The 5-Minute Sports Medicine Consult 2nd Edition 2011

2011
Lippincott Williams & Wilkins

Philadelphia
Two Commerce Square, 2001 Market Street, Philadelphia, Pa. 19103 USA
978-1-60547-668-1
Copyright 2011 by LIPPINCOTT WILLIAMS & WILKINS a WOLTERS KLUWER business

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Library of Congress Cataloging-in-Publication Data
The 5-minute sports medicine consult / editors, Mark D. Bracker … [et al.]. 2nd ed.
p. ; cm.
Five minute sports medicine consult
Includes bibliographical references and index.
ISBN 978-1-60547-668-1
1. Sports medicine—Handbooks, manuals, etc. I. Bracker, Mark D.
II. Title: Five minute sports medicine consult.
[DNLM: 1. Sports Medicine–Handbooks. 2. Athletic Injuries–Handbooks. QT 29]
RC1211.A145 2011
617.1′027–dc22
2010039966
Care has been taken to confirm the accuracy of the information presented and to describe
generally accepted practices. However, the authors, editors, and publisher are not responsible
for errors or omissions or for any consequences from application of the information in this book
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10 9 8 7 6 5 4 3 2 1
Editor
Mark D. Bracker MD
Professor
Department of Family and Preventative Medicine University of California, San Diego San
Diego, California
Co-Editors
Suraj A. Achar MD, FAAFP
Associate Professor
Department of Family and Preventive Medicine University of California School, San Diego
San Diego, California
Andrea L. Pana MD, MPH

Team Physician
University of Texas Athletics Austin, Texas
Kenneth S. Taylor MD
Associate Professor
Department of Family and Preventive Medicine Director Sports Medicine University of
California, San Diego San Diego, California
Section Editors
Holly J. Benjamin MD, FAAP, FACSM
Associate Professor of Pediatrics and Surgery
Section of Academic Pediatrics, Section of Orthopedic Surgery and Rehabilitation Medicine,
Director of Primary Care Sports Medicine, The University of Chicago, Chicago, Illinois
David T. Bernhardt MD
Professor
Department of Pediatrics/Orthopaedics & Rehabilitation, University of Wisconsin, Madison,
Wisconsin
Delmas J. Bolin MD, PhD

Associate Professor
Sports and Family Medicine, Virginia College of Osteopathic, Medicine, Blacksburg, Virginia,
Head Team Physician, Radford University, Radford, Virginia
Jeffrey R. Bytomski DO, FAOASM

Associate Professor
Department of Community and Family Medicine, Head Medical Team Physician, Director,
Primary Care Sports Medicine, Fellowship, Duke University Medical Center, Durham, North
Carolina
James M. Daniels II MD, MPH, FAAFP, FACPM, FACOEM

Director
Sports Medicine Fellowship, Professor of Family and Community Medicine, Adjunct Professor
of Orthopedic Surgery, Southern Illinois University School of Medicine, Springfield, Illinois
Mark I. Ellen MD, FABPMR, CAQ-SM

Clinical Associate Professor
Sept of Physical Medicine and Rehabilitation, UAB School of Medicine, Birmingham VAMC,
Birmingham, Alabama
Kim Fagan MD, FACP

Private Practice, Fagan Sports Medicine, Birmingham, Alabama
Matthew Gammons MD
Assistant Clinical Professor
Department of Family and Community Medicine, Medical College of Wisconsin, Milwaukee,
Wisconsin, Vermont Orthopaedic Clinic, Rutland, Vermont
George D. Harris MD, MS

Professor
Assistant Dean Year 1 and 2 Medicine, University of Missouri Kansas City—School of
Medicine, Kansas City, Missouri
Marc I. Harwood MD
Assistant Professor
Department of Family & Community, Medicine, Rothman Institute, Thomas Jefferson
University, Philadelphia, Pennsylvania
Suzanne Hecht MD
Assistant Professor
University of Minnesota, Department of Family Medicine & Community Health, Division of
Sports Medicine, Team Physician; UM Athletic Department, Minneapolis, Minnesota
Shawn F. Kane MD, LTC, MC, US Army

US Army Special Operations Command (Airborne) Staff Family Physician
Womack Army Medical Center, Ft. Bragg, North Carolina, Assistant Professor, Department of
Military and Emergency Medicine Uniformed Services, University of the Health Sciences,
Bethesda, Maryland
Chris Koutures MD, FAAP

Pediatrics and Sports Medicine, Anaheim Hills, California, Medical Team Physician, Cal
State, Fullerton and USA National Volleyball Teams
Kim Edward LeBlanc MD, PhD, FAAFP, FACSM

Marie Lahasky Professor and Chairman
Department of Family Medicine, Director of Rural Education, LSUHSC School of Medicine,
New Orleans, Louisiana
Jim Moeller MD
Sports Medicine Associates, Auburn Hills, Michigan
Trish Palmer MD
Associate Director, Sports Medicine Fellowship, Assistant Professor
Departments of Orthopaedic Surgery and Family Medicine, Rush University Medical Center,
Chicago, Illinois
Deepak S. Patel MD, FAAFP

Director of Sports Medicine
Rush-Copley Family Medicine Residency, Aurora, Illinois, Assistant Professor, Rush Medical
College, Chicago, Illinois, Family Medicine and Sports Medicine, Yorkville Primary Care,
Yorkville, Illinois
George G.A. Pujalte MD, CAQSM

Assistant Professor
Primary Care Sports Medicine, Department of Family and Community, Medicine, The
Pennsylvania State University, Hershey, Pennsylvania
Margot Putukian MD, FACSM

Director of Athletic Medicine
Princeton University, McCosh Health Center, Princeton, New Jersey, Associate Clinical
Professor, RWJ-UMDNJ
Sam Rifat MD, FACSM

Sports Medicine Associates, Auburn Hills, Michigan
Brent S. E. Rich MD, ATC

Utah Valley Sports Medicine, Fellowship Director, Team Physician, Bringham Young
University, Provo, Utah
Stephen Simons MD
Co-Director South Bend Sports Medicine, Fellowship, Saint Joseph Regional Medical Center,
South Bend, Indiana
Kevin N. Waninger MD, MS
Department of Family and Community, Medicine, Temple University School of Medicine,
Director, Sports Medicine Fellowship, St. Luke's Hospital and Health Network, Bethlehem,
Pennsylvania
David Webner MD
Co-Director
Sports Medicine Fellowship, Crozer-Keystone Health System, Suburban, Philadelphia
Contributors
Adam Abdulally MD, UPMC
St. Margaret, Family Medicine Residency, Pittsburgh, Pennsylvania
Suraj A. Achar MD, FAAFP

Associate Professor
Department of Family and Preventive Medicine, University of California, San Diego, San
Diego, California
Ayo Adu MD
University of Oklahoma College of Medicine, Department of Family Medicine & Sports
Medicine, Tulsa, Oklahoma
Arturo J. Aguilar MD
Sports Medicine, Family Medicine, Boston University Medical Center, Boston, Massachusetts
Safdar Akbar MD
Medical Emergency Professionals, Hagerstown, Maryland
Keith A. Anderson MD
Sports Medicine Fellow
Department of Family Medicine, Carolinas Medical Center, Charlotte, North Carolina
Chad A. Asplund MD, FACSM

Assistant Professor
Family Medicine, Division of Sports Medicine, Team Physician, The Ohio State University,
Columbus, Ohio
Elizabeth Austin MD
Epidemiology Unit, Medical Center, University of California at San Diego, San Diego,
California
Robert J. Baker MD, PhD, ATC

Program Director Primary Care Sports Medicine Fellowship
MSU/Kalamazoo Center for Medical Studies, Associate Professor Michigan State University,
Team Physician Western Michigan University
James Bales MD
Orthopaedic Surgeon
U.S. Air Force, Wilford Hall Medical Center, Lackland AFB, Texas
Karrn Bales DO, CAQSM, Board Certified ABFM

Sports Medicine Associates of San Antonio, San Antonio, Texas
Kenneth Barnes MD, MSc, CAQSM

Director
Sports Medicine, Head Athletic Team Physician, Internal Medicine, Pediatrics & Sports
Medicine, Elon University, Elon Adjunct Faculty, Moses Cone Sports Medicine Fellowship,
Clinical Assistant Professor, UNC Chapel Hill School of Medicine
Evan Bass MD
Associate Program Director
Harbor-UCLA/Team to Win Sports Medicine Fellowship, Harbor City, California, Kaiser
Permanente Family Medicine/Sports Medicine, Harbor City, California
David E. J. Bazzo MD, FAAFP

Clinical Professor of Family Medicine
University of California, San Diego, School of Medicine, Department of Family and Preventive
Medicine, San Diego, California
Tricia Beatty DO
Crozer Keystone Sports Medicine Fellowship, Healthplex Sports Medicine Institute, Crozer
Keystone Health System, Springfield, Pennsylvania
Clint Beaver MD
Carolinas Medical Center, Charlotte, North Carolina
Brent R. Becker DO
Sports Medicine Physician
Senior Medical Officer, SMART Clinic, Marine Corps Recruiting Depot, San Diego, California,
Naval Medical Center, San Diego, California
Jonathan A. Becker MD
Director
Primary Care Sports Medicine Fellowship, University of Louisville and Jewish Hospital Sports
Medicine, Louisville, Kentucky
Holly J. Benjamin MD, FAAP, FACSM

Associate Professor of Pediatrics and Surgery
Section of Academic Pediatrics, Section of Orthopedic Surgery and Rehabilitation Medicine,
Director of Primary Care Sports Medicine, The University of Chicago, Chicago, Illinois
David T. Bernhardt MD
Professor
Department of Pediatrics/Orthopaedics & Rehabilitation, University of Wisconsin, Madison,
Wisconsin
Kenneth M. Bielak MD
Associate Professor
Department of Family Medicine, University of Tennessee, Knoxville, Tennessee
Krystian Bigosinski MD
Division of Sports Medicine, Primary Care Sports Medicine, RUSH University Medical Center,
Chicago, Illinois
W. Scott Black MD, MS

Associate Professor
Department of Family & Community Medicine, University of Kentucky, Lexington, Kentucky
Brandon A. Bockewitz MD
Department of Family and Community Medicine, Wake Forest University School of Medicine
Warren Bodine DO
Department of Family and Community Medicine, Christiana Care Health System, Wilmington,
Delaware
Blake Boggess DO
Assistant Professor
Department of Orthopedics and Family Medicine, Duke University Medical Center, Durham,
North Carolina
Delmas J. Bolin MD, PhD

Associate Professor
Sports and Family Medicine, Virginia College of Osteopathic Medicine, Blacksburg, Virginia,
Head Team Physician, Radford University, Radford, Virginia
James R. Borchers MD, MPH

Director, Primary Care Sports Medicine Fellowship, Department of Family Medicine, The
Ohio State University
Anne S. Boyd MD
Director
UPMC Primary Care Sports Medicine Fellowship Program, St. Margaret, Assistant Professor,
Department of Family Medicine, University of Pittsburgh School of Medicine, Pittsburgh,
Pennsylvania
Matthew P. Boyd MD
Metro Health Family Medicine/Sports Medicine Physician
Robert Bramante MD
Emergency Medicine Resident, North Shore University Hospital, Manhasset, New York
James E. Bray MD
Associate Professor of Family Medicine
Texas A&M Medical School, Consulting Physician for University of Texas at Austin and
Southwestern University Athletics, Scott and White Georgetown Central Clinic, Associate
Director, Georgetown, Texas
William W. Briner Jr. MD, FACSM, FAAFP CAQ

Sports Medicine Director
Sports Medicine Fellowship, Lutheran General Hospital, Park Ridge, Illinois
Stacey L. Brown Brocklehurst MD

UPMC St. Margaret Family Medicine Residency, Pittsburgh, Pennsylvania
Steve Burdine MD
Palmetto Health Sports Medicine Fellowship, Department of Family and Preventive Medicine,
University of South Carolina School of Medicine
Michelle Burke MD
Fellow, Pediatric Primary Care Sports Medicine, Akron Children's Hospital, Sports Medicine
Center, Akron, Ohio
Seth M. Burkey MD
Emergency Medicine, Sports Medicine Fellow, St. Luke's Primary Care Sports Medicine
Fellowship, St. Luke's Hospital, Bethlehem, Pennsylvania
Kevin E. Burroughs MD
Sports Medicine & Injury Center, Concord, North Carolina
Jeffrey R. Bytomski DO, FAOASM

Associate Professor
Department of Community and Family Medicine, Head Medical Team Physician, Director,
Primary Care Sports Medicine Fellowship, Duke University Medical Center, Durham, North
Carolina
Greg Canty MD
Fellow, Sports Medicine, University of Colorado, Denver, Colorado
Matthew D. Capuano MD
Resident Physician
Highland Family Medicine, University of Rochester
David Carfagno DO, CAQSM

Owner/Director Scottsdale Sports
Medicine Institute, Scottsdale, Arizona
Rebecca L. Carl MD
Assistant Professor of Pediatrics
Institute for Sports Medicine, Children's Memorial Hospital, Northwestern University, Chicago,
Illinois
Nick Carter MD
Fellow, Specialist in Rheumatology, Allan McGavin Sports Medicine Centre, University of
British Columbia, Vancouver, British Columbia, Canada
Kyle J. Cassas MD, GHS

Assistant Professor of Clinical Sports Medicine
Department of Orthopaedic Surgery and Family Medicine, Steadman Hawkins Clinic of the
Carolinas, Greenville Hospital System, University Medical Center, Greenville, South Carolina
Joseph N. Chorley MD
Associate Professor of Pediatrics
Section of Adolescent Medicine and Sports Medicine, Baylor College of Medicine, Houston,
Texas
Yvonne Chow MD
Primary Care Sports Medicine Fellow, Department of Family Medicine, University of
Pennsylvania Health System, Philadelphia, Pennsylvania
Julie J. Chuan MD, FAAFP

Clinical Instructor
Department of Family Medicine, University of California, San Diego
Christopher Cieurzo MD
Fellow, St Luke's Primary Care Sports Medicine Fellowship, St Luke's Hospital, Bethlehem,
Pennsylvania
Kristen Samuhel Clarey MD

Moses Cone Health System, Greensboro, North Carolina
Justin A. Classie MD
Clinical Instructor
Department of Family Medicine, The Ohio State University Sports Medicine Center,
Columbus, Ohio
Rachel A. Coel MD, PhD

Pediatric Primary Care Sports Medicine, Sports Medicine for Young Athletes, The Children's
Hospital, Department of Orthopedics, Aurora, Colorado
Philip H. Cohen MD
Clinical Assistant Professor of Internal Medicine and Family Medicine
UMDNJ-Robert Wood Johnson Medical School, Assistant Team Physician, Rutgers University,
Sports Medicine, Piscataway, New Jersey
Douglas Comeau DO
Primary Care Sports Medicine, Boston Medical Center, Assistant Professor, Family Medicine,
Boston University School of Medicine, Team Physician, Boston University
Kara D. Cox MD, FAAFP

University of Kansas SOM-Wichita, Department of Family and Community Medicine, Sports
Medicine Fellowship at Via Christi, Family Medicine Residency at Via Christi, Via Christi
Sports Medicine, Wichita, Kansas
Steven C. Cuff MD, FAAP

Assistant Clinical Professor of Pediatrics
Division of Sports Medicine, Nationwide Children's Hospital, The Ohio State University
College of Medicine, Columbus, Ohio
Sean A. Cupp MD
Primary Care Sports Medicine, OrthoKansas, P.A., Lawrence, Kansas, Team Physician,
University of Kansas Athletics
Rafael daFonseca MD
Clinical Attending, Family Medicine, Mount Sinai Hospital and Clinics, Chicago, Illinois
Claudia Dal Molin DO

Internam Medicine Resident, Christiana Care Health System, Newark, Delaware
Jeffrey W. R. Dassel MD
Associate Director
Sports Medicine Fellowship, Department of Family and Community Medicine, Christiana Care
Health System, Wilmington Delaware
Marjorie Delo MD, CAQSM

Mercy Sports Medicine and Sports Medicine Fellowship, Lake Geneva, Wisconsin
Rania L. Dempsey MD, MS

Wisconsin
Matt DesJardins MD
Non-surgical Sports Medicine and Orthopaedics, Commonwealth Orthopaedic Centers,
Edgewood, Kentucky
Rajwinder Deu MD
Instructor
Department of Family and Community Medicine, Thomas Jefferson University, Philadelphia,
Pennsylvania
Kevin deWeber MD, FAAFP, LTC(P), Medical Corps, Army, USUHS

Sports Medicine Fellowship Director, Family Physician
William W. Dexter MD
Director
Maine Medical Center Sports Medicine Fellowship Program, Department of Family Practice,
Portland, Maine
Alex B. Diamond DO
Assistant Professor of Orthopaedics and Rehabilitation
Assistant Professor of Pediatrics, Vanderbilt Sports Medicine, Vanderbilt, University Medical
Center, Nashville, Tennessee
Masha Diede MD
Douglas J. DiOrio MD
Max Sports Medicine, Fellowship Director Riverside Sports Medicine
Laura Distel MD
Clinical Instructor
Department of Family Medicine, The Ohio State University Sports Medicine Center,
Columbus, Ohio
Martha A. Dodson DO
Sports Medicine, El Paso, Texas
Jonathan Drezner MD
Associate Professor
Department of Family Medicine, Associate Director, Sports Medicine Fellowship, Team
Physician, Seattle Seahawks & University of Washington Huskies, University of Washington,
Seattle, Washington
Anna Dumont DO
Family Medicine, Sports Medicine, Ohio Health
Kevin E. Elder MD, FAAFP

Partner Physician
HealthPoint Medical Group Affiliate, Assistant Professor, University of South Florida Team
Physician, Tampa Bay Buccaneers, Tampa, Florida
Kevin Eerkes MD
Clinical Assistant Professor
Department of Medicine, New York University School of Medicine, New York, New York
Benjamin D. England MD
Department of Family Medicine, University of Tennessee, Knoxville, Tennessee
Robyn Fean MD
Primary Care Sports Medicine Fellow, University of Washington, Seattle, Washington
Jeffrey Feden MD
Assistant Professor of Emergency Medicine
Department of Emergency Medicine, Alpert Medical School of Brown University, Providence,
Rhode Island
William Felix-Rodriguez MD
Department of Surgery, Division of Emergency Medicine, Duke University Medical Center,
Durham, North Carolina
Karl B. Fields MD
Professor of Family Medicine and Sports Medicine
University of North Carolina, Director Sports Medicine Fellowship, Moses Cone Health
System, Greensboro, North Carolina
Anastasia N. Fischer MD
Division of Sports Medicine, Nationwide Children's Hospital, Westerville, Ohio
Ryan C. Fowler MD, LCDR, MC, USN

Primary Care Sports Medicine/Senior Medical Officer, Bradley Branch Medical Clinic at
USMC Officer Candidate School, Naval Health Clinic, Quantico, Virginia
David Z. Frankel MD
Clinical Assistant Professor of Family Medicine
Hall Health Primary Care Center, University of Washington, Seattle, Washington
R. Michael Galbraith DO
South Bend Sports Medicine Fellowship Program, South Bend, Indiana
Anne M. Garrison DO
Team Physician
Arizona State University, Tempe, Arizona
Coley Gatlin MD
Moses Cone Hospital, Family Practice Residency, Greensboro AHEC, Greensboro, North
Carolina
Kevin B. Gebke MD
Co-Chair
Department of Family Medicine, Director, Primary Care Sports Medicine Fellowship, Director,
IU Center for Sports Medicine, Associate Professor of Clinical Family Medicine, Indiana
University School of Medicine, Indianapolis, Indiana
Christopher A. Gee MD
Assistant Professor (Clinical)
Division of Emergency Medicine, University of Utah Health Sciences Center, Salt Lake City,
Utah
Nicole Y. Gesik DO
Family Medicine Resident, Oregon Health and Science University, Portland, Oregon
Andrew Getzin MD
Clinical Director
Cayuga Medical Center Sports Medicine and Athletic Performance, Ithaca, New York
Gordon Givan MD
Resident
St. Joseph Regional Medical Center, South Bend, Indiana
Jason Glowney MD
Primary Care Sports Medicine Fellow, University of Colorado School of Medicine, Denver,
Colorado
Orlando V. Gonzalez MD
Mountainside Hospital Program, Montclair, New Jersey, University of Medicine and Dentistry-
New Jersey
Rodney S. Gonzalez MD, FAAFP

Doctor of Medicine
Family Medicine Teaching Staff, Martin Army Community Hospital, Ft. Benning, Georgia,
Assistant Professor of Family Medicine, Uniformed Services University of Health Sciences
(USUHS), Bethesda, Maryland
Alysia L. Green MD
Assistant Professor of Family Medicine
Primary Care Sports Medicine, Department of Family Medicine, Boston University, Boston
Medical Center, Boston, Massachusetts
Steven A. Greer MD, CAQ Sports Medicine

Assistant Professor
Departments of Family Medicine and Orthopaedics, Medical College of Georgia, Augusta,
Georgia
Andrew Gregory MD
Assistant Professor
Orthopedics & Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee
Sunny Gupta DO
Crozer-Keystone Center for Family Health, Springfield, Pennsylvania
Tarek Hadla MD
Sports Medicine Fellow 2009–2010, MacNeal Hospital-Berwyn, IL, University of Chicago
Tanya J. Hagen MD
Assistant Professor
University of Pittsburgh School of Medicine, Orthopedics. UPMC Sports Medicine, Director,
Sports Medicine Fellowship, UPMC Shadyside
Mark Halstead MD
Assistant Professor
Orthopedic Surgery, Department of Orthopedic Surgery, Washington University School of
Medicine, St. Louis, Missouri
Michael Hanna MD
Resident
Internal Medicine, Rush University Medical Center, Chicago, Illinois
Andrew Harcourt MD
Adjunct Assistant Professor of Family Medicine
Department of Family Medicine, University of South Alabama, Mobile, Alabama
John Hariadi MD
Assistant Chief Medical Officer
United States Coast Guard Personnel Service Center, Arlington, Virginia
Kimberly Harmon MD
Departments of Family Medicine and Orthopedics, University of Washington, Seattle,
Washington
COL Mark D. Harris MD, MPH, Medical Corps, Army, USUHS

Family Physician
Natasha Harrison MD, MPP, PGY-2
University of Pennsylvania Family Medicine Residency
Marc I. Harwood MD
Assistant Professor
Department of Family & Community Medicine, Rothman Institute, Thomas Jefferson
University, Philadelphia, Pennsylvania
Benjamin A. Hasan MD
Assistant Clinical Professor of Family Medicine University of Chicago NorthShore
University Health System Glenbrook Hospital, Glenview, Illinois
Suzanne Hecht MD
Assistant Professor
University of Minnesota, Department of Family Medicine & Community Health, Division of
Sports Medicine, Team Physician; UM Athletic Department, Minneapolis, Minnesota
Quynh Hoang MD
Pediatric Sports Medicine Fellow, University of Colorado, Denver
Eugene Hong MD
Hamot and Sturgis Endowed Chair, Chief Division of Sports Medicine, Department of Family,
Community and Preventive Medicine, Drexel University College of Medicine, Philadelphia,
Pennsylvania
Michal “Kalli” Hose MD

Clinical Professor
University of California, Staff Physician, VA San Diego Health Care System, San Diego,
California
Robert G. Hosey MD
Associate Professor
Family and Community Medicine/Orthopaedics, Director Primary Care Sports Medicine
Fellowship, University of Kentucky, Chandler Medical Center, Lexington, Kentucky
Stephen Huang MD
Warren Clinic Orthopaedic Surgery and Sports Medicine, Tulsa, Oklahoma
Shane Hudnall MD
Moses Cone Sports Medicine Fellowship Program, Greensboro, North Carolina
Tudor Hesketh Hughes MD, FRCR

Professor of Clinical Radiology
Radiology Resident Program Director, Department of Radiology, UCSD Medical Center, San
Diego, California
Andrew Hunt MD
Illinois Bone & Joint Institute, Sports Medicine Division, Medical Director, USA Triathlon
Nadim Ilbawi MD
Family Medicine Resident, Department of Family Medicine, University of Wisconsin Family
Medicine Residency Program, Madison, Wisconsin
Arthur Islas MD, MPH, FAWM, CAQSM

Associate Professor
Department of Family & Community Medicine, Paul L. Foster School of Medicine, Texas Tech
Health Science Center, El Paso, Texas
Carrie A. Jaworski MD, FACSM, FAAFP

Director of Intercollegiate Sports Medicine, Head Team Physician, Assistant Professor of
Family & Community Medicine, Northwestern University, Evanston, Illinois
Sandeep Johar DO, MS

Department of Emergency Medicine, University of Florida
Matthew John MD
Fellow in Sports Medicine, Sports Medicine Fellowship Program, University of Missouri-
Kansas City School of Medicine, Kansas City, Missouri
Christopher Johnson MD
Memorial Family Medicine Residency, South Bend, Indiana
Rob Johnson MD
Professor
Department of Family Medicine and Community Health, University of Minnesota, Minneapolis,
Minnesota
Scott Fister Johnson MD

Bethesda Sports Medicine Fellowship Program, Cincinnati, Ohio
Robert L. Jones MD
Director
Primary Care Sports Medicine Fellowship, Department of Family Medicine, Carolinas Medical
Center, Team Physician, UNC Charlotte, Charlotte, North Carolina
Vijay Jotwani MD
Indiana University Primary Care Sports Medicine Fellowship, Department of Family Medicine,
Indiana University School of Medicine, Indianapolis, Indiana
Amy Kakimoto MD
North Coast Family Medical Group, Encinitas, California
Rahul Kapur MD, CAQSM

Assistant Professor
Family Medicine and Sports Medicine, University of Pennsylvania, Department of Family
Medicine and Community Health
Pankaj Kaw MD
Consultant, Sports Medicine, Crystal Run Health Care, Middletown, New York
Roberta Kern MD
Bethesda Family Practice, Cincinnati, Ohio
Thomas Kern MD
Eastern Oklahoma Orthopedic Center, Tulsa, Oklahoma
Julie M. Kerr MD
Clinical Assistant Professor of Pediatrics
NEOUCOM, Program Director, Pediatric Primary Care Sports Medicine Fellowship, Akron
Children's Hospital, Sports Medicine Center, Akron, Ohio
Razib Khaund MD
Clinical Assistant Professor of Medicine
Department of Internal Medicine, Warren Alpert School of Medicine, Brown University,
Providence, Rhode Island
Jacklyn Kiefer DO
Primary Care Sports Medicine Fellow, The Toledo Hospital Primary Care Sports Medicine
Fellowship, Toledo, Ohio
Jane Kim DO
Sports Medicine, Sharp-Rees Stealy Medical Group
Jeff Kindred DO
South Bend Sports Medicine Fellowship, Saint Joseph Regional Medical Center, South Bend,
Indiana
Kari Kindschi MD
Duke University, Primary Care Sports Medicine Fellow, Department of Community and Family
Medicine
Robert B. Kiningham MD, FACSM

Director
Sports Medicine Fellowship, Associate Professor, Department of Family Medicine, University
of Michigan Health System, Ann Arbor, Michigan
K. Michele Kirk MD, CAQ Sports Medicine

Assistant Director of Sports Medicine Fellowship
Department of Family Medicine, John Peter Smith Hospital Network, Fort Worth, Texas
Jennifer Scott Koontz MD, MPH

Pinnacle Sports Medicine and Orthopaedics, Clinical Instructor, Department of Family and
Community Medicine, University of Kansas School of Medicine-Wichita, Newton, Kansas
Chris Koutures MD, FAAP

Pediatrics and Sports Medicine, Anaheim Hills, California, Medical Team Physician, Cal State
Fullerton and USA National Volleyball Teams
Michael A. Krafczyk MD
St. Luke's Primary Care Sports Medicine Fellowship, St. Luke's Hospital, Bethlehem,
Pennsylvania
Jeffrey B. Kreher MD, FAAP

Primary Care Sports Medicine, Pediatrics & Internal Medicine, Emerson Hospital, Concord
Massachusetts
Steve Kroll MD
Georgia Sports Medicine, Atlanta, Georgia
Sebastian Ksionski MD
John Peter Smith Sports Fellow
Geoffrey Kuhlman MD, CAQSM, FAAFP

Hinsdale Family Medicine Residency, Hinsdale, Illinois
Michele LaBotz MD FAAP
InterMed Sports Medicine, Portland, Maine
Michael Ladewski DO
Adjunct Faculty, Department of Family Medicine, University of Chicago, Chicago, Illinois
Mike LaGrange MD
IMA Sports Medicine/Indiana University Sports Medicine, Bloomington, Indiana
Shanyn Lancaster MD
Department of Orthopedics, Aurora Advanced Healthcare, Milwaukee, Wisconsin
Mark E. Lavallee MD, CSCS, FACSM

Director
Sports Medicine, Memorial Hospital of South Bend, Co-Director, South Bend Sports Medicine
Fellowship Program, Assistant Clinical Professor, Indiana University School of Medicine, Co-
Chairman, USA Weightlifting, Sports Medicine Committee, Head Team Physician, Indiana
University South Bend, Head Team Physician, Holy Cross College, Volunteer Team Physician,
University of Notre Dame
Adrian Lavina MD
Retina Care Specialists, LLP, Palm Beach Gardens, Florida
Aaron Lee DO
Lutheran General Hospital, Park Ridge, Illinois
Jason Lee DO
Resident
Department of Physical Medicine and Rehabilitation, Rush University Medical Center,
Chicago, Illinois
Lt Col (P) Jeffrey C. Leggit MD, CAQSM

Commander
Barquist Army Health Community Center, Fort Detrick, Maryland
Jason M. Leinen MD
Department of Family Medicine, University of Oklahoma-Tulsa, Tulsa, Oklahoma
Aaron P. Leininger MD
Moses Cone Health System, Greensboro, North Carolina
Amy Leu DO
UCSD Primary Care Sports Medicine Fellow, Department of Family and Preventative
Medicine, UCSD
Daniel Lewis MD
Adjunct Clinical Faculty
ETSU Quillen College of Medicine, Johnson City, Tennessee
Brian Lindenmayer MD
John Peter Smith Sports Fellow, Fort Worth, Texas
Michael M. Linder MD
Associate Professor of Family Medicine
Department of Family Medicine, University of South Alabama, Mobile, Alabama
Kelsey Logan MD, FAAP

Assistant Professor of Internal Medicine
Medical Director, Sports Concussion Program, The Ohio State University Sports Medicine
Center, Columbus, Ohio
Emily Lott MD
University of Missouri-Kansas City, School of Medicine, Kansas City, Missouri
James H. Lynch MD, MS

Fellow, Military Primary Care Sports Medicine Fellowship, Uniformed Services University of
the Health Sciences, Bethesda, Maryland
Brian Macy MD
Fellow, Family and Community Medicine, University of Kentucky, Lexington, Kentucky
Christopher C. Madden MD
Private Practice, Sports Medicine at Longs Peak Family Practice, Longmont, Colorado,
Assistant Clinical Professor, Department of Family Medicine, University of Colorado, Health
Sciences Center, Denver, Colorado
Danielle L. Mahaffey MD
Cornerstone Healthcare, High Point Family Practice, High Point, North Carolina
Navid Mahooti MD, MPH

University of Connecticut
Aaron V. Mares MD
Internal Medicine Resident, Department of Internal Medicine, University of Pittsburgh Medical
Center, Medical Education Program, Pittsburgh, Pennsylvania
Peter D. Marshall MD
Private Practice, Sports Medicine at Longs Peak Family Practice, Longmont, Colorado
Catharine Mayer MD
Department of Family, Community, and Preventive Medicine, Drexel University College of
Medicine, Philadelphia, Pennsylvania
Kevin J. McAward MD
Associate Director
South Bend Sports Medicine Fellowship, Associate Director, Memorial Family Medicine
Residency Program, South Bend, Indiana
Derek McCoy MD
Private Practice
Jeffrey McDaniel MD
Palmetto Health Sports Medicine Fellowship, Department of Family and Preventive Medicine,
University of South Carolina School of Medicine
Emily C. McDevitt DO
Resident
Family Medicine, Memorial Hospital, South Bend Indiana
Christopher McGrew MD
Professor
Department of Family and Community Medicine, Department of Orthopedics and
Rehabilitation, University of New Mexico Health Sciences Center, Albuquerque, New Mexico
Paul B. McKee IV MD
Fellow, Sports Medicine, University of Louisville, Lousiville, Kentucky
Sean McKeown MS, PT, Cred MDT

Center Director, PRN Physical Therapy, San Diego and La Jolla Facilities
Dominic McKinley MD
Guilford Orthopaedics and Sports Medicine Center, Greensboro, North Carolina
Holly McNulty MD
Assistant Fellowship Director
University of Arizona, Primary Care Sports Medicine Fellowship, Clinical Assistant Professor',
Department of Family and Community Medicine, Coordinator Primary Care Arizona Institute
for Sports Medicine, Staff Physician Primary Care Sports Medicine, Arizona Institute for
Sports Medicine
Robert D. Menzies MD
Assistant Director
John Peter Smith Pain Medicine Fellowship, Fort Worth, Texas
Tara Merritt MD
Primary Care Sports Medicine Fellow, Steadman Hawkins Clinic of the Carolinas, Greenville
Hospital System University Medical Center, Greenville, South Carolina
Brent H. Messick MD, MS

Cabarrus Family Medicine, Adjunct Instructor, Department of Family Medicine, UNC-Chapel
Hill School of Medicine
Christopher D. Meyering DO
Assistant Director
Primary Care Sports Medicine Fellowship, Medical College of Georgia, Augusta, Georgia,
Director Sports Medicine, Family Medicine Residency Program, DD Eisenhower Army
Medical Center, Ft. Gordon, Georgia
Mark H. Mirabelli MD
Assistant Professor
Primary Care Sports Medicine, Departments of Family Medicine and Orthopaedics, University
of Rochester
Jennifer J. Mitchell MD, FAAFP

Associate Professor
Sports Medicine Fellowship Director, Department of Family and Community Medicine, Texas
Tech University Health Sciences Center, Lubbock, Texas
Kelly T. Mitchell MD
Associate Professor
Ophthalmology Residency Program Director, Co-director Retina Service, Department of
Ophthalmology and Visual Sciences, Texas Tech University Health Sciences Center, Lubbock,
Texas
Jeffrey M. Mjaanes MD
Assistant Professor
Departments of Pediatrics and Orthopedic Surgery, Rush University Medical Center, Chicago,
Illinois
Jason Mogonye MD
Department of Family Medicine, John Peter Smith Health Network, Fort Worth, Texas
Anna G. Monroe MD
Department of Family and Community Medicine, Wake Forest Baptist Medical Center,
Winston Salem, North Carolina
Kinshasa Morton MD, CAQSM

Department of Family Medicine, University of Medicine and Dentistry of New Jersey-RWJ,
New Brunswick, New Jersey
Carter W. Muench MD
Primary Care Sports Medicine, Hennepin County Medical Center, Minneapolis, Minnesota
John Munyak MD
Director
Sports Medicine Fellowship Program, North Shore University Hospital, Manhasset, New York
Greg Nakamoto MD
Physician, Department of Orthopedics and Sports Medicine, Virginia Mason Medical Center,
Seattle, Washington, Clinical Instructor, Department of Medicine, University of Washington,
Seattle, Washington
Vikram Narula MD
LMT Rehabilitation Associates, P.C.
Rodolfo R. Navarro MD
Primary Care Sports Medicine Fellow, Department of Family and Community Medicine,
University of New Mexico Health Sciences Center, Albuquerque, New Mexico
Melissa Nayak MD
Department of Orthopaedics, Division of Sports Medicine, Assistant Program Director,
Primary Care Sports Medicine Fellowship, Henry Ford Health Systems, Detroit, Michigan
Mark W. Niedfeldt MD
Associate Clinical Professor
Wisconsin
Rochelle M. Nolte MD, CDR, USPHS

Senior Medical Officer, US Coast Guard, San Diego, CA
David Olson MD, CAQ Sports Medicine

Assistant Professor
Department of Family Medicine and Community Health, University of Minnesota
Richard A. Okragly MD
Director of Sports Medicine, Bethesda Sports Medicine Fellowship Program, Cincinnati, Ohio
Ross Osborn MD
Center for Health and Sports Medicine, Jacksonville, Florida
Lisa Palazollo DPT, ATC, ART certified, Physical Therapist

Athletic Trainer, Assistant Facility Manager, Athletico, Evanston, Illinois
Kyle D. Parish MD, CAQ Sports Medicine

Family and Sports Medicine, Private Practice, Paducah, Kentucky
Susan Park MD
Family and Sports Medicine Fellow, University of California, San Diego, San Diego, California
Eric D. Parks MD
Primary Care Sports Medicine, Watauga Orthopaedics, Kingsport, Tennessee
Stephen Paul MD
Fellowship Director, University of Arizona Primary Care Sports Medicine Fellowship, Clinical
Assistant Professor, Department of Family and Community Medicine, Clinical Assistant
Professor, Department of Orthopedics, Staff Physician Campus Health, Staff Physician
Primary Care Sports Medicine, Arizona Institute for Sports Medicine, Coordinator Department
of Sports Medicine, Campus Health, Assistant Team Physician, University of Arizona
Intercollegiate Athletics
Matthew Pecci MD
Director of Primary Care Sports Medicine Boston Medical Center, Director of Sports Medicine
Boston University, Boston, Massachusetts
Bernadette Pendergraph MD
Program Director, Harbor-UCLA/Team to Win Sports Medicine Fellowship, Harbor City,
California, Associate Professor, Department of Family Medicine, David Geffen School of
Medicine
K. Brooke Pengel MD
Director
Sports Medicine for Young Athletes, Assistant Professor, Department of Orthopaedic Surgery,
University of Colorado School of Medicine
Jayson Pereira MD, CAQSM

Physician, Department of Emergency Medicine, North Memorial Medical Center,
Robbinsdale, Minnesota
Ryan C. Petering MD
Clinical Instructor of Family Medicine, Department of Family Medicine, Oregon Health and
Sciences University, Portland, Oregon
Andrew R. Peterson MD
Assistant Professor
Departments of Pediatrics and Orthopedics/Rehabilitation, University of Wisconsin, Madison,
Wisconsin
Deena C. Petrocelli MD
Department of Family Medicine, University of Connecticut Health Center, Saint Francis
Hospital and Medical Center
Thomas A. Phipps MD
Primary Care Sports Medicine, Ani Orthopedics, Hazlet, New Jersey
Sourav K. Poddar MD
Director
Primary Care Sports Medicine, University of Colorado School of Medicine, CU Sports
Medicine Center, Denver, Colorado
Thomas L. Pommering DO, FAAFP

Assistant Clinical Professor of Pediatrics and Family Medicine
Division Chief for Sports Medicine, Nationwide Children's Hospital, The Ohio State University
College of Medicine, Columbus, Ohio
Emily Porter MD
Primary Care Sports Medicine Fellow, Department of Community and Family Medicine,
Medical College of Wisconsin, Milwaukee, Wisconsin
Mitchell Pratte DO, CAQSM

Head Team Physician, Brigham Young University, Provo, Utah
David E. Price MD
Associate Director
Primary Care Sports Medicine Fellowship, Carolinas Medical Center, Charlotte, North
Carolina
Aaron J. Provance MD
Assistant Professor of Pediatric Sports Medicine
Department of Orthopaedics, The Children's Hospital, Aurora, Colorado
James C. Puffer MD
President and Chief Executive Officer, American Board of Family Medicine, Professor,
Department of Family and Community Medicine, College of Medicine, University of Kentucky,
Lexington, Kentucky
George G.A. Pujalte MD, CAQSM

Assistant Professor
Primary Care Sports Medicine, Department of Family and Community Medicine, The
Pennsylvania State University, Hershey, Pennsylvania
Anna P. Quan MD
Professor of Medicine
UCSD/San Diego VA, San Diego, California
Catherine Rainbow MD
Resident Physician
Department of Family Medicine, Carolinas Medical Center, Charlotte, North Carolina
Neha P. Raukar MD, MS

Assistant Professor
University Emergency Medicine Foundation/University Orthopedics, Department of
Emergency Medicine/Primary Care Sports Medicine, Warren Alpert School of Medicine,
Brown University
Reno Ravindran MD
Nationwide Children's Hospital Sports Medicine, The Ohio State University College of
Medicine, Columbus, Ohio
Tracy Ray MD
Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama
Steven G. Reece MD
Department of Medicine, Virginia Commonweatlh University School of Medicine, Richmond,
Virginia, Medical Director, Randolph Macon College Student Health Services, Ashland,
Virginia
Paul Reehal MD
Indiana University Primary Care Sports Medicine Fellow, Indiana University School of
Medicine, Indianapolis, Indiana
L. Shay Richardson MD
Fellow, John Peter Smith Pain Medicine Fellowship, Fort Worth, Texas
Brent S. E. Rich MD, ATC

Utah Valley Sports Medicine, Fellowship Director, Team Physician, Brigham Young University,
Provo, Utah
Allen Richburg MD, MS, FAAFP

San Diego Sports Medicine and Family Health Center, Head Team Physician U.S. Olympic
Training Center, Chula Vista, Assistant, Professor, Volunteer, U.C. San Diego, School of
Medicine, Team Physician and Clinical Instructor, San Diego State University
Leland S. Rickman MD
Associate Clinical Professor of Medicine
University of California at San Diego, San Diego, California
Tara Robbins MD
Department of Family and Preventative Medicine, University of California San Diego, San
Diego, California
James Robinson MD
PGY2, St. Joseph Regional Medical Center, South Bend, Indiana
Richard E. Rodenberg MD, FAAP

Assistant Clinical Professor of Pediatrics and Internal Medicine
Primary Care Sports Medicine Fellowship Director, Nationwide Children's Hospital, The Ohio
State University College of Medicine, Columbus, Ohio
Jorge O. Rodriguez DO, CAQSM
Assistant Professor
Department of Orthopaedics, Emory Health Care, Emory Orthopaedics and Spine Center,
Atlanta, Georgia
Stephen J. Rohrer DO, CAQ Sports Medicine

University of California-San Diego, Assistant Clinical Professor, San Diego State University,
Assistant Team Physician, San Diego State University
Daryl A. Rosenbaum MD, CAQSM

Assistant Professor
Sports Medicine Fellowship Director, Department of Family and Community Medicine, Wake
Forest University School of Medicine, Winston-Salem, North Carolina
Jeffrey Rosenberg MD
Director Mountainside Sports Medicine Fellowship, Mountainside Family Medicine Residency
Program, Verona New Jersey
Matt Roth MD
Associate Director Sports Care
The Toledo Hospital Primary Care Sports Medicine Fellowship, Toledo, Ohio
Mark Rowand MD
Moses Cone Health System
Cherise Russo DO
Northwestern Orthopaedic Institute, LLC, Primary Care Sports Medicine, Clinical Instructor,
Northwestern University, Feinberg School of Medicine, Chicago, Illinois
Darin Rutherford MD
Mercy Sports Medicine and Rehabilitation Center, Mercy Health System, Janesville,
Wisconsin
Mark Sakr DO
Department of Community and Family Medicine, Duke University Medical Center, Durham,
North Carolina
Tomoya Sakai MD
Department of Family Medicine, John Peter Smith Health Network
Bradley Sandella DO
Saint Joseph Regional Medical Center, Mishawaka, Indiana
Thomas Sargent DO
Resident
Family Medicine, Department of Family and Community Medicine, Christiana Care Heath
System, Wilmington, Delaware
Michael Schettino MD
Christiana Care Health System, Department of Family and Community Medicine, Section of
Sports Medicine, Wilmington, Delaware
David A. Scott MD
Primary Care Sports Medicine Fellow, Steadman Hawkins Clinic of the Carolinas, Greenville
Hospital System University Medical Center, Greenville, South Carolina
W. Franklin Sease Jr MD, GHS

Assistant Professor of Clinical Sports Medicine
Department of Orthopaedic Surgery and Family Medicine, Steadman Hawkins Clinic of the
Carolinas, Greenville Hospital System, University Medical Center, Greenville, South Carolina
Nilesh Shah MD
Medical Director
Summa Center for Sports Medicine, Summa Health System, Akron, Ohio, Assistant Clinical
Professor of Family Medicine, Northeast Ohio Universities College of Medicine, Rootstown,
Ohio
Ramsey Shehab MD
Senior Staff Physician, Division of Sports Medicine, Dept of Orthopaedics, Henry Ford Health
System, Detroit, Michigan
John Shelton MD
Program Director
Halifax Sports Medicine Fellowship, Associate Program Director, Halifax Family Medicine
Residency Program, Assistant Clinical Professor of Family Medicine, Florida State University
School of Medicine, Tallahassee, Florida
Matthew D. Shores MD
Arizona State University, Primary Care Sports Medicine Fellowship, Tempe, Arizona, Sports
Medicine Express, Chandler, Arizona
Ian Shrier MD, PhD

Assistant Professor
McGill University, Centre for Clinical Epidemiology and Community Studies, SMBD-Jewish
Hospital, Montreal, Quebec, Canada
Robby S. Sikka MD
TRIA Orthopaedic Center, University of Minnesota Dept. of Anesthesiology
Stephen Simons MD
Co-Director South Bend Sports Medicine Fellowship, Saint Joseph Regional Medical Center,
South Bend, Indiana
David V. Smith MD
University of Wisconsin, Department of Pediatrics/Ortho & Rehab, Division of Sports
Medicine, Madison, Wisconsin
M. Kyle Smoot MD
Department of Family and Community Medicine, University of Kentucky, Lexington. Kentucky
Dan Somogyi MD
Program Director
University of Pennsylvania Medical Center at Shadyside, Primary Care Sports Medicine
Fellowship, Pittsburgh, Pennsylvania
Luke M. Spellman DO
Fellow, Pediatric Primary Care Sports Medicine, Akron Children's Hospital, Sports Medicine
Center, Akron, Ohio
Jason E. Spring DO
Department of Family and Sports Medicine, UCSD Medical Center, La Jolla, California
Tim Sprockel MD
Texas Tech Sports Medicine Fellowship, Texas Tech Department of Family Medicine,
Lubbock, Texas
Jason J. Stacy MD
Associate Professor Team Physician
Director, Palmetto Health Sports Medicine Fellowship, Department of Family and Preventive
Medicine, University of South Carolina School of Medicine
Harry Stafford MD
Assistant Professor Sports Medicine Family Medicine and Orthopedics
University of North Carolina Chapel Hill, Chapel Hill, North Carolina
David A. Stone MD
Assistant Professor
Orthopaedic Surgery, University of Pittsburgh Medical Center
Mark Stovak MD
University of Kansas School of Medicine Wichita, Department of Family and Community
Medicine, Director, University of Kansas School of Medicine-Wichita Family Medicine
Residency Program and Sports Medicine Fellowship Program at Via Christi Health
Paul Stricker MD
Director
Associate Professor and Team Physician, Vanderbilt Sports Medicine Center, Vanderbilt
University, Nashville, Tennessee
Keith A. Stuessi CDR, MC, USN

Fellowship Director, Primary Care Sports Medicine, Department Head, Physical Medicine,
Naval Hospital Camp Pendleton
Jessica Stumbo MD
University of Louisville & Jewish Hospital, Sports Medicine, Assistant Professor of Medicine
University of Louisville, Louisville, Kentucky
Payal Sud MD
Tod Sweeney MD
Family Practice Department, Maine Medical Center, Portland, Maine
John T. Swisher IV DO
Sports Medicine Fellow HCMC/University of Minnesota
Michael Devin Taylor DO

Utah Valley Sports Medicine, Sports Medicine Fellow, Provo, Utah
Kirk Tieman MD, DSc

Texas Tech University Health Sciences Center, Lubbock, Texas
Todd Toriscelli MA, ATC
Director of Sports Medicine and Performance, Tampa Bay Buccaneers, Tampa, Florida
Christopher C. Trigger MD
UPMC Shadyside Sports Medicine Fellow, University of Pittsburgh Medical Center, Pittsburgh,
Pennsylvania
Thomas Trojian MD, MMB

Sports Medicine Fellowship Director, Associate Professor Department of Orthopaedics and
Family Medicine, University of Connecticut Health Center, Director of Injury Prevention and
Sports Outreach Programs, New England Musculoskeletal Institute, Team Physician
University of Connecticut, Sports Medicine Consultant to Connecticut Interscholastic Athletic
Conference
Priscilla Tu DO
Duke Family Medicine/Sports Medicine, Department of Community and Family Medicine
Philipp Underwood MD, FAAEM, FACEP, FAAFP

Sports Medicine Fellowship, Department of Emergency Medicine, North Shore University
Hospital, Manhasset, New York, Assistant Professor, Clinical Emergency Medicine, NYU
School of Medicine, New York, New York
Verle Valentine MD
Sports Medicine Physician
Sanford Orthopedics & Sports Medicine, Medical Director, Sanford Sports Medicine, Medical
Director, National Institute for Athletic Health & Performance & Center for Youth Sports &
Health, Assistant Professor, Sanford School of Medicine at the University of South Dakota,
Sioux Falls, South Dakota
Jake Veigel MD
Cayuga Medical Center Sports Medicine and Athletic Performance, Ithaca, New York
Nadya Volsky MD
General Practice Physician, Totara Health, Hastings, New Zealand
Natalie Voskanian MD
University of California, San Diego Sports Medicine, Department of Orthopaedic Surgery, San
Diego, California
Bryant Walrod MD
The Medical College of Wisconsin
Jason Wander DO
Primary Care Sports, Medicine Fellow, UPMC Sports Medicine, Pittsburgh, Pennsylvania
Kevin N. Waninger MD, MS

Department of Family and Community Medicine, Temple University School of Medicine,
Director, Sports Medicine Fellowship, St. Luke's Hospital and Health Network, Bethlehem,
Pennsylvania
Anna Waterbrook MD
Assistant Fellowship Director
University of Arizona, Primary Care Sports Medicine Fellowship, Clinical Assistant Professor,
Department of Emergency Medicine, Staff Physician Primary Care Sports Medicine, Arizona
Institute for Sports Medicine, Assistant Team Physician, University of Arizona Intercollegiate
Athletics
Charles W. Webb DO
Assistant Professor of Family Medicine and Orthopedics
Director, Primary Care Sports Medicine Fellowship, Oregon Health & Science University,
Portland, Oregon
Kathleen Weber MD, MS

Assistant Professor, Departments of Internal Medicine & Orthopaedic Surgery, Rush
University Medical Center, Chicago, Illinois
C. Thayer White MD
Resident in Family Medicine, Department of Family Medicine, Oregon Health & Science
University, Portland, Oregon
Nancy White MD
Senior Staff Physician, Departments of Orthopedic Surgery and Family Medicine, Henry Ford
Health System, Detroit, Michigan, Program Director, Primary Care Sports Medicine
Fellowship Program, Henry Ford Health System, Detroit, Michigan
Russell D. White MD
Professor of Medicine
Director, Sports Medicine Fellowship Program, Medical Director, Sports Medicine Center,
University of Missouri-Kansas City School of Medicine, Kansas City, Missouri
John J. Wilson MD, MS

Assistant Professor
University of Wisconsin School of Medicine and Public Health, Departments of Family
Medicine and Orthopedics, Division of Sports Medicine, Madison, Wisconsin
Kristina M. Wilson MD
Clinical Instructor of Orthopaedics and Rehabilitation, Department of Orthopaedics and
Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee
Jason P. Womack MD
Assistant Professor
Department of Family Medicine and Community Health, UMDNJ - Robert Wood Johnson
Medical School, New Brunswick, New Jersey
Lauren Wood
Fourth-Year Medical Student, University of Virginia College of Medicine, Charlottesville,
Virginia
Shannon Woods MD
UPMC Sports Medicine, Pittsburgh, Pennsylvania
Justin Wright MD
Crozer-Keystone Sports Medicine Fellowship Program, Springfield, Pennsylvania
Ronald Yee MD
Hennepin County Medical Center Sports Medicine Department
Ramon Ylanan MD CAQSM

Team Physician
University of South Carolina, Assistant Director, Palmetto Health Sports Medicine Fellowship,
Assistant Professor, Department of Family and Preventative Medicine, Adjunct Clinical
Associate Professor, Department of Orthopedic Surgery, Clinical Instructor University of South
Carolina Athletic Training Education Program, University of South Carolina School of
Medicine
Craig C. Young MD
Professor of Orthopaedic Surgery & Community and Family Medicine
Medical Director of Sports Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin
Alan Zakaria DO, MS

Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan
Carrie B. Zaslow MD
Ophthalmology Housestaff, North Shore-Long Island Jewish Medical Center
Tracy L. Zaslow MD, FAAP, CAQSM

Team Physician
Los Angeles Galaxy Men's League Soccer, Attending Physician, Los Angeles Ballet
Company, Clinical Instructor, Primary Care Sports Medicine, Encino, California
Dedication
This book is dedicated to the entire team of health care professionals who work with athletes of
all ages and stages of training in an atmosphere where time becomes essential, and an
accurate diagnosis and treatment plan are expected. The 5-Minute Sports Medicine Consult in
both printed and Web-based format is ideal for this setting.
It is our hope that the information contained in this body of work will help guide you and your
patients along the path to recovery and peak performance.
Preface
In the 8 years since the publication of the first edition of the 5-Minute Sports Medicine Consult
(5MSMC), much has changed in how we practice medicine. To a large degree, this change can
be attributed to how we receive and apply quality medical information in a timely fashion, and
the rapid integration of the electronic medical record keeping system into our daily work.
As the computer continues to permeate our lives, health care professionals have increasingly
turned to web-based formats as a source of medical information in their busy practices.
Building on our success with the first edition of the 5MSMC, progress with the second edition
was streamlined by utilizing a new online writing and editing format adopted by our publisher.
Users of the first edition will be pleased to note that the overall format of the second edition has
remained by and large the same with a few new headings now being used throughout the entire
5-Minute Consult series.
The basic concept for this book parallels a teaching technique that we have used at the
University of California, San Diego (UCSD) since 1991 for Sports Medicine Fellows in training
called the “How I Manage Series.”
As part of our regular weekly Sports Medicine didactic program, fellows and faculty are asked
to present lectures on a single topic related to their sports medicine clinical practice covering
the essential elements in the diagnosis and management of problems as seen through the eyes
of a primary care physician.
The audience will consist of experienced clinicians, including orthopaedic surgeons, radiologists,
physical therapists, athletic trainers and other members of the “Sports Medicine team.”
Organization and presentation of these didactics follows those found in this book with an
emphasis on evidence-based medicine.
Perhaps the most significant advancement with the second edition has taken place behind the
scenes: The publisher has negotiated a formal relationship with the American Medical Society
for Sports Medicine (AMSSM) to assure the highest possible content quality utilizing the
combined experience of its members to draft and edit each chapter. It is my continued belief
that the AMSSM is in the best position to assure a project such as this is completed in a timely
fashion, represents the latest thinking on each topic, and remains focused on the needs of the
primary care sports medicine physician as the team leader.
Finally, I would like to express my sincerest gratitude to my co-editors: Ken Taylor, Suraj Achar,
and Andrea Pana. These three young academic physicians have worked tirelessly with me from
the beginning to keep this project moving forward and completed on time. As the roman orator
Cicero said many years ago:
“The first way for a young man to set himself on the road towards glorious reputation is to win
renown.”
It is with pleasure and security that I can pass the editorial torch on to these outstanding
physicians, and future generations of physicians to come, knowing that it will be kept burning
brightly in their hands.
Mark D. Bracker, MD
Professor, Department of Family and Preventive Medicine, University of California, San Diego,
San Diego, California
Forward
The American Medical Society for Sports Medicine (AMSSM) is proud to partner in the second
edition of the 5-Minute Sports Medicine Consult. Since it's inception in 1991, the AMSSM has
been the group of physicians with expertise in the breadth of sports medicine.
Over the past 18 years, the AMSSM has grown to over 1,600 members and is leading sports
medicine into the future. Many of the chapters in the first edition were written by members of
the AMSSM; however, the second edition is almost exclusively written by AMSSM members.
The chapter editors for this edition were chosen from a large group of qualified and
experienced AMSSM members; both the editors and authors have done an excellent job in
helping make this a high-quality reference book.
The AMSSM feels that the expertise and experience of our writers and editors is reflected in
the quality of the material in this book.
AMSSM recommends the 5-Minute Clinical Consult as a outstanding reference book for Sports
Medicine Physicians as well as nurse practitioners, physician assistants, athletic trainers,
primary care doctors, orthopaedists and anyone else who cares for those with sports medicine
injuries or illnesses. AMSSM plans to continue to partner with the publisher and editors in the
future to maintain the best quality, up-to-date, evidence-based information available to the
reader. We are excited to continue to expand the book with additional topics being added online
between the publishing of future editions.
Andrea L. Pana, MD
AMSSM Board of Directors, Publications Committee Chair
FRONT OF BOOK ↑
[+] Editors
[+] Authors
- Dedication
- Preface
- Forward
TABLE OF CONTENTS ↑
[+] Abdominal Muscle Strains

[+] Achilles Tendinitis
[+] Achilles Tendon Rupture
[+] ACL Injuries
[+] ACL Tear: Management in Skeletally Immature Athletes
[+] Acromioclavicular Separations (Types 1–6)
[+] Adductor Thigh Strain
[+] Adhesive Capsulitis
[+] Anaphylaxis
[+] Ankle Sprains, Lateral
[+] Ankle Sprains, Medial
[+] Ankylosing Spondylitis
[+] Anterior Interosseous Syndrome
[+] Anterior Metatarsalgia (Submetatarsal Head Pain)
[+] Aortic Stenosis
[+] Athletic Heart Syndrome
[+] Atlantoaxial Instability
[+] Auricular Hematomas
[+] Avascular Necrosis of the Proximal Femoral Epiphysis (Legg-Calve-Perthes Disease)
[+] Axillary Nerve Injury
[+] Barotitis Media
[+] Biceps Tendinitis
[+] Biceps Tendon Rupture
[+] Bites and Stings
[+] Brachial Plexus Injuries (Burners and Stingers)
[+] Bursitis
[+] Calcium Pyrophosphate Deposition Disease (CPPD) (Pseudogout)
[+] Calluses and Corns
[+] Cardiac Arrhythmias: Atrial Fibrillation, SVT
[+] Carpal Tunnel Syndrome
[+] Cellulitis
[+] Central Slip Avulsion and Pseudoboutonniere Deformities
[+] Cervical Disk Disease
[+] Cervical Stenosis
[+] Cervical Strains
[+] Channelopathies, Long QT, CPVT
[+] Claudication
[+] Cluster Headache
[+] Compartment Syndrome, Anterior
[+] Complex Regional Pain Syndrome
[+] Concussion
[+] Congenital Cervical Disease
[+] Contact Dermatitis
[+] Corneal Abrasions
[+] Cubital Tunnel Syndrome
[+] Cuboid Subluxation and Fracture
[+] Dentoalveolar Trauma
[+] DeQuervain Tenosynovitis
[+] Developmental Dysplasia of the Hip
[+] Diabetes
[+] DIP Dislocation
[+] Discoid Meniscus
[+] Dislocation, Hip, Posterior
[+] Distal Clavicular Osteolysis
[+] Dupuytren's Contracture
[+] Eating Disorders
[+] Elbow Dislocation
[+] Epistaxis
[+] Exercise-Induced Anaphylaxis
[+] Exercise-Induced Asthma
[+] Exercise-Induced Diarrhea
[+] Exercise-Induced Urticaria
[+] Exertional Headache
[+] Extensor Tendon Avulsion from the Distal Phalanx/Mallet Finger
[+] External Ear Chondritis/Abscess
[+] External Genital Trauma
[+] Felon
[+] Female Athlete Triad
[+] Flexor Carpi Ulnaris and Flexor Carpi Radialis Tendonitis
[+] Flexor Tendon Avulsion/Jersey Finger
[+] Folliculitis
[+] Foot Osteochondroses (Accessory Navicular, Navicular Asceptic Necrosis-Kohler, Islin—
Apophysitis of Base 5th MT)
[+] Fracture, Avulsion: ASIS, AIIS, Ischial Tuberosity, Iliac Crest
[+] Fracture, Blow Out
[+] Fracture, Calcaneus
[+] Fracture, Carpal Bone (Other)
[+] Fracture, Clavicle
[+] Fracture, Coccyx
[+] Fracture, Compression
[+] Fracture, Coronoid
[+] Fracture, Distal Femur
[+] Fracture, Distal Phalanx
[+] Fracture, Distal Radius
[+] Fracture, Fibula
[+] Fracture, Fifth Metatarsal (Avulsion, Jones Fractures)
[+] Fracture, Frontal Sinus
[+] Fracture, Hamate: Hook, Body
[+] Fracture, Humeral Head
[+] Fracture, Humeral Shaft
[+] Fracture, Lateral and Medial Malleoli
[+] Fracture, Le Fort
[+] Fracture, Lisfranc
[+] Fracture, Lunate/Kienböck Disease
[+] Fracture, Mandibular
[+] Fracture, Metacarpal Base/Shaft: I-V
[+] Fracture, Metacarpal Neck: I-V
[+] Fracture, Metatarsal
[+] Fracture, Middle Phalanx
[+] Fracture, Nasal
[+] Fracture, Olecranon
[+] Fracture, Orbital
[+] Fracture, Patella
[+] Fracture, Pelvic
[+] Fracture, Posterior Malleolus
[+] Fracture, Proximal Phalanx
[+] Fracture, Proximal Tibia
[+] Fracture, Radial Head
[+] Fracture, Rib
[+] Fracture, Sacral
[+] Fracture, Scaphoid
[+] Fracture, Spinous and Transverse Processes
[+] Fracture, Sternum
[+] Fracture, Stress: Metatarsal, Navicular
[+] Fracture, Talus
[+] Fracture, Tibial Plateau
[+] Fracture, Tibial Spine Avulsion
[+] Fracture, Volkmann: Posterolateral Tibiofibular Ligament Avulsion
[+] Fracture, Zygoma
[+] Freiberg's Disease
[+] Glenohumeral Dislocation, Anterior
[+] Glenohumeral Dislocation, Posterior
[+] Glenoid Labral Tears/SLAP Lesions
[+] Gout
[+] Greenstick Fracture
[+] Haglund's Deformity (Pump Bump)
[+] Hallux Valgus (Bunions)
[+] Hammer/Claw/Mallet Toe
[+] Hamstring Strain
[+] Hand Infection
[+] Heel Pain: Heel Fat Pad Syndrome, Lateral Plantar Nerve Entrapment
[+] Hematomas, Epidural and Subdural
[+] Hematuria
[+] Hemoglobinopathies in Sport: Thalassemia, Sickle Cell Trait
[+] Herpes Gladiatorum
[+] High-Altitude Illness
[+] Hip Pointer
[+] Hyperthermia: Heat Stroke, Exhaustion, and Cramps
[+] Hypertrophic Cardiomyopathy
[+] Hyphema
[+] Hyponatremia
[+] Hypothenar Hammer Syndrome
[+] Hypothermia and Frostbite
[+] Iliopsoas
[+] Iliotibial Band Friction Syndrome
[+] Impetigo
[+] Impingement, Subacromial Bursitis and Rotator Cuff Tendinitis
[+] Inner Ear Injuries (Tympanic Membrane Perforation)
[+] Intermetatarsal (Morton's) Neuroma
[+] Interphalangeal Collateral Ligament Sprain
[+]
Intersection Syndrome
[+] Intraocular Foreign Bodies
[+] Klippel-Fiel Syndrome: Fusion of Cervical Vertebrae
[+] Knee Dislocation
[+] Kohler Disease (Aseptic Necrosis of the Tarsal Navicular)
[+] Kyphosis
[+] Lacerations and Soft Tissue Injuries
[+] Lateral Collateral Ligament Tear
[+] Lateral Epicondylitis
[+] Lightning Injuries
[+] Little Leaguer's Elbow (Medial Apophysitis)
[+] Little League Shoulder (Proximal Humeral Epiphysiolysis)
[+] Low Back Pain and Lumbar Strains
[+] Lumbar Disc Disease
[+] Lunate Dissociation
[+] Marfan's Syndrome
[+] MCP (MetaCarpophalangeal) Collateral Ligament Sprain
[+] MCP (Metacarpophalangeal) Dislocation
[+] Medial Collateral Ligament Tear
[+] Medial Epicondylitis
[+] Medial Gastrocnemius Injury, Tennis Leg
[+] Medial Tibial Stress Syndrome
[+] Meniscal Tears
[+] Menstrual Disorders in the Athlete
[+] Migraine Headache
[+] Molluscum Contagiosum
[+] Mononucleosis
[+] Motion Sickness
[+] Nasal Septal Hematomas
[+] Near-Drowning/Drowning
[+] Neck Lacerations and Penetrating Injuries
[+] Nonsteroidal Anti-Inflammatory Drug Poisoning
[+] Nursemaid's Elbow
[+] Obesity and Weight Management
[+] Olecranon Bursitis
[+] Onychocryptosis
[+] Onychomycosis
[+] Oral Lacerations
[+] Osgood-Schlatter Disease
[+] Osteitis Pubis
[+] Osteoarthritis
[+] Osteochondritis Dissecans
[+] Osteomyelitis
[+] Osteoporosis
[+] Otitis Media/Externa
[+] Overtraining
[+] Panner Disease and OCD of Elbow Capitellum
[+] Paronychia
[+] Patellar Dislocation and Instability
[+] Patellar/Quadriceps Tendinitis
[+] Patellar/Quadriceps Tendon Rupture
[+] Patellofemoral Pain Syndrome (PPS)
[+] Pectoralis Major Tendon Rupture
[+] Pericarditis
[+] Periorbital and Orbital Cellulitis
[+] Peroneal Tendon Dislocation/Subluxation
[+] Pes Anserine Bursitis
[+] Phalangeal Injuries
[+] Photodermatitis
[+] Physeal Injuries in Children Salter-Harris Classification
[+] Pigmented Villonodular Synovitis (PVNS)
[+] PIP Joint Dislocations
[+] Piriformis Syndrome
[+] Plantar Fasciitis
[+] Pneumothorax and Hemothorax
[+] Popliteal Tendonitis
[+] Posterior Cruciate Ligament (PCL) Tear
[+] Posterior Interosseous Nerve Syndrome
[+] Posterolateral Capsular Tear
[+] Pregnancy
[+] Pronator Syndrome
[+] Proteinurea in Sports
[+] Pseudoanemia
[+] Pulmonary Contusion
[+] Quadriceps Contusion
[+] Quadriceps Tear
[+] Radial Tunnel Syndrome
[+] Red Eye
[+] Redundant Plica
[+] Renal Trauma
[+] Retinal Detachments and Tears
[+] Rhabdomyolysis
[+] Rheumatoid Arthritis in Sports
[+] Rotator Cuff Tears
[+] Scapholunate Dissociation
[+] Sciatica
[+] Scoliosis
[+] SCUBA Diving Injuries: DCS and AGE
[+] Seizures and Epilepsy
[+] Septic Arthritis and Bursitis
[+] Sesamoid Dysfunction
[+] Sever Disease/Calcaneal Apophysitis
[+] Shoulder Instability, Anterior
[+] Shoulder Instability, Multidirectional
[+] Sinus Tarsi Syndrome
[+] Slipped Capital Femoral Epiphysis
[+] Snapping Scapula and Winging of the Scapula
[+] Spinal Stenosis
[+] Splenic Contusion and Rupture
[+] Spondyloarthropathies (Seronegative RA)
[+] Spondylolysis and Spondylolisthesis
[+] Sports Hernias
[+] Sternoclavicular Joint Injury
[+] Subconjunctival Hemorrhage
[+] Subungual Exostosis and Hematoma
[+] Sudden Cardiac Arrest: Commotio Cordis
[+] Superficial Radial Nerve (Wartenberg Disease)
[+] Suprascapular Nerve Palsy
[+] Surfer's Ear
[+] Syncope
[+] Syndesmodial Injury of the Lower Leg
[+] Tarsal Tunnel Syndrome/Posterior Tibial Nerve Entrapment
[+] Temporomandibular Joint Injury
[+] Testicular Torsion
[+] TFCC (Triangular Fibrocartilage Complex) Tears
[+] Thoracic Outlet Syndrome
[+] Thoracic Spine Injury
[+] Thrombophlebitis, Superficial
[+] Thrombosis, Deep Vein (DVT)
[+] Thumb Ulnar Collateral Ligament Sprain (Skier's Thumb)
[+] Tibialis Posterior Tendonitis
[+] Tibial Stress Fracture
[+] Tillaux Fractures: Anterior Tibia-Fibula Ligament Avulsion
[+] Tinea Gladiatorum (Capitis, Corporis, Cruris, Pedis)
[+] Tinea Versicolor
[+] Tracheal and Laryngeal Injuries
[+] Triceps Tendinitis
[+] Triceps Tendon Rupture
[+] Trigger Finger
[+] Trochanteric Bursitis
[+] Turf Toe
[+] Ulnar Collateral Ligament Injuries of the Elbow
[+] Ulnar Tunnel Syndrome
[+] Ultraviolet Keratitis
[+] Ureteral, Bladder, and Urethral Trauma
[+] Warts
[+] Wolff-Parkinson-White (WPW) Syndrome
BACK OF BOOK ↑
[+] Appendix A
[+] Index
Abdominal Muscle Strains
Jonathan A. Becker
Basics
Description
Injury to the abdominal wall musculature:
Typically a noncontact injury, but may be caused by trauma
Acute or subacute injury
Acute injury result of an abrupt movement of the trunk
Subacute injury caused by repetitive activity
The abdominal wall musculature includes rectus abdominus, internal/external obliques, and
transverse abdominus.
Epidemiology
Somewhat uncommon injuries, but specific sports have a higher prevalence:
Account for <2% of athletic injuries (1)
Sports with repetitive trunk rotation have higher rates:
Soccer, tennis, ice hockey, gymnastics, pole vault
Seen in runners, as the abdominal muscles are used for pelvic stabilization
Attributed to weight training and abdominal workouts as well
Risk Factors
Poorly conditioned abdominal musculature or deficits in core strength
Previous abdominal wall muscle strain/tear
Poor weight training or conditioning techniques
Participation in activities that require abrupt and/or repetitive movements of the torso
General Prevention
Appropriate weight training and conditioning techniques with attention to core strength
Etiology
Acute or chronic muscle-tendon injury of the abdominal wall musculature
Diagnosis
History
Acute abdominal wall pain associated with stretching or twisting mechanism
Chronic pain due to repetitive activity of the trunk or torso
Direct trauma associated with a minority of these injuries
Pain usually focal and exacerbated by specific movements or positions
Pain with active contraction of affected muscle during sneezing or coughing
Symptoms generally subside in the absence of activity.
Physical Exam
Appearance is typically normal with swelling and evidence of contusion rare in the absence of
preceding trauma.
Splinting may be noted if pain is severe.
Tenderness of the abdominal wall is usually focal and discrete, but may be more diffuse in
overuse type injury.
Muscle defect may be notable if an associated tear or herniation is present.
Peritoneal signs are absent.
Symptoms are reproduced by contraction of the affected muscle.
Diagnostic Tests & Interpretation

Imaging
Plain films, CT scan indicated if there is concern for rib fracture or intra-abdominal process
MRI can be utilized to assess for muscle tear or to assess the extent of injury:
Reserved for more severe injuries
Musculoskeletal US may prove to be the diagnostic procedure of choice.
Differential Diagnosis
Abdominal wall contusion
Abdominal wall hematoma:
Swelling, periumbilical contusion, and a mass with rigidity and/or guarding are signs of a
rectus sheath hematoma
Abdominal wall hernia (umbilical, Spigelian)
Intra-abdominal injury (contusion, laceration, perforation)
Intra-abdominal process (eg, infection, mass, etc.)
Iliac apophysitis
Osteitis pubis
Treatment
Acute treatment:
Remove the athlete from the offending activity.
Ice
Compressive wrap
NSAIDs or acetaminophen
Once pain subsides, a rehabilitation program may be initiated (1,2)[C].
Medication
First Line
NSAIDs or acetaminophen:
Avoid NSAIDs if there is concern for bleeding or hematoma.
Second Line
Narcotics or muscle relaxants may be utilized for more severe injuries, but are
rarely needed.
Additional Treatment
General Measures
Rehabilitation:
Assess abdominal muscle strength and core strength/stability.
Initiate a rehab program once pain has subsided:
Start with passive stretching.
Advance to strengthening activities.
Progress to sport-specific activities (1,2)[C].
Additional Therapies
Modalities such as US or muscle stimulation may help alleviate symptoms.
Corticosteroid injection at the site of muscle tear/strain may be considered for
acute pain relief or refractory cases.
Surgery/Other Procedures
Surgery may be necessary in cases of rectus sheath hematoma, hernia, or intra-
abdominal process.
Ongoing Care
Follow-Up Recommendations
The athlete may return to activity once pain subsides and they can engage
in sport-specific activity.
Prognosis
Overall prognosis for recovery is excellent:
Duration of symptoms is variable and may persist for months.
Recurrence rates are high (>20%).
References
1. Johnson R. Abdominal wall injuries: rectus abdominis strains, oblique
strains, rectus sheath hematoma. Curr Sports Med Rep. 2006;5:99–103.
2. Maquirriain J, Ghisi JP, Kokalj AM. Rectus abdominis muscle strains in

tennis players. Br J Sports Med. 2007;41:842–848.
Codes
ICD9
848.8 Other specified sites of sprains and strains
Clinical Pearls
Athletes can return to play when there is minimal-to-no tenderness, normal
muscle strength and stamina, and can perform sport-specific tasks.
Usual duration of symptoms varies from weeks to months.
Achilles Tendinitis
Craig C. Young
Mark W. Niedfeldt
Basics
Description
Achilles tendinitis is an overuse injury of the Achilles tendon (from the musculotendinous
junction of the gastrocnemius/soleus complex proximally to its insertion on the calcaneous)
that causes pain in the posterior calf and heel.
Synonym(s): Achilles tendinosis; Achilles tendinopathy
Epidemiology
Accounts for 6.5–18% of injuries in runners
Accounts for up to 4% of patients in sports medicine clinics
Most common site is mid-portion (80–90%); pure insertional is rare (5%)
Incidence
Lifetime incidence in competitive athletes is estimated to be 24%:
Athletes in running and jumping sports are especially at risk; lifetime incidence in competitive
runners may be as high as 50%.
Risk Factors
Training errors: Recent increase in distance, intensity, or length of activity
Worn, old shoes
Inflexibility, especially tight heel cords
Obesity
Hypertension
Malalignment of the leg (excessive genu valgum, external tibial torsion) or ankle/foot (pes
planus)
Fluoroquinolones: Recent use of these antibiotics has been associated with increased risk for
Achilles tendinopathy and rupture (1)[B].
Estrogen exposure from hormone replacement therapy and oral contraceptives may cause
changes in microvascularity that may predispose a woman to Achilles tendinopathy (2)[C].
Etiology
Tendinosis: Chronic degenerative condition is more common than tendinitis, which is an
inflammatory condition.
Disruption of normal tendon architecture:
Chronic intratendinous degeneration, collagen disorientation, and increases in mucoid
ground substance
Neovascularization
Commonly Associated Conditions

Retrocalcaneal bursitis
Posterior ankle impingement syndrome
Superficial Achilles bursitis (“pump bump” or Haglund's deformity)
Achilles tendon rupture: Chronic changes in tendon may predispose to rupture.
Diagnosis
History
Pain that initially subsides with use but returns with continued use or after use suggests an
overuse injury.
Morning stiffness is a hallmark of Achilles tendinitis.
Training errors are a factor in a large percentage of cases.
Worn shoes: Shoes need to be changed every 250–500 miles because of shoe padding
breakdown.
Patients may report weakness and intermittent swelling.
Physical Exam
Pain and stiffness 2–6 cm above Achilles tendon insertion
Pain with running, especially sprinting
Tenderness over the distal Achilles tendon (2–6 cm above the insertion):
Tenderness near insertion suggests insertional Achilles tendinopathy (enthesopathy) or
bursitis.
Thickening of the distal Achilles tendon (chronic injury)
Tenderness with resisted plantar flexion
Crepitus with ankle motion
Negative Simmonds-Thompson test: Compression of the calf will cause normal passive
plantar flexion of the foot:
A positive test (absence of plantar flexion with calf compression) suggests complete
Achilles tendon rupture.
Decreased ankle dorsiflexion (from tight heel cord)

Imaging
Not usually needed for initial evaluation. X-rays should be obtained if other potential injuries
are suspected (eg, fracture or tumor) or if injury is not responding to appropriate treatment.
Standard ankle series (anteroposterior, lateral, and mortise) may show calcification of
tendon; however, presence of calcification does not affect initial treatment.
US (3)[C]:
Hypoechoic regions, intratendinous calcifications, disorganization of fibers, fusiform
expansion, intrasubstance/partial-thickness tears, and neovascularization may be seen with
Achilles tendinopathy:
Degenerative changes may be seen in 60% of healthy uninjured persons.
Individuals who were more active are more likely to have changes.
Neovascularization at baseline does not predict clinical outcome of nonoperative
treatment.
MRI shows thickening of the tendon with intratendinous changes.
Superficial Achilles bursitis
Calcaneal apophysitis (Sever's condition) in adolescents
Haglund deformity: Prominent superior tuberosity of calcaneus
Achilles tendon rupture
Gastroc-soleus tear
Overuse myositis
Chronic exertional compartment syndrome
Os trigonum irritation or posterior ankle impingement syndrome
Vascular/neurogenic claudication
Deep venous thrombosis
Hematoma
Infection
Treatment
Acute tendinopathy (4,5,6,7,8)[C]:
Ice after activity; proper warm-up prior to activity
NSAIDs: May be useful as an adjunct for pain control and in cases of acute
injury
Modalities: Consider the use of US or phonophoresis. Although some studies
have shown that these modalities are useful in returning an athlete to activity
sooner, they also show no long-term benefit.
Short-term immobilization (7–10 days) with walking boot for severe acute
symptoms or recalcitrant symptoms
Heel lift (or high-heeled shoes)
Chronic tendinopathy (4,5,6,7,8)[C]:
Hamstring and calf stretching and strengthening program:
Progression to eccentric exercise programs has been shown to shorten
time to return to full activity. Results of randomized, controlled trials have
not consistently shown short- or long-term benefit, though.
Orthotics or arch supports may be useful in patients with pes planus and
those who overpronate.
Short-term use of night splints or walking boots may be useful in patients with
recalcitrant symptoms.
Nitric oxide via topical nitroglycerin particularly for noninsertional chronic
Achilles tendinopathy (9)[C]
Autologous blood or platelet-rich plasma injections: Theoretically make the
environment of fibroblasts more conducive to healing (10)[C]
Injection of sclerosing agents to destroy the sensory nerves that travel with
the blood vessels of neovascularization
Avoid injection of cortisone into the Achilles tendon because of risk of
rupture.
Extracorporeal shock wave therapy: Thought to induce neovascularization
and a new inflammatory process that leads to tissue healing (11)[C]
Low-level laser therapy: Thought to modulate inflammation and regeneration
of collagen (12)[C]
Surgery for recalcitrant cases
Referral
Consider referral for surgical debridement for individuals whose symptoms have
not responded to 3–6 or more months of nonoperative treatment.
Stretching: Ensure athlete is on appropriate conditioning program, pre-activity
warm-up, and post-activity cool-down programs.
Strengthening: Including a gastrocnemius and soleus strengthening program
with emphasis on eccentric exercises
Ongoing Care
Relative rest: Especially eliminate sprinting, speed work, and running hills or stairs. Overall
decrease in running intensity, duration, and/or frequency.
New shoes: Avoid shoes with high heel counters or other structures that place pressure over
irritated area. Running shoes should be changed every 250–500 miles.
Use of heel lifts or high heels often can acutely decrease symptoms.
References
1. Sode J, Obel N, Hallas J, et al. Use of fluroquinolone and risk of Achilles tendon rupture:
a population-based cohort study. Eur J Clin Pharmacol. 2007;63:499–503.
2. Holmes GB, Lin J. Etiologic factors associated with symptomatic achilles tendinopathy.
Foot Ankle Int. 2006;27:952–959.
3. Nicol AM, McCurdie I, Etherington J. Use of ultrasound to identify chronic Achilles

tendinosis in an active asymptomatic population. J R Army Med Corps. 2006;152:212–216.
4. Gottschlich LM, Eerkes KJ, Lin D, et al. Achilles tendonitis.

http://emedicine.medscape.com/article/85115-overview, 2009.
5. Ham P, Maughan KL. Achilles tendinopathy and tendon rupture.

http://www.uptodate.com/online/content/topic.do?topicKey=ad_orth/11653, 2009.
6. Magnussen RA, Dunn WR, Thomson AB. Nonoperative treatment of midportion Achilles
tendinopathy: a systematic review. Clin J Sport Med. 2009;19:54–64.
7. Marks RM. Achilles tendinopathy: peritendinitis. Foot Ankle Clin. 1999;4(4):789–809.
8. Solan M, Davies M. Management of insertional tendinopathy of the Achilles tendon. Foot

Ankle Clin. 2007;12:597–615.
9. Paoloni JA, Murrell GA. Three-year followup study of topical glyceryl trinitrate treatment
of chronic noninsertional Achilles tendinopathy. Foot Ankle Int. 2007;28:1064–1068.
10. Mishra A, Woodall J, Vieira A. Treatment of tendon and muscle using platelet-rich
plasma. Clin Sports Med. 2009;28:113–125.
11. Furia JP. High-energy extracorporeal shock wave therapy as a treatment for insertional
Achilles tendinopathy. Am J Sports Med. 2006;34:733–740.
12. Stergioulas A, Stergioula M, Aarskog R, et al. Effects of low-level laser therapy and
eccentric exercises in the treatment of recreational athletes with chronic Achilles
tendinopathy. Am J Sports Med. 2008;36:881–887.
Codes
ICD9
726.71 Achilles bursitis or tendinitis
ICD10
M76.6 Achilles tendinitis
Clinical Pearls
Because of the high stresses placed upon the Achilles tendon with weight-
bearing activities and the risk of rupture, corticosteroid injection into the Achilles
tendon should be avoided.
Achilles Tendon Rupture
Carrie A. Jaworski
Lisa Palazollo
Basics
Achilles tendon ruptures are caused by laceration or by indirect forces applied to the
tendon.
3 types of indirect forces have been described:
Pushing off with the weight-bearing forefoot while extending the knee, such as with sprint
starts and the pushoff in basketball
Sudden, unexpected dorsiflexion of the ankle, as when the foot slips in a hole
Violent dorsiflexion of a plantar flexed foot, as with a fall from a height
Description
Achilles tendon rupture is a complete disruption of the Achilles tendon, usually occurring 2–6
cm proximal to its calcaneal insertion, where blood supply is the poorest.
It can be associated with preexisting tendon degeneration and microtrauma.
It most commonly occurs in 30- to 40-year-old men.
Synonym(s): Heel-cord rupture; Achilles tear
Epidemiology
>75% of Achilles tendon ruptures occur in patients 30–40 yrs old while they partake in sports
activities.
Males > Females: Ratio ranges from 1.7:1–19:1.
Left Achilles > right Achilles: Thought to be due to higher prevalence of right-side dominant
individuals using left lower limb to push off during activity
Risk Factors
Disease processes: Connective tissue disorders, seronegative spondylopathies, rheumatoid
arthritis, collagen vascular disease, diabetes mellitus, gout, hyperparathyroidism, renal
insufficiency
Medications: Anabolic steroids or prolonged oral corticosteroid usage leads to degradation of
collagen fibrils and decreased Achilles tendon strength. Corticosteroid injections weaken
tendon structure. Fluoroquinolone antimicrobials lead to ischemia of tendon.
Disuse atrophy and sedentary lifestyle
Prolonged immobilization
Advanced age
History of Achilles tendonitis/tendinosis, regardless of history of injection therapy
Mechanical imbalances (ie, decreased flexibility of gastrocnemius-soleus complex)
Body weight/obesity
Possibility of genetic predisposition (possibility of association with HLA-B27, blood group 0)
Etiology
Is the largest tendon in the human body. It is designed to endure stresses up to 10 times the
body's weight.
Is formed by the confluence of the tendons of the gastrocnemius and soleus muscles. The
gastrocnemius medial and lateral heads originate from the medial and lateral femoral
condyles, respectively. The soleus originates from a large attachment on the posterior tibia
and fibula. Together, these tendons insert onto the calcaneus to form the Achilles tendon.
Receives its blood supply intrinsically from both the musculotendinous junction and the
osteotendinous insertion site.
Additional vascular supply comes from an external source known as the paratenon. The
paratenon is a thin layer of areolar tissue that encases the Achilles tendon. The further the
tendon is from its musculotendinous origin and calcaneal insertion, the more it relies on the
paratenon for vascular support.
The area with the poorest vascular supply is 2–6 cm proximal to the calcaneal insertion site.
Prior to inserting into the calcaneus, the Achilles tendon internally rotates, which imparts a
structural torque stress in the tendon. This is thought to contribute to decreased vascularity in
the tendon and ensuing tendon failure.
Diagnosis
History
Patients commonly report feeling as if they have been kicked or struck in the back of the
heel, only to find no one is nearby.
May feel or hear a “pop” or snap
Pain with weight-bearing
Weakness or stiffness of posterior ankle
May give history of chronic Achilles tendinitis with or without history of injection therapy
Physical Exam
Acute complete rupture of the Achilles tendon involves a sudden, sharp pain behind the ankle,
usually associated with a painful, palpable defect in the tendon.
Swelling and/or ecchymosis
“Hatchet strike” defect: Palpable, tender defect, usually 2–6 cm from the tendon insertion site
Positive Thompson test is diagnostic. Have patient lie prone or kneel with ankles clear of the
table. Squeeze bulk of calf muscle and observe for plantar flexion. Perform on uninvolved
side 1st for comparison. Absence of plantar flexion is consistent with complete tendon
rupture.
Note that for the Achilles to function normally, only 25% of the fibers are needed; therefore,
partial tears may be missed on examination.
Plantar flexion strength and ability to toe rise may be decreased compared to unaffected
side.
Passive dorsiflexion may be increased compared to unaffected side.
These signs may be absent because of recruitment of other intact muscles, such as tibialis
posterior, peroneus longus and brevis, and flexor digitorum and hallucis longus.

Imaging
Routine plain films should be obtained to avoid missing a calcaneal avulsion rupture, which
would require surgical treatment. This finding usually can be appreciated on the lateral ankle
radiograph.
US and MRI should be reserved for when the diagnosis of a complete rupture is questionable
or if one is considering a partial tear.
Achilles tendinitis
Ankle sprain
Peritendinitis
Superficial Achilles bursitis
Periostitis
Plantar tendon rupture
Calcaneal avulsion
Treatment
Analgesia should be based on the patient's degree of pain.
Rest, ice, compression, and elevation (RICE) should be used in the initial
treatment of complete and partial tears.
Both treatment approaches should be followed by a well-outlined rehabilitation
program.
Advances in therapy should be supervised by the treating physician.
Cardiovascular fitness during treatment can be sustained through arm
ergometer use, then recumbent cycling once no longer using crutches.
Once the cast is removed, active movement is initiated with the knee bent to 90
degrees; wound care and edema reduction is administered.
Progress to passive movement, but focus on limiting maximum stretch on the
tendon while restoring normal ankle range of motion.
Slowly start strength exercises with isometrics, then progress to resisted range
of motion exercises.
To restore functional activity, progress to closed kinetic chain exercises
focusing on eccentric gastrocnemius strength.
Ongoing Care
Controversy in the literature exists as to the best treatment approach for Achilles tendon
rupture.
Careful patient selection is based on the patient's activity level and goals.
The 2 treatment options are surgical repair and casting.
Casting:
Offers quicker return to work
Fewer complications than surgery
Risk of re-rupture greater than with surgical repair: 10–30% for nonsurgical vs 1–4% for
surgical repair
Risk of deep venous thrombosis (DVT) with prolonged casting; warfarin prophylaxis for
high-risk patients
Usually recommended for less active or elderly patients, those with medical
contraindications to surgery, or those with a history of multiple, chronic tears (1,2,3)[A]
Partial tears, or a tear in continuity diagnosed by MRI, also treated conservatively
The option exists to use a functional dorsal block splint that restricts dorsiflexion and
gradually increases the amount of plantar flexion. Functional splints have been shown to
help prevent gastrocnemius atrophy, quicker return to full dorsiflexion and better tolerance
by patients than casting (4,5).
0–4 wks: Long-leg cast with knee at 45 degrees and foot in gravity equinus. Can use
short-leg cast non–weight-bearing (SLC NWB) if patient avoids any leg extension. This
prevents pull on the Achilles from the gastrocnemius attachment at the femoral condyles.
4–8 wks: Short-leg walking cast (SLWC) in slightly less equinus/neutral position
8–10 wks: Continuous active motion (CAM) walker with gradual increases in dorsiflexion as
tolerated. 10 degrees every 2–3 days. Discontinue CAM walker when full dorsiflexion is
achieved.
10 wks: 2–2.5-cm heel lift gradually decreased over next several weeks/months and
aggressive rehabilitation for range of motion, then strengthening
6 mos: Return to full activity
Open repair or closed, percutaneous technique:
Associated with a lower incidence of re-rupture (1,2,3,6)[A]
Increased restoration of calf strength/less loss of pushoff power
More likely to return to preinjury level: 57% surgical vs 29% nonsurgical
Surgical complications can include infection, DVT, pulmonary embolism, and death.
Other postoperative risks include delayed healing, scar adhesions, infection, persistent
equinus, overlengthening, and fistulas.
Usually recommended for high-level athletes, those returning to high-risk activities
(basketball, tennis, soccer, and sprinting), and for treatment of re-rupture
0 wks: Surgical repair
0–2 wks: SLC NWB in gravity equinus
2–4 wks: CAM walker in 20 degrees plantar flexion and crutches
4–8 wks: CAM walker with free plantar flexion and 0 degree dorsiflexion
8 wks: Heel lift or elevated shoe and NWB resistive exercises
12 wks: Resisted calf strengthening
6 mos: Return to sports
The foot should be kept in slight plantar flexion and crutches should be used.
No activity until definitive treatment is under way and cleared by physician.
References
1. Cetti R, Christensen SE, Ejsted R, et al. Operative versus nonoperative treatment of
Achilles tendon rupture. A prospective randomized study and review of the literature. Am J
Sports Med. 1993;21:791–799.
2. Khan RJ. Treatment of acute Achilles tendon ruptures: a meta-analysis. J Bone Joint
Surg Am. 2005;87:2202–2210.
3. Khan RJK, Fick DP, Keogh A, et al. Interventions for treating acute Achilles tendon
ruptures. Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD003674.
DOI: 10.1002/14651858. CD003674.pub3 Accessed 8/31/09.
http://www.cochrane.org/reviews/en/ab003674.html(A)
4. Saleh M, Marshall PD, Senior R, et al. The Sheffield splint for controlled early
mobilisation after rupture of the calcaneal tendon: a prospective, randomised comparison
with plaster treatment. J Bone Joint Surg Br. 1992;74:206–209.
5. Weber M, et al. Nonoperative treatment of acute rupture of the Achilles tendon. Results
of a new protocol and comparison with operative treatment. Am J Sports Med.
2003;31:685–691. (B)
6. Metz R, Verleisdonk EJ, van der Heijden GJ, et al. Acute Achilles tendon rupture:
minimally invasive surgery versus nonoperative treatment with immediate full weightbearing
—a randomized controlled trial. Am J Sports Med. 2008;36:1688–1694.
Additional Reading
Metzl JA, Ahmad CS, Levine WN. The ruptured Achilles tendon: operative and non-operative
treatment options. Curr Rev Musculoskelet Med. 2008;1:161–164.
Codes
ICD9
727.67 Nontraumatic rupture of Achilles tendon
845.09 Other ankle sprain
Clinical Pearls
The literature varies in its reported success and failure rates for both the
surgical and nonsurgical approaches. Physicians need to be aware of both
treatment options and their risks/benefits in order to help their patients make an
informed decision (see “Long-Term Treatment”).
If casting is the treatment choice, typically 4 wks of non-weight-bearing, then 4
wks in an SLWC. After a patient has surgery, use of the CAM walker is
preferred. Earlier mobilization can be utilized with these special braces to
accelerate the healing by decreasing leg edema, increase range of motion, and
restore normal gait pattern to return to functional activity. However, it is best to
discuss surgical treatment approaches with your local orthopedic group to
determine their philosophy (see “Long-Term Treatment”).
ACL Injuries
Suraj A. Achar
Basics
Description
The anterior cruciate ligament (ACL) is a critical stabilizer of the knee.
The ACL provides stability against anterior translation of the knee.
The ACL has 2 important bundles: The posterolateral bundle is tight in extension, whereas
the anteromedial bundle is tight in flexion.
The ACL is a secondary stabilizer of tibial rotation and provides some restraint to varus and
valgus rotation if the primary lateral structures have been disrupted.
ACL tears can occur with trauma or noncontact hyperextension or twisting injuries.
Epidemiology
The ACL is the most commonly injured knee ligament.
An estimated 200,000 ACL injuries occur annually in the U.S.
100,000 ACL reconstructions are performed each year.
The incidence of ACL injury is greater in active adults and children participating in cutting
sports such as basketball, football, skiing, soccer, and gymnastics.
Noncontact ACL tears account for 2/3 of injuries.
Female gender confers higher risk. A meta-analysis in 2007 noted a roughly 3× greater
incidence of ACL tears in female soccer and basketball players versus male athletes. Year-
round female athletes who play soccer and basketball have an ACL tear rate approaching
5%.
Risk Factors
High-risk sports and female gender appear to be the most clear risk factors for ACL injuries:
70% of ACL injuries occur in the high-risk sports, such as football (ie, soccer), American
football, basketball, volleyball, gymnastics, and downhill skiing. Hewson and colleagues
found a 100-fold increase in the incidence of ACL injury in college football players
compared with the general population.
Female risk factors being evaluated include differences in training, different strength-to-
weight ratios, limb alignment, joint laxity, muscle recruitment patterns, and notch index.
Kinematics and electromyography studies suggest that females prepare for landing with
decreased hip and knee flexion, increased quadriceps activation, and decreased hamstring
activation, which may result in increased ACL loading and the risk for noncontact ACL
injury.
Data have shown that ACL laxity does not vary with the menstrual cycle, making hormonal
differences a less likely etiology.
Factors that increase traction have been associated with a higher incidence of ACL tears:
Early studies of artificial turf (“Astroturf”) in the National Football League noted an
increased risk.
Cleats that have a predominant grip on the periphery may also increase the risk, especially
when used with artificial turf.
General Prevention
Neuromuscular training programs:
A meta-analysis of 6 prospective studies demonstrated a significant effect of
neuromuscular training programs on ACL incidence in female athletes (p < .0001). One
potential limitation of the meta-analysis is publication bias. The reviewers noted the
following:
All 3 studies that incorporated high-intensity plyometrics reduced ACL risk, whereas the
studies that failed to use this regimen did not reduce ACL injuries.
Training sessions need to be performed more than once a week.
Duration: Minimum of 6 wks
Plyometrics, balance, and strengthening exercises all need to be incorporated into a
comprehensive training protocol.
A consensus statement issued by the American College of Sports Medicine and the
American Academy of Orthopedic Surgeons supports the use of ACL injury prevention
programs for female athletes.
Bracing:
Bracing has been used to reduce knee injuries in American football for many years. Studies
on the use of prophylactic knee bracing have had mixed results. Early research in the
1980s revealed an increased number of ACL injuries during a prospective period of time
that prophylactic braces were used.
A larger prospective study at West Point showed no difference in overall ACL injuries but
showed a decrease in the severity of knee injuries overall.
As brace technology changes, new studies will be needed to access potential benefits and
risks.
Injuries to the medial and lateral meniscus are commonly associated with an ACL tear.
50% of ACL injuries are associated with meniscal tears.
Chondral and subchondral injuries are often noted.
These associated injuries can be identified on both physical examination and MRI.
Diagnosis
History
Many patients with an ACL tear feel a “pop” in their knee, followed by an acute swelling of
the knee within hours.
According to Noyes and colleagues, in the absence of bony trauma, an immediate effusion is
believed to have a 72% correlation with an ACL injury of some degree.
Symptoms of an ACL-deficient knee include feeling of “giving out” and instability aggravated
by squatting, pivoting, and stepping laterally or bearing the entire body weight when walking
down stairs.
Physical Exam
If evaluated within 12 hrs of an acute injury, the athlete will have difficulty bearing weight and
will have an effusion.
An athlete with an ACL injury likely will have difficulty achieving full knee extension because
the ACL stump gets caught in the notch.
Other causes of loss of range of motion (ROM) are a possible associated bucket-handle
meniscal tear or loose bony fragment.
Examination should begin with inspection to look for an effusion or bony abnormalities.
Palpation of bony structures is important to evaluate for associated tibial plateau fractures or
growth plate injuries in the case of growing adolescents.
Palpation of the joint line is critical to evaluate for meniscal tears or medial collateral ligament
(MCL) injuries.
Valgus stress testing can be of further help in evaluating the MCL.
Specific tests to determine an ACL tear include the Lachman test, the pivot shift, the anterior
drawer test, and the flexion-rotation drawer examination:
The anterior drawer test was found to be only 50% positive, especially if the posterior horn
of the medial meniscus is intact.
The flexion-rotation drawer examination is performed by cradling the calf and flexing the
knee. A posteriorly directed force on the tibia will cause reduction of the tibia as the femur
rotates from an externally rotated position.
The pivot shift test, although useful, is often painful and leads to guarding.
The Lachman test, performed under anesthesia, was 98% accurate in predicting anterior
cruciate injury. The sensitivity of this test decreases with hemarthrosis, guarding, and
experience of the performer but is still reported to have a sensitivity of 87%. One key to
using the Lachman test is to 1st examine the uninjured side for comparison. Patients may
have increased laxity that is not pathologic.
The Lachman test should be the 1st special test performed for evaluation of a possible
ACL-injured athlete. Performance of the test is described below:
Allow the hip to rotate externally, and support the knee in slight flexion to facilitate
relaxation.
One hand should firmly grasp the femur, while the other is positioned below the joint,
grasping the tibia to allow anterior translation.
The knee should be flexed around 20–30 degrees.
A quick, firm motion pulling the tibia anteriorly while stabilizing the femur should be
performed.
The examiner will appreciate the degree of translation and quality of endpoint.
A soft endpoint has a greater specificity for a positive ACL tear.
It is more important to interpret the Lachman test as positive or negative rather than to
quantify the degree of laxity.

Imaging
Standard radiography:
Plain radiography should be performed on all patients suspected of acute ACL tears
because of the risk of fractures.
X-ray studies have a pivotal role in the evaluation of adolescents and children because of
the risk of growth plate fractures and tibial spine fractures.
In children, plain x-rays should be performed before aggressive maneuvers are performed,
especially in the case of decreased active ROM or tenderness at the distal femoral physis.
X-rays should include anteroposterior (AP), lateral, and oblique views to better visualize
fractures.
Advanced imaging:
MRI should be used to evaluate for other concomitant injuries and, in some cases, either to
confirm the diagnosis or help to plan surgery.
The surgical consent and plan will depend on associated injuries, such as meniscal or MCL
injuries.
MRI, if used for evaluation of a presumed ACL tear, should be non-contrast-enhanced.
The accuracy and sensitivity of MRI are excellent when compared with arthroscopic
findings.
US is another modality that can be used to assess the ACL. Research in Europe and
Australia shows US to have 88–91% sensitivity and 98–100% specificity when used to
detect rupture of the ACL.
Sonography is a useful and inexpensive method of detecting the presence of rupture of the
ACL in the clinical setting of a traumatic hemarthrosis.
Sonography has limited use in the US owing the widespread use of MRI in this setting.
Treatment
Most patients who sustain an ACL injury are active in some type of sports.
Expectations after injury vary, however, based on age and activity.
Reconstruction is an elective procedure for most individuals. Many can
maintain an active lifestyle with an ACL-deficient knee. High-level athletes and
the young do the worst without surgery and have frequent episodes of
instability.
The adolescent with open growth plates poses a significant challenge. There is
some concern about damaging the growth plates in adolescents with tunnels.
However, studies are ongoing, and more procedures on adolescents to
reconstruct the ACL are being performed.
To date, there is a lack of evidence to support a protective role of
reconstructive surgery of the ACL against osteoarthritis development. At 10–
20 yrs, 50% of those diagnosed with an ACL tear have osteoarthritis and
functional impairment—“the young patient with an old knee.”
No studies have shown that bracing an ACL-deficient knee will prevent
episodes of instability when an athlete returns to cutting and pivoting sports.
The data on bracing do show a decrease in anterior tibial translation at low
levels of force. Activity modification provides the best method outside of
surgery to prevent “giving way” episodes. If an athlete attains and maintains full
ROM and at least 90% strength of the contralateral lower extremity, low-risk
sports such as running, bicycling, and swimming can be performed.
Daniels and colleagues found that an athlete's inability to return to sports
determines whether that athlete elects surgery. KT-1000 measurements of
more than 5 mm have been shown in some studies to predict instability and the
need for surgery. A positive pivot-shift test at 3 mos after injury in an awake
patient is a strong predictor of the future need for reconstruction. Dynamic
functional testing (a series of hopping tests) may be a useful adjunct to predict
who may be a “coper” and can continue nonoperative treatment.
Operative treatment: The procedure selected for ACL reconstruction must
restore normal stability and full ROM. Primary ACL suturing does not restore
stability and has been abandoned. One exception to primary repair is a bony
avulsion, seen mostly in adolescents.
Graft selection:
Autogenous tissue:
Patellar tendon (with bone attached both proximally and distally)
Hamstring tendons
Allograft tissue: The use of synthetic materials such as Dacron and Gore-
Tex has been abandoned because of long-term failure and complications
secondary to wear of the material.
Patellar tendon autograft: The patellar tendon autograft is an example of bone-
to-bone ACL reconstruction and has been used more for high-demand
athletes. Of all the procedures, it appears to have the least laxity on KT-1000
testing on follow-up. The potential bone-to-bone fixation promotes earlier graft
fixation. Long-term follow-up shows no difference in return to full participation
for either autograft procedure.
Hamstring tendon autograft: The hamstring graft has several advantages. Use
of the hamstring tendon avoids patellar tendon morbidity. As of 2001, studies
have shown a decrease in anterior knee pain among those who undergo a
hamstring autograft compared with those undergoing bone-to-bone fixation
(relative risk 0.49, 95% confidence interval 0.32–0.76, p = .001, I2 = 0%).
Hamstring donor-site pain heals within 3 mos.
New techniques that go beyond the scope of this chapter, including double-
bundle reconstruction, yield even greater stability.
Allografts: Allografts are used commonly for ACL reconstruction. These are
often employed as 2nd-option surgeries in those who have already had a
hamstring or bone-to-bone patellar graft.
The risks of infection are extremely low. The benefits of decreased surgical
morbidity and easier rehabilitation must be weighed against the potential for
greater failure of biologic incorporation, infection, and possibly slower return
to activities.
The overall risk of infection is extremely low because donors are tested and
the grafts are irradiated.
Significant bacterial infections occur in fewer than 1%, and no reports of HIV
or hepatitis transmission have occurred after 2002.
Perhaps the newest and most concerning risk of allograft use is bone
resorption noted on follow-up.
The significance of this resorption has yet to be completely understood.
New data now suggest increased failure rates with allografts compared with
hamstring tendon or patellar tendon autografts.
Timing of surgery:
The timing of surgery is controversial because some surgeons perform
surgery at the site where patients are injured, ie, the ski area.
Negative outcomes, especially arthrofibrosis, are not directly associated with
surgical timing but rather with signs of inflammation marked by periarticular
swelling, effusion, and hyperthermia.
Other factors that predict arthrofibrosis include decreased ROM and
perioperative pain.
Surgery should be delayed until these factors are improved.
Early surgery is absolutely indicated only in bony avulsions.
Graft placement:
Placement of the grafts is critical because the ACL performs a role in
rotatory stability and with valgus torque.
Double-tunnel ACL reconstructions have been postulated to improve this
stability, but the early results are limited to animals.
Ongoing research may lead to improved placement of the graft and potential
use of multiple bundles.
Ongoing Care
Patients are now returning to activity sooner after reconstruction. Return to sport
depends more on strength and proprioception than on time from surgery. Usual return to
sport may fall between 6 and 12 mos or longer after surgery. Early return prior to full
proprioception and strength may lead to prolonged instability and possible reinjury.
Therapy protocols may be divided into 4 categories, as per Shelbourne and Nitz:
Phase 1: Preoperative; maintain ROM.
Phase 2 (0–2 wks): Achieve full extension; maintain quadriceps strength, reduce swelling,
and achieve flexion to 90 degrees.
Phase 3 (3–5 wks): Maintain full extension and increase flexion up to full ROM; stair
climbers and exercycles may be used.
Phase 4 (6 wks–9 mos): Increase strength and agility; progressive return to sports.
The use of custom ACL bracing has also been controversial. A systemic review of several
randomized, controlled trials (level I evidence, 12 trials) found no evidence that pain, ROM,
graft stability, or protection from subsequent injury was affected by postoperative bracing.
If arthrofibrosis is evident after surgery, early surgical intervention (<1 yr) improves the
outcome.
Full ROM should be achieved to prevent degenerative joint disease.
Prognosis
Most patients with ACL injuries do well with activities of daily living even after follow-up in the
range of 5–15 yrs. Most can participate in some sports activity if they are inclined to do so,
but most will have some limitations in vigorous sports, and only a few will be entirely
asymptomatic.
The presence of clinically significant chondral and meniscal injuries that occur at the time of
injury or after injury determines long-term prognosis more than the ACL injury itself. Over
time, the prevalence of meniscal injuries increase, leading to increasing disability, surgery,
and arthrosis in high-risk patients.
Ligament reconstruction has not been shown to prevent arthrosis, but in prospective studies,
it appears to reduce the risk of subsequent meniscal injury, to improve passive AP knee
motion limits, and to facilitate return to high-level sporting activities.
Additional Reading
Chappell JD, Creighton RA, Giuliani C, et al. Kinematics and electromyography of landing
preparation in vertical stop-jump: risks for noncontact anterior cruciate ligament injury. Am J
Sports Med. 2006;36:e3.
Daniel DM, Malcom LL, Losse G, et al. Instrumented measurement of anterior laxity of the
knee. J Bone Joint Surg Am. 1985;67:720–726.
Daniel DM, Stone ML, Dobson BE, et al. Fate of the ACL-injured patient. A prospective
outcome study. Am J Sports Med. 1994;22:632–644.
Fithian DC, Paxton LW, Goltz DH. Fate of the anterior cruciate ligament-injured knee.
Orthop Clin North Am. 2002;33:621–636, v.
Guelich DR, Lowe WR, Wilson B. The routine culture of allograft tissue in anterior cruciate
ligament reconstruction. Am J Sports Med. 2007;35:1495–1499.
Hewett TE, Ford KR, Myer GD. Anterior cruciate ligament injuries in female athletes: part 2,
a meta-analysis of neuromuscular interventions aimed at injury prevention. Am J Sports
Med. 2006;34:490–498.
Hewson GF, Mendini RA, Wang JB. Prophylactic knee bracing in college football. Am J
Sports Med. 1986;14:262–266.
Huston LJ, Greenfield ML, Wojtys EM. Anterior cruciate ligament injuries in the female
athlete. Potential risk factors. Clin Orthop Relat Res. 2000;372:50–63.
Kostogiannis I, Ageberg E, Neuman P, et al. Clinically assessed knee joint laxity as a

predictor for reconstruction after an anterior cruciate ligament injury: a prospective study of
100 patients treated with activity modification and rehabilitation. Am J Sports Med.
2008;36:1528–1533.
Lohmander LS, Englund PM, Dahl LL, et al. The long-term consequence of anterior cruciate
ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35:1756–1769.
Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and
outcome. Arch Orthop Trauma Surg. 2004;124:518–522.
Miller SL, Gladstone JN. Graft selection in anterior cruciate ligament reconstruction. Orthop
Clin North Am. 2002;33:675–683.
Noyes FR, Bassett RW, Grood ES, et al. Arthroscopy in acute traumatic hemarthrosis of
the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am.
1980;62:687–695, 757.
Poolman RW, Farrokhyar F, Bhandari M. Hamstring tendon autograft better than bone
patellar tendon bone autograft in ACL reconstruction: a cumulative meta-analysis and
clinically relevant sensitivity analysis applied to a previously published analysis. Acta Orthop.
2007;78:350–354.
Prodromos CC, Han Y, Rogowski J, et al. A meta-analysis of the incidence of anterior
cruciate ligament tears as a function of gender, sport, and a knee injury-reduction regimen.
Arthroscopy. 2007;23:1320–1325.e6.
Ptasznik R, Feller J, Bartlett J, et al. The value of sonography in the diagnosis of traumatic
rupture of the anterior cruciate ligament of the knee. AJR Am J Roentgenol.
1995;164:1461–1463.
Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in college football. Am J Sports
Med. 1987;15:111–116.
Shelbourne KD, Nitz P. Accelerated rehabilitation after anterior cruciate ligament

reconstruction. Am J Sports Med. 1990;18:292–299.
Sitler M, Ryan J, Hopkinson W, et al. The efficacy of a prophylactic knee brace to reduce
knee injuries in football. A prospective, randomized study at West Point. Am J Sports Med.
1990;18:310–315.
Up-to-date
Wright RW, Fetzer GB. Bracing after ACL reconstruction: a systematic review. Clin Orthop
Relat Res. 2007;455:162–168.
Codes
ICD9
717.83 Old disruption of anterior cruciate ligament
844.2 Sprain of cruciate ligament of knee
Clinical Pearls
Nearly all patients with an acute ACL tear have an effusion.
Noncontact injuries account for the majority of ACL tears.
ACL Tear: Management in Skeletally Immature
Athletes
Holly J. Benjamin
Michael Ladewski
Basics
Description
Injury sustained by known mechanism that leads to instability with significant effect on the
athlete's ability to perform at the highest levels of sport
Considerable controversy exists regarding treatment in the skeletally immature population.
Epidemiology
Higher incidence in female basketball and soccer players than in their male counterparts
The higher incidence in females is thought to be due to differences in biomechanics, joint
laxity, hormonal influences, intercondylar notch dimensions, and ligament size.
Other sports associated with anterior cruciate ligament (ACL) injury are skiing and football.
Incidence
16/1,000 high school athletes annually
38,000 high school students yearly
General Prevention
Neuromuscular balance training and core strengthening have been shown to decrease the
incidence in female athletes.
Etiology
Midsubstance tear most common
Tibial spine avulsion fracture more frequent in the skeletally immature athletes
Femoral ACL avulsion fractures are rare causes of ACL injury.
Mechanisms of injury:
Hyperextension, sudden deceleration, or a valgus and rotator force with a planted foot
External rotation of the femur on a fixed tibia combined with a valgus load often the result
of a noncontact pivoting injury
Bone bruise: Lateral compartment more than medial compartment
Meniscus tears: Lateral more commonly in acute knee injury; medial more common in athlete
with chronic ACL deficiency
Associated medial meniscus tears and medial collateral ligament injury in patient with valgus
stress mechanism
Diagnosis
History
May be a “pop” sensation at the time of injury
Effusion usually develops acutely.
Athlete unable to continue play
Instability of knee after injury
Physical Exam
It can be difficult to perform an accurate physical exam after significant hemarthrosis
develops.
Ecchymosis and loss of normal knee contour secondary to effusion are often present.
The Lachman test is the most sensitive physical examination test and is the “gold standard”
for diagnosis.
Anterior drawer and pivot-shift tests are positive but are less sensitive tests.
Palpate the distal femur and proximal tibia physes for tenderness.
Tenderness at the ends of long bones is a fracture until proven otherwise in skeletally
immature patients.

Imaging
Knee radiographs to rule out tibial spine avulsion fracture, physeal fractures, Segond
fracture, and osteochondral fractures
MRI to evaluate ACL and concomitant meniscal, posterior cruciate ligament, collateral
ligament, and chondral injuries:
95% sensitivity and 88% specificity when correlated with arthroscopic findings
Tear imaging shows increased signal intensity with a disrupted pattern.
May have a higher false-positive rate in adolescents
Consider wrist x-rays to assess bone age, which may influence surgical approach.
Diagnostic Procedures/Surgery
Diagnostic arthroscopy is sometimes required when physical exam and imaging studies are
equivocal.
KT-1000 device may be helpful in quantifying relative ACL laxity.
Tibial spine avulsion fractures
Physeal fractures of the distal femur or proximal tibia
Meniscal injury
Patellar subluxation
Other ligamentous injury of the knee
Treatment
Compression
Ice
Pain management
Weight bearing as tolerated unless physeal fracture is suspected
Therapeutic aspiration is rarely performed on the hemarthrosis.
If fat is noted in the hemarthrosis, then a fracture is present.
Nonoperative therapy may be considered depending on physical demands and
age of athlete.
Not a definitive treatment choice owing to risk of recurrent instability and further
meniscal damage
Bracing with derotational ACL-stabilizing brace does not restore stability when
athlete returns to high-demand sport.
Restoration of range of motion
Strengthening quadriceps and hamstrings
Activity modification
May be recommended if ACL reconstruction delayed owing to skeletal
immaturity
Controversy related to approach and risk for early physeal closure:
Related to skeletal maturity
Undertaken only after restoration of range of motion (ROM)
Acute repair not proven to be successful
Considered with unsuccessful nonoperative treatment, high-level adolescent
athlete
Associated meniscal tear an indication for surgical treatment
Options include physeal sparing and partial or complete transphyseal
reconstructions.
Ongoing Care
Patients with suspected ACL injuries should be referred to an orthopedic or sports medicine
specialist.
Preference would include specialist with experience in surgical approaches in the skeletally
immature athlete.
Prognosis
Typical postoperative recovery and rehabilitation period is usually 9–12 mos.
Up to 78% risk of radiographic evident osteoarthritis within 14 yrs of injury ± surgery.
Natural history of the ACL-deficient knee is chronic instability, chondral injury, subsequent
meniscal pathology, pain, and joint arthrosis.
Complications
Associated medial collateral ligament (MCL) and meniscal injuries
Surgical complications:
Graft failure
Premature physeal closure
Slow recovery in ROM
Usual risks of infection and anesthesia
Additional Reading
Fehnel DJ, Johnson R. Anterior cruciate injuries in the skeletally immature
athlete: a review of treatment outcomes. Sports Med. 2000;29:51–63.
Murray MM. Current status and potential of primary ACL repair. Clin Sports
Med. 2009;28:51–61.
Schachter AK, Rokito AS. ACL injuries in the skeletally immature patient.
Orthopedics. 2007;30:365–370; quiz 371–372.
Siow HM, Cameron DB, Ganley TJ. Acute knee injuries in skeletally immature
athletes. Phys Med Rehabil Clin N Am. 2008;19:319–345, ix.
Codes
ICD9
Clinical Pearls
Injury that is increasing in incidence in the adolescent population
Surgical therapies vary in their approach and timing.
Type of ACL reconstruction and timing of surgery in the skeletally immature
athletic population are extremely controversial, and cases should be decided
on an individual basis.
Acromioclavicular Separations (Types 1–6)
Anne S. Boyd
Shannon Woods
Basics
Separation of the clavicle and acromion due to injury of the acromioclavicular (AC) and
coracoclavicular (CC) ligaments
Classified based on the degree of separation and the anatomical structures that are involved
(types I–VI)
AC ligament is the main static stabilizing force for the AC joint in the anterior-posterior
direction:
This ligament blends with the trapezius and deltoid fascia to form the AC capsule and
provide static stability to the joint (1).
CC ligament is the main static stabilizing force for the AC joint in the superior and inferior
direction:
This ligament comprises the trapezoid and conoid ligaments (2).
Synonym(s): Shoulder separation; Shoulder sprain; AC sprain; AC dislocation; Shoulder
dislocation (misname; term primarily refers to glenohumeral dislocation)
Description
Type I:
Mild sprain of the AC ligament, some fiber disruption
Position of clavicle: No change
Type II:
Complete tear of the AC ligament with an intact CC ligament
Position of clavicle: Slight subluxation of the AC joint
Type III:
Complete AC and CC ligament tear
Position of clavicle: 100% AC joint dislocation in a superior direction, representing 25–
100% increase in coracoclavicular separation vs the noninvolved side
Type IV:
Clavicle displaced posteriorly into trapezius
Deltoid and trapezius detached
Axillary view on radiographs reveals injury extent
Surgical referral immediately
Type V:
Position of clavicle: Also thought of as a large type III, there is 100–300% change in CC
separation and may see disruption of the deltoid and trapezius attachments to the clavicle
Type VI:
Position of clavicle: 100% inferior AC joint displacement, usually with distal clavicle wedged
underneath coracoid process. There is potential damage to the underlying brachial plexus
and subclavian vessels.
Epidemiology
Direct trauma to an unprotected shoulder, such as when tackling an opponent without
shoulder pads
Falling directly upon the “point” of shoulder, such as when diving for a baseball
Upward indirect force, fall on outstretched hand, force directed cranially through humeral
head to AC joint
Downward indirect force, sudden change in load through upper extremity, usually heavier
weight
Incidence
Males are 5 times more likely to suffer injuries than females.
Nearly 45% of all AC dislocations occur to individuals in their 20s.
Type I and II injuries account for the majority of AC dislocations.

Fracture injuries are associated with a type III–V AC dislocation in 5% of patients (3).
Intra-articular injuries are associated with a type III–V AC dislocation in 18% of patients:
Shoulder labrum/SLAP tears reported in 5–14% (3).
Rotator cuff tears reported in 4% (3).
Diagnosis
History
Exact mechanism of injury (to assess the severity of the injury and the possibility of
associated injuries)
Neurologic symptoms or vascular symptoms (which indicate a more severe injury and may
require immediate surgery)
Physical Exam
Pain at the AC joint
Pain during forward flexion and/or adduction of the shoulder, over shoulder motions, direct
weight-bearing, abduction of shoulder
Deformity (step-off) of AC joint with type III injuries and higher
Inspection (asymmetry of the shoulders)
Palpation (point tenderness of the affected AC joint) (2)
Range of motion decrease due to pain adduction > abduction > flexion
Crossover or scarf test: Flexion of shoulder to 90 degrees and forced adduction across chest
to reproduce pain over the AC joint (2)
Careful neurovascular examination

Imaging
True shoulder anteroposterior (AP), scapular Y, and axillary views are the standard views for
the shoulder:
Zanca views of both shoulders (try to get on same cassette): To identify fractures of the
clavicle, acromion, or coracoid, and to preliminarily evaluate AC joint separation and CC
ligament disruption (2)
Axillary lateral view helps to distinguish a type III dislocation from a type IV. A type IV will
show the scapula anterior to the clavicle. Many patients may be unable to tolerate this
view, and a computed tomography scan may be required (2).
Zanca view: An AP of the shoulder with the central beam directed 10–15 degrees cephalad
towards the clavicle, and with slightly reduced penetration (since the AC joint is superficial
and will be overpenetrated with regular beam strength).
Stress views (weighted views) can be used to differentiate types I–III, but are not
recommended, as the results do not affect treatment, and disruption of the CC ligament
(larger space between coracoid and clavicle on the affected side) can be seen on the
standard AP.
Stryker notch views to assess for coracoid fracture when indicated (2)
The average distance between the inferior aspect of the clavicle and the coracoid is 1.1–1.3
cm. This value can vary, so it is important to compare to the unaffected side.
CT scan may be required to assess for other bony injuries not well visualized on plain
radiographs.
Magnetic resonance imaging (MRI) may be utilized to assess for concomitant soft tissue
injuries, especially in older patients or those with systemic ailments that may make the
patient at increased risk, such as diabetes.
Rarely is an injection required to confirm diagnosis.
Fractures of the coracoid, acromion, or clavicle
Rotator cuff injuries
SLAP/shoulder labrum lesion
Glenohumeral dislocation
Burner/stinger (neurogenic)
Cervical spine injuries
Pneumothorax (rare)
Gorhams massive osteolysis
Gout
Neoplasm (multiple myeloma)
Treatment
Types I and II:
Shoulder sling for several days (average of 3–7 days) for pain reduction and
comfort
Ice and analgesics for pain and swelling:
Generally, fewer than 1–2 wks of analgesia are needed.
Range of motion exercises early in course; the sooner the better (4).
Rotator cuff, scapular stabilization, and trunk strengthening exercises as pain
resolves
Type III:
Dependent upon patient usage/expectations: Nonsurgical vs surgical repair.
Studies indicate good outcome with nonsurgical management, as detailed
under types I and II:
80% of individuals are subjectively satisfied with their nonoperative
outcomes based on pain and function.
Some strength loss might occur after injury, particularly with bench press.
Some evidence to suggest less strength loss with operative treatment (4).
Consider surgical referral, particularly in throwers, heavy manual laborers,
high-level athletes, patients unwilling to tolerate cosmetic deformity, and those
who fail nonoperative management (4).
Types IV–VI:
Surgical referral
Types I and II: Shoulder range of motion and strengthening exercise are
introduced as pain subsides. Full return to contact when full, painless range of
motion and normal strength resumes.
Type III: Shoulder strengthening exercises are introduced when range of
motion and pain are improved. Return to contact sports usually is anticipated in
6 wks–6 mos, depending on resumption of full painless range of motion and
normal strength.
Types IV–VI usually require operative treatment.
Ongoing Care
Type IV–VI refer to orthopedics.
Refer type III in high-level athletes, patients unwilling to have conservative therapy, heavy
manual laborers, patients unwilling to tolerate the deformity, and patients who have failed
nonoperative treatment after 3–6 mos
Prognosis
Reports suggest that up to 40% of individuals with type I or II injures will go on to develop
osteoarthritis at the AC joint (1).
Complications
Cosmetic deformity and AC joint arthritis are common complications.
Many patients note intermittent pain and/or clicking, often referred to as
nuisance symptoms. These symptoms may require an injection or further
physical therapy.
Rarely, distal clavicle osteolysis may occur.
References
1. Rudzki JR, Matava MJ, Paletta GA. Complications of treatment of
acromioclavicular and sternoclavicular joint injuries. Clin Sports Med.
2003;22:387–405.
2. Mazzocca AD, Arciero RA, Bicos J. Evaluation and treatment of

acromioclavicular joint injuries. Am J Sports Med. 2007;35:316–329.
3. Tischer T, Salzmann GM, El-Azab H, et al. Incidence of associated injuries

with acute acromioclavicular joint dislocations types III through V. Am J Sports
Med. 2008;37:136–139.
4. Buss DD, Watts JD. Acromioclavicular injuries in the throwing athlete. Clin
Sports Med. 2003;22:327–341, vii.
Codes
ICD9
831.04 Closed dislocation of acromioclavicular (joint)
Clinical Pearls
In general, full return to contact sports is possible when painless range of
motion and normal strength are achieved. However, type I sprains are stable,
so the athlete may return immediately if strength is normal and pain is tolerable
and will not limit his athletic abilities.
Cosmetic deformity and AC joint arthritis are common complications.
Adductor Thigh Strain
K. Michele Kirk
Brian Lindenmayer
Sebastian Ksionski
Basics
Description
Medial thigh/adductor pain and weakness resulting from injury to muscle
Usually adductor longus muscle, but may include gracilis, iliopsoas, rectus femoris, or
sartorius
Synonym(s): Groin strain; Pulled groin
Epidemiology
Most common cause of groin pain in athletes, but symptoms overlap with a wide differential.
Risk Factors
Eccentric loading of muscle (muscle is passively being stretched while it is contracting) is
usual mechanism of injury.
Inactive or fatigued muscles have less ability to absorb energy and are more likely to
undergo acute strain.
Diagnosis
History
Acutely, often a stretch injury with an abrupt cutting motion as in slide tackling in soccer (1),
or straddling injury as in gymnastics, cheerleading, or horseback riding
Also can result from overuse, as in skating or rollerblading
May have only minor discomfort with walking, but pain and weakness develop with cutting or
running
If symptoms do not respond to initial therapy, need to consider other diagnoses.
Physical Exam
Classic triad of tenderness to palpation in the muscle and its insertion, pain with passive
stretching, and pain with resisted contraction
Usually acute episode is noted, but symptoms may become chronic after initial injury if
undertreated and repeatedly strained.
Tenderness along proximal 1/3 of medial thigh and tendinous origin in pubic region
Pain with passive abduction
Pain with resisted adduction
Swelling and ecchymosis increase suspicion for tear
With complete rupture, palpable depression and knot of torn muscle may be present.

Imaging
Generally not necessary in straightforward cases, but may be part of workup if appropriate
Hip and pelvis films recommended to rule out other conditions (1,2)
Musculoskeletal US to evaluate for tendon fiber discontinuity or hematoma if there is a
palpable mass (1,2)
Bone scan if stress fracture suspected
Osteitis pubis
Stress fracture of femoral neck or pubic ramus
Iliopsoas bursitis
Avascular necrosis of femoral head
Groin disruption (aka, sports hernia, Gilmore's groin, athletic pubalgia)
Myositis ossificans
Adductor tendinitis
Avulsion fracture (especially in an adolescent)
Slipped capital femoral epiphysis (usually seen in early teens)
Inguinal hernia
Lymphadenopathy
Nerve entrapment, specifically obturator nerve (2)
Referred pain from spine or genitourinary tract
Conjoined tendon lesions (2)
Treatment
OTC analgesics usually are sufficient.
Some sources recommend avoiding nonsteroidal anti-inflammatory drugs with
antiplatelet properties to help prevent bleeding into tissue.
Topical anesthetics
Muscle relaxants may provide some benefit.
Strict immobilization generally is not recommended, and rehabilitation should be
initiated early in the 1st few days.
Limited activity as tolerated for 1–2 wks; longer for more protracted cases
Gentle compression with compression shorts, Neoprene sleeve, or elastic
wrap
For severe, incomplete tears, crutches for walking while symptomatic with
ambulation
Additional Treatment P.
Ice for 20 min every 2–3 hrs for the 1st 2–3 days.
Heat may be added after 2–3 days.
Gentle stretching exercises may be instituted after the 1st few days.
Gentle (pain-free) stretching and low-intensity isotonic strengthening can be
instituted as symptoms subside (3,4)
Progress to active strength training and stretching (3,4). Balance
training/proprioceptive exercises of hip and groin musculature.
If full flexibility and pain-free, may increase to full loading (2,5)
Physical therapy modalities, such as US or electrical stimulation, may benefit in
more chronic cases.
Correction of predisposing factors, such as muscle tightness, weakness, or
imbalance, should be addressed.
Adequate stretching and warmup may help prevent reinjury.
Surgical repair may be required for complete avulsion from the femur.
Early repair is generally recommended.
Ongoing Care
Except for significant tears, referral to a specialist generally is not necessary unless another
diagnosis is being considered and requires evaluation.
References
1. Gilmore J. Groin pain in the soccer athlete: fact, fiction, and treatment. Clin Sports Med.
1998;17:787–793, vii.
2. Lacroix VJ. A complete approach to groin pain. Physician Sports Med. 2000;28(1):online.
3. Ruane JJ, Rossi TA. When groin pain is more than “just a strain.” Physician Sports Med.
1998;26(4):online.
4. Anderson M, Hall S, Martin M. Foundations of Athletic Training Prevention, Assessment

and Management. 2005:475–477.
5. Sim FH, Nicholas JA, Hershman EB. The Lower Extremity and Spine in Sports Medicine.
St. Louis: Mosby, 1995.
Additional Reading
Johnson D, Mair S. Adductor strain. Clin Sports Med. 2006:659.
Fry B, Brunner R. Adductor strain. http://emedicine.medscape.com/article/307308-overview.

February 21, 2007.
Macleod DA, Gibbon WW. The sportsman's groin. Br J Surg. 1999:86(7):849–850.
Dahan R. Rehabilitation of muscle tendon injuries to the hip, pelvis, and groin. Vol 5.
1997:326–333.
Baha R, Machlum S. Clin Guide Sports Injur. 2004:266–268.
Garrett WE. Muscle strain injuries. Am J Sports Med. 1996;24:S2–S8.
Codes
ICD9
843.8 Sprain of other specified sites of hip and thigh
Clinical Pearls
Decision on return to play depends on extent of injury and underlying
predisposing factors. Pain is usually a fair measure, so unrestricted play is
generally permitted if pain-free, which may take weeks.
Although initial symptoms may not be debilitating enough to impair performance,
pain is a marker for injury. Left untreated condition can become chronic and
ultimately take longer to rehabilitate.
Adhesive Capsulitis
Yvonne Chow
Natasha Harrison
Rahul Kapur
Basics
Description
Commonly known as “frozen shoulder”
Painful restriction of glenohumeral joint range of motion
Caused by thickening and contraction of shoulder capsule
Classified into 2 categories:
Primary, which has an insidious idiopathic onset with no precipitating event
Secondary, which follows trauma, immobilization, or underlying systemic illness
Epidemiology
Slight predominance in females (1.4:1)
Mean age of onset is 55 yrs of age.
15% experience bilateral disease.
Prevalence
2–3% of the general population; prevalence is 11% in patients with diabetes mellitus.
Risk Factors
Shoulder immobilization increases risk by 5–9× over the general population.
Diabetes mellitus: 40% lifetime risk in type 1 diabetics
Hyperthyroidism
Hypertriglyceridemia
Female gender
Age >40 yrs old
General Prevention
Avoidance of prolonged shoulder immobilization
Etiology
Exact pathophysiology of condition is unclear.
Increasing evidence suggests the process involves synovial inflammation with subsequent
reactive fibrosis.
Initial synovial inflammation causes pain.
Resultant capsular fibrosis restricts range of motion (ROM).
Generally idiopathic
Can result from period of shoulder immobilization
Rarely, also arises from clinically significant trauma to shoulder, cervical radiculopathy,
brachial plexus pathology, or rotator cuff tendonitis
Autoimmune theory of disease: Microvascular disease causes abnormal collagen repair,
leading to capsular fibrosis.

Diabetes
Hyperthyroidism
Hypertriglyceridemia
Cervical spondylosis
Diagnosis
History
Progressive shoulder pain over weeks to mos. Patients will tend to have symptoms of pain
and stiffness for weeks to months prior to presentation to a physician.
Pain worse with any shoulder movement, both active and passive. Pain is worse at night and
may interfere with sleep. Pain usually is present in the region of the deltoid, but also may
radiate into the upper arm and neck regions.
Common functional impairments include difficulty dressing, combing one's hair, reaching into
one's back pocket for a wallet, or fastening a brassiere.
A careful medical history to exclude associated conditions should be conducted.
3 clinical phases:
Phase 1: Painful phase, insidious onset of nocturnal pain, progresses to pain at rest, no
restriction of ROM, may last 2–9 mos
Phase 2: Frozen or adhesive phase, progressive limitation of ROM in all directions, lasts
3–9 mos or longer
Phase 3: Thawing or regressive phase, symptoms gradually improve over 12–24 mos
Physical Exam
The hallmark of adhesive capsulitis is a decreased glenohumeral range of motion associated
with pain. The loss of motion occurs earliest in external rotation, but later in the disease
course, all ranges of motion are affected.
Observation usually reveals limited use of the limb and lack of arm swing in walking.
Pain at extremes of ROM may be the only finding in the early phase. The greatest limitation
is usually seen in external rotation initially. In later stages, all ranges of motion usually are
limited. The loss of motion commonly occurs in the following order: external rotation →
abduction → internal rotation → forward flexion
There is a limitation of both active and passive ROM.
Active ROM may show inverted scapulothoracic motion to compensate.
Impingement (Neer, Hawkins) and biceps tendinopathy (Speed's) maneuvers may be
positive.
The scapula usually is elevated, laterally placed, and protracted. Wasting of the shoulder
girdle muscles may be present due to disuse atrophy.

Lab
None indicated, but may consider thyroid-stimulating hormone, glucose, triglycerides if patient
presents with bilateral symptoms or is <45 yrs of age.
Imaging
No imaging is indicated, as the diagnosis primarily is clinical.
Radiographs are useful to assess the presence of alternate diagnoses. No specific findings
on radiographs correlating with a diagnosis of adhesive capsulitis have been reported, though
there may be periarticular osteopenia as a result of disuse.
Arthrography has been described as sensitive in making the diagnosis where the joint capsule
volume is decreased 5–10 mL in comparison to 25–30 mL in a normal joint. However, a loss
of volume of the shoulder capsule is not always present, and the test carries risks that have
led some authors to recommend avoiding its use in diagnosis.
MRI may reveal slight thickening in the joint capsule and the coracohumeral ligament.
Rotator cuff disease
Impingement syndrome
Biceps tendinopathy
Posterior shoulder dislocation
Arthritis/degenerative arthrosis of the glenohumeral joint
Cervical radiculopathy
Polymyalgia rheumatica
Fracture of the humerus or glenoid
Referred pain from the cervical spine, thorax, or abdomen
Treatment
A high rate of spontaneous recovery within 18–30 mos for this condition
should be kept in mind when choosing treatment options. Treatment should be
focused on relief of symptoms and optimization of ranges of motion.
NSAIDs can be used, if tolerated, to aid with pain control in the initial painful
phase.
Distention with saline and steroid can reduce pain and improve ROM and
function in the short-term. At 2 yrs of follow-up, distention was as effective as
manipulation under anesthesia (MUA) without the risks associated with MUA.
Oral steroids also can provide short-term benefits in pain relief and improved
ROM and function. However, oral steroids have side effects that limit the
patient population for which they can be used.
Intra-articular corticosteroid injections have been shown to decrease pain,
improve function, and increase ROM. Multiple injections have been shown to
be beneficial, specifically up to 3 injections within a 16-wk period. There is a
theoretical risk of weakening ligaments, tendons, and/or other capsular
structures with repetitive cortisone injections though.
A program of therapeutic exercise comprising gentle range of motion
exercises, stretching, and graded resistance training has been associated with
increased range of motion and decreased pain. The program should be guided
by the patient within the limits of his or her pain, and vigorous programs that
increase symptoms should be avoided.
Suprascapular nerve blocks may decrease pain.
Manipulation under anesthesia is recommended if conservative measures fail.
Surgical capsular release also may be utilized for refractory cases.
Additional Reading
Buchbinder R, Green S, Youd JM, et al. Arthrographic distension for adhesive
capsulitis (frozen shoulder). Cochrane Database Syst Rev. 2008;
(1):CD007005.
Buchbinder R, Green S, Youd JM, et al. Oral steroids for adhesive capsulitis.
Cochrane Database Syst Rev. 2006:CD006189.
Dias R, Cutts S, Massoud S. Frozen shoulder. BMJ. 2005;331:1453–1456.
Jacobs LG, Smith MG, Khan SA, et al. Manipulation or intra-articular steroids
in the management of adhesive capsulitis of the shoulder? A prospective
randomized trial. J Shoulder Elbow Surg. 2009;18:348–353.
Shah N, Lewis M. Shoulder adhesive capsulitis: systematic review of

randomised trials using multiple corticosteroid injections. Br J Gen Pract.
2007;57:662–667.
Codes
ICD9
726.0 Adhesive capsulitis of shoulder
Anaphylaxis
Kristina M. Wilson
Basics
The causative agent in anaphylaxis remains unknown in up to 1/3 of cases.
Food is the most common causative agent (about 1/3 of known cases) in children.
Pharmacotherapeutic agents are the most common cause in adults.
Other common causes include Hymenoptera stings and latex.
Key to management and treatment is early recognition and immediate initiation of appropriate
medical therapy.
Epinephrine is the undisputed initial therapy for anaphylaxis, and its administration never
should be delayed.
Failure to inject epinephrine promptly has been identified as the most important factor
contributing to death in patients experiencing anaphylaxis.
Description
Serious allergic reaction that is rapid in onset and may cause death
A systemic condition caused by an IgE-mediated reaction that is often life-threatening and
almost always unanticipated:
Involves the respiratory and/or cardiovascular systems
Patients may have a history of less severe reaction previously on exposure to relevant
allergen.
Exercise-induced anaphylaxis (EIAn):
Occurs in response to physical exertion
Subset of patients must have associated food trigger—food-dependent exercise-induced
anaphylaxis (FDEIAn).
Cold urticaria:
Reproducible, rapid onset of erythema, pruritus, and edema after exposure to cold
Most idiopathic
Occasionally involves abnormal circulating proteins (ie, cryoglobulins or cryofibrinogens);
agglutinate or precipitate at lower temperatures
Epidemiology
Death rates from the most common causes of anaphylaxis have varied:
Food-induced has remained stable.
Insect sting has declined.
Drug-induced has increased significantly—300% over past decade.
Exercise-induced anaphylaxis:
Female-to-male ratio 2:2.5
Most reported cases in young adults and adolescents
Most patients have a reduction in the number of attacks over time (2)[B].
Incidence
8–50/100,000 person-years in Western countries
Incidence rates vary widely owing to differences in sample populations, data-collection
methods, and varying definitions of anaphylaxis.
Prevalence
Lifetime prevalence of 0.05–2.0% in Western countries, rising especially in children
Exercise-induced anaphylaxis and food-dependent, exercise-induced anaphylaxis:
Difficult: Few systematic attempts to determine
Best estimates are from a cross-sectional survey of school nurses in Japan (3)[B]:
EIAn 0.03%
FDEIAn 0.017%
Risk Factors
Prior anaphylaxis event can predict subsequent anaphylaxis:
As the only risk factor, prior anaphylaxis has a poor ability to identify patients who might
develop anaphylaxis.
14% of anaphylaxis admissions for peanut sensitivity have a prior history of anaphylaxis.
Often occurs following a previous mild allergic reaction to the same allergen.
Most proposed risk factors have limited value owing to a low specificity.
Coexisting atopic disease; particularly poorly controlled asthma
Older age at 1st reaction to food allergy
Clinical risk factors for fatality in anaphylactic reactions (1)[B]:
Food-induced:
Coexisting asthma (90–100%)
Age >10 yrs at the time of anaphylactic episode (54–65%)
Absence of or delayed access to an adrenaline autoinjector (80–87%)
Peanut or tree-nut allergy (38–81%)
Drug-induced:
Elderly age group (75% were 55–85 yrs old)
Presence of cardiovascular (33%) or respiratory (17%) comorbidity
Insect sting: Male predominance (95% male)
General Prevention
Avoidance of known allergen
No available tests exist to predict the likelihood of a person developing anaphylaxis.
Neither size of skin prick test wheal nor the level of serum-specific IgE correlates with
reaction severity.
Immunotherapy:
Hymenoptera venom and penicillin: Currently available
Food allergens: Being investigated
Exercise-induced anaphylaxis:
Daily administration of an H1 antihistamine
Food restriction 2–6 hrs prior to athletic activity
Cold-induced anaphylaxis:
Avoidance of:
Cold water and air
Cold food and beverages
Promising outlooks: Characterization of β-cell epitope responses:

Specific allergenic epitopes may correlate with severity of reaction.
Individuals have a unique fingerprint of IgE-specific allergenic epitopes, and
characterization of this profile may help to determine risk of anaphylaxis.
Etiology
Allergic: IgE-mediated:
Drugs
Venom
Latex
Vaccines
Food
Nonallergic: Direct basophil/mast cell mediated
Radio-contrast dye
Opioid drugs
Diagnosis
Diagnosis is made based on clinical symptoms:
Do not underestimate the potential severity of an allergic reaction in its early stages.
Symptoms may progress rapidly.
Suspicion of anaphylaxis requires immediate medical intervention and should not be delayed
by diagnostic tests.
Clinical criteria for diagnosing anaphylaxis (1)[C]:
Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal
tissue, or both (eg, generalized hives; pruritus or flushing; swollen lips, tongue, and/or
uvula) and at least one of the following:
Respiratory compromise (eg, dyspnea, wheeze/bronchospasm, stridor, reduced peak
expiratory flow (PEF), hypoxemia)
Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia/collapse,
syncope, incontinence)
2 or more of the following that occur rapidly after exposure to a likely allergen for that
patient:
Involvement of the skin–mucosal tissue (eg, generalized hives; itch or flush; swollen lips,
tongue, and/or uvula)
Respiratory compromise (eg, dyspnea, wheeze/bronchospasm, stridor, reduce PEF,
hypoxemia)
Reduced BP or associated symptoms (eg, hypotonia/collapse, syncope, incontinence)
Persistent GI symptoms (eg, crampy abdominal pain, vomiting)
Reduced BP after exposure to known allergen for that patient:
Infants and children: Low systolic BP (age-specific) or >30% decrease in systolic BP
Adults: Systolic BP of <90 mm Hg or >30% decrease from that person's baseline
History
Previous history of anaphylaxis
Symptoms
Fatigue
Pruritus
Urticaria
Angioedema
Wheezing
Rhinitis
GI distress
Cardiovascular collapse
Time between exposure or suspected exposure and event, may happen within seconds
Recent changes in baseline health
Contributing environmental factors:
Extremes of temperature
Elevated humidity
Increased pollen count
Contributing personal factors:
Physical exertion
Ethanol consumption
Insect sting
Food consumption
Stress
Menses
Medications:
NSAIDs
Aspirin
Antibiotics
ACE inhibitors
Comorbid medical conditions:
Asthma
COPD
Cardiovascular disease
Mastocytosis
If patient has a history of anaphylaxis: Previous treatments and their effects
Physical Exam
Respiratory: Bronchospasm, laryngeal edema
Cardiovascular: Hypotension, dysrhythmias, myocardial ischemia
GI: Nausea, vomiting, diarrhea
Cutaneous: Urticaria, angioedema
Hematologic: Activation of intrinsic coagulation pathway sometimes leading to disseminated
intravascular coagulation (DIC), thrombocytopenia
Neurologic: Seizures
Death can occur from airway obstruction or circulatory collapse.

Lab
There are no specific tests to make the diagnosis of anaphylaxis, and evaluation should not
delay diagnosis and treatment.
For respiratory distress after administration of epinephrine, an arterial blood gas analysis
may be helpful in evaluating ventilatory status.
These changes can be noted during anaphylaxis:
Elevation of plasma histamine level
Increase in hematocrit secondary to fluid extravasation
May obtain tryptase levels:
Must be drawn within 3 hrs of symptom onset
Must be placed on ice
Rarely elevated in food-induced anaphylaxis
ECG: Abnormalities including dysrhythmias, ischemic changes, infarction
Pulmonary embolism
Acute myocardial infarction
Airway obstruction
Asthma
Tension pneumothorax
NSAID reaction
Vasovagal collapse
Septic shock
Hereditary angioedema
Serum sickness
Systemic mastocytosis
Pheochromocytoma
Carcinoid syndrome
Treatment
Pre-Hospital
ABCs
Remove trigger (ie, stinger from insect).
Early administration of epinephrine IM in the anterolateral thigh positively
affects outcome (4)[B].
If preloaded epinephrine is available, it is prudent to administer prior to
emergency personnel arriving if anaphylaxis is suspected.
May be administered every 5–15 min as needed based on patient's
condition.
Call 911 for emergent transfer to hospital.
Recumbent position with legs elevated (5)[B]: Maintenance of central vascular
compartment volume
Albuterol: Metered-dose inhaler (MDI) or nebulized solution if bronchospasm
not relieved by administration of epinephrine: Every 20 min or continuously
Diphenhydramine: Cochrane Review 2007 of H1 antihistamines in anaphylaxis
revealed no studies that provided evidence for the use of H1 antihistamines in
anaphylaxis (6)[B].
Onset of action takes 1–2 hrs.
Relieves pruritus, urticaria, and angioedema
Works synergistically with epinephrine
Does not relieve upper or lower respiratory tract obstruction or circulatory
collapse
Does not prevent fatality
ED Treatment
Continuous cardiac and vital sign monitoring until stable.
Persistent bronchospasm can be treated with β-agonist bronchodilators.
Hypotension should be treated with isotonic volume. Vasopressors and
Trendelenburg positioning are useful adjuncts.
Antihistamines (both H1 and H2 blockers) have been shown to be helpful in
preventing histamine interactions with target tissues.
Not a 1st-line treatment
Does not treat life-threatening symptoms of anaphylaxis (6)[B]
Most helpful treating cutaneous symptoms
Corticosteroids have never been shown in placebo-controlled trials to affect
the course of anaphylaxis but are used to treat associated conditions (eg,
asthma, allergic rhinitis):
Onset 4–6 hrs
May decrease the chance of having a biphasic reaction:
2nd episode of anaphylaxis after treatment for 1st episode
Occurs 2–72 hrs after onset of 1st episode
80% occur within the 1st 4 hrs of initial episode.
Glucagon is useful in epinephrine-resistant anaphylaxis from β-adrenergic
blocking agents.
Medication
First Line
Epinephrine (EpiPen):
Adult: 0.3–0.5 mg (use 1:1,000 dilution for SC route)
Children: 0.01 mg/kg SC (maximum dose 0.3 mg)
Preloaded syringe: 0.15 mg per injector (EpiPen Jr) and 0.30 mg per injector
(EpiPen)
Refractory hypotension:
Epinephrine drip 0.1–1 mcg/kg/min (maximum 10 mcg/min)
Titrated based on clinical effect; must be on cardiac monitor owing to risk of
lethal cardiac arrhythmias
Second Line
β-agonist: Albuterol:
MDI
Continuous nebulizer treatment
H1 antagonist: Diphenhydramine:
Adult: 50 mg IV
Children: 1–2 mg/kg slow IV pump (IVP)
Steroids:
Methylprednisolone: Severe reactions:
Adult: 125 mg IV
Children: 1–2 mg/kg IV (maximum single dose 60–80 mg)
Prednisone: Mild reactions:
Adult: 60 mg PO
Children: 1–2 mg/kg PO (maximum single dose 60–80 mg)
Hydrocortisone:
Adults: 500 mg IV
Children: 4–8 mg/kg per dose IV
Oxygen: Respiratory distress/hypoxia
H2 antagonist:
Ranitidine: Adult: 50 mg IV or
Cimetidine: 300 mg IV; children: 1–2 mg/kg (maximum dose 75–150 mg)
Glucagon: For refractory hypotension, especially if patient is on a beta blocker:
Adult: 1 mg IV
Children: 20–30 mcg/kg (maximum dose 1 mg) given over 5 min; followed by
an infusion of 5–15 mcg/min titrated to effect
In-Patient Considerations
Initial Stabilization
ABCs:
Ensure adequate ventilation.
Endotracheal intubation may be required but is difficult because of laryngeal
edema or spasm.
Transtracheal jet insufflation or cricothyrotomy may be necessary to control
the airway.
Epinephrine IM
Aggressive volume resuscitation with crystalloids to maintain BP; transfer of as
much as 50% of the intravascular fluid into the extravascular space may occur
within 10 min.
In volume-refractory hypotension, may need continuous IV epinephrine or other
vasopressors (eg, vasopressin or dopamine)
Monitor for biphasic reaction
P.
Admission Criteria
Intubated patients, patients in respiratory distress, and patients with refractory
hypotension should be admitted to an ICU setting.
A monitored bed may be necessary for the patient who has not had substantial
response to initial therapy.
Patients with significant generalized reactions and persistent symptoms should
be admitted for observation for 24 hr.
Discharge Criteria
Individualized based on the following criteria (7)[C]:
Initial presentation
Response to therapy
Availability of close observation at home
Accessibility of a medical facility from home
Patients with complete resolution of symptoms may be discharged after 4–6 hr
of ED observation.
Epinephrine duration—1 hr
Majority of biphasic reactions occur within the 1st 4 hr of initial episode.
Continuation of H1 antagonist, H2 antagonist, and corticosteroids for minimum
48 hr after discharge
Patients with allergic reactions should have follow-up within 48 hr of discharge
to evaluate effectiveness of outpatient therapy.
Severity of the reaction should be emphasized to each patient and family.
Anaphylaxis action plans:
Education about prevention and prehospital management
Prescription for self-administered epinephrine and instructions on its use
Patients with a known trigger should be counseled on strict avoidance of that
trigger.
Limited evidence on their impact on recurrence of anaphylaxis or reduction in
fatal events (8)[B]
A follow-up visit with an allergist is also recommended for consideration of
allergy testing exercise ± food provocation test.
References
1. Shadick NA, Liang MH, Partridge AJ, et al. The natural history of exercise-
induced anaphylaxis: survey results from a 10-year follow-up study. J Allergy
Clin Immunol. 1999;104:123–127.
2. Aihara Y, Takahashi Y, Kotoyori T, et al. Frequency of food-dependent,

exercise-induced anaphylaxis in Japanese junior-high-school students. J
Allergy Clin Immunol. 2001;108:1035–1039.
3. Tang ML, Osborne N, Allen K. Epidemiology of anaphylaxis. Curr Opin

Allergy Clin Immunol. 2009;9:351–356.
4. Sheikh A, Shehata YA, Brown SG, et al. Adrenaline for the treatment of
anaphylaxis: Cochrane systematic review. Allergy. 2009;64:204–212.
5. Oswalt ML, Kemp SF. Anaphylaxis: office management and prevention.

Immunol Allergy Clin North Am. 2007;27:177–191.
6. Sheikh A, ten Broek VM, Brown SGA, et al. H1 antihistamines for the
treatment of anaphylaxis with and without shock. Cochrane Database Syst
Rev. 2007;1:CD006160.
7. Soar J, Pumphrey R, Cant A, et al. Emergency treatment of anaphylactic

reactions—guidelines for healthcare providers. Resuscitation. 2008;77:157–
169.
8. Nurmatov U, Worth A, Sheikh A. Anaphylaxis management plans for the

acute and long-term management of anaphylaxis: a systematic review. J
Allergy Clin Immunol. 2008;122:353–61, 361.e1–361.e3.
Additional Reading
Liberman DB, Teach SJ. Management of anaphylaxis in children. Pediatr
Emerg Care. 2008;24:861–866.
Lieberman P. Epidemiology of anaphylaxis. Curr Opin Allergy Clin Immunol.

2008;8:316–320.
Pumphrey RSH. When should self-injectible epinephrine be prescribed for

food allergy and when should it be used? Curr Opin Allergy Clin Immunol.
2008;8:254–260.
Soar J, Guideline Development Group. Emergency treatment of anaphylaxis in

adults: concise guidance. Clin Med. 2009;9:181–185.
See Also
Exercise-induced Anaphylaxis
Exercise-induced Urticaria
Codes
ICD9
995.0 Other anaphylactic shock, not elsewhere classified
995.60 Anaphylactic shock due to unspecified food
Ankle Sprains, Lateral
Christopher A. Gee
Basics
Description
Lateral ankle sprains are the most common injury sustained by athletes and comprise 14%
of all sports-related injuries (1).
80% of sprains are due to an inversion type of mechanism that injures the lateral ankle
restraints.
While the medial side of the ankle has the broad, strong deltoid ligament as a restraint, the
lateral side of the ankle has 3 smaller ligaments that act as the static restraint system.
Primary static restraints to ankle inversion:
Anterior talofibular ligament (ATFL): Passes from the tip of the fibula to the lateral talar
neck; taut in plantar flexion; injured most commonly
Calcaneofibular ligament (CFL): Passes inferior and posterior from the tip of the fibula to
the lateral calcaneous; usually injured with the ATFL
Posterior talofibular ligament (PTFL): Passes posteriorly from the fibula to the talus; injured
less commonly
These ligaments are injured in a sequential pattern as extreme inversion and plantarflexion
forces are placed on the ankle. The ATFL is injured 1st (isolated ATFL injuries occur in 2/3
of injuries). After the small ATFL is injured, the CFL then is stressed and injured, followed by
the PTFL. The ankle joint capsule is also sprained during an inversion injury. Given this
pattern, isolated CFL injuries are uncommon.
Bony support of the distal fibula assists the deltoid ligament in restricting eversion stress to
the ankle. However, the medial malleolus is smaller than the lateral malleolus and, as such,
more easily allows inversion stress to injure the lateral ankle ligaments.
Ankle sprain grading:
Grade 1: Stretching to partial tearing of ligaments but with no gross laxity
Grade 2: Partial tear of ligaments with increased laxity of ankle but still with firm endpoint
Grade 3: Complete rupture of ligaments; gross laxity of ankle with no endpoint
Epidemiology
Incidence
Very common injury in athletes and the general population, with 23,000 cases every day (2)
Risk Factors
Athletes (especially those involved in sports with jumping near other players and quick
“cutting” motions) (3)
Dancers
Congenital tarsal coalition
Prior ankle injury (4)
Etiology
Lateral ankle sprains occur when the ankle is stressed with extreme inversion and plantarflexion
forces that overcome the static restraints (ligaments). Spraining and tearing of the ligaments
lead to pain, swelling, and varying degrees of disability.
Diagnosis
History
Patients report history of inversion-type injury often with an audible pop. This is followed by
rapid swelling, pain, and an inability to walk.
Physical Exam
Physical examination reveals ecchymosis and diffuse swelling about the ankle joint.
Tenderness to palpation is noted along the course of injured ligaments and can be diagnostic
of which ligaments are injured.
Palpation of the anterior ankle joint and the talar dome with the foot in full plantarflexion can
help to diagnose other forms of pathology.
It is important to palpate both the medial and lateral malleoli and the base of the 5th
metatarsal to examine for possible fracture.
Occasionally, the ankle ligaments can be disrupted and the stress passed up the tibiofibular
syndesmosis. This leads to syndesmotic injuries or the so-called high ankle sprain.
Assess neurovascular status by feeling distal pulses and manually testing appropriate muscle
groups.
Grading of ankle injury can be accomplished by testing the integrity of various ligaments.
Examiner also should take into account the fact that prior ankle sprains may have left residual
laxity on either side.
Anterior drawer:
Tests stability of ATFL; performed by holding the distal tibia and pulling the heel forward.
Increased laxity relative to the opposite side indicates a tear of the ATFL.
Inversion tilt: Tests stability of CFL; performed by holding the distal tibia and moving the
foot from a neutral position to an inversion position. Increased laxity compared with
opposite side indicates a tear of the CFL.

Imaging
Plain radiographs of affected ankle (including anteroposterior, lateral, and Mortise views) to
rule out fracture
May not need to perform x-rays if patient doesn't have tenderness along posterior 6-cm edge
of lateral and medial malleoli and can bear weight initially after injury (Ottawa ankle rules) (5).
CT scans may be performed to evaluate for occult fracture.
MRI is rarely useful in ankle sprains but may be useful in assessing integrity of various
ligaments in patients with chronic ankle instability.
Tibia fracture
Pilon fracture
Fibula fracture
Osteochondral defect in talar dome
Anterior ankle impingement
Talus fracture
Calcaneal fracture
Treatment
Initial therapy focuses on RICE (rest, ice, compression, elevation) protocol
to decrease pain and swelling.
Crutches can be used until patient is able to bear weight as tolerated.
Various kinds of braces, compression devices, stirrup splints, and walking
boots can be used to provide protection and support and to encourage walking.
Severe sprains may be best treated with more motion restriction in devices
such as casts or walking boots (6).
Progressive therapy through a 3-phase approach may best promote rapid
recovery:
Phase 1 consists of RICE protocols to improve pain and swelling (often wks
1–2).
Phase 2 consists of progressive range-of-motion exercises to improve
motion and decrease swelling. Patients should continue to use a protective
brace when walking to prevent further injury. Patients should be working
toward full weight bearing during this stage (wks 2–4).
Phase 3 begins more aggressive strengthening and rehabilitation exercises.
Specifically, patients should work on proprioception and endurance. This can
be a formalized physical therapy program as needed (wks 4–6).
Medication P.
NSAIDs can be used after initial injury for pain. They should be avoided in
patients at risk for GI bleeding.
Physical therapy can be used to assist patients in strengthening and generally
rehabilitating the injured ankle.
Electrical stimulation and iontophoresis may have a role in pain and swelling
control.
Often general rehabilitation principles and conservative therapy are adequate
to return athletes to their sport without more aggressive interventions. Patients
rarely need primary repair of ligaments after an acute lateral ankle sprain.
Occasionally, severe laxity of lateral ankle restraints may lead to recurrent
ankle injuries and chronic ankle instability. These patients may benefit from
ligament repair or ankle reconstruction to improve stability.
Ongoing Care
Patient Monitoring
Patients may return to play once they have achieved a full range of motion and strength, as
well as being able to perform their sport-specific activities without limitations. Some may be
able to return to play with a supportive device to protect from further injury depending on the
sport and the patient's position.
Depending on the sport, certain patients may need to go through a progression of sport-
specific activities to return to play.
Prognosis
Prognosis depends on the extent of injury and any concurrent injuries, but for most patients,
prognosis is excellent. More severe injuries may require more extensive rehabilitation for
patients to return to full function and prevent recurrence.
Patients with recurrent instability and those in high-risk sports (eg, volleyball, basketball) may
benefit from functional bracing or taping.
Patients who fail to undergo proper rehabilitation are often left with chronic instability and
recurrent ankle injuries.
Complications
Stiffness from prolonged immobilization
Recurrent instability
Osteochondral defects
References
1. Fong DT, Chan YY, Mok KM, et al. Understanding acute ankle ligamentous
sprain injury in sports. Sports Med Arthrosc Rehabil Ther Technol.
2009;1:14.
2. Kannus P, Renström P. Treatment for acute tears of the lateral ligaments of

the ankle. Operation, cast, or early controlled mobilization. J Bone Joint Surg
Am. 1991;73:305–312.
3. Nelson AJ, Collins CL, Yard EE, et al. Ankle injuries among United States
high school sports athletes, 2005–2006. J Athl Train. 2007;42:381–387.
4. Malliaropoulos N, Ntessalen M, Papacostas E, et al. Reinjury after acute

lateral ankle sprains in elite track and field athletes. Am J Sports Med.
2009;37:1755–1761.
5. Stiell IG, Greenberg GH, McKnight RD, et al. A study to develop clinical
decision rules for the use of radiography in acute ankle injuries. Ann Emerg
Med. 1992;21:384–390.
6. Lamb SE, Marsh JL, Hutton JL, et al. Mechanical supports for acute,
severe ankle sprain: a pragmatic, multicentre, randomised controlled trial.
Lancet. 2009;373:575–581.
Codes
ICD9
845.02 Calcaneofibular (ligament) ankle sprain
Clinical Pearls
Extremely common injury that can present with swelling, ecchymosis, and
inability to walk
Thorough exam and proper imaging can help to avoid missing associated
fractures.
Treatment involves progression from RICE protocol to progressive weight
bearing and range of motion and finally to strengthening and proprioceptive
exercises.
Ankle Sprains, Medial
Anne S. Boyd
Jason Wander
Basics
Description
Injury to the deltoid ligament complex of the medial ankle occurs primarily from a
pronation/external rotation injury of the foot.
Grade I sprain results from mild stretching of the deltoid ligament with microscopic tears (1).
Patients have mild swelling and tenderness. There is no joint instability on exam, and the
patient is able to bear weight and ambulate with minimal pain. Owing to their benign nature,
these injuries are not seen frequently in the office.
Grade II sprain is a more severe injury involving an incomplete tear of the deltoid ligament.
Patients have moderate pain, swelling, tenderness, and ecchymosis. There is mild to
moderate joint instability on exam with some restriction in the range of motion and loss of
function. Weight bearing and ambulation are painful.
Grade III sprain involves a complete tear of the deltoid ligament. Patients have severe pain,
swelling, tenderness, and ecchymosis. There is significant mechanical instability on exam and
significant loss of function and motion. Patients are unable to bear weight or ambulate.
Synonym(s): Medial ankle sprain; deltoid ligament sprain
Epidemiology
Isolated deltoid ligament injuries are rare and constitute <10% of all ankle sprains (2).
Deltoid ligament sprains are often accompanied by a lateral malleolar fracture and/or
syndesmotic injury (2).
Risk Factors
Previous ankle sprain
High-risk sports, including football, basketball, and long jumping
Low arch of the foot
Dysfunction of the posterior tibialis
Extreme fatigue of peroneus (fibularis) longus muscle
General Prevention
Ankle braces and taping both appear to be somewhat effective, but braces appear to be
superior to taping (1).
Proprioceptive training appears to be equally effective in primary and secondary prevention
of ankle injuries (3).

Syndesmosis sprain
Fracture of the fibula and/or tibia
Avulsion fracture of the medial malleolus
Severe lateral ligament injury
Posterior tibial tendon injury
Flexor hallucis longus injury
Posterior tibial and/or saphenous nerve traction injury
Diagnosis
History
Athlete reports an eversion, external rotation injury with the foot abducted/pronated.
Should inquire about previous ankle injury and history of “giving way.” This would suggest that
there is an acute injury superimposed on chronic ankle instability.
Physical Exam
Signs and symptoms include:
Medial ankle pain
Swelling on the medial aspect of the ankle
Ecchymosis around the medial aspect of the ankle
Sensation of a “pop”
Inability to walk
Physical examination includes:
Evaluation of the ability to bear weight
Careful palpation to identify tender structures
Determination of tenderness over the deltoid ligament
A check for tenderness over the anterior syndesmosis ligament, lateral ankle, and fibula
(distal and proximal)
A check of posterior tibial tendon function with resisted inversion
A check of extensor hallucis longus tendon function with resisted extension of the great toe
A check of range of motion of the ankle joint
A check of flexor hallucis longus tendon function with resisted flexion of the great toe
A squeeze test and external rotation test to rule out syndesmotic injury
A valgus talar tilt test to determine the stability of the deltoid ligament; this is done with
passive eversion of the ankle.

Imaging
Anteroposterior, lateral, and mortise views of the injured ankle are essential to rule out
fracture (60% of patients with a deltoid rupture have an associated avulsion fracture of the
medial malleolus, syndesmotic injury, or a fibular fracture).
>3 mm of medial clear space between the lateral border of the medial malleolus and the
medial border of the talus at the level of talar dome is abnormal and suggestive of a medial
ankle sprain.
Consider a valgus talar tilt stress radiograph to assess for significant instability and possible
surgical treatment: >10 degrees difference in abduction tilt of the talus compared with
opposite ankle is abnormal (perform this test only if there are no associated fractures).
Consider MRI if the extent of deltoid ligament rupture is unclear (partial vs complete), and
surgical treatment is being considered.
In the setting of acute injury, MRI has no advantage over plain x-ray (1).
Syndesmosis tear or sprain
Posterior tibial tendon tear or subluxation
Flexor hallucis longus tendon tear or sprain
Distal tibia fracture
Osteochondral fracture of the talar dome
Fracture of the calcaneus
Fracture of the lateral process of the talus
Medial ankle sprain with associated proximal fibular fracture (Maisonneuve fracture)
Treatment
Pre-Hospital
Prevent/reduce inflammation and swelling with rest, ice, compression, and
elevation (RICE protocol).
Prevent further injury or worsening of current injury.
Rest is achieved by limiting weight bearing by having patients use crutches or
other assistive devices until they are able to walk with a normal gait.
Ice or cold-water immersion is recommended for 15–20 min q2–3h for the 1st
48 hr or until swelling improves, whichever comes 1st.
Compression to control and decrease swelling should be applied early, usually
with an Ace wrap or stirrup brace. Compression should be supportive but not
constrictive.
The injured ankle should be kept elevated above the level of the heart to further
alleviate swelling.
Grade I sprain: Functional rehabilitation and possibly a splint or a brace, with
the recognition that return to sports generally is more delayed (3–6 wks) than
with a lateral sprain (1–3 wks)
Grade II sprain: Same as grade 1, but in addition, may need a short period of
immobilization in posterior splint or walking boot
Grade III sprain: Treatment is controversial; requires immobilization (6–8 wks)
or may need operative repair (see “Referral”).
Referral
>4 mm of medial clear space on the mortise view
Significant instability on reverse talar tilt stress radiograph or weight-bearing
views
Grade III injury may need operative repair to prevent long-term complications.
Medial malleolus fracture
Displaced lateral malleolus fracture
Wound penetrating into the joint
Uncertain diagnosis
Patients with neurovascular compromise
Functional rehabilitation is of great importance in aiding return to activity and
preventing chronic instability. The exercises should begin as soon as the initial
pain and swelling have subsided sufficiently to allow the patient to perform
simple exercises and should continue until the patient has returned to pain-free
activity (1)[A].
Achilles tendon stretch
Foot circles
Alphabet exercises: While leg is stable, patient should use the great toe and
foot to “write” the letters of the alphabet in the air.
Isometric and isotonic plantar flexion, dorsiflexion, inversion, eversion, and toe
curls
Marble pickups (using toes)
Heel walks
Toe walks
Circular wobble board
Walking on different surfaces
Walk-jog, jog-run
During functional rehabilitation, it may be of benefit to use splints, braces, and
taping to try to reduce instability, protect the ankle from further injury, and limit
swelling.
Complementary and Alternative Medicine
Neither US therapy, low-level laser therapy, nor hyperbaric therapy appears to be
effective in the treatment of medial ankle sprains (1)[B].
Ongoing Care
Prognosis
Pain decreases rapidly during the 1st 2 wks following injury.
5–33% of patients report some pain after 1 yr.
Healing rates vary widely among studies, with 36–85% of patients reporting full recovery over
the 1st 3 yrs.
Lack of proper rehabilitation contributes to recurrent and/or chronic ankle symptoms,
complaints, and problems.
Complications
Deltoid ligament injury generally is a more serious injury than lateral ankle sprain
and frequently is associated with concomitant injury to the lateral ligaments or
fibula.
References
1. Maughan DL. Ankle sprain. In: UpToDate, Eiff P (Ed), UpToDate, Waltham,
MA, 2009.
2. Clanton TO, Porter DA. Primary care of foot and ankle injuries in the
athlete. Clin Sports Med. 1997;16:435–466.
3. McGuine TA, Keene JS. The effect of a balance training program on the
risk of ankle sprains in high school athletes. Am J Sports Med. 2006;34:1103.
Additional Reading
Birrer RB, Fani-Salek MH, Totten VY, et al. Managing ankle injuries in the
emergency department. J Emerg Med. 1999;17:651–660.
Mei-Dan O, Kahn G, Zeev A, et al. The medial longitudinal arch as a possible

risk factor for ankle sprains: a prospective study in 83 female infantry recruits.
Foot Ankle Int. 2005;26:180–183.
Codes
ICD9
845.01 Deltoid (ligament), ankle sprain
Clinical Pearls
An athlete may return to full activity once he or she is able to do a progressive
rehabilitation program without pain and instability. Return to sports may be
prolonged over several months depending on the degree of injury.
To prevent future injuries, athlete should wear an ankle brace for sporting
activities and complete rehabilitation.
Untreated, severe sprain may result in chronic pain, instability, and the
possibility of ankle arthritis.
Effect of external ankle support on performance:
Dependent on the specific brace or method (such as taping) used
Decrease in performance ≤5%
Ankylosing Spondylitis
Catharine Mayer
Eugene Hong
Basics
Description
Ankylosing spondylitis (AS) is a chronic inflammatory, seronegative autoimmune arthritis
characterized by inflammatory back pain.
It is the most common and potentially severe subtype of the spondyloarthritis (SpA), which
includes:
Reactive (Reiter) arthritis
Arthritis/spondylitis with inflammatory bowel disease (IBD)
Arthritis/spondylitis with psoriasis
Unspecified spondylitis
AS causes inflammation of the sacroiliac joints, peripheral joints, and entheses (sites where
ligaments or tendons attach to bone).
Common sites for enthesopathy include:
Calcaneus
Patella
Tibial tubercle
Vertebral bodies
The involvement of vertebral body entheses leads to the characteristic findings of ankylosis
(fusion) and syndesmophytes (vertical bony growths) responsible for the classic radiographic
“bamboo” appearance of the spine in advanced disease.
Synonym(s): Axial spondyloarthritis; Inflammatory spine disease
Epidemiology
Incidence
Overall incidence: 0.5–8.2/100,000/yr (1)
Incidence rate varies directly with prevalence of HLA-B27 in given population.
Commonly presents in young adulthood
Predominant age:
80% of patients with AS develop symptoms before age 30.
<5% of patients with AS present after age 45.
Predominant gender: Male > Female ( 3:1).
Prevalence
Prevalence of AS in a given population depends on HLA-B27 prevalence in the population.
Overall prevalence in U.S. is 0.10–0.12% for AS and 0.21% for all SpAs including AS.
Higher in Alaskan Eskimos and some Native American populations owing to higher than
average HLA-B27 rate
Lower in African Americans secondary to a lower HLA-B27 rate
Up to 5% of patients evaluated for chronic low back pain are ultimately diagnosed with AS.
Risk Factors
Positive family history of SpA or HLA-B27
90% or more of individuals with AS are HLA-B27-positive.
Reactive arthritis triggered by Chlamydia trachomatis and certain enteric infections (eg,
Shigella, Salmonella, Yersinia, and Campylobacter spp.) predisposes to development of
AS.
10–20% of HLA-B27-positive patients with reactive arthritis develop AS.
Genetics
Expression of HLA-B27 antigen is clearly linked to the development of AS, but the exact
mechanism is unknown.
Prevalence of HLA-B27 in African Americans is 2–4% and in Caucasians is 8%.
Etiology
A clear etiologic pathway has not been established.
Research suggests that some interplay among environmental/infectious exposure, genetic
predisposition, and immune response is responsible for the development of AS and all SpAs.
It is likely that an autoimmune response triggered by an immunologic event causes an
inflammatory cell infitrate (predominately T cells and macrophages) in the sacroiliac joints,
peripheral joints, and entheses leading to ongoing inflammation that results in bony
proliferation, erosions, sclerosis, and destruction.
Uveitis/iritis
IBD
Psoriasis
Rarely, cardiac valve/aortic root involvement
Diagnosis
Must recognize the features of inflammatory back pain (IBP) to distinguish from
mechanical back pain. New York criteria are the traditional diagnostic criteria for AS. New
criteria to diagnose all causes of IBP, not just AS, have been developed by the Assessment
for SpondyloArthritis International Society (ASAS).
ASAS-endorsed criteria for IBP (SOR-A: Validated clinical rule) (2):
Age of onset <40 yrs
Insidious onset
Improvement with exercise
No improvement with rest
Nighttime pain with improvement on getting up
Requires 4 of 5 parameters
77% sensitive, 92% specific for IBP (not only AS)
Modified 1984 New York criteria for AS:
Clinical criteria:
Low back pain and stiffness of at least 3 mos' duration that improves with exercise but is
not relieved by rest
Limited lumbar spinal motion in sagittal (sideways) and frontal (forward and backward)
planes
Chest expansion decreased relative to normal values corrected for age and sex
Radiologic criteria:
Bilateral sacroiliitis grades 2–4 or
Unilateral sacroiliitis grade 3 or 4
A patient is considered to have definite AS if one radiologic criterion is associated with at

least one clinical criterion.
A patient is considered to have probable AS if 3 clinical criteria are present or one radiologic
criterion is present without any clinical criterion.
History
Signified by back pain of insidious onset that has been present for at least 3 mos
Physical Exam
Physical exam should include assessment of:
Entire spine: Range of motion, tenderness. Shober's test: Mark area on patient's back at L5
and 10 cm above that point. Once patient bends forward, remeasure that distance. In normal
persons, it should be >5 cm greater in flexion; <5 cm suggests loss of motion in lumbar
spine.
Peripheral joints, especially in the lower extremity: Limited range of motion, inflammatory
signs such as effusion, warmth, tenderness
Major entheses: Calcaneous for Achilles and plantar fascia attachments, patella, tibial
tuberosity
Eyes: Inflammatory findings
Skin: Rash characteristic of psoriasis

Lab
Laboratory studies that can aid in the diagnosis include:
HLA-B27
C-reactive protein (CRP)
Erythrocyte sedimentation rate (ESR)
CRP and ESR can be elevated in 50–70% of patients with AS, but normal values do not
negate presence of disease. Further, normal or elevated levels in patients with established
disease do not correlate with disease activity.
Imaging
Imaging of sacroiliac joints is required for the diagnosis and classification of AS.
Plain radiographs:
Sacroiliitis is a hallmark of disease.
20–30% of patients with the 1st 2 yrs of developing IBP will have structural changes
detectable by radiographs, confirming diagnosis.
In established AS, 95% of patients have detectable structural changes; however, structural
changes may take several years or longer to become apparent radiographically.
Absence of radiographic findings in patients with IBP does not imply a lack of inflammation,
nor does it negate the possibility of AS.
MRI (T2 and STIR):
May be useful when plain radiographs are noncontributory

Able to detect active and acute inflammation of sacroiliac joints in early disease prior to
onset of structural changes
Also can predict the future development of structural changes
Not as sensitive as plain radiographs to assess degree of structural changes
CT scan:
Useful for detecting chronic changes in the sacroiliac joints
Role is limited owing to high radiation exposure.
Mechanical low back pain
Myofascial low back pain
Lyme arthritis
Herniated nucleus pulposus
Degenerative disk disease
Degenerative joint disease
Spondylolysis
Diskitis
Other causes of IBP
Treatment
Management is individualized based on degree of disease, severity of
symptoms, and patient expectations.
Typically is long term, if not lifelong
Medication
Depending on location and severity of disease, the following treatment modalities
may be indicated:
NSAIDs
Tumor necrosis factor (TNF) blockers
Disease-modifying antirheumatic drugs (DMARDs)
Corticosteroid injections
First Line
NSAIDs (SOR-A) (3):
Diclofenac, naproxen, celecoxib, and others
Full dose and regular scheduling maximize symptom relief.
Randomized trials have demonstrated that the anti-inflammatory properties of
NSAIDs suppress symptoms.
Beneficial for both axial (spine) and peripheral (joint, enthesis) involvement
Data suggest that long-term therapy may have disease-controlling properties
evidenced by suppression of radiographic progression.
Most, but not all, patients will respond to NSAIDs. Try another NSAID class
before considering 2nd-line therapy.
Must monitor for GI, cardiovascular, renal, and hepatic side effects with
ongoing NSAID use.
Second Line
TNF blockers (SOR-A) (4):
Infliximab, adalimumab, and etanercept
Clear guidelines on indication and use
Randomized trials demonstrate significant improvement in pain, function, and
disease activity.
With extended therapy, up to 1/3 of patients may develop remission.
Studies are ongoing investigating long-term use and disease progression.
Cochrane Review underway but unpublished as of 2009
DMARDs:
Limited role for sulfasalazine; some benefit with peripheral disease only
(SOR-A) (5)
No role for methotrexate (SOR-A) (6)
Local corticosteroid injections: May be useful for symptomatic relief of inflamed
peripheral joints
Referral
Rheumatology evaluation may be helpful to confirm presence and severity of
disease, as well as to guide treatment indications for use of TNF blockers and
other DMARDs.
Consider early referral in patients with IBP and the presence of HLA-B27,
radiographic findings, or positive family history of AS or other SpA.
Education (absolute indication)
Exercise (absolute indication)
Physical therapy/rehabilitation (absolute indication)
Self-help groups
AS associations
A Cochrane Review of physiotherapy determined that a home or supervised
exercise program performed better at improving function and decreasing pain
than no exercise at all (7).
A Cochrane protocol for review of self-management programs for patients with
AS is underway. No review of findings has been published as of 2009.
Hip arthroplasty as indicated for progressive arthropathy∏
Knee arthroplasty as indicated for progressive arthropathy∏
Ongoing Care
Duration of therapy: Long term or lifelong
When to expect improvement:
Many patients experience significant improvement of symptoms within 1 wk of initiating
NSAID therapy.
Continued improvement occurs over weeks to several months in pain, stiffness, and range
of motion, as well as function.
Signs to watch for that indicate problems:
Worsening stiffness despite maximal NSAID therapy
Side effects of NSAID therapy
Vision, skin, or cardiovascular complaints
Pitfall: Overdiagnosis in HLA-B27-positive individuals in whom other causes for joint swelling
should be considered.
Prognosis
AS has an unpredictable clinical course independent of age of onset or sex.
Most patients have a fluctuating course with flares and periods of relative remission.
Chronic symptoms can range from mild, medically controllable inflammation to debilitating
progression that is refractory to treatment.
Complications
Fusion of vertebrae leading to loss of function or restrictive lung disease
Uveitis can occur in 40% of patients.
Aortitis or aortic insufficiency, rare
Hip arthritis with refractory pain or disability requiring arthroplasty
References
1. Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of
SpondyloArthritis international Society (ASAS) handbook: a guide to assess
spondyloarthritis. Ann Rheum Dis. 2009;68 (Suppl 2):ii1–44.
2. Sieper J, van der Heijde DM, Landewé RB, et al. New criteria for
inflammatory back pain in patients with chronic back pain—a real patient
exercise of the Assessment in SpondyloArthritis international Society (ASAS).
Ann Rheum Dis. 2009;68:784–788.
3. Song IH, Poddubnyy DA, Rudwaleit M, et al. Benefits and risks of

ankylosing spondylitis treatment with nonsteroidal antiinflammatory drugs.
Arthritis Rheum. 2008;58:929–938.
4. Braun J, Davis J, Dougados M, et al. First update of the international ASAS

consensus statement for the use of anti-TNF agents in patients with
ankylosing spondylitis. Ann Rheum Dis. 2006;65:316–320.
5. Chen J, Liu C. Sulfasalazine for ankylosing spondylitis. Cochrane

Database Syst Rev. 2005:CD004800.
6. Chen J, Liu C, Lin J. Methotrexate for ankylosing spondylitis. Cochrane

Database Syst Rev. 2006:CD004524.
7. Dagfinrud H, Kvien TK, Hagen KB. Physiotherapy interventions for

ankylosing spondylitis. Cochrane Database Syst Rev. 2008:CD002822.
Additional Reading
Braun J, Sieper J. Ankylosing spondylitis. Lancet. 2007;369:1379–1390.
Sieper J, Rudwaleit M, Khan MA, et al. Concepts and epidemiology of

spondyloarthritis. Best Pract Res Clin Rheumatol. 2006;20:401–417.
Codes
ICD9
720.0 Ankylosing spondylitis
Clinical Pearls
Consider features of IBP that can distinguish it from other causes of chronic
back pain.
If plain radiographs are not diagnostic, consider further imaging (eg, MRI).
In a patient <45 yrs of age at symptom onset with low back pain for >3 mos,
consider determining the presence of IBP clinical symptoms, HLA-B27
serology, or radiographic/MRI evidence of sacroiliac inflammation. Each of
these findings may increase the likelihood of AS.
With early recognition, diagnosis, and appropriate management, AS symptoms
and disease progression can be improved.
Anterior Interosseous Syndrome
David Z. Frankel
Basics
The anterior interosseous nerve (AIN) is a motor branch of the median nerve that
innervates the pronator quadratus, flexor pollicis longus, and flexor digitorum profundus
serving the index finger.
Anterior interosseous syndrome is a catch-all term for neuropathies that result in paralysis of
these muscles secondary to a number of causes.
Etiology
The most frequent causes of anterior interosseous syndrome are direct traumatic nerve
damage and external compression.
Traumatic causes:
Penetrating trauma
Blunt injury
Traction injury
Fracture
Surgery
Venipuncture
Injection
Cast pressure
External compression:
Bulky tendinous origin of the deep head of the pronator teres
Soft tissue mass such as lipoma, ganglion, or tumor
Accessory muscle
Fibrous band originating from the superficial flexor
Vascular abnormality
Diagnosis
History
Pain in the forearm
Sensory loss not noted
Weakness noted as difficulty with writing or with fine-pinch activities
Physical Exam
The signature finding is weakness of the flexor pollicis longus, flexor digitorum profundus
indicis, and pronator quadratus.
Weakness of the flexor pollicis longus and flexor digitorum profundus to the index finger is
indicated by an inability to make the “OK sign.” Rather the distal interphalangeal (DIP) joint of
the index finger and interphalangeal (IP) joint of the thumb are hyperextended during
attempted tip-to-tip pinch.
The pronator quadratus is difficult to isolate clinically. Weakness may be detected by asking
the patient to forcibly pronate the forearm against resistance (resist supination) with the
elbow flexed at 90 degrees.
The AIN provides no sensory fibers to the skin; therefore, abnormal sensation testing rules
out anterior interosseous neuropathy.

Electrodiagnostic testing:
Should include electromyography (EMG) of the flexor pollicis longus, pronator quadratus,
and flexor digitorum profundus indicis
The latency and amplitude of compound muscle action potential are compared with those
of the unaffected side.
Sensory nerve action potentials are normal.
Imaging modalities:
Both MRI and US may be helpful in confirming the clinical diagnosis of anterior
interosseous syndrome.
MRI findings of edema in the muscles innervated by the AIN on T2-weighted fat-
suppressed images
The AIN may appear swollen on US when compared with the normal contralateral nerve.
US of the AIN-innervated muscles may show a loss of bulk, increased reflectivity, reduced
perfusion on Doppler sonography, and lack of active contraction of the affected muscles.
Tendon rupture
Brachial plexus neuritis (Parsonage-Turner syndrome)
Congenital absence of the flexor digitorum longus and flexor pollicis longus
Partial lesion of the median nerve
Treatment
Once an accurate diagnosis of anterior interosseous syndrome is made,
treatment must be guided by the underlying etiology.
Penetrating trauma suggests nerve disruption or compression and is best
treated with surgical exploration and nerve decompression or repair.
With blunt trauma, an EMG suggestive of a complete lesion may mandate early
surgical exploration. Partial injuries may be given an opportunity to recover
spontaneously. If no improvement is noted after 6–12 wks of conservative
management, surgical exploration is necessary.
The typical nonsurgical treatment regimen includes rest, splinting, and
observation.
Spontaneous paralysis of the AIN may be treated nonsurgically for 12 wks, with
surgical exploration if no clinical or EMG improvement is evident.
Spontaneous recovery after 12 mos is documented, and some advocate
nonsurgical management for at least this long before proceeding with surgical
exploration.
Tendon transfers allow functional reconstruction of the thumb and index finger
should the AIN fail to recover, be unreconstructable, or irreversible muscle
atrophy is present after prolonged muscle denervation.
Additional Reading
Chin DH, Meals RA. Anterior interosseous nerve syndrome. J Am Soc Surg
Hand. 2001;1:249–257.
Dang AC, Rodner CM. Unusual compression neuropathies of the forearm,

part II: median nerve. J Hand Surg Am. 2009;34:1915–1920.
Dunn AJ, Salonen DC, Anastakis DJ. MR imaging findings of anterior

interosseous nerve lesions. Skeletal Radiol. 2007;36:1155–1162.
Hide IG, Grainger AJ, Naisby GP, et al. Sonographic findings in the anterior
interosseous nerve syndrome. J Clin Ultrasound. 1999;27:459–464.
Martinoli C, Bianchi S, Pugliese F, et al. Sonography of entrapment

neuropathies in the upper limb (wrist excluded). J Clin Ultrasound.
2004;32:438–450.
Codes
ICD9
354.1 Other lesion of median nerve
354.9 Mononeuritis of upper limb, unspecified
Clinical Pearls
Dysfunction of the AIN is characterized by weakness of the pronator
quadratus, flexor pollicis longus, and flexor digitorum profundus serving the
index finger.
On examination, the patient cannot make the “OK sign” with the thumb and
index finger.
The AIN does not provide sensory nerves to the skin; therefore, abnormal
sensation rules out anterior interosseus syndrome.
Penetrating trauma or blunt trauma with an EMG suggestive of a complete AIN
lesion mandates surgical exploration.
Anterior Metatarsalgia (Submetatarsal Head Pain)
Kenneth M. Bielak
Benjamin D. England
Basics
Description
Refers to pain in the plantar aspects of the metatarsal heads. Metatarsalgia is not an
anatomical diagnosis. It can be divided into primary and secondary metatarsalgia.
Primary metatarsalgia develops from intrinsic factors, such as a long 1st ray, hallux valgus,
and other congenital deformities.
Secondary metatarsalgia may result from trauma, sesamoiditis, or neurogenic disorders.
Epidemiology
Common in athletes with high-impact sports involving the lower extremities (dancing, running,
jumping)
Risk Factors
Overpronation
Foot deformities: Pes planus (flat foot), pes cavus, tight Achilles tendon, tarsal tunnel
syndrome, hallux valgus, prominent metatarsal heads, hammertoe deformity, tight toe
extensors, Morton's foot with a short 1st metatarsal and a relatively long 2nd metatarsal
Old or poorly fitted shoes
Competitive athletes in weight-bearing sports (soccer, ballet, basketball, baseball, football,
etc.)
High heels or narrow, pointed shoes
Abnormal gait or stance due to intrinsic or extrinsic factors
Obesity
Fat pad atrophy or displacement
Soft tissue dysfunction: Intrinsic muscle weakness, laxity in the Lisfranc ligament
Dermatologic issues: Calluses and warts
Involvement of lesser metatarsals: Freiberg infarction (aseptic necrosis of metatarsal head,
as seen in adolescent sprinters)
General Prevention
Wear properly fitted shoes with adequate padding.
Gradual progression of weight-bearing exercise programs
Etiology
Specific etiology variable, but repetitive/excessive stress combined with intrinsic and extrinsic
factors (see “Risk Factors”)
Due to the 2 sesamoid bones, the 1st metatarsal (MT) head usually carries 30% of the load
when walking. A normal metatarsal arch also ensures this balance with adequate padding
around the 1st MT head. A pronated or splayfoot can disturb this balance, resulting in
changed load bearing by the other metatarsal heads. Reactive tissue can build up a callus
around the metatarsal head, which further compounds the discomfort.
Excessive or repetitive stress, such as wearing high heels or ballet dancers

Soft tissue dysfunction: Intrinsic muscle weakness, laxity in the Lisfranc ligament
Dermatologic issues: Calluses and warts
Hallux valgus or rigidus
Involvement of lesser metatarsals: Freiberg infarction (aseptic necrosis of metatarsal head,
as seen in adolescent sprinters)
Hammertoe or clawtoe
Morton syndrome (long 2nd metatarsal)
Diagnosis
History
Gradual chronic onset is more common than acute presentation.
Patient may have history of repetitive stress with unaccustomed walking and running.
Symptoms located typically to plantar surface of metatarsal heads
Typical pain described as walking with a “pebble in the shoe”
Aggravated during midstance or propulsion phases of walking or running
Physical Exam
Pain is predominantly located in the plantar forefoot, especially in the distal half of the
metatarsal shaft and head.
Calluses may indicate areas of excessive friction/pressure.
Palpation for tenderness may differentiate soft tissue injury from the bony metatarsal head.
Pain in interdigital space or positive metatarsal squeeze test suggests Morton neuroma.
Examination for the presence of callus, edema, erythema, swelling, gross deformity, breaks
in the skin, and/or abnormal foot mechanics should be performed.
Range of motion of the phalanges, metatarsophalangeal joint, and ankle, especially to
dorsiflexion, should be examined.
Gait analysis should be performed.
Diagnostic injection (metatarsophalangeal joint) with local anesthetic sometimes can help
differentiate intra-articular pathology (synovitis, capsulitis) from extra-articular pathology
(neuroma).

Lab
Not required, but may be considered to rule out additional pathology (differential diagnosis)
WBC count may be elevated in infection, but is normal in metatarsalgia.
Sedimentation rate will be normal, barring infection or arthritis.
Consider testing for:
Gout—Uric acid level
Pseudogout—Synovial fluid
Systemic disease—Human leukocyte antigen, rheumatoid factor
Imaging
Not required, but may be considered to rule out additional pathology (differential diagnosis)
Weight-bearing anteroposterior and lateral foot and oblique radiographs should be normal.
Metatarsal and sesamoid axial films to rule out sesamoid fracture or skyline view of the
metatarsal heads (MTP joints in dorsiflexion to view alignment) may be considered.
Bone scan is indicated if there is a high index of suspicion for stress fracture. Triple-phase
bone scan will help delineate soft tissue from bony pathology.
MRI is indicated if a mass lesion is suspected.
Increasing use of ultrasonography, especially with effusions or neuromas.
Diagnostic injection (metatarsophalangeal joint) with local anesthetic sometimes can help
differentiate intra-articular pathology (synovitis, capsulitis) from extra-articular pathology
(neuroma).
Plantar pressure distribution analysis may help to distinguish patterns of pressure distribution
due to malalignment.
Neuroma (plantar or Morton's)
Idiopathic metatarsophalangeal joint synovitis
Freiberg disease: Ischemic epiphyseal necrosis of the 2nd metatarsal
Inflammatory arthritis of metatarsophalangeal joints (rheumatoid arthritis, seronegative
spondyloarthropathy, crystalline-induced arthritis, osteoarthritis, septic arthritis)
Stress fracture
Salter I fracture (pediatric population)
Sesamoiditis or sesamoid fracture
Lisfranc injury
Traumatic arthritis
Foreign body
Cellulitis or infection (diabetic foot, Lyme disease, leprosy)
Ganglion cyst
Vasculitis (diabetes)
Cavovarus foot
Tumor (rare)
Treatment
Acute treatment:
Ice and rest with activity modification
Well-cushioned athletic shoes correctly fitted for the athlete's foot type (1)[C]
Calluses should be pared down, preferably after soaking the foot in warm
water and using a stone or emery board.
A metatarsal pad may be placed just proximal to the metatarsal heads to
relieve pressure. A common error is to place the pad directly beneath the
metatarsal heads, which will exacerbate the symptoms.
Analgesics such as acetaminophen or NSAIDs may be of benefit
symptomatically.
Stretching a tight Achilles tendon may help reduce metatarsal loading acutely.
Long-term treatment:
Prescriptive orthotics are beneficial:
Pes cavus (2)[C]
Hallux valgus (2)[C]
Arch support and a well-fitted, low-heel shoe for daily wear (1)[C]
Energy-absorbing sole on shoe
Enhance gastroc-soleus mechanism flexibility
Correction of postural or gait imbalance
Physical therapy may be helpful.
Rarely, a cam walker boot, cane, or crutch may be necessary.
Progressive return to sports activities as tolerated
Replace daily and sports shoes after 350 miles of running or when they show
early wear, such as creasing in the midsole under the ball of foot or heel.
Avoid hard surfaces and prolonged standing.
Medication
Analgesics for symptom control
NSAIDs (ibuprofen, naproxen) or acetaminophen
Referral
Athletes may warrant early podiatric or orthopedic evaluation.
If no improvement with conservative therapy for 3 mos, consider referral to
foot/ankle orthopedic or surgical podiatrist.
If a correctable anatomic abnormality exists, bunionectomy, partial osteotomy,
or surgical fusion may be considered. Success rates vary, depending on
procedure.
Surgery is considered a last resort if no anatomic abnormality is present.
Corticosteroid injection should be avoided because it may cause fat pad atrophy.
Ongoing Care
Patient Education
Instruct patient about wearing proper shoes and gradual return to activity.
Cross training until symptoms subside
Biomechanical evaluation by appropriately skilled clinician
Complications
Back, knee, and hip pain owing to compensatory gait change
Transfer metatarsalgia following surgical intervention as stress transfers to
other areas
References
1. Espinosa N, Maceira E, Myerson MS. Current concept review:
metatarsalgia. Foot Ankle Int. 2008;29:871–879.
2. Hockenbury RT. Forefoot problems in athletes. Med Sci Sports Exerc.

1999;(7 suppl):S448–S458.
Additional Reading
Baker CL. Reactive synovitis of the foot—metatarsalgia. In The Hughston
Clinic sports medicine field manual. Baltimore: Williams & Wilkins, 1996:270.
Birbilis T, Theodoropoulou E, Koulalis D. Forefoot complaints—the Morton's

metatarsalgia. The role of MR imaging. Acta Medica (Hradec Kralove).
2007;50:221–222.
Gregg J, Marks P. Metatarsalgia: an ultrasound perspective. Australas Radiol.

2007;51:493–499.
Gregg JM, Schneider T, Marks P. MR imaging and ultrasound of metatarsalgia

—The lesser metatarsals. Radiol Clin North Am. 2008;46:1061–1078.
Tóth K, Huszanyik I, Kellermann P, et al. The effect of first ray shortening in

the development of metatarsalgia in the second through fourth rays after
metatarsal osteotomy. Foot Ankle Int. 2007;28:61–63.
Weber PC. Resolution of metatarsalgia following oblique osteotomy. Clin

Orthop Relat Res. 2007;458:248.
Codes
ICD9
355.6 Lesion of plantar nerve
726.70 Enthesopathy of ankle and tarsus, unspecified
ICD10
M77.4 metatarsalgia
Clinical Pearls
Common especially in athletes with high-impact sports involving the lower
extremities (running, jumping, dancing, etc.)
Pain of the plantar surface of the forefoot in the metatarsal head region
Point tenderness over plantar metatarsal heads
Athletes may warrant early podiatric or orthopedic consultation.
Abnormal pressure distribution to plantar aspect of metatarsal heads
Aortic Stenosis
Charles W. Webb
Ryan C. Petering
Basics
Description
Aortic stenosis is the most prevalent valvular heart disease. There are several terms that are
used to describe different variants of aortic valve abnormalities.
Aortic sclerosis: Calcification or thickening of the aortic valve without outflow obstruction
Calcific aortic stenosis: Calcification on the aortic valve cusps that leads to outflow
obstruction; most common etiology of aortic stenosis
Congenital bicuspid aortic valve: Aortic stenosis resulting from 2-leaflet aortic valve with
symptoms developing in 1st or 2nd decade of life; frequently associated with coarctation of
the aorta
Congenital aortic stenosis: Various valve structural abnormalities that lead to symptoms in
childhood; less likely to be associated with heart failure and angina than adult onset aortic
stenosis (1)
System(s) affected: Cardiovascular
Epidemiology
Incidence
Calcific aortic stenosis is frequency associated with age:
Ages 65–74: 1–3% prevalence
Ages 75–84: 2–4% prevalence
Age >85: >4% prevalence
Predominant gender: Male > Female (slightly)
Bicuspid aortic valve present in 1–2% of newborns
Bicuspid aortic valve occurs predominantly in males (1).
Risk Factors
The exact mechanism of aortic stenosis is unclear.
Proposed mechanisms include lipid accumulation, inflammation, and calcification.
Risk factors include:
Increasing age
Male gender
Hyperlipidemia
Active inflammation (2)
Diagnosis
Classic triad of (1) dyspnea, (2) angina, and (3) syncope
Symptoms of heart failure (dyspnea on exertion, orthopnea, lower extremity edema)
Murmur: Harsh crescendo-decrescendo systolic murmur loudest over the right 2nd intercostal
space with radiation toward the carotid artery
Parvus tardus: Slow, delayed carotid upstroke
Absent or diminished aortic component of 2nd heart sound (3)

Lab
There are no specific laboratory studies related to aortic stenosis.
Imaging
CXR and electrocardiogram frequently will be abnormal, but changes are not specific nor
sensitive in the diagnosis of aortic stenosis.
Transthoracic echocardiogram (TTE):
Mainstay for diagnosis and staging of aortic stenosis
Key measurements include left ventricular systolic function, hypertrophy, transvalvular
pressure gradient, and aortic valve area.
Normal: Aortic jet velocity <2.5 m/s2, aortic valve area 3–4 cm2
Mild: Aortic jet velocity 2.5–2.9 m/s2, aortic valve area 1.5–2 cm2
Moderate: Aortic jet velocity 3–4 m/s2, aortic valve area 1–1.5 cm2
Severe: Aortic jet velocity >4 m/s2, aortic valve area <1 cm2 (3)
Cardiac catheterization is commonly performed as part of the diagnostic workup of aortic
stenosis to rule out coexisting coronary artery disease (1).
Coronary artery disease
Congestive heart failure
Other valvular heart disease
Treatment
Some patients will present with hemodynamic instability that requires
aggressive intervention.
Aortic valve replacement surgery is the only treatment for symptomatic aortic
stenosis and is recommended for most symptomatic patients.
Nonurgent intervention is usually guided by patient symptoms.
Congestive heart failure symptoms (ie, shortness of breath, orthopnea, and
dyspnea on exertion) are associated with increased mortality (4).
Close follow-up and observation is generally recommended for patients with
aortic stenosis unless categorized as severe by TTE or symptoms exist.
Medication P.
No medications have been shown to influence the course or symptoms of
aortic stenosis.
Coexisting hypertension, congestive heart failure, hyperlipidemia, and coronary
artery disease should be treated according to individual guidelines (1).
Aortic valve replacement surgery is recommended for asymptomatic patients with
severe aortic stenosis and left ventricular dysfunction (TTE finding of an ejection
fraction of <50%) (4).
Ongoing Care
Activity recommendations need to be individualized owing to often complicated picture of
coexisting conditions in aortic stenosis patients.
Asymptomatic, mild aortic stenosis: No restrictions in activity
Asymptomatic, moderate–severe aortic stenosis: Avoid competitive and vigorous activity with
high dynamic and static muscle demands. Otherwise, exercise is generally permitted.
Symptomatic aortic stenosis: Activity contraindicated (1)
Patient Monitoring
TTE monitoring by aortic stenosis severity:
Severe: Every 6–12 mos
Moderate: Every 1–2 yrs
Mild: Every 3–5 yrs
Treadmill stress testing can be used to help guide management of asymptomatic patients
with moderate–severe aortic stenosis (3).
Patient Education
All asymptomatic patients who are being monitored need detailed education about the
symptoms of heart failure.
Prognosis
1% annual risk of sudden death with asymptomatic aortic stenosis
Average overall survival rate for symptomatic patients is 2–3 yrs without aortic valve
replacement.
Aortic valve replacement surgery perioperative overall mortality is roughly 4%. There is great
variability in risk based on patient age and coexisting conditions.
Patients without coexisting conditions and age 55–65 yrs: 1% risk
Patients with coexisting hypertension and coronary artery disease and age 85 yrs: 7% risk
Patients with coexisting hypertension, coronary artery disease, and previous cardiac
catheterization and age 85 yrs: 24% risk (4)
References
1. Carabellow BA, Paulus WJ. Aortic stenosis. The Lancet. 2009;373:956–966.
2. Dal-Bianco JP, et al. Management of severe asymptomatic aortic stenosis. J Am Coll

Cardiol. 2008;52:1279–1292.
3. Gimard BH, Larson JM. Aortic stenosis: diagnosis and treatment. Am Fam Physician.
2008;78(6):717–725.
4. Otto CM. Valvular aortic stenosis. J Am Coll Cardiol. 2006;47:2141–2151.

Codes
ICD9
424.1 Aortic valve disorders
440.0 Atherosclerosis of aorta
746.4 Congenital insufficiency of aortic valve
Athletic Heart Syndrome
Justin Wright
Basics
Description
A benign condition consisting of physiologic adaptations to the increased cardiac workload of
exercise. Its primary features are biventricular hypertrophy and bradycardia associated with
normal systolic and diastolic function.
Many characteristics overlap with serious pathologic conditions. This makes the
differentiation challenging and of paramount importance.
Synonym(s): Athlete's heart; Physiologic cardiac hypertrophy
Epidemiology
These changes are almost universal in highly trained athletes.
Often mistaken for pathologic conditions
Risk Factors
Chronic endurance exercise
Genetic predisposition
Etiology
Changes in cardiac structure vary based on type of exercise (1).
Dimensions of athlete's heart rarely exceed upper limits of normal
Dynamic exercise (eg, distance running):
Increased heart rate and stroke volume
Adaptive responses in the heart due to volume overload and increased systolic BP
Increase in left ventricular end-diastolic diameter with proportional increases in septal and
free-wall thickness to normalize wall stress
Static exercise (eg, weight lifting, bodybuilding):
Marked increased peripheral resistance with smaller increases in heart rate and cardiac
output
Increase in septal and free-wall thickness without increase in left ventricular end-diastolic
diameter
Combined exercise (eg, cycling, rowing):
Extreme volume load and extreme pressure load
Largest increases in left ventricular end-diastolic diameter and septal and free-wall
thickness
Diagnosis
History
Used to differentiate benign physiologic change from pathologic conditions
History of chest pain, dizziness, or syncope associated with exercise may be suggestive of
pathology.
Inquire about heart disease risk factors, including HTN, hyperlipidemia, tobacco use, and
family history of sudden cardiac death.
History of previously identified murmur should be investigated.
Physical Exam
Decreased body fat and increased muscle mass (generally very physically fit)
Pulse slow and often irregular (sinus bradycardia or bradycardia with 1st- and 2nd-degree
blocks)
Grade 1 or 2 midsystolic murmurs (benign functional ejection murmur resolves with Valsalva
maneuver)
3rd and 4th heart sounds very common (benign filling sounds)
BP typically remains normal.
Laterally displaced left ventricular impulse

Imaging
Electrocardiography (2)[B]:
Rhythm:
Sinus bradycardia of 40–55 beats/min while at rest
Sinus pauses of more than 2 sec due to increased vagal tone
Wandering atrial pacemaker, found only in dynamic athletes
Atrioventricular block:
1st-degree atrioventricular block present only at rest; P-R interval normalizes with
exercise
2nd-degree atrioventricular block present only at rest; Mobitz I (Wenckebach block)
common in marathon runners
Higher-grade atrioventricular blocks (Mobitz II, 3rd-degree) rare in athletes; may be
indicative of underlying heart disease
Voltage:
Left ventricular hypertrophy
Right ventricular hypertrophy, common in dynamic athletes, but rarely seen in sedentary
controls and static athletes
Repolarization:
S-T segment elevation with peaked T waves, normalizes with exertion
S-T segment depression with depressed J points, rarely found in athletes
T-wave inversion in lateral leads associated with interventricular septal hypertrophy in
static athletes (can be normal finding in dynamic athletes)
Chest radiography (2)[C]:
Heart is globular in appearance, particularly in endurance athletes.
Cardiomegaly (cardiothoracic ratio >0.50)
Echocardiography:
Biventricular hypertrophy
Left ventricular wall thickness >13 mm uncommon in highly trained athletes; values >15 mm
indicative of hypertrophic cardiomyopathy (3)
Dynamic athletes: Left and right ventricular dilation with left, right ventricular and septal
hypertrophy (eccentric hypertrophy)
Static athletes: Left ventricular and septal hypertrophy with either decrease or no change
in left ventricle chamber size (concentric hypertrophy); similar changes occur with chronic
HTN (2)[B]
Cardiac magnetic resonance (1,3)[B]:
Precise assessment of chamber size, myocardial mass, systolic function
Capable of measuring both ventricles
Useful in differentiating athlete's heart from hypertrophic cardiomyopathy and
arrhythmogenic right ventricular cardiomyopathy (ARVC)
Detraining leads to a decrease in wall thickness and a reversal of electrocardiographic
abnormalities (2,3)[B]:
Reversal happens over several weeks.
Can be used to differentiate from hypertrophic cardiomyopathy if other methods are
unrevealing
Hypertensive cardiac hypertrophy
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
ARVC
Treatment
If pathologic evidence of heart disease is absent, then reassure the athlete
that the observed changes are normal physiologic adaptations to exercise.
Do not encourage the athlete to stop exercising.
Ongoing Care
Many of the physiologic adaptations observed in athletic heart syndrome resolve when
exercise is stopped.
Because the adaptations that occur in the resistive or static athlete are similar to those
caused by chronic HTN, the long-term effects could be damaging. Therefore, these
individuals should be encouraged to incorporate dynamic components to their weight-lifting
routine.
Patients with overlapping features of athletic heart and a pathologic process (ie, exertional
symptoms or family history) should be evaluated by a cardiologist prior to being allowed to
return to sport or exercise.
References
1. La Gerche A, Taylor AJ, Prior DL. Athlete's heart: The potential for multimodality imaging
to address the critical remaining questions. JACC Cardiovasc Imaging. 2009;2:350–363.
2. Rich BS, Havens SA. The athletic heart syndrome. Curr Sports Med Rep. 2004;3:84–88.
3. Lauschke J, Maisch B. Athlete's heart or hypertrophic cardiomyopathy? Clin Res Cardiol.
2009;98:80–88.
Additional Reading
Pluim BM, et al. The athlete's heart. A meta-analysis of cardiac structure and function.
Circulation. 2000;101:336–344.
Maron BJ. Sudden death in young athletes. New Engl J Med. 2003;349:1064–1075.
Codes
ICD9
429.3 Cardiomegaly
Clinical Pearls
Physiologic response to exercise; no increased risk with participation
Important to differentiate from pathologic conditions that place athlete at risk for
sudden cardiac death
Electrocardiography and echocardiography can help distinguish physiologic
from pathologic
Detraining can aid in differentiation.
Atlantoaxial Instability
Rebecca L. Carl
Basics
Description
Atlantoaxial instability (AAI) is the term for increased motion at the joint between the 1st and
2nd cervical vertebrae (the atlas and the axis).
Congenital, inflammatory, traumatic, or infectious conditions may weaken the structures
supporting the C1–2 joint leading to atlantoaxial instability.
Many patients who meet the radiographic definition of AAI are asymptomatic and at low risk
for neurological sequelae.
Synonym(s): Atlantoaxial subluxation
Epidemiology
The incidence of radiographic/asymptomatic AAI in individuals with Down syndrome is
estimated between 10 and 20%.
The incidence of symptomatic AAI is much lower at 2.6%.
Incidence of AAI increases with age and progression may occur during growth spurts.
For individuals with Down syndrome, males over the age of 10 are most likely to have
progression of AAI.
Risk Factors
Down syndrome
Rheumatoid arthritis
Juvenile idiopathic arthritis
Many forms of dwarfism/skeletal dysplasias
Marfan syndrome: Increased incidence of C1-C2 hypermobility but symptoms are rare.
Diagnosis
Lateral cervical radiographs with flexion and extension views are used for screening. AAI
is defined radiographically as an increased distance between the odontoid process and the
anterior arch of the axis.
Obtaining screening x-rays for AAI in asymptomatic patients with Down syndrome is
controversial.
Because of poor radiographic reproducibility and because many radiographic signs of AAI
often resolve over time in asymptomatic patients, the American Academy of Pediatrics
retired a position statement that had previously endorsed routine screening.
The Special Olympics continues to require radiographic screening in all athletes with Down
syndrome.
Some suggest screening lateral x-rays in patients with Down syndrome during periods of
rapid growth at ages 5, 12, and 18.
History
Most individuals with AAI are asymptomatic.
AAI can be acute or chronic. However, acute AAI without a history of preceding symptoms is
rare.
Patients with acute AAI often present after injury. Injury can be due to direct or indirect
trauma. Mechanisms of injury include hyperextension, hyperflexion, direct loading.
In patients who have an acute worsening of AAI, participation in organized sports is an
uncommon triggering event.
Patients with chronic AAI often present with gait changes, progressive weakness, and
fatigue. Neck pain, bowel and bladder incontinence, ataxia, spasticity, and quadriplegia can
be present with longstanding, severe chronic AAI.
Physical Exam
Hyperreflexia
Sensory changes
Weakness
Gait changes
Cervical spine range of motion is often normal

Imaging
Lateral neck radiographs with flexion/extension views:
AAI is defined as a space of 5 mm or more between the odontoid process of the axis and
the anterior arch of the atlas.
Further evaluation with CT or MRI in cervical flexion and extension is often needed to assess
for spinal cord compression in patients with AAI on plain radiographs.
Neck sprain/strain
Cervical disc herniation
Torticollis
Vertebral fracture
Ligamentous laxity
Spinal contusion
Epidural hemorrhage
Treatment
Management of athletes with acute worsening of AAI symptoms
If worsening occurs with trauma, assume a potentially unstable injury is present
until proven otherwise.
The cervical spine must be stabilized in the field.
Protect the airway if respiratory difficulties arise.
Anesthesia administration:
Blind endotracheal intubation of a patient with AAI should be avoided.
Tracheal intubation with a flexible bronchoscope under topical anesthesia
avoids neck flexion and maintains cervical spine stability.
For elective procedures, consider regional anesthesia with minimal sedation.
Atlantoaxial fusion should be considered for patients with progressive,
symptomatic AAI and/or cervical myelopathy.
Because atlantoaxial fusion is a very high-risk procedure, nonoperative
management is recommended for patients without neurologic symptoms.
Ongoing Care
Long-term management:
Individuals who exhibit signs and symptoms should be restricted from contact sports and
other activities that place stress on the neck.
Restriction of asymptomatic patients with only radiographic evidence of AAI is somewhat
controversial, particularly for noncontact activities:
Special Olympics requires that patients with radiographic evidence of atlantoaxial instability
be temporarily restricted from the following:
Butterfly stroke
Diving (including diving starts in swimming)
Pentathlon
High jump
Squat lifts
Equestrian sports
Artistic gymnastics
Soccer
Skiing
These restrictions can be removed if an asymptomatic athlete (or the athlete's parents in
the case of a minor) signs a waiver after having the risks of AAI explained by 2 physicians.
Primary care physicians should counsel families of patients with Down syndrome, rheumatoid
arthritis, juvenile inflammatory arthritis, and skeletal dysplasias about possible signs and
symptoms of atlantoaxial instability.
Additional Reading
Atlantoaxial instability in Down syndrome: subject review. American Academy of Pediatrics
Committee on Sports Medicine and Fitness. Pediatrics. 1995;96:151–154.
Cremers MJ, Bol E, de Roos F, et al. Risk of sports activities in children with Down's
syndrome and atlantoaxial instability. Lancet. 1993;342:511–514.
Laiho K, Savolainen A, Kautiainen H, et al. The cervical spine in juvenile chronic arthritis.
Spine J. 2002;2:89–94.
Torg JS, Ramsey Emrhein JA. Suggested management guidelines for participation in
collision activities with congenital, developmental, or postinjury lesions involving the cervical
spine. Med Sci Sports Exerc. 1997;29:S256–S272.
Wills BP, Dormans JP. Nontraumatic upper cervical spine instability in children. J Am Acad
Orthop Surg. 2006;14:233–245.
Winell J, Burke SW. Sports participation of children with Down syndrome. Orthop Clin North
Am. 2003;34:439–443.
Codes
ICD9
718.88 Other joint derangement, not elsewhere classified, involving other specified sites
Clinical Pearls
Athletes with radiographic evidence of AAI who are asymptomatic appear to be at
low risk for experiencing acute worsening during participation in organized sports
(particularly noncontact activities). Each individual athlete should discuss sports
participation guidelines with his/her physician(s).
Auricular Hematomas
Kevin E. Elder
Todd Toriscelli
Basics
Alert
Failure to diagnose and promptly treat this condition with evacuation of the hematoma may lead
to permanent deformation of the ear.
Description
Auricular hematoma is an injury caused by trauma or friction of the ear that often occurs in
contact sports such as rugby, wresting, boxing, and judo.
Trauma or continuous friction to the auricle leads to bleeding into the soft tissues of the ear.
Bleeding often occurs anteriorly at the junction of the perichondrium and elastic cartilage of
the ear.
Recognition of this condition as a result of trauma led to the development of treatments
during the latter half of the 20th century.
Epidemiology
Incidence
The incidence of this condition is higher in young males owing to their predilection to
participate in the sports most often producing this injury. One study of collegiate wrestlers
found a statistically significant difference in wrestlers developing auricular hematoma while
wearing headgear (26%) versus those who were not wearing headgear (52%) (1).
This is a reported 50% decrease in incidence of the condition in wrestlers who consistently
wore protective headgear during training and competition (1).
Prevalence
This condition is more prevalent in young males because they are most often the participants
in the specific organized team sports associated with the injury, but it may occur in males or
females.
There are no well-established records of the exact prevalence of this condition.
Risk Factors
Failure to wear headgear while participating in sports such as wresting, rugby, or martial arts
disciplines such as judo may increase the risk of ear trauma.
General Prevention
General prevention is based on proper use of headgear during participation.
Ill-fitting headgear may provide inadequate protection to the auricle.
Awareness of the importance and use of proper fitting headgear by athletes, coaches, and
athletic training staff may prevent this injury.
Etiology
The condition is caused by trauma owing to a direct blow or frictional forces to the auricle.
Bleeding into the auricle, specifically between the skin and auricular cartilage, results in a
hematoma in this space.
Untreated, the hematoma can cause pressure, necrosis, and scarring of the auricular
cartilage leading to a “cauliflower ear,” which is the name given to the characteristic deformity
to the ear.
Neocartilage formation at the site of the clot also plays a role in the associated deformity.
This deformity is disfiguring and permanent.

Auricle laceration
Rupture of tympanic membrane owing to associated trauma
Concussions related to head trauma
Cellulitis and perichondritis may mimic or be associated with this disorder.
Diagnosis
Diagnosis is made based on clinical exam and history of trauma/excessive friction to the
ear (2)[C].
The absence of associated factors that may lead to cellulitis of the ear may aid in the correct
diagnosis.
History
History of direct and recent trauma to the auricle with resulting hematoma
Lack of protective head gear while participating in high-risk sports for this injury should raise
level of suspicion.
The athlete complains of a painful ear and may have associated hearing loss.
Physical Exam
Examination of the auricle reveals a soft hematoma with tenderness of the auricle presenting
within a few hours after the inciting injury.
Loss of the normal architecture of the auricle compared with the contralateral side
Exam should include an assessment of the athlete's hearing.
Associated ear drainage should prompt consideration for rupture of the tympanic membrane.
Assessment to rule out signs and symptoms of concussion should be performed.

Diagnosis of this condition is based on history and clinical exam.
Lab
No specific lab tests confirm diagnosis.
CBC or ESR may aid in the diagnosis of associated infection.
Ear laceration
Cellulitis of ear
Perichondritis
Treatment
Once frictional and/or direct pressures have resulted in a hematoma
between the skin and auricular cartilage, the initial goal in treatment is to
aspirate this area to prevent further complications.
Following anesthesia with lidocaine without epinephrine, aspiration can be
attempted with a 25-gauge needle and syringe (2)[C].
This aspiration must be done in the acute phase when the hematoma is
palpable.
Later evacuation of the hematoma may require an 18–22-gauge needle (3)
[C].
If left untreated, the hematoma can lead to neocartilage formation, scarring,
and necrosis, all of which can lead to permanent deformity.
Antibiotics are sometimes given as a preventative measure because infection
of the auricle will result in further poor outcomes. Antibiotics should cover
common skin bacteria. Cephalexin is used commonly.
To prevent reaccumulation of the hematoma and the need for additional
aspirations, a compression dressing must be applied to the area.
Incision and drainage followed by mattress suture placement also have been
described. This method is more time- and labor-intensive but allows for better
cosmetic results.
Medication
Consider antibiotics for prophylactic coverage (eg, cephalexin ×7 days). If
suturing or incision and drainage are done, antibiotics definitely should be used
(4)[C].
NSAIDs and aspirin should be avoided to minimize hematoma recurrence risk.
The importance of acute aspiration of hematoma has been described, as well
as the possible need for attempted hematoma evacuation with a larger-bore
needle.
On occasion, a pressure dressing may not be needed if the hematoma does
not recur within 1 hr of successful aspiration (5).
To prevent reaccumulation of the hematoma and the need for additional
aspirations, a compression dressing commonly is placed over the area.
Compression must stay over the ear until it is fully healed.
Compression dressing may be needed for 3 days or more.
Owing to the shape of the ear, firm and even compression can be challenging.
The most widely used method of compression is the application of a collodion
cast dressing (6)[C].
This is accomplished by mixing collodion, a topical adhesive, with sterile
gauze. The resulting adhesive cast then is formed around the auricle. The
cast hardens in a short period of time and, if performed properly, can result in
uniform compression (7)[C].
Another treatment involves a mold of the ear being taken and a compression
cast made from silicone of the mold (8)[C].
Another method that may provide to be the best uniform compression but is
more time- and labor-intensive is through-and-through mattress sutures (9)
[C].
These maintain pressure, sometimes with use of dental rolls or a button.
A small incision is made along the helical or anthelical rim for hematoma
evacuation, and sutures are placed afterward (3)[C].
The ear's natural contour is maintained.
This method is more technically difficult and may more appropriate for ENT
or plastic surgery.
These type of sutures may remain for up to 7–10 days.
The possibility of surgery may be entertained, as mentioned earlier, in
consultation with ENT or plastic surgery.
Ongoing Care
Daily follow-up is needed to observe for signs of hematoma redevelopment, pressure necrosis,
allergic reaction to materials, and infection.
Patient Monitoring
Follow-up with ENT or plastic surgery after acute treatment is recommended because of the
risk of poor cosmetic result even with proper treatment of the condition.
Patient Education
Return to play too early, prior to fully healing of the injury, will increase the risk of a poor
outcome.
No definitive return-to-play protocol exists.
Some authors recommend no competition while wearing ear compression dressing,
whereas others allow full activity with ear protection being worn (10).
The decision should be made in consultation with the athlete, recognizing the potential for
poor cosmesis with recurrence of the injury.
Ear protectors and headgear always should be worn in high-risk sports.
Ice and pressure applied at the end of practices and matches may help to prevent
recurrence of injury.
Prognosis
Best prognosis is achieved by prompt aspiration and compression if needed.
Poorer outcomes are associated with repeated need for aspiration and earlier return to
contact sports/reinjury.
Complications
Permanent scarring and cosmetic deformity.
Chondritis and perichondritis.
Prompt treatment including aseptic technique may prevent these
consequences.
References
1. Schuller DE, et al. Auricular injury and the use of headgear in wrestlers.
Arch Otolaryngol Head Neck Surg. 1989;115:714–717.
2. Mudry A, Pirsig W. Auricular hematoma and cauliflower deformation of the

ear: from art to medicine. Otol Neurotol. 2009;30:116–120.
3. Wu TS. Tricks of the trade: head and neck procedures. American College
of Emergency Physicians Scientific Assembly, 2008.
4. Sallis RE, Massimino F. ACSM's Essentials of Sports Medicine. General

Medicine. Mosby, 1997:120–121.
5. Davidson TM, Neuman TR. Managing ear trauma. Phys Sports Med.
1994;22(7):27–32.
6. Inside Surgery.com. Treatment of hematoma of the auricle. July 16, 2009.
7. Macdonald DJ, Calder N, Perrett G, et al. Case presentation: a novel way

of treating acute cauliflower ear in a professional rugby player. Br J Sports
Med. 2005;39:e29.
8. Lane SE, Rhame GL, Wroble RL: A silicon splint for auricular hematoma.
Phys Sports Med. 1998;26:9.
9. Giles WC, Iverson KC, King JD, et al. Incision and drainage followed by
mattress suture repair of auricular hematoma. Laryngoscope.
2007;117:2097–2099.
10. Schuller DE, Dankle SD, Strauss RH: A technique to treat wrestler's
auricular hematoma without interrupting training or competition. Arch
Otolaryngol Head Neck Surg. 1989;115:202–206.
Additional Reading
Dallas B: Cauliflower ear: the trademark worn by a competitive wrestler.
ACC.com; Wrestling. Dec 2004.
Kaufman BR, Heckler FR: Sports related facial injuries. Clinics Sports Med.
1997;16(3):543–562.
Mellion et al, eds. Team Physician's Handbook, 3rd ed. Wrestling, 617.
Hanley & Belfus, 2002.
Codes
ICD9
380.31 Hematoma of auricle or pinna
Clinical Pearls
Diagnosis of this condition is based on history and clinical exam.
Early recognition and treatment of this condition with hematoma aspiration may
prevent long-term sequelae and disfigurement.
Return to contact sports without sufficient time for injury to fully heal/allow
adequate retreatment increases the risk for a poor cosmetic result.
Compression treatment options include collodion cast, silicon cast, and
horizontal mattress suture repair.
ENT/plastic surgery consultation may be required.
Use of ear protection/headgear is effective in prevention of this condition.
Avascular Necrosis of the Proximal Femoral
Epiphysis (Legg-Calve-Perthes Disease)
Christopher McGrew
Basics
Description
Juvenile idiopathic avascular necrosis of the capital femoral epiphysis of the femoral head
Synonym(s): Perthes disease; Aseptic necrosis of the femoral head; Osteochondritis
deformans juvenilis; Osteonecrosis of capital femoral epiphysis of the femoral head
Epidemiology
Incidence in general population 1/1,200 to 1/12,000
Prevalence 75/100,000 person-years
Predominant age: Affects children 3–12 yrs of age but is most common between the ages of
4 and 9 yrs; median age 7 yrs
Predominant gender: Male > Female (4–5:1)
Most prevalent among whites and Chinese; rare in blacks and Native Americans
Bilateral hip involvement in 15–20% of patients
Risk Factors
Low birth weight
Short stature
Delayed bone maturation
Involved family member (after index sibling, incidence 1/35)
Familial thrombophilia and hypofibrinolysis (controversial)
Etiology
Etiology of Legg-Calve-Perthes disease (LCPD) is unclear, but the following has been
proposed as a theoretical sequence of events:
Blood supply to the capital femoral epiphysis is interrupted.
Bone infarction occurs, especially in the subchondral cortical bone, whereas the articular
cartilage continues to grow (articular cartilage receives its nutrients from synovial fluid).
Revascularization occurs, and new bone ossification starts. At this point, a percentage of
patients develops LCPD, whereas others have normal bone growth and development.
LCPD is present when a subchondral fracture occurs. This is the result of normal physical
activity, not direct trauma to the area.
Changes to the epiphyseal growth plate occur secondary to the subchondral fracture.
Diagnosis
History
Symptoms of LCPD usually have been present for weeks because the child often does not
complain.
Hip or groin pain, which may be referred to the thigh
Mild or intermittent pain in anterior thigh or knee
Limp worsened by activity, usually most pronounced at end of day
Usually no history of trauma
Inflammatory synovitis can mimic LCPD but usually resolves in 10–14 days.
Physical Exam
Examine the musculoskeletal system with a focus on the pelvis and lower extremities.
Include range-of-motion (ROM) testing, limited abduction and internal rotation, presence or
absence of hip flexion contracture.
Evaluate for muscle atrophy of the thigh, calf, and buttocks, which is seen in long-standing
cases.
Measure for possible leg-length discrepancy, which indicates advanced involvement of the
femoral head.
Evaluate gait. Trendelenburg gait is observed with abductor weakness.
Perform log-roll test of extended leg on examining table; painful and reduced ROM is
observed compared with the opposite side.
Short stature: Children with LCPD often have delayed bone age.

Imaging
Anteroposterior and frog-leg lateral views of pelvis; can appear normal early in course
Femoral head appears smaller then opposite head with a widened articular cartilage space.
With disease progression, a crescent-shaped radiolucent line may be seen in the central
portion of the femoral head, especially on the lateral view.
Fracture, fragmentation, and resorption
Extent of femoral head involvement determines severity of disease.
Bone scan and MRI can be used to evaluate before radiographic changes are apparent.
MRI may be used to evaluate disease progression and/or resolution over time if radiographs
provide inadequate detail.
Inflammatory: Septic arthritis, osteomyelitis, transient synovitis
Trauma: Fracture
Neoplasm
Congenital: Limb abnormality
Developmental: Hip dysplasia, slipped capital femoral epiphysis
Sickle cell anemia: Osteonecrosis secondary to vascular infarcts
Gaucher disease: Osteonecrosis secondary to cerebroside and infarcts
Treatment
The healing process involves revascularization of the femoral head,
removal of necrotic bone, and replacement with viable bone. It is a biologic
process that requires many months. No current interventions accelerate this
process.
Nonsurgical treatment:
Treatment may involve simple observation, especially in children <6 yrs of
age.
Analgesia: Nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen
Activity restriction, crutches for non-weight-bearing, abduction stretching
exercises, bed rest
Abduction bracing/casting can be used for symptom relief and to hold the
femoral head in the acetabulum.
Casting/bracing may be discontinued when there is radiographic evidence of
subchondral reossification, usually after 12–18 mos.
Both surgical and nonsurgical treatments are aimed at symptom reduction,
prevention of capital femoral epiphysis destruction, and attainment of a
spherical femoral head at healing.
Rehabilitation:
Formal therapy program is recommended during and after bracing owing to
extensive atrophy, contracture, and loss of motion.
A home stretching program is encouraged to maintain ROM.
Goal is containment of femoral head leading to round femoral head.
Techniques vary depending on age of child and severity of femoral head
involvement.
Advantages include less time required in a brace and earlier return to activity.
Disadvantages include necessity of two operations.
Ongoing Care
All patients with suspected LCPD should be referred to a pediatric orthopedic surgeon
immediately.
Prognosis
The younger the age of onset of LCPD, the better is the prognosis.
Children >10 yrs of age have a very high risk of developing osteoarthritis.
Most patients have a favorable outcome.
Prognosis is proportional to the degree of radiologic involvement.
Complications
LCPD may result in femoral head deformity and degenerative joint disease
(onset of severe arthritis varies from adolescence to more commonly in
geriatric years).
Femoral head may be distorted permanently.
Additional Reading
Kocher MS, Tucker R. Pediatric athlete hip disorders. Clin Sports Med.
2006;25:241–253, viii.
Nochimson G. Legg-Calve-Perthes Disease. emedicine.medscape updated
9/24/08 http://emedicine.medscape.com/article/826935-overview.
Roy DR. Current concepts in Legg-Calvé-Perthes disease. Pediatr Ann.

1999;28:748–752.
Codes
ICD9
732.1 Juvenile osteochondrosis of hip and pelvis
Axillary Nerve Injury
Laura Distel
James R. Borchers
Basics
Originates from the C5–6 rami (and occassionally C4) and is a branch of the posterior
cord of the brachial plexus (1)
Courses from the brachial plexus and below the coracoid process along the anterior surface
of the subscapularis and then heads posteriorly and through the quadrilateral space (1)
The quadrilateral space is an anatomic entity created by the teres minor muscle inferiorly, the
long head of the triceps medially, the neck of the humerus laterally, and the subscapularis
and teres major muscles superiorly. The axillary nerve and posterior humeral circumflex
artery travel within the space (1).
Once through the space, the nerve travels further posteriorly and branches into an anterior
and posterior trunk.
The anterior trunk courses around the posterolateral (surgical) neck of the humerus and
innervates the anterior and middle deltoid.
The posterior trunk bifurcates into a motor branch, the teres minor and posterior deltoid
muscles, and a sensory branch innervating the superolateral brachial cutaneous nerve, which
innervates the lateral upper extremity.
Epidemiology
Has been reported to encompass <1% of all nerve injuries (2)
Incidence
True incidence unknown owing to underrecognition of the diagnosis.
Risk Factors
Anterior shoulder (glenohumeral) dislocation
Humeral neck fracture
Direct blunt trauma to the anterior lateral deltoid, which is common in contact sports such as
hockey, football, or rugby
Repetitive overhead sports (eg, volleyball, tennis, or baseball): This can lead to quadrilateral
space syndrome.
Iatrogenic damage (eg, shoulder instability surgery, rotator cuff surgery, and rarely, shoulder
arthroscopy)
Etiology
Traction injury to the nerve during an anterior dislocation or fracture (2)
Presumed compression injury of the nerve as a result of a direct blow to the anterolateral
deltoid (2)
Quadrilateral space syndrome: Proposed mechanisms include compression of the nerve by
fibrous bands, hypertrophied muscles that border the space, any space-occupying lesion (eg,
aneurysm or cyst), or shear between the teres minor and major (2).
Iatrogenic damage to the nerve during shoulder surgery (2)

Anterior glenohumeral dislocation
Humeral neck fracture
Diagnosis
Nerve injury should be suspected in any athlete with anterior shoulder dislocation or
humeral neck fracture.
History
Easy fatigability with overhead activities or heavy lifting (3)
Decreased strength with shoulder abduction (3)
Paresthesias or loss of sensation in the lateral upper arm (sensation is spared after anterior
shoulder dislocation)
Quadrilateral space syndrome: Vague, nonspecific aching or burning of the posterolateral
shoulder and/or generalized weakness with overhead activities (1)
Physical Exam
Assess for deltoid or teres minor atrophy compared with the unaffected side (more common
in chronic cases).
Active and passive range of motion (ROM) about the shoulder, including abduction, forward
elevation, and external rotation
Strength testing of abduction and forward elevation (deltoid function) and external rotation
(teres minor function)
Neurovascular exam, especially assessing for sensation over the lateral deltoid area known
as the “sergeant's patch”
Perform the Spurling maneuver (rotate the patient's head to the affected side and
hyperextend the neck) to assess for cervical radiculopathy.
Tenderness to palpation of the posterior shoulder at the quadrilateral space (often the only
positive finding in quadrilateral space syndrome)

Imaging
Plain x-rays of the shoulder to evaluate glenohumeral dislocation or evidence of fracture (3)
Consider cervical spine x-rays to rule out cervical spine causes of deltoid paresthesias,
weakness, or atrophy (1).
MRI can be helpful in chronic cases to identify a combined nerve injury, to determine
prognosis of functional recovery by evaluating fatty replacement of the muscle, or to evaluate
other soft tissue causes of shoulder weakness but is often not needed (3).
Electromyography (EMG) and nerve conduction velocity (NCV) should be obtained no sooner
than 3 wks after injury to establish baseline dysfunction (3)[A].
Repeat EMG and NCV after 3 mos if no clinical improvement to assess for nerve recovery
(2)[A].
Arteriogram of the posterior circumflex humeral artery to evaluate for quadrilateral space
syndrome, but there are conflicting recommendations regarding the use of this test (1)[B].
Brachial plexus syndromes:
Thoracic outlet syndrome
Neuralgic amyotrophy (Parsonage-Turner syndrome)
Quadrilateral space syndrome
Cervical spine lesions
Aneurysm, neoplasm, or cystic mass near the axillary nerve
Treatment
Nonoperative treatment is preferred initially (2)[A].
Emphasize active and passive ROM of the shoulder.
Relative rest
Strengthening exercises of the shoulder
Avoidance of exacerbating triggers or activities
ED Treatment
Reduction of glenohumeral dislocation or treatment of fracture
Electrical stimulation of the deltoid is an option to prevent atrophy while the nerve
is recovering (3)[C].
Appropriate interval for surgical intervention is unclear, but there is some
evidence to suggest that surgery within 6 mos of injury yields superior return of
function and strength (3)[B].
Generally indicated if no improvement using nonoperative treatments or if
EMG/NCV shows no interval nerve recovery in 3–12 mos postinjury (2)[A]
Operative procedures include (2)[A]:
Neurolysis
Sural nerve grafting
Neurorrhaphy
Nerve transfer
Neurotization
Surgical decompression can be performed for quadrilateral space syndrome to
release fibrous bands (3)[B].
Ongoing Care
Routine clinical follow-up every 4–8 wks while patient is undergoing therapy to assess for
return of strength and sensation
Repeat EMG/NCV if no improvement in 3 mos
Return to contact sports once full ROM and adequate strength of the shoulder are achieved.
Prognosis
Depends on mechanism and severity of nerve damage
Functional shoulder recovery is usually excellent (2).
85–100% of axillary nerve injury owing to fracture or dislocation will recover fully by 6–12
mos with nonoperative treatment (1).
Poorer prognosis for functional recovery in symptomatic patients who undergo surgical
intervention >12 mos after date of injury (3)
References
1. Safran MR. Nerve injury about the shoulder in athletes, part 1: suprascapular nerve and
axillary nerve. Am J Sports Med. 2004;32:803–819.
2. Perlmutter GS, Apruzzese W. Axillary nerve injuries in contact sports: recommendations

for treatment and rehabilitation. Sports Med. 1998;26:351–361.
3. Steinmann SP, Moran EA. Axillary nerve injury: diagnosis and treatment. J Am Acad
Orthop Surg. 2001;9:328–335.
Codes
ICD9
955.0 Injury to axillary nerve
Clinical Pearls
Axillary nerve injury should be suspected in individuals with a glenohumeral
dislocation or humeral neck fracture.
Normal sensation of the lateral upper arm does not rule out axillary nerve injury.
EMG/NCV tests should be performed in a suspected axillary nerve injury, but
no sooner than 3 wks postinjury.
Despite variable recovery rates of the axillary nerve and deltoid muscle,
functional recovery of the shoulder is excellent.
Barotitis Media
Carter W. Muench
Rob Johnson
Basics
Injury to the body as a result of the expansion and contraction of gas in an enclosed
space
Boyle's law states that at a constant temperature, pressure (P) is inversely related to volume
(V):
PV = K (constant) or P1V1 = P2V2.
Increase in pressure mandates a reduction in volume by same factor.
Gas-filled cavities in the body are subject to expansion/contraction:
Lung
Middle ear
Sinus
Solid and liquid-filled spaces distribute the pressure equally.
Volume changes experienced during diving are greatest in the few feet nearest the surface.
Alert
For barotrauma of descent, unless an air-filled cavity has ruptured, no progression of the
disease on return to normal atmospheric pressure expected.
If patient transport requires air evacuation, maintain air cabin pressure at 1 atm or fly below
1,000 ft to avoid aggravating barotrauma.
General Prevention
Avoid diving with upper respiratory infection, which may not allow for equalization of
pressures across the tympanic membrane because of eustachian tube blockage.
Predive medical examination can help to identify individuals at increased risk for barotrauma.
Taking pseudoephedrine 60 mg PO 30 min prior to diving was shown to decrease the
incidence and severity of middle ear barotrauma.
Etiology
Middle ear:
Barotrauma of descent
Most common type of barotrauma
Seen in 30% of inexperienced divers and 10% of experienced divers
Results from inadequate equalization of pressure between the middle ear and the external
ear canal
Eustachian tube provides the sole route of pressure equalization for the middle ear.
Upper respiratory infections may cause blockage or dysfunction of the eustachian tube.
External ear:
Due to the presence of a tight-fitting hood, ear plugs, or a cerumen plug
Pressure cannot equalize throughout the canal, and a relative intracanal vacuum is created
as the pressure differential across the obstruction increases.
Inner ear:
Results from forceful attempts at equalizing middle ear pressure
Increased middle ear pressure can raise intracranial pressure and cause rupture of the
round or labyrinth windows, allowing perilymph to enter the middle ear.
Paranasal sinus:
Nasal ostia act as a valve to regulate sinus pressure.
If the ostia fail to allow pressure equalization, congestion, edema, and hemorrhage can
occur.
External objects: Air pockets in dive suit/mask expand and contract.
Teeth: Air trapped inside a filling
GI:
Barotrauma of ascent
Swallowed air in the GI tract expands as external pressure decreases.
Pulmonary barotrauma [PBT or pulmonary overpressurization syndrome (POPS)]:
Occurs with ascent
Lungs expand against a closed glottis.
Cause for arterial gas embolism
Divers with decrease lung compliance/increased lung volumes at increased risk [chronic
obstructive pulmonary disease (COPD), asthma]
Taking a breath from a SCUBA tank at a shallow depth and surfacing without exhaling is
enough to cause pulmonary barotrauma.
Diagnosis
Essential Workup
Essential Workup
HEENT exam with particular attention paid to the tympanic membrane to determine if rupture
has occurred
Pulmonary exam looking for signs of SC emphysema and pneumothorax
Neurologic exam looking for signs of inner ear pathology or arterial gas embolism
Physical Exam
Signs and symptoms:
Middle ear (barotitis media):
Begins as a clogged sensation
Increasingly painful as the pressure differential across the tympanic membrane (TM)
increases
Associated symptoms include nausea, vertigo, tinnitus, conductive hearing loss, and
occasionally, facial nerve palsy.
Progresses to rupture of the TM: Appearance: TM congestion → TM edema → gross
hemorrhage → TM rupture
External ear: Canal mucosa becomes edematous, then hemorrhagic, and ultimately may tear.
Inner ear:
Sudden, severe vertigo
Tinnitus
Sensorineural hearing loss in the affected ear
Symptoms begin or are associated with forceful attempt to equalize pressures of middle
ear during descent.
Normal external canal and TM exam with isolated inner ear barotrauma
Paranasal sinuses:
Sinus congestion
Pain
Epistaxis
External objects:
Mask: Conjunctival hemorrhage, facial edema, and swelling
Tight-fitting dive suit: Edema and erythema of the skin
Teeth (barodontalgia): Severe tooth pain
GI (aerogastralgia):
Excessive belching
Flatulence
Abdominal distension
Pulmonary:
Dyspnea
Chest pain
Cough with a frothy red sputum
SC emphysema of the neck and chest
Delayed symptoms including a bull neck appearance, dysphagia, and changes in voice
character

Sinus imaging:
CT scan
Plain films
Chest X-ray for pneumothorax and pneumomediastinum
Abdominal series (upright, decubitus) for free air from a ruptured viscus
Lab
Arterial blood gas determinations for pulmonary symptoms
Decompression sickness
Otitis media
Otitis externa
Sinusitis
Arterial gas embolism
Treatment
Hospital admission criterion: Pulmonary barotrauma
ED Treatment
Establish IV access for unstable patients.
Control bleeding from the ear or nose.
Oral decongestants for middle ear or sinus congestion
Antibiotics with TM or sinus rupture
Analgesics
Consult Divers Alert Network (DAN): 1–919–684–4DAN (4326).
Medication
Amoxicillin 250–500 mg (children: 40 mg/kg/24 hr) PO t.i.d.
Bactrim DS 1 tablet (children: 40/200 per 5 mL-5 mL/10 kg/dose) PO b.i.d.
Pseudoephedrine (Sudafed) 60 mg (children: 6–12 yrs of age, 30 mg; 2–5 yrs
of age, 15 mg/dose) PO q4–6h
Airway, breathing, and circulation (ABCs):
100% oxygen for ill-appearing patients
Intubation in patients with massive SC emphysema of the neck
Immediate needle thoracostomy for evidence of tension pneumothorax
Admission Criteria
Pulmonary barotrauma
Discharge Criteria
Nonpulmonary barotrauma
ENT follow up for severe TM or sinus pathology
Ongoing Care
No diving until TM has healed and other symptoms have resolved
Predive medical clearance is recommended for anyone with prior pulmonary barotrauma or
decompression illness.
ENT referral for severe TM, inner ear, or sinus pathology
Additional Reading
Bradley ME. Pulmonary barotrauma. In: Bove AA, Davis JC. Diving medicine. 2nd ed.
Philadelphia: WB Saunders, 1990:188–191.
Brown M, Jones J, Krohmer J. Pseudoephedrine for the prevention of barotitis media: a

controlled clinical trial in underwater divers. Ann Emerg Med. 1992;21:849–852.
DeGorordo A, Vallejo-Manzur F, Chanin K, et al. Diving emergencies. Resuscitation.

2003;59:171–180.
Edmonds C, Lowry C, Pennefather J. Diving and subaquatic medicine. Oxford:

Butterworth-Heinemann, 1992.
Jerrard DA. Diving medicine. Emerg Med Clin North Am. 1992;10:329–338.
McMullin AM. Scuba diving: what you and your patients need to know. Cleve Clin J Med.
2006;73:711–712, 714, 716 passim.
Raymond LW. Pulmonary barotrauma and related events in divers. Chest. 1995;107:1648–
1652.
www.diversalertnetwork.org
Codes
ICD9
993.0 Barotrauma, otitic
993.1 Barotrauma, sinus
Biceps Tendinitis
Stephen Huang
Jason M. Leinen
Basics
Description
Overuse injury of the long head of the biceps
Initially begins as inflammation in the tendon sheath known as tenosynovitis and then
progresses to tendon degeneration and disordered arrangement of collagen fibers, otherwise
known as tendinosis or biceps tendinopathy
Primary biceps tendinitis (inflammation of the tendon) is estimated to represent only 5% of
cases.
Risk Factors
Repetitive use of upper extremities (especially overhead), such as throwing/hitting, swimming,
racquet sports, and gymnastics
Etiology
Anatomy:
The long head of the biceps arises from the superior glenoid labrum and the supraglenoid
tubercle of the scapula.
It is an intraarticular but extrasynovial structure.
Primary blood supply proximally is the anterior humeral circumflex artery.
Biomechanics:
Primary function of the biceps at the elbow is as a flexor and supinator.
In the shoulder, the biceps tendon may act as a humeral head depressor and a secondary
stabilizer of the glenohumeral joint.
During throwing, it assists in deceleration of the humerus.

Rotator cuff pathology (tendinopathy, impingement, tears)
Glenoid labral tears (SLAP lesions)
Subluxation/dislocation of the long head of the biceps
Biceps tendon rupture
Diagnosis
History
Anterior shoulder pain localized over the bicipital groove, which may radiate distally toward
the biceps
Pain is aggravated by overhead activities or lifting objects.
Physical Exam
Point tenderness over the bicipital groove
An audible or palpable snap during arc of motion while throwing may indicate instability or
subluxation of the biceps tendon.
A large mass (“Popeye deformity”) in the upper arm, ecchymosis, and swelling following a
painful audible pop with quick resolution of pain could indicate biceps tendon rupture.
Any positive testing for biceps tendon pathology may also signify a glenoid labral tear (SLAP
lesion).
Special tests:
Speed test: With the patient's shoulder elevated to 90 degrees of forward flexion, elbow
extended and forearm supinated, the patient flexes the shoulder against resistance. Pain in
or about the bicipital groove is considered a positive test.
Yergason test: With the patient's elbow flexed to 90 degrees, the patient supinates against
resistance. Pain over the biceps tendon in the bicipital groove is considered a positive test.

Imaging
Plain-film radiographs are not helpful in the diagnosis of biceps tendon pathology but may
reveal abnormalities of the acromion process such as hooking or spurring associated with
rotator cuff impingement.
MRI may show increased signal on T2-weighted images in the area of the biceps tendon.
MRI is also useful in detecting pathology of the superior labrum and rotator cuff and is
noninvasive.
MR arthrography is superior to conventional MRI in evaluating the glenoid labrum and rotator
cuff but is invasive.
Dynamic US is becoming more popular in diagnosing biceps tendon rupture, subluxation, and
dislocation. It is not reliable in evaluating intra-articular tears or the glenoid labrum. US is very
operator- and facility-dependent. Advantages include low cost and lack of radiation exposure.
Rotator cuff tendinopathy
Impingement syndrome
Glenoid labral tears
Biceps tendon subluxation/dislocation
Subacromial bursitis
Acromioclavicular joint separation or arthritis
Pectoralis minor strain
Glenohumeral joint arthritis
Cervical disk disease
Brachial plexus injuries
Pancoast tumor
Treatment
Acute treatment:
Conservative measures include rest, ice, and NSAIDs.
Rest should not include prolonged immobilization because this may lead to
adhesive capsulitis (frozen shoulder).
Gentle stretching and range-of-motion (ROM) exercises should be initiated
early, once symptoms begin to improve.
Consider physical therapy for persistent symptoms.
Surgery is reserved for refractory cases.
Physical therapy:
Gentle ROM exercises are begun 1st.
Scapulothoracic stabilization exercises
Rotator cuff strengthening
Biceps strengthening
Include:
US: Uses sound waves to heat up the affected tissues
Phonophoresis: Uses US waves to drive topical corticosteroid medication
into the affected tissue
Iontophoresis: Uses electric current to drive a corticosteroid into the affected
tissue
Injections:
Corticosteroid injection into the biceps tendon sheath may be considered, but
controversy exists regarding the accuracy of such injections.
Injection into the tendon itself has been associated with tendon rupture and
should be avoided.
Surgical options may be considered for patients who fail conservative
treatment or have refractory pain.
Tenotomy: Surgical release of the long head of the biceps tendon at or near
its superior glenoid labral origin:
Recommended in older patients with low activity requirements
Disadvantage includes a cosmetic “Popeye deformity” and possible loss of
some strength with supination.
Minimal rehabilitation is required.
Tenodesis: Fixation of the long head of the biceps tendon in the bicipital
groove
Minimal loss of function compared with tenotomy
No cosmetic defect
Recommended in younger, more active individuals
Disadvantages include a more complex operation, a period of
immobilization, and longer postoperative rehabilitation.
Proximal rupture of the long head of the biceps typically relieves symptoms of
pain without significant loss of function. Surgery may be considered if there is
significant loss of strength or function.
Reference
1. Longo UG, Franceschi F, Ruzzini L, et al. Characteristics at haematoxylin
and eosin staining of ruptures of the long head of the biceps tendon. Br J
Sports Med. 2007.
Additional Reading
Ahrens PM, Boileau P. The long head of biceps and associated tendinopathy.
J Bone Joint Surg Br. 2007;89-B:1001–1009.
Churgay CA. Diagnosis and treatment of biceps tendinitis and tendinosis. Am

Fam Physician. 2009;80:470–476.
Friedman DJ, Dunn JC, Higgins LD, et al. Proximal biceps tendon: injuries and
management. Sports Med Arthrosc. 2008;16:162–169.
Patton WC, McCluskey GM. Biceps tendinitis and subluxation. Clin Sports
Med. 2001;20:505–529.
Simmon SM, Dixon JB. Biceps tendinopathy and tendon rupture.

www.uptodate.com. version 17.2. March 5, 2009. 1–14.
Codes
ICD9
726.12 Bicipital tenosynovitis
Clinical Pearls
Primary biceps tendinitis is very rare and thought to be 5% of cases.
Studies involving biopsies of biceps tendons show an absence of inflammatory
cells in the tendon itself.
Instead they have shown collagen degeneration and disordered arrangement
of collagen fibers (1).
Biceps Tendon Rupture
Peter D. Marshall
Christopher C. Madden
Basics
Description
Complete or partial tear of the long bicipital tendon at a proximal or distal location from
repetitive microtrauma or acute traumatic injury
Epidemiology
Occurs most commonly in middle-aged males as a result of impingement
Occurs most commonly concomitantly with rotator cuff disease (eg, tendinopathy, tear)
rather than in isolation (1)[C]
90–97% of biceps tendon ruptures are proximal, at the intertubercular sulcus.
3–10% occur distally at the elbow.
Risk Factors
Male
Age >30 yrs
Known bicipital tendinopathy
Known rotator cuff tendinopathy or tear (biceps tendon pathologically loaded)
Overhead athlete (contributes to anterior shoulder stability with repeated abduction/external
rotation)
Prior corticosteroid injection into biceps tendon sheath
Anabolic steroid use

Rotator cuff impingement: Subacromial impingement in combination with repetitive overhead
motion, such as with throwing, can lead to proximal biceps tendon degeneration.
Superior labrum anterior-to-posterior (SLAP) lesions: Lesions of the superior glenoid labrum
from the 10 o'clock to the 2 o'clock position. SLAP lesions may involve the biceps anchor (2)
[C).
Subscapularis rupture/partial rupture: Following subscapularis tears, the biceps tendon can
sublux medially out of the bicipital groove, causing a painful clicking sensation.
Rotator interval lesions: The biceps tendon can sublux medially over the lesser tuberosity
after tears to the rotator interval, but there usually is an associated subscapularis injury.
Diagnosis
History
Mechanism is usually forceful eccentric biceps contraction, and it may be acute or chronic.
Pain is usually located more proximal than distal.
Prior symptoms are indicative of prior rotator cuff or bicipital tendinopathy.
Prior biceps tendon sheath corticosteroid injection is risk factor.
An injury with minimal symptoms in elderly patients showing acceptable strength may be
managed conservatively.
Physical Exam
Proximal rupture:
Patient may report a sudden tearing or “pop” in the shoulder.
Acute pain (may not be extreme) and later ecchymosis and swelling about the anterior
shoulder
Visible lump-type of deformity in the mid-upper arm anteriorly, secondary to muscle belly
retracting distally (“Popeye sign”)
In some cases of chronic shoulder pain, there may be notable improvement after
inflammation subsides.
Patients with accompanying rotator cuff pathology may complain of overhead pain and
weakness and night pain.
Inspect for “Popeye sign” deformity in anterior brachium.
Ecchymosis may involve entire anterior biceps.
Elbow function generally is preserved. Patient may have mild weakness of elbow flexion
and supination.
Shoulder function may be diminished, and careful evaluation of rotator cuff integrity is
advised.
Specialized tests for biceps pain include the Speed, Yergason, and Ludington tests.
Distal rupture:
History is usually of a sudden eccentric load with elbow at 90 degrees of flexion.
Acute tearing sensation with sudden loss of elbow flexion and supination strength
Pain, ecchymosis, and swelling localized over the antecubital fossa
Antecubital fossa with swelling and ecchymosis
May visualize absence of distal biceps tendon as it crosses the flexion crease
A palpable defect usually can be felt in antecubital fossa.
Usually significant losses in strength on resisted elbow flexion and supination
A partial rupture may have many of the same features as a complete rupture, but generally
the tendon still can be palpated in continuity.

Imaging
Plain films of shoulder are often negative with isolated tendon rupture. They are helpful in
ruling out proximal humerus fracture in elderly patients, however.
Shoulder MRI confirms diagnosis if clinical exam not straightforward and if rotator cuff
pathology is suspected.
MRI findings may include absence of the tendon within the intertubercular groove as a result
of tendon retraction. Partial rupture may show increased T2-weighted signal extending
partially through the tendon (3)[C].
Standard elbow x-ray series for distal injuries:
Check for avulsion fragment of radial tuberosity.
Degenerative changes or lipping at the radial tuberosity can be associated with biceps
tendinopathy.
Proximal rupture:
Superior labral lesion (ie, SLAP tear)
Subscapularis injury
Rotator cuff/rotator interval injury
Biceps tendon subluxation (rupture of transverse ligament)
Long head of biceps tendinitis or tendinosis; onset usually insidious
Greater or lesser tuberosity fractures may occur following shoulder dislocation.
Distal rupture:
Distal biceps tendinitis or tendinosis; onset usually insidious
Partial distal biceps tendon rupture
Anterior capsule strain; occurs with hyperextension injuries, and tenderness is more diffuse
anteriorly.
Coronoid process fractures directly tender over coronoid process; no palpable biceps
defect
Lateral antebrachial cutaneous nerve entrapment syndrome
None of these problems demonstrates absence of a palpable biceps tendon in the
antecubital fossa.
Partial ruptures can be difficult to diagnose, and MRI often is required.
Treatment
Proximal rupture:
Acute immobilization in posterior elbow splint with the elbow at 90 degrees for
comfort and forearm in full supination; add sling for comfort.
Younger patients should begin immediate shoulder and elbow passive range
of motion (ROM) exercises.
Strengthening can begin in 4–5 wks or when there is resolution of pain (4)[C].
Return to unrestricted activities after 2–3 mos
Patients over 50 yrs of age may require longer period of immobilization prior
to strengthening rehab.
Younger patients may prefer surgical treatment (tenodesis) for cosmetic
reasons or to return to their previous level of functioning.
Most patients are older and will have little to no change in elbow
flexion/supination strength; they may opt for surgery, however, if there is
additional rotator cuff pathology.
Distal rupture:
Acute management is the same as for proximal injuries.
Trial of nonoperative treatment for partial ruptures and elderly or sedentary
patients
Most patients require surgical repair because there is more significant loss
of elbow flexion and supination strength and endurance with distal injuries.
The main complaint after conservative management of biceps tendon ruptures,
especially distal ruptures, is loss of elbow flexion and forearm supination
strength, especially endurance.
Most young people and athletes require surgical repair of complete biceps
tendon injuries. Many advocate surgical repair of partial ruptures in this
population, especially if the ruptures are distal.
References
1. Phillips BB, Canale ST, Sisk TD, et al. Ruptures of the proximal biceps
tendon in middle-aged patients. Orthop Rev. 1993;22:349–353.
2. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps
muscle and superior glenoid labrum in anterior stability of the shoulder. Am J
Sports Med. 1994;22:121–130.
3. Zanetti M, Weishaupt D, Gerber C, et al. Tendinopathy and rupture of the

tendon of the long head of the biceps brachii muscle: evaluation with MR
arthrography. AJR Am J Roentgenol. 1998;170:1557–1561.
4. Baker BE, Bierwagen D. Rupture of the distal tendon of the biceps brachii:
operative versus non-operative treatment. J Bone Joint Surg Am.
1985;67:414–417.
Additional Reading
Anzel SH, Covey KW, Weiner AD, et al. Disruption of muscles and tendons:
an analysis of 1,014 cases. Surgery. 1959;45:406–414.
Mariani EM, Cofield RH, Askew LJ, et al. Rupture of the tendon of the long
head of the biceps brachii: surgical versus nonsurgical treatment. Clin Orthop.
1988;228:233–239.
Rokito AS, McLaughlin JA, Gallagher MA, et al. Partial rupture of the distal
biceps tendon. J Shoulder Elbow Surg. 1996;5:73–75.
Codes
ICD9
727.62 Nontraumatic rupture of tendons of biceps (long head)
840.8 Sprain of other specified sites of shoulder and upper arm
Bites and Stings
Steven A. Greer
Basics
Arthropods affect man as pests, by inoculating poison or invading tissue, or by
transmitting disease. Inoculation of poison may occur as either a bite or a sting. This discussion
is limited to the irritative, poisonous, allergic effects of these pests.
Description
Harmful arthropods of the U.S. include (1,2,3):
Ants: Fire ants, harvester ants
Bees: Bumblebees, sweat bees, honeybees, Africanized (killer) bees
Bugs: Kissing, bed, wheel
Caterpillars: Puss, browntail, buck, moth saddleback
Centipedes
Fleas: Human, cat, dog
Flies: Deer, horse, black, stable, and biting midges
Lice: Body, head, pubic
Mites: Itch mite (scabies), red bugs (chiggers)
Mosquitoes
Scorpions
Spiders: Brown recluse, black widow, hobo
Ticks: Deer, lone star
Wasps: Hornets, wasps
Characteristic reactions include:
Local tissue irritation, inflammation, and destruction
Systemic effects related to inoculated poisons
Allergic reactions: Immediate or delayed
System(s) affected: Skin/Exocrine
Epidemiology
Affects all ages with 0- to 4-yr-olds and 20- to 24-yr-olds at highest risk for nonfatal
bites/stings (4)
Males = Females
Incidence
Common, with 1 million nonfatal and 50 fatal cases per year (4,5)
Anaphylaxis is estimated at 3% in adults and 0.4–0.8% in children
Individual stings from Africanized (killer) bees are no more potent than other bees; the
danger lies in their predilection to swarm, causing death by multiple stings.
Prevalence
Ubiquitous, varies by region and season (4)
Risk Factors
Living environment (5,6)
Climate
Season
Clothing
Lack of protective measures
Perfumes, colognes
Previous sensitization
Young or elderly at more risk for morbidity/mortality
Genetics
No genetic predilection
General Prevention
Prevention/avoidance (5,6,7):
Avoid re-exposure in known hypersensitive individuals.
Prescribe anaphylactic (ANA kit) or self-administered epinephrine (Epi-Pen), if indicated.
Educate on risks of increasing anamnestic responses in the future.
Consider desensitization with immunotherapy in severe cases.
Cover as much skin as possible.
Use repellants on uncovered areas.
Apply sunscreen 1st, then repellant.
DEET, epicardin, or other proven insect repellants
Oil of lemon eucalyptus, PMD, and IR3535 are considered biopesticides by the
Environmental Protection Agency (EPA), but be sure to use EPA-approved products, as
many versions have not been tested.
Permethrin applied to clothes is effective through multiple washings.
Permethrin-infused clothing is commercially available and effective.
Consider immunization/prophylaxis for travel to endemic areas.
Etiology
Local tissue inflammation and destruction from poison (5)
Allergic reaction from previous sensitization (0.4–3%)
Toxic reaction from large inoculation of poison
Diagnosis
Physical Exam
Signs and symptoms (2,3,5,6,8):
Erythema
Pain
Heat
Swelling
Itching
Blisters
Secondary infection: Cellulitis, abscess
Necrosis
Ulceration
Drainage
Toxic reactions (nonantigenic):
Nausea
Vomiting
Headache
Fever
Diarrhea
Lightheadedness
Syncope
Drowsiness
Muscles spasms
Edema
Convulsions
Systemic reactions (allergic):
Itching eyes
Facial flushing
Generalized urticaria
Dry cough
Chest/throat constriction
Wheezing
Dyspnea
Cyanosis
Abdominal cramps
Diarrhea
Nausea
Vomiting
Vertigo
Chills/fever
Stridor
Shock
Loss of consciousness
Involuntary bowel/bladder action
Frothy sputum
Respiratory failure
Death
Delayed reaction:
Serum-sickness-like reactions
Fever
Malaise
Headache
Urticaria
Lymphadenopathy
Polyarthritis
Unusual reactions:
Encephalopathy
Neuritis
Vasculitis
Nephrosis
Extreme fear/anxiety

Lab
Leukocytosis, thrombocytopenia, hypofibrinogenemia, abnormal coagulation, disseminated
intravascular coagulation, proteinuria, hemoglobinemia, hemoglobinuria, myoglobinemia,
myoglobinuria, and azotemia are uncommon but possible manifestations in severe reactions.
Pathological Findings
Inflammation, ulceration, vesiculation, pustulation, rupture, eschar, swelling (3,5)
Local reaction: Infection, cellulitis, dermatoses, punctures, foreign bodies
Toxic reaction: Chemical exposure/ingestion, medications, IV drug abuse, environmental,
plants
Allergic reaction: Medications, illicit drugs, foods, topical products, environmental, plants,
chemicals
Treatment
Long-term treatment (5):
Recommended for those with hypersensitivity reaction, but may be
considered for individuals with large local reactions
Self-administered epinephrine device
Hypersensitivity identification
Venom immunotherapy for 3–5 yrs is 80–90% effective even after cessation
of treatment.
Acute treatment (1,2,3,5,8,9):
Outpatient or inpatient, depending on individual response to injury
Hospitalize for severe systemic reactions with threatened airway obstruction,
bronchospasm, hypotension, severe angiodermatitis, or pain
Medication P.
First Line
Local (depending on severity):
Analgesics
Antihistamines: Diphenhydramine (Benadryl) 25–50 mg q.i.d.
Steroids topical or oral: Prednisone 20–40 mg/day is unproven but may be
helpful for large local reactions.
Antibiotics only if there is a secondary infection
Systemic (depending on severity and reaction type):
Epinephrine [1:1,000] SC: To combat urticaria, wheezing, angioedema—child
0.01 mL/kg, adult 0.3–0.5 mL
Diphenhydramine: 25–50 mg IV or IM to combat urticaria, wheezing,
angioedema
Albuterol 5 mg inh and ipratropium bromide 0.5 mg inh: Bronchospasm
IV fluids (Ringer's lactate): If needed for hypotension, hypovolemia
Dopamine: 200 mg in 250 mL at 5 mcg/kg/min to correct vascular collapse
Titrate to maintain systemic BP over 90 mm Hg:
Hydrocortisone: 100–250 mg IV, if needed, for severe urticaria or spider bite
Tetanus prophylaxis and antibiotics: Only if secondary infection, rarely
indicated
Diazepam (Valium): 5–10 mg, if needed, for severe muscle spasms
Morphine or meperidine (Demerol): If needed for pain
Antivenins may be appropriate based on availability, identification of organism,
and previous sensitivity.
Topical insecticides:
Lice: 1% permethrin (Nix, Elimite) is still considered first line despite up to
50% resistance. 0.5% Malathion (Ovide) may be used as initial choice or for
permethrin failure. 1% lindane (Kwell) or pyrethrin (Rid) is also effective.
Scabies: 5% permethrin is drug of choice, but 10% crotamiton (Eurax) and
lindane are effective.
Contraindications: Refer to manufacturer's literature.
Precautions:
Dosing appropriate to age
If severe reaction, don't delay treatment.
Severe vascular collapse may require central pressure monitor.
Significant possible interactions: Refer to manufacturer's literature.
Second Line
Alternative drugs (9):
Other H1 antihistamines (eg, loratadine [Claritin], fexofenadine [Allegra], etc.)
H2 blockers (eg, ranitidine [Zantac], cimetidine [Tagamet], famotidine
[Pepcid], etc.)
Oral ivermectin (Mectizan) appears effective for lice and scabies, but is not
FDA-approved for this purpose.
General Measures
First aid measures, local treatment, activate emergency services in severe
reactions. If history of allergy or large envenomations, don't wait to seek
emergency care (2,3,5,6).
Use ANA kit and over-the-counter antihistamines, if available and required.
Local (depending on severity):
Remove stinger (scrape it out—don't squeeze with tweezer).
Cleanse wound.
Ice packs to bite or sting site (alternate 10 min on/10 min off)
Elevation of affected part
Debride ulcers.
Drain abscesses.
Systemic (depending on severity and type of reaction): Home use—Epi-Pen:
Adequate airway (intubation, tracheostomy): If needed to bypass obstruction
Oxygen (4–6 L/min): If needed for respiratory distress
Hospitalize and observe 24–48 hrs.
Oil of lemon eucalyptus, PMD, and IR3535 are considered biopesticides by the
EPA, but be sure to use EPA-approved products, as essential oils have not
been tested (6,11).
Tumeric may help inflammation. Animal studies show promise, but no proof in
humans and no dose data.
Optimal treatment of necrotic spider bites is not well defined. Surgical repair may
be required for severe ulcerative lesions, but not until primary necrotizing
process is complete (2,3,6).
Ongoing Care
No activity restrictions
Patient Monitoring
Follow-up wound care
Diet
No special diet; nothing by mouth if severe systemic reaction
Patient Education
Protective measures, ANA kit/Epi-Pen use, risks (5,6)
Individuals with known sensitivity should wear medical identification (bracelet, tag) or carry a
card.
Prognosis
Expected course (2,5):
Minor reactions—excellent
Severe reactions—excellent with early, appropriate treatment
Complications
Infection (2,5,9):
Bacterial
Arthropod-associated diseases with tick, fly, bug, and mosquito bites (eg,
lyme borreliosis, rickettsial disease [Rocky Mountain spotted fever], arboviral
encephalitis, malaria, leishmaniasis, trypanosomiasis, dengue)
Scarring
Drug reactions
Multisystem failure
Death
References
1. Isselbacher KJ, et al., eds. Harrison's principles of internal medicine. 13th
ed. New York, McGraw-Hill, 1994.
2. Tintinalli JE, Krome RL, eds. Emergency medicine. New York, McGraw-Hill,
1988.
3. MMWR: Necrotic arachnidism-Pacific Northwest, 1996;45(21).
4. Center for Disease Control and Prevention National Center for Injury
Prevention and Control http://www.cdc.gov/injury/wisqars/index.html
5. Moffitt JE, Golden DBK, Reisman RE, et al. Stinging insect hypersensitivity:
a practice parameter update. J Allergy Clin Immunol. 2004;114:869–886.
6. Burnette GW, et al., eds. CDC health information for international travel
2010, Mosby, 2009.
7. Mosquitoes and mosquito repellants: a clinician's guide. Ann Int Med.

1198;128(ll):931–940.
8. Schroeder SA, Krupp MA, Tieme LM, et al. eds. Current medical diagnosis
and treatment. Norwalk, CT: Appleton & Lange, 1989.
9. Pickering L, ed. 2009 red book: report of the committee on infectious

diseases, 28th ed. American Academy of Pediatrics, 2009.
10. The Medical Letter. Vol 40 (issue 1017) Jan 2, 1998.

11. Jurenka JS: Anti-inflammatory properties of curcumin, a major constituent
of Curcuma longa: a review of preclinical and clinical research. Altern Med
Rev. 2009;14(2):141–153.
Pediatric Considerations
Not a contraindication to appropriate management
Codes
ICD9
919.5 Insect bite, nonvenomous, of other, multiple, and unspecified sites, infected
989.5 Toxic effect of venom
Brachial Plexus Injuries (Burners and Stingers)
Geoffrey Kuhlman
Basics
Traction to the plexus when the shoulder is depressed and the head is forced away from
the injured side
Compression of cervical nerve roots when the head is forced toward the side of injury
Direct blow to the brachial plexus at the supraclavicular fossa
Description
Acute trauma to the neck and shoulder area injuring the brachial plexus
Typically causes burning or stinging pain in the upper shoulder radiating down the entire
upper extremity, hence the names “burner” and “stinger”
Most commonly involves the upper trunk of the plexus or cervical nerve roots C5 and C6
Epidemiology
Incidence
Exact incidence unknown due to underreporting by athletes
Common in contact sports (football, wrestling, hockey); football career incidence reported
between 49% and 65%
Frequent recurrence, reported as high as 87% (1)
Risk Factors
Previous burner
Limited range of motion of the neck or shoulder
General Prevention
Neck roll, shoulder pad lifter, or rigid collar (eg, Cowboy Collar) in football might reduce injury
risk.
SORT-C (strength of recommendation taxonomy, level C)
Etiology
Most are limited to neurapraxia, nerve dysfunction with demyelination
Minority involve axonotmesis, with subsequent Wallerian degeneration and eventual
regeneration of axons
Diagnosis
History
Mechanism of injury (falling on an outstretched arm suggests alternative injury) (2)
Details of symptom quality, severity, and location (bilateral or lower extremity symptoms
indicate cervical fracture or cord injury until proven otherwise; symptoms not typical of
burners mandate search for an alternative diagnosis)
Modifying factors (limitation or pain with shoulder motion suggests alternative shoulder
diagnosis)
Initial vs recurrent injury (recurrence typically requires more aggressive rehabilitation)
Physical Exam
Signs and symptoms (2):
Burning or stinging pain radiating down 1 arm circumferentially (ie, nondermatomal pattern)
Sometimes numbness, paresthesias, and weakness in the extremity
Athlete often immediately holds the arm close to the body
Symptoms often last a few minutes, but can persist for weeks, particularly in recurrent
episodes.
Physical examination (2):
Inspection (asymmetry or postural abnormality to address in therapy)
Palpation (tenderness suggests alternative diagnosis; spasm is common but nonspecific)
Neurologic examination (strength, sensation, reflexes to localize injury, rule out cord injury)
Weakness most common in deltoid, biceps, and rotator cuff
Tinel sign at the supraclavicular fossa (positive result indicates plexus injury)
After serious cervical injury is ruled out, Spurling's neuroforaminal compression test (disc
herniation, burner from cervical foraminal stenosis)

Not routine
X-ray cervical spine if fracture, dislocation, or cervical instability suspected (anteroposterior,
lateral, oblique, flexion, extension)
MRI or CT typically not needed; many false-positive results
Imaging
Cervical spine x-rays if recurrent injury, findings localizing to 1 cervical level, or symptoms in
more than 1 extremity (3)
MRI cervical spine if x-rays are unrevealing to identify neuroforaminal stenosis, disk
herniation, or mass as possible causes of nerve root impingement (3)
Electromyogram/nerve conduction velocity (EMG/NCV) if symptoms last 3 wks for confirmation,
localization, and prognosis (EMG normalization lags far behind clinical and neurologic recovery,
so follow-up EMG generally not indicated) (3)
Cervical injury (fracture, dislocation, spinal cord injury, disc herniation)
Acromioclavicular separation
Clavicle fracture
Thoracic outlet syndrome (when chronic, recurrent)
Treatment
Stretch tight muscles at neck and shoulder
Strengthen neck, shoulder, and muscles weakened by injury
These strategies apply, regardless of injury mechanism.
General Measures
Chest-out posture
Ensure correct playing technique.
Maintain strength and flexibility of neck and shoulder.
No contact sports until asymptomatic and normal neurologic examination (3,4)
Football players can consider neck roll, shoulder pad lifter, or rigid collar when
returning to play.
Ongoing Care
Schedule follow-up until symptoms and examination normalize.
References
1. Sallis RE, Jones K, Knopp W. Burners: an offensive strategy for an underreported injury.
Physician Sports Med. 1992;20:47–55.
2. Kuhlman GS, McKeag DB. The “burner”: a common nerve injury in contact sports. Am
Fam Physician. 1999;60:2035–2040, 2042.
3. Standaert CJ, Herring SA. Expert opinion and controversies in musculoskeletal and sports
medicine: stingers. Arch Phys Med Rehabil. 2009;90:402–406.
4. Safran MR. Nerve injury about the shoulder in athletes, part 2: long thoracic nerve, spinal
accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med.
2004;32:1063–1076.
Additional Reading
Aval SM, Durand P Jr, Shankwiler JA. Neurovascular injuries to the athlete's shoulder: part
I. J Am Acad Orthop Surg. 2007;15(4):249–256.
Aval SM, Durand P Jr, Shankwiler JA. Neurovascular injuries to the athlete's shoulder: part
II. J Am Acad Orthop Surg. 2007;15(5):281–289.
Dimberg EL, Burns TM. Management of common neurologic conditions in sports. Clin
Sports Med. 2005;24(3):637–662. PMID 16004923
Dimberg EL, Burns TM. Management of common neurologic conditions in sports. Clin
Sports Med. 2005;24:637–662, ix.
Rihn JA, Anderson DT, Lamb K, et al. Cervical spine injuries in American football. Sports
Med. 2009; 39(9):697–708.
Codes
ICD9
953.4 Injury to brachial plexus
Clinical Pearls
Nerve damage is generally not permanent, but a few patients have symptoms
lasting months to years.
Conditioning and rehabilitation should begin immediately. You can return to
contact activity when the symptoms are gone and your strength and sensation
are back to normal.
Continue stretching and strengthening at least the rest of the season.
Continuance of exercises throughout your career will lower the chance of
having another burner.
Bursitis
Sandeep Johar
Basics
Alert
May be difficult to distinguish from fractures. Suspicious joints should be immobilized,
particularly in the setting of trauma.
Inflammation or irritation of the bursa (a sac filled with lubricating fluid, located between
tissues such as bone, muscle, tendons, and skin, which decreases rubbing, friction, and
irritation)
Potentially any bursa may be affected:
Subacromial (subdeltoid) bursitis: Lies between the acromion and the rotator cuff
Olecranon bursitis: Lies between the olecranon process and the overlying skin (usually
secondary to trauma)
Iliopsoas bursitis: Lies between the iliopsoas tendon and the lesser trochanter (largest
bursa in the body)
Trochanteric bursitis: Has superficial and deep components. The superficial bursa lies
between the tensor fascia lata and skin; the deep bursa is located between the greater
trochanter and the tensor fascia lata.
Prepatellar bursitis: Lies between the patella and the skin (usually secondary to trauma or
frequent forward kneeling)
Calcaneal bursitis: 2 bursae at the level of insertion of the Achilles tendon. The superficial
one is located between the skin and the tendon, and the deep one is located between the
calcaneus and the tendon.
Description
Bursae are flattened sacs that serve as a protective buffer between bones and overlapping
muscles (deep bursae) or between bones and tendons/skin (superficial bursae). In the
normal state, they contain minimal amounts of fluid to reduce friction and facilitate pain-free
movement during muscle contraction.
Humans have 160 bursae.
Risk Factors
If you work in a profession or have a hobby that requires repetitive motion or pressure on
particular bursae (ie, carpet laying, tile setting, gardening, bicycling, baseball, ice skating)
Osteoarthritis
Gout
Thyroid disease
Diabetes
Etiology
Trauma (acute and chronic): Most common cause
Septic bursitis: Direct introduction of microorganisms through traumatic injury or through
contiguous spread from cellulitis
Predisposing factors for septic bursitis include diabetes, alcoholism, steroid therapy, uremia,
trauma, and skin disease.
For septic bursitis: Staphylococcus aureus causes 80%, followed by Streptococcus
Crystal deposition: Gout or pseudogout
Systemic diseases: Rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis,
scleroderma, systemic lupus erythematosus, pancreatitis, Whipple disease, oxalosis, uremia,
hypertrophic pulmonary osteoarthropathy, idiopathic hypereosinophilic syndrome
Diagnosis
Full assessment of regional musculoskeletal function
Any suspicion of infection warrants aspiration of bursae (especially olecranon and prepatellar
bursae)
Aspiration of hip and other deep bursae should be deferred to orthopedics or rheumatology,
or may be guided in emergency department by US
Physical Exam
Localized tenderness
Decreased range of motion or pain with movement
Erythema or edema (seen in superficial bursitis)
Traumatic bursitis often follows traumatic event or overuse of related joints.

Lab
CBC with differential, erythrocyte sedimentation rate, serum protein electrophoresis,
rheumatoid factor, serum uric acid
Aspiration and analysis of bursa fluid: Cell count with differential, glucose and total protein,
crystal determination, gram stain, and culture
Normal fluid: Fluid is clear yellow with 0–200 WBCs, 0 RBCs, low protein, and glucose is
same as serum.
Traumatic bursitis: Fluid is bloody/xanthochromic with <1,200 WBCs, many RBCs, low
protein, and normal glucose.
Infective bursitis: Fluid is cloudy yellow with >50,000 WBCs, few RBCs, slightly increased
protein, and decreased glucose; bacteria on gram stain.
Rheumatoid and microcrystalline inflammation: Fluid is yellow, can be cloudy, and has 1,000–
40,000 WBCs, few RBCs, slightly increased protein, and variable glucose; use polarizing
microscope to identify crystals.
Chronic or recurrent bursitis should be sent for acid-fast staining and cultured on special
media for mycobacteria, Brucella, and algae.
Monosodium urate crystals seen in gout; calcium pyrophosphate crystals seen in pseudogout
Imaging
X-rays to exclude other suspected pathologies (ie, fractures, dislocations)
X-rays may demonstrate chronic arthritic changes or calcium deposits
US for diagnostic aspiration or treatment injections
MRI helps depict bursa/prebursa fluid, associated abscesses, and adjacent soft tissue
structures.
Arthritis: Rheumatoid, septic, osteo-
Cellulitis
Gout and pseudogout
Fracture, tendon/ligament tear, contusion, sprain
Tendonitis
Treatment
ED Treatment
Shoulders should not be immobilized for more than 2–3 days due to the risk of
adhesive capsulitis.
Aseptic bursitis: Rest, ice, compression, elevation, NSAIDs, bursa aspiration,
and intrabursa steroid injections
Septic bursitis: If suspected, treat with antibiotics while awaiting culture results
and drain bursae.
Superficial septic bursitis can be treated with oral therapy.
Septic bursitis with systemic symptoms or who are immunocompromised
require IV antibiotics.
Staphylococcus aureus 80%, followed by streptococcal species
Penicillinase-resistant penicillin (oxacillin) or 1st-generation cephalosporin
(cefazolin). In penicillin-allergic patients or in carriers of methicillin-resistant
Staphylococcus aureus, vancomycin
Medication
NSAIDs: Ibuprofen: Adult: 800 mg PO q8h; peds: 10 mg/kg PO q8h. Naproxen:
Adult: 250–500 mg PO b.i.d. Ketorolac: Adult: 30 mg IV/IM q6h or 10 mg PO
q4–6h
Most patients may be treated as an outpatient.
Antibiotics (for an infected bursitis): Oxacillin: Adult: 500–1,000 mg PO q4–6h,
1–2 g IV/IM q6h; peds: 50–100 mg/kg/day PO divided q6h, 150–200 mg/kg/day
IV/IM divided q6h Cefazolin: Adult: 2 g IM/IV; peds: 20 mg/kg IM/IV.
Vancomycin: Adult: 1 g IV q12h; peds: 10–15 mg/kg IV q6h
In general, bursitis is not treated surgically. However, surgical release may be
indicated when adhesive bursitis develops, severely limiting joint motion. During
surgery, the adhered bursa is removed and the contiguous tissues are released.
Immobilize joint if pain is severe.
Admission Criteria
Septic bursitis with high fevers, surrounding cellulitis, unable to take oral
antibiotics, failed outpatient therapy, or immunocompromised
Ongoing Care
Most patients respond to therapy within 1 wk.
Rheumatology or orthopedic referral is recommended for patients with repetitive acute bouts,
necessitating repeated joint/bursa aspirations or, eventually, surgical excision of involved
bursa.
Additional Reading
Costantino TG, Roemer B, Leber EH. Septic arthritis and bursitis: emergency ultrasound
can facilitate diagnosis. J Emerg Med. 2007;32(3):295–297.
Torralba KD, Quismorio FP Jr. Soft tissue infections. Rheum Dis Clin North Am.
2009;35(1):45–62.
Valeriano-Marcet J, Carter JD, Vasey FB. Soft tissue disease. Rheum Dis Clin North Am.
2003;29(1):77–88, vi.
Codes
ICD9
726.19 Other specified disorders of bursae and tendons in shoulder region
726.33 Olecranon bursitis
727.3 Other bursitis disorders
Calcium Pyrophosphate Deposition Disease (CPPD)
(Pseudogout)
Kenneth M. Bielak
Benjamin D. England
Basics
Description
Calcium pyrophosphate deposition disease (CPPD) is a crystal arthropathy characterized by
deposition of calcium pyrophosphate dihydrate crystals in joints.
Synonym(s):
Pseudogout: Describes an acute attack of CPPD crystal-induced synovitis (similar to gout),
but many will not experience such intense symptoms
Chondrocalcinosis: As evidenced by radiographic calcification, but is not absolutely specific
for CPPD and not universal among all patients with CPPD
Pyrophosphate arthropathy: Specifically associated with inorganic pyrophosphate
metabolism as the etiology for CPPD
Epidemiology
Prevalence of chondrocalcinosis is 5–8% in the general population, but 15% by the 9th
decade
Female-to-Male ratio: 2–7:1
Peak age: 65–75 yrs
Risk Factors
Gout (20% may be hyperuricemic)
Hemochromatosis
Hypothyroidism
Trauma
Osteoarthritis
Hyperparathyroidism
Hemosiderosis
Hypophosphatasia
Hypomagnesemia
Aging
Amyloidosis
Genetics
<1% of cases may show an autosomal dominant inheritance pattern.
General Prevention
There are no absolute prevention measures, but mainstays include adequate hydration (to
prevent crystal precipitation) and decreasing purine-rich foods, such as organ meats,
mushrooms, legumes, asparagus, and coffee.
For individuals who have experienced 3 or more attacks in 1 yr, colchicine has been found to
reduce the recurrence rate (1)[B].
Etiology
CPPD crystal formation is initiated in cartilage located near the surface of chondrocytes, which
are embedded in and contribute to the collagen- and proteoglycan-containing cartilage matrix of
joint surfaces. The CPPD crystal formation may be a combination of elevated levels of either
calcium or pyrophosphate and/or matrix changes that enhance local CaPPi (calcium
pyrophosphate) supersaturation. Many cases of CPPD deposition are idiopathically sporadic,
but more commonly are precipitated by trauma or various metabolic disorders.

Pseudorheumatoid arthritis: A nonerosive, inflammatory arthritis with demonstrable CPPD
crystals in the joint fluid. The clinical picture resembles rheumatoid arthritis with morning
stiffness, fatigue, synovial thickening, edema, and loss of motion. The 2 may coexist and
must be differentiated as the treatment options vary.
Pseudoarthritis: Progressive joint degeneration involving multiple joints. CPPD crystal
deposition can be differentiated by radiographic evidence of calcifications in the absence of a
preceding trauma.
Case reports of CPPD associated with Charcot joints.
CPPD, especially familial patterns, can be found along the spine and resemble ankylosing
spondylitis.
Diagnosis
History
Acute joint swelling in 1 or more joints with previous episodes involving the same joint
(characteristic of crystal arthropathies)
The most common joint is the knee, followed by the wrist, shoulder, and hip.
May be severe and associated with malaise and fever
Period of previous episodes (typically several days to weeks)
Patients often are symptom-free between attacks.
Physical Exam
Involved joint:
Hot
Edema, tender
Limited range of motion
Uncommon presentations include tendinopathy, tenosynovitis, and bursitis.
Chronic CPPD: Symmetrical polyarthritis affecting knees, metacarpophalangeal joints, wrists,
ankles, and shoulders:
May involve the spine
Affected joints show signs of osteoarthritis with varying degrees of synovitis.
Predominantly affects women

Lab
Any newly diagnosed CPPD should be followed with laboratory evaluations of calcium,
magnesium, thyroid-stimulating hormone, ferritin, transferrin, iron, phosphorus, and alkaline
phosphatase.
Synovial fluid microscopy with compensated polarized light microscopy showing weakly
positive birefringent rhomboidal shaped crystals is diagnostic; gram stain and culture should
be considered to rule out differential diagnoses.
Erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, uric acid, white cell
count (leukocytosis), and blood cultures may be considered to rule out differential diagnoses.
Leukocyte concentration typically in the range of 15,000–30,000 per cubic millimeter with
90% neutrophils
Imaging
Plain radiography has diagnostic utility in the crystal-induced arthropathies, which illustrates
calcium crystal deposition (2).
X-ray: Calcification of articular fibrocartilage (chondrocalcinosis) in menisci of the knee,
triangular fibrocartilage complex in the wrist. Other sites include glenoid and acetabular labra
and symphysis pubis.
X-ray changes of osteoarthritis often are pronounced.
X-ray hands (2nd/3rd metacarpophalangeal chookd osteophytes in hemochromatosis)
High-resolution US may improve noninvasive diagnosis of the crystal-induced arthropathies
and allow monitoring of intra-articular tophi in clinical trials.
CT provides excellent definition of tophi and bone erosion, and 3D CT assessment of tophus
volume is a promising outcome measure in gout.
MRI is also a reliable method for assessment of tophus size in gout, and has an important
role in detection of complications of disease in clinical practice.
Emerging imaging techniques include 3D US and dual-energy CT. Advanced imaging
modalities also offer new insights into the mechanisms of cartilage and bone damage in the
crystal-induced arthropathies (3)[B].
Tissue sections are best examined with alizarin red, looking for crystals as the hematoxylin and
eosin stains may cause dissolution of the crystalline CPPD due to their acidity.
Gout (can coexist)
Septic arthritis (can coexist)
Osteoarthritis
Trauma (hemarthrosis)
Human leukocyte antigen B27-related peripheral arthritis (psoriatic arthritis, ankylosing
spondylitis, reactive arthritis)
Hypertrophic osteoarthropathy
Pseudorheumatoid arthritis: Severe synovitis in rheumatoid pattern
Treatment
Acute treatment (4)[C]:
Joint aspiration (often significantly reduces pain) (4)[C]
Intra-articular corticosteroid injection can be effective.
Joint rest and splinting
NSAIDs and oral analgesia
Colchicine and systemic corticosteroids can be used if other treatments are
contraindicated.
For patients suffering recurrent attacks of pseudogout, oral daily colchicine
may be effective as a prophylactic agent at a usual dosage of 0.6 mg b.i.d.
(1)[B].
Repeat joint aspiration may be required.
Once acute attacks have settled, the aims of treatment are to relieve
symptoms and regain function.
No specific treatment exists for chronic CPPD, and no treatments are
available that reverse joint damage.
Medication
NSAIDs are first-line treatment.
Antibiotics if septic arthritis is suspected until joint and blood cultures return
negative
There have been anecdotal reports of cured acute attacks by the consumption of
dark cherries or cherry juice or herbs that contain xanthene oxidase inhibitors to
decrease urate formation, but none have been well studied.
Joint arthroplasty may be required for severely damaged joints.
Ongoing Care
Primary metabolic disorders or familial predisposition are uncommon, but should be
considered if CCPD occurs before 55 yrs of age or if there is florid polyarticular CCPD.
After the age of 55 yrs, hyperparathyroidism should be considered in all patients.
Complications
Although acute pseudogout usually responds well to therapy, chronic CPPD often
is progressive and may cause considerable disability.
References
1. Alvarellos A, Spilberg I. Colchicine prophylaxis in pseudogout. J Rheumatol.
1986;13:804–805.
2. Ciapetti A, Filippucci E, Gutierrez M, et al. Calcium pyrophosphate dihydrate

crystal deposition disease: sonographic findings. Clin Rheumatol. 2008.
3. Dalbeth N, McQueen FM. Use of imaging to evaluate gout and other crystal
deposition disorders. Curr Opin Rheumatol. 2009;21:124–131.
4. Announ N, Guerne PA. Treating difficult crystal pyrophosphate dihydrate

deposition disease. Curr Rheumatol Rep. 2008;10:228–234.
Additional Reading
Couto AR, Brown MA. Genetic factors in the pathogenesis of CPPD crystal
deposition disease. Curr Rheumatol Rep. 2007;9:231–236.
Doherty M. Crystal arthropathies: calcium pyrophosphate dihydrate. In: Klippel

JH, Dieppe PA, eds. Rheumatology. London: Mosby-Year Book Europe
Limited, 1994:7.13.1–7.13.12.
Ea HK, Lioté F. Advances in understanding calcium-containing crystal

disease. Curr Opin Rheumatol. 2009;21:150–157.
Fodor D, Albu A, Gherman C. Crystal-associated synovitis-ultrasonographic

feature and clinical correlation. Ortop Traumatol Rehabil. 2008;10:90–102.
Richette P, Bardin T, Doherty M. An update on the epidemiology of calcium

pyrophosphate dihydrate crystal deposition disease. Rheumatology (Oxford).
2009.
Ryan LM, McCarty DO. Calcium pyrophosphate crystal deposition disease,

pseudogout and articular chondrocalcinosis. In: Koopman WJ, ed. Arthritis
and allied conditions: a textbook of rheumatology, 13th ed. Baltimore:
Williams & Wilkins, 1997:2103–2125.
Shah K, Spear J, Nathanson LA, et al. Does the presence of crystal arthritis
rule out septic arthritis? J Emerg Med. 2007;32:23–26.
Codes
ICD9
275.49 Other disorders of calcium metabolism
712.20 Chondrocalcinosis, due to pyrophosphate crystals, involving unspecified site
Clinical Pearls
The cause of CPPD is unknown (unlike gout, in which hyperuricemia leads to
precipitation of uric acid crystals into joints). Therefore, there is no preventative
treatment for recurrent attacks, although colchicine may be useful as prophylaxis
in those with frequent recurrences.
Calluses and Corns
Kathleen Weber
Basics
Calluses and corns are common skin conditions.
They result from increased pressure or friction; typically located on the hands and feet.
A callus is an adaptive response to repetitive friction.
Calluses and corns may lead to considerable discomfort and pain.
Description
A callus is a plaque of hyperkeratosis of relatively even thickness caused by repetitive
friction, pressure, or trauma, and commonly occurs over bony prominences (1).
A corn is a localized, tender, sharply defined area of hyperkeratosis found usually on the foot
(1).
A corn has a central core that penetrates into the dermis.
Epidemiology
Calluses and corns are common skin conditions.
Risk Factors
Activity: Occupational (eg, manual workers); musicians (eg, guitarists); athletic activities that
apply increased stress to the skin (ie, racquet sports—hands, runners—feet, rowers—hands,
sacrum) (2)
Ill-fitting footwear: Tight, loose irregularities in shoe, or not wearing shoes (3)
Bony prominences (4)
Faulty foot mechanics or foot structure (3)
Toe deformities
General Prevention
Proper footwear (low-heeled, a soft upper portion, and wide toebox)
Orthotics
Toe separators
Place felt pads over bony prominences or areas of increased friction to the skin.
Wear gloves to protect the hands.
Keep the hands and feet skin soft by applying a moisturizer (5).
Etiology
Calluses and corns develop as a result of hyperkeratosis, a normal physiologic response of
the skin to chronic friction, pressure, or trauma and commonly occur over bony prominences
(1).
Calluses commonly develop overlying bony prominences as a normal adaptation of the body
to protect the skin when chronic pressure or friction is encountered (3,4).
Abnormal stresses may be either extrinsic (eg, tight toebox) or intrinsic (eg, hammertoe) or a
combination of both (3).
Diagnosis
The diagnosis of calluses and corns is based upon their clinical appearance.
Radiographs may be obtained if your physician suspects an underlying bony prominence is a
contributing factor.
History
Corns and calluses are typically located at sites of friction, pressure, repetitive trauma, or at
bony prominences.
Factors that typically provoke the formation of corns and calluses are:
Sports that require cutting, turning, and sudden stops
Occupations that are categorized as manual labor requiring the repetitive use of the hands
or kneeling, such as a carpenter or landscaper
Leisure activity that involves activities that cause repeated friction or pressure
Poorly fitting footwear
Coexisting illnesses (eg, diabetes)
Inherited disposition (autosomal-dominant inheritance)
Physical Exam
The most common site for calluses is under the metatarsal heads and over bony
prominences; may occur anywhere on the skin as a result of friction (4).
A callus may be asymptomatic or painful, often appearing as a thick yellowish plaque that
retains the natural skin lines (helps distinguish from warts) (2).
A hard corn is a dry horny mass found commonly over the interphalangeal joints (dorsally) or
the 5th toe (dorsolaterally).
Soft corns are extremely painful; occur interdigitally; skin appears white and macerated;
commonly located between the 4th interdigital space (often mistaken for tinea).
Observe gait and the alignment of the feet for any faulty mechanics.
Note the location and appearance of the hyperkeratotic lesions:
Common sites for corns and calluses: Plantar surface (over the metatarsal heads, sides of
the arch, and the heel) and dorsum of the foot (over the interphalangeal joints)
Common sites for calluses on hands: Palmar surface and over metacarpophalangeal joints
Palpate for any abnormal bony prominences.
Assess for pain or tenderness.

Physical examination of the area is typically all that is necessary to make the diagnosis.
Imaging
Usually not necessary
Radiographs: Hands and weight-bearing views of the feet used to identify bony prominences
or abnormalities (3)
Verruca vulgaris or plantaris (differentiated by paring the skin: The corn becomes more
normal in appearance and the wart displays the characteristic tiny red dots when pared)
Tinea pedis (interdigital)
Psoriatic plaque: Hyperkeratosis with red base
Treatment
Treatment is aimed at providing symptomatic relief and avoiding the
underlying mechanical forces that caused the development of the callus or
corn (1,2,3,5)[C]:
Careful and regular paring
Use an emery board or a pumice stone daily, if necessary, to remove excess
thickened skin.
The pumice stone works best after bathing when the thickened skin has
softened.
Soft corn: Toe separator or lamb's wool
Doughnut-shaped corn pads
Proper footwear with soft upper and a roomy toebox
Orthotics can reduce pressure by redistributing forces.
Use a skin-softening cream to prevent cracking of the callus or corn.
Medication
Antibiotics are only indicated when there is evidence of an infected corn or
callus.
First Line
Salicylic acid (40%): Careful application or pads containing keratolytic agents (2)
Surgery may be required to correct the bony abnormalities or deformities, and is
indicated only if all conservative measures have failed (3).
Ongoing Care
Follow-up is needed for ongoing corns and calluses despite conservative management, signs of
infection, or severe pain.
Patient Monitoring
Diabetics, the elderly, and individuals with peripheral arterial disease or peripheral neuropathy
should consult with their healthcare providers before initiating treatment for calluses or corns.
These individuals should be monitored closely for signs of nonhealing or infection.
References
1. Freeman DB. Corns and calluses resulting from mechanical hyperkeratosis. Am Fam
Physician. 2002;65:2277–2280.
2. Cordoro KM, Ganz JE. Training room management of medical conditions: sports
dermatology. Clin Sports Med. 2005;24:565–598, viii–ix.
3. Singh D, Bentley G, Trevino SG. Callosities, corns, and calluses. BMJ. 1996;312:1403–
1406.
4. Spink MJ, Menz HB, Lord SR. Distribution and correlates of plantar hyperkeratotic
lesions in older people. J Foot Ankle Res. 2009;2:8.
5. Robbins JM. Recognizing, treating, and preventing common foot problems. Cleve Clin J
Med. 2000;67:45–47, 51–52, 55–56.
Codes
ICD9
700 Corns and callosities
Cardiac Arrhythmias: Atrial Fibrillation, SVT
Charles W. Webb
Nicole Y. Gesik
Basics
Any deviation from normal (sinus) heart rhythm broadly classified as bradyarrhythmias
(slow) or tachyarrhythmias (fast) (1)
Epidemiology
Incidence
Bradyarrhythmias (2,3):
Common in aerobically trained athletes secondary to elevated resting vagal tone
Sinus bradycardia (50–65% of athletes vs 23% in general population)
Sinus arrhythmias (13.5–69% of athletes vs 2.4–20% in general population)
Sinus pause of >2 sec (37.1% of athletes vs 5.7% in general population)
1st-degree AV block (6–33% of athletes vs 0.65% in general population)
2nd-degree AV block, Mobitz I (2.4–10% of athletes vs 0.003% in general population)
3rd-degree AV block (0.017% in athletes vs 0.00002% in general population)
Junctional rhythms (0.031–7% of athletes vs 0.06% in general population)
These changes are readily reversed in athlete's heart as increased sympathetic drive
overcomes resting vagal tone. If presents with symptoms (impaired consciousness or
fatigue) or not readily reversed, often associated with underlying cardiac disease.
Tachyarrhythmias (2,3):
Atrial fibrillation more common in competitive athletes (0.063%) than general population
(0.004%)
Other supraventricular atrial or AV nodal tachyarrhythmias are not more common in athletes
in comparison to the general population.
Wolff-Parkinson-White syndrome (EKG showing short PR interval with wide QRS and slurred
upstroke or delta wave) equal in athletes and general population (0.15%)
Premature ventricular contractions occur at similar rates in athletes vs general population.
Complex ventricular arrhythmias are always pathologic and should seek prompt cardiology
examination.
Risk Factors
Structural heart disease (hypertrophic cardiomyopathy, anomalous coronary syndrome,
arrhythmogenic right ventricular dysplasia, Marfan's syndrome, aortic stenosis, dilated
cardiomyopathy) (1,3)
Myocarditis
Atherosclerotic coronary artery disease (especially if >35 yrs old)
Drugs (amphetamines, cocaine, ephedrine)
Long QT syndrome with QTc >0.46 sec (congenital vs iatrogenic, including medications such
as class Ia antiarrhythmics, antifungals, nonsedating antihistamines, antibiotics, promotility
agents).
Commotio cordis (direct nonpenetrating trauma to chest wall)
Metabolic abnormalities (electrolyte disturbances, hyperthyroidism)
Etiology
Special considerations (1,2):
Systematic training may cause physiologic adaptations, including a variety of abnormal EKG
findings, in about 40% of elite athletes, termed the “athlete's heart”
Increased QRS voltage, incomplete right bundle branch block, early repolarization, and
peaked T waves related to increase in overall cardiac mass.
Diagnosis
Wide range of clinical presentations, from occasional palpitations to sudden cardiac
death (3)
Bradyarrhythmias can present with impaired consciousness or fatigue.
Tachyarrhythmias can cause palpitations, chest pain, and exertional dyspnea.
Unstable ventricular tachyarrhythmias may cause lightheadedness or syncope.
Supraventricular tachycardia (SVT):
Evaluation:
Identify rate response of SVT during activity or exercise.
If unable to induce SVT with exercise, can induce with either atrial/esophageal pacing,
then monitor with exercise stress test
Atrial fibrillation:
May be present intermittently or chronically
More common with diseases such as coronary artery disease or hypertension
Evaluation:
Determination of ventricular response with athletic activity
12-lead EKG
Long-term 24-hr EKG
Echocardiogram
History
Based on AHA Consensus Panel Recommendations for Preparticipation Athletic Screening
(1,3):
Family history:
Premature sudden cardiac death
Heart disease in relatives <50 yrs old
Personal history:
Heart murmur, fatigue, systemic hypertension, exertional chest pain, syncope/near syncope
during or after exercise, unexplained or disproportionate exertional dyspnea
Presence of palpitations, chest pain, lightheadedness, syncope, and relation of symptoms
to activity or rest
Note prescription and OTC medications, especially cold or diet remedies (especially those
containing ephedra), nutritional supplements, recreational drugs (especially cocaine).
Physical Exam
Vital signs (pulse, temperature, BP, respiration rate)
Dynamic heart evaluation looking for heart murmur, documented in at least 2 positions
(usually supine and standing) to discern murmurs with outflow obstruction
Hypertrophic cardiomyopathy murmur INCREASES with maneuvers that decrease venous
return (such as Valsalva or moving from squat or stand)
Aortic stenosis murmur DECREASES with the same maneuvers.
Pathologic murmur identified as any systolic murmur graded 3/6 or greater, or any diastolic
murmur or any holosystolic murmur.
Palpation of radial and femoral pulses to exclude coarctation of the aorta (3,4)

Workup for athletes with significant arrhythmia includes (3,4):
12-lead EKG
Echocardiogram (evaluate for hypertrophic cardiomyopathy and structural disease such as
valvular problems)
Exercise stress test to identify exertional arrhythmias or induced ischemia; may need to be
adapted specifically for athlete (ie, at peak energy for sprinter) as well as sport (maximal
ergometer stress test for rower reproducing training conditions that produce symptoms):
Nonpathologic bradycardias in athlete usually resolve with exercise testing.
Nonpathologic premature ventricular complexes usually resolve with exercise testing.
Holter 24 or 48 cardiac monitoring if possible during specific type of participation exercise
Implanted loop recorder, cardiac MRI, electrophysiologic studies rarely required
Anxiety disorder, panic attacks
Angina
Costochondritis
Neurocardiogenic syncope
Heat stroke
Seizure
Thyroid dysfunction
Treatment
Acute treatment (1,2):
Symptomatic athletes should initially have ABCs assessed and stabilized
(airway, breathing, circulation).
If athlete is unstable, may require advanced cardiac life support, immediate
DC cardioversion, and emergent transport to a medical facility.
Suspected supraventricular tachycardias may respond to efforts to increase
parasympathetic tone, including Valsalva maneuver, carotid massage, and
ice applied to face/neck.
Antiarrhythmic medications, electrophysiologic cardiac ablation, treatment of
underlying cardiac disease
Should be re-evaluated every 6–12 mos after trained to determine if
conditioning affects arrhythmia
Beta-adrenergic blocking agents banned in some competitive sports
Ongoing Care
Return to play guidelines (2,5):
Important for thorough cardiac examination, as underlying structural heart disease may
place athlete at increased risk for sudden cardiac death with exertion
Athletes with syncope or near syncope should not participate in sports where the likelihood
of loss of consciousness could be hazardous until the cause has been determined and
treated.
Athletes with symptoms such as impaired consciousness and fatigue attributed to
arrhythmias should be treated and if asymptomatic for 2–3 mos during treatment, may
participate in all sports.
Athletes with symptomatic tachy/brady arryhythmias should be treated, if no structural
heart disease, for 2–3 mos, then they can return to sports.
Atrial flutter:
Athletes with atrial flutter without absence of structural heart disease if without flutter for
2–3 mos may participate in all sports.
Athletes with structural heart disease who have atrial flutter can participate in sports such
as billiards, bowling, cricket, curling, golf, and rifle (Bethesda Guidelines class 1A sports).
Athletes without structural heart disease who have had ablation or surgery can participate
in all sports after 2–4 wks without recurrence.
Athletes who require anticoagulation cannot participate in competitive sports where the
chance of collision is present.
Atrial fibrillation (a-fib):
Athletes with asymptomatic atrial fibrillation without structural heart disease who maintain a
ventricular rate that appropriately increases and slows, with or without treatment, can
participate in all sports. (Use caution, as beta-blockers are banned in some sports.)
Athletes with a-fib and structural heart disease who have rate control can participate to the
limits and recommendations of the structural disease.
Athletes who require anticoagulation cannot participate in competitive sports where the
chance of collision is present.
SVT:
Athletes without structural heart disease who have controlled SVT may participate in all
sports.
Athletes with syncope, near syncope, or significant symptoms due to arrhythmia, or who
have structural heart disease may participate in class 1A sports once treated and have no
recurrence for 2–4 wks.
Asymptomatic athletes with SVT ranging 5–10 sec without increased duration with exercise
can play in all sports.
References
1. Giada F, Barold SS, Biffi A, et al. Sport and arrhythmias: summary of an international
symposium. Eur J Cardiovasc Prev Rehabil. 2007;14:707–714.
2. Pelliccia A, Zipes DP, Maron BJ. Bethesda Conference #36 and the European Society of
Cardiology Consensus Recommendations revisited a comparison of U.S. and European
criteria for eligibility and disqualification of competitive athletes with cardiovascular
abnormalities. J Am Coll Cardiol. 2008;52:1990–1996.
3. Goldberger JJ, Cain ME, Hohnloser SH, et al. American Heart Association/American
College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive
risk stratification techniques for identifying patients at risk for sudden cardiac death: a
scientific statement from the American Heart Association Council on Clinical Cardiology
Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and
Prevention. Circulation. 2008;118:1497–1518.
4. Maron BJ, Haas TS, Doerer JJ, et al. Comparison of U.S. and Italian experiences with
sudden cardiac deaths in young competitive athletes and implications for preparticipation
screening strategies. Am J Cardiol. 2009;104:276–280.
5. Mitchell JH, Haskell W, Snell P, et al. Task Force 8: classification of sports. J Am Coll
Cardiol. 2005;45:1364–1367.
Codes
ICD9
427.9 Cardiac dysrhythmia, unspecified
427.31 Atrial fibrillation
427.89 Other specified cardiac dysrhythmias
Clinical Pearls
Document pertinent negatives in history (1,4).
Document a dynamic heart exam during physicals.
Consider EKG as 1st step in evaluation of arrhythmias.
Carpal Tunnel Syndrome
Anne S. Boyd
Adam Abdulally
Stacey L. Brown Brocklehurst
Basics
Description
Clinical condition caused by entrapment of the median nerve in the carpal tunnel at the wrist
Classically presents as pain, weakness, and paresthesias on the palmar surface on the first
3½ digits
Can be acute or chronic (idiopathic)
Epidemiology
Carpal tunnel syndrome (CTS) accounts for 90% of all entrapment neuropathies (1).
Predominant gender: Female > Male (from 3:1 to as high as 10:1).
Predominant age: Peak prevalence is among women aged 55 yrs and older; prevalence
increases with age.
More likely to occur in the dominant extremity and is bilateral up to 50% of the time.
Pregnancy Considerations
Common during pregnancy; usually in the 3rd trimester and often bilateral; usually symptoms
will resolve spontaneously after delivery or with conservative treatment during pregnancy.
Incidence
Lifetime incidence is 10%.
It is estimated that 1 million adults annually in the U.S. require medical treatment (1).
Prevalence
Prevalence is 1–16% of the population depending on the criteria for diagnosis.
Risk Factors
Repetitive wrist motion is the most widely recognized risk factor for occupational CTS.
Narrow bony measurements of the wrist, elevated body mass index, increased age, female
gender, and pregnancy are other common risk factors.
Etiology
Exact pathogenesis of CTS is not clear. Most popular theories are mechanical compression,
microvascular insufficiency, and vibration.
Acute:
Uncommon and caused by rise in pressure in carpal tunnel
Most commonly with radial fracture
Also with burns, coagulopathy, local infection, and injections
Chronic:
Idiopathic: Only 50% of cases have an identifiable cause, which can be local, regional, or
systemic in origin.
Local: Inflammation, trauma, tumors, and anatomic anomalies
Regional: Osteoarthritis, rheumatoid arthritis, amyloidosis, and gout
Systemic: Diabetes, obesity, hypothyroidism, pregnancy, menopause, systemic lupus
erythematosus (SLE), scleroderma, dermatomyositis, renal failure, long-term hemodialysis,
acromegaly, multiple myeloma, sarcoidosis, leukemia, alcoholism, and hemophilia (1)

Diabetes, thyroid disease, advancing age, and rheumatoid arthritis all have been associated
with the development of CTS.
Activities involving repetitive wrist motion, vibration, and excessive forces through the wrist
Traumatic carpal bone dislocation or wrist fracture can disrupt the median nerve through the
carpal tunnel.
Lipomas, ganglion cysts, and other anatomic anomalies can grow and directly compress the
median nerve.
Proximal upper extremity nerve entrapment or nerve root compression—the “double crush”
syndrome
Diagnosis
History
Complaints of pain, weakness, and paresthesias on the palmar surface on the 1st 3.5 digits
Exacerbated by specific wrist motion in sport, occupational task, sleeping, driving, etc.
Nighttime symptoms
Improved with “shaking of the hands” (aka flick sign)
Consider cervical root pathology or radiculopathy if complaint of “shooting pain” down arm.
Consider generalized peripheral polyneuropathy if complaint of “sock and glove” distribution
of pain in upper and lower extremities.
Physical Exam
Classically presents as pain, weakness, and paresthesias on the palmar surface on the first
3½ digits; however, there can be variations.
Nocturnal acroparesthesia (ie, extremity numbness, tingling, or other abnormal sensation) is
the symptom most characteristic of CTS (2).
Flick sign, in which a patient may demonstrate vigorous shaking of the hand and wrist in
order to relieve symptoms, may be present.
Pain or paresthesia evoked by hand grip
Observe and palpate region of thenar muscle mass for atrophy (late finding).
Usually normal ROM
Strength testing of the abductor pollicis brevis muscle
Sensory testing, especially in median nerve distribution
Provocative tests:
Tinel sign: Percuss over the region of the carpal tunnel at wrist to elicit paresthesias in the
distribution of the nerve; 38–100% sensitive and 80% specific (2)[A].
Phalen test: Position wrists adjacent to each other in complete flexion for at least 60 sec to
elicit paresthesias; 42–85% sensitive and 80% specific (2)[A].
Carpal compression test: Press with thumbs over the carpal tunnel for 30 sec to elicit
symptoms; reported 87% sensitivity and 90% specificity for CTS (2)[A].
Other tests: Square wrist sign, tethered median nerve stress test, pressure provocation
test, and tourniquet test

Diagnosis usually can be made on history and physical examination alone.
Imaging
Indicated when the classic defining features of CTS are not present
Plain films generally are normal. Occasionally, carpal tunnel views may be helpful to rule out
anatomic variants, fractures with trauma, and narrowing or calcification in the carpal tunnel.
US of the wrist depicts structural abnormalities of nerve swelling.
A recent study showed that a change in cross-sectional area of the nerve as it travels
distally through the carpal tunnel is more useful than just one measurement of the nerve.
Sensitivity of diagnosis may increase with use of nerve conduction velocity (NCV) together
with US.
US is painless, noninvasive, and inexpensive. The sensitivity and specificity of US vary
among studies (3)[B].
MRI has been used to visualize structural abnormalities in and around the nerve.
There are few studies examining the sensitivity and specificity of MRI for this purpose.
One small study showed no difference in diagnostic accuracy between MRI and US.
MRI is costly and cumbersome.
MRI cannot assess the physiologic integrity of the median nerve across the carpal tunnel
segment.
Electrodiagnostic examinations can confirm/support the diagnosis of CTS.
Nerve conduction studies provide a highly sensitive (>85%) and specific (>95%) means for
assessing the physiologic integrity of the median nerve across the carpal tunnel segment (2)
[A].
Can be used to classify severity of CTS and to monitor progression of median nerve
entrapment
Needle electromyography is useful for documenting the presence of axonal loss to intrinsic
hand muscles innervated by the median nerve distal to the carpal tunnel segment and, if the
study includes structures proximal to the carpal tunnel, identifying other or coexisting
neuromuscular pathology (eg, cervical radiculopathy).
Clinical prediction rule (CPR): One recent prospective diagnostic study evaluated a
developed CPR for the diagnosis of CTS.
CPR: Shaking hand for symptom relief, wrist ratio index of 0.67, symptom severity scale
>1.9, reduced median sensory field of digit 1, and age >45 yrs (LR = 18.3)
de Quervain tenosynovitis
Cervical radiculopathy, C6–7
Proximal median nerve entrapment, pronator teres syndrome, or anterior interosseous
syndrome
Ulnar neuropathy at the elbow or wrist
Brachial plexus neuropathy
Wrist arthritis or other lesions in the wrist
Colles fracture, lunate dislocation
Generalized peripheral polyneuropathy
Angina pectoris
Upper motor neuron pathology
Syringomyelia
Mononeuritis multiplex
Multiple sclerosis
Treatment
Conservative treatment:
Splinting:
Splinting the wrist at a neutral angle helps to decrease repetitive flexion and
rotation, thus relieving mild soft tissue swelling or flexor tenosynovitis.
Compared with nighttime-only splint use, full-time use has been shown to
provide greater improvement of symptoms and electrophysiologic
measures; however, compliance with full-time use is more difficult (4)[B].
Corticosteroids:
Oral corticosteroids have been shown to be more effective than NSAIDs
or diuretics in short-term treatment (4).
Corticosteroid injection into or proximal to the carpal tunnel provides
greater clinical improvement at 1 mo than placebo (4)[A].
Surgery should be considered if patient needs more than 2 injections.
Other conservative treatments and their evidence:
Level 1 (strong evidence of efficacy): Local and oral steroids (5)[A]
Level 2 (moderate evidence of efficacy): Splints are effective; vitamin B6 is
ineffective (5)[A].
Level 3 (limited/conflicting evidence of efficacy): NSAIDs, diuretics, yoga,
laser, and US are effective. Botulinum toxin B injection is ineffective (5)[A].
80% of patients with CTS respond initially to conservative treatment;
however, symptoms recur in 80% after 1 yr (4).
Surgical treatment:
Patients who fail conservative therapy or who have severe symptoms (eg,
nerve entrapment on nerve conduction studies, thenar atrophy, or motor
weakness)
Surgical decompression of the carpal tunnel segment by sectioning of the
transverse carpal ligament has been reported to result in good symptomatic
improvement in 80–90% of patients and may prevent further median nerve
axon loss.
Both open and endoscopic carpal tunnel surgical procedures currently are
used.
Recent Cochrane database review did not show a difference in
postoperative complications and early return to work between the 2
techniques (1)[A].
Complications of surgery include injury to median nerve, scar tenderness,
hypotrophic scarring, loss of grip strength, pillar pain (ie, tenderness on the
base of the palm), reflex sympathetic dystrophy, and bow stringing of flexor
tendons.
Geriatric Considerations
In the geriatric population, surgery has been found to provide better symptom
relief, functional status, and general satisfaction than nonoperative therapy.
Restriction of precipitating activities may relieve symptoms.
Ongoing Care
Patient Education
Use of wrist wraps and taping may minimize forces through the carpal tunnel by limiting
excessive motion through the wrist in upper extremity weight-bearing sports such as
gymnastics and weight lifting.
Improvements in wrist pain and paresthesias may be noted within a few weeks after CTS
surgery, but maximal improvements in thenar strength and numbness may take as long as 9
mos.
References
1. Aroori S, Spence RA. Carpal tunnel syndrome. Ulster Med J. 2008;77:6–17.
2. Wilder-Smith EP, Seet RC, Lim EC. Diagnosing carpal tunnel syndrome-clinical criteria
and ancillary tests. Nat Clin Pract Neurol. 2006;2:366–374.
3. Klauser AS, Halpern EJ, De Zordo T, et al. Carpal tunnel syndrome assessment with US:
value of additional cross-sectional area measurements of the median nerve in patients
versus healthy volunteers. Radiology. 2009;250:171–177.
4. Viera AJ. Management of carpal tunnel syndrome. Am Fam Physician. 2003;68:265–

272.
5. Piazzini DB, Aprile I, Ferrara PE, et al. A systematic review of conservative treatment of
carpal tunnel syndrome. Clin Rehabil. 2007;21:299–314.
Additional Reading
Wainner RS, et al. Development of a clinical predition rule for the diagnosis of carpal tunnel
syndrome. Arch Phys Med Rehabil. 2005;86:609–617.
Gerritsen AAM, et al. Splinting vs surgery in the treatment of carpal tunnel syndrome.
JAMA. 2002;288:1245–1251.
Codes
ICD9
354.0 Carpal tunnel syndrome
Clinical Pearls
CTS is a very common compressive neuropathy of the upper extremity.
It classically presents as pain, weakness, and paresthesias on the palmar
surface on the 1st 3½ digits.
Patients also complain of nighttime symptoms and needing to shake their
hands to help the pain.
Diagnosis often can be made based on history and physical examination
findings alone.
Corticosteroids (oral and injection), splinting, and surgery have the best
evidence for treatment.
Cellulitis
Kenneth Barnes
Shane Hudnall
Basics
An inflammation of the skin and underlying subcutaneous tissues (specifically the dermal
and subcutaneous fat layers) caused by a spreading infiltration of bacteria through the skin
surface
Description
Typically results from entry of bacteria through a break in the skin, from a contiguous foci
(abscess), or from metastatic dissemination via bacteremia
Most commonly involves the lower extremities where venous stasis predisposes to infection
Can occur anywhere on the body, including periorbital area, upper extremities, and abdominal
wall
Gram positives (beta-hemolytic streptococcus, strep pyogenes especially, and
Staphylococcus aureus) comprise >80% of the organisms responsible.
Methicillin-resistant Staphylococcus aureus (MRSA) is a concern due to increasing
prevalence in the community setting.
Epidemiology
Incidence
1 case per 500 patient years (1)
Risk Factors
Disruption of skin from trauma or scratching
Eczema or other inflammation
Underlying skin infections (ie, tinea pedis)
Elderly (thrombophlebitis)
IV drug use
Human or animal bites
Edema (related to venous insufficiency)
Surgeries
MRSA risk factors:
Recent antibiotics
Recent hospitalization
Homelessness
Previous MRSA infection
IV drug abuse
Contact sports (2,3)

Consider treating for the specific organisms identified in these populations (2):
Diabetes: Anaerobes and gram negatives
Neutropenia: Pseudomonas
Human bite: Eikenella corrodens, Fusobacterium species
Cat bite: Pasteurella multocida
Dog bite: Pasteurella multocida, Capnocytophaga canimorsus
Hot tub: Pseudomonas
Fresh water: Aeromonas hydrophila
Salt water: Vibrio species
IV drug abuse: MRSA, Pseudomonas
Immunocompromised: Cryptococcus neoformans
Diagnosis
History
Breakdown in normal skin barriers almost always precedes this infection.
Preexisting venous stasis alone may predispose to cellulitis.
Physical Exam
Area of involvement denoted by spreading erythema, warmth, and swelling with ill-defined
margins
Associated pain and tenderness
Streaks of erythema and tenderness indicative of lymphatic spread
Bullae may develop, but generally rash is not raised.
Fever, sweats, shaking chills common, but bacteremia infrequent
Regional lymphadenopathy
Look for evidence of predisposing factors: Lower extremity venous stasis, tinea infection, IV
drug abuse track marks, eczema, radiation (irritation and thinning of skin)
Use of pen/marker to demarcate the leading edge of cellulitis is helpful in monitoring during
follow-up.

Lab
Current recommendations are to culture all wounds for bacterial identification and
antimicrobial sensitivity testing.
Blood cultures rarely helpful (<5%) (3,4)
Needle aspiration of abscess or bullae most likely to be helpful if present
Culture of overlying intact skin is not helpful and recommended against.
Imaging
Generally, imaging not recommended unless concerned about osteomyelitis, gas gangrene,
underlying abscess, or other conditions in differential (ie, deep vein thrombosis)
Erysipelas (infection of the superficial layers of the skin, usually caused by group A
streptococci)
Fasciitis/necrotizing fasciitis
Myonecrosis/gas gangrene
Toxic epidermal necrolysis
Osteomyelitis
Cutaneous candidal infection
Septic arthritis
Gout
Zoster
Erythema migrans
Contact dermatitis
Eczema
Ruptured baker's cyst
Drug rash
Insect bite
Treatment
If staph is isolated, consider treating for MRSA if patient has MRSA risk
factors and/or if local prevalence of MRSA is high.
Medication
Treat presumptively with close follow-up.
Duration of therapy 10–14 days total
Improvement anticipated in 1–2 days
If no improvement or clinical deterioration, admit for parenteral antibiotics and
broaden differential diagnosis to include possibility of potentially fatal infections
such as necrotizing fasciitis.
Treatment recommendations:
Outpatient for non-MRSA infections: Dicloxacillin 500 mg PO q.i.d.,
cephalexin 500 mg PO q.i.d. May use clindamycin 300–450 mg PO q6–8h or
fluoroquinolones if allergic to penicillins.
Inpatient for non-MRSA infections: Nafcillin 1–2 g IV q4h
Outpatient for MRSA infections: Bactrim DS 2 tabs PO b.i.d. or doxycycline
100 mg PO b.i.d. (not recommended for children <8 yrs old) or clindamycin
300–450 mg PO q6–8h (check local resistance patterns)
Inpatient for MRSA infections: Vancomycin (15 mg/kg/dose IV q12h), linezolid
600 mg PO b.i.d. (expensive and need to monitor for thrombocytopenia) (3,5)
Human bites: Augmentin (outpatient), ampicillin/sulbactam (inpatient); penicillin
allergy: Moxifloxacin + clindamycin or Bactrim + Flagyl
Animal bites: Augmentin (outpatient), ampicillin/sulbactam (inpatient); penicillin
allergy: (doxycycline or moxifloxacin or Bactrim) + (clindamycin or Flagyl) (3)
General Measures
If abscess present, incision and drainage required
If bullae noted, typically do not rupture as part of treatment
If underlying venous stasis noted, elevation of affected limb and, if possible,
compression stockings (not over area of skin involvement) recommended
Referral
If patient not responding to antibiotic treatment in timely manner
If development of crepitance suggesting a gas-forming organism
If the cellulitis is on the face, there is a low threshold for referral.
If a high-risk patient or immunocompromised for any reason, have a low
threshold for involvement of an infectious disease specialist if not readily
responding to treatment.
Recently recognized that use of cell-wall active antibiotics (ie, β-lactams) cause
an initial worsening prior to improvement due to rapid release of a bolus of
exotoxins (6)
Ongoing Care
Patient Education
Early identification is important.
If infection considered contagious, must not participate in contact or collision sports
MRSA becoming more prevalent in locker rooms as well as in the community.
Do not share towels, razors, other products.
Frequent skin inspections
Cover all wounds.
Disinfect all shared athletic equipment and whirlpools.
Education and posters recommended in all training rooms and locker rooms
Liberal use of antibacterial soap or alcohol-based hand sanitizer
Return to play:
Mild to moderate skin lesions: 72 hr after initiation of therapy, with clinical improvement and
no new lesions for 48 hr
Before and during sports participation: Cover completely with occlusive dressing.
Multiple wound checks: If leakage, remove athlete, cleanse skin with soap and water,
apply new dressing
Removal of dressing once firm, adherent crust develops (7,8)
References
1. McNamara DR, Tleyjeh IM, Berbari EF, et al. Incidence of lower-extremity cellulitis: a
population-based study in Olmsted county, Minnesota. Mayo Clin Proc. 2007;82:817–821.
2. Eron LJ, Laine C, Goldmann DR, Sox HC. Cellulitis and soft-tissue infections. Ann Intern
Med. 2009;150:ITC1–1.
3. Stevens DL, et al. Practice guidelines for the diagnosis and management of skin and soft-
tissue infections. Clin Infect Dis. 2005;41:1373–1406.
4. Perl B, Gottehrer NP, Raveh D, et al. Cost-effectiveness of blood cultures for adult
patients with cellulitis. Clin Infect Dis. 1999;29:1483–1488.
5. Gilbert DN, Moellering RC Jr, Sande MA, eds. The Sanford guide to antimicrobial
therapy 2000, 30th ed. Hyde Park, VT: Antimicrobial Therapy, 2000.
6. Melzer M, Eykyn SJ, Gransden WR, et al. Is methicillin-resistant Staphylococcus aureus

more virulent than methicillin-susceptible S. aureus? A comparative cohort study of British
patients with nosocomial infection and bacteremia. Clin Infect Dis. 2003;37:1453–1460.
7. American Academy of Pediatrics, Committee on Sports Medicine and Fitness. Medical

Conditions Affecting Sports Participation. Pediatrics. 2008;121:841–848.
8. Minooee A, Arezou, Rickmans LS, et al. Transmission of infectious diseases during

sports. In: Schlossberg D, ed. Infections of leisure, 2nd ed. Washington, DC: American
Society for Microbiology, 1999.
Additional Reading
Benjamin HJ, Nikore V, Takagishi J. Practical management: community-associated
methicillin-resistant Staphylococcus aureus (CA-MRSA): the latest sports epidemic. Clin J
Sport Med. 2007;17(5):393–397.
Reese RE, Betts RF, eds. A practical approach to infectious diseases, 4th ed. Boston:
Little Brown, 1996.
Stevens DL. Cellulitis, pyoderma, and other skin and subcutaneous infections. In: Armstrong
D, Cohen J, eds. Infectious diseases. Vol. 1. Mosby/Harcourt Publishers, 1999:2.2.6–2.2.8.
Swartz NN. Cellulitis and subcutaneous tissue. In: Mandell GL, Bennet JE, Dolin R, eds.
Mandell, Douglas, and Bennetts principles and practice of infectious disease, 5th ed. Vol.
1. Philadelphia: Churchill Livingstone, 2000.
Codes
ICD9
682.2 Cellulitis and abscess of trunk
682.3 Cellulitis and abscess of upper arm and forearm
682.9 Cellulitis and abscess of unspecified sites
Central Slip Avulsion and Pseudoboutonniere
Deformities
Jeffrey Feden
Razib Khaund
Basics
Description
Boutonniere deformity describes a characteristic flexion deformity of the proximal
interphalangeal (PIP) joint and hyperextension deformity of the distal interphalangeal (DIP)
joint; it results from disruption of the central slip at or near its insertion onto the dorsal aspect
of the base of the middle phalanx.
Mechanism of injury is often forced flexion of an extended PIP joint or volar dislocation of the
middle phalanx, causing avulsion of the central slip.
Deformity of the finger may develop several weeks after an untreated injury.
Pseudoboutonniere deformity results from hyperextension of the PIP joint; the volar plate is
ruptured, whereas the central slip remains intact.
Epidemiology
Unknown incidence but relatively uncommon
Risk Factors
Ball-handling sports
Etiology
Boutonniere deformity:
Following avulsion of the central slip, the intact lateral bands slowly migrate in a volar
direction as the central slip retracts.
The head of the proximal phalanx “buttonholes” through the injured extensor mechanism.
The lateral bands become flexors of the PIP joint and extenders of the DIP joint.
Pseudoboutonniere deformity: Contracture and fibrosis of the volar plate following injury
leads to a flexion deformity of the PIP joint.
Diagnosis
History
Always consider injury to the central slip when an athlete “jams” a finger or has a PIP joint
dislocation reduced.
Knowledge of the mechanism of injury and/or direction of a PIP joint dislocation also may
localize the injury and guide treatment.
Forced flexion of an extended PIP joint or volar dislocation of the middle phalanx may
cause central slip injury.
Hyperextension of the PIP joint or dorsal dislocation of the middle phalanx may cause volar
plate injury.
Physical Exam
Early: Swollen PIP joint with dorsal tenderness, weak active extension, full passive extension;
classic deformity is rarely seen in the acute setting.
Late: Flexion deformity of the PIP joint with hyperextension of the DIP joint
Unlike a true boutonniere deformity, pseudoboutonniere deformity is characterized by a fixed
flexion contracture of the PIP joint, inability to achieve passive extension, and mild or absent
DIP joint hyperextension.

Imaging
Plain radiographs (especially a true lateral view) to evaluate for fracture, dislocation, and volar
plate injury
Fracture
PIP joint dislocation
Volar plate disruption
Collateral ligament tears
Treatment
Boutonniere deformity:
Strict immobilization of the PIP joint in continuous extension for 4–6 wks;
nighttime splinting for another 2–3 wks (1,2,3)[C]
Allow active and passive flexion of the DIP joint without immobilization (1,2,3)
[C].
Gentle active and passive range of motion after splinting is completed (1,2,3)
[C]
Splinting is appropriate initial treatment even for chronic deformity (3)[C].
Safety-pin splints are most practical for flexion contractures of >40 degrees;
dynamic spring splints may be used for greater contractures (4)[C].
Pseudoboutonniere deformity: P.
May be treated with progressive extension splinting if the flexion contracture
is <45 degrees; otherwise, surgical release should be considered (5)[C].
Acute volar plate injuries should be treated initially with an extension block
splint and active flexion for 3 wks, followed by gradual extension (5)[C].
Referral
Referral is recommended for:
Inability to reduce a PIP joint dislocation or a large, displaced intra-articular PIP
joint fracture
Failure of nonoperative treatment with splinting
Chronic flexion contractures of >45 degrees
Consider surgical management for:
Interposed soft tissue preventing congruent reduction of a volar PIP dislocation
Large, displaced intra-articular PIP fracture at the base of the middle phalanx
Flexion contractures of >45 degrees
Symptomatic, chronic deformities
Ongoing Care
The athlete's sport and position will dictate his or her ability to participate with the injured
finger immobilized.
References
1. Hong E. Hand injuries in sports medicine. Prim Care. 2005;32:91–103.
2. Peterson JJ, Bancroft LW. Injuries of the fingers and thumb in the athlete. Clin Sports
Med. 2006;25:527–542, vii–viii.
3. Lee SJ, Montgomery K. Athletic hand injuries. Orthop Clin North Am. 2002;33:547–554.
4. Aronowitz ER, Leddy JP. Closed tendon injuries of the hand and wrist in athletes. Clin
Sports Med. 1998;17:449–467.
5. Rettig AC. Athletic injuries of the wrist and hand: part II: overuse injuries of the wrist and
traumatic injuries to the hand. Am J Sports Med. 2004;32:262–273.
Additional Reading
Coons MS, Green SM. Boutonniere deformity. Hand Clin. 1995;11:387–402.
Hogan CJ, Nunley JA. Posttraumatic proximal interphalangeal joint flexion contractures. J
Am Acad Orthop Surg. 2006;14:524–533.
Codes
ICD9
736.21 Boutonniere deformity
Clinical Pearls
An acutely injured PIP joint with dorsal tenderness and weak active extension
should be treated empirically even in the absence of a classic boutonniere
deformity.
Accidental flexion of the PIP joint during the treatment period must be avoided
to prevent disruption of the healing process.
The majority of central slip injuries can be treated nonoperatively with
satisfactory results.
The mechanism and direction of injury at the PIP joint may help to differentiate
boutonniere from pseudoboutonniere deformities.
Cervical Disk Disease
Kevin Eerkes
Basics
Description
Cervical radiculopathy is defined as neurogenic pain in a dermatomal distribution ± numbness,
weakness, and decreased reflexes in the upper limb.
This is caused by compression or irritation of the nerve root.
The most common location is the neural foramen.
Epidemiology
Predominant age: Peak age for cervical radiculopathy is 50–54 yrs.
Predominant gender: Female > Male; women are more likely to suffer from cervical disk
disease than men at an earlier age.
Incidence
Annual incidence rates of cervical radiculopathy:
107.3 cases/100,000 men
63.5 cases/100,000 women (1)
Etiology
Cervical radiculopathy occurs when the nerve root becomes dysfunctional from compression,
stretching, and/or irritation.
The most common cause is degenerative changes of the cervical spine. Degenerative
changes become more prominent with age and encompasses the following:
Desiccation and bulging of the disks
Osteophyte formation at the uncovertebral and facet joints
Loss of disk height
These all may lead to narrowing of the neural foramen through which the nerve exits.
Disk herniation is the 2nd most common cause of cervical radiculopathy.
This also tends to occur in an older population with some disk degeneration.
Can occur in younger population (<45 yrs old), but more force generally is needed because
their disks are more resilient.
Pathophysiology:
The annulus fibrosis becomes weakened, allowing the nucleus pulposus to herniate
through.
The herniated disk material may compress the nerve root and incite the production of
various inflammatory cytokines that irritate the nerve.
Pathoanatomy:
Cervical nerve roots exit above their correspondingly numbered pedicles.
C7 nerve root exits between C6 and C7.
C6 nerve root exits between C5 and C6.
Most common level for the herniation is C6–7 (70%), which affects the 7th cervical
nerve.
C5–6 is the next most common level. Herniation here typically affects the 6th cervical
nerve.
Most disk herniations occur in a posterolateral direction into the foramen.
The disk occasionally can herniate posteriorly, which may result in myelopathy (cord
compression).
The presence of osteophytes narrows the canal, so a disk herniation (which further
narrows the canal) more than likely would be symptomatic.
Diagnosis
History
Ask about prior neck or low back problems.
Usually the onset of symptoms is spontaneous or with only minor force to the disk.
The annulus is usually already weakened, so major force is not necessary for herniation.
Occasionally, the onset of symptoms is coincident with trauma such as axial loading and/or
hyperflexion.
Pain radiates into the neck and the ipsilateral upper limb in a myotomal pattern.
A myotome is the muscle(s) innervated by a nerve. The myotome for the 6th and 7th
cervical nerves would be the arm and forearm.
The upper limb pain may be greater than the neck pain.
Pain also may be referred to the upper trapezius, periscapular area, and shoulder girdle.
Patient may report relief by abducting the upper limb. This decreases the amount of
stretch on the nerve root.
Numbness and paresthesia often occur in a dermatomal distribution.
For the 7th cervical nerve, this would occur down the limb to the middle finger.
For the 6th cervical nerve, this would occur down the limb to the thumb and index finger.
Note that this classic dermatomal pattern is not always present.
Weakness often develops in the muscles supplied by the nerve.
Red flags:
Gait disturbance, bowel/bladder dysfunction, or hand clumsiness (possible myelopathy)
Fever, chills, unexplained weight loss
Unremitting night pain
Immunosuppression
History of cancer
IV drug abuse
Physical Exam
Range of motion of the neck is decreased.
Neck tenderness is often present.
Muscle spasm may be present.
Strength and/or reflexes often decreased.
For the 7th and 8th cervical nerves, triceps weakness and diminished triceps reflex
For the 5th and 6th cervical nerves, weak deltoid, wrist extensors, and biceps;
brachioradialis and biceps reflexes diminished
Sensation in dermatome may be decreased (see “History”).
Spurling's maneuver may be positive.
Neck extension combined with side bending and rotating to the ipsilateral side
This further narrows the neural foramen and may reproduce symptoms down the upper
limb.
Accuracy is poor.
May check for signs of myelopathy:
Hoffmann sign: Flexion and adduction of the thumb when the examiner passively flexes the
distal phalanx of the middle finger (while stabilizing the middle phalanx)
Hyperreflexia
Babinski sign
Lhermitte sign: Shocklike sensation radiating down the spine with simultaneous neck and
hip flexion

Imaging
X-rays:
Obtain on initial visit if red flags; otherwise, optional
Anteroposterior, lateral, and oblique views
Images usually are not very helpful.
Often normal
May show nonspecific spondylosis
Athletes with a long history of involvement in collision sports have a higher rate of x-ray
abnormalities.
Disk space narrowing occasionally may be seen at the level of the disk herniation.
MRI:
Provides excellent visualization of disks and nerves
Indications:
Symptoms or signs of myelopathy
Red flags suggestive of tumor or infection
Progressive or disabling neurologic deficit
No improvement after 4–6 wks of treatment
T2 images best show disk herniation.
Caution should be used when interpreting MRIs in contact athletes and older adults.
They have a high frequency of abnormal findings on MRI, many of which are
asymptomatic.
MRI results should correspond with the physical findings to be significant.
The nerve root compromised on MRI must correspond to location of pain and
weakness/reflex loss in the patient.
CT myelogram:
Only done if need information the MRI doesn't provide
Differentiates a soft disk (disk herniation) from a hard disk (osteophyte disk ridge complex)
Shows foraminal stenosis better than MRI
Disadvantage is that it is invasive.
Electrodiagnostic studies (nerve conduction study and/or electromyogram):
Obtain only if diagnosis is unclear or want to rule out peripheral nerve entrapment.
Wait until symptoms have been present at least 3 wks before testing. Testing sooner may
result in false-negative result.
Cervical spondylosis
Osteophyte disk ridge complex (the remnants of a herniated disk combined with an
osteophyte)
Annular tear
Peripheral nerve entrapment
Brachial plexus neurapraxia (“stinger”)
Parsonage-Turner syndrome/brachial plexopathy
Myelopathy (with massive central disk herniation)
Spinal tumor
Spinal infection
Complex regional pain syndrome
Herpes zoster
Rotator cuff disorders
Pancoast tumor
Vascular disturbance
Treatment
Because of a relatively high rate of spontaneous resolution, initial treatment
is usually nonoperative. Exceptions that may require further workup and
subspecialty consultation include:
Progressive neurologic deficit
Disabling weakness
Infection or tumor
Vertebral fracture or subluxation from trauma
There are no controlled trials comparing the various nonsurgical treatment
regimens with the natural history (ie, no treatment at all); therefore, it remains
unclear whether nonsurgical management actually improves the natural history
of the disorder or simply treats the symptoms as the disorder runs its course
(2)[C].
Treatment recommendations are from case series and anecdotal experience.
The aim of treatment of disk herniation is to relieve pain and improve
neurologic function while the herniated disk is absorbed by the body and the
nerve dysfunction subsides. Resolution of the symptoms correlates with
attenuation of the herniation on imaging studies.
Patients should be reevaluated at regular intervals during the treatment
process so that worsening symptoms can be identified promptly.
P.
Medication
First Line
NSAIDs:
Use at anti-inflammatory doses (eg, ibuprofen 600 mg q.i.d.).
Block formation of inflammatory mediators at the site of the disk herniation
Use cautiously if:
Risk factors for GI bleeding
Risk factors for renal disease
Oral steroids:
More potent anti-inflammatory agents than NSAIDs, although greater
potential side effects
May consider using if:
Not responding to NSAIDs
Severe pain
Weakness
Avoid using with NSAIDs.
Have not been shown to alter the natural history of cervical radiculopathy
Dose:
Often corresponds to the degree of weakness
Typical regimen: Start with 50–70 mg/day of prednisone; taper over next 10
days (3)[C].
Side effects: Numerous, but significant side effects are rare if drug is taken
in small doses for a limited length of time.
Second Line
Narcotics:
May be considered for short-term use if pain is severe and not controlled by
other medications and modalities
Have additive effect with NSAIDs on pain relief
Typical prescription: Oxycodone (Vicodin) 1–2 pills q4–6h PRN for pain
Potential side effects: Drowsiness, vomiting, constipation, dependency
Antispasmodic agents (muscle relaxants):
Consider using if muscle spasm is prominent.
Additive effect on pain relief when used with a NSAID or narcotic; drowsiness
when combined with a narcotic may be intolerable.
Typical prescription: Cyclobenzaprine (Flexeril) 5–10 mg t.i.d.
Avoid using for >2–3 wks.
Potential side effects: Sedation, dependency
Rest:
“Relative rest” is typically recommended. Patient is encouraged to be as
active as the pain allows.
Bed rest:
Reserved for only the worst cases
Elevate head of bed
Limit to <7 days
Cervical collar to limit motion:
Theoretical function:
Diminish inflammation around an irritated nerve root
Decrease muscle spasm
Provide warmth
Data on efficacy are unclear.
May consider initially if severe pain when moving head
May aid sleep by limiting motion of the head
Try to limit use to <1–2 wks (to avoid weakness and stiffness).
Come out of the collar several times per day for range-of-motion (ROM)
exercises within limits of pain.
Physical therapy:
May start as pain is improving (within 1–2 wks)
Heat/cold, active ROM, isometric strengthening as tolerated
As condition improves, ROM and resistive exercises are advanced.
May add nonimpact aerobic exercise; gear toward an activity that allows the
neck to remain in neutral position (eg, walking, stationary bike).
Postural education
Ergonomic adjustments
Traction:
Theoretically distracts the vertebra, enlarges the neural foramen, and allows
more room for exiting nerves
Conflicting reports regarding benefit
Spinal manipulation (chiropractic treatment):
Not routinely recommended
No evidence of benefit, and there are reports of complications such as spinal
cord and vertebral artery injury.
Epidural steroid injections:
Sometimes used to treat radiculopathy that persist despite NSAIDs, oral
steroids, and time
A high concentration of steroid is deposited at the site of inflammation.
Well-designed studies supporting this treatment are lacking (2)[C]. Have not
been shown to change the natural history.
Potential side effects:
Bleeding
Infection
Dural puncture
Nerve damage
Spinal cord and brain stem infarction (4)[C]
P.
Consider referring to spine surgeon if:
Progressive or severe neurologic deficit
Recalcitrant radicular pain or numbness despite nonoperative treatment for
6–12 wks; no data on the optimal timing
Instability of the spine with radicular symptoms
Moderate to severe myelopathy
Muscle atrophy
Surgical outcomes for relief of arm pain range from 80–90% (2)[C].
Typical procedure for cervical radiculopathy:
Anterior cervical discectomy and fusion (ACDF): Allows removal of the disk
and uncovertebral spur without neural retraction
Bone graft or plate is placed anteriorly.
Total disk arthroplasty (experimental):
Diseased disk is removed, and an artificial disk is placed.
Allows preservation of motion, thereby theoretically decreasing the incidence
of adjacent segment disease (5)[B]
Preliminary results have been favorable.
No significant complications have been associated with this procedure thus
far.
Further study is needed.
Ongoing Care
Patient Education
In attempt to decrease recurrence of symptoms:
Keep the neck muscle strong.
Use correct posture when sitting (head centered over shoulders).
Workstation setup ergonomically correct
Avoid forcing the neck into extremes of motion.
Regular aerobic exercise
Prognosis
Resolution of all or most symptoms occurs within 6–12 wks in most patients.
Acute cervical radiculopathy has up to a 75% rate of spontaneous improvement (2).
Complications
Waiting too long to treat: If weakness is present for too long, patient may never
regain full strength and function.
References
1. Radhakrishnan K, Litchy WJ, O'Fallon WM, et al. Epidemiology of cervical
radiculopathy. A population-based study from Rochester, Minnesota, 1976
through 1990. Brain. 1994;117 (Pt 2): 325–335.
2. Rhee JM, Yoon T, Riew KD. Cervical radiculopathy. J Am Acad Orthop

Surg. 2007;15:486–494.
3. Carette S, Fehlings MG. Clinical practice. Cervical radiculopathy. N Engl J

Med. 2005;353:392–399.
4. Malhotra G, Abbasi A, Rhee M. Complications of transforaminal cervical

epidural steroid injections. Spine. 2009;34:731–739.
5. Nabhan A, Ahlhelm F, Shariat K, et al. The ProDisc-C prosthesis: clinical

and radiological experience 1 year after surgery. Spine. 2007;32:1935–1941.
Additional Reading
Acosta FL, Ames CP. Cervical disc arthroplasty: general introduction.
Neurosurg Clin N Am. 2005;16:603–607, vi.
Albright JP, Moses JM, Feldick HG, et al. Nonfatal cervical spine injuries in
interscholastic football. JAMA. 1976;236:1243–1245.
Brown S, Guthmann R, Hitchcock K, et al. Clinical inquiries. Which treatments

are effective for cervical radiculopathy? J Fam Pract. 2009;58:97–99.
Ellis JL, Gottlieb JE. Return-to-play decisions after cervical spine injuries.
Curr Sports Med Rep. 2007;6:56–61.
Young IA, Michener LA, Cleland JA, et al. Manual therapy, exercise, and
traction for patients with cervical radiculopathy: a randomized clinical trial.
Phys Ther. 2009.
Zmurko MG, Tannoury TY, Tannoury CA, et al. Cervical sprains, disc
herniations, minor fractures, and other cervical injuries in the athlete. Clin
Sports Med. 2003;22:513–521.
Codes
ICD9
722.0 Displacement of cervical intervertebral disc without myelopathy
723.4 Brachial neuritis or radiculitis nos
839.00 Closed dislocation, cervical vertebra, unspecified
Clinical Pearls
Weakness is the most serious effect of cervical radiculopathy and should be
followed closely.
MRI is the test of choice for imaging the disks and nerves.
Treatment in most patients is nonoperative.
The timing of surgical intervention for cervical radiculopathy has not been
established, but surgery should be considered if there is significant weakness
or symptoms that are refractory to nonoperative treatment.
Don't miss the red flags: Cervical myelopathy, tumor, infection.
Cervical Stenosis
Robert D. Menzies
L. Shay Richardson
Basics
Description
A congenital or acquired narrowing of the cervical spinal canal. However, this problem has
several definitions. This definition is based on MRI evidence from the National Center for
Catastrophic Sports Injury Research (NCCSI).
Functional spinal stenosis is the loss of the CSF cushion around the spinal cord or a clear
deformation of the cord demonstrated by CT scan, MRI, or myelography.
Synonym(s): Cervical cord neurapraxia; Any transient neurologic deficits
Epidemiology
Incidence
The incidence of cervical stenosis is unknown.
However, Torg reported that in a single football season, 6 of 10,000 exposures resulted in
transient paresthesia in all 4 extremities and 1.3 of 10,000 exposures resulted in transient
quadriplegia (1).
This describes cervical cord neurapraxia (CCN), which is thought to be a sequela of stenosis.
Prevalence
In a cadaveric study, Lee et al. estimated the prevalence of cervical spinal stenosis to be
4.9% of the adult population based on radiographic measurement of canal diameter <12 mm
(2).
Cervical stenosis also was found to increase with age.
Risk Factors
Congenital or acquired defects, which include bulging disk, hypertrophied or unstable
ligaments, and degenerative changes
Involvement in sports that engage in potential axial loading, such as football, ice hockey,
diving, head-first sliding in baseball, wrestling, soccer, gymnastics, and rugby
Diagnosis
History
During preparticipation physical examination, determination of any prior history of neurologic
events, such as burners/stingers or transient neurologic events, is critical.
If the athlete gives a positive response, all data from previous evaluations must be reviewed.
If no workup has been done, then seriously consider starting one before allowing the athlete
to begin contact/collision sports.
If the athlete has a condition such as Down syndrome, odontoid abnormality, atlantooccipital
fusion, or Klippel-Feil anomaly, these may predispose him or her to cervical stenosis, and the
athlete must be further evaluated.
Physical Exam
Unfortunately, cervical stenosis is asymptomatic until forced hyperflexion or hyperextension
occurs with an axial load, which causes CCN.
The athlete develops acute transient sensory paresthesia and/or motor paresis.
Findings are always bilateral.
Paresthesia is described as burning pain, numbness, or tingling of the affected region.
Motor changes can range from weakness to complete paralysis.
Neurapraxia commonly lasts 10–15 min but can take up to 48 hr to resolve (3).
During the preparticipation physical examination, the Spurling foraminal compression test can
be done. If symptoms are elicited, further workup can be started. The yield is very low unless
the patient already has stenosis. It should be done on any athlete who gives a history of
neurologic events.
If the initial event occurs on the field, start with assessment of the athlete's level of
consciousness. If unconscious, immobilize and transport. If conscious, proceed to assess
neck pain.
If neck pain is present or absent and the athlete has neurologic symptoms, immobilize and
transport for further workup.

Imaging
The initial radiographic examination should start with cervical spine x-rays, which can be used
to evaluate for gross fracture or dislocation. In addition, some measurements of the spinal
canal can be done. The normal canal measures >15 mm; <13 mm is considered spinal
stenosis (4).
On the lateral x-ray, the Torg ratio can be calculated. Measure (in millimeters) the distance
from the posterior aspect of the vertebral body to the spinolaminar line (a) and the width of
the vertebral body (b); then calculate the ratio a/b. A value <0.8 is abnormal and needs
further evaluation (5).
A large vertebral body can result in a false-positive result; the false-positive rate has been
reported as high as 88%. If the patient has spinal stenosis, the ratio almost always is
abnormal.
Cervical x-ray limitations include the failure of roentgenography to appraise the width of the
cord and an inability to appreciate stenosis resulting from ligamentous hypertrophy,
ligamentous laxity, or disk protrusion.
Therefore, the next step is to use MRI or CT myelography.
MRI can evaluate spinal stenosis caused by most abnormalities. It is not as effective as CT
myelography in evaluating bony lesions. MRI is sufficient in most cases (4,6).
MRI is done in a neutral position. With hyperextension, spinal canal diameter decreases by
30% owing to infolding of the interlaminar ligaments.
“Functional” spinal stenosis, defined as loss of CSF around the cord or, in more extreme
cases, deformation of the spinal cord, whether documented by CT myelography, MRI, or
standard myelography, is a more accurate measure of stenosis (4,6).
Stable spinal fracture
Any cause of permanent spinal cord injury
Spear tackler's spine
Unstable fracture
Spinal fracture with dislocation
Ligamentous injury
Herniated cervical disk
Treatment
After the 1st episode of CCN, if the initial workup is negative for stenosis, a
generalized neck strengthening program should be started.
Athletes involved in collision sports should be able to support their body weight
with the cervical spine in neutral and in all directions when positioned at a 45-
degree angle.
If an acquired cause for spinal stenosis is detected, consultation with a
neurosurgeon or orthopedic spine surgeon for consideration of surgery can be
undertaken.
However, after surgery, the athlete probably cannot participate in
contact/collision sports.
Ongoing Care
Team physicians should be concerned with functional spinal stenosis. If present, and the
athlete incurs spinal cord symptoms, the athlete should not continue in contact/collision sports
because such activities predispose athletes to a worse neurologic outcome in the context of
cervical spine injuries (4,6).
Data collected by the NCCSI from 1987 to 1996 showed that no athlete with functional spinal
stenosis and cervical spinal fracture recovered from quadriplegia.
This finding needs to be compared with nearly 20% of athletes with cervical spinal fracture
and normal canal sizes who had initial quadriplegia and recovered fully.
During the same period, in all cases of quadriplegia without cervical spinal fracture
dislocation, severe spinal stenosis was present.
If the athlete redevelops CCN, the workup should proceed again, from plain radiographs to
MRI or CT myelography.
According to a review performed by Torg et al., 56% of National Football League players
with one episode of CCN went on to develop a repeat episode after return to play (3).
Given the excellent sensitivity of the Torg ratio, any athlete with an abnormal ratio along with
spinal cord symptomatology should undergo MRI, myelography, or CT myelography (4).
References
1. Torg JS, Pavlov H, et al. Neurapraxia of the cervical spinal cord with transient
quadriplegia. J Bone Joint Surg. 1986;21:1354–1370.
2. Lee Michael J, et al. Prevalence of cervical spine stenosis: Anatomic study in cadavers. J
Bone Joint Surg. 2007;892:376–380.
3. Eddy, Derrick, et al. A review of spine injuries and return to play. Clin J Sports Med.
2005;15(6):453–458.
4. Cantu RC. Cervical spine injuries in the athlete. Semin Neurol. 2000;20:173–817.
5. Torg JS. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin
Sport Med. 1990;9:279–296.
6. Cantu RC. The cervical spinal stenosis controversy. Clin Sport Med. 1998;17:121–126.
7. Cantu RC. Stingers, transient quadriplegia, and cervical stenosis: return to play criteria.
Med Sci Sports Exerc. 1997;29[7 Suppl]:233–235.
Additional Reading
Cantu RC, Bailes JE, Wilberger JE Jr. Guidelines for return to contact or collision sport after
a cervical spine injury. Clin Sport Med. 1998;17:137–146.
Maroon JC, Bailes JE. Athletes with cervical spine injury. Spine. 1996;21:2294–2299.
Wilberger JE Jr. Athletic spinal cord and spine injuries. Clin Sport Med. 1998;17:111–120.
Zachazewsia JE, Magee DJ, Quillen WS. Athletic injury and rehabilitation. Philadelphia: WB
Saunders, 1996.
Codes
ICD9
723.0 Spinal stenosis in cervical region
742.59 Other specified congenital anomalies of spinal cord
756.10 Congenital anomaly of spine, unspecified
Clinical Pearls
Return-to-play guidelines (7):
Canal/vertebral body ratio ≤0.8 in asymptomatic individuals: No
contraindication
Ratio of ≤0.8 with one episode of CCN: Relative contraindication
Documented episodes of CCN associated with intervertebral disk disease
and/or degenerative changes: Relative contraindication
Documented episode of CCN associated with MRI evidence of cord defect or
cord edema: Relative/absolute contraindication
Documented episode of CCN associated with ligamentous instability,
symptoms, or neurologic findings lasting >36 hr and/or multiple episodes:
Absolute contraindication
Any episode in which, during the evaluation, functional stenosis is detected:
Absolute contraindication
Athletes with significant bone or ligamentous spinal instability, spinal cord
contusion, or significant spinal stenosis should not return to contact sports.
Cervical Strains
Jeffrey M. Mjaanes
Jason Lee
Basics
Description
Cervical strain refers to a stretch-type injury within the muscle substance or at the
myotendinous junction of the cervical and upper back muscles. In addition to the muscle and
tendons, injury commonly involves the ligamentous structures of the cervical spine.
Synonym(s): Cervical sprain; Whiplash (whiplash-associated disorders)
Epidemiology
Most frequently caused by whiplash injury, ie, hyperextension of the cervical spine from a
rear-end motor vehicle collision
More than 1 million cases per year are reported in the U.S. More common in urban areas
with a greater number of motor vehicles.
Higher incidence seen in females
More common in adults than children (especially persons ages 30–50 yrs)
Incidence associated with sports is unknown.
In general, collision sports are responsible for a high number of injuries to the head and neck.
Risk Factors
Speculated: Age, level of conditioning, prior history of neck injury, cervical degenerative disc
disease, head position at time of impact, mechanism of injury, personality traits, and
psychosocial factors
Etiology
Acutely, cervical strain occurs as the result of a blow to the head or neck during muscular
contraction. In motor vehicle accidents, the causative force is usually a rear-end collision
leading to a hyperextension then hyperflexion of the neck. The applied force often creates an
eccentric contraction causing microscopic or gross tensile failure, most often at the
myotendinous junction and in ligamentous structures.
Muscles with high ratios of type II or fast-twitch muscle fibers demonstrate a higher risk for
strains or shearing-type injuries.
Healing process divided into 3 stages:
Destructive phase: Starting with hematoma formation, myofibrillar necrosis, and the
initiation of the inflammatory response
Repair phase: Involves phagocytosis of necrotic tissue and regeneration of myofibers and
the formation of fibrous tissue in areas of damages
Remodeling: Entails maturation of the regenerated muscle tissues and reorganization of
scar tissue based on the stresses placed on the zone of injury
Cervical strains can also be chronic in nature and related to repetitive stress or abnormal
postural biomechanics.
Diagnosis
History
When taking the history, it is essential to determine the mechanism of injury. For example, if
the injury is the result of a motor vehicle accident, important information includes the
approximate speed of the vehicles, the location of the patient within the vehicle (driver, front
seat passenger, etc.), and whether the patient was restrained.
Onset, time course, and location of symptoms (anatomical pain drawings may be helpful in
providing an overview of the pain pattern)
Presence of any neurological symptoms and course: Upper or lower extremity sensory
changes, pain radiating into the arms past the elbows, or weakness in upper extremities
Activities and head positions that aggravate or alleviate symptoms
Prior episodes of similar symptoms, previous neck injury or surgery
Previous treatment, including modalities, medications, physical therapy, traction,
manipulation, injection, and surgical treatments
Social history, including level of physical activity, occupation, job satisfaction, ongoing
litigation, and use of nicotine, alcohol, and/or other substances
Pain is the most common presenting complaint in cervical strains. Frequently, patients may
have minimal pain immediately after the injury but have increasing pain severity several hours
to days later. Pain may be referred to the shoulder, upper limb, and head.
Soft tissue swelling may be present.
Muscle spasm or tightness
Limitation in range of motion at the neck
Neck fatigue, stiffness, pain at rest and/or with movement
Other symptoms may include unusual skin sensations at head/face, dizziness,
lightheadedness, concentration and memory deficits, tinnitus, blurred vision, hearing
difficulties, and other cranial nerve deficit complaints.
Physical Exam
Observation: Head and neck posture, movement during normal conversation, weak or stiff
movement
Range of motion: Active range of motion, usually reduced, particularly in directions stretching
the injured muscles
Palpation: Tenderness, usually noted along the cervical paraspinal muscles; may be present
along muscles where symptoms are referred, muscles with associated hypertonicity, or
“spasm”
Generally normal neurologic examination, although subjective sensory deficits may be present
Careful manual muscle testing for evidence of deficits in myotomal distribution
Sensory examination for dermatomal deficits in sensation, hyperesthesia, inconsistent or
“nonanatomical” pattern
Deep tendon reflexes/muscle stretch reflexes and Hoffman or Babinski signs helpful in
identifying myelopathy, radiculopathy, and brachial plexopathy
By definition, all provocative tests are negative.
Spurling's test is performed by extending the neck and rotating the head, and then applying
downward pressure on the head. Considered positive if pain radiates into the limb ipsilateral
to the side the head is rotated. Specific but not sensitive in diagnosing acute radiculopathy.
Lhermitte's sign is performed by passively flexing the neck. Considered positive if “electric-
like” sensation radiates down the spine. Positive with cervical stenosis, myelopathy, spinal
cord injury due to tumor, multiple sclerosis, and other conditions.
Axial compression test is performed by gently applying an axially directed pressure on top of
the seated patient's head. The patient's neck is in neutral. Pain radiating distal to the elbow is
considered positive for likely radicular origin. Manual distraction often greatly reduces neck
and limb symptoms in patients with radiculopathy.

Imaging
In the management of cervical strain, radiographs are usually not necessary. In trauma
patients, however, plain radiographs are used to rule out other potentially serious conditions,
such as fractures or dislocations.
Minimum views include anteroposterior, lateral, and oblique cervical spine views for evidence
of acute fracture or subluxation with trauma.
Open mouth view for evidence of atlantoaxial instability and odontoid fractures. Flexion and
extension lateral views are helpful to look for evidence of spinal instability.
According to the National Emergency X-Radiography Utilization Study (NEXUS) (1992), Low-
Risk Criteria (NLC) cervical-spine radiography is indicated for patients with trauma unless
they meet all of the following 5 criteria:
No posterior midline cervical spine tenderness
No evidence of intoxication
A normal level of alertness
No focal neurologic deficit
No painful distracting injuries
CT offers superior sensitivity for detection of acute fractures than plain radiographs. When
combined with myelography, CT has significant sensitivity and specificity for radiculopathy
and stenosis.
Relatively low cost and able to be performed quickly, so ideal in emergency room setting with
trauma and vehicular accident victims
Performed as indicated
MRI is the study of choice to detect soft tissue pathology, including disc and ligament
disruption and nerve root or spinal cord compression/injury.
Indicated in the acute setting of the patient with multiple injuries to rule out cervical instability
Also indicated for patients with deterioration in neurologic findings in order to detect spinal
cord changes
Electrodiagnostic studies used to diagnose nerve root dysfunction when the diagnosis is
uncertain or to distinguish a cervical radiculopathy from other lesions that are unclear on
physical examination
Ideally performed 3 or more wks after injury, as diagnostic abnormalities will first be seen
18–21 days after the onset of radiculopathy
Diagnostic fluoroscopic-guided medial branch anesthetic block may be performed to assess
for facet-mediated pain in patients resistant to treatment.
In evaluation of the patient with acute and subacute neck pain, it is essential to rule out more
serious conditions, such as fractures, dislocations, instability, and spinal cord injury. In chronic
neck pain, other diagnoses, such as neoplasia, must be considered.
Differential diagnosis includes:
Cervical fracture
Cervical instability, subluxation, or dislocation
Disc annulus fibrosis injury
Facet joint injury
Myofascial pain
Myelopathy
Brachial plexus injury
Peripheral nerve entrapment (eg, suprascapular nerve)
Treatment
Acute treatment directed at reducing pain and inflammation. Therapies
include local icing, NSAIDs, relative rest, and avoidance of positions that
increase symptoms. Patient should be encouraged to be as active as pain
allows; bed rest is discouraged.
In addition to NSAIDs, other pharmacologic therapies include muscle relaxants
to decrease spasm and tonicity and other analgesics such as acetaminophen.
Narcotic analgesics are often used for pain relief, but in general their use
should be limited due to the potential of opioid-associated side effects.
Consider myofascial trigger point injections for severe pain not controlled by
initial therapies in the acute phase.
Modalities such as electrical stimulation may be helpful in reducing the
associated muscle pain and spasm. Should be limited to the initial pain control
phase of treatment.
P.
Gentle stretching; first passive mobilization and then active to begin to
reestablish nonpainful range of motion
Gentle strengthening: Isometric cervical strengthening in a single plane (flexion,
extension, lateral flexion, rotation), scapular stabilization, and cervicothoracic
stabilization programs. All exercises should be performed without pain.
Low-level aerobic cross-training (eg, stationary bike, stair stepper, treadmill,
aquatic running, etc.) begun as soon as tolerated to avoid deconditioning
Use of soft and rigid collars for cervical strain management is controversial
and has not been proven effective. Several randomized studies, including one
by Kongsted et al. in 2007, showed no significant difference in outcomes
(headache and neck pain intensity, disability, and work capability) between
those treated with immobilization and those treated with an “act-as-usual”
approach (1)[A].
Recover phase directed toward normalizing active range of motion,
neuromuscular control, strength, and posture
Progressive passive and active stretching, mobilization, and manipulation as
appropriate
Progressive strengthening (isometric to isotonic) with independent single-plane
and complex multiple-plane coordinated motions to include cervicothoracic,
scapulothoracic, and scapulohumeral stabilization activities
Continued aerobic cross-training
Maintenance phase directed toward sport/activity-specific training
Protected padding often helpful: Neck rolls/collars, interval pads, and
customized orthoses
Flexibility and strength balance postural training
Power and endurance training, including strenuous upper extremity
strengthening and plyometric activities
Patterned motion training
Continued aerobic training
Stretching and strengthening should be continued indefinitely to minimize injury
recurrence.
Guidelines for returning to competition: No pain at rest, full pain-free range of
motion, normal posture, normal strength, and normal physical examination;
athletes should not return to competition until they can perform at the level of
their pre-injury abilities.
Pre-Hospital
Any victim of blunt cervical trauma who is unconscious or conscious and
complaining of neck pain or extremity paresthesias/paralysis should be assumed
to have a cervical spine injury. The cervical spine must be stabilized and the
patient transported to the emergency department on a backboard and with a
semi-rigid cervical collar in place (2)[B].
ED Treatment
All post-trauma patients with cervical pain should be “clinically cleared” using
NEXUS or the Canadian C-Spine Rule as decision rules to guide the use of
cervical spine radiography to rule out cervical fractures, dislocations, or spinal
cord injury.
Initial treatments include:
Ice
Analgesics or NSAIDs
Muscle relaxants
Medication
Analgesics, such as acetaminophen, can be used in the acute phase for pain
relief.
NSAIDs have anti-inflammatory as well as analgesic effects, and are often
used successfully in the management of cervicalgia. Examples include
ibuprofen and naproxen.
Muscle relaxants are often prescribed acutely as adjunct therapy to decrease
the spasm and hypertonicity experienced in acute muscle strain.
Follow-up is recommended to ensure there has been no deterioration in
symptoms or exam findings. Ideally, patients should follow up with their primary
care physician within 1 wk.
Often, referral to physical therapy may be necessary, especially in patients who
have significant spasm and decreased cervical motion.
Aggressive, specialized referrals may not be the best-suited approach for most
patients. In a recent cohort study by Pape et al., patients who were treated
initially with conservative management showed improved long-term outcomes
compared with those who received multidisciplinary care (3)[B].
General Measures
Therapy focusing on progressive motion, stretching, and finally strengthening is
often beneficial. Vassiliou et al. demonstrated in a randomized controlled trial
involving 200 patients with whiplash injury that those who participated in a
consistent physical therapy regimen had decreased pain intensity scores after 6
wks and 6 mos compared to controls (4)[A].
Osteopathic manipulation may be helpful in treating cervical strains. Avoid
manipulation in the following scenarios: Focal neurological deficits, severe
cervical spasm or pain, advanced age, rheumatoid arthritis, point tenderness
over bone, cervical fusion or fracture, osteoporosis, and cervical laxity.
Acupuncture
US
Topical analgesic creams
Ongoing Care
Complications
Neck strain can result in stiffening in the cervical region with resultant decreased
motion. The prolonged muscle spasm itself can become a source of long-term
pain and disability. Morbidity from cervical strains comes from disuse, weakness,
and spasm. Cervical strain can lead to chronic pain syndromes in certain
patients.
References
1. Kongsted A, Qerama E, Kasch H, et al. Neck collar, “act-as-usual” or active
mobilization for whiplash injury? A randomized parallel-group trial. Spine.
2007;32:618–626.
2. Dorshimer GW, Kelly M. Cervical pain in the athlete: common conditions

and treatment. Prim Care. 2005;32:231–243.
3. Pape E, Hagen KB, Brox JI, et al. Early multidisciplinary evaluation and
advice was ineffective for whiplash-associated disorders. Eur J Pain. 2009.
4. Vassiliou T, Kaluza G, Putzke C, et al. Physical therapy and active

exercises—An adequate treatment for prevention of late whiplash syndrome?
Randomized controlled trial in 200 patients. Pain. 2006.
Additional Reading
Bogduk N, Teasell R. Whiplash: the evidence for an organic etiology. Arch
Neurol. 2000;57:590–591.
Cantu R, Bailes J, Wilberger JE. Guidelines for return to contact or collision

sport after a cervical spine injury. Clin Sports Med. 1998;17:137–146.
Cole AJ, et al. Cervical spine athletic injuries. Phys Med Rehabil Clin North
Am. 1994;5:37–68.
Gore DR, Sepic SB, Gardner GM, et al. Neck pain: a long-term follow-up of
205 patients. Spine. 1987;12:1–5.
Johnson G. Hyperextension soft tissue injuries of the cervical spine—a

review. J Accid Emerg Med. 1996;13:3–8.
Jónsson H, Cesarini K, Sahlstedt B, et al. Findings and outcome in whiplash-
type neck distortions. Spine. 1994;19:2733–2743.
Lagattuta FP, Falco FJE. Assessment and treatment of cervical spine

disorders. In: Braddom RL, ed. Physical medicine rehabilitation, 1st ed.
Philadelphia: WB Saunders, 1996:747–748.
Malanga GA. The diagnosis and treatment of cervical radiculopathy. Med Sci
Sports Exerc. 1997;29:S236–S245.
Panjabi M, et al. Cervical spine biomechanics. Semin Spine Surg. 1994;5:10–

16.
Pettersson K, Hildingsson C, Toolanen G, et al. Disc pathology after whiplash

injury. A prospective magnetic resonance imaging and clinical investigation.
Spine. 1997;22:283–287; discussion 288.
Phull PS. Management of cervical pain. In: De Lisa JA, ed. Rehabilitation
medicine: principles and practice, 1st ed. Philadelphia: JB Lippincott,
1988:757–758.
Ronnen HR, de Korte PJ, Brink PR, et al. Acute whiplash injury: is there a role
for MR imaging?—a prospective study of 100 patients. Radiology.
1996;201:93–96.
Squires B, Gargan MF, Bannister GC. Soft-tissue injuries of the cervical

spine. 15-year follow-up. J Bone Joint Surg Br. 1996;78:955–957.
Sturzenegger M, DiStefano G, Radanov BP, et al. Presenting symptoms and

signs after whiplash injury: the influence of accident mechanisms. Neurology.
1994;44:688–693.
Torg JS, Glasgow SG. Criteria for return to contact activities following cervical
spine injury. Clin J Sports Med. 1991;1:12–26.
Zmurko M, Tannoury T, Tannouty C, et al. Cervical sprains, disc herniations,

minor fractures, and other cervical injuries in the athlete. Clin Sports Med.
2003;22:514.
Codes
ICD9
847.0 Neck sprain
Clinical Pearls
Cervical strain is common and is usually a benign, self-limited condition.
Conservative management is the key to treatment. Modalities include ice,
analgesics, and occasionally muscle relaxants.
Care must be taken not to miss more serious conditions such as fractures or
dislocations, especially in patients with acute neck pain.
Victims of trauma with neck pain or tenderness, and unconscious victims, need
to be treated with cervical stabilization until the spine can be fully evaluated with
imaging.
At 1–10 yrs after whiplash injury associated with motor vehicle trauma: 60–
80% of patients are asymptomatic and only 5–15% are severely symptomatic.
Prognosis associated with sports activities is believed to be excellent, although
no data are available.
Channelopathies, Long QT, CPVT
Amy Kakimoto
Basics
Description
Channelopathies are inherited disorders that affect the movement of ions (ie, sodium,
calcium, and potassium) through channels in the cardiac cell.
The channelopathies include long QT syndrome (LQTS), Brugada syndrome, and
catecholaminergic polymorphic ventricular tachycardia (CPVT). They are each characterized
by specific ECG abnormalities and may present clinically as syncope or sudden cardiac
death.
LQTS:
LQTS includes a diverse group of myocardial repolarization disorders that all result in a
prolonged QT interval.
There are 2 clinical phenotypes of inherited LQTS.
Romano-Ward syndrome:
Transmitted as an autosomal dominant trait
Characterized by LQTS without deafness. Also called the cardiac phenotype.
Can be the result of any of the mutations found thus far.
The more common phenotype
Jervell and Lange-Nielsen syndrome:
Transmitted as an autosomal recessive trait
Characterized by LQTS and sensorineural deafness
Caused by mutations in KCNQ1 (LQT1) or KCNE1 (LQT5), which affect only the
slow-acting component of the outward-rectifying potassium current
Typically has a more malignant course
Brugada syndrome: Brugada syndrome is an inherited disorder that mostly commonly affects
the cardiac sodium channel and is characterized by ECG findings of a pseudo–right bundle
branch block (RBBB), ST-segment elevation in leads V1–V3, and an increased risk of sudden
cardiac death.
CPVT: Also called familial catecholaminergic polymorphic ventricular tachycardia, this is a
congenital disorder that results from mutation in one of 2 cardiac genes and results in life-
threatening ventricular tachycardia (VT) or ventricular fibrillation (VF).
Epidemiology
LQTS:
Although more than 10 different types of congenital LQTS have been identified, LQT1,
LQT2, and LQT3 account for over 90% of cases of congenital LQTS.
Often presents in childhood but may be as early as the newborn period or go undiagnosed
into middle age
Brugada syndrome:
Most commonly presents in the 3rd or 4th decades of life. Average age at diagnosis is 41
yrs.
Majority of affected individuals are Asian.
Up to 9× more common in men than in women
CPVT: Generally presents for the 1st time in childhood or adolescence
Prevalence
Congenital LQTS:
Incidence estimated at 1/2,500–10,000; however, the true incidence of mutations in the
population is likely much higher.
Accounts for 3,000–4,000 sudden cardiac deaths annually in children in the U.S.
Most cases of LQTS can be attributed to 3 particular genotypes: LQT1 (40–55%), LQT2
(35–45%), and LQT3 (8–10%).
Brugada syndrome: Prevalence 0.4% in the U.S. but may be up to 1% in Japan and other
Asian countries.
CPVT: Prevalence is generally unknown but estimated at 1/10,000.
Risk Factors
The primary risk factor for most channelopathies is genetic.
LQTS:
Acquired LQTS can be caused by medications and metabolic or electrolyte abnormalities,
particularly hypokalemia and hypomagnesemia.
It is not uncommon for a patient with undiagnosed congenital LQTS to be become clinically
apparent only after exposure to a particular drug.
Risk factors for precipitating a fatal arrhythmia in a patient with LQTS include swimming
(primarily LQT1) and any strenuous exercise.
Brugada syndrome:
Risk factors for precipitating a fatal arrhythmia are swimming, fever or any cause of
hyperthermia, cocaine use, and overdose of psychotropic drugs (neuroleptics, tricyclic
antidepressants).
Risk factors for sudden cardiac death (SCD) in patients with Brugada syndrome are male
sex, a personal history of sudden cardiac arrest or syncope, and a family history of SCD.
CPVT: Physical effort (including swimming) and emotional stress are the most common
precipitants of VT or VF.
Genetics
LQTS:
There are hundreds of possible mutations in more than 10 genes. Distinct genetic types
have been labeled LQT1 through LQT10.
Both autosomal dominant and recessive inheritance patterns
Brugada syndrome: The most common cause is the autosomal dominant inheritance of a
mutation that affects the cardiac sodium channel with variable penetrance.
CPVT:
Mutations in 2 genes have been identified: The cardiac ryanodine receptor and
calsequestrin 2.
Mutations may be inherited or sporadic.
The autosomal dominant form of CPVT results from a mutation on chromosome 1q42-q43
in the gene for the cardiac ryanodine receptor (RyR2), also called the cardiac
sarcoplasmic calcium release channel.
General Prevention
While there is no way to prevent the channelopathy itself, SCD resulting from a
channelopathy may be prevented by carefully screening and identifying athletes with the
condition. The preparticipation physical is the most important tool for identifying athletes with
symptoms that may represent an inherited channelopathy. Any athlete with symptoms of
palpitations, syncope, presyncope, any collapse, or with a family history of SCD or
“accidental” death should be further evaluated with the tools reviewed below.
While some countries, such as Italy, practice the use of ECG routinely as part of the
preparticipation physical, in the U.S., initial screening for channelopathies relies heavily on a
careful history and physical examination.
Automatic external defibrillators (AEDs) are another important tool in preventing SCD from
undiagnosed channelopathies.
Antiarrhythmic Drugs Psychotropic Drugs Other Drugs
Quinidine Thioridazine Diuretics
Motility drugs: Cisapride,

Procainamide Phenothiazines
domperidone
Disopyramide Tricyclic antidepressants Droperidol
Amiodarone Haloperidol HIV protease inhibitors
Selective serotonin reuptake Vasodilators: Prenylamine,

Sotalol
inhibitors (SSRIs) bepridil, mibefradil
Dofetilide, ibutilide, azimilide, sematilide Risperidone Ketanserin
Antimicrobial Drugs Methadone Ranolazine
Macrolide antibiotics: Erythromycin,

Antihistamines Organophosphate insecticides
telithromycin, clarithromycin,
azithromycin (minor) Terfenadine Cocaine
Pentamidine Astemizole Papaverine
Fluoroquinolones: Moxifloxacin, gatifloxacin,

Chloral hydrate
levofloxacin,
sparfloxacin Arsenic trioxide
Spiramycin Some Chinese herbs
Chloroquine
Halofantrine mefloquine
Etiology
LQTS:
Cardiac phenotype: Caused by a variety of mutations in genes that code for cardiac ion
channels, including sodium and potassium channels
Jervell and Lange-Nielsen phenotype: Caused by a mutation in the genes that encode
either the α or β subunits of the slow-acting component of the outward-rectifying potassium
channel
Brugada syndrome: Autosomal dominant inheritance of a mutation affecting the cardiac
sodium channel gene
CPVT:
Sporadic or inherited mutations in the cardiac ryanodine receptor or calsequestrin 2
The exact mechanism by which the arrhythmia is triggered is unclear, but it may be a
reentry phenomenon with delayed afterdepolarizations owing to calcium overload and/or
changes in autonomic tone.
With β-adrenergic stimulation, the mutated cardiac ryanodine receptor has increased
calcium channel activity or becomes “leaky,” resulting in increased calcium release and
potentially an arrhythmia.

For certain patients with LQTS only, sensorineural hearing loss is associated.
Diagnosis
LQTS: Diagnosis is based mostly on ECG pattern because patients may be
symptomatic or asymptomatic.
Brugada syndrome:
Brugada pattern is used to describe those with typical ECG features but no other clinical
criteria.
Brugada type 1 is diagnosed on the basis of:
Type 1 ST-segment elevation (coved type) in >1 right precordial lead (V1–V3) in the
presence or absence of a sodium channel blocker plus at least 1 of the following:
Documented VF
Self-terminating polymorphic VT
Family history of SCD at <45 yrs
Type 1 ST-segment elevation in family members
Electrophysiologic inducibility of VT
Unexplained syncope suggestive of a tachyarrhythmia
Nocturnal agonal respiration
Brugada type 2 or 3 is diagnosed on the basis of:
Type 2 or 3 ST-segment elevation (saddleback type) in >1 right precordial lead under
baseline conditions with conversion to type 1 ST-segment elevation following challenge
with a sodium channel block plus at least 1 of the following:
Documented VF
Self-terminating polymorphic VT
Family history of SCD at <45 yrs
Type 1 ST-segment elevation in family members
Electrophysiologic inducibility of VT
Unexplained syncope suggestive of a tachyarrhythmia
Nocturnal agonal respiration
CPVT:
Unfortunately, most patients come to attention only after experiencing life-threatening VT or
VF.
Since the arrhythmia is not usually reproducible in the electrophysiology lab, the diagnosis
is made clinically on the basis of documented spontaneous stress-induced ventricular
arrhythmias.
Pre Hospital
In the case that any patient with a channelopathy coverts into a life-threatening arrhythmia in
the field, the most useful immediate tool and treatment is an AED.
History
Pertinent history in screening athletes: Gathering a detailed and careful history during the
preparticipation physical or during the evaluation of an athlete who comes to your attention is
critical. The following questions should be included when interviewing an athlete:
Have you ever passed out, become dizzy, or had chest pain during or after exercise?
Do you get tired more quickly than others during exercise?
Has anyone in the family died suddenly and unexpectedly before the age of 50?
(Remember to ask about family members who died of accidental causes such as sudden
infant death syndrome, drownings, and motor vehicle accidents because they may be clues
to an undiagnosed family history of channelopathy.)
Have you ever had a heart abnormality or murmur diagnosed by a doctor?
Have you ever had an abnormal heart rate, palpitations, or irregular heartbeats?
Have you had high BP or high cholesterol?
Has a physician ever denied or restricted your participation in sports for heart problems?
Have any of your relatives ever had cardiomyopathy, Marfan syndrome, LQTS, or
significant heart arrhythmias?
Pertinent history in potentially affected athletes:

LQTS:
Most commonly asymptomatic
Common symptoms include palpitations, syncope, presyncope, seizures, and cardiac
arrest.
Hearing loss (occurs in Jervell and Lange-Nielsen phenotype patients only)
Arrhythmias are most commonly precipitated by exercise, followed by exercise and
emotion together, emotion alone, and less commonly, loud noise or anesthesia.
Swimming and diving also have been described as triggers.
Family history of SCD
Use of any medications that may cause LQTS or torsades de pointes
Brugada syndrome:
Most common clinical presentation is life-threatening arrhythmia.
More common at night and while sleeping
Not usually related to exercise
Inquire about a history of syncope, presyncope, past history of sudden cardiac arrest or a
family history of sudden cardiac arrest or SCD
CPVT:
Most commonly asymptomatic until initial presentation with syncope or life-threatening VT
or VF
May have a family history of sudden cardiac arrest or SCD
Physical Exam
The most important elements of the exam are general (including level of consciousness),
cardiac, and pulmonary examinations and, in the case of a patient who has sustained a life-
threatening arrhythmia, complete trauma examination.
Since patients with channelopathies typically have structurally normal hearts, it is not
uncommon to observe a completely normal examination when a life-threatening arrhythmia is
not present.
When arrhythmias are present, the examination may be notable for bradycardia or
tachycardia, either regular or irregular, depending on the patient's rhythm.

Lab
In the setting of a life-threatening arrhythmia, it may be indicated to rule out ischemic or
metabolic causes with a basic or comprehensive metabolic panel and cardiac enzymes.
For LQTS specifically, genetic testing has become available to identify specific mutations that
result in LQTS, which may affect management and exercise restrictions slightly.
Electrocardiogram is the most important initial diagnostic tool. During the initial evaluation of an
athlete, Holter monitoring may be important, as well as echocardiograms to rule out any
structural abnormalities.
LQTS:
Prolonged QTc (>0.44 s)
Common ventricular arrhythmias, when they occur, are torsades de pointes (type of
polymorphic VT), multiform ventricular premature beats, uniform ventricular premature
beats, monomorphic VT.
Also common to see bradycardia (20–30% of patients) and less so atrioventricular block
Some mutations have low penetrance, resulting in normal electrocardiograms with normal
QT intervals.
Brugada syndrome:
Classic Brugada type 1: Elevated ST segment (≥2 mm) descends with an upward
convexity to an inverted T wave—“coved type” Brugada pattern.
Brugada types 2 and 3:
“Saddle back” ST-T wave: Elevated ST segment descends toward the baseline and then
rises again to the upright or biphasic T wave.
ST segment elevated ≥1 mm in type 2 and <1 mm in type 3
Moving the right precordial chest leads up to the 2nd or 3rd intercostal space may
increase the sensitivity.
The electrocardiogram findings may be transient and not present each time an
electrocardiogram is performed.
Electrophysiology testing may be used in evaluating Brugada syndrome but is not heavily
relied on.
CPVT:
Usually the baseline electrocardiogram will be completely normal until a life-threatening
electrocardiogram pattern of VT or VF develops.
Reported findings in baseline electrocardiograms of patients with CPVT include sinus
bradycardia, U waves, or a short PR interval, but none is diagnostic.
Acquired LQTS with its many reversible metabolic and drug-induced causes, acute coronary
syndrome, true RBBB, pericarditis, drug-induced VT or VF
Treatment
Congenital LQTS:
All symptomatic patients should be treated owing to the high risk for SCD.
This risk may be up to 50–60% in 10 yrs.
Major risk factors for SCD are congenital deafness, history of syncope,
documented history of ventricular arrhythmias, family history of SCD, female
gender, QTc >0.60 sec, medical noncompliance after an event.
The longer the QTc, the higher is the risk of SCD.
The decision whether to treat asymptomatic patients is less clear, but most
experts recommend treatment because the initial clinical presentation can be
SCD. Treatment may be more likely to be important in the following
asymptomatic patients: newborns and infants, patients with sensorineural
hearing loss, patients with siblings with LQTS and SCD, patients with QTc
>0.60 sec.
Treatment includes lifestyle modification and medical therapy with β blockers
or other agents and may include surgical options such as an implantable
cardioverter-defibrillator (ICD).
Brugada syndrome: The only treatment with proven efficacy is ICD, but there is
some role for pharmacotherapy.
CPVT: The primary treatment is ICD.
Medication
LQTS:
β blockers reduce the risk of syncope and SCD (1)[B].
Efficacy of β blockers varies by LQTS genotype.
Adjunctive treatments include potassium, flecainide, mexiletine, and
nicorandil.
Brugada syndrome:
Pharmacotherapy with quinidine alone has been attempted but is unproven.
Adjunctive pharmacotherapy for patients with frequent ICD discharges
includes amiodarone and quinidine.
Electrical storm in Brugada syndrome is treated with isoproterenol or
quinidine.
CPVT:
β blockers are recommended for all patients who have been affected
clinically and usually for those with the mutation but no history of arrhythmia,
particularly children.
β blockers may be used alone or in conjunction with ICD.
Flecainide also has been shown to be effective.
LQTS:
Cardiac pacing is an option for high-risk patients (2)[C].
ICD
Recommended for patients who fail β blockers (syncope or VT), have
survived cardiac arrest, or have risk factors for SCD (2)[B]
Left cardiac sympathetic denervation:
Rarely performed in the U.S.; more common elsewhere
Reserved for patients who fail all other treatments or who continue to
receive many ICD shocks despite medical therapy
P.
Brugada syndrome:
ICD implantation can prevent SCD in Brugada syndrome (3)[B].
Selection of patients for ICD is not entirely clear, but ICD may be used in
higher-risk patients such as those with syncope or with VT without cardiac
arrest (2)[C].
CPVT:
ICD is recommended for patients who continue to experience syncope
and/or documented VT despite treatment with β blockers (2)[C].
Sympathetic denervation may be used in patients with CPVT, but not
commonly.
As always, all patients who present with a life-threatening arrhythmia should be
treated emergently with cardioversion and/or pharmacotherapy as dictated by
standard ACLS.
Ongoing Care
All patients with channelopathies should be followed regularly by a cardiologist.
Education and restrictions regarding exercise are crucial to survival.
Return-to-play decisions:
LQTS:
Competitive athletes with a history of SCD or syncope should be limited to only low-
intensity competitive sports such as billiards, bowling, cricket, curling, golf, and riflery.
Competitive athletes who are asymptomatic but with a QTc >0.47 sec in men and >0.48
sec in women should be limited to the same low-intensity sports.
Restriction may be loosened for those with proven LQT3 mutation because they are less
susceptible to exercise.
Recreational athletes should not participate in high-intensity sports, but most low- and
moderate-intensity sports are thought to be safe.
Recreational swimming should be avoided by all patients unless proven to be a genotype
other than LQT1.
Caution should be used to avoid sports where impaired consciousness would be
dangerous or lethal, such as with SCUBA diving, swimming, weight lifting with free weights,
and horseback riding.
All patients with LQTS should be counseled to avoid all medications known to be potential
triggers for life-threatening arrhythmias. These are listed in the table above.
Brugada syndrome:
SCD in Brugada syndrome usually is not related to exercise.
Competitive athletes should be restricted to low-intensity sports, primarily owing to the
potential impact of hyperthermia.
Recreational athletes may participate in low- and moderate-intensity exercise. They should
avoid or participate very cautiously in high-intensity exercise.
Caution should be used to avoid sports where impaired consciousness would be
dangerous or lethal, such as with SCUBS diving, swimming, weight lifting with free weights,
and horseback riding.
CPVT:
Patients should be restricted from all competitive sports, except possibly the lowest-
intensity sports such as billiards, bowling, cricket, curling, golf, and riflery.
Patients should be restricted from all competitive swimming because it is a common
precipitant of fatal arrhythmias.
Recreational athletes should be excluded from all types of vigorous exercise.
References
1. Moss AJ, Zareba W, Hall WJ, et al. Effectiveness and limitations of beta-blocker therapy
in congenital long-QT syndrome. Circulation. 2000;101:616–623.
2. 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 Guidelines (Writing
Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of
Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the
American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation.
2008;117:e350–e408.
3. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second

consensus conference. Heart Rhythm. 2005;2:429–440.
Additional Reading
Beckerman J, Wang P, Hlatky M. Cardiovascular screening of athletes. Clin J Sport Med.
2004;14:127–133.
Behr E, Wood DA, Wright M, et al. Cardiological assessment of first-degree relatives in

sudden arrhythmic death syndrome. Lancet. 2003;362:1457–1459.
Brukner P, White S, Shawdon A, et al. Screening of athletes: Australian experience. Clin J

Sport Med. 2004;14:169–177.
Esperer HD, Hoos O, Hottenrott K. Syncope due to Brugada syndrome in a young athlete.
Br J Sports Med. 2006.
European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, 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 (Writing Committee to Develop Guidelines for Management of Patients With
Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol.
2006;48:e247–e346.
Maron BJ, Chaitman BR, Ackerman MJ, et al. Recommendations for physical activity and
recreational sports participation for young patients with genetic cardiovascular diseases.
Circulation. 2004;109:2807–2816.
Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations
related to preparticipation screening for cardiovascular abnormalities in competitive athletes:
2007 update: a scientific statement from the American Heart Association Council on
Nutrition, Physical Activity, and Metabolism: endorsed by the American College of
Cardiology Foundation. Circulation. 2007;115:1643–1455.
Miyasaka Y, Tsuji H, Yamada K, et al. Prevalence and mortality of the Brugada-type

electrocardiogram in one city in Japan. J Am Coll Cardiol. 2001;38:771–774.
Monroe MH, Littmann L. Two-year case collection of the Brugada syndrome

electrocardiogram pattern at a large teaching hospital. Clin Cardiol. 2000;23:849–851.
Sangwatanaroj S, Prechawat S, Sunsaneewitayakul B, et al. New electrocardiographic

leads and the procainamide test for the detection of the Brugada sign in sudden unexplained
death syndrome survivors and their relatives. Eur Heart J. 2001;22:2290–2296.
Codes
ICD9
426.82 Long QT syndrome
746.89 Other specified congenital anomalies of heart
Claudication
Bernadette Pendergraph
Basics
Claudication is a symptom of peripheral artery disease (PAD).
Description
The feeling of fatigue, discomfort, or pain in extremity muscles during exertion due to
inadequate arterial blood flow that is relieved with rest. The lower extremities, the calves
more often than the thighs, are more commonly involved than the upper extremities, and the
discomfort reproduced with a similar intensity and length of exercise.
System(s) affected: Cardiovascular; Musculoskeletal
Epidemiology
8 million Americans affected with peripheral artery disease. 60% of people with PAD
experience claudication. Men more commonly affected than women.
Incidence
Younger than 44 yrs: 6 males and 3 females per 10,000 person-years; >65 yrs: 61 males and
54 females per 10,000 person-years
Prevalence
Age >55 yrs: 9–23%
Risk Factors
Tobacco use
Diabetes/prediabetes
HTN
Hyperlipidemia
Obesity
Preexisting heart disease
Chronic renal insufficiency
Metabolic factors: Elevated C-reactive protein, homocysteine, D-dimer
Genetics
African Americans at higher risk than Caucasians
General Prevention
Avoid/cease smoking.
Heart-healthy diet
Etiology
Claudication is often a symptom of widespread atherosclerotic disease (95%) or some other
process that narrows the artery, such as embolus, popliteal entrapment, adventitious cystic
disease of popliteal artery, thromboangiitis obliterans
Location of blockages and symptoms:
Lower extremity claudication: Blockage of superficial femoral artery (upper calf), popliteal
artery (lower calf), peroneal or tibial arteries (foot)
Thigh and hip claudication: Blockage of aortic and iliac vessels
Upper extremity claudication: Similar blocks of subclavian, axillary, and brachial artery

Other manifestations of arteriosclerotic vascular disease: Coronary artery disease, carotid
artery disease, renal artery stenosis
Diagnosis
Most with claudication will be managed with medical therapy and an exercise program.
Advanced imaging is necessary when revascularization is considered.
History
Muscle cramping may start suddenly or gradually and progresses gradually.
Discomfort reported as muscle fatigue, heaviness, weakness, or cramp of muscle group
below level of blocked artery
Physical Exam
Decreased or absent pedal pulses
Foot pallor on elevation or rubor on dependency
Skin may appear shiny.
Loss of hair on foot or leg
Ankle:brachial index (ABI): Measurement of BP of the dorsalis pedis and tibial arteries in the
ankle with Doppler divided by the measured BP of the brachial artery in the upper extremity
with Doppler while the patient is in the supine position.

Lab
Laboratory studies are used to identify underlying risk factors: Complete blood count
(anemia), electrolytes/creatinine (renal disease), prothrombin time/thromboplastin time
(hypercoagulable state), fasting lipid profile (dyslipidemia), hemoglobin A1c/urinalysis
(diabetes)
Consider in hypercoagulable patients <50 yrs: Homocysteine, activated protein C, lipoprotein
A
Imaging
Duplex US: Good for assessing arteries above the knee
CT angiography: Avoid in renal insufficiency
Magnetic resonance angiography: Avoid in patients with pacemakers, defibrillators, and
metal aneurysm clips; caution when GFR <30 mL/min because of risk of nephrogenic
systemic fibrosis
Digital substraction arteriography: Gold standard for delineating arterial tree prior to
revascularization procedure; risks of bleeding, allergic reaction to contrast
Interpretation of ABI:
0.9–1.2 Normal
0.6–0.89 Mild PAD
0.4–0.59 Moderate PAD
<0.4 Severe PAD/rest pain
Perform toe-brachial artery index (TBI) if diabetes or kidney disease (decreased
compressibility of calcified arteries), ankle systolic BP >290 mm Hg, ankle systolic BP >240
mm Hg when brachial systolic BP <160 mm Hg or ABI >1.3
TBI <0.5 indicates PAD
Pseudoclaudication: Spinal stenosis causes exercise-induced leg symptoms relieved by
squatting, sitting, and leaning forward. Individuals can continue to walk leaning over a cart
(shopping cart sign), which relieves tension on spinal nerve roots.
Osteoarthritis of hips and knees: Pain starts immediately on weight-bearing and localizes
over involved joint on exam
Peripheral neuropathies: Normal ABI
Restless leg syndrome: Symptoms improve with leg movement
Arterial embolus: Acute development of leg pain with pallor and decreased pulses; limb
emergency
Deep venous thrombosis: Lower extremity swelling
Popliteal entrapment syndrome: Normal ABI at rest
Chronic exertional compartment syndrome: Normal ABI at rest; elevated compartment
pressures during exertion
Treatment
Long-term treatment: Modify risk factors by tobacco cessation, BP
reduction, weight loss, diabetes control if applicable, cholesterol reduction, and
a walking program
Acute treatment: Evaluation for rest pain and acute ischemia with limb threat:
Pain, poikilothermia pulselessness, paralysis, paresthesias, and pallor
ED Treatment
Acute ischemic limb: Unless contraindicated, heparin IV (100 units/kg) for
embolic/thrombotic event and emergent vascular surgeon evaluation
Medication
All individuals should have antiplatelet therapy, cholesterol therapy, and an
exercise program combined with tobacco cessation.
First Line
Antiplatelet therapy:
Aspirin: 81 mg/day or
Clopidogrel: 75 mg/day
Cholesterol therapy: Statin
Claudication therapy: For lifestyle-limiting claudication:
Cilostazol (Pletal): 100 mg b.i.d.: Vasodilates and decreases platelet
aggregation, thrombus formation, and vascular smooth muscle proliferation:
Contraindicated in congestive heart failure
Headache occurs in up to 1/3 of patients
Metabolized via the cytochrome P-450 isoenzymes. Use caution during
coadministration of other inhibitors of CYP3A4 (eg, grapefruit juice,
ketoconazole, itraconazole, erythromycin, and diltiazem) and during
coadministration of inhibitors of CYP2C19 (eg, omeprazole).
Second Line
Antiplatelet therapy:
Pentoxifylline 400 mg t.i.d.: Decreases blood viscosity and improves RBC
flexibility:
May increase theophylline levels
Ticlopidine 250 mg b.i.d.: Inhibits adenosine diphosphate-induced platelet
fibrinogen binding:
Concern for neutropenia/pancytopenia: CBC every 2 wks for 3 mos
Claudication therapy:
Vasodilators: Ramipril
Calcium channel blockers
Anticoagulants
General Measures
Conservative measures: Stop smoking, initiate walking and exercise program,
control of hyperlipidemia
Reduce risk factors.
Referral
Refer to a vascular specialist if severe PAD, symptoms suggestive of PAD with
normal ABI, need for specialized tests such as exercise ABI, and evaluation for
revascularization procedure.
Ginkgo biloba extract, EGb 761, increased pain-free walking distance when
compared to placebo
Surgical treatment is appropriate for patients with rest pain secondary to
ischemia, nonhealing ischemia ulcers, and lifestyle-limiting claudication despite
maximal medical therapy.
Surgical options:
Endovascular treatments: Less invasive, patency at 5 yrs about 52%:
Angioplasty with stenting
Subintimal recanalization
Atherectomy
Surgical bypass (autologous tissue or prosthetic conduit): Long segment
lesions not amenable to endovascular treatments
Common complications: Arterial thrombosis, lymph leakage, wound infection,
hematoma, pseudoaneurysm
Ongoing Care
Patient Monitoring
Periodically evaluate symptoms of claudication, physical exam, ABI measurement; and
evaluate control of hypertension, lipids, glucose, and tobacco use
Peripheral noninvasive vascular studies every 6 mos
Diet
DASH (Dietary Approaches to Stop Hypertension) diet
Patient Education
http://familydoctor.org/online/famdocen/home/common/heartdisease/basics/008.html
http://www.padcoalition.org/about-pad/
Prognosis
Gradual improvement in walking distance and pain or progression to rest pain and/or gangrene
Complications
30% will die of vascular causes within 5 yrs.
15% of people with PAD will develop critical limb ischemia with rest pain and
ischemia ulcer.
20–40% of people with critical limb ischemia will require amputation.
Additional Reading
Bendermacher BLW, Willigendael EM, Teijink JAW, Prins MH. Medical
management of peripheral artery disease. J Thromb Haemost. 2005;3:1628–
1637.
Arain FA, Cooper LT. Peripheral arterial disease: Diagnosis and management.
Mayo Clin Proc. 2008;83(8):944–950.
Laine C, Goldmann D. In the clinic: Peripheral artery disease. Ann Int Med.
2007;ITC3–ITC16.
Codes
ICD9
440.21 Atherosclerosis of native arteries of the extremities with intermittent claudication
443.9 Peripheral vascular disease, unspecified
ICD10
173.9 Peripheral vascular disease, unspecified
Cluster Headache
Kyle D. Parish
Basics
Description
A primary headache disorder characterized by recurrent attacks of excruciating, short-lasting
unilateral headache typically localized to the periorbital and temporal area. Disorder is
associated with signs of ipsilateral autonomic dysfunction such as conjunctival injection,
lacrimation, rhinorrhea or nasal congestion, facial diaphoresis, miosis, ptosis, and eyelid
edema.
Attacks last 15–180 min if left untreated.
2 types exist:
Episodic: 1 or 2 episodes per year separated by a pain-free interval of at least 1 mo;
account for 80% of all cases
Chronic: Ongoing attacks of headaches for 1 yr or more without more than 1 mo of
remission; represent the remaining 20% of cases
System(s) affected: Nervous
Synonym(s): Horton's headache; Erythromelalgia of the head; Histaminic cephalalgia; Ciliary
or migrainous neuralgia; Erythroprosopalgia of Bing; Petrosal neuralgia of Gardner;
Hemicrania periodica neuralgiformis; Sphenopalatine, Vidian, or Sluder neuralgia
Epidemiology
Incidence
Predominant age: Most often affects young adults; average age of onset occurs after 30 yrs.
A significant diagnostic delay has been reported in most cases (median of 3-yr delay).
Symptoms are rare in children.
Decrease is often noted after age 70.
Predominant gender: Male > Female (reported at just higher than 2:1)
Prevalence
Affects 0.05–0.1% of adults
Risk Factors
Male gender
Age between 20 and 40 yrs
Alcohol use
Tobacco use, particularly cigarette smoking
History of head injury
Family history of headaches
Shift work
Nitroglycerin use
Genetics
Genetic aspects have been noted in twin studies, but no clear locus or transmission mode has
been established.
General Prevention
Abstinence from alcohol and tobacco, especially during headache bouts
Regular sleep cycle
Etiology
Exact cause is currently unknown.
PET scan and functional MRI studies have established a fundamental role of the
hypothalamus in the pathophysiology of cluster headaches.

Tobacco use
Sleep apnea
Seasonal allergic rhinitis
Suicidal ideation
Diagnosis
At least 5 attacks fulfilling the following criteria (1,2)[C]:
Severe or very severe unilateral periorbital and/or temporal pain lasting 15–180 min if
untreated
Headache accompanied by at least one of the following (ipsilateral) symptoms:
Conjunctival injection and/or lacrimation
Nasal congestion and/or rhinorrhea
Eyelid edema
Facial sweating
Miosis and/or ptosis
A general sense of restlessness or agitation
Attacks from 1 every other day to 8 per day
Not attributed to another disorder
History
Diagnosis generally is made through history alone.
Physical Exam
Few distinguishing features outside active bout
Signs or trigeminal autonomic dysfunction ipsilateral to side of headache during attack
Restless and agitated behavior (pacing and rocking while holding head in hands)

Lab
Useful only to rule out diagnosis included in differential
Imaging
In most cases normal, but used to exclude other diagnosis and/or for individuals not responding
to appropriate therapy
Migraine headache
Paroxysmal hemicrania
Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)
syndrome
Hemicrania continua
Trigeminal neuralgia
Intracranial tumor or bleed
Orbital tumor or infection
Sinusitis
Carotid dissection
Temporal arteritis
Herpes zoster
Treatment
Pre-Hospital
Treatment in most cases is outpatient.
Medication
Avoid treatment with analgesics, particularly narcotics, for acute attacks
because they are generally ineffective and risk side effects such as GI
bleeding, hepatic injury, and/or opioid dependence.
For contraindications, warnings, cautions, and possible drug interactions for
each medication listed, please refer to manufacturers' literature.
First Line
Acute attacks:
Oxygen 100% at a rate of 7 L via face mask for at least 15 min (3)[A]
Sumatriptan 20 mg via nasal spray or 6 mg via SC injection, with repeat dose
if needed once in a 24-hr period (1)[A]
Treatments may be used in combination.
Prophylaxis: Verapamil 120–160 mg PO t.i.d. (3)[A]
Second Line
Acute attacks:
Lidocaine 1 mL of 10% solution placed intranasally with a cotton swab (3)[B]
Dihydroergotamine 0.5 mg via nasal spray placed in each nostril (3)[B]; must
not be combined with any of the triptans
Capsaicin intranasal, ipsilateral nostril t.i.d. ×7 days (3)[B]
Prophylaxis:
Prednisone 50–80 mg PO daily tapered over 10–12 days (3)[B]
Topiramate 100–200 mg PO daily (3)[B]; dose must be tapered up from
starting dose of 25 mg.
Ergotamine 2–4 mg PO daily in divided doses (3)[B]; should be avoided if
current active treatment with a triptan.
Divalproex 600–2,000 mg daily (3)[B]
Methylergonovine maleate 0.2 mg PO t.i.d. to q.i.d. (3)[B]
Lithium 600–1,200 mg PO in divided doses; blood levels must be checked
periodically to avoid intoxication.
Melatonin 10 mg taken at night (3)[B]
Massotherapy, physiotherapy, and acupuncture all have been described but not
adequately studied to determine effect.
Destructive approaches have variable results and irreversible complications
(1)[B].
Trigeminal section
Thermocoagulation of gasserian ganglion
Glycerol rhizotomy
Radiosurgery of the trigeminal nerve
Hypothalamic deep brain stimulation (1)[B]
Neurostimulation of the greater occipital nerve
Greater occipital nerve blocks (1)[B]
Admission Criteria
Concern that patient is a high risk for suicide
Intercranial pathology is considered, requiring inpatient workup.
Ongoing Care
Diet
Avoidance of alcohol is highly recommended during bouts because it is the only known dietary
trigger.
Patient Education
Little research is available to assess the effectiveness of lifestyle modifications, but exercise,
relaxation techniques, biofeedback, and smoking cessation have been suggested to improve
quality of life.
There is no evidence that exercise or athletic participation is contraindicated during an acute
bout of cluster headache, but severity of headache may limit ability of individual participation
during episode.
Prognosis
Very unpredictable course:
Recurrent attacks
Prolonged remission
Episodic type can evolve to chronic type.
Total remission has been described.
Complications
Medication side effects
Self-injury or suicide during attacks
Potential for prescription drug abuse
References
1. Leroux E, Ducros A. Cluster headache. Orphanet J Rare Dis. 2008;3:20
2. The International Classification of Headache Disorders 2nd Edition.

Cephalalgia. 2004;24: 1–160.
3. Beck E, Sieber WJ, Trejo R. Management of cluster headache. Am Fam

Physician. 2005;71:717–724.
Additional Reading
Bussone G. Cluster headache: from treatment to pathophysiology. Neurol Sci.
2008;29 (Suppl 1):S1–S6.
Codes
ICD9
339.00 Cluster headache syndrome, unspecified
339.01 Episodic cluster headache
339.02 Chronic cluster headache
Clinical Pearls
Patients are often misdiagnosed with secondary cause of headache, delaying
definitive diagnosis.
Once diagnosis is made, effort should be directed toward avoidance of
narcotic analgesic treatment, which may prolong bouts and risk patient
dependence.
There is currently no known curative treatment.
Compartment Syndrome, Anterior
Andrew Getzin
Jake Veigel
Basics
Description
Compartment syndrome is a condition caused by an increase in interstitial pressure in a
closed fascial compartment that leads to microvascular compromise and ischemic pain over
the anterior lower leg and possibly associated numbness and muscular dysfunction.
It can come on acutely owing to a rapid increase in training.
It can present as chronic activity-related pain owing to repetitive activity over months.
The anterior compartment consists of the tibialis anterior, extensor hallicis longus, extensor
digitorum longus, peroneus tertius, and deep peroneal nerve. It is bounded by the tibia, fibula,
and a thick inelastic fibrous septum.
Epidemiology
Incidence
Occurs in runners and in sports that involve a lot of running. It is not seen in cyclists because
there is no eccentric contraction of the muscle in the anterior compartment in cycling.
Bilaterality is common.
Predominant gender: Male = Female
Prevalence
Present in 27–33% of athletes with chronic lower leg pain (1)
Risk Factors
Rapid increase in activity
Large, muscular lower legs
Use of creatine supplements (2)
Participation in high-risk sport activities
Etiology
It is caused by an increase in interstitial pressure in a closed fascial compartment that leads to
microvascular compromise and ischemic pain.
Diagnosis
History
Signs and symptoms include (1)[C]:
Asymptomatic at rest
Cramping, burning, or pain felt over anterior lower leg with exercise
Symptoms in a crescendo–decrescendo pattern, increasing until usually necessitating
termination of activity, followed by gradual recovery
Muscle hernias seen in 40–50% of patients
Athletes may develop paresthesias distally and may develop motor problems (eg, foot
drop) as a late finding.
History:
Patients usually don't report a one-time injury.
Pain is usually progressive with continued exercise or increased intensity and begins to
occur sooner into the activity as time progresses.
Physical Exam
Exam is usually normal at rest. The key to the exam at rest is to help exclude other potential
causes of lower leg pain (1)[C].
Examination immediately after exercise can be helpful. Compartments can be very rigid, or
there may be fascial defects (1)[C].
Tender anterior compartment on direct palpation
Tender with passive stretching
Tender with resisted strength testing
Muscle hernias may be present (1)[C].

Imaging
Radiographs and MRI images are helpful to exclude stress fractures.
Intracompartmental pressure measurements before, during, and after exercise provide
helpful information and are considered the gold standard. Most clinicians use the modified
Pedowitz criteria to indicate a positive test: ≥15 mm Hg at rest, ≥30 mm Hg immediately after
exercise (1 min), and ≥20 mm Hg 5 min after exercise (3)[C].
However, there is considerable testing variability between clinicians (4). Compartment
pressure measurement should be used only to validate the clinical diagnosis.
For atypical presentations, consider MRI/MRA of the knee with attention to the popliteal
fossa with the foot in neutral, plantarflexion, and dorsiflexion or arteriogram to rule out
popliteal artery entrapment syndrome. Electromyography (EMG) with attention to the
superficial peroneal nerve should be considered to rule out superficial peroneal nerve
entrapment.
MRI has been looked at and does not appear to be as useful as the gold standard
compartment pressure measurement. Near-infrared spectroscopy, a noninvasive means of
measuring IM oxygen content, holds promise as a future possibility for diagnosing
compartment syndrome.
Consider performing duplex US of the lower extremities and ABIs with the foot in neutral,
dorsiflexion, and plantarflexion and MRI/MRA of the popliteal fossa to exclude popliteal artery
entrapment syndrome. EMG of the lower extremities is useful to exclude superficial peroneal
nerve entrapment syndrome.
Tibia or fibula stress fracture
Periostitis
Popliteal artery entrapment syndrome
Superficial peroneal nerve entrapment (1)[C]
Treatment
Rest and activity modification (volume and intensity of training, training
activity, practice surface, footwear) (1)[C]
Elevation when not exercising
Physical therapy to address any biomechanical predisposition; orthosis may
help to address biomechanical issues.
Nonsurgical treatment is usually not effective for competitive athletes.
Special considerations:
Acute compartment syndrome is a different entity from exercise-induced
compartment syndrome. It usually follows acute lower leg trauma, such as a
crush injury, but can occur after sudden, extreme exertion.
Acute compartment syndrome is a surgical emergency that must be treated
with emergent fasciotomy to avoid muscle necrosis.
Medication P.
There is no consensus as to the role Tylenol or NSAIDs prior to exercise for pain
control.
After surgery, the athlete is encouraged to walk as tolerated to decrease risk of
the release fascia closing.
Full return to participation is gradual over 6–12 wks.
Surgery is the definitive treatment (5)[C].
Surgery consists of a fasciotomy of the affected anterior compartment
(4,5,6,7)[C].
81–100% of patients report good to excellent long-term results (6,7)[C].
6% recurrence rate (8)
Ongoing Care
Postoperative care:
Initial weight bearing as tolerated and early range of motion to prevent postoperative scarring
Light jogging at 2–4 wks
Full participation in 6–12 wks
References
1. Edwards PH, Wright ML, Hartman JF. A practical approach for the differential diagnosis
of chronic leg pain in the athlete. Am J Sports Med. 2005;33:1241–1249.
2. Schroeder C, Potteiger J, Randall J, et al. The effects of creatine dietary

supplementation on anterior compartment pressure in the lower leg during rest and following
exercise. Clin J Sport Med. 2001;11:87–95.
3. Pedowitz RA, Hargens AR, Mubarak SJ, et al. Modified criteria for the objective
diagnosis of chronic compartment syndrome of the leg. Am J Sports Med. 1990;18:35–40.
4. Tzortziou V, Maffulli N, Padhiar N. Diagnosis and management of chronic exertional

compartment syndrome (CECS) in the United Kingdom. Clin J Sport Med. 2006;16:209–
213.
5. Detmer DE, Sharpe K, Sufit RL, et al. Chronic compartment syndrome: diagnosis,
management, and outcomes. Am J Sports Med. 1985;13:162–170.
6. Schepsis AA, Fitzgerald M, Nicoletta R. Revision surgery for exertional anterior

compartment syndrome of the lower leg: technique, findings, and results. Am J Sports Med.
2005;33:1040–1047.
7. Schepsis AA, Martini D, Corbett M. Surgical management of exertional compartment

syndrome of the lower leg. Long-term followup. Am J Sports Med. 1993;21:811–817;
discussion 817.
8. Turnipseed WD. Diagnosis and management of chronic compartment syndrome. Surgery.

2002;132:613–617; discussion 617–619.
Additional Reading
Eisele SA, Sammarco GJ. Chronic exertional compartment syndrome. In: Instructional
course lectures. Rosemont, IL: American Academy of Orthopedic Surgeons, 1993:213–
217.
Codes
ICD9
729.72 Nontraumatic compartment syndrome of lower extremity
958.92 Traumatic compartment syndrome of lower extremity
Clinical Pearls
Activity-related lower leg pain that escalates during a workout but usually
resolves shortly afterward
There are no long-term sequelae, but the phenomenon is progressive and
usually inhibits successful participation in running sports.
Condition is not usually responsive to conservative measure but instead
requires surgical compartment release.
Treatment success rate is high, with 90% of athletes returning to full sports
participation.
There is no evidence that long-term tissue damage occurs with repetitive bouts
of exercise-associated pain from compartment syndrome. However, runners
usually are unable to compete successfully once the problem has progressed.
Athletes who play stop-and-go sports are usually able to complete their season
but have to limit their training so that the compartment stays calm.
Surgical compartment release can be done open or endoscopically using 1 or
2 incisions. They seem to provide the same degree of symptom release with
only a minimal difference in postoperative scarring.
There is overlap with medial tibial stress syndrome, tibial stress fractures, and
compartment syndrome. The same inappropriate rate of increase in forces
placed on the lower legs can result in more than one problem occurring at the
same time.
Complex Regional Pain Syndrome
Andrew R. Peterson
David T. Bernhardt
Basics
Description
Exaggerated response to injury manifested by 4 clinical characteristics:
Intense and/or prolonged pain
Vasomotor disturbances
Delayed functional recovery
Various associated trophic changes
1995 consensus statement grouped several previously identified syndromes as “complex
regional pain syndrome” (CRPS):
Complex regional pain syndrome type I
Complex regional pain syndrome type II (previously “causalgia”)
Reflex sympathetic dystrophy
Shoulder-hand syndrome
Sudeck atrophy
Neurovascular dystrophy
Pain dysfunction syndrome
Transient osteoporosis
Acute atrophy of bone
Epidemiology
Adult:
Female: Male, 4:1
Median age at onset: 46 yrs
Upper limb twice as common as lower limb
Most report a triggering event
Fracture most common trigger (46%)
Distal radius most common triggering fracture, but only 1% of radius fractures develop
CRPS
Incidence following peripheral nerve injury: 2–14%
Children:
Female: Male lower than in adults, but majority are female (67–86%)
Symptoms typically start just prior to puberty:
Mean age 12.4 in girls
Mean age 13.4 in boys
Lower limb more likely to be involved than upper limb (5:1)
Often less clear inciting event
Higher recurrence rate
More responsive to treatment than adults
Incidence
5.46 per 100,000 person-years at risk
Prevalence
20.57 per 100,000 person-years
Risk Factors
Precipitating event (adults):
Usually painful, but not always
Fracture
Surgery (especially arthroscopic procedures)
Sprain
Myocardial infarction
Hemiplegia
Immobilization following stroke
Placement of arteriovenous graft for hemodialysis
Peripheral nerve injury
Up to 35% have no history of precipitating event.
Precipitating event (children):
50% have a vague, minor, or no precipitating event:
Sprains
Strains
Minor contusions
Surgery (especially arthroscopic procedures of the knee)
Henoch-Schönlein purpura
Emotional stress
Hepatitis B vaccination
Constitutional or psychiatric predisposition:
Suspected by many clinicians, but no evidence to support
Clearly not present in most patients with CRPS
“Sympathetic hyper-reactors” described as those with a history of increased sweating in
the palms, poor cold tolerance, and emotional liability
Genetics
Human leukocyte antigen (HLA) type:
Increased incidence in those with HLA-A3, B7, and DR2 (15)
HLA-DR2 (15) may predict poor treatment outcome.
HLA testing has no role in clinical management of CRPS.
No specific single-gene polymorphisms have been clearly linked to CRPS.
General Prevention
Stroke:
Early mobilization following stroke decreases risk of developing CRPS (1)[A].
Limited evidence supports early mobilization following injury and myocardial infarction.
Fracture:
Vitamin C supplementation (500 mg/day in most studies, but 200 mg and 1,500 mg have
also shown effect) decreases rate of CRPS following distal radius fractures (2)[A].
Mechanism is unclear
Regional anesthesia:
IV regional anesthesia (IVRA) is commonly used to provide anesthesia during extremity
surgery.
IVRA with or without clonidine may decrease the chance of developing postsurgical CRPS
(3)[B].
Etiology
Pathogenesis is unclear, but several theories exist:
Reflex arc following inciting event
Sympathetic nerve reflex arc causes central sympathetic dysfunction, causing peripheral
vascular dysfunction
Increased sensitivity of injured nerves to endocrine and paracrine substances
Inappropriate inflammatory mediator control (especially IL-6, IL-1β, TNF-alpha, substance P,
neuropeptide, and calcitonin gene-related peptide)
Several studies have demonstrated CNS modulation as cause of CRPS.
A recent model of “neurogenic inflammation” attempts to tie the above theories together into
a unifying theory of pathogenesis.

Precipitating injury or event
Possible psychiatric or personality disorders
Other pain syndromes have been reported as associated conditions:
May represent heterogeneity of a single disease or susceptible phenotype
Fibromyalgia most commonly associated pain syndrome
Diagnosis
Clinical diagnosis
Laboratory and imaging studies are only indicated if diagnosis is uncertain.
History
Stage 1: Early disease following inciting event or spontaneous:
Progressive limb pain
Burning pain
Occasional throbbing
Diffuse aching
Sensitivity to cold and/or touch
Localized edema
Stage 2: Progressive physical changes (see “Physical Exam”)
Stage 3: Severe disease:
Worsening pain
Increasingly dramatic physical findings (see “Physical Exam”)
Other symptoms (not stage-specific): Urinary urgency, frequency, and/or incontinence
Physical Exam
Stage 1:
Localized edema
Vasomotor disturbances:
Color changes
Temperature changes (usually cool, but can be warm)
Stage 2:
Progressively worsening soft tissue edema
Thickening of the skin
Muscle wasting
Stage 3:
Joint contractures
Waxy appearance to skin
Brittle nails
Other findings (not stage-specific):
Allodynia
Hyperhidrosis
Abnormal hair growth (patchy, sparse, or excessive hair)
Urinary retention

CRPS is a clinical diagnosis.
The tests and imaging studies listed below should only rarely be performed when the
diagnosis is uncertain.
Lab
Tests to exclude other systemic causes of pain:
CBC
ESR
Fasting blood glucose
Serum ionized calcium level
Thyroid-stimulating hormone and free T4 levels
Imaging
Bone scan (triple-phase technitium-99m bone scintigraphy):
Increased uptake in 2/3 of adult patients with reflex sympathetic dystrophy
Findings vary by phase:
30 sec: Increased flow, but decreased tracer uptake in affected limb
3 min: Capillary leak around affected joint
3 hr: Increased uptake of tracer at periarticular bone of affected joint
Findings less reliable in pediatric patients:
1/3 exhibit increased uptake (usually in late stages of disease).
1/3 exhibit normal findings.
1/3 exhibit decreased uptake (usually in early stages).
Can also be used to help rule out other diagnoses, such as stress fracture or tumor
Plain radiography (x-ray):
Initially normal
After 3 mos, may show patchy subchondral osteopenia
Late stages show profound bone demineralization.
X-ray findings are less common in children.
MRI:
Multiple nonspecific changes (edema, skin thickening)
Useful to rule out constant stimulants (such as meniscal tear or loose body)
Thermography:
Significant skin temperature asymmetry
Cold challenge may increase sensitivity and specificity
CT scan:
Focal areas of osteoporosis
Swiss cheese appearance of bone in stage 3 CRPS can be dramatic.
Costs, radiation dose, and poor sensitivity and specificity limit use
Autonomic testing:
Resting sweat output (RSO)
Resting skin temperature (RST)
Quantitative sudomotor axon reflex test (QSART)
Abnormal RSO and QSART are highly sensitive for CRPS.
Use of these tests should be limited to patients with uncertain diagnosis
Sympathetic blockade:
Typically causes abrupt improvement in symptoms
In those with cool affected limbs, typically have increase of 1–3°C in skin temperature
Lack of response has high negative predictive value.
Relief is typically transient.
Stellate or lumbar sympathetic blocks more diagnostically useful than regional blocks (eg,
Bier block), although both may provide relief of symptoms
Fracture/stress fracture
Infection
Tumor (especially Pancoast syndrome)
Nerve root impingement
Vasculitis
Peripheral neuropathy
Deep vein thrombosis
Angioedema
Other pain syndromes
Treatment
Usually more effective early in disease (4)[A]
Follow a stepwise approach, starting with least risky/invasive and progressing
to more invasive as needed (3)[C]
An interdisciplinary program seems to be the most effective approach to CRPS
(3)[B]:
Physical therapy
Occupational therapy
Psychotherapy
Medications
Interventional procedures
Medication
First Line
Vitamin C 500 mg daily for prevention in patients with distal radius fractures (2)
[A]
Tricyclic antidepressants have been shown to decrease pain in multiple studies
and should be considered in all patients with CRPS (3)[A].
Second Line
Antiepileptic drugs:
Thoroughly tested for other pain syndromes, but cannot extrapolate results to
CRPS.
Gabapentin most widely used, but studies have demonstrated variable
efficacy
Pregabalin is also widely used, but has not been studied for treatment of
CRPS.
Selective serotonin and norepinephrine reuptake inhibitors have not been
studied for treatment of CRPS.
Systemic glucocorticoids may be useful for improving the clinical course of
CRPS early in the disease (3)[B].
Bisphosphonates are effective for preventing bone loss in CRPS, but they
have an unclear effect on the overall disease course:
Widely used
Several clinical studies have demonstrated variable efficacy.
Pamidronate, alendronate, and clodronate have been most studied.
Topical capsaicin cream is effective in other types of neuropathic pain. It is
generally safe and may be a useful adjuvant treatment for CRPS (3)[C].
Opioid use should be limited [C].
Several other medications have been reported to be effective in small trials, but
are rarely used:
Free radical scavengers (dimethylsulfoxide and N-acetylcysteine)
Topical clonidine
Ketamine
Baclofen
Physical therapy mainstay of RSD treatment
Tactile desensitization is most effective if used early.
Joint mobilization, progressive weight-bearing, strengthening, and return to
daily activities are important aspects of care directed by physical therapy.
Transcutaneous electrical nerve stimulation can be beneficial.
Behavioral management
Relaxation techniques
Stress management
P.
Acupuncture:
Popular complementary therapy
High patient satisfaction
Well-designed studies have shown no difference when compared to placebo
(4).
May have a role as part of an interdisciplinary approach to CRPS
Nerve blockade:
Sympathetic nerve blockade can be both therapeutic and diagnostic.
Lumbar sympathetic block for lower extremity
Stellate ganglion blocks for upper extremity
Unclear which patients are good candidates for sympathetic blocks
Unpredictable response to repeated sympathetic blocks
Other interventional procedures:
Used less frequently and less proven than sympathetic blockade
Peripheral nerve stimulation
Spinal cord stimulation
Chemical and surgical sympathectomy
Implanted spinal infusion pumps and/or intrathecal injections:
Baclofen may be useful if significant dystonia.
Clonidine has frequent side effects, such as hypotension and significant
sedation.
Deep brain stimulation
Ongoing Care
A strong partnership with the patient and all participating caregivers is essential.
Patient Monitoring
Weekly or biweekly follow-up is appropriate.
Have a flexible treatment plan:
Stepwise approach to care
Therapeutic trials of only 1–2 wks before moving on to the next treatment modality
Prognosis
Early diagnosis and treatment can lead to resolution by 6–12 mos.
Late diagnosis is associated with permanent residual symptoms.
Children are more likely to relapse than adults.
3 distinct phases (described above):
Patients in stage 1 and 2 respond better to therapy.
Stage 3 disease is often more refractory to treatment.
References
1. Petchkrua W, Weiss DJ, Patel RR. Reassessment of the incidence of complex regional
pain syndrome type 1 following stroke. Neurorehabil Neural Repair. 2000;14:59–63.
2. Stevermer JJ, Ewigman B. Give vitamin C to avert lingering pain after fracture. J Fam
Pract. 2008;57:86–89.
3. Hsu ES. Practical management of complex regional pain syndrome. Am J Ther.

2009;16:147–154.
4. Dowd GS, Hussein R, Khanduja V, et al. Complex regional pain syndrome with special
emphasis on the knee. J Bone Joint Surg Br. 2007;89:285–290.
Additional Reading
Barbier O, Allington N, Rombouts JJ. Reflex sympathetic dystrophy in children: review of a
clinical series and description of the particularities in children. Acta Orthop Belg.
1999;65:91–97.
Codes
ICD9
337.20 Reflex sympathetic dystrophy, unspecified
337.22 Reflex sympathetic dystrophy of the lower limb
355.9 Mononeuritis of unspecified site
Clinical Pearls
Clinical diagnosis of an exaggerated response to injury of a limb with intense
prolonged pain, vasomotor disturbances, delayed functional recovery, and
trophic changes
Pathology is unclear, but there is an obvious central sympathetic disregulation
that causes or modulates peripheral symptoms.
Diagnostic tests should be reserved for unclear cases and to rule out other
diagnoses.
Treatment should be initiated immediately at diagnosis and follow a rapid
stepwise approach from least to most invasive.
A partnership between providers, therapists, and the patient is essential for
effective treatment.
Concussion
Daryl A. Rosenbaum
Anna G. Monroe
Basics
Description
“Concussion is defined as a complex pathophysiologic process affecting the brain, induced by
traumatic biomechanical forces” (1).
Common features include the following:
The blow may be directly to the head, face, or neck, or the force may be transmitted
indirectly after a blow elsewhere on the body.
Neurologic signs and symptoms present quickly and disappear spontaneously, although in
a small number of cases the symptoms may be prolonged.
Symptoms result from a functional disturbance in the absence of structural pathology, and
imaging studies are usually normal.
Concussion symptoms may or may not include loss of consciousness (LOC).
Synonym(s): “Bell ringer”; “Ding”; Mild traumatic brain injury (TBI); Minor head trauma;
Commotio cerebri
Epidemiology
207,830 ED visits for nonfatal sports-related traumatic brain injuries per year between 2001
and 2005 (2)
Children ages 5–18 yrs represented 65% of those ED visits (2).
Estimated 1.6–3.8 million sports-associated traumatic brain injuries (2)
Incidence likely higher because athletes, coaches, or medical providers may fail to recognize
the signs and symptoms of a concussion or athletes try to minimize the symptoms in order to
continue to play (3,4).
In a study of high school football players, only 47.3% reported their concussion. 2/3 withheld
information because they did not think their symptoms needed medical care. Almost 1/2
wanted to avoid being withheld from play, and a little more than 1/3 simply lacked
understanding of concussion (5).
Possible underreporting of concussion especially in children because many do not seek
medical care (4)
Some evidence of a higher incidence of concussion in female high school and college athletes
even when comparing the same sports; the reason is unclear but could be due to more
honest reporting of concussion in females (4,6).
572 concussions per year for college athletes between 1988 and 2004 (7)
54.8% of the total concussions during that period of time occurred in football (7).
Women's soccer, men's ice hockey, men's soccer, and women's basketball each represented
between 5% and 7% of total college concussions for the same time period (7).
Risk Factors
Participation in contact and collision sports (2,3,4,7)
An athlete with a previous concussion may be more likely to have a repeat concussion than
an athlete without a history of a concussion (3).
Improper technique (eg, leading with the head, or “spearing,” in football) (7)
Genetics
Investigations ongoing as to the significance of apolipoprotein (Apo) E4, ApoE promoter gene,
tau polymerase, and others in concussion (1,8)
General Prevention
Evidence does not support prevention of concussion in football or rugby with current helmet
technology, but helmets do prevent skull fractures and other head injuries. Likewise, while
mouth guards do not prevent concussion, they do decrease dental and orofacial injuries
(1,4,9).
Rules that promote safe and proper techniques (eg, outlawing “spearing” in football, leading
with the head, and head-to-head contact) should be coached and enforced to limit
concussion (1,7,10).
Encourage fair competition but discourage violent behavior in sports, especially among young
athletes (1).
Etiology
Complicated pathophysiology that is incompletely understood (1,4,8)
Impact and resulting forces create shear injury to vessels and neurons (4,8).
Biochemical chain reactions are set in place, some of which may involve the release of
excitatory amino acids (4,8,10).
Resulting decrease in cerebral metabolism occurs (4,8,10).
Alternatively, the blow may create immediate neuronal depolarization followed by a refractory
period where neural transmission does not happen (8).
Diagnosis
Historically, numerous classification systems for grading severity have existed (4).
Systems were based mainly on the presence of LOC and/or amnesia (4).
More recent consensus statements recommend against concussion grading systems
(1,10,11,12)[C].
Judge treatment for and severity of concussion on an individual basis according to the
burden, nature, and duration of symptoms.
The presence of certain “modifiers” also may indicate the need for a more detailed workup or
different management strategies (1)[C].
Modifiers include the following: Number, duration, or severity of symptoms; LOC for more
than a minute; amnesia; concussive convulsions; frequent concussions or those occurring in
close proximity; sustaining subsequent concussions with less impact; concussions in those
<18 yrs of age; the presence of other comorbid or premorbid conditions such as mental
health or learning disorders, including attention deficit hyperactivity disorder (ADHD); taking
psychoactive drugs or anticoagulants; having a dangerous style of play; or participating in
high-risk activities (1)[C].
Pre Hospital
Address airway, breathing, and circulation (ABCs) (4)[C].
Consider cervical spine (C-spine) immobilization (all unconscious athletes should have C-
spine immobilization) (4)[C].
Do not remove the helmet in football or ice hockey players if C-spine injury is suspected (13)
[C].
Assess level of consciousness with the Glasgow coma scale (GCS) (13)[C].
Evaluate for other trauma such as skull fractures (including basilar skull fractures) or
lacerations (13)[C].
Perform a neurologic exam including cognitive evaluation and balance assessment (13)[C].
Conscious athletes in whom C-spine trauma is not suspected may exit the field and undergo
a more thorough exam (13)[C].
Immediately transfer athletes with prolonged LOC, focal neurologic deficits including
asymmetric pupils and declining GCS or worsening symptoms, athletes with comorbidities
(eg, hemophiliacs), and those with persistent vomiting (3)[C].
History
Direct blow to the head, sudden rotational or acceleration-deceleration force to the head in
the absence of direct trauma, or transmitted force to head (13)
Athletes often fail to recognize or report their symptoms. Concussion should be considered in
anyone demonstrating signs of a concussion (4).
Standardized symptom checklists such as the one found in the Sport Concussion Assessment
Tool 2 (SCAT 2) that allow the athlete to score his or her complaints on a scale of 0–6 may
be useful when evaluating the concussed athlete (1)[C].
Athletes may complain of any of the following: headache (HA) or neck pain; feeling off-
balance or dizzy; nausea or vomiting; problems with vision or hearing including ringing in the
ears; confusion; slowness, fatigue, or sleepiness; irritability or other emotional problems;
concentration difficulty; memory problems; “dinged”; “dazed”; or “don't feel right” (3)[B].
Prospectively validated symptoms include HA, dizziness, blurred vision, attention deficit,
memory problems, and nausea (3)[A].
Physical Exam
Physical signs: LOC, amnesia, or balance problems (1,3)[A]
Behavioral changes such as irritability (1,3)[B]
Cognitive problems such as slowed reaction times (1,3)[B]
Sleep disturbances such as drowsiness (1,3)[B]
After addressing emergency medical issues, formal concussion assessment should occur (1)
[C].
Perform a detailed neurologic exam including cognitive evaluation and balance assessment
(13)[C].
Consider administering the SCAT 2 or other standardized test (1)[C].
The SCAT 2 was developed by the 3rd International Conference on Concussion in Sport and
incorporates 2 prospectively validated tests, the Maddocks Score and the Standardized
Assessment of Concussion (SAC), into a comprehensive tool (1,3).
The SCAT 2 contains 8 sections and assesses the following domains: Subjective rating of
symptoms; physical signs; GCS; Maddocks score (which assesses recent memory about the
game but is not used in the final score); cognitive testing such as orientation, immediate
memory, and concentration; balance examination using the modified Balance Error Scoring
System (BESS); coordination test (finger to nose); and repeated cognitive testing focusing on
delayed memory (1).
An overall score is calculated out of 100 possible points (1).
Cut-off scores are not currently known, and the test has not yet been validated (1).
Score is useful with repeat testing or with known baseline (1)[C].
The SCAT 2 should not be used as the only tool to diagnose concussions, determine whether
recovery has occurred, or decide when to allow an athlete to return to play (1)[C].

Lab
Research conducted on more severe head injury suggests that many genetic and cytokine
factors are induced (1).
These include insulin-like growth factor 1 (IGF-1), IGF-binding protein 2, fibroblast growth
factor, copper-zinc superoxide dismutase 1 (SOD-1), nerve growth factor, glial fibrillary acidic
protein (GFAP), and S-100 (1).
As yet, the significance of these factors in concussion is not fully known, and no routine
laboratory testing is occurring (1).
Imaging
Cranial CT scan: Useful in acute imaging to rule out intracranial bleed. Consider if prolonged
LOC or if symptoms are worsening or failing to resolve in a timely manner (1,3)[C].
Imaging usually contributes little to routine concussion management (1,3).
MRI modalities such as gradient echo and perfusion and diffusion imaging may diagnose
structural lesions better than CT scan, but again, routine use of MRI does not add to
concussion evaluation (1)[C].
Functional MRI (fMRI) may illustrate degree of symptoms and their resolution but is not yet
part of standard concussion management (1).
Experimental imaging technology includes positron emission tomography (PET), diffusion
tensor imaging, MRI spectroscopy, and functional connectivity (1).
Neuropsychological (NP) testing is used to assess cognitive function and help with return to
play (RTP) decisions (1)[A].
Usually conducted when the athlete is asymptomatic as a final measure before clearance for
RTP (3)[C]
Cognitive function often resolves after other symptoms, so NP evaluation can add helpful
information (1)[A].
Should never be used as the only factor in deciding if an athlete should RTP (1,3)[C]
Consider in the case of a concussion with modifiers (1)[C].
Computerized tests such as the Automated Neuropsychological Assessment Metrics
(ANAM), CogState, Concussion Recovery Index (CRI), Immediate Post-Concussive
Assessment and Cognitive Testing (ImPACT), and HeadMinder, among others, facilitate
administration and interpretation, especially among nonneuropsychologists (3).
In addition to a postconcussion symptom scale, the tests evaluate the following: attention,
memory, processing speed, and reaction time (3).
The most effective use of NP testing involves comparing preinjury baseline testing with
postinjury testing and using a test that accounts for confounding factors (eg, a practice
effect) that occur with serial tests (3,10,14)[C].
The Reliable Change Index describes test-retest reliability and is a feature available with
computerized tests (14).
A neuropsychologist may administer other formal NP testing if necessary, and
neuropsychologists are often the most qualified to interpret any NP test (1)[C].
Balance testing adds valuable information to concussion assessment, especially when the
athlete is having signs or symptoms of postural instability (1)[A].
The Sensory Organization Test is a computerized force plate system to evaluate postural
sway under changing visual and somatosensory information (3).
The Balance Error Scoring Test (BESS) evaluates the ability of a person to hold without
“error” 3 positions (legs together, single-leg stance, and tandem stance) with eyes closed
and hands on the hips. The test is conducted on a firm and a foam surface (3).
BESS has been prospectively validated (3)[A].
A modified BESS is part of the SCAT 2 test.
Subdural hematoma, which may be acute or subacute (15)
Epidural hematoma, which can result in rapid deterioration after a “lucid interval” (15)
Intraparenchymal hemorrhage (15)
Diffuse axonal injury (DAI) or shear injury to white matter that leads to prolonged LOC and
often causes residual deficits (15)
Second impact syndrome (SIS) is a rare yet often fatal process that occurs when an athlete
who has not recovered completely from one concussion sustains a 2nd blow to the head.
Cerebral edema and increased intracranial pressure result. The patient can decline rapidly as
cerebral herniation occurs (4).
Trauma-induced migraine
Treatment
On-field management (1,3,13)[C]:
Evaluate and treat ABCs as necessary.
Perform C-spine immobilization if indicated, taking care to leave helmet in
place.
Perform baseline GCS and quick neurologic evaluation.
Evaluate athlete for associated and other injuries (C-spine).
If athlete is conscious and C-spine injury has been reasonably ruled out, take
athlete to sideline for further testing, reevaluation, and/or observation.
Immediately transfer athlete to a hospital when indicated (eg, prolonged LOC
>5 min, focal neurologic deficit, decreased or deteriorating mental status,
uncontrolled vomiting, suspected skull fracture).
P.
Sideline management:
Continue to address first aid and exclude associated injuries such as a C-
spine injury (1)[C].
Physical and cognitive rest until asymptomatic (1)[C]
A trained healthcare professional should conduct a detailed medical and
neurologic assessment that includes balance assessment and cognitive
evaluation (1,3)[C].
Consider the administration of a test such as the SCAT 2 (1)[C].
An athlete with any symptoms at rest or with exertion should not RTP (1)[C].
Nonadult athletes (<18 yrs old) should not RTP the same day a concussion
occurs (1)[C].
Some evidence suggests that when assessing recovery by NP evaluation,
high school students with concussion may take longer to recover than college
students with concussion (16).
Consider “modifiers” (symptom severity; associated signs such as LOC,
amnesia, or concussive convulsions; a history of prior concussions;
comorbid conditions such as ADHD; etc.) may dictate a more conservative
approach (1).
Consideration of same-day RTP can occur with adult athletes (1)[B].
Arrange for observation (in-hospital for severe cases or situations where
there is a lack of adequate supervision or by a medical provider, trustworthy
friend, or family member) and serial examinations of the athlete several times
over the 1st few hours after a concussion to monitor for deterioration or
delayed symptoms (1,3)[C].
Ongoing Care
A 6-step graduated RTP protocol is endorsed in the work of the Concussion in Sport
Group and by the American College of Sports Medicine (1,10,11,12)[C].
Athletes progress through each step for a period of at least 24 hr. Before moving forward in
the protocol, athletes must be asymptomatic and not taking any drugs that would change or
hide their symptoms.
If symptoms develop at one stage, the athlete should go back one level. Another attempt to
progress to the next level can occur after a 24-hr rest period.
The 6 steps are as follows: No activity, light aerobic exercise, sport-specific training,
noncontact training drills, full contact practice, and return to play.
This protocol sometimes may be expedited in an adult athlete.
An augmented RTP protocol might be appropriate in the situation of a concussion with
modifying features, including in children.
After sustaining a concussion, an athlete should be evaluated by a medical professional prior
to RTP (13)[C].
Emergent follow-up should be sought in the case of any of the following: focal neurologic
deficit, declining mental status or LOC, uncontrolled vomiting, or worsening headache (3,13)
[C].
Tylenol may be used to treat HA or other pain, but NSAIDs and aspirin should be avoided
initially.
Athletes also should avoid sedating medicines or substances such as alcohol that may affect
cognitive function.
An athlete should rest from all physical and mental activity while still having symptoms of a
concussion. Physical rest includes avoiding activities such as physical education class or
riding a bike to school, and mental rest includes school work, video games, texting, computer
usage, etc. (1)[C].
After all symptoms have resolved without the use of medicine to mask complaints and an
athlete sees a medical provider, a gradual RTP prescription likely will be recommended. This
program might include starting with light aerobic activity and progressing from noncontact
drills to contact drills over at least a 24-hr period per step provided that no symptoms appear
with the addition of exercise (1).
It is important to be honest about the presence of symptoms because there is some
evidence that if someone is incompletely recovered from a concussion and sustains another
blow to the head, SIS, a rare yet often fatal process, can occur (4).
Patient Monitoring
A patient should not be left unsupervised following a concussion (1)[C].
A patient should be monitored for the following: focal neurologic deficit, declining mental
status or LOC, and uncontrolled vomiting (3)[C].
Emergent medical care should be sought if any of the preceding occur (3)[C].
Prognosis
80–90% of concussions resolve within 7–10 days (1).
Complications
Depression is reported in retired former professional football players at higher
incidence in those with a history of concussion compared with those without
(1).
Chronic traumatic encephalopathy or cognitive impairment is more common
among retired National Football League (NFL) players who sustained
increasing numbers of concussions (17).
A small number of patients may develop postconcussion syndrome (PCS)
(8,18).
There are limited data on the incidence and characterization of PCS, especially
with respect to sports-related concussions (8,19).
This syndrome is characterized by persistent cognitive trouble (concentration
deficits, memory difficulty), physical complaints (headache, fatigue), or
emotional disturbances (irritability, depression) (15,18).
NSAIDs and antidepressants are used commonly to treat PCS, and
psychological treatment also may help (19).
Athletes should not RTP when still symptomatic (1,3,4,10,11,12).
No evidenced-based guidelines exist for temporary or permanent
disqualification after concussion (20).
Retirement from sports participation may be considered in the case of
continued symptoms or objective exam findings, situations where a lesser
impact creates concussion symptoms and the athlete takes longer to recover,
or when an athlete sustains multiple concussions in one season (20).
References
1. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on
concussion in sport—The 3rd International Conference on concussion in
sport, held in Zurich, November 2008. J Clin Neurosci. 2009;16:755–763.
2. Centers for Disease Control and Prevention (CDC). Nonfatal traumatic

brain injuries from sports and recreation activities—United States, 2001–
2005. MMWR Morb Mortal Wkly Rep. 2007;56:733–737.
3. Goldberg LD, Dimeff RJ. Sideline management of sport-related

concussions. Sports Med Arthrosc. 2006;14:199–205.
4. Meehan WP, Bachur RG. Sport-related concussion. Pediatrics.
2009;123:114–123.
5. McCrea M, Hammeke T, Olsen G, et al. Unreported concussion in high

school football players: implications for prevention. Clin J Sport Med.
2004;14:13–17.
6. Dick RW. Is there a gender difference in concussion incidence and

outcomes? Br J Sports Med. 2009;43(Suppl 1):i46–i50.
7. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15

sports: summary and recommendations for injury prevention initiatives. J Athl
Train. 2007;42:311–319.
P.
8. McCrory P, Johnston KM, Mohtadi NG, et al. Evidence-based review of
sport-related concussion: basic science. Clin J Sport Med. 2001;11:160–165.
9. McIntosh AS, McCrory P, Finch CF, et al. Does Padded Headgear Prevent
Head Injury in Rugby Union Football? Med Sci Sports Exerc. 2009.
10. Concussion (mild traumatic brain injury) and the team physician: a
consensus statement. Med Sci Sports Exerc. 2006;38:395–399.
11. Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of

the First International Conference on Concussion in Sport, Vienna 2001.
Recommendations for the improvement of safety and health of athletes who
may suffer concussive injuries. Br J Sports Med. 2002;36:6–10.
12. McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement

statement of the 2nd International Conference on Concussion in Sport,
Prague 2004. Clin J Sport Med. 2005;15:48–55.
13. Wojtys EM, Hovda D, Landry G, et al. Current concepts. Concussion in

sports. Am J Sports Med. 1999;27:676–687.
14. McCrory P, Makdissi M, Davis G, et al. Value of neuropsychological

testing after head injuries in football. Br J Sports Med. 2005;39 (Suppl 1):i58–
i63.
15. Bailes JE, Cantu RC. Head injury in athletes. Neurosurgery. 2001;48:26–
45; discussion 45–46.
16. Field M, Collins MW, Lovell MR, et al. Does age play a role in recovery
from sports-related concussion? A comparison of high school and collegiate
athletes. J Pediatr. 2003;142:546–553.
17. Guskiewicz KM, Marshall SW, Bailes J, et al. Association between

recurrent concussion and late-life cognitive impairment in retired professional
football players. Neurosurgery. 2005;57:719–726; discussion 719–726.
18. Lee LK. Controversies in the sequelae of pediatric mild traumatic brain
injury. Pediatr Emerg Care. 2007;23:580–583; quiz 584–586.
19. Ryan LM, Warden DL. Post concussion syndrome. Int Rev Psychiatry.
2003;15:310–316.
20. Kirkwood MW, Yeates KO, Wilson PE. Pediatric sport-related concussion:
a review of the clinical management of an oft-neglected population. Pediatrics.
2006;117:1359–1371.
Additional Reading
Access the SCAT 2 at the following Web site:
www.sportconcussions.com/html/SCAT2.pdf.
Codes
ICD9
850.0 Concussion with no loss of consciousness
850.11 Concussion, with loss of consciousness of 30 minutes or less
850.12 Concussion, with loss of consciousness from 31 to 59 minutes
Clinical Pearls
No one should RTP while still having the signs or symptoms of a concussion. In
general, an athlete <18 yrs of age should not RTP the same day because there
may be unrecognized symptoms initially or a delay in the development of
symptoms. Also, the younger you are, the longer you will likely need to recover
fully from a concussion. Receiving a 2nd blow to the head (even a minor one)
while still suffering from the effects of the original concussion can lead to SIS,
which results in severe brain swelling and often death.
The physician likely will prescribe a stepwise and gradual return to activity to
begin after the patient is no longer experiencing symptoms. Developing any
symptoms during this program will require additional rest before proceeding. In
some cases, the physician may recommend additional testing such as balance
testing or formal cognitive testing before a patient can RTP.
As yet, there is no specific cutoff number of concussions used to permanently
disqualify an athlete. However, mounting evidence exists that the more
concussions a person suffers, the worse he or she tends to do on various
tests of brain function. Long-term data from retired professional football
players suggest that increased numbers of concussions are associated with
depression and permanent memory difficulty. Athletes should consider this risk
of cumulative brain injury from multiple concussions when deciding whether or
not to RTP.
While helmets cannot necessarily prevent concussions, proper headgear for
sports should be worn to prevent other head injuries. Learning safe
fundamentals of a given sport, such as the proper head-up tackling position in
football, can help to reduce the occurrence and severity of concussions.
Athletes should engage in respectful competition and should refrain from violent
behavior.
Congenital Cervical Disease
Jeffrey B. Kreher
Basics
Uncommon group of diseases
Majority asymptomatic
May have only slight restricted cervical range of motion (ROM)
Upper cervical anomalies: More likely younger onset of instability and neurologic problems
after minor trauma
Lower cervical anomalies: More likely adult presentation owing to degenerative changes in
hypermobile segments adjacent to fused segments
Klippel-Feil syndrome: Most common disease: Con-genital fusion of cervical vertebrae (2
segments, congenital block vertebrae, or entire cervical spine)
Description
Craniovertebral junction diseases: Occipitoatlantal fusion, basilar impression and invagination
(odontoid is more cephalad and may protrude into foramen magnum), occipital vertebrae and
condylar hypoplasia, occipitoatlantal instability
Atlantoaxial anomalies: Aplasia/hypoplasia of the atlas, familial cervical dysplasia,
aplasia/hypoplasia of the odontoid, os odontoideum
Lower cervical spine anomalies: Primarily Klippel-Feil syndrome
Klippel-Feil syndrome: Most common: Classic triad (congenital cervical fusion, decreased
neck ROM, and short neck with low hairline) found in 50%
Epidemiology
Rare occurrence but potential for cervical spine instability and neurologic injury
Often discovered incidentally in workup of trauma, sports-related cervical cord neurapraxia,
or symptomatic cervical disk disease
Prevalence
Klippel-Feil syndrome, or congenital fusion of cervical vertebrae: 0.60–0.71%:
Most often asymptomatic and C2–3 fusion
Next most common level C5–6 fusion
75% of cases C1–3
50% involve ≤3 vertebrae.
Prevalence of others unknown but very low
Much higher prevalence in associated conditions
Risk Factors
Trisomy 21 and Morquio syndrome (odontoid anomalies)
Genetics
Klippel-Feil syndrome:
Can be autosomal dominant (commonly C2–3)
Can be autosomal recessive (commonly C5–6)
Familial form gene locus on long arm of chromosome 8
Familial cervical dysplasia: Often autosomal dominant
Mutations in the Homeobox, or Hox, genes may play a role.
Possibly due to teratologic insult (ie, maternal smoking, alcohol)
Etiology
Acute occipitoatlantal, or C1–2, instability owing to:
Disruption of transverse atlantal ligament (runs posterior and limits excursion of odontoid
into spinal cord)
Disruption of alar ligaments (attached to odontoid and limits posterior excursion)
Chronic occipitoatlantal, or C1–2, instability (as seen in trisomy 21): Relies on checkrein
effect of alar liga-ments to limit spinal cord compression by odontoid

Scoliosis/kyphosis/lordosis (>50%)
Hearing impairment (30%)
Sprengel deformity (congenital elevation of the scapula, 25–35%)
Genitourinary anomalies (most common unilateral renal agenesis followed by malrotation of
normal kidney, 2–64%)
Cardiovascular anomalies (more common in females, ventricular septal defect most
common lesion, 4.2–14%)
Rib abnormalities (including fusion, abnormal joints and/or spacing)
Omovertebral bone (limits neck and shoulder movement)
Lower cervical fusion more likely with other syndrome/condition (eg, fetal alcohol
syndrome, Alpert syndrome, Crouzon syndrome, Goldenhar syndrome, cervico-
oculoacoustic dysplasia, congenital cervicothoracic deformity)
Occipitocervical junction anomalies (most commonly occipitoatlantal fusion):
Achondroplasia, diastrophic dwarfism, spondyloepiphyseal dysplasia, Larsen syndrome,
Morquio syndrome
Pes cavus/excavatum, syndactylies, jaw anomalies, cleft palate, congenital ear
deformities, hypospadias
Primary basilar impression: Occipitoatlantal fusion, atlas hypoplasia, bifid posterior arch of
atlas, odontoid anomalies, Klippel-Feil syndrome, achondroplasia
Occipitoatlantal instability: After trauma in trisomy 21, familial cervical dysplasia, and
hyperlaxity syndromes (eg, Marfan and Ehlers-Danlos syndromes)
Diagnosis
History
Often asymptomatic or nondescript symptoms:
Neck pain, headaches, syncope, weakness, numbness
Wry neck (torticollis)
Weakness, numbness, or pain in the upper extremities
Possible transient paresis following trauma
Possible synkinesis (mirror movements, often <5 yrs old and tends to improve with age)
Occasionally, vertebrobasilar insufficiency symptoms: Nausea, vomiting, vertigo/dizziness,
seizures, mental deterioration, and syncope
Occasionally, pyramidal tract symptoms: Spasticity, hyperreflexia, muscle weakness/atrophy,
and gait disturbances
Rarely, cranial nerve disturbance: Diplopia, tinnitus, dysphagia, and auditory disturbances
Rarely, posterior column disturbance: Loss of proprioception, vibration, and tactile
discrimination
Occipitoatlantal fusion:
Symptom onset usually 5th–6th decade and slowly progressive
May be precipitated by trauma or inflammatory process
Decreasing frequency: Pain in the occiput/neck, vertigo, unsteady gait, paresis,
paresthesias, speech disturbances, hoarseness, diplopia, syncope, auditory disturbance,
and dysphasia
Basilar impression and invagination:
May not present until 2nd–3rd decade of life
May be precipitated by minimal trauma
Symptoms depend on impinged structures.
Commonly, neck pain, headaches in occipital nerve distribution, and weakness and
paresthesias of the limbs
Occasionally, ataxia, vertigo, and sexual dysfunction
Nontraumatic occipitoatlantal instability: Neck pain, headache, torticollis, weakness, and
vertebrobasilar symptoms
Odontoid anomalies: Hypoplasia/aplasia, os odontoideum:
Average age at diagnosis: 19–30 yrs
Symptomatic 50% of time
Neck pain, weakness, loss of balance, transitory paresis following trauma, and myelopathy
Few with vertebrobasilar symptoms and/or progressive myelopathy
Physical Exam
Pterygium colli, nuchal webbing:
Shortened neck appearance when bilateral or torticollis when unilateral
<20% in Klippel-Feil syndrome, occipitoatlantal fusion, basilar impression
Torticollis ± facial asymmetry:
<20% in Klippel-Feil syndrome, basilar impression
Rarely, initial flexibility at craniovertebral junction progressing to rigidity, no sensory motor
cortex, tightness, and aplasia of nuchal cavity on affected side; atlas hypoplasia/aplasia
Painful (±restricted) cervical ROM: Flexion/extension generally better preserved than rotation
and lateral bending
Scoliosis: Significant in 60% of Klippel-Feil syndrome patients
Radiculopathy: Nerve root irritation from osteophytes at hypermobile segments adjacent to
fused vertebrae
Upper extremity weakness, numbness, or pain: More common with occipitoatlantal fusion,
basilar impression
Possible long-tract signs owing to pyramidal compression:
Long-standing spinal cord compression
Frequent with occipitoatlantal fusion
Posterior column signs: Altered sensation to deep touch, vibration, and proprioception
Posterior impingement of occipitoatlantal fusion: Possible nystagmus, ataxia, and imbalance
from cerebellar herniation
Occipitoatlantal, basilar impression: Rarely, respi-ratory and autonomic dysfunction or
sudden death

Imaging
X-rays: Cervical spine anteroposterior (AP) view; open-mouth odontoid view; lateral views in
neutral, flexion, and extension ± thoracolumbar posteroanterior and lateral views:
AP: May show accessory vertebrae, especially of lateral masses or condylar
hypoplasia/dysplasia
Open-mouth: Odontoid anomalies
Lateral neutral: Spinal stenosis (sagittal diameter of the canal and ratio of Pavlov, both
limited by projection and possible abnormal vertebrae)
Lateral flexion/extension: Translational instability (anterior or posterior translation >5 mm)
or fusion (no change in distance between spinous processes)
Thoracolumbar: Other associated spinal deformities
In Klippel-Feil syndrome: Vertebrae widened, flattened, “wasp-waist appearance”
(concave anterior and posterior cortices) ± foraminal osteophytes; absent or narrowed
disk spaces possible ± posterior element fusion ± instability
With C1–2 instability: Abnormal atlas-dens interval (ADI; ≤4 mm in children and <3 mm in
adults) but not as helpful in chronic atlantoaxial instability (ie, trisomy 21, rheumatoid
arthritis, or congenital anomalies), where space available for the cord (SAC), posterior
aspect odontoid to anterior aspect of posterior arch atlas or posterior lip of foramen
magnum is used
In os odontoideum (or odontoid nonunion post trauma), ADI may be normal but SAC
significantly reduced in flexion or extension
In occipitoatlantal fusion, SAC ≤13 mm associated with neurologic symptoms
With basilar impression, interpretation may be difficult owing to various techniques and
associated deformities, but McGregor's line (upper surface of posterior hard palate to the
most caudal point of the occipital curve) is the best screen—odontoid ≥4.5 mm above
McGregor's line warrants more investigation; if the odontoid lies below McRae's line
(defined by opening of foramen magnum), symptoms are less likely.
CT scan: Helpful for defining bone anatomy
MRI:
Identifies intraspinal lesions (syringomyelia, meningioma, and lipoma) or Arnold-Chiari type
I malformation (isolated or associated)
May pick up disk protrusion, osteophytes, cord impingement, and narrowing at
craniovertebral junction not seen on x-ray
Obtain if will change clinical management
Arteriography (or MRA) if surgery is planned or if symptoms warrant (basilar impression,
occipitoatlantal fusion, atlas aplasia)
Owing to increased incidence of vertebral artery anomalies
Neurologic abnormalities: Extensive but include cervical disk disease, congenital spinal
stenosis, vascular disease, Arnold-Chiari malformation, and odontoid nonunion
Torticollis: Congenital muscular torticollis [sternocleidomastoid tumor (SMT), muscular
torticollis, postural torticollis without SMT mass or tightness], ocular deficiency, hearing
deficit, Grisel and Sandifer syndromes, tumor of posterior fossa, syringomyelia/Arnold-Chiari
malformation, Klippel-Feil syndrome, rotatory cervical instability, infection, cervicothoracic
scoliosis
Basilar impression:
Secondary basilar impression (owing to softening of osseous skull base): Not congenital
disease
Occasionally, secondary to rickets, osteomalacia, osteogenesis imperfecta, Paget
disease, neurofibromatosis, skeletal dysplasia, ankylosing spondylitis, and rheumatoid
arthritis
Occasionally, erroneously diagnosed as multiple sclerosis, posterior fossa tumors,
amyotrophic lateral sclerosis, or traumatic injury
Treatment
Symptomatic treatment for headaches and occiput/neck pain not
associated with neurologic symptoms
Conservative treatment such as cervical collar, braces, and traction indicated
for:
Signs and symptoms associated with C1–2 instabi-lity without posterior
column signs and symptoms
Odontoid anomalies without neurologic symptoms
Before surgery for occipitoatlantal fusion owing to higher morbidity and
mortality of surgical procedures in this condition
Medication
Analgesics (ie, acetaminophen, NSAIDs) for headache
Referral
Generally, all congenital cervical disease referred to neurosurgeon and/or
neurologist for concurrent observation and management
Most common surgical indication: Posterior column signs and symptoms
Decompression of the posterior elements:
Posterior fusion of occiput-atlas complex in occipitoatlantal fusion
Suboccipital decompression with decompressive laminectomies of atlas and
axis with posterior fusion in basilar impression
Atlantoaxial arthrodesis for odontoid abnormalities with the following:
Myelopathy, instability of ≥10 mm in flexion and extension, progressive
instability, or persistent neck pain with C1–2 instability
Includes possible resection for os odontoideum
Arthrodesis extended (occiput to atlas) for occipitoatlantal instability
Anterior stabilization required for anterior impingement
Rarely, posterior fusion of C1–2 required for familial cervical dysplasia
Preoperative reduction with traction or positioning (atlantoaxial instability owing
to odontoid anomalies):
If neurologic symptoms reduced or alleviated, prognosis after surgery
improved and used postoperative for immobilization
Preoperative angiography of vertebral vessels for possible associated
anomalies
Especially with atlas hypoplasia/aplasia
Postoperative halo device after stabilization procedures
Ongoing Care
Patient Monitoring
Return to play recommendations are primarily expert opinions:
Absolute contraindications to contact/collision sports: Odontoid abnormalities, occipitoatlantal
fusion, Klippel-Feil syndrome with fusions above C3 (1)[C]
No contraindications for Klippel-Feil syndrome with fusion of 1 or 2 interspaces below C3, full
cervical range of motion, and absence of occipital cervical anomalies, instability, disk
disease, or degenerative changes (1)[C]
Patient Education
Minimally affected patient can expect normal, active life with minor restrictions.
With major areas of synostosis or high-risk patterns of cervical motion, advise patient to
avoid activities that stress the cervical spine.
All congenital cervical diseases: Trauma can be catastrophic (more often with translational
instability and maybe with stenotic cervical canal).
Prognosis
Hypermobility of upper cervical spine: Increased risk for neurologic issues
Lower cervical spine involvement: Increased risk for degenerative disease
Overall, prognosis is good, with most patients remaining relatively asymptomatic with
occasional mild complaints of headaches, nonradicular weakness, and numbness.
Complications
May be absent or include paresis or sudden death
Reference
1. Torg JS, Ramsey-Emrhein JA. Management guidelines for participation in
collision activities with congenital, developmental, or postinjury lesions
involving the cervical spine. Clin J Sport Med. 1997;7:273–291.
Additional Reading
Guille JT, Sherk HH. Congenital osseous anomalies of the upper and lower
cervical spine in children. J Bone Joint Surg Am. 2002;84-A:277–288.
Guille JT, Miller A, Bowen JR, et al. The natural history of Klippel-Feil
syndrome: clinical, roentgenographic, and magnetic resonance imaging
findings at adulthood. J Pediatr Orthop. 1995;15:617–626.
Hensinger RN. Congenital anomalies of the cervical spine. Clin Orthop Relat
Res. 1991:16–38.
See Also
Congenital Cervical Stenosis
Codes
ICD9
756.13 Absence of vertebra, congenital
756.15 Fusion of spine (vertebra), congenital
756.16 Klippel-Feil syndrome
Clinical Pearls
Symptoms in Klippel-Feil syndrome originate at the open segments from
compensatory hypermobility.
Upper cervical disease tends to present in pediatric/adolescent patients with
neurologic symptoms from instability.
Lower segment hypermobility and resulting degenerative changes present in
adulthood and are less severe if they involve the lower cervical spine and 2 or
more segments between fused segments
Flexion views are most helpful in determining maximal odontoid excursion into
SAC and through foramen magnum.
When evaluating high thoracic congenital scoliosis, include lateral views of the
cervical spine to look for associated Klippel-Feil syndrome.
Instability at the occipitoatlantal joint is usually due to deficiency of the
transverse atlantal ligament.
Prophylactic surgery in asymptomatic patients is controversial but often
recommended for athletes.
Contact Dermatitis
Jennifer J. Mitchell
Kirk Tiemann
Basics
Allergic contact dermatitis (ACD)
Irritant contact dermatitis (ICD): Causes about 80% of contact dermatitis
Description
ACD:
Delayed cell-mediated hypersensitivity reaction
Requires previous exposure and sensitization
Indirect exposure to allergen from pet, clothing, smoke, dust
Cross-sensitization when exposed to chemically related antigen
Entire skin becomes hypersensitive to the contact allergen
Pruritic erythematous lesions usually rapid but can be delayed for days following exposure
and may appear to spread over time
ICD:
Inflammatory response to contact with irritant (chemical and physical)
Requires no previous exposure
Direct injury to skin usually limited to the site of contact
Erythematous lesions may occur minutes to days from exposure.
Epidemiology
Predominant age:
All ages
Extremes of age less likely to sensitize to plants.
Pediatric considerations:
ACD less frequent in young children than adults
Major sources of pediatric contact allergy:
Metals (nickel most common)
Shoes
Preservatives
Fragrances
Topical medications
Plants
Risk Factors
Increased activities related to contact or exposure to irritant or allergen
Common sports-related contact dermatitis (1):
Baseball: Friction and/or moisture with clothing and gear
Basketball: “Pebble fingers” associated with ball surface
Canyoning: “Canyoning hand”:
ICD
Irritation of hands from cold water and rock abrasions
Cycling: Friction or moisture with clothing and gear
Fishing:
Epoxy or resin in rod
Fish bait
Nickel
Football:
Moisture
Friction
Adhesives and athletic tape
Chemicals associated with equipment
Golf: Chemicals in glove, club grip
Hockey:
Gloves
Epoxy or resin in equipment
Moisture with clothing and gear (“gonk”)
Running:
Friction or moisture with clothing and gear
Shoe dermatitis associated with synthetic rubber, glues, dyes in athletic shoes
Skiing:
Clothing
Epoxy or resin
Metals: Nickel, cobalt
Formaldehyde
Soccer:
Friction or moisture with gear
Resin in shin guards
“Cement burns” associated with alkaline lime of field markings
Swimming/snorkeling/diving:
Brominated pool water
Formaldehyde or synthetic rubber compounds in goggles, head caps, and wet suits
Larvae of parasitic flatworm schistosomes from snails; “swimmer's itch”
Red coral
Seawater
Seaweed
Tennis: “Tennis player's thigh”:
Friction or moisture with clothing
Epoxy or resin in equipment
Weightlifting:
Chalk
Gloves
Metal: Nickel/chromium in weights/bar
Disabled athletes (2): Prosthetic equipment, including:
Epoxy resin
Friction
Formaldehyde
Moisture
Plastic
Synthetic rubber
Clothing and gear
General Prevention
Avoidance of irritants or causative agents (3):
ACD prevention:
No good-quality studies
Toxicodendron (Rhus): Severity reduced or prevention: Quaternium-18-bentonite
(organoclay) lotion
Nickel, cobalt, copper prevention and reduction of reaction: Diethylenetriamine pentaacetic
acid
ICD prevention: Good evidence from good-quality studies:
Barrier creams
Moisturizing creams, high-lipid content
Fabric softeners
Cotton glove liners (fair quality)
Etiology
Common causes include (3,4):
Plants: Toxicodendron (formerly Rhus) genus:
Poison ivy, most common
Poison sumac
Poison oak, 2 types
Most common cause of ACD in U.S.
More common than all other causes combined
Allergen: Urushiol:
Pentadactyl catechol from plant sap
Cross-reaction with similar catechol derivatives in several other plants
Contact may be:
Primary with plant (leaves/roots/stems)
Secondary via clothing, pets, equipment
Chemicals:
Alkaline lime for field marking (rarely used now)
Cement
Formaldehyde: Clothing, gear, paper products
Fiberglass: Equipment
Fragrances/perfumes: Cosmetics, soaps, lotions, sunscreen, insect repellant
Glues and adhesives: Epoxy, resins, colophony (tree sap resin)
Latex: Natural compounds; may cause immediate hypersensitivity reaction
Mercaptobenzothiazole: Athletic shoe rubber
Paraphenylenediamine (PPD): Dyes, henna, hair dye, neoprene
Potassium dichromate: Leather tanning
Preservatives:
Thimerosal, methylchloroisothiazolinone, parabens
Lotions, cosmetics, cleaning agents, moisturizers
Soaps, strong detergents
Solvents (eg, turpentine): Cleaning agents, polishes, waxes
Thiuram (rubber accelerator): Black rubber, gloves, basketballs, tubing, waistbands,
contraceptive devices
Waterless hand cleaners
Metals:
Chromium: Cement, pigments in tattoos, vitamins, chrome-covered metals/equipment
Cobalt: Buckles, snaps, dental amalgams, jewelry
Copper: Jewelry, equipment, IUD
Gold: Jewelry, some liqueurs, some food items
Mercury: Organic forms, dental amalgams
Nickel:
Most common cause of metal dermatitis
Snaps, clips, jewelry, earrings
Topical medications:
Merthiolate: Preservative in topical medications
Topical antibiotics: Neomycin, bacitracin, polymyxin
Topical anesthetic:
Ester class (benzocaine, tetracaine)
Amide class (lidocaine, dibucaine), less frequent
Shoe dermatitis:
Allergic or irritant
Dorsal aspect of foot, sparing interdigit spaces
Chemicals/dyes from processing of leather, adhesives, or rubber compounds
Photocontact dermatitis:
Inflammatory reaction from exposure to an irritant
Frequently plant sap or photoallergic drug and sunlight
Diagnosis
Typically made from history and physical exam
Often difficult to distinguish between ACD and ICD
History
Lesion characteristics: Vesicles, pruritus, rash (5)[B]
Date of onset
Time course
Treatment
Possible exposure to irritating substance:
Acute or chronic
New skin products: Cosmetics, sunscreen, soaps, perfumes, hygiene products
New equipment use: Braces, clothing, shoes
New jewelry, body piercing
Recent use of medications:
Topical
Systemic
Recent travel: Camping, hiking, mountain biking
Recent change in environment: Running, hiking, snorkeling
Recent change in occupation
Keep in mind cross-sensitization: Reaction to different allergen with similar properties
Physical Exam
Acute lesions:
Erythematous rash
Fever
Edema
Pruritus
Stinging
Pain
Papules
Vesicles
Erosions
Serous drainage
Subacute lesions:
Erythema
Pruritus
Scaling
Firm papules
Chronic lesions:
Erythema
Scaling
Firm papules
Excoriations
Plaques of lichenification
Pigmentation changes
Appearance of lesions:
Borders of lesions: Sharp demarcated, linear when caused by rubbing against plant
Edema
Erythema and rubor associated with secondary infection
Vesicles may coalesce into bullae, rupture, or ooze.
Lichenification/scaling/fissures in chronic exposure
Common clues to causative agents associated with distribution:
Head: Hair dyes, shampoos, sunscreen, cosmetics, body piercing, jewelry, medications,
swim caps, headgear
Oral mucosa: Piercing, dental appliances
Neck: Perfumes, cosmetics, jewelry, clothing
Torso: Clothing, elastic in bra line or waistline
Extremities: Environmental exposure, insect repellant, metal in rings or watches, pocketed
items (coins, keys) in striking area of thighs, shoe components, sunscreen

Diagnosis based on history and physical findings; no specific acute testing helpful (6)[A]
Potassium hydroxide slide: Rule out possible fungal causes.
Patch testing: Placement of known concentrations of common antigens on the skin to help
identify responsible causes
Serum IgE: Radioallergosorbent test (RAST) helps to identify specific causes; safer than
patch test because performed with blood in lab
Skin prick: Small quantities of antigen (eg, latex) introduced into skin via small needle
Atopic dermatitis: Associated family history of atopy, scaly eczematous lesion
Bullous pemphigoid: Diffuse bullous lesions
Cellulitis: Warm, blanching, painful lesion
Erythrasma: Pink patches may turn brown and scale, red fluorescence with Wood's lamp
Herpes simplex: Groups of vesicles, painful, burning lesions
Herpes zoster: Painful vesicular lesions following dermatome
Impetigo: Yellow crusting lesions
Infectious eczematous dermatitis: Usually associated with secondary bacterial infection,
typically Staphylococcus aureus
Intertrigo: Dermatitis in areas where skin is in apposition
Lichen simplex: Scaly eczematous lesions
Molluscum contagiosum: Skin-colored papule with central umbilication, caused by poxvirus
Nummular dermatitis: Coinlike lesions
Pityriasis alba: Discrete asymptomatic hypopigmented lesions
Psoriasis: Silvery adherent scaling lesions, well demarcated, typically on extensor surfaces,
scalp, and genital regions
Scabies: Intensely pruritic lesions, frequently interdigital or in waistband regions, associated
“tracks” from mite sometimes noted
Seborrheic dermatitis: Scaly or crusting “greasy” lesions
Tinea (corpus, pedis): Maximal involvement at margins of lesion, fluoresces with Wood's lamp
Urticaria: Pruritic raised lesions (wheal) frequently with surrounding erythema (flare)
Treatment
General measures (3)[A],(7)[A]:
Primarily directed at symptomatic relief
Avoidance of irritants or causative agents: Wash and clean any possible
irritant-containing clothing or equipment with nonallergenic cleaners.
Protective barriers if irritant or allergen cannot be avoided
Mild nonallergenic soap and water cleansing with cool to tepid water; avoid
hot water.
Cool, wet compresses: Especially effective during acute blistering phase
Burrow's solution soaks
Calamine- or oatmeal-containing creams: May soothe acute lesions
Nonallergenic, high-lipid-content barrier moisturizing creams may be applied.
Acute treatment:
Follow general measures plus:
Aseptic aspiration of larger vesicles or bullae with tops left in place may
relieve discomfort.
Severe reaction: Systemic corticosteroids for 2–3 wks with gradual taper
Premature termination of corticosteroid therapy may result in rapid rebound
of symptoms.
Shoe dermatitis: Follow general measures plus:
Wear open-toe, canvas, or vinyl shoes.
Control perspiration: Change socks; use absorbent powder.
P.
Medication
Topical (3)[A],(7)[A]:
Aluminum acetate (Burrow's) solution: Apply topically for 20 min t.i.d. until skin
is dry.
Calamine lotion: q.i.d. PRN
Corticosteroid: Low- to medium-high-potency for both ACD and ICD;
beneficial for:
Mild to moderate localized lesions
<20% body surface area involved
Avoid in thinner skin areas (eyelids, face, flexural surfaces) and prolonged
use
Hydrocortisone:
Forms: Cream (c)/lotion (l)/ointment (o)/solution (s)/spray (sp)
Low potency: Hydrocortisone acetate 0.5% (c/o) or 1% (c/o/sp) b.i.d., t.i.d.,
or q.i.d.
Medium potency:
Hydrocortisone butyrate 0.1% (c/o/s) b.i.d. or t.i.d.
Hydrocortisone valerate 2% (c/o) b.i.d. or t.i.d.
Triamcinolone:
Forms: Cream (c)/lotion (l)/ointment (o)/solution (s)
Medium potency: Triamcinolone (Kenalog) 0.1% (c/l/o/s) b.i.d., t.i.d.
High potency: Triamcinolone (Kenalog) 0.5% (c/o) b.i.d., t.i.d.
Topical tacrolimus 0.03–0.1% b.i.d.
Effective with ACD
Carries a black box warning for potential risk for developing malignancies
Not recommended for children <2 yrs old
Topical antibacterial ointment for secondary infections
OTC meds:
No good information on efficacy
Examples: Mean Green hand scrub, Tecnu, Zanfel
Avoid benzocaine-containing products.
May further sensitize skin
Systemic:
Antihistamine (H1-receptor antagonist, 1st and 2nd generation)
Diphenhydramine hydrochloride:
Adult: 12.5–50 mg PO/IM q6h PRN
Children: 5 mg/kg/24 hr divided q6h PRN
Hydroxyzine hydrochloride:
Adult: 25–50 mg PO/IM up to q.i.d. PRN
Children: 2 mg/kg/24 hr PO divided q.i.d. or 0.5 mg/kg IM q4–6h PRN
Loratadine:
Adult and children >6 yrs of age: 10 mg PO daily
Children ages 2–5 yrs: 5 mg PO daily
Cetirizine:
Adult and children >6 yrs of age: 5–10 mg PO daily
Children ages 2–5 yrs: 2.5 mg PO daily b.i.d.
Fexofenadine:
Adult and children >12 yrs of age: 60 mg PO b.i.d. or 180 mg PO daily
Children ages 6–12 yrs: 30 mg PO b.i.d.
Corticosteroids useful in extensive lesions, >20% body surface area: Oral
adult dose 0.5–2 mg/kg, depending on severity, daily ×5–7 days, tapered by
50% over next 5–7 days, tapered thereafter depending on severity and
duration
Methylpreclnisolone:
Solu-Medrol: Dose varies 4–48 mg PO daily.
Medrol Dosepack: Taper from 24 mg over 6 days.
Prednisone: Dose varies 5–60 mg PO daily.
Sterapred 5-mg tablets: Taper 30–5 mg over 6 days.
Sterapred DS 10-mg tablets: Taper 60–10 mg over 6 days.
Oral pediatric dose 0.04–1 mg/kg/24 hr, depending on severity, divided b.i.d.
or t.i.d.
Orapred: Suspension 5 mg/5 mL, 15 mg/5 mL; orally disintegrating tablets 10,
15, 30 mg
Oral antibiotics for secondary infections against Staphylococcus or β-
hemolytic Streptococcus bacterial infections until culture results obtained
Ongoing Care
Return to play:
Athlete stable with symptomatic relief
Dressing may be applied:
Reduce irritation, if needed.
May be required for aesthetics
Contagious causes for lesion ruled out
If contagious agent suspected:
Prompt treatment
Isolation from skin contact to inhibit spread to others
References
1. Kockentiet B, Adams BB. Contact dermatitis in athletes. J Am Acad Dermatol. 2007.
2. Meulenbelt H, Geertzen J, Dijkstra P, et al. Skin problems in lower limb amputees: an

overview by case reports. J Eur Acad Dermatol Venereol. 2007;21:147–155.
3. Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment

and prevention. J Am Acad Dermatol. 2005;53:845.
4. Mark BJ, Slavin RG. Allergic contact dermatitis. Med Clin North Am. 2006;90:169–185.
5. Slodownik D, Lee A, Nixon R. Irritant contact dermatitis: A review. Australas J Dermatol.

2008;49:1–11.
6. Bourke J, Coulson I, English J. Guidelines for the management of contact dermatitis: an

update. Br J Dermatol. 2009.
7. Beltrani VS, Bernstein IL, Cohen DE, et al. Contact dermatitis: a practice parameter. Ann
Allergy Asthma Immunol. 2006;97:S1–S38.
Codes
ICD9
692.0 Contact dermatitis and other eczema due to detergents
692.1 Contact dermatitis and other eczema due to oils and greases
692.9 Contact dermatitis and other eczema, unspecified cause
Corneal Abrasions
Nilesh Shah
Basics
Description
Removal or scraping away of the superficial layers of the cornea (stratified squamous
epithelium) without penetration of Bowman's membrane.
In some cases, the bulbar conjunctiva is also involved.
In the general population, injury usually results from contact lens misuse but also can be
attributed to foreign bodies, tangential shearing injuries, and contusion to the globe.
In the workplace, both physical trauma and chemical trauma may be an etiology for corneal
abrasions.
In sports, the mechanism is more commonly direct trauma.
Severe corneal injuries also can involve the deeper, thicker stromal layer; in this situation, the
term corneal ulcer may be used.
Epidemiology
Most common eye injury after soft tissue injuries
More common in sports with projectiles/balls
More common in collision sports
Risk Factors
Collision/contact sports
Contact lens use, especially soft lenses
Failure to wear eye protection
Sports with projectiles/balls
General Prevention
Single-piece-construction protective eyewear with 3-mm polycarbonate lenses will reduce the
risk of eye injuries.

Hyphema (blood in the anterior chamber)
Scleral rupture: Look for vitreous leak.
Intraocular foreign body
Rust ring
Perforation: Look for vitreous leak.
Orbital fracture
Iridodialysis: Defect of the iris caused by its separation from the scleral spur
Superinfection
Recurrent erosion syndrome
Diagnosis
History
Mechanism of injury guides physical exam for associated injuries and delineates the need for
further studies.
History of previous injuries: Possible viral keratitis or recurrent erosion syndrome
Contact lens history (hard, soft, overuse): Symptoms are usually better with contact in place,
acting as a bandage.
Risk of foreign body: Particular sports, windy conditions, etc.
Physical Exam
Pain
Redness
Lacrimation
Foreign-body sensation
Photophobia
Blepharospasm
General bony orbital exam
Cranial nerve assessment
Ocular movements
Topical anesthetic and cycloplegic agents: May be needed to decrease pain and
photophobia for optimal exam
Visual acuity
Loupe with good light or slit lamp (preferable)
Fluorescein drops/strips: Sharply demarcates defects in corneal epithelium and helps to
differentiate from herpes keratitis (dendritic pattern)
Anterior chamber and corneal exam: Slit lamp preferred to rule out associated injuries
(hyphema, perforation)
Eversion of upper and lower lids: Identify any foreign bodies under tarsal plate.
Intraocular pressure (IOP): Unless perforation/scleral rupture is suspected

Imaging
Orbital series: Only if history or physical exam suggests fracture
US (B-scan)/CT scan/MRI: If occult intraocular foreign body is suspected
Foreign body
Corneal laceration
Perforation
Viral keratitis (usually herpes)
Conjunctivitis: Infectious/allergic
Iridocyclitis
Optic neuritis
Retinal detachment
Keratitis
Scleritis/episcleritis
Blepharitis
Keratoconjunctivitis
Canaliculitis
Globe injury
Orbital fracture
Photokeratitis/retinitis
Periorbital cellulitis
Trichiasis
Treatment
Long-term treatment
Alert
Long-term use of topical anesthetics may compromise epithelial healing.
Acute treatment
Analgesia:
Topical anesthesia: For exam only; see warning above. These agents should
not be prescribed for home use because they can cause secondary keratitis,
compromise healing of the epithelial wound, and block protective corneal
reflexes and sensation.
Oral analgesia as needed
Medication
Antibiotics:
Broad-spectrum topical antibiotics: Aid with lubrication and are used for
infection prophylaxis (eg, sulfacetamide/quinolones)
Contact lens–associated: Gram-negative coverage is essential (eg,
gentamicin/cefazolin); also consider coverage for Pseudomonas (eg,
gentamicin/quinolones).
Water sport–associated: Pseudomonal coverage (eg,
gentamicin/quinolones)
Topical NSAIDs (1)[A]: May be used for pain associated with the corneal
abrasion
Anticholinergic medications: Long-acting cycloplegic agents can provide relief
from photophobia and blepharospasm. Caution should be used in patients with
narrow angles because mydriatic medications can lead to acute angle-closure
glaucoma.
Oral analgesics: Oral anti-inflammatory medications and narcotic pain
medications may be used for pain control.
General Measures
Daily monitoring until reepithelialization (48–72 hr) and no infection potential
exists
Topical antibiotics continued for 1 wk after reepithelialization
Watch for recurrent erosion—sudden pain, redness, tearing—which may lead
to recurrent erosion syndrome, requiring débridement and further specialized
treatment.
Referral
Referral for recurrent abrasions, erosions, larger abrasions, infections, and
corneal ulcers
Additional Therapies P.
Cycloplegic agent for comfort, optional (initially given for first few days and then
discontinued). Examine to exclude narrow angles.
Pressure patch: Patching is for patient comfort and prevents retearing of
healing epithelium. However, most corneal abrasions do not need patching. For
small, uncomplicated corneal abrasions, patching has not been shown to
decrease pain or increase healing rates. Patching also creates loss of
binocular vision. Patching should not be used if the injury is contact lens-
induced because of the potential for harboring of infecting organisms and
promoting infection.
Ongoing Care
Hyphema
Intraocular foreign body/rust ring
Perforation
Patient Monitoring
Eye rest (ie, minimize reading or heavy computer work that requires substantial eye
movement): This helps to minimize interference with reepithelialization.
Avoid light or wear sunglasses for comfort owing to photophobia.
Patient Education
Eye protection during the healing process is important, especially in patients whose jobs put
them at increased risk of corneal abrasions or ultraviolet (UV) exposure.
If the patient is unconscious or cannot voluntarily close his or her eyelids (eg, Bell palsy or
other neuropathies), eyelids may be taped closed and use of lubrication considered.
Prognosis
The prognosis is usually good, with healing and full recovery of vision if prompt evaluation and
treatment are initiated.
Some deep abrasions heal with a scar. If this occurs in the central visual axis (the central
area of the cornea directly over the pupil), visual acuity may be permanently lost. Deep
abrasions within the central visual axis should be considered for ophthalmologic referral.
Healing of minor abrasions is expected within 24–48 hr. Extensive or deep abrasions may
require a week to heal.
Complications
Deep corneal involvement may result in facet formation in the epithelium or
scar formation in the stroma.
Progression of abrasions into corneal ulcers may lead to devastating
outcomes.
Abrasions involving exposure to vegetable matter are at risk of fungal ulcers.
Abrasions from contact lens use are at risk for pseudomanas and amoebic
keratitis.
Recurrent erosions
Allergic reactions to treatment medications
Loss of school and work time/productivity
Use of mydriatics in patients with glaucoma may lead to acute angle-closure
glaucoma.
References
1. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do
ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated
with simple corneal abrasion without delaying healing? Ann Emerg Med.
2003;41:134–140.
2. American Academy of Pediatrics Committee on Sports Medicine and

Fitness. Protective eyewear for young athletes. Pediatrics. 2004;113:619–
622.
Additional Reading
Aslam SA, Sheth HG, Vaughan AJ. Emergency management of corneal
injuries. Injury. 2006.
Calder LA, Balasubramanian S, Fergusson D. Topical nonsteroidal anti-
inflammatory drugs for corneal abrasions: meta-analysis of randomized trials.
Acad Emerg Med. 2005;12:467–473.
Hart A, White S, Conboy P, et al. The management of corneal abrasions in

accident and emergency. Injury. 1997;28:527–529.
Heimmel MR, Murphy MA. Ocular injuries in basketball and baseball: what are
the risks and how can we prevent them? Curr Sports Med Rep. 2008;7:284–
288.
Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database Syst

Rev. 2006;CD004764
Watson SL, Barker NH. Interventions for recurrent corneal erosions.

Cochrane Database Syst Rev. 2007;CD001861.
Wilson SA, Last A. Management of corneal abrasions. Am Fam Physician.

2004;70:123–128.
Zagelbaum BM. Treating corneal abrasions and lacerations. Physician Sports

Med. 1997;25:38–44.
Codes
ICD9
370.00 Corneal ulcer, unspecified
371.82 Corneal disorder due to contact lens
918.1 Superficial injury of cornea
ICD10
E91.4 Corneal foreign body
H16.0 Corneal ulcer, unspecified
H18.9 Corneal disorder, unspecified
H19.2 Corneal keratitis
H19.2 Herpes zoster keratoconjunctivitis
S05.0 Corneal abrasion
Clinical Pearls
Return to play is based on patient comfort. Once the pain is under control and
the patient is not having any visual difficulties, he or she may return to play.
Patients may wear their contact lenses again when the abrasion has healed
fully without complications (usually 3–5 days). Furthermore, if the abrasion is
related to old, worn contact lenses, they need to be replaced and new ones not
started until complete healing of the abrasion has occurred.
There is no increased risk of another corneal abrasion after an initial injury, but
anyone in a collision/contact sport or a sport with a projectile/ball may want to
wear protective eyewear.
Optimal protective eyewear is made of a sturdy frame single-piece
construction that will not allow posterior dislocation of the lens of the eyewear.
The lenses should have a 2–3-mm center thickness and be made of
polycarbonate. Different sports have differing eyewear regulations. They
should have American Society for Testing and Materials (ASTM) certification
(2).
Cubital Tunnel Syndrome
Jeffrey Rosenberg
Thomas A. Phipps
Basics
Compression, traction, or irritation of the ulnar nerve as it passes through the cubital
tunnel of the medial elbow
The cubital tunnel is bounded by the medial trochlea, the medial epicondylar groove, and the
posterior portion of the ulnar collateral ligament and is roofed by the triangular arcuate
ligament.
Primary complaints are medial elbow and forearm pain.
Additional complaints are paresthesias in the ring and little fingers.
Synonym(s): Ulnar tunnel syndrome
Epidemiology
Incidence
The elbow is the most common site of compression of the ulnar nerve.
Predominant gender: Male > Female (3–8:1)
The 2nd most common compressive neuropathy (after carpal tunnel syndrome)
Overhead throwing athletes are most at risk.
Risk Factors
Overhead throwing athletes
Repetitive upper extremity activities
Diabetes
Obesity
Peripheral neuropathies
General Prevention
Avoid prolonged pressure on the medial elbow.
Etiology
Possible causes of the compression of the ulnar nerve as it passes the medial elbow include:
Subluxation of the ulnar nerve over the medial epicondyle
Enlarged medial head of the triceps muscle
Cubitus valgus
Ulnar collateral ligament instability/tears
Triangular arcuate ligament tears in baseball pitchers
Osteophytes
Ganglia or lipomas
Tumors
Repetitive elbow flexion and extension
Anconeus epitrochlearis: Anomalous muscle in 70% of population

Ulnar neuritis
Ulnar collateral ligament instability
Diagnosis
History
Vague, aching pain in the region of the elbow, worsening with overhead activities
Paresthesias over the 4th and 5th digits
Numbness of the 4th and 5th digits
Weakness of interosseous muscles of the hand
Worsening grip and clumsiness
Snapping or popping sensation of medial elbow
Overhead throwing athletes will complain of loss of control of ball with activity.
Physical Exam
Pain with palpation of cubital tunnel of affected elbow
Positive Tinel sign: Tapping over the ulnar nerve at the elbow will cause a reproduction of
symptoms (1).
Elbow flexion test: Placing the elbow in full flexion and the wrist in maximal extension will
cause pain or paresthesias after 1 min (1).
Scratch test: Patient faces examiner with arms adducted, elbows flexed, and hands
outstretched with wrists in a neutral position. Patient resists adduction/internal rotation to the
forearms applied by the examiner. The examiner scratches or wipes fingertips over the
cubital tunnel, and resistance to adduction/internal rotation is again applied. In a positive test,
the patient has immediate and temporary loss of external resistance tone, which resolves
within 5 sec (1).
Sensory changes in ulnar nerve distribution can be detected with Semmes-Weinstein
monofilament testing and, in more advanced cases, with 2-point discrimination tests.
Asymmetric hypothenar atrophy, decreased pinch and grip strength, abducted little finger, or
severe claw deformity of little finger only (Wartenberg sign)
Intrinsic muscle weakness and wasting (especially 1st dorsal interosseous muscle)
Patient will exhibit decreased sensation in the ulnar nerve distribution.

Complete medical history and physical exam
Nerve conduction velocity (NCV) to determine how fast neurologic signals travel down nerve
to detect site of compression or constriction. Studies must be performed with elbow at 45
degrees of flexion to lessen chance of erroneous results (2).
Electromyogram (EMG) to evaluate nerve and muscle function
Imaging
Radiograph of elbow to evaluate for bony changes or spurs
MRI of elbow to evaluate cubital tunnel for soft tissue masses and continuity of ulnar
collateral ligament
Diagnostic US: Ratio of ulnar nerve cross-sectional area at maximal enlargement to cross-
sectional area at unaffected site >2.8:1; ratio in control subjects 1.1:1 (3)
At decompression, specific sites of nerve compression usually can be found.
Inspect the arcade of Struthers, intermuscular septum, cubital tunnel, and Osborne fascia
(between 2 heads of flexor carpi ulnaris).
Systemic: Diabetes, renal disease, multiple myeloma, amyloidosis, chronic alcoholism,
malnutrition
Compression: Postoperative occupational or recreational activities requiring repetitive flexion
and extension, supracondylar process, ligament of Struthers, medial head of triceps, ulnar
nerve compression at Guyon canal
Medial epicondylitis
Ulnar collateral ligament injury
Carpel tunnel syndrome
Treatment
Conservative treatment is effective in up to 90% of patients irrespective of
EMG/NCV results (4,5,6,7).
The most effective treatment is cessation of activity that is causing the
problem.
A splint or foam elbow pad worn at night (to limit movement and reduce
irritation)
Elbow pad (to protect against chronic irritation from hard surfaces)
NSAIDs
Physical therapy with attention to nerve-gliding exercises
Consider surgery if symptoms continue after 3 mos of conservative therapy or
multiple recurrences in a throwing athlete (8,9,10).
Address ulnar collateral ligament instability if coexisting.
Decompression of the nerve in the canal, especially in setting of bone spurs
Transposition of the nerve out of the canal in an anterior direction
Multiple meta-analyses have been inconclusive and differ in results; none
specifically for athletes (11,12,13).
No clinical or NCV differences between simple compression and ulnar nerve
transposition
No statistically significant difference but rather a trend toward improved
clinical outcomes with transposition of the ulnar nerve (combining 2 types of
transposition) compared with simple decompression
Preference for overhead athlete is transposition of the ulnar nerve to allow for
improved movement of the nerve throughout the range of motion (8).
Subcutaneous technique: Anterior transposition of nerve without detachment
of flexor mass; fascial sling used to prevent subluxation of nerve
Submuscular technique: Allows inspection and treatment of ligament and
osseous pathology; nerve stabilized deep to flexor-pronator muscles but
more morbidity and potential for deep scarring
References
1. Cheng CJ, Mackinnon-Patterson B, Beck JL, et al. Scratch collapse test for
evaluation of carpal and cubital tunnel syndrome. J Hand Surg [Am].
2008;33:1518–1524.
2. Sattari S, Emad M. Changes in ulnar nerve conduction velocity across the

elbow in different angles of elbow flexion. Electromyogr Clin Neurophysiol.
2007;47:373–376.
3. Yoon JS, Walker FO, Cartwright MS. Ultrasonographic swelling ratio in the
diagnosis of ulnar neuropathy at the elbow. Muscle Nerve. 2008.
4. Szabo RM, Kwak C. Natural history and conservative management of

cubital tunnel syndrome. Hand Clin. 2007;23:311–318, v–vi.
5. Svernlov B, Larsson M, Rehn K, et al. Conservative treatment of the cubital

tunnel syndrome. J Hand Surg Eur Vol. 2009.
6. Gellman H. Compression of the ulnar nerve at the elbow: cubital tunnel

syndrome. Instr Course Lect. 2008;57:187–197.
7. Padua L, Aprile I, Caliandro P, et al. Natural history of ulnar entrapment at

elbow. Clin Neurophysiol. 2002;113:1980–1984.
8. Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder

and elbow in the athlete. Clin Sports Med. 2006;25:465–487, vi–vii.
9. Keefe DT, Lintner DM. Nerve injuries in the throwing elbow. Clin Sports
Med. 2004;23:723–742, xi.
10. Charles YP, Coulet B, Rouzaud JC, et al. Comparative clinical outcomes
of submuscular and subcutaneous transposition of the ulnar nerve for cubital
tunnel syndrome. J Hand Surg Am. 2009;34:866–874.
11. Mowlavi A, Andrews K, Lille S, et al. The management of cubital tunnel

syndrome: a meta-analysis of clinical studies. Plast Reconstr Surg.
2000;106:327–334.
12. Zlowodzki M, Chan S, Bhandari M, et al. Anterior transposition compared

with simple decompression for treatment of cubital tunnel syndrome. A meta-
analysis of randomized, controlled trials. J Bone Joint Surg Am.
2007;89:2591–2598.
13. Macadam SA, Gandhi R, Bezuhly M, et al. Simple decompression versus

anterior subcutaneous and submuscular transposition of the ulnar nerve for
cubital tunnel syndrome: a meta-analysis. J Hand Surg [Am].
2008;33:1314.e1–1314.e12.
Additional Reading
Cuts S. Cubital tunnel syndrome. Postgrad Med. 2007;83(975):28–31.
Mowlavi A, et al. The management of cubital tunnel syndrome: a meta-analysis

of clinical studies. Plast Reconstr Surg. 2000;106:327.
Codes
ICD9
354.2 Lesion of ulnar nerve
Clinical Pearls
Most important part of treatment is to minimize elbow flexion and pressure on
the elbow and to engage in relative rest from repetitive activity.
Screen overhead athletes for ulnar collateral ligament instability.
Cuboid Subluxation and Fracture
Aaron P. Leininger
Danielle L. Mahaffey
Karl B. Fields
Basics
Description
Subluxation and dislocation: Midfoot injury that disrupts the ligamentous structures around the
cuboid, allowing subluxation and, rarely, complete dislocation of the cuboid. Typically,
subluxation and dislocation occur in the plantar direction, but one case of dorsal subluxation
(1)[C] has been reported. Mechanism of injury is often an inversion ankle sprain, although
alternative mechanisms have been described (2)[A].
Fracture: Typically, tarsal cuboid bone fractures arise from indirect “nutcracker” compression,
usually after significant traumatic force that causes abduction of the forefoot. Other types of
cuboid fractures include avulsion fractures and stress fractures.
Synonym(s):
Subluxation and dislocation: Cuboid syndrome; Locked cuboid; Dropped cuboid; Calcaneal
cuboid fault syndrome; Lateral plantar neuritis
Fracture: Nutcracker fracture
Epidemiology
Incidence
Subluxation: Subluxation is considered rare, but some propose that it is underdiagnosed. 2
studies found the prevalence of cuboid instability to be 4–6.7% in patients with foot problems
and inversion injury, respectively (3,4)[B].
Dislocation: Rare
Fracture: Rare; in one study, 38% (58/155) of traumatic midfoot fractures involved the cuboid
(5)[C].
Risk Factors
Subluxation:
Pronated feet
Tight peroneal longus tendon
Ballet dancing (2)[A]
Trail running or running on uneven surfaces
Fracture and dislocation:
Activities at high risk for foot trauma (eg, motorsports, equestrian, etc.)
Long-distance running (stress fracture)
Diagnosis
History
Subluxation:
May follow inversion ankle injury
Subluxation may be precipitated by increased routine activity, increased activity on uneven
terrain, or initiation of new activity, especially for patient with excess pronation.
Pain in lateral midfoot proximal to and involving the base of the 4th and/or 5th metatarsal,
exacerbated with activity
Often with symptom-free intervals
Associated with foot weakness or difficulty with ambulation
Fracture and dislocation:
Substantial traumatic force needed owing to stable ligamentous attachments
Most patients with fractures are unable to bear weight.
Dislocations often are associated with severe weakness and markedly antalgic gait if
patient is able to bear weight.
Midfoot deformity may be present with fracture or dislocation.
Physical Exam
Subluxation:
Tenderness to palpation over cuboid (dorsal and/or plantar surface)
Increased mobility to manipulation of the cuboid at the Lisfranc joint
Dislocation and fracture:
Midfoot swelling
Tenderness to palpation over cuboid (dorsal and/or plantar surface)
With dislocation, abnormal indentation in lateral midfoot may be noted with concomitant
fullness in the plantar surface.
May be unable to bear weight

Imaging
Radiographs: Recommend anteroposterior, lateral, and oblique views.
Oblique view usually demonstrates a cuboid fracture, and dislocation can be seen if medial
border of 4th metatarsal is not aligned to medial border of the cuboid.
Subluxation often is not seen.
CT scan is often beneficial if fracture is present.
MRI is the most sensitive test for stress fracture.
Peroneus longus tenosynovitis
Base of 4th and 5th metatarsal stress fracture
Calcaneonavicular coalition
Peroneal longus tendon subluxation
Os peroneum fracture
Treatment
Subluxation:
Literature suggests repeated manipulation with the “cuboid whip” or “cuboid
squeeze” attempting to reestablish proper alignment of the calcaneocuboid
joint. One case series of 7 patients reported good results with this technique
(6)[C].
Patient stands with support, affected leg with knee bent to 90 degrees.
Examiner grasps forefoot with fingers and places thumbs (one over the
other) on plantar aspect of cuboid. Cuboid is manipulated with a quick
downward thrust of the thumbs in a dorsal and lateral direction.
Orthotics, use of cuboid pad, and arch straps/taping recommended (2)[C]
Strength and proprioception rehabilitation (2)[C]
Dislocation:
Controversial
Open fixation followed by short-leg splinting/casting and non-weight-bearing
for 6 wks or more depending on stability (7)[C]
Closed reduction with local anesthesia (7)[C]
Fracture:
Controversial
Open reduction with internal fixation, possibly requiring a bone graft, is the
most commonly accepted treatment (8)[C].
Other options include conservative treatment with cast immobilization for 6–8
wks, surgical arthrodesis, and external fixation (9)[C].
Ongoing Care
Subluxation:
Return to play depends on the severity of the athlete's symptoms.
Most athletes should be able to return to play almost immediately given proper treatment
with orthotics/cuboid pad/arch supports.
Some patients may need a period of relative rest with return to play after physical therapy
and symptom improvement.
Some patients also learn to self-treat in the field after instruction in self-administration of
the cuboid whip maneuver.
Fracture/dislocation:
Return to play for cuboid stress fractures is similar to other foot stress fractures.
Athletes should follow a slow, incremental, symptom-free return-to-play protocol with rest
and regression of intensity of symptoms develop.
Return to play for most fractures and dislocations should proceed only after clearance by
the orthopedic surgeon and would be slow and incremental.
Depending on the severity of the injury, there may be chronic damage ultimately limiting
return to play.
Athletes who underwent ankle arthrodesis will be very limited in the types of sports they
can play because of lack of motion at the ankle joint.
Complications
Subluxation and dislocation: Chronic instability can be a problem for both
dislocation and subluxation.
Fracture: Nonunion, particularly if diagnosis/treatment is delayed
References
1. Mooney M, Maffey-Ward L. Cuboid plantar and dorsal subluxations:
assessment. J Orthopaed Sports Phys Ther. 1994;20(4):220–226.
2. Patterson SM. Cuboid syndrome: a review of the literature. J Sports Sci &
Med. 2006;(5):597–606. Available at: http://www.jssm.org/vol5/n4/18/v5n4–
18pdf.pdf
3. Newell SG, Woodle A. Cuboid syndrome. Phys Sports Med. 1981;9:71–76.
4. Blakeslee TJ, Morris JL. Cuboid syndrome and the significance of midtarsal
joint stability. J Am Podiatr Med Assoc. 1987;77:638–642.
5. Richter M, Wippermann B, Krettek C, et al. Fractures and fracture

dislocations of the midfoot: occurrence, causes and long-term results. Foot
Ankle Int. 2001;22:392–398.
6. Jennings J, Davies GJ. Treatment of cuboid syndrome secondary to lateral

ankle sprains: a case series. J Orthop Sports Phys Ther. 2005;35:409–415.
7. Littlejohn SG, Line LL, Yerger LV Jr. Complete cuboid dislocation.

Orthopedics. 1995;19:175–176.
8. Sangeorzan BJ, Swintkowski MF. Displaced fractures of the cuboid. J Bone

Joint Surg. 1990;72-B:376–378.
9. Manoj-Thomas A, Gadgil A. Nutcracker fracture of the cuboid: a case

report. Eur J Orthop Surg Traumatol. 2006;16:178–180.
Additional Reading
Hunter JC, Sangeorzan BJ. A nutcracker fracture. Am J Roentgenol.
1996;4:888.
Main BJ, Jowett RL. Injuries of the midtarsal joint. J Bone Joint Surg.
1975;57-B:89–97.
Omey ML, Micheli LJ. Foot and ankle problems in the young athlete. Med Sci
Sports Exerc. 1999;31:S470–S486.
Codes
ICD9
825.23 Fracture of cuboid bone, closed
838.01 Closed dislocation of tarsal (bone), joint unspecified
Dentoalveolar Trauma
Mark H. Mirabelli
Matthew D. Capuano
Basics
Description
Dentoalveolar injuries include dental avulsion, dental luxation, extrusion and intrusion, enamel
and crown fractures, root fracture, and alveolar bone fracture.
Epidemiology
25% of all respondents between the ages of 6 and 50 yrs reported suffering at least one
traumatic dental injury to their anterior teeth for all causes in the U.S. (1).
30% of children have experienced dental injuries (2).
The peak period for trauma to the primary teeth is 18–40 mos of age because this is a time
of increased mobility for the relatively uncoordinated toddler. Injuries to primary teeth usually
result from falls and collisions as the child learns to walk and run (2).
With the permanent teeth, school-aged boys suffer trauma almost twice as frequently as
girls.
Sports accidents and fights are the most common cause of dental trauma in teenagers.
The upper (maxillary) central incisors are the most commonly injured teeth.
Data show that these orofacial injuries occur primarily during recreational sports and
organized athletic events. Individuals who incur facial trauma during noncompetitive sporting
events go vastly underreported, which skews the reporting. 2 independent retrospective
studies show that at least 60% of the injuries were incurred by males in the age range of 8–
18 yrs.
90.3% of crown fractures or crown-root fractures occur from direct trauma (3).
The most commonly involved teeth were the central incisors (58.3%), and the 2nd most
commonly involved teeth were the maxillary lateral incisors.
The previous study showed a seasonal variation in incidence. These data demonstrate the
probable correlation between outdoor activities and predominance of dental trauma during
warmer times of the year (in the northern hemisphere) (1).
5–35% of the population; 75% under 15 yrs of age
Predominant gender: Male > Female (3:1); equal or higher rates sometimes reported for
females than males when corrected for exposure rates.
Risk Factors
Protection: mouth guards are associated with a 7–10-fold reduction in risk.
Sports: Baseball, basketball, cycling, hockey, soccer, skiing, rugby, football, wrestling, boxing
and martial arts
Anatomy: Protruding maxillary incisors, lip incompetence, class II malocclusion
Previous injury
General Prevention
Face masks, in sports such as hockey and football, provide protection against trauma to the
mouth and face.
Mouth guards reduce oral lacerations and tooth fractures and displacement and cushion
impacts that could result in condylar displacement and subsequent injury. They dramatically
reduced injury rates when mandated.
Stock mouth guards are the most inexpensive but lack customized fit. The athlete has to
continuously bite down on mouth guard for it to not become loose and free in the mouth.
These mouth guards come with the risk that if the patient becomes unconscious, the mouth
guard may be extruded from the oral cavity or obstruct the airway. They are often bulky and
may interfere with speech and breathing.
Mouth-formed or boil and bite mouth guards are the most commonly commercially sold mouth
guards, and many types are available. These mouth guards are best fit by a dentist but may
be fit at home. Inconsistent retention, fit, and quality make these mouth guards still not the
most desirable option, although a better option than stock mouth guards. They are molded to
the mouth after being placed in boiling water and then are set in cold water after being
placed in the athlete's mouth.
Custom-fitted mouth guards are fit in a 2-stage process by a dentist for maxillary (class I or
II occlusion) or mandibular (class III occlusion) arches. They provide increased comfort,
compliance, and protection. They may last several years and are impractical for children
under 13 yrs of age owing to rapid dental changes. They may be formed by vacuum or
pressure lamination (preferred) processes. These mouth guards exhibit the most reliable
retention rates and limit the incidence of dental trauma. The high cost of these mouth guards
can be easily justifiable economically relative to the cost of cosmetic or restorative dentistry.
Etiology
Etiology (2):
Falls made up 49% of cases (including uncoordinated childhood falls).
Sports-related injuries occurred in 18% of cases.
Bicycle and scooter accidents accounted for 13% of cases.
Assaults made up 7% of cases.
Road traffic accidents resulted in 1% of cases.
All others 12%
Pathophysiology:
Enamel fracture only (Ellis class I), 15.8%:
Roughness of chipped tooth on tongue
May go unnoticed by athlete
Not a dental emergency
Enamel and dentin fracture (Ellis class II), 39.9%:
Exposure of yellow dentin
Pain with dentin exposure to air, cold drinks, or touch
Not a dental emergency
Enamel, dentin, pulp exposed (Ellis class III), 25.7%:
Dental emergency (within 3 hr)
Exposure of red-pink dental pulp
Vital with closed root apex: Less complex treatment
Vital pulp with open root apex: More complex but viable
Dental pulp opening appears dry or oozes putrescent exudates and no pain: Nonviable
Root fractures (Ellis class IV):
Middle (1/3) root fractures have a good prognosis depending on time of evaluation and
treatment. This root fracture can be identified by its longer visible coronal segment and it
being partially extruded compared with other teeth. The tooth is likely to bleed from the
gingival sulcus, and with gentle finger pressure it may be rotated in the socket.
Cervical 3rd fractures have the worst prognosis of all root fractures.
Apical root fractures have the best prognosis for maintaining viability, especially if lacking
segmental mobility.
Extrusion, intrusion, lateral luxations:
Displacement (not fracture) involving periodontal ligament (ie, stretch, compress, rupture
ligament)
Lateral luxation involves movement of tooth in anterior/posterior plane: Follow up with
dentist within 24 hr for splinting or immediately if tooth cannot be repositioned.
Intrusion involves movement of tooth inward:
May be extremely painful, painless, or numb depending on the extent of nerve root
injury.
Extrusion is movement of the tooth out of the socket: Follow up with dentist within 24 hr
for splinting or immediately if tooth cannot be repositioned.
Avulsion (tooth exarticulation): Dental emergency (immediate): Time inversely related to
viability.
Associated soft tissue injury (abrasions, lacerations, contusions):
Lacerations of the lip: 55.8%
Abrasions of face constituted 34.2%
Abrasions of lip constituted 30.2%
Abrasions of mentum constituted 21%
Abrasions of nose constituted 13%
Abrasions of other regions constituted 1.5%

Facial contusion, laceration, fracture
Mandible fracture
Intraoral laceration (tongue, buccal mucosa, gingiva)
Concussion
Diagnosis
Suspicions for dental trauma:
Impact to jaw, face, or any part of skull or neck leaving bruising or ecchymosis, diffuse or
focal
Facial swelling, bleeding from mouth or gums
Patient complains of ear, jaw, or neck pain or headache
Patient intolerant of drinking hot or cold fluids ± inability to chew
Pre Hospital
Evaluate patient for signs of shock or acute blood loss.
Determine the extent of injury because this dictates how quickly action must be taken.
Response time is paramount when discussing viability of teeth affected by dental trauma.
Better outcomes result from proper interventions done early in the time course.
Assess all lacerations for severity and necessity of intervention by dentist or oral maxillofacial
surgeon.
History
Mechanism of injury and associated injuries (4)
Force and vector of injury: This is paramount to identify all injuries visible or potentially
concealed by soft tissue injury and swelling.
Time since injury, time tooth was out of mouth, method of storage and transport
Past dental history, past general medical and surgical history
Medications and allergies
Last tetanus shot
Physical Exam
Pain and tenderness to percussion or palpation
Temperature sensitivity
Color changes
Tooth loosening
Assess levels of consciousness, and ensure that airway, breathing, and circulation are
intact.
Begin with general examination of the head and neck, including skull, eyes, ears, nose,
cervical spine, and anterior neck.
Proceed with extraoral exam. Palpate the mandible, zygoma, temporomandibular joint, and
mastoid region. Check for any mandibular or maxillary fractures that are present. Find
mandibular fractures by feeling the lower border of the mandible for a step-down fracture.
Identify any extraoral lacerations, bruises, or swelling. If a laceration is present in the
upper or lower lip, the area must be inspected for foreign bodies such as gravel or tooth
fragments. Any foreign bodies must be débrided from the soft tissue.
The mandibular condyles and maxilla should be carefully palpated. Check jaw movements
for normal range of movements. Chin lacerations require careful evaluation of the cervical
spine and mandibular condyles. Indications of condylar fractures include an anterior open
bite, a malocclusion, or limited mandibular opening. Confirmation of condylar fractures
requires a panoramic radiograph with closed- and open–mouth views.
Follow this with a detailed intraoral exam. Identify and account for all missing teeth, if
possible. Explore oral cavity to identify extent of dental and oral mucosa damage. The
labial and buccal mucosa, maxillary frenum, gingival tissues, and tongue should be
examined for bruising or lacerations. All intraoral lacerations must be cleaned and
explored, looking for any foreign bodies. Palpate the alveolus to detect any fractures. Have
the patient clench the teeth so that the dental occlusion can be evaluated. Each tooth
should be examined for damage or mobility. Multiple types of injuries to each tooth must be
suspected. Excess mobility suggests root and alveolar fractures; this is also seen with
luxation injuries to a lesser degree. Malalignment may indicate luxation injury or fracture.
Modular movement of adjacent teeth suggests alveolar fractures.

Imaging
Radiographic examination: For evaluating injuries to the maxillary or mandibular teeth, an
occlusal radiograph is the film of choice.
2 periapical views at different angles if a root fracture is suspected are required for a
definite diagnosis.
For deep tooth structure evaluation (ie, Ellis class III, root, jaw fractures, intruded teeth), a
lateral anterior radiograph provides additional useful information.
Chest radiograph if dyspneic, hemoptysis, or missing tooth to evaluate for aspirated tooth
fragment
Panorex (panoramic radiograph) helps to evaluate suspected mandibular or condylar
fractures.
Routine radiographs may not show root fractures; dental films (panoramic film with selected
periapical views at multiple angles) are indicated with a low index of suspicion. Fractures may
not be evident initially; negative films may be repeated 1–2 days after injury.
Postreduction views are needed to rule out root or alveolar fractures and confirm placement
after reimplantation or splinting of an avulsed tooth.
Photographic documentation: The use of preoperative and postoperative photography may
be useful for documentation purposes.
Associated trauma: Ruled out by history, physical examination, and radiography
Mandibular fractures and temporomandibular joint (TMJ) damage: Check occlusion, limitation
of jaw motion, mobility of multiple teeth or jaw fragments, maxillary/hard palate mobility,
anesthesia/paresthesia of the cheek and lip, as well as radiography.
Soft tissue injuries: Include radiographs if not all tooth fragments are accounted for.
Treatment
Treatment depends on rapid identification of injury type.
Initial stabilization:
Establish airway, breathing, and circulation.
Control soft tissue bleeding: Pressure from gauze, fabric, or any other
moldable material
Provide analgesia:
Injection of 1–2 mL lidocaine (0.5–1 mL for primary teeth) into the buccal
gingival mucosa over the injured tooth and root apex, with epinephrine if not
contraindicated; less effective with mandibular teeth
Inferior alveolar nerve block may be required for pain relief of mandibular
teeth, with 2–4 mL lidocaine injected just superior to the lingula of the
mandible.
Orthodontic wax may be applied to protect exposed dentin or pulp and
sharp edge.
Oral pain medications are not recommended initially owing to the possibility
of ingesting blood and fragments of teeth.
P.
Tooth avulsions (5):
Avulsed primary teeth should not be replaced owing to the risk of injury to
permanent teeth.
Locate all teeth or tooth fragments, and prepare to replace and reposition
tooth immediately.
Handle the tooth only by the crown. Any contact with the root may render the
tooth nonviable.
Inspect the tooth to ensure that no foreign material is left on the surface
(especially at the root). If any foreign material is present, flush or swish the
tooth in a sterile balanced salt solution (Hank's balanced salt solution, Earl's
balanced salt solution) or milk for 10 sec. Do not brush.
Replantation should be performed as soon as possible (good prognosis
within 20 min but poor after 2 hr) (6).
Do not attempt to replace tooth in obtunded patient.
After exam, flush socket with saline, and prepare to replace tooth.
Firmly (but not forcefully) reinsert tooth into the socket after local anesthesia
and saline irrigation. Have patient bite gently on gauze to seat tooth in
socket. Patient may feel a click or a give and then increased resistance.
Once the tooth is firmly implanted in the alveolar socket and is anatomically
consistent (labial and lingual surfaces align) with adjacent teeth, place an
oversized piece of gauze atop the reimplanted tooth, and have the patient
bite down firmly on the gauze.
Transport immediately to dental office or emergency department with on-call
dentistry, whichever is available at that time.
Place nonimplantable teeth or tooth fragments in preserving system such as
sterile balanced salt solution (Hank's balanced salt solution, Earl's balanced
salt solution) or milk if available.
Tooth may be stored in milk for 3–6 hr and even longer in sterile balanced salt
solution and in saliva for up to 2 hr. If low risk for aspiration and no other
alternatives are available, store sublingually or in buccal vestibule to prevent
drying.
Do not store in plain water because this causes osmotic lysis of periodontal
ligament cells.
Do not allow tooth to dry.
Dental treatment:
5–10 days of antibiotics (penicillin V or alternatives) reduce the risk of root
resorption.
Splinting/immobilization: Acid-etch resin is used with wire along the labial
surface to passively splint the injured tooth.
Duration of splinting varies with injury: Semirigid splints should be applied
for 7–10 days after avulsion.
Tooth fractures (7):
Enamel only (Ellis class I): Locate fragment, if possible. If fragment cannot be
reattached or securely replaced, place the fragment in a balanced salt
solution. May be reattached up to 48 hr later by a dentist with resin or
bonding. If nonviable, smoothing and contouring the rough edge are tactilely
therapeutic and aesthetically pleasing; nonurgent referral to smooth rough
edges, with cosmetic repair 4–8 wks later if needed.
Enamel and dentin (Ellis class II): Fragment may be reattached with bonding
agent or composite resin materials. Transport tooth fragments in tooth-
preserving system. Arrange dental referral as soon as possible for best
results (same day). Dentist may place composite resin or glass ionomer
bandage. Exposed dentin should be sealed as soon as possible; delay may
allow bacterial contamination of the pulp via dentinal tubules, especially in
immature teeth. Acid-etch composite is used (possibly with tooth fragments)
for definitive restoration.
Enamel, dentin, and pulp (Ellis class III): Emergent evaluation within 3 hr
before proceeding with treatment by dentist. Treatment based on pulp status
and dental age of tooth. Direct pulp capping may allow pulp vitality with small
pulp exposures. Partial pulpotomy with calcium hydroxide treatment may be
indicated in immature teeth to delay root canal treatment until after apex
maturation (if pulp remains vital). Teeth with moderate pulp exposure and
closed apices necessitate root canal treatment.
Crown-root fractures (cleave fractures): Fractures near the alveolar crest
rarely heal without either root canal therapy and post/crown placement or
extraction and prosthodontic treatment.
Root fracture (Ellis class IV): Coronal portion should be repositioned after
local anesthesia with radiographic confirmation and rigid immobilization for
2–3 mos (shorter for more apical fractures) (8).
Root fractures, as mentioned previously, have poorer prognosis the more
distal from the apical segment. Apical root fractures may heal by cementum
union alone.
Middle 3rd fractures require urgent care. Immediate intervention includes
using gentle pressure coupled with instructing the athlete to bite down on
sterile gauze after repositioning. Subsequent dental evaluation emergently as
well as periodically over the next 6–8 wks is necessary. The patient may
require a root canal if indicated by a dentist.
Urgent management remains the same as for middle 3rd injuries, but a
dentist's evaluation will determine viability of affected tooth and possible need
for extraction and replacement with a dental implant.
Luxation:
For lateral luxation (subluxation of the dentoalveolar joint), if minor, it may be
appropriate to attempt reduction if possible.
If reduction is possible and successful, provider may approximate and suture
any gingival injury. Splint for 2–4 wks, and follow up with pulp vitality testing,
local anesthesia, firm repositioning, and splinting with close follow-up
Urgent referral (same day) only if repositioning cannot be done.
Extrusion injuries: Repositioning and splinting with anesthesia as needed
Urgent referral (same day) only if repositioning cannot be done
Intrusion injuries are dental emergency. Record the distance of intrusion, use
local anesthesia, and luxate the tooth with gentle twisting if it is not already
slightly mobile. Do not splint. Intrusive luxation with deciduous teeth may need
to be extracted or may be left in and may re-erupt. Teeth also may ankylose.
Urgent repositioning is necessary.
Refer within 3 hr to ED or dentist's office for treatment.
Alveolar fractures:
Immediate reduction with manual pressure after clinical diagnosis followed by
radiographs and rigid splinting for 1–2 mos reduces pulp necrosis.
Empirical antibiotic therapy against oral flora is recommended to reduce
contamination.
Medication
Immunizations: Tetanus. Consider administration of immunization in cases of
lacerations or tooth injuries with exposed pulp or for avulsions in patients for
whom immunizations are due (last immunization >5 yrs).
Antibiotic therapy: Consider prophylactic antibiotics in cases of exposed pulp
or avulsion. Penicillin VK or clindamycin may be used (9).
Pain medications: Consider use of NSAIDs (ibuprofen) and/or analgesic
(acetaminophen, tramadol, codeine, hydrocodone) as needed.
Referral
Patients should be advised to see their dentist in the time frame outlined earlier.
Urgent oral surgical referral may be necessary owing to associated injuries.
P.
Photographs and meticulous documentation are particularly important in cases
of assault or motor vehicle accidents.
Aspiration: If an avulsed tooth is not accounted for, a chest film may be
indicated. Swallowed teeth rarely require treatment and should not be retrieved
unless there is concern for GI obstruction.
Damage to primary teeth may result in damage to permanent teeth in 25–70%
of injuries.
Dental splinting is used as an initial treatment for subluxed or avulsed teeth that
are replaced.
Root canal might be considered as delayed treatment in cases of injury
resulting in damage to the root.
Hospital admission or observation is rarely required. Criteria may include:
Multiple, complicated trauma
Vital signs instability
Abuse or violence suspected in injury history
Concern for aspirated tooth
Ongoing Care
Tooth avulsion:
Endodontic treatment is usually required at 1–2 wks in teeth with a closed apex (after
pulpal ischemic necrosis, before infection) to prevent periapical abscess formation and root
resorption. Teeth with an open apex may reestablish blood supply; thermal sensitivity
testing is performed every 3–4 wks, with root canal treatment delayed until clinical or
radiographic signs of disease. Calcium hydroxide treatment also may be considered to
prevent inflammatory root resorption.
Follow-up is essential at least every 6 mos for several years; potential root resorption must
be monitored and alveolar bone optimized for prosthetic implantation considerations.
Tooth fractures:
Crown fractures: Definitive restoration should be performed as soon as possible,
especially if the arch is crowded, because delay may allow encroachment of adjacent teeth
and necessitate orthodontic treatment before restoration. Root canal treatment may be
required in 1–2 wks in cases of pulp exposure.
Root fractures: Monthly clinical and radiographic evaluation should be performed during
splinting and then every 3–6 mos for at least 2 yrs; 20–45% have pulpal necrosis and
require pulpotomy, root canal treatment, or prosthesis. Hard tissue union is more likely with
pulpal vitality, younger patients, closer fragment opposition, and increased root diameter.
Tooth luxation:
Intrusion: Radiographic monitoring for pulp necrosis or root resorption should occur every 3
wks. Orthodontic extrusion is required if re-eruption is not satisfactory after 3 mos. Root
canal treatment is required in 2–3 wks for 95% of teeth with mature roots and 65% of
teeth with immature roots owing to pulp necrosis.
Lateral luxation requires follow-up with radiographs every 3 mos for 2 yrs to ensure that
root resorption or loss of pulp vitality is not evident.
Diet
Soft or liquid diet may be necessary for a time to further protect teeth and allow for healing.
References
1. Ranalli DN. Sports dentistry and dental traumatology. Dent Traumatol. 2002;18:231–236.
2. Wright D, Bell A, McGlashan G, et al. Dentoalveolar trauma in Glasgow: an audit of

mechanism of injury. Dental Traumatology. 2007: doi: 10.1111/j.1600–9657.2006.00430
3. Castro JCM, Poi WR, Manfrin TM, et al. Analysis of the crown fractures and crown root
fractures due to dental trauma assisted by the Integrated Clinic from 1992 to 2002. Dental
Traumatology. 2005:21:121–126.
4. Torg JS, Greenberg MS, Springer PS. Diagnosis and management of oral injuries. St.
Louis: Mosby-Year Book, 1991.
5. Dewhurst SN, Mason C, Roberts GJ. Emergency treatment of orodental injuries: a

review. Br J Oral Maxillofac Surg. 1998;36:165–175.
6. Trope M. Clinical management of the avulsed tooth. Dental Clin North Am. 1995;39:93–
112.
7. Donly KJ. Management of sports-related crown fractures. Dental Clin North Am.
2000;44:85–94.
8. Camp JH. Management of sports-related root fractures. Dental Clin North Am.
2000;44:95–109.
9. Mark DG, Granquist EJ. Are prophylactic oral antibiotics indicated for the treatment of
intraoral wounds? Ann Emerg Med. 2008;52:368–372.
Codes
ICD9
873.62 Open wound of gum (alveolar process), uncomplicated
873.63 Open wound of internal structures of mouth, tooth (broken) (fractured) (due to
trauma), uncomplicated
873.72 Open wound of gum (alveolar process), complicated
Clinical Pearls
If the pulp becomes devitalized, the tooth will rapidly change color, along with
associated symptoms. If root canal treatment is needed, a slight and gradual
darkening may be noticed.
Depending on the type of injury and promptness of care, chances are good for
a successful recovery.
DeQuervain Tenosynovitis
William W. Briner Jr
Basics
Description
de Quervain tenosynovitis is a stenosing tendinosis of the 1st dorsal compartment of the
wrist.
The abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons course through
this compartment.
It is the most frequently encountered tendinosis on the dorsal side of the wrist.
de Quervain tenosynovitis is typically an overuse injury, but may result from direct trauma.
Synonym(s): Extensor tendonitis; Stenosing tenosynovitis; Stenosing tendinitis; Peritendinitis;
Styloid tenovaginitis; Stenosing tendovaginitis
Epidemiology
Usually seen in adults aged 30–50 yrs
More common in females than males
Risk Factors
Activities requiring forceful grasp with excessive ulnar wrist deviation or repetitive use of the
thumb (eg, golfing, bowling, wrestling, fly fishing, racquet sports [squash, badminton, tennis],
javelin or discus throwing)
Direct trauma with associated scarring
Also can be seen as systemic component of rheumatologic disorders such as rheumatoid
arthritis
Etiology
Repetitive or sustained tension on tendons of the 1st dorsal compartment cause an
inflammatory, then fibroblastic response.
There is thickening and swelling of the extensor tendons and retinaculum.
Pain is produced from resisted gliding of the APL and EPB tendons in the narrowed
fibroosseous canal.
Histopathology is consistent with collagen disorientation and mucoid changes (tendinosis), not
inflammation.
Diagnosis
History
Gradual onset of pain along the radial styloid of the wrist for several weeks to months
Acute onset of pain over the radial styloid after trauma
Pain is aggravated by moving the wrist or thumb.
Pain may radiate to the thumb, up the dorsoradial aspect of the forearm, or occasionally into
the shoulder.
Physical Exam
Swelling, tenderness, and/or crepitus to palpation of the APL and EPB tendons near the
radial styloid process
Positive Finkelstein test is pathognomonic and confirms the diagnosis.
To perform the Finkelstein test, the examining physician grasps the thumb of the patient and
the hand is ulnar-deviated sharply. A positive test produces sharp pain along the distal radius.
A similar test was previously described by Eichoff, in which the thumb is placed in the palm of
the hand and held with the fingers; the hand is then ulnar-deviated, causing intense pain over
the radial styloid. (This test is often confused with the Finkelstein test.)
Uncommon presentations include extensor triggering or locking of the thumb and dorsal
ganglion cyst formation.

Imaging
Usually none needed
If patient has history of trauma or other bone pathology is suspected, obtain wrist x-rays.
US and US-guided injection may help confirm the diagnosis, identify anatomical variants, and
ensure proper placement of medication, which may increase efficacy and decrease
complications and possibly recurrences.
Trigger thumb
Thumb carpometacarpal joint arthritis
Intersection syndrome
Flexor carpi radialis tendonitis
Radial styloid fracture
Scaphoid fracture
Avascular necrosis of the scaphoid
Radial neuritis
Wartenburg's syndrome
Treatment
Rest from offending activity.
Ice massage is beneficial when used early.
Corticosteroid injection is effective treatment:
Place a rolled-up towel under the wrist to position it in slight ulnar deviation.
Use a 2-mL mixture of 1/3 each: lidocaine, bupivacaine, and dexamethasone
phosphate.
Inject into the 1st dorsal compartment at the radial styloid through a 27-gauge
needle at a 45-degree angle to the skin.
Inject along the axis of the sheath.
Infiltrate the sheath from distal to proximal.
Fusiform swelling occurs in the 1st dorsal compartment if properly placed.
Pain relief is often immediate.
Patient must be cautioned against overuse following an injection.
If no improvement is seen in 2 wks, patient may have an anatomical variant with
2 tendon sheaths or a septation in the 1st dorsal compartment. In addition,
there can be multiple slips of the APL or EPB tendon. Anatomic variants may
be seen in as many as 40–60% of patients who fail injections.
Can inject again in the same manner, but redirect needle to enter both tendon
sheaths, or under US guidance to assess for anatomic variants
Consider surgical referral if 2nd injection fails.
Water-soluble corticosteroid decreases local complications, including SC
atrophy and hypopigmentation.
Medication
NSAIDs may benefit some patients.
Using a thumb spica splint may relieve pain, but there is some suggestion that
immobilization could increase recovery time.
There is little research supporting other therapeutic modalities, including
stretching, strengthening, iontophoresis, and US.
If conservative therapy is ineffective, surgical release of the fibrous 1st dorsal
compartment may be considered. Repair of the extensor retinaculum is rarely
required.
Ongoing Care
Complications
Complications of injection:
SC fat atrophy
Hypopigmentation
Pain
Neuritis
Fat necrosis
Postinjection flare
Local infection
Complications of surgery:
Radial sensory nerve injury
Incomplete decompression
Volar subluxation of the APL and EPB tendons
Additional Reading
Ilyas A, Ast M, Schaffer AA, et al. De Quervain tenosynovitis of the wrist. J
Ilyas AM. Nonsurgical treatment for de Quervain's tenosynovitis. J Hand Surg

[Am]. 2009;34:928–929.
Jeyapalan K, Choudhary S. Ultrasound-guided injection of triamcinolone and

bupivacaine in the management of de Quervain's disease. Skeletal Radiol.
2009.
Peters-Veluthamaningal C, van der Windt DA, Winters JC, et al.

Corticosteroid injection for de Quervain's tenosynovitis. Cochrane Database
Syst Rev. 2009:CD005616.
Richie CA, Briner WW. Corticosteroid injection for treatment of de Quervain's

tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam
Pract. 2003;16:102–106.
Codes
ICD9
727.04 Radial styloid tenosynovitis
Clinical Pearls
Recurrence can be prevented by changing technique when doing repetitive
wrist activities.
Why did the injection fail? Failure of injection may fail as a result of anatomic
variant. Sometimes more than one injection is necessary, even in cases
without variant.
Developmental Dysplasia of the Hip
Sunny Gupta
Basics
Developmental dysplasia of the hip (DDH) is the most common disorder of the hip in
children.
Description
Dysplasia refers to an acetabulum that is shallow or underdeveloped.
Subluxation refers to a femoral head that is not centered within the acetabulum.
Dislocation refers to a femoral head that is completely out of the acetabulum.
Teratologic dislocation refers to a femoral head that is in a fixed dislocated position usually
associated with a genetic, developmental, or neuromuscular disorder.
An unstable hip refers to a femoral head that can be subluxed or dislocated on physical
examination.
DDH refers to a wide spectrum of hip disorders from mild underdevelopment of the
acetabulum to frank teratologic dislocation of the femoral head from the acetabulum.
Epidemiology
Incidence
Incidence varies with gender, age, and race.
Incidence of hip dysplasia is 0.5–2% of live births; however, true dislocation occurs in 0.1–
0.2% of live births.
Late dysplasia, subluxation, and dislocation occur in 0.04% of children.
Risk Factors
Predominant race: More common in Caucasians of European descent; rare in African
Americans
Predominant gender: Females > Males (6:1)
Birth order: Increased risk with firstborns.
Family history: Very strong risk factor
Risk 13% with 1 parent with hip dysplasia and 35% with affected parent and sibling.
Intrauterine factors: Increased risk with breech presentation and oligohydramnios
General Prevention
There is no true way to prevent occurrence.
Early diagnosis is key to management.
Thorough examination of hips of newborns and infants is the mainstay of early diagnosis.
Etiology
Caused by any mechanism that prevents femoral head from being positioned correctly within
the acetabulum, resulting in a shallow acetabulum.
Firstborn
Intrauterine factors:
Abnormal intrauterine positioning: Breech presentation positions hip in such a way that the
femoral head is forced out of the acetabulum.
Oligohydramnios
Underlying ligamentous laxity
Collagen-vascular disorders
Infection
Environmental: Culture-associated neonatal swaddling
Congenital:
Arthrogryposis
Lumbosacral agenesis
Spina bifida
Neonatal Marfan syndrome
Fetal hydantoin syndrome
Larsen syndrome

Commonly associated with other “packaging” problems, such as torticollis (20% coexistence)
and metatarsus adductus (10% coexistence)
Diagnosis
History
Determine risk:
Breech delivery?
Female?
Firstborn?
Family history?
Race?
Is the baby moving both lower extremities symmetrically?
Any abnormal position of lower extremities noticed by parents?
Physical Exam
All infants require clinical screening by primary care provider who has experience in
examining the hip.
Examine patient in supine position.
Every attempt should be made to examine the infant when he or she is not crying to avoid
tensing of lower extremity muscles.
Observe for signs of asymmetries:
Decrease in abduction of hip with adduction contracture
Asymmetric gluteal, anterior upper thigh, and popliteal skin folds
Galeazzi sign: Apparent femoral shortening with hips and knees flexed together
Ortolani test:
Abduction and external rotation of hip with examiner's middle finger over greater trochanter
Palpable clunk is positive sign produced by reduction of dislocated hip.
Barlow test:
Adduction and internal rotation of hip
Palpable clunk is positive sign as hip dislocates.
Examination may be normal initially despite the presence of hip dysplasia. Consequently, hip
evaluation should be performed as part of neonatal physical examination through 4 mos of
age.

Lab
False-positive results: Hip clicks will be present in 10% of infants; only a small percentage
will have hip dysplasia.
Overdiagnosis is a problem because avascular necrosis of femur can occur (rarely) as a
result of therapeutic interventions.
Imaging
X-rays:
Not useful prior to 4 mos, when the femoral head epiphysis ossifies and acetabular
parameters are better defined.
Various reference lines (Hilgenreiner's, Shenton's, and Perkin's) and angles (acetabular
index) are useful to detect frank dislocation.
US:
Most sensitive and effective form of screening
Recommended to screen with US starting at age 4–6 wks in patients with risk factors,
persistent clunk on hip exam, or asymmetric hip exam.
Static and dynamic imaging (with Barlow and Ortolani maneuvers) to assess femoral head
displacement
Useful in monitoring progress of therapy
Requires experienced ultrasonographer
CT scan and MRI are not useful in diagnosis.
Treatment
Subluxation at birth often resolves spontaneously and therefore may be
observed for 3 wks.
Indication for treatment: Subluxation of hip persists beyond 3 wks, confirmed on
physical exam or US. Refer to a pediatric orthopedist.
Pavlik harness:
Indicated for infants from ages 3 wks to 6 mos
Applied by orthopedist; hips positioned in flexion and abduction
Requires weekly evaluation of straps and radiologic confirmation of hip
reduction; if hip is stable at 2 wks, reevaluation every 2 wks.
Gradually weaned as hip stability continues
Duration of treatment: 3 mos after hip stability achieved
Hip spica cast:
Indicated for children from ages 6–18 mos
Applied by orthopedist under general anesthesia; hips positioned in flexion
and abduction with cutouts for perineal care
Cast changes every 6 wks
Duration of treatment: 3–4 mos
Open reduction:
Indicated if closed reduction fails or excess abduction (>60 degrees)
required for concentric reduction
Corrects barriers to reduction, and safely increases stability
Femoral/pelvic osteotomies:
Indicated if all prior closed and open reductions fail
Usually considered in children from ages 18–36 mos
Ongoing Care
Prognosis
If diagnosed early, prognosis is uniformly excellent.
Complications
Missed early diagnosis can result in more complicated management and less
favorable outcome.
Failed reduction and redislocation
Osteonecrosis of femoral head
Hip labral pathology in adolescence or adulthood
Osteoarthritis in adulthood
Additional Reading
Beaty JH. Congenital and Developmental Anomalies of Hip and Pelvis.
Campbell's Operative Orthopaedics. 10th ed. 2003: Mosby, Inc. 1079–1117.
Bennet GC. Screening for congenital dislocation of the hip. J Bone Joint Surg
Br. 1992;74:643–644.
Cotillo JA, Molano C, Albiñana J. Correlative study between arthrograms and

surgical findings in congenital dislocation of the hip. J Pediatr Orthop B.
1998;7:62–65.
Darmonov AV, Zagora S. Clinical screening for congenital dislocation of the
hip. J Bone Joint Surg Am. 1996;78:383–388.
Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from
birth to six months. J Am Acad Orthop Surg. 2000;8:232–242.
Vitale MG, Skaggs DL. Developmental dysplasia of the hip from six months to
four years of age. J Am Acad Orthop Surg. 2001;9:401–411.
Codes
ICD9
718.75 Developmental dislocation of joint, pelvic region and thigh
754.30 Congenital dislocation of hip, unilateral
755.63 Other congenital deformity of hip (joint)
Diabetes
Russell D. White
Matthew John
Basics
Description
Group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin
secretion, insulin action, or both. This hyperglycemia produces both long-term microvascular
and macrovascular complications.
Synonym(s):
Type 1: Autoimmune diabetes; Insulin-dependent diabetes mellitus (IDDM)
Type 2: Non-insulin-dependent diabetes mellitus (NIDDM)
Epidemiology
Type 1:
5–10% of patients with diabetes
Diagnosis usually before age 30 yrs
Type 2:
90–95% of patients with diabetes
Diagnosis usually after age 40 yrs
Incidence
Most common endocrine disorder
Increasing in incidence
Estimated 23.6 million patients in U.S. (8% of the population)
Risk Factors
Type 1:
With or without family history
Frequently, the patient or a 1st-degree relative has an autoimmune disease process.
Autoantibodies often present before clinical diagnosis.
Diagnosis or exacerbation of disease during adolescence or periods of stress
Type 2:
Genetic factors:
Family history
Familial hyperlipidemia
Environmental factors:
Sedentary lifestyle
Inappropriate, calorie-laden diet
High association with insulin resistance
Gestational diabetes mellitus (GDM)
General Prevention
Primary prevention:
Exercise:
Persons with diabetes should perform at least 150 min per week of moderate-intensity
physical activity (50–70% of maximum heart rate) (1)[A].
In the absence of contraindications, persons with type 2 diabetes should be encouraged
to perform resistance training 3× per week (1)[A].
Weight loss and calorie restriction
Medical therapy
Secondary prevention:
Same as primary prevention
Treat HTN, lipids
Smoking cessation
Screen/treat retinopathy
Cardiac evaluation if indicated: Performing >4 hr/wk of moderate to vigorous aerobic
and/or resistance exercise physical activity is associated with greater cardiovascular
disease reduction than with lower volumes of activity in persons with type 2 diabetes (2)
[B].
Aspirin for prevention of myocardial infarction/stroke
Excellent foot care
Select appropriate exercise: Persons with type 2 diabetes should include resistance
exercise 3× weekly, targeting all major muscle groups and progressing to 3 sets of 8–10
repetitions at a weight that cannot be lifted more than 8–10× (8–10 RM) (2)[A].
Etiology
Type 1: Autoimmune disease characterized by antibodies against islet cells, insulin, and
enzymes
Type 2: Hepatic and peripheral insulin resistance with triad of:
Impaired insulin secretion
Increased hepatic glucose production
Decreased muscle glucose uptake

Dyslipidemia
HTN:
In patients with type 1 diabetes, HTN and any degree of albuminuria, angiotensin-
converting enzyme (ACE) inhibitors have been shown to delay the progression of
nephropathy (1)[A].
In patients with type 2 diabetes, HTN, and microalbuminuria, both ACE inhibitors and
angiotensin-receptor blockers (ARBs) have been show to delay the progression of
macroalbunimuria (1)[A].
Nephropathy
Nonproliferative/proliferative retinopathy
Neuropathies
Infections
Coronary artery disease/peripheral arterial disease
Diabetic ketoacidosis
Nonketotic hyperosmolar coma
Other autoimmune disorders associated with type 1 diabetes (eg, autoimmune thyroiditis,
vitiligo, gluten-sensitive enteropathy, etc.)
Diagnosis
Fasting plasma glucose >125 mg/dL or
Casual plasma glucose >199 mg/dL together with classic symptoms of disease or
2-hr oral glucose tolerance test glucose >199 mg/dL following 75-g glucose load
Definitive diagnosis requires any 2 of the preceding abnormal values preferably on 2
separate days or
A1C ≥6.5%
Prediabetes is defined as a blood glucose ≥100–125 mg/dL.
Medical risks of exercise:
Hypoglycemia
Hyperglycemia/ketoacidosis in insulinopenic patients
Asymptomatic coronary artery disease
Peripheral arterial disease
Exacerbation of retinopathy (weight lifting, high-altitude sports)
Foot injuries
Autonomic dysfunction (abnormal sweating mechanisms, asymptomatic heart disease or
hypoglycemia, lack of normal heart rate response to exercise, orthostatic hypotension)
Specific activities (rock climbing, SCUBA diving)
Type 1:
Metabolically unstable with classic symptoms
3 P's: Polyuria, polyphagia, polydipsia
Fatigue
Weight loss
Type 2:
Weight gain/loss
Complications often present at time of diagnosis of:
Serious infection
Pregnancy
Acute coronary syndrome (14% of patients)
Retinopathy (16%)
History
Classic symptoms: Polyuria, polydipsia, polyphagia
Unexplained weight loss and ketoacidosis (type 1)
Family history
Coexisting problem, eg, serious infection, acute coronary syndrome, pregnancy, major
trauma
Physical Exam
May be normal in mild or controlled cases
Acute signs:
Ketoacidosis
Weight loss
Volume depletion
Mental status changes
Hypotension
Abdominal pain
Chest pain
Chronic signs:
Obesity (type 2)
Diabetic retinopathy (microaneurysms, retinal hemorrhages)
Cardiac arrhythmia
Chronic infections, fever
Neurologic sensation loss to monofilament testing
Foot ulcers/infections
HTN
Microalbuminuria
Renal failure
“Stiff man” syndrome, ie, limited joint mobility

Lab
Undiagnosed/uncontrolled cases:
Elevated plasma glucose
Elevated A1C
Glycosuria, ketonuria
Microalbuminuria/proteinuria (>30 µg albumin/mg creatinine in a random spot urine collection)
Abnormal lipid profile
Acidosis/decreased HCO3-
Decreased K+ and Mg2+
Elevated blood urea nitrogen (BUN) and Na+
Imaging
Plain films, bone scan, or MRI to rule out stress fracture, Charcot foot, foreign body
MRI is the diagnostic test of choice for osteomyelitis.
Exercise testing should be considered in patients with diabetes who are considering
activity/exercise greater than the activities of daily living.
One may determine the 10-yr risk of cardiovascular disease using either of the statistical
sites below to determine the relative risk of cardiac disease. Those with a 10-yr risk of 10%
or greater should undergo exercise testing for further evaluation. Web site 1 is used for either
type 1 or type 2 diabetes; Web site 2 is used for those with type 2 diabetes.
American Diabetes Association's PHD (Personal Health Decisions):
www.diabetes.lorg/phd/profile/default.jsp
UKDPS Risk Engine: www.dtu.ox.ac.uk/index.html?maindoc%20=%20/riskengine/
Secondary causes:
Other pancreatic disease (eg, trauma, drug- or chemical-induced), genetic syndromes,
Cushing syndrome, and acromegaly
Steroid-induced
Treatment
Long-term treatment
Acute treatment
Pre-Hospital
Check for hypoglycemia, hyperglycemia, and volume depletion.
Measure glucose; administer oral glucose, SC/IM glucagon, IV glucose, and IV
fluids as indicated.
Precompetition anxiety may mimic hypoglycemia: Check glucose.
Check blood sugar before exercise:
Ideal range for type 1 athlete is 120–180 mg/dL.
If <100 mg/dL, snack before exercise (20 g carbohydrate)
If 100–250 mg/dL, exercise
If >250 mg/dL, delay exercise, check ketones, and treat hyperglycemia and
dehydration.
If >250 mg/dL with no ketones, be cautious, and check blood sugar frequently
during exercise.
Consume 15 g carbohydrate/15 min during exercise <45 min; 15 g
carbohydrate every 30 min if exercise >45 min.
Consume 1.5 g/kg carbohydrate within 30 min of exercise completion; repeat
1–2 hr later. Fine-tune management based on training history.
Delayed hypoglycemia occurs 6–28 hr after exercise. Check blood sugar 1–2×
during the night after event.
Medication
Insulin secretagogues (ie, sulfonylureas, meglitinides): Decrease dose by 50%
on exercise days.
Biguanides (ie, metformin)
Alpha-glucosidase inhibitors (ie, acarbose)
DPP-IV inhibitors (ie, sitagliptin)
Incretin mimetics (ie, exenatide, pramlintide)
P.
Insulin, SC:
Decrease rapid-acting insulin dose by 30% for <1 hr of activity, 40% for 1–2
hr, 50% for >2 hr.
Decrease intermediate-acting insulin dose by 50% prior to activity.
When exercise lasts several hours, decrease basal insulin dose by 50%
prior to activity.
Very important to monitor frequently and determine individual insulin need
according to type and duration of activity.
Avoid regular or NPH insulin if possible owing to variability in absorption.
Insulin pump therapy:
Decrease basal rate by 50% 1 hr before intense activity and for 1–2 hr
afterward.
Reduce subsequent mealtime bolus by 30–50%.
May temporarily suspend (discontinue) insulin pump therapy for 60 min for:
Water sports (SCUBA, swimming, sailing)
Contact sports (rugby, football, wrestling)
Dozen diabetic tips:
Have preexercise evaluation and exercise test, if indicated.
Always exercise with a partner.
Wear identification (Med-Alert) and have strategy for treating hypoglycemia.
Use, do not simply possess, glucose-monitoring device with exercise.
Athletes with well-controlled type 1 diabetes of <10 yrs' duration usually have
few complications.
Type 1 athletes of >10 yrs' duration often have dysregulation.
Injection sites in type 1 athletes may affect absorption rate with exercise;
certain medications in type 2 athletes may cause hypoglycemia.
Meals should be ingested 3–4 hr before exercise.
Avoid exercising during times of peak insulin activity (consider rapid-acting
insulin).
Check blood sugar before, during, and after exercise.
Be aware of delayed hypoglycemia. Replenish glycogen stores in the “golden
hour” after exercise based on duration/intensity of activity.
Each diabetic athlete must be aware of personal pattern in blood glucose
response to exercise based on training experience.
Hypoglycemia:
Admit for severe refractory hypoglycemia.
Treat volume depletion.
Administer parenteral or IV glucose, glucagon.
Glucagon is ineffective if glycogen stores are depleted.
Correct associated electrolyte abnormalities.
Nonketotic hyperglycemia:
Treat sometimes profound dehydration with isotonic crystalloid.
IV or scheduled SC insulin
Treat associated electrolyte abnormalities (ie, hypokalemia,
hypomagnesemia).
Diabetic ketoacidosis:
Treat hypovolemia with isotonic crystalloid; transition to dextrose-containing
fluid until acidosis resolves.
IV or scheduled SC insulin until acidosis resolves
Treat associated electrolyte abnormalities (ie, hypokalemia,
hypomagnesemia).
Ongoing Care
Treatment goals:
Control blood glucose:
Avoid blood glucose <70 mg/dL or >200 mg/dL.
Maintain A1C within 1% of the upper limits of normal for reference laboratory.
No severe hypoglycemia
Treat associated problems:
Strive to normalize weight.
Avoid excessive alcohol use.
Cease smoking.
Treat associated diseases:
HTN:
Maintain BP <130/80 mm Hg.
Select ACE inhibitors, ARBs, or some calcium-channel blockers (eg, amlodipine or
diltiazem) for treatment.
Avoid use of diuretics, β blockers, and verapamil in exercising persons.
Hyperlipidemia: Maintain total cholesterol <200 mg/dL. Strive for low-density lipoprotein
(LDL) cholesterol <100 mg/dL, <70 mg/dL in individuals with established cardiovascular
disease. Strive for high-density lipoprotein (HDL) cholesterol >50 mg/dL in women and >40
mg/dL in men.
Monitor/prevent macrovascular complications:
Coronary artery disease:
Common but often asymptomatic
Screen with exercise testing according to ADA/ACSM recommendations.
Use aspirin therapy in primary prevention for type 1 or type 2 patients with family history
of coronary artery disease, cigarette smoking, HTN, obesity, micro- or
macroalbuminuria, hyperlipidemia, or age >30 yrs or in secondary prevention for
diabetics with macrovascular disease.
Peripheral arterial disease
Cerebrovascular disease
Monitor/prevent microvascular complications:
Retinopathy:
Type 1 patients >10 yrs of age should have a comprehensive dilated eye exam within 3–
5 yrs of diagnosis and then yearly thereafter.
Type 2 patients should have a comprehensive dilated eye exam soon after diagnosis and
then yearly thereafter.
Avoid activities in patients with moderate nonproliferative retinopathy (power lifting,
heavy Valsalva), severe nonproliferative retinopathy (boxing, heavy competitive sports),
and proliferate retinopathy (weight lifting, jogging, high-impact aerobics, racquet sports).
Nephropathy:
Screen diabetic patients for microalbuminuria: type 1 at puberty, after 5 yrs' duration,
and then yearly thereafter; type 2 at diagnosis and yearly thereafter.
Screening can be done as either a 24-hr urine collection, timed urine collection, or spot
urine collection in the morning.
Treat nephropathy with BP control, good glycemic control, use of ACE inhibitors, and
mild protein restriction.
Neuropathy:
Annual 10-g monofilament testing
Routine foot care education
Treat special foot problems.
References
1. American Diabetes Association: Standards of Medical Care in Diabetes-2009. Diabetes
Care. 2009;32(Suppl 1):S13–S61.
2. Sigal RJ, Kenny GP, Wasserman DH, et al. Physical Activity/Exercise and Type 2
Diabetes: A consensus statement of the American Diabetes Association. Diabetes Care.
2006;29:1433–1438.
Additional Reading
American College of Sports Medicine and American Diabetes Association. Joint position
statement: diabetes mellitus and exercise. Med Sci Sports Exerc. 1997;29:i–vi.
American Diabetes Association. Diabetes mellitus and exercise. Diabetes Care. 2000;23
(Suppl 1):S50–S54.
Sigal RJ, Kenny GP, Boule N, et al. Effects of aerobic training, resistance training, or both
on glycemic control in type 2 diabetes; a randomized trial. Ann Int Med. 2007;147:357–369.
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
Clinical Pearls
Some diabetic athletes in good metabolic control can carbohydrate-load without
ill effects.
The ideal time to exercise is early morning or when in basal state (>3 hr since
last meal).
Physiologic factors that predispose to hypoglycemia include reduced fitness
level, longer exercise time, greater exercise intensity, higher insulin dosage,
insulin injection into or over exercising muscle, and massage or heat
application to area of insulin injection.
For exercise, avoid short- and intermediate-acting insulin owing to variability of
absorption from day to day in the same person. Rapid-acting insulin is
decreased by 25–75%; long-acting basal insulin is reduced in athletes with type
1 diabetes by as much as 50% with long periods of exercise (cycling, triathlons,
tournament play). Further insulin adjustments are tailored to the individual
athlete's response and are based on glucose patterns with exercise.
As type 2 patients begin training, improve physical fitness, reduce body fat, and
improve insulin resistance, the dosage of medications may be decreased.
Anaerobic exercise may cause hyperglycemia secondary to catecholamine
release. Type 1 patients who are insulinopenic may become hyperglycemic with
exercise.
The best way to determine metabolic needs is through careful testing during
training to determine the individual's metabolic response to exercise.
Insulin and insulin secretagogues (sulfonylureas and meglitinides) can cause
hypoglycemia.
Regulate an insulin pump during exercise by decreasing basal infusion rate by
50% and for 1–2 hr afterward; reduce subsequent meal-time bolus by 30–50%.
The most common error among diabetic athletes is not measuring glucose
before, during, and after exercise.
DIP Dislocation
Jason J. Stacy
Jeffrey McDaniel
Basics
Description
Dislocations of distal interphalangeal (DIP) or 1st interphalangeal (IP) joints
Mechanism is typically a hyperextension injury of the DIP joint.
Synonym(s): Jammed finger
Epidemiology
Incidence
Pure DIP dislocations are uncommon. They are usually accompanied by a bony avulsion
fracture.
Most dislocations are primarily dorsal in direction.
Volar dislocations are often associated with disruption of the terminal extensor tendon at its
insertion point, making management more difficult.
Simultaneous DIP and proximal interphalangeal (PIP) dislocations are rare, occurring most
commonly in ring and small fingers.
Diagnosis
History
Mechanism of injury (ie, hyperextension)
Presence of an obvious deformity (eg, distal phalanx positioned above or below the plane of
the middle phalanx)
Often self-reduced by the patient on the playing field
Physical Exam
Obvious deformity if not already reduced: Distal phalanx sitting above (dorsal dislocation) or
below (volar dislocation) the plane of the middle phalanx.
Careful examination: Check flexor and extensor function (with the PIP joint held in extension)
of the DIP joint and sensation at the tip of the finger.
Check collateral ligament: Place radial and ulnar stress across DIP joint with joint in full
extension and 30 degrees flexion looking for increased laxity.
Check volar plate: Increased hyperextension of the joint is indicative of a volar plate injury.

Imaging
Radiographs: 3 views preferred (anteroposterior, lateral, and oblique views)
Look carefully for any bony avulsion, especially of the volar plate.
Fracture of distal or middle phalanx
Flexor digitorum profundus (FDP) rupture (ie, jersey finger)
Extensor mechanism rupture (ie, mallet finger)
Bony mallet finger (bony avulsion of the insertion of the extensor mechanism at the dorsal
base of the distal phalanx)
Fracture-dislocation
Collateral ligament disruption
Chronic instability
Treatment
Reduction techniques:
On-field reduction should be attempted to reduce pain and usually is easily
performed when done acutely.
Technique for reduction: Maintaining proximal countertraction to the DIP joint,
apply a steady longitudinal traction force of the distal finger. Recreating the
injury initially may help in reduction.
Sometimes sweat causes slick skin, making reductions acutely difficult. Try
using a towel or gauze pad for additional grip.
Reduction may require a digital block if dislocation is prolonged or associated
with significant pain.
Postreduction evaluation: P.
Careful examination as above, especially checking neurovascular status
Postreduction radiographs from at least 2 views
Complications:
Dislocation may be irreducible. This is thought to happen for several
reasons:
Trapped volar plate
FDP entrapment behind a single condyle of P2
P2 has buttonholed through the volar plate.
Extensor tendon displacement around the head of P2
Immobilization:
Dorsal dislocations should be placed in a splint with the DIP joint in slight
flexion (20 degrees) for 1–2 wks.
Volar dislocations should be placed in a splint with the DIP joint in extension
for 8 wks, allowing the extensor tendon to heal.
Duration of immobilization depends on degree of joint stability.
When splinting, use caution with regard to the dorsal skin segment between
the extensor crease and the nail fold because pressure can cause necrosis.
Referral
A referral to an orthopedic surgeon or hand specialist should be made when
the dislocation is irreducible or an open injury has occurred with joint exposure.
In addition, chronic dislocations, FDP tendon ruptures, and unstable collateral
ligaments should be referred to a specialist.
Start range-of-motion (ROM) exercises after splint removal.
Use both active and passive ROM initially.
Start resisted ROM as soon as active and passive motions are pain-free.
Closed reduction and percutaneous pinning (CRPP): Some degree of joint
instability may require immobilization with use of a Kirschner wire for
stabilization.
Open reduction:
May be required in a chronically (>3 wks) dislocated or subluxated joint to
remove scar tissue and release tension to facilitate reduction.
Use of a Kirschner wire depends on degree of stability.
Additional Reading
Browner BD, et al. Skeletal trauma: Basic science, management, and
reconstruction, vol. 2, 3rd ed. Philadelphia: Saunders Publishing, 2003.
Bucholz RW, et al. Rockwood and Green's fractures in adults, vol. 1, 6th ed.
Philadelphia: Lippincott Williams & Wilkins, 2006.
Eiff MP, Hatch RL, Calmbach WL. Fracture management for primary care:
finger fractures. Philadelphia: WB Saunders, 1998.
Green DP, Strickland JW. Orthopaedic sports medicine: principles and

practice, the hand. Philadelphia: WB Saunders, 1994.
Palmer RE. Joint injuries of the hand in athletes. Clin Sports Med.
1998;17:513–531.
Wang QC, Johnson BA. Fingertip injuries. Am Fam Physician.

2001;63:1961–1966.
Codes
ICD9
834.02 Closed dislocation of interphalangeal (joint), hand
Clinical Pearls
Athlete can return to play immediately if dislocation is uncomplicated and
reduced and the athlete is allowed to play with a splint.
Thumb IP dislocations should be treated exactly the same as DIP dislocations.
Discoid Meniscus
Melissa Nayak
Basics
Description
Menisci are fibrocartilaginous structures that are C-shaped (axial plane) and wedge-shaped
(coronal plane).
Discoid meniscus lacks C-shaped configuration.
Completely filled in center or small void in center with thicker outer rim
Anatomic variation alters normal mechanics and predisposes to tearing.
Most common abnormal meniscal variant in children (1)
Predominantly lateral; may be medial or bilateral
May not be symptomatic until adolescence or adulthood
Watanabe classification (1,2,3)[C]:
Most widely accepted classification system
Type I (complete):
Most common
Disk-shaped thickened meniscus with thin center, complete tibial plateau coverage
Type II (incomplete): Semilunar-shaped meniscus with partial tibial plateau coverage
Type III (Wrisberg type):
Least common
Hypermobile meniscus resulting from deficient posterior tibial plateau attachments
Presence of ligament of Wrisberg (from posterior horn lateral meniscus to posterior
aspect medial femoral condyle)
Unstable and may displace
Epidemiology
Incidence
1–3% (pediatric population) (1)
Bilateral (lateral) in 10–20% of patients (1,3)
Increased incidence in Asian populations (1,3)
Up to 17% in Korean and Japanese populations (1)
Prevalence
0.4–20% in patients undergoing arthroscopy (2)
Risk Factors
Asian ancestry
Genetics
Genetic/familial transmission may play a role.
Etiology
Exact cause unknown
May be congenital anomaly or malformation
Discoid lateral menisci:
Thicker, poorer vascularity
Some have unstable peripheral attachments (Wrisberg type) and thus increased
susceptibility to tearing.

Associated meniscal tears (70% of time; incidence increases with age) (4)
Osteochondritis dissecans, lateral femoral condyle
High fibular head
Hypoplasia of lateral femoral condyle
Hypoplasia of tibial spines
Abnormal shape of lateral malleolus
Enlarged inferior lateral geniculate artery
Diagnosis
History
Patients may be asymptomatic.
Signs and symptoms (in absence of trauma) include:
Pain
Clunking
Giving way
Popping
Snapping
Swelling
Locking
Decreased knee extension
Physical Exam
Palpable click near complete extension
Quadriceps atrophy
Lack of full extension
Joint-line tenderness
Effusion less common
Positive McMurray test (with associated meniscal tears)

Imaging
Radiographs (weight-bearing AP, lateral, tunnel, and Merchant views):
May be normal
Widened lateral joint space
Squared off appearance of lateral femoral condyle
Cupping of lateral tibial plateau
Flattening of tibial eminence
MRI:
Test of choice
May not show abnormal signal intensity
Lateral meniscal height greater than medial, with high intrameniscal signal
Abnormal thickened “bow tie” appearance of meniscus
Meniscal tear
Popliteus tendinitis
Osteochondritis dissecans
Loose body
Any condition that causes a “snapping” knee:
Subluxation or dislocation of patellofemoral joint
Snapping of tendons around knee
Congenital subluxation of tibiofemoral joint
Subluxation/dislocation of proximal tibiofemoral joint
Meniscal cyst
Treatment
No treatment or surgical indications for asymptomatic patients
Referral
Orthopedic surgical consultation is indicated in patients still symptomatic after
conservative measures.
Goal is meniscal preservation (2,3)[C].
Arthroscopic partial meniscectomy with saucerization (reshape meniscus) and
repair of unstable or detached peripheral attachments to the capsule
Arthroscopic total meniscectomy not recommended owing to complication of
osteoarthrosis; reserved for large or complex tears not amenable to
saucerization or repair.
Ongoing Care
Postoperative physical therapy for knee range of motion, quadriceps strengthening,
hamstring stretching, and gait training
Patient Education
Asymptomatic discoid meniscus needs no treatment.
Surgery is recommended if mechanical symptoms present: Pain, locking, swelling, giving
way, functional limitations, inability to participate in sports.
Prognosis
Good prognosis when asymptomatic
Poorer prognosis when osteochondritis dissecans present
Complications
Osteochondritis dissecans of lateral femoral condyle
Postoperative complications:
Recurrence of meniscal instability
Cartilage remains thickened and more susceptible to developing tear.
Scuffing of articular surface
Osteoarthrosis
References
1. Hart ES, Kalra KP, Grottkau BE, et al. Discoid lateral meniscus in children.
Orthop Nurs. 2008;27: 174–179.
2. Good CR, Green DW, Griffith MH, et al. Arthroscopic treatment of

symptomatic discoid meniscus in children: classification, technique, and
results. Arthroscopy. 2007;23:157–163.e1.
3. Yaniv M, Blumberg N. The discoid meniscus. J Child Orthop. 2007;1:89–

96.
4. http://www.posna.org/education/StudyGuide/DiscoidMeniscus.asp
Codes
ICD9
717.5 Derangement of meniscus, not elsewhere classified
Dislocation, Hip, Posterior
Greg Nakamoto
Basics
Description
Hip dislocations can be classified into congenital and traumatic (1):
Congenital hip dislocations occur in 2–4 cases per 1,000 live births.
80–85% of congenital dislocations occur in girls.
Congenital hip dislocations are commonly the result of femoral head or acetabular
dysplasia.
The remainder of this topic is dedicated to the evaluation and management of traumatic
(posterior) hip dislocations:
Posterior hip dislocation is an orthopedic emergency in which the femoral head is displaced
posteriorly relative to the acetabulum.
Of primary concern when evaluating the patient with a posterior hip dislocation is the
attainment of early reduction (within 6 hr) to prevent long-term sequelae and the search for
additional injuries (often life- or limb-threatening due to the excessive forces necessary to
create this injury).
In the case of posterior dislocation without fracture, the experienced physician may
perform 1 attempt at closed reduction. If reduction is not accomplished with ease, or if
there is an associated fracture of the hip, then emergent orthopedic consultation is
warranted.
Epidemiology
Because of the forces required for this injury, it is relatively uncommon in contact sports.
Seen more often in high-energy trauma, such as with motor sports, equestrian events, and
high-speed mountain sports.
Posterior dislocations account for 90% of all hip dislocations.
More common in young males because these injuries are associated with risk-taking behavior
(1)
Age (1):
Trauma (such as motor vehicle accident) is a more common cause in patients younger than
35 yrs than in older patients.
Falls are a more common cause in those older than 65 yrs than in younger patients.
Risk Factors
High-energy trauma
Mechanism is forced adduction, internal rotation, and some degree of flexion of the hip (2).
Most common cause is knee striking the dashboard in a head-on motor vehicle accident:
Depending on the position of the hip, this can result in either anterior or posterior
dislocation.
This mechanism of injury is associated with an incidence of simultaneous severe knee injury
in 26% of patients (including patellar fracture in 4%) (2).
In athletic competition, low-energy mechanisms of injury include a forward fall onto the knee
with a flexed hip or a blow from behind while down on all 4 limbs (3).

Life-threatening internal organ damage, bleeding, and shock
Ipsilateral sciatic nerve injured in 10–14% of cases; changes a posterior hip dislocation from
an orthopedic urgency to a true surgical emergency
Irreducible dislocations occur in up to 16% of simple posterior dislocations.
Fractures of the pelvis, acetabulum, femoral head, neck, and shaft:
81% of adult posterior hip dislocations have an associated posterior acetabular fracture
(2).
Ligamentous injury to the ipsilateral knee is not uncommon when the mechanism of injury
involves a blow to the anterior knee.
Delayed reduction increases risk of avascular necrosis (AVN).
Other chronic complications include recurrent posterior dislocation, post-traumatic arthritis,
and heterotopic bone formation (myositis ossificans) of the thigh or buttocks.
Diagnosis
History
Mechanism? Can help guide the search for associated visceral and orthopedic injuries.
Position at time of injury? Simple posterior dislocation most commonly occurs with force on a
flexed knee with the hip in varying degrees of flexion and adduction. Addition of hip abduction
increases the risk of associated acetabular fracture or anterior dislocation.
Physical Exam
Immediate, severe pain and disability
Limb shortening with hip flexion, internal rotation, and adduction
Classic position may be absent if there is an associated femoral shaft fracture.
Vital signs and complete trauma evaluation essential because of the high association with life-
threatening injuries
Look for classic presenting position as described above. Femoral head may be palpable in
the buttocks.
Pelvic rocking and pubic compression tests to examine for associated pelvic rim fractures
Distal neurovascular examination to assess for sciatic nerve or vascular injures, which merit
more urgent reduction

Lab
Laboratories are ordered as needed on the basis of the trauma assessment and for
preoperative planning.
Type and cross of blood products may be necessary.
Imaging
Initial x-rays: Anteroposterior (AP) and lateral views of the pelvis (4)[A]. AP often reveals the
dislocation, but a true lateral may be needed to confirm the direction.
Search for associated pelvic rim, acetabular, femoral head, neck, and shaft fractures
generally merits additional x-rays, including 3/4 internal and external obliques of the pelvis as
well as femur films.
Of particular importance is the ruling out of femoral neck fractures before reduction
procedures are performed (3).
Anterior dislocation of the hip
Combined fracture-dislocation
Fracture of the pelvis, acetabulum, or femur
Traumatic hip subluxation
Hip pointer
GI or genitoureteral visceral injury
Treatment
Pre-Hospital
Patients suffering a high-energy trauma sufficient to cause hip dislocation
commonly have associated injuries that take precedence for overall patient
stabilization. Attempts to reduce the dislocation in the field are ill advised (1):
Establish ABCs with appropriate spinal stabilization.
If the hip dislocation is detected in the field, the patient should be placed on a
backboard and allowed to assume the leg position of maximal comfort (ie, hip
slightly flexed with leg adducted).
Transport to a center with trauma care appropriate to patient's overall clinical
status.
One might consider attempt at early reductions in the field if significant
transport time will occur (eg, wilderness or backcountry situations) (5)[C].
ED Treatment
Initial management focuses on achieving rapid reduction of the dislocation. A
2nd phase of management focuses on performing definitive care (3).
Will often require IV analgesics, muscle relaxants, and/or sedation to
overcome severe pain and muscular spasm before closed reduction can be
attempted
May require spinal or general anesthesia to achieve closed reduction
Simple posterior dislocation without fracture should be reduced by closed
reduction as early as possible, as reduction under 6 hr reduces the rate of
AVN (3,6)[A].
Some authors advise orthopedic consultation for any dislocated hip and that
the orthopedist should be present when attempting closed reduction (5)[C].
For the experienced treating physician, 1 attempt at reduction of a simple
dislocation might be reasonable. However, urgent orthopedic consultation
should be obtained for simple dislocations that are not easily reducible with 1
attempt, as multiple attempts at closed reduction are also associated with
poorer outcomes (6)[A].
Fracture-dislocations or dislocations with associated sciatic nerve injury also
merit urgent orthopedic consultation.
Numerous methods of reduction have been described, with no one method
having been proven superior. 3 of the more common methods include:
Allis method: An assistant stabilizes the pelvis of the supine patient with
downward pressure on the anterior superior iliac spine. The operator applies
axial traction in line with the deformity by pulling with his or her hands from
behind the flexed knee. While maintaining this traction, the hip is gently flexed
to 90° and then gently internally and externally rotated until reduction occurs.
Requires 2 operators (1,6,7,8).
Stimson method: Patient placed prone, with affected hip hanging down over
edge of bed. Downward traction is applied to the leg while an assistant
applies stabilizing pressure to the pelvis. Requires 2 operators; might be
difficult to move multiply injured patient into proper position and difficult to
monitor the airway in the prone position (1,6,7,8).
Whistler method: Patient supine with unaffected knee flexed to 120° such
that the unaffected foot is placed firmly on the bed. Standing on the affected
side, the operator reaches his hand under the affected knee and places his
hand onto the unaffected flexed knee. By straightening his arm and lifting his
shoulder, the operator adducts the patient's leg and applies traction until the
hip reduces. Requires only 1 operator and airway easily monitored in supine
position (1,8).
If closed reduction cannot be accomplished, the dislocated hip should be held
in a position of relative extension with the ipsilateral knee in flexion until open
reduction can be performed. This position puts the least strain on the sciatic
nerve (2)[C].
P.
Postoperatively, repeat neurovascular examination of the injured limb
Repeat AP and lateral x-rays immediately (4).
CT scan with fine cuts (2–3 mm) through the hips:
To evaluate for presence of osteochondral or intra-articular fragments,
femoral head injuries, and acetabular fractures (any of which might make the
reduction unstable)
Essential in assigning proper classification of posterior fracture-dislocations
of the hip, which in turn determines optimal treatment
CT scan should be part of the standard postreduction evaluation of a
traumatic posterior hip dislocation (3,4,7)[A].
MRI may aid in the diagnosis of labral injuries, femoral head
contusions/microfractures, sciatic nerve injury, and intra-articular fragments (3)
[C].
After successful closed reduction, immobilize in slight abduction (pad between
legs) to prevent adduction until further orthopedic evaluation is completed and
traction instituted (1).
After initial reduction, further orthopedic examination and radiographic
evaluation as above helps determine presence of coexisting fractures, other
injuries, and the likelihood of stability with the current reduction.
Patients with stable, concentric reductions without associated significant
fractures may be treated nonoperatively (6,7)[A].
Patients with unstable reductions, displaced fractures, or acetabular fractures
that would likely compromise stability are generally treated operatively (6,7)[A].
General Measures
Dislocation of the prosthetic hip is a special concern (1)[C]:
Hip prostheses can deteriorate over time and consequently dislocate with
minimal force (eg, crossing of legs, standing up).
Prosthesis is most susceptible to dislocation at 3–4 mos after initial surgery.
Reduction of a prosthetic hip dislocation is less urgent than for a native hip if
neurovascular status is intact:
Concern for AVN or osteoarthritis is nonexistent.
Reduction is accomplished with same maneuvers as for native hip:
However, less force is used so as to avoid iatrogenic fracture.
Given this injury often occurs in the setting of high-energy trauma, orthopedic
evaluation usually occurs in conjunction with the initial trauma evaluation.
In the case of pure dislocations without other trauma, as sometimes occurs
with a low-energy mechanism, a single attempt at reduction may be attempted if
orthopedic consultation is delayed. However, urgent orthopedic referral should
be made for any patient in whom closed reduction does not result in easy
reduction, as reduction in <6 hr is the goal to reduce the risk of AVN, and
multiple attempts at reduction results in poorer long-term outcomes. More
urgent reduction is needed if there is associated neurovascular compromise.
Postreduction, orthopedic, and radiographic evaluations as above are needed
to guide surgical decision making.
Indications for open reduction include (1)[A]:
Irreducible dislocation ( 10% of all dislocations)
Persistent instability following closed reduction (eg, fracture-dislocation of the
posterior acetabulum)
Fracture of the femoral head or shaft
Neurovascular deficits that occur after closed reduction
Ongoing Care
Given the high-energy mechanism of injury, most patients require
admission, often to a trauma service, for continued evaluation and treatment of
associated injuries.
The duration of traction and nonweight-bearing immobilization is controversial
(1)[C]:
Evidence suggests early weight-bearing (eg, 2 wks after reduction) may
increase severity of AVN in patients at risk.
However, early weight-bearing decreases the incidence of other
complications (eg, venous thromboembolism, decubiti)
P.
Physical therapy as directed by the orthopedist often starts with range-of-
motion exercises while the patient is still in traction, and continues to include
muscle rehabilitation and strengthening once out of traction.
Consider MRI at wk 6 to assess for signs of AVN (5)[C]:
If evidence of AVN, keep patient partial weight-bearing and return to range-
of-motion exercises only.
If no evidence of AVN, the patient may continue to progress through therapy.
Complications
Complication rate increases directly with time elapsed before relocation.
Up to 50% of patients will have limited use or chronic pain as a result of hip
dislocation (1).
The main complications are AVN, osteoarthritis, and heterotopic bone
formation (8):
Risk of avascular necrosis is the reason that traumatic posterior hip
dislocations represent an orthopedic emergency.
Incidence of AVN is between 6% and 27% in timely reductions, and up to
48% in delayed reductions (2).
Sciatic neurapraxia occurs in up to 5% of pediatric dislocations and 10–15%
of adult dislocations. Symptoms partially or entirely resolve in 60–70% of
cases (2):
New neurologic deficits that occur postreduction warrant immediate
surgical intervention. Hence, the importance of a complete neurovascular
exam before and after reduction (5)[C].
References
1. Tham E, Doty C. Dislocation, hip. 2008. eMedicine. Retrieved Aug 10,
2009 from http://emedicine.medscape.com/article/823471-overview
2. Davenport M. Joint reduction, hip dislocation, posterior. eMedicine.

2009. Retrieved Aug 10, 2009, from
http://emedicine.medscape.com/article/109225-overview
3. Shindle MK, Ranawat AS, Kelly BT. Diagnosis and management of

traumatic and atraumatic hip instability in the athletic patient. Clin Sports
Med. 2006;25:309–326, ix–x.
4. Brooks RA, Ribbans WJ. Diagnosis and imaging studies of traumatic hip
dislocations in the adult. Clin Orthop Relat Res. 2000;337:15–23.
5. Gammons M. Hip dislocation. eMedicine. 2009. Retrieved Aug 10, 2009,

from http://emedicine.medscape.com/article/86930-overview
6. Yang EC, Cornwall R. Initial treatment of traumatic hip dislocations in the

adult. Clin Orthop Relat Res. 2000;337:24–31.
7. Alonso JE, Volgas DA, Giordano V, et al. A review of the treatment of hip
dislocations associated with acetabular fractures. Clin Orthop Relat Res.
2000;337:32–43.
8. Newton EJ, Love J. Emergency department management of selected

orthopedic injuries. Emerg Med Clin North Am. 2007;25:763–793, ix–x.
Additional Reading
Kum CK, Tan SK. Traumatic posterior dislocation of the hip—a local
experience and review of the literature. Singapore Med J. 1990;31:22–25.
Rockwood C, Green D, Bucholz R, et al., eds. Rockwood and Green's

fractures in adults, 4th ed. Philadelphia: Lippincott-Raven Publishers, 1996.
Schlickewei W, Elsässer B, Mullaji AB, et al. Hip dislocation without

fracture: traction or mobilization after reduction? Injury. 1993;24:27–31.
Codes
ICD9
835.01 Closed posterior dislocation of hip
835.11 Open posterior dislocation of hip
Clinical Pearls
Of primary concern when evaluating the patient with a posterior hip dislocation
is the attainment of early reduction (within 6 hr) to prevent long-term sequelae
and the search for additional injuries (often life- or limb-threatening due to the
excessive forces necessary to create this injury).
In the case of posterior dislocation without fracture, the experienced physician
may perform 1 attempt at closed reduction. If reduction is not accomplished
with ease, or if there is an associated fracture of the hip, then emergent
orthopedic consultation is warranted.
Postreduction, orthopedic and radiographic evaluations are needed to guide
surgical decision making. CT scan should be part of the standard postreduction
evaluation.
In an isolated posterior dislocation without fracture treated with closed
reduction within 6 hr of injury, the managing orthopedist might allow the patient
to start weight-bearing as soon as comfort allows. This may be as early as 2
wks after injury.
Whereas a significant delay between dislocation and reduction may increase
the risk of AVN, the overall long-term prognosis is most dependent on the
severity of the initial trauma.
Distal Clavicular Osteolysis
Ryan C. Fowler
Keith A. Stuessi
Basics
Description
A loss of subchondral bone detail with osteoporosis, cystic changes, osteolysis, and
osteophyte formation of the distal clavicle while sparing the acromion
Most commonly associated with atraumatic mechanism but can be trauma-related
Epidemiology
Incidence
True incidence of distal clavicular osteolysis (DCO) is unknown.
Associated with repetitive heavy lifting and occasionally as a result of trauma
Rare reports of idiopathic cases (1)
Risk Factors
Any activity putting excessive repetitive force on the acromioclavicular (AC) joint may
increase risk.
Weight lifting appears to be a significant risk factor in nontraumatic cases (2,3).
Occasionally will result from blunt trauma to the shoulder
Traumatic injuries include AC joint dislocation and separation, as well as clavicle fractures.
General Prevention
Atraumatic causes are potentially prevented by limiting repetitive lifting, but no studies
address this issue.
Athletes generally are reluctant to decrease training.
Etiology
Although the specific pathophysiologic cause has not been determined, atraumatic osteolysis
is thought to start as a stress fracture of the distal clavicle from repetitive microtrauma (2,4).
Common MRI findings include bone edema and evidence of subchondral injury (2,4).
The pathophysiologic process in traumatic injuries is unknown.
Diagnosis
History
Insidious onset of aching in the AC joint
Athletes may have a history of remote trauma.
Activities placing repetitive stress to the joint may increase the risk.
In weight lifters, bench press, military press, shoulder shrugs, pushups, and clean-and-jerk
may cause pain.
Physical Exam
Signs and symptoms:
Patient complains of a dull ache over the AC joint.
Mild swelling of the joint may be present.
Pain usually is worse at the beginning of the exercise period.
Any movement of the arm requiring 90 degrees or more of abduction causes pain.
Pain can radiate to the adjacent superior trapezius border and deltoid muscles.
Physical examination:
Tenderness over the AC joint
Positive cross-arm test: Forward flexion to 90 degrees and adduction of the arm cause
pain. This compresses the AC joint.
Paxinos test: Arm at side resting against chest and hand over top of shoulder; thumb on
acromion and fingers on clavicle and compressing them together; pain is a positive test.
Sometimes a trapezius spasm will be palpated.
Because it is common to have other shoulder pathology in conjunction with DCO, a local
anesthetic injection to the AC joint can be helpful in achieving an accurate diagnosis (2)[C].

Imaging
Clavicular or Zanca view: 10 degrees of cephalic tilt; distal clavicular end will appear frayed;
will see bony osteolysis, cystic changes, and translucency of the bone. Bilateral Zanca views
are helpful in comparing the involved and uninvolved sides.
Technetium bone scan can be helpful as an additional test.
MRI can be used to rule out other pathology and often shows bone edema in the distal
clavicle (4)[C].
Diagnostic injection into the AC joint with local anesthetic can be helpful in differentiating the
cause of pain (2,5)[C].
AC joint trauma, osteoarthritis
Other shoulder pathology should be considered (eg, instability, impingement, rotator cuff
tears, tendinitis, and labral disease).
Also includes hyperparathyroidism, rheumatoid arthritis, multiple myeloma, scleroderma,
infection (septic arthritis, tuberculosis), rickets, eosinophilic granuloma, and other, more rare
diseases including cleidocranial dysplasia, progeria, and pycnodysostosis.
Treatment
Acute treatment:
NSAIDs or other pain medications can be used as needed (2,5)[C].
Cessation of activity is often very effective in reducing pain (2,5)[C].
Therapeutic corticosteroid injection to the AC joint is often effective at
reducing painful symptoms (2,5)[C].
Other symptomatic treatment such as ice can be helpful (2,5)[C].
Activity modification (2,5)[C]
Often difficult in athletes
Activity modification by weight lifters should include decreased weight with
increased repetitions or substitution of exercises.
Physical therapy should be instituted if there is evidence of other shoulder
pathology. Rehabilitation also should include range-of-motion (ROM) therapy
and strengthening exercises for the rotator cuff and scapulothoracic
stabilizer muscles (5)[C].
Surgical resection may be considered for those not responding to
conservative therapy.
Surgery is recommended for those who fail conservative treatment (2,5)[C].
Surgery may be performed open or arthroscopic.
Arthroscopic surgery involves less tissue dissection and faster rehabilitation
times (2)[C].
Arthroscopic surgery can be completed directly through the AC joint or
indirectly through the subacromial space. The direct approach allows faster
return to activity (21 vs 42 days) (6)[B].
Ongoing Care
Referral to an orthopedic surgeon for failure of conservative treatment
Postoperative physical therapy:
Active ROM as tolerated
Shoulder strengthening
Return to sports as soon as symptoms allow; time frame depends on surgical approach.
References
1. Hawkins BJ, Covey DC, Thiel BG. Distal clavicle osteolysis unrelated to trauma, overuse,
or metabolic disease. Clin Orthop Relat Res. 2000;370:208–211.
2. Schwarzkopf R, Ishak C, Elman M, et al. Distal clavicular osteolysis—a review of the

literature. Bull NYU Hosp Jt Dis. 2008;66:94–101.
3. Scavenius M, Iversen BF. Nontraumatic clavicular osteolysis in weight lifters. Am J Sports

Med. 1992;20:463–467.
4. Kassarjian A, Llopis E, Palmer WE. Distal clavicular osteolysis: MR evidence for

subchondral fracture. Skeletal Radiol. 2006.
5. Rios CG, et al. Acromioclavicular joint problems in athletes and new methods of
management. Clin Sports Med. 2008;27:763.
6. Charron KM, Schepsis AA, Voloshin I. Arthroscopic distal clavicle resection in athletes: a
prospective comparison of the direct and indirect approach. Am J Sports Med. 2006.
Codes
ICD9
No specific ICD-9 code
716.91 Shoulder arthritis
810.03 Closed fracture of acromial end of clavicle
840.9 Shoulder sprain
Clinical Pearls
Can resolve without surgery, but only a minority of cases produce satisfactory
results, particularly when the athlete does not stop training long enough for the
AC joint to heal.
Athletes can return to their former level of competition after surgical resection.
Dupuytren's Contracture
Thomas Trojian
Basics
Description
Contracture of the palmar fascia owing to fibrous proliferation and resulting in flexion
deformities and loss of function. Similar changes rarely may occur in plantar fascia.
Dupuytren contracture (DC) usually appears simultaneously.
Genetics:
Autosomal dominant with variable penetrance
10% of patients have a positive family history.
System(s) affected: Musculoskeletal
Abbreviations: MP = metacarpophalangeal; PIP = proximal interphalangeal
Epidemiology
Incidence
Predominant age: 50 yrs for males; 60 yrs for females
Predominant gender: Male = Female (ranges from 2:1 to 10:1)
Prevalence
Prevalence is about 306/100,000.
Disease prevalence varies from 2–42% depending on population and risk factors.
Overall prevalence is 8.8% in Northern European population.
African Americans are less likely to get the disease.
Japanese and Taiwanese have a prevalence equal to that in Northern Europe. These patients
usually present with a less severe form of the disease.
Risk Factors
Smoking (mean 16 pack-years; odds ratio = 2.8)
Alcohol intake
Both alcohol and cigarette use has a higher risk than individual use.
Increasing age (>40 yrs of age)
Male (increase in androgen receptors in nodules)
Northern European, Japanese, Taiwanese
Diabetes mellitus (1/3 affected, increases with time, usually mild; middle and ring fingers
involved)
Epilepsy (may be medication or disease)
HIV infection (may or may not be associated)
Vibration work exposure (Some studies show increased risk, and other studies show no risk.)
Rheumatoid arthritis (lower risk)
Genetics
Autosomal dominant with variable penetrance; in one family, the gene has been mapped to
chromosome 16q.
>30 unique genes were upregulated, and 6 unique genes were downregulated by 4-fold or
greater.
Upregulated genes include ones that code for fibronectin, tenascin C, transforming growth
factor β2 (TGF-β2), collagen III, collagen IV, and collagen VI.
All 3 forms of TGF-β are upregulated. TGF-β2 is upregulated 10–20 times. As in
tendinopathy, it may be a TGF receptor lack of response, so TGF continues to be made.
Musculoaponeurotic fibrosarcoma oncogene homologue B, or MafB, in the family of
oncogenes is found in the cord but not paracord fascia of normal control individuals.
General Prevention
None known; avoid risk factors when possible.
Etiology
Unknown
Ischemia to the fascia with oxygen free-radical formation
Possibly related to release of angiogenic basic fibroblast growth factor
Related to microhemorrhage and release of growth factors

Alcoholism
Smoking
Epilepsy
Diabetes mellitus
Occupational hand trauma (vibration white finger)
Diagnosis
Physical Exam
Signs and symptoms:
Typical:
Caucasian male aged 50–60 yrs
Bilateral with one hand more involved
Family history
Unilateral or bilateral (50%)
Right hand more frequent
Ring finger more frequent
Ulnar digits more affected than radial
Mild pain early
Later painless plaques or nodules in palmar fascia
Extends into a cordlike band in the palmar fascia
Skin adheres to fascia and becomes puckered.
Nodules can be palpated under the skin.
Digital fascia becomes involved as disease progresses.
Web space contractures
Dupuytren diathesis can involve plantar (Ledderhose 10%) and penile (Peyronie 2%)
fascia.
Knuckle pads
Atypical:
No age, gender differences
No family history
May have systemic disease (see “Risk Factors”)
May have a history of trauma
More common unilateral
No ectopic manifestations (Ledderhose or Peyronie)
Nonprogressive
A firm nodule in the palm of the hand proximal to the metacarpophalangeal (MCP) joint
Hueston tabletop test
Test is positive if patient is unable to flatten his or her hand on the table.

Lab
Drugs that may alter lab results: N/A
Disorders that may alter lab results: N/A
Imaging
Not needed except in rare cases
US can be used in diagnosis.
MRI can assess cellularity of lesions, which correlate with higher recurrence after surgery.
Rarely is a biopsy needed to differentiate Dupuytren nodule from a soft tissue tumor.
Myofibroblasts
1st stage (proliferative): Increased myofibroblasts
2nd stage (residual): Dense fibroblast network
3rd stage (involutional): Myofibroblasts disappear.
Callus formation
Nodule on flexor tendon
Camptodactyly—early teens tight facial bands ulnar side of small finger
Soft tissue tumor
Treatment
10% of patients will have disease regression without treatment.
Intralesional steroid injection (triamcinolone) has been shown to reduce the
need for surgery.
Although surgical intervention has been shown to be very helpful in cases of
advanced DC, there are inherent risks to surgery, such as nerve injury,
hematoma, skin necrosis, and infection.
Although partial fasciectomy has long been the mainstay of treatment for
patients with advanced DC, office procedures such as percutaneous needle
aponeurotomy and collagenase injections may represent alternatives to
surgery in certain patients.
Whatever the method selected to treat the contracture, each technique carries
with it a significant risk of recurrence.
Medication
First Line
Steroid injection (triamcinolone) for an acute tender nodule, painful knuckle pad
Second Line
Radiation therapy, 5-fluorouracil, and hyperbaric oxygen have been used.
General Measures
Steroid injection for acute tender nodule
Physiotherapy is ineffective alone.
Isolated involvement of palmar fascia can be followed.
MCP joint involvement can be followed if flexion contracture is 30 degrees.
Collagenase injections to the nodules and cords under US guidance may be
approved for use. Phase III clinical trials have been completed.
Surgery: Partial fasciectomy:
Surgical referral should be made when MCP joint contractures reach 30
degrees or any degree of PIP joint contracture develops.
May require skin grafts for wound closure with severe cutaneous shrinkage
80% have full range of movement if operated on early.
Continuous elongation technique is useful to prepare a severely contracted
PIP joint for surgery. The digit frequently can be completely extended but will
relapse if surgery is not performed.
Amputation of little finger, if severe and deforming (rare)
Needle aponeurotomy (NA), also called percutaneous needle fasciotomy
(PNF), is a minimal invasive technique.
Done under local anaesthetic
Type I DC
Done through the skin usually blind with 18-gauge or special tool
US may be beneficial.
Recurrence rates can be high, but recovery is faster and procedure is
inexpensive.
Ongoing Care
No activity restrictions
Physical therapy after surgery: Started 3–5 days after surgery (passive and active exercises,
posterior dynamic extension splints)
Patient Monitoring
Follow patient in early stages of disease.
Diet
No special diet
Patient Education
Avoid risk factors, especially with a strong family history.
Regular follow-up by physician every 6 mos to 1 yr
Prognosis
Typical:
Unpredictable but usually slowly progressive
Patients likely to have aggressive disease (one or more): age 40 at onset, knuckle pads,
positive family history, bilateral disease involving radial side of hand
Reports of clinical regression with continuous passive skeletal traction in extension and
under a skin graft
Recurrence rate after surgery is 10–34%.
Prognosis better for MCP joint vs PIP joint after surgery.
Atypical:
Nonprogressive
Surgery rarely needed
Recurrence unlikely if surgery performed
Complications
Postoperative stiffness (common)
Postoperative recurrence or extension 46–80% (common)
Postoperative development of reflex sympathetic dystrophy (uncommon)
Postoperative hematoma or infection (rare)
Intraoperative neurovascular injury (rare)
Digital infarction (rare)
Additional Reading
Rayan GM. Dupuytren's disease: anatomy, pathology, presentation, and
treatment. Instr Course Lect. 2007;56:101–111.
Burke FD, Proud G, Lawson IJ, et al. An assessment of the effects of

exposure to vibration, smoking, alcohol and diabetes on the prevalence of
dupuytren's disease in 97,537 miners. J Hand Surg Eur Vol. 2007;32:400–
406.
Hueston J. Dupuytren's contracture. J Hand Surg [Br]. 1993;18:806.
Rayan GM. Dupuytren's disease: anatomy, pathology, presentation, and

treatment. Instr Course Lect. 2007;56:101–111.
Saboeiro AP, Porkorny JJ, Shehadi SI, et al. Racial distribution of Dupuytren's
disease in Department of Veterans Affairs patients. Plast Reconstr Surg.
2000;106:71–75.
Shaw RB, Chong AK, Zhang A, et al. Dupuytren's disease: history, diagnosis,
and treatment. Plast Reconstr Surg. 2007;120:44e–54e.
Thurston AJ. Dupuytren's disease. J Bone Joint Surg Br. 2003;85:469–477.
Trojian TH, Chu SM. Dupuytren's disease: diagnosis and treatment. Am Fam
Physician. 2007;76:86–89.
Codes
ICD9
728.6 Contracture of palmar fascia
Clinical Pearls
DC is an inherited disease of progressive fibrous tissue contracture of the
palmar fascia.
The disease predominantly affects males of Northern European decent over
the age of 40 yrs who are smokers, alcohol drinkers, or diabetics.
Patients present with a small lump or multiple lumps with pits in the palm of the
hand progressing to contractures of the fingers.
Intralesional steroid injections have been shown to reduce the need for
surgery.
Surgical referral should be made when MCP joint contractures reach 30
degrees or if any degree of PIP joint contracture is present.
Surgery usually is done in advanced disease in order to restore function to the
hand.
Percutaneous needle aponeurotomy and the emerging therapy of collagenase
injections are significant therapeutic alternatives to surgery.
Eating Disorders
Kelsey Logan
Basics
There are 3 diagnosable eating disorders (EDs) under the American Psychiatric
Association DSM IV criteria: Anorexia nervosa (AN), bulimia nervosa (BN), and eating
disorder not specified (EDNOS).
Disordered eating is a spectrum of behaviors that focus on controlling eating and weight.
Athletes often do not meet the stringent criteria for ED diagnosis but have disordered eating
nonetheless.
Description
Diagnostic criteria (DSM-IV and DSM IV-TR) (1):
AN:
Weight <85% of normal for age and height, either due to loss or by failure to gain
Intense fear of gaining weight even though patient is underweight
Body image disturbance and/or denial of seriousness of current low-weight status
Secondary amenorrhea (missing at least 3 consecutive menstrual cycles in a woman with
established menses)
2 types:
Restricting type: Mainly restricts intake to achieve weight loss; does not regularly
engage in binge eating or purging behavior
Binge-eating/purging type: Regularly uses binge eating/purging to lose weight
BN:
Recurrent episodes of binge eating, with binge eating defined as:
Eating an amount of food in a discrete time period (eg, 2 hr) that would be larger than
most people would eat and
Feeling unable to stop eating or control the amount of food eaten during this time
Consistently uses abnormal compensatory behavior to prevent weight gain (eg, self-
induced vomiting, laxative or enema misuse, diuretics, fasting, excessive exercise)
Binge eating and compensatory behaviors occur at least twice weekly for 3 mos (on
average).
Body image disturbance
The disturbance does not occur exclusively during episodes of AN.
2 types:
Purging type: Regularly uses self-induced vomiting, laxatives, diuretics, and/or enemas in
the current episode of illness
Nonpurging type: Uses behaviors other than purging during the episode of illness, such
as fasting or excessive exercise
EDNOS:
Disorders that do not meet the full criteria for AN or BN
Includes binge-eating disorder: Similar to bulimia except that individuals do not perform
compensatory behaviors to avoid weight gain; these individuals are more likely to be
overweight.
Epidemiology
Some research has shown an increased prevalence in athletes compared with nonathletes.
Prevalence is higher in female athletes than their male counterparts.
In adolescent girls, AN is the 3rd most common chronic illness.
Undiagnosed in 50% of cases, so true impact is unknown
Prevalence
Studies have shown that up to 47% of female athletes have diagnosable ED, depending on
sport (2).
Studies have found that 0–5% of male athletes have diagnosable ED.
Particularly in males, seasonal disordered eating practices may be present in over 50% of
athletes.
AN is present in 0.5–1% of older adolescent or adult women; 1–2% of this general population
meets the criteria for BN.
Males account for 5–15% of patients with AN or BN and 35% of those with binge eating
disorder in the general population.
Risk Factors
Higher body mass index (BMI)
Low self-esteem
Perfectionism
Depression and other manifestations of negative affect
Body dissatisfaction
Pubertal stage and timing
Pressure to conform to cultural body ideals; attempting to mimic media personalities
In males, negative weight comments by fathers
Frequent dieting in both genders
Attempting to meet unrealistic body weight goals for sport performance, especially in
endurance sports
Sports with weight restrictions/classes
While lean sports (eg, gymnastics, diving, ice skating) traditionally are associated with more
DE problems, that risk factor is being lessened; nearly all sports present a risk.
Genetics
Young female adolescents/children of mothers with ED history are 3 times more likely than
controls to purge weekly; not true in older adolescents.
Largely influenced by maternal psychological influence in young women; genetics unclear (3)
General Prevention
Educational and behavioral programs for the athletic community
Open communication about appropriate body composition for sport
Education about abnormal weight-control methods and appropriate nutrition guidelines
Focus on healthy eating and energy balance rather than weight

Female athlete triad
Depression, anxiety, and other psychological disorders
Diagnosis
History
Body image and weight concerns
Disordered eating practices
Athletes with EDs tend to hide them: Getting information from family, coach, athletic trainer,
and friends is helpful.
Amenorrhea/oligomenorrhea, especially during sport training or season
History of stress fractures
Dysfunctional bowel (eg, constipation, diarrhea)
Orthostatic symptoms
Cold intolerance
Dental and gum disease
Fatigue
Mild cognitive impairment
Mild neuropathy
May see performance decreases, but some athletes perform well despite the illness
Physical Exam
BMI (<17.5 is concerning), documentation of weight loss (weights should be done privately,
often with the results masked from the patient)
Bradycardia
Orthostatic hypotension
Poor skin turgor
Emaciation/muscle wasting
Lanugo hair
Swollen parotid glands (chubby cheeks)
Poor dentition; tooth enamel erosion
Russell sign (callous on fingers owing to self-induced vomiting)
Hypercarotenemia
Neuropathy
Cognitive impairment

Lab
High urine specific gravity
Electrolytes reflecting metabolic effects of purging: Hypokalemia, hypochloremic alkalosis,
hypomagnesemia, hyponatremia
Thyroid function: Low triiodothyronine and thyroxine with normal thyroid-stimulating hormone
Leukopenia, pancytopenia (if severe AN)
Low glucose
Labs often normal
Body composition testing, handled in sensitive manner (4); some athletes respond poorly to
knowing body composition, but it can be helpful to have objective evidence of malnutrition.
iDXA (intelligent dual energy x-ray absorptiometry) and bioelectric impedance are more
accurate than skinfold calipers in measuring body composition.
ECG to evaluate for dysrhythmias
DXA if amenorrheic for >3 mos or with stress fracture history; if <18 yrs old, use Z-score (-1
or less is concerning).
Psychiatric conditions (depression, anxiety, etc.)
GI malabsorption syndromes
Diabetes mellitus
Malignancies
Prolactinoma
Thyroid disease
Treatment
AN and BN have high relapse rates; focus on long-term management, not
cure.
BN: Help patient to establish control over eating, become educated about
nutrition and weight regulation, and restructure unrealistic body image.
BN: Up to 75% comorbid depression or anxiety; important to treat
Alcohol and drug problems commonly associated
Medication
Treatment of comorbid psychiatric disorders with pharmacotherapy as indicated
Referral
Psychology for cognitive-behavioral therapy
Psychiatry for pharmacotherapy management of comorbid psychiatric
disorders
Nutrition for eating strategies
Sport participation issues:
Motivation for treatment: Monitor performance (ED usually decreases
performance).
Refusal of treatment despite objective evidence (performance, physical or lab
abnormalities, etc.) of illness: Consider sport restriction/suspension.
Sport participation: Allowed if healthy enough to compete; keeping the athlete
out of sport may be psychologically detrimental.
Develop written contract for sport participation and diet and exercise practices
signed by treatment team and athlete.
Consider keeping minimum weight “guideline” with caloric intake needed to
sustain that weight (4)[C].
Consider hospitalization if medically unstable. This includes, but is not limited
to:
Cardiac dysrhythmias (including bradycardia)
Electrolyte disturbances
Severe dehydration
Severe malnutrition (<75% of expected average body weight for adolescents
and <85% for adults)
Psychiatric emergencies
Food refusal and uncontrolled binging and purging may result in hospitalization.
Hospitalization is for medical stabilization, does not cure disorder
Ongoing Care
Frequent follow-up and routine monitoring by all in treatment team (nutritionist, mental health
providers, physician) (5)[C]
Open communication among team members
Weight is monitored routinely, as are BP and pulse.
Prognosis
Prognosis is poor for complete recovery. Many patients relapse after initial improvement.
Complications
Cardiac dysrhythmias
Electrolyte disturbances
Stress fractures
Lack of fertility
References
1. Beals KA, Meyer NL. Female athlete triad update. Clin Sports Med.
2007;26:69–89.
2. Torstveit MK, Rosenvinge JH, Sundgot-Borgen J. Prevalence of eating

disorders and the predictive power of risk models in female elite athletes: a
controlled study. Scand J Med Sci Sports. 2007.
3. Field AE, Javaras KM, Aneja P, et al. Family, peer, and media predictors of
becoming eating disordered. Arch Pediatr Adolesc Med. 2008;162:574–579.
4. Bonci CM, Bonci LJ, Granger LR, et al. National athletic trainers'
association position statement: preventing, detecting, and managing
disordered eating in athletes. J Athl Train. 2008;43:80–108.
5. The female athlete triad. Med Sci Sports Exerc. 2007;39:1867–1882.
See Also
Female Athlete Triad
Menstrual Disorders in the Athlete
Codes
ICD9
307.1 Anorexia nervosa
307.50 Eating disorder, unspecified
307.51 Bulimia nervosa
Elbow Dislocation
John Munyak
Robert Bramante
Basics
Description
Separation/disruption of the articulations between distal humerus, proximal radius, and
proximal ulna. Typically resulting from trauma and injury to the supporting soft tissue
structures.
Subtypes: Anterior (rare) vs posterior (common) and simple (soft tissue injury) vs complex
(fracture-dislocation)
Complete (dislocation) or partial (subluxation)
System(s) affected: Musculoskeletal
Epidemiology
The elbow is the second most frequently dislocated major joint after the shoulder.
Comprises 10–25% of all elbow injuries
More frequently seen in wrestling, gymnastics, football, falls, and motor vehicle accidents
Incidence
Adults: 6–8/100,000
10–50% sports-related
Usually on the nondominant side
Prevalence
Predominate age:
Mean 30 yrs old
2nd most common dislocation in adults
Predominate sex: Males > Females
Risk Factors
Anatomical risk factors include a shallow olecranon fossa and a prominent olecranon tip.
Age and sports activity
Fall on an outstretched hand
General Prevention
Sport protective padding may provide a benefit.
Avoidance of falls
Etiology
Progression of injury from lateral collateral ligament to capsule to medial collateral ligament in
posterior dislocation
Anterior dislocation from trauma to the posterior portion of a flexed elbow
Fall on outstretched hand
Axial loading and rotation upon impact

Common: Radial head/neck fracture, epicondyle avulsion fracture, soft tissue edema,
coronoid process fracture
Rare: Neurovascular injury (brachial artery and median nerve), compartment syndrome
Diagnosis
History
Mechanism of fall
Type of activity leading to injury (sports, fall, work, accident)
Time since injury
Reduction attempts
Physical Exam
An obvious visual deformity usually is present.
Note the condition of the skin: Look for wounds indicating an open dislocation.
Palpation of deformity and effusion:
Prominent olecranon: Posterior
Long extended forearm: Anterior
Neurovascular evaluation, especially brachial artery and ulnar, interosseous and median nerve
function
Consult orthopedics/vascular surgery urgently for any signs of neurovascular injury.
Rule out additional injuries, especially in contiguous musculoskeletal structures.
In reduced elbows: Lateral pivot-shift apprehension test is highly sensitive (1)[C]
Sensation of dislocation is a positive test.

Imaging
Initial anteroposterior and lateral radiographs: Evaluate relationship between distal humerus
and radio-ulnar complex. Identify associated fracture (2)[C].
Maintain a high index of suspicion for additional injuries and obtain radiographs of the
humerus, forearm, or wrist as indicated.
Exception: On-field reduction by a medical professional can precede initial films (3)[C].
Postreduction radiographs: All dislocations (3)[C]
CT: Reserved for complex fracture dislocations or reconstruction planning
Angiography for suspected arterial injury
Elbow subluxation
Spontaneous elbow dislocation and reduction
Be especially cautious in the pediatric age group, as supracondylar humerus fractures are
common in 5–10-yr-olds.
Nursemaid's elbow (pediatrics)
Other elbow joint/forearm fracture
Treatment
In experienced hands, reduction may be performed on the field without
analgesia. Otherwise, transport patient to a medical facility that can treat this
injury.
Appropriate monitoring is required, and proper resuscitation equipment should
be available.
In rare instances, general anesthesia in the operating room may be required.
Postreduction, check elbow stability with range of motion.
Obtain postreduction radiographs.
Immobilize the elbow in a posterior splint as close to 90 degrees of flexion as
possible using avoidance of a diminishing radial pulse as a guide.
Perform a postreduction neurovascular examination.
Duration of elbow immobilization is a controversial issue. Recommendations
vary from 1 day to 2 wks.
Closed reduction of dislocation: Goal is atraumatic reduction with minimal
attempts. There are several techniques:
Option #1: Supine patient, forearm traction, humeral counter traction, anterior
force on olecranon, and forearm supination (2) [C]
Option #2: Prone patient, apply counter traction while extending the arm at
the elbow, manipulate the coronoid process past the trochlea (3)[C]
Option #3: (1-person reduction) Patient's arm across the chest, 1 hand
braces the injured distal arm, the other holds the elbow and olecranon while
providing traction to allow the coronoid to pass the trochlea (4)[C]
Full passive range of motion will signify a successful reduction.
Postreduction evaluation:
Postreduction radiographs to confirm position of radial head and ulna in
relation to the capitate and distal humerus. Also to exclude iatrogenic
fracture.
Neurovascular reassessment to confirm no nerve impingement
Assess joint stability:
Range of motion (ROM): No locking or crepitation
Joint should be examined under gentle stresses (valgus stress/laxity most
common following dislocation) (3)[C]
Lateral pivot-shift apprehension test for joint stability (1)[C]
Stable joint: Arm sling for comfort and early mobilization
Unstable joint that stabilizes with pronation: Splint in pronation/flexion (2)[C]
Joint unstable needs >45 degrees of flexion: Consider surgery (2)[C]
Issues for referral: Initial follow-up with orthopedics/sports medicine for splint
removal and early mobilization
Additional therapies: P.
ROM exercises after initial immobilization for comfort if joint is stable (2)[C]
Unstable joints should have a splint that blocks full extension with
encouragement of flexion as tolerated (2)[C]
Extended therapy required if ROM not improved by 6–8 wks post injury (3)[C]
Stability should be confirmed prior to full ROM therapy (5)[C].
Medication
Analgesia:
Reduction can be attempted without analgesia (4)[C].
Narcotics:
Morphine 0.1 mg/kg IVP usually 10 mg/dose (pediatric 0.1 mg/kg/dose)
Fentanyl 25–50 mcg IVP initially, shorter-acting, preferred narcotic for
conscious sedation (pediatric 2 mcg/kg/dose)
Reversible with naloxone
Multiple oral narcotics available for use
Postreduction NSAIDs are recommended, as they also decrease risk of
heterotopic ossification (2)[C].
Anxiolysis:
Benzodiazepines:
Midazolam 1 mg/dose (pediatric 0.05 mg/kg/dose), short acting, rapid
onset, preferred for conscious sedation
Lorazepam 0.05 mg/kg/dose (pediatrics 0.05 mg/kg/dose), longer duration
not ideal for procedural sedation use
Conscious/procedural sedation (multiple options): Goal of adequate pain
control and muscle relaxation:
Versed/Fentanyl: As above
Ketamine: Pediatric >3 mos 1.5 mg/kg IV with 0.5 mg/kg repeat doses.
(Rarely used in adults due to emergence reactions and agitation.)
Multiple other options, including propofol, barbiturates, and nitrous oxide
General sedation:
Occasionally required for difficult/painful reductions
Local anesthesia by joint infiltration can reduce needed analgesic doses (2)[C].
Precautions:
Be aware of respiratory and airway reflex depression with narcotics and
benzodiazepines.
Thorough preparation required for procedural sedation, including airway
management devices, bag-valve mask for ventilation, reversal agents
(naloxone/flumazenil) as appropriate, cardiovascular monitoring equipment
A follow-up radiograph should be obtained 1 and 2 wks after injury. A small
percentage of patients will develop recurrent instability, which can be due to
insufficiency of the lateral ulnar collateral ligament. These patients may require
surgical reconstruction to restore stability.
Rehabilitation after simple elbow dislocation requires 1–3 mos to return to
preinjury status. Typically, the outcome is good, with most athletes experiencing
little morbidity or loss of function. The most common problem is loss of
extension, which is minimized with an active, aggressive, early rehabilitation
program.
Surgery is limited to select cases, as conservative management is preferred
(5)[C].
Open dislocation, compartment syndrome, nerve injury/impingement, unstable
fractures, and unstable reductions require operative intervention (2)[C].
Grossly unstable elbows may require acute ligament repair to confer early
stability to allow for range of motion and enhanced rehabilitation.
Complex dislocations with fractures, including significant radial head,
olecranon, and coronoid fractures, may require surgical stabilization via open
reduction internal fixation (ORIF) of fracture segments (2)[C].
Isolated lateral collateral ligament repair in recurrent dislocation has shown
success (1)[B]. Chronically unstable elbows may require reconstruction of the
lateral ulnar collateral ligament.
Admission Criteria
Fracture dislocation requiring operative intervention
Nonreducible dislocation
Neurovascular injury
Edema with concern for compartment syndrome development
Nursing
Providing ordered medications for patient comfort or sedation as necessary
Monitoring of vitals for sedation procedures if needed
Reinforcing discharge instructions/plan
Discharge Criteria
Elbow dislocation confirmed by postreduction radiograph
Normal postreduction neurovascular exam documented
Supply orthopedic follow-up
Reduced elbow splinted for comfort or to maintain stability as needed
Ongoing Care
Consultation with an orthopedic surgeon should be obtained in most cases.
Patient Education
Avoid activities that specifically stress the elbow joint (eg, throwing) until ready upon re-
evaluation.
Prognosis
Generally full recovery
Poor outcome related to stiffness/decreased ROM:
Early physical therapy/ROM exercises decrease stiffness.
Complications
Neurovascular compromise
Stiffness
Compartment syndrome
Recurrent dislocation
Heterotopic ossification
References
1. Burra G, Andrews J. Acute elbow and shoulder dislocations in the athlete.
Orthop Clin N Am. 2002;33:479–495.
2. Kuhn MA, Ross G. Acute elbow dislocations. Orthop Clin North Am.
2008;39(2):155–161.
3. O' Driscoll SW. Classification and evaluation of recurrent instability of the
elbow. Clin Orthop Relat Res. 2007;370:34–43.
4. Mehta JA, Bain GI. Elbow dislocations in adults and children. Clin Sports
Med. 2004;23(4):609–627.
5. Kumar A, Ahmed M. Closed reduction of posterior dislocation of the elbow:

a simple technique. J Orthop Trauma. 1999;13(1):58–59.
Additional Reading
Krul M, van der Wouden JC, et al. Manipulative interventions for reducing
pulled elbow in young children. Cochrane Database of Systemic Reviews.
2009;2.
Ristic S, Strauch R, Rosenwasser M. The assessment and treatment of

nerve dysfunction after trauma around the elbow. Clin Orthop Relat Res.
2000;370:138–153.
Ross G, Chronister R, Ove P, et al. Treatment of elbow dislocation utilizing an

immediate motion protocol. Am J Sports Med. 1999;3:308–311.
Taylor F, Sims M, et al. Interventions for treating acute elbow dislocations in

adults. Cochrane Database of Systemic Reviews. 2009;3.
Work Loss Data Institute. Elbow (acute & chronic). Corpus Christi, TX: Work
Loss Data Institute; 2008.
Codes
ICD9
832.00 Closed dislocation of elbow, unspecified site
832.01 Closed anterior dislocation of elbow
832.10 Open dislocation of elbow, unspecified site
Clinical Pearls
Recognize neurovascular injury early.
Confirm relocation with a radiograph.
Early mobilization reduces postreduction stiffness.
Evaluate for other injuries in all traumas.
Epistaxis
David Z. Frankel
Basics
Description
Bleeding from injured nasal mucosa overlying a blood vessel
Self-induced digital trauma (nose picking) is the most common etiology, particularly among
children.
Affected persons usually do not seek medical attention, especially if bleeding is minor or self-
limited.
Synonym(s): Nosebleed; Nasal bleeding
Epidemiology
Common problem that is estimated to occur in 60% of the general population
90% of cases occur along the anterior nasal septum at Kiesselbach's plexus.
Bimodal age distribution with incidence peaks at ages <10 yrs and >50 yrs
Etiology
Local causes:
Local digital trauma
Low moisture content in ambient air
Nasal septal deviation
Intranasal neoplasm or polyps
Chemical irritants (eg, cigarette smoke)
Medications (eg, intranasal steroids)
Allergic or viral rhinitis
Chronic sinusitis
Facial trauma
Foreign body
Septal perforation
Illicit drug use (eg, cocaine)
Aneurysm
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)
Iatrogenic instrumentation
Systemic causes:
Coagulopathies (eg, Von Willebrand disease, hemophilia)
Renal failure
Platelet dysfunction
Thrombocytopenia
Hematologic malignancies (eg, leukemia)
Alcoholism
Hypertension
Liver disease (eg, cirrhosis)
Medications (eg, aspirin, NSAIDs, anticoagulants)
Diagnosis
History
Laterality of nosebleed
Amount of blood loss
Severity
Duration
Frequency
Presence of nasal obstruction: May indicate a neoplasm, especially with recurrent bleeding
from the same side
Trauma: Consider other associated injuries.
Other medical conditions that predispose to bleeding:
Tumors and coagulation disorders
Cirrhosis
HIV infection
Intranasal cocaine use
The presence of chronic medical conditions that can be exacerbated by blood loss:
Chronic obstructive pulmonary disease
Medications:
Aspirin
NSAIDs
Anticoagulants
Intranasal steroids
Alcohol use
History of severe nosebleeds or easy bruising
Family history of bleeding disorders
Physical Exam
Initial evaluation should focus on airway assessment and cardiovascular stability, looking for
signs of airway compromise or hypovolemia.
Pretreatment/initial tamponade:
The patient should blow his or her nose to remove blood and clots.
Local anesthetic and vasoconstrictor should be applied as a topical spray or via saturated
cotton pledgets.
Drugs commonly used for this purpose are lidocaine and oxymetazoline (Afrin).
One small retrospective study found that oxymetazoline spray stopped the bleeding in
65% of consecutive patients with epistaxis presenting to the ED.
The patient should be sitting up and leaning forward to prevent blood from tracking into the
pharynx.
The patient should apply direct pressure over the upper lip for 5 min and by tightly pinching
the nasal alae (soft cartilaginous part of the nose) against the septum continuously for 10–
15 min.
A cold compress applied over the bridge of the nose may help with hemostasis.
The examination should take place in a well-lighted room, preferably with a headlamp or
mirror.
The patient should be seated comfortably in an upright position with head movement
restricted.
An adequate examination for the source of bleeding requires use of a nasal speculum.
Clots and foreign bodies in the anterior nasal cavity can be removed with suction (Frazier
suction catheter), irrigation, forceps, and cotton-tipped applicators.
If no anterior source is identified, a nasal endoscope can be used to visualize the
remainder of the nasal cavity.
Posterior bleeding may be subtle, and the general location of the source of bleeding should
be determined (eg, behind the middle turbinate, roof of the nasal cavity, submucosal
masses).
This is important because different arteries supply the floor and roof of the posterior nasal
cavity.
Epistaxis from nasal trauma warrants an evaluation for fracture.
Deformity of the bony structures may be notable, and palpation of the bony structures may
reveal tenderness.
Evaluate extraocular muscle movements and stability of the teeth to rule out orbital or
maxillary fracture.
CSF leak should be ruled out using the ring test, if indicated.
In patients with recurrent nosebleeds, evaluate for signs of coagulopathy (eg, ecchymoses,
petechiae, telangiectatic lesions).

Lab
Laboratory studies should be dictated by the history, physical examination, and severity of
bleeding.
For severe bleeding, a CBC should be performed in addition to blood type and crossmatching
for possible transfusion.
In anticoagulated patients, coagulation studies may be required to determine if
anticoagulation levels are supratherapeutic.
In patients with systemic conditions that could lead to coagulopathy, testing for hepatic or
renal dysfunction may be required.
Even when testing is done selectively, the results are normal in nearly 80% of patients.
Imaging
Radiographic studies are usually not helpful unless nasal or facial fracture is suspected.
Unexplained recurrent unilateral epistaxis should raise suspicion for neoplasm and warrants
consideration of CT scan or MRI and endoscopic evaluation.
Pulmonary hemoptysis
Upper GI bleed such as bleeding esophageal varices
Tumor bleeding from the pharynx, larynx, or trachea
Treatment
Anterior bleed:
Minor anterior nosebleeds may resolve without intervention prior to clinical
evaluation or with initial tamponade.
Epistaxis that is refractory to pressure and topical vasoconstrictors may
require cautery.
If an anterior bleeding source is visualized, 1st-line treatment consists of
chemical or electrical cautery.
Chemical cautery is usually performed with silver nitrate.
Most useful for minor active bleeds or after active bleeding has stopped
and prominent vessels have been identified.
Apply the cautery for 10 sec.
Begin at the periphery of a small area surrounding the bleeding site and
move centrally.
Exercise caution with silver nitrate because it cauterizes everything that it
touches.
Never cauterize both sides of the nasal septum in the same session to
reduce the risk of iatrogenic septal perforation.
Electrical cautery is useful for more aggressive bleeding or larger vessels
of the anterior nasal septum.
The nose must first be anesthetized using injected local anesthetic
because electrical cautery can be extremely painful.
Anesthetize bilaterally because the electrical current is transmitted
through the septum.
Electrocautery must be performed cautiously to avoid excessive
destruction of healthy tissue.
The use of electrocautery on both sides of the septum may increase the
risk of septal perforation.
Laser cautery has little role in the treatment of acute epistaxis, although it
is used commonly for patients who have chronic epistaxis secondary to
hereditary hemorrhagic telangiectasias.
If cautery is unsuccessful, or if no obvious site of bleeding is seen, nasal
packing should be considered to tamponade the epistaxis.
A number of absorbable and nonabsorbable packing materials are available
for anterior nasal packing.
Traditional packing products consist of nondegradable materials.
Gauze impregnated with petroleum jelly (eg, Xeroform) may be inserted in
layers from the floor of the nasal cavity to tamponade the epistaxis.
A preformed nasal tampon made of polyvinyl alcohol that expands when wet
(eg, Merocel) will swell and fill the nasal cavity, applying pressure over the
bleeding area.
An inflatable carboxymethylcellulose pack consisting of a balloon catheter
and hydrocolloid coating (eg, Rapid Rhino) that forms a lubricant on
contact with water and remains in contact with mucosa on balloon deflation
may cause less discomfort and be easier to insert and remove.
Absorbable or degradable materials that do not require formal removal are
useful.
Oxidized cellulose (eg, Surgicel) and gelatin foams (eg, Gelfoam) increase
clot formation and provide a degree of tamponade.
Bovine-derived thrombin gel (eg, FloSeal) is conformable to the contours of
the nasal cavity, easy to apply, and less painful. Higher costs of its use may
be offset by the lack of need for packing removal.
Packing generally is left in place for 1–5 days to ensure adequate clot
formation.
Topical or oral antibiotics typically are used with prolonged nasal packing
because of the possibility of toxic shock syndrome.
Other complications of nasal packing include septal hematomas, abscesses,
or pressure necrosis from traumatic packing; sinusitis from blockage of sinus
drainage; hypoxia from nasal airway blockage or apneic spells; stimulation of
the nasovagal reflex causing syncope during packing; and acute airway
obstruction from pack displacement into the oropharynx.
Failure to control anterior bleeding with cautery or packing may necessitate
embolization or surgical ligation of the offending vessels.
Referral to an otolaryngologist is appropriate when bleeding is refractory,
complications are present, or specialized treatment is required.
Continued bleeding despite an anterior pack may be due to a posterior bleed.
Posterior bleed:
These bleeds can be difficult to treat and may require either balloon insertion
or a formal posterior pack.
If a specialized balloon device (eg, Brighton balloon, Simpson plug, Epistat
nasal catheter) is not available, posterior tamponade can be achieved using
a Foley catheter.
Posterior packing usually necessitates hospitalization out of concern for
hypoxic complications, cardiopulmonary events, and the risk of asphyxiation
should the packing become dislodged.
Posterior packing can be quite uncomfortable and may require significant
anesthesia.
A posterior pack may be an emergent temporizing measure before surgery
or angiographic embolization.
Ongoing Care
Once epistaxis is controlled, conservative measures may prevent recurrent bleeding
owing to local factors.
Refrain from activities that may stimulate bleeding:
Blowing or picking nose
Heavy lifting
Strenuous activity
Patient should abstain from alcohol or hot drinks that may cause vasodilatation of the nasal
vessels.
Nasal saline washes and water-soluble ointments assist in humidification of the nasal mucosa
and promote healing.
Humidified air, especially for patients using oxygen via nasal canula, may improve local
conditions within the nose.
Patients should meet with their primary care physician to search for and address underlying
causes and risk factors for epistaxis.
All patients with recurrent epistaxis, particularly if unilateral, require formal evaluation with
radiographic studies and nasal endoscopy to rule out a neoplastic lesion.
Additional Reading
Alter H. Approach to the adult with epistaxis. In: UpToDate, Basow DS (Ed), UpToDate,
Waltham, MA, 2009.
Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am. 2008;41:525–536, viii.
Kucik CJ, Clenney T. Management of epistaxis. Am Fam Physician. 2005;71:305–311.
Leong SC, Roe RJ, Karkanevatos A. No frills management of epistaxis. Emerg Med J.
2005;22:470–472.
Pope LE, Hobbs CG. Epistaxis: an update on current management. Postgrad Med J.
2005;81:309–314.
Schlosser RJ. Clinical practice. Epistaxis. N Engl J Med. 2009;360:784–789.
Codes
ICD9
784.7 Epistaxis
Clinical Pearls
Athletes with an anterior bleed that is easily controlled and without significant
facial trauma or underlying condition may return to play during the same event
after cessation of bleeding and appropriate counseling.
Exercise-Induced Anaphylaxis
Robert G. Hosey
Basics
Description
Distinct form of physical allergy characterized by a spectrum of exercise-induced symptoms
ranging from mild skin symptoms such as pruritus and urticaria to angioedema, hypotension,
syncope, and death.
A subgroup may develop food-dependent exercise-induced anaphylaxis (EIA).
Epidemiology
Incidence
Incidence seems to be increasing (1). A few deaths have been attributed to EIA in the
literature (2).
Predominant gender: Female > Male ( 2:1) (1).
Prevalence
1,000 cases have been reported (3).
Risk Factors
Previous episodes
Atopic individuals may be at slightly increased risk.
Associated factors include:
Ingestion of certain foods or medications (particularly aspirin or NSAIDs) before exercise
may be a predisposing factor.
Hormonal fluctuations during menstrual cycle may play a role in women with EIA (1).
Family variant may exist.
General Prevention
Preventive medications include (3):
Nonsedating antihistamines on a daily basis have been shown to be at least partially effective
in prevention of symptoms (cetirizine 5–10 mg PO every day, loratidine 10 mg PO every day)
(3)[C].
Cromolyn sodium metered-dose inhaler (MDI) 2–4 puffs q.i.d. may be helpful.
Possible role for use of leukotriene inhibitors (montelukast 10 mg PO in the evening,
zafirlukast 20 mg PO b.i.d.)
Some clinicians advocate for avoiding antihistamines because they may block cutaneous
manifestations of EIA that often serve as a “warning” of impending anaphylaxis (1,4)[C].
Avoid food/medication triggers.
Etiology
Release of histamine and tryptase by mast cells has been implicated as a possible cause of
EIA.

Eczema
Asthma
Diagnosis
Careful clinical history documentation of attacks is often required to make a diagnosis.
History
Transient exercise-induced itching and cutaneous erythema ± urticaria is suggestive of EIA.
Progression of these symptoms to dyspnea, dizziness, GI colic, or syncope is further
suggestive of EIA.
History of previous EIA
Identify possible provocative agent: Urticaria with warm shower or anxiety is consistent with
cholinergic urticaria. Cold, ultraviolet rays, or water also may induce urticaria. Diagnosis may
require an exercise diary.
Identify any ingestions prior to exercise: Specific food or NSAID may be a trigger.
EIA does not occur with every bout of exercise but may occur at any level of physical activity.
Generalized itching
GI colic
Headache
Choking sensation
Urticaria or angioedema with hypotension or respiratory obstruction is hallmark of classic
EIA.
Patient may present in full anaphylactic shock.
Physical Exam
Assess ABCs:
Hypotension or respiratory difficulty may signify impending anaphylactic shock.
Dermatologic examination may reveal wheals.
Identifying urticarial size and presence of angioedema aids in diagnosis (5).

Lab
Abnormal laboratory tests include elevated serum histamine and serum tryptase levels.
Serum tryptase levels should be determined within 2–3 hr of the event (2).
Passive warming test (eg, warm shower or sauna) can be helpful in differentiating cholinergic
urticaria from EIA.
Exercise challenge test using a treadmill or stationary bike can be performed. A positive test
(reproduction of symptoms and urticaria) is helpful in diagnosis, but a negative test does not
exclude a diagnosis of EIA because reproducibility of symptoms is variable. Emergency
equipment should be immediately available if exercise test is performed.
Allergy testing for potential food and common allergen triggers should be done in all patients
with EIA.
Cholinergic urticaria
Exercise-induced asthma
Environmental allergy
Treatment
Pre-Hospital
ABCs
SC administration of 0.3–0.5 mL epinephrine 1:1,000 if systemic symptoms of
anaphylaxis are present; then call 911.
Trendelenburg position
ED Treatment
Treat symptoms of anaphylactic shock as necessary in appropriate medical
setting (eg, fluid support for hypotension, assisted ventilation for respiratory
obstruction).
General Measures
Cease physical activity if any symptoms arise.
Avoid exercise for 4–6 hr after eating.
Avoid anti-inflammatory drugs before exercise.
Always exercise with a partner and carry injectable epinephrine.
Possible role for desensitization to physical activity
Ongoing Care
Referral to an allergist for identification of possible associated triggers may be beneficial.
Follow-up to assess recurrence of symptoms and success of drug therapy
Patient Education
Advise patient on Epipen use (should have access to one at all times).
Renew Epipen annually.
Advise patient to avoid any triggers, if known.
Recommend wearing a medical alert device.
References
1. Castells MC, Horan RF, Sheffer AL. Exercise-induced anaphylaxis. Curr Allergy Asthma
Rep. 2003;3:15–21.
2. Sheffer AL, Soter NA, McFadden ER, et al. Exercise-induced anaphylaxis: a distinct form
of physical allergy. J Allergy Clin Immunol. 1983;71:311–316.
3. Briner WW. Physical allergies and exercise. Clinical implications for those engaged in
sports activities. Sports Med. 1993;15:365–373.
4. Schwartz LB, Delgado L, Craig T, et al. Exercise-induced hypersensitivity syndromes in

recreational and competitive athletes: a PRACTALL consensus report (what the general
practitioner should know about sports and allergy). Allergy. 2008;63:953–961.
5. Nichols AW. Exercise-induced anaphylaxis and urticaria. Clin Sports Med. 1992;11:303–
312.
Additional Reading
See Also
Anaphylaxis
Exercise-Induced Urticaria
Codes
ICD9
995.0 Other anaphylactic shock, not elsewhere classified
995.1 Angioneurotic edema, not elsewhere classified
Clinical Pearls
Because symptoms may vary significantly from episode to episode and among
patients, some patients may not feel comfortable returning to activity knowing
that they could have repeat attacks. In addition, patients who have experienced
an anaphylactic response to exercise should be cautioned about returning to
activity. For those whose symptoms are controlled with medication, it is
recommended they continue to carry injectable epinephrine and exercise with a
partner.
EIA can occur with any level of activity and may be precipitated by the ingestion
of many foods. Unless a specific trigger is identified, there are no restrictions
placed on diet or type of activity. A general rule of thumb is to avoid eating for
4–6 hr before exercise.
Exercise-Induced Asthma
Michael A. Krafczyk
Christopher Cieurzo
Basics
Description
Airway bronchoconstriction characterized by wheezing, coughing, shortness of breath, and/or
chest tightness occurring during or after exercise
If the athlete has underlying asthma, then it is called exercise-induced asthma; otherwise, it
is exercise-induced bronchoconstriction.
Usually within 5–15 min of the onset of exercise, an acute episode of airway obstruction
begins. This is usually followed by recovery within 30–90 min on completion of the exercise.
Synonym(s): Exercise-induced bronchoconstriction
Epidemiology
10–50% of recreational and elite athletes
70–80% of asthmatics
40% of patients with allergic rhinitis
35–50% of cold-weather athletes
No gender or age differences have been noted.
A high level of fitness does not confer immunity from either asthma or exercise-induced
bronchocon-striction (EIB).
Risk Factors
Cold-weather sports such as ice hockey, figure skating, and cross-country skiing
Sports with a long duration of high-intensity exercise such as running, bicycling, swimming,
soccer, and rugby
Environmental factors such as tobacco smoke, chlorine, sulfur dioxide, nitrogen oxide, carbon
monoxide, pollens and molds, cold weather, and low humidity
Etiology
Hyperosmolarity theory posits that increased airflow, particularly of unhumidified air, causes
water loss from the surface liquid of the airways. This causes a hyperosmolar state in the
airways, leading to inflammation and bronchoconstriction.
Airway rewarming theory suggests that increased respiratory rate cools the cells on the
surface of the airways. Once exertion subsides, the airways rewarm, causing dilatation of the
airway blood vessels, leading to hyperemia and fluid leakage into the bronchioles. This, in
turn, causes inflammation and airway constriction.

Asthma
Allergic rhinitis and hay fever
Diagnosis
Direct testing with pulmonary function tests (PFTs) done before and after albuterol
should be done 1st (1)[A].
If negative, then move on to indirect testing with one of the following.
PFTs before and after exercise (1)[A]:
Spirometry more accurate than peak expiratory flow rate
10–15% reduction in preexercise forced expiratory capacity in 1 sec (FEV1) confirms the
diagnosis of EIB.
Best to test athletes during sport-specific exercise or at temperatures of 20–25°C and
<50% relative humidity
Exercise at a workload of 80–90% of predicted VO2,max for 6–8 min during testing
Eucapnic voluntary hyperventilation (1)[A]:

Recommended by IOC Medical Commission for diagnosing athletes
Hyperventilation of a gas mixture with 21% O2 and 5% CO2 for 6 min at 85% maximum
voluntary ventilation
FEV1 is measured prior to the test and 5, 10, and 15 min after the test.
90% sensitive when 10% drop in FEV1 is used as cutoff; 100% sensitive when a drop of
15% is used.
Inhaled mannitol testing shows high sensitivity and specificity for exercise-induced asthma
(EIA) and is likely to become another diagnostic tool (2,1)[A].
History
Personal or family history of allergies or asthma
Symptoms are often a poor predictor of who has EIA.
Symptoms occur during or after exercise, typically appearing after 6–8 min of exercise.
Physical Exam
Coughing
Wheezing
Shortness of breath
Chest tightness
Abdominal pain
Headache
Fatigue
Feeling out of shape
Chest pain or discomfort
Physical examination should include the following:
Look for evidence of allergic disease such as pale nasal mucosa or allergic “shiners.”
Cardiac exam to evaluate for cardiac abnormalities
Lung examination typically normal; if wheezing, consider chronic asthma.
On the field or after exercise challenge, physical examination is more likely to reveal
wheezing.
Pulmonary:
Asthma with exercise exacerbation
Exercise-induced hyperventilation
Restrictive lung disease
Cystic fibrosis
Cardiac:
Congenital/acquired heart defects
Arrhythmias
Cardiomyopathy
ENT:
Vocal cord dysfunction
Laryngeal prolapse
Exercise-induced laryngeal dysfunction
Laryngomalacia
Chronic sinusitis
GI: Gastroesophageal reflux disease
Allergic: Exercise-induced anaphylaxis/urticaria
Other:
General state of deconditioning
Anxiety disorders, panic attacks
Treatment
Warm-up of 15 min at moderate exertion 15–30 min prior to exercise can
induce a refractory period preventing bronchoconstriction.
Avoidance of triggers
In cold weather, a mask can be used to warm the air.
Nose breathing can help to warm and moisturize the air.
Athletes with underlying asthma should be well controlled before beginning a
sport/exercise program.
Medication P.
Short-acting beta agonists
Oral steroids for severe exacerbation
Treat as per asthma guidelines (National Heart, Blood, and Lung Institute),
particularly for patients with underlying asthma.
Inhaled corticosteroids do not typically help in the acute setting.
First Line
Prophylactic (preexercise) medication:
Short-acting beta agonist: 2–4 puffs 15–30 min before exercise; may repeat
during exercise as needed (3)[A]
Second Line
If not responding adequately to a short-acting beta agonist, can add:
Cromolyn 4–10 puffs 10–20 min before exercise (3)[A]
Nedocromil 2–4 puffs 10–20 min before exercise (3)[A]
Montelukast 10 mg PO up to 2 hr before exercise (3)[A]; consider in athletes
with allergic rhinitis.
Long-acting beta agonist (LABA), such as formoterol and salmeterol, in
conjunction with inhaled corticosteroids 30–60 min before exercise (3)[A]
Avoid use of LABA without inhaled corticosteroids based on a recent study
showing increased incidence of asthma-related events when LABAs are used
alone (4).
For elite athletes, check the U.S. Olympic Committee or National Collegiate
Athletic Association list of banned substances to be sure that the medications
used are in compliance with their rules.
High-dose omega-3 fish oil
Pycnogenol 30–100 mg/day or 10 mg/kg/day taken 2–3 times a day
Breathing exercises/relaxation techniques may be tried.
Ongoing Care
Daily medication:
Cromolyn: 2 puffs q.i.d. or 4 puffs b.i.d. (3)[A]
Nedocromil: 2 puffs q.i.d. (3)[A]
Montelukast 10 mg daily (3)[B]
Zafirlukast 20 mg b.i.d.
Zileuton 1,200 mg b.i.d.
Inhaled corticosteroid with or without long-acting beta agonist (dose varies depending on
which product is used) (3)[A]
Begin treatment with inhaled short-acting beta agonist before exercise.
Cromolyn and nedocromil best used in conjunction with a short-acting beta agonist (3)[B]
Tachyphylaxis to short-acting beta agonists can occur with daily use (3)[B].
Maximize therapy of underlying asthma.
Nonpharmacologic:
For cold-weather athletes, wearing a mask to prewarm the inhaled air may help to reduce
symptoms.
Adequate warm-up (1)[B]:
At least 15 min of warm-up at a level of exertion sufficient to provoke symptoms
May take inhaler after warm-up is complete and rest for 15–30 min
This can place the bronchospasm in a refractory period and reduce constriction during
competition.
Educate on proper use of inhalers and spacers.
If allergies play a role in triggering asthma, then avoidance of triggers and consideration for
immunotherapy (allergy shots)
If not responding to inhaled short-acting beta agonist, consider other diagnoses.
Have patient return if use of short-acting beta agonist increases.
Patient Education
All athletes with EIA should have a short-acting beta agonist inhaler with them during
practices and games.
All athletes should be taught proper use of an inhaler.
Spacers can help to improve delivery of the inhaler medication.
The athlete should know the difference between his or her controller and as-needed
medication.
Teach to avoid triggers.
Consider allergy testing.
Prognosis
Good
Complications
Poorly controlled athletes with EIA can progress to airway remodeling that
becomes unresponsive to short-acting beta agonists.
References
1. Parsons JP, Mastronarde JG. Exercise-induced bronchoconstriction in
athletes. Chest. 2005;128:3966–3974.
2. Holzer K, Douglass JA. Exercise induced broncho-constriction in elite

athletes: measuring the fall. Thorax. 2006;61:94–96.
3. Carlsen KH, Anderson SD, Bjermer L, et al. Treatment of exercise-induced
asthma, respiratory and allergic disorders in sports and the relationship to
doping: Part II of the report from the Joint Task Force of European
Respiratory Society (ERS) and European Academy of Allergy and Clinical
Immunology (EAACI) in cooperation with GA(2)LEN. Allergy. 2008;63:492–
505.
4. Nelson HS, Weiss ST, Bleecker ER, et al. The Salmeterol Multicenter
Asthma Research Trial: a comparison of usual pharmacotherapy for asthma
or usual pharmacotherapy plus salmeterol. Chest. 2006;129:15–26.
Additional Reading
Schwartz LB, et al. Exercise-induced hypersensitivity syndromes in
recreational and competitive athletes: a PRACTALL consensus report (what
the general practitioner should know about sports and allergy). Allergy.
2008;63:953–961.
Storms WW. Review of exercise-induced asthma. Med Sci Sports Exerc.

2003;35:1464–1470.
Storms WW. Exercise-induced asthma: diagnosis and treatment for the

recreational or elite athlete. Med Sci Sports Exerc. 1999;31:S33–S38.
Codes
ICD9
493.81 Exercise induced bronchospasm
Clinical Pearls
1st-line treatment is a short-acting beta agonist before exercise.
Avoid daily use of short-acting beta agonists because tachyphylaxis may
develop. Have athlete use during high-intensity practice and competition.
It is no longer recommended to use long-acting beta agonists without an
inhaled corticosteroid.
Exercise-Induced Diarrhea
Kimberly Harmon
Basics
Description
Increased stool frequency or volume often accompanied by lower abdominal cramping, or
urge to defecate associated with strenuous physical activity:
Normal physical examination
Normal laboratory and diagnostic studies
Synonym(s): Runner's diarrhea; Runner's trots
Epidemiology
Primarily associated with running sports, but also common in cycling and reported in
swimming, wrestling (1,2,3)
Difficulty with existing research:
Difficult to control all variables (diet, exercise intensity, underlying pathology such as
irritable bowel syndrome)
Studies often lack a denominator, making a true incidence of symptoms difficult to
determine.
Many studies are surveys with low response rates, which introduces a selection bias.
Subject's dietary recall often is inaccurate.
Prevalence
Prevalence of diarrhea reported from 8–60% in athletes
Prevalence of diarrhea in control subjects reported up to 40%
Risk Factors
Underlying bowel pathology may worsen with strenuous exercise.
Dehydration
Occurs more frequently with increased exercise intensity
Occurs more frequently in untrained participants
Type of exercise (running > cycling, swimming, speed skating, cross-country skiing)
Meals rich in fat, protein, and fiber taken shortly before exercise worsen symptoms.
Etiology
Proposed mechanisms (1,2,3):
Mesenteric ischemia:
With strenuous exercise, blood is shifted away from the gut and to the working muscle.
Exercising at 70% VO2 max decreases blood flow to GI tract by 60–70%.
May lead to the production of endotoxin
Causes a cascade of inflammatory events that can further impair the mucosal integrity
Increased activity of the sympathetic nervous system leads to decreased sphlanic blood
flow and is caused by:
Mental stress
Hyperthermia
Dehydration
Hypoglycemia
Increased sympathetic nervous system activity:

Suppresses parasympathetic activity
Decreased gut tone and resistance
Increased colonic transit times
Secretion of gastroenteropancreatic hormones
Mechanical stimulation of the colon due to intra-abdominal jostling
Enteric fluid and electrolyte balance
Diagnosis
History
Increased stool frequency or volume, or loose stools after exercise
Often accompanied by abdominal cramping and urge to defecate
May occur just with competition and not with training
Normal bowel function at other times
Physical Exam
Increased stool frequency
Increased stool volume
Loose or explosive stools
Urge to defecate, often necessitating the athlete to cease exercise
Abdominal cramping
Rectal bleeding
Unremarkable physical examination

Exercise-associated diarrhea is a diagnosis of exclusion.
Workup is used to rule out other causes of diarrhea.
Lab
Stool cultures, including Clostridium difficile
Consider antigliadin and tissue transaminase antibodies to rule out celiac sprue.
Thyroid-stimulating hormone
Consider stool osmolar gap if eating disorder and/or laxative abuse is suspected:
Increased osmotic gap is suspicious for laxative use.
Imaging
Imaging studies should be obtained as clinically indicated:
Consider barium enema
Contrast-enhanced CT scan
Diagnostic procedures such as sigmoidoscopy or colonoscopy may be considered as clinically
indicated.
Irritable bowel disease
Inflammatory bowel disease
Infection
Colon cancer
Superior mesenteric or portal venous thrombosis
Malabsorption
Microscopic colitis
Laxative abuse
Lactose intolerance
Hyperthyroidism
Treatment
Treatment is generally conservative and should include (1,2,3)[C]:
Training modification:
Increase volume and intensity of training slowly.
Try to evacuate prior to exercise.
Diet modification
Acute symptoms usually rapidly resolve with cessation of activity:
Hyoscyamine (Levsin) 0.125 mg sublingually sometimes is helpful in stopping
abdominal cramping after exercise.
Medication
All athletes should consult with the governing bodies of their sports regarding
banned substances.
First Line
Antispasmodics may be helpful, but have anticholinergic side effects and
should be used with caution:
Dicyclomine (Bentyl) 20 mg PO q.i.d.
Hyoscyamine (Levsin) 0.125–0.25 mg PO/s.l. q4h PRN:
The athlete should remain well hydrated.
Use in hot/humid conditions is not ideal
Loperamide (Imodium) decreases intestinal motility and affects water and
electrolyte absorption:
Loperamide 2–4 mg 30 min before exercise
Side effects are rare.
Second Line
Opiate/atropine combinations (diphenoxylate [Lomotil]) should be used with
caution:
Opiates are habit-forming.
May be banned depending on governing body of the sport
May adversely affect performance
Atropine may cause hyperthermia, tachycardia, and heat regulation problems.
Ongoing Care
Diet
Dietary modification can be helpful (1,2,3)[C]:
Stay well hydrated.
Avoid caffeine, which is both a diuretic and a cathartic.
Avoid foods that exacerbate symptoms (eg, lactose in lactose-intolerant athlete).
Limit intake of gas-forming foods (broccoli, onions, beans).
Eat a small, low-fat, low-fiber meal several hours before competition:
Use low-osmolar sports drink between meal and competition or training.
Avoid large doses of vitamin C, sodium bicarbonate, and carbohydrate drink prior to
exercise.
If athlete still has difficulty with diarrhea or urge to defecate, try complete nutritional liquid
that is low in fiber during the day preceding competition.
Prognosis
Most athletes can learn how to manage their symptoms through the use of diet and training.
References
1. Casey E, Mistry DJ, MacKnight JM. Training room management of medical conditions:
sports gastroenterology. Clin Sports Med. 2005;24:525–540, viii.
2. Ho GW. Lower gastrointestinal distress in endurance athletes. Curr Sports Med Rep.
2009;8:85–91.
3. Simons SM, Kennedy RG. Gastrointestinal problems in runners. Curr Sports Med Rep.
2004;3:112–116.
Additional Reading
Green GA. Gastrointestinal disorders in the athlete. Clin Sports Med. 1992;11:453–470.
Swain RA. Exercise-induced diarrhea: when to wonder. Med Sci Sports Exerc.
1994;26:523–526.
Codes
ICD9
306.4 Gastrointestinal malfunction arising from mental factors
564.5 Functional diarrhea
787.91 Diarrhea
Exercise-Induced Urticaria
Mark Halstead
David T. Bernhardt
Basics
Description
Spectrum of allergic response to exercise ranging from itching, flushing, and cutaneous
warmth to development of well-circumscribed wheals (large papular lesions with pale centers
and an erythematous ring) and angioedema to severe anaphylactic shock
Elevation of serum histamine levels with exercise
Mast cell degranulation seen in skin biopsies suggesting immunoglobulin E–mediated
sensitization
Described with almost any type of physical exercise
Distinguishable from cholinergic urticaria, which also has exercise as a possible trigger
Certain foods in combination with exercise may cause symptoms in susceptible individuals.
Synonym(s): Exercise-induced anaphylaxis; Hives
Epidemiology
Incidence and prevalence unknown
Predominant gender: Male = Female.
Predominant age: Seen more frequently in young adults but has been described as early as 4
yrs of age
Risk Factors
Atopic history (eczema, asthma, allergic rhinitis)
Other forms of physical allergy
Food allergy
General Prevention
Stop exercise with first onset of symptoms.
Avoid foods 6–8 hr before exercise. Exercising 1st thing in the morning after evening fast is
preferable.
Avoid known problematic food or medication triggers for at least 12 hr before exercise.
Preventive antihistamine therapy may be useful.
Patients always should have an epinephrine kit with them while exercising; Benadryl also may
be reasonable to have.
Exercising with a companion knowledgeable in CPR is recommended.
Recommend wearing medical alert device
Diagnosis
History
Diagnosis usually is made by history.
Initially patients describe generalized feeling of tingling, warmth, and itching.
May start as early as 5 min after initiating exercise or can occur after exercise has been
completed
May have history of food or medication ingestion within previous 6–8 hr before exercise
Patients often (>50%) have atopic history (ie, eczema, asthma, allergic rhinitis).
Foods reported to be associated include eggs, lentils, shellfish, hazelnuts, wheat, peaches,
apples, grapes, celery, and cheese sandwiches. Cases have been reported with many other
foods.
Medications: NSAIDs, aspirin, antibiotics
Usually resolves within 30 min to 4 hr after exercise
Headaches may continue for up to 3–4 days after a severe reaction.
Physical Exam
Signs and symptoms:
Pruritus
Urticaria
Wheezing
Hypotension
Flushing
Angioedema
Headaches
Nausea
Choking
Profuse sweating
Generally distinguished from cholinergic urticaria because larger (>10 mm) wheals are
seen in exercise-induced urticaria, whereas fine punctate (<5 mm) lesions are seen in
cholinergic urticaria
Wheals are not reproducible with generalized heat application or sweating, which is more
characteristic of cholinergic urticaria, or cold application (ice cube) common to cold
urticaria.
Respiratory examination may demonstrate stridor, wheezing, and retractions during acute
attack.
Angioedema seen in more severe acute attacks

Lab
Not necessary in acute attacks
Allergy testing may be beneficial as an outpatient.
Positive skin testing does not always mean a cause-and-effect relationship. Suspicious
positive skin tests may need to be followed by an exercise challenge because patients with
positive food skin tests may not always develop urticaria with exercise and consumption of
that food.
Physical urticarias (cold, dermographic, delayed pressure, solar, aquagenic, vibratory)
Cholinergic urticaria (induced by increased body temperature)
Vocal cord dysfunction
Insect bites
Drug eruption
Urticaria pigmentosa
Systemic lupus erythematosus
Erythema multiforme
Treatment
Medication
Epinephrine (Epi-Pen) 0.3 mg IM for severe anaphylactic reaction
Diphenhydramine (Benadryl) 25–50 mg PO q4–6h (children: 5 mg/kg/day
divided q6–8h, not exceeding 300 mg/day)
Hydroxyzine (Atarax) 25–100 mg PO q6h (children: 2 mg/kg/day divided q6–
8h)
During exercise, patients should carry an epinephrine kit (Epi-Pen) with them at
all times.
H1 antihistamines as prophylaxis have shown mixed results (fexofenadine 60
mg PO b.i.d., loratadine 10 mg PO daily, and cetirizine 10 mg PO daily).
Cromolyn taken orally has been reported to be of some benefit.
H2 antihistamines may be of help (eg, cimetidine, ranitidine, and famotidine).
Doxepin, which has both H1- and H2-blocking abilities, may be of value.
General Measures
Acutely, care is targeted toward ensuring airway protection if severe
anaphylaxis is present.
Trendelenburg position
Ongoing Care
Referral to an allergist may be beneficial for skin testing and controlled exercise challenge
testing.
Additional Reading
Briner WW. Physical allergies and exercise. Clinical implications for those engaged in sports
activities. Sports Med. 1993;15:365–373.
Briner WW, Sheffer AL. Exercise-induced anaphylaxis. Med Sci Sports Exerc.
1992;24:849–850.
Horan RF, Sheffer AL, Briner WW. Physical allergies. Med Sci Sports Exerc.
1992;214:845–848.
Kaplan AP. Allergy: principles and practice, 5th ed. St. Louis: Mosby-Year Book, 1998.
Nichols AW. Exercise-induced anaphylaxis and urticaria. Clin Sports Med. 1992;11:303–
312.
Tilles S, Shocket A, Milgrum H. Exercise-induced anaphylaxis related to specific foods. J

Pediatrics. 1995;27:587–589.
Tilles SA, Schocket AL. Food allergy: adverse reactions to foods and food additives.
Cambridge: Blackwell Science, 1997.
Codes
ICD9
708.8 Other specified urticaria
Clinical Pearls
Exercise may be continued as long as precautions are taken by avoiding all
food 6–8 hr before exercise and 12 hr after eating food suspected of causing
reactions.
Epinephrine should be carried at all times with the patient when exercising, and
a companion who knows CPR ideally would be exercising with the patient.
Patients who had severe life-threatening reactions likely need counseling to
discuss curtailing exercise.
These reactions are not always preventable. Despite premedication with
various antihistamines, patients still can develop urticarial lesions and have
anaphylaxis.
Initiating antihistamine therapy on a daily basis for those who exercise
frequently is a worthwhile start to hopefully reduce the number of occurrences
of this phenomenon.
Each individual may react to different foods. Reported reactions occur more
frequently with celery and shellfish, but also with hazelnuts, eggs, apples,
peaches, grapes, wheat, and even cheese sandwiches.
Some patients have been reported to react to any food they eat, so avoid
eating 4–6 hrs prior.
If a food seems to be a trigger a reaction, it is best to avoid that food for at
least 12 hr before exercise.
It is reasonable to see an allergist for testing and an exercise challenge with
suspicious food items.
Exertional Headache
Natalie Voskanian
Basics
There are 2 types of exertional, or exercise-associated, headaches seen in athletes: 1)
benign exertional headache (BEH); and 2) weightlifter's headache.
These headache syndromes are not associated with intracranial lesions or systemic
disorders, and are distinct from migraines, tension headaches, concussion, and cervicogenic
headaches, all of which are also seen in athletes.
Weightlifter's headache, also known as cough headache, is a short-lasting headache that
results abruptly from Valsalva maneuvers, such as from weightlifting or resistance training. It
has also been called sexual headache because it can result from an orgasm in some
individuals.
BEH is believed to be distinct from weightlifter's headache because it lasts longer, has a
different population profile, results from more sustained intense exercise, and is usually not
associated with Valsalva maneuvers.
Description
BEH occurs typically in young athletes (age range 10–48 yrs old, average age of 24) and
lasts several hours on average (1).
BEH is brought on by sustained physical exertion, such as running or doing running drills,
rugby, swimming, soccer, swimming, etc.
Weightlifter's headache is usually short-lived and brought on by sudden strains, such as
coughing, sneezing, crying, or lifting a heavy object.
Weightlifter's headache lasts only several minutes and is more commonly seen in older
individuals (1).
Though historically, the classification of these entities has been vague, most agree that these
2 are distinct entities.
Epidemiology
Exertional headaches occur more often in men (2).
Incidence
BEH affects 1% of the general population (2).
Up to 50% of athletes report regular headaches from sport activity (3).
Risk Factors
Male gender (2)
History of migraine (4)
General Prevention
Avoidance of intense, sustained physical exertion
Etiology
Pathophysiology is largely unknown, but several theories have been postulated:
Systemic BP changes or increases in intra-abdominal/intrathoracic pressures during exercise
may lead to increased cerebral arterial pressure or cause dilatation of pain-sensitive venous
sinuses (3).
BP changes during exercise in individuals with impaired cerebrovascular autoregulation may
lead to inappropriate cerebrovascular dilation (5).
Incompetence of the jugular venous valve may be a potential mechanism (6).

Up to 40% of individuals who experience cough headaches also experience BEH (4).
Diagnosis
History
BEH:
Is characterized as bilateral, throbbing, pulsatile headache of acute onset
Begins during or soon after exercise
Not associated with any head trauma
Lasts anywhere from 5 min to 24 hr (3)
Can be prevented by avoidance of exercise or decreased intensity
Is not associated with vomiting, but may have nausea
Weightlifter's headache:
Results from a sudden, explosive activity
Is described as “stabbing”
Lasts seconds to minutes
Thorough history should aim to:
Elicit details that may alert to a focal neurologic cause and rule out any history of head
trauma
Identify any red flags suggesting other cause of headache, such as confusion,
disorientation, fatigue, blurry vision, seizure activity, numbness or focal weakness, memory
or speech impairment, aura, phonophobia, photophobia, blurry or double vision, febrile
illness, dizziness, ataxia, or history of head trauma
Distinguish exertional headache from migraine or tension headache (by identifying if it is
unilateral or bilateral, “throbbing,” or “stabbing,” and whether it lasts seconds, minutes, or
hours)
Identify history of migraine disorder in the patient or his/her family
Identify any past history of bleeding disorders or blood clots
Physical Exam
A complete neurologic examination must be performed.
This should include a funduscopic exam to look for any papilledema, testing of visual fields,
and pupillary reflex.
Check bilateral extremity strength, coordination, balance, gait, reflexes, sensation, and
cranial nerve function.
Assess mental status. If there are any signs of altered mental status, then it is not BEH.
Look for signs of meningismus or neck stiffness.
Check vital signs, including BP, temperature, pulse, and respiratory rate.
By definition, the neurologic examination will be normal in BEH.
The rest of the exam should be determined by any red flags or key components of the
history, which may suggest a systemic cause.

Imaging
If there are any focal findings or any concern for a structural lesion or a stroke, then
neuroimaging, such as CT or MRI, must be done.
Due to increased risk for intracranial pathology with increasing age, many experts
recommend doing neuroimaging on any headache that develops above age 40 [Class C].
At younger ages with classic history of BEH and normal exam, imaging is typically not
necessary to make the diagnosis.
The decision whether to neuroimage the 1st episode of weightlifter's or cough headache can
be a difficult one, due to the fact that this type of headache often develops abruptly and
cannot be easily distinguished from SAH on a clinical basis. This decision should be made on
a case-by-case basis, depending on risk factors, associated signs and symptoms, and age
[Class C].
MRI can better evaluate the posterior fossa than CT scan, but CT more quickly rules out
hemorrhage.
An MRA (MR angiogram) can be considered in appropriate circumstances that require
assessment of intracranial vasculature.
Consider lumbar puncture if there is a suspicion for subarachnoid hemorrhage (SAH) and the
CT scan is negative.
Concussion
Cervicogenic headache
Tension headache
Migraine disorder
Systemic disorder, such as a viral illness
Drug-induced headache
Heat illness
Dehydration
HTN
CNS infection
Intracranial lesion, such as a brain tumor
Subarachnoid hemorrhage (SAH)
Cerebral aneurysm
Treatment
Medication
NSAIDs are typically used to treat BEH as well as to prevent recurrence.
They should be taken 30–60 min prior to the headache-causing physical
exertion.
Indomethacin (25 mg PO t.i.d.) and naproxen have been used with success
7[C].
Ergotamine can be used for prophylaxis in cases where NSAIDs are not well
tolerated [C], but caution needs to be exercised because of its side effects and
drug interaction profile.
Propranolol is another option for prophylactic therapy, although efficacy in BEH
has not been proven.
General Measures
NSAIDs can cause peptic ulcer disease, stomach irritation, and nausea. In
high doses, they can cause renal dysfunction and renal failure. They should be
taken with food and used sparingly.
Ergotamine has known complications, including vascular stasis and peripheral
vascular constriction, thrombosis, worsening of vascular disease, fibrosis, and
increased uterine contractility. It is contraindicated in coronary artery disease,
hypertension, liver disease, renal disease, pregnancy, and Raynaud's
syndrome. It should be used with caution.
Referral
Consider referral to a neurologist if headache symptoms are atypical or
recalcitrant to treatment.
Ongoing Care
Patient Education
Patients should be advised to avoid exercising in the heat and to stay hydrated.
A sudden, severe headache described as “the worst headache” of a patient's life should lead
to evaluation in an emergency room.
Prognosis
BEH tends to recur with exercise.
In 1 study that followed 93 patients, 32% of patients with exertional headache sustained
complete remission within 5 yrs, and 78% underwent complete remission or significant
improvement in 10 yrs (8).
In a small study of patients with sexual headache, 41% had recurrence within 5 yrs (4).
References
1. Pascual J, Iglesias F, Oterino A, et al. Cough, exertional, and sexual headaches: an
analysis of 72 benign and symptomatic cases. Neurology. 1996;46:1520–1524.
2. Rasmussen BK, Olesen J. Symptomatic and nonsymptomatic headaches in a general
population. Neurology. 1992;42:1225–1231.
3. McCrory P. Headaches and exercise. Sports Med. 2000;30:221–229.
4. Silbert PL, Edis RH, Stewart-Wynne EG, et al. Benign vascular sexual headache and
exertional headache: interrelationships and long term prognosis. J Neurol Neurosurg
Psychiatry. 1991;54:417–421.
5. Heckmann JG, Hilz MJ, Mück-Weymann M, et al. Benign exertional headache/benign

sexual headache: a disorder of myogenic cerebrovascular autoregulation? Headache.
1997;37:597–598.
6. Doepp F, Valdueza JM, Schreiber SJ. Incompetence of internal jugular valve in patients
with primary exertional headache: a risk factor? Cephalalgia. 2007.
7. Diamond S. Prolonged benign exertional headache: its clinical characteristics and

response to indomethacin. Headache. 1982;22:96–98.
8. Rooke ED. Benign exertional headache. Med Clin North Am. 1968;52:801–808.
Additional Reading
Green MW. A spectrum of exertional headaches. Med Clin North Am. 2001;85:1085–1092.
Headache Classification Committee of the International Headache Society. The international

classification of headache disorders. Cephalgia. 2004;24(Suppl 1):9–160.
Turner J. Exercise-related headache. Curr Sports Med Rep. 2003;2:15–17.
Codes
ICD9
339.84 Primary exertional headache
Clinical Pearls
BEH occurs during or soon after intense physical activity and can be prevented
by avoiding intense exertion.
It is typically characterized as bilateral, throbbing, and pulsatile. It lasts 5 min to
24 hr, and the average age of onset is 24.
Weightlifter's (or cough) headache is quick in onset, “stabbing,” lasts seconds
to minutes, and is associated with the Valsalva maneuver. It more commonly
affects older individuals.
Neuroimaging should be considered if there are any signs or symptoms
suggestive of intracranial pathology.
Evidence behind diagnosis and management of exertional headaches is
limited.
Extensor Tendon Avulsion from the Distal
Phalanx/Mallet Finger
Rachel A. Coel
Quynh Hoang
Basics
Description
Mallet finger is defined as a stretching or tearing of the extensor tendon or a complete
avulsion of the tendon insertion from the dorsal base of the distal phalanx with or without
bony avulsion.
The injury results in the inability to completely extend the distal interphalangeal (DIP) joint.
It is most commonly caused by sudden forced flexion of the fingertip while the DIP joint is
actively extended.
Less commonly, it can occur when the DIP joint is forcefully hyperextended with a resulting
fracture at the dorsal base of the distal phalanx (1,2)[C].
Epidemiology
Usually occurs during sports participation when an extended finger is struck on the tip by a
ball.
Also occurs in the work environment or with minor household trauma.
The most commonly injured digit is the 3rd (middle) finger of the dominant hand, although any
digit, including the thumb, can be involved.
Risk Factors
Sports, especially those involving ball contact and hand-to-hand contact
Diagnosis
History
Patient reports axial loading and/or hyperflexion of the DIP joint while the finger is held in
extension. Classically, the extended finger is struck on the tip by a ball.
Patient complains of pain and swelling at the DIP joint of the affected finger, especially the
dorsal aspect, with inability to actively extend the DIP joint.
Physical Exam
There is tenderness to palpation over the dorsum of the DIP joint.
Patient is unable to actively extend the DIP joint, although passive extension is possible.
To effectively establish the diagnosis, hold the proximal interphalangeal (PIP) joint in a fixed
position, and then have the patient extend at the DIP joint.
An extensor lag at the DIP joint generally is present immediately after injury, but the deformity
may be delayed by hours and even days or weeks.
In general, also evaluate for open skin lesions, collateral stability, and digit rotation or
angulation.

Using the Doyle classification scheme (3), mallet finger injuries can be divided into four types:
Type I: Closed injury ± small dorsal avulsion fracture
Type II: Open injury/laceration at DIP joint with loss of tendon continuity
Type III: Open injury with deep abrasion causing loss of skin, subcutaneous tissue, and
tendon substance
Type IV: Mallet fracture
Transepiphyseal injury fracture in children
Fracture fragment involving 20–50% of articular surface
Fracture fragment involving >50% of articular surface
Imaging
Radiographs are recommended in all cases to evaluate for accompanying fracture or joint
subluxation.
Three views of the affected finger: posteroanterior, lateral, and oblique
Three patterns: No avulsion fracture, small avulsion fracture (<30% articular surface), large
avulsion fracture (>30% articular surface)
Consider obtaining repeat radiographs at conclusion of continuous splinting to evaluate
fracture healing.
Tuft or distal phalanx fracture with deformity
In the pediatric age group, injury to the epiphysis at the base of the distal phalanx may mimic
a mallet finger.
Treatment
The involved finger should be splinted in full extension or slight
hyperextension at the DIP joint.
No flexion should occur at any time until treatment is complete.
Splint continuously for 6–8 wks, followed by an additional 2 wks of nighttime
splinting (1)[C],(4)[B],(5)[A].
If bone avulsion fracture, extension splint should be applied for 6 wks.
If tendon injury without bone involvement, splint in extension for 8 wks.
If large avulsion fracture, consider surgical consultation.
Compliance should be assessed at 2-wk intervals until healing has occurred.
Monitor dorsal skin for signs of vascular compromise owing to compressive
splinting.
Controversy still exists regarding the optimal treatment of each type of mallet
finger with respect to the type of splint used, the length of immobilization, and
the surgical technique used if operative repair is indicated.
A recent Cochrane Review (2009) concluded that there is insufficient evidence
from existing studies to establish the relative effectiveness of different types of
finger splints used versus the standard Stack splint. Additionally, there is
insufficient evidence to determine when surgery is indicated (5)[A].
A systematic review by Geyman and colleagues suggested that conservative
treatment with splinting was safe and effective in more than 80% of mallet
finger injuries (4)[B].
Most quantitative research studies indicated that splinting is the treatment of
choice and is effective for most mallet finger injuries involving less than a third
of the articular surface or without DIP joint subluxation.
DIP joint often is stiff after prolonged immobilization.
After 6–8 wks of continuous splinting, start DIP joint gentle active and passive
range-of-motion (ROM) exercises.
At the end of continuous immobilization, if a mallet deformity of >20 degrees
recurs, continue splinting for an additional 1–2 mos.
Consider extension splinting during athletic activities for an additional 2 mos
after continuous splinting has been completed.
For chronic mallet finger injury (patients who present more than 4 wks after
injury), treatment with continuous splinting for 10 wks followed by 2 wks of
nighttime splinting has been shown to be successful (2)[C].
Surgical treatment with direct repair of the tendon or with open reduction and
internal fixation is usually reserved for open injuries or for unstable mallet
fractures involving more than a third of the articular surface or with associated
DIP joint subluxation (1)[C].
However, based on a recent Cochrane Review, there is insufficient evidence
to determine when surgery is specifically indicated (5)[A].
Ongoing Care
Regular physician assessment and diligent patient compliance are critical for successful
nonoperative treatment.
Assess compliance with continuous splinting at follow-up visits at 2-wk intervals.
Consider repeat radiographs at the conclusion of continuous splinting to assess for bone
healing.
Patient Education
This injury requires careful patient compliance.
The patient must understand the necessity of keeping the finger in extension for the entire
duration of treatment, including during splint changes and skin care.
The patient must monitor dorsal skin for signs of vascular compromise from continuous
extension splinting.
Complications
Patients may develop a slight extensor lag (5–10 degrees) with a mild loss of
total motion, but it should not result in a functional deficit.
Complications tend to be related to splinting and typically are short term, such
as skin ulcerations, splint-related pain, and tape allergies.
Other complications include permanent DIP joint stiffness and deformity.
If patient has failed 10 wks of continuous splinting, he or she may require
surgical consultation.
Surgical complications may be long term, including pain, deformity, and
treatment failure.
References
1. Bendre A, Hartigan B, Kalainov D. Mallet finger. J Amer Acad Orthop Surg.
2005;13:336–344.
2. Tuttle HG, Olvey SP, Stern PJ. Tendon avulsion injuries of the distal
phalanx. Clin Ortho and Related Research. 2006:157–168.
3. Doyle JR. Extensor tendons—acute injuries. Green DP, Hotchkiss RN,

Pederson WC, eds. Green's operative hand surgery. 4th ed. Philadelphia,
PA: Churchill Livingstone; 1999:1962–1971.
4. Geyman JP, Fink K, Sullivan S. Conservative versus surgical treatment of

mallet finger: a pooled quantitative literature review. J Amer Board of Fam
Pract. 1998;11(5):382–390.
5. Handoll H, Vaghela M. Interventions for treating mallet finger injuries.

Cochrane Database of Systematic Reviews. 2009;2.
Codes
ICD9
736.1 Mallet finger
Clinical Pearls
Special considerations for the pediatric population:
Physeal and epiphyseal involvement at the base of the distal phalanx is
common in pediatric mallet finger injuries.
Children <12 yrs of age are more likely to have a Salter-Harris type I or II injury
rather than a true mallet finger injury.
In the pediatric age group, nondisplaced mallet finger injury may be treated with
continuous splinting of the DIP joint in extension or slight hyperextension for 4–
6 wks, with 2 additional weeks of nighttime splinting. Extension splints should be
worn for sports activities for an additional 4 wks.
Reduction is necessary for displaced fractures.
If closed reduction is unsuccessful, then referral for surgical repair is indicated.
External Ear Chondritis/Abscess
Arturo J. Aguilar
Basics
Description
Inflammation and infection of the pinna
Commonly a complication of otic trauma, burns, or neighboring infection
It may present as a complication of draining a periauricular hematoma (cauliflower ear) in
sports such as wrestling and rugby.
Occasionally, chondritis may be a complication of untreated or resistant otitis externa in
swimmers.
Cartilage of the external ear is easily damaged and at risk for infection owing to:
Lack of overlying subcutaneous tissue
Relative avascularity
Exposed position
Etiology
Common causes of chondritis include:
Chemical or thermal burns
Otitis externa
Deep abrasions
Frostbite
High piercing of the earlobe
Human bites
Iatrogenic from incision and drainage treatment of hematoma
Mastoid surgery
Bacteria involved:
Pseudomonas aeruginosa
Staphylococcus spp.
Proteus spp.
Diagnosis
Typical physical findings in combination with preceding causes
Physical Exam
Initially a dull pain that increases in severity
Pinna:
Painful
Exquisite tenderness
Erythematous
Warmth
Loss of contours caused by edema often with sparing of the lobule
Increase in the auriculocephalic angle
Fluctuant areas develop with eventual breakdown and suppuration.
Entire ear involvement if untreated: Disfigurement can occur.
Fever/chills

Lab
CBC with differential for systemic symptoms
Wound culture for signs of localized infection
Blood culture if systemic signs of infection
Periauricular hematoma: “Cauliflower ear”
Malignant otitis externa
Treatment
Acute treatment
General postinjury preventive measures:
Prevention of chondritis is of the utmost importance.
Difficult management and disfiguring potential
Avoid pressure to the injured ear
Minimize active débridement of eschars and crusts
Gentle washing twice daily with antibacterial soap and water followed by
complete drying and application of topical antibiotics
Keep hair away from the ear.
Complications: Disfiguration of the pinna:
Occurs without proper treatment
Ranges from being shriveled, cauliflower-like ear to complete loss of the
external ear and possible stenosis of the auditory meatus
ENT consult:
For treatment of chondritis, abscess, and necrosis of the involved cartilage
Early surgical drainage
Aggressive early management may prevent gross ear deformity.
Medication
Oral antibiotics for minor cases of early ear lobe inflammation:
Ciprofloxacin preferred (<18 yrs old)
1st-generation cephalosporin or dicloxacillin
IV antibiotics for severe infection
Apply topical antibiotics when break in skin barrier.
Medications:
Ciprofloxacin: 500 mg PO t.i.d. (adult)
Cephalexin: 500 mg (children: 50 mg/kg/day) PO q.i.d.
Dicloxacillin: 500 mg (children: 25 mg/kg/day) PO q.i.d.
Admission Criteria
Parenteral antibiotics and early surgical drainage for patients with complicated
chondritis
Toxic patient with fever and chills
Immunocompromised patient
Unreliable patient or caretaker
Additional Reading
Bentrem DJ, Bill TJ, Himel HN, et al. Chondritis of the ear: a late sequela of
deep partial thickness burns of the face. J Emerg Med. 1996;14:469–471.
Leybell I, Regan L. Drainage, auricular hematoma: treatment and medication.
Emedicine. 2008. Medscape. 7 Sept. 2009
Osguthorpe D, Nielsen D. Otitis externa: review and clinical update. Am Fam

Phys. 2006;74:1510–1516.
Staley R, Fitzgibbon JJ, Anderson C. Auricular infections caused by high ear

piercing in adolescents. Pediatrics. 1997;99:610–611.
Codes
ICD9
380.03 Chondritis of pinna
380.10 Infective otitis externa, unspecified
380.11 Acute infection of pinna
External Genital Trauma
David V. Smith
David T. Bernhardt
Basics
Injuries in males:
Lacerations, hematomas, avulsions of penis/scrotum
Urethral injury
Testicular rupture
Hematocele
Penetrating injury to penis/scrotum
Injuries in females:
Lacerations, hematomas, avulsions of vagina/soft tissue
Vaginal impalement injuries
Vaginal insufflation injuries
Pelvic fracture
Genital trauma from sexual abuse
Consider nonaccidental trauma or sexual abuse.
Sexual abuse is a common etiology in females.
Urethral damage is frequently caused by traumatic mechanisms similar to those in adults.
Description
Females:
Injuries to the urethra are rare owing to the short, unexposed, and mobile urethra. Most
occur at the bladder neck.
Most traumatic injuries are secondary to accidental falls onto objects resulting in
impalement or blunt trauma.
Blunt trauma:
Vulvar lacerations, ecchymosis, hematoma
Can result in crush injury or pelvic fractures
Impalement:
Physical findings can mimic penetration by blunt forceful trauma, so must evaluate for
possible sexual abuse.
Vagina, urethra, bladder, anus, rectum, and peritoneal cavity can be pierced by a
sharp object.
Insufflation with high-pressure water (eg, falls off jet skis or water skis) can result in
vaginal tears.
Males:
Blunt trauma:
Penile/soft tissue:
Urethral injuries are more common in prostatic urethra vs bulbar or penile urethra.
95% of posterior urethral injuries are caused by pelvic fractures.
As many as 25% of pelvic fractures have concomitant urethral injuries.
Laceration, ecchymosis, hematoma, avulsion injuries
Scrotal trauma:
Most testicular injuries are from blunt trauma in athletics.
Scrotal ecchymosis, hemorrhage
Hematoceles: Blood accumulation in space between tunica albuginea and tunica
vaginalis.
Testicular rupture: Disruption of the tunica albuginea
Traumatically induced hydroceles
Traumatically induced testicular torsion
Pelvic fracture with significant blunt trauma
Penetrating injury: Can cause significant injury to soft tissues and scrotum
Diagnosis
If an examination of the introitus and perineum cannot be performed easily, examination under
anesthesia should occur.
An examination in the OR, in addition to being better tolerated by the patient, can help the
physician to evaluate for sexual abuse and to confirm that the injury is consistent with the
history.
The workup of male pediatric patients also should include an examination in the OR if an
adequate ED examination does not occur or if suspicion of abuse exists.
History
Mechanism of injury
Prior history of trauma
Pelvic pain, bleeding, inability to void
Blood at the urethral meatus or hematuria
History of possible sexual abuse
Physical Exam
Females:
Genitourinary (GU) examination to determine extent of injury
Collection of laboratory and forensic specimens if history of sexual abuse
If injury is minor superficial laceration or hematoma and no history of penetrating injury,
normal exam is sufficient.
Vaginal lacerations with active bleeding should be repaired by provider with experience to
avoid urethra, bladder, and rectal injury.
Indications for exam under anesthesia:
Young or uncooperative patient
Transection of the hymen with inability to see the full extent of injury
Vaginal hemorrhage
Expanding vulvar or vaginal hematoma
History of significant blunt, forceful, or penetrating trauma
Significant vaginal laceration or soft tissue injury
Complex vaginal and perineal lacerations associated with pelvic fracture or rectal injury
Perforation into peritoneal cavity requires exploratory laparotomy/laparoscopy.
Males:
GU examination to determine extent of injury
Examine for high-riding prostate, perineal or genital swelling, blood at meatus.
Examine testicles for pain or swelling concerning for rupture, hematocele, torsion.
Evaluate for rectal injuries.
Lab
Urinalysis
Hematocrit
Blood urea nitrogen (BUN) and creatine (Cr)
Consider screen for sexually transmitted infections if history or exam is consistent with sexual
abuse.
Imaging
Scrotal imaging: Scrotal ultrasound (SUS):
Scrotum exam can be difficulty with significant swelling.
SUS is the most sensitive and specific imaging for detecting intrascrotal injury (1)[B].
SUS assesses the integrity and vascularity of the testes.
SUS can distinguish testis rupture from hematocele, hydrocele, torsion, and epididymitis
(1).
Urethral injury: Retrograde urethrography (RUG):
Inability to void, blood at meatus, and any degree of hematuria are absolute indications for
RUG (1)[B].
Recommended with any penetrating genital injuries (1)[C]
Water-soluble contrast material is injected at the urethral meatus.
Extravasation of contrast material and location of extravasation can diagnose presence of
tear as well as degree of tear.
Cystography: 40% of urethral injuries have concomitant bladder injuries.
Proctoscopy: In the female when there is a possibility of impalement injury or pelvic fracture,
proctoscopy can aid in evaluating the extent of injury (2).
Perineal and vaginal trauma
Bladder trauma
Ureter or kidney trauma
Pelvic fracture
Treatment
Pre-Hospital
Similar considerations as for major trauma victims
ED Treatment
Initial stabilization, control of bleeding, pain control
After appropriate evaluation and workup, urologic or gynecologic consult if
warranted
Urethral contusions, lacerations, and avulsions are best managed by an
experienced urologist.
Scrotal hematomas, hydroceles, and contusions can be managed with rest,
ice, and elevation.
Tetanus immunization if warranted for laceration or avulsion.
Medication
Anytime there is injury to the female mucosal genital surfaces, application of
topical estrogen cream can benefit the healing process and decrease scarring.
Males:
When physical exam findings and mechanism of injury suggest significant
testicular injury, operative exploration should be undertaken even with
equivocal SUS (1)[B].
When testicular rupture is suspected, prompt surgical intervention is advised
(1)[B].
Prompt drainage of large hematoceles is recommended to prevent infectious
complications and prevent prolonged pain (1)[B].
Following blunt scrotal trauma, probability of testicular salvage decreases
significantly if not explored in 72 hr (1).
Posttraumatic testicular torsion and testicular dislocation require immediate
surgical intervention.
Penetrating trauma to the scrotum or penis warrants prompt surgical
exploration (1)[C].
Complex avulsions are best managed with initial débridement and delayed
reconstruction (1)[B].
Minor avulsions are managed as simple lacerations with irrigation and
primary closure (1)[B].
Females:
Simple perineal and vulvar lacerations usually can be repaired in the ED (2).
Large hematomas should be incised and drained (2).
See “Physical Exam” for indications for exam under anesthesia.
In exam under anesthesia, if peritoneal or rectal cavities are entered,
exploratory laparotomy is indicated (3).
ABCs of trauma care take precedence.
Admission Criteria
Concurrent closed head injury, blunt abdominal trauma, or pelvic fracture
Need for operative management of urethral, penile, vaginal, pelvic, or bladder
injuries
Discharge Criteria
Isolated urethral injuries frequently may be managed in the outpatient setting after
appropriate urinary catheterization or suprapubic cystostomy with urologic follow-
up.
Ongoing Care
Complications
Impotence
Incontinence
Strictures
Infection
Disfigurement
Pain
Scarring
Infertility
References
1. Morey AF, Metro MJ, Carney KJ, et al. Consensus on genitourinary trauma:
external genitalia. BJU Int. 2004;94:507–515.
2. Wessells H, Long L. Penile and genital injuries. Urol Clin North Am.
2006;33:117–126, vii.
3. Merritt DF. Genital trauma in children and adolescents. Clin Obstet
Gynecol. 2008;51:237–248.
Additional Reading
Carter CT, Schafer N. Incidence of urethral disruption in females with
traumatic pelvic fractures. Am J Emerg Med. 1993;11:218–220.
Lee SH, Bak CW, Choi MH, et al. Trauma to male genital organs: a 10-year
review of 156 patients, including 118 treated by surgery. BJU Int. 2007.
Codes
ICD9
867.0 Injury to bladder and urethra without mention of open wound into cavity
878.2 Open wound of scrotum and testes, without mention of complication
959.14 Other injury of external genitals
Felon
Michael M. Linder
Andrew Harcourt
Basics
Description
Infection of the palmar pulp space of the distal finger or thumb (1)
Progresses rapidly to a severe throbbing pain and swelling in the distal pulp space
If left untreated, swelling may lead to ischemia and distal nerve damage.
Epidemiology
Usual cause is penetrating trauma with a subsequent bacterial infection
The most common pathogen is Staphylococcus aureus, but it may be caused by
Streptococcus or gram-negative organisms (1).
Risk Factors
Penetrating trauma
Etiology
Small vertical septa divide the volar pulp space into small fascial compartments (2).
These compartments provide a closed space for infection but help to prevent spread to the
flexor tendons, distal phalanx, or joint capsule.
Diagnosis
Physical Exam
Complete neurovascular exam of distal digit
Examination of function of affected digit
Examination for evidence of flexor tenosynovitis
Signs and symptoms:
Commonly present with affected hand overhead in an effort to reduce pain
Erythematous and swollen distal pulp space
Exquisite tenderness over distal pulp space
Loss of sensation indicates advanced state and likely tissue necrosis.

Lab
Wound cultures should be obtained to help direct antibiotic coverage because osteomyelitis can
develop quickly.
Imaging
Anteroposterior (AP) and lateral radiographs assist in the assessment of a retained foreign
body or if osteomyelitis is suspected.
Herpetic whitlow
Flexor tenosynovitis
Treatment
ED Treatment
The hallmark of treatment is early and complete incision and drainage of the
affected pulp space.
Lateral approach (3):
Digital nerve block with long-acting anesthetic agent
Tourniquet with Penrose drain to promote a bloodless field
Simple longitudinal incision is preferred to minimize long-term complications.
Begin incision 3–5 mm distal to distal interphalangeal (DIP) joint to avoid
injury to flexor tendon sheath or joint capsule.
Incision should be made dorsal to the neurovascular bundle and extend just
distal to the free edge of nail.
The incision should be made on the ulnar aspects of digits 2–4 and on the
radial aspect of digits 1 and 5.
A blunt probe or hemostat is used to dissect the fibrous septa.
Care is used to irrigate and remove all necrotic and purulent material.
The wound tis hen packed with sterile gauze for 24–48 hr.
The finger then is splinted for protection.
Alternatively, a simple vertical volar incision may be made for felons that P.
appear to point at the whirl of the fingertip.
Incisions carried all the way across the fingertip may result in an unstable
fingertip and are now discouraged (2).
Medication
Increasing prevalence of community-acquired methicillin-resistant S. aureus
(MRSA) requires knowledge of local patterns and susceptibilities.
Treatment should include coverage for MRSA until culture results are available.
Adults:
Trimethoprim-sulfamethoxazole DS 1 pill PO b.i.d. × 7–10 days
Clindamycin 300 mg PO q6h × 7–10 days
Children:
Trimethoprim-sulfamethoxazole 20 mg/kg/day PO divided b.i.d. × 7–10 days
Clindamycin 25 mg/kg/day PO q6–8h × 7–10 days
Complicated felons, those where osteomyelitis or tenosynovitis is suspected or
where incision and drainage needs operating room débridement, necessitate
orthopedic consultation.
Ongoing Care
Most patients can be treated and followed as outpatients.
Examination in 24–48 hr for repacking is indicated.
Adjustment of antibiotic coverage is dictated by culture results.
Complications can include frank disruption of the digital nerve and subsequent
loss of sensation in distal digit, painful neuromas, and an unstable finger pad
(4).
Incorrectly placed incisions can leave scars that interfere with sensation and
pincer grasp function.
References
1. Clark DC. Common acute hand infections. Am Fam Physician.
2003;68:2167–2176.
2. Hauck RM, Camp L, Ehrlich HP, et al. Pulp nonfiction: microscopic anatomy
of the digital pulp space. Plast Reconstr Surg. 2004;113:536–539.
3. Roberts, et al. Clinical procedures in emergency medicine, 4th ed.;
Chapter 38, (2004).
4. Marx, et al. Rosen's emergency medicine: concepts and clinical practice,

6th ed.; Chapter 47, (2005).
Codes
ICD9
681.01 Felon
Kelsey Logan
Basics
Description
A condition of female athletes that refers to disordered eating, functional hypothalamic
amenorrhea, and osteoporosis; this condition is a manifestation of the interrelationship of
energy availability, menstrual function, and bone mineral density.
Epidemiology
Prevalence
Female athlete triad: Largely unknown; 1–4% in various studies (1)
Disordered eating: 25–62% depending on sport
Amenorrhea: 3–66% (secondary amenorrhea) depending on sport
Osteoporosis: 0–13%
Risk Factors
Sports emphasizing leanness or endurance, such as gymnastics, figure skating, cross-
country running or skiing, and diving
Individual sports as opposed to team sports
Early sport-specific training
Punitive measures imposed for weight gain
Unreasonable performance expectations by self or others
Poor body self-image
Social isolation
Etiology
Reduced energy availability or an imbalance between intake and output of calories is the
ultimate cause of the disorder.
Restriction of calories may be inadvertent (not taking in enough calories for the demand of
the sport) or intentional (to try to lose weight).
Purging of calories may manifest as vomiting, laxative use, or excess exercise/training with
little or no recovery periods.
This energy deficit leads to disruption of normal estrogen production through the
hypothalamic–pituitary axis, which decreases bone formation and bone production and, in
women, a change in menstrual function. Men may demonstrate reduced energy availability
and thus a decrease in bone density, also owing to the preceding risk factors.
The etiology is multifactorial.
There is a psychological difference between those misusing exercise, laxatives, or calorie
restriction to manage/lose weight and those who inadvertently do not match their calories to
their sport.
In many women, the emphasis on leanness in sport, along with the perceived benefits of low
body weight (eg, better fitness, agility, speed) causes increased focus on weight-control
measures (2).

Psychological disorders such as depression and anxiety
Diagnosis
High index of suspicion required
History
One component of the triad raises suspicion for the others.
Presence of primary (absence of menses by age 15) or secondary amenorrhea (absence of
menses for 3 consecutive months)
Presence of stress fracture or history of stress fracture
Review exercise habits and nutritional history for abnormal weight-control behavior involving
food and/or exercise.
Review life stressors.
Patient may have fear of weight gain and/or poor body image.
Patient may have comorbid psychological problem (eg, depression).
Symptoms include:
Amenorrhea
Stress fracture
Weight-control behaviors and/or weight loss
Cold intolerance
Sore throat/gastroesophageal reflux
Constipation/GI motility problems
Light-headedness
Fatigue
Depression
Introversion
Worsened athletic performance
Physical Exam
Height, weight, body mass index (BMI <18.5 kg/m2 considered underweight for women ≥18
yrs of age)
Vital signs for evidence of bradycardia and/or orthostatic hypotension
Observe for fat depletion and muscle wasting.
Integumentary exam for dry skin, lanugo, brittle hair/nails
Ocular exam to evaluate for pituitary and thyroid disorders
Dental examination for evidence of lingual enamel erosion secondary to vomiting
Parotid gland observation/palpation for hypertrophy secondary to vomiting
Thyroid palpation
Cardiac auscultation for evidence of dysrhythmia
Complete neurologic examination, especially cranial nerves and reflexes
Tanner staging
Consider pelvic examination if amenorrheic.
Careful examination of any musculoskeletal pain, looking for stress fracture

Laboratory results may be normal, even in very undernourished women.
Lab
Pregnancy test
Urinalysis for specific gravity (should be normal unless dehydration is present)
CBC (normal; possibility of anemia)
Erythrocyte sedimentation rate (normal)
Serum electrolytes, blood urea nitrogen, and creatinine (normal, except possibly in the case
of bulimia, which may cause electrolyte abnormalities or severe dehydration associated with
malnutrition)
Thyroid function tests (normal)
Luteinizing hormone and follicle-stimulating hormone levels (low or normal)
Estradiol level (low)
Serum prolactin (normal)
Serum cortisol (mildly elevated)
Serum testosterone and dehydroepiandrosterone sulfate if concern for androgen excess,
such as with polycystic ovary syndrome or adrenal tumors
Imaging
Bone mineral density (BMD) testing with dual-energy x-ray absorptiometry (DXA) if patient
has had stress fracture from mild trauma or 6 mos' evidence of hypoestrogenism and/or
disordered eating (3)[C]
Reevaluation on same DXA machine yearly if chronic
DXA of posteroanterior spine and hip using lower Z-score to base diagnosis of low BMD
Progesterone challenge (eg, medroxyprogesterone acetate 10 mg PO daily × 7–10 days): If a
period occurs, there is sufficient estrogen to stimulate the endometrium.
Pregnancy
Pituitary disease
Hyperthyroidism
Hypogonadism
Hyperparathyroidism
Polycystic ovary disease
Adrenal dysfunction
Autoimmune disease
Anabolic steroid use/abuse
Excess glucocorticoid administration
Malabsorption syndromes
Treatment
Main goal of treatment is to increase energy availability and preserve
normal BMD; the normal estrogenic state requires adequate caloric intake to
match energy expenditure (4).
Athlete often resists treatment if negative energy balance is intentional.
Treatment discussion requires good patient rapport.
Requires team approach (ie, physician, psychologist, athletic trainer, parents,
nutritionist, coach) and open communication among all involved
Counsel athlete that achieving energy balance may require increasing caloric
intake and/or decreasing caloric expenditure (through decreased exercise).
Identify and modify specific behavior triggers or stressors.
Emphasize performance and injury issues related to negative energy balance
(eg, stress fractures are related to low BMD).
Monitor progress closely, as indicated by severity and response to treatment.
May need to restrict patient from sport/training if not making progress or
participating in treatment plan
Prevention is best accomplished through education of athletes, coaches,
trainers, and parents.
Medication
There is no strong evidence to support either hormone-replacement therapy or
oral contraceptive use to increase or protect BMD in athletes with functional
hypothalamic amenorrhea, even if they remain amenorrheic (5).
Bisphosphonates are not recommended for women of reproductive age (6).
Treating comorbid psychiatric conditions is essential, and pharmacotherapy for
the specific disorder may be useful here.
Multivitamin supplements are commonly recommended.
Supplement calcium at 1,500 mg/d and vitamin D at 400–800 IU/d.
Referral
Psychology referral is recommended for cognitive-behavioral therapy; consider
family therapy to help identify and cope with stressors.
Nutrition consultant with disordered-eating experience recommended
Electrolyte disturbance
Severe bradycardia or dysrhythmia
Severe dehydration
Significant psychiatric pathology
Ongoing Care
Frequent follow-up to gauge compliance with treatment plan
Monitor weight; address nutritional concerns and goals at each visit.
Consistent education regarding energy balance and sport performance
Assess physiological and psychological functioning, sport performance (if
participating).
Coordinate care with psychology and nutrition consultants.
Menstruation usually occurs (may take a year or more) with improved nutrition
and decreased exercise intensity.
Patient Education
Body weight and caloric intake below what is necessary for normal
physiological function are detrimental to athletic performance.
BMD may be permanently lowered in adolescents by decreasing bone
formation and increasing bone resorption.
Fertility is decreased with amenorrhea but is not totally impaired; it is possible
to conceive without having a period. Fertility issues are not thought to be
permanent and may normalize with resumption of menses.
Prognosis
Diagnosable eating disorders (eg, anorexia nervosa and bulimia nervosa) are
very difficult to treat and rarely are totally resolved. Prognosis is guarded.
Athletes who have perfectionist-driven tendencies are less likely to comply with
treatment and have difficulty with recovery.
Appropriate increase in energy availability has the potential to restore normal
estrogenic state, normalize menstrual function, and improve BMD.
Complications
Injury forcing the athlete to take time from exercising can exacerbate
disordered eating practices (eg, caloric restriction or purging).
References
1. Nichols JF, Rauh MJ, Lawson MJ, et al. Prevalence of the female athlete
triad syndrome among high school athletes. Arch Pediatr Adolesc Med.
2006;160:137–142.
2. Beals KA, Meyer NL. Female athlete triad update. Clin Sports Med.
2007;26:69–89.
3. The female athlete triad. Med Sci Sports Exerc. 2007;39:1867–1882.
4. Dimarco NM, Dart L, Sanborn CF. Modified activity-stress paradigm in

an animal model of the female athlete triad. J Appl Physiol. 2007.
5. Falsetti L, Gambera A, Barbetti L, et al. Long-term follow-up of functional

hypothalamic amenorrhea and prognostic factors. J Clin Endocrinol Metab.
2002;87:500–505.
6. Lebrun CM. The female athlete triad: what's a doctor to do? Curr Sports
Med Rep. 2007;6:397–404.
See Also
Eating Disorders
Codes
ICD9
626.0 Absence of menstruation
733.00 Osteoporosis, unspecified
Clinical Pearls
Female athlete triad represents a disorder of negative energy balance where,
for whatever reason, the body's energy intake does not keep up with energy
output.
When one aspect of the triad is found, the others should be investigated (eg, if
a woman presents with a bony stress injury, inquiry about menstrual function
and eating habits should be made).
Treatment with oral contraceptives or other hormonal supplementation does not
improve BMD in these athletes. The goal of treatment should be positive
energy balance, with increased nutritional intake and decreased physical
activity resulting in resumption of normal periods through nonpharmacologic
methods.
Treatment of the triad involves many members of a medical team, including
physician, nutritionist, psychologist, athletic trainer, and others. Involving a
support system, including coaches, teammates, friends, and family, is often
helpful.
Flexor Carpi Ulnaris and Flexor Carpi Radialis
Tendonitis
Kevin Eerkes
Basics
Description
Flexor carpi radialis (FCR) and flexor carpi ulnaris (FCU) tendons are located on the radial
and ulnar aspects of the wrist, respectively.
Tendonitis of these tendons may occur from trauma or repetitive use.
Epidemiology
FCU tendonitis is more common than FCR tendonitis.
FCR tendonitis is considered rare.
Risk Factors
Diabetes mellitus
Sports with grip: Tennis, racquetball, golf, cycling, weightlifting, etc.
Etiology
Anatomy and function:
FCR inserts on the volar aspects of the trapezium and 2nd and 3rd metacarpal bases.
It is difficult to palpate the insertion point owing to overlying thenar muscles.
It palmar flexes and radially deviates the wrist.
FCU inserts mainly on the pisiform, with some fibers extending to the hamate hook and
bases of the 4th and 5th metacarpals.
The pisiform is a sesamoid imbedded in the FCU tendon.
It palmar flexes and ulnarly deviates the wrist.
Pathology:
With trauma or repetitive use, the synovium of the tendon can become inflamed.
Even though the term tendonitis is commonly used, tenosynovitis is a more appropriate
term.
Over the long term, trauma and overuse can cause the tendon to degenerate, a condition
called tendinosis.
Etiology of tendonitis:
Direct injury can trigger tendonitis.
A single macrotraumatic event or
Repeated microtraumatic events (eg, racquet sports, baseball, golf, hammering, typing,
mousing)
Improper technique can cause tendonitis.

Other overuse injuries of the wrist and hand
Median nerve irritation because of close proximity of FCR tendon to the median nerve
Diagnosis
History
Pain and possible swelling on volar aspect of wrist
Increase in pain with activity and gripping
Limited motion
Possible crepitus at the site with movement or palpation
Possible acute or repeated trauma to the area
Overuse:
Repetitive and forceful activity
Sudden increase in activity
Change in technique or equipment
FCR tendonitis: Pain radially, may radiate into forearm or thumb
FCU tendonitis: Pain ulnarly
Physical Exam
Possible swelling at the volar aspect of wrist
Tenderness near insertion points:
FCR tendonitis:
Locate the FCR tendon to the ulnar side of the scaphoid tubercle.
Follow the course of tendon about 3 fingerbreadths distally to find the approximate
insertion point.
FCU tendonitis: Tenderness at the pisiform or just distal at the 4th and 5th metacarpal
bases
Pain with active contraction:
FCR tendonitis: Palmarflex and radially deviate the wrist.
FCU tendonitis: Palmarflex and ulnarly deviate the wrist.
Also may have pain with passive dorsiflexion of the wrist
Pain with pisotriquetral grind test may suggest osteoarthritis of the pisotriquetral joint.

Imaging
Radiographs:
Usually not needed for diagnosis
Views: Posteroanterior, lateral, oblique, and lateral in slight supination of wrist
Usually normal but may see:
Degenerative changes in the pisotriquetral joint
Calcium in the tendon in calcific tendonitis
MRI:
Use when diagnosis is unclear (especially for ulnar-sided wrist pain)
Use when not improving with conservative treatment
Findings:
High fluid signal within the tendon sheath
Tendon sheath thickening
Tendon may be enlarged.
US:
FCR tendonitis: Fluid distending the synovial sheath
FCU calcific tendonitis: Calcium deposition in the tendon proximal to the pisiform
FCR/FCU tendinosis:
Hypoechoic thickening of tendon
May show neovascularization on color-flow Doppler
Pain relief with lidocaine injection into the tendon sheath aids in diagnosis.
Radial side of wrist:
Fracture of scaphoid, trapezium, or 1st or 2nd metacarpal bases
de Quervain tenosynovitis
Osteoarthritis at 1st carpometacarpal joint or other joints of the carpus
Strain or tendonitis of thenar muscles
Ganglion: Usually located to the radial side of the FCR tendon
Carpal tunnel syndrome
Ulnar side of wrist:
Fracture of pisiform, ulnar styloid, hamate hook, or other carpal bone
Triangular fibrocartilage complex tear
Osteoarthritis of the pisotriquetral joint or other nearby joints
Strain or tendonitis of hypothenar muscles
Hypothenar hammer syndrome
Ulnar nerve entrapment in Guyon canal
Miscellaneous:
FCR/FCU tendinosis
FCR/FCU tendon rupture
Tenosynovitis from rheumatologic disorder
Treatment
Initial treatment:
Avoiding provocative activities
Wrist splint in 25 degrees of palmar flexion (1)[C] × 1–2 wks or until
symptoms improve
Icing
NSAIDs
Subsequent treatment as condition improves:
Occupational therapy:
Stretching and strengthening program
Ergonomic improvements
Coaching:
Improve technique/mechanics.
Consider changing racquet grip (2)[C].
Refractory cases: Injection of steroid and local anesthetic into tendon sheath:
Resolution of symptoms in 35–40% of patients (3)[C]
Calcific tendonitis responds particularly well to steroids.
If symptoms are prominent and not responding to nonoperative treatment,
consider surgical consultation.
Surgical procedure:
Surgical release of the tendon
Excision of inflamed tenosynovium
Z-plasty lengthening if needed
Pisiform excision
Surgery is usually curative, with return to racquet sports in 6–8 wks (3)[C].
Ongoing Care
Patient Education
When introducing a new activity or increasing a current activity, do so slowly to help prevent
an overuse injury.
Allow time for recovery between practices and competition.
Warm up the area well before playing.
Maintain proper strength, flexibility, and endurance of the forearms, wrists, and hands.
Use proper technique.
Prognosis
Usually resolves with conservative treatment within 6 wks
References
1. Rettig AC. Athletic injuries of the wrist and hand: part II: overuse injuries of the wrist and
traumatic injuries to the hand. Am J Sports Med. 2004;32:262–273.
2. Tagliafico AS, Ameri P, Michaud J, et al. Wrist injuries in nonprofessional tennis players:
relationships with different grips. Am J Sports Med. 2009;37:760–767.
3. Palmieri TJ. Pisiform area pain treatment by pisiform excision. J Hand Surg [Am].
1982;7:477–480.
Additional Reading
Bencardino JT, Rosenberg ZS. Sports-related injuries of the wrist: an approach to MRI
interpretation. Clin Sports Med. 2006;25:409–432, vi.
Osterman AL, Moskow L, Low DW. Soft-tissue injuries of the hand and wrist in racquet
sports. Clin Sports Med. 1988;7:329–348.
Parellada AJ, Morrison WB, Reiter SB, et al. Flexor carpi radialis tendinopathy: spectrum of
imaging findings and association with triscaphe arthritis. Skeletal Radiol. 2006.
Young D, Papp S, Giachino A. Physical examination of the wrist. Orthop Clin North Am.
2007;38:149–165.
Codes
ICD9
727.05 Other tenosynovitis of hand and wrist
Clinical Pearls
FCR and FCU tendonitis usually responds to conservative treatment.
Steroid/lidocaine injection can be diagnostic as well as therapeutic.
Surgery is rarely needed.
Flexor Tendon Avulsion/Jersey Finger
Jason E. Spring
Amy Kakimoto
Basics
3 primary injury patterns have been described based on the degree of tendon retraction,
vascular disruption, and the presence of a bony fragment (1):
Type I: Retraction of the tendon into the palm of the hand with nearly complete disruption of
the blood supply (1)
Type II: Retraction of the tendon to the proximal interphalangeal (PIP) joint, held in place by
the intact vincula longa (1)
Type III: Avulsion of a large bony fragment attached to the tendon, causing retraction to stop
at the distal interphalangeal (DIP) joint due to a “hang-up” at the A4 pulley, maintaining full
vascular supply to the tendon (1)
A Type IV (also known as a type IIIb) injury has been described in the literature and refers to
a condition where both an avulsion of a bony fragment at the insertion of the FDP and an
avulsion of the tendon from the bony fragment exists. This condition frequently results in
retraction of the tendon similar to that of a type I injury (2).
Description
An avulsion of the flexor digitorum profundus (FDP) tendon from its insertion at the base of
the distal phalanx (3)
Synonym(s): Jersey finger; FDP avulsion
Epidemiology
A relatively uncommon injury seen primarily in sports where tackling and grasping of the
jersey is probable; these sports include rugby, football, and hockey (1)
The classic scenario occurs when a player grabs or attempts to grab the back of another
player's uniform causing forced extension to a strongly flexed distal phalanx, resulting in the
avulsion of the FDP tendon at its insertion (4).
Although any digit can sustain this injury, the “ring” finger is by far the most commonly
affected, accounting for over 75% of all cases (3).
Frequently misdiagnosed as a jammed or strained finger (4)
Risk Factors
Participation in any sport where tackling occurs by grabbing another player's jersey
Etiology
The FDP tendon travels along the volar side of the palm and finger. It passes distally through a
split in the flexor digitorum superficialis tendon and inserts at the base of the distal phalanx. The
jersey finger injury occurs when the FDP tendon is avulsed from its attachment on the distal
phalanx (2).
Diagnosis
History
The mechanism of injury frequently involves a sudden forceful extension of the finger while
grasping another player's jersey (1)[C].
FDP avulsions are typically seen in football, rugby, and hockey players, but rarely in other
athletes (1)[C].
The time lapse between initial injury and presentation will dictate the urgency of surgical
intervention (2)[C].
Physical Exam
INSPECTION: Swelling and discoloration may be present along the distal phalanx and DIP
joint (1)[C].
PALPATION: Tenderness may be present along the length of the flexor tendon, particularly at
the site of FDP tendon insertion. A palpable lump may be present at any point along the
proximal digit, frequently at the PIP joint or on the palm of the hand at the A1 pulley (2)[C].
RANGE OF MOTION: The loss of active flexion at the DIP joint is the most reliable exam
finding in an FDP avulsion injury. To assess the integrity of the FDP tendon, hold the PIP joint
in full extension and ask the patient to actively flex the DIP joint (2)[C]. Alternatively, ask the
patient to make a fist and look for loss of flexion at the affected DIP joint (5)[C]. Active
flexion of the PIP joint and metacarpophalangeal (MCP) joint is preserved in the injured digit.
NEUROVASCULAR EXAM: Should always be assessed and should be normal in jersey
finger injuries

Imaging
3 view radiographs (anteroposterior, lateral, and oblique) are necessary to determine the
presence and degree of bony avulsion and to potentially assess the level of tendon retraction
(5)[C].
Avulsion fractures can be seen on the volar aspect of the distal phalangeal base at the FDP
attachment site (3)[C].
Some avulsion fractures may be nothing more than a small flake of bone (common in type II
injuries) (1)[C].
DIP joint dislocation
Distal phalanx fracture
Flexor digitorum superficialis avulsion
Treatment
All FDP avulsion injuries require surgical intervention (5)[C]; however, a few
initial interventions can minimize pain and swelling while surgery is being
arranged. The urgency of hand surgery referral varies depending on the
classification of injury.
Ice
NSAIDs
The injured finger should be dorsally splinted to maintain slight flexion at the DIP
and PIP joints (5)[C].
Patients should avoid any DIP extension (5)[C].
Time between injury and treatment
Degree of tendon retraction
Presence and size of bony avulsion
Level of blood supply to the avulsed tendon (1)[C]
Several treatment options exist for athletes who present outside the window for
primary repair. These include no treatment, tendon grafting, or terminal
interphalangeal joint tenodesis or arthrodesis (2)[C].
Flexor tendon grafting may be offered if deemed necessary to the athlete's
performance (1)[C].
Arthrodesis may be offered in cases of DIP instability or articular surface
disruption (1)[C].
If symptoms are minimal, many athletes do not require any surgical
intervention, and the loss of flexion at the DIP joint usually results in minimal
functional loss. Forgoing surgery may be the optimal choice for patients with a
neglected FDP avulsion (2)[C].
The player may deem the injury as minor and not seek care.
The athlete may forego treatment in favor of completing the season, accepting
the loss of DIP flexion.
The injury may be initially misdiagnosed.
Type I:
Surgical repair should be conducted within 7–10 days of the injury (2)[C].
Surgery involves retrieval of the retracted tendon, feeding it back through the
pulley system, and reattaching the tendon to its insertion via suture or pullout
wire (1)[C].
Type II:
Early surgical repair within 7–10 days is preferred; however, due to the intact
vincula longa, surgery can be delayed 6–8 wks (2)[C].
Surgery involves feeding the tendon under the fourth annular pulley followed
by suture/pullout wire reattachment to the insertion site (1)[C].
Type III:
Early surgical intervention is preferred, but satisfactory results are possible
with delayed repair of 2 wks, due to an intact blood supply to the tendon (2)
[C].
Surgery involves open reduction and internal fixation of the avulsed bony
fragment via removable wires (1)[C].
Wires can be removed after 3–4 wks postoperatively (1)[C].
Type IV or IIIb:
Surgical repair involves the combination of bony fragment fixation and
reattachment of the retracted tendon with suture/pullout wire (2)[C].
The degree of tendon retraction and loss of vascular supply can be similar to
a type I injury, requiring surgical intervention within 7–10 days (2)[C].
Ongoing Care
Following surgery, the affected hand should be placed in a dorsal blocking splint with the
wrist in midflexion, the MCP joints at 75 degrees of flexion, and the PIP/DIP joints in
extension or near extension (1)[C]. The hand should remain in this splint for 6 wks (2)[C].
Passive flexion of the PIP and DIP joints can be started within days of the surgery (1)[C].
Utilizing an experienced hand therapist early in the postoperative period is recommended (2)
[C].
Strengthening activities can usually begin at 12 wks postoperatively (2)[C].
A mitten-type splint/cast that keeps the wrist slightly flexed with the fingers flexed into the
palm may allow an athlete to return to play early, provided no grasping of the hand is
required (2)[C].
Return to play with full grasping capabilities usually takes 4–6 mos (2)[C].
Immediate referral to an orthopedic/hand surgeon is recommended for all types of FDP
avulsion injuries.
References
1. Aronowitz ER, Leddy JP. Closed tendon injuries of the hand and wrist in athletes. Clin
Sports Med. 1998;17:449–467.
2. Jaworski CA, Krause M, Brown J. Rehabilitation of the wrist and hand following sports
injury. Clin Sports Med. 2010;29:61–80.
3. Peterson JJ, Bancroft LW. Injuries of the fingers and thumb in the athlete. Clin Sports
Med. 2006;25:527–542, vii–viii.
4. Lee SJ, Montgomery K. Athletic hand injuries. Orthop Clin North Am. 2002;33:547–554.
5. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the emergency department:
closed tendon injuries of the hand. Am J Emerg Med. 2001;19:76–80.
Codes
ICD9
842.13 Sprain of interphalangeal (joint) of hand
959.5 Other and unspecified injury to finger
Clinical Pearls
Delaying surgical treatment, particularly for type I injuries, can result in
irreparable scarring of the flexor tendon and permanent loss of flexion at the
DIP joint. While delayed surgical intervention may be offered in certain
circumstances, favorable results are not guaranteed. Type II and III injuries
frequently can be delayed several weeks without significant changes to surgical
outcome, but this is not advised (1).
If the sport does not require grasping, it may be possible for the patient to
return to play early, provided that a playing splint/cast is worn. Otherwise, return
to full play usually takes 4–6 mos (2).
Folliculitis
Elizabeth Austin
Leland S. Rickman
Basics
Description
Infection of hair follicles usually caused by Staphylococcus aureus
May be caused by gram-negative organisms, as in the case of “hot tub” folliculitis
Epidemiology
Lesions usually occur on areas of skin traumatized by maceration occurring under shoulder
pads or sweaty garments.
May develop on the legs, arms, and trunk of wrestlers
Infection does not spread in epidemic proportions but may be transmitted through skin
trauma.
“Hot tub” folliculitis is associated with the use of hot tubs, whirlpools, Jacuzzis, and swimming
pools.
Risk Factors
Furuncles occur in skin areas containing hair follicles subject to friction and perspiration.

Deep folliculitis lesions ultimately may produce furuncles or boils.
Boils may combine to form a large, exquisitely painful group of furuncles called a carbuncle.
Furunculosis, an infection pertaining to hair follicles, sebaceous glands, or skin compromised
by abrasions, wounds, or burns, may arise from existing areas of folliculitis.
Diagnosis
History
Maceration caused by sports equipment is a common cause of folliculitis. This knowledge may
lead to a definitive diagnosis.
Folliculitis lesions consist of small (2–5 mm) erythematous, sometimes pruritic papules often
topped by a central pustule.
Cultures (if taken) will show the presence of S. aureus (or Pseudomonas aeruginosa for
suspected “hot tub” folliculitis).
Furuncles appear as deep, inflammatory nodules.
Carbuncles extend into the subcutaneous fat; multiple abscesses are separated by
connective tissue septa.
Treatment
Acute treatment
Mild folliculitis:
Most cases of mild folliculitis heal spontaneously within 5 days.
To prevent furuncle formation, astringent lotions or drying agents that remove
the tops of pustules can be used.
“Hot tub” folliculitis is self-limiting and lasts only 7–10 days. It requires no
specific treatment other than avoiding persistent hot tub use.
Furuncle or carbuncle formation:
Aspiration or incision and drainage may be required for fluctuant lesions.
Cleanse affected area with benzoyl peroxide.
Oral antibiotics may be prescribed, but usually no more than 14 days of use
are necessary to prevent recurrence. Agents effective against S. aureus
include penicillinase-resistant penicillins such as oral dicloxacillin, cephalexin,
and erythromycin (or other macrolides). Fluoroquinolones such as
moxifloxacin, levofloxacin, and gatifloxacin may be effective.
Warm compresses can be applied.
Clothing and dressings that have come in contact with the affected area
should be cleansed daily at high temperatures.
Hand-washing should be performed regularly by all who come into contact
with the affected area.
Additional Reading
Adler AI, Altman J. An outbreak of mud-wrestling-induced pustular dermatitis in
college students. Dermatitis palaestrae limosae. JAMA. 1993;269:502–504.
Bartlett PC, Martin RJ, Cahill BR. Furunculosis in a high school football team.
Am J Sports Med. 1982;10:371–374.
Chandrasekar PH, Rolston KV, Kannangara DW et al. Hot tub-associated
dermatitis due to Pseudomonas aeruginosa. Case report and review of the
literature. Arch Dermatol. 1984;120:1337–1340.
Decker MD, Lybarger JA, Vaughn WK et al. An outbreak of staphylococcal

skin infections among river rafting guides. Am J Epidemiol. 1986;124:969–
976.
Heeb MA. Deep soft tissue abscesses secondary to nonpenetrating trauma.

Surgery. 1971;69:550–553.
Minooee A, Rickman LS. Transmission of infectious diseases during sports.

In: Scholssberg D, ed. Infections of leisure, 2nd ed. Washington, DC:
American Society for Microbiology, 1999.
Sosin DM, Gunn RA, Ford WL, et al. An outbreak of furunculosis among high
school athletes. Am J Sports Med. 1989;l:828–832.
Stevens DL. Cellulitis, pyoderma, and other skin and subcutaneous infections.
In: Armstrong D, Cohen J, eds. Infectious diseases, vol. 1. St. Louis:
Mosby/Harcourt Publishers, 1999:2.2.3–2.2.4.
Swartz NN. Cellulitis and subcutaneous tissue. In: Mandell GL, Bennett JE,
Dolin R, eds. Mandell, Douglas, and Bennett's principles and practice of
infectious disease, vol. 1, 5th ed. Philadelphia: Churchill Livingstone; 2000.
Codes
ICD9
704.8 Other specified diseases of hair and hair follicles
Clinical Pearls
Personal contact rarely causes transmission of S. aureus from a patient with
folliculitis, but cases of transmission through skin trauma have been
documented.
Infected areas should be kept clean and covered. To prevent spread of
infection, athletes with furuncles or carbuncles should be strongly discouraged
from participation in contact sports until lesions have resolved.
Foot Osteochondroses (Accessory Navicular,
Navicular Asceptic Necrosis-Kohler, Islin—
Apophysitis of Base 5th MT)
Jeffrey B. Kreher
Basics
Description
Accessory navicular: Unfused accessory ossification center at posterior tibialis tendon (PTT)
insertion
Geist classification:
Type I: Small sesamoid bone in PTT (usually 2–3 mm)
Type II: Synchondrosis between navicular and os naviculare (usually 8–12 mm triangular or
heart-shaped); 70% of symptomatic lesions
Type III: Cornuate navicular (questionable end stage of type II with ossification across
synchondrosis)
Synonym(s): Os tibiale (externum); Os naviculare (secundarium); Symptomatic accessory
tarsal navicular; Accessory scaphoid bone; Accessory tarsal scaphoid; Navicular secundum
Köhler disease: Articular osteochondrosis with secondary involvement of articular and
epiphyseal cartilage as a consequence of avascular necrosis of tarsal navicular bone;
synonyms: Aseptic necrosis of tarsal navicular; Avascular necrosis of navicular; Koehler
disease; Idiopathic osteonecrosis of navicular in children
Osteonecrosis of tarsal navicular in adults: Mueller-Weiss disease
Iselin disease: Nonarticular osteochondrosis of the 5th metatarsal at site of ligament and
tendon attachment and trauma; synonym: Traction apophysitis of 5th metatarsal
Traction apophysitis at base of the 5th metatarsal bone: Peroneus brevis insertion
Epidemiology
Accessory navicular:
Most often symptoms found in active children and females in 4th decade
2nd most common accessory bone of foot
Accessory bones in 36% of asymptomatic feet
Köhler disease: Rare:
Age of onset 2–9 yrs
Mean age of diagnosis: Males 6 yrs, females 4.5 yrs
Occasionally bilateral Iselin disease: Rarely reported but probably more common than
appreciated:
Age of onset in late childhood or early adolescence
Apophysis appears: Males 11–12 yrs, females 10 yrs
Apophysis fuses about 2 yrs later.
Prevalence
4–21% of general population: Most asymptomatic
50–90% bilateral
In skeletally immature, 64% symptomatic
Köhler disease: Prevalence unknown
Iselin disease: Prevalence unknown
Risk Factors
Accessory navicular: May be worse with hyperpronation
Köhler disease: May be more common in late ossification of tarsal navicular
Iselin disease:
May be more common with tight calf muscles
Seen most commonly in soccer, basketball, gymnastics, and dance
Etiology
Accessory navicular: Becomes symptomatic in the following:
Adolescent patients from chondroosseous disruption owing to tension and shear forces
from PTT and foot dynamics (type II)
From pressure of overlying footwear (all types)
Older patients owing to posttraumatic disruption of synchondrosis (type II) ± PTT avulsion
or rupture
Symptomatic type II: Microfracture, acute and chronic inflammation, and cellular
proliferation
Köhler disease:
Tarsal navicular is last bone to ossify and believed to be more susceptible to compression
injury.
May be due to ischemia from recurrent cumulative microtrauma or acute macrotrauma
Iselin disease:
Repetitive traction from peroneus brevis
Acute avulsion fracture with widening of chondroosseous junction

Köhler disease: Occasionally with other osteochondroses such as Osgood-Schlatter or Legg-
Calve-Perthes disease
Diagnosis
Symptomatic or asymptomatic
Most often clinically relevant accessory navicular is symptomatic type II.
Köhler disease:
Based on history and x-ray findings
Does not equal asymptomatic feet with abnormal x-ray findings: Multiple ossification
centers or other process
Iselin disease: Based on history and x-ray findings
History
Asymptomatic or medial foot pain with navicular bump
If painful, onset gradual or acute
If painful, onset may be secondary to ankle sprain or contusion.
Worse with activity (during or after) and compression with shoes
May have limp/antalgic gait
Köhler disease:
Medial foot pain (tenderness at tarsal navicular)
Usual gradual in onset
Worse with activity
Limp/antalgic gait
Iselin disease:
Lateral foot pain (tenderness at proximal 5th metatarsal)
Usual insidious onset
May be acute after significant trauma; often inversion injury
Worse with weight-bearing, lateral movements, cutting, and jumping
Limp/antalgic gait
Physical Exam
Protuberant tarsal navicular (posteromedial aspect)
Normal range of motion (ROM) of foot, ankle, hindfoot
Possible overlying swelling
Tender to palpation over tarsal navicular ± PTT distally
Pain with resisted plantarflexion and inversion
Köhler disease:
Antalgic gait with shifting of weight to lateral aspect of foot
Possible overlying swelling
Less likely overlying warmth
Tender to palpation over tarsal navicular
May have pain with resisted plantarflexion and inversion
Iselin disease:
Perhaps prominent proximal 5th metatarsal
Very little or no erythema, edema, or ecchymosis
May show mild pronation
Tender to palpation at peroneus brevis insertion
Pain with resisted eversion, extreme inversion, and extreme plantar- or dorsiflexion

Imaging
Radiographs:
Anteroposterior and lateral foot often miss.
Must include external oblique view
Findings depend on type (see “Geist classification” in “Description”)
US:
More for tendinous abnormalities
May see heterogeneous synchondrosis (compared with asymptomatic side)
May see diastasis in older patient
MRI:
Rarely needed
STIR images show increased signal within accessory navicular at PTT insertion.
Bone scan:
Increased uptake in region
Only 50% specific but 100% sensitive
Köhler disease:
Radiographs:
Anteroposterior and lateral foot
Commonly, narrowing/flattening of the tarsal navicular and/or loss of trabecular pattern
Possibly, apparent fragmentation or diffusely increased density in normal-shaped tarsal
navicular
Do not confuse with multiple ossification centers without increased density.
Bone scan:
Decreased uptake, or “cold area”
May be present before x-ray changes (1)
MRI:
Rarely needed
Low signal on T1 and high signal on T2
Iselin disease:
Radiographs:
Anteroposterior and lateral foot often miss.
Must include medial oblique view
Consider comparing with unaffected side
Apophyseal widening and often fragmentation of ossification center
Found almost parallel to long axis of shaft
Occasionally, with cystic changes of physis
Accessory navicular: Histologically, microfracture, acute and chronic inflammation, and cellular
proliferation in symptomatic lesions
Navicular pathology (stress fracture, tuberosity avulsion fracture)
PTT pathology (tendinopathy, tenosynovitis, rupture, dysfunction)
Less commonly: Deltoid/spring ligament injury, tarsal tunnel syndrome, Köhler disease (in
younger patients), tarsal coalition, plantar fasciitis, tight heel cord
Systemic: Infection, malignancy
Köhler disease:
Accessory navicular, trauma, stress fracture, infection, malignancy
If not better with conservative treatment, rarely tarsal coalition (congenital or acquired)
Iselin disease:
Fractures: 5th metatarsal (acute Jones and stress more transverse line), avulsion fracture
(more common with lateral ankle sprains and more oblique line)
Os vesalianum (incidence 0.1–1%; most often asymptomatic; found within peroneus brevis
tendon)
Treatment
Accessory navicular: Rest, shoe insert/orthotic (soft orthotic initially until
pain-free; then assess mechanics to see if semirigid orthotic is better for
longer-term support), analgesics, physical therapy, occasionally cast
immobilization
Köhler disease:
If mild disease, soft arch supports only
Short-leg cast (10–15 degrees of varus, 10–20 degrees of equinovarus) for
6–8 wks followed by arch support if mild pain persists
Casting may lead to shorter length of pain.
No significant difference in final outcome between short-leg cast and shoe
correction, rest, or non-weight-bearing with crutches (2,3)[C]
Symptom duration: 8+ wks of casting: 2.5 mos; <8 wks of casting: 4 mos;
noncasting: 15.2 mos (3)[C]
Iselin disease:
Rest, ice, calf stretching
If severe pain, immobilization × 2–4 wks (aircast, walking cast, or short-leg
cast with crutches)
Physical therapy to improve strength and coordination when pain-free
Medication
Analgesics (eg, acetaminophen and NSAIDs) for pain
General Measures
Accessory navicular: Application of doughnut pad over bony prominence
Indication: No improvement with nonoperative treatment
Resection of symptomatic bone with Kidner procedure ± reattachment of
PTT (4)[C]
Possible percutaneous drilling in young athletes (5)[C]
Iselin disease:
Indication: Failure of conservative treatment and symptomatic nonunion
Very rarely indicated
Resection or fixation of symptomatic bone (6)[C]
Ongoing Care
Prognosis
Most do not become painful.
Painful lesions in adolescents often improve with growth.
Uncertain prognosis for symptomatic lesion treated nonoperatively
Continued symptoms more likely with recurrent stresses of athletics
Anecdotally, less likely to improve in physically active youth owing to repeated injury
Uncertain if bony union is natural course (10–50% fusion reported)
Köhler disease:
Self-limiting and excellent prognosis
Full reconstitution of tarsal navicular (6–13 mos, average 8 mos) (2)[C]
No evidence of arthritis long term (2,3)[C]
Potentially, minor faceting of tarsal navicular (3)[C]
Iselin disease:
Pain resolves with relative rest, immobilization, or eventual bony union.
Rare reports of nonunion and prolonged symptoms
References
1. Khoury J, Jerushalmi J, Loberant N, et al. Kohler disease: diagnoses and assessment by
bone scintigraphy. Clin Nucl Med. 2007;32:179–181.
2. Ippolito E, Ricciardi Pollini PT, Falez' F. Köhler's disease of the tarsal navicular: long-term
follow-up of 12 cases. J Pediatr Orthop. 1984;4:416–417.
3. Williams GA, Cowell HR. Köhler's disease of the tarsal navicular. Clin Orthop Relat Res.
1981;53–58.
4. Ray S, Goldberg VM. Surgical treatment of the accessory navicular. Clin Orthop Relat
Res. 1983;61–66.
5. Nakayama S, Sugimoto K, Takakura Y, et al. Percutaneous drilling of symptomatic

accessory navicular in young athletes. Am J Sports Med. 2005;33:531–535.
6. Ralph BG, Barrett J, Kenyhercz C, et al. Iselin's disease: a case presentation of nonunion
and review of the differential diagnosis. J Foot Ankle Surg. 1999;38:409–416.
Additional Reading
Canale ST, Williams KD. Iselin's disease. J Pediatr Orthop. 1992;12:90–93.
Sella EJ, Lawson JP, Ogden JA. The accessory navicular synchondrosis. Clin Orthop Relat
Res. 1986;280–285.
Ugolini PA, Raikin SM. The accessory navicular. Foot Ankle Clin. 2004;9:165–180.
Codes
ICD9
732.5 Juvenile osteochondrosis of foot
755.67 Congenital anomalies of foot, not elsewhere classified
Clinical Pearls
Symptomatic type II accessory navicular may respond less favorably to
conservative treatment in adolescent athletes.
Asymptomatic radiologic abnormalities without pain or antalgic gait are not
Köhler disease.
Avascular necrosis of the tarsal navicular in an adolescent or an adult is not
Köhler disease.
Iselin disease is probably missed often but has a good prognosis.
Fracture, Avulsion: ASIS, AIIS, Ischial Tuberosity,
Iliac Crest
K. Michele Kirk
Jason Mogonye
Tomoya Sakai
Basics
Description
Injury that typically occurs at the unfused apophysis (secondary growth center) in an
adolescent athlete
Results from sudden, forceful, concentric or eccentric muscular contraction without external
trauma
Also may occur from sudden excessive passive lengthening of a muscle
Chronic injury may occur as a result of repetitive microtrauma or overuse.
Epidemiology
Prevalence
Account for 13–40% of pediatric pelvic fractures
Ischial tuberosity most commonly avulsed and accounts for 38% of all pelvic avulsion
fractures.
Anterosuperior iliac spine (ASIS) accounts for 32% and anteroinferior iliac spine (AIIS) for
18% (1).
Generally more common in males but also common in female gymnasts (2).
More common among adolescents than young children or adults
May occur in adults (“weekend warriors”)
Can occur bilaterally
Risk Factors
Athletes involved in strenuous sporting activities (soccer, football)
Sprinters (ASIS type I, AIIS) (1)
Batting in baseball (ASIS type II) (1)
Gymnasts, hurdlers, long jumpers, tennis players (ischial tuberosity) (3)
“Weekend warriors”
Etiology
ASIS:
Type I: Sudden, forceful contraction of sartorius muscle with hip in extension and knee in
flexion (1)
Type II: Sudden, forceful contraction of tensor fasciae latae (1)
Ischial tuberosity: Sudden, forceful contraction of hamstring with knee extended and hip
flexed (3)
Iliac crest: Avulsion of abdominal muscles
Diagnosis
History
Athlete often reports popping or snapping with immediate onset of severe pain.
Acute injury may be preceded by prodrome of low-level pain for up to several months owing
to chronic apophysitis (1).
Activity at time of injury helps to define mechanism of injury.
Attempting to kick a ball (ASIS)
Clearing a hurdle (ischial tuberosity)
Being tackled from behind (iliac crest) (4)
Pattern of pain helps to localize site of avulsion fracture.
Ischial tuberosity avulsion fracture may radiate to posterior thigh.
AIIS avulsion fracture may radiate to anterior thigh.
Physical Exam
Pain with localized tenderness and swelling at avulsion site
Limitation of motion about the site of avulsion injury
Difficulty (sometimes inability) bearing weight
Physical examination includes the following:
Palpate regions of suspected avulsion. Acute localized tenderness to palpation is present
over involved apophysis; avulsed apophyseal fragment may be palpated.
Assess active and passive range of motion of involved muscle(s).
ASIS type I: Pain with passive extension or active flexion of hip; also pain with passive
internal rotation and active external rotation of hip
ASIS type II: Pain with passive extension and active flexion of hip; also pain with passive
external rotation and active internal rotation; pain also can be seen with active abduction
and passive adduction of hip.
AIIS: Pain with passive extension and active flexion of hip; also pain with passive knee
flexion and active knee extension
Ischial tuberosity: Pain with passive hip flexion and active hip extension
Iliac crest: Pain with contraction of abdominal muscles, lateral bending of torso, resisted
hip abduction

Imaging
Anteroposterior view of pelvis: May demonstrate avulsion of a portion of involved apophysis;
fragments may be mildly to severely displaced. Chronic avulsions may result in prominent
bone formation and nonunion. Radiographic appearance of exostosis may be confused with
osseous malignancy or osteomyelitis.
Oblique view of pelvis: May better demonstrate avulsions of iliac crest
CT scan: May be helpful in chronic cases or those without a clear history; may aid in
management of ischial tuberosity avulsions complicated by impingement of sciatic nerve (4)
US: May visualize ASIS or AIIS avulsion fractures
Apophysitis
Muscle strain
Tendon avulsion without fracture
Malignancy, especially in an adult with nontraumatic pelvic avulsion fracture (4)
Treatment
Ice application
Analgesics
Immobilization
Rest
Positioning of the limb to relieve tension on the involved muscle group
Crutch therapy may be required initially, with progressive weight-bearing as
pain decreases and range of motion improves.
Start with non-weight-bearing for ischial tuberosity avulsion fractures. Proceed
with progressive weight-bearing when pain-free with abduction and extension of
hip (5).
Gradual increase in active and passive excursion of involved muscle group to
achieve full active range of motion
Progressive resistance exercise program, followed by integration of injured
musculotendinous unit with the other muscles of the hip and pelvis
Sport-specific training followed by return to sport when pain-free and with
normal motion and strength of involved muscle
Surgery generally is not needed.
Open reduction and internal fixation (ORIF) is considered when fragment is
displaced >2 cm (some even say up to 3 cm), especially for ischial tuberosity
avulsion (4).
ORIF may be considered for nonunion or exostosis causing pain or functional
impairment.
Ongoing Care
Most fractures heal with conservative treatment.
Prognosis
Athletes typically are able to return to full activity without restrictions or long-term sequelae;
however, this may take up to 6 mos.
Complications
Exostosis is the most commonly reported complication following nonoperative
management.
Nonunion of fracture fragment
ASIS fractures may cause meralgia paresthetica owing to associated injury to
the lateral femoral cutaneous nerve. This typically resolves spontaneously (1),
but surgical intervention may be considered for severe, persistent symptoms.
References
1. White KK, Williams SK, Mubarak SJ. Definition of two types of anterior
superior iliac spine avulsion fractures. J Pediatr Orthop. 2002;22:578–582.
2. Rossi F, Dragoni S. Acute avulsion fractures of the pelvis in adolescent

competitive athletes: prevalence, location and sports distribution of 203 cases
collected. Skeletal Radiol. 2001;30:127–131.
3. Vandervliet JM, Vanhoenacker FM, Snoeckx A, et al. Sports-related acute

and chronic avulsion injuries in children and adolescents with special
emphasis on tennis. Br J Sports Med. 2007;41:827–831.
4. Sanders TG, Zlatkin MB. Avulsion injuries of the pelvis. Semin

Musculoskeletal Radiol. 2008;12:42–53.
5. Steerman JG, Reeder MT, Udermann BE, et al. Avulsion fracture of the iliac
crest apophysis in a collegiate wrestler. Clin J Sports Med. 2008;18:102–103.
Additional Reading
Paletta GA, Andrish JT. Injuries about the hip and pelvis in the young athlete.
Clin Sports Med. 1995;14:591–628.
Rossi F, Dragoni S. Acute avulsion fractures of the pelvis in adolescent

competitive athletes: prevalence, location and sports distrivution of 203 cases
collected. Skeletal Radiol. 2001;30:127–131.
Stevens MA, El-Khoury GY, Kathol MH, et al. Imaging features of avulsion
injuries. Radiographics. 1999;19:655–672.
Winfield C, Salis RE, Massimino F, eds. ACSM's essentials of sports

medicine. St. Louis: Mosby, 1997.
Codes
ICD9
808.41 Closed fracture of ilium
808.42 Closed fracture of ischium
Clinical Pearls
Depending on fracture location, most can return to some sort of activity by 4–8
wks.
Full return to activity can take up to 6 mos.
Fracture, Blow Out
Jayson Pereira
Basics
Orbital floor fractures: Extremely unlikely before 7 yrs of age
Lack of pneumatization of the paranasal sinuses: Orbital floor is not a weak point in the orbit.
Orbital roof fractures with associated CNS injuries more common
Description
Defined as an orbital wall fracture without orbital rim involvement owing to blunt trauma to the
orbit
Force transmitted through the orbital structures to the weakest structural point—most
commonly the orbital floor or medial wall—resulting in fracture
Trapdoor fracture (more common in children) is a linear fracture of the orbital bone that
reduces spontaneously to original position, entrapping and strangulating infraocular soft
tissue.
Usually an intraoperative diagnosis
Open door fracture is more common in adults.
Orbital floor serves as roof to air-filled maxillary and ethmoid sinuses. Communication
between the spaces results in orbital emphysema.
Orbit contains fat, which holds the globe in place.
Orbital floor fracture may result in herniation of the fat on the inferior orbital surface into
the maxillary or ethmoid sinuses.
Leads to enophthalmos owing to orbital volume loss
Sinus congestion and fluid collection occur secondary to edema.
Infraorbital nerve runs through the bony canal 3 mm below the orbital floor.
Injury results in hypoesthesia of the ipsilateral cheek.
Distinguished from hypoesthesia owing to swelling by testing for decreased sensation on
the ipsilateral gingiva, which is within the infraorbital nerve distribution
Inferior rectus and inferior oblique muscles run along the orbital floor.
Restriction of these extraocular muscles occurs owing to entrapment within the fracture or
contusion or cranial nerve dysfunction.
Diplopia on upward gaze
Inability to elevate the affected eye normally on examination
Medial rectus muscle is located above the ethmoid sinus.
Less commonly entrapped
Diplopia on ipsilateral lateral gaze
Oculocardiac reflex is defined as an increased vagal tone secondary to soft tissue
entrapment. Signs and symptoms include nausea, vomiting, bradycardia, and syncope.
Epidemiology
Observed in any sport that puts the athlete at risk for forceful contact to the face.
Most common: Boxing, mixed martial arts, wrestling, rugby, soccer, basketball, action sports
Less common: Diving, gymnastics, cheerleading, baseball, handball
Object striking the orbital region is usually larger than orbital rim, such as a baseball or fist
(1).
Diagnosis
Immature facial skeleton with lack of pneumatization of the paranasal sinuses makes plain
radiographs of limited value.
Orbital CT scan: Study of choice
Thorough ophthalmologic examination:
Visual acuity (should not be affected)
Test extraocular movements for disconjugate gaze or diplopia.
Palpate bony structures for evidence of step-off.
Test sensation in inferior orbital nerve distribution.
Examine lid and adnexa.
Careful attention not to place pressure on the globe until ruptured globe excluded
Slit-lamp and funduscopic examination help to identify associated injuries.
Associated injuries:
Ocular injuries:
Ruptured globe (incidence 5–10% of blowout fractures) (2)
Subconjunctival hemorrhage
Corneal abrasion/laceration
Hyphema
Iridodialysis
Traumatic iridocyclitis (uveitis)
Traumatic mydriasis
Retinal detachment
Vitreous hemorrhage
Compressive orbital emphysema
Retrobulbar hemorrhage
Optic nerve injury
Central retinal artery occlusion
Acute angle glaucoma
Extraocular muscle entrapment:
Inferior rectus
Inferior oblique
Medial rectus (less common)
Infraorbital nerve injury
Facial fractures:
Nasal bones
Zygomatic arch fracture
Neck injuries
Intracranial injury
Physical Exam
Periorbital tenderness, swelling, ecchymosis
Impaired ocular mobility or diplopia:
Upward gaze impaired owing to inferior rectus entrapment
Ipsilateral lateral gaze impaired with medial rectus entrapment
Infraorbital hypoesthesia: Owing to compression/contusion of infraorbital nerve
Enophthalmos or hypoophthalmos: Owing to herniation of orbital fat through fracture
Periorbital emphysema
Normal visual acuity (unless associated ocular injury)
Epistaxis (indicative of medial wall injury)

Plain radiographs:
Facial films
Orbits
Water's view and exaggerated Water's view:
Classic “teardrop sign” illustrates herniated mass of orbital contents in the ipsilateral
maxillary sinus.
Opacification of or air–fluid level in the ipsilateral maxillary sinus (less specific)
Orbital floor bony fracture
Lucency in orbits consistent with orbital emphysema (1)
CT scan of orbits:
If diagnosis in question and for follow-up
Defines involved anatomy
Obtain 1.5-mm cut (2).
Trapdoor type of fractures may be difficult to identify, even with CT scan
Forced duction test:
Distinguishes nerve dysfunction from entrapment
Topical anesthesia is applied to the conjunctiva on the opposite side, and the globe is
pulled away from the expected point of entrapment. If the globe is not mobile, the test is
positive.
Lab
Preoperative laboratory studies if indicated
Periorbital contusion/ecchymosis
Cranial nerve palsy
Ruptured globe
Orbital cellulitis
Periorbital cellulitis
Treatment
Pre-Hospital
Metal protective eye shield if possible globe injury
Place in supine position.
ED Treatment
Apply cool compresses for the 1st 24–48 hr to decrease swelling in order to
minimize/reverse herniation and avoid surgical intervention.
Avoid Valsalva maneuvers and nose blowing to prevent compressive orbital
emphysema.
Prophylactic antibiotics (eg, amoxicillin, cephalexin, or erythromycin) to prevent
infection
Nasal decongestants (eg, phenylephrine nasal spray)
Analgesics
Tetanus prophylaxis
Medication
Phenylephrine nasal spray: b.i.d. × 10–14 days
Amoxicillin: 250–500 mg PO t.i.d. × 10–14 days
Cephalexin: 250–500 mg PO q.i.d. × 10–14 days
Erythromycin: 250–500 mg PO q.i.d. × 10–14 days
Initial approach and immediate concerns:
Rule out ruptured globe.
Assess for associated intracranial or cervical spine injuries.
Test visual acuity: Decreased visual acuity is suggestive of associated ocular
injury.
Admission Criteria
Rarely indicated except with:
Severe herniation of orbital contents threatening vision
Cosmetically, enophthalmos typically 5 mm
Associated injuries that mandate admission
Discharge Criteria
Consultation with facial trauma service: Arrange follow-up evaluation within 1–2
wks of injury and to determine need for surgery.
Immediate ophthalmology evaluation if patient has evidence of visual loss or
within 24 hr for complete retinal evaluation
Need for surgical intervention:
Rarely indicated immediately
85% resolve without surgical intervention (2).
Typically observe for 10–14 days until swelling resolves.
Earlier surgical intervention in children owing to higher incidence of trapdoor
fracture
Surgery indications:
Persistent diplopia
Restricted extraocular movements
Cosmetically significant enophthalmos or hypoophthalmos
Persistent oculocardiac reflex
Progressive infraorbital hypesthesia
Ongoing Care
Complications
Sinusitis
Orbital infection
Permanent restriction of extraocular movement
Enophthalmos
References
1. O'Hare TH. Blow-out fractures: a review. J Emerg Med. 1991;9:253–263.
2. Linden JA, Renner GS. Trauma to the globe. Emerg Med Clin North Am.
1995;13:581–605.
Additional Reading
Anderson PJ, Poole MD. Orbital floor fractures in young children. J
Craniomaxillofac Surg. 1995;23:151–154.
Burnstine MA. Clinical recommendations for repair of orbital facial fractures.
Curr Opin Ophthalmol. 2003;14:236–240.
Joondeph BC. Blunt ocular trauma. Emerg Med Clin North Am.
1988;6(1):151.
Koltai PJ, Amjad I, Meyer D. Orbital fractures in children. Arch Otoiaryngol

Head Neck Surg. 1995;121(12):1375–1379.
Levin LM, Kademani D. Clinical considerations in the management of orbital

blow-out fractures. Compend Contin Educ Dent. 1997;18:593, 596–598,
600; quiz 602.
Theologie-Lygidakis N, Iatrou I, Alexandridis C. Blow-out fractures in children:

six years' experience. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2006.
Codes
ICD9
802.6 Closed fracture of orbital floor (blow-out)
802.7 Open fracture of orbital floor (blow-out)
Fracture, Calcaneus
Greg Nakamoto
Basics
Description
Calcaneus fractures can occur secondary to either acute trauma or recurrent stress (ie,
calcaneal stress fracture). The focus here is on the management of acute traumatic fractures
of the calcaneus.
Of primary concern when evaluating the acute calcaneus fracture is determining whether the
fracture is extra- or intraarticular.
Most extraarticular fractures can be managed conservatively.
Current practice is for most intraarticular fractures to be treated surgically. Such fractures
consequently should be referred for orthopedic evaluation.
Having said that, no universally accepted guidelines exist as to the optimal treatment of
calcaneal fractures.
It should be noted that most calcaneal fractures (other than stress fractures) involve the
articular surface.
Secondarily, one should be aware that many patients with acute calcaneus fractures have
other coexisting lower extremity or vertebral injuries.
Synonym(s): Os calcis fracture; Heel bone fracture
Epidemiology
Prevalence
Most commonly seen in young men, representing 2% of all fractures seen in adults (1,2,3)
Calcaneal fractures are relatively rare in children, who account for only 5% of all calcaneal
fractures (4).
The calcaneus is the most frequently fractured tarsal bone, accounting for 60% of all tarsal
fractures (1).
25–30% of calcaneal fractures are extraarticular; 70–75% are intraarticular (1,2,3).
2% are open fractures (1).
Risk Factors
Fall from a height directly onto the heel
Other force of impact directly onto the heel (eg, motor vehicle accident)
Osteoporosis can predispose to calcaneal fractures despite a seemingly trivial mechanism of
injury.
Extraarticular fractures of the calcaneal body and plantar tuberosity also can be caused by
blunt-force trauma or a twisting injury (1).
Avulsion fractures of the calcaneal tuberosity can occur with abrupt contraction of the Achilles
tendon (1).
Stress fractures of the calcaneus can occur as an overuse injury in athletes (1).

High-energy mechanism of injury usually is required for these fractures, resulting in a high
incidence of coexisting lower extremity or spinal injury.
Calcaneal fractures occur bilaterally in 5–9% of patients (1,4).
10% of patients will have sustained a spinal compression fracture as well (1,4).
Often associated with significant local soft tissue injury
Alert
Acute compartment syndrome of the foot occurs in up to 10% of patients and is a surgical
emergency (4).
Diagnosis
History
Mechanism of injury:
Extraarticular fractures are more commonly due to an indirect mechanism such as a twisting
injury or muscular avulsion.
Intraarticular fractures are due to high-energy accidents.
History of a fall from a height is particularly concerning for additional lower extremity and
lumbar spine injury.
Physical Exam
Heel pain
Swelling
Ecchymosis
Look for associated soft tissue injury. Blisters may occur when swelling is substantial.
Excessive soft tissue injury will influence duration of splinting before placing into a cast for
those being treated conservatively or may delay definitive surgical treatment in those being
treated operatively (1,5)[C].
Assess function of the nerves of the foot. With significant swelling, pulses may be difficult
to assess; check capillary refill of the toes.
Ecchymosis that tracks distally to the sole of the foot, known as the Mondor sign, is
pathognomonic for calcaneal fracture (1).
Check for evidence of lower extremity compartment syndrome. Significant swelling in the
plantar arch may suggest plantar compartment syndrome. This requires emergent surgical
referral even if the fracture itself is nonoperative (1)[A].
Look for associated lower extremity and vertebral fracture because of high incidence of
coexisting injury.

Imaging
Goal of imaging is to confirm diagnosis of calcaneus fracture and to determine whether the
fracture is intra- or extraarticular (5,6)[B].
Standard initial x-rays: Anteroposterior, lateral, and axial calcaneus (Harris) views; consider
obtaining views of the contralateral heel for comparison purposes.
Böhler tuber joint angle (Figure 1):
A line is drawn between the posterosuperior aspect of the calcaneus and the highest
point of the posterior subtalar articular surface; a second line, which intersects the first,
is drawn from the highest point of the anterior process to the posterior margin of the
subtalar surface (4).
Measures between 25 and 40 degrees, with a similar angle found in the two calcanei in
any one person.
Decrease of 10 degrees versus the uninjured side is considered a significant difference.
“Crucial angle” of Gissane (Figure 2): On the lateral x-ray, the angle formed by the
wedge in which the lateral process of the talus sits; this angle is disrupted when axial
compressive forces drive the talus as a wedge into this space. Radiograph of the
uninjured side is useful for comparison; may not be as helpful as the Böhler angle in
determining the presence of a calcaneus fracture (6).
Oblique (Broden) views can be helpful in assessing involvement of the articular surfaces.
Additional x-rays to consider based on history and physical examination include views of
the contralateral foot (because of the significant incidence of bilateral injury and to
compare Böhler and Gissane angles with the injured foot), ipsilateral ankle, and lumbar
spine and pelvis (because of high frequency of associated fractures).
CT scan (4,5,6)[A]:
In patients in whom x-rays are inconclusive, CT scan is considered the gold standard for
confirming the diagnosis of calcaneal fracture.
Additionally, if plain films show articular involvement or if suspicion of articular
involvement remains high despite equivocal plain films, then a CT scan is essential for a
more specific analysis of the subtalar and calcaneocuboid joints because displacement
of either likely will require surgical management.
Should include axial and coronal cuts
MRI: While not generally used for the evaluation of traumatic calcaneus injuries, MRI may
be the preferred imaging modality in patients with suspected stress fractures, particularly
in patients with severe osteoporosis, in whom a bone scan may appear falsely negative
(4,6)[C].
Follow-up and special considerations: For extraarticular fractures being treated
nonoperatively, postreduction imaging involves repeating the standard radiographs to
assess adequacy of reduction after closed manipulation. Comparison with the opposite
foot often is useful.
Talar fracture
Cuboid fracture
Malleolar fracture
Ankle dislocation
Ankle sprain
Treatment
Ice and oral analgesics are useful in the prehospital setting, and oral
analgesics may be required for some time after casting.
Extraarticular calcaneal body fractures with minimal displacement:
Mediolateral compression of the heel with the palms of the hands can be
applied to reduce displaced extraarticular body fractures being treated
nonoperatively.
P.
Other extraarticular fractures or any intraarticular fractures: Surgical
consultation for possible open reduction and internal fixation (ORIF). For
details, see “Ongoing Care.”
Postreduction evaluation: Repeat x-rays in 1 wk in any patient being treated
nonoperatively.
Immobilization:
Usually begins with splinting or bulky Jones dressing to accommodate
changes in soft tissue swelling.
In patients who require casting (see “Ongoing Care”), the splint can be
changed to a short-leg cast after the initial soft tissue injury has stabilized
after 3–5 days.
In patients who require operative treatment, splinting is appropriate until the
patient can see an orthopedic surgeon.
Intraarticular fractures and certain extraarticular fractures as listed below (see
“Ongoing Care”) should undergo orthopedic evaluation for possible surgical
treatment.
In patients requiring operative treatment, referral should be made promptly so
that fixation can occur within 5–7 days.
In patients with significant associated soft tissue injury, prompt orthopedic
referral allows for early interventions to reduce edema, which can take 7–14
days to accomplish. In such cases, operative treatment within the 1st 3 wks,
before early consolidation of the fracture fragments, is preferred (5)[C].
All cases of compartment syndrome require emergent referral (1)[A].
Ongoing Care
Optimal management of calcaneal fractures, particularly of intraarticular fractures,
remains controversial (2,5,6,7)[B]. New techniques, such as arthroscopically assisted
percutaneous pinning, are being developed that may lead to more consistently improved
outcomes.
Some general guidelines include:
Nondisplaced or minimally displaced extraarticular fractures of the body of the calcaneus
can be treated with short-leg casting and no weight bearing for 2 wks, followed by range-
of-motion exercises. Progressive weight bearing may start at 8 wks, with full weight
bearing by 12 wks (1)[C].
Exceptions (extraarticular fractures that might best be treated surgically) (1,8)[C]:
Extraarticular fractures with a decrease of Böhler angle by 10 degrees versus the
contralateral side
Fractures of the sustentaculum tali with >2 mm of displacement
Displaced avulsions of the Achilles tendon insertion from the calcaneal tuberosity
Significant fractures of the calcaneal body
Intraarticular fractures or extraarticular fractures as listed should be referred for orthopedic
consultation (2)[B].
An intraarticular fracture still might be treated nonoperatively if it is completely
nondisplaced (5)[C].
Conservative treatment should be reserved for extraarticular fracture only. All intraarticular
fractures or the specific extraarticular fractures listed earlier should be referred for
consideration of surgical fixation.
In patients treated conservatively, removal from splinting/casting should be followed by
referral to physical therapy to restore normal flexibility and strength before allowing return to
play.
Patient Education
Patients should be informed early on that treatment can be difficult and that adverse
outcomes can be potentially severe and disabling at times.
Chronic pain and posttraumatic arthritis are not uncommon.
Complications
In both operatively and nonoperatively treated patients, chronic disability owing
to pain from an improperly functioning or arthritic subtalar or calcaneocuboid
joint may occur (1,6).
Complications specifically seen in patients undergoing ORIF include (1):
Infection
Pain
Swelling
Delayed would healing
Nonunions of the fracture fragments
Lateral impingement of the peroneal tendon
Sural nerve injury
P.
References
1. Nickelbur S, Dixon T, Probe R. Calcaneus fractures. eMedicine. Retrieved
Aug 10, 2009, from http://emedicine.medscape.com/article/1232246-
overview; 2008.
2. Bajammal S, Tornetta P, Sanders D, et al. Displaced intra-articular

calcaneal fractures. J Orthop Trauma. 2005;19:360–364.
3. Ibrahim T, Rowsell M, Rennie W, et al. Displaced intra-articular calcaneal

fractures: 15-year follow-up of a randomised controlled trial of conservative
versus operative treatment. Injury. 2007.
4. Khan A, Rahim R, Irion K, et al. Calcaneus fractures. eMedicine. Retrieved

Aug 10, 2009, from http://emedicine.medscape.com/article/388031-overview;
2008.
5. Sanders R. Displaced intra-articular fractures of the calcaneus. J Bone

Joint Surg Am. 2000;82:225–250.
6. Simpson RB. Fractures of the calcaneus. Curr Opin Orthop. 2007;18:124–

127.
7. Randle JA, Kreder HJ, Stephen D, et al. Should calcaneal fractures be

treated surgically? A meta-analysis. Clin Orthop Relat Res. 2000;377:217–
227.
8. Thermann H, Krettek C, Hüfner T, et al. Management of calcaneal fractures

in adults. Conservative versus operative treatment. Clin Orthop Relat Res.
1998;353:107–124.
Additional Reading
Buckley R, Tough S, McCormack R, et al. Operative compared with
nonoperative treatment of displaced intra-articular calcaneal fractures: a
prospective, randomized, controlled multicenter trial. J Bone Joint Surg Am.
2002;84-A:1733–1744.
Lewis G. Biomechanics as a basis for management of intra-articular fractures

of the calcaneus. J Am Podiatr Med Assoc. 1999;89:234–246.
Miric A, Patterson B. Pathoanatomy of intra-articular fractures of the

calcaneus. J Bone Joint Surg. 1998;80A:207–212.

Swanson SA, Clare MP, Sanders RW. Management of intra-articular fractures

of the calcaneus. Foot Ankle Clin. 2008;13:659–678.
Codes
ICD9
733.95 Stress fracture of other bone
825.0 Fracture of calcaneus, closed
825.1 Fracture of calcaneus, open
Clinical Pearls
During the initial evaluation of a patient with a calcaneus fracture, be aware that
many patients will have a coexisting lower extremity or vertebral fracture. 10%
will have coexisting compartment syndrome of the foot, which is a surgical
emergency.
Proper management of calcaneus fractures requires determining if the fracture
is intraarticular or extraarticular. Intraarticular fractures generally are best
treated surgically, whereas extraarticular fractures (with the exceptions noted
under “Ongoing Care”) are often treated nonoperatively. If x-rays are
equivocal, CT scan is used to determine if the fracture is intraarticular.
Optimal treatment of calcaneal fractures is still controversial, with posttraumatic
arthritis being the cause of most cases of chronic disability.
In nonoperative cases, athletes may be ready to return to play in as little as 8–
12 wks depending on the severity of the original injury. In operative cases, the
duration of immobilization and recovery is more variable and depends on the
particulars of the fracture.
Consensus suggests that long-term outcome is determined mainly by the
degree of joint destruction at the time of injury (8).
It seems poorer outcomes are seen more commonly in patients who develop
arthritis of the subtalar joint; consequently, there might be a link between
preservation of the subtalar joint at the time of initial treatment conferring a
better long-term prognosis (6).
There seems to be a subset of calcaneal fractures that has a poor outcome
regardless of treatment (1).
Fracture, Carpal Bone (Other)
Thomas Trojian
Deena C. Petrocelli
Basics
Description
Fracture of the carpal bones of the wrist, excluding those of the hamate and scaphoid
Includes Kienböck disease, a disease of the lunate where the blood supply is compromised
and possible osteonecrosis occurs
Synonym(s): Wrist fracture
Epidemiology
The carpal bones consist of the scaphoid, lunate, triquetrum, and pisiform in the proximal row
and the trapezoid, trapezium, capitate, and hamate in the distal row.
Since 1990, 8–19% of hand injuries have resulted in a carpal fracture.
Frequency of fracture seen in carpal bones is scaphoid 80%, triquetrum 6%, hamate 5%,
trapezium 4%, lunate 3%, capitate 1%, and trapezoid and pisiform, <1% each.
Carpal fractures are caused by trauma from either a fall on the extended wrist or a direct
blow.
Kienböck disease in 75% of the cases is preceded by severe trauma with the wrist in
extreme dorsiflexion.
Risk Factors
Fractures of the carpal bones other than the scaphoid and lunate bones are often seen in
sports using a stick (eg, hockey, lacrosse).
Diagnosis
History
Athlete usually will present with a fall on the outstretched hand in the hyperextended position.
However, direct trauma or a fall on a flexed wrist can also cause a fracture. Pain and
restricted motion often are presenting complaints.
Mechanism of injury can help localize the injury to a specific carpal bone.
Determine when the wrist began to hurt; recent vs prolonged is important.
Determine location of pain, whether ulnar or radial, at rest or with motion.
An occult fracture often will present as a persistent wrist sprain. Carefully examine the
patient, as Kienböck disease and small chip fractures of the triquetrum can present in this
manner.
Physical Exam
Pain and tenderness over the dorsum of the wrist
Localized swelling and limited range of motion; a prominence may be present.
Strength testing of the muscles whose tendons insert on or are supported by the injured
structure may help localize the injury.
Neurovascular signs are unusual, except for fracture of the pisiform, which may affect the
ulnar nerve and artery.
Inspect for swelling, deformity, and ecchymosis (the latter usually not seen with carpal
fractures).
Evaluate movement of wrist in flexion, extension, and ulnar and radial deviation.
Palpate individual carpal bones to determine location of tenderness.
Test strength of muscles that attach to carpal bones.
Assess neurovascular integrity (fracture of the pisiform may affect the ulnar nerve and a
lunate dislocation may compress the median nerve).
Axial loading of metacarpals above the carpal bones may help in diagnosis.

Imaging
Radiographs consisting of 6 views: Anteroposterior (AP) and lateral, each taken in an exact
neutral position; motion views of maximal radial deviation and maximal ulnar deviation; lateral
views in maximal flexion and maximal extension
Additional radiographic views may be needed if a fracture is suspected for certain carpal
bones: Pisiform (carpal tunnel views, oblique view with forearm in 20 degrees supination),
triquetrum (slightly oblique, pronated lateral view), trapezium (carpal tunnel views and true AP
[Robert] view), and trapezoid (oblique views)
CT scanning should be considered if a fracture of the capitate, lunate, pisiform, trapezium, or
trapezoid is suspected and negative plain films are seen.
Postreduction views should be obtained to confirm reduction and correct anatomical
alignment.
Ligamentous injury (wrist sprain)
Contusion
Carpal dislocation
Metacarpal fracture
Distal radioulnar fracture
Treatment
Immobilization of the wrist should eliminate the pain of the fracture.
NSAIDs or narcotics can be added as needed.
There are theoretical concerns about the adverse effects of NSAIDs on
fracture healing; there is not enough clinical evidence to deny patients with
simple fractures their analgesic benefits.
Reduction techniques should not be necessary. All displaced or dislocated
fractures should be splinted and referred for surgery.
Lunate dislocation may need immediate reduction if median nerve or artery is
involved.
All treatments are for nondisplaced fractures.
Triquetrum: Short arm cast for 4–6 wks for transverse body fracture; short arm
cast or splint for 2–4 wks for dorsal avulsion
Trapezium: Short arm thumb spica cast for 4–6 wks
Pisiform: Short arm cast or splint for 3–6 wks
Trapezoid: Short arm thumb spica cast for 4–6 wks
Capitate: Short arm thumb spica cast for 6–8 wks. Some recommend long arm
with finger extension. Consider referral because of possible avascular
necrosis (AVN).
Lunate: Short arm cast, or at least splint until referred; prolonged immobilization
of 12–16 wks, may need long arm cast with finger extension.
Triquetrum:
2nd most commonly fractured carpal bone
Dorsal rim chips of the triquetrum are easily missed on AP view and may be
the only sign of a fracture.
May have tenderness distal to the ulnar styloid while the hand is in radial
deviation
Persistent pain after appropriate treatment should alert the treating physician
that a concurrent injury (pisiform fracture, triangular fibrocartilage complex
injury, and/or lunate-triquetrum ligament tear) was initially not noticed.
Capitate:
Most often fractured with the scaphoid or metacarpal
Consider all capitate fractures unstable because of the high likelihood of
surrounding carpal instability.
Consider serial radiographs in patients with persistent pain.
High incidence of delayed nonunion in these fractures
Referral to hand specialist is reasonable.
Trapezium: P.
Easily missed; patients will describe a localized pain at base of the thenar
eminence and pain with wrist flexion.
Missed fractures cause ongoing pain at base of the thumb.
Carpal tunnel view demonstrates fracture of the palmar ridge.
When displaced, may affect the integrity of the trapeziometacarpal joint,
which is responsible for pinch and grasp motions.
Pisiform:
Sesamoid bone located within the flexor carpi ulnaris tendon, which can be
disrupted if a fracture is present
Usually caused by direct blow to hand
Can compress the ulnar nerve or artery at Guyon's canal
The pisiform can be excised in chronically symptomatic cases.
Trapezoid:
Least commonly fractured
Patients describe pain at the base of the second metacarpal.
Axial compression of second metacarpal will elicit tenderness.
Lunate:
Lunate fractures can be occult.
AVN is seen in 20% of lunate fractures.
Kienböck disease may be secondary to lunate injury.
Kienböck disease has a high association with ulna-minus variant.
In the early stages of Kienböck disease, plain radiographs are usually not
diagnostic; MRI is usually needed for definitive diagnosis.
Referral to hand specialist is reasonable.
Initially, while in cast, the athlete needs to continue fitness training. Constant
monitoring of the cast and frequent (weekly) changes may be needed to
maintain skin and cast integrity.
Once out of the cast, range of motion (ROM) then strengthening of the wrist
need to be done until restoration of a painless, functional arc of wrist motion
and near-normal strength are obtained.
Surgery is needed for displaced fractures(s) through the metacarpocarpal joint
articulation.
Ongoing Care
Any displaced fracture of the carpal bones should be referred to an orthopedic surgeon.
Lunate fractures may develop AVN (avascular necrosis, Kienböck disease) and should be
considered for referral even if not displaced.
Additional Reading
Cooney WP III, Linscheid RL, Dobyns JH. Fractures and dislocations of the wrist. In
Rockwood A Jr, Green DP, eds. Rockwood and Green's fractures in adults, 4th ed.
Philadelphia: Lippincott-Raven Publishers, 1996:822–827.
Culver JE, Anderson TE. Fractures of the hand and wrist in the athlete. Clin Sports Med.
1992;11:101–128.
DeHaven KE, Lintner DM. Athletic injuries: comparison by age, sport, and gender. Am J
Sports Med. 1986;14:218–224.
Eisenhauer MA. Wrist and forearm. In: Rosen P, ed. Emergency medicine: concepts and
clinical practice, 4th ed. St. Louis: Mosby-Year Book, 1998:673–677.
Geissler WB. Carpal fractures in athletes. Clin Sports Med. 2001;20:167–188.
Papp S. Carpal bone fractures. Orthop Clin North Am. 2007;38:251–260.
Rettig AC. Epidemiology of hand and wrist injuries in sports. Clin Sports Med.
1998;17:401–406.
Rettig ME, Dassa GL, Raskin KB, et al. Wrist fractures in the athlete. Distal radius and
carpal fractures. Clin Sports Med. 1998;17:469–489.
Slade JF, Milewski MD. Management of carpal instability in athletes. Hand Clin.
2009;25:395–408.
Vigler M, Aviles A, Lee SK. Carpal fractures excluding the scaphoid. Hand Clin.
2006;22:501–516; abstract vii.
Wright PE II. Wrist. In: Canale T, ed. Campbell's operative orthopaedics, 9th ed. St. Louis:
Mosby, 1998:3455–3476.
Codes
ICD9
814.00 Closed fracture of carpal bone, unspecified
814.02 Closed fracture of lunate (semilunar) bone of wrist
814.03 Closed fracture of triquetral (cuneiform) bone of wrist
Clinical Pearls
Return to play varies with the degree of injury and casting. In lunate fractures, it
is up to 6 mos; in triquetrum fractures, it is 4 wks, possibly less, in cast.
General requirements for returning to play are complete healing of the fracture
and any concurrent soft tissue injuries. Thorough rehabilitation with restoration
of a painless, functional arc of wrist motion and near-normal strength are
essential.
Wrist stiffness is a common problem after casting, and physical therapy for
ROM and strengthening is essential after cast removal. When rehabilitation is
done, the wrist is most often free of pain.
Fracture, Clavicle
Christopher C. Trigger
Tanya J. Hagen
Basics
The clavicle is a subcutaneous S-shaped bone.
1st bone to ossify in the human body (5th wk of gestation)
Functionally acts as a strut that connects the shoulder girdle to the axial skeleton
Description
Allman classification based on fracture site (1,2)
Craig further subdivided group II and III fractures:
Group I: Fracture of the middle third
Group II: Fracture of the lateral (distal) third:
Type I: Lateral to coracoclavicular (CC) ligament (typically nondisplaced)
Type II: Medial to the CC ligaments; causes superior displacement of the medial
fragment relative to the lateral fragment
Type III: Fracture extends into the acromioclavicular (AC) joint.
Type IV: Proximal fragment displacement out of periosteal tube (only in children)
Type V: Comminuted where CC ligaments remain attached to an inferior bone fragment
only
Group III: Fracture of the medial (proximal) third:
Type I: Nondisplaced
Type II: Displaced with ligamentous rupture
Type III: Fractures extend into the sternoclavicular (SC) joint.
Type IV: Fracture causes epiphyseal separation (children and adolescents).
Type V: Comminuted
Epidemiology
Incidence
Most commonly fractured bone in children and adolescents
Bimodal age distribution with peaks in children/adolescents and the elderly
Predominant gender: Male > Female (2.5:1)
80% are group I; 15% group II; 5% group III.
Risk Factors
Direct trauma and fall onto the shoulder are the most common mechanisms of injury.
Highest-risk sports in the U.S. are football, lacrosse, and hockey.

AC joint injury
Labral tears
Rotator cuff injuries
Proximal humeral fractures
Rib fractures
Pneumothorax/hemothorax
SC joint dislocation
Brachial plexus, vascular injuries (uncommon)
Diagnosis
Diagnosis is easily made by history, physical exam, and appropriate imaging.
History
Direct trauma or a fall
Middle-third fractures are frequently seen with fall on an outstretched arm.
Distal-third fractures most often are associated with loads transmitted to the lateral aspect of
the shoulder.
Physical Exam
With or without ecchymosis or tenting of the skin over the fracture
Tenderness to palpation at fracture site
Pressure along the clavicle may reveal fracture motion or crepitus.
Careful pulmonary and neurovascular exam must be performed to identify possible
associated injury.
Imaging
Radiographs:
An anteroposterior (AP) view of the clavicle including the AC and SC joints and the
shoulder girdle
A 30–45-degree cephalic-tilt (Zanca) view is recommended to delineate displacement and
comminution in all fracture types.
A 40-degree cephalic-tilt view of the SC joint (serendipity view) can rule out SC
dislocations.
An axillary view can be useful in distal clavicle fractures.
CT scan:
Articular fractures of the medial or lateral clavicle may require a CT scan.
A CT angiogram or standard angriogram can be used if distal vascular deficit is suspected
(1,2).
Special considerations: The proximal clavicular epiphysis is the last growth plate in the body to
fuse (approximately age 20 yrs). Therefore, many injures involving the SC joint in athletes
probably are physeal injuries and should be evaluated by thin-cut CT scan.
AC joint injury
Rotator cuff contusion/tear
Labral injury
Rib fracture
Humeral head fracture
SC joint injury
Treatment
The primary goal in treating clavicular fractures is to obtain bony union and
restore shoulder function to preinjury level with little or no residual pain,
dysfunction, or cosmetic deformity (2,3,4).
Most fractures can be treated nonoperatively (80–90%).
Most clavicle fractures (when treated nonsurgically) will heal clinically in 3–6
wks; radiographic healing usually takes longer.
Arm sling and sling-and-swathe are the most common forms of immobilization
(2,3,4)[B].
Figure-of-eight harness is used less frequently because of discomfort,
noncompliance, and worse complication rates.
Range of motion (ROM) and active shoulder flexion (up to 40°) as well as
isometric deltoid and rotator cuff strengthening can begin once pain is
improved.
Avoid ROM >45° of forward flexion until clinical evidence of healing is seen.
As union progresses, increase ROM and resistive exercises.
When radiographic union is present, full active use of the arm is allowed.
Surgery is rarely required.
Indications for early operative treatment include (1,2,3):
Displaced or shortened (>1.5 cm) and comminuted middle-third fractures of
the clavicle
Type II distal clavicle fractures are typically managed surgically owing to the
high rate of nonunion; also, operative treatment is recommended in type IV
and V fractures.
Any open fractures
Tenting of skin over an irreducible fracture
Concomitant glenoid neck fracture, also known as floating shoulder
Posterior fracture dislocations of the medial clavicle should be reduced in the
presence of a thoracic surgeon owing to risk of vascular injury.
Surgical techniques used include open reduction with rigid fixation (ORIF) with
plates and screws or intramedullary fixation.
Primary operative fixation is becoming much more common in healthy, young
athletes, as well as professional athletes with a goal of possibly expediting
return to play.
Secondary operative treatment is considered for
Persistent (>6 wks) displacement and shortening despite immobilization
Malunion
Ongoing Care
Follow-up should be scheduled 1–2 wks after injury to assess clinical symptoms and then
every 2–4 wks until clinical and radiographic union occur (2).
Radiographic union progresses more slowly than clinical union.
Radiographs should be performed at intervals of 4–6 wks to assess healing.
A final radiograph to assess callus formation and clinical union can be useful.
Athletes should not be allowed to return to play until the fracture is clinically and
radiographically healed (typically 6–8 wks) (2,4)[C].
Noncontact and throwing athletes should have full, painless ROM and at least 90% strength
compared with the uninjured arm (usually requires 6 wks).
Return to contact/collision sports may take up to 8–12 wks.
Complications
Posttraumatic arthritis
Nonunion:
Degree of displacement and comminution most important factors
More common in women and the elderly
Recent studies show a 2% rate of nonunion in patients managed surgically
and a 4.5% rate of nonunion in nonoperative patients.
Historically, 0.1–1% of nonunions occurred for nonoperative treatment and
3.5–5% for operative treatment. Improved surgical technique and better
reporting presumably are the reasons for the change.
Malunion resulting in angulation, shortening, and a poor cosmetic appearance
Neurovascular injury (uncommon): Medial branch (ulnar nerve) of the brachial
plexus most commonly affected
References
1. Kim W, McKee MD. Management of acute clavicle fractures. Orthop Clin
North Am. 2008;39:491–505, vii.
2. Pujalte GG, Housner JA. Management of clavicle fractures. Curr Sports

Med Rep. 2008;7:275–280.
3. Jeray KJ. Acute midshaft clavicular fracture. J Am Acad Orthop Surg.

2007;15:239–248.
4. Pecci M, Kreher JB. Clavicle fractures. Am Fam Physician. 2008;77:65–
70.
Additional Reading
Smekal V, Oberladstaetter J, Struve P, et al. Shaft fractures of the clavicle:
current concepts. Arch Orthop Trauma Surg. 2008.
Codes
ICD9
810.00 Closed fracture of clavicle, unspecified part
810.01 Closed fracture of sternal end of clavicle
810.02 Closed fracture of shaft of clavicle
Clinical Pearls
Most fractures are managed nonoperatively.
Most patients can return to noncontact sports within 6–8 wks.
Typical return to contact sports is 8–12 wks.
Protective donut pads may be useful in protecting the clavicle from reinjury or
pain from a direct blow.
Fracture, Coccyx
John Munyak
Payal Sud
Basics
The coccyx is the last bony structure at the caudal end of the vertebral column and is
triangular in shape.
Coccygeal fractures can be caused by trauma such as falling and landing on the buttocks
(eg, during skating) or in newborns during passage through the vaginal canal.
Coccyx fractures are also known as a “broken arse” and “broken tailbone.”
Although the mechanism may be low impact, immobilization should be considered until other
spine injuries are properly evaluated.
Description
Fall landing in sitting position is most common.
Also can occur during childbirth
Surgical procedures performed in area of coccyx
Fractures of the coccyx are usually transverse.
More common in women
Risk Factors
Predominantly occur in females because the female pelvis is broader, and the coccyx is more
exposed.
Advanced age
Osteoporosis
Decreased balance causing more falls
Congenital bone disorder such as osteogenesis imperfecta
Involvement in activities such as skating or skateboarding
General Prevention
Calcium and vitamin D supplements to prevent osteoporosis
Refraining from activities that would predispose to falling on the buttocks, especially if elderly
or if underlying medical conditions such as osteogenesis imperfecta are present
Etiology
The coccyx is made up of 3–5 fused vertebrae with attachments of several important
muscles and ligaments. The muscles include the levator ani group, which supports the pelvic
floor and aids in maintaining fecal continence, and the gluteus maximus, which aids in thigh
extension.
The coccyx has limited movement at the sacrococcygeal junction and a curvature such that
the tip curves into the pelvis.
Coccyx injuries are often belittled by physicians, but it should be kept in mind that the pain
can be extremely severe and debilitating to the patient. Additionally, the coccyx is a weight-
bearing structure in the seated position, and an ill-managed coccyx fracture can cause the
patient to apply more weight on the ischial tuberosities, causing bursitis.
Diagnosis
Mechanism of Injury
Look for ecchymosis and palpate for tenderness in the gluteal fold.
Pre Hospital
Evaluate for other associated injuries (other potential life-threatening injuries such as head
injuries may be missed if the focus is on the pain from the coccyx injury).
History
Mechanism of injury (fall vs assault vs childbirth)
Factors leading up to the fall (mechanical fall vs syncope)
Other associated injuries (other potential life-threatening injuries such as head injuries may be
missed if the patient is focusing on the pain from the coccyx injury)
Use of blood thinners (for severity of injury)
The PQRST of pain: Palliative or Precipitating factors, Quality, Region or Radiation, Severity
(1–10), and Timing
Risk for cancer (pathologic fracture): Bright Red Blood Per Rectum (BRBPR), abnormal
vaginal bleeding, weight loss
Physical Exam
Low back pain, buttock pain, rectal bleeding (if associated rectal tear)
Pain when sitting or defecating
Palpation of the sacrococcygeal joint for pain
Digital rectal examination can be diagnostic with mobility and/or crepitus of the coccyx.
Assess sacrococcygeal joint mobility by palpating the coccyx anteriorly (digital rectal exam)
and posteriorly (externally).
Anoscopy should be performed if gross blood is present to evaluate for possible rectal
perforation (very rare).
Examination of entire spine is necessary to evaluate for concomitant injury.
Neurologic exam of the lower extremities to assess radiculopathy

Radiographs will identify other suspected spinal injuries.
Displaced coccyx fractures can be seen best on the lateral view.
Radiographs are not necessary if isolated coccyx fracture is apparent on rectal exam.
Nondisplaced fractures are difficult to see on x-ray.
When x-rays are used in the diagnosis, 3 views needed: anteroposterior (AP), lateral, and
cone-down (focused) coccyx view.
More extensive diagnostic imaging is unnecessary in traumatic coccyx injuries.
Contusion, hematoma
Coccyx dislocation
Pilonidal cyst
Treatment
ED Treatment
Symptomatic treatment
Rarely, bed rest until ambulation can be tolerated
Oral analgesics are key; may range from OTC acetaminophen or ibuprofen to
prescription oxycodone-APAP or hydrocodone-APAP combinations based on
severity of pain.
Attempted manipulation and reduction of the displaced fracture by digital rectal
approach is not necessary and futile because the coccyx cannot be stabilized.
If there is an associated rectal injury, call for a surgical consult immediately.
Prescribe antibiotics to cover enterics: cefoxitin, cefotetan, metronidazole.
Cushions (“doughnuts”)
Sitz baths
Stool softeners may help to reduce pain during bowel movements.
Medication
Cefotetan: Adult: 2 g IV; children: 80 mg/kg/day divided q6–8h (used with rectal
injury)
Cefoxitin: Adult: 2 g IV; children: 80–160 mg/kg/day divided q6h (used with
rectal injury)
Metronidazole: Adult: 500 mg–1 g IV; children: 30 mg/kg/day divided q12h (used
with rectal injury)
Acetaminophen
Ibuprofen
Oxycodone
Hydrocodone
General Measures
Prescription “donut pillows” provide comfort until the fracture heals. They are
helpful even if only a contusion is present.
Surgery is usually not required. Very rarely, severe trauma results in a
comminuted fracture requiring coccygectomy.
Spine immobilization for suspected concomitant cervical, thoracic, or lumbar
injuries
Pain control with NSAIDs or narcotic analgesics
Admission Criteria
Nearly all patients can be managed on an outpatient basis.
Only patients with severe pain, an inability to walk or to take care of
themselves, other serious injury, or requiring surgery need to be admitted.
Discharge Criteria
Most patients can be managed as outpatients with appropriate follow-up.
The patient is discharged home when other conditions are ruled out and pain is
under control.
Ongoing Care
Healing is slow.
Pain may become chronic.
Orthopedic consultation and possible coccygectomy may be required in severe cases.
Patient Education
Avoid activities requiring prolonged sitting such as horseback riding, long travel, biking, etc.
Lean forward while sitting to avoid weight bearing on the coccyx.
Prognosis
Pain usually resolves about a week after callous forms.
Complications
Rarely, chronic pain may require coccygectomy.
Additional Reading
Cwinn AA. Pelvis and hip. In Rosen P, et al., eds. Emergency medicine:
concepts and clinical practice. 4th ed. St. Louis: CV Mosby, 1998:739–762.
Foye P, et al. Coccyx pain, Emedicine, 2009.
Pollack C. Pelvic trauma. In: Harwood-Nuss A, et al., eds. The clinical

practice of emergency medicine. 2nd ed. Philadelphia: Lippincott-Raven,
1996.
Rockwood C, Green D, eds. Fractures in adults. 4th ed. Philadelphia:

Lippincott-Raven, 1996.
Simon R, Koenigsknecht SJ. Emergency orthopedics: The extremities. 4th

ed. E. Norwalk, CT: Appleton & Lange, 1996.
Codes
ICD9
805.6 Closed fracture of sacrum and coccyx without mention of spinal cord injury
805.7 Open fracture of sacrum and coccyx without mention of spinal cord injury
Clinical Pearls
More common in women
May occur owing to falls or during childbirth
A self-limited condition
Treatment includes pain management with oral anti-inflammatory medications
and doughnut pillows.
Fracture, Compression
David E. J. Bazzo
Tara Robbins
Basics
Description
A compression fracture is defined as failure of the anterior vertebral column of the spine.
The thoracolumbar spine is divided into 3 columns:
Anterior column (anterior portion of vertebral body, anterior longitudinal ligament, and
anterior annulus fibrosus)
Middle column (posterior longitudinal ligament, posterior annulus fibrosus, and posterior
wall of vertebral body)
Posterior column (posterior arch and posterior ligamentous complex)
2 subtypes: Anterior, caused by anterior flexion, and lateral, caused by lateral flexion
3 locations: Cervical, thoracolumbar (transition between thoracic and lumbar from T10–L2),
and lower lumbar vertebrae
If anterior AND middle columns are involved, the fracture is termed “burst.”
Synonym(s): Wedge fracture
Epidemiology
Spinal column injuries occur at 4–5.3 injuries per 100,000 households or 50,000 annually in
the U.S.
45% result from motor vehicle accidents, 20% from falls, 15% from sports-related activities,
15% from violence, and 6% from miscellaneous causes.
Spine injuries make up 10% of all athletic injuries.
Compression fractures make up 48% of thoracolumbar spinal fractures. L1 is the most
commonly fractured vertebrae (1).
Most common cervical compression fracture is anterior wedge fracture, usually at C5, as a
result of axial loading, as might occur in football or diving
10% of cervical spine fractures have an associated, noncontiguous spinal column fracture.
15% of female population >50 yrs will suffer a compression fracture secondary to
osteoporosis, usually nontraumatic.
Risk Factors
Cervical spine injuries are most common in diving, American football (poor tackling technique),
and wrestling.
Diagnosis
History
Hyperflexion and axial loading injuries, such as with “spear tackling” in football or striking the
forehead on the bottom of the pool, typically cause cervical compression fractures.
Hyperextension mechanism suggests a “teardrop” fracture or defect of posterior spinal
elements or pars interarticularis.
Transient or permanent paralysis and/or sensory deficits can occur with compression
fractures, but are rare. Neurologic deficits imply spinal cord injury due to retropulsion of disk
material or the fracture fragment (ie, burst fracture).
Physical Exam
Sudden, localized pain immediately following direct trauma or axial loading injury
Palpate the spinal column for “step-off” defect or tenderness.
Careful neurologic examination, including sensation, motor function, and reflexes. Should be
completely intact, but occasionally transient neurologic symptoms occur in an isolated
compression fracture.

Imaging
Anteroposterior (AP) radiograph: Buckling of lateral vertebral cortex next to end-plate with
decreased interspinous distance. May show lateral wedging with lateral flexion injury.
Lateral radiograph: Height of anterior vertebral body is decreased while posterior height is
unchanged, causing increased density of vertebral body from bony impaction and
prevertebral swelling. No subluxation of vertebral bodies.
Flexion-extension views: Evaluate cervical ligamentous instability (>3.5 mm horizontal or 11-
degree angular displacement between adjacent vertebrae).
CT scan: To confirm intact vertebral ring (posterior wall, pedicles, and lamina). 25% of
compression fractures identified on plain films will be reclassified as burst fractures after CT
scanning.
Myelography: Rules out osseous protrusion into spinal canal and better evaluates neural
compression than CT.
MRI: Recommended to evaluate spinal cord or nerve root compression and intrinsic spinal
cord abnormalities if neurologic symptoms persist or plain films are abnormal.
Burst fracture (anterior and middle column disrupted, with or without posterior involvement)
Fracture-dislocation (anterior, middle, and posterior columns disrupted)
“Teardrop” fracture (triangular fracture of anteroinferior vertebral body)
Transverse process or spinous process fracture
Lumbar or cervical strain or sprain
Spondylolysis and/or spondylolisthesis
Scheuermann disease: Kyphosis >50 degrees, wedging of at least 3 vertebral bodies by at
least 5 degrees, disk space narrowing, irregularity of end-plates
Spear tackler spine: Radiographic evidence of:
Developmental narrowing of the cervical spinal canal (<13-mm AP diameter of spinal canal
on plain film or impedance of contrast medium on myelography)
Straightening or reversal of the normal cervical lordotic curve
Preexisting minor post-traumatic radiographic evidence of bony or ligamentous injury
History of repeated spear tackling. Some authors believe that these findings absolutely
prohibit return to contact sports. Others believe that if normal cervical lordosis is restored
by treatment and the athlete refrains from further spear tackling, then there is not a high
risk of injury in returning to athletic activity.
Burning hands syndrome: A variant of central cord syndrome with characteristic complaint of
burning paresthesia and dysesthesia in both arms or hands and occasionally legs. Associated
with bony or ligamentous spine injury in 50% of cases.
Treatment
Pre-Hospital
It is estimated that 3–25% of spinal cord injuries may result from improper
stabilization of the spinal column during the transportation period.
Initial full spinal immobilization with a firm cervical orthosis and backboard are
necessary in all cases of suspected spine injury until radiographs can confirm
the extent of the injury.
If spinal cord injury is suspected, then management should be with advanced
trauma life support procedures: Airway should be established and protected,
breathing maintained, and circulation supported.
The possible administration of IV methylprednisolone (30 mg/kg) should be
discussed with neurosurgical consultants prior to use.
If the player is wearing a helmet, it should not be removed.
ED Treatment
All suspected spinal cord injuries warrant emergency department evaluation as
soon as possible. Radiographs should be obtained as soon as possible, and full
neurological exam should be documented.
Medication
NSAIDs
Consider narcotics for acute treatment. If narcotics are used, then patient
should also be put on a bowel movement program to prevent constipation.
Less severe injuries may be managed with bracing and serial imaging to
evaluate healing and alignment.
Unstable injuries mandate urgent surgical treatment.
A portion of injuries may require delayed surgical intervention.
General Measures
Cervical compression fractures in the absence of subluxation are treated with
a rigid brace for 8–12 wks with or without halo (2).
Thoracic fractures are relatively stable because of surrounding chest cage and
strong costovertebral ligaments, and can be treated conservatively with relative
rest.
Thoracolumbar injuries (T10–L2) are inherently more unstable and require a
longer recumbency and possible immobilization in thoracolumbar spinal
orthosis.
Isolated fractures with <25% anterior compression are considered stable and
can be treated with thoracic lumbosacral orthosis brace immobilization.
A >50% loss of anterior vertebral height, multiple adjacent compression
fractures, or angulation >20 degrees at the thoracolumbar junction are
associated with segmental instability due to posterior ligamentous injury. This
requires surgery to prevent formation of chronic instability and possible further
kyphotic deformity. The procedure of choice is usually posterior short-segment
pedicle screws or interspinous wiring and fusion.
Kyphotic deformities may be managed with a posterior approach with
osteotomies or a combined anterior approach and posterior procedure,
although anterior approaches are associated with higher morbidity and
complications.
Vertebroplasty and kyphoplasty are routinely used for pain associated with
osteoporotic and pathologic compression fractures. Recent study has shown
that percutaneous vertebroplasty and kyphoplasty are 2 safe and effective
techniques for treatment of thoracolumbar traumatic fractures and allow good
pain control and return to normal working activity and social life.
Ongoing Care
Any patient with unstable radiographic abnormalities should be seen by an orthopedist or
neurosurgeon for complete evaluation.
References
1. Denis F. The three column spine and its significance in the classification of acute
thoracolumbar spinal injuries. Spine. 1983;8:817–831.
2. Khoueir P, Oh BC, Wang MY. Delayed posttraumatic thoracolumbar spinal deformities:

diagnosis and management. Neurosurgery. 2008;63:117–124.
Additional Reading
Cantu RC, Bailes JE, Wilberger JE. Guidelines for return to contact or collision sport after a
cervical spine injury. Clin Sports Med. 1998;17:137–146.
Costa F, Ortolina A, Cardia A, et al. Efficacy of treatment with percutaneous vertebroplasty

and kyphoplastic for traumatic fracture of thoracolumbar junction. J Neurosurg Sci.
2009;53:13–17.
Maroon JC, Bailes JE. Athletes with cervical spine injury. Spine. 1996;21:2294–2299.
McGirt MJ, Parker SL, Wolinsky JP, et al. Vertebroplasty and kyphoplasty for the treatment
of vertebral compression fractures: an evidenced-based review of the literature. Spine J.
2009.
Nicholas J, Nuber G, eds. The lower extremity and spine in sports medicine. St. Louis:
Mosby, 1995.
Oner FC, Dhert WJ, Verlaan JJ. Less invasive anterior column reconstruction in
thoracolumbar fractures. Injury. 2005;36 (Suppl 2):B82–B89.
Tatsumi RL, Hart RA. Cervical, thoracic and lumbar fractures. Current Therapy of Trauma
and Surgical Critical Care. Philadelphia: Mosby; 2008:513–519.
Codes
ICD9
733.13 Pathologic fracture of vertebrae
805.00 Closed fracture of cervical vertebra, unspecified level
805.10 Open fracture of cervical vertebra, unspecified level
Clinical Pearls
Compression fractures without neurologic injuries are considered stable and,
once healed completely, should allow the player to return to action when neck
pain is gone, range of motion is complete, muscle strength is normal, and
fusion is solid (if done).
Athletes with significant vertebral injury requiring a halo brace or surgical
stabilization are considered not to have adequate strength to return to contact
sports.
Fracture, Coronoid
David A. Stone
Delmas J. Bolin
Basics
The coronoid process:
An important stabilizer of the elbow to varus stress and posterior ulnar displacement.
Part of the sigmoid notch, the portion of the proximal ulna that articulates with the humerus.
Has several important soft tissue insertions:
The brachialis muscle inserts anteriorly, distal to the capsule; the anterior joint capsule
inserts very close to the tip of the coronoid; the anterior bundle of the medial collateral
ligament and the lateral collateral ligament complex insert at the base of the coronoid.
When the coronoid is fractured at the base, the ligament insertion sites are often preserved
because failure occurs through bone, not the ligament insertions. Smaller fractures are likely
to be associated with ligament injury.
Usual mechanism of injury is elbow dislocation as a result of a fall on an outstretched hand.
Description
Coronoid fractures are classified based on anatomic location of the fracture; subclassification
according to the associated soft tissue injuries and fractures to determine treatment (1,2):
Type 1: Fracture of the tip of the coronoid:
Tip subtype 1 fractures involve <2 mm of coronoid and may be isolated or associated with
a fracture dislocation.
Tip subtype 2 fractures involve >2 mm and generally is associated with “terrible triad”
injuries (ie, elbow dislocation, radial head fracture, and coronoid fractures).
Type 2: Fracture of the anteromedial facet:
Anteromedial subtype 1 fractures extend from just medial to the tip of the coronoid to the
anterior half of the sublime tubercle (the insertion of the medial band of the medial
collateral ligament).
Anteromedial subtype 2 fractures extend to the tip of the coronoid.
Anteromedial subtype 3 fractures extend to the anteromedial rim and the entire sublime
tubercle but do not always extend to the tip of the coronoid.
Type 3: Fracture of the basal aspect of the coronoid involving >50% of the coronoid:
Basal subtype 1 fractures involve the basal coronoid alone.
Basal subtype 2 fractures are associated with fractures of the olecranon.
Epidemiology
Uncommon, rarely occurring as an isolated injury
In elbow dislocations, 2–15% of cases have coronoid process fractures.
Risk Factors
Displacement of large coronoid process fracture fragments has been associated with
recurrent dislocation.
No known significant risk factors to date

Elbow instability
Radial head fracture
Olecranon fracture
Loss of range of motion
Degenerative joint disease (posttraumatic arthritis)
Ulnar, median, radial, and anterior interosseous nerve injury
Brachial artery injury
Heterotopic ossification
Diagnosis
History
Common mechanism is fall on outstretched hand.
Most patients with coronoid fractures present with elbow dislocations.
Direct impact is a less common cause.
Physical Exam
Diffuse edema within and around the elbow joint
Tenderness is usually multifocal. Look for radial head tenderness as well as olecranon
tenderness.
Range of motion (ROM) is limited, and crepitus on ROM should be noted.
Anteroposterior instability may be present.
Neurovascular examination is paramount, especially if there is elbow deformity.
If elbow is dislocated, perform neurologic and vascular examinations before reduction.
Repeat neurovascular examination after elbow dislocation is reduced, and assess for elbow
instability.
Palpate radial head and olecranon to look for accompanying fractures.

Imaging
Standard elbow x-ray series (anteroposterior, lateral, and 1 or both obliques) should be
requested at the time of evaluation.
Evaluate for comminuted fractures, where reduction may not be advisable.
Repeat plain radiographs after elbow relocation.
If radial head tenderness is present, radial head view should be added to x-ray series.
Advanced imaging: Small coronoid fractures can be difficult to distinguish from radial head
fractures, and both CT scanning and MRI should be considered if radiographs are not
definitive.
Elbow subluxation
Posterior lateral rotatory instability
Acute ulnar collateral ligament sprain
Hyperextension injuries to joint capsule
Treatment
Acute treatment (1,3)[B]:
Elbow dislocations with coronoid fractures should be evaluated for instability
and splinted in position of stability.
Tip subtype 1 fractures do not involve the insertion of the anterior capsule
and can be treated with immobilization for 1–2 wks.
Tip subtype 2 fractures almost always involve the anterior capsule insertion
and are often seen in terrible triad injuries. They should be referred to
orthopedics; they often will require suture fixation because the fragments are
too small to be secured with screws.
Anteromedial subtype fractures are associated with incongruent articulation
of the ulnohumeral joint and may lead to posttraumatic degenerative joint
disease. These fractures require surgical stabilization.
Basal coronoid fractures generally have less soft tissue disruption than tip or
anteromedial fractures but require stabilization to prevent recurrent instability
and traumatic degenerative joint disease.
Posttraumatic degenerative joint disease correlates with patient age.
Ulnar nerve injuries occur from handling of nerve and do not always resolve.
Subluxation or repeat dislocation usually requires repeat surgery.
Contractures and heterotopic ossification are common after treatment.
Rehabilitation:
Early mobilization with active and active assistive ROM should begin as soon
as comfort allows, generally after 1 wk.
A hinged brace to protect the elbow from varus and valgus stress generally is
prescribed for the 1st month, and blocking of the terminal 30 degrees of
extension during early rehabilitation is common.
Prophylaxis for heterotopic ossification is not routine (eg, indomethacin or
Naprosyn).
Resistive exercises generally are delayed for 6 wks.
Serial radiographs are commonly obtained to confirm maintenance of
concentric reduction.
Surgery to repair soft tissue injuries associated with coronoid fractures is being
performed increasingly.
Ongoing Care
Prognosis
Joint stiffness and limited ROM are common with prolonged immobilization.
Presence of posttraumatic arthritis correlates with patient age.
Pain is a common complaint in at least half of all patients after treatment.
Complications
Vascular and neurologic injuries associated with elbow dislocations
Complex dislocations with loss of ROM and stability
Persistent pain and loss of ROM after treatment
References
1. Ring D. Fractures of the coronoid process of the ulna. J Hand Surg [Am].
2006;31:1679–1689.
2. Doornberg JN, Ring D. Coronoid fracture patterns. J Hand Surg [Am].

2006;31:45–52.
3. Wells J, Ablove RH. Coronoid fractures of the elbow. Clin Med Res.
2008;6:40–44.
Codes
ICD9
813.02 Fracture of coronoid process of ulna, closed
813.12 Fracture of coronoid process of ulna, open
Clinical Pearls
Coronoid fractures can be managed conservatively with meticulous diagnosis.
Athletes with associated soft tissue injuries or instabilities should be referred
early for orthopedic evaluation.
Athletes return to play when fractures are healed and when they have restored
painless ROM with normal strength and flexibility.
Recovery can be prolonged, and careful follow-up is important.
Patients with type 1 tip fractures generally can return to play within 6–8 wks.
Patients with injuries requiring surgery frequently require longer rehabilitation
time prior to return to play.
Lockout elbow bracing should be considered because it can help to stabilize
the elbow and can be an important adjuvant to healing and rehabilitation.
Fracture, Distal Femur
Sandeep Johar
Basics
Description
Fracture involves the distal 15 cm of the femur.
Fractures may be
Supracondylar: Zone is from the femoral condyles to the junction of the metaphysis and
femoral shaft.
Intracondylar
Condylar
Many classification systems (Neer, Stewart, Schatzker, etc.): AO/OTA is the most commonly
used and complete classification system.
Epidemiology
Distal femur fractures represent 7% of all fractures of the femur (1).
No data on the incidence in the athletic population
Up to 60% of femoral fractures in children 3 yrs old or younger may be the result of
nonaccidental trauma (2).
Spiral fractures of the femur strongly suggest child abuse (2).
Risk Factors
High-energy sports such as motor sports and downhill skiing
Osteoporosis
Etiology
Fractures generally occur from significant axial loading with associated varus, valus, or
rotation force.
May occur from direct trauma as well
In young adults, fractures are usually associated with high-energy trauma such as:
Motor vehicle accidents, falls from heights, direct impact
Motor sports, downhill skiing
In older individuals, a slip and fall may be enough force to cause injury.
Muscle attachments, quadriceps, hamstring, and gastrocnemius cause the observed
deformity in distal femur fractures.

Fractures are generally from high-energy mechanism, so a full trauma survey should be
performed.
Complications may include:
Proximal or shaft fractures of the femur
Ligament and cartilage injuries of the knee
Proximal tibia fractures
Open fractures: 5–10% of all supracondylar fractures
Quadriceps tendon injury
Vascular injuries are relatively uncommon.
Diagnosis
Cartilaginous components of the proximal and distal ends of the developing femur alter the
fracture patterns seen in hip and knee injuries in children.
Essential workup:
Radiographs
Assess distal pulses, palpate compartments, and evaluate sensation and motor function.
If pulses are not equal or palpable, bedside Doppler may be necessary.
Search for associated injuries.
In suspected child abuse, obtain skeletal survey or bone scan.
History
History will help to guide examination and workup.
High-energy injuries require full examination and search for associated injuries.
Direct trauma and low-energy mechanism do not necessarily require a more comprehensive
evaluation.
Physical Exam
Tenderness on examination, deformity, thigh shortening, swelling (secondary to hematoma),
and crepitus with movement
Limited movement of hips and knees
Commonly presents with associated injuries: Chest or abdominal trauma, hip or knee injury,
direct blow to the extremity
Vascular compromise (arterial injury): Expanding hematoma, absent or diminished pulses,
progressive neurologic deficits in a closed fracture
Hypotension and tachycardia secondary to significant blood loss

Radiographs:
Anteroposterior (AP) view of pelvis, true lateral of hip, AP and lateral views of femur, and
complete knee series
Other imaging as indicated by trauma protocols
CT scan: Complex intraarticular injuries generally necessitate CT scan for operative planning.
Arteriography: Should be performed for evidence or suspicion of vascular compromise
Lab
CBC, type, and crossmatch
Hip fracture or dislocation
Knee dislocation
Proximal tibia fracture
Thigh contusion or hematoma
Treatment
Assess markers for nonaccidental trauma.
Delay in presentation; history of mechanism inconsistent with the injury
Isolated trauma to the thigh; associated burns, bruises, or linear abrasions
Assess for dislocation of the femoral capital epiphysis.
Depending on the age of the patient and the fracture type, pediatric femoral
fractures may not require operative treatment.
Pre-Hospital
Long-leg splint should be applied to the extremity in the position it was found.
If signs of neurovascular compromise, reduce limb with in-line traction.
Use analgesia when possible.
Do not attempt to reduce open fractures in the field.
Apply wet sterile dressing over an open fracture.
If wound is grossly contaminated, use sterile saline irrigation.
Apply wet sterile dressing over an open fracture.
If wound is grossly contaminated, use sterile saline irrigation.
ED Treatment P.
Primary and secondary trauma surveys
If surgical treatment will be delayed or for selected patients in whom
nonoperative management is the treatment of choice, consider fracture
reduction.
Reduce fractures to near-anatomic alignment by using in-line traction (Hare,
Buck, or long posterior splint): Reduces pain and helps to prevent hematoma
formation.
Pain management: Parenteral or IV opiate-type analgesia
Infection prophylaxis: With open fractures, tetanus toxoid if indicated, cefazolin
with gentamicin
For injuries with highly contaminated wounds, add penicillin G to cover
Clostridium spp.
Emergently consult an orthopedic surgeon
Femur fractures with vascular (expanding hematoma, absent or diminished
pulses) or progressing neurologic compromise require immediate angiography
or vascular consultation for femoral artery exploration.
Consider transferring patients with a femur fracture if:
Necessary orthopedic consults are not available.
There are associated serious injuries that may require a trauma center for
management.
Medication
Cefazolin: Adult: 2 g IM/IV; children: 20 mg/kg IM/IV
Gentamicin: 1.5 mg/kg IV
Penicillin G: Adult: 2 million IU IV; children: 25,000 IU/kg/day IV divided q8h
Surgical reconstruction should be performed as soon as possible (3)[C].
If surgery will be delayed more than 24 hr (closed fractures), tibial pin traction
should be applied to maintain limb length (3)[C].
Multiple surgical techniques can be performed to obtain reduction and fixation
and depend on both surgeon experience and the specific fracture.
Anatomic reduction of the fracture with particular attention to the articular
surface is more closely related to positive outcomes than the actual surgical
technique.
Children aged 6 mos to 5 yrs with a diaphyseal fracture and <2 cm of
shortening may be treated with early spica casting or traction and delayed
spica casting (4)[B].
There is unclear benefit of surgery versus casting in fractures with >2 cm
shortening or varying degrees or rotation and angulation (4)[C].
Monitor heart rate and BP continuously because large volumes of blood (ie, 4–6
units) may be contained within the thigh.
Admission Criteria
Most femur fracture patients should be admitted.
Conservatively treated fractures in a pediatric patient may not require
hospitalization.
Ongoing Care
Prognosis
Depends on multiple factors:
Fracture type
Associated injuries
Patient comorbidities
Fracture with intra-articular involvement carries a high risk of posttraumatic arthritis.
Complications
Hemorrhagic shock secondary to significant blood loss
Infection secondary to open fractures
Fat embolism and adult respiratory distress syndrome can cause respiratory
failure.
References
1. Arneson TJ, Melton LJ, Lewallen DG, et al. Epidemiology of diaphyseal and
distal femoral fractures in Rochester, Minnesota, 1965–1984. Clin Orthop
Relat Res. 1988;188–194.
2. Hui C, Joughin E, Goldstein S, et al. Femoral fractures in children younger

than three years: the role of nonaccidental injury. J Pediatr Orthop.
2008;28:297–302.
3. Albert MJ. Supracondylar fractures of the femur. J Am Acad Orthop Surg.

1997;5:163–171.
4. Kocher MS, Sink EL, Blasier RD, et al. Treatment of pediatric diaphyseal
femur fractures. J Am Acad Orthop Surg. 2009;17:718–725.
Additional Reading
Macnicol MF. Fracture of the femur in children. J Bone Joint Surg Br.
1997;79:891–892.
Starr AJ, Hunt JL, Reinert CM. Treatment of femur fracture with associated
vascular injury. J Trauma. 1996;40:17–21.
Codes
ICD9
821.20 Fracture of lower end of femur, unspecified part, closed
821.21 Fracture of femoral condyle, closed
821.22 Fracture of lower epiphysis of femur, closed
Clinical Pearls
Be aware of potential associated injuries in all femur fractures.
Evaluate for signs of child abuse in children <3 yrs.
Fracture, Distal Phalanx
Thomas L. Pommering
Basics
Fractures of the distal tip (Tuft fracture):
Open
Closed
Fractures of the shaft:
Longitudinal
Transverse
Fractures of the base:
Mallet fracture
Reverse mallet fracture (jersey finger)
Pediatric epiphyseal fractures:
Salter-Harris type I or type II
Seymour fracture (pediatric jersey finger)
Description
Mallet finger: A pure tendon injury where there is disruption of the extensor tendon caused by
forced flexion of the fingertip while the distal interphalangeal (DIP) joint is in extension; the
result is that the active extension of the DIP joint is lost, leaving the fingertip in slight flexion
Mallet fracture: A disruption of the terminal extensor tendon from its insertion onto the
proximal aspect of the distal phalanx dorsally with a bony avulsion
Jersey finger: Flexor digitorum profundus (FDP) rupture from its insertion onto the palmar
distal phalanx; can be a pure tendinous injury or include a bony avulsion
Swan-neck deformity: Reverse boutonniere deformity; hyperextension of the proximal
interphalangeal (PIP) joint caused by disruption of the volar plate attachment to the middle
phalanx causing relaxation of the extensor mechanism and allowing the unopposed flexor
digitorum to draw the distal phalanx into flexion; often the result of an undiagnosed or
untreated mallet finger or mallet fracture
Seymour fracture: Extraarticular transverse fracture of the base of the distal phalanx usually
involving the distal physis (SH I or II) or 1–2 mm distal to the physis; this fracture mimics
mallet finger deformities but does not involve the articular surface. The FDP tends to pull the
distal metaphyseal fragment volarly, whereas the extensor tendon insertion onto the proximal
aspect of the distal phalanx pulls the epiphysis dorsally, in the opposing direction.
Tuft fracture: A fracture of the distal tip of the distal phalanx; usually from a crush injury and
associated with a subungual hematoma and/or a nail bed injury; can be an open or closed
injury.
Epidemiology
Incidence
Most common peak incidence is during early teenage years, followed by a second peak
during toddler years (crush injury in doors)
In the pediatric population, physeal fractures of the phalanges account for 37% of all physeal
fractures, with the small finger being affected most often (30%), followed by the thumb
(20%).
Hand injuries, in general, account for 9% of all sports injuries.
Seen more often with contact sports, where direct trauma is more likely (eg, football), or with
sports where the hand is exposed to projectiles (eg, baseball)
Risk Factors
Crush injury to tip of finger (eg, getting stepped on by opponent's spiked shoes) results in
comminuted fracture or tuft injury.
Acute flexion of an extended DIP joint (eg, catching a ball on the tip of the finger or striking an
object with the finger extended) results in mallet finger.
Forced extension while actively flexing the DIP joint (eg, grabbing a jersey of a ball carrier in
football or catching the rim while dunking a basketball) results in jersey finger.
General Prevention
Seen more often with contact sports where direct trauma is more likely (eg, football) or with
sports where the hand is exposed to projectiles (eg, baseball)
Buddy taping to the adjacent digit or interphalangeal joint taping for high-risk athletes
Etiology
The tip of the distal phalanx ends with broad, spadelike ungual tuberosity that provides a
stable and protective base for the distal digital pulp.
On the palmar surface, the FDP inserts onto the midportion of the distal phalanx.
On the dorsal side, the terminal extensor tendon attaches to the proximal aspect of the distal
phalanx (or the epiphyseal plate in children), blending with the joint capsule and periosteum.
Collateral ligaments span the DIP joint (or the epiphyseal plate in children) and insert onto the
metaphysis of the distal phalanx.
Lateral interosseous ligaments originate on and span the distance of the distal phalanx,
protecting the neurovascular bundle as they pass dorsally from the pulp to the nail bed.
Diagnosis
History
Crush, torsional, or hyperflexion/hyperextension mechanism (“jammed finger”)
Blunt trauma or projectile force against the fingertip resulting in forced flexion: Mallet
finger/fracture
Forced extension on a flexed distal phalanx (eg, grabbing a jersey during a tackle): Jersey
finger
Physical Exam
Pain, swelling, and ecchymosis
Loss of range of motion (ROM), malalignment or angular deformities noted with flexion
Obvious deformity, especially if associated with dislocation
Subungual hematomas
Traumatic swelling and tenderness over the volar aspect of the distal phalanx with
additional palmar pain is a rupture of the FDP until proven otherwise.
Sites of tenderness, loss of active ROM, evidence of instability, and neurovascular
examination
Radiographs should be obtained before any manipulative examination.
Mallet finger: 40–45-degree loss of extension at the DIP joint with inability to extend the
distal phalanx; there also is pain and swelling over the dorsal aspect of the joint.
Jersey finger: Inability to flex the distal phalanx, with tenderness over the volar aspect of
the joint and in the palm secondary to retraction of the tendon after rupture

Imaging
Imaging should be obtained before any manual reduction attempts.
Three views of the affected digit: Anteroposterior (AP), lateral, and oblique views
Consider comparison views of the unaffected side when skeletal immaturity is involved.
Rarely do MRI, CT scan, or US add useful diagnostic information for distal phalangeal
injuries.
MRI is occasionally useful to delineate soft tissue ligamentous or tendon injury.
CT scan is occasionally useful to delineate osseous injury for preoperative planning.
Fracture
Sprain
Tendon rupture or avulsion
Interphalangeal dislocations
Treatment
Distal phalanx or tuft fractures:
Closed with minimal to no displacement:
Inherently stable
Often have an associated subungual hematoma that may need evacuated
(see “Other Procedures”) for pain control
Ice for swelling and pain control
Simple moldable aluminum splint covering the tip of the finger for support
and protection; usually not needed for more than 3 wks
Union by 6–8 wks
Open:
Inherently unstable because of disruption of the supporting pulp and nail
bed
Require careful débridment, irrigation, and soft tissue repair often with loop
magnification
Oral antibiotics and tetanus prophylaxis
Consider surgical consultation.
Shaft fractures:
Closed longitudinal or transverse shaft:
Usually inherently stable
Longitudinal fractures: Heal within 3–4 wks; splint for protection
Transverse fractures: Take longer, requiring slightly longer support until
clinical discomfort abates or radiographic union is evident
Open shaft fractures:
Unstable; also often associated with underlying nail bed injury
Proper alignment is necessary.
Surgical consultation is recommended.
Base-of-phalanx fractures:
Tend to be unstable regardless of the overlying soft tissue involvement owing
to the deforming traction of the extensor or flexor tendons
Lack the intrinsic support of the overlying nail and nail plate
Tend to angulate with the apex pointing dorsally
If >1/3 to 1/2 of the articular surface is involved or if displaced, consider
Closed nondisplaced fracture of the dorsal surface in adults (mallet fracture):
Continuous 24 hr/day splinting with the DIP joint in extension using a molded
volar aluminum splint or properly fitted polythene (Stack) splint for 6–8 wks;
night splinting is recommended for an additional 2–6 wks.
Hyperextension of the DIP joint should be avoided.
PIP joint is always left free.
Any momentary loss of extension (eg, during changing or removal of splint for
hygiene) mandates restarting back at day 1 of immobilization.
Some extension lag after treatment is expected.
The goal is to prevent a hyperextension PIP joint deformity (swan-neck
deformity).
Because the surgery often is deceptively difficult to perform and is
associated with several complications, operative management is reserved
for injuries with volar subluxation of the distal phalanx or if displaced and
involving >50% of the joint surface.
Discussion with your surgical consultant is advised.
P.
Mallet finger:
Pure tendon injury with normal radiographs
Treated similarly to mallet fracture with 6–8 wks of continuous 24 hr/day DIP
joint splinting followed by night splinting
Failed or interrupted treatment can be restarted because extended splinting
time will not alter clinical outcomes and may even yield good results.
Conservative treatment is preferred owing to the complication risks of
surgical treatment.
Closed nondisplaced fracture of the volar surface in adults (jersey finger):
Essentially opposite of mallet finger
Ring finger involved 75% of the time
Avulsed fragment from the volar surface is attached to the FDP, which tends
to promote displacement.
Prompt surgical referral (within 7–10 days) should be the rule to optimize full
functional outcome and avoid late complications.
Rare injury in children (see below); when present, usually occurs in
adolescents near skeletal maturity
Children <5 yrs of age often have a SH I or II fracture (Seymour fracture).
The FDP tendon is attached to the distal shaft, pulling it in the volar direction,
whereas the epiphysis remains extended owing to the traction of the
extensor tendon.
Extraarticular fracture of the base of the distal phalanx before closure of the
epiphysis
Clinically, mimics mallet fracture or DIP joint dislocation (although is not an
intraarticular injury)
Splint application for up to 6 wks in slight hyperextension
Close follow-up with weekly lateral radiographs for the 1st 2 wks to confirm
alignment and stability to prevent permanent deformity
Surgical referral for open fractures, those not amenable to closed reduction,
or if unfamiliar with treatment of this injury in children
Transverse or comminuted distal phalanx fractures: No reduction usually is
required, only protective splinting for 3–4 wks, elevation, and analgesics.
Treat associated subungual hematomas.
Displaced distal phalanx fractures with AP displacement: Apply traction to the
distal aspect, and mold the fragments by squeezing the end of the finger
between your thumb and index finger. Lateral displacement is corrected by
compressing the lateral borders of the terminal phalanx with your thumb and
index finger. Be aware that these can be difficult to reduce when soft tissues
become interposed between fragments. If uncorrected, this may lead to
nonunion.
Repeat radiographs
Neurovascular examination
Pre-Hospital
Protect and splint
Medication
If reduction is needed or repair of associated soft tissue injuries (eg, nail bed
laceration), a hematoma block, digital block, or wrist block can be used.
Conscious sedation or reduction under general anesthesia may be needed.
Second Line
Chronic pain control usually can be achieved with nonnarcotic analgesics or mild
narcotic pain medication.
Hematoma evacuation from the nail bed when >30–50% of the nail is involved
or there is a need for pain control
Usually accomplished using either a heated paper clip or electric cautery
device
Referral
Displaced fractures not responsive to manual reduction
Anytime there is suspected flexor tendon involvement
Open fracture of the shaft or intraarticular fracture
Open tuft fractures are often unstable and involve complex injuries to the nail
bed requiring skilled repair under loop magnification.
Suspected neurovascular injury or secondary infection
With fractures associated with subungual hematomas involving >30–50% of
the nail, concomitant nail bed lacerations should be suspected and repaired if
present. This is usually done using 5–0 or 6–0 dissolvable sutures and
replacing the nail plate if possible. This is treated as an open fracture in the
sense that it should be done under sterile conditions followed by antibiotic
coverage for 7–10 days.
Physical therapy with a qualified hand therapist is recommended in
postoperative cases, after prolonged immobilization, and after splinting mallet
finger if return to full ROM is not progressing.
With mallet finger, patients should be warned against strong passive ROM in an
attempt to hasten flexion owing to the risk of additional damage to the extensor
insertion. Gradual progression is usually the rule.
FDP tears or jersey finger
Mallet finger with volar subluxation of the distal phalanx
Comminuted distal phalanx fracture with significant displacement (Tuft fracture)
Any distal phalanx fracture with malalignment that is not reducible by closed
methods
Generally reserved for severe, infected, or complicated injuries requiring surgical
intervention
Ongoing Care
Repeat radiographs:
Mallet fractures: Consider at 1–2 wks to document stability (x-ray in splint) and possibly at
4–6 wks if there is any evidence of extension lag
Pediatric epiphyseal fractures (including Seymour fracture): At 1–2 wks to document stability;
optional at 4 wks as the clinical picture dictates
Longitudinal and transverse shaft fractures: At 2 wks
Prognosis
In general, distal phalanx fractures are usually stable and heal with an uneventful course.
Complications
Nonunion or malunion
Infection for open fractures
Joint stiffness or arthrofibrosis
Permanent loss of flexor tendon function or dysfunction with undiagnosed or
delayed treatment for flexor tendon avulsions or disruptions
Physeal arrest in children
Avascular necrosis with displaced unicondylar fractures, especially in children
Swan neck deformity
Skin necrosis from splints applied too tightly
Skin hypersensitivity with distal injuries
Osteoarthritis for late, undiagnosed, or inadequately healed intraarticular
fractures
Additional Reading
Flynn JM, Nagda S. Upper extremity injuries. In: Dormans JP, ed. Pediatric
orthopaedics and sports medicine. 1st ed. St. Louis: Mosby, 2004:21–25.
Heaps RJ, Levin LS. In: Garrett WE, Speer KP, Kirkendall DT, eds. Principles
and practice of orthopaedic sports medicine. 1st ed. Philadelphia: Lippincott
Williams & Wilkins, 2000:235–236.
Jobe MT, Calandruccio JH. Fractures, dislocations and ligamentous injuries.

In: Canale ST, ed. Campbell's operative orthopedics. 10th ed. Philadelphia:
Mosby, 2003:3515–3516.
Jupiter JB, Axelrod TS, Belsky MR. Fractures and dislocations of the hand. In:
Browner BD, Jupiter JB, Levine AM, et al. eds. Skeletal trauma: basic
science, management, and reconstruction. 4th ed. Philadelphia: W.B.
Saunders, 2008:121–141. (accessed on line www.mdconsult.com, 8/25/09).
Leggit JC, Meko CJ. Acute finger injuries: part II. Fractures, dislocations, and
thumb injuries. Am Fam Physician. 2006;73:827–834, 839.
Lindley SG, Rulewicz. Hand fractures and dislocations in the developing

skeleton. Hand Clin 2006;22:253–268.
Papadonikolakis A, Zhongyu L, Smith BP et al. Fractures of the phalanges and

interphalangeal joints in children. Hand Clin. 2006;22:11–18.
Peterson JJ, Bancroft LW. Injuries of the fingers and thumb in the athlete. Clin
Sports Med. 2006;25:527–542.
Shepler T. The pediatric hand. In: DeLee JC, Drez D, Miller MD, eds. DeLee
and Drez's orthopaedic sports medicine. 3rd ed. Philadelphia: Saunders,
2009:1–43 (accessed on line www.mdconsult.com, 8/25/09).
Waters PM. The upper limb. In: Morrissy RT, Weinstein SL, eds. Lovell and
Winter's pediatric orthopaedics. 5th ed. Philadelphia: Lippincott Williams &
Wilkins, 2001:886–887.
Codes
ICD9
736.1 Mallet finger
816.02 Closed fracture of distal phalanx or phalanges of hand
816.12 Open fracture of distal phalanx or phalanges of hand
Clinical Pearls
Patients who remove a stack splint even for a moment (eg, during the treatment
of mallet finger) must start treatment over at day 1.
Proper healing depends on continuous splinting of the DIP joint for 6–10 wks.
To ensure this, patients are shown how to change their splints while keeping
the DIP joint extended against a hard surface before splint application.
Patients are seen again after 1–2 wks to be sure that they have complied or
can comply with the strict protocol.
Late, untreated mallet fingers with no functional problems need not be treated.
With mallet finger, some experts recommend a second course (8 wks) of full-
time splinting in the event of significant extensor lag after initial splinting.
Return to play with uncomplicated distal phalanx fracture depends on several
factors:
Athlete's (and parent's, if a minor) wishes and expectations. They need to be
involved in the decision and understand the risks and benefits.
Rules governing the athlete's sport and whether an effective splint that meets
the safe play criteria be fabricated.
Athlete's sport and/or position: Will splint protect the DIP joint and allow the
athlete to play at a competitive level?
Depending on the athlete and his or her age and maturity, many times he or
she can return to play in a protective splint once the initial swelling and pain
have subsided.
Fracture, Distal Radius
Kevin B. Gebke
Vijay Jotwani
Basics
Description
Classically, the fractured distal portion will be dorsally displaced and angulated (“silver-fork
deformity”); commonly referred to as Colles fracture
Other variations include:
Smith fracture (volar displacement and angulation)
Barton fracture (dorsal fracture-dislocation involving displacement of carpus with distal
fragment)
Reverse Barton (Barton fracture with volar displacement)
Hutchinson fracture (lateral-oriented fracture through radial styloid process extending into
radiocarpal articulation)
Galeazzi fracture-dislocation (fracture of distal third of radius with associated dislocation of
distal radioulnar joint)
Key is to always describe fracture location, angulation, displacement, and involvement of
either radiocarpal or radioulnar joints
Synonym(s): Colles fracture; Smith fracture; Barton fracture; Reverse Barton fracture;
Hutchinson fracture; Galeazzi fracture-dislocation
Epidemiology
General (1):
Most common fracture of the upper extremity
Seen in all age groups, with peaks between 6 and 10 yrs of age and 60 and 69 yrs of age
Female predominance in the general population, but male predominance in sports (1,2)
Sports:
True incidence in sports is unknown:
Distal radius fractures represent 12.5% of fractures caused by sporting activity in 1
study (2): Percentages of total fractures by sport that were distal radius: Snowboarding
34.8%, ice skating 36.4, soccer 19.1%, rugby 14.7%, mountain biking 14%
Distal radius fractures represent 14.5% of injuries in snowboarders (3).
Risk Factors
General:
Decreased bone mineral density
Unsteady gait
Sports:
Activities with high risk of falls and impact: Snowboarding, football, ice skating, etc.
General Prevention
Wrist guards can decrease the rates of wrist injury, including distal radius fractures in
snowboarders (4)[B]:
50 snowboarders have to wear wrist guards to prevent 1 wrist injury.
Beginner snowboarders get the most benefit from wrist guards.
Unclear if these results can be generalized to other sports
Etiology
Commonly sustained by falling onto an outstretched hand with the wrist in extension

Vascular injury
Nonunion
Arthrosis secondary to poor joint approximation at radioulnar or radiocarpal joint
Joint stiffness or weakness
Median nerve dysfunction
Reflex sympathetic dystrophy
Diagnosis
Pre Hospital
If a distal radial fracture is suspected during event coverage, splinting should be applied after
careful neurovascular assessment.
Transport for radiographic evaluation
History
Elicit specific details regarding fall or trauma involved:
High- or low-energy mechanism
Comorbid conditions such as osteoporosis or malignancy
Physical Exam
Pain, swelling, and limitation of movement of distal upper extremity
Paresthesias, weakness, or coolness to touch:
Associated neurologic or vascular injury
Gross visualization of the involved extremity for bony deformity and evidence of open injury
Neurologic evaluation, including radial, median, and ulnar nerve testing
Vascular evaluation, including radial and ulnar pulses

Multiple classification systems have been described, Frykman, Melone, A-O, etc., but none
have been found to be reliable and reproducible, nor do they add prognostic value to treatment
or outcomes (1).
Imaging
Posteroanterior (PA) view: Useful for identifying Colles and Hutchinson fractures and Galeazzi
fracture-dislocation
Lateral view: Useful for identifying Colles, Smith, Barton, and reverse Barton fractures and
Galeazzi fracture-dislocation
Ancillary imaging techniques, including CT, arthrography, bone scan or MRI: May be
necessary in subtle or complex cases for further evaluation:
CT can be useful for evaluation of the articular surface in fractures that have an intra-
articular component.
PA and lateral views should be obtained after reduction to evaluate correction of radial length
and angulation of distal articular surface.
Carpal fracture
Ulnar fracture
Radiocarpal sprain
Radioulnar sprain
Soft tissue/bony contusion
Treatment
General:
Most studies that compare conservative vs surgical management do not
involve younger patients. This makes it difficult to determine the best
treatment option in many cases.
Treatment of the fractures may vary significantly based on the type of
fracture, patient demands, and physician experience.
Analgesia:
Adequate pain relief using oral and/or IV narcotics
For pediatric fractures, ibuprofen is equal to Tylenol with codeine (5)[A].
Hematoma blocks can provide pain relief for closed reductions:
May be less effective than IV regional anesthesia (6)[B]
Nondisplaced fractures:
Nondisplaced fractures can be immobilized in a sugar tong splint or radial
gutter splint (7)[B].
Pediatric torus fracture can be treated safely with a wrist immobilizer (8)[B].
Displaced fractures/unstable fractures:
No defined criteria for displacement, but it is generally accepted as (1)[C]:
>20° dorsal angulation
>5 mm of radial shortening
>2 mm of articular displacement
No defined criteria for unstable fractures, but risk fractures for instability may
include (1):
Dorsal angulation >20°
Comminution
Intra-articular involvement
Age >60
It is unclear which fractures may benefit from closed reduction vs surgical
techniques.
There are multiple surgical techniques, percutaneous pinning, external
fixation, volar or dorsal plating, etc.:
No clear superiority of one technique over the other
The decision for surgery and the choice of surgical technique is based on
multiple factors and the individual patient.
Goal is to achieve anatomical alignment to allow proper healing of the
fragments and eventual restoration of normal function.
Reduction should always be accomplished in a timely manner before soft
tissue inflammatory changes progress.
Reduction should be attempted urgently for signs of neurovascular
compromise.
Closed reduction of displaced distal radial fractures frequently can be P.
accomplished using manual traction of the extremity in combination with
manipulative maneuvers to restore alignment.
No evidence to suggest superiority of any one method of closed reduction
(9): Manual vs finger traps, etc.
More than 2 attempts at closed reduction in pediatric fractures involving the
physis increases the risk of growth arrest (10)[B].
Pinning, external fixation, and open reduction and internal fixation are
frequently used when there is concern of loss of reduction or instability,
especially for intra-articular fracture requiring maintenance of anatomic
alignment (1)[C].
Repeat neurovascular examination.
Postreduction x-rays (PA and lateral) after application of immobilizing device
to assure maintenance of reduction
Medication
Acetaminophen and NSAIDs can be used for mild-to-moderate pain:
Although there is some theoretical concern about NSAIDs inhibiting bone
healing, there are no clinical studies addressing this question.
Narcotic pain medications are commonly used in the first few weeks following
injury.
Referral
Referral patterns will vary on treating physician experience level.
Orthopedic referral for:
Open fractures
Unstable fractures
Intra-articular involvement
Significant comminution
Fractures involving the physis
Overall there is unclear benefit of rehabilitation of distal radius fractures in adults
(11):
Limited evidence to suggest a short-term benefit of physical therapy after distal
radius fracture (<3 mos) (11)[B]:
May be more important in athletes in terms of functional recovery and faster
return to play, but no studies address this specifically
A single visit with a physical therapist for instruction may be as effective as
multiple visits (11)[B].
Home-based exercise program is effective after volar plating for distal radius
fractures (12)[B].
Vitamin C 500 mg 1 × day for 50 days decreased the incidence of complex
regional pain syndrome (13)[A].
Surgery is indicated for unstable and significantly displaced fractures (1)[C].
Multiple surgical techniques, percutaneous pinning, external fixation, volar or
dorsal plating, etc., are used in the treatment of distal radius fractures:
The choice of techniques is based on many factors and the individual patient.
No evidence exists to suggest one technique is superior in the management
of these fractures (14).
Ongoing Care
Most patients should be re-examined and x-rays repeated in 7–10 days to ensure fracture
stability:
Pediatric torus fractures do not require repeat radiographs in most cases (15)[B]:
Consider repeat x-rays for pain >3–4 wks
Splint removed and cast applied at 7–10 days:
There appears to be no benefit of long arm casting vs short arm (16)
Final radiographs are generally done at 6–8 wks.
Healing time is generally:
6–8 wks adults
3–4 wks children
Some athletes may be able to return to sports with protection as soon as pain allows:
This will depend on the type of fracture, intervention, athlete, and the sport.
Prognosis
Generally good, with most patients regaining full function and motion at the wrist
Complications
Severe acute complications, such as neurovascular injuries and compartment
syndrome, are associated with high-energy trauma and are, fortunately, rare
(1).
Degenerative changes, stiffness, and pain are more common in intra-articular
fractures (1).
Complex regional pain syndrome (CRPS) is relatively common after distal
radius fractures (13):
24% of patients with Colle's fracture in a cohort study met all clinical criteria
for CRPS at 2 wks post fracture
Vitamin C 500 mg 1 × day for 50 days reduces the incidence of CRPS (13)
[A]:
Number needed to treat = 13
Growth arrest in pediatric fractures is relatively common (up to 7%), but
generally asymptomatic (10,17):
Risk increases with more than 2 attempts at closed reduction.
References
1. Wulf CA, Ackerman DB, Rizzo M. Contemporary evaluation and treatment
of distal radius fractures. Hand Clin. 2007;23:209–226, vi.
2. Court-Brown CM, Wood AM, Aitken S. The epidemiology of acute sports-

related fractures in adults. Injury. 2008.
3. Matsumoto K, Sumi H, Sumi Y, et al. Wrist fractures from snowboarding: a

prospective study for 3 seasons from 1998 to 2001. Clin J Sport Med.
2004;14:64–71.
4. Russell K, Hagel B, Francescutti LH. The effect of wrist guards on wrist and
arm injuries among snowboarders: a systematic review. Clin J Sport Med.
2007;17:145–150.
5. Drendel AL, Gorelick MH, Weisman SJ, et al. A randomized clinical trial of
ibuprofen versus acetaminophen with codeine for acute pediatric arm fracture
pain. Ann Emerg Med. 2009.
6. Handoll HH, Madhok R, Dodds C. Anaesthesia for treating distal radial

fracture in adults. Cochrane Database Syst Rev. 2002:CD003320.
7. Bong MR, Egol KA, Leibman M, et al. A comparison of immediate

postreduction splinting constructs for controlling initial displacement of
fractures of the distal radius: a prospective randomized study of long-arm
versus short-arm splinting. J Hand Surg [Am]. 2006;31:766–770.
8. Firmin F, Crouch R. Splinting versus casting of “torus” fractures to the distal

radius in the paediatric patient presenting at the emergency department (ED):
a literature review. Int Emerg Nurs. 2009;17:173–178.
9. Handoll HH, Madhok R. Closed reduction methods for treating distal radial
fractures in adults. Cochrane Database Syst Rev. 2003:CD003763.
10. Lee BS, Esterhai JL, Das M. Fracture of the distal radial epiphysis.
Characteristics and surgical treatment of premature, post-traumatic
epiphyseal closure. Clin Orthop Relat Res. 1984;185:90–96.
11. Handoll HH, Madhok R, Howe TE. Rehabilitation for distal radial fractures
in adults. Cochrane Database Syst Rev. 2006;3:CD003324.
12. Krischak GD, Krasteva A, Schneider F, et al. Physiotherapy after volar
plating of wrist fractures is effective using a home exercise program. Arch
Phys Med Rehabil. 2009;90:537–544.
13. Zollinger PE, Tuinebreijer WE, Breederveld RS, et al. Can vitamin C
prevent complex regional pain syndrome in patients with wrist fractures? A
randomized, controlled, multicenter dose-response study. J Bone Joint Surg
Am. 2007;89:1424–1431.
14. Handoll HH, Madhok R. Surgical interventions for treating distal radial
fractures in adults. Cochrane Database Syst Rev. 2003:CD003209.
15. Farbman KS, Vinci RJ, Cranley WR, et al. The role of serial radiographs
in the management of pediatric torus fractures. Arch Pediatr Adolesc Med.
1999;153:923–925.
16. Handoll HH, Madhok R. Conservative interventions for treating distal

radial fractures in adults. Cochrane Database Syst Rev. 2003:CD000314.
17. Cannata G, De Maio F, Mancini F, et al. Physeal fractures of the distal

radius and ulna: long-term prognosis. J Orthop Trauma. 2003;17:172–179;
discussion 179–180.
Codes
ICD9
813.40 Closed fracture of lower end of forearm, unspecified
813.41 Colles' fracture, closed
813.42 Other closed fractures of distal end of radius (alone)
Clinical Pearls
Swelling and pain over the physis may indicate a physeal injury even with
normal radiographs.
Complex regional pain syndrome is relatively common after distal radius
fractures, and vitamin C can help prevent this complication.
Fracture, Fibula
Anna Waterbrook
Stephen Paul
Holly McNulty
Basics
Description
Isolated fracture of the shaft of the fibula without evidence of associated ligamentous injury
Synonym(s): Fibula shaft fracture; Fibula diaphyseal fracture
Epidemiology
Isolated fibula shaft fractures are rare.
Risk Factors
Direct blow or trauma to the lateral leg leading to injury of the fibular shaft
Contact sports or sports that require high repetitive axial loading may make some athletes
more susceptible (1,2,3)[C].
Diagnosis
History
Patients usually will describe direct trauma to the lateral leg and complain of pain and swelling
in that area. They may be able to bear weight with minimal or no pain.
Physical Exam
Tenderness to palpation over the fracture site with evidence of swelling and possible
ecchymosis
It is important to examine the ankle and the knee for concomitant injuries, including proximal
fibula fracture, distal fibula or tibia fracture, or injury to the syndesmosis.
Detailed neurovascular exam with particular attention to the peroneal nerve

Imaging
Radiographs of the tibia/fibula with anteroposterior and lateral views
Stress views or radiographs of the knee and ankle if suspicion for associated injuries exists.
No further imaging is necessary for isolated fibular shaft fractures.
Fracture or injury to the knee, ankle, tibia, proximal or distal fibula, peroneal nerve, and/or
anterior syndesmosis.
Treatment
Treatment is based on patient comfort.
If patient is having pain with ambulation, then a splint, cast, or walking boot
should be used.
Otherwise, a compression dressing is sufficient.
Immobilization for 3–4 wks generally is recommended, followed by graded
progression back to sport.
Healing time usually takes about 6–8 wks but may be prolonged in some
athletes (3)[C].
Patient should be referred to an orthopedic surgeon if fracture is communited,
significantly displaced, there is an associated fracture of the tibia, or there is
evidence of neurovascular injury or painful nonunion.
Special attention should be given to evaluation of the syndesmosis and
peroneal nerve (1,4,5)[C].
References
1. Al-Kashmiri A, Delaney JS. Fatigue fracture of the proximal fibula with
secondary common peroneal nerve injury. Clin Orthop Relat Res. 2007.
2. King WD, Wiss DA, Ting A. Isolated fibular shaft fracture in a sprinter. Am J
Sports Med. 1990;18:209–210.
3. Slauterbeck JR, Shapiro MS, Liu S, et al. Traumatic fibular shaft fractures
in athletes. Am J Sports Med. 1995;23:751–754.
4. Cheung Y, Perrich KD, Gui J, et al. MRI of isolated distal fibular fractures
with widened medial clear space on stressed radiographs: which ligaments
are interrupted? AJR Am J Roentgenol. 2009;192:W7–W12.
5. Mino DE, Hughes EC. Bony entrapment of the superficial peroneal nerve.
Clin Orthop Relat Res. 1984;203–206.
Codes
ICD9
823.21 Closed fracture of shaft of fibula
823.31 Open fracture of shaft of fibula
Clinical Pearls
Patients will need to be in a cast for 3–4 wks.
The fracture will heal in 6–8 wks.
Depending on symptoms, rehabilitation may begin at 4–6 wks and training at 6–
8 wks. Return to contact activities may take longer and has increased risk of
refracture (3)[C].
Usually there are no complications, but a small percentage may result in
nonunion, peroneal nerve injury, or associated damage to the interosseus
membrane (1,2,3,4,5)[C].
Careful evaluation of the mechanism of injury should be made to avoid missing
pronation–external rotation injuries that often have associated ligamentous
injury (Weber C fractures). Such fractures may be unstable, and prompt
orthopedic referral should be made if they are suspected.
Fracture, Fifth Metatarsal (Avulsion, Jones Fractures)
Mark E. Lavallee
R. Michael Galbraith
Basics
Description
Fractures of the proximal 5th metatarsal of the foot occur at different locations, often with
different etiologies. Prognosis and treatment differ vastly, and there is potential to have
chronic pain and instability of the foot if not treated properly. Proximal 5th metatarsal
fractures are classified into 3 types by region, especially in relation to the joint at the base of
the 4th/5th metatarsals (1,2,3,4):
Avulsion fracture of the tuberosity:
Near splayed insertion of the peroneus brevis tendon (within 0.5 cm from proximal tip of
5th metatarsal)
Located extra-articular and do not extend into the joint between the 4th and 5th
metatarsal (cubometatarsal joint)
Jones fracture (metaphyseal–diaphyseal junction):
Fracture line extends into or towards the articulation between the bases of the 4th and
5th metatarsals (measuring from the proximal tip of the 5th metatarsal, >0.5 cm and
<1.5 cm)
Have relative poor blood supply, heal more slowly, and are prone to delayed union and
nonunion
Diaphyseal stress fractures:
Most commonly occur just distal to the 4th and 5th intermetatarsal articulation to
midshaft
Result of chronic, repetitive microtrauma, especially in younger athletes
Heal most slowly and have greatest risk of delayed union, nonunion, and recurrence
Subtypes according to healing potential (5):
Type I (acute): Acute without prior pain. X-rays show clean fracture without sclerosis.
Type II (delayed union): Involve prior symptoms or a known stress fracture. X-rays show
medullary sclerosis and a widened fracture line.
Type III (nonunion): Involves prior symptoms or a known stress fracture. X-rays show
evidence of repeated trauma, widened fracture line, and exuberant sclerosis (suggesting
fracture nonunion).
Synonym(s): Dancer's or tennis fracture: avulsion fracture of base of the 5th metatarsal
Epidemiology
Fractures of the proximal 5th metatarsal are common foot fractures.
Avulsion fractures are the most common type of fracture.
Diaphyseal stress fractures are the least common type of fracture.
Risk Factors
Previous fracture to the proximal 5th metatarsal
Lateral ankle instability

Lateral ankle sprain: Tuberosity avulsion fractures are commonly associated with ankle
sprains with the foot inverted and plantar flexed. The anterior talofibular and calcaneofibular
ligaments often are injured, and there may be swelling and ecchymosis just anterior and
distal to the lateral malleolus.
Proximal 5th metatarsal stress fracture: Patient may have had a previously undiagnosed and
slightly symptomatic stress fracture of the proximal 5th metatarsal.
There is a high incidence of delayed union, nonunion, and refracture with Jones and
diaphyseal stress fractures.
Diagnosis
Postreduction views are only applicable when clinician attempts to reduce a significantly
displaced fracture of the 5th metatarsal. Most displaced fractures are best treated operatively.
Views would be anteroposterior, lateral, and oblique
History
How and when did it occur? Mechanism of injury is important to determine.
Did athlete injure this foot previously? Determine presence of fracture of the 5th metatarsal.
Was there a recent history of ankle sprain prior to this injury? Loss of proprioception and
reflex inhibition may have predisposed athlete to this injury.
History of other medical conditions? Diabetes or other causes of peripheral neuropathy.
Physical Exam
Patient may complain of pain over the lateral aspect of foot, especially when weight-bearing
on plantar-flexed foot.
Jones fractures often occur as a result of a pivot in the direction opposite the planted foot.
Patient is tender to palpation over the proximal 5th metatarsal.
Often there may be swelling or ecchymosis of the proximal 5th metatarsal.
Check neurovascular status: Posterior tibial and dorsalis pedis pulses and normal capillary
refill
Palpate the peroneus brevis tendon to assess its integrity.
Resisted external rotation of foot activates the peroneus brevis muscle and checks its
strength.
Full examination of the distal fibular, lateral ligaments, and foot helps identify associated
ankle or foot injury.
Check sensation: If decreased around lateral aspect of foot, the lateral dorsal cutaneous
nerve, a branch off the sural nerve, may be injured.

Imaging
Standard x-ray films: Anteroposterior (AP), lateral, and oblique views of the foot. If findings are
suggestive of ankle trauma meeting the Ottawa criteria for radiographs, ankle films (AP, lateral,
and oblique views) also should be taken. The Ottawa Ankle rules state that radiographs are
indicated for patients between the ages of 15 and 55 yrs old with inability to walk 5 steps after
an ankle injury OR tender over posterior 3rd of distal fibula.
Peroneus brevis tendon injury
Apophysis (secondary ossification center closes between ages 9 and 11 yrs in girls, 11 and
14 yrs in boys)
Apophysitis (Iselin disease)
Accessory ossicles
Hematoma of lateral proximal foot
Midshaft diaphyseal fracture of the 5th metatarsal
Sprain of the cubometatarsal joint
Treatment
Apply ice, rest, and elevate foot.
Oral pain relief (acetaminophen, tramadol, or narcotics) or topical lidocaine is
often sufficient if reduction not necessary.
If reduction is needed, give oral pain relief before performing a hematoma
block (2–5 mL of 1% lidocaine).
Significantly displaced fracture warrants an orthopedic referral for possible
surgery.
Reduction techniques generally not recommended if surgical fixation is an
option
Grab the 5th toe and distract in a longitudinal plane. Apply plantar or dorsal
pressure to the proximal portion of the 5th metatarsal.
Check alignment via postreduction radiographs.
Avulsion fractures:
Place in a hard-soled shoe or post-op shoe for 3–4 wks (2,3)[A].
Can place in a walking boot or walking cast if worried about patient
compliance. May weight-bear as tolerated (1,2)[A].
Jones (metaphyseal–diaphyseal) fractures and diaphyseal stress fractures:
Type I (acute): For nondisplaced or minimally displaced fractures (<2 mm),
can place patient in short leg cast and make strict non-weight-bearing for 6–8
wks (or longer). Otherwise, consider surgical fixation (1,2)[A].
Type II (delayed union/stress): Consider surgical fixation because of better
prognosis and quicker return to activity. Occasionally can consider prolonged
immobilization (up to 16 wks) with non-weight-bearing for selective patients
(1,2)[A].
Type III (nonunion): Consider surgical fixation (1,2)[A].
When deciding on treatment for type II fractures, take into account athlete's
timetable and previous medical history.
Occasionally after conservative treatment, a nonunion develops secondary to
“distal to proximal” vascular supply to the bone.
Bone stimulation (electrical or US) has shown in some cases to improve
healing for delayed union and nonunion fractures (1)[B]. Progression to surgery
may be indicated instead of using bone stimulation or if there is inadequate
healing with bone stimulation.
Avulsion fractures: Start with range of motion and progress to strengthening of
the peroneus brevis (external rotation and pronation of the foot). Patient may
return to play after 3–4 wks and when no longer symptomatic.
Jones fractures: Once no longer immobilized, start with range of motion and
progress to strengthening. Electrical stimulation may help patient initially learn
to reactivate musculature. Resume weight-bearing activities slowly.
Avulsion fractures rarely require surgery (2)[A].
Jones (metaphyseal–diaphyseal) and diaphyseal stress fractures:
Type I: Consider surgical fixation (open reduction, internal fixation with a
cannulated screw) for athletes and active patients who wish quicker return to
play (1,2,4)[A].
Type II (delayed union) and type III (nonunion): Refer for surgical evaluation
(1,2)[A].
Ongoing Care
Orthopedic referral for surgery as indicated above and for avulsion fractures that are
displaced (rare), comminuted (rare), or involve >30% of the cubometatarsal articulation
Patients not responding to home exercise programs after immobilization is complete may
benefit from referral to physical therapy.
Type I Jones or diaphyseal stress fractures should be referred to an orthopedist if patient
prefers surgery in order to return to play quicker or the fracture is displaced or comminuted.
References
1. Brown SR, Bennett CH. Management of proximal 5th metatarsal fractures in the athlete.
Curr Opin Ortho 2005;16:95–99.
2. Fetzer GB, Wright RW. Metatarsal shaft fractures and fractures of the proximal 5th
metatarsal. Clin Sports Med. 2006;25:139–150, x.
3. Hatch RL, Alsobrook JA, Clugston JR. Diagnosis and management of metatarsal
fractures. Am Fam Physician. 2007;76:817–826.
4. Mologne TS, Lundeen JM, Clapper MF, et al. Early screw fixation versus casting in the
treatment of acute Jones fractures. Am J Sports Med. 2005;33:970–975.
5. Torg JS, Balduini FC, Zelko RR, et al. Fractures of the base of the 5th metatarsal distal
to the tuberosity. Classification and guidelines for non-surgical and surgical management. J
Bone Joint Surg Am. 1984;66:209–214.
Codes
ICD9
733.94 Stress fracture of the metatarsals
825.25 Fracture of metatarsal bone(s), closed
825.35 Fracture of metatarsal bone(s), open
Clinical Pearls
Return to play:
Avulsion fractures: About 3–4 wks
Jones and diaphyseal stress fractures: Up to 20 wks with conservative therapy
Type 1: ≥8 wks
Types 2 and 3: If casted, 3–5 mos and 8 wks for surgery
Fracture, Frontal Sinus
Martha A. Dodson
Basics
Frontal sinuses are not present at birth and begin to develop around 7 yrs of age, continuing
to develop until puberty.
Ethmoid and maxillary sinuses are present at birth.
Sphenoid sinuses develop around 5 yrs of age.
Airway control takes precedence.
Associated facial injuries may preclude the use of oral intubation.
Nasotracheal intubation is contraindicated in massive facial or nasal trauma.
Cricothyrotomy is the airway of choice if intubation using rapid sequence intubation cannot
be performed.
Many patients with frontal sinus fractures have associated facial and/or neurologic injuries
owing to the amount of force needed to create the injury.
Consider the need for cervical spine immobilization, especially in the presence of
multitraumatic fractures and/or high-velocity trauma.
The presence of rhinorrhea and/or otorrhea should suggest the possibility of frontal sinus
fracture.
Frontal sinus fracture is not the immediate concern in a multitrauma victim.
Description
Typically owing to high-velocity blunt trauma localized to the face/head/frontal sinus area
The most common mechanisms of injury are motor vehicle collisions, assaults, falls, and
other accidents.
Because the anterior table is thick, it requires 800–2,200 lb of force to cause frontal sinus
fracture (twice the force required to fracture other facial bones).
Most common classification identifies involved frontal sinus anatomy:
Anterior wall/table
Posterior wall/table
Anterior and posterior walls/table
Nasofrontal duct (NFD) involvement
Epidemiology
Frontal sinus fractures account for 5–12% of all facial fractures.
35% have concomitant orbital fractures.
17% have zygomatic fractures.
15% have naso-orbitoethmoid fractures.
0.7–2.1% have involvement of both anterior and posterior walls of the frontal sinus.
Risk Factors
High-velocity trauma to the face, especially in presence of other facial bone fractures
Acromegaly: Size and extension of frontal sinuses enlarged
General Prevention
Avoidance of motor vehicle collisions
Proper use of vehicle safety restraints

Laceration of the supraorbital ridge, glabella, or lower forehead
Frontal ecchymosis
Disruption of the NFD
Intracranial injuries in 12–17% of patients with frontal sinus fractures
Associated cerebrospinal fluid (CSF) leak in 15% of patients with frontal sinus fractures
Ocular injuries are present in up to 59%.
Periorbital fractures
Traumatic subcutaneous emphysema (TSE)
Concussion
Potential sequelae:
Brain abscess
Contour deformity
Osteomyelitis
Hematoma
Meningitis
Mucocele
Diagnosis
Look for and treat life-threatening injuries first.
Carefully palpate the frontal area for crepitus or depression.
Lacerations over the frontal sinus area should raise suspicion of frontal sinus fracture and
mandate digital palpation for a fracture.
Perform a nasal speculum examination looking for blood, septal hematoma, or CSF high in
the nasal cavity.
Perform otoscopic exam looking for otorrhea and/or hemotympanum.
Perform a careful neurologic examination to look for CNS injury, including concussion.
Perform a careful ophthalmologic exam.
Pre Hospital
Cervical spine immobilization considerations
Identify concomitant life-threatening injuries.
History
Victim of motor vehicle collision, assault to head/face, fall, or other high-velocity trauma
May or may not have loss of consciousness
Physical Exam
The physical examination is the most important aspect of the evaluation. Failure to diagnose a
frontal sinus fracture can lead to abscess formation, meningitis, mucocele formation,
osteomyelitis of the calvarium, or permanent cosmetic deformity.
Laceration on the supraorbital ridge, glabella, or lower forehead
Ecchymosis of periorbital region
Periorbital edema
Depression or step-off identified on palpation of frontal sinus area
Crepitus over the frontal sinus area
Subcutaneous emphysema of periorbital region
Associated facial trauma with supraorbital, orbital, nasal, frontonasoethmoid, or maxillary
fractures
Associated ocular trauma may be present.
Bloody discharge from the nose without visible nasal source
Clear rhinorrhea or otorrhea indicative of CSF leak
Absent tearing that may be indicative of nasofrontal duct injury
Diplopia with upward or downward gaze
Supraorbital ridge anesthesia
Loss of consciousness or altered mental status secondary to associated brain injury or
posterior table fracture
May complain of double vision, anesthesia to skin surrounding eye, “postnasal drip” sensation
(owing to CSF leak)
May present with facial subcutaneous emphysema following Valsalva maneuver owing to
previously undiagnosed paranasal fracture following facial trauma.

CT scanning is the imaging modality of choice.
Serial 1.5-mm cuts in both the axial and coronal planes
Identification of frontal sinus fractures and concomitant paranasal and facial fractures
Anterior table fracture, displaced or nondisplaced; displacement is defined as bony
displacement more than or equal to the width of the outer table.
Posterior table fracture identification: Associated intracranial injuries on CT scan may
include subdural hemorrhage or pneumocephalus.
Frontonasal duct integrity
Caldwell and lateral radiographic views are good for preliminary evaluation, but frontal sinus
fractures can be subtle on these films. Sinus pathology is strongly suspected when the x-rays
show air-fluid levels, a diffusely cloudy sinus, or pneumocephalus.
Lab
None recommended
Imaging
Requires acute examination and imaging
CT scanning is the imaging modality of choice.
Serial 1.5-mm cuts in both the axial and coronal planes
Identification of frontal sinus fractures and concomitant paranasal and facial fractures
Anterior table fracture, displaced or nondisplaced; displacement is defined as bony
displacement more than or equal to the width of the outer table.
Posterior table fracture identification: Associated intracranial injuries on CT scan may
include subdural hemorrhage or pneumocephalus.
Frontonasal duct integrity
Caldwell and lateral radiographic views are good for preliminary evaluation, but frontal sinus
fractures can be subtle on these films. Sinus pathology is strongly suspected when the x-rays
show air-fluid levels, a diffusely cloudy sinus, or pneumocephalus.
Nasofrontoethmoid fractures
Cribriform plate fractures
Facial fractures, including the orbits, maxilla, nasal, and zygomatic bones
Frontal fractures not involving the frontal sinus (may have a similar presentation)
Treatment
Pre-Hospital
Physical examination including complete neurologic exam
High suspicion for fracture given nature of trauma and physical findings
Airway, breathing, and circulation (ABCs)
Cervical immobilization as needed
ED Treatment
If while irrigating a laceration overlying the frontal sinus the patient can taste the
irrigating solution or notes the irrigating fluid in the nose, the frontal sinus is
disrupted.
Lacerations overlying frontal sinus fractures involving only the anterior table
may be sutured in the ED. ENT or plastic surgery should evaluate lacerations
associated with more complex sinus injuries.
If an isolated simple anterior table fracture is noted without a posterior table
fracture and intracranial injuries are rules out, the presence of a frontonasal
duct injury should be evaluated by instilling fluorescein into the frontal sinus.
Lack of visualization of the fluorescein in the nose is indicative of disruption of
the duct.
Antibiotics are indicated in all patients with frontal sinus fractures. IV antibiotics
are indicated in patients with posterior table fractures or CSF leaks.
Nondisplaced frontal sinus fracture with a patent nasofrontal duct and no
neurologic involvement usually can be managed nonsurgically.
All displaced anterior wall fractures, all posterior wall fractures, all frontal sinus
fractures with involvement/obstruction of the nasofrontal duct, and all frontal
sinus fractures with neurologic involvement require further surgical evaluation
and probable surgical repair.
Medication
Cefotaxime: Adult: 2 g IV; children: 50 mg/kg IV single dose
Cephalexin: Adult: 250–500 mg PO q.i.d.; children: 25–50 mg/kg/day divided
q.i.d.
The approach to each patient should be individualized but, in general, is based on
3 clinical factors:
Fracture location and displacement
Dural and cerebral involvement
Damage to the frontal sinus drainage system
ABCs of trauma care: Attend to the airway as the 1st priority.
RSI is the initial airway management of choice.
Massive facial injuries may require a surgical airway if RSI is unsuccessful.
If associated injuries are present, protect the cervical spine until cleared.
Other major injuries and life threats take precedence over the frontal sinus
fracture.
Admission Criteria
Patients with other significant associated trauma
Patients with posterior table fractures (neurosurgery or ENT evaluation)
Patients with associated intracranial injuries (neurosurgery)
Patients with CSF leak
Discharge Criteria
Patients with frontal sinus fractures who may be discharged are those with
isolated frontal sinus fracture, those who have no involvement of the posterior
table or evidence of an intracranial injury on CT scan.
Oral antibiotics are indicated in these patients.
Referral to ENT in 24–36 hr is appropriate.
Patients with complex fractures may be discharged when cleared by
neurosurgery and/or ENT.
Ongoing Care
Patient Education
Avoid Valsalva maneuvers (eg, sneezing, nose blowing, etc.) to minimize risk of
subcutaneous emphysema.
Avoid air travel for a period (individualize for each patient) after frontal sinus fracture.
Complications
Early complications:
Contour deformity postoperatively
Sinusitis: Treat with antibiotics and decongestants. If swelling and/or pain to
periorbital region persists, may need to refer for surgical sinus mucosal
obliteration.
Meningitis
Late complications:
Thrombosis of cavernous sinus
Encephalitis
Mucocele
Mucopyocele
Osteomyelitis
Brain abscess
Surgical referral for any of these
Additional Reading
Bell RB, Dierks EJ, Brar P, et al. A protocol for the management of frontal
sinus fractures emphasizing sinus preservation. J Oral Maxillofac Surg.
2007;65:825–839.
Bell RB. Management of frontal sinus fractures. Oral Maxillofac Surg Clin
North Am. 2009;21:227–242.
Brasileiro BF, Cortez AL, Asprino L, et al. Traumatic subcutaneous

emphysema of the face associated with paranasal sinus fractures: a
prospective study. J Oral Maxillofac Surg. 2005;63:1080–1087.
Kalavrezos N. Current trends in the management of frontal sinus fractures.
Injury. 2004;35:340–346.
Kaufman BR, Heckler FR. Sports-related facial injuries. Clin Sports Med.
1997;16:543–562.
Keefe SO, et al. Frontal sinus fractures. In: English GM, ed. Otolaryngology.
Vol 4. Rev ed. Philadelphia: JB Lippincott, 1994:342–364.
Manson PN. Maxillofacial injuries. Emerg Med Clin North Am. 1984;2:761–
782.
Rohrich RJ, Hollier LH. Management of frontal sinus fractures. Changing

concepts. Clin Plast Surg. 1992;19:219–232.
Tiwari P, Higuera S, Thornton J, et al. The management of frontal sinus

fractures. J Oral Maxillofac Surg. 2005;63:1354–1360.
Codes
ICD9
801.00 Closed fracture of base of skull without mention of intra cranial injury, with state of
consciousness unspecified
801.50 Open fracture of base of skull without mention of intracranial injury, with state of
consciousness unspecified
Clinical Pearls
For lacerations, ecchymosis, and/or edema to frontal sinus region following
trauma, consider and evaluate with CT scan for frontal sinus fracture.
Fracture, Hamate: Hook, Body
Mark Stovak
Basics
Description
A fracture through the hook or the body of the hamate
Epidemiology
Hamate fractures occur in 3 patterns:
Type 1: Hook
Type 2a: Coronal (dorsal oblique and splitting)
Type 2b: Transverse (1)
Incidence
Hook fracture:
Hook of the hamate fractures account for <2% of all carpal bone fractures (2).
The number of hook of the hamate fractures reported in the literature is low because
routine x-rays usually are normal, and symptoms are nonspecific (2).
Average length of time from injury to correct diagnosis is 10 mos (3).
Fractures most commonly occur at the base of the hook (1).
Body fracture: Body of the hamate fractures is rare and much less common than hook
fractures.
Risk Factors
Hook fracture: Sporting activities that involve a bat, club, or racket (2)
General Prevention
Avoid holding the handle end of the bat, club, or stick in the palm to prevent it from creating
pressure on the hook of the hamate.
Etiology
Acute traumatic injury
Repetitive stress leads to a stress fracture.
Diagnosis
History
Hook fracture:
Type 1
Hook of the hamate fractures occurs in athletes who use equipment with a handle (eg, golf
clubs, baseball bats, and rackets) (2).
Athlete grips the handle of the club, bat, or racket over the distal ulnar aspect of the palm,
placing the handle in close proximity to the hook of the hamate (2).
In golf, the fracture often occurs when the club head accidentally strikes too much ground
and a large divot is taken. In baseball, most fractures occur at the end of forceful check
swings as opposed to swings that make contact with the ball (2).
A less common mechanism of injury is a fall on an outstretched hand (2).
Stress fractures are also possible of the hook and are likely if no traumatic event can be
identified in the history.
Body fracture:
Body fractures often result from punching a hard stationary object, such as a wall, with a
closed fist (type 2a). The 4th and 5th metacarpals are driven back into the hamate, leading
to a fracture. Body fractures may accompany a boxer's fracture (1).
They also may occur when the hamate is smashed between two objects in a dorsopalmar
fashion (type 2b) (1).
Stress fractures have been described from repetitive military-style knuckle push-ups (4).
Physical Exam
Point tenderness occurs in the palm over the hook of the hamate. The hook is located by
projecting a line from the pisiform to the center of the head of the index metacarpal. Rarely, if
the fracture is at the base of the hook, pain may be greater over the dorsal hamate than over
the hook in the palm (because the hamate is covered on the volar aspect with thick skin,
subcutaneous fibrofatty tissue, and parts of the palmaris brevis muscle and transverse carpal
ligament, making palpation difficult) (2).
Painful and weak grasp (2)
Check pulses: An Allen test will help to rule out ulnar artery thrombosis (2).
Signs of partial or complete 4th/5th flexor digitorum profundus (FDP) tendon rupture may be
present. Pain with grip, decreased grip strength, crepitance with 4th/5th finger motion, and
eventually, loss of active flexion at the 4th/5th finger distal interphalangeal joints may indicate
FDP injury; a small percentage of all hook fractures are correctly diagnosed only after FDP
tendon rupture (2).
Decreased sensation or weakness may be due to ulnar or median nerve injury. The fracture
fragments may injure the nerves directly, or swelling and inflammation may injure them
indirectly (2).

Imaging
Hook fracture:
The routine wrist series (anteroposterior [AP], lateral, and oblique views) usually are
negative, often delaying diagnosis (2).
Ring of the hook can be visualized on AP view; if it is not present, this may be a clue to a
hook fracture (5).
Carpal tunnel view often will aid in making the diagnosis. However, to obtain this view, the
wrist must be forcefully hyperextended. During the acute phase of the injury, pain and
limited range of motion may not allow proper positioning to make this x-ray possible (2).
Another useful view is the radially deviated thumb-abducted lateral view (the hook is seen
in profile between the 1st and 2nd metacarpals) (6).
An additional view is the hamate hook lateral view. This view places the film on a 30-
degree slant board and rests the hand on the film with the thumb abducted and the beam
perpendicular to the table (the hook is seen in profile between the 1st and 2nd
metacarpals) (7).
CT scanning is the gold standard for diagnosis but often is unnecessary if plain films show
the fracture. CT scans are useful if plain films are negative and a fracture is highly
suspected. CT scanning has the advantage of visualizing both hamates at the same time
and can be used to evaluate the extremely rare case of a bipartite hamate, which usually is
bilateral and is a normal variant. CT scan is performed with both hands in the praying
position (palm to palm) (2).
Body fracture:
The routine wrist series (AP, lateral, and oblique views) is more useful for diagnosis of
body fractures than for hook fractures. The oblique and lateral views are the most useful.
However, many fractures are still missed by plain films (1,8,9).
CT scan may be needed to delineate further the exact fracture pattern and degree of
fragment displacement. CT scan should be considered when routine films are negative but
a fracture is highly suspected (1,8,9).
Flexor/extensor carpi ulnaris tendon injury
Metacarpal/carpal bone fracture or contusion
Ulnocarpal ligament sprain
Triangular fibrocartilaginous complex tear
Ulnar artery thrombosis
Ulnar nerve entrapment/neuropathy
Treatment
Hook fracture:
Acute treatment (<2 wks)
One option is excision of the hook distal to the fracture. Most patients
return to their previous level of functioning in their sport or occupation by 8
wks. Excision has been the favored approach for both displaced and
nondisplaced fractures (10)[C].
Conservative option for nondisplaced fractures is a short-arm cast. The
cast should immobilize the metacarpophalangeal joints of the 4th/5th
fingers and be a thumb spica to decrease micromotion at the hook. Cast
should be worn for 6–8 wks to prevent nonunion. If pain is still present after
cast removal, then excision for nonunion is the treatment of choice (11)[C].
Decision between casting and surgery is based on the lifestyle demands of
the patient. The athlete who does not want to risk having a nonunion after
casting may opt for surgery to minimize the time away from sport. Similarly,
a patient with a job that requires repetitive grabbing, gripping, or lifting may
elect for excision to reduce the risk of an extended period of time away
from work (10)[C].
Delayed treatment (>2 wks): P.
Nonunion of the hook of the hamate is very common. Nonunion is related
to micromotion from the soft tissue attachments to the hook but also may
be related to a tenuous blood supply similar to the scaphoid (10)[C].
Excision of the hook is the treatment of choice for these injuries to prevent
a nonunion. The sooner the fragment is removed and the base smoothed,
the less likely is the chance for tendon rupture and/or neurovascular
damage (12)[C].
An alternative approach is open reduction and internal fixation (ORIF); the
goal is to maintain maximal grip strength by preserving the pulley system for
the 4th/5th FDP tendons. Although this seems logical, the loss of grip
strength associated with excision has been minimal, resulting in excision
being the most popular surgical treatment method (10)[C].
Treatment for painless nonunion is excision to reduce the risk of tendon
rupture and/or neurovascular injury (2)[C].
Body fracture:
Coronal fractures are often associated with 4th and 5th metacarpal
dislocations that require reduction. Once reduced, stability must be
assessed. If the reduction is stable and the fracture nondisplaced, then a
short-arm cast can be used for 4–6 wks. If the fracture is displaced, then
ORIF or closed reduction with pinning must be used to obtain congruent joint
surfaces to prevent degenerative joint disease (1)[C].
Transverse fractures, if not displaced, can be treated in a short-arm cast for
4–6 wks or by ORIF or closed reduction and pinning if displacement has
occurred (1)[C].
Ongoing Care
Prognosis
Prognosis of hook fractures is generally good if they are diagnosed and treated (cast,
excision, ORIF) early before tendon injury/rupture occurs (13).
Prognosis for hamate body fractures is generally good if they are diagnosed and treated
(cast, ORIF, closed reduction and pinned) early enough to maintain congruent joint surfaces
(8,9).
Complications
Complete rupture of the FDP tendon is reported to occur in 15–20% of cases
of nonunion. The FDP of the little finger ruptures more commonly than that of
the ring finger (2)[C].
Excision is associated with a 3% complication rate; complications include
ulnar/median nerve injury, ulnar palmar arch vessel injury, weakness, painful
grip, altered sensation, flexor tendon adhesions, and scar tenderness (2)[C].
References
1. Hirano K, Inoue G. Classification and treatment of hamate fractures. Hand
Surg. 2005;10:151–157.
2. Binzer T, Carter P. Hook of the hamate fracture in athletes. Op Tech Sports

Med. 1996;4:242–247.
3. Murray PM, Cooney WP. Golf-induced injuries of the wrist. Clin Sports
Med. 1996;15:85–109.
4. Busche MN, Knobloch K, Rosenthal H, et al. Stress fracture of the hamate

body and fourth metacarpal base following military style push-ups: an unusual
trauma mechanism. Knee Surg Sports Traumatol Arthrosc. 2008.
5. Boulas H, Milek M. Hook of the hamate fractures: diagnosis, treatment, and

complications. Orthop Rev 1990;XIX:518–529.
6. Bhalla S, Higgs PE, Gilula LA. Utility of the radial-deviated, thumb-abducted

lateral radiographic view for the diagnosis of hamate hook fractures: case
report. Radiology. 1998;209:203–207.
7. Akahane M, Ono H, Sada M, et al. Fracture of hamate hook–diagnosis by

the hamate hook lateral view. Hand Surg. 2000;5:131–137.
8. Chase JM, Light TR, Benson LS. Coronal fracture of the hamate body. Am
J Orthop. 1997;26:568–571.
9. Ebraheim NA, Skie MC, Savolaine ER, et al. Coronal fracture of the body of
the hamate. J Trauma. 1995;38:169–174.
10. Scheufler O, Andresen R, Radmer S, et al. Hook of hamate fractures:

critical evaluation of different therapeutic procedures. Plast Reconstr Surg.
2005;115:488–497.
11. Carroll RE, Lakin JF. Fracture of the hook of the hamate: acute treatment.
J Trauma. 1993;34:803–805.
12. David TS, Zemel NP, Mathews PV. Symptomatic, partial union of the hook
of the hamate fracture in athletes. Am J Sports Med. 2003;31:106–111.
13. Bishop A, Beckenbaugh R. Fracture of the hamate hook. J Hand Surg.

1988;13A:135–139.
Codes
ICD9
814.08 Closed fracture of hamate (unciform) bone of wrist
814.18 Open fracture of hamate (unciform) bone of wrist
Clinical Pearls
The treatment option that will allow the quickest return to play with the least
amount of residual symptoms is excision of the hook of the hamate.
Routine plain-film radiographs are not sensitive for identifying hook of the
hamate fractures. A specialized view (eg, carpal tunnel; radial-deviated, thumb-
abducted lateral; or hamate hook lateral) or a CT scan is usually needed for
identification.
Surgery is recommended to prevent tendon rupture even in the absence of
pain related to fracture.
Fracture, Humeral Head
Julie J. Chuan
Basics
Caution: Excessive movement of the arm may produce further neurovascular injury.
Controversy: Prehospital reduction is not recommended because manipulation may lead to
neurovascular compromise or further displacement of a fracture.
Description
Proximal humeral fractures involve fractures of the humeral head, lesser tuberosity, greater
tuberosity, bicipital groove, and proximal humeral shaft.
Fall onto an outstretched hand
High-energy direct trauma
Excessive rotation of the arm in the abducted position
Electrical shock or seizure
Pathologic fracture from metastatic disease (1)
Epidemiology
Incidence
Typically seen in adults >65 yrs old
Proximal humeral fractures account for 5% of all fractures.
Predominant gender: Female > Male
Prevalence
Proximal humerus fractures are the 2nd most common upper extremity fractures (2).
In patients >65, they are the 3rd most common fracture after radius and hip fractures.
Risk Factors
Risk factors for humeral head fractures include low bone mass and falls.
Indirect risk factors include those that increase the risk for falls, such as depression,
epilepsy, diabetes with neuropathy, and hearing impairment.
Physical activity, menopausal hormone treatment, and fewer number of fractures since age
45 are associated with a decrease risk of fracture (2).
General Prevention
Increased moderate physical activity, calcium supplementation to optimize bone density, and fall
prevention minimize the risk of proximal humerus fractures.
Diagnosis
In children, proximal humeral fractures consist of metaphyseal fractures and physeal
separations. Three fracture patterns tend to vary depending on the age group.
Children <5 yrs: Salter-Harris type I fractures are seen.
Neonatal fractures occur from obstetric trauma, and pseudoparalysis is seen often.
Physeal separation in an infant also may be the result of physical abuse.
Children 5–10 yrs: Metaphyseal fractures tend to occur in this age group because rapid
growth causes thinning of the metaphyseal cortex. Most fractures are transverse or short
oblique.
Children >11 yrs: Salter-Harris type II fractures tend to be seen in adolescents.
Careful history and physical examination to localize the injury and to rule out any other
significant injuries
Assessment of neurovascular status:
Assess function of radial, median, ulnar, axillary (sensation to the lateral aspect of the
shoulder), and musculocutaneous nerves (sensation to the extensor aspect of the
forearm).
Presence of radial, ulnar, and brachial pulses and good capillary refill in all digits
Shoulder radiographs: Try to obtain orthogonal views (3).
Physical Exam
Signs and symptoms include (4):
Pain, swelling, and tenderness about the shoulder, especially around the greater tuberosity
Difficulty in initiating active motion
Position of the arm is often adducted and held closely against the chest.
Crepitus may be present.
Shoulder effusion owing to hemarthrosis developing into ecchymoses within 24–48 hr at the
area of fracture and may spread to chest wall, flank, and distal extremity
Diminished peripheral pulses or decreased sensation, especially over the deltoid muscle
(axillary nerve)
Remember to examine:
Nerve: Sensation over the deltoid muscle (axillary nerve) and distal motor and sensory
function in the hand and fingers
Vascular: Radial and ulnar pulse, capillary refill time
Associated injuries: Clavicle, scapula, wrist, and elbow for range of motion and tenderness
for concomitant injury (1)

Standard radiographs:
Anteroposterior (AP), lateral, and axillary views or transscapular Y view
AP view shows the articular surface of the humeral head, glenohumeral joint space, and
the greater and lesser tuberosities.
The axillary view provides better assessment of shoulder dislocations, humeral head
compression fractures, and glenoid, coracoid, and lesser tuberosity fractures.
CT scan: Consider CT scan if articular involvement is suspected to evaluate the glenoid and
humeral head (5).
Imaging
Standard radiographs (trauma series) can be taken while in sling:
AP, lateral Y, and axillary views allow for 3 orthogonal views.
True AP view, taken 35–40 degrees from the sagittal plane, shows the articular surface of
the humeral head, glenohumeral joint space, and the greater and lesser tuberosities.
Scapular Y view, taken 90 degrees from the true AP and 40 degrees from the coronal
plane, shows the scapular contour and position of the humeral head in the glenoid.
Axillary view, taken with the shoulder abducted 70–90 degrees with the beam cephalad,
shows shoulder dislocations, humeral head compression fractures, and glenoid and lesser
tuberosity fractures; may need to use trauma axillary view or Velpeau view.
CT scan:
Intra-articular fractures to evaluate the glenoid and humeral head
Suspected occult fractures
Posterolateral compression fractures
Evaluate for multipart fractures of humeral head (5).
Shoulder dislocation
Acute hemorrhagic bursitis
Traumatic rotator cuff tear
Calcific tendinitis
Pathologic fracture
Treatment
In children nearing skeletal maturity, determining the degree of displacement or
separation of the proximal humeral epiphysis is essential because exact
reduction is important to prevent later growth disturbance.
Pediatric patients are often less compliant with immobilization and less able to
verbalize complaints and may benefit from admission to the hospital for
observation and neurovascular checks.
ED Treatment P.
Proper immobilization, orthopedic consultation, and pain management
Operative versus nonoperative treatment is decided in conjunction with
orthopedics.
Neer classification: This system identifies the number of fragments and their
location.
The fractures consist of 2–4-part fractures, and the locations include the
anatomic neck, the surgical neck, the greater tuberosity, and the lesser
tuberosity.
Displacement is defined as >1 cm of separation or >45 degrees of
angulation between fragments.
In general, the higher the number of fragments in the fracture and the greater
the degree of displacement, the more difficult it is to manage the patient with
a closed reduction.
AO (Arbeitsgemeinschaft fur Osteosynthese-fragen) classification:
A: Unifocal, extraarticular, 2-part fracture with an intact blood supply
B: Bifocal, extraarticular, 2-part fracture with possible injury to the blood
supply
C: Articular fracture involving the anatomic neck, high likelihood of injury to
the blood supply, and risk of avascular necrosis of the humeral head.
Nonoperative treatment:
Initial immobilization and early motion: Succeeds in many cases because
most proximal humeral fractures are minimally displaced
Use a sling, swathe, and axillary pad to immobilize.
Closed reduction should be performed with consultation of an orthopedic
surgeon.
Conscious sedation should be used for all closed reductions.
Following reduction, the stability of the fracture can be tested in different
positions to ascertain that significant displacement requiring surgical
intervention will not occur.
Surgical referral:
1- and 2-part fractures are often treated successfully with closed reduction,
but 3- and 4-part fractures are unstable and may need open reduction and
internal fixation (ORIF).
If the blood supply is compromised, there is a risk of avascular necrosis of
the humeral head, and surgical intervention should be considered (5).
Medication
Pain medications are indicated for comfort.
Conscious sedation should be used if attempting a closed reduction.
A fracture is considered a nonunion if it is not clinically healed after 3 mos.
Risk factors for nonunions include:
Displacement of the fracture
Aggressive rehabilitation
Patient noncompliance
Comorbidities that can be a risk factor for nonunions include:
Osteoporosis
Alcoholism
Tobacco usage
Mental illness
Systemic corticosteroids
Rheumatologic disease (6)
Airway, breathing, and circulation (ABCs) and secondary survey for associated
injuries
Immediate immobilization is important to prevent further fracture displacement
or neurovascular injury.
Sling with arm supported at the side or in the Velpeau position
Axillary pad also may be used for comfort.
After immobilization, perform another neurovascular examination.
Admission Criteria
Open fractures for operative management and parenteral antibiotic therapy
Displaced fracture that cannot be treated through closed reduction and
therefore require operation
Significant associated injuries that require admission and observation
Discharge Criteria
Patients with either a nondisplaced fracture or a fracture that is treated
successfully through closed reduction and who have no associated injuries
Ongoing Care
The proximal humerus is supplied by the axillary artery, which is often disrupted with
displaced fractures resulting in avascular necrosis of the humeral head.
Prognosis
Nonunions can be treated nonoperatively if pain is minimal with adequate range of motion and
function.
Nonunions can be surgically reduced with internal fixation if the glenohumeral articular surface
is preserved.
Arthroplasty is preferred when the articular surface is disrupted.
References
1. Rockwood CA, Green DP, Bucholz RW, et al. In: Rockwood CA, Green DP, eds.
Rockwood and Green's fractures in adults. 4th ed. Philadelphia: Lippincott-Raven, 1996.
2. Chu SP, Kelsey JL, Keegan TH, et al. Risk factors for proximal humerus fracture. Am J
Epidemiol. 2004;160:360–367.
3. Morrissy RT, Weinstein SL. Lovell and Winter's pediatric orthopaedics. Vol. II. 4th ed.
Philadelphia: Lippincott-Raven, 1996.
4. Neer CS. Displaced proximal humeral fractures: i. classification and evaluation. J Bone
Joint Surg. 1970;52A:1077–1089.
5. Robinson BC, Athwal GS, Sanchez-Sotelo J, et al. Classification and imaging of proximal
humerus fractures. Orthop Clin North Am. 2008;39:393–403, v.
6. Cheung EV, Sperling JW. Management of proximal humeral nonunions and malunions.
Orthop Clin North Am. 2008;39:475–482, vii.
Additional Reading
Hawkins RJ, Angelo RL. Displaced proximal humeral fractures. Selecting treatment,
avoiding pitfalls. Orthop Clin North Am. 1987;18:421–431.
Rasmussen S, Hvass I, Dalsgaard J, et al. Displaced proximal humeral fractures: results of

conservative treatment. Injury. 1992;23:41–43.
Codes
ICD9
812.00 Fracture of unspecified part of upper end of humerus, closed
812.09 Other closed fractures of upper end of humerus
812.19 Other open fracture of upper end of humerus
Clinical Pearls
Axillary artery is the most common neurovascular injury and can result in
avascular necrosis of the humeral head.
When evaluating shoulder dislocations, consider associated humeral head
fractures.
When the fracture is stable with some callus on radiograph, consider initiating
gentle range-of-motion exercises as early as tolerated.
Fracture, Humeral Shaft
Julie J. Chuan
Basics
Direct trauma from a fall
Direct blow to the upper arm
Fall on elbow or outstretched arm
Motor vehicle or industrial accident
Pitching a ball (torque causes a spiral fracture)
Bone malignancy (pathologic fracture) (1)[B]
Description
Transverse fractures occur from a bending force.
Spiral fractures occur from torsion.
Oblique fractures occur from bending and torsion and may have an associated butterfly
fragment.
Proximal or distal comminuted fractures occur from compressive forces.
Spiral fractures in children are concerning for child abuse.
Epidemiology
Bimodal distribution in the 3rd and 7th decades
3rd decade male predominance owing to sports and vehicular trauma
7th decade female predominance owing to simple falls (1)[B]
Types:
Midshaft: 60%
Proximal shaft: 25%
Distal shaft: 10% (1)[B]
Diagnosis
History and physical examination with special attention to a thorough neurovascular and
skin examination
Consider associated injuries such as ipsilateral shoulder, elbow, wrist, or hand fractures or
dislocations.
Diagnosis is confirmed by x-ray.
Pre Hospital
Immobilize with sling and swath for transport.
Evaluate for open fracture.
Evaluate for distal neurologic and vascular deficit.
Rapid transport in presence of neurologic or vascular deficits
History
History of fall: Simple trip and fall, a low-impact force, is often associated with older (70+
yrs), osteoporotic women.
Collision or direct blow: Higher impact, occurring more commonly in younger men
Pain after throwing or pitching
History of malignancy
Consider as pathologic fractures any humerus fracture produced by low-energy
mechanism; the humerus can be a common site of metastatic disease.
“Falls” in toddlers or infants are concerning for abuse
Check for other bruises and injuries suggesting abuse.
Examine the elbow in children who are guarding their arm.
Elbow dislocations are more common in toddlers (nursemaid's elbow).
Supracondylar fractures are more common in children when they sustain a fall.
Physical Exam
Pain and swelling over the area of the humeral shaft
Shortening, deformity, or decreased mobility
Crepitus on gentle passive range of motion (ROM)
Neurologic deficit (2)[C],(3)[B]:
Radial nerve is most commonly injured, occurring in 15% of humeral shaft fractures:
It is tethered down and emerges through the intermuscular septum at the middle to distal
shaft.
Injury will affect active extension in the wrist, hand, and fingers.
Occurs most frequently in middle and distal shaft fractures and spiral fractures
Usually a neurapraxia or axonotmesis (perineurium and epineurium intact)
Ulnar nerve injury will affect finger abduction (spreading the fingers apart).
Median nerve injury will affect thumb opposition (thumb and small finger pinch).
Vascular injury: Presenting as decreased pulse, slow distal capillary refill, or a cool extremity:
Brachial artery
Cephalic and basilic veins
Open fracture: If the skin is disrupted over the site of the fracture, there is a high risk of
infection and need for surgical evaluation.

Anteroposterior (AP) and lateral views of the entire humerus are mandatory to assess for
fracture pattern.
Displacement, including angulation and shortening type of fracture: Transverse, spiral,
oblique
Location of the fracture on the humeral shaft in relation to muscle attachments
Number of fracture segments (butterfly fragments) and comminution
Include shoulder and elbow views to exclude associated joint involvement.
Imaging
The AO/ASIF system defines humeral shaft fractures as follows (3)[B]:
Type A: Simple fractures:
A1: Simple spiral
A2: Simple short oblique
A3: Simple transverse
Type B: Wedge fractures:
B1: Spiral wedge
B2: Bending wedge
B3: Fragmented wedge
Type C: Complex pattern fractures:
C1: Complex spiral
C2: Segmental fracture
C3: Irregular comminuted fracture
Pathologic fractures of the humeral shaft are associated with the following malignancies (1)[B]:
Women:
Breast 40%
Myeloma 23%
Lung 9%
Kidney 9%
Men:
Prostate 33%
Kidney 25%
Myeloma 8%
Lung 8%
Bone contusion
Muscle contusion: Primarily the biceps, triceps, or deltoid
Hematoma
Tendon rupture: Primarily the biceps
Neurapraxia: Primarily the radial nerve
Abscess
Treatment
These fractures usually do not require elaborate reduction or
immobilization.
Fractures without neurovascular compromise can be treated conservatively;
see immobilization options below.
Immobilize for 4–6 wks until clinically and radiographically healed.
Pre-Hospital
With the introduction of functional (Sarmiento) bracing, conservative treatment
has become more popular and can be managed in the office.
Conservative care can be undertaken with 90% healing rates for adults with low
to moderate functional demands. The degree of displacement accepted in
these studies was up to 20 degrees and 2 cm of shortening.
Fractures can displace further after injury owing to contraction of the
surrounding muscles (see below).
No randomized, controlled trials support these recommendations, so they are
class C recommendations.
Open fractures or fractures associated with neurovascular compromise
require immediate orthopedic consultation.
Children remodel well and usually are able to compensate with overgrowth for
fractures up to 1.5 cm shortening and 20 degrees of angulation.
Anyone with high functional demands such as elite athletes, mechanics, and
carpenters should be considered for surgical fixation for optimal anatomic
alignment.
Of the nonunions, 90% ultimately heal with surgical intervention.
The carrying angle (valgus angle at the elbow when the arm is fully extended) is
most often affected in displaced humeral shaft fractures (4)[C].
ED Treatment
Specific injuries will warrant further surgical intervention and should be referred
immediately to the ED if seen in the office (5)[B].
Radial nerve palsy at any evaluation
Multisite trauma
Open or segmental fractures
Floating elbow: Occurs when there is a fracture above and below the elbow and
is considered an “unstable” injury
Ipsilateral arm injuries
Vascular injury: Refer for urgent vascular surgery evaluation.
Medication
Immobilization: Immobilize to limit movement at the site of the fracture, which is
one of the most effective methods of pain control.
Ice: Icing the fracture site intermittently (15 min q.i.d.) for the first few days will
reduce swelling and help to control pain.
Elevation: After immobilization, try to elevate the arm above the level of the
heart as much as possible to minimize swelling.
Analgesic medications:
Narcotic analgesics: Initially may be needed for adequate pain control
Nonnarcotic analgesics: After the fracture stabilizes (about 1 wk), NSAIDs
and/or acetaminophen should provide sufficient pain relief.
Consider displacing forces of the contracted muscles around the site of fracture
when immobilizing the injury:
Supraspinatus, infraspinatus, and teres minor externally rotate the humeral
head.
Subscapularis internally rotates the humeral head.
Pectoralis pulls fragments toward the chest (medially) and forward (anteriorly).
Latissimus and teres major pull fragments inward toward the chest.
Deltoid displaces the fracture outward (abducts) away from the chest.
P.
Referral
Surgical indications (4)[B]:
Unacceptable alignment after closed reduction
Radial nerve palsy at any evaluation, including after closed reduction
Multisite trauma
Open or segmental fractures
Floating elbow: Occurs when there is a fracture above and below the elbow and
is considered an “unstable” injury
Ipsilateral arm injuries
Pathologic fractures
Fracture with significant gap between segments usually represents muscle or
fat separating the bone fragments and is unlikely to heal.
Vascular injury: Refer for urgent vascular surgery evaluation.
Surgical options:
Intermedullary nailing
External fixation
Plate fixation
Immobilization options for conservative management (3)[B],(3)[C]:
Sling immobilization: Best for nondisplaced fractures that do not need
distraction but can predispose to further shortening
Sugar-tong, coaptation, or U-shaped splint: Best for limitation of transverse
fracture displacement; limits shoulder and elbow motion, predisposing to
stiffness after prolonged immobilization
Hanging cast: Better for displaced or comminuted fractures needing
distraction:
Needs closer follow-up after injury to evaluate for signs of compartment
syndrome
Cannot keep arm elevated to minimize swelling because gravity aids with
distraction of the fracture
Functional bracing: Allows for elbow mobility and earlier ROM; applied after
initial swelling subsides and fracture starts to stabilize, usually 2 wks after
injury
Always repeat the vascular and neurologic examination after splint or cast
application.
Surgical treatment:
Benefits:
More predictable alignment
Immediate stability
Risks:
Infection
Nerve and vascular injury
Nonunion
Anesthesia risks
Conservative treatment (5)[B]:
Benefits:
Functional bracing usually allows for full or nearly full shoulder and elbow
mobility.
Less infection and neurovascular injury risk
Risks:
Skin breakdown
Angular or translational malalignment/deformity
Nonunion (higher in simple fractures or type 1)
Shoulder or elbow stiffness
Pain control with NSAIDs or narcotic analgesics
Immobilization with sling and swath or shoulder immobilizer pending definitive
diagnosis
Application of ice to limit swelling
Open humerus fractures require covering with a sterile dressing, tetanus
prophylaxis, and parenteral prophylactic antibiotics.
Admission Criteria
Open fractures
Associated neurovascular compromise
Multisite trauma
Discharge Criteria
Uncomplicated humeral shaft fractures should be referred to an orthopedic
surgeon for follow-up.
Orthopedic consultation in the ED is required for patients with grossly displaced
or comminuted fractures.
Ongoing Care
Immobilize until clinical healing pain-free with bony callus on radiographs, usually 4–6
wks.
Start passive ROM after 2 wks to minimize shoulder and elbow stiffness.
Nonunion is most common with proximal shaft fractures, with overall nonunion rate of about
6%.
Radial nerve injury is most common in distal shaft fractures.
Varus angulation is most common in transverse fractures.
Nonunion risk factors:
Open fracture
Segmental (more than 2 fragments)
Transverse (tend to displace into varus owing to displacing forces)
Highly comminuted (unable to hold alignment)
Associations: Smoking, use of NSAIDs
Comorbidities: Diabetes, hypothyroid, infection, metabolic bone disease (2)[C]
Patient Monitoring
Weekly follow-up: Initially, every week to assess for displacement of the fracture
Every other week: Once the fracture is stable on consecutive radiographs (usually 2–3 wks
after injury). follow every 2 wks.
Once callus is noted on radiograph and no pain on examination, splint can be removed, and
shoulder and elbow should be mobilized with gentle ROM exercises.
Continue to follow clinically until ROM is restored and healing noted on radiographs (usually
8–12 wks).
At 12–14 wks, if union is not complete clinically and radiographically, consider referral to
surgery for intervention.
Patient Education
Compartment syndrome signs and symptoms if casted
Monitor for new neurologic deficit.
Monitor for new vascular deficit.
Encourage wrist, hand, and shoulder ROM exercises.
Sleep upright (recliner) if in a hanging cast until fracture is stable to minimize displacement.
Complications
Compartment syndrome:
Pressure increases in a contained space with the potential for severe nerve
and soft tissue injury (muscle ischemia and necrosis).
Present with:
Pain out of proportion to the injury
Paresthesias or numbness
Pulselessness (decreased pulse distally, slow capillary refill time, cool
extremity), loss of motion distally (hand or fingers)
Pain worse with passive ROM
Distally continued swelling
Pallor
References
1. Ekholm R, Adami J, Tidermark J, et al. Fractures of the shaft of the
humerus. An epidemiological study of 401 fractures. J Bone Joint Surg Br.
2006;88:1469–1473.
2. Anglen JO, Archdeacon MT, Cannada LK, et al. Avoiding complications in

the treatment of humeral fractures. Instr Course Lect. 2009;58:3–11.
3. Papasoulis E, Drosos GI, Ververidis AN, et al. Functional bracing of

humeral shaft fractures. A review of clinical studies. Injury. 2009.
4. Ekholm R, Tidermark J, Törnkvist H, et al. Outcome after closed functional

treatment of humeral shaft fractures. J Orthop Trauma. 2006;20:591–596.
5. Jawa A, McCarty P, Doornberg J, et al. Extra-articular distal-third

diaphyseal fractures of the humerus. A comparison of functional bracing and
plate fixation. J Bone Joint Surg Am. 2006;88:2343–2347.
Additional Reading
Magnusson AR. Humerus and elbow. In: Rosen P, et al., eds. Emergency
medicine: concepts and clinical practice. 4th ed. St. Louis: CV Mosby, 1998.
Simon R, Koenigskhecht S. Emergency orthopedics, the extremities. 3rd ed.

Norwalk, CT: Appleton & Lange, 1993.
Zuckerman J, Koval K. Fractures of the shaft of the humerus. In: Rockwood

CA, Green DP, eds. Rockwood and Green fractures in adults. 4th ed.
Philadelphia: Lippincott-Raven, 1996.
Codes
ICD9
812.21 Fracture of shaft of humerus, closed
812.31 Fracture of shaft of humerus, open
Clinical Pearls
Radial nerve injury is the most common neurovascular injury, occurring in about
15% of humeral shaft fractures.
10–20 degrees of angulation and 1–2 cm of shortening generally are well
tolerated owing to compensated overgrowth and the surrounding muscles.
Contraction of the muscles around the humerus can displace the fracture after
the initial injury and should be considered when immobilizing the fracture.
Consider close weekly follow-up after immobilization to monitor for fracture
displacement.
Fracture, Lateral and Medial Malleoli
Thomas Sargent
Jeffrey W. R. Dassel
Basics
Description
Any fracture involving the most distal portions of the fibula or tibia, commonly known as the
lateral and medial malleoli, respectively
Synonyms: Ankle fracture
Epidemiology
Very common: 187 ankle fractures per 100,000 people each year (1)
Fractures to ankle or midfoot occur in <15% of ankle sprains.
Most ankle fractures are malleolar fractures: 60–70% are unimalleolar (lateral being most
common), 15–20% are bimalleolar, and 7–12% are trimalleolar (medial, lateral, and posterior
malleoli) (2).
Risk Factors
History of prior ankle injury
Inadequate rehabilitation of injury
Skeletal immaturity
Weakness in dynamic (muscles) and/or static (ligamentous) stabilizers of the ankle
Abnormal gait and/or foot biomechanics
Foot and ankle proprioceptive dysfunction (dysfunction in the ability of the foot and ankle to
adapt to uneven terrain)
Cigarette smoking
Obesity

Pilon fracture
Maisonneuve fracture
Diagnosis
History
Elicit mechanism: Inversion vs eversion and external vs internal rotation of the ankle and foot
Most frequent injury is inversion
Occasionally caused by direct blow to the affected malleolus
Patient may hear or feel a “pop.”
Immediate, disabling pain and difficulty bearing weight
Acute onset of swelling
Development of ecchymosis
Assess for neurovascular symptoms.
Physical Exam
Swelling and/or deformity about the ankle
Ecchymosis
Limited range of motion of the ankle
Tenderness to palpation over the affected malleolus
Difficulty or inability to bear weight and/or ambulate
May note instability of the ankle joint on examination
Check for signs of neurovascular compromise (pulses/sensation in the foot).

Imaging
Ottawa Ankle Rules are used to determine whether x-rays are necessary. Obtain x-rays for
pain in the malleolar zone associated with any of the following:
Bony tenderness along distal 6 cm of posterior tibia or fibula, or at medial or lateral
malleolar tip.
Inability to bear weight (4 steps) on ankle immediately after injury and at time of evaluation.
The Ottawa Ankle Rules have a sensitivity for fracture near 100% and a modest specificity
(3)[B].
X-rays include anteroposterior (AP), lateral, and mortise (AP with foot in 15 degrees of
adduction) views.
Some ankle fractures may not be initially seen. Presence of a large ankle effusion on the
lateral radiograph may indicate an occult fracture and the need for further evaluation (4)[C].
On the mortise view, the joint space between the talus and lateral malleolus and the distal
tibia and medial malleolus should be equal. Inequality should raise suspicion of an unstable
ankle injury.
CT not indicated in most ankle fractures; however, is performed when an occult fracture is
suspected or to further evaluate pilon (comminuted distal tibial fracture), triplane (tibial
fracture in sagittal, coronal, and axial planes), or suspected talar fractures (5)[C]
When performed, order thin-cut CT in case coronal or sagittal reconstructions are required.
Contusion
Ankle sprain
Tear of ankle retinacular structures
Syndesmosis injury (“high ankle sprain”)
Foot fracture
Posttraumatic subluxation of peroneal tibialis posterior tendons
Treatment
Acetaminophen at recommended age- or weight-based dosages every 6–8
hr as needed
Consider NSAIDs, although controversy exists as to their effect on bone
healing.
Narcotics as needed for severe pain only
Cryotherapy applied 20–30 min every 2–4 hr for the 1st 24–48 hr after injury.
Use caution to avoid thermal injury to the skin.
Relative rest and elevation of affected limb for 1st 48–72 hr
Isolated lateral malleolar fractures with 2 mm or less of displacement do not
need reduction. Refer to orthopedist for >2 mm displacement (6)[C].
Isolated medial malleolar fractures with any displacement other than small
avulsion injuries should be referred to an orthopedist. Do not attempt to reduce.
Check neurovascular status of foot post reduction. P.
Post-reduction x-rays are same views as initial films
Non-weight-bearing in stirrup or posterior splint, with ankle in neutral position,
for 3–5 days
Isolated, minimally displaced lateral malleolar fracture: Short leg walking cast
with ankle in a neutral position or fracture boot with (eg, Cam walker) or without
adjustable ankle range of motion for 4–6 wks
Isolated simple avulsion fracture of the medial malleolus: Stirrup splint or Cam
walker can be used short-term for comfort, typically 2–4 wks
Referral
Any open fracture or fracture associated with neurologic or vascular deficits
requires emergent surgical evaluation.
Ankle injuries that are unstable or incongruent should be evaluated by an
orthopedic surgeon (1)[C].
Patients should seek attention immediately for pain that is increasing, new or
worsening numbness, or skin pallor/duskiness distal to the fracture or
splint/cast.
Repeat x-rays at 2 wks to ensure maintained alignment and at 6 wks to assess
bony healing (1)[C].
Repeat x-rays every 2 wks if not healing.
Total healing time: 6–8 wks. May take months to see complete radiographic
healing.
Athletes should cross-train while healing to maintain fitness.
Proper rehabilitation of these injuries with a home instructional program or with
formal physical therapy guidance is crucial to successful healing and return to
full function.
After period of immobilization is complete, start standard ankle rehabilitation
range of motion exercises, strengthening exercises, and proprioceptive
training.
The shorter the period of immobilization, the easier it should be for the patient
to regain ankle motion and strength.
Follow up every 2–3 wks to assess progress of rehabilitation.
The following injuries are frequently managed with surgical intervention:
Disrupted mortise joint
Fracture-dislocations
Bimalleolar fractures
Trimalleolar fractures
Unimalleolar fracture with contralateral ligament rupture
Lateral malleolar fractures with >2 mm displacement (1)[C]
Lateral malleolar fractures above the tibio-talar joint line (as they are frequently
associated with syndesmotic disruption)
Medial malleolar fractures with >2 mm displacement (6)[C]
Posterior malleolus fractures involving >25% of the articular surface or >2 mm
displacement (6)[C]
Admission Criteria
Open fracture
Fracture-dislocations in which adequate reduction is not achieved with manual
manipulation
Evidence of/concern for neurovascular compromise (severely comminuted
pilon fracture, compartment syndrome)
References
1. Koehler SM, Eiff P. Overview of ankle fractures. UpToDate. 2009.
www.uptodate.com
2. Court-Brown CM, McBirnie J, Wilson G. Adult ankle fractures—an

increasing problem? Acta Orthop Scand. 1998;69:43–47.
3. Bachmann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to
exclude fractures of the ankle and mid-foot: systematic review. BMJ.
2003;326:417.
4. Clark TW, Janzen DL, Ho K, et al. Detection of radiographically occult ankle

fractures following acute trauma: positive predictive value of an ankle effusion.
AJR Am J Roentgenol. 1995;164:1185–1189.
5. Mulligan ME. Fractures, Ankle. eMedicine. 2009.

emedicine.medscape.com/article/398578-imaging
6. Michelson JD. Fractures about the ankle. J Bone Joint Surg Am.
1995;77:142–152.
Additional Reading
Eiff MP, Hatch RL, Calmbach WL. Fracture management for primary care.
Philadelphia: WB Saunders, 1998.
Rockwood CA, Green DP, Bucholz RW, eds. Rockwood and Green's
fractures in adults. Philadelphia: JB Lippincott, 1996.
Codes
ICD9
824.0 Fracture of medial malleolus, closed
824.1 Fracture of medial malleolus, open
824.2 Fracture of lateral malleolus, closed
Fracture, Le Fort
Amy Leu
Basics
Maxillofacial fractures occur less frequently in children.
Because of the smaller facial skeleton, there is a higher incidence of skull fractures and
head trauma compared with midface injuries.
Le Fort fractures are particularly uncommon in young children. By ages 10–12 yrs, as
facial morphology becomes adult-like, more mid- and lower facial fractures are seen.
Be suspicious of child abuse or family violence as possible causes of midfacial injuries,
especially in children under age 6.
Cautions:
Airway management:
Airway compromise is common.
Bag valve mask (BVM) ventilation may be difficult.
Avoid nasotracheal intubation.
Strict cervical spine precautions
Multisystem injury is likely with high-energy trauma.
Description
Maxillofacial fractures caused by high-energy blunt trauma to the midface: The most common
causes include motor vehicle accidents, physical assault, sports injuries, and domestic
violence.
On traction of the maxillary arch/hard palate, you should find:
Le Fort I (horizontal): Movement of the hard palate and maxillary dentition only; can arise
from a blow low on the maxillary alveolar rim
Le Fort II (pyramidal): Movement of the hard palate, maxillary dentition, and the nose; can
arise from a blow to the lower to middle maxilla
Le Fort III (transverse): Movement of the entire midface including orbital rims (inferior and
lateral aspects); can arise from a blow to the nasal bridge or upper maxilla
Epidemiology
Prevalence
Midface fractures have been reported to make up 30% of all facial fractures.

Le Fort III fractures are commonly associated with lateral rim and zygomatic breaks.
Visual changes may signify a disturbance of the optic canal, problems within the globe or
retina, or other neurologic lesions.
Disturbances of extraocular motion or enophthalmos may signify a blowout in the orbital floor.
Consultation with an ophthalmologist is appropriate when extensive involvement of the orbit or
globe is suspected.
Le Fort III fractures also can extend to the base of the sphenoid and can result in a CSF
leak.
Diagnosis
Young children are often frightened and in pain. Through kindness, patience, and distraction,
cooperation can be gained.
Sedation may be required to perform a thorough exam after ruling out head injury.
Incomplete (greenstick) fractures with minimal or no displacement can occur.
Be cognizant of possible child abuse, and evaluate for prior nonaccidental trauma, if
appropriate.
Evaluate the patency of the airway and need for immediate airway control.
There is a high incidence of cervical spine injuries associated with facial trauma; thus cervical
spine precautions always must be taken (1).
Le Fort fractures can be diagnosed by careful intraoral examination and the pattern of facial
movement.
If fracture fragments are impacted, there may be little or no midface mobility.
Carefully evaluate the patient for CSF rhinorrhea and malocclusion.
If any disturbance of vision or extraocular motion is suspected, consider the presence of a
blowout fracture and/or ophthalmologic involvement.
Pre Hospital
Establishing airway patency is of utmost importance.
In severe Le Fort II and III cases, the maxillary plate can be displaced posteriorly and
inferiorly, possibly occluding the airway.
There is a high incidence of cervical spine injuries associated with facial trauma; thus, cervical
spine precautions always must be taken (1).
History
History may be difficult to obtain directly from the patient, but these types of fractures typically
arise from a high-energy force directed at different aspects of the face. Situations can include
motor vehicle accidents, altercations, sports injuries, and falls.
Physical Exam
Facial injury with massive swelling and ecchymosis
Facial hemorrhage/epistaxis
Airway obstruction may be present.
Dyspnea (especially when supine)
Malocclusion
Vision disturbance (diplopia)
Facial lengthening or flattening, periorbital ecchymosis (raccoon's eyes), periorbital swelling
CSF rhinorrhea
Facial anesthesia, midface mobility on traction, open bite
Frequently associated with multisystem injury (especially head and cervical spine)

Imaging
Facial imaging may be delayed for 24–72 hr in patients requiring care of other life-threatening
conditions.
CT scanning is the diagnostic standard for defining midface fractures with thin (2-mm) cuts in
the coronal and axial planes.
Conventional radiographs may be used as a screening test. The occipitomental (Waters') and
lateral views of the skull may reveal bony fracture/asymmetry, subcutaneous emphysema, or
layering of blood in the maxillary sinuses. Sinus films and cervical spine films usually are
included as part of the screening examination.
Le Fort fracture classification:
Le Fort I: Transverse (horizontal) through the maxilla above the roots of the teeth
Le Fort II: Pyramidal dysjunction including the nasal bridge, maxilla, lacrimal bones, and
orbital floor and rim
Le Fort III: Craniofacial dysjunction
Le Fort IV: Involves the frontal bone in addition to a Le Fort III maxillary fracture
Different-grade Le Fort fractures may be found on opposite sides of the face.
Treatment
Surgical cricothyroidotomy should not be considered in children under age 10.
Needle cricothyroidotomy with jet ventilation may be attempted if intubation
attempts fail.
There is a higher incidence of multiple injuries in children, especially head
trauma, skull fractures, and orthopedic injuries.
Cervical spine injuries tend to involve upper levels more commonly in children. P.
Also, spinal cord injury without radiographic abnormality (SCIWORA) syndrome
may be seen.
Definitive repair of pediatric facial fractures should not be delayed for more
than 3–4 days. The facial bones heal rapidly, and delayed repair may result in
malunion and cosmetic deformity.
ED Treatment
Cervical spine: Owing to the risk of cervical spine injury in patients with head
and maxillofacial trauma, it is imperative that radiographic clearance of the
cervical spine is obtained.
Hemorrhage control: Direct pressure should be applied to areas of bleeding,
and nasal packing (anterior and posterior) may be necessary for epistaxis. In
some cases, manual reduction of the midface may be required to control
intractable hemorrhage. Although blood loss from facial bleeding may be
significant, it is rarely a primary cause of hemorrhagic shock.
Early consultation with oral maxillofacial or plastic surgeon
Analgesics, antibiotics, and tetanus prophylaxis
Medications:
Adult Dose (mg/kg IV) Pediatric Dose (mg/kg IV)
Sedative/analgesics*
Diazepam 0.1–0.2 0.1–0.2
Droperidol 2.5-mg aliquots 1- to 1.5-mg aliquots
Etomidate 0.2–0.3 0.2–0.3
Fentanyl 2–10 µg 2–3 µg
Ketamine 2 1–2
Meperidine 1–2 1–2
Midazolam 0.1 0.15
Morphine sulfate 0.1–0.2 0.1–0.2
Defasciculating drug
Vecuronium 0.01 0.01
Paralytic agents
Pancuronium 0.1–0.15 0.1–0.15
Rocuronium 0.6 0.6
Succinylcholine 1.5 1.5–2
Vecuronium 0.1–0.3 0.1–0.3
*All these sedatives/analgesics should be titrated to effect.
Often, maxillomandibular fixation (MMF) is used in conjunction with open
reduction and internal fixation (ORIF) of maxillofacial injuries to maintain
optimal immobilization.
In the pediatric population, several considerations are taken into account,
including duration of MMF, use of smaller hardware, and avoiding injury to
developing teeth.
Aggressive airway control is paramount.
Orally suction patients to minimize aspiration of blood, saliva, and stomach
contents.
Remove any foreign matter or teeth from the airway.
After cervical spine clearance, stable and alert patients may be allowed to sit
up and suction themselves.
When airway management is needed, rapid-sequence induction is
recommended to maximize airway control and minimize rise of intracranial
pressure (ICP) in patients with head injuries (2).
If there is concern that paralysis will result in loss of airway tone and inability to
intubate because of subsequent distortion of airway anatomy in patients with
severe facial injuries, oral intubation under sedation with midazolam, etomidate,
droperidol, or ketamine is an option.
Emergency cricothyroidotomy may be necessary if orotracheal intubation is
unsuccessful. Recall that BVM ventilation may be difficult owing to loss of bony
support and altered anatomy.
Nasotracheal intubation is not recommended in patients with midface trauma
because of the lack of success and danger of intracranial placement (2,3,4).
Admission Criteria
All patients are admitted for ORIF of maxillofacial injuries.
Patients should be admitted to an ICU setting.
Ongoing Care
Complications
Infection can emerge from multiple stages during the treatment process,
particularly if there is extensive soft tissue involvement.
Scarring can occur depending on the suturing technique used, as well as the
patient's ability to keep the repaired area immobilized.
Nerve damage can arise from the original trauma as well as a result of the type
of surgery used to repair the fractures.
Malunion and, less commonly, nonunion also can result if adequate
immobilization is not achieved.
References
1. Mithani SK, St-Hilaire H, Brooke BS, et al. Predictable patterns of
intracranial and cervical spine injury in craniomaxillofacial trauma: analysis of
4786 patients. Plast Reconstr Surg. 2009;123:1293–1301.
2. Porras LF, Cabezudo JM, Lorenzana L, et al. Inadvertent intraspinal

placement of a Foley catheter in severe craniofacial injury with associated
atlanto-occipital dislocation: case report. Neurosurgery. 1993;33:310–311;
discussion 311–312.
3. Pawar SJ, Sharma RR, Lad SD. Intracranial migration of Foley catheter–an
unusual complication. J Clin Neurosci. 2003;10:248–249.
4. Engel M, Reif J, Moncrief E. Inadvertent intracranial placement of a Foley

catheter. A rare iatrogenic complication of severe frontomaxillary trauma. Rev
Stomatol Chir Maxillofac. 1992;93:333–336.
Additional Reading
Colucciello SA, Sternbach G, Walker SB. The treacherous and complex
spectrum of maxillofacial trauma: etiologies, evaluation, and emergency
stabilization. Emerg Med Rep. 1995;16;7:59–69.
Hehmann RJ, Sargent LA. Maxillary fractures. Trauma Q. 1992;9:67–75.
Hunter JG. Pediatric maxillofacial trauma. Pediatr Clin North Am.

1992;39:1127–1143.
Le Fort R. Experimental study of fractures of the upper jaw. Rev Chir de

Paris. 1901;23:208, 360, 479. Reprinted in Plast Reconstr Surg.
1972;50:497, 600.
Moe KS, Byrne P, Kim DW, et al. Facial Trauma, Maxillary and Le Fort
fractures. 2008 Dec http://emedicine.medscape.com/article/1283568-
overview
Shimoyama T, Kaneko T, Horie N. Initial management of massive oral bleeding

after midfacial fracture. J Trauma. 2003;54:332–336; discussion 336.
Subhashraj K, Nandakumar N, Ravindran C. Review of maxillofacial injuries in

Chennai, India: a study of 2748 cases. Br J Oral Maxillofac Surg. 2007.
Codes
ICD9
802.4 Closed fracture of malar and maxillary bones
802.5 Open fracture of malar and maxillary bones
Fracture, Lisfranc
Kenneth M. Bielak
Benjamin D. England
Basics
Description
Injury occurs from direct or indirect mechanisms.
Direct injury occurs with crush injury to the tarsometatarsal joint.
Indirect injury occurs:
When the hindfoot is placed in a fixed position, and the forefoot is forcefully abducted,
producing lateral displacement of the metatarsals with associated fracture of the second
metatarsal base
From an axially applied force to a plantar flexed foot (“tiptoe” position) causing disruption
of the dorsal ligament complex
From a force applied to the heel in the axis of the foot with the toes in a fixed plantar
position
Synonym(s): Lisfranc fracture; Tarsometatarsal fracture; First-second metatarsal-cuneiform
fracture
Epidemiology
1/50,000–60,000 orthopedic injuries per year; 67% occur in motor vehicle accidents.
0.2% of all fractures per year
Rare in the athletic population
2nd tarsometatarsal joint is most frequently injured.
Risk Factors
Slips, falls, motor vehicle accidents
Motorcycle accidents continue to be a source of severe injury, especially to the foot. The
most common foot injury is a metatarsal fracture; however, there must be a high index of
suspicion for associated injuries (1).
Although these injuries are associated with a low mortality rate, they require prompt
assessment and treatment to limit long-term morbidity and disability.

Cuneiform and cuboid fracture dislocations
Compartment syndrome of the foot
Late recognition and treatment: Posttraumatic arthritis with resulting pes planus and forefoot
abduction, which may require tarsometatarsal arthrodesis
Diagnosis
History
Is there midfoot pain? A high index of suspicion for these injuries needed. Up to 20% of
subtle injuries may be missed on initial examination.
Was the injury associated with low- or high-velocity trauma? High-velocity trauma usually will
have obvious deformity; low-velocity trauma may cause only minor discomfort in the midfoot.
Physical Exam
Midfoot pain and swelling
Pain with weight-bearing on involved foot or inability to bear weight
Plantar ecchymosis
Evaluate the integrity of the soft tissue, and perform neurovascular examination. Marked
swelling and deformity may indicate complete dislocation and risk for compartment
syndrome.
Palpate each articulation for tenderness and swelling. Medial cuneiform-1st metatarsal joint
is the most frequent site of pain and swelling.
Stress 2nd metatarsal joint by elevating and depressing the 2nd metatarsal head relative to
the 1st metatarsal head; elicits pain in Lisfranc joint.
Compression of midfoot from side to side reproduces pain in the interval between the
bases of the 1st and 2nd metatarsals.

Imaging
Standard anteroposterior (AP) view:
Medial shaft of 2nd metatarsal should be aligned with medial aspect of the middle
cuneiform.
Any malalignment indicates Lisfranc dislocation.
Small fractures in and around the Lisfranc joint should cause suspicion of significant injury
in this area.
“Fleck sign” avulsion fracture in medial cuneiform-2nd metatarsal space represents rupture
of Lisfranc ligament.
Compression fracture of cuboid (“nutcracker” injury) may be apparent.
30-degree oblique view: Medial shaft of 4th metatarsal should align with the medial aspect of
the cuboid. Any malalignment indicates disruption of the joint. Malalignment of 1st metatarsal
joint is seen frequently.
Lateral view: Dorsal or plantar displacement of the metatarsals relative to the tarsal bones
Weight-bearing lateral (both feet): Flattening of longitudinal arch; seen with subtle Lisfranc
injuries
Weight-bearing AP (both feet): Diastasis >1–2 mm between 1st and 2nd metatarsal bases
indicates rupture of Lisfranc ligament.
Stress views: Valgus stress can be applied to accentuate the injury.
CT scan may be helpful in defining the extent of injury.
MRI can show isolated ligamentous injury and bone marrow edema as another important
differentiating feature.
Lisfranc fracture dislocation
Tarsometatarsal sprain
Treatment
Bulky posterior splint for fracture ± dislocation
Lisfranc injuries with <2 mm of diastasis on weight-bearing radiographs can be
treated without weight-bearing in a short-leg cast or a walking boot for 6 wks
(2).
Lisfranc injuries with more significant displacement or instability require
operative intervention.
Pre-Hospital
Immobilize with posterior splint, non-weight-bearing, elevation, and
ice/compression
Any diastasis (>1 mm) or fracture requires operative reduction and screw
fixation.
Primary treatment by open reduction and internal fixation (ORIF) of
tarsometatarsal fracture dislocations leads to improved functional results,
earlier return to work, and greater patient satisfaction than secondary
corrective arthrodesis (remains a useful salvage procedure providing
significant relief of pain and improvement in function) (3).
Ongoing Care
Early orthopedic referral is indicated for any fracture, dislocation, or instability of the Lisfranc
joint.
References
1. Jeffers RF, Tan HB, Nicolopoulos C, et al. Prevalence and patterns of foot injuries
following motorcycle trauma. J Orthop Trauma. 2004;18:87–91.
2. Lattermann C, Goldstein JL, Wukich DK, et al. Practical management of lisfranc injuries in
athletes. Clin J Sport Med. 2007;17:311–315.
3. Rammelt S, Schneiders W, Schikore H, et al. Primary open reduction and fixation

compared with delayed corrective arthrodesis in the treatment of tarsometatarsal (Lisfranc)
fracture dislocation. J Bone Joint Surg Br. 2008;90:1499–1506.
Additional Reading
Clanton TO, Porter DA. Primary care of foot and ankle injuries in the athlete. Clin Sports
Med. 1997;16:435–466.
Coetzee JC. Making sense of Lisfranc injuries. Foot Ankle Clin. 2008;13:695–704.
Crim J. MR Imaging evaluation of subtle Lisfranc injuries: the midfoot sprain. Magn Reson
Imaging Clin N Am. 2008;16:19–27.
Desmond EA, Chou LB. Current concepts review: lisfranc injuries. Foot Ankle Int.
2006;27:653–660.
Codes
ICD9
825.24 Fracture of cuneiform bone of foot, closed
825.25 Fracture of metatarsal bone(s), closed
825.29 Other fracture of tarsal and metatarsal bones, closed
Clinical Pearls
Generally, surgically repaired injuries initially are immobilized in a non-weight-
bearing cast for 6 wks, followed by progressive weight-bearing in a cast or
range-of-motion boot for another 3–6 wks.
Athletes typically can return to sports at 4–5 mos after injury.
Fracture, Lunate/Kienböck Disease
Kevin E. Burroughs
Basics
Description
Kienböck (pronounced “Keen-bock”) disease, or lunatomalacia, is a painful disorder of the
wrist in which there are histologic and radiologic changes showing avascular necrosis of the
lunate.
1st described in 1910 by Robert Kienböck
Synonym(s): Lunatomalacia; Lunate avascular necrosis
Epidemiology
Most commonly seen between the ages 20 and 40 yrs
Predilection for the right hand in manual laborers
Bilateral changes occur less frequently than unilateral changes.
A 2% incidence of asymptomatic cases was reported in a large study of African patients.
Risk Factors
Previous wrist trauma including lunate fracture
Negative ulnar variance
Repetitive trauma (manual labor)
Anatomic and biomechanical features, including vulnerable blood supply or fixed position of
the wrist (loss of range of motion)
Etiology
A true etiology of Kienböck disease is unknown; however, the end result of lunate
fragmentation and collapse is definitively osteonecrosis.
Essentially two theories exist: Vascular and mechanical.
Increased intraosseous pressures have been recorded in Kienböck disease, supporting
impaired venous outflow as a potential etiology. Revascularization success with vascular
pedicle grafts also supports the circulatory etiology.
Mechanical theory describes necrosis secondary to progressive trabecular collapse of the
lunate owing to excessive loads and repetitive microfractures. Anatomic factors that would
lead to abnormal pressure on the lunate would include negative ulnar variance, uncovering of
the lunate by the distal radius, the shape of the lunate (trapezoidal), the existence of a
midcarpal facet on the lunate to articulate with the hamate, and radial inclination of the distal
radius.
Diagnosis
Lichtman classification of staging for Kienböck disease (via x-ray):
Stage I: Normal architecture and bone density; may be either a linear or a compression
fracture
Stage II: Definite density changes, but size, shape, and anatomic relationship of the bones
not altered; later in this stage, anteroposterior (AP) view shows loss of height on radial side
of lunate.
Stage IIIa: Entire lunate collapse, but the carpal height is relatively unchanged.
Stage IIIb: There is additionally proximal migration of the capitate and disruption of the carpal
architecture, including a fixed hyperflexion of the scaphoid (cortical ring sign). On lateral view,
a dorsovolar ribbon-like elongation of the lunate is seen.
Stage IV: In addition to stage III changes, generalized degenerative changes in the carpus
History
Longer duration of pain increases probability.
Both an inciting traumatic event and repetitive trauma have been linked with the occurrence of
Kienböck disease.
Physical Exam
Painful, stiff, and often swollen wrist joint
Usually >1 mo of pain at presentation
Pain most often mild to moderate in severity
Asymptomatic presentation can occur.
Look for swelling, erythema, and calor at the radioulnar joint. Erythema and calor are not
associated with Kienböck disease.
Evaluate range of motion; decreased in Kienböck disease, especially dorsiflexion.

Lab
Laboratory tests for the diagnosis of common arthritides can be used in those with wrist
symptoms, but no radiographic findings can be used to determine other possible causes.
Imaging
Standard AP and lateral radiographs
Initially, the lunate may have normal architecture and density.
Subsequently, increasing density of the lunate; then altered shape and diminished size
Adjacent arthritic changes and carpal row collapse
CT scan may be useful to detect early changes, including fracture lines.
Radiographic measures such as a smaller lunate diameter and height, a more radially inclined
lunate tilting angle, and a flatter radial inclination have been shown in those with Kienböck
disease (see Thienpont reference for descriptors).
MRI:
T1-weighted images show loss of signal intensity (corresponding to osteonecrosis).
T2-weighted images initially may show hyperintensity (early signs of osteonecrosis).
If negative, can rule out Kienböck disease in a patient with wrist symptoms; may show
alternative diagnosis better than plain films.
Wrist arthroscopy has been used to assess and classify Kienböck disease.
Assessment of the surfaces of the lunate is used to stage disease and plan appropriate
surgical interventions.
Triangular fibrocartilage complex tear (more lateral)
Scapholunate ligament instability
Distal radioulnar joint complex ligament instability
Monarticular arthritides (multiple)
X-ray:
Lunate fracture
Degenerative joint disease carpals
Treatment
Acute treatment
Immobilization:
In early stages, immobilization for 7 days is a reasonable 1st step because
synovitis and tenosynovitis usually resolve, and examination may become
more focused.
After classification is established, in stage I, initial treatment consists of up to
3 mos of casting or similar form of immobilization.
Arthroscopy with synovectomy also can be used for intervention in stages I and
II.
Over time, it has become evident that immobilization will not prevent long-term
collapse of the lunate. Some studies showed similar pain relief in conservative
versus surgical treatment.
If the patient still has pain after conservative measures or has more advanced
disease, there are a few other options.
In stage II or IIIA with positive ulnar variance: Direct revascularization plus
external fixation or temporary scaphotrapeziotrapezoid pinning (stage II only),
radial wedge or dome osteotomy, capitate shortening with or without
capitohamate fusion, combination of joint leveling and direct revascularization
procedures.
In stage II and IIIA with negative or neutral ulnar variance: Radius-shortening
osteotomy, ulnar lengthening, capitate shortening
In stage IIIB: Scaphotrapeziotrapezoid or scaphocapitate fusion with or without
lunate excision with palmaris longus autograft, radius-shortening osteotomy,
proximal row carpectomy
In stage IV: Proximal row carpectomy, wrist arthrodesis, wrist denervation
Silicone arthroplasty is no longer performed because of poor long-term results.
Lunate excision can reduce symptoms but does not prevent carpal collapse.
Ongoing Care
Prompt referral to an orthopedist after detection to evaluate, accurately stage, and discuss with
the patient available current treatments
Complications
A continuum from wrist stiffness to a fused and immovable wrist
Persistent pain
Nonunion in attempted arthrodesis
Additional Reading
Alexander AH, Lichtman DM. Kienböck's disease. Orthop Clin North Am.
1986;17:461–472.
Allan CH, Joshi A, Lichtman DM. Kienböck's disease: diagnosis and

treatment. J Am Acad Orthop Surg. 2001;9:128–136.
Bain GI, Begg M. Arthroscopic assessment and classification of Kienböck's

disease. Tech Hand Up Extrem Surg. 2006;10:8–13.
Beckenbaugh RD, Shives TC, Dobyns JH, et al. Kienböck's disease: the
natural history of Kienböck's disease and consideration of lunate fractures.
Clin Orthop Relat Res. 1980;149:98–106.
Bonzar M, Firrell JC, Hainer M, et al. Kienböck disease and negative ulnar
variance. J Bone Joint Surg Am. 1998;80:1154–1157.
Gelberman RH, Szabo RM. Kienböck's disease. Orthop Clin North Am.
1984;15:355–367.
Jackson MD, Barry DT, Geiringer SR. Magnetic resonance imaging of the
avascular necrosis of the lunate. Arch Phys Med Rehab. 1990;71:510–513.
Kuschner SH, Brien WW, Bindiger A, et al. Review of treatment results for
Kienböck's disease. Orthop Rev. 1992;21:717–728.
Lichtman DM, Mack GR, MacDonald RI, et al. Kienböck's disease: the role of
silicone replacement arthroplasty. J Bone Joint Surg 1977;59A:899–908.
Luo J, Diao E. Kienböck's disease: an approach to treatment. Hand Clin.

2006;22:465–473; abstract vi.
Mennen U, Sithebe H. The incidence of asymptomatic Kienböck's disease. J
Hand Surg Eur Vol. 2009;34:348–350.
Peltier LF. The classic. Concerning traumatic malacia of the lunate and its
consequences: degeneration and compression fractures. Privatdozent Dr.
Robert Kienböck. Clin Orthop Relat Res. 1980;149:4–8.
Schuind F, Eslami S, Ledoux P. Kienböck's disease. J Bone Joint Surg Br.

2008;90:133–139.
Thienpont E, Mulier T, Rega F, et al. Radiographic analysis of anatomical risk

factors for Kienböck's disease. Acta Orthop Belg. 2004;70(5):406–409.
Codes
ICD9
732.3 Juvenile osteochondrosis of upper extremity
814.02 Closed fracture of lunate (semilunar) bone of wrist
Fracture, Mandibular
Harry Stafford
Blake Boggess
Basics
First priority is to protect the airway, as severe fractures of facial structures may result
in airway obstruction from lack of glossal-supporting structures, blood clots, loose teeth,
dentures, or bony fragments.
Protect the C-spine.
Description
Fracture of the mandible is usually due to a direct force.
Frequently injured because of the mandible's prominence and relative lack of support
The most common area to be fractured is the angle, followed by the condyle, molar, and
mental regions.
Because of its thickness, the mandibular symphysis is rarely fractured.
Epidemiology
The mandible is the third most common facial fracture following nasal and zygomatic fractures.
Incidence
The incidence of mandibular fractures is lowest in children younger than 5 yrs of age (1.2 per
100,000), and peaks between 16 and 20 yrs of age (26.5 per 100,000).
Prevalence
Fractures of the mandible have been reported to account for 36–70% of all maxillofacial
fractures.
Risk Factors
43% of mandible fractures are caused by vehicular accidents, 34% by assaults, 7% work-
related, 7% the result of a fall, 4% from sporting accidents, and the remainder were
unspecified (1).
Etiology
Usually result from a direct force applied to the mandible by motor vehicle accidents,
personal violence, contact sports, or industrial accidents
The most common area to be fractured is the angle, followed by the condyle, molar, and
mental regions.

Additional traumatic facial fractures and other injuries
Patients may be intoxicated and unable to give a complete history of the injury.
Diagnosis
History
The source, size, and direction of traumatic force are helpful in diagnosis.
Patients involved in motor vehicle accidents tend to sustain compound, comminuted fractures.
Localized trauma (eg, pipe, stick, hammer, fist) tends to cause a single comminuted fracture
since the force is concentrated in a small area.
Trauma distributed to a larger surface area may cause several fractures (eg, symphysis,
condyle) secondary to distribution of the force throughout the mandible. These fractures are
classified by the anatomic location. More than 50% of patients have multiple fractures.
Direction of the force can help in making the diagnosis of concomitant fractures. Trauma
directed to the chin often results in a symphyseal fracture with concomitant unilateral or
bilateral condylar fractures.
Physical Exam
Patient complaints include:
Facial asymmetry, deformity, dysphagia, and mandibular pain
Malocclusion, decreased range of motion of the temporomandibular joint, or a grating
sound conducted to the ear with movement of the mandible
Inspect the maxillofacial area for obvious deformity:
Note facial lacerations, swelling, and hematomas.
A common site for a laceration is under the chin, and is associated with subcondylar or
symphysis fracture.
From behind the supine or seated patient, bimanually palpate the inferior border of the
mandible from the symphysis to the angle on each side. Note areas of swelling, step
deformity, or tenderness.
Loose, fractured, or missing teeth, gross malalignment of teeth; separation of tooth
interspaces; and ecchymosis or hematoma of the floor of the mouth
Protrusion or lateral excursion of the jaw. Interference with normal mandibular function,
including decreased range of motion or deviation of the mandible with opening:
The examiner should be able to insert 3 fingers between the mandible and maxilla.
Suggested by inability of the patient to break a tongue depressor placed between the teeth
and forced downward
Paresthesia of the lower lip or gums strongly indicates a mandibular fracture with secondary
damage to the inferior alveolar nerve.
Standing in front of the patient, palpate the movement of the condyle through the external
auditory meatus. Pain elicited through palpation of the preauricular region should alert the
clinician to a possible condylar fracture.
Observe any deviation on opening of the mouth, or for an inability to chew or open mouth:
Deviation on opening is typically toward the side of the mandibular condyle fracture.
Note any limited opening and trismus that may be a result of reflex muscle spasm,
temporomandibular effusion, or mechanical obstruction to the coronoid process resulting
from depression of the zygomatic bone or arch.
Changes in occlusion are highly suggestive of a mandibular fracture.
Look for intraoral mucosal or gingival tears:
Floor of the mouth ecchymosis may indicate a mandibular body or symphyseal fracture. If
a fracture site along the mandible is suggested, grasp the mandible on each side of the
suspected site and gently manipulate it to assess mobility.
Inability of the examiner to note motion of the mandibular condyles when palpated through the
external ear canals with motion of the jaw is highly suggestive of a mandibular fracture.

Imaging
The following types of radiographs are helpful in diagnosis of mandibular fractures:
Panoramic radiograph
Bilateral oblique radiographs
Posteroanterior mandibular view
Reverse Towne view
Mandibular occlusal view
Mandibular views are best for evaluating the condyles and neck of the mandible.
Dental panoramic views are best for evaluating the symphysis and body.
If the plain films are negative and a condylar fracture is still suspected, obtain a CT of the
condyles in the coronal plane.
Contusions
Dislocation of the mandible
Isolated dental trauma
Treatment
Mandibular fractures are uncommon in children <6 yrs of age. When they do
occur, they are usually greenstick fractures and can be managed with soft diet
alone. Parents should be informed that any fracture of the mandible has the
potential to damage permanent teeth and cause facial asymmetry; long-term
follow-up with a specialist is advisable.
20–40% of patients have associated injuries, and treatment should address
the most lethal concerns from airway obstruction, aspiration, major
hemorrhage, cervical spine or cord injury, and/or intracranial injury.
Airway compromise can occur from intraoral edema and hematoma, bony
fragments, loose teeth, and loss of tongue support.
C-spine precautions should be maintained.
If intubation is needed, an oral trachea tube should be placed.
Nasotracheal or cricothyrotomy may be indicated, depending on the extent of
the injuries.
ED Treatment P.
With the exception of condylar fractures, many mandibular fractures are
associated with mucosal, gingival, or tooth socket disruption, and should be
considered open fractures:
Patients should receive antibiotics such as penicillin or erythromycin to cover
intra-oral anaerobic pathogens.
Tetanus prophylaxis if appropriate
Definitive care usually consists of reduction and fixation by wiring upper and
lower teeth in occlusion for 4–6 wks:
This may not be possible initially due to patient instability or local edema.
Linear, nondisplaced, or greenstick fractures may be treated with soft diet
without wiring.
If mandible dislocation is present, bilateral downward pressure while the jaw is
open placed on the occlusal surface of the posterior lower teeth while grasping
the mandible:
The goal is to free the condyle from its anterior position to the eminence.
The operator's thumbs are placed on the external oblique line of the mandible
(lateral to the third molar area) or, after wrapping the thumbs in gauze, on the
occlusal surface of the lower molars. The other fingers are curled under the
mandible. The patient is asked to open wide, as if yawning, and the operator
then applies downward force on the molars while applying upward force over
the chin until the mandible reduces (2).
Once reduced, the patient should be placed in a Barton bandage for
temporary immobilization until they receive definitive care.
Reduction is facilitated by muscle relaxants (diazepam or midazolam), or
anesthetic injection of mastication muscles.
A bite block should be used or examiner's fingers should be wrapped in
gauze to prevent injury.
Medication
Use of preoperative and perioperative antibiotics in mandible fractures with
dentate involvement is well established to reduce the risk of infection (3).
Diazepam: Adult: 10 mg IV; peds: 0.1–0.2 mg/kg/dose IV
Midazolam: Adult: 2–5 mg IV; peds: Safety not established, but 0.02–0.05
mg/kg/dose have been used
Penicillin: Adult: 500 mg PO q.i.d.; peds: 25–30 mg/kg/24 hr divided q6h PO
Erythromycin: Adult: 500 mg PO q.i.d.; peds: 30–50 mg/kg/24 hr divided q6–8h
PO
With the exception of condylar fractures, many mandibular fractures are
associated with mucosal, gingival, or tooth socket disruption and should be
treated as open fractures.
Patients should receive antibiotics such as penicillin or erythromycin to cover
oral anaerobic microbes.
Patients should have their tetanus updated if needed.
Definitive care usually consists of reduction and fixation by wiring upper and
lower teeth in occlusion for 4–6 wks.
Linear, nondisplaced, or greenstick fractures may be treated with a soft/liquid
diet without wiring.
Admission Criteria
Those fractures in which there is significant displacement or associated dental
trauma, or those fractures that are thought to be open, require urgent specialty
consultation for admission.
The severity of associated trauma may indicate admission.
Any patient with the potential for airway compromise, including oropharyngeal
edema or bilateral mandibular body fractures, should be admitted.
An unreliable patient with nondisplaced fractures should be admitted for
definitive fixation.
In the pediatric population, if the mechanism of injury is not appropriate to the
injuries seen, evaluate for child abuse.
Discharge Criteria
Relatively asymptomatic patients with nondisplaced, closed fractures may be
discharged on analgesics and a soft diet. They should be referred to an
otorhinolaryngologist or an oral maxillofacial surgeon within 1–2 days.
Ongoing Care
Patient Education
Alcohol abuse plays a major role in the etiology of mandibular fractures. It results in a higher
rate of complications either secondary to noncompliance or as a result of metabolic
dysfunction.
Prognosis
Patients will usually be immobilized for 4–6 wks, and can resume contact sports within 1–2
mos after treatment with appropriate protective equipment (eg, customized headgear to
provide protection).
A better prognosis is achieved with removal of grossly diseased teeth.
Physical therapy is also recommended to improve jaw opening.
Complications
Treatment should occur as soon as possible. Prolonged delay in treatment
contributes to infection.
Immobilization of the fracture segments is perhaps the most important aspect
in avoiding delayed union, nonunion, and infection.
References
1. Alonso LL, Purcell TB. Accuracy of the tongue blade test in patients with
suspected mandibular fracture. J Emerg Med. 1995;13:297–304.
2. Ellis E, Moos KF, el-Attar A. Ten years of mandibular fractures: an analysis

of 2,137 cases. Oral Surg Oral Med Oral Pathol. 1985;59:120–129.
3. Busuito MJ, Smith DJ, Robson MC. Mandibular fractures in an urban

trauma center. J Trauma. 1986;26:826–829.
Additional Reading
Luyk NH, Ferguson JW. The diagnosis and initial management of the
fractured mandible. Am J Emerg Med. 1991;9:352–359.
Miles BA, Potter JK, Ellis E. The efficacy of postoperative antibiotic regimens
in the open treatment of mandibular fractures: a prospective randomized trial.
J Oral Maxillofac Surg. 2006;64:576–582.
Shepherd SM, Lippe MS. Maxillofacial trauma. Evaluation and management by

the emergency physician. Emerg Med Clin North Am. 1987;5:371–392.
Shorey CW, Campbell JH. Dislocation of the temporomandibular joint. Oral

Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:662–668.
Codes
ICD9
802.20 Closed fracture of unspecified site of mandible
802.21 Closed fracture of condylar process of mandible
802.22 Closed fracture of subcondylar process of mandible
Clinical Pearls
Consider a mandibular fracture for any athlete that has facial deformity,
dysphagia, and mandibular pain after direct trauma to the face.
The first priority is to maintain the airway and the C-spine.
This fracture must be treated as an open fracture with antibiotics.
Fracture, Metacarpal Base/Shaft: I-V
Tara Robbins
Basics
Description
Metacarpal shaft and base fractures are defined by their location, pattern, and displacement:
3 types of metacarpal shaft fractures: Transverse, oblique or spiral, and comminuted
2 types of metacarpal base fractures: Intra-articular and extra-articular
Metacarpal fractures involving the 1st metacarpal (thumb) are considered separately from
those involving the 2nd to 5th metacarpals.
Two intra-articular fractures of the thumb deserve special mention:
Bennett's fracture: Fracture combined with a subluxation or dislocation of the metacarpal
joint
Rolando fracture: T- or Y-shaped fracture involving the joint surface
Epidemiology
Metacarpal fractures account for 1/3 of all hand fractures.
Small finger is the most commonly injured (50%), followed by the thumb, index, long finger,
and ring finger (1)
Fractures of metacarpal base occur most commonly in the 4th and 5th metacarpals.
Metacarpal fractures account for 10–39% of pediatric hand injuries.
Incidence
Lifetime incidence of metacarpal fracture is 2.5%.
Risk Factors
Gymnastics, contact sports, racquet sports, boxing, karate
Etiology
Transverse and comminuted metacarpal shaft fractures usually result from a direct blow:
Dorsal angulation is common.
Spiral metacarpal fractures result from indirect trauma or rotational torque applied to a digit:
Fracture fragments tend to shorten and rotate, especially in the index and small fingers.
Intra-articular metacarpal base fractures are high-energy injuries and usually result from a
direct blow over the base of the metacarpal or a significant axial force or torque applied to
the digit:
Associated with carpometacarpal (CMC) dislocations
Most frequently occur in ring and small fingers
Uncommon in index and middle fingers
Avulsion fractures usually occur due to tractional forces from tendons that insert into the
base of the metacarpals.
Extra-articular metacarpal base fractures occur from same forces as intra-articular
metacarpal base fractures:
Most are stabilized by intermetacarpal ligament resulting in only minimal displacement
Can be associated with CMC dislocation of adjacent digit
Diagnosis
History
Direct blow vs indirect blow with rotational torque: Rotational torque often leads to spiral
fractures.
Nerve injury or damage to the extensor tendon frequently is associated with crush injuries.
Physical Exam
Tenderness and swelling over the dorsal hand
Pain with motion
Inability to make a fist
All patients require a thorough neurovascular examination distal to the fracture site. 4th and
5th metacarpal base fractures may cause injury to the motor branch of the ulnar nerve,
resulting in paralysis of the intrinsic hand muscles.
Evaluate for rotational malalignment:
All the fingers of a closed fist should point to the scaphoid tubercle.
No crowding or digital overlap should be present when the digits are fully flexed.
The plane of the fingernails should be parallel on the injured and normal hand.
Function of the flexor and extensor tendons must be documented.
Imaging
Radiographic evaluation with 3 views is mandatory because many fractures are overlooked
or misinterpreted.
Standard anteroposterior and lateral views: Pronation of 10–30° in lateral view facilitates
view of the second and third metacarpals; supination of 10–30° aids in viewing the ring and
small fingers.
Oblique views allow better visualization of intra-articular fractures, spiral fractures, and
epiphyseal plate injuries.
Robert view with the hand in maximal pronation is helpful for differentiating between intra-
articular and extra-articular fractures, as it allows for visualizing intra-articular extension of an
epibasilar fracture.
Tomograms or computed axial tomographic scans help define CMC relationships, and are of
benefit for defining comminuted intra-articular fractures (1).
Malrotation should be suspected if there is metacarpal shortening or a discrepancy in the
shaft diameter.
Metacarpal head and neck fractures
Metacarpophalangeal collateral ligament injuries
Carpometacarpal fracture dislocation
Treatment
Once thorough neurovascular examination is complete, wrist or hematoma
block may facilitate reduction.
Fractures amenable to closed manipulative reduction are transverse fractures,
isolated spiral/oblique fractures with <3 mm of shortening, and extra-articular
fractures of the thumb.
Closed reduction of metacarpal shaft fractures is performed with longitudinal
traction, dorsal pressure at the fracture site, and rotation as needed.
Closed reduction of extra-articular base fractures typically require only
longitudinal traction.
Postreduction films are mandatory. Limits of angular deformity depend on
mobility of different metacarpals at base: <10° for 2nd and 3rd metacarpals;
<20° for 4th and 5th metacarpals; <25° of both angulation and rotation are
acceptable for the thumb.
Orthopedic referral is required if satisfactory reduction cannot be performed or
maintained.
Radiographs should be repeated 1 wk after injury to reevaluate for angulation,
rotation, and shortening.
Dorsal and volar splints must include all metacarpal shafts and wrist while
avoiding immobilization of the metacarpophalangeal joint. Splint should be left in
place for 3–4 wks (1)[B].
Ulnar gutter splint for 3–4 wks for extra-articular metacarpal base fractures if
ring and/or little finger(s) are involved.
Volar or radial gutter for 3–4 wks for extra-articular metacarpal base fractures
of index and long finger
Functional brace (Galveston) if fracture requires significant reduction P.
Thumb spica cast for extra-articular fractures of the thumb for 4–6 wks
Bulky compressive dressing for unstable fractures
Closed reduction with local block or conscious sedation and immobilization is
generally effective for children (1)[B].
Referral is needed for unstable or unsatisfactory reductions in children.
Long oblique and spiral fractures typically require closed reduction and
percutaneous pinning in children (1)[B].
Fractures involving the physis and epiphysis are uncommon in children:
Usually Salter type II, which almost always are treatable with closed reduction
and immobilization
Salter type III fractures are rare. These require open reduction, since
osteonecrosis of the metacarpal head can result if inadequately reduced.
Children can be immobilized longer due to additional flexibility.
Referral
Any rotational deformity
>3 mm of shortening
>10° angulation for 2nd and 3rd metacarpals; >20° angulation for 4th and 5th
metacarpals; >25° angulation of the thumb
Intra-articular base fractures
Inability to perform or maintain satisfactory closed reduction
All surgical cases, including special situations such as multiple fractures, nerve
or tendon injury, and open fractures
Field management: Splint immobilization provides comfort and minimizes soft
tissue injury.
Ice packs should be used proximal to the metacarpals to prevent digital injuries.
Active motion as soon as 3–4 wks for fractures treated with immobilization and
closed reduction
Buddy taping may provide stability when mobilization begins.
Clinical union is manifest by absence of tenderness at the fracture site with
palpation and range of motion. Radiographic union will lag behind clinical union
by several weeks.
Open reduction internal fixation or closed reduction with percutaneous pinning is
advocated for patients with malunion or unstable fractures (Bennett, Rolando,
comminuted, intra-articular, spiral/oblique with shortening and rotation).
Ongoing Care
Follow up 1 wk after injury with radiographs to evaluate for angulation, rotation, and
shortening.
Splint should remain in place for 3–4 wks.
Rehabilitation should be delayed until 3–4 wks post injury for distal metacarpal shaft fractures
(2).
Both active and passive range of motion (ROM) at interphalangeal joints can be started
immediately for metacarpal base and proximal shaft fractures (2).
Gentle active ROM at the MCP joint is allowed in most proximal stable shaft fractures 3–4
wks after injury (2).
Passive ROM at MCP joint can be added when there are signs of clinical union, usually 5–6
wks after the injury (2).
Strengthening exercises should be added at 8 wks (2).
Complications
Stiffness can develop after prolonged immobilization or delayed rehabilitation.
Chronic CMC joint stiffness is associated with intra-articular fractures.
Malunion usually manifests as malrotation or dorsal angulation, so confirm that
the patient's fingertips point toward the scaphoid tuberosity in flexion at each
visit:
5 degrees of malrotation can result in 1.5 cm of digital overlap and cause a
decrease in grip strength.
Nonunion is uncommon in metacarpal fractures.
References
1. Chin SH, Vedder NB. MOC-PSSM CME article: metacarpal fractures. Plast
Reconstr Surg. 2008;121:1–13.
2. Weinstein L, Hanel D. Metacarpal fractures. J Am Soc Surg Hand.

2002;2(4):168–180.
Additional Reading
Capo JT, Hastings H. Metacarpal and phalangeal fractures in athletes. Clin
Sports Med. 1998;17:491–511.
Harrison BP, Hilliard MW. Emergency department evaluation and treatment of

hand injuries. Emerg Med Clin North Am. 1999;17:793–822.
Lyn E, Antosia R. Chapter 47: Hand. Marx: Rosen's emergency medicine:

concepts and clinical practice, 6th ed. Philadelphia: Mosby, 2006.
Mastey RD, Weiss AP, Akelman E. Primary care of hand and wrist athletic
injuries. Clin Sports Med. 1997;16:705–724.
Peterson JJ, Bancroft LW. Injuries of the fingers and thumb in the athlete. Clin
Sports Med. 2006;25:527–542, vii–viii.
Simon RR, Koenigsknecht SJ, eds. Emergency orthopedics. Stamford, CT:

Appleton Lange, 1996.
Codes
ICD9
815.00 Closed fracture of metacarpal bone(s), site unspecified
815.01 Closed fracture of base of thumb (first) metacarpal
815.02 Closed fracture of base of other metacarpal bone(s)
Clinical Pearls
Boxer's fractures are metacarpal neck fractures involving the small finger.
Return to play needs to be individualized, depending on the type of fracture,
mobility, and clinical healing.
Fracture, Metacarpal Neck: I-V
Quynh Hoang
Chris Koutures
Basics
Description
The metacarpal neck (distal metaphysis) is the aspect of the metacarpal shaft immediately
underneath the metacarpal head.
The weakest point of the metacarpal is located at the distal metaphysis, so metacarpal
fractures frequently involve the neck (1)[C].
The mechanism of injury is usually an axial load on the metacarpal phalangeal (MCP) joint
while in a flexed position, such as when throwing a punch.
Fractures about the metacarpal neck must be scrutinized for malrotation and angulation.
As 2nd and 3rd metacarpals are necessary for handgrip power, much less angulation is
tolerated in these injuries.
Synonym(s): Boxer's fracture; 5th metacarpal neck fracture
Epidemiology
5th metacarpal neck fractures (boxer's fractures) are the most common hand fracture,
accounting for 20% of all hand fractures (1)[C],(2)[B].
Fractures of the 1st metacarpal neck are uncommon.
Risk Factors
Out-of-control tempers: Boxer's fractures usually are due to striking an opponent or a wall with
a clenched fist.
Etiology
Due to the action of the interosseus muscles, the distal fracture fragment (metacarpal head)
displaces volarly, resulting in an apex dorsal angulation.
The index and long fingers cannot tolerate angulation deformities given their relatively fixed
articulations with the distal carpal bones.
The ring and small fingers, however, have limited flexion and extension, so angular
deformities are better tolerated and they heal with minimal loss of function.
Diagnosis
History
Axial load or direct trauma, often to clenched fist or dorsum of the hand
Immediate pain and swelling noted
Physical Exam
Swelling and tenderness on the dorsum of the hand, often accompanied by
metacarpophalangeal (MCP) joint depression
Extreme angulation may lead to pseudoclawing, ie, hyperextension of the MCP joint along
with proximal interphalangeal (PIP) joint flexion as the patient attempts to extend the finger.
Tenderness and swelling about the dorsal aspect of the distal metacarpals. Examine skin
closely for teeth marks or other injuries.
Evaluate the digits for malrotation, which occurs more in 4th and 5th metacarpal neck
fractures. Have the patient bring all the fingernails into the palm and compare with the
noninjured hand. All the nails should point toward the base of the 1st metacarpal. If the
injured finger is out of this alignment, strongly suspect significant fracture malrotation.

Imaging
Anteroposterior, oblique, and true lateral views of the hand usually are sufficient.
Normally, the metacarpal neck is situated with a baseline of 15 degrees of volar angulation.
Ensure adequate visualization on the lateral view to evaluate the degree of fracture
angulation.
A conservative rule for limits of acceptable angulation of the 2nd through 5th digits is 10–30.
Thus, the 2nd digit can only tolerate 10 degrees of angulation (in addition to the baseline 15
degrees); the 5th metacarpal can accept 30 degrees above the baseline. Many other experts
will tolerate a greater degree of angulation of the 5th metacarpal; this decision often is
influenced by the particular activity or sport of the patient.
Degrees of acceptable angulation vary in current literature. For the index or long finger, some
authors report that angulations of >15 degrees above baseline are not tolerated due to the
lack of carpal metacarpal motion (1)[C]. Others report that for the ring finger up to 30
degrees of excessive angulation (above baseline) at the metacarpal neck is acceptable, and
for the small finger, up to 40 degrees of excessive angulation (above baseline) at the 5th
metacarpal neck is acceptable (3)[C],(2)[B].
Metacarpal head fracture
Metacarpal shaft fracture
Open fracture
MCP joint dislocation
MCP joint sprain
Treatment
NSAIDs can be used along with ice for immediate analgesia.
Narcotic analgesics may be necessary for sleep during the first few nights
after the injury.
Closed reduction is considered in cases of significant angulation of 4th (>20
degrees above baseline) and 5th (>30 degrees above baseline) metacarpal
neck fractures.
Anesthesia can be obtained by hematoma block or ulnar nerve block.
Flex the MCP, PIP, and distal interphalangeal joints all to 90 degrees. Apply
dorsally directed pressure along the proximal phalanx shaft through the flexed
PIP joint while simultaneously applying volarly directed pressure over the
proximal fracture fragment (3)[C].
Obtain a postreduction lateral view of the hand to ensure adequate reduction
and immobilization.
Nondisplaced and nonangulated fractures of the 2nd or 3rd metacarpal necks
can be immobilized in a radial gutter splint with the wrist in 30 degrees
extension, MCP joint in 70–90 degrees of flexion, and PIP/DIP joints near full
extension.
Mildly angulated 4th (<20 degrees above baseline) and 5th (<30 degrees)
metacarpal neck fractures can be immobilized in ulnar gutter splints with the
same positions.
Alternatively, some literature recommends functional treatment by casting
(glove cast) or by taping with pressure bandage (3)[C],(2)[B]. For functional
casting, the cast is applied circularly around the metacarpals, and it starts distal
to the palmar crease of the wrist and ends just proximal to the MCP joint. This
allows maximal range of motion of the finger and wrist while providing
immobilization and protection of the fracture fragment.
Elevate the hand and apply ice for 20-min intervals on a regular basis over the
first 24–48 hr after injury.
Splints should be applied to injuries requiring orthopedic referral (see below), P.
unless that consultant is immediately available.
Controversy still exists regarding the optimal management for metacarpal neck
fractures, particularly for fracture of the 5th metacarpal neck.
There is no consensus on:
How much angulation is acceptable (recommendations in literature vary from
20–70 degrees for the 5th metacarpal)
Which splinting method is most optimal
What length of immobilization is optimal (literature varies anywhere from no
immobilization to 1 wk of immobilization followed by functional treatment, to
pure immobilization ranging from 2–4 wks)
In a randomized controlled trial by Muller et al., no differences in functional
outcome were found between boxer's fractures treated with immobilization in
an ulnar gutter cast for 3 wks and those treated with functional taping for 1 wk.
Furthermore, range of motion of the 5th CP joint was not affected in fractures
with angulation <70 degrees that were not reduced (2)[B].
In a 2005 Cochrane Review, the authors concluded that there is no single
nonsurgical treatment method that can be recommended as superior to
another (4)[B].
Referral
Open reduction and internal fixation is indicated for:
Significant angulation of 2nd (>10 degrees above baseline) and 3rd (>10
degrees above baseline) metacarpal neck fractures, or those with any
displacement
Failure to achieve acceptable angles after reduction of the 4th and 5th
metacarpals
Any metacarpal neck fracture with rotational malalignment or comminution
Any potential open fracture
Degree of residual angulation that is unacceptable to the patient
Inability to hold reduction position
Athlete who desires immediate return to play in cast orthosis
Ongoing Care
Fractures should remain splinted for a minimum of 3–4 wks.
Clinical healing is defined as no tenderness with palpation of the fracture site.
Once the splints are removed, begin range of motion work with emphasis on handgrip and
manipulation strength. Key to prevent stiffness of the MCP joint.
For 2nd and 3rd metacarpal neck fractures, follow-up radiographs should be obtained in 5–7
days to monitor fracture alignment.
For 4th and 5th metacarpal neck fractures, follow-up radiographs should be taken at 7–10
days.
Perform follow-up visits at 2-wk intervals to monitor for malalignment, rotational deformity,
angulation, and progress of healing.
Patient Monitoring
Return to sports participation recommended when there is pain-free range of motion and
when strength approaches that of the contralateral hand.
In general, conservative guideline for return to contact sports with splint/orthotic protection is
after 2–4 wks of immobilization. Some experts may allow immediate return to play with a
protective cast or splint.
Use of orthotic protection during contact sports should continue for 8–10 wks after the initial
injury.
Patient Education
Patients should be warned that despite reduction and splinting, loss of knuckle prominence
may result.
After splint removal, educate patient on range of motion exercises to prevent MCP joint
stiffness.
Complications
MCP joint stiffness due to prolonged immobilization, interosseus muscle
contractures, or tendon adhesions
Cosmetic deformity without functional loss still may ensue.
Although uncommon, delayed union or nonunion of the fracture site may occur.
Pseudoclawing
References
1. Capo J, Hastings H. Metacarpal and phalangeal fractures in athletes. Clin
Sports Med. 1998;17: 491–511.
2. Muller M, Poolman R, et al. Immediate mobilization gives good results in
boxer's fractures with volar angulation up to 70 degrees: a prospective
randomized trial comparing immediate mobilization with cast immobilization.
Arch Orthop Trauma Surg. 2003;123:534–537.
3. Leggit J, Meko C. Acute finger injuries: part II. Fractures, dislocations, and
thumb injuries. Am Fam Physician. 2006;73:827–834.
4. Poolman RW, Goslings JC, et al. Conservative treatment for closed fifth
(small finger) metacarpal neck fractures. Cochrane Database Syst Rev.
2005;3:CD003210.
Codes
ICD9
815.04 Closed fracture of neck of metacarpal bone(s)
815.14 Open fracture of neck of metacarpal bone(s)
Fracture, Metatarsal
Andrew Hunt
Basics
The anatomy of the foot is divided into the hind-foot, the mid-foot, and the forefoot:
The hind-foot includes the calcaneus and talus.
The mid-foot includes the navicular, cuboid, and cuneiform bones.
The forefoot includes the metatarsals and phalanges:
The forefoot functions to transmit ground reaction forces to the mid-foot with weight-
bearing activities.
Fractures in the forefoot, specifically to the metatarsals, can alter the normal distribution of
weight and lead to secondary metatarsalgia (pain) as well as transfer lesions such as
plantar callouses and stress lesions.
Description
A metatarsal fracture can be described as being extra-articular, partial intra-articular, or
articular, depending on where on the metatarsal the fracture occurs. Extra-articular fractures
may be transverse (straight across the long axis), oblique, or spiral. An articular or partial
intra-articular may be a simple isolated fracture extending into the joint, comminuted, or an
avulsion fracture.
A stress injury with normal radiographs but a positive exam (pain to palpation) may be
categorized as macrotrabecular (visible fracture lines on MRI) or stress reaction (T2 signal
change on MRI without visible fracture lines).
Epidemiology
Metatarsal fractures are likely more common in athletes involved in weight-bearing exercise
such as dancers, runners, or contact sport athletes.
Any direct trauma, however, can cause fracture, and lower-risk athletes such as swimmers
or bikers still may present with this injury.
Incidence
Overall incidence of metatarsal fractures is unclear, as a wide variety of physicians treat this
injury:
This includes internists, pediatricians, family practice physicians, emergency physicians, and
orthopedic surgeons.
Risk Factors
Same as for bone fractures in general
Those with osteopenia or osteoporosis have a greater risk.
Any activity that increases the likelihood of direct trauma to the foot increases the risk of
metatarsal injury.
Excessively rapid progressions of training volume and/or stress on the foot can also increase
the risk of metatarsal stress injury.
General Prevention
Gradual increases in workload allow a bone to adapt to mechanical stress and become
stronger.
Bone is a dynamic organ that is subject to anabolic forces tending to build it up, as well as to
catabolic forces tending to break it down.
This balance allows a bone to remodel and adapt to stress, but may also cause progressive
weakening if catabolic forces outweigh the anabolic ones, such as with too-rapid progression
of training load.
Etiology
When the cortical bone's mechanical strength is exceeded acutely by direct trauma, such as
a heavy object falling on the foot, it will fracture.
When this acute stress is a shear force secondary to twisting on a plantar flexed foot, the
fracture pattern may be a spiral in shape.
A fracture may also occur when the bone-tendon interface is acutely stressed past its
mechanical failure point.
A typical example of this is at the base of the 5th metatarsal where the peroneus brevis
muscle inserts and acts to evert the foot.
An additional mechanism for fracture occurs when repetitive subthreshold forces are
incompletely healed and the additive damage eventually causes an overt fracture.
Prior to an overt fracture, however, such stress may cause macrotrabecular fracturing not
evident on plain radiographs but seen on MRI.

The same forces that cause fracturing of the metatar-sals may also injure adjacent structures
such as the mid-foot joint (between the row of cuneiform bones articulating with the 1st
through 4th metatarsals and the cuboid articulating with the 4th and 5th metatarsal). At the
other end, the metatarsophalan-geal joints (MTP joint) may be involved when a fracture
extends into the joint or when the joint capsule or ligamentous structures are disrupted.
Other injuries to consider:
Mid-tarsal joint injury (calcaneo-cuboid or talo-navicular): Can include lateral process of
talus or anterior process of calcaneus
Navicular or cuboid contusion/fracture
Metatarso-cuneiform/cuboid injury (MTC): Lisfranc joint injury may include ligamentous
disruption and/or fracture of surrounding bone.
Metatarso-phalangeal joint (MTP) injury: Can include capsular or ligamentous sprain (turf
toe) or fracture of adjacent bone
Phalangeal fracture
Sesamoid contusion or fracture
Predisposing conditions:
Hallux valgus/hallux rigidus: Altered mechanics at the 1st MTP joint leads body weight
shifting laterally over the lesser caliber 2nd metatarsal
Osteopenia/osteoporosis: Decreased mechanical strength of the bone increases
susceptibility to stress fracture and acute fracture
Diagnosis
Diagnosis of overt metatarsal fracture is by radiograph.
Standard views include the anteroposterior (AP), lateral, and oblique views.
Addition of weight-bearing views may help identify subtle lesions as well as Lisfranc injuries if
the patient tolerates them.
Diagnosis of radiographically negative stress injury is via a technetium-99 bone scan or by
MRI.
Advantages of MRI over bone scan include differentiation of stress reaction without
fracture lines vs macrotrabecular fracture.
Pre Hospital
Prehospital/on-field care includes minimizing weight bearing on the affected extremity as well
as icing to reduce swelling and inflammation.
If there is no evidence for open fracture or vascular compromise, plain radiographs may be
obtained at the patient's convenience.
If there is visible bone penetrating the skin or the extremity is cool indicative of vascular
compromise, immediate transport to the emergency room is advisable.
History
With acute injury, the patient will usually be able to point to a direct trauma to the foot or a
twisting injury causing pain.
More subtle stress injuries will typically have a history of recent increases in training volume
or impact load and possibly a prior history of other stress fractures, disordered eating, or
menstrual irregularities.
Physical Exam
Point-tenderness directly over the metatarsal is the typical finding on exam.
The foot will usually show some swelling in comparison to the unaffected foot and possibly
some bruising as well.
Gross displacement is not common. Open fractures will present with bone penetrating
through the skin.

Focal tenderness and/or swelling over the metatarsals after an injury is a clear indication for
plain radiographs to rule out a fracture.
Chronic symptoms of foot pain with weight bearing and negative radiographs warrants further
imaging such as bone scan or MRI.
An urgent need for a clear diagnosis after an acute injury and negative radiographs also
suggests the need for further imaging.
Imaging
Plain radiographs will show cortical disruption if a significant fracture has occurred.
The findings may be subtle with mild injury.
A stress fracture may show subtle sclerotic borders/periosteal elevation or be entirely
normal.
Plain films only become positive once healing has progressed enough to produce visible bony
callus. In the interim, an MRI should show changes on T2 images and a bone scan should be
positive for focal hot spot over the painful area.
A CT scan may be indicated for an intra-articular fracture to delineate any articular step-off.
MTP joint synovitis: Inflammation of the joint rather than stress reaction in the bone itself.
Bone scan will show distal uptake around MTP joint. MRI is diagnostic. Claw toe may also
cause synovitis with plantar displacement of metatarsal head or a metatarsal stress reaction.
MTP capsular strain and/or chip fracture of 1st metatarsal head (turf toe)
Lisfranc sprain/fracture: Injury to the 2nd MTC articulation. Any pain at the proximal 2nd
metatarsal in association with a twisting injury in plantar flexion should raise concern for this
injury.
Mid-foot sprain: Injury to MTC ligamentous structures
Forefoot mass (ganglion or tumor)
Metatarsalgia
Morton's neuroma (interdigital neuroma)
Freiberg's infarction: Osteonecrosis of 2nd metatarsal head. More common in adolescent
athletes with unilateral (usually) pain in 2nd metatarsal head.
Treatment
The goal of treatment is to stabilize the fracture such that normal length,
rotation, and declination of the metatarsal is maintained and the area is
protected from further injury until healing has occurred.
Pre-Hospital
If possible, the foot should be elevated and cooled with ice as soon as possible
after injury.
Limited or crutch-assist weight bearing is advisable until emergency
department (ED) or physician evaluation has occurred.
Chronic complaints can be evaluated in a physician's office rather than an ED.
ED Treatment
Evaluation of acute injury to the foot in the ED includes AP, lateral, and oblique
plain radiographs. Good neurovascular status must be verified, as
compartment syndrome can occur with a forefoot crush injury. The need for
closed or open reduction is then assessed. Multiple metatarsal fractures with
more than 4 mm of displacement or an apical angulation of the metatarsal head
of more than 10° on the lateral view could require open/closed reduction to
ensure a normal weight-bearing position of the metatarsal head.
Open reduction of metatarsal, phalangeal, and MTP joint injuries can cause
scarring and stiffness in addition to the original trauma. It is used to largely to
maintain a plantigrade foot for normal weight bearing. An open fracture
requires surgical intervention for debridement and stabilization.
Nondisplaced fractures of the metatarsal neck and shaft may be treated with a
short leg cast, fracture brace, or a cast shoe. Weight bearing is permitted as
tolerated on discharge from ED. The minimum amount of immobilization
necessary for comfort should be used. Fractures at the base of the 5th
metatarsal may be treated with an ankle stirrup brace, cast shoe, or fracture
brace to maintain comfort.
Medication
Depending on the severity of the injury, NSAIDs are a 1st-line drug to treat
pain.
Acetaminophen is also used.
More severe pain may require narcotic pain relief.
First Line
NSAIDs
Acetaminophen
Second Line
Oral low- to mid-potency narcotics such as hydrocodone, codeine, or
propoxyphene
Tramadol is also an option.
Proximal 5th metatarsal avulsion fracture (pseudo-Jones Fx):
Mechanism is usually due to an acute inversion injury to the ankle in plantar
flexion. This can cause avulsion of the peroneus brevis or lateral plantar
aponeurosis at the metatarsal tuberosity. May be a stress injury. They tend to
be nondisplaced and experience relatively rapid union with symptomatic
treatment. More distal injuries (without being a Jones Fx) may require short
leg casting with nonweight-bearing (NWB) status for up to 6–8 wks. Use
open reduction/internal fixation (ORIF) for delayed union or nonunion,
significant displacement, or if cuboid 5th metatarsal joint involved.
Jones fracture (proximal shaft of 5th metatarsal):
The metaphyseal/diaphyseal junction is a watershed zone for blood flow and
is susceptible to delayed union or nonunion. Consider ORIF in higher-level
athletes primarily and if nonunion occurs. Treat initially with short leg
cast/fracture brace with no weight bearing until evidence of bony callus
formation is seen. Progress to weight bearing at that point. May present with
preinjury symptoms similar to stress fracture exacerbated by inversion injury.
Spiral fracture of 5th metatarsal:
This is typically treated nonsurgically with a fracture brace or cast shoe.
Weight bearing is allowed as tolerated. Radiographic healing may take up to
12 wks. Called a “dancer's fracture” when it occurs in the distal part of the
bone.
Referral
Multiple metatarsal fractures
Single metatarsal fracture with >4 mm of displacement
Single metatarsal fracture with >10° of dorsal angulation of distal segment
Possible compartment syndrome
Displaced/comminuted fracture of the 1st metatarsal
Open fracture
Proximal 5th metatarsal fracture nonunion after 12 wks of conservative care
Proximal 5th metatarsal Fx/Jones Fx: ORIF with malleolar screw Kirschner
wires.
Bone grafting may be required in nonunions.
Lisfranc fracture/dislocation: Involves 2nd through 5th MTC joints. ORIF with
cortical screws and kirschner wires
Metatarsal fractures rarely require inpatient care.
Open fractures and multiple traumatic injuries that include a metatarsal likely
require IV antibiotics and observed care.
Ongoing Care
Upon discharge from the ED or after initial diagnosis, a patient with a metatarsal fracture
should be seen in the office for follow-up radiographs in 1 wk to document correct bony
alignment and adequacy of the treatment mode. Assuming radiographs show stability, follow-
up films can be obtained at 6 wks, when full healing should be expected.
The least-limiting form of immobilization should be considered. With the exception of a Jones
fracture, most metatarsal fractures tolerate weight bearing with use of a cast shoe/wooden-
soled shoe fairly quickly, if not at the time of diagnosis. If fracture brace/CAM boot use is
required initially, transition to a stiff-soled or cast shoe should be considered when tolerated.
A steel shank insert into a gym shoe may also be used.
Restriction from full weight-bearing stress without protection should continue for at least 4
wks for a stress fracture and for 4–6 wks for a nondisplaced metatarsal fracture. Pain to
palpation and forefoot swelling should subside as the fracture heals. Evidence for
radiographic healing, resolution of edema, and pain-free direct palpation are needed for
return to sports.
Jones fracture:
Once diagnosis is made, an NWB fracture brace/cast is used for 6 wks to allow for healing
to occur. Repeat radiographs are done at this point to assess progress, but up to 12 wks
may be needed. Nonunions at 12 wks may require ORIF. The decision to pursue ORIF for
a Jones fracture in a competitive athlete may occur at the time of initial diagnosis.
Patient Education
The patient should be advised to:
Elevate the leg frequently to minimize forefoot edema
Use ice up to 20 min/hr to control swelling
Notify the physician if there is any significant increase in pain/swelling during the recovery
process
Reduce their activity level to remain pain-free and use stiff-soled shoe for all weight-bearing
activity until healing is complete
Prognosis
Good
Complications
Nonunion
Malunion with painful plantar calluses under the metatarsal head
Dorsal corns secondary to friction over prominent metatarsal head
Additional Reading
Brockwell J, Yeung Y, Griffith JF. Stress fractures of the foot and ankle. Sports
Med Arthrosc. 2009;17:149–159.
Garrick JG. Athletic foot disorders. Orthopedic knowledge update-sports

medicine, 3rd ed. American Academy of Orthopedic Surgeons. 2004:249–
261.
Goulart M, O'Malley MJ, Hodgkins CW, et al. Foot and ankle fractures in
dancers. Clin Sports Med. 2008;27(2):295–304.
Greene WB. Ed., Essentials of Musculoskeletal Care, 2nd ed. American

Academy of Orthopedic Surgeons, 2001:453–455.
Judd DB, Kin DH. Foot fractures frequently misdiagnosed as ankle sprains.
Am Fam Physician. 2002;66(5):785–794.
Kaeding CC, Yu JR, Wright R, et al. Management and return to play of stress
fractures. Clin J Sport Med. 2005;15(6):442–447.
Koval KJ. Orthopedic Knowledge Update 7 2002 American Academy of

Orthopedic Surgeons. Chapter 45 Ankle and Foot: Pediatric Aspects pgs
537–545, Chapter 46 Ankle and Foot: Trauma pgs 547–563.
Koval KJ, Zuckerman JD. Handbook of Fractures 2nd Ed. Lippincott Williams
& Wilkins; 2002:267–287, 402–406.
Meardon SA, Edwards B, Ward E, et al. Effects of custom and semi-custom

foot orthotics on second metatarsal bone strain during dynamic gait
simulation. Foot Ankle Int. 2009;30:998–1004.
Ribbans WJ, Natarajan R, Alavala S. Pediatric foot fractures. Clin Orthop

Relat Res. 2005;(432):107–115.
Safran MR, McKeag DM, Van Camp SP. The foot. Manual of Sports
Medicine. Lippincott-Raven Publishers. 1998:476–486.
Codes
ICD9
825.0 Fracture of calcaneus, closed
825.20 Fracture of unspecified bone(s) of foot (except toes), closed
825.21 Fracture of astragalus, closed
Fracture, Middle Phalanx
Michael M. Linder
Andrew Harcourt
Basics
Description
Represents 5% of all metacarpal and phalangeal fractures (1)
Shaft is the most common location for fracture.
Etiology
The flexor digitorum superficialis (FDS) and the central extensor slip (CES) insert onto the
middle phalanx and account for the primary deforming forces on shaft fractures.
Fractures proximal to the insertion of the FDS result in volar angulation of the distal fragment.
Fractures distal to the insertion of the FDS will result in volar angulation of the proximal
fragment.
The CES may also pull the proximal fragment in dorsal angulation if the fracture is proximal to
the FDS insertion.
Interphalangeal collateral ligament injuries may result in avulsion fractures affecting articular
surfaces.

Distal interphalangeal (DIP) or proximal interphalangeal (PIP) joint dislocations
Distal artery or nerve injury
Extensor mechanism injuries
Volar plate injuries and resulting swan neck deformities
Diagnosis
History
Elicit mechanism of injury:
Grabbing a jersey, jammed finger, crush, traction, or twisting
Document occupation and hand dominance.
Probe for initial deformity or excessive blood loss.
Physical Exam
Inspect for deformity, ecchymosis, swelling, and open wound.
Assess range of motion.
Assess rotational alignment (all digits should point to scaphoid tuberosity).
Assess sensation (touch, pinprick, and 2-point discrimination).
Assess capillary refill.
Assess integrity of all joint structures.
All should be compared either to contralateral side or adjacent finger.

Imaging
All fractures require anteroposterior, true lateral, and oblique with affected finger in isolation.
May require preimaging anesthesia
PIP dislocation
DIP joint dislocation
Tendon rupture
Volar plate disruption
Bone contusion
Soft tissue contusion
Treatment
Open, unstable, spiral, comminuted, or those that fail to maintain reduction
require orthopedic referral
Fractures at the base (2):
Usually result from an axial load (jammed finger)
Nondisplaced fractures should be splinted for 2 wks with a dorsal extension
block splint and then buddy-taped for wks 2–4.
Volar fractures that result from a dorsal dislocation, are nondisplaced, and
involve <30% of the articular surface are considered stable and may be
splinted for 4–6 wks.
Fractures affecting the dorsum of the base are frequently associated with
central slip attachment and may result in a boutonniere deformity; treatment
of these requires 6 wks in extension splinting.
Fractures of the shaft (2): P.
Transverse:
Nondisplaced may be treated with buddy taping for 2–4 wks.
Displaced: May attempt reduction under anesthesia (orthopedic referral
recommended); longitudinal traction and gentle manipulation of distal
fragment; a tape splint may be necessary for postreduction radiographs,
generally 15-degree angulation in the plane of motion is tolerated; if
postreduction films show adequate alignment, splint for 4–6 wks.
Fractures of the condyles (3):
Nondisplaced fractures may be managed with buddy taping for 2–4 wks.
Displaced fractures require orthopedic consultation.
Open fractures necessitate careful management:
Appropriate antibiotic coverage, sterile dressing, elevation, and splinting
maybe necessary until orthopedic consultation can be obtained.
Ongoing Care
Repeat radiographs at 2 wks may add to follow-up.
Deformity may result from no treatment or improper reduction.
Stiffness may result from overtreatment.
Referral to hand or occupational therapy is indicated for loss of function.
Return to play may be as early as 2 wks for nondisplaced simple transverse fracture, but as
long as 6 wks for more complicated fractures (4).
A goal of lifelong function should take precedence when making return-to-play decisions.
References
1. Koval KJ, Zuckerman JD. Handbook of Fractures, 3rd Ed. Philadelphia: Lippincott
Williams and Wilkins, 2006.
2. Eiff MP, Hatch RL, Calmbach WL. Fracture management for primary care, 2nd ed.
3. Browner, et al. Skeletal Trauma, 3rd ed. Philadelphia: WB Saunders, 2003.
4. DeLee JC, Drez D. Orthopaedic Sports Medicine, 2nd ed. Philadelphia: WB Saunders,
2003.
Codes
ICD9
816.01 Closed fracture of middle or proximal phalanx or phalanges of hand
816.11 Open fracture of middle or proximal phalanx or phalanges of hand
Fracture, Nasal
Daryl A. Rosenbaum
Brandon A. Bockewitz
Basics
Epidemiology
Most frequently injured and fractured facial structure due to its prominence:
3rd most commonly fractured structure of the skeleton
Most fractures occur in the lower half of the nasal bones, where they are thinner and
broader.
Etiology
The upper third of the nose is a bony tripod formed by a pair of nasal bones that meet in the
midline, with the thin perpendicular plate of the ethmoid as a weak center strut.
A pair of upper and lower lateral cartilages supported by the central quadrangular septal
cartilage make up the lower 2/3.

Fracture of other facial bones
Septal hematoma
Septal dislocation
Cribriform plate injury with leakage of cerebrospinal fluid
Laceration
Orbital fracture
Concussion
Cervical spine injury
Diagnosis
History
Force: Low-velocity trauma, such as a blow from an elbow, usually causes a simple fracture
pattern. High-velocity trauma from a stick or fast-moving ball/puck more likely causes a
complex comminuted fracture as well as associated injuries to the face, head, and cervical
spine.
Direction of blow: Lateral is most common and can cause fracture displacement and
dislocation of the septum. Direct blows can lead to nasal obstruction. Inferior blows can
disrupt the septal cartilage and nasal tip.
Physical Exam
Nasal deformity
Epistaxis
Nasal airway obstruction
Periorbital swelling and ecchymosis
Nasal bone reduction: Best if done either immediately after the injury or 3–5 days later when
swelling will not interfere with assessment
Palpate nasal bones for deformity and crepitus.
Ring test to rule out cerebrospinal fluid (CSF) leak by collecting fluid from the nose onto filter
paper to see if a clear ring of CSF diffuses out beyond the central area of blood.
Intranasal examination must be performed on each side to evaluate for a bulging septal
hematoma or septal dislocation. Use suction and a topical decongestant to control bleeding,
then a nasal speculum, otoscope, or rigid nasal endoscope along with a light source for
adequate visualization.
Palpate all bony structures of the face, including teeth, to assess for associated trauma.

Imaging
Diagnosis is clinical, as radiographs have not been shown to be helpful for diagnosis or
management (1)[A].
If suspicious for fracture of other facial bones, CT is study of choice.
Treatment
Head-up position; lean forward to aid expectoration of blood
Direct pressure, ice
Topical decongestant
Cautery of visible bleeding sites in Kiesselbach plexus using silver nitrate sticks
For refractory epistaxis, may have to pack both sides of the anterior nose with
a tampon or antibiotic-soaked petrolatum gauze
Posterior epistaxis can require inflation of a Foley bulb within the nasal fossa in
addition to anterior packing to achieve hemostasis.
In-Patient Considerations P.
Can consider immediate closed reduction before swelling develops if the nose
is severely displaced and health care provider is well trained
In most cases, simply provide analgesics and re-examine in 2–5 days.
Adults with nondisplaced fractures that cause minimal deformity may not
require reduction.
Ongoing Care
Closed reduction (2)[B]:
Ideally performed in 1st 3–6 hr after injury, before significant swelling occurs
If delayed, should be done within 10–14 days of the injury, before significant bone healing
occurs.
Indications for adult population:
Unilateral or bilateral nasal bone fracture
Nasal deviation <½ the width of the nasal bridge
Local anesthesia using a 5% or 10% topical cocaine solution is highly effective for both
analgesia and vasoconstriction, but rarely available.
Topical nasal sprays, including lidocaine, bupivacaine, and Pontocaine, are alternatives for
adequate anesthesia.
Topical vasoconstrictors, such as phenylephrine hydrochloride and oxymetazoline, provide
adequate hemostasis and decrease edema.
A 1:1 mixture of topical oxymetazoline or phenylephrine and 4% topical lidocaine has been
cited as an equally efficacious alternative to topical cocaine (3).
Blunt probe is placed within the nose and used to elevate the depressed nasal bone.
Forceps are used to reduce septal deformity.
External splint and packing for 1–2 wks
Open reduction (2)[B]:
Indications for adult population:
Extensive/complicated fracture-dislocation of nasal bones and septum
Nasal deviation <50% the width of the nasal bridge
Open fracture
Persistent nasal deformity after closed reduction
Involvement of the caudal septum
References
1. Nigam A, Goni A, Benjamin A, et al. The value of radiographs in the management of the
fractured nose. Arch Emerg Med. 1993;10:293–297.
2. Mondin V, Rinaldo A, Ferlito A. Management of nasal bone fractures. Am J Otolaryngol.

2005;26:181–185.
3. Kucik CJ, Clenney T, Phelan J. Management of acute nasal fractures. Am Fam

Physician. 2004;70:1315–1320.
4. Procacci P, Ferrari F, Bettini G, et al. Soccer-related facial fractures: postoperative

management with facial protective shields. J Craniofac Surg. 2009;20:15–20.
Additional Reading
Rubinstein B, Strong EB. Management of nasal fractures. Arch Fam Med. 2000;9:738–742.
Codes
ICD9
802.0 Closed fracture of nasal bones
802.1 Open fracture of nasal bones
Clinical Pearls
Physician responses to common patient questions:
When can I return to play after a broken nose?
It can take 6 wks for a nasal fracture to completely heal. An athlete should be
advised that returning to competition before complete healing means that
even minor contact could disrupt a minimally displaced or previously reduced
fracture and require additional intervention. A general guideline is no contact
for 1–2 wks followed by return to play while wearing a nasal protective device
for another 2–4 wks. Case reports have been published of return to play
within 7–10 days with nasal protective device worn for 4 wks post-reduction
with encouraging results (4)[C].
Fracture, Olecranon
Greg Nakamoto
Basics
Issue of fundamental concern when evaluating fractures of the olecranon is determining
whether the fracture is displaced or nondisplaced.
Nondisplaced fractures can be managed with immobilization.
Displaced fractures should be referred to an orthopedic surgeon for fixation.
Description
The olecranon is the curved process extending from the posterior proximal surface of the
ulna. It forms a large portion of the articulating surface between the ulna and the trochlea of
the humerus. The triceps inserts into the posterior third of the olecranon.
For a fracture of the olecranon to be considered nondisplaced and stable, it must be
displaced <2 mm, must not change in position with gentle flexion to 90 degrees, and must not
change in position with extension against gravity (1).
Epidemiology
Account for 10% of fractures of the adult elbow (1)
Olecranon fractures can range from simple nondisplaced fractures to complex fracture
dislocations of the elbow (1).
Olecranon fractures are uncommon in children because early in life the olecranon process is
short, thick, and relatively stronger than the distal humerus (2).
Risk Factors
Direct trauma, such as a fall onto the tip of the elbow, may cause a fracture directly and is
most often associated with isolated injuries (1).
Indirect trauma, such as a fall onto the hand with the elbow partially flexed, may cause an
avulsion owing to eccentric contraction of the triceps (1).
Fracture dislocation also is possible with a high-energy mechanism of injury. The olecranon
fragment usually displaces posteriorly (1).

Ulnar nerve injury: Occurs in 2–5% of cases (2)
Discontinuity of the triceps mechanism
Fracture dislocation of the elbow
Open fracture
Can lead to chronic pain and arthritis
Diagnosis
History
Mechanism of injury (1):
A fall or blunt trauma to the posterior elbow may cause the fracture directly.
A fall onto an outstretched hand may cause a fracture indirectly, often through avulsion by the
triceps.
A high-energy mechanism of injury increases the likelihood of fracture dislocation.
Physical Exam
Pain and swelling over the posterior elbow
Elbow effusion owing to the intraarticular component of the fracture
Painful and limited motion at the elbow
Determine if patient can extend the elbow against gravity. Inability to extend suggests either
discontinuity of the triceps mechanism or a mechanical block. Either problem merits surgical
consultation (1)[C].
Perform distal neurovascular examination. The ulnar nerve may be injured; more common in
comminuted fractures (1).
Excessive soft tissue injury, swelling, or ecchymosis may influence the timing of surgery (1).

Imaging
Standard radiographs: Anteroposterior (AP), lateral, and oblique views (1)[C]
A true lateral view is necessary to evaluate for fracture displacement and articular disruption;
slightly obliqued views are inadequate substitutes for a true lateral.
Fat pad signs: Collection of intraarticular fluid (eg, caused by intraarticular fracture) causes
displacement and hence visualization of the fat pads around the elbow. The anterior fat pad
sometimes may be visible in the normal elbow; the posterior fat pad usually is not visible on a
normal lateral radiograph and may be the only radiographic evidence of occult fracture.
Children: Often helpful to obtain radiographs of the contralateral elbow for comparison
Good-quality standard radiographs as just listed are essential for accurate diagnosis,
classification, and operative planning. In cases of isolated olecranon fracture, they also
should be sufficient, and CT scan in such cases rarely provides additional information that
alters decision making. CT scan generally is reserved for more complex fracture
combinations (1,2)[C].
Coronoid process fracture
Olecranon bursitis
Treatment
There are several systems used for classification of olecranon fractures,
including the AO classification, the Schatzker classification, and the Mayo
classification. No single classification is used universally.
The Mayo classification is useful in determining whether an olecranon fracture
should be treated surgically (1,2)[C].
Mayo type I fractures (undisplaced [<2 mm] ± communition) can be treated
nonoperatively.
Mayo type II (stable fractures with >3 mm displacement) and type III fractures
(unstable, displaced fracture dislocations) should be treated surgically.
In the specific case of avulsion fractures, treatment is generally operative (1,3)
[C].
Nondisplaced fractures: Unnecessary
Displaced fractures: Surgical reduction and fixation
Fracture dislocation: See “Elbow Dislocation.”
Immobilization of nondisplaced fractures: While it is generally agreed that
stable nondisplaced fractures of the olecranon can be managed
nonoperatively, there are varying protocols for the duration of strict
immobilization.
Traditionally, a more conservative approach treated all nondisplaced olecranon P.
fractures in a long-arm cast with the elbow in 90 degrees of flexion for 3–4 wks,
followed by protected range-of-motion exercises (1,2)[C].
Follow-up x-rays are obtained 5–7 days after cast application to ensure that
displacement has not occurred.
Flexion past 90 degrees is avoided until complete radiographic bony healing
at 6–8 wks.
To avoid excessive stiffness, elderly patients are allowed to start range of
motion before 3 wks if pain allows.
Other authors advocate even earlier motion (3)[C].
Patient is immobilized at 90 degrees in a splint or cast for 7–10 days.
After 7–10 days, the patient starts gentle motion, beginning with pronation
and supination.
At 2–3 wks, limited flexion and extension exercises can begin.
Flexion past 90 degrees can occur when radiographs show complete bone
healing.
Repeat standard x-rays weekly until evidence of healing to ensure that there
is no displacement requiring surgical referral.
Splinting: If there is a delay until definitive treatment can be accomplished, then
temporary splinting may be done for patient comfort and protection.
Undisplaced fractures should be splinted with the elbow flexed at 90 degrees
and hand in neutral position.
Displaced fractures should be splinted in a comfortable position with the
elbow between 45 and 90 degrees and hand in neutral position; prompt
orthopedic consultation should be obtained.
Elderly patients with undisplaced fractures: Because of their propensity to
develop stiffness at the elbow, elderly patients should spend much less time
immobilized. In patients most prone to stiffness, joint immobilization can be
achieved with a sling initially, and careful range of motion can begin once the
patient is comfortable as soon as a few days later.
Ice and oral analgesics are useful in the prehospital setting. Oral analgesics
may be required for several days after casting.
Nondisplaced fractures: Protected range of motion advanced as described
earlier. If the patient still has stiffness, then dynamic splinting and physical
therapy referral for elbow range of motion may be of benefit.
Displaced fractures: Range of motion to be initiated as determined by the
operating surgeon.
Referral is required for all displaced fractures, including avulsion fractures,
unstable fractures, and fracture dislocations (1,2)[C].
Ongoing Care
Nondisplaced fractures (Mayo type I): Can be released to home in a splint or cast with
follow-up x-rays in 1 wk
Displaced fractures: Disposition determined in consultation with an orthopedic surgeon
Complications
Loss of motion:
Typically 10–15 degrees of extension in isolated olecranon fractures (1)
Motion may improve somewhat for up to 2 yrs after injury (2).
Nonunion is reported in 1–5% of patients (1,2).
Heterotopic calcification occurs in 13–14% of patients (2).
Painful hardware requiring subsequent removal is one of the most common
complications after internal fixation; reported in up to 80% of patients (1,2).
References
1. Veillette CJ, Steinmann SP. Olecranon fractures. Orthop Clin North Am.
2008;39:229–236, vii.
2. Pritchett J, Porembski M. (2006) Olecranon fractures. eMedicine.

Retrieved Aug 11, 2009, from
http://emedicine.medscape.com/article/1231557-overview.
3. Sanchez-Sotelo J, Barwood S, Blaine T. Current concepts in elbow fracture

care. Curr Opin Orthop. 2004;15:300–310.
Additional Reading
Bartlett III C. Elbow fractures. Curr Opin Orthop. 2000;11:290–304.
Karlsson MK, Hasserius R, Karlsson C, et al. Fractures of the olecranon: a

15- to 25-year followup of 73 patients. Clin Orthop Relat Res. 2002;403:205–
212.
Morrey BF. Current concepts in the treatment of fractures of the radial head,
the olecranon, and the coronoid. Instr Course Lect. 1995;44:175–185.
Nork SE, Jones CB, Henley MB. Surgical treatment of olecranon fractures.
Am J Orthop. 2001;30:577–586.

Schippinger G, Seibert FJ, et al. Management of single elbow dislocations.

Arch Surg. 1999;384(3):294–297.
Codes
ICD9
813.01 Fracture of olecranon process of ulna, closed
813.11 Fracture of olecranon process of ulna, open
Clinical Pearls
The goal when evaluating fractures of the olecranon is determining whether the
fracture is nondisplaced and stable versus displaced and/or unstable.
For a fracture of the olecranon to be considered nondisplaced and stable, it
must be displaced <2 mm, must not change in position with gentle flexion to 90
degrees, and must not change in position with extension against gravity.
The assessment of stability and displacement usually can be made with
standard radiographs and clinical examination. CT scan is rarely necessary for
isolated olecranon fractures.
Stable, nondisplaced fractures (Mayo type I) can be treated nonoperatively.
Other fractures merit orthopedic consultation for consideration of surgical
treatment.
Physician response to common patient question:
How long do I need to wear this cast/sling?
Nondisplaced fractures: In the case of a stable fracture in a reliable
patient, immobilization is for comfort and can be discontinued after initial
pain and swelling have resolved in 7–10 days (even less in the elderly
patient prone to stiffness). If the patient is at particular risk for displacing an
otherwise stable fracture, immobilization in a long-arm cast for up to 3 wks
may be required.
Displaced fractures: Depends on the extent of injury and type of repair
required
Fracture, Orbital
Kelly T. Mitchell
Basics
Description
Types of orbital fractures:
Orbital rim: Caused by direct blow to bony orbit
Orbital wall: Caused by blunt trauma to globe
Blowout fracture: Most common; fracture fragment is directed away from the bony orbit.
Blow-in fracture: Trauma typically directed against frontal bone or maxilla; fracture
fragment(s) is displaced toward the orbital space.
Orbital anatomy:
Bony orbit is a conical structure.
Base faces anterolaterally.
Apex originates posteromedially.
Seven bones
Anterior rim comprised of maxilla, zygoma, frontal bones
Orbital roof:
Frontal bone, orbital process
Sphenoid bone, lesser wing
Forms floor of frontal sinus
Medial wall:
Ethmoid bone
Lamina papyracea
Thinnest portion of the orbit
Sphenoid bone
Maxillary bone
Lacrimal bone
Forms walls of ethmoid sinus, sphenoid sinus, and nasal cavity
Orbital floor:
Zygomatic bone
Maxillary bone
Palatine bone
Forms roof of maxillary sinus
Most commonly fractured area of orbit
Lateral wall:
Sphenoid bone
Zygomatic bone
Frontal bone
Unique aspects: Not bordered by a sinus; thickest of the orbital walls
Epidemiology
1/3 of orbital blowout fractures are sustained during sport. Other causes include motor
vehicle accidents, assaults, and falls.
Eye injury is the second leading cause of visual impairment after cataract.
40% of monocular blindness is due to eye trauma.
57% of eye injuries were sustained by individuals under 30 yrs of age.
Males sustain around 80% of eye injuries.
13% of serious eye injuries are related to sports and recreation.
Estimated 1,400 of every 100,000 U.S. citizens will sustain an eye injury in their lives (1).
Incidence
Trauma to the eye represents 3% of all ED visits in the U.S. (2).
The eye represents 0.3% of the body's total surface area.
Whole-person impairment or disability from loss of vision:
One eye, 24%
Both eyes, 85%
Prevalence
Around 2.5 million new eye injuries occur annually.
Eye trauma is the cause of 40,000–60,000 new cases of blindness each year.
Annually, 11,000 eye injuries sustained by children are caused by toys or home playground
equipment (1).
Risk Factors
Most common causes of orbital fracture:
Sporting events
Falls
Assaults
Sports most commonly associated with orbital fracture (3):
U.S.:
Baseball
Football
Basketball
Racquetball
United Kingdom and Australia:
Soccer
Rugby
Cricket
General Prevention
Use of eye protection for any sport where an object or another participant may impact the
globe.
Etiology
Blowout fractures:
Occur within bony orbit
Usually along:
Medial wall and/or
Orbital floor
Orbital rims are intact.
2 proposed theories:
Hydraulic theory (3):
Blunt object of larger than diameter of the orbital entrance strikes the eye.
Compresses globe, resulting in sudden increase in intraorbital hydraulic pressure
Globe does not rupture.
Increased intraocular pressure dissipates via soft tissues to weakest portions of orbit:
Posteromedial orbital floor, lamina papyracea of ethmoid bone, or medial orbital wall.
Buckling theory (4):
Fractures occur as a result of direct trauma to the inferior orbital rim.
Causes buckling of the orbital floor
Thinnest area fractures

Ocular injury is associated with blowout fracture 14–40% of the time (5).
Potential associated injuries:
Mild ocular injuries:
Conjunctival laceration
Corneal abrasion
Vision threatening injuries:
Corneal laceration
Globe rupture
Hyphema
Traumatic iridocyclitis
Acute glaucoma
Lens subluxation/dislocation
Posttraumatic cataract
Vitreous hemorrhage
Retinal detachment/tear
Commotio retinae, traumatic retinal swelling
Foreign body: Intraocular or intraorbital
Optic nerve injury
Orbital emphysema with ocular vascular compromise
Injuries to ocular adnexa:
Eyelid contusion ± ecchymosis
Eyelid laceration ± margin involvement
Canthal injury, laceration or avulsion
Traumatic ptosis
Intracranial injuries:
Pneumocephalus
Cerebral injury
Cerebrospinal fluid leak
Delayed complications:
Enophthalmos
Hypoglobus
Diagnosis
History
Timing
Mechanism:
Penetrating trauma:
Energy/velocity
Type of material
Size of object
Nonpenetrating trauma
Location
Protective eyewear in use
Visual symptoms:
Change in vision
Diplopia
Discharge
Flashing lights
Floaters
Pain
Photophobia
Prior ocular history:
Contact lens use
Previous visual impairment/visual correction
Prior trauma
Surgical history
Tetanus status
AMPLE history:
Allergies
Medications
Past medical history
Last meal
Events/environment related to injury (2)[C]
Physical Exam
Signs and symptoms include (4)[B]:
Decreased vision
Diplopia
Enophthalmos
Exophthalmos
Hypoesthesia in V2 distribution:
Infraorbital
Cheek
Lateral nose
Upper lip
Intraorbital emphysema
Nosebleed
Periorbital ecchymosis
Step-off abnormality of bony structures
Physical examination includes the following (2)[C]:
Neurologic survey first
If neurologically intact, then initial visual acuity (VA) to evaluate for emergent visual
changes
Perform exam in systematic manner.
Avoid placing pressure on globe; risk of vitreous herniation if globe is ruptured
If no emergency visual changes, more detailed VA determination
Visual acuity before manipulation of eye
Near vision (near-reading card or other readily available reading material)
Far vision (Snelling chart)
Patient should use his or her corrective lenses (not contacts).
Use pinhole occluder if not available
Patient unable to see well enough to read
Display number of fingers
Detection of hand motion
Light perception or lack of
Examine head, scalp, face, periorbital tissues
Lacerations: Location, depth, length
Lid edema
Foreign body
Sensory deficit
Bony tenderness to palpation around orbital rim
Orbital rim fracture
Step-offs: Blowout fracture
Exophthalmos
Enophthalmos
Deformity of external eye structures:
Conjunctiva:
Blood (subconjunctival hemorrhage)
Chemosis (swelling)
Foreign bodies
Exposed tissue
Cornea:
Fluorescein stain/cobalt blue light
Irregularities (abrasion, laceration, ulceration)
Foreign bodies
Extraocular motility: Generally decreased motility may be due to edema.
Impaired upward gaze: Orbital floor fracture
Impaired downward gaze: Inferior rectus or oblique muscle entrapment
Internal structures: Iris/pupil:
Size, shape, symmetry
Reaction to light
Swinging flashlight test: Afferent pupillary defect is present if the pupil of the affected eye
dilates when exposed to the light source.
Intraocular pressure: Use tonopen; do not use Schiotz tonometer or manual pressure.
Funduscopic exam:
Red reflex presence or absence
Decreased intensity can imply vitreous hemorrhage or large retinal detachment
Central retinal artery pulsations
Slit-lamp exam:
If available: Anterior chamber, cornea, iris, lens
If not available, use penlight to look for:
Hyphema
Obvious laceration
Shrunken-appearing globe

Imaging
Plain-film radiographs:
Rarely used for diagnosis in orbital trauma
High false-negative rate: 50%
Nondiagnostic rate 30% (3)[B]
If ordered:
Waters' view best displays inferior orbital rims, nasoethmoid bones, maxillary sinuses.
Teardrop sign represents orbital contents herniated into maxillary sinuses.
Air–fluid levels/opacifications of sinuses that may indicate fracture
Orbital emphysema: Medial wall blowout fracture
CT scan:
Reference standard imaging modality
Thin-sliced helical CT with coronal reconstructions:
Improved image quality
Reduced radiation to lens
If helical CT scan not available (5)[B]:
CT scan with slices of 3 mm or less
Axial plane and
Coronal plane
Only way to assess orbital floor and roof
Sagittal reconstruction helpful
Sensitivity 79–96%
Vegetable or other organic foreign bodies may not be visualized. Increased risk of
endophthalmitis
May help distinguish between orbital edema and entrapment of extraocular muscles
Findings may predict future enophthalmos or diplopia: May play a role in prompting surgery
US:
Useful when:
CT scan impractical
Unable to retract eyelids
May see periorbital emphysema with orbital fracture
Contraindicated if high suspicion of rupture
MRI:
Limited usefulness in acute stages of ocular trauma
Do not perform if metallic intraocular foreign body may be present.
Helpful if suspicion of optic nerve injury
May identify organic foreign body
Treatment
Not emergent unless:
Visual impairment
Globe injury
Immediate referral to ophthalmology for open globe injury, facial fracture,
symptomatic orbital emphysema, orbital compartment syndrome, retrobulbar
hemorrhage, and optic neuropathy and to rule out other ophthalmologic injuries
Pre-Hospital
Airway, breathing, and circulation (ABCs) first priorities
Cervical spine immobilization and neurologic evaluation
Control active bleeding with direct pressure.
No direct pressure to orbit if open globe is possible or suspected.
Cover with a protective shield, and refer to ophthalmologist immediately.
Medication
The use of prophylactic antibiotics is controversial.
Prudent when fracture communicates with sinus.
Nose blowing increases the risk of orbital cellulitis.
General Measures
Cold packs for at least 48 hr (4)[B]
Nasal decongestants
Elevate head of bed.
Avoid nose blowing.
Avoid Valsalva maneuvers such as coughing.
Sneeze with mouth open.
Tetanus booster if not current
Pain control to include acetaminophen, NSAIDs, narcotics, and local
anesthetics
Avoid aspirin.
P.
Surgical goal (4)[B]:
Reconstruct the defect area of the fractured wall
Does not attempt to achieve bone healing
Strong surgical indications:
Diplopia, not improving
Enophthalmos >2 mm
Fracture >50% of floor
Increase in orbital volume >1 cm3
Lack of ocular motility
Significant hypoglobus
Lesser degrees of trauma indications controversial
Timing of surgery is controversial.
Rarely urgent:
Oculocardiac reflex present
Ocular motility lesions in children
Muscle entrapment in trapdoor fracture
Penetrating craniocerebral injuries
Concern for optic nerve compression
Appropriate timing important for achieving good results:
Delay allows for:
Orbital swelling resolution
Assisting in ensuring accurate diagnosis
Strengthens indications for surgery
No consensus on best material for repair
Ongoing Care
Return to play:
Based on significance of ocular injury and associated findings
Fracture only:
Noncontact sport: 2 wks
Contact sport: 4–6 wks
Surgery for fracture:
Return will vary.
Depends on specific repair required
Return to activities with proper eye protection
Patient Education
Return sooner than planned follow-up for:
Intense eye pain
Change in vision
Proptosis
Tense globe
References
1. May DR, Kuhn FP, Morris RE, et al. The epidemiology of serious eye injuries from the
United States Eye Injury Registry. Graefes Arch Clin Exp Ophthalmol. 2000;238:153–157.
2. Bord SP, Linden J. Trauma to the globe and orbit. Emerg Med Clin North Am.
2008;26:97–123, vi–vii.
3. Petrigliano FA, Williams RJ. Orbital fractures in sport: a review. Sports Med.
2003;33:317–322.
4. Jatla KK, Enzenauer RW. Orbital fractures: a review of current literature. Curr Surg.
2004;61:25–29.
5. Go JL, Vu VN, Lee KJ, et al. Orbital trauma. Neuroimaging Clin N Am. 2002;12:311–
324.
Additional Reading
Kontio R, Lindqvist C. Management of orbital fractures. Oral Maxillofac Surg Clin North
Am. 2009;21:209–220, vi.
Codes
ICD9
801.00 801.50 Open fracture of base of skull without mention of intracranial injury, with state
of consciousness unspecified
802.6 Closed fracture of orbital floor (blow-out)
802.7 Open fracture of orbital floor (blow-out)
802.8 Closed fracture of other facial bones
Clinical Pearls
Significant changes in visual acuity or vision loss: Possible optic nerve
compromise:
Ophthalmic emergency
Immediate ophthalmology consultation
Significant other exam abnormality: Immediate ophthalmology consultation
All other abnormalities: Ophthalmology consultation within 48 hr
To diagnose orbital fracture, helical CT scan with coronal reconstructions or
CT scan with 3-mm or smaller slices in both axial and coronal planes to assess
orbit floor and roof is essential.
Most orbital fractures will resolve without significant visual sequelae or need for
Pitfalls: Failure to diagnose orbital fracture and/or associated intracranial or
cervical spine injuries
Fracture, Patella
Aaron J. Provance
Basics
Direct trauma: Often comminuted but minimally displaced; associated with fractures of the
tibia, femur, and hip, as well as posterior hip dislocation
Indirect trauma: Exertional loading of the extensor mechanism beyond the tensile strength of
the patella; often with unexpected knee flexion; frequently transverse with significant
displacement and disruption of the extensor retinaculum
Pediatric sleeve fractures: Cartilage of the inferior pole of the patella is pulled off, often with
a small avulsed bone fragment. This occurs with a vigorous contraction of the quadriceps
muscle group when the knee is in a flexed position (1)[C].
Patellar subluxation or dislocation: Associated with osteochondral fractures of the medial
facet of the patella; avulsion fractures of the medial aspect of the patella can occur at the
attachment of the medial retinaculum.
Epidemiology
Incidence
1% of all fractures
Usually 20–50 yrs of age
Patellar sleeve fractures occur between 8 and 12 yrs of age.
Osteochondral fractures are common in the adolescent years.
Incidence of osteochondral fractures (patellar and femoral) in patients with first-time
traumatic dislocations was found to be 24% in a recent systematic review (2)[A].
Predominant gender: Male > Female (2:1)
Diagnosis
Transverse (50–80%): Usually displaced, of the middle and lower thirds; in the adult
population, most patellar fractures sustained during sports participation are of the transverse
type (3)[C]. They often result from a strong quadriceps contraction, such as in a partial fall or
in jumping sports; also with associated direct trauma.
Stellate (30%): Usually comminuted and nondisplaced; often secondary to high-impact direct
trauma in sport or motor vehicle accidents
Longitudinal (12–25%): Due either to trauma (especially of the lateral facet) or to
subluxation/dislocation of the patella; often in adolescents, with resulting osteochondral
fragments
Sleeve fractures: Significant articular cartilage and a small bony fragment avulsed from the
distal pole; often difficult to see on plain films; may have an ipsilateral patella alta
Stress fractures: Usually elderly, osteopenic patients with anterior knee pain after minor
trauma
History
Activity (partial fall, exertional strain, etc.)
Trauma (object, direction, force)
Subluxation or dislocation
Popping or snapping
Locking or joint instability
Difficulty weight-bearing
Speed and extent of swelling
Characterization of pain
Constitutional symptoms, especially with delayed presentation or evidence of infection
Previous knee injuries
Past medical and surgical history
Medications and allergies
Physical Exam
Tenderness to palpation and pain with passive motion of the patella
Hemarthrosis or diffuse soft tissue swelling of the knee
Limited range of active leg extension owing to disruption of soft tissues
Pain and tenderness with palpation
Pain with passive motion
Palpable step-off defect
Effusion or soft tissue swelling
Distal neurovascular status
Full range of active knee extension implies preservation of extensor mechanism.
Rule out associated injuries, especially hip, femur, leg, and ankle.
Soft tissue injuries, contamination, or signs of infection
Stress testing of ligaments should be delayed until after radiographic evaluation if there are
concerns of growth plate injury in children.
Open fractures should be ruled out owing to the risk of osteomyelitis and septic arthritis;
saline may be injected intraarticularly after aspiration of hemarthrosis to test for suspected
communication with soft tissue injuries.
Patellar apprehension test is used to help identify acute patellar dislocation.

Imaging
Anteroposterior (AP) and lateral radiographs: Used to evaluate patella, distal femur, proximal
tibia, and soft tissues. The AP view can help to determine fracture lines, and the lateral view
can help to determine the number of fragments and commination (3)[C].
Axial (sunrise, merchant) views: Help to identify osteochondral medial patellar avulsion and
other longitudinal fractures. Comparison views of the contralateral side should be used to
help determine fractures. Sunrise view (90 degrees of flexion) can be very difficult to obtain
with lack of range of motion (ROM) and pain. Merchant view (30–60 degrees of flexion) may
be easier to obtain acutely.
CT scan: Used to detect suspected occult fractures
Bone scan: Used to evaluate stress reactions, stress fractures, and osteomyelitis
MRI: Used to evaluate suspected soft tissue injuries and patellar sleeve and osteochondral
fractures. MRI is a critical tool for evaluating the severity of an osteochondral defect and
assessing the true extent of injury to the extensor mechanism with patellar sleeve fractures
(1)[C].
All patients with first-time traumatic dislocations should be suspected of having an
osteochondral injury until proven otherwise by MRI, CT scan, or continued clinical examination
(2)[A].
Osteochondral fractures have been reported to be missed on 30–40% of initial radiographs
based on MRI studies and surgical findings (2)[A].
Bipartite patella: Usually bilateral and not associated with point tenderness, with rounded
edges at the proximal lateral corners of the patellae
Acute patellar dislocation: Moderate to large hemathrosis and positive apprehension sign;
may or may not have underlying osteochondral defect
Proximal tibia or distal femur fractures: Should be ruled out radiographically with plain films
Occult physeal injuries: May require MRI if not apparent on plain films
Anterior cruciate ligament tears: May present with moderate to large hemarthrosis; similar
mechanism of injury as patellar dislocation, but with usually less extraarticular swelling
Meniscal tears: May present with hemathrosis and lack of ROM; tenderness usually along
medial or lateral joint line
Treatment
Acute management:
Analgesia
Aspiration of hemarthrosis may be followed by injection of local anesthesia to
facilitate assessment of the extensor mechanism. Presence of fatty globules
is indicative of an osteochondral defect or occult patellar fracture (2)[A].
Consider aspiration of tense anterior hematomas.
Ice and elevation to control swelling (avoiding prolonged, direct application)
Anti-inflammatory and/or low-potency narcotic medications for pain control
Immobilization: Splinting and support in position of comfort (usually slight
flexion) to minimize quadriceps contraction and fracture distraction
Nonoperative treatment: P.
Displacement of <3 mm in any plane and <2 mm of the articular surface, as
well as full range of active knee extension
The athlete's ability to straight-leg raise against gravity is crucial when
selecting treatment options (3)[C].
Compressive dressings and aspiration of hemarthrosis (if present) before
cast application may help to control edema and discomfort.
Immobilization in full extension in a long-leg cast with weight-bearing as
tolerated for 3–6 wks
Weekly radiographs should be obtained to evaluate for possible fracture
displacement and appropriate healing (3)[C].
Progressive ROM and strengthening are used until the patient can perform a
straight-leg raise against gravity without extension lag (3)[C].
Special considerations: Open fractures: IV antibiotics and emergent referral for
extensive irrigation and debridement, usually followed by internal fixation
Displacement of >2 mm of articular step-off or >3 mm in any plane of fracture
separation
Disruption of extensor mechanism is indicated by lack of full extension against
gravity.
Open reduction with internal fixation (ORIF): Modified tension-band wiring with
either circumferential wire loops or infragmentary wires or screws (depending
on fragment configuration) in conjunction with repair of medial and lateral
retinaculum; small fragments might not be amenable to surgical fixation and
need to be resected (3)[C].
Partial patellectomy: Indicated with severe patellar comminution or inability to
restore a smooth articular surface; involves repair of retinaculum and
reinsertion of patellar or quadriceps tendon into remaining patellar fragment
near its articular surface
Total patellectomy: Reserved for severe comminution precluding retention of
any significant (>25%) patellar fragments; involves soft tissue repair with
shortening of the quadriceps tendon; loss of knee extension strength (up to
40%) is frequently reported.
Inferior pole avulsion fractures: The normal height of the patella can be
maintained by preserving the patellar pole. In a recent study, internal fixation
with use of a basket plate provided better clinical results than pole resection
and patellar tendon repair (4)[B].
Osteochondral fractures: Difficult to detect on plain films; usually heal if
nondisplaced but require arthroscopic removal or screw fixation if displaced;
associated patellar instability may be surgically corrected at the same time.
Surgery may be delayed with extensive or contaminated soft tissue injury.
Ongoing Care
Immobilization: Long-leg cast for nonoperative treatment and for 3–6 wks after partial or
total patellectomy; immediate joint motion if intraoperative fracture stability is achieved (3)[C]
Weight bearing as tolerated in a cast or locked brace: Reduces quadriceps contraction and
fragment distraction
Isometric exercises and straight-leg raises: Started within days of cast application or surgical
fixation.
ROM exercises such as continuous passive motion may be started immediately after stable
internal fixation with a delay of 3–6 wks for immobilization in nonoperative treatment and after
unstable fracture repair. Exercises should be delayed no more than 6 wks to reduce pain and
improve ROM. Active flexion and passive extension are performed until the fracture is healed
and then progress with resistance exercises (3)[C].
Resistance exercises: Several months of resistance exercises may be required to achieve full
strength and ROM.
Return to play when bony healing is demonstrated on AP, lateral, and merchant radiograph
views, complete extension is obtained, complete and painless range of motion are achieved,
90% of quadriceps strength is achieved, and balance and proprioception are restored (3)[C].
Check ROM and strength as compared with the contralateral side.
Repeat plain films (AP, lateral, and merchant) to document signs of healing with callus
formation and periosteal reaction.
Functional testing prior to return to sport.
Orthopaedic referral whenever criteria for nonoperative treatment are not met
Emergent referral with evidence of an open fracture
Anti-inflammatory and/or low-potency narcotic medications for pain control
Complications
Patellofemoral arthritis is the most common complication. Risk factors include
incongruence of the articular surface and damage to articular cartilage.
Treatment includes anti-inflammatory medications and physical therapy, with
patellectomy and tibial tubercle elevation reserved for severe cases.
A slight decrease in flexion is common but not usually clinically significant. Early
postoperative motion and physical therapy help to maintain ROM, with
manipulation under anesthesia and arthroscopic lysis of adhesions required if
unsuccessful.
Painful hardware: Common complication; managed by removal after fracture
union (minimum 6 mos) or tendon healing (minimum 3 mos)
Infection: Local care for superficial infections; osteomyelitis or septic
osteoarthritis may require IV antibiotics with surgical irrigation and
debridement, removal of loose hardware, and delayed closure.
Radiographic evidence of avascular necrosis consists of a sclerotic area
evident 1–2 mos after injury, usually of the proximal fragment; mostly
asymptomatic, resolving spontaneously.
Loss of fixation: Often owing to unrecognized comminution; requires surgery if
fragments are significantly displaced
Nonunion: Very uncommon; repeat surgery indicated if symptomatic.
References
1. Dupuis CS, Westra SJ, Makris J, et al. Injuries and conditions of the
extensor mechanism of the pediatric knee. Radiographics. 2009;29:877–886.
2. Stefancin JJ, Parker RD. First-time traumatic patellar dislocation: a

systematic review. Clin Orthop Relat Res. 2007;455:93–101.
3. Bharam S, Vrahas MS, Fu FH. Knee fractures in the athlete. Orthop Clin
North Am. 2002;33:565–574.
4. Veselko M, Kastelec M. Inferior patellar pole avulsion fractures:

osteosynthesis compared with pole resection. Surgical technique. J Bone
Joint Surg Am. 2005;87 (Suppl 1):113–121.
Additional Reading
Cohn SL, Sotta RP, Bergfeld JA. Fractures about the knee in sports. Clin
Sports Med. 1990;9:121–139.
Codes
ICD9
822.0 Closed fracture of patella
822.1 Open fracture of patella
Clinical Pearls
Most athletes with patellar fractures return to play the following season (3–6
mos) with little residual deficit. Return of function is more limited with
comminuted, high-impact mechanisms of injury. Strength of terminal knee
extension will be reduced by 15–30% if patellectomy is required.
If criteria for nonoperative treatment are met, studies have shown a failure rate
of <5% for fractures managed nonoperatively.
Many patients have some residual complaints, but most report good to
excellent results overall after ORIF. Slightly fewer achieve this level of
satisfaction after partial patellectomy, and fewer still after total patellectomy.
Fracture, Pelvic
David Carfagno
Basics
Children can have proportionately greater hemorrhage.
Nonaccidental trauma is a concern.
The most widely utilized classification scheme is the Young-Burgess system, which focuses
on the mechanism of injury.
Lateral compression (LC): Anterior injury-rami fractures:
The most common mechanism of pelvic fractures
This usually involves rami fractures anteriorly with a sacral impaction iliac wing fracture.
This type of injury is rotationally unstable but usually vertically stable. LC I: Sacral fracture
on side of impact; LC II: Crescent fracture on side of impact (iliac wing fracture); LC III:
Type I or II injury on side of impact with contralateral open-book injury.
Fracture of individual pelvic bone with no break in ring continuity
Isolated rami fractures: Commonly seen in falls in the elderly
Avulsion fractures: 4 types: Anterior superior, inferior iliac spine, and ischial tuberosity: The
ischial tuberosity is the most common location for apophyseal avulsion injury in the pelvis
and usually results from a forceful contraction of the hamstring muscles. Avulsion of the
ischial tuberosity is most often associated with intense athletic activity, such as sprinting, or
with excessive passive lengthening of the hamstring muscles, as often occurs during
cheerleading or gymnastics. The patient may experience a popping sensation at the time of
injury and typically presents with severe posterior thigh or gluteal pain and complains of
difficulty walking:
Iliac wing fractures (Duverney's fractures) due to direct trauma or lateral compression
Sacral fractures
Coccygeal fractures
Anterior-posterior compression (APC): Anterior injury = symphysis diastasis/rami fractures:

The 1st point of failure is the symphysis pubis. As increasing external rotation is applied,
the sacrotuberous, sacrospinous, and anterior sacroiliac (SI) ligaments fail under tension.
APC I: Minor opening of symphysis and SI joint anteriorly; APC II: Opening of anterior SI,
intact posterior SI ligaments; APC III: Complete disruption of SI joint.
Significant urogenital, vascular, and neurological injury is accompanied by the APC and
vertical shear (VS) injuries due to the stretch and traction placed on these structures as the
injuring forces are applied.
Open book fracture:
Wide separation of symphysis pubis (often >2.5 cm) associated with sacroiliac joint
disruption from anterior/posterior pelvic compression
2 ipsilateral ischiopubic rami fractures; most common Type II fracture
Symphysis pubis fracture: often associated with genitourinary injury
Vertical shear (VS type): Vertical displacement of hemipelvis with symphysis diastasis or rami
fractures anteriorly, iliac wing, sacral facture, or SI dislocation posteriorly
Combination (CM type): Any combination of above injuries:
Multiple breaks in pelvic ring continuity
High risk for associated injuries and pelvic hemorrhage
Malgaigne fracture
Anterior and posterior break in the ring on the same side
Straddle fracture:
Fractures of all 4 pubic rami or ipsilateral fracture of 2 pubic rami with dislocation of
symphysis pubis
Due to lateral compression or straddle injury (ie, fall on object)
Severe multiple fractures and crush injuries or falls resulting in multiple fractures and gross
instability
Cautions:
Pneumatic antishock garment (PASG) is an option, particularly when faced with a
prolonged transport time or hemodynamically instability.
Aggressive fluid resuscitation must occur before deflation of the PASG.
Risk Factors
Etiologies of pelvic fractures in descending order of frequency:
Motorcycle crash
Vehicle-pedestrian collision
Side-impact motor vehicle collision
Fall >15 feet
Motor vehicle crash
Etiology
The incidence of pelvic fractures in the U.S. is estimated to be more than 100,000 per year.
60% of pelvic fractures occur from motor vehicle accidents, most commonly pedestrians
struck by automobiles.
30% are due to falls from heights.
Represent the third most common cause of death in motor vehicle accidents
Mortality rate from pelvic fractures reported is 5–42%.
Increases to nearly 50% with hemorrhagic shock
Significant pelvic hemorrhage can occur in unstable pelvic fractures, particularly Type III
fractures:
Bleeding most commonly arises from the venous plexuses.
Significant hemorrhage results in retroperitoneal hematoma formation that may tamponade
in the enclosed pelvic space.
Diagnosis
Pelvic radiology is the most valuable initial diagnostic test.
A single anteroposterior (AP) view of the pelvis should be obtained as early as possible.
Most significant unstable pelvic fractures will be seen on the single AP view.
Other views include:
Inlet projection: 30° caudal view, allows visualization of posterior arch
Outlet projection: 30° cephalic angulation, allows visualization of sacrum
Judet oblique views (internal and external): Allows evaluation of acetabulum
Physical Exam
Does the patient have pelvic pain?
Are there neurologic deficits involving sciatic, femoral, or obturator nerves?
Are there contusions, ecchymoses, or abrasions at or near the bony prominences of the
pelvis?
Are there ecchymoses of the scrotum or perineum?
Is there blood at the urethral meatus?
Is there blood in or around the rectum, and is the prostate normal?
Are there open wounds of the groin, buttock, or perineum?
Is there a leg length difference, or is the resting position of one leg different from the other?
Is there pain or abnormal pelvic motion on compression of the anterior iliac spines, lateral
compression of the iliac crests, rotation of the lower extremity, or hip flexion-extension?

CT scan may further delineate pelvic fracture(s) and retroperitoneal hematoma.
MRI is indicated when there is evidence of neurologic injury.
Abdominal US or diagnostic peritoneal lavage (DPL) are rapid bedside evaluations for
intraperitoneal hemorrhage:
There is a high mortality rate in victims with pelvic fractures who undergo celiotomy;
caution must be exercised to avoid false-positive results.
In the setting of pelvic fracture, the supraumbilical open approach for DPL should be used.
Angiography may be necessary in complicated pelvic fractures where vascular concern is
an issue:
According to the Pelvic Injury Symposium in 2000, physicians can determine when
interventional radiology may be needed based on certain scenarios.
Hemodynamic instability, poorly responsive to fluid challenge, no hemoperitoneum, pelvic
fracture
Hemodynamic stability, little hemoperitoneum, pelvic fracture, more than 4–6 units
transfusion over 24 hr to 48 hr, respectively
Large or expanding retroperitoneal hematoma encountered at laparotomy or active
bleed on CT scan
Angiography is usually used in these above scenarios within the first few hours with a
90% rate of finding extravasation.
Lab
Type and crossmatch
Hemoglobin/hematocrit, platelet count, and coagulation studies (prothrombin time/partial
thromboplastin time)
Clinical signs that suggest an increased risk of ongoing pelvic fracture bleeding:
Pre-hospital hypotension
Admission base deficit >5
Persistent tachycardia in face of normal oxygenation and adequate pain control
Recurrent hypotension during resuscitation
Requirement for 6 U blood during first 24 hr
Normal variants (ie, os acetabuli epiphyseal line can mimic type I fracture on x-ray)
Ligamentous injury
Spinal injury
Intra-abdominal injury and hemorrhage
Treatment
LC-1/AP-1:
Protected weight-bearing on the affected side and treated conservatively with
bed rest, analgesics, and comfort measures
Further surgical treatment may be needed if displacement of the fracture
occurs after the patient starts to bear weight.
Follow-up x-rays can determine displacement after 2–5 days of physical
therapy.
AP-2/LC-1:
Marked displacement of the anterior ring without complete ring disruption.
Consult orthopedic surgery.
LC-II, LC-III, AP-III, and VS:
Complete disruption of the posterior ring, and in general, require stabilization
of both the anterior and posterior rings. Consult orthopedic surgery; patient
should remain NPO.
May require emergency department pelvic stabilization measures
Assess for pelvic hemorrhage (see below).
Pelvic hemorrhage:
Angiography and selective vessel embolization
Direct operative control of pelvic bleeding
Prioritization of studies: CT, angiography, or surgery:
In the hemodynamically unstable patient, a rapidly performed DPL or US can
determine treatment course:
If the DPL or US is positive, the patient should go for celiotomy with
external pelvic fixation followed by selective angiography.
If the DPL or US is negative, the patient should go to angiography.
In the hemodynamically stable patient, the patient can go to CT scan for
evaluation of the abdomen, pelvis, and retroperitoneum.
ED Treatment
Determine which pelvic fractures are stable and unstable (see “Treatment”).
Medication
Crystalloid fluids: Normal saline or Lactated Ringers, IV bolus 2 L; peds: 20
cc/kg
Blood products: Cross-matched, type-specific, or 0-negative 4–6 IU; peds: 10
cc/kg
Several factors play into the initial approach to bony stabilization, including
hemodynamic status and response to resuscitation, fracture pattern,
associated injury, and inflammatory status.
Hemodynamic status is of particular concern, as the pelvis may be the primary
source of bleeding or be contributing very little to bleeding. In the presence of
ongoing thoracic or abdominal hemorrhage, orthopedic management beyond
placement of a pelvic binder is delayed. Associated long bone fractures should
be immediately splinted with coverage of open wounds.
ABCs of trauma care:
Avoid using lower extremity IV sites.
Aggressive resuscitation with blood or crystalloid, 0-negative or type-specific
blood if hemodynamically unstable
Immobilize the pelvis to prevent further injury and decrease bleeding.
PASG: Use in emergency department (ED) is controversial, but allows rapid
pelvic immobilization and pelvic compression to slow bleeding
External fixator requires more time to place than PASG, but “splints” pelvis in a
similar manner; contraindicated in severely comminuted pelvic fracture
Placement of a stabilization device should not interfere with further workup and
care (DPL, etc.).
Admission Criteria
Hemodynamic instability, and pelvic hemorrhage to the ICU
“Triad of death” is a term coined to describe patient decompensation in the
presence of acute blood loss, resulting in hypothermia, coagulopathy, and
acidosis.
Type III or IV pelvic fracture
Other related injuries (genitourinary, intra-abdominal, neurologic, etc.)
Intractable pain
Discharge Criteria
Type I or II fractures; hemodynamically stable with no evidence of other injuries
Ongoing Care
Complications
Vascular injury leading to blood loss
Closed head injuries
Visceral injury (bladder and urethral, small bowel, diaphragm)
Nerve injury
Atelectasis/pneumonia
Musculoskeletal back pain
Sexual dysfunction
Malunion/nonunion of pelvic fracture
Additional Reading
Berger JJ, Britt LD. Pelvic fracture hemorrhage. Current strategies in
diagnosis and management. Surg Annu. 1995;27:107–112.
Cryer HM, Miller FB, Evers BM, et al. Pelvic fracture classification: correlation
with hemorrhage. J Trauma. 1988;28:973–980.
Cwinn AA. Pelvis and hip. In: Rosen P, et al., eds. Emergency medicine:
concepts and clinical practice. 4th ed. St. Louis: CV Mosby, 1998:739–762.
Fulkerson EW, Egol KA. Timing issues in fracture management—a review of

current concepts. Bull NYU Hosp Jt Dis. 2009;67:58–67.
Jerrard DA. Pelvic fractures. Emerg Med Clin North Am. 1993;11:147–163.
Kobziff L. Traumatic pelvic fractures. Orthop Nurs. 2006;25:235–241.
Rice PL, Rudolph M. Pelvic fractures. Emerg Med Clin North Am.
2007;25:795–802, x.
Sanders TG, Zlatkin MB. Avulsion injuries of the pelvis. Semin Musculoskelet
Radiol. 2008;12:42–53.
Codes
ICD9
808.0 Closed fracture of acetabulum
808.2 Closed fracture of pubis
808.41 Closed fracture of ilium
Fracture, Posterior Malleolus
Steven G. Reece
Basics
Description
Ankle fracture involving the posterior malleolus
Isolated posterior malleolus fractures result from vertical loading or anterior displacement of
the tibia when the foot is planted.
Epidemiology
Isolated posterior malleolus fractures are very uncommon.
1% of all ankle fractures
Risk Factors
Osteoporosis
Repetitive vertical loading
Etiology
Abduction or external rotation, posterior displacement of the talus, vertical loading, or
combinations of these forces, cause fractures of the posterior malleolus.

Associated soft tissue ankle injuries (lateral, deltoid, and syndesmotic injuries)
Bimalleolar or trimalleolar (posterior malleolus fractures in conjunction with lateral malleolus
fractures, medial malleolus fractures, or both)
Fracture patterns can be suggestive of posterior malleolar involvement:
Tibial spiral fractures often associated with occult posterior malleolar involvement; use CT
scan to evaluate
Diagnosis
Diagnosis of posterior malleolar fractures hinges on high degree of suspicion in the right
acute or chronic clinical setting.
History
Very important to obtain exact mechanism of injury:
Posterior malleolus fracture has been described in association with external rotation-
abduction injuries (1).
History should address chronic vs acute.
Physical Exam
Consider a fracture if patient is unable to bear weight or has significant swelling or
ecchymosis in acute setting.
Chronic presentation: “Sprain” that persists in being painful but is not unstable
Observe for obvious deformity, ecchymosis, and swelling.
Palpate for pain, starting away from area of maximal tenderness, and compare to uninvolved
foot.
Check for ligamentous laxity.
Assess neurovascular status.
Assess ability to bear weight and gait.

Imaging
X-rays needed to confirm diagnosis 2:
Anteroposterior (AP), lateral, and mortise views should be obtained.
Use of stress views remains controversial because there are no standard techniques for
anesthesia, positioning, or force used to elicit instability.
External-rotation lateral view of the ankle often helpful
CT and MRI sometimes used to evaluate complex ankle fractures:
CT recommended if high clinical suspicion and negative plain films (3)
Acute setting:
High-grade ankle sprain
Lateral/medial malleolus fractures
Achilles' tendon injury
Peroneal tendon subluxation and dislocation
Chronic setting:
Os trigonum syndrome
Treatment
Posterior splint with compression wrap
Ice, elevation
Crutches and make nonweight-bearing
Opioid analgesics vs NSAIDs (4):
NSAIDs use with fractures in question
Follow-up in 1 wk if no emergent surgical indications present
If >25% of the articular surface is involved, or if the fracture is displaced >2
mm, then open reduction internal fixation (ORIF) is recommended.
If ORIF is not chosen, closed reduction still is needed
Oblique plain films postreduction, in addition to AP, lateral, and mortise views
CT scan may be indicated.
Nonweight-bearing posterior splint for 1 wk:
Cast for total of 6 wks if fracture nondisplaced
If fracture is displaced, then surgical repair (ORIF)
Medication
Opioid use vs NSAIDs (4):
Use of NSAIDs recently brought into question in fracture care pain
management
NSAIDs shown to potentially negatively affect fracture repair
Physical therapy after both operative and nonoperative care:
Regain full range of motion, strength, and proprioception
If >25% of the articular surface is involved, or if the fracture is displaced >2
mm, then ORIF is recommended.
When associated with syndesmosis injury, fixation of posterior malleolus may
be preferred over syndesmotic screw (5).
Ongoing Care
Orthopedic referral should be considered for any isolated fractures of the posterior malleolus
because they often are complicated by other injuries.
Patient Education
It is important to discuss that ankle sprains and fractures often are difficult to differentiate.
If diagnosed ankle sprain, persistent symptoms (pain, swelling, limp) warrants follow-up and
further workup
Many different outcomes exist, depending on the severity and type of ankle fracture:
Compliance is critical.
Prognosis
Isolated posterior malleolar fractures have an excellent prognosis.
Those posterior malleolar fractures associated with significant comorbid fractures and/or
syndesmotic injuries are much more likely to have long-term issues:
Post-traumatic arthritis
Loss of normal range of motion
Complications
See “Prognosis.”
References
1. Clanton TO, Porter DA. Primary care of foot and ankle injuries in the
athlete. Clin Sports Med. 1997;16:435–466.
2. Leddy JJ, Smolinski RJ, Lawrence J, et al. Prospective evaluation of the

Ottawa Ankle Rules in a university sports medicine center. With a modification
to increase specificity for identifying malleolar fractures. Am J Sports Med.
1998;26:158–165.
3. Boraiah S, Gardner MJ, Helfet DL, et al. High association of posterior

malleolus fractures with spiral distal tibial fractures. Clin Orthop Relat Res.
2008.
4. Harder AT, An YH. The mechanisms of the inhibitory effects of nonsteroidal
anti-inflammatory drugs on bone healing: a concise review. J Clin Pharmacol.
2003;43:807–815.
5. Gardner MJ, Brodsky A, Briggs SM, et al. Fixation of posterior malleolar

fractures provides greater syndesmotic stability. Clin Orthop Relat Res.
2006;447:165–171.
Additional Reading
Prokuski LJ, Saltzman CL. Challenging fractures of the foot and ankle. Radiol
Clin North Am. 1997;35:655–670.
Wedmore IS, Charette J. Emergency department evaluation and treatment of

ankle and foot injuries. Emerg Med Clin North Am. 2000;18:85–113, vi.
Codes
ICD9
824.4 Bimalleolar fracture, closed
824.6 Trimalleolar fracture, closed
824.8 Unspecified fracture of ankle, closed
Clinical Pearls
Posterior malleolar fractures rarely occur in isolation, so a high index of
suspicion is necessary when lateral or medial malleolar fractures and/or
syndesmotic injuries are diagnosed.
An undiagnosed posterior malleolus fracture can be the source of chronic pain
in the setting of ongoing pain associated with an ankle “sprain.”
Apply the Ottawa rules coupled with a few additional tips to catch these on x-
ray. If not seen on x-ray, consider CT scan.
ORIF if >25% articular surface or >2 mm displacement; otherwise,
nonoperative options are appropriate.
Fracture, Proximal Tibia
Steven G. Reece
Basics
Tibial plateau fractures occur as a result of:
Force directed either medially (valgus deformity) or laterally (varus deformity)
Axial compressive force
Combination of both
An axial compressive force, as with a fall from a height, landing on an extended knee, usually
results in a bicondylar type of fracture.
Associated ligamentous injuries have been postulated to occur owing to continued deforming
force after the fracture has been sustained.
68% of tibial plateau fractures have posterolateral ligamentous corner injury (1).
These ligamentous injuries may not always occur after the fracture but may be coincident
with the tibial plateau fracture.
Description
Fracture that includes the articular surface of the medial and/or lateral tibial condyles
Synonym(s): Tibial plateau fracture
First coined a “fender fracture” by Cotton in 1929
40–60% of tibial plateau fractures involve an automobile hitting a pedestrian. Fracture results
from a medially directed (valgus-deforming) force.
Epidemiology
Tibial plateau fractures account for 1% of all fractures and 8% of fractures in the elderly.
Lateral tibial plateau fractures account for 55–70%.
Bilateral plateau fractures account for 11–31%.
Medial plateau fractures account for 10–23%.
Risk Factors
Osteoporosis
Perioperative fracture associated with total or unicompartmental knee arthroplasty (2)
Sports: Skiing, football
Tibial plateau fractures often accompany a predictable pattern of associated soft tissue knee
injury.
Medial tibial plateau fracture: Lateral collateral ligament and medial meniscus injuries
Lateral tibial plateau fracture: Medial collateral ligament and lateral meniscus injuries
Anterior cruciate ligament injuries can be seen with either medial or lateral plateau
fractures.
Owing to brisk hemorrhage and swelling, tibial plateau fractures can be associated with
acute compartment syndrome.
Diagnosis
X-ray: Anteroposterior (AP), lateral, oblique
MRI: Better assessment of associated ligamentous injury and osteochondral injury
CT scan: Best to assess bone deformity
Schatzker classification system for tibial plateau fractures (3):
Type I: Lateral split
Type II: Split with depression
Type III: Pure lateral depression
Type IV: Pure medial depression
Type V: Bicondylar
Type VI: Split extends to metadiaphysis.
Ancillary studies: Knee aspirate may help to reveal the presence of fat globules (indicating
osteochondral injury) and to reduce pain.
History
An accurate history will help to determine the direction of the force, velocity (high vs low),
and initial deformity produced.
Swelling can be an immediate effusion or delayed ± lower leg swelling.
Physical Exam
Signs and symptoms:
Painful swollen knee
Unable to bear weight
Also may have compartment syndrome signs and symptoms
Key to diagnosing compartment syndrome is pain out of proportion to physical examination
findings.
Most accurate way to evaluate the extent of the soft tissue injuries
Allows for evaluation of the vascular and neurologic status of the extremity
Gives insight into any associated ligamentous injuries and subsequent stability of the
extremity
Pain and swelling about the knee may be associated with varus or valgus knee deformity.
Visible knee deformity indicates a severe injury.
Tenderness to palpation is noted over the medial and/or lateral tibial plateau.
Associated ligamentous injuries may show tenderness to palpation and instability of the
collateral or cruciate ligaments.
Key finding is excursion of endpoint movement.
Large hemarthrosis usually is present.
If not present, it may indicate a torn capsule if the plateau is depressed.
Document distal pulses.
Check neurologic status with focus on the peroneal nerve and tendon function.
Check for abrasions or possible open fracture.
Watch for compartment syndrome findings:
Pain out of proportion to the physical examination findings
Pressure or tightness in the compartment
Pallor
Paresthesias
Paralysis: Sign of cell death and need for immediate compartment release

Imaging
Standard radiographs in anteroposterior (AP), lateral, and 2 oblique views;
Initial x-rays may miss a small tibial plateau fracture.
High index of suspicion must be maintained based on mechanism of injury,
presence/absence of an effusion, and joint instability.
Series provides information allowing for accurate assessment of the fracture pattern.
Internal oblique view improves assessment of the lateral plateau.
External oblique view improves assessment of the medial plateau.
Tunnel view helpful if suspicious for intercondylar eminence fractures
Lateral view gives information on depression.
Medial side is concave.
Lateral side is convex.
Posterior collateral ligament injury may show avulsion fracture.
Tomography in the AP and lateral planes:
Reveals extent and position of the fracture lines.
Allows visualization of areas of depression.
CT scan:
Image of choice if negative films but high index of suspicion for fracture
Provides cross-sectional and sagittal assessment of the fracture pattern
If necessary, three-dimensional reconstructions can be provided to enhance the
understanding of the fracture.
MRI: Allows for assessment of associated ligamentous injuries; may not show fracture well
Arteriography:
Should be considered in any tibial plateau fracture where the stability of the joint is in
question.
Also may use ABI If <0.8, then indicates arterial insult.
Medial plateau fractures have a high incidence of vascular insult (owing to greater energy
injuring force).
Arteriography/ABI should be seriously considered.
Presence of a palpable pulse does not exclude the possibility of intimal tear.
May lead to intraoperative occlusive thrombosis that could jeopardize the extremity
Intercondylar eminence fracture ± anterior cruciate ligament (ACL) tear: Segond sign on plain
film indicates lateral capsule avulsion.
Collateral ligament avulsion
Tibial tubercle avulsion
Proximal fibular fracture
Patella fracture
Hemarthrosis from patellar dislocation, ACL tear, or meniscal tear (if in the red or red-white
zone)
Treatment
No more than 5 mm of depression/displacement is acceptable on for
conservative treatment.
ED Treatment
Acute treatment:
Non–weight bearing
Long leg splint with knee in full extension, ankle splinted at 90 degrees
Ice, elevation
Pain management with narcotics
If plain films show <5 mm of displacement, then nonoperative management is
acceptable.
Medication
Recent studies suggest possible negative effects of NSAIDs on bone healing
in fracture care (4).
Reasonable to consider narcotics as 1st-line agents in favor of NSAIDs
Use TROM brace locked in extension, and make the patient non–weight
bearing to improve pain control.
General Measures
Patient's age, medical condition, history of osteoporosis, and expected level of
activity should be taken into consideration on a case-by-case basis in terms of
operative vs nonoperative management.
There are no specific recommendations regarding patient age or comorbid
arthritis to dictate operative vs nonoperative management.
Nonoperative treatment is possible with hinged TROM-style bracing and strict
non–weight bearing for 2–6 wks if:
Under adequate sedation there is no varus/valgus instability through a full arc
of motion.
The fracture shows no elements of depression or <5 mm of displacement.
Referral
Emergent referral and treatment if there is associated acute compartment
syndrome and/or vascular injury
Referral recommended within 48 hr if fracture is depressed or displaced (5
mm) or associated with significant ligament/meniscal injuries
Physical therapy: See “Postoperative Management” below.
Key to good outcome is early range of motion and non–weight bearing
compliance.
Important to encourage quadriceps strengthening after bracing discontinued
The goals of treating an intraarticular fracture of the tibia are to preserve pain-
free joint mobility, stability, axial alignment, and articular cartilage congruity and
avoid posttraumatic osteoarthritis.
Best accomplished by anatomic reduction of the joint surface and restoration
of axial alignment.
Intraarticular fractures, regardless of open or closed treatment, must be
mobilized quickly to achieve the best range of motion (ROM).
Only percutaneous or open reduction and stable fixation allow early motion
without loss of articular cartilage.
Fractures treated initially by closed reduction often will show persistent
displacement of articular cartilage fragments.
If open reduction cannot be achieved owing to mitigating circumstances, then
treatment should consist of skeletal traction and early mobilization.
Bicondylar tibial plateau fractures are best managed with locked plating in favor
of external fixation (5).
Absolute surgical indications:
Open fractures
Acute compartment syndrome
Acute vascular injury
Timing of surgery: Immediate if open fractures, associated compartment
syndrome, and fractures with associated vascular injuries
Careful evaluation of fractures with tomography/CT scan/MRI is
recommended.
Delay of 24–48 hr will not compromise the outcome.
Evaluation of soft tissue injury is important.
Patients delayed >48 hr can be placed in skeletal traction.
Postoperative management:
Depends on the degree of stability achieved with fixation and the findings at
surgery
If stable, early motion by continuous passive motion (CPM) is beneficial.
Motion from full extension to 40–60 degrees of flexion on postoperative night
1.
CPM is increased to 90 degrees as quickly as possible.
If CPM is not available, immobilization of the knee in 60–90 degrees of
flexion is recommended for the first 48–72 hr, followed by active motion.
Immobilization in flexion greatly affects postoperative motion.
Non–weight-bearing ambulation is encouraged postoperatively.
Stable type I–V fractures may start partial weight bearing at 8 wks.
More comminuted fractures should be held non–weight bearing for 10–12
wks.
Early motion and non–weight bearing are critical keys to long-term
success.
Ongoing Care
Prognosis
High rate of arthritis associated with tibial plateau fractures (6)
Prognosis for full return of motion in the presence of OA is poor.
Complications
Posttraumatic arthritis
Infection
Wound slough
Loss of ROM
Compartment syndrome (preoperative and postoperative)
Fixation failure
Loss of articular reduction
Malunion
Nonunion (rare)
Deep vein thrombosis
Pseudoarthrosis
References
1. Gardner MJ, Yacoubian S, Geller D, et al. The incidence of soft tissue injury
in operative tibial plateau fractures: a magnetic resonance imaging analysis of
103 patients. J Orthop Trauma. 2005;19:79–84.
2. Kim KI, Egol KA, Hozack WJ, et al. Periprosthetic fractures after total knee
arthroplasties. Clin Orthop Relat Res. 2006;446:167–175.
3. Schatzker J. Tibial plateau fractures. Skeletal Trauma 1992;1745–1769.
4. Boursinos LA, Karachalios T, Poultsides L, et al. Do steroids, conventional

non-steroidal anti-inflammatory drugs and selective Cox-2 inhibitors adversely
affect fracture healing? J Musculoskelet Neuronal Interact. 2009;9:44–52.
5. Krupp RJ, Malkani AL, Roberts CS, et al. Treatment of bicondylar tibia
plateau fractures using locked plating versus external fixation. Orthopedics.
2009;32.
6. Ding C, Cicuttini F, Jones G. Tibial subchondral bone size and knee

cartilage defects: relevance to knee osteoarthritis. Osteoarthritis Cartilage.
2007.
Additional Reading
Stanitski CL, Harvell JC, Fu F. Observations on acute knee hemarthrosis in
children and adolescents. J Pediatr Orthop. 1993;13:506–510.
Codes
ICD9
823.00 Closed fracture of upper end of tibia
Clinical Pearls
Need to have a high index of suspicion with ligamentous injury, especially in the
setting of large swelling shortly after injury
Though tibial plateau fractures have a low overall incidence, these injury
patterns must be thought of in trauma owing to the risk of associated vascular
insult (see discussion on arteriography under “Diagnostic Tests”).
Liberal use of advanced imaging is encouraged for full understanding of the
extent of the injury, although x-ray evaluation is still considered the “gold
standard” for imaging assessment.
The keys—both for early treatment and for long-term reasonable prognosis—
lie in compliance with non–weight bearing and ROM.
Anticipate the development of osteoarthritis, and educate these patients
accordingly.
Fracture, Proximal Phalanx
James H. Lynch
Kevin deWeber
Basics
Epidemiology
2nd most common phalangeal fracture in adults
Base of proximal phalanx fracture is most common pediatric hand injury
Little finger is the most common ray involved, followed by the thumb.
Males affected 3x as often as females
Crush or direct blow to the finger accounts for more than 80% of injuries.
Etiology
Intrinsic muscles of the hand (interossei) insert into the extensor expansion on the dorsum of
the proximal phalanx.
Proximal phalangeal fractures usually angulate volarly due to the proximal fragment flexed by
interossei and the distal fragment extended by the central slip's insertion on the base of the
middle phalanx.
Normally, flexed fingertips should all point toward the scaphoid without significant overlap.
Metacarpophalangeal (MCP) joint collateral ligaments are taut in 70–90° of flexion and
provide stabilization of the MCP joint.

Digital nerve injury: Contusion, transection
Digital artery injury: Open or closed fracture; usually does not require treatment
Tendon injury: Complete or partial rupture; infrequent with proximal phalangeal fracture
Thumb avulsion fracture common with ulnar collateral ligament injury (skier's thumb)
Diagnosis
History
Mechanism of injury: Direct blow, axial load, axial traction, twisting/torque, or “grabbing a
jersey”
History of previous injury, surgery, or deformity
Review treatment rendered
Physical Exam
Pain, swelling, bruising, tenderness, loss of motion, and function are typical findings.
Gross deformity in some cases
Open (compound) fractures usually are obvious and require emergent care.
May be mistaken for metacarpophalangeal (MCP) or proximal interphalangeal (PIP) joint
dislocation
Malrotation is common with spiral and oblique shaft fractures, and must be detected and
corrected early.
Inspection/observation: Location and degree of deformity, swelling, and ecchymosis
Rotational malalignment: With MCP and PIP flexed to 90°, all fingers should point toward the
scaphoid. When viewed “end on,” the plane of all fingernails should be symmetrical.
Range of motion (ROM): Usually decreased. Compare with contralateral side.
Palpation: Feel for crepitus. Determine point of maximal tenderness.
Provocation: Axial loading or distraction often results in pain at the fracture site.
Adjacent structures: MCP and PIP joints, tendon function, and soft tissues
Neurocirculatory function: Sensation, capillary refill, skin color, and temperature

Imaging
Radiographs should be obtained before any manipulative examination.
Anteroposterior (AP), true lateral, and oblique views are diagnostic.
For the thumb, which is out of plane from the fingers, obtain Robert's view and Bett's view
(1).
Describe rotation of fragments, angulation, and intra-articular vs extra-articular.
Differences in diameter of fragments suggest rotation.
MCP joint dislocation
PIP joint dislocation
Soft tissue contusion, sprain, strain, or rupture
Treatment
Open (compound) fractures: Sterile wet dressing, ice, elevate, splint, refer
to orthopedic surgeon:
Antibiotics not routinely necessary if aggressive irrigation/debridement is
adequate (2)[C].
Cephalosporin or penicillin to cover Staphylococcus aureus for
contaminated wounds
Tetanus toxoid and/or immune globulin if indicated
Reduction of fracture fragments to anatomical positions is desired to speed
healing and maximize hand function. Closed reduction is often successful and
should usually be attempted.
After reduction, immobilization should be applied and postreduction imaging
should be obtained.
Pre-Hospital
Apply sterile dressing over any open wounds.
Splint in a position of comfort, apply ice if available, and transport for
radiographs and definitive treatment.
ED Treatment
Stable, nondisplaced without angulation or rotational deformity:
Dynamic splinting (“buddy taping”) to an adjacent normal digit
Use absorbent material between digits for padding and to prevent
maceration.
Early ROM: Patient should use the hand normally as comfort allows.
Nondisplaced and impacted fractures:
Some degree of intrinsic stability; do not require surgery
Splint or short arm cast in the safe position (wrist dorsiflexed 30°, MCP joint
flexed 70–90°, IP joints extended) for 3 wks. This position of function shifts
the extensor aponeurosis distally to cover the majority of the proximal
phalanx dorsally, which compresses and stabilizes the fracture.
Displaced or angulated transverse midshaft:
Volar angulation common, generally unstable, with variable response to
closed reduction, which should be attempted
Technique:
Metacarpal or digital block
Longitudinal traction and flexion of the MCP joint with manual realignment of
fracture fragments
If reduction achieved/maintained, apply gutter splint or Burkhalter splint
(dorsal slab of stabilizing material placed from the end of a short arm cast
to just proximal to the PIP, with MCP joints flexed 70–90°)
If reduction not achieved after splinting, refer to ortho/hand.
Displaced fractures of the base:
Significant volar angulation requires reduction
Technique:
Metacarpal or digital block
Longitudinal traction and flexion of the MCP joint and correct volar
angulation with direct pressure
If reduction achieved/maintained, apply gutter or Burkhalter splint; if not,
refer to ortho/hand.
Unstable: oblique—condylar (lateral or medial aspect of base), displaced or
angulated—and displaced intra-articular fractures:
Refer to ortho/hand for pin fixation or open reduction internal fixation (ORIF).
AP, true lateral, oblique to confirm reduction P.
Unacceptable, unstable, or unsure alignment: Early consultation with orthopedic
surgeon advised
Persistence of significant displacement, angulation of more than 10°, intra-
articular component, or any degree of rotational malalignment necessitates an
orthopedic surgeon consultation(3)[C]
Medication
Oral analgesics may be used if needed; NSAIDs should be used with caution in
acute fractures since they may impair acute fracture healing.
Digital or metacarpal block with local anesthetics may be used if reduction or
repair of associated soft tissue injury is required.
Referral
The following phalangeal fractures in children warrant prompt orthopedic
consultation, since many will require immediate surgery (4)[B]:
Phalangeal neck or condyle fractures: Failure to treat this injury with pin
stabilization can result in a malunion that limits digital flexion.
Malrotation fractures
Widely displaced, irreducible proximal phalanx base fractures (due to
entrapment of soft tissue)
Avulsion fractures of the thumb MCP ulnar collateral ligament insertion
(pediatric equivalent of skier's thumb, usually a displaced Salter-Harris Type III
intra-articular fracture)
Ongoing Care
On follow-up x-rays, any malalignment should prompt an orthopedic surgeon consultation.
Patient Monitoring
Monitor specific fractures as follows (5)[B]:
Stable, nondisplaced without angulation or rotational deformity, treated with buddy taping:
Dynamic splinting for 3 wks; x-ray at 7–10 days to check alignment and stability
Daily ROM exercises after 1 wk as comfort allows
Continued dynamic splinting for athletic activities for another 4–6 wks
Nondisplaced and impacted fractures treated with splint or cast:
Recheck radiographs in 7–10 days to assess healing.
After 3 wks, early protected mobilization with buddy taping
Displaced or angulated transverse midshaft treated with closed reduction and splint or cast:
X-ray at 5 and 10 days to assure reduction is maintained; if not, refer to ortho/hand.
If reduction maintained, continue splint for 3–4 wks; if reduction fails, refer to ortho/hand
for ORIF or percutaneous fixation.
Displaced fractures of the base:
X-ray at 5 and 10 days to assure reduction is maintained; if not, refer to ortho/hand.
Complications
Joint stiffness and subsequent functional disability. Adhesions between
extensor mechanism and periosteum may result in loss of motion requiring
surgical intervention. Adhesions between flexor superficialis and flexor
profundus may follow prolonged immobilization and require surgical intervention
to restore function.
Arthritis can result from intra-articular fractures.
Nonunion is rare except for improperly immobilized or open fractures.
References
1. Carlsen BT, Moran SL. Thumb trauma: Bennett fractures, Rolando
fractures, and ulnar collateral ligament injuries. J Hand Surg [Am].
2009;34:945–952.
2. Suprock MD, Hood JM, Lubahn JD. Role of antibiotics in open fractures of
the finger. J Hand Surg [Am]. 1990;15:761–764.
3. Henry MH. Fractures of the proximal phalanx and metacarpals in the hand:
preferred methods of stabilization. J Am Acad Orthop Surg. 2008;16:586–
595.
4. Waters PM. Operative carpal and hand injuries in children. J Bone Joint
Surg Am. 2007;89:2064–2074.
5. Stanton JS, Dias JJ, Burke FD. Fractures of the tubular bones of the hand.
J Hand Surg Eur Vol. 2007;32:626–636.
Additional Reading
Cornwall R, Ricchetti ET. Pediatric phalanx fractures: unique challenges and
pitfalls. Clin Orthop Relat Res. 2006;445:146–156.
Vadivelu R, Dias JJ, Burke FD, et al. Hand injuries in children: a prospective
study. J Pediatr Orthop. 2006;26:29–35.
Codes
ICD9
816.01 Closed fracture of middle or proximal phalanx or phalanges of hand
816.11 Open fracture of middle or proximal phalanx or phalanges of hand
Clinical Pearls
Return-to-play decision based on stability, ROM, current clinical and
radiographic healing status, and specific demands of sport.
Most athletes with stable fractures are able to return as early as 1–2 wks after
the injury with protection such as buddy taping.
For unstable fractures, early surgical intervention may be desirable for better
outcome and earlier return.
Fracture, Radial Head
Keith A. Stuessi
Ryan C. Fowler
Basics
As classified by modified Mason classification (Johnston adding type IV and Morey
adding displacement and percentage affected):
Type I: Nondisplaced or minimally displaced fracture of head or neck:
Intra-articular displacement of the fracture <2 mm and fragment size ≤30% of articular
surface
Forearm rotation (pronation/supination limited only by acute pain and swelling
Nonoperative treatment
Type II: Displaced fracture of the head or neck:
Fracture displaced >2 mm and fragment size >30% of articular surface
Motion may be mechanically limited.
If fracture involves more than a marginal lip of the radial head and is not severely
comminuted, repair by open reduction with internal fixation should be considered.
Type III: Severely comminuted fracture of the radial head and neck:
Not reconstructible
Requires excision, with or without arthroplasty
Type IV (added to Mason's classifications by Johnston):
Radial head fracture with an associated elbow dislocation
Description
Fracture of the head of the radius, most often caused by direct axial loading, as with a fall on
outstretched hand (FOOSH) injury
Can also be caused by posterior lateral rotary force, any injury causing posterior dislocation
to the elbow that may result in radial head fracture (such as Monteggia fracture or coronoid
fracture-dislocation), or rarely, a direct blow.
Epidemiology
Radial head fractures are the most common fracture about the elbow, accounting for about
30% of all elbow fractures in adults and 1.7–5.4% of all adult fractures (1). Uncommon in
children, accounting for only 1% of all fractures.

1/3 of patients will have a concomitant injury.
Essex-Lopresti lesion: Disruption of triangular fibrocartilage complex of the wrist and
interosseous membrane of the forearm resulting in instability of the forearm and subluxation
of the distal radioulnar joint
Concomitant capitellar, olecranon, and coronoid fractures (often associated with elbow
dislocation)
Posterior Monteggia fractures: Proximal 1/3 ulna fracture with radial head dislocation
The terrible triad is known as posterior dislocation of the elbow with radial head fracture and
associated coronoid process fracture.
Medial collateral ligament tear
Presence or absence of mechanical block with rotation. Examination achieved after aspiration
of hematoma, with or without intra-articular injection of anesthetic. Mechanical block
associated with displaced fragment of radial head and affects surgical treatment.
Diagnosis
History
Determining the mechanism of injury (FOOSH vs. direct trauma to elbow) may help differentiate
radial head fracture versus other fractures of the elbow.
Physical Exam
Patient usually holds injured arm gently against the chest with elbow flexed.
Typically there is pain and moderate swelling over the lateral side of the elbow.
Any attempt to flex or extend the elbow or rotate the forearm may accentuate pain.
Of note, a recent study reaffirmed that preservation of active elbow range of motion (ROM)
was 97% specific for absence of a fracture.
Well-localized tenderness over the radial head (located just distal to the lateral epicondyle)
Palpation of radial head with passive rotation of the forearm typically elicits pain and
occasionally crepitation.
Forearm and wrist always need to be palpated. Rule out associated injuries such as acute
radioulnar dissociation and injury to the interosseous ligament of the forearm.
Palpation of medial ligament necessary for signs of possible disruption
Neurovascular status checked distally, especially with history of elbow dislocation
Imaging
Anteroposterior and lateral radiographs of the elbow are usually sufficient.
If fat pad sign present (either anterior “sail sign” or posterior fat pad sign) and fracture not
apparent, radiocapitellar views are helpful, taken with forearm in neutral rotation and x-ray
beam angled 45° cephalad.
CT scans are helpful in estimating fracture size, degree of fragmentation, and displacement.
If wrist or forearm pain present, x-rays of the wrist in neutral rotation view should be taken.
Patient may have limited ROM due to pain and effusion. It is important to perform an intra-
articular joint aspiration and subsequent ROM testing to ensure no mechanical block
(although uncommon) is found, which may change treatment.
A recent study found no benefit in ROM, pain, or function comparing arthrocentesis alone vs
arthrocentesis followed by anesthetic instillation (1).
Joint aspiration is performed at the lateral elbow in the soft spot at the center of the dorsal
olecranon, radial head, and lateral epicondyle.
If diagnostic hemarthrosis is avoided, serial exams may be helpful.
Any questions should be referred for orthopedic consideration.
Other fractures of the elbow, including capitellar, olecranon, and coronoid
Supracondylar fractures much more prevalent in children
Treatment
Aspiration alone may provide some pain relief vs aspiration with local
anesthetic instillation.
Type I:
Treated nonoperatively
Sling for pain control no longer than 3–4 days
Active ROM can begin as soon as pain permits. Flexion and extension of the
elbow and supination and pronation of the forearm should be taken to the
point where mild pain begins.
Ice therapy for 2–5 days
Acetaminophen and oral narcotics as necessary for pain control
Type II:
Orthopedic consultation should be obtained with any type II patient, as there
is still considerable controversy as to proper treatment and no specific
criteria have been defined to differentiate who responds better to which
treatment. Recent studies show better results with specific type II injuries as
below with nonoperative vs open reduction internal fixation (ORIF), but
randomized trials are still lacking.
Without associated injuries and moderate displacement (2–5 mm), can be
treated nonoperatively such as type I
With associated injuries, especially causing elbow instability or with
mechanical block, should be referred for orthopedic consultation and
possible open ORIF
Type III:
ORIF vs resection and arthroplasty vs resection alone
Type IV:
Treated as above, with obvious attention paid to reduction of dislocation and
surgical repair of both fractures and associated ligamentous injuries
Initiate ROM exercises early.
More aggressive strength and flexibility exercises added progressively as
tolerated
If ROM does not improve on a weekly basis, a mechanical block should be
excluded. Once excluded, formal therapy may be needed.
Only mild restriction of extension and rotation should be expected at 6 wks.
Ongoing Care
Contractures and loss of motion may develop if early active ROM is not initiated.
Increased sensitivity to cold, which may persist for up to 1 yr
Long-term pain is rarely a complication.
Nonunion is possible, but is frequently asymptomatic.
Nerve injuries in the form of partial ulnar nerve and posterior interosseus nerve injury have
been documented, mainly associated with surgical exploration.
Early orthopedic input is essential in all but type I fractures due to potential need for surgical
correction and controversy surrounding treatment.
Reference
1. Kaas L, et al. The incidence of associated fractures of the upper limb in fractures of the
radial head. Strategies Trauma Limb Reconstr, 2008.
Additional Reading
Akesson T, et al. Primary nonoperative treatment of moderately displaced two-part
fractures of the radial head. J Bone Joint Surg Am. 2006;88:1909–1914.
Chalidis BE, Papadopoulos PP, Sachinis NC, et al. Aspiration alone versus aspiration and
bupivacaine injection in the treatment of undisplaced radial head fractures: A prospective
randomized study. J Shoulder Elbow Surg. 2009.
Darracq MA, et al. Preservation of active range of motion after acute elbow trauma predicts
absence of elbow fracture. Am J Emerg Med. 2008;26:779.
Herbertsson P, et al: Uncomplicated Mason type-II and III fractures of the radial head and
neck in adults. A long-term follow-up study. J Bone Joint Surg Am. 2004;86-A:569.
Pike JM, Athwal GS, Faber KJ, et al. Radial head fractures—an update. J Hand Surg [Am].
2009;34(3):557–565.
Ring D. Fractures and dislocations of the elbow: radial head fractures. In: Rockwood CA,
Green DP, Bucholz RW, et al. Rockwood and Green's fractures in adults, 6th ed.
Philadelphia: Lippincott, Williams & Wilkins, 2006;1011–1019.
Rosenblatt Y, et al. Current recommendations for the treatment of radial head fractures.
Orthop Clin North Am. 2008;39:173.
Codes
ICD9
813.05 Fracture of head of radius, closed
Clinical Pearls
In type I fractures, typically athletes can return to play as early as 6–8 wks,
depending on pain, ROM, and strength.
Protection of the elbow may be needed if returning to contact sports. In type II–
IV fractures, return to play is based on extent of associated injuries and
surgical correction.
Fracture, Rib
Robert J. Baker
Basics
Description
May be the result of acute chest trauma, especially in contact sports
Stress fractures can occur as a result of chronic overuse of the upper body (1,2,3,4)[B].
Fractures may be complete, incomplete, or stress-related (1)[C].
Rib fractures may often be associated with other fractures, soft tissue injuries, and deep
organ trauma (5)[C].
Synonym(s): Broken ribs; Double fractures of the chest: Steering wheel injury, flail chest,
stove-in chest (6)[C]
Epidemiology
Isolated fractures of the upper 4 ribs are rare because they are well protected by the
shoulder complex (1,6,7)[B].
When injury occurs, trauma can be significant enough to fracture other bones of the shoulder,
and injury to the deep organs such as lungs, heart, bronchus, blood vessels, and/or
esophagus must be considered (5)[C].
Blunt trauma to the lower 8 ribs commonly results in fractures, most commonly related to
blunt trauma of contact sports, such as football, hockey, and rugby (6,8)[C].
Forceful contraction, usually against a significant amount of resistance, of muscles with an
attachment to the ribs may result in incomplete, complete, or avulsion fractures of the ribs
(2,3)[B].
Chronic stress of upper body muscles, which attach to the ribs, can result in stress fractures
of the ribs. Commonly seen in rowing, tennis, golf, gymnastics, and baseball (2,3,9)[B].
1st rib fractures have been reported as a result of falling on an outstretched arm, as well as
direct trauma. 1st rib stress fractures also reported in the literature (1,7,8,10)[B].
Avulsion fractures of the lower 3 floating ribs often occur at the attachment of the external
oblique muscles. Known to occur in baseball pitchers and batters (4,11,12)[B].
Multiple rib fractures occur in high-impact trauma such as automobile, motorcycle, mountain
biking, and bicycle racing (6)[B].
Rib fractures more common in adults compared to children due to the relative inelasticity of
the adult chest wall compared to children (6,13)[C].
Risk Factors
Rib fractures most likely occur in contact and collision sports such as football, hockey,
boxing, wrestling, rugby, and soccer (1)[A].
As with any trauma, injuries can be more severe in athletes unprepared, either from lack of
conditioning or contact from the back or blind side.
Stress fractures of the ribs more likely occur in sports with increased upper body demands
such as golf, rowing, gymnastics, baseball, tennis, racquet sports, and weight-lifting.
Overuse and poor technique can contribute to rib stress fractures (2,3,7)[B].
Other predisposing factors include a history of bone or joint disease, bone tumors, metastatic
cancer, poor nutrition, and calcium deficiency (6,7)[C].
Genetics
There is no known genetic link for rib fractures. Those pathological fractures can occur in
association with other bone tumors and metastatic cancer.
General Prevention
Protective equipment for contact sports is available for high-risk athletes. Rib protectors are
available in football. Flack jackets are available for use in other contact sports.
Appropriate conditioning and technique in upper extremity sports is recommended for
prevention of stress fractures (2,3,13)[C].
Etiology
Most acute rib fractures occur as a result of direct trauma, either blunt or penetrating missile
(ie, ball, gunshot) (6)[C].
Relative long, thin shape of the rib predisposes to fractures. Common specific location is
posterior lateral bend (6)[C].
Because of the rib's thin bony structure compared to other long bones, fracture may occur
earlier due to pathological causes (13)[C].
Because there are multiple muscle attachments of the rib to the neck and upper extremities,
stress can lead to fatigue fractures of the ribs (1,2,3,13)[B].

Organ injuries that may occur with acute rib fractures include:
Pulmonary contusion
Pneumothorax
Tension pneumothorax
Hemothorax
Liver laceration, especially with lower rib fractures
Spleen laceration, especially with lower rib fractures
Esophageal rupture
Great vessel injury, aorta and superior vena cava with upper and middle rib fractures (5)[C]
Diagnosis
Pre Hospital
Prehospital care is directed at stabilizing the athlete.
Evaluate and treat for shock in penetrating wounds, open fractures, and suspected internal
injuries where blood loss is likely.
Evaluate and treat for respiratory distress where tension pneumothorax, unstable multiple rib
fractures, or flail chest is present (5)[A].
In the case of tension pneumothorax, diagnosis and aspiration may be life-saving prior to
transfer (5)[C].
History
Acute rib fracture usually presents after chest trauma. Can result from a fall on an
outstretched arm.
Athletes may experience the sensation of having the “the wind knocked out of them.”
Athlete may recall feeling a “pop” when the trauma occurred.
Athlete may complain of abdominal pain if the lower (11th and 12th) ribs are involved.
Stress fractures usually occur in elite athletes who train intensely. These fractures tend to be
more gradual in onset (7)[C].
Physical Exam
Localized pain over the involved rib(s)
Sensation of crepitus over the fracture site(s)
Pain generally exacerbated by deep inspiration, resulting in shallow, rapid breathing
Pain aggravated by coughing and sneezing
Other symptoms, such as increasing shortness of breath, increasing pain, cyanosis, and SC
emphysema, may indicate serious life-threatening conditions requiring emergent attention.
Palpable deformity may be present in complete displaced fracture.
Swelling and ecchymosis may be present in the area of rib fractures.
In athletes involved in sports with heavy upper extremity activity, stress fractures may
present as gradual-onset localized rib pain, with or without deformity. Pain may radiate
backward (2,3,8)[B].
Localized rib tenderness is the cardinal finding.
Obvious deformity or crepitation at the fracture site may be present.
Palpable swelling, with or without ecchymosis, may be present at the fracture site.
SC emphysema may be present, especially with associated pneumothorax.
With significant chest trauma, a thorough cardiopulmonary examination must be performed to
rule out complications or associated injuries (14)[B].
If trauma occurred to the upper chest, special attention should be given to the neck,
shoulders, and major vessels (5,14)[B].
If trauma occurred to the lower chest, a thorough abdominal examination should be
performed to rule out injury to the liver, spleen, GI tract, and kidneys (6)[C].

Lab
In the case of pathologic fractures, other blood work, such as CBC, comprehensive
metabolic panel, and isoenzymes of alkaline phosphatase may be directed by history and
physical (15)[B].
Appropriate blood work directed at associated injury of internal organs may be indicated;
however, no direct blood work is necessary to diagnose the rib fracture.
Imaging
Most rib fractures heal without need for reduction or immobilization; thus, postreduction films
are not required (6)[C].
Healing 1st rib fractures may compromise the vasculature to the upper extremity (8,10)[B].
Repeat films may be performed to monitor this complication during healing ()[B].
Other than in cases of complications, continued pain, and poor healing, routine repeat films
are not necessary.
Chest radiographs should be taken after chest trauma to rule out complications such as
pneumothorax and hemothorax (6,14)[B].
Rib series radiographs are not necessary for suspected isolated fractures of ribs 5–9.
Rib series radiographs are indicated if ribs 1–2 or ribs 9–12 are involved.
US has been used to diagnose and manage rib fractures (13)[B].
Rib series radiographs should be performed if there are suspected multiple rib fractures or
pathologic fracture, the athlete is elderly, or there is preexisting pulmonary disease (15)[B].
With upper thoracic rib fractures, arteriography is indicated if there is evidence of vascular
insufficiency, hemorrhage, or concomitant brachial plexus injury; marked displacement of the
rib fragments; fractures of the scapula, vertebrae, or sternum; widening of the mediastinum;
left apical cupping; or downward displacement of the left mainstem bronchus (10,5,8)[B].
ECG, echo, or stress testing if cardiac complications are considered
IV pyelogram if renal complications are suspected
Abdominal CT scan may be necessary if hepatic or splenic injury is suspected.
Rib/chest wall contusion
Muscle strain
Rupture of pectoralis major
Costochondral separation
Sternoclavicular separation
Costochondral sprain
Sternal fracture (anterior)
Intervertebral joint sprain
Intervertebral disc injury
Apophyseal joint sprain
Paraspinal muscle strain
Costovertebral joint sprain
Scheuermann disease (posterior)
Other causes of chest pain, such as cardiac causes, peptic ulcer disease, gastroesophageal
reflux disorder, pneumothorax, pulmonary embolism, asthma, pleurisy, herpes zoster
Treatment
Treatment is generally supportive.
Pain control is the cornerstone of treatment and may be required for up to 3–6
wks after injury.
Ice and NSAIDs may control symptoms, but stronger oral pain medications
often are required.
Local intercostal nerve blocks remain an option if other pain control techniques
fail (9)[B].
Epidural anesthesia is also an option for pain control (13)[C].
Strapping or a chest binder has been advocated to help with pain. Caution
should be exercised because immobilization techniques may result in inhibition
of deep breathing, leading to atelectasis and possibly pneumonia (1,6,13)[C].
If immobilization is deemed necessary for comfort, its use should be minimized.
Flail chest occurs when ≥3 ribs are fractured in 2 locations.
Nonunion of rib fractures is rare but has been reported.
Rib stress fractures may respond well to rehabilitation exercises, such as
push-ups, serratus press, upper extremity step-ups, and serratus rhythmic
stabilization (1)[C].
Biomechanics of throwing, rowing, batting, or weight-lifting should be evaluated
and corrected if necessary (2,11,16)[C].
Need for surgery is rare in cases of isolated rib fractures (6)[C]
Exception is in the case of flail chest. Open reduction internal fixation may be
required (6)[C].
Suspected internal injuries associated with rib fractures should be referred for
possible surgical repair.
Chronic pain due to recurrent stress fracture, nonunion, or recurrent
dislocation or subluxation may improve with surgical excision of the involved rib
(4)[B].
Admission Criteria
Patients over the age of 45 are at increased risk for complications, which may
require hospitalization (6,14)[C].
Athletes with multiple rib fractures should be considered for admission to the
hospital.
Ongoing Care
The athlete should be encouraged to continue activi-ties as tolerated, except for contact
sports (7)[C].
Contact should be limited for the 1st 3 wks following injury. Consider rib protection in contact
sports after return (1)[C].
Monitor regularly for signs of delayed complications (8)[B].
Patient Education
Athletes should be educated that it is common to have significant pain. They should not be
reluctant to take pain medication early on. This allows for more normal breathing and less
chance of complications like pneumonia (13)[C].
Athletes should be educated when to follow up. Especially if they experience fever, chills,
worsening pain, dizziness, lightheadedness, fatigue, persistent cough, or respiratory distress.
Prognosis
Full healing usually takes 4–6 wks; however, athletes may return to participation in
noncontact sports when pain-free.
Early return to contact sports may be possible prior to 6 wks if pain is controlled and the
area can be protected adequately (13)[C].
Complications
Nonunioun of the ribs is rare in general. Symptomatic nonunion can occur and
would be an indication for surgery (4,8,11)[B].
Pseudoarthrosis of the 1st rib is described in the literature and has been a
cause for discontinued participation (4,8,11)[B].
References
1. Brukner P, Karim K. Clinical sports medicine. New York: McGraw-Hill,
1997.
2. Davis BA, Finnoff JT. Diagnosis and management of thoracic and rib pain in
rowers. Curr Sports Med Rep. 2003;2:281–287.
3. Lord MJ, Ha KI, Song KS. Stress fractures of the ribs in golfers. Am J
Sports Med. 1996;24:118–122.
4. Mithöfer K, Giza E. Pseudarthrosis of the first rib in the overhead athlete.

Br J Sports Med. 2004;38:221–222.
5. George RB, Light RW, Matthay RA, eds. Chest medicine: essentials of
pulmonary and critical care medicine. Baltimore: Williams & Wilkins, 1995.
6. DePalma AF. DePalma's the management of fractures and dislocations.
7. Miles JW, Barrett GR. Rib fractures in athletes. Sports Med. 1991;12:66–
69.
8. Proffer DS, Patton JJ, Jackson DW. Nonunion of a first rib fracture in a
gymnast. Am J Sports Med. 1991;19:198–201.
9. Orchard JW. Benefits and risks of using local anesthetic for pain relief to
allow early return to play in professional football. Br J Sports Med.
2002;36:209–213.
10. Barrett GR, Shelton WR, Miles JW. First rib fractures in football players. A
case report and literature review. Am J Sports Med. 1988;16:674–676.
11. O'Neal MO, Ganey TM, Ogden JA. First rib fracture and psuedoarthrosis
in the adolescent athlete: The role of costosternal anatomy. Clin J Sports Med
2009;19:65–67.
12. Sakellaridis T, Stamatelopoulos A, Andrianopoulos E, et al. Isolated first rib

fracture in athletes. Br J Sports Med. 2004;38:e5.
13. Karlson KA. Rib fractures. UpToDate. On-line: www.uptodate.com

accessed 8/29/2009.
14. Kleckner K, DelRios M, Lewiss RE. Fracture of the third rib. Ann Emerg
Med. 2008;51:e1–e2.
15. Smoljanovic T, Bojanic I. Ewing sarcoma of the rib in a rower: a case

report. Clin J Sports Med. 2007;17:510–512.
16. Sik EC, Batt ME, Heslop LM. Atypical chest pain in athletes. Curr Sports
Med Rep. 2009;8:52–58.
Additional Reading
O'Kane J, O'Kane E, Marquet J. Delayed complication of a rib fracture.
Physician Sportsmed. 1998;26:69–77.
Rosen P, Barkin R, Danzl D, eds. Emergency medicine: concepts and

clinical practice. St Louis: Mosby-Year Book, 1998.
Codes
ICD9
807.00 Closed fracture of rib(s), unspecified
807.09 Closed fracture of multiple ribs, unspecified
807.10 Open fracture of rib(s), unspecified
Clinical Pearls
To combat pain associated with fractured ribs, patients should:
Start with icing.
Sometimes pushing against and supporting the injured rib, especially with
coughing or sneezing, will decrease pain.
If necessary, a binder may be used for a very limited time.
In most cases of isolated rib fractures, simple chest films are all that are
required. If the 1st or the bottom couple of ribs are involved, other x-rays may
be ordered.
Patients should continue to be as active as they can tolerate and should not
hesitate to take medication prescribed for pain.
Collision or contact sports should be avoided until return to play is approved
by a doctor, usually in 3 wks.
It is important allow the stress fracture to heal, as well as to determine what
might have contributed to it. Training, technique, and nutritional status should all
be evaluated. Once contributing factors are identified and corrected, patients
can return to their previous level of activity.
Fracture, Sacral
Michele LaBotz
Basics
Sacral injuries are rare, but most authors believe that sacral fractures are generally
under-recognized.
A high degree of suspicion is required to make the diagnosis:
Standard radiographs of the lumbar spine and pelvis are often normal.
Advanced imaging is often required to appreciate sacral injury.
Description
Traumatic fractures of the sacrum are most commonly described using the Denis system of
fracture orientation:
Zone I:
Fracture line usually vertically through the sacral ala
Entirely lateral to foramina
Typically, strength of sacroiliac (SI) ligaments spares SI joint from injury, but fractures
that enter SI joint at greater risk for instability
Neural elements typically spared; 6% with neurologic involvement
Zone 2:
Fracture line involving the neural foramen, but sparing the central spinal canal
28% with neurologic injury
Zone 3:
Fracture line involving the spinal canal; typically includes transverse fractures
58% with neurologic injury
Atraumatic injuries result from a mismatch between bone stress and bone strength:
Nomenclature is typically broken down into the following categories:
Stress fractures in athletes; typically unilateral fracture of sacral ala
Insufficiency fractures in elderly or infirm; often bilateral fractures of sacral alae; may
also have horizontal component
Epidemiology
Sacral fractures need to be considered in several clinical scenarios:
Multitrauma patients with other pelvic or thoracolumbar injury:
Sacral fractures rarely occur as isolated injury (<5%)
Osteoporotic patients with low back or gluteal pain:
Atraumatic or trivial injury
Athletes with activity-related pain of low back/SI region:
Usually in running based sports:
Often after increases in training intensity
May produce thigh pain as well
Risk Factors
Insufficiency fractures are most common in elderly osteoporotic females:
May occur in others at risk for poor bone density, including the following:
Chronic corticosteroid use
History of pelvic irradiation
Stress fractures occur most commonly in running athletes:
As with other stress fractures, risk probably increases with the following:
Training errors (inadequate recovery, increasing training, etc.)
Biomechanical factors (leg length discrepancy, poor core and pelvic stabilization)
Increased impact forces (footwear, training surface)
Nutritional/hormonal impacts on bone density (disordered eating/female athlete triad,
inadequate calcium/vitamin D)
Etiology
Sacral fractures may occur by the following mechanisms:
Post-traumatic injuries:
Producing large forces and fracture across healthy bone:
Typically motor vehicle accidents or falls from a height
Atraumatic injuries:
Normal stresses (or trivial injury) producing fractures across relatively weakened bone:
Insufficiency fractures in the elderly/ill
Fractures often bilateral
Increased stress or overuse, producing fracture across relatively normal bone:
Stress fractures in the younger, athletic population
Fractures often unilateral

Acute sacral fractures may be seen in conjunction with:
Other bony injury:
Other pelvic ring disruptions
Other spinal fractures:
May be noncontiguous
Fracture-dislocations of lower facet joints or disruption of lumbosacral junction
Neurologic injury:
Should be described according to the Gibbons grading system:
Grade 1: No neurologic deficit
Grade 2: Paresthesias/sensory changes only
Grade 3: Motor deficit, but gastrointestinal (GI)/genitourinary (GU) function normal
Grade 4: Loss of GI/GU function
Injury to other pelvic contents:

Rectal perforation most common
Diagnosis
Pre Hospital
Traumatic sacral fractures typically occur in the multitrauma patient.
Initial assessment and treatment should proceed as per Advanced Trauma Life Support for
patients with suspected spine injury:
ABCs/resuscitation
Spine precautions/backboard
Transport
History
Injury to sacrum is suggested by pain in lower back, buttocks, perirectal region, and posterior
thigh
Important to inquire about possible nerve root involvement:
Incontinence of bowel or bladder, sexual dysfunction
Sciatica
Paresthesias, especially of saddle region
Patients without history of trauma should be asked about:
Change in activity or footwear, especially in running-based sports
Risk factors for poor bone density:
Osteopenia/osteoporosis in patient or family members
Past or present disordered eating pattern
Oligo- or amenorrhea in females
Physical Exam
Trauma patient:
Inspect for ecchymosis/bruising over sacral prominence
Palpate entire spinal column and bony pelvis in addition to the sacrum.
Neurologic testing of L5–S5 nerve root function should be completely assessed initially then
periodically re-evaluated:
Pinprick sensation, rectal sphincter contraction and tone, as well as cremasteric,
bulbocavernosus, perianal wink reflexes
L5 injuries most common with Zone 2 injuries
Sacral roots have bilateral input, and unilateral injuries to S2–5 are difficult to detect.
Digital rectal and vaginal evaluation to exclude open fractures
Atraumatic patient with possible insufficiency or stress fracture:
No pathognomonic findings
Typically with tenderness over sacrum, paraspinal, or over region of SI joint
FABER test (with hip in flexion, abduction, external rotation) often positive
Distal neurovascular assessment typically normal
Gait may be antalgic and may have pain with a hop test

Lab
Trauma patients should have stool assessed for occult blood.
Otherwise, assessment should proceed as directed by other possible injury.
Imaging
Traumatic injury:
Although radiographs typically only reveal about 30% of sacral fractures, they may be
useful for initial assessment of suspected sacral injury:
AP views of the pelvis are standard in multitrauma patients
Visualization of suspected sacral injuries may be enhanced with the addition of pelvic
inlet view: 35–40 degree caudal tilt of radiograph tube; pelvic outlet view: 45-degree
cranial tilt of radiograph tube; lateral view of sacrum
Look for transverse L5 fractures, which can be seen in up to half of pelvic and sacral
fractures.
CT scanning is now standard for definitive assessment of suspected acute sacral fracture:
Routine CT scans often not satisfactory
Close consultation with radiologist on gantry alignment recommended
Thin section (1.0–1.5 mm cuts) with coronal and sagittal reconstructions; relatively high
radiation exposure: 10–20 mSV
MRI may help delineate neural compression or injury:
Multiplanar nature may also better assess fracture alignment
Atraumatic injury:
Since typical presentation is of lumbar or gluteal pain, initial lumbar spine series as well as
anteroposterior views of the pelvis are often obtained:
Usually unremarkable
MRI of sacrum appropriate for diagnosis:
Some authors report not as sensitive as bone scan
Most bony stress injuries will have high signal on T2-weighted images, low signal on T1-
weighted images.
Fracture line may or may not be present.
Bone scan most sensitive, but not specific for bony stress injury:
Stress fractures in athletes; typically with unilateral uptake sacral ala
Insufficiency fractures; often with multiple sites of injury; classic “H” sign seen in about
40% of patients; bilateral vertical fractures with horizontal component
Uptake can be obscured by residua in bladder; outlet views in addition to standard
anterior and posterior projections
Differential diagnosis for acute fractures:
Contusion
Other pelvic or lumbar fractures
Nerve root injuries
Differential diagnosis for atraumatic/stress fractures:
Lumbar disc disease
Sacroiliac dysfunction
Spondylolysis
Treatment
Acute fracture:
See below for surgical indications
Stable injuries without neurologic involvement treated with initial bed rest and
gradual ambulation and activity advancement as tolerated:
Fractures through S3 and distally often require protection with sitting until
pain-free
Stress fracture: Average +/-6 wks for return to sport (but some may take up to
3 mos)
Protected weight-bearing if limp or pain with ambulation:
Advance weight-bearing as tolerated
Discontinue painful activity/relative rest
Maintain cardiovascular conditioning with pain-free activity:
May need to begin with non-weight-bearing activity (typically swimming or
cycling)
Begin progressive rehabilitation typically after 3–5-day pain-free interval:
Core/pelvic stabilization; address underlying biomechanical deficiencies
Cardiovascular cross-training progression through following sequence
when activity is pain-free: Non-weight-bearing (ie, pool running, bicycling),
weight-bearing/nonimpact (ie, elliptical-type trainer), impact (ie, running),
sports-specific functional progression
Insufficiency fractures in elderly may have prolonged symptoms (up to 9 mos):
Initial treatment is usually nonoperative, even for patients with neurologic
deficit:
Many authors recommend initial period bed rest followed by progressive
ambulation
Neurologic symptoms appear to improve as pain resolves.
Consider surgery if severe pain after 3-mon trial conservative treatment
Medication
Analgesics should be titrated for symptom relief:
Scheduled doses for first several days of diagnosis may allow for pain-free
rest:
Over-the counter analgesics often sufficient for stress fractures:
Acetaminophen, up to 1,000 mg q4h PRN; pediatric dosage 10–15 mg/kg
up to q4h Nonsteroidals often beneficial. Theoretically may impair bony
healing, but no consensus on effect on clinical outcomes. Naproxen 500
mg q12h; pediatric dosage 10–20 mg/kg/day divided b.i.d.
Patients with severe pain may need stronger medications for first several
days:
Hydrocodone/acetaminophen 5/500 1–2 PO. q4–6h PRN; pediatric
suspension 7.5/500/15 mL; patient weight 32–45 kg: 10 mL q4–6h PRN
Tramadol 50 mg 1–2 tabs q4–6h PRN; maximum dose 400 mg/day;
caution in elderly and with renal or hepatic impairment
Analgesics should not be used specifically to allow for progression of activity or
sport participation
Surgical consideration for traumatic sacral fractures:
Unstable injuries
Severe disruption of sagittal or coronal alignment:
In AP plane displacement, >1 cm generally recognized as unstable
Neurologic impairment
Injuries with persistent pain after about 6 mos
Insufficiency fractures considered for surgery if with persistent, severe pain
after 3 mos conservative treatment
Stress fractures and insufficiency fractures are generally managed in
outpatient setting.
Acute traumatic sacral fractures often require hospitalization for additional
injury:
Isolated and stable Zone 1 or 2 fractures with no neurologic deficit and
adequate pain control may be considered for outpatient treatment.
Ongoing Care
Sacral stress or insufficiency fractures may be a bellwether for underlying metabolic
bone disease:
Bone density testing or other laboratory evaluation should be considered.
Diet
Patients with insufficiency or stress fractures should be counseled on appropriate intake of
calcium and vitamin D.
Patient Education
Education should focus on biomechanical issues and training errors predisposing to injury:
Importance of maintaining adequate strength and flexibility of core and pelvic musculature
Advance training volume by 10%/wk to minimize risk of additional overuse injury
Especially in the running athlete, the importance of appropriate footwear selection:
Effective lifespan of most running shoes is 300–400 miles
Prognosis
Healthy athletes with sacral stress injury:
Usually able to return to normal activity 4–6 wks
Usually able to return to sport 6–10 wks
Elderly patients with insufficiency fractures may have pain for many months.
Fractures requiring surgery often with instrumentation:
Up to 1/3 may have hardware failure.
Complications
Deformity or bony callus formation after acute injury may lead to nerve root
entrapment.
Prolonged pain common in elderly with insufficiency fractures.
Additional Reading
Micheli LJ, Curtis C. Stress fractures in the spine and sacrum. Clin Sports
Med. 2006;25:75–88.
Shah MK, Stewart GW. Sacral stress fractures: an unusual cause of low back
pain in an athlete. Spine. 2002;27:E104–E108.
White JH, Hague C, Nicolaou S, et al. Imaging of sacral fractures. Clinical

Radiology. 2003;58: 914–921.
Kuklo TR, Potter BK, Ludwig SC, et al. Radiographic measurement techniques
for sacral fractures consensus statement of the Spine Trauma Study Group.
Spine. 2006;31:1047–1055.
Levine AM. Fractures of the sacrum in browner: skeletal trauma, 4th ed.
Philadelphia: Saunders, 2008.
Shah MK, Stewart GW. Sacral stress fractures: an unusual cause of low back
pain in an athlete. Spine. 2002;27:E104–E108.
See Also
Fracture, Pelvic
Codes
ICD9
805.6 Closed fracture of sacrum and coccyx without mention of spinal cord injury
806.60 Closed fracture of sacrum and coccyx with unspecified spinal cord injury
806.70 Open fracture of sacrum and coccyx with unspecified spinal cord injury
Clinical Pearls
Consider sacral injury in any acute injury resulting in other pelvic or spinal injury.
Consider sacral injury in chronic cases of low back, thigh, or buttock pain.
Sacral fractures are typically occult on plain radiographs and often require
advanced imaging for definitive diagnosis.
Fracture, Scaphoid
Brent R. Becker
Keith A. Stuessi
Basics
Most commonly fractured of the 8 carpal bones of the hand
Usual mechanism of injury is a fall onto an outstretched hand
Scaphoid fractures, particularly fractures of the proximal pole, have an increased risk of
nonunion.
Synonym: Fracture, carpal navicular
Epidemiology
Fractures of the carpal bones account for 6% of all fractures.
Fracture of the scaphoid accounts for 70% of all carpal fractures:
75–80% of scaphoid fractures occur through the waist of the bone.
15–20% through the proximal pole
10–15% through the distal pole
Young adult males are the most common patient (children: Distal radial physis fails before
scaphoid fracture; older adults: Distal radial metaphysis fails before scaphoid fracture).
Incidence
Incidence in athletes is unknown.
4-fold greater incidence in men compared to women (1)
Etiology
Most commonly described mechanism is hyperextension of wrist with radial deviation and
axial loading of scaphoid onto radial rim
Usually associated with falls, athletic injuries, or motor vehicle injuries
Increased risk of nonunion in proximal pole fractures due to tenuous blood supply
Diagnosis
History
Patients report falling on the extended wrist or other wrist trauma.
Pain at the wrist, near base of the 1st metacarpal
Pain located at the “anatomical snuffbox”: Area on radial side of wrist between extensor
pollicis brevis and extensor pollicis longus
Pain described as deep and dull made worse with gripping or squeezing
Physical Exam
Tenderness in anatomical snuffbox (waist fracture or distal pole fracture):
Bordered dorsally by tendon of extensor pollicis longus and volarly by extensor pollicis
brevis and abductor pollicis longus
Sensitivity 90%, specificity 40% (2)
False positives may occur by compression of a sensory branch of the radial nerve as it
crosses the snuffbox.
Tenderness of scaphoid tubercle:
Extend patient wrist and apply pressure at proximal wrist crease
Sensitivity 87%, specificity 57% (2)
Scaphoid compression test: Axially/longitudinally compressing patient's thumb along a line of
the 1st metacarpal:
Some studies show poor predictive value (2).

Imaging
3 views of the wrist: Posteroanterior (PA), lateral, and “scaphoid” view, ie, anteroposterior
view of wrist with 30 degrees supination and ulnar deviation
May request additional views: Radial oblique, ulnar oblique, and PA wrist with clenched fist in
radial and ulnar deviation
Plain radiographs may be normal immediately after injury.
Fracture may become apparent 10–14 days after injury (immobilization allows
demineralization of the fracture line).
Examine radiographs for evidence of the “Terry Thomas” sign (ie, widening of the
scapholunate distance). Evidenced by >3 mm between the scaphoid and the lunate:
Indicates ligamentous injury to the scapholunate ligament
Bone scan:
Consider in patients with persistent snuffbox tenderness but negative plain radiographs
Cost-effective when compared to repeat radiographs (2)
Positive scan shows increased uptake at the scaphoid focally after 72 hr.
Excellent sensitivity (97%), but specificity (87%) is less than CT and MRI (3)
CT scan:
May be used to accurately help diagnose and delineate the fracture line and displacement
Sensitivity (93%) and specificity (99%) is similar to MRI (3).
MRI:
Consider when initial radiographs are negative and/or other ligamentous injury is suspected.
Sensitive (96%) and specificity (99%) (3)
Cost-effectiveness is unclear (2).
MRI shows diminished signal in T1-weighted and increased signal in T2-weighted images.
Scapholunate dissociation
Distal radius fracture
Wrist sprain
Arthritis
Treatment
Scaphoid fractures or suspected fractures with negative radiographs (2)
[C]:
Immobilize in a thumb spica splint
Sling for comfort
Ice and elevation
Medication
Tylenol or NSAIDs as needed
Narcotics for breakthrough pain
Classification systems exist (Herbert, Mayo, etc.); however these
classifications are not prognostic.
<1 mm separation of the fracture is generally considered nondisplaced (1).
Most nondisplaced fractures can be treated successfully with cast
immobilization (1,2,4)[B].
Time to fracture union varies by location:
Distal pole (6 wks) < Waist (12 wks) < Proximal pole (3–6 mos) (1)
Thumb immobilization does not appear to reduce healing time or increase the
risk of nonunion (2)[B].
Long arm cast (vs short arm) may decrease healing time but does not improve
nonunion rates (1,2,4)[C].
Displaced fractures should be referred for surgical fixation (1,2)[B].
Associated injuries include fracture of the distal radius, radial head, and lunate;
soft tissue ligamentous injury leading to scapholunate dissociation; and
possible injury to the median nerve
Postoperative or postcasting hand therapy
Surgical intervention should be undertaken for displaced fractures (1,2,4)[B].
Also consider surgery for nondisplaced fractures in high-demand
athletes/patients where the necessary length of casting would interfere
significantly with competition, training, or work (1)[C].
Multiple surgical techniques can be used (dorsal open reduction internal
fixation [ORIF], volar ORIF, percutaneous, arthroscopic assisted):
No current evidence to suggest one technique is superior:
Each has advantages and disadvantages.
Surgeon preference and experience is often the deciding factor in operative
technique.
Ongoing Care
Avascular necrosis of the proximal fracture fragment, leading to wrist dysfunction and
early osteoarthritis
High incidence of fibrous nonunion at the fracture site (8–10%)
Frequent malunion
Carpal instability
Post-traumatic arthritis
Nondisplaced waist or distal pole fracture can be treated closed by primary care physician.
Refer patients with displaced scaphoid fracture.
Consider referring patient with proximal pole fracture (prone to nonunion and avascular
necrosis).
Consider referring high-demand patients with nondisplaced fractures.
References
1. Rizzo M, Shin AY. Treatment of acute scaphoid fractures in the athlete. Curr Sports Med
Rep. 2006;5:242–248.
2. Phillips TG, Reibach AM, Slomiany WP. Diagnosis and management of scaphoid
3. Yin ZG, Zhang JB, Kan SL, et al. Diagnosing suspected scaphoid fractures: a systematic
review and meta-analysis. Clin Orthop Relat Res. 2009.
4. Grewal R, King GJ. An evidence-based approach to the management of acute scaphoid

fractures. J Hand Surg [Am]. 2009;34:732–734.
Additional Reading
Beeres FJ, Rhemrev SJ, den Hollander P, et al. Early magnetic resonance imaging
compared with bone scintigraphy in suspected scaphoid fractures. J Bone Joint Surg Br.
2008;90:1205–1209.
Ram AN, Chung KC. Evidence-based management of acute nondisplaced scaphoid waist
fractures. J Hand Surg [Am]. 2009;34:735–738.
Codes
ICD9
814.01 Closed fracture of navicular (scaphoid) bone of wrist
814.11 Open fracture of navicular (scaphoid) bone of wrist
Clinical Pearls
A scaphoid fracture is unlikely in the absence of tenderness in the anatomic
snuffbox and at the scaphoid tubercle.
High-demand athletes may do better with early surgical fixation of even
nondisplaced fractures, as this allows earlier return to activity.
Fracture, Spinous and Transverse Processes
David E. J. Bazzo
Tara Robbins
Basics
Description
Transverse and spinous process fractures are considered minor spine injuries and usually are
stable and benign. Both types can be markers of considerable trauma and should encourage
the physician to look for additional injury.
Fractures of the spinous process typically occur at C7 or any of the lower cervical or upper
thoracic vertebrae. They are commonly avulsion-type injuries resulting from contraction of the
trapezius, rhomboid minor, and/or serratus posterior.
Traditionally referred to as “clay shoveler injuries,” but now are found mostly after sudden
deceleration in motor vehicle accidents or forced flexion of the neck, often in football players
and weightlifters
Synonym(s): Minor spinal fracture
Epidemiology
Spinous process fractures are relatively rare since mechanization replaced clay shovelers.
“Sentinel spinous process fractures” are associated with fractures of lamina and facets,
which can lead to instability.
Up to 21% of transverse process fractures resulting from high-energy trauma (eg, motor
vehicle accidents) are associated with visceral injuries, most commonly to the spleen and
liver (1).
Up to 11% have other spine injuries not detected by plain radiographs but identified on CT
scanning (1).
Transverse process fractures resulting from low-energy trauma (eg, playing football) do not
generally have associated spinal, nerve root, or visceral injuries.
Risk Factors
Growth spurts, training errors, improper technique, and repetitive trauma predispose the athlete
to spine fractures.
Diagnosis
History
Forceful hyperflexion of the neck (eg, spearing in football) is associated with lower cervical
spinous process fractures. Lumbar transverse process fractures usually result from direct
trauma.
Pain with hip flexion indicates possible lumbar transverse process fracture. Pain with neck
flexion suggests cervical spinous process fracture.
Physical Exam
Localized pain over injured area without radiation
Pain increased with neck flexion (lower cervical spinous process fracture) or hip flexion
(lumbar transverse process fracture)
Careful neurologic examination for weakness, reflex changes, or sensory changes in a
dermatomal distribution. As neurologic injuries are not commonly associated with minor
fractures, abnormal results should raise suspicion of additional spinal injury.
Pain worse with hip flexion (site of iliopsoas origin) seen in lumbar transverse process
fractures
Benign abdominal examination does not exclude coexistent intra-abdominal injury.

Imaging
CT scan: Superior to plain films to evaluate extent of spinal fractures and rule out serious
spine injury, but has limited field of view and high radiation dose
MRI: Only necessary if neurologic symptoms are present to evaluate extrinsic spinal cord
compression or intrinsic cord injury
Radiographic appearance often lags behind clinical healing and should not be used as the
primary criterion for return to play.
Cervical lateral radiograph:
Very important to visualize C7 spinous process, which often is obscured by the shoulders
Obtain “swimmer's view” if necessary to visualize C7–T1 junction.
Anteroposterior (AP) radiograph may show double shadow of spinous process due to
avulsion.
Flexion-extension films to rule out ligamentous instability and lamina or facet injury
Thoracolumbar AP radiograph:
Relatively insensitive at identifying transverse process fractures
May show double shadow of spinous process due to avulsion
Hematoma may obscure evidence of transverse process fracture. Loss of normal psoas
shadow may be most prominent finding.
Oblique radiograph to rule out defects in pars interarticularis
“Burst” fracture
Lumbar strain
Disc herniation
Spondylolysis and/or spondylolisthesis
Treatment
Rest is often the most effective treatment for isolated injury.
Cryotherapy repeated frequently within initial 36–48 hr may help prevent
muscle spasm.
NSAIDs and gentle exercises may be helpful.
In all cases of suspected spine injury, immobilization with a backboard and rigid
cervical collar is mandatory until the patient can be cleared radiographically.
If transverse process fractures result from high-energy trauma, there should
be a high index of suspicion for associated visceral injuries. Urinalysis should
be performed; if >8 RBCs per high-power field are seen, perform cystogram
and IV pyelogram to evaluate for possible urinary tract injury (1).
If transverse process fractures are identified on plain radiographs, abdominal
CT should be performed due to possible associated visceral and abdominal
injuries (1).
With cervical injury, protection against flexion with an orthosis should be
provided for 4–6 wks:
Obtain flexion/extension radiographs at end of immobilization period.
Return to play once fracture is healed and patient has full, painless range of
motion and no neurological deficits (2)[B].
There is controversy whether bracing is beneficial in thoracolumbar fractures
without associated spinal injury. Some authors have suggested the use of
bracing for symptomatic relief. Others have shown that it is not effective in
immobilization and can result in complications such as skin breakdown. At the
time of publication, there is no evidence for the effectiveness of bracing in
patients with thoracolumbar fractures (3,4)[B].
If there is associated spinal injury, a rigid orthosis is needed. The patient should
be limited to isometric exercises, with restricted upper extremity exercises, until
full range of motion and no tenderness to palpation are present.
Isolated fractures of the transverse process usually cause disability for a few
weeks and carry a very low likelihood of long-term sequelae. Early mobilization
and physical therapy is important in rehabilitation:
Healing of the transverse process often does not occur because of
distraction of the fracture fragment from muscle pull. Healing is often
determined by radiographs and palpation at site of injury.
Return to play once range of motion is painless and the trunk has been
strengthened.
Likely no equipment changes will be needed in noncontact sports, but padded
equipment modification may be helpful in reducing the risk for reinjury in
contact sports.
Contiguous transverse process fractures should be observed carefully for
development of pseudoarthrosis or myositis ossificans.
Nonunion of fractured fragments is common in both injuries, but most authors
advocate avoiding excision of fragments unless pain persists beyond the period
of immobilization.
Ongoing Care
Patients with isolated fractures do not need orthopedic or neurosurgical referral.
References
1. Patten RM, Gunberg SR, Brandenburger DK. Frequency and importance of transverse
process fractures in the lumbar vertebrae at helical abdominal CT in patients with trauma.
Radiology. 2000;215:831–834.
2. Boden BP, Jarvis CG. Spinal injuries in sports. Neurol Clin. 2008;26:63–78.
3. Giele BM, Wiertsema SH, Beelen A, et al. No evidence for the effectiveness of bracing in
patients with thoracolumbar fractures. Acta Orthop. 2009;80:226–232.
4. Homnick A, Lavery R, Nicastro O, et al. Isolated thoracolumbar transverse process
fractures: call physical therapy, not spine. J Trauma. 2007;63:1292–1295.
5. Tewes DP, Fischer DA, Quick DC, et al. Lumbar transverse process fractures in
professional football players. Am J Sports Med. 1995;23:507–509.
Additional Reading
Krueger M, Green D, Hoyt D, et al. Overlooked spine injuries associated with lumbar
transverse process fractures. Clin Orthop Rel Research. 1996;327:191–195.
Nicholas J, Nuber G, eds. The lower extremity and spine in sports medicine. St. Louis:
Mosby, 1995.
Sturm JT, Perry JF. Injuries associated with fractures of the transverse processes of the
thoracic and lumbar vertebrae. J Trauma. 1984;24:597–599.
Codes
ICD9
805.00 Closed fracture of cervical vertebra, unspecified level
805.2 Closed fracture of dorsal (thoracic) vertebra without mention of spinal cord injury
Clinical Pearls
The average time lost from sports reported in a National Football League study
was 25 days for lumbar transverse process fractures, but varies from case to
case, depending on the number of vertebral levels involved and any associated
injury (5).
Athletes involved in contact sports may feel more comfortable in a flak jacket,
although there is no evidence that they prevent reinjury or accelerate return to
competition.
Most common occurrence is at the levels of C7>C6>T1
Forced hyperflexion is the usual mechanism of injury.
Fracture, Sternum
Steven C. Cuff
Thomas L. Pommering
Basics
Description
Direct:
Results from direct force applied to the sternum, most often from a blow to the body of the
sternum in the lower part; usually from a motor vehicle accident (MVA)
Fracture typically occurs near manubrium.
Indirect:
Results from an indirect flexion-compression injury of the cervicothoracic spine, usually a
forced flexion of the cervical spine that causes the upper 2 ribs to pull the manubrium
posteriorly (downward and posterior force on the manubrium and upper 2 ribs)
May be exacerbated by chin striking the manubrium
Always involves the upper 2 segments of the sternum
Muscular:
Results from violent muscular action that causes fracture through opposing muscle groups,
ie, tetanus
Extremely rare
Epidemiology
Very rare, especially in children and adolescents, due to elasticity of sternum and costal
cartilage
Accounts for about 3–8% of all blunt trauma
More common in men (60–80%)
Etiology
In adults, most commonly related to automobile accidents, typically from a direct mechanism:
Striking the steering wheel or dashboard
Flexion of the sternum across the diagonal part of the seat belt, which acts as a fulcrum
While seatbelts decrease the risk of serious injury, they do not seem to decrease the risk of
sternal fractures during MVAs; however they do decrease the risk of internal injury, likely
because of the fracture mechanism.
In children, more likely related to a fall off a bicycle (direct) or from a height (indirect)

Vertebral fracture: Especially from indirect mechanism. Most commonly thoracic vertebrae,
but also may occur in lower cervical or upper lumbar vertebrae.
Rib fracture: Most often associated with a direct mechanism. Can cause flail chest.
Trauma to heart, mediastinum, great vessels, tracheobronchial tree, lung parenchyma, or
liver: Mediastinal injury much less common with an indirect mechanism. Always consider
cardiac contusion, especially with double or comminuted fracture and in fracture involving the
sternal angle.
Pneumothorax
Tamponade
Head injury
Limb fracture
Diagnosis
Chest posteroanterior and lateral radiographs postreduction
History
Direct blow to chest wall
Forced flexion of cervical spine (heavy blow to back of head or fall onto head or upper back)
Pain with inspiration
Crepitus with respiratory excursion
Dyspnea, usually transient. If persistent, consider more severe underlying injury.
Physical Exam
Pain
Tenderness
Bruising
Swelling
Deformity
Possible dyspnea
Localized tenderness
Palpable or visible step-off (deformity present with displaced fracture)
Palpable crepitus with respirations (more rare)
Edema, ecchymosis
Screen for associated rib fracture, clinical evidence of pulmonary contusion, vascular injury,
pneumothorax, and pericardial friction rub.

Imaging
Care must be taken not to confuse nonossified intrasternal cartilage in young patients with
fractures.
Chest posteroanterior (PA) and lateral radiographs (fracture missed in >80% of
anteroposterior views): Possible pneumothorax or mediastinal injury. Widened mediastinum
should not be attributed to hematoma, but instead to underlying vascular injury until ruled out.
Sternal fracture displacement and sternal dislocation occur in the sagittal plane.
ECG: May see ECG changes in >50%, especially if from a direct mechanism. No single test
is consistently reliable for diagnosis of myocardial contusion. If initial ECG is normal, consider
repeat in 24 hr. May see ST or T-wave abnormalities or bundle branch block. May see major
arrhythmia in 1st 24 hr (rare).
Cervical, thoracic, lumbar spine radiographs: Especially if from an indirect mechanism
Consider other modalities (echocardiogram, CT, aortography, serial creatine phosphokinase
levels) if underlying injury is suspected.
Costochondral dislocation
Sternoclavicular dislocation
Sternal contusion
Costochondritis
Cardiac contusion
Cardiac ischemia
Treatment
Narcotics appropriate once associated injuries are ruled out
Consider hematoma block if reduction is necessary.
Most nondisplaced fractures are treated conservatively with rest and analgesia
until symptoms subside.
Some displaced fractures can be reduced by having the patient lay supine and
hyperextending the thoracic spine by placing a sandbag transversely under the
shoulders, slightly below the level of the spines of the scapulae. Extension can
be maintained by bracing or bed rest.
For simple displaced fractures, some authors recommend having the patient
lay supine and simultaneously lifting the head and the extended lower
extremities, thus separating the upper and lower parts of the sternum. Use
thumb to place pressure on the anteriorly displaced fragment (should infiltrate
with local anesthetic first).
Open reduction internal fixation: Primary indication is pain with respiration that
limits respiratory excursion; also flail chest. If not stabilized, can have
pseudoarthrosis that can be source of ongoing pain or instability.
Consider 24-hr inpatient observation and monitoring due to the relatively high
likelihood of associated underlying injuries.
Immobilization typically is not necessary with nondisplaced fractures.
Short-term immobilization may be necessary after surgical repair.
Consider cardiac monitoring while performing reduction if available.
Avoid aggravating activities and contact sports.
May start general conditioning within the limits of discomfort
Surgical treatment for displaced fractures as above
Consider surgical repair if nonunion (rare).
Ongoing Care
Usually heals without any sequelae
Consider early orthopedic referral if displaced fracture, open fracture, or flail chest.
Early consultation as appropriate if there are associated underlying thoracic injuries
(pneumothorax, cardiac contusion, etc.)
Additional Reading
Athanassiadi K, Gerazounis M, Moustardas M, et al. Sternal fractures: retrospective
analysis of 100 cases. World J Surg. 2002;26:1243–1246.
Buckman R, Trooskin SZ, Flancbaum L, et al. The significance of stable patients with sternal
fractures. Surg Gynecol Obstet. 1987;164:261–265.
Ferguson LP, Wilkinson AG, Beattie TF. Fracture of the sternum in children. Emerg Med J.
2003;20:518–520.
Jones HK, McBride GG, Mumby RC. Sternal fractures associated with spinal injury. J
Trauma. 1989;29:360–364.
Kitchens J, Richardson JD. Open fixation of sternal fracture. Surg Gynecol Obstet.
1993;177:423–424.
Lyons FR, Rockwood CA. Orthopaedic sports medicine: principles and practice.
Mayba II. Sternal injuries. Orthop Rev. 1986;15:364–372.
Metaxas EK, Condilis N, Tzatzadakis N, et al. Sternal fracture with or without associated
injuries. Assessment of the difference in the diagnosis, management and complications.
Eighteen years of experience. Ann Ital Chir. 2006;77:379–383.
Recinos G, Inaba K, Dubose J, et al. Epidemiology of sternal fractures. Am Surg.

2009;75:401–404.
Santos GH. Treatment of displaced fractures of the sternum. Surg Gynecol Obstet.
1988;166:273–274.
Codes
ICD9
807.2 Closed fracture of sternum
807.3 Open fracture of sternum
807.4 Flail chest
Clinical Pearls
Contact sports should be avoided until symptoms subside, typically 6–12 wks.
General conditioning or training program permitted within the limits of
discomfort posed by the injury.
When returning to play, should consider chest protector if likelihood of reinjury.
Fracture, Stress: Metatarsal, Navicular
Stephen Simons
Gordon Givan
James Robinson
Basics
Description
Overload, repetitive stress injury to bone
Manifest as fatigue fractures to otherwise normal bone
Epidemiology
Stress fractures account for 0.7–15.6% of athletic injuries (1).
Metatarsal fractures are the second most common stress fractures; most frequent in track,
running, and dance (1).
Tarsal navicular stress fractures were thought to be rare, but they may be more common
than first thought. They occur mostly in running and jumping sports, with 73% occurring in
track (2).
Tarsal navicular stress fractures have been reported in athletes as young as 13 (3).
Risk Factors
Training errors: Number, frequency, intensity, and duration of strain cycles
Impact attenuation: Muscle fatigue, training surfaces, footwear
Gait mechanics: Foot type, lower extremity alignment, altered gait
Bone health: Nutrition, genetics, hormones, bone disease
Diagnosis
History
Pain onset acute or insidious? Usually insidious.
Pain location? Site of fracture; forefoot for metatarsal stress fractures and dorsomedial
midfoot for tarsal navicular stress fractures. Some patients may report ankle pain related to
the tarsal navicular stress fractures.
Associated findings? There is usually minimal or no swelling with stress fractures.
Does pain improve or worsen during the activity?
Tendinitis pain often improves as the injured tissue warms up, but stress fracture pain
persists or worsens during the activity.
Physical Exam
Metatarsals: Forefoot pain that progressively worsens with activity
Tarsal navicular: Vague, dorsal midfoot pain sometimes radiating along the medial arch or
into the ankle
Minimal or no forefoot swelling
Tenderness at the base, head, or midshaft of the metatarsal
Axial load applied to head of the metatarsal causes pain at the fracture site and distant to the
examination site.
Examine callous patterns, which may clue the examiner to excessive loads to individual
metatarsals.
Tender over the dorsum of the navicular at the “N” spot in the space between the anterior
tibial tendon and the extensor hallucis longus tendon
Biomechanical examination, joint range of motion, strength, and flexibility to assess
predisposing conditions

Imaging
Radiographs:
Metatarsals: Anteroposterior and lateral radiographs are often initially normal; 2–3 wks
following symptom onset, periosteal thickening and sometimes a radiolucent line can be
appreciated (1,4)[A].
Tarsal navicular: Plain radiographs often are normal throughout the course of a navicular
stress fracture (5,6,7)[A].
Bone scan:
Metatarsals: Very sensitive, but necessary only if a diagnosis is needed quickly, as with a
competitive athlete. Not specific and must be correlated with clinical history and
examination (1).
Navicular: Characteristically show radioactive uptake throughout the entire navicular (5,8)
[B]
CT scan:
Metatarsals: Not helpful
Navicular: Thin sliced cuts in the plane of the talonavicular joint reveal the curvilinear
fracture extending from the dorsal cortex surrounded by exuberant bony sclerosis. CT is
helpful to determine an incomplete fracture vs a complete dorsoplantar transection of the
navicular. CT scan can also help differentiate between navicular stress fracture and a
stress reaction (5,7)[A].
MRI:
Although generally not necessary, metatarsals will demonstrate intramedullary edema.
For tarsal navicular, alternative to bone scan considering cost and ionizing radiation. MRI
may distinguish an active tarsal navicular stress fracture from a mature fracture as
sometimes seen on CT.
Navicular fracture types (5):
Type I fractures involve only the dorsal cortex.
Type II fractures are fractures that extend into the navicular body.
Type III fractures traverse the entire navicular and extend into the plantar cortex.
Tendinitis
Tendon rupture, partial or complete
Metatarsalgia
Symptomatic accessory ossicle
Treatment
Metatarsals (1,4,9)[A]:
Cease sporting activities
Non-weight-bearing only needed for pain control
Rest period, average 6 wks
Navicular:
Non-weight-bearing on crutches with below-the-knee cast or removable
brace for 6–8 wks. High failure rate with weight-bearing rest (6,7,10)[A].
Studies continue to show poorer outcomes with early weight-bearing (7)[B].
Follow-up clinical assessment for tenderness at the “N” spot. Radiographic
assessment not helpful. Continued tenderness should extend non-weight-
bearing another 2–3 wks (6)[B].
Surgery is rarely required for metatarsal stress fractures (1,4,9)[B].
90% of navicular stress fractures can be managed with non-weight-bearing
cast. However, type III fractures should be referred for surgical management
[C].
Surgical fixation with internal screw, bone grafting, or both is necessary for
fractures not clinically healed by nonoperative means.
Recent studies show comparative long-term outcomes between conservative
non-weight-bearing and surgery (10,2)[B].
Ongoing Care
Metatarsals (1)[C]:
Non-weight-bearing aerobic training by swimming and pool running during the rest period
Advance to biking and stair climbing before running
Return to progressive gradual training only after pain-free walking and no local tenderness
at the fracture site.
Consider biomechanical control with custom orthotic to address excessive lesser
metatarsal loading.
Navicular (8)[C]:
1st 2 wks following cast removal: Activities of daily living, swimming, water running
2nd 2 wks: Assess “N” spot; if nontender, then 5 min jogging on grass every other day.
Gradually increase to 10 min per session.
3rd 2 wks: Assess “N” spot; if nontender, then faster running for short distances, ie, 50
meters on alternate days. Gradual speed increase.
4th 2 wks: Assess “N” spot; if nontender, then gradual return to full training over several
weeks. Average time to return to sport is 5–6 mos from diagnosis.
Attention throughout the rehabilitation time to soft-tissue massage and joint mobilization to
the talocrural, subtalar, and midtarsal joints.
Strength training to reverse the atrophy acquired during immobilization
Metatarsal stress fractures not healing in a reasonably expected period should be referred to
orthopedic surgery or podiatry. Consider referring for biomechanical evaluation for recurrent
stress fractures.
Navicular: Refer the persistently symptomatic navicular stress fracture that does not heal by
the above outlined protocol.
References
1. Brukner P, Bennell K, Matheson G, eds. Stress fractures. Champaign, IL: Human
Kinetics, 1999.
2. Potter NJ, Brukner PD, Makdissi M, et al. Navicular stress fractures: outcomes of
surgical and conservative management. Br J Sports Med. 2006;40:692–695; discussion
695.
3. Ostlie DK, Simons SM. Tarsal navicular stress fracture in a young athlete: case report
with clinical, radiologic, and pathophysiologic correlations. J Am Board Fam Pract.
2001;14:381–385.
4. Hatch RL, Alsobrook JA, Clugston JR. Diagnosis and management of metatarsal
5. Kiss ZS, Khan KM, Fuller PJ. Stress fractures of the tarsal navicular bone: CT findings in
55 cases. AJR Am J Roentgenol. 1993;160:111–115.
6. Khan KM, Brukner PD, Kearney C, et al. Tarsal navicular stress fracture in athletes.
Sports Med. 1994;17:65–76.
7. Burne SG, Mahoney CM, Forster BB, et al. Tarsal navicular stress injury: long-term
outcome and clinicoradiological correlation using both computed tomography and magnetic
resonance imaging. Am J Sports Med. 2005;33:1875–1881.
8. Quirk R. President's guest lecture: stress fractures of the foot. Ankle Int. 1998;19:494–
496.
9. Wienfeld SB, Haddad SL, Myerson MS. Metatarsal stress fractures. Clin Sports Med.
1994;16:319–338.
10. Torg J, Moyer J, Gaughan J. Management of tarsal navicular stress fractures—

conservative vs. surgical treatment: a meta-analysis. Presented at the AOSSM 2009
Annual Meeting.
Codes
ICD9
733.94 Stress fracture of the metatarsals
733.95 Stress fracture of other bone
Clinical Pearls
Risk factors for stress fractures include overuse or training errors,
biomechanical factors, choice or age of shoe, nutrition, and menstrual issues
for women.
Careful attention to the risk factors, particularly training errors, will minimize the
risk of reinjury.
Surgery is rarely indicated for metatarsal and tarsal navicular stress fractures.
Fracture, Talus
Mark Rowand
James E. Bray
Karl B. Fields
Basics
Description
Relatively uncommon fracture usually involving the talar neck, lateral process, or
osteochondral fracture of talar dome
Excluding smaller osteochondral fractures, talar neck fractures account for 50% of talar
fractures, talar body fractures 40%, and talar head fractures 5–10%.
Osteochondral fractures (a subset of talar body fractures) can occur in up to 6.5% of acute
ankle sprains.
Shepherd fracture (posterior tubercle fracture) represents the largest single group of talar
body fractures.
“Snowboarder's ankle,” a lateral process fracture, is the second most common type of talar
body fracture.
Stress fractures of the talus have been reported, but are rare (1).
Epidemiology
Talar fractures constitute 3–6% of all foot fractures, and are estimated at 1% of all fractures
in the entire human body.
“Snowboarder's ankle” (lateral process fracture) appears to be increasing in frequency.
Risk Factors
In general, fractures of the talar head and neck are the result of high-energy trauma.
Snowboarding is associated with acute dorsiflexion/inversion injuries to the ankle, which can
cause lateral process fractures.
Etiology
60–70% of the talar surface consists of cartilage, accommodating 7 different articulations.
The talus has no muscular insertions or origins, and is held in place by its osseous neighbors
and constraining ligamentous attachments.
The talar neck is the only section of the talus that is primarily extra-articular (2).
The tibiotalar articulation is responsible for hindfoot motion in the plantar/dorsiflexion plane;
the subtalar joint provides hindfoot inversion/eversion motion.
The talus transmits axial force.
The tibiotalar joint has more loads per unit area than any other joint in the body (3).
Only 40% of the talus can be perfused by blood vessels. The other 60% is covered by
articular cartilage. As a result, talus fractures are at a high risk of avascular necrosis (4).
Diagnosis
History
Fractures of the talar head and neck usually are found after high-velocity trauma, eg,
motorcycle accidents.
Fractures of the talar neck occur as a result of hyperdorsiflexion and axial loading of the foot
against a stationary tibia.
Crush fractures of the talar head occur via a compressive load through the calcaneous
sustentaculum tali.
Shear fractures of the talar head occur via an axial load through the navicular (5).
Anterolateral osteochondral fractures are associated with an inversion-dorsiflexion injury of
the ankle.
Posterolateral osteochondral fractures are associated with plantar flexion, inversion, and
external rotation of the ankle.
Lateral process fractures are the result of ankle dorsiflexion, inversion, and external rotation
(6).
Chronic osteochondral fractures present with pain following an adequate healing time for
ligamentous injury, complaints of ankle “giving out,” catching, or locking up.
Physical Exam
Talar head fractures cause swelling and tenderness at the talonavicular joint.
Talar neck fractures present with swelling and tenderness of the proximal dorsal foot. With
displaced fractures, the normal ankle contours will be changed.
Acute inversion injuries of the ankle that remain painful after conservative treatment should
make the clinician suspicious for osteochondral lesion of the talus or a lateral process
fracture.
Thoracolumbar spinal fractures have been found in association with fractures of the talar
neck and talar body (4).
Lateral talar process fractures have the same symptoms as an acute sprain of the anterior
talofibular ligament. Findings may include tenderness inferior and anterior to the tip of the
lateral malleolus, associated with pain on active and passive range of motion of the ankle and
subtalar joints.
Acute osteochondral fractures present with edema, ecchymosis, range of motion limited by
guarding, and pain to palpation.
Displaced talar neck fractures can lead to skin necrosis due to significant stretching of the
soft tissues (4).

Imaging
Initial radiographic workup of most talar fractures should include ankle mortise views with
routine anteroposterior (AP) and lateral views.
The Canale view (foot internally rotated 15 degrees with x-ray angled at 75 degrees from the
plane of the table) gives a direct AP view of the talus, and is very useful in evaluating talar
neck fractures (2).
To best view lateral osteochondral lesions with plain x-rays, films should be obtained with 10–
35 degrees of internal rotation and maximal plantar flexion.
Lateral osteochondral fractures have a thin, waferlike appearance; medial osteochondral
lesions have a deep, cup-shaped appearance.
If plain x-rays show abnormalities of the talar dome, CT scan should be performed to
determine size and nature of lesion, essential in preoperative planning.
Bone scan is indicated if history and physical are suspicious for osteochondral fracture but x-
rays are negative. If the bone scan is positive, MRI is required to evaluate the extent of the
osteochondral lesions (7).
Conditions that can mimic osteochondral fractures of the talar dome include osteochondritis
desiccans, degenerative joint disease, and/or loose bodies.
Treatment
Intra-articular corticosteroid injections may offer temporary relief of
osteochondral fractures, but have no beneficial effect on healing and are not
generally recommended.
Displaced talar fractures require anatomical reduction to prevent arthrosis and
avascular necrosis, and usually require surgical fixation.
Reduction of a displaced talar neck fracture can be attempted by plantar flexion
of the foot, bringing the head and body into line. This is an orthopedic
emergency if there are signs of skin necrosis.
Clinical signs and symptoms correlated with repeated radiographic examination
are important during conservative treatment to assure proper healing.
Nondisplaced acute talar fractures may be treated in a short, nonweight-
bearing leg cast for 6–12 wks. There should be evidence of healing before
weight-bearing is resumed.
Subacute nondisplaced osteochondral fractures can be treated initially with
cast immobilization and limited weight-bearing, with follow-up radiographs in 4–
6 wks and progression to full ambulation after 12–16 wks (3).
Stress fractures are treated with 3–6 wks of nonweight-bearing immobilization
with a CAM walker, followed by progressive mobilization, rehabilitation, and
return to activity based on case reports.
50% of talar neck fractures go on to avascular necrosis, as do 25–50% of
talar body fractures.
Treatment of osteonecrosis is primarily conservative, and patient can begin
weight bearing once there is evidence of stable changes on x-ray. Failure of
conservative measures to allow weight bearing may require surgery (4).
Talar head fracture complications include midtarsal instability, talonavicular
arthritis, and avascular necrosis of the talar head.
Standard range of motion, strengthening, and proprioceptive rehabilitation are
appropriate after the fracture has healed.
Any talar fracture that is displaced, even minimally, requires surgical treatment,
given the risks of avascular necrosis and future arthritis.
Nondisplaced osteochondral fractures can be managed conservatively for up
to 12 mos without compromising subsequent surgical outcomes.
Any loose body associated with a fracture may require arthroscopic removal.
References
1. Ahmad J, Raikin SM. Current concepts review: talar fractures. Foot Ankle
Int. 2006;27:475–482.
2. Boon AJ, Smith J, Laskowski ER. Snowboarding injuries. Physician

Sportsmed. 1999;27:94–104.
3. Boon AJ, Smith J, Zobitz ME, et al. Snowboarder's talus fracture.

Mechanism of injury. Am J Sports Med. 2001;29:333–338.
4. Fortin PT, Balazsy JE. Talus fractures: evaluation and treatment. J Am

Acad Orthop Surg. 2001;9:114–127.
5. Grossman JP, Lyons MC. A review of osteochondral lesions of the talus.

Clin Podiatr Med Surg. 2009;26:205–226.
6. Higgins TF, Baumgaertner MR. Diagnosis and treatment of fractures of the

talus: a comprehensive review of the literature. Foot Ankle Int. 1999;20:595–
605.
7. Juliano PJ, Dabbah M, Harris TG. Talar neck fractures. Foot Ankle Clin.
2004;9:723–736, vi.
Additional Reading
Mandracchia VJ, Buddecke DE, Giesking JL. Osteochondral lesions of the
talar dome. A comprehensive review with retrospective study. Clin Podiatr
Med Surg. 1999;16:725–742.
Mayer D. Isolated talus fractures: description of a new clinical sign. Am J

Emerg Med. 1997;15:412–414.
Schachter AK, Chen AL, Reddy PD, et al. Osteochondral lesions of the talus.
J Am Acad Orthop Surg. 2005;13:152–158.
Shea DJ, Feder JM, Boylan JP. Fractures of the lateral process of the talus:
two case reports and a comprehensive literature review. Foot Ankle Int.
1998;19:1646.
Shea MP, Manoli A II. Recognizing talar dome lesions. Physician Sportsmed.
1993;21:109–121.
Sormaala MJ, Niva MH, Kiuru MJ, et al. Outcomes of Stress Fractures of the
Talus. Am J Sports Med. 2006.
Codes
ICD9
825.21 Fracture of astragalus, closed
825.31 Fracture of astragalus, open
Fracture, Tibial Plateau
Ramon Ylanan
Steve Kroll
Basics
Tibial plateau fractures are rare in children because of the dense cancellous bone of the tibial
plateau (1).
Schatzker classification system:
Type 1 is a split-off fracture of the lateral tibial plateau without compression of the plateau
(2).
Occurs in younger patients where the plateau resists depression (2)
Usually occurs from a valgus force to the knee in combination with axial load
Type 2 is a combination of a split fracture and depression of all or a portion of the
remaining lateral plateau. The mechanism is similar to the preceding, but these patients
tend to be older and have weaker bones; the plateau can be depressed by the femoral
condyle (2).
Type 3 is a local depression of the articulating surface of the lateral plateau (2).
Type 4 is a fracture/depression of the medial plateau (2).
It requires much more force for this injury to occur (2).
Be suspicious for other concomitant injuries, such as damage to the popliteal artery,
peroneal nerve, lateral collateral ligament, medial meniscus, and cruciate ligaments
Type 5 is a bicondylar fracture (2). High-impact injury associated with popliteal vessel
injury, peroneal nerve injury, and possible development of compartment syndrome
Type 6 is a bicondylar, grossly comminuted fracture involving both the plateau and the
metaphysis (2). Occurs from a violent force, usually a fall from a height; it is typically
associated with neurovascular compromise and compartment syndrome.
Cautions:
With high-energy mechanisms, associated major life-threatening injuries take precedence.
Immobilize to prevent further neurologic or vascular injury.
Description
Fracture or depression of the proximal tibial articulating surface
Also referred to as tibial condylar fractures
Valgus or varus force applied in combination with axial loading (3):
A pedestrian struck by an automobile (fender fracture, where the bumper of a vehicle
strikes the lateral aspect of the proximal tibia) is the most common mechanism of injury.
This usually results in splitting or depression of the lateral plateau.
The younger the patient, the more resistant the plateau is to depression.
Elderly patients present more often with depression-type fractures.
Fall from a height causing femoral condyles to impact on tibial surface
Violent twisting force, eg, skiing
Medial plateau fractures are much less common and require significant force to occur (3).
Associated injuries include ligamentous damage (lateral collateral, posterior cruciate, and
medial meniscus) and neurovascular injury (peroneal nerve and popliteal vessels) to that
knee.
Epidemiology
Incidence
1% of all fractures (4).
Of tibial plateau fractures, 55–70% are lateral, 10–23% are medial, and 11–31% are
bicondylar (4).
Rate of associated ligamentous injury varies from 7–15.7% (5).
Diagnosis
Include oblique views as part of routine radiography (6).
Neurovascular examination:
High-energy mechanism (medial plateau or bicondylar fractures) carries risk of
neurovascular damage and compartment syndrome.
Check popliteal, posterior tibial, and dorsalis pedis arterial pulses.
Check integrity of peroneal nerve and ankle and toe dorsiflexion and sensation in the
webspace between the great and second toes.
Plain radiography:
Anteroposterior and lateral views of the knee and proximal tibia
Include oblique views
Cross-table lateral view may demonstrate lipohemarthrosis (fat-fluid level).
Pay attention to areas of ligamentous attachment, where avulsion fractures may take
place, ie, medial and lateral femoral condyles, intercondylar eminence, and fibular head.
Physical Exam
Painful, swollen knee
Inability to bear weight on the injured leg
Knee effusion (hemarthrosis)
Decreased (both active and passive) range of motion (ROM) of the knee
Tenderness along the proximal tibia (either medial or lateral tibial plateau)
Possible varus or valgus deformity of the knee
Possible joint instability owing to associated ligamentous injury

Imaging
Tibial plateau view–anteroposterior (AP) view with the knee in 10–15 degrees of flexion helps
to visualize depressions (6).
Oblique: Internal and external: May help to determine the location and degree of depression
that may not apparent on other films (6)
MRI can be used to better view soft tissue injuries and classify using the Schatzker system,
especially in the pediatric population (6).
CT scan: May help to determine the size of the fracture and depression of the fragments (6)
Angiography is indicated if:
High-energy mechanism
Schatzker type 4, 5, or 6 fracture
Alteration in distal pulses
Expanding hematoma
Bruit
Injury to anatomically related nerves
Compartment pressures if suspected compartment syndrome:
Pain not over fracture site
Pain on passive stretch
Paresthesias
Abnormality of pulses
Pressures >30 mm Hg are an indication for fasciotomy.
Arthrocentesis to look for fat globules if mechanism strongly suggests that fracture and
effusion are present without x-ray findings
Knee dislocation
Cruciate ligament tears/avulsion
Meniscal tears
Quadriceps tendon rupture
Patellar fracture
Patellar dislocation
Treatment
Pre-Hospital
ABCs/ATLS protocol in multiple-trauma victim
Long-leg splint
Ice
Elevation
ED Treatment
Non-weight-bearing
Pain control
Nondisplaced fractures or minimally displaced lateral plateau fractures without
ligamentous injury:
Aspiration of hemarthrosis and injection of local anesthetic
Examination for ligamentous instability
If knee is stable:
Compressive dressing
Ice and elevation for 48 hr
Non-weight-bearing/crutches
Early orthopedic follow-up if knee is not stable
Blokker and colleagues recommended open reduction with internal fixation
(ORIF) for fractures with >5 mm of depression or 1 mm of displacement (5).
Open fractures:
Remove contaminants.
Apply moist sterile dressing.
Assess tetanus immunity.
Antibiotics
Emergent orthopedic consultation
Admission Criteria
Open fractures for débridement, irrigation, and IV antibiotics
Comminuted bicondylar fractures for traction
High-energy mechanism for observation of neurovascular status
Suspected compartment syndrome
Pain control (7)
Discharge Criteria
Nondisplaced fractures
Minimally displaced, stable fractures of the lateral plateau
Ongoing Care
Nonoperative management:
Fractures with <5 mm of depression or 1 mm displacement (5)
Non-weight-bearing and early ROM are critical (3).
Average time to heal is 12–20 wks (3).
Timetables:
Initially, patient in brace with full extension for 10–14 days (3)
Begin gradual ROM, with goal of 90 degrees of flexion by 4 wks (3).
Non-weight-bearing for 4–6 wks or until radiographic evidence of healing is noted; then
may proceed with partial weight-bearing with crutch assistance (3)
Follow-up every 2–3 wks, repeating radiographs at each visit to document healing (3)
Formal physical therapy early can help to restore function (3).
Hinged knee brace for support should be used during the healing process (3).
References
1. Rang M. Children's fractures. 2d ed. Philadelphia: JB Lippincott, 1984.
2. Simon RR, Sherman SC, Koenigsknecht SJ. Proximal Tibia Fractures. In: Simon RR,
Sherman SC, Koenigsknecht eds. Emergency orthopedics: the extremities 5th ed. Norwalk
CT: Appleton and Lange, 2007:396–403.
3. Eiff MP, Hatch RL, Calmbach WL: Fracture management for primary care. Saunders.
2003:269–273.
4. Wiss DA, Watson JT, Johnson EE. Fractures of the knee. In: Rockwood CA, Green DP,
Bucholz RW, et al. eds. Rockwood and Green's fractures in adults. 4th ed. Philadelphia:
Lippincott-Raven, 1996:1593–1652.
5. Blokker CP, Rorabeck CH, Bourne RB. Tibial plateau fractures. An analysis of the results
of treatment in 60 patients. Clin Orthop Relat Res. 1984:193–199.
6. Markhardt BK, Gross JM, Monu JU. Schatzker classification of tibial plateau fractures:
use of CT and MR imaging improves assessment. Radiographics. 2009;29:585–597.
7. Torrey SB. Lower extremity and pelvis trauma. In: Barkin ed. Pediatric emergency
medicine. St. Louis: CV Mosby. 1992:357–365.
Additional Reading
Wheeless III, Clifford R. January 18, 2008.
[http://www.wheelessonline.com/ortho/tibial_plateau_fractures]
Codes
ICD9
Fracture, Tibial Spine Avulsion
Quynh Hoang
Chris Koutures
Basics
Description
Avulsion fractures occur when either the tendon-bone or ligament-bone interface is ruptured
by forceful muscle contraction or undue ligament stress.
In children, the weaker, incompletely ossified bone will fail before the ligament or tendon is
injured.
Thus an injury that typically would result in an anterior cruciate ligament (ACL) tear in an adult
instead would cause a fracture through the anterior tibial spine via pull of the ACL.
Fracture through the posterior tibial spine (where the posterior cruciate ligament attaches) is
rare and generally occurs in skeletally mature patients.
Hyperextension ± valgus stress or rotation about the knee
Fracture also can occur with a direct blow to the distal end of the femur with the knee
flexed.
Synonym(s): Tibial eminence fracture; Intercondylar eminence fracture
Epidemiology
Avulsion fractures of the ACL attachment to the tibial spine are most prevalent in children 8–
14 yrs of age but are seen in adults >35 yrs of age who have low bone density.
ACL avulsion from the femoral attachment is less common, as is posterior cruciate ligament
avulsion from the posterior tibial eminence.
Tibial spine fractures classically have been associated with a fall from a bicycle or motorcycle
on an outstretched leg (1)[B],(2)[C],(3)[C].
The injury is now also commonly seen in sporting activities (1)[B],(2)[C],(3)[C].
Risk Factors
Children <16 yrs of age
Adults >35 yrs of age who are osteopenic

In adolescents and adults, tibial spine avulsion fractures are commonly associated with a
concomitant injury to the medial collateral ligament (1)[B],(2)[C].
Diagnosis
History
In children aged 8–11 yrs, often due to hyperflexion injury
Above this age, owing to either hyperextension injury or single-leg landing from a jump, both
associated with a rotational or twisting stress to the knee
Audible “pop” at the time of injury
Immediate (within 1–2 hr) prominent swelling of the knee (acute hemarthrosis)
Frequently unable to bear weight after injury
Physical Exam
Signs and symptoms:
Presence of a large, tense knee effusion (especially in a child <16 yrs of age) should raise
concern for a potential ACL avulsion fracture.
Examination findings of an ACL tear should raise suspicion.
Large, tense effusion noted with loss of full range of motion (ROM).
ACL stress tests (Lachman, anterior drawer, and pivot shift) show more forward
translation of the tibia compared with the noninjured side.
A positive posterior drawer sign or if the tibia is displaced posteriorly relative to the femur
when compared with the noninjured knee may suggest posterior cruciate ligament avulsion
from the tibial spine.
Evaluate other ligamentous and meniscal structures, particularly the medial collateral
ligament, for concomitant pathology.

Imaging
Plain radiographs should include anteroposterior (AP), lateral, and tunnel views. The latter
outlines the femoral notch and tibial eminence.
The lateral view is most helpful to assess fracture position and degree of displacement.
Grades of anterior tibial spine avulsion fractures are based on degree of displacement. The
Meyers and McKeever classification scheme is the most widely accepted.
Type I: Minimal displacement of the anterior eminence
Type II: Elevation of the anterior third to half of the eminence with hinging on posterior
eminence
Type IIIA: Complete displacement and separation of fragment without rotational
malalignment
Type IIIB: Complete displacement and separation of fragment with rotational malalignment
Types II and III are of equal incidence and are more common than type I.
With negative plain radiographs, nondisplaced fracture or ligament injury still must be
suspected in patients with acute hemarthrosis. MRI should be obtained in these instances to
further evaluate extent of injury.
Midsubstance ACL tear
Congenital absence or deficiency of the ACL
Midsubstance tear of the posterior cruciate ligament
Tibial plateau fracture
Patellar dislocation or subluxation
Osteochondral fracture of the femoral condyle
Treatment
Acute treatment
Analgesia:
NSAIDs and narcotic medications are used initially for pain control.
Frequent application of ice for 20-min periods is recommended.
Aspiration of the joint may enhance comfort and allow further knee extension.
Lack of full knee extension may imply a mechanical block (ie, fracture fragment
or meniscal tear).
Immobilization:
Initial care includes complete knee immobilization with minimal knee flexion
for 2–3 days until effusion begins to resolve.
Crutch ambulation is recommended in this initial stage.
Type I fracture: After effusion resolves, type I fractures are best managed by
long-leg-cast immobilization with knee flexed at 10–20 degrees for 4–6 wks
(1)[B].
Type II and III fractures:
Controversy still exists regarding optimal treatment for fractures with greater
degrees of displacement.
Type II tibial spine fractures can be managed by either closed reduction with
the knee immobilized in full extension or surgically with arthroscopy or open
reduction and internal fixation (1)[B].
Numerous studies have shown no significant differences in outcome
measures of residual ACL laxity between closed vs open reduction methods
so long as fracture reduction is maintained (1)[B].
Type III fractures generally require open or arthroscopic reduction with
fragment fixation (1)[B].
If requiring open reduction, better results are obtained if surgery is done
within the 1st wk after injury. Prompt surgical referral is essential.
The knee should be immobilized while awaiting surgical consultation.
Referral
All suspected ACL avulsion fractures should be referred to an orthopedic
surgeon.
Patients with open growth plates would benefit from consultation with a pediatric
orthopedist.
After completion of cast immobilization, focus should be on recovering full knee
ROM followed by strengthening of knee extensors.
Proprioception is another key part of the rehabilitation process.
Arthroscopic or open reduction with internal fixation should be performed for
displaced type II fractures if closed methods fail to obtain or maintain reduction
of fracture fragment. Type III fractures generally require arthroscopic or open
reduction with internal fixation.
Many authors prefer arthroscopic reduction owing to less surgical trauma and
easier postoperative rehabilitation course.
Ongoing Care
In the immediate postinjury or postoperative period, follow-up radiographs are necessary to
evaluate for loss of fracture reduction.
Prognosis
Tibial spine fractures generally have an excellent prognosis, even when the fracture fragment
is completely displaced.
Despite true anatomic reduction, about 50% of pediatric patients may have mild objective,
measurable ACL laxity owing to interstitial ligament damage that occurs before the avulsion.
However, it does not result in functional instability.
Fewer data on treatment outcome are available for skeletally mature patients, with one study
by Aderinto and colleagues reporting symptomatic knee instability as the main complication of
nonoperative treatment of tibial spine fractures (2)[C].
Complications
Although overall prognosis is remarkably good, some complications may include
Loss of full knee extension owing to arthrofibrosis from immobilization or from
mechanical block secondary to loss of reduction or malunion of fracture
fragment (1)[B]
Knee stiffness, particularly in skeletally mature patients who underwent tibial
spine fixation (2)[C]
References
1. Accousti WK, Willis RB. Tibial eminence fractures. Ortho Clin N Am.
2003;34:365–375.
2. Aderinto J, Walmsley P, Keating JF. Fractures of the tibial spine:

epidemiology and outcome. The Knee. 2008;15:164–167.
3. Wiley JJ, Baxter MP. Tibial spine fractures in children. Clin Ortho Relat
Res. 1990:54–60.
Additional Reading
Lastihenos M, Nicholas SJ. Managing ACL injuries in children. Physician
Sportsmed. 1996;24:59–70.
Stanitski C, Sherman C. How I manage physeal fractures about the knee.
Physician Sportsmed. 1997;25:108–121.
Codes
ICD9
823.10 Open fracture of upper end of tibia
Fracture, Volkmann: Posterolateral Tibiofibular
Ligament Avulsion
Matt DesJardins
Basics
Volkmann fracture is a rare injury in children <14 yrs of age, given the relative weak physis of
the tibia.
Salter-Harris fractures occur during external rotation and abduction injuries, which only
occasionally involve the posterior tubercle. The fracture fragment usually is contiguous with
the medial malleolar fragment.
The Lauge-Hansen (L-H)1, Danis-Weber, and Orthopaedic Trauma
Association/Arbeitsgemeinschaft für Osteosynthesefragen systems have been used to
describe ankle injury patterns. The L-H system can aid in closed reduction maneuvers.
Volkmann fracture is classified by the L-H system as supination external rotation (SER) stage
III, pronation external rotation (PER) stage IV, and pronation abduction (PA) stage II.
In SER injuries, anterior inferior talofibular ligament (AITFL) rupture and spiral fracture of the
fibula precede Volkmann fracture.
In PER injuries, deltoid ligament rupture, medial malleolar fracture, AITFL disruption, and
oblique fibular fracture may precede Volkmann fracture.
In PA injuries, deltoid ligament rupture or avulsion of the medial malleolus may occur first.
Description
Ankle fracture involving avulsion of the posterior lip of the tibia at its articular surface
(Volkmann tubercle)
Fracture occurs via a force through the PITFL at its tibial attachment.
Epidemiology
Few data exist regarding incidence or prevalence of isolated posterior malleolar fracture.
Volkmann fracture generally occurs concurrently with other malleolar fractures, deltoid and
syndesmotic membrane injuries.
Associated with spiral tibia fractures (2,3)
Etiology
Volkmann tubercle is part of the posterior aspect of the medial malleolus of the ankle,
commonly referred to as the posterior malleolus.
The posterior malleolus extends from the fibular notch of the tibia to the medial malleolus.
The PITFL's attachment to the posterior malleolus resists posterior translation of the talus.
The PITFL is 1 of 4 syndesmotic ligaments that maintain integrity between the tibia and
fibula. Also referred to as the posterior tibiofibular ligament.
Diagnosis
History
Ankle injury involving a Volkmann fracture is rarely subtle, given typical concomitant fractures
and ligament tears.
A mechanism of injury involving external rotation or abduction and the presence of associated
injuries should evoke suspicion.
Any floor or field sport, particularly those with contact, can result in posterior malleolar
fracture.
Patients should be questioned for elapsed time since injury, mechanism, associated sounds
such as “pops” or “cracks,” and weight-bearing ability.
Physical Exam
Emergent examination:
Should focus on neurovascular compromise secondary to joint dislocation or calf
compartment syndrome and skin integrity
Doppler US should be used if pulses are nonpalpable, and a detailed sensorimotor
examination of the foot should be done.
Concern for early compartment syndrome should prompt measurement of calf
compartment pressures.
Nonemergent examination:
Systematic ankle, foot, leg, and knee examination should be performed.
Observation, palpation, and careful range of motion should be done, followed by stability
testing.
Acute examination will reveal a painful, tender, and swollen ankle consistent with a
moderate or severe injury.
Possible findings include an increased posterior drawer test, increased internal rotation,
and, with associated syndesmotic instability, a positive squeeze and external rotation test.
Imaging
Anteroposterior, lateral, and mortise views are standard.
Lateral films generally show the posterior malleolar fracture, but do not reliably estimate the
size of the avulsion or the articular surface involvement (4). Some authors recommend an
external rotation lateral view (45–50 degrees) to estimate fragment size (5).
Standard views will diagnose associated injuries that are almost always present.
Stress radiographs are controversial and not routinely indicated.
If Volkmann fracture is seen on plain film evaluation, CT is recommended to elucidate the
extent of articular involvement and size of the fragment, which are instrumental in determining
treatment.
MRI reserved for evaluation of soft tissues and generally not indicated unless CT films are
inadequate.
Treatment
Closed reduction generally not indicated for definitive treatment
Closed reduction is indicated prior to definitive treatment if the neurovascular
structures or skin are compromised.
Fracture of posterior malleolus usually is accompanied by fracture of lateral
and/or medial malleoli, and involves significant articular surface or fibular
displacement.
Small (<25% of distal tibia), nondisplaced, incomplete fractures can be
considered for a short-leg walking cast with appropriate orthopedic
consultation.
Use of a modified Jones compression dressing and posterior splint is
important to reduce swelling, which when untreated, can increase risk of poor
surgical outcome.
Compression dressing with frequent icing and elevation can allow for operative
intervention in the 1st 2–3 days.
General Measures
Usually occurs with external rotation or abduction
Given that the PITFL is markedly stronger than the anterior inferior tibiofibular
ligament (AITFL), the torsional/rotational forces rupture the AITFL but avulse
the posterior tibial tubercle through an intact PITFL.
Complicated ankle fractures require immediate assessment of the
neurovascular status of the foot.
If compromised, reduction of dislocation or deformity should be accomplished
immediately by closed reduction using the L-H classification to reverse order of
injury.
Ongoing Care
Controversy exists as to whether all posterior malleolar fractures need to be internally
fixated (6).
Volkmann tubercle often reduces spontaneously with reduction of the fibula and/or medial
malleolus.
Size of the fragment and its proportion of the articular surface are predominant factors in
determining the need for internal fixation.
Most recommend internal fixation if 25–35% of the articular surface is fractured (4,6).
If factors such as displacement of malleoli, talar subluxation, plafond articular incongruity, or
syndesmotic instability exist, internal fixation is recommended.
Prognosis
Posterior tubercle fractures adversely affect the prognosis of ankle fractures compared to
single or bimalleolar fractures (7).
These fractures have an increased risk of joint dislocation and osteoarthritis.
Postoperative arthritis varies with the size of the fragment and amount of articular surface
involvement, but those requiring internal fixation have ≥35% likelihood of osteoarthritis.
References
1. Lauge-Hansen N. Fractures of the ankle. II. Combined experimental-surgical and
experimental-roentgenologic investigations. Arch Surg. 1950;60:957–985.
2. Boraiah S, Gardner MJ, Helfet DL, et al. High association of posterior malleolus fractures
with spiral distal tibial fractures. Clin Orthop Relat Res. 2008.
3. Hou Z, Zhang Q, Zhang Y, et al. A occult and regular combination injury: the posterior
malleolar fracture associated with spiral tibial shaft fracture. J Trauma. 2009;66:1385–
1390.
4. Haraguchi N, Haruyama H, Toga H, et al. Pathoanatomy of posterior malleolar fractures

of the ankle. J Bone Joint Surg Am. 2006;88:1085–1092.
5. Ebraheim NA, Mekhail AO, Haman SP. External rotation-lateral view of the ankle in the
assessment of the posterior malleolus. Foot Ankle Int. 1999;20:379–383.
6. Clare MP. A rational approach to ankle fractures. Foot Ankle Clin. 2008;13:593–610.
7. Fitzpatrick DC, Otto JK, McKinley TO, et al. Kinematic and contact stress analysis of
posterior malleolus fractures of the ankle. J Orthop Trauma. 2004;18:271–278.
Additional Reading
Mandracchia DM, Mandracchia VJ, Buddecke DE. Malleolar fractures of the ankle. A
comprehensive review. Clin Podiatr Med Surg. 1999;16:679–723.
Michelson JD. Fractures about the ankle. J Bone Joint Surg. 1995;77A:142–152.
Stanitski CL. Pediatric and adolescent sports injuries. Clin Sport Med. 1997;16:613–633.
van den Bekerom MP, Haverkamp D, Kloen P. Biomechanical and clinical evaluation of
posterior malleolar fractures. A systematic review of the literature. J Trauma. 2009;66:279–
284.
Vander Griend RA, Savoie FH, Hughes JL. Fractures of the ankle. In: Rockwood CA Jr,
Green DP, Bucholz RW, eds. Rockwood and Green's fractures in adults, vol. 2, 3rd ed.
Philadelphia: JB Lippincott, 1991:1983–2039.
Vander Griend R, Michelson JD, Bone LB. Fractures of the ankle and the distal part of the
tibia. Instr Course Lect. 1997;46:311–321.
Codes
ICD9
824.0 Fracture of medial malleolus, closed
Fracture, Zygoma
Martha A. Dodson
Basics
Maxillofacial fractures are rarely seen in the pediatric population.
Children have a comparatively larger cranium than facial skeleton, leading to a higher
incidence of head trauma.
Falls and motor vehicle accidents account for the majority of facial trauma in children.
Consider nonaccidental trauma, particularly in children under age 6.
Description
Fractures of the zygoma result from blunt trauma to the side of the face.
The most common mechanisms include motor vehicle accidents, falls, and physical assault.
The direction and magnitude of force will determine the fracture type and degree of
displacement.
A blow to the side of the face directed posteriorly and medially will produce a zygomatic
body (tripod) fracture.
A lateral blow often results in an isolated zygomatic arch fracture.
Zygoma fractures may have associated paranasal sinus fractures.
Risk Factors
Motor vehicle collisions
Falls
Assault
Blunt-force trauma from athletic equipment including ball(s)
General Prevention
Appropriate use of athletic helmet/face shield
Proper use of vehicle safety restraints

Facial lacerations
Ecchymosis
Edema
Palpable defect
Trismus
Orbital floor fracture
Maxillary sinus fracture
Diagnosis
Sedation may be required to properly examine some children.
If a head injury is suspected, sedation is not recommended.
If circumstances or injuries raise suspicions of child abuse, a comprehensive investigation for
previous nonaccidental trauma is essential.
If a high-velocity or severe blunt-force mechanism is suspected, a thorough evaluation for
associated injuries (cervical spine, head, globe, other maxillofacial bones, etc.) is imperative.
Radiographs:
The submental vertex (jug-handle) view is used to diagnose fractures of the zygomatic
arch.
Plain films are not as useful in the evaluation of zygomatic body fractures.
The Waters (occipitomental) view shows the inferior orbital rims and possibly layering of
blood in the maxillary sinus.
The articulation between the zygoma and frontal bone can be evaluated on the Caldwell
view.
Pre Hospital
ABCs:
Airway
Breathing
Circulation
Cervical spine: Immobilization PRN.
Cautions:
Airway compromise may occur with severe maxillofacial injuries.
Assume that the patient with face or head injury has also sustained a cervical spine injury
until proven otherwise.
History
Direct blow to face with ball, elbow, or sports equipment
May or may not have loss of consciousness
May complain of double vision owing to orbital floor disruption
May complain of trismus
Physical Exam
Signs and symptoms:
Malar edema or flattening
Periorbital ecchymosis, drooping lateral canthus
Lateral subconjunctival hemorrhage, diplopia
Infraorbital anesthesia, trismus/open bite
Intraoral palpation of the zygomatic body and arch for bony step deformity
Palpation of arch for crepitance and/or step-off deformity
Assess sensation of the inferior orbital area (cheek, upper lip, and gingiva).
Examine the globe and orbit carefully.
Periorbital ecchymosis and lateral subconjunctival hemorrhages are common.
Assess visual acuity, pupillary function, and extraocular movements.
Inferior displacement of the globe may lead to diplopia and enophthalmos. Carefully
evaluate extraocular movements.
Mandibular movement may be restricted.
Trismus may be seen if there is impingement of the mandibular coronoid process by
displacement of the zygomatic body.
Zygomatic arch fractures may impede the temporalis muscle or coronoid process.
Lastly, temporalis muscle contusion or temporomandibular joint (TMJ) effusion may cause
pain that limits range of motion (ROM).
Unilateral epistaxis may be present and typically resolves spontaneously.

Imaging
CT scan is the diagnostic standard for evaluation of zygomatic body fractures.
CT scan is not usually needed for isolated fractures of the zygomatic arch.
Facial contusions
La Forte fractures
Treatment
Multiple injuries are often seen in children, including head trauma, skull fracture,
and orthopedic injuries.
Definitive repair of facial fractures should not be delayed beyond 3 or 4 days.
The facial bones heal rapidly in children, and delays of more than 3–4 days
may result in malunion and cosmetic deformity.
Consult social services and local child welfare agency if needed.
ED Treatment
Assume that the patient with head and maxillofacial trauma has a cervical spine
injury. The neck should be immobilized until radiographic clearance is obtained.
Do not blindly clamp bleeding vessels because this may cause inadvertent
damage to the facial nerve, parotid duct, etc.
Early consultation with oral maxillofacial or plastic surgeon
Analgesics, antibiotics, and tetanus prophylaxis if open injury P.
Airway management is particularly important if there are associated
maxillofacial or mandibular injuries causing airway compromise. Isolated
zygoma fractures do not typically require aggressive airway intervention.
Medication
Perioperative antibiotics for contaminated field
Referral
Refer all open and/or displaced and comminuted fractures to oral and
maxillofacial surgery.
Open reduction with internal fixation (ORIF): Secured with plates and screws
and occasionally wire.
Delayed fracture displacement, poor cosmetic outcome, and difficulty with
mandibular movement are indications for ORIF.
Isolated arch fractures are amenable to outpatient treatment. These typically
require open reduction of fracture fragments. If the reduction is unstable,
internal fixation is then performed.
Nondisplaced tripod fracture can be treated conservatively as an outpatient
with close follow-up.
ABCs
Cervical spine immobilization PRN
Admission Criteria
Displaced or comminuted zygomatic body fractures require open reduction and
internal fixation.
Associated head, neck, or other traumatic injuries requiring admission
IV Fluids
Medications:
Sedative/Analgesics* Adult Dose (mg/kg IV) Pediatric Dose (mg/kg IV)
Diazepam 0.1–0.2 0.1–0.2
Fentanyl 2–10 (µg/kg) 2–3 (μg/kg)
Ketamine 2 1–2
Meperidine 1–2 1–2
Midazolam 0.1 0.15
Morphine sulfate 0.1–0.2 0.1–0.2
*All these sedative/analgesics should be titrated to effect.
Ongoing Care
Consider custom face mask for return to play.
Diet
As tolerated safely given extent of oral/maxillary involvement
Patient Education
Proper usage of safety equipment
Additional Reading
Bell RB, Dierks EJ, Brar P, et al. A protocol for the management of frontal sinus fractures
emphasizing sinus preservation. J Oral Maxillofac Surg. 2007;65:825–839.
Colucciello SA, Sternbach G, Walker SB. The treacherous and complex spectrum of
maxillofacial trauma: etiologies, evaluation, and emergency stabilization. Emerg Med Rep.
1995;16;7:59–69.
Covington DS, Wainwright DJ, Teichgraeber JF, et al. Changing patterns in the epidemiology
and treatment of zygoma fractures: 10-year review. J Trauma. 1994;37:243–248.
Hunter JG. Pediatric maxillofacial trauma. Pediatr Clin North Am. 1992;39:1127–1143.
Kaufman BR, Heckler FR. Sports-related facial injuries. Clin Sports Med. 1997;16:543–562.
Rumsey C, Sargent LA. Zygomatic fractures. Trauma Q. 1992;9:76–85.
Codes
ICD9
802.4 Closed fracture of malar and maxillary bones
802.5 Open fracture of malar and maxillary bones
Freiberg's Disease
Christopher McGrew
Rodolfo R. Navarro
Basics
Description
Osteonecrosis of the superior portion of the metatarsal head of unknown etiology
Freiberg 1st described this entity in 1914 in 6 patients as an infraction (incomplete fracture
without displacement of the fragments).
4th most common osteochondrosis
Affects women more commonly than men
Synonym(s): Freiberg's infraction; Eggshell fracture; Koehler's second disease; Peculiar
metatarsal disease; Malakopathy
Epidemiology
Incidence unknown
Male: Female ratio is 1:5
Peak onset around 11–17 yrs, but may happen up into 30s
Most common involvement is the 2nd metatarsal head
2nd most common involvement is the 3rd metatarsal head
Usually affects the longest metatarsal
Occasionally seen in sports requiring sprinting and jumping
Risk Factors
No known risk factors
May be related to repetitive microtrauma vs vascular deficiency or both
Genetics
Unknown
General Prevention
None
Etiology
No single clear etiologic factor exists.
The process is postulated to be a combination of traumatic and vascular factors:
Traumatic factors include metatarsal stress during normal activity and/or abnormal
biomechanics of the forefoot intrinsically or as a result of footwear, causing repetitive
microtrauma upon the dorsal aspect of the distal metatarsal head.
Vascular factors include abnormal metatarsal head vascular variations, as well as trauma-
induced vessel damage, spasm, and eventual ischemia.

None known
Diagnosis
History
Slow development of significant, dull, aching pain over affected metatarsal head
Patient may notice loss of motion.
Pain increases with activity and motion.
Pain worsens with weight bearing.
Pain often relieved by rest, but pain may awaken patient from sleep.
Physical Exam
Surrounding soft tissue swelling and warmth
Tenderness over metatarsal head
May be painful with motion
As disease progresses, osteophytes may be palpable.
May be limited motion of metatarsophalangeal (MTP) joint
Palpable crepitus in advanced disease
Other foot deformities may be present, such as hallux valgus.

Imaging
Radiography normal in early stages
As the disease progresses, osteonecrotic changes are seen on the superior/central head.
Eventually the superior/central head collapses and flattens.
Medial and lateral dorsal osteophytes develop.
Osteophytes may break free, becoming loose bodies, best seen on the oblique.
Cystic changes may be seen in the head.
The inferior portion of the metatarsal head is usually not involved.
Radiographic staging of disease, based on correlation with Smillie's classification:
Stage I: MTP joint space widening, with increased subchondral bone density
Stage II: MT head flattening (anteroposterior view)
Stage III: Collapse of the central portion of the dorsal part of the distal MT head.
Stage IV: Medial and lateral fractures of the projections of the remaining metatarsal head
(multiple loose bodies in the joint).
Stage V: Complete loss of joint anatomy and integrity.
Hot spot over metatarsal head
Classic osteonecrotic changes seen in MRI
May be useful in early detection prior to radiographic changes (1) [B]
Fracture: Acute or stress
Septic joint
Neuroma
Gout
Metatarsalgia
Treatment
Symptomatic relief for early stages of disease prior to collapse and loose
body formation
Goal is to restrict weight bearing a sufficient time to allow healing to take place.
Immediate cessation of sports
Use of crutches to restrict weight-bearing may be indicated in early stages
when most painful
As symptoms subside, may progressively bear weight with use of metatarsal
pads, bars, and/or a custom orthosis
Occasionally may need a walking boot or short leg walking cast with a toe plate
By restricting weight bearing, the lesion may heal over a period of 6–12 wks.
Return to sports when asymptomatic with custom foot orthosis
Operative treatment indicated if nonoperative treatment fails or if disease is
advanced
Joint debridement with dorsal osteophyte excision, synovectomy, and loose
body excision
Other operative options include dorsiflexion osteotomy or metatarsal head
excision in an older, less demanding patient
Medication
Symptomatic treatment with acetaminophen or NSAIDs as indicated (2)[C].
Referral
Orthopedic surgery referral indicated if nonoperative treatment fails or if disease
is advanced.
None
Surgery is reserved for those patients who fail conservative therapies, or those
with late-stage and demonstrated degenerative joint progression.
In general, surgical procedures that preserve the articular interaction of the
MTP joint have shown the most benefit. Examples include metatarsal
osteotomy and excisional and incisional arthroplasty (2[C],3[B]).
Ongoing Care
No standard return to participation protocol has been established. Protocol should be
individualized and based on radiographic confirmation of healing as well as symptom resolution
(2)[C].
Patient Education
Patient education should focus on the need for activity modification and a functional symptom-
based rehabilitation program.
Prognosis
For most nondegenerative lesions, conservative therapy is likely to lead to healing and
resolution of symptoms.
Current surgical procedures are demonstrating satisfactory results, but continue to be an
investigative topic.
Complications
Joint degeneration or destruction with resultant chronic pain and/or loss of
function.
References
1. Torriani M, Thomas BJ, Bredella MA, et al. MRI of metatarsal head
subchondral fractures in patients with forefoot pain. AJR Am J Roentgenol.
2008;190:570–575.
2. Carmont MR, Rees R, Blundell C. Current concepts review: Freiberg's

disease. Foot & Ankle International. 2009;30(2):167–176.
3. Sproul J, Klaaren H, Mannarino F. Surgical treatment of Freiberg's

infraction in athletes. Am J Sports Med. 1993;21:381–384.
Additional Reading
Manusov EG, Lillegard WA, Raspa RF. Pediatric foot problems. American
Family Physician. 1996;54(2):592–606.
Codes
ICD9
Clinical Pearls
Typical presentation is a teenage female in a growth spurt who presents with
forefoot pain with walking or activity.
Glenohumeral Dislocation, Anterior
Jason Glowney
Sourav K. Poddar
Basics
Description
Humeral head is displaced anteriorly beyond the glenoid fossa due to external rotation while
arm is in abduction.
Sometimes (less commonly) caused by direct contact to the posterior aspect of the shoulder.
Epidemiology
Most commonly dislocated diarthrodial joint; 45% of all dislocations are of the shoulder.
Bimodal incidence with peaks in the 2nd and 6th decades of life
2% lifetime incidence between 18 and 70 yrs of age
96% of glenohumeral dislocations are anterior.
Risk Factors
History of previous dislocation
Generalized ligamentous laxity
Sports such as wrestling, football, rugby, skiing, and skateboarding

Bankart lesions: Detachment of inferior glenohumeral ligament-labral complex from anterior
glenoid rim. Very common in younger patients. Strongly associated with dislocation
recurrence.
Rotator cuff tears: Between 14 and 63% of anterior dislocations are associated with rotator
cuff tears, with increasing frequency in older individuals. Often the subscapularis muscle with
anterior dislocation.
Fractures: Humeral head and neck (significant displacement may be a contraindication to
closed reduction), glenoid rim, and greater tuberosity avulsions. Seen especially with
traumatic etiology.
Hill-Sachs lesion: Depression fracture of posterolateral humeral head. More than 50% of
anterior dislocations in patients younger than 40 yrs old are associated with this type of
lesion. Presence of a Hills-Sachs lesion associated with recurrent dislocation.
Neurologic injury: Common complication with 10% suffering injury to the axillary nerve. Less
frequently injured are the brachial plexus or musculocutaneous nerve.
Vascular injury: Infrequent complication (1–2%), axillary artery most frequently injured in
anterior dislocation, higher incidence in older individuals given the loss of arterial elasticity
secondary to atherosclerosis.
Recurrent dislocation: Rate varies inversely with age, with up to 95% recurrence in athletic
patients, with initial dislocation at younger than 20 yrs old without surgical intervention.
Diagnosis
West Point view (reverse axillary lateral) helps in showing bony Bankart lesions.
Styker notch (anteroposterior internal rotation of humerus) good to demonstrate Hill-Sachs
deformity
History
Often occurs after a fall on the outstretched arm or with reaching (making a tackle) and
having arm forcibly abducted
1st time event vs recurrence (may affect ease of reduction and long-term treatment plan)
Amount of trauma involved (traumatic vs atraumatic) can give clues as to whether there is a
component of ligamentous instability.
Duration shoulder has been dislocated (helps in decision concerning analgesia)
Physical Exam
Anterior fullness of the shoulder
Forearm of affected arm often cradled with shoulder in externally rotated, partially abducted
position
Patient usually guarding and very uncomfortable
Sulcus sign (depression in the skin below the acromion)
Perform neurovascular exam, both before and after reduction, to check for previously
mentioned nerve injuries.
Check deltoid muscle strength and lateral shoulder sensation to assess axillary nerve function
(former not always practical prior to reduction of dislocated shoulder).
Check proximal and distal muscle function and range of motion before and after relocation.
No crepitus should be felt or heard during relocation.

Imaging
At least 2 views orthogonal to each other are required.
Normally acute traumatic shoulder dislocations are evaluated with a trauma series that
includes an axillary view, a trans-scapular (Y) lateral view, and a true shoulder anterior-
posterior view
Standard anteroposterior: Head of humerus displaced medially on glenoid; difficult to
distinguish anterior from posterior dislocations
True lateral (trans-scapular, Y) view: Humeral head displaced toward coracoid process
Axillary view: Allows easier visualization of associated injuries, but requires movement of an
already uncomfortable patient
May utilize advanced imaging, such as CT scan, MRI, or musculoskeletal US, to assess if
associated injuries suspected
Acute subluxation
Acromioclavicular joint separation
Fractures of humeral head, coracoid, acromion, proximal humerus, clavicle, rib
Rotator cuff injury
Posterior dislocation
Treatment
Analgesia often not needed if reduction is performed immediately after
dislocation.
Verbal coaching to relax the patient is helpful.
Narcotic and benzodiazepine medications may be required, if reductions are
not performed early, to relax spasm and ease relocation.
Some sources recommend local glenohumeral joint anesthesia using 10–20
mL of 1% lidocaine.
Intra-articular lidocaine has been shown to have similar relocation success
rates vs IV analgesia and sedation, and a significant decrease in cost and
length of stay in the emergency department, although patient satisfaction tends
to be higher with the use of IV agents [A].
Traction methods: Stimson (prone traction with weight applied to arm hanging P.
down); supine traction/countertraction (gentle traction at 45 degrees of
abduction while countertraction applied with folded sheet under axilla)
Leverage techniques: Hennepin or modified Kocher maneuver (with patient
supine, externally rotate arm to 90 degrees; slowly abduct arm until dislocation
reduced)
Axillary pressure by assistant's hand may help guide the humeral head over the
glenoid.
Scapular manipulation: Patient prone or seated with arm at 90 degrees of
flexion with mild traction applied (10–15 lbs), apply medially directed force to
inferolateral border of scapula; may also do when patient is supine to assist
with other techniques.
Combinations
Experience, familiarity, and available resources (time and help) are important
considerations when deciding which technique to use.
More than 2 dozen different described techniques, but only 1 randomized
controlled trial exists that compared Kocher and Milch techniques. In this study,
the authors did not detect a statistically significant different success rate
between the 2 techniques. They did, however, find a greater relocation success
rate in those under 40 yrs old vs those older than 40 yrs (1)[A].
Recheck neurovascular exam and rotator cuff; post-reduction radiographs
Controversy exists as to best approach to postdislocation management, but
many authors at this time would recommend immobilization in a sling for
comfort about 1 wk (2)[A], followed by range-of-motion exercises and then
progression to strengthening exercises, with an emphasis placed on
periscapular muscle strengthening. Shorter immobilization period decreases
the risk of adhesive capsulitis in the older patient (age over 30).
Recent reports have suggested that immobilization in external rotation instead
of traditional internal rotation may be associated with a lower rate of
recurrence. In clinical practice, patients may find it difficult to function with their
arm immobilized in external rotation (3)[B].
Immobilization theoretically allows time for “scarring” of injured anterior
structures and healing of pathologic lesions.
Humeral head and neck fractures contraindications to closed reduction, as
are:
Significantly displaced (<1 cm) greater tuberosity fractures
Severe scapula fractures
Intrathoracic humeral head fractures
Early range of motion in older patients (age >30) to prevent adhesive capsulitis
Strengthening of rotator cuff muscles and scapular stabilizers help in
maintaining dynamic stability.
Most helpful in nontraumatic dislocations in patients who have multidirectional
instability or generalized ligamentous laxity (TUBS [traumatic unilateral Bankart
lesions] vs AMBRI [atraumatic, multidirectional, bilateral shoulders])
Immobilization and postimmobilization rehabilitation have not been shown to be
effective in preventing recurrence in young, traumatic, 1st-time dislocators.
Surgical stabilization recommended for many athletic 1st-time disclocators,
especially if “throwing shoulder.”
Surgery recommended for those with recurrent dislocations, especially if the
episodes appear to require less “trauma” than prior episodes.
Ongoing Care
Little data exist as to when it is safe for an athlete to return to play after sustaining a
dislocation.
Most experts would recommend waiting until athlete has full range of motion and strength
before their return (4)[C].
Athletes returning to play with history of instability are at risk for recurrence, with 1 study
showing 37% incidence of repeat dislocation during the ongoing season (4)[B].
Growing consensus for early arthroscopic stabilization after primary anterior shoulder
dislocation in young athletic patients unwilling to modify their risk factors, as numerous
studies have shown a high rate of recurrence in nonoperative treated subjects in this group.
When surgically stabilized, athletes show significant decreased rates or dislocation
recurrence (2)[A].
Recurrent instability patients likely to benefit from orthopedic referral for arthroscopic or open
surgical repair as warranted
Patients with multidirectional instability should be treated with traditional methods, although
surgical repair is often necessary with recurrences.
Early orthopedic referral indicated for all except uncomplicated, recurrent anterior
dislocations.
Orthopedic referral with humeral head or neck fractures and irreducible dislocations
References
1. Cox CL, Kuhn JE. Operative versus nonoperative treatment of acute shoulder dislocation
in the athlete. Curr Sports Med Rep. 2008;7:263–268.
2. Dodson CC, Cordasco FA. Anterior glenohumeral joint dislocations. Orthop Clin North
Am. 2008;39:507–518, vii.
3. Kuhn JE. Treating the initial anterior shoulder dislocation—an evidence-based medicine
approach. Sports Med Arthrosc. 2006;14:192–198.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl.
2009;91:2–7.
Additional Reading
Arciero RA, St Pierre P. Acute shoulder dislocation. Indications and techniques for operative
management. Clin Sports Med. 1995;14:937–953.
Wen DY. Current concepts in the treatment of anterior shoulder dislocations. Am J Emerg
Med. 1999;17:401–407.
Codes
ICD9
831.01 Closed anterior dislocation of humerus
Clinical Pearls
TUBS vs AMBRI:
TUBS usually responds better to surgical fixation.
AMBRI: Rehabilitation for 3–6 mos or more (patient needs to perform
exercises independently); if fails prolonged exercise program, may benefit from
inferior capsular shift
Glenohumeral Dislocation, Posterior
Tracy Ray
Eric D. Parks
Basics
Description
A posterior glenohumeral dislocation occurs when the humeral head disarticulates from the
glenoid and rests posteriorly to its normally seated position on the glenoid.
Glenohumeral instability is classified by:
Mechanism (traumatic vs atraumatic)
Direction (anterior, posterior, superior, inferior, or multidirectional)
Circumstance (acute, chronic, or recurrent)
Degree (subluxation vs dislocation)
Other names:
Posterior shoulder dislocation
Shoulder instability
Epidemiology
The shoulder is the most commonly dislocated joint in the human body. Glenohumeral
instability affects 2% of the general population, ranging from mild subluxation to frank
dislocation. Recurrent, unidirectional posterior subluxation is the most frequent form of
posterior instability (1)[C].
Anterior dislocations are much more common than posterior dislocations.
Posterior shoulder dislocations account for only 2–5% of all traumatic shoulder dislocations.
However, trauma is associated with 50% of all posterior dislocations.
A posterior shoulder dislocation is the most commonly missed shoulder pathology. 60–79%
of these dislocations are not diagnosed at initial presentation, which may compromise the
potential effectiveness of orthopedic intervention. Proximal and diaphyseal humeral fractures
are often associated with posterior dislocation. Compared to anterior dislocations, posterior
dislocations associated with vascular or neurologic compromise are unusual.
In the absence of trauma, posterior dislocations occur most often as a result of a seizure
(contraction of the internal rotators) or electrical shock injury. Dislocation can occur when an
axial load is applied to the upper extremity in the “at risk” position: forward flexion, adduction,
and internal rotation.
Injury can occur in athletes with a fall upon a flexed elbow and adducted arm, or by a direct
axial load to the humerus.
Extremely rare in pediatrics because force necessary to cause a dislocation will instead
cause a proximal humerus fracture
Risk Factors
History of seizure disorder
History of electric shock (2)[C]
History of posterior shoulder dislocation or instability
Disorders such as Charcot shoulder and Ehlers-Danlos syndrome have been well
documented.
Congenital anomalies, such as scapular aplasia, increase the risk of dislocation.
Glenoid hypoplasia and excessive glenoid retroversion increase risk.
At-risk sports/positions for posterior instability and/or dislocation include offensive linemen
with arms in blocking position, backhand stroke in racket sports, pull-through phase of
swimming, and follow-through phase in golf or throwing motion (2)[C].
Diagnosis
History
Mechanism of injury? Generally direct trauma to anterior aspect of shoulder.
Direction of applied force and position of the arm (the “at-risk” position)
Acute vs chronic in nature?
Overhead athletes may have insidious onset of weakness and pain, especially with muscle
fatigue.
History of previous injury or pain in affected shoulder?
Previous or present description of pain, including location, intensity, and duration
Previous or present history of tingling, weakness, catching, locking
Any aggravating or alleviating factors?
Physical Exam
Severe shoulder pain that increases with movement
Cardinal sign: An arm held in internal rotation and adduction with inability to externally rotate
or abduct the arm
Mild flattening of the anterior shoulder with an anterior glenohumeral void and loss of normal
deltoid contour may be present.
There may be prominence of the coracoid process and squaring-off of the anterior-lateral
acromion.
The humeral head may be visible or palpable posteriorly.
Routine observation, gentle palpation, range of motion, and strength of the affected extremity
should be performed.
Limitation with passive external rotation and abduction may be noted
It is of utmost importance to monitor the neurovascular status of the affected arm. Injury to
the axillary vessels is rare but potentially catastrophic.
Examine axillary nerve function by testing active contraction of the deltoid as well as
sensation over the lateral aspect of the shoulder.
Neurologic involvement is often in the form of a neurapraxia.
Evaluate for atrophy of posterior rotator cuff muscles as an indication of chronic posterior
instability.
Assess for generalized ligamentous laxity.
Scapulothoracic mechanics and rhythm should be observed, if position not “fixed.”

Imaging
Plain radiographs for a suspected posterior shoulder dislocation should include an
anteroposterior view, a trans-scapular lateral view (Y view), and a modified axillary lateral
view.
The normal lateral projection of the greater tuberosity is lost in a posterior shoulder
dislocation.
With disarticulation of the humeral head posteriorly, the anterior rim of the glenoid is void of
the humeral head, which is displaced medial to the glenoid convexity.
A reverse Hill-Sachs lesion may be visible as an indentation of the anterior articular surface of
the humeral head caused by the posterior rim of the glenoid.
Axillary view is helpful for evaluating for glenoid rim fracture and morphology (hypoplasia,
retroversion).
Advanced imaging (CT, MRI, or arthrography) should be reserved for evaluating the extent of
associated humeral head fractures/impression defect, glenoid fractures, rotator cuff tears,
labral pathologies, version and morphology of the glenoid, and articular surface integrity.
However, if surgery is warranted, CT scan for preoperative planning is acceptable (1,3)[B].
Acute subluxation
Fractures (clavicle, scapula, and humerus)
Rotator cuff pathology (strain, partial or complete tear)
Adhesive capsulitis/frozen shoulder
Acromioclavicular joint pathology
Intra-articular pathology (labral, glenoid, or ligamentous)
Scapular winging/instability
Treatment
Multiple factors influence the choice of anesthesia (ie, analgesia for an on-
the-field chronic and recurrent dislocator is very different from an electrical
shock injury).
Whenever possible, an analgesic and muscle relaxant should be administered
prior to any reduction attempt.
Conscious sedation or general anesthesia may be necessary if a gentle and
atraumatic reduction cannot be obtained.
Early attempts at reduction should be performed in all cases, except ones with
associated fractures of the anatomic or surgical neck of the humerus.
With the patient supine, gentle longitudinal traction is applied to the affected
arm while the elbow is flexed at 90 degrees.
While traction is applied, gentle internal rotation of the arm often unlocks the
humeral head from the rim of the glenoid.
It may be necessary to also use direct anterolateral pressure on the humeral
head to unlock it from the glenoid rim.
If an atraumatic reduction cannot be achieved, reduction in the operating room
under general anesthesia should be considered.
An alternative technique is to apply gentle internal rotation and lateral traction to
disimpact the humeral head.
If this dislocation is seen hours or even days after occurring, it may be
impossible to reduce nonsurgically.
Open reduction should also be considered for persistent dislocation (>6 wks),
chronic dislocations, and humeral head involvement >25%.
Associated fractures also may require operative intervention, and open
reduction may be necessary.
Confirm intact neurovascular status after any reduction attempt.
Obtain postreduction radiographs to confirm reduction and to evaluate humeral
or glenoid fractures.
Consider repeat physical exam, taking care not to cause repeat dislocation.
Immobilization should not include the use of a sling and swathe because
internal rotation should be avoided.
Immobilize in neutral to external rotation, allowing for healing of the posterior
capsulolabral complex.
A shoulder spica cast or commercial brace for posterior shoulder dislocation;
arm held in 20 degrees of external rotation and 0–20 degrees of abduction
Duration of immobilization depends on age, chronicity, associated fractures,
and operative intervention.
For 1st-time uncomplicated dislocations, 7–14 days of immobilization for
patients >45 yrs of age to avoid shoulder stiffness. Younger patients are
immobilized 4–6 wks to allow capsular scarring to occur.
Referral
Orthopedic referral should be considered for all posterior shoulder dislocations.
Potential associated injuries of fractures, rotator cuff tears, and labral pathology
require evaluation.
Independent of the duration of immobilization, aggressive physical therapy
should be completed.
Isometric external rotation strengthening can occur during the immobilization
stage in the brace.
Progressive range of motion with strengthening of the internal and external
rotators
Advanced rehabilitation program for athletes concentrating on sport-specific
activities and proprioception
Return to athletics for 1st-time nonoperative dislocators in 6–12 wks to
reduce likelihood of future dislocations
Repeat nonoperative dislocators may return to activity once pain-free and full
strength has been recovered. These patients are very likely to have recurrent
dislocations.
A conservative nonoperative trial of physical therapy may allow an individual
with an uncomplicated dislocation to resume pain-free daily activities.
Dislocations with large defects involving the articular surface of the humeral
head (>20–25%) may require operative intervention to prevent recurrent
instability.
Athletes (specifically overhead athletes) may continue to have disability that is
not amenable to an extended conservative trial of rehabilitation (3–6 mos). In
these patients, operative intervention should be considered following the initial
dislocation.
Surgical intervention is indicated with associated injuries, such as fractures,
rotator cuff tears, and suspected labral pathology, after an initial dislocation.
While the posterior capsulolabral complex often heals with nonoperative
management, recurrent instability may necessitate the need for surgical repair,
and possibly additional soft tissue repair for improved posterior stability.
Operative interventions often include examination under anesthesia, diagnostic
arthroscopy, and arthroscopic or open stabilization procedures.
Open stabilization procedures (such as the Bankart repair, Putti-Platt, and
Neer capsular shift) have historically had superior results to arthroscopic
endeavors.
Recent advances in arthroscopic stabilization procedures have documented
recurrence rates at 5%. Long-term results are still unavailable on
arthroscopic stabilizations (4)[B].
There is continued interest in the use of thermally assisted arthroscopic
capsular shifts in shoulder instability. Outcomes remain pending.
References
1. Millett PJ, Clavert P, Hatch GF, et al. Recurrent posterior shoulder instability.
2. Bradley JP, Forsythe B, Mascarenhas R. Arthroscopic management of

posterior shoulder instability: diagnosis, indications, and technique. Clin
Sports Med. 2008;27:649–670.
3. Kowalsky MS, Levine WN. Traumatic posterior glenohumeral dislocation:

classification, pathoanatomy, diagnosis, and treatment. Orthop Clin North Am.
2008;39:519–533, viii.
4. Savoie FH, Holt MS, Field LD, et al. Arthroscopic management of posterior
instability: evolution of technique and results. Arthroscopy. 2008;24:389–396.
Additional Reading
Andrews OR, Wilk KE. The athlete's shoulder. New York: Churchill
Livingstone, 1994.
Canale TS. Campbell's operative orthopaedics. St. Louis: CV Mosby, 1998.
Dee R, Mango E, Hurst LC. Principles of orthopaedic practice. New York:

McGraw-Hill, 1989.
Codes
ICD9
831.02 Closed posterior dislocation of humerus
Clinical Pearls
Because so many posterior dislocations are reported missed within the office or
emergency department, one must have a low threshold for advanced imaging,
such as a CT scan, to make sure of appropriate diagnosis.
Glenoid Labral Tears/SLAP Lesions
Aaron V. Mares
Tanya J. Hagen
Basics
Glenohumeral joint is a dynamic spheroid (‘ball and socket’) articulation:
The glenoid labrum, in addition to the glenohumeral ligaments, the rotator cuff, and the
scapular rotators, provide joint stability.
The labrum is a fibrocartilaginous “lip” that surrounds the circumference of the glenoid fossa:
Increases the depth and surface area of the joint, increasing joint stability
The long head of the biceps brachii attaches to the superior portion of the labrum.
Because of the mechanisms of injury involved, superior tears (“SLAP” lesions) and anterior-
inferior tears (Bankart lesions) are more common than posterior labral tears.
Description
SLAP lesions (superior labrum anterior posterior lesions):
Typically caused by repetitive overhead motion (eg, baseball pitcher in late cocking phase)
or from a fall onto an outstretched arm
Presently, 10 types of lesions are described by some experts.
Traditionally, there have been 4 main types of lesions as listed:
Type I: Fraying or degeneration of the superior capsulolabral structures sparing the
origin of the biceps brachii tendon (long head); joint remains stable.
Type II: Detachment of superior labrum and the origin of the long head of the biceps
brachii tendon (most common)
Type III: Bucket-handle tear of the superior labrum sparing the origin of the biceps
brachii tendon (long head)
Type IV: Bucket-handle tear of the superior labrum as well as the origin of the biceps
brachii tendon (long head).
Bankart lesions:
Usually involve anterior and inferior portion of the glenoid labrum
Typically caused by anterior shoulder instability
May be associated with a fracture of the glenoid rim (“bony Bankart”)
Epidemiology
In addition to labral tears, common shoulder injuries in sports include:
Rotator cuff contusions/tendonitis/tear
Fractures
Glenoid labral tears frequently occur in combination with other shoulder injuries.
Incidence
SLAP lesions: Reported rates range from 6–20%
Bankart lesions: When associated with acute anterior dislocation, reported rates up to 78%
incidence and with chronic instability up to 93% (1)
Risk Factors
Repetitive overhead motion (sports or occupational):
Baseball (pitchers)
Football (quarterbacks)
Weight lifters (military press)
Swimmers
Tennis
Shoulder instability/trauma
Anatomic variation (eg, Buford complex) or underlying generalized laxity/instability
General Prevention
Per USA Swimming and the Network Task Force on Injury Prevention (2002):
Stretching (eg, capsular stretch in throwers with “GIRD” = glenohumeral internal rotation
deficiency)
Rotator cuff and periscapular strengthening
Core strength training
Ensure proper overhead (throwing/swimming, etc.) mechanics.
Etiology
Mechanisms of injury to the glenoid labrum are acute trauma and repetitive microtrauma from
overhead activity:
Acute: Trauma:
Shoulder dislocation/subluxation: Anterior → Bankart, posterior (less common, eg, blocking
football lineman) → posterior labral tear/“reverse Bankart”
Falling on an outstretched arm
Abrupt jerk on the upper extremity:
Traction when breaking a fall
Sudden pull on the arm (ie, when trying to lift a heavy object)
Chronic: Microtrauma:
Secondary to repetitive overhead shoulder motion
SLAP lesions typically occur in overhead athletes during acceleration in the late cocking
phase.
Chronic instability, without true traumatic dislocation, can cause labral tearing.

Labral tears can be associated with other, underlying shoulder problems and anatomic
variability. In addition, forces that cause labral tearing can cause other injury. Finally, there
are frequently secondary problems that may arise as a result of labral tears.
Conditions that may be found in conjunction with labral tears include but are not limited to (1):
Instability
Bony injury (particularly in the setting of traumatic dislocation): Bony Bankart, Hill Sacks
Rotator cuff injury, tendinosis, impingement
Internal impingement, glenohumeral internal rotation deficiency
Ganglion cysts
Buford complex
Scapulothoracic dysrhythmia
Diagnosis
The diagnosis of a glenoid labral tear is made by history, physical, and appropriate
imaging. Occasionally, arthroscopy is necessary for definitive diagnosis.
History
Most individuals complain of nonspecific shoulder pain. Location depends on the site of the
tear.
Persons with SLAP lesions most commonly complain of anterior/superior shoulder pain.
Other pertinent positives in the history may include:
Acute trauma or repetitive motion (sport, hobby, occupational)
Mechanical symptoms: “Click, pop, or catch” with circumferential motion
Decrease in athletic performance (strength, velocity, accuracy, precision)
Weakness in the upper extremity
Sense of instability
Physical Exam
Numerous examination techniques have been described, but no single test is both sensitive
and specific enough to accurately diagnose glenoid labral tears (2)[A].
A study by Parentis and colleagues in 2006 found that the O'Brien's active compression test,
Jobe test, Speed's test, Hawkins test, and Neer's test were the most sensitive, though not
specific, in the evaluation for SLAP lesions (3)[B].
Other exam findings will depend on associated issues (instability, RTC weakness, etc).
Examples of commonly used labral exam techniques:
Labral “clunk” test:
Original test for glenoid labral tears 1st described in the 1980s
Patient lies supine with examiner abducting the shoulder past 90 degrees with one hand
while pressing the proximal humeral head anteriorly. The clinician then internally and
externally rotates the shoulder.
(+) test = pain or catch prior to a “click” felt by the patient
O'Brien's active compression test:
Examiner resists forward flexion while the patient's arm is flexed to 90 degrees and
adducted 15 degrees across midline. Initially, the shoulder is internally rotated (thumb
down) and then externally rotated (palm up).
(+) test = pain that improves with external rotation (palm up)
Speed's test:
Examiner resists forward flexion while the patient's arm is flexed to 90 degrees, externally
rotated (palm up), with the elbow in full extension.
(+) test = pain experienced at the proximal biceps with resistance

Because the physical exam is both nonsensitive and nonspecific, imaging (x-ray and MRI
arthrogram) is frequently relied upon for definitive diagnosis when the history and physical is
suggestive.
Imaging
Plain radiographs:
Aid in ruling out other pathology, such as fractures, calcific tendinitis, and degenerative joint
disease
Minimum 3 views: True AP of glenohumeral joint, axillary lateral, outlet view:
Consider other “instability” views as appropriate: Stryker notch view, west point axillary
lateral, etc.
MR arthrogram (4)[A]:
Labral pathology best appreciated on coronal oblique sequences
Sensitivity 82–100%, specificity 71–98%
At most centers, MR arthrography provides improved sensitivity (without loss of specificity)
when compared to MRI without intra-articular contrast.
Glenohumeral arthroscopy:
Gold standard
Most sensitive and specific test for labral pathology
Instability (traumatic/atraumatic)
Rotator cuff contusion/tendinitis/tear, impingement
Bicipital tendinitis/rupture (long head)
Arthritis (osteoarthritis, inflammatory, crystalline arthropathies)
Cervical radiculopathy and other referred pain
Septic joint
Pain syndromes (complex regional pain syndrome, Parsonage Turner)
Treatment
Current recommendations support an initial conservative approach, but
depending on location and degree of injury, surgery is often required:
Initial therapy (nonoperative) (5)[B]:
Relative rest from overhead/aggravating activity
Pain management: Ice, NSAIDs, acetaminophen
Physical therapy to improve strength and flexibility and to address
predisposing/associated issues (eg, scapulothoracic dysrhythmia in patients
with instability or capsular tightness in patients with GIRD)
Evaluate and address underlying biomechanical problems (eg, kinetic
chain/core weakness in thrower).
Medication
Pain control: NSAIDs or acetaminophen
In the setting of associated impingement, a subacromial corticosteroid injection
could be considered.
A brace that limits shoulder motion may be of some value to athletes attempting
to “get through a season.” The efficacy of such brace use depends on many
factors, including type and severity of lesion, sport, and position. It should be
noted that there is no current research to support this.
Surgical repair and/or debridement for the majority of labral tears is definitive
therapy when nonoperative management fails.
The decision to repair (vs debridement) is primarily based on the degree of
injury, specifically for SLAP tears, whether there is significant
capsuloligamentous detachment.
Surgical intervention may include:
Labral debridement
Labral repair (stapling, suture anchors, biodegradable implants)
Subacromial decompression
Acromioplasty
Cyst decompression
Biceps tenotomy
Other intervention may be required depending on associated conditions such
as rotator cuff tears or instability.
Ongoing Care
Postoperative care varies among individuals and depends on overall surgical intervention.
Example of postoperative care after a posterior portal approach (5)[C]:
Immobilization in a sling for 4 wks
Elbow and wrist range of motion exercises immediately
Resistance strength exercises at 3 mos postoperatively
Avoidance of extreme positions of abduction and external rotation during the 1st 3 mos
Initiation of formal throwing in overhead athletes at 4 mos
Typical return to full throwing by 9–12 mos
Rigorous follow-up is recommended.
Prognosis
Bendi and colleagues reviewed recent data and reported a 63–94% satisfaction score in
symptoms after surgical intervention, with 45–96% returning to their pre-injury level of
performance, depending on the extent of injury and surgical intervention required (debridement
vs comprehensive surgery) (5)[A].
Complications
Potential complications for labral tears that are treated both operatively and
nonoperatively include:
Occult instability
Persistent pain
Chondral injury
Adhesive capsulitis
Operative complications may include (in addition to those listed above):
Synovitis
Infection
Hemarthrosis
Mechanical failure
Broken or dislodged tack/suture
Chondrolysis
References
1. Yiannakopoulos CK, Mataragas E, Antonogiannakis E. A comparison of the
spectrum of intra-articular lesions in acute and chronic anterior shoulder
instability. Arthroscopy. 2007;23:985–990.
2. Hegedus EJ, Goode A, Campbell S, et al. Physical Examination Tests of the

Shoulder: A Systematic Review with Meta-analysis of Individual Tests. Br J
Sports Med. 2007.
3. Parentis MA, Glousman RE, Mohr KS, et al. An evaluation of the

provocative tests for superior labral anterior posterior lesions. Am J Sports
Med. 2006;34:265–268.
4. Chang D, Mohana-Borges A, Borso M, et al. SLAP lesions: Anatomy,

clinical presentation, MR imaging diagnosis and characterization. Eur J
Radiol. 2008.
5. Bedi A, Allen AA. Superior labral lesions anterior to posterior-evaluation and

arthroscopic management. Clin Sports Med. 2008;27:607–630.
Additional Reading
McKeag, DB, Moeller JL. ACSM's Primary care sports medicine.
McMahon PJ, ed. Current diagnosis & treatment in sports medicine. New
York: Lange Medical Books/McGraw Hill Medical Pub., 2007.
Sallis RE, Massimino F, eds. Essentials of sports medicine. St. Louis: Mosby-
Year Book, 1997.
See Also
http://www.acsm.org
http://orthoinfo.aaos.org
Codes
ICD9
718.01 Articular cartilage disorder involving shoulder region
718.31 Recurrent dislocation of joint of shoulder region
Clinical Pearls
Glenoid labral tears are relatively common in overhead athletes and those who
participate in contact sports.
Patients frequently complain of vague pain, decreased performance, and
mechanical symptoms. Physical exam, while helpful, is unreliable for definitive
diagnosis, so have a low threshold for imaging (MRI arthrogram) in appropriate
cases.
An initial trial of conservation management is reasonable, but the majority of
these injuries require surgical intervention. Keep this and the required
recovery/rehabilitation time in mind with regard to timing of surgery and return
to sport.
After surgical management, 63–94% of individuals report a satisfaction score
in their symptoms, with 45–96% returning to their pre-injury level of
performance (5)[A].
The labrum is unlikely to heal as the result of shoulder exercises. Exercises
can, however, improve the biomechanics of the shoulder, which may reduce the
stress on the labrum and, ultimately, reduce or resolve symptoms. Because
some exercises may aggravate the injury, therapy should be tailored to each
patient.
If the symptoms are minor and the injury does not interfere with athletic
performance, nonsurgical management is a reasonable option.
Without surgery, however, long-term consequences include:
Continued stress to the damaged labrum may extend the tear
Glenoid labrum problems are similar to meniscus tears in the knee.
Catching or locking symptoms may be intermittent
If the symptoms are minor and the injury does not interfere with athletic
performance, nonsurgical management is a reasonable option.
Without surgery, however, continued stress to the damaged labrum may
extend the tear.
Gout
Natalie Voskanian
Basics
Gout is an acute disease that eventually progresses to a chronic state.
Consists of painful inflammatory deposition of monosodium urate crystals into joints and,
eventually, soft tissues (tophaceous gout)
Pseudogout is a similar but distinct entity in which the inflammatory process is instigated by
calcium pyrophosphate dihydrate (CPPD) crystal deposition instead of monosodium urate.
Description
Gout has 3 stages:
Acute phase: Inflammatory monarthritis; resolves within several days to a week
Intercritical or interval phase: The patient is asymptomatic.
Chronic phase: Intermittent repeated flairs of monarticular or polyarticular gout and soft
tissue deposition of tophi.
Common joints affected by gout: 1st metatarsophalangeal (MTP) joint (most common site of
initial presentation; also known as podagra), olecranon, ankle, wrist, knee, tarsal joints, and
interphalangeal joints of the hand
Much less commonly affected joints include shoul-der, sternoclavicular joint, spine, and
sacroiliac joints.
Tophaceous gout can extend to periarticular structures (tendons and soft tissue) and rarely
can affect visceral organs.
Up to 20% of gout patients may present with polyarticular or tophaceous gout at initial
presentation.
Epidemiology
Incidence
Typically presents in middle-aged men (30–50 yrs old).
Seen 2nd most commonly in elderly men and postmenopausal women, typically in those with
multiple medical comorbidities.
Predominant gender: Male > Female (2–4:1).
Prevalence
Prevalence of gout in U.S. is 1% and increases with increasing age (1).
Others have found a prevalence of 8.4/1,000 (2).
Risk Factors
Excessive alcohol intake (especially beer and spirits)
Chronic diuretic use
Recent trauma
Recent surgery
Hyperuricemic state (from either overproduction or underexcretion of uric acid)
Rapid changes in uric acid level
Diets high in purine-containing products
Diets low in dairy or high in meat or fish (hazard ratio up to 1.41 in high-quantity meat-eaters
and 1.51 in high-quantity fish-eaters) (3); total protein intake is not correlated with risk for
gout.
Risk factors for the presence of tophaceous gout at initial diagnosis:
Postmenopausal women
Coexisting chronic renal disease
Diuretic therapy
General Prevention
Factors that can reduce risk of gout:
High-quantity dairy product intake (hazard ratio of 0.56) (3)
Minimizing diuretic use and dose
Minimizing alcohol intake
Urate-lowering agents are used for the prevention of chronic gout. See “Medications.”
Etiology
Chronic hyperuricemia for many years results in concentrated extracellular deposition of
monosodium uric acid.
This leads to a localized inflammatory process in which the body tries to eradicate the foreign
crystals.
This inflammatory process results in localized pain, swelling, and erythema of the affected
joint.
This disease process mimics infection.

Hypertension
Chronic diuretic therapy
Obesity
Hyperlipidemia
Chronic nephropathy and renal disease
Hyperuricemic syndromes such as myeloproliferative or lymphoproliferative disorders,
psoriasis, cyclosporine A use (in organ transplant patients), and inherited defects in purine
metabolism
Patients with gout are at increased risk for uric acid nephrolithiasis.
Diagnosis
History
Initially a severely painful, erythematous, and swollen joint (noninfectious monarthritis)
There is no significant trauma of the joint preceding the attack.
Rarely there may be polyarticular involvement at 1st onset.
Maximal pain reaches peak at 24–48 hr (4).
Often symptoms resolve within 5–7 days even without treatment (5).
Physical Exam
Gout:
Fever
Swelling, erythema, warmth, and tenderness of affected joint
Sometimes overlying skin can be erythematous and desquamated, resembling cellulitis.
Tophi:
Subcutaneous nodules (resembling rheumatoid arthritis) or a bulky mass overlying a joint
±Tenderness or erythema of tophi
Aspirated tophi contents appear as white pasty or chalky material.
Lab
Distinction from an infectious process may be difficult.
CBC: Leukocytosis may be extremely high.
C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are often elevated as
well.
Chemistry panel to assess renal function: Not only is renal impairment associated with gout,
but chronic hyperuricemia can lead to urate nephropathy.
Uric acid level often will be high during an acute gout attack but may be normal.
Incidence of gout in patients with uric acid levels >9 mg/dL is 6 × greater than in patients at
7–8.9 mg/dL (5).
In a group of 339 patients with acute gout, 14% had uric acid levels ≤6 mg/dL and 32%
were ≤8 mg/dL (6).
Thus uric acid level on its own cannot be used to diagnose or rule out gout, but a high uric
acid level in the appropriate clinical context can be suggestive of gout (5,7)[B].
Imaging
Although sometimes helpful, imaging is not necessary to make a diagnosis of gout (8)[A].
Can be used to rule out alternate diagnoses such as rheumatoid arthritis
Chronic gout is often characterized by subcortical cysts, bony erosions, overhanging edges,
and diffuse soft tissue calcifications on x-ray or MRI (8).
Large tophi can be identified on MRI but often will need to be aspirated to confirm the
diagnosis (8)[A].
Pseudogout, on the other hand, does not typically have bony abnormalities but instead
consists of chondrocalcinosis (calcification of cartilage).
The “gold standard” diagnosis of gout is made by aspiration (arthrocentesis) of the affected
joint's synovial fluid (9)[A].
Characteristic needle-shaped negatively birefringent monosodium urate crystals are seen
under polarized light microscopy.
In contrast, pseudogout consists of rhomboid-shaped crystals with weakly positive
birefringence.
Aspirate: Check cell count, Gram stain, and bacterial culture to rule out infection (with a
negative Gram stain and negative culture).
Aspirate WBC count: 2,000–50,000 seen in gout (also pseudogout or rheumatoid arthritis);
>50,000 is suspicious for septic arthritis.
It is important to rule out septic arthritis, which can mimic gout (and rarely may coexist with
gout).
Pseudogout
Septic arthritis
Osteoarthritis
Reactive arthritis
Osteomyelitis
Malignancy
Joint trauma
Treatment
Medication
First Line
NSAIDs are 1st-line therapy; typically naproxen (500 mg b.i.d.) or indomethacin
(50 mg t.i.d.) is used (10)[A]. Should be given within 24–48 hr of symptom onset
for best results (4)[B]
COX-2 inhibitors are equally effective according to recent studies (11)[B].
P.
Duration of treatment varies, often ranging from 3–10 days until the attack
subsides.
Within several days of treatment, the dosing can be decreased if clinical
improvement (5)[B].
Corticosteroids (IV, oral, or intra-articular) are an effective alternative 1st-line
agent if NSAIDS are contraindicated (12)[A].
Begin oral prednisone at 30–40 mg/day × 2–3 days; then taper over total of
7–10 days (5,9)[C].
If doing intra-articular injection instead, can use methylprednisolone 20–40
mg (5,9)[C].
Septic arthritis is an absolute contraindication to intraarticular corticosteroid
treatment.
Second Line
Colchicine is a very effective 2nd-line agent for treatment of acute gout (13,14)
[A]. Colchicine has fallen out of favor as a 1st-line agent owing to its high side-
effect profile and contraindication in renal disease (5,13).
Use oral colchicine 0.6 mg t.i.d. or b.i.d.; choose b.i.d. or daily regimen in
patients with renal impair-ment or elderly patients (or avoid entirely) (5,9).
For best results, colchicine should be given within 24–48 hr of symptom
onset (14)[B].
The hourly dosing of colchicine used in the past was poorly tolerated
(nausea, vomiting, and diarrhea) and resulted in poor compliance (13).
IV colchicines should not be used and are no longer approved by the FDA
owing to the high level of toxicity (14)[A].
In a randomized, controlled trial that compared colchicine with placebo, the
number needed to treat (NNT) for colchicine was 3, whereas the NNT with
resulting toxicity for colchicine was 2 (13).
Preventive therapy can substantially reduce future episodes but should be
avoided during acute attacks (10,14)[B].
Indications for chronic preventative therapy include (7,15)[B]
Recurrent or disabling gout attacks (specifically >2 gout attacks/yr)
Persistent tophi
Joint damage noted on imaging
Uric acid nephropathy or nephrolithiasis
The symptom-free period required prior to starting prophylactic therapy once
the acute attack has resolved is unclear.
Some advocate using concomitant colchicine treatment the 1st 3–6 mos of
urate-lowering treatment (16)[C].
Some suggest waiting about 4–6 wks after the acute attack before starting
prophylactic medication (5)[C].
If a gout attack occurs while on urate-lowering treatment, the urate-lowering
medication should not be stopped (4)[B].
Uric acid level should be monitored for a goal of <6 mg/dL (355 µmol/L)
because this is associated with a significantly lower incidence of gout (5)[B].
Allopurinol is a xanthine oxidase inhibitor that decreases uric acid production.
Used most commonly
Therapeutic dose is 100–300 mg/day: Start at a lower dose (50 or 100
mg/day), and titrate up slowly over several weeks (eg, by 100 mg every 2–4
wks) to target uric acid goal of <6 mg/dL (9)[C].
Patients with renal insufficiency require lower doses.
Periodic laboratory testing (liver enzymes and CBC) should be considered.
Febuxostat is a newer medication.
Cleared through the liver and therefore an appropriate alternative in renal
disease.
Recent studies suggest that it might be superior to allopurinol, but more
studies are needed (17).
Probenecid is a uricosuric agent that increases uric acid secretion.
2nd-line medication for prophylaxis (10)
Ineffective in patients with impaired creatinine clearance
Avoid in patients with nephrolithiasis.
Caution for multiple medication interactions
NSAIDs (naproxen 250 mg b.i.d.) or colchicine (≤0.6 mg/day or b.i.d.) can be
used as chronic suppression therapy in the place of or in addition to urate-
lowering agents (4)[B].
Low-dose prednisone (≤10 mg) also can be considered, but it has long-term
side effects (4)[B].
General Measures
See “Risk Factors” for what to avoid.
Therapy for gout includes diet modification (see “Risk Factors”), using
medications that reduce overall uric acid levels (such as losartan and
fenofibrate), and minimizing medications that are known to increase gout flairs
(such as diuretics and aspirin) when appropriate.
Referral
Rheumatology if refractory condition, multiple comorbities, or unusual
presentation
Orthopedics if suspected septic arthritis
Consider for severe cases of gout, especially if needed for pain control or for
diagnostic confirmation.
Suspected septic arthritis requires IV antibiotics and orthopedic referral.
Ongoing Care
Prognosis
60% of patients undergoing a gout attack will have another one within 12 mos (18).
Complications
It takes, on average, about 10 yrs for chronic top-haceous gout to develop
after the initial attack (4).
Chronic gout can lead to joint damage and destruction.
Frequent attacks can be very painful and disabling and have a negative impact
on quality of life.
References
1. Wallace KL, Riedel AA, Joseph-Ridge N, et al. Increasing prevalence of
gout and hyperuricemia over 10 yrs among older adults in a managed care
population. J Rheumatol. 2004;31:1582–1587.
2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence
of arthritis and other rheumatic conditions in the United States: Part II. Arthritis
Rheum. 2008;58:26–35.
3. Choi HK, Atkinson K, Karlson EW, et al. Purine-rich foods, dairy and protein
intake, and the risk of gout in men. N Engl J Med. 2004;350:1093–1103.
4. Keith MP, Gilliland WR. Updates in the manage-ment of gout. Am J Med.

2007;120:221–224.
5. Eggebeen AT. Gout: an update. Am Fam Physician. 2007;76:801–808.
6. Schlesinger N, Norquist JM, Watson DJ. Serum urate during acute gout. J
Rheumatol. 2009.
7. Zhang W, Doherty M, Pascual E, et al. Eular evidence based

recommendations for gout—Part I Diagnosis: Report of a task force of the
Standing Committee for International Clinical Studies Including Therapeutics
(ESCISIT). Ann Rheum Dis. 2006.
8. Schumacher HR, Becker MA, Edwards NL, et al. Magnetic resonance

imaging in the quantitative assessment of gouty tophi. Int J Clin Pract.
2006;60:408–414.
9. Terkeltaub RA. Clinical practice. Gout. N Engl J Med. 2003;349:1647–

1655.
10. Zhang W, Doherty M, Bardin T, et al. EULAR Evidence based

recommendations for gout— part II management: report of a task force of the
EULAR Standing Committee for International Clinical Studies Including
Therapeutics (ESCISIT). Ann Rheum Dis. 2006.
11. Wortmann RL. Recent advances in the management of gout and

hyperuricemia. Curr Opin Rheumatol. 2005;17:319–324.
12. Janssens HJ, Janssen M, van de Lisdonk EH, et al. Use of oral
prednisolone or naproxen for the treatment of gout arthritis: a double-blind,
randomised equivalence trial. Lancet. 2008;371:1854–1860.
13. Schlesinger et al. Cochrane database of systemic reviews: Colchicine

for acute gout. CD006190, Issue 4, 2006.
14. Terkeltaub RA. Colchicine Update: 2008. Semin Arthritis Rheum. 2008.
15. Shoji A, Yamanaka H, Kamatani N. A retrospective study of the

relationship between serum urate level and recurrent attacks of gouty arthritis:
evidence for reduction of recurrent gouty arthritis with antihyperuricemic
therapy. Arthritis Rheum. 2004;51:321–325.
16. Borstad GC, Bryant LR, Abel MP, et al. Colchicine for prophylaxis of acute
flares when initiating allopurinol for chronic gouty arthritis. J Rheumatol.
2004;31:2429–2432.
17. Becker MA, Schumacher HR, Macdonald PA, et al. Clinical efficacy and
safety of successful longterm urate lowering with febuxostat or allopurinol in
subjects with gout. J Rheumatol. 2009.
18. Gutman AB. The past four decades of progress in the knowledge of gout,
with an assessment of the present status. Arthritis Rheum. 1973;16:431–
445.
Additional Reading
Li-Yu J, Clayburne G, Sieck M, et al. Treatment of chronic gout. Can we
determine when urate stores are depleted enough to prevent attacks of gout?
J Rheumatol. 2001;28:577–580.
20. Sutaria S, Katbamna R, Underwood M. Effectiveness of interventions for

the treatment of acute and prevention of recurrent gout—a systematic review.
Rheumatology (Oxford). 2006.
Codes
ICD9
274.00 Gouty arthropathy, unspecified
274.01 Acute gouty arthropathy
274.9 Gout, unspecified
Clinical Pearls
Gout is an acute inflammatory arthritis that can mimic infection and progresses
to a chronic disease.
A painful, warm, erythematous, swollen joint should be aspirated to rule out
septic arthritis versus gout.
Tophaceous gout is the chronic form of gout that, in rare cases, can present
acutely as well.
Prophylactic treatment should be considered in recurrent patients because it
has been shown to reduce chronic flairs and joint damage.
Many medications that treat gout have side effects, and care must be taken in
choosing the right medication while maintaining close follow-up.
Pseudogout is a disease that is distinct from gout but has various similarities,
is less debilitating, and is less common.
Greenstick Fracture
Greg Canty
K. Brooke Pengel
Basics
Description
Greenstick fractures are incomplete fractures that occur when a bone is exposed to bending
forces. The bending forces are strong enough that the bone begins to fracture, but the force is
not sufficient enough to result in a complete fracture:
The fracture appears on the tension (convex) side of the bone as a break in the periosteum
and the cortex.
The compression side of the bone, or the concave surface, remains intact and appears as a
hinge.
This fracture pattern is most commonly described in forearm fractures of growing children.
Greenstick fractures may be isolated or may coexist with other complete fractures in forearm
injuries.
Epidemiology
Most recent study states up to 5% of childhood and adolescent fractures are of the
greenstick variety (1)
Previous studies have estimated even greater percentages of childhood fractures are of the
greenstick variety.
Although extremely rare, there have actually been a few case reports of greenstick fractures
in the young adult population (2)
Forearm (radius or ulna) = most common
Proximal humerus
Tibia
Etiology
Greenstick fractures occur in children and adolescents because the bone is more:
Porous
Compliant
Resilient
Soft
Complete fracture of an accompanying bone (common)
Fracture/dislocation like a Monteggia variant (proximal 3rd ulna fracture with anterior
disruption of radial head) (rare)
Diagnosis
Pre Hospital
Suspect with any forearm injury having a mild angular deformity, swelling, and pain
History
Establish mechanism of injury, which is often a fall on outstretched hand with some rotational
force.
Inquire about any numbness, tingling, or pain out of proportion to exam findings.
Physical Exam
Pain and localized tenderness to palpation
Unwillingness to use or mobilize the affected extremity
Mild to moderate angular deformity
Swelling
Ecchymosis
Palpation of bony deformities
Crepitus
Assess the distal portion of the affected extremity for:
Circulation (capillary refill and pulses)
Motor function
Sensation
Assess proximal and distal joints/bones for related injuries.

Imaging
Anteroposterior and lateral radiographs required for diagnosis
Look for tearing of the periosteum and cortex on the convex side of affected bone.
Concave surface of affected bone should have intact periosteum.
Plastic deformation of bone may also be apparent.
Oblique views may occasionally be helpful.
Repeat radiographs after reduction.
Complete fracture
Compound fracture
Plastic deformation/Bowing deformity
Torus (buckle) fracture
Contusion
Sprain
Treatment
Pre-Hospital
Ice to affected region for pain control and swelling
Splint in comfortable position using:
Air splint or board
Tape
Rolled towels
ED Treatment
Pain control (see “Medications”)
Fracture reduction (3)[C]:
Most greenstick fractures of the forearm are reduced by rotating the palm
toward the apex of the fracture.
Greenstick fractures are incomplete fractures, and may require completing
the fracture in order to obtain adequate reduction.
Immobilize the injury with either a cast or splint:
Immobilize in reduced position.
Long arm cast/splint with elbow at 90° if fracture of proximal or middle 3rd of
forearm
May consider below-the-elbow cast if fracture is in distal 3rd of forearm (4)
[B]
Ensure proper 3-point molding to maintain reduction.
Immobilize the joints proximal and distal to the injury.
Postreduction films after casting/splinting
Ensure reduction is maintained with immobilization prior to discharge from
emergency department.
Medication
First Line
Ibuprofen (10 mg/kg) with max of 800 mg every 6–8 hr (5)[B]
Hydrocodone/acetaminophen (available as an elixir containing 7.5 mg
hydrocodone/500 mg acetaminophen/15 mL):
12–15 kg = 3.75 mL every 4–6 hr (max 22.5 mL/day)
16–22 kg = 5 mL every 4–6 hr (max 30 mL/day)
23–31 kg = 7.5 mL every 4–6 hr (max 45 mL/day)
32–45 kg = 10 mL every 4–6 hr (max 60 mL/day) P.
>46 kg = 15 mL every 4–6 hr (max 90 mL/day)
Oxycodone (available as an elixir containing 1 mg/1 mL) (6)[B]:
0.05–0.15 mg/kg every 4–6 hr
Second Line
Fentanyl 1–2 mcg/kg every 1–4 hr (max 100 mcg)
Morphine 0.1–0.2 mg/kg every 2–4 hr (max 10 mg)
Referral
Refer if unable to maintain reduction
Refer for any signs of median nerve or tendon entrapment
Refer for any progressive deformity
Rarely indicated unless nerve/tendon entrapment or inability to maintain reduction
Admission Criteria
Any suspicion of a nonaccidental injury (NAI):
History is best predictor of NAI.
Best predictor of NAI is whether history is consistent with injury pattern/severity
Discharge Criteria
Pain is well controlled.
Orthopedic referral within 1 wk
Splint or cast care instructions:
Ice/cold pack application
Elevation of the injured limb
Analgesic medication
Return precautions
Ongoing Care
Patient Monitoring
Repeat radiographs should be obtained at 1 and 2 wks to ensure alignment is being
maintained.
Beware of the risk for greenstick fractures of the tibia to result in a valgus deformity (follow
for 1–2 yrs)
Loss of reduction or progression of any deformity warrants surgical consideration, although
younger patients have excellent capability of remodeling and rarely require surgery.
Prognosis
Greenstick fractures are expected to heal completely.
Complications are rare.
Remodeling capabilities are tremendous in young patients.
Excellent prognosis
Complications
10–15% of greenstick fractures may lose reduction after immobilization.
Nerve or tendon sheath entrapment
An unrecognized accompanying injury
References
1. Cheng JC, Shen WY. Limb fracture pattern in different pediatric age groups:
a study of 3,350 children. J Orthop Trauma. 1993;7:15–22.
2. Casey PJ, Moed BR. Greenstick fractures of the radius in adults: a report
of two cases. J Orthop Trauma. 1996;10:209–212.
3. Noonan KJ, Price CT. Forearm and distal radius fractures in children. J Am
4. Bohm ER, Bubbar V, Yong Hing K, et al. Above and below-the-elbow plaster
casts for distal forearm fractures in children. A randomized controlled trial. J
5. Drendel AL, Gorelick MH, Weisman SJ, et al. A Randomized Clinical Trial
of Ibuprofen Versus Acetaminophen With Codeine for Acute Pediatric Arm
Fracture Pain. Ann Emerg Med. 2009.
6. Koller DM, Myers AB, Lorenz D, et al. Effectiveness of oxycodone,

ibuprofen, or the combination in the initial management of orthopedic injury-
related pain in children. Pediatr Emerg Care. 2007;23:627–633.
Additional Reading
Rang's children's fractures. Wenger DR, Pring ME, eds. 3rd edition,
Lippincott Williams & Wilkins, 2005.
Rockwood and Wilkins' fractures in children. Beaty JH, Kasser JR. 6th
edition, Lippincott Williams & Wilkins, 2005.
Skeletal trauma in children. Green NE, Swiontkowski MF. 4th edition,

Saunders, 2008.
Codes
ICD9
812.00 Fracture of unspecified part of upper end of humerus, closed
813.81 Fracture of unspecified part of radius (alone), closed
813.82 Fracture of unspecified part of ulna (alone), closed
Clinical Pearls
Examine surrounding bones/joints closely for accompanying injuries such as a
both-bone forearm fracture or a Monteggia-variant fracture/dislocation.
Incomplete fractures, like the greenstick, may require completing the fracture
for adequate reduction.
Reduce radial greenstick fractures by rotating the forearm so that the palm is
pointing toward the apex of the fracture.
Follow greenstick fractures closely after reduction to ensure adequate
reduction is maintained.
Beware of the long-term risk for a valgus deformity following greenstick
fractures of the tibia.
Haglund's Deformity (Pump Bump)
Brent S. E. Rich
Michael Devin Taylor
Basics
Description
Haglund's deformity is an abnormal prominence of the posterosuperior surface of the
calcaneus. It can give rise to Haglund's disease, which consists of retrocalcaneal bursitis,
insertional Achilles tendinitis, and pre-Achilles bursitis or superficial bursitis. These occur due
to compression of the distal Achilles tendon and the surrounding soft tissues, between the os
calcis and the posterior shoe counter.
Synonyms(s): Haglund's disease; Haglund's syndrome; Pump bump
Epidemiology
More common in females who start wearing high heels and shoes with restrictive heel
counters
Haglund's syndrome occurs in both sexes and is seen in all active age groups.
Women age 20–30 yrs seem to have a slightly higher prevalence.
More commonly seen in individuals/athletes wearing shoes with rigid heel counters (eg,
pumps, ice skates, work boots)
Risk Factors
Heel varus
Cavus foot
Rigid plantarly flexed 1st ray
Rigid or poorly shaped heel counters
Diagnosis
History
Increase in training program, specifically number of miles run
Change in shoe wear (shoes with rigid heel counters can irritate the subcutaneous tissues,
and can inflame the underlying bursae)
Physical Exam
Dull, achy, exertional posterior heel pain
Tenderness and thickening of the overlying skin at the Achilles tendon attachment
Palpable swelling anterior or posterior to the Achilles tendon
Pain is intensified with active or passive dorsiflexion of the ankle.
Prominent-appearing posterosuperior portion of the calcaneus
Careful, discreet palpation to differentiate between swelling in the Achilles tendon and
swelling in the retrocalcaneal bursa
Palpation medially as well as laterally within the retrocalcaneal bursa

Imaging
Lateral radiographs may show a 2–3-mm bony extrusion on the posterosuperior angle of the
calcaneus.
Calcaneal body index assesses the shape of the calcaneus, and the calcaneal inclination
angle assesses the orientation of the calcaneus. Good predictors of posterior heel pain.
Parallel pitch lines and Fowlers lines have been used in the past for diagnosis, but in recent
studies have been found to have no statistically significant relationship to posterior heel pain
Consider ordering MRI or musculoskeletal US to evaluate the integrity of the Achilles tendon
and the retrocalcaneal bursa.
Pre-Achilles bursitis
Achilles tendinitis/tendinosis
Calcaneal stress fracture
Ankle impingement
Tibiotalar degenerative joint disease
Treatment
Shoe modification
Achilles stretching program
U-shaped pad
Heel pad
Soft tissue modalities (ie, ice, US, iontophoresis)
Decrease in mileage and hill work
Minimization of hard-surface running
NSAIDs
Immobilization with a short-leg walking cast
Aspiration and injection with corticosteroids
Achilles stretching program
Soft tissue modalities (ie, ice, US, iontophoresis)
Partial calcaneal osteotomy (open or endoscopic): Complete resection of the
bursal projection
Postoperative course: Short-leg walking cast provided for 8 wks, 2 wks partial
weight-bearing, full weight-bearing over succeeding 6 wks, until cast removal.
Course shortened with endoscopic procedure.
Rehabilitation program consisting of conditioning exercises and functional
retraining
Ongoing Care
Surgery as indicated above
Complications
Chronic heel pain
Additional Reading
Aronow MS. Posterior heel pain (retrocalcaneal bursitis, insertional and
noninsertional Achilles tendinopathy). Clin Podiatr Med Surg North Am.
2005;22:19–43.
Heneghan MA, Pavlov H. The Haglund painful heel syndrome. Experimental

investigation of cause and therapeutic implications. Clin Orthop Relat Res.
1984:228–234.
Hoberg M, Gradinger R, Rudert M. [Heel pain] MMW Fortschr Med.

2007;149:36–39; quiz 40
Lu CC, Cheng YM, Fu YC, et al. Angle analysis of Haglund syndrome and its
relationship with osseous variations and Achilles tendon calcification. Foot
Ankle Int. 2007;28:181–185.
Ortmann FW, McBryde AM. Endoscopic bony and soft-tissue decompression

of the retrocalcaneal space for the treatment of Haglund deformity and
retrocalcaneal bursitis. Foot Ankle Int. 2007;28:149–153.
Codes
ICD9
Clinical Pearls
When can I return to play? The time to return to play is dependent on the
severity and number of associated conditions involved. Return to play after
conservative treatment ranges from 2–8 wks, whereas surgery and
postoperative course limits and prevents strenuous activity for 4–6 mos.
Athletes may return to strenuous activity when local symptoms have resolved at
this time.
Hallux Valgus (Bunions)
Robyn Fean
Jonathan Drezner
Basics
Description
Hallux valgus refers to a subluxation of the 1st metatarsophalangeal (MTP) joint with lateral
or valgus deviation of the great toe and medial or varus deviation of the 1st metatarsal,
leading to a bony prominence at the medial aspect of the joint (medial eminence or bunion).
Synonym(s): Bunion; Metatarsus primus varus
Epidemiology
More common in females; Female: Male = 10:1
Familial tendency
Almost exclusively seen in shoe-wearing societies
Prevalence is highest in women in their 4th through 6th decades of life.
Risk Factors
Constrictive footwear and high-heeled shoes
Pes planus and forefoot pronation lead to increased pressure on the medial aspect of the
great toe and attenuation of the medial capsular structures at the 1st MTP joint.
A rounded MTP articulation is more prone to lateral subluxation then a flat articulation.
Metatarsus primus varus and an increased 1st and 2nd intermetatarsal angle are often
implicated in juvenile or adolescent hallux valgus.
Tight Achilles tendon
Hypermobility of the 1st metatarsocuneiform joint
Neuromuscular disorders and collagen-deficient disorders
General Prevention
Avoid tight-fitting shoes and shoes with an excessively high heel (ie, >1 inch).
Correct for overpronation with orthotics.
Etiology
Pes planus and forefoot pronation lead to increased pressure on the medial aspect of the
great toe and attenuation of the medial capsular structures at the 1st MTP joint.
The abductor hallucis is located medially and provides support to the alignment of the great
toe.
A hallux valgus deformity develops, the abductor hallucis tendon is displaced in a plantar
direction, and the joint loses most of its medial support.
The adductor hallucis then pulls the proximal 1st phalanx laterally and exerts a rotational
force, resulting in pronation of the 1st phalanx.
With worsening of the hallux valgus deformity, the extensor hallucis longus shifts into the 1st
metatarsal interspace and becomes a lateral force on the great toe.
With continued lateral pull of the 1st phalanx, the 1st metatarsal deviates medially in relation
to the sesamoids and leads to the appearance of subluxation of the sesamoids.

Hammer toe deformity of the 2nd toe
Pes planus
Ingrown toenails in the great toe or the 2nd toe
Metatarsalgia
Plantar keratosis beneath the 2nd metatarsal head
Diagnosis
History
Pain over the medial eminence aggravated by tight or rigid footwear is the most common
complaint.
Pain under the 2nd metatarsal head with a plantar keratosis is also common.
Blisters, swelling, callus formation, or bursitis over the medial eminence may occur with
athletic activities.
Patients may describe forefoot widening or difficulty wearing shoes comfortably.
Numbness or tingling of the medial aspect of the great toe may occur from pressure on the
medial dorsal cutaneous nerve to the hallux.
Physical Exam
Note the severity of hallux valgus and rotational deformity of the great toe in both the
standing and nonweight-bearing positions.
Assess for pes planus and excessive pronation.
Check active and passive range of motion at the 1st MTP joint (normal extension is 70
degrees).
Evaluate sensation of the great toe.
Evaluate for tightness of the Achilles tendon.

Imaging
Radiographs are typically unnecessary for conservative management of hallux valgus.
Weight-bearing anteroposterior (AP) and lateral radiographs are helpful in the preoperative
assessment of the severity of the deformity (1)[C].
Using the AP radiographs, the hallux valgus angle can be measured. The hallux valgus angle
is the angle subtended by the axis of the proximal phalanx and the 1st metatarsal (normal
<15 degrees, mild to moderate <30 degrees, severe <40 degrees).
The 1st–2nd intermetatarsal angle is formed by the intersection of the longitudinal axis of the
1st and 2nd metatarsals (normal <9 degrees, mild to moderate <14 degrees, severe >14
degrees).
Radiographs also assess MTP joint congruity or subluxation, lateral sesamoid subluxation,
the shape of the metatarsal head, and degenerative changes of the MTP joint.
Axial films may be helpful to assess lateral displacement of the sesamoids, and lateral films
are helpful for evaluating arthritic changes of the MTP joint and identifying hallux rigidus.
Hallux rigidus (degenerative arthritis of the great toe MTP joint with dorsal bunion)
Hallux interphalangeus (valgus at the interphalangeal joint, not the MTP joint)
Gout
Osteoarthritis of the 1st MTP joint
Treatment
Initial treatment consists of footwear modification and patient education.
Wider footwear with a roomy toe box will help decrease pressure and friction
on the medial eminence.
Shoes with flexible and nonconstricting stitching over the medial eminence are
recommended (shoes can be professionally stretched to provide additional
room).
High-heeled shoes (which place increased pressure on the forefoot) should be P.
avoided.
Medial longitudinal arch support may decrease pressure on the 1st metatarsal,
especially in patients with pes planus.
Activity modification in joggers and runners (substituting bicycling or other
nonimpact activities) may significantly decrease symptoms and stress on the
forefoot.
Medication
NSAIDs may be beneficial in decreasing pain and inflammation (2)[C].
Properly fitting shoes with appropriate forefoot width (ie, wide toe box) and
avoidance of high-heeled shoes (2)[C]
Felt pads to protect the medial eminence (2)[C]
Metatarsal pads to help unload the joint (2)[C]
Orthotic arch supports (3)[A]
Ice (2)[C]
Treatment of an athlete with hallux valgus should be nonoperative until pain and
symptoms are significantly affecting athletic performance.
Stiffness, decreased range of motion, pain, and reduced function of the MTP
joint are potential risks of surgery and may hamper athletic performance
(particularly in sprinters and dancers, who require MTP motion for strength in
toe push-off).
Surgery should be considered after conservative treatment has failed (4)[C].
Numerous surgical procedures have been developed to correct hallux valgus.
Operative procedures include medial eminence resection, proximal phalangeal
osteotomy, distal metatarsal osteotomy, medial capsular reefing, lateral
capsular and adductor hallucis release, and joint fusion or replacement (4)[C].
Proximal crescentic osteotomy of the 1st metatarsal and distal soft tissue
repair may be beneficial in alleviating pain in moderate-to-severe cases (3)[B].
Ongoing Care
Patients should be referred for surgical consideration when nonoperative treatment, including
footwear and activity modification, have not adequately relieved symptoms.
Complications
Increased risk of falls secondary to pain and postoperative footwear, especially
in the elderly
Stiffness, decreased range of motion, and reduced function of the MTP joint
are potential risks of surgery and may hamper athletic performance (especially
in sprinters and dancers, who require MTP motion for strength in toe push-off).
References
1. Snider RK, ed. Essentials of musculoskeletal care. Chicago: American
Academy of Orthopaedic Surgeons, 1997.
2. DeLee JC, Drez D. Orthopaedic sports medicine. Philadelphia: WB

Saunders, 1994.
3. Coughlin MJ, Smith BW. Hallux valgus and first ray mobility. A prospective
study. J Bone Joint Surg. 2007;89-A:1887–1898.
4. Vanore JV, et al. Diagnosis and treatment of first metatarsophalangeal joint

disorders. Section 1: hallux valgus. J Foot Ankle Surg. 2003:112–120.
Additional Reading
Coughlin MF. Hallux valgus: demographics, etiology and radiographic
assessment. Foot Ankle Int. 2007;28(7):759–777.
Coughlin MJ. Instructional course lectures, The American Academy of

Orthopedic Surgeons—hallux valgus. J Bone Joint Surg. 1996;78-A:932–966.
Donley BG, Tisdel CL, Sferra JJ, et al. Diagnosing and treating hallux valgus:
a conservative approach for a common problem. Clev Clin J Med
1997;64:469–474.
Hawke F, et al. Custom-made foot orthoses for the treatment of foot pain. In:
The Cochrane Library, Issue 3, 2009. Chichester: Wiley. Updated quarterly.
Codes
ICD9
735.0 Hallux valgus (acquired)
Clinical Pearls
Without appropriate treatment, hallux valgus deformities typically progress.
However, with activity modification, proper footwear, and selective use of orthotic
arch supports, symptoms and complications can largely be controlled.
Hammer/Claw/Mallet Toe
Robyn Fean
Jonathan Drezner
Basics
Description
Mallet toe is a flexion contracture of the DIP joint with normal alignment of the MTP and PIP
joints. The 2nd toe is most commonly affected
Hammer toe is a plantar flexion contracture of the proximal interphalangeal (PIP) joint.
Passive extension of the metatarsophalangeal (MTP) joint is common. The distal
interphalangeal (DIP) joint is neutral or slightly extended. The 2nd toe is most commonly
affected.
Claw toe is an extension contracture of the MTP joint with a flexion contracture of the PIP
joint and sometimes the DIP joint. Claw toe usually results from weakness in the intrinsic
muscles of the foot secondary to a neurologic condition and commonly affects multiple toes.
Epidemiology
Hammer, claw, and mallet toes are the most common deformities of the lesser toes.
Incidence increases with age.
Predominant gender: Female > Males ( 9:1).
Risk Factors
Hammer and mallet toe deformities are usually the result of long-term use of poorly fitting
and constricting footwear.
Abnormally long ray or digital length
Pressure or deforming force from adjacent digits (ie, hallux valgus)
Inflammatory joint disease
Pes cavus may indicate an associated neuromuscular disorder.
Claw toes are found in associated neurologic conditions such as peripheral neuropathies
(diabetes and alcoholism), Charcot-Marie-Tooth disease, cerebral palsy, muscular dystrophy,
and spinal cord tumors.
General Prevention
Avoidance of constrictive footwear.
Etiology
Long-term use of poorly fitting and constricting footwear
Idiopathic
Congenital anatomic dysfunction
Trauma
Inflammatory arthropathy
Neuromuscular dysfunction resulting in weakness in intrinsic muscle function
Diagnosis
History
Painful callus formation over the dorsal aspect of the PIP or DIP joint (from rubbing against the
undersurface of the shoe). Callus formation also may take place at the tip of the toe (1)[C].
Physical Exam
Hammer toe:
Painful callus over the dorsal aspect of the PIP joint (from rubbing against the undersurface
of the shoe) is most common.
Secondary metatarsalgia with plantar keratosis (callus) under the metatarsal head may
occur if MTP joint subluxation is present.
Claw toe: Painful callus formation over the dorsal PIP joint, beneath the metatarsal head, or
on the end of the toe
Mallet toe: Painful callus at the tip of the toe
Patients should be evaluated both standing and non–weight bearing. (In hammer toe
deformities, extension of the MTP joint is common in the standing position but may largely
resolve when non–weight bearing.)
Toes should be passively stretched to determine if the deformity is flexible (reducible to
neutral position), semirigid (partially reducible), or rigid (nonreducible). A flexible hammer or
claw toe deformity may appear to resolve when passively bringing the ankle from
dorsiflexion to plantarflexion.
Inspection for the presence of calluses, ulcers, adventitious bursa, infection, and interdigital
maceration
Calluses are common on the dorsum of the PIP joint and under the metatarsal head
(hammer and claw toes) or on the tip of the toe (hammer, claw, and mallet toes).
Dorsal dislocation of the proximal phalanx onto the metatarsal head may occur in advanced
cases.
A crossover deformity of the 2nd toe resting on top of the great toe may exist with medial
subluxation of the 2nd MTP joint.

Imaging
Radiographs typically are unnecessary for conservative management in most cases.
Weight-bearing anteroposterior (AP) radiographs are helpful to assess for the presence of
MTP joint subluxation or dislocation.
Lateral radiographs best confirm the deformity.
Advanced imaging (bone scan or MRI) may be indicated when ulceration is present and
osteomyelitis is suspected.
Electromyography and nerve conduction studies may be useful to evaluate for peripheral
neuropathies in claw toe deformities.
Hammer toe (flexion of the PIP joint)
Claw toe (extension of the MTP joint and flexion of the PIP and DIP joints)
Mallet toe (flexion of the DIP joint)
Hard corn (keratosis over the lateral aspect of the 5th toe)
Interdigital (soft) corn (keratosis and maceration resulting from pressure between 2 adjacent
toes)
Treatment
Long-term treatment
Acute treatment:
Shoes with a roomy toe box are recommended to accommodate the
deformity (an elevated toe box may eliminate dorsal pressure on the PIP
joint).
High-heeled shoes should be avoided.
Passive manual stretching and strengthening exercises for the intrinsic foot
muscles (laying a towel flat on the floor and using the toes to crumple it
beneath the foot) may be helpful for flexible deformities.
Débridement of hyperkeratotic lesions and home use of a pumice stone may
reduce painful calluses.
Foam pads used over the callosity or a cushioned toecap to protect the end
of the toe may reduce symptoms.
Metatarsal pads placed proximal to the MTP joint may reduce pressure on
the metatarsal heads.
Taping the toe in a corrected position may stabilize a subluxed MTP joint.
Medication
First Line
NSAIDs may be appropriate to relieve pain and inflammation
General Measures
Shoes with a roomy toe box are recommended to accommodate the deformity
(an elevated toe box may eliminate dorsal pressure on the PIP or DIP joint) (2)
[C].
High-heeled shoe should be avoided (2)[C].
Foam pads used over the callosity or a cushioned toe cap to protect the end of
the toe may reduce symptoms.
Metatarsal pads placed proximal to the MTP joint may reduce pressure on the
metatarsal heads.
A toe crest placed beneath the toes may be used to diminish pressure on the
tip of the toe (2)[C].
Surgery is indicated when nonoperative treatment is unsuccessful in relieving
symptoms (2)[C].
Flexible hammer/claw toes may be repaired with flexor and extensor
percutaneous tenotomies (3)[C].
Rigid deformities require a capsulotomy or treatment with arthroplasty (joint
resection) or arthrodesis (joint fusion) (3)[C].
Flexible mallet toes may be treated with percutaneous release of the flexor
digitorum longus tendon (4)[C].
Ongoing Care
Referral for surgical consideration is recommended when conservative treatment has not
adequately relieved symptoms.
Prognosis
Surgery usually can be avoided if conservative treatment is started early.
When needed, surgery can be very effective in alleviating pain and improving the deformity.
Complications
Toe and toenail deformity
Chronic pain/metatarsalgia
If surgery is performed, persistent numbness of the toe and surrounding areas
may occur as a result of nerve injury.
Malalignment of the digits may occur after surgery.
Flexor digitorum longus tendon transfer results in the inability to actively flex the
affected toe.
References
1. DeLee JC, Drez D. Orthopaedic sports medicine. Philadelphia: WB
Saunders, 1994.
2. Coughlin MJ. Lesser-toe abnormalities. J Bone Joint Surg-Am.

2002;84:1446–1469.
3. Migues A, Campaner G, Slullitel G, et al. Minimally invasive surgery in hallux

valgus and digital deformities. Orthopedics. 2007;30:523–526.
4. Coughlin MJ. Operative repair of the mallet toe deformity. Foot Ankle Int.
1995;16:109–116.
Additional Reading
Bade H, Tsikaras P, Koebke J. Pathomorphology of the hammer toe. Foot
Ankle Surg. 1998;4:139–143.
Barakat MJ, Gargan MF. Deformities of the lesser toes. How should we
describe them? The Foot. 2006;16:16–18.
Hammer toe syndrome. American College of Foot and Ankle Surgeons. J

Foot Ankle Surg. 1999;38:166–178.
Snider RK, ed. Essentials of musculoskeletal care. Chicago: American
Academy of Orthopaedic Surgeons, 1997.
Codes
ICD9
735.4 Other hammer toe (acquired)
735.5 Claw toe (acquired)
Clinical Pearls
The distinction between hammer toe and claw toe deformities can be difficult
because both have flexion contractures of the PIP joint.
However, in claw toe, deformities of multiple toes are involved, and there is
always an extension deformity of the MTP joint and often a flexion contracture
of the DIP joint.
Hamstring Strain
Kara D. Cox
Basics
Description
Hamstring strain is a common injury in athletes that can be painful and disabling. The
musculotendinous unit (biceps femoris, semitendinosus, and semimembranosus) can be injured
at multiple sites, including the proximal bony attachment, the musculotendinous junction, the
central muscle belly, and the distal tendon. The injury occurs due to an excessive load during an
eccentric contraction, such as with running or jumping. Treating hamstring strain can be
frustrating due to slow healing, persistent symptoms, and high recurrence rates.
Epidemiology
Hamstring strains are among the most common injuries in running, jumping, and kicking sports,
particularly those that involve sprinting. The biceps femoris is the most commonly injured
muscle, and strain most commonly occurs at the muscle-tendon junction.
Prevalence
Prevalence rates vary due to differing definitions and underreporting:
Prevalence rates vary from 8–25% (1).
Single-season prevalence has been reported to be as high as 50% (1).
Reinjury is common and is reported at rates of 12–31% (2).
Risk Factors
Nonmodifiable risk factors:
Increased age: Athletes between 23 and 25 yrs were between 1.3 and 3.9 times more
likely to suffer strains, and in increasing age groups, the risk was shown to increase by
30% annually (1)[A].
Black racial background: Studies suggest that this is not specific to any one nationality, but
to all athletes of black racial background (1)[A].
Higher levels of competition: Hamstring strain was infrequently reported in amateur sport,
but prevalence was significantly greater (p <.01) in higher levels of competition (1)[A].
Modifiable risk factors:
Previous history of hamstring strain injury: Previously injured athletes were 2–6 times more
likely to suffer subsequent strains (1)[A].
Strength imbalances, including 10% difference between right to left hamstring or low
hamstring to quadriceps ratio (H:Q ratio) have been quoted as risk factors, but have not
been shown to be significant predictors of future injury (1,3)[C]
Poor flexibility: Inflexible hip flexors is a significant risk factor, and increased quadriceps
flexibility is inversely related to hamstring strain incidence; however, hamstring flexibility
does not demonstrate significant association (1)[C]
A proposed multifactorial model for hamstring injury includes poor flexibility, strength
imbalances, inadequate warm-up, and muscle fatigue (1,2,3,4)[C]
General Prevention
Balanced strength of hamstrings from side to side and of hamstrings to quadriceps
Eccentric strengthening programs
Flexible hamstrings and, just as important, flexible hip flexors and quadriceps
Proper warm-up
Proper recovery following hamstring injury and avoidance of premature return to play
Etiology
Muscle injuries can be as simple as a muscle cramp or as complicated as a complete
rupture, and in between are the muscle strains.
Strains are classified by severity of muscle fiber injury (2,4):
Mild strain (1st degree): Stretch type injury with few muscle fibers injured, causing only
minor swelling/pain and minimal loss of strength/motion
Moderate strain (2nd degree): Partial tear with strength loss and functional limitations due
to more extensive muscle injury
Severe strain (3rd degree): Extensive or complete tear across whole muscle with disabling
loss of muscle function
The healing process in muscle injury includes initial muscle fiber injury with immediate
hemorrhage followed by inflammatory cell introduction to the damaged tissue, production of
connective scar tissue, and regeneration of damaged muscle fibers.
The hamstring musculotendinous unit (biceps femoris, semitendinosus, and
semimembranosus) is susceptible to injury for many reasons (5):
The hamstrings cross 2 joints, which can be moving in opposing directions.
The short head of the biceps femoris has a long, inconstant origin along the femur.
The hamstrings (specifically the biceps) have dual innervation, which causes forceful,
uncoordinated contractions (the hamstrings, including the long head of the biceps, are
innervated by the tibial branch of the sciatic nerve, with the exception being the short head
of the biceps, which alone is innervated by the peroneal branch of the sciatic nerve).
During the gait cycle, the hamstrings have differing activity (the semimembranosus has
increased eccentric activity to slow hip flexion during the swing phase, while the biceps are
most active during take-off).
The usual mechanism of injury occurs in the later part of the swing phase as the hamstrings
rapidly change from eccentrically working to decelerate knee extension to concentrically
becoming an extensor of the hip (2).

Apophyseal injury, such as traction apophysitis (found in children when the ischial apophysis
appears at ages 13–15 and up to ages 20–25 when it fuses with the pelvis) (5)
Complete tendon rupture, with or without avulsion fracture (found mostly in adults, more
commonly proximal at the ischium vs distal, which is rare) (5)
Development of myositis ossificans
Diagnosis
Most hamstring strain injuries occur in an acute setting with sudden onset of posterior
thigh pain that often limits participation. Typical hamstring strain injury can be diagnosed based
on thorough history and physical exam.
History
Hamstring strain is most commonly seen in kicking or speed athletes (2,3,4)[C].
In cases of avulsion injury other activities are reported, such as water skiing, dance, weight
lifting, and ice skating (2,3,4)[C].
Often the athlete can relay information about fatigue or improper warm-up (3)[C].
Acute or chronic:
Some hamstring strain injuries are more chronic in nature with recurring “tightness” or
muscle “pull” complaints (3)[C].
Treatment protocol is different for acute injury vs chronic as well as for initial injury vs
recurrent injury (3,4)[C].
Mechanism: Increased risk of avulsion if there is extreme hip flexion with the knee in full
extension (3)[C]
Severity: Discontinuation of activity, inability to ambulate following the injury, or describing an
audible pop at the time of injury can point toward a more severe strain or an avulsion injury
(3)[C].
Physical Exam
Position patient prone, knee in flexion, and palpate entire muscle from origin to insertion (3)
[C]:
Biceps femoris is most commonly injured.
Examine the patient with the muscles relaxed and also with mild tension (3)[C].
Inspect for swelling, induration, tenderness, and/or ecchymosis (3)[C].
An abnormality can be difficult to palpate even with more diffuse injury (3)[C].
Active range of motion, strength, flexibility, and neurovascular testing of bilateral lower
extremities (3)[C]
Note severity of injury using maximal tolerance of passive straight leg raise/knee extension
(3)[C].

Imaging
Further examination beyond the physical exam is not typically necessary, but if needed,
radiographs, MRI, and sonography have been found useful (2).
Radiographs: Anteroposterior pelvis can be helpful acutely if an avulsion is suspected or
chronically to look for development of myositis ossificans (3,4).
US and MRI can help determine more accurate location and extent of injury (4,5):
US is as useful as MRI for acute hamstring injury and has added benefit of low cost.
MRI images of an acute injury appears as high signal in or around the muscle on T2-
weighted images.
Remodeling phase of muscle includes muscle regeneration and fibrous scar formation (3).
Chronic tendinopathy can develop if the healing process forms a disorganized scar.
In addition to the associated injuries listed above, consider these in the differential diagnosis:
Direct hamstring injury, including muscle laceration or contusion (common direct mechanism
for injury as opposed to indirect sprain mechanism) (2)
Posterior lateral corner knee injury (rare, can have associated distal hamstring injury) (3)
Pelvic or proximal femoral stress fracture
Piriformis syndrome, gluteus medius injury, adductor strain
Pain radiating from the lumbar back, sacroiliac joint, or hip
Treatment
The treatment protocol is different for acute vs chronic injury as well as for
initial vs recurrent injury (4)[C].
The protocol must be individualized for the patient based on sport-specific
needs, risk factors, and location of the injury (4)[C].
Acute:
Goals: Control pain, swelling, hemorrhage, and muscle fiber adhesion; work
toward restoration of normal active range of motion and gait (may require
crutches early) (3,4)[C]
Treatment:
24–72 hr: Rest, ice, compress, elevate, early immobilization in extension,
passive gentle range of motion (2,3,4)[C]
NSAIDs: Standard NSAID precautions apply:
Begin after acute injury and continue for a limited time (3–7 days) (3,4)
[C].
May be beneficial to delay treatment for 2–4 days to allow for the normal
inflammatory response needed for healing (2)[C]
Limit prostaglandin-mediated inflammation, allowing for earlier/more
effective rehab
When used early in muscle injury, NSAIDs have been shown to decrease
pain/strength loss and improve recovery, though limited studies in
hamstring injuries (4)[C]
There are concerns for delay of muscle regeneration and functional
losses related to the use of NSAIDs (4)[C].
Corticosteroids not routinely recommended (4)[C]:
There is controversy about injection after acute muscle injury.
Consider within 72 hr if severe injury and palpable defect (4)[C]
Concerns include delayed healing, tendon rupture (several case series),
and infection (4)[C]
1 retrospective study showed favorable results with no complications and
limited time lost with quick return to play (1,4)[C].
Subacute/rehab (day 3 up to 6 wks)
Goals: Control pain and swelling, promote muscle fiber alignment, strength,
and repair; restore flexibility and muscle imbalances; begin muscle
conditioning and advance over time while maintaining cardiovascular fitness
(3,4)[C]
Treatment:
Pain-free passive range of motion, then pain-free active range of motion
(3)[C]
Maintain cardiovascular conditioning with pool activities or stationary bike
(3,4)[C].
Therapeutic modalities may assist in rehab (3,4):
Electric stimulation can decrease pain and swelling.
Moist heat or US can warm muscle.
Deep friction massage or myofascial release can resolve adhesions and
stimulate repair.
Proceed with flexibility and strength restoration in a slow progression (4)
[C]:
Back off intensity if painful (2,4)[C]
Stretch all lower extremity musculature, with focus on quads and hip
flexors.
Strengthen the gluteals and correct thigh muscle imbalances.
Progress hamstring strengthening from early concentric to more
advanced eccentric conditioning (2,4)[C].
Functional (2 wks up to 6 mos)
Goals: Perform functional rehab in a progressive fashion to minimize reinjury
(1,2,3,4)[C]
Treatment:
Functional rehabilitation programs that incorporate sport-specific drills
should be used in combination with traditional interventions (1)[B].
Walk to jog to run to sprint, then sport-specific drills
Return to play:
Goals: Safe and timely return to play with best possible functionality
Treatment:
May return when able to perform pain-free sport-specific activity, has
normal flexibility, and normal strength (often measured as within 10% of
uninjured leg) (4)[C]
Maintain strength and flexibility (2,3,4)[C]
Newer therapies aimed at the treatment of tendinopathy may play a role in
treatment of hamstring strain injury, especially in chronic and recurrent hamstring
strain injury. These therapies include US-guided needle tenotomy, prolotherapy,
autologous blood, or platelet-rich plasma injections.
Surgical referral should be considered to prevent poor outcome in complete soft
tissue ruptures or bony avulsions that are >2 cm displaced (2,3,4,5)[C].
Ongoing Care
Recovery time after hamstring strain injury can be as short as 3 wks and as long as 6 mos,
depending on the severity and chronicity of the injury.
Although reinjury is common, proper functional rehab and appropriate return to play can
minimize the risk.
Maintenance and prevention protocols should focus on the modifiable risk factors outlined
above.
References
1. Prior M, Guerin M, Grimmer K. An evidence based approach to hamstring strain injury: a
systematic review of the literature. Sports Health: A Multidisciplinary Approach.
2009;1:154–164.
2. Petersen J, Hölmich P. Evidence based prevention of hamstring injuries in sport. Br J

Sports Med. 2005;39:319–323.
3. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. J Am
4. Drezner JA. Practical management: hamstring muscle injuries. Clin J Sport Med.
2003;13:48–52.
5. Mann G, Shabat S, Friedman A, et al. Hamstring injuries. Orthopedics. 2007;30:536–

540; quiz 541–542.
Additional Reading
Evidence-based material is lacking for interventions for prevention and treatment of
hamstring strain injury (1).
Further high-quality prospective studies with large samples from broad populations
investigating risk factors and management are needed to provide better framework to target
interventions for hamstring injury (1)[A].
Davis KW. Imaging of the hamstrings. Semin Musculoskelet Radiol. 2008;12:28–41.
Lempainen L, Sarimo J, Mattila K, et al. Proximal hamstring tendinopathy: results of surgical

management and histopathologic findings. Am J Sports Med. 2009.
Codes
ICD9
843.9 Sprain of unspecified site of hip and thigh
Clinical Pearls
Previous history of hamstring injury is a significant risk factor for hamstring
strain injury.
Functional rehab programs with sport-specific drills along with traditional
interventions can be used for both prevention and treatment of hamstring strain
injury.
Hand Infection
Michael M. Linder
Andrew Harcourt
Basics
Description
Infection present in any structure in the hand
Generally caused by penetrating trauma, but any trauma can introduce pathogens.
Early recognition is key, as infections caught early are amenable to splinting, elevation, and
rest.
Risk Factors
Diabetes mellitus: More likely to have gram-negative infections and are more susceptible to
infection in general
Immunocompromised: More susceptible to N. gonorrhea and candidal infections
Sexually transmitted disease exposure: Increased incidence of flexor tenosynovitis caused by
disseminated N. gonorrhea
Tropical fish aquarium injury: Exposure to Mycobacterium marinum
Etiology
Paronychia: Infection involving the tissue surrounding the nail:
Acute: Staph and strep
Chronic: Commonly due to Candida
Children: Anaerobes or fungal secondary to thumb sucking or nail biting
Felon: Infection of the distal pulp space of the finger:
Primarily staph
Herpetic Whitlow: Autoinoculation of broken skin with type 1 or 2 herpes simplex virus
Flexor tenosynovitis: Infection in one or more of the flexor tendon sheaths:
While flexor tendon sheath anatomy varies greatly, generally the tendon sheath of the
index, middle, and ring finger extends from the distal phalanx to the distal palmar crease
and is isolated.
The tendon sheath of the 5th digit extends from the distal phalanx and communicates with
the ulnar bursa, while the thumb tendon sheath extends from the distal phalanx to the radial
bursa.
Once present, infection can spread easily to all communicating spaces.
Most commonly staph and strep
Clenched fist injury: Infection following human bite or fight injury to the dorsum of the hand:
Typically involves both anaerobes and aerobes
Palmar space infection: Can be isolated to the thenar and hypothenar spaces, or midpalmar
space:
Usually staph or strep
Can be secondary to high-pressure injection injury
Diagnosis
History
A careful history should be taken to determine mechanism of injury, past medical history, and
other associated risk factors.
Physical Exam
A complete physical exam is indicated, with particular attention to the neurovascular status
and function status of the affected structures.
Paronychia: Pain and swelling at the edge of the nail
Felon: Significant pain and swelling of the distal pulp
Herpetic Whitlow: Abrupt onset, pain out of proportion to exam, small clear vesicles early,
which coalesce
Flexor tenosynovitis: Kanavel's signs:
Fusiform swelling
Partial flexion at rest
Excessive uniform tenderness along the tendon sheath
Pain with passive extension
Clenched fist injury: Laceration over metacarpophalangeal (MCP) joint, swollen and
erythematous dorsum of the hand
Palmar space infections: Redness, tenderness, and fluctuance

Paronychia: Culture if incision and drainage performed
Felon: Radiographs to evaluate for osteo or foreign body
Herpetic Whitlow: Tzanck smear or viral culture can confirm diagnosis, but are rarely needed.
Clenched fist injury: Radiographs are indicated to evaluate for fracture, subcutaneous gas, or
foreign body.
Palmar space infections: Radiographs to evaluate for foreign body and fracture
Treatment
Paronychia:
Early infections can be treated conservatively with antibiotics, elevation, and
rest.
If fluctuance is present, the eponychium may be sharply elevated and
irrigated; if infection is evident under the nail, the proximal 1/4 of the nail is
removed.
1st-generation cephalosporin, clindamycin if gram-negative organism is
suspected
Felon:
May be drained with either a lateral incision or vertical volar incision;
knowledge of neurovascular structures is key when making a lateral incision.
Care is taken to debride all purulent material and the wound packed with
sterile gauze for 24–48 hr
Antibiotic coverage should include methicillin-resistant Staphylococcus
aureus (MSRA)
Herpetic Whitlow:
Self-limited, may be treated with antivirals if started in 1st 48 hr
Recur 30–50%
Flexor tenosynovitis:
Early infections may be amenable to conservative treatment with IV
antibiotics, splinting, elevation, and rest.
All rings should be removed if tenosynovitis is suspected.
If no improvement in 12–24 hr, surgical consultation is mandated.
Clenched fist injury:
All wounds should be irrigated and explored for signs of penetrating trauma,
retained foreign body, extensor tendon injury or metacarpophalangeal (MCP)
joint capsule damage.
If seen in 1st 24 hr and there is no evidence of secondary injury, may be
irrigated and placed on prophylactic antibiotics, typically amoxicillin-
clavulanate and recheck in 24 hr
Do not primarily close wound.
All other injuries should be considered for hospital admission and IV antibiotics.
Palmar space infection: Urgent consultation for evaluation and debridment
Pre-Hospital
Early consultation/admission is indicated for flexor tenosynovitis, infections in the
deep structures of the hand, and complicated clenched fist injuries:
IV antibiotics and operative drainage are generally indicated for all of the
above.
Ongoing Care
Paronychia and felon should be followed up at 24 hr if irrigation and drainage was done.
Additional Reading
American Family Physician. Common Hand Infections. 2003;68:2167–2176.
American Family Physician. Hand and wrist injuries: part II. Emergent Evaluation.
2004;69:1949–1956.
Townsend: Sabiston textbook of surgery, 18th ed.; Chapter 74—Hand surgery, infections.
Canale & Beaty: Campbell's Operative Orthopedics, 11th ed. 2006.
Antosia RE, Lyn E. The hand. In: Rosen P, et al., eds. Emergency medicine: Concepts and
clinical practice. 4th ed. St. Louis: CV Mosby, 1998:625–668.
Brown DM, Young VL. Hand infections. South Med J. 1993;86:56–66.
Hausman MR, Lisser SP. Hand infections. Orthop Clin North Am. 1992;23:171–185.
Codes
ICD9
686.9 Unspecified local infection of skin and subcutaneous tissue
Heel Pain: Heel Fat Pad Syndrome, Lateral Plantar
Nerve Entrapment
Reno Ravindran
Richard E. Rodenberg
Thomas L. Pommering
Basics
Description
Heel fat pad syndrome:
The heel pad is composed of columns of adipose tissue separated by fibrous septae. It is
located directly below the calcaneus and acts as a hydraulic shock-absorbing layer (1).
The encapsulated fat acts in a hydraulic fashion to absorb shock by resisting compressive
loads.
Degeneration or trauma may cause local loss of the heel pad or rupture of the fibrous
tissue septa, which may result in loss of the heel pad compressibility.
Cause is often multifactorial
The syndrome may result from a direct blow to the bottom of the heel, resulting in a bruise
and loss of heel pad elasticity.
Displacement, loss, or atrophy of fat pads causes pain from excessive pressure.
Lateral plantar nerve entrapment:
Lateral plantar nerve (LPN) and the 1st branch of the LPN are branches of the tibial nerve,
which supplies autonomic, sensory, and motor fibers to the plantar foot. The LPN is the
most common cause of plantar heel pain of neural origin (2).
Synonym(s): Calcaneodynia; Heel pain syndrome; Calcaneal neuritis; Policeman's heel;
Runner's heel; Tennis heel; Stone bruise; Tuber calcanei pain; Subcalcaneobursitis
Epidemiology
1 in 10 people develop heel pain in their lifetime.
Peak age 40–60 yrs (3)
15% of all adults with foot problems are thought to be related to heel pain.
More common with increasing age, obesity, and diabetes
Relationship with athletic overuse injuries (stress-related pathogenesis)
More common with occupations requiring prolonged standing or walking on hard surfaces (4)
Risk Factors
Elderly, advancing age
Obesity, body mass index >30
Occupations requiring prolonged standing or walking
Repetitive trauma, such as in distance runners, hurdlers, long jumpers, triple jumpers,
gymnasts, or dancers
Overuse in recreational or professional athletic activities (4)
Etiology
LPN entrapment can occur at different sites:
Where the nerve passes at the sharp edge of the deep fascia of the abductor hallucis
Distal to the medial edge of the calcaneus
Between the abductor hallucis and the medial head of quadratus plantae muscle (2)
Diagnosis
History
Gradual onset of plantar heel pain, which may be unilateral or bilateral
May have a history of local trauma
Pain may radiate into the arch or proximally to the medial heel area.
If pain is severe enough, a patient may walk on the ball or lateral aspect of the foot.
Pain primarily with weight-bearing and relieved with rest
Pain is usually nonspecific and occurs diffusely over the heel pad.
Pain does not tend to radiate or increase with dorsiflexion (1).
LPN entrapment:
Burning, sharp, shooting, shocklike pain; localized to the medial inferior aspect of the heel
and proximally into the medial ankle region. Pain may radiate across the plantar aspect of
the heel to the lateral aspect of the foot.
Pain worse during or after weight-bearing activities and improves with rest, but can also
occur at rest and in non-weight-bearing positions
Pain at night may be due to nerve compression as a result of venostasis and venous
engorgement.
Post-static dyskinesia: Plantar heel pain when patient 1st stands after periods of rest. Can
be typical in patients with heel pain of neural origin, but this can also occur in plantar
fasciitis.
Sensory deficit may not be common, but occasionally can cause tingling and/or numbness
in the heel or foot (2).
Physical Exam
Thorough examination of the lower extremity, including neurovascular exam, is
recommended.
Exam is facilitated by having the patient lie prone
Tenderness directly over the weight-bearing part of the calcaneus rather than on the distal
tuberosity
May have palpable absence or diminution of a compressible pad
In prolonged cases, the underlying bone can be felt underneath the skin due to significant
fat pad atrophy.
LPN entrapment:
Palpation over 1st branch of the LPN deep to the abductor hallucis muscle or medial
calcaneal tuberosity with reproduction of pain/symptoms proximally and distally. Should
have minimal tenderness over the plantar fascia origin.
Dorsiflexion with eversion of the ankle can reproduce symptoms. Although not specific, can
help with diagnosis.
Plantar flexion-inversion may reproduce symptoms, although not specific
Negative Tinel's test (2)

Imaging
Anteroposterior, lateral, and oblique plain radiographs. Radiographs may reveal calcaneal
spurs or calcifications, fractures, tumors, arthrosis, or other unusual causes of heel pain.
High-resolution US or MRI to look for benign tumors or neuromas entrapping a nerve
Lumbar spine radiographs and MRI to rule out causes of lumbar radiculopathy
Consider bone scan or MRI to rule out suspected stress fracture.
LPN:
Electromyography and nerve conduction studies can reveal abnormalities in LPN.
Quantitative sensory testing, also known as the pressure-specified sensory device,
determines pain mechanisms by assessing function of large and small sensory nerve fibers.
If nerve entrapment is suggested by history and exam, a diagnostic injection with local
anesthetic providing complete pain relief can help with diagnosis (2,5).
Calcaneal spurs
Local inflammatory conditions (plantar fasciitis, subcalcaneal bursitis, periostitis,
tenosynovitis, blister)
Systemic inflammatory conditions (ankylosing spondylitis, Reiter's syndrome, psoriatic
arthritis, rheumatoid arthritis, sarcoidosis, gout, and pseudogout)
Calcaneal fracture or stress fracture
Entrapment (tarsal tunnel syndrome, medial calcaneal nerve)
Infectious (osteomyelitis, tuberculosis)
Tumors (glomus tumor of heel pad, osteoid osteoma, osteoblastoma, chondromyxoid
fibroma, chondrosarcoma, simple and aneurysmal cysts)
Neuropathy (diabetes mellitus, alcoholism, reflex sympathetic dystrophy)
Metabolic (osteomalacia, Paget disease)
Calcaneal apophysitis (4)
Treatment
NSAIDs of choice
Modified weight-bearing activities
Injections of local anesthetics/steroids at site of nerve entrapment for LPN.
Caution should be exercised with repeated injections or improper technique,
due to the risk of irreversible damage to the heel pad by mechanical disruption
of the heel septae and by steroid-induced fat necrosis.
Immobilization rarely necessary, symptom-directed
Treatment of other associated conditions (eg, night splints in plantar fasciitis)
Taping of the heel in fat pad syndrome can provide support and limit movement
of the heel's fat pad. This can also help confirm diagnosis (5).
Various methods for altering the biomechanical forces on the heel have been
advocated:
Weight control
A well-fitted heel cup cushions the heel and prevents the heel pad from
splaying, thereby improving the intrinsic cushioning of the calcaneus. There is
no consensus as to which type of orthosis is best. Regardless of whether over-
the-counter heel cups or custom orthoses are used, consistent features should
be support of the arch, presence of adequate cushioning material, recess for
area of pain beneath the heel, and slight medial elevation.
Shoes with softer midsoles, which provide more cushioning of the fat pad
Raising the heel may thereby transfer the weight-bearing anteriorly with heel
strike and in midstance.
Medial heel wedge to relieve the pressure on the medial tuberosity, causing
more lateral pressure
Physical therapy may be useful for patients not adequately responding to other
conservative modalities. US, extracorporeal shock wave therapy, laser
modalities.
Surgery reserved for patients when conservative treatment fails to provide
adequate pain relief
Some experts advocate that symptoms be present for more than 1 yr,
despite appropriate conservative treatment, before surgery is considered.
Surgical options are directed towards the cause of heel pain and include spur
resection, wide release of plantar fascia, drilling decompression, and
neurolysis.
It is important to have an exact diagnosis of the pain before surgical
intervention, due to the multifactorial and often recurrent nature of plantar
heel pain (6).
LPN entrapment:
Considered after failure of conservative treatment for 6–12 mos
Surgical decompression of the 1st branch of LPN (2)
Ongoing Care
Heel fat pad syndrome responds very well to conservative treatment and is usually self-limited.
References
1. Aldridge T. Diagnosing heel pain in adults. Am Fam Physician. 2004;70:332–338.
2. Alshami AM, Souvlis T, Coppieters MW. A review of plantar heel pain of neural origin:
Differential diagnosis and management. Man Ther. 2007.
3. Toomey EP. Plantar heel pain. Foot Ankle Clin. 2009;14:229–245.
4. Alvarez-Nemegyei J, Canoso JJ. Heel pain: diagnosis and treatment, step by step. Cleve
Clin J Med. 2006;73:465–471.
5. Franson J, Baravarian B. Tarsal tunnel syndrome: a compression neuropathy involving

four distinct tunnels. Clin Podiatr Med Surg. 2006;23:597–609.
6. Bateman JE. Disorders of the foot and ankle, medical and surgical management.
Additional Reading
Bordelon RL. Orthopedic sports medicine, principles and practice. Philadelphia: WB
Saunders, 1994.
Cailliet R, ed. Foot and ankle pain. Philadelphia: FA Davis, 1997.
Karr SD. Subcalcaneal heel pain. Orthop Clin North Am. 1994;25:161–175.
Simons SM. Foot injuries of the recreational athlete. Phys Sports Med. 1999;27:57–70.
Turgut A, Gokturk E, Kose N, et al. The relationship of heel pad elasticity and plantar heel
pain. Clin Orthop Rel Res. 1999;360:191–196.
Codes
ICD9
Clinical Pearls
Both soft heel cups and more rigid ones have been used with some success.
The hard cups are intended to encompass the heel pad beneath the calcaneus,
helping to restore some of its compressibility. The softer cups are designed
primarily to cushion the fat pad. Athletes who run a lot in their sport often prefer
softer heel cups or orthotics.
To prevent heel fat pad syndrome, training errors should be identified and
corrected. The athlete should be certain to wear proper shoes with an energy-
absorbing heel cushion, avoiding excessive wear of the shoes. Mileage should
be increased gradually, and running on steep hills should be avoided. Training
on safe and shock-absorbing surfaces is essential (eg, running on an all-
weather track or on a surface softer than concrete or asphalt).
Hematomas, Epidural and Subdural
Greg Nakamoto
Basics
Description
Traumatic brain injury (TBI) can result in direct brain parenchymal damage as well as
intracranial hematomas. The 2 main categories of intracranial hemorrhage are epidural
hematoma and acute subdural hematoma. Both are seen in the setting of traumatic brain
injury, but can follow different clinical courses and have different prognoses.
In epidural hematoma (EDH), blood is confined to the space between the inner table of the
calvaria (inner surface of the skull) and the dura mater.
In subdural hematoma (SDH), localized bleeding occurs below the dura mater, directly
adjacent to brain parenchyma.
SDH can be acute or chronic (this topic focuses on acute SDH, commonly defined as an SDH
diagnosed within 14 days of TBI [1]).
Alert
EDH and acute SDH are neurosurgical emergencies. With prompt appropriate treatment, a
patient with an EDH can often achieve complete neurologic recovery, whereas a missed
diagnosis may result in death within hours. Mortality for patients with acute SDH is much higher
(50–90%), presumably due to greater underlying injury to the brain tissue itself.
Synonym(s):
SDH: Subdural hemorrhage
EDH: Epidural hemorrhage, extradural hematoma, extradural hemorrhage
SDH and EDH: Intracranial hematoma, intracranial hemorrhage
Epidemiology
EDH: Incidence is reported between 2.7% and 4% of head trauma admissions (2):
Peak incidence is in the 2nd decade, with mean age between 20 and 30 yrs (2).
More frequently located in temporoparietal and temporal regions of the skull, with a slight
predominance of right-sided lesions (2)
Bilateral in 2–5% of patients (2)
Typically attributed to bleeding from the middle meningeal artery as a result of a temporal
skull fracture. Other sources of EDH blood include the middle meningeal vein, the diploic
veins, or the venous sinuses (2).
Acute SDH: Incidence is reported between 12% and 29% of head trauma admissions (1):
Mean age reported to be between 31 and 47 yrs, with the vast majority being male (1)
Most common mechanism of injury for SDH depends on age. Overall, most SDH are
caused by motor vehicle accidents (MVA), falls, and assaults (1):
1 study found that in younger patients (18–40 yrs), 56% were caused by MVA and only
12% were caused by falls (1).
In the same study, older patients (>65 yrs) suffered SDH as a result of MVA 22% and
falls 56% of the time (1).
Other studies of comatose patients describe MVA as the cause of injury in 53–75% of
SDH, suggesting that MVA causes more severe injury, possibly because of a higher-energy
mechanism of injury and a greater association with diffuse axonal injury (1).
Acute SDH occurs either secondary to a parenchymal laceration (which implies a severe
underlying brain tissue injury) or due to disruption of a surface or bridging vessel (in which
case underlying brain injury may be less severe). This latter mechanism is more common in
older individuals and in athletes such as boxers.
SDH is the most common athletic injury resulting in death.
Risk Factors
High-energy trauma is a risk factor for both EDH and SDH.
SDH: Bridging veins can also be torn during acceleration-deceleration injuries without actual
head impact.

EDH: Associated temporal or other skull fracture
SDH: Underlying brain parenchymal injury
EDH and SDH:
Sequelae of increased intracranial pressure (ICP), including obtundation, Cushing's reflex,
respiratory distress, and death
Due to high-energy mechanisms of injury, cervical spine and other orthopedic trauma are
often seen in EDH and SDH.
Diagnosis
Pre Hospital
<50% the patients suffering EDH have the classically described “lucid interval” that is
commonly associated with EDH (2):
Patient suffers TBI, which is often followed by an initial period of altered consciousness.
The patient subsequently improves, exhibiting for a period the appearance of recovery.
The period of improvement, however, ends with secondary deterioration of the patient's
mental status, ending the so-called “lucid interval.”
Studies report only 47% of patients with EDH exhibit a lucid interval (2).
Between 12% and 42% of patients remain con-scious throughout the time between trauma
and surgery, and 3–27% are neurologically intact (2).
On the other hand, between 22% and 56% are comatose on admission or immediately
before surgery (2).
In patients admitted for SDH, a lucid interval has been described in between 12% and 38%
of patients (1):
Between 37% and 80% of patients with acute SDH present with initial Glasgow Coma
Scale (GCS) scores of 8 or less (thus meeting criteria for a severe head injury) (1).
Pupillary abnormalities reported in 30–50% of patients upon admission or before surgery
(1).
History
Mechanism: Higher-energy trauma resulting in skull fracture is a risk factor for EDH;
alternatively, acute SDH due to high-energy trauma implies more underlying brain tissue
damage. Also, mechanism of injury can guide the search for associated traumas in the poorly
responsive patient.
Lucid interval: Presence of a lucid interval is more common with EDH.
Deterioration in mental status: Regardless of mechanism or level of recovery after initial
unconsciousness, any patient with a deterioration of mental status after a head trauma
should be evaluated for a possible neurosurgical emergency.
Physical Exam
EDH: Classic presentation involves brief post-traumatic loss of consciousness followed by a
lucid interval lasting several hours, often with headache, followed by rapid deterioration;
classic presentation occurs in up to 47% of patients.
SDH: Typically presents with immediate loss of consciousness followed by only incomplete
recovery of mental status, then further deterioration; incomplete recovery due to underlying
brain parenchymal damage; slower course due to slower accumulation of venous blood
EDH: Skull exam to look for fracture
EDH and SDH:
Complete neurologic exam initially, followed by serial exams to assess for herniation
(ipsilateral pupillary dilatation, contralateral hemiparesis) and signs of increased intracranial
pressure (obtundation, hypertension, bradycardia, respiratory depression)
Trauma assessment as necessitated by search for coexisting injuries

Lab
Perform appropriate laboratories for any associated trauma (3,4)[C].
Coagulation studies are of particular importance (3,4)[C]:
Knowledge of coagulation status is important for neurosurgical planning.
In the head-injured patient, breakdown of the blood–brain barrier with exposed brain tissue
is a potent cause of disseminated intravascular coagulation, and is thus a marker for
severe brain injury.
In adults, EDH rarely causes a significant drop in hematocrit due to the rigidity of the skull. In
infants, EDH in an expansile cranium with open sutures can result in significant blood loss and
resultant hemodynamic instability. Therefore, in infants with EDH, careful monitoring of the
hematocrit is also warranted (5)[C].
Imaging
CT is the study of choice for diagnosing EDH and SDH (1,2,3,4,5,6)[A]:
In EDH, lesion is hyperdense (acute blood), biconvex, sharply demarcated, and adjacent to
the skull; mass effect is common.
In SDH, lesion can be slightly less dense than in EDH (from mixing with cerebrospinal fluid),
concave, and conforming to the underlying brain; accompanying parenchymal injury and
edema may be seen; may become isodense with brain parenchyma as early as 4 days.
X-rays: Skull films do not show acute blood and so are not useful for ruling out EDH or SDH.
Moreover, plain x-rays in 40% of patients with EDH show no fracture.
Concussion
Uncomplicated skull fracture
Intracerebral hemorrhage/cerebrovascular accident
Subarachnoid hemorrhage
2nd impact syndrome
Treatment
No strong evidence exists regarding the benefits of any treatment to
reduce complications of moderate-to-severe head injury (7)[C].
Evidence as to the efficacy of hyperventilation, hypothermia, and mannitol (all
employed to lower intracranial pressure) has been inconclusive with regard to
improving mortality.
Anticonvulsants, specifically carbamazepine and phenytoin, while reducing
early seizures in patients with head injury, have not been shown to reduce late
seizures, neurologic disability, or death.
Barbiturates have not been shown to either reduce ICP or to prevent adverse
neurologic outcome.
Prophylactic antibiotics have not been shown to reduce death or meningitis in
patients with moderate-to-severe head injury and skull fracture.
Alert
Corticosteroids have been shown to increase mortality when used acutely in
people with head injury.
Pre-Hospital
As would be expected for any trauma patient:
Stabilize vital signs, achieve airway control, support BP, and address acute life-
threatening injuries (3)[C].
Establish IV access, and administer oxygen and crystalloids (3)[C].
Consider intubation, sedation, and neuromuscular blockade vs bag-valve-mask
ventilation (3)[C].
ED Treatment
Complete prehospital care steps not already addres-sed as per Advanced
Trauma Life Support guidelines
Intubation using rapid sequence induction (which minimizes rises in ICP and
catecholamine release), and allow for hyperventilation as needed if clinical
signs of increased ICP or incipient herniation (with the caveat that
hyperventilation to decrease ICP has not been shown to decrease mortality)
(3)[C]
Once spine is cleared, elevate the head of the bed to 30° or use reverse
Trendelenburg positioning to reduce ICP and increase venous drainage (3)[C].
Consider phenytoin to reduce early posttraumatic seizures, with the caveat that
it does not reduce late seizures, poor neurologic outcome, or death (3,7)[C].
Head CT for diagnosis and staging of head injury
Rapid neurosurgical consultation for any symptomatic EDH or SDH, or for any
asymptomatic EDH or SDH meeting the CT criteria listed under “Surgical
Treatment”
Given lack of strong evidence showing a benefit, institution of medical
interventions to control elevated ICP should not delay definitive neurosurgical
treatment.
If there is a high index of suspicion of EDH or SDH but a negative CT scan,
such patients should be admitted for 24 hr observation because EDH and SDH
can evolve slowly. If headache or other symptoms persist, repeat CT or MRI
before considering discharge:
Delayed EDH (hematoma not present on initial CT, but found on follow-up
scan) comprises up to 10% of cases in most series. Theoretical risk factors
include rapidly correcting shock, lowering ICP (either medically or surgically,
including evacuating a contralateral hematoma), and coagulopathies. A high
index of suspicion is necessary to make the diagnosis.
P.
Drilling burr holes (trephination) is generally reserved for the following patients
(5)[C]:
Patients with definitive localizing signs and clinical evidence of intracranial
hypertension who are unable to tolerate a CT scan because of severe
hemodynamic instability, or
Patients who meet criteria for surgical treatment of their hematoma, but in
whom such treatment must be delayed for immediate surgical intervention for
other systemic injuries
In addition, consider performing burr hole if patient is herniating, all other
treatments prove insufficient, neurosurgery is unavailable for urgent
consultation, and air or ground transport is prolonged (3)[C].
Burr hole procedure (3):
Drill hole adjacent to, but not over, skull fracture in the area located by CT
scan.
In the absence of CT scan, place burr hole on the side of the dilated pupil,
2 fingerwidths anterior to tragus of ear and 3 fingerwidths above.
Acute neurosurgical referral is merited for any patient suffering a TBI who is
found to have either an EDH or acute SDH:
For both EDH and acute SDH: The decision to operate [on an acute EDH or
SDH] is based on the patient's GCS score, pupillary exam, comorbidities, CT
findings, age, and, in delayed decisions, the patient's ICP. Neurological
deterioration over time is also an important factor influencing the decision to
operate (1,2)[A].
CT guidelines for management of EDH (2)[A]:
Patients who are not comatose, without focal neurological deficits, and with
an acute EDH with a thickness of <15 mm, a midline shift (MLS) of <5 mm,
and a hematoma volume <30 cm3 may be managed nonoperatively with serial
CT scanning and close neurological evaluation in a neurosurgical center
(2,6)[A].
In patients initially being treated nonoperatively, the 1st follow-up CT scan
should be obtained within 6–8 hr after TBI (2)[C]:
Enlargement of an EDH is common, resulting in the need for follow-up CT
scans in patients initially being treated nonoperatively.
Mean time to enlargement in 1 study was 8 hr after TBI, with no
enlargement after 36 hr (6).
CT guidelines for management of SDH (1)[A]:
Patients with SDH presenting with a clot thickness >10 mm or an MLS >5 mm
should undergo surgical evacuation, regardless of their GCS (1,6)[B].
Patients who present with coma (GCS <9) but with an SDH with a thickness
<10 mm and an MLS <5 mm can be treated nonoperatively, providing they
undergo ICP monitoring, are neurologically stable since the injury, have no
pupillary abnormalities, and have no intracranial hypertension (ICP >20 mm
Hg) (1)[B].
Surgical management decisions should take into consideration the
recommendations for both lesion types (1).
Any patient with known EDH or SDH who is initially stable but later develops
new symptoms suggestive of mass effect, herniation, or increased ICP is a
candidate for emergent neurosurgical intervention:
Time from neurological deterioration, as defined by onset of coma, pupillary
abnormalities, or neurological deterioration to surgery, is more important than
time between trauma and surgery.
Surgical evacuation should be performed as soon as possible; delays in
surgery are associated with progressively worse outcomes (2)[A].
Ongoing Care
Neurosurgical referral for EDH or SDH as described under “Surgical Treatment”
EDH: In the case of nonsurgical EDH, the consulting neurosurgeon may consider discharge if
the patient is neurologically stable after 24 hr of observation. Follow-up CT scan in 1 wk if
stable, then again in 1–3 mos until documented resolution.
SDH: Because of underlying brain injury, period of observation required before determination
of clinical stability may be longer than for EDH. Furthermore, more likely to need rehabilitation
or temporary/permanent skilled nursing care.
Physical therapy or occupational therapy as determined by the particular neurological deficit
Prognosis
EDH:
Mortality in patients in all age groups and across all GCS scores undergoing surgery for
evacuation of EDH is 10% (range 7–12.5%) (2):
Mortality rates are near 0 for patients not in coma preoperatively, 10% for obtunded
patients, and 20% for patients in deep coma (3).
If treated early, prognosis is generally excellent, as the underlying brain injury is often
limited (3,5).
Mortality in comparable pediatric case series is 5% (2).
SDH:
Studies of patients from all age groups with GCS scores between 3 and 15 with SDH
requiring surgery report mortality rates between 40 and 60% (1).
Mortality for patients presenting to the hospital in coma who subsequently undergo surgery
is between 57 and 68% (1).
Delay of surgery over 4 hr from time of injury, or over 2 hr from onset of coma, associated
with significantly increased mortality (1)
Complications
Complications seen in patients with TBI include:
Neurologic deficits associated with parenchymal brain injury, which is more
commonly seen in acute SDH than EDH
Neurologic deficits associated with increased ICP and subsequent herniation
Posttraumatic seizures, which can occur early or late after TBI
Postoperative complications include:
Recurrent or residual hematoma, which may require repeat operations
Wound infection, meningitis, or cerebral abscess after craniotomy
CSF leak
References
1. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute
subdural hematomas. Neurosurgery. 2006;58:S16–S24; discussion Si–Siv.
2. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute

epidural hematomas. Neurosurgery. 2006;58:S7–S15; discussion Si–Siv.
3. Price D, Wilson S. Epidural hematoma. eMedicine. Retrieved Aug 21,

2009, from http://emedicine.medscape.com/article/824029-overview, 2008.
4. Engelhard III H, Sinson G. Subdural hematoma. eMedicine. Retrieved Aug

21, 2009, from http://emedicine.medscape.com/article/247472-overview,
2009.
5. Ullman J, Sin A. Epidural hemorrhage. eMedicine. Retrieved Aug 21, 2009,

from http://emedicine.medscape.com/article/248840-overview, 2007.
6. Servadei F, Compagnone C, Sahuquillo J. The role of surgery in traumatic

brain injury. Curr Opin Crit Care. 2007;13:163–168.
7. Maconochie I, Ross M. Head injury (moderate to severe). Clin Evid

(Online). 2007.
Additional Reading
Scaletta T. Subdural hematoma. eMedicine. Retrieved Aug 21, 2009, from
http://emedicine.medscape.com/article/828005-overview, 2008.
Codes
ICD9
852.20 Subdural hemorrhage following injury, without mention of open intracranial wound,
with state of consciousness unspecified
with no loss of consciousness
with brief (less than one hour) loss of consciousness
Clinical Pearls
EDH and acute SDH are neurosurgical emergencies that merit rapid
neurosurgical evaluation.
CT is the study of choice in evaluating intracranial lesions in a patient with head
injury.
While CT criteria exist to guide the management of EDH and acute SDH, the
decision to operate is ultimately determined by GCS score, pupillary exam,
age, and ICP, as well as the associated CT findings.
Neurologic deterioration is an important factor influencing decision to operate.
In patients who need operative treatment, delay of surgery is associated with
poorer outcomes.
What is the mortality rate of EDH and SDH?
About 10% (range 7–12%) for EDH, as low as 5% if treated optimally within
a few hours. The mortality rate is twice as high if there was no lucid interval,
presumably because of associated brain parenchyma injury. Mortality in
SDH is more varied, but generally worse than for EDH. Ranges from 40–
60% in those requiring surgery, and up to 68% in surgical cases presenting
to the hospital in coma.
Hematuria
Charles W. Webb
C. Thayer White
Basics
Exercise-induced hematuria (1):
Occurs with or without trauma in males and females; resolves with rest in 2–3 days
Although a benign condition, it is a diagnosis of exclusion.
Directly correlated with intensity and duration of exertion
Traumatic mechanisms:
Direct kidney trauma
Contusion of the mobile bladder wall with the fixed wall in an empty bladder during running
Atraumatic mechanisms:
Physiologic decreased renal blood flow during exercise causing hypoxic damage to the
nephron and leading to increased permeability for RBCs and proteins
Relatively more marked constriction of the efferent arteriole leads to increased filtration
pressure favoring excretion of RBCs and protein.
Hydration and a partially full bladder during exercise may help to prevent or minimize this
condition (2).
Description
Microscopic hematuria or microhematuria: Presence of 3 or more RBCs per high-powered
field (RBCs/HPF) on microscopic analysis of at least 2 of 3 properly collected urine samples:
A urine dipstick of 1+ blood or greater usually corresponds to at least 3–5 RBCs/HPF but
also can be caused by free hemoglobin, myoglobin, or other interfering substances in
foods or drugs. A dipstick test is not diagnostic of hematuria.
A clean-void specimen for males and nonmenstruating females
May require catheterized or carefully collected sample in menstruating or postpartum
women
The RBC count drops 5–9% over 5 hr and 11–28% over 24 hr, so immediate microscopic
analysis is important.
Gross hematuria: Red to brown discoloration of the urine with numerous RBCs seen on
microscopy
Exercise-induced hematuria (EIH): Transient appearance of usually microscopic hematuria
following physical exertion with no history of trauma. It typically resolves within 48–72 hr.
Symptomatic hematuria: Either gross or microscopic hematuria in the presence of any lower
or upper urinary tract symptoms (eg, flank pain, renal colic, dysuria, urgency, etc.)
Asymptomatic hematuria: Either gross or microscopic hematuria in the absence of any
urinary tract symptoms
Note: 1 mL of blood per liter of urine can produce a visible color change.
Persistent recurrent, symptomatic, or traumatic hematuria warrants further evaluation (1,2,3).
Epidemiology
EIH: Unknown
All other causes:
Age <40 yrs: Usually infection
Age >40 yrs: Increasing incidence of tumor
Males >60 yrs: Usually prostatic obstruction, calculi, or tumor
Females >60 yrs: Usually malignancy (1,2)
Prevalence
Prevalence of hematuria in the general population is 2.5–20% depending on the population
studied and the criteria for diagnosis.
Prevalence in the general pediatric population is 0.5–2%.
Prevalence increases to 18–80% following athletic competition and usually resolves in 48 hr
(1,3).
Risk Factors
Chronic urinary tract infection
Anticoagulation
Strenuous exercise
History of calculi, prostatitis, trauma, malignancy, coagulopathy, or sexually transmitted
disease
Family history of renal failure
Travel to Africa, India, or the Middle East (1,2,3)
General Prevention
There are currently no recommendations to screen any population for hematuria.
There are currently no recommendations to screen any populations using urine dipsticks.
Diagnosis
Hematuria itself is rarely a medical emergency but may be a sign of underlying
pathology, such as malignancy or medical renal disease.
Microscopic hematuria is usually transient and benign, but this is a diagnosis of exclusion.
History and exam features will help to guide which patients need further workup.
Confirm the diagnosis as asymptomatic microscopic hematuria with microscopic examination
at least 2 separate urine samples before initiating further workup.
>50 RBCs/HPF is generally considered significant hematuria and may warrant immediate
further investigation, depending on the situation.
Any symptomatic or gross hematuria warrants further evaluation.
Causes:
Unexplained/idiopathic: No urologic cause is found in 87% of microhematuria and 72% of
gross hematuria seen at a referral clinic.
Spurious:
Menstruation
Sexual intercourse
Pseudohematuria (aka dipstick hematuria)
Rhabdomyolysis
Foods (beets, rhubarb, blackberries)
Drugs (doxorubicin, chloroquine, rifampin)
UTI: Acute cystitis or pyelonephritis:
If UTI is suspected as a cause, send urine for culture to confirm, treat infection, and
repeat test in 6 wks before initiating workup.
Recurrent UTI could signal pathology.
Prostatitis or urethritis
Urinary tract calculi
Exercise-induced
Trauma to flank or abdomen (renal fracture)
Cancer: Renal, bladder, prostate, ureter:
Present in 19–25% of gross hematuria but <1.5% of microhematuria in the general
population:
Exceedingly rare under age 40
Transient hematuria and intermittent hematuria are common.
Benign prostatic hyperplasia (BPH)
Glomerular disease (many causes; consider nephrology referral if suspected); IgA
nephropathy and thin basement membrane (TBM) disease most common
Sickle-cell disease
Rare causes:
Polycystic kidney disease
Schistosoma haematobium infection
Radiation cystitis
Urethral strictures
Tuberculosis
Medullary sponge kidney
Cyclophosphamide-induced cystitis
Arteriovenous malformation
Renal artery thrombosis
Papillary necrosis of any cause
Loin pain hematuria syndrome
EIH (4):
Diagnosis of exclusion
Can make the diagnosis without further workup in athletes <40 yrs old who have hematuria
within 12 hr of vigorous activity that resolves completely within 48–72 hr.
Not fully understood; thought to be multifactorial
More common with increased intensity of exercise
Epinephrine and norepinephrine release cause renal vasoconstriction and decreased
glomerular filtration rate (GFR), which results in increased glomerular filtration and
permeability.
Bladder trauma can occur in runners as the posterior bladder wall repeatedly strikes the
base. This can be alleviated by keeping a small amount of urine in the bladder.
Cyclist can experience direct trauma to the prostate and urethra.
Hemoglobinuria can be caused by RBC lysis for a number of reasons.
Dehydration and increased blood viscosity
Increased body temperature
Oxidative-damage myoglobinuria
March, or foot-strike, hematuria is thought to occur from trauma to the foot capillaries.
Can result from muscle breakdown (3)
Traumatic hematuria:
More likely to present as gross hematuria
Children are more likely to have renal injury following trauma owing to lack of perinephric
fat and less protection by the ribs.
There is a lower threshold for imaging of children.
Serious renal injury is much more likely to occur after a fall, bike, or motor vehicle accident
(high-velocity accidents and/or collisions) than with athletic participation.
A pediatric database of 49,651 trauma cases also includes 813 renal injuries with 28 lost
kidneys. There were 85 sports-related renal injuries with no lost kidneys. Football was the
most common sport causing traumatic renal injury.
The presence of any one of the following: (1) gross hematuria, (2) hypotension, or (3)
significant mechanism (eg, fall from a height or rapid deceleration) should prompt imaging
in an adult. In a large review, no significant injuries were missed with these criteria.
In children, additional criteria for imaging include >50 RBCs/HPF and abdominal/flank pain
or ecchymosis.
All penetrating trauma needs a surgical consultation.
The severity of injury is graded I to V on the organ Injury Severity Scale (ISS). Grades I
and II are considered minor, and grades III through V are considered major (4).
History
Recent physical activity: Type, intensity, and duration; EIH can occur up to 12 hr after activity.
Trauma
Urinary tract symptoms: Flank pain, renal colic, dysuria, weak stream, etc.
Medication use, including herbals and over-the-counter drugs: Anticoagulants do not increase
the risk of hematuria and should not influence the workup.
Family history of sickle cell disease/trait or hematuria. PCKD and TBM can have autosomal
dominant inheritance.
Red flags for malignancy or tuberculosis such as fevers, night sweats, and weight loss
Assess risk factors for significant urologic disease.
Abuse of analgesic drugs (NSAIDs)
Age >40 yrs increases likelihood of cancer.
Cyclophosphamide use
Exposure to pelvic radiation
History of urinary tract infections
Irritative voiding symptoms
Occupation exposure to chemicals or dyes
Smoking
Personal urologic history
Recent sore throat could suggest poststreptococcal glomerulonephritis or immunoglobulin
A nephropathy
Travel to developing nations increases risk of urinary schistosomiasis.
Unilateral flank pain suggests calculi or pyelonephritis.
Physical Exam
Many patients will not have any signs or symptoms. Nearly all patients with EIH will have no
symptoms whatsoever. The symptoms listed below suggest something other than benign
EIH.
Fever
Urethral discharge
Flank ecchymosis
Painless red or brown urine
Dysuria
Frequency
Hesitancy
Flank pain
Suprapubic pain
Vitals (ie, fever, hypotension, hypertension, tachycardia)
Thorough abdominal and flak exam including auscultation for bruits
Genital and prostate exam in males
Pelvic exam in females
Additional exam as indicated by history
Inspection of urethral meatus, flank, and abdomen for signs of trauma
Stepwise approach to the patient:
Step 1: History and physical examination (HPE) as above:
If HPE reveals only a history of exercise in a patient <40 yrs of age, observe and repeat
urinalysis after 48–72 hr.
If urinalysis is normal, no further studies are warranted. Observe the patient for
recurrence.
If hematuria persists or HPE suggest cause other than EIH, proceed to step 2.
Step 2: Obtain the following laboratory tests:
Urine culture and serum creatinine, BUN, CBC, prothrombin time (PT), partial
thromboplastin time (PTT), sickle-cell preparation
Consider serum creatine kinase to rule out rhabdomyolysis.
If serum creatinine is normal, obtain intravenous pyelogram (IVP) to evaluate for
obstruction, mass, and kidney function.
If results of these tests are normal, proceed to step 3.
Step 3: Cystoscopy. If normal, proceed to step 4.
Step 4: US or CT scan:
Include bladder, especially if patient >40 yrs of age
CT scan can detect early bladder tumors missed on cystoscopy.
If normal, proceed to step 5.
Step 5: Consider renal arteriogram.
Evaluate for vasculitis, atrioventricular (AV) malformation, and renal infarction/thrombosis
If normal, proceed to step 6.
Step 6: Consider renal biopsy.
Evaluate for interstitial kidney disease.
If at any time concurrent proteinuria, dysmorphic RBCs, or casts are present, obtain 24-
hr urine for protein, creatinine, calcium, citrate, and uric acid.
Consider serum antistreptolysin O titer, Venereal Disease Research Lab (VDRL),
antineutrophil cytoplasmic antibody complement levels, antiglomerular basement
membrane antibody levels, hepatitis B serology.
Consider renal biopsy if results of all preceding tests are negative.

Lab
Initial testing: Urinalysis: To observe for clearing of the hematuria within 48–72 hr. Further
testing is indicated if it does not clear.
Follow-up testing: To be done if urinalysis does not clear in 48–72 hr.
Analyze within 30 min or refrigerate immediately to prevent change in bacterial count and
hemolysis.
Must include cell count to rule out pseudohematuria
RBCs alone suggest prostatic disease, pelvic or ureteral calculi, trauma, heavy exercise,
or malignancy. Dysmorphic RBCs can be seen in EIH as well as intrinsic renal disease.
WBCs + RBCs suggests infection.

RBCs + protein/casts/dysmorphic RBCs or absence of clots suggests glomerular disease.
RBC casts are virtually diagnostic of glomerulonephritis or vasculitis.
RBC clots usually indicate extraglomerular bleeding (urokinase in the glomeruli prevents
clotting).
Proteinuria suggests medical renal disease.
Urine culture (consider acid-fast bacilli culture if suspect tuberculosis)
24-hr urine for protein (consider electrophoresis for Bence-Jones protein/multiple myeloma),
creatinine, calcium, uric acid, and citrate
Protein excretion can be quantified accurately with a spot protein:creatinine ratio instead of a
full 24-hr urine collection.
CBC, PT, and PTT to evaluate for coagulopathy, anemia, and leukocytosis
Serum creatinine/BUN/electrolytes to evaluate renal function
3-tube test may help to isolate the specific origin of bleeding in isolated hematuria.
Collection and comparative evaluation of the number of RBCs in 3 urine specimens of
roughly equal volume
1st few milliliters (indicates a urethral lesion), a midstream sample, and the last few
milliliters (possible lesion at the trigone region of the bladder if this sample alone has most
RBCs)
If all 3 samples have similar levels of RBCs, the lesion more likely is renal, ureteric, or
diffuse bladder disease.
Urine cytology is rarely helpful.
Imaging
Imaging is needed only for further workup should the hematuria not clear after 48–72 hr of
rest on urinalysis and the 2nd-line testing is also negative (ie, urine culture).
Imaging is rarely needed unless there is a traumatic incident or suspected nephrolithiasis or
tumor.
Non-contrast-enhanced CT scan is the preferred modality for evaluating calculi with a
sensitivity of 98–100% and a specificity of 92–100%. Many institutions have a renal stone CT
scan protocol to minimize radiation exposure.
CT urography is the preferred test to evaluate urologic pathology such as malignancy or
obstruction. Images are collected in 3 phases:
Unenhanced
Nephrographic phase done shortly after administration of contrast material
Pyelographic phase done several minutes later to visualize the collecting system
Direct visualization with cystoscopy is necessary to rule out bladder cancer.
The combination of CT urography and cystoscopy generally is considered sufficient to rule
out serious urinary tract pathology.
Plain radiographs have the benefit of being inexpensive and easily available but have only a
60% sensitivity for calculi and a limited utility for diagnosing malignancy.
US has the benefit of no radiation exposure, so it can be used safely in children and pregnant
women. It has a low sensitivity for detection of calculi or tumors, especially tumors <3 cm in
size.
IV urography is used to visualize the collecting system but is being rapidly replaced by CT
urography owing to much higher sensitivity.
Retrograde pyelography also can be used to visualize the bladder and collecting system.
Voiding cystourethrogram (VCUG) is used to detect vesicoureteral reflux.
MR urography can be used in place of CT scan to minimize radiation or contrast material
exposure but is more expensive and time-consuming.
Arteriography detects renovascular hypertension, polyarteritis nodosa, thromboemboli, mass,
and aneurysm (4,5).
Painless:
EIH
Malignancies
Glomerulonephropathy, especially in children
PCKD
Sickle-cell trait or disease
Coagulation defect (clotting factor deficiency, thrombocytopenia, polycythemia)
Vasculitis (lupus, Goodpasture syndrome)
Infection (endocarditis, tuberculosis, syphilis)
Iatrogenic: Anticoagulation, catheterization, NSAID) nephritis: Decrease in vasodilating
prostaglandin causes decreased renal blood flow leading to nephron damage and
hyperfiltration
Early calculi formation (cause of microscopic damage): Hypercalciuria (>4 mg Ca/kg/day in
a 24-hr urine specimen); hyperuricosuria (>750 mg uric acid/day); hypocitruria (<450 mg
citrate/day for men, <650 mg/day for women; citrate helps to prevent stone formation)
Painful:
Pyelonephritis
Prostatitis
Cystitis
Urethritis
Calculi
Trauma
Bladder tumor
Renal tumor
Renal artery aneurysm
Renal vein thrombosis
Pseudohematuria
Myoglobinuria owing to rhabdomyolysis (no RBCs in HPF)
Hemolysis and/or “march hematuria” (no RBCs in HPF; RBCs are hemolyzed in foot
capillaries during marching)
Medications: Phenothiazine, phenolphthalein laxatives, rifampin, phenazopyridine
(Pyridium), phenytoin, quinine
Porphyria
Vegetable dyes (beets, rhubarb)
Vaginal blood contamination
Treatment
General:
Treatment is targeted to the underlying condition.
Antibiotics for infection
Pain control, if applicable; avoid NSAIDs until renal injury and nephritis are
ruled out.
Pyridium can be given for cystitis.
EIH:
Reassurance that this is a benign condition
Proper hydration can ensure adequate renal blood flow and minimize bladder
trauma.
Traumatic hematuria:
Be sure to perform a full primary and secondary survey to assess life-
threatening and coexisting injuries.
Immediate surgical consultation for signs of shock or severe trauma
Evaluate need for imaging.
All grades of traumatic kidney injury can be managed conservatively initially
with the assistance of a urologist.
Management of asymptomatic microscopic hematuria (AMH):
Confirm in 2–3 properly collected specimens.
No further workup needed if present in only one sample or no RBCs seen on
microscopic analysis (dipstick hematuria)
Consider further workup if >50 RBCs/HPF in single sample, unless clear
diagnosis of EIH.
Rule out transient (urinary tract infection or calculi) or spurious causes; treat
if present.
If age ≥40 yrs, refer for urologic evaluation with imaging and cystoscopy.
If age <40 yrs, assess for:
GFR <60 mL/min
Proteinuria (albumin:creatinine ratio ≥30 or protein:creatine ratio ≥50)
Hypertension (BP ≥140/90 mm Hg)
If any of the above are abnormal, refer to nephrology.
If no diagnosis is found, monitor GFR, proteinuria, and hypertension yearly.
Management of symptomatic microscopic hematuria (SMH):
Less well defined than for AMH
Rule out transient and spurious causes; treat if present.
Consider immediate referral to urology. One small study showed a
nonstatistically significant increase in cancer diagnosis with SMH vs AMH.
Alternatively, you may follow the same algorithm as for AMH.
Management of gross hematuria:
All patients should be considered for urologic evaluation.
Evaluate and treat transient causes.
Assess renal function, and consider imaging before referral (1,4).
Signs of shock (ie, tachycardia, hypotension), expanding flank mass, or oliguria
require emergent urologic referral.
Prescribe rest until hematuria resolves if EIH is suspected.
Emphasize hydration during exercise and avoidance of urination within 15–20
min of onset of exercise.
Ongoing Care
Referral to urology or nephrology is rarely needed to assist with diagnosis.
It is useful when other etiologies cannot be found and the hematuria persists.
Referral to a urologist or nephrologist where appropriate
Prognosis
Based on underlying diagnosis, if known.
Unexplained hematuria is relatively common in the general population and does not carry a
negative prognosis as long as an appropriate diagnostic workup has been done (2,4).
References
1. Rao PK, Jones JS. How to evaluate dipstick hematuria: what to do before you refer. Clev
Clin J Med. 2008;75:227.
2. Kelly JD, Fawcett DP, Goldberg LC. Assessment and management of non-visible
haematuria in primary care. BMJ. 2009;338:a3021.
3. Mercieri A. Exercise-induced hematuria. Up To Date. 21 Aug 2009 www.uptodate.com.
4. Bernard JJ. Renal trauma: evaluation, management, and return to play. Curr Sports Med
Rep. 2009;8:98–103.
5. O'Connor OJ, McSweeney SE, Maher MM. Imaging of hematuria. Radiol Clin N Am.
2008;46:113–132.
Codes
ICD9
599.70 Hematuria, unspecified
599.71 Gross hematuria
599.72 Microscopic hematuria
Clinical Pearls
Physician response to common patient question: When can I return to play?
Return to play is acceptable if hematuria resolves after 48–72 hr of rest;
otherwise, counsel patients on an individual basis depending on the diagnosis.
Transient hematuria is usually benign but should be worked up further in people
≥40 yrs of age.
Persistent hematuria always should be evaluated further.
Painless gross hematuria should be considered bladder cancer until proven
otherwise.
Hemoglobinopathies in Sport: Thalassemia, Sickle
Cell Trait
Bernadette Pendergraph
Evan Bass
Basics
Description
Thalassemia and sickle cell trait are genetic disorders of hemoglobin production. Thalassemias
are a mixed collection of quantitative abnormal production, leading to either absent or
decreased production of normal alpha or beta subunits. Sickle cell trait produces an abnormal
beta subunit in normal amounts.
Epidemiology
Incidence
Thalassemia: 1 in 1,000 people has thalassemia in the U.S.
Sickle cell trait: 8–10% of American blacks and 0.05% of American whites; 1 in 3 persons in
West Africa and 1 in 5 persons in the eastern province of Saudi Arabia have sickle cell trait
(1).
Prevalence
Thalassemia is the most common single genetic disorder known. In the thalassemia belt
(Mediterranean, Turkey, Iran, India, Thailand, Cambodia, and southern China), the prevalence
is 2.5–15% (2); 2.5 million people in the U.S., and 300 million people worldwide have sickle cell
trait (1).
Risk Factors
Genetics
The condition is caused by the inheritance of an autosomal-recessive gene.
General Prevention
Genetic screening and preconception counseling
Etiology
Thalassemia occurs when there is an abnormal gene on chromosome 11 or 16 that impairs
the production of alpha or beta subunits of hemoglobin. Abnormalities include point mutations,
total deletions, or the rearrangement of gene loci. Thalassemia minor occurs when a single
abnormal gene is inherited, resulting in normal or low-normal hemoglobin measurement with
significant microcytosis. More severe forms of beta thalassemia impair erythropoietin
production, cause hemolytic anemia, and reduce oxygen capacity (2).
Sickle cell trait occurs from the inheritance of 1 normal hemoglobin gene (HbA) and 1
abnormal B1 globin gene (HbS). In this carrier state, hemoglobin A1 and hemoglobin S is
produced in a 60:40 ratio. The B1 gene is found on the short arm of chromosome 11. RBCs
will sickle and polymerize under certain conditions, such as severe tissue hypoxia, acidosis,
dehydration, increased viscosity, and hypothermia (3).

Sickle cell trait: Increased incidence of hyposthenuria, microhematuria, renal papillary
necrosis, exertional rhabdomyolysis, exercise-related sudden death, and renal medullary
carcinoma; 2-fold increase in venous thrombosis; splenic infarcts reported at high altitude
(>7,000 feet) (1)
Thalassemia minor is usually asymptomatic. Other forms of thalassemia are associated with
erythroid hyperplasia (extramedullary erythropoietic tissue development in face, chest,
abdomen, and pelvis), resulting in frontal bossing, coarse facies, and splenomegaly. Heart
failure occurs secondary to hemolytic anemia. Other bone abnormalities include shortened
upper extremities, pathological fractures of long bones and vertebral bodies, notching, and
osteolytic lesions of the ribs because of marrow masses. Growth retardation, delayed
pubertal development, insulin resistance, hypothyroidism, and hypoparathyroidism are also
possible complications.
Diagnosis
Pre Hospital
Sickle cell trait: Usually asymptomatic; may present with cramping or sudden collapse,
usually within the 1st 30 min of intense practice and initial conditioning with normal core
temperature.
Thalassemia minor: Usually asymptomatic.
History
Sickle cell trait: Muscle cramps with exertion
Physical Exam
Sickle cell trait: Muscles are soft and nontender to palpation; no visible contractions.

Lab
Hemoglobin electrophoresis: Sickle cell trait shows hemoglobin AS (hemoglobin A1, 55–60%,
and hemoglobin S, 40–45%) (3,4).
CBC: Sickle cell trait leads to microcytosis and hypochromia.
Reticulocyte count: Normal in sickle cell trait but increased when combined with alpha or beta
thalassemia.
Indirect bilirubin: Normal in sickle cell trait but increased when combined with alpha or beta
thalassemia.
Alpha thalassemia:
1 gene deletion
Asymptomatic; normal hematologically
Alpha thalassemia:
2 gene deletion
Microcytosis and mild anemia, not reversed with iron
Beta minor thalassemia:
1 normal gene and 1 abnormal
Microcytosis and mild anemia not reversed with iron
Sickle cell trait combined with beta minor thalassemia or alpha thalassemia:
Usually symptomatic
Sickle cell trait combined with hemoglobin C
Iron deficiency anemia:
Microcytosis, decreased iron stores; improves with iron repletion
Dilutional pseudoanemia:
Increased volume expansion related to exercise; normal RBC indices and iron stores
Treatment
No treatment for asymptomatic sickle cell trait; focus is on prevention of
exertional rhabdomyolysis and exertional collapse
Collapse in sickle cell athlete:
Occurs from sickling of RBCs in exerting limbs, with resultant rhabdomyolysis
from continued exertion in the face of ischemia.
Severe lactic acidosis from anaerobic metabolism of ischemic muscles can
develop, leading to eventual shock.
Rapid diagnosis and treatment are necessary to prevent acute renal failure
from the rhabdomyolysis, subsequent hyperkalemia, eventual ventricular
fibrillation, and death.
Pre-Hospital
Sickle cell trait: If cramping or collapse, check vital signs, administer high-flow
oxygen, cool athlete if necessary, and activate emergency medical services if
patient is obtunded or vital signs are unstable.
ED Treatment
Continued support: Oxygen, IV fluids
Evaluation for rhabdomyolysis: CBC, electrolytes, BUN, creatinine, liver
function tests, coagulation panel
Correction of hyperkalemia
General Measures
Sickle cell trait:
Education of the athlete on importance of conditioning and identification of
cramping as a sign of sickling.
All athletes with the sickle cell trait should be counseled on preseason
strength and conditioning programs, gradual progression during session
training, and stopping activity if cramping, difficulty catching breath,
weakness, or pain.
When performing repetitive sprints/interval training, longer periods should be
allowed for athlete to recover in between exertional activities.
Exertion should be limited when conditions exist that may precipitate sickling:
Illness, high ambient temperature, dehydration, asthma, altitude (5)
Thalassemia: In severe cases, transfusions to keep the hemoglobin 9–10.5
g/L; chelation therapy in those receiving transfusions with deferoxamine,
deferasirox, or deferiprone
Referral
Hematology referral: Patients with symptomatic sickle cell trait; concern for
misdiagnosis and need for more advanced testing
Ongoing Care
Patient Education
Sickle Cell Disease Association of America:
http://www.sicklecelldisease.org/about/scd/index.phtml
Information Center for Sickle Cell and Thalassemia Disorders: http://sickle.bwh.harvard.edu/
Prognosis
Excellent, if prevention measures are instituted.
References
1. Tsaras G, Owusu-Ansah A, Boateng FO, et al. Complications associated with sickle cell
trait: a brief narrative review. Am J Med. 2009.
2. Giardina PJ, Forget BJ. Thalassemia syndromes. In Hoffman: Hematology: basic

principles and practice, 5th ed. Churchill Livingstone, 2008:
3. Hebbel RP. Variant sickle cell syndromes. In Hoffman: Hematology: basic principles and
practice, 5th ed. Churchill Livingstone, 2008.
4. www.scinfo.org/sicklecelltrait.htm accessed October 12, 2009
5. NATA Consensus statement: sickle cell trait and the athlete. Accessed on 8/7/09 at
http:/www.nata.org/statements/consensus/sicklecell.pdf
Additional Reading
Mercer KW, Densmore JJ. Hematologic disorders in the athlete. Clin Sports Med.
2005;24:599–621.
Codes
ICD9
282.41 Sickle-cell thalassemia without crisis
282.42 Sickle-cell thalassemia with crisis
282.49 Other thalassemia
Herpes Gladiatorum
Luke M. Spellman
Julie M. Kerr
Basics
Description
Variant of cutaneous herpes disease caused by herpes simplex virus type 1 (HSV-1) or type 2
(HSV-2) occurring among wrestlers and transmitted by direct skin-to-skin contact
Epidemiology
Affects 2.6% of high school wrestlers and 7.6% of collegiate wrestlers
Risk Factors
Abrasions increase the likelihood of acquiring infection.
Stresses of weight loss, competition, and school responsibilities can lead to recurrence.
General Prevention
Isolate infected wrestler to prevent skin contact with other wrestlers.
Used to control outbreaks among previously infected wrestlers
Acyclovir 200 mg b.i.d.
Valacyclovir 500 mg or 1 g daily
Famciclovir 250 mg b.i.d.
Consider using prophylactic antiviral medications during the wrestling season or before
important tournaments.
Teach skin hygiene and protect other skin abrasions from secondary contact with HSV.
Educate athletes to identify lesions/recurrence and seek early treatment in these situations.
Diagnosis
History
Initial vs recurrent eruption
Similar location as previous infection
Previous treatment and length of infection
History of recent stressors (eg, school, sleep, weight loss, emotional)
Physical Exam
Incubation period for primary infection is 2–14 days.
Prodrome of burning, stinging pain, or itching at the infected site, followed by clusters of
vesicles on an erythematous base
Common locations include head, neck, and upper body
Symptoms of fever, localized lymphadenopathy, malaise, myalgia, or pharyngitis may
accompany infection, especially with 1st episode.
Repeated outbreaks usually are less severe and involve a smaller area.
Infections around the eye increase the risk of corneal or retinal involvement, such as
keratoconjunctivitis or retinal necrosis.
Erythema and grouped vesicles, ulcers, or crusts on head, face, neck, or upper extremities
most common, but may occur anywhere on the body
Impetigo
Herpes zoster
Folliculitis
Allergic or contact dermatitis
Tinea gladiatorum
Cellulitis
Think herpes if infection fails to improve after 3–4 days of oral antibiotic therapy and if lesions
cross the midline and involve the face and scalp.
Diagnosis can be made by viral culture or Tzanck smear of vesicle fluid.
According to a recent study, polymerase chain reaction testing is a sensitive and cost-
effective method to determine viral presence and should be considered the gold standard for
detecting HSV-1 or HSV-2 in individuals with a rash suggestive of a herpes infection.
Treatment
Initial infection:
Started early in the clinical course, during vesicle formation, oral antiviral
medications can arrest viral replication and shorten the duration of infection.
Acyclovir 200 mg 5 times a day or 400 mg 3 times a day for 10 days
Valacyclovir 1 g b.i.d. for 10 days
During the ulcer stage, benzoyl peroxide and use of a hair dryer can help dry
crusts more rapidly and minimize secondary bacterial infections.
Recurrent infection: P.
Antiviral medications begun during the prodromal phase can effectively
shorten the duration of recurrent infections.
According to a recent study, treatment with 1 g valacyclovir daily reduced
herpes gladiatorum (HG) outbreaks by 92% in individuals with a <2-yr history
of recurrent HG, and treatment with 300 mg valacyclovir daily reduced HG
outbreaks in 88% of those with a longer than 2-yr history of recurrent
infection.
Acyclovir 200 mg 5 times a day for 5 days
Valacyclovir 500 mg b.i.d. for 5 days
Famciclovir 125 mg b.i.d. for 5 days
Valacyclovir 1 g b.i.d.
Famciclovir 250 mg 3 times daily
Valacyclovir 2 g × 1 dose; repeat in 12 hr
Additional Reading
Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of
herpes gladiatorum in wrestlers. Clin J Sports Med. 1999;9:86–90.
Anderson BJ. Managing herpes gladiatorum outbreaks in competitive

wrestling: the 2007 Minnesota experience. Curr Sports Med Rep.
2008;7:323–327.
Anderson BJ. Prophylactic valacyclovir to prevent outbreaks of primary

herpes gladiatorum at a 28-day wrestling cAMP. Jpn J Infect Dis. 2006;59:6–
9.
Anderson BJ. The epidemiology and clinical analysis of several outbreaks of

herpes gladiatorum. Med Sci Sports Exerc. 2003;35:1809–1814.
Annunziato PW, Gershon A. Herpes simplex virus infections. Pediatr Rev.

1996;17:415–423; quiz 424.
Becker TM, Kodsi R, Bailey P, et al. Grappling with herpes: herpes

gladiatorum. Am J Sports Med. 1988;16:665–669.
Belongia EA, Goodman JL, Holland EJ, et al. An outbreak of herpes
gladiatorum at a high-school wrestling camp. N Engl J Med. 1991;325:906–
910.
Dienst WL Jr, Dightman L, Dworkin MS, et al. Pinning down skin infections:
diagnosis, treatment, and prevention in wrestlers. Physician Sportsmed.
1997;25:45–50.
Stacey A, Atkins B. Infectious diseases in rugby players: incidence, treatment

and prevention. Sports Med. 2000;29:211–220.
Codes
ICD9
054.9 Herpes simplex without mention of complication
Clinical Pearls
Return to play: National Federation of State High School Associations Sports
Medicine Advisory Committee guidelines:
Herpetic lesions (simplex, fever blisters/cold sores, zoster, gladiatorum): To
be considered “noncontagious,” all lesions must be scabbed over with no
oozing or discharge and no new lesions should have occurred in the
preceding 48 hr. For primary (1st episode of HG), wrestlers should be
treated and not allowed to compete for a minimum of 10 days. If general body
signs and symptoms like fever and swollen lymph nodes are present, that
minimum period of treatment should be extended to 14 days. Recurrent
outbreaks require a minimum of 120 hr or 5 full days of oral antiviral
treatment, again so long as no new lesions have developed and all lesions
are scabbed over.
NCAA guidelines on Herpes simplex:
Primary infection: 1. Wrestler must be free of systemic symptoms of viral
infection (fever, malaise, etc.). 2. Wrestler must have developed no new
blisters for 72 hr before the examination. 3. Wrestler must have no moist
lesions; all lesions must be dried and surmounted by a FIRM
ADHERENT CRUST. 4. Wrestler must have been on appropriate
dosage of systemic antiviral therapy for at least 120 hr before and at the
time of the meet or tournament. 5. Active herpetic infections shall not be
covered to allow participation. See above criteria when making decisions
for participation status.
Recurrent infection: 1. Blisters must be completely dry and covered by a
FIRM ADHERENT CRUST at time of competition, or wrestler shall not
participate. 2. Wrestler must have been on appropriate dosage of
systemic antiviral therapy for at least 120 hr before and at the time of the
meet or tournament. 3. Active herpetic infections shall not be covered to
allow participation. See above criteria when making decisions for
participation status.
Questionable cases:
Tzanck prep and/or HSV antigen assay (if available)
Wrestler's status deferred until Tzanck prep and/or HSV assay results
complete
Wrestlers with a history of recurrent herpes labialis or herpes gladiatorum
could be considered for season-long prophylaxis. This decision should be
made after consultation with the team physician.
High-Altitude Illness
Arthur Islas
Basics
Altitude illness is a spectrum of symptoms ranging from nausea and headache to
pulmonary edema, cerebral edema, and potentially death, due to change in altitude:
High altitude: 1,500–3,500 m
Very high altitude: 3,500–5,500 m
Extreme altitude: Above 5,500 m
Altitude illness can be seen at any of these levels, precipitated not only by the altitude
achieved, but by a rapid change in altitude. Generally, prevention consists of slow ascent to
altitude. Treatment may include medications such as acetazolamide, and always consists of
descent to a lower altitude.
Sports issues to consider:
Train low: Lower-altitude training is optimally below 1,500 m; allows for achievement of
high VO2 max, absolute workload, heart rate, and blood lactate concentration.
Live (sleep) high: Optimally at an altitude of 2,500–3,000 m will maximize the
acclimatization response. The acclimatization response is in part due to increased
erythropoietin production, which may require increased iron stores or supplementation:
Sea level performance can be enhanced by the physiological effects of acclimatization to
altitude. The acclimatization process causes an increase in red cell mass (due to
increased erythropoietin production) and accordingly increases the oxygen-carrying
capacity of blood, resulting in increases in aerobic power and exercise performance at
sea level.
There is a further increase in capillary density and ratio of mitochondrial volume to
contractile protein.
Tissue myoglobin concentration and 2,3-diphosphoglyceric acid increase, which results in
increased oxygen uptake of exercising muscle
Competition at altitude:
VO2 max will decrease at altitude.
Acclimatizing at altitude adequately for 1–2 wks can maximize aerobic performance.
Improved performance at high altitude is dependent on the athlete's acclimatization,
altitude of residence, and the type of athletic event participated in.
Athletes in highly anaerobic events such as power lifting or throwing events do not benefit
from acclimatization and require only event time arrival.
Description
Clinical spectrum of signs and symptoms resulting from ascent to high altitudes are due to
hypobaric hypoxia.
Hypobaric hypoxia is the physiologic basis for the major altitude illnesses; acute mountain
sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema
(HACE).
These high-altitude illnesses frequently overlap in presentation.
AMS and HACE are considered as a continuum from mild AMS to HACE.
Each syndrome can present independently and progress rapidly, with or without the initial
warning of milder symptoms.
Untreated HAPE or HACE may end in death.
Epidemiology
As many as 38% of unacclimatized individuals may experience symptoms of AMS.
The largest study on children and high altitude showed no difference in incidence when
compared to adults, though a much smaller study showed that children 6–48 mos had a
higher incidence of AMS.
Incidence and severity increase with higher altitude and speed of ascent.
Risk Factors
Rapid ascent
Sleeping at altitude (typically >3,000 ft/night (>1,000 m/night))
Inadequate acclimatization
Strenuous exertion upon arrival to high altitude
Previous history and/or individual susceptibility to altitude illness
Low altitude of residence
Obesity
Chronic illness such as moderate to severe chronic obstructive pulmonary disease, sickle cell
disease, uncompensated congestive heart failure, or pulmonary hypertension
Well-controlled hypertension and asthma are not considered risk factors.
Physically fit individuals have shown a predilection toward altitude illness because of a
tendency to exert themselves more upon arrival at altitude and a faster rate of ascent.
Physical fitness can be advantageous in performing at altitude when altitude illness is not
present, but does not prevent altitude illness.
General Prevention
Graded ascent is the best way to prevent high altitude illnesses.
Avoid sleeping at altitudes >3,000 m.
Spend 2–3 nights at 2,500–3,000 m before going higher.
Spend an extra night of acclimatization for every 600–900 m above 3,000 m planned.
Avoid 600-m increases in sleeping altitudes above the 2,500-m mark.
Etiology
Hypobaric hypoxia:
Describes the decrease in the barometric pressure as altitude is gained. This decrease in
atmospheric pressure also decreases the partial pressure of oxygen, though the
percentage of oxygen in the atmosphere remains stable. This decrease in the partial
pressure of oxygen is what precipitates the hypoxia at altitudes, as there is not as much
pressure in the atmosphere to drive oxygen into the alveoli and consequently the
bloodstream.
As altitude is gained and the partial pressure of oxygen is decreased, some very unique
physiological responses occur. The carotid body senses the decrease in the partial
pressure of oxygen and compensates for this by signalling the respiratory centers in the
medulla to increase ventilation. This hypoxic ventilatory response (HVR) is commonly seen,
but the extent of the response is genetically determined. This increase in ventilation causes
hypocapnia and an alkalosis, which is compensated for by an increase in the excretion of
bicarbonate by the kidneys.
The HVR also causes hyperpnea resulting in respiratory alkalosis. The central respiratory
center responds with periods of apnea, called Cheyne-Stokes breathing, and is one of the
factors causing disturbed sleep.
HACE:
Vasogenic cerebral edema, caused by a myriad of responses to hypobaric hypoxia,
including endothelial activation and sympathetic activity.
HAPE:
A response to hypoxia through multiple mechanisms, which may include microemboli,
sympathetic discharge, pulmonary and peripheral vasoconstriction, which all in turn cause
increased capillary pressure, which leads to capillary leakage and then to pulmonary
edema.
Diagnosis
AMS: Any symptom of AMS at altitude should be considered due to altitude until proven
otherwise:
Headache
Insomnia
Nausea
Anorexia
Lassitude
Fatigue
Weakness
Malaise
Dizziness
Lightheadedness
Memory impairment
Concentration difficulties
HAPE: Half of HAPE victims experience symptoms of AMS in addition to severe dyspnea on
exertion progressing to dyspnea at rest:
Nonproductive and persistent cough
Chest tightness
Fatigue
Weakness
HACE: Ataxia and confusion are widely accepted as the symptoms that signal the
progression from AMS to HACE:
Headache
Lethargy
Incoordination
Vomiting
Disorientation
Irrational behavior
Visual or auditory hallucinations
Seizures
Semicoma
Unconsciousness (coma may ensue in as little as 24 hr after the onset of ataxia)
History
Altitude syndromes:
The more rapid the ascent and the higher the altitude attained, the more prevalent and
severe the altitude illnesses in those susceptible.
AMS:
Ascent to high altitude with onset of symptoms in 12–24 hr (symptoms can start as soon
as 2 hr after arrival but rarely after 36 hr)
HAPE:
Symptoms usually begin 2–4 days after arrival to high altitude and classically the 2nd night
sleeping at high altitude.
Characterized by insidious onset with decreased exercise performance and recovery time,
cough, dyspnea on exertion, and progressive worsening of symptoms, especially at night.
Pink frothy sputum is usually a late finding.
May have a sudden onset, especially in sedentary individuals at altitude
HACE:
Previous symptoms of AMS, with progressive worsening of neurologic symptoms, including
ataxia, extreme lassitude, mental status changes, and coma

Is commonly associated with HAPE
Progression from mild AMS to HACE at altitude may be as fast as 12 hr but usually
requires 1–3 days
HACE usually occurs above 3,000 m but has occurred as low as 2,100 m.
Physical Exam
AMS:
Specific physical findings are missing in mild AMS.
Tachycardia or bradycardia is possible.
BP can be normal.
Localized rales can be present but are not diagnostic.
Tortuous and dilated retinal veins and retinal hemorrhages may be present but are not
diagnostic.
HAPE:
Cyanosis is common.
Crackles in right middle lobe are classic but can be anywhere in the lung field.
Tachycardia
Tachypnea
Low-grade fever
Orthopnea
HACE:
Inability to perform activities such as dressing or eating
Truncal ataxia demonstrated by poor heel-toe walking.
Mental status changes
Occasionally focal neurologic deficits
Fundoscopic examination can demonstrate papilledema and retinal hemorrhages (not
diagnostic).

Imaging
HAPE:
Chest x-rays demonstrate fluffy and patchy infil-trates in the periphery of the lung fields
with a pre-dilection for the right middle lobe; normal heart size.
HACE:
Brain MRI is not necessary for diagnosis, but T2 images show an increased signal in the
white matter, especially at the splenium of the corpus callosum.
AMS:
Dehydration
Exhaustion
Viral syndrome
Gastroenteritis
Hangover
Hypothermia
Carbon monoxide intoxication
Hyponatremia
HAPE:
Pneumonia
Asthma
Mucus plugging
Pulmonary embolus
Myocardial infarction
Uncomplicated HAPE usually does not present with high fever >101°F, chills, or
mucopurulent sputum.
HACE:
Same as those for AMS as above
Cerebrovascular accident
Intoxication
Brain tumors
CNS infection
Acute psychosis
Treatment
Altitude illnesses in general: Descent to a lower altitude is the mainstay of
treatment.
Mild AMS:
No further ascent until symptoms resolve; consider descent of at least 500
m.
Limit physical exertion and maximize hydration.
Symptomatic medications: NSAIDs, aspirin, acetaminophen for headache
and antiemetics for nausea/vomiting
Acetazolamide 125–250 mg PO b.i.d. to help speed the acclimatization
process
Moderate-to-severe AMS or continued mild symptoms:
In addition to treatment of mild AMS, consider low-flow oxygen at 2–4 L/min.
Acetazolamide 125–250 mg b.i.d. with or without dexamethasone 4 mg PO,
IM or IV q6h
After stopping dexamethasone, ensure the patient remains symptom-free for
24–48 hr before re-ascending, as rebound symptoms of AMS can occur
after discontinuation of steroid.
Consider use of Gamow bag if O2 is not available or if symptoms are severe
or not improving or if immediate descent is not possible. A Gamow bag is a
fabric pressure (hyperbaric) bag that the patient is placed in that can be
manually inflated. When inflated to 2 psi, the internal environment of the bag
simulates a descent of 1,000–3,000 m, depending on starting altitude.
HAPE:
Assisted descent immediately
Minimize exertion; keep patient warm.
Early recognition of HAPE symptoms is essential to initiate immediate
descent and oxygen.
Concomitant use of high-flow oxygen at 4–6 L/min is essential, if available.
Consider nifedipine 10 mg PO every 4 hr by titration to response or 10 mg
PO once followed by 30 mg extended-release q12–24h.
Inhaled beta agonist
Consider sildenafil 50 mg PO q8h
Gamow bag: Hyperbaric therapy for 4–6 hr can be used if immediate
descent is impossible and oxygen is unavailable or symptoms not improving;
symptomatic medications as for AMS can be used.
Observe for symptoms of HACE.
HACE:
Immediate descent is mandatory.
Oxygen at 2–10 L/min
Dexamethasone 4 mg PO, IM or IV every 6 hr
Gamow bag can be used if descent is delayed or if athlete is unable to
descend.
Observe for symptoms of HAPE.
After descent, hospitalization is recommended.
Ginkgo biloba and antioxidants have both been looked at as possible alternative
treatments and/or preventative measures for AMS. Results for both have been
mixed, and both deserve further study.
Ongoing Care
General preventative measures:
Avoid heavy exertion for 2–3 days upon arrival to high altitude.
Maintain adequate hydration.
Eat frequent, small, high-carbohydrate meals.
Avoid alcohol.
Avoid sedatives/hypnotics.
Avoid smoking.
Avoid daytime sleeping.
Acclimatization:
Planned acclimatization is the physiologic method of progressively increasing sleeping
altitude.
Proper acclimatization can prevent serious altitude illness.
“Climb high and sleep low.” See the “General Prevention” section above for specific
acclimatization guidelines.
If a rapid ascent to 3,000 m or more is unavoidable, or if there is a previous history of
AMS or HAPE, acetazolamide can be used to help prevent or speed up the acclimatization
process. Acetazolamide 125 mg PO b.i.d.–t.i.d. is most commonly supported for
prevention means.
Additional Reading
1991 International Hypoxia Symposium held at Lake Louise in Alberta Canada.
International Society of Mountain Medicine Web site
Sutton JR, Coates G, Houston CS, eds. 1992. “The Lake Louise Consensus on the
Definition and Quantification of Altitude Illness.” In Hypoxia and mountain medicine.
Burlington, Vermont: Queen City Printers.
Hackett PH, Roach RC. High altitude cerebral edema. High Alt Med Biol. 2004;5:136–146.
Hackett PH, Roach RC. High altitude medicine. In: Auerbach PS, ed. Wilderness medicine
5th ed. St. Louis: Mosby, 2007.
Levine BD, Stray-Gundersen J. “Living high-training low”: effect of moderate-altitude

acclimatization with low-altitude training on performance. J Appl Physiol. 1997;83:102–112.
Levine BD, Stray-Gundersen J. A practical approach to altitude training: where to live and
train for optimal performance enhancement. Int J Sports Med. 1992;13(Suppl 1):S209–
S212.
Schoene RB. Illnesses at high altitude. Chest. 2008;134:402–416.
Stray-Gundersen J, Chapman RF, Levine BD. Hi lo altitude training improves performance in

elite runners. Med Sci Sports Exerc. 1998;30:s35.
Codes
ICD9
993.2 Other and unspecified effects of high altitude
Clinical Pearls
Proper acclimatization (a graded ascent) is the best method for preventing
altitude-related illnesses.
Athletes who participate in highly aerobic sports/events at low altitudes will
benefit most from the “train low, sleep high” method of training.
Athletes who participate in aerobic sports/activities above 2,000 m will benefit
from a short period of acclimatization before participation (5–20 days).
For athletes performing above 4,000 m, acclimati-zation at an intermediate
altitude is recommended.
When at altitude, think altitude.
Early diagnosis of altitude illnesses is key, as treatment is much more
successful the earlier the illness is diagnosed.
Acetazolamide given at 125–250 mg PO b.i.d. is a safe and effective way to
help the acclimatization process and to treat AMS.
Hip Pointer
Brent S. E. Rich
Basics
Description
Iliac crest contusion
Synonym(s): Bruised hip or contusion
Epidemiology
Most common in contact/collision sports such as football, wrestling, soccer, and lacrosse
Risk Factors
Collision sports
Inadequate iliac crest protection
Diagnosis
History
Direct blow to the iliac crest
Physical Exam
Signs and symptoms:
Acute, severe pain at the site of contusion
Athlete usually not able to continue activity
Posture often flexed to side of injury
Inspect for swelling, deformity, or ecchymosis.
Tenderness to palpation over iliac crest
Abdominal exam may reveal muscle spasm but should not be tender to palpation.
Weakness and pain with active abdominal contraction, trunk rotation, side bending, and/or
hip flexor contraction
Imaging
Plain anteroposterior (AP) pelvis radiographs to rule out fracture
Oblique views may be helpful.
Compression fracture to iliac crest
Avulsion fracture of anterosuperior iliac spine
Intra-abdominal injury
Avulsion of internal/external oblique, latissimus dorsi, and/or paraspinals
Treatment
Analgesia:
Minimize bleeding and swelling with compression and ice.
Narcotics may be appropriate for 1st 48–72 hr.
NSAIDs are indicated at onset until resolution.
Some clinicians prefer to give corticosteroid burst to decrease symptoms.
Modalities per certified athletic trainer or physical therapist in acute phase
Crutches for partial or non–weight-bearing may be necessary for 1st few days
of treatment.
Some clinicians prefer to inject with local anesthetic and corticosteroid to
decrease symptoms and speed recovery; increases risk of infection and
bleeding
Rehabilitation:
Gentle abdominal and hip stretching when tolerated
Gradual abdominal and hip strengthening
Progressive functional activity
Protection with padding on return to play
Ongoing Care
For evidence of intraabdominal trauma or displaced iliac crest fracture
Additional Reading
Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med.
2001;29:521–533.
Codes
ICD9
924.01 Contusion of hip
Clinical Pearls
Return to play can take place when there is minimal to no tenderness at the
contusion site, near-normal or normal abdominal and hip muscle strength, full
range of motion to hip flexion, trunk rotation, and sidebending. Athlete then should
be given adequate protection/padding.
Hyperthermia: Heat Stroke, Exhaustion, and Cramps
Christopher C. Trigger
Tanya J. Hagen
Basics
Description
Heat illness is the result of increased heat production and impaired heat dissipation.
Exertional heat illness is a continuum, but based on signs and symptoms can be divided into
the following groups:
Heat cramps
Heat exhaustion
Heat stroke
Epidemiology
Incidence
400 deaths per year can be attributed to all types of heat illness in the U.S.
Exertional heat stroke is the 3rd leading cause of death in athletes (1).
Prevalence
Football has been identified as the sport with the greatest number of heat-related fatalities.
From 1995–2005, 26 deaths were reported in high school, collegiate, and professional
football due to heat stroke (1).
Risk Factors
Hot, humid weather
Dehydration
Sickle trait
Age (<15 yrs or >65 yrs)
Poorly trained and/or overweight athletes
Cumulative heat load from previous days' exposures
Improper attire (plastic suits)
Equipment (football pads/helmet)
Poor acclimatization
Medications:
Dietary supplements (ie, ephedra, diet pills)
Antihypertensives (ie, diuretics, beta-blockers, calcium channel blockers)
Tricyclic antidepressants
Monoamine oxidase inhibitors
Antihistamines
Amphetamines
Illicit drugs (ie, cocaine, heroin, phencyclidine)
Concurrent illness (viral illness, skin disorders, cardiac disease)
General Prevention
Pre/post hydrate
Modify time, intensity, and exposure in hot, humid weather:
Exercise in the early morning or evening.
Limit sun exposure if possible.
Remove unnecessary equipment and/or clothing.
Heat acclimatization (usually takes 10–14 days) (2)[C]
Increase electrolyte intake, mainly sodium (Na), using sports drinks.
Etiology
Heat dissipation occurs via 4 processes (1,3):
Radiation is the direct release of heat from the body to the environment.
Conduction occurs with direct transfer of heat during contact with a cooler object.
Convection is when cooler air passes over the warmer exposed skin, lifting the heat away.
Evaporation through perspiration is the body's most effective way of eliminating heat,
although limited when humidity is high.
Diagnosis
History
Heat cramps:
Painful involuntary contractions of muscles, most commonly the calf, quadriceps, and
abdomen
Heat cramps are more commonly thought of as an electrolyte problem than a heat issue.
Heat exhaustion:
Fatigue
Shortness of breath
Dizziness or syncope
Nausea and vomiting
Normal mental status
Heat stroke:
CNS symptoms with the correct environmental conditions (hot and humid)
Previous history of heat exhaustion
Physical Exam
Heat cramps:
Normal temperature and vital signs
Tense, tender, involuntary contraction of the muscle belly
Heat exhaustion:
Normal or elevated core temperature but <40°C (104°F)
Vital signs usually normal, but can be variable depending on severity
Normal mental status
Flushed skin
Profuse sweating
Cold, clammy skin
Heat stroke:
Core (rectal) temperature >40°C (104°F) (2)[B]
CNS disturbances (confusion, ataxia, irritability, coma)
Tachycardic, tachypneic, and hypotensive
Hot skin with or without sweating
End organ damage/failure
Lab
Routine lab work typically unnecessary for minor heat illness, but depending on the clinical
picture, you may need to check the following:
CBC
Basic metabolic panel
Urinalysis to detect myoglobin
Serum creatine kinase to evaluate for rhabdomyolysis
Toxicology screen
Cardiac enzymes
Liver function tests
Coagulation studies to evaluate disseminated intravascular coagulation
EKG: Consider in heat stroke to look for cardiac damage/dysfunction
Dehydration
Electrolyte abnormality
Exercise-associated collapse
CNS lesion
Thyroid dysfunction
Infection
Treatment
Acute treatment:
Use basic or advanced cardiac life support for all unstable patients and
transfer them to the nearest medical facility.
Common theme in treating all heat illnesses is to lower the core temp to an
acceptable (38°C) level as quickly as possible
Heat cramps (2,13):
Rest
Oral replacement of fluids and electrolytes (Na) using sports drinks (1)
IV fluids if unable to tolerate by mouth
Passive stretching and/or ice massage of the affected muscles
Heat exhaustion (1,2,3):
More aggressive cooling techniques:
Move to cool environment.
Rest and remove excess clothing.
Apply ice bags to neck, axilla, and groin (2)[C].
Place in supine position and elevate legs.
Replacement of fluids and electrolytes
IV fluids if unable to tolerate oral rehydration
Heat stroke (1,2,3):
Support airway, breathing, and circulation.
Rapid cooling of the patient is first line:
Cold/ice water immersion most rapid form of cooling (2)[A]
If immersion unavailable, place wet towels/sheets and ice bags to neck,
axilla, and groin (1,2,3)[C]
IV fluids
Danger Apparent
Heat Syndrome
Category Temperature (°F)
IV. Extreme
130°F or higher Heat stroke highly likely with continued exposure
danger
Heat cramps or heat exhaustion likely, and heat stroke possible with prolonged exposure
III. Danger 105–130°F
and/or physical activity
II. Extreme Heat stroke, heat cramps, and heat exhaustion possible with prolonged exposure and/or
90–105°F
caution physical activity
I. Caution 80–90°F Fatigue possible with prolonged exposure and/or physical activity
ED Treatment
Any person exhibiting signs of worsening heat illness, specifically those with
mental status changes and a temperature >40°C, should be immediately
cooled and transferred for improved monitoring and management.
Once in the emergency department, the patient will undergo similar cooling
techniques as noted above.
Ongoing Care
Return to play recommendations (1,2):
Heat cramps [C]:
May return immediately after symptoms resolve with rest and fluid replacement
Depending on severity, may require 24 hr of relative rest
Heat exhaustion [C]:
Immediate return not recommended
Generally can return to activity within 24–48 hr
Gradually increase intensity and volume of training
Heat stroke [B]:
Consider at least 7 days of rest or until asymptomatic and lab values have normalized.
Consider follow-up no later than 1 wk after event or even sooner based on severity of
symptoms and lab abnormalities.
When cleared, begin training in cool environment and acclimate to heat over a 2-wk period.
Clear the athlete for full competition if heat tolerance exists after 2–4 wks of training.
If athlete does not tolerate return to play progression or has recurrent heat illnesses,
consider laboratory exercise-heat tolerance test.
Patient Education
Avoid risks listed above.
“Salty sweaters” may be at higher risk for heat cramps due to loss of Na; encourage
increased salt intake with meals and hydration with electrolytes.
Complications
End organ failure
Seizures
Acute respiratory distress syndrome
Liver failure
Acute renal failure
Rhabdomyolysis
Disseminated intravascular coagulation
References
1. Howe AS, Boden BP. Heat-related illness in athletes. Am J Sports Med.
2007;35:1384–1395.
2. Armstrong LE, Casa DJ, Millard-Stafford M, et al. Exertional heat illness

during training and competition. Med Sci Sports Exerc. 2007;39:556–572.
3. Wexler RK. Evaluation and treatment of heat-related illnesses. Am Fam

Physician. 2002;65:2307–2314.
Codes
ICD9
992.0 Heat stroke and sunstroke
992.1 Heat syncope
992.2 Heat cramps
Clinical Pearls
General Heat Stress Index (1,3)
Hypertrophic Cardiomyopathy
Matthew P. Boyd
Anne M. Garrison
Vikram Narula
Basics
Description
Asymmetric nondilated left ventricular hypertrophy (LVH), with or without outflow obstruction
Mostly inherited autosomal-dominant disease, but many cases are sporadic.
Primary cause (35%) of sudden atraumatic death in athletes <35 yrs
Death results from ventricular tachycardia either due to or in the absence of LV outflow
obstruction (some patients have arrhythmogenic foci).
Synonym(s): Idiopathic subaortic stenosis; Asymmetric septal hypertrophy
Epidemiology
Incidence of hypertrophic cardiomyopathy (HCM) is 0.2% or 1:500 in the general population.
Incidence of sudden cardiac death in athletes <35, mostly due to HCM, is 1:250,000.
Risk Factors
Family history of unexplained or early (<40 yrs) cardiac death
Age from 12–30 yrs old
Prior history of syncope
Abnormal BP response to exercise
Diagnosis
History
History is negative for most patients.
Direct and specific questions are important, and parents should be questioned as well.
Providers should also inquire about prescription medications and drugs of abuse.
Physical Exam
Most common initial presentation is syncope or sudden cardiac death (SCD) with exertion
Palpations
Exertional chest pain
Most patients with HCM have a completely normal physical examination.
Murmur:
In rare cases where murmur is detected, it usually is midsystolic and heard at the mid left
sternal border.
Murmur is ominous if it increases with maneuvers to decrease LV end-diastolic (LVED)
filling. These maneuvers cause dynamic obstruction in the LV outflow tract.
Maneuvers include rising from squatting to standing, moving from supine to vertical
position, and performing the Valsalva maneuver.
Murmur decreases when LVED filling increases, while moving from standing to squatting
(LV free wall moves away from the septum with increased filling).
Benign murmurs usually become louder while squatting and decrease on rising.
Such murmurs are common with improved fitness from training, as described with the AHS.
Athletes with significant outflow obstruction eventually may have pansystolic blowing
murmur of mitral regurgitation radiating to the axilla.
Any diastolic murmur indicates other cardiac pathology requiring workup.

Lab
Genetic family screening is available.
Clinicians may be increasingly faced with the dilemma of making recommendations regarding
sports participation for subjects who have only preclinical evidence of HCM (genotype
positive-phenotype negative).
Imaging
Electrocardiogram:
LVH findings
Increased voltage
Repolarization abnormalities
Prominent deep Q waves in left precordial leads
Ischemic ST changes in 90% of cases
Holter:
Not commonly used for screening, but may reveal paroxysmal atrial fibrillation and
ventricular tachycardia, which frequently are symptomatic.
Echocardiogram:
Echocardiogram usually shows LV wall thickening measured on the free wall as >15 mm.
The wall thickness is characteristically asymmetric, with the interventricular septum and
anterolateral thicker than the posterior wall.
Unlike patients with HCM, athletes with AHS (fit, young adults who also have murmurs)
have right ventricular hypertrophy and increased LV volumes or total LV diameter. These
findings represent physiologic adaptations to increased plasma volume.
Exercise stress testing is useful for evaluation of symptomatic patients, but its value in
screening asymptomatic subjects is controversial.
Athletic heart syndrome (AHS)
Myocarditis/pericarditis
Coronary artery anomalies
Aortic stenosis
Prolonged QT syndrome
Marfan syndrome
Wolff-Parkinson-White syndrome
Arrhythmogenic right ventricular dysplasia
Costochondritis
Gastroesophageal reflux
Treatment
Acute treatment:
Cardiopulmonary resuscitation (CPR) for syncope or arrest and defibrillation
with automated external defibrillator (AED) as soon as possible if indicated
Implantable cardiac defibrillator (ICD) along with modifications of activities
Ongoing Care
36th Bethesda Conference recommendations for activity for individuals with HCM:
Athletes with a probable or unequivocal clinical diagnosis of HCM should be excluded from
most competitive sports, except possibly low-intensity sports. This recommendation includes
athletes with and without symptoms or LV outflow obstruction.
Given that the risk of SCD may be reduced in older individuals (>40 yrs) with HCM, an
alternative of individual judgment may be used in selected older athletes only when each of
the following clinical features is absent:
Ventricular tachycardia (sustained or nonsustained) on ambulatory electrocardiogram
Family history of SCD due to HCM, particularly if <40 yrs old
History of syncope or other clinically relevant episodes of impaired consciousness
Severe hemodynamic abnormalities, including dynamic LV outflow tract gradient >50 mm
Hg
Exercise-induced hypotension
Moderate-to-severe mitral regurgitation, enlarged left atrium (>50 mm), or paroxysmal
atrial fibrillation
Presence of abnormal myocardial perfusion
These recommendations are not altered if medical or surgical treatment is undertaken in a
given athlete.
Although the clinical significance and natural history of genotype positive-phenotype negative
individuals remains unresolved, no compelling data are available at present with which to
preclude these patients from competitive sports in the absence of cardiac symptoms or
family history of sudden death.
Additional Reading
Beckerman J, Wang P, Hlatky M. Cardiovascular screening of athletes. Clin J Sport Med.
2004;14:127–133.
Maron BJ, Ackerman MJ, Nishimura RA, et al. Task Force 4: HCM and other
cardiomyopathies, mitral valve prolapse, myocarditis, and Marfan syndrome. J Am Coll
Cardiol. 2005;45:1340–1345.
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes: analysis
of 1866 deaths in the United States, 1980–2006. Circulation. 2009;119:1085–1092.
Rizvi AA, Thompson PD. Hypertrophic cardiomyopathy: who plays and who sits. Curr Sports
Med Rep. 2002;1:93–99.
Rowland TW. Evaluating cardiac symptoms in the athlete: is it safe to play? Clin J Sport
Med. 2005;15:417–420.
Codes
ICD9
425.1 Hypertrophic obstructive cardiomyopathy
425.4 Other primary cardiomyopathies
Clinical Pearls
Avoid physical activities that require exertion while awaiting diagnosis as this
may exacerbate your potential condition.
HCM is a rare genetic disease that can cause abnormal beating of the heart,
especially with exercise. It is difficult to control, and even those who are treated
probably should avoid all strenuous exercise unless HCM is proven not to be
the diagnosis.
There is a significant risk of death in people who have true HCM. Exercise
increases this risk in some athletes. Certain exercises may be permitted after
the true diagnosis and extent of the problem are clear.
Only very low-intensity exercises (Class IA sports) are considered possibly
acceptable, including golf, billiards, bowling, cricket, curling, and riflery.
Hyphema
Jorge O. Rodriguez
Adrian Lavina
Basics
Blood in the anterior chamber of the eye
Description
Traumatic hyphema grading:
Microhyphema:
Circulating RBCs seen by slit lamp exam only
Grade I:
<33% anterior chamber filling
Grade II
33–50% anterior chamber filling
Grade III
>50% anterior chamber filling
Grade IV
100% anterior chamber filling (often referred to as a blackball or 8-ball hyphema)
Epidemiology
Blunt or lacerating trauma (projectile or punch)
During or after intraocular surgery
Spontaneously secondary to neovascularization, neoplasm, uveitis, vascular anomalies of the
iris
Use of substances that alter platelet or thrombin function
Bleeding disorders
Incidence
Annual incidence of traumatic hyphema: 12/100,000 (1)
Males 3–5 times > Females
77% occur in people >30 yrs, with peak incidence between 10 and 20 yrs of age (1)
Risk Factors
Spontaneous hyphema:
Diabetes mellitus
Iris melanoma, retinoblastoma, other eye tumors
Juvenile xanthogranuloma
Clotting disorders
Anticoagulants or medications that inhibit platelet function
Uveitis
Iris neovascularization due to retinal or ocular ischemia
Scar formation (cicatrix)
Uveitis, glaucoma, hyphema syndrome
General Prevention
Protective eyewear should be worn during any high-risk sport such as racquetball or ice
hockey.
One-eyed athletes should wear eye protection during sports where there is any risk of eye
injury.
Etiology
Blunt trauma:
Bleeding results from tears in the vessels of the ciliary body, iris, and other anterior
segment structures
Elevated intraocular pressure:
Results from RBCs obstructing outflow through trabecular meshwork
Prolonged intraocular hypertension results in optic nerve atrophy
Secondary glaucoma
Rebleeding:
Secondary hemorrhage occurs 2–5 days after initial injury:
Predisposing factors include: Initial hyphema Grade II or greater, high intraocular
pressure (>22 mm Hg), pediatric age group, sickle hemoglobinopathy, African American
race, with and without hemoglobinopathy. It is more common in African Americans both
with and without sickle cell disease.
Systemic bleeding dyscrasia
Antiplatelet and anticoagulant medications
Predisposes to increased intraocular pressure, secondary glaucoma, corneal blood
staining with resultant risk of permanent vision loss
Ocular hypotony
Penetrating trauma
Spontaneous hyphema

Corneal abrasion
Scleral rupture
Perforation
Orbital fracture
Iridodialysis
Diagnosis
History
May accompany multiple trauma or serious head injury
Often associated with open globe, posterior segment injury, orbital fracture
Patients with sickle cell disease/trait, bleeding tendencies are at high risk for poor visual
outcome.
If mechanism does not match degree of injury, evaluate for child abuse, diabetes mellitus,
clotting disorder, tumors.
Physical Exam
Acute exam (2):
Sports-related ocular trauma evaluated on site
Obtain adequate history.
Best corrected visual acuity is checked with an eye chart if possible.
Check confrontation visual fields.
Examine pupils.
Penlight exam of the anterior chamber
Ocular motility
External exam looking for orbital injury
Funduscopic exam if possible
Topical anesthetic may be used to facilitate exam.
Eversion of upper and lower eyelids: Identify foreign bodies under tarsal plate.
If suspect globe rupture, place protective shield over affected eye, make NPO, refer
immediately.
Appears as a layering of RBCs in the anterior chamber
Physical findings associated with traumatic hyphema:
Photophobia
Decreased visual acuity
Anisocoria
Elevated intraocular pressure

Lab
Sickle cell rapid preparation and HgB electrophoresis
CBC, prothrombin time, partial thromboplastin time, international normalized ratio to screen
for bleeding dyscrasias
Imaging
Orbital series: If history and physical suggests fracture
B scan US if posterior segment exam limited by a large hyphema
Orbital CT scan if concern for globe rupture, intraocular foreign body, orbital fracture
A fluorescein angiogram is not usually indicated in the setting of a hyphema. Once there is an
adequate view to take photos of the retina, and if a retinal problem was suspected (such as
an arterial occlusion, a choroidal rupture, or contusion necrosis), an angiogram should be
done.
A gonioscopy puts pressure on the eye and is contraindicated with an acute hyphema.
Once the blood is completely resolved, probably around 6 wks after injury, gonioscopy is
performed to check for angle recession (trauma to the angle) to determine whether there is
increased risk for glaucoma. Gonioscopy can precipitate rebleeding if done too early before
the hyphema has resolved.
Hemolytic glaucoma
Ghost cell glaucoma
Iris injury
Ruptured globe injury
Treatment
Pre-Hospital
Place rigid eye shield to protect the eye.
Minimize mobility of the patient.
Head of transport bed elevated 30–45 degrees so blood will tend to settle
inferiorly
Do not give any NSAIDs.
Keep NPO in case surgery is required.
ED Treatment
Assess and treat life-threatening injuries.
Assess carefully for ocular perforation (open globe)
Avoid succinylcholine if rapid sequence intubation is required and globe rupture
suspected.
Treat any underlying bleeding dyscrasias.
Treat emesis and pain to prevent sudden intraocular hypertension with
extrusion of ocular contents.
Elevate head of bead to 30–45 degrees and place an eye shield over the
affected eye.
Instill cyclopentolate, scopolamine, or 1% atropine to dilate the pupil for exam
and pain relief after visual acuity has been assessed. If an ophthalmologist is
available, they should evaluate the patient prior to pupillary dilatation.
Control any ocular hypertension.
Provide additional pain control with proparacaine or tetracaine ophthalmic,
oxycodone with acetaminophen, morphine, fentanyl
Do not give NSAIDs due to the platelet-inhibiting properties.
Medication
Proparacaine will facilitate examination of the patient with hyphema if they have
pain.
Fluorescein dye will help detect a corneal abrasion.
In terms of controlling intraocular pressure (IOP), take the IOP and treat as
described in “Treatment” section.
Wear eye shield and restrict activity for 1 wk or until hyphema resolves.
Use cycloplegic eye drops: Atropine 1% b.i.d.–t.i.d. (patients without narrow
angle glaucoma) (3)[B]:
May prevent formation of posterior synechiae
Decreases pain from ciliary spasm
Topical corticosteroid eye drops (prednisolone acetate 1% q.i.d.) for traumatic
hyphema preferred over systemic (3)[C]
Traumatic hyphema and intraocular hypertension require medication to
decrease intraocular pressure (3)[C]:
Use topical beta-adrenergic blocker eye drops.
Use topical carbonic anhydrase inhibitor (CAI), such as dorzolamide if sickle
cell hemoglobinopathy has been ruled out. In sickle cell, CAIs may cause
increased sickling in anterior chamber due to increased ascorbic acid levels
in anterior chamber.
Use acetazolamide 250 mg PO q.i.d. if necessary as long as sickle cell
hemoglobinopathy has been ruled out.
It is a consideration to give systemic or topical antifibrinolytic therapy
(aminocaproic acid) for patients with traumatic hyphema who are at low risk for
thrombotic complications to reduce occurrence of secondary hemorrhage, and
for patients who have already rebled (3)[B].
Indications for surgical intervention after hyphema:
Intraocular pressure ≥50 mm Hg for 5 days
Intraocular pressure ≥35 mm Hg for 7 days
Total hyphema unresolved for 9 days
Microscopic corneal blood staining
Because of high incidence of late complications with hyphemas, referral to an
ophthalmologist for follow-up is recommended.
Outpatient follow-up is usually adequate, but close follow-up is necessary.
After resolution of hyphema, complete eye exam by an ophthalmologist with
gonioscopy (contact lens exam of angle) and ophthalmoscopy with scleral
depression is recommended.
Referral
Any hyphema should be referred for ophthalmologic follow-up.
Sickle cell disease/trait, bleeding dyscrasia, concern for open globe injury
necessitate urgent referral.
5% require surgery.
Surgical clot evacuation (3)[C]:
Large persistent hyphemas (Grade III or greater for more than 10 days)
Early corneal blood staining
Uncontrolled intraocular pressure despite maximal medical therapy
Inpatient management is recommended for (3)[C]:
Bleeding dyscrasias or sickle hemoglobinopathy
Other ocular injuries requiring hospital care
Suspected child abuse
Active young children
Intraocular hypertension on initial exam
Delayed presentation
Large hyphemas (Grade III or IV)
Discharge Criteria
Grade I hyphemas and microhyphemas can be managed as an outpatient if
intraocular pressure is stable.
Ongoing Care
Patient Education
Review symptoms of rebleeding or elevated intraocular pressure (sudden decreased vision
and pain).
Review symptoms of retinal detachment (flashes, floaters, shade descending over vision).
Provide medications and medication schedule prior to discharge to improve adherence.
Minimize activity.
Prognosis
Final visual acuity depends on size of hyphema and related complications.
Secondary hemorrhages usually result in hyphemas that are larger than the initial injury.
Grade I resolve in 4–5 days.
A final vision of 20/50 or worse is seen in 10% of patients with Grade I and in 50–75% with
Grade III or IV.
14% of hyphema patients have poor visual outcomes as a result of associated sequelae
(vitreous hemorrhage, retinal detachment, ocular rupture).
Blunt eye injury and hyphema increase risk of traumatic glaucoma.
References
1. Andreoli CM. Traumatic hyphema: epidemiology, anatomy, and pathophysiology.
Retrieved June 22, 2009 from www.uptodate.com, 2009.
2. Rodriguez JO, Lavina AM, Agarwal A. Prevention and treatment of common eye injuries
in sports. Am Fam Physician. 2003;67:1481–1488.
3. Andreoli CM. Traumatic hyphema: clinical features and management. Retrieved June
22, 2009 from www.uptodate.com, 2009.
Additional Reading
Ashaye AO. Traumatic hyphaema: a report of 472 consecutive cases. BMC Ophthalmol.
2008;8:24.
Irak-Dersu I. Glaucoma, hyphema. Retrieved November 23, 2009 from

http://emedicine.medscape.com/, 2007.
Walton W, Von Hagen S, Grigorian R, et al. Management of traumatic hyphema. Surv

Ophthalmol. 2002;47:297–334.
Weber TS. Training room management of eye conditions. Clin Sports Med. 2005;24:681–
693, x.
Codes
ICD9
364.41 Hyphema of iris and ciliary body
Clinical Pearls
Protective devices (2):
The American Society for Testing and Materials has established
performance standards for selected eyewear that are most appropriate for
sports with a risk of ocular injury.
Return to play (2):
The injured eye should feel comfortable with adequate return of vision.
Eye protectors must be worn for sports at high risk for ocular injury.
Hyponatremia
Tod Sweeney
William W. Dexter
Basics
Description
Decrease in serum sodium concentration to <136 mmol/L
Serum sodium concentration and serum osmolarity normally are maintained under precise
control by homeostatic mechanisms involving thirst, antidiuretic hormone (ADH), and renal
handling of filtered sodium.
Increased serum osmolarity above normal (280–300 mOsmol/kg) stimulates hypothalamic
osmoreceptors, which then cause increased thirst and circulating levels of ADH.
Can be associated with low, normal, or high tonicity
Effective osmolality or tonicity refers to the contribution to osmolality of solutes such as
sodium and glucose that cannot move freely across cell membranes, thereby inducing
transcellular shifts in water.
Most common form is hypotonic (dilutional) hyponatremia.
Excess of water in relation to existing sodium stores, which can be decreased, normal, or
increased.
Retention of water most commonly reflects presence of conditions that impair renal
excretion of water.
Less commonly caused by excessive water intake, with normal or near-normal excretory
capacity.
Hypertonic hyponatremia results from a shift of water from cells to the extracellular fluid that
is driven by solutes confined in the extracellular compartments (as occurs with hyperglycemia
or retention of hypertonic mannitol).
Pseudohyponatremia is a form of iso-osmolar and isotonic hyponatremia identified when
severe hypertriglyceridemia or paraproteinemia is present, which affects accurate laboratory
measurement of sodium concentration.
Epidemiology
Occurs in 10–40% of ultraendurance athletes after a race
7% of healthy elderly persons
Predominant gender: Male = Female.
More common in the very young and very old, who are less able to experience and express
thirst and less able to autonomously regulate fluid intake.
Risk Factors
Elite endurance athletes who consume excessive fluids
In marathoners, more common in women, slower runners, and finishers who maintain or
increase their body weight
Excess fluid losses (eg, excessive sweating, vomiting, diarrhea, GI fistulas or drainage tubes,
pancreatitis, burns) that have been replaced primarily by hypotonic fluids
Infants given inappropriate amounts of free water
Thiazide diuretics, chlorpropamide, cyclophosphamide, clofibrate, carbamazepine, opiates,
oxytocin, desmopressin, vincristine, selective serotonin reuptake inhibitors, or tolbutamide
Those with history of hepatic cirrhosis, congestive heart failure, or nephrotic syndrome, who
are subject to increases in total body sodium and free water stores
Acute or chronic renal insufficiency in patients who may be unable to excrete adequate
amounts of free water or those with salt-wasting nephropathy
Syndrome of inappropriate ADH secretion (SIADH)
Uncorrected hypothyroidism or cortisol deficiency
Consumption of large amounts of beer or use of the recreational drug methylenedioxy-
methamphetamine (“ecstasy”)
NSAID use

Hyponatremic encephalopathy associated with noncardiogenic pulmonary edema in healthy
marathon runners
Cerebral edema leading to brain stem herniation and death
Permanent CNS dysfunction
Central pontine myelinolysis characterized by weakness, muscle spasms, diplopia, confusion,
delirium, or dysphagia
Seizures
Rhabdomyolysis
Diagnosis
History
Thorough past medical, past surgical, medication, and social history, with special attention to
signs, symptoms, and differential diagnosis as listed above
Physical Exam
Signs and symptoms:
Varying range depending on the chronicity, cause, and the individual
Overhydration in athletes characterized by edema of the hands with swelling of the fingers
Anorexia
Headache
Muscle cramps
Nausea and vomiting
Difficulty concentrating
Confusion
Lethargy
Agitation
Obtundation
Coma
Status epilepticus
Most abnormalities are neurologic in origin.
Assess level of alertness.
Assess degree of cognitive impairment.
Depressed deep tendon reflexes, ataxia, asterixis, pathologic reflexes, or pseudobulbar
palsy (bilateral hemiplegia, dysarthria, dysphagia)
Look for signs of focal or generalized seizure activity.
In patients with acute severe hyponatremia, signs of brain stem herniation may be
apparent, including coma; fixed, unilateral, dilated pupil; decorticate or decerebrate
posturing; and respiratory arrest.

Imaging
Measure serum sodium level, and always consider possibility of laboratory error or improper
sampling technique.
Measure blood urea nitrogen, creatinine, uric acid, urinary osmolality, and urinary sodium.
Measure serum osmolality (low <280 mOsmol).
If normal (280–285 mOsmol), measure blood sugar, lipid, and protein levels.
If elevated (>280 mOsmol), measure blood sugar.
If serum hyperglycemia is present, then serum sodium must be corrected by a factor of 1.6
mEq/L for each 100 mg/dL increase in serum glucose.
Consider chest x-ray, electrocardiogram, head CT scan, or other laboratory work based on
history and physical examination.
Adrenal insufficiency and adrenal crisis
Congestive heart failure and pulmonary edema
Gastroenteritis
Hypothyroidism and myxedema coma
Renal failure, acute
Renal failure, chronic
SIADH
Cirrhosis
Nephrotic syndrome
Psychogenic polydipsia
Pseudohyponatremia
Iatrogenic
Medication related
Treatment
Long-term treatment
Acute treatment
Triathlete considerations:
Unconscious athlete should have bladder catheterized and should be moved
promptly to a hospital for definitive management.
For severe hyponatremia (<126 mEq/L), patient should not receive fluids
either orally or intravenously, except perhaps 3% saline solution (these
athletes usually are volume overloaded).
For less severe hyponatremia (>130 mEq/L), watchful waiting is the
cornerstone of therapy because most will self-correct.
Calculations:
Change in serum Na = (infusate Na – serum Na)/total body water + 1.
Estimates effect of 1 L of any infusate on serum Na.
Total body water (in liters) is calculated as a fraction of body weight.
Fraction = 0.6 in children; 0.6 and 0.5 in nonelderly men and women,
respectively; and 0.5 and 0.45 in elderly men and women, respectively.
Normally, extracellular and intracellular fluids account for 40% and 60% of
total body water, respectively.
General Measures
Airway, breathing, and circulation (ABCs)
Establish IV access.
Determine cause by history, physical examination, and laboratory data, and
direct treatment accordingly.
There is no consensus about the optimal treatment of symptomatic
hyponatremia. Increase serum sodium rapidly by 1–2 mEq/L/hr over the 1st 1–
2 hr for levels <120 mEq/L.
Patients with seizures or impending brain stem herniation should receive 3%
saline (see “Calculations” above) to accomplish rapid correction, but only
enough to arrest progression of symptoms; usually 4–6 mEq/L is sufficient. Be
aware of cardiac status with aggressive IV therapy.
Patients with mild symptoms and serum sodium <125 mEq/L often have chronic
hyponatremia and must be managed cautiously.
Rapid increase in serum sodium can lead to central pontine myelinolysis, but
risk appears minimal if correction is at a rate <0.5 mEq/L/hr or 12 mEq/L/day.
Isolated cases of osmotic demyelination after correction at 9–10 mEq/L/day
have been reported; therefore, maximum correction of 8 mEq/L/day is a more
conservative approach.
Hypovolemic hyponatremia with mild to moderate symptoms is treated with
normal saline (see “Calculations” above), and frequent monitoring of serum
sodium levels is important to assess rate of correction.
Hypervolemic hyponatremia treatment consists of sodium and water restriction
and attention to the underlying cause.
Euvolemic hyponatremia treatment consists of free water restriction and
correction of the underlying condition.
Patients with severe, symptomatic hyponatremia should be admitted to an ICU,
with close monitoring of serum sodium levels.
Proper management of underlying cause with close clinical follow-up
Discontinue medications known to be associated with hyponatremia.
Clozapine appears to be effective in long-term treatment of schizophrenic
patients with compulsive water drinking.
Ongoing Care
Although uncertainty about the diagnosis occasionally may justify a limited trial of isotonic
saline, attentive follow-up is needed to confirm the diagnosis before substantial deterioration
occurs.
Isotonic saline is unsuitable for correcting the hyponatremia of SIADH.
Great vigilance is required to recognize and diagnose hypothyroidism and adrenal
insufficiency, which tend to masquerade as SIADH.
Presence of hyperkalemia always should alert the physician to the possibility of adrenal
insufficiency.
Patients with persistent asymptomatic hyponatremia require slow-paced management, but
those with symptomatic hyponatremia must receive rapid but controlled correction.
Education on fluid intake and appropriate placement of support stations was associated with
a decreased incidence of symptomatic hyponatremia at ultraendurance sporting events.
Hypotonic fluids and excessive isotonic fluids should be avoided after surgery.
Additional Reading
Adrogue HJ, Madias N. Hyponatremia. N Engl J Med. 2000;342:1581–1589.
Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary
edema in marathon runners. Ann Intern Med. 2000;132:711–714.
Craig S. http://www.emedicine.com/emerg/topic275.htm (hyponatremia).

http://dynamicmedical.com Hyponatremia (hypotonic)
Kugler JP, Hustead T. Hyponatremia and hypernatremia in the elderly. Am Fam Physician.
2000;61:3623–3630.
Noakes TD, Mayers LB. A guide to treating ironman triathletes at the finish line. Physician
Sportsmed. 2000;28.
Speedy DB, Rogers IR, Noakes TD, et al. Diagnosis and prevention of hyponatremia at an
ultradistance triathlon. Clin J Sports Med. 2000;10:52–58.
Codes
ICD9
276.1 Hyposmolality and/or hyponatremia
Clinical Pearls
In ultraendurance athletes, IV should not be used unless there are signs of
dehydration, including cardiovascular instability.
Hypothenar Hammer Syndrome
Tarek Hadla
Holly J. Benjamin
Basics
Description
Lesion of the superficial palmar arch of the ulnar artery in the hand mainly owing to repetitive
compression or blunt trauma or even a single severe trauma over the hook of the hamate (1,2)
Epidemiology
Traditionally regarded as a rare condition, though may be underdiagnosed
Etiology
Etiology (1,2):
Trauma: By frequent use of the hand as a “hammer”
Vascular pathology: Thrombosis, abnormal anatomy, or aneurysm of the ulnar artery,
prothrombotic factors
Work-related: Auto mechanics, metal workers, lathe operators, miners, machinists,
butchers, bakers, carpenters, and brick layers
Sport-related: Golf, baseball catchers, heavy weight lifting, martial arts, mountain biking
Anatomy and pathophysiology: Hypothenar relates to the muscles of the 5th finger: AFO:
Abductor digiti minimi
Flexor digiti minimi
Opponens digiti minimi
The hand obtains its arterial supply through the ulnar and radial arteries. The ulnar artery and
nerve pass through Guyon's canal next to the hamate bone before dividing into the superficial
and deep palmar branches. Just distal to the canal, a short segment of the superficial branch
that forms the origin of the superficial palmar arch is unprotected between the skin and the
bone in the hypothenar area. Chronic trauma to this area can lead to pathology of the ulnar
artery.
Types of hypothenar hammer syndrome (HHS): Arteriographic patterns of HHS:
Type 1: Stenosis of superficial palmar arch around the hook of the hamate
Type 2a: Occlusion of the superficial palmar arch around the hook of the hamate
Type 2b: Occlusion of superficial and deep palmar arches around the hook of the hamate
Type 3a: Occlusion of the ulnar artery at the proximal part of the wrist
Type 3b: Occlusion of the ulnar artery near the wrist
Diagnosis
History
Symptoms (2,3):
Paresthesias in fingers with “pins and needles” sensation
Pain in fingers caused by cold or repetitive movements
Reynaud-like phenomenon that spares thumb
Physical Exam
Signs:
A hypothenar mass or callus
Tenderness of the hypothenar eminence
Raynaud phenomenon in the fingers and on the ulnar side of the hand (as above) (3)
Positive Allen test (see below)
Dependent rubor
Ulceration of fingertips or gangrene
Allen test: The Allen test is often used before cannulating the radial artery or in assessment
of hand trauma. The technique is as follows:
Patient elevates the hand and makes a fist for 20 sec.
Firm pressure is held against both the radial and ulnar arteries.
The patient opens the hand, and it should blanche white.
The examiner releases compression of the ulnar but not radial artery.
A normal hand flushes within 5–7 sec.
If the hand remains white, there is abnormal circulation.

Lab
CBC and international normalization ratio (INR) if thrombosis is suspected
Imaging
Doppler US
MR angiography (4)
CT angiography
Arteriography (“gold standard”)
Hand-arm vibration syndrome (5)
Raynaud phenomenon (3)
Treatment
Nonsurgical:
Avoidance of further trauma or modification of sport activity
Urokinase has been used to clear obstruction, as has prostaglandin E1 with
heparin.
Calcium channel blockers, vasodilators. and platelet inhibitors also have
been used (6).
Treat underlying atherosclerotic and prothrombotic factors, eg, smoking and
lipids.
Surgical:
Surgical reconstruction (end-to-end anastomosis of the ulnar artery) requires
microsurgical techniques. Arteries may be transplanted from other sites, or a
venous graft may be used (7).
Sympathectomy appears to give poor results.
Ongoing Care
Complications: Gangrene of the fingers in severe cases, which may require surgery
Prognosis: Many patients improve with nonsurgical treatments (see above). Results of
reconstructive surgery were variable, and recurrence was fairly common (2).
Prevention: Prevention should focus at improving work practices, sports modification, and
avoiding use of the palm of the hand as a hammer to pound, push, or twist objects (2).
References
1. Ferris BL, Taylor LM, Oyama K, et al. Hypothenar hammer syndrome: proposed etiology.
J Vasc Surg. 2000;31:104–113.
2. Jagenburg A, Goyen M, Hirschelmann R, et al. [Hypothenar hammer syndrome: causes,

sequelae and diagnostic aspects] Rofo. 2000;172:295–300.
3. Pineda CJ, Weisman MH, Bookstein JJ, et al. Hypothenar hammer syndrome. Form of
reversible Raynaud's phenomenon. Am J Med. 1985;79:561–570.
4. Van de Walle PM, Moll FL, De Smet AA. The hypothenar hammer syndrome: update and
literature review. Acta Chir Belg. 1998;98:116–119.
5. Cooke RA. Hypothenar hammer syndrome: a discrete syndrome to be distinguished from

hand-arm vibration syndrome. Occup Med (Lond). 2003;53:320–324.
6. Conn J, Bergan JJ, Bell JL. Hypothenar hammer syndrome: posttraumatic digital
ischemia. Surgery. 1970;68:1122–1128.
7. Brodmann M, Stark G, Aschauer M, et al. Hypothenar hammer syndrome caused by

posttraumatic aneurysm of the ulnar artery. Wien Klin Wochenschr. 2001;113:698–700.
Codes
ICD9
904.9 Injury to blood vessels of unspecified site
923.20 Contusion of hand(s)
Hypothermia and Frostbite
Rania L. Dempsey
Craig C. Young
Basics
Description
Frostbite:
Severe local cold-related injury resulting in freezing of soft tissue:
Superficial: Partial or complete freeze of skin
Deep: Involvement of skin and underlying tissue (may include muscles, vessels, nerves,
fat, and bone)
Hypothermia:
Systemic cold injury, classified as:
Mild: Core body temperature 32–35°C (90–95°F)
Moderate: 30–32°C (86–90°F)
Severe: <30°C (86°F)
Epidemiology
Incidence
True incidence of hypothermia and frostbite is unknown in athletes:
Mild cases of both are likely common in cold environments.
Hypothermia reported in up to 69% of athletes in cold water swimming events (1).
Annual incidence of hypothermia-related deaths 4 per 1,000,000 general population in the
U.S. (2):
More common in men (67% of hypothermia deaths) and those aged ≥65 yrs (49% of
hypothermia deaths)
Risk Factors
Hypothermia:
Environmental factors: Cold temperature, wind chill, prolonged exposure, high altitude
Wet clothing (increases heat loss 2–5 times) or immersion (increases heat loss 10–25
times)
Fatigue
Low body fat
Alcohol use (inhibits shivering, enhances heat loss through peripheral vasodilation, and may
lead to false sense of warmth)
Extremes of age (very young or old)
Underlying medical disease (eg, sickle cell anemia, peripheral vascular disease, diabetes,
seizure disorder, hypothyroidism)
Use of neuroleptic drugs
Frostbite:
Environmental factors:
Cold temperature, wind chill, prolonged exposure, high altitude
Risk of frostbite is <5% with temperatures >5°F (-15°C), but significant risk of
frostbite increases with temperatures ≤18°F (-27°C) (3).
Wet clothing (increases heat loss 2–5 times) or immersion (increases heat loss 10–25
times)
Prior cold injury
Petroleum or oil lubricants
Constrictive clothing
Smoking
Vasospastic disorders, ie, Raynaud's syndrome
General Prevention
Best treatment for hypothermia and frostbite is prevention (3)[C]:
Event planning based on the potential temperature ranges
Proper clothing, including hats, mittens, and multiple layers, as necessary
Avoid alcohol and other mood-altering drugs.
Recognize the signs and symptoms of hypothermia that indicate a need to seek shelter
(shivering, slurred speech, somnolence)
Etiology
Frostbite:
Fluids in body tissues and cellular spaces freeze and crystallize.
Cyclic vasodilation and vasoconstriction contribute to hypoxia/ischemia of affected tissue
Severe or prolonged exposure can lead to irreversible tissue damage.
Hypothermia:
Body heat is lost to the environment at a rate that overwhelms normal temperature
homeostasis, resulting in decreased core body temperature.
With decreasing temperature, heart rate, cardiac output, and cerebral blood flow
decrease:
May lead to cardiac rhythm disturbance and death
Diagnosis
Frostbite:
Skin may appear erythematous and swollen, or waxy, white, yellow, or blue-purple.
Vesicles/blisters may be present.
Patients with superficial frostbite complain of numbness and pain in affected area, but in
severe/deep frostbite, pain may be absent.
Hypothermia:
Mild: Patient displays shivering and mild mental status changes, including confusion,
amnesia, dysarthria, and ataxia.
Moderate: As core temperature declines, patient may develop severely impaired judgment
or stupor, loss of deep tendon reflexes, loss of shivering with muscle rigidity, and cardiac
arrhythmias.
Severe: Patient may have dilated pupils and appear comatose, with nearly undetectable
BP and respiration.
History
Duration and severity of cold exposure (prolonged exposure to very cold temperatures
increases risk of severe frostbite or hypothermia)
Recent alcohol or drug use (impairs judgment and increases susceptibility to cold injury)
History of cold water immersion (wet clothing and skin significantly increase continued heat
loss)
Underlying medical conditions (increases risk of severe frostbite or hypothermia)
Pain in affected area suggests superficial vs deep frostbite.
Physical Exam
Measure core body temperature:
For greatest accuracy, should be taken rectally with a thermometer capable of measuring
hypothermic temperatures (4)[A]
Assess pulse and cardiac rhythm:
Tachycardia may be seen with mild hypothermia.
May progress to bradycardia, atrial fibrillation, or ventricular fibrillation with more severe
hypothermia
In severe hypothermia, may be difficult to manually palpate pulse
Assess mental status:
Degree of mental status alteration correlates with severity of hypothermia
Perform complete neurologic examination:
Intact sensation to pinprick indicates a better prognosis for patients with frostbite.
Decreased muscle coordination, delayed deep tendon reflexes, and slowed pupillary
reflexes suggest more severe hypothermia.
Focal neurologic deficit suggests etiology of mental status changes other than
hypothermia.
Inspect appearance of skin:
Cold, yellow-white, or purple skin suggests frostbite.
Tissue pliability suggests superficial frostbite; hard tissue without pliability suggests deep
frostbite.

EKG: May see tachycardia; bradycardia; atrial fibrillation; ventricular fibrillation; prolonged
PR, QRS, and QT intervals, and J waves (positive deflection occurring at junction of QRS
complex and ST segment)
Electrolytes and basic chemistries: Hypothermic patients are at high risk for acid-base
disturbances.
Frostbite:
Frostnip: Freezing injury to superficial skin layers
Trenchfoot: Swelling, cyanosis, and erythema of extremity without freezing of tissue
Chilblains: Local cold-related erythematous skin lesions
Hypothermia:
Altered mental status from metabolic abnormalities, alcohol/toxic ingestion, or closed head
injury
Treatment
Pre-Hospital
Frostbite:
Avoid thawing until no further risk of refreezing, then immerse affected part in
40°C (104°F) water for 15–30 min (5)[C].
Remove wet clothing and protect from further cold injury (5)[C].
Avoid rubbing or massaging skin, which may compound tissue damage (4,5)
[A].
Monitor and treat for hypothermia (4)[C].
Arrange transport to medical facility for moderate or severe frostbite.
Hypothermia:
Mild:
Passive external rewarming: Prevent further heat loss with blankets, dry
clothing, shared body heat, and moving patient to shelter (4)[C].
Active external rewarming: Direct application of heat sources (heating pad,
hot water bottle, warm water immersion, electric blanket) applied to trunk
and used cautiously. Application of heat sources to extremities can result in
rapid reversal of cold-induced peripheral vasoconstriction, leading to
hypotension (rewarming shock) and further decreases in core temperature
(“afterdrop”).
Hot drinks for patients with normal gag reflex (4)[C].
Obtain rectal temperature when possible (4)[B]:
Athletes with oral or axillary temperatures >95°F are not likely to be
hypothermic.
Moderate/severe: In addition to the above measures:
Active emergency medical system. Perform a primary survey and institute
cardiopulmonary resuscitation (CPR) if needed (4)[C].
Attempts at field rewarming should not delay transport to emergency facility for
patients with moderate or severe hypothermia (4)[C].
Avoid agitation or jarring due to high risk of arrhythmias (4)[B].
ED Treatment
Frostbite:
After rewarming, debride white blisters and apply topical aloe vera. For
hemorrhagic blisters, apply aloe vera without debridement (5)[C].
Hypothermia (moderate or severe):
Continuous cardiac monitoring (6)[C]
Active external rewarming with forced-air rewarming blanket (6)[C]
Active internal rewarming with heated [43°C (109°F)] IV fluid or heated
humidified air or oxygen (6)[C]:
Peritoneal, gastric, pleural, or bladder lavage with heated [40°C (104°F)]
fluids may be used.
For severe cases, cardiopulmonary bypass may improve survival in young,
otherwise healthy individuals.
Monitor electrolytes; rewarming usually corrects electrolyte and acid-base
disturbances (6)[C].
Hypothermia with cardiac arrest requires a modified Advanced Cardiac Life
Support protocol (hypothermic heart less responsive to defribrillation and
cardioactive drugs; slowed drug metabolism with hypothermia) (7)[C]:
Establish airway; start CPR.
For ventricular fibrillation or ventricular tachycardia, attempt difibrillation
once; withhold cardioactive drugs until core temperature >30°C but
continue basic life support
For core temperature between 30°C and 34°C, administer cardioactive
drugs with increased intervals between doses
Medication
Frostbite:
Administer tetanus prophylaxis and analgesics (5,6)[C].
Administration of penicillin G (500,000 U every 6 hr for 48–72 hr)
prophylactically (5,6)[C]:
Controversial
Administration of intra-arterial tissue plasminogen activator within 24 hr of
injury may decrease amputation rate (5,6,8)[B].
Hypothermia:
No evidence to support routine use of antibiotics, steroids, or barbiturates
Range of motion and strengthening exercises may benefit frostbite-affected
limbs (5)[C].
Surgical debridement or amputation may be indicated for late treatment of
necrotic or gangrenous tissue due to frostbite (6)[C].
Ongoing Care
Prognosis
Mild-to-moderate cases of both hypothermia and frostbite generally
recover fully without complication.
Severe cases may lead to significant disability and death.
Complications
Frostbite:
Limb and digit loss
Premature closure of the epiphysis (younger athletes) (9)
Autonomic dysfunction of affected extremity
Permanent cold sensitivity and susceptibility to cold injury
Hypothermia:
Cardiac arrhythmias
Electrolyte and acid-base disorders
Inefficient clotting leading to disseminated intravascular coagulation
References
1. Brannigan D, Rogers IR, Jacobs I, et al. Hypothermia is a significant
medical risk of mass participation long-distance open water swimming.
Wilderness Environ Med. 2009;20:14–18.
2. Centers for Disease Control and Prevention (CDC). Hypothermia-

related deaths–United States, 1999–2002 and 2005. MMWR Morb Mortal
Wkly Rep. 2006;55:282–284.
3. Castellani JW, Young AJ, Ducharme MB, et al. Prevention of cold injuries
during exercise. Med Sci Sports Exerc. 2006;38:2012–2029.
4. Cappaert TA, Stone JA, Castellani JW, et al. National Athletic Trainers'
Association position statement: environmental cold injuries. J Athl Train.
2008;43:640–658.
5. Imray C, Grieve A, Dhillon S, et al. Cold damage to the extremities:

frostbite and non-freezing cold injuries. Postgrad Med J. 2009;85:481–
488.
6. Ulrich AS, Rathlev NK. Hypothermia and localized cold injuries. Emerg
Med Clin North Am. 2004;22:281–298.
7. ECC Committee, Subcommittees and Task Forces of the American

Heart Association. 2005 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2005;112:IV1–IV203.
8. Bruen KJ, Ballard JR, Morris SE, et al. Reduction of the incidence of
amputation in frostbite injury with thrombolytic therapy. Arch Surg.
2007;142:546–551; discussion 551–553.
9. Sallis R, Chassay CM. Recognizing and treating common cold-induced

injury in outdoor sports. Med Sci Sports Exerc. 1999;31:1367–1373.
Codes
ICD9
991.0 Frostbite of face
991.3 Frostbite
991.6 Hypothermia
Clinical Pearls
Hypothermia can occur even at moderate temperatures [50–65°F (10–18°C)]
if wind, rain, sweat, or wet clothing lead to heat loss that is greater than
metabolic heat production.
Prolonged exposure to cold temperatures, wet clothing, drug or alcohol use,
and underlying medical conditions increase risk of hypothermia and frostbite.
Prevention is the best treatment for hypothermia and frostbite.
Avoid cotton clothing: It retains sweat, does not dry quickly, and provides very
little insulation when wet:
Instead, use clothing made from wool or synthetic fabric.
Iliopsoas
Kevin E. Burroughs
Basics
Aching pain; can be in groin or over the anterior thigh
Occasionally, onset of pain is acute or subacute, with sharp lancinating or burning pain.
More often, it is insidious in onset, with pain exacerbated by climbing stairs, getting in/out of
bed, or rising from a seated position.
Description
Bursitis is inflammation and secondary pain in a bursal structure.
It is a common cause of lower extremity pain in people of all ages and activity levels.
2 types of bursae have been described, constant and adventitial. Constant bursae are
formed in embryogenesis and are endothelial-lined saclike structures (eg, iliopsoas and
trochanteric). Adventitial bursae form later in life through myxomatous degeneration of fibrous
tissues at sites of friction (eg, a bunion).
The iliopsoas bursa is the largest synovial bursa in the body and is present in over 95% of
adults. It averages 3 cm (width) × 6 cm (length) in size. There often is communication with
the hip joint capsule (14% of adults).
Synonym(s): Snapping hip syndrome
Snapping hip syndrome is usually broken down into intraarticular and extraarticular.
Extraarticular is subclassified into medial (internal). which is associated with iliopsoas
pathology, and lateral (external), which is associated with iliotibial band and greater
trochanteric pathology.
Epidemiology
Bursitis is reported to account for 0.4% of all visits to primary care, but in runners the
incidence may be as high as 10%.
In a 6-yr study of ballet dancers, 21 of 73 hip problems reported were attributed to iliopsoas
bursitis/tendonitis.
Reported in patients of all ages, but average age is 25 yrs, with a range of 12–56 yrs.
Risk Factors
Rheumatoid arthritis, osteoarthritis, acute trauma, overuse, or mechanical factors (tightened
hip flexors)
Common sports associated: Strength training, rowing, uphill running, competitive track and
field, aerobics
Etiology
The psoas and iliacus muscles originate from the lumbar spine and the internal aspect of the
pelvic brim, respectively. They converge to form the iliopsoas muscle-tendon complex and
insert distally on the lesser trochanter. It is a hip flexor and external rotator.
The muscle-tendon complex crosses over the anterior pelvic brim and hip capsule. The
iliopsoas bursa lies between the tendon and the bony pelvic brim.
Frictional compression of the bursa between these structures leads to an inflammatory
reaction.

Osteoarthritis
Pigmented villonodular synovitis
Synovial chondromatosis
Infection
Trauma
Status post total hip arthroplasty
Avascular necrosis of the femoral head
Leg-length discrepancy
Diagnosis
Pain can be present ± snapping.
If pain is the predominant feature, it will be in the groin or anterior thigh.
Irritation of the femoral nerve can be a cause of anterior thigh pain.
If there is remarkable bursal swelling, a pelvic or inguinal mass may be palpated.
Stride may be abbreviated during gait to avoid extension.
History
Pain is typically achy but may be sharp and is located in the groin or anterior thigh. One must
differentiate from L1 disk disease (uncommon).
Hip flexion and/or extension may cause pain. Stride length of gait may be shortened.
Physical Exam
Local tenderness to pressure beneath the midpoint of the inguinal ligament may be present.
The hip may be passively held in flexion, and the gait may be shortened to avoid hip
extension.
Pain is present in the inguinal region with resisted external rotation in a seated position. Pain
also should be in same location with passive hip extension or internal rotation, but there
should not be a fixed limitation of motion.
Positive Thomas test

Imaging
X-rays: Anteroposterior (AP) view of the pelvis and lateral view of the affected hip may show
osteoarthritis (associated cause) or other bony pathology to be considered in the differential
diagnosis.
US: Static or conventional US is a rapid, noninvasive, cost-effective diagnostic modality that
can demonstrate the fluid nature of an enlarged bursa. Dynamic US can demonstrate
abnormal snapping or movement of the tendon over the anterior pelvic brim. Also can be
used to guide aspiration/injection of the bursa.
Contrast bursography: Not often used. It will not show communication with hip joint if present,
and it is difficult to interpret.
Arthrography: Clearly shows if there is communication of bursa with hip joint.
CT scan: Seldom used; can demonstrate abnormal boney pathology causing friction at the
pelvic brim or a malpositioned lesser trochanter
MRI/MR arthrogram: MRI is a more sensitive and specific means of identifying lesions other
than bursa as the source of hip pain. MR arthrography may be required to increase the
sensitivity of detecting an acetabular labral tear.
Inguinal mass present: Lymphadenopathy, malignant tumor, hernia, vascular malformation,
hematoma
Pain or paresthesia present: L1 disk disease, meralgia paresthetica, hip arthritis, stress
fracture of the hip, acetabulum labral tear, proximal rectus femoris avulsion fracture at the
anteroinferior iliac spine in an adolescent
Treatment
In mild cases, relative rest, NSAIDs, and heat or other physical therapy
modalities
If there is a palpable mass or remarkable enlargement of the bursa by imaging
or CT scan, US-guided aspiration and instillation of a steroid preparation may
be indicated.
General Measures
2 basic premises: Reduce pain and inflammation and rehabilitation and
prevention of reinjury
Treatment depends on the severity and nature of the underlying cause.
Stretching of the hip flexors including iliopsoas and quadriceps
Strengthening of same and of hip rotators (internal and external)
Modification of any underlying mechanical abnormality (ie, correcting leg-length
discrepancy)
Typically only as a last resort after several attempts at conservative measures
May be necessary if bony pathology causes the bursal irritation
Partial surgical release or lengthening of the distal tendinous portion has
demonstrated good outcomes.
Mild hip weakness and loss of sensation in the lateral femoral cutaneous nerve
distribution have occurred following surgical release.
Ongoing Care
Patient Education
A study by Johnston and colleagues showed that a home-based exercise program lead to the
majority of individuals being pain-free or essentially pain-free.
The program included:
Exercises performed in a seated position with an elastic resistance strap. 3 sets of 20
repetitions of both internal and external rotation of the hip were performed. These were
performed daily for 2 wks.
The patient continued these exercises, but with the hip in less flexion, and now only 2–3
days per week. The patient added a side-lying abduction/external rotation with the hip at
45 degrees of flexion. These again were performed daily for 2 wks.
At 1 mo, an additional exercise of a 1-legged minisquat on the affected side was added. 3
sets of 20, 2 to 3 times per week.
Daily stretching targeting the hip flexor, quadriceps, and lateral hip/piriformis and hamstring
muscles was performed.
Prognosis
Good prognosis with reduction of inflammation, appropriate rehabilitation, and proper attention
to alteration of mechanical issues
Additional Reading
Adler RS, Buly R, Ambrose R, et al. Diagnostic and therapeutic use of sonography-guided
iliopsoas peritendinous injections. AJR Am J Roentgenol. 2005;185:940–943.
Butcher JD, Salzman KL, Lillegard WA. Lower extremity bursitis. Am Fam Physician.
1996;53:2317–2324.
Flanagan FL, Sant S, Coughlan RJ, et al. Symptomatic enlarged iliopsoas bursae in the
presence of a normal plain hip radiograph. Br J Rheumatol. 1995;34:365–369.
Johnston CA, Lindsay DM, Wiley JP. Treatment of iliopsoas syndrome with a hip rotation
strengthening program: a retrospective case series. J Orthop Sports Phys Ther.
1999;29:218–224.
Johnston CA, Wiley JP, Lindsay DM, et al. Iliopsoas bursitis and tendinitis. A review. Sports
Med. 1998;25:271–283.
Lachiewicz PF, Kauk JR. Anterior iliopsoas impingement and tendinitis after total hip
arthroplasty. J Am Acad Orthop Surg. 2009;17:337–344.
Pelsser V, Cardinal E, Hobden R, et al. Extraarticular snapping hip: sonographic findings.

Penkava RR. Iliopsoas bursitis demonstrated by computed tomography. AJR Am J

Roentgenol. 1980;135:175–176.
Schon L, Zuckerman JD. Hip pain in the elderly: evaluation and diagnosis. Geriatrics.
1988;43:48–62.
Taylor GR, Clarke NM. Surgical release of the ‘snapping iliopsoas tendon’. J Bone Joint
Surg Br. 1995;77:881–883.
Toohey AK, LaSalle TL, Martinez S, et al. Iliopsoas bursitis: clinical features, radiographic
findings, and disease associations. Semin Arthritis Rheum. 1990;20:41–47.
Codes
ICD9
726.5 Enthesopathy of hip region
Iliotibial Band Friction Syndrome
Natasha Harrison
Rahul Kapur
Basics
Description
Iliotibial band friction syndrome (ITBS or ITBFS) is an overuse tendonitis that occurs from
compression of the iliotibial band (ITB) against the lateral femoral epicondyle.
Pain is especially sharp after foot strike in the gait cycle, usually at 30 degrees of knee
flexion.
Synonym(s): Iliotibial band tendonitis
Epidemiology
Incidence as high as 12% of all running-related overuse injuries
Second to patellofemoral syndrome as the most common running injury
Risk Factors
Training factors: Higher weekly mileage, downhill running, disproportionate running on a track
in the same direction
Increased peak hip adduction (possibly owing to significant weakness of the hip abductors of
one limb as compared with the other) and increased knee internal rotation with running (1)
Etiology
The iliotibial band is composed of dense fibrous connective tissue that originates off the iliac
crest. Its course runs inferiorly, passing over the lateral femoral epicondyle prior to insertion
distally on the tibia at Gerdy's tubercle.
The iliotibial band is compressed against the lateral femoral epicondyle with knee flexion, with
the greatest compression at 30 degrees of knee flexion.
Etiology is unclear, but it appears that the repetitive compression leads to inflammation of the
band as well as inflammation of the connective tissue and fat pad between the band and the
epicondyle (2).
Diagnosis
History
Lateral knee sharp pain or burning
Pain is not present when the patient starts exercising but begins at a predictable time or
distance within the workout.
Symptoms that subside shortly after the workout but return with the next workout
Pain worse with downhill running, stride lengthening, or sitting for long periods of time with a
flexed knee
Involvement in sports that require continuous running or repetitive knee flexion (ie, bicycling)
Physical Exam
Lateral knee pain made worse with running (3)[C]
Pain with ascending and descending stairs
Stiff-legged walking in advanced cases
Extensive musculoskeletal exam with particular attention to the lower extremities: With a
patient with ITBS, the clinician may notice local tenderness and swelling, as well as
crepitation, snapping, or pitting edema over the distal ITB where it passes over the lateral
femoral epicondyle, and there may be pain or paresthesia along the length of the band (3)
[C].
Perform Obers' test: Position the patient on the unaffected side with the involved knee in 90
degrees of flexion. The leg is abducted at the hip, and the examiner then grasps the ankle,
allowing the knee to return to an adducted position. A person with ITBFS remains abducted
owing to a contracture of the ITB.
Perform Noble's compression test: With the patient on his or her side with the affected knee
up and flexed at 90 degrees, apply pressure on the ITB at the lateral femoral epicondyle and
extend the knee. A positive test occurs when pain occurs as the knee approaches 30
degrees of flexion.
Evaluate for excessive ankle pronation and causes of it, including evaluation for tight
gastrocnemius or soleus muscles, pes planus, or femoral or tibial torsion. Excessive ankle
pronation increases knee flexion.
Evaluate for muscle imbalances, especially pelvic and core musculature.
Exclude lumbar spine pathology.
Feet and footwear should be evaluated closely. Footwear can give clues to the pronation
pattern.
Evaluate iliac crests and leg length. Discrepancies of leg length can cause tightening of the
ITB.

Imaging
Generally not needed except to rule out other disease processes
Consider a standing anteroposterior (AP) view of pelvis (in adult) to assess leg-length
discrepancy if clinically indicated.
Patellofemoral syndrome
Lateral meniscal damage or pathology
Lateral collateral ligament sprain
Superior tibiofibular joint sprain
Popliteal or biceps femoris tendinitis
Peroneal nerve injury
Gout and other metabolic arthritides
Referred pain
Treatment
Rest or modification of activities may be sufficient, but often all potentially
exacerbating activities, notably running and cycling, must be avoided (3)[C].
Appropriate doses of NSAIDs along with modalities including ice,
phonophoresis, and iontophoresis (3)[C]
Address muscle imbalances as necessary, specifically pelvic and core
musculature.
Address pronation as well as other comorbidities (eg, patellofemoral
dysfunction, leg-length discrepancy) if present.
Relative rest is very important, but no forms of immobilization are used.
Steroid injections can be considered after appropriate interventions are used.
Research has shown steroid injections to be especially useful if given within 2
wks of the development of ITBS (4)[B].
Rehabilitation should involve an aggressive stretching and strengthening
program targeting the ITB and the muscles attached, with goals to restore
range of motion and improve flexibility while increasing strength.
Only after exhaustive nonoperative therapy
Often involves resection of a portion of the ITB, lengthening of the ITB, or
resection of the connective tissue and fat between the ITB and the lateral
femoral epicondyle (5)[B]
All toward a goal of reducing the compression of the ITB on the lateral femoral
epicondyle
Ongoing Care
If no improvement is seen after extensive therapy and training modification, then referral to an
orthopedic surgeon is warranted.
References
1. Noehren B, Davis I, Hamill J. ASB Clinical Biomechanics Award Winner 2006 Prospective
study of the biomechanical factors associated with iliotibial band syndrome. Clin Biomech
(Bristol, Avon). 2007.
2. Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band
during flexion and extension of the knee: implications for understanding iliotibial band
syndrome. J Anat. 2006;208:309–316.
3. Fredericson M, Wolf C. Iliotibial band syndrome in runners: innovations in treatment.

Sports Med. 2005;35:451–459.
4. Gunter P, Schwellnus MP. Local corticosteroid injection in iliotibial band friction syndrome
in runners: a randomised controlled trial. Br J Sports Med. 2004;38:269–272; discussion
272.
5. Michels F, Jambou S, Allard M, et al. An arthroscopic technique to treat the iliotibial band
syndrome. Knee Surg Sports Traumatol Arthrosc. 2008.
Codes
ICD9
728.89 Other disorders of muscle, ligament, and fascia
Clinical Pearls
An attempt to return too early with pain can result in significant delay. Activity
can be resumed when symptoms have improved nearly 100% or have
resolved. Earlier return can be accomplished using non-weight-bearing
activities such as swimming or running in the deep end of a pool. Return should
be gradual with gentle buildup on level ground progressing in
distance/resistance and elevation.
Most patients recover in about 6 wks and are able to resume full activity at that
time.
To prevent ITBFS, maintain flexibility with adequate warm-up periods and
stretching before and after exercise.
Impetigo
Arturo J. Aguilar
Basics
Description
Superficial skin infection of the epidermis with Staphylococcus aureus or group A beta-
hemolytic streptococcus or a combination of the 2, classically characterized as well-defined
erythematous papules and pustules with honey-colored crust (1)
Divided into bullous and nonbullous types (1)
Bullous (2):
Caused by epidermolytic toxin from Staphylococcus aureus
Favors intertriginous areas
Is a localized form of scalded skin syndrome
Starts as a vesicular eruption that develops into bullae and then may rupture to form honey
crusts
Nonbullous (more contagious) (2):
Caused by Staphylococcus aureus and group A beta-hemolytic streptococcus (GAS)
Starts as macules or papules and progresses to vesicular eruption, which rupture to form
erosions with honey crusts
Impetiginous (or common) impetigo is a nonbullous subtype that is a complication of systemic
diseases such as diabetes mellitus or HIV. It may also develop as a secondary infection of a
cut, scrape, or insect bite (1).
May be transmitted person to person or person to athletic equipment by direct contact (1)
Can also be spread by autoinoculation from skin excoriations in contact with other parts of
the body (1)
Synonym(s): Scrum strep (1)
Epidemiology
Most common bacterial skin infection in children (2)
3rd most common skin infection overall (2)
Most common in areas of skin-to-skin contact between athletes (1)
Most common on face and upper extremities (1)
Incidence is greatest in the summer months (1)
14.2% of skin infections in men's wrestling practices (3)
Risk Factors
Abrasions or open cuts allow passage of bacteria through the epidermis (1).
Sweat- and water-soaked clothes allow easy passage of bacteria through the 1st protective
layer of the epidermis (stratum corneum) (1).
Poor hygiene (1,3)
General Prevention
Techniques (1):
Avoid sharing equipment, towels, tape, and ointments.
Avoid dispensing ointments from common containers.
Clean equipment and clothes daily.
Shower immediately after sports activity with antibacterial soap.
Shower before using communal hot tubs.
Wear moisture-wicking, synthetic clothing.
Discourage body shaving in contact sports.
Frequent skin checks by athletic trainers and athletes in contact sports
Frequent handwashing by athletic trainers and affected athletes
Cover any injured skin immediately.
Use topical triple antibiotic for skin wounds.
Etiology
Bullous (2):
Epidermolytic toxin from Staphylococcus aureus
Nonbullous (2):
Staphylococcus aureus and/or GAS
Diagnosis
History
Mild itching and soreness (1)
May be an infection of a minor skin injury or occur on unimpaired skin (1)
May have accompanying pharyngitis (2)
Bullous (1,2):
Starts with superficial vesicles, which progress to flaccid bullae without surrounding
erythema
When the bullae rupture, they ooze and create honey-colored crusts.
Self-limited and may spontaneously resolve in weeks if left untreated
Nonbullous (more contagious) (1,2):
Starts as a single macule or papule that develops into a vesicle
Vesicle may rupture and form an erosion, and the contents become honey-colored crusts
that are often pruritic.
May spontaneously resolve without scarring if left untreated for weeks
Physical Exam
Findings (1,2,4):
Clear vesicles in the early stages
Some may progress to pustules and/or bullae
When vesicles or pustules/bullae break, they will have a honey-colored crust with
erythematous papules or erosions.
Lesions may range from millimeters up to several centimeters in diameter.
Mainly located on face and upper extremities
Regional lymphadenopathy

Diagnosis is based on history and clinical appearance (1).
Cultures can be done if history or epidemic of methicillin-resistant Staphylococcus aureus
(MRSA)
Lab
Wound culture to confirm or rule out MRSA if recent epidemic on the athletic team (1)
Throat culture if symptoms of pharyngitis for GAS (2)
Acne vulgaris (1)
Folliculitis (2)
Poison ivy (2)
Atopic dermatitis (2)
Herpes gladiatorum (1)
Tinea corporis gladiatorum (1)
Treatment
Methods (1):
Soak affected skin in warm water for 5–10 min 3 times daily until cleared.
Manually remove honey-colored crusts to improve antibiotic penetration.
Wash area with povidone-iodine liquid soap.
Medication
First Line
Mild (1,4):
Topical 2% mupirocin twice a day for 10 days
Topical fusidic acid (not available in the U.S.)
Bacitracin/neomycin found to be less effective in a 2003 meta-analysis
Moderate or widespread (adult dosing) (1,4):
Topical therapy in combination with oral antibiotic coverage
Amoxicillin/clavulanate 250–500 mg 2 times a day for 10 days
Dicloxacillin 250–500 mg 3–4 times a day for 10 days
Cephalexin 250–500 mg 3–4 times a day for 10 days
Penicillin-allergic oral therapy (4):
Erythromycin
Clindamycin
MRSA-positive lesions (1):
Topical 2% mupirocin with trimethoprim/sulfamethoxazole or clindamycin for
at least 14 days
Second Line
Tetracycline (4)
Vancomycin (4)
Linezolid (4)
Dactinomycin (4)
Clean clothes in bleach and water at a temperature of at least 71°C (1).
Clean equipment with diluted bleach solution (1).
Ongoing Care
Return-to-play guidelines (3):
College:
National Collegiate Athletic Association wrestling rules for competition:
Oral antibiotics for at least 72 hr prior to competition
No new lesions for 48 hr before a meet or tournament
No moist, exudative, or purulent lesions at the meet or tournament time
Active purulent lesions shall not be covered to allow participation
Firm adherent crusts may be covered with a nonpermeable dressing that will not
dislodge.
High school:
Each state's high school association has varying guidelines for competition.
Patient Monitoring
Recurrent infection should be considered for evaluation and possible treatment for
Staphylococcus aureus carrier state (2).
Patient Education
Educate athletes and athletic staff regarding the importance of good hygiene (3).
Prognosis
Untreated, may last several weeks to months but ultimately self-limiting (1).
Complications
Secondary (1,2,4):
Poststreptococcal glomerulonephritis up to 3 wks after skin infection:
Occurs in 20% of nonbullous-type impetigo
Risk not decreased with antibiotic treatment
Hyperpigmented area after healed lesions mostly in dark-skinned athletes
Cellulitis
Lymphangitis
Guttate psoriasis
Toxic shock syndrome
Staphylococcal scalded skin syndrome
Sepsis
Osteomyelitis
Pneumonia
References
1. Adams BB. Bacterial skin infections. Sports Dermatology. New York:
Springer, 2006:3–8.
2. Habif PT. Bacterial infections. Clinical dermatology. Mosby, 2004:267–

272.
3. National Collegiate Athletic Association. Skin infections in athletics. 2009–

10 NCAA Sports Medicine Handbook. National Collegiate Athletic
Association, 2009:56–63.
4. Cole C, Gazewood J. Diagnosis and treatment of impetigo. American

Family Physician. 2007;75:859–864.
Codes
ICD9
684 Impetigo
Impingement, Subacromial Bursitis and Rotator Cuff
Tendinitis
Mark E. Lavallee
Emily C. McDevitt
Basics
Description
Repetitive shoulder activity causes breakdown in the rotator cuff muscles from tensile
overload and results in tendinopathy.
Weakness in the rotator cuff muscles (supraspinatus, infraspinatus, teres minor, or
subscapularis) results in loss of effective dynamic glenohumeral movement.
This causes impingement of the cuff muscles under the acromion, enhancing the pain and
inflammation.
Synonym(s): Calcific tendonitis of the shoulder; Subacromial bursitis; Shoulder impingement
syndrome
Epidemiology
Very common in athletes, especially in those with repetitive motion of the arms (ie, throwing,
racquet sports, swimming, weight lifting)
In individuals <25 yrs of age, impingement is usually related to laxity caused by instability.
In those 25–40 yrs of age, impingement is usually due to overuse of the rotator cuff.
In those >40 yrs of age, impingement is caused by use of the cuff muscles over threshold.
This may result in partial- or full-thickness tears in addition to impingement (1)[C].
Risk Factors
Weight lifting (Olympic style)
Throwing or racquet sports
“Industrial” athletics (repetitive, overhead motion)
Shoulder instability
Previous shoulder surgery or trauma (to ipsilateral or contralateral shoulder)
Individuals with more “hooked” acromions (type III > type II > type I)
Smoking
Rotator cuff tear (partial or full)
Adhesive capsulitis
Axillary nerve entrapment
Pancoast tumor
Diagnosis
History
Rule out cervical spine disease, neck pain.
Symptoms: Weakness, crepitation, numbness, “slipped out,” night pain, dead arm (3)[B]
Exacerbation: Pain presents more at rest or with activity
Duration: Chronic (overuse) versus acute (traumatic)
Activation: Right or left handed, type of job, sports, hobby
History of previous trauma or surgery
Physical Exam
Shoulder pain with overhead activity
Weakness in the shoulder musculature
Crepitations
Numbness/paresthesias (usually between the lateral neck to the elbow)
Night pain
Pain at rest (usually in more severe cases)
Medial upper scapular border or medial upper trapezius pain (2)[C]
Observation:
How the athlete carries arm/shoulder (ie, recent dislocation, guarding)
Deltoid atrophy (ie, C5 plexus injury)
Scapular winging (ie, long thoracic nerve palsy) (3)[C]
Infraspinatus fossa scalloping (inferior branch of the suprascapular nerve)
Palpation:
Cervical spinous process: Rule out cervical neck pathology as cause of shoulder pain (4)
[A].
Subacromial bursa: Distal to acromion
Biceps tendon (long head)/bicipital groove
Insertion of the deltoid on the humerus: Pain at site but no pain with palpation; axillary
nerve pain referral site
Coracoid process: Pain referral site for impingement
Range of motion (ROM) (2):
Abduction (0–180 degrees)
Adduction (0–50 degrees)
Flexion: Forward (0–180 degrees) and horizontal (0–130 degrees)
Extension (0–90 degrees)
Internal rotation (0–100 degrees) (adduction and internal rotation: “Bra strap”)
External rotation (0–60 degrees) (abduction and external rotation: “Shampoo hair”)
Manual muscle testing:
Deltoid: Full abduction, resist at 90 degrees
Supraspinatus: Abduction to 90 degrees, 30 degrees forward flexion, resist downward
pressure
Infraspinatus and teres minor: Arm at side, 90 degrees at elbow, resist external rotation
(ie, “opening the door”)
Subscapularis: Hand behind back, push-off; Gerber's lift-off test
Special tests:
Hawkin's test: 90 degrees of forward flexion at the shoulder and elbow, support elbow,
pain with internal rotation of arm (4)[B]
Arc test: Shoulder abduction, gets “stuck” or painful at 60–120 degrees (2)[B]
Infraspinatus test: 90 degrees of flexion at the elbow, elbow held against body while
patient attempts to externally rotate arm against examiner's resistance, pain in shoulder
with external rotation (4)[B]
Neer test: Arm straight, thumb down, passive forward flexion (pain at 60–120 degrees) (2)
[B]
Impingement test: Inject subacromial bursa with lidocaine; helps to differentiate between
impingement and tear; after injection, pain, ROM, and strength should improve if
impingement and not a tear (2)[B].
Drop arm test: Patient cannot hold arm at 90 degrees of abduction; indicates cuff tear (2)
[A].
Speed test: Arm straight, forward flexion to 90 degrees, palm up, resisted downward
pressure; palpate the bicipital tendon at groove; pain indicates bicipital tendonitis (2)[B].

Imaging
Imaging is often not needed in light of good history and physical exam and a straightforward
case.
Radiography:
Anteroposterior (AP) view and axillary (transscapular) views bare minimum to order;
radiographs helpful for acute injuries to rule out fractures, dislocations; with impingement,
may be helpful to get additional views (1)[C]
Internal and external AP rotational views help to visualize humerus (ie, Hill-Sacks lesions)
(3)[C].
Stryker notch view helps to visualize posterolateral humeral head deformity (ie, Hill-Sacks
lesions) (3)[C].
West Point (modified axillary) view allows visualization of the anterior/inferior glenoid (ie,
Bankhart lesions) (1)[C].
Outlet or Alexander view allows for visualization of subacromial space; helpful in elderly
patients with severe impingement (3)[C].
Calcification on the tendon is associated with bicipital tendonitis or severe impingement.
US:
Though dependent on skill and comfort of practitioner, can be cost-effective in-office
imaging choice for static and dynamic view of soft tissue structures of the shoulder (ie,
rotator cuff muscles, biceps tendons, subacromial bursa, calcification in tendons) (3)[C],(5)
[A]
Also can be used to guide injections into biceps tendon sheath, subacromial bursa, or
intraarticular area
MRI:
In severe or confusing cases, MRI is helpful in diagnosis of rotator cuff tears, labrum tears,
biceps tendon rupture, as well as assessing volume and capsule thickening in adhesive
capsulitis.
An MRI arthrogram is often useful to further displace a torn labrum, thus improving
visualization of the anatomy (1)[C].
Electromyography/nerve conduction study: Helpful if there is weakness in addition to an
altered neurologic exam (sensation, reflexes) etc.; has the highest sensitivity when symptoms
have persisted >3 wks
Rotator cuff tear (partial or full thickness)
Adhesive capsulitis
Acromioclavicular sprain/injury
Labral tear
Bicipital tendonitis
Fracture: Clavicle, humerus, scapula
Subluxation of glenohumeral joint
Axillary nerve entrapment
Pancoast tumor
Bankhart lesion (avulsion fracture of glenoid)
Hill-Sacks lesion (impact fracture of humeral head)
Septic arthritis
Glenohumeral arthritis
Thrombosis of subclavian or brachial artery
Treatment
Medication
Oral analgesia: NSAIDs, acetaminophen, tramadol; in severe cases, short-
term pain relief with narcotics. Prednisone: Short course of 40 mg daily × 5
days (1)[A]
Dermal: Topical cream or transdermal patches (NSAID- or lidocaine-based)
Injectable: Subacromial bursa injection (5–10 mL 2:2:1 mixture of lidocaine,
Marcaine, corticosteroid; use a 22–25-gauge, 1.5-in-long needle) (1)[A]
Management of acute phase:
Relative rest: Decrease use of affected shoulder (1)[C]
Home exercise program (HEP): Exercise done daily, 3 sets per exercise
ROM: Dangling arm circles, finger wall-walking, broom-handle exercises
Strengthening: Sword-from-sheath exercises, posterior dumbbell raises,
proprioceptive neuromuscular facilitation (PNF), augmented soft tissue
mobilization (ASTM), scapular stabilizing exercises using light weights or
flexible elastic cords (1)[C]
Rehabilitation for long-term treatment:
Formal physical therapy: Pain relief via contrast baths, hydrocollator, ice,
mobilization/manipulation, modalities (e-stim, US) (1)[C]
ROM strengthening: Deltoid, rotator cuff musculature, scapular stabilizers,
biceps
ROM flexibility: Biceps, triceps, glenohumeral joint
Transmembrane corticosteroid (ie, phono-phoresis, iontophoresis)
Return to normal function
Sports-specific retraining
In the younger athlete, impingement is often due to another underlying problem
(ie, instability).
Certain athletes (ie, mentally challenged, unmotivated, etc.) may need
assistance of formal physical therapy without a trial of HEP.
Mentioned in literature for recalcitrant cases: Prolotherapy, platelet-rich plasma
injections, acupuncture, and topical nitrates
Anterior acromioplasty: The acromion is “shaved” to allow more space for the
rotator cuff. It is used only if conservative measures fail. There is a less
favorable outcome in younger (50% success rate) than older athletes (1)[C].
Surgical débridement/repair of rotator cuff: Often accompanies an anterior
acromioplasty
Surgical débridement/repair of labrum
Ongoing Care
Presence of a fever and a tense joint capsule (ie, a potentially septic joint)
Severe disease that is refractory to physical therapy, modalities, and steroid injections
Rotator cuff tear, full or partial thickness, nonresponsive to conservative care
Extra cervical rib, causing shoulder symptoms
SLAP lesion
Gross instability of shoulder not improved with physical therapy
References
1. Burbank KM, Stevenson JH, Czarnecki GR, et al. Chronic shoulder pain: part II.
Treatment. Am Fam Physician. 2008;77:493–497.
2. McFarland E, Tanaka M, Papp D. Examination of the shoulder in the overhead and

throwing athletes. Clin. Sports Med. 2008;(27):553–578.
3. Burbank KM, Stevenson JH, Czarnecki GR, et al. Chronic shoulder pain: part I.
Evaluation and diagnosis. Am Fam Physician. 2008;77:453–460.
4. Parker B, Zlatkin M, Newman J, et al. Imaging of shoulder injuries in sports medicine:

current concepts and protocols. Clin Sports Med. 2008;(27):579–606.
5. Iannotti J, et al. Accuracy of office-based ultrasonography of the shoulder for the

diagnosis of rotator cuff tears. J Bone Joint Surg. 2005;(87-A)6:1305–1311.
Codes
ICD9
726.10 Disorders of bursae and tendons in shoulder region, unspecified
726.11 Calcifying tendinitis of shoulder
726.12 Bicipital tenosynovitis
Clinical Pearls
If caught early with no other shoulder pathology and treated with aggressive
conservative therapy, many athletes are able to return to their prior level of
competition.
With cortisone treatment, pain relief is often immediate owing to the analgesia.
This will wear off. Cortisone starts working within 3 days.
If no other shoulder pathology is present, and the injury is treated with
aggressive conservative therapy, most athletes respond and avoid surgery.
Inner Ear Injuries (Tympanic Membrane Perforation)
Rochelle M. Nolte
John Hariadi
Basics
Description
Blunt trauma (slap to the ear)
Penetrating trauma (Q-tip)
Rapid pressure change (diving, flying)
Extreme noise (blast)
Lightning
Spontaneous perforation of acute otitis media
Acute necrotic myringitis
Epidemiology
Incidence
Incidence in general population has not been studied.
A study found that 3% of children with ventilation tubes had tympanic membrane perforations.
Etiology
Infection (such as acute otitis media) is the principal cause of tympanic membrane
perforations.
Ear canal infections rarely cause perforations.
Presence of perforation renders ear more susceptible to infection if water enters the canal.
Perforation therefore is an absolute contraindication to irrigation for cerumen removal.
Diagnosis
Direct visualization of tympanic membrane with otoscope
Test hearing in both ears.
Note any nystagmus with changes of position or pressure on the tragus occluding the canal
(fistula sign).
Physical Exam
Ear pain (mild)
Decreased hearing (partial)
Severe pain or complete hearing loss in the affected ear suggests additional injuries.
Purulent or bloody discharge from ear canal
Tinnitus
Vertigo
Otorrhea

Insufflation via pneumatic otoscope:
Will not cause the perforated tympanic membrane to move normally
Holding pressure for 15 sec (the fistula test) may cause nystagmus or vertigo if the
pressure is transmitted through the middle ear and into a labyrinthine fistula.
Weber test (tuning fork on midline bone):
Sound should be equal or louder in the injured ear, consistent with decreased conduction.
Sound localizing to the opposite side of injury indicates possible otic nerve injury.
Rinne test: Usually normal (air conduction detected after bone conduction fades) or shows a
small conductive loss (1)
Imaging
Radiography and MRI are of no value unless the clinical picture suggests ossicular
destruction and/or cholesteatoma.
Asymptomatic perforations, especially if hearing is near normal, require no imaging studies
(1).
Temporal bone fracture
Serous otitis media
Suppurative otitis media
Otitis externa
Cerumen impaction
Barotrauma
Acoustic trauma
Foreign body
Child abuse
Treatment
ED Treatment
Medical treatment for perforations is directed at controlling otorrhea.
Clean debris from the ear canal.
Prescribe antibiotics if there is evidence of infection.
Acute otitis media with tympanic membrane perforation should be treated with
an oral antibiotic (2)[A].
Oral antibiotic choices (administered for 7–10 days):
Amoxicillin
Trimethoprim-sulfamethoxazole
Cefixime
Augmentin
Prophylactic antibiotics not indicated P.
Use topical antibiotics with low acidity/ototoxicity, such as ofloxacin or
ciprofloxacin otic, in combination with oral systemic antibiotics.
Topical quinolones (±steroids) are the best treatment for chronic suppurative
otitis media (2)[A].
Analgesics if needed for pain
Do not prescribe topical ototoxic eardrops such as gentamicin, neomycin
sulfate, or tobramycin.
Arrange ENT follow-up.
After detailed examination and formal audiometric tests, most
otolaryngologists follow the perforation with monthly examinations.
Operative repair reserved for the 10–20% that do not heal spontaneously.
Provide detailed discharge instructions.
Occlude the ear canal with cotton coated in petroleum jelly or antibiotic ointment
when showering to prevent entry of water into the middle ear, which can be
painful.
Swim only with fitted earplugs.
Avoid forceful blowing of the nose.
Expected outcome:
Most perforations heal spontaneously over a few months (68% within 1 mo,
94% within 3 mos).
A few require operative repair such as a collagen foam splint or a flap from
the canal wall.
Perforations caused by molten metal or electrical burns are less likely to heal
spontaneously.
Forceful entry of water, as in a water skiing accident, is more likely to lead to
infection.
Complications include infection, dislocation of ossicles, perilymph leak, and
cholesteatoma.
Medication
Amoxicillin: 250–500 mg (children: 20–40 mg/kg/24 hr) PO t.i.d.
Trimethoprim-sulfamethoxazole (Bactrim DS): 1 tablet (children: 6–12 mg/kg/24
hr) PO b.i.d.
Cefixime: 400 mg (children: 8 mg/kg/24 hr) daily
Augmentin: 250–500 mg (children: 20–40 mg/kg/24 hr) PO t.i.d.
Ofloxacin otic topical solution 0.3%: 10 drops in affected ear b.i.d. × 14 days
Ciprofloxacin 0.3% and dexamethasone 0.1% otic solution (Ciprodex): 4 drops
in affected ear b.i.d. × 7 days (2)
Office procedures such as paper patch method (67% success) and fat plug
(87% success)
Surgical tympanoplasty under local or general anesthesia (90–95% success)
(3)
Initial stabilization: Airway, breathing, and circulation (ABCs of trauma care)
Immobilize cervical spine, and investigate for intracranial injury when indicated.
Admission Criteria
Associated injuries requiring admission
Severe vertigo impairing ambulation
References
1. Howard ML, et al. Middle ear, tympanic membrane, perforations. eMedicine
update 25 September 2009.
2. Wright D, Safranek S. Treatment of otitis media with perforated tympanic

membrane. Am Fam Physician. 2009;79:650, 654.
3. Dursun E, Dogru S, Gungor A, et al. Comparison of paper-patch, fat, and

perichondrium myringoplasty in repair of small tympanic membrane
perforations. Otolaryngol Head Neck Surg. 2008;138:353–356.
Additional Reading
Gladstone HB, Jackler RK, Varav K. Tympanic membrane wound healing. An
overview. Otolaryngol Clin North Am. 1995;28:913–932.
Golz A, Netzer A, Joachims HZ, et al. Ventilation tubes and persisting

tympanic membrane perforations. Otolaryngol Head Neck Surg.
1999;120:524–527.
Codes
ICD9
382.01 Acute suppurative otitis media with spontaneous rupture of eardrum
384.20 Perforation of tympanic membrane, unspecified
872.61 Open wound of ear drum, uncomplicated
Intermetatarsal (Morton's) Neuroma
Alan Zakaria
Robert B. Kiningham
Basics
Description
An inflammatory fibrosing process of the interdigital nerve characterized by pain on the
plantar surface of the foot
Most commonly occurs between the heads of the 3rd and 4th metatarsals, although may also
involve the 2nd and 3rd intermetatarsal space
Occurs just before the nerve bifurcates at the metatarsal area to innervate sides of 2
adjacent toes
Usually unilateral symptoms
Epidemiology
Occurs more often in women than men
Found in kickboxers, ballet dancers, and runners
Etiology
Caused by nerve thickening from repetitive dorsiflexion of the toes, causing microtrauma to
the nerve as it is compressed either under the transverse metatarsal ligament or by an
inflamed intermetatarsal bursa (1)
The repetitive trauma causes swelling of the plantar digital nerve that pathologically
resembles other nerve entrapment syndromes
Diagnosis
Physical Exam
Intermittent, episodic pain, usually on the plantar surface of the foot between the 3rd and 4th
metatarsals
Forefoot pain radiating to the affected interspace, toes, and ankle (1)[C]
Paresthesias in the toes and interdigital space are common (1)[C].
Pain exacerbated with exercise and relieved with rest
Tenderness to palpation on the plantar surface of the foot, usually between the 3rd and 4th
metatarsals
Mulder's click: Audible, painful click after compressing the metatarsal heads and releasing
the forefoot (1)[C]
No weakness noted on strength testing of the foot

Primarily a clinical diagnosis
Imaging usually not needed
Imaging
X-ray imaging can be used to exclude other causes of foot pain.
Electromyography and nerve conduction studies are not helpful.
MRI may show neuroma and edema surrounding the interdigital nerve (2)[A].
Metatarsalgia
Metatarsal stress fracture
Ganglion cyst
Neuropathies (diabetic, alcoholic, toxic, nutritional)
Freiberg's disease (osteochondrosis of the head of the metatarsal in teenagers)
Treatment
Conservative treatment is almost always indicated initially.
Wide toe box shoes or open footwear
Avoid repetitive toe dorsiflexion activities.
Metatarsal pad proximal to the affected interspace may be helpful (1)[B].
If conservative measures are unsuccessful or unhelpful, injection of the
intermetatarsal bursa with corticosteroid may help (3)[B].
NSAIDs for pain
If nonpharmacologic and acute treatments do not give sufficient relief, surgical
treatment has been shown to be successful (4)[A].
References
1. McKean KA. Neurologic running injuries. Neurol Clin. 2008;26:281–296;
xii.
2. Zanetti M, Weishaupt D. MR imaging of the forefoot: Morton neuroma and

differential diagnoses. Semin Musculoskelet Radiol. 2005;9:175–186.
3. Shapiro BE, Preston DC. Entrapment and compressive neuropathies. Med

Clin North Am. 2009;93:285–315, vii.
4. Akermark C, Saartok T, Zuber Z. A prospective 2-year follow-up study of

plantar incisions in the treatment of primary intermetatarsal neuromas
(Morton's neuroma). Foot Ankle Surg. 2008;14:67–73.
Additional Reading
Toth C. Peripheral nerve injuries attributable to sport and recreation. Neurol
Clin. 2008;26:89–113.
Codes
ICD9
Interphalangeal Collateral Ligament Sprain
Matt Roth
Basics
Description
Injury to a collateral ligament at the interphalangeal joint of the finger, usually the proximal
interphalangeal joint (PIP):
1st degree: Pain, but no laxity with stress
2nd degree: Pain and laxity but firm endpoint with stress
3rd degree: Pain and loss of firm endpoint with stress
Mechanisms: Abduction or adduction force applied to the finger, usually while extended
Synonym(s): Mild injuries: Jammed finger
Epidemiology
Incidence
1st- and 2nd-degree sprain much more common than 3rd-degree sprain
Index finger most often affected
Radial collateral ligament (RCL) more often affected than ulnar collateral ligament (UCL)
Risk Factors
Ball-handling and contact sports: Football, basketball, volleyball, wrestling
Prior injury or dislocation of the PIP joint
Diagnosis
History
Finger struck by player or ball during play
Axial trauma causing forced ulnar or radial deviation of joint
Usually presents acutely in 1st few weeks but may become chronic
Physical Exam
Pain and swelling over lateral aspects of PIP joint
Decreased range of motion (ROM) secondary to pain and swelling
Instability in more severe injuries
Confirm neurovascular integrity, especially with on-field assessment.
Ensure that maximum tenderness is over lateral aspects and not dorsal (suggestive of central
slip injury, which can have significant consequences if missed).
Stability is best evaluated for with the metacarpophalangeal (MCP) joint kept in 90 degrees
of flexion and the PIP joint stressed in both extension and 20–30 degrees of flexion (1)[C].
Compare with uninjured fingers.
Use gentle force to avoid overstressing joint and extending partial tear into a complete tear.
Instability with lateral stress (opening beyond 20 degrees or lack of firm endpoint) suggests
loss of integrity.
Assess function of flexor and extensor tendons by isolating MCP, PIP, and distal
interphalangeal (DIP) joints separately to rule out tendon injury.
Loss of active ROM may be due to either pain or volar plate/central slip injury, so digital
block may be necessary to test ROM (2)[C].

Imaging
Plain radiographs are generally not required for 1st-degree injuries but may be considered
for 2nd- or 3rd-degree injuries or to rule out additional bone injury.
Minimum requirement of posteroanterior, true lateral, and oblique radiographs of involved
fingers (2)[C]
May be associated with avulsion fracture at ligamentous insertion
Look for dorsal subluxation to suggest instability
US is an emerging diagnostic tool in the evaluation of finger ligament integrity (1)[C].
Phalangeal fracture
IP dislocation
Central slip injury
Volar plate injury
Often associated with one or more of above
Treatment
Immobilization:
Treatment is guided by which finger is involved, level of activity, and degree of
pain and disability.
In general, finger should be “buddy taped” to finger adjacent to injured
ligament, except that the ring finger should be secured to 5th digit (small
finger)—regardless of ligament affected— to avoid unprotected 5th digit (3)
[C].
Mild injures may be “buddy taped,” and patient may consider return to play
depending of function and sport requirements (1)[C].
1st degree: “Buddy tape” continuously for 10–14 days; then during physical
activity for an additional 2–4 wks (3)[C].
2nd degree: Splint in 30 degrees of flexion acutely; decrease flexion by 10
degrees per week; once full extension, “buddy tape” during physical activity
for an additional 4–6 wks (3)[C].
3rd degree: Some treat as severe 2nd degree, but surgery may be warranted
if “unstressed instability,” tissue interposition limiting joint motion, or lack of
joint congruity is observed on radiographs (3)[C].
Rehabilitation: Depending on severity, begin passive ROM exercises in 1st
week and active ROM after 1–2 wks, later for more severe injuries (3)[C].
Displaced intraarticular and large avulsion fractures with displacement may
require open reduction and internal fixation (ORIF) (2)[C].
Hyperextension and/or dorsal dislocation injuries and central tenderness over
the volar aspect should raise concern for volar plate injuries.
Central tenderness over the dorsal PIP joint suggests central slip injury, which
can lead to a chronic boutonniere deformity.
Collateral ligament injury in children should raise concern for growth plate
involvement, and there should be a low threshold for referral to a hand specialist
(1)[C].
Generally necessary if instability with active ROM, tissue interposition limiting
joint motion, or lack of joint congruity is observed on radiographs (2)[C].
Routine surgical repair for all complete tears is controversial (2)[C].
Pro: Helps to ensure stability of pinch (especially in radial collateral ligament
of index finger), shorter duration of disability
Con: Most complete tears heal well with conservative treatment; operative
trauma may limit joint motion.
ORIF usually necessitates 4 wks of activity limitation following surgery (2)[C].
Ongoing Care
Follow up in 1–2 wks for reevaluation of laxity.
Refer significant fractures for possible ORIF (2)[C].
If uncertain of possible central slip/volar plate injury, refer to surgeon or follow up in 7–10
days for reevaluation (2)[C].
Chronic disability may be seen in athletes with delayed presentation or multiple dislocations
(2)[C].
Chronic symptoms may respond to extended splinting and “buddy taping” with protected
ROM exercises for several weeks to months (2)[C].
Surgical repair may be indicated if disability and instability persist after a sufficient trial of
conservative treatment (2)[C].
Patient Education
Advise patients that some persistent deformity may be noted after injury has healed.
References
1. Leggit JC, Meko CJ. Acute finger injuries: part I. Tendons and ligaments. Am Fam
Physician. 2006;73:810–816.
2. Freiberg A, Pollard BA, Macdonald MR, et al. Management of proximal interphalangeal

joint injuries. Hand Clin. 2006;22:235–242.
3. Morgan WJ, Slowman LS. Acute hand and wrist injuries in athletes: evaluation and
management. J Am Acad Orthop Surg. 2001;9:389–400.
Additional Reading
Alexy C, De Carlo M. Rehabilitation and use of protective devices in hand and wrist injuries.
Clin Sports Med. 1998;17:635–655.
Palmer RE. Joint injuries of the hand in athletes. Clin Sports Med. 1998;17:513–531.
Codes
ICD9
842.13 Sprain of interphalangeal (joint) of hand
Clinical Pearls
Ensure active ROM in all affected and surrounding joints to rule out more
significant ligamentous injuries.
Return to play depends on finger affected and demands of sport, but frequently,
immediate return to play can be accomplished with “buddy taping” and/or
splinting with some risk for further injury.
Some residual soreness can be expected for months and sometimes up to a
year.
The joint affected may appear permanently enlarged owing to scarring during
the healing process.
Intersection Syndrome
Jennifer Scott Koontz
Basics
Description
Intersection syndrome is an inflammatory condition located in the distal radial forearm where
the tendons of the 1st extensor compartment cross over the tendons of the 2nd
compartment.
Patient usually presents with pain, crepitus, and squeaky sensation in the dorsal distal
forearm. May have localized swelling.
Pain usually occurs about 4 cm (range of 4–8 cm) proximal to the radial styloid.
Synonym(s): Oarsman's wrist; Crossover syndrome; Squeaker's wrist; Peritendinitis
crepitans
Epidemiology
Most common in rowers and weight lifters
Skiers, other athletes, or workers that do repetitive forceful wrist flexion and extension
activities are also at risk.
Risk Factors
Sports with increased risk include:
Rowing (1)
Weightlifting
Skiing
Racquetball
Tennis
Any activity with repetitive forceful flexion and extension of the wrist
Etiology
The abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons comprise the
1st compartment.
The extensor carpi radialis longus (ECRL) and brevis (ECRB) tendons comprise the 2nd
compartment.
Friction occurs at the intersection where the APL and EPB of the 1st compartment cross over
the tendon sheath of the ECRL and ECRB in the 2nd compartment.
This results in a tenosynovitis of the 2nd compartment.
Diagnosis
History
Commonly misdiagnosed as de Quervain's tenosynovitis
History of increase in activity that requires repetitive wrist flexion/extension
Athletes will report pain in the distal forearm or radial side of wrist, typically 4 cm (range of
4–8 cm) proximal to the radial styloid. May complain of localized swelling and a squeaking
sensation.
Physical Exam
Localized swelling 4–8 cm proximal to the radial styloid may be present.
Crepitus on palpation is classic for intersection syndrome.
Pain exacerbated by ulnar deviation of the hand
Movement of wrist typically causes more pain than movement of thumb, as seen in de
Quervain's
Bony palpation is typically nontender, and neurovascular status should be intact.

Imaging
Radiographs should be taken to rule out any underlying abnormalities. Anteroposterior,
lateral, and oblique views of the wrist and distal forearm should be obtained.
If US is available, this could be helpful for differentiating intersection syndrome from other
disorders (2)[C].
MRI would not be indicated in the initial evaluation of this syndrome. If diagnosis is not clear
or pain is persistent, MRI could be considered to evaluate for soft tissue masses or bony
abnormalities. The MRI may need to be extended to include the forearm in addition to the
wrist (3)[B].
De Quervain's tenosynovitis
Extensor pollicis longus tendinitis (drummer boy palsy)
Wartenberg's syndrome (neuritis of superficial radial nerve)
Degenerative joint disease of carpometacarpal joint
Radial styloid fracture
Scaphoid fracture
Treatment
Initial treatment (for 2–3 wks):
Rest
Ice
NSAIDs
Thumb spica splint in 15–20 degrees of extension
All treatment requires subsequent activity modification to prevent recurrence.
Occupational therapy may be helpful for stretching program, local swelling
reduction, and to help with activity modification.
If no relief with NSAIDs, a short course of oral prednisone may be given.
Injection is usually reserved after no improvement with 2–3 wks of splinting and
activity modification.
2–3 mL of a local anesthetic and steroid combination may be injected into the
area of maximal swelling.
Surgery is reserved for recalcitrant cases.
Surgery may include tenosynovectomy or bursectomy.
Ongoing Care
If no improvement after adequate course of conservative therapy, surgical referral is
warranted.
Surgery may be needed if fibrosis of the tendon sheath has occurred (4).
Prognosis
Recovery is usually achieved after initial treatment of activity modification, splinting, and
NSAIDs for 2–3 wks. A 60% recovery response to conservative therapy has been reported
(5).
If surgery is necessary, postoperative rehabilitation typically lasts 4–6 wks.
Return to play may occur once symptoms have resolved.
References
1. Rumball JS, Lebrun CM, Di Ciacca SR, et al. Rowing injuries. Sports Med. 2005;35:537–
555.
2. De Maeseneer M, Marcelis S, Jager T, et al. Spectrum of normal and pathologic findings

in the region of the first extensor compartment of the wrist: sonographic findings and
correlations with dissections. J Ultrasound Med. 2009;28:779–786.
3. Lee RP, Hatem SF, Recht MP. Extended MRI findings of intersection syndrome. Skeletal
Radiol. 2008.
4. Fulcher SM, Kiefhaber TR, Stern PJ. Upper-extremity tendinitis and overuse syndromes
in the athlete. Clin Sports Med. 1998;17:433–448.
5. Grundberg AB, Reagan DS. Pathologic anatomy of the forearm: intersection syndrome. J
Hand Surg [Am]. 1985;10:299–302.
Additional Reading
Rettig AC. Wrist and hand overuse syndromes. Clin Sports Med. 2001;20:591–611.
Codes
ICD9
726.4 Enthesopathy of wrist and carpus
Clinical Pearls
Intersection syndrome is an overuse syndrome.
Pain is located 4–8 cm proximal to radial styloid.
Athletes will often report a squeaking sensation in their wrist.
Be able to consider both intersection syndrome and de Quervain's
tenosynovitis in the differential of distal forearm pain.
The mainstay of treatment is conservative, utilizing activity modification and a
short course of NSAIDs and thumb-spica splinting.
Intraocular Foreign Bodies
Kevin N. Waninger
Basics
Epidemiology
The presentation, outcome, and prognosis of intraocular foreign bodies (IOFBs) are variable.
Adults: Often in industrial accidents (hammering, metal on metal contact, blast injury, high-
speed machines like drills, grinding wheels, saws, windy weather)
Children: Often with explosives, weapons, windy weather
Similar to most other traumatic injuries, the peak incidence is found in the 2nd and 3rd
decades and generally in males younger than 40 yrs of age.
Mostly accidental work-related injuries, although increasingly related to home and leisure
activity accidents
Risk Factors
Protective eyewear of appropriate quality (3 mm of polycarbonate) prevents virtually all injuries
from IOFBs (1).
General Prevention
Wear appropriate protective eyewear in any situation (sports, construction, workshops,
industries) that may lead to a higher risk of particles or objects getting into the eyes.
The eyes should not be rubbed while working with wood or metal pieces. If a foreign body
should enter an eye, no attempt should be made by the patient to remove the foreign body if
perforation is suspected. If perforation is not suspected, eye irrigation may be attempted to
wash out any potential foreign bodies.
Use particular caution with explosives.
Diagnosis
Superficial foreign bodies that are removed after the injury typically leave no permanent
sequelae. However, corneal scarring and infection may occur, and the longer the time interval
between the eye injury and subsequent treatment, the greater the likelihood that
complications may occur.
Morbidity greatly increases if the foreign body penetrates into the anterior or posterior
chambers, as damage to the iris, lens, and retina can occur and severely affect visual acuity.
Any IOFB can lead to infection and endophthalmitis, which can threaten loss of the eye.
Pre Hospital
Place a shield over the eye, both eyes if IOFB with globe perforation is suspected.
Position patient sitting upright.
History
The activities of the patient and their surroundings at the time of injury are important and
should lead to a high index of suspicion for IOFB.
Common complaint: “Something flew into my eye”
Past medical history should be obtained, including prior surgeries, medications, allergies,
tetanus status, last meal (if surgery is a possibility).
Visual acuity and correction with contacts (daily- or extended-wear) or glasses
Inquire whether the patient was wearing eye protection at the time of injury. Try to find out
what type of eyewear, if so, and whether they are still intact.
Composition of suspected foreign body is important:
Organic: Wood, soil, plants, insect parts
Inorganic material: Oxidizes (iron, copper)
Inert material: Paint, glass, plastic, fiberglass, nonoxidizing metals, sand
Physical Exam
Note that IOFBs can be deceptively subtle on initial presentation. The symptoms of an ocular
foreign body may range from irritation to intense, excruciating pain. This is dependent on the
location, material, and type of injury.
Note that high-speed projectiles may not produce pain or visual acuity problems initially, as
the foreign body may be located below the epithelial or conjunctival surface. A fully dilated
eye exam may be necessary to visualize all aspects of the eye.
Eye pain/foreign body sensation (typically relieved significantly by topical anesthesia)
Redness
Tearing
Blurred/decreased vision
Light sensitivity (photophobia)
Visible foreign body or rust ring
Difficulty opening the eye
A complete examination of both eyes is necessary, including visual acuity and fields, lid
eversion to check for retained FB, pupil size, shape, and reactivity.
Slit lamp, fluorescein, and funduscopic examinations should be performed as soon as
possible. Perform intraocular pressures if there is no evidence of perforation.
Minimize manipulation of the globe and exercise caution during examination if perforation is
suspected to prevent prolapse of ocular contents.
Document corneal irregularities, wound location and size, if visible, as well as blood in the
anterior chamber or vitreous.
Note normal or decreased visual acuity, any conjunctival injection, ciliary injection (especially if
an anterior chamber reaction occurs), any visible foreign body, any rust ring (especially if a
metallic foreign body has been embedded for at least several hours), any epithelial defect
that stains with fluorescein, any corneal edema, and anterior chamber cells/flare.
If a corneal infiltrate is present, an infectious cause needs to be considered.
Use the Seidel's sign to look for globe penetration that is not so obvious. In the case of a
positive Seidel's sign, the oozing aqueous humor at the site of the penetration through the
cornea appears under ultraviolet light as a “dark waterfall,” clearing away excess fluorescein
on the cornea.
Minimize manipulation of the globe and exercise caution during examination to prevent
prolapse of ocular contents.
Document baseline visual acuity, visual fields, pupillary size, shape and reactivity, corneal
irregularities, wound location and size, depth of the anterior chamber, iris and lens condition,
blood in the anterior chamber or vitreous, gaze restriction, and external examination.
History, physical, and imaging studies should be used to assess number, size, shape,
location, composition, visibility, trajectory, and accessibility of the IOFB.

Lab
Unless an infectious corneal infiltrate/ulcer or an intraocular foreign body is suspected, no
laboratory work is indicated.
Infectious corneal infiltrates/ulcers generally require scrapings for smears and cultures.
Imaging
Orbital CT with 0.5-mm axial and coronal cuts
Radiographs have low sensitivity for small and nonmetallic objects, but can be used for
metallic FBs if CT not available.
β-scan US, with caution due to risk of ocular prolapse
MRI: Initially contraindicated due to risk of magnetic properties, but may be used to localize
small nonmetallic IOFBs after metallic IOFBs ruled out by CT scan
Ultrasound biomicroscopy
Corneal abrasion
Conjunctival and corneal foreign bodies
Corneal perforation
Ruptured globe
Other trauma without retained IOFB
Corneal ulcer
Keratitis, bacterial and/or fungal
Treatment
No topical medications or ointments if globe perforation is suspected
Topical anesthetic to assist examination and decrease discomfort
(proparacaine/tetracaine) unless with obvious globe perforation
Minimize nausea and vomiting to prevent resultant increase in intraocular
pressure.
Pediatric patients may require sedation to facilitate examination and FB
removal.
Shield should be placed over involved eye, avoiding any pressure on the globe.
Both eyes should be shielded to prevent contralateral eye movement if globe
perforation is suspected.
Topical antibiotics may be started until the epithelial defect heals to prevent
infection.
If perforation is suspected, systemic antibiotics prior to surgical intervention
may be started.
Topical corticosteroids may be used to decrease inflammation (controversial,
must rule out herpes infection)
Initiate topical cycloplegic agents for pain and photophobia. P.
Update tetanus if indicated
Liberal use of pain medications; these injuries may be very painful.
Corneal patching is no longer recommended (2)[A].
ED Treatment
Deep penetrating foreign bodies:
Deep penetrating foreign bodies require immediate referral to an
ophthalmologist, because endophthalmitis and permanent scarring may
occur, and delayed surgical removal is associated with significantly worse
outcomes.
Superficial foreign bodies:
Superficial foreign bodies can be removed manually by those who are trained
in the technique. Anesthesia (topical anesthetic ophthalmic solution) is
necessary prior to foreign body removal and usually facilitates initial eye
examination.
The procedure's benefits, risks, and complications must be explained to the
patient, or to the patient's representative, and an informed consent obtained.
A negative Seidel's sign must be obtained.
If the foreign body is superficial, the eye should be irrigated to moisten the
cornea. Removal of the foreign body should be attempted by using a gentle
rolling motion with a wetted cotton-tipped applicator. Pressure should not be
applied, as this may push the foreign body deeper into the cornea or scrape
it, creating a large corneal abrasion. An attempt to wash the foreign body off
the cornea should be done by directing a stream of normal saline at an
oblique angle to the cornea.
An embedded foreign body should not be removed with irrigation or with a
cotton-tipped applicator.
An embedded foreign body should be removed by using a gentle flicking
motion with an eye spud, if available, or with a 25- or 27-gauge needle. Using
a slit lamp to visualize the FB and to immobilize the patient's head, the hub of
the needle may be placed on the tip of a cotton swab or a 3-mL syringe. The
cornea may be approached from the side, with the needle in a plane tangent
to the cornea and the bevel away from the corneal surface. This minimizes
the chance of corneal perforation. Once dislodged from its embedded
position on the cornea, remaining corneal debris can be removed with a
wetted cotton-tipped applicator.
Within 3 hr, iron-containing foreign bodies oxidize, leaving a rust stain on
adjacent epithelial cells, which can delay healing and act as an irritant focus.
Removal with 25-gauge needle or a pothook burr at the same time as FB
removal, or within 24 hr, is recommended. Rust rings that remain in the
cornea after removal of a metallic foreign body that cannot be manually
removed will require ophthalmology removal with a rust ring drill (1,3,4)[B].
Documenting a negative Seidel's sign after the removal of a corneal foreign
body is good practice, especially after using a sharp instrument, to confirm
that no iatrogenic penetration of the cornea occurred during the procedure
(5,6)[C].
Medication
Topical anesthetics prolong epithelial healing and should never be prescribed
for home pain relief (1,4,7)[C].
Ophthalmic NSAIDs appear to be useful for decreasing pain in patients with
corneal injury (8)[A].
Referral
Patients who present to the emergency department with emergent conditions
should be referred to an ophthalmologist on the day of presentation. Patients
with urgent conditions can be seen the following day.
Emergent conditions:
Hyphema (blood in the anterior chamber)
Diffuse corneal defect or opacity
Laceration of the cornea or sclera
Single dilated pupil or an abnormally shaped pupil
A more deep or shallow anterior chamber (when compared to the other eye)
Possible penetration of the globe
Positive Seidel's sign
Multiple foreign bodies
Extremely uncooperative patient (eg, young child, intoxicated individual,
patient with mental disability)
Urgent conditions:
Significant lid edema
Diffuse subconjunctival hemorrhage
Large corneal abrasion
Corneal ulceration
If the examination in the office or the emergency department is not good enough
to rule out a foreign body or ocular perforation, then an examination under
anesthesia should be considered. This is especially true for children, where there
should be a low threshold to examine the patient in the operating room.
Admission Criteria
Foreign bodies that present any potential for intraocular penetration must by
explored in the operating room. These injuries should be explored within 24 hr of
initial examination.
Discharge Criteria
All corneal foreign bodies: Follow-up in 24–48 hr for reexamination.
If rust rings were not completely removed, follow-up should be made with
ophthalmology within 24 hr.
Ongoing Care
Patient Monitoring
Follow up every 1–2 days until the epithelial defect is well healed and corneal infiltrates have
resolved.
No activity or positioning restrictions are necessary once the wound heals.
A gonioscopy should be performed after resolution of the problem. Annual follow-up care for
intraocular pressure should be planned if the severity of trauma raises a suspicion for angle-
recession glaucoma in later life.
A dilated fundus examination should be performed on a routine basis after any injury severe
enough to potentially damage the retina.
Patient Education
Eye protection when taking part in risky activities (eg, hammering, mowing the lawn) is strongly
recommended.
Prognosis
Prognosis is good unless a rust ring or scarring involves the visual axis. If infection develops,
prognosis is more guarded. Globe-penetrating injuries and intraocular foreign bodies have much
worse prognoses, but reading vision is usually retained/regained, if properly treated.
Complications
Endophthalmitis, corneal scarring, elevated intraocular pressure, cataract, retinal
detachment, proliferative vitreoretinopathy, and metallosis (eg, chalcosis,
siderosis) are possible complications.
References
1. Kuhn F, Wong DT, Giavedoni L. Foreign body, intraocular. Updated
December 3, 2008. Accessed: September 19, 2009.
2. Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database

Syst Rev. 2006;CD004764
3. Weichel ED, Yeh S. Techniques of intraocular foreign body removal. Tech

Ophthalmology. 2009;7:45–52.
4. Bashour M. Corneal foreign body. Emedicine.medscape.com. Updated

June 30, 2008. Accessed September 19, 2009.
5. Yeh S, Colyer MH, Weichel ED. Current trends in the management of

intraocular foreign bodies. Curr Opin Ophthalmol. 2008;19:225–233.
6. Coa CE, Hackett TS. Foreign body removal, cornea.

Emedicine.medscape.com. Updated May 21, 2009. Accessed on September
19, 2009.
7. Greven CM, Engelbrecht NE, Slusher MM, et al. Intraocular foreign bodies:
management, prognostic factors, and visual outcomes. Ophthalmology.
2000;107:608–612.
8. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do

ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated
with simple corneal abrasion without delaying healing? Ann Emerg Med.
2003;41:134–140.
Additional Reading
Peate WF. Work-related eye injuries and illnesses. Am Fam Physician.
2007;75:1017–1022.
Codes
ICD9
930.0 Corneal foreign body
930.1 Foreign body in conjunctival sac
930.2 Foreign body in lacrimal punctum
Klippel-Fiel Syndrome: Fusion of Cervical Vertebrae
Tracy L. Zaslow
Basics
A malformation sequence
Clinical triad of short neck, low hairline, and fusion of multiple cervical vertebrae resulting in
decreased range of motion (ROM)
Description
First described independently by Maurice Klippel and Andre Feil in 1912. They described
patients who had the triad of short, webbed neck; decreased ROM in the cervical spine; and
a low hairline.
Original classification by Gunderson et al (1):
Type I: Massive fusion of cervical spine
Type II: Fusion of 1 or 2 cervical interspaces
Type III: Thoracic or lumbar vertebrae involved
A newer classification system by Samartzis (2,3) modifies the classification system as: Type
I patients have a single-level fusion; Type II patients have multiple, noncontiguous fused
segments; and Type III patients have multiple, contiguous fused segments.
Epidemiology
Occurrence is sporadic.
However, cases with autosomal-dominant and autosomal-recessive inheritance with variable
expression have been reported.
Incidence
The true incidence of Klippel-Feil syndrome is unknown.
Estimated as 1:40,000–42,000
General Prevention
Prevention of complications can be done by initial broad evaluation of systems commonly
affected by Klippel-Feil and regular evaluation of associated features.
Motion at each intervertebral space should be evaluated annually by lateral flexion-extension
radiographs of the cervical spine.
Etiology
Etiology of Klippel-Feil syndrome and its associated conditions are unknown.
The sequence may be a part of a serious neural tube development caused by a failure in the
normal segmentation or division of the cervical vertebrae during the early weeks (3rd and 8th
wks) of fetal development.
Other possible etiologies include vascular disruption and global fetal insult.

Klippel-Feil triad is associated with congenital abnormalities of the genitourinary tract,
musculoskeletal system, spinal cord/neurological system, cardiovascular system, and
auditory system.
Genitourinary tract:
Genitourinary (GU) tract structure abnormalities, occur in 30–40% of patients with Klippel-
Feil; double collecting systems, renal aplasia, horseshoe kidney, and recurrent
pyelonephritis are common; however, absence of a kidney is the most common finding.
The extent of cervical abnormality does not correlate with severity of GU abnormalities;
thus, thorough GU evaluation is indicated in all patients.
Musculoskeletal:
Short stature
Atlanto-axial instability
Scoliosis is present in 60% of patients with Klippel-Feil syndrome.
Scoliosis may be due to fusion in the thoracic or lumbar spine, or a developmental
compensation for the cervical/cervicothoracic scoliosis.
Cervical spinal stenosis can also occur in association with Klippel-Feil syndrome; although
uncommon, when present, cervical stenosis can increase risk of neurological involvement.
Sprengel anomaly (congenital elevation of the scapula) occurs in 20–30% of those with
Klippel-Feil. A higher than expected incidence of scoliosis occurs in those with Sprengel
anomaly.
Upper extremity abnormalities, including syndactyly, hypoplastic thumb, supernumerary
digits, and hypoplasia of the upper extremity
Cardiovascular:
Septal defects
Situs inversus
Coarctation of the aorta
Pulmonary:
Lobar agenesis
Neurological:
Chiari I malformation
Syringomyelia
Diastematomyelia
Sleep-disordered breathing
Dermoid cyst in the posterior fossa
Hereditary neuropathies
Auditory system:
Hearing impairment: Occurs in more than 1/3 of Klippel-Feil patients
Other:
Ptosis of the eye
Duane's eye contracture
Lateral rectus palsy
Facial nerve palsy
Cleft palate
Synkinesia, or mirror movement
Facial asymmetry
Craniosynostosis
Diagnosis
Clinical presentation is variable due to the presence/absence of different associated
anomalies.
Often Klippel-Feil syndrome is discovered incidentally on physical examination.
The complete triad is present in <50% of cases.
History
Often asymptomatic
Neck/back pain +/- neurological symptoms, including numbness, tingling, weakness
Decreased hearing
Physical Exam
Low hairline
Short neck
Decreased cervical range of motion; rotational loss is usually more pronounced than loss of
flexion and extension
Torticollis
Facial asymmetry
Heart examination to evaluate for heart position and murmurs
Chest examination to evaluate for rib fusion and other chest wall anomalies
Back examination for Sprengel's deformity and scoliosis

Imaging
Plain radiography (anteroposterior/lateral of the cervical spine) is the basis for the diagnosis
of Klippel-Feil syndrome.
Flexion-extension radiographs are indicated if instability is suspected at the craniocervical
junction or if 2 fused segments are separated by an open segment.
Plain radiographs of the entire spine must be obtained to detect other spinal anomalies.
Rib series radiography to evaluate for possible rib anomalies, such as multiple rib fusions,
also is necessary.
CT scanning may be done in patients being evaluated for surgery, but is not required for
diagnosis.
MRI is indicated in patients with neurologic deficits to most accurately assess subluxation,
cord compression, spinal stenosis, and additional CNS anomalies.
US of the kidneys: Indicated to screen for renal anomalies. IV pyelography should be
performed if further definition of a kidney abnormality is required.
Full age-appropriate hearing screening: Due to the high incidence of hearing loss
Congenital muscular torticollis
Acquired spinal fusion (postinfection, spine inflammatory disorders)
Wilder-Vanck (cervico-oculo-acoustic) syndrome
Mayer-Rokitansky-Kaster syndrome
Cervical spina bifida
Congenital scoliosis
CNS lesion (brain tumor)
Iniencephaly
Dyssegmental dysplasia
Treatment
No known treatment for underlying etiology
Treatment is symptomatic, which includes modification of activities, bracing,
and, for subluxation, traction. Response to traction may also predict the
success of surgery.
Surgical interventions should be delayed as long as possible. Indications for
surgery include progressive symptomatic segmental instability and neurological
compromise.
Physical therapy may help to maximize range of motion and minimize functional
limitations.
General activity limitations, even without presence of symptoms or instability:
Avoid contact sports.
Avoid occupations and recreational activities with risk of head and neck
trauma.
Sports participation limitations (4):
All types: Avoid contact sports and activities with risk of head and neck
trauma.
Type I: Absolute contraindication to participation in contact sports.
Type II:
Fusion of 1 or 2 interspaces at C2 or above with limited cervical range of
motion, occipitocervical anomalies, involvement of C2, instability, disc
disease, or degenerative changes → Absolute contraindication.
Fusion of 1 or 2 interspaces at C3 or below with full cervical range of
motion AND no occipitocervical anomalies, no involvement of C2, no
instability, no disc disease, and no degenerative changes → No additional
contraindications.
Surgical interventions should be delayed as long as possible.
Indications for surgery include progressive symptomatic segmental instability,
neurological compromise, and/or severe scoliosis.
Surgical techniques involve occipitocervical arthrodesis, halo immobilization,
and atlantoaxial arthrodesis.
Ongoing Care
Patient Monitoring
Annual cervical spine radiographs to evaluate for instability
Additional follow-up studies based on individual system involvement
Patient Education
If hypermobility is noted in the upper cervical segment, there is increased risk of developing
neurological impairment and patients should not be cleared for activities that increase risk of
neck injury (ie, gymnastics, cheerleading, contact sports).
Prognosis
Prognosis is good if features of the disorder are treated early and appropriately.
If hypermobility is noted in the upper cervical segment, there is increased risk of developing
neurological impairment and patients should not be cleared for activities that increase risk of
neck injury (ie, gymnastics, cheerleading, contact sports).
If hypermobility is noted in the lower cervical segment, there is increased risk for
degenerative disk disease and patients should be treated symptomatically and held from
sports based on symptoms.
References
1. Gunderson CH, Greenspan RH, Glaser GH, et al. The Klippel-Feil syndrome: genetic and
clinical reevaluation of cervical fusion. Medicine (Baltimore). 1967;46:491–512.
2. Samartzis D, Herman J, Lubicky JP, et al. Sprengel's deformity in Klippel-Feil syndrome.

Spine. 2007;32(18):E512–E516.
3. Samartzis DD, Herman J, Lubicky JP. Classification of congenitally fused cervical patterns
in Klippel-Feil patients: epidemiology and role in the development of cervical spine-related
symptoms. Spine. 2006;31(21):E798–E804.
4. Wheeless, CR. Klippel Feil Syndrome. In Wheeless' textbook of orthopaedics. Data

Trace Internet Publishing, 1995–2009.
Additional Reading
Brown MW, Templeton AW, Hodges FW III. The incidence of acquired and congenital
fusions in the cervical spine. Am J Roentgenol. 1964;94:1255–1259.
Driscoll DJ, Rigamonti D, Gailloud P. Klippel-Feil Syndrome, Chapter 20. In The National
Organization of Rade Disorders, NORD Guide to Rare Disorders. Philadelphia, PA:
Lippincott Williams and Wilkins, 2003:720.
Gjorup PA, Gjorup L. Klippel-Feil's syndrome. Dan Med Bull. 1964;11:50–53.
Hensinger RN, Lang JE, MacEwen GD. Klippel-Feil syndrome; a constellation of associated
anomalies. J Bone Joint Surg Am. 1974;56(6):1246–1253.
Klippel-Feil Sequence. In Jones KL. Smith's Recognizable Patterns of Human

Malformation, 5th Edition. Philadelhia, PA: W.B. Saunders Company, 1997;618–619.
Klippel-Feil Syndrome, 686.2. In Behrman RE, Kliegman RM, Jenson HB. Nelson Textbook
of Pediatrics, 16th Edition, Philadelphia, PA: W.B Saunders Company, 2000;2090.
McGaughran JM, Kuna P, Das V. Audiological abnormalities in the Klippel-Feil syndrome.

Arch Dis Child. 1998;79(4):352–355.
Thomsen MN, Schneider U, Weber M, et al. Scoliosis and congenital anomalies associated
with Klippel-Feil syndrome types I–III. Spine. 1997;22:396–401.
Codes
ICD9
756.16 Klippel-Feil syndrome
Clinical Pearls
When examining the back, always look at the scapula for Sprengel's deformity.
If Sprengel's deformity is observed, consider C-spine x-rays to rule out fusion
associated with Klippel-Feil syndrome.
Knee Dislocation
Jane Kim
Basics
Knee dislocation is a rare but potentially devastating injury. It may lead to amputation or
inability to return to full function.
The true incidence of knee dislocations is unknown owing to frequent spontaneous reduction.
Missed spontaneous reductions may cause detrimental neurovascular damage. It is
unnecessary to have complete dislocation for injury to the intimal wall of the popliteal artery
(1,2,3).
High-velocity mechanism is a sudden violent force such as in a motor vehicle accident, falls
from skiing, and injuries from gymnastics and extreme sports. They are usually associated
with increased risk for neurovascular damage owing to more extensive disruption to the joint
capsule.
Low-velocity injuries are usually due to sports such as football or rugby and usually have less
soft tissue damage with better prognosis.
There are 6 structures within the knee that are at risk of injury with knee dislocation: Anterior
cruciate ligament (ACL), posterior cruciate ligament (PCL), medial cruciate ligament (MCL),
lateral cruciate ligament (LCL), medial meniscus, and lateral meniscus.
The popliteal artery sits within the popliteal fossa with branches to the collateral artery
supply. The geniculate collateral arteries cannot compensate for a ruptured popliteal artery.
The peroneal nerve wraps around the fibular head.
The definition of a knee dislocation is complete displacement of the tibia in regard to the
femur with 3 or more stabilizing ligaments torn.
It is unnecessary to have complete dislocation for injury to the intimal wall of the popliteal
artery.
Traditionally, 2 cruciate ligaments and 1 collateral ligament are torn; however, both cruciates
do not have to be torn. Any 3 stabilizing ligaments torn is considered a dislocated knee.
The popliteal artery is damaged owing to the close proximity to the knee joint. It passes
under the adductor canal cephalad and attaches to the soleus muscle caudad, which restricts
its ability to stretch. Damage to the intimal wall of the popliteal artery may not be physically
evident initially.
If vascular repair is not performed within 8 hr of injury, above-knee amputations are near
90% (1,3,4).
Cautions:
Documentation of pulses and motor response is essential.
Splint in slight flexion to prevent traction or compression of the popliteal artery.
Description
Defined by the position of the tibia in relationship to the distal femur
Anterior dislocation:
Most common dislocation; accounts for 60%
Hyperextension of the knee
Rupture of the posterior capsule at 30°
Rupture of the PCL and popliteal artery (PA)
Posterior dislocation:
Direct blow to the anterior tibia with the knee flexed at 90 degrees
ACL is usually spared.
Medial dislocation: Varus stress causing tear to ACL, PCL, and LCL
Lateral dislocation: Valgus stress causing tear to ACL, PCL, and MCL
Rotary dislocation:
Twisting mechanism (planted foot and body twis-ting in opposite direction) that can be
further divided into anteromedial, anterolateral, posterolateral
Posterolateral dislocations are nearly impossible to be reduced by closed method.
Popliteal artery injury:
PA injury occurs in up to 30% of dislocations.
If vascular injury is not reversed within 6–8 hr, amputation rate approaches 90%.
Anterior dislocations place traction on the PA and cause contusion or intimal injury, which
may result in delayed thrombosis.
Posterior dislocations cause direct intimal fracture or transection of the artery with
immediate thrombosis.
Peroneal nerve injury:
Less common than arterial injury: If present, must rule out concomitant arterial insult.
Characterized by hypesthesia at 1st web space and lack of dorsiflexion of the foot
Poor prognosis for recovery
Medial dislocations cause injury by traction to the nerve.
Rotatory injuries have a high incidence of traction and transection.
Epidemiology
Up to 50% of knee dislocations reduce spontaneously; therefore, the actual incidence is
unknown (2,3,4).
The most common mechanism of injury is a motor vehicle accident.
>50% of dislocations occur owing to anterior/posterior dislocation; most common cause for
PA damage.
There is 10–40% PA injury rate with any knee dislocation
The peroneal nerve is injured close to 25% of the time; up to 50% of patients have
permanent deficit (3,4).
Prevalence
Motor vehicle accidents (MVAs; 50–60%)
Falls (30%)
Industrial accidents (3–30%)
Sports (7–20%); on the rise owing to more extreme sports
Risk Factors
Morbid obesity is a potential risk factor for posterior dislocations.
Contact or high-velocity sports
Etiology
High-energy injuries such as MVAs, auto versus pedestrian accidents, and athletic injuries
Football is the most common source of athletic injuries.
Diagnosis
Suspect a relocated knee dislocation if the patient had a high-impact injury with
excessive knee laxity in full extension.
The initial physical exam may be difficult owing to excessive swelling and pain.
If peripheral pulses are normal initially, it is essential to do serial, frequent exams with
documentation of pulses (1)[C].
Estimated 5–15% of knee dislocations may have a strong distal pulse initially with delayed
expansion of intimal tear (1,5,6)[B].
Complete and careful physical exam, including:
Pulses: By palpation, Doppler, ankle-brachial pressure indexes, and distal perfusion (1)[C]
Neurologic: Sensation to the 1st web space and great toe, movement of the toes,
dorsiflexion of the foot
Knee x-rays: Fractures common (periarticular, avulsion fracture, tibial plateau)
MRI
Repeat examination if any closed reduction is attempted.
Arterial imaging (“gold standard”) if any signs of limb ischemia (1,3)[A]
Pre Hospital
If covering a game or event with potential high-impact injuries, initially assess for life-
threatening injuries.
Basic life support: ABCs; assess for head and neck injury.
If knee dislocation is suspected, immediate neurovascular assessment becomes the focus of
the evaluation. Remove shoes and socks for better neurovascular exam only if safe.
Compare posterior and dorsal pedal pulses bilaterally. Compare dermatomes, capillary refill,
skin color, skin temperature, and motor strength (3,4)[C].
Splint in slight flexion (15–20 degrees) (1,3)[C].
Transfer to a facility capable of immediate reduction.
History
Patient will usually hear a pop at time of injury.
There is usually significant pain and swelling to knee immediately with decreased range of
motion. However, there may be delayed swelling and effusion depending on the amount of
capsular damage and fluid extravasation (4).
Have patient describe mechanism of injury, if possible.
Physical Exam
Subjective pain, instability, and swelling
Look at skin, palpate for pulses (DP/PT/popliteal)
Sensation, motor examination
Grossly deformed knee/asymmetry
Grossly unstable knee in anterior/posterior plane or on varus/valgus stress:
ACL and PCL, collateral ligament injuries
Suspect dislocation if having valgus/varus laxity with knee in extension or lack of distal
pulses.
Popliteal thrill or expanding pulsatile hematoma
Signs of distal ischemia: Pallor, paresthesias (stocking glove or 1st web space), pain,
paralysis
Unequal temperature of lower extremities

Patients with abnormal pulses who have symptoms or signs of ischemia should undergo
immediate intraoperative arteriogram or surgical exploration (1,5,7)[C].
Patients with abnormal pulses but well-perfused limb should undergo arteriography (5)[C].
Those with normal pulses and well-perfused limb should undergo either arteriography or
serial examinations depending on surgeon's preference (1,5)[C].
If no arteriogram is performed initially, observation for 24–48 hr is recommended for all
cases of knee dislocation or multiligament injury (1)[C].
Frequent neurovascular checks should be performed, usually in the ICU.
A protocol that uses serial exams that include the dorsal medial pulse for 24–48 hr has been
found to be highly sensitive and specific to detect vascular studies; however, it depends on
the examiner and consistency (1,5)[C].
Currently there is a trend toward protocols that include serial physical exams and adjunctive
studies (arterial-brachial index, duplex US) versus selective arteriography.
Adjunctive tests:
Duplex US may be able to detect injury that is non-flow-limiting (subclinical) and therefore
may increase the sensitivity for a selective angiography protocol.
Arterial-brachial index (ABI): Systolic BP from all 4 extremities with Doppler probe and BP
cuff. ABI = highest pressure from dorsal pedal pulse or posterior tibial pulse/highest
brachial BP.
Prospective study: Mills and colleagues: 11/38 patients who required vascular surgery had an
ABI <0.90.
No patients with an ABI >0.90 required vascular intervention surgery.
1 patient had normal pulses and no hard signs of ischemia but had an ABI >0.90 and was
found to have a positive arteriogram. This patient would have been missed without an ABI
study.
3 patients in this study would have undergone unnecessary arteriography.
Negative predictive value with an ABI >0.90 was 100%.
However, study is small and with no long-term follow-up.
Currently there is no conclusive evidence demonstrating any single selective angiography
protocol to be superior. Therefore, any equivocal exam must have an arteriogram
performed (1)[C].
Imaging/special tests:
Anteroposterior (AP) and lateral plain x-rays
Angiogram is indicated for any patient with poor distal perfusion, pulse return after
reduction, abnormal pulses, signs of peroneal nerve injury, and ischemic symptoms despite
normal pulse (1,3,4)[C].
Lab
CBC
Basic metabolic protein with BUN/Cr
International normalization ratio (INR)/coagulation studies
Imaging
Radiographs
Duplex Doppler
ABI
MRI
Supracondylar femoral fracture
Treatment
ABCs
Get history/mechanism of injury
Take off shoe/expose limb if stable (4)[C].
Assess distal pulses/popliteal pulses bilaterally, capillary refill, sensory, motor
exam, range of motion (ROM), if able.
Splint knee in slight flexion or in position of comfort (1)[C].
Get pre- and postsplint distal pulses (1)[C].
Plan for reduction in ED.
ED Treatment
Closed reduction by longitudinal traction and lifting femur into normal alignment
without placing pressure on the popliteal artery
Posterior leg splint in 15 degrees of flexion at knee (to avoid stretch of PA)
IV analgesia for patient comfort
Vascular and orthopedic surgical consultation for open injury, evidence of PA
injury, or unable to reduce dislocation
If medial furrow on knee exam, suspect posterolateral dislocation, which cannot
be reduced closed (3)[C].
Medication
Pain control with opiates
Avoid NSAIDs if possible need for surgery.
Physical therapy will be essential for conservative and postoperative treatment.
Rehabilitation depends on specific ligaments torn.
On average, 9 mos of arduous therapy (4)[C]
Knee dislocation complications: Chronic stiffness, pain, arthrosis, and
instability (3,4)[C]
Unlikely to compete at same level
Peroneal nerve damage decreases likelihood of recovery to full activity (3,4)
[C].
All vascular injuries will need a vascular surgeon consult.
Orthopedic consult
Ligamentous repair/reconstruction vs conservative treatment with splinting
alone depends on activity level of patient.
Surgical treatment decreases stiffness.
Arthroscopic surgery is usually contraindicated until >2 wks after injury owing to
capsular tears and extravasation of fluid. There is an increased risk for
compartment syndrome (3).
Conservative treatment:
An option only for very sedentary patients, elderly, or if not able to undergo
surgery
Knee immobilizer plus Jones compression dressing
Hinged knee brace locked in extension when good quadriceps strength
6 wks average time of immobilization; if longer, complicated by stiffness (4)
ABCs
Fluid resuscitation because hypotension may alter distal pulses and perfusion
Closed reduction must be performed as soon as possible in the ED.
Early surgical consultation in an open injury or a high suspicion of arterial injury
Admission Criteria
All patients with knee dislocation require admission for either arterial injury repair
or observation of limb perfusion.
Ongoing Care
Prognosis
Return to full competitive sport or activity is unlikely (3,4).
Prognosis depends on neurovascular damage, which depends on velocity of injury.
Peroneal nerve damage portends a worse prognosis.
Chronic stiffness, arthrosis, pain, and instability are common complaints (3,4).
Complications
Amputation
Neurovascular deficit
Chronic pain
Stiffness
Instability
References
1. Nicandri GT, Chamberlain AM, Wahl CJ. Practical management of knee
dislocations: a selective angiography protocol to detect limb-threatening
vascular injuries. Clin J Sport Med. 2009;19:125–129.
2. Twaddle BC, Bidwell TA, Chapman JR. Knee dislocations: where are the
lesions? A prospective evaluation of surgical findings in 63 cases. J Orthop
Trauma. 2003;17:198–202.
3. Green J, Shahrdar C, Owens Brett. Knee dislocations.
http://emedicine.medscape.com/article/1250829. updated 8/25/08.
downloaded 7/12/09.
4. Henrichs A. A review of knee dislocations. J Athl Train. 2004;39:365–369.
5. Barnes CJ, Pietrobon R, Higgins LD. Does the pulse examination in

patients with traumatic knee dislocation predict a surgical arterial injury? A
meta-analysis. J Trauma. 2002;53:1109–1114.
6. Mills WJ, Barei DP, McNair P. The value of the ankle-brachial index for
diagnosing arterial injury after knee dislocation: a prospective study. J
Trauma. 2004;56:1261–1265.
7. Stannard JP, Sheils TM, Lopez-Ben RR, et al. Vascular injuries in knee
dislocations: the role of physical examination in determining the need for
arteriography. J Bone Joint Surg Am. 2004;86-A:910–915.
8. Ibrahim SA, Ahmad FH, Salah M, et al. Surgical management of traumatic

knee dislocation. Arthroscopy. 2008;24:178–187.
Codes
ICD9
836.0 Tear of medial cartilage or meniscus of knee, current
836.1 Tear of lateral cartilage or meniscus of knee, current
836.2 Other tear of cartilage or meniscus of knee, current
Clinical Pearls
Up to 50% knee dislocations reduce spontaneously.
If high-impact injury with knee deformity/gross swelling/laxity with valgus/varus
stress testing, suspect knee dislocation.
Document pulses on serial exams prehospital, in ED, and as inpatient.
Normal pulse does not necessarily indicate normal PA.
Arteriogram is “gold standard” for diagnosis.
Duplex US and ABI are adjunctive studies to serial physical exams.
Neurologic deficit indicates worse injury and prognosis.
Address life-threatening conditions 1st.
When splinting, avoid full/hyperextension.
PA damage that is not surgically repaired within 8 hr is likely results in above-
knee amputation (1,3,4).
Recovery to good function of the knee to perform daily activities of living is
likely but to demanding sports is not predictable (8).
On average, extension loss is 0–2 degrees; flexion loss is 10–15 degrees (8).
Kohler Disease (Aseptic Necrosis of the Tarsal
Navicular)
Kevin E. Burroughs
Basics
Description
Osteochondrosis of the tarsal navicular, 1st described by Alban Kohler in 1908 (1)
Osteochondrosis is a disease process that causes necrosis of the ossification center of a
developing bone and is followed by regeneration.
Epidemiology
Predominant age: Occurs in children 2–7 yrs of age (average age 5 yrs and 10 mos)
Predominant gender: Males > Females (4–6:1)
Usually occurs unilaterally; bilateral in only 15–20% of cases.
Appears to be no relation between weight and incidence.
Risk Factors
May be caused by repetitive microtrauma to the maturing navicular ossification center
Compression of the bony nucleus at a critical phase of growth may occlude the penetrating
blood vessels and produce ischemia and aseptic necrosis of the bone.
Delayed ossification leading to irregular ossification centers may predispose to this condition.
Occurrence is not related to acute macrotrauma, age at 1st walking, foot type, or family
history.
Etiology
Navicular development:
The navicular becomes evident on radiographs between 18 and 24 mos in girls and
between 30 and 36 mos in boys.
A more irregular and more dense navicular is often present in children whose navicular
ossifies at later times than these, and these findings are similar to those in Kohler disease.
The navicular ossifies from a single center in 2/3 of children and from multiple centers in
the remainder. Those ossifying later than the norm tend to be from multiple centers.
A dense perichondral network of blood vessels has been described on the nonarticular
surfaces, with numerous penetrating arteries.
Theories of etiology:
Questionably a normal variant but does not explain why some individuals are
asymptomatic.
Some believe that it is avascular necrosis. However, this wouldn't explain acute onset of
pain, lack of correlation with radiographic changes in the short amount of time, and no
matter the treatment, a normal navicular is the end result (true necrosis should cause
deformity).
Most likely a syndrome or continuum of disease because radiographic changes can be
seen in asymptomatic individuals. Perhaps those who are symptomatic have experienced a
stress injury to the ossifying bone. This would explain radiographic changes, with
remodeling to a normal-appearing bone.
Diagnosis
Although variations in morphology of the navicular have been described, the diagnosis of
Kohler disease is made on the basis of both clinical and radiographic findings.
History
It is often difficult for young children to localize pain, but it should be over the midfoot area.
Repetitive microtrauma may be a risk factor in sport activities.
A history of macrotrauma should lead the practitioner to consider other causes of foot pain.
Physical Exam
Signs and symptoms:
Insidious onset of foot pain and limp aggravated by activity
Time to presentation varies from days to months after onset of pain.
Look for localized edema and warmth in the area of the tarsal navicular.
Palpate the entire foot and ankle; tenderness should be localized to the medial midfoot.
Check the range of motion of the ankle and subtalar joints, which should be normal.
Examine the knee and hip, which can be the source of referred pain and limp.

Imaging
Radiographs: Standard anteroposterior, lateral, and oblique radiographs of the foot should be
obtained.
Findings:
Varying degrees of navicular sclerosis
Diminished size or flattening of the navicular (“Alka-Seltzer-on-end” appearance)
Occasional loss of trabecular pattern and fragmentation
A person with an asymptomatic foot with abnormal radiographic features found incidentally
does not have Kohler disease.
Bone scintigraphy: Not recommended but will show decreased uptake in the navicular
indicating decreased or interrupted blood supply.
Patchy areas of bone destruction and dead trabeculae with interference of normal ossification
Normal variants: Variations of size and shape of the navicular ossification center may be
indistinguishable from Kohler disease except for the absence of symptoms.
Localized involvement on the articular surface
Well demarcated from the normal bone by a crescent-shaped area of radiolucency
Treatment
Acute treatment:
Apply ice to midfoot.
NSAIDs or acetaminophen can be used for analgesic effect.
Immobilization to effect relief of symptoms, although the type and duration of
treatment do not influence long-term outcomes.
Immobilization:
Despite not altering the long-term outcome, immobilization has been shown to
decrease the duration of symptoms.
Patients with cast immobilization are typically pain-free at 3 mos, whereas
those treated without casting were symptomatic until 15 mos on average.
Those casted for at minimum 2 mos were asymptomatic in the shortest time.
Weight-bearing status does not appear to affect outcome.
Orthoses have not been found to be effective.
Rehabilitation: Usually not indicated
Rarely required
Ongoing Care
Orthopedic referral is indicated if symptoms do not resolve with conservative management.
Patient Monitoring
In a study of 12 cases, complete restoration of normal bone structure occurred in 8 mos
(minimum 6 mos and maximum of 13 mos).
At 30-yr follow-up, no patient showed degenerative changes at the tarsonavicular joint, and
no radiographic differences were seen with the unaffected foot.
Prognosis
Complete resolution of symptoms with reconstitution of the navicular can be expected in all
patients.
No evidence of cartilage degeneration in long-term follow-up studies
Reference
1. Kohler A. A frequent disease of individual bones in children. Munch Med Wochenschr.
1908;55:1923–1925.
Additional Reading
Borges JL, Guille JT, Bowen JR. Köhler's bone disease of the tarsal navicular. J Pediatr
Orthop. 1995;15:596–598.
Gips S, Ruchman RB, Groshar D. Bone imaging in Kohler's disease. Clin Nucl Med.
1997;22:636–637.
Ippolito E, Ricciardi Pollini PT, Falez' F. Köhler's disease of the tarsal navicular: long-term
follow-up of 12 cases. J Pediatr Orthop. 1984;4:416–417.
Manusov EG, Lillegard WA, Raspa RF, et al. Evaluation of pediatric foot problems: the
forefoot. Am Family Physician. 1996;54:592–606.
Sharp RJ, Calder JD, Saxby TS. Osteochondritis of the navicular: a case report. Foot Ankle
Int. 2003;24:509–513.
Stanton BK, Karlin JM, Scurran BL. Köhler's disease. J Am Podiatr Med Assoc.
1992;82:625–629.
Williams GA, Cowell HR. Köhler's disease of the tarsal navicular. Clin Orthop Relat Res.
1981:53–58.
Codes
ICD9
Clinical Pearls
Although all patients eventually will have complete resolution of symptoms,
immobilization with a cast for at least 8 wks shortens the duration of symptoms
by 1 yr.
Sports may be resumed once symptoms have resolved.
Long-term follow-up studies have found no increase in the rate of arthritis or
other chronic foot problems in adults who had Kohler disease during childhood.
Kyphosis
Mark E. Lavallee
Christopher Johnson
Basics
Description
Kyphosis is a fixed exaggerated convex anteroposterior (AP) curvature of the thoracic spine.
Scoliosis is a fixed lateral curvature of the spine (>10 degrees by Cobb angle) and vertebral
rotation.
Lordosis is a fixed concave exaggerated AP curvature of the lumbar spine.
Kyphoscoliosis is a combination of lateral and AP curvatures of the spine.
Scheuermann's juvenile kyphosis is osteochondrosis of the secondary ossification center of a
vertebrae causing thoracic kyphosis.
Synonym(s): Curvature of the spine; Hunchback; Dowager's hump; Postural roundback
Epidemiology
Most commonly seen in postmenopausal women who have osteoporosis. Rare occurrence in
skeletally maturing patients; occasionally seen in adolescents as they transition through their
secondary growth spurt.
Females > Males
Kyphosis has an incidence of 1 in 1,000, while scoliosis is about 2 in 100.
Scheuermann's juvenile kyphosis occurs in 0.4–0.8% in the U.S.
Idiopathic scoliosis occurs in 2–4% of school-aged children (1).
Risk Factors
Female gender and remaining growth potential
Family history is the primary risk. Inheritance patterns are still being actively elucidated.
Myelodysplasia, Marfan syndrome, Ehlers-Danlos syndrome, and achondroplasia have all
been associated with kyphosis and/or scoliosis.
Genetics
In 2007, CHD7 was identified as the 1st gene with polymorphisms associated with susceptibility
to scoliosis. No consistent genetic loci has been associated purely with kyphosis (2).
Osteoporosis
Vertebral fracture
Scoliosis
Scheuermann's juvenile kyphosis
Marfan syndrome
Ehlers-Danlos syndrome
Diagnosis
History
Upper back curvature, often painless
Often noticed by an observer, such as a parent, partner, or spouse
Cases of nonpainful, nontraumatic kyphosis are often discovered in school-based screenings,
preparticipation examinations, or general wellness exams.
A family history of kyphosis, scoliosis, connective tissue disorder, or neurological disorder
should be sought.
Physical Exam
Subtle findings, such as noticeable “hump” on back
Pain is not often a feature for idiopathic kyphosis, but if present, other causes of kyphosis
need to be ruled out.
Check posture, leg length discrepancy, muscle tone, and abdominal reflexes.
A complete neuro-orthopedic exam (ie, cavus feet seen in Charcot-Marie-Tooth syndrome)
Assess patient's ability to “correct” deformity with attempted thoracic hyperextension.
Postural roundback will improve, whereas true kyphosis will have minimal improvement.
Marfanoid body habitus, hypermobile joints, or hyperextensible skin (ie, Marfan or Ehlers-
Danlos syndrome)
Café-au-lait spots (ie, neurofibromatosis)
Adams' forward bending test (to look for associated scoliosis): Patient stands with legs
locked, bends at the waist, arms toward feet. Examiner stands behind patient, lowers head
and views across patient's back, looking for elevated and rotated vertebral segments.
A scoliometer may also be used to assess if patient has scoliosis. Measure the angle of trunk
rotation (ATR). An ATR of 7 degrees or greater correlates (83% sensitivity, 86% specificity)
to a clinically significant curve. The ATR multiplied by 3 estimates the curvature (Cobb angle).
Imaging
Kyphosis: AP/lateral chest x-ray is usually the 1st imaging test. Able to assess for
degenerative joint disease, fractures, Schmorl's nodes, angle of kyphosis. Secondary or
more complete view is a lateral standing radiograph of entire spine. Look for Schmorl's
nodes (protrusions of intervertebral disc cartilage through vertebral body end plate of
adjacent vertebra that are pathognomonic for Scheuermann's.
If scoliosis is associated with kyphosis: Standing posteroanterior and lateral radiographs of
the entire spine. Pelvis is analyzed to determine Risser score.
In children and adolescents, make sure with radiographs to image the iliac crests, including
the iliac apophyses to help with the Risser scoring.
Indications for MRI:
Age <10
Rapid progression of a curve
Abnormal neurologic examination
Atypical pain with inconclusive radiograph (1)[C]
Congenital kyphosis: Anomalies of vertebral segmentation and/or formation (Klippel-Feil
syndrome, VACTERL syndrome).
Neuromuscular scoliosis: Upper motor neuron (Friedrich's ataxia, cerebral palsy, Charcot-
Marie-Tooth syndrome, syringomyelia, muscular dystrophy) or lower motor neuron
(poliomyelitis, spina bifida), spinal dysraphism (myelomeningocele)
Scheuermann's juvenile kyphosis: Pathognomonic Schmorl's nodes on at least 2 consecutive
levels
Kyphosis secondary to bone demineralization (osteoporosis)
Vertebral fractures/trauma
Benign or malignant tumors (ie, Paget's disease of bone)
Parkinson's disease: “Stooping posture”
Spinal tuberculosis
Rickets
Marfan syndrome
Achondroplasia
Ehlers-Danlos syndrome, especially kyphoscoliotic type
Ankylosing spondylitis
Treatment
Management options include observation, bracing, physical therapy, oral
medicine (osteoporosis), and surgical invention (in rare cases).
Idiopathic kyphosis in adolescence and Scheuermann kyphosis rarely need
Treatment of painful kyphosis is 1st to determine cause.
<50 degrees in young adolescents without evidence of progression may be
observed. Strengthening and stretching of abdominals, hamstrings, and
paraspinal muscles are recommended to prevent excessive lordosis and
hamstring contractures (1)[C].
Painful curves between 50 and 70 degrees or progressive deformity >65
degrees may be braced (many associated with Scheuermann's) (1)[C].
Literature supports surgical correction indicated at >75 degrees with P.
Scheuermann's kyphosis and 60 degrees for congenital kyphosis.
Observation:
Juveniles/adolescents with moderate curves of <60 degrees: Manage by
following with serial radiographs every 4–6 mos, depending on skeletal
maturity (Risser score; see scoliosis chapter)
Skeletally mature with curves <40: Follow with history, physical, and
occasional radiograph.
Check bone densitometry (dual energy x-ray absorptiometry) on patient with
vertebral fracture, nontraumatic, and those with osteoporosis. Treatment of
osteoporosis with bisphosphonates has been shown to improve kyphosis-
related back pain.
Standing lateral radiographs of whole spine every 6 mos
Brace:
Immature with curve >60 degrees or in those who progresses >10 degrees
during observation to a curve >40
Bracing options include:
Preliminary hyperextension plaster cast
Milwaukee brace (for curves above T7)
May use an underarm rigid brace (if curve is below T7)
Once the curve is supported, the patient should use 20 hr/day. The brace use
may be tapered to nighttime use once the progression of the curve is
controlled.
Goal is to delay/prevent curve progression until skeletally mature
Contraindication to bracing: Curves >80 degrees, extreme thoracic
hypokyphosis, high thoracic or cervical curves
Standing radiograph images every 6 mos (or 4 mos if progressing and
skeletally immature)
Surgery:
Wedge osteotomies of the posterior aspect of the vertebrae have been done
to correct those with severe kyphosis in skeletally mature patients without
osteoporosis.
Vertebroplasty and balloon kyphoplasty are procedures available to patients
who develop kyphosis related to osteoporosis or trauma-related collapse of
thoracic vertebral body.
Once a curve reaches 80 degrees, it is assumed it is not controlled by
bracing; operative correction with posterior instrumentation/fusion is
recommended. Upper thoracic kyphosis with curves >100 cause significant
restrictive lung disease.
Some clinicians advocate following juvenile patients with exaggerated kyphotic
curves of >40 degrees at 4–6-mo intervals until iliac crest growth plates close.
Postural roundback, not true kyphosis, has been shown to improve with
physical therapy focused on postural control and core/shoulder girdle
strengthening.
Bracing in juvenile/adolescent patients should be continued as long as there is
no progression of curvature and vertical growth is still occurring. In young
women, this means a Risser stage of at least 3; in young men, a Risser stage
of 4.
Ongoing Care
Refer to orthopedic/spine specialist when there is a:
Nonbraceable curve of the thoracic spine (apex of curve higher than T6)
Worsening curvature despite bracing
Curvature in the newborn and infant; any children under 10 yrs old
Curvature associated with severe trauma/vertebral fracture
Curvature-associated malignancy
Juvenile/adolescent kyphosis is often diagnosed or progresses during a sensitive time of life.
Studies have demonstrated a negative effect on body image, self-esteem, and attitude with
treatment. This may affect compliance. Treatment is time-consuming, confining, and can be
uncomfortable. The adolescent is faced with many lifestyle changes. Providers should be
aware of the possible psychological impact from new demands on the patient and family.
Discussions about patient's thoughts/feelings on treatment as well as support groups should
be considered (3)[C].
References
1. Schiller JR, Eberson CP. Spinal deformity and athletics. Sports Med Arthrosc.
2008;16:26–31.
2. Gao X, Gordon D, Zhang D, et al. CHD7 gene polymorphisms are associated with
susceptibility to idiopathic scoliosis. Am J Hum Genet. 2007;80:957–965.
3. Reichel D, Schanz J. Developmental psychological aspects of scoliosis treatment. Pediatr

Rehabil. 2003;6:221–225.
4. Wood KB. Spinal deformity in the adolescent athlete. Clin Sports Med. 2002;21:77–92.
Additional Reading
Dobbs MB, Weinstein SL. Infantile and juvenile scoliosis. Orthop Clin North Am.
1999;30:331–341, vii.
Miller NH. Cause and natural history of adolescent idiopathic scoliosis. Orthop Clin North
Am. 1999;30:343–352, vii.
Roach JW. Adolescent idiopathic scoliosis. Orthop Clin North Am. 1999;30:353–365, vii–viii.
Staheli LT, Song K. Practice of pediatric orthopaedics, 2nd ed. Lippincott, Williams &
Wilkins; 2006:220–224.
Codes
ICD9
737.10 Kyphosis, acquired, postural
737.30 Kyphoscoliosis, idiopathic
756.19 Kyphosis, congenital
Clinical Pearls
Sports and athletic activity is allowed and encouraged for all patients with
nonpainful kyphosis in nonoperative treatment. Those with painful causes of
their kyphosis should consult with their doctor prior to starting an exercise
program. Postoperative patients' return to play is at the discretion of the
surgeon. Level/extent of fusion, time from surgery, and type of sport usually
dictates the decision (4)[C].
Braces are used to prevent progression and are not intended to correct the
curve. Compliance is essential to treatment success.
Most studies support results with brace wear of 18–20 hr per day. Night-only
braces have also been shown to have success (4)[A].
Braces for juvenile/adolescent patients should be worn until the Risser score is
4 (closed growth plates).
Further studies are still needed to elucidate the effect of exercises. Favorable
effects have been shown, however, on strength, postural stability, and balance.
This may be valuable as an adjunct to treatment. Exercise has been shown to
help postural roundback.
Manipulation therapy has not been proven to help correct curvature of the
spine. Few articles such as case studies advocate the role on manipulation, but
more data and controlled studies are needed to support their use in curve
correction.
Lacerations and Soft Tissue Injuries
Ross Osborn
Basics
Alert
Lacerations and abrasions are a disruption of the skin resulting from trauma.
Description
Soft tissue injuries include blisters, chaffing, burns, hematomas, abrasions, and lacerations:
Blisters are a separation of the epidermis from the dermis and caused by repetitive friction.
Chaffing is caused by repetitive friction of the skin without separation of the dermis from
the epidermis.
Hematomas are caused by blunt trauma to the skin and underlying structures, which cause
extravasation into surrounding soft tissue.
Abrasions describe a superficial skin wound caused by tangential friction, and involve
stripping of the epidermis from the underlying dermis.
Lacerations are full-thickness skin wounds involving the epidermis and dermis, and may
occur with injury to connective tissue, cutaneous nerves, and vasculature.
Soft tissue injuries can occur on any part of the body:
Blisters generally occur at sites where the skin encounters friction from equipment (ie, feet
vs shoes, hand vs club or racquet)
Chaffing most commonly occurs in areas of skin-to-skin contact (ie, groin, axilla) or where
clothes rub (ie, “jogger's nipple”)
Abrasions most commonly occur on the knees and elbows.
Lacerations most often occur on the head and neck (50%) or upper extremities (35%).
Epidemiology
11 million lacerations are treated in emergency departments, but this number doesn't include
those injuries treated in an office or on the sideline.
Location of skin injuries is sports-specific.
Risk Factors
Most common preventable cause of skin trauma is improper equipment use or lack of use.
Etiology
Hematomas, lacerations, and abrasions are most commonly caused by blunt trauma.
Lacerations caused by sharp objects are common and usually involve the equipment used for
the sport (ie, shoe spikes, sticks, skates)
Any nonaccidental trauma in a child should raise the suspicion for abuse.

Associated symptoms can include:
Bleeding
Foreign body
Paresthesia
Loss of motor function
Diminished vascularization
Diagnosis
Regardless of situation, observe standard universal precautions.
Assess the ABCs.
Control bleeding before obtaining more complete history and physical.
Determine the time, mechanism, and circumstances of injury.
History of foreign body (glass, splinter, teeth, field material):
Avoid digital exploration if the object is believed to be sharp.
Evaluate nerve and motor function, as well as possibility of underlying fracture.
Assess presence of devitalized tissue.
Obtain medical history for co-morbid conditions that may impede wound healing.
History
Estimate the amount of blood loss.
Assess tendon, muscle, or nerve injury:
Complaints of weakness, numbness, or tingling
Local sensory nerve/peripheral nerve function should be assessed by 2-point discrimination
prior to administration of anesthetic.
Medication history:
Aspirin, NSAIDs, clopidogrel (Plavix), Coumadin, or other blood-thinning medications and/or
supplements
Allergies:
Latex, lidocaine, iodine, or pain medications
Immunization status:
Assess if tetanus status is up-to-date.
In minors, parental consent should be obtained prior to procedure if possible.
Have a consent form in sideline bag.
Physical Exam
Vitals:
BP and pulse should be assessed for hemodynamic stability.
General:
Pallorous, ashen, or faint (hemodynamic vs vagal)
Cardiovascular:
Peripheral pulses distal to the site of injury:
Decreased or absent pulses should initiate prompt referral.
Capillary refill
Pulmonary:
Assess ease of respiration after chest wall trauma.
Adequate and equal breath sounds:
Unequal breath sounds necessitates further evaluation for pneumothorax
Head/eyes/ears/nose/throat:
Cranial nerve assessment in cases of trauma to the head
Assess for concussion.
Musculoskeletal:
Deformities or concerns for fracture under an open wound should prompt referral.
Neurologic:
Sensory exam distal to site of injury to evaluate underlying nerve damage
Skin:
Patients with thin skin may require adapting the repair modality.
Psychological:
Psychomotor agitation may make following universal precautions more challenging.
May also signify underlying head trauma

Imaging
Radiographs:
For concerns of underlying fracture
Plain radiography may help to identify some foreign bodies.
US is emerging as a useful tool in the imaging of suspected foreign bodies:
A few small clinical studies show increasing reliability in the detection of foreign bodies (1).
The portability of some US units makes them a readily available imaging modality.
US is useful to identify foreign bodies with the same density as soft tissue (eg, splinters).
Skin avulsion
Contusion
Abrasion
Laceration
Hematoma
Rash/dermatitis
Treatment
Initial stabilization:
Assess ABCs.
Ensure hemostasis prior to further evaluation, treatment, or repair.
Initial examination:
Explore wound for foreign body.
Removal of any devitalized tissue
Assess for injury to underlying structures.
Irrigation and preparation:
Clean surrounding skin with soap and water if superficial, or copious
irrigation:
Do not use povidone iodine, hydrogen peroxide, or detergents, as they
have been shown to impede healing (2)[B].
Employ appropriate universal precautions.
Remove foreign bodies or other contaminants in wound:
A fine-pore sponge may be used in cases of significant contamination or
fine particulate matter.
Indications for removal of a foreign body include: Potential or actual injury
to tendons, nerves, vasculature; toxic substance or reactive agent; source
of pain
Retained foreign bodies in abrasions may result in “tattooing” of the skin.
Irrigate wound with sterile water, saline, or clean tap water:
Sterile saline and tap water have been found to have equivalent infection
rates (3)[B].
Incidence of infection relates inversely to the amount of irrigation used (3).
A “rule of thumb” is to use 50–100 mL of irrigant per centimeter of
laceration.
Debride devitalized tissue and revise wound edges if necessary to achieve a
good closure.
Clip hair growing near the wound, but avoid shaving, as it may introduce
bacteria into the wound.
Larger blisters can be drained to prevent expansion or rupture, but should
have the epidermal “roof” kept intact to act as a biological dressing.
Time to treatment:
Blisters, chaffing, and abrasions can be treated immediately and the athlete
can return to play.
Lacerations may heal by primary closure, delayed primary closure, or
secondary intention:
All “clean” wounds can be closed primarily except puncture wounds not able
to be adequately irrigated.
Wounds presenting for treatment after a delay, contaminated wounds, and
noncosmetic animal bites should be irrigated, debrided, and have bleeding
controlled.
Delayed primary closure can be performed after 3–5 days in order to allow
the patient's immune system to decrease the bacterial load. The lowest
approximate bacterial load will occur 96 hr after the initial injury (3).
Secondary closure is allowing a wound to heal by granulation. This is
appropriate for partial-thickness avulsions, contaminated small wounds,
and infected wounds (3).
Analgesia:
Topical anesthesia:
Can be useful to treat abrasions, chaffing, and blisters as well as to further
evaluate skin lacerations (4).
Options include 1% or 2% lidocaine jelly, LET (4% lidocaine, 0.1225%
epinephrine, and 0.5% tetracaine), or EMLA (eutectic mixture of local
anesthetics: 2.5% lidocaine and 2.5% prilocaine), or LMX (formerly known
as Ela-Max-liposomal lidocaine) (3).
Local or regional anesthesia:
Preferred type of anesthesia for lacerations: Amide agents (lidocaine and
bupivacaine) and ester agents (procaine) are the 2 basic types. Allergy to
one group is not associated with allergy to anesthetic from the other group
(3). Most allergies are caused by the preservatives used in the anesthetic,
so a pure agent, such as cardiac lidocaine, could be used as an alternative
(3). Intradermal diphenhydramine can be used for those patients allergic to
the above anesthetics (2).
Epinephrine will improve the duration of injected anesthetics (5) and will
promote vasoconstriction. Should be used with caution in fingers, toes,
nose, ears, or the penis, as vasoconstriction may result in tissue necrosis.
Can limit immune cell migration into the wound because of
vasoconsrtiction.
Patient comfort can be increased by using a smaller gauge needle to inject,
injecting subcutaneously through the open wound, using a slower injection
rate, and with the addition of sodium bicarbonate to the anesthetic (1:10 of
total volume injected).
P.
Modalities for closure:
The location of the laceration should determine the type of material used for
closure because of differences in skin tension.
Modalities include surgical tapes, skin adhesives, staples, and sutures:
Surgical tape: Advantages: Rapid application, patient comfort, lower
infection rates, least tissue reactivity, low cost. Disadvantages: Can't apply
to areas with hair, must remain dry, highest dehiscence rates, low tensile
strength. Application: Use benzoin tincture, apply only to dry skin edges,
ensure adequate approximation of skin edges.
Skin adhesives: Advantages: Rapid application, resists bacterial growth, no
need for removal, no anesthesia needed, good cosmetic results, excellent
for children. Disadvantages: Not adequate for moderate or heavy tension
areas of the skin. Application: Apply on to dry skin edges, approximate skin
edges.
Staples: Advantages: Rapid application, low tissue reactivity, low cost, can
be used in areas with a lot of hair. Disadvantages: Inability to provide a
meticulous closure, interference with imaging (CT or MRI), removal
required. Application: Sterilize area, anesthesia, roughly approximate
edges.
Sutures: Advantages: Meticulous closure, most tensile strength, lowest
dehiscence rate. Disadvantages: Anesthesia required, slow application,
most tissue reaction, removal required. Application: Determine single or
multiple layer closure, remove foreign material or devitalized tissue, create
sterile field.
Skin closure:
Single vs multiple layer closure:
Single layer can be performed with staples, adhesives, surgical tape, or
sutures. Choice should depend on location of laceration.
Multiple layer closure: Closes deep tissue dead space; lessens tension at
the epidermal level, improving the cosmetic result; absorbable suture
should be used to close SC tissue.
Wound dressing:
Blisters: Should be covered with protective membrane or dressing, or a
semipermeable membrane, or hydrocolloidal dressing if draining:
Blisters <1 cm in size can be left intact and covered with a protective
dressing or membrane (5).
Blisters >1 cm can be aspirated to prevent expansion, but the epidermal
“roof” should be left intact (5). After drainage, they should be covered with
a protective dressing or membrane.
Abrasions can be covered by a nonstick dressing, such as Telfa or Adaptic,
then covered by an absorbent gauze dressing:
Alternative dressings include Tegaderm, zinc oxide-impregnated gauze,
and occlusive hydrocolloidal dressings such as Duoderm.
Hematomas can be covered by a pad or padded dressing for comfort if the
athlete is able to return to play.
Lacerations should be covered with a sterile gauze or nonadherent pad until
the stitches or staples are removed:
The initial dressing should be kept on for 48 hr following repair.
Athlete can shower within the 1st 24 hr, but should avoid prolonged
exposure to water for 72 hr.
After 48 hr, dressing should be changed daily
Antibiotic ointment has not been proven to prevent infection, but may
improve wound healing. Ointments should not be used more than 48 hr, as
they may macerate the skin. White petrolatum ointment has been shown to
be equally as effective as antibiotic ointment to prevent infection and
promote healing (2)[B].
Antibiotic prophylaxis should be considered for contaminated wounds.
Medication
Antibiotics:
Uncomplicated lacerations, abrasions, blisters, and chaffing do not require
systemic antibiotics.
There are no studies to support antibiotic prophylaxis in simple, nonbite
wounds.
Choice of antibiotics should be based on suspected pathogen:
Normal skin flora (S. aureus and S. pyogenes): 1st-generation
cephalosporin, dicloxacillin, macrolides, or amoxicillin/clavulanate
Bite wounds (Pasteurella): Amoxicillin/clavulanate or clindamycin for
penicillin-allergic patients
Contaminated waterborne vectors: 1st-generation cephalosporin +
Levaquin + doxycycline or metronidazole
Open fractures, exposed tendon injuries, or exposed joint injuries typically
require systemic antibiotics.
P.
Tetanus prophylaxis guidelines are listed below (5).
Tetanus Clean, minor wounds All other wounds
Vaccination History Td TIG Td TIG
<3 doses or unknown status Yes No Yes Yes
≥3 doses
Last dose within 5 yr No No No No
Last dose within 5–10 yr No No Yes No
Last dose >10 yr Yes No Yes No
Admission Criteria
Soft tissue injuries themselves do not necessitate hospital admission, but the
following exceptions apply:
Grossly contaminated wounds or wounds requiring extensive debridement
Open fractures
Hemodynamically unstable patient
Comorbid conditions such as a head injury or abdominal trauma
Wounds requiring ongoing IV antibiotics
Lacerations to the eyelid should prompt a referral to an ophthalmologist.
References
1. Blankenship RB, Baker T. Imaging modalities in wounds and superficial skin
infections. Emerg Med Clin North Am. 2007;25:223–234.
2. Forsch RT. Essentials of skin laceration repair. Am Fam Physician.

2008;78:945–951.
3. Moreira ME, Markovchick VJ. Wound management. Emerg Med Clin North
Am. 2007;25:873–899, xi.
4. Cordoro KM, Ganz JE. Training room management of medical conditions:

sports dermatology. Clin Sports Med. 2005;24:565–598, viii–ix.
5. Honsik KA, Romeo MW, Hawley CJ, et al. Sideline skin and wound care for
acute injuries. Cur Sports Med Reports. 2007;6:147–154.
Codes
ICD9
709.8 Other specified disorders of skin
879.8 Open wound(s) (multiple) of unspecified site(s), without mention of complication
949.0 Burn of unspecified site, unspecified degree
Clinical Pearls
Traumatic skin lesions are commonly seen in the athletic arena, and their
proper management can facilitate a safe and rapid return to play.
Proper assessment and preparation will allow the best possible outcome for
skin injuries.
Materials for treatment should be based on the location and type of injury, as
well as the experience of the treating provider.
Return-to-play decisions should be based on the ability to treat the injury and
dress the wound to limit the exposure of bodily fluids.
Antibiotics use should be based on the degree and source of contamination.
Also ensure adequate tetanus prophylaxis.
Lateral Collateral Ligament Tear
Brent S. E. Rich
Mitchell Pratte
Basics
Description
Partial or complete sprain of the lateral collateral ligament (LCL) owing to an acute force,
usually from a medial direction
Consists of a cordlike fiber bundle that runs from the lateral femoral condyle to the lateral
aspect of the fibular head about 1 cm anterior to the apex: discrete extracapsular structure.
Primary restraint to varus stress with the knee in extension
Isometric between 0 and 70 degrees of flexion, followed by slackening trend with deeper
flexion
Epidemiology
Least commonly injured knee ligament; isolated injuries are rare.
Infrequent site of overuse injury or rupture
Wrestling is the most likely associated sport.
May be associated with injury to other ligaments [anterior cruciate ligament (ACL) or
posterior cruciate ligament (PCL)] or structures of the posterolateral corner (popliteus
tendon, biceps femoris, iliotibial band, popliteofibular ligament) and peroneal nerve injuries
Risk Factors
Unclear if previous LCL injuries predispose to recurrent injury
Varus knee, otherwise normal, does not seem to be predisposed to LCL injury.
PCL deficiency may increase risk of LCL injury.
Diagnosis
History
Contact or noncontact varus stress to partially flexed knee in internal tibial rotation from
direct force or, more rarely, distal indirect stress (eg, stepping into a hole) with fixed foot
Acute lateral knee pain
Many hear/feel an associated “pop.”
LCL is extraarticular; mild to moderate swelling is associated with isolated injury.
Mild disability with low-grade injury; difficult weight bearing with high-grade injury/associated
injuries owing to pain and instability
Instability with high-grade or moderate injury
Check for possible peroneal nerve symptoms.
Physical Exam
Signs and symptoms:
Acute lateral knee pain associated with a mechanism of varus stress with knee in flexion of
25–30 degrees
Patient may feel or hear a “pop” at time of injury.
Swelling variable, effusion not common with low-grade injuries; associated ligamentous
injuries may cause significant effusion.
Instability symptoms in high-grade injury or with associated underlying varus knee
Possible peroneal nerve symptoms
Local swelling over ligament
Tender to palpation over ligament
Readily palpated in “figure-of-4 position”: Normally a pencil-like structure but less distinct
with partial tears (grade II) or complete tears (grade III)
Varus stress testing: Grade I sprain, no increased laxity; grade II sprain, increase in laxity
with semifirm endpoint at 25–30 degrees of flexion isolates the LCL; grade III sprain,
increase in laxity with soft or no endpoint compared with the uninjured knee indicates injury.
Careful assessment of ACL (Lachman test) and PCL (posterior drawer test),
posterolateral structures (external rotation recurvatum test, external rotation roll-out test at
90 and 30 degrees, posterolateral drawer sign), and pivot shift if possible. Grade I injuries
may be confused with lateral meniscal tears.
Peroneal nerve sensory and motor function should be checked as well.

Imaging
Plain films to rule out occult fracture of tibial plateau, lateral femoral condyle, or fibular head
on all patients
MRI to better assess integrity of LCL and associated knee structures (ACL, PCL, lateral
meniscus, popliteus tendon, posterolateral corner)
Proximal fibula avulsion fracture
Biceps femoris strain
Iliotibial band strain
Popliteus strain/tear
Associated anterior or posterior cruciate injury
Lateral meniscus tear
Lateral compartment chondral/osteochondral injury
Associated loose body
Peroneal nerve injury
Treatment
Acute treatment
Analgesia:
Ice and compression in acute setting
NSAIDs until acute pain subsides
Narcotics appropriate for 24–72 hr for grade II or III injuries or combined
ligamentous injuries
Immobilization:
Grade I injury: No immobilization needed, but hinged bracing limiting flexion to
45–60 degrees is beneficial.
Grade II or III: Limited short-term use of knee immobilizer (<1 wk) followed by
hinged brace, progressing through to full ROM over 4–6 wks
Bracing continues for contact or collision sport for the remainder of that
season.
May consider more prolonged immobilization and bracing in varus knee, which
is thought to increase stress on the injured ligament. This is somewhat
controversial.
Rehabilitation:
In the acute setting, start isometric quadriceps exercises and straight-leg
lifts.
Electrical stimulation/biofeedback to VMO quads
Gentle hamstring and calf strengthening in protective ROM
ROM exercises with progression to full ROM over 4–8 wks to allow ligament
to heal without too much stress
Stair stepper or similar for CV conditioning can be added, limiting knee
flexion to 45–60 degrees when tolerated.
Stationary bike later in rehabilitation when able to flex knee to 115 degrees
without pain or residual swelling afterwards
When gait is normal, begin jogging and enhanced resistance exercises.
Progress to half sprints, full sprints, and cutting maneuvers once ligament
fully healed.
Surgery is considered for grade III/combined ligamentous injuries.
Ongoing Care
Referral to orthopedic surgery for any fracture, associated ligament injury, complex meniscal
tear, or grade III injury that is not amenable to the initial 2–4 wks of rehabilitation
Associated neurovascular injuries should be considered emergent, and appropriate
surgical/radiographic consultations should be initiated and performed on the same day.
Additional Reading
Kozanek M, et al. Posterolateral structures of the knee in posterior cruciate ligament
deficiency. Am J Sports Med. 2009;3.
Van de Velde S, et al. The effect of anterior cruciate ligament deficiency on the in vivo
elongation of the medial collateral and lateral collateral ligament. Am J Sports Med.
2007;35.
Victor J, et al. How isometric are the medial patellofemoral, superficial medial collateral, and
lateral collateral ligaments of the knee? Am J Sports Med. 2009;37.
Wheeless' Textbook of Orthopaedics, Duke University, 2009,
http://www.wheelessonline.com/ortho/lateral/collateral/ligament
Codes
ICD9
844.0 Sprain of lateral collateral ligament of knee
Clinical Pearls
Average return to play for grade I injury is 1–2 wks; grade II, 4–6 wks. Return to
play is greatly dependent on the type of activity.
Once healed, there are no data to suggest that the ligament is more
predisposed to recurrent injury.
Lateral Epicondylitis
Craig C. Young
Bryant Walrod
Basics
Description
Lateral epicondylitis, or lateral elbow tendinosis, is an overuse injury of the forearm and wrist
extensor muscles, which causes pain at the lateral elbow.
Synonym(s): Tennis elbow
Epidemiology
Accounts for 90% of elbow epicondylitis
Precipitated by tennis and other activities that require repetitive wrist extension, radial
deviation, and forearm supination
Occurs in dominant arm 75% of the time
Risk Factors
Age 40–60 yrs
Improper equipment (eg, inappropriate grip size, overstrung racquet, inappropriate-weight
racquet)
Poor technique (eg, backhand with excessive wrist extension)
Playing tennis for more than 2 hr per wk (1)

Posterior interosseous nerve entrapment (radial tunnel syndrome) may coexist in up to 15% of
cases.
Diagnosis
History
Pain pattern: Patients typically report an insidious onset, but they will often relate a history of
overuse without specific trauma. Pain can vary from mild (eg, present only with aggravating
activities like tennis or the repeated use of a hand tool), or it can be severe (eg, holding a
coffee cup will act as a trigger for the pain).
Numbness or tingling: Radicular symptoms suggest nerve entrapment or radiculopathy.
2-handed backhand: Most tennis players with lateral epicondylitis use a 1-handed backhand.
Improper technique: Hitting late in the backhand or improper positioning when striking the ball
Equipment used, location, and frequency of play: Many cases of lateral epicondylitis are
associated with improper equipment, old or wet tennis balls, racquets that are strung too
tightly or too heavy, and fast surfaces.
Poor conditioning: Poor general conditioning leads to fatigue of the core and shoulder
muscles, which puts an overemphasis on the extensor muscles of the forearm.
Physical Exam
Pain at lateral elbow
Pain with wrist and forearm movements
Pain with gripping objects (“coffee cup sign”) and shaking hands (“politician's sign”)
Localized tenderness over lateral epicondyle. Also pain just distal and anterior to lateral
epicondyle 1–2 cm distal to the origin of the extensor carpi radialis brevis
Tenderness with resisted wrist extension with wrist pronated and radially deviated
Tenderness with resisted middle finger extension
Tenderness with resisted supination
Decreased internal rotation of ipsilateral shoulder causing compensatory excessive wrist
flexion

Imaging
Not usually needed for initial treatment
Standard elbow radiography series (anteroposterior and lateral) should be obtained if other
potential injuries are suspected (eg, fracture, tumor, degenerative joint disease) or if injury is
not responding to appropriate treatment.
Up to 25% of cases have associated calcification in extensor aponeurosis; however,
presence of these deposits does not affect initial treatment.
Consider additional imaging like MRI or US to evaluate for intrasubstance tears. MRIs are
also helpful in diagnosing OCD lesions and stress fractures.
A local anesthetic block may lead to symptom resolution and confirmation of the diagnosis.
Microscopic evaluation of the tendons does not show signs of inflammation, but rather
angiofibroblastic degeneration and collagen disarray.
Light microscopy reveals both an excess of fibroblasts and blood vessels that are consistent
with neovessels or angiogenesis.
The tendons are relatively hypovascular proximal to the tendon insertion. This hypovascularity
may predispose the tendon to hypoxic tendon degeneration and has been implicated in the
etiology of tendinopathies.
These findings support a failed healing response rather than a true inflammatory process.
Posterior interosseous nerve entrapment (radial tunnel syndrome)
Osteoarthritis
C7 radiculopathy
Musculocutaneous nerve entrapment
Chronic compartment syndrome of anconeus muscle
Radiocapitellum OCD lesion
Lateral collateral ligament strain
Stress fracture
Humeral fracture
Treatment
Acute treatment:
Ice after activity.
Anti-inflammatory medications: Consider NSAIDS, either topical or by mouth.
Corticosteroid injections have proven effectiveness for short-term relief of
symptoms, but no major differences were seen at 1 yr compared to NSAID
treatment (2).
Modalities: Consider the use of US, phonophoresis, or iontophoresis. Some
studies have shown them to be useful in returning an athlete to activity
sooner, but they show no long-term benefit (3).
Long-term treatment: P.
Watchful waiting: 83% of patients symptom-free at 1 yr (2)
Autologous blood, platelet-rich plasma, prolotherapy, topical nitrates,
botulinum toxin have demonstrated effectiveness in small studies (4,5,6)
Extracorporeal shock wave therapy and low-intensity laser therapy have not
demonstrated effectiveness (2,7)
Surgical intervention: 30 of 36 people reported improvement after surgery
(8).
Physical therapy consisting of forearm stretching and strengthening program
with progression to eccentric muscle strengthening of the common extensor
tendon
A forearm counterforce brace during activities may help some patients; the
use of a night wrist splint can be helpful for patients with morning pain.
Referral
Consider referral for surgical debridement for individuals whose symptoms do not
respond to a high-quality nonoperative treatment program.
Technique modification: Lessons from a professional instructor or coach about
proper serve and backhand techniques
Improve ergonomics in the work environment.
Equipment: Ensure athlete is using properly sized, weighted, and strung
racquet.
Stretching and strengthening: Ensure athlete is on appropriate conditioning
program, preactivity warm-up, and postactivity cool-down programs.
Ongoing Care
Relative rest: Limit activities that cause pain
Equipment modifications: Decrease racquet string tension; use only new, dry tennis balls;
play on grass court if available.
References
1. Gruchow HW, Pelletier D. An epidemiologic study of tennis elbow. Incidence, recurrence,
and effectiveness of prevention strategies. Am J Sports Med. 1979;7:234–238.
2. Smidt N, van der Windt DA, Assendelft WJ, et al. Corticosteroid injections,
physiotherapy, or a wait-and-see policy for lateral epicondylitis: a randomised controlled
trial. Lancet. 2002;359:657–662.
3. Bisset L, Paungmali A, Vicenzino B, et al. A systematic review and meta-analysis of

clinical trials on physical interventions for lateral epicondylalgia. Br J Sports Med.
2005;39:411–422; discussion 411–422.
4. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich

plasma. Am J Sports Med. 2006.
5. Paoloni JA, Appleyard RC, Nelson J, et al. Topical nitric oxide application in the treatment
of chronic extensor tendinosis at the elbow: a randomized, double-blinded, placebo-
controlled clinical trial. Am J Sports Med. 2003;31:915–920.
6. Placzek R, Drescher W, Deuretzbacher G, et al. Treatment of chronic radial epicondylitis

with botulinum toxin A. A double-blind, placebo-controlled, randomized multicenter study. J
7. Buchbinder R, Green SE, Youd JM, et al. Shock wave therapy for lateral elbow pain.
Cochrane Database Syst Rev. 2005:CD003524
8. Grewal R, MacDermid JC, Shah P, et al. Functional outcome of arthroscopic extensor

carpi radialis brevis tendon release in chronic lateral epicondylitis. J Hand Surg [Am].
2009;34:849–857.
Additional Reading
Calfee RP, Patel A, Dasilva MF, et al. Management of lateral epicondylitis: current concepts.
Faro F, Wolf JM. Lateral epicondylitis: review and current concepts. J Hand Surg [Am].
2007;32:1271–1279.
Kraushaar BS, Nirschl RP. Tendinosis of the elbow (tennis elbow). Clinical features and
findings of histological, immunohistochemical, and electron microscopy studies. J Bone Joint
Surg Am. 1999;81:259–278.
Plancher KD, Halbrecht J, Lourie GM. Medial and lateral epicondylitis in the athlete. Clin
Sports Med. 1996;15:283–305.
Thurston AJ. Conservative and surgical treatment of tennis elbow. Aust N ZJ Surg.
1998;68:568–572.
Walrod B, Young C. Lateral Epicondyitis. emedicine.com. July, 2009.
Codes
ICD9
726.32 Lateral epicondylitis
Clinical Pearls
The lateral elbow serves as the origin of the forearm muscles and thus elbow
pain may result
Histologic biopsies of chronic lateral epicondylitis reveal no inflammation, but
rather signs of poor and disordered healing, a term called angiofibroblastic
degeneration. Chronic lateral epicondylosis is not an inflammatory condition.
Consider other treatments such as physical therapy and proinflammatory
modalities in this case.
Lightning Injuries
Justin A. Classie
Chad A. Asplund
Basics
Description
Injury from lightning strike has variable severity
Individuals need to adhere to proper precautions. Lightning safety remains primarily an
individual responsibility that requires individual decisions for prevention.
3rd most common environmental cause of death after heat-related injury and floods (1)
Direct strike: The charge of lightning may pass through or over the person's body. Passing
over the body, or “flashover” phenomenon, causes less damage than a strike that passes
directly through the individual.
Side flash: Lightning strike “jumps” from an object to the victim.
Contact injury: The victim is in contact with an object that is struck.
Ground current: Current will flow across 2 separate points on the victim on the ground;
most frequent occurrence; 40–50% of lightning injuries (1)
Blunt injury: Caused by shock wave production and/or muscle contractions produced (2,3)
Lightning injures are caused by:
High voltage
Heat production
Explosive force
Blunt trauma
May all cause:
Head injury
Burns
Fractures
Neurological problems
Contusions
Hematologic abnormalities
Cardiopulmonary injuries (2,4)
Risk Factors
Lightning incidence increases as you move closer to the equator.
Tropical and subtropical areas of the world have a higher rate of injuries and fatalities.
Improvements in a region's economic system, urbanization, and housing decreases lightning
victim incidence:
Secondary to advancements in plumbing and wiring providing protection
3 factors determine whether something is statistically more likely to be hit by lightning:
Isolation
Height
Narrowness of the tip of the object facing the cloud:
Only 1st 2 apply to humans (1)
General Prevention
Formalize a lightning safety policy.
Identification of a chain of command, a weather watcher, and a means to monitor forecast
Designate safe locations within a building with plumbing and wiring that aid in grounding the
building:
Cars are a safe location as long as you are not in contact with metal frame.
Use flash to bang (“30–30” rule): If the time between a visible lighting flash and associated
thunder bang is 30 sec or less, all involved should have already sought out appropriate
shelter:
Lightning may strike as far as 10 miles in any direction.
At least 10% of lightning hits when blue sky is visible
Wait 30 min after last lightning or thunder strike before resuming activity. Postpone or
suspend activity if thunderstorm is imminent.
Avoid using plumbing facilities and landline phones during a thunderstorm (good conductors of
electricity).
Avoid highest point in area (ie, trees).
Keeping participants and patrons aware of lightning safety procedures (when lightning strike
seems imminent, assume lightning-safe position). See “Patient Education” section (3,4).
Diagnosis
Confirmatory history from bystanders or rescuers of the circumstances of the injury
Cardiac asystole:
Due to direct current injury
May resolve spontaneously as the heart's intrinsic automaticity resumes
Respiratory arrest:
Due to paralysis of medullary respiratory center
May persist longer than cardiac asystole and lead to hypoxic-induced ventricular fibrillation
Acute myocardial infarction rare
Shock:
Neurogenic (spinal injury)
Hypovolemic (trauma-related hemorrhage)
Mottled or cold extremities due to autonomic vasomotor instability:
Usually resolves spontaneously in a few hours
Confusion
Memory defects
Alteration of level of consciousness (>70% of cases)
Flaccid motor paralysis
Seizures
Fixed dilated pupils may be evident; however, fixed and dilated pupils may be a manifestation
of the lightning injury and not indicative of true neurologic function, and should not be used as
an indication in these patients to stop the resuscitative efforts.
Blunt trauma:
To the head or spine
Fractures, dislocations, muscle tears, and compartment syndromes
Ruptured tympanic membrane with ossicular disruption (up to 50%); also temporary hearing
loss due to shock wave/thunder
Burns:
Discrete entrance and exit wounds uncommon
Thermal burns due to evaporation of water on skin, ignited clothing, heated metal objects
(buckles/jewelry)
Feathering (fern-like pattern) “burns” (Lichtenberg figures):
Cutaneous imprints from electron showers that track over skin
Pathognomonic of lightning injury
Resolve within 24 hr
Cataracts occur days to years postinjury
Corneal lesions
Intraocular hemorrhages
Retinal detachment
Physical Exam
Lichtenberg figures (superficial feathering or ferning pattern on skin)
Punctate burns
Linear burns (2,4)
Consider lightning strike in unwitnessed falls, cardiac arrests, or unexplained coma in an
outdoor setting.
Other causes of coma, cardiac dysrhythmia or trauma:
Hypoglycemia
Intoxication
Drug overdose
Treatment
Pre-Hospital
In cases with multiple lightning injuries, treat the patients who are not moving
1st, as they are in need of Advanced Trauma Life Support management.
Typically, all lightning strike victims who do not experience cardiac or
respiratory arrest survive. Normal triage properties are reversed in this case.
You should treat those who are not moving 1st, as the resuscitation should be
directed to those with cardiac or respiratory arrest.
Survey scene for safety (ie, continued lightning strikes)
ABCs (airway, breathing, circulation)
Perform basic life support.
Use advanced life support as necessary (4).
Activate emergency protocol.
Move victim to safe location.
Conduct primary and secondary survey.
Calculate and treat specific injury (ie, apnea, asystole, hypothermia, shock,
fractures, and burns) (3).
ED Treatment
Treatment should be directed towards life-threatening injuries (ie,
cardiopulmonary arrest, neurological deterioration, or severe burns).
Continue supportive measures.
Evaluate and treat for hypothermia and shock (3).
Evaluate and treat for fractures and/or burns (3).
Obtain laboratory tests, including urinalysis, CBC, electrolytes, serum
myoglobin, blood urea nitrogen, creatinine, creatine phosphokinase with
cardiac isoenzymes, and ECG (2).
ECG finding: Prolonged QT, generally resolves without treatment
Medication
Medications for pain relief if no other significant pathology noted
Referral to specialist will depend on type and severity of symptoms after lightning
strike.
It has been hypothesized, yet not proven, that burn surgeons may use vitamin C
and vitamin E to decrease scarring for electrical burns.
ABCs
Standard Advanced Cardiac Life Support measures for cardiac arrest
Diligent primary and secondary survey for traumatic injuries:
Maintain cervical spine precautions until cleared
Treat altered mental status with glucose, naloxone, or thiamine if person found
down with unexplained history of injury and unconscious; not true if lightning
strike witnessed
Hypotension requires volume expansion, pressor agents, and recognition on
any source of bleeding.
Admission Criteria
All victims need to be transported to hospital and evaluated in the emergency
department.
Standard of care for any complications noted (ie, chest pain, seizures,
respiratory distress)
Large majority of lightning strike victims are not admitted.
Provide reassurance once cleared and all further evaluations if indicated (1,4)
Ongoing Care
Patient Monitoring
Victims usually benefit from support network:
Lightning Strike and Electric Shock Survivors http://lightning-strike.org
http://www.struckbylightning.org/
Neuropsychology battery of testing as indicated for mental status assessment (2)
Patient Education
All persons must understand the severity of a threatening storm:
Know warning signs of imminent lightning strike (3):
Hair standing on end
“Bacon sizzling” sounds
Assume safe position if this occurs: Crouch with feet together, weight on balls of feet, head
lowered while covering ears
Lightning myths that are NOT true (4):
Metal attracts lightning: Despite popular belief, nothing attracts lightning.
Rubber tires protect you in a car: While you are protected in a car, tires have nothing to do
with it.
Dangerous to make contact with victims of lightning strike
Lightning never strikes same location twice.
Lighting always hits the highest object.
No place outside is totally safe when thunderstorms are in the area.
National Weather Service: www.lightningsafety.noaa.gov
Prognosis
Dependent on mechanism of lightning strike and subsequent systemic involvement
Complications
Headache
Sleep disorders
Irritability
Psychomotor impairment
Sympathetic nervous system dysfunction
Posttraumatic stress disorder (2)
References
1. Cooper MA. eMedicine, June 12, 2009. Lightning injuries.
2. DeFranco MJ, Baker III CL, DaSilva JJ, et al. Environmental Issues for
Team Physicians. Am J Sports Med. 2008;36:2234–2235.
3. Walsh KM, Bennett B, Cooper MA, et al. National Athletic Trainers'

Association Position Statement: Lightning Safety For Athletics and
Recreation. J Athl Train. 2000;35:471–477.
4. Zafren K, Durrer B, Herry JP, et al. Lightning injuries: prevention and on-site
treatment in mountains and remote areas. Official guidelines of the
International Commission for Mountain Emergency Medicine and the Medical
Commission of the International Mountaineering and Climbing Federation.
Resuscitation. 2005;65:369–372.
Additional Reading
Cooper MA, Andrews CJ, Holle RL, et al. Lightning injuries. In: Auerbach PS,
ed. Wilderness medicine. 4th ed. St. Louis: Mosby, 2001:73–110.
Holle RL, Lopez RE, Howard KW, et al. Safety in the presence of lightning.
Semin Neurol. 1995;15:375–380.
Bennett BL, Holle RL, Lopez RE. Lightning safety guideline 1D. 2009–2010
National Collegiate Athletic Association Sports Medicine Handbook.
Overland Park, KS: National Collegiate Athletic Association; 2009–2010:12–
14.
Codes
ICD9
994.0 Effects of lightning
Clinical Pearls
Preparedness is the only prophylactic measure that can reduce injuries due to
lightning strikes.
Use of the “30–30 rule” (when time between seeing the lightning and hearing
the thunder is 30 sec or less) as the signal to seek appropriate shelter.
Initiation of cardiopulmonary resuscitation as soon as safely possible is
essential (important to remember victims are safe to touch as they no longer
carry electrical charge).
Little Leaguer's Elbow (Medial Apophysitis)
Robert G. Hosey
Brian Macy
Basics
Description
Classic definition: Valgus stress lesion of the medial epicondylar physis
On a continuum with avulsion fracture of the medial epicondyle
Now used as a catch-all phrase for elbow pain in a young athlete:
Medial epicondylar fragmentation and avulsion
Delayed or accelerated apophyseal growth of the medial epicondyle
Delayed closure of the medial epicondylar growth plate
Osteochondrosis and osteochondritis of the capitellum (Panner's disease)
Deformation and osteochondritis of the radial head
Hypertrophy of the ulna
Olecranon apophysitis
Epidemiology
In a longitudinal study, 26% of 9–12-yr-old pitchers report “elbow pain” following a game.
Of the symptomatic elbows, about 67% were referred to the medial aspect.
In total, 1% of pitchers during a season saw a physician for “elbow pain,” and these were
diagnosed with medial epicondylitis.
Risk Factors
Position: Shows magnitude of stress (pitcher > catcher > infielder > outfielder)
Activity level: Types of pitches, number of pitches, innings pitched, typical pitching rotation
Increased age and weight
Handedness: Occurs most commonly in the dominant arm, unless it is a traumatic event
Family history of osteochondrosis
Glenohumeral internal rotation deficit (GIRD)
Etiology
There are 6 distinct secondary centers of ossification in the elbow.
The medial epicondyle may arise from more than one ossific nucleus and is commonly the
last epiphyseal center to fuse with the humeral shaft in the normal child; it may fuse as late
as 17 yrs of age.
The medial epicondyle is the site of attachment for the flexor muscle origins and the ulnar
collateral ligament.

Flexion contracture
If avulsion fragment is incarcerated in the joint, it can severely damage the articular surface.
Diagnosis
History
Age: Important because of the different ages at which each growth center appears and/or
closes
Location: Most commonly, pain is located in the medial epicondyle; however, sometimes pain
presents laterally or posteriorly.
Duration (pain characteristics): The length of time that the athlete has had pain is usually an
indirect measure of the severity of the problem. If the pain occurs during and after throwing
as well as when the athlete is not throwing, it is an ominous sign.
Radiation: If pain or numbness radiates into the last 2 fingers, consider ulnar nerve damage.
Mechanism (acute vs chronic): Acute pain in the young athlete in the medial elbow is more
consistent with avulsion fracture of the medial epicondyle.
Physical Exam
Pain in medial elbow
Pain accentuated during early and late cocking of throwing motion
Decrease in control of pitches or throwing distances
Bilateral comparison of the elbows
Inspection: Note presence of swelling, muscle atrophy/hypertrophy, symmetry, carrying angle
(normal = 5–10 degrees in males, 10–15 degrees in females); ecchymosis is indicative of an
avulsion.
Palpation: Medial/lateral epicondyles (point tenderness along medial epicondyle consistent
with avulsion fracture), olecranon process, radial head, collateral ligaments, ulnar nerve
Range of motion: Flexion/extension (flexion contracture >15 degrees consistent with avulsion
fracture); supination/pronation usually normal; assess for ulnar collateral ligament stability
with valgus stress at 20 degrees of flexion
Evaluation of the shoulder to assess for scapular dyskinesia, GIRD, and rotator cuff strength
Neurologic: Check sensation along the ulnar nerve distribution; check Tinel's sign at the
cubital tunnel; check interosseous muscle strength in the hand.

Imaging
Radiography is indicated if there is decreased range of motion, or there is a suspicion of an
avulsion fracture.
Anteroposterior/lateral views of the elbow
Appearance of growth centers: CRITOE:
Capitellum: Appears at 1–2 yrs of age
Radial epiphysis (3–4 yrs)
Inner epicondyle (medial epicondyle, 5–6 yrs)
Trochlea (9–10 yrs)
Outer epicondyle (lateral epicondyle >10 yrs)
Obtain bilateral elbow views if needed for comparison.
Assess for presence of anterior and especially posterior fat pads, which signify the presence
of an effusion.
Compare medial epicondylar ossification centers.
Assess for displacement of epicondylar fragment.
Medial epicondylitis
Avulsion fracture
Ulnar collateral ligament sprain/tear
Ulnar nerve injury
Osteochondritis dissecans (may have lateral pain)
Avascular necrosis of the capitellum (may have lateral pain)
Neoplasms
Referred pain: Neck vs shoulder vs wrist
Treatment
Pitch-count guidelines
Acute treatment:
Typically, 4–6 wks of rest
Followed by progression of noncompetitive throwing program
Ice and NSAIDs as needed
Treatment depends on the amount of displacement of the medial epicondylar
physis.
If fragment is minimally displaced (2–5 mm):
Apply posterior splint until acute symptoms resolve (2–3 wks)
Gradual active motion
Radiologic healing by 6 wks; at this time start aggressive active motion
When union is obvious, allow the patient to throw if pain-free
Allow return to competitive play when there is normal range of
motion/strength/endurance while throwing
If fragment is displaced more than 5 mm:
Open reduction and internal fixation
2 cancellous screws to prevent rotation
Allow early gradual active motion
After 6 wks, aggressive rehabilitation program
Ongoing Care
Closed reduction is associated with pseudoarthrosis, causing pain and instability, as well
as formation of double epicondylar epiphyses.
Additional Reading
Benjamin HJ, Briner WW. Little league elbow. Clin J Sport Med. 2005;15:37–40.
DaSilva MF, Williams JS, Fadale PD, et al. Pediatric throwing injuries about the elbow. Am J
Orthop. 1998;27:90–96.
Klingele KE, Kocher MS. Little league elbow: valgus overload injury in the paediatric athlete.
Sports Med. 2002;32:1005–1015.
Lyman S, Fleisig GS, Waterbor JW, et al. Longitudinal study of elbow and shoulder pain in
youth baseball pitchers. Med Sci Sports Exerc. 2001;33:1803–1810.
Papavasiliou VA. Fracture-separation of the medial epicondylar epiphysis of the elbow joint.
Clin Orthop Relat Res. 1982:172–174.
Codes
ICD9
726.31 Medial epicondylitis
732.6 Other juvenile osteochondrosis
Clinical Pearls
In the adolescent, the type of pitch affects incidence because proper technique
and muscle control have not yet been learned. Breaking pitches, such as the
screwball, in the untrained adolescent pitcher will place more stress on the
medial aspect of the elbow, increasing the likelihood of developing medial elbow
pain.
At present, most youth baseball leagues have rules that limit the number of
innings per week and length of time between pitching appearances. In addition,
specific pitch count recommendations have been published and been adopted
by the Little League (see
http://www.littleleague.org/Assets/forms/pubs/RR/Changes/BB/09.pdf).
Best prevention is to follow established pitching guidelines set forth by Little
League. An offseason conditioning and throwing program may also be helpful.
If pain does begin to occur, the player should stop throwing and see a
physician.
Little League Shoulder (Proximal Humeral
Epiphysiolysis)
Mike LaGrange
Tracy Ray
Basics
Description
Remodeling and deformation of the proximal humeral physis
Overuse injury from recurrent, excessive torque placed on the growth plate
Typically seen in overhead athletes, especially adolescent baseball pitchers. Results from
recurrent, excessive overhead activity.
1st described in 1966 as osteochondrosis of the proximal humeral epiphysis and then
reported again in 1974 as proximal humeral epiphysiolysis in adolescent baseball players
Epidemiology
Uncertain exact prevalence due to under-reporting of pain with throwing
Most common in male baseball players between ages of 11 and 13
Has also been reported in swimming, volleyball, and cricket
Can occur in any adolescent athlete involved in repetitive overhead rotational activities
Risk Factors
The following risk factors are based on expert opinion, as no studies have evaluated this to the
author's knowledge:
Year-round pitching without 3 mos of rest from throwing during the course of the year
Playing in multiple leagues at the same time
Going over recommended age-specific pitch count for game, season, or year
Inadequate rest between pitching outings
Improper throwing mechanics
Throwing with a fatigued shoulder
Genetics
No known genetic disposition
General Prevention
Prevented by avoiding excessive, repetitive overhead activities; having adequate rest between
outings; and not throwing with shoulder fatigue or pain
Etiology
Unknown exact etiology
Biomechanical studies have revealed shear stress arising from high torque during late
cocking phase is large enough to lead to deformation of the proximal humeral growth plate.
Diagnosis
Diagnosis based on history, physical, and classic radiographic findings
History
Patients typically complain of pain while throwing or with overhead activity.
Pain with throwing is typically constant throughout throwing cycle.
Most commonly presents with pain laterally over the proximal humeral physis, but can
present with diffuse pain all over shoulder or referred pain to upper arm.
Insidious onset of pain
Patients may report recent increase in number of pitches thrown or recent change to playing
on a larger field.
Physical Exam
Typical physical exam finding is tenderness to palpation over the proximal humeral physis
without erythema, increased warmth, or soft tissue swelling.
Can present with painful range of motion, including pain with abduction or forward flexion
>150 degrees
Can present with decreased strength of the rotator cuff musculature secondary to pain. Most
common is reduced strength and pain with resisted external rotation.

Standard x-rays are the diagnostic gold standard.
Imaging
Anteroposterior of the affected shoulder in external rotation and internal with comparison
films of the unaffected side are standard.
Typical findings are widening of the affected growth, plate especially on the lateral side of the
growth plate.
May also see osteolysis and cortical irregularity of the bone surrounding the physis
MRI will also show widening of the growth plate on the T1-weighted images with possible
extension of signal into the metaphysis on T1 and gradient echo images.
Rotator cuff tendonitis/impingement
Multidirectional instability
Labral tear (usually SLAP tear)
Salter Harris I fracture of the proximal humeral physis
Biceps tendonitis
Osteochondral fragment of the glenoid
Treatment
Treatment consists of rest from throwing and limited use of OTC pain
medications such as acetaminophen or NSAIDs as needed for pain.
Recommend rest from throwing for 3 mos
Physical therapy during rest period should focus on rotator cuff strengthening
and improved range of motion at the shoulder.
Recommended to complete an interval throwing program after finishing
physical therapy/3 mos rest before returning to full activity
Medication
Age-appropriate dose of any NSAID or acetaminophen can be used as needed
for pain during initial period of rest.
No surgical correction required
Ongoing Care
Recommended to re-evaluate the patient in office again after 3 mos
rest/physical therapy to reassess exam and give guidance on starting an
interval throwing program
Repeat x-rays are not necessary at return visit, as it can take up to a year for
growth plate to return to normal.
Patient Education
Patients, parents, and coaches should be educated on age-appropriate
pitching recommendations, including pitch counts and age restrictions on
throwing specialty pitches.
Should also stress importance of not throwing with a fatigued arm or painful
shoulder as this can lead to future injury
Prognosis
Patients treated with appropriate rest have an excellent long-term prognosis.
Complications
Alteration of throwing mechanics from throwing with pain may lead to other
injuries, such as labral tears or injuries to the elbow of the same arm.
Additional Reading
Adams JE. Little league shoulder: osteochondrosis of the proximal humeral
epiphysis in boy baseball pitchers. Calif Med. 1966;105:22–25.
Drescher WR, Falliner A, Zantop T, et al. Little league shoulder syndrome in

an adolescent cricket player. Br J Sports Med. 2004;38:E14
Johnson JN, Houchin G. Adolescent athlete's shoulder: a case series of

proximal humeral epiphysiolysis in nonthrowing athletes. Clin J Sport Med.
2006;16:84–86.
Kocher MS, Waters PM, Micheli LJ. Upper extremity injuries in the
paediatric athlete. Sports Med. 2000;30:117–135.
Obembe OO, Gaskin CM, Taffoni MJ, et al. Little Leaguer's shoulder
(proximal humeral epiphysiolysis): MRI findings in four boys. Pediatr Radiol.
2007.
Sabick MB, Kim YK, Torry MR, et al. Biomechanics of the shoulder in youth
baseball pitchers: implications for the development of proximal humeral
epiphysiolysis and humeral retrotorsion. Am J Sports Med. 2005;33:1716–
1722.
Codes
ICD9
Clinical Pearls
An adolescent should never throw with shoulder pain or fatigue.
Loss of velocity or pitch control during an outing are signs of shoulder fatigue.
Low Back Pain and Lumbar Strains
Robert G. Hosey
M. Kyle Smoot
Basics
Description
Acute low back pain is pain of <3 mos' duration localized below the costal margin but above
the inferior gluteal folds with or without leg pain.
Synonym(s): Lumbar strain; Lumbar sprain; Lumbago; Low back syndrome
Acute pain is felt in the low lumbar, lumbosacral, or sacroiliac region. It is often accompanied
by sciatica, pain radiating down the distribution of the sciatic nerve.
Chronic low back pain is the same unremitting pain that has been present for more than 3
mos.
Epidemiology
The total costs of low back pain in the U.S. exceed $100 billion per year from direct and
indirect costs.
The most common musculoskeletal reason for office visits to primary care providers
Most common between the ages of 35 and 55
1% of the U.S. population is chronically disabled because of back problems, and another
1% is temporarily disabled.
Incidence
70% of people in developed countries will experience low back pain at some time in their
lives.
90% of people experience low back pain in their lifetime, and 5–10% will develop chronic
back pain.
Various authors have reported incidences of 16–22% in populations 8–14 yrs of age.
Prevalence
Annual prevalence in the U.S. population is 15–20%.
Increases with age, peaking during the 6th decade of life
Risk Factors
Age
Activity
Occupation
Obesity
Smoking
Sedentary lifestyle
Psychosocial factors
Poor posture
Chronic flexion injuries
General Prevention
Exercise programs, posture training, body mechanics training, and weight loss have been
advised.
U.S. Preventive Services Task Force has concluded that current evidence is not adequate to
recommend for or against the routine use of interventions to prevent low back pain in adults.
Diagnosis
History
Initial history should focus on the patient's age and pain characteristics (onset, duration,
severity, quality, radiation, aggravating factors, alleviating factors).
Question patient about mechanism of injury and occupation.
Determine if serious underlying conditions (red flags) are responsible for the back pain:
Fracture (steroid use, trauma, menopausal status); infection (fever, IV drug use, adenopathy,
immunosuppression); cancer (weight loss, adenopathy, previous cancer); cauda equina
syndrome (bowel or bladder incontinence, saddle anesthesia, major limb motor weakness).
Assess psychological and socioeconomic problems.
The patient should be assessed for the following red flags:
Is patient under 20 or over 55 with no prior history of back pain? Most low back pain (LBP)
occurs in patients 30–50 yrs of age.
Known or previous cancer? Assume bone metastasis until otherwise proven.
IV drug abuse? Assume spinal abscess if tender.
Is pain worse when you lie down? LBP is relieved by bed rest.
Is pain associated with fever, chills, or weight loss? Look for infection or tumor.
Loss of bowel or bladder control and/or caudal anesthesia? Look for cauda equina
syndrome.
Physical Exam
Pain located below the costal margin but above the inferior gluteal folds
Possible radiation of pain to buttocks and lower extremity
Pain aggravated by movement and alleviated by rest
Limited range of motion of back
Paraspinal muscular spasm is common.
Assess severity of pain by observing the patient's gait, posture, and demeanor.
Prior to examining the back, check the temperature, weight, skin, abdomen, pelvis, groin,
peripheral pulses, and lymph nodes for pathology that may mimic spinal disease. A rectal
exam should be performed to assess sphincter tone.
With the patient standing, assess stance, spinal curvature, range of motion, heel-walk, toe-
walk, and squat. Locate area of maximal pain.
With patient sitting, assess deep tendon reflexes of the knee and ankle.
With the patient supine, assess the straight-leg raise, ankle and great toe dorsiflexion, hip
range of motion, sacroiliac joint stability, muscle strength testing, and sensory testing.
With the patient in the prone position, assess buttock symmetry and perform femoral stretch
test.
Pain in low back is exacerbated by movement and is often accompanied by focal muscle
spasm in the lumbar extensors.
Patients prefer to stand in a semiflexed position and move slowly rather than sit motionless
on the exam table.
Walk on heels (L4–5), then toes (S1–2).
Back muscles uncoordinated or guarding (signs for spasm)
Ankle and knee reflexes (objective data without reliance upon patient's volition)
Straight-leg raising and crossed straight-leg raising (possible acute disc herniation)

Imaging
In the absence of red flag symptoms, imaging can usually be delayed until 30 days after the
initial assessment. This approach allows 90% of patients to recover spontaneously and
avoids unneeded procedures.
If symptoms persist >30 days, consider plain radiographs, CT scan, MRI, and bone scan.
If no red flags are identified in the history, then no imaging tests or laboratory tests are
indicated.
If a red flag is identified, then proceed with diagnostic testing as indicated.
Herniated disc
Musculoskeletal sprains and strains
Posterior facet syndrome
Spondylolisthesis
Spinal stenosis
Osteoporosis
Referred pain
Tumor
Infection
Fracture
Genitourinary
Gynecologic
Psychogenic
85% mechanical back pain (MBP)
5% symptomatic herniated disc
4% compression fracture
4% spondylolysis/spondylolisthesis
2% tumor, infection, rheumatologic disease, or referred pain
Treatment
Natural history of MBP, regardless of treatment:
33% resolves within 1 wk.
70% resolves by 3 wks.
90–95% resolves in 3 mos.
Analgesia:
Tylenol for 2 wks (as effective as NSAIDs if given on schedule)
NSAIDs provide pain relief and allow early ambulation (caution for renal
insufficiency, pregnancy, HTN, GI intolerance)
Short-term nonopioid on a schedule basis (Ultram 50 mg 3 times daily)
Short-term muscle relaxants or opioids to assist sleep (potential for
dependence)
Bedrest:
Relative bedrest for 2 days (longer bedrest delays recovery)
Manipulative medicine:
Manual therapy aimed at restoring maximal pain-free movement of the
musculoskeletal system has significant proven benefit for acute low back
pain.
Passive therapy such as massage, physical therapy modalities, and traction
have no proven benefit.
Systemic corticosteroids:
Contraindicated
No proven benefit and significant potential harm (avascular necrosis of the
hip)
Antidepressants:
Antidepressants do not reduce pain or improve functional status in patients
with nonspecific LBP.
Injection therapy:
A Cochrane review has concluded that the evidence regarding the efficacy of
prolotherapy injections is conflicting for patients with chronic low back pain. In
addition, prolotherapy has not been found to be an effective treatment for
chronic low back pain.
Acupuncture:
A randomized controlled trial has demonstrated that acupuncture can
improve pain symptoms in comparison to placebo; however, more data are
needed.
Long term:
Systematic review of the literature of chronic LBP concluded that
individualized, exercise therapy programs that incorporated stretching or
strengthening and supervision may improve pain and function in chronic
nonspecific low back pain.
Cochrane review of the literature added that there is evidence that a graded
activity program improves absentee outcomes in subacute LBP. In acute low
back pain, exercise therapy is as effective as either no treatment or other
conservative treatments.
Medication
NSAIDs are the agents of choice to treat acute low back pain. Tylenol may be
used as an alternative.
Prolonged opioid use (>2 wks) should be avoided.
Muscle relaxants may be beneficial.
Avoid debilitation—keep activity as normal as possible. It takes twice as long to
regain conditioning as it does to lose it.
Goal of therapy is increasing function, not absence of pain.
General Measures
Bedrest for 2–4 days may be required in patients with severe initial symptoms
of sciatica. Prolonged bedrest (>4 days) should be avoided.
Patients should be advised to stay active because this speeds recovery and
reduces time away from work. Begin with low-stress aerobic activity such as
walking, riding a bicycle, swimming, and eventually jogging.
After 2 wks of general activity, specific conditioning exercises for trunk
muscles may be helpful.
Physical therapy may be helpful during the 1st month of symptoms.
Referral
Rapidly progressive neurologic deficits, symptoms of cauda equina syndrome or
cord compression, acute vertebral collapse, suspicion of infection
Considered only when serious spinal pathology or nerve root dysfunction due
to a herniated lumbar disc is detected
Patients with acute LBP alone, without findings of serious conditions or
significant nerve root compression, rarely benefit from surgery.
Surgery has not been proven to help back pain without radiculopathy.
Ongoing Care
Early osteopathic or chiropractic referral is often beneficial.
Early orthopedic or physical therapy referral is rarely indicated.
Begin walking as soon as possible.
Additional Reading
Acute low back problems in adults. AHCPR Publication No. 95–0642, December 1994.
Brinkhaus B, Witt CM, Jena S, et al. Acupuncture in patients with chronic low back pain: a
randomized controlled trial. Arch Intern Med. 2006;166:450–457.
Dagenais S, Yelland MJ, Del Mar C, et al. Prolotherapy injections for chronic low-back pain.
Cochrane Database Syst Rev. 2007:CD004059.
Hayden JA, van Tulder MW, Malmivaara A, et al. Exercise therapy for treatment of non-
specific low back pain. Cochrane Database Syst Rev. 2005:CD000335.
Jones GT, Macfarlane GJ. Epidemiology of low back pain in children and adolescents. Arch
Dis Child. 2005;90:312–316.
Katz JN. Lumbar disc disorders and low-back pain: socioeconomic factors and
consequences. J Bone Joint Surg Am. 2006;88(Suppl 2):21–24.
Rakel RR. Essentials of family practice, 2nd ed. Philadelphia: WB Saunders, 1998.
Taylor RB. Manual of family practice: manual of family practice. Boston: Little, Brown,
1996.
U.S. Preventive Services Task Force. Primary care interventions to prevent low back pain in
adults: recommendation statement. Am Fam Physician. 2005;71:2337–2338.
Urquhart DM, Hoving JL, Assendelft WW, et al. Antidepressants for non-specific low back
pain. Cochrane Database Syst Rev. 2008:CD001703.
Codes
ICD9
724.2 Lumbago
847.2 Lumbar sprain
Lumbar Disc Disease
Matthew D. Shores
Basics
Description
In regard to terminology, lumbar disc disease may represent a broad spectrum of pathology,
including disc herniations, disc space narrowing, disc desiccation, and sclerosis of the end
plates, as well as many lumbar spine abnormalities with various etiologies:
Most commonly, the term refers to lumbar disc herniation, and this topic most specifically
addresses lumbar disc herniation.
Lumbar disc herniations are the most common cause of sciatica, although not the only cause.
Epidemiology
Incidence
Approximate lifetime incidence is 5% in males and 2.5% in females.
Peak incidence is between the 4th and 6th decades of life (30s to 50s).
Risk Factors
Lifestyle risks include sedentary occupations, physical inactivity, and smoking.
Increased tendency in families with acquired spinal disorders, such as ankylosing spondylitis
and degenerative arthritis.
In addition, more common in patients with increased height and weight.
Etiology
Compromise in the integrity of the annulus fibrosus may allow herniation of the nucleus
pulposus.
Herniation of the nucleus pulposus of the disc may compress and irritate the adjacent nerve
root.
Most common site of herniation is L5–S1, affecting the S1 nerve root. 2nd most common site
of herniation is L4–L5, affecting the L5 nerve root.
Diagnosis
History
Often presents with history of multiple episodes of back pain that vary in severity and
duration:
This accumulated recurrent back pain can lead to disc herniation.
May present following an acute lifting or twisting injury
Often worsened by coughing, sneezing, and Valsalva
Presents with sciatic pain, that is, pain originating in the low back and radiating from the
buttock down the posterior or lateral thigh to the ankle or foot:
Patients may have a difficult time finding a position of comfort.
Sciatica has a high sensitivity for lumbar disc herniation but low specificity:
More specific for disc herniation if pain is greater in the leg than in the back or pain that is
worse with the Valsalva maneuver.
Can present with back pain that does not radiate, but patient may note motor or sensory
deficits.
Red flag symptoms that may indicate an alternative diagnosis, including cauda equina
syndrome, infection, or neoplasm:
Fecal incontinence
Loss of motor function
Perianal numbness
Radicular symptoms lasting >6 wks
Saddle anesthesia
Urinary retention
Unexplained fever
Weight loss
Physical Exam
A full physical exam of the back, pelvis, and lower extremities should be done, including a
detailed neurological exam.
Provocative tests should include a straight leg raise test, the most sensitive test for lumbar
disc herniation (1):
Straight leg raise can be done seated or supine, although for lumbar disc herniation, supine
test has higher sensitivity (1).
Crossed straight leg raise is highly specific for lumbar nerve root entrapment, including that
caused by lumbar disk herniation.
Other findings may include:
Sensory loss:
Medial foot, including plantar aspect of 1st toe sensory loss (L4 involvement)
Dorsum of the foot sensory loss (L5 involvement)
Lateral heel sensory loss (S1 involvement)
Tendon reflex changes:
Diminished or lost patellar tendon reflex (L4 involvement)
Please note: There is no L5 tendon reflex
Diminished or lost Achilles reflex (S1 involvement)
Motor finding (often late findings):
Weak tibialis anterior and quadriceps (L4 involvement)
Weak foot inversion, eversion, dorsiflexion, and 1st toe extension (L5 involvement)
Weak hamstrings or gastrocnemius (S1 involvement)
Please note Waddell's signs to assess malingering:
Tenderness:
Superficial tenderness with light palpation or tenderness on deep palpation but
nonanatomic over a large area
Simulated tests:
Axial loading causes low back pain, or rotation of the hips and shoulders together
causes low back pain
Distraction:
Formal straight leg raise is positive, but when distracted, straight leg raise does not
produce pain.
Regional sensory or motor changes:
Glove and stocking sensation loss or nonanatomic muscular weakness (various muscles
innervated by different nerve roots)
Overreaction:
Exaggerated response or emotions

Imaging
MRI is the preferred imaging modality; however, in the absence of red flag symptoms, MRI
should be delayed for a 6-wk trial of conservative treatment. If symptoms persist beyond 6
wks, MRI may then be considered (1)[A]:
Please note, it has been demonstrated that in asymptomatic patients under the age of 60
with no history of back complaints, 50% of patients had bulging discs and nearly 25% had
herniated discs on MRI (2,3).
Emergent imaging may be considered for red flag symptoms such as urinary retention, fecal
incontinence, saddle anesthesia, progressive neurologic changes, and intractable pain.
Plain radiographs may be beneficial to rule out bony abnormalities (such as metastic disease
or fractures); in addition, they may demonstrate age-related degenerative changes.
Cauda equina syndrome
Hip arthritis
Knee arthritis
Meralgia paresthetica
Piriformis syndrome
Sacroiliitis
Spinal neoplasms
Spinal stenosis
Trochanteric bursitis
Vascular insufficiency
Vertebral fracture or infection
Treatment
Medication
First Line
NSAIDs, acetaminophen, and muscle relaxants may be effective for
nonspecific low back pain, but studies for lumbar disc herniation are limited (1)
[B].
In the treatment of pain associated with lumbar disc herniation, systemic
steroids are no better than placebo (1)[A].
Opioid medications and opioid agonists, such as tramadol, are often included
as a standard component in the conservative treatment of patients with severe
pain, although their use has not been extensively studied.
Second Line
In lumbar disc herniation, epidural steroid injections can improve pain in the short
term, but do not provide long-term relief (1,4)[A].
Physical therapy is often incorporated as a component of conservative therapy:
However, evidence shows little to support physical therapy in improving pain or
functional status.
Modalities such as US and transcutaneous electrical nerve stimulation (TENs)
do not have enough quality evidence to clearly assess their effectiveness,
although they may provide some short-term benefit.
Traction produces conflicting evidence, but systemic reviews indicate that
traction is not effective.
Aerobic conditioning and trunk muscle strengthening are important for good
outcomes.
Immediate indications for surgery include:
Acute myelopathy
Severe motor deficits
Intractable pain
In addition, surgery may be considered with the failure of conservative therapy
to provide relief within 6–12 wks (1)[A].
Surgical techniques include:
Open discectomy
Microdiscectomy
In comparison to conservative management, surgical discectomy has been
shown to provide quicker and better relief of pain associated with lumbar disc
herniation in the 1st 2 yrs:
This benefit has been documented up to 2 yrs, after which there is no
difference between surgery and conservative management (no long-term
benefits with surgery) (1,5,6)[A].
References
1. Gregory DS, Seto CK, Wortley GC, et al. Acute lumbar disk pain: navigating
evaluation and treatment choices. Am Fam Physician. 2008;78:835–842.
2. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans
of the lumbar spine in asymptomatic subjects. A prospective investigation. J
3. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance

imaging of the lumbar spine in people without back pain. N Engl J Med.
1994;331:69–73.
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;68:723–729.
5. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical vs nonoperative

treatment for lumbar disk herniation: the Spine Patient Outcomes Research
Trial (SPORT) observational cohort. JAMA. 2006;296:2451–2459.
6. Peul WC, van Houwelingen HC, van den Hout WB, et al. Surgery versus
prolonged conservative treatment for sciatica. N Engl J Med.
2007;356:2245–2256.
Additional Reading
Greer S, Chambliss L, Mackler L, et al. Clinical inquiries. What physical exam
techniques are useful to detect malingering? J Fam Pract. 2005;54:719–722.
Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on
imaging. Ann Intern Med. 2002;137:586–597.
Kerr RS, Cadoux-Hudson TA, Adams CB. The value of accurate clinical
assessment in the surgical management of the lumbar disc protrusion. J
Neurol Neurosurg Psychiatry. 1988;51:169–173.
Codes
ICD9
722.10 Displacement of lumbar intervertebral disc without myelopathy
722.52 Degeneration of lumbar or lumbosacral intervertebral disc
722.73 Intervertebral disc disorder with myelopathy, lumbar region
Clinical Pearls
Although the specificity is low, straight leg raise in the supine position is the
most sensitive physical exam test for lumbar disc herniation.
In the absence of red flag symptoms, conservative management may be
attempted for 6 wks prior to obtaining diagnostic imaging such as MRI.
Conservative management may include NSAIDs, muscle relaxants, and opoid
analgesics for severe pain:
Oral steroids have not been shown to be beneficial compared to placebo.
Epidural steroids may provide short-term relief, but have not been shown to
provide long-term relief.
Although in the 1st 2 yrs, surgery offers better improvement in pain in
comparison to conservative management, there is no difference in outcome
beyond 2 yrs.
Lunate Dissociation
Navid Mahooti
Thomas Trojian
Basics
Description
Dissociation, or dislocation, is classified by the pattern of carpal collapse, either dorsal or
volar in nature, after wrist trauma or injury.
The carpal bones in the wrist are stabilized by multiple extrinsic and intrinsic ligaments. The
scaphoid, lunate, and triquetrum have no tendon insertions and are described as an
intercalated segment (motion depends on mechanical signals from ligamentously intact
neighboring articulations) (1).
The dorsal component of the scapholunate interosseous ligament (SLIL) is the primary
stabilizer of the lunate. Important secondary stabilizers include the short radiolunate ligament
(SRL), which maintains the position of the lunate adjacent to the radius, and the dorsal
intercarpal (DIC) ligament. Several other extrinsic ligaments serve as secondary restraints
(1,2).
Injury typically occurs when an extended wrist undergoes a forced axial load, such as in a fall
on an outstretched hand (FOOSH) with the hand in ulnar deviation or when pushing a heavy
object.
Isolated carpal dislocations are rare. Most information on them comes from case reports and
surgical technique papers (2).
A number of injury patterns can occur with this mechanism, depending on several factors:
Position of the extremity at impact, quality of the bone, ligamentous strength, and direction of
the force (2).
Disruption of the SLIL eliminates the scaphoid's flexion (volar) force on the lunate and allows
the triquetrum to push the lunate into an extended (dorsal) position. Disruption of the SLIL
and at least one other secondary ligament (eg, the DIC) is required to show static changes in
scaphoid and lunate position [known as dorsal intercalated segment instability (DISI)] (3).
The lunotriquetral interosseus ligament (LTIL) is another important lunate stabilizer. LTIL
disruption causes an unopposed volarly directed force on the lunate by the scaphoid. Volar
intercalated segment instability (VISI) results (4).
The terms lunate dissociation, scapholunate dissociation, and perilunar dissociation and
dislocation have overlapping features. Similarly, injury patterns to the lunate and adjacent
structures have overlapping characteristics and nomenclatures.
Perilunate injuries are severe disruptions of carpal anatomy defined by dislocation of the
capitate head from the concavity of the distal lunate. The spectrum of injury ranges from a
perilunate dislocation (PLD), a soft tissue circumferential disruption around the lunate, to the
transscaphoid perilunate dislocation (TSPLD), which involves a scaphoid fracture rather than
a scapholunate ligamentous injury (5).
Mayfield initially described 4 stages of perilunate instability in 1980 that have since been
modified (2,5):
Stage 1: Disruption of scapholunate articulation
Stage 2: Lunocapitate dislocation
Stage 3: Lunotriquetral disruption
Stage 4: Volar lunate dislocation
A 4-stage classification system is used commonly to describe scapholunate dissociation
(SLD) (3):
Stage 1: Predynamic instability consists of the earliest scapholunate injury, typically a
partially torn or attenuated scapholunate membrane that causes abnormal motion,
synovitis, and wrist pain. Plain and stress radiographs are normal; arthroscopy may show
attenuation of the SLIL or hemorrhage within the scapholunate joint. Untreated, secondary
stabilizers may become attenuated and progress to dynamic or static instability.
Stage 2: Dynamic instability is characterized by ligamentous tear of the palmar or dorsal
aspect of the SLIL. Plain radiographs will be normal, but stress views show widening of the
scapholunate interval. An arthrogram may show abnormalities within the ligament.
Stage 3: Static instability occurs with injury to the SLIL and a secondary stabilizer and is
evident on plain radiography (gap of 3 mm or greater between the lunate and scaphoid or
a scapholunate angle >70 degrees on lateral views). DISI is often present.
Stage 4: SLAC refers to the final stage of SLD, the result of continued loads to a
biomechanically altered joint that lead to progressive articular cartilage deterioration and
eventually arthritis.
Synonym(s): Wrist sprain; Perilunate dissociation; Scapholunate dissociation; Scapholunate
instability
Dislocation is often used interchangeably with dissociation; a dislocated bone is always
dissociated, but a dissociated bone is not always dislocated.
Epidemiology
PLDs are the most common carpal dislocation (2).
More common in men in the 2nd and 3rd decades of life; less common in the elderly (distal
radius fails/fractures before ligamentous injury occurs) and children (radial physis is weaker,
resulting in Salter-Harris fractures) (2)
SLD is more common in football than in any other sport.
Wrist injuries account for an estimated 3–9% of all athletic-related injuries (4).
A 10-yr study done at the Cleveland Clinic revealed that 14.8% of athletic participants under
the age of 16 yrs sustained upper extremity injuries, and of these, 9% involved the wrist.
The incidence of lunate dissociation is uncommon, but failure to identify the injury results in
long-term disability.
Risk Factors
Any injury involving excessive wrist extension and ulnar deviation with intracarpal supination,
typically a FOOSH injury
Chronic crutch-walkers, gymnasts, American football players, collision sports
Increased ulnar negative variance
General Prevention
Controversy exists as to whether braces or wrist guards effectively prevent wrist injuries (4).
One cadaveric model showed decreased carpal fractures, ligament, and capsular tears with
bracing.
In-line skating-type guards have not been shown to prevent wrist fractures.
European studies of snowboarders show a significant decrease in the incidence of wrist
fractures and injuries with wrist guards.
Some are concerned that bracing/guards simply alter the area of force transmission.

Scaphoid fractures occur with a similar mechanism of injury (FOOSH) and therefore must be
ruled out.
Failure to diagnose and treat lunate dissociation increases the risk of arthritic degeneration
and development of SLAC wrist.
Diagnosis
History
Determine duration of pain: Most patients present acutely, but some report a history of
painful clicking, reduced grip strength, and giving way with activities.
Obtain detailed mechanism of injury to determine if SLD is a possible injury (typically a
FOOSH with ulnar deviated wrist).
Rule out any distracting injuries (elbow, forearm, etc.).
Physical Exam
Signs and symptoms:
100% of patients have dorsal wrist pain, 91% have decreased grip strength, and 71%
have decreased range of motion (ROM).
Clicking with wrist motion (nonspecific)
Inspect for swelling and deformity; compare with contralateral wrist.
Tenderness is typically on radial aspect of the wrist; palpate just distal to Lister's tubercle,
which is often tender as well.
Scaphoid tenderness (anatomic snuffbox) is a scaphoid fracture until proven otherwise.
Document ROM of wrist and neurovascular status (pulses, sensation, particularly median
nerve distribution because it can be diminished in severe dissociations owing to mechanical
forces).
Finger extension test: Hold wrist in flexion, and test active finger extension against
resistance; causes pain over lunate.
Watson's scaphoid test may be positive. The examiner places the thumb on the scaphoid
tubercle, and the 4 fingers wrap around the distal radius. While the wrist is in ulnar
deviation, pressure is directed dorsally with the thumb at the volar scaphoid. The wrist is
then radially deviated. Pain is the hallmark of a positive test result, although a dramatic
“clunk” may be felt or heard.
Kleinman's shear stress test for lunotriquetral instability: Wrist in neutral position,
examiner's contralateral thumb is placed over dorsal lunate while ipsilateral thumb loads
the pisotriquetral joint with a dorsally directed force. Pain is a positive test.
The Reagan shuck test and Linscheid compression test are other maneuvers to determine
lunotriquetral instability.

Imaging
Radiographs: Posteroanterior (PA), lateral, and oblique views of the wrist, clenched-fist view:
Gap of 3 mm on PA films (“Terry Thomas” or “Dave Letterman” sign, in reference to their
gapped teeth) is classically used. However, Cautilli obtained PA radiographs on 100 normal
wrists and found the mean gap in males was 4.0 mm and in females it was 3.6 mm. Zhu
performed a similar study and found the mean gap to be 3.14 mm. Both studies revealed
that gaps up to 5 mm were not necessarily indicative of carpal instability. Consequently,
contralateral wrist films should be obtained for comparison.
Lateral views: Dorsal extension of the lunate is referred to as DISI and is highly suggestive
of injury to the SLIL and at least one secondary stabilizer.
Scapholunate angle is normally 30–60 degrees on lateral view; an angle >70 degrees is
diagnostic (6); clenched-fist view accentuates injury.
Follow-up and special considerations:
3-phase bone scintigraphy is sensitive but nonspecific but has a high negative predictive
value (3).
MRI (1,6):
Complete SLIL tears are characterized by distinct area of discontinuity within the
ligament, outlined by fluid-like T2 hyperintensity, or by complete absence of the ligament.
Fluid signal at attachments also can be seen.
Detection of LTIL tears is more difficult, with a decreased sensitivity and specificity given
the smaller size of this structure.
MRI arthrography appears to have greater sensitivity at detecting partial tears of the SLIL
than does MRI or traditional arthrograms. Extravasation of contrast material indicates a
full-thickness ligamentous defect.
MRI arthrography has a sensitivity of 83–92% and a specificity of 46–100%.
Arthroscopic evaluation is the “gold standard” for identifying and grading scapholunate injuries
(3).
Scaphoid fracture
Colles' fracture
Scaphoid impaction syndrome
Dorsal wrist ganglion cyst
Other carpal bone injury
Treatment
Acute treatment
Analgesia; NSAIDs, narcotics
Only for least severe injury (eg, dynamic instability; see above)
Recommended for experienced providers only
Immobilization:
Partial tears of SLIL can be treated conservatively with splinting. Immobilize
with splint in correct anatomic position. Symptoms guide management.
Patients with suspected ligamentous injury should be referred promptly to an
orthopedist, preferably a hand specialist, because misdiagnoses can have
significant consequences.
Long-term treatment
Surgical referral:
Standard of care is operative repair.
Prolonged immobilization for weeks to months after surgery is necessary to
maintain carpal bone alignment and to prevent SLAC wrist.
Rehabilitation: Physical therapy after immobilization to improve ROM and
strength
Referral
Timely referral to hand surgeon if any question in the diagnosis
Immediate referral to hand surgeon if abnormal neurovascular status
Typically considered a season-ending injury
Standard of care typically involves open reduction, ligament repair, and internal
fixation (2).
References
1. Lau, Steven et al. Scapholunate dissociation: an overview of the clinical
entity and current treatment options. Eur J Orthop Surg Traummot.
2009;19:377–385.
2. Grabow RJ, Catalano L. Carpal dislocations. Hand Clin. 2006;22:485–500;

abstract vi–vii.
3. Manuel J, Moran SL. The diagnosis and treatment of scapholunate

instability. Orthop Clin North Am. 2007;38:261–277.
4. Slade JF, Milewski MD. Management of carpal instability in athletes. Hand

Clin. 2009;25:395–408.
5. Sauder DJ, Athwal GS, Faber KJ, et al. Perilunate injuries. Orthop Clin
North Am. 2007;38:279–288.
6. Bencardino JT, Rosenberg ZS. Sports-related injuries of the wrist: an

approach to MRI interpretation. Clin Sports Med. 2006;25:409–432, vi.
Additional Reading
Cohen MS. Ligamentous injuries of the wrist in the athlete. Clin Sports Med.
1998;17:533–552.
Mastey RD, Weiss AP, Akelman E. Primary care of hand and wrist athletic
injuries. Clin Sports Med. 1997;16:705–724.
Nguyen DT, McCue FC, Urch SE. Evaluation of the injured wrist on the field
and in the office. Clin Sports Med. 1998;17:421–442.
Rettig AC. Epidemiology of hand and wrist injuries in sports. Clin Sports Med.
1998;17:401–406.
Ritchie JV, Munter DW. Emergency department evaluation and treatment of

wrist injuries. Emerg Med Clin North Am. 1999;17:823–842, vi.
Young D, et al. Physical examination of the wrist. Orthop Clin North Am.
2007;38:149–165.
Codes
ICD9
833.03 Closed dislocation of midcarpal (joint)
Clinical Pearls
Surgery results in 35% loss of flexion and extension. This should still allow an
athlete to return to activity in most cases.
The ligament in the wrist has torn in this injury and the bones have shifted, so
they cannot heal correctly without surgery.
Marfan's Syndrome
Rebecca L. Carl
Basics
Description
An autosomal dominant genetic disorder of connective tissue affecting primarily the
musculoskeletal system, the cardiovascular system, and the eye
System(s) affected: Musculoskeletal, cardiovascular, ocular, skin/integument,
endocrine/metabolic, pulmonary
Genetics: Autosomal dominant with high penetrance; 15–25% spontaneous mutation
Incidence/prevalence in U.S.: 1/5,000 to 1/15,000
Predominant age: Genetic condition. Generally, clinical manifestations become apparent
during late childhood or adolescence. There is a more severe neonatal form of this condition;
affected individuals are generally diagnosed in the newborn period.
Predominant gender: No gender, ethnic, or racial predilection
Risk Factors
Advanced paternal age gives rise to a slightly increased risk only in cases that are not clearly
familial.
General Prevention
No prenatal diagnosis yet available, but presymptomatic diagnosis may be possible at research
centers using linkage analysis techniques.
Etiology
Genetic: 75% of affected individuals have an affected parent; the remainder have a
spontaneous mutation in the fibrillin 1 (FBN-1) gene.
Diagnosis
Genetic testing, looking for mutations in the FBN-1 gene, is available. Mutations can be
identified in 90% of affected individuals.
The mainstay of diagnosis is clinical evaluation and application of established diagnostic
criteria. These criteria, now known as the Ghent nosology, were revised most recently by De
Paepe and colleagues in 1996.
Individuals who have a 1st-degree relative with the diagnosis of Marfan syndrome or
documented FBN-1 mutation must have a major manifestation in one organ system with
involvement of one other system.
Individuals with no significant family history or genetic diagnosis must have major
manifestations involving 2 organ systems with involvement of an additional system.
Echocardiography, spine radiographs, and slit-lamp examination may be helpful in making the
diagnosis.
Physical Exam
Musculoskeletal:
Major criteria:
Pectus carinatum
Pectus excavatum requiring surgery
Upper-segment-to-lower-segment ratio of >1.05
Positive thumb sign (thumb can protrude from ulnar side of a clenched fist) and wrist sign
(thumb and 5th finger can encircle wrist and overlap)
Elbow hyperextension
Pes planovalgus with medial displacement of the medial malleolus
Protrusio acetabulae on radiographs
Scoliosis of >20 degrees or spondylolisthesis
Minor criteria:
Pectus excavatum
Joint hypermobility
High arched palate with crowding of teeth
Facial appearance
Cardiovascular:
Major criteria:
Aortic root dilatation
Dissection of the ascending aorta
Minor criteria:
Mitral valve prolapse
Dilatation of the main pulmonary aorta (age <40)
Calcification of the mitral valve annulus (age <40)
Dilatation or dissection of the descending or abdominal aorta (age <50)
Ocular:
Major criterion: Ectopia lentis (lens subluxation)
Minor criteria:
Flat cornea
Decreased miosis owing to hypoplastic iris or ciliary muscles
Pulmonary (minor criteria only):

Spontaneous pneumothorax
Apical blebs
Skin/integument (minor criteria only):
Striae
Recurrent hernia or hernia at an incision site
Dura (major criterion only): Lumbosacral dural ectasia

Lab
Genetic testing to look for FBN-1 mutation
Imaging
Plain radiographs of the spine are useful prior to skeletal maturity to detect and quantify
scoliosis.
Initial diagnostic echocardiogram, followed by serial screening echocardiograms, is
recommended beginning in adolescence to look for dilatation of the aorta and valvular
changes.
Cystic medial necrosis of the aorta
Myxomatous degeneration of the cardiac valves
Homocystinuria
Marfanoid habitus
Marfanoid skeletal and skin features (MASS) phenotype
Ehlers-Danlos syndrome
Beal syndrome (congenital contractural arachnodactyly)
Loeys-Dietz syndrome
Treatment
Long-term treatment
Acute treatment: Outpatient
Medication
First Line
No specific medical therapy is available. Medications may be used to treat
manifestations of Marfan syndrome.
Beta blockers have been used to slow progression of aortic root dilatation.
ACE inhibitors and calcium channel blockers have been used in patients who
don't tolerate or fail to respond to beta blockers.
Recent studies using animal models suggest that angiotensin II receptor
blockers may be effective in slowing aortic root dilatation as well; clinical
studies are currently in progress.
Contraindications: For beta blockers: Asthma, depression, Raynaud
phenomenon
Precautions: Refer to the manufacturer's profile for each drug.
Significant possible interactions: Refer to the manufacturer's profile for each
drug.
General Measures
In addition to health supervision visits with primary care physicians, individuals
with Marfan syndrome should have regular follow-up with cardiology and
ophthalmology.
Geneticists generally are involved in making the initial diagnosis.
Orthopedic consultation is often helpful.
Athletes should have echocardiograms every 6 mos to screen for the
presence of aortic root dilatation and worsening valvular insufficiency.
Skeletally immature patients should be offered the opportunity to meet with an
endocrinologist if they would like to consider hormonal therapy to limit growth.
Antibiotic prophylaxis for endocarditis prior to medical and dental procedures is
no longer uniformly recommended for Marfan patients with mitral valve
prolapse.
Individuals with significant valvular regurgitation/insufficiency should consult
their cardiologists about the necessity of infective endocarditis prophylaxis for
their specific conditions.
Antibiotic prophylaxis should be given to individuals with a prior history of
infective endocarditis or a history of valve replacement or repair of the aorta
using graft material.
Cardiac surgery is often required for people with Marfan syndrome who have
aortic root diameter >5 cm, rapid rate of aortic root dilatation, or significant aortic
valve regurgitation.
Ongoing Care
Athletes with Marfan syndrome can participate in low–moderate static/low dynamic sports as
long as they do not have moderate or severe mitral regurgitation, have no evidence of aortic
root dilatation, and have no family history of aortic dissection or sudden death owing to
Marfan syndrome.
Individuals with Marfan syndrome should not participate in contact sports or weightlifting.
Patient Monitoring
Routine health maintenance visits with a primary care physician.
Regular follow-up with cardiology; athletes should have screening echocardiograms every 6
mos.
Yearly ophthalmology follow-up owing to high rate of retinal detachment. Patients also have
higher rates of myopia and glaucoma.
Diet
No special diet
Patient Education
Information is available from the National Marfan Foundation, 382 Main St., Port Washington,
NY 11959; 800–8MARFAN, www.marfan.org.
Prognosis
Life-threatening complications are cardiovascular. With the advancement of techniques to
replace the aortic root, individuals with Marfan have a near-normal life span.
Complications
Aortic dissection or aortic rupture
Aortic valvular insufficiency owing to aortic root dilatation
Mitral valve insufficiency, often associated with myxomatous change
Bacterial endocarditis
Retinal detachment
Early medical or surgical intervention may reduce the degree of scoliosis.
Pregnancy Considerations
Pregnant women with the Marfan syndrome need to be managed as high-risk patients,
preferably with involvement of a cardiologist. The outcome is usually excellent.
Additional Reading
De Paepe A, Devereux RB, Dietz HC, et al. Revised diagnostic criteria for the Marfan
syndrome. Am J Med Genet. 1996;62:417–426.
Faivre L, Masurel-Paulet A, Collod-Béroud G, et al. Clinical and molecular study of 320

children with Marfan syndrome and related type I fibrillinopathies in a series of 1009
probands with pathogenic FBN1 mutations. Pediatrics. 2009;123:391–398.
Maron BJ, Chaitman BR, Ackerman MJ, et al. Recommendations for physical activity and
recreational sports participation for young patients with genetic cardiovascular diseases.
Circulation. 2004;109:2807–2816.
Codes
ICD9
759.82 Marfan syndrome
Clinical Pearls
Clinicians should be on the lookout for the musculoskeletal manifestations of
Marfan syndrome when performing preparticipation screening.
Physicians should carefully evaluate individuals with increased wing span,
characteristic facial features, and other stigmata of Marfan syndrome and
consider referral to genetics, cardiology, and/or ophthalmology when
appropriate.
MCP (MetaCarpophalangeal) Collateral Ligament
Sprain
Kathleen Weber
Basics
Description
Injury to the collateral ligaments of the metacarpophalangeal (MCP) joints; most commonly
the MCP joint of the thumb
An injury to the MCP ligament may result in a simple strain to a complete tear of both proper
and accessory ligaments (1).
Epidemiology
Isolated injuries to collateral ligaments of the MCP joints are uncommon, except for those of
the MCP joint of the thumb, which is the focus of this chapter.
Ulnar collateral ligament (UCL) injuries of the MCP joint of the thumb (gamekeeper's thumb or
skier's thumb) occur more often than radial collateral ligament (RCL) injuries.
UCL sprain is the 2nd most common injury encountered by skiers and most common
ligamentous injury to the thumb.
The ligamentous injury can occur either at the proximal or more commonly the distal
attachment of the ligament.
50% of these injuries will have an associated base of the proximal phalanx fracture.
Acute UCL injury is seen frequently in football players, ball-handling athletes, and other
contact sports participants.

Complete rupture of the collateral ligament (proper and accessory) and volar plate (2)
Stener lesion: The adductor pollicis aponeurosis is interposed between the torn end of the
UCL (thumb) and its insertion into the base of the proximal phalanx, inhibiting healing (not
seen in RCL complete tears) (2,3).
3 types of avulsion fractures: Small fragment at the base of the proximal phalanx; a large,
intraarticular fracture that involves at least 25% of the articular surface of the base of the
proximal phalanx; and an avulsion fracture involving the volar plate (2)
Dislocation of the thumb MCP joint
Diagnosis
History
MCP collateral ligament sprain is most commonly an acute injury related to trauma.
Mechanism of injury to the UCL of the MCP joint of the thumb is sudden, forced, radial
deviation (abduction) and extension resulting in partial or complete tear of the ligament.
Mechanism of injury to the RCL of the MCP joint of the thumb is force adduction or twisting of
the flexed joint.
Prompt diagnosis is the key to a good outcome.
Chronic MCP collateral ligament sprain is usually secondary to a missed diagnosis from an
earlier acute injury.
Physical Exam
Hallmark symptom of acute UCL injury is pain and swelling localized to the ulnar aspect of the
MCP joint along the UCL.
Acute injury: Ecchymosis and pain over the ligament
Chronic injuries: May not be painful
A palpable mass may be present.
Weakness of thumb; weakness with pinch noted with UCL injury (1)
RCL injuries have pain and swelling localized to the radial aspect of the metacarpal head, and
activities such as twisting open a jar lid can exacerbate the symptoms.
A careful physical exam differentiates a sprain from a complete tear (2).
Always compare with asymptomatic thumb.
Examine the joint for swelling, ecchymosis, and areas of tenderness.
Anteroposterior (AP) and lateral radiographs should be obtained prior to stressing the joint
because a nondisplaced fracture can be displaced as a result of the stress.
If radiographs are negative, the stability of the ligament should be tested.
Test the ligaments by applying radial stress (UCL) or ulnar stress (RCL) to the MCP joint in
full extension and in 30 degrees of flexion.
A collateral ligament injury should be suspected if during stress testing a firm endpoint is
lacking.
Valgus stress of the flexed MCP joint with opening of ≥30 degrees or 15 degrees greater
than the contralateral thumb indicates collateral ligament proper complete rupture; <30
degrees of laxity assumes a partial tear (2,4).
Valgus stress of the extended MCP joint with opening of ≥30 degrees suggests an accessory
collateral ligament tear (2).
If unable to make a clear distinction on clinical exam, stress radiographs are indicated.

Imaging
AP and lateral radiographs of the thumb to evaluate for a fracture (2,3)
Stress radiographs in full extension and in 30 degrees flexion if no fracture (always compare
with the contralateral thumb)
Additional radiographic signs that indicate a complete rupture are volar subluxation of the
proximal phalanx seen on lateral view and radial deviation of the proximal phalanx seen on AP
view.
Stress films are contraindicated in children with Salter-Harris fractures.
MRI and US may be used to evaluate for a ligament injury and Stener lesion (3,4).
Complete tear of collateral ligament
Dislocation of the thumb MCP joint
Fracture
Treatment
Analgesia (5): NSAIDs, ice
Non-thumb-related collateral ligament sprains, depending on severity, can be
splinted immobilized or “buddy taped” (2)[C].
No detectable instability: Immobilization (thumb spica splint) for 2 wks (6)[C]
Partial tear with stable joint: Thumb spica splint or cast for 4–6 wks depending
on severity of the injury (2)[C]; thumb is immobilized in slight flexion in the spica
cast; the interphalangeal joint is not immobilized to allow active motion and
prevent scarring of the extension mechanism.
Complete tear: Repair surgically (2)[C].
Avulsion fracture: Small avulsions that are not intraarticular can be treated
nonoperatively; nondisplaced fractures, thumb spica cast (application as
above) for 4–6 wks (2)[C].
Avulsion fracture: Rotated, displaced, or large intraarticular fragments require
surgical repair (2)[C].
Surgical repair is necessary for Stener lesion; failure to recognize this injury or
inadequate treatment can result in chronic instability (1)[C].
Referral
Prompt referral to an orthopedist or hand surgeon is indicated for all but
uncomplicated injuries and when a Stener lesion cannot be ruled out on the basis
of physical examination and standard radiographs.
When the cast is removed, range of motion (ROM) exercises are performed
several times a day; a removable splint is worn for an additional 2–3 wks.
Sports participation: Protect the thumb for 3 mos either by “buddy taping” it in
adduction to the index finger or by using a splint.
Surgical treatment is recommended for fractures that are displaced, rotated, or
have significant articular involvement.
Surgical repair is necessary for complete ligament tears and Stener lesions.
The goal of surgery is restoration of anatomy and joint stability.
Ongoing Care
Complications
Inadequate treatment of UCL thumb injuries may result in chronic painful
instability, weakness of pinch, and arthritis.
References
1. Rettig A, Rettig L, Welsch M. Anatomic reconstruction of thumb
metacarpophalangeal joint ulnar collateral ligament using an interference
screw docking technique. Tech Hand Up Extrem Surg. 2009;13:7–10.
2. Carlsen BT, Moran SL. Thumb trauma: Bennett fractures, Rolando

fractures, and ulnar collateral ligament injuries. J Hand Surg [Am].
2009;34:945–952.
3. Ebrahim FS, De Maeseneer M, Jager T, et al. US diagnosis of UCL tears

of the thumb and stener lesions: technique, pattern-based approach, and
differential diagnosis. Radiographics. 2006;26:1007–1020.
4. Papandrea RF, Fowler T. Injury at the Thumb UCL: is there a stener lesion?
JHS. 2008;33A:1882–1884.
5. Baskies MA, Lee SK. Evaluation and treatment of injuries of the ulnar
collateral ligament of the thumb—metacarpophalangeal joint. Bull NYU Hosp
Jt Dis. 2009;67:68–74.
6. Fricker R, Hintermann B. Skier's thumb. Treatment, prevention and

recommendations. Sports Med. 1995;19:73–79.
Codes
ICD9
842.12 Sprain of metacarpophalangeal (joint) of hand
MCP (Metacarpophalangeal) Dislocation
Jessica Stumbo
Basics
The metacarpophalangeal (MCP) joints are relatively stable joints, especially in flexion.
Stability is provided by collateral ligaments on either side of the joint and the volar plate. The
collateral ligaments are lax in extension and taut in flexion. The volar plate has a firm distal
attachment to the proximal phalanx and a less stable proximal attachment to the metacarpal.
It is the proximal attachment that is disrupted in a dislocation (1,2,3).
The index finger, thumb, and 5th finger are most vulnerable to dislocations.
Description
An MCP joint dislocation involves dislocation of the proximal phalanx in relation to the distal
metacarpal.
Requires disruption of stabilizing structures
Dislocations may occur dorsally (most common), laterally (uncommon), or volarly (rare).
The typical mechanism for a dorsal dislocation is hyperextension at the MCP joint. With
hyperextension, there is rupture of the volar plate from its proximal attachment, and due to
the anatomy of the joint, there is also proximal dorsal translocation of the base of the
proximal phalanx over the distal metacarpal (3).
Classification of dislocations: (3)
Simple dorsal: Articular surfaces are in partial contact, and there is no soft tissue
interposed in the joint.
Complex dorsal: The volar plate or other tissue is interposed between articular surfaces
and is, by definition, an irreducible dislocation.
Lateral: Results from an injury to the collateral ligament, either ulnar (UCL) or radial
collateral ligament (RCL). The collateral ligaments of the thumb are more commonly injured
than the collateral ligaments of the fingers (4).
Volar: Rare, but may result from severe or repetitive blows to knuckle, leading to rupture of
dorsal capsule with subsequent volar displacement of the proximal phalanx
Epidemiology
MCP dislocations are much less common than proximal interphalangeal dislocations because
of support from surrounding structures and protected position (2,3).
Usually occurs in index finger, thumb, or 5th finger.
Nearly always a single digit, but multiple digits may be involved.
Risk Factors
Contact and ball-handling sports
Prior history of injury or dislocation
Diagnosis
History
Will complain of pain, loss of function, and usually an obvious deformity
Dorsal dislocation generally results from forced hyperextension of digit, as in striking the heel
of an opponent while diving to make a tackle, or a fall on an outstretched hand (1,3,5)[C].
Lateral dislocation is caused by an ulnarly or radially directed blow to the MCP joint, usually
while in a flexed position (3,5)[C].
Volar dislocation may be seen with punching in boxing and martial arts.
Physical Exam
Evaluate and document neurovascular status before and after reduction attempts.
With dorsal dislocations, the metacarpal head is volarly displaced and will be easily palpable
in the palm (1)[C].
Simple dorsal: There is obvious deformity, with the phalanx resting at 60–90 degrees of
hyperextension over the head of the metacarpal (2)[C].
Complex dorsal: Much more subtle deformity, with only slight hyperextension (10–15
degrees) of the phalanx; may find dimpling or puckering of the palmar aspect of the finger
where the volar plate is caught between the ends of the bones (proximal phalanx and head of
metacarpal). This is pathognomonic for a complex dislocation; slight ulnar deviation of the
involved digit also may be noted (1,2,6)[C].
Lateral: Swelling and tenderness along the ulnar or radial side of the MCP joint; assess for
injury and laxity of the collateral ligaments by stressing the ligament with the MCP joint in
flexion (4,5)[C].
Volar: Obvious deformity, with the phalanx positioned palmar to metacarpal

Imaging
Anteroposterior (AP), lateral, and oblique views of involved digit (not the entire hand)
generally show deformity, joint space widening, and any accompanying fracture.
Brewerton view (MCP joint flexed to 65 degrees, with the dorsum of the proximal phalanx flat
against the film cassette and the beam angled 15 degrees ulnar to radial) helpful in identifying
collateral ligament avulsion fractures and fractures of the metacarpal head (2,3,4)[C]
Presence of a sesamoid in the widened joint space of the involved digit is pathognomonic for
a complex dorsal dislocation (because sesamoids are embedded in the volar plate) (1,2)[C].
In skeletally immature patients, it is important to image the contralateral side in order to
adequately evaluate for growth plate injuries.
In skeletally mature patients, stress radiographs are sometimes utilized. Stress x-rays should
only be done after static x-rays to prevent nondisplaced fractures from becoming displaced
fractures. In the thumb, MCP joint laxity >30–35 degrees on stress x-rays is usually
associated with a complete collateral ligament tear. Stress x-rays are not typically utilized in
the skeletally immature patient because those patients are more likely to have a growth plate
injury.
Postreduction views: AP, lateral, and oblique to evaluate for joint congruity and/or fracture
Up to 50% of MCP joint dislocations may have a concomitant fracture of the proximal phalanx
base and/or the metacarpal head.
Fracture of phalanx or metacarpal
Tendon rupture
Disruption of volar plate
Treatment
Various methods of anesthesia can be utilized for reduction, including local
intra-articular, regional block, or IV sedation. Typically for intra-articular
injections, a short-acting local anesthetic such as 1% lidocaine without
epinephrine is used, although a longer-acting agent such as bupivacaine may
also be used. It is important to document neurovascular status prior to the
administration of the anesthetic agent.
Usually not necessary for simple dislocations, but intra-articular anesthesia or
wrist block may facilitate reduction and prevent false conclusion that dislocation
is complex if patient prevents reduction due to pain.
For complex dislocations, digital block or general anesthesia in the operating
room may be necessary if closed reduction is to be attempted.
Document neurovascular status before and after reduction.
In general, reduction of dorsal MCP dislocations differs from most other
dislocations in that distal traction should be avoided. By using traction, a simple
dislocation can be converted to a complex one because the volar plate gets
displaced and locked within the joint space (1,6)[C].
Simple dorsal: 1st, relax flexors by placing wrist and IP joints into flexion; next,
accentuate dislocation slightly by hyperextending proximal phalanx to 90
degrees (controversial), and then push base of proximal phalanx distally over
the articular surface of the metacarpal into flexion while maintaining contact
with metacarpal head to prevent entrapment of the volar plate (thus converting
a simple dislocation into a complex one) (5,6)[C].
Complex dorsal: Attempt at closed reduction is warranted, but usually not P.
successful; reduction technique is similar to that of a simple dislocation (2)[C].
Lateral: Closed reduction is usually accomplished with gentle longitudinal
traction, taking care not to interpose any soft tissue.
Volar: Generally is performed open because concomitant dorsal hood injury
needs repair.
Reasons for failed closed reductions: Volar plate is interposed in the joint
space or metacarpal head has buttonholed through the palmar structures (1)[C]
Evaluate and document neurovascular status post reduction.
Evaluate tendon and ligament function. With thumb MCP dislocations, it is very
important to assess the integrity and stability of the UCL.
AP, lateral, and oblique radiographs of the involved digit to evaluate for joint
congruity and/or fracture
Simple dorsal: Dorsal blocking splint to prevent extension beyond neutral with
the MCP joint in 50–70 degrees of flexion for 7–10 days if no evidence of
significant instability; buddy taping also may be implemented. Active flexion
exercises are permitted. With thumb MCP dislocations, a thumb spica splint is
used for immobilization (1,2)[C].
Complex dorsal: Postoperative immobilization is at the prerogative of the
surgeon (ranges from buddy taping for 4–6 wks to immobilization in 60 degrees
of flexion).
Lateral: Majority of complete ligamentous injuries are splinted in 30–50
degrees of MCP flexion for 2–4 wks followed by buddy taping; with significant
instability especially of the border digits, primary surgical repair of the collateral
ligament may be considered. Incomplete MCP collateral ligament injuries and
complete tears in nonborder digits are usually treated with buddy taping and
early range of motion exercises (2,4,5)[C].
Volar: Postoperative management varies and is at the prerogative of the
surgeon.
Medication
NSAIDs for pain relief and to decrease inflammation.
If surgery is planned, may consider acetaminophen to avoid potential bleeding
risks.
General Measures
PRICE: Protection, Rest, Ice, Compression, Elevation
In dislocations of the thumb, assessment of the UCL is essential. With a
hyperextension/hyperabduction injury, a Stener lesion can result. A Stener
lesion occurs when the adductor aponeurosis becomes interposed between
the torn end of the UCL and its bony attachment on the proximal phalanx.
Spontaneous healing cannot occur since the ligament is no longer in contact
with its bony attachment (7).
Occupational therapy may be indicated in more severe injuries.
Dorsal dislocations that are stable post-reduction need to be placed in a dorsal
extension blocking splint to prevent extension beyond neutral and
hyperextension. This position allows the volar plate to heal. Time frame is
variable but typically 2–3 wks. While in the extension blocking splint, active
range of motion (ROM) is encouraged to prevent joint stiffness.
Thumb MCP dislocations require immobilization in a forearm-based thumb
spica splint or cast for 4–6 wks.
Initial therapy will focus on control of pain and swelling. General progression
through rehab includes regaining full active ROM, followed by strengthening,
and then function (activities of daily living and work-/sport-specific functions).
If the injury can be properly protected in a splint or cast, an athlete may be able
to return to activities immediately. Otherwise, after the injury has healed (3–6
wks), an athlete can return to play with buddy taping for 1–3 more wks for
additional protection.
Surgery is often necessary for reduction, specifically for the complex dorsal and
volar dislocations, as discussed above, and may be indicated for repair of
severely damaged structures in other forms of dislocation (ie, complete tear of
UCL or RCL in lateral MCP joint dislocation).
Ongoing Care
After successful closed reduction, most MCP dislocations should be followed up with an
orthopedic surgeon or hand surgeon within a week.
Patient Education
Warn patients that finger and hand swelling can take months to resolve.
Prognosis
Prognosis of most MCP dislocations is good as long as identified early and managed
appropriately.
Complications
Joint stiffness and/or flexion contracture
Degenerative/post-traumatic arthritis
Avascular necrosis
Osteochondral fracture
Tendon adhesions/stiffness
Ligamentous laxity
Damage to the neurovascular bundle during open reduction
Premature closure of the physeal plate (rare) (1,3)
References
1. Dinh P, Franklin A, Hutchinson B, et al. Metacarpophalangeal joint
dislocation. J Am Acad Orthop Surg. 2009;17:318–324.
2. Ashkenaze DM, Ruby LK. Metacarpal fractures and dislocations. Orthop

Clin North Am. 1992;23:19–33.
3. Hubbard LF. Metacarpophalangeal dislocations. Hand Clin. 1988;4:39–44.
4. Lourie GM, Gaston RG, Freeland AE. Collateral ligament injuries of the
metacarpophalangeal joints of the fingers. Hand Clin. 2006;22:357–364, viii.
5. Lee SJ, Montgomery K. Athletic hand injuries. Orthop Clin North Am.
2002;33:547–554.
6. Wolov RB. Complex dislocations of the metacar-pophalangeal joints.
Orthop Rev. 1988;17:770–775.
7. Miller RJ. Dislocations and fracture dislocations of the

metacarpophalangeal joint of the thumb. Hand Clin. 1988;4:45–65.
Additional Reading
1998;17:513–531.
Rettig AC. Athletic injuries of the wrist and hand: part II: overuse injuries of the
wrist and traumatic injuries to the hand. Am J Sports Med. 2004;32:262–273.
See Also
Thumb Ulnar Collateral Ligament Sprain and MCP Collateral Ligament Sprain
Codes
ICD9
834.01 Closed dislocation of metacarpophalangeal (joint)
Clinical Pearls
Dorsal dislocations are the most common type of MCP joint dislocations.
When attempting to reduce a dorsal MCP joint dislocation, do not use distal
traction; risk converting simple dislocation to a complex one.
In general, complex dorsal and volar MCP joint dislocations require surgery.
Medial Collateral Ligament Tear
Claudia Dal Molin
Delmas J. Bolin
Basics
Superficial component is primary restraint to valgus stress.
Deep portion has tight connection to medial meniscus.
Medial collateral ligament (MCL) connects with the posteriomedial corner structures and is a
secondary stabilizer in resisting external rotation and anterior-posterior translation of the
knee.
Description
Tension injury to the MCL occurs most commonly with a valgus stress (ie, a blow to the
lateral knee).
Grade of injury classified by symptoms and physical exam by degree of joint opening with
applied valgus stress at 0° and 30° of knee flexion:
Grade I: minimal fiber tearing, localized tenderness, no instability (0–5 mm of laxity)
Grade II: greater degree of ligamentous tearing, slight-to-moderate abnormal motion (6–
10 mm of laxity)
Grade III: complete tear, demonstrable instability (>10 mm of laxity)
Epidemiology
Incidence
MCL is most frequently injured ligament of the knee (1).
General Prevention
Prophylactic knee bracing is controversial; most studies demonstrate bracing protects MCL and
increases force required to produce failure. Some studies suggest athletes perceive decreased
performance while using brace (1,2).

Medial meniscus tear, commonly in the posterior horn
Anterior cruciate ligament (ACL) tear
Posterior oblique ligament injury; anteromedial rotatory instability
Dislocation of the knee (rare)
Diagnosis
History
In contact/collision sports, an acute blow to the lateral aspect of the knee when the foot is
planted results in a valgus stress:
The medial joint line is under tension and can open, producing “buckling” and an injury to
the MCL (closed-chain injury).
The injury may be seen in soccer players who are struck on the instep while passing the ball
(open-chain injury).
Skiers can injure MCL by noncontact valgus external rotation injury.
Overuse injuries to the MCL have been reported in breaststroke swimmers.
History of a “pop” should suggest associated meniscus or ACL injury.
Physical Exam
Observe for antalgic gait; inquire about a sense of the knee being “loose.”
Inspect the knee for ecchymosis, swelling, effusion, and presence of deformity. Presence
suggests greater extent of injury. In pediatric patients, ecchymosis and swelling necessitate
evaluation for physeal injury.
Palpate for localized tenderness over medial joint line and course of MCL, including adductor
tubercle and proximal medial tibia.
Assess range of motion for deficit at full extension (MCL) or flexion (MCL and joint effusion).
Perform valgus stress at full extension and 30° of knee flexion. Valgus laxity at 30° alone
indicates an isolated MCL injury. Laxity at both 0° and 30° indicates injury to the MCL and
posterior oblique ligament, knee capsule, and/or anterior cruciate ligaments. Always compare
the exam to the unaffected knee.
Degree of injury (as opposed to grade) assessed by findings: 1st degree, pain but no laxity;
2nd degree, pain and laxity but firm endpoint present on valgus stress test at 30°; 3rd
degree, no end point is present on valgus stress test at 30°.
Determine the amount of joint line opening. If >10 mm, coexisting intra-articular pathology
(torn ACL or meniscus) will be present 80% of the time.
Posterior oblique ligament injury can lead to anteromedial rotatory instability and posterior
horn medial meniscus tears. Anterior drawer testing with the foot in external rotation can
assess anteromedial translation, but may be difficult to perform in acute injury.
Lachman's exam to evaluate a concomitant ACL tear; McMurray's exam to evaluate the
menisci for injury
Assess neurovascular status of the extremity; popliteal nerve and artery injuries associated
with instability can be limb-threatening and should not be missed.

Imaging
Standard radiographic knee series (45-degree flexion weight-bearing, lateral, and sunrise
views) usually normal, but used to identify avulsions or osteochondral fragments
Stress radiographs are useful in adolescents to exclude Salter-Harris (physeal) injuries; used
when tenderness presents completely around physis.
Calcification of the MCL (Pellegrini-Stieda lesion) is seen in chronic MCL injury (3).
T2 MRI is gold standard and demonstrates acute intrasubstance edema and fiber
discontinuity with acute MCL tears, and identifies associated bone contusions (45% of MCL
injuries) and associated injuries, including ACL and meniscal tears (1).
Medial meniscus tear
Medial knee contusion
Patellar instability, subluxation, or dislocation
Fracture of the distal femoral physis
Treatment
Grade I injuries:
Ice applied 20 min every 3–4 hr; avoid lateral knee, as more vigorous icing
has led to cryoinjury of common peroneal nerve
Weight-bearing as tolerated, with or without assistive device, when able to
walk without limp
Active range of motion (ROM) exercises and achievement of full ROM as
soon as tolerated
Strengthening exercises (open- and closed-chain) as tolerated
Progression towards agility, proprioceptive, and sport-related drills as
tolerated
In both grade I and II MCL injuries, PRICE (protection, rest, ice,
compression, elevation) and NSAIDs are first-line treatments.
Grade II injuries:
Weight-bearing as tolerated with long-leg brace. Brace may be locked in
extension for 1–2 wks, depending on comfort level and degree of valgus
opening. Discontinuation of brace is dependent on pain, anatomic alignment,
and degree of laxity present.
Active ROM exercises are started immediately.
Quadriceps strengthening and electrical stimulation, as well as straight leg
raises, are started immediately. Stationary cycling and resistive exercises
are initiated as tolerated.
Proprioception and agility drills can begin once full ROM and functional
strength are achieved.
Grade III injuries: P.
Long-leg brace is worn and locked in extension for 3–6 wks, depending on
anatomic alignment. Non-weight-bearing is recommended in patients with
more severe valgus alignment for no more than 3 wks.
For patients with normal alignment, immediate ROM out of the brace 2–3
times/day is performed. For patients who are “knock-kneed,” ROM out of the
brace begins at 3 wks. The brace should remain locked in extension for 6
wks.
Weight-bearing is determined by the degree of laxity. Progressive weight-
bearing begins after the determined non-weight-bearing period as tolerated.
Strengthening of quadriceps is done with quad sets, straight leg raise, and
electrical stimulation. Closed-chain exercises are initiated, depending on the
patient's weight-bearing status.
Proprioception, agility drills, bracing, and return to sport are the same as in
grade II injuries. Isolated grade III injuries with tolerable symptoms can be
rehabilitated similarly.
There is no difference in outcome for immobilization, early mobilization, and
surgery, although patients treated with early rehabilitation were able to return
to sport faster and were slightly more unstable at follow-up.
Combined MCL/ACL injuries:
Early referral to orthopedics, especially if rotatory instability is suspected
MRI is helpful to delineate pathology.
Surgical approach remains controversial. Initial rehab mirrors that of grade III
MCL injuries for the 1st 6 wks. ACL reconstruction is performed after 6 wks
and when full ROM has been achieved. If excessive valgus laxity is present,
combined ACL-MCL reconstruction may be recommended. ACL
reconstruction alone: Weight-bearing as tolerated with long-leg brace locked
in extension for 10–14 days. ROM exercises are permitted, and
strengthening exercises are initiated. ACL-MCL reconstruction: Non-weight-
bearing for 6 wks with brace locked in extension for 3 wks. Brace is unlocked
at 3 wks, and ROM exercises are initiated as tolerated. Partial weight-
bearing is initiated at the end of wk 6 and progressed to full by wk 10.
Functional brace is used and strengthening exercises begun after wk 10, and
proprioception is permitted once full weight-bearing is achieved. Return to
sports is the same as in grade II injuries.
Aggressive rehabilitation is undertaken to restore knee motion and get
through the inflammatory phase of the injury. Then the ACL is usually
reconstructed and the MCL is permitted to scar down on its own. This
approach has minimized postoperative arthrofibrosis.
Rehabilitation protocols after surgery are similar to ACL protocols. If there is
significant rotational instability, repair of the MCL is often performed as well.
Medication
Short-term use of NSAIDs is helpful in decreasing pain and swelling. The authors
use piroxicam 20 mg daily for 2–3 wks because of its collagen-synthesis
stimulation as well as NSAID properties (4).
Ongoing Care
Grade I injuries:
Bracing is preferable for contact-related sports; football lineman at the college and
occasionally at the high school levels will wear prophylactic MCL braces (1,5)
Return to sport is acceptable when level of strength, agility, and proprioception is
equivalent (usually 90% of) to the uninvolved extremity.
Grade I injuries may be able to return to play in as little as 10 days to 2 wks.
Grade II injuries:
Return to play based on functional ability similar to that of grade I injuries; a hinged or
custom MCL brace may be used for comfort and confidence of the athlete.
Grade II usually return to play in 21–28 days.
Grade III: Conservative management:
May require more than 28 days to return to full function. Consider surgical consultation for
those athletes who fail conservative management or who develop pain with chronic
instability.
Referral is suggested when there is suspicion of ACL or meniscal injury.
Some clinicians have suggested arthroscopy for all complete MCL injuries with more than 6
mm of joint opening.
Complications
The Pellegrini-Stieda lesion can be seen on radiographs; represents calcification
of the previously injured MCL.
References
1. Miyamoto RG, Bosco JA, Sherman OH. Treatment of medial collateral
ligament injuries. J Am Acad Orthop Surg. 2009;17:152–161.
2. Chen L, Kim PD, Ahmad CS, et al. Medial collateral ligament injuries of the
knee: current treatment concepts. Curr Rev Musculoskelet Med.
2008;1:108–113.
3. Reider B. Medial collateral ligament injuries in athletes. Sports Med.

1996;21:147–156.
4. Hanson CA, Weinhold PS, Afshari HM, et al. The effect of analgesic
agents on the healing rat medial collateral ligament. Am J Sports Med.
2005;33:674–679.
5. Albright JP, Powell JW, Smith W, et al. Medial collateral ligament knee
sprains in college football. Effectiveness of preventive braces. Am J Sports
Med. 1994;22:12–18.
Additional Reading
Azar FM. Evaluation and treatment of chronic medial collateral ligament
injuries of the knee. Sports Med Arthrosc. 2006;14:84–90.
Ballmer PM, Jakob RP. The non operative treatment of isolated complete
tears of the medial collateral ligament of the knee. A prospective study. Arch
Orthop Trauma Surg. 1988;107:273–276.
Edson CJ. Conservative and postoperative rehabilitation of isolated and

combined injuries of the medial collateral ligament. Sports Med Arthrosc.
2006;14:105–110.
Schweitzer ME, Tran D, Deely DM, et al. Medial collateral ligament injuries:
evaluation of multiple signs, prevalence and location of associated bone
bruises, and assessment with MR imaging. Radiology. 1995;194:825–829.
Codes
ICD9
844.1 Sprain, medial collateral, knee
Clinical Pearls
How long until I can return to play? For most sports, athletes with grade I
injuries return in an average of 10 days. Those with grade II sprains return in
2–3 wks. Those with grade III sprains return in 3–6 wks. Soccer players may
require several more weeks because the use of the instep to kick and pass the
ball exerts a valgus force that subjects the injured MCL to recurrent stress.
Operative treatment of combined injuries can require 6–12 mos of
rehabilitation prior to full return.
Bracing is recommended for all grades of MCL injury. Grade III injuries may
require up to a full year of bracing, depending on residual laxity.
A 10-yr follow-up on isolated MCL injuries suggests that most patients have
excellent function and no major radiographic evidence of arthritis.
After rehabilitation, most patients note only minor symptoms; 10-yr studies
show most perform well with only minor decreases in physical ability.
Medial Epicondylitis
Craig C. Young
Emily Porter
Basics
Description
Medial epicondylitis is clinically defined as pain at the medial epicondyle due to repetitive flexion
and pronation at the elbow. It is usually an overuse injury that can affect both athletes and
nonathletes. Golfer's elbow is a common term used for medial epicondylitis.
Epidemiology
Diagnosed less often than lateral epicondylitis, a similar condition affecting the origin of the
common extensor tendon on the lateral epicondyle
Estimated prevalence of 0.4% in 2006 observational study in Finland (1)[C]
Diagnosis is often made in the 4th and 5th decades, although the condition has been seen in
patients ranging from 12–80 yrs of age.
Men and women are affected equally.
The dominant hand is most often affected.
Etiology
Initially thought to be an inflammatory process.
Inflammation may play a role in the initial acute injury when microtearing of the tendon occurs
Histologic studies of chronic epicondylitis have shown abnormal collagen architecture due to a
fibroblastic and immature vascular response, which causes incomplete tendon repair.
Notable lack of acute and chronic inflammatory cells in chronic epicondylitis.
Degenerative changes often seen in the pronator teres and flexor carpi radialis muscles and
their tendons.
Palmaris longus, flexor digitorum superficialis, and flexor carpi ulnaris may also be involved.
Common causes:
Activities that involve forceful and/or continuous flexion and pronation at the wrist or a large
amount of stabilization applied by the wrist, such as racquet sports, swimming, swinging a
golf club, throwing, playing tennis, using a computer keyboard or playing piano.
Certain occupations (carpenters, plumbers, meat cutters, etc.) may be more at risk.
Diagnosis
History
Pain and tenderness along the medial elbow, extending into the forearm, which worsens with
resisted forearm pronation or wrist flexion at 90° of elbow flexion and/or full elbow extension.
Difficulty gripping without pain
Decreased wrist strength
Tightness/stiffness when stretching elbow and wrist
Physical Exam
Tenderness to palpation over the medial epicondyle, pronator teres and flexor carpi radialis
Local swelling and warmth may be present
Active and resisted range of motion may be full or limited depending on the severity of the
injury.

Imaging
Generally not needed for initial evaluation
In cases that are refractory to treatment or where the diagnosis is in question, basic elbow x-
rays followed by US or MRI may be considered (2)[C].
Entrapment neuropathy (ie, cubital tunnel syndrome, carpal tunnel syndrome)
Ulnar neuritis
UCL insufficiency
Medial elbow apophysitis (ie, “Little leaguer's elbow”)
Inflammatory arthritis
Myofascial pain
Treatment
Initial treatment includes relative rest, ice, acetaminophen or OTC NSAIDs
as needed.
The mainstay of treatment involves stretching and strengthening with
progression to eccentric training exercise with or without formal physical
therapy.
Bracing may be helpful.
If no improvement in 6 wks, consider obtaining x-rays and initiating formal
physical therapy.
If still symptomatic, consider injection. Various techniques have been proposed
including dry needling of tendon, corticosteroid injection, or use of newer
techniques including prolotherapy or injection of platelet-rich plasma or
autologous blood (3)[C].
Other treatments to consider include nitric oxide via topical nitroglycerin or
extra-corporeal shock wave therapy (4,5)[C].
If symptoms persist, consider advanced imaging with US or MRI to confirm
diagnosis.
Rarely, recalcitrant symptoms >6 mos in duration may require surgical
intervention.
Ongoing Care
Home exercise program as follows:
Strengthening:
Continue regular breathing during the exercises
Stay below the level of pain
Perform 2 to 3 sets of 10–15 repetitions, 2–4 times a week. Once 3 sets of 15 repetitions
can be performed easily, increase the weight, reduce the repetitions to 10, and build back
up to 15.
Exercises:
Wrist extension curls: With the forearm supported on a firm surface and the palm facing
downward, lift and lower the weight.
Wrist flexion curls: With the forearm supported on a firm surface and the palm facing
upward, lift and lower the weight.
Forearm pronation/supination: With the forearm supported on a firm surface, turn the
palm up and then down while holding onto a weight.
Gripping: Gently grip a rubber ball, a towel, or putty and then advance to items with
more resistance. Perform 10–30 repetitions, increasing in intensity once 30 repetitions
can be performed.
Finger extension: Wrap a rubber band around the outside of all the fingers and thumb,
gently extend the hand by opening the fingers, and then close the fingers. Perform 10–30
repetitions.
Stretching:
Keep the stretch to a comfortable level.
Continue regular breathing during the exercises.
Hold each stretch for 30 sec.
Repeat each stretch 3–6 times.
Exercises:
Wrist flexion stretch: Bend the involved wrist down gently by grasping it with the other
hand until a pulling sensation is felt. Keep the elbow straight.
Wrist flexion stretch (advanced): Same as for the wrist flexion stretch, but with the
addition of wrist movement toward the side of the little finger.
Wrist extension stretch: Bend the involved wrist up gently by grasping it with the
opposite hand until a pulling sensation is felt. Keep the elbow straight.
References
1. Shiri R, Viikari-Juntura E, Varonen H, et al. Prevalence and determinants of lateral and
medial epicondylitis: a population study. Am J Epidemiol. 2006.
2. Park G, Lee S, Lee M. Diagnostic value of ultrasonography for clinical medial

epicondylitis. Arch Phys Med Rehabil. 2008;89:738–742.
3. Suresh SP, Ali KE, Jones H, et al. Medial epicondylitis: is ultrasound guided autologous
blood injection an effective treatment? Br J Sports Med. 2006;40:935–939.
4. Paoloni JA, et al. Topical nitric oxide application in the treatment of chronic extensor
tendinosis at the elbow: a randomized, double-blinded, placebo-controlled clinical trial. Am J
Sports Med. 2003;31:915–920.
5. Rompe JD, et al. Repetitive low-energy shock wave treatment for chronic lateral
epicondylitis in tennis players. Am J Sports Med. 2004;32:734–743.
Additional Reading
Ciccotti MC, Schwartz MA, Ciccotti MG. Diagnosis and treatment of medial epicondylitis of
the elbow. Clin Sports Med. 2004;23:693–705.
Jayanthi N. (2009). Epicondylitis. Accessed online on August 12, 2009 from UpToDate Web
site: www.uptodate.com
Codes
ICD9
Clinical Pearls
Wrist splints are often more helpful then counter-force bracing if the patient
has significant pain upon awakening. However counter-force braces are often
better tolerated during the day.
The cost of nitroglycerin patches can be decreased by cutting them in half or
quarters.
Medial Gastrocnemius Injury, Tennis Leg
Sandeep Johar
Basics
Description
Musculotendinous disruption of varying degrees in the medial head of the gastrocnemius muscle
that results from an acute, forceful push-off with the foot
Risk Factors
Male
4th to 6th decades of life
High-risk sports, including hill running, jumping, and tennis
Muscles that have not been properly warmed up may be greater at risk.
Recurrent calf strains
Diagnosis
Audible pop when the injury to the medial calf occurs
Pain in the area of the calf with radiation to the knee or the ankle
Pain with range of motion (ROM) of the ankle
Swollen leg that extends down to the foot or ankle
Bruising of the calf
History
Athlete reports audible pop when the injury to the medial calf occurred, and the patient
complains of feeling like a stick struck his or her calf.
Physical Exam
Asymmetric calf swelling and discoloration
Visible defect may be present in the medial gastrocnemius muscle.
Tenderness on palpation of the medial gastrocnemius muscle (more painful at the medial
musculotendinous junction)
A palpable defect may be evident at the medial musculotendinous junction.
Palpation of the Achilles tendon demonstrates an intact tendon.
Peripheral pulses should be normal.
Pain with passive ankle dorsiflexion
Pain with active resistance to ankle plantarflexion
Thompson test is negative: Thompson test should always be performed in the clinical setting
of atraumatic, acute-onset pain in the posterior lower leg associated with an audible “pop.”

Imaging
X-ray films of the tibia/fibula may be ordered to rule out an avulsion fracture.
MRI: The most sensitive and specific imaging method to show the area of disrupted soft
tissue
US: Will aid in ruling out a deep vein thrombosis (DVT)
Baker cyst rupture
DVT
Plantaris tendon rupture
Acute compartment syndrome after rupture of the medial head of the gastrocnemius
Chronic exertional compartment syndrome (posterior)
Posterior tibial tendon rupture or tendonitis
Anomalous gastrocnemius muscle rupture
Treatment
Prevention/reduction of swelling: Elevation, compression, and ice for 20
min 3–4 × a day
Early weight bearing (may need crutches and/or bilateral heel lifts for normal
gait)
Ankle/foot bracing to keep the ankle in maximal tolerable dorsiflexion: In the
early stages of treatment, using the splint at night may be helpful.
Medication
NSAIDs: Clinicians must carefully consider pain therapy in the 1st 48 hr, as
decreased platelet activity may result in increased bleeding and larger hematoma
formation with resultant effects on healing.
Ibuprofen: Adult: 600 mg PO q8h; children: 10 mg/kg PO q8h
Naproxen: Adult: 250–500 mg PO b.i.d.
Ketorolac: Adult: 30 mg IV/IM q6h or 10 mg PO q4–6h
Ice therapy for control of pain and swelling
Active resistance dorsiflexion exercises until the athlete is pain-free
Apply compression dressing from the metatarsal heads to the gastrocnemius
for the 1st 2 wks.
Partial weight-bearing ambulation as soon as tolerable to maximize the contact
of the sole of the foot to the ground
Stationary cycling, leg presses, and heel raises
Proprioception and balance training
Ongoing Care
Prognosis
Prognosis is excellent for the tennis leg sufferer to return to sports endeavors.
Noncompliance can prevent players from returning to sports for 3–4 mos.
Early and aggressive rehabilitation allows most patients to recover within a few weeks.
Additional Reading
Best TM, McCabe RP, Corr D, et al. Evaluation of a new method to create a standardized
muscle stretch injury. Med Sci Sports Exerc. 1998;30:200–205.
Bianchi S, Martinoli C, Abdelwahab IF, et al. Sonographic evaluation of tears of the

gastrocnemius medial head (“tennis leg”). J Ultrasound Med. 1998;17:157–162.
Delgado GJ, Chung CB, Lektrakul N, et al. Tennis leg: clinical US study of 141 patients and
anatomic investigation of four cadavers with MR imaging and US. Radiology.
2002;224:112–119.
Millar AP. Strains of the posterior calf musculature (“tennis leg”). Am J Sports Med. 1979;
7:172–174.
Zarins B, Ciullo JV. Acute muscle and tendon injuries in athletes. Clin Sports Med.
1983;2:167–182.
Codes
ICD9
844.8 Sprain of other specified sites of knee and leg
Medial Tibial Stress Syndrome
Benjamin A. Hasan
Basics
Description
Typically an overuse injury, with pain over the posteromedial border of the middle to distal
thirds of the tibia, but there may be pain in other locations circumferentially around the lower
leg.
Historically attributed to degenerative tendinopathy or periostitis
Newer evidence points to repetitive bony overload of the posteromedial tibial border (1)
May be on a continuum with stress fracture
Synonym(s):
“Shin splints,” a misnomer widely accepted in the running and sports medicine communities
(2)
Medial tibial stress syndrome, the most medically appropriate term (3)
Tibialis posterior myofasciitis
Soleus syndrome
Posterior tibial tendinitis
Epidemiology
Shin splints is the diagnosis in 13% of injuries to runners (2).
Incidence has been reported between 4 and 35% in military studies, 4% in currently training
U.S. Navy recruits (3).
Risk Factors
Risks for development of lower extremity overuse syndromes have been commonly observed
by runners, coaches, trainers, therapists, and physicians (1,3,4,5,6):
Repetitive stress, especially running and jumping
<5 yrs of experience in running (1)[B]
Overpronation or other lower extremity alignment abnormalities (7,8)[B]
Increase in training intensity
Change in running/playing surface
Training on surfaces
Inability to decrease intensity or duration of training
Female sex
Elevated body mass index (BMI)
History of prior medial tibial stress syndrome
General Prevention
Prevention methods often encouraged [C]:
Achilles tendon stretches
Foam or rubber heel pads
Shock-absorbing insoles: Most promising in studies (9)
Footwear specific to foot type
Gradually increasing running programs
Systematic review shows now statistical benefit from any reported prevention (9).
Diagnosis
History
Often insidious and progressive
Temporally related to sudden increase in intensity/duration of activity, or change in
playing/running surface from a softer surface to a harder surface such as concrete
Early in course: Pain with onset of exertion, usually relieved by rest:
Sometimes relieved as activity continues
Often worse with toe-off
Late in course: Pain through full duration of activity:
Pain may continue after cessation of inciting activity.
Physical Exam
Tenderness to palpation along the middle to distal thirds of the tibia, along the posteromedial
border
Lower extremity kinetic chain examination may reveal excessive pronation or other alignment
abnormalities
Chronic cases: Induration, soft tissue swelling, or nodularity
Shoe examination reveals wear pattern, age of shoes

Imaging
Plain films of anteroposterior and lateral tibia are often normal; may show cortical
hypertrophy or demineralization (2)
Bone scan: Diffuse uptake along the posteromedial border of the tibia, often seen better on
delayed images, involves radiation, shows whole body (if concern for bilateral or other
associated areas of bony tenderness as in multiple stress fractures)
MRI: Bone marrow edema and periosteal signal may be seen, similar sensitivity and
specificity to bone scan, no radiation, single body part at a time (10)
Stress fracture
Muscular strain
Nerve entrapment
Fascial defects
Effort-induced venous thrombosis
Treatment
Acute treatment (2,6)[C]:
NSAIDs most beneficial in acute stages
No benefit to immobilization
Ice most beneficial in acute stage
Complete rest if possible
Otherwise, 20–50% reduction in mileage/inciting activity, with slow return to
previous level of activity as symptoms resolve (9)[C]
Cross-training with nonimpact activities: Swimming, water running, bicycling
Special considerations [C]:
Special taping techniques by athletic trainers may improve symptoms.
For very flat feet (pes planus), consider more supportive shoes or supportive
inserts.
For very high-arched feet (pes cavus), consider increased cushioning in
shoes or shock-absorbing inserts.
Rehabilitation (9)[C]:
Target-specific stretching and strengthening exercises
Towel calf stretches
Tracing alphabet with toes
Alternate heel/toe walking
Generally limited success, but in some studies, success rates of 29–93% have
been reported (11)[B].
Surgical procedures for recalcitrant cases:
Surgical release of the investing fascia around the soleus insertion on the
posteromedial aspect of the tibia. Medial tibial stress syndrome is not a
compartment syndrome, but releasing this fascia has helped.
Surgical division of the insertion of the soleus on the periosteum can relieve
associated periostitis.
Cauterization of the periosteum over the posteromedial tibia allows scarring
and reattachment of the periosteum.
Ongoing Care
Changes in training techniques:
Increase rest days.
Add in cross-training days with nonweight-bearing activity such as swimming and biking.
Slow increase in training intensity/duration, with no more than a 10% increase per week
Correct shoe type for foot type:
Some people benefit from custom orthotics.
Most people just need the right shoe for pes planus or pes cavus foot type.
Patient Education
Much education required
Advance training intensity gradually to prevent overuse (9)[C].
Rest sufficiently to overcome symptoms.
Return slowly to avoid recurrence.
New shoes every 3–6 mos, 200–300 miles of wear (9)[C]
References
1. Hubbard TJ, Carpenter EM, Cordova ML. Contributing factors to medial tibial stress
syndrome: a prospective investigation. Med Sci Sports Exerc. 2009.
2. Andrish JT. In DeLee JC, Drez D, Miller MD, eds. Orthopedic sports medicine. 2nd ed.
Philadelphia: Saunders, 2003:2155–2161.
3. Moen MH, Tol JL, Weir A, et al. Medial tibial stress syndrome: a critical review. Sports
Med. 2009;39:523–546.
4. Beck BR. Tibial stress injuries. An aetiological review for the purposes of guiding
management. Sports Med. 1998;26:265–279.
5. Bennett JE, Reinking MF, Pluemer B, et al. Factors contributing to the development of
medial tibial stress syndrome in high school runners. J Orthop Sports Phys Ther.
2001;31:504–510.
6. Cosca DD, Navazio F. Common problems in endurance athletes. Am Fam Physician.

2007;76:237–244.
7. Tweed JL, Avil SJ, Campbell JA, et al. Etiologic factors in the development of medial
tibial stress syndrome: a review of the literature. J Am Podiatr Med Assoc. 2008;98:107–
111.
8. Tweed JL, Campbell JA, Avil SJ. Biomechanical risk factors in the development of medial
tibial stress syndrome in distance runners. J Am Podiatr Med Assoc. 2008;98:436–444.
9. Thacker SB, Gilchrist J, Stroup DF, et al. The prevention of shin splints in sports: a
systematic review of literature. Med Sci Sports Exerc. 2002;34:32–40.
10. Haims A, Jokl P. In Johnson TR, Steinbach LS. Essentials of musculoskeletal imaging.
Rosemont, IL: AAOS; 2004:516–519.
11. Abramowitz AJ, Schepsis A, McArthur C. The medial tibial syndrome. The role of
surgery. Orthop Rev. 1994;23:875–881.
Additional Reading
Locke S. Exercise-related chronic lower leg pain. Aust Fam Physician. 1999;28:569–573.
Touliopolous S, Hershman EB. Lower leg pain. Diagnosis and treatment of compartment
syndromes and other pain syndromes of the leg. Sports Med. 1999;27:193–204.
Codes
ICD9
844.9 Sprain of unspecified site of knee and leg
Clinical Pearls
Activity should be avoided until pain and tenderness resolve, followed by a slow,
structured return to prior level of activity.
There is no good evidence that special taping or an ACE bandage will shorten
recovery, but it may help to improve symptoms.
If time cannot be taken off from training, relative rest, with a 20–50% decrease
in training intensity/duration. Work in cross-training days, with nonweight-
bearing activity.
Rehabilitation exercises should aim at stretching and strengthening involved
musculotendinous units.
Use a towel to pull your foot toward you and stretch your calf. Trace the
alphabet with your feet. Alternate walking on toes and heels. “Toe raises” to
strengthen lower leg while standing on stairs or steps [C].
Meniscal Tears
Michael Schettino
Basics
Description
Menisci are the cartilaginous structures that serve in transmitting tibiofemoral load, shock
absorption, lubrication, and passive stabilization of the knee.
The peripheral 1/3 zone has a vascular supply, while the central 2/3 zone is avascular.
Tears are classified as longitudinal, radial, oblique, horizontal, degenerative, complex, flap, or
bucket-handle.
Meniscal tears can disrupt knee biomechanics, causing varying degrees of symptoms and
predisposing the knee to other short- and long-term sequelae, including quadriceps or
hamstring inhibition, patellofemoral pain syndrome, altered gait, and osteoarthritis.
Synonym(s): Cartilage tear (common usage by patients for a meniscal tear)
Epidemiology
One of the most common knee problems; annual incidence is 60–70 per 100,000 persons
(1).
Traumatic tears typically occur in 13–40-yr-old individuals with sports-related injuries.
Degenerative tears typically develop in patients over 40.
Posterior horn of medial meniscus is most commonly affected location.
More common in males than females, with ratio between 2.5:1 and 4:1 (1)
Risk Factors
Abnormal mechanical axis
Ligament deficiency
Discoid meniscus
Poor quadriceps control
Etiology
A meniscal tear may occur following twisting, shearing, or compressive forces from contact or
noncontact mechanisms.

1/3 of traumatic meniscal tears associated with anterior cruciate ligament (ACL) injury
Tibial plateau and femoral shaft fractures
Diagnosis
History
With a skilled practitioner, diagnosis can be correctly made in 75% by history alone (2)[B].
Traumatic tears in the younger, athletic population are most frequently associated with a
significant cutting/twisting injury, whereas degenerative tears in older patients usually lack
identifiable trauma.
Pain in area of medial or lateral joint line
Pain with weight-bearing and twisting/turning of knee or squatting
Degree of pain usually such that individual is able to ambulate after acute injury and may be
able to continue sports participation
May be associated with slow onset of effusion over several hours
Catching, locking, or clicking sensation
Episodes of giving way
Symptoms may wane, but typically recur with resumption of activities.
Subsequent intermittent effusions not uncommon
Physical Exam
With a skilled history and physical, clinical examination can reach 88–92% accuracy (3)[C].
Exam findings suggestive of meniscal tear:
Effusion/hemarthrosis may be a sign of meniscal, ligament, or osteochondral injury.
Locked knee is suggestive of bucket-handle meniscal tear, ligament tear, or loose body.
Valgus/varus instability suggestive of medial collateral ligament (MCL)/lateral collateral
ligament sprain, which may have associated meniscal injury.
Positive anterior/posterior drawer or Lachman test indicates cruciate ligament injury, which
may have associated meniscal injury.
Tenderness to palpation isolated over the medial or lateral joint line is the most common
finding on physical exam (sensitivity 71–85%, specificity 86–93%) (2)[B].
Positive McMurray's test: Palpable click and pain over joint line produced when meniscal
fragment catches during test (sensitivity 48–80%, specificity 86–94%) (2)[B]
Positive Apley test: Pain over the respective joint line with the patient prone and the knee
flexed to 90 degrees, while the leg is internally and externally rotated under an axial load
(sensitivity 41%, specificity ranges 80–93%) (2)[B]
Positive Thessaly test: Pain over the respective joint line with the patient standing on the
affected leg at 5 and 20 degrees of knee flexion, followed by internal and external rotation
of the leg and torso (sensitivity 66–92%, specificity 91–97%) (2)[C]
Atrophic quadriceps suggestive of chronic inhibition by pain or effusion
May have decreased range of motion secondary to pain or effusion

Imaging
Standard weight-bearing anteroposterior/lateral/tunnel/patellar (sunrise, merchant) views to
rule out other conditions such as loose body, arthritis, osteochondritis dissecans, or fracture
MRI useful to evaluate for concomitant structural damage when the diagnosis is in question
or for operative planning
Should be performed quickly for locking symptoms or suspicion for substantial injury.
Otherwise, is typically reserved for symptoms persisting >4–8 wks in the otherwise healthy
knee
MRI findings of meniscal tear include meniscal cleavage signal, which extends to the meniscal
surface.
Synovitis
Intra-articular loose body
Articular cartilage defect
Ligamentous injury, particularly ACL and/or MCL
Patellar subluxation/dislocation
Chondromalacia patellae
Treatment
Initial treatment is RICE—rest, ice (20 min several times per day),
compression, elevation—and NSAIDs.
Immobilization is not recommended unless evaluating for fracture or major
ligamentous injury; however, a hinged knee brace may offer support,
protection, and symptom relief.
While infrequently required, crutches with partial weight-bearing may provide
relief.
Sports activity should be restricted until symptoms resolve or (if indicated) MRI
is performed.
Further management decisions are based upon patient's age, symptomatology,
type of tear, and co-existing knee conditions.
Younger patients with traumatic tears should be thoroughly evaluated and more
aggressively treated.
Referral
Expedited surgical referrals should be made for:
Traumatic longitudinal or radial peripheral tears measuring ≥1 cm (4)[B]
Locking symptoms, flap tears, and bucket-handle tears
Associated cruciate ligament injury, osteochondral defect, loose bodies, or
fracture
Nonurgent referrals include tears treated nonoperatively but that continue to
cause pain or disability.
Individuals with degenerative joint disease will likely have meniscal tears, and
the presence of one is not necessarily a cause for a surgical referral.
Small (<1 cm) peripheral meniscal tears often spontaneously heal. Even if they
persist, they will likely become asymptomatic. Pain typically improves over 6–12
wks (4)[B].
For discomfort persisting several weeks, intra-articular corticosteroid injections
often provide significant relief.
Stationary bicycle riding or a home exercise program/physical therapy
addressing balance, quadriceps and hamstring strength can reduce pain,
increase range of motion, and help protect the knee from further injuries.
While surgery is not contraindicated, nonoperative interventions (including
NSAIDs and corticosteroid injections) are appropriate initial treatment for:
Smaller central tears
Complex/degenerative tears
Tears in setting of degenerative joint disease
Both partial meniscectomy and meniscal repair are outpatient-based
procedures.
Partial meniscectomy is frequently performed for flap and bucket-handle tears
or for tears failing nonoperative treatment.
Horizontal tears are typically degenerative tears and have a minimal chance of
healng. As they may progress to flap tears, they may be excised.
Meniscal repair is attempted most commonly for traumatic longitudinal or radial
tears in the periphery (4)[C].
Occasionally bucket-handle tears are amenable to repair.
Ongoing Care
Prognosis
20% of meniscal tears may heal without surgical intervention. These are typically small (<1
cm), traumatic longitudinal or radial tears along the meniscal periphery (4)[B].
Younger patients are more likely to spontaneously heal than older patients, and have better
outcome with meniscal repair (5)[C].
In the carefully chosen patient, meniscal repair is successful in up to 80% (6)[B].
Successful repair compared to resection has a lower incidence of degenerative change after
5 yrs (6)[B].
Regardless of healing, many meniscal tears become asymptomatic (4)[B].
Greatest factor affecting long-term outcome after meniscectomy is presence of articular
cartilage damage. 80–90% of patients without articular cartilage damage have good to
excellent results with partial meniscectomy within 1st 5 yrs (6)[B].
Total meniscectomy in previously normal knees results in significant arthrosis in 2/3 of
patients by 15 yrs from surgery.
Complications
Injury to peroneal nerve possible with lateral meniscus repair
Injury to infrapatellar branch of saphenous nerve possible with medial meniscus
repair
Repair could fail, resulting in repeat arthroscopy
Infection
References
1. Arendt EA, ed. Orthopaedic knowledge update: sports medicine 2.
Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1999.
2. Karachalios T, Hantes M, Zibis AH, et al. Diagnostic accuracy of a new

clinical test (the Thessaly test) for early detection of meniscal tears. J Bone
Joint Surg Am. 2005;87:955–962.
3. Mohan BR, Gosal HS. Reliability of clinical diagnosis in meniscal tears. Int
Orthop. 2006.
4. DeHaven KE. Meniscus repair. Am J Sports Med. 1999;27:242–250.
5. Stärke C, Kopf S, Petersen W, et al. Meniscal Repair. Arthroscopy.

2009;25:1033–1044.
6. Greis PE, Holmstrom MC, Bardana DD, et al. Meniscal injury: II.
Management. J Am Acad Orthop Surg. 2002;10:177–187.
7. Ryzewicz M, Peterson B, Siparsky PN, et al. The diagnosis of meniscus

tears: the role of MRI and clinical examination. Clin Orthop Relat Res.
2007;455:123–133.
Additional Reading
Andersson-Molina H, Karlsson H, Rockborn P. Arthroscopic partial and total
meniscectomy: A long-term follow-up study with matched controls.
Arthroscopy. 2002;18:183–189.
Greis PE, Bardana DD, Holmstrom MC, et al. Meniscal injury: I. Basic science
and evaluation. J Am Acad Orthop Surg. 2002;10:168–176.
Klimkiewicz JJ, Shaffer B. Meniscal surgery 2002 update: indications and

techniques for resection, repair, regeneration, and replacement. Arthroscopy.
2002;18:14–25.
Codes
ICD9
836.0 Tear of medial cartilage or meniscus of knee, current
836.1 Tear of lateral cartilage or meniscus of knee, current
836.2 Other tear of cartilage or meniscus of knee, current
Clinical Pearls
Not all patients with meniscal tears require surgery. Clinical evaluation by a skilled
examiner identifies patients with surgically amenable meniscus tears with equal
or better reliability than MRI (7)[C].
Anastasia N. Fischer
Thomas L. Pommering
Basics
Description
Primary amenorrhea is the lack of spontaneous uterine bleeding:
By the age of 14 yrs without development of secondary sexual characteristics OR
By the age of 16 yrs with otherwise normal development.
Secondary amenorrhea is as a 3-mo absence of menstrual bleeding in a woman with
previous regular menses or a 9-mo absence with previous oligomenorrhea.
Suspect Female Athlete Triad.
Epidemiology
Amenorrhea occurs in 3–64% of female college athletes compared with 2–5% of the general
population.

Diagnosis
History
With amenorrhea, history is directed toward other causes besides hypothalamic amenorrhea:
Thyroid disease, androgen excess, anabolic steroids, and autoimmune and pituitary
disorders.
Menstrual history:
Age of menarche
Last menstrual period
Frequency and duration of menses
Longest time between menses
Physical signs of ovulation (cervical mucous change or menstrual cramps)
Previous or current hormonal therapy
Diet history
Exercise history
Sexual history
Physical Exam
Tanner stage
Acne
External genitalia abnormalities
Lanugo, or hirsutism
Bradycardia
Behavioral signs of disordered eating: Preoccupation with food and weight, self-criticism,
eating alone, excessive water/soda drinking, compulsive and excessive exercise, poor self-
image, frequent bathroom trips during and after meals
If anorexia nervosa is present, cachexia, hypotension, alopecia, pruritus, cold intolerance,
and yellow skin (hypercarotenemia) also may be observed.
Any other findings consistent with differential diagnosis

Initial: Pregnancy test, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating
hormone, prolactin
If patient is hirsute, has acne, or polycystic ovary syndrome is suspected, add free
testosterone and dehydroepiandrosterone sulfate to the list of studies.
If TSH/prolactin is normal, consider progesterone challenge.
Imaging
Pelvic US if suspect anatomic abnormality
MRI Sella turcica if suspect pituitary problem
Pregnancy
Hypothalamic dysfunction:
Gonadotropin-releasing hormone (GnRH) deficiency
Hypogonadotropic hypogonadism (psychogenic, stress, weight loss, or exercise-induced)
Eating disorder/Female Athlete Triad
Drugs (GnRH analogues, medroxyprogesterone acetate, danazol, or oral contraceptives)
or systemic illness
Kallmann syndrome
Idiopathic (eg, head trauma)
Space-occupying lesion or infection
Pituitary dysfunction:
Pituitary neoplasm or prolactin-secreting tumor
Sheehan syndrome
Empty-sella syndrome
Granulomatous disease (eg, sarcoidosis)
Lawrence-Moon-Biedl syndrome
Thalassemia major
Mumps encephalitis
Ovarian dysfunction:
Menopause or premature ovarian failure
Polycystic ovary syndrome
Ovarian neoplasm
Turner syndrome (45,X)
Gonadal dysgenesis
Autoimmune disease
Uterine dysfunction:
Asherman syndrome
Absence of uterus or transverse vaginal septum:
Androgen insensitivity
Imperforate hymen
Mayer-Rokitansky-Kuster-Hauser syndrome (müllerian agenesis)
Endocrine disease:
Hypothyroidism
Cushing syndrome
Adrenal hyperplasia
Adrenal tumors
Treatment
Treat underlying condition if found
Otherwise, consider hormonal manipulation of menses
Additional Reading
American Academy of Pediatrics. Committee on Sports Medicine and Fitness.
Medical concerns in the female athlete. Pediatrics. 2000;106:610–613.
Fagan KM. Pharmacologic management of athletic amenorrhea. Clin Sports

Med. 1998;17:327–341.
Ireland ML, Ott SM. Special concerns of the female athlete. Clin Sports Med.
2004;23:281–298, vii.
Manore MM. Dietary recommendations and athletic menstrual dysfunction.

Sports Med. 2002;32:887–901.
Marshall LA. Clinical evaluation of amenorrhea in active and athletic women.

Clin Sports Med. 1994;13:371–387.
Master-Hunter T, Herman D. Amenorrhea: evaluation and treatment. Am Fam

Physician. 2006;73:1374–1382.
Rickenlund A, Eriksson MJ, Schenck-Gustafsson K, et al. Amenorrhea in

female athletes is associated with endothelial dysfunction and unfavorable
lipid profile. J Clin Endocrinol Metab. 2005;90:1354–1359.
Rumball JS, Lebrun CM. Preparticipation physical examination: selected

issues for the female athlete. Clin J Sport Med. 2004;14:153–160.
Warren MP, Goodman LR. Exercise-induced endocrine pathologies. J

Endocrinol Invest. 2003;26:873–878.
Codes
ICD9
626.0 Absence of menstruation
626.1 Scanty or infrequent menstruation
Clinical Pearls
If patient is amenorrheic just during her competitive years, she is at risk for
irreversible bone loss after only 6 mos of amenorrhea. This is especially
important because adolescence and early adulthood are times when the patient
should be building bone for later life to prevent osteoporosis and its
complications. Also, the amenorrhea may just be a symptom of more important
issues that may prevail beyond the competitive years and should be
addressed, such as Female Athlete Triad.
Migraine Headache
Tim Sprockel
Basics
Description
Common cause of benign episodic headache:
Sensory sensitivity
Frequently altering activities of daily living
Characterized by at least 2 of the following (1):
Chronic
Unilateral
Throbbing or pulsating
Worsened by movement or activity
Moderate-to-severe pain intensity
Including at least 1 of the following:
Nausea
Vomiting
Photophobia
Phonophobia
Subtypes:
Migraine without aura:
Common migraine
Most frequent variant
No sensory, motor, or visual disturbances
Migraine with aura:
Classic migraine
Characteristically with sensory, motor, and/or visual disturbances at onset
Acephalgic migraine (less common subtype):
Typical aura occurs, but no headache
Basilar migraine (less common subtype):
Headache with aura
Disturbances in brainstem function; diplopia, dysarthria, paresthesias, tinnitus, vertigo
No motor weakness
Familial hemiplegic migraine (less common subtype):
Headache with aura
Hemiparesis or hemiplegia
Patient with a 1st- or 2nd-degree relative with similar symptoms
Medication overuse migraine (less common subtype):
Excessive use or consumption of analgesic medications
Menstrual migraine (less common subtype):
Headaches present 2 days before through 1st 3 days of menses
Retinal migraine (less common subtype):
Headache with recurrent monocular visual disturbances
Normal ophthalmologic exam in between migraine attacks
Sporadic hemiplegic migraine (less common subtype):
Headache with aura
Hemiparesis or hemiplegia
Epidemiology
Females > Males (2)
Before puberty, Males > Females
Throughout puberty and adolescence, prevalence and incidence increase rapidly in females.
Risk Factors
Family history of migraine headaches
Female gender, in particular after onset of menses
Certain foods (red wine, cheese, deli meats, MSG)
Sleep cycle disturbances (lack of sleep)
Emotional or psychological disturbances
Oral contraceptive pills; estrogen therapy
Missing or skipping meals
Genetics
Migraine with aura has a hereditary component,
Chromosome 19 associated with familial hemiplegic migraine
MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes):
Extremely rare progressive neurological disorder leading to dementia:
May present with migraine-like headaches
Linked to a mutation in a mitochondrial gene
General Prevention
Identify and avoid triggers:
Foods—cheeses, meats, MSG
Red wine:
Postulated causative agents tyramines and tannins (plant polyphenols)
Inadequate sleep patterns
Irregular eating times/skipping meals
Consider discontinuation of:
Oral contraceptive pills
Hormone replacement therapy
Establish and implement ways to manage emotional and/or psychological stressors.
Evaluate association with menstrual cycle.
Use medications for prophylactic treatment.
Etiology
2 potential causes:
Vascular theory:
Vasodilation and vasoconstriction of cerebral blood vessels
Neurovascular theory:
Neuronal excitation in the gray matter with simultaneous vasodilation and
vasoconstriction
Excitation of sensory neurons in the occipital region, brainstem, hypothalamus, and
thalamus
Ongoing research examining the role of serotonin and calcitonin gene-related peptide as
possible etiologies

Anxiety (2)
Asthma/allergy
Atrial septal aneurysm
Bipolar disorder
Cerebrovascular accident: Ischemic, subclinical, or white matter abnormality
Depression
Epilepsy
Fluctuations in BP
Irritable bowel syndrome
Panic disorder
Patent foramen ovale
Reynaud's phenomenon
Sleep apnea/snoring
Tourette's syndrome
Diagnosis
History
Migraine without aura:
Episodic headaches lasting 4–72 hr
Includes at least 2 of the following:
Unilateral
Throbbing
Worsened by movement
Moderate or severe
And includes at least 1 of the following:
Nausea
Vomiting
Photophobia
Phonophobia
Migraine with aura:

Headache consistent with migraine without aura AND
Includes at least 1 temporary disturbance: Visual, sensory, speech
Includes at least 2 of the following:
Each disturbance lasts at least 5 min, not >60 min, and is fully reversible.
1 disturbance develops slowly over time, and other disturbances appear in succession
over time.
Homonymous visual symptoms and/or unilateral sensory symptoms
Aura is characterized, in order of incidence, by visual, sensory, language, motor
disturbances
Other associated symptoms include:
Diarrhea
Lightheadedness
Muscular tenderness
Vertigo
Syncope
Paresthesias
Physical Exam
General physical examination
Detailed neurological examination

Lab
Typically not needed, especially in those with established migraines with typical symptoms
Labs to consider if concern for other diagnoses:
Pseudotumor cerebri:
Lumbar puncture (LP) with opening pressure
No LP until after cerebral imaging to rule out intracranial mass, which could cause
cerebral herniation
Meningitis:
CT or MRI 1st as above, then LP
Temporal arteritis:
Erythrocyte sedimentation rate
C-reactive protein
Hypoxia from carbon monoxide poisoning:
Carbon monoxide level
Imaging
CT scan or MRI to rule out intracranial hemorrhage or tumor
MRI is preferred over CT (3)[B].
Red flags to prompt imaging:
1st or worst headache
Subacute headaches with increased frequency and/or severity
Progressively worsening headache
Headache always on the same side
Not responding to treatment
New-onset headache in immunocompromised individuals or with history of malignancy
New-onset headache after age 50
Seizures with headaches
Headache with:
Signs of meningitis:
Fever
Stiff neck
Altered mental status
Sick contacts
Focal neurological deficits
Papilledema
Cognitive impairment
Personality changes
Acid/base disturbance
Acute ischemic cerebrovascular accident (CVA)
Cerebral aneurysm/vascular malformation
Cluster headache
Dental abscess
Exertional headache
Head trauma
Hemorrhagic CVA
Hypoglycemia
Hypoxia
Intracranial infection
Intracranial malignancy
Medication side effects (eg, nitroglycerin, sildenafil)
Nonintracranial infections
Poor visual acuity
Pseudotumor cerebri
Psychiatric disorder
Secondary gain
Sinus infection or congestion
Substance withdrawal or exposure
Temporal arteritis
Temporomandibular joint disorders
Transient ischemic attack
Tension headache
Uncontrolled HTN
Treatment
Preventive treatment (4)[A]:
Determining initiation:
Significantly impacting patient's daily life
Failure or contraindication to abortive medications
Overuse of abortive medications
Patient preference
Start at low dose and increase slowly until desired effect
Allow adequate time for medication to work:
6–8 wks for some
Examples of preventive medications with recommended doses:
Anticonvulsants:
Topiramate 15–25 mg PO at bedtime
Antidepressants:
Amitriptyline 10 mg PO at bedtime
Venalfaxine 37.5 mg PO in morning
Beta-blockers:
Atenolol 50 mg PO daily
Propranolol 40 mg PO b.i.d.
Calcium channel blockers:
Verapamil 80 mg PO b.i.d. or t.i.d.
Flunarizine 5 mg PO at bedtime
Selective serotonin reuptake inhibitors not effective (5)
Medication
Medication contraindications/cautions:
Serotonin agonists contraindicated in patients with:
Peripheral vascular disease
Uncontrolled HTN
Patients with a complicated migraine course
Do not use serotonin agonists in patients who:
Have taken ergotamine derivatives within 24 hr
Have taken other serotonin agonists within 24 hr
Utilize monamine oxidase inhibitors.
Do not use NSAIDs or ASA in patients with known gastric ulcers.
Do not use NSAIDs in patients with liver or renal compromise.
Do not use narcotics if suspected secondary gain.
Avoid medications in patients with suspected or documented allergy to that
substance.
Consider that frequent use of a medication may lead to overuse headache or
rebound headache.
Pregnancy:
Serotonin agonists are not FDA-approved for use during pregnancy,
Category C
Ergot derivatives are contraindicated, Category X
Narcotic medications are Category B and C
Serotonin agonists pass through breast milk.
Pediatrics:
Serotonin agonists are not recommended for use in patients under 18 yrs of
age.
First Line
OTC medications:
NSAIDs
Aspirin (ASA)
Acetaminophen (APAP)
Combination medications that include caffeine, ASA, and APAP
P.
Prescription medications:
Ketorolac 30–60 mg IM/IV
Midrin 2 caps PO at onset of headache
Serotonin agonists (triptans) chosen based on:
Onset of action
Mode of delivery
Cost to patient
Examples:
Sumatriptan 25 mg PO or 5 mg nasal spray or 4 mg SC
Zolmitriptan 2.5 mg PO or 5 mg nasal spray
Ergotamine use has declined since the introduction of serotonin agonists
Potential problems with medication use:
Medication overuse
Withdrawal/rebound headaches (6)[A]
Second Line
Use of narcotic in refractory migraine headaches:
Morphine 2–4 mg IV
Meperidine 50–100 mg IM/IV
Caution advised with use of narcotics (6)[A]
Adjunct therapy (antiemetics) (6)[A]:
Promethazine 25–50 mg PR/IM/IV
Metoclopramide 10 mg IV/IM
Prochlorperazine 5–10 mg PO
Ondansetron 4 mg IV/IM
Some antiemetics themselves treat migraine pain.
Otherwise, used as adjunctive treatment to allow patient to tolerate oral
abortive medications
Remove from known environmental stimuli or stressors.
Encourage sleep.
Avoid known triggers.
Preventive therapies (4)[A]:
Evidence of efficacy in reducing frequency:
Riboflavin 400 mg (vitamin B2) daily
Butterbur extract 75 mg b.i.d.
Acupuncture effective as prophylaxis alone or in conjunction with analgesics,
antidepressants, beta-blockers or anticonvulsants (7)
No evidence of efficacy:
Botulinum toxin type A (Botox)
Herbal supplements such as feverfew
ABCs
IV fluids
Medications:
Analgesics
Antiemetics
Removal from environmental stimuli
Admission Criteria
Unstable vital signs
Neurologic exam with focal deficits that do not resolve
Unclear diagnosis or to exclude life-threatening illness
Intractable migraine despite appropriate therapy
Intractable nausea and vomiting
Electrolyte imbalance
Potential self-harm or harm to others due to symptoms or medications
Discharge Criteria
Resolution or improvement of symptoms
Certain of diagnosis
Life-threatening pathology ruled out
Able to tolerate oral liquids/food and medications
Ongoing Care
Return to play criteria:
No neurological or cognitive deficits
Resolution of symptoms:
Movement or activity can worsen migraine symptoms
Play with ongoing symptoms could create difficulty in evaluation if the athlete sustains a
concussion.
Migraine headache after concussion:
May not return to play until all symptoms resolved (increased risk for 2nd impact syndrome
if still symptomatic)
High school and college athletes with migraine after concussion may have increased
neurocognitive impairment.
Consider potential medication side effects and how these may affect performance.
Patient education on:
Etiology
Natural course of illness
Cautions concerning progression of illness
Use of medications/avoiding overuse
Headache journal to identify potential triggers
Discuss lifestyle modifications:
Avoidance of triggers
Abortive treatment
Follow-up visits based on patient's:
Understanding of condition
Ability to self-assess and self-treat
Frequency of headaches
Prognosis
Most migraines last from 4–72 hr:
If persisting, must consider other pathology
Most patients dramatically reduce the number of migraine episodes by avoiding triggers.
Remission increases with age.
Complications
Status migrainous:
Migraine lasting >72 hr
Severely alters patient's activities
Migrainous stroke:
Presence of 1 or more aura symptoms
Associated lesion demonstrated on brain imaging
Chronic migraine:
Headache without aura
Present for at least 15 days per month
Over a time span >3 mos (8)
Medication overuse migraines
Medication side effects
References
1. Headache Classification Subcommittee of the International Headache
Society. The international classification of headache disorders: 2nd edition.
Cephalgia. 2004;24(Suppl 1):1–160.
2. Bigal ME, Lipton RB. The epidemiology, burden, and comorbidities of

migraine. Neurol Clin. 2009;27:321–334.
3. Evans RW. Diagnostic testing for migraine and other primary headaches.
Neurol Clin. 2009;27:393–415.
4. Silberstein SD. Preventive migraine treatment. Neurol Clin. 2009;27:429–

443.
5. Moja L, Cusi C, Sterzi R, et al. Selective serotonin re-uptake inhibitors

(SSRIs) for preventing migraine and tension-type headaches. Cochrane
Database of Systematic Reviews 2005;3:CD002919. DOI:
10.1002/14651858.CD002919.pub2.
6. Tepper SJ, Spears RC. Acute treatment of migraine. Neurol Clin.

2009;27:417–427.
7. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for migraine prophylaxis.

Cochrane Database of Systematic Reviews. 2008;2:CD001218. DOI:
10.1002/14651858.CD001218.pub2.
8. Vargas BB, Dodick DW. The face of chronic migraine: epidemiology,

demographics, and treatment strategies. Neurol Clin. 2009;27:467–479.
Additional Reading
Goadsby PJ. Pathophysiology of migraine. Neurol Clin. 2009;27:335–360.
Lay CL, Broner SW. Migraine in women. Neurol Clin. 2009;27:503–511.
Codes
ICD9
346.00 Migraine with aura, without mention of intractable migraine without mention of status
migrainosus
346.10 Migraine without aura, without mention of intractable migraine without mention of
status migrainosus
346.20 Variants of migraine, not elsewhere classified, without mention of intractable migraine
without mention of status migrainosus
Clinical Pearls
Differentiate benign-natured migraine headache and more serious intracranial
pathology.
Key to prevention is avoiding known triggers
Allow enough time for prophylactic therapies to work; up to 6–8 wks
If imaging is needed, MRI is preferable to CT.
Serotonin agonists are not approved in:
Peripheral vascular disease
Uncontrolled HTN
Pregnancy
Patients under 18 yrs of age
Excessive medication use can promote rebound headaches.
Molluscum Contagiosum
Paul Stricker
Basics
Associated Complications
STDs possible
Description
Definition
Superficial pox virus skin infection
Risk Factors
Close physical contact/sports (ie, wrestling)
Sexual contact
Autoinoculation
Diagnosis
Nonpruritic rash
Located at the axilla/arm, chest wall, perineum, and upper thigh
1.5-mm, smooth, pearly, flesh-colored papules with umbilication
No associated prodrome, fever, or illness
History
How long has it been there?
Does it itch?
Any blisters? (usually more associated with herpetic lesions)
Do new lesions keep appearing?
Sexually active or previous STD?
Contact sports participation?
Physical Exam
Small, raised, 1–2-mm, flesh-colored umbilicated lesions containing white core substance
Acne/ectopic sebaceous glands
Warts
Ingrown hairs
Molluscum contagiosum
Basal. cell epithelioma
Treatment
Acute Treatment
Gentle destruction. Options include:
Deroofing the lesion individually, which hastens resolution
Cryotherapy with liquid nitrogen
Chemical therapy, using retinoic acid or salicylic acid
Other:
Refrain from contact activities until lesions are healed
Cover lesions
If untreated, usually last 6–9 mos but can persist for years
Additional Reading
Levandowski R, Keogh G, Mullane J. Sports dermatology. In: Mellion MB, ed.
Sports medicine secrets. Philadelphia: Hanley & Belfus, 1994:189–193.
Mellman MF, Podesta L. Common medical problems in sports. Clin Sports

Med. 1997;16:635–662.
Codes
ICD9
078.0 Molluscum contagiosum
Clinical Pearls
Molluscum contagiosum can be contracted from another athlete via close
contact, such as football or wrestling.
Molluscum contagiosum is contagious and it is spread by physical or sexual
contact. Should keep them covered when participating; ideally, athletes should
wait to resume contact sports for 24–48 hr after lesions are gone.
Mononucleosis
Christopher McGrew
Basics
Description
Acute viral syndrome classically resulting from infection with the Epstein-Barr virus (EBV)
EBV is a lymphotrophic γ-herpesvirus that replicates in epithelial cells and B lymphocytes.
Characterized by classic triad of fever, pharyngitis, and lymphadenopathy
Synonym(s): “Mono”; Glandular fever
Epidemiology
Peak incidence in the U.S. is between the ages of 15 and 19
Estimated prevalence 1–3% of adolescent/young adult population. U.S. incidence is
45:100,000.
Evidence of infection via EBV antibody seroconversion occurs earlier in lower socioeconomic
groups.
In all populations, >90% seroconversion by the end of the 3rd decade of life, although many
are not aware of having the disease.
No evidence to suggest that infectious mononucleosis is more or less prevalent in student
athletes than among the general student population.
Risk Factors
Transmission via passage of infected mucous membrane secretions, most commonly saliva
(“the kissing disease”); incubation period typically 30–50 days
EBV also felt to be passed via respiratory tract secretions, blood, rectal, and potentially
genital secretions, raising the possibility of sexual transmission. No aerosol transmission has
been found.
Lack of mononucleosis epidemics supports concept of low-level contagiousness.
Relative risk of contracting EBV increased by factors negatively affecting the overall status of
the immune system: Baseline fatigue, overtraining, poor nutritional status
General Prevention
General handwashing/hygiene measures
Avoidance of sharing of water bottles, food, other utensils
Proper rest/avoid overtraining
Good nutrition
Etiology
Infectious mononucleosis (IM) is caused by the EBV, which is a lymphotrophic γ-herpesvirus
that replicates in epithelial cells and B lymphocytes.

Group A beta hemolytic streptococcal pharyngeal/tonsillar infection coexistent in up to 30% of
cases
Diagnosis
IM remains a clinical diagnosis based on history, physical, and selected laboratory
testing.
Hoagland's criteria are frequently cited for establishing diagnosis
CBC shows at least 50% lymphocytes, of which 10% are atypical.
Presence of fever, pharyngitis, and adenopathy
Serologic confirmation
Only 50% of patients with suggestive symptoms and serologic confirmation meet all of
Hoagland's criteria.
History
Prodrome of malaise/fatigue followed by development of the classic triad of fever, sore
throat, and enlarged lymph nodes
Headache in many cases
Patient often does not have known history of EBV exposure.
Athlete may complain of poor exercise performance.
Fatigue is often disabling, even for activities of daily living.
Physical Exam
Classic triad: Fever, pharyngitis, and cervical lymphadenopathy (anterior and posterior)
Many patients manifest a prodrome of disabling fatigue/malaise.
Pharyngitis characterized by yellow-gray tonsillar exudate and palatal edema
Fevers of 39°–40°C with evening peaks, typically for 10–14 days
Abdominal pain
Notable decline in exercise tolerance
Fever often demonstrable
Patient may appear fatigued and mildly to moderately ill but generally nontoxic.
Exudative pharyngitis
Palatal petechiae
Periorbital edema
Prominent anterior and posterior cervical lymphadenopathy (lymphadenopathy may also
involve axillary and inguinal regions)
Although splenomegaly is probably present in nearly all patients, peaking in the 2nd and 3rd
wks, physical exam for splenomegaly has poor sensitivity and specificity, and interexaminer
reliability is poor.
Overzealous abdominal exam may precipitate splenic injury in rare cases.
With splenic rupture, may develop Kehr sign (patient supine, raise left leg, intra-abdominal
blood tracks up to diaphragm, creates referred pain to left shoulder)
Maculopapular, urticarial or petechial rash (petechial rashes should raise suspicion for
potential aplastic anemia, thrombocytopenia or DIC)
Maculopapular rash may often develop after antimicrobial administration: Most commonly
ampicillin or amoxicillin, but has also been reported with the use of azithromycin, levofloxacin,
and cephalexin.

Lab
Primary means of laboratory testing via nonspecific heterophile antibody studies (ie,
monospot qualitative agglutination slide test)
Heterophile antibody (+) 60–70% at 1 wk, 80–90% by 3–4 wks
Definitive diagnosis: EBV viral capsid antigen (VCA) immunoglobulin M (+) for acute
infections, (-) for recent or past infections
EBV VCA immunoglobulin G confirms past infection and generation of protective antibody.
May use more specific EBV-associated antigens if necessary to determine exact phase of
illness
Classic hematologic findings include >10% atypical lymphocytes [Downey cell-activated
cytotoxic suppressor (CD8) T lymphocytes], relative leukocytosis (up to 20,000), followed by
mild neutropenia during wk 2 of illness, mild hemolytic anemia, and mild thrombocytopenia
(100,000–140,000/mm3)
Mild hepatitis (2–3-fold increase in liver function tests) may be seen in week 2–3 of illness.
Imaging
No routine imaging used for diagnosis or management of mononucleosis
One-time imaging of the spleen for assessment of splenomegaly at the time of illness is not
recommended because of the wide variability encountered in normal values (1)[A].
Contrasted abdominal CT for concerns about splenic rupture (incidence of 1–2 per 1,000
cases of mononucleosis, often spontaneous)
Primarily must be differentiated from nonspecific viral syndromes, lymphoma, leukemia, and
Streptococcus pharyngitis
Many infectious agents may cause mononucleosis-like syndromes: Cytomegalovirus,
adenovirus, hepatitis A, human herpesvirus 6, HIV, rubella, toxoplasmosis
Medications causing mononucleosis-like syndromes: phenytoin, sulfa drugs
Treatment
General Measures
Care is primarily supportive/symptomatic.
No effective treatment presently is available.
Care should be taken to avoid splenic trauma; avoid exercise and activities
with jarring movements; use stool softeners to avoid increasing intra-abdominal
pressure.
Avoid alcohol and other liver toxins.
Referral
Splenic rupture
Acyclovir has been shown to decrease viral shedding, but has no effect on the
natural course of the illness, and no clinical benefit has been demonstrated.
Corticosteroids may be clinically indicated in cases with airway compromise,
severe dysphagia, massive/painful spleen enlargement, myocarditis, or
hemolytic anemia.
A Cochrane Review evaluating the use of corticosteroids for symptom control
in IM concluded that although symptoms were decreased for the 1st 12 hr,
these benefits were lost at 2–4 days. Since there was no clear evidence on the
effectiveness of steroids and, given the potential for adverse effects from the
use of steroids, the Cochrane Review recommended that corticosteroid use be
avoided in uncomplicated cases (2)[A].
None
Splenic rupture may be treated with either splenectomy or observation in
selected situations.
Earlier return to play with splenectomy, but must be weighed against risks of
asplenia
If splenectomy chosen, H flu, pneumococcal, and meningococcal vaccination
should be provided prior to splenectomy
Ongoing Care
Diet
No special recommendations other than balanced diet with adequate fluids and fiber to avoid
constipation; avoid alcohol.
Prognosis
Most patients who contract IM have an uneventful clinical course with an unremarkable
recovery.
Some athletes may take as long as 3 mos to return to their pre-illness levels of activity.
Adult form of mononucleosis is different from the disease in children and adolescents:
Most adults: Pharyngitis or lymphadenopathy
Fever is often more prolonged.
Abnormal liver function more frequent
Lymphocytosis/presence of atypical lymphocytes less common
Complications
A wide variety of complications can occur, involving virtually all organ systems:
Edema of Waldeyer's ring, resulting in airway compromise and/or severe
dysphagia
Splenomegaly: Nearly universal in IM, so not truly a complication
Splenic rupture: Reported in 0.1–2% of cases; most cases occur in 1st 3–4
wks of illness; in 1 study, 50% nontraumatic
Guillain-Barré syndrome
Cranial nerve palsies
Aseptic meningitis
Meningoencephalitis
Aplastic anemia
Hemolytic-uremic syndrome
Jaundice
Myocarditis
Conjecture that chronic fatigue syndrome may be associated with chronic EBV
infection is not well supported in the literature.
Immunocompromised (eg, HIV, transplant patients, etc.): Lymphoma and other
lymphoproliferative disorders are potential severe complications.
References
1. Hosey RG, Mattacola CG, Kriss V, et al. Ultrasound assessment of spleen
size in collegiate athletes. Br J Sports Med. 2006;40:251–254.
2. Candy B, Hotopf M. Steroids for symptom control in infectious

mononucleosis. Cochrane Database Syst Rev. 2006;3:CD004402.
3. Putukian M, O'Connor FG, Stricker P, et al. Mononucleosis and athletic

participation: an evidence-based subject review. Clin J Sport Med.
2008;18:309–315.
Additional Reading
Peter J, Ray CG. Infectious mononucleosis. Pediatr Rev. 1998;19:276–279.
Codes
ICD9
075 Infectious mononucleosis
Clinical Pearls
In most cases, athletes will not feel well enough to participate in activity for
several weeks. In addition, although the risk for splenic rupture is extremely low,
given that most of these occur within the 1st 3 wks of illness, independent of
spleen size, it is generally felt that it is safe to resume light activity 3 wks from
the onset of symptoms, as long as the athlete is afebrile, has a good energy
level, and does not have any significant associated abnormalities. The risk of
splenic rupture likely diminishes as more time progresses; therefore, delaying
return to play should be considered if clinical features, lack of athlete
readiness, and/or associated complications are present. Treatment must,
therefore, be individualized to account for all of these issues (3)[C].
The appropriate time for safe return to contact play is unclear, although, given
the risk for splenic rupture, a time frame of at least 3 wks commonly is
recommended. Return can occur only after the athlete has no remaining clinical
symptoms, is afebrile, and has a normal energy level. The risk for splenic
rupture likely decreases as more time passes, allowing for individualized
return-to-play decisions, depending on the athlete, sport, and other factors (3)
[C].
It is unclear what role exercise has on the natural history of IM disease.
Although many athletes can self-regulate on return to ad lib activity if afebrile, it
would appear that premature return to heavy exertion might prolong the
duration of symptoms, most notably fatigue, and also be associated with a
decrease in performance (3)[C].
Fortunately, because of the nature of transmission, epidemics of
mononucleosis are uncommon. Care should be taken to avoid shared water
bottles, utensils, etc. Teams that travel extensively together have greater
potential contacts for transmission. As the incubation period is lengthy,
identifying index cases is difficult. It is not practical or necessary to exclude
infected teammates if appropriate measures are taken to avoid spread of the
virus. Appropriate rest, proper nutrition, and avoiding overtraining may reduce
susceptibility to IM.
Motion Sickness
Derek McCoy
Mark I. Harwood
Basics
Description
Not a true “sickness” but a situation in which there is a sensory conflict about body position
among the visual receptors, vestibular receptors, and body proprioceptors. It can also be
induced when patterns of motion differ from those previously experienced.
Also can be induced when patterns of motion differ from those previously experienced
System(s) affected: Nervous
Synonym(s): Car sickness; Sea sickness; Air sickness
Epidemiology
Incidence
Predominant sex: Female > Male
Risk Factors
Motion
Travel
Visual stimuli (ie, moving horizon)
Poor ventilation (fumes, smoke, carbon monoxide)
Emotions (fear, anxiety)
Zero gravity
Pregnancy
Age
Gender (Females > Males [1.7:1])
Other illness or poor health
General Prevention
Pediatric alert:
Rare in children <2 yrs of age
Incidence peaks between the ages of 3 and 12 yrs
Antihistamines may cause excitation in children.
Gerontologic alert:
Age confers some resistance to motion sickness.
Elderly at increased risk of anticholinergic side effects from treatment
Pregnancy alert:
Pregnant patients more likely to experience motion sickness
Treat with medications thought to be safe during morning sickness (eg, meclizine,
dimenhydrinate).
Prevention/avoidance:
Minimize exposure (seat in middle of plane or boat)
Improve ventilation
Semirecumbent seating
Fix vision at 450-degree angle above horizon
Avoid fixation of vision on moving objects (ie, waves)
Avoid reading while traveling.
Minimize food intake prior to travel.
Etiology
Precise etiology unknown; thought to be due to a mismatch of vestibular and visual
sensations
Nausea and vomiting occur as a result of increased levels of dopamine and acetylcholine,
which stimulate chemoreceptor trigger zone and vomiting center in CNS.
Diagnosis
Physical Exam
Nausea
Vomiting
Diaphoresis
Pallor
Hypersalivation
Yawning
Hyperventilation
Anxiety
Panic
Malaise
Fatigue
Weakness
Confusion
Mountain sickness
Vestibular disease
Gastroenteritis
Metabolic disorders
Toxin exposure
Treatment
Premedicate before travel with antidopaminergic, anticholinergic, or
antihistamine agents.
For extended travel, consider treatment with scopolamine transdermal patch.
2nd-generation (nonsedating) antihistamines are not effective at preventing
motion sickness.
Serotonin (5-HT3) antagonists (eg, ondansetron) do not appear effective in
preventing motion sickness.
Conflicting data exist on the efficacy of acupressure for nausea and vomiting
associated with motion sickness.
Benzodiazepines suppress vesibular nuclei, but would not be considered 1st
line owing to sedation and addiction potential.
Medication P.
First Line
Scopolamine transdermal where available; apply patch 6 hr before travel and
replace every 3 days or 0.4 mg to 0.8 mg PO q.i.d. PRN with 1st dose 1 hr
prior to event (1)[C]
Dimenhydrinate (Dramamine) given 30 min prior to motion; adults and
adolescents 25–50 mg q4–6h, maximum 300 mg/day; children 6–12 yrs 12.5–
25 mg q4–6h, maximum 150 mg/day; children 2–5 yrs 6.25 mg PO/IM/IV q4–
6h, maximum 37.5 mg/day (1)[C]
Meclizine (Antivert) 25–50 mg q24h Start 1 hr prior to travel (1)[C]
Contraindications: Glaucoma, hypersensitivity to drug class
Precautions:
Young children
Elderly
Pregnancy
Urinary obstruction
Pyloric obstruction
Significant possible interactions:
Sedatives (antihistamines, alcohol, antidepressants)
Anticholinergics (belladonna alkaloids)
Adverse reactions:
Drowsiness
Dry mouth
Blurred vision
Confusion
Headache
Urinary retention
Second Line
Ginger: 1 g PO Take 4 hr prior to travel (2)[C].
Stimulation of the P6 (pericardium 6) acupressure point with placement of fingers
(3)[D]
Ongoing Care
Diet
Decrease oral intake or small frequent feedings
Avoid alcohol
Prognosis
Symptoms should resolve when motion exposure ends.
Resistance to motion sickness seems to increase with age.
Complications
Hypotension
Dehydration
Depression
Panic or anxiety
References
1. Nachum Z, Shupak A, Gordon C. Transdermal scopolamine for prevention
of motion sickness. Clinical Phamacokinetics. 2006;45:543–566.
2. White B. Ginger: An overview. American Family Physician. 2007;75:1689–

1691.
3. Miller K, Muth E. Efficacy of acupressure and acustimulation bands for the

prevention of motion sickness. Aviation, Space and Environmental Medicine.
2004;75:227–234.
Additional Reading
Dundee JW, McMillan C. Positive evidence for P6 acupuncture antiemesis.
Postgrad Med. 1991;67:417–422.
Joseph J, Griffin M. Motion sickness: effect of changes in magnitude of

combined lateral and roll oscillation. Aviation, Space Environ Med.
2008;79:1019–1027.
Klosterhalfen S, et al. Nausea induced by vection drum: contributions of body

position, visual pattern, and gender. Aviation, Space Environ Med.
2008;79:384–389.
Kohl RL, Calkins DS. Control of nausea & autonomic dysfunction with
terfenadine, a peripherally acting antihistamine. Aviation, Space Environ Med.
1991;62(5):392–396.
Shupak A, Gordon C. Motion Sickness: Advances in Pathogenesis,
Prediction, Prevention, and Treatment. Aviation, Space Environ Med.
2006;77:1213–1223.
Codes
ICD9
994.6 Motion sickness
Clinical Pearls
Nonpharmacologic means for prevention should be tried 1st, which include
sitting in the front of moving objects and toward the middle of the vehicle, if
possible. Improving ventilation and sitting semirecumbent may be helpful. In
addition, avoidance of food prior to travel and avoidance of reading during
travel are recommended. It is also recommended to avoid visual fixation on
moving objects.
The preferred treatment method is pretreatment with scopolamine transdermal,
dimenhydrinate, or meclizine. Alternatively, acupressure (P6), ginger, or
promethazine can be tried. If motion sickness develops, removing the noxious
stimulus is curative for that exposure.
Nasal Septal Hematomas
Brandon Bockewitz
Daryl A. Rosenbaum
Basics
Hematoma contained in the tight submucosal space can lead to pressure necrosis or
abscess. This results in cartilage destruction and collapse of the nasal dorsum, or a saddle
nose deformity.
Dorsal nose deformity causes significant cosmetic and functional morbidity that usually is
permanent. Although rare, monitor for the presence of septal hematoma in every case of
nasal trauma, and treat promptly when it is diagnosed.
Description
Bleeding between cartilaginous and mucosal layers of the nasal septum resulting from trauma
to the nose that collects to form a hematoma
Septal hematomas can occur bilaterally or unilaterally.
Diagnosis
History
Trauma to the nose, most often an inferior blow, because the supportive structure of the lower
2/3 of the nose is composed entirely of cartilage
Physical Exam
Signs and symptoms:
Epistaxis, nasal deformity and swelling, ecchymosis, pain, and crepitant to palpation,
usually from associated nasal fracture
Difficulty breathing through one or both sides of the nose
Septal hematoma will appear as a bluish red bulge from the septum into the nasal vestibule
or as an asymmetric mucosal fold. Newly formed hematomas may lack the classic bluish
red discoloration, making direct palpation a more reliable exam finding.
Control bleeding with direct pressure, topical decongestants, or cautery, as indicated for
optimal visualization.
Patient positioning: Drainage of blood from the nose is best achieved with the patient in a
supine position with the head elevated.
Visualize the anterior septum, preferably using a nasal speculum or otoscope with the tip
inserted past the nasal vestibule. If necessary, a rigid nasal endoscope may be needed.
Sufficient lighting and suction are helpful.
Direct palpation: Using a gloved finger, gently palpate along the entire nasal septum,
feeling for swelling, fluctuance, widening of the septum, or any other abnormalities.
Blood clots adjacent to the nasal septum can falsely represent a septal hematoma and
should be evacuated before examining the nasal septum.
Masses located deep within the nasal cavity, out of the reach of a gloved finger, may
require palpation by a cotton swab, again, feeling for a soft mass as opposed to the firm
cartilaginous septum.

Lab
Rarely necessary for routine cases
Delayed presentation to health care providers or failed drainage can lead to nasal septal
abscess.
Purulent specimens should be sent for Gram stain and culture, both aerobic and anaerobic.
Treatment
Acute treatment
Prompt intervention:
Needle aspiration or sharp incision and drainage under local or general
anesthesia followed by suction of the clot, if needed, and irrigation (1,2,3):
Mucosal incision should be made over the area of greatest fluctuance, with
care taken not to damage the underlying cartilage.
Bilateral hematomas should be treated with staggered incisions to
decrease risk of possible through-and-through perforation.
Wick or drain placement is unnecessary unless suspicious for septal
abscess (4)[C].
If a drain was placed, it can be removed when drainage has stopped for 24
hr.
Bilateral anterior nasal packing to approximate the perichondrium and P.
prevent recurrence of the hematoma (3)[C]
Usually 2–4 days
Systemic antibiotic coverage with clindamycin or amoxicillin–clavulanic acid
provides appropriate coverage against the most common abscess
pathogens (1,2,3)[C], including:
Staphylococcus aureus
Streptococcus pneumoniae
Group A β-hemolytic Streptococcus
Haemophilus influenzae
Ongoing Care
Patients and parents should be instructed on signs and symptoms of nasal septal hematoma
because formation may be delayed up to 14 days after the initial trauma (3).
Close follow-up after diagnosis and drainage for evaluation of possible failed drainage or
reaccumulation of blood after successful drainage
Children should be followed for 12–18 mos for cartilaginous changes and cosmetic defects
(3).
Complications
Reaccumulation of hematoma
Nasal septal abscess
Saddle nose deformity
References
1. Menger DJ, Tabink I, Nolst Trenité GJ. Treatment of septal hematomas and
abscesses in children. Facial Plast Surg. 2007;23:239–243.
2. Lopez MA, Liu JH, Hartley BE, et al. Septal hematoma and abscess after
nasal trauma. Clin Pediatr (Phila). 2000;39:609–610.
3. Savage RR, Valvich C. Hematoma of the nasal septum. Pediatr Rev.

2006;27:478–479.
4. Perkins SW, Dayan SH. Management of nasal trauma. Aesthetic Plast

Surg. 2002;26 (Suppl 1):3
Additional Reading
Kaufman BR, Heckler FR. Sports-related facial injuries. Clin Sports Med.
1997;16:543–562.
See Also
Incision and drainage of a septal hematoma or abscess
Codes
ICD9
920 Contusion of face, scalp, and neck except eye(s)
Clinical Pearls
Special populations: Children (4)[C]:
Increased incidence of septal hematoma secondary to highly cartilaginous
nasal skeleton
Minor trauma can lead to hematoma formation, even without signs of external
injury.
Any history of nasal trauma warrants intranasal examination.
The nasal packing usually is left in for about 2–4 days so that the mucosa can
heal and fill in the space where the hematoma formed.
Return to play is not advised until the packing is removed owing to impaired
breathing and the need to protect the septal mucosa while it heals.
After removal of packing, return to play is based on consideration of the
associated nasal fracture and whether or not an infection is present.
Near-Drowning/Drowning
Kevin N. Waninger
Basics
The terms “drowned” and “near-drowned” have been used to describe the outcomes
dead or alive, respectively. The term “near-drowned” has also been used to describe patients
who subsequently died from drowning. This usage has led to uncertainty about the meaning of
the term. Therefore, the term “near-drowning” has lost favor. The term “drowned” will continue
to refer to a person who died or suffered injury from drowning.
Description
Drowning is a process resulting in primary respiratory impairment from submersion or
immersion in a liquid medium. The pathophysiology is primarily related to abnormal gas
exchange, with resultant hypoxia.
Hypoxia may result from laryngospasm causing no pulmonary gas exchange, or aspiration of
fluids causing pulmonary injury and subsequent disruption of productive gas exchange.
The drowning process is a continuum that begins when the victim's airway lies below the
surface of a liquid, usually water, at which time the victim voluntarily holds their breath.
Breath-holding is usually followed by an involuntary period of laryngospasm secondary to the
presence of liquid in the oropharynx or larynx, resulting in hypoxemia, hypercarbia, and
acidosis.
During this laryngospasm, there is no exchange of air, and the victim may swallow large
quantities of water. As arterial oxygen tension drops further, laryngospasm abates, and the
victim actively breathes liquid. The amount of liquid inhaled varies considerably from victim to
victim.
Changes occur in the lungs, body fluids, blood-gas tensions, acid-base balance, and
electrolyte concentrations, which are dependent on the composition and volume of the liquid
aspirated and the duration of submersion. Surfactant washout, pulmonary HTN, and shunting
also contribute to the development of hypoxemia.
The clinical presentation and prognosis vary due to different water temperatures, different
fluid properties (fresh water, seawater, Dead Seawater, water contaminated with chemicals
and bacteria), and the variety of environments (from toilets to hurricane sea conditions) in
which drowning occurs.
The heart and brain are the organs at greatest risk for permanent, detrimental changes from
relatively brief periods of hypoxia. Posthypoxic encephalopathy, with or without cerebral
edema, is the most common cause of death in hospitalized drowning victims.
Reinstitution of adequate ventilation and oxygenation before the occurrence of circulatory
arrest and irreversible nervous system damage results in complete and dramatic restoration
of function (if aspiration does not occur).
When aspiration occurs, due to ventilation/perfusion mismatch and shunting, prolonged
hypoxemia and subsequent complications are more likely to occur.
Epidemiology
Drowning incidents occur in swimming pools, lakes, rivers, streams, storm drains, hot tubs,
bathtubs, and even toilets and buckets in toddlers.
In 2005, there were 3,582 fatal unintentional drownings in the U.S., averaging 10 deaths per
day.
>25% of fatal drowning victims were children <15 yrs old, and of all children 1–4 yrs old who
died, almost 30% died from drowning. An additional 710 people died from drowning and
other causes in boating-related incidents.
A swimming pool is 14 times more likely than a motor vehicle to be involved in the death of a
child age 4 and under.
For every child who dies from drowning, another 4 receive emergency department care for
nonfatal submersion injuries.
Male: Female ratio in drowning is 4:1.
Although drowning rates have slowly declined, fatal drowning remains the 2nd-leading cause
of unintentional injury-related death for children ages 1–14 yrs.
19% of drowning deaths involving children occur in public pools with certified lifeguards
present. Of all preschoolers who drown, 70% are in the care of 1 or both parents at the time
of the drowning, and 75% are missing from sight for <5 min.
The majority of children who survive without sequelae are discovered within 2 min following
submersion, and most children who die are found after 10 min.
Incidence
In 2005 there were 3,582 fatal unintentional drownings in the U.S., averaging 10 deaths per
day.
Children under 5 and adolescents (ages 15–24) have the highest drowning rates.
Prevalence
Rates of fatal drowning are notably higher among African Americans (1.3×) and American
Indians and Alaskan Natives (1.8×) compared to Caucasians.
For children ages 5–14, the fatal drowning rate of African American children (3.2×) and
American Indian and Alaskan Native children (2.4×), is higher than for white children.
Risk Factors
Unattended children at water sites; inadequate adult supervision
Alcohol and/or drug abuse (50% cases involving adolescents and adults)
Limited swimming ability and exhaustion
Trauma
Risky behavior in the water; rough play
Deliberate prolonged submersion, intentional hyperventilation before breath-hold diving; young
children more susceptible to the diving reflex, triggered by submersion of face in cold water,
with bradycardia and redistribution of blood flow to heart and brain
Exacerbation of existing medical problems (seizure disorder, cardiac disease, diabetes,
syncope, cerebrovascular accident)
Cold-water immersion or hypothermia; cold shock response; young children more
susceptible, due to larger body surface-to-mass ratio; decreases the metabolic rate, survival
to full recovery possible
Scuba: Contamination of air supply with toxic gases (ie, carbon monoxide), running out of air
at depth
Oxygen-induced seizures in divers using oxygen-enriched air mixtures
Panic/anxiety
Improper fencing of pools (at least 5 feet high with self-closing latches)
General Prevention
Drowning is preventable! Prevention is the key:
Parental supervision of children around water; watch empty pails, buckets, toddlers around
toilets.
Carefully watching children while they bathe
Swimming lessons: Children 1–4 yrs old who drowned were significantly less likely to have
attended swimming classes than matched controls (1)[B].
The American Academy of Pediatrics recommends that all children be taught to swim after
age 5, but makes no recommendation for younger children.
Adequate pool fencing; wearing properly sized life jackets
Improved pool design preventing children from being trapped when submerged
Poor pool maintenance resulting in murky or cloudy water
Instruction/supervision of lifeguards in methods of waterfront surveillance and resuscitation
techniques
Education of public in prudent consumption of alcoholic beverages
Impose severe sanctions against boaters who are intoxicated.
Encourage people to learn to swim, understand the limits of their swimming ability, and never
swim alone.
Restricted swimming areas; post proper signage in areas of dangerous underwater tow; pay
attention to the weather, tides and water conditions, and especially currents. Currents are
usually perceived from the outside as weaker than they actually are.
Understand the water environment where you are swimming, diving, or boating.
Instruct greater numbers of the public in Basic Life Support (BLS) or Cardiopulmonary
Resuscitation (CPR).
Bring a cordless telephone to the pool so children are not left unsupervised while answering a
phone call.
Etiology
Unexpected submersion. Struggle does not always occur.
Aspiration of variable amounts of water. Grossly contaminated water poses a risk of
pulmonary infection.
Laryngospasm
Hypoxia
Metabolic acidosis
Myocardial dysfunction
Coagulation abnormalities
Multisystem organ dysfunction with renal failure
CNS dysfunction
Diagnosis
Hypothermia may be protective.
Family history of sudden death by drowning may suggest a genetic cause for syncope, such
as long QT.
History
See “Risk Factors.”
Information from witnesses or emergency medical services personnel at the scene
Physical Exam
Cardiac presentation depends on severity of exposure; ranging from sinus tachycardia to
cardiac arrest and apnea. It is not uncommon for these patients to require but respond to
prolonged CPR. Children who still require CPR at the time they arrive at the emergency
department have a poor prognosis, with at least half of survivors suffering significant
neurologic impairment.
The process of drowning is characterized by a gradual decrease in arterial oxygen saturation

with a simultaneous decrease in cardiac output. Cardiac arrest is, therefore, not sudden but
is preceded by a brief period of tachycardia and HTN, followed by bradycardia with
hypotension and electromechanical dissociation (pulseless electrical activity).
Ventricular fibrillation is rare after submersion, unless resulting from acute hypothermia or
triggered by mechanical irritation, and will frequently not respond to defibrillation. The
automated external defibrillator will not play a major role in improving the success of
resuscitation after drowning (2,3)[A].
Whether the drowning event occurs in fresh water or seawater, the end result is pulmonary
edema, a decrease in pulmonary compliance, and an increase in the ventilation/perfusion
mismatch.
Patients with water aspiration may present with minimal symptoms, severe pulmonary
edema, or frank cardiopulmonary arrest. Cyanosis, dyspnea, and/or copious pulmonary
secretions may be present.
Cerebral edema/injury
Evidence of trauma/cervical spine injury
Hypothermia; full vital signs with rectal temperature required

Lab
Most drowning victims do not aspirate enough fluid to cause life-threatening changes in blood
volume.
Life-threatening electrolyte abnormalities occur when the amount of aspirated fluid is >22
mL/kg of body weight.
Aspiration of this volume of water is unlikely in humans who survive the drowning process
(<15%).
Rarely is there a need for emergent treatment of electrolyte abnormalities unless very large
volumes of water are aspirated or the drowning event occurs in a highly concentrated liquid
medium such as the Dead Sea.
Arterial blood gases
CBC; significant changes of hemoglobin and hematocrit are seldom seen in human drowning
victims.
Chemistry panels usually normal, but rule out hyperkalemia, hypernatremia, hyponatremia, or
signs of renal failure
Urinalysis
Prothrombin time/international normalized ratio (coagulation panel)
Alcohol and toxicology screen
Imaging
Chest x-rays may be normal initially, or show infiltrates ranging from a patchy distribution to
global pulmonary edema.
CT scan of head may be needed to rule out acute or chronic intracranial process in
unconscious patients.
Obtain cervical spine films if you suspect head/neck trauma.
Consider a potential underlying cause of submersion injury, such as alcohol or drug
intoxication, myocardial infarction, syncope (long QT syndrome), seizure (including O2-
induced), stroke, hypoglycemia, or trauma.
Head or spinal cord injury/trauma
Venomous stings by aquatic animals
Decompression sickness or arterial gas embolism, nitrogen narcosis from scuba diving
Consider child abuse/neglect
Treatment
Pre-Hospital
ABCs, remove wet clothing, initiate rewarming as soon as possible, IV with
0.9% normal saline (watch fluids in patients with pulmonary edema)
Initiate cardiopulmonary resuscitation as soon as possible if indicated; begin in
the water if can be done without putting rescuer at risk; although unusual,
recovery with normal neurologic function has been reported even after
prolonged cardiac arrest.
Basic life support, and sometimes rescue breathing alone, performed by
laypersons, play a key role in the survival of the drowning victim (3)[A].
Avoid further aspiration; apply cricoid pressure during bag-valve-mask
ventilation.
Secure airway and protect against aspiration of stomach contents; intubation
with 100% oxygen
Strict cervical spine precautions (2,3)[A]
The subdiaphragmatic thrust (Heimlich) maneuver to remove water from the
abdomen is not recommended unless a foreign body is suspected of
obstructing the airway (2,3)[A].
ED Treatment
Correct hypoxia, titrate to oxygen saturation, intubation with positive end-
expiratory pressure can be effective in reversing the abnormal V/Q
relationships. In patients who are alert, nasal continuous positive airway
pressure may be needed for ventilation support.
P.
The risk for aspiration from water and stomach contents is still present, so
strict aspiration precautions with elevation of head of bed if possible are
recommended.
If bronchospasm is present or suspected, give nebulized beta-2-agonist
treatments.
Evaluate and treat traumatic injuries.
If in cardiopulmonary arrest, initiate Advanced Cardiac Life Support measures;
continue resuscitation until core temperature >32°C, or until spontaneous pulse
and respirations return.
Follow temperature and continue rewarming efforts if indicated.
Insert a nasogastric tube to decompress the stomach.
Insert Foley catheter, if needed.
Check and correct severe electrolyte abnormalities and monitor acid-base
balance. Correct acidosis with sodium bicarbonate administration for pH <7.1.
Antibiotics needed only in those patients who become febrile, develop new
pulmonary infiltrates, or have purulent secretions. Prophylactic antibiotics do
not improve morbidity or mortality (3)[A].
Steroids have been shown to be ineffective in treating the pulmonary issues of
drowning, and may worsen outcome by interfering with the normal healing
process (3)[A].
Management of patients with suspected hypoxic brain injury includes
hyperventilation (maintain PaCO2 at 25–30 mm Hg), head elevation (if no C-
spine injury is present), diuretics, and muscle relaxants.
It appears that in the absence of hypothermia that may have occurred during
the drowning process, aggressive brain resuscitation in the neurologically
impaired drowning patient, using current techniques, is of limited benefit in
returning patients to normal neurologic function.
Admission Criteria
ICU:
Patients who required CPR or artificial resuscitation
Abnormal chest x-ray
Arterial blood gas abnormalities
Glasgow Coma Scale (GCS) <13
Admit observation:
Submersion unknown or >1 min
History of cyanosis or apnea
Required brief assisted ventilation
GCS >13
Delayed pulmonary edema (up to 12 hr)
Delayed neurologic abnormalities
Discharge Criteria
Questionable history of submersion, after observation in emergency
department for 6–8 hr
Normal chest x-ray
No respiratory distress
No neurologic deterioration
Discharge to reliable home, with instructions to return for shortness of breath
or mental status changes
Ongoing Care
Prognosis
Prognosis of resuscitated drowning victim is related to degree of damage secondary to the
anoxic episode and the duration of immersion and pulmonary insult.
Residual complications of near-drowning may include intellectual impairment, convulsive
disorders, and pulmonary or cardiac complications.
References
1. Brenner RA, Taneja GS, Haynie DL, et al. Association between swimming lessons and
drowning in childhood: a case-control study. Arch Pediatr Adolesc Med. 2009;163:203–210.
2. Bierens JJ, Knape JT, Gelissen HP. Drowning. Curr Opin Crit Care. 2002;8:578–586.
3. Layon AJ, Modell JH. Drowning: Update 2009. Anesthesiology. 2009;110:1390–1401.
Additional Reading
Centers for Disease Control and Prevention, National Center for Injury Prevention and
Control. Web-based Injury Statistics Query and Reporting System (WISQARS) [online].
(2008) [cited 2008 March 23]. Available from: URL: www.cdc.gov/ncipc/wisqars. Accessed
on September 12, 2009.
Idris AH, Berg RA, Bierens J, et al. Recommended guidelines for uniform reporting of data
from drowning: the “Utstein style.” Circulation. 2003;108:2565–2574.
Papa L, Hoelle R, Idris A. Systematic review of definitions for drowning incidents.

Resuscitation. 2005;65:255–264.
Codes
ICD9
994.1 Drowning and nonfatal submersion
Clinical Pearls
Medical authorities traditionally made a great distinction between salt water and
fresh water drowning. The theory was that because of its high salt content,
seawater in the lungs would affect the body very differently from fresh water in
a variety of ways. Although this is true in theory, very few survivors of near-
drowning ingest enough water to make a difference, and this rarely becomes
an issue in treating patients who arrive at the hospital. In practice, water
temperature and the presence of any contaminants are much more important
considerations.
Hypoxia is the main threat in drowning victims, and resuscitation efforts should
be directed toward restoration of optimal oxygenation.
Neck Lacerations and Penetrating Injuries
Neha P. Raukar
Basics
Esophageal and venous injuries present with very subtle findings, and the diagnosis of injuries
to these structures is often delayed.
Alert
Unstable patients with penetrating neck trauma receive definitive care in the operating room.
Stable patients should be transferred to a trauma center.
Occlusive dressings that are soaked in petroleum jelly should be applied to lacerations over
major veins to prevent air embolism. If possible, patients should also be placed in
Trendelenburg.
Before attempting to secure the airway, be sure to have a surgical airway kit at the bedside.
Do not be fooled by the seemingly stable patient. These patients can decompensate rapidly
and without warning.
Surgical intervention is required in 15–20% of cases of penetrating neck injury (1).
Description
Penetrating neck trauma is defined as a wound that violates the platysma muscle.
The neck is divided into 3 zones based on superficial landmarks, and are numbered from
most caudal to cephalad:
Zone I extends from the top of the sternum to the sternal notch or cricoid cartilage:
Penetrating trauma in this zone carries the highest mortality due to injury to thoracic
structures.
An isolated Horner's syndrome may be the only presenting sign of injury to this zone.
Zone II extends from the cricoid cartilage to the angle of the mandible:
The majority of penetrating neck wounds occur in this zone.
However, since injured structures are more easily identified, treatment, both in the
emergency department and the operating room, is more often successful. Therefore,
mortality rates are the lowest in this zone.
Zone III extends cephalad from the angle of the mandible to the base of the skull:
Least commonly injured
Injuries to the distal carotid artery can mimic a stroke.
Etiology
Gunshot wounds
Stab wounds
Miscellaneous (glass shards, metal fragments)
Sports trauma (cleat spikes, hockey stick laceration, shattered baseball bat fragments, etc.)
Diagnosis
Careful examination of the wound to determine integrity of the platysma
Wounds should never be blindly probed, as this may result in uncontrolled hemorrhage.
Lateral neck radiograph to evaluate soft tissue injury and detect foreign bodies
Chest radiograph for suspected Zone I injuries to detect hemopneumothorax, mediastinal air,
or bleeding that extends into the upper mediastinum
Physical Exam
Signs and symptoms vary depending on the specific structures injured.
Vascular injury:
Active hemorrhage or hematoma
Tracheal deviation
Loss of normal anatomic landmarks
Pulse deficits in upper extremities
Thrills or bruits in neck
An intact pulse does not rule out a vascular injury.
Laryngotracheal injury:
Respiratory distress
Hoarseness, voice changes
Hemoptysis
Neck pain or tenderness
Crepitus/SC emphysema
Pharyngoesophageal injury:
Dysphagia
Odynophagia
Hematemesis
Neurologic injury:
Central or peripheral nervous system deficits
Horner's syndrome

Can be divided by best tests to detect damage to a particular system; however, since there is
no consensus on the best diagnostic approach, all decisions should be made in cooperation
with the trauma service.
Aerodigestive:
Multidetector helical CT with esophageal studies (contrast swallow with endoscopy)
Laryngotracheal injury:
Multidetector helical CT in stable patients
Vascular injuries:
Stable patients can undergo multidetector helical CT with angiography (MDCT-A). The
sensitivity and specificity of this approaches traditional angiography, which was the former
gold standard. However, MDCT-A is faster and more readily available (2)[B].
Color flow Doppler combined with frequent, repeated physical exam is a fast, noninvasive
therapeutic modality; however, this does not fully evaluate injuries to Zone I or III, is
operator-dependent, and can miss subtle findings.
Pharyngoesophageal injury:
Obvious clinical findings are frequently absent in esophageal injuries requiring surgical
intervention.
Should always suspect esophageal injury in Zone I injuries.
MDCT is being used increasingly to evaluate esophageal injury.
The chest x-ray can demonstrate nonspecific findings, but does not rule out esophageal
injury.
100% sensitivity is reached only with the combination of esophagography and flexible
endoscopy (3)[B].
Lab
Type and crossmatch
Baseline complete blood panel and chemistry panel
Coagulation studies
Vascular injury
Pharyngoesophageal injury
Laryngotracheal injury
Peripheral or central nervous system injury
Cervical spine injury
Associated head or thoracic trauma
Treatment
Airway management:
Although penetrating neck trauma often does not involve the cervical spine,
the cervical spine should be evaluated and cleared appropriately. Airway
management should be done with the patient in cervical spine precautions
until cleared.
Patients who are comatose or in respiratory distress require immediate
intubation.
Stable patients without evidence of respiratory distress may be aggressively
managed with prophylactic intubation or closely observed with airway
equipment at the bedside.
Bag-valve-mask can force air through fascial planes and should be done
carefully.
Orotracheal intubation with rapid sequence induction is the method of choice
for securing the airway.
Nasotracheal intubation is contraindicated with apnea, severe facial injury, or
airway distortion because of the risk of puncturing an expanding hematoma.
Fiber-optic intubation is contraindicated with active bleeding that may
obscure the scope.
Percutaneous transtracheal ventilation may be useful when oral or
nasotracheal intubation fails and should be used only as a temporizing
measure until a more secure airway is obtained. Care should be taken to
ensure proper placement:
Leaves the airway unprotected and is contraindicated in cases of upper
airway obstruction, as it may cause barotrauma
If the trachea is exposed due to a complete or partial transection, the caudal
end should be directly intubated.
In all patients in whom intubation is attempted, there should be a surgical
airway kit at the bedside. The physician must be prepared for a
cricothyroidotomy or tracheostomy, as these are required in cases of severe
facial injury, laryngotracheal injury, and uncontrolled upper airway
hemorrhage.
Breathing:
Zone I injury can cause pneumothorax or subclavian vein injury and
hemothorax, requiring needle decompression and tube thoracostomy.
Circulation:
2 large-bore IVs should be placed contralateral to the side of the injury to
avoid ipsilateral venous injury.
External hemorrhage should be controlled with direct pressure. Blind
clamping of vessels is contraindicated due to the risk of further
neurovascular injury.
If bleeding cannot be controlled, a Foley catheter can be inserted and inflated
with saline to help tamponade the bleeding.
Patients with uncontrolled bleeding or hemodynamic instability must go
directly to the operating room.
Pre-Hospital
Impaled objects should not be removed.
Gently suction to clear the airway of blood, secretions, or vomitus.
Lateral decubitus or prone positioning may be required to prevent aspiration.
The airway must be vigilantly monitored, as edema or expanding hematoma
can progress to airway compromise.
Early oral intubation is indicated for clinical signs of respiratory distress, such
as stridor, air hunger, or labored breathing, or if an expanding neck hematoma
is present.
ED Treatment
Alert and seemingly stable patients are known to rapidly decompensate;
therefore, an airway setup should be at the bedside.
Nasogastric tube should not be placed due to risk of rupturing a pharyngeal
hematoma.
Prophylactic antibiotics are recommended (cefoxitin, clindamycin, penicillin G
plus metronidazole).
Surgical consult for all wounds that penetrate the platysma muscle
There is controversy regarding mandatory vs selective surgical exploration in
stable patients, especially in those with Zone II injuries:
Mandatory approach:
Surgical exploration is indicated in all cases of penetrating neck trauma
because significant injury may not manifest outward signs or symptoms.
Selective approach:
Supported by the research
Surgical exploration for specific indications, including expanding or pulsatile
hematoma, active bleeding, absence of peripheral pulses, hemoptysis,
Horner's syndrome, bruit, SC emphysema, respiratory distress, or air
bubbling through a wound
Tetanus prophylaxis
Traumatic arrest in patients with penetrating neck injury is an indication for the
emergency department thoracotomy.
Medication
Cefoxitin: Adult: 2 g IV q8h; peds: 80–160 mg/kg/day IM/IV div q6h or
Clindamycin: Adult: 600–900 mg IV q8h; peds: 25–40 mg/kg/day IV div q6–8h
or
Penicillin G: Adult: 24 million IU/day div q4–6h; peds: 150,000–250,000
IU/kg/day div q4–6h plus
Metronidazole: Adult: 1 g load, then 500 mg IV q6h; peds: 30 mg/kg/day IV div
q12h
General Measures
Esophageal and venous injuries are subtle and often missed.
Admission Criteria
All patients with penetrating neck trauma should be admitted and observed for
at least 24 hr.
Observation must take place in a facility capable of providing definitive surgical
care.
Patients with possible airway or vascular injury must be admitted to the
intensive care unit.
Discharge Criteria
Asymptomatic patients who have negative studies may be discharged after at
least 24 hr of observation.
References
1. Kendall JL, Anglin D, Demetriades D. Penetrating neck trauma. Emerg Med
Clin North Am. 1998;16:85–105.
2. Biffl WL, Moore EE, Rehse DH, et al. Selective management of penetrating
neck trauma based on cervical level of injury. Am J Surg. 1997;174:678–682.
3. Arantes V, Campolina C, Valerio SH, et al. Flexible esophagoscopy as a

diagnostic tool for traumatic esophageal injuries. J Trauma. 2009;66:1677–
1682.
Additional Reading
Inaba K, Munera F, McKenney M, et al. Prospective evaluation of screening
multislice helical computed tomographic angiography in the initial evaluation of
penetrating neck injuries. J Trauma. 2006;61:144–149.
Thal ER, Meyer DM. Penetrating neck trauma. Curr Probl Surg. 1992;29:1–
56.
Codes
ICD9
874.00 Open wound of larynx with trachea, uncomplicated
874.01 Open wound of larynx, uncomplicated
874.02 Open wound of trachea, uncomplicated
Nonsteroidal Anti-Inflammatory Drug Poisoning
Kenneth Barnes
Shane Hudnall
Basics
Primary effect is competitive inhibition of cyclooxygenase (COX) enzyme, thus inhibiting
production of prostaglandins, thromboxanes, and prostacyclin from arachidonic acid
There are 2 COX isoforms, COX-1 and COX-2.
COX-1 is expressed in most tissues.
COX-2 is induced more in inflammation and pain.
Most adverse effects are attributed to COX-1 inhibition.
Class of drugs works as antipyretics, analgesics, and anti-inflammatory agents.
Reduction of circulating prostacyclin and thromboxane results in platelet aggregation and
vasodilation, respectively.
OTC NSAIDs include ibuprofen, naproxen, and aspirin.
Classification:
Carboxylic acids:
Salicylates: Aspirin, diflunisal
Propionic acids: Ibuprofen, naproxen, ketoprofen
Acetic acids: Indomethacin, etodolac, ketorolac, sulindac, diclofenac
Fenamates: Meclofenamate, mefenamic acid
Enolic acids:
Oxicams: Piroxicam, meloxicam
Pyrazolones: Phenylbutazone
COX-2 inhibitors: Celecoxib
Meloxicam and etodolac have slightly greater inhibition of COX-2 than COX-1 at low doses
(1).
Epidemiology
Incidence
Up to 20 million Americans take NSAIDs on a regular basis.
It is estimated that >30 billion OTC NSAID tablets are sold annually in the U.S.
70 million NSAID prescriptions are written each year in the U.S.
NSAID poisoning is rare despite their extensive use.
Aspirin caused 63 fatalities and other NSAIDs 44 fatalities in 2007 in the U.S.
Most poisonings are attributable to ibuprofen (nearly 80,000 total) (2).
Risk Factors
Suicidal ideation
Untreated pain
Patients unclear of maximum allowed dosage of NSAIDs
Etiology
Toxicity (3,4,5):
Only a small percentage of overdoses (<1%) lead to serious harm (ie, GI bleeding, renal
failure).
Most are asymptomatic or have nonspecific symptoms (eg, nausea, vomiting, dizziness,
somnolence).
Generally doses >400 mg/kg of an NSAID are needed to cause severe toxicity.
COX-2 inhibitors have been shown to decrease HTN, edema, and hepatotoxicity in addition
to the other benefits listed below.
GI:
Most common adverse effects are GI related (ie, vomiting, abdominal pain, dyspepsia,
diarrhea, constipation).
Gastric, duodenal, and large intestinal ulceration may occur (1–4% of users annually).
3–10× more likely to have serious hemorrhage with NSAIDs
COX-2 inhibitors have been shown to delay ulcer healing in animal studies, but this has not
been elucidated in humans (6).
Celecoxib may be associated with decreased colon adenomas and cancer from inhibiting
COX-2 and tumor growth. More studies are being done on this to assess the validity of this
finding (7).
Renal:
2nd most common adverse effects
Inhibition of prostaglandins interferes with renal blood flow and glomerular filtration rate.
Leads to vasoconstriction (from blocking prostaglandin synthesis) and possibly acute renal
failure or acute interstitial nephritis
Retention of sodium, potassium, and water may lead to CHF exacerbation.
COX-2 inhibitors: Little toxicity demonstrated at renal level, but use caution in patients who
are dehydrated, have renal insufficiency, heart failure, or cirrhosis (8).
CNS:
Elderly particularly at risk
Can cause headache, confusion, delirium, psychosis, hallucinations, nightmares, tremor,
seizures, tinnitus, transient hearing loss, and aseptic meningitis
Cardiovascular:
Can raise BP and worsen control of HTN
Controversy exists regarding whether or not NSAIDs in combination with aspirin leads to
increased mortality and cardiovascular events (9,10).
COX-2 inhibitors may increase cardiovascular risk, although celecoxib has not yet been
shown at recommended doses to confer this risk. Rofecoxib and valdecoxib were
withdrawn from the market (September 2004).
All are associated with increased risk of CHF exacerbation in those with a history of CHF.
Pulmonary:
Respiratory arrest is rare.
Asthmatics are at increased risk for bronchospasm owing to increased production of
leukotrienes.
COX-2 inhibitors are much less likely to trigger bronchospasm.
Pulmonary infiltrates with eosinophilia are also possible.
Patients with clinical triad of asthma, nasal polyps, and allergic rhinitis are at increased risk
of anaphylaxis to both salicylates and NSAIDs.
Hepatic:
Possibility (though rare) of fulminant hepatic failure, hepatitis, elevated transaminases
Generally this is reversible and only rarely fatal.
Hematologic:
Aplastic anemia (now rare with decreased use of phenylbutazone and indomethacin),
agranulocytosis, neutropenia, hemolytic anemia, thrombocytopenia possible
Decreased platelet aggregation may lead to increased GI bleeding.
COX-2 inhibitors have not been shown to decrease platelet function and are associated
with a decreased risk of bleeding compared with nonselective NSAIDs.
Skin: Toxic epidermal necrolysis and Stevens-Johnson syndrome are uncommon, but relative
risk is increased slightly with NSAID use compared with placebo.
Metabolic: May lead to anion-gap metabolic acidosis
Drug interactions:
Increased risk of GI bleeding when used with anticoagulants
Digoxin, lithium, sulfonylurea, and aminoglycoside levels are all increased with use of
NSAIDs.
NSAIDs reduce antihypertensive effects of diuretics, beta blockers, and ACE inhibitors.
Celecoxib contains a sulfa moiety and thus is contraindicated in patients allergic to sulfa-
containing agents.
Diagnosis
History
There is a poor correlation between the amount ingested and toxic poisoning, although
significant symptoms may occur after 5–10× the maximum dose has been ingested.
Timing of ingestion
Past medical history (ie, peptic ulcer disease, chronic renal insufficiency)
Physical Exam
ABCs
Vital signs: Monitor BP, respiratory rate, and oxygen saturation.
Thorough neurologic examination (especially monitoring mental status)
Rectal examination for gross or occult blood

Lab
CBC, comprehensive metabolic panel (attention to transaminases), prothrombin time/partial
thromboplastin time (PT/PTT; coagulation studies), arterial blood gases (if patient has anion
gap on CMP or altered mental status), fingerstick glucose (rule out hypoglycemia),
pregnancy test (if child-bearing female)
Consider salicylate and acetaminophen levels, but do not check serum or urine levels of other
NSAIDs. Just treat presumptively.
ECG to look for prolongation of QRS or QTc
Imaging
Generally not necessary unless concern for perforated ulcer is present
Treatment
Acute treatment:
Supportive measures:
Call poison control.
Secure the ABCs.
There is no antidote for NSAID poisoning.
Close monitoring is warranted for almost all patients, and usually this is the
only treatment necessary.
Consider giving IV fluids if there is any volume deficit clinically.
Benzodiazepines IV if patient has seizures
Decontamination:
Gastric lavage if patient presents within 1 hr of ingestion or patient has
massive overdose
Activated charcoal (1 g/kg adults, 0.5–1 g/kg in children) should be given to
all patients with acute NSAID ingestion unless contraindicated (eg, bowel
perforation) (11).
Dialysis is unnecessary and ineffective.
Long-term treatment: Disposition:
Admit patient for any signs of toxicity (eg, renal failure, vital sign changes,
somnolence, electrolyte abnormalities).
Asymptomatic patients should be monitored for 4–6 hr to ensure that they do
not have any signs of toxicity before discharging home (possibly longer for
drugs such as naproxen that have longer half-lives).
Obtain psychiatric consultation for suicide attempts once medically stable.
References
1. Glaser K, Sung ML, O'Neill K, et al. Etodolac selectively inhibits human
prostaglandin G/H synthase 2 (PGHS-2) versus human PGHS-1. Eur J
Pharmacol. 1995;281:107–111.
2. American Association of Poison Control Centers 2008 Annual Report.

http://www.aapcc.org/DNN/Portals/0/NPDS%20reports/2008%20AAPCC%20Annu
3. Carson JL, Willett LR. Toxicity of nonsteroidal anti-inflammatory drugs. An

overview of the epidemiological evidence. Drugs. 1993;46 (Suppl 1):243–248.
4. Hall AH, Smolinske SC, Stover B, et al. Ibuprofen overdose in adults. J Clin
Toxicol. 1992;30:23–37.
5. Keller KH. In: Olson KR, ed. Poisoning and drug overdose. Stamford:
Appleton & Lange, 1999.
6. Mizuno H, Sakamoto C, Matsuda K, et al. Induction of cyclooxygenase 2 in

gastric mucosal lesions and its inhibition by the specific antagonist delays
healing in mice. Gastroenterology. 1997;112:387–397.
7. Sheehan KM, Sheahan K, O'Donoghue DP, et al. The relationship between

cyclooxygenase-2 expression and colorectal cancer. JAMA. 1999;282:1254–
1257.
8. Perazella MA, Eras J. Are selective COX-2 inhibitors nephrotoxic? Am J

Kidney Dis. 2000;35:937–940.
9. García Rodríguez LA, Varas-Lorenzo C, Maguire A, et al. Nonsteroidal

antiinflammatory drugs and the risk of myocardial infarction in the general
population. Circulation. 2004;109:3000–3006.
10. Kurth T, Glynn RJ, Walker AM, et al. Inhibition of clinical benefits of aspirin
on first myocardial infarction by nonsteroidal antiinflammatory drugs.
Circulation. 2003;108:1191–1195.
11. Donovan JW. In: Haddad LM, ed. Clinical management of poisoning and
drug overdose. Philadelphia: WB Saunders, 1998.
Additional Reading
Andreoli TE, Carpenter CCJ, Griggs RC, et al. Cecil Essentials of Medicine.
6th Ed. 2004.
Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal

Medicine, 15th Ed. 2001.
Bruno GR, Carter WA. In: Tintinalli JE, ed. Emergency medicine: a
comprehensive study guide. New York: McGraw-Hill, 2000.
Hall AH, Smolinske SC, Conrad FL, et al. Ibuprofen overdose: 126 cases.
Ann Emerg Med. 1986;15:1308–1313.
Halpern SM, Fitzpatrick R, Volans GN. Ibuprofen toxicity: A review of adverse

reactions and overdose. Adverse Drug Reac Toxicol Revi. 1993;12:107–128.
Palmer ME, Howland MA. In: Goldfrank LR, ed. Gotdfrank's toxicologic
emergencies. Stamford: Appleton & Lange, 1998.
Patrignani P, Panara MR, Greco A, et al. Biochemical and pharmacological

characterization of the cyclooxygenase activity of human blood prostaglandin
endoperoxide synthases. J Pharmacol Exp Ther. 1994;271:1705–1712.
Polisson R. Nonsteroidal anti-inflammatory drugs: practical and theoretical

considerations in their selection. Am J Med. 1996;100:31S–36S.
20. Seger DL, Murray L. In: Rosen P, ed. Emergency medicine: concepts
and clinical practice. St. Louis: Mosby, 1998.
21. Silverstein FE, Faich G, Goldstein JL, et al. Gastrointestinal toxicity with
celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and
rheumatoid arthritis: the CLASS study: A randomized controlled trial.
Celecoxib Long-term Arthritis Safety Study. JAMA. 2000;284:1247–1255.
22. Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper
gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomized
controlled trial. JAMA. 1999;282:1921–1928.
Codes
ICD9
965.7 Poisoning by other non-narcotic analgesics
965.9 Poisoning by unspecified analgesic and antipyretic
965.61 Poisoning by propionic acid derivatives
965.69 Poisoning by other antirheumatics
Clinical Pearls
Studies have shown that there is no additional benefit to giving >1 dose of
activated charcoal.
Ipecac generally has fallen out of favor for most if not all acute ingestions. It is
no longer recommended for NSAID toxicity.
Nursemaid's Elbow
John Munyak
Masha Diede
Basics
Description
Results from a traumatic subluxation of the radial head, which is produced by sudden forcible
traction on the pronated hand or wrist with the relaxed elbow extended
Subluxation of the radial head only occurs in pronation, which is the position in which the
diameter of the radial head is the most narrow in the anteroposterior plane.
As the radial head subluxes, there is an interposition of the annular ligament in the
radiocapitellar joint where it becomes entrapped.
Synonym(s): Pulled elbow; Radiocapitellar subluxation; Subluxation of the head of the radius;
Subluxation of the radius by elongation; Temper tantrum elbow; Malgaigne's injury;
Epidemiology
One of the most common musculoskeletal injuries in children age 4 and under
Uncommon in children over 5 yrs of age secondary to the distal attachments of the orbicular
ligament are sufficiently strong to prevent its proximal migration
Peak incidence is from age of 1–3 yrs old
Risk Factors
Frequently, the traction force occurs when the child suddenly attempts to pull away from a
parent or drops to the ground.
The necessary force also can occur while a child is being pulled by the hand or forearm, such
as in pulling a child as he or she stumbles, lifting him or her up by the hand, or swinging the
child by the hand.
Diagnosis
Postreduction views not usually indicated
Postreduction views may be indicated if the child's arm does not return to normal function
after reduction attempts are made.
Consider additional imaging of the forearm, wrist, or humerus in young children.
History
In more than 80% of cases, there is a history of sudden longitudinal traction to a pronated,
extended forearm.
May be a history of a “click” felt or heard by the person who pulled the child's arm
May be a history of an incidental fall in which the arm, elbow, and forearm were impacted
between the ground and the child's trunk
Immediately following the injury, the child is usually tearful due to the pain and refuses to use
the affected arm.
Pain, if vocalized, may be referred toward the wrist.
The child holds the forearm by his or her side, always in a pronated and partially flexed
position (nursemaid's position).
Occasionally, there is no history of trauma and the parents may notice the affected extremity
not being used.
Physical Exam
Child refuses to use the affected limb.
The forearm is always pronated and the elbow is partially flexed.
The child typically holds the affected limb by his or her side, sometimes supporting the
forearm with the other hand.
The child may be tearful during physical exam.
The child also may appear content and playful, but declines to move the affected arm.
Gentle palpation can reveal local tenderness over the anterolateral aspect of the radial head.
By carefully avoiding movements involving the elbow and forearm, one can note painless
range of motion of the wrist, hand, and shoulder.
Typically no obvious swelling or deformity
There is minimal restriction to flexion and extension of the elbow, but supination of the
forearm is markedly limited and resisted.
Often, the appearance is that of a wrist injury with the wrist flexed and pronated.
It is imperative to examine the joints above and below the suspected injury to increase the
likelihood of identifying the primary injury site.

Diagnosis is based on history alone.
Consider prereduction radiographs if there is a history of trauma.
Posterior elbow dislocation
Distal radial buckle fracture (torus) or other radial fracture
Septic elbow
Ulnar fracture
Supracondylar fracture or other fracture of the humerus
Avulsion of the medial or lateral epicondyle
Treatment
Analgesia:
Not typically necessary for reduction
Consider acetaminophen (15 mg/kg) or ibuprofen (5–10 mg/kg) as needed.
The thumb is placed in the region of the radial head for palpation and the
exertion of mild pressure (anterior to posterior).
The child's forearm is gently but firmly rotated into full supination.
The elbow is then flexed to 90 degrees by holding the child's forearm above
the wrist and stabilizing the humerus and elbow with the other hand to prevent
rotation of the shoulder. If any resistance is met, one should continue flexing
the elbow to the point of maximal flexion.
As reduction is achieved, a palpable and sometimes audible “click” can be
felt in the region of the radial head.
This maneuver will typically achieve instantaneous reduction of the radial
head and sometimes instant relief of pain.
Consider a hyperpronation maneuver if supination/flexion fails.
The child should typically be observed for 15 min for a return of full function
and use of the affected arm.
If function has not normalized in 15 min, a repeated attempt at reduction is
recommended.
In some studies, the delay until normal use of the arm is achieved is longer
when there has been a delay in treatment from the time of injury.
If there is no evidence of recovery after several reduction attempts, the
diagnosis must be reconsidered.
Immobilization:
Immobilization is not necessary for the 1st occurrence of subluxation.
If reduction is delayed for more than 12 hr following injury, an attempt is made
to support the limb with a sling for 10 days with the elbow in 90 degrees of
flexion and the forearm in full supination, but most toddlers discard the sling
within minutes.
For cases of multiple recurrences of nursemaid's elbow, some clinicians
recommend a trial of immobilization of the upper limb in an above-elbow cast
for 2–3 wks after evaluation by a pediatric orthopedist.
In a child under 6 mos of age, consider abuse from a caretaker while
evaluating the child. However, subluxation can occur while simply rolling over
in this age group.
Recurrence of subluxation as a result of subsequent pulls occurs in 5–40%
of cases.
Rehabilitation:
Prevention is key. The parent should be advised to avoid longitudinal traction
strains on the arm by not pulling on the hand or wrist, but rather pick the child
up by the trunk.
For the child who recovers fully after 1 or 2 reduction maneuvers, further
therapy or intervention is unnecessary.
Very rarely, the subluxed radial head may be irreducible by manipulation,
especially in recurrent cases, requiring surgical intervention.
The need for open reduction is extremely rare.
Ongoing Care
Even when multiple attempts at closed reduction fail, spontaneous reduction almost always
occurs.
Usually no long-term sequelae
Consider an occult fracture or cartilaginous injury if the response to treatment is not typical.
Additional Reading
Bachman D, Santora S. Textbook of pediatric emergency medicine. Baltimore: Williams &
Wilkins, 1993.
Christoph RA. Emergency medicine, a comprehensive study guide. New York: McGraw-
Hill, 1996.
Rand FF. Emergency medicine. Boston: Little, Brown, 1992.
Schunk JE. Radial head subluxation: epidemiology and treatment of 87 episodes. Ann
Emerg Med. 1990;19:1019–1023.
Tachdjian MO, ed. Pediatric orthopedics. Philadelphia: WB Saunders, 1990.
Codes
ICD9
832.2 Nursemaid's elbow
Clinical Pearls
Possibility of recurrence can be minimized by avoidance of pulling on the child's
hand or arm.
Long-term sequelae unlikely
Obesity and Weight Management
David Carfagno
Basics
Description
World Health Organization definitions:
Overweight = body mass index (BMI) >25
Obesity = BMI >30
Obesity is caused by a complex interplay between genetic and environmental factors.
Ultimately, a cumulative positive energy balance causes obesity. Energy balance is
determined by the difference between energy intake (calories consumed) and energy
expenditure (calories expended through resting energy metabolism, the thermic effect of
food, and physical activity).
Weight gain occurs when energy intake exceeds energy expenditure (ie, positive energy
balance).
1 lb of fat is equivalent to 3,500 kcal of energy.
Epidemiology
Prevalence
Overweight (BMI ≥25) or obesity (BMI ≥30) now affects almost 2/3 of Americans.
The National Health and Nutrition Examination Survey, 2003–2004, showed prevalences of
obesity in U.S. men and women of 31.1% and 33.2%, respectively, with particularly high
rates among non-Hispanic black Americans and Mexican Americans.
The most recent data released in November 2007 demonstrates that over the last several
years there has been a plateau in the prevalence in obesity in the U.S., with over 72 million
adults having a BMI >30 kg/m2. This represents 33.3% of men and 35.3% of women.
The WHO monitors the prevalence of obesity around the world. Although prevalence rates
vary dramatically from country to country, the WHO estimates that over 1.7 billion people
around the globe are overweight and 310 million are obese.
The problem of obesity is growing in many developing countries. Rates of obesity have
tripled in the last 20 yrs in the developing world, with 10% of the world's children currently
overweight or obese. The Middle East, Pacific Islands, Southeast Asia, and China are facing
the greatest challenges.
The effect of obesity on mortality has shown that there is a 20–40% increase in mortality in
both men and women who were overweight in midlife, and a 2–3-fold increased risk of
mortality among obese individuals. This is according to the National Institutes of Health-
American Association of Retired Persons (NIHAARP) cohort in 2006.
Extremely obese people—those who are ≥80 lb over a normal weight—live 3–12 fewer yrs
than their normal-weight peers. 6% of people are extremely obese—that is, they have a
BMI ≥40.
Nonsmokers who are obese—those who are about 30 or more pounds over a healthy weight
—have a shorter life span by a year or less.
Nonsmokers who are overweight— 29 lb over a healthy weight—do not have shortened
lives.
Smoking takes a toll, too, and very heavy smokers are affected most. An 18-yr-old white
male who is normal weight and does not smoke can expect to live to age 81. If he's
extremely obese and a smoker, his life expectancy is 60, a difference of 21 yrs.
The effect of extreme obesity appears to be greater for men than women and for whites than
blacks.
Risk Factors
Genetics
Genetic linkage to obesity comes from the data on the FTO gene (fat mass and obesity-
associated) gene.
A number of variant alleles of the FTO have been shown in several independent genome-wide
association studies to be strongly and significantly associated with obesity-related traits.
Individuals who are homozygous for the high-risk alleles weigh roughly 3 kg more than those
individuals homozygous for the low-risk allele. Homozygosity appears to occur in roughly 16%
of several populations that have been studied.
Etiology
Hormones in the regulation of body weight:
Leptin: A hormone made in the hypothalamus, is activated when there is a decrease in
appetite and when insulin is secreted. It's also made when there is an increase in the
metabolic rate. Obese individuals are known to have elevated levels of leptin and become
leptin-resistant.
Ghrelin is the key appetite hormone of the stomach. It is secreted at high levels by an
empty stomach, but is decreased with feeding.
Other hormones involved in the regulation of appetite and satiety include adiponectin,
resistin, glucagon-like peptide-1, tumor necrosis factor, plasminogen activator inhibitor type
1, and peptide YY.
Metabolic syndrome comprises obesity, carbohydrate intolerance or type 2 diabetes, HTN,
dyslipidemia, and a prothrombotic inflammatory vascular environment:
It is more prevalent in males over females worldwide. Male accumulation of body fat,
predominantly in the trunk and visceral rather than the SC fat. It is the visceral fat that is
the metabolically active fat, which produces adipokines, which increase insulin resistance.
Insulin resistance is closely related to the amount of visceral fat deposition and is poorly
correlated with BMI.

Obesity contributes to excess mortality from HTN, type 2 diabetes, coronary artery diseases,
stroke, gallbladder disease, sleep apnea, and osteoarthritis.
Cancers occurring more commonly in these individuals include endometrial, breast, prostate,
colon, esophageal, and liver.
Centripetal obesity, in which the waist-to-hip ratio is high, indicates a subset of individuals at
much higher risk of cardiovascular diseases.
Relative risk of HTN among obese adults aged 20–45 is 5–6 times that of their nonobese
counterparts.
Relative risk of diabetes and of hypercholesterolemia is increased 2.9 and 1.5 times,
respectively, in obese individuals.
Secondary causes of obesity include a number of endocrinopathies and syndromes, which
result in abnormalities of systems regulating feeding behavior and/or energy expenditure:
Hypothyroidism
Hypercortisolism
Hypothalamic dysfunction
Growth hormone deficiency
Prader-Labhart-Willi syndrome
Bardet-Biedl syndrome
Pseudohypoparathyroidism
Diagnosis
History
Obtain weight history, diet history, eating patterns, activity history.
Search for trigger factors, medications.
Physical Exam
Vital signs, including BP, heart rate, weight, height, waist circumference
Appearance, including android or gynoid fat deposition. Android has a higher predisposition to
cardiovascular disease.
Body mass index and waist-to-hip ratio. In the office, are the most reliable methods to
determine body fat in the office. The gold standard test is the dual energy x-ray
absorptiometry (DEXA) body composition.
Eye exam: Fundoscopic exam to evaluate for arteriosclerosis. Visual fields to screen for
homonymous hemianopsia, presence of a pituitary tumor.
Oropharynx: Tooth enamel evaluation for chronic gastric reflux disease. Craniofacial
abnormalities seen in conditions like Prader-Willi syndrome. A small posterior pharynx due to
hypertrophic fat may be a clue for obstructive sleep apnea.
Neck: Thyroid abnormalities, including asymmetrical or enlarged. Carotid bruits indicating
atherosclerosis.
Chest: Heart examination may reveal findings such as an enlarged heart, displaced PMI, S3,
S4, all corresponding with cardiovascular disease and HTN. Atelectasis and bibasilar rales
occur due to decreased lung compliance.
Abdomen: Appearance of SC and visceral fat deposition. Liver may be more prominent due
to fatty liver.
Pelvis, rectal, and genitalia: Manually may be difficult to examine. Android obesity raises
suspicion of testicular failure, Stein-Leventhal syndrome in women.
Musculoskeletal: Joint arthritis may be prevalent in obese patients. Careful to evaluate every
joint, especially weight-bearing joints for effusion, range of motion abnormalities.
Skin: Maceration of the intertriginous skin folds. Acanthosis nigricans can be seen in
Cushing's, polycystic ovarian syndrome, and diabetes.
Breast: Gynecomastia in men must be differentiated from pseudogynecomastia, an increase
in subareolar fat. Careful inspection in women due to larger breasts and adipose tissue.

Lab
CBC, complete metabolic panel, including glucose, liver function tests, lipid panel, thyroid-
stimulating hormone with T4, morning cortisol, urinalysis
Imaging
DEXA scan body fat composition. The gold standard test for determining body fat.
Other reliable tests include hydrostatic weighing, air displacement, skin calipers, body
impedance.
Chest x-ray, mammogram, colonoscopy (per routine screening guidelines, age and medically
appropriate)
Nocturnal pulse oximetry or formal sleep study
Electrocardiogram, graded exercise treadmill Bruce ACSM protocol.
Exercise testing may be beneficial for obese patients. When performing standard exercise
testing, the level of deconditioning typically observed in this population will necessitate a low
initial workload (2–3 metabolic equivalents [METS]) and small workload increments per test
stage (0.5–1.0 METs).
Other comorbidities (eg, HTN and other chronic diseases) or concerns (orthopedic limitations
or elderly) may dictate modifications to the testing procedures.
Use of leg or arm ergometry may enhance testing performance.
Special attention to proper cuff size is necessary for accurate BP measurements.
Treatment
Medication
Pharmacologic therapy is appropriate for patients as an adjunct to lifestyle
interventions to facilitate weight loss and prevent weight regain. Current criteria
for the use of pharmacologic therapy for obesity are a BMI >30 or a BMI >27 in
the presence of coexisting conditions.
Only 4 drugs have been approved by the Food and Drug Administration for
weight reduction. Phentermine and diethylpropion are adrenergic stimulants
that enhance the release of norepinephrine in the brain and reduce food intake.
Efficacy and safety data are limited. In randomized trials, a weight reduction
was 3–4% greater in the medication groups than in the placebo. The drugs are
classified by the Drug Enforcement Agency as Schedule IV controlled
substances. Limited data suggest that these stimulants may be effective for
more than 10 yrs, but they have been approved only for short-term use.
Sibutramine is a serotonin-norepinephrine reuptake inhibitor that reduces
appetite. In several randomized trials, weight loss was 5% greater for subjects
taking sibutramine than for those taking placebo. The combination of a group
taking sibutramine and lifestyle modification resulted in weight loss at 12 mos of
12.1 kg than did the sibutramine group alone (5 kg) or lifestyle intervention
alone (6.7 kg). Common side effects include HTN and tachycardia.
Orlistat is a triacylglycerol lipase inhibitor that reduces fat absorption by about
30%. One study showed that in combination with lifestyle changes, orlistat
reduced body weight by 3% more than intervention alone. Common side effects
include fecal incontinence, oily stools, and flatus. It's now available OTC.
Referral
Ancillary services may be needed for a multidisciplinary approach, including
psychotherapists, registered dietician, exercise physiologist, physical therapy.
Referral at times necessary for morbidly obese to bariatric surgery consult.
Bariatric surgical treatments reduce calorie intake by restrictive or
malabsorptive operations on the GI tract.
The 2 main procedures are the Roux-en-Y bypass and the laparoscopic
adjustable gastric banding.
The National Institutes of Health guidelines for adults recommended
consideration of bariatric surgery with BMI at least 40 kg/m2 or a BMI at least
35 kg/m2 with significant obesity-related comorbidities.
Bariatric surgery in adults improved diabetes (77% of patients), hyperlipidemia
(83%), HTN (66%), and sleep apnea (88%).
Adverse effects include perioperative complications, dehydration, bowel
obstruction, anastomotic leaks, ulcers, cholelithiasis, and vitamin deficiencies.
Mortality rates are reported as 0.5% for bypass, 0.1% for gastric banding, and
1.1% for malabsorptive procedures.
Ongoing Care
Diet
The U.S. Department of Agriculture puts out the Dietary Guidelines for Americans every 5 yrs,
last published in 2005. For long-term weight maintenance, individuals should follow these
dietary guidelines:
Diet rich in fruits and vegetables. Intake a variety from all 5 vegetable subgroups (dark
green, orange, legumes, starchy vegetables, and other vegetables) several times a week.
Consume 3-oz servings of whole-grain products daily, and >50% of grain products
consumed should come from whole grains.
Goal of a fiber intake of 25–30 g/day. Will contribute to increased satiety, reduced hunger,
and improved weight loss.
Limit total fat intake to 20–35% of daily calories, with most fats coming from polyunsaturated
or monounsaturated sources.
Patient Education
Exercise prescription is based on working on the model of frequency, intensity, duration with
goal in mind to encourage greater overall energy expenditure within the program for the
obese individual.
Primary mode should be large muscle group aerobic activities.
The initial exercise training intensity should be moderate (eg, 40–60% VO2R or HRR) with
more emphasis placed on increased duration and frequency. Eventual progression to higher
exercise intensities (50–75% VO2R or HRR) allows for further increases in VO2max, which in
turn allows for a more efficient exercise session.
Frequency of training: 5–7 d/w
Duration of training session: 45–60 min
Volume of training: Initial training volume should focus on attainment of 150 min of moderate
intensity exercise weekly. However, the optimal maintenance dose of physical activity is
>2,000 kcal/w.
Special considerations: Obese individuals are at an increased risk for orthopedic injury, and
this may require that the intensity of exercise be maintained at or below the intensity
recommended for improvement of fitness. Nonweight-bearing activities may be necessary.
Obese individuals are at an increased risk of hyperthermia during exercise. Equipment
modifications may be needed (ie, wide seats on cycle ergometers and rowers).
In 2007, the CDC published Evidence-Based Recommendations for Promoting Physical
Activity:
Creating information approaches: Large-scale, visible campaigns via television, radio,
newspaper, etc.
Point of decision prompts: Signs in elevators to promote stair usage
Behavioral and social approaches: Teach behavioral skills to help incorporate physical
activity into daily routines.
Environmental and policy approaches: Social networks of exercise groups
Future directions of obesity research lie in the field of genetics and of responsiveness to
lifestyle and pharmacologic interventions.
Since identification of the leptin gene, new hormones and metabolic pathways involved in the
regulation of body weight have been discovered (eg, ghrelin). This may lead to the
development of new classes of drugs that can alter/modify energy balance.
Additional Reading
Barness LA, Opitz JM, Gilbert-Barness E. Obesity: genetic, molecular, and environmental
aspects. Am J Med Genet A. 2007.
Bessesen DH. Update on obesity. J Clin Endocrinol Metab. 2008;93:2027–2034.
Davy BA, Franklin NF, Gordon IM, et al. ACSM's guidelines for exercise testing and
prescription. Baltimore, MD: Lippincott Williams and Wilkins, 2006:216–219.
Eckel RH. Clinical practice. Nonsurgical management of obesity in adults. N Engl J Med.
2008;358:1941–1950.
Lenz A, Diamond FB. Obesity: the hormonal milieu. Curr Opin Endocrinol Diabetes Obes.
2008;15:9–20.
O'Gorman DJ, Krook A. Exercise and the treatment of diabetes and obesity. Endocrinol
Metab Clin North Am. 2008;37:887–903.
Uli N, Sundararajan S, Cuttler L. Treatment of childhood obesity. Curr Opin Endocrinol

Diabetes Obes. 2008;15:37–47.
Whitlock EA, O'Connor EP, Williams SB, et al. Effectiveness of weight management
programs in children and adolescents. Evid Rep Technol Assess (Full Rep). 2008;1–308.
Wolf AM, Woodworth KA. Obesity prevention: recommended strategies and challenges. Am
J Med. 2009;122:S19–S23.
Codes
ICD9
278.00 Obesity, unspecified
278.01 Morbid obesity
278.02 Overweight
Olecranon Bursitis
Catherine Rainbow
Robert L. Jones
Basics
Description
Inflammation of the superficial olecranon bursa
3 different types of olecranon bursitis exist: acute, chronic, and septic.
Acute:
Caused by direct trauma to the bursa
Usually hemorrhagic bursitis that causes swelling within a few hours
Often seen in sports such as football, wrestling, and volleyball
Chronic:
Most common form of olecranon bursitis
Due to repetitive trauma or rubbing of the bursa
Bursal linings become thickened by fibrosis.
Also may be caused by systemic inflammatory processes (eg, rheumatoid arthritis) or
crystal deposition disease
Septic:
Superimposed infection of acute or chronic olecranon bursitis
Develops from skin wounds, dermatitis, or hematogenous seeding
Synonym(s): Miner's elbow; Student's elbow
Risk Factors
Acute: Direct elbow trauma
Chronic:
Multiple episodes of elbow trauma
Illnesses that cause crystal deposition or systemic inflammatory conditions
Septic:
History of elbow trauma
Skin lesions
General Prevention
High-quality elbow pads
Softer playing surfaces (natural turf)
Avoiding repetitive elbow motions
Etiology
Acute:
Synovial cell inflammatory response following direct trauma to the bursa
Hemorrhagic fluid collects in the bursa from capillary destruction.
Chronic:
Synovial cell inflammatory response to repetitive microtrauma of the bursa
May be associated with systemic inflammatory processes or crystal deposition disease
Septic:
Synovial cell and systemic inflammatory response to an infectious agent
Infectious agent is either inoculated directly into the bursa via trauma or arrives by
hematogenous spread.
Polymorphonuclear cells infiltrate the infected bursa.
May be more likely to occur in immunocompromised patients
Diagnosis
History
Acute:
History of recent direct trauma to the elbow
Rapid swelling and pain
Chronic:
Multiple episodes of elbow trauma
Certain occupations requiring repetitive pressure to the bursa (eg, carpenters)
Chronic swelling
Septic:
Likely history of superficial elbow trauma
Swelling and erythema of the bursa (overlying cellulitis or peribursal cellulitis)
Pain over the olecranon bursa with range of motion and palpation
May have systemic symptoms such as fever
Physical Exam
All forms present with a swollen, fluctuant fluid collection of the superficial olecranon bursa.
Acute:
Afebrile
Tenderness to palpation of the bursa
Preserved range of motion
Chronic:
Afebrile
Nontender to palpation
Preserved range of motion
Fibrotic trabeculae and villi may form a SC mass that is palpable.
Septic:
Often tender along the olecranon bursa ± elbow motion
Overlying skin abrasions and erythema often present
Possible systemic symptoms such as fever
If complicated, may have decreased range of motion of the elbow

Lab
Acute: No labs indicated
Chronic:
Assess for systemic inflammatory diseases such as rheumatoid arthritis with a rheumatoid
factor, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).
Assess for gout with uric acid level or crystal analysis of the bursal fluid (1)[C].
Septic:
Assess for infection with a CBC with differential, ESR, and CRP (1)[C].
Perform diagnostic bursal aspiration, and send fluid for Gram stain, crystals, cell count,
and culture (2)[C].
Perform a blood culture to rule out sepsis if systemic symptoms are present.
Imaging
Plain films of the elbow should be obtained to rule out fracture and/or dislocation, especially if
trauma precipitated olecranon bursitis.
US may be helpful to assess integrity of the triceps tendon, and it may demonstrate
inflammation of the olecranon bursa.
Sonography also may be helpful during aspiration if fluid is loculated.
MRI is used as a last resort to rule out other pathology, including triceps tear, tendinopathy,
and/or stress fractures.
Acute:
Aspiration of bursa is not a necessary procedure but is helpful for athletes attempting to
return to play (3)[C].
Hemorrhagic fluid is usually aspirated.
Chronic:
Aspiration of bursa is not a necessary procedure but is often done for patient comfort,
aesthetics, and return to play.
Aspirated synovial fluid may show crystals, as seen in gout or pseudogout.
Steroid injection via the lateral approach followed by a light compression dressing is
controversial (3)[C].
Must be performed after bursal fluid aspiration
More recent studies suggest that steroid injections facilitate healing and decrease
recurrence (3)[C].
Septic:
Must aspirate synovial fluid from the olecranon bursa for Gram stain and culture to identify
the infectious agent (4,5)[C]
Purulent fluid obtained
Never perform a steroid injection in a suspected infected olecranon bursa.
Acute:
Hemorrhagic synovial fluid
WBC count between 2,000 and 100,000 WBCs/µL consistent with inflammatory response
(1)[C]
Negative Gram stain and culture
Chronic:
Possible crystals owing to gout or pseudogout
WBC count ranges depending on whether the patient has a systemic inflammatory
disease.
Negative Gram stain and culture
Septic:
Purulent synovial fluid
WBC count >100,000 WBCs/µL (1)[C]
Positive/negative Gram stain with positive culture
Cellulitis
Fracture of the olecranon process of the ulna
Osteoarthritis
Septic arthritis
Overuse injury of the elbow
Ligamentous injury
Triceps avulsion, tear, or tendinitis
Triceps enthesopathy owing to chronic tendinosis
Contusion
Gout and pseudogout
Systemic inflammatory disease such as lupus and rheumatoid arthritis
Synovial cyst of the elbow joint
Treatment
Ice
NSAIDs
Compression
Elevation
Avoidance of repetitive elbow movements
Frequent monitoring
Aspiration:
Perform when distension causes significant discomfort and loss of motion
(2)[C].
Always perform on painful bursa with suspected infection. Fluid should be
analyzed for cell count, crystals, Gram stain, and culture.
Aseptic fluid typically is straw-colored, whereas septic fluid is purulent.
Staphylococcus aureus is the most common organism detected in septic
bursitis (4)[C].
Perform aspiration through healthy, intact skin so as to not cause an
iatrogenic infection.
Steroid injections (5)[C]:
Always aspirate bursal fluid prior to steroid injection.
Used by some clinicians for acute and chronic bursitis with mixed results;
may decrease healing time and recurrences (3)[C]
Contraindicated if infection suspected
Antibiotics:
Antibiotics are given when septic bursitis is suspected.
Must aspirate bursal fluid prior to initiation of antibiotic therapy for cell
count, Gram stain, and culture
Typically cover for S. aureus and streptococci, but treatment is usually
directed by Gram stain and culture results (4)[C].
If no systemic illness is identified, may proceed with oral antibiotics for 4
wks (4)[C]
If systemic illness is identified, one must initiate therapy with IV antibiotics
followed by oral antibiotics for a total of 4 wks of antibiotic therapy (4)[C].
Incision and drainage: May be needed in some cases of septic bursitis
Surgery: Bursectomy is performed for refractory cases that limit activity.
Medication
NSAIDs: May use NSAID of choice
Antibiotics:
IV antibiotics if systemic symptoms present initially; then switch to oral
antibiotics based on culture results for a 4-wk course of therapy (4)[C].
Suggested empirical IV therapy: Oxacillin 2 g IV q6h (3)[C]
Oral antibiotics for 4 wks if no systemic signs are present (4)[C]
Suggested empirical oral therapy:
Oxacillin 500 mg PO q6h (3)[C] or
Dicloxacillin 1 g q6h with 2 g probenecid daily (3)[C]
Cover for S. aureus and streptococci:
Usually a penicillinase-resistant penicillin such as oxacillin or cefazolin
May include MRSA coverage if patient is immunocompromised
In refractory cases, consider TB and Brucella as rare causative agents (4)
[C].
Immunocompromised patients often will require longer antibiotic treatment (4)
[C].
Referral
Chronic:
Consider rheumatology consultation if systemic inflammatory disease is
identified.
Consider orthopedic surgery consultation if refractory bursitis for
bursectomy.
Septic: Consider surgical evaluation if systemic symptoms persist despite
antibiotic treatment.
Physical therapy may benefit patients who have undergone a bursectomy.
Bursectomy may be needed for cases of refractory bursitis or for patients with
persistent septic bursitis despite antibiotic therapy.
Septic: Patients with systemic symptoms such as fever must be hospitalized to
receive IV antibiotics.
Ongoing Care
Patient Monitoring
Patient follow-up guidelines have not been established.
Follow-up for patients with septic bursitis should be frequent to ensure that no complications
such as septic arthritis develop.
Patient Education
Use NSAIDs regularly if no contraindications.
Ice the bursa frequently.
Use a light compression stocking over the bursa initially.
Elevate the elbow.
Avoid repetitive elbow motions.
Contact a physician if systemic symptoms develop.
Prognosis
Very good
Most cases of aseptic olecranon bursitis respond very well to conservative treatment.
Some recurrence may be seen, especially after repeated trauma.
Septic olecranon bursitis resolves in most cases when treated with appropriate antibiotics.
Severe cases of infection and refractory cases of bursitis often require bursectomy, which
has good postoperative results.
Complications
Can develop chronic olecranon bursitis with repetitive injuries
Rarely develop chronic pain at olecranon bursa (1)[C]
Complications of a corticosteroid injection include bleeding, bruising, infection,
skin atrophy, allergic reactions, and hyperglycemia in diabetic patients (1)[C].
References
1. Foye PM, Stitik TP, Nadler SF. Olecranon bursitis. emedicine. Medscape.
Updated March 27, 2009. http://emedicine.medscape.com/article/97346-
overview.
2. Deu RS, Carek PJ. Common sports injuries: upper extremity injuries.
Clinics in Family Practice. 2005;7:249–265.
3. Salzman KL, Lillegard WA, Butcher JD. Upper extremity bursitis. Am Fam
Physician. 1997;56:1797–1806,1811–1812.
4. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis
Clin North Am. 2005;19:991–1005, xi.
5. McFarland EG, Gill HS, Laporte DM, et al. Miscellaneous conditions about
the elbow in athletes. Clin Sports Med. 2004;23:743–763, xi–xii.
Codes
ICD9
Clinical Pearls
Olecranon bursitis is usually caused by some form of trauma to the elbow.
Treatment includes NSAIDs, ice, compression, elevation, and therapeutic
aspiration for comfort.
The bursa must be aspirated if there is concern for infection and the fluid sent
for cell count, crystals, Gram stain, and culture.
Patients with suspected septic bursitis need to be started on antibiotic therapy
with S. aureus and streptococcal coverage until culture results are obtained.
Most cases of olecranon bursitis resolve with appropriate therapy, but
refractory cases may require a bursectomy.
Onychocryptosis
Rodney S. Gonzalez
Basics
Description
Puncturing of the periungual skin by the nail plate; this leads to a foreign body (the nail plate),
inflammatory, and (possibly) infectious processes.
Alteration in the proper fit of the nail plate into the lateral or medial nail groove.
Improper fit leads to callous formation, edema, and perforation in the nail groove as a result
of the rubbing of the nail plate against the nail groove.
3 stages:
Stage 1 (mild): Erythema, slight edema, and pain when pressure is applied to the lateral
nail groove
Stage 2 (moderate): Increased stage 1 symptoms, drainage, and infection
Stage 3 (severe): Worsening stage 1 symptoms, presence of granulation tissue, and
lateral wall hypertrophy
Recurrence is not uncommon.
Synonym(s): Ingrown toenail; Unguis incarnatus; In-fleshed toenail; Embedded toenail
Epidemiology
Most commonly affects the great toe
Lateral nail edge more common than medial nail edge
26% of pathologic nail conditions
Most cases occur in males in their 2nd and 3rd decades.
Predominant gender: Male > Female (2:1 <30 yrs of age 1:1 >30 yrs of age).
Risk Factors
Shoes with tight-fitting toe box
Improperly fitting cleats
Poor stance and gait
Improper nail-trimming techniques (including tearing of nails)
Senior athletes
Onychomycosis
Diabetes
Hyperhidrosis
Obesity
Subungual neoplasms
Arthritis
Immune deficiency
Trauma, acute and repetitive
Skeletal abnormalities
Family history of in-curveted nails
Congenital and acquired nail disorders
General Prevention
Properly fitting footwear
Proper nail trimming
Etiology
Nail spicules form on the medial or lateral nail plate owing to trauma, disease processes, or
improper hygiene.
Nail plate punctures the periungual skin, causing a foreign-body and inflammatory reaction.
Biologic agents (eg, bacteria and fungi) may cause an infection of the periungual skin.

Paronychia
Cellulitis
Osteomyelitis
Diagnosis
History
Ask about tight-fitting shoes: Small toe boxes predispose to onychocryptosis.
Signs of infection: Erythema, edema, and pain
Ask about recurrence and previous treatment: May affect treatment choice
History of immune deficiency or abnormal wound healing: Increased chance for severe
infection and possibly require the use of antibiotics
Physical Exam
Signs and symptoms:
Pain, swelling, and limitation of activities
Cardinal signs of inflammation (redness, warmth, and drainage)
In-curveted nail margin
Tenderness, erythema, edema, drainage
Inspect for foreign bodies
Cardinal signs of ascending infection
Presence of excess medial or lateral wall tissue

Lab
Usually not necessary
Consider CBC, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) ± blood
cultures if there is concern for a more severe infection (eg, osteomyelitis).
Imaging
Plain films and/or bone scan may be required for a severely infected toe if osteomyelitis is
suspected.
Osteomyelitis
Cellulitis
Felon
Paronychia
Foreign body
Tumor
Treatment
Long-term treatment
Acute treatment
Analgesia:
Depends on planned treatment option and patient discomfort level
Recommend performing local anesthesia or a digital block with 1–2%
lidocaine without epinephrine before manipulation
Ibuprofen or acetaminophen for postoperative pain control
Immobilization: P.
Patients may be full weight bearing after nonsurgical treatment.
Partial weight bearing for 24–48 hr after surgery may be needed, but
generally, weight bearing is well tolerated.
There are no trials that compare the cost-benefit of nonsurgical versus
surgical treatment options.
Patients should be instructed in maintenance of proper foot hygiene,
avoidance of shoes with a tight-fitting toe box, soaking the feet, properly
trimming nails (cutting the nail straight across), and avoidance of repetitive
trauma.
Conservative treatment options:
Foot soaking: 10–20 min in warm, soapy water, followed by application of
topical antibiotic ointment for a few days until resolution
Cotton wisps: Place cotton under the ingrown nail edge (also may be done
with dental floss).
Gutter splint: Using plastic tubing (eg, IV infusion tubing) with a vertical slit
and placing this over the ingrown nail edge
Cure rates can be as high as 75% with good patient compliance for stage
1 lesions.
If infection is suspected, it is important to remove the source of the
infection. Antibiotics are usually not required when doing surgical treatment;
when using antibiotics, they should be directed against gram-positive
bacteria (eg, Staphylococcus aureus and Streptococcus spp.).
Surgery may be recommended for recurrent stage 1 lesions as below for stage
2 lesions.
Stage 2: Remove with a wedge excision the distal outer nail edge without
matricectomy.
Stage 2 or 3: Partial removal of the medial or lateral nail with matricectomy
(medial/lateral nail avulsion) ± electrosurgical or phenol cauterization
Stage 3: In addition to the preceding, ablation of medial or lateral wall tissue
to promote normalization of the medial/lateral nail fold
Major contraindications include disorders causing digital ischemia, eg,
diabetes, peripheral vascular disease, and collagen diseases.
Studies shows that antibiotics before or after surgery do not affect healing time
and should be withheld in most cases.
Partial nail removal with phenolization decreases the risk of recurrence;
however, there may be a slight increase in postoperative infections.
Matricectomy with electrocautery and radiofrequency and carbon dioxide laser
is also effective; the high cost of these procedures may be prohibitive,
however.
Ongoing Care
Immune-compromised individuals with a severe infection may require hospitalization for
administration of IV antibiotics.
Patient Education
Properly fitting footwear
Proper nail trimming (and foot hygiene)
Online patient handouts:
http://familydoctor.org/online/famdocen/home/common/skin/disorders/208.html
www.aafp.org/afp/20090215/311ph.html
Complications
Osteomyelitis
Narrowing of nail (when matrix ablation performed)
Recurrence
Additional Reading
Heidelbaugh JJ, Lee H. Management of the ingrown toenail. Am Fam
Physician. 2009;1579:303–308.
Peggs JF. Ingrown toenails. In: Pfenninger and Fowler's procedures for
primary care, 2nd ed. St. Louis: Mosby, 2003.
Bos AM, van Tilburg MW, van Sorge AA, et al. Randomized clinical trial of
surgical technique and local antibiotics for ingrowing toenail. Br J Surg.
2007;94:292–296.
Heidelbaugh JJ, Lee H. Management of the ingrown toenail. Am Fam

Physician. 2009;79:303–308.
Ikard RW. Onychocryptosis. J Am Coll Surg. 1998;187:96–102.
Mann JL, Coughlin MJ. Surgery of the foot and ankle. St. Louis: Mosby-Year
Book, 1993.
Peggs JF. Ingrown toenails. In: Pfenninger and Fowler's procedures for
primary care 2nd ed. St. Louis: Mosby, 2003.
Codes
ICD9
703.0 Ingrowing nail
Clinical Pearls
Antibiotics have not been shown to change the healing from ingrown toenails
when using surgical treatment options.
Impact activities should be avoided until the patient is pain-free and clear of
infection.
The frequencies of symptomatic nail regrowth following distal nail wedge
resection, nail avulsion, and phenol and electrosurgical cauterization are distal
nail wedge resection, 70%; nail avulsion, 50–80%; phenol cauterization, 4–
25%; and electrosurgical cauterization, <5%.
Onychomycosis
John T. Swisher IV
Suzanne Hecht
Basics
Description
A fungal infection of the toes and/or fingernails involving the nail bed, matrix, or plate
Synonym(s): Nail ringworm; Tinea unguium
Epidemiology
22–130 cases/1,000 population
Accounts for 1:3 of integumentary infections
Incidence of infection increasing worldwide
Accounts for 50% of toenail dystrophies
Adults 30× more likely to be affected than children
2% prevalence in children
Risk Factors
HIV
Immunosuppressive states
Diabetes mellitus (DM)
Contact with infected individuals
Peripheral vascular disease (PVD)
Trauma
Communal bathing
Occlusive footwear
General Prevention
Appropriate foot hygiene:
Wear absorbent cotton socks.
Wear breathable footwear.
Protect feet in community areas.
Keep feet dry throughout day.
Discard old shoes that may harbor fungi.
Control chronic health conditions.
Etiology
Pathophysiology:
Distal/lateral subungual onychomycosis (most common): Fungal invasion begins at
hyponychium and spreads along nail bed proximally, concomitantly involving the inferior nail
plate.
White superficial onychomycosis: Fungal invasion develops from dorsal nail plate invasion.
Proximal subungual onychomycosis (associated with immunocompromised state): Fungal
invasion of cuticle and subsequent nail fold that penetrates dorsal nail plate
Endonyx onychomycosis (least common): Fungal invasion of nail surface with eventual
deep penetration
Candidal onychomycosis: Yeast infection via onycholysis, paronychia, or chronic
mucocutaneous disease
Total dystrophic onychomycosis: End-stage fungal infection of entire nail unit that may
easily fragment and lead to permanent scarring
Etiology:
Dermatophytes (>90% occurrence rate)
Yeast
Nondermatophytes
Diagnosis
History
Identify digits involved.
History of predisposing factors: Trauma, tinea, and immunocompromised state
Discuss bathing footwear habits
Historical clues in regard to secondary infection
Physical Exam
Distal/lateral subungual onychomycosis: Thickened/opacified nail with possible subungual
hyperkeratosis and/or onycholysis
White superficial onychomycosis: White patches on nail surface that can coalesce
Proximal subungual onychomycosis: Nail fold leukonychia with white proximal nail plate
Endonyx onychomycosis: White nail plate without subungual hyperkeratosis or onycholysis
Candidal onychomycosis: Paronychia, onycholysis, and/or subungual hyperkeratosis
Total dystrophic onychomycosis: Thick, opaque, yellow-brown nail involving entire plate/matrix

Diagnosis made when both clinical and laboratory results are positive
Essential that causative organism is identified
Avoid topical antifungals for 2 wks prior to testing.
Cleanse nail with alcohol swab prior to testing.
Utilize potassium hydroxide (KOH) and fungal culture to determine therapy for initial screen.
Owing to a high false-negative rate, you may need to repeat KOH or use histologic
analysis with fungal culture.
Histologic analysis with periodic acid–Schiff (PAS) is more sensitive than KOH or culture
(1)[A].
Lab
KOH prep with light microscopy:
20% KOH with 40% dimethyl sulfoxide (DMSO)
Use a 1-mm curette to obtain most proximal sample
Use a No. 15 blade scalpel for superficial fungi.
Immediate results
Fungal culture:
Cycloheximide medium for dermatophytes and noncycloheximide medium for yeasts and
nondermatophytes
Nail clippings or scrapings for specimen
May take weeks to grow on medium
Species identification
Histologic analysis with PAS:
High sensitivity
Prompt results
Pathogen not identified
Distal nail clipping from attachment to nail bed in formalin
Immunohistochemistry:
Identifies pathogen via labeled antibody to specific fungi
Complicated and costly
In vivo confocal microscopy:
Uses light to penetrate nail to analyze reflection of fungi
Inability to distinguish pathogen
Costly
Scanning electron microscopy:
Expensive
Detailed imaging of fungi elements
Polymerase chain reaction (PCR):
Fungal species identification by DNA sequence analysis
Sufficient nail material required for testing
Flow cytometry:
Sorts by DNA, protein, cell size, and granulosity to identify fungi
Complicated and costly
Eczema
Endocrine disease
Herpes whitlow
Malignant melanoma
Medications
Paronychia
Psoriasis
Squamous cell carcinoma
Trauma
Yellow nail syndrome
Treatment
Indications for treatment consist of pain, functional limitation, aesthetic
purposes, and secondary infection.
Discuss costs, side effects, and continuous/pulse dosing.
Confirm past medical history to determine appropriate medication.
Treat tinea pedis as soon as possible.
Explain that it may take 12–18 mos for resolution of toenail infections and 4–6
mos for resolution of fingernail infections.
Despite successful eradication of fungi, the nail may remain abnormal in
appearance. This is not considered a treatment failure.
Clinical cure is based on the absence of physical exam findings.
Mycologic cure is when no fungal elements remain; however, the nail
appearance still may be abnormal.
Repeat testing may be required at completion of treatment to confirm cure.
High recurrence (relapse/reinfection) rates: 15–20% within 1 yr
Treatment failure may require repeat treatment.
Return to play ± oral, topical, or surgical treatment is based on symptoms.
Medication
First Line
Terbinafine:
Fungicidal against dermatophytes with fungistatic properties against some
yeast and nondermatophytes
Mycologic cure 76% ± 3%; clinical cure 66% ± 5%
Fingernail: 250 mg/day × 6 wks (2)[A]
Toenail: 250 mg/day × 12 wks (2)[A]
Monitor pretreatment AST/ALT and every 6 wks for hepatotoxicity
Contraindications: Hypersensitivity
Precautions: Hepatotoxicity, GI upset, immunodeficiency, systemic lupus
erythematosus (SLE), renal insufficiency, Steven-Johnson syndrome, and drug
interactions
Second Line
Itraconazole:
Fungistatic against dermatophytes, yeast, and nondermatophytes
Mycologic pulse cure 63% ± 7%; mycologic continuous cure 59% ± 5%;
clinical pulse cure 70% ± 11%; clinical continuous cure 70% ± 5%
Fingernail continuous therapy: 200 mg/day × 6 wks (3)[A]
Toenail continuous therapy: 200 mg/day × 12 wks (3)[A]
Fingernail pulse therapy: 200 mg b.i.d. × 7 days, off 21 days (2–3 pulses may
be required)
Toenail pulse therapy: 200 mg b.i.d. × 7 days, off 21 days (3–4 pulses may
be required)
Monitor pretreatment AST/ALT and every 6 wks for hepatotoxicity for
continuous therapy; not required for pulse therapy
Contraindications: Hypersensitivity, pregnancy, ventricular dysfunction,
concomitant use of CYP3A4 drugs
Precautions: Hepatotoxicity, GI upset, hearing loss, neuropathy, drug
interactions
Griseofulvin:
Fungistatic against dermatophytes
Mycologic cure 60% ± 6%; clinical cure 2% ± 2%
Fingernails: 1,000 mg/day × 4 mos or more (3)[A]
Toenails: 1,000 mg/day × 6 mos or more (3)[A]
Contraindications: Hypersensitivity, porphyria, hepatocellular dysfunction,
pregnancy
Precautions: Penicillin allergy, photosensitivity
Ciclopirox 8%:
Mechanism of action unproven
Mycologic cure 32%; treatment cure 7%
Apply daily × 48 wks; remove lacquer once a week (2)[A].
Consider when oral medication isn't indicated or nail plate has been removed.
Contraindication: Hypersensitivity
Precautions: DM, immunosuppressed state, and concomitant systemic
antifungal use
Nail plate removal (total or partial)
Chemical removal (40% urea)
Use concomitant oral or topical antifungal with surgical approach (4)[C].
Consider in recalcitrant cases.
References
1. Bell SS, Hall JB. Oral treatments for toenail onychomycosis (protocol). The
Cochrane Collaboration 2009.
2. Gupta AK, Tu LQ. Therapies for onychomycosis: a review. Dermatol Clin.

2006;24:375–379.
3. Internet Resource: Thompson Micromedix Healthcare Series.
4. Blumberg M, Kantor GR. www.emedicine.com. Onychomycosis. 2007.
Codes
ICD9
110.1 Dermatophytosis of nail
112.3 Candidiasis of skin and nails
Clinical Pearls
Not all nail dystrophies are due to fungi.
Clinical and lab confirmation is essential for appropriate diagnosis and
treatment.
Oral is favorable to topical treatment.
High recurrence rates exist.
Advise patient on prevention techniques.
Oral Lacerations
Brent H. Messick
Kevin E. Burroughs
Basics
Description
Soft tissue injury in the orofacial area
Typically results from a direct blow to the mouth resulting from a fall or impact by an
opponent or object
Lacerations may be an indirect result of an individual biting the cheek or lip.
Epidemiology
Most common in contact sports not requiring face protection (basketball, hockey, soccer,
baseball, wrestling)
Other at-risk sports include bicycling, in-line skating, and gymnastics.
Children are most susceptible between the ages of 7 and 11.
Incidence
As high as 1.06/100,000 athlete exposures (1)
Prevalence
1.4/10,000 athlete exposures in football and 18.3/10,000 in basketball; 58–75% of these
injuries are soft tissue lacerations (2).
Risk Factors
Participation in collision or contact sports
Not using a mouth guard

Fracture of the mandible, dental arch, palate
Dental luxation or avulsion
Tooth fracture
Temporomandibular joint (TMJ) trauma
Vessel injury
Nerve transection
Salivary gland duct injury
Diagnosis
History
Determine where and how the injury was sustained. Common in sports, but also seen as
result of fighting, assault, and abuse.
Determine areas of numbness or loss of muscle control to evaluate for nerve injury.
Determine last tetanus immunization, as wounds often are contaminated from the
environment as well as from the oral cavity.
Sensitivity of teeth (assess for occult dental trauma)
Physical Exam
Significant hemorrhage due to the abundant blood supply in the face and maxillofacial areas
Visible defects with “through and through” lacerations (lacerations involving all layers:
Mucosa, muscular, SC, and skin)
Patient distress
Head and neck examination for signs of neural injury
Palpate over TMJ joint to evaluate for subcondylar mandibular fracture
Test mobility of jaw
Evaluate laceration for length and depth as well as for affected structures, including nerves
and vessels (transected nerves need to be referred for surgical repair)
Buccal lacerations need to be evaluated for parotid salivary flow from the Stenson's duct.
Parotid orifice is located opposite the maxillary 1st molar. Saliva should flow from opening
when parotid gland is palpated (disruptions of the duct should be referred for repair).
Evaluate for normal occlusion of the teeth. Dental examination should be performed to check
for fractured, loose, or avulsed teeth.

Imaging
If there is a clinical suspicion of a fracture or foreign body such as a tooth fragment,
appropriate studies should be ordered: Panorex for teeth, plain radiographs for foreign
bodies or CT for facial fractures, etc.
Bone fixation/repair, if needed, should be performed before soft tissue closure.
Contusion
Abrasion
Dental trauma (luxation, avulsion, fracture)
Treatment
Most oral lacerations can be left to heal by secondary intention. Only those
that are >1 cm, gapping at rest, or require hemostasis may need to be
repaired.
Copious irrigation of the wound to remove foreign debris and wound
contaminants
Clean with antiseptic scrub
Regional anesthesia via nerve block is preferred over local injection to
minimize tissue distortion, making approximation easier (especially for the
vermilion border).
Infraorbital nerve block numbs the upper lip.
Mental nerve block numbs the anterior lower lip and teeth.
Maxillary nerve 2nd division numbs the entire maxilla on the blocked side.
Interrupted stitches using 3–0 chromic or similar absorbable suture material
Inside-out and bottom-up technique; eliminating dead spaces helps prevent
hematoma and subsequent infection
Muscular layer: 4–0 slow-absorbing suture; polyglactic suture breaks down
more slowly than chromic suture, maintaining wound strength for 30 days.
Oral mucosa: 3–0 or 4–0 chromic or other absorbable suture material on a P.
cutting needle
Small intraoral lacerations may be left to heal by secondary intention.
SC layer: 3–0 or 4–0 plain gut on a cutting needle
Skin: 4–0 to 6–0 nylon
Suture orbicularis oris 1st; see above suture suggestions
Loosely approximate the vermilion border (very important for cosmetic
appearance) with a suture at the junction with the skin
Proceed in layers as above
Superficial lacerations <1 cm and not gaping at rest do not require sutures
unless required for hemostasis.
Lacerations involving the muscular layer or labial margin require sutures.
Lacerations involving the tip may require sutures to prevent a “forked tongue.”
Most can be left alone. Anterior tongue lacerations are rare and are often self-
inflicted. Small ones can close, but large ones will require sutures. If the tongue
heals “forked,” it can also be corrected later if necessary.
Repair in layers: 4–0 slow-resorbing polyglactic suture for the muscle and
chromic suture for the mucosa
Typically “V” shaped
Small lacerations can be allowed to close by secondary intention.
Hemorrhage typically from disruption of the muscular layer may require a stitch
to obtain hemostasis.
Large gaping lacerations can be repaired with 1 or 2 vertical sutures.
Tetanus immunization status
Prophylactic antibiotics for severe or grossly contaminated laceration
(coverage for the oral flora includes amoxicillin, penicillin, clindamycin, or
erythromycin)
If fracture is present, leave wound open until fixation is completed.
Evaluate ABCs.
Control hemorrhage.
Protect the airway if compromised.
Ongoing Care
Laceration associated with fracture or involving nerves or salivary ducts should be referred
for definitive care as soon as possible.
Refer dental trauma to a dentist or oral surgeon.
Patients receiving antibiotics should be rechecked in 48 hr to ensure improvement and
antibiotic susceptibility.
References
1. Labella CR, Smith BW, Sigurdsson A. Effect of mouthguards on dental injuries and
concussions in college basketball. Med Sci Sports Exerc. 2002;34:41–44.
2. Flanders RA, Bhat M. The incidence of orofacial injuries in sports: a pilot study in Illinois.
J Am Dent Assoc. 1995;126:491–496.
Additional Reading
Echlin P, McKeag DB. Maxillofacial injuries in sport. Curr Sports Med Rep. 2004;3:25–32.
Echlin PS, Upshur RE, Peck DM, et al. Craniomaxillofacial injury in sport: a review of
prevention research. Br J Sports Med. 2005;39:254–263.
Ranalli DN, Demas PN. Orofacial injuries from sport: preventive measures for sports
medicine. Sports Med. 2002;32:409–418.
Ud-din, Zia and Aslam, Musarrat. Should minor tongue lacerations be sutured in children.
Best Evidence Topics. 2007. Accessed 10/05/2009. http://www.bestbets.org/home/bets-
introduction.php
Using mouthguards to reduce the incidence and severity of sports-related oral injuries. J Am
Dent Assoc. 2006;137:1712–1720.
Codes
ICD9
873.60 Open wound of mouth, unspecified site, uncomplicated
873.61 Open wound of buccal mucosa, uncomplicated
873.62 Open wound of gum (alveolar process), uncomplicated
Clinical Pearls
Stitches placed inside the mouth will dissolve on their own. Sutures in the skin
should be removed in 4–5 days to prevent significant scarring.
Return to play depends on the severity of the injury, chance of reinjury, and
availability/feasibility of protection for the wound.
Osgood-Schlatter Disease
Stephen Huang
Ayo Adu
Basics
Description
Traction apophysitis of the tibial tubercle at the insertion of the patellar tendon
Overuse injury due to repetitive strain or microtrauma of the secondary ossification center of
the tibial tuberosity
Epidemiology
One of the most common causes of knee pain in active adolescents
More prevalent in male gender
Age of onset coincides with growth spurts, males age 10–15, females age 8–13
Risk Factors
Adolescents
Male sex
Sports that involve running and jumping
Activities that involve direct contact with the knee (eg, kneeling)
Etiology
Chronic repetitive strain and microtrauma cause chronic avulsion of the secondary ossification
center (1).
The force is increased after periods of rapid growth.
Chronic avulsion may cause separation of the patellar tendon insertion from the tibial
tubercle, swelling, and enlargement.
Diagnosis
History
Anterior knee pain and swelling
Symptoms are bilateral in 20–30% of patients.
Pain begins as a dull ache that gradually increases with continued activity.
Pain is worsened by running, jumping, direct trauma, kneeling, and squatting.
Pain is improved with rest.
Physical Exam
Enlarged prominent tibial tubercle
Tenderness of the proximal tibial tubercle at the patellar tendon insertion
Poor flexibility of the quadriceps and hamstrings
Pain is exacerbated by knee extension against resistance, flexion of the knee actively or
passively, or by direct trauma to the tibial tubercle.

Imaging
Osgood Schlatter disease is a clinical diagnosis, and radiographs are not required for
diagnosis. However, they may be helpful in ruling out other conditions, such as acute tibial
apophyseal fracture, osteomyelitis, and tumors.
X-ray:
Lateral view may show an elevated tibial tubercle with anterior soft tissue swelling,
fragmentation of the tibial tubercle, or calcification and ossicle formation in the distal
patellar tendon (2).
Patellar tendonitis
Sinding-Larsen-Johansson syndrome
Tibial tubercle avulsion fracture
Patellar fracture
Patellofemoral syndrome
Pes anserine bursitis
Patellar tendon rupture
Patellar subluxation
Chondromalacia patellae
Hoffa's disease (infrapatellar fat pad impingement)
Osteomyelitis
Tumor
Treatment
Pre-Hospital
Relative rest or activity modification is recommended.
Activity as tolerated, including sports, is allowed as long as symptoms are
tolerable and resolve within 24 hr.
Pain control with NSAIDs or acetaminophen
Protective pad may be worn over tibial tubercle to prevent direct trauma
Ice application especially after exercise
If significant symptoms, consider physical therapy consult
General Measures
Osgood-Schlatter disease is usually a benign and self-limited condition that
resolves once growth plate closes.
Usual course is 6–18 mos (2)
Symptoms may continue into adulthood despite conservative measures in 5–
10% of patients.
Stretching exercises of the quadriceps and hamstring and strengthening of the
quadriceps
Surgical excision of the enlarged tibial tubercle and free ossicles may be
considered in skeletally mature patients if conservative treatment has failed.
References
1. Gholve PA, Scher DM, Khakharia S, et al. Osgood Schlatter syndrome.
Curr Opin Pediatr. 2007;19:44–50.
2. Kienstra AJ, Macias CG. Osgood-Schlatter disease. www.uptodate.com.

version 17.1. Spetember 8, 2008. 1–17.
Additional Reading
Bloom OJ, Mackler L, Barbee J. Clinical inquiries. What is the best treatment
for Osgood-Schlatter disease? J Fam Pract. 2004;53:153–156.
Codes
ICD9
732.4 Juvenile osteochondrosis of lower extremity, excluding foot
Clinical Pearls
Athletes may participate in athletic activity as tolerated. Pain level should
generally be tolerable, without a decrease in performance, and resolve within
24 hr of activity. If performance is decreased, the athlete should discontinue
activity.
Athlete should not “play through the pain.” Instead, pain should be used as a
measure of when to stop activity.
Pain will resolve when the growth plate closes.
Future complications can include persistent enlargement of the tibial tubercle,
pain with kneeling, and possibly some limitation of activities.
Prognosis is excellent, provided the athlete demonstrates good compliance
with the physician's recommendations.
Osteitis Pubis
Nadya Volsky
Robert L. Jones
Basics
Description
Chronic inflammatory, painful condition secondary to stress forces through the anterior pelvis
involving the pubic bones, pubic symphysis, and adjacent structures as a result of either
chronic overloading or impaction trauma
Anterior pelvic ache or sharp pain that is worse with activities involving twisting/kicking
Located over the symphysis
May radiate into the lower abdominal muscles, perineum, and thigh adductors
May have associated adductor spasm
Can be provoked by standing on one leg or resisted hip adduction
Synonym(s): Pubic symphysis enthesopathy; Pubic symphysitis; Osteochondritis of pubic
symphysis; Athletic pubalgia
Epidemiology
Incidence
Depends on type of sport; groin pain in general is seen in 2–5% of all sports injuries.
In sports that involve excessive twisting and turning movements such as soccer, ice and field
hockey, tennis, and Australian-rules football, groin injuries may rise to 5–7% of all injuries.
Difficult to separate from possible coexisting conditions and to diagnose
Pure incidence for osteitis pubis alone is not clear.
Risk Factors
Sports involving kicking, interval sprinting, and rapid changes of direction such as soccer, ice
and field hockey, Australian-rules football, tennis
Skeletal immaturity, especially coupled with high training volume/competition demands
Hip adductor/abductor muscle imbalance (abductors normally are 20% stronger than
adductors)
Possibly hip stiffness and decreased range of motion (ROM) in the hip joint
Sacroiliac (SI) joint dysfunction
Pelvic asymmetry
History of prior groin injury
Pregnancy and/or postpartum
Rheumatologic disorders, such as ankylosing spondylitis or rheumatoid arthritis involving SI
joint
Infection following urologic or gynecologic procedure
Etiology
Poorly understood; poorly studied
Likely includes combination of following: Adductor muscles injury or overuse, anterior pelvic
instability
Possible correlation between decreased preseason hip rotational ROM and the development
of osteitis pubis
Diagnosis
Physical Exam
Tenderness with palpation over the symphysis and pubic rami
Pain with resisted adduction, stretching hip flexors, and rising from a seated position

Imaging
X-rays:
Anteroposterior view of pelvis
1-legged stance
In relatively acute cases, plain radiographs may be normal; in chronic cases, radiographs
can show cystic changes, sclerosis, and widening or narrowing at the symphysis,
osteophytes, bony irregularities, or resorption.
Instability may be evident on a 1-legged stance film (step-off >2 mm between the pubic
rami in the vertical plane and/or symphyseal gap >7 mm between the pubic bones).
MRI:
Bone edema spanning the symphysis with cystic or other degenerative changes, adductor
microtears, and fluid in symphysis area may be visible.
Associated pathologies such as tendon injuries, stress fractures, and SI or sacral injuries
may be evident.
Bone scan: May show increased uptake at the symphysis, although it can take months to
become positive
Most common:
Adductor dysfunction (adductor complex tendinopathy, adductor tendinitis, adductor strain)
and sports hernia
Both also could coexist or proceed osteitis pubis.
Other:
Femoral neck stress fracture
Labral tear of hip
Sacroiliitis
Lumbar disk pathology
Inguinal hernia
Genitourinary disorders: Prostatitis in males, UTI in females, passing renal stones
Gynecologic problems in females: Ovarian cyst, endometriosis
Pelvic soft tissue tumors
Treatment
Treatment modalities: No randomized, controlled trials with level 4 evidence
for any treatment regimen
Rest, ice, and NSAIDs are the 1st-line treatment.
Physical therapy including hip ROM and pelvic and core stabilization modalities
Manual therapy/massage
Corticosteroid injection in the symphysis
Prolotherapy with dextrose solution
Surgery:
Wedge resection at the symphysis
Symphysiodesis
Posterior wall mesh repair
Pubic symphysis curettage
Polypropylene mesh repair has provided the quickest return to play with level
4 evidence studies only.
Rehabilitation:
Core stabilization
Hip ROM
Correction of biomechanical errors such as poor/inefficient kicking technique
in soccer player
Correction of pelvic asymmetry
Correction of SI joint dysfunction
Rest, ice, and NSAIDs
Work on the biomechanical weakness, hip ROM, abdominal strengthening, and
pelvic stabilizers.
Corticosteroid injection into the symphysis pubis and surrounding tissue can be
beneficial.
Functional progress back to sport
General return to sport in 4–8 wks
Additional Reading
Choi H, McCartney M, Best TM. Treatment of osteitis pubis and osteomyelitis
of the pubic symphysis in athletes: a systematic review. Br J Sports Med.
2008.
Cunningham PM, Brennan D, O'Connell M, et al. Patterns of bone and soft-

tissue injury at the symphysis pubis in soccer players: observations at MRI.
AJR Am J Roentgenol. 2007;188:W291–W296.
Kunduracioglu B, Yilmaz C, Yorubulut M, et al. Magnetic resonance findings of

osteitis pubis. J Magn Reson Imaging. 2007;25:535–539.
Paajanen H, Hermunen H, Karonen J. Pubic magnetic resonance imaging

findings in surgically and conservatively treated athletes with osteitis pubis
compared to asymptomatic athletes during heavy training. Am J Sports Med.
2007.
Pizzari T, Coburn PT, Crow JF. Prevention and management of osteitis pubis
in the Australian football league: a qualitative analysis. Phys Ther Sport.
2008;9:117–125.
Tibor LM, Sekiya JK. Differential diagnosis of pain around the hip joint.
Arthroscopy. 2008;24:1407–1421.
Codes
ICD9
733.5 Osteitis pubis
Clinical Pearls
Return to play depends on how long the condition persisted prior to starting
treatment (average time frame is 8–10 wks) and when the patient is pain free
or mostly pain free with sports-specific activities (range of recovery between 2
wks and 5 mos).
To speed up recovery and to prevent this from happening again, work on hip
ROM and flexibility and strengthening of muscles around hip joint, and core and
pelvic stabilization exercises; maintain good and efficient sport-specific body
mechanics (kicking for soccer, skating for hockey, etc.); and make sure to
progress slowly and only if pain free with sport-specific activities.
Surgery is reserved for athletes who have failed to show improvement with a
consistent trial of nonoperative treatment for at least 8 wks. Main reasons
include the perioperative risks; just as with any other surgery, success rate, on
average, is 80%, although techniques continue to improve. Recovery after
surgery is also long and demands adherence to physical therapy regimen.
Recovery from surgery generally lasts 8 wks at a minimum with gradual return
to play, but it may vary based on surgeon and the type of surgery.
Osteoarthritis
Kevin deWeber
Basics
Description
A predominantly noninflammatory, slowly progressing, degenerative condition of articular
cartilage, sometimes known as “degenerative joint disease”
Epidemiology
Prevalence
Radiographic osteoarthritis (OA) seen in about 40 million Americans, although only 10–30%
of them have significant pain or disability.
Prevalence of symptomatic OA significantly increases with age and varies with affected joint
(1):
Knee: 6% of adults >30, and 10–15% >60
Hip: 1–4% of adults
Hand: 10–15% of the elderly
Risk Factors
Systemic risk factors (1) contribute to development of OA by creating an environment where
the joint is vulnerable:
Age (10-fold increase from 30–65 yrs of age)
Gender:
Men <50 have higher incidence than women (may be related to risk of joint injury)
Women >50 have higher incidence than men (possible protective role of estrogen is
gone after menopause)
Genetics
Nutritional factors:
Lower risk of OA in persons with middle and highest tertiles of vitamin C intake or
highest levels of vitamin D (Framingham data)
Ethnicity:
Chinese have lower rates of hip and hand OA.
African Americans have higher rates of hip and knee OA.
Joint biomechanical risk factors (1) cause direct trauma to articular cartilage:
Joint injury (fractures, dislocations, ligament and meniscal ruptures, articular surface
damage)
Obesity (knee, hip, even hand OA)
Occupations involving high physical demands: Repetitive use of joints, heavy lifting,
frequent squatting
Sports with significant risk of acute joint injury
Abnormal joint biomechanics (dysplasia, malalignment, instability, abnormal innervation)
Excessive running (>60 miles a wk) has relative risk of 2–12 times for hip OA (Systematic
Review 2003)
Genetics
OA has a genetic component, especially in women. Primary, generalized OA is polygenic and
multifactorial; environmental factors play a significant role in gene expression.
General Prevention
Avoidance of joint trauma
Weight management:
50% reduction in OA risk with 11-lb weight loss in women (1)[C]
Adequate vitamin C and D intake (1)[C]
Avoid extremes of joint activity (joint immobilization or gross overuse)
Estrogen replacement after menopause may be protective (1)[C].
Etiology
OA is caused by an imbalance between breakdown and repair of joint tissue, usually due to
multiple risk factors:
Cartilage matrix (collagen, water, proteoglycans) slowly degrades
Chondrocytes are unable to maintain adequate repair.
Mechanical forces contribute to progressive cartilage loss.
Early stages: Cartilage fibrillation (fine fraying)
Middle and late stages: Formation of extra subchondral bone and cysts and osteophytes
(usually at joint margins)
Predominantly noninflammatory, but occasional mild inflammatory clinical flares

Degenerative meniscal tears in knee OA
Labral tears in hip OA
Diagnosis
Primary classification (idiopathic): Usually generalized
Secondary classification: Causes include previous trauma/internal derangement, metabolic
disorder, and deposition diseases
Most commonly affected joints include the distal interphalangeal (DIP) and proximal
interphalangeal (PIP) joints of the hands; metacarpophalangeal joints of the thumb; and the
hallux, hips, knees, cervical, and lumbar spine
History
Insidious onset over months to years is typical.
Most common symptoms are pain (especially after excessive activity), crepitus or grinding,
and joint swelling
There is typically short-lived (<30 min) stiffness after immobilization (ie, upon awakening),
improving with mobilization.
Some patients experience muscular weakness in the surrounding soft tissue.
There may be a personal history of antecedent joint trauma or a family history of OA.
Physical Exam
Joint line tenderness is common in hands and knees.
Joints may have crepitus, decreased range of motion (ROM), effusion, and atrophy of
surrounding muscles
In hands, may see nodules in the DIP and PIP joints, termed Heberden and Bouchard nodes,
respectively
In the hips, decreased and painful internal rotation are early signs.
Severely affected joints may appear misshapen or deformed due to osteophytes or
malalignment.

OA is diagnosed primarily through history and physical examination and confirmed by plain
films.
Lab
Laboratory assessment only used to rule out other disorders, if clinically suspected:
CBC, chemistry profile, and urinalysis are normal.
Markers of inflammation (erythrocyte sedimentation rate, C-reactive protein) usually are
normal, but may be slightly elevated during inflammatory flare-ups.
Rheumatoid factor and antinuclear antibody titers are negative.
Imaging
Plain films are the modality of choice (2)[D]:
Weight-bearing films are most sensitive in early knee and hip OA.
X-ray characteristics include osteophytes, joint space narrowing, subchondral sclerosis, and
cyst formation.
Radiographic severity does not correlate with symptom severity.
CT and MRI do not play a large role in diagnosis of 0A. May be used if other conditions
suspected.
Arthrocentesis and joint fluid examination are not routinely necessary unless the diagnosis is in
question, there is a possibility of septic arthritis/crystal deposition disease, or for treatment of
tense effusion.
Collagen vascular diseases
Crystal deposition disease
Gout
Calcium pyrophosphate deposition disease
Meniscal or labral tears
Treatment
Optimal management requires a combination of nonpharmacological and
pharmacological modalities (3)[D].
A multidisciplinary approach may help patients make the most of available
therapies:
Providers, physical therapists, personal exercise trainers, health care
educators, nutritionists
Surgical therapy is best reserved for patients with severe pain that affects
quality of life or activities of daily living who have failed multiple conservative
measures (3)[C].
Medication P.
No disease-modifying agents are yet available.
First Line
Acetaminophen (up to 4 g/day) is modestly effective and should be encouraged
as the first-line medication due to its relative safety (3)[A].
Oral glucosamine sulfate (not hydrochloride) 1,500 mg/day is modestly
effective in reducing pain in some patients (3)[A]:
Use for several years can slow progression of joint space narrowing;
consider use even if no symptomatic benefit (3)[A].
Oral NSAIDs effective, but have higher risks; reserved for short-term therapy
(3)[A].
COX-2 inhibitors are not more effective; less GI toxicity, but not without risks.
Discourage chronic use of NSAIDs; if necessary, add gastroprotection with a
proton pump inhibitor or misoprostol.
Viscosupplementation with intra-articular injection of hyaluronate derivatives is
modestly effective in pain reduction (3)[A]:
3–5 weekly injections
2–5-wk delay in effects
1–6-mo duration of effects
Second Line
Tramadol 50–100 mg t.i.d. is effective but has sedating and constipating
properties similar to narcotics (3)[A].
Topical NSAIDs are effective; effect takes 1–2 wks (3)[A].
Topical capsaicin is effective; high incidence of local irritation (3)[A].
Weak opioids or narcotics can be considered for short-term refractory pain;
those requiring long-term use may benefit from maximization of
nonpharmacologic therapies and/or surgery (3)[A].
Intra-articular injections with corticosteroids are effective for 2–4 wks (3)[A]:
Reserve for patients not responding to oral medications or inflammatory
flare-ups.
Limit to 2–3 injections per year per joint.
Observe for significant incidence of systemic side effects.
General Measures
Patient education is effective (3)[A]:
Set reasonable expectations on outcome (pain reduction, increased function,
not cure)
Modification of activities to minimize pain and risk of joint trauma
Importance of nonpharmacologic therapies
Weight reduction is paramount (3)[A].
Aerobic conditioning with nonpainful activities (walking, deep-water running and
other aquatic exercise, cycling) (3)[A]
ROM and muscle strength exercises are effective (3) for hip [D] and knee [A]
OA.
Physical therapy referral may be effective (3)[D].
Walking aids for knee and hip OA may be effective (cane, crutch in
contralateral hand; walkers for bilateral OA) (3)[D].
Knee brace for patients with varus or valgus instability improves stability and
reduces fall risk (3)[A].
Footwear with lateral wedge insoles for medial knee compartment OA (3)[A]
Thermal therapies (heat, cold) may be effective (3)[A].
Transcutaneous electrical nerve stimulation can provide short-term relief (3)
[A].
Acupuncture may be effective in knee OA (3)[A].
Pulsed electromagnetic field therapy may be effective in improving function 4
[A].
Balneotherapy (spa, mineral baths) may be effective 5 [A].
Static magnets: No evidence for support; effectiveness cannot be ruled out 6
[A].
Intra-articular autologous platelet-rich plasma injection: Success in 1 series;
under study
Indicated in patients with recalcitrant pain and interference with activities of
daily living despite maximizing conservative management (3)[C]
Arthroscopic lavage and debridement NOT effective (3)[A]; only indicated for
concomitant non-OA conditions
Medial or compartment knee OA:
Wedge osteotomomy may be effective (7)[B].
Unicompartmental arthroplasty (replacement) effective (7)[B]
Interposition arthroplasty (joint spacer insertion); no data on safety/efficacy
Total knee arthroplasty (TKA): Very effective (3)[C]:
Hardware durable 10–15 yrs
Try to delay TKA until after 55 by maximizing other treatments.
Rate of hardware failure <10 yrs is 3 time in <55 vs >70 yrs of age
Patellofemoral joint (PFJ) OA in isolation (rare):
Elevation of tibial tubercle may be effective
PFJ arthroplasty sometimes used
Total hip arthroplasty or joint resurfacing is effective in hip OA (3)[B].
Glenohumeral OA: Total shoulder replacement more effective/durable than
humeral head replacement (8)[B], but both are effective.
Cartilage replacement techniques gaining in popularity and evidence:
Autologous cartilage implantation: Arthroscopy harvests patient's cartilage,
chondrocytes are replicated in culture, and 2nd arthroscopy fills cartilage
defect with cells.
Osteoarticular cartilage transplant: Cartilage from patient's nonweight-
bearing surface in knee joint is placed into defect.
Cartilage allografts (cadaver cartilage) to fill defects
Ongoing Care
As needed based on symptoms and function
Diet
Ensure adequate vitamin C and D intake.
Patient Education
Good education has proven benefit for successful management:
In office by professionals
Public education materials (eg, www.myosteoarthritiscentral.com)
Prognosis
OA is a progressive arthropathy with highly variable course
Oral glucosamine shown to slow rate of radiographic progression over >3 yrs
References
1. Garstang SV, Stitik TP. Osteoarthritis: epidemiology, risk factors, and pathophysiology.
Am J Phys Med Rehabil. 2006;85:S2–S11.
2. American College of Radiology Expert Panel on Musculoskeletal Imaging, 2008.

http://74.125.93.132/search?
q=cache:Up16N8YvlbEJ:www.acr.org/SecondaryMainMenuCategories/quality/safety/app/criteri
3. Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of
hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines.
Osteoarthritis Cartilage. 2008;16:137–162.
4. Vavken P, Arrich F, Schuhfried O, et al. Effectiveness of pulsed electromagnetic field

therapy in the management of osteoarthritis of the knee: A meta-analysis of randomized
controlled trials. J Rehabil Med. 2009;41:406–411.
5. Harzy T, Ghani N, Akasbi N, et al. Short- and long-term therapeutic effects of thermal
mineral waters in knee osteoarthritis: a systematic review of randomized controlled trials.
Clin Rheumatol. 2009;28:501–507.
6. Pittler MH, Brown EM, Ernst E. Static magnets for reducing pain: systematic review and
meta-analysis of randomized trials. CMAJ. 2007;177:736–742.
7. Richmond JC. Surgery for osteoarthritis of the knee. Med Clin North Am. 2009;93:213–
222.
8. Radnay CS, Setter KJ, Chambers L, et al. Total shoulder replacement compared with
humeral head replacement for the treatment of primary glenohumeral osteoarthritis: A
systematic review. J Shoulder Elbow Surg. 2007.
Codes
ICD9
715.91 Osteoarthrosis, unspecified whether generalized or localized, involving shoulder
region
715.92 Osteoarthrosis, unspecified whether generalized or localized, involving upper arm
715.93 Osteoarthrosis, unspecified whether generalized or localized, involving forearm
Osteochondritis Dissecans
Susan Park
Basics
Description
Osteochondritis dissecans (OCD) is an acquired defect in the articular cartilage and
subchondral bone.
It is classified into juvenile and adult forms, depending on growth plate status.
It often affects the femoral condyles (most common: posterolateral portion of medial
condyle), talar dome, and humeral capitellum but can occur in all large joints.
Epidemiology
Incidence estimated to be 15–30/100,000 persons
Predominant gender: Male > Female (5:3).
Occurs most commonly in ages 10–20 yrs but can occur from 5–50 yrs of age
Risk Factors
Repetitive microtrauma or overuse
Familial predisposition
Endocrine abnormalities
Anomalies of ossification
Impaired blood supply
OCD in 1 joint is risk factor for contralateral involvement; 20–30% of patients with OCD of
the knee have bilateral involvement.
Sports involving jumping, pivoting, cutting movements
Throwing sports and gymnastics are specific risk factors for OCD of the elbow.
General Prevention
Learning proper mechanics of sports/activities
Strength and stability training
Etiology
Repeated microtrauma may lead to microfractures, which may cause some focal ischemia
and may result in alteration of growth.
May lead to cartilage separation and fragmentation
Diagnosis
MRI staging classification:
Stage I: Subchondral lesion of low signal intensity (subchondral compression fracture); stable
Stage II: Hypointense rim on images indicating demarcation but not separation of lesion
(osteochondral fragment attached by osseous bridge); stable
Stage III: High signal intensity and underlying cystic changes indicative of instability (detached
nondisplaced fragment); unstable
Stage IV: Partial or complete dislocation of osteochondral fragment into the joint space
(displaced fragment, loose body); unstable
History
Insidious onset of symptoms
Preceding injury to joint surface seen in <50% of patients
Stiffness after periods of rest
If symptoms in knee, may have pain going up and down stairs or hills
Physical Exam
Signs and symptoms:
Vague joint pain, aching
Locking
Restricted range of motion (ROM)
Sense of giving way or weakening
Pain with activity or weight bearing
Effusion and/or crepitus may be present.
Decreased or painful ROM
Poorly localized joint-line tenderness
Point of maximal tenderness
Mild antalgic gait
Ipsilateral quad atrophy if symptom in knee

Imaging
X-ray is standard for diagnosis. For knee, obtain anteroposterior (AP), lateral, and tunnel
views.
Bone scan occasionally is useful for diagnosis if onset is acute and x-rays are negative; may
help to predict healing if physis is open.
US is unreliable.
CT scan can be used.
MRI is “gold standard” for staging after diagnosis; also good for assessment of loose body;
may help to predict prognosis of nonoperative management.
Knee:
Meniscal or ligamentous injury
Tendinitis
Patellofemoral pain syndrome
Osteoarthritis
Posttraumatic osteochondral defect
Spontaneous osteonecrosis of the knee
Crystal-induced arthropathies
Elbow:
Panner's disease
Ligament sprains
Fractures
Posttraumatic asteochondral defect, “loose body”
Ankle:
DJD
Ligament sprains
Fractures
Arthropathies
Posttraumatic osteochondral defect, “loose body”
Treatment
Long-term treatment
Acute treatment
Immobilization:
Stage I OCD is treated nonoperatively with either activity restriction or
immobilization. Phase I: Weight bearing is restricted for 6–8 wks. Phase II: If
repeat radiographs are stable and patient is pain-free, may proceed to weight
bearing as tolerated and physical therapy for ROM. Phase III: If radiographic
and clinic signs of healing at 3–4 mos after initial diagnosis, may slowly
initiate activities of running, jumping, and cutting.
Stage II OCD is treated nonoperatively in juveniles with open joint physis.
Treatment of adults is controversial but usually requires surgery and may
depend on the size of the lesion.
Stage III–IV patients and those who fail nonoperative therapy should be
referred for surgical management.
Early recognition of condition is important. If not treated, it can lead to
degenerative osteoarthritis.
Prognosis depends on growth plate status. Children with open physis should be
considered for nonoperative management if lesion is stable.
Progression of symptoms to joint stiffness or locking necessitates arthroscopy
to evaluate and treat for possible loose bodies.
NSAIDs are useful adjunctive therapy.
Rehabilitation:
Physical therapy may be initiated for conservatively managed patients.
Stretching, ROM exercises, conditioning exercises, and quadriceps
strengthening are beneficial.
Postoperative physical therapy can be tailored to the procedure.
Patients with larger lesions, greater skeletal maturity, and high signal on MRI
likely will do better with surgery.
Arthroscopy has better outcomes than open procedures.
Comparing excision, curettage, and drilling, the highest success rates were
seen when all 3 therapies were used together.
Surgical procedures may also include pinning and grafting.
Ongoing Care
Orthopedic referral is indicated for all patients with unstable OCD and for those who fail
Additional Reading
Bohndorf K. Osteochondritis dissecans: a review and new MRI classification. Eur Radiol.
1998;8:103–112.
Ganley TJ, Flynn JM. Osteochondritis dessicans of knee. The pediatric and adolescent
knee. 2006;273–293.
Hixon AL, Gibbs LM. Osteochondritis dissecans: a diagnosis not to miss. Am Fam
Physician. 2000;61:151–156, 158.
Kocher MS, Tucker R, Ganley TJ, et al. Management of osteochondritis dissecans of the
knee: current concepts review. Am J Sports Med. 2006;34:1181–1191.
Stäbler A, Glaser C, Reiser M. Musculoskeletal MR: knee. Eur Radiol. 2000;10:230–241.
Tol JL, Struijs PA, Bossuyt PM, et al. Treatment strategies in osteochondral defects of the
talar dome: a systematic review. Foot Ankle Int. 2000;21:119–126.
Codes
ICD9
732.7 Osteochondritis dissecans
Clinical Pearls
Patients with stable lesions require a break from competitive sports for at least
6–8 wks.
Patients must be pain-free before return to sports.
MRI and/or bone scan may be useful to evaluate healing.
Depending on the severity of the lesion and treatment, healing can take up to
10–18 mos.
The juvenile form of OCD has a good potential for full recovery if treated
appropriately but still may lead to early degenerative joint disease.
Adult forms tend to be more complicated and often lead to early degenerative
joint disease.
Osteomyelitis
Alex B. Diamond
Basics
Description
Inflammatory process of bone and its components secondary to infection by pyogenic
organism
Categorized as acute, subacute, or chronic
Other classification systems have emerged:
Waldvogel: Hematogenous, contiguous, or chronic
Cierny-Mader: Based on dynamic status of disease process
Acute osteomyelitis develops within 2 wks of disease onset:
Predominantly in children
Typically the result of hematogenous dissemination
Metaphysis of long bones the most commonly involved location
Subacute osteomyelitis presents within 1 to several months of disease onset
Diagnosis difficult, as characteristic signs and symptoms of acute form absent
Brodie abscess most common type of subacute form:
Cavitary lesion in epiphysis or metaphysis characterized by small, localized lucency
surrounded by reactive, dense-appearing bone
Subacute form represents favorable host-pathogen response, as dependent on balanced
interplay between infecting bacteria and host immune mechanisms
Subacute form mimics various other conditions, which results in delayed diagnosis and
treatment:
Most frequent incorrect diagnosis is that of tumor, either benign or malignant
Chronic osteomyelitis develops after few months of disease onset:

May be recurrent or intermittent in presentation
Direct contamination frequent cause of chronic form (open fracture, penetrating wound,
surgical manipulation)
Simultaneous presence of microorganisms and necrotic bone (sequestra) is hallmark
Epidemiology
Overall prevalence in children is 1 per 5,000
Overall incidence higher in developing countries
Most prevalent type is result of injury (associated with open fracture, surgical reconstruction
of bone)
Males: Females = 2:1; no association with race
Special populations:
Annual incidence in sickle cell patients is 0.36%.
Prevalence after foot puncture in diabetic patients is 30–40%.
Incidence of subacute osteomyelitis has increased since use of antibiotics:
Most common form in East Africa
Long-term recurrence rate of chronic osteomyelitis is 20–30%.
Secondary hematogenous infections more common in adults:
Represent reactivation of quiescent focus of primary hematogenous osteomyelitis from
childhood
Deep musculoskeletal infection incidence from open fracture as high as 23%
Spine becomes most common site of infection in patients >45 yrs old
Culture more likely positive if history of trauma, shorter duration of symptoms, higher WBC
count and erythema, swelling or cellulitis overlying infected bone
Morbidity significant:
Pain, disability, amputation, extension of infection and sepsis
10–15% with vertebral osteomyelitis develop neurologic symptoms or spinal cord
compression
30% of pediatric cases may develop deep vein thrombosis.
Mortality low unless associated sepsis
Risk Factors
Open or compound fracture
Surgical manipulation (orthopedic, colorectal, genitourinary procedures)
IV drug abuse
Immunosuppression (AIDS, chronic steroid use)
Peripheral vascular disease (diabetes mellitus)
Sickle cell disease
Genitourinary or biliary tract infection
Chronic joint disease
Presence of prosthetic orthopedic device
Low socioeconomic status
Infancy
Elderly
Alcoholism
History of tuberculosis (Pott disease)
General Prevention
Timely diagnosis and treatment of primary infections to avoid seeding of bone
Appropriate wound management and possible use of prophylactic antibiotics with injury or
manipulative surgery
Etiology
Normal bone highly resistant to infection unless result of very large inocula, trauma, or
presence of foreign bodies
Microorganisms adhere to bone/devices; survive intracellularly in osteoblasts; express
resistance to antimicrobial treatment (high failure rate of short courses of therapy); form
inflammatory markers (potent osteolytic factors) and phagocytes (generate toxic oxygen
radicals and release enzymes that lyse surrounding tissues); pus develops and spreads into
vascular channels increasing intraosseous pressure and impairing blood flow; ischemic
necrosis of bone
Infectious agents include bacteria, mycobacteria, and fungi.
Routes of infection include hematogenous, contiguous focus, and direct inoculation.
Primary hematogenous osteomyelitis occurs mainly in infants and children:
Sluggish circulation at highly vascular metaphyseal-physeal barrier predisposes vessels to
thrombosis and bone to localized necrosis and bacterial seeding.
Metaphyseal arteries lack phagocytic lining cells and sinusoidal veins (in growth plate)
contain functionally inactive phagocytic cells.
Usually monomicrobial
Manifestations more localized, but can involve multiple organisms when result of contiguous
or direct inoculation
Subacute osteomyelitis occurs in much wider variety of bones:
Femur > tibia > remaining lower limb > upper limb
Metaphyseal-equivalent locations (pelvis, vertebrae, calcaneus, clavicle, talus)
Chronic osteomyelitis characterized by sequestrum of necrotic bone harboring bacteria
Capability to persist or recur, regardless of initial cause/mechanism and despite aggressive
intervention
Pathogen isolated in 35–40% of cases
Fungal agent usually result of catheter-related complication, use of illicit drugs, or prolonged
neutropenia
Bacterial agents:
Most common include Staphylococcus aureus, coag-negative staph and aerobic gram-
negative bacilli; others include strep, enterococci, and anaerobes
Increasing MRSA
Age of patient and inoculation method important factor in species prevalence:
Hematogenous: Children and adolescents: S. aureus (80%), group A streptococcus
species, H. influenzae. Adults: Staph, occasional Enterobacter or strep species
Direct or contiguous: Generally staph (75% of cultures), Enterobacter, pseudomonas
Puncture wound through sneaker typically staph, pseudomonas
Chronic osteomyelitis most likely S. epidermidis or S. aureus, pseudomonas, serratia, E.
coli
Consider anaerobes if “fight bite” injury
Staph and salmonella predominate sickle cell disease
Diagnosis
History
Children with acute hematogenous osteomyelitis may present with abrupt-onset high fever,
chills, fatigue, irritability, lethargy, restricted motion and local pain, edema, erythema, and
tenderness.
In a young child, inability to get to seated position, limp, and refusal to walk may be observed
if the spine, pelvis, or lower extremity is involved; pseudoparalysis if upper extremity
50% of children and most adults present with vague complaints, nonspecific pain of involved
limb, and minimal if any temperature elevation or constitutional symptoms.
Limitation of joint motion usually present if primary lesions particularly close to joint spaces
leading to sympathetic effusions
Osteomyelitis due to contiguous focus often presents with painful or unstable joint, little or no
fever
Subacute osteomyelitis presents with mild pain, minimal fever, and few constitutional
symptoms.
In chronic osteomyelitis, there is local bone loss, persistent drainage through fistulas or sinus
tracts, nonhealing ulcers, recurrent pain, possibly low-grade fever, and mild systemic
symptoms (ie, chronic fatigue).
An insidious onset with history of acute bacteremic episode, local tenderness, erythema, and
edema is common in vertebral osteomyelitis.
Physical Exam
Fever (temperature >100.4°F), but not always present
Tenderness to palpation, swelling, erythema, warmth over involved area
Fluctuance
Decreased use of extremity, refusal to bear weight
Limited movement of adjacent joint
Other possible foci of infection
Sinus tract drainage
Passive range of motion tolerated, unlike septic arthritis

Lab
CBC may reveal elevated WBC or left shift, but frequently normal
C-reactive protein (CRP) and erythrocyte sedimentation rate almost always elevated, but
nonspecific tests:
Changes in CRP detected sooner
Blood culture positive 50% of cases
Aspiration from affected site normal 25% of the time
Bone biopsy can be achieved by percutaneous needle, radiographic guided instruments, or
open surgical procedure:
Send for Gram stain and culture (aerobic, anaerobic, mycobacterial, and fungal)
Obtain 2nd specimen for histopathology
Imaging
In early disease, x-rays may be normal or show only soft tissue swelling.
Osseous changes usually appear 7–14 days after symptom onset; 90% with changes on x-
ray by 28 days:
Include periosteal elevation and/or destruction of bone with radiolucency, fading cortical
margins, and no surrounding reactive bone. Periosteal elevation followed by cortical or
medullary lucencies.
In acute osteomyelitis in children, classic findings include deep, circumferential soft tissue
swelling with obliteration of muscular planes.
In adults, plain radiographs are of less value because 50% of the bone matrix must be
destroyed before lytic changes are visible.
Radioisotope bone scan (triple phase with technetium 99m) is highly sensitive and initial test
of choice for early diagnosis of osteomyelitis, especially if x-ray studies are ambiguous
(Termaat MF, et al. JBJS Am, 2005. LOE = III).
MRI effective in early detection and localization. Reported 90–100% sensitivity.
Consider MRI if bone scan is negative or when very minor destructive changes present.
Spatial resolution of MRI makes it useful in differentiating between bone and soft tissue
infection. Good for diagnosis and assessment of extension. IV contrast useful in
differentiating vascularized and inflamed tissue from abscess.
CT scanning may play role in diagnosis and assisting the surgeon in operative planning. Most
useful in evaluation of spinal vertebral lesions or other areas with complex anatomy (pelvis,
sternum, calcaneous). May reveal small areas of osteolysis, gas, or foreign bodies.
US may show periosteal thickening and elevation, soft tissue abscess, or fluid collection.
Provides direction for aspiration. May demonstrate changes earlier, but can't evaluate bone
cortex.
Histopathologic and microbiologic exam of bone is gold standard:
Requires 2 of 4:
Purulent material on aspiration of affected bone
Positive findings of bone tissue or blood culture
Localized classic physical findings of bony tenderness, overlying soft tissue erythema, or
edema
Positive radiological imaging study
Principal histiologic findings in acute osteomyelitis include microorganisms, infiltrations of
neutrophils, and congested or thrombosed blood vessels
Distinguishing feature of chronic osteomyelitis is necrotic bone
Acute leukemia
Acute rheumatic fever
Rheumatoid arthritis (adult or juvenile)
Acute gout, pseudogout
Cellulitis
Malignant bone tumors (Ewing sarcoma, osteosarcoma)
Septic arthritis
Multiple myeloma (elderly)
Sepsis
Deep vein thrombosis, thrombophlebitis
Intervertebral disc disorders
Fracture
Aseptic bone infarction
Neuropathic joint disease
Transient synovitis
Treatment
Immobilization of the affected part, hydration, fever control, and IV
antibiotics directed by culture and sensitivity results (when available)
Involvement of specialists (orthopedic surgeon, infectious disease specialist)
Empiric treatment is guided by the age of the patient, severity of disease, and
suspected organisms:
Use broad-spectrum antibiotics until lab results, then tailor to culture and
sensitivities
Stengel D et al. Lancet Infect Dis, 2001. (LOE = II-III)
For children >4 yrs, nafcillin or oxacillin is recommended. If allergic to penicillin,
use vancomycin or clindamycin. If community-acquired MRSA is suspected,
use vancomycin or clindamycin as 1st choice. Add a 3rd-generation
cephalosporin for gram-negative bacteria coverage if needed.
In adults >21 yrs, recommended antibiotics include nafcillin, oxacillin, or
cefazolin. If allergic to penicillin, use vancomycin or clindamycin. Add a 3rd-
generation cephalosporin or ciprofloxacin plus rifampin for gram-negative
bacilli coverage.
For suspected Pseudomonas aeruginosa, administer ceftazidime or
cefepime; alternatively, use ciprofloxacin, except in children.
Duration of treatment is usually 4–6 wks IV, but may be longer, depending on
the clinical response and laboratory values
For sickle cell patients, use fluoroquinolone except in pediatric population.
Alternative is 3rd-generation cephalosporin (ceftriaxone).
Possibility for children with Albright hereditary osteodystrophy to receive 2 wks
IV therapy followed by 4 wks of PO antibiotics if responding well
Recommend treatment with IV antibiotics 6 wks from last debridement
Failure of symptoms to resolve after an up-to-6-wk course of antibiotics or
worsening of the condition during treatment should lead to reevaluation and a
definite tissue diagnosis, followed by surgical treatment and appropriate
antibiotics.
Other indications for surgery are impending sinus formation, drainage into a
synovial joint, and signs of subperiosteal pus or synovitis, which indicate that
the subacute infection has transformed into an acute component.
Surgical drainage and debridement is needed for tissue culture identification of
the offending organism, evacuation of abscesses, and removal of necrotic
bone and nidus of infection.
Surgical decompression may release intramedullary and subperiosteal pus.
Chronic osteomyelitis requires primarily surgical treatment, as complete
debridement of all devitalized bone and soft tissue is essential for cure
(Simpson AH et al. JBJS Br, 2001. LOE = II).
Reconstruction of large bony defects may be required, and success entails
both filling the space created by the loss of tissue due to debridement and
revascularization of poorly perfused regions.
Grafting wounds (bone, soft tissue) and revascularization procedures are the
best means of fighting recurrent infection.
Remove infected prosthetic devices and hardware.
Hyperbaric oxygen therapy has shown some promising results in treating
chronic or refractory osteomyelitis, but no convincing evidence, especially in
diabetic patients with vascular insufficiency (Goldman RJ. PMR, 2009. LOE =
Moderate – High via GRADE criteria).
Provides oxygen to promote collagen production, angiogenesis, and ultimately
wound healing
With skeletal tuberculosis, any bone can be involved.
Usually involves the metaphysis of long bones in children and adolescents
In adults, the axial skeleton most often is involved, followed by the proximal
femur, knee, and small bones of the hands and feet.
Tissue for histologic examination is almost always required for diagnosis.
With fungal osteomyelitis, bone infections may be caused by
coccidioidomycoses, blastomycosis, cryptococcosis, candidiasis, or
sporotrichosis.
Most common presentation is a cold abscess overlying an osteolytic lesion.
Treatment involves surgical debridement and antifungal chemotherapy.
Vertebral osteomyelitis primarily in adults, rare disease overall
Involves 2 adjacent vertebrae and disc spaces between them
Focal neck or back pain, fever
Blood culture often negative; needle biopsy with multiple specimens is
diagnostic procedure of choice
Biopsy and debridement cultures dictate choice of antibiotic(s).
Surgical intervention reserved for management of complications or for medical
therapy failure.
Percutaneous transpedicular debridement and discectomy by removing
infected necrotic bone accelerates healing and prevents progression of bone
destruction and deformity in the early stages of vertebral osteomyelitis and
spondylodiscitis.
Ongoing Care
Protection of the joint with traction or splinting and starting protected motion early is a
consideration.
Limitation of weight-bearing until x-ray evidence of defect's partial healing due to risk of
collapse
Follow-up based on response to therapy and overall health of patient after completion of
treatment regimen.
Should continue for at least 2 yrs in subacute cases:
Closely monitor at 1st for signs of response to treatment (clinical and laboratory).
Then ensure compliance with antibiotic therapy for 6 wks. Clinical response is usually within
a few days of initiation of treatment.
For next 6 mos, monitor for signs of recurrence. Most recurrences occur within this time,
but recurrence after up to 18 mos has been reported.
Radiologic healing is slower than clinical healing and usually occurs within 3–12 mos.
Metaphyseal and epiphyseal cavities usually heal, leaving either a small area of sclerosis or a
small, indistinct lucency in the cortex.
The purpose of follow-up after a year is for assessment of bone growth and alignment.
Prognosis
Variable, but markedly improved with timely diagnosis and aggressive treatment
Complications
Include bone abscess, bacteremia, fracture, loosening of hardware, overlying
cellulitis, and draining soft tissue tracts
Sinus tract formation may be associated with neoplasms, especially with long-
standing infection:
Squamous cell carcinoma most common tumor associated with chronic
osteomyelitis. Other tumors reported.
Recalcitrant infection that does not respond should prompt biopsy evaluation
for malignancy from multiple sites.
Despite localized transgression of the epiphyseal plate by subacute
osteomyelitis, growth disturbances are exceedingly rare.
Most common complication is recurrence.
Additional Reading
Carek PJ, Dickerson LM, Sack JL. Diagnosis and management of
osteomyelitis. Am Fam Physician. 2001;63:2413–2420.
Conterno LO, da Silva Filho CR. Antibiotics for treating chronic osteomyelitis
in adults. Cochrane Database Syst Rev. 2009;CD004439.
Goldman RJ. Hyperbaric oxygen therapy for wound healing and limb salvage:
a systematic review. PM R. 2009;1:471–489.
Lew DP, Waldvogel FA. Osteomyelitis. Lancet. 2004 Jul 24–30;364:369–379.

Lew DP, Waldvogel FA. Osteomyelitis. N Engl J Med. 1997;336:999–1007.
Pineda C, Vargas A, Rodríguez AV. Imaging of osteomyelitis: current

concepts. Infect Dis Clin North Am. 2006;20:789–825.
Sharif I, Adam H. Current Treatment of Osteomyelitis. Pediatrics in Review.

2005;26:38–39.
Stengel D, Bauwens K, Sehouli J, et al. Systematic review and meta-analysis

of antibiotic therapy for bone and joint infections. Lancet Infect Dis.
2001;1:175–188.
Codes
ICD9
730.00 Acute osteomyelitis, site unspecified
730.01 Acute osteomyelitis involving shoulder region
730.02 Acute osteomyelitis involving upper arm
Clinical Pearls
The most common pathogens implicated in development of osteomyelitis are
MRSA, coagulase-negative staph, aerobic gram-negative bacilli
Often, abrupt high fever presents with acute hematogenous osteomyelitis. It is
not uncommon to have no fever or a low-grade fever with the other forms of the
disease.
The test of choice and gold standard for diagnosis of osteomyelitis are bone
biopsy and histopathologic and microscopic examination.
Chronic osteomyelitis primarily requires surgical treatment for cure.
Recalcitrant infection that does not respond to treatment should spur biopsy
evaluation from multiple sites for concern of malignancy development following
long-standing infection.
Osteoporosis
Julie M. Kerr
Basics
Description
Systemic disorder characterized by decreased bone mass and microarchitectural
deterioration of bone leading to bone fragility and increased susceptibility to fractures of the
hip, spine, and wrist
World Health Organization definition:
Bone mineral density (BMD) >2.5 SD below the mean for a particular age on dual-energy
x-ray absorptiometry (DEXA) scan
(T-score = -2.5)
Osteopenia:
BMD between -1.0 and -2.5 SD below the mean for a particular age on DEXA scan
T-score = -1 to -2.5
Classifications:
Primary
Age-related (postmenopausal estrogen deficiency, age-related vitamin D deficiency)
Secondary (drug or concurrent medical condition etiology)
Epidemiology
In the U.S., 13–18% of women aged 50 or older:
37–50% have osteopenia
Lifetime risk of fractures: 40–50% for postmenopausal Caucasian women
1 in 8 men >50
Risk Factors
Female sex
Non-Hispanic Caucasian race
Asian race
Family history
Age 65 yrs or older
Diet low in calcium; low in vitamins C, D, and K; and decreased copper, manganese, and zinc
mineral content
Estrogen deficiency: Postmenopausal or premenopausal secondary to overexercising and/or
eating disorder
Sedentary lifestyle, lack of weight-bearing exercise
History of falls
Female athlete triad: Disordered eating, amenorrhea, and osteoporosis
Medications: Corticosteroids, anticonvulsants, cyclosporine, heparin, thyroid replacement
drugs
Excessive alcohol (>2 drinks per day) and tobacco intake
Other diseases: Diabetes, hyperparathyroidism, hyperthyroidism, multiple myeloma
Impaired absorption of calcium, phosphate, and vitamin D from the GI tract, as in inflamed
bowel disease, gastrectomy, celiac disease, jejunoileal bypass, or pancreatic insufficiency
General Prevention
Identification and treatment of risk factors/secondary causes of osteoporosis
Weight-bearing exercise with additional resistance training can maintain bone mass and can
help prevent falls when coupled with adequate calcium and vitamin D intake.
Fall prevention addressing vision deficits, balance and gait abnormalities, cognitive
impairment, dizziness, and home safety assessment
When counseling young females, emphasize importance of achieving peak bone mass via
calcium and vitamin D supplementation, good overall nutrition, and regular menstrual cycles.
Diagnosis
History
Atraumatic fracture/stress fracture
Risk factor assessment
Physical Exam
Usually late findings, such as an exaggerated kyphotic curvature (dowager's hump) indicating
anterior wedge fractures of thoracic vertebrae
Usually not evident on exam unless advanced stage and subsequent fracture

Assessment of biochemical markers of bone turnover: Osteocalcin, total and bone-specific
alkaline phosphatase useful in monitoring response to treatment
Serum type I collagen propeptide, pyridinoline levels in blood and urine, and plasma tartrate-
resistant acid phosphatase levels are markers used in research settings.
Imaging
DEXA measures bone mineral content of lumbar spine, femoral neck, and distal radius
yielding BMD (g/cm2).
DEXA uses lower dose of radiation and costs less than quantitative CT.
US of the calcaneus may be useful as screening tool to identify patients at risk and those
who would benefit from DEXA evaluation.
Treatment
Medication
Pharmacologic interventions act by decreasing bone resorption, thus providing at
most a 10% increase in BMD at any given site.
First Line
Calcium carbonate and calcium citrate are essential adjuncts to other
treatments: 1,500 mg for postmenopausal women, 1,000 mg for
premenopausal women, 1,500 mg for female athletes.
Vitamin D: Particularly useful in vitamin D-deficient elderly (≥700–800 IU daily);
current studies suggest that the desirable serum concentration of at least 75
nmol/L 25(OH)D may require a daily dose of over 1,000 IU; due to seasonal
fluctuations of 25(OH)D levels, a desirable range during the summer months
may not be sustained in the winter months.
Bisphosphonates: Most commonly prescribed therapy for the prevention and P.
treatment of osteoporosis; inhibit both osteoblast and, to a greater extent,
osteoclast activity, thus decreasing bone turnover and increasing BMD;
alendronate (Fosamax), risedronate (Actonel), ibandronate (Boniva),
zoledronic acid (Reclast):
Alendronate and risedronate reduce vertebral and hip fractures; oral dosing
daily or weekly
Ibandronate has antifracture effectiveness in the spine only; IV 3 mg every 3
mos increases BMD or oral
Zoledronic acid was effective over a 3-yr period in reducing the risk of
vertebral and hip fractures; has been shown to have effectiveness in
reducing risk of several other types of fractures in patients with
postmenopausal osteoporosis or recent low-trauma hip fracture; more long-
term studies are currently underway; 5 mg IV, yearly
Cost for IV medications is high, but may be indicated in high-risk women who
cannot tolerate or are noncompliant with oral therapy due to pre- and
postdose fasting and posture requirements
Risk of osteonecrosis of jaw a rare complication
Selective estrogen receptor modulators: Raloxifene (Evista); estrogen agonist
activity in bone tissue and on lipids, with antagonist activity in breast and uterine
tissue; especially useful in women at high risk for breast cancer; effective in
reducing the incidence of vertebral fracture; oral, 60 mg daily
Teriparatide (Forteo): Recombinant human parathyroid hormone with potent
bone anabolic activity; 20 mcg SC daily for 2 yrs decreases vertebral and
nonvertebral fractures; indicated for postmenopausal women with severe bone
loss, men with osteoporosis at high risk of fracture, and in persons not
improved with bisphosphonate therapy
Second Line
Calcitonin: Antiresorptive treatment:
Decreases occurrence of vertebral compression fractures but not
nonvertebral or hip fractures
100 IU SC/IM daily or every other day
200 IU intranasal spray daily with 1,000 mg calcium and 400 IU vitamin D
Hormone therapy:
Women's Health Initiative: Estrogen, with or without progesterone, slightly
reduces risk of hip and vertebral fractures, but benefit did not outweigh the
increased risk of stroke, deep vein thrombosis, heart disease, and breast
cancer, even in women at high risk of fracture
FDA recommends hormone replacement therapy for osteoporosis only in
women with moderate or severe vasomotor symptoms using the lowest
effective dose for the shortest time
Combination oral contraceptives may be useful in treating amenorrhic
females with osteopenia
Soy phytoestrogens: Efficacy as bone-protective agents in vivo remains unclear
Ongoing Care
Patient Monitoring
Changes in BMD levels indicative of real biological change can be measured after 1 yr of
treatment.
Changes in bone turnover marker levels in treated patients can be observed within 3 mos of
treatment initiation.
Additional Reading
http://osteoed.org/tools.php?type=score for Simple Calculated Osteoporosis Risk
Estimation (SCORE) tool to predict which women may benefit from DEXA screening.
http://www.nos.org.uk “Building Healthy Bones” for detailed list of dietary sources of

calcium.
Holick MF. Optimal vitamin D status for the prevention and treatment of osteoporosis. Drugs
Aging. 2007;24:1017–1029.
Keen AD, Drinkwater BL. Irreversible bone loss in former amenorrheic athletes.
Osteoporosis Int. 1997;7:311–315.
Lim LS, Hoeksema LJ, Sherin K, et al. Screening for osteoporosis in the adult U.S.
population: ACPM position statement on preventive practice. Am J Prev Med. 2009;36:366–
375.
Otis CL, Drinkwater B, Johnson M, et al. American College of Sports Medicine position
stand on the female athlete triad. Med Sci Sports Exerc. 1997;29:i–ix.
Poulsen RC, Kruger MC. Soy phytoestrogens: impact on postmenopausal bone loss and
mechanisms of action. Nutr Rev. 2008;66:359–374.
Sweet MG, Sweet JM, Jeremiah MP, et al. Diagnosis and treatment of osteoporosis. Am
Fam Physician. 2009;79:193–200.
Voss LA, Fadale PD, Hulstyn MJ. Exercise-induced loss of bone density in athletes. J Am
West RV. The female athlete. The triad of disordered eating, amenorrhoea and
osteoporosis. Sports Med. 1998;26:63–71.
Codes
ICD9
733.00 Osteoporosis, unspecified
733.90 Disorder of bone and cartilage, unspecified
Otitis Media/Externa
Darin Rutherford
Craig C. Young
Basics
Description
Acute otitis media (AOM): Rapid onset of signs and symptoms in the presence of a middle-
ear effusion and with the signs and symptoms of middle-ear inflammation
Synonym(s): Suppurative otitis media
Recurrent otitis media: ≥3 episodes of acute otitis media in 6 mos
Otitis externa: Acute or chronic (>6 mos) infection or inflammation of the external auditory
canal
Synonym(s): Swimmer's ear
Secretory otitis media
Catarrh of the middle ear, catarrhal otitis media, tubal catarrh, hydrops ex vacuo
Epidemiology
AOM:
Almost all (93%) children experience ≥1 episode of otitis media by age 6 yrs.
Most frequent primary diagnosis at U.S. office visits in children <15 yrs
Most common infection for which antibacterial agents are prescribed for children in the
U.S.
Direct and indirect cost $3 billion in 1995
Peak incidence in children age 6–18 mos
Otitis externa:
Acute (bacterial): 4 in 1,000 persons U.S. 90% unilateral
Chronic (fungal or allergic): 3–5% of population
Risk Factors
AOM:
Recent upper respiratory infection (URI) with eustachian tube dysfunction
Bottle feeding
Pacifier use after 6 mos of age
Passive smoking
Group child-care facility attendance
Previous episodes of acute otitis media, especially if first when <1 yr old
Sibling history of recent infection
Nonmodifiable risk factors: Genetic predisposition, male gender, premature birth, Native
American or Inuit ethnicity, family history of recurrent otitis media, presence of siblings in
the household
Otitis externa:
Aquatic athletes
High humidity, warm temperature
Local trauma (cotton swab use or hearing aids)
Eczema, allergic rhinitis, asthma, diabetes
General Prevention
Otitis externa:
Measures that are related to ear hygiene:
Avoid using cotton swabs or inserting objects into the external canal, including earplugs.
Avoid frequent washing of the ears with soap (leaves an alkali residue that neutralizes
the acidic pH of the ear canal).
Avoid swimming in polluted waters.
Empty water from the ear canals after swimming or bathing.
Prophylactic eardrops with a 2:1 ratio of 70% isopropyl alcohol and acetic acid assist in
drying and acidifying the ear canal after swimming.
Etiology
Usually eustachian tube dysfunction after viral URI, which results in fluid in the middle ear that
acts a culture medium for bacterial superinfection:
Most common bacterial causes (account for 95% of bacterial AOM):
Streptococcus pneumoniae (increased incidence of drug resistance 30–60% in some
communities)
Haemophilus influenzae
Moraxella catarrhalis
Less common bacterial causes:
Streptococcus pyogenes
Mycoplasma pneumoniae
Otitis externa:
Bacterial (91%): Pseudomonas aeruginosa (50%), Staphylococcus aureus (23%),
anaerobes and gram-negative organisms (12.5%)
Fungal: Aspergillus (90%) and Candida
Diagnosis
AOM:
Abrupt, rapid onset of signs and symptoms
Presence of middle ear effusion indicated by any of the following:
Bulging tympanic membrane (TM)
Limited/absent TM mobility
Air fluid level behind TM
Otorrhea: more specific to AOM
Signs or symptoms of middle ear inflammation indicated by:
Distinct erythema of TM, OR
Otalgia that interferes with normal activity or sleep, OR
Otalgia, irritability in an infant or toddler, fever, and URI symptoms (cough, nasal
discharge, or stuffiness) are nonspecific and occur in 90% with AOM and 72% without
AOM
Otitis media with effusion:
Absence of signs and symptoms of acute infection
Reduced hearing may be present
TM neutral or retracted in appearance; fluid in middle-ear space
Otitis externa:
Otalgia and discharge from external canal
History
AOM:
Patient with or without recent URI symptoms complains of otorrhea, otalgia, fever,
decreased hearing, or occasional vertigo
Other complaints: Anorexia, irritability, vomiting, diarrhea
May have history of otitis media
TM may spontaneously rupture, leading to resolution of pain.
Clinical history alone is poorly predictive of AOM, especially in younger children.
Otitis externa:
Otalgia
Aural fullness
Itching
Discharge: Initially clear and odorless, but then becomes purulent and foul-smelling
Tinnitus
Physical Exam
AOM:
TM bulging, full, red, and immobile; may be cloudy
TM rupture may lead to signs of otorrhea on examination.
May have tenderness in mastoid area
TM neutral or retracted
Fluid behind TM may be present.
May need tympanometry or acoustic reflectometry to confirm diagnosis
Otitis externa:
Tragal tenderness with manipulation
Erythematous and edematous external auditory canal
Purulent discharge
Eczema of auricle
Periauricular and cervical adenopathy

Tympanocentesis may be helpful in selected refractory or recurrent cases to make
microbiologic diagnosis.
AOM:
Redness: Crying, fever, cerumen removal with irritation of external canal
Earache: Referred pain from throat, jaw, teeth, other nearby structures
Tympanosclerosis
Mastoiditis:
Tenderness in mastoid area may be due to otitis media.
Otitis externa:
Foreign body
Mastoiditis
Herpes zoster
Treatment
AOM:
Usually treated empirically with antibiotics (see “Etiology”)
First line: Amoxicillin: 500 mg t.i.d. Peds: 80–90 mg/kg/day (American
Academy of Pediatrics/American Academy of Family Physicians 2004
treatment guidelines). Not effective against H. influenzae or M. catarrhalis
(B-lactamase producers).
Penicillin allergy: Erythromycin or trimethoprim-sulfamethoxazole. Cefdinir,
cefpodoxime, or cefuroxime if no type I hypersensitivity reaction.
Acetaminophen or ibuprofen for mild pain, and narcotic analgesics for
moderate-to-severe pain.
Tympanostomy
AOM with tympanic membrane rupture:
Oral antibiotics (amoxicillin or amoxicillin-clavulanate)
AOM treatment failures:
Switch in empiric therapy recommended after 48–72 hr if not responding
Drugs of choice: Amoxicillin-clavulanate (Augmentin), cefuroxime axetil
(Ceftin), and IM ceftriaxone (Rocephin)
Initial diagnosis may be confirmed with tympanometry; usually observe or
treat with oral antibiotic.
Decongestants, antihistamines, and oral steroids not indicated
May need tympanostomy tube following complete ear, nose, and throat (ENT)
evaluation
Otitis media and tympanostomy tubes:
Ciprofloxacin 0.3%/dexamethasone 0.1% 4 drops b.i.d. × 7 days
Otitis externa:
Bacterial: Gentamicin/betamethasone otic drop 2–3 drops q.i.d. × 7–10 days
or ciprofloxacin 0.3%/dexamethasone 0.1% 4 drops b.i.d. × 7 days
Fungal: Clotrimazole 1% otic sol 4 drops q.i.d. × 7–10 days
General Measures
Outpatient management except in cases requiring surgical intervention.
Modification of environmental risk factors (see “Risk Factors”)
Consider tympanocentesis for treatment failures, especially if several recent
courses of antibiotics; allows for pathogen-directed treatment.
Ongoing Care
Age 1–3 yrs:
If effusion present for >6 wks, consider hearing evaluation
If effusion present for >3 mos, need hearing evaluation and possible ENT referral for
tympanostomy tube (grommet) placement
Older individuals:
May need grommet placement after 3 mos following complete ENT evaluation to exclude
other causes of effusion
Complications
Otitis externa: Local purulent extension of disease, such as the following:
Necrotizing otitis externa
Mastoiditis
Chondritis of the auricle
Bony erosion of the base of the skull
CNS infection
Additional Reading
Gary JP. Otitis Externa. eMedicine. Updated Nov 30 2007.
Neff MJ, AAP, AAFP et al. AAP, AAFP, AAO-HNS release guideline on
diagnosis and management of otitis media with effusion. Am Fam Physician.
2004;69:2929–2931.
Neff MJ, American Academy of Pediatrics, American Academy of Family

Physicians. AAP, AAFP release guideline on diagnosis and management of
acute otitis media. Am Fam Physician. 2004;69:2713–2715.
Osguthorpe JD, Nielsen DR. Otitis externa: Review and clinical update. Am
Fam Physician. 2006;74:1510–1516.
Ramakrishnan K, Sparks RA, Berryhill WE. Diagnosis and treatment of otitis

media. Am Fam Physician. 2007;76:1650–1658.
Wright D, Safranek S. Treatment of otitis media with perforated tympanic

membrane. Am Fam Physician. 2009;79:650, 654
Sexton S, Natale R. Risks and benefits of pacifiers. Am Fam Physician.

2009;79:681–685.
Codes
ICD9
380.10 Infective otitis externa, unspecified
380.11 Acute infection of pinna
380.12 Acute swimmers' ear
Clinical Pearls
Diving should be avoided until normal TM mobility because of increased risk of
rupture at depths >4.3 ft.
Be careful with over-the-counter decongestants. Drugs containing ephedrine or
pseudoephedrine are banned by the International Olympic Committee. Sedating
antihistamines are banned by the IOC for shooting sports. If in doubt, call the
United States Anti-Doping Agency Drug Reference Line at 1–800–233–0393.
There is no evidence that athletes with grommets are at greater risk of
developing otorrhea; possible decreased incidence in swimmers vs
nonswimmers. Decreased incidence of infection with use of polymyxin B-
Neosporin-hydrocortisone (2 drops at night after swimming).
There is no evidence of decreased infection rate with earplug use. Surface
swimming only; increased pressure in diving may increase infection rate.
Overtraining
W. Scott Black
Robert G. Hosey
Basics
Description
Overreaching:
The accumulation of training and/or nontraining stress, which results in a short-term
decrease in performance capacity and may be accompanied by psychological symptoms.
Recovery of performance capacity and resolution of psychological symptoms can take
from several days to several weeks to occur (1).
Overtraining:
The accumulation of training and/or nontraining stress, which results in a long-term
decrease in performance capacity and may be accompanied by psychological symptoms.
Recovery of performance capacity and resolution of psychological symptoms can take
from several weeks to several months to occur. When being used to describe a clinical
entity, this is often referred to as the “overtraining syndrome” (OTS). Synonym(s) include
“unexplained underperformance syndrome,” “staleness,” and “burnout” (1).
Epidemiology
Overreaching is common and may be intentionally induced as part of a training regimen (1,2).
The prevalence of overtraining is not known, but it is thought to be uncommon (2) given the
large number of athletes participating in training programs at any given time. It is thought to
be most common among endurance athletes.
Risk Factors
Highly motivated athletes who respond to poor athletic performance by increasing training
loads
Athletes subjected to generic overload stimuli, without individualized training
Additional “nonathletic” stressors (social, economic, scholastic, relationship, etc.)
General Prevention
Daily training logs:
Helpful in determining the cumulative strain involved with training
To be useful in early detection of OTS, systematic documentation of subjective and
objective factors must be completed at baseline (when the athlete has no signs or
symptoms) and reevaluated regularly.
Although small daily variations occur in athletes, training logs can identify an individual
athlete's abnormal response to training at an early stage.
Once identified, interventions can be made to prevent further deterioration of performance
and normalization of subjective and objective criteria.
Training logs should include:
Daily workout schedule (including intensity, duration, and mode of training)
Rating of perceived exertion (RPE) for the entire training session on a specific day. This
can be done using the modified (category-ratio) Borg scale, which rates perceived effort
from 0 (nothing at all) to 10 (almost maximal) (3)
The product of the session RPE and session duration can be recorded and represents
an objective measurement of daily “training load” (3).
Some general description of sense of fatigue or overall state of well-being of the athlete
Proper coaching and training techniques:

Recognize overtraining early and intervene.
Avoid monotony in training.
Avoid punishing poor training performance with higher levels of training.
Training goals should be formulated on a week-to-week basis during times of increased
training.
Training loads should display day-to-day variability.
Alternate hard day/easy day and include 1 rest day per week (hard day = RPE >5; easy
day = RPE <5)
If athlete begins to show strain (performance decrements, increasing RPE at low-level
training), reduce training to a lower level.
Etiology
Historically, multiple pathophysiologic mechanisms have been proposed as causes for OTS:
Dysfunction of the autonomic nervous system (sympathetic or parasympathetic forms of
OTS), hypothalamic dysfunction (hypothalamic-pituitary-adrenal axis and hypothalamic-
pituitary-gonadal axis), reduced blood glutamine levels, decreased blood levels of branched-
chain amino acids, and glycogen depletion (1,4)
More recently, muscle trauma with resulting cytokine-mediated systemic inflammation has
been implicated (5).
Currently, there is no universally accepted hypothesis as to the cause of OTS.
Diagnosis
There is no single diagnostic test for OTS.
Blood testing if clinically indicated to rule out organic disease/“other” causes of fatigue
Profile of Mood States questionnaire may show an “inverse iceberg profile” (2).
Standardized Overtraining Questionnaire from the French Society for Sports Medicine scores
>20 are suggestive of overtraining. An English translation of this questionnaire has been
published (6).
Reduced performance on speed-endurance or short, high-intensity exercise tests (decreased
performance on time trials) is consistently found (1,2).
VO2MAX may be reduced, but unchanged values are not unusual.
Blood lactate at submaximal steady-state exercise and at maximal exercise may be reduced
from baseline.
Performance cerements when evaluating maximum sport-specific performance.
Increased perceived exertion at given workload
Decreased coordination
History
Consider:
Current training load: Intensity, frequency, duration, and/or mode of training
Historical training load over past several months
Any changes in “nonathletic” stressors (eg, financial problems, family illness, relationship
problems, scholastic concerns)
Any changes in sleep pattern
Recent exposure to infection
Changes in menstruation
Physical Exam
Because OTS is a spectrum of diseases, the clinical presentation varies among individual
athletes.
Subjective complaints of fatigue or “heavy legs”
Sleep disturbance
Oral temperature to rule out systemic infection
Evaluate resting heart rate and BP, including orthostatics.
Head/eyes/ears/nose/throat exam to evaluate possible upper respiratory infection/infectious
mononucleosis
Neck exam for adenopathy or thyroid abnormalities
Chest auscultation to evaluate for cardiopulmonary disease
Abdominal examination to evaluate spleen and liver
Neurologic examination to evaluate for neuromuscular disease
Major depression or other psychologic disorder
Eating disorder
Organic disease (mononucleosis, hypothyroidism, anemia)
Drug abuse
Treatment
General Measures
The primary treatment for OTS is relative or absolute rest, depending on the
severity of overtraining.
Mild cases may improve with a relative decrease in training load (frequency
and/or intensity), an increase in rest between training sessions, and/or an
increase in training variety (cross-training).
More severe cases may need weeks to months of absolute rest.
Occasionally, athletes never return to their previous level of function.
It has been suggested that some of the newer antidepressant medications
(selective serotonin reuptake inhibitors, noradrenaline reuptake inhibitors,
combination serotonin and noradrenaline reuptake inhibitors) might offer a
pharmacologic approach to the treatment of OTS (4).
Antidepressant medications are not approved for the use of OTS, and their use
for this purpose would be strictly off-label.
Antidepressant medications may cause problems with thermoregulation, so
caution should be used when treating athletes who will exercise in the heat (4).
References
1. Halson SL, Jeukendrup AE. Does overtraining exist? An analysis of
overreaching and overtraining research. Sports Med. 2004;34:967–981.
2. Urhausen A, Kindermann W. Diagnosis of overtraining: what tools do we
have? Sports Med. 2002;32:95–102.
3. Foster C. Monitoring training in athletes with reference to overtraining

syndrome. Med Sci Sports Exerc. 1998;30:1164–1168.
4. Armstrong LE, VanHeest JL. The unknown mechanism of the overtraining

syndrome: clues from depression and psychoneuroimmunology. Sports Med.
2002;32:185–209.
5. Smith LL. Cytokine hypothesis of overtraining: a physiological adaptation to

excessive stress? Med Sci Sports Exerc. 2000;32:317–331.
6. Elloumi M, El Elj N, Zaouali M, et al. IGFBP-3, a sensitive marker of physical

training and overtraining. Br J Sports Med. 2005;39:604–610.
Codes
ICD9
780.79 Other malaise and fatigue
Panner Disease and OCD of Elbow Capitellum
John J. Wilson
Nadim Ilbawi
Basics
Panner's disease and osteochondritis dissecans, conditions of the pediatric elbow, are
commonly the result of overuse, particularly in the young throwing athlete and gymnasts.
Description
Panner's disease (osteochondrosis) and osteochondritis dissecans (OCD) of the capitellum are
overuse injuries of the elbow found in children and adolescents (respectively) that involve
disordered endochondral ossification of the humeral capitellum.
Epidemiology
Occur most commonly in the dominant arm
Boys affected more often than girls
Panner's disease occurs most commonly before the age of 10
OCD of the capitellum mainly in adolescents:
Average patient age is between 12 and 17 yrs
<5% are bilateral
Lesions of the capitellum are most common, but disorders of the radial head, trochlea,
olecranon, and olecranon fossa have also been described.
Risk Factors
Precise etiology is not well established.
Lateral compression and shear forces are applied to the radiocapitellar joint during the late
cocking and early acceleration phases of throwing and racquet sports.
Increased weight-bearing and axial impact loads across the upper extremity are seen in
young gymnasts and weightlifters.
Repetitive compressive forces may compromise vulnerable blood supply to capitellum and
result in articular cartilage breakdown and fragmentation of subchondral bone.
Genetics
A genetic predisposition has been hypothesized.
General Prevention
Proper throwing technique in overhead throwing athletes
Adequate rest from activities that cause repetitive microtrauma to the lateral elbow
Etiology
Panner's disease:
Articular osteochondrosis
Articular chondrocyte viability may be compromised by repetitive compressive loading.
Ossific nucleus of capitellum has a tenuous blood supply, which may be vulnerable to
stresses at the elbow.
OCD of the elbow capitellum:
Disordered growth of articular cartilage and subchondral bone resulting in spontaneous
osteonecrosis and formation of osteochondral fragments
Histopathological examination has failed to demonstrate inflammatory reaction.
Likely a result of repetitive compressive forces exerted across the radiocapitellar joint
during a time of epiphyseal vulnerability
Diagnosis
History
Often insidious onset of elbow pain with activity:
Acute, sudden onset is rare.
Pain is relieved with rest.
Pain is often lateral, but diffuse pain can occur.
Restricted range of motion is common.
Other symptoms: Stiffness, swelling, clicking, catching, grinding, locking
Physical Exam
Tenderness over radiocapitellar joint
Loss of extension; 15–30° is common:
Loss of flexion less common
Pronation, supination usually unaffected
Effusion may be present.
Crepitus may be present with active or passive pronation and supination.
Pain with radiocapitellar compression test:
Arm actively pronated and supinated with elbow fully extended

Lab
Not indicated unless other underlying etiology suspected (eg, infectious, endocrine)
Imaging
Plain radiographs:
Obtain anteroposterior and lateral elbow radiographs:
May be compared to contralateral elbow to detect subtle changes of capitellum
Able to demonstrate interval healing
Panner's disease: Fissuring, radiolucency, decreased size, flattened articular surface,
sclerosis, and loose bodies may be visualized at capitellum:
Grade I: Translucent shadow in middle or lateral capitellum
Grade II: Clear line or demarcation between lesion and subchondral bone
Grade III: Presence of loose bodies
OCD of capitellum:
Focal lucency in subchondral bone in anterolateral capitellum
Similar appearance to Panner's; loose bodies and capitellar flattening more common in
OCD
Low sensitivity to detect OCD and loose bodies; 66% and 57%, respectively:
MRI considered standard imaging modality for additional assessment.
MRI (1):
Imaging modality of choice
Capable of detecting early lesions not visible on plain radiographs
Useful for lesion characterization of size and extent
Allows assessment of lesion stability and integrity of articular cartilage:
Unstable lesions demonstrate peripheral ring of high-signal intensity or an underlying
fluid-filled cyst on T2-weighted images
Able to demonstrate interval healing and lesion resolution
CT arthrography:
Useful for confirming presence of intra-articular loose bodies
Depicts cartilage integrity and fissuring
US:
Able to assess subchondral bone and overlying cartilage integrity
Operator-dependent imaging modality
Radionucleotide bone scan:
Very sensitive, but nonspecific for Panner's and OCD of the capitellum
Limited usefulness in the diagnosis and staging of these conditions
Elbow arthroscopy allows direct visualization of the articular cartilage surface for staging:
May fail to identify changes of the capitellum not evident at joint surface
Trochlear lesions (avascular necrosis, osteochondritis dissecans of the elbow trochlea)
Distal humerus fracture
Posterolateral elbow impingement
OCD of the radial head
Angular deformity of the radial neck
Treatment
Medication
Analgesics and NSAIDs may be used as necessary for pain relief.
Little evidence exists for duration of treatment, bracing, or physical therapy for
these conditions:
Panner's disease:
Rest from offending activities and avoidance of radiocapitellar joint loading
for 3–6 mos
Immobilization for 3–4 wks may provide early pain relief.
Nonoperative treatment provides excellent long-term prognosis.
Surgery rarely necessary
OCD of the capitellum:
Rest from offending activities and avoidance of radiocapitellar joint loading
for 3–6 mos:
Some advocate for hinged unloader elbow brace to avoid excessive valgus
stress.
Immobilization for 3–4 wks may provide early pain relief.
Nonoperative treatment is recommended for early, intact, and stable lesions.
Conservative monitoring with serial radiographs is reasonable in skeletally
immature patients, often with successful resolution of stable OCD lesions
over a period of weeks to months.
Patients with stage 3–4 lesions on MRI, particularly in the presence of a
loose body, is an indication for early surgical referral.
In skeletally mature patients with symptomatic OCD, early referral for surgical
consultation is recommended.
Referral
Panner's disease:
Persistent pain or symptoms despite appropriate conservative care
OCD of the capitellum:
Persistent pain or symptoms despite appropriate conservative care
Symptomatic loose bodies
Articular cartilage fracture
Unstable, loose, or displaced osteochondral lesion
Operative management is indicated for the following reasons (2)[C]:
Failure of appropriate conservative management
Mechanical symptoms
Intra-articular loose bodies
Unstable lesions
Operative techniques vary, include the following:
Loose body or unstable fragment removal
Fixation of unstable osteochondral fragment
Chondroplasty
Autologous chondrocyte implantation
Subchondral drilling
Closing wedge osteotomy of the lateral epicondyle
Ongoing Care
Patient Monitoring
Return to activity:
Gradual progressive return to activity and sports can begin after a period of rest when
patient is asymptomatic.
Physical therapy may begin when symptoms improve:
Range of motion, stretching, and gentle strengthening while avoiding radiocapitellar stress
Evidence of healing should be evident on follow-up radiographs or MRI before return of
elbow loading:
Serial radiographs performed at 6-wk intervals are useful to document healing or
progression.
MRI follow-up 6 mos after initiation of conservative management to document lesion
healing; consider imaging at 1 yr
Athlete should be monitored closely by health care team during return to sport:
Progress activity as tolerated, gradually increasing weight-bearing and load across lateral
elbow.
Rest and resumption of activity avoidance if symptoms return
For pitchers, recommend strict adherence to established pitch count recommendations.
It is important to establish good core strength to improve sport mechanics and potentially
decrease loading of the radiocapitellar joint.
Patient Education
Instruct patients on importance of proper sport technique.
Strict adherence to pitch counts upon return to pitching
Re-evaluation is necessary for return of elbow symptoms after return to sport.
Consider activity modification to decrease elbow loading following recovery.
Prognosis
Favorable prognostic factors (3)[C]:
Open capitellar physis
Age <10
Normal elbow range of motion
Absence of mechanical symptoms
Stable lesion with radiographic findings of subchondral lucency or flattening
Poor prognostic factors:
Closed capitellar physis
Age >10
Loss of elbow extension
Mechanical symptoms
Unstable lesion or loose bodies
Large fragment involving >50% of capitellum
Complications
Many patients will have persistent loss of extension despite good clinical
outcome with return to sport.
Early degenerative joint disease and continued symptoms of pain and stiffness
are more likely in advanced cases.
References
1. Kijowski R, De Smet AA. MRI findings of osteochondritis dissecans of the
capitellum with surgical correlation. AJR Am J Roentgenol. 2005;185:1453–
1459.
2. Baker CL, Romeo AA, Baker CL. Osteochondritis dissecans of the

capitellum. Am J Sports Med. 2010.
3. Kobayashi K, Burton KJ, Rodner C, et al. Lateral compression injuries in

the pediatric elbow: Panner's disease and osteochondritis dissecans of the
capitellum. J Am Acad Orthop Surg. 2004;12:246–254.
Codes
ICD9
Clinical Pearls
Panner's disease and OCD of the elbow capitellum are common causes of
elbow disability in young adolescent athletes.
Repetitive overuse of the elbow, such as in throwing sports, gymnastics, and
weightlifting, are known risk factors.
Clinical suspicion warrants evaluation with plain radiographs and MRI.
Early, stable lesions can be treated with prompt rest and nonoperative
treatment with favorable results and return to activity.
Patients with advanced unstable lesions, loose bodies, mechanical symptoms,
or failed conservative management are candidates for operative treatment.
Paronychia
Krystian Bigosinski
Basics
Description
Infectious inflammation of the folds of skin surrounding the fingernail or toenail; may be acute
or chronic
System(s) affected: Skin/Exocrine
Genetics: No known genetic pattern
Synonym(s): Eponychia; Perionychia
Epidemiology
Incidence
Incidence/prevalence in U.S.: Common
Predominant age: All ages
Predominant gender: Female > Male (3:1)
Risk Factors
Acute: Trauma to skin surrounding nail, retained foreign body, ingrown nails
Chronic: Frequent immersion of hands in water, diabetes mellitus, artificial nail placement
May be considered work-related in bartenders, waitresses, nurses, and others who often
wet their hands
General Prevention
Chronic: Avoid frequent wetting of hands. Wear rubber gloves with cloth liner.
Good diabetic control
Etiology
Acute: Staphylococcus aureus; less frequently, Streptococcus spp., Pseudomonas spp., and
herpes simplex
Chronic: Candida albicans; less frequently, fungi—dermatophytes and, occasionally, molds
(Scytalidium, Fusarium)
Diabetes mellitus
Diagnosis
Special tests: None
Diagnostic procedures: N/A
Physical Exam
Separation of nail fold from nail plate
Red, painful swelling of skin around nail plate
Purulent and fluctuant
Deformity of nail plate
Green changes in nail (Pseudomonas)

Lab
Gram stain
Culture and sensitivity
Potassium hydroxide preparation plus fungal culture
Drugs that may alter lab results: Use of OTC antimicrobials or antifungals
Herpetic whitlow
Felon
Reiter disease
Psoriasis
Treatment
Long-term treatment
Medication
First Line
Acute (if diabetic, suppurative, or more severe cases):
Amoxicillin-clavulanate 500–875 mg q12h
Clindamycin 150–450 mg q6h
Trimethoprim-sulfamethoxazole 160 mg/800 mg q12h
Dicloxacillin 125–500 mg q6h
Cloxacillin 250–500 mg q6h
Erythromycin 500 mg q6h
Cephalexin (Keflex) 250 mg q6h
Chronic:
Bacterial: Mupirocin (Bactroban)
Yeast or dermatophyte: Topical imidazoles (econazole, ketoconazole,
terbinafine)
Systemic: P.
Itraconazole (Sporanox) 200 mg/day × 90 days (may have longer action
because incorporated in nail plate); pulse therapy may be useful: 200 mg
b.i.d. × 7 days, repeated monthly for 2 mos
Terbinafine (Lamisil) 250 mg/day × 90 days
Fluconazole (Diflucan) 150 mg/wk × 4–6 mos
Viral (consider in wrestlers, rugby players): Acyclovir 400 mg q8h
Contraindications: Allergy to antibiotic
Precautions: Erythromycin may cause significant GI upset.
Significant possible interactions:
Erythromycin affects levels of theophylline and effects of carbamazepine,
digoxin, and corticosteroids. Cardiac toxicity is seen with terfenadine or
astemizole.
Ketoconazole, astemizole, itraconazole, fluconazole, terfenadine
Second Line
Antipseudomonal drugs, eg, 3rd-generation cephalosporin, aminoglycosides
General Measures
Acute: Warm compresses, protection of affected digit with splint
Chronic: Keep fingers dry.
Incision and drainage (I&D) of abscess, if present
If a subungual abscess or ingrown nail is present, will need partial or complete
removal of nail
Ongoing Care
Full activity
Patient Monitoring
Routine follow-up until healed
Diet
No special diet
Patient Education
Chronic: Keep fingers dry.
Prognosis
With adequate treatment and prevention, healing can be expected.
Complications
Acute: Subungual abscess
Chronic: Secondary ridging, thickening, and discoloration of nail, nail loss
Additional Reading
Baran R, Dawber RPR, eds. Diseases of the nail and their management. 2nd
Ed. Boston: Blackwell Scientific, 1994.
Brook I. Aerobic and anaerobic microbiology of paronychia. Ann Emerg Med.

1990;19:994–996.
Fitzpatrick TB, et al, eds. Dermatology in general medicine. 3rd Ed. New
York: McGraw-Hill, 1987.
Hochman LG. Paronychia: more than just an abscess. Int J Dermatol.

1995;34:385–386.
Moschella SC, Hurley HJ, eds. Dermatology. 3rd Ed. Philadelphia: W.B.
Saunders Co., 1992.
Anaerobes may be involved in patients with thumb/finger sucking.
Codes
ICD9
112.3 Candidiasis of skin and nails
681.02 Onychia and paronychia of finger
Patellar Dislocation and Instability
Keith A. Stuessi
Brent R. Becker
Basics
Description
Patellar instability is defined as hypermobility of the patella in either the medial or lateral
direction.
Medial instability is extremely rare.
Complete dislocation and subluxation represent variations in severity of instability.
Acute dislocation typically occurs with a twisting injury and strong contraction of the
quadriceps; rarely it is due to direct trauma to the medial aspect of the patella.
Risk Factors
Prior history of subluxed or dislocated patella
Recurrence rate 15–50% after initial dislocation
Adolescent females
Patella alta (“high-riding patella”)
Excessive genu valgum
Weak vastus medialis
Excessive tibial torsion
Family history of patellar instability
Trochlear dysplasia
Lateralized tibial tuberosity
Risk factors associated with developmental dysplasia (1st-born girl, high birth weight, deliver
by C-section, breech delivery)

Avulsion fracture of the superior medial pole of the patella
Osteochondral fractures of the lateral femoral condyle or posterior patellar articular surface
Tear of the medial patellofemoral ligament
Concomitant major ligamentous or meniscal injury
Diagnosis
Pre Hospital
Patient has severe pain and may have heard a pop at time of dislocation.
Knee is usually held in 20–30 degrees of flexion, and patella is palpable laterally.
Acutely swollen knee
Hemarthrosis
Tenderness to palpation over the medial edge of patella
Tenderness just proximal to medial femoral epicondyle
Consider subluxation if:
History is consistent of a dislocation but pain and examination findings have resolved
Look for patella alta (high-riding patella) or laterally displaced patella.
History
Initial or recurrent?
History of previous knee injury or patellofemoral pain syndrome?
Does your patella feel like it is slipping or moving laterally on certain movements?
Do you have swelling?
Physical Exam
Immediately after dislocation, may show patella dislocated laterally and prominence medially
due to uncovered medial femoral condyle
Obvious effusion
Tenderness most apparent over the medial retinaculum and vastus medialis
Limited range of motion with knee in extended position
Fear of redislocation when knee is flexed
Positive apprehension sign with movement of patella laterally
Check ACL and meniscus, as up to 12% of patellar dislocations have associated major
ligamentous or meniscal injury.
“J” sign: Seated patient straightens the knee; the patella moves outward instead of straight
upward.

Imaging
Standard anteroposterior, lateral, and patellar views (“sunrise” or “tunnel” view)
Sunrise view mandatory. Rule out presence of associated osteochondral fractures. Avulsion
fracture or calcification along the medial edge of the patella is considered pathognomonic for
patellar dislocation
CT more sensitive than plain films for identifying patellar malalignment
MRI more informative than CT, as it can evaluate articular cartilage
Subluxation vs dislocation
Although history of patellar dislocation is fairly classic, consider other entities that cause early
effusions, eg, anterior cruciate ligament (ACL) tear, meniscal tear, and tibial plateau
fractures.
Treatment
If not reduced spontaneously, may require conscious sedation for pain
control and muscle relaxation
Alternatively, arthrocentesis performed with instillation of 10–15 mL of lidocaine
and/or bupivacaine
Extension of the leg with hip flexed (reduces tension of quadriceps tendon)
Gentle pressure on patella directed lateral to medial
Postreduction radiographs to confirm reduction and rule out fractures
Examine anterior ACL and medial and lateral menisci to rule out accompanying
tears.
After reduction, rest, ice, focal compression, and elevation are indicated for the
1st 24–48 hr.
Knee immobilization is maintained for 2–3 wks, although early passive range
of motion in terminal extension is allowed to minimize disuse atrophy.
Hinged brace may be substituted for knee immobilizer as early as 1 wk.
Medication
Trial of NSAIDs drugs
Tylenol
Referral
Orthopedic referral indicated if:
Osteochondral fracture noted on either plain radiographs or MRI
Recurrent patellar dislocations despite adequate rehabilitation, especially in
younger patients (<14 yrs old), in whom recurrence rates can reach 60%
Evidence of joint locking
High-risk athlete participates in activities involving pivoting and is at increased
risk of recurrent patellar dislocation
A significant number of patients develop large hemarthrosis. Aspiration may be
considered after 48–72 hr, both to relieve pain and to check for fat globules,
which might help diagnose an occult osteochondral fracture.
Isometric quadriceps exercises are begun as soon as possible, although it is
often difficult and painful for the athlete to produce a contraction that involves
the vastus medialis.
Active range of motion exercises (closed chain) are started at 1 wk and
physical therapy consultation given for medial quadriceps strengthening (vastus
medialis oblique).
Knee immobilizer or hinged brace is used for ambulation until 100 degrees of
painless flexion is present, there is no effusion, and a normal heel-to-toe gait is
possible.
Immobilizer or hinged brace ultimately is replaced with a neoprene sleeve with a
lateral buttress until normal, painless activities of daily living are possible.
Rehabilitation alone appears to be effective as operative treatment that is
followed by rehabilitation in children under 16 yrs with patellofemoral instability
(1)[A].
Typically patients who fail a conservative trial of 6 mos become surgical
candidates.
Surgical management includes lateral retinacular release alone, proximal
extensor mechanism realignment alone, or combined proximal and distal
realignment.
Minimally invasive patellar realignment includes lateral retinacular release and
plication of the medial retinaculum.
Minimally invasive patellar realignment improves morbidity and recovery when
compared with open realignments (2)[C].
References
1. Palmu S, Kallio PE, Donell ST, et al. Acute patellar dislocation in children
and adolescents: a randomized clinical trial. J Bone Joint Surg Am.
2008;90:463–470.
2. Andrish J. The management of recurrent patellar dislocation. Orthop Clin

North Am. 2008;39:313–327, vi.
Additional Reading
Drez D, Delee JC, eds. Orthopaedic sports medicine: principles and
practices. Philadelphia: WB Saunders, 1994.
Garth WP, Pomphry M Jr, Merrill K. Functional treatment of patellar dislocation

in an athletic population. Am J Sports Med. 1996;24:785–791.
Iobst CA, Stanitski CL. Acute knee injuries. Clin Sports Med. 2000;19:621–
635, vi.
Kilgore KP. The knee: patellar dislocation. In: Ruiz E, Cicero JJ, eds.
Emergency management of skeletal injuries, 1st ed. St. Louis: Mosby-Year
Book, 1995.
Roberts DM, Stallard TC. Emergency department evaluation and treatment of

knee and leg injuries. Emerg Med Clin North Am. 2000;18:67–84, v–vi.
Codes
ICD9
718.86 Other joint derangement, not elsewhere classified, involving lower leg
836.3 Dislocation of patella, closed
Clinical Pearls
Return to sports: Evidence of adequate healing (absence of sensations of
instability, lack of effusion, and absence of pain on patellofemoral compression)
and adequate function (able to perform rotational movements such as pivoting,
cutting, and twisting without evidence of instability). Athlete may need McConnell
taping or patellar stabilizing braces to accomplish this.
Patellar/Quadriceps Tendinitis
Stephen Huang
Thomas Kern
Basics
Description
Overuse syndrome of the patellar tendon/quadriceps complex
Anterior knee pain worsened by activity such as jumping or running
Also termed “jumper's knee”
Epidemiology
Prevalence
Commonly seen in athletes who participate in sports with excessive jumping or running
(volleyball, basketball, soccer, track and field)
Prevalence is estimated to be 40–50% among high-level volleyball players, and 35–40%
among elite basketball players (1,2)
Affects males and females equally
Risk Factors
Participation in a sport with excessive “jumping” (volleyball, basketball)
Risk increases with training volume and intensity (3).
Poor flexibility of quadriceps and hamstrings
Etiology
Histopathology shows (4):
Collagen degeneration and disorganization
Increase in mucoid ground substance
Fibroblast proliferation
Neovascularization
Absence of inflammatory cells
More accurately termed tendinosis or tendinopathy
Diagnosis
History
Anterior knee pain exacerbated by activity or by prolonged knee flexion
Participation in a sport with excessive jumping
A progressive condition of anterior knee pain (Blazina classification) (5):
Phase 1: Pain after activity
Phase 2: Pain during and after activity not affecting performance
Phase 3: Pain during and after activity impeding performance
Physical Exam
Localized tenderness at the inferior pole of the patella and patellar tendon
Pain reproduced with extension of the knee vs resistance, or with maximal stretching of the
quadriceps
Poor flexibility of the quadriceps and hamstrings

Imaging
Patellar tendinopathy remains a clinical diagnosis, and routine imaging is neither required nor
recommended.
Plain film radiographs may show occasional intratendinous calcification.
MRI may reveal increased signal within the patellar tendon at the junction with the patella (4).
US may reveal focal hypoechoic areas in the patellar tendon or neovascularization on color
Doppler flow (4).
The study of choice and relevance of abnormalities remains controversial.
Hoffa's disease (fat pad impingement)
Osgood-Schlatter disease
Chondromalacia
Treatment
Medication
Conservative measures typically include relative rest (reduction in amount or
intensity of training to achieve pain-free state), ice, and NSAIDs
NSAIDs are commonly used as analgesics and may be beneficial for acute
symptoms. However, there is a lack of evidence showing benefits in cases of
chronic patellar tendinopathy.
Consider physical therapy for chronic symptoms.
General Measures
Stretching exercises of the quadriceps and hamstrings to improve flexibility
Eccentric strengthening exercises of the quadriceps
Correction of biomechanical abnormalities or training errors
The early results are promising for several other types of treatments, which
theoretically re-create the inflammatory response or restart the failed healing
process:
Deep friction massage
Platelet-rich plasma injections
Prolotherapy
Patellar tenotomy may be considered for patients who fail conservative
measures for 6 mos.
No randomized trials have been able to show the efficacy of one surgical
technique over others.
Ongoing Care
Steroid injections into a tendon should be avoided due to the risk of tendon rupture.
References
1. Bahr R, Fossan B, Løken S, et al. Surgical treatment compared with eccentric training for
patellar tendinopathy (jumper's knee). A randomized, controlled trial. J Bone Joint Surg Am.
2006;88:1689–1698.
2. Lian OB, Engebretsen L, Bahr R. Prevalence of jumper's knee among elite athletes from
different sports: a cross-sectional study. Am J Sports Med. 2005;33:561–567.
3. Peers KH, Lysens RJ. Patellar tendinopathy in athletes: current diagnostic and
therapeutic recommendations. Sports Med. 2005;35:71–87.
4. Khan KM, Bonar F, Desmond PM, et al. Patellar tendinosis (jumper's knee): findings at
histopathologic examination, US, and MR imaging. Victorian Institute of Sport Tendon Study
Group. Radiology. 1996;200:821–827.
5. Blazina ME, Kerlan RK, Jobe FW, et al. Jumper's knee. Orthop Clin North Am.
1973;4:665–678.
Additional Reading
Rees J, Maffulli N, Cook J. Management of Tendinopathy. Am J Sports Med. 2009.
Codes
ICD9
726.64 Patellar tendinitis
Patellar/Quadriceps Tendon Rupture
Warren Bodine
Basics
Description
Partial or complete rupture of the patellar or quadriceps tendon
Synonym(s): Extensor mechanism disruption
Epidemiology
In the general population, quadriceps and patellar tendon ruptures are the 2nd and 3rd most
common cause of extensor mechanism disruption, respectively (following patellar fracture).
Both have increased in prevalence in recent decades but remain rare.
True incidence and prevalence not known, but in a higher-risk active-duty military population,
the incidences of patellar and quadriceps tendon ruptures were 13 and 4 per 100,000,
respectively (1).
Patellar tendon ruptures are more common in athletes and individuals <40 yrs of age.
Complete quadriceps tendon ruptures are more common in those >40 yrs of age.
Ruptures most commonly occur unilaterally; systemic disease increases the risk of bilateral
ruptures.
Ethnicity may influence incidence and prevalence, with blacks and Hispanics more
predisposed to tendon ruptures than whites (1).
Risk Factors
Trauma
History of patellar/quadriceps tendinosis or patellar spurs
High-power sports (eg, high jump, basketball, weight lifting)
Steroid injection in the patellar or quadriceps tendon
Fluoroquinolone use in previous 6 mos
Diabetes mellitus
Hyperparathyroidism
Chronic kidney disease
Uremia
Obesity
Gout
Previous total-knee arthroplasty, ACL reconstruction using patellar autograft or excision of
tendinosis
Etiology
Most commonly due to eccentric overload of myotendinous unit with foot planted and knee
partially flexed, as occurs in landing from a jump or fall.
Patellar tendon ruptures usually are complete, occurring most commonly at the
osseotendinous junction in athletic trauma versus midsubstance in those with systemic
disease (2).
Quadriceps tendon ruptures usually occur distally, through pathologic tissue 0–2 cm from the
superior patellar pole. Pathologic changes are most commonly degenerative in nature (2).
Chronic tendinosis, corticosteroids, fluoroquinolones, and systemic disease change tendon
structure, decreasing its failure point.

Jumper's knee/tendinopathy
Patellar spurs
Quadriceps injury
Diagnosis
History
Mechanism of injury: Specifically jumping, stumbling, or slipping
Hearing or feeling “pop” or tearing sensation
Immediate, disabling pain
Difficulty straightening or bearing weight on affected extremity
Acute onset of swelling
History of chronic patellar or quadriceps tendinosis
History of steroid injection in tendon
Recent fluoroquinolone use
Physical Exam
Diffuse swelling or effusion
Ecchymosis, possible hemarthrosis
Patella alta in complete patellar tendon rupture
Patella baja in complete quadriceps tendon rupture
Palpable defect (may be masked by swelling acutely or by scar tissue in delayed evaluation)
Tenderness to palpation over patellar poles, retinaculum, or tibial tuberosity
Pain with knee flexion
Inability to actively achieve full extension/having significant extension lag
Absence of/altered patellar tendon reflex
Altered gait if able to bear weight
Quadriceps atrophy (in chronic cases)

Lab
Laboratory studies are rarely indicated but, depending on history and physical exam, may be
performed to evaluate for associated risk factors.
Imaging
Plain radiographs:
Diagnosis usually based solely on history, physical exam, and plain radiographs.
Obtain anteroposterior, lateral, tunnel, and patellar (sunrise or Merchant) views.
Contralateral films allow comparison of patellar height.
Superior or inferior patellar migration without fracture is conclusive for rupture.
Avulsion fractures may occur at the superior or inferior patellar poles or the tibial
tuberosity.
US:
More commonly performed in Europe than U.S.
High-resolution US shows hypoechogenicity in acute tears, tendon thickening, and
heterogeneous echotexture in chronic tears.
MRI:
May be performed if diagnosis cannot be made by clinical and radiographic examination
Findings include tendon fiber disruption with associated edema or hemorrhage.
Pathologic changes usually are degenerative, including hypoxic degenerative tendinopathy,
mucoid degeneration, tendolipomatosis, and calcifying tendinopathy (2)[B].
Fracture
Muscular strain (grade I or II)
Meniscal or ligamentous pathologies
Treatment
Immobilization of knee with straight-leg immobilizer, ice, elevation, and
crutch-assisted ambulation in the immediate setting.
Immobilization and crutch use should be continued until evaluation and, if
indicated, surgical intervention is completed (3)[C].
Incomplete tendon ruptures:
Most can be treated nonoperatively with immobilization and protected
ambulation for 6 wks (3)[B].
Immobilizer can be discontinued when patient can perform straight-leg raise
without discomfort (3)[B].
Surgery is indicated for complete ruptures or for incomplete ruptures failing
to respond to nonoperative treatment.
Referral
Patients should be referred for orthopedic evaluation as soon as a
patellar/quadriceps tendon rupture is suspected to decrease complications (4)
[B].
Surgery is necessary for all complete ruptures to restore the extensor
mechanism of the knee; it is also indicated for partial ruptures failing
nonoperative treatment.
Repair should occur as soon as possible, preferably within 2 wks. Delays >6
wks complicate surgical intervention and lead to poorer outcomes (3)[B].
The exact surgical intervention depends on which portion of the extensor
mechanism was disrupted and the acuity of the injury.
If ruptures are several months old, semitendinosus tendon or synthetic graft
may be used in the repair.
Postoperative rehabilitation:
Based on quality of tissue and extent of repair
Traditionally, a straight-leg cast was in place for 6 wks regardless of repair
technique; postoperative knee braces with motion control and extension
locks are now favored, with motion increased by 10–15 degrees weekly (3)
[C].
Weight-bearing as tolerated is permitted.
Straight leg raising typically begins at 3 wks, with cast or brace advancement
at 6 wks (3)[C].
Ambulation without assistance is initiated when motion and strength have
returned (3)[C].
Comprehensive physical therapy program should be completed before return
to athletics.
Ongoing Care
Patient Education
Reasonable function can be obtained in most individuals, especially in the acute tendon
rupture that is repaired immediately.
Most patients can return to their previous occupation, but many have difficulty returning to
their preinjury athletic level, particularly with quadriceps tendon ruptures.
Prognosis
Outcome after repair is closely related to the length of time between injury and repair, the
quality of the preexisting tissues, and the tendon healing at the proper length and tension.
If the tendon is repaired immediately, most patients experience nearly full return of knee
motion.
Complications
Loss of flexion is common after quadriceps tendon rupture.
Extensor mechanism weakness
Postoperative infection
Degenerative change at the patellofemoral joint
References
1. White DW, Wenke JC, Mosely DS, et al. Incidence of major tendon
ruptures and anterior cruciate ligament tears in U.S. Army soldiers. Am J
Sports Med. 2007.
2. Kannus P, Józsa L. Histopathological changes preceding spontaneous

rupture of a tendon. A controlled study of 891 patients. J Bone Joint Surg Am.
1991;73:1507–1525.
3. Greis PE, Holmstrom MC, Lahav A. Surgical treatment options for patella
tendon rupture, Part I: Acute. Orthopedics. 2005;28:672–679; quiz 680–681.
4. Ilan DI, Tejwani N, Keschner M, et al. Quadriceps tendon rupture. J Am

Additional Reading
Griffin LY, ed. Sports Medicine. Rosemont, IL: American Academy of
Orthopaedic Surgery, 1994.
Hardy JR, Chimutengwende-Gordon M, Bakar I. Rupture of the quadriceps

tendon: an association with a patellar spur. J Bone Joint Surg Br.
2005;87:1361–1363.
Matava MJ. Patellar tendon ruptures. J Am Acad Orthop Surg. 1996;4:287–

296.
Shah MK. Outcomes in bilateral and simultaneous quadriceps tendon rupture.

Orthopedics. 2003;26:797–798.
Codes
ICD9
727.65 Nontraumatic rupture of quadriceps tendon
727.66 Nontraumatic rupture of patellar tendon
Clinical Pearls
Rupture of the extensor mechanism is an uncommon yet disabling injury
requiring prompt diagnosis and early surgical management.
Misdiagnosis of quadriceps tendon rupture is common, occurring in 10–50%
(4).
Suspect patellar or quadriceps tendon rupture in any patient with acute knee
pain and inability to actively extend the knee.
Patellofemoral Pain Syndrome (PPS)
Christopher D. Meyering
Basics
Description
Overuse injury with pain located around or behind the patella
Multifactorial in origin resulting in biomechanical changes in normal alignment of the patella
Synonym(s):
Chondromalacia patella (term frequently used synonymously in older literature; a subset of
anterior knee pain related to softening and damage to the articular cartilage)
“Runner's knee”
Epidemiology
Anterior knee pain represents 20–40% of all knee problems.
Most common running injury presenting to a sports medicine clinic
Risk Factors
Recent increase or change in training/activity
Deviations of normal rollover pattern of foot (ie, excessive or insufficient pronation)
Patellar hyper- or hypomobility
“Miserable malalignment syndrome” (ie, increased femoral anteversion, inward-looking
patella, external tibial torsion, pronated feet, and bayonet sign)
Valgus deformity of the leg
Vastus medialis oblique (VMO) muscle strength deficit relative to vastus lateralis
Varus position of the subtalar joint
Gluteus medius inhibition or dysfunction; leads to decreased hip control and greater femoral
adduction and/or internal rotation
Family history of patellofemoral or anterior knee pain
Q-angle formerly felt to be a significant risk factor, but multiple studies have not seen any
significant correlation when comparing symptomatic and asymptomatic individuals

Chondral injury, especially with history of blunt trauma
Increased residual laxity or tearing of the medial patellar stabilizers with lateral dislocation of
the patella
Diagnosis
History
Recent changes in activity frequency, type, and intensity
Duration of wearing and changes to current exercise footwear
Past effusion, if knee currently not swollen. Effusion is not a typical finding of patellofemoral
pain syndrome (PFPS). Its presence is likely related to other pathology, although PFPS
cannot be excluded.
Subluxation vs dislocation episodes and/or history of direct trauma
Prior treatments, including NSAIDs, taping, physical therapy, orthotics, injections, or surgery
The presence of crepitus is not helpful to make a diagnosis, as most healthy women and
almost half of healthy men also have crepitus on exam.
Physical Exam
Insidious onset of anterior knee pain with activity
Pain around or behind the patella with one or more of the following activities: prolonged
sitting, squatting, stair climbing, running, kneeling, hopping/jumping
In-line “giving way” of the knee secondary to pain and not ligamentous or tendinous deficiency
Physical examination tests have been reported to have sensitivities <50%, although
specificity for some tests have ranged from 72–100% (1)[B].
Evaluate gait and overall limb alignment, as mentioned in “Risk Factors.”
Note any atrophy of the lower extremity, especially VMO.
Assess strength of gluteus medius using Trendelenburg test or side-lying hip abduction test.
Examine flexibility of quadriceps (Thomas' test), iliotibial band (Ober's test), hamstring
(popliteal angle test), hip (Thomas' test), and gastrosoleus (ankle range of motion).
Assess for presence of crepitus or J-sign (abrupt lateral motion of patella with full extension)
during active flexion and extension of the knee.
Assess for patella alta, patella baja, squinting patella, or grasshopper eyes (proximal and
lateral patellar rotation).
Rule out patellar and quadriceps tendinopathy, ligamentous instability, and meniscal
pathology.
Evaluate the prepatellar, infrapatellar, and pes anserine bursae and presence of joint
effusion.
Examine for patellar facet and retinaculi tenderness. Tenderness over lateral retinaculum
present in 90% of patients.
Evaluate patellar glide and apprehension:
Divide patella into quadrants.
If moves 1 quadrant or less laterally or medially, a tight medial or lateral retinaculum is
present.
If able to translate >3 quadrants medially or laterally, the patella is hypermobile.
Hypermobility usually results in apprehension as the patient senses impending patellar
dislocation.
Perform patellar tilt test: With knee in full or 30 degrees of flexion, if examiner cannot get the
lateral border of patella to horizontal with posterior pressure on medial edge, a tight lateral
retinaculum is present.

Imaging
Imaging studies are not required for an accurate diagnosis of patellofemoral pain syndrome.
Multiple studies have evaluated sulcus angle, patellar height (determined by Insall-Salvati
index), patellar tilt (determined by Laurin angle), and patellar displacement (determined by
Merchant angle) and have found no significant difference between symptomatic and
asymptomatic patients (1)[A].
Imaging studies are recommended if there is clinical suspicion of another diagnosis or if a
patient has failed initial conservative management. Most radiographs will appear normal. Any
structural abnormalities may need to be addressed when determining the appropriate care
plan for an individual patient.
CT, MRI, and bone scintigraphy are recommended to determine presence of additional
pathology causing anterior knee pain or to assist with surgical options when conservative
management has failed.
Plain films:
Anteroposterior bilateral standing: May show varus or valgus orientation of femur, knee, or
tibia
Lateral view of affected knee: Evaluate for patella alta (patella length to patellar tendon
length <0.8) or patella baja (patella length to patellar tendon length >1.2) with Insall
method.
Merchant view of bilateral patellofemoral joints, as this view does not distort the
trochlea/patella appearance. Evaluate for a shallow sulcus angle, subluxation degree, and
femoral condyle appearance.
Tunnel view if osteochondral deficit lesion suspected
CT:
Useful to evaluate patellofemoral relationships (eg, tilt and subluxation), especially in
patients with suspected subluxation at <30–45 degrees of flexion that cannot be visualized
well on plain film
Useful to evaluate intraosseous lesions
Useful to plan selective surgical realignment procedures
MRI:
Provides information similar to CT
May add evaluation of articular cartilage (stage III and IV chondromalacia can be
evaluated reliably with accuracy of 89%), presence of loose bodies, and integrity of
surrounding soft tissue structures such as the medial and lateral patellar retinacula
Bone scintigraphy:
Increased uptake at patella and distal femur believed to indicate poor prognosis with
prolonged pain (average 6–9 mos)
Positive bone scan correlates with chondromalacia, with positive predictive value of 72%.
Patellar or quadriceps tendinopathy
Patellofemoral osteoarthritis
Patellar instability with subluxation or dislocation
Osteochondral defect of the trochlear or patellar surface
Iliotibial band syndrome
Anterior fat pad inflammation
Synovial plica
Retinacular strain
Sinding-Larsen-Johansson disease
Referred pain from the hip, often affecting the anterior distal thigh and knee
Multiple other sources of knee pain and arthritis (eg, gout, infection, reflex sympathetic
dystrophy, neuroma, or sickle cell disease)
Pigmented villonodular synovitis
Treatment
Because patellofemoral pain syndrome is typically multifactorial in origin,
adequate treatment should address multiple facets of care:
80% of patients respond to conservative management.
Reduce activities that may have led to onset of symptoms, such as
resistance training (lunges or full squats), increased mileage with running, or
plyometric exercises.
Encourage relative rest using alternate exercises (ie, pool running, bicycling,
swimming, or using an elliptical trainer).
Evaluate footwear with focus on excessive deterioration, inadequate support,
or excessive support.
Ice application after activity can help with pain symptoms, but will not treat any
underlying cause of the pain.
Effective therapy must focus on the physical findings or deficits seen for each
individual patient (ie, strength training for those with muscle weakness and
flexibility training for those with decreased range of motion. Physical therapy
program should be individualized for maximal results:
Strength training consists of closed chain (end of limb is in contact with a
surface) or open chain (limb end is not in contact). Typical muscle strength
deficits will be in the quadriceps muscle group, but can also be in the gluteus
medius or core muscle groups.
Witvrouw et al. evaluated the long-term effects of an open vs a closed kinetic
chain training program and concluded that both training programs lead to
good functional outcome. On initial evaluation and 3 mos later, the closed
chain exercises produced less pain, better functional improvement, and less
subjective clicking. At the 5-yr follow-up, however, 3 of 18 evaluations by
visual analog scales revealed the open chain group showed fewer complaints
than the closed group (2).
Flexibility training should address the hamstrings, quadriceps, hip flexors,
iliotibial band, and gastrocsoleus.
Hazneci et al. determined that isokinetic exercise (variable resistance
applied so movement remains at a constant speed) has positive effects on
knee joint position sense, which in turn increases strength and work capacity
(3).
Medication
Medication management should focus on pain, not inflammation control.
Acetaminophen or NSAIDs may be used initially to provide relief of pain
symptoms during daily activities.
Steroid injections are of limited value.
P.
Bracing:
Lun et al. randomly assigned patients diagnosed with PFPS to 1 of 4
treatment groups consisting of a home exercise program, patellar bracing
alone, home exercise program with patellar bracing, and home exercise
program with knee sleeve, and found no significance in the pain or function
between the groups (4).
Finestone et al. evaluated the subjective pain of military recruits using a
simple knee sleeve, a brace with a patellar ring, or no treatment, and found
no significant differences (5).
Miller et al. compared a dynamic patellar brace, a counterforce knee strap,
and no brace in patients receiving medication and physical therapy, but found
no significant difference with the groups (6).
Studies evaluating the change in patellar tracking patterns using kinematic
MRI have not supported the proposed mechanisms of action in the
patellofemoral braces (7).
Regardless of the reason for benefit, patellar bracing can potentially improve
the symptoms of patellofemoral pain syndrome and can be tried, as not all
patients may be willing or able to complete an adequate trial of physical
therapy.
Orthotics:
Collins et al. compared patients treated with off-the-shelf foot orthoses, flat
inserts, physical therapy, or foot orthoses plus physical therapy. Foot
orthoses were found to be better than the flat inserts, but no significant
improvement was found compared to therapy with or without orthoses (8).
The overall recommendation is that an orthotic may improve pain symptoms
for patients who cannot complete therapy.
Taping:
Multiple studies have evaluated the effects of patellar taping and found
decreased pain, increased exercise tolerance, and improvement in timing of
quadriceps contraction (9).
Whittingham, Palmer, and Macmillan performed a randomized controlled trial
and found that a combination of daily patella taping and exercise was
superior to exercise alone (10).
After at least 6–12 mos of adequate conservative therapy has been tried,
surgery may be considered.
Isolated lateral retinacular release of the patella has not been shown to provide
long-term benefit for treatment of patellar instability, but may be used along with
proximal or distal realignment of the extensor mechanism.
Patients with Q-angles >20 degrees plus abnormal congruence angles may
undergo distal realignment procedures such as an anterior medial tibial
tubercle transfer.
Dislocators are operated on if symptoms of patellofemoral instability were
present before their dislocation.
Patellectomy and derotational osteotomies are last resorts.
References
1. Haim A, Yaniv M, Dekel S, et al. Patellofemoral pain syndrome: validity of
clinical and radiological features. Clin Orthop Relat Res. 2006.
2. Witvrouw E, Danneels L, Van Tiggelen D, et al. Open versus closed kinetic

chain exercises in patellofemoral pain: a 5-year prospective randomized
study. Am J Sports Med. 2004;32:1122–1130.
3. Hazneci B, Yildiz Y, Sekir U, et al. Efficacy of isokinetic exercise on joint

position sense and muscle strength in patellofemoral pain syndrome. Am J
Phys Med Rehabil. 2005;84:521–527.
4. Lun VM, Wiley JP, Meeuwisse WH, et al. Effectiveness of patellar bracing
for treatment of patellofemoral pain syndrome. Clin J Sport Med.
2005;15:235–240.
5. Finestone A, Radin EL, Lev B, et al. Treatment of overuse patellofemoral

pain. Prospective randomized controlled clinical trial in a military setting. Clin
Orthop Relat Res. 1993:208–210.
6. Miller MD, Hinkin DT, Wisnowski JW. The efficacy of orthotics for anterior
knee pain in military trainees. A preliminary report. Am J Knee Surg.
1997;10:10–13.
7. Chew KT, Lew HL, Date E, et al. Current evidence and clinical applications
of therapeutic knee braces. Am J Phys Med Rehabil. 2007;86:678–686.
8. Collins N, Crossley K, Beller E, et al. Foot orthoses and physiotherapy in

the treatment of patellofemoral pain syndrome: randomised clinical trial. Br J
Sports Med. 2009;43:163–168.
9. Post WR. Patellofemoral pain: results of nonoperative treatment. Clin

Orthop Relat Res. 2005:55–59.
10. Whittingham M, Palmer S, Macmillan F. Effects of taping on pain and

function in patellofemoral pain syndrome: a randomized controlled trial. J
Orthop Sports Phys Ther. 2004;34:504–510.
Additional Reading
Arroll B, Ellis-Pegler E, Edwards A, et al. Patellofemoral pain syndrome. A
critical review of the clinical trials on nonoperative therapy. Am J Sports Med.
1997;25:207–212.
Bellemans J, Cauwenberghs F, Witvrouw E, et al. Anteromedial tibial tubercle

transfer in patients with chronic anterior knee pain and a subluxation-type
patellar malalignment. Am J Sports Med. 1997;25:375–381.
Blond L, Hansen L. Patellofemoral pain syndrome in athletes: a 5.7-year

retrospective follow-up study of 250 athletes. Acta Orthop Belg.
1998;64:393–400.
Brushoj C, Albrecht-Beste E, Bachmann M, et al. Acute Patellofemoral pain:

Aggravating activities, clinical examination, MRI and US findings. Br J Sports
Med. 2007.
Cowan SM, Crossley KM, Bennell KL. Altered hip and trunk muscle function in
individuals with patellofemoral pain. Br J Sports Med. 2008.
Davis W, Fulkerson J. Initial evaluation of the athlete with anterior knee pain.
Op Tech Sports Med. 1999;7:55–58.
P.
Fredericson M, Yoon K. Physical examination and patellofemoral pain
syndrome. Am J Phys Med Rehabil. 2006;85:234–243.
Gerbino PG, Zurakowski D, Soto R, et al. Long-term functional outcome after

lateral patellar retinacular release in adolescents: an observational cohort
study with minimum 5-year follow-up. J Pediatr Orthop. 2008;28:118–123.
Hartig DE, Henderson JM. Increasing hamstring flexibility decreases lower

extremity overuse injuries in military basic trainees. Am J Sports Med.
1999;27:173–176.
20. Kannus P, et al. An outcome study of chronic patellofemoral pain

syndrome: seven-year follow-up of patients in a randomized, controlled trial. J
Bone Joint Surg. 1999;81:355–363.
21. Kaufman KR, Brodine SK, Shaffer RA, et al. The effect of foot structure
and range of motion on musculoskeletal overuse injuries. Am J Sports Med.
1999;27:585–593.
22. Kelly M. Proximal realignment and medial tibial tubercle transfer. Op Tech
Sports Med. 1999;7:76–80.
23. Laprade J, Culham E. Radiographic measures in subjects who are

asymptomatic and subjects with patellofemoral pain syndrome. Clin Orthop
Relat Res. 2003:172–182.
24. Lattermann C, Toth J, Bach BR. The role of lateral retinacular release in
the treatment of patellar instability. Sports Med Arthrosc. 2007;15:57–60.
25. Macintyre JG, Taunton JE, Clement DB, et al. Running injuries: a clinical
study of 4,173 cases. Clin J Sport Med. 1991;1(2):81–87.
26. Merchant A. Radiography of the patellofemoral joint. Op Tech Sports Med.

1999;7:59–64.
27. Natri A, Kannus P, Järvinen M. Which factors predict the long-term

outcome in chronic patellofemoral pain syndrome? A 7-yr prospective follow-
up study. Med Sci Sports Exerc. 1998;30:1572–1577.
28. Nigg BM, Nurse MA, Stefanyshyn DJ. Shoe inserts and orthotics for sport
and physical activities. Med Sci Sports Exerc. 1999;31:S421–S428.
29. Papagelopoulos PJ, Sim FH. Patellofemoral pain syndrome: diagnosis and
management. Orthopedics. 1997;20:148–157; quiz 158–159.
30. Powers CM, Landel R, Sosnick T, et al. The effects of patellar taping on
stride characteristics and joint motion in subjects with patellofemoral pain. J
Orthop Sports Phys Ther. 1997;26:286–291.
31. Presswood L, Cronin J, Keogh JWL, et al. Gluteus medius: applied

anatomy, dysfunction, assessment, and progressive strengthening. Strength
Cond J. 2008;30:41–53.
32. Schreiber S. Arthroscopic surgery and the lateral release for

patellofemoral disorders. Op Tech Sports Med. 1999;7:69–75.
33. Stiene HA, Brosky T, Reinking MF, et al. A comparison of closed kinetic
chain and isokinetic joint isolation exercise in patients with patellofemoral
dysfunction. J Orthop Sports Phys Ther. 1996;24:136–141.
34. Thijs Y, Tiggelen DV, Roosen P, et al. A prospective study on gait-related

intrinsic risk factors for patellofemoral pain. Clin J Sport Med. 2007;17:437–
445.
35. Timm KE. Randomized controlled trial of protonics on patellar pain,

position, and function. Med Sci Sports Exerc. 1998;30:665–670.
36. Witvrouw E, Sneyers C, Lysens R, et al. Reflex response times of vastus

medialis oblique and vastus lateralis in normal subjects and in subjects with
patellofemoral pain syndrome. J Orthop Sports Phys Ther. 1996;24:160–165.
Codes
ICD9
719.46 Pain in joint involving lower leg
Clinical Pearls
Return to activity:
If patient has patellofemoral pain during, immediately following, or the day
after exercising:
Decrease activity. Avoid strength training exercises such as full squats and
lunges.
Consider alternate activities, such as an elliptical trainer, bicycling, or
swimming.
Runners who need to maintain running-specific conditioning, utilize a
floatation belt for pool running.
80% of patients respond to a nonoperative therapy, most within 4 wks
Complete resolution of symptoms may take longer.
In athletes with patellofemoral pain followed for 5–7 yrs, 27–75% were pain-
free at 6–8 mos, and 50% had a significant decrease in pain at 6–8 mos;
70% of patients remained pain-free at 7 yrs in 1 study.
Correlates of improvement at 7 yrs include maintenance of quadriceps strength
and function, young age, short stature, negative findings of patellar pain and
crepitation, and absence of bilateral symptoms during the follow-up period.
Most patients (65%) with patellofemoral pain do not get patellofemoral
osteoarthritis.
Pectoralis Major Tendon Rupture
Ramsey Shehab
Basics
Most commonly refers to complete avulsion of the pectoralis tendon at the humeral
insertion (1)
Ruptures at the myotendinous junction, muscle belly, or bony avulsion are possible but less
likely (2).
Associated with weightlifting (bench press) mostly, but possible with falls as well as direct
trauma to tendon (3)
Pectoralis is a powerful adductor, internal rotator, and flexor of humerus.
Main source of power to the torso during strenuous activity
2 heads:
Superior/clavicular: Originates at medial clavicle and upper sternum
Inferior/sternal: Originates at distal sternum, external oblique fascia, costal cartilage of 1st
6 ribs
Fibers converge, rotate 90 degrees, and insert lateral to bicipital groove on humerus.
Innervation: Medial and lateral pectoral nerves
Blood supply: Pectoral branch of thoracoacromial artery
Epidemiology
1st reported in 1822 by P. Patssier
Increasing incidence with increase in health and fitness activities
More than 200 cases reported in medical literature
Risk Factors
Medications:
Steroid use: Muscle strength increases disproportionately to tendon strength leaving it
vulnerable to injury (4).
Corticosteroid injection: Weakens tendon structure
Systemic diseases: Connective tissue disorders, collagen vascular disease, diabetes (1)
Advanced age
Disuse atrophy
Etiology
Indirect mechanism most common with excessive tension on a maximally contracted muscle
(5)
Weightlifting (bench press specifically) is a common mechanism (3).
Direct trauma to muscle in wrestling, rugby, and auto accidents also reported (4)
Diagnosis
History
Men 20–40 yrs of age (2)
Usually report a pop or tearing in the shoulder (2,4)
Complain of pain/weakness in chest or shoulder (1,4)
Physical Exam
Swelling and ecchymosis in anterior shoulder/chest most common (4)
May have loss of axillary fold accentuated by abduction to 90 degrees (1)
Shoulder motion limited by pain
Weakness in abduction and internal rotation

Imaging
Plain radiographs initially to rule out bony avulsions, fracture, or dislocations (1)
Characteristic finding on x-ray is soft tissue swelling and loss of pectoralis major shadow (1)
US can identify tears by uneven echogenicity and muscle thinning.
MRI is optimal; assesses grade, muscle retraction, acuity, and presence of adhesions in
chronic tears (3)
Long head biceps subluxation
Proximal humerus fracture
Rotator cuff tear
Treatment
Acute treatment:
Analgesics
Ice
Sling immobilization
Long-term care:
Tear type, patient age, activity level, and cosmetic desires determine care
(1).
Most partial tears, sternoclavicular tears, and muscle belly tears are treated
nonsurgically (2).
Complete sternal tears require surgical repair to restore function and
strength (3).
Conservative treatment may be enough in elderly/inactive population
irrespective of type of tear (1).
Ongoing Care
Begin shoulder mobilization and unresisted stretching when tolerated (1).
Advance to resisted strengthening exercises at 6–8 wks post injury (1).
Unrestricted activity at 3–4 mos after injury (2)
Instruct in proper weightlifting technique to decrease re-rupture rate (5).
Surgical management:
Provides best outcomes in terms of patient satisfaction, strength, cosmesis, and return to
sport (1,2)
Acute repair within 8 wks is optimal (3).
Delayed repairs do better than nonsurgical treatment (1).
References
1. Petilon J, Carr D, Sekiya J: Pectoralis major muscle injuries: evaluation and management.
2. http://www.eorif.com/Shoulderarm/PectoralisRupture.html
3. Potter BK, Lehman RA, Doukas WC: Pectoralis major ruptures. Am J Orthop.
2006;35(4):189–195.
4. Hasegawa K, Schofer J: Rupture of the pectoralis major: a case report and review. J Em
Med. 2008;01.025.
5. Dodds SD, Wolfe SW: Injuries to the pectoralis major. Sports Med. 2002;32:945–952.
Codes
ICD9
727.69 Nontraumatic rupture of other tendon
Clinical Pearls
Usually a complete avulsion of pectoralis major tendon at humerus
Most commonly occurs during weightlifting; specifically bench press
Patients may report a pop and present with swelling, ecchymosis, and palpable
tendon deformity.
MRI is gold standard for diagnosis.
Type of tear, patient age, and activity level dictate treatment.
Surgical repair provides best outcomes in terms of strength, return to play, and
patient satisfaction.
Pericarditis
Kevin J. McAward
Basics
Description
Inflammation of the pericardial sac owing to multiple etiologies
Acute pericarditis:
Rapid in onset
Potentially complicated by effusion, which may lead to cardiac tamponade
Constrictive pericarditis: Results from chronic inflammation causing thickening and adherence
of the pericardium to the heart
Epidemiology
Incidence and prevalence are essentially unknown owing to lack of epidemiologic studies.
Prevalence
Acute pericarditis is noted in 0.1% of hospitalized patients and 5% of ED-admitted patients with
non-myocardial infarction (non-MI) chest pain.
Etiology
Idiopathic (most common)
Infectious: Viral most common:
Viral: Echovirus, coxsackievirus, adenovirus, varicella virus, Epstein-Barr virus,
cytomegalovirus, hepatitis B virus, HIV
Bacterial: Staphylococcus, Streptococcus, Haemophilus, Salmonella, Legionella,
tuberculosis
Fungal: Candida, Aspergillus, Histoplasma, Coccidomyces, Blastomyces, Nocardia
Parasitic: Amebiasis, Toxoplasmosis, Echinococcosis
Neoplastic: Lung cancer, breast cancer, lymphoma, leukemia, melanoma, primary
neoplasm of peri/myocardium
Cardiac/aortic:
MI (Dressler syndrome)
Aortic dissection
Autoimmune diseases:
Connective tissue disease (systemic lupus erythematosus, rheumatoid arthritis,
scleroderma)
Metabolic:
Uremia
Myxedema
Trauma:
Blunt
Penetrating
Iatrogenic
Drugs (rare):
Antiarrhythmics: Procainamide
Antibiotics: Isoniazid, penicillin
Antihypertensives: Hydralazine
Cromolyn sodium
Muscle relaxants: Dantrolene
Anticoagulants and thrombolytics
Chemotherapeutics: Doxorubicin
Anticonvulsants: Phenytoin
Amyloidosis
Diagnosis
2 of 4 major criteria should be present to make diagnosis:
Chest pain
Friction rub
ECG changes (described below)
Pericardial effusion
History
Chest pain: Classically described as worsened by lying flat and relieved by leaning forward
Typically sharp and constant pain located substernally
May radiate to bilateral trapezius owing to phrenic nerve innervation of the pericardium
May have pleuritic component
Fever and palpitations are described occasionally.
Physical Exam
Tachypnea
Tachycardia
Friction rub (noise of 2 inflamed layers of pericardium rubbing against each other):
Heard best at lower left sternal border with diaphragm of stethoscope
Intermittent and exacerbated by leaning forward
Muffled heart sounds
Signs of cardiac tamponade: Much less common in idiopathic cases:
Increased venous pressure (distended neck veins)
Pulsus paradoxus
Hypotension

Cardiac tests:
ECG:
Evolves over days/weeks
Initially, diffuse ST elevation with ST depression in aVR and V1, as well as depressed PR
segments in most leads except aVR and V1
Later, ST segments normalize, and diffuse T-wave inversion is seen that may last
indefinitely.
ECG changes eventually resolve over months.
Uremic patients may not have characteristic patterns.
Echocardiogram:
Recommended on every patient with pericarditis to check for effusion
Effusion not necessary for diagnosis
Imaging/special tests:
CXR:
Can be normal
May show enlargement of the cardiac silhouette
No change in heart size until >200 mL of fluid has accumulated in the pericardial sac
Chest CT scan: Useful for the detection of calcifications or thickening of the pericardium
Pericardiocentesis:
Only for severe cases with tamponade or unknown etiology
Used mainly for therapeutic treatment of tamponade and for diagnosis of suspected
nonviral infectious pericarditis
Lab
Standard:
CBC
Erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP) may be elevated; helpful in
following treatment.
Cardiac enzymes:
Helpful in distinguishing pericarditis from MI and myopericarditis
Reported elevated with the inflammation of pericarditis, typically to a lesser degree than
infarction
Other considerations:
Viral serology including HIV
Blood cultures if high fever
Antinuclear antibodies (ANAs)
Metabolic profile
Tuberculin skin test may be done if tuberculosis is a diagnostic consideration.
Myopericarditis
Acute MI
Pulmonary embolism
Pneumothorax
Aortic dissection
Pneumonia
Empyema
Cholecystitis
Pancreatitis
Musculoskeletal chest wall pain
Treatment
Idiopathic etiology (1,2):
Low risk:
NSAIDs or aspirin
Adding colchicine may be of benefit.
High risk: Admit for observation and treatment.
Recurrent:
Add colchicine to normal NSAID regimen
Prednisone for severely symptomatic recurrent disease
Tamponade: Pericardiocentesis for hemodynamic stabilization with testing of
fluid for etiology
Underlying disease
Infectious: Antimicrobials if known organism
Neoplasm: Treat malignancy
ED Treatment
Treatment depends on the underlying etiology.
Idiopathic, viral, rheumatologic, and posttraumatic:
NSAID regimens effective
Corticosteroids reserved for refractory cases
Bacterial:
Aggressive treatment with IV antibiotics along with drainage of the pericardial
space
Search for primary focus of infection
Therapy guided by determination of pathogen from pericardial fluid tests
Neoplastic: Treat underlying malignancy.
Uremia:
Intensive 2–6-wk course of dialysis
Caution should be used if using nonsteroidal medications.
Expected course/prognosis:
Majority of patients will respond to treatment within 2 wks.
Most have complete resolution of symptoms.
Small number progresses to recurrent bouts with eventual development of
constrictive pericarditis or cardiac tamponade.
Medication
First Line
Ibuprofen 300–800 mg q6–8h until symptoms improve
Aspirin 800 mg q6–8h; preferred treatment in Dressler syndrome
May need to taper down over weeks to prevent recurrence (2)
Second Line
Colchicine 0.6 mg b.i.d.
Prednisone 1–1.5 mg/kg daily
Pericardiectomy for recurrent pericarditis has been found to be largely
unsuccessful.
Admission Criteria
Fever >38°C
Subacute onset
Immunocompromised state
Anticoagulant use
Myopericarditis
Larger pericardial effusion
Tamponade
Trauma
Discharge Criteria
Most patients can be discharged quickly as long as they remain
hemodynamically stable.
Close follow-up is recommended.
Ongoing Care
Return to play: Based on 36th Bethesda Conference guidelines (3):
No participation during acute phase regardless of etiology
Return is allowed when active disease has resolved.
Normalization of serum inflammatory markers (CRP, ESR)
No effusion per echocardiogram
If myocardial involvement, need to check eligibility requirements based on myocarditis
Residual constrictive pericarditis disqualifies an athlete from most sports.
Prognosis
Most patients do very well without any long-term sequelae.
1% of acute idiopathic pericarditis patients go on to constrictive pericarditis; increased
numbers if proven etiology.
15–30% of acute idiopathic pericarditis patients go on to have recurrent disease.
NSAID treatment has no bearing on potential for complications.
References
1. Adler Y, Finkelstein Y, Guindo J, et al. Colchicine treatment for recurrent pericarditis: a
decade of experience. Circulation. 1998;97:2183–2185.
2. Maisch B. Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology,

new diagnostic imaging methods, and treatment. Curr Opin Cardiol. 1994;9:379–388.
3. 36th Bethesda Conference. J Am College Cardiol. 2005;45.
Additional Reading
Ariyarajah V, Spodick DH. Acute pericarditis: diagnostic cues and common
electrocardiographic manifestations. Cardiol Rev. 2007;15:24–30.
Braunwald et al. Harrison's manual of medicine. 15th Edition. McGraw-Hill 2002
Imazio M. Evaluation and management of acute pericarditis. UpToDate. 2008

Lange RA, Hillis LD. Acute pericarditis. N Engl J Med. 2004;351:2195–2202.
Launbjerg J, Fruergaard P, Hesse B, et al. Long-term risk of death, cardiac events and
recurrent chest pain in patients with acute chest pain of different origin. Cardiology.
1996;87:60–66.
Maisch B, Seferovi PM, Risti AD, et al. Guidelines on the diagnosis and management of
pericardial diseases executive summary; The task force on the diagnosis and management
of pericardial diseases of the European society of cardiology. Eur Heart J. 2004;25:587–
610.
Permanyer-Miralda G. Acute pericardial disease: approach to the aetiologic diagnosis.

Heart. 2004;90:252–254.
Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684–690.
Codes
ICD9
074.21 Coxsackie pericarditis
115.03 Histoplasma capsulatum pericarditis
115.13 Histoplasma duboisii pericarditis
Clinical Pearls
Consider pericarditis as etiology of nonexertional chest pain.
Usually a benign course
Often complete resolution with course of oral NSAIDs
Important to rule out other causes of acute chest pain, eg, MI
Periorbital and Orbital Cellulitis
COL. Mark D. Harris
Kevin deWeber
Basics
Description
Periorbital (preseptal) cellulitis:
Inflammatory process, such as acute infection of the dermis and SC tissue anterior
(superficial) to the orbital septum
Orbital (postseptal) cellulitis:
Inflammatory process, such as acute infection in the structures posterior (deep) to the
orbital septum
Orbital septum: Connective tissue extension of the orbital periosteum into the upper and
lower eyelids. It is nearly impervious to the spread of infection into the orbit.
Unlike what is commonly understood, periorbital cellulitis does not progress to orbital
cellulitis.
Epidemiology
Mean age cited in many case studies of orbital cellulitis is 7.4 yrs.
Adults are more likely to be affected with periorbital cellulitis.
Rarely, recurrent periorbital cellulitis occurs.
Incidence
The incidence of periorbital cellulitis is roughly equal in males and females (1).
The incidence of orbital cellulitis is roughly 2:1 for Males: Females.
Risk Factors
Risk factors for periorbital and orbital cellulitis include (2):
Conjunctivitis
Infected wound or trauma
Insect bite
Sinusitis (acute or chronic)
Dacryostenosis, adenitis, and cystitis
Bacteremia
Genetics
No known genetic pattern
General Prevention
Immunization against H. influenzae provides good protection against periorbital and orbital
cellulitis caused by H. influenzae. Children who have received at least 2 Hib immunizations
are unlikely to have H. influenzae b infection.
Avoiding periorbital skin trauma is important for prevention. Protective goggles and other
American National Standards Institute-approved eyewear may help decrease the risk.
Etiology
Prior to H. influenzae type b (Hib) immunization, H. influenzae accounted for 80% of
bacteremic periorbital cellulitis cases. Now it is more common in younger and in
nonvaccinated children.
Currently, both Staphylococcal (methicillin-sensitive Staphylococcus aureus [MSSA] and
methicillin-resistant Staphylococcus aureus [MRSA]) and Streptococcal infections (group A
and pneumococcus) are important causative organisms.
Consider M. catarrhalis, anaerobes, and nonbacteremic causes.
Infectious causes of preseptal cellulitis (3):
Localized infection of the eyelid or adjacent structures:
Conjunctivitis
Hordeolum
Chalazion
Dacryoadenitis
Dacryocystitis
Bacterial cellulitis from trauma
Surrounding skin disruptions (minor trauma, insect bites, dermatologic disorders)
Hematogenous dissemination:
Bacteremic periorbital cellulitis
Acute sinusitis:
Inflammatory edema
Infectious causes of orbital (postseptal) cellulitis:
Acute sinusitis
Hematogenous dissemination
Traumatic inoculation
Diagnosis
Clinical diagnosis is based on signs and symptoms and the neurological exam. It is very
important to assess for orbital involvement because orbital cellulitis is much more dangerous
than periorbital cellulitis.
History
Periorbital cellulitis:
Recent or current viral upper respiratory infection
Dermatologic trauma
Recent conjunctivitis
Fever
Orbital cellulitis:
Above, plus:
Recent sinusitis
Other serious infections
Physical Exam
Periorbital swelling, erythema, warmth, and tenderness
Unilateral
Orbital cellulitis:
Physical findings above, plus:
Proptosis
Ophthalmoplegia
Loss of visual acuity
Chemosis (bulbar conjunctival edema)
Lab
WBCs >15,000 can be associated with bacteremic periorbital cellulitis.
Blood culture if sepsis is suspected
Gram stain and culture of either a tissue aspirate or swab of draining purulent material.
Specimens can be difficult to get, and specimens obtained during surgery often have the best
results.
Lumbar puncture/cerebrospinal fluid evaluation if the child appears markedly ill, has
insufficient Hib immunization, or meningitis must be ruled out.
Imaging
Sinus x-rays can be helpful to diagnose sinusitis.
Orbital/sinus/facial CT scan with contrast:
Should be strongly considered in most cases to differentiate between periorbital and orbital
cellulitis
Definitely indicated if there is a concern for orbital cellulitis, traumatic penetration of the
orbital septum, or if the patient fails to respond to parenteral antimicrobial therapy
Best confirmation of orbital cellulitis is by CT scan with contrast infusion of the orbit.
Can show sinusitis, proptosis, foreign body, and subperiosteal abscess
Lack of fever and leukocytosis suggest noninfectious causes:
Trauma (including insect bite)
Local edema (hypoproteinemia, congestive heart failure)
Allergy (including angioneurotic edema and contact hypersensitivity)
Tumor (such as choroidal melanoma, retinoblastoma, rhabdomyosarcoma, neuroblastoma)
Early orbital cellulitis:
May have the same appearance as periorbital cellulitis
Treatment
ED Treatment
Establish IV access and administer oxygen for serious complications, including
sepsis, meningitis, and cavernous sinus thrombosis.
Consider vancomycin in geographic areas with prevalent penicillin-resistant
pneumococci or prevalent MRSA.
Children with orbital cellulitis require:
Parenteral antibiotics
CT scan
Ophthalmologic consultation
Prompt surgery may be necessary.
Medication
First Line
There is no evidence that IV antibiotics are generally better than oral
antibiotics for periorbital cellulitis (1) [A].
Augmentin: 500 mg (peds: 45–90 mg/kg/24 hr) PO b.i.d.
Cephalexin: 500 mg (peds: 50–100 mg/kg/24 hr) PO q.i.d.
Clindamycin: 600 mg (peds: 40 mg/kg/24 hr) IV q6h; 300 mg (peds: 30
mg/kg/24 hr) PO q.i.d.
Dicloxacillin: 500 mg (peds: 100 mg/kg/24 hr) PO q6h
Orbital cellulitis:
MSSA:
Nafcillin: 2 g (peds: 150 mg/kg/24 hr) IV q4h or oxacillin: 2 g (peds: 150
mg/kg/24 hr) IV q4h
MRSA:
Vancomycin: 1 g IV q12h, PLUS
Ceftriaxone: 2 g IV (peds: 50–100 mg/kg/24 hr) q24h, PLUS
Metronidazole 1 g IV q12h
If penicillin/cephalexin allergy, vancomycin + levofloxacin 750 mg IV q24h +
metronidazole IV
Symptomatic treatments:
Sinus decongestion
Nasal sprays
Oral decongestants
Oral antihistamines
Second Line
Immunocompromised patients: Gentamicin and piperacillin
Complicated or resistant cases: Linezolid (Zyvox)
Referral
Patients with orbital cellulitis should be referred for ophthalmologic consultation.
Orbital cellulitis patients with complete ophthalmoplegia, an abscess, or vision
loss should undergo surgical drainage (2).
Most patients with orbital cellulitis should be admitted for 24–48 hr of IV
antibiotics. If significant improvement occurs, switch to oral antibiotics. If no
significant improvement results, consider repeat CT scan and surgical
intervention.
0.9% NS IV bolus (500 cc or 20 cc/kg) for dehydration, sepsis, hypotension
Admission Criteria
Toxicity
Orbital cellulitis should usually be treated in the hospital. Outpatient treatment
should only be attempted if the eye is at least 50% open and very close follow-
up can be guaranteed (2).
Progression of infection on oral antibiotics
Uncertainty that patient can get adequate care at home
Discharge Criteria
No more than modest swelling, tolerating oral antibiotics well with progressive
improvement, nontoxic appearance, and reliable caregivers
Monitor for progressive swelling, irritability, increased fever, or vision changes.
Ongoing Care
Return-to-play guidance:
Athlete must be asymptomatic and the physical exam must be normal.
Athlete must pass sport-specific functional assessment.
Medical personnel should closely observe the athlete's performance in practice prior to
clearing him or her for competition.
Patient Monitoring
Repeat imaging in patients with orbital cellulitis if there is any question about resolution after
treatment.
Complications
Possible complications of orbital cellulitis include:
Blindness
Cavernous sinus thrombosis
Meningitis
Subdural empyema
Brain abscess
References
1. Goldman RD, Dolansky G, Rogovik AL. Predictors for admission of children
with periorbital cellulitis presenting to the pediatric emergency department.
Pediatr Emerg Care. 2008;24:279–283.
2. Nageswaran S, Woods CR, Benjamin DK, et al. Orbital cellulitis in children.

Pediatr Infect Dis J. 2006;25:695–699.
3. Wald ER. Periorbital and orbital infections. Pediatr Rev. 2004;25:312–320.

Additional Reading
Robinson A, Beech T, McDermott A, et al. Investigation and management of
adult periorbital and orbital cellulitis. J Laryng Otol. 2007;121:545–547.
Rimon A, Hoffer V, Prais D, et al. Periorbital cellulitis in the era of haemophils

influenzae type B vaccine: predisposing factors and etiologic agents in
hospitalized children. J Pediatr Ophthal Strabis. 2008;45:300–304.
Codes
ICD9
376.01 Orbital cellulitis
Peroneal Tendon Dislocation/Subluxation
Orlando V. Gonzalez
Jeffrey Rosenberg
Basics
Description
The peroneus longus and brevis tendons pass through a single tendon sheath in the fibular
groove in the posterior fibula. They are fixed in place by the superior peroneal retinaculum.
The peroneals' primary actions are plantar flexion, foot eversion, and to provide dynamic
lateral stability to the lateral ankle.
Elevation of the posterior periosteal attachment of the superior peroneal retinaculum off the
fibula allows the peroneal brevis tendon to sublux over the posterior ridge of the fibula.
Injury occurs from a forceful contraction of the peroneal muscles, usually with the ankle in
forced plantarflexion with inversion.
Subluxation can be a chronic overuse injury.
Subluxation of the tendon is temporary and quickly reduced, but a dislocated tendon remains
permanently out of the posterior fibular groove.
Epidemiology
Generally a rare injury in most sports
Nontraumatic
Usually occurs with quick stopping or cutting movement
Risk Factors
Field sports with tackling or regular body contact
Ice skating with excessive pushing off during jumps
Gymnastics and ballet with excessive plantarflexion and plié
Gait abnormalities such as excessive eversion
Severe pes planus or hindfoot deviation (valgus or varus)
Equinus or restricted ankle dorsiflexion
Anterolateral ankle impingement, particularly immediately following acute ankle sprain, which
can lead to peroneal overcompensation
Etiology
A sudden dynamic reflexive contraction during foot inversion with ankle dorsiflexed
A forced dorsiflexion on the everted foot, often occurring when being tackled
Classically occurs in athletes participating in sports such as skiing, football, ice skating,
soccer, basketball, rugby, and gymnastics
Nontraumatic subluxations associated with anatomically shallow, flat, or absent retrofibular
groove, neuromuscular disease, calcaneovalgus foot type, chronic lateral ankle instability

Neuromuscular diseases such as cerebral palsy
Congenital absence of superior peroneal retinaculum
Diagnosis
Any trauma to the ankle while falling to ground, tripping, or being tackled
Athlete of above-mentioned sports with lateral, painful snapping of the ankle
Recurrent ankle instability or snapping after prior ankle injury
Ankle instability on uneven ground
Chronic posterolateral ankle pain in setting of prior ankle injury
History
Snapping or popping at time of injury over lateral ankle (1)
Intensely painful posterior or inferior to the lateral malleolus and above the joint line
Snapping and/or popping sensation with ambulation
Unable to continue play or bear weight
In recurrent dislocations, snapping or clicking in distal fibula
Often misdiagnosed as ankle sprain
Physical Exam
Acute injury:
Very difficult to distinguish from ankle sprain especially, because of the swelling and pain
(2)
Ecchymosis, swelling, and pain posterior and/or distal to lateral malleolus and along path
of tendons (vs tenderness over the anterior talofibular ligament in ankle sprain)
Locate and palpate the peroneals. These tendons may palpably sublux out of their groove
and over the fibula with eversion against resistance on a dorsiflexed ankle.
Limited dorsiflexion or plantarflexion
Assess lateral ligament stability: Anterior drawer test and inversion tilt test.
Pain elicited with active eversion with the foot held in dorsiflexion
Chronic injury;
Examiner may be able to reproduce subluxation with dorsiflexion and eversion against
resistance.
Possible tenderness or swelling over the lateral malleolus
Chronic instability

Lab
No laboratory tests
Imaging
Plain radiographs:
After acute injury, anteroposterior view of ankle to rule out other bony lesion
Pathognomonic is a thin rim of avulsed cortical bone from the lateral aspect of the lateral
malleolus, best seen on mortise view (15–20 degrees of internal rotation).
MRI:
Tearing of the retinaculum, fluid in the peroneal sheath, or a longitudinal tear (split) of the
peroneus brevis
Rules out other ligamentous or cartilage lesions
Peroneals may switch position within the sheath.
Diagnostic US: Dynamic real-time imaging of ankle can reveal fluid distending the tendon
sheath, tendinopathy, longitudinal peroneal splits, and frank subluxation of peroneal tendon.
Findings at time of surgery:
Tears of superior retinaculum
Unroofing of retinaculum from lateral fibular edge
Tendinosis
Midsubstance tendon tears
Longitudinal split
Adhesions of synovial sheath
Lateral ankle ligament tear
Shallow or absent peroneal groove
Lateral ankle instability
Varus hindfoot alignment
Ankle fracture
Talar osteochondral lesion
Talofibular ligament injury
Calcaneofibular ligament injury
Achilles tendinitis
Tarsal coalition
Sural neuritis
Sinus tarsi syndrome
Treatment
Acute treatment:
Analgesia
Ice
NSAIDs
Crutches to aid with ambulation and prevent need for weight-bearing, which is
very painful acutely
Conservative treatment: 5–6 wks
Immobilization may relieve symptoms and reduce inflammation.
RICE (rest, ice, compression and elevation) and NSAIDS
Ankle bracing may limit the excursion of the foot and may decrease the
episodes of painful subluxation.
Activity modification may reduce the occurrence of subluxation in certain
patients if the subluxation is activity-specific.
Options include non-weight-bearing cast for 5–6 wks with the ankle in
midplantar flexion (to relax the tendons), strapping the ankle with lateral
crescent- or J-shaped pads, or compression bandages.
Nonoperative approach: Always should be the initial intervention, although elite
and high-level athletes likely will need surgical intervention to return to preinjury
level of athletics.
Algorithm for nonsurgical treatment is not well established; 50% failure of
nonsurgical treatment with persistent pain, instability, and redislocation.
No studies to compare surgical vs nonsurgical treatment in any population
Repeat dislocations and chronic pain are indications for surgical intervention.
Surgery should be considered in all cases secondary to the high incidence of
recurrence with nonoperative treatment.
Repeated dislocations cause bone changes that further exacerbate recurrent
instability.
Surgery allows a quick return to normal lifestyle and athletics with no instability.
Surgical procedure has very low morbidity.
Surgery should be considered in all high-level athletes with acute injury and is
the only appropriate management in chronic dislocations.
Many techniques exist; all attach the superior peroneal retinaculum and the
periosteum back to the bone when repositioning the peroneal tendon. Tendon
dèbridement and repair of longitudinal split tears also are accomplished (3,4).
Retromalleolar groove impaction with reattachment of peroneal retinaculum
provided complete return to activity by 1 yr in a case series of 23 active
athletes (average age 34 yrs) with acute peroneal subluxation. No functional
differences were noted between the ankles, and there were no further
subluxation episodes (5).
Postoperative below-the-knee cast in relaxed plantar flexion and slight eversion
for 6 wks; physical therapy once cast is removed
No studies comparing differing surgical techniques
10–20% failure rate of surgical repair may require further salvage procedure.
Can take 6–9 mos to return to preinjury level of activity
Many now questioning need for deepening of fibular groove because the
fibrocartilagous periosteal cushion is now thought be the attachment of the
retinaculum.
Ongoing Care
Some chronic cases are minimally symptomatic and do not significantly alter athletic
performance.
J-shaped pad with compression and lateral heel wedge occasionally useful
Immediate referral for surgical evaluation is appropriate for most athletes.
Prognosis
Full return to high-level athletics may not be possible with conservative treatment, but operative
repair has 10–20% failure rate.
References
1. Omey ML, Micheli LJ. Foot and ankle problems in the young athlete. Med Sci Sports
Exerc. 1999;31:S470–S486.
2. Safran MR, O'Malley D, Fu FH. Peroneal tendon subluxation in athletes: new exam
technique, case reports, and review. Med Sci Sports Exerc. 1999;31:S487–S492.
3. Cerrato RA, Myerson MS. Peroneal tendon tears, surgical management and its
complications. Foot Ankle Clin. 2009;14:299–312.
4. Oliva F, Del Frate D, Ferran NA, et al. Peroneal tendons subluxation. Sports Med
Arthrosc. 2009;17:105–111.
5. Walther M, Morrison R, Mayer B. Retromalleolar groove impaction for the treatment of

unstable peroneal tendons. Am J Sports Med. 2008.
Additional Reading
Mason RB, Henderson JP. Traumatic peroneal tendon instability. Am J Sports Med.
1996;24:652–658.
Philbin TM, Landis GS, Smith B. Peroneal tendon injuries. J Am Acad Orthop Surg.
2009;17:306–317.
Codes
ICD9
Clinical Pearls
High recurrence rate of 50–75%.
Nonoperative treatment can take 2–3 mos to return to play; 6–9 mos after
surgical repair.
Conservative treatment can be attempted but patient still may not return during
same season. Immediate surgical repair will have a longer recovery but less
likelihood of recurrent subluxations and chronic pain.
Snapping over lateral ankle with plantar flexion or with dorsiflexion and eversion
at time of initial on the field evaluation guides to peroneal subluxation as cause
of injury.
Conservatively treat with RICE and non-weight-bearing for in-season athlete;
ankle taping with J-shaped pad may allow for eventual return to play prior to
surgical repair.
Surgical repair is indicated after the season or if conservative treatment fails.
Pes Anserine Bursitis
Shanyn Lancaster
Melissa Nayak
Basics
Description
Pes anserine bursitis is an acute or chronic inflammatory condition that affects the medial
aspect of the knee at the insertion of the conjoined pes anserine tendon onto the anteromedial
proximal tibia. The pes anserine tendon, which is comprised of the tendons of the sartorius,
gracilis, and semitendinosus muscles, is superficial to a bursa, which may become inflamed
and/or distended. This bursa does not typically communicate with the knee joint.
Epidemiology
The exact incidence is unknown.
Risk Factors
Incorrect training techniques (ie, sudden increase in mileage, excessive hill running, no
stretching routine)
Tight hamstrings
Abnormal gait
Obesity
Osteoarthritis of the knee (1)[C]
Etiology
Any abnormal force on the insertion point of the 3 tendons caused by a change in the
mechanical relationship between the knee, hip, and pelvis, such as an abnormal gait, can
cause pes anserine bursitis, though it may also result from trauma.
Athletes who perform side-to-side and cutting motions

Medial collateral ligament (MCL) pathology
Osteoarthritis
Obesity
Pes planus
Valgus knee deformity
Diagnosis
History
Episodes are typically characterized by:
Pain, tenderness, and acute swelling within the well-localized area of the tendon and bursa
along the medial tibia
Pain may be exacerbated by rising from a seated position and ascending or descending
stairs.
Pain is generally worse at night.
Patients may deny pain when walking on level surfaces.
May be bilateral
Physical Exam
Tenderness at the insertion of the pes anserine tendon at the proximal medial tibia, 2–5 cm
below the anteromedial joint line of the knee
Palpable crepitus of the bursa may be felt, but the bursa is usually not palpable unless
effusion and thickening are present.
Pain occasionally is reproduced with resisted internal rotation and flexion of the knee.
Pain may also be reproduced when a valgus stress is applied. This may make it difficult to
distinguish this problem from an MCL injury; however, MCL injuries are typically superior and
posterior to this type of bursitis.
Hamstring-popliteal angle should be measured to assess hamstring flexibility. This is done by
having the patient flex the hip to 90° and then passively extend the leg. The angle is formed
by a perpendicular line to the femoral shaft and the tibial shaft.
Chronic cases are marked by local pain at the site of the bursa.

Diagnosis of pes anserine bursitis can be made on clinical grounds, and further workup is not
necessarily indicated, although normal radiographs of the knee will rule out bony pathology.
In refractory cases, workup is dictated based on suggested diagnosis and may include lab
work to rule out a rheumatoid disorder or further imaging such as a MRI.
Imaging
MRI is the preferred imaging study for pes anserine bursitis (2)[C].
The pes anserine bursa is observed to show a collection of fluid with low signal intensity on
T1-weighted images and homogenous increased signal intensity on T2-weighted images.
Aspiration of the bursa is typically not required.
In difficult cases, a local anesthetic block may be used to confirm the diagnosis. Relief of
pain with the injection is diagnostic.
Medial collateral ligament injury
Osteoarthritis
Medial meniscus tear
Medial plica and discoid medial meniscus
Medial hamstring strain (semitendinosus) and tendonitis
Myofascial pain
Stress fracture
Fibromyalgia
Regional tumors, including villonodular synovitis, osteochondromatosis, and synovial sarcoma
Prepatellar bursitis
Treatment
The mainstay of treatment for patients with pes anserine bursitis is to
reduce pain and inflammation through the following (3)[C]:
Activity modification (decreased distance)
Hamstring stretching
Closed kinetic chain quadriceps strengthening
Anti-inflammatory medications
Ice massage
Use of a protective pad over the affected area
Addressing gait abnormalities
Older patients and those with chronic pain should be encouraged to maintain
activity levels to prevent disuse atrophy. Obesity counseling should also occur.
Medication
First Line
NSAIDs are recommended, including both nonselective NSAIDs as first line and
the selective COX-2 inhibitors if there are tolerance issues.
Second Line
Corticosteroid injections are traditionally utilized as first- or second-line
medications, as the blood supply to the bursa is limited.
Physical therapy can be beneficial for patients with pes anserine bursitis.
Modalities such as US, phonophoresis, ice massage, and stretching can also be
helpful in relieving pain and inflammation.
Injection with local anesthetics and corticosteroids is an option in cases that fail
to improve with more conservative measures.
The patient is placed supine with the leg extended and hip externally rotated.
The area of maximal tenderness is marked, and ethyl chloride is sprayed on
the skin for local anesthesia.
A smaller-gauge needle is inserted into the skin and directed toward the
bursa until the periosteum is contacted.
The needle should be withdrawn 1/8″ to prevent injection into the medial
collateral ligament, and a mixture of corticosteroid and local anesthetic is
injected.
Patients may experience immediate, though not complete, relief.
The injection should be free flowing with little resistance.
This injection may be repeated in 6 wks if swelling recurs or persists.
Surgery is a rare option in chronic cases and includes bursectomy and/or
excision of bony exostoses.
Ongoing Care
In general, patients experience success with conservative treatments, including
hamstring stretching, quadriceps strengthening, activity modification, and oral NSAIDs.
Most patients will experience alleviation of pain within 6–8 wks.
Patients may return to their activities based on their level of pain and function.
Patient Education
The following recommendations can be made to the patient:
Minimize the use of stairs and climbing.
Eliminate squatting.
Prevent direct pressure on the bursa by using a pillow between the legs at night.
Avoid crossing the legs.
Limit repeated bending of the knee.
Patients and their coaches should be counseled on the gradual increase in activity based on
symptoms.
Prognosis
Pes anserine bursitis is usually a self-limiting condition, with few complications if the individual
decides to participate through the pain. In general, pain resolves after 6–8 wks of conservative
treatment (4)[C].
References
1. Alvarez-Nemegyei J. Risk factors for pes anserinus tendinitis/bursitis syndrome: a case
control study. J Clin Rheumatol. 2007;13:63–65.
2. Rennie WJ, Saifuddin A. Pes anserine bursitis: incidence in symptomatic knees and
clinical presentation. Skeletal Radiol. 2005;34:395–398.
3. http://utdonline.com/online/content/topic.do?
topicKey=st/rheum/6373&selectedTitle=2 45&source=search/result.
4. http://emedicine.medscape.com/article/90412-overview.
Additional Reading
Nokes SR, Smith T. Acute pes anserine bursitis. J Ark Med Soc. 2007;104:112.
Codes
ICD9
726.60 Enthesopathy of knee, unspecified
Clinical Pearls
Pes anserine bursitis is a cause of medial-sided knee pain.
Diagnosis can be made with local tenderness over the bursa, located 2–5 cm
distal to the joint line, a negative valgus stress test, and negative radiographs.
Treat any underlying gait abnormalities; use activity modification, ice, NSAIDs,
and steroid injection to decrease pain and inflammation.
Phalangeal Injuries
Lt. Col (P) Jeffrey C. Leggit
Basics
Attempt to reduce dislocations immediately if neurovascular compromise is suspected.
All finger phalangeal injuries require radiographic evaluation.
Description
Typically results from direct trauma, crushing injury to the distal phalanx
High likelihood of concomitant soft tissue injury (ie, nail bed trauma)
Epidemiology
Prevalence
10–15% of all sports-related injuries
50% of all hand fractures are distal phalanx fractures.
Risk Factors
Middle finger and thumb are the most commonly affected digits, due to the fact that they tend
to be more exposed than the other digits.
Etiology
Crushing injury

Nail bed trauma
Soft tissue injury
Tendon injuries
Dislocations have high risk for concomitant ligamentous injuries/disruptions
Diagnosis
Posteroanterior (PA), lateral, and oblique radiographs
Oblique or spiral fractures may also be associated with malrotation (1)[C].
History
Hand dominance
Occupation and/or athletic position
Environment surrounding injury (risk of infection)
Mechanism of injury
Associated symptoms (ie, numbness, tingling)
Physical Exam
Pain, swelling, and ecchymosis are common findings.
Subungual hematoma frequently encountered with distal phalanx fracture
Gross deformity
Malrotation (flex distal interphalangeal and proximal interphalangeal while keeping
metacarpophalangeal extended; all fingers should point toward scaphoid; if they do not,
malrotation is present)

Imaging
PA, lateral, and oblique radiographs
Oblique or spiral fractures may also be associated with malrotation (1)[C].
Inspection of nail bed for suspected laceration or hematoma
Treatment
Nondisplaced fractures:
Buddy tape nondisplaced fractures: Never leave 5th finger isolated, as tends
to get snagged (remember to place absorptive padding between digits)
Drain subungual hematoma if >50% nail bed, and repair nail bed if lacerated
Splint to avoid inadvertent trauma to fingers
Hard-sole shoe for toe fractures and weight-bearing as tolerated with
crutches or cane
Oral analgesics
Pain improves over 2–3 wks
Displaced intra-articular fractures of interphalangeal joint:
Closed reduction with longitudinal traction
Short-leg walking cast with toe platform
Acceptable reduction is <6 mm of shortening, <15 degrees of angulation, and
no rotational deformity
If unstable after closed reduction, then open reduction internal fixation is
required.
Interphalangeal joint dislocations:
Digital block anesthesia
Longitudinal traction with gentle downward pressure on distal phalanx to
reduce dislocation
Buddy tape to next digit for 2–3 wks (caution with 5th finger)
Unstable reductions require operative management (2)[C].
Surgery/Other Procedures P.
Unstable fractures
Irreducible dislocations
Consider referral for intra-articular fractures >30% surface area
Ongoing Care
Buddy tape/splint continuously for 2 wks and then during sporting events for another 4
wks
Soft shoe or splint for comfort
Patient Monitoring
Fractures that required reduction should be seen within 1 wk and repeat radiographs should
be obtained to check for fracture stability.
Subungual hematoma: 24 hr
Prognosis
Most heal well, but may remain sensitive for months (3)
Complications
Chronic pain
Chronic deformity
References
1. Lee SG, Jupiter JB. Phalangeal and metacarpal fractures of the hand.
Hand Clin. 2000;16:323–332.
2. Walsh JJ. Fractures of the hand and carpal navicular bone in athletes.
South Med J. 2004;97:762–765.
3. Peterson JJ. Clin Sports Med. 2006;25(3):527–542, vii–viii Injuries of the

fingers and thumb in the athlete.
Additional Reading
Rettig AC. Athletic injuries of the wrist and hand. Part I: traumatic injuries of
the wrist. Am J Sports Med. 2003;31:1038–1048.
Codes
ICD9
826.0 Closed fracture of one or more phalanges of foot
959.5 Other and unspecified injury to finger
959.7 Other and unspecified injury to knee, leg, ankle, and foot
Clinical Pearls
Obtain radiographs in all finger injuries.
High suspicion for concomitant soft tissue injury
Photodermatitis
Allen Richburg
Basics
Photodermatitis is an abnormal skin reaction to light or ultraviolet (UV) rays.
The reaction may be acute or chronic, allergy-mediated, or irritative and often is associated
with substances or conditions that create an increase in photosensitivity.
Description
Light-induced eruptions seen in a pattern of photodistribution on the skin
Exogenous:
Phototoxic reactions (nonallergic): Result of acute toxic effect on skin by UV light alone
(sunburn) or together with a photosensitizing substance; occurs in 100% if exposed to
enough of the agent and light
Photoallergic eruptions (allergic, delayed hypersensitivity): A form of allergic dermatitis
resulting from combined effects of a photosensitizing substance (drugs or chemical) plus
UV light
Endogenous:
Porphyria cutanea tarda: Defect in uroporphyrinogen decarboxylase, inherited and
acquired types
Erythropoietic protoporphyria: Autosomal dominant deficiency in ferrochelatase, diagnosed
in childhood
Idiopathic and immunologic:
Polymorphous light eruption: Chronic, intermittent light-induced eruption with erythematous
papules, urticaria, or vesicles owing to a certain threshold of UV light; presents in 20s and
30s; spring and summer most common
Chronic actinic dermatitis: Lichenified papules or plaques on sun-exposed areas; pruritic;
older adults
Solar urticaria: IgE formation with mast cell degranulation; urticaria minutes after sun
exposure; disappears within hours
Photoaggravated conditions:
Lupus erythematosus
Dermatomyositis
Atopic dermatitis
Seborrheic dermatitis
Ultraviolet (UV) radiation:
Both UVA and UVB are responsible for photodermatitis (light-induced eruptions); therefore,
both UVA and UVB should be blocked during outdoor sport activities.
UVA range 320–400 nm: Penetrates skin deepest; can penetrate window glass; 360-nm
wavelength is peak for many photosensitizing drugs.
UVB range 290–320 nm: Penetrates skin superficially; responsible for most acute skin
erythema
Epidemiology
Can affect patients from all backgrounds and races who are exposed to UV light
Most frequently identified photoallergens by photopatch testing: Medications, sunscreen
agents, fragrances, and antiseptics
Incidence
Up to 29.7% of persons who use sensitizing agents will get a reaction.
Prevalence
Estimated 25% of white-skinned persons in the U.S. are Fitzpatrick skin type I or II and have an
increased risk of sunburn with limited exposure.
Risk Factors
Fitzpatrick skin types:
Type I: Never tan, always burn
Type II: Occasionally tan, usually burn
Type III: Usually tan, occasionally burn
Type IV: Easily tan, rarely burn
Type V: Brown skin
Type VI: Black skin
Genetics
Skin types I and II will exceed sunburn threshold tolerance in 10–20 min of noontime-
temperature summer sunlight.
3–8 times minimal erythema dose will produce moderate to severe burn.
Other genetic conditions increase risk (eg, xeroderma pigmentosa, porphyrias).
General Prevention
Avoid sun from 10 a.m. to 2 p.m. when 2/3 of total daily UV radiation reaches the earth.
Avoid being outdoors during high UV index days.
Avoid indoor tanning beds.
Use protective clothing: Long sleeves, wide-brim hats, sunglasses.
Use tinted glass windows.
Identify and avoid sun-sensitizing drugs and agents (see under “Causes”).
Sunscreens:
No. 15 sun protection factor (SPF) or greater recommended
Apply 30 min before exposure and every 2 hr, especially after sweating and swimming.
1 oz to cover whole body
Physical blocking agents: Zinc oxide, titanium dioxide, iron oxide, kaolin
Sunscreen with ingredients that filter out both UVA and UVB rays is recommended.
UVB filters:
PABA derivatives
Cinnamates
Salicylates
Octocrylene
UVA filters:
Benzophenones
Avobenzone (Parsol 1789)
Anthranilates
Physical blocking agents:
Iron oxide
Kaolin
Titanium dioxide
Zinc oxide
Etiology
Exogenous photosensitizers:
Antiarrhythmics
NSAIDs
Phenothiazines
Diuretics
Quinolones
Tetracyclines
Thiazides
Sulfonamides
Sulfonylureas
Oral contraceptives
Topicals: Psoralens, coal tars, photoactive dyes (eg, eosin, acridine orange)
Phytophotosenitizing agents:
Citrus fruits (Rutaceae): Lemon, lime, grapefruit; furocoumarins are more concentrated in
the peel.
Fig (Moraceae)
Cayenne pepper, paprika, chili, Tabasco (Solanaceae)
Nettle (Urticaceae)
Photoallergens:
Antiseptics
Fragrances
Medications
Sunscreen filters
Diagnosis
History of previous sun or UV light exposure
Exposure to or ingestion of the many sun-sensitizing agents
Family history of similar disorders
Type of sunscreen and how the sunscreen has been used prior to reaction
Physical Exam
Phototoxic:
Erythema
With increasing severity: Vesicles and bullae
Classic example: Sunburn
Nails may exhibit onycholysis.
Chronic: Epidermal thickening, elastosis, telangiectasia, and pigmentary changes
Sharp lines of demarcation between involved and uninvolved skin (sunlight exposure)
Phototoxic eruption owing to topicals: Area of application
Usually develops shortly after sun exposure.
Hyperpigmentation may follow resolution.
Pain
Photoallergic:
Papules with erythema and occasionally vesicles
Area exposed to light with less distinct borders
Usually delayed: 24 hr or more after exposure
May spread to unexposed areas
Pruritus
Polymorphous light eruption:
Erythematous papules
Occasionally urticaria or vesicles
Scattered over sun-exposed areas with normal skin in between
Can spread to nonexposed areas
Often flares in spring or early summer
Desensitization affect (less over the course of the summer)
Burning or pruritus may precede lesions.
Chronic actinic dermatitis:
Lichenified papules on sun-exposed areas in older person
Usually pruritic
Biopsy and phototesting confirm diagnosis.
Solar urticaria:
Urticaria within minutes of UV exposure
Unidentified photosensitizing agent
Wheals itch and burn and disappear within hours.
Porphyria cutanea tarda:
Skin fragility
Blisters, crusts, milia
Mottled skin pigmentation
Hypertrichosis on periorbital area
Erythropoietic protoporphyria:
Presents by age 2
Child cries or screams in pain when exposed to sun
Burning feeling, induration, and purpura
Waxy thickening of skin on knuckles

Lab
Antinuclear antibody and other rheumatologic tests when systemic lupus erythematosus and
dermatomyositis are suspected
Check serum, urine, and stool porphyrin if porphyria is suspected.
Photopatch test: Test a small patch of a potentially photosensitive substance on the skin to
find out if this is the substance that caused the reaction. Examples of substances tested
include medications, sunscreens or other lotions, fragrances, antiseptics, and plant products.
Phototest: Test the skin for a photoreaction to UV light after normal diet and/or after ingestion
of a possible photosensitizing agent such as an NSAID, a sulfa drug, a diuretic, or an oral
contraceptive pill.
Skin biopsy: Used to determine the type of skin inflammation and the potential disease
process or malignancy
Lymphohistiocytic dermal infiltrates and spongiosis seen in the more common condition of
phototoxicity
Phototoxicity
Photoallergic reaction
Cellulitis
Pityriasis rosea
Viral exanthem
Drug eruption
Polymorphorous light eruption
Chronic actinic dermatitis
Solar urticaria
Porphyria
Atopic dermatitis
Dermatomyositis
Steven-Johnson syndrome
Treatment
Sun and light radiation protection and avoidance
Identification and avoidance of photoenhancing, -sensitizing, and -allergic
substances
Medication
Drugs of choice for phototoxic and photoallergic reactions (1,2):
Topical corticosteroids class I or II within 4–48 hr of exposure × 3 days (eg,
betamethasone valerate 0.1% cream)
NSAIDs, topical or oral (eg, indomethacin topical 5% or oral 25 mg t.i.d.;
aspirin; others)
Prednisone for severe reactions (0.5–1 mg/kg/d × 3–10 days)
Antihistamines for pruritus (eg, hydroxyzine 25–50 mg q.i.d.)
Sunscreens for prevention: Use broad-spectrum sunscreen to block both
UVA and UVB.
Treatment for polymorphous light eruption:
Desensitization with UVB or UVA (PUVA) phototherapy for 15 min 2–3 × per
week during the spring
Antimalarial drugs for protections during the spring and summer
Topical or oral steroids once the outbreak has occurred
Treatment for chronic actinic dermatitis:
Topical and oral corticosteroids
Topical tacrolimus
Low-dose PUVA
Mycophenolate mofetil
Cyclosporine
Azathioprine
Treatment for solar urticaria:
Antihistamines
Low-dose PUVA
Treatment for porphyria cutanea tarda:
Phlebotomy
Avoid hepatotoxins and iron.
Antimalarial drugs
Treatment for erythropoietic protoporphyria:
β-Carotene
Narrow-band UVB
PUVA
Contraindications: Refer to manufacturer's profile for each drug.
Precautions: para-Aminobenzoic acid (PABA), benzophenones, and
cinnamates may cause contact dermatitis. Also, if allergic to benzocaine,
procaine, paraphenylenediamine, or sulfonamides, one may have allergy to
PABA. Refer to manufacturer's profile for each drug.
Significant possible interactions: Refer to manufacturer's profile for each drug.
General Measures
Avoid sunlight/limit exposure.
Protective clothing/sunscreens
Ice packs/cold water compresses
Ongoing Care
Avoid sunlight.
Patient Monitoring
Monitor as necessary for persistence or recurrence.
Diet
No special diet
Patient Education
Avoidance of sunlight
Avoidance of photosensitizing drugs
Protective clothing
Use sunglasses that wrap around and absorb UVA and UVB rays.
Use lip balm sunscreens.
Sunscreens:
SPF 15–30 with both UVA and UVB protection
Apply 15–30 min before exposure.
Reapply generously every 1–2 hr and especially after swimming or sweating.
Stress application to be sure to cover neck and ears (one study showed that 60% of
people miss these areas).
Children:
Avoid midday sun.
For those younger than 6 mos of age, use titanium dioxide, which is less likely to irritate
the skin.
Prognosis
Good with avoidance/protection measures
Complications
Geriatric Considerations
Geriatric: More likely to experience adverse reactions to causative drugs.
References
1. Arndt KA, Hsu JTS. Sun reactions and sun protection. In: D'Amelio Miller, ed. Manual of
dermatologic therapeutics. Lippincott Williams & Wilkins, 2007:212–221.
2. Hall JC. Dermatologic reactions to ultraviolet radiation and visible light. In: Linden L, Lim
HW, eds. Sauer's manual of skin diseases. Lippincott Williams & Wilkins, 2006:364–372.
Additional Reading
Fitzpatrick TB, et al. Color atlas and synopsis of clinical dermatology: common and
serious diseases, Second ed. McGraw-Hill, 1992:210–213.
McKee PH, Calonje E, Granter SR. Pathology of the skin: with clinical correlations, Vol 1,
3rd ed. Elsevier Mosby, 2005:630–633.
Scalf LA, Davis MD, Rohlinger AL, et al. Photopatch testing of 182 patients: a 6-year
experience at the mayo clinic. Dermatitis. 2009;20:44–52.
Tyring SK, Lupi O, Hengge UR. Tropical dermatology. Elsevier Inc., 2006:441–443.
Codes
ICD9
692.72 Acute dermatitis due to solar radiation
Clinical Pearls
Use sunscreens that block UVA and UVB rays.
Consider phototoxic, photoallergic, or polymorphous light eruption as a
diagnosis for any rash in sun-exposed areas.
Physeal Injuries in Children Salter-Harris
Classification
Rachel A. Coel
Basics
Description
In pediatric bone, the primary areas of growth include the physis and the epiphysis.
Physeal injuries may occur in the skeletally immature population from acute trauma, as well
as from chronic overuse and repetitive loading.
In 1963, Salter and Harris described a classification scheme for acute injuries to the physis
(1)[C].
Although most physeal fractures heal well, growth plate injuries can lead to complications
including avascular necrosis, premature growth arrest, or angular deformities.
Epidemiology
Occurs most commonly after 10 yrs of age but can be seen in any skeletally immature
patient
Typical age range: 10–16 yrs of age; median age: 13 yrs
Predominant gender: Boys > Girls
Most common time frame: Spring through summer months (more outdoor playtime)
Most common bone location: Distal radial physis
Most common type of physeal injury: Salter-Harris type II (75%)
Prevalence
Current estimates suggest that from 15–30% of all pediatric fractures involve the physis.
Risk Factors
Skeletal immaturity
Falls, especially while running or playing
Competitive organized sports, especially contact sports
Recreational sports, including skiing/snowboarding, skateboarding, and bicycling
Overuse training activities that cause repetitive loading and stress, such as gymnastics,
cheerleading, throwing, and running
General Prevention
Monitor training demands, especially in young athletes during periods of heightened growth
Cross-training to avoid overuse and repetition
Overtraining prevention: Alternate periods of heavy training with designated periods of rest.
Etiology
There are 2 types of epiphyses: Traction epiphyses (apophyses), where major tendons
originate or insert into bone, and pressure epiphyses, at the ends of long bones.
Traction epiphyses shape and strengthen bone but do not add longitudinal growth; hence
their injury typically does not cause longitudinal growth arrest.
Pressure epiphyses add longitudinal growth to long bones.
The physis, located between the epiphysis and the metaphysis of long bones, serves as the
area of rapid longitudinal bone growth.
Injury to the physis or pressure epiphyses may result in growth disturbance.
The active physis consists of 4 zones of cells separated by cartilage matrix; the 3rd zone
(hypertrophic zone) is the area most susceptible to injury and cleavage.
The epiphysis provides the nutrient blood supply to the physis; epiphyseal injury can cause
disruption of normal growth and maturation owing to compromised vascular supply.
Diagnosis
Salter-Harris classification of epiphyseal plate injuries (1)[C]:
Type I: Complete separation of epiphysis from metaphysis without bone fracture
Type II: Separation occurs partially along physis and out through an associated metaphyseal
bone fracture.
Type III: Intraarticular epiphyseal fracture extending out through partially separated physis
Type IV: Intraarticular epiphyseal fracture extending through the full thickness of physis and
out through metaphyseal bone fracture
Type V: Severe crush injury at one area of physis
History
Fall onto an outstretched hand (FOOSH) is a common mechanism of distal radius growth
plate injury (2)[C].
Abduction, adduction, and twisting mechanisms are especially common in tibial physeal
injuries and other lower extremity growth plate injuries (1,2)[C].
Severe abduction or adduction mechanisms in the ankle or knee can cause type V crush
injury to the physis (1,2)[C].
Patient often reports “sprain” of a joint.
Chronic stress injuries to the physis may present with a history of intense training with
minimal rest or with overuse repetitive motion, such as baseball pitchers or gymnasts.
Patients complain of focal pain at the area of the physis (2,3,4)[C].
Physical Exam
Swelling
Ecchymosis
Focal tenderness to palpation
Limited range of motion owing to pain
Refusal to bear weight

Salter-Harris type I injuries are often a clinical diagnosis owing to the radiolucent nature of
physis on radiographs.
Imaging
Initial approach:
Plain x-ray trauma series: Typically 3–4 views of injured joint (anteroposterior, lateral, and
oblique) (4)[C]
Type I fractures and chronic stress injuries may appear as physeal widening, epiphyseal
displacement, or irregularity and sclerosis at the metaphysis; however, no radiographic
abnormality is common (3,4)[C].
Comparative plain films of the opposite side may be helpful (4)[C].
Stress radiography may worsen physeal injury and should be used with caution (2,4)[C].
Type II–IV fractures are usually evident on plain x-rays and demonstrate associated bone
fracture lines or bone fragmentation (Thurston-Holland sign) (1,2,3)[C].
Evaluate fractures for angulation and displacement.
Follow-up:
Growth recovery lines, or Harris lines, appear in the metaphysis on plain films typically 12
wks after trauma (4)[C].
If they are parallel to the epiphysis and extend entirely across the metaphysis, future
growth disturbance is unlikely.
If they are angled, curved, or highly irregular, subsequent growth disturbance is more likely.
If growth plate injury is suspected but plain radiographs are negative, advanced diagnostic
measures may be employed.
Further evaluation typically is advocated only if initial management of the injury will be
altered by definitive radiographic diagnosis (2)[C].
MRI: Preferred method; can identify intact versus separated growth plate, physeal
bridging, growth arrest, and avascular necrosis, as well as cartilage,
ligamentous/tendinous, and soft tissue imaging (4,5)[C].
CT scan: Useful in further defining known physeal injuries and aids in treatment planning,
such as alignment and displacement of fractures at the articular surface, growth arrest,
physeal bridging, and surgical planning (4,5)[C].
Other options include US and bone scintigraphy (2,5)[C].
Bone fractures
Sprains: Physeal injuries most commonly mistaken for sprains
Ligamentous rupture
Dislocation
Treatment
ED Treatment
Nondisplaced or minimally displaced type I and II fractures: Splint
immobilization, ice, elevation, and orthopedic referral (2)[C]
Type III and IV fractures: Obtain orthopedic consultation in ED owing to intra-
articular fracture (2)[C].
If diagnosed in ED, type V fractures require orthopedic consultation (2)[C].
Medication
Pain management should be addressed (OTC versus prescription pain
medications).
General Measures
Diagnosed type I fractures: Closed reduction and rigid immobilization (cast
versus brace) for 3–4 wks
Suspected type I fractures: Immobilization for 1–2 wks; then reexamination and
repeat radiographs for periosteal reaction. If healing reaction is evident,
immobilize for 1–2 more wks.
Type II fractures: Typically closed reduction and rigid immobilization with
casting for 3–4 wks; if unstable, refer to orthopedic surgery.
Type III and IV fractures: Refer to orthopedic surgery; often require open
reduction and internal fixation to ensure stability and joint surface congruity (1)
[C].
Diagnosed type V fractures: Non-weight-bearing cast for 3–4 wks followed by
another 2–3 wks of weight-bearing casting; refer to orthopedic surgery (1,4)
[C].
Late-diagnosis type V fractures: Frequently a missed diagnosis acutely and
diagnosed after growth disturbance has occurred; refer to orthopedic surgery
(5)[C].
Multiple attempts at reduction and reductions performed 7 days after the date
of injury are not recommended owing to increased risk of physeal injury (1)[C].
Consider bracing for sports activity for another 3–4 wks after initial rigid
immobilization is complete and while the patient is in rehabilitation.
Consider physical therapy prior to return to play for ankle and knee physeal
injuries.
May be required for significantly displaced or unstable type I or type II fractures
or, more commonly, for intraarticular type III and IV fractures
Ongoing Care
Consider bracing for sports activity for another 3–4 wks after initial rigid immobilization is
complete.
Patient Monitoring
Patients should be monitored for growth disturbance or deformity every 6 mos for the 1st yr
after physeal injury.
Thereafter, patients should be reevaluated annually until skeletal maturity owing to risk of
growth disturbance complications until adolescent growth spurt has been completed.
Patient Education
Patients and their parents should be informed of the risk of complications with growth plate
injury, including late-onset avascular necrosis, growth arrest, or deformity.
Prognosis
Estimates range from 30–75% of all physeal injuries lead to some type of growth disturbance
or angular deformity (1,3,4)[C].
However, current estimates predict only 1–10% of these patients demonstrate significant
functional deficits requiring surgical intervention (4,5)[C].
Typically, Salter-Harris type I and II fractures have a good to excellent prognosis. Types III
and IV have a poorer prognosis, and type V injury invariably results in growth disturbance
with the worst prognosis (1,2,4,5)[C].
Younger children have a worse prognosis owing to longer duration of remaining growth that
may be affected (1)[C].
Other indicators of poor prognosis include compromised epiphyseal blood supply, repeated
or forceful manipulation of physis during reduction, and open physeal fracture (1)[C].
Complications
Partial or complete growth arrest/limb-length discrepancy
Fibrous bone bar/physeal bridging
Angular deformity
Avascular necrosis
Regardless of age of onset of physeal injury, growth disturbances may not
manifest until the adolescent growth spurt (5)[C].
Risk of complications (3,5)[C]:
Greatest risk in early adolescence (pubescence) during periods of rapid
growth
Increases with higher grade acute Salter-Harris injury (types III–V) (type V
has nearly 100% focal growth arrest rate)
Increases with high-velocity, high-energy injury
Increases in lower extremity injury, especially distal femur, proximal tibia, and
distal tibia
Also may occur with chronic repetitive stress injury to physis
References
1. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint
Surg Am. 1963;45: 587–622.
2. Perron AD, Miller MD, Brady WJ. Orthopedic pitfalls in the ED: pediatric
growth plate injuries. Am J Emerg Med. 2002;20:50–54.
3. Caine D, Difiori J, Maffulli N. Physeal injuries in children's and youth sports:

reasons for concern? Br J Sports Med. 2006.
4. Rogers LF, Poznanski AK. Imaging of epiphyseal injuries. Radiology.

1994;191:297–308.
5. Khoshhal KI, Kiefer GN. Physeal bridge resection. J Am Acad Orthop

Surg. 2005;13:47–58.
See Also
Calcaneal apophysitis (Sever disease)
Codes
ICD9
813.42 Other closed fractures of distal end of radius (alone)
821.22 Fracture of lower epiphysis of femur, closed
Clinical Pearls
The Salter-Harris classification system of physeal injuries in children describes
growth plate injuries by the level of involvement of the physis, the bone, and the
joint.
Growth plate injury can occur from both acute trauma and chronic stress.
Although most physeal injuries have a favorable prognosis, up to 10% may
result in significant growth arrest, angular deformity, or avascular necrosis.
There are numerous prognostic indicators, such as age at onset of injury,
location of injury, and severity of injury.
Orthopedic surgery consultation is recommended for unstable, displaced, or
angulated fractures.
Pigmented Villonodular Synovitis (PVNS)
Nancy White
Basics
Pigmented villonodular synovitis (PVNS) is a proliferative disorder of the synovium.
There are 2 forms described, localized and diffuse, which are likely both ends of a spectrum
of the same disorder.
The synovial lesions are composed of lipid-laden macrophages, giant cells, and hemosiderin.
The knee is the most commonly involved joint.
PVNS also can involve the hip, ankle, shoulder, and elbow.
Epidemiology
Predominant age: Most commonly seen in 3rd and 4th decades; can be seen in patients as
young as 10 yrs of age or as old as the 70s
Incidence: 1.8/1 million (general population)
Risk Factors
Risk factors are unknown.
Genetics
No genetic component
Etiology
Etiology not fully understood; theories include the following:
Trauma and recurrent local hemorrhage to affected joint
Abnormal metabolic activity within the joint to cause inflammatory response (macrophages,
giant cells, hemosiderin)
Neoplastic process: Rare cases of malignant transformation have been reported.
Synovial lesions contain lipid-laden macrophages, giant cells, hemosiderin, and stromal and
fibroblast proliferation.
There are 2 forms:
Localized PVNS:
Lesions are pedunculated/lobular and localized to 1 area of synovium.
Knee is the most common joint involved.
Diffuse PVNS:
Histology is similar to localized PVNS; however, involvement is noted throughout most or
all of the involved joint, bursa, or affected tendon sheath.
Knee is the most commonly affected joint; however, can involve the hip, ankle, shoulder,
elbow.
More common than localized PVNS
Higher recurrence rate following treatment than local form
More destructive course and consequently leads to more end-stage joint disease than
localized PVNS
Diagnosis
History
Insidious onset with a history of associated trauma unusual
Symptoms are often vague and may be intermittent and are typically slowly progressive.
Swelling and stiffness out of proportion to pain
Monarticular involvement is the norm, with the knee the most commonly involved joint.
Localized PVNS symptoms most commonly involve locking/catching/instability; also can have
pain/swelling.
Diffuse PVNS symptoms include insidious onset of pain, swelling, stiffness (often mistaken
for early arthritis, meniscal or ligamentous injuries).
Physical Exam
Localized PVNS:
Effusion
Palpable synovial mass:
Most common in anterior compartment of the knee (anterior horn of medial meniscus)
Infrapatellar fat pad, suprapatellar pouch, intercondylar notch, anterior horn of lateral
meniscus also common
Tenderness to palpation
Loss of motion
Diffuse PVNS:
Global effusion of joint
Decreased range of motion (ROM)

Imaging
Plain radiographs:
Often are normal
May see periarticular erosions/subchondral cysts
Reciprocal erosions on opposite sides of the joint, with a preserved joint space, are highly
suggestive of PVNS.
CT scan:
PVNS is a high-density soft tissue mass compared with skeletal muscle.
Bone erosion and cysts may be seen.
CT scan with contrast material displays the synovial changes.
MRI:
Improved sensitivity/specifity for PVNS.
Helps to determine extent of disease
Local PVNS: MRI reveals synovial nodular mass with bone erosion; T1/T2-weighted images
show low signal owing to hemosiderin.
Diffuse PVNS:
T1/T2-weighted images show diffuse mass/synovial thickening with periarticular “dark on
dark” erosions.
Fat-suppressed images show high signal synovial mass (hemosiderin deposits not seen).
Fast field echo shows hemosiderin deposits.
Thallium-201 uptake also useful
Aspiration/joint fluid evaluation:
Blood-tinged aspirate is common, but aspirate may be clear.
Blood-tinged aspirate without a history of trauma is highly suggestive of PVNS.
Aspirate may show hemosiderin pigment and macrophages.
Aspirate may be normal.
Osteoarthritis: Similar exam/radiographs, but PVNS does not have osteophytes.
Hemophilia: Similar exam/radiographs but without history of hemophilia
Synovial hemangioma: Similar exam/radiograph but age of presentation different (PVNS 3rd–
4th decades, synovial hemangioma 1st–3rd decades)
Rheumatoid arthritis: Similar exam/radiographs but PVNS monarticular
Tuberculous arthritis: Similar exam but without periarticular osteoporosis/abscesses on
radiographs/MRI
Lipoma arborescens: Similar exam and MRI findings, but lesions show low signal
enhancement with contrast versus no enhancement
Treatment
Surgery is treatment of choice.
Localized PVNS: Arthroscopic partial synovectomy of lesion with margin of
healthy synovium is recommended.
Lesions in anterior compartment allow for surgeon to use standard
arthroscopy approach.
Lesions in posterior compartment require additional portals.
Recurrence rate is low.
Diffuse PVNS: Arthroscopy is an option, but open arthrotomy is often selected.
Extent of disease/location of lesions/surgeon's preference determine if
arthroscopy or open arthrotomy is selected.
Open arthrotomy is recommended when lesion is posterior to posterior
collateral ligament, extraarticular, or located within a cyst.
Complete synovectomy is treatment of choice.
Radiation may be combined with surgical techniques for extensive or recurrent
disease.
Joint replacement also is considered for severe or recurrent disease where
significant joint space narrowing is involved.
Ongoing Care
Patient Monitoring
No clear-cut guidelines
Recurrence is common especially with diffuse PVNS.
Consider monitoring with MRI.
Complications
Recurrence
Joint erosion
End-stage joint disease as result of erosion
Additional Reading
Adelani MA, Wupperman RM, Holt GE. Benign synovial disorders. J Am Acad
Orthop Surg. 2008;16:268–275.
Tyler WK, Vidal AF, Williams RJ, et al. Pigmented villonodular synovitis. J Am
Codes
ICD9
719.20 Villonodular synovitis, site unspecified
719.21 Villonodular synovitis involving shoulder region
719.22 Villonodular synovitis involving upper arm
PIP Joint Dislocations
Safdar Akbar
Basics
Description
Dislocation of the proximal interphalangeal (PIP) joint
Hinge joint allowing flexion and extension with little lateral movement because collateral
ligaments are tight through entire range of motion (ROM)
Dislocations may be dorsal (most common), ventral, or rotary subluxation, where the twisting
injury to the finger causes buttonholing of the head of the proximal phalanx through a tear in
the central slip and lateral band.
Synonym(s): Finger dislocation
Epidemiology
Most commonly injured joint in the hand
Risk Factors
Playing sports
General Prevention
Wear appropriate sport-specific padding and safety equipment when participating in sports or
activities.
Diagnosis
History
Ascertain the direction of dislocation if already reduced.
Determine mechanism: Dislocated finger may be due to forced hyperextension or
hyperflexion of digit from traumatic athletic injury, entrapment of finger between objects, or a
fall.
Physical Exam
Swelling and deformity if not already reduced by coach or friend
Deformity will indicate direction of dislocation.
Careful palpation about the joint to locate the most tender area can help to differentiate
between injuries.
Volar tenderness: Volar plate
Lateral joint-line tenderness: Collateral ligaments
Dorsal tenderness: Central slip injury
Neurologic examination before and after reduction: Check sensation in distal finger.
Check extensor tendon function: Have patient actively extend PIP and distal interphalangeal
(DIP) joints.
If able to extend DIP but not PIP joint, consider central slip rupture, which may lead to a
boutonniere deformity. Extended DIP and flexed PIP with late loss of DIP flexion is the most
disabling problem.
Check flexion.
Have patient actively flex PIP joint with other fingers held in extension.
Check DIP flexion with PIP held in extension.
If unable to flex DIP joint, consider flexor digitorum profundus rupture, which requires
Check collateral ligaments.
Apply radial and ulnar stress with PIP joint in full extension and 30 degrees of flexion.
Look for increased laxity.
Check volar plate.
Excessive hyperextension is consistent with volar plate injury.
If volar plate is unstable and not treated properly, it will lead to hyperextension of the PIP
joint and flexion of DIP joint, a swan-neck deformity.

Imaging
X-rays: 2 views, including anteroposterior and lateral, before reduction if possible
Oblique view if initial x-rays are negative but high suspicion of fracture
Ensure joint congruity to rule out fracture-dislocation.
May see small volar avulsion fracture
With rotary subluxation, will see true lateral view of middle phalanx with oblique view of
proximal phalanx, or vice versa
Fracture-dislocation: Large dorsal fracture-dislocations can be missed, with the volar fracture
involving >75% of joint surface with dorsal subluxation of the remaining portion of the middle
phalanx.
Central extensor tendon rupture (boutonniere injury) rupture of central slip allows lateral
bands to slip below PIP joint and cause PIP flexion with distal interphalangeal (DIP)
extension.
Treatment
Long-term treatment
Acute treatment:
Dorsal dislocation: Reduction:
If reduced before onset of swelling, reduction is easier.
Reduce with longitudinal traction and gentle pressure to the dorsal aspect
of the midphalanx.
X-rays: 2 views if not already obtained
Rule out dorsal fracture-dislocation.
Check collateral ligament stability after reduction.
Immobilization:
If dorsally dislocated and stable, simple, and reduced quickly, patient can
continue sporting activity after “buddy taping” fingers if injury is to
nondominant hand.
Stable: Splint for 1–2 wks in 15–20 degrees of flexion (also may use
extension block splint) until pain-free. Often have volar plate injury; if so,
consider splint in flexion for 4–5 wks.
Splint should include only PIP joint; may be dorsal or volar.
“Buddy tape” for an additional 3–4 wks.
Can treat with “buddy taping” alone for 3–6 wks if no volar plate injury
Volar dislocation: Reduction:
Same as for dorsal dislocation
Closed treatment if minimally displaced avulsion fracture
Avulsion fracture reduces with full extension.
X-rays: 2 views
Immobilization:
Splint PIP joint in full extension for 6 wks (dorsal or volar splint) because
central slip is often involved, DIP and metacarpophalangeal joints free.
Need to actively and passively flex DIP joint
Night splint for an additional 3–4 wks
Splint until full active extension of PIP joint and active flexion of DIP joint
Rotary subluxation: Reduction:
Sometimes difficult to reduce closed
Closed reduction:
Digital block
Gentle traction with metacarpophalangeal and PIP joints at 90 degrees of
flexion
Dorsiflex wrist (relaxes extensor mechanism).
Apply gentle rotatory and traction force.
X-rays: 2 views
Immobilization: “Buddy tape” after closed reduction.
Rehabilitation:
Dorsal dislocation: Work on ROM when out of splint.
Volar dislocation: Work on ROM of DIP and metacarpophalangeal joints while
in splint.
Rotary subluxation: Start active and passive ROM when out of splint; add
resisted ROM when pain-free, active and passive ROM.
Unable to reduce closed
Dorsal fracture-dislocation carries significant risk of long-term disability if
treated improperly.
Volar dislocation with significant avulsion fracture or fracture does not reduce
with extension and carries high risk of disability if treated improperly.
Additional Reading
Eiff MP, Hatch RL, Calmbach WL. Finger fractures. In: Fracture management
for primary care. Philadelphia: WB Saunders, 1998.
Green DP, Butler TE. Fractures and dislocations in the hand. In: Rockwood
CA, Green DP, Bucholz RW, Heckman JD, eds. Rockwood and Green's
fractures in adults, vol. 1, 4th ed. Philadelphia: Lippincott-Raven Publishers,
1996.
Green DP, Strickland JW. The hand. In: Delee JC, Drez D, eds. Orthopaedic
sports medicine: principles and practice. Philadelphia: WB Saunders,
1994:945–1017.
1998;17:513–531.
Codes
ICD9
834.02 Closed dislocation of interphalangeal (joint), hand
Clinical Pearls
Return to play can be immediate with “buddy taping” or if able to play in splint.
Volar lip fracture involves >20–70% of articular surface. Joint is unstable after
reduction and requires referral.
Recurrent dorsal dislocations occasionally can result in pseudo-boutonniere
deformity. Treat with dynamic splinting.
Piriformis Syndrome
Douglas Comeau
Alysia L. Green
Basics
Description
Sciatic nerve irritation as it courses underneath or through the piriformis muscle causing
buttock pain with or without radiation into the leg
The piriformis muscle acts as an external rotator in hip extension and an abductor in hip
flexion.
Piriformis muscle spasm or hypertrophy can occur in certain motions, such as running
downhill or repetitive motions.
Direct irritation of the sciatic nerve may be caused by inflammatory agents released from an
injured piriformis muscle.
Synonym(s): Pyriformis syndrome; Sciatica; Sciatic neuritis; “Hip pocket neuropathy”; “Wallet
neuritis”
Epidemiology
Incidence
6/100 cases of sciatica
Predominant gender: Female > Male (6:1 in some trials).
The incidence of piriformis syndrome is skewed secondary by the lack of evidence-based
guidelines. The ratio is likely higher.
Risk Factors
In roughly 20% of the population, the sciatic nerve passes through the piriformis muscle,
which may irritate the nerve and cause pain.
Leg-length discrepancy may predispose a patient to development of symptoms.
A Morton foot can predispose a patient from the change in ambulation.
General Prevention
Maintaining an appropriate lumbar core stabilization can decrease the recurrence of
symptoms.
A core stabilization program includes the anterior pelvis, posterior back, and buttocks.
Etiology
The piriformis muscle originates at the S2–3 vertebrae, sacrotuberous ligament, and upper
margin of the greater sciatic foramen.
The piriformis muscle then passes through the greater sciatic notch, inserting on the greater
trochanter.
It is innervated by L5, S1, and S2.
In hip extension, the piriformis serves as an external rotator.
In hip flexion, it serves as a hip abductor.

Sciatica
Gluteal strain
Diagnosis
History
Trauma to the gluteal region is seen in <50% of patients.
Sitting on hard surfaces exacerbates pain.
Location of referred pain; not likely piriformis syndrome if below the knee
Complaint of pain with movements that cause external hip rotation
Women may complain of dyspareunia.
Physical Exam
Cramping or aching pain in the buttock ± pain radiating into the hamstrings
Sensation of “tight hamstrings”
Point tenderness to deep palpation over any part of the piriformis muscle
Pain increased with sitting
Full range of motion and 5/5 strength in active and passive forward flexion and extension
Negative stork test
Negative straight-leg raise and negative flexion, abduction, and external rotation
Buttock pain ± radiation to hamstrings produced by combination of hip flexion, adduction, and
internal rotation; this maneuver stretches the piriformis muscle.
Pace sign: Weakness in resisted abduction and external rotation
Tenderness to palpation over the piriformis muscle
Sciatic notch tenderness
Usually normal neurologic examination
Pelvic and/or digital rectal examination elicits pain ipsilaterally proximal to the ischial
tuberosity.

Lab
No laboratory tests are recommended in the workup.
Imaging
Diagnostic imaging is rarely helpful in confirming the diagnosis.
Clinical history and physical examination are key to diagnosing piriformis syndrome.
Further diagnostic tests may be needed to rule out other potential diagnoses.
MRI and CT scanning can be used if history and physical examination are not conclusive.
Atrophy or fibrous tissue replacement of the piriformis muscle on MRI or CT scan supports
the diagnosis.
Musculoskeletal US demonstrating hypertrophy of the muscle is a newer radiologic technique
that may be used in difficult cases.
Electromyographic (EMG) findings of peronaei and/or tibial H reflex prolongation in the
adducted, internally rotated, flexed hip strongly anecdotally supports the diagnosis in some
studies; however, EMG is typically normal and not a recommended diagnostic tool.
Lumbar facet arthropathy
Lumbar spondylolysis and spondylolisthesis
Lumbosacral radiculopathy
Myofascial pain
Achilles tendonitis
Cord tumor
Spinal stenosis
Aneurysm of the inferior or superior gluteal artery
Fibrotic band around the sciatic nerve
Hematoma
Gluteal abscess
Pelvic tumor
Endometriosis and other pelvic diseases
Bursitis: Obturator internus, trochanteric or ischial
Treatment
ED Treatment
Low back pain is one of the top 10 causes of acute emergency visits.
Typically, a lumbar spine film will be taken and is negative.
The patient should be treated with NSAIDs and muscle relaxants and sent for
primary care and/or sports medicine follow-up.
Medication
First Line
NSAIDs for 10–14 days
Short course of analgesics and/or muscle relaxants may be beneficial (1)[C].
Ice
Acetaminophen
Relative rest for a short period, but should begin piriformis stretch and physical
therapy as soon as possible
Physical therapy incorporating stretching and strengthening of the piriformis
muscle; also should incorporate correction of pelvic obliquities and leg-length
discrepancies (1)[A]
Deep muscle massage with US
Continued lumbar stabilization program
Continued piriformis stretching
Injections:
With no improvement after conservative therapy, consider local injection of
anesthetic (1–2% lidocaine hydrochloride ± bupivacaine 4–6 mL) under
fluoroscopic or US guidance into the tender area within the piriformis muscle.
Botulinum toxin has shown benefit in nonrandomized, controlled trials. The
mechanism of action would be decreasing the piriformis spasm by injecting
Botox (2)[C].
Surgery as indicated earlier for recalcitrant cases of piriformis syndrome
Osteopathic manipulative treatment (OMT) may be used in conjunction with
physical therapy.
Techniques include muscle energy technique and myofascial release to help
with piriformis strengthening and stretching.
If conservative treatment fails, surgical release of the piriformis muscle around
the sciatic nerve should be used as a last resort.
Patients with documented EMG nerve impairment have the best outcome after
surgical release.
A patient typically is admitted only if preoperative for surgical correction.
Ongoing Care
Patient Monitoring
Initially, a patient should follow up with primary care or sports medicine 6–8 wks after starting
physical therapy.
On follow-up, close interaction should be maintained to ensure compliance with the home
exercise program (lumbar stabilization).
Patient Education
Patient education may include home exercise program handouts to ensure compliance.
Showing the patient a diagram of the piriformis and its closeness to the sciatic nerve may
help in patient recognition.
Prognosis
Prognosis is predicated on compliance with home exercise program and core stability.
Although compliance with core stabilization cannot guarantee lifelong relief of symptoms, a
stronger core can decrease the chance of recurrence.
Complications
Complications typically occur without early diagnosis and treatment.
Chronic low back pain may be debilitating and multifactorial.
References
1. Rouzier P. “Piriformis Syndrome.” The Sports Medicine Patient Advisor.
Amherst, MA: McKesson, 2004.
2. Kirschner JS, Foye PM, Cole JL. Piriformis syndrome, diagnosis and
treatment. Muscle Nerve. 2009.
See Also
For exercise handouts, please see The Sports Medicine Patient Care Advisor.
Codes
ICD9
355.0 Lesion of sciatic nerve
Clinical Pearls
Prevention: A strong core stabilization program to increase strength and range
of motion
Any activities that involve prolonged sitting (ie, biking) should be avoided.
Return to play: Weight-bearing as tolerated 5–10 days after surgery with
gradual return to full activity; avoidance of prolonged sitting for 4–6 wks after
surgery is recommended.
Plantar Fasciitis
Anna Dumont
Douglas J. DiOrio
Basics
Description
Degeneration and irritation of the plantar fascia origin at the medial calcaneal tuberosity on
the anteromedial side of the heel and surrounding perifascial structures
Synonym(s): Enthesopathy of plantar fascia; Plantar fasciosis
Epidemiology
Plantar fasciitis accounts for 80% of patients with plantar heel pain.
Nearly 2 million patients receive treatment each year in the U.S.
In the running population, plantar fasciitis accounts for 10% of running injuries.
Peak age of incidence is between 40 and 60 yrs, but can occur in adults of all ages.
Risk Factors
Excessive torsion and hyperpronation with poor supporting footwear
Poor shock dissipation with cavus foot
Hindfoot valgus with pronation deformity
Limited ankle dorsiflexion
Obesity and those who are on their feet most of the day
Etiology
50% of patients with plantar fasciitis will have heel spurs. Up to 19% of patients without
plantar fasciitis will also have heel spurs. Heel spurs can occur with plantar fasciitis, but they
are not the cause.
Histologic findings include myxoid degeneration, microtears in the fascia, collagen necrosis,
and angiofibroblastic hyperplasia.
Diagnosis
History
Insidious and progressive pain in the inferior heel
Worst with 1st few steps out of bed in the morning
Worsens after period of prolonged standing
Pain tends to lessen with activity and worsens at the end of the day.
Pain exacerbated with walking barefoot, on toes, or up stairs
Physical Exam
Pain at the anteromedial aspect of the heel
Worsens with activity such as running or walking
Worst pain with 1st few steps in the morning
Pain intensity increases with prolonged weight-bearing, especially while walking barefoot and
in dress shoes.
Pain can radiate across the medial side of the heel and less so to the lateral aspect.
Pain can involve both feet.
Pain can be described as throbbing, searing, or piercing.
Tenderness localized to anteromedial aspect of the heel with palpation
Tight Achilles heel cord
Pes planus or pes cavus foot deformity
Passive range of motion: Hypermobility of subtalar joint, midtarsal joint, and 1st ray
Pain with passive dorsiflexion of toes
Gait evaluation: Calcaneus everted at heel lift

Imaging
Imaging plays a limited role in routine clinical evaluation and is rarely needed. Radiographic
evaluation would be appropriate in patients who fail to improve with appropriate treatment in
a reasonable amount of time or if patient presents with an atypical history or physical exam.
X-rays may show calcifications in the soft tissues around the heel or osteophytes on the
anterior calcaneus (ie, heel spurs). US may show thicker heel aponeurosis.
Triple-phase bone scan can differentiate between plantar fasciitis and a calcaneal stress
fracture. A bone scan or MRI should be ordered when heel pain has not improved after 4–6
mos of nonsurgical treatment.
Skeletal:
Bone contusion
Subtalar arthritis
Inflammatory arthropathies
Infections (osteomyelitis/subtalar pyoarthrosis)
Soft tissue:
Intrinsic muscle strain (abductor hallucis, flexor digitorum brevis, quadratus plantae)
Plantar fibromatosis
Plantar fascia rupture
Achilles tendinitis
Posterior tibial tendinitis
Fat pad atrophy
Neurologic:
Entrapment of branches of the posterior tibial nerve usually at or after passage through the
posterior tarsal tunnel: Medial plantar nerve, lateral plantar nerve, or medial calcaneal
nerve
Radicular symptoms of L4–S1 (sciatic nerve)
Abductor digiti quinti nerve entrapment
Treatment
NSAIDs of choice for analgesic effect
Early morning stretching of heel cord as well as throughout the day
Ice massage and deep friction massage of the arch and insertion
Shoe inserts: Prefabricated insoles (ie, soft heel pads/Silastic), custom
orthotics, or medial heel wedges
Arch taping during athletic activities
Motion-control shoes with rigid heel counters
Posterior-tension night splints
Supination strap
Judicious use of long-acting steroid injections for the in-season athlete (1–3/yr)
Risk of fat pad atrophy must be noted
Dexamethasone (Decadron) iontophoresis
Physical therapy with plantar fascia: Specific stretching and Achilles tendon
stretching programs
Extracorporeal shock wave therapy
Walking cast
Conservative therapy should be used for a minimum of 6 mos and, preferably,
for 12 mos because >90% respond positively to nonsurgical management.
Acupuncture
Surgery can be considered after failure of extensive conservative therapy,
even up to 2 yrs: Operative release of proximal fascia of deep abductor fascia
Plantar fasciotomy can be either partial or complete and is a common surgical
procedure for treating recalcitrant cases of plantar fasciitis.
Postoperative therapy includes splint for 2 wks, mild stretching and ambulation
with crutches and walking boot, pool running for 3 wks, and return to activity in
3–4 mos.
Additional Reading
Clanton TO, Porter DA. Primary care of foot and ankle injuries in the athlete.
Clin Sports Med. 1997;16:453–466.
Cole C, Seto C, Gazewood J. Plantar fasciitis: evidence-based review of

diagnosis and therapy. Am Fam Phys. 2005;72:2237–2242.
Neufeld SK, Cerrato R. Plantar fasciitis: evaluation and treatment. J Am Acad

Orth Surg. 2008;16:338–346.
Codes
ICD9
728.71 Plantar fascial fibromatosis
Clinical Pearls
Surgery should only be considered after exhaustive conservative treatment of
at least 6 mos to 1 yr has failed.
A Cochrane review showed that corticosteroid injections improved plantar
fasciitis at 1 mo but not at 6 mos when compared with control groups.
Pneumothorax and Hemothorax
Russell D. White
Emily Lott
Basics
Description
Air (pneumothorax), blood (hemothorax), or both (hemopneumothorax) in the pleural space
between the lung and chest wall
Tension pneumothorax: Progressive accumulation of air in the pleural space causing
compression of chest structures including heart and restricting venous return and the
contralateral lung; can lead to cardiac arrest. Differentiated from simple pneumothorax by
mediastinal shift toward the uninvolved lung on x-ray and/or ipsilateral diaphragm flattening or
inversion on x-ray.
Pneumothorax can be categorized as:
Spontaneous: No obvious precipitating factor present; further divided into:
Primary: No apparent underlying disease
Secondary: Clinically apparent underlying disease (such as COPD or cystic fibrosis)
Catamenial: Occurs in conjunction with menstruation
Nonspontaneous or traumatic: Caused by trauma; can be further divided into penetrating or
nonpenetrating chest injury
Iatrogenic: Secondary to a procedure such as transthoracic or transbronchial biopsy,
subacromial injections, central line placement, pleural biopsy, or thoracentesis
Synonym(s): Collapsed lung
Epidemiology
Rare, but potentially serious
<4% of all sports injuries involve the chest or abdomen.
Incidence
20,000 new cases of spontaneous pneumothorax are reported each year in the U.S.
Primary spontaneous pneumothorax affects 9,000 persons in the U.S. each year.
Activity reported to be related to pneumothorax in <10% of cases
Predominant gender: Male > Female (6:1)
Risk Factors
Tall, thin, young (20s–40s), males (primary spontaneous pneumothorax)
Smoking (spontaneous pneumothorax)
Substance use such as heroine, ecstasy, marijuana, speed, and cocaine (spontaneous
pneumothorax)
Congenital apical lung blebs
Underlying lung disease (eg, COPD, cystic fibrosis, TB)
Connective tissue disorder (Marfan)
Homocystinuria
Trauma, especially rib fractures (most commonly 1st 4 and last 2, multiple, or flail segments)
or scapular fractures
Preparticipation recommendations:
If patients want to SCUBA dive, should perform assessment of expiratory flow rates and
conventional spirometry in those with underlying lung disease
MEF50 and MEF25 or MEF25-75 should be at least 80% of predicted values.
Genetics
Some reports of familial clustering of primary spontaneous pneumothorax: Autosomal
dominant, autosomal recessive, polygenic, and X-linked recessive inheritance mechanisms all
have been proposed.
Birt-Hogg-Dube syndrome:
Autosomal dominant
Predisposes to skin tumors and renal cancer
Associated with increased incidence of primary spontaneous pneumothorax
Gene responsible for this familial cancer syndrome (called FLCN) has been mapped to
chromosome 17p11.2. Other mutations of FLCN have been associated with spontaneous
pneumothorax and bullous lung disease in the absence of the oncologic manifestations.
General Prevention
Avoid smoking and substance use.
If history of pneumothorax, avoid contact sports and trauma.
Etiology
Spontaneous pneumothorax:
Theorized to be caused by the rupture of subpleural blebs
Rupture caused by increased intrathoracic pressure
Traumatic pneumothorax and iatrogenic pneumothorax:
Caused by tear in visceral pleura resulting in air leak into the pleural space
Trauma may be penetrating or nonpenetrating.
Hemothorax: Caused by virtually any disruption of the tissues of the chest wall and pleura
with subsequent bleeding
Precipitating factors may include atmospheric pressure changes and exposure to loud music.

COPD
Cystic fibrosis
Diagnosis
Pre Hospital
Initial evaluation should include vital sign assessment and auscultation in a quiet setting.
History
Trauma to thoracic wall
Persistent pain at injury site
Shortness of breath
Localized chest pain, especially on deep inspiration, frequently present: May radiate to neck,
shoulder, back, or abdomen
Dyspnea and/or tachypnea frequently present
Up to 25% of patients are asymptomatic.
Physical Exam
Decreased or absent breath sounds on affected side
Decreased tactile fremitus on side of pneumothorax
Unequal expansion of right and left sides of chest with inspiration
Hyperresonance to percussion in the case of pneumothorax; dullness to percussion in the
case of hemothorax
In tension pneumothorax, tracheal deviation away from site of pneumothorax, neck vein
distension, and laterally displaced cardiac impulse all may be present.
Crepitation or SC emphysema may be present, especially in traumatic pneumothorax.
Possible pallor or cyanosis (usually with tension pneumothorax)
Tachycardia may be present.

Imaging
Upright posteroanterior and lateral chest films:
Inspiratory and expiratory films have equal sensitivity in detecting pneumothoraces, so a
standard inspiratory chest radiograph is sufficient in most cases (1).
Pneumothorax is demonstrated by a white visceral pleural line on the chest radiograph.
The visceral pleural line defines the interface of the lung and pleural air and is either
straight or convex toward the chest wall with no pulmonary vessels usually visible beyond
the visceral pleural edge.
Rib x-rays on affected side
CT scanning generally is not necessary unless abnormalities are noted on the plain chest
radiograph that require further evaluation or poor chest tube placement is suspected (1).
ECG often demonstrates right-axis deviation, decreased QRS amplitude, and precordial T-
wave inversion.
If hemodynamically unstable and findings are consistent with a pneumothorax (most likely
tension pneumothorax), may consider emergency needle aspiration, which is both diagnostic
and therapeutic
Diagnosis is confirmed by rapid gush of air coming through the needle.
Chest wall/rib contusion
Lung contusion
Costochondral separation
Muscle strain
Fracture
Treatment
Pre-Hospital
Acute treatment:
Determine if patient is hemodynamically stable because primary job is to
stabilize.
ABCs of basic life support, especially airway management
Determine diagnostic possibilities; transfer to hospital (x-ray) facility if
suspicious for pneumothorax
Semi-Fowler position
Oxygen if available and if patient is dyspneic
If unstable and/or findings consistent with a tension pneumothorax,
emergency needle decompression (thoracostomy) should be performed.
Needle decompression is performed by inserting a large-caliber needle
(usually 14 or 18 gauge), preferably with a catheter over needle, into the 2nd
intercostal space at the midclavicular line just above the 3rd rib.
If catheter over needle, then remove needle and leave plastic sheath; may
attach a syringe
Flail chest may accompany rib fractures; if present, stabilize flail segment
with manual pressure or a bulky dressing to the segment
Emergency personnel:
Oxygen
IV line placement
Transport to emergency facility
P.
ED Treatment
Obtain chest x-ray.
Further treatment depends on patient characteristics and clinical
circumstances.
When pneumothorax small (<20%) tension-free pneumothorax (no
mediastinal shift) and patient is hemodynamically stable, treat expectantly
without chest tube and with supplemental oxygen and observation only (1)[C].
Must be observed in the ED for at least 6 hr with follow-up films obtained
before discharge showing no progression of pneumothorax and again in
12–48 hr (1)[C]
Must have access to emergency medical services (1)[C]
Exception is when associated with underlying lung disease: Requires
urgent and immediate treatment (1)[C].
When pneumothorax is large (>20%) and clinically stable, treat initially with
pleural aspiration (1)[A].
If aspiration fails, treat with closed thoracostomy chest tube insertion with
Heimlich valve or, preferably underwater seal (1)[A].
Should also consider video-assisted thoracoscopic surgery (VATS) with
aerosolized talc during the same hospitalization based on the high success
rate of VATS, both short and long term (1)[A].
Chemical pleurodesis with talc slurry should be performed through the
chest tube if VATS is indicated and is not readily available or patient
refuses (1)[A].
In cases of recurrent primary spontaneous pneumothorax when patient is
clinically stable, treat with VATS after chest tube insertion; should perform
recurrence prevention at the same time (pleurodesis) (1)[B]. Chemical
pleurodesis with talc slurry should be performed through the chest tube if
VATS is indicated and is not readily available or patient refuses (1)[A].
If patient is clinically unstable, he or she should undergo chest tube insertion
(1)[C].
If the chest tube insertion is delayed, decompression can be performed as
a bridge by advancing a standard 14-gauge IV catheter into the pleural
space at the junction of the midclavicular line and the 2nd or 3rd intercostal
space (1)[C].
The chest tube can be connected to a water-seal device. Suction should be
applied to the chest tube if the pneumothorax fails to resolve (1)[C].
Chest tube size recommendations:
Patients who require mechanical ventilation or who may have a large air leak
should be managed with a 24–32Fr chest tube.
All other patients who require chest tube insertion can be managed with a
16–22Fr chest tube or a ≤14Fr chest catheter.
Hemothorax with even a small pneumothorax requires a chest tube to preclude
development of “trapped lung,” which eventually may require decortication.
Medication
Lidocaine (Xylocaine) 1% for chest tube insertion
Oral or IV medication prior to chest tube insertion and after as needed for
comfort
May consider Tylenol 3 or other narcotic for oral use, especially around time of
chest tube insertion
Referral
Should refer to cardiothoracic surgeon in cases of persistent air leak or
recurrent pneumothorax requiring further intervention.
Avoid chest binders, taping, etc., which tend to compromise deep inspiration and
may contribute to the development of atelectasis.
Video-assisted thoracoscopic surgery (VATS):
Should consider, along with chest tube placement, if pleural aspiration alone
is unsuccessful (1)[A]
Should perform in cases of recurrent primary spontaneous pneumothorax
after chest tube insertion (1)[B].
Should perform pleurodesis with aerosolized USP talc at the same time (1)
[B].
Consider in patients being managed with a chest tube who have a persistent
air leak (1)[B].
If preventive procedure is required, VATS with pleurodesis is recommended
over tube thoracostomy with chemical pleurodesis because it reduces the
recurrence rate to <5% (1)[B].
Thoracotomy:
Alternative to VATS
Rarely necessary
As a general rule of thumb, air from the pleural space is absorbed at a rate of
1.25% per day.
Supplemental oxygen can accelerate this rate 3-fold.
Hospital treatment:
If aspiration fails, treat with closed thoracostomy–chest tube insertion with
Heimlich valve or, preferably, underwater seal (1)[A].
Should also consider VATS during the same hospitalization based on the high
success rate of VATS, both short and long term (1)[A].
Chemical pleurodesis with talc slurry should be performed through the chest
tube if VATS is indicated and is not readily available or patient refuses (1)[A].
In cases of recurrent primary spontaneous pneumothorax when patient is
clinically stable, treat with VATS after chest tube insertion; should perform
recurrence prevention at the same time (pleurodesis) (1)[B].
Chemical pleurodesis with talc slurry should be performed through the chest
tube if VATS is indicated and is not readily available or patient refuses (1)[A].
The chest tube can be connected to a water-seal device. Suction should be
applied to the chest tube if the pneumothorax fails to resolve (1)[C].
For patients being managed with a chest tube whose lung is at least 90%
expanded but who have an air leak that persists longer than 3 days, the chest
tube may be attached to a Heimlich valve, and the patient may be discharged
home if the patient is responsible and is easily followed on an outpatient
basis (1)[C].
For patients being managed with a chest tube who have a persistent air leak
and whose lung is <90% expanded, consider VATS (1)[B].
Should be accomplished in ED, but continue to be mindful.
Airway management, if change in condition
Chest tube placement, if not done in ED
Continue supplemental oxygen.
Admission Criteria
Hemodynamically unstable
Tension pneumothorax and/or chest tube placement
Pneumothorax with >15–20% volume loss
All patients with secondary spontaneous pneumothorax
P.
IV Fluids
With pneumothorax, needed only if hemodynamically unstable
Recommended in case of hemothorax because there is likely to be volume
loss, which may lead to shock if not treated appropriately
Isotonic fluids, such as normal saline or lactated Ringer's
Discharge Criteria
Resolution of pneumothorax with removal of chest tube
Chest tube can be removed when air leak has stopped and x-ray confirms lung
expansion; usually within 24–72 hr.
Re-x-ray after removal of chest tube (prior to discharge) to check for
recurrence.
Ongoing Care
Preventative intervention with VATS or chemical pleurodesis with tube
thoracostomy recommendations:
If recurrence occurs, consider VATS, pleurodesis, or on occasion,
thoracotomy.
For patients who are not operative candidates or who refuse VATS, tube
thoracostomy with chemical pleurodesis is recommended over tube
thoracostomy drainage alone because it reduces the recurrence rate to <25%
(1)[A].
Advise patient that pain likely will be present for at least 6 wks, especially if rib
fracture produced the pneumothorax.
May return to conditioning 3–4 wks after pneumothorax resolved, provided no
evidence of pneumothorax on chest x-ray
May return to play soon after
Should consider extra padding
Patient Monitoring
Recheck chest x-ray in 4–6 wks.
Diet
No special considerations
Patient Education
Counsel on high risk of recurrence: For traumatic pneumothorax, there is no
increased risk of recurrence compared with other types.
Counsel against smoking.
Air travel recommendations (2):
Commercial air travel is contraindicated in the presence of an acute,
unresolved pneumothorax or congenital pulmonary cysts.
Avoid during exacerbations of chronic lung disease.
For commercial travelers, no travel for 4–6 wks after resolution of
pneumothorax
For the military, air travel may be restricted for 6–9 mos
Take all prescribed pulmonary medications before and during flight as
scheduled.
May restrict air travel in persons with a history of pneumothorax with
underlying lung disease
SCUBA diving absolute contraindications:
A history of a spontaneous pneumothorax (3)[A]
Diving within 3 mos after any type of nonspontaneous pneumothorax (4)
Expert divers with recurrent pneumothorax following a pleurectomy (4)
Prognosis
Depends on type and extent: Small (<20%) usually resolve on own without
treatment.
When associated with underlying disease, even when small, is more serious
and has a mortality rate of 15%.
Recurrence rate is 40% for both primary and secondary pneumothoraces.
Most recurrences occur within 1.5–2 yrs; recurrence is at its highest likelihood
in the 1st few months after the initial pneumothorax.
For traumatic pneumothorax, there are no data to suggest that there is an
increased risk of recurrence with or without return to play.
Recurrence rate increases with each recurrence.
Most recurrences are seen on the same side, but not always.
Complications
Recurrence: If it occurs, consider VATS pleurodesis or thoracotomy.
References
1. http://uptodateonline.com/online/content/topic.do?
topicKey=pleurdis/9228&selectedTitle=2 150&source=search/result,
accessedon August 30, 2009.
2. http://uptodateonline.com/online/content/topic.do?
topicKey=pleurdis/9127&selectedTitle=7 150&source=search/result,
accessed on August 30, 2009.
3. http://diversalertnetwork.org/medical/faq/faq.aspx?faquid=36
4. http://scuba-doc.com/spntpnu.htm
Additional Reading
Amaral JF. Thoracoabdominal injuries in the athlete. Clin Sports Med.
1997;16:739–753.
Codes
ICD9
512.0 Spontaneous tension pneumothorax
512.1 Iatrogenic pneumothorax
512.8 Other spontaneous pneumothorax
Clinical Pearls
Return to activity:
Return to play: 3–6 wks
Air travel: 4–6 wks after chest tube removal (if repeat x-ray is okay)
SCUBA diving: Contraindicated, if spontaneous pneumothorax
Popliteal Tendonitis
Michael A. Krafczyk
Seth M. Burkey
Basics
The popliteus muscle originates from the popliteal saddle on the lateral femoral condyle.
It then runs deep to the lateral collateral ligament (LCL) and then goes intraarticular. It
courses through the popliteal hiatus of the coronary ligament and inserts on the posterior tibia
under the tibial condyles (1).
There are also attachments to the fibula (popliteofibular ligament) as well as the lateral
meniscus, posterior cruciate ligament (PCL), and posterior capsule.
The femoral origin of the popliteus is consistently anterior and distal to the femoral
attachment of the LCL.
Its primary function is that of internal rotation of the tibia on the femur.
Also an important structure in preventing external tibial rotation
Also may help the PCL prevent forward displacement of the femur during deceleration and
downhill running
Description
Popliteal tendinitis involves irritation, swelling, and pain along the length of the tendon that
courses lateral around the femoral condyle.
It is often seen with downhill running. It presents as posterolateral knee pain that is worse
with downhill running and sitting cross-legged.
Epidemiology
Uncommon
Risk Factors
May occur as overuse injuries or acutely such as in trauma.
Commonly seen in downhill running (cross-country), walking (backpacking)
Poor conditioning
Pes planus foot (hyperpronation)
Quadriceps weakness
General Prevention
Appropriate warm-up and stretching
Adequate rest and recovery during sports participation
Proper training technique
Foot orthoses for pes planus
Maintain good quadriceps strength.
Etiology
Usually due to repetitive stress, such as seen in runners
Almost always a result of quadriceps overuse
Also may be due to a blow to the anteromedial border of the knee, a hyperextension injury,
or a varus noncontact injury
Diagnosis
History
The patient will complain of insidious lateral or posterolateral knee pain.
May elicit a history of walking, backpacking, and running, such as downhill or cross-country
Can be intermittent or constant
Worse with weight bearing when the knee is between 15 and 30 degrees of flexion
The patient also may describe trauma directed to the anteromedial border of the knee,
hyperextension, or a varus injury.
Physical Exam
Palpation of the tendon insertion along the lateral femoral condyle will reveal pain. Tendon is
best palpated with the patient in a figure-of-4 (cross-legged) position and palpating just
posterior and just anterior to the LCL (2).
The Garrick test involves testing the popliteus with the patient supine and the hips and knees
flexed to 90 degrees, in which resisted internal rotation of the knee provokes pain. Passive
external rotation with the knee in the same position also can provoke pain (3)[C].
Shoe-removal maneuver, in which the sitting patient internally rotates the injured lower leg
and foot to push the contralateral shoe off, also may produce pain.

Imaging
Plain films may reveal calcific deposits of the tendon in cases of calcific tendonitis or signs of
possible avulsion fracture as in trauma.
MRI will reveal fluid and inflammation of the popliteus sheath and tendon.
Arthroscopic examination of the knee can reveal synovitis of the sheath or hydroxyapatite
deposits (4).
Iliotibial tract tendinitis
Biceps femoris tendinitis
Lateral meniscal tear
Lateral collateral ligament injury
Treatment
Initial treatment: Rest, ice, anti-inflammatory medications
Followed by stretching and intensive strengthening exercises of the quadriceps
and hamstrings (4)[C]
Modify activity: Limit downhill running or aggravating activity.
Arch support if pes planus is present
Medication
Anti-inflammatory medications, such as NSAIDs, either orally or topically
Glucocorticoids, either injected or via iontophoresis, may be beneficial for
acute tendinitis of <3 mos (however, they should be avoided in chronic
tendinopathies, possibly leading to tendon rupture) (5).
Topical glyceryl trinitrate patches placed directly over the tendon act as a
potent signaling molecule that stimulates collagen synthesis in tendon cells.
Activity modification to limit the volume and intensity of loads placed on the
tendon, such as running on more level ground or running in the opposite
direction on a track
Eccentric and heavy-load exercises, guided by a therapist, appear to stimulate
tissue remodeling and normalization of tendon structure.
Static or dynamic stretching following activity, when muscles are warm
Ice and/or heat may be beneficial for reduction in swelling and improved pain.
Joint mobilization may decrease stiffness, which can contribute to altered
movement patterns and abnormal tendon loading.
Friction massage has been shown in animal studies to increase tendon
fibroblast activity.
As with other injuries, gradual return to activities is encouraged.
Referral
Ruptured tendon
Calcific tendinitis
Failed conservative therapy
Additional treatment options include:
Prolotherapy
Sclerotherapy
Dry needling
Platelet-rich plasma therapy
Shock wave therapy
Acupuncture
Manipulative therapy
Surgery is indicated for tendon avulsion or complete tears.
For chronic tendinopathies, surgery includes incising the paratendon and
removing the adhesions, followed by macroscopically degenerate tissue.
Longitudinal incisions can be made in the tendon in hopes of promoting a repair
response.
Resection or drilling of the tendon's attachment points also has been
described.
Minimally invasive arthroscopic surgical procedures have been developed to
limit lengthy rehabilitation and include débriding the area of neovascularization.
In cases of calcific tendinitis, arthroscopic washout and removal of calcium
deposits have proven helpful.
Ongoing Care
Complications
Tendon rupture
Calcific tendinitis
References
1. Blake SM, Treble NJ. Popliteus tendon tenosynovitis. Br J Sports Med.
2005;39:e42; discussion e42.
2. Mayfield GW. Popliteus tendon tenosynovitis. Am J Sports Med.

1977;5:31–36.
3. Olson WR, Rechkemmer L. Popliteus tendinitis. J Am Podiatr Med Assoc.

1993;83:537–540.
4. Radhakrishna M, Macdonald P, Davidson M, et al. Isolated popliteus injury

in a professional football player. Clin J Sport Med. 2004;14:365–367.
5. Khan K. Overview of the management of overuse (chronic) tendinopathy.

UpToDate; June 2009.
Codes
ICD9
726.69 Other enthesopathy of knee
Posterior Cruciate Ligament (PCL) Tear
Priscilla Tu
Basics
Description
Rupture of any or all parts of the posterior cruciate ligament (PCL) of the knee (anterolateral
portion and posteromedial portion)
Epidemiology
Incidence
All knee injuries in general population 3%
Knee injuries in trauma patients 38%
Knee injuries in athletes <1%, although may be underreported and/or underdiagnosed
Risk Factors
Contact sports, especially American football
Other sports, specifically soccer, skiing, and wrestling

Lateral or medial collateral ligament tears
Meniscal derangement
Posterolateral corner injury
Tibial plateau fractures
Bony avulsions at the insertions of the cruciate ligament
Avulsion fracture at the tibial tubercle
Fibular head fracture
Chondral injury
Posterior knee subluxation or dislocation caused by hamstring force in the PCL-deficient knee
Diagnosis
History
“Dashboard injury”: Traumatic injury, often seen in motor vehicle accidents, with posteriorly
directed force to the anterior proximal tibia in a flexed knee
Similar mechanism to preceding in sports, particularly in American football and wrestling, with
opponent's hit to lower leg driving tibia backwards and rupturing PCL
Often in sports, fall onto flexed knee, particularly with foot plantarflexed
Less commonly, cutting, twisting, and hyperextension injury in sports; often accompanied by
other ligament injuries
Physical Exam
Mild to moderate pain in the knee
Rapid onset (within few hours) of swelling and tenderness in knee
May have difficulty walking or walk with slight limp
May experience feeling of instability in the knee
Pain with kneeling, squatting, twisting, or walking up or down stairs and inclines
Discomfort felt with flexion
Anterior patellar contusions may be seen.
Posterior knee or popliteal ecchymosis may be found.
Neurovascular examination:
Perform neurovascular examination before other provocative tests.
Important to determine and document associated nerve damage or vascular injury
(particularly popliteal artery injury)
Comprehensive knee examination:
Rule out dislocation.
Rule out other ligament or meniscus injuries.
Posterior drawer test:
Perform with the patient supine and knee flexed at 90 degrees and hip flexed at 45
degrees
Examiner stabilizes foot.
A posteriorly directed force is applied to the proximal tibia to elicit abnormal posterior tibial
translation.
Posterior translation of 0–5 mm (grade 1), 5–10 mm (grade 2), and >10 mm (grade 3)
90% sensitive and 99% specific for diagnosing PCL tears
Posterior sag test:
degrees
Examiner stabilizes both heels.
Observe the knee from lateral perspective.
Normally, the tibial plateau sits 1 cm anterior to the femoral condyles.
An abnormal contour, or sag, of the tibial plateau in relation to the femoral condyles is
consistent with PCL deficiency.
Quadriceps active test:
degrees
Examiner stabilizes the foot, and the patient attempts to extend the knee while the
examiner applies a counter force against the ankle.
Patient also may be asked to activate quadriceps by sliding foot down the table.
In a PCL-deficient knee, the posteriorly subluxed tibia will translate anteriorly with
quadriceps activated.
Dynamic posterior shift test:
Patient is supine with knee and hip flexed at 90 degrees.
Examiner slowly extends knee.
With a PCL tear, there will be “clunk” near full extension when the posteriorly subluxed tibia
is reduced.

Imaging
Radiographic evaluation with anteroposterior (AP), lateral, sunrise, and tunnel views to rule
out bony avulsions, other fractures, or patellar subluxations
Oblique views are sometimes helpful to rule out tibial plateau fractures.
Flexion weight-bearing posteroanterior and patellar radiographs can help to distinguish early
degenerative changes from chronic PCL deficiencies.
Stress radiographs: 8 mm or more posterior tibial translation is indicative of complete PCL
tear.
Radionuclide bone scans are able to distinguish early degenerative changes in medial and
patellofemoral compartments from chronic PCL deficiencies.
MRI:
Reported to be up to 100% sensitive and specific in evaluating complete PCL rupture.
Only about 67% sensitive in identifying partial PCL tears
Proton density sequence is more sensitive than T2-weighted images for identifying isolated
PCL tears.
Also can evaluate other soft tissue pathology of the affected knee
ACL tear
Tibia or fibular fracture
Medial or lateral collateral ligament tear
Meniscal derangement
Posterolateral corner injury
Knee dislocation
Treatment
Acute treatment:
Ice
NSAIDs
Compression
Elevation
Immobilization:
Partial weight-bearing
Possible immobilization in full extension for grade 3 lesions
Early surgical repair is indicated for patients with associated avulsion fractures
or other ligament involvement.
Indications include:
Associated bony avulsion fractures
Multiple ligament injuries
Persistent pain in grade 3 lesions
Chronic symptomatic instability with activities of daily living or with sports
Acute grade 3 injury in young, active patient
Ongoing Care
Grade 1 and 2 lesions:
Early range of motion
Aggressive quadriceps strengthening
Protection of knees against posterior sag
PCL brace may be useful but not proven effective.
Grade 3 lesions:
2–4 wks of immobilization in full extension to protect posterolateral structures from
posterior tibial translation
Early range of motion
Quadriceps strengthening with quadriceps sets and straight-leg raises
Hamstring strengthening
Functional PCL brace may be useful during activity but not proven effective.
Referral to orthopedic surgery if indicated, as above
Early orthopedic referral except in uncomplicated, isolated grade 1 and 2 lesions
Early physical therapy referral may be beneficial because loss of proprioception and sprint
speed are major problems with return to play.
Complications
Nonoperative:
Chronic PCL laxity
Progressive medial compartment and patellofemoral degeneratative changes
Operative:
Most common: Residual laxity
Iatrogenic neurovascular injury (especially of the popliteal artery)
Loss of motion
Infection
Medial femoral condyle osteonecrosis
Anterior knee pain
Painful hardware
Additional Reading
Colvin AC, Meislin RJ. Posterior cruciate ligament injuries in the athlete—
diagnosis and treatment. Bull NYU Hosp Jt Dis. 2009;67:45–51.
Cosgarea AJ, Jay PR. Posterior cruciate ligament injuries: evaluation and
management. J Am Acad Orthop Surg. 2001;9:297–307.
Harner CD, Höher J. Evaluation and treatment of posterior cruciate ligament

injuries. Am J Sports Med. 1998;26:471–482.
St Pierre P, Miller MD. Posterior cruciate ligament injuries. Clin Sports Med.
1999;18:199–221, vii.
Codes
ICD9
Clinical Pearls
In isolated grade 1 and 2 PCL tears, uncomplicated patients may be able to
return to play within 2–4 wks depending on the sport.
In grade 3 injuries, uncomplicated patients may take up to 3 mos of
rehabilitation before return to play.
Posterior Interosseous Nerve Syndrome
Roberta Kern
Richard A. Okragly
Basics
Description
Compression/entrapment of the posterior interosseous nerve under the extensor carpi
radialis longus that presents with variable weakness to loss of function of finger and thumb
extensors
Initially pain and weakness may have been noted about the elbow and/or forearm.
Epidemiology
Dominant arm is involved twice as much as the nondominant arm
Risk Factors
Repetitive pronation and supination (usually strenuous activity)
Trauma
Monteggia fracture
Synovitis
Soft tissue masses:
Thickened arcade of Frohse
Lipoma
Neuroma/ganglia
Fibroma
Tight arm bands, eg, holding a rifle sling wrapped around the forearm for prolonged periods,
as seen in military recruits
General Prevention
Avoidance of preventable risk factors
Etiology
The posterior interosseous nerve is a continuation of the motor branch of the deep radial
nerve, tracking distally across the surface of the abductor pollicis longus and yielding
branches to the extensor pollicis longus (EPL) and adductor pollicis longus (APL) and the
extensor indicis.
Nerve roots, mainly C6, C7, and C8, with main contribution from C7

Direct trauma to the nerve, as with laceration
May be associated with synovitis of the radiocapitellar joint
Entrapment of the fibrous edge of the extensor carpi radialis brevis (ECRB)
Compression of the radial recurrent artery
Diagnosis
History
Weakness or inability to extend the wrist and digits
Pain in the deep exterior muscle group distal to the radial head:
Can be dull or sharp pain
Not a primary complaint
May precede the weakness
No sensory deficits
Physical Exam
Sensation intact
Radial deviation of the hand on wrist extension owing to paralysis of the extensor carpi
ulnaris muscle
Intact extensor carpi radialis longus and brevis, which are innervated distal to the posterior
interosseous nerve
Unable to extend digits at the metacarpophalangeal joint
Tenderness on deep palpation along proximal radius

Imaging
Plain radiographs: Obtained to exclude fractures, dislocations, healing callus, arthrosis, or
tumor as causes of the symptoms
MRI/CT scan/US:
To detect soft tissue masses (such as lipomas and ganglions) as well as aneurysms
Also to look for rheumatoid synovitis
Electromyelography (EMG)/nerve conduction studies (NCSs): See next section.
Electrodiagnostic testing: Typically need to wait 17 days to see electrophysiologic response to
Wallerian degeneration of motor fibers.
Normal sensory nerve action potentials (SNAPs)
Drop in compound muscle action potential (CMAP) amplitude or conduction when stimulated
between brachialis and brachioradialis muscles and recorded proximal to extensor indicus
proprius
Needle examination reveals membrane instability (positive sharp waves) in muscles distal to
supinator muscle.
Triceps, brachioradialis, and extensor carpi radialis longus and brevis are spared.
Supinator muscle may or may not be affected.
Serial exams can document recovery (every 3–6 mos).
Other radial nerve injuries, including:
Radial nerve palsy
Radial tunnel syndrome
Wartenberg syndrome
C7 radiculopathy
Lateral epicondylitis (tennis elbow)
Rupture or dislocation of any of the extensor tendons
Treatment
Conservative management that includes:
Rest
Ice
Anti-inflammatory medications
Immobilization
Time frame for conservative treatment varies from 1–6 mos.
ED Treatment
Immobilize with a cock-up wrist splint.
Medication
First Line
NSAIDs [C]:
Use for 4–6 wks.
Help with pain relief
If no resolution of symptoms, then may proceed to steroid injection.
Second Line
Corticosteroid injection [C]:
Place injection 4 cm distal to lateral epicondyle.
Doses and types of corticosteroids vary but can include 1 mL of local
anesthetic with 1 mL of corticosteroid.
Physical therapy that includes:
Range-of-motion exercises that increase strength, endurance, and postural
awareness
Progressive strengthening and modified work simulated tasks
Application of heat and/or US
Massage
Duration of therapy varies from 1–6 mos.
Done in adjunction with treatment with medications
Referral
Refractory cases (3 mos without improvement)
Progressive symptoms despite treatment
If severe, a dynamic splint is needed to hold the fingers in extension.
Occupational therapy consult
Surgical decompression may be necessary in refractory cases.
Ongoing Care
Will need close follow-up with a surgeon after surgery to prevent any postoperative
complications (eg, flexion contracture at the elbow)
It is important to start physical therapy/rehabilitation 7–10 days postoperatively to prevent
contractures and stiffness.
Additional Reading
Alba CD. Therapist's management of radial tunnel syndrome. In: Mackin E, Callahan A,
Skirven T, et al. eds. Rehabilitation of the hand and upper extremity 5th ed. Philadelphia,
PA: Mosby, 2002.
O'Connor FG, Ollivierre CO, Nirschl RP. Elbow and forearm injuries. In: Lillegard WA,
Butcher JD, Rucker KS, eds. Handbook of sports medicine 2nd ed. Boston: Butterworth
Heinemann, 1999:150–151.
Stern, Mark. Radial Nerve Entrapment. www.emedicine.com. September 2, 2009.
Wheeless III, Clifford R. Posterior Interosseous nerve compression syndrome. Wheeless

Textbook of Orthopaedics. www.wheelessonline.com. Updated Janurary 3, 2010.
Codes
ICD9
354.3 Radial nerve lesion
Clinical Pearls
Function usually returns with conservative therapy in a few weeks.
Surgery is rarely necessary.
Posterolateral Capsular Tear
Matt Roth
Jacklyn Kiefer
Basics
Description
Posterolateral corner (PLC) of the knee is composed of the posterior lateral capsule and its
supporting structures.
The supporting structures of the PLC are composed of the popliteus muscle/tendon complex,
the popliteofibular ligament, the lateral collateral ligament complex, and the arcuate-
fabellofibular ligament complex.
Biomechanically, the PLC is a primary restraint to both varus motion and external rotation of
the tibia, and helps to resist posterior translation (1)[C].
When some or all of these structures are damaged, a pathologic laxity occurs that can result
in varus and rotational instability and chronically can lead to post-traumatic arthritis (1)[C].
Grading system:
Address both varus opening and rotational instability compared to unaffected side
Grade I: Posterolateral pain, varus opening/break 0–5 mm, 0–5 degrees of laxity on dial
test
Grade II: Varus opening 6–10 mm, 6–10 degrees of laxity on dial test
Grade III: Varus opening >10 mm, >10 degrees of laxity on dial test
Epidemiology
Isolated PLC injuries are uncommon (<2% of all acute ligamentous knee injuries).
May occur in conjunction with cruciate or lateral collateral ligament injury or any
multiligamentous knee injury
High association of chronic PLC insufficiency in the setting of failed cruciate ligament
reconstruction and/or chronic instability
Risk Factors
Any collision sport or recreational activity where running and cutting may cause an
anteromedially directed blow or a noncontact hyperextension with external twisting of the knee
Etiology
Various mechanisms of injury can occur:
Posterolateral directed blow onto a nearly fully extended tibia, which results in knee
hyperextension
Noncontact hyperextension with an external rotation twisting injury
A posterior directed blow to the proximal tibia of a flexed knee (dashboard injury)
Complete knee dislocation from varus force with hyperextension

Posterior cruciate ligament (PCL) tear
Tibial plateau fracture or contusion
Lateral collateral ligament (LCL) ligament injury
Peroneal nerve injury (as high as 30%)
Diagnosis
History
Mechanism of injury
Acutely, pain and swelling to posterolateral knee
Feelings of knee instability, hyperextension, or knee “giving out”
Difficulty with twisting, pivoting, or cutting
Pain with kneeling
History of cruciate repair failure
Physical Exam
Assess for effusion.
Assess the vascular status of the leg and foot. Diminished pulses may indicate a vascular
injury and warrant an arteriogram (2)[C].
Assess neurologic status of leg and foot, particularly the common peroneal nerve and its
branches (weakened ankle dorsiflexion and great toe extension or diminished dorsal foot
sensation).
Assess alignment and gait. Inspection in standing position may reveal asymmetrical varus
involvement on the affected side. In chronic injury, varus thrust ambulatory pattern or
ambulation with flexed knee (1)[C].
Perform a complete ligamentous examination:
Cruciate and collateral ligaments must be evaluated to rule out a multiple ligamentous injury
(2)[C].
Test anterior and posterior translation with the knee in 30 degrees of flexion (Lachman
examination) and 90 degrees of flexion (drawer test).
Test varus and valgus laxity with the knee fully extended at 30 degrees of flexion. Laxity
with full extension suggests PLC injury (3)[C]
Specialty testing of the PLC:
Dial test or posterolateral rotation test most helpful (1)[C]:
With the patient in the supine position, the foot is passively externally rotated and the
degree of rotation, measured by thigh-foot angle, is compared to the contralateral limb.
Test should be performed with the knee in both 30 and 90 degrees of flexion.
>10-degree increase in external rotation with the affected knee in 30 degrees of flexion
represents a pathologic state.
If improvement occurs with 90 degrees of flexion, suggestive of isolated PLC injury (no
PCL involvement)
External rotation recurvatum test:
Lift great toe while stabilizing thigh, looking for increased recurvatum compared to
unaffected knee.
Posterolateral drawer test:
Knee flexed 80 degrees, foot stabilized in 15 degrees of external rotation, looking for
increased translation when posterior force applied to tibia (2)[C]
Reverse pivot shift test addresses tibial plateau subluxation:
With the patient supine, knee flexed, and foot externally rotated 45–60 degrees.
Valgus force applied as knee extended
Visible shift or clunk near 30 degrees of flexion implies reduction of the subluxation.
If PLC is insufficient, the lateral tibial plateau will be subluxed posteriorly relative to the
lateral femoral condyle (1)[C].

Imaging
Plain radiographs: Minimum of anteroposterior and lateral to rule out associated fractures (1)
[C]:
Segond sign (see ACL Injury), avulsion fracture of the fibular head or styloid, or tibial
plateau fracture may be associated with injury to posterolateral structures (1)[C].
Low threshold for MRI in case of suspected PLC injury:
Higher-powered magnets (1.5 T or greater) helpful for viewing variable structures of PLC
(1)[C]
Injuries to 2 or more structures of PLC (especially popliteus complex, LCL, or
postererolateral capsule) strongly suggests PLC insufficiency (4)[C].
Thin-slice coronal oblique view through fibular head and styloid may improve PLC structure
visibility (4)[B].
US may be an emerging tool for evaluating posterolateral corner structures (5)[C].
Posterior cruciate ligament injury
ACL injury
Lateral collateral ligament complex injury
Knee dislocation
Treatment
Acute treatment:
Recognize that a serious knee injury has occurred.
Treatment depends on degree of laxity or instability, timing from injury, and
concomitant ligament involvement (2)[C].
Acute PLC injuries are amenable to surgical repair if treated early. Surgical
options for treatment include primary repair, advancement, or reconstruction
(2)[C].
Immobilization with pain and swelling control comprise initial treatment.
Grade I injuries:
No abnormal motion or instability.
Nonoperative treatment results in good functional outcomes (2)[B].
Hinged knee brace locked in extension for 2–4 wks with protected weight-
bearing for the 1st 2 wks (3)[C]
Followed by progressive range of motion and rehabilitation program. Closed
chain exercises (2) initiated at 6–8 wks (3)[C].
Gradual progression as strength improves. Full release to activities
anticipated at 12–14 wks (3)[C].
Grade II injuries:
Mild to moderate abnormal joint motion
Nonoperative or surgical treatment, depending on associated injuries (2)[C]
Isolated injury can be treated like grade I injuries with prolonged protected
weightbearing (2)[C]:
Residual laxity may persist with nonoperative treatment (1)[C].
Unrestricted return to full activity may take up to 3–4 mos for nonoperative
cases (3)[C].
More significant injuries or those associated with cruciate injury should be
fixed surgically (2)[C]:
Primary repair may be possible if surgery performed within 3 wks of injury
(2)[C].
Delayed treatment requires anatomic reconstruction and addressing
malalignment issues (2)[C].
Grade III injuries:
Requires operative intervention to prevent long-term instability and expedited
development of osteoarthritis (6)[C]
Early on, primary repair may be possible depending on quality of injured
structures (2)[C].
After 4–6 wks, reconstruction necessary because of associated scarring (3)
[C]
Return to unrestricted sports participation usually 10–12 mos post surgical
repair (1)[C]
Chronic posterolateral rotatory instability:
Management of chronic PLC instability is more difficult than an acute PLC
(injury) (1)[C].
Primary repair of structures usually is impossible (2)[C].
Assessment of both gait and lower extremity alignment is important (1)[C].
Patient with preexisting varus malalignment and varus thrust during gait may
not have a successful reconstruction because the lateral structures may be
attenuated and nonfunctional (1)[C].
In this setting, proximal tibial osteotomy may be indicated before ligamentous
reconstruction. The most critical structures to reconstruct are the
popliteofibular ligament, popliteus, and LCL (1)[C].
A variety of surgical procedures described without consensus or evidence-
based outcomes (4)[C]
Recreating damaged structures favored over nonanatomical reconstructions
(1)[C]
Rehabilitation emphasis on quadriceps strengthening (1)[C]
Early immobilization should not preclude protected strengthening. Best results
are achieved with early intervention (1)[C].
Progressive resistance exercises and sports-specific drills initiated as range
of motion advanced (2)[C]
Patients who develop excessive knee hyperextension or varus thrust during
gait may benefit from gait retraining before reconstruction (7)[C].
Ongoing Care
Complications
Peroneal nerve dysfunction secondary to primary injury or surgery (1)[C]
Residual laxity, persistent pain, or osteoarthritis may occur even with surgical
intervention (1)[C].
References
1. Ranawat A, Baker CL, Henry S, et al. Posterolateral corner injury of the
knee: evaluation and management. J Am Acad Orthop Surg. 2008;16:506–
518.
2. Ricchetti ET, Sennett BJ, Huffman GR. Acute and chronic management of
posterolateral corner injuries of the knee. Orthopedics. 2008;31:479–488;
quiz 489–490.
3. Cooper JM, McAndrews PT, LaPrade RF. Posterolateral corner injuries of

the knee: anatomy, diagnosis, and treatment. Sports Med Arthrosc.
2006;14:213–220.
4. Vinson EN, Major NM, Helms CA. The postero-lateral corner of the knee.
5. Barker RP, Lee JC, Healy JC. Normal sonographic anatomy of the
posterolateral corner of the knee. AJR Am J Roentgenol. 2009;192:73–79.
6. Kannus P. Nonoperative treatment of grade II and III sprains of the lateral

ligament compartment of the knee. Am J Sports Med. 1989;17:83–88.
7. Covey DC. Injuries of the posterolateral corner of the knee. J Bone Joint
Surg Am. 2001;83-A:106–118.
Additional Reading
Malone AA, Dowd GS, Saifuddin A. Injuries of the posterior cruciate ligament
and posterolateral corner of the knee. Injury. 2006;37:485–501.
Codes
ICD9
844.0 Sprain of lateral collateral ligament of knee
Clinical Pearls
Appropriate management depends on injury severity and timing of diagnosis.
Significant posterolateral capsular and PLC injuries causing varus and
rotational instability require expedited evaluation and treatment, as surgery is
ideally performed within 3 wks from injury onset.
Isolated PLC injuries are rare, and concomitant cruciate and bony injuries must
be ruled out.
Chronic injuries associated with feeling of instability or hyperextension and can
cause abnormal gait and expedited medial osteoarthritis.
Diagnosis and treatment of this injury continue to evolve.
Pregnancy
Suzanne Hecht
David Olson
Ronald Yee
Robby S. Sikka
Basics
American College of Obstetricians and Gynecologists (ACOG) 2002 recommendations
for exercise in pregnancy:
In the absence of either medical or obstetrical complications pregnant women should
participate in 30 min or more of moderate intensity exercise on most, if not all days of the
week.
Thorough clinical evaluation required for recommendation of exercise program. In the
absence of contraindications regular, moderate intensity exercise is advised. Women should
be counseled for warning signs of when to stop exercise.
Avoid the following:
Activities with a high risk of falling or trauma.
Hockey, soccer, basketball, gymnastics, horseback riding, downhill skiing, and vigorous
racquet sports, scuba diving
Women should avoid exercises where they will be in the supine position or exposed to
prolonged motionless standing.
Women who plan to exercise at altitudes of >6,000 feet should be made aware of signs of
altitude sickness.
Recommended exercises include walking, hiking, jogging/running, aerobic dance, swimming,
cycling, rowing, cross-country skiing, and dancing.
Athletes participating in NCAA or professional sports may continue to participate in sports
during the early phases of pregnancy, but should be made aware of the risks and benefits of
continued participation in high-level sports and should be monitored more closely.
As pregnancy progresses athletic performance tends to decline. The physical demands of
high intensity training should be balanced with close monitoring of body temperature,
hydration status, and weight. These patients should be seen more frequently than their
routine prenatal visits.
Gradual resumption of exercise in the post partum period is advised.
Return to physical activity after pregnancy has been associated with decreased incidence of
postpartum depression if the exercise is felt to be stress relieving (1,2,3).
General Prevention
Warning signs to terminate exercise while pregnant (1,3,4):
Vaginal bleeding
Dyspnea prior to exertion
Dizziness
Headache
Chest pain
Muscle weakness
Calf pain or swelling
Preterm labor
Decreased fetal movements
Amniotic fluid leakage
Absolute contraindications to exercise in pregnancy (1,3,4):
Incompetent cervix
Intrauterine growth restriction
Multiple gestations (>triplets)
Persistent 2nd or 3rd trimester bleeding
Placenta previa after 25–28 wks of gestation
Preeclampsia
Pregnancy-induced HTN
Premature labor during current or prior pregnancy
Premature rupture of membranes
Risk of premature labor
Etiology
Thermoregulation:
In active nonpregnant women, exercise can elevate body temperature >103°F (39.2°C).
Current recommendations are that core body temperature should not rise more than 1.5°C
above resting temperature or >38.9°C during exercise in pregnancy (4,5).
Studies show that women appear well protected against hyperthermia even during
prolonged exercise when the intensity is low. However, nearly all studies have been
performed in women who trained prior to the study, and no prospective trials exist
evaluating the risk of elevated temperatures. Nonetheless, no human study has elicited an
increase of more than 1.1°C in maternal core temperature during pregnancy in response to
exercise (4,6,7,8).
Metabolic changes:
Utilization of glucose is potential concern for the fetus. However, no studies have shown
an actual decrease in fetal growth during exercise as there is likely increased glucose
delivery after exercise, and women who exercise may have an increased placental size.
Regular aerobic exercise has been shown to lower fasting and postprandial glucose
concentrations in several small studies of previously sedentary individuals with GDM
(2,7,9,10).
Lower back pain and pelvic pain:

Commonly associated with hormonal change. Increased ligamentous laxity is commonly
seen in pregnancy and is thought to be related to the effects of estrogen and relaxin.
Exacerbated with weight bearing and activity.
Sitting, rest, and recumbency often ameliorate symptoms, and good results have been
seen following acupuncture and use of a pelvic binder.
Hyperlordosis of pregnancy is associated with ligamentous laxity and pubic symphysis pain
is caused by widening of the pubic symphysis caused in part by the effects of relaxin and
can cause tenderness and pain over the pubic symphysis.
Rupture of the pubic symphysis is a rare complication.
Treatment of this is generally conservative.
Consideration of operative intervention is needed if diastasis is >4 cm. Careful
monitoring of women who become pregnant within a few months of ACL reconstruction
is recommended (11,12).
Cardiopulmonary changes:
Cardiac output may increase up to 40% by as early as 24 wks' gestation.
After 30 wks gestation, cardiac output is greatly influenced by body position; specifically
recumbent position may decrease the cardiac output.
Decreased splanchnic blood flow may result from exercise potentially compromising uterine
or umbilical artery blood flow.
Doppler US has shown no change in either arteries perfusion.
Increase in fetal heart rate may occur during maternal exercise.
Small percentage of fetuses that have bradycardia or decelerations in response to
maternal exercise. Episodes of bradycardia resolved within 2 min and were not thought
to be substantial enough to result in fetal hypoxia, and there were no adverse birth
outcomes (13).
Iron supplementation is advised. It is not uncommon for a pregnant female to have a
hemoglobin of 12.5 m/dL (2,7).

Orthopedic considerations during pregnancy include:
Soft tissue swelling in the 2nd and 3rd trimesters; may manifest as carpal tunnel syndrome
(CTS).
Elevated prolactin, fluid retention, and hand positioning during nursing may worsen
symptoms.
De Quervain's tenosynovitis and Meralgia paresthetica, neuropathy of the lateral femoral
cutaneous nerve, are often seen.
Symptoms from nerve compression syndromes typically resolve after pregnancy and are
treated conservatively.
Night splints can relieve CTS and steroid injections are useful in patients with recalcitrant
symptoms. Similar treatments are recommended for de Quervain's patients. For patients
with meralgia paresthetica, loose-fitting clothes, positional changes, and activity
modification often relieve symptoms (11).
In late pregnancy and after delivery, transient changes in cortisol and clotting factors can lead
to femoral head osteonecrosis:
Symptoms include antalgic gait, pain at rest, and painful range of motion.
Treatment: Restricted weight bearing; avoid surgery until after delivery.
Transient osteoporosis of pregnancy should be suspected in any patient with an antalgic gait
and complaints of pain with activity, with minimal pain at rest (5,6,9,14).
Diagnosis: Usually presents in the 3rd trimester and plain AP radiographs with appropriate
shielding often show diffuse osteopenia of the pelvis.
MRI may show high-intensity signal in the bone marrow on T2 images.
Treatment: Protected weight bearing; Use of calcitonin is controversial but may shorten the
duration of symptoms; bisphosphonate exposure during gestation may lead to decreased
fetal bone growth.
Outcomes and follow-up:
Usually results in a self-limited course with no long-term sequelae; failure to diagnose
transient osteoporosis could lead to fracture.
Serial exams are important to distinguish between these conditions. The clinician should
try to avoid unnecessary radiographs, as hip pain is common in pregnancy.
Ongoing Care
Specific sport recommendations include (13):
Stationary upright cycling is recommended by the Society of Obstetricians and Gynecologists
of Canada (SOGC) and American College of Sports Medicine (ACSM).
Fetal heart rate (FHR) and maternal temperature are not negatively affected. However
there may be more variability of FHR and maternal temperature with higher intensity and
longer duration exercise.
No negative fetal outcomes have been reported.
Recommended: Cycling for 30 min at a maternal heart rate around 140 beats per min
(bpm), or exercising for 15 min at a rate of 155 bpm.
Swimming is an optimal exercise during pregnancy due to buoyant effects and the thermally
conductive properties of water; recommended by ACOG, SOGC, and ACSM.
Baseline fetal heart rate may be less affected by swimming than cycling (1,3,10).
Walking: Many women use walking as a primary means of exercise throughout pregnancy.
Recommended by ACOG, SCOG and ACSM.
Increases maternal sense of well-being and decreases physical complaints.
Has not been shown to have a negative effect on maternal weight gain or on labor
outcomes (13).
Weight training: Conditioning exercises and physical therapy to help maintain posture and
prevent low back pain have been recommended by ACOG.
No reports of adverse effects with light to moderate weight training with free weights or
weight machines.
Moderate strength conditioning has been shown to be safe in a healthy pregnancy with no
obvious positive or negative effects; minimal fetal heart rate changes from baseline and
fetal wakefulness is increased.
Avoid weight training in the supine position late in gestation (10,13).
Scuba diving is not endorsed by the ACOG.
Those who dive frequently and professionally are at 3–6 times greater risk for
spontaneous abortion, IUGR, and fetal malformation (1,13).
High altitude exercise: Few reported cases of injury with high altitude exercise such as skiing,
hiking, mountain biking, and running.
Pregnancy complications such as low birth weight occur at a higher rate at altitudes above
10,000 ft. SOGC has suggested women modify or avoid mountain climbing all together.
Cycling with short bursts of moderate to high intensity at altitude levels of 6,000 and 7,300
ft have been reported without injury to mother or fetus (10,13).
Sports with abdominal trauma risk from contact or falling are discouraged (eg, downhill
skiing, waterskiing, horseback riding, road cycling, surfing, basketball, racquet sports, ice
hockey, soccer, and gymnastics) (3,13).
Running:
Can become uncomfortable later in gestation.
Jogging is supported by ACOG; may enhance placental growth, indicating a healthy
pregnancy outcome (12).
Women who continue to exercise throughout pregnancy generally maintain their training
regimens and level of fitness; cardiovascular risk level is well below those of the general
populace and women who temporarily stopped exercise during pregnancy (10,12).
References
1. American College of Obstetricians and Gynecologists Committee Opinion Number 267.
Exercise during pregnancy and the postpartum period. Washington, DC: The American
College of Obstetricians and Gynecologists; January 2002.
2. Artal R, O'Toole M, White S. Guidelines of the American College of Obstetrics and

Gynecologists for exercise during pregnancy and the postpartum period. Br J Sports Med.
2003;37:6–12.
3. Kramer MS, McDonald SW. Aerobic exercise for women during pregnancy. Cochrane
Database Syst Rev. 2006;(1):CD000180.
4. Olson DA, Sikka RS, et al. Exercise in Pregnancy. Curr Sport Med Rep. 2009;8(3):147–
153.
5. Ritchie JR, et al. Orthopaedic considerations during pregnancy. Clin Obstet Gynec.
2003;46:456–466.
6. Artal R, Fortunato V, et al. A comparison of cardiopulmonary adaptations to exercise in

pregnancy at sea level and altitiude. Am J Obstet Gynecol. 1995;172:1170–1178.
7. Clapp JF. Exercise during pregnancy: An Update. Clin Sports Med. 2000;19:273–286.
8. Soultanakis-Aligianni HN. Thermoregulation during exercise in pregnancy. Clin Obstet

Gynec. 2003;46:442–455.
9. Borg-Stein J, Dugan S, et al. Musculoskeletal aspects of pregnancy. Am J Phys Med

Rehab. 2005;84:180–192.
10. Clapp JF. Long-term outcome after exercising throughout pregnancy: fitness and
cardiovascular risk. Am J Obstet Gynecol. 2008;199:489.e1–489.e6.
11. Artal R, Wiswell RA, et al. Exercise in pregnancy: heat stress and pregnancy.
Phiadelphia: Lippincott Williams & Wilkins, 1991.
12. Guerra JJ, Steinberg ME. Distinguishing transient osteoporosis from avascular necrosis
of the hip. J Bone Joint Surg. 1995;77:616–624.
13. Blecher AM, Richmond JC. Transient laxity of an anterior cruciate ligament
reconstructed knee related to pregnancy. Arthros. 1998;14:77–79.
14. Cunningham F, et al. Williams obstetrics 21st ed. McGraw-Hill: Medical Publishing
Division. 2001:109–195.
Codes
ICD9
V22.0 Supervision of normal first pregnancy
V22.1 Supervision of other normal pregnancies
Clinical Pearls
Positive effects include potential risk reduction for development of gestational
diabetes and pregnancy-induced HTN, decrease in post partum depression
symptoms, and a decreased incidence of urinary incontinence, preeclampsia;
no increased risk of pre-term birth.
The cardiovascular benefits of exercise are the same for pregnant women as
they are for nonpregnant women.
Exercise in morbidly obese women may have a preventative effect on
development of gestational diabetes.
All pregnant women should be evaluated for medical and/or obstetrical
contraindications prior to beginning an exercise regimen.
Recreational and competitive athletes with uncomplicated pregnancies should
remain active. They should be monitored by regular prenatal visits unless
participating in high-intensity exercise.
Sedentary individuals without contraindications should be encouraged to begin
exercising for the health benefits.
Women with a history of or risk for preterm labor or fetal growth restriction
should be advised to reduce their activity in the 2nd and 3rd trimesters.
Women participating in higher-intensity sports should be monitored closely.
Pronator Syndrome
Kevin E. Burroughs
Basics
Seyffarth 1st described compression of the median nerve as it passes through the
pronator teres just distal to the elbow in 1951.
Description
Median nerve entrapment that occurs (1) within the ligament of Struthers, (2) within the
lacertus fibrosis, (3) between the humeral and ulnar heads of the pronator teres muscle, or
(4) at a tight fibrous arch proximally between the heads of the flexor digitorum superficialis,
the sublimis arch.
Compression between the heads of the muscle is the most common etiology, with the
sublimis arch the 2nd most common.
Synonym(s): Lacertus fibrosis syndrome; Pronator teres syndrome; Sublimis bridge
syndrome
Epidemiology
Relatively uncommon but should be considered in any patient with carpal tunnel symptoms or
volar hand numbness
Carpal tunnel syndrome is responsible for over 90% of cases of median nerve entrapment
neuropathies.
Prevalence
Usually presents in the 5th decade, and 4× more common in women
Delay in diagnosis ranging from 9 mos to 2 yrs
Risk Factors
Repetitive occupational pronation/supination
Acute forceful pronation or wrist flexion
Weight lifters with hypertrophied pronator-flexor mass
Etiology
In over 80% of individuals, the pronator teres arises from 2 heads, superficial (humeral) and
deep (ulnar), and the median nerve travels between as it enters the antecubital area.
Variants have been demonstrated where the nerve travels posterior to both heads, under a
single head, or pierces the superficial head.
Compression can occur proximally in individuals with a supracondyloid process. This is an
anomalous bone spur on the anteromedial distal 1/3 of the humerus and occurs in 1% of
people of European ancestry.
Diagnosis
History
Typically patients complain of an aching or fatigue-like pain in proximal forearm. Other
symptoms may include occasional hand pain, dysesthesias of the radial 3½ digits, cramping
in the hand (writer's cramp).
Many report an increase in pain with exercise or an increase in activity.
Frank hand weakness occurs only in long-standing or severe cases.
Motor and sensory symptoms can be poorly defined.
Onset typically is insidious, but a specific event may cause a sudden increase in pain.
Typically, pain does not occur at night, as it would with carpal tunnel syndrome.
Physical Exam
Thickened or hypertrophied pronator muscle mass
Tenderness or positive Tinel sign in the proximal anterior forearm over the pronator muscle,
with radiation to the palm and/or radial 3½ digits
May have weakness or atrophy of the hand intrinsics innervated by the median nerve (LOAF
muscles): lumbricals (1st 2 on radial side of hand), opponens pollicis, abductor pollicis brevis,
and flexor pollicis brevis
May have weakness of the extrinsic finger flexors, wrist flexors, and pronator quadratus
Tests of Spinner can determine location of median nerve entrapment.
Pain or paresthesia reproduced with resisted flexion of the forearm in a position of >120
degrees of elbow extension, maximal supination: Lacertus entrapment of median nerve
Reproduction of pain or paresthesia with resisted pronation (forearm in neutral) as the
elbow is extended: Pronator entrapment of median nerve
Reproduction of symptoms with resisted proximal interphalangeal (PIP) joint flexion of the
middle finger with forearm fully supinated and elbow extended: Flexor digitorum
superficialis entrapment of median nerve

Imaging
Plain radiographs of the elbow rule out bone involvement such as a supracondyloid process
(exostosis that attaches to ligament of Struthers).
MRI:
Since the median nerve often is poorly depicted at the elbow because of the minimal
amount of perifascial fat in this region, MRI is not indicated for the diagnosis of pronator
syndrome but may be used for excluding other etiologies. The nerve can look normal at the
site of entrapment.
The pronator teres and other muscles innervated by the median nerve distally to the site of
the lesion may show abnormally high signal intensity on T2-weighted fat-suppressed, STIR
(Short TI Inversion Recovery), or T1-weighted images in more advanced cases.
Electrodiagnostic testing:
Needle electromyography (EMG) is the most helpful to identify evidence of denervation.
Symptoms often must persist for minimum of 4–6 wks before positive findings on EMG.
Nerve conduction may be normal despite compressive pathology.
Some report that only 10% of patients show abnormal EMG findings that support the clinical
diagnosis.
In the electrodiagnostic evaluation of carpal tunnel syndrome, EMG of muscles innervated by
the median nerve proximal to the wrist should be performed to decrease unnecessary carpal
tunnel surgeries.
Carpal tunnel syndrome (common): Double crush phenomena can occur.
C6 or C7 radiculopathy (common)
Anterior interosseous syndrome (Kiloh-Nevin syndrome) (uncommon)
Thoracic outlet syndrome (rare)
Neuralgic amyotrophy (brachial neuritis, Parsonage-Tuner syndrome) (rare)
Treatment
Rehabilitation is the initial treatment and can be summarized using the
acronym APORIM:
Activity modification: Avoidance of provocative activities
Protection from external compression
Orthoses: Night splints to prevent excessive elbow flexion
Rehabilitation: Assess proximal and distal kinetic chain (shoulder girdle and
wrist) for strength, flexibility, and movement.
Injections can be considered at point of compression, but exercise caution to
avoid direct injection into nerve bundle.
Medication: Nonsteroidal or steroid anti-inflammatory medications
If conservative measures fail, or if muscle atrophy or denervation occurs, one
should consider exploration.
For a proven supracondyloid process, excision of the bone prominence and
release of the ligament of Struthers should provide resolution.
For evaluation of entrapment within the forearm, an incision begins in the distal
arm about 5 cm above the elbow and along the medial aspect of the biceps
muscle. The incision curves toward the lacertus fibrosus at the elbow crease
and then continues distally over the flexor-pronator mass. Dissection distally
should ensure visualization of the nerve to its course at the flexor superficialis
origin.
Additional Reading
Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and
elbow in the athlete. Clin Sports Med. 2006;25:465–87, vi–vii.
Dawson DM, Hallett M, Wilbourn AJ, eds. Median nerve entrapment in

entrapment neuropathies. Philadelphia: Lippincott-Raven Publishers,
1999:99–111.
Dumitru D. Etectrodiagnostic medicine. Philadelphia: Hanley & Belfus,

1994:856–867.
Hartz CR, Linscheid RL, Gramse RR, et al. Pronator teres syndrome:
compressive neuropathy of the median nerve. J Bone Joint Surg.
1981;63A:885–890.
Kopell HP, Thompson WA. Pronator syndrome: a confirmed case and its
diagnosis. N Engl J Med. 1958;259:713–715.
Tetro AM, Pichora DR. High median nerve entrapments. An obscure cause of
upper-extremity pain. Hand Clinics. 1996;12:691–703.
Werner CO, Rosen I, Thorngren KG. Clinical and neurophysiologic

charateristics of the pronator syndrome. Clin Ortho Related Res.
1985;197:231–236.
Wiggins CE. Pronator syndrome. South Med J. 1982;75:240–241.
Codes
ICD9
354.1 Other lesion of median nerve
Clinical Pearls
Prognosis usually depends on the severity of median neuropathy. Worse
prognosis with extensive axon loss and atrophy. Expect some reinnervation of
distal musculature once the median nerve is free from compromising
structures.
Symptoms of pronator syndrome typically do not occur at night. Also, wrist
splints typically do not improve symptoms.
Proteinurea in Sports
Justin Wright
Basics
Description
Proteinuria is defined as the excretion of >150 mg/day of urinary protein.
Present in 17% of asymptomatic individuals (1)
Exercise-induced proteinuria (2):
Transient increase in urine protein following exercise; resolves over 24–48 hr
Relatively common, benign finding
Proteinuria more related to exercise intensity than duration
Due to increased glomerular permeability and decreased tubular resorption of protein as a
result of reversible physiologic change in the kidney
May also be due to a decrease in the intravascular volume from acute dehydration in
athletes partaking in severe or extreme exercise
No known long-term sequelae
Epidemiology
Proteinuria seen in up to 17% of asymptomatic individuals in general population
In the athletic population, prevalence between 18% and 100%, depending on type of activity
and intensity (2)
Seen in activities with higher exercise intensity, such as boxing, wrestling, gymnastics,
football, and rowing
Also seen in long-distance running, swimming, and track
Etiology
Proteins seen in the urine include:
Plasma proteins such as albumin, transferrin, kappa, and lambda chains
Tubular proteins such as secretory IgA, Tamm-Horsfall protein
3 categories of proteinuria (2,3):
Glomerular:
Increased filtration of macromolecules across the glomerular capillary wall
Permeability affected by increased organic acid production, renin-angiotensin system,
prostaglandins, and catecholamine activation
Urine protein components similar to plasma proteins
Seen with mild-to-moderate exercise
Tubular:
Decreased resorption of filtered proteins
Presence of low-molecular-weight proteins
Due to saturation of reabsorbing mechanisms caused by a higher quantity of proteins
filtered at the glomerular level
Seen in strenuous exercise in combination with glomerular proteinuria
Overflow:
Increased production of low-molecular-weight proteins (eg, multiple myeloma)
Unless pre-existing condition is present, not seen in exercise-induced proteinuria
Diagnosis
The history and physical are important to differentiate benign and transient exercise-
induced proteinuria from pathologic causes of proteinuria.
History
Exercise type, intensity, and duration
Prior history of renal disease
Underlying conditions that may cause proteinuria
History of recent illness
Family history of renal disease
Physical Exam
Identifying signs of underlying renal disease or process, including (4)[C]:
Elevated BP
Peripheral edema
Flank pain
Abdominal bruits

Lab
Urinalysis/dipstick:
Inexpensive, quick screening test for proteinuria
Standard dipstick test measures albumin concentration via a colorimetric reaction.
False-positive results seen with alkaline urine; highly concentrated urine; gross hematuria;
presence of certain medications (penicillin, sulfonamides, tolbutamide); and the presence
of pus, semen, or vaginal secretions
False-negative results seen with dilute urine or when urine proteins are nonalbumin or low
molecular weight
In exercise-induced proteinuria, dipstick may become positive within 30 min of onset of
exercise and is positive for 24–48 hr.
Usually no more than 2+ on dipstick
For dipstick-positive proteinuria lasting >48 hr after a period of rest, further workup is
required (2,4)[C].
Further workup (2,4)[C]:
Blood urea nitrogen and creatinine
CBC
24-hr urine collection for creatinine and total protein or spot protein-to-creatinine ratio
Imaging
Not routinely used in exercise-induced proteinuria
For persistent proteinuria or suspicion of renal parenchymal disease, a renal US should be
performed (4)(C).
Transient proteinuria:
Orthostatic proteinuria:
Elevated protein excretion in upright position, with normal excretion in recumbent position
Occurs mostly in pediatric population
Diagnosis made by collecting urine throughout the day, then again in the morning after
recumbent all night. If orthostatic proteinuria is present, protein level in overnight sample
will be within normal limits. Elevated protein in overnight sample should prompt workup
for persistent proteinuria (1,4)[C].
Fever
Stress
Pregnancy
Glomerular causes (eg, minimal change disease, membranous glomerulonephritis)
Tubular causes (eg, hypertensive nephrosclerosis)
Overflow (eg, multiple myeloma, hemoglobinuria)
Treatment
Exercise-induced proteinuria is transient and self-limited; no specific
therapy indicated
For underlying renal disease, treatment aimed at specific cause
Referral
Evaluation by nephrologist should be considered for:
Persistent proteinuria, especially in patients older than 30
Elevated serum creatinine
Evidence of underlying medical disease or glomerular process
Ongoing Care
Prognosis
There is no evidence that suggests these athletes are at increased risk for chronic renal
disease or have any reason to limit their physical activity.
References
1. Carroll MF, Temte JL. Proteinuria in adults: a diagnostic approach. Am Fam Physician.
2000;62:1333–1340.
2. Bellinghieri G, Savica V, Santoro D. Renal alterations during exercise. J Ren Nutr.

2008;18:158–164.
3. Naderi AS, Reilly RF. Primary care approach to proteinuria. J Am Board Fam Med.
2008;21:569–574.
4. Kane SF, Cohen MI. Evaluation of the asymptomatic athlete with hepatic and urinalysis
abnormalities. Curr Sports Med Rep. 2009;8:77–84.
Codes
ICD9
791.0 Proteinuria
Clinical Pearls
Exercise-induced proteinuria is transient, lasting 24–48 hr.
Repeat testing in 48 hr after a period of rest to ensure clearance of protein.
Persistent proteinuria requires workup for underlying renal disease.
Pseudoanemia
Michelle Burke
Julie M. Kerr
Basics
Description
Dilutional phenomenon in endurance athletes causing hemoglobin and hematocrit values that
are lower than established limits of normal
Plasma volume expansion by 10–20% with little change in red cell numbers (ie, oxygen-
carrying capacity; red cell mass remains unchanged) (1)
Contributing factors include:
Exercise-induced release of aldosterone, renin, and vasopressin
Increased size of vascular bed owing to muscle hypertrophy
Retention of crystalloids and colloids governed by hormones
Theoretically, this increased blood volume decreases viscosity, thereby maximizing stroke
volume, cardiac output, and subsequent oxygen delivery (2).
Hemodilution occurs over the 48 hr after every episode of endurance exercise and may
persist for as long as 1 wk after discontinuing training.
If training continues, red cell mass will catch up with plasma volume expansion over the span
of few weeks, causing hemoglobin and hematocrit values to normalize (3).
Synonym(s): Sports anemia; Athletes' pseudoanemia
Epidemiology
Incidence
Elite athletes involved in endurance training
Previously sedentary individuals starting an exercise program
Athletes increasing intensity of training
Diagnosis
History
Check exercise schedule, type of training activity, and occurrence of any symptoms.
Physical Exam
Hemoglobin levels 13–14 g/100 mL in men and 11–12 g/100 mL in women; dose-response
relationship between amount/intensity of exercise and hemoglobin drop (4)
Elite endurance athletes have a greater degree of dilutional pseudoanemia than more
moderate endurance athletes.
Females are more likely than males to have iron-deficiency anemia with sports ± presence of
pseudoanemia.
No particular symptoms or physical findings

Laboratory studies are performed if etiology unclear or symptoms are present.
Normal mean corpuscular volume
No hematuria or hemoglobinuria on urinalysis
Normal bilirubin and haptoglobin
Ferritin may be lower in endurance athletes owing to the same relative dilutional effect.
Values often <60 µg/L, occasionally <30, but <15 = iron deficiency.
Iron-deficiency anemia
GI bleeding
Hematuria
Foot-strike hemolysis
Treatment
Rule out iron-deficiency anemia.
Self-limited condition; indexes return to pretraining levels after training is
discontinued (5).
Normal physiologic response; no treatment required (6)
References
1. Eichner ER. Sports medicine pearls and pitfalls: Nature's anticoagulant.
Curr Sports Med Rep. 2009;8:2–3.
2. El-Sayed MS, Ali N, El-Sayed Ali Z. Haemorheology in exercise and
training. Sports Med. 2005;35:649–670.
3. Sawka MN, Convertino VA, Eichner ER, et al. Blood volume: importance
and adaptations to exercise training, environmental stresses, and
trauma/sickness. Med Sci Sports Exerc. 2000;32:332–348.
4. Chatard JC, Mujika I, Guy C, et al. Anaemia and iron deficiency in athletes.
Practical recommen-dations for treatment. Sports Med. 1999;27:229–240.
5. Shaskey DJ, Green GA. Sports haematology. Sports Med. 2000;29:27–38.
6. Carlson DL, Mawdsley RH. Sports anemia: a review of the literature. Am J

Sports Med. 1986;14:109–112.
Additional Reading
Balaban EP. Sports anemia. Clin Sports Med. 1992;11:313–325.
Raunikar RA, Sabio H. Anemia in the adolescent athlete. Am J Dis Child.

1992;146:1201–1205.
Watts E. Athletes' anaemia. A review of possible causes and guidelines on

investigation. Br J Sports Med. 1989;23:81–83.
Weight LM, Darge BL, Jacobs P. Athletes' pseudoanemia. Eur J Appl Physiol.
1991;62:358–362.
Codes
ICD9
285.9 Anemia, unspecified
Clinical Pearls
Iron supplementation does not affect occurrence or improve lab values, nor is it
necessary unless there is a coexisting iron-deficiency anemia.
Pulmonary Contusion
John Shelton
Basics
The clinical syndrome, following blunt chest trauma of chest pain and respiratory
difficulty, with or without hemoptysis, confirmed by findings on chest radiographs (CXR) or
other imaging:
Specific symptoms may include persistent and progressive shortness of breath, tachypnea,
or decreasing pulse oximetry.
CXR or CT demonstrate focal or diffuse infiltrates that do not conform to pulmonary lobes
or segments.
While rarely reported in sports, the true incidence is not well known:
3 case studies since 1997 (1,2)
Most of the literature reviews severe trauma and injury, such as motor vehicle accidents,
that generally require more intervention than those reported in sports (3,4,5).
While pulmonary contusion is dramatic in presentation, athletes appear to recover and return
to play within 1 wk limited primarily by chest wall pain rather than respiratory status.
Description
Blunt trauma to the chest causing disruption of alveolar capillary interface, resulting in
collection of blood, edema, and protein in the interstitium and alveoli
Clinical diagnosis is suggested by hemoptysis or progressive respiratory distress and
confirmed by imaging.
Synonym(s): Bruised lung
Epidemiology
In contact sports, chest wall contusions occur frequently and are managed by athletic
trainers without being reported.
There are only 3 reported cases of pulmonary contusion in the literature since 1997 (1,2).
In all comers to an emergency department during the 1990s (6):
26% of rib fractures are associated with pulmonary contusion.
32% are associated with hemothorax/pneumothorax.
Risk Factors
Collision/contact sports
Sports with high speeds or where the athlete is airborne:
Cycling, equestrian, alpine skiing, snowboarding, extreme sports, etc.
General Prevention
Use protective equipment and padding appropriate for the activity, such as seat restraints in
motor sports to prevent ejection (5):
Padding may diffuse force on impact.
Padding after the injury can decrease pain of subsequent impacts:
Military data not sport-specific.
Etiology
Blunt trauma to the chest causing disruption of alveolar capillary interface, resulting in collection
of blood, edema, and protein in the interstitium and alveoli

Chest wall contusion
Rib fracture
Diagnosis
Diagnosis is suspected when an athlete sustains a blunt trauma to the chest and has
respiratory difficulty:
Hemoptysis after an injury is highly suggestive of a pulmonary contusion.
History
Blunt nonpenetrating trauma
Chest wall contusion is often the initial diagnosis.
Hemoptysis may be present, but its absence does not rule out a contusion.
Pain in the shoulder or scapular angle suggests abdominal or diaphragmatic injury.
If fever is present, consider infectious differential.
Consider pulmonary parenchymal contusion when dyspnea is progressive over hours or days
or if hemoptysis occurs.
Nasal or facial trauma supports consideration of epistaxis as the etiology of bleeding possibly
instead of pulmonary injury in the absence of obvious chest trauma.
High-energy/velocity injuries should increase suspicion for associated injuries.
Physical Exam
High-velocity/energy injuries should prompt full trauma evaluation:
Both primary and secondary surveys should be performed in these cases.
Dyspnea or tachypnea must be present for diagnosis, unless hemoptysis occurs.
Palpable and pleuritic chest wall pain are present due to the impact force required to produce
a pulmonary contusion.
Arm or trunk movement may worsen chest pain.
Dyspnea may persist after rest.
Chest wall region is tender.
Ecchymosis usually will not be present initially, but crepitus or more severe point tenderness
often is present when ribs are fractured.
Auscultation is generally normal:
Consider hemopneumothorax if abnormal lung sounds are present.
Inspect and record naso-oropharyngeal findings, as hemoptysis may be reported later:
Note any evidence of bleeding in the nose or mouth.
Evaluate nose and posterior pharynx for sites of bleeding, as nasal trauma or bites of
cheeks or tongue are more common than pulmonary contusion as the source of blood in
suspected hemoptysis.
Inspect range of motion of neck and palpate to rule out other injury in the presence of
significant blunt trauma to chest.
Record vital signs serially if athlete is unable to return to play to observe for deterioration:
Pulse oximetry <91% suggests contusion with A/V shunting.
Abdominal examination for tenderness or guarding is critical:
Penetrating injury occurring anteriorly at rib interspace 5 or below may penetrate the
abdomen
Observe the chest closely for paradoxical movement of a segment of ribs indicative of flail
chest.

Lab
Decreasing pulse oximetry (<91%) suggests pulmonary contusion with A/V shunting:
Consider pneumothorax with low pulse oximetry as well.
Imaging
Posterior, anterior, and lateral CXR:
May not be required for chest pain in absence of dyspnea or hemoptysis
Rib films do not contribute to management in absence of pulmonary symptoms or clinical
flail fracture.
Clinically significant hemopneumothorax and pneumothorax can generally be ruled out with
negative radiographs; however, additional imaging should be considered based on the
mechanism of injury and clinical findings, as normal radiographs do not definitively exclude
underlying lung injury (7)[B].
Posterior/anterior and lateral CXR reveals peripheral infiltrate in area of trauma when
significant contusion occurs:
Generally seen within 6 hr, but may take up to 48 hr for radiographic changes (8)
The infiltrate may not correlate to lobular architecture.
CT and other imaging will be guided by the clinical picture:
Ventilation perfusion scan may show matched ventilation perfusion defect, unlike pulmonary
embolus, which shows ventilation perfusion mismatch.
Chest US may be comparable to CT for pulmonary contusion (9)[B].
Follow-up imaging guided by clinical symptoms and severity of injury:
Isolated contusion in the athlete generally does not require repeat radiographs
Consider if symptoms are not resolving over 5–7 days or worsen
If hemoptysis is recurrent over >48 hr, bronchoscopy may be considered, depending on clinical
status (10):
Hemoptysis should generally clear within 1 wk.
Epistaxis
Rib fracture or contusion
Naso-oropharyngeal trauma
Pulmonary laceration or hematoma
Traumatic pneumothorax or hemothorax
Diaphragmatic, splenic, or hepatic injury
Tracheobronchial mucosal avulsion
Pulmonary emboli
Treatment
Pre-Hospital
Primary on-field concerns:
Multiple traumas in motor sports or high-velocity sports (downhill skiing) should
be stabilized and transported immediately by emergency services to a
designated trauma center:
Primary concerns with severe trauma are airway, breathing, and circulation.
Evaluate for C-spine injury; immobilize as indicated.
Expose by removing equipment as needed.
Report any increase in dyspnea; may need support, oxygen, and ventilation.
Mild to moderate injuries may be observed on site and reevaluated frequently P.
for signs of decompensation.
Transport for worsening symptoms:
Dyspnea and tachypnea are the most important signs of deterioration (3).
ED Treatment
In cases of multiple trauma due to motor vehicle accident or high-velocity
impact, general trauma protocols should be followed.
In contact sports, trauma with isolated pulmonary contusion may be treated with
observation and minimal support as needed:
Pain medication
Oxygen
Penetrating injuries and flail chest are associated with a much higher risk of
complications, including the need for mechanical support (6).
Medication
Acetaminophen and NSAIDs can be used as first line for mild to moderate
pain:
Consider avoiding NSAIDs in patients with hemoptysis.
Narcotic pain medications may be needed in more severe cases:
Monitor use closely, as these may cause respiratory depression
Isolated pulmonary contusion in stable patients does not require additional
treatment:
Rest from strenuous exercise as needed to allow pulmonary healing
Additional supportive and treatment measures will be dictated by the severity of
injuries:
Chest tube may be required emergently if hemopneumothorax is present.
Light exercise or walking promotes deep breathing and retards atelectasis.
When asymptomatic, begin stepwise return to play as tolerated by symptoms.
Rib taping and other attempts at immobilization are generally not effective and
should be used with caution, as they could possibly increase the risk of
atelectasis and pneumonia.
Admission criteria:
Traumatic injuries requiring stabilization and support
Patient with respiratory difficulty and oxygen saturations <90%
Patients with uncontrolled pain
Special considerations (8,11):
Rib fractures can be associated with severe blunt trauma, but these cases
generally involve high-energy mechanism.
Flail chest is a rare but serious complication requiring hospitalization to
observe for pulmonary deterioration and need for intubation with respiratory
support.
Pulmonary laceration:
Transfer of energy from the chest wall; shear forces often are generated
that can tear the lung.
Most lacerations heal without complications, but elastic recoil of the lung
may extend the laceration to form a pulmonary pseudocyst, which may
result in infection, abscess, hemoptysis, air leak, adult respiratory distress
syndrome, and death.
Airway avulsion or rupture:
Most common site is within 2.5 cm of the carina between tracheal rings
Findings include SC emphysema and hemoptysis.
Isolated pneumothorax is uncommon with blunt trauma due to dense
fibroconnective tissue surrounding carina and mainstem bronchi.
Discharge Criteria
Stable patients can be discharged home with observation and instructions to
return for worsening symptoms:
Pain controlled
No significant dyspnea
Stable oxygen saturation on room air:
No concensus, but generally >90% for an otherwise healthy individual
Ongoing Care
Return to play (1,2)[C]:
Simple chest wall contusions:
Same day
Athlete must be nondyspneic, able to perform usual movements as required for the
sport, and able to tolerate pain without narcotics or local anesthetic
On return to play, rib pads, flak jacket, or equestrian chest protector may decrease
discomfort and reinjury during contact.
Remove from activity for recurrent dyspnea; consider chest x-ray
Pulmonary contusions:
Field-side diagnosis with hemoptysis or persistent pain precludes return to that contest.
Athlete may return to full activity at 1 wk if they tolerate progressive training without
dyspnea, hemoptysis, or limited performance after the last episode.
After strenuous exercise is tolerated for 48 hr and athlete is able to perform at a level
appropriate for contact sports, return to play in contact sports may be allowed.
Report any deterioration in performance or dyspnea.
Pulmonary consultation for bronchoscopy if hemoptysis persists
Prognosis
Most isolated pulmonary contusions will resolve without complication.
Chest wall pain usually persists for 6 wks, but generally will not interfere with function.
Isolated pulmonary contusion in young, healthy patients is not associated with mortality (4).
Complications
Factors associated with a poor outcome in severe pulmonary contusion (multiple
traumas/motor vehicle accident):
Poor outcome = death, prolonged hospitalization >7 days, severe
complications (pneumonia, empyema, atelectasis requiring bronchoscopy or
bronchopleural fistula) (4):
Pulmonary contusion on admission chest x-ray
3 or more rib fractures
Chest tube insertion
Hypoxia on admission (PO2 <70 torr)
References
1. Lively MW, Stone D. Pulmonary contusion in foot-ball players. Clin J Sport
Med. 2006;16:177–178.
2. Meese MA, Sebastianelli WJ. Pulmonary contusion secondary to blunt

trauma in a collegiate football player. Clin J Sport Med. 1997;7:309–310.
3. Kollmorgen DR, Murray KA, Sullivan JJ, et al. Predictors of mortality in

pulmonary contusion. Am J Surg. 1994;168:659–663; discussion 663–664.
4. Hoff SJ, Shotts SD, Eddy VA, et al. Outcome of isolated pulmonary
contusion in blunt trauma patients. Am Surg. 1994;60:138–142.
5. Cohn SM. Pulmonary contusion: review of the clinical entity. J Trauma.

1997;42:973–979.
6. Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J
Trauma. 1994;37:975–979.
7. Brink M, Kool DR, Dekker HM, et al. Predictors of abnormal chest CT after
blunt trauma: a critical appraisal of the literature. Clin Radiol. 2009;64:272–
283.
8. Wanek S, Mayberry JC. Blunt thoracic trauma: flail chest, pulmonary
contusion, and blast injury. Crit Care Clin. 2004;20:71–81.
9. Soldati G, Testa A, Silva FR, et al. Chest ultrasonography in lung contusion.

Chest. 2006;130:533–538.
10. Bidwell JL, Pachner RW. Hemoptysis: diagnosis and management. Am

Fam Physician. 2005;72:1253–1260.
11. Miller DL, Mansour KA. Blunt traumatic lung injuries. Thorac Surg Clin.
2007;17:57–61, vi.
Additional Reading
Dubinsky I, Low A. Non-life-threatening blunt chest trauma: appropriate
investigation and treatment. Am J Emerg Med. 1997;15:240–243.
Codes
ICD9
861.21 Contusion of lung without open wound into thorax
Clinical Pearls
Blunt thoracic trauma with high-energy mechanism should always prompt a
thorough evaluation, as pulmonary contusions and rib fractures are com-monly
associated with significant internal injuries:
This is in contrast to most sports-related injuries, which are usually lower
energy and are generally associated with good outcomes.
Significant morbidity in clinically stable patients has not been reported. One
episode of hemoptysis in an asymptomatic athlete will likely not recur and
imaging is not required. Pulmonary dysfunction associated with a contusion
may take 24–48 hr to develop as fluid accumulates in the air spaces. Serial
reevaluations daily may be needed to detect worsening tachypnea and
tachycardia. Get emergency follow-up evaluation if delayed deterioration
occurs rapidly.
Future ability to play is only as limited by chest wall pain. Return to peak
conditioning depends on ability to reach maximum exertion effort. Involuntary
guarding of pleuritic pain during healing may delay recovery to peak form for up
to 6 wks.
Quadriceps Contusion
Kinshasa Morton
Jason P. Womack
Basics
Description
Traumatic thigh injury resulting in muscle fiber damage along with capillary rupture and
subsequent bleeding into the quadriceps muscle tissue. Usually the result of a blunt force blow
to the anterior, medial, or lateral thigh, most commonly occurring in contact sports:
Recurrent quad contusions predispose to more severe injury and development of
complications.
Delay in onset of therapy leads to a higher percentage of complications and delay in
recovery.
Synonym(s): Charley horse; Thigh bruise; Dead leg; Quadriceps hematoma
Epidemiology
Percentage of participants that will sustain a quad contusion in 1 yr (per sport) (1):
Rugby = 4.7%
Karate/judo = 2.3%
Football = 1.6%
All other sports are <1%.
Muscle contusion injuries are 2nd only to strain injuries as a major cause of morbidity in the
modern athlete (2).
Risk Factors
More prevalent in contact sports (rugby, mixed martial arts, football)
Inappropriately sized, thinly cushioned, or nonuse of thigh pads (football)
Bleeding disorders predispose to hematoma formation.

Myositis ossificans traumatica (MOT):
Benign formation of heterotopic bone and cartilage in soft tissue that previously sustained
trauma or contusion injury:
Development related to severity of injury
Incidence with muscle contusion injury reported as 9–17% (2)
Suspect when contusion injuries do not resolve within 2 wks (2)
Suspect when contusion injuries worsen rather than improve over time (2)
May be confused with osteosarcoma on imaging (2)
Acute compartment syndrome (ACS):

Rare complication of quadriceps contusions in which increased pressure within the fascial
compartments of the thigh results in circulatory failure. If severe and left untreated, it may
lead to nerve damage and tissue necrosis:
Suspect when pain is out of proportion to injury
Suspect with finding of paresthesia, which may be progressive
Most commonly occurs with femur fracture, rarely with quadriceps contusion
Diagnosis
History
Patients give history of blunt force trauma to the thigh sustained during collision, usually while
playing a sport. Complaint of pain and swelling in the area of trauma and also difficulty in
ambulation are common:
Collison may have been with another person or playing object (baseball, field hockey ball,
hockey puck).
Pain and/or swelling may be immediate or delayed.
History or rapid, progressive swelling accompanied by numbness and exquisite pain may
signify the development of ACS. This may necessitate quick intervention (compartment
pressures, neurochecks, fasciotomy).
Relevant past medical history/history of previous injury:
Has there been a previous similar injury to the same area?
Recurrent injury may result in the development of MOT.
What has been the duration of the injury?
Contusion injuries that linger and have not resolved within 2 wks may be progressing to
MOT.
Is there a history of bleeding/coagulation disorders or current use of anticoagulants?
If so, may lead to increased bleeding and large hematoma formation that again may lead
to MOT or delayed recovery
Physical Exam
Observation:
May ambulate with antalgic gait or has reluctance to bear weight
Appearance:
May have area of ecchymosis
Swelling in the anterior thigh, which may extend to proximal knee:
Patients with severe quad contusions may get knee effusion without intra-articular
pathology
Serial thigh circumference measurements taken to assess expansion or resolution of
swelling
Palpation:
Tense and tender to palpation over anterolateral thigh
Range of motion (ROM):
Reduced ability to actively flex the knee
Quad contusions are graded by ROM deficit with active knee flexion (3)[C]:
Mild (>90 degrees of active flexion)
Moderate (45–90 degrees of active flexion)
Severe (<45 degrees of active flexion)
Strength:
Reduced ability to perform straight leg raise
Reduced ability to perform knee extension against resistance
Sensation:
Sensation deficits along anterolateral thigh are rare. If present must consider ACS.

Imaging
Plain radiographs:
Rarely needed acutely unless concern for femur fracture
Useful in assessing for MOT if prolonged symptoms (>2 wks) or progressive symptoms:
Radiographic abnormalities can be seen within 18–21 days (2).
US:
Rarely needed acutely unless trying to differentiate between quad contusion or quad
tendon rupture
May be used to differentiate between diffuse muscle edema and acute hematoma
formation
Can be used to assess for size of hematoma
MRI:
Again, rarely needed unless contusion injury is moderate to severe, or slow to resolve
Helpful when patient's symptoms do not match physician's clinical findings (4)
Imaging modality of choice for the visualization of quad contusion injuries:
Reveals injuries that may be missed by US (4)
Allows for more accurate assessment of site and extent of injury (4)
Better assessment of size and extension of hematomas
Serial MRIs may be done to follow resolution
Resolution of MRI abnormalities usually lag behind clinical resolution by up to 2 wks.
Caution, as early MOT is difficult to differentiate from osteosarcoma
Quadriceps strain
Quadriceps tendon rupture
Quadriceps spasm/cramp
Acute compartment syndrome of the thigh
Femur fracture
Treatment
Acute treatment (1st 24 hr):
R.I.C.E. (Rest, Ice, Compression, Elevation) (4)[C]:
Rest reduces retraction of ruptured myofibrils, preventing large gaps in the
muscle.
Icing associated with smaller hematoma formation, less inflammation, and
early muscle regeneration
Compression reduces IM bleeding.
Elevation reduces interstitial fluid accumulation (swelling).
Collectively, these measures limit the severity of quad contusions.
Immobilization:
Immobilize in 120 degrees of knee flexion with either brace or figure of 8 Ace
bandaging for 1st 24 hr (3)[B]:
Shown to decrease time to return to play compared with traditional
treatment
Also functionally compresses injury
Use crutches to aid in ambulation and to rest injury.
Discontinue immobilization after 24 hr.
NSAIDs treatment:
Early use (24–48 hr after injury) is controversial because of theoretic
increased risk of bleeding and worsen of hematoma formation
Early short-term use has shown no adverse effects on healing process (5,6)
[B].
For moderate-to-severe quad contusions, a 7-day course of NSAID
treatment recommended to help prevent MOT (5):
Consider waiting 48–72 hr to reduce theoretical risk of increased bleeding.
Subacute treatment (after 1st 24 hr):
Ensure thigh circumference has stabilized (3)[C].
Discontinue immobilization and begin stretching (3)[C]:
Passive flexion with goal of 120 degrees of pain-free flexion
Begin active quad stretching and strengthening exercises once pain
decreases and motion improves.
Strengthening should progress from isometric to isotonic to isokinetic training
(6).
Discontinue crutch use when pain-free ambulation achieved
Long-term treatment/rehabilitation:
May return to sports-specific training when (3,6)[C]:
ROM on injured quad side and uninjured side are equal.
Use of injured quad is pain-free with basic movement.
Prior to return to sport, player should be fitted for oversized quad pad (3)[C]:
Helps to protect from recurrent injury, which could lead to MOT
Wear for 3–6 mos or until end of season
Rarely do quad contusions and hematomas require surgery or percutaneous
aspiration (7)[C].
Use of corticosteroids is generally contraindicated for treatment of muscle
contusion injuries (8)[C].
Athletes with MOT who have persistent pain and limited motion may have the
heterotopic bone removed when it has matured (2)[C]:
Should not be performed until at least 12 mos after the initial injury
Bone scan or plain films determine maturity of the tumor.
ACS of thigh almost always can be treated conservatively. When unresponsive
to conservative measures, then requires fasciotomy (7)[C].
References
1. Ryan JB, Wheeler JH, Hopkinson WJ, et al. Quadriceps contusions. West
Point update. Am J Sports Med. 1991;19:299–304.
2. Beiner JM, Jokl P. Muscle contusion injury and myositis ossificans

traumatica. Clin Orthop Relat Res. 2002;403(suppl):S110–S119.
3. Aronen JG, Garrick JG, Chronister RD, et al. Quadriceps contusions:

clinical results of immediate immobilization in 120 degrees of knee flexion.
Clin J Sport Med. 2006;16:383–387.
4. Järvinen TA, Järvinen TL, Kääriäinen M, et al. Muscle injuries: biology and
treatment. Am J Sports Med. 2005;33:745–764.
5. Mehallo CJ, Drezner JA, Bytomski JR. Practical management: nonsteroidal

antiinflammatory drug (NSAID) use in athletic injuries. Clin J Sport Med.
2006;16:170–174.
6. Järvinen TA, Järvinen TL, Kääriäinen M, et al. Muscle injuries: optimising

recovery. Best Pract Res Clin Rheumatol. 2007;21:317–331.
7. Diaz JA, Fischer DA, Rettig AC, et al. Severe quadriceps muscle
contusions in athletes. A report of three cases. Am J Sports Med.
2003;31:289–293.
8. Beiner JM, Jokl P, Cholewicki J, et al. The effect of anabolic steroids and
corticosteroids on healing of muscle contusion injury. Am J Sports Med.
1999;27:2–9.
Codes
ICD9
924.00 Contusion of thigh
Clinical Pearls
Think MOT when a quadriceps contusion is not improving as expected over 2–
3 wks.
Early flexion splinting will aid in faster return to play.
Quadriceps Tear
Jason P. Womack
Kinshasa Morton
Basics
Quadriceps strains are graded based on the degree of injury:
Grade I: Stretch injury of muscle fibers
Grade II: Partial tearing of muscle fibers
Grade III: Complete tear of muscle fibers:
Grade III tears most commonly involve the distal rectus femoris muscle.
Grade III tears may involve complete rupture of the extensor mechanism if the distal
quadriceps tendon is involved (1).
Proximal ruptures may involve avulsion of anterior inferior iliac spine.
Epidemiology
Rectus femoris is the most common location of clinically significant quadriceps strains (2):
Majority of injuries around the muscle body, with distal and proximal injuries being rare (1)
Tears occur predominantly in males (3).
Partial tears occur on average at 28 yrs old (3).
Represents 10% of injuries to soccer players
Proximal rupture/avulsion is rare:
More commonly seen in adolescent, kicking athletes
Represents 1.5% of hip injuries (0.05% of all injuries) to National Football League (NFL)
players since 1997 (4)
Distal quadriceps rupture is a rare event:
88% of ruptures occur in those >40 yrs of age.
Risk Factors
Distal tendon rupture (5):
Age over 40
Hemodialysis patients
Diabetes
Gout
Hyperparathyroidism
Hypocalcemia
Etiology
Commonly affects athletes with repetitive functional overloading of the extensor mechanism
(3):
The dominant kicking leg is at risk for quadriceps strain (2).
Complete tears most likely seen in basketball, weightlifting, and high jump (6).
Diagnosis
History
Strain to quadriceps muscle is most commonly associated with kicking or sprinting.
Strains are a noncontact injury. History of contact leads to diagnosis of quadriceps contusion.
Physical Exam
Appearance:
There may be swelling and possible ecchymosis around the area of injury.
Palpation:
Tenderness, spasm, or both at the area of muscle injury
A defect in the muscle tissue may be felt in Grade III strains.
If distal ruptured, the intercondylar notch may be palpated, as the quadriceps tendon is not
present
Range of motion:
The extensor mechanism must be evaluated in all knee and quadriceps injuries.
Inability of any active extension of the knee is concerning for quadriceps rupture.
Strains show pain with active extension and passive knee flexion:
Grade I will show pain with resisted active extension.
Grade II and III will show pain with unopposed active extension.
Alert
Lack of active extension of the knee should raise concern of complete tendon rupture that
requires prompt diagnosis and surgical consultation.
Strength exam:
Weakness of knee extension secondary to the injured muscle tissue
Neurological exam:
Sensation and reflexes are intact:
No reflex will be present in complete rupture.

Imaging
Plain radiographs:
Not helpful in the diagnosis of acute quadriceps strain
Complete ruptures may show patellar baja on lateral views.
MRI:
Not necessary in quadriceps strain, but will likely show edema and possible defects in the
musculature (1)
Proximal ruptures may show avulsion of the anterior inferior iliac spine (AIIS) and degree of
retraction from the pelvis.
US (7):
Partial tearing:
Hypoechoic cleft in the tendon
Scanning in the long and short axis helps to determine the extent of the strain.
Complete rupture:
Complete discontinuity in the long axis of scanning
Quadriceps tendonitis
Patellar tendinitis
Patellar dislocation/subluxation
Sinding-Larsen-Johansson disease
Treatment
Acute phase:
Rest, ice, compression, and pain control
Gentle stretching as permitted to maintain range of motion
Early surgery is indicated for complete distal rupture:
Proximal rupture/avulsion may be treated nonoperatively
NSAIDs:
NSAIDs may be used acutely to help with pain.
Controversy exists as to whether NSAIDs delay healing and collagen
formation.
Alert
Be careful if there is a suspected quadriceps contusion NSAID used could
theoretically increase bleeding.
Recovery phase:
Recovery of range of motion with stretching
Exercise to regain strength of the quadriceps and hamstring tendons
Padding should be worn to protect the injured portion of the quadriceps
musculature.
Surgery indicated for quadriceps rupture at the patellar insertion as noted
above. A recent study of NFL players with proximal quad tendon avulsion
showed that conservative measures lead to good outcomes in these injuries.
Acute rupture of the distal quadriceps tendon:
Requires prompt surgical repair
Time from injury to repair is the greatest determinant of outcome in athletes
with quadriceps tendon ruptures. Repair within 1–2 wks yields significantly
better outcomes.
End-to end repairs and tendon-to-bone repairs are used, depending on the
level of the rupture.
Proximal avulsion of the AIIS:
Vast majority are successfully treated nonoperatively
Surgery to reattach the avulsed AIIS may be successful treatment if there is
continued pain, disability, or both after conservative measures have failed
(8).
Intrasubstance rectus femoris Grade III strains:
Removal of the tear may benefit those who continue to have pain or
dysfunction after physical therapy.
Ongoing Care
Return to play:
When quadriceps has 120 degrees of flexion
No signs of quadriceps weakness
May take days to months based on the degree of injury
References
1. Armfield DR, Kim DH, Towers JD, et al. Sports-related muscle injury in the lower
extremity. Clin Sports Med. 2006;25:803–842.
2. Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football.
Am J Sports Med. 2001;29:300–303.
3. DeBerandino T, Milne l, DeMaio M. “Quadriceps Injury.” eMedicine. 2006 Jun 5.

4. Gamradt SC, Brophy RH, Barnes R, et al. Nonoperative treatment for proximal avulsion
of the rectus femoris in professional American football. Am J Sports Med. 2009.
5. Johnson AE, Rose SD. Bilateral quadriceps tendon ruptures in a healthy, active duty
soldier: case report and review of the literature. Mil Med. 2006;171:1251–1254.
6. Rooks YL, Corwell B. Common urgent musculoskeletal injuries in primary care. Prim
Care. 2006;33:751–777.
7. Miller T. Common tendon and muscle injuries: lower extremity. Ultrasound Clinics.
2007;2:595–615.
8. Irmola T Heikkila JT, Orava S, et al. Total proximal tendon avulsion of the rectus femoris
muscle. Scand J Med Sci Sports. 2007;17:378–382.
Additional Reading
Ramseier LE, Werner CM, Heinzelmann M. Quadriceps and patellar tendon rupture. Injury.
2006;37:516–519.
Codes
ICD9
Radial Tunnel Syndrome
Pankaj Kaw
Rajwinder Deu
Basics
Description
Radial tunnel syndrome (RTS) is a compressive neuropathy (without any motor deficits)
involving one of the terminal branches of the radial nerve, the posterior interosseous nerve
(PIN), as it passes through the radial tunnel:
Controversy exists as to the exact definition and existence of this condition (1,2).
Sometimes separated into radial tunnel syndrome and PIN syndrome (3):
RTS: Painful condition without motor deficits
PIN syndrome: PIN motor neuropathy
Significant overlap in many cases, making some question the differentiation
The symptoms are diffuse, not well defined, overlap those of the much more prevalent lateral
epicondylitis, and therefore have caused confusion as to what actually constitutes radial
tunnel syndrome. A careful history and examination are required to differentiate the 2.
Epidemiology
Incidence
Incidence ranges between 1% and 2% of all peripheral nerve entrapments (1)
Risk Factors
Patients often perform repeated pronation and supination or forceful extension of the
forearm.
Most common presentation is that of a heavy manual laborer. Others at risk include tennis
players, swimmers, rowers, housewives, welders, conductors, and violinists (3).
Patients between 40 and 60 yrs old; no gender predilection (1,3)
Etiology
Over a distance of 5 cm in the radial tunnel, the PIN can be compressed at the following
sites:
Dynamically by the conjoint tendon of origin of the wrist and finger extensors
By fibrous bands that arise between the brachioradialis and joint capsule
By recurrent radial vessels (the leash of Henry)
By the fibrous edge of the extensor carpi radialis brevis
By the fibrous proximal border of the superficial portion of the supinator (arcade of Frohse)
By the distal edge of the supinator
At any level, the PIN also may be compressed by a ganglion or lipoma, or by marked
swelling of the elbow capsule resulting from rheumatoid synovitis.
Diagnosis
History
Pain in the lateral elbow and/or proximal dorsal forearm that typically radiates distally
Heaviness in upper forearm
Occasional vague dorsal wrist pain
Increase in symptoms with repetitive activities such as forearm rotation, elbow extension, and
maximum wrist flexion-extension
Acute: Pain usually absent at rest, provoked by powerful grasping and lifting activities, worse
at end of the day
Chronic: Baseline pain is present but is augmented by activation of the extensor-supinator
group.
Physical Exam
Much overlap between lateral epicondylitis and radial tunnel syndrome exam findings
Tenderness to palpation over the radial tunnel—4 fingerbreadths distal to the lateral
epicondyle—rather than at the common extensor origin on the lateral epicondyle
Symptoms are exacerbated with active supination with the elbow extended against
resistance, passive pronation, passive elbow extension, resisted wrist extension, and
resisted middle finger extension (“middle finger test”).

Imaging
Radiographs are helpful to exclude cervical spondylosis and degenerative changes in the
elbow joint.
MRI manifestations include muscle denervation edema or atrophy along the PIN. Increased
T2 signal in the muscles supplied by the PIN for acute denervation and increased T1 signal
for chronic denervation (3).
Electrodiagnostic studies are generally not useful (1,4)[C].
Relief of symptoms after localized injection of an anesthetic into the radial tunnel and PIN
confirms the diagnosis and is indicative of the pain relief that can be expected after surgical
decompression (1,4,5)[C].
Lateral epicondylitis
Radial neuropathy (other than in the radial tunnel)
Posterolateral instability of the elbow
Compression of the lateral antebrachial cutaneous nerve
Osteoarthritis of the elbow
Intra-articular loose bodies
Extensor tenosynovitis
Treatment
Nonoperative treatment (4,5)[C]:
Anti-inflammatory medications, rest, and avoidance of provocative activities
A splint can be used to maintain forearm supination and wrist extension.
Physical therapy focused on ergonomic retraining, stretching, and eventual
strengthening of the extensor-supinator group
Injections of local anesthetic can be helpful diagnostically and may relieve
pain in the short term:
Addition of a corticosteroid is sometimes considered, but no data are
available to support effectiveness
Conservative treatment is highly recommended because delay of surgery
has never been reported to compromise the final recovery.
Operative treatment:
Patient selection is very important. Clear differentiation must be made
between radial tunnel syndrome and lateral epicondylitis. Best surgical
candidates are those who complain of pain in association with resisted
supination, positive middle finger test, positive electrodiagnostic findings, and
pain relief after anesthetic injection into the radial tunnel.
Surgical decompression should be considered for patients who fail 12 wks of
conservative treatment (4,5)[C].
Multiple surgical approaches; dependent on the site of offending anatomical
structures
Rates of improvement range from 50–90% (1,4,5)[C].
Successful surgery should result in full recovery over a period of 9 mos (1)
[C].
Ongoing Care
Return to activity should be undertaken slowly as symptoms improve.
Rehabilitation program should be continued for both nonoperative and
postoperative patients.
References
1. Stanley J. Radial tunnel syndrome: a surgeon's perspective. J Hand Ther.
2006;19:180–184.
2. Huisstede B, Miedema HS, van Opstal T, et al. Interventions for treating the
radial tunnel syndrome: a systematic review of observational studies. J Hand
Surg [Am]. 2008;33:72–78.e3.
3. Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder

and elbow in the athlete. Clin Sports Med. 2006;25:465–487, vi–vii.
4. Henry M, Stutz C. A unified approach to radial tunnel syndrome and lateral

tendinosis. Tech Hand Up Extrem Surg. 2006;10:200–205.
5. Tsai P, Steinberg DR. Median and radial nerve compression about the
elbow. J Bone Joint Surg Am. 2008;90:420–428.
Codes
ICD9
354.3 Lesion of radial nerve
Clinical Pearls
Compressive neuropathy of the posterior interosseous nerve (PIN) at the
radial tunnel
No motor deficits
Symptoms overlap with more prevalent lateral epicondylitis.
No definitive diagnostic tests
Nonoperative treatment (anti-inflammatory medications, physical therapy,
and/or injection) is first line.
Surgical decompression is an option for those who fail 12 wks of nonoperative
treatment.
Red Eye
Jeffrey R. Bytomski
William Felix-Rodriguez
Basics
Ocular inflammation
Dilation of the anterior ciliary arteries
Concomitant inflammation of the cornea, iris, or ciliary body
Description
Pain (especially on movement of the eye)
Blurred vision
Diplopia
Diminished visual fields
Photophobia
Floaters or flashes
Epiphora
Altered facial sensations
Anisocoria
Hyphema
Exophthalmos/enophthalmos
SC emphysema
Irregular-shaped pupil
Etiology
Canaliculitis:
Common pathogens are Actinomyces israelii, Candida, and Aspergillus.
It also may be iatrogenic, after instrumentation, or placement of silicone plugs in the
treatment of dry eyes.
Redness and tenderness are most prominent at the side of the eye near the nose.
Conjunctivitis (viral, bacterial, or allergic):
Usually self-limited
Systemic manifestations depend on patient's status at presentation (age,
immunocompromised state).
Obtain cultures and smear.
Blepharitis:
Usually self-limited
Seborrheic or staphylococcal infection
Mildly red eye (unilateral), slight discharge (clear)
Obtain cultures and smears.
Corneal injury:
Infective, toxic, degenerative, traumatic, or allergic
Assess for abrasions and visual acuity.
Ophthalmologic assessment within 48 hr of injury
Dacryocystitis:
Inflammation and/or obstruction of nasolacrimal duct
In children, Haemophilus influenzae
Adults: Staphylococcus aureus or β-hemolytic Streptococcus
Episcleritis:
Autoimmune/inflammatory systemic condition
Most often, unknown etiology
Inflammation well localized, not diffuse
Recurrence common
Corneal complications (15%) and uveitis (7%) (1)
Keratoconjunctivitis sicca:
Eye appears normal.
Deficiency of tear film components and lid surface
Epithelial abnormalities with autoimmune systemic disorders
Symptoms include itching, burning, irritation, and photophobia.
Narrow-angle glaucoma:
Pre-existing narrowing of the anterior chamber angle
Haloes around lights
Patients >50 yrs of age
Intraorbital pressure (IOP) is elevated (>21 mm Hg).
Nausea and vomiting common
Pupil mid-dilated and nonreactive to light
Scleritis:
Insidious decrease in vision
Globe tenderness
Swollen sclerae
Systemic disease (eg, rheumatoid arthritis, herpes-zoster ophthalmicus, gout) in 40% of
cases (2)
Beware of the white eye; may be ischemic changes
Subconjunctival hemorrhage:
May occur spontaneously or with trauma
Flat, thin hemorrhage or a thicker collection of blood
Iritis:
Autoimmune/inflammatory systemic condition
Unknown etiology
Correlation of 50% with presence of HLA-B27 or HLA-B8 (3)
Trauma
Direct and consensual photophobia
Unilateral
Foreign body:
Detect evidence of corneal abrasion.
Penetration of the globe should be excluded.
Eversion of lid to exclude retained material
Iridodialysis:
Avulsion of a portion of the iris root in severe blunt trauma
Always associated with hyphema (manage as such)
Exclude retinal dialysis.
Orbital injury:
Fracture of orbital bones
Increased IOP
Intraorbital contents herniate/entrap through the fracture site.
Orbital floor and the medial wall are the most common fracture sites.
Hordeolum/chalazion:
Localized nodule at lid margin
Hordeolum: Staphylococcal infection of the glands of Zeis
Chalazion: Obstruction of the meibomian glands
Diagnosis
Visual acuity
Extraocular movements
Pupil reactivity
Pupil shape
Direct and consensual photophobia
Slit-lamp examination of the cornea for edema, defects, or opacification ± fluorescein
Anterior chamber evaluation for depth, cells, and flare
IOP measurements
Eyelid inspection with eversion
CT of the head/orbits for foreign bodies or orbital fractures
Culture/smears of purulent secretions; assess sexual history and potential contacts.
If recurrent and bilateral, search for autoimmune systemic conditions (CBC, ESR, ANA,
purified protein derivative, angiotensin-converting enzyme levels, Lyme/cytomegalovirus titers)
Consult ophthalmologist for:
Dacryocystitis
Corneal ulcer
Scleritis
Angle-closure glaucoma
Uveitis
Proptosis
Orbital cellulitis
Vision loss
Uncertain diagnosis
History
Time and speed of onset
Ocular associations (eg, photophobia, blurry vision, discharge, etc.)
Systemic associations (eg, headaches, nausea, rash on the forehead)
Symptoms in the other eye, because a number of patients will fail to describe them if not
asked
Specifically inquire about trauma.
Prior surgeries
Lazy eye (guide as to whether the recorded visual acuity is worrying or not)
Recently worn contact lenses
Ask about level of hygiene.
Ask if the patient forgot to take out daily disposable contact lenses.
Ask about prior similar episodes.
Physical Exam
Lids:
Note position with regard to contralateral eye.
Redness ± swelling
Lacerations (full thickness vs partial thickness, involvement of the puncta)
Note any skin abnormality, rashes, ill-defined thickening.
Note eyelashes.
Lid eversion
Lacrimal system: Look for swelling medial to the canthus and any evidence of redness, pain,
or discharge.
Conjunctiva:
Look at color (injected, pale concretions or ulcerations).
Look for foreign bodies embedded up or down in the fornices.
Cornea:
Check if the patient is wearing contact lenses.
Look for corneal haziness.
Check for white dots visible before fluorescein staining (infiltrates suggestive of infective
keratitis).
Anterior chamber:
Using a slit lamp; assess by narrowing the beam to 1 mm and putting it on its brightest light
setting.
Angle it at 30–45 degrees to the cornea, and focus in past the cornea.
Look for cells (particles passing through the shaft of light) and flare (cloudiness).
Pupils:
Look at their relative sizes.
Elicit the red reflex in both eyes, and compare the size of these directly rather than shifting
from one to the other close up.
Look for change in shape and any abnormal oscillations.
Visual acuity: Essential examination; should be carried out on every patient presenting with an
eye problem.
Visual fields
IOP
Pupillary reactions:
Direct response to light
Light-near dissociation
Adult blepharitis
Chemical burns
Orbital cellulitis
Preseptal cellulitis
Chalazion
Acute hemorrhagic conjunctivitis
Allergic conjunctivitis
Bacterial conjunctivitis
Giant papillary conjunctivitis
Viral conjunctivitis
Contact lenses (complications)
Corneal abrasion
Dacryocystitis
Distichiasis
Ectropion
Dry-eye syndrome
Bacterial endophthalmitis
Entropion
Herpes simplex
Hordeolum
Pterygium
Acute angle-closure glaucoma
Episcleritis
Treatment
Canaliculitis:
Topical penicillins and cephalosporins
Surgery if not resolved with topical treatment
Conjunctivitis (viral, bacterial, or allergic): Topical treatment depending on
etiology (antibiotics, antivirals, or antihistamines)
Blepharitis:
Treat with application of heat to warm the eyelid.
The eyelid margin is washed mechanically to remove adherent material.
Lid hygiene is essential. Apply warm compresses to closed lid 5–10 min twice
daily 4 times a day.
Follow lid cleansing with topical antistaphylococcal treatment. Bacitracin or
erythromycin ophthalmologic ointment is 1st line; apply to lids twice daily 4
times a day immediately after cleansing.
Dacryocystitis:
Treat with oral antibiotics (Augmentin).
Treat involvement with orbital cellulitis with IV antibiotics (Vancomycin).
Episcleritis: Self-limiting disease; no treatment needed
Corneal injury:
Topical antibiotics
Tetanus toxoid
Keratoconjunctivitis sicca:
Topical cyclosporine, artificial tears
Patch with lubrication at night.
Artificial tears insert in the mornings
Surgery for severe cases (ulceration, decreased visual acuity)
Narrow-angle glaucoma:
Topical α-adrenergic agonists, β-blockers, miotic agents, prostaglandin
analogues, carbonic anhydrase inhibitors
Definitive treatment is laser iridotomy.
Scleritis: NSAIDs, glucocorticoids
Subconjunctival hemorrhage:
Self-limiting disease; no treatment needed
Treat with artificial tears
Iritis: Topical steroids and cycloplegics
Foreign body:
Removal; topical antibiotic drops and cycloplegics
Avoid removal if penetration to cornea >25%.
Iridodialysis: Observation and bed rest
Orbital injury: Rapid surgical intervention if a significant fracture is present, with
possible herniation of intraorbital contents
Hordeolum/chalazion: Warm compresses and topical antibiotics
N/A
Admission Criteria
Endophthalmitis
Perforated corneal ulcers
Orbital cellulitis
Discharge Criteria
Depends on the diagnosis: If the diagnosis is certain and visual loss will not
result, the patient may be discharged without consultation.
References
1. Red Eye Evaluation: Gino A Farina, MD, Program Director, Associate
Professor of Clinical Emergency Medicine, Department of Emergency
Medicine, Long Island Jewish Medical Center, Albert Einstein College of
Medicine. Coauthor(s): Gregory I Mazarin, MD, Assistant Professor,
Department of Emergency Medicine, Department of Emergency Medicine,
Montefiore Medical Center, Albert Einstein College of Medicine; Consulting
Staff, St Vincent's Midtown, North Shore University Hospital Updated 2006.
2. Wilhelmus KR. The red eye. Infectious conjunctivitis, keratitis,

endophthalmitis, and periocular cellulitis. Infect Dis Clin North Am. 1988;2:99–
116. Review.
3. Nishimoto JY. Iritis. How to recognize and manage a potentially sight-

threatening disease. Postgrad Med. 1996;99:255–257, 261–262. Review.
Additional Reading
Bertolini J, Pelucio M. The red eye. Emerg Med Clin North Am. 1995;13:561–
579.
Cullom R, Chang B. The Wills eye manual: office and emergency room
diagnosis and treatment of eye disease. 2nd ed. Philadelphia: JB Lippincott,
1994.
Juang PS, Rosen P. Ocular examination techniques for the emergency

department. J Emerg Med. 1997;15:793–810.
Subconjunctival Hemorrhage: Robert H Graham, MD, Senior Associate

Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona
Coauthor(s): Vivian Monsanto, MD, Consulting Staff, The Mackool Eye
Institute and Laser Center; Norvin Perez, MD, Clinical Assistant Professor of
Emergency Medicine, Albert Einstein College of Medicine; Consulting Staff,
Department of Emergency Medicine, Montefiore Medical Center Updated
2007.
Codes
ICD9
379.93 Redness or discharge of eye
Redundant Plica
Sean A. Cupp
Basics
Description
A plica is a redundant fold of embryonic synovium adjacent to the patella.
3 common locations for plicae are superior, medial, and inferior.
A 4th, lateral location is very rare and controversial.
The inferior location is the most common, and the medial is the least common, but the medial
plica is the most clinically relevant and most studied (1)[C].
Synonym(s): Patellofemoral syndrome; Synovitis of the knee
Epidemiology
Incidence
Present in 18–80% of knees
Prevalence
Predominant gender: Female > Males.
Predominant age: Occurs more often in growing adolescents
Risk Factors
Congenital presence of plica
Extensor mechanism malalignment, eg, quadriceps/vastus medialis oblique (VMO) weakness,
increased Q-angle
Repetitive flexing and extending of the knee, eg, running, jumping
Etiology
Normal elastic synovial tissue becomes thickened and swollen owing to inflammation and is
replaced by fibrotic tissue that is tight and inelastic.
This causes impingement between the patella and medial femoral condyle, resulting in
mechanical synovitis.
This secondary synovitis can alter the normal patellofemoral joint mechanism, leading to
articular cartilage softening and degeneration and chondromalacia.
Direct shearing forces from the inflamed plica on the articular cartilage may worsen the
chondromalacia (2)[C].
Diagnosis
History
Complaint of intermittent, dull anterior knee pain
Pain over suprapatellar or medial peripatellar region
Pain worse after long periods of knee flexion (eg, sitting), especially when accompanied by a
distinct snap or pop when knee is extended
May have a history of overuse or direct trauma
Painful catching or pseudolocking episodes over medial patellofemoral joint
May describe feeling of instability with episodes of pain
Physical Exam
Episodes of anterior knee pain
May be associated with swelling of the knee
Patient may describe a feeling of knee instability, “catching,” “buckling,” or “giving way” with
episodes of pain.
Palpation over the medial patellofemoral joint may demonstrate a tender thickened band in
the anterior synovium.
Often difficult to palpate; best done while passively flexing and extending the knee while
holding the tibia in internal rotation
Kick test:
Patient lies supine with knees flexed to 90 degrees
Patient quickly extends knee, imitating a soccer kick
Test is positive if it reproduces pain (3)[C].
Mediopatellar plica test:
Patient lies supine with knees in full extension
Examiner's thumb applies manual force between medial femoral condyle and patella while
knee is flexed to 90 degrees
Test is positive if pain in extension resolves or diminishes with knee in flexion (4)[A].
May find other problems associated with extensor mechanism malalignment, eg,
chondromalacia patella, patellar subluxation
Assess hamstring and heel cord tightness because these conditions tend to aggravate the
problem.

Imaging
X-ray studies do not usually show any bony abnormality. They are helpful to exclude other
sources of pathology: Osteochondritis dissecans, loose bodies, osteoarthritis, fractures,
osteophytes (1)[C].
Patellar views (eg, sunrise, Merchant, Hughston patellar views) may demonstrate a lateral
patellar tilt consistent with weakness of the vastus medialis or an increased Q-angle.
MRI may demonstrate inflammation and thickening of the anteromedial synovium of the knee
in extreme chronic cases; helps to exclude meniscal and articular cartilage pathology.
US imaging may have limited use in evaluating thickening of the synovial plica but is very
dependent on operator experience and expertise.
Other painful patellofemoral conditions, eg, chondromalacia patella, osteochondritis
dissecans of the medial femoral condyle, patellar instability/subluxation
Medial meniscus tear, pes anserine bursitis, medial collateral ligament sprain
Treatment
Analgesia: NSAIDs
Protection:
Consider external patellar support.
Rest:
Relative rest to reduce repetitive flexion of the knee
May consider short-term straight-leg immobilization (1–3 days) if pain is
severe
Ice: 20 min every 2–3 hr to reduce inflammation until swelling and pain have
resolved.
Compression: Elastic bandage can be used for comfortable level of
compression during the acute phase to help to reduce swelling.
Elevation: Elevating the knee above the level of the heart as much possible P.
may help to reduce swelling within the plica.
Support:
Consider using an open patellar knee brace with a patellar support to reduce
patellar mobility and recurrent “pinching” of the plica; may help to reduce the
chance of recurrent trauma to the plica when the patient returns to activity.
McConnell taping (a physical therapy taping technique using strong
supportive tape surrounding the patella) may be used for short-term
improvement in patellar alignment and reduction in patellar hypermobility.
Foot orthotics if patient has significant pes planus or overpronation; may help
symptomatic knee valgus deformity and decrease the Q-angle
6–8 wks of home exercises or formal physical therapy (1,5)[C]
VMO strengthening (quad sets, straight-leg raises, terminal arc extensions of
the knee)
Hamstring stretching
Heel-cord stretching
Ice for 15–20 min after exercise
Consider phonophoresis.
Injection:
Intraarticular corticosteroid injection into the knee often produces a decrease
in inflammation of the plica and associated symptoms and may be
considered if initial conservative treatment has failed.
Corticosteroid injection may help to resolve the problem and negate the need
for arthroscopic intervention.
Intraplical injection is difficult, and needle placement is unreliable and
therefore not recommended (5)[C].
Surgery:
If plica is fibrotic and symptoms persist, arthroscopic removal of the plica is
indicated.
For chronic painful plica, arthroscopic removal often provides good relief of
symptoms and return to normal function.
Surgery should be combined with rehabilitative strengthening of the VMO to
reduce the chance of recurrence.
Arthroscopy can result in further irritation and scarring of synovial plica, thus
worsening symptoms (1,5)[C].
References
1. Sznajderman T, Smorgick Y, Lindner D, et al. Medial plica syndrome. Isr
Med Assoc J. 2009;11:54–57.
2. Lyu SR, Hsu CC. Medial plicae and degeneration of the medial femoral
condyle. Arthroscopy. 2006;22:17–26.
3. Irha E, Vrdoljak J. Medial synovial plica syndrome of the knee: a diagnostic

pitfall in adolescent athletes. J Pediatr Orthop B. 2003;12:44–48.
4. Kim SJ, Lee DH, Kim TE. The relationship between the MPP test and
arthroscopically found medial patellar plica pathology. Arthroscopy.
2007;23:1303–1308.
5. Griffith CJ, Laprade RF. Medial plica irritation: diagnosis and treatment.
Curr Rev Musculoskelet Med. 2008;1:53–60.
Additional Reading
Boyd CR, Eakin C, Matheson GO. Infrapatellar plica as a cause of anterior
knee pain. Clin J Sport Med. 2005;15:98–103.
Calmbach WL, Hutchens M. Evaluation of patients presenting with knee pain:

Part II. Differential diagnosis. Am Fam Physician. 2003;68:917–922.
Codes
ICD9
727.83 Plica syndrome
Clinical Pearls
Plica bands are congenital. An inflamed plica usually occurs after chronic and
repetitive pinching of the lining of the knee caused by weakness of the
quadriceps (vastus medialis) muscle or a larger than normal angle from the hip
to the knee pulling the kneecap more sideways (commonly seen in growing
adolescent females) or after an acute trauma to the front of the knee.
Unless the inflammation has been present for a long time and scar tissue has
formed, the symptoms of an inflamed plica often will resolve with ice, NSAIDs,
and rehabilitative exercises. The plica band can only be removed with surgery,
and often the resulting scar tissue can mimic the inflamed plica symptoms.
Pain that occurs with plica irritation usually occurs only after the plica becomes
inflamed, often from being pinched between the kneecap and thigh bone from
such activities as running, jumping, going up and down stairs, or sitting with the
knee flexed for an extended period of time.
Renal Trauma
Nick Carter
Basics
Description
Back or abdominal trauma due to collision with other players or equipment may result in injury
to the kidney and its collecting system. Because signs and symptoms may initially be subtle,
a high level of suspicion is warranted, especially if other commonly associated injuries such
as splenic trauma, rib fractures, or vertebra fractures are present.
Synonym(s):
Nephroptosis: Floating kidney, mobile kidney
Renal trauma: Kidney trauma, nephric trauma
Epidemiology
5–10% of renal trauma occurs in sports.
8–10% of all blunt and penetrating injuries to the abdomen involve the kidney. The kidney is
the most commonly injured organ in the urogenital system. Blunt trauma accounts for 80–
90% of kidney injuries.
The most common blunt trauma mechanism is rapid deceleration, especially to the upper
abdominal area.
Vascular injury of renal vessels has been reported in 1–3% of patients with blunt trauma.
Venous injuries following blunt or penetrating trauma to the kidney can result in rapid and
massive blood loss with relatively few symptoms.
Injuries to the renal pedicle can lead to life-threatening blood Loss. Fortunately, these injuries
account for only 1–2% of all renal injuries.
Among children, 16–25% of renal trauma is sports-related. The majority of injuries involve
boys 11–17 yrs of age. Of children with renal trauma, 8–22% have congenital anomalies.
Risk Factors
Multiple fractures and injuries to abdominal organs, the vascular system, chest, and head
make kidney trauma more likely.
Ectopic placement of kidneys elsewhere in the abdomen may predispose to injury due to lack
of protection usually afforded by the ribs.
Pre-existing renal anomalies have been shown to be associated with injury in 0.1–23% of
adult cases and in 0.4–23% of pediatric cases.
Diagnosis
History
Flank pain and tenderness are usually present.
The athlete may complain of gross hematuria.
History of a collision or fall is described.
Physical Exam
Diffuse abdominal tenderness with or without hematuria is the most common sign and
symptom of kidney trauma.
Associated injuries such as lower rib fractures, vertebral body fractures, and flank trauma
with or without other internal injuries are common.
Major injury to the renal vasculature may occur in the absence of hematuria. Hematuria, when
present, is usually an early indicator of renal injury. The degree of hematuria, however, does
not correlate with the severity of the injury.
Significant renal trauma may result in hypovolemic shock.
The athlete may initially present as pale, perspiring, tachycardic, and nauseated.
Tenderness to palpation of the flank and back is usually present.
Muscle guarding may be present.
Reflex ileus may occur with a loss of bowel sounds.
A mass may be palpable representing either a hematoma or other renal abnormality.
Hypotension and shock may be present if there is significant blood loss.
Assess for associated injuries to the abdomen, chest, and back.

Lab
Blood counts may show slight leukocytosis with a left shift. Hematocrit may be normal or
decreased depending on fluid status. Serum BUN and creatine, as a baseline, help evaluate
for pre-existing renal abnormalities.
Gross or microscopic hematuria has been reported in over 95% of patients with kidney
injuries.
Athletes with hematuria, gross or microscopic, following blunt trauma should undergo
radiologic assessment.
Microscopic hematuria without shock does not necessarily require radiographic evaluation,
but can be managed conservatively.
Renal imaging is required in all pediatric patients.
Renal imaging is required in all adult patients with penetrating trauma and hematuria, gross or
microscopic.
If physical exam or associated injuries suggest renal injury, renal imaging should be
performed for staging.
High-resolution CT scan with contrast is the preferred method of renal evaluation following
trauma.
CT scan is noninvasive, sensitive to hematoma, and sensitive to urine extravasation, and
provides additional information regarding other possible organ damage.
CT scan is not reliable in evaluating possible renal vein injuries. If venous injury is suspected,
venography should be performed.
Arteriography is the definitive study to identify parenchymal and vascular injuries.
Sonography provides less information compared with CT scan and does not accurately
detect vascular injuries.
Radionuclide scanning gives limited information and is not especially helpful in staging renal
injuries.
Although retrograde pyelography is useful in evaluating ureteral injuries, it is not helpful in
evaluating renal injuries.
Hematuria:
Renal: Congenital anomalies, polycystic kidney, tumor, pyelonephritis, glomerulonephritis,
Alport's syndrome, nephrolithiasis
Collecting system: Bladder rupture, exercise-induced, tumor, ureteral laceration, urethral
laceration, blood dyscrasias
Organ injury: Splenic fracture, ruptured viscera, pulmonary contusion, liver fracture
Musculoskeletal injury: Fractured rib(s), fractured vertebral body, fractured posterior spinal
elements, contusion, muscle strain
Treatment
Aggressive fluid resuscitation in athletes with hypotension or shock
Often conservative management if renal contusion is present
If staging evaluation of the kidneys shows evidence of vascular involvement,
surgical intervention may be required.
Evidence of renal venous compromise necessitates emergent intervention.
Athletes should be followed until hematuria resolves. Some recommend IV
pyelogram (IVP) at 3 mos.
Athletes with serious renal trauma should be followed at 3-mo intervals with
urinalysis and IVP for at least 1 yr.
Renal injuries are classified according to 5 grades:
Grade I: Renal contusion
Grade II: Minor lacerations
Grade III: Lacerations >1.0 cm without collecting system rupture
Grade IV: Parenchymal laceration through renal cortex, medulla, and
collecting system
Grade V: Complete kidney fracture with vascular compromise
Generalized return to conditioning may be required following prolonged
convalescence.
Specific rehabilitation of chest, abdomen, and back muscles for associated
injuries
Contusions represent 85–90% of blunt renal injuries. These can be managed
nonoperatively.
Surgical management of minor and major renal lacerations is controversial.
Most clinicians avoid operating unless bleeding is life-threatening.
In those cases when surgery is performed, a nephrectomy is usually required.
Indications for surgical intervention of complications include expanding
uncontained hematoma, pulsatile hematoma, urinary extravasation, vascular
injury, nonviable parenchyma, and incomplete staging.
Renal exploration is required in 2.5% of cases of blunt trauma.
Of those requiring renal exploration, the salvage rate is 87%.
Ongoing Care
Athletes with renal contusions should refrain from participating in contact sports for 6
wks after hematuria resolves.
Athletes with extensive renal trauma should be withheld from contact or collision sports for 6–
12 mos.
Although athletes with a solitary kidney may participate in sports, the decision to participate
in contact and collision sports should be weighed on an individual basis.
Athletes with solitary kidneys or previous kidney trauma should seriously consider special
protective equipment use when they return.
Vascular injuries to the main renal artery carry a poor chance of reconstruction if diagnosis is
delayed or the patient is older.
Additional Reading
Armstrong PA, Litsher LJ, Key DW, et al. Management strategies for genitourinary trauma.
Hosp Physician. 1998;34:19–25.
Cianflocco AJ. Renal complications of exercise. Clin Sports Med. 1992;11:437–451.
Danzl DF, Rosen P, Barkin R. Emergency medicine: concepts and clinical practice. St.
Louis: CV Mosby, 1998.
Feliciano DV, Moore EE, Mattox KL. Trauma. Stamford, CT: Appleton & Lange, 1996.
Gillenwater JY, Grayhack JT, Howards SS, et al. Adult and pediatric urology. St Louis: CV
Mosby, 1998.
Mandell J, Cromie WJ, Caldamone AA, et al. Sports-related genitourinary injuries in

children. Clin Sports Med. 1982;1:483–493.
Moeller JL. Contraindications to athletic: participation. Physician Sportsmed. 1996;24:57–

75.
Codes
ICD9
866.00 Unspecified injury to kidney without mention of open wound into cavity
866.01 Hematoma of kidney, without rupture of capsule, without mention of open wound into
cavity
866.02 Laceration of kidney without mention of open wound into cavity
Clinical Pearls
Return to sports: Depends on the seriousness of the injury. If surgery
(particularly nephrectomy) was required, patient may want to consider avoiding
contact or collision sports.
Follow-up: Frequent until all symptoms clear then, depending on seriousness of
injury, periodic monitoring of kidney function
Retinal Detachments and Tears
Jorge O. Rodriguez
Adrian Lavina
Basics
The retina is a multilayer of neurons that line the back of the eye and convert photons
into neural impulses that travel to the visual cortex.
Retinal detachment occurs when the neurosensory retina separates from the underlying
retinal pigment epithelium and choroid.
Retinal detachments can be rhegmatogenous (caused by a break in the retina; rhegma is
Greek for “tear”), exudative (caused by leakage or exudation from beneath the retina), or
tractional (vitreous, fibrous, or fibrovascular traction pulling on the retina).
Description
3 distinct classifications of retinal detachments:
Rhegmatogenous retinal detachment (RRD)
Tractional retinal detachment (TRD)
Exudative retinal detachment (ERD)
RRD:
Most common
Occurs when a break in the sensory retina allows fluid from the vitreous to separate the
rods and cones from the villi of the pigment epithelium
Occurs as an acute event, with symptoms of flashes owing to the separation of the nerve
fibers and spots owing to bleeding from the rupturing of retinal blood vessels
Posterior vitreous detachment (PVD) is the most common cause of RRD. A PVD occurs
when the vitreous liquefies and then separates from the back of the eye. Although this is
usually a normal part of aging, 2% of the time that a PVD occurs forcefully enough to
cause symptoms, a retinal tear occurs (1).
TRD:
Occurs because of contraction of fibrous vitreous bands pulling the sensory retina off of
the pigment epithelium
Chronic progressive disorder
May remain without symptoms unless hemorrhage or retinal tear occurs
ERD:
Abnormal collections of fluid are produced, separating the layer of the retina.
Usually asymptomatic until involvement of the macula occurs, with impairment of central
vision
Occasionally, the retina can become so elevated and anteriorly displaced by underlying
fluid as to be visible with a penlight just behind the lens.
Epidemiology
Incidence
Incidence increases with age
Nontraumatic RRD: 1/10,000 per year (1)
Prevalence
After cataract surgery, 1–3% of patients will develop a retinal detachment.
Risk Factors
Myopia
Cataract surgery
PVD and associated conditions (trauma, inflammation, aphakia); ages 50–75 yrs
Aphakia
Trauma
Retinal detachment in fellow eye
Lattice degeneration: Present in 6–8% of population and in 30% of patients with nontraumatic
RRD (1)
Glaucoma
Vitreoretinal tufts: Caused by focal areas of vitreous traction
Meridional folds: Redundant retina
Family history of retinal detachment
Vitreohyaloidopathy: Hereditary abnormality of the vitreous body
Genetics
Most cases are sporadic.
General Prevention
Impossible to prevent spontaneous PVD
Patient education is key.
Early identification of retinal tears and treatment may prevent retinal detachment and
significant vision loss.
Etiology
RRD occurs as a result of either structural or developmental abnormalities of the eye; by
definition, they are caused by a full-thickness retinal hole or tear.
High myopia
Marfan syndrome
Structural degeneration of the underlying anatomy of the eye (including the pigment
epithelium, the sensory retina, and the vitreous body or occasionally as a result of trauma)
PVD: Most common cause of RRD
Traumatic retinal detachment: Much less common than spontaneous RRD
TRD occur in association with:
Diabetes
Vasculopathy
Perforating injury
Severe chorioretinitis
Retinopathy of prematurity, sickle-cell retinopathy, or toxocariasis
ERD arise from
Tumors of the choroid (eg, melanoma) or retina (eg, retinoblastoma)
Inflammatory disorders such as Coats or Harada disease
Central serous chorioretinopathy

Lattice degeneration
High myopia
Cataract surgery
Glaucoma
History of retinal detachment in other eye
Trauma
Diagnosis
History, especially:
Age
Speed of onset of symptoms
Associated symptoms
Previous episodes
Complete ophthalmologic examination, especially:
Assessment of pupillary function
Evaluation of the vitreous for cells
Dilated retinal exam
360-degree scleral depressed examination using indirect ophthalmoscope
B-scan US
History
Floaters
Sudden loss of vision
Bright flashes of light (photopsias)
Expanding shadow
Progressive peripheral visual field defect
Physical Exam
Slit-lamp exam
Dilated fundus exam with binocular indirect ophthalmoscopy

Visual field testing
Lab
As indicated for underlying disease
Imaging
B-scan US
Elevation of the neurosensory retina from the underlying retinal pigment epithelium
Elevation of retina associated with retinal tears in RRD or elevation of the retina without tears
in exudative detachment
In 3–10% of patients with presumed RRD, no definite retinal break is found (2).
Tenting of the retina without retinal tears in traction detachment
Pigmented cells within the vitreous “tobacco dust” (1)[C]
Senile retinoschisis (retinoschisis, a splitting of the retina)
Juvenile retinoschisis
Choroidal detachment
Vitreous hemorrhage
Vitreous inflammation (eg, Toxoplasma chorioretinitis)
Ocular lymphoma
Treatment
Sports-related ocular trauma evaluated on site (3)
Obtain adequate history.
Best corrected visual acuity is checked with an eye chart.
Check confrontation visual fields.
Examine pupils.
Penlight exam of the anterior chamber
Ocular motility
External exam looking for orbital injury
Funduscopic exam
If suspecting globe rupture, place protective shield over the eye, put on NPO
status, and refer.
ED Treatment
Bed rest
Urgent ophthalmologic consultation
A retina specialist ultimately will need to care for the patient if retinal
detachment is present.
Referral
Sudden decrease in or loss of vision
Loss of field of vision
Pain on movement of the eye
Photophobia
Diplopia
Proptosis of the eye
Light flashes or floaters
Irregularly shaped pupil
Foreign-body sensation/embedded foreign body
Red and inflamed eye
Hyphema
Halos around light (corneal edema)
Laceration of the lid margin or near medial canthus
Broken contact lens or shattered eyeglasses
Suspected globe perforation
PVD management:
Most patients who present with PVD and do not have any retinal breaks or
tears require only reassurance and education.
Full dilated exam with indirect ophthalmoscopy at least twice during the 6 wks
following onset of symptoms
Retinal hole or tear: Laser photocoagulation or cryoretinopexy to prevent
retinal detachment (1)[A]
RRD:
Laser photocoagulation or cryoretinopexy for smaller detachments
Pneumatic retinopexy
Scleral buckle
Vitrectomy
TRD: Pars plana vitrectomy (1)[C]
ERD (1)[C]: Identify and treat etiology; surgical repair is not recommended in
most cases.
Bed rest prior to surgery
Postoperatively, if intraocular gas has been used, the patient may need specific
head positioning and may need to avoid all air travel or high altitudes.
N/A
Admission Criteria
RRDs require emergent referral to a retina specialist, particularly if the macula
is not yet detached (macula on retinal detachment).
Surgery may be done in a hospital or ambulatory surgery center, and this will be
the retinal specialist's decision.
Admission may be required until a retina specialist is found.
Discharge Criteria
RRDs that do not yet involve the macula (macula on retinal detachment)
require repair within 24 hr.
RRDs involving the macula (macula off retinal detachment) may be repaired
within 3–7 days because there is no evidence that urgent repair affects the
outcome.
TRDs are repaired within 1–2 wks depending on the chronicity.
ERDs generally will resolve with successful treatment of the underlying
condition.
Ongoing Care
Prognosis
RRD:
Pneumatic retinopexy is an in-office procedure for which certain patients are candidates.
Pneumatic retinopexy leads to successful retinal attachment 70–80% of the time after 1
procedure (1,4).
In cases of failure, treat with scleral buckle placement and/or vitrectomy.
Scleral buckle placement is successful 80–90% of the time after 1 procedure (1).
Failed cases usually are treated with vitrectomy (5).
Vitrectomy has an 80–90% success rate after 1 surgery (1).
In failed cases, more extensive vitreoretinal procedures are required.
Virtually all patients over age 50 will develop progressive cataract following vitrectomy (1).
References
1. Arroyo JG. (2009). Retinal tear and detachment. Retrieved June 17, 2009 from
www.uptodate.com
2. Coffee RE, Westfall AC, Davis GH, et al. Sympto-matic posterior vitreous detachment
and the incidence of delayed retinal breaks: case series and meta-analysis. Am J
Ophthalmol. 2007.
3. Rodriguez JO, Lavina AM, Agarwal A. Prevention and treatment of common eye injuries
in sports. Am Fam Physician. 2003;67:1481–1488.
4. Chan CK, Lin SG, Nuthi AS, et al. Pneumatic retinopexy for the repair of retinal
detachments: a comprehensive review (1986–2007). Surv Ophthalmol. 2008;53:443–478.
5. Heimann H, Bartz-Schmidt KU, Bornfeld N, et al. Scleral buckling versus primary

vitrectomy in rhegmatogenous retinal detachment: a prospective randomized multicenter
clinical study. Ophthalmology. 2007;114:2142–2154.
Codes
ICD9
361.00 Retinal detachment with retinal defect, unspecified
361.01 Recent retinal detachment, partial, with single defect
361.02 Recent retinal detachment, partial, with multiple defects
Clinical Pearls
Protective devices: The American Society for Testing and Materials has
established performance standards for selected eyewear that are most
appropriate for sports with a risk of ocular injury.
Return to play:
The injured eye should feel comfortable and have adequate return of vision.
Eye protectors must be worn.
Rhabdomyolysis
Cherise Russo
Basics
Description
Syndrome associated with muscle injury and systemic release of intracellular contents, such
as creatine phosphokinase (CPK)
A combination of myoglobinuria, hypovolemia, and aciduria leads to acute renal failure.
Direct release of potassium from damaged muscle tissue may lead to dysrhythmias and
sudden death.
Epidemiology
Occurs in up to 85% of trauma patients
10–50% of patients with rhabdomyolysis will develop acute renal failure.
26,000 people are affected in the U.S. each year.
Exact incidence of exertional rhabdomyolysis is unknown, but is likely comparable to military
reports of 0.3–3%
Risk Factors
Heritable muscle enzyme deficiencies
Electrolyte abnormalities
Infections
Drugs
Toxins
Endocrinopathies
Exercise in high heat
Exercise in high humidity
Sudden increase in physically demanding exercise
Exercise in dehydrated state
Genetics
Metabolic myopathies:
Small percentage of total cases
Inherited disorders:
Disorder of glycogenolysis
Disorder of glycolysis
Disorder of lipid metabolism
Disorder of purine metabolism
Mitochondrial myopathies
Increased suspicion when patients have recurrent episodes of rhabdomyolysis associated
with exercise
Etiology
Muscle damage and/or necrosis that results in elevation in CPK levels, electrolyte disturbances,
and renal compromise:
Trauma/crush injuries (motor vehicle accidents, fall from seizure or stroke, struggle against
restraints, abuse, prolonged tourniquet)
Exercise
Hyperthermia (heat stroke, malignant hyperthermia, and neuroleptic malignant syndrome)
Hypothermia
Prolonged immobile state
Drugs/toxins (alcohols, cocaine, amphetamines, opiates, antihistamines, barbiturates,
phencyclidine, caffeine, carbon monoxide, cholesterol-lowering agents, succinylcholine, snake
venom, bee/hornet venom, etc.)
Chronic electrolyte disturbances (hypokalemia, hypophosphatemia, hypoxia)
Infections (viral, bacterial, parasitic, protozoan, rickettsial)
Endocrinopathies (hyperthyroid state, diabetic ketoacidosis, hyperosmolar)
Burn or electrical injury
Genetic disorders/metabolic myopathies (McArdle's disease, Tarui's disease)
Hematologic disorder (sickle cell trait)
Immunological disorders (dermatomyositis, polymyositis)
Idiopathic
Diagnosis
General symptoms include: Malaise, fever, tachycardia, nausea/emesis along with
myalgia
Typically, the patient demonstrates decreased flexibility and decreased strength secondary to
pain.
Muscle pain, reduced flexibility, decreased/painful strength
History and physical are insensitive in making the diagnosis.
Serum CPK level is criterion standard and must be sent if any clinical suspicion exists.
Serum electrolytes, BUN, creatinine, calcium, and liver enzyme levels should be obtained.
Urine dipstick that is positive for heme but absent for RBCs suggests rhabdomyolysis
(myoglobinuria):
Because of rapid urinary excretion of myoglobin, up to 26% of patients with
rhabdomyolysis have negative urine dipstick.
History
Wide range of severity of symptoms
Classic features: Myalgia, weakness, and dark urine (seen in <10% of patients)
General symptoms include: Malaise, fever, tachycardia, nausea/emesis
Physical Exam
Signs and symptoms can vary dramatically, reflecting underlying disease process.
Obvious crushing injury
Hypothermia/hyperthermia
Patient may be either alert or obtunded
Muscle tenderness, swelling (calves and lower back most commonly involved)
Change in urine color; orange to cola-colored to black
Hypovolemic state, dry mucous membrane, poor skin turgor, tachycardia, hypotension
Decreased urine output

Lab
CPK levels are the most sensitive; CK-MM isoenzyme is most elevated
CPK levels rise within 12 hr, peak in 1–3 days, and reduce 3–5 days after underlying cause
of muscle injury is addressed.
CPK levels >5,000 U/L relate to renal failure.
Serum and urine myoglobin levels useful in acute phase; has short half-life and may return to
normal within 6–8 hr
Perform urine dipstick to evaluate for myoglobinuria and urine analysis to detect casts,
protein, and uric acid crystals.
Arterial blood gas
Carbonic anhydrase III more specific for skeletal muscle
Metabolic profile (hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia)
Blood urea nitrogen level to creatinine ratio decreases to 6:1 or less
Serum glucose, lactate dehydrogenase, serum glutamic oxaloacetic transaminase, albumin
Toxicology screen in absence of physical injury
Prothrombin time/partial thromboplastin time, platelet count, fibrinogen, fibrin-split products if
disseminated intravascular coagulopathy is suspected
Imaging
MRI is 90–95% sensitive in visualizing muscle injury.
MRI is not typically ordered because the imaged muscle damage does not change initial
treatment.
Forearm ischemic test:
To differentiate genetic causes of rhabdomyolysis
Performed after rhabdomyolysis is resolved
Obtain baseline ammonia and lactic acid levels.
Inflate sphygmomanometer to >200 mm Hg.
Patient performs hand-grip exercises to fatigue.
Cuff is removed and serial blood tests are drawn.
Minimal or no rise in lactic acid suggests carbohydrate metabolism disorder or McArdle's
disease.
Delayed rise or no rise in the ammonia level suggests myoadenylate deaminase deficiency.
Normal rise in ammonia and lactic acid levels suggests the presence of a disorder of lipid
metabolism.
The following conditions may present with elevated serum CPK but may not lead to
complications of rhabdomyolysis:
Nontraumatic myopathies
Renal failure
IM injections
Myocardial injury
Hypothyroidism
Hyperthyroidism
Stroke
Surgery
Treatment
Aggressive fluid resuscitation is paramount to reducing renal compromise.
Pre-Hospital
Need for rapid extrication in case of crush injury
Early IV fluids to prevent complications (hypovolemia, acute renal failure [ARF],
hyperkalemia, etc.)
ED Treatment
Directed toward treating or reversing the underlying cause of rhabdomyolysis
Prevent ARF:
Immediate IV isotonic saline (1,2)[B]
Mannitol following IV saline promotes diuresis, acts as renal vasodilator, and
may act as free-radical scavenger), but clinical effects are unproven (1,2)
[C].
Furosemide administration is controversial (3).
Hyperkalemia: IV fluid, dextrose, insulin, monitor/electrocardiogram
Acidosis: Bicarbonate administration is debated, may worsen hypocalcemia
(1,2)[C]
Overdose: Activated charcoal, lavage, antidote
Infection: Broad-spectrum antibiotics
Compartment syndrome: Fasciotomy (compartment pressure >35 mm Hg)
Neuroleptic malignant syndrome: Dantrolene, bromocriptine
Need for hemodialysis: Refractory to treatment, hyperkalemia,
hyperphosphatemia, hyperuricemia, volume overload, overdose
Medication
Medication guidelines (1,2):
Administer IV isotonic saline at 1,000–1,500 mL/hr initially.
Goal: To achieve urine output of 300 mL/hr until myoglobinuria resolves
Dextrose may be added after initial resuscitation to 0.45NS
Bicarbonate and mannitol have been recommended but have unproven benefit.
Furosemide administration is also controversial.
First Line
IV fluids: Isotonic saline
Second Line
Bicarbonate and mannitol have been recommended but have unproven benefit.
Furosemide administration is also controversial.
ABCs
Immobilization of trauma/crush injuries
IV fluids for hypotension and hypovolemia
Admission Criteria
Because it is impossible to predict which patients will develop complications, all
patients with significant elevated CPK or suspicion for rhabdomyolysis must be
admitted.
Admit to monitored bed for patients with electrolyte abnormalities.
Admit to intensive care unit bed for patients who might require hemodialysis or
closer fluid and electrolyte monitoring.
IV Fluids
Plasma volume resuscitation with isotonic saline is first-line treatment.
Nursing
Frequency of hemodynamic monitoring determined by stability of patient
Monitor urinary output closely.
Discharge Criteria
No patients suspected of having rhabdomyolysis should be discharged from
the emergency department.
Patient must be hemodynamically stable before discharge from hospital.
Stable electrolytes and adequate renal function before discharge from hospital
Patient should follow up within 1 wk after discharge.
Ongoing Care
Underlying cause of rhabdomyolysis should be determined if etiology was not discovered
during hospital stay.
Genetic testing and muscle biopsies should be considered when warranted.
Medications, if implicated, should be stopped.
Metabolic-modifying supplements and enhancing agents should be stopped.
Activity modification if exercise-induced
No specific guidelines exist for return to exercise after exertional rhabdomyolysis.
Areas to consider:
Symptoms should be completely resolved.
All bloodwork and urine tests should be within normal limits.
Examination should demonstrate clinical resolution.
Patient should be able to demonstrate full strength.
Gradual return to exercise with acclimatization and adequate hydration
Return to exercise should begin with mild to moderate intensity.
Patient Monitoring
Initially, patient should be monitored clinically at regular short intervals.
For example, the physician may want to re-evaluate the athlete every 48 hr as intensity
increases.
Diet
Education should be provided about hydration.
Specific diet recommendations may be considered for specific myopathies.
Patient Education
Prevention strategies for return to sports after rhabdomyolysis:
Appropriate hydration counseling should be provided.
Gradual return to exercise may include acclimatization.
Return to exercise should begin with mild to moderate intensity.
Advise against significant dietary changes initially.
Athlete should be advised to stop activity if he or she experiences similar symptoms and
physician should be contacted immediately.
Complications
Early complications:
Hyperkalemia
Hypocalcemia
Cardiac arrhythmia
Cardiac arrest
Hepatic inflammation
Late complications (past 12 hr):
Acute life-threatening renal failure
References
1. Bagley WH, Yang H, Shah KH. Rhabdomyolysis. Intern Emerg Med. 2007.
2. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review:

Rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9:158–169.
3. Sauret JM, Marinides G, Wang GK. Rhabdomyo-lysis. Am Fam Physician.

2002;65:907–912.
Additional Reading
Miller, Marc L. Rhabdomyolysis. www.uptodate.com. April 30, 2009.
Codes
ICD9
728.88 Rhabdomyolysis
Clinical Pearls
Classic features: Myalgia, weakness, and dark urine
Aggressive fluid resuscitation is paramount to treatment.
Rheumatoid Arthritis in Sports
Kenneth Barnes
Shane Hudnall
Basics
Chronic systemic inflammatory autoimmune disorder that primarily affects the small joints
of the body causing a symmetric polyarthritis
Description
Polyarthritis most commonly affecting the joints of the wrist, the proximal interphalangeal
(PIP) and metacarpophalangeal (MCP) joints of the hands, and the metatarsophalangeal
(MTP) joints of the feet.
Less commonly affects cervical spine (though higher risk of atlantoaxial instability than
general population), ankles, knees, hips, elbows, and shoulders
Extraarticular manifestations: Anemia, rheumatoid nodules (20–30%), pleuritis, pericarditis,
entrapment neuropathies (carpal tunnel syndrome), episcleritis and scleritis (<1%),
splenomegaly, renal disease, interstitial lung fibrosis, pericarditis, interstitial lung disease,
vasculitis, Sjögren syndrome, Felty syndrome [rheumatoid arthritis (RA), splenomegaly,
neutropenia]
Epidemiology
Incidence
Annual incidence roughly 3/10,000
Prevalence overall 1%; varies from 0.1–5% based on ethnic background
Predominant gender: Female > Male (2–5:1; increases in patients >60 yrs).
Mean age of onset is 52 yrs.
Peak age of onset is between 35 and 70 yrs, although possible in all ages.
Risk Factors
Female gender (pregnancy and oral contraceptive use may be protective)
Nulliparity
Family history (identical twins 3–4× more likely to share disease than fraternal twins)
HLA-DR4 (also tend to have more severe disease)
Cigarette smoking
Silica or asbestos exposure
Electrical workers
Wood workers
Etiology
RA is characterized by the presence of pannus (a proliferative mass of inflammatory
vascularized tissue that may erode bone or cartilage).
Macrophages produce cytokines [eg, tissue necrosis factor α (TNF-α)], which produce many
of the systemic features [eg, fatigue, weight loss, elevated C-reactive protein (CRP) and
ESR, and joint damage].
Diagnosis
History
Clinical diagnosis: Usually symmetric synovitis (warmth, swelling, tenderness) of small joints
(MCPs, PIPs, MTPs, wrists) with morning stiffness >1 hr that improves with activity
Progression to joint destruction and deformities (ulnar deviation at MCPs, volar subluxation at
MCPs and wrists, swan-neck and/or boutonniere deformities of fingers)
Constitutional symptoms are very common (eg, low-grade fever, fatigue, myalgia, weight
loss).
American Rheumatism Association (ARA) criteria (must have 4 of 7): Morning stiffness,
symmetric arthritis, arthritis in 3+ joints, involvement of hand joints (all of these must have
occurred >6 wks), rheumatoid nodules, serum rheumatoid factor positive, and/or radiographic
changes
Note that 25% of patients have monarticular involvement at initial presentation.
Extraarticular manifestations (eg, chest pain, shortness of breath, skin changes, nodules, dry
eyes or mouth)
Physical Exam
Examine joints thoroughly for synovitis (warmth, swelling, tenderness, erythema).
Look for deformities (swan-neck, boutonnieres, ulnar deviation of digits/wrists, volar
subluxation at MCP or wrist).
Nail fold infarcts
Splinter hemorrhages
Rheumatoid nodules
Splenomegaly
Pericardial rub
Pleural effusions

Lab
Joint fluid exam most helpful: >10,000 WBCs with neutrophilic predominance characteristic
but nondiagnostic
Rheumatoid factor positive >80% of the time but is not sufficient for diagnosis or to rule out
diagnosis; if positive, more likely to have severe disease and extraarticular involvement than if
was negative
Antinuclear antibodies (ANAs) also not diagnostic
ESR and CRP not specific but may be elevated
CBC: Anemia: Hemoglobin generally >9; level correlates with disease severity, leukocytosis,
thrombocytosis.
Abnormal liver function tests: Low albumin: Directly linked to disease severity; elevated
alkaline phosphatase
Anticyclic citrullinated peptide (anti-CCP) antibodies: Sensitivity of 67%, specificity of 95% for
diagnosis of RA (1)
Imaging
X-rays: Erosions or bony decalcification in wrist or posteroanterior hand radiographs
Early: Obtain posteroanterior (PA) view of hands and wrists, anteroposterior (AP) view of
both feet so that you have comparison for later bony destruction.
CT scan, MRI, and US much more sensitive for detecting early signs of damage and
revealing erosions or edematous bony lesions. These studies may detect destruction earlier
even in patients with normal findings on radiography (2,3).
Systemic lupus erythematosus (SLE)
Osteoarthritis (typically involves distal interphalangeals, knees, hips)
Reactive arthritis
Lyme disease
Gout
Pseudogout
Hypothyroidism
Hypertrophic osteoarthropathy
Colitis
Treatment
Nonpharmacologic treatment: Patient education, relative rest, routine
exercise, physical and occupational therapy, dietary therapy
Pharmacologic treatment:
Combination therapy is preferred and has shown greater efficacy than
monotherapy.
Generally combine a nonbiologic DMARD with a biologic DMARD + burst of
corticosteroids (intraarticular if single or few joints involved) for active
disease, with continuation of DMARDs after flare is over (4).
Review specific side-effect profiles and monitoring parameters for the
medications that are chosen.
Medication
Analgesia: NSAIDs helpful in controlling pain and inflammation, improving daily
function, but they do not alter natural course of disease.
Consider COX-2 inhibitors in those who have GI side effects.
High-dose aspirin (12–16 tabs/day) or ibuprofen (2,400 mg/day)
DMARDs: Many of these agents inhibit progression of erosive disease; offer
to all patients as early as possible in disease course; divided into nonbiologic
and biologic agents (5).
Nonbiologic agents: P.
Methotrexate most commonly used nonbiologic agent and is generally
preferred; takes effect as early as 4 wks; not to take in pregnancy; monitor
for hematologic, hepatic, or pulmonary side effects (use folic acid
supplementation 1 mg daily with methotrexate) (6).
Methotrexate
Sulfasalazine
Hydroxychloroquine
Minocycline
Azathioprine
Gold
Biologic agents:
Effective at modifying disease and preventing erosions but increased risk of
infection
Tuberculosis skin test prior to initiation because can reactivate mycobacterial
infections
As general rule, do not combine biologic agents with one another.
Etanercept: Inhibits action of TNF-α; SQ injection 50 mg every week or 25
mg twice weekly
Infliximab: Antibody to TNF-α; periodic IV infusion
Other biologic agents include adalimumab, rituximab, anakinra, abatacept,
certolizumab, pegol, golimumab
Corticosteroids:
Oral, IV, and intra-articular forms
Prednisolone <7.5 mg/day is relatively safe; greater doses should be used
only for short periods of time.
Referral
Consider total joint replacement for severe disability or pain that is unresponsive
to medical therapy.
Ongoing Care
Patient Education
Exercise and increase in activity are associated with decreased level of pain, increased
function, and better outcomes in patients with RA (best data shown for whole-body low-
intensity group and individual exercise) (7).
Athletes with a history of cervical spine involvement need flexion/extension radiographs of C1
and C2 to assess risk of motion (atlantoaxial instability) and subsequent spinal cord injury.
Generally can play most sports, although contact sports and sports with a trampoline confer
much greater risk and may be discouraged.
Athletes with ocular involvement should be screened by ophthalmologist before being allowed
to play; may need eye protection.
If have systemic juvenile RA or HLA-B27-associated RA, must have cardiovascular
assessment.
Prognosis
Clinical course and severity highly variable, ranging from insidious onset, slowly progressive
disease with little destruction of joint spaces and few deformities (majority of cases), to a
rapidly progressive disease leading to severe bony destruction and deformities (roughly 10–
15%)
Poor prognostic factors:
Functional limitation
Extraarticular disease
Rheumatoid factor (RF) positivity or anti-CCP antibody positive
Bony erosions by x-ray
Cigarette smoking
Complications
50% increased risk of cardiovascular disease death in those with RA (8)
Increased risk of stroke (especially ischemic) with RA (9)
70% higher risk for developing infection (most likely related to immune
dysfunction) (10)
Increased likelihood to develop lymphoma; correlates directly with RA disease
severity (11)
References
1. Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic
accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for
rheumatoid arthritis. Ann Intern Med. 2007;146:797–808.
2. Ostergaard M, et al. New radiographic bone erosions in the wrists of

patients with rheumatoid arthritis are detectable with magnetic resonance
imaging a median of two years earlier. Arthritis Rheum. 2003;48:2128–2131.
3. Terslev L, et al. Doppler ultrasound and magnetic resonance imaging of

synovial inflammation of the hand in rheumatoid arthritis: a comparative study.
4. Goekoop-Ruiterman YP, et al. Clinical and radiographic outcomes for four

different treatment strategies in patients with early rheumatoid arthritis (the
BeSt study): a randomized, controlled trial. Arthritis Rheum. 2005;52:3381–
3390.
5. Saag KG, et al. American College of Rheumatology 2008
recommendations for the use of nonbiologic and biologic disease-modifying
antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum. 2008;59:762–
784.
6. Rantalaiho V, et al. The good initial response to therapy with a combination

of traditional disease-modifying antirheumatic drugs is sustained over time:
the eleven-year results of the Finnish rheumatoid arthritis combination therapy
trial. Arthritis Rheum. 2009;60:1222–1231.
7. Ottawa Panel. Ottawa Panel evidence-based clinical practice guidelines for

therapeutic exercises in the management of rheumatoid arthritis in adults.
Phys Ther. 2004;84:934–972.
8. Aviña-Zubieta JA, Choi HK, Sadatsafavi M, et al. Risk of cardiovascular

mortality in patients with rheumatoid arthritis: a meta-analysis of observational
studies. Arthritis Rheum. 2008;59:1690–1697.
9. Nadareishvili Z, Michaud K, Hallenbeck JM, et al. Cardiovascular,

rheumatologic, and pharmacologic predictors of stroke in patients with
rheumatoid arthritis: a nested, case-control study. Arthritis Rheum.
2008;59:1090–1096.
10. Doran MF, Crowson CS, Pond GR, et al. Frequency of infection in patients
with rheumatoid arthritis compared with controls: a population-based study.
11. Zintzaras E, Voulgarelis M, Moutsopoulos HM. The risk of lymphoma

development in autoimmune diseases: a meta-analysis. Arch Intern Med.
2005;165:2337–2344.
Additional Reading
Andreoli TE, Carpenter CCJ, Griggs RC, et al. Cecil essentials of medicine.
6th ed. 2004.
Baecklund E, Iliadou A, Askling J, et al. Association of chronic inflammation,

not its treatment, with increased lymphoma risk in rheumatoid arthritis. Arthritis
Rheum. 2006;54:692–701.
Braunwald E, Fauci AS, Kasper DL, et al. Harrison's principles of internal

medicine. 15th ed. 2001.
Solomon DH, Goodson NJ, Katz JN, et al. Patterns of cardiovascular risk In
rheumatoid arthritis. Ann Rheum Dis. 2006.
Van der Heijde DM. Overview of radiologic efficacy of new treatments.

Rheum Dis Clin North Am. 2004;30:285–293.
Codes
ICD9
714.0 Rheumatoid arthritis
714.30 Chronic or unspecified polyarticular juvenile rheumatoid arthritis
714.31 Acute polyarticular juvenile rheumatoid arthritis
Clinical Pearls
RA can go into remission; must have 5+ to qualify for >2 mos: <15 min morning
stiffness, no fatigue, no joint pain, no joint tenderness or pain with activity, no soft
tissue swelling, ESR <30 in women or <20 in men.
Rotator Cuff Tears
Kenneth M. Bielak
Benjamin D. England
Basics
Description
Partial or complete tears or disruption of any one or combination of the 4 rotator cuff muscles
of the glenohumeral joint
Supraspinatus and infraspinatus muscle-tendon complexes are the most common tears.
Rotator cuff muscles are the supraspinatus, infraspinatus, teres minor, and subscapularis
muscles.
Synonym(s): Tear of the supraspinatus; Tear of the infraspinatus; Tear of the teres minor;
Tear of the subscapularis muscle
Epidemiology
Rare in young athletes
More common in athletes >40 yrs of age, especially those with a history of many years of
repetitive overhead sports
More common than osteoarthritis (shoulder is the only joint where soft tissue often wears out
before joint)
Risk Factors
Over-40 “weekend warrior” with years of repetitive overhead use (eg, swimming, tennis,
volleyball, gymnastics, weight lifting, and throwing sports)
Previous trauma
Sports with potential fall risk, such as equestrian, skiing, and body surfing
Etiology
Can present following specific trauma (acute traumatic tear)
Usually degenerative (chronic impingement syndrome), especially in older athlete with
overarm sports
Diagnosis
History
Acute traumatic events such as a fall, direct blow, or forceful boxing punch
Traumatic hyperextension of abducted arm
Traumatic external or internal rotation of abducted arm
Anterior dislocation
Chronic overhead arm use may develop insidiously.
Nocturnal pain and pain on sleeping on the affected side are common.
Pain location can be variable (anterior, lateral, or posterior shoulder).
Pain may radiate to elbow.
Pain typically is aggravated with reaching motions: laterally, toward the back and/or
overhead.
Physical Exam
Diminished range of motion (ROM)
Pain with arm abduction, especially at 80–120 degrees of arc (1)[B]
Atrophy of cuff muscles, especially if chronic
Crepitus of supraspinatus muscle during abduction
Rotator cuff muscle weakness
Drop-arm test is positive for partial-thickness tear (14.3% sensitive, 88.4% specific) and full-
thickness tear (34.9% sensitive, 87.5% specific) (1)[B]:
Arm is passively abducted to 90 degrees.
Patient is instructed to slowly return the arm to the side.
Severe pain or inability to do so is positive test for a torn rotator cuff complex.
Empty-can test is positive for large or full-thickness tears (88% sensitive, 70% specific) (2)
[B]:
Resistance applied to arm abducted 90 degrees, angled 30 degrees anteriorly with a
medially rotated forearm (thumbs down, “empty can”)
Test is positive for inability to do so or severe pain, indicating a tear of the supraspinatus
tendon.
Test external rotation strength (partial tear 68.9% specific, 19.4% sensitive; full tear 84%
specific, 50.5% sensitive) (1)[B]:
Perform test with elbow flexed 90 degrees at the side.
Pinpoints infraspinatus and teres minor involvement.
Lift-off test for subscapularis is positive (3)[B]:
Inability to lift the dorsum of the hand off the back hip.
Modified lift-off test (cannot maintain lift-off position and springs back toward the back) is
more accurate (3)[B].
Significant pain with internal rotation can preclude an accurate test.
Poor scapular stability is often present.
Anterior glenoid-humeral laxity may be noted.
Comprehensive testing of active and passive ROM, strength testing, and adequate
neurovascular testing are recommended.

Imaging
Plain radiographs, although not specific for rotator cuff tears, may show some findings that
are suggestive:
Calcifications along the tendons of the rotator cuff muscle (repetitive/chronic injury)
Subacromial osteophytes (may predispose to tears)
Superior or anterior migration of the humeral head (indicates full-thickness tear) (4)[B]
MRI demonstrates an 80–97% sensitivity in detecting full-thickness rotator cuff tears. Partial
tears are more difficult to detect, with a sensitivity of 67–89%. This improves if fat
suppression is used (5)[B].
Double-contrast arthrotomography (DCAT) is 100% sensitive and 94% specific in diagnosing
complete rotator cuff tears. This study is much less sensitive for partial tears. The study is
more appropriate in patients with signs of instability rather than pain alone.
US is gaining attention as an imaging modality because it can be done relatively inexpensively
and can localize areas of tenderness and dysfunction with patient present and in dynamic
examination (technician-dependent) (6)[B].
Diagnostic injection: Subacromial bursa injection (10 mL of 1% lidocaine) may distinguish bursal
pathology and minor impingement from distinct tears of the rotator cuff (no pain relief or
strength improvement from the injection).
Rotator cuff strains
Glenoid labrum tear
Subluxation or unstable shoulder
Subacromial impingement
Isolated bicipital tendonitis
Acromioclavicular joint disorders
Glenohumeral arthritis
Rare subacromial abscess or tumors
Adhesive capsulitis
Cervical radiculopathy can radiate to the shoulder.
Treatment
Acute treatment
Analgesia:
NSAIDs are the drugs of choice initially (level II-2).
More potent analgesics may be necessary temporarily to relieve nocturnal
symptoms.
Immobilization: Sling may provide some relief for the acutely injured shoulder.
Prolonged rehabilitation emphasizing increased ROM and strengthening is
indicated for a partial tear.
Normalizing scapulothoracic stabilization and posterior capsular flexibility with a
1:1 strength ratio for rotator cuff to anterior/middle cuff deltoid muscles
For complete tears, surgery may be warranted in the young patient or active
athlete.
Early operative repair provides the best chance for functional recovery (level II-
3).
Ongoing Care
Acute full-thickness tears should be referred early on.
Partial tears after failed conservative therapy
Patient Education
Overhead athletes undergoing surgical repair may require 6 mos or longer before being able to
return to full active sports participation.
References
1. Park HB, Yokota A, Gill HS, et al. Diagnostic accuracy of clinical tests for the different
degrees of subacromial impingement syndrome. J Bone Joint Surg Am. 2005;87:1446–
1455.
2. Holtby R, Razmjou H. Validity of the supraspinatus test as a single clinical test in

diagnosing patients with rotator cuff pathology. J Orthop Sports Phys Ther. 2004;34:194–
200.
3. Hertel R, Ballmer FT, Lombert SM, et al. Lag signs in the diagnosis of rotator cuff
rupture. J Shoulder Elbow Surg. 1996;5:307–313.
4. Weiner DS, Macnab I. Superior migration of the humeral head. A radiological aid in the
diagnosis of tears of the rotator cuff. J Bone Joint Surg Br. 1970;52:524–527.
5. Burks RT, Crim J, Brown N, et al. A prospective randomized clinical trial comparing
arthroscopic single- and double-row rotator cuff repair: magnetic resonance imaging and
early clinical evaluation. Am J Sports Med. 2009.
6. Teefey SA, Middleton WD, Yamaguchi K. Shoulder sonography. State of the art. Radiol
Clin North Am. 1999;37:767–785, ix.
Additional Reading
Allen GM, Wilson DJ. Ultrasound of the shoulder. Eur J Ultrasound. 2001;14:3–9.
Bearcroft PW, Blanchard TK, Dixon AK, et al. An assessment of the effectiveness of
magnetic resonance imaging of the shoulder: literature review. Skeletal Radiol.
2000;29:673–679.
Breazeale NM, Craig EV. Partial-thickness rotator cuff tears. Pathogenesis and treatment.
Orthop Clin North Am. 1997;28:145–155.
Chang D, Mohana-Borges A, Borso M, et al. SLAP lesions: anatomy, clinical presentation,
MR imaging diagnosis and characterization. Eur J Radiol. 2008.
Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med.
2007;74:473–474, 477–478, 480–482 passim.
Farid N, Bruce D, Chung CB. Miscellaneous conditions of the shoulder: anatomical, clinical,
and pictorial review emphasizing potential pitfalls in imaging diagnosis. Eur J Radiol. 2008.
Firestein: Kelley's Textbook of Rheumatology, 8th ed. 2008: W. B. Saunders Company
Fritz RC, Stoller DW. MR imaging of the rotator cuff. Magn Reson Imaging Clin N Am.
1997;5:735–754.
Howard TM, O'Connor FG. The injured shoulder. Primary care assessment. Arch Fam Med.
1997;6:376–384.
Hulstyn MJ, Fadale PD. Shoulder injuries in the athlete. Clin Sports Med. 1997;16:663–679.
Jost B, Zumstein M, Pfirrmann CW, et al. MRI findings in throwing shoulders: abnormalities
in professional handball players. Clin Orthop Relat Res. 2005;130–137.
Meister K. Injuries to the shoulder in the throwing athlete. Part two: evaluation/treatment.
Am J Sports Med. 2000;28:587–601.
Opsha O, Malik A, Baltazar R, et al. MRI of the rotator cuff and internal derangement. Eur J
Radiol. 2008.
Stetson WB, Phillips T, Deutsch A. The use of magnetic resonance arthrography to detect
partial-thickness rotator cuff tears. J Bone Joint Surg Am. 2005;87(Suppl 2):81–88.
Teefey SA, Rubin DA, Middleton WD, et al. Detection and quantification of rotator cuff
tears. Comparison of ultrasonographic, magnetic resonance imaging, and arthroscopic
findings in seventy-one consecutive cases. J Bone Joint Surg Am. 2004;86-A:708–716.
Toyoda H, Ito Y, Tomo H, et al. Evaluation of rotator cuff tears with magnetic resonance
arthrography. Clin Orthop Relat Res. 2005;439:109–115.
Codes
ICD9
726.10 Disorders of bursae and tendons in shoulder region, unspecified
726.11 Calcifying tendinitis of shoulder
726.19 Other specified disorders of bursae and tendons in shoulder region
Clinical Pearls
Surgery is an option, especially for the young and/or active athlete, and should
be considered early on for diagnosis of complete tears of the rotator cuff.
Rehabilitation of a partial tear of the rotator cuff is a prolonged process that
may take months to return to preinjury status.
Scapholunate Dissociation
Keith A. Anderson
Robert L. Jones
Basics
Description
Complete tear of the scapholunate interosseous ligament (SLIL) with an additional tear of 1 or
more secondary ligament restraints
Epidemiology
Most common ligamentous instability in the wrist
More precise epidemiologic data are lacking.
Risk Factors
Active individuals who have ulnar-negative variance; shorter distal ulna compared with the
radius on a neutral anteroposterior (AP) radiograph of the wrist (1)
Etiology
Often a fall on an outstretched hand, with hyperextension and ulnar deviation
Axial compression can force the capitate between the scaphoid and lunate.
May result from minor repetitive trauma (2)
Repetitive motion after an isolated SLIL injury may produce attritional changes in the
secondary stabilizers, leading to their eventual failure, thus completing the scapholunate
dissociation (3).
Diagnosis
Early diagnosis offers the best chance for successful surgical outcome.
There are different levels of instability, which can be classified by increasing severity of wrist
instability (4):
Occult instability: Isolated tear or attenuation of a portion of the SLIL. There is no
radiologic evidence, and wrist pain is with mechanical loading.
Dynamic scaphoid instability: Subtotal or complete tear of the SLIL, including the dorsal
portion, with a partial extrinsic ligament injury. May have normal static radiographs, but
instability will be apparent on stress radiographs.
Scapholunate dissociation: Involves a complete tear of the SLIL with additional tear of 1 or
more secondary ligaments. The scaphoid usually rotates into flexion, and the lunate rotates
into extension. This is apparent on plain static radiographs.
Dorsal intercalated segment instability (DISI): Term used to describe the shifted positions
of the bones of the carpus due to lack of association between the lunate and scaphoid.
Abnormalities include flexion of the scaphoid, extension of the lunate and triquetrum, and
dorsal and proximal translation of the capitate and distal carpal row. Apparent on lateral
static radiograph.
Scapholunate advanced collapse (SLAC): End stage of the spectrum of instability. There is
predictable and progressive degeneration and arthritis of the carpus due to the irreversible
postural changes of the scaphoid, capitate, and lunate.
History
Need to establish the timing of the injury (2):
Acute <4 wks
Subacute 4 wks to 6 mos
Chronic >6 mos
Patient may report a fall or sudden load applied to the wrist, but may not recall any specific
fall or injury.
May report pain or weakness with hyperextension loading of the wrist
Often will not seek immediate care because initial injury seems too trivial (3)
Subacutely, there may be symptoms of painful popping or clicking with activities, or
decreased grip strength
Later on, limited motion may be a complaint (1,4).
Physical Exam
In the acute setting, pain may be poorly localized about the periscaphoid area and preclude
most provocative wrist ligament testing. Swelling may be diffuse or localized to the
scapholunate region (4)[C].
In the subacute setting, there is usually well-localized tenderness about the scaphoid and
dorsal scapholunate interval distal to Lister's tubercle.
The patient may have weakness of grip and pinch strength (2).
Watson scaphoid shift test should be performed:
Patient places wrist in ulnar deviation, and the physician puts dorsal pressure on the
scaphoid tubercle with the thumb. The physician then radially deviates the patient's wrist.
Relief of thumb pressure will allow the scaphoid to reduce, often with an audible or
palpable clunk. Pain with a clunk may represent scapholunate instability.
Imaging
Imaging should be obtained in individuals with appropriate history and positive scaphoid shift
test.
Radiographs of the opposite wrist should always be obtained (2,5)[C].
Initial views should include AP, lateral
Initial radiographs may appear normal, so stress radiographs should be obtained when
carpal instability is suspected but static radiographs are normal.
Normal static and stress films in the acute situation do not always rule out serious injury (4)
[C].
Key findings on the lateral film (wrist in neutral):
Scapholunate angle >70° is considered highly suggestive of diagnosis (normal 30–60°)
(2,3,4)[C]
Radiolunate angle exceeding 15° indicates DISI (3,4)[C].
Key findings on the AP film:
Increased scapholunate joint space (>2 mm, increased compared to contralateral),
referred to as scapholunate diastasis or the “Terry Thomas sign” (3)[C]
Scaphoid ring sign: Distal scaphoid tubercle is superimposed on the scaphoid waist when
scaphoid is flexed more than 70°
AP grip (clenched fist) view is the most frequent stress view. It profiles the scapholunate joint
and demonstrates pathologic scapholunate widening (>2 mm) under axial loaded conditions
(4)[C]. Additional stress view could include AP in ulnar deviation (2).
CT arthrography has been reported as having a 95% sensitivity and 86% specificity for
detecting SLIL tears when compared with arthroscopy (4)[B].
MRI with average of 71% sensitivity and 88% specificity in detecting scapholunate tears, but
high variability between individuals. Many authors conclude that MRI is not reliable for
diagnosing SLIL injury (1,3,4)[B].
Arthrography and MRI are anatomic and not functional evaluations.
Simple fluoroscopy is a helpful functional ancillary study (2,4)[C].
Wrist arthroscopy is the gold standard for diagnosis.
Differential diagnosis (2,3):
Scaphoid or other carpal fracture
Radial styloid or distal radius fracture
Synovitis
Radioscaphoid impingement
Occult ganglion
Lunotriquetral instability
Triangular fibrocartilage complex tear
Osteoarthritis or rheumatoid arthritis
Kienböck's disease
Treatment
Treatment must be predicated by the patient's symptoms and clinical exam,
not imaging.
The treatment is most often surgical, so do not delay referral.
Proper treatment may be challenging due to delay in recognition (3).
ED Treatment
Stabilize with a thumb spica splint (5).
Medication
NSAIDs or Tylenol for pain
There has been some success with casting, splinting, NSAIDs, and therapy
without surgical intervention for dynamic instability (4)[C]. This would include a
short arm cast for 2–6 wks, followed by removable splint for active range of
motion (ROM) exercises and gentle strengthening across the wrist (2)[C].
For acutely injured scapholunate joint, some will use closed reduction and K-
wire fixation.
There has also been some success with external reduction of the scaphoid
followed by immobilization of the wrist in plaster, but most consider this
unreliable for reduction (3)[C].
In general, in wrists without fixed bony deformity, attempts should be made to
restore the bony relationships with soft tissue augmentation; in wrists with fixed
deformity, salvage procedures are needed to alleviate pain (3).
There are many opinions as to the specifics of surgical intervention, but in
general, the procedures performed are dictated based on the severity
classification of the wrist instability:
Occult instability:
There has been some success with arthroscopic debridement with or
without pinning, but usually this is treated with conservative measures (4).
There is also some new evidence for electrocautery for electrothermal
collagen shrinkage following arthroscopic debridement (3)[C].
Dynamic instability and scapholunate dissociation with a repairable SLIL:
Treatment of choice is open reduction with scapholunate repair and a
dorsal capsulodesis. Delayed repair is somewhat controversial, but there
has been reported success 8 wks after injury if the SLIL is adequate for
repair (1,4)[C].
Scapholunate dissociation without repairable SLIL:
In subacute or chronic injuries, the goal is to reestablish the critical
scapholunate linkage.
DISI:
A salvage procedure is performed to restore alignment, improve load
distribution, and attempt to slow degenerative changes.
SLAC:
Salvage procedures appear to be the only option, such as excision of
scaphoid, capitate-lunate-hamate-triquetral arthrodesis, or carpectomy (4)
[C].
Ongoing Care
Following repair, immobilize wrist for 8 wks then slow rehabilitation program
No return to competitive sports for 4–6 mos postoperatively (1)[C]
Avoid power gripping and weight-bearing exercises of the upper extremity.
Gentle putty or sponge gripping can help improve grasp.
Physical therapy should be performed within pain tolerance (2).
Decisions about return to play must be individualized based on sport-specific demands.
In general, an athlete may return after demonstrating progression in strength and ROM in a
supervised rehabilitation program.
Complications
Arthritis of the wrist, which can be chronic and debilitating
Inherent complications of surgery
References
1. Cohen MS. Ligamentous injuries of the wrist in the athlete. Clin Sports
Med. 1998;17:533–552.
2. Lewis DM, Osterman AL. Scapholunate instability in athletes. Clin Sports

Med. 2001;20:131–140, ix.
3. Manuel J, Moran SL. The diagnosis and treatment of scapholunate

instability. Orthop Clin North Am. 2007;38:261–277.
4. Kuo CE, Wolfe SW. Scapholunate instability: current concepts in diagnosis

and management. J Hand Surg [Am]. 2008;33:998–1013.
5. Daniels JM, Zook EG, Lynch JM. Hand and wrist injuries: Part I.
Nonemergent evaluation. Am Fam Physician. 2004;69:1941–1948.
Codes
ICD9
842.09 Other wrist sprain
Clinical Pearls
Most common ligamentous instability in the wrist
Normal static and stress films in the acute situation do not always rule out
serious injury.
Radiographs of the opposite wrist should always be obtained.
Terry Thomas sign: Gap >2 mm between scaphoid and lunate on AP, indicative
of scapholunate dissociation
Most often needs surgical intervention
Sciatica
Kathleen Weber
Basics
Sciatica is referred to in the medical literature as lumbosacral radicular syndrome,
radiculopathy, or nerve root pain.
Sciatica pain radiates from the lower back into the leg. It usually radiates below the knee into
the foot in a dermatomal pattern corresponding to the affected nerve root.
Description
Radicular pain in the distribution of a sciatic nerve root (L4, L5, S1, S2, or S3), usually
producing symptoms along the posterior or lateral aspect of the lower extremity and extending
to the ankle or foot
Epidemiology
Lower back pain (LBP) is extremely common in the general population and the athletic
population (eg, football, gymnastics, tennis).
General population: 5% annual occurrence; 60–90% lifetime incidence (1):
Men and women equally affected
Common reason to visit primary care physician
Leading cause of job-related disability in the U.S.
Sciatica:
Sciatica is a common cause of pain and disability.
Prevalence rates reported in different studies and reviews vary considerably, ranging from
1.2–43% (1).
Peaks in the 4th to 5th decades of life
Risk Factors
Occupations or activities that require repetitive lifting or movement in the forward bent-and-
twisted position
Etiology
The usual etiology of sciatica pain is the result of direct mechanical compression to the affected
nerve root and in part from chemical irritation of the nerve root by chemical substances resulting
from the herniated nucleus pulposus.
Urinary retention
Motor loss
Intractable pain
Diagnosis
History
Determine any red flags: Warning signs to increase your clinical suspicion as cited by the
Agency for Health Care Policy and Research:
Age <20 yrs or >50 yrs
History or signs and symptoms of infection or malignancy
Unexplained weight loss
Immunosuppression
Severe or atypical pain
Trauma
Fracture
IV drug use
Abdominal pain
Significant neurologic deficit
Bowel/bladder dysfunction
Saddle anesthesia
Evaluate and manage any positive red flags.
Determine any constitutional signs.
Mechanism of injury or inciting incident
Length of symptoms
Is the pain worsened by Valsalva maneuver, coughing, sneezing?
Is the pain unilateral or bilateral?
Does the pain radiate below the knee? Into the foot or toes?
Psychosocial issues that may add to symptoms and prolong pain
Physical Exam
Signs and symptoms:
Sharp or “electrical” pain radiating along the sciatic nerve dermatomal distribution (most
commonly L4, L5, and S1), usually to the ankle or foot
Often associated with dermatomal sensory disturbances, motor weakness, and hypoactive
deep tendon reflexes
Onset of pain is variable because it can be immediate or within a few hours or days of the
inciting event.
May complain of radicular symptoms and not localized back pain
95% involve the L5 (most common) or S1 nerve root.
Aggravating factors are trunk flexion or rotation, prolonged sitting or standing, coughing,
sneezing, or straining during defecation.
Muscle atrophy reflects long-standing condition.
Detailed neurologic (motor, sensory, and reflexes) and vascular examination includes rectal
tone and anal sensation.
Criterion for abnormal findings is reproduction of pain in radicular distribution rather than
reproducing lower back pain.
Straight-leg raise (SLR) of involved leg: Performed in supine position; reproduces sciatic-
type pain between 30 and 60 degrees
Crossed SLR: Raising the contralateral leg results in reproduction of pain on the affected
side and is specific for a herniated disk.
Sitting knee extension: Performed while patient is sitting; passive extension of the knee
reproduces pain (modification of SLR).
Ankle dorsiflexion or chin to the chest: Performed either with SLR or crossed SLR;
exacerbates the pain
Test specific nerves.
Sensory loss:
L4: Anteromedial leg, medial malleolus
L5: Lateral lower leg, web space between the great and 2nd toes
S1: Back of lower leg, lateral aspect of foot, little toe
Motor weakness:
L4: Knee extension (quads)
L5: Extensor hallucis longus (great toe)
S1: Foot plantar flexion (toe raises)
Reflex (hypoactive):
L4: Patellar
L5: None
S1: Achilles tendon

Imaging
Anteroposterior and lateral radiographs of lumbar sacral spine usually are not indicated
unless
Red flags are present (see “History”).
Unresolved back pain for 6 wks
Back pain with constitutional symptoms and history of IV drug abuse, cancer, or diabetes
MRI (preferred study) or CT scan (used primarily when MRI is contraindicated, ie, hardware,
pacemaker) or CT myelography:
Suspected cauda equina syndrome
Abscess
Neoplasm
6 wks of failed conservative therapy for sciatica or intractable pain
MRI is typically not necessary unless there is intractable pain or neurologic deficits.
CT scan is the study of choice for identifying bony vertebral injuries.
Abdominal US or CT scan to evaluate for abdominal aortic aneurysm
Extrinsic nerve compression, eg, from wallet or prolonged cycling
Facet arthropathy
Pathologic, traumatic, or osteoporotic compression fracture
Herniation of the nucleus pulposus
Infection, eg, osteomyelitis, epidural abscess
Neoplasm, primary or metastatic
Osteoarthritis
Paget disease
Piriformis syndrome
Sacroiliitis
Spinal stenosis
Spondylolisthesis
Synovial cyst
Trauma, eg, hematoma, musculoligamentous strain, fracture
Nonspinal causes, eg, abdominal aortic aneurysm, herpes zoster, hip arthritis or bursitis,
iliotibial band syndrome, psychogenic, vascular claudication
Treatment
NSAIDs, acetaminophen (2)[B]
Acute LBP: Avoid inactivity; sciatica: Activity level not found to make a
difference (3)[B]
6 wks of conservative management should be tried before obtaining imaging or
invasive procedures unless red flags are present or develop (4)[A].
Physical therapy may provide benefit in subacute and chronic LBP; studies are
inadequate to draw definitive recommendations (5)[B].
Epidural steroid injections may provide short-term improvement in pain but do
not affect long-term outcomes (6)[A].
Patients with lumbar disk herniations that are not responding to conservative
management should be considered for diskectomy (4,7)[A].
Surgery referral for any suspicion of cord compression, bilateral sciatica,
significant or progressive neurologic deficit, or disabling sciatica (7)[A]
In the absence of severe intractable pain, neurologic deficits, and/or severe
disease, surgery should be avoided.
Physical therapy directed toward restoring motor or strength deficits (5).
For the best physical therapy outcomes, both aerobic conditioning and core
strengthening are essential.
Alternative therapies such as acupuncture, traction, and/or manipulative therapy
have not been proven effective in randomized, controlled trials (Cochrane
reviews).
Ongoing Care
Patient Education
Weight loss is beneficial in overweight and obese individuals.
Avoid opioids.
Stop smoking.
Prognosis
Acute pain is almost always self-limited.
Estimated recovery time: 90% within 4–6 wks (4)
References
1. Konstantinou K, Dunn KM. Sciatica: review of epidemiological studies and prevalence
estimates. Spine. 2008;33:2464–2472.
2. Roelofs PD, Deyo RA, Koes BW, et al. Nonsteroidal anti-inflammatory drugs for low back
pain: an updated cochrane review. Spine. 2008;33:1766–1774.
3. Hagen KB, Jamtvedt G, Hilde G, et al. The updated cochrane review of bed rest for low
back pain and sciatica. Spine. 2005;30:542–546.
4. Gibson JNA, Waddell G. Surgical interventions for lumbar disc prolapse. Cochrane
Database of Systematic Reviews. 2007;2:CD001350.
DOI:10.1002/14651858.CD001350.pub4.
5. Hayden J, van Tulder MW, Malmivaara A, et al. Exercise therapy for treatment of non-
specific low back pain. Cochrane Database of Systematic Reviews. 2005;3:CD000335.
DOI:10.1002/14651858.CD000335.pub2.
6. 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;34:1078–1093.
7. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical versus nonoperative treatment for
lumbar disc herniation: four-year results for the Spine Patient Outcomes Research Trial
(SPORT). Spine. 2008;33:2789–2800.
Additional Reading
Caragee EJ. Persistant lower back pain. NEJM. 2005;352:1891–1898.
Codes
ICD9
724.3 Sciatica
Scoliosis
Cherise Russo
Basics
Not a diagnosis but a description of a structural change in anatomy
Description
Lateral curvature of the spine measuring 10° of curvature by Cobb angle, usually
accompanied by rotation
3 categories:
Neuromuscular scoliosis develops in patients with neurologic or musculoskeletal
abnormalities and may be structural or nonstructural.
Congenital scoliosis is usually evident before adolescence and is a result of congenital
asymmetry in the vertebrae.
Idiopathic scoliosis is a diagnosis of exclusion; infantile (0–3 yrs) and juvenile (4–9 yrs) are
considered early-onset, and children 10 yrs and older are considered to have adolescent
idiopathic scoliosis (AIS):
AIS is the most common type of idiopathic scoliosis (80–85%).
Epidemiology
Generally considered 1.9–3% for curves exceeding 10°
Only 10% of adolescents with AIS require treatment: 0.3% of the population.
Males and females affected equally, but the risk of curve progression is 10 times higher in
females.
Prevalence
Cobb angle 10–19°: 2–3%
Cobb angle 20–29°: 0.3–0.5%
Cobb angle 30–39°: 0.1–0.3%
Cobb angle >40° is ≤0.1%
Risk Factors
Etiology of AIS is unclear at this time.
Believed to be multifactorial
Genetics have been proposed to play a role.
Other proposed factors: Growth hormone secretion, connective tissue structure, paraspinal
musculature, vestibular function, melatonin secretion, platelet microstructure
Genetics
2 studies show a higher concordance rate in the incidence of scoliosis in monozygotic twins
vs dizygotic twins.
Chromosomes 17 and 19 have been identified as having genetic loci for AIS.
Inheritance pattern is not known.
Expression of familial AIS may be linked to the X chromosome, with a dominant inheritance
pattern.
General Prevention
No prevention recommendations exist at this time.
Benefit of preclinical detection not proven at this time
U.S. Preventive Services Task Force recommends against the routine screening of
asymptomatic adolescents for idiopathic scoliosis (1)[D].
Etiology
Lateral curvature of the spine with rotation
By definition, causes are unknown; listed are some theories, none proven in isolation.
Genetic:
Positive familial history for scoliosis in 30% (not predictive for severity)
Connective tissue disorder:
Platelet calmodulin levels may be predictive of curve progression.
Neurological (equilibrium system):
Most widely supported theory
Abnormalities noted in vestibular, ocular, proprioceptive, and vibratory functions.
Hormonal:
Lower levels of melatonin secreted from pineal body in those with AIS.
Growth-stimulating hormone: More of an influential factor than etiologic factor studies
Diagnosis
Neuromuscular scoliosis:
Occurs in patients with neurologic or musculoskeletal conditions
May be seen with cerebral palsy, myelomeningocele, muscular dystrophy, or leg length
discrepancy
Congenital scoliosis:
Occurs from vertebral asymmetry secondary to congenital abnormalities
Hemivertebrae, wedge vertebrae, failure of segmentation
Usually manifests before adolescence
Idiopathic scoliosis:
No definite etiology
Age 0–3 yrs: Infantile
Age 4–9 yrs: Juvenile
Age ≥10 yrs: Adolescent
Criteria for AIS:
Age ≥10 yrs
Curvature of spine in coronal plane that has a Cobb angle of ≥10°
Exclusion of neuromuscular and congenital causes
Pre Hospital
Identify underlying etiologies
Assessment of the curve clinically
Determine need for radiographs
Determine risk of progression
History
Consider:
Onset: Consider when 1st noted, by whom, rate of worsening, previous treatment,
associated signs or symptoms, familial history, etc.
Rate of progression: Rapid progression is suggestive of a nonidiopathic cause.
Pain: Patients with idiopathic scoliosis should not have pain.
Night pain: If pain, consider tumor such as osteoid osteoma or other tumor
Are there symptoms suggestive of neuromuscular etiology? Bowel or bladder problems?
Muscle weakness? Headache? Neck pain?
Neurologic symptoms increase likelihood of nonidiopathic causes.
Does the patient have difficulty breathing?
Severe thoracic scoliosis may affect respiratory function.
Has the pubertal growth spurt started?
Important for determining remaining linear growth and need for intervention
Has the patient entered puberty?
Tanner grade 2 precedes the onset of pubertal growth spurt in boys. Tanner 2 follows the
onset of pubertal growth spurt in girls.
Has menarche occurred?
Pubertal growth spurt occurs just before menarche.
Is there a history of lower limb fracture, joint infection, or arthritis?
This may result in a leg length discrepancy.
Is there a family history of scoliosis?
A family history may suggest AIS.
Other signs or symptoms?
Review of systems (especially neurological)
Physical Exam
Plot height and weight on growth curve.
Spine inspection, head should be balanced in line over the center of the sacrum
Assess Tanner stage (risk for progression is greatest during the pubertal spurt)
General inspection to look for skin changes such as:
Café au lait, pigmentation, or other signs of neurofibromatosis, for example, dysraphic
signs (hairy patches, etc.)
Assess for maturity, hyperelasticity, contracture, congenital anomalies.
Assess for deformity, symmetry of spine, symmetry of iliac crests, shoulders and trunk,
including decompensation, abnormalities of thoracic kyphosis, or cervical or lumbar lordosis.
The Adam forward bending test is used to look for rib or paraspinous elevations,
demonstrates rotational component
Assess for leg length discrepancy, congenital anomalies, and neurological abnormalities
(including abdominal reflex).
Findings:
Crankshaft phenomenon: Progression of curve size and rotation following posterior spinal
fusion due to continued anterior spinal growth
Patient is Risser 0, open triradiate cartilages, <10 yrs old, and is prior to the occurrence of
peak height velocity (the time of maximum spinal growth).
Consider anterior fusion in addition to posterior fusion.
Physical examination tools:

Scoliometer: To measure trunk rotation, an angle of 7° generally corresponds to Cobb
angle of 20°.
Important note: Not all patients with radiographic scoliosis have trunk rotation.
Abnormal abdominal reflex: May suggest intraspinal pathology, including syrinx

Lab
Usually not helpful unless to rule out associated metabolic conditions
Pulmonary function testing is useful preoperatively.
Imaging
Plain standing full-length PA and lateral scoliosis films on a long 3-foot x-ray cassette (2)[B].
Direction of curve labeled by convexity (left thoracic curves have been associated with
nonidiopathic causes)
Location is identified by vertebra that is most deviated and rotated from midline.
Cobb angle, formed by the intersection of a line parallel to the superior end plate of the most
cephalad vertebra that has the greatest tilt with the line parallel to the inferior endplate of the
most caudad vertebra of the curve. Not proportionate to the severity.
Curve patterns are classified according to the King-Moe and Lenke classification systems.
Risser sign is a visual grading of the degree of ossification and fusion of the iliac apophysis
(lower Risser grade indicates more growth remaining).
MRI is not routinely necessary, but indicated in patients with neurologic symptoms, early age
of onset with rapid progression, and for abnormalities found on plain radiographs.
Renal US or IV pyelogram are for evaluation of patient with congenital scoliosis.
Scoliosis: Neuromuscular, congenital, idiopathic
Postural abnormalities
Leg length discrepancy
Pain that results in splinting
Treatment
Concepts for treatment are based on the severity of the deformity present
and on the likelihood of progression:
Risk for progression:
Gender: Females have a 3–10-fold increased risk for progression.
Curve magnitude: Initial Cobb angles of 20–29° are more likely to increase
by at least 5°.
Curve pattern: Double and thoracic curves have a 3-fold increased risk of
progression.
Maturity (remaining growth potential): For example, the lower the Risser sign,
the greater the risk for progression
Options for treatment include observation, bracing, and surgery.
Guidelines for management (3)[B]:
Patients with trunk rotation <7° are followed every 6 mos and standing full-
length PA views are repeated if trunk rotation increases.
Cobb angles <20° may be observed every 6–8 mos; younger children and
patients with curves closer to 20° should be followed more frequently.
Risser sign 0–2 with Cobb 20–29° should be followed closely and brace if
angle increases by 5° or more over 3–6 mos.
Risser sign 0–2 with Cobb angles of 30–40° should be braced.
Risser sign 0–2 with Cobb angles between 40° and 50° may be braced or
considered for surgery.
Risser sign 0–2 with Cobb angle >50° at time of diagnosis typically require
surgical evaluation and intervention.
Risser sign ≥3 should be followed for at least 1 yr past skeletal maturity with
radiographs every 6–9 mos.
Skeletally mature with Cobb angles <40° can be reassured and discharged
Skeletally mature with Cobb angles between 40° and 50° are managed on an
individual basis
Medication
Postoperative continuous epidural infusion helpful for pain control
General Measures
Bracing recommendation:
Does not correct curve, but may prevent further progression
Only indicated for skeletally immature
Indicated if patient has a Risser sign of 0–2 and Cobb angle of 30–40° at time
of diagnosis
Indicated if patient has Risser sign of 0–2 and has progression of 5° or more
over 6–8-mo period of observation
No need for bracing if skeletally mature or Cobb angle ≥50°
Thoraco-lumbar-sacral orthosis underarm brace is useful for most curves.
Cervico-thoraco-lumbar-sacral orthosis (Milwaukee brace) indicated for
curves with apex above T8 and double thoracic curves
Braces should be worn for 23 hr/day until the end of growth.
After discontinuation of brace, monitor patient every 6–8 mos.
Referral
Trunk rotation angle >7° and inability to assess Cobb angle
Cobb angle between 20° and 29° in premenarchal girls and boys 12–14 yrs of
age
Cobb angle >30°
Progression of Cobb angle <5°
Surgical referral for skeletally immature patients with curves ≥50°
Posterior spinal fusion (PSF) with instrumentation and bone grafting
Current implants are segmental as opposed to older Harrington rods.
Segmental instrumentation affords the surgeon a better option for positioning.
Thorascopic procedures utilized for restrictive anterior soft tissue barriers
Anterior spinal fusion and PSF is needed at times to prevent the anterior spine
from continuing to grow after the PSF (crankshaft phenomenon).
Bony fusion is paramount; pseudoarthrosis or failure to fuse is a complication
of surgery.
Sports restriction for 9–12 mos following surgery, and contact sport clearance
should be assessed by surgeon.
Ongoing Care
Follow-up 2 yrs after onset of skeletal maturity.
Skeletally mature patients do not need routine follow-up if Cobb angle >40°; beyond 40°
should be individualized.
Back pain associated with idiopathic scoliosis
Pain in 23% at time of initial evaluation (additional 9% during follow-up)
Of those with back pain, only 9% found to have identifiable cause, such as spondylolysis,
Scheuermann, syrinx, disc herniation, tumor, tether cord
Increased suicidal thoughts and self-image concerns among patients; address on individual
basis
Pregnancy does not impact curve progression, nor does curve progression affect pregnancy
outcome.
Prognosis
Risk of curve progression is related to patient's maturity (Risser sign, menarcheal status) and
to the size of the curve.
Curves l <20–25° have a low risk of progression, even if patient is Risser 0 or Risser I.
Curves 25–45° have higher risk of progression, particularly in the immature.
Curves >45–50° have much higher risk of progression, regardless of maturity.
Overall, good prognosis for the majority of patients
Complications
Reduced pulmonary function for patients with thoracic curves >60°
Progression of lumbar curves >50° in adult life with degenerative disc disease
and pain
Psychosocial factors
No increased mortality rates compared with general population
References
1. U.S. Preventative Task Force. Screening for idiopathic scoliosis in
adolescents: recommen-dation statement. Am Fam Physician. 2005;71:
1975–1976.
2. Scherl SA. Clinical features; evaluation; and diagnosis of adolescent
idiopathic scoliosis. www.uptodate.com. May 21, 2009.
3. Scheral SA. Treatment and prognosis of adolescent idiopathic scoliosis.

www.uptodate.com. June 9, 2009.
Additional Reading
Greiner KA. Adolescent idiopathic scoliosis: radiologic decision-making. Am
Fam Physician. 2002;65:1817–1822.
Reamy BV, Slakey JB. Adolescent idiopathic scoliosis: review and current
concepts. Am Fam Physician. 2001;64:111–116.
Weinstein SL. Adolescent idiopathic scoliosis: prevalence and natural history.

Instr Course Lect. 1989;38:115.
Codes
ICD9
737.30 Scoliosis (and kyphoscoliosis), idiopathic
737.31 Resolving infantile idiopathic scoliosis
737.32 Progressive infantile idiopathic scoliosis
Clinical Pearls
If any of the signs mentioned are seen in conjunction with significant back pain,
an x-ray or referral is indicated. The scoliometer is also a useful tool in
screening patients.
Scoliosis associated with osteoid osteoma is the suggested diagnosis for
children who present with scoliosis and back pain that occurs especially at night
and is relieved with aspirin.
SCUBA Diving Injuries: DCS and AGE
Paul B. McKee
Basics
Description
Decompression sickness (DCS): Formation of nitrogen gas bubbles in the blood and body
tissues caused by inadequate elimination of the nitrogen gas. As a diver descends and
breathes air, the tissues can become saturated with nitrogen due to the increased pressure.
As the diver ascends, the excess nitrogen must be eliminated. If the nitrogen is not
eliminated, it can become trapped in the tissue, thus resulting in the symptoms of DCS. The
term DCS is used in a general sense to denote all forms of injury due to bubble formation
occurring as a consequence of a sudden reduction in ambient pressure.
Type I DCS is characterized by musculoskeletal pain (vague, intense pain), dermal
complications (pruritus, rash, blebs), and constitutional symptoms (fatigue, malaise,
anorexia). Extreme fatigue may be a sign or forerunner of a more severe decompression
illness.
Type II DCS is characterized by neurologic symptoms (paresthesias, weakness, poor
sphincter control, paralysis), cardiorespiratory symptoms (dyspnea, nonproductive cough,
hemoptysis), and vestibular symptoms (tinnitus, dizziness, hearing loss) (1)[C].
Arterial gas embolism (AGE): A CNS injury (usually cerebral) or systemic injury (usually
cardiac) as a consequence of pulmonary barotrauma. Barotrauma refers to injury produced
by mechanical forces caused by a change of pressure in a gas-filled space (the lungs). Air
released from an overpressurized alveolus enters the pulmonary circulation and causes
occlusion of the organ's blood supply. Venous gas emboli reach the arterial circulation
paradoxically via a patent foramen ovale or a right to left shunt (2,3,4)[C]. AGE can be
confused with type II DCS.
It is sometimes difficult to tell the difference between type II DCS and AGE, because both
can cause similar symptoms. The time of onset of symptoms may be more informative. The
time course of air embolism symptoms from lung overexpansion is usually short (immediately
or within minutes after surfacing), whereas decompression sickness usually develops later
after a dive (hours to days).
Some clinicians advocate grouping type II DCS and AGE into 1 clinical entity called
decompression illness (DCI). The 2 are treated the same (recompression).
Synonym(s): The bends; Air embolism; Caisson disease; Decompression illness
Epidemiology
DCI is estimated to occur in 4 in 100,000 sport divers per year (Divers Alert Network
statistics).
Predominant age is young adulthood (20–29 yrs).
Predominant sex is male; however, there is no evidence to suggest that men are more
susceptible (5)[C].
Risk Factors
Rapid ascent from SCUBA diving
Flying too soon after SCUBA diving
Inexperienced divers (6)[C]
Multiple/repetitive dives
Tunnel work (Caisson disease)
Inadequate pressurization/denitrogenation when flying
Prolonged dive at depth of >33 ft
Taking a warm shower after diving
Obesity (nitrogen is lipid-soluble)
Fatigue
Dehydration
Poor physical conditioning
Acute illnesses (pulmonary or GI)
Breath-hold diving
Holding breath while ascending
Patent foramen ovale
Intracardiac septal defects
COPD (increases risk for pulmonary barotrauma)
Strenuous physical activity while diving (commercial diving)
Physical activity before or after diving
Panicking while diving
Diving in cold water
Rough sea conditions
General Prevention
Follow the dive profile.
Only dive nondecompression dives or perform adequate safety stops.
Avoid flying or traveling to higher altitudes for 24 hr after diving.
Maintain good hydration.
Avoid holding breath while diving.
Diagnosis
History
The history should include the dive profile, rate of ascent, time of onset of symptoms, and
changes in the type or intensity of symptoms.
An independent account from a dive buddy or dive instructor is often useful, especially if the
patient's consciousness is impaired.
Obtaining information from a dive computer (if the patient was using one) is also very useful.
Note any history of previous dives in the past few days, any exposure to altitude (which can
precipitate decompression sickness), and any previous health problems.
Physical Exam
Gas deposition in joints and soft tissues may manifest as a “pain only” syndrome (limb
bends), or simple pruritus (cutis marmorata), blebs (or skin bends), fatigue, or vague
soreness.
Gas deposition in the cerebral circulation causes strokelike symptoms (cerebral bends).
Gas deposition in the spinal cord (or autochthonous bubbles) can cause transverse paresis
(spinal cord bends or spinal decompression sickness).
Development of bubbles in the inner ear can cause deafness or equilibrium dysfunction,
nausea, vomiting, and nystagmus (inner ear bends or “staggers”).
Excessive venous bubbles develop and release vasoactive substances causing pulmonary
irritation and bronchoconstriction. Symptoms may include chest pain, dyspnea, and cough
(lung bends or “chokes”).
Other symptoms include headache, ataxia, delirium, coma, convulsions, confusion, patchy
numbness, coughing paroxysms (Behnken's sign), arrhythmias, cardiac arrest, tachy- or
bradycardia, vertigo, aphasia, blindness, and rapidly ascending paraplegia.
Skin lesions: Painful, pruritic, red rash on torso; burning blebs on skin; lymphedema. Also
palpate skin for SC emphysema.
Joints: Erythema and edema on periarticular surfaces. There is usually pain with movement.
Neurologic: Various manifestations of a cerebrovascular accident, including numbness,
weakness, aphasia, paresthesias, paralysis, paraplegia, confusion, personality changes, etc.
Cardiac: Arrhythmias, tachy- or bradycardia, findings of congestive heart failure
Pulmonary: Decreased breath sounds if pneumothorax present

Imaging
Chest radiography to look for pneumothorax, mediastinal emphysema, heart enlargement
CT scan of the brain to look for cerebral abnormalities
US to look for gas bubbles in joints, tendons, bursae, muscles
Diagnostic repressurization (place the patient in a hyperbaric chamber, descend to 60 ft or
2.8 ATA; symptoms should improve within 15 min if DCS is truly the correct diagnosis)
Traumatic injury to extremity
Acute myocardial infarction
Musculoskeletal strains
Urticaria/anaphylaxis
Malingering
Contaminated breathing gas (carbon monoxide)
Near drowning and hypoxic brain injury
Seafood toxin poisoning (ciguatera, puffer fish, paralytic shellfish, sea snake, cone shell)
Migraine
Guillain-Barre syndrome
Multiple sclerosis
Transverse myelitis
Spinal cord compression (from disk protrusion, hematoma, or tumor)
Middle ear or sinus barotrauma with cranial nerve compression
Inner ear barotrauma
Unrelated seizure (hypoglycemia, epilepsy) and postictal state from unrelated seizure
Cold water immersion pulmonary edema
Treatment
DCS type I: Mild cases of DCS type I may be treated by breathing 100%
oxygen via a nonrebreather mask. Close observation is necessary, and if
conservative measures fail to alleviate symptoms, strong consideration for
hyperbaric oxygen therapy (HBOT) should be considered.
DCS type II: Definitive treatment of DCS type II and unresolved DCS type I
after conservative treatment is recompression in a hyperbaric oxygen
chamber. HBOT involves compression of the nitrogen gas bubbles that caused
the symptoms of DCS while the oxygen administered replaces the nitrogen in
the blood. The nitrogen gas then defuses slowly out of the affected tissues
over time, thereby alleviating the symptoms. Treatment is administered based
on the U.S. Navy treatment protocols arranged in a table format. Tables 5 and
6 are the most commonly used methods and take 3–4.5 hr, respectively, to
complete. Treatment should continue until symptoms completely resolve.
Patients often experience significant improvement of symptoms as the trapped
nitrogen gas bubbles shrink, which generally occurs soon after the patient
arrives to depth of 60 ft (2.8 ATA).
AGE: Initial treatment is the same as any emergency: Airway, breathing, and
circulation. Once ABCs have been accounted for, 100% oxygen via a
nonrebreather mask is indicated. Position the patient in left lateral decubitus
position and begin HBOT treatment using U.S. Navy Table 6 (100% oxygen at
2.8 ATA). Table 6 may be preceded by a 30-min period of (40–50% oxygen at 6
ATA) for those whose symptoms don't improve significantly at the traditional 2.8
ATA. Less oxygen is used in order to prevent oxygen toxicity. Treatment is
continued until symptoms resolve or plateau.
Pre-Hospital
Administer 100% oxygen by nonrebreather mask.
Give IV fluids; isotonic solutions are preferred. Glucose solutions may worsen
neurologic outcome in patients with CNS conditions and should be avoided
unless treating known hypoglycemia.
Trendelenburg position or left lateral decubitus (Durant's maneuver) if CNS is
affected in DCS type II or AGE.
Give diazepam 5–15 mg IV for inner ear bends (symptomatic relief from
vertigo, nausea, and vomiting).
Transport (via ground preferably) to nearest hyperbaric facility. Aircraft that can
be pressurized to sea level also can be used for transport.
General Measures
Deep venous thrombosis and pulmonary embolism prophylaxis are
recommended for patients with severe CNS bends with leg weakness.
Do not give NSAIDs to patients with pain-only symptoms of DCS until
hyperbaric treatment has been instituted.
The cause of a fever in a patient with DCS should be determined and
vigorously treated (outcome is significantly worsened by hyperthermia).
Call the Diver's Alert Network [DAN; (919) 684–4326] for referral to nearest
hyperbaric facility for recompression.
DAN Latin American Hotline [DAN; 1–919–684–9111]
Patients may be sent home if only cutaneous symptoms are present and the
patient responded to conservative therapy administered in the emergency
department.
Rehabilitation of the injured diver is more successful than that of the patient
with a traumatic spinal cord injury or stroke. The patient may continue to
improve slowly after recompression treatments for up to 2 yrs.
Ongoing Care
Referral to the nearest hyperbaric chamber facility should be done as soon as possible.
Follow-up should be made with a physician knowledgeable in dive medicine.
Prognosis
The prognosis is excellent for early symptomatic presentation, referral, and treatment.
The duration and severity of symptoms prior to presentation and treatment negatively affects
outcome.
Complications
Oxygen toxicity
Myopia due to oxygen toxicity to the lens (older patients) generally resolves in
about 6 wks.
Residual neurologic deficits in CNS bends (46–75%) despite treatment
Residual paralysis may occur if recompression is not carried out immediately.
Residual paralysis may occur even in adequately treated patients if initial
presentation is severe.
References
1. Newton HB. Neurologic complications of scuba diving. Am Fam Phys.
2001;63:2211–2218, 2225–2226.
2. Gerriets, T, Tetzlaff, K, Hutzelmann A, et al. Association between right-to-

left shunts and brain lesions in sport divers. Aviation Space Environ Med.
2003;74:1058.
3. Gerriets T, Tetzlaff K, Liceni T, et al. Arteriovenous bubbles following cold

water sport dives: relation to right-to-left shunting. Neurology. 2000;55:1741.
4. Schwerzmann M, Seller C, Lipp E, et al. Relation between directly detected

patent foramen ovale and ischemic brain lesions in sport divers. Ann Intern
Med. 2001;134:21.
5. St Leger, Dowse M, Bryson P, et al. Comparative data from 2250 male and
female sports divers: diving patterns and decompression sickness. Aviation
Space Environ Med. 2002;73:743.
6. Klingmann C, et al. Decompression illness reported in a survey of 429

recreational divers. Aviation Space Environ Med. 2008;79:123.
Additional Reading
USN Dive Manual Revision 6
Codes
ICD9
993.3 Caisson disease
958.0 Air embolism as an early complication of trauma
Clinical Pearls
DCS should be at the top of the differential diagnosis in any patient with recent
history of diving and clinical symptoms.
HBOT is the definitive treatment for any patient diagnosed with DCS.
Proper diagnosis of DCS is supported if the patient's symptoms improve within
a relatively short period of time after recompression.
Table 6 is the preferred method of treatment.
In general, 24 hr is recommended as a safe duration to flying after any dive.
After suffering from decompression sickness, those diagnosed with type I
DCS characterized by musculoskeletal pain, dermal complications, and/or
constitutional symptoms, 2 wks is recommended before returning to diving.
For those diagnosed with type II DCS characterized by only minor neurologic
symptoms, 6 wks is recommended before returning to diving. For those
diagnosed with type II DCS characterized by severe neurologic symptoms,
diving is no longer recommended.
After treatment of DCS or AGE, exposure to altitude can precipitate
symptoms. After reaching a clinical plateau with treatment, an additional
period of 3–4 days at sea-level pressure is usually sufficient. In-flight oxygen
supplementation may prevent a treated patient from developing reoccurring
symptoms.
Seizures and Epilepsy
Nilesh Shah
Basics
Complications:
Status epilepticus: Recurrent generalized seizures without return to consciousness
Seizure types:
Generalized: Sudden onset involving an altered level of consciousness, usually bilateral and
symmetrical
Partial: Either simple (no alteration of consciousness) or complex (alteration/loss of
consciousness often with semipurposeful inappropriate movements)
Description
A seizure is an abnormal paroxysmal electrical discharge in the brain, usually with mental
status changes.
Individuals who have 2 or more seizures are deemed to have epilepsy.
Synonym(s): Convulsions; Epilepsy; Fits; Spells
Epidemiology
>10% of the population will have at least one seizure during their lifetime.
3% will have epilepsy by age 70.
100,000 new cases of epilepsy per year in the U.S., many in pediatric patients (1)[C]
70–80% of patients with epilepsy will go into remission (1)[C].
Risk Factors
Cerebrovascular disease
Brain tumors
Alcohol
Previous head injury
Malformations of cortical development
Infections
Idiopathic
Low seizure threshold is impossible to quantify. It may represent a genetic or acquired brain
disorder.

Abrasions, lacerations, contusions: Occur from uncontrolled contact with objects during
seizure
Tongue lacerations: Tongue is often bitten during a seizure.
Blunt head trauma
Syncope
Diagnosis
History
Actual account by 1st-hand observer is extremely helpful.
Previous history of seizure
Previous history of head trauma
Medications
Social/family history
Physical Exam
Fever: Suggests infectious etiology
Focal neurologic deficit: Possible localized trauma or tumor
Meningismus: May be present in meningitis
Papilledema: Secondary to increased intracranial pressure
Look for injuries that may have occurred during the seizure.
Look for evidence of acutely increased intracranial pressure, such as pupillary dilatation or
posturing, indicating an emergency.
Expect postictal confusion that gradually clears after a seizure.
Thorough neurologic exam to document focal deficits

Lab
Electrolytes, including glucose, calcium, magnesium, and phosphorus
Liver function tests, including ammonia level
Blood toxicology
Urine toxicology
Anticonvulsant level: Inadequate levels are a significant cause of recurrent seizures.
Imaging
CT scan: Rule out acute bleeding or intracranial masses.
MRI: May better define posterior fossa tumors, vascular abnormalities, and temporal lobes
Electroencephalography (EEG): May define true seizure activity and focus, although a
negative EEG result does not rule out seizure disorder. Sometimes a sleep-deprived patient
EEG may be required.
Spinal tap to rule out infectious etiology, elevated intracranial pressure, some congenital
etiologies
Alcohol withdrawal
Arteriovenous malformation
Electrolyte abnormalities (hypoglycemia, hyponatremia)
Fever
Hepatic failure
Idiopathic
Illicit drug use/abuse/withdrawal
Infection
Intracranial swelling/2nd-impact syndrome
Primary/secondary brain tumor
Posttraumatic (impact) seizure
Stroke
Syncope
Uremia
Vascular disease
Treatment
Immediate actions:
Supportive: ABCs
Keep area clear: Ensure that the patient does not injure self or others.
If in the setting of trauma, stabilize C-spine.
Once stable, workup begins as above.
ED Treatment
Immediate ED treatment includes benzodiazepines or other antiepileptic drugs
if patient is in status epilepticus.
Workup as above for etiology
Consider neurology consultation.
Medication
A number of drugs are available.
Use depends on etiology of seizures.
First Line
Benzodiazepines for status epilepticus
Second Line
Depends on etiology of seizure
General Measures
If no reversible cause is found, place patient on antiepileptic drugs (AEDs).
Monitor levels of AEDs, especially in 1st couple months of training.
Follow up with neurologist.
Transfer to ED if the patient has no known seizure disorder.
Hospitalization recommended for immediate care of uncontrolled seizures
Abnormal mental status associated with seizures
Ongoing studies (ie, sleep study or 24-hr EEG monitoring)
IV Fluids
IV drug administration
Correction of electrolyte abnormalities
Correction of dehydration
Ongoing Care
If no reversible cause is found, the patient should be referred to a neurologist for an initial visit
and EEG.
Patient Education
Recommendations on specific sports (2)[C]:
Activities to be avoided:
Scuba diving
Parachuting
High-altitude climbing
Gliding
Hand-gliding
Aviation
Motor-racing
Boxing
Activities requiring precautions or supervision:
Water-skiing
Swimming
Canoeing
(Wind) surfing
Sailing
Activities requiring knowledge of seizure type and sports:
Cycle racing
Skating
Horse-riding
Gymnastics
Prognosis
Prognosis is generally good with well-controlled seizures.
Complications
Preparticipation Physical Evaluation (PPE) clearance for some sports in cases
of uncontrolled or poorly controlled seizure disorders.
References
1. Arida RM, Cavalheiro EA, da Silva AC, et al. Physical activity and epilepsy:
proven and predicted benefits. Sports Med. 2008;38:607–615.
2. van Linschoten R, Backx FJ, Mulder OG, et al. Epilepsy and sports. Sports
Med. 1990;10:9–19.
3. Dimberg EL, Burns TM. Management of common neurologic conditions in

sports. Clin Sports Med. 2005;24:637–662, ix.
Additional Reading
Cantu RV, Cantu R. Epilepsy and athletics. Clin Sports Med. 1998;17:61–69.
Fountain NB, May AC. Epilepsy and athletics. Clin Sports Med. 2003;22:605–
616, x–xi.
Howard GM, Radloff M, Sevier TL. Epilepsy and sports participation. Curr
Sports Med Rep. 2004;3:15–19.
Miele VJ, Bailes JE, Martin NA. Participation in contact or collision sports in
athletes with epilepsy, genetic risk factors, structural brain lesions, or history
of craniotomy. Neurosurg Focus. 2006;21:e9
Sirven JI, Varrato J. Physical activity and epilepsy— what are the rules?
Physician Sports Med. 1999;27:63, 64, 67–70.
Codes
ICD9
345.10 Generalized convulsive epilepsy, without mention of intractable epilepsy
345.11 Generalized convulsive epilepsy, with intractable epilepsy
780.39 Other convulsions
Clinical Pearls
There is no definitive evidence of any relationship between repetitive minor
head injury and deterioration of the epileptic patient; therefore, most
collision/contact sports are acceptable (but no boxing). Swimming is acceptable
only with a certified lifeguard who should be made aware of the situation. Motor
sports should be undertaken only by individuals with well-controlled seizures.
Sports in which falling is a potential (eg, gymnastics, rock climbing, hang gliding)
should be judged on an individual basis based on the type and frequency of
seizure.
Sports need not be avoided for children who experience seizures. Improving
overall health may reduce the number of seizures experienced by a child. He or
she also may benefit from the increased self-esteem and social integration, so
important to all youngsters, available with participation in sports. Children will
obtain all the physiologic benefits of exercise, including increased
cardiovascular fitness, stronger muscles, and weight control.
Many antiepileptic medications have side effects that may impair concentration
or coordination. Most are approved by the NCAA and IOC.
The following questions need to be asked when deciding if participation in
sports is OK (3)[C]:
Are there any other impairments to modify the athlete's participation (ie,
ventricular shunts or vascular malformations)? What type of seizures occur?
How often do seizures occur?
Do AEDs significantly impair the athlete's perception and alertness?
Overall, the decision is individualized, but the physiologic and psychological
benefits of sport and exercise usually far outweigh the risk to athletes or their
competitors.
Risk factors of exercise include fatigue, psychic stress, hypoxia,
hyperhydration, hyperthermia, and hypoglycemia.
Hypoxia is usually an issue at high altitudes (>2,000 m).
Hyperhydration can occur with vigorous hydration in combination with sodium
loss.
Hyperthermia, a known seizure trigger, can occur with exercise in the heat,
especially with high humidity.
Certain AEDs can place athletes at risk for heat illnesses as well.
Hyperventilation is a common trigger of seizures but is rarely seen as a
trigger in exercise because this is a compensatory mechanism owing to
exercise, and respiratory alkalosis does not occur.
Septic Arthritis and Bursitis
Kevin B. Gebke
Paul Reehal
Basics
Description
Infection of articular joints or bursae with a bacterial, mycobacterial, spirochetal, fungal, or
viral source
May be an indication of systemic infection
Synonym(s): Infectious arthritis; Infectious bursitis
Epidemiology
Usually a monarticular or oligoarticular pattern for acute bacterial infection, chronic
mycobacterial infection, or fungal infection
Acute polyarticular involvement usually signifies disseminated neisserial infection or acute
hepatitis B.
Neisserial involvement is responsible for 50% of infectious arthritis.
Risk Factors
Sexually active person at risk for STDs
Joint penetration or recent surgery
Trauma
Immunocompromised patient
History of arthritis in affected joint (greatest incidence in patients with rheumatoid arthritis)
IV drug abuse
Significant comorbid diseases (diabetes, malignancy, hepatic failure, sickle-cell disease,
immunocompromised states)
Diagnosis
History
Rapid or insidious onset (patient may describe crescendo-like throbbing pain)
Single joint involvement in more than 90% of patients
Most commonly involves knee > hip > shoulder, wrist, or elbow joints
Presence of infection leading to bacterial seeding of joint (skin infection, pneumonia,
pyelonephritis, or gonorrhea are commonly the source)
Physical Exam
Various degrees of pain in region of joint or bursa
Swelling
Decreased range of joint motion
Erythema overlying joint or bursa
Localized or systemic fever
Possible associated skin lesions (petechial or pustular rash, Kaposi sarcoma)
Concomitant urethral discharge
Erythema and tenderness to palpation of affected joint or bursa
Joint effusion
Decreased range of motion (usually secondary to pain or effusion/swelling)
Local warmth or generalized fever
Cutaneous lesions (Lyme disease, meningococcal infection, gonorrhea)

Lab
Laboratory evaluation of joint or bursal aspirate is essential for diagnosis.
Laboratory specimens should be collected prior to antibiotic administration.
CBC, blood cultures, erythrocyte sedimentation rate, C-reactive protein
Prompt collection of joint or bursal aspirate if clinical suspicion of infectious process
Contaminated overlying tissue (ie, cellulitis) should be avoided during arthrocentesis or bursal
aspiration.
Synovial or bursal fluid aspirate should be sent for Gram stain and examination for crystals,
chemistry (lactate dehydrogenase, protein, and glucose), and culture.
In acute septic arthritis, synovial WBC counts typically average 100,000 WBC/mL with >90%
neutrophils.
Imaging
Plain radiographs may show soft tissue swelling, joint space widening, or displacement,
radiolucent areas indicating presence of gas, erosions, or joint space loss.
US is useful for identifying hip effusions.
CT scan and MRI are useful for evaluation of sacroiliac joint and vertebral joints.
Bone scan is indicated for identification of region affected by inflammatory process.
Cellulitis
Osteomyelitis
Gout
Pseudogout (calcium pyrophosphate deposition disease)
Juvenile rheumatoid arthritis
Rheumatic fever
Lyme disease
Spondyloarthropathy (Reiter syndrome, psoriatic arthritis, ankylosing spondylitis, irritable
bowel disease)
Sarcoidosis
Synovitis
Synovial papilloma
AIDS
Treatment
Septic bursitis:
Most common organisms include Staphylococcus aureus, β-hemolytic
Streptococcus, and Staphylococcus epidermidis. Rarely mycobacterial
infection is identified.
Potential exists for overwhelming sepsis or extension of infection into the
adjacent joint.
Primary therapy includes penicillinase-resistant penicillins (nafcillin or
dicloxacillin) or 1st-generation cephalosporins.
Therapy should be continued for a minimum of 2–3 wks.
Hospitalization for parenteral therapy is required when signs of systemic or
bony extension of infection are observed.
Septic arthritis:
Usually requires hospitalization for parenteral antibiotics
Owing to potential for rapid joint destruction, treat with broad-spectrum
antibiotics while culture results are pending.
Choice of broad-spectrum antibiotic coverage is based on Gram stain result.
If Gram stain shows gram-positive cocci, treat with a 1st-generation
cephalosporin such as cefazolin.
If Gram stain shows gram-negative bacilli, treat with a 3rd-generation
cephalosporin such as ceftriaxone, and add an aminoglycoside such as
gentamicin if Pseudomonas is suspected.
Infection eradication is complicated by the presence of joint prostheses, and
removal of the prosthesis may be necessary.
No indication for intraarticular antibiotics
Antibiotics are to be continued for 1–2 wks after resolution of symptoms.
Patients treated for gonorrhea also should receive doxycycline 100 mg PO
b.i.d. × 7 days to cover possible concurrent Chlamydia infection.
Longer treatment is required for joints affected by arthritis.
Surgical intervention via arthroscopic lavage or arthrotomy is indicated only if
needle drainage is ineffective (fluid loculation or inaccessible joint).
Ongoing Care
Complete resolution and restoration of joint function is the goal.
Possible adverse outcomes include death, impaired joint function (eg, decreased motion,
fusion, dislocation), septic necrosis, sinus formation, ankylosis, osteomyelitis, synovitis, and
limb-length changes.
Recurrent arthrocentesis is recommended as joint fluid reaccumulates to rule out
persistent/recurrent infection.
Regular office visits are recommended after hospital discharge for revaluation and early
recognition of persistent or new problems.
Prosthesis replacement is possible in the future after clearance of infection.
Additional Reading
Dambro MR, Rothschild BM. Griffith's 5-minute clinical consult. Philadelphia: Lippincott
Williams & Wilkins, 1999.
García-De La Torre I. Advances in the management of septic arthritis. Infect Dis Clin North
Am. 2006;20:773–788.
Gilbert DN, Moellering RC Jr, Sande MA. The Sanford guide to antimicrobial therapy. Hyde
Park, NY: Antimicrobial Therapy, Inc., 2000.
Goldman L, Ausiello D (eds). Cecil Medicine, 23rd Ed. Philadelphia: Saunders Elsevier,
2008.
Pioro MH, Mandell BF. Septic arthritis. Rheum Dis Clin North Am. 1997;23:239–258.
Stell IM, Gransden WR. Simple tests for septic bursitis. BMJ. 1998;316:187–189.
Thaler SJ, Maguire JH. Harrison's principles of internal medicine. 14th ed. New York:
McGraw-Hill, 1998.
Codes
ICD9
711.00 Pyogenic arthritis, site unspecified
711.01 Pyogenic arthritis involving shoulder region
711.02 Pyogenic arthritis involving upper arm
Clinical Pearls
Septic arthritis is considered an emergency, and prompt drainage and
administration of IV antibiotics can prevent joint damage.
If joint cannot be drained, do not simply treat with antibiotics; immediately
consult orthopedic surgery or other service for drainage and/or further
management.
Complete restoration of joint function is expected if early diagnosis and
treatment occur before articular damage is seen.
Prophylaxis may be indicated in certain conditions.
Protection from sexually transmitted diseases should be discussed with all
high-risk patients.
Sign of hip infection, more common in children, is hip held in flexed and
externally rotated position.
Sesamoid Dysfunction
Laura Distel
James R. Borchers
Basics
Anatomy:
2 sesamoid bones, the larger tibial (medial) sesamoid and fibular (lateral) sesamoid
Located on the plantar side of the 1st metatarsophalangeal (MTP) joint, just proximal to
the metatarsal head, embedded within the flexor hallucis brevis tendon and connected by
the intersesamoid ligament
The sesamoids' articular surfaces are located dorsally and articulate with the plantar
facets on the 1st metatarsal head
Blood supply is usually from a single artery, with a lack of significant secondary blood
supply (which increases risk for nonunion of fractures) (1).
Can have multiple ossification centers that may lead to a bipartite sesamoid, which can be
difficult to distinguish from an acute fracture (1)
Vitally important in the biomechanics of the foot
When the 1st MTP joint dorsiflexes, the sesamoids are pulled distally, covering and
protecting the plantar surface of the 1st metatarsal head and absorbing the weight-bearing
forces on the medial aspect of the forefoot.
Flexor hallucis brevis provides the active plantarflexion force at the 1st MTP joint, but the
sesamoid complex provides an increased mechanical advantage in plantarflexion.
Sesamoid function:
Protect the tendon of the flexor hallucis longus
Absorb a majority of the weight on the medial aspect of the forefoot:
Sesamoid bones bear up to 3 times body weight during normal gait.
Medial (or tibial) sesamoid bears the majority of this weight and thus is at higher risk for
injury.
Dissipate the forces on the metatarsal head
Increase the power of the flexor hallucis brevis and thus plantarflexion (1)
Description
Stress fractures:
Most common sesamoid pathology (1)
More common in athletes than in general population (2)
Sesamoiditis:
Generic term that encompasses multiple conditions including osteonecrosis,
chondromalacia, or inflammatory changes (1)
Usually involves the medial (tibial) sesamoid (1)
Acute fracture:
Typically caused by forced dorsiflexion (1)
Often a transverse fracture line with sharp edges (3)
Epidemiology
Sesamoiditis is seen more commonly in young, active adults.
Stress fractures are more common in athletes.
Risk Factors
Repetitive, forceful dorsiflexion, or loading (pushing off) of the MTP joint
At-risk sports include dancing (especially ballet), running, gymnastics, volleyball, basketball,
high-impact aerobics, and soccer (1).
Asymmetrical sesamoids
Pes cavus (3)
Playing on artificial turf (1)
Wearing shoes without adequate forefoot support, ie, high heels
General Prevention
Wearing shoes with adequate forefoot support
Use of orthotics to offload the 1st MTP joint
Diagnosis
History
Gradual onset of pain on the plantar surface of the hallux.
Pain with dorsiflexion or weight-bearing (1).
Unilateral symptoms are typical.
Pain typically is located at the medial sesamoid.
Acute fracture usually occurs with a history of hyperextension injury of the big toe (1).
Physical Exam
Tenderness with direct palpation of the sesamoids ± swelling or ecchymosis
Pain with resisted plantarflexion of the hallux
Pain with passive dorsiflexion of the 1st MTP
Pain with “pushing off” while walking or running
Decreased range of motion and/or strength of the 1st MTP
Occasional erythema or swelling of the sesamoids
An enlarged bursa on the plantar surface may be present
Presence of significant pes cavus, pes planus, or cock-up deformity of the hallux

Imaging
X-ray examination of the foot should include weight-bearing anteroposterior, lateral, medial,
and lateral oblique views. Comparison views of the contralateral foot may be helpful (2)[A].
If possible, an axial view of the 1st MTP joint in dorsiflexion, known as the “sesamoid view”
(2)[A]:
Presence of a bilateral bipartite sesamoid is more likely a normal variant rather than an
acute fracture; acute fractures are almost always unilateral.
A bipartite sesamoid may be seen in 25% of the population.
85% of bipartite sesamoids are bilateral (1)
An acutely fractured sesamoid is characterized by sharp, irregular edges, comminution, or
widely spaced fragments in contrast to the sclerotic edges of a nonunion or the smooth
edges of a bipartite sesamoid (1)
MRI is more specific in diagnosing sesamoid disorders because it can differentiate soft
tissue from bony abnormalities (4)[C].
Bone scan may show a stress fracture or osteochondritis before radiographically evident (5)
[C]; can help differentiate a bipartite sesamoid from an acute fracture because a bipartite
sesamoid will have a normal bone scan (1).
Also can also consider CT scan for evaluation of acute or stress fracture (2)[C]
Turf toe
Flexor hallucis longus tendonitis
Hallus rigidus
Hallus valgus
Neuroma
Metatarsalgia
Osteochondritis (more common in young women)
Osteoarthritis or inflammatory arthritis
Osteonecrosis
Avascular necrosis of the sesamoids
Neoplasm
Nerve impingement (less common)
Nonunion of a sesamoid fracture
Treatment
Sesamoiditis or stress fracture/nonunion:
Initially, conservative therapy is recommended (1)[A]:
Relative rest with immobilization by offloading the 1st MTP complex with
orthotics, a dancer's pad, or metarsal bar; taping the great toe in
plantarflexion may be considered for severe symptoms. This may require
4–6 wks of such treatment for adequate relief of symptoms (3)[A].
Ice
Pain control (oral NSAIDs or other analgesics) (3)[C]
Rarely, injections with corticosteroids can be considered (3)
Avoid wearing high-heeled shoes.
Long-term treatment includes:
Correction of any mechanical abnormalities with the use of taping,
orthotics, or a stiff-soled shoe to limit dorsiflexion of the 1st MTP joint
Eliminating or minimizing the stressing activity (1)[C]
Surgery, usually to excise the sesamoid, prolonged symptoms despite
several months of conservative management (see below).
Acute fractures:
Non-weight-bearing immobilization with a short-leg cast/AFO for 6–8 wks,
followed by protected weight-bearing in cast/AFO for 4–6 additional weeks
(2)[B]
Open reduction and internal fixation is controversial.
Percutaneous fixation may be an option (2)[B].
Surgical options are available if nonoperative treatment fails, but mechanical
defects can lead to long-term problems.
Sesamoidectomy (surgical excision) (1):
Most common procedure for sesamoid pathology
Can be partial or complete
Can result in overload of the metatarsal head or flexor hallucis longus tendon
Excision of both sesamoids generally is not recommended owing to
development of cock-up deformity and biomechanical morbidity (1).
Curettage and bone grafting (1)
Shaving of the sesamoid (1)
Ongoing Care
Custom orthotics ± cutouts for the sesamoid bones (3)
Short-leg walking cast can be considered for recalcitrant cases (1).
Corticosteroid injection into the sesamoid area can be considered with caution.
Periodic follow-up every 4–8 wks until the patient is asymptomatic
Continued modification of activities and use of orthotics
Referral to orthopedic surgeon or podiatrist if symptoms persist >6 mos
Prognosis
Conservative management generally is successful in treating most sesamoid pathology.
More severe cases that require surgical intervention are at risk for iatrogenic complications.
Complications
Nonunion of fractures
Development of stress fractures or avascular necrosis in untreated
sesamoiditis
References
1. Dedmond BT, Cory JW, McBryde A. The hallucal sesamoid complex. J Am
2. Mittlmeier T, Haar P. Sesamoid and toe fractures. Injury. 2004;35(Suppl

2):SB87–SB97.
3. Cohen BE. Hallux sesamoid disorders. Foot Ankle Clin. 2009;14:91–104.
4. Waizy H, Jäger M, Abbara-Czardybon M, et al. Surgical treatment of AVN

of the fibular (lateral) sesamoid. Foot Ankle Int. 2008;29:231–236.
5. Garrido IM, Bosch MN, González MS, et al. Osteochondritis of the hallux
sesamoid bones. Foot Ankle Surg. 2008;14:175–179.
Codes
ICD9
733.99 Other disorders of bone and cartilage
825.20 Fracture of unspecified bone(s) of foot (except toes), closed
Clinical Pearls
Medial sesamoid is injured most commonly.
Acute fractures are almost exclusively unilateral.
Bilateral bipartite sesamoids are usually benign.
Tenderness over the sesamoids or pain with dorsiflexion that improves with
non-weight-bearing should arise suspicion for sesamoid pathology.
Nonoperative treatment, especially immobilization, is the mainstay of therapy.
Sever Disease/Calcaneal Apophysitis
Stephen Simons
Jeff Kindred
Basics
Description
Sever disease, also known as calcaneal apophysitis, is an overuse syndrome causing late
childhood and adolescent heel pain.
This traction apophysitis is the foot equivalent to Osgood-Schlatter disease.
Synonym(s): Calcaneal apophysitis
Epidemiology
Incidence
Typically occurs during an adolescent growth spurt
Predominant age: Described most often between the ages of 9 and 12 yrs; most frequent at
age 11 in girls and at age 12 in boys
Predominant gender: Male > Female
Occurs bilaterally in just over 60% of cases
Risk Factors
Adolescent growth spurt
Increased or excessive sport and play activity
Tight gastrocsoleus complex
Weak ankle dorsiflexors
Biomechanical factors such as genu varum and forefoot varus
Poor-quality or worn-out athletic shoes
Poorly cushioned or low-heeled shoes such as soccer, baseball, track, or cycling cleats
Running on hard surfaces
High-impact sports
Etiology
The posterior calcaneus develops as a secondary ossification center.
This secondary ossification center provides attachment for the tendoachilles.
This secondary ossification site is not contiguous with a diarthrodial joint; therefore, this
portion of bone is called an apophysis instead of an epiphysis.
A physis (open growth plate) separates the apophysis from the body of the calcaneus.
The calcaneal physis typically closes between the ages of 12 and 15 yrs.
Diagnosis
History
An 8–13-yr-old child presents with heel pain worsened with increased activity (1)[C].
Recent growth spurt coincides with vigorous sport or play activities (1)[C].
Sports requiring a lot of running and jumping activities are particularly prone to cause this
overuse syndrome (2)[C].
Pain can be unilateral or bilateral and is relieved with rest (2)[C].
The pain may become severe enough to stop sport activity and even require crutch walking
(2)[C].
Physical Exam
Intermittent or continuous posterior heel pain during or following increased sport or play
activity (1)[C]
Pain can be bilateral or unilateral (1)[C].
Pain is usually absent in the morning.
No swelling
No ecchymoses or skin changes
Absence of swelling or erythema
Tenderness just anterior to the Achilles insertion on the heel (2)[C]
Tenderness with medial and lateral compression of the heel to the posterior 3rd of the
calcaneus (2)[C]
Pain aggravated by standing on tiptoe (Sever sign)
Heel cord inflexibility with sometimes <10 degrees of dorsiflexion
Biomechanical contributors such as forefoot varus, hallux valgus, pes cavus, and pes
planus (1)[C]

Imaging
Radiographs may show fragmentation, sclerosis, and increased density of the apophysis, but
these radiographic changes can be normal (2,3)[C].
Imaging is not necessary to make this clinical diagnosis but may be helpful to rule out other
causes of heel pain (2)[C].
MRI has been used to evaluate persistent heel pain that does not respond to conservative
treatment and has shown many of these patients to have bone bruising and edema on the
calcaneal metaphysis and apophysis (4)[C].
Calcaneal bursitis
Insertional Achilles tendonitis
Fat pad syndrome
Plantar fasciitis
Tarsal tunnel syndrome
Tarsal coalition
Calcaneal osteomyelitis
Treatment
Rest or reduce activity to a pain tolerance level (2,3)[C].
Ice (2,3)[C]
NSAIDs for pain control (2,3)[C]
Heel lifts (2,3)[C]
Viscoelastic heel cups (2,3)[C]
If not responsive to conservative treatment, a short-leg cast or boot walker or
even immobilization may be necessary (2,4)[C].
Gastrocsoleus stretching exercises: Knee straight and knee flexed stretch with
the heel maintained on the floor or ground (2)[C]
Strengthening of the quadriceps and gastrocsoleus to better equip these
muscle groups to act as shock absorbers (2)[C]
Strengthening of the foot dorsiflexors
Shoe orthotics may be helpful to correct significant biomechanical
abnormalities. Off-the-shelf orthoses are much more cost-effective and can be
tried 1st before custom orthoses are considered.
Good-quality shoe with adequate shock absorption and firm heel counter (2)[C]
Time to symptom resolution varies, but symptoms abate totally with skeletal
maturity (2)[C].
No reports of long-term sequelae from Sever disease (2)[C]
Not indicated
Ongoing Care
Referral/disposition necessary only when clinician is uncertain of diagnosis
Complications
Persistent pain that does not respond to conservative measures may indicate
there is a calcaneal stress fracture and may require a 3–4-wk period of
immobilization (4)[C].
References
1. Micheli LJ, Ireland ML. Prevention and management of calcaneal
apophysitis in children: an overuse syndrome. J Pediatr Orthop. 1987;7:34–
38.
2. Hendrix CL. Calcaneal apophysitis (Sever disease). Clin Podiatr Med Surg
North Am. 2005;22:55–62, vi.
3. Cassas KJ, Cassettari-Wayhs A. Childhood and adolescent sports-related

overuse injuries. Am Fam Physician. 2006;73:1014–1022.
4. Ogden JA, Ganey TM, Hill JD, et al. Sever's injury: a stress fracture of the
immature calcaneal metaphysis. J Pediatr Orthop. 2004;24:488–492.
Additional Reading
Madden CC, Mellion MB. Sever's disease and other causes of heel pain in
adolescents. Am Fam Physician. 1996;54:1995–2000.
Stanitski CL. Pediatric and adolescent sports injuries. Clin Sports Med.
1997;16:613–633.
Codes
ICD9
Clinical Pearls
Total rest may hasten the recovery from this heel pain but may not be
necessary. Reducing the amount of activity may allow sports participation
without worsening the heel pain.
Current evidence does not suggest any long-term sequelae.
Shoulder Instability, Anterior
Tricia Beatty
Basics
Description
A symptomatic anteroinferior subluxation or dislocation of the glenohumeral (GH) joint
Synonym(s): Glenohumeral dislocation; Glenohumeral subluxation; Dead-arm syndrome
Epidemiology
The most dislocated joint in the body. In a study of 8,056 dislocations, 45% involved the GH
joint.
Anterior GH dislocations are the most common. In a study of 394 shoulder dislocations and
separations, 84% were anterior GH dislocations.
Recurrence rate for athletes under age 25 is over 85% in those who have suffered an initial
traumatic event.
Risk Factors
History of previous dislocation
Younger patients
Athletes participating in repetitive overhead activities such as throwing or volleyball
Diagnosis
History
Patients usually give a history of prior dislocation/subluxation event. The symptoms will be
reported to occur when the arm is placed in the provocative position of abduction and
external rotation.
Patients also may complain of a “dead arm,” which typically occurs with subluxation.
Physical Exam
Patients note the feeling of impending dislocation with the arm in a provocative position. Pain
itself is generally not a sign of pure dislocation.
A thorough exam of the cervical spine, proximal humerus, and scapula should be performed
when evaluating anyone with shoulder pain. If multidirectional instability is suspected, an
assessment of ligamentous laxity should be addressed. A complete neurologic exam should
be performed to identify any central or peripheral neuropathy.
Apprehension test: Arm is placed at 90 degrees of abduction and gently externally rotated. A
sense of “impending” dislocation is regraded as a positive test.
Relocation test: With the patient supine, the apprehension test is repeated. A posteriorly
directed force is applied to the proximal humerus with the scapula stabilized by the
examiner's opposite hand. If symptoms abate, the test result is positive.
Load and shift test: The patient is seated while the examiner stabilizes the scapula with one
hand and with the thumb and forefinger of the free hand on the proximal humerus attempts to
sublux the head anteriorly and posteriorly. In general, this test works better with thinner
patients and requires a fair amount of patient relaxation.

Imaging
Imaging studies should include orthogonal views to rule out associated bony injuries and to
ensure that the humeral head is reseated within glenoid.
Radiography: The initial series includes an anteroposterior (AP), true shoulder AP, axillary
lateral, and scapular Y. Additional views, if necessary, may include the Westpoint view (good
for identifying a bony Bankart/anteroinferior glenoid rim fracture) and Stryker notch view
(good for identifying a Hill-Sachs lesion/posterolateral humeral head compression fracture).
Velpeau view (if required to stay in sling) if initial radiographs are inconclusive or patient is
unable to be appropriately positioned.
MRI can identify rotator cuff tears, biceps abnormalities, and occasionally lesions associated
with humeral avulsion of the GH ligament. Because of the normal variation of the labrum and
GH ligaments, most studies overestimate the frequency of labral tears.
Postreduction views are necessary for the acute treatment of a shoulder dislocation to
ensure relocation and assess for possibility of a fracture.
Diagnoses that can mimic anterior instability include multidirectional instability,
acromioclavicular instability, superior labral anteroposterior (SLAP) lesions, biceps tendon
subluxation, and subscapularis tear.
One always should rule out referred pain from the cervical spine.
Treatment
Early treatment consists of brief immobilization of up to 3 wks for younger
patients, followed by early protected ROM and strengthening. The anterior
capsular structures must be protected throughout rehabilitation, and therefore,
all stressors to the anterior structures should be limited.
Rotator cuff strengthening: Initial strengthening should begin in the plane of the
scapula. Internal and limited-range external rotation exercises can be begun
with light free weights or therabands.
Scapular stabilization: Exercises include rowing, modified push-ups with
maximal protraction, scaption (elevation of the humerus in external rotation in
the scapular plane), modified flies and press-ups (later stage).
Indications for surgery include more than 3 dislocations per year, dislocation at
rest, or failed nonoperative therapy.
Relative indications for surgery depend on patient demand, such as 1st-time
dislocations in young (<30 yrs) athletes or laborers.
Surgical technique: Repair the traumatic lesion by reattaching the torn labrum
and GH ligaments. Avoid compromised motion by not overtightening the
capsule.
Arthroscopic stabilization: Has advantage of easier postoperative rehabilitation
and less restriction of motion secondary to scarring; has disadvantage of a
higher recurrence rate of 12%. To reduce rate of recurrence, capsular laxity
must be addressed with either capsular imbrication or thermal capsulorrhaphy.
Open stabilization (Bankart procedure): Has more successful outcome, with
recurrence rates of <5%; Has the disadvantage of slowed rehabilitation
secondary to injury to the subscapularis tendon.
Ongoing Care
Any patient with recurrent anterior dislocations or a young, athletic, 1st-time dislocator should
have the opportunity to discuss all options, including surgery, and therefore may be referred
to an orthopedic surgeon for evaluation.
Any patient failing nonoperative modalities also should be referred.
Additional Reading
Bankart AS. Recurrent or habitual dislocation of the shoulder. BMJ. 1923;2:1132–1133.
Bedi A, Ryu RK. The treatment of primary anterior shoulder dislocations. AAOS
Instructional Course Lectures. 2009;58:293–301.
Cave EF, Burke JF, Boyd RJ. Trauma management. Chicago: Year Book Medical, 1974.
Jobe FW, ed. Operative techniques in upper extremity sports injury. St. Louis: Mosby Year
Book, 1996.
Kazár B, Relovszky E. Prognosis of primary dislocation of the shoulder. Acta Orthop Scand.
1969;40:216–224.
Ludewig PM, Reynolds JF. The Association of Scapular Kinematics and Glenohumeral Joint
pathologies. J Ortho & Sports Phys Ther. 2009;39:90–101.
Matthews LS, Pavlovich LJ. Disorders of the shoulder: diagnosis and management.
Neviaser RJ, Neviaser TJ, Neviaser JS. Anterior dislocation of the shoulder and rotator cuff
rupture. Clin Orthop Relat Res. 1993;291:103–106.
Ochoa E, Burkhart SS. Glenohumeral bone defects in the treatment of anterior shoulder
instability. AAOS Instructional Course Lectures. 2009;58:323–333.
Rowe CR, Patel D, Southmayd WW. The Bankart procedure: a long-term end-result study.
J Bone Joint Surg Am. 1978;60:1–16.
Codes
ICD9
718.81 Other joint derangement, not elsewhere classified, involving shoulder region
Clinical Pearls
In general, surgery is required only when physical therapy has failed. Most
young patients (<30 yrs of age) require surgical intervention.
In the hands of a good arthroscopist with experience in shoulder stabilizations,
the success rate of arthroscopy probably has improved beyond the previously
reported rate of 85%. The open procedure is still the “gold standard,” with a
success rate of 95%.
Shoulder Instability, Multidirectional
David E. J. Bazzo
Tara Robbins
Basics
Description
Multidirectional instability (MDI) is an increase in glenohumeral translation in more than one
direction causing either subluxation (any partial loss of normal articulation) or dislocation (a
complete loss of glenohumeral articulation) in more than one direction, such as anterior,
inferior, superior, or posterior.
The extent of laxity can be described objectively by the measured amount in millimeters of
which the humeral head can be translated on the glenoid. Some individuals may be
symptomatic with minimal millimeters of laxity, whereas others may have minimal symptoms
with 3+ laxity.
Hallmark pathology of MDI is a large, patulous inferior capsule, although this is not always
the case.
Epidemiology
MDI is much more common than previously realized but still represents <5% of all shoulder
instability.
Most patients are in their 3rd decade of life but range in age from teenagers to middle age.
Risk Factors
Repetitive microtrauma (especially overhead motion): Butterfly and backstroke swimmers,
gymnasts, baseball pitchers, and weight lifters
Generalized ligamentous hyperlaxity
Etiology
Etiology is thought to be multifactorial, with current theories focusing on anatomic, biochemical,
and neuromuscular abnormalities.
Anatomic:
Patients with MDI have been shown to have a large, patulous inferior pouch and wide
rotator interval that are both common manifestations of inferior instability.
Pathologic changes in labral height and Bankart lesions also are observed in patients with
MDI (1).
Biochemical:
Patients with MDI have been shown to have alterations in the type and quantity of collagen,
specifically types III and IV collagen, as seen in Ehlers-Danlos syndrome (1).
Neuromuscular:
Loss of strength or neuromotor coordination of rotator cuff and scapular stabilizing muscles
also contributes to MDI.
Recent studies have shown that when compared with controls, patients with MDI have
altered functioning of the musculature of the shoulder girdle and the dynamic stabilizers of
the glenohumeral joint during movement.
Loss of proprioception also can contribute to MDI because proprioceptive feedback is
important in maintaining stability.
It still needs to be elucidated whether the proprioceptive defect is a cause or effect of the
instability (1).
Diagnosis
History
MDI is associated with recurrent or “low-energy” trauma.
Unilateral versus bilateral shoulder problems: 30–70% of patients with MDI have symptoms in
the opposite shoulder as well.
MDI of the humeral head reduces spontaneously or is self-reduced.
Previously unsuccessful shoulder reconstruction for presumed unidirectional instability may
indicate MDI.
Patients with emotional problems who can purposely cause repeated dislocation typically will
not benefit from surgery until their emotional problems are resolved. However, patients who
dislocate voluntarily and do not have emotional problems may benefit from surgery.
Physical Exam
Most common complaint is vague pain radiating to the deltoid insertion, initially occurring after
activity and progressing to pain at rest, and in late stages, patients may develop night pain.
Transient neurologic symptoms, such as numbness (“dead arm”) or tingling owing to transient
subluxation, usually affecting ulnar > median nerve distribution
Rotator cuff weakness
Inferior instability: Pain, numbness, tingling while carrying briefcase or heavy suitcase; this is
caused by traction on the brachial plexus.
Posterior instability: Pain while arm in forward-flexed, internally rotated position (eg, pushing
open a heavy door, performing push-ups or bench press, blocking in football, or during pull-
through phase of rowing stroke)
Anterior instability: Pain with arm in overhead, abducted, externally rotated position (eg,
during wind-up or early acceleration of a throw)
Often general ligamentous laxity is present (eg, thumb to forearm), elbow hyperextension,
metacarpophalangeal joint hyperextension, genu recurvatum, patellofemoral subluxation (40–
75%)
Sulcus test involves inferior traction on the arm while at the side. Inferior translation of at
least 1–2 cm causing concavity of skin inferior to acromion (positive sulcus sign) indicates
inferior instability.
Anterior and posterior load and shift test and/or drawer test usually result in anterior and
posterior displacement (graded trace to III). Always remember to stabilize the scapula with
one hand while the patient remains in either a seated or supine position.
Apprehension test involves placing the shoulder in the position of instability (throwing position:
abduction and external rotation for anterior instability; adduction, flexion, and internal rotation
for posterior instability). A positive test is seen when the patient senses pending subluxation
or has involuntary guarding. It is apprehension that is most reliable in confirming shoulder
instability, not pain.
Relocation test involves relief of apprehension and symptoms when applying a stabilizing
counterforce (posterior force on humeral head for anterior instability; anterior force on
humeral head for posterior instability) to the arm in the provocative position with the scapula
stabilized.
Cervical range of motion, upper extremity strength, sensory function (including axillary nerve),
and reflexes also should be evaluated.
Muscle guarding may make the examination difficult, and repeat exams may be necessary for
confirmation of diagnosis.

Imaging
MDI is a clinical diagnosis based on the history and physical exam; orthogonal plain
radiographs should be obtained to evaluate for bony defects such as Bankart and Hill-Sachs
lesions as well as glenoid dysplasia.
Stryker notch: Patient supine, cassette under shoulder, arm flexed, palm to head, elbow
pointing straight upward, beam 10 degrees cranially centered over coracoid; reported to
show defect in 90% of 20 patients studied
Axillary view: Clear delineation of glenoid-humerus relationship; evaluation of anteroposterior
displacement of humeral head on glenoid and Hill-Sachs lesions as well as larger glenoid rim
and humeral head compression fractures
West Point (reverse axillary lateral): Patient placed prone on table, involved shoulder place
on raised (8 cm) pad, head and neck rotated away, cassette against superior aspect of
shoulder, beam centered at axilla with 25 degrees down/25 degrees medial angulation;
allows view of anteroinferior glenoid rim; this view is usually used for traumatic anterior
dislocations.
Weight-bearing traction films typically not performed routinely because diagnostic yield is
quite low
More sophisticated imagery is now accepted as routine preoperatively or for persistent
symptoms. Most shoulder surgeons prefer an MRI arthrogram to help detect capsular
redundancy, but MRI remains more useful in ruling out other pathology. Double-contrast CT
arthrography may show increased capsular volume.
Unilateral instability (anterior, posterior, inferior)
Acute dislocation or subluxation
Voluntary dislocator
Primary impingement
Cervical disc disease
Brachial plexitis
Treatment
Analgesia: NSAIDs can decrease pain and inflammation acutely, but long-
term analgesic usage typically is not necessary.
Reduction: Usually reduce spontaneously or self-reduce
Immobilization:
Usually immobilize with a sling for 3 wks for young (<30 yrs of age) acute,
1st-time true dislocation. There has not been a well-demonstrated
association between length of immobilization and recurrence.
Immobilization for recurrent dislocators is of less value, although some
authorities suggest short-term immobilization for each occurrence.
Use caution in immobilizing older patients, who are more likely to develop
adhesive capsulitis.
1st-line treatment is prolonged course of physical therapy/independent
exercise program with emphasis on strengthening anterior deltoid and rotator
cuff muscles for at least 6 mos and probably up to 1 yr. Symptomatic relief is
gradual.
2 phases have been suggested: Phase I focuses on strengthening the
anterior deltoid and rotator cuff muscles and usually lasts 6–12 wks. Phase II
focuses on continuing to strengthen deltoid and rotator cuff muscles with the
addition of strengthening scapular stabilizers and improving proprioception
(1)[B].
Recent data suggest that most patients will begin to improve within 3 mos of
physical therapy (2)[B].
It is important to continue a maintenance exercise program indefinitely.
If patient is pain-free with normal strength after 6 mos, prior activity may be
resumed.
May develop secondary impingement syndrome, which can be relieved by a
subacromial injection of a steroid preparation, if necessary, to allow
continuation of physical therapy
May need to change prior activity (ie, a butterfly stroke swimmer may need to
choose a different stroke or a pitcher may need to change his or her delivery
or position)
Surgery is indicated only for symptomatic, painful shoulders after the patient
fails aggressive, prolonged physical therapy (usually minimum 6 mos) (1)[C].
Laxity alone is not a typical indication for surgery.
Some authorities advocate earlier surgery if there is a documented
glenohumeral ligament avulsion on double-contrast CT or MRI arthrogram.
Neer et al. described the open inferior capsular shift repair technique with good
success in 1974, and it continues to be a reasonable choice of surgical
interventions for MDI.
Recently, several arthroscopic approaches have been described, including
transglenoid capsular shift and capsular plication with bone anchors and
adjunctive thermal capsulorrhaphy and/or rotator interval closure. The
arthroscopic techniques produce clinical results equivalent or superior to open
techniques. Arthroscopic treatment results in less surgical time and presumed
less morbidity (1,3)[B].
Thermal capsulorrhaphy (capsular shrinkage through laser or radiofrequency
energy) has been used to treat shoulder instability for centuries; however,
clinical studies have not shown favorable results. In isolated thermal
capsulorrhaphy, a high failure rate and complications of glenohumeral
chondrolysis and axillary nerve injuries have been reported. However, thermal
capsulorraphy may be useful as adjunctive therapy (4)[B].
Note: Probably the earliest “sports surgery” was thermal capsulorraphy for
anterior instability in ancient Egypt, where warriors with instability were treated
with a hot poker to thermally shrink anterior structures to try to allow them to
throw a spear.
Ongoing Care
Most patients with MDI should be referred for physical therapy. Patients who fail physical
therapy can be referred to an orthopedist for consideration of surgical treatment.
Asymptomatic, pain-free voluntary dislocators with emotional problems who purposely
dislocate their shoulder repeatedly for shock value do not benefit from surgery and may need
a psychiatric referral.
References
1. Bahu MJ, Trentacosta N, Vorys GC, et al. Multidirectional instability: evaluation and
treatment options. Clin Sports Med. 2008;27:671–689.
2. Miniaci A, Codsi MJ. Thermal capsulorrhaphy for the treatment of shoulder instability. Am
J Sports Med. 2006.
3. Caprise P, Sekiya J. Open and arthroscopic treatment of multidirectional instabilty of the

shoulder. Arthroscopy: J Arthroscopic Related Surg. 2006;22:1126–1131.
4. Mahaffey BL, Smith PA. Shoulder instability in young athletes. Am Family Phys.
1999;59:2773–2782.
Additional Reading
Foster CR. Multidirectional instability of the shoulder in the athlete. Clin Sports Med.
1983;2:355–368.
Misamore GW, Sallay PI, Didelot W. A longitudinal study of patients with multidirectional
instability of the shoulder with seven- to ten-year follow-up. J Shoulder Elbow Surg.
2005;14:466–470.
Schenk TJ, Brems JJ. Multidirectional instability of the shoulder: pathophysiology, diagnosis,
and management. J Am Acad Orthop Surg. 1998;6:65–72.
Yamaguchi K, Flatow EL. Management of multidirectional instability. Clin Sports Med.

1995;14:885–902.
Codes
ICD9
718.81 Other joint derangement, not elsewhere classified, involving shoulder region
755.59 Other congenital anomalies of upper limb, including shoulder girdle
831.00 Closed dislocation of shoulder, unspecified site
Clinical Pearls
Regardless of whether the treatment is conservative physical therapy or
surgery, the time until resumption of full sports generally is 6 mos. If surgery is
required, then postoperative immobilization with a sling is typically for 3–6 wks,
with early supervised range-of-motion exercises. Light sports and throwing can
start at 4 mos postoperatively if strength is at least 90% and full range of
motion is achieved.
10–13% of patients require bilateral surgical repair.
Sinus Tarsi Syndrome
George G. A. Pujalte
Rafael DaFonseca
Basics
Sinus tarsi syndrome is refractory pain, often chronic, over the anterolateral aspect of an
ankle, often associated with previous ankle injury (1).
Description
Sinus tarsi is the lateral extension of the tarsal canal formed by the sulcus of the talus and
calcaneus (2).
Within the sinus tarsi are the talocalcaneal interosseous ligament; cervical ligament; the
subtalar joint capsule; synovium; and the medial, intermediate, and lateral roots of the inferior
extensor retinaculum (2).
Talocalcaneal interosseous ligament is involved in movements of the subtalar joint (2). It
functions to maintain apposition of the talus and calcaneus in all positions (2). Its rich
innervation suggests that the sinus tarsi may be susceptible to neurogenic inflammation and
may be a center of articular nociception (2).
Epidemiology
Patients with sinus tarsi syndrome are usually between their 3rd and 4th decades of life
(3,4).
Often associated with dancers, volleyball players, basketball players, overweight individuals,
and patients with foot deformities, usually flexible flat feet (5).
Risk Factors
Forefoot and calcaneal valgus, mechanical factors predisposing to supination ankle injuries,
may lead to sinus tarsi syndrome after such injuries (6). In the majority of cases, the lateral
ankle pain follows a history of an inversion ankle sprain (7).
Etiology
Soft tissue inversion injuries of the ankle most commonly involve the ligamentous structures of
the lateral aspect of the ankle and sinus tarsi (8).
Posttraumatic fibrotic changes in the wall and surrounding tissue of veins, causing
disturbance of venous outflow and increased intrasinusal pressure, may be a factor in the
pathogenesis of sinus tarsi syndrome (7).
Sinus tarsi is not only a talocalcaneal joint space with interosseous ligaments, but also a
source of nociceptive and proprioceptive information on the movements of the foot and ankle
(2).
Sinus tarsi syndrome may result from disorders of nociception and proprioception of the foot
(2).

70% of cases are posttraumatic
30% can be attributed to causes including systemic disease, structural abnormalities, and
soft tissue masses, such as ganglions (3,9).
Diagnosis
4 clinical characteristics have been used to describe and diagnose the syndrome (3,4):
Pain at the lateral opening of the sinus tarsi, increasing with pressure, usually ceasing at rest
Perception of instability of the rear foot on uneven ground
Marked reduction of pain and discomfort following an injection of local anesthetic into the
sinus tarsi
Clinical and stress radiographic examination showing no or minimal instability
History
Deep aching, throbbing, or sharp pain within the sinus tarsi may be associated with a sense
of rear foot instability (3).
Pain over the lateral part of the ankle and hindfoot, over the sinus tarsi, is often the primary
complaint (10).
A previous sprain or other injury is often the inciting event (3).
Initial injury may have responded to conservative therapies, but recurrent pain or pain
settling into the sinus tarsi may be experienced with activities of daily living (3).
Can result in severe pain and instability of the ankle and the subtalar joints, particularly in
athletes (8)
Pain and paresthesia may also be felt over the dorsolateral aspect of the foot (11).
Intermittent pain often radiates into the leg, with resulting paresthesia over the distal aspect
of the foot (11). Swelling may and may not be present (10).
Patients most often complain of “ankle” pain, when in reality, the pain is emanating from the
subtalar area (3). When asked to identify the site of maximal tenderness, patients often point
directly to the sinus tarsi region (3).
Pain may involve the anterior and lateral ankle, although this pain is less intense (3).
The perception of ankle symptoms may be secondary to previous trauma, referred pain, or
an altered gait in an attempt to reduce pain (3).
Physical Exam
Diagnosis is often clinical; tenderness over the sinus tarsi often leads to the diagnosis of
sinus tarsi syndrome (10).
Discomfort usually worsens with pressure over the lateral opening of the sinus tarsi,
becoming more severe with the foot in varus position (7).
Symptoms are usually alleviated when the foot is immobilized in a valgus position (7).
Injury to the ligaments may result in laxity of the joints of the ankle complex, neuromuscular
deficits are also likely to occur due to the injury to the nervous and musculotendinous tissue
(12).
Neuromuscular deficits may be manifested as impaired balance, reduced joint position sense,
slower firing of the peroneal muscles on inversion, slowed nerve conduction velocity, impaired
cutaneous sensation, strength deficits, and decreased dorsiflexion range of motion (12).
Assessment of patients with lateral ankle sprain must address not only joint laxity and
swelling, but should also include examination for neuromuscular deficits (2).

Imaging
Radiological examination usually will not reveal a bone lesion or any insufficiency of the ankle
ligaments, and dynamically, there is usually no restriction of talocalcaneonavicular joint range
of motion (7).
MRI, with or without arthrography, can lead to better definition of abnormalities in the sinus
tarsi and tarsal canal (9).
Pain and functional instability in the region have been found to be reduced for a few hours
after the injection of a local anesthetic into the opening of the sinus tarsi (6).
A reduction in electrical activity or complete electrical silence of both the peroneus brevis and
longus muscles have been noted on electromyographic studies (2).
Peripheral mononeuropathies
Radiculopathy
Lateral ankle sprain
Anterolateral soft tissue impingement
Bifurcate ligament injury
Stress fractures of the cuboid, talus, or calcaneus (3,13)
Treatment
Relative rest, avoidance of aggravating activities, and use of NSAIDs as
needed for pain may give temporary relief (3).
Orthotics may be used to address forefoot valgus and calcaneal valgus,
mechanical factors predisposing to supination ankle sprains (6).
Referral to physical therapy for ankle and leg strength and proprioception
exercises is often quite appropriate (6).
Conservative treatment includes corticosteroid injections, immobilization in a
cast, application of local anti-inflammatory gels or local irritants such as
Capsaicin, and systemic drugs aimed at reducing neuralgic pain.
Physical therapy treatments may include mobilization, friction massage, and
deep massage using US, soft laser, transcutaneous electrical stimulation, or
any other method of deep massage. When there is ankle instability or a feeling
of giving way, physical therapy should be tried 1st.
Corticosteroid injections mixed with local anesthetics have been shown to be
effective (14).
Conservative treatment has been shown to be effective in up to 2/3 of patients
(4). There seem to be no clear studies that delineate the length of time
conservative measures should be tried, and the determination appears to be
on a case-to-case basis for the most part, although, in our practice, a time
frame of 4–6 wks is the most commonly used length of time for any
conservative treatment chosen and applied to sinus tarsi syndrome.
Medication
A local anesthetic injection may be given as initial treatment for the pain of
sinus tarsi syndrome; may also be diagnostic (6).
A mixed local anesthetic and corticosteroid injection may also be given as
treatment for the pain of sinus tarsi syndrome, with 5–6 injections at weekly
intervals usually sufficient (4,6).
Referral
Referral to orthopedic surgery may be appropriate after failure of conservative
measures (6).
Surgical treatment of sinus tarsi syndrome may involve excision of the lateral half
of the sinus tarsi contents, followed by below-knee casting for 3 wks and physical
therapy (6).
Ongoing Care
Postoperatively, patients may be immobilized with a walking caliper for around 4 wks, then
made to undergo physical therapy, usually for another 4–6 wks (4).
Prognosis
2/3 of sinus tarsi syndrome cases respond to conservative treatment.
In the remaining 1/3 of cases, surgical intervention has been shown to cure or improve 90%
of patients (4).
A 15-yr retrospective study on conservative treatment of sinus tarsi syndrome showed that
most of these patients eventually required surgical intervention after nonoperative treatment
failed to alleviate their symptoms, whereupon long-term follow-up revealed relief from pain
after surgery (15).
Complications
Sinus tarsi syndrome responds well to therapeutic interventions, often mixed
local anesthetic and corticosteroid injections (14).
Should surgery be required, there are usually few postoperative complications
(1,16).
The most common reported complication from surgical intervention is a
transient neurapraxia involving branches of the superficial peroneal nerve (17).
References
1. Lowy A, Schilero J, Kanat IO. Sinus tarsi syndrome: a postoperative
analysis. J Foot Surg. 1985;24:108–112.
2. Akiyama K, Takakura Y, Tomita Y, et al. Neurohistology of the sinus tarsi and

sinus tarsi syndrome. J Orthop Sci. 1999;4:299–303.
3. Schnirring-Judge M, Perlman M. Chronic ankle conditions: Sinus tarsi

syndrome. In: Banks A, ed. Foot and ankle surgery, 3rd Ed, Vol 1; 35:1091–
1092.
4. Taillard W, Meyer JM, Garcia J, et al. The sinus tarsi syndrome. Int Orthop.
1981;5:117–130.
5. Herrmann M, Pieper KS. [Sinus tarsi syndrome: What hurts?] Unfallchirurg.

2008.
6. Duddy RK, Duggan RJ, Visser HJ, et al. Diagnosis, treatment, and
rehabilitation of injuries to the lower leg and foot. Clin Sports Med.
1989;8:861–876.
7. Schwarzenbach B, Dora C, Lang A, et al. Blood vessels of the sinus tarsi

and the sinus tarsi syndrome. Clin Anat. 1997;10:173–182.
8. Mabit C, Boncoeur-Martel MP, Chaudruc JM, et al. Anatomic and MRI study
of the subtalar ligamentous support. Surg Radiol Anat. 1997;19:111–117.
9. Dozier TJ, Figueroa RT, Kalmar J. Sinus tarsi syndrome. J La State Med
Soc. 2001;153:458–461.
10. Mann R, Coughlin MJ. Athletic injuries to the soft tissues of the foot and
ankle. In: Surgery of the foot and ankle, 6th ed. 1993;1165–1166.
11. Giorgini RJ, Bernard RL. Sinus tarsi syndrome in a patient with talipes
equinovarus. J Am Podiatr Med Assoc. 1990;80:218–222.
12. Rab M, Ebmer J, Dellon AL. Innervation of the sinus tarsi and implications
for treating anterolateral ankle pain. Ann Plast Surg. 2001;47:500–504.
13. Shear MS, Baitch SP, Shear DB. Sinus tarsi syndrome: the importance of
biomechanically-based evaluation and treatment. Arch Phys Med Rehabil.
1993;74:777–781.
14. Zwipp H, Swoboda B, Holch M, et al. [Sinus tarsi and canalis tarsi
syndromes. A post-traumatic entity] Unfallchirurg. 1991;94:608–613.
15. Kuwada GT. Long-term retrospective analysis of the treatment of sinus

tarsi syndrome. J Foot Ankle Surg. 1994;33:28–29.
16. Oloff LM, Schulhofer SD, Bocko AP. Subtalar joint arthroscopy for sinus
tarsi syndrome: a review of 29 cases. J Foot Ankle Surg. 2001;40:152–157.
17. Frey C, Feder KS, DiGiovanni C. Arthroscopic evaluation of the subtalar

joint: does sinus tarsi syndrome exist? Foot Ankle Int. 1999;20:185–191.
Codes
ICD9
726.79 Other enthesopathy of ankle and tarsus
Slipped Capital Femoral Epiphysis
Tara Merrit
W. Franklin Sease Jr.
Basics
Description
A disorder of unknown cause in which the proximal femoral epiphysis (head of the femur)
begins to “fall off” the femoral neck.
The slippage occurs at the epiphyseal plate, which begins to weaken as it matures.
There are 4 presentation patterns for SCFE:
Preslip
Acute
Acute-on-chronic
chronic
SCFEs are classified based on the intensity and duration of symptoms present as well as the
radiographic findings.
Epidemiology
The disorder affects 0.2–10/100,000 children.
Predominant age: The mean age at which it occurs is 12 yrs in girls and 13.5 yrs in boys.
Age decreases with increasing obesity.
The disorder is bilateral in 18–63% of affected children.
The disorder frequently occurs in 2 distinct body types: (1) slender, tall, rapidly growing boys
and (2) large, obese boys ± undeveloped sexual characteristics. The 2nd body type is more
prevalent than the 1st.
Pacific Islanders have the highest incidence, followed by African Americans, Hispanics,
Native Americans, Americans, and children of Indonesian/Malay descent.
Risk Factors
Occurs during the rapid growth spurt
Endocrine disorders that weaken the physis are associated with slipped epiphyses and are
particularly prevalent in preadolescent children.
Radiation therapy and renal failure are also associated with slipped capital femoral epiphysis
(SCFE).
Obesity
Etiology
Biomechanical and biochemical factors play a role in SCFE.
Biomechanical factors include obesity, femoral retroversion, and increased physeal obliquity.
Biochemical factors include increased growth hormone during puberty, which increases the
height of the zone of hypertrophy, and increased testosterone, which decreases physeal
strength.

GH deficiency
Hyperthyroidism
Hypothyroidism
Multiple endocrine neoplasia
Panhypopit
Renal failure
Radiation therapy
Diagnosis
Determined by history, physical examination, and anteroposterior (AP) and frog lateral
view radiographs.
It is important to always examine both sides owing to possibility of bilateral disease.
Physical Exam
The most common presenting complaint is hip pain and a limp (antalgic gait). Trendelenburg
test is positive when the patient stands on the affected leg and a downward pelvic tilt occurs
due to hip weakness on the affected side.
The pain typically is located in the groin area and very commonly presents as referred medial
knee pain ± thigh pain.
Pain is usually gradual in onset, and symptoms occur even when minimal displacement is
present. Pain also may occur acutely with a dramatic onset of injury and sudden severe hip
or knee pain and inability to bear weight.
The physical exam reveals tenderness over the hip joint capsule, and an external rotation
deformity of the lower extremity may be present.
There is restricted hip motion, especially internal rotation, abduction, and forward flexion.
The hip tends to rotate externally and abduct as it is flexed (Whitman sign).
In chronic cases, the affected leg may be 1–3 cm shorter than the normal leg, and the thigh
muscles may be atrophied.

Imaging
CT is occasionally useful for grading chronic slips.
MRI is useful for detecting preslips that may be symptomatic but have normal radiographs.
AP and frog-leg lateral views confirm the diagnosis. The affected side always should be
compared with the unaffected leg. Up to 10% of SCFE patients have normal radiographs
initially.
The capital epiphysis is seen to displace posteriorly and downward, whereas the femoral
neck displaces upward and anteriorly. In some patients, displacement is not obvious, but the
physeal plate is widened (preslipping stage).
Classification is based on the severity of the slip. Type 1 slips involve <33% of the width of
the femoral epiphysis. Type 2 involves a 33–50% slip, and a type 3 involves >50% of the
width of the femoral epiphysis.
Femoral cutaneous nerve entrapment (more common in muscular girls)
Proximal femur fracture
Avascular necrosis
Juvenile rheumatoid arthritis
Chondrolysis
Psoas abscess
Legg-Calve-Perthes disease (in younger age range)
Septic joint
Toxic synovitis
Intra-abdominal tumor
Treatment
Long-term treatment
Acute treatment: Orthopedic referral should be made immediately on diagnosis.
Surgical stabilization is the mainstay of treatment for all types of slippages.
Acute treatment involves cessation of weight bearing and surgical stabilization.
A displaced epiphysis may require reduction before fixation.
In the preslip phase, with widening of the physeal plate evident on radiographs,
in situ operative fixation is recommended.
Weight bearing is begun at 6 wks postoperatively.
Ongoing Care
Orthopedic referral should be made immediately on diagnosis.
Prognosis
Prognosis is usually good, except in patients with acute traumatic separation.
Slight shortening of the leg of <1.25 cm may result, along with a mild external rotation
deformity.
The internal fixation devices are removed after the physeal plate closes in 1–2 yrs.
Additional Reading
Aronsson DD, Loder RT, Breur GJ, et al. Slipped capital femoral epiphysis: current
concepts. J Am Acad Orthop Surg. 2006;14:666–679.
Mercier L. Practical orthopedics. St. Louis: Mosby-Year Book, 1995.
Paletta GA, Andrish JT. Injuries about the hip and pelvis in the young athlete. Clin Sports
Med. 1995;14:591–628.
Snider RK, Greene WB, Johnson TR, et al. Essentials of musculoskeletal care. Rosemont,
IL: American Academy of Orthopedic Surgeons, 1998.
Stanitski CL, DeLee JC, Drez D Jr. Pediatric and adolescent sports medicine. Philadelphia:
WB Saunders, 1994.
Codes
ICD9
732.2 Nontraumatic slipped upper femoral epiphysis
Clinical Pearls
In acute traumatic separations, avascular necrosis of the femoral head is a
common complication, and this usually results in severe arthritis of the hip.
Another complication is acute cartilage necrosis or lysis of the articular
cartilage of the hip joint. A painful fibrous ankylosis of the hip joint is frequently
the end result.
All adolescent patients with thigh or hip pain should get x-rays. SCFE can
present unilaterally or bilaterally with only knee or thigh pain; not all cases have
hip pain. Abnormal range of motion may be noted on physical examination. The
recommended radiographs are AP and frog-leg lateral pelvis views, not
individual hip radiographs.
Acute SCFE: Sudden onset severe pain usually of <3 wks' duration that
prevents weight bearing. Usually associated with trauma. Joint effusion and no
metaphyseal remodeling. Examination reveals external rotational deformity,
shortening of the affected limb, decreased range of motion at the hip and
severe pain with attempted manipulation.
Treatment: Immediately make patient non–weight bearing; refer urgently to
pediatric orthopedic surgery
Acute on chronic SCFE: History of at least 3 wks of hip pain and/or limp with a
sudden increase in pain and inability to bear full weight. Patients usually have a
joint effusion and metaphyseal widening.
Treatment: Treat like an acute SCFE. Make patient non–weight bearing, and
refer to pediatric orthopedic surgery.
Chronic SCFE: Most common presentation; vague intermittent symptoms of
hip, thigh, or knee pain, worsened by activity and relieved by rest. Exam reveals
antalgic gait and even a Trendelenburg or waddling depending on whether
unilateral or bilateral. Often the affected foot is turned outward. Often pain with
internal rotation, abduction, and flexion of the hip with reduced movement in
these planes. Metaphyseal modeling is present but no effusion.
Treatment: Make patient non–weight bearing, and refer to pediatric orthopedic
surgery.
Snapping Scapula and Winging of the Scapula
Joseph N. Chorley
Basics
Description
Snapping scapula syndrome (SSS) is a disorder of the scapulothoracic articulation resulting in
crepitation that may or may not be painful. It can be the result of anatomic impediment to
normal scapular motion from weakness, inflexibility, or inadequate proprioception of 1 or more
of the 17 muscles that insert on the scapula. Winging scapula (WS) results from a nerve injury,
usually of the long thoracic (LTN) or spinal accessory nerves (SAN). This results in profound
weakness of the serratus anterior or trapezius muscles, respectively, producing functional
shoulder pain and dysfunction.
Epidemiology
Incidence
SSS is relatively common.
Altered scapular position and motion has been reported in 68–100% of patients with shoulder
injuries.
Prevalence
SSS:
Relatively common
Altered scapular position and motion has been reported in 31% of asymptomatic
individuals.
WS:
Rare
Long thoracic nerve palsy has been reported 15/7,000 electromyelogram (EMG) patients,
1/38,500 orthopedic patients, 3/12,000 neurologic evaluations
Spinal accessory nerve palsy prevalence is difficult to assess.
Etiology
SSS:
Anatomic:
Thoracic rib disorders (fracture with prominent callus or displacement)
Thoracic spine disorder (costovertebral dysfunction, scoliosis, Scheuermann's kyphosis)
Scapular disorders (fracture with prominent callus or displacement, hooked superior
medial edge, osteochondroma)
Soft tissue tumor (elastofibroma)
Inadequate strength, flexibility, and proprioception:
Weakness (mostly in serratus anterior, middle, and lower trapezius)
Inflexibility (mostly in pectoralis minor, levator scapulae, and upper trapezius)
Abnormal firing patterns associated with repetitive motion (asymmetric strength training,
throwing mechanics, swimming technique, etc.)
WS:
Blunt trauma:
LTN: Sudden depression of the shoulder
SAN: Blow over the posterior cervical triangle
Sports related: Archery, ballet, baseball, basketball, bowling, football, golf, gymnastics,
hockey, soccer, tennis, weightlifting, wrestling
Iatrogenic:
LTN: chiropractic manipulation, crutches, surgery
SAN: Surgery to the neck area
Other: Postviral, exposure to toxin or drugs, muscular dystrophy
Diagnosis
History
SSS:
Mechanical sensation, with or without pain, usually along the medial scapular border
(superior inferior > middle)
Classic anterior impingement complaints (pain with overhead activities)
Involved in higher incident sports (baseball, swimming, tennis)
WS:
LTN: Shoulder pain that usually is more toward the upper medial scapula. It may occur a
few weeks after onset of palsy when the trapezius starts to stretch from the unopposing
serratus anterior. Severe pain may occur with postviral neuritis. Burning neuralgic pain at
the inferior scapular pole may occur with acute trauma.
SAN: Stiffness, heaviness, pain, and weakness, especially with overhead activities or
prolonged exertion
Physical Exam
Cervical spine evaluation, including range of motion of the cervical spine, strength, sensation,
deep tendon reflexes in the upper extremity, Spurling's maneuver
Spine and shoulder inspection: Standing and forward flexed, analyzing for asymmetry and
posture
Scapular position:
SSS (may be normal scapular position with classic “teenager posture” with rounded
shoulders, dynamic thoracic kyphosis, forward flexed head, and suboccipital extension)
LTN (scapula is superior and adducted medially)
SAN (drooping shoulder with scapula abducted laterally)
Scapular winging tests:
LTN (entire medial scapula will protrude with shoulder forward flexion or wall push-up)
SAN (superior medial scapula will laterally displace causing downward rotation with
shoulder abduction or resisted external rotation; no winging with shoulder forward flexion)
Range of motion deficit:
LTN (<120 degrees of forward flexion [FF] and 110 degrees of abduction)
SAN (normal FF and <90 degrees of abduction)
Scapular motion with shoulder movement:
Lateral scapular slide test: Patient will place the arms in the resting position (1), hands on
iliac crest (2), and shoulders at 90 degrees abduction in the scapular plane (3). Distance
from the inferior scapular pole to a fixed point on the midline thoracic spine (usually spinous
process of T9) is measured in each position. Scapular dyskinesis is diagnosed when there
is 1.5 cm difference from the opposite side.
Scapular assistance tests: Perform the classic Neer impingement test, which is painful.
Repeat the test with the examiner holding the superior medial scapula down (assisting
serratus anterior) and gliding the inferior scapular pole medially assisting the lower
trapezius), and the pain will not be provoked.
Repeat the test with the examiner holding the medial scapula retracted, and the pain will
not be provoked.
Scapular dyskinesis classification (SSS) based on scapular prominence at rest and with
lateral scapular slide test:
Inferior medial
Entire medial
Superior medial and superior translation
Slightly lower (normal in the dominant arm)

Imaging
Radiographs of the cervical spine, shoulder, chest, and ribs will usually be normal.
CT scans and MRI are rarely necessary unless concern about bone or soft tissue masses.
Isolated left thoracic scoliosis should be evaluated with cervical spine MRI secondary to its
association with congenital anomalies (syringomyelia, Arnold-Chiari malformations).
Electromyography (EMG) is the only definitive diagnostic test for nerve dysfunction and muscle
paralysis associated with WS. Abnormalities such as resting denervation potentials, decreased
motor unit recruitment, and polyphasic motor unit potential with volitional activities.
Electromyography does not correlate with clinical improvement and cannot be used to predict
extent of recovery.
Cervical discogenic neuropathy
Rotator cuff tear
Glenohumeral instability
Suprascapular nerve entrapment
Primary neuromuscular disease
Neurofibromatosis
Primary pulmonary pathology
Treatment
ED Treatment
Acute injury may result in WS, but the symptoms of pain and nerve dysfunction
may not present for a few weeks.
Avoiding painful activities, especially overhead activities, is important.
Brief sling immobilization may be necessary for pain control.
Medication
Analgesic medications may be necessary for acute injuries and severe pain,
like with postviral neuritis.
Subacromial bursa steroid injection and oral anti-inflammatories may be used
with SSS in order to decrease pain while physical therapy is retraining normal
muscle firing patterns.
General Measures
SSS (treat the etiology):
Anatomic lesions (fracture callus, fracture displacement, mass lesion):
Assessment for surgical consultation, depending on their contribution to the
pain and dysfunction.
Thoracic dysfunction: Thoracic scoliosis and Scheuermann's kyphosis may
require bracing and surgery. Segmental thoracic dysfunction (resulting in
malalignment) may benefit from manual manipulation followed by stabilization
rehabilitation.
Scapular dyskinesis: Requires an astute clinician to direct the subtle
relationships that need to be restored. Outlined below are the most common
components of most scapular dyskinesis:
Release the muscular and capsular restrictions:
Glenohumeral posterior capsule tightness with decrease internal rotation
can be improved using the side lying “sleeper stretch.”
Pectoralis minor muscular shortening can be improved with the patient
supine with a towel roll under thoracic spine and a steady posteriorly
directed force on the anterior shoulder.
Improve muscular strength and scapular force couples:
Early rehabilitation will include closed chain exercises like low, middle,
and high rows, and advancing to “scapular clocks,” “wall washes,” and
“punches.”
When a stable scapular base is achieved, open chained exercises can
be incorporated (classic rotator cuff with increasing abduction, scapular
4 directions against manual resistance).
“Pushups with a plus” are effective in strengthening serratus anterior and
plyometrics, and proprioceptive neuromuscular facilitation will complete
most of this phase of rehab.
Return to activity: Correcting technique, overload, and other problems in
the kinetic chain are important as return to activity is considered.
Incorporating the new biomechanics into often-entrenched biomechanics
takes time and an astute team, including the coach, patient, therapist,
and clinician.
WS:
LTN: 75% will respond to conservative management, but will take anywhere
from 6–24 mos. There are some that do not improve serratus anterior firing
but improve their function by muscular compensation with other
scapulothoracic stabilizers (usually trapezius):
In the early phase of rehabilitation, avoid further injury by limiting any
overhead or painful activities.
As pain decreases, progress to gentle range of motion of the shoulder and
scapula to avoid adhesive capsulitis. Avoid stretching the serratus anterior
muscle by limiting passive scapular retraction.
As the serratus strength improves, shoulder girdle strengthening exercises
can be started. Reducing the amount of winging during rehab and everyday
activities is important during conservative treatment.
Scapular bracing may help, but is often restrictive and has poor
compliance. Doing rehab while lying supine will stabilize the winged scapula.
SAN: Conservative management is not as effective. A trial of protection,
bracing, and progression as above is advised for 6–12 mos.
WS: If symptoms continue despite compliant conservative management for 12
(SAN) to 24 mos (LTN), surgical intervention must be considered. Dynamic
muscle transfer procedures show improved function, fewer symptoms of pain
and winging, and are replacing many of the older procedures.
Additional Reading
Forthomme B, Crielaard JM, Croisier JL. Scapular positioning in athlete's
shoulder: particularities, clinical measurements and implications. Sports Med.
2008;38:369–386.
Kibler WB, McMullen J. Scapular dyskinesis and its relation to shoulder pain. J
Manske RC, Reiman MP, Stovak ML. Nonoperative and operative

management of snapping scapula. Am J Sports Med. 2004;32:1554–1565.
Martin RM, Fish DE. Scapular winging: anatomical review, diagnosis, and
treatments. Curr Rev Musculoskelet Med. 2008;1:1–11.
Codes
ICD9
736.89 Other acquired deformity of other parts of limb
Clinical Pearls
Scapular dyskinesis should be considered in patients with shoulder pain.
Whether it is a primary cause or a secondary problem, it is an important
component of restoring shoulder function.
Spinal Stenosis
Stephen J. Rohrer
Basics
Description
Stenosis of the spinal canal is defined as narrowing of the available space within the spinal
canal causing impingement on the neural and/or vascular elements of the spine.
A general consensus defines spinal stenosis as an anteroposterior diameter of <13 mm from
C3 to C7.
Spinal stenosis is also divided into congenital and acquired forms.
It appears to affect men more than women (1).
Epidemiology
Most often occurs in the lumbar spine but can occur in the cervical spine
Rarely occurs in the thoracic spine
Incidence
The absolute incidence of spinal stenosis is unknown, but lumbar spinal stenosis is an
increasing cause of disability in older patients.
Risk Factors
Degenerative changes in the intervertebral disks, ligaments, and facet joints, as well as
osteophyte formation surrounding the canal
Older age
Spondylitic disease of the spine may contribute to stenosis.
Genetics
Genetics play a role in some cases of spinal stenosis in conditions such as
spondyloarthropathies, dwarfism, and spina bifida.
General Prevention
Degenerative changes may not be able to be prevented, but symptom severity may be
limited by maintaining a healthy back.
Core strengthening, appropriate flexibility and posture, and maintaining a healthy body weight
may slow the progression of symptoms.
Etiology
Spondylosis, or degenerative arthritis affecting the spine, is the most common cause of lumbar
spinal stenosis and typically affects individuals over the age of 60 yrs.

Degenerative arthritis
Disk bulging
Facet osteophytes
Ligamentum flavum hypertrophy
Spondylolisthesis
Diagnosis
History
Typically, the earliest complaint is back pain.
Bilateral leg pain often involving the buttocks and thighs and spreading toward the feet
The pain may be described as burning, cramping, or dull fatigue.
Classically, the symptoms of lumbar canal stenosis worsen with ambulation or standing and
are relieved by sitting.
In severe late-stage cases where the sacral roots are impinged, visceral disturbance may
manifest with urinary incontinence.
The history for cervical spinal stenosis may include transient quadriplegia after a tackle or
just bilateral “stingers” (numbness and pain down both arms).
Physical Exam
A broad-based gait is often present.
Abnormal Romberg test
The spine must be examined for abnormal curvature or limitation in range of motion (ROM).
Commonly, flexion relieves symptoms, and extension is painful.
The back should be examined for tenderness, which may suggest a fracture, neoplasm, or
infection.
The straight-leg test should be done to rule out disk herniation. Generally, patients with
lumbar spinal stenosis do not have a positive straight-leg test.
A femoral stretch test where the knee is flexed in a prone position may elicit pain in patients
with spinal stenosis at L3–4.
The physical examination also should include an examination of the skin, nails, and distal
pulses of the feet to evaluate for possible vascular claudication. Patients with vascular
claudication often will have pallor, nail dystrophy, absence of hair, and distal pulses in their
feet. Popliteal and femoral pulses need to be examined.
Cervical spinal stenosis requires a careful active ROM exam of the neck and an upper
extremity neurologic exam.

Imaging
Plain films are not diagnostic but may demonstrate degenerative spine disease or
spondylolisthesis.
In the C-spine, a vertebral canal–vertebral body ratio under 0.8 was defined by Torg as
spinal stenosis. The Torg ratio, however, is not used exclusively to evaluate cervical spinal
stenosis. Even though it carries about a 93% sensitivity, it leads to many false-positive results
and has a poor positive predictive value for predicting cervical cord neurapraxia (2)[C].
CT scans ± intrathecal contrast material injection (CT myelogram) may demonstrate
encroachment of the canal by osteophytes, hypertrophied lamina, or other degenerative
changes.
MRI is currently the preferred method to establish a diagnosis and exclude other conditions.
MRI is both noninvasive and visualizes the soft tissue structures that may be obstructing the
canal (3)[B].
Vascular claudication
Space-occupying lesion such as a neoplasm
Herniated disk
Trauma, eg, compression fracture
Degenerative subluxation of the vertebrae (spondylolisthesis)
Infectious process, eg, diskitis or epidural abscess
Spear tackler's spine:
Developmental narrowing of the cervical spinal canal
Straightening or reversal of the normal cervical lordotic curve
Preexisting minor posttraumatic x-ray evidence of bony or ligamentous injury
Documentation of using spear-tackling techniques
Treatment
Nonsurgical management of lumbar stenosis may be attempted initially in
patients who do not have severe pain or significant weakness. Patients on
warfarin sodium or those who have severe risks for complications with
decompressive surgery may not be candidates for invasive procedures.
NSAIDs and exercises may provide some relief for patients with lumbar spinal
stenosis. Flexion exercises that reduce lumbar lordosis are especially useful.
Morbidly obese patients should be encouraged to lose weight.
Research is limited to suggest support for or against specific nonsurgical
approaches, but studies are currently ongoing.
Pre-Hospital
Management of acute symptomatic cervical spinal stenosis after trauma includes
stabilization of the spine with a cervical collar and transport to an emergency
setting.
Medication
There is little evidence that pharmacologic therapy provides long-term relief in
spinal stenosis (3)[B].
Epidural steroid injections may provide short-term relief (2–3 wks), but long-term
efficacy results are conflicting (3)[B].
Though a systematic review of the literature failed to support physical therapy or
exercises as a stand-alone treatment for lumbar spinal stenosis, experts believe
it to be beneficial for certain patients (3)[V].
In a Cochrane review, spinal manipulation associated with exercise has been
shown to be beneficial for mechanical neck pain (1)[B].
Lumbosacral corset bracing may provide symptomatic relief while walking, but
the symptoms return once the brace is removed (3)[C].
Most patients benefit from decompression of the lumbar canal.
Typically, multilevel decompressive laminectomies are needed because the
canal stenosis often occurs at multiple levels.
Multilevel laminotomies, foraminotomies, and even decompression of the
lateral recesses may be alternative methods of treatment.
Most patients with radiographic and clinical evidence of spinal stenosis get
significant long-term relief from decompressive surgery.
Ongoing Care
Prognosis
According to the North American Spine Society, patients followed for 2–10 yrs with mild to
moderate stenosis have a 20–40% chance of requiring surgical intervention.
Of those who do not have surgery, 50–70% will have improvement in their pain (3)[C].
References
1. Gross AR, Hoving JL, Haines TA, et al. A Cochrane review of manipulation and
mobilization for mechanical neck disorders. Spine. 2004;29:1541–1548.
2. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J
Bone Joint Surg Am. 2002;84-A:112–122.
3. Snyder, D, et al. Treatment of degenerative lumbar spinal stenosis. Am Fam Physician,

August 1, 2004.
Additional Reading
Alvarez JA, Hardy RH. Lumbar spine stenosis: a common cause of back and leg pain. Am
Fam Physician. 1998;57:1825–1834, 1839–1840.
Atlas SJ, Delitto A. Spinal stenosis: surgical versus nonsurgical treatment. Clin Orthop Relat
Res. 2006;443:198.
Bronfort G, Nilsson N, Haas M, et al. Non-invasive physical treatments for chronic/recurrent

headache. Cochrane Database Syst Rev. 2004;CD001878
Cantu RC. The cervical spinal stenosis controversy. Clin Sports Med. 1998;17:121–126.
Garfin SR, et al. Spinal stenosis. J Bone Joint Surg [Am]. 1999;81:573–583.
Martinelli TA, Wiesel SW. Epidemiology of spinal stenosis. Instr Course Lect. 1992;41:179–
181.
Waters, W, et al. Clinical guidelines for multidisciplinary spine care, diagnosis and treatment
of degenerative lumbar spinal stenosis. Nor Am Spine Society, 2007.
Codes
ICD9
723.0 Spinal stenosis in cervical region
724.00 Spinal stenosis of unspecified region
724.01 Spinal stenosis of thoracic region
Clinical Pearls
Experience with the National Center for Catastrophic Sports Injury Research
suggests that athletes with significant cervical spinal stenosis are at increased
risk of quadriplegia and should not participate in contact or collision sports.
Referral to a spine specialist is indicated for competitive athletes wishing to
return to play.
To evaluate a patient with surgical hardware for spinal stenosis, use a CT
myelogram.
Splenic Contusion and Rupture
Eugene Hong
Basics
Description
Splenic injury spectrum includes contusion, hematoma, laceration, and rupture.
Not uncommon in contact and collision sports or with falls during activities, including football,
hockey, lacrosse, biking, skiing, horseback riding, and motorsports.
Epidemiology
Most common abdominal organ injury in sports (1)
May represent up to 50% of all sports-related abdominal organ injuries
1.5 million adults are admitted to hospitals each year in the U.S. following an injury; 2.6%
will have a blunt splenic injury (2).
Risk Factors
Recent or distant history of trauma that may have caused a prior splenic injury that did not
completely resolve (see “Delayed splenic rupture” in “Complications” section below)
Overlying rib fracture
Recent infectious mononucleosis infection resulting in splenomegaly
Etiology
Trauma mechanism resulting in direct or indirect force on the spleen

Liver injury
Rib injury
Kidney injury
Diagnosis
History
Symptoms of hypovolemia: Dizziness, light-headedness, syncope, palpitations, shortness of
breath
Abdominal pain: May be localized to left upper quadrant
Left shoulder pain: Referred via the left phrenic nerve from intraabdominal diaphragmatic
irritation (Kerr sign)
Pain elsewhere also should raise suspicion for concurrent injuries elsewhere, eg, liver, rib,
kidney.
Physical Exam
Vital signs including orthostatics: Serial measurements; assess for stability; relative
tachycardia may be an early sign.
Abdominal tenderness
Abdominal rebound or guarding, consistent with peritoneal irritation from bleeding
Decreased or absent bowel sounds
Avoid palpating spleen aggressively or deeply.
Decreased breath sounds
Rib tenderness, crepitus, or deformity
Costovertebral angle tenderness
Skin discoloration in the periumbilical area (Cullen sign) or flank (Turner sign) may take 24 hr
to appear; both signs are consistent with intra-abdominal bleeding.

Lab
CBC
Type and screen or type and crossmatch in the event that a transfusion is needed.
Serum electrolytes
Consider serial hemoglobin/hematocrits as indicated clinically.
Imaging
Consider abdominal CT scan if splenic injury suspected.
US may not be as sensitive as CT scan in determining severity in splenic injury.
Imaging results will help to assess for the presence and severity of splenic injury.
Severity grading will help to guide management by the American Pediatric Surgical
Association (APSA) Guidelines 2000.
American Association for the Surgery of Trauma Splenic Injury Scale (revised 1994):
Grade I:
Hematoma, subcapsular: <10% surface area
Laceration, capsular tear: <1 cm parenchymal depth
Grade II:
Hematoma, subcapsular: 10–50% surface area, intraparenchymal, <5 cm diameter
Laceration, capsular tear: 1–3 cm parenchymal depth; does not involve trabecular vessel
Grade III:
Hematoma, subcapsular: >50% surface area or expanding; ruptured subcapsular or
parenchymal hematoma; intraparenchymal hematoma >5 cm or expanding
Laceration: >3 cm parenchymal depth or involving trabecular vessels
Grade IV: Laceration: Involving segmental or hilar vessels producing major
devascularization (>25% of spleen)
Grade V:
Laceration: Completely shattered spleen
Vascular: Hilar vascular injury that devascularizes spleen
Advance 1 grade for multiple injuries up to grade III.
Treatment
Pre-Hospital
Transport all patients with suspected splenic injuries to hospital for further
evaluation.
Assess vital signs, and perform complete physical examination.
Assess for other injuries, especially in a trauma setting.
Obtain medical history, if possible.
If the patient is unstable, place 2 large-bore IVs, and begin fluid resuscitation.
Call ahead to advise ED/trauma team of clinical situation.
ED Treatment
Assess hemodynamic stability of patient.
Thorough trauma assessment and workup
Begin resuscitation as indicated clinically.
Type and screen or type and crossmatch in case transfusion is required.
Trauma surgery consultation
Medication
Consider not giving pain medications until after ED/trauma team initial evaluation.
General Measures
Emergent surgical consult and evaluation for all unstable patients with known or
suspected splenic injury for consideration of emergency exploratory surgery
and possible splenectomy
Admission for observation and management for all known splenic injuries
ICU admission for more severe splenic injuries or as indicated clinically
American Pediatric Surgical Association (APSA) Guidelines in Children with
Isolated Spleen Injury Guidelines 2000 [B]: Guidelines for 5 parameters in
management (excludes grade V injuries and unstable patients) (3).
CT grade I:
ICU stay: None
Hospital stay: 2 days
Predischarge imaging: None
Postdischarge imaging: None
Activity restriction: 3 wks*
CT grade II:
ICU stay: None
CT grade III: P.
ICU stay: None
CT grade IV:
ICU stay: 1 day
*Return to full-contact, competitive sports should be at the discretion of the
individual pediatric trauma surgeon. The proposed guidelines for return to
unrestricted activity include “normal” age-appropriate activities (Stylianos, APSA
Trauma Committee, 2000).
Referral
Surgical consultation is indicated for all suspected splenic injuries.
Consider referral to trauma center or pediatric trauma center for evaluation
and management of suspected or known splenic injuries.
Consider emergency exploratory surgery for possible splenectomy for all
hemodynamically unstable patients with known or suspected splenic injury.
Consider surgery for patients with known splenic injury whose clinical course is
worsening.
Splenic artery embolization is being used in some trauma centers in some
select patients (4).
Laparoscopic surgery, if surgery is to be performed, in the nonemergent patient
may be considered.
Ongoing Care
If splenectomy is performed, patient will need pneumococcal [A], meningococcal [B], and
Haemophilus influenzae (Hib) [B] vaccines; give at or after 14 days for emergency
splenectomy, and consider boosters every 5 yrs (5). Also, CDC recommends annual
influenza vaccination in the asplenic population.
Need for follow-up imaging is controversial in the clinically improving patient with a
nonoperatively managed isolated splenic injury. In pediatric patients engaged in normal age-
appropriate activities, follow-up imaging may not be needed after isolated splenic injury (6)
[C]. Further research studies may be required to determine if serial imaging is needed, and
when, before acceptable return to contact and collision sports.
If indicated clinically, consider follow-up or serial imaging with abdominal CT scan in any age
group.
Nonoperative management of stable isolated splenic injuries is appropriate in the majority of
patients.
95–99% of pediatric patients with stable isolated splenic injury grades I–IV can be managed
nonoperatively (7).
70–90% of adult patients with stable isolated splenic injuries can be managed nonoperatively.
Prior recommendation for return to play was 3 mos, in part based on studies looking at
radiographic healing in splenic injuries.
For return to play in pediatric patients, see APSA Guidelines 2000 in “Treatment” section
above.
There are no return-to-play guidelines similar to the APSA Guidelines for the adult population;
it may be reasonable to use APSA Guidelines in this population as well.
As noted in the APSA Guidelines, return to play for full-contact and collision sports should be
based on the individual clinical case and in discussion with the treating physician.
Complications
Possible reinjury or worsening of injury if return to activity too soon or if further
trauma is sustained prior to full recovery
Unknown whether radiologic healing actually equals or translates to full
physiologic healing
Delayed splenic rupture is main complication after nonoperative management
of splenic injury. Occurrence rates vary from <1% to 2% in children and adults.
Delayed splenic rupture, if it occurs, has a 5–15% mortality rate (compared
with the 1% mortality rate with primary splenic rupture) (8).
References
1. Rifat SF, Gilvydis RP. Blunt abdominal trauma in sports. Curr Sports Med
Rep. 2003;2:93–97.
2. Zarzaur BL, Vashi S, Magnotti LJ, et al. The real risk of splenectomy after
discharge home following nonoperative management of blunt splenic injury. J
Trauma. 2009;66:1531–1536; discussion 1536–1538.
3. Stylianos S, et al. Evidence-based guidelines for resource utilization in

children with isolated spleen or liver injury. J Pediatric Surg. 2000;35:164–
169.
4. Rajani RR, Claridge JA, Yowler CJ, et al. Improved outcome of adult blunt
splenic injury: a cohort analysis. Surgery. 2006;140:625–631; discussion
631–632.
5. Webb CW, Crowell K, Cravens D. Which vaccinations are indicated after

splenectomy? J Fam Pract. 2006;55:711–712.
6. Stylianos S. Compliance with evidence-based guidelines in children with

isolated spleen or liver injury: a prospective study. J Pediatr Surg.
2002;37:453–456.
7. Davies DA, Pearl RH, Ein SH, et al. Management of blunt splenic injury in
children: evolution of the nonoperative approach. J Pediatr Surg.
2009;44:1005–1008.
8. Brown, Rebeccah, et al. Observation of splenic trauma: when is a little too

much? J Pediatric Surg. 1999;34:1124–1126.
Additional Reading
Harbrecht BG, Zenati MS, Ochoa JB, et al. Evaluation of a 15-year
experience with splenic injuries in a state trauma system. Surgery.
2007;141:229–238.
Putukian M, O'Connor FG, Stricker P, et al. Mononucleosis and athletic

participation: an evidence-based subject review. Clin J Sport Med.
2008;18:309–315.
Savage SA, Zarzaur BL, Magnotti LJ, et al. The evolution of blunt splenic
injury: resolution and progression. J Trauma. 2008;64:1085–1091; discussion
1091–1092.
Stylianos S, Egorova N, Guice KS, et al. Variation in treatment of pediatric

spleen injury at trauma centers versus nontrauma centers: a call for
dissemination of American Pediatric Surgical Association benchmarks and
guidelines. J Am Coll Surg. 2006;202:247–251.
Codes
ICD9
865.00 Unspecified injury to spleen without mention of open wound into cavity
865.01 Hematoma of spleen, without rupture of capsule, without mention of open wound into
cavity
865.02 Capsular tears to spleen, without major disruption of parenchyma, without mention of
open wound into cavity
Spondyloarthropathies (Seronegative RA)
Brent H. Messick
Kevin E. Burroughs
Basics
Description
Spondyloarthropathy (SpA) is a term applied to the clinical, radiologic, and immunogenetic
features shared by a group of diseases that include:
Ankylosing spondylitis (AS)
Reactive arthritis (ReA)
Psoriatic arthritis (PsA)
Arthritis associated with inflammatory bowel disease (IBD)
Juvenile onset spondyloarthritis
Undifferentiated spondyloarthropathy (USpA):
These conditions are variably associated with the HLA B27 antigen. Individuals with
these conditions frequently exhibit overlapping clinical and radiologic features.
Synonym(s): Seronegative spondyloarthropathies; HLA B27-related spondyloarthropathy
Epidemiology
AS and USpA are the most common types of SpA.
AS and ReA are more common in males.
SpA is seen in all age groups, but most cases present at 20–50 yrs of age.
Incidence
ReA incidence: 0.6–3.1/100,0007 (Level of Evidence 1c)
Prevalence
SpA: 0.5–2% of the Caucasian population
AS: 1–2/1,000
ReA: 1/1,000
PsA develops in 5% of patients with psoriasis.
Risk Factors
Male
Caucasian
Unprotected sex
Positive family history
ReA is significantly increased in persons with HIV.
Genetics
HLA B27 positivity:
AS 90–95%
ReA 80%
USpA: 70%, PsA 40%
IBD-associated 30%
8% of Caucasians and 4% of African Americans are HLA B27-positive.
<20% of HLA B27-positive individuals will develop SpA.
Etiology
Most cases of SpA are associated with HLA B27.
ReA is triggered by an infectious agent (Chlamydia, Ureaplasma, Shigella, Salmonella,
Campylobacter, and others).
Diagnosis
There are 2 criteria for research purposes: European Spondyloarthropathy Study Group
(ESSG) and Amor. However, diagnosis of SpA remains clinical.
History
Inflammatory back pain:
Insidious onset of low back pain before the age of 40
Morning stiffness (>30 min)
Often associated with night pain
Persists for more than 3 mos
Improved with exercise and NSAIDs (inflammatory vs mechanical back pain)
Other joint or enthesis involvement, eye, bowel, skin, mucous membrane, gut, genitourinary
symptoms
Physical Exam
Low back pain at night with prominent early morning stiffness (sacroiliitis, spondylitis)
Peripheral joint pain and swelling (often lower limb and asymmetric)
Pain and inflammation at the insertion of tendons or ligaments (enthesitis), sausage digits
(dactylitis)
Ocular: Conjunctivitis, iritis
GI: Oral ulcerations, gut inflammation
Skin and nails: Psoriasis, keratoderma blennorrhagica, psoriatic nail dystrophy
Genitourinary: Urethritis, cervicitis, circinate balanitis
Constitutional: Fever and weight loss (ReA)
Lumbar spine: Restricted range of motion:
Schober's test: Mark the spinous process of L5 and make a mark 10 cm above that point.
Ask the patient to bend forward. The distance between the 2 points should increase by
more than 5 cm in a normal subject.
Peripheral joints: Tender and/or warm
Enthesitis: Tenderness around the heel (Achilles or plantar fascia)
Skin and nails: Psoriatic nail changes and plaques (scalp, extensor surface of knees)

Lab
Elevated ESR or C-reactive protein
Elevated WBCs in peripheral and synovial fluid:
Note: These studies have poor sensitivity and specificity.
Imaging
Joint space narrowing, signs of inflammation, multiple joint involvement, and distal involvement
in the hands and feet with added features of bone proliferation suggest seronegative
spondyloarthropathy:
Differentiation of these relies on the distribution of radiographic abnormalities and clinical
information.
Peripheral arthritis with soft tissue swelling, juxta-articular osteopenia, joint space narrowing,
and erosions
Areas of periostitis or osteitis are not uncommon (PsA, ReA).
Psoriatic arthritis:
Typically involves the hands, wrists, and feet. Bilateral or unilateral, symmetric or
asymmetric.
Involvement of several joints in a single digit produces the classic “sausage digit.”
Irregular and indistinct appearance of marginal bone about the joint, characterized as
“fuzzy” or “whiskering.” May also see one side of joint thinned, the other broad (“pencil-
and-cup”).
In foot sclerosis, enthesitis, periostitis, and soft tissue swelling can give an “ivory phalanx”
appearance.
At the sacroiliac (SI) joint, advanced changes are usually bilateral and show bone erosions
and narrowing to the point of fusion.
Reactive arthritis:
Similar features to psoriatic arthritis
Lower extremity involvement more common than upper. Sausage digit and pencil-and-cup
deformities can also occur.
In the spine, large, comma-shaped, paravertebral ossification may also be seen.
Ankylosing spondylitis:
More commonly involves the axial skeleton, although peripheral joints can be affected.
The spine findings are characterized by osteitis, syndesmophyte formation, facet
inflammation, and eventual facet joint and vertebral body fusion (bamboo spine of AS).
SI joint disease is bilateral and symmetric, and typically precedes spine involvement.
MRI may detect up to 75% of early sacroiliitis not seen on plain radiography.6 (Level of
Evidence 1b)
Spine involvement is centered at the thoracolumbar or lumbosacral junction. Focal areas of
osteitis become sclerotic and are termed “the shiny corner sign.”
US may show areas of abnormal vascularization of the entheses.
Osteoarthritis
Psoriatic arthritis
Seronegative arthritis
Gout
Septic (gonococcal) arthritis
Sarcoidosis
Treatment
The goal of treatment is to reduce pain and stiffness and maintain posture
and function.
Eye, skin, genitourinary, and bowel involvement should be treated accordingly.
Patients with spondylitis should engage in a lifelong program of exercise to
preserve posture and mobility.
Antibiotic therapy is indicated for proven acute bacterial infections, but does
not reduce arthritis.
Medication
First Line
NSAIDS and topical/intra-articular steroids for acute pain
Second Line
Sulfasalazine for patients that do not respond to NSAIDs.
Disease-modifying antirheumatic drugs: Methotrexate, etanercept, and
infliximab are used for chronic pain and inflammation.4 (Level of Evidence 3a)
Pamidronate for refractory cases
Joint splinting and rest may be indicated for acute flares.
Physical therapy and home exercise plans
Referral
Referral to an ophthalmologist for ocular symptoms because these may require
additional treatments
Joint arthroplasty may be required for those with severe peripheral joint disease.
Additional Reading
Gardner GC, Kadel NJ. Ordering and interpreting rheumatologic laboratory
tests. J Am Acad Orthop Surg. 2003;11:60–67.
Jacobson JA, Girish G, Jiang Y, et al. Radiographic evaluation of arthritis:

degenerative joint disease and variations. Radiology. 2008;248:737–747.
Kataria RK, Brent LH. Spondyloarthropathies. Am Fam Physician.

2004;69:2853–2860.
Mease PJ. Disease-modifying antirheumatic drug therapy for

spondyloarthropathies: advances in treatment. Curr Opin Rheumatol.
2003;15:205–212.
Olivieri I, Salvarani C, Cantini F, et al. Ankylosing spondylitis and

undifferentiated spondyloarthropathies: a clinical review and description of a
disease subset with older age at onset. Curr Opin Rheumatol. 2001;13:280–
284.
Oostveen J, Prevo R, den Boer J, et al. Early detection of sacroiliitis on

magnetic resonance imaging and subsequent development of sacroiliitis on
plain radiography. A prospective, longitudinal study. J Rheumatol.
1999;26:1953–1958.
Townes JM, Deodhar AA, Laine ES, et al. Reactive arthritis following culture-
confirmed infections with bacterial enteric pathogens in Minnesota and
Oregon: a population-based study. Ann Rheum Dis. 2008.
Codes
ICD9
696.0 Psoriatic arthropathy
720.0 Ankylosing spondylitis
721.90 Spondylosis of unspecified site without mention of myelopathy
Clinical Pearls
In most patients, the initial episode of reactive arthritis is short-lived and settles
within weeks to months.
Some may go on to experience recurrent attacks, and these occur more
frequently in HLA B27-positive individuals.
<30%, however, develop a chronic arthritis.
Spondylolysis and Spondylolisthesis
David A. Scott
Kyle J. Cassas
Basics
Description
From Greek, spondylo vertebra + lysis loosening, listhesis slippage
Spondylolysis:
Involves a defect in the pars interarticularis of the vertebral complex
Usually an acquired stress fracture or stress reaction of the lower lumbar spine
Most common cause of significant back pain in athletes
Most commonly involves L5 (85–95% of cases) and L4 (5–15% of cases)
Spondylolisthesis:
Results from anterior displacement of a vertebral body on the subjacent vertebra
Most common segment involved is the L5–S1 level, followed by L4–5. Most cases (80%)
are bilateral.
Defect may be secondary to fracture, arthrosis, or systemic disease.
Epidemiology
Incidence up to 11% in athletic populations; 2–5% in the general population.
Highest incidence in sports emphasizing extension activities (eg, gymnastics, ballet, volleyball,
weightlifting, football, and wrestling)
Peak age of symptomatic onset is 10–15 yrs, although spondylolysis usually originates
between ages 5 and 10 yrs.
By the end of childhood, incidence is estimated to be 6% overall (1).
In the general adult and elderly population, the incidence is roughly 11.5% as measured by
CT (2).
Risk Factors
Possible genetic component
Eskimo population
Male: Female, ratio 2:1
Association with high-risk sports involving repetitive hyperextension forces and rotational
movement on the spine (ie, diving, weightlifters, wrestlers, football lineman, gymnastics, and
track high jump)
Anatomic variations: Spina bifida occulta, transitional vertebrae, and elongated pars intra-
articularis
Etiology
Physical shear forces may account for the etiology of spondylolysis.
Shear forces on the normal lumbar lordosis are increased in extension and accentuated by
combined extension and lateral side-bending.
Genetic factors may play a role:
High incidence (25–69%) demonstrated in studies on twins and 1st-degree relatives
Spondylolysis may be either an overuse injury to the affected vertebral level or a traumatic
fracture.
Vertebral translation can be a source of pain, radiculopathy (spinal nerve injury), or spinal
cord injury.
Degenerative spondylolisthesis is associated with arthritic changes and is seen in adults and
elderly patients.
Isthmic spondylolisthesis is a result of fracture, and is the most common form in athletes.
Diagnosis
Classification of spondylolisthesis:
Isthmic (spondylolytic):
Listhesis caused by breakdown of the pars interarticularis
Most common cause of listhesis, representing up to 50% in some series
Dysplastic (congenital):
Failure of development of the superior facets
Represents 20% of all cases of listhesis
Major slippage can occur.
Degenerative:
Degeneration of the superior facets or disc material
Major cause of spinal stenosis
Traumatic:
Disruption of the posterior elements of the neural arch other than pars (pedicles or
lamina)
Pathologic:
Due to osteoporosis, rheumatoid arthritis, tumor, or infection
Grading of spondylolisthesis:
Grading system proposed by Meyerding in 1932:
Grade I: L5 vertebral body has slipped forward on the sacrum a distance of up to 25%
of its length (or the length of the subadjacent vertebrae).
Grade II: L5 vertebral body has slipped forward a distance of 25–50% of its length.
Grade III: L5 vertebral body has slipped a distance of 50–75% of its length.
Grade IV: L5 vertebral body has slipped a distance of >75% of its length.
Some add grade V to include L5 vertebral body that has slipped off the sacrum; also
termed spondyloptosis.
In addition to grading slips as described above, when monitoring a slip, specific
percentages of listhesis relative to the subadjacent vertebrae should be documented to
track changes.
History
Insidious onset of low back pain is the most common complaint of symptomatic patients.
May note increase in symptoms with an increase in intensity or volume of training
Pain may radiate into the buttocks or thigh, but patients rarely experience radicular signs or
symptoms.
Pain is usually worse with activity, especially extension/lateral side-bending, and alleviated
with rest.
May progress to having pain that becomes more constant and associated with daily activities
Should not usually report numbness, paresthesias, weakness, bowel or bladder changes,
gait disturbance, or constitutional symptoms (fever, weight loss, night pain, or rashes)
Physical Exam
Symptomatic patient may be tender to palpation of the paraspinal musculature or affected
spinal level.
Patient often exhibits hamstring tightness, hyperlordosis.
May exhibit limited range of motion and pain with extension.
Some suggest performing the “stork” test or single leg lumbar hyperextension test:
Pain when a patient stands on one leg and hyperextends the back may indicate active
spondylolysis.
This maneuver creates combined extension/lateral side-bending, which may produce pain.
If significant listhesis is present (grade III or more, see below), may appreciate a step-off
when palpating the spinous processes.
Gait abnormality
Neurological findings are rare.

Imaging
The following are different imaging modalities. Although plain films are valuable, and should be
the starting point for an evaluation, subsequent tests should be chosen on a case-by-case
basis. Influential factors may include duration of pain, index of suspicion for soft tissue lesions,
patient age, and radiation exposure:
Plain films:
May include erect anteroposterior (AP), lateral, and oblique views
Evaluate for number of lumbar vertebrae, scoliosis, spina bifida occulta, transitional
vertebrae, etc.
May be normal in the acute or subacute stage
Oblique films may allow visualization of the “scotty dog.” When visualizing this image,
attention should be paid to the dog's neck. A radiolucent line through the neck may
represent a defect through the pars interarticularis. AP and lateral images may be useful
as well, showing sclerosis and listhesis in some cases, respectively.
Standing lateral x-ray can help with grading of listhesis.
Weight-bearing x-rays may worsen the apparent slip by up to 25%.
On standing AP view, when a large slip has occurred (grade IV/V), an “inverted Napoleon's
hat sign” can be seen, representing the radiographic appearance of spondyloptosis.
Clinically, this puts the cauda equina at risk for compromise.
Triple-phase bone scan:
Often necessary to evaluate the acuity of the injury
Defect may be present on x-ray and not be the cause of symptoms.
X-ray may be negative, while the bone scan demonstrates the defect.
Bone scan can be positive as soon as 48–72 hr after injury.
Test less helpful in older patients, especially those with significant osteoarthritis of the L-
spine due to high-false positive rate.
Not recommended in asymptomatic patients or in patients with symptoms >1 yr
Single-photon emission computed tomographic (SPECT) scan:
Improves resolution of bone scans, especially with SPECT fusion scan
May be more helpful in demonstrating stress reactions at the pars
Advantage: May also help delineate the acute “hot” lesion with potential to heal, vs more
chronic “cold” lesion that may not heal or progress to a fibrous union.
Disadvantage: May not be widely available, and much greater radiation exposure
CT scan:
Useful after SPECT to help stage and determine treatment stratification
Reverse Gantry thin-cut CT at the level seen on bone scan or SPECT activity
Delineates bony pars defect or neural compression
May detect osseus fragments near the pars defect
Advantage: Visualization of bony anatomy, assessment of healing at later interval (6 mos)
Disadvantage: Radiation exposure (50 × plain films)
MRI:
Advantages: Lack of radiation, ability to detect other pathology (diskitis, disc pathology,
tumor).
Sagittal short T1 inversion recovery sequences may reveal early stress reaction or pars
defect.
May see false positives in younger patients secondary to normal bone marrow edema
Some would consider MRI first line vs SPECT scan.
Infection
Tumor
Herniated nucleus pulposus
Spinal stenosis
Treatment
Goal is to return the athlete to pain-free participation in sports along with the
prevention of further slippage and spondylolisthesis. Low-grade slips can often
be treated conservatively; higher-grade listhesis or listhesis in the context of
neurological findings should be referred for surgical opinion.
Relative rest to allow healing has been shown to be effective in young soccer
players (3):
A period of at least 3 mos is generally recommended for acute lesions (4).
Depending upon acuity of lesion, rest may or may not allow healing, but
should help symptoms (4).
For lesions with chronic features on CT, healing is unlikely and rest should
continue until full resolution of symptoms (4).
Some advocate use of braces, such as the thoracolumbar sacral orthosis.
When to use these braces remains controversial
Most suggest using the brace if initial attempts at relative rest, NSAIDs, and
ice do not significantly improve pain.
>83% of patients treated conservatively for spondylolysis and Grade 1
spondylolisthesis had clinical improvement at 1 yr (1)
Reported duration of bracing is variable, ranging from 6 wks to 6 mos. If
bracing is used, it should continue until patient is asymptomatic with all
activities (3).
Patients with positive x-ray and negative bone scan demonstrate a chronic
injury that usually does not need to be braced.
For advanced cases creating substantial pain or neural compromise, surgical
intervention may be indicated, and may include vertebral body fusion. This
procedure carries a risk of “adjacent segment” disease, or arthritic change
above or below the surgical level. Laminectomy and segmental fixation may
also be performed.
Spondylolisthesis:
Higher-grade listhesis, specifically beyond 50%, and any neurological
findings should be evaluated by a surgeon (3).
For cases of higher-grade listhesis, and specifically those with canal
stenosis, surgical intervention has been shown to provide more lasting relief
of pain (5).
Standard surgical intervention in the presence of canal compromise is
decompressive laminectomy with fusion (5)
Initial treatment will include modalities followed by strengthening activity.
Typical rehabilitation includes hamstring stretching and core strengthening (low
back, hip, and abdominal musculature).
Water therapy, including water running, is very helpful when available.
Aerobic conditioning with progression to sport-specific drills.
Indications include:
Slip progression
Persistent pain or gait abnormality despite treatment
Neurologic deficit
High amount of slip in the skeletally immature patient (Grade III/IV or high slip
angle >55 degrees)
Surgical procedure:
Most suggest in situ fusion (ie, fusion of one level of vertebral body to
another).
Postoperative casting/bracing is not generally indicated.
Return to noncontact sports permissible
PRICES: Protection (and Pain medications), Rest Ice, Compression,
Elevation, Support (and strengthening/stretching exercises)
Anti-inflammatory drugs:
Will help decrease symptoms
If one class of NSAIDs does not work, try a different class.
Allow adequate trial of NSAIDs (up to 7 days).
Ongoing Care
Monitor symptoms, gait abnormalities, and radiographic progression.
In the skeletally immature, monitoring is more important, as changes are common during
growth (4).
Some recommend plain x-ray every 6–12 mos in skeletally immature (4).
Most patients with spondylolysis eventually will have mild-to-no symptoms.
X-rays: Data on the timing and frequency of follow-up x-rays are not clear. After skeletal
maturity, progression is less likely.
Risk factors to consider when assessing for slip progression of listhesis:
Clinical factors: Age (10–15 yrs), gender (female), recurrent symptoms, and postural
deformity (gait disturbances)
Radiographic factors: Type of slip (dysplastic spondylolisthesis), degree of slip (Grades
III/IV), and increasing angle of slip
References
1. Klein G, Mehlman CT, McCarty M. Nonoperative treatment of spondylolysis and grade I
spondylolisthesis in children and young adults: a meta-analysis of observational studies. J
Pediatr Orthop. 2009;29:146–156.
2. Kalichman L, Kim DH, Li L, et al. Spondylolysis and spondylolisthesis: prevalence and

association with low back pain in the adult community-based population. Spine.
2009;34:199–205.
3. Purcell L, Micheli L. Low back pain in young athletes. SportsHealth: A Multidisciplinary

Approach. 2009;1:212–222.
4. Standaert CJ, Herring SA. Expert opinion and controversies in sports and musculoskeletal
medicine: the diagnosis and treatment of spondylolysis in adolescent athletes. Arch Phys
Med Rehabil. 2007;88:537–540.
5. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical compared with nonoperative
treatment for lumbar degenerative spondylolisthesis. four-year results in the Spine Patient
Outcomes Research Trial (SPORT) randomized and observational cohorts. J Bone Joint
Surg Am. 2009;91:1295–1304.
Additional Reading
Comstock CP, Carragee EJ. Spondylolisthesis in the young athlete. Phys Sport Med.
1994;22:39–46.
Frymoyer JW. Degenerative spondylolisthesis: diagnosis and treatment. J Am Acad Orthop

Surg. 1994;2:9–15.
Hensinger RN. Current concepts review: spondylolysis and spondylolisthesis. J Bone Joint
Surg. 1989;71A:1098–1107.
Hilibrand AS, Urquhart AG, Graziano GP, et al. Acute spondylolytic spondylolisthesis: risk of
progression and neurological complications. J Bone Joint Surg. 1995;77A:190–196.
Ikata T, Miyake R, Katoh S, et al. Pathogenesis of sports-related spondylolisthesis in

adolescents. Radiographic and magnetic resonance imaging study. Am J Sports Med.
1996;24:94–98.
Jimenez CE. Advantages of diagnostic nuclear medicine. Phys Sports Med. 1999;27.
Johnson RJ. Low-back pain in sports: managing spondylolysis. Phys Sports Med.
1993;21:53–68.
Muschik M, Hähnel H, Robinson PN, et al. Competitive sports and the progression of
spondylolisthesis. J Pediatr Orthop. 1996;16:364–369.
Pizzutillo PD, Hummer CD. Nonoperative treatment for painful adolescent spondylolysis or
spondylo-listhesis. J Pediatr Orthop. 1989;9:538–540.
Radcliff KE, Kalantar SB, Reitman CA. Surgical management of spondylolysis and
spondylolisthesis in athletes: indications and return to play. Curr Sports Med Rep.
2009;8:35–40.
Renshaw TS. Managing spondylolysis: when to immobilize. Phys Sports Med. 1995;23:75–
80.
Stinson JT. Spondylolysis and spondylolisthesis in the athlete. Clin Sports Med.
1993;12:517–528.
Codes
ICD9
738.4 Acquired spondylolisthesis
756.11 Congenital spondylolysis, lumbosacral region
756.12 Spondylolisthesis, congenital
Sports Hernias
Aaron Lee
William W. Briner Jr.
Basics
Description
The sports hernia is a syndrome of chronic pain owing to weakness or injury to the posterior
inguinal canal, conjoined tendon, and common adductor origin.
Described as a “phenomenon of chronic activity-related groin pain that is unresponsive to
conservative therapy and significantly improves with surgical repair” (1)[C]
Historically, it was considered to be an early direct inguinal hernia, but more recently this has
been called into question because there is no palpable hernia on physical exam, and hernia
has not been evident at surgery in these patients. Thus the term sports hernia may in fact be
considered a misnomer (1,2,3)[C].
Synonym(s): Athletic pubalgia; Sportsman's hernia; Inguinal ligament sprain; Gilmore groin;
Footballer's groin/hernia
Epidemiology
Incidence
Unknown; far more common in soccer players
Also described in football, hockey, and baseball players in the U.S. and rugby players abroad
Predominant gender: Males account for >90% of cases.
Risk Factors
Activities with high-speed twisting and turning, such as soccer and rugby
General Prevention
Strength and conditioning programs that stress flexibility, core strength and sport specific
movements have been suggested. There may be a strength imbalance of musculature below
the pubic symphysis over muscles above, so abdominal oblique and rectus strengthening may
be beneficial, however research is currently lacking (1)[C]
Etiology
Pathogenesis is unclear but:
May involve some aspect of congenital inguinal wall weakness
Likely related to overuse with some combination of muscle strength, balance, stability, or
endurance inequality between the abdominal musculature and the adductor muscle group
A resulting tear in the rectus complex and conjoined tendon may extend into the internal or
external ring of the inguinal canal, causing pain and weakness and contributing to the sports
hernia.

Groin pain is often multifactorial. In particular, chronic adductor strain may coexist with athletic
pubalgia.
Diagnosis
History
Early in course, groin pain is felt after activity or toward the end of activity.
As condition progresses, pain is more severe and occurs earlier in activity. Decreased ability
to twist, turn, or stride out is observed. Later in course, pain occurs with running and may
progress to affect daily activities.
Pain may radiate to uninvolved side or scrotum.
Painful intercourse
Pain with coughing/Valsalva maneuver
Often more intense and felt more “internally” than groin strains
Resolves with prolonged abstinence from training but recurs with return to activity
Groin pain with exercise
Exacerbated by sudden movements
Usually unilateral
Often insidious in onset but may occur after sudden tearing sensation
Chronic in nature; may progress to affect daily activities, even getting out of bed
In soccer players, pain worse with long kicks and hard shots
Physical Exam
Inversion of scrotal skin and palpation along inguinal canal is the essential physical exam
technique.
Most tender posteriorly in midinguinal canal and at pubic tubercle
Dilated superficial ring
Inguinal floor tear that may be palpable and cause tenderness inside the external inguinal
ring
Pain worse with Valsalva or sit-ups, with minimal bulging occasionally palpable
Lack of palpable hernia
Also have tenderness of the conjoined tendon
Hip adductor origin tenderness and pain with resisted adduction suggest chronic adductor
strain.
Careful hip/genitourinary exam should be performed.
Palpate pubic symphysis for tenderness that would be consistent with osteitis pubis.

Imaging
There is no diagnostic imaging test for athletic pubalgia. Imaging studies likely will all be
negative if this is the lone diagnosis.
Primarily to rule out other causes of chronic groin pain
Plain films to rule out fracture and pubic symphysis asymmetry
Bone scan/CT scan may identify stress fractures, osteitis pubis.
MRI/MR arthrography may be helpful to identify muscle, tendon, or intraarticular pathology.
MRI survey of the pelvis is recommended initially to identify areas of possible pathology that
allow a more specific, high-resolution, small field of view study to take place (3)[C].
US is emerging as a diagnostic tool, particularly in Europe, but it is highly operator-
dependent; allows dynamic visualization of tissues.
Herniography used in Europe
Inguinal hernia
Chronic adductor strain
Chronic rectus abdominis strain
Bursitis: Especially iliopectineal bursa
Ilioinguinal nerve entrapment
Snapping hip syndrome
Femoral hernia
Femoral neck stress fracture
Pubic ramus fracture
Osteitis pubis
Intraarticular hip pathology
Testicular/ovarian pathology
Referred pain from herniated disk or spondyloarthropathy
Chronic groin pain is often multifactorial. Sports hernia often coexists with one or more of
these diagnoses owing to the close proximity of anatomic structures.
Treatment
Long-term rehabilitation
Special considerations (1)[C]:
Conservative measures may not be effective.
A rest period of 6–8 wks followed by a rehabilitation program focusing on
abdominal oblique and rectus strengthening and hip adductor stretching with
sport-specific functional exercises may be beneficial.
A gradual return to full sports activity should be attempted.
Entire process may take as long as 10–12 wks.
Rehabilitation (1)[C]:
Mainly postoperative
Pelvic strength/flexibility exercises
Non-weight-bearing exercises as tolerated
Return to running at 3–5 wks, avoiding twisting and cutting movements
Return to prior level of activity at 6–8 wks, possibly sooner with close
attention to functional rehabilitation
Herniorrhaphy is the definitive treatment. Anatomic repair of all layers of tissue
must be undertaken. Anchoring sutures to the pubic symphysis are usually
necessary.
Open or laparoscopic surgical techniques have both been reported to be
effective at similar rates.
Laparoscopic technique generally allows for an earlier return to functionality but
may have a slightly lower success rate because the involved structures may
not be fully visualized and repaired (1,2)[C].
References
1. Caudill PH, Nyland JA, Smith CE, et al. Sports hernias: a systematic
literature review. Br J Sports Med. 2008.
2. Johnson JD, Briner WW: Primary care of the sports hernia: Recognizing
an often-overlooked cause of pain. The Physician and Sportsmedicine,
2005;33:35–39.
3. Meyers WC, McKechnie A, Philippon MJ, et al. Experience with “sports

hernia” spanning two decades. Ann Surg. 2008;248:656–665.
Additional Reading
Omar IM, Zoga AC, Kavanagh EC, et al. Athletic pubalgia and “sports hernia”:
optimal MR imaging technique and findings. Radiographics. 2008;28:1415–
1438.
Codes
ICD9
848.8 Other specified sites of sprains and strains
Clinical Pearls
In a true hernia, there is protrusion of bowel into the inguinal canal. A sports
hernia is a weakness or injury of the posterior inguinal canal with no protrusion
of bowel into the canal.
Symptoms are likely to resolve with prolonged rest. Rehabilitation to strengthen
the abdominal muscles may be helpful. However, symptoms often recur with
resumption of activity. Therefore, surgery with herniorrhaphy is the treatment of
choice.
Prognosis:
Studies seem to indicate at least an 80–90% rate of return to prior level of
activity. Although groin pain is often multifactorial, if sports hernia is the only
source of pain, surgery is curative. Although there is no definitive diagnostic
test readily available, surgery is often both diagnostic and therapeutic. If
there are other components to the pain, they also need to be addressed,
ideally prior to surgery.
Sternoclavicular Joint Injury
Alysia L. Green
Douglas Comeau
Basics
The sternoclavicular joint (SCJ) is a saddle-type joint that participates in all movements
of the upper extremity.
The SCJ provides free movement of the clavicle in nearly all planes.
The joint is weakest inferiorly and reinforced superiorly, anteriorly, and posteriorly by the
interclavicular, anterior, and posterior sternoclavicular and costoclavicular ligaments.
Description
Sternoclavicular joint injuries are graded into 3 types:
Grade I: Incomplete tear or stretching of the sternoclavicular and costoclavicular ligaments
Grade II: Complete tear of the sternoclavicular ligament and a partial tear of the
costoclavicular ligament secondary to an anterior or posterior subluxation of the clavicle
from the manubrium
Grade III: Complete rupture of the sternoclavicular and costoclavicular ligaments
The ligaments and capsule of the SCJ contribute to its stability, making it one of the least
dislocated joints in the body.
Dislocations are primarily due to trauma from vehicular or athletic injuries; congenital
dislocations are extremely rare.
Epidemiology
Incidence
Overall incidence is higher in males than in females.
Incidence is increased in young adult males.
Etiology
Anterior dislocation is much more common than posterior dislocation (9:1 ratio):
Caused by an anterolateral force compressing the shoulder that rotates the shoulder
backward and transmits stress to the joint
Posterior dislocation is caused either from a direct anterior-to-posterior blow to the medial
clavicle or from a posterolateral force compressing the shoulder followed by forward rolling.
Posterior dislocation is a surgical emergency and has an estimated 25% complication rate:
Compression of trachea, esophagus, and great vessels in the mediastinum demand
immediate reduction.
Diagnosis
Elicit mechanism of injury, time from injury, and initial symptoms.
Respiratory, neurologic, and vascular assessments mandatory
Appropriate analgesia for patient comfort
History
Mechanism of injury: Direct trauma (motor vehicle accident, athletic injury), falls, dislocations
can also be secondary to congenital, degenerative, and inflammatory processes
Symptoms: Chest and/or shoulder pain exacerbated by arm movement or by lying down,
dyspnea, dysphagia, or paresthesias
Physical Exam
Patient presents with the affected arm foreshortened and supported across the chest by
opposite hand
Inability to abduct or externally rotate the affected arm because of severe pain over
sternoclavicular junction
In anterior dislocation, medial end of the clavicle is visibly prominent, palpable, and may be
fixed or mobile
In posterior dislocation, loss of normal inner prominence of the clavicular head may be
masked by significant local swelling:
Head tilted toward injured side because of spasm of the sternocleidomastoid muscle
Venous congestion in the neck or upper extremities, diminished pulses on affected
extremity, shortness of breath, hoarseness, dysphagia, or signs of shock may suggest life-
threatening impingement of the posteriorly displaced clavicle upon vascular structures in
the mediastinum.
Check vital signs and perform a complete neurovascular examination of the affected
extremity.
True dislocations of the SCJ are extremely rare in children because of the strong ligamentous
attachments about the medial physis.
The medial physeal growth plates of the clavicles may not be radiographically apparent until
age 18 and generally fuse between ages 22 and 25. It is the last physis to close.
Presumed SCJ dislocations are often actually fractures through the medial physis.
In patients <25 yrs of age, SCJ dislocations are classified as Salter-Harris type I or type II
fractures.

Routine radiographs can be difficult to interpret and may appear normal.
In patients with posterior dislocations, a plain chest radiograph is needed to rule out possible
pneumothorax.
Rockwood view (serendipity view): A specialized view that allows for better visualization of
the position of the medial clavicle:
X-ray beam aimed at manubrium in a 40° caudal tilt
CT scan is the best study to evaluate the SCJ:
Useful in the emergency department when plain films are inconclusive
Accurately differentiates fractures from dislocations
Demonstrates the position of the medial end of the clavicle in relation to the structures in
the mediastinum
Shows detailed anatomy of the structures of the thoracic outlet and mediastinum
Sternoclavicular sprain/subluxation
Medial clavicle fracture
Rib fracture
Septic joint
Osteoarthritis
Treatment
During childhood, the medial physeal growth plate of the clavicle provides 80%
of longitudinal bone growth.
Fractures in the medial clavicle have tremendous capability for healing and
remodeling.
Nonunion and significant malunion rarely occur.
Anteriorly displaced fractures of the medial clavicle that mimic SCJ dislocation
can be placed in a figure-8 splint without reduction.
Posteriorly displaced fractures uniformly require reduction and should be
considered a surgical and orthopedic emergency.
Pre-Hospital P.
The close proximity of the sternum and clavicle to vital structures of the neck
and chest predispose patients with sternoclavicular joint injuries to additional
severe and life-threatening injuries.
ABCs must 1st be addressed in these patients.
Vital signs and an initial neurovascular examination should be completed.
For patients with isolated sternoclavicular joint injuries, the affected extremity
should be splinted and immobilized to stabilize the joint and minimize pain prior
to transport to the hospital.
ED Treatment
Anterior dislocations may be reduced in the emergency department (ED) (1)
[A].
Conscious sedation is necessary for pain control and muscle relaxation.
A rolled towel is placed between the shoulder blades in the supine position:
Longitudinal traction is applied to the ipsilateral arm in the extended position
with the shoulder abducted at 90°.
An assistant can maintain gentle inward pressure over the displaced medial
end of the clavicle.
After reduction, immobilization is achieved using a well-padded figure-8
dressing.
Many anterior dislocations remain unstable after reduction; however, open
reduction and internal fixation is rarely indicated, as the deformity is mainly
cosmetic without functional loss.
Posterior dislocations require prompt reduction, best achieved in the operating
room (OR) under general anesthesia (1)[A]:
If an appropriate surgeon is not immediately available to reduce a posterior
dislocation in the OR, reduction may be attempted in the ED to relieve
serious airway, neurologic, or vascular compromise.
After adequate sedation, a small incision is made directly over the medial
head of the clavicle.
A sterile towel clamp can carefully be used to encircle the medial clavicular
head and gentle anterior traction applied to reduce the dislocation.
A surgical consultant should subsequently evaluate the patient.
Medication
Anti-inflammatory agents and analgesics are the drugs of choice to decrease
inflammation and reduce pain:
Acetaminophen: 500–1,000 mg q6–8h PRN
Ibuprofen: 400–800 mg q4–8h PRN with meals
Acetaminophen 300 mg with codeine: 30 mg q6h PRN
Propoxyphene and acetaminophen: 1–2 tabs q4h PRN
Hydrocodone and acetaminophen: 1–2 tabs q4–6h PRN
Patients in respiratory distress require endotracheal intubation and immediate
reduction.
Emergent reduction is also needed in patients with hoarseness, dysphagia, or
neurovascular compromise (upper extremity weakness, paresthesia,
diminished pulses, signs of shock).
Patients with posterior dislocations represent true orthopedic and surgical
emergencies, and appropriate consults should be obtained promptly.
Appropriate analgesia (eg, narcotics or NSAIDs) necessary for pain control
Admission Criteria
All posterior dislocations of the SCJ require admission for prompt reduction in the
operating room and evaluation for potential intrathoracic complications.
Discharge Criteria
Anterior dislocations of the SCJ that can be reduced and splinted, in the absence
of neurovascular compromise, may be discharged with appropriate orthopedic
follow-up.
Ongoing Care
Patient Monitoring
Patients with sprains should initially restrict activity, and depending on the amount of pain or
discomfort, a sling can be used for immobilization.
Reductions performed in the ED require stabilization of the affected shoulder with a soft
figure 8 or sling. Immobilization for 4 wks.
Anterior dislocations should restrict activity and follow up with their physician as directed.
Patients with posterior dislocations who are discharged home should return for medical care
if they exhibit symptoms of mediastinal injury.
Prognosis
Prognosis depends on extent and type of joint damage, but most patients have adequate upper
extremity function following SCJ injuries.
Complications
Tracheal rupture
Pneumothorax
Laceration of superior vena cava
Occlusion of the subclavian artery
Recurrent dislocation
Deformity
References
1. Cope R, Riddervold HO, Shore JL, et al. Dislocations of the
sternoclavicular joint: anatomic basis, etiologies, and radiologic diagnosis. J
Orthop Trauma. 1991;5:379–384.
Additional Reading
Bicos J, Nicholson GP. Treatment and results of sternoclavicular joint injuries.
Clin Sports Med. 2003;22:359–370.
Cope R. Dislocations of the sternoclavicular joint. Skeletal Radiol.

1993;22:233–238.
Gardner MA, Bidstrup BP. Intrathoracic great vessel injury resulting from blunt
chest trauma associated with posterior dislocation of the sternoclavicular joint.
Aust N Z J Surg. 1983;53:427–430.
Gobet R, Meuli M, Altermatt S, et al. Medial clavicular epiphysiolysis in

children: the so-called sterno-clavicular dislocation. Emerg Radiol.
2004;10:252–255.
Lewonowski K, Bassett GS. Complete posterior sternoclavicular epiphyseal
separation. A case report and review of the literature. Clin Orthop Relat Res.
1992;84–88.
Winter J, Sterner S, Maurer D, et al. Retrosternal epiphyseal disruption of

medial clavicle: case and review in children. J Emerg Med. 1988;7:9–13.
Codes
ICD9
839.61 Closed dislocation, sternum
848.41 Sternoclavicular (joint) (ligament) sprain
Subconjunctival Hemorrhage
Holly McNulty
Steven Paul
Anna Waterbrook
Basics
Description
Rupture of small vessels leading to an accumulation of blood in the subconjunctiva, the
potential space between the conjunctiva and the sclera
Synonym(s): Conjunctival hemorrhage
Epidemiology
One of the most frequently encountered eye problems in primary care offices; accounted for
2.9% of visits to outpatient eye clinics in 1 study.
Risk Factors
Sudden increase in ocular pressure, which may result from coughing, sneezing, vomiting, or
straining
Uncontrolled HTN
Acute conjunctivitis
Vigorous eye rubbing
Aspirin or other anticoagulant use
Underlying hematologic or systemic disease
Diagnosis
History
No visual changes
Eye trauma, including rubbing
Use of aspirin or other anticoagulant
Medical conditions leading to increased intraocular pressure or straining, including
uncontrolled HTN, constipation, prostatic hypertrophy, cough, sneezing, and vomiting
Exercise or activities involving exertional straining (ie, weightlifting, etc.)
Diagnosis of or symptoms suggestive of bleeding disorders, such as easy bruising,
menorrhagia, etc.
Physical Exam
Asymptomatic
Extreme redness of eye without change in vision
Extensive subconjunctival hemorrhage may cause a protruding sac of blood, possibly beyond
the lid margin.
Bright red area of blood, either focally or diffusely in potential space under conjunctiva
BP measurement to evaluate for uncontrolled HTN (1)[C]
Stigmata of bleeding or other hematologic disorders (petechiae, bruising, etc.)
Associated signs suggestive of acute hemorrhagic conjunctivitis
Acute hemorrhagic conjunctivitis: A highly contagious disease caused by enterovirus 70 and
coxsackievirus A24. Pain, photophobia, blurred vision, and epiphora develop acutely, with
80% developing bilateral disease within 24 hr. Ocular signs may include subconjunctival
hemorrhage as well as discharge, punctate corneal epithelial keratitis, and lid edema.
Patients also may complain of fever, headache, upper respiratory infection symptoms, and
myalgia, and may have tender preauricular lymphadenopathy. Symptoms usually resolve
without treatment over 5–7 days, with persistent subconjunctival hemorrhages resolving over
an additional 1–2 wks.
Scleral rupture should be suspected in a posttraumatic patient with a bullous subconjunctival
hemorrhage, especially in the presence of blood in the vitreous, decreased intraocular
pressure, or a shallow anterior chamber.
Orbital hemorrhage may present with massive subconjunctival hemorrhage as well as
proptosis and limitation of extraocular movements, usually after trauma.
Infrequently, adenoviral conjunctivitis, bacterial conjunctivitis, and even allergic conjunctivitis
may present with an associated subconjunctival hemorrhage.
Treatment
No analgesia; condition is self-limited.
Condition is nonpainful, so the presence of pain should alert examiner to more
serious condition
Topical steroids are contraindicated, especially with suspicion of acute
hemorrhagic conjunctivitis, due to risk of clinical deterioration and permanent
side effects.
General Measures
Reassurance: Hemorrhages usually resolve spontaneously in 1–3 wks.
Further treatment should be directed at reduction of risk factors and treatment
of any identified underlying etiology (bleeding problems, HTN).
Treat secondary bacterial conjunctivitis and allergic conjunctivitis as indicated.
Ongoing Care
Consider ophthalmology consultation if history of ocular trauma is present or in the presence
of associated ocular injury.
Consider hematology consultation if hemorrhages are idiopathic and recurrent.
References
1. Pitts JF, et al. Spontaneous subconjunctival haemorrhage a sign of hypertension? Br J
Ophthalmology. 1992;76:297–299.
Additional Reading
Fukuyama J, Hayasaka S, Yamada K, et al. Causes of subconjunctival hemorrhage.
Ophthalmologica. 1990;200:63–67.
Goroll AH, May LA, Mulley AG Jr, eds. Primary care medicine. Philadelphia: JB Lippincott,
1995.
Kaimbo W, Kaimbo D. Epidemiology of traumatic and spontaneous subconjunctival

hemorrhage in Congo. Bull Soc Belge Opthalmol. 2009;311:31–36.
Pavan-Langston D, ed. Manual of ocular diagnosis and therapy, 4th ed. Boston: Little,
Brown, 1996.
Tatsuya M, et al. Subconjunctival hemorrhage and conjunctivochalasis. Opthalmology,

Article in Press, 2009.
Wright PW, Strauss GH, Langford MP. Acute hemorrhagic conjunctivitis. Am Fam
Physician. 1992;45:173–178.
Codes
ICD9
372.72 Conjunctival hemorrhage
Clinical Pearls
Most cases resolve completely over the course of 1–3 wks.
Subungual Exostosis and Hematoma
Kathleen Weber
Basics
Description
Subungual exostosis: Solitary, benign, bony growth from the distal phalanx's terminal tuft
commonly causing deformity of the nail (1)
Subungual hematoma: Acute, traumatic, subungual collection of blood, manifested by an area
of black or blue discoloration, usually caused by a direct blunt impact or chronic, repetitive
stresses to the nail unit (2)
Synonym(s) for subungual hematoma: Tennis toe; Jogger's toe; Sportsman's toe
Epidemiology
Subungual exostosis:
Relatively uncommon (1,3)
Seen more commonly after the 2nd and 3rd decades of life (1)
Usually affects the great toe, but can occur on the lesser toes or, rarely, a finger (1)
Risk Factors
The cause of subungual exostosis is unknown (3).
Suggested causal factors include trauma (3), tumor, chronic infection, or hereditary
abnormality.
General Prevention
Subungual hematoma:
Well-fitted footwear with a snug midfoot and a wide toe box
Keep nails trimmed.
Orthotic devices
Etiology
Repeated contact of the toes with the front of the shoebox causes toenail dyshesion and
subsequent hemorrhage (4).
If the activity continues, it may lead to chronic nail dystrophy, nail loss, and callus formation of
the tip of the toe (4).
Subungual hematomas are seen more commonly in sports that require frequent pivoting,
abrupt stops, or repetitive kicking (eg, basketball, handball, racquet sports, soccer, football,
running).
Trauma (eg, fingertip slammed in a car door, hammer blow, or blunt trauma)
Diagnosis
Pain and swelling over the exostosis can affect gait.
Pain associated with trauma is common because the tumor protrudes and is easily
traumatized.
History
Inquire whether the pigment was present at birth or acquired.
Specific questions pertaining to athletic activities, recent trauma, and physical exertion
Obtaining a thorough medication history of any medications may help identify drugs that may
contribute to abnormal nail pigmentation.
Physical Exam
Gait may be affected secondary to pain and swelling related to the subungual bony
growth.
Direct trauma to a protruding exostosis may elicit significant pain.
Subungual hematoma:
Collection of blood, reddish to reddish-black pigmentation, under the nail with or without
edema/erythema
Can be extremely painful with throbbing pain
Hematoma may be painless with minor trauma.
Presence of a firm mass noted at the distal portion of the terminal phalanx
Nail plate can be elevated laterally by the tumor, but is rarely injured.
Pain elicited with direct pressure
Subungual hematoma:
Examine nail unit and the periungual skin (5).
May note a callus on the skin distal to the affected nail.
Observe for any extension of discoloration from under the nail plate into the proximal
nailfold and nail matrix (Hutchinson melanotic whitlow sign); suspect subungual melanoma.
The pigment in a subungual hematoma is homogenous in distribution, while melanocytic
lesions have cellular inclusions (5).
Toes most likely affected in sport-specific pattern are:
“Tennis toe”: More commonly lateral nail of the hallux or 2nd toe, depending on which is
longer
“Jogger's toe”: 2nd through 5th toes
Kicking sports: 2nd or 3rd toe

Imaging
Radiograph mandatory if hard subungual mass noted on examination
A subungual exostosis and an enchondroma may involve the distal portion of a phalanx with
associated nail changes.
Radiographs differentiate an exostosis from an enchondroma.
Radiographically, an exostosis is a bony outgrowth projecting from the distal phalanx's tuft,
while a radiolucent enchondroma results in expansion of the phalanx itself.
Subungual hematoma:
Anteroposterior, lateral, and oblique radiographs should be obtained when a hematoma
involves >25% of the visible nail to assess for fracture.
Obtain radiographs when a fracture is suspected.
A chronic nontraumatic lesion may require a biopsy of the underlying nail matrix and/or nail bed
to rule out a pigmented lesion.
Subungual exostosis (1):
Subungual osteochondroma: Histologically, the exostosis has a fibrous cartilage cap over
the bony growth and the osteochondroma has hyaline cartilage (6).
Fibroma
Subungual verruca vulgaris
Glomus tumor
Enchondroma
Multiple exostosis: Consider an autosomal-dominant multiple exostosis syndrome.
Subungual hematoma (5):
Subungual benign and malignant tumors (eg, melanoma)
Onychomycosis
Glomus tumor (extremely painful nodule under the nail; pain worse when exposed to cold
temperatures)
Subungual exostosis
Treatment
Excision of tumor (1)[C]
Subungual hematoma:
Immediate elevation and application of ice or immersion in ice water may
reduce pain and bleeding.
An acute subungual hematoma can be evacuated by puncturing the nail plate
overlying the hematoma using thermal cautery, laser, or a drill (ie, 18-gauge
needle, scalpel blade, dental bur) (2,4,7)[C].
Evacuation is performed by directing the preferred heated trephine
perpendicular to the nail plate overlying the hematoma; slow and gentle
pressure is applied until blood is expressed from the nail plate.
Nail removal if the normal architecture of the nail plate or its surrounding
structures has been damaged (2,7)[C]
Wound repair if needed (7)[C]
Referral
Chronic lesions should be referred for evaluation for the possibility of a
subungual melanoma.
Ongoing Care
Further evaluation with radiographs (exclude exostosis) and possibly a biopsy are required
when a suspected subungual hematoma does not grow out distally as the nail plate grows, or if
there is recurrence of the hematoma (5).
Patient Education
Subungual hematoma:
To prevent infection following a trephination of the hematoma, instruct the patient on proper
wound care, including:
Observing and reporting any signs of infection
Keeping the area clean and dry
Avoidance of swimming, hot tub, and whirlpool use
Inform the patient that they will eventually lose the affected nail and a new nail will grow out,
typically within 2–6 mos.
Wear well-fitted footwear with a snug midfoot and a wide toe box.
Keep nails trimmed.
Orthotic devices if appropriate
Prognosis
Prognosis for both a subungual exostosis and a hematoma is excellent.
Complications
Infection, although an uncommon complication, following an excision of a
subungual exostosis or an evacuation of the hematoma of a subungual
hematoma may occur.
Recurring subungual hematomas of the same nail bed secondary to repetitive
trauma may predispose the nail bed to onychomycosis.
References
1. Guarneri C, Guarneri F, Risitano G, et al. Solitary asymptomatic nodule of
the great toe. Int J Dermatol. 2005;44:245–247.
2. Salter SA, Ciocon DH, Gowrishankar TR, et al. Controlled nail trephination
for subungual hematoma. Am J Emerg Med. 2006;24:875–877.
3. Campanelli A, Borradori L. Images in clinical medicine. Subungual
exostosis. N Engl J Med. 2008;359:e31.
4. Cordoro KM, Ganz JE. Training room management of medical conditions:

sports dermatology. Clin Sports Med. 2005;24:565–598, viii–ix.
5. Braun RP, Baran R, Le Gal FA, et al. Diagnosis and management of nail
pigmentations. J Am Acad Dermatol. 2007.
6. Lee SK, Jung MS, Lee YH, et al. Two distinctive subungual pathologies:
subungual exostosis and subungual osteochondroma. Foot Ankle Int.
2007;28:595–601.
7. Batrick N, Hashemi K, Freij R. Treatment of uncomplicated subungual

haematoma. Emerg Med J. 2003;20:65.
Codes
ICD9
726.91 Exostosis of unspecified site
923.3 Contusion of finger
924.3 Contusion of toe
Clinical Pearls
Remember that not all dark patches under the nail are subungual hematomas.
Consider the diagnosis of melanoma and other tumors when the history of
trauma and the physical examination are not consistent with a simple subungual
hematoma.
Sudden Cardiac Arrest: Commotio Cordis
Kevin E. Elder
Basics
Alert
Early resuscitation with cardiopulmonary resuscitation (CPR)/defibrillation improves survival;
however, even with early resuscitation within 2–3 min survival is only 25%.
Description
Commotio cordis (CC), Latin for “disturbance of the heart,” is blunt, nonpenetrating trauma to
the precordium, which results in an irregular heart rhythm such as ventricular tachycardia or
ventricular fibrillation (VF). This is a rare event, but must be considered secondary to its lethal
nature.
Epidemiology
This condition occurs primarily in young males, with the highest incidence in sports such as
baseball and hockey; however, it can be seen in sports such as softball, lacrosse, and
soccer as well. It may occur in any sport with male or female participants whereby a blow,
via contact with another player, or via the ball/puck exerts a sudden impact to the precordial
region.
Commotio cordis was 1st described in 1763, and at least 190 cases have been documented
in the U.S. alone.
It is the 2nd most common cause of sudden cardiac death in athletes younger than 35.
Greater recognition of this condition has led to improved reporting of it.
The prevalence is higher in competitive sports, with nearly half of the cases occurring during
competitive sports. The mean age is 15.6 ± 6.5 yrs, with young males 4–18 at greatest risk
(1).
Youth baseball accounts for most of the cases.
Incidence
60% of reported CC events involve sports.
>190 cases of CC in the U.S. Only 5 reported prior to 1983; thought to be related to lack of
recognition/underreporting.
20% of sudden cardiac death (SCD) cases (77 of 387)
Occurs mostly in competitive sports, with highest incidence in youth baseball (1)
25% of CC cases in youth baseball were from a pitch traveling 30–50 mph.
Prevalence
CC is the 2nd most common cause of SCD in young athletes, 2nd only to hypertrophic
cardiomyopathy.
There has been an increase in reported cases of this condition, with only 5 cases reported
prior to 1983; however, there are more than 180 cases reported in the CC registry today (2).
Decreased prevalence of CC prior to 1983 felt to be related to lack of
recognition/underreporting.
47% of cases occur during competitive sports, with total of 60% occurring with all sports
participation.
Risk Factors
Participation in competitive sports known to have a greater risk of CC.
Harder projectiles used in certain sports are more likely to cause CC, with use of standard
baseballs and pitches with speeds between 30 and 50 mph carrying the highest incidence of
developing the insult.
Velocities above and below this range did not seem to carry the same risk.
Use of protective equipment has not been demonstrated to offer adequate protection from
CC.
Genetics
No specific genetics have been attributed to the condition. Increased chest wall pliability in
the most vulnerable age group of young males may play a role.
It is unclear why there is a male predilection for this condition, aside from increased relative
participation in competitive youth baseball relative to females.
General Prevention
The U.S. Consumer Product Safety Commission recommends use of softer “safety
baseballs” to reduce the risk of soft tissue trauma (3). These “safety baseballs” reduced the
risk of onset of VF after precordial impact in a swine model study, and there is a linear
correlation between CC events and the relative hardness of a baseball (4)[B]. However,
safety baseballs have not been proven to eliminate risk of CC.
Doerer et al. and Weinstock et al. have demonstrated that chest protectors (commonly worn
by catchers) in baseball did not prove to be effective in eliminating cases of CC (5). Only
13% of victims who were wearing chest protectors survived a CC event. It is theorized that
malpositioning of equipment (when the athlete moves or raises his hands) may contribute to
this failure. A swine model by Link et al. revealed that commercially available chest
protectors did not prevent CC (6).
Changes in coaching techniques to eliminate chest blocking are theorized to potentially
reduce CC events.
Public health measures, such as parents/coaches learning CPR, and the increased availability
and use of automated external defibrillator (AED) may provide the biggest impact on
improving CC outcomes, but cannot necessarily prevent onset of CC due to the
pathophysiology of condition.
Etiology
Impact to the precordium during the vulnerable period of the repolarization upslope of the T-
wave (10–30 ms before the T-wave peak) may lead to VF. VF is the most common initial
rhythm in CC.
A study by Link et al. demonstrated that low energy impact, directly over the heart,
specifically over the center of the left ventricle (LV), carries the highest risk. Blows at
noncardiac sites in this study did not generate VF (7).
The role of projectile speed and projectile hardness has been discussed. The ideal projectile
speed and hardness create an ideal energy transfer that potentiates this often-lethal
condition.
Causative theories on predisposition to VF/CC include rapid rises in LV pressures to forces
between 250 and 450 mm Hg that may potentiate the associated arrhythmia. Stretch
channels may be activated due to associated myocardial stretch with impact, and potassium
adenosine triphosphate channel activation has been implicated (8).
Critical mass of projectile leading to higher velocity impacts tends to lead to myocardial
damage as opposed to myocardial activation.
Sympathetic activation occurring during sports participation may increase the likelihood of
CC, but this has not been substantiated in research studies.

Contusio cordis
Myocardial contusion with tissue damage
Rule out other causes of SCD causing arrhythmia such as hypertrophic cardiomyopathy
(HCM).
Diagnosis
History
Witnessed trauma to the precordium followed by collapse should elicit suspicion of CC,
especially when occurring during highest-risk sports in young athletes.
Physical Exam
Physical exam is best aided by use of an AED to determine that the athlete has developed the
potentially lethal arrhythmia associated with CC. A more thorough physical exam in the acute
setting is impractical. Any physical exam should be focused on institution of advanced cardiac
life support (ACLS) protocols, with use of AED as soon as possible.

There are no specific labs/imaging tests to aid in diagnosis.
CC is a diagnosis made based on witnessed precordial blow and confirmed by AED
recognition of subsequent arrhythmia.
Autopsy is notable for absence of any significant cardiac or thoracic injury.
HCM
Long QT syndrome
Wolff-Parkinson-White syndrome
Arrhythmogenic right ventricle dysplasia
Brugada syndrome
Dilated cardiomyopathy
Marfan syndrome
Aortic valve stenosis
Myositis
Asthma
Heat stroke
Drug abuse (1)[C]
Treatment
Treatment consists of immediate institution of ACLS protocols, including
implementation of an AED after a witnessed event. Early defibrillation is
critical to survival with CC, as empirically demonstrated in swine models.
However, the total survival of CC is only 15% (9,10)[C].
All CC survivors should be referred to a cardiologist for evaluation to include 12-
lead electrocardiogram, ambulatory Holter monitor, exercise stress test, and
echocardiogram (1)[C].
Ongoing Care
Patient Monitoring
All patients should be admitted to the hospital for observation and monitoring after a CC
event to undergo complete cardiac evaluation (11)[C].
Patients should be followed after discharge to assess for potential cardiac or neurologic
deficit.
Patient Education
An individual athlete's susceptibility to CC should be considered in any return to play
decisions regarding contact sports.
Decisions are made on a case-by-case basis, with consideration given to residual cardiac
deficit, neurologic deficit, or other morbidity. Cardiology consultation should be involved in
these decisions (4)[C].
Maron et al. demonstrated that 71% of CC survivors achieved complete physical recovery
(10).
Prognosis
CC is a condition that carries a grave prognosis. Despite use of ACLS protocols, the
condition is often lethal. Immediate recognition of condition and use of AED to abolish cardiac
arrhythmia may allow improved survival and decreased subsequent morbidity.
As the availability and use of AEDs during athletic participation occurs, their effectiveness
may be further measured in future studies.
Complications
Neurologic impairment may occur secondary to cerebral hypoperfusion.
Cardiac injury resulting in decreased left ventricular ejection fraction
References
1. Palacio LE, Link MS. Commotio Cordis. Sports Health. 2009;1:174–179.
2. U.S. National Registry for Sudden Death in Athletes:

www.suddendeathathletes.org
3. Link MS, et al. An experimental model of sudden death due to low-energy

chest-wall impact (commotio cordis). N Eng J Med. 1998;338:1805–1811.
4. Link MS, et al. Reduced risk of sudden death from chest wall blows
(commotio cordis) with safety baseballs. Pediatrics. 2002;109:873–877.
5. Doerer JJ, et al. Evaluation of chest barriers for protection against sudden
death due to commotio cordis. Am J Cardiol. 2007;99:857–859.
6. Weinstock J, et al. Failure of commercially available chest wall protectors to

prevent sudden cardiac death induced by chest wall blows in an experimental
model of commotio cordis. Pediatrics. 2006;117:e656–662.
7. Link MS, et al. Impact directly over the cardiac silhouette is neccessary to
produce ventricular fibrillation in an experimental model of commotio cordis. J
Am Coll Cardiol. 2001;37:649–654.
8. Link MS, et al. Upper and lower limits of vulnerability to sudden arrythmic
death with chest wall impact (commotio cordis). J Am Coll Cardiol.
2003;41:99–104.
9. Link MS: Mechanically induced sudden death in chest wall impact

(commotio cordis). Prog Biophys Mol Biol. 2003;82:175–186.
10. Maron BJ, et al. Clinical profile and spectrum of commotio cordis. JAMA.
2002;287:1142–1146.
11. Maron BJ, Estes NA, Link MS. Task force 11: commotio cordis. J Am Coll
Cardiol. 2005;45:1371–1373.
Additional Reading
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive
athletes: analysis of 1866 deaths in the United States, 1980–2006.
Circulation. 2009;119:1085–1092.
Sharma N, Andrews S. Commotio cordis. Br J Hosp Med (Lond).

2009;70:48–49.
Codes
ICD9
861.01 Contusion of heart without mention of open wound into thorax
Clinical Pearls
Witnessed precordial impact to a young athlete with resultant distress/collapse
should elicit consideration of CC. Immediate institution of ACLS protocols with
use of AED provides the best chance of survival.
Use of age-appropriate safety baseballs has been shown to reduce CC
events.
Chest wall protective devices should be used in high-risk positions
(catchers/goalies) but have not been proven to prevent CC.
Thorough evaluation of all CC survivors should be undertaken, with return to
play considerations made on a case-by-case basis.
The prognosis of this condition at this time is very poor.
Superficial Radial Nerve (Wartenberg Disease)
Kristen Samuhel Clarey
Dominic McKinley
Coley Gatlin
Karl B. Fields
Basics
Description
Compression mononeuropathy of the superficial branch of radial nerve in the distal forearm
Radial nerve, arises from C5–8, provides motor function to the extensors of the forearm,
wrist, and fingers. Provides motor function for supinators of forearm. Superficial radial nerve
provides sensory function to posterior forearm via posterior cutaneous nerve and the web of
skin between the thumb and index finger.
Superficial radial nerve (SRN) becomes susceptible to injury as it pierces deep fascia to
become SC between the tendons of the extensor carpi radialis longus and brachioradialis
muscles.
Synonym(s): Wartenberg syndrome entrapment; Cheiralgia paresthetica; Prisoner's palsy;
Handcuff disease; Radial sensory nerve entrapment
Epidemiology
The incidence is not known.
It is rare, although often is not recognized.
Risk Factors
Wrist compression (ie, tight bands, tape, watches, archery guards, gloves, or straps of a
racquetball racquet, cast, soft tissue mass)
Direct trauma in contact sports
Laceration and post surgical injury
Sports involving repetitive pronation and supination at the wrist (eg, batting, throwing, and
rowing)

De Quervain's syndrome
Diagnosis
History
Determine whether pain or sensory deficit is the primary symptom. If pain is the main
complaint, then De Quervain's disease seems a more likely diagnosis (1)[C].
Duration of symptoms
Location of symptoms
Characteristics of symptoms to suggest sensory involvement
Physical Exam
Symptoms primarily limited to the dorsoradial aspect of the distal forearm and hand (wrist,
hand, dorsal thumb, and index finger)
Paresthesias (numbness and tingling)
Hyperesthesia
Less commonly, pain or burning
Positive Tinel sign along the radial aspect of the midforearm
Wrist flexion, ulnar deviation, and pronation place traction on the nerve and increase
symptoms.
Sensation deficit on the dorsoradial aspect of the forearm and/or hand
Finkelstein test typically negative, as opposed to De Quervain's syndrome, which usually has
positive Finkelstein test
With SRN injury, pain can be present with thumb abduction and adduction, differentiating this
from De Quervain's syndrome in which extension and flexion create more symptoms.

Lidocaine test: Because the terminal branch of the lateral antebrachial cutaneous nerve often
shares distribution with the SRN, its compression can mimic that involving the SRN.
Diagnostic nerve block to the cutaneous nerve in the proximal forearm just distal to the cubital
crease and adjacent to the cephalic vein may help define its contribution to any pathology (2)
[C].
Nerve conduction study may be inconsistent, but helpful. Indicated if the symptoms are
persistent, surgery is being considered, or if the diagnosis is in doubt (2)[C].
The most common technique records the sensory nerve action potentials from the web space
between the thumb and index finger with stimulation originating in the distal forearm.
Sensory action potential, conduction velocity, and amplitude are decreased.
Motor testing of radial nerve is normal.
De Quervain's syndrome
Intersection syndrome
Lateral antebrachial cutaneous neuropathy
Thumb carpometacarpal arthritis
C6 radiculopathy
Treatment
Almost all patients do well with conservative treatment (3)[C].
Remove constricting bands/devices.
Avoid repetitive trauma to the area. Consider padding the area if unable to
avoid trauma during the athletic season.
Avoid repetitive pronation, wrist flexion, and ulnar deviation.
Thumb spica splint in 20 degrees of wrist extension with the thumb in 45
degrees of metacarpal phalangeal flexion (2)[C]
NSAIDs
Steroid injection and anesthetic in the area of maximum pain can be helpful.
Desensitization
No information exists about neuropathic pain agents, and use of vitamin B6 is
anecdotal.
No studies of acupuncture or other alternative products reported
Provides variable response, so is usually treated nonoperatively (1)[C]
Ongoing Care
If conservative treatment fails after about 6–12 mos, then surgical exploration/decompression
should be considered (1)[C].
References
1. Dang AC, et al. Unusual compression neuropathies of the forearm, part I: radial nerve. J
Hand Surg. 2009;34:1906–1914.
2. Stern M. Radial nerve entrapment. Emedicine online. Jan 3, 2008.
3. Upton SD, et al. Causes of wrist pain in children and adolescents. Uptodate.com. Sept
2009.
Additional Reading
Anto C, Aradhya P. Clinical diagnosis of peripheral nerve compression in the upper
extremity. Orthop Clin North Am. 1996;27:227–236.
Nuber GW, et al. Neurovascular problems in the forearm, wrist, and hand. Clin Sports Med.
1998;17:585–610.
Plancher KD, Peterson RK, Steichen JB. Compressive neuropathies and tendinopathies in
the athletic elbow and wrist. Clin Sports Med. 1996;15:331–371.
Steinberg GG, Akins CM, Baran DT. Orthopedics in primary care, 2nd ed. Philadelphia:
Lippincott, Williams & Wilkins, 1992:73.
Terrono AL, Millender LH. Management of work-related upper-extremity nerve entrapments.

Orthop Clin North Am. 1996;27:783–793.
Codes
ICD9
354.3 Lesion of radial nerve
Clinical Pearls
If the symptoms are present >3 days, the neurapraxic injury may require up to
3 mos to reach maximum improvement.
The splint usually needs to be worn 2–4 wks or until symptoms resolve.
The protective padding needs to be worn until symptoms resolve or if engaging
in sports with repetitive forearm trauma.
Suprascapular Nerve Palsy
Philip H. Cohen
James C. Puffer
Basics
Epidemiology
Relatively uncommon; true incidence unknown
May occur in up to 45% of international-level volleyball players
Ganglion cyst found at spinoglenoid notch in 1% of cadavers in one study
Spinoglenoid ligament present in 50–60% of shoulders
Suprascapular neuropathy in 7% of athletes with peripheral nerve injuries
Risk Factors
More common in volleyball players and overhead throwing athletes, possibly owing to traction
injury or scar formation from overuse
May be particularly associated with “floating serve” in volleyball, which requires intense
eccentric contraction of infraspinatus to decelerate the arm and stabilize the shoulder; this
can stretch the suprascapular nerve across the lateral edges of the scapular spine.
Sudden downward depression of shoulder (traction injury to nerve near plexus origin)
Compression by ganglion cyst, tumor, posttraumatic calcification, vascular malformation, or
ligament at scapular or spinoglenoid notch
Direct trauma, eg, scapular fracture
Etiology
Suprascapular nerve arises from the upper trunk of the brachial plexus at Erb's point,
carrying fibers from the C5 and C6 nerve roots with variable contributions from C4.
It crosses the posterior triangle of the neck, runs deep to the trapezius, and passes under
the transverse scapular ligament via the scapular notch.
Crossing the supraspinatus fossa, it sends 2 branches to the supraspinatus and sensory
branches to the acromioclavicular and glenohumeral joints.
The nerve makes a sharp turn around the spinoglenoid notch and passes into the
infraspinatus fossa, where its branches terminate.
3 main sites of injury:
Scapular notch
Spinoglenoid notch
Near the origin from the upper trunk of brachial plexus
Diagnosis
History
Traumatic versus atraumatic? May yield clues to mechanism of injury; traction injury caused
by blunt trauma has a good prognosis.
Painful versus painless? Painless weakness suggests distal lesion.
Overhead-throwing athlete? If yes, this may increase risk of suprascapular nerve lesion.
Physical Exam
Signs and symptoms depend on level of injury.
If proximal, may have posterior/lateral shoulder pain along with weakness and atrophy of
supraspinatus and infraspinatus
If lesion is distal to sensory branches at spinoglenoid notch, painless, isolated infraspinatus
atrophy and weakness of external rotation may be seen.
Inspection is key. Look for supraspinatus or (especially) infraspinatus atrophy.
Rule out cervical radiculopathy and other C-spine pathology (complete neck exam, including
the Spurling maneuver)
External rotation testing against resistance to evaluate infraspinatus strength
Jobe test to evaluate supraspinatus strength
Complete neurologic examination to determine type, origin, and extent of injury; note that
deep tendon reflexes should not be affected in isolated suprascapular neuropathy.
Thorough shoulder examination to evaluate for associated injury
Tenderness to palpation at scapular notch present in up to 77% patients
Cross-body adduction test (forward flexed arm externally rotated and adducted across body)
puts tension on suprascapular nerve at spinoglenoid notch; may help to differentiate from
rotator cuff lesion
Injection into scapular notch may help to determine source of pain but is rarely necessary.

Imaging
Plain films of the neck and shoulder evaluate for bony abnormalities.
30-degree cephalic tilt view helps to visualize the scapular notch; obtain especially if scapular
fracture.
MRI may be used to detect ganglion cysts and tumors affecting the suprascapular nerve, as
well as other shoulder pathology (rotator cuff injury, labral tears, etc.).
US can be similarly useful in detecting lesions affecting the suprascapular nerve; it also can
be quickly used to evaluate the rest of the shoulder girdle during the same exam. However, it
is extremely operator-dependent.
Electromyography of entire shoulder girdle
Nerve conduction velocity studies from Erb's point to the supraspinatus, with comparison to
unaffected side
Wait minimum 3–4 wks after onset of complaint before neurodiagnostics because false-
negative results may occur if done earlier.
Brachial plexopathy/“stinger”
Rotator cuff tendonitis/tear
Labral pathology
Turner-Parsonage syndrome/neuritis
Treatment
Unless there is a well-defined lesion causing suprascapular nerve
compression, nonoperative therapy is recommended. This includes:
Rest from overhead movements/throwing/exacerbating activities
Physical therapy to strengthen external rotation and stabilize scapula
NSAIDs or analgesics if needed
If labral tear with associated ganglion cyst causes symptoms,
repair/débridement of Labral tear may allow cyst to resolve, thereby relieving
pressure on the suprascapular nerve.
If conservative management not beneficial after 3–6 mos, refer for surgical
exploration.
Ongoing Care
Complications
Ganglion cysts at the spinoglenoid notch may be secondary to labral injuries,
especially superior labrum anterior and posterior lesions.
Secondary impingement may develop owing to loss of
supraspinatus/infraspinatus function.
Additional Reading
Butters KP. Nerve lesions of the shoulder. In: DeLee JC, Drez D, eds.
Orthopaedic sports medicine: principles and practice. Philadelphia: WB
Saunders, 1994:657–663.
Chochole MH, Senker W, Meznik C, et al. Glenoid-labral cyst entrapping the

suprascapular nerve: dissolution after arthroscopic debridement of an
extended SLAP lesion. Arthroscopy. 1997;13:753–755.
Toth C. Peripheral nerve injuries attributable to sport and recreation. Neurol

Clin. 2008;26:89–113.
Codes
ICD9
354.8 Other mononeuritis of upper limb
Clinical Pearls
Return to play depends on severity and cause of the neuropathy. As strength
increases and atrophy and symptoms resolve, a gradual return to play may be
initiated.
Return of muscle strength usually occurs over time once the cause of the injury
has been treated. However, especially with long-standing, severe lesions,
muscle atrophy may not fully resolve.
Surfer's Ear
Steve Burdine
Jason J. Stacy
Basics
Surfer's ear, or external auditory exostosis, is a benign overgrowth of the temporal bone
in the external auditory meatus that occurs after prolonged exposure to cold water.
Patients are usually asymptomatic but may present with recurrent ear infections, conductive
hearing loss, and/or pain.
Description
Benign overgrowth of temporal bone into external auditory meatus
Usually bilateral
May have multiple exostoses in a canal
Broad-based
Occurs after prolonged exposure to cold water
Epidemiology
Rates are highly correlated with time spent in the associated activities. Typically, condition
becomes symptomatic after 5–7 yrs of surfing or other cold water activities (1,2).
Prevalence
Prevalence increases with time spent in the associated activities. Surfers have higher rates of
exostoses with increasing years of surfing experience.
Risk Factors
Occurs after prolonged and/or repetitive exposure to cold water (2)
Most common in surfing; also seen in kayaking, white water rafting, diving (breath holding
and SCUBA), etc. (3)
General Prevention
Best method of prevention is molded earplugs worn during activity.
Special headbands that cover ears are also preventive.
Ear plugs and headbands may be used in combination.
Etiology
Increasing size of exostoses can lead to recurrent infections, conductive hearing loss, and/or
pain.

Otitis externa
Furunculosis
Acute cellulitis
Rare: Perichondritis, chondritis, bullous myringitis
Diagnosis
Visual diagnosis during otoscopic exam
History
Key points:
Amount of cold water exposure
Use of preventive aids
Previous surgeries
Presence of recurrent infections or progressive hearing loss
Fibrous dysplasia
Otitis externa
Acute otitis media
Cholesteatoma
Osteoma
Mastoiditis
Referred pain
Temporomandibular joint syndrome
Treatment
Medication
Medications typically are not needed, unless to treat related bacterial infection or
cerumen impaction.
Referral
Referral to ENT indicated for recurrent infections, pain, or hearing loss (4)
Surgery is definitive care for exostoses.
Reserved for severe, symptomatic cases; presence of exostoses without
symptoms would not necessitate surgical intervention.
Several approaches are used; postauricular is the most common and seems to
minimize complications (5).
If hearing loss is present, generally there is a good response to surgery with
restored hearing.
Some patients require repeated surgeries if cold water exposure continues
(usually after ≥5 yrs of additional exposure).
Ongoing Care
Prognosis
Correctable with surgery but may recur with continued exposure
References
1. Chaplin JM, Stewart IA. The prevalence of exostoses in the external auditory meatus of
surfers. Clin Otolaryngol Allied Sci. 1998;23:326–330.
2. Kroon DF, Lawson ML, Derkay CS, et al. Surfer's ear: external auditory exostoses are
more prevalent in cold water surfers. Otolaryngol Head Neck Surg. 2002;126:499–504.
3. Sheard PW, Doherty M. Prevalence and severity of external auditory exostoses in breath-
hold divers. J Laryngol Otol. 2008;122:1–6.
4. Mlynski R, Radeloff A, Brunner K, et al. [Exostoses of the external auditory canal: Is the
cold water hypothesis valid for patients in continental areas?] HNO. 2007.
5. House JW, Wilkinson EP. External auditory exostoses: evaluation and treatment.
Otolaryngol Head Neck Surg. 2008;138:672–678.
Additional Reading
Cooper A, Tong R, Neil R, et al. External auditory canal exostoses in white water kayakers.
Br J Sports Med. 2008.
Codes
ICD9
380.81 Exostosis of external ear canal
Clinical Pearls
Benign bony overgrowth of the temporal bone into the external auditory meatus
Causes repeated ear infections, hearing loss, or pain in surfers (or other cold
water athletes)
Preventable with earplugs and/or headbands
Surgery is definitive treatment.
Syncope
Justin A. Classie
Chad A. Asplund
Basics
Description
Exercise-related syncope (ERS) is syncope that can occur either during or immediately after a
period of exercise.
Epidemiology
Syncope does not typically occur with exertion.
ERS represents only 3–20% of syncope cases (1).
In a study of 7,500 athletes, 6.2% had reported a syncopal episode in the preceding 5 yrs.
Of these cases of syncope, 87.7% were unrelated to exercise, 12% were postexertional,
and only 1.3% were exertional (2,3).
Prevalence
To date, ERS has not been explicitly characterized in any major epidemiologic studies on
syncope (4).
Risk Factors
Genetics
The occurrence of ERS in multiple members of the same family suggests that there could be a
genetic basis for the unexpected loss of consciousness during exercise (5).
Etiology
Only a minority of syncopal events are associated with physical activity, accounting for only
3–20% of cases.
Athletes who present with exertional syncope (during exertion) have a greater probability of
cardiac causes.
Stroke volume may be an important pathophysiologic factor in ERS.

Exercise-associated collapse (EAC) is defined as occurring when an athlete essentially
collapses and is unable to stand or walk unaided as a result of light-headedness, faintness,
dizziness, or syncope.
Victims of EAC are often able to assist in their own recovery, as opposed to those of a true
ERS event.
Diagnosis
Pre Hospital
In the field, immediately following an event:
Postsyncopal athletes are best evaluated in a head-down, legs-up position because this may
be therapeutic for EAC.
Begin with assessment of mentation and circulatory status.
If pulseless and unresponsive, basic life support (BLS) should be started, as suggested by
the new cardiopulmonary resuscitation guidelines.
Once cardiorespiratory status has been established, a thorough history should be obtained,
with a particular focus on any presyncopal symptoms and prior episodes.
History
Is it a true syncope?
Does the initial evaluation lead to certain diagnosis, suspected diagnosis, or unexplained
diagnosis?
Is heart disease present?
Physical Exam
According to the guidelines on syncope of the European Society of Cardiology and a similar
statement of the American Heart Association, the initial evaluation of patients with syncope is
based on a thorough history and physical examination, supine and upright BP measurement,
and standard ECG.
Comprehensive neurologic assessment, especially with regard to cognitive function
Vital statistics should be obtained, with the caveat that a rectal temperature is the most
reliable means of assessing core temperature after exertion if heat stroke is suspected as a
cause for the syncopal episode.
BP in both arms, pulse, and hydration status will provide additional immediate clues.
Cardiac and pulmonary examinations should attempt to identify any structural cardiac
abnormalities.
Careful evaluation of the carotid or radial pulse may demonstrate the bifid pulse (2 systolic
peaks) of hypertrophic cardiomyopathy or the slow rising pulse (pulsus parvus et tardus) of
aortic stenosis.
Chest palpation in an attempt to identify the point of maximal impulse, as well as any thrills or
heaves that may identify pathologic conditions
Auscultation should be performed with the patient in the supine, seated, and standing
positions.
Murmurs, gallops, and pathologic splitting all should be noted.
Listening to the patient during squatting, while standing, and during a Valsalva maneuver may
help to rule out dynamic outflow obstruction.
A systolic murmur that gets louder with standing or during a Valsalva maneuver suggests the
obstruction of hypertrophic cardiomyopathy.
A patient with an identified systolic murmur and a systolic pressure gradient between the
upper and lower extremities of >10 mm Hg should suggest a diagnosis of aortic stenosis.

Lab
If arrhythmia, anemia, or underlying metabolic disorders are suspected, focused lab studies
may be appropriate (eg, electrolyte studies and basic chemistries, as well as blood counts).
Imaging
In the setting of an abnormal ECG or with a high suspicion for structural heart disease,
echocardiography should be considered.
ECG offers additional information for the physician evaluating syncope.
It has been recognized, however, that abnormal ECGs are common in athletes.
Tilt-table testing has significant limitations in utility for the evaluation of athletes and is not
recommended.
The major causes of syncope among athletes would be cardiac, neurologic, or metabolic.
Neurologic tests include EEG, brain imaging (MRI, MRA, CT scans), and neurovascular
studies (Doppler, US).
Metabolic syncope is seen frequently during the event and has readily identifiable conditions.
Most patients suffer from cardiac syncope.
Drugs could precipitate a syncopal attack, and a detailed medication history including
recreational drug use is essential. The drugs most likely to induce syncope include nitrates,
vasodilators, and β-blockers.
Treatment
Pre-Hospital
In the field, immediately following an event:
Postsyncopal athletes are best evaluated in a head-down, legs-up position
because this may be therapeutic for EAC.
Assessment of the collapsed athlete should, of course, begin with assessment
of mentation and circulatory status.
If the patient is unresponsive and no pulse is confirmed, chest compressions
should be started until an automatic or manual defibrillator can be applied and a
stable rhythm is confirmed, as suggested by the new cardiopulmonary
resuscitation guidelines.
ED Treatment
Once cardiorespiratory status has been established, a thorough history should
be obtained, with a particular focus on any presyncopal symptoms and prior
episodes.
Medication
While pharmacologic therapy may be warranted in carefully selected patients, the
use of any medication in the management of neurally mediated syncope is
controversial, and physicians should be reluctant to prescribe any drugs in these
conditions.
Referral
Patients with obvious structural heart disease, eg, a history of ischemic heart
disease or cardiomyopathy, should be referred immediately. If syncope or
presyncope remains unexplained, the patient should be referred to a
cardiologist.
Management of neurally mediated syncope in competitive athletes is
controversial. The condition is optimally managed by a consultant who is
familiar with this population.
Ongoing Care
Patient Monitoring
Long-term ECG monitoring with Holter monitors can be useful in patients with frequent of
reproducible symptoms.
Athletes with intermittent symptoms are best evaluated with a continuous-loop monitor.
Diet
The treatment should be aimed initially at increasing salt and fluid intake.
The patient should be encouraged to maintain hydration.
Patient Education
If the prodrome of an episode is recognized, the patient should lie flat until the episode
passes.
These measures, along with patient education, frequently will be all that is required.
Prognosis
Generally, in athletes without structural cardiac defects, in whom syncope occurred after
exercise, return to play is likely.
In fact, athletes with syncope had a low recurrence rate and no major adverse events in a
follow-up period of >6 yrs (2,3).
Complications
Most patients with syncope will recover without significant sequelae, but this in no
way excludes the possibility of activity-limiting or life-threatening pathology.
References
1. Kapoor W. Evaluation and outcome of patients with syncope. Medicine.
1990;69:160–175.
2. Colivicchi F, Ammirati F, Santini M, et al. Epidemiology and prognostic

implications of syncope in young competing athletes. Eur Heart J.
2004;25:1749–1753.
3. Colivicci F, Ammirati F, Biffi A, et al. Exercise-related syncope in young

competitive athletes without evidence of structural heart disease: clinical
presentation and long-term outcome. Eur Heart J. 2002;23:1125–1130.
4. Sarasin FP, Louis-Simonet M, Carballo D, et al. Prospective evaluation of
patients with syncope. Am J Med. 2001;111:177–184.
5. Fox WC, Lockett W. Unexpected syncope and death during intense

physical training: evolving role of molecular genetics. Aviat Space Environ
Med. 2003;74(12):1223–1230.
Additional Reading
Mitchell JH, Haskell W, Snell P, et al. Task Force 8: Classification of sports.
36th Bethesda Conference: Eligibility recommendations for competitive
athletes with cardiovascular abnormalities. J Am Coll Cardiol. 2005;45:1364–
1367.
Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF scientific

statement on the evaluation of syncope: from the American Heart Association
Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular
Disease in the Young, and Stroke, and the Quality of Care and Outcomes
Research Interdisciplinary Working Group, and the American College of
Cardiology Foundation in collaboration with the Heart Rhythm Society;
endorsed by the American Autonomic Society. Circulation. 2006;113:316–
327.
Codes
ICD9
780.2 Syncope and collapse
Clinical Pearls
Any athlete with exertional syncope/presyncope should be evaluated with a
thorough history and physical examination and an ECG (LOE = C).
Any athlete with unexplained syncope/presyncope should be excluded from
participation until a diagnosis is established (LOE = C).
Tilt-table testing is not recommended in the evaluation of young athletes with
exertional syncope/presyncope (LOE = C).
Unexplained exertional syncope/presyncope warrants evaluation by a
cardiologist prior to return to play (LOE = C).
Syndesmodial Injury of the Lower Leg
Delmas J. Bolin
Lauren Wood
Basics
Involves disruption of ligaments supporting the integrity of the mortise joint
Associated with prolonged symptoms of pain and dysfunction
Relevant injured structures can include anterior tibiofibular, posterior tibiofibular and
transverse tibiofibular ligaments, interosseous membrane, and interosseous ligament, which
serve to prevent lateral displacement of distal fibula during weight bearing
Synonym(s): High ankle sprain
Description
Mechanism of injury involves sudden, forceful external rotation of the dorsiflexed ankle.
The talus is pressed against the fibula, opening the distal tibiofibular articulation and rupturing
the tibiofibular syndesmosis.
Epidemiology
10–20% of all ankle sprains
Higher percentage of ankle sprains involve the syndesmosis when occurring in collision sports
such as football, rugby, and lacrosse.
Risk Factors
Collision sports are at higher risk:
Football
Rugby
Lacrosse
Sports that immobilize the foot in a high ankle shoe or boot:
Hockey
Slalom skiing; catching inner ski on gate
Sports played on turf, eg, soccer

Deltoid ligament tear
Fibular or medial malleolar fracture
Heterotopic ossification or synchondrosis of the syndesmosis in 25–100% of cases
Tibiofibular synostosis resulting in prolonged pain and chronic disability
Longer healing time and more missed practices
Occult talar dome fracture
Diagnosis
History
Patient is often unable to adequately or completely describe mechanism; patients commonly
report an inversion mechanism.
Focus history on mechanism of injury; raise index of suspicion with history of forceful external
rotation, hyperdorsiflexion, or hyperplantarflexion.
Examples of common mechanisms include soccer (player tackling ball), football (player
prone, has foot stepped on, leading to forceful external rotation), and skiing (slalom skiers,
catch ski on gate)
Pain is usually between anterior distal tibia and fibula; also posteromedially at ankle joint.
Patients complain of pain with weight bearing, pushing off, or with external rotation.
Physical Exam
Less swelling than anticipated with severe lateral ankle sprain
Palpation of the tibia and fibula helpful to rule out fracture:
Anterior joint line and anterior syndesmosis are often tender.
Squeeze test: Compression above mid-calf produces distal pain in the anterior ankle joint
(syndesmosis).
External rotation test: Distal lower leg is stabilized with ankle in neutral position while
mediolateral force/external rotation of the foot is performed. Positive test noted by pain
and/or increased rotation relative to unaffected side.
Push-off test: Push-off/heel raise on affected side may be weak or absent.
Fibular translation (drawer) test: Increased translation of fibula from anterior to posterior or
loss of firm end-point relative to uninjured side
Stabilization test: Distal syndesmosis is stabilized with athletic tape and assess if symptoms
are decreased with running and jumping.
Cotton test: Increased translation or pain with translation of talus from medial to lateral (may
indicate deltoid ligament tear)
Crossed-leg test: Pain at syndesmosis with gentle pressure exerted on the medial side of the
knee while resting the mid-tibia of affected leg on uninjured knee
Evaluate distal neurovascular status with any lower leg injury to rule out acute compartment
syndrome (1)[B].

Imaging
X-rays: Initial studies are static films. 50% of syndesmotic injuries have avulsion fractures
associated:
Weight-bearing anteroposterior view:
Tibiofibular clear space is among most sensitive indicators of syndesmotic injuries.
Measured 1 cm proximal to ankle joint; widening demonstrated by >6 mm between
medial border of fibula and medial cortical density of tibia.
Tibiofibular overlap; measured 1 cm proximal to joint; normal is >6 mm overlap between
medial border of fibula and lateral border of tibia
Medial clear space should be <4 mm; >4 mm termed diastasis
Standing mortise view to evaluate talocrural angle; the angle of a line drawn across tips of
malleoli intersecting with a line perpendicular to a line drawn across the superior aspect of
tibial plafond. Variation from contralateral side of >5° is significant.
Lateral
Dynamic radiographs:
Cotton test: Grasp distal fibula and pull laterally; modified cotton test: Push or pull fibula in
sagittal plane. Comparison to contralateral side is frequently required.
Varus and valgus ankle stress views are essential to assess instability.
External rotation stress views not considered reliable indicators of syndesmotic injury
MRI can clarify diagnosis and extent of soft tissue injury:
Compared with ankle arthroscopy, had sensitivity 100%/100% and specificity 93%/100%
for anterior inferior/posterior inferior tibiofibular ligament disruption, respectively
CT helpful for bony detail of suspected talar dome injuries (2)[B].
Pronation-external rotation ankle fracture (Weber type C)
Supination-external rotation ankle fracture (Weber type B)
Fracture of the proximal fibula (Maisonneuve)
Ossification of the syndesmosis
Calcification of the syndesmosis
Deltoid ligament tear
Talar dome fracture
Tibiofibular synostosis resulting in prolonged pain and chronic disability
Treatment
Syndesmosis injuries without fracture (1)[B]: Consensus is 3–4-phase
rehabilitation protocol. If no frank diastasis, most injuries result in inability to
bear weight without symptoms.
Phase I is to limit inflammatory response and protect the joint, usually with
NSAIDs and short-term (10 days–2 wks) nonweight-bearing protection in a
cast, boot, or brace with crutches. Include protection, rest, ice, compression,
and elevation and modalities to minimize edema.
Phase II is typically restoration of range of motion and normalization of gait
pattern. In this phase, high ankle braces (Donjoy Velocity and others) may
facilitate rehabilitation.
Phase III progression once patient can ambulate and hop without
dysfunction. Progress to agility drills, plyometrics, sports-specific tasks, and
strengthening. Return to play when patient can demonstrate tasks such as
backward pedaling, vertical hopping, or running in figure 8 pattern.
Return to play is variable, usually 3–6 wks.
Syndesmosis injuries with fracture or diastasis noted on radiographs:
Referral to orthopedic surgeon indicated if frank diastasis is noted on stress
radiographs or if fracture is present.
Screw fixation followed by nonweight-bearing cast immobilization for 6 wks,
followed by appropriate rehabilitation (1)[B].
References
1. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in
athletes. Am J Sports Med. 2007;35:1197–207.
2. Herscovici D, Anglen JO, Archdeacon M, et al. Avoiding complications in

the treatment of pronation-external rotation ankle fractures, syndesmotic
injuries, and talar neck fractures. J Bone Joint Surg Am. 2008;90:898–908.
Additional Reading
Amendola A, Williams G, Foster D. Evidence-based approach to treatment of
acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc.
2006;14:232–236.
Hopkinson WJ, St Pierre P, Ryan JB, et al. Syndesmosis sprains of the ankle.
Foot Ankle. 1990;10:325–330.
Porter DA. Evaluation and Treatment of Ankle Syndesmosis Injuries. Instr

Course Lect. 2009;58:575–581.
Codes
ICD9
845.03 Tibiofibular (ligament) sprain, distal
Clinical Pearls
A high ankle sprain involves ligaments that stabilize the ankle mortise joint. It is
not a “routine ankle sprain” and must be treated differently.
High ankle sprains should be immobilized as soon as the diagnosis is made for
a variable period ranging from a few days in elite professional and collegiate
athletes to 2 wks for high school athletes. Suspect a high ankle sprain in a
“regular ankle sprain” that is not improving as you expect.
Although there is little evidence for it, some have found high ankle stirrup
braces helpful in the subacute setting for stabilizing the mortise joint, limiting
rotational stress at the ankle, and permitting a more vigorous rehabilitation.
Tarsal Tunnel Syndrome/Posterior Tibial Nerve
Entrapment
Stephen Simons
Bradley Sandella
Basics
Description
A peripheral compression neuropathy that results in foot pain and paresthesias along the
medial and plantar aspects of the foot and toes secondary to posterior tibial nerve
entrapment in the tarsal tunnel (1)[C]
Synonym(s): Posterior tibial nerve entrapment
Epidemiology
Unknown; rare compared with other peripheral mononeuropathies (upper extremity) (2)[C]
Risk Factors
Space-occupying lesions (eg, ganglion or lipoma)
Local trauma
Scar tissue
Abnormal foot/ankle mechanics (eg, excessive pronation)
Hindfoot deformities (eg, heel valgus or varus)
Repetitive activity
Weight gain
Lower extremity edema
Previous foot or ankle surgery
Accessory muscles (eg, accessory soleus)
Hypertrophic flexor retinaculum
Osteophytes/bone spurs
Varicose veins
Fat pad dysfunctions
Systemic diseases (eg, diabetes)
Etiology
Tarsal tunnel is a fixed anatomic space bordered by the calcaneus and talus superiorly,
inferiorly, and laterally and by the flexor retinaculum medially. The flexor retinaculum (or
laciniate ligament) runs obliquely from posterior to anterior and forms the roof of the tunnel.
Structures passing through the tunnel include the tibialis posterior, flexor digitorum longus,
and flexor hallucis longus tendons, as well as the posterior tibial artery, veins, and tibial
nerve.
Tibial nerve branches at various locations through the tunnel, forming the medial and lateral
plantar nerves, along with the medial calcaneal nerve. The medial and lateral plantar nerves
then enter their own tunnels.
The medial plantar nerve runs deep to the abductor hallucis and flexor hallucis longus
muscles.
The lateral plantar nerve passes directly through the abductor hallucis muscle.
Medial calcaneal nerve pierces through the flexor retinaculum to the medial side of the heel,
providing sensory innervation to the posterior and medial heel.
Tarsal tunnel can be viewed as an upper tunnel or a lower tunnel, which are different clinical
entities based on nerve branching locations.
Diagnosis
History
Tarsal tunnel syndrome presents with a nonspecific, highly variable clinical picture.
History of trauma or repetitive activity (eg, running)
Numbness, tingling, and burning to the medial aspect and sole of the foot; can include calf
symptoms and radiation to the toes
Foot cramping
Prolonged standing or walking often exacerbates the symptoms.
Habit of removing shoes to obtain relief
Patients lack morning pain and often lack heel pain.
Nocturnal pain may awaken the patient, especially after excessive activity.
Rest and lower extremity elevation are often helpful in relieving the symptoms.
Physical Exam
Numbness/tingling that progresses to a burning sensation at the plantar aspect of the foot;
intermittent initially; can become constant
Plantar foot pain accentuated by walking and foot dorsiflexion
Nocturnal pain often relieved with walking
Pain worse at the end of the day
Occasional fusiform swelling over the nerve course
Motor weakness or loss as late finding: Poor prognostic indicator
Muscle fasciculations
Tenderness distal or proximal to area of entrapment (Valleix sign)
Inspect for biomechanical abnormalities such as excessive heel varus or valgus positioning.
Observe for swelling.
Observe for toe contractures, which can occur late.
Palpate for soft tissue thickening or lesions.
Light touch–induced paresthesias
Diminished 2-point discrimination often occurs early.
Diminished pinprick sensation to plantar foot
Intrinsic muscle weakness, although possibly present, is difficult to assess.
Atrophy of abductor hallucis or abductor digiti minimi as a late finding
Percussion sign (Tinel sign)
Cuff sign: Pain with pneumatic pressure device around leg
Dorsiflexion-eversion test: Pain elicitated when placing the foot in maximum dorsiflexion and
eversion and then maximally dorsiflexing the metatarsophalangeal joints and holding this
position for 5–10 s (sensitivity of 97%, specificity of 100%) (3)[A]

Imaging
Plain x-ray and CT scan to rule out displaced fractures, accessory ossicles, coalition, and
bony exostoses
Electrodiagnostic studies, if positive, may be helpful but frequently are insensitive and
negative.
Electromyography (EMG) to evaluate for motor latencies
Nerve conduction studies (NCSs) evaluating for sensory action potentials may increase
sensitivity (1)[C].
Diagnostic US (using a high-frequency machine and 10–15 MHz linear array transducer) can
be used to evaluate for tendinopathies and space-occupying lesions (1)[C].
MRI is test of choice to evaluate tunnel contents. Bony and soft tissue structures can be
viewed (eg, ganglion cysts, accessory or hypertrophied muscles, bone spurring).
Pressure-specified sensory device (PSSD) is a computer-assisted device for quantitative
sensory testing of peripheral nerves that may allow for earlier recognition of syndrome (1)[C].
Plantar fasciitis
Calcaneal bursitis
Tendinitis/tenosynovitis [flexor hallucis longus (FHL), posterior tibialis tendon (PTT), flexor
digitorum longus (FDL)]
S-1 radiculopathy
Peripheral vascular disease, including popliteal artery entrapment
Systemic disease (eg, Reiter disease, rheumatoid arthritis, gout) (4)[C]
Bony abnormalities (eg, degenerative changes, previous fractures)
Treatment
Long-term treatment
Acute treatment: Immobilization:
Rigid ankle-foot orthosis
Walking cast
Medial longitudinal arch supports
There is no arbitrary length of time to trial the preceding acute treatment
options; it has been reported that lasting nerve damage can occur with a
prolonged episode (1)[C].
Medication
NSAIDs
Corticosteroid injection
General Measures
Ice
Relative rest
Shoe modification
Untreated patients risk nerve atrophy from continued pressure by space-
occupying lesions.
Tunnel pressures >80 mm Hg can cause irreversible damage to the nerve
(3)[A].
Rehabilitation:
Correct abnormal foot mechanics with shoe orthoses, especially in runners.
Well-fitted and supportive shoes
Flexibility training
Physiotherapy to strengthen foot intrinsic and extrinsic muscles
Therapeutic modalities including massage and US
Weight loss for obese patients
Stockings to decrease swelling and venous stasis
Indicated for acute cases with space-occupying lesions and recalcitrant
conservatively treated cases
Flexor retinaculum release
Dissection of lateral and medial plantar nerves beyond their tunnels and
compression site (5)[C]
Early mobilization after surgery decreases scar formation (1)[C].
Best surgical results in patients with tumor or coalition
Poor surgical results in patients with idiopathic or posttraumatic cases, along
with patients who have experienced long-standing symptoms
Long-term surgical results vary, with reported success rates of 75–91% (1)[C].
Ongoing Care
Surgical referral should be considered for patients recalcitrant to a high-quality nonoperative
treatment program.
References
1. Franson J, Baravarian B. Tarsal tunnel syndrome: a compression neuropathy involving
four distinct tunnels. Clin Podiatr Med Surg. 2006;23:597–609.
2. Kinoshita M, Okuda R, Yasuda T, et al. Tarsal tunnel syndrome in athletes. Am J Sports
Med. 2006.
3. Dellon AL. The four medial ankle tunnels: a critical review of perceptions of tarsal tunnel
syndrome and neuropathy. Neurosurg Clin N Am. 2008;19:629–648.
4. Diers DJ. Medial calcaneal nerve entrapment as a cause for chronic heel pain. Physiother
Theory Pract. 2008;24:291–298.
5. Mullick T, Dellon AL. Results of decompression of four medial ankle tunnel in the
treatment of tarsal tunnels syndrome. J Reconstr Microsurg. 2008.
Additional Reading
Bailie DS, Kelikian AS. Tarsal tunnel syndrome: diagnosis, surgical technique, and functional
outcome. Foot Ankle Int. 1998;19:65–72.
Lau JT, Daniels TR. Tarsal tunnel syndrome: a review of the literature. Foot Ankle Int.
1999;20:201–209.
Codes
ICD9
355.5 Tarsal tunnel syndrome
Clinical Pearls
Many cases of tarsal tunnel syndrome can be managed with relative rest from
exercise, biomechanical control, and anti-inflammatory drugs.
Identification of a surgically treatable cause is necessary to avoid permanent
nerve compression, sensory deficits, and motor weakness.
Temporomandibular Joint Injury
Daniel Lewis
Basics
Temporomandibular joint (TMJ) injuries, while relatively uncommon, do occur in sport.
Players in collision sports (eg, football, field hockey, soccer, lacrosse) may be at particular risk,
along with divers.
Description
The cause of TMJ pain dysfunction syndrome (TMPDS) is unclear in most patients.
May be related to an abnormality in neuromuscular mechanics: Trauma, dentoskeletal
malocclusion, and bruxism are important contributors.
Up to 70% of sufferers may have displacement of the articular disk, made up of
fibrocartilage.
Osteoarthrosis is another common cause of TMJ pain.
May be related to whiplash injuries or related acceleration-deceleration injuries in sport
Epidemiology
Incidence
10–20 million adults suffer TMPDS (up to 3–7% of the adult population may seek treatment
at some point in their lives).
Patients typically present in 4th decade of life, unless problem is related to injury. 1/3 of
TMPDS sufferers report a previous history of macrotrauma.
Predominant gender: Female > Male (2:1, although this ratio may be reversed in athletes)
General Prevention
Use of mouth guards in sport may provide protection against traumatic causes.
Proper technique in sports-specific activitis
Avoidance of repetitive or unilateral chewing

In cases of trauma, other facial injuries may be related:
Mandibular or other orofacial fractures
Cervical neck injury may occur in whiplash-type injuries.
Diagnosis
Diagnosis based on clinical presentation
Exclude other causes of unilateral facial or head pain
History
History of pain with chewing, particularly repetitive chewing
May have related history of trauma
Physical Exam
Dull, aching unilateral jaw, ear, or head pain: Exacerbated by opening the mouth
A “popping” or “clicking” sensation may be noted with chewing.
Limited range of motion of the mandible
Symptoms more conspicuous in the evening and less prominent on awakening
Pain may refer to a variety of locations on the ipsilateral hemicranium and supraclavicular
region.
Dentoskeletal malocclusion
Mandibular deviation with opening and closing of the mouth
TMJ capsule tenderness
Tenderness over the muscles of mastication
A palpable click often can be palpated with opening and closing of the mouth.

Plain radiographs are of little value.
Tomograms, bone scintigraphy, CT scan, and MRI are not necessary during the initial
evaluation of TMPDS in the ED.
Lab
No specific laboratory tests are indicated.
Imaging
Not necessary for diagnosis; may be helpful to rule out other disorders with similar symptoms
Mandibular fracture
Myocardial ischemia
Carotid or vertebral artery dissection
Intracranial hemorrhage (subarachnoid hemorrhage)
Temporal arteritis
MS may present with pain similar to trigeminal neuralgia.
Trigeminal or glossopharyngeal neuralgia
Vascular headache
Dental abnormalities
Herpes zoster
Salivary gland disorder, otitis media, external otitis, and sinusitis
Elongated styloid process pain often is precipitated by swallowing or turning the head.
Treatment
Typically treated as outpatients with pain medication, muscle relaxants, and
warm compresses
In general, symptoms from acute injury resolve within 7–10 days, although a
significant percentage of patients may have long-term sequelae.
Pre-Hospital
Evaluate patient to rule out other more serious injuries:
Cervical spine injuries
Orofacial fractures
In acute injuries, conservative measures are applied:
Protection from further injury
Icing
NSAIDs for pain relief if indicated
Decreased stimulation (ie, chewing) on affected side
ED Treatment P.
Pain control
Radiographs to rule out other injuries as clinically indicated (plain film, CT)
Refer to dentist or oral-maxillofacial surgeon for occlusal splints.
Medication
Oral or parenteral analgesics (NSAIDs, occasionally narcotics)
Muscle relaxants
Additional adjunct therapies:
Tricyclic antidepressants
Intra-articular and local injections of anesthetics or steroids
Hyaluronic acid injection has not been widely studied.
Vapocoolant spray with physiotherapy
Warm/cold compresses
Behavior modification
Physical therapy exercises to strengthen muscles of mastication, maintain
range of motion
US or massage also may be beneficial.
While not studied extensively, a mouthpiece or mouthguard may help to relieve
some postinjury pain.
Referral
Pain or loss of function uncontrolled by the preceding may benefit from referral
to maxillofacial or orofacial surgeons.
Surgery is rarely required, but may consist of:
Arthrocentesis and arthroscopy
Hemiarthroplasty
Osteotomy
Total joint replacement is considered a salvage procedure.
N/A
Ongoing Care
Diet
A soft diet may be effective in reducing pain severity during episodes.
Chewing gum also may make symptoms worse.
Prognosis
Typically self-limited but can progress to a chronic state of inflammation and pain
Additional Reading
Marbach JJ. Tempomandibular pain dysfunction syndrome: history, physical examination and
Treatment. Rheum Dis Clin North Am. 1996;22:47–98.
Marbach JJ. Temporomandibular pain and dysfunction syndrome. History, physical

examination, and treatment. Rheum Dis Clin North Am. 1996;22:477–498.
Tanaka E, Detamore MS, Mercuri LG. Degenerative disorders of the temporomandibular

joint: etiology, diagnosis, and treatment. J Dent Res. 2008;87:296–307.
Codes
ICD9
524.60 Temporomandibular joint disorders, unspecified
848.1 Jaw sprain
959.09 Other and unspecified injury to face and neck
Testicular Torsion
Anne M. Garrison
Vikram Narula
Matthew P. Boyd
Basics
Testicular torsion is a surgical emergency. Prompt diagnosis with restoration of blood
flow within 6 hr is required to save testicular viability.
Description
Testicular torsion results from twisting of the spermatic cord causing ischemia to the testicle
by obstructing venous return.
Rotation generally occurs medially and ranges from incomplete (eg, 90–180 degrees) to
complete (540–720 degrees) torsion.
Depending on the degree of torsion, vascular occlusion occurs, and the result is infarction of
the testicle after 6 hr.
Testicular infarction leads to atrophy and ultimately may decrease fertility.
Epidemiology
Incidence
The annual incidence of testicular torsion for males under the age of 25 is about 1/4,000 (1).
90% are caused by a congenital malformation of the process vaginalis (1)
The peak age of occurrence is 14 yrs of age, with 2/3 of torsions noted in males between 10
and 20 yrs of age (2).
The 2nd most common group is neonates (2).
Testicular torsion rarely occurs after age 30 (2).
Risk Factors
Congenital malformation of the tunica vaginalis inserted high on the spermatic cord, known as
the “bell-clapper deformity”
Increased testicular size often related to puberty
Testicular tumor
Testicles with a horizontal lie
Spermatic cord with long intrascrotal portion
Cryptorchidism
General Prevention
No known primary prevention measures
Secondary prevention: Ipsilateral orchidopexy can prevent recurrent torsion. This is often
done on the contralateral testicle at the same time to prevent potential future torsion (2)[C].
Etiology
Most patients have a congenital abnormality of the genitalia with a high insertion of the tunica
vaginalis on the spermatic cord and a redundant mesorchium that permits increased mobility
and twisting of the testicle on its vascular pedicle.
The anatomic abnormality generally is bilateral, so both testicles are susceptible to torsion.
Only 4–8% of torsions are the result of trauma; most occur without a precipitating event (1).
Diagnosis
The presentation of an “acute scrotum” in a child or adolescent requires rapid
assessment and strong consideration for consultation with an urologist (3)[C].
Patients who present clinically with testicular torsion should go immediately to surgery.
If the diagnosis of torsion is uncertain, then Doppler US can be done rapidly to assess the
blood flow in the testis.
25–30% of these patients ultimately will prove to have testicular torsion.
History
Sudden onset of severe scrotal pain or trauma: Unilateral testicular pain and tenderness
followed by scrotal swelling and erythema
Less commonly, torsion may present with pain in the inguinal or lower abdominal area.
1/3 of patients have had a previous episode of testicular pain (2).
Physical Exam
Nausea and vomiting occur in 50% of patients, and low-grade fever occurs in 25% (2).
Symptoms of urinary infection (ie, dysuria, frequency, and urgency) are absent.
In distinguishing torsion from epididymitis, localization of tenderness is helpful early in the
course. However, once significant scrotal swelling occurs, the anatomy becomes indistinct,
and some form of testicular flow study or surgical exploration is required.
The affected testicle may ride higher than the contralateral testicle.
The affected testicle may be found to lie transversely as opposed to the normal vertical lie.
The cremasteric reflex is the most sensitive (99%) physical finding (1).
Reflex is elicited by stroking the medial thigh, which causes the cremaster muscle to
contract, elevating the testis.
Reflex is considered positive if the testicle moves at least 0.5 cm.
The classic Prehn sign, which consists of relief of pain on elevation of the testicle in
epididymitis, and worsening or no change in the pain with torsion, is considered unreliable (2).
Torsion of the appendix testis may present with a palpable hard, tender nodule 2–3 mm in
diameter in the upper pole of the testicle. Blue discoloration in this area is called the “blue dot
sign” (1).

Radionuclide scan: The criterion standard imaging modality traditionally has been 99m TC-
pertechnetate radionuclide scan, which shows decreased flow in the torsed testicle
compared with the unaffected side (1).
Epididymitis will reveal increased flow owing to inflammation.
This technique has an overall sensitivity and specificity of 98% and 100%, respectively.
US: Because of the frequent time delays in obtaining nuclear scans and the importance of a
rapid and accurate diagnosis, use of Doppler US to assess testicular blood flow has
essentially replaced nuclear scanning as a less invasive, more readily available test with
comparable accuracy (1,2)[C].
Overall sensitivity and specificity for color-flow Doppler range from 86–100% and 97–
100%, respectively, although the accuracy tends to be lower in infants owing to the smaller
anatomy.
US does not expose the patient to ionizing radiation.
There are limitations of all flow studies in that they reflect only the current state of
perfusion. Consequently, a spontaneously detorsed testicle may show normal or even
increased flow and yet still be at high risk for recurrent torsion.
Lab
Generally laboratory tests are not helpful.
Urinalysis is usually normal; some patients with torsion may have pyuria.
Elevated WBC count with a left shift is present in 50% of patients.
There are no laboratory tests specific for testicular torsion.
Epididymitis/orchitis
Torsion of the appendix testis
Testicular trauma or rupture of the testicle
Incarcerated inguinal hernia
Testicular tumor
Acute hydrocele
Henoch-Schönlein purpura
Other intra-abdominal conditions (eg, appendicitis, pancreatitis, renal colic) rarely may
present with testicular pain.
Treatment
Pre-Hospital
Acute onset of testicular pain should prompt immediate referral for further
evaluation.
If transportation will be delayed and torsion is suspected, manual detorsion
should be attempted.
ED Treatment
If history and physical exam findings are consistent with the diagnosis of
torsion, surgical care should not be delayed for imaging studies (1,2)[C].
If the diagnosis is uncertain, imaging and/or consultation with a specialist is
appropriate (1,2)[C].
US generally is the imaging study of choice: US is faster and more readily
available, but it is less sensitive than radionuclide scanning.
In situations in which definitive care is likely to be delayed beyond 4–5 hr after
the onset of torsion, manual detorsion may be attempted (1,2)[C].
Do not delay surgical consultation to attempt manual detorsion.
Surgical exploration is still necessary even with successful detorsion.
Attempt usually requires anesthesia: IV sedations or local anesthesia
Manual detorsion is accomplished by externally rotating the affected testicle
laterally (away from midline, as if opening as book, because 2/3 of torsions
are medial) until pain is relieved or normal anatomy is restored. All patients
who undergo manual detorsion still should have blood flow documented and
orchidopexy to prevent recurrences.
Rotation in the opposite direction, toward the midline, should be attempted if
lateral rotation is not successful.
Surgical consultation should be obtained in all suspected cases of testicular
torsion (1,2,3)[C].
Surgical exploration of the affected and contralateral testes is recommended in
all cases (1,2,3)[C].
Orchiopexy, fixation of the testicle within the scrotum, is the surgical
procedure of choice.
The procedure is performed prophylactically on the contralateral side.
Nonviable testes should be removed.
IV fluid
Analgesics as appropriate
Admission Criteria
Any patient with confirmed testicular torsion must be admitted for scrotal
exploration and bilateral orchiopexy.
Flow studies that are inconclusive or technical failures mandate further
investigation by surgical exploration of the scrotum.
Admission for urgent surgical exploration of an acute scrotum is mandatory if
there will be any potential delay in obtaining a flow study.
Discharge Criteria
Patients with negative scrotal exploration or normal flow studies can be
discharged with appropriate urologic follow-up.
Appropriate parameters for return to ED must be discussed because of the
possibility of intermittent torsion.
Patients with an obvious diagnosis other than testicular torsion (eg, a
nonincarcerated inguinal hernia) can be referred for elective care.
Ongoing Care
Patients may return to full activity once the surgical wounds have healed and pain has
resolved.
Patients who have a testicle removed should be advised of the risk of injury to the remaining
testicle and strongly consider protective equipment for contact sporting activity.
Complications
Delayed recognition and treatment may lead to testicular atrophy, decreased
fertility, and possibly the need to remove the affected testicle.
References
1. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician.
2006;74:1739–1743.
2. Lavallee ME, Cash J. Testicular torsion: evaluation and management. Curr

Sports Med Rep. 2005;4:102–104.
3. Leslie JA, Cain MP. Pediatric urologic emergencies and urgencies. Pediatr
Clin North Am. 2006;53:513–527, viii.
Additional Reading
Gatti JM, Murphy JP. Acute testicular disorders. Pediatr Rev. 2008;29:235–
241.
Codes
ICD9
608.20 Torsion of testis, unspecified
608.21 Extravaginal torsion of spermatic cord
608.22 Intravaginal torsion of spermatic cord
Clinical Pearls
Obtain surgical consultation early in suspected cases of testicular torsion.
Do not delay surgical intervention for imaging studies when clinical suspicion is
high.
US can be useful in cases where clinical suspicion is low because it can
evaluate for torsion as well as other pathology.
TFCC (Triangular Fibrocartilage Complex) Tears
Stephen Paul
Holly McNulty
Anna Waterbrook
Basics
3–9% of all athletic injuries involve the wrist and hand (1).
TFCC tears are part of the spectrum of ulnar-sided pain, often with clicking, and they can be
disabling to the athlete.
The TFCC acts as a primary stabilizer to the distal radioulnar joint (DRUJ) and a cushion to
the ulnar-sided carpal bones, transmitting up to 18% of the load on the wrist (2).
TFCC tears are either traumatic or degenerative.
Traumatic tears may be acute or acute on chronic, repetitive events.
Tears are either from acute collision (axial load with rotation, hyperpronation-supination, or
traction) or repetitive injury (chronic loading of ulnar wrist).
Description
The TFCC has 5 major components as described by Palmer (2):
TFC proper, the articular disc distal to the ulna
Meniscus homologue (ulnocarpal meniscus)
Radioulnar ligaments (dorsal and volar)
Sheath of the extensor carpi ulnaris
Ulnar collateral ligament
Fibers of the TFCC originate on the distal radius, inserting on the distal ulna, base of the
ulnar stylus, and extending to lunate, triquetrum, and base of the 5th metacarpal
The periphery of the TFCC is vascular, and the central aspect is avascular.
Epidemiology
No studies have addressed the epidemiology of TFCC tears.
Degenerative tears often are seen in an older, general population.
Traumatic tears are seen frequently in the athletic population.
Risk Factors
Type of sport can lead to tears from collision, falling on outstretched hand, and hyperrotation
or traction.
Racquet sports (tennis, racquetball), pole vault, gymnastics, golf, weight training (bench
press), hockey (collision and hyperrotation with a slapshot), and water skiing (traction)
Positive ulnar variance is associated with TFCC tears.
Distal radius fractures and fractures of the base of the ulnar stylus are associated with TFCC
tears.
Etiology
The thickness of the TFCC is inversely related to the ulnar variance (the more ulnar plus, the
thinner the TFCC).
In neutral mechanics, with axial load on, the load on the forearm is 82% at the distal radius
and 18% at the TFCC; with removal of the TFCC, the radius takes 95% of the load (3).
Palmer classified TFCC tears in to 2 types: traumatic and degenerative (2):
Traumatic:
1A: Central perforation
1B: Ulnar avulsion ± distal ulnar fracture
1C: Avulsion from lunate or triquetrum
1D: Avulsion from sigmoid notch of radius
Degenerative:
2A: TFCC wear
2B: TFCC wear + lunate and/or ulnar chondromalacia
2C: TFCC perforation + lunate and/or ulnar chondromalacia
2D: TFCC perforation + lunate and/or ulnar chondromalacia + ligament tear
2E: TFCC perforation + lunate and/or ulnar chondromalacia + ligament tear + ulnocarpal
arthritis
Several mechanisms have been described to cause TFCC tears.

Axial loading the ulnar side of the wrist with a rotational force (often a fall on an outstretched
hand)
Hyperrotation with hyperpronation or hypersupination
Traction to the ulnar side of the wrist
Chronic repetitive loading the ulnar carpus

Positive ulnar variance (repetitive loading of ulnar carpus)
Distal radius fractures
Fracture/nonunion of base of the ulnar stylus: Base of stylus fractures tear the TFCC.
Instability (subluxation or dislocation) of the DRUJ, midcarpus, or triquetrum-lunate
Ulnar impaction syndrome (abutment syndrome, impingement syndrome) with positive ulnar
variance and risk factors (sport, repetitive trauma): There is central tear to TFCC, and
chondromalacia develops in the lunate, triquetrum, and ulnar head.
Diagnosis
History
In athletes, there is a history of:
Acute trauma such as a fall on an outstretched hand, especially with ulnar load or ulnar
deviation
Traction or hyperrotation
Previous Colles fracture
Previous dislocated/subluxed DRUJ
“Insignificant” wrist injury
Overuse and repetitive trauma to the ulnar side of the wrist as seen in club and racquet
sports
Patients often report ulnar-sided pain ± clicking.
Weak hand grip
Subjective sense of wrist instability
Pain with pronation, supination, or extension with axial load
Physical Exam
Point tenderness at the recess of the TFCC [area between the dorsal aspect and distal ulnar
styloid and between the pisiform and the extensor carpi ulnaris (ECU) and flexor carpi ulnaris
(FCU)]: Described as fovea sign
TFCC impaction/load/compression test: Axially load the wrist and ulnar deviate; reproduces
pain ± click
May have pain/weakness with isometric resisted wrist flexion (patient tries to lift table in
supination); this is seen with dorsal-sided peripheral tears.
Pain/weakness pushing out of a chair (wrist extension with axial load)
Tests to rule out associated instability:
Distal ulnar movement in anteroposterior (AP) plane with fixed distal radius
AP translation of triquetrum to fixed lunate
AP translation of triquetrum to fixed hamate
Ulnar compression test: Squeeze ulnar head against sigmoid notch of distal radius.
Diagnostic test: Injection with lidocaine: ECU, FCU, TFCC space, DRUJ, midcarpus, or
lunotriquetrum; may help to differentiate pain

Imaging
Radiographs: Posteroanterior (PA) neutral zero rotation and lateral to rule out associated
fractures and determine ulnar variance (preoperative assessment of ulnar variance may be
augmented with PA pronation with hand-grip views)
The standard is arthroscopy, which is still diagnostic and therapeutic (can successfully
diagnose peripheral tears with trampoline sign: Lack of spring to TFCC with probe).
MR arthrogram and high-resolution dedicated MRI are improving in accuracy to diagnose
TFCC tears.
Peripheral lesions are difficult to diagnose with imaging.
Diagnostic injection with lidocaine in to ECU, FCU, TFCC space, DRUJ, midcarpus, or
lunotriquetrum may help to differentiate pain.
Tendinopathy (ECU, FCU)
DRUJ instability (dislocation, subluxation) and arthritis
Carpal instability (lunotriquetral, midcarpal)
Fracture (distal radius, ulnar styloid nonunion, triquetrum, hamate, pisiform)
Ulnar carpal impingement (ulnar abutment syndrome)
Kienböck disease
Treatment
Initial treatment for traumatic and symptomatic degenerative tears for up to
8–12 wks (4):
Immobilization in slight flexion and ulnar deviation in a short-arm cast for 4–6
wks, followed by removable wrist splints and physical therapy
Initial treatment with long-arm casting for 4–6 wks for traumatic tears and 3–4
wks of short-arm casting for degenerative tears recommended by some
McAdams (5)[C] and Rettig (1)[C] recommend more aggressive approach for
high-level athletes:
A trial of immobilization of the wrist for 2–3 wks if distal DRUJ is stable
Arthroscopic surgery if that fails or there is any associated instability
Care to not load the ulnar wrist or load in pronosupination is important.
Peripheral lesions often will heal owing to the improved vascularity.
Injections with corticosteroids are often tried, but there is no evidence for
efficacy to support this approach.
Medication
Trial of NSAIDs for pain
Referral
For competitive athletes, a more aggressive approach has been recommended
(1,5)[C].
If any instability to the DRUJ or lunotriquetrum is noted, refer for arthroscopy
(1,5)[C].
If the wrist is stable and not responding to initial immobilization, refer for
arthroscopy (1,5)[C].
For traumatic type 1A lesions, arthroscopic débridement/repair is
recommended (5)[C].
For traumatic type 1B–D peripheral ulnar and radius lesions, arthroscopic
repair is recommended (5)[C].
For degenerative type 2 lesions, ulnar variance is assessed as well as
midcarpal stability and wear.
If ulnar variance is 3 mm or less, wafer procedure is recommended (5)[C].
If ulnar variance is >3 mm, wafer + ulnar shortening is recommended
(1,5,6,7)[C].
Wafer procedure is arthroscopic decompression of the ulnocarpal joint with
débridement of the TFCC.
Ongoing Care
After initial injury, follow-up should be at 2–3 wks to gauge response to immobilization.
Prognosis
Return to play:
McAdams (5) recommends a conservative approach postoperatively to avoid ulnar
synovitis: 6 wks of immobilization in a short-arm or Muenster cast followed by 6 wks of
progressive range of motion and strength, with full return to sport at 3 mos postoperatively.
Rettig (1) recommends return to restricted sport (golf and tennis) 4–6 wks after
débridement of central TFCC tear (1A) and 3–4 mos after repair.
Prognosis:
McAdams (5) reported excellent results for return to play with improvement in pain relief
after arthroscopic surgery in 14 of 16 high-level athletes.
The 2 who did not return to play at 3 mos had DRUJ instability and ulnar-carpal abutment;
both returned to play after an additional period postoperatively.
Complications
Previously undiagnosed carpal or DRUJ instability or ulnar-carpal abutment
syndrome
References
1. Rettig AC. Athletic injuries of the wrist and hand: part II: overuse injuries of
the wrist and traumatic injuries to the hand. Am J Sports Med. 2004;32:262–
273.
2. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J

Hand Surg [Am]. 1989;14:594–606.
3. Palmer AK, Werner FW. Biomechanics of the distal radioulnar joint. Clin
Orthop Relat Res. 1984;26–35.
4. emedicine: Verheyden JR, Palmer AK: Triangular fibrocartilage complex

injuries, emedicine > orthopedic surgery > hand & upper extremity, updated
June 23, 2009.
5. McAdams TR, Swan J, Yao J. Arthroscopic treatment of triangular
fibrocartilage wrist injuries in the athlete. Am J Sports Med. 2008.
6. Steinberg B. Acute wrist injuries in the athlete. Orthop Clin North Am.
2002;33:535–545, vi.
7. Ahn AK, Chang D, Plate AM. Triangular fibrocartilage complex tears—a

review. Bull Hosp Jt Dis. 2006;64:114–118.
8. Coggins CA. Imaging of ulnar-sided wrist pain. Clin Sports Med.

2006;25:505–526, vii.
Additional Reading
eMedicine Specialties > Orthopedic Surgery > Hand & Upper Extremity >
Ulnar-Sided Wrist Pain Author: David M Lichtman, MD, Chair, Department of
Orthopedic Surgery, John Peter Smith Hospital; Clinical Professor,
Department of Orthopedic Surgery, University of Texas Southwestern Medical
Center; Professor, Department of Surgery, Uniformed Services University of
the Health Sciences; Professor and Chair, Department of Orthopedic Surgery,
University of North Texas Health Science Center. Coauthor(s): Atul Joshi,
MD, MCh, FRCS, Consulting Staff, Department of Orthopedics, Covenant
Medical Center. Contributor Information and Disclosures Updated: July 9,
2009 (8).
Palmer AK, Werner FW. The triangular fibrocartilage complex of the wrist–
anatomy and function. J Hand Surg [Am]. 1981;6:153–162.
Codes
ICD9
842.09 Other wrist sprain
Clinical Pearls
Ulnar-sided wrist pain has been described as the “low back pain” of the wrist.
A careful history and exam can demystify this condition.
Not solely relying on radiographs is important in correct diagnosis.
Early referral (arthroscopy) or advanced imaging (MR arthrogram, high-
resolution MRI) when suspecting TFCC tears or after failure to improve in a
short period of immobilization will improve the outcomes for the athlete.
Thoracic Outlet Syndrome
Kari Kindschi
Jeffrey R. Bytomski
Basics
Description
Neurogenic or vascular symptoms in the upper extremity due to compression of the
neurovascular bundle (brachial plexus and subclavian vessels) by skeletal and/or muscular
structures above the 1st rib and behind the clavicle
Symptoms are variable and based on the structure that is compressed or irritated.
3 types:
Neurogenic: >95% of cases
Venous: 4% of cases
Arterial: <1% of cases
Risk Factors
Repetitive work
Overhead athletes: Swimmers, pitchers, weightlifters, volleyball and tennis players
Poor posture
Middle-aged female
Congenital abnormalities:
Cervical rib
Abnormally long transverse process of C7
Anomalous fibromuscular band in the thoracic outlet
Trauma
Obesity
Etiology
Brachial plexus nerve roots, subclavian artery, and subclavian vein pass through the scalene
triangle formed by the 1st rib, anterior scalene muscles, and middle scalene muscles.
Increased risk of positional compression of the neurovascular bundle at the thoracic outlet
due to:
Congenital anatomic predisposition (cervical rib, abnormally long transverse process of C7,
anomalous fibromuscular band)
Acquired extrinsic factors (anterior scalene hypertrophy, pectoralis minor tightness, poor
posture causing decreased diameter of the costoaxillary canal, trauma, shortening of the
scalene muscles due to active trigger points)
Upper extremity venous thrombosis or Paget-Schroetter Syndrome:
Overhead athletes may develop “effort thrombosis” due to repetitive shoulder
hyperabduction and external rotation which can compress the axillary-subclavian veins,
damage the intimal lining, and transiently restrict venous flow. Over time, this creates a
favorable environment for thrombus formation.
Diagnosis
Thoracic outlet syndrome is largely a clinical diagnosis.
History
Neurogenic and vascular symptoms related to certain positions
Worse with lifting heavy objects, overhead activities, shoulder abduction, and external
rotation
Neurogenic:
Arm, shoulder, and neck pain
Paresthesias and numbness:
Frequently seen in the ulnar distribution
Headaches
Cramping of forearm muscles
Difficulty with fine motor skills of the hand
Sensory loss, motor weakness, atrophy (late findings)
Gilliatt-Sumner hand: Severe wasting of the abductor pollicis brevis and, to a lesser extent,
the interossei and hypothenar muscles
Venous:
Pain
Edema
Cyanosis
Feeling of heaviness in the arm or hand
Venous distension of the arm and hand
Arterial (often asymptomatic until embolization occurs):
Ischemic pain
Paresthesias and numbness
Claudication
Cool extremity
Pallor
Decreased distal pulse
Pulsating lump above the clavicle
Physical Exam
Swelling or discoloration of the affected extremity
Muscle atrophy
Decreased or absent distal pulse with activity or position changes
Bruit auscultated in the supraclavicular space
Provocative testing (low overall sensitivity and specificity):
Elevated arm stress test: (1)[C]
Arms abducted above the head in a “stick-em-up” position
Patient opens and closes fists at moderate speed for 3 min
Positive test if position reproduces pain or paresthesias
Upper limb tension tests: (1)[C]
Position 1: Abduct arms to 90°
Position 2: Extend wrists
Position 3: Tilt head to 1 side—ear to shoulder—then tilt head to other side
Positions 1 and 2 should cause ipsilateral pain, and position 3 should cause contralateral
pain.
Strongest response is an onset of symptoms with position 1 and an increase in severity
with positions 2 and 3.
Adson maneuver (original diagnostic test described in the 1920s) (1)[C]:
Neck extended and turned to the affected side while the shoulder is slightly abducted
and extended
Feel for radial pulse while patient takes a deep breath.
Positive test if pulse lost and symptoms reproduced
False positives are common.
Wright test:
Affected arm is progressively hyperabducted and externally rotated
Positive test if radial pulse lost
Allen test:
Flex elbow to 90°, abduct and externally rotate the shoulder
Patient rotates head away from the test arm
Positive test if radial pulse lost

Lab
Consider hypercoagulable workup in venous thoracic outlet syndrome and patients with arterial
thrombosis (2,3)[C].
Imaging
X-rays of the cervical spine and chest: Useful to evaluate for a cervical rib or other thoracic
pathology (2)[C]
X-rays of the shoulder (2)[C]
MRI: Helpful to determine the location and cause of compression or to identify an anomalous
fibrous band (3)[C]
Duplex US: To document degree of stenosis, presence of an aneurysm, or confirm
thrombosis (2,3)[C]
Electromyogram (3)[C]
Nerve conduction studies (3)[C]
Arteriography/venography: Reserved for cases of suspected arterial or venous thoracic outlet
syndrome and for surgical planning (2)[C]
Cervical disc disorders
Rotator cuff tear/impingement syndrome
Brachial plexus neuritis
Ulnar nerve entrapment
Complex regional pain syndrome
Fibromyalgia
Subclavian steal
Vasculitis
Raynaud's disease
Multiple sclerosis
Tumors of the spinal cord
Pancoast tumor
Neurofibroma
Treatment
Conservative therapy is the initial approach, except in cases of
thromboembolic phenomena with acute vascular occlusion, stenosis, arterial
dilatation or progressive neurologic deficits.
Medications (2)[C]:
NSAIDs
Muscle relaxants
Tricyclic antidepressants or SSRIs
Activity modification (2)[C]
Weight loss (2)[C]
Physical therapy (2,3,4)[C]:
Postural retraining
Pectoral and scalene stretching/strengthening
Scapulothoracic mobility
Trigger point treatment
Soft tissue mobilization
Botox injections (3)[C]:
CT-guided injections into the scalene muscles
Consider as a short-term adjunct to nonoperative therapy with physical
therapy or as a bridge to surgery
Venous thoracic outlet syndrome with thrombus present (3)[C]:
Thrombolytics and anticoagulation
Surgery is an option for neurogenic thoracic outlet syndrome that has not
responded to aggressive nonoperative treatments or for patients with vascular
compromise/thrombus formation (2,3)[C].
CT-guided scalene block with local anesthetic to relax the anterior scalene
muscle and lower the 1st rib to relieve the tension on the brachial plexus. If the
injection provides symptomatic relief, it indicates likely benefit of a 1st rib
resection/anterior scalenectomy (2,3)[C].
Ongoing Care
Surgical referral if signs of vascular compromise or severe neurogenic symptoms are present
Surgical referral when a cervical rib or extra-long transverse process of C7 is associated with
loss of sensation, muscle atrophy, or weakness
Surgical referral if symptoms persist despite an adequate course of aggressive therapy
Complications
Poststenotic dilatation of the subclavian artery resulting in aneurysm formation
and the potential for thromboembolism to the affected upper extremity (arterial
thoracic outlet syndrome)
Pulmonary embolism, residual symptoms and high recurrence rate (venous
thoracic outlet syndrome)
Progressive motor deficits (neurogenic thoracic outlet syndrome)
References
1. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet
syndrome. J Vasc Surg. 2007;46:601–604.
2. Fugate MW, Rotellini-Coltvet L, Freischlag JA. Current management of

thoracic outlet syndrome. Curr Treat Options Cardiovasc Med. 2009;11:176–
183.
3. Nichols AW. Diagnosis and management of thoracic outlet syndrome. Curr

Sports Med Rep. 2009;8:240–249.
4. Vanti C, Natalini L, Romeo A, et al. Conservative treatment of thoracic

outlet syndrome. A review of the literature. Eura Medicophys. 2006.
Codes
ICD9
353.0 Brachial plexus lesions
Thoracic Spine Injury
Karrn Bales
James Bales
Basics
Cautions:
In a traumatic injury suspicious for a thoracic spine fracture, immobilize the patient on a spine
board immediately.
Patients with a neurologic deficit should be transported directly to a trauma center.
Description
Thoracic spine fracture:
Rarely seen in sports but potentially very catastrophic when it occurs: Seen in collision
sports such as hockey, football, and wrestling
The spinal column can be divided into three anatomically distinct columns. If 2 of the 3
columns are disrupted, then the spinal column is unstable.
Posterior column: Posterior bony arch and interconnecting ligamentous structures
Middle column: Posterior aspects of the vertebral bodies, posterior annulus fibrosis, and
posterior longitudinal ligament
Anterior column: Anterior longitudinal ligament, anterior annulus fibrosis, and anterior
vertebral body
Fracture types:
Isolated articular fracture
Transverse process fracture
Spinous process fracture
Pars interarticularis fracture (more commonly seen in the lumbar spine)
Compression fracture (anterior or lateral flexion forces)
Fracture of anterior portion of vertebral body with intact middle column of spine: May
have posterior column disruption
Burst fracture (axial loading forces)
Fracture through middle column of spine: May have spreading of posterior elements and
lamina fractures
Fracture dislocations: Failure of all 3 columns following compression, tension, rotation, or
shear forces
Thoracic diskogenic pain:
The 3 basic structures of normal vertebral disks:
Nucleus pulposus: Gelatinous core of the disk, composed mostly of water and
proteoglycans
Annulus fibrosus: Surrounds the nucleus pulposus, composed of water and concentric
layers of collagen; tears in the innervated outer 3rd aspect may be clinically significant.
Vertebral endplates: Lie on the superoinferior aspect of the disks adjacent to the
vertebral bodies and aid in the diffusion of nutrients into the disks
Four categories of thoracic disk herniations:
Central: May cause spinal cord compression; patients may present with increased
muscle tone, hyperreflexia, abnormal gait, and/or urinary/bowel incontinence.
Centrolateral: May result in a presentation resembling Brown-Sequard syndrome, with
ipsilateral weakness and contralateral pain or sensory disturbances
Lateral: May cause nerve root compression and radiculopathy
Intradural: Rare, <10% of cases
Muscular contusions: Caused by a direct blow that results in bleeding in the muscle fibers;
seen especially in contact sports with potential for falling (football and wrestling)
Muscular strains:
Stretch tear of at least one of the back muscles or ligaments
Seen most frequently in sports involving twisting and turning
Facet syndrome:
Back pain associated with an overriding of the facets
Usually diagnosed by exclusion when there is no evidence of disk herniation or spinal
stenosis
Scheuermann kyphosis (juvenile diskogenic disease):
Anterior wedging of at least 5 degrees of 3 consecutive thoracic vertebral bodies
Hyperkyphosis of thoracic spine and hyperlordosis of lumbar spine
Spinal tumors;
Maintain a high index of suspicion in younger patients with night pain, fevers, and systemic
symptoms.
Primary tumors that occur in posterior elements are usually benign.
Osteoid osteoma, osteoblastoma, giant cell tumor, hemangioma, aneurysmal bone cyst,
eosinophilic granuloma
Vertebral body tumors are often malignant in the younger population.
Solitary plasmacytoma, Ewing sarcoma, osteosarcoma, chondrosarcoma, chordoma,
lymphoma
Epidemiology
Thoracic spinal fractures:
19–50% of fractures in the thoracolumbar spine region are associated with neurologic
damage and compression to the spinal cord.
15% of spinal fractures are seen in sports, the 3rd most common general cause after
motor vehicle accidents (45%) and falls (20%).
In sports-related injuries, the most common cause of fracture is water sports (65%).
Of the water sports, diving is the most common cause (60%).
Male-to-Female ratio of spinal fractures 4:1
Mean age: 24 ± 12 yrs
Scheuermann kyphosis: Seen between the ages of 10 and 15 yrs
Facet syndrome: Up to 40% of back pain is caused by facet inflammation.
Sport-specific injuries:
Football players have increased risk of degenerative disk disease, facet degeneration, and
chronic back pain that is proportional to their years of involvement in their sport.
Weight lifting is also associated with degenerative disk disease as well as sprains/strains
of the spinal musculature and ligaments.
Endurance athletes also may be at risk. Butterfly swimmers and rowers are at risk for rib
subluxation from the transverse processes of the thoracic spine, usually at the 6th or 7th
level.
Disk herniation is seen in any athletes participating in sports involving axial rotation of the
spine, such as golf.
Incidence
Scheuermann kyphosis:
1–8% of the general population
True incidence is probably underreported because the diagnosis is often missed or attributed
to poor posture.
Prevalence
Scheuermann kyphosis: Prevalence is approximately equal in males and females.
Etiology
The thoracic spine is very rigid owing to the rib cage and the costovertebral articulations. The
spinal canal is narrowest in the thoracic spine
Little flexion-extension motion
Strong flexion-extension forces combined with axial load are not tolerated well
biomechanically and may lead to injury.
Cervicothoracic junction and thoracolumbar junction are susceptible to shear and flexion-
extension forces.
The thoracic spine, enclosed and protected by the rib cage, has vertically oriented facets to
facilitate rotation.
Most thoracic spine fractures occur in the lower thoracic spine or at the thoracolumbar
junction.
Rotational or extension forces may fracture the pars interarticularis and damage facet
joints.
Up to 90% of herniated disks are due to a degenerative process. With aging, water
content of the disk decreases, leading to decreased disk height and loss of function of
absorbing axial loads.
Trauma can be implicated in 10–20% of patients, specifically a twisting or torsional
movement.
Facet syndrome:
Overuse of the facet joint
Spinal osteoarthritis
Sudden and excessive movement that traumatizes the joint
Commonly seen in athletes who engage in sports involving excessive spinal movements
such as gymnasts and figure skaters
Exact etiology unknown
74% heritability, indicating a major genetic contribution
Disorganized enchondral ossification, collagen reduction, increase in mucopolysaccharides
in the endplate
Diagnosis
Rapid evaluation of ABCs
Primary and secondary trauma survey
Detailed neurologic exam with specific attention to evidence of spinal cord injury
Thorough spine exam noting any deformity or tenderness
Any midline tenderness elicited on examination, distracting injury, or intoxication mandates
plain-film spine radiography (1,2)[A].
History
Significant force is required to produce thoracic vertebral fractures, so other injuries may
obscure those directly related to thoracic fractures.
Primary symptoms of thoracic vertebral fracture occur from pain at the fracture site or
impingement of nearby structures by bone fragments.
Common signs and symptoms:
Localized soft tissue defect
Pain or tenderness:
Localized—pain and tenderness over spinous process
Referred—paraspinal, anterior chest or abdomen
Paraspinal muscle spasm
Paresthesia or dysesthesia
Weakness (focal or global)
Distal areflexia, flaccid plegia
Bowel or bladder incontinence
Priapism
Loss of temperature control
Spinal shock—hypotension with bradycardia (1)[A]

Most commonly manifests insidiously with no significant history of trauma
Pertinent historical features: Duration of symptoms, extent of pain/weakness, and
presence of bowel or bladder symptoms
Pain is the most common symptom, the presenting symptom in 60% of patients. It may be
dull and localized to the thoracic spine or referred to retrogastric, retrosternal, or inguinal
areas.
Sensory disturbances, presenting symptom in 25% of patients
Numbness, dysesthesias, paresthesias in a dermatomal distribution

Weakness is the presenting symptom in 17% of patients, usually lower extremities,
occasionally abdominal and intercostal muscles.
Bladder symptoms are the presenting symptoms in only 2% of patients (3)[B].
Muscular strains: Typically mild pain following a sporting activity
Symptoms are typically insidious and slow in onset with no reported history of trauma.
Often seen in repetitive microtrauma, osteoporosis, osteochondrosis, necrosis of the ring
apophysis, and tight hamstrings (2)[A]
Physical Exam
Thoracic spine fracture: Focus on paresthesia and transient weakness, both of which may be
indicative of cord involvement.
Musculoskeletal findings often nonspecific but may reveal myofascial pain or patterns of
weakness or inflexibility
Sensory deficits to light touch or pinprick along a dermatomal pattern
Motor examination should include testing muscle strength, flexibility, and tone.
Include abdominal muscles because T9 and T10 lesions can paralyze the lower
abdominal muscles but spare the upper abdominal muscles.
Lower extremity weakness associated with spasticity or hyperactive reflexes is a serious
finding, indicative of myelopathy.
Reflexes: Hyperactive reflexes signify an upper motor neuron lesion, whereas hypoactive
reflexes signify a lower motor neuron lesion.
In purely thoracic diskogenic pain, upper extremity reflexes should be normal (otherwise
suspect cervical pathology) and patellar and Achilles reflexes should be normal (otherwise
suspect lumbosacral pathology) (3)[B].
Round back deformity that does not correct with passive extension
Hyperlordosis of the lumbar spine
Tight hip flexors, hamstrings, and lumbar fascia (2)[B]
Pain or tenderness, severe motor vehicle accident, or falls from height are indications for
anteroposterior (AP) and lateral plain-film views of the spine.
Thin-cut CT scanning is indicated in any patient with evidence of spinal fracture or
ligamentous injury on plain films to assess spinal canal integrity or in patients with normal
plain films and significant pain or tenderness and mechanism for severe injury (4)[B].
Lab
Spinal tumors:
Rule out tumor when patient has nocturnal back pain or constitutional symptoms.
CBC with differential
ESR
C-reactive protein
Imaging
CT scan is more sensitive and specific than plain radiographs for the detection of thoracic
spine fractures and should be used in any patient with a traumatic injury suspicious for
fracture based on history, exam, or initial plain films.
Plain radiographs are used to rule out fracture, tumor, or infection.
Signs of disk degeneration on x-ray:
Disk calcification: Present in up to 70% of patients with thoracic disk herniation and only
4–6% of patients without herniation
Osteophyte formation
Disk space narrowing
Kyphosis
MRI: Screening test of choice, better visualization of soft tissues, earlier recognition of disk
degeneration, and ability to evaluate in the sagittal plane
CT myelography: Less optimal study than MRI but good for diagnosing lateral herniations
and calcification (3,5)[A]
Scheuermann kyphosis: Plain radiographs are usually diagnostic.
Irregular upper and lower vertebral end plates
Apparent loss of disk space height
Wedging of >5 degrees in at least 1 vertebrae
Presence of hyperkyphosis >40 degrees, apex between T7 and T9 (5)[B]
Spinal tumors: Start with plain radiographs.
May not show abnormality until there is 30–50% loss of cancellous bone
Technetium-99m bone scan is sensitive but not specific.
18F positron emission tomography shows improved specificity.
MRI, especially with gadolinium, demonstrates excellent definition of soft tissue and
osseous changes (5)[B].
Arthritis (degenerative and rheumatoid)
Spina bifida
Congenital malformation
Neoplasm
Pathologic fracture
Treatment
General:
Most thoracic injuries respond well to rest, NSAIDs, physical therapy, and
stretching.
Limit bed rest to 1 or 2 days.
Return to play may occur gradually as the athlete achieves painless range of
motion (ROM) (1)[A].
P.
Stable fractures are often treated with brace immobilization.
Thoracolumbosacral orthosis immobilizes a stable thoracic compression
fracture (<50% loss of height).
Unstable fractures may be a consideration for surgical stabilization.
Muscular contusions: Conservative treatment:
Ice to limit bleeding and swelling
Moist heating pad after 72 hr
Massage after initial pain has resolved
Analgesics as needed for pain
Restrict activity until pain-free.
Physical therapy consisting of ROM exercises (5)[A]
Muscular strains: Conservative treatment:
Physical therapy regimen of gradual mobilization as well as stabilization
NSAIDs
Facet syndrome: Conservative treatment:
NSAIDs
Postural correction
Rest
If no response to above treatment, consider an intraarticular facet injection
of corticosteroid and long-acting local anesthetic
Physical therapy (PT) to stretch tight hamstring muscles, hip flexors, and
lumbar fascia
PT to strengthen abdominal and upper back postural musculature
Consider a brace in a skeletally immature patient with fixed thoracic kyphosis
>50 degrees.
Milwaukee brace for high thoracic curves
Boston brace with sternal pads for curves with apex below T7
Surgery is rarely indicated, and indications are unclear.
Decision for surgery needs to be an individual one based on patient's
symptoms and self-perception (2)[B].
ED Treatment
Perform all needed resuscitation and diagnostic tests with the patient in full
spinal immobilization.
If spinal cord injury is suspected, administer high-dose steroids and consult a
neurosurgeon or orthopedic surgeon.
If spinal fracture or ligamentous injury is suspected without neurologic
impairment, arrange CT scan or MRI while simultaneously consulting
neurosurgery or orthopedic surgery.
Pain control should be administered as soon as possible. NSAIDs, opiates,
and benzodiazepines are the mainstays of treatment.
Medication
Thoracic spine fracture with neurologic deficit:
High-dose steroid protocol: Solumedrol 30 mg/kg IV bolus within 8 hr of injury,
followed by an infusion of 5.4 mg/kg/hr for the next 23 hr (4)[A]
Other causes of back pain: NSAIDs
Follow the ABCs of trauma resuscitation.
Airway intervention should be done with inline cervical immobilization.
Preserve residual spinal cord function and prevent further injury by stabilizing
the spine.
Admission Criteria
Patients with significant spinal cord or column injury should be treated in a
regional trauma center.
Unstable spinal column injury
Cord or root injury
Ileus
Pain control
Concomitant traumatic injury
Discharge Criteria
Stable minor fractures after orthopedic or neurosurgical evaluation
References
1. Khan N, Husain S, Haak M. Thoracolumbar injuries in the athlete. Sports
Med Arthrosc. 2008;16:16–25.
2. Lowe TG, Line BG. Evidence based medicine: analysis of Scheuermann

kyphosis. Spine. 2007;32:S115–S119.
3. Brown CW, Deffer PA, Akmakjian J, et al. The natural history of thoracic
disc herniation. Spine. 1992;17:S97–S102.
4. Chiles BW, Cooper PR. Acute spinal injury. N Engl J Med. 1996;334:514–
520.
5. Curtis C, d'Hemecourt P. Diagnosis and management of back pain in
adolescents. Adolesc Med State Art Rev. 2007;18:140–164, x.
Additional Reading
Diaz J, Cullinane D, Altman D, et al. Practice management guidelines for the
screening of thoracolumbar spine fracture. J Trauma. 2007;63:709–718.
Karlson K. Thoracic region pain in athletes. Curr Sports Med Rep. 2004;53–
57.
Papagelopoulos P, Mavrogenis A, Savvidou O, et al. Current concepts in

Scheuermann's kyphosis. Orthopedics. 2008;31;52–58.
Ye C, Sun T, Li J, et al. Patterns of sports and recreation related spinal cord

injuries in Beijing. Spinal Cord. 2009; May 12.
Codes
ICD9
722.11 Displacement of thoracic intervertebral disc without myelopathy
805.2 Closed fracture of dorsal (thoracic) vertebra without mention of spinal cord injury
805.3 Open fracture of dorsal (thoracic) vertebra without mention of spinal cord injury
Thrombophlebitis, Superficial
Jeffrey M. Mjaanes
Michael Hanna
Basics
Description
Superficial thrombophlebitis is an inflammatory condition of the veins with clinical findings of
pain, tenderness, induration, and erythema of a superficial vein with secondary thrombosis.
Septic (suppurative) thrombophlebitis types:
Iatrogenic
Infectious: Mainly syphilis and psittacosis
Aseptic thrombophlebitis types:
Primary hypercoagulable states: Disorders with measurable defects in the proteins of the
coagulation and/or fibrinolytic systems
Secondary hypercoagulable states: Clinical conditions with a risk of thrombosis
System(s) affected: Cardiovascular
Synonym(s): Phlebitis; Phlebothrombosis; Superficial venous thrombosis
Abbreviations: DVT = deep vein thrombosis; LMWH = low-molecular-weight heparin
Pediatric: Subperiosteal abscesses of adjacent long bone may complicate.
Geriatric: Septic thrombophlebitis is more common; prognosis poorer.
Others: N/A
Warfarin and NSAIDs are contraindicated.
Associated with increased risk of aseptic superficial thrombophlebitis
Alert
Note: Potentially lethal misnomer is use of now abandoned term superficial femoral vein
thrombosis, which is actually a DVT and should be treated as such.
Epidemiology
Incidence
Septic:
Up to 10% of all nosocomial infections
Incidence of catheter-related thrombophlebitis is 88/100,000.
Develops in 4–8% if cutdown is performed
More common in childhood
Aseptic primary hypercoagulable state:
Antithrombin III and heparin cofactor II deficiency incidence is 50/100,000.
Antithrombin III and heparin cofactor II deficiency: Neonatal period, but 1st episode usually
at age 20–30 yrs
Proteins C and S deficiency: Before age 30
Aseptic secondary hypercoagulable state:
Trousseau syndrome incidence in malignancy 5–15%
Trousseau syndrome incidence in pancreatic carcinoma 50%
In pregnancy, 49-fold increased incidence of phlebitis
Superficial migratory thrombophlebitis in 27% of patients with thromboangiitis obliterans
Mondor disease (superficial phlebitis of the breast): Women ages 21–55 yrs; also can
occur in dorsal penile vein in men
Thromboangiitis obliterans onset: 20–50 yrs
Predominant gender: Mondor: Female > Male (2:1); thromboangiitis obliterans: Female >
Male (1–19% of clinical cases)
Risk Factors
Nonspecific:
Immobilization
Obesity
Advanced age
Postoperative states
Septic:
IV catheter
Duration of IV catheterization (68% of cannulas have been left in place for 2 days)
Emergent placement of catheter
Cutdowns
Cancer, debilitating diseases
Steroids
Incidence is 40 times higher with plastic cannulas (8%) than with steel or scalp cannulas
(0.2%)
Thrombosis
Dermal infection
Burn patients
Lower extremities IV catheter
IV antibiotics
AIDS
Varicose veins
Antithrombin II and heparin cofactor II deficiency:
Pregnancy
Oral contraceptives
Surgery, trauma, infection
In pregnancy;
Increased age
HTN
Eclampsia
Increased parity
Thromboangiitis obliterans: Persistent smoking
Mondor disease:
Breast abscess
Antecedent breast surgery
Breast augmentation
Reduction mammoplasty
Genetics
Septic: No known genetic pattern
Antithrombin III deficiencies: Autosomal dominant
Proteins C and S deficiency: Autosomal dominant with variable penetrance
Disorders of fibrinolytic system: Congenital defects, inheritance variable
Dysfibrinogenemia: Autosomal dominant
Factor XII deficiency: Autosomal recessive
General Prevention
Use of scalp vein cannulas
Avoidance of lower extremity cannulations
Insertion under aseptic conditions
Secure anchoring of the cannulas
Replacement of cannulas, connecting tubing, and IV fluid every 48–72 hr
Neomycin-polymyxin B-bacitracin ointment in cutdown
Etiology
Septic:
Staphylococcus aureus in 65–78%
Enterobacteriaceae, especially Klebsiella
Multiple organisms in 14%
Anaerobic isolate rare
Candida spp.
Cytomegalovirus in AIDS patients
Aseptic primary hypercoagulable state:
Antithrombin III and heparin II deficiency
Protein C and protein S deficiency
Disorder of tissue plasminogen activator
Abnormal plasminogen and coplasminogen
Dysfibrinogenemia
Factor XII deficiency
Lupus anticoagulant and anticardiolipin antibody syndrome
Aseptic secondary hypercoagulable states:
Malignancy (Trousseau syndrome: Recurrent migratory thrombophlebitis): Seen most
commonly in metastatic mucin or adenocarcinomas of the GI tract (pancreas, stomach,
colon, and gall bladder), lung, prostate, ovary
Pregnancy
Oral contraceptives
Infusion of prothrombin complex concentrates
Behçet disease
Buerger disease
Mondor disease

DVT: Superficial and deep vein thromboses (DVTs) can occur together from direct extension
or noncontiguous findings.
Incidence: Coexisting conditions 15% of time (1)[C]
Both more likely in a hypercoagulable state
Lower extremity superficial thrombophlebitis of great saphenous vein thought to be
associated with DVTs (especially above knee) (1)[C]
Varicose veins
Systemic diseases such as pancreatic or other abdominal cancers
Hypercoagulable states such as Factor V Leiden, prothrombin gene mutation, antithrombin III
(AT-III), protein C and protein S deficiencies
Surgery
Trauma, burns
Obesity, pregnancy
Thromboangiitis obliterans
Diagnosis
Pre Hospital
Treat initially with support stockings, elevation, and OTC analgesics, such as acetaminophen, or
NSAIDs, such as ibuprofen.
History
Swelling over affected vein: May feel firm and “cordlike”
Redness and warmth of affected vein and area
Pain and tenderness to palpation
Physical Exam
Swelling, tenderness, mild erythema along the course of the affected vein(s); palpable “cord”
May look like cellulitis or erythema nodosa
Fever in 70% of patients
Warmth, significant erythema, tenderness, or lymphangiitis in 32%
Signs of systemic sepsis in 84% in suppurative thrombophlebitis (hypotension, tachycardia,
shallow respirations, altered mental status, multiorgan failure)

Lab
CBC
Blood culture
Coagulation assay and special tests (eg, Factor V Leiden) may be indicated.
Other tests:
Doppler or duplex US
Venography
Septic:
Bacteremia in 80–90%
Culture of IV fluid bag and tip
Leukocytosis
Aseptic:
Acute-phase reactant
Patients with single episode of superficial thrombophlebitis do not require
hypercoagulable screening. Screen for recurrent cases without known risk factors (2)
[C].
Factor levels
Protein C and S
Thrombin activity
Platelet function test
Doppler or duplex US
Venography
Septic:
Bacteremia in 80–90%
Culture of IV fluid bag and tip
Leukocytosis
Aseptic:
Acute-phase reactant
Patients with single episode of superficial thrombophlebitis do not require hypercoagulable
screening. Screen for recurrent cases without known risk factors (2)[C].
Factor levels
Protein C and S
Thrombin activity
Platelet function test
Drugs that may alter lab results: In sepsis, broad-spectrum antibiotics

Imaging
US of veins reveals an increase in the diameter of the lumen (can detect extension of
thrombus but less useful in regions deep to the clavicle or mandible).
Upper extremity superficial thrombophlebitis and saphenous thrombophlebitis below the
knee do not require imaging in absence of risk factors for DVT (2)[C].
Saphenous thrombophlebitis above the knee is more likely to progress to DVT and requires
diagnostic US and follow-up US in 3–7 days (2)[C].
Chest x-ray: Multiple peripheral densities or a pleural effusion consistent with pulmonary
embolism, abscess, or empyema
Bone and gallium scan: For associated subperiosteal abscess in septic thrombophlebitis
High-resolution CT scan with contrast material: Most useful for jugular or vena caval septic
thrombophlebitis
Venography (more invasive than above)
Evaluation of complications (DVT and others)
Leukocyte imaging
Skin biopsy helpful in recurrent and migratory types as well as unclear cases
The affected vein is enlarged, tortuous, and thickened.
Associated perivascular suppuration and/or hemorrhage
Vein lumen may contain pus and thrombus.
Endothelial damage, fibrinoid necrosis, and thickening of the vein wall
Cellulitis
Erythema nodosa
Cutaneous polyarteritis nodosa
Sarcoid granuloma
Kaposi sarcoma
Hyperalgesic pseudothrombophlebitis
Panniculitis
Insect bite
Treatment
Septic: Inpatient
Aseptic: Outpatient
Medication
First Line
Septic:
Initially, antistaphylococcal agent (vancomycin 30 mg/kg/day in 2 equally
divided doses) plus an aminoglycoside (eg, gentamicin 1.7–2.0 mg/kg IV as a
loading dose, followed by 1.5 mg/kg per renal function). If MSSA, change
vancomycin to oxacillin 2 g IV q4h (3)[C].
Duration of therapy is empirical.
If due to Candida albicans, consider a short course of amphotericin B, 200
mg cumulative dose
If osteomyelitis documented, antibiotic therapy for at least 6 wks
Aseptic:
NSAIDs for upper extremity and below-the-knee clots without DVT risk
factors
Systemic LMWH or unfractionated heparin ×4 wks suggested for all above-
the-knee superficial or large leg thromboses (4)[B],(5)[A]
Oral anticoagulant warfarin with bridging as alternative (4)[C]
Antithrombin III and heparin cofactor II deficiency:
IV heparin
Antithrombin III concentrate
Prophylaxis: Warfarin
Proteins C and S deficiency: Long-term warfarin, lower dose, no loading
Disorder of tissue plasminogen activator:
Phenformin and ethylestrenol
Stanozolol and phenformin
Stanozolol alone
Ethylestrenol alone
Second Line
Factor XII deficiency: Streptokinase or alteplase [tissue plasminogen activator
(tPA)]
Behçet: Oral anticoagulants plus cyclosporine
Thromboangiitis obliterans: Corticosteroid, antiplatelets, and vasodilating drugs
General Measures
Heat application
Extremity elevation
Compression stockings
Continue ambulation: Bed rest is counterproductive. Patients tend to do better
with early and continued mobilization (6)[C].
If occurs in setting of IV catheter, remove the catheter.
Referral
In high-risk patients (ie, patients with varicosities and a history of superficial
thrombophlebitis), referral to a surgeon may be indicated. Vein stripping,
phlebectomy, or sclerotherapy may be required to prevent further episodes.
Treatment with a therapeutic or prophylactic dose of LMWH or an NSAID
reduces the incidence of SVT extension or recurrence but not the incidence of
venous thromboembolic disease (7)[B].
An intermediate dose of LMWH for a month plus use of elastic compression
stockings may be the best preventive approach, although more studies are
needed (5)[A].
Septic:
Surgery is always necessary in peripheral thrombophlebitis.
If central vein is involved, surgical resection may not be possible.
If septic thrombophlebitis is suspected, exploratory surgery should be
performed (3)[C].
Excision of the involved vein segment and all involved tributaries
Excision from ankle to groin may be required in some burn patients.
If systemic symptoms persist after vein excision, reexploration is necessary
with removal of all involved veins.
Drainage of contiguous abscesses
Remove all cannulas.
Aseptic:
Mondor disease: Consider surgical transection of the phlebitic cord.
Management of underlying conditions
Ongoing Care
Activity
Patient Monitoring
Septic:
Routine WBC count and differential and culture
Repeat culture from the phlebitic vein
Aseptic:
For above-the-knee clots of the great saphenous vein, monitor with US after 3–7 days to
exclude progression (1).
Clinical follow-up to rule out secondary complications and improvement
Repeat of blood studies for fibrinolytic system, platelets, and factors
Diet
No restrictions
Patient Education
Avoid trauma.
Be alert to change in skin color.
Be alert to tenderness over extremities.
Prognosis
Septic: High mortality (50%) if untreated
Aseptic:
Usually benign course: Recovery in 7–10 days
Antithrombin III and heparin cofactor deficiency: Recurrence rate is 60%.
Proteins C and S: Recurrence rate is 70%.
Prognosis depends on development of DVT and early detection of complications.
Aseptic thrombophlebitis can be isolated, recurrent, or migratory.
Complications
Complications of superficial thrombophlebitis are relatively rare. Risk of
embolism is uncommon compared with DVT.
Septic:
Systemic sepsis, bacteremia (84%)
Septic pulmonary emboli (44%)
Metastatic abscess formation
Gangrene
Pneumonia (44%)
Subperiosteal abscess of adjacent long bones in children
Aseptic:
DVT
Thromboembolic phenomena
Treatment/prevention of complications:
Dysfibrinogenemia:
Acute attack: Anticoagulation
Prophylaxis: Stanozolol
Abnormal plasminogen and plasminogenemia:
Acute attack: Anticoagulation
Prophylaxis: Warfarin
Factor XII deficiency: Standard therapy
Lupus anticardiolipin: Prophylaxis: Warfarin
Trousseau syndrome: Heparin
For pregnancy: Heparin
Behçet disease:
Phenformin
Ethylestrenol
Stanozolol
Thromboangiitis obliterans:
Stop smoking
Pentoxifylline
Contraindications: Refer to manufacturers' literature.
Precautions: Refer to manufacturers' literature.
Significant possible interactions: Refer to manufacturers' literature.
References
1. Decousus H, Epinat M, Guillot K, et al. Superficial vein thrombosis: risk
factors, diagnosis, and treatment. Curr Opin Pulm Med. 2003;9:393–397.
2. Fernandez L. Superficial phlebitis. In: UpToDate, Sarkar R, Ed. UpToDate,

Waltham, MA, 2009.
3. Spelman D. Suppurative (septic) thrombophlebitis. In: UpToDate, Sexton

DJ, Ed. UpToDate, Waltham, MA, 2009.
4. Kearon C, Kahn SR, Agnelli G, et al. Antithrombotic therapy for venous
thromboembolic disease: American College of Chest Physicians Evidence-
Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133:454S–
545S.
5. Di Nisio M, Wichers IM, Middeldorp S. Treatment for superficial

thrombophlebitis of the leg. Cochrane Database Syst Rev. 2007;CD004982.
6. Cesarone MR, Belcaro G, Agus G, et al. Management of superficial vein

thrombosis and thrombophlebitis: status and expert opinion document.
Angiology. 2007;58(Suppl 1):7S–14S; discussion 14S–15S.
7. Wichers IM, Di Nisio M, Büller HR, et al. Treatment of superficial vein

thrombosis to prevent deep vein thrombosis and pulmonary embolism: a
systematic review. Haematologica. 2005;90:672–677.
Additional Reading
Mandell GL, ed. Principles and practice of infectious diseases. 4th Ed. New
York: Churchill Livingstone, 1995.
Samlaskie CP, James WD. Superficial thrombophlebitis I. Primary

hypercoagulable states. J Am Acad Dermatol 1990;22:975–989.
Samlaskie CP, James WD. Superficial thrombophlebitis II. Secondary

hypercoagulable states. J Am Acad Dermato. 1990;23:1–18.
Superficial Thrombophlebitis Treated By Enoxaparin Study Group. A pilot

randomized double-blind comparison of a low-molecular-weight heparin, a
nonsteroidal anti-inflammatory agent, and placebo in the treatment of
superficial vein thrombosis. Arch Intern Med. 2003;163:1657–1663.
See Also
Thrombosis, deep vein (DVT)
Cellulitis
Codes
ICD9
451.0 Phlebitis and thrombophlebitis of superficial vessels of lower extremities
451.11 Phlebitis and thrombophlebitis of femoral vein (deep) (superficial)
451.82 Phlebitis and thrombophlebitis of superficial veins of upper extremities
Clinical Pearls
Superficial thrombophlebitis is an inflammatory condition of the veins with
clinical findings of pain, tenderness, induration, and erythema of a superficial
vein with secondary thrombosis.
Risk factors include hypercoagulable states, venous stasis, and IV catheters.
Diagnosed clinically and confirmed by finding a thrombus with Doppler US
Aseptic type is usually benign, and treatment is based on location and risk
factors.
Conservative therapy with heat, compression, elevation, and NSAIDS for
upper extremity and lower leg clots
Upper leg clots and those with risk factors for DVTs require anticoagulation
×4 wks.
Septic type more serious and requires IV antibiotics and usually surgical
exploration with resection of affected vessels.
Thrombosis, Deep Vein (DVT)
Harry Stafford
Blake Boggess
Jake Veigel
Basics
Description
Venous thrombosis is a condition in which a blood clot (thrombus) forms in a vein.
This clot can limit blood flow through the vein, causing swelling and pain.
Most commonly, venous thrombosis occurs in the “deep veins” in the legs, thighs, or pelvis.
Associated with inflammation of the vessel wall
This is called a deep vein thrombosis, or DVT.
Roughly 2 million cases of thrombophlebitis occur in the U.S. annually.
Most significant complication is pulmonary embolism (PE), from which an estimated 60,000
Americans die annually
Lower extremity DVT is divided into distal (to the popliteal vein) or proximal.
DVT can also occur in upper extremity veins.
Epidemiology
Venous thrombosis can form anywhere in the venous system. However, DVT is the most
common type of venous thrombosis. If a part or all of the blood clot in the vein breaks off
from the site where it was created, it can travel through the venous system; this is called an
embolus.
If the embolus lodges in the lung, it is called a pulmonary embolism (PE).
In most cases, PE is caused by a DVT when part of a blood clot breaks off and lodges in the
lung.
Incidence
Affects 1 in 1,000 people every year. Rates increase with age and are higher in males
compared to females.
Prevalence
2 million cases of deep venous thrombosis occur in the U.S. annually.
Risk Factors
Independent risk factors (1):
Increasing age
Surgery
Trauma: Fractures of long bones or crush injuries
Hospitalization or nursing home confinement
Malignancy
Indwelling or prior indwelling central venous catheter or pacemaker
Prior superficial vein thrombosis
Neurologic disease with paresis
Liver disease
Other risk factors:
Oral contraceptive use
Pregnancy/postpartum period
Hormone replacement therapy
Tamoxifen therapy
Selective estrogen receptor modulator therapy
Travel
Inherited hypercoagulable states
Other hypercoagulable states
High altitude (>14,000 feet)
Prior DVT or pulmonary embolism
Obesity
Nephrotic syndrome
Heparin-induced thrombocytopenia
Polycythemia vera
Myeloproliferative disorders
Paroxysmal nocturnal hemoglobinuria
Thromboangiitis obliterans
Thrombotic thrombocytopenic purpura
Behçet disease
Genetics
Genetic defects such as factor V Leiden mutation or protein C or S deficiencies are associated
with DVTs.
General Prevention
Avoid prolonged immobility.
Caution when using birth control; use low-estrogen pills when possible.
Prophylaxis for hospitalized patients
Etiology
Virchow's triad of venous stasis, vessel wall injury, and coagulation abnormality is considered
the primary mechanism for the development of venous thrombosis.

Malignancy accounts for 1/5 of all cases.
The list of risk factors is inclusive of associated conditions.
Diagnosis
Wells criteria (2)[A]
Active cancer within 6 mos +1
Paralysis or immobilization of lower extremity +1
Recent bedridden >3 or surgery <4 wks +1
Tenderness/cord along vein +1
Entire leg swollen +1
Calf circumference >3 cm vs other leg +1
Alternative diagnosis likely -2
Interpretation
High probability +3
Moderate probability +1–2
Low probability 0
History
Many patients are asymptomatic; however, the classic symptoms are swelling, pain, and
discoloration in the involved extremity.
Clinical signs and symptoms of PE as the primary manifestation occur in 10% of patients with
confirmed DVT.
The pain and tenderness associated with DVT do not usually correlate with the size, location,
or extent of the thrombus.
Physical Exam
Inspection of the extremity may reveal ipsilateral edema, erythema:
>1–2-cm circumferential difference in leg
Palpation of the extremity may reveal a palpable cord, increased warmth, and superficial
venous dilation.
Homans' sign: Passive dorsiflexion of the ankle elicits pain in the calf.
Phlegmasia cerulean dolens: Reddish purple lower extremity from venous engorgement and
obstruction
Evaluate for signs of pulmonary embolus: Tachycardia, tachypnea, low-grade fever, and a
cardiac exam

Duplex scanning (combination of color Doppler and B-mode US):
Rapid, inexpensive, and highly accurate in detecting proximal DVT
Impedance plethysmography:
Nearly as accurate as duplex scanning
Not as routinely available as US
Venography is the historic gold standard:
Accurate but invasive
Associated with dye reactions
Can precipitate phlebitis
Lab
No blood test diagnoses or excludes DVT with certainty:
D-dimer (ELISA technique) has sensitivities around 95% (3)[A].
All D-dimer assays have been evaluated in various validation studies that determine the
assay's sensitivity, specificity, and negative predictive value (NPV). An assay with a sensitivity
of 80% has an NPV of 97.6% in a low-risk patient. However, the NPV of the same assay is
only 33% in high-risk patients with a pretest probability of 90% for DVT.
CBC and prothrombin time (PT)/partial thromboplastin time (PTT) as baseline measurements
Labs for idiopathic DVT include factor V Leiden, prothrombin, serum homocysteine, factor
VIII level, lupus anticoagulant, protein C and S levels, antithrombin activity, and anticardiolipin
antibodies.
Imaging
US (3)[A]:
Sensitivities and specificities vary by vein with more accuracy in the proximal veins.
Sensitivities of 89–96%
Specificities of 94–99%
US is recommended for patients with high pretest probability (Wells criteria) in the lower
extremities (4)[A].
Helical CT scan
Contrast venography has long been considered the reference test for the diagnosis of DVT.
Superficial thrombophlebitis
Cellulitis
Torn muscles and ligaments
Ruptured baker's cyst
Bilateral edema (seen with heart, kidney, or liver disease) is rarely caused by DVT.
Prior DVT and postphlebitic syndrome
Arterial insufficiency
Arthritis
Cellulitis, lymphangitis
Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess
Hematoma
Lymphedema
Neurogenic pain
Prolonged immobilization or limb paralysis
Stress fractures or other bony lesions
Varicose veins
Treatment
ED Treatment
Anticoagulation:
Contraindications:
Active internal bleeding
Uncontrolled HTN
Significant recent trauma or surgery
CNS tumor
Initiate in the emergency department
Duration of oral anticoagulation in unprovoked venous thromboembolism
should be extended (longer than 12 mos, level 1 evidence), whereas
provoked venous thromboembolism may be well served with just 3 mos of
therapy (level 2 evidence) (5).
Recurrent thromboembolism despite documented adequate anticoagulation
(defined as an aPTT of <1.5 times control for heparinized patients and an
international normalized ratio (INR) of <2 for warfarinized patients) requires
vena caval interruption.
Low molecular-weight heparin (LMWH) is treatment of choice if cost is less
important or outpatient management is considered:
Enoxaparin
Does not require laboratory monitoring
May be administered as an outpatient
Initiate oral warfarin therapy same day
Medication
Enoxaparin: 1 mg/kg SC b.i.d.
Heparin: 80 IU/kg bolus followed by a drip of 18 IU/kg/hr (aPTT should be
checked in 6 hr and tile infusion rate adjusted accordingly)
Warfarin: 10 mg PO, then 5 mg PO every day; monitor PT
Referral
Cardiology, pulmonary, or anticoagulation clinic is appropriate if the physician is
unable to monitor the INR levels or is uncomfortable with managing patients with
DVT.
Patients with DVT rarely require immediate stabilization:
Phlegmasia alba dolens (painful white leg) or phlegmasia cerulea dolens
(painful blue leg)
Hypoperfusion with blanching and cyanosis
May require fluid resuscitation, immediate anticoagulation, and thrombolysis or
thrombectomy
Admission Criteria
Severely ill patients
Patients with significant comorbid conditions
Patients without the means for appropriate home administration of LMWH
Discharge Criteria
Isolated DVT
No significant comorbid conditions
Resources available for home administration of LMWH
Appropriate follow-up assured
Ongoing Care
Patient Monitoring
INR levels should be evaluated frequently until stable with a target range between 2 and 3.
Diet
Patients should also be aware that certain foods high in vitamin K may diminish the
anticoagulation effects of warfarin.
Patient Education
When patients are traveling, they should sit in seats that allow leg extension, take hourly
walking breaks, wear loose clothing, and not cross their legs.
Prognosis
Pulmonary embolism will occur in 50% of untreated patients with DVT within days or weeks. If
the DVT was caused by a thrombophilic disorder, the risk of repeat episode may be high.
Complications
Review all secondary disease or negative reactions that may occur during the
course of an illness, that usually aggravate the illness, and any possible
preventive measures. In addition, differentiate between acute/chronic, likelihood
of complication, and common/rare.
References
1. Heit JA. Risk factors for venous thromboembolism. Clin Chest Med.
2003;24:1–12.
2. Wells PS, Anderson DR, Bormanis J, et al. Value of assessment of pretest

probability of deep-vein thrombosis in clinical management. Lancet.
1997;350:1795–1798.
3. Segal JB, Eng J, Tamariz LJ, et al. Review of the evidence on diagnosis of
deep venous thrombosis and pulmonary embolism. Ann Fam Med.
2007;5:63–73.
4. Qaseem A, Snow V, Barry P, et al. Current diagnosis of venous

thromboembolism in primary care: a clinical practice guideline from the
American Academy of Family Physicians and the American College of
Physicians. Ann Intern Med. 2007;146:454–458.
5. Segal JB, Streiff MB, Hoffman LV, et al. Management of venous

thromboembolism: a systematic review for a practice guideline. Ann Intern
Med. 2007;146:211–222.
Additional Reading
Hirsh J, Hoak J. Management of deep vein thrombosis and pulmonary
embolism. A statement for healthcare professionals. Council on Thrombosis
(in consultation with the Council on Cardiovascular Radiology), American
Heart Association. Circulation. 1996;93:2212–2245.
Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis

by real-time B-mode ultrasonography. N Engl J Med. 1989;320:342.
Levine M, et al. A comparison of LMWH administered primarily at home with

unfractionated heparin administered in the hospital for proximal DVT. N Engl J
Med. 1996;334:677–681.
Meyering C, Howard T: Hypercoagulability in athletes. Curr Sports Med Rep.

2004;3:77–83.
Pearson SP, et al. A critical pathway to evaluate suspected DVT. Arch Int
Med. 1995;155:1773–1778.
Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the

diagnosis of suspected deep-vein thrombosis. N Engl J Med.
2003;349:1227–1235.
Codes
ICD9
451.11 Phlebitis and thrombophlebitis of femoral vein (deep) (superficial)
451.19 Phlebitis and thrombophlebitis of other
453.40 Acute venous embolism and thrombosis of unspecified deep vessels of lower
extremity
Clinical Pearls
A DVT is associated with risk factors noted in Virchow's triad of:
Venous stasis of an alteration in normal blood flow
Vascular endothelial injury
Hypercoagulability
Essential workup includes a Doppler US (duplex scanning) of the affected
extremity.
Treatment with anticoagulation
Thumb Ulnar Collateral Ligament Sprain (Skier's
Thumb)
Ian Shrier
Dan Somogyi
Basics
Description
Synonym(s): Gamekeeper thumb; Skier's thumb
Sprain of the ulnar collateral ligament (UCL) of the 1st metacarpophalangeal (MCP) joint with
or without a bony avulsion from the insertion on the phalanx
Stener lesion:
Proximal end of the ligament becomes trapped superficial to the adductor pollicis
aponeurosis
Incidence with a complete tear is reported between 64 and 87% (1)
Epidemiology
5–7% of all skiing injuries (2)
Risk Factors
Ski poles likely increase the risk of UCL injury:
Wrist straps on the ski poles do not likely increase the risk of UCL injury further.
Diagnosis
Avulsion of bony fragment at the insertion of UCL on the phalanx may be associated with
this condition.
History
Stress to the thumb in extended and/or abducted position
Usually in skiing, but often occurs in other sports, such as football and judo
Physical Exam
Diagnosis may be made based on physical examination if the examination is done within a
couple of hours.
Pain, swelling, and muscle spasm may make clinical diagnosis of a complete tear difficult if
the examination is performed later:
Local anesthetic may be helpful in the diagnosis in these cases (3)[C].
Pain at the origin and insertion of the UCL
Swelling and tenderness over the ulnar aspect of the 1st MCP joint
Mild-to-complete instability on stress testing of UCL with MCP joint in flexion, depending on
whether it is a 1st-, 2nd-, or 3rd-degree sprain:
Tested at 0° and 30° of metacarpal phalangeal joint flexion
There is significant side to side variability in UCL testing noninjured individuals (4)[B]:
Most important physical finding is lack of an endpoint, as this indicates complete
ligament disruption.

Imaging
X-rays (posteroanterior/lateral) (3):
Rule out bony avulsion or other fractures.
Stress x-rays to determine if the tear is partial (usually treated conservatively) or complete
(often treated surgically)
Because of associated muscle spasm, many clinicians advise local anesthetic infiltration
before x-rays:
Unclear benefit of stress views
“Sag sign”: Volar subluxation of the proximal phalanx in relation to the metacarpal at the
MCP joint may indicate UCL injury (3).
US:
Appears to have excellent accuracy, but is operator-dependent and requires experience
(5,6):
Can be used to delineate partial from complete tears as well as identification of a Stener
lesion
MRI (7,8):
Ordered to diagnose whether there is a complete tear or if there is a Stener lesion
present:
96% sensitivity and 95% specificity
Unclear whether arthrography provides additional benefit over simple MRI
Radial collateral ligament sprain
Metacarpal fracture
Proximal phalanx fracture
MCP sprain
Treatment
Ice, elevation, and immobilization should be used immediately after the
injury for protection and pain control.
Partial tears:
Nonsurgical treatment is generally successful for these injuries (1,3)[C].
Protection with thumb spica splint or cast:
2–4 wks of immobilization followed by 2–4 wks of protection during activity
Start range of motion after period of immobilization.
Progress to strengthening exercises as symptoms allow
Complete tears:
If a Stener lesion can be ruled out with MRI or magnetic resonance
arthrography, good results can be expected with conservative treatment (ie,
brace or cast) (1,3)[C].
If a Stener lesion is present, treatment should be surgical (1,3)[C].
If presence of a Stener lesion cannot be determined, management is
controversial. As early surgical repair yields superior results compared with
conservative treatment, surgery is preferred by many clinicians. However,
most late repairs are successful; therefore, some clinicians will treat patients
with a trial of conservative treatment and reserve surgery for patients who
continue to have symptoms:
In the absence of a Stener lesion, there is no data evaluating outcomes of
surgical vs conservative treatment of complete UCL injuries.
Surgical repairs within 3 wks have good results.
Avulsion fractures: P.
If avulsion-type fracture is present, treatment is a thumb spica cast for 4–6
wks (1,3)[C]:
Casting may be modified to a hand-based thumb spica (wrist out) as
symptoms allow.
Studies on outcomes of UCL injuries with avulsion injuries are mixed, so
these should be followed closely to ensure joint stability is regained (1,3).
Medication
Acetaminophen or NSAIDs are generally adequate for pain control.
Some cases may require short-term, short-acting narcotic use.
Rehabilitation may be helpful in regaining full range of motion and strength
postoperatively or in those with difficulty regaining motion and strength after
Early range of motion may be acceptable postoperatively (3)[C].
Acute operative treatment (1,3):
Primary repair is best performed in the 1st 3 wks (1)[C].
Several different surgical techniques are used and will depend on the exact
nature of the injury and surgeon experience.
Cast or splint is used for 4–6 wks at which time range of motion and
strengthening exercises are initiated.
Full unrestricted activity is generally allowed at 12 wks.
Protected activity may be allowed sooner depending on the surgical
technique and surgeon preference.
Chronic operative treatment (1)[C]:
Generally requires surgical reconstruction of the UCL
Several different surgical techniques are used and will depend on the exact
nature of the injury and surgeon experience.
Surgical repair becomes less reliable the more time that has passed from the
injury.
Ongoing Care
Surgery is the preferred treatment for chronic instability, but is not as successful as when
performed acutely (1)[C].
Conservative treatment is limited to bracing and strengthening exercises, but the majority of
patients do not obtain satisfactory results.
Prognosis
Prognosis is excellent for partial UCL injuries (1,3)[C].
Prognosis is excellent for complete tears treated surgically (1,3)[B]:
In the absence of a Stener lesion, there is no data evaluating outcomes of surgical vs
conservative treatment of complete UCL injuries.
Complications
Most common complication is instability, resulting in difficulty pinching the 2nd
and 1st fingers together:
Long-term instability may increase the risk of osteoarthritis.
Other complications are related to surgical interventions (local numbness,
infection).
References
1. Baskies MA, Lee SK. Evaluation and treatment of injuries of the ulnar
collateral ligament of the thumb—metacarpophalangeal joint. Bull NYU Hosp
Jt Dis. 2009;67:68–74.
2. Deibert MC, Aronsson DD, Johnson RJ, et al. Skiing injuries in children,
adolescents, and adults. J Bone Joint Surg Am. 1998;80A:25–32.
3. Johnson JW, Culp RW. Acute ulnar collateral ligament injury in the athlete.
Hand Clin. 2009;25:437–442.
4. Malik AK, Morris T, Chou D, et al. Clinical testing of ulnar collateral ligament
injuries of the thumb. J Hand Surg Eur Vol. 2009;34:363–366.
5. Ebrahim FS, De Maeseneer M, Jager T, et al. US diagnosis of UCL tears

of the thumb and stener lesions: technique, pattern-based approach, and
differential diagnosis. Radiographics. 2006;26:1007–1020.
6. Schnur DP, DeLone FX, McClellan RM, et al. Ultrasound: a powerful tool in
the diagnosis of ulnar collateral ligament injuries of the thumb. Ann Plast Surg.
2002;49:19–22; discussion 22–23.
7. Plancher KD, Ho CP, Cofield SS, et al. Role of MR imaging in the

management of “skier's thumb” injuries. Magn Reson Imaging Clin N Am.
1999;7:73–84, viii.
8. Harper MT, Chandnani VP, Spaeth J, et al. Gamekeeper thumb: diagnosis

of ulnar collateral ligament injury using magnetic resonance imaging, magnetic
resonance arthrography and stress radiography. J Magn Reson Imaging.
1996;6:322–328.
Additional Reading
Ballas MT, Tytko J, Mannarino F. Commonly missed orthopedic problems. Am
Fam Physician. 1998;57:267–274.
Husband JB, McPherson SA. Bony skier's thumb injuries. Clin Orthop Relat
Res. 1996;327:79–84.
Richard OR. Gamekeeper's thumb: ulnar collateral ligament injury. Am Fam

Physician. 1996;53:775–780.
Codes
ICD9
841.1 Ulnar collateral ligament sprain
Clinical Pearls
When one can return to play depends on severity and whether surgery is
performed. Incomplete tears usually are treated with splinting for 4–8 wks, with
range of motion exercises and strengthening beginning after 3 wks. A protective
splint should be worn for sports until range of motion and strength have returned
to normal, usually within 6–8 wks of injury. If surgery is performed, range of
motion and strengthening exercises usually begin 6 wks after surgery. A
protective splint usually is prescribed until range of motion and strength have
returned to normal.
Tibialis Posterior Tendonitis
Christopher D. Meyering
Basics
Description
Overuse injury resulting in tendon degeneration with pain typically located posterior to the
medial malleolus
Various presentations of condition divided into 3 stages:
Stage 1: Mild swelling, medial ankle pain, normal but painful heel rise, and no foot or ankle
deformity
Stage 2: Progressive flattening of the arch, flexible hindfoot, abducted midfoot,
incompetent or ruptured tendon, and inability to perform a heel rise
Stage 3: All signs of stage 2 except the hindfoot deformity is fixed
Synonym(s): Posterior tibial tendon dysfunction; Posterior tibial tendinopathy
Epidemiology
Incidence of 2.3–3.6% in runners presenting to sports medicine clinics in earlier studies (1)
Posterior tibial tendon dysfunction is the major cause of acquired flatfoot deformity in adults.
Risk Factors
Recent increase or change in training or type of activity
Surgical or accidental trauma to the foot
60% of cases in patients over 50 yrs of age associated with HTN, diabetes, and obesity; no
association of these factors with younger patients
Severe pronation of the foot with planovalgus foot deformity
Association with rheumatoid arthritis and seronegative inflammatory disease
Prior exposure to steroids; local injection reported as a possible cause of rupture
Diagnosis
History
Patients mostly complain of pain along the length of the posterior tibialis tendon, particularly
near the medial malleolus.
May relate a recent change in activity frequency, type, and intensity
Medial arch pain
Occasional radiation of pain into the medial calf area
Usually symptoms worsen with prolonged or strenuous activity, especially activities with a
strong push-off motion.
Initially painful but normal heel raise progressing to gait changes and inability to toe-raise
Physical Exam
Pain with palpation over the posterior tibialis tendon with greatest tenderness posterior to the
medial malleolus
Medial ankle and possible foot swelling
Flattened longitudinal arch compared with unaffected foot
Increased hindfoot valgus and “too many toes sign,” where more toes are seen laterally
when viewing the patient from behind (late finding)
Single-limb heel-rise test: Patient stands on affected foot and attempts to rise up on the ball
of the foot while the other foot is off the ground. With tendinopathy, patients will be able to
raise the affected heel, but with medial ankle pain. Repetitive heel raises may show some
weakness in the tendon with persistent valgus hindfoot position through the toe raise or
decreased function owing to pain.
Tendon strength can be further tested by placing the foot in a plantarflexed and everted
position. The patient then is instructed to attempt to invert the foot. If the foot is dorsiflexed
or moves past the neutral position, the anterior tibialis may help to invert the foot.

Imaging
Sensitivity, specificity, and accuracy for detection of surgically created longitudinal tears in
cadaveric models were similar for MRI and dynamic US (2)[B].
Clinicians assessing for tendon dysfunction or alignment issues are likely able to identify
tendinopathy, but if the clinician is inexperienced or uncertain, US can confirm an abnormality.
MRI is preferred by some clinicians to establish anatomic diagnosis, but it was more
sensitive for posterior tibialis tears (3)[B]. One study published opposite results, finding that
US was 100% sensitive and 89.9% specific compared with MRI, which was 23.4% sensitive
and 100% specific, when evaluating intrasubstance or complete tendon tears.
Weight-bearing anteroposterior and lateral plain radiographs of the foot, plus anteroposterior,
lateral, and mortise views of the ankle, should be obtained. These likely will show normal
findings or minimal angular changes in earlier stages. Plain films may be helpful to rule out
other differential diagnoses.
Flexor hallucis or flexor digitorum longus tendinopathy
Subluxation or dislocation of the posterior tibialis tendon
Tarsal tunnel syndrome or other entrapment neuropathy
Stress fracture to the navicular or accessory navicular (will present as point tenderness over
the navicular)
Fracture of sustentaculum, medial talar process, or talar dome (with acute trauma)
Treatment
Care must be taken that a patient with stage 1 findings does not progress
to stage 2 or 3 with conservative care.
Use the Education, Unloading, Reloading, and Prevention (EdUReP) Model for
nonsurgical management of tendinopathy (4)[A]:
Education: 5 A's construct for behavioral counseling: Assess, advise, agree,
assist, and arrange.
Unloading: OTC or custom-made orthotics to provide medial arch support;
relative rest using alternative exercises such as pool running or swimming,
where there is limited weight bearing during activity. The alternative activity
should not result in continued or worsening pain.
Reloading: Controlled reloading of the tendon through focused concentric or
eccentric exercises, transition to weight-support training (treadmill in pool),
and weaning from unloading braces or orthotics. One randomized controlled
trial evaluated 36 patients with posterior tibial tendon dysfunction randomly
assigned to 1 of 3 groups: Custom orthoses and calf stretching; custom
orthoses, calf stretching, and a concentric exercise program; or custom
orthoses, calf stretching, and an eccentric exercise program. All 3 groups
showed significant reduction in pain after 3 mos, with the greatest
improvement seen in the eccentric exercise group (5)[B].
Prevention: Prevention of disease progression and disease recurrence
through gradual resumption of activity
One study found that treatment with an orthosis, gastrocsoleus stretches, and P.
structured exercises is effective for patients with stage 1 or 2 posterior tibial
tendon dysfunction (6)[B].
Some authors advocate aggressive treatment using immediate immobilization
with a short-leg cast or cam walker for 2–8 wks (7)[C]. If symptoms are
improved with immobilization, then patients are fitted with a custom orthotic or
an ankle-foot orthosis (AFO). Physical therapy then is added, focusing on
Achilles tendon stretching and posterior tibialis tendon strengthening.
Medication
Medication management should focus on pain control and not inflammation
control because changes are associated more with a degenerative process.
Local steroid injections into the synovial sheath are not recommended and
have been associated with tendon rupture.
Glyceryl trinitrate patches, extracorporeal shock wave therapy, and sclerotherapy
have not been evaluated specifically with posterior tibialis tendinopathy, and a
recommendation cannot be made for their use.
Patients with stage 1 or 2 disease should be managed with conservative
therapy for 3–4 mos before surgery is considered.
Tendon sheath release, scar tissue excision, and partial synovectomy are
the typical surgical management approach.
Posterior tibial tendon sheath endoscopy has been shown to be effective,
with less postoperative pain, smaller scars, and shorter hospital stays (8)[C].
Patients with stage 3 disease have a fixed deformity, and tendon
reconstruction will not correct the problem. Subtalar or triple arthrodesis is
usually needed to block hindfoot motion.
References
1. Macintyre JG, Taunton JE, Clement DB, et al: Running injuries: a clinical
study of 4,173 cases. Clin Sports Med. 1991;1:81–87.
2. Gerling MC, Pfirrmann CW, Farooki S, et al. Posterior tibialis tendon tears:
comparison of the diagnostic efficacy of magnetic resonance imaging and
ultrasonography for the detection of surgically created longitudinal tears in
cadavers. Invest Radiol. 2003;38:51–56.
3. Perry MB, Premkumar A, Venzon DJ, et al. Ultrasound, magnetic

resonance imaging, and posterior tibialis dysfunction. Clin Orthop Relat Res.
2003;408:225–231.
4. Davenport TE, Kulig K, Matharu Y, et al. The EdUReP model for nonsurgical
management of tendinopathy. Phys Ther. 2005;85:1093–1103.
5. Kulig K, Reischl SF, Pomrantz AB, et al. Nonsurgical Management of
Posterior Tibial Tendon Dysfunction With Orthoses and Resistive Exercise: A
Randomized Controlled Trial. Phys Ther. 2008.
6. Alvarez RG, Marini A, Schmitt C, et al. Stage I and II posterior tibial tendon
dysfunction treated by a structured nonoperative management protocol: an
orthosis and exercise program. Foot Ankle Int. 2006;27:2–8.
7. Fink BR, Mizel MS. Management of posterior tibial tendinitis in the athlete.
Oper Tech Sports Med. 1999;7:28–31.
8. van Dijk CN, Kort N, Scholten PE. Tendoscopy of the posterior tibial tendon.
Arthroscopy. 1997;13:692–698.
Additional Reading
Andres BM, Murrell GA. Treatment of tendinopathy: what works, what does
not, and what is on the horizon. Clin Orthop Relat Res. 2008.
Augustin JF, Lin SS, Berberian WS, et al. Nonoperative treatment of adult
acquired flat foot with the Arizona brace. Foot Ankle Clin. 2003;8:491–502.
Chao W, Wapner KL, Lee TH, et al. Nonoperative management of posterior

tibial tendon dysfunction. Foot Ankle Int. 1996;17:736–741.
Geideman WM, Johnson JE. Posterior tibial tendon dysfunction. J Orthop

Sports Phys Ther. 2000;30:68–77.
Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop
Relat Res. 1989;239:196–206.
Krause F, Bosshard A, Lehmann O, et al. Shell brace for stage II posterior

tibial tendon insufficiency. Foot Ankle Int. 2008;29:1095–1100.
Lysholm J, Wiklander J. Injuries in runners. Am J Sports Med. 1987;15:168–

171.
Premkumar A, Perry MB, Dwyer AJ, et al. Sonography and MR imaging of

posterior tibial tendinopathy. AJR Am J Roentgenol. 2002;178:223–232.
Richie DH. Biomechanics and clinical analysis of the adult acquired flatfoot.
Clin Podiatr Med Surg. 2007;24:617–644.
Codes
ICD9
726.72 Tibialis tendinitis
Clinical Pearls
The main tendon that supports the arch in your foot has been overworked and
needs relative rest. This includes using the orthotic or brace you are given by
your clinician, performing any home exercise program as directed, and
avoiding weight-bearing activities other than daily living. Cardio training
activities such as swimming or pool running are safe because no excessive
stress is being placed on the damaged tendon.
Most patients will need 3–4 mos of therapy and treatment before they are
able to return to previous activities.
Even patients with a flattened arch and functionally incompetent tendon can be
treated nonoperatively. The need for surgery hinges on the progression of
symptoms and adherence to treatment and therapy. Definitive treatment for
patients with a fixed hindfoot deformity is surgery, however.
Tibial Stress Fracture
Andrew Gregory
Basics
Stress fracture of the tibia refers to a fatigue injury of the bone as a result of repetitive
loading that overwhelms its capacity to heal and must be differentiated from medial tibial stress
syndrome, which is not a stress fracture. In general, stress fractures of the tibia can be
classified into low-risk or high-risk stress fractures. The more common low-risk stress fracture
of the tibia occurs on the posterior medial aspect of the bone (compression side) and usually
heals if treated appropriately. The less common high-risk stress fracture of the tibia occurs on
the anterior aspect of the bone (tension side) and often does not heal well even when treated
appropriately.
Epidemiology
Incidence unknown, but fairly common
Prevalence unknown, but fairly common
19–64% of all stress fractures (1)
Predominantly younger athletes (<20 yrs old)
Predominantly female athletes
No difference in race
Incidence
Incidence of tibial stress fractures is not known and varies greatly among sports and studies
(1).
Prevalence
Prevalence of tibial stress fractures is not known and varies between sports and studies (1).
Risk Factors
Previous history of stress fractures
Track and field athletes
Female gender
Younger age
Change in training volume or intensity (1)
Multisport athletes
Osteopenia
Disordered eating
Amenorrhea
Chronic steroid use
Genetics
Little is known about the genetic predisposition for stress fracture other than osteopenia.
General Prevention
Most stress fractures can be prevented by:
Gradual increases in activity (The 10% Rule: No more than a 10% increase in intensity,
duration, or frequency per week)
Appropriate footwear (properly fitted running shoes, orthotics if indicated)
Appropriate nutrition (matching energy intake with expenditure; nutrition consult may be
appropriate)
Etiology
Insoles may reduce femoral and tibial stress fractures (2)[B].

Female athlete triad or any of the signs:
Osteopenia/osteoporosis: Chronic steroid use
Amenorrhea/oligomenorrhea: Either primary or secondary
Energy imbalance: Disordered eating, excess exercise
Diagnosis
Primarily based on history and physical examination and a high index of suspicion based
on risk factors
Imaging studies can be helpful if positive, but are often unremarkable.
Hallmark is point tenderness on physical examination
It is important to distinguish anterior stress fractures (the dreaded black line) from
posteromedial ones, as the prognosis is much worse.
History
Pain in the shin area:
Severe enough to limit activity
Worse with activity and better with rest
Worsens over time if the activity is continued
Often associated with an increase in training duration or intensity
Often no associated injury
Assess for risk factors:
Training history should include days per week, hours per day and intensity, and footwear
(how often changed and what type).
Dietary history (calories, foods avoided, and vitamin D and calcium intake, weight changes)
Menstrual history (frequency, birth control pills, prior to birth control)
Family or personal history of stress fractures or osteoporosis/osteopenia
Medications known to decrease bone density (contraceptives, glucocorticoids, antiseizure
medications)
Supplements (sex hormones or precursors, vitamin D, calcium)
Physical Exam
Focal tenderness to palpation on examination is the primary method for diagnosis of a stress
fracture.
Palpate for fracture callus, stepoff, or crepitus.
Hop test: Pain at the site with hopping on one leg
Fulcrum test: Pain at the site with bending the long bone over a fulcrum (table edge or
examiner's leg)
Tuning fork test: Pain at the site when applying the tuning fork to another bony prominence of
the same bone
Examine foot function for biomechanical factors that predispose to stress fracture (heavy
heel strike).

Imaging can be helpful in diagnosing stress fractures, but is often negative initially.
History and clinical examination is often all that is necessary.
MRI is the gold standard for diagnosis.
Imaging
Initial approach:
X-rays:
May be negative for 2–3 wks; shows crack or fracture callus
For anterior cortical fractures, shows the “dreaded black line”
Bone scan:
Good sensitivity (74%), especially early (3)
Good specificity (100%)
Poor accuracy (52%)
Helpful in multiple areas of concern, such as bilateral tibial stress fracture
MRI:
Gold standard; sensitivity is better than bone scan (88%) (3)
Best at demonstrating the exact location and extent of injury; specificity (100%), accuracy
(90%) (3)[B]
Shows fracture line on T1 and edema on T2
CT scan:
Not useful in the acute setting; poor sensitivity (42%) (3)
Useful in assessing healing of high-risk stress fractures
Follow-up and special considerations:
X-rays will show the fracture healing in most cases; look for callus formation.
Bone scan can remain positive for over a year; therefore, not useful for follow-up, only for
diagnosis
MRI may continue to show edema after the fracture is asymptomatic.
CT is useful for assessing fracture healing for fractures that are difficult to see on plain
film.
Occasionally, stress fractures can be confused with tumor on imaging and a biopsy may be
obtained.
Medial tibial stress syndrome (shin splints)
Chronic exertional compartment syndrome
Pes anserine bursitis
Posterior tibialis tendonitis
Superficial nerve entrapment
Other bony processes: Bone cysts, osteoid osteoma, tumor, infection
Treatment
Treatment of most stress fractures of the tibia is the same as other stress
fractures, which is to remove the offending activity (usually impact training).
However, the treatment of anterior tibial and posterior medial tibial stress
fractures is quite different:
Posterior medial tibial stress fractures can be allowed to continue to
participate in limited activity as pain allows. Decrease practice to allow more
participation in games.
Anterior tibial stress fractures (the dreaded black line) should not continue to
participate because of the risk of fracture progression and/or nonunion.
Often requires surgery for internal fixation and bone grafting to heal.
Pre-Hospital
RICE:
Rest
Ice
Compression
Elevation
Acetaminophen
Walking boot or long Aircast, crutches if necessary based on the amount of
pain with weight-bearing
ED Treatment
Continued RICE
Acetaminophen
Avoidance of NSAIDs
Walking boot
Crutches as needed
Consider surgery for anterior tibial stress fractures or nonunion of other tibial
stress fractures
Addressing other risk factors: Nutritional, menstrual, osteopenia
Medication
No medications currently available to help stress fracture healing, but can treat
with pain medications.
Pain medications with anti-inflammatory drugs may be contraindicated, as they
may delay the healing of fractures.
Measures to alleviate the pain associated with stress fractures include ice,
Tylenol, a Cam Walker boot, and crutches.
Some evidence that use of a pneumatic or stirrup brace may shorten the time
to return to activity [B]
Referral
Most athletes with anterior tibial stress fractures should be referred for surgical
treatment (4).
Conservative treatment with casting and strict nonweight-bearing for 2–3 mos
can be considered, but still may result in nonunion.
Physical therapists can check and possibly correct poor biomechanics.
Bone stimulators: Current evidence is insufficient to conclude a benefit in
improving the rate of union in patients with a fresh fracture, osteotomy, delayed
union, or nonunion or on time to healing in tibial stress fractures or a reduction in
pain (5)[A].
Surgical treatment of anterior tibial stress fractures consists of intermedullary
nailing, with or without bone graft (4).
Not applicable in most cases
Ongoing Care
Low-risk stress fractures of the tibia: Ongoing activity modification and pain management
is usually sufficient.
High-risk stress fractures of the tibia require intermedullary nailing and grafting or nonweight-
bearing and casting for 8–12 wks, after which intermedullary nailing and grafting still may be
necessary.
Diet
Nutritional evaluation is important, not only for healing of the current fracture but also for
prevention of recurrence.
Current recommendations from the National Osteoporosis Foundation are 1,000 mg of
calcium and 400–800 IU of vitamin D daily for adults under age 50.
Patient Education
Athletes should understand that training, nutrition, biomechanical, and footwear errors must
be remedied.
Athletes with a prior stress fracture are at increased risk for a future stress fracture.
Prognosis
Good for low-risk stress fractures of the tibia
Poor for high-risk stress fractures of the tibia
Complications
Posteromedial stress fractures of the tibia: Potential for slower healing if
continued participation is allowed
Anterior stress fractures of the tibia: Risk of nonunion or delayed or partial
union is high, requiring surgery
References
1. Snyder RA, Koester MC, Dunn WR. Epidemiology of stress fractures. Clin
Sports Med. 2006;25:37–52, viii.
2. Snyder RA, Deangelis JP, Koester MC, et al. Does shoe insole modification
prevent stress fractures? A systematic review. HSS J. 2009.
3. Gaeta M, Minutoli F, Scribano E, et al. CT and MR imaging findings in

athletes with early tibial stress injuries: comparison with bone scintigraphy
findings and emphasis on cortical abnormalities. Radiology. 2005;235:553–
561.
4. Kaeding CC, Yu JR, Wright R, et al. Management and return to play of

stress fractures. Clin J Sport Med. 2005;15:442–447.
5. Mollon B, da Silva V, Busse JW, et al. Electrical stimulation for long-bone

fracture-healing: a meta-analysis of randomized controlled trials. J Bone Joint
Surg Am. 2008;90:2322–2330.
Additional Reading
Aoki Y, Yasuda K, Tohyama H, et al. Magnetic resonance imaging in stress
fractures and shin splints. Clin Orthop Relat Res. 2004;(421):260–267.
Busse JW, Kaur J, Mollon B, et al. Low intensity pulsed ultrasonography for
fractures: systematic review of randomised controlled trials. BMJ.
2009;338:b351.
Spits DJ, Newberg AH. Imaging of stress fractures in the athlete. Radiol Clin
North Am. 2002;40:313–331.
Whitelaw GP, Wetzler MJ, Levy AS, et al. A pneumatic leg brace for the
treatment of tibial stress fractures. Clin Orthop Relat Res. 1991;(270):301–
305.
See Also
Other stress fracture chapters
Codes
ICD9
733.93 Stress fracture of tibia or fibula
Clinical Pearls
Distinguish low-risk from high-risk stress fracture based on imaging.
Tenderness to palpation is the main physical examination finding.
MRI is the imaging study of choice.
Evaluate for training errors.
Evaluate for additional risk factors.
Tillaux Fractures: Anterior Tibia-Fibula Ligament
Avulsion
Kyle J. Cassas
Basics
Description
1st described by Paul Jules Tillaux in 1892 (1)
Avulsion fracture of the lateral distal tibia epiphysis
Occurs in adolescents with a partially closed physes (girls 13–15 and boys 15–17 yrs of age)
During the 18-mo period when the distal tibial physis has begun to fuse centrally
Results in either a Salter Harris type III or IV physeal avulsion fracture
Synonym(s): Juvenile Tillaux fracture; Transitional fracture of distal tibia
Epidemiology
2.9% (2)
Relatively uncommon
Should be considered in adolescents with ankle injuries
Risk Factors
Girls 13–15 yrs of age with a partially closed physis
Boys 15–17 yrs of age with a partially closed physis
Rapid, forceful external rotation of the foot
Diagnosis
History
Forceful external rotation of the foot or internal rotation of the lower leg on a firmly planted
foot
Stress applied to the anterior tibiofibular ligament, which inserts on the anterolateral aspect
of the distal tibial epiphysis
Physical Exam
Signs and symptoms:
Acute anterolateral ankle pain
May report difficulty bearing weight
Swelling and ecchymosis: Generally mild
Inspection: Mild swelling and/or ecchymosis
Limited active ankle range of motion (ROM)
Pain with passive ankle motion
Tenderness over the anterolateral ankle and syndesmosis region
Usually unable to fully bear weight
Palpate entire length of the fibula for associated injury
Neurovascular examination

Imaging
Initial radiographs: Ankle anteroposterior (AP), lateral, and mortise views
Comparison films of the uninjured ankle to evaluate physeal closure and displacement
CT scan often needed to determine fracture pattern, amount of displacement, and need for
surgery
Ankle sprain
Syndesmosis injury/sprain (high ankle sprain)
Triplanar fracture: More severe version of Tillaux fracture
Talar dome injury/osteochondritis dissecans
Distal fibular physeal injury
Treatment
Nondisplaced or minimally displaced fractures (1 mm) can be treated
nonoperatively.
Analgesia:
Immobilization, ice, elevation, acetaminophen/NSAIDs
Narcotics for breakthrough pain
Reduction technique: Gently position the foot in internal rotation
Neurovascular check
Radiography: Ankle AP, lateral, and mortise views
CT scan may be needed to determine the fracture pattern and the amount of
displacement, and assess the need for surgery (see “Surgical Criteria”
below).
Immobilization:
Consider posterior splint or fracture boot initially for significant swelling.
A long-leg cast (owing to the intra-articular component) with knee partially
flexed
Non–weight bearing for 4 wks and weight bearing as tolerated for 2–4 wks in
a cam walker or rigid shell boot
Prognosis is good for those treated nonoperatively if displacement <2 mm
(3).
Anatomic alignment of the articular surface is essential to minimize the risk of
posttraumatic arthritis.
Physeal arrest typically is not a concern.
Evaluate for varus or valgus deformity.
Rehabilitation:
ROM
Strengthening of dynamic stabilizers
Proprioception
Sport-specific drills
Indicated if 2 mm of displacement or greater
Open reduction with internal fixation of fracture, typically using two cannulated
screws
Successful treatment also described using percutaneous fixation assisted
arthroscopically (4)
Good reported surgical outcomes (3,5)
Ongoing Care
For nonsurgically treated:
Follow-up with x-rays, typically every 2 wks.
After 4 wks of immobilization, progress to walking cast or cam walker for 2–4 wks.
Prognosis
Good
Most patients are able to return to full activity at 3 mos after injury.
References
1. Cassas KJ, Jamison JP. Juvenile Tillaux fracture in an adolescent basketball player. Phys
Sportsmed. 2005;33:30–33.
2. Spiegel PG, Cooperman DR, Laros GS. Epiphyseal fractures of the distal ends of the
tibia and fibula. A retrospective study of two hundred and thirty-seven cases in children. J
3. Pannier S, Odent T, Milet A, et al. [Tillaux fractures in teenagers: a review of nineteen

cases.] Rev Chir Orthop Reparatrice Appar Mot. 2006;92:158–164.
4. Thaunat M, Billot N, Bauer T, et al. Arthroscopic treatment of a juvenile tillaux fracture.

Knee Surg Sports Traumatol Arthrosc. 2006.
5. Kaya A, Altay T, Ozturk H, et al. Open reduction and internal fixation in displaced juvenile
Tillaux fractures. Injury. 2006.
Additional Reading
Churchill JA, Mazur JM. Ankle pain in children: diagnostic evaluation and clinical decision
making. J Am Orthop Surg. 1995;3:183–193.
Codes
ICD9
Clinical Pearls
Possible complications include posttraumatic arthritis and asymmetric physeal
growth.
If the intra-articular fracture is treated nonoperatively, 4 wks non–weight
bearing followed by 2–4 wks in a walking cast or cam walker is the rule. If the
intra-articular fracture is stabilized with internal fixation, 3 wks non–weight
bearing followed by 3 wks of weight bearing in walking cast is appropriate.
Return to sports in 12 wks at minimum is usual. Patient must be healed on x-
ray, be pain-free with activity, and have full ROM and strength.
Peroneal strengthening and proprioception training are essential after this
injury; proper mechanics in sport and proper shoe wear should be emphasized
to prevent excessive stress to the anterior tibiofibular ligament. Consider use
of an ankle support during early return-to-activity phase.
Tinea Gladiatorum (Capitis, Corporis, Cruris, Pedis)
Philipp Underwood
Basics
Description
This group of topical fungal infections commonly affects athletes, particularly swimmers,
soccer players, and wrestlers. They are classified by site of infection: Tinea capitis involves
the scalp and hairline; tinea corporis involves the trunk, face, or extremities; tinea cruris
involves inguinal folds; tinea pedis involves the feet. Infection is caused by a dermatophyte,
most commonly from the Trichophyton, Epidermophyton, and Microsporum species. This is
typically an infection of the stratum corneum that results in thickening of the epidermis and
scale formation. Majocchi's granuloma is an infection of the dermis, usually as a result of
fungal entry through hair follicles.
Synonym(s): Ring worm (tinea corporis); Jock itch (tinea cruris); Athlete's foot (tinea pedis);
Tinea gladiatorum (most commonly Trichophyton tonsurans and T. rubrum)
Epidemiology
Varies from 25–35% of all wrestlers during any given season
10–20% lifetime risk for nonathletes
More common in African Americans and Asians
2–20 days from inoculation to subsequent development of identifiable skin lesions
Risk Factors
Spread by direct contact with a pet or human carrier
Fomite transmission may occur from wrestling mats, pieces of athletic equipment, shower
floor, etc.
Diagnosis
Scraping of the leading edge of the skin plaque and preparation with potassium
hydroxide (KOH) 5–20% can be examined under the microscope. This will reveal hyphae and
pseudohyphae, which are diagnostic of tinea infection. For Tinea capitis, spores are visualized
by KOH preparation of the hair shaft. Microsporum canis may fluoresce bright green under a
Wood's lamp. Fungal culture using Sabouraud dextrose agar also can be used, but in athletes,
use is limited by time and expense involved. Most tinea infections do not fluoresce under
Wood's light examination.
History
Determine when and where lesions appeared and exposure history.
Other wrestlers on the team are infected
Physical Exam
Lesions present with erythema, pruritus, and scaling.
Tinea capitis: 2 distinct types:
Black dot: Most common form seen in U.S. and most commonly caused by T. tonsurans.
Usually children and elderly. Erythematous, scaling patch that enlarges slowly. Hairs break
off flush with scalp causing alopecia, which may be permanent.
Gray patch: Uncommon in U.S. and caused by Microsporum canis contracted usually from
dogs and cats. Erythematous, scaling patch that enlarges slowly. Hairs break off 1–2 mm
above the scalp.
Tinea corporis: Circular, erythematous, scaling plaques with central clearing on trunk, face,
and extremities
Tinea cruris: Pruritic, scaling, erythematous patches in inguinal folds and/or medial thighs. If
lesions present on penis or scrotum, consider candidal infection rather than tinea.
Tinea pedis: Pruritic, erythematous scaly skin along the sole of foot. Cracking and maceration
of the web spaces also may be present. Bullous form will have bullae or vesicles filled with
clear fluid.
Tinea capitis: Alopecia areata, impetigo, psoriasis, seborrhea, trichotillomania
Tinea corporis: Impetigo, eczema, psoriasis, contact or atopic dermatitis, drug eruption,
cutaneous herpes, lupus, pityriasis rosea
Tinea cruris: Contact dermatitis, candidal intertrigo, erythrasma, psoriasis, seborrhea
Tinea pedis: Eczema, contact or atopic dermatitis, dyshidrosis, pitted keratolysis, psoriasis
Treatment
Medication
Primary treatment for tinea corporis, cruris, and pedis is with topical antifungal
agents. Primary treatment for tinea capitis is oral antifungal agents.
Initial treatment also may include a topical corticosteroid. This may help reduce
the associated pruritus and erythema; however, this may exacerbate tinea
infections and lead to treatment failure.
Tinea capitis and diffuse, multiple lesions in other areas should be treated with
oral antifungal agents.
When using oral agents, give consideration to drug interactions, potential for
toxicity, and cost of medication.
Prevention is key: Emphasize proper personal hygiene; use dry, cotton clothing;
and keep athletic equipment disinfected properly.
Tolnaftate and clotrimazole only suppress the fungus and are not cidal.
Shampooing hair and body with selenium (Selsun Blue) may be useful
prophylaxis.
Failure to treat all areas simultaneously may result in treatment failure.
Tinea capitis requires oral treatment: P.
Griseofulvin: Treat for 6 wks. Monitor CBC, liver function tests (LFTs). Side
effects: Photosensitivity, headache, neutropenia, elevated LFTs, paresthesia,
rash. Pregnancy Category C.
Adults: 500 mg microsize or 330–375 mg ultramicrosize daily for 6 wks
Children: 11 mg microsize/kg/d or 7.3 mg ultramicrosize/kg/d for 6 wks
Terbinafine: Treat for 4 wks. Monitor CBC, LFTs. Pregnancy Category B.
10–20 kg: 62.5 mg daily
20–40 kg: 125 mg daily
Above 40 kg: 250 mg daily
Itraconazole: Treat for 2–6 wks. Monitor LFTs. Caution: Hypoglycemia with
sulfonylureas, rhabdomyolysis with HMG-CoA reductase inhibitors.
Pregnancy Category C.
Adults: 100 mg daily up to 200 mg b.i.d.
Children: 3–5 mg/kg daily
Fluconazole: Treat for 2–4 wks. Increased international normalized ratio
(INR) on warfarin. Pregnancy Category C.
Adults: 200 mg daily
Children: 6 mg/kg/d
Tinea corporis, cruris, and pedis: Topical antifungals are first-line treatment.
Topical nystatin is ineffective. Oral therapy for failed topical, extensive lesions
or immunocompromised.
Topical therapy: Treat for 2–6 wks (continue treatment additional week after
resolution of rash):
Ciclopirox: Apply twice daily
Clotrimazole: Apply twice daily
Econazole: Apply once daily
Ketoconazole: Apply once daily
Miconazole: Apply twice daily
Naftifine: Gel, apply twice daily; cream, apply once daily
Oxiconazole: Apply once to twice daily
Sertaconazole: Apply twice daily
Sulconazole: Apply once to twice daily
Terbinafine: Apply once to twice daily
Tolnaftate: Apply twice daily
Oral therapy: Treat for 2–6 wks:
Griseofulvin: 500 mg daily OR 500 mg b.i.d. OR 250 mg t.i.d.
Fluconazole: 150–200 mg once weekly for 2–4 wks or 400 mg one-time
dose
Itraconazole: 100–200 mg daily
Terbinafine: 250 mg daily
Prophylaxis for tinea gladiatorum:
Recommended for recurrent episodes (exclude immunocompromised state)
Use by some prior to wrestling tournaments or during season:
Fluconazole: 200 mg once weekly
Itraconazole: 400 mg once every 2 mos
Ongoing Care
Wrestling return to play:
NCAA: A minimum of 2 wks of systemic antifungal therapy is required for scalp lesions. A
minimum of 72 hr of topical therapy is required for skin lesions. Wrestlers with extensive and
active lesions will be disqualified. Activity of treated lesions can be judged either by use of
KOH preparation or a review of therapeutic regimen. Wrestlers with solitary or closely
clustered, localized lesions will be disqualified if lesions are in a body location that cannot be
“properly covered” (a gas-permeable dressing, eg, Op-site, Tegaderm, Bioclusive, Duoderm,
then covered by elastic/stretch tape). The disposition of tinea cases will be decided on an
individual basis as determined by the examining physician and/or athletic trainer. (NCAA
Sports Medicine Handbook 2009–2010)
NFHS: Tinea lesions (ringworm scalp, skin): Oral or topical treatment for 72 hr on skin and 14
days on scalp (NFHS revised/approved April 2008)
Most infections are easily treated with topical or oral antifungal agents; therefore, referral is
rare. However, for cases that do not respond as expected, further evaluation to rule out an
immunocompromised state or other systemic illness should be considered.
Additional Reading
Doncker PD, Gupta AK, Marynissen G, et al. Itraconazole pulse therapy for onychomycosis
and dermatomycoses: an overview. J Am Acad Dermatol. 1997;37:969–974.
Goldstein AO, Goldstein BG. Dermatophyte (tinea) infections. Available at:

www.uptodate.com/online/content/topic.do?topicKey=dermatol/5934&view=print Accessed
August 24, 2009.
González U, Seaton T, Bergus G, et al. Systemic antifungal therapy for tinea capitis in
children. Cochrane Database Syst Rev. 2007;CD004685.
Hazen PG, Weil ML. Itraconazole in the prevention and management of dermatophytosis in
competitive wrestlers. J Am Acad Dermatol. 1997;36:481–482.
Kohl TD, Martin DC, Berger MS. Comparison of topical and oral treatments for tinea
gladiatorum. Clin J Sport Med. 1999;9:161–166.
Lesher JL. Oral therapy of common superficial fungal infection. J Am Acad Dermatol
1999;40(suppl):31–34.
Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea infections.
Am Fam Physician. 1998;58:163–174, 177–178.
Codes
ICD9
110.0 Dermatophytosis of scalp and beard
110.3 Dermatophytosis of groin and perianal area
110.4 Dermatophytosis of foot
110.5 Dermatophytosis of the body
Clinical Pearls
All areas of tinea infection need to be treated simultaneously to reduce risk of
reinfection.
Tinea Versicolor
Mark Sakr
Jeffrey R. Bytomski
Basics
Description
Tinea versicolor, also known as pityriasis versicolor, is a common superficial skin infection
that is caused by the lipophilic yeast Pityrosporum.
Pityrosporum is found in the normal skin flora. The primary species in tinea versicolor is
Pityriasis ovale (formerly named Malassezia furfur) (1).
Hot and humid weather, excessive sweating, use of oils, and immunosuppression can cause
the transformation from the benign yeast spores to the hyphal form that causes clinical
disease.
Skin lesions manifest as hypo/hyperpigmentation or light pink/salmon, brown, or white
colored patches. They occur primarily on the upper extremities and trunk, less frequently on
the face and intertriginous areas (2).
The lesions are often small macules but can coalesce into larger papules. The lesions have a
fine scaly appearance and may be mildly pruritic.
Synonym(s): Sun spots; Pityriasis versicolor
Epidemiology
Disease may occur at any age but is much more common during the years of higher sebaceous
activity (ie, adolescence and young adulthood).
Incidence
2–8% of the population
The exact incidence in the U.S. is difficult to assess because many individuals who are
affected may not seek medical attention.
Prevalence
40% prevalence in tropical areas (2)
Occurs worldwide, with prevalences reported to be as high as 50% in the humid, hot
environment of western Samoa and as low as 1.1% in the colder temperatures of Sweden
3% of all dermatologist visits during the summer months in temperate areas (2)
90–100% of adults are colonized (2).
Occurs most commonly during adolescence and young adulthood but is seen in childhood as
well.
Adults who present with this disease are likely to suffer from recurrent episodes from early
adulthood.
Most commonly seen in the summer months, when patients perspire more and sun exposure
leads to skin color changes that highlight the lesions
Risk Factors
Excess heat and humidity
Adrenalectomy
Cushing disease
Pregnancy
Malnutrition
Burns
Corticosteroid therapy
Immunosuppression
Oral contraceptives
Individuals with oily skin
Diabetes mellitus
General Prevention
Avoid using oil or oily products on the skin.
Avoid constrictive or unvented clothing in warm weather.
Prophylactic topical or oral antifungal therapy in patients with recurrent lesions (2)
Etiology
The discoloration is secondary to damage of the melanocytes and the body's inflammatory
response to the yeast.
Tinea versicolor is not contagious.

Diabetes mellitus
Immunosuppression
HIV
Chronic corticosteroid use
Cushing disease
Hyperhidrosis
Pregnancy
Oral contraceptives
Malnutrition
Adrenalectomy
Diagnosis
History
The lesions are usually asymptomatic, but they may be pruritic.
Patients may present with areas of skin that do not tan with sun exposure.
Older patients will sometimes have a history of similar skin lesions since early adolescence.
Physical Exam
Multiple small circular macules of various colors that enlarge radially
Lesions may be hyper- or hypopigmented; the color is uniform in each individual.
The upper trunk is most commonly involved, but lesions may spread to the upper arms, neck,
face, and abdomen.

An overlying powdery scale can be easily removed with a number 15 surgical blade or
transparent tape. The scale is then evaluated by direct microscopy.
Wood's light examination shows irregular yellow to white fluorescence; some lesions may not
fluoresce.
Direct microscopic examination of skin scrapings in 10% potassium hydroxide (KOH)
Classic pattern of “spaghetti and meatballs” of yeast hyphae and spores (1)
Skin biopsy yielding stratum corneum with abundant short hyphae and round budding cellular
fungal elements is also diagnostic, but this is an invasive means of diagnosis.
Vitiligo
Psoriasis
Pityriasis rosea
Pityriasis alba
Secondary syphilis
Tinea corporis
Treatment
Medication
First Line
Topical therapy:
Selenium sulfide lotion/shampoo 2.5% applied to the skin for 10–15 min a day
for 7–14 days
Alternately, apply lotion to affected area for 24 hr before washing off, repeating
weekly for 4 wks.
Ketoconazole 2% shampoo applied 1 time or daily for 3 days is also effective
(69% cure rate) (3).
Miconazole, clotrimazole, ketoconazole, econazole, or ciclopirox lotions can be
applied to affected area twice daily for 2–4 wks ( 76–100% cure rates for
these therapies) (3).
Second Line
Systemic therapy:
Fluconazole 400 mg is effective as a single oral dose (80% cure rate) (1).
Itraconazole 200 mg/day PO for 5 days (92% cure rate) (3)
Ketoconazole may be given as a single 400-mg dose or in as 200 mg/day for 5
days ( 77% cure rate) (4).
Systemic treatments may be given to patients who fail topical therapies.
Caution is advised with the use of oral antifungals in patients with liver disease.
Selenium sulfide 2.5% shampoo applied to affected areas on the 1st and 3rd
days of each month for 6 mos is a topical prophylactic therapy (2).
Itraconazole 200 mg PO administered twice a day for 1 day each month is an
effective oral prophylactic treatment (3).
Ketoconazole 400 mg PO once a month or 200 mg for 3 consecutive days at
the beginning of each month is an alternate treatment (2).
General Measures
Keep skin dry and clean during warm seasons.
Avoid using oily products on the skin.
Avoid constrictive or unvented clothing in warm weather.
Wash skin immediately after exercise and accumulation of sweat.
Referral
Unclear diagnosis
Failure to respond to therapy
Resistance to treatment may point to other underlying medical conditions that
deserve proper evaluation.
Ongoing Care
Repeat above treatments as necessary.
If patient has multiple recurrences and requires systemic treatments each time, check
baseline liver function tests (especially with ketoconazole).
Patient Monitoring
Skin color does not reverse immediately.
Return to normal pigmentation takes 1–2 mos on average with adequate treatment.
The inability to produce a powdery scale with a number 15 surgical blade or transparent tape
indicates that the fungus has been eliminated.
Recurrence rates are high, estimated at 40–60% in the 1st yr and up to 80% in the 2nd yr
(2).
Exposure to sunlight will help to accelerate repigmentation when hypopigmented lesions
predominate.
Re-evaluate for treatment each spring, prior to prolonged outdoor activities or tanning
season.
Prognosis
Treatments have high success rates, but recurrences are common.
Lesions may last for months.
References
1. Usatine RP. Variations in color. J Fam Pract. 2003;52:481–484.
2. Schwartz RA. Superficial fungal infections. Lancet. 2004;364:1173–1182.
3. Faergemann J, Gupta AK, Al Mofadi A, et al. Efficacy of itraconazole in the prophylactic

treatment of pityriasis (tinea) versicolor. Arch Dermatol. 2002;138:69–73.
4. Kose O, Bülent Taştan H, Riza Gür A, et al. Comparison of a single 400 mg dose versus
a 7-day 200 mg daily dose of itraconazole in the treatment of tinea versicolor. J Dermatol.
Treat. 2002;13:77–79.
Additional Reading
Crawford F, Hollis S. Topical treatments for fungal infections of the skin and nails of the foot.
Cochrane Database Syst Rev. 2007;CD001434
Stulberg DL, Clark N, Tovey D. Common hyperpigmentation disorders in adults: Part II.
Melanoma, seborrheic keratoses, acanthosis nigricans, melasma, diabetic dermopathy,
tinea versicolor, and postinflammatory hyperpigmentation. Am Fam Physician.
2003;68:1963–1968.
Codes
ICD9
111.0 Pityriasis versicolor
Clinical Pearls
Skin lesions manifest as hypo/hyperpigmentation or light pink/salmon, brown, or
white colored patches.
Occur primarily on the upper extremities and trunk, less frequently on the face
and intertriginous areas
The lesions are often small macules but can coalesce into larger papules.
Fine scaly appearance
May be mildly pruritic
Most commonly seen in the summer months, when patients perspire more and
sun exposure leads to skin color changes that highlight the lesions
Classic pattern of “spaghetti and meatballs” of yeast hyphae and spores on
direct microscopy
Mainstay of treatment involves topical or systemic antifungals.
Recurrence rates are high.
Tracheal and Laryngeal Injuries
Jeffrey Feden
Razib Khaund
Basics
Description
Injuries to the larynx and trachea may result from either blunt or penetrating trauma involving
the head, neck, or upper chest.
Although they are relatively uncommon and sometimes subtle, these potentially life-
threatening injuries must not be overlooked.
Epidemiology
Laryngotracheal (LT) trauma occurs at an estimated frequency from 1/5,000 to 1/30,000 ED
visits.
Laryngeal injuries comprise <1% of blunt and 7% of penetrating trauma cases; only 10%
result from athletic trauma (1).
Mortality is as high as 20% and 40% for penetrating and blunt injuries, respectively (2).
Risk Factors
Contact and collision sports
Sports with high-velocity projectiles (ie, baseball, hockey, lacrosse)
Motor sports
Etiology
Laryngotracheal trauma may cause obstructive edema, submucosal hematomas, cartilage
fractures, mucosal tears, or complete laryngotracheal separation.
Low-velocity trauma may cause soft tissue swelling, lacerations, contusions, abrasions.
High-velocity trauma may injure laryngeal muscles and nerves.
Forceful compression to the chest against a closed glottis may cause laryngeal fractures and
mucosal disruption.

Penetrating trauma is associated with additional injury to the chest, esophagus, vasculature,
or nerves in 86% of cases; esophageal injury occurs 50% of the time.
Blunt trauma is associated with intracranial injury (17%), cervical spine injury (13%), chest
injury (13%), and esophageal injury (13%) (2).
Pneumothorax may accompany distal tracheal injuries.
Diagnosis
History
Signs or symptoms may be absent initially in up to 1/3 of those with LT trauma.
Physical Exam
Dysphonia (ie, hoarseness) and dyspnea are most common.
Cough, hemoptysis, odynophagia, respiratory distress, stridor
Loss of anatomic landmarks, anterior cervical tenderness, SC crepitus, cervical ecchymosis,
or hematoma

Imaging
Chest radiograph to evaluate for associated trauma
Cervical spine radiographs to evaluate for cervical spine injury
Plain radiographs may show hyoid bone elevation or prevertebral air.
CT scan of the cervical region may be performed if the airway is stable and provides
additional anatomic detail that may help to guide management decisions.
Flexible bronchoscopy is the preferred initial method for evaluating the stable airway.
Fiberoptic laryngoscopy may provide more detail about laryngeal anatomy and vocal cord
function.
Treatment
Pre-Hospital
Initial treatment focuses on the primary survey and ABCs in accordance with
Advanced Trauma Life Support guidelines.
Control the airway and immobilize the cervical spine.
Rapidly transport to the nearest ED while continuing to manage the airway.
Oral airways, combitubes, and laryngeal mask airways fail to provide a
definitive airway by virtue of not passing below the larynx.
Orotracheal intubation and cricothyroidotomy may be contraindicated in cases
of significant trauma or complete LT separation; either must be undertaken with
extreme caution to avoid losing the airway or causing greater injury.
ED Treatment
Prompt assessment of the stable airway includes flexible bronchoscopy and/or
fiberoptic laryngoscopy in consultation with ENT, followed by close observation,
further imaging with CT scan, or surgical management in the operating room.
Preferred management of an unstable airway includes awake tracheotomy
under local anesthesia in the operating room (2).
Observation in an ICU for at least 24 hr is indicated for significant LT that does
not require emergent surgical intervention.
Some patients may develop signs or symptoms up to 48 hr after injury.
Monitor for signs of progressive airway compromise, and prepare for the
possibility of urgent tracheotomy.
Humidified air and head of the bed elevation P.
Serial bronchoscopic examinations
Cryotherapy with wet ice for treatment of soft tissue injury
Vocal rest
Minimize laryngeal irritation from gastric acid with H2 blockers or proton pump
inhibitors.
Antibiotics and systemic corticosteroids are controversial.
Use narcotic pain medications and sedatives with caution to avoid their effects
of respiratory depression.
Following initial treatment, prompt phoniatric evaluation is mandatory for all
patients.
Speech therapy may be required to restore vocal quality or to avoid permanent
restrictions of phonation.
Indications for surgery include initial airway instability, progressive airway
decline despite conservative treatment, and complex LT injuries.
Operative interventions range from tracheotomy to open reduction and internal
fixation (ORIF) of the injured cartilaginous structures.
25–80% of patients with LT trauma will require surgery.
Ongoing Care
Long-term treatment goals involve restoring the anatomy, airway patency, and vocal
quality.
All athletes should be sent for phonic and speech therapy evaluations; speech therapy may
be necessary to restore vocal quality.
Patient Education
Dysphonia is the most common and problematic complication after LT trauma.
Phoniatric evaluation is essential, and speech therapy may be important even after minor
injuries.
Prognosis
Prognosis depends on injury severity, but complications may be avoided by early diagnosis
and proper initial management.
Voice disorders typically are associated with the most severe injuries, but even minor injuries
can cause permanent problems with phonation.
Most patients can expect excellent airway patency and good voice quality following LT
trauma that has been recognized and treated appropriately.
Prognosis is worse for those with late presentations (who already may have laryngeal
stenosis).
Complications
Dysphonia, hoarseness, voice fatigue, poor vocal control are most common.
Vocal cord paralysis owing to recurrent laryngeal nerve injury
Permanent phonic disorders owing to laryngeal scarring or infection
References
1. Paluska SA, Lansford CD. Laryngeal trauma in sport. Curr Sports Med
Rep. 2008;7:16–21.
2. Atkins BZ, Abbate S, Fisher SR, et al. Current management of

laryngotracheal trauma: case report and literature review. J Trauma.
2004;56:185–190.
Additional Reading
Bhojani RA, Rosenbaum DH, Dikmen E, et al. Contemporary assessment of
laryngotracheal trauma. J Thorac Cardiovasc Surg. 2005;130:426–432.
Brosch S, Johannsen HS. Clinical course of acute laryngeal trauma and

associated effects on phonation. J Laryngol Otol. 1999;113:58–61.
Mussi A, Ambrogi MC, Ribechini A, et al. Acute major airway injuries: clinical
features and management. Eur J Cardiothorac Surg. 2001;20:46–51,
discussion 51–52.
Codes
ICD9
807.5 Closed fracture of larynx and trachea
807.6 Open fracture of larynx and trachea
925.2 Crushing injury of neck
Clinical Pearls
Laryngotracheal trauma may be immediately life-threatening.
Diagnosis often requires a high index of suspicion.
Prompt recognition and airway management are essential.
Complications and airway compromise may not develop until 24–48 hr following
injury.
Consideration of associated traumatic injuries is also important.
Triceps Tendinitis
Clint Beaver
David E. Price
Robert L. Jones
Basics
Description
Inflammation of the triceps tendon at or above the insertion onto the olecranon
Classically an overuse injury due to repetitive extension of the elbow or extreme force placed
on the tendon
May result from direct trauma
Epidemiology
Uncommon, but higher prevalence observed in certain groups (see “Risk Factors”)
Male predominance of 2:1 (1)[B]
Has been described through a wide range of ages (1)[B]
Risk Factors
Commonly associated with posterior impingement presence of loose bodies, or classic tennis
elbow
Activities such as hammering, weightlifting (specifically pushups and dips), throwing
(baseball), platform diving, and playing guitar
Use of anabolic steroids may also predispose to injury.
General Prevention
Proper form when lifting weights
Avoid excessive weight or force when utilizing triceps.
Appropriate stretching prior to repetitive use of triceps or weightlifting
Etiology
Inflammation or swelling of the triceps tendon due to excessive force or repetitive use

Olecranon bursitis (2)[C]
Triceps tendon rupture (1,3)[B]
Diagnosis
History
Increasing pain in the posterior elbow over several weeks that worsens over course of the
day and associated with occasional morning stiffness
Improvement can be seen with periods of inactivity.
Physical Exam
Pain in the posterior elbow
Pain on full extension/flexion of the elbow
Swelling at or above the tendinous insertion
Weakness with extension of elbow
Tenderness at or above the triceps insertion onto the olecranon
Swelling in the same area
Increased pain with resisted extension of the elbow
Weakness with elbow extension (may be indicative of tendon rupture)

Imaging
Anterior/posterior and lateral plain films may be helpful; specifically may be useful to evaluate
for tendon avulsions (2)[B].
US may be useful in distinguishing between triceps tendonitis and olecranon bursitis if the
physical exam is unclear; may also show calcifications within the triceps tendon (3)[B].
MRI is rarely needed.
Olecranon fracture/stress fracture
Olecranon bursitis
Triceps rupture
Subtendinous bursitis
Treatment
Prevention is vital in high-risk populations such as weightlifters,
carpenters/construction workers, or guitar players; the key to prevention is
proper stretching before activity, avoiding excessive force, and taking
frequent breaks within activity.
Acute treatment:
R.I.C.E.: Rest, Ice, Compression, Elevation:
Rest: Avoid any that which may exacerbate symptoms.
Ice: Use ice packs in the painful area for 20–30 min 3–4 times/day. May
also perform ice massage, which includes freezing water in a Styrofoam or
plastic cup, tearing back the sides to the edge of the ice, and rubbing over
the affected area.
Compression: Wrapping the affected area with an elastic bandage, strap,
or brace
Elevation: If swelling is present, elevation will help alleviate the swelling.
Anti-inflammatories are also a mainstay of therapy. Ibuprofen 2 or 3
times/day, or other NSAIDs, may reduce the inflammatory process and
hasten healing.
Medication P.
Anti-inflammatories: NSAIDs (ibuprofen, etodolac)
Referral
If history, physical exam, or other imaging studies suggest signs of tendon
rupture, including profound weakness with elbow extension, referral to
orthopedic surgery is necessary for potential surgical intervention (2)[B].
For high-risk patients, physical therapy may be beneficial to ensure proper
form and stretching.
Limit ice to 20 min 3 or 4 times daily to avoid cubital tunnel damage of the
ulnar nerve.
Rehabilitation:
Graduated stretching and strengthening following period of rest
French stretch: (1) Clasp fingers together with hands above head; (2) keep
elbows close to head; (3) reach down behind head attempting to touch back;
(4) hold, then repeat
French press: As with stretch, except holding a dumbbell
Towel stretch: (1) Injured arm overhead with uninjured reaching behind back;
(2) one end of towel in each hand; (3) pull, hold, and repeat
Rare, but operative treatment described with elliptical resection of diseased
tissue
Ongoing Care
Return to sport/activity when no longer tender at or above tendon insertion, strength regained,
and full range of motion
References
1. Vidal AF, Drakos MC, Allen AA. Biceps tendon and triceps tendon injuries. Clin Sports
Med. 2004;23:707–722, xi.
2. Blankstein A, Ganel A, Givon U, et al. Ultraschall Med. 2006.
3. Rineer CA, Ruch DS. Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and
triceps ruptures. J Hand Surg [Am]. 2009;34:566–576.
Codes
ICD9
727.09 Other synovitis and tenosynovitis
Clinical Pearls
Evidence suggests that the increased risk of rupture with injection serves as a
contraindication to direct tendon injection. New evidence for the advent of
prolotherapy, which is direct stimulation to injured areas to increase the
inflammatory process, promoting faster healing, may be beneficial in these types
of injuries.
Triceps Tendon Rupture
Mark H. Mirabelli
Ramsey Shehab
Basics
Description
Triceps tendon ruptures are defined as a partial or complete tear of the triceps muscle or
tendon at one of several sites, including the musculotendinous junction or the tendinous
insertion into the bone. The latter scenario occasionally includes a piece of bone from the
olecranon insertion (1). There also have been several cases of tears of the muscle belly (2).
Synonym(s): Triceps tendon rupture; Triceps tendon avulsion; Triceps tendon tear; Avulsion
fracture of the olecranon; Triceps muscle tear
Epidemiology
Triceps tendon ruptures are rare and have been described as the least common of all tendon
injuries.
This injury is more commonly seen in men and affects individuals in the age range of 7–70
yrs.
Least common of all major tendon injuries (1.9% of all tendon ruptures) (3)
Equal predominance in both sides, and no correlation with dominant or nondominant hand
Risk Factors
Several predisposing factors have been described (4):
Hyperparathyroidism secondary to chronic renal failure
Both local and systemic corticosteroid injection; the former sometimes secondary to
olecranon bursitis (5)
Chronic tendinosis at the area may also be a risk factor.
Recent use of fluoroquinolones is also a risk factor for all types of tendon ruptures.
Etiology
Usual mechanism of injury involves a fall on an outstretched arm (causing a deceleration-type
injury).
Direct blow to the posterior arm or elbow, especially if flexed
Olecranon fracture (intra-articular)
Triceps tendinosis
Triceps contusion
Avulsion fracture of the olecranon
Olecranon bursitis
Diagnosis
History
Injury history is of an acute trauma, usually from direct blow or fall.
There may be antecedent history of problems with the elbow.
Patients usually complain of pain and swelling of the posterior elbow.
May have ecchymosis over area of triceps insertion
Can also have decreased active elbow extension
Physical Exam
Presentation includes swelling, pain, bruising over posterior arm and elbow
Activities can be significantly limited, including those requiring pushing and reaching overhead.
Begin with a general exam of upper extremity and contralateral side, including shoulder and
wrist exams, to exclude other concomitant injuries and establish a basis for comparison.
Specifically examine affected side and compare to contralateral.
Patients have localized swelling at the posterior elbow.
Tenderness in the area of the triceps tendon insertion is typical.
Sometimes a palpable defect can be appreciated just proximal to the olecranon.
Test triceps function; pain and weakness with resisted elbow extension should be noted.
Verify integrity of neurovascular status.
Modified Thompson test can help determine the integrity of the musculotendinous unit. This
test is best accomplished with the upper arm supported, the elbow flexed to 90 degrees, and
the forearm and hand hanging relaxed. This can be done by allowing the forearm to hang
over the side of a table or the back of a chair. Upon squeezing the triceps muscle belly, the
elbow should reflexively extend if the tendon is intact. If there is a complete rupture of the
tendon, the elbow will not extend.
Imaging
Radiographs occasionally show 1 or several bony flecks from the tip of the olecranon that
have been avulsed with the tendon.
Sometimes a larger fracture of the olecranon can be seen.
Associated injuries and findings may include radial head or neck fractures, as well as wrist
fractures (probably secondary to the common mechanism of injury, a fall on an outstretched
hand).
US can be used to diagnose triceps tendon ruptures, but may be operator-dependent (6).
MRI can be helpful in the diagnosis and can differentiate between complete and partial
tendon ruptures (7).
Olecranon fracture (intra-articular)
Triceps tendonitis or strain
Triceps contusion
Avulsion fracture of the olecranon
Olecranon bursitis
Treatment
Ice and NSAIDs are the mainstay of acute therapy.
If injury is associated with a larger olecranon fracture or radial head or wrist
fracture, narcotic pain medication may be warranted.
Arm should be placed in sling with ≤90 degrees of flexion initially after the injury.
A posterior splint may be used if necessary.
When a triceps tendon rupture is diagnosed, it is imperative to determine
whether the tear is partial or complete. This will determine whether operative or
nonoperative therapy is appropriate. As noted, MRI is useful for making this
determination when correlated with clinical findings.
Loss of elbow motion and triceps strength (the inability to extend the elbow
against even minor resistance) is consistent with a complete tendon rupture.
The treatment for this is surgery.
If there is some active elbow extension, particularly against resistance, the
more likely diagnosis is a partial tendon rupture.
Although some clinicians suggest surgical repair for both partial and complete
tears because of its low morbidity and high success rate, others support
nonsurgical treatment of partial tendon ruptures with close clinical observation.
Platelet-rich plasma and autologous whole blood injections are currently
investigational adjuvants in both operative and nonoperative treatment.
If nonoperative treatment is appropriate, the elbow should be immobilized in a
posterior splint in 30–40 degrees of flexion for up to 6 wks.
After a period of immobilization (for either operative or nonoperative cases),
patients should be sent to physical therapy for increased range of motion and
progressive strength recovery.
Pain control modalities and shoulder, forearm and wrist range of motion (ROM)
exercises may be started immediately.
Passive elbow ROM should be started after 2–3 wks.
Active assist and then full active ROM exercises should be initiated after
completion of immobilization period.
Recovery is often slow.
Unrestricted activity should be considered no sooner than 3–4 mos (dependent
upon recovery from either operative or nonoperative intervention) due to risk of
rerupture.
Full recovery may take up to 1 yr.
This is the recommended treatment for complete rupture (8).
Surgical repair can be more easily accomplished during the 1st 2 wks after the
injury.
There are several methods of repairing triceps tendon ruptures that yield
excellent results.
A common repair technique reattaches the tendon with wire or suture through
drill holes in the olecranon.
For 3–4 wks postoperatively, the elbow is splinted in 30–40 degrees of flexion.
Ongoing Care
Prognosis
Prognosis is generally good for complete tears treated surgically and incomplete tears
treated either nonoperatively or operatively.
Athletes can expect to return to their previous level of activity with preserved motion and
normalized strength.
References
1. Viegas SF. Avulsion of the triceps tendon. Orthop Rev. 1990;19:533–536.
2. Aso K, Torisu T. Muscle belly tear of the triceps. Am J Sports Med. 1984;12:485–487.
3. Anzel SH, Covey KW, Weiner AD, et al. Disruption of muscles and tendons; an analysis
of 1,014 cases. Surgery. 1959;45:406–414.
4. Bach BR, Warren RF, Wickiewicz TL. Triceps rupture. A case report and literature
review. Am J Sports Med. 1987;15:285–289.
5. Stannard JP, Bucknell AL. Rupture of the triceps tendon associated with steroid
injections. Am J Sports Med. 1993;21:482–485.
6. Kaempffe FA, Lerner RM. Ultrasound diagnosis of triceps tendon rupture. Clin Orthop
Rel Res. 1996;332:138.
7. Tuite MJ, Kijowski R. Sports-related injuries of the elbow: an approach to MRI

interpretation. Clin Sports Med. 2006;25:387–408, v.
8. Rineer CA, Ruch DS. Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and
triceps ruptures. J Hand Surg [Am]. 2009;34:566–576.
Additional Reading
Farrar EL, Lippert FG. Avulsion of the triceps tendon. Clin Orthop Rel Res. 1981;161:242.
Pantazopoulos T, Exarchou E, Stavrou Z, et al. Avulsion of the triceps tendon. J Trauma.

1975;15:827–829.
Strauch RJ. Biceps and triceps injuries of the elbow. Orthop Clin North Am. 1999;30:95–
107.
Codes
ICD9
727.60 Nontraumatic rupture of unspecified tendon
841.8 Sprain of other specified sites of elbow and forearm
Clinical Pearls
When can I resume my usual work/play activities? Treatment for triceps tendon
rupture commonly yields excellent return of motion and strength. Rehabilitation,
after the period of immobilization, is the key to attaining full recovery, and
patients should be able to resume full activity in 3–4 mos.
Trigger Finger
Yvonne Chow
Rahul Kapur
Basics
Description
Also called flexor tenosynovitis
Type of stenosing tenosynovitis
Nodule on flexor tendon catching on A1 pulley
Can affect any digit; occasionally, multiple digits
Ring and middle digit involvement most common in adults
Almost exclusively thumb in children
Diffuse versus nodular versus “congenital” (pediatric trigger thumb)
Epidemiology
Predominant gender: Female > Male (3–6× more common in females).
Predominant age: Bimodal: Age <8 yrs and 55–60 yrs
Seen more commonly in dominant hand
Lifetime risk 2.6% in general population but 10% in diabetics
Incidence
28 cases/100,000 population
Risk Factors
Diabetes, rheumatoid arthritis (RA), connective tissue disorders
Repetitive trauma with compressive force against metacarpophalangeal (MCP) area (eg, arc
welding)
General Prevention
Etiology
Inflammation of flexor digitorum superficialis (FDS) tendon leading to nodule formation
1st annular (A1) pulley spans from volar plate of distal metacarpal to base of proximal
phalanx.
Nodule catches on A1 pulley during finger flexion, leading to pain.
Pain often greatest at MCP joint
Generally idiopathic
Can result from repetitive trauma or sepsis from secondary infection (eg, tuberculosis)

Diabetes
RA
Hypothyroidism
Amyloidosis
Mucopolysaccharidosis
Connective tissue disorders
Diagnosis
History
Painful catching/clicking with finger flexion or extension
Pain over MCP; may refer to palm or proximal interphalangeal (PIP) joint
Digit may be locked, usually in flexion.
Stiffness develops with prolonged symptoms.
Physical Exam
Tender, palpable nodule on flexor tendon
Active fist closing reproduces lock/snap.

Lab
None indicated, except to evaluate associated systemic disease.
Imaging
None indicated; x-rays may be considered to rule out differentials.
None; steroid injection is both therapeutic and diagnostic.
Dupuytren contracture
Gamekeeper's thumb
RA
Tendon sheath ganglion
Suppurative tenosynovitis
Treatment
Splinting of MCP joint at 10–15 degrees of flexion ×6–10 wks:
Reduces tendon motion in sheath
Allows resolution of surrounding synovitis
93% with partial or full symptom resolution after 10 wks (1)[B]
Medication P.
First Line
Injected corticosteroids (see “Surgery/Other Procedures” below)
Second Line
NSAIDs may help with pain relief; no specific evidence but commonly
recommended.
Corticosteroid injection into tendon sheath:
Palmar or dorsolateral approach to avoid neurovascular bundle
US guidance may maximize accuracy (2)[B].
SC infiltration equal or superior to intrasheath injection (3)[B].
May require repeat injection in 1 mo
Up to 93% complete or partial reduction of symptoms in nodular type (4)[A]
Only 50% response in diffuse type or diabetes
Surgical release of A1 pulley:
Open or percutaneous procedure
1st-line treatment for locked digit or pediatric trigger thumb, although there is
increasing argument toward conservative management for the latter
Indicated if repeat injections ineffective
97% complete resolution of symptoms (4)[A]
Ongoing Care
Patient Monitoring
May see increased glucose level following steroid injection in diabetes
Prognosis
Excellent; over 90% symptom resolution with steroid or surgical therapy
23–63% of pediatric trigger digits may resolve spontaneously.
Complications
If untreated:
PIP joint flexion contracture
Distal triggering from FDS tendon degeneration
Of injection:
Fat atrophy and necrosis
Local skin depigmentation
Theoretical risk of tendon rupture
Of surgical release:
Bowstringing of flexor tendon
A2 pulley injury
Digital nerve injury
Infection
Long-term scar tenderness
References
1. Colbourn J, Heath N, Manary S, et al. Effectiveness of splinting for the
treatment of trigger finger. J Hand Ther. 2008;21:336–343.
2. Bodor M, Flossman T. Ultrasound-guided first annular pulley injection for
trigger finger. J Ultrasound Med. 2009;28:737–743.
3. Kazuki K, Egi T, Okada M, et al. Clinical outcome of extrasynovial steroid

injection for trigger finger. Hand Surg. 2006;11:1–4.
4. Nimigan AS, Ross DC, Gan BS. Steroid injections in the management of
trigger fingers. Am J Phys Med Rehabil. 2006;85:36–43.
Additional Reading
Akhtar S, Bradley MJ, Quinton DN, et al. Management and referral for trigger
finger/thumb. BMJ. 2005;331:30–33.
Ryzewicz M, Wolf JM. Trigger digits: principles, management, and

complications. J Hand Surg [Am]. 2006;31:135–146.
Codes
ICD9
727.03 Trigger finger (acquired)
Clinical Pearls
Clinical diagnosis by painful catching at MCP joint
Corticosteroid injection is safe and highly effective 1st-line treatment.
Surgical release provides excellent results when conservative measures fail.
Trigger finger in diabetics is less likely to respond to steroid therapy.
Trochanteric Bursitis
Verle Valentine
Basics
Description
Historically, the condition of pain and tenderness in the area of the greater trochanter had
been referred to as trochanteric bursitis. Recent literature has referred to this condition as
greater trochanteric pain syndrome. This change has come about owing to the recognition
that the etiology of this pain can be from multiple sources that include the bursae in the area
but also can include tendinosis or tendinopathy. These include the tendons of the gluteus
medius and gluteus minimus that insert on the greater trochanter (1,2,3,4,5,6,7).
Bursitis refers to inflammation of the bursae.
Tendinosis refers to chronic degenerative changes within the tendon.
Tendinopathy refers to any anomaly of a tendon. This can include inflammation or
degeneration.
Epidemiology
More common in adults
Incidence peaks between the 4th and 6th decades of life.
Predominant gender: Female > Male (4:1)
Common in runners
Risk Factors
Ipsilateral or contralateral hip arthritis
Degenerative changes of the lumbar spine
Degenerative changes of the knees
Leg-length discrepancy
Total hip arthroplasty
Obesity
Fibromyalgia
Iliotibial band syndrome
Weakness of hip abductors and/or external rotators of the hip
Pes planus
Excessive or rapidly increased activity
Training on hard or banked surfaces
Poorly cushioned shoes
Limitation of internal rotation of the hip
Local trauma
Genetics
No genetic predisposition is known.
General Prevention
Strengthening of hip external rotators and hip abductors
Stretching of muscles around the hip
Avoid sudden increase in activity (including intensity, duration, or pace)
Avoid exercise on banked surfaces
Proper shoe wear
Avoid direct trauma (use protection when appropriate).
Weight loss (if appropriate)
Etiology
Etiology of bursitis:
Inflammation of the bursae can come from repetitive friction between the bony structures
of the trochanter and the muscle, tendon, or fascial tissue that overlies the bursae.
Inflammation of the bursae also can come about owing to direct trauma to the lateral hip.
Etiology of tendinopathy:
Tendon changes can come about from acute or chronic overuse of a muscle tendon unit.
Weakness or tightness of the muscle tendon unit contributes to this condition.

See “Risk Factors.”
Diagnosis
History
Pain localized to the area of the lateral hip is the key historical finding. This pain may radiate
down the lateral thigh or into the groin (8).
Pain is often aggravated by (8):
Prolonged walking
Rising after sitting
Lying on affected side
Squatting
Climbing
Patient also may report other related conditions as seen in “Risk Factors.”
Physical Exam
Tenderness over the greater trochanter is the key diagnostic finding (6).
Other exam tests may be positive but are less specific and lack sensitivity (9):
Pain with extremes of passive rotation, abduction, or adduction
Pain with resisted hip abduction and external or internal rotation
Positive Trendelenburg sign
Other testing to evaluate for associated conditions:
Positive Patrick-FABERE (flexion, abduction, external rotation, extension) testing for
sacroiliac joint dysfunction or hip joint pathology
Ober test for iliotibial band flexibility
Flexion and extension of hip for hip joint pathology
Leg-length measurement for leg-length discrepancy
Foot inspection for pes planus or overpronation
Lower extremity neurologic assessment for lumbar radiculopathy or neuromuscular
disorders

Lab
Blood tests are not altered by this condition.
Imaging
Imaging is not essential for the diagnosis.
If radiography is done, it should include anteroposterior view and frog-leg lateral view of the
affected hip.
Radiographs typically are normal but can show irregular bone formation or bony spurring at
the greater trochanter owing to chronic bursitis or chronic tendinopathy.
Radiographs also may show associated degenerative disease of the hip joint or the lumbar
spine.
Advanced imaging is rarely necessary.
Detection of abnormalities on MRI is a poor predictor of clinical syndrome (9).
Bone scan may show inflammatory component of this condition but is not needed as a
diagnostic tool (7).
A wide variety of conditions should be considered (6,8):
Lumbosacral disk disease
Spinal stenosis
Radiculopathy
Degenerative disease of the hip
Osteonecrosis of the hip
Stress fracture of the hip
Slipped capital femoral epiphysis
Fracture
Contusion
Soft tissue infection
Treatment
Ice
Analgesics
NSAIDs
Corticosteroid injection (4,10,11)
Minimize aggravating activities such as running or prolonged standing or
walking.
Avoid lying on affected side, and consider placing a pillow between knees while
sleeping.
Strengthening (including hip abductors and external rotators of the hip)
Stretching (including the piriformis and iliotibial band)
Address flexibility of hip and low back.
US
Electrical stimulation
Deep friction massage of greater trochanteric, gluteal, and iliotibial band areas
Weight loss (if applicable)
Address leg-length discrepancy (if applicable).
Address pes planus or overpronation (if applicable).
Medication
Analgesics:
Acetaminophen 1,000 mg PO q.i.d.
NSAIDs
Ibuprofen 800 mg PO t.i.d.
Naprosyn 500 mg PO b.i.d.
Others
Injectable corticosteroids:
1 mL of dexamethasone 4 mg/mL
1 mL of Kenalog 40 mg/mL
Anesthetics:
Injection of anesthetic alone can be diagnostic.
Should be used along with corticosteroids during injection
5 mL of 1% lidocaine, 5 mL of 0.5% bupivacaine, or a combination of both
can be used.
Referral
Recalcitrant pain and failure of conservative treatments
Septic bursitis
Various alternative treatments exist. They include:
Accupuncture
Prolotherapy (12)
Extracorporeal shock wave therapy (13)
Platelet-rich plasma (PRP) injections
Surgery is rarely needed and should be reserved for recalcitrant cases that
have failed conservative measures.
Various surgical procedures have been described. They include:
Open surgery with fenestration or release of the iliotibial band and excision of
the subgluteal bursae (14)
Arthroscopic bursectomy (9)
Ongoing Care
Complications
Bursal thickening and fibrosis
Tendon thickening, fibrosis, or tearing
References
1. Gordon EJ. Trochanteric bursitis and tendinitis. Clin Orthop. 1961;20:193–
202.
2. Segal NA, Felson DT, Torner JC, et al. Greater trochanteric pain syndrome:
epidemiology and associated factors. Arch Phys Med Rehabil. 2007;88:988–
992.
3. Shbeeb MI, Matteson EL. Trochanteric bursitis (greater trochanter pain

syndrome). Mayo Clin Proc. 1996;71:565–569.
4. Brinks A, van Rijn RM, Bohnen AM, et al. Effect of corticosteroid injection
for trochanter pain syndrome: design of a randomised clinical trial in general
practice. BMC Musculoskelet Disord. 2007;8:95.
5. Silva F, Adams T, Feinstein J, et al. Trochanteric bursitis: refuting the myth

of inflammation. J Clin Rheumatol. 2008;14:82–86.
6. Alvarez-Nemegyei J, Canoso JJ. Evidence-based soft tissue

rheumatology: III: trochanteric bursitis. J Clin Rheumatol. 2004;10:123–124.
7. Bird PA, Oakley SP, Shnier R, et al. Prospective evaluation of magnetic

resonance imaging and physical examination findings in patients with greater
trochanteric pain syndrome. Arthritis Rheum. 2001;44:2138–2145.
8. Schapira D, Nahir M, Scharf Y. Trochanteric bursitis: a common clinical

problem. Arch Phys Med Rehabil. 1986;67:815–817.
9. Baker CL, Massie RV, Hurt WG, et al. Arthroscopic bursectomy for
recalcitrant trochanteric bursitis. Arthroscopy. 2007;23:827–832.
10. Shbeeb MI, O'Duffy JD, Michet CJ, et al. Evaluation of glucocorticosteroid
injection for the treatment of trochanteric bursitis. J Rheumatol.
1996;23:2104–2106.
11. Cohen SP, Narvaez JC, Lebovits AH, et al. Corticosteroid injections for
trochanteric bursitis: is fluoroscopy necessary? A pilot study. Br J Anaesth.
2005;94:100–106.
12. Rabago D, Best TM, Beamsley M, et al. A systematic review of

prolotherapy for chronic musculoskeletal pain. Clin J Sport Med.
2005;15:376–380.
13. Furia JP, Rompe JD, Maffulli N. Low-energy extracorporeal shock wave
therapy as a treatment for greater trochanteric pain syndrome. Am J Sports
Med. 2009.
14. Slawski DP, Howard RF. Surgical management of refractory trochanteric

bursitis. Am J Sports Med. 1997;25:86–89.
Additional Reading
Paluska SA. An overview of hip injuries in running. Sports Med. 2005;35:991–
1014.
Schon L, Zuckerman JD. Hip pain in the elderly: evaluation and diagnosis.
Geriatrics. 1988;43:48–62.
Williams BS, Cohen SP. Greater trochanteric pain syndrome: a review of

anatomy, diagnosis and treatment. Anesth Analg. 2009;108:1662–1670.
Codes
ICD9
726.5 Enthesopathy of hip region
Turf Toe
Matthew Pecci
Basics
Sprain of the 1st metatarsophalangeal (MTP) joint
Description
Hyperdorsiflexion of the 1st MTP joint, causing sprain of the supporting structures, most
notably the plantarcapsuloligamentous complex
Historically, playing on artificial turf was felt to be a significant contributing factor, but in
actuality, it is believed to be related more to the flexible shoe wear that is typically worn on
these surfaces.
Epidemiology
1st described in the 1970s
Incidence seems to have increased since the late 1960s, related to the more widespread use
of artificial turf fields
Common in football, but also seen in soccer, basketball, tennis, volleyball, and wrestling
Risk Factors
Playing on hard surfaces such as artificial turf combined with shoes with flexible soles, which
are commonly worn on these surfaces
Any condition that limits motion in 1st MTP joint can predispose to injury, such as baseline-
poor MTP range of motion with dorsiflexion <60°, degenerative joint disease of the 1st MTP,
hallux rigidus
Foot mechanical issues that place increased stress on MTP joint during the gait cycle may
predispose to injury, such as poor ankle flexibility, pes planus, and overpronation.
The greater the years of sports participation, the greater the chance of sustaining a 1st MTP
injury.
General Prevention
Careful choice of shoe wear, specifically use of stiff-soled shoes, especially when training or
competing on hard surfaces such as artificial turf
During the preparticipation exam, identify those with a predisposition to injury, specifically
those with limited 1st MTP joint motion (dorsiflexion <60°) or limited ankle flexibility
Those with prior injury or those with predisposing factor may benefit from a stiff orthotic or
insole prophylactically.
Etiology
Most common mechanism is hyperextension of the 1st MTP joint, which injures the
plantarcapsuloligamentous complex
During sports, this mechanism can occur with the foot in a position of push-off with the
forefoot and 1st MTP joint dorsiflexed and the heel off the ground. If an axial force is applied
to the foot at the heel, this can cause hyperdorsiflexion of the 1st MTP joint and injury.
If the hyperextension force is severe, it can lead to dorsal dislocation of the MTP joint and
injury to the joint articular cartilage.
Less common mechanisms include hyperflexion and valgus type injuries.

Severe injuries can be associated with dorsal dislocation of the 1st MTP joint, articular cartilage
injury, plantar plate rupture, and sesamoid fractures.
Diagnosis
History
Excessive dorsiflexion of 1st MTP, causing injury
Pain localized to 1st MTP and increases with range of motion and ambulation, particularly
toeing off
Localized swelling
May describe ecchymosis
Physical Exam
Metatarsophalangeal (MTP) periarticular swelling
May have ecchymosis
MTP tenderness to palpation, commonly on the plantar aspect, but with more severe injuries
can be present dorsally as well
Painful range of motion of MTP, particularly dorsiflexion
May have decreased range of motion
Difficulty weight bearing, may walk with everted foot to avoid toe-off
May have laxity of the ligamentous capsule or collateral ligaments, depending on mechanism
of injury
May have positive Lachman test of toe with plantar plate rupture
Grading system:
Grade 1 sprain: Pain over plantar or medial aspect, no ecchymosis, minimal swelling,
limited pain with weight-bearing
Grade 2 sprain: More intense and diffuse pain, pain with motion, ecchymosis, swelling,
significant pain with weight-bearing
Grade 3 sprain: Severe pain with motion, considerable swelling and ecchymosis, restricted
range of motion, inability to bear weight

Imaging
Anteroposterior, lateral, and oblique radiographic views to rule out associated fractures
Radiographs may show avulsion fracture of capsule or ligamentous complex.
If there is an associated metatarsal compression fracture, radiographs may show intra-
articular loose bodies.
MRI may be performed if suspected plantar plate rupture or other soft tissue injury.
Bone scan may be useful to differentiate associated sesamoid fracture from a bipartite
sesamoid.
Fracture of the 1st metatarsal or proximal phalanx
Sesamoiditis
Exacerbation of degenerative joint disease
Tendonitis of flexor or extensor hallucis tendons
Plantar plate rupture
Treatment
Grade 1:
Ice
Elevation
NSAIDs
Taping of toe to limit dorsiflexion
Early controlled range of motion
May be allowed to continue sports participation if the pain is minimal when
taped
Grade 2:
Treated similar to grade 1, except needs to refrain from activity until minimal
pain, which may take 1–2 wks
May benefit from rigid-soled shoe or rigid forefoot orthotic when returns to
play
Grade 3:
Treated similar to grade 2, except may need crutches for weight-bearing until
walking produces little discomfort
Slow progressive return to participation when symptoms allow, which may
take 4–8 wks
Medication
NSAIDs
Physical therapy referral for aggressive range of motion in chronic cases with
limitations in motion
Surgery is rarely indicated acutely except in cases of significant fracture-
dislocations or plantar plate injury.
Surgery is only considered in chronic cases with nonunion or osteonecrosis of
a sesamoid fracture, persistent pain, restricted motion, or inability to return to
sports participation.
Ongoing Care
More severe or recurrent cases may require a rigid-soled shoe or rigid forefoot orthotic
when participating in sports.
Prognosis
Most cases can return to previous level of function with proper conservative treatment.
Complications
Chronic or severe cases can lead to significantly limited range of motion, which
can predispose to recurrent injury, so early controlled range of motion is
recommended after injury to minimize the risk of this complication.
Additional Reading
Allen LR, Flemming D, Sanders TG. Turf toe: ligamentous injury of the first
metatarsophalangeal joint. Mil Med. 2004;169:xix–xxiv.
Clanton TO, Ford JJ. Turf toe injury. Clin Sports Med. 1994;13:731–741.
Crain JM, Phancao JP, Stidham K. MR imaging of turf toe. Magn Reson
Imaging Clin N Am. 2008;16:93–103.
Kubitz ER. Athletic injuries of the first metatarsophal-angeal joint. J Am

Podiatr Med Assoc. 2003;93:325–332.
Mullen JE, O'Malley MJ. Sprains–residual instability of subtalar, Lisfranc joints,

and turf toe. Clin Sports Med. 2004;23:97–121.
Rodeo SA, O'Brien S, Warren RF, et al. Turf-toe: an analysis of

metatarsophalangeal joint sprains in professional football players. Am J
Sports Med. 1990;18:280–285.
Sammarco GJ. Turf toe. Instr Course Lect. 1993;42:207–212.
Watson TS, Anderson RB, Davis WH. Periarticular injuries to the hallux
metatarsophalangeal joint in athletes. Foot Ankle Clin. 2000;5:687–713.
Codes
ICD9
845.12 Metatarsaophalangeal (joint) sprain
Clinical Pearls
Return to play:
An athlete typically must pass a functional progression for his/her given sport
without pain to return to play. This progression typically begins when an
athlete is pain free with ambulation and daily activity, which may take 1–8 wks,
depending on the degree of initial injury.
Returning to participation too soon may delay full healing and can lead to
chronic symptoms. This lack of healing can also cause loss of MTP motion,
which can lead to recurrent injury.
Corticosteroid injections merely mask symptoms and do not hasten healing.
Ulnar Collateral Ligament Injuries of the Elbow
Marjorie Delo
Basics
Description
Sprain or tearing of the ulnar collateral ligament (UCL) of the elbow secondary to acute or
chronic valgus stress leading to pain, instability, and dysfunction
2 main mechanisms: chronic deterioration of the UCL owing to repetitive valgus overload or,
less commonly, an acute traumatic rupture
Epidemiology
Most UCL injuries are seen in baseball players, but they also can be seen in wrestlers, javelin
throwers, tennis players, football players, volleyball players, and in acute trauma victims.
UCL injuries typically are seen in skeletally mature athletes; skeletally immature athletes with
open physes sustain medial apophyseal avulsion injuries but typically maintain an intact UCL.
Predominant gender: Male > Female.
Although the exact prevalence of UCL injury is unknown, there has been a definite increase in
the number of surgical reconstructions performed in professional, collegiate, and high school
athletes in recent years. This rapid increase has been attributed to overuse as well as
improved diagnostics.
Risk Factors
Participation in sport that demands repetitive excessive valgus stress to the elbow, such as
high-velocity throwing or overhead activity, is a risk factor for chronic injury.
Throwers who become front-on too early in the throwing motion are at increased risk.
Contact sports or sports with significant fall risk are a factor in acute injury.
General Prevention
Athletes who participate in throwing or overhead sports should be on a conditioning program
that includes core stabilization, rotator cuff and forearm muscle strengthening, and posterior
capsule stretching.
Athletic technique should be reviewed to minimize valgus stress to the elbow.
Single-sport athletes should have a 3-mo rest within a year.
Etiology
The UCL is the primary restraint to valgus stress of the elbow in flexion.
The UCL is composed of 3 ligaments: The anterior bundle, posterior bundle, and transverse
ligament.
The anterior bundle, which is composed of an anterior and posterior band with reciprocal
functions, is the most important medial stabilizer of the elbow (1)[A]. Rupture of the anterior
bundle is considered a complete tear of the UCL.
The posterior bundle provides secondary restraint beyond 90 degrees of flexion.
The transverse ligament is an extension of the joint capsule and does not contribute to valgus
stability (2)[A].
Repetitive valgus load to the elbow is absorbed primarily by the UCL.
Over time, the UCL becomes overloaded, and microtraumatic tears occur, leading to altered
elbow kinematics.
Cumulative microtrauma can lead to rupture of the UCL; altered mechanics lead to
decreased throwing or hitting accuracy and velocity.
Acute rupture can occur in a previously attenuated ligament or in a normal ligament subjected
to extreme valgus stress, such as an elbow dislocation.

Valgus-extension overload syndrome: Radiocapitellar and posteromedial olecranon
impingement
Ulnar neuritis or subluxation
Loose osteochondral bodies
Diagnosis
History
In acute rupture, the athlete may experience sudden pain, sometimes with an audible pop,
and cannot resume play.
Chronic injuries present as persistent, insidious medial elbow pain, often accompanied by
decreased command and velocity of throwing or hitting.
Physical Exam
Tenderness along the UCL
Joint effusion and ulnar nerve tenderness may be present.
Flexion contracture with pain at terminal extension is common.
Valgus stress test: The examiner stabilizes the arm and flexes the elbow to 30 degrees;
valgus stress is applied. The test is positive if the athlete has pain, apprehension, or
instability.
Milking maneuver: The forearm is supinated and the elbow flexed to 90 degrees; the
examiner applies a valgus stress by pulling on the thumb while palpating along the UCL. Pain,
apprehension, or instability indicate MCL injury, but this test can give a high number of false-
positive results (3)[B].
Moving valgus stress test: This test is highly sensitive and specific for UCL injury (3)[A]. A
constant valgus stress is placed on the elbow as the joint is moved through the arc of flexion
and extension. The test is positive if the athlete's pain is reproduced between 70 and 120
degrees of flexion.

Imaging
X-rays: 3-view series of the elbow should be performed to evaluate for osteophytes,
calcifications within the ligament or soft tissues, osteochondral damage, and loose bodies.
Stress x-rays may show joint widening compared with the contralateral elbow; a difference in
joint opening of 1–3 mm suggests UCL injury (1)[B].
Stress US is a relatively new method that can demonstrate joint space opening with
application of valgus stress. US also can reveal disruption of the UCL in the hands of an
experienced user (4)[B].
CT arthrography can visualize partial tears of the UCL but is used less frequently with the
improving quality of MRI.
MRI can visualize attenuation, partial tearing, or complete tearing of the UCL, as well as
evaluate the articular surface and surrounding soft tissue structures. Image enhancement is
possible with saline or gadolinium.
Arthroscopy can evaluate and treat associated articular injuries but cannot visualize the UCL
well. Stress testing under arthroscopy, however, can be diagnostic of UCL tear (5)[C].
Flexor/pronator tendonitis or rupture
Ulnar neuritis or subluxation
Medial triceps subluxation
Loose bodies
Olecranon osteophytosis
Medial epicondyle avulsion
Pronator syndrome
Treatment
Acute treatment: Acute injuries should be treated with rest from sport, ice,
NSAIDs, and sling immobilization if pain is substantial with movement.
Grade 1 injuries, consisting of edema seen on imaging but no definitive tear,
should be treated with rehabilitation, including sports-specific training.
Grade 2 and 3 injuries are treated with a hinged elbow brace followed by
prolonged rehabilitation and sports-specific training.
Surgical reconstruction is indicated for athletes who fail conservative
management. Surgery should be considered early in the high-demand
throwing athlete.
Rehabilitation:
Range of motion (ROM) exercises begin after pain decreases.
Once pain-free, strengthening begins with wrist flexor and extensor groups
followed by scapular stabilizers.
Throwing and valgus stresses are restricted for at least 6 wks.
A structured sports-specific program, such an interval throwing program, is
begun when the athlete has full strength and painless valgus testing.
Athletes are rested at any period when they experience pain.
Surgery is indicated for complete rupture or failure of 3–6 mos of conservative
management in a high-demand competitive athlete.
Surgical reconstruction of the UCL is performed using the palmaris longus, toe
extensor, or other tendon graft through a muscle-splitting approach in the
flexor-pronator bundle.
Surgery is followed by lengthy postoperative rehabilitation.
After 10–14 days of immobilization, ROM exercises are initiated.
Hinged bracing is usually recommended until 6 wks.
At that time, strengthening exercises begin.
Valgus stress is avoided until 4 mos postoperatively.
An interval throwing program is initiated at 4 mos with soft ball tosses.
This is advanced in intervals, with return to competitive throwing allowed at 9–
12 mos if the athlete is pain-free with full strength and ROM.
Athletes are rested at any step if pain recurs.
Return to play after reconstruction ranges from 9–18 mos.
Most modern techniques allow 80–90% of athletes to return to play (1)[A].
References
1. Lynch JR, et al. Medial collateral ligament injury in the overhand-throwing
athlete. Journal of Hand Surg Am. 2008;33:430–437.
2. Creighton RA, Bach BR, Bush-Joseph CA. Evaluation of the medial elbow
in the throwing athlete. Am J Orthop. 2006;35:266–269.
3. Erne HC, Zouzias IC, Rosenwasser MP. Medial collateral ligament

reconstruction in the baseball Pitcher's elbow. Hand Clin. 2009;25:339–346.
4. Nassab PF, Schickendantz MS. Evaluation and treatment of medial ulnar

collateral ligament injuries in the throwing athlete. Sports Med Arthrosc Rev.
2006;14:221–231.
5. Rahman RK, Levine WN, Ahmad CS. Elbow medial collateral ligament
injuries. Curr Rev Musculoskelet Med. 2008;1:197–204.
Codes
ICD9
841.8 Sprain of other specified sites of elbow and forearm
Clinical Pearls
UCL injuries are predominantly seen in high-velocity throwing or overhead
athletes.
Pain, apprehension, or laxity seen on valgus testing of the elbow should lead to
MRI or US imaging to evaluate the integrity of the UCL.
Most UCL injuries respond to rehabilitation and sports-specific training, but
surgical reconstruction should be considered in high-level athletes.
Ulnar Tunnel Syndrome
Richard A. Okragly
Scott Fister Johnson
Basics
Description
Compression of the distal ulnar nerve as it passes through Guyon's canal:
Guyon's canal or the ulnar canal is located at the base of the hand.
The superficial sensory branch and/or the deep motor branch of the ulnar nerve can be
involved.
Synonym(s): Handlebar palsy; Guyon's canal syndrome
Types (based on the Shea and McClain classification):
I—Combined sensory and motor deficit
II—Motor deficit only
III—Sensory deficit only
Risk Factors
Environmental trigger factors:
Repetitive occupational wrist trauma (occupational neuritis)
Baseball catchers
Cyclists
Hockey goalies
Golf and racquet sports
Martial arts
Anatomical
Ganglion cyst
Hamate fracture
Lipoma
General Prevention
Avoid excessive pressure to ulnovolar aspect of palm.
Avoid repetitive wrist trauma.
Etiology
Guyon's canal is located in the base of the hand on the ulnar side:
The borders of Guyon's canal are:
Pisiform (medially)
Hook of the hamate (laterally)
Volar carpal ligament/pisohamate ligament (roof)
Transverse retinacular ligament (floor)
Injury to the nerve is caused by trauma to wrist and pressure over the hypothenar eminence.
A true motor, true sensory, or mixed injury pattern can be seen, depending on the location of
the compression.
The mixed (motor and sensory) type is due to compression in the proximal aspect of Guyon's
canal before the division of the ulnar nerve into superficial and deep branches (type I).
True motor type is due to compression of the ulnar nerve at the level of the lower wrist (type
II).
True sensory type is due to compression of the superficial branch of the ulnar nerve at the
distal aspect of Guyon's canal (type III).

Ulnar cubital syndrome
Radial nerve compression
Hook of hamate fractures
Martin-Gruber ulnar-median anastomosis (15% of population)
Riche-Cannieu deep ulnar-median anastomosis
Diagnosis
History
Ring (4th) and small (5th) finger paresthesias with variable weakness of grip
Localized pain and tenderness over Guyon's canal
Paresthesias or vascular symptoms (coldness and pallor of the 4th and 5th digits, cyanosis,
and pain) if the ulnar artery is involved
Coincident involvement of the median nerve is common (tingling or numbness or weakness or
pain in the 2nd and 3rd digits and the lateral aspect of the 4th digit) (1,2,3)[C].
Physical Exam
Depending on the location of the lesion, motor, sensory, or mixed signs may be elicited.
Sensory (1,2,3)[C]:
Positive Tinnel's sign at the pisiform, affecting the medial aspect of the 4th digit and all of
the 5th digit
Sensory loss at tip of little finger
Hypoesthesia on volar sensory branch without involvement of dorsal sensory branch
Motor (1,2,3)[C]:
Weakness with resistance of adductor pollicis and all interossei muscles
Late atrophy of the 1st dorsal interosseus muscle
Positive Wartenberg sign: Abduction of the small finger due to interosseous and lumbrical
compromise
Positive Froment sign: Activation of flexor pollicis longus to substitute for adductor pollicis
Decreased grip strength (40% due to ulnar-innervated muscles)
Ulnar claw hand with paralysis of the deep motor branch

Imaging
Generally, imaging is not need to make the diagnosis, but can be used to establish the etiology
or rule out other diagnoses (1,2,3,4)[C]:
Radiographs to exclude carpal instability
CT scan to exclude hook of the hamate fractures
Doppler US to exclude thrombosis
MRI to exclude ganglion cyst or lipoma
Electromyogram (EMG) studies to document ulnar nerve pathology (1,2,3,4)[C]
Proximal ulnar entrapment (elbow, cervicothoracic spine)
Calcific tendonitis of flexor carpi ulnaris tendon
Carpal instability
Arthropathy of pisotriquetral joint
Ligamentous wrist injury
Hypoesthesia on dorsal sensory branch does NOT involve compression in Guyon's canal.
Treatment
Pre-Hospital
Avoid aggravating activities, including but not limited to (2,3)[C]:
Repetitive hand motions
Heavy grasping
Resting the palm against hard surfaces
Medication
First Line
NSAIDs (2,3)[C]
Second Line
Local injection of corticosteroids (2,3)[C]
General Measures
Conservative treatment to include (2,3)[C]:
Splinting
Physical therapy
Rest
Adjust handlebar positions or increase padding with gloves (2,3)[C].
Avoid repetitive wrist trauma (2,3)[C].
Fascial release to free the aponeurosis around Guyon's canal (2,3,5)[C]
Surgery to remove compressive ganglion (2,3,5)[C]
Ongoing Care
Following surgery, proper wound care and pain control are essential.
Return to full activity 4–8 wks following surgical decompression (3)[C]
References
1. Anto C, Aradhya P. Clinical diagnosis of peripheral nerve compression in the upper
extremity. Orthop Clin North Am. 1996;27:227–236.
2. Plancher KD, ed. The athletic elbow and wrist, part II: common overuse injuries. Clin
Sports Med. 1996;15:347–353.
3. Baker CL Jr, ed. Overuse injuries in the upper extremity. Clin Sports Med. 2001;20:603–
605.
4. Beltran J, Rosenberg ZS. Diagnosis of compressive and entrapment neuropathies of the

upper extremity: value of MR imaging. AJR Am J Roentgenol. 1994;163:525–531.
5. Green DP. Operative hand surgery, 2nd Ed., Vol. 2. Churchill Livingstone Publishing,
1988:1452–1454.
Codes
ICD9
354.2 Lesion of ulnar nerve
Clinical Pearls
Numbness and tingling in the hand are not always signs of carpal tunnel
syndrome.
A good history and physical examination are needed to accurately diagnose
this condition.
Serial EMGs can be used to determine if conservative treatment is effective.
Ultraviolet Keratitis
Carrie B. Zaslow
Tracy L. Zaslow
Basics
Also known as photokeratitis
Acute syndrome occur after exposure of the eyes to ultraviolet (UV) radiation.
Painful but usually self-limited
Description
Exposure to various forms of UV radiation leads to corneal edema and sloughing, followed by
secondary inflammation of the iris.
Risk Factors
UV exposure to unprotected eyes associated with various recreational and occupational
activities
Sources of exposure:
Welder's arc burns
Snowblindness
High-voltage-line short circuits
Other solar exposure
Sunlamps
Damaged metal halide lamps
Aquaria disinfection lamps
Laboratory or germicidal UV lamps
Genetics
No genetic association
General Prevention
The mode of prevention depends on the type of exposure.
Recreational sun exposure: Well-fitting sunglasses that meet the American National
Standards Institute (ANSI) standards with protection against most UV-A and UV-B radiation
Occupational exposure to solar and artificial-solar UV sources: UV-blocking safety goggles in
accordance with ANSI
Occupational exposure to metal halide or mercury vapor lamps: Adherence to the Food and
Drug Administration (FDA) radiologic health program is recommended.
Etiology
Cornea transmits light in visible spectrum.
Cornea absorbs light UV spectrum.
10–20% of light in UV-A spectrum is absorbed.
Nearly 100% of UV-C light is absorbed.
Damage to the cornea in UV keratitis:
Results from absorption of light at the transition point between UV-B and UV-C (290 nm)
Occurs from absorption in the corneal epithelium, the most anterior part of the cornea,
which is several layers thick
Causes surface epithelial cells to die and desquamate
Damaged cells contain epithelial nociceptor terminal axons that are destroyed, leading to
corneal pain secondary to stimulation of the subepithelial nerve plexus.

Facial edema and erythema, resulting from the same UV exposure injury
Diagnosis
Accurate history, including:
Type of exposure
Timing and duration of exposure
Use of protective eyewear
Visual acuity
Complete ocular exam, including:
Extraocular movements
Conjunctiva/sclera/corneas with fluorescein
Anterior chambers (checking for cell and flare)
Lenses
Eversion of the lids to check for foreign bodies
pH exam
History
Exposure without protective eyewear 6–12 hr prior to onset of symptoms
Symptoms (usually bilateral):
Intense pain
Photophobia
Mild to moderate decrease in visual acuity
Increased lacrimation
Physical Exam
Topical anesthetic generally is needed to obtain a good physical exam.
Penlight exam:
Tearing, injection, chemosis of the bulbar conjunctiva and corneal haziness
No discharge present in the tarsal conjunctiva; lack of discharge distinguishes
photokeratitis from conjunctivitis.
Pupils are usually relatively miotic and react sluggishly.
Fluorescein exam: Confluent superficial punctuate staining between the lids
Slit-lamp exam:
Eversion of the eyelids should not reveal a foreign body.
Corneal edema and anterior chamber reaction (cell and flare) may be seen.

A thorough eye exam including fluorescein staining and slit-lamp exam generally is sufficient for
diagnosis.
Imaging
Orbit radiographs/US/CT scan/MRI for suspected intraocular foreign body
pH of tear lake: To distinguish from a chemical burn, check pH of tear lake in lower conjunctival
fornix; pH should be normal in UV keratitis.
Foreign body of the cornea or eyelids
Corneal abrasion
Thermal burns
Toxic epithelial keratopathy (from exposure to chemicals or drugs)
Exposure keratopathy
Nocturnal lagophthalmos
Conjunctivitis
Stevens-Johnson syndrome
Infectious keratitis
Neurotrophic keratopathy
Contact lens–related problems
Trauma
Dry eye syndrome
Dacryocystitis
Canaliculitis
Scleritis
Treatment
Treatment is supportive.
Severe pain from the syndrome should be treated with oral analgesics.
Although they do have a role in the physical exam, topical anesthetics should
not be prescribed.
ED Treatment
Oral analgesics:
Mild oral narcotics may be necessary.
Pain control is important to allow patient to sleep, thus creating an anatomic
patch.
Cycloplegic drops:
Will help to relieve photophobia
Short-acting agents preferable to avoid long-lasting pupil dilation that can be
uncomfortable for patient
Antibiotic ointment:
To provide prophylaxis against superinfection
Has secondary effect of providing lubrication and increasing comfort
Pressure patch:
On the worse eye for 24 hr
May provide some relief
Has not been proven to aid in expeditious healing
Medication
Antibiotic ointment (prescribed 3–4×/day for 2–3 days):
Erythromycin
Bacitracin
Polymyxin-bacitracin
Cycloplegics:
Cyclopentolate 1%
Homatropine 2–5%
Scopolamine 0.25%
Topical anesthesia helps to obtain:
More accurate documentation of visual acuity
More thorough eye exam and fluorescein staining
Do not prescribe on outpatient basis: Interferes with healing and worsens
keratitis
Admission Criteria
Patients requiring bilateral patching with severely decreased visual acuity and
whose social circumstances make it impossible for the patient to take care of his
or her own needs
Discharge Criteria
Nearly all patients may be discharged from the ED following treatment with
cycloplegics, topical antibiotics, and patching.
Lesions usually heal completely within 24 hr.
Ophthalmologist referral for patients who have other eye disorders or for those
who fail to improve significantly after 24 hr
Ongoing Care
Corneal surface regenerates in 24–72 hr.
Surface regeneration leads to symptom resolution.
Reexamination in 24–48 hr
If symptoms improved: Patient can continue with topical antibiotics q.i.d.
If symptoms not improved and superficial punctate staining is still present: Continue treatment
with cycloplegics, antibiotics, and possibly pressure patch.
If new symptoms develop or symptoms persist: Refer to an ophthalmologist.
Patient Monitoring
Long-term monitoring is generally unnecessary with the exception of counseling patients on
using protective eyewear.
Patient Education
Depending on their daily activities, patients should be referred to the appropriate resource to
learn about protective eyewear:
American National Standards Institute (www.ANSI.org)
FDA Radiological Health Program (www.FDA.gov)
Prognosis
Generally, acute, single episodes heal without long-term sequelae.
Complications
Chronic UV exposure can lead to other sequelae:
Cutaneous melanoma
Ocular melanoma
Erythema
Cataract
Nonmelanocytic skin cancer
Additional Reading
Banerjee S, Patwardhan A, Savant VV. Mass photokeratitis following exposure
to unprotected ultraviolet light. J Public Health Med. 2003;25:160.
Lerman S. Direct and photosensitized ultraviolet radiation. In: Fraunfelder FT,

Roy FH, eds. Current ocular therapy. Sec. 16. 3rd ed. Philadelphia: WB
Saunders, 1990:315–320.
Lubeck D, Greene JS. Corneal injuries. Emerg Med Clin North Am.
1988;6:73–94.
Newell FW. Injuries caused by radiant energy. In: Newell FW, ed.
Ophthalmology: Principles and concepts. Chap. 8. 7th ed. St. Louis: CV
Mosby, 1992:184–185.
Podskochy A. Protective role of corneal epithelium against ultraviolet radiation

damage. Acta Ophthalmol Scand. 2004;82:714–717.
Ehlers JP, Shah CP, eds. The Wills eye manual: office and emergency room
diagnosis and treatment of eye disease, 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2008.
Turner A, Rabiu M. Patching for corneal abrasion. Cochrane Database Syst

Rev. 2006;CD004764.
Verma AS, Dwarika D, Bhola RM, et al. Photokeratitis following the

manipulation of aquaria disinfection lamps. Emerg Med J. 2007;24:232.
Codes
ICD9
370.24 Photokeratitis
Clinical Pearls
A patient with eye pain should not be prescribed topical anesthetic eye drops.
Abuse of these drops can lead to neurotrophic keratopathy, a loss of corneal
sensation leading to epithelial defects.
Ureteral, Bladder, and Urethral Trauma
Robert J. Baker
Basics
Description
Sports-related trauma to the trunk and/or perineum can result in contusion, laceration, or
complete transection of the ureter, bladder, or urethra.
Ureteral, bladder, and urethral injuries may be associated with pelvic fractures.
Epidemiology
Fractures of the pelvis can result in injuries to the urethra, bladder, and ureters.
Ureteral injuries rarely occur as isolated injuries following blunt abdominal trauma.
Ureteral injuries account for 1% of all genitourinary injuries (1,2,3)[A].
Bladder contusion or rupture may occur as a result of lower abdominal blunt trauma and
pelvic fractures.
Although males are susceptible to blunt injury of the urethra, this type of injury is uncommon
in females (2)[A].
Urethral injuries in children may result from a straddle mechanism (ie, direct trauma to the
perineum commonly due to contact with the cross-bar of a bicycle) (4,5)[B].
Impingement of the bulbous urethra against the pubic symphysis results in urethral injuries
from the straddle mechanism (3)[C].
Straddle injuries in females may result in labial hematoma and urinary retention. These
injuries have been reported in in-line skating (3)[B].
Most posterior urethral injuries occur by a shearing mechanism (6)[C].
Patients admitted with multiple trauma injuries will have associated genitourinary injuries as
well 10% of the time (1)[C].
Risk Factors
Especially in children with multiple injuries, genitourinary (GU) injuries are common (7)[C].
Although rare, avulsion of the ureter secondary to blunt trauma is known to occur in children
(8)[C].
Rupture of the bladder may occur following blunt or penetrating trauma. The bladder is
especially at risk for injury when full (9)[C].
The abdominal position of the bladder in childhood places it at great risk for traumatic injury
(8)[C].
Bladder injuries often occur in association with pelvic fractures (6)[B].
Genetics
There is no specific genetic predisposition for GU injuries.
However, genetic malformations and solitary kidney are often diagnosed in young children
after workup for GU trauma (7)[C].
Diagnosis
Pre Hospital
Since these injuries are often associate with multiple trauma, stabilization of the patient is
important.
Signs of shock may be present and should be addressed immediately.
Other more life-threatening organ trauma, renal injuries, for example, likely will need to be
addressed 1st.
History
Ureter: Trauma to the back or flank, hematuria, expanding flank mass (2)[C]
Bladder: Hematuria, urethrorrhagia, or inability to void following a traumatic injury to the
abdomen (2)[C]
Urethra: Trauma to the pelvis possibly resulting in fracture, urethrorrhagia, hematuria, inability
to void, lower abdominal or perineum pain (2)[C]
Physical Exam
Ureter: Flank pain, flank mass (urine or hematoma), hematuria, fever, chills, rarely shock (1)
[C]
Bladder: Hematuria, urethrorrhagia, or inability to void (1)[C]
Urethra: Urethrorrhagia and inability to void, especially if pelvic fracture is present or
suspected (1)[C]
Localized tenderness: Ureter, flank pain; bladder, abdominal pain; urethra, perineum pain
Extravasation, especially of the bladder, may result in peritoneal signs (10)[C].
Ecchymosis in the pubic area or perineum (10)[C]
Findings consistent with pelvic fracture
Ureter: Flank mass; lower abdominal pain, chills, fever, urgency, frequency, and pyuria (6)[C]
Urethra: Blood at the meatus; rectal exam reveals a floating or absent prostrate; ecchymosis
and swelling of the external genitalia (10)[C].

Lab
Hematuria on urinalysis, though nonspecific, can be an indication of lower collecting system
injury (urethra, bladder, ureter) (2)[C].
The degree of hematuria is not necessarily correlated with the degree of injury. Small urethral
injuries may present with significant gross blood. Large ureteral injuries may present with
microscopic hematuria (3)[C].
Imaging
Plain x-rays can identify associated injuries (eg, pelvic fractures, lower rib fractures, and
spinal vertebrae fractures), which may raise suspicion of a GU injury (6)[C].
Ureter: IV pyelography (IVP) or retrograde pyelography is diagnostic (10)[B].
Bladder: Retrograde cystography can establish presence of bladder rupture (9)[B].
Urethra: Retrograde urethrography is diagnostic (3)[C].
Children: Some recommend all children with or not stable should be imaged if they have
gross hematuria or >50 RBCs per high-power field (7)[C].
US is not reliable at differentiating urine and blood. Thus US is not the imaging technique to
use in patients with high risk of bladder injury (3)[B].
Pelvic fractures patterns associated with high risk of GU injury are pubic rami fractures of all
4 rami, ipsilateral rami fracture with massive posterior disruption of the sacrum, sacroiliac
joint, or ilium (2)[B].
Pelvic fracture patterns associated with low risk are single rami fractures, ipsilateral rami
fractures without ring disruption (2)[B].
Very little risk of ureteral injury with isolated fractures of acetabulum, ilium, and sacrum (3)
[C].
Hematuria: Kidney contusion, kidney laceration, sports-induced hematuria, kidney failure,
renal calculi, cystitis
Inability to void: Kidney failure, renal calculi, kidney laceration
Treatment
Acute treatment
Analgesia: Oral analgesia may be adequate; however, pain from associated
trauma may require IM or IV administration of strong narcotics (3)[C].
Prognosis is good for full recovery if the injury is diagnosed early and treated
appropriately.
Most patients will require urologic consultation and possible surgical
intervention.
Ureteral fistulas and strictures can occur as a result of missed injuries or
from entrapment associated with fibrosis from healed dislocation of
sacroiliac joints (3)[C].
IV pylorogram should be performed prior to the cystogram (10)[C].
Retrograde urethrography should be performed prior to catheterization in the
male athlete who has sustained a pelvic fracture and is unable to void
following the trauma (1)[C].
Rehabilitation:
No specific rehabilitation, but general reconditioning is usually required
following the period of convalescence.
Following surgical procedures, rehabilitation exercises directed at the back
or pelvic musculature may be necessary.
Transection of the ureter requires prompt repair, ureteropyelostomy (1)[C].
Any bladder rupture associated with pelvic fracture where penetration of the
bladder by a bony spicule is possible is best managed with surgical
débridement (1)[C].
Intraperitoneal rupture of the bladder is appropriately treated with
transperitoneal exploration, débridement, and repair (3)[C].
Initial management of urethral injuries remains controversial. Although early
exploration and realignment have been successful, lower complication rates
have been found with conservative treatment and delayed realignment (3)[C].
Ongoing Care
Delayed diagnosis of ureteral injury can result in nephrectomy (3)[C].
Small, uncomplicated extraperitoneal rupture of the bladder may be managed nonoperatively
with a urethral catheter for 7–14 days (2)[C].
References
1. Lynch TH, Martínez-Piñeiro L, Plas E, et al. EAU guidelines on urological trauma. Eur
Urol. 2005;47:1–15.
2. Morey AF, Metro MJ, Carney KJ, et al. Consensus on genitourinary trauma: external
genitalia. BJU Int. 2004;94:507–515.
3. Runyon MS. Blunt genitourinary trauma. UpToDate. On-line: www.uptodat.com accessed

8/28/2009.
4. Asplund C, Barkdull T, Weiss BD. Genitourinary problems in bicyclists. Curr Sports Med
Rep. 2007;6:333–339.
5. Yelon JA, Harrigan N, Evans JT. Bicycle trauma: a five-year experience. Am Surg.
1995;61:202–205.
6. Gillenwater JY, Grayshack JT, Howards SS, et al. Adult and pediatnc urology. St. Louis:
CV Mosby, 1998.
7. Livne PM, Gonzales ET. Genitourinary trauma in children. Urol Clin North Am.
1985;12:53–65.
8. Mandell J, Cromie WJ, Caldamone AA, et al. Sports-related genitourinary injuries in

children. Clin Sports Med. 1982;1:483–493.
9. Bryan ST, Coleman NJ, Blueitt D, et al. Bladder problems in athletes. Curr Sports Med
Rep. 2008;7:108–112.
10. Rosen P, Barkin R, Danzl DF. Emergency medicine: concepts and clinical practice. St.
Louis: CV Mosby, 1998.
Codes
ICD9
867.0 Injury to bladder and urethra without mention of open wound into cavity
867.1 Injury to bladder and urethra with open wound into cavity
867.2 Injury to ureter without mention of open wound into cavity
Clinical Pearls
Using sport-specific protective equipment, along with appropriate coaching and
officiating, will decrease the likelihood of these rare sports injuries.
Usually these injuries occur after significant trauma. Avoiding high-risk
behaviors may decrease the occurrence. However, there is no specific
limitation to participation.
Warts
Kathleen Weber
Basics
Description
Warts are caused by a human papillomavirus (HPV) infection, resulting in a variety of lesions on
the skin and mucous membranes.
Epidemiology
More than 130 different genotypes of HPV have been identified (1).
Cutaneous HPV infections, 3 types:
Common warts (verruca vulgaris): 70%
Plantar warts (verruca plantaris): 25–30%
Flat warts (verruca plana): 3–4%
10–20% of children will develop cutaneous warts, with the peak incidence occurring between
12 and 16 yrs.
Mucosal HPV infections:
Most common are genital warts (condyloma acuminatum)
Estimated prevalence rate of HPV genital infection in the U.S. adult population is 10–20%
(2).
Risk Factors
Cutaneous HPV infections:
Transmission: Direct or indirect contact; minor superficial abrasions of the skin promote
infection
Autoinoculation occurs especially in younger children.
Risk factors: Immunocompromised
Mucosal HPV infections:
Transmission: Sexual contact; contact with contaminated objects; autoinoculation; vertical
transmission during vaginal delivery (2)
Risk factors: Unprotected sexual relations; multiple sex partners
General Prevention
Cutaneous lesions: No restrictions for participation; coverage recommended (3)
Mucosal lesions: Condoms recommended, but not completely effective
Anogenital warts: The importance of Pap smears should be stressed; screen for other
sexually transmitted diseases (1)
HPV vaccination is indicated for use in women who are between 9 and 26 yrs of age; not
recommended for pregnant women (1)[A]
Ideally, young women should be vaccinated before they have sexual intercourse for the 1st
time (1).
Etiology
HPV infects epithelial tissues and mucous membranes.
The virus infects the mucosa or the basal layer of the skin, causing cellular proliferation and
vascular growth, resulting in a mucosal or skin lesion.
Incubation period, once exposed, varies from weeks to more than a year.

Cutaneous HPV infection: Warts may regress spontaneously; immunocompromised
individuals may be refractory to all treatment.
Condylomata recurs commonly despite therapy.
Condylomata is associated with cervical dysplasia and cervical squamous cell carcinoma,
invasive carcinoma of genitalia, and anal squamous cell carcinoma.
Diagnosis
Warts are usually diagnosed based on their appearance (4).
History
Cutaneous and anogenital warts are usually asymptomatic, but plantar warts can cause
discomfort during activities.
Without treatment, the wart can remain for months to years.
Diagnosis is usually made by characteristic appearance of lesions.
Physical Exam
Verruca vulgaris (common warts):
Skin-colored papule, hyperkeratotic with horny surface
Normal skin markings are disrupted.
Pathognomonic for warts are red-black dots seen on the surface
Can be 1 or multiple lesions
Typically asymptomatic, but may be painful, especially if located over areas of pressure
Distribution: Fingers, hands (most common), knees, may occur anywhere
Verruca plantaris (plantar warts):
Skin-colored papule with coarse, keratotic surface; has characteristic red-black dots
Normal skin markings are disrupted.
Painful, especially if located over areas of pressure
Distribution: Plantar surface of foot
Verruca plana (flat warts):
Skin-colored or lightly pigmented; well-defined, smooth, flat, or slightly elevated papules
Variety of shapes: Round, oval, linear
Sizes vary from pinhead to a few millimeters.
Numbers range from a few to hundreds.
Distribution: Face; dorsum of the hands; extremities, especially shins
Most commonly seen in children and less common in adolescents and adults
Condylomata acuminata (anogenital warts):
Skin-colored, slightly pigmented, or pink
Range from soft, tiny isolated papules, filiform and often pedunculated sessile papules to
cauliflower masses (2)
Distribution: Glans penis, prepuce, shaft, labia, vagina, cervix, perianal area, urethra,
bladder, rectum, and oral cavity (2)
Most asymptomatic or subclinical; may go unrecognized
Subclinical lesions on the genital skin can be visualized as white patches by applying 5%
acetic acid to the suspected area.
Confirmed by biopsy if diagnosis unclear by exam
Verruca vulgaris: Callus, guttate psoriasis, molluscum contagiosum, seborrheic keratosis
Verruca plantaris: Callus, corn
Verruca plana: Lichen planus, molluscum contagiosum, seborrheic keratosis, moles, skin tags
Condylomata acuminata: Lichen planus, pearly penile papules, skin tags, squamous cell
carcinoma, condyloma lata due to secondary syphilis
Treatment
Salicylic acid preparations (10–70%) (5)[A]
Cryosurgery (liquid nitrogen): Apply to wart and surrounding normal tissue (1
mm) for 10–15 sec; repeat every 4 wks (may be painful) (5)[B]
Alternative therapies: Excision, electrocautery, CO2 laser surgery (6)[A], or
pulsed dye laser (PDL) (6)[A]
Duct tape (4)[C]
For mucosal lesions: Cryosurgery as described above; repeat weekly
Podophyllotoxin (7)[A], podophyllin (2)[B] contrai-ndicated during pregnancy
Trichloroacetic acid 80–90% (2)[B]
Imiquimod 5% (7)[A]
CO2 laser, PDL (6)[A]
Alternative therapies: Electrocautery or excision (2)[A]
Referral
Referral to a dermatologist should be considered in recalcitrant warts or
immunocompromised patients.
Ongoing Care
Papanicolaou tests screening for cervical cancer at age 18 or at the onset of sexual activity
In cases of extensive or recalcitrant anogenital warts, consider immune deficiency, especially
HIV.
References
1. Kahn JA. HPV vaccination for the prevention of cervical intraepithelial neoplasia. N Engl J
Med. 2009;361:271–278.
2. Scheinfeld N, Lehman DS. An evidence-based review of medical and surgical treatments

of genital warts. Dermatol Online J. 2006;12:5
3. Cordoro KM, Ganz JE. Training room management of medical conditions: sports
dermatology. Clin Sports Med. 2005;24:565–598, viii–ix.
4. Herman BE, Corneli HM. A practical approach to warts in the emergency department.
Pediatr Emerg Care. 2008;24:246–251; quiz 252–254
5. Gibbs S, Harvey I. Topical treatments for cutaneous warts. Cochrane Database Syst
Rev. 2006;3:CD001781.
6. Ockenfels HM, Hammes S. [Laser treatment of warts.] Hautarzt. 2008.
7. Yan J, Chen SL, Wang HN, et al. Meta-analysis of 5% imiquimod and 0.5%
podophyllotoxin in the treatment of condylomata acuminata. Dermatology. 2006;213:218–
223.
Codes
ICD9
078.10 Viral warts, unspecified
078.12 Plantar wart
078.19 Other specified viral warts
Wolff-Parkinson-White (WPW) Syndrome
Tricia Beatty
Basics
Alert
Supplemental oxygen
Monitor
Synchronized cardioversion if signs of instability (1)
Controversies:
Prehospital use of adenosine:
Stable patients should be treated with adenosine.
Unstable patients should undergo cardioversion.
Catheter radiofrequency ablation:
Use in asymptomatic children and adults is controversial.
Risks and benefits of treating or not treating should be weighed carefully.
Description
The presence of paroxysmal arrhythmias in a patient with ventricular preexcitation caused by
one or more accessory pathways (2).
Epidemiology
Incidence
New cases are diagnosed in the general population at a rate of 0.004% per year.
Prevalence
0.1–0.3% of general population affected
No difference in the athletic population
Predominant gender: Male > Female (3)
Risk Factors
Genetics
3–4% of the cases are familial.
Inheritance pattern is autosomal dominant (2).
Etiology
Type A (orthodromic) is the most common (95%).
Antegrade limb is the atrioventricular (AV) nodal conduction system, and the retrograde
limb is the accessory pathway.
A circuit is created that potentiates reentrant tachycardia.
Type B (antidromic):
Less common than type A
The circuit operates in the opposite direction.
Risks associated with reentrant tachycardia:
Development of atrial fibrillation in 20–25% of cases
Degeneration into ventricular fibrillation
Sudden cardiac death (4)

Ebstein anomaly
Ventricular septal defect
Hypertrophic cardiomyopathy
Atrial septal defect
Anomalous pulmonary venous return
Corrected transposition of the great arteries
Aortic regurgitation
Tetralogy of Fallot
Tricuspid atresia
Neoplasm (rhabdomyosarcoma)
Polycystic kidney disease
Rheumatic heart disease
Genetic abnormality (PRKAG2 gene) (4)
Diagnosis
Wolff-Parkinson-White (WPW) syndrome should be considered as the underlying
etiology in all cases of tachydysrhythmias.
The diagnosis should be based on the characteristic ECG findings once the patient has
converted to a sinus rhythm.
Electrophysiology studies to assess for reentrant tachydysrhythmia inducibility (2)
History
Asymptomatic
Palpitations
Chest pain
Dyspnea
Dizziness
Weakness
Fatigue
Nausea
Light-headedness
Syncope
Physical Exam
Abnormal heart rate:
Narrow QRS complex:
Rapid and regular [supraventricular tachycardia (SVT)]
Irregular (atrial fibrillation)
Wide QRS complex:
Ventricular fibrillation
Ventricular tachycardia
Signs of instability:
Chest pain
Hypotension
Change in mental status
Rales

Lab
CBC
Thyroid function test
Basic metabolic panel
ECG (2):
PR interval <120 ms during sinus rhythm in adults and <90 ms in children
Delta wave: Slurring of initial portion of the QRS complex
QRS duration >120 ms in adults and >90 ms in children
Secondary ST- and T-wave changes
Echocardiogram: Structural heart disease
Holter monitor or external event monitor: Useful in documenting paroxysmal tachydysrhythmia
Electrophysiology study:
Elucidate the accessory pathway(s)
Determine inducibility of AV reciprocating tachycardia (AVRT).
Indications:
All competitive athletes or high-risk recreation athletes
Patients with high-risk professions (pilot, truck or bus driver, etc.)
All children >10 yrs of age
AV nodal reentry SVT
Atrial fibrillation
Ventricular fibrillation
Ventricular tachycardia (4)
Treatment
ED Treatment
Stable patients with narrow complex, regular tachycardia (2):
Vagal maneuvers such as a Valsalva
Right carotid artery massage for no more than 10 s: Auscultate the artery 1st
for a bruit, which would be a contraindication to right carotid artery massage.
Fluid replacement and Trendelenburg position if the patient has mild
hypotension
Pharmacologic conversion if carotid massage fails: Adenosine; monitor for
development of atrial fibrillation.
Stable patients with irregular wide-complex tachycardia:
Procainamide is the drug of choice.
Never use calcium channel blockers, β-blockers, or digoxin. These
medications block the AV node and lead to conduction occurring exclusively
down the faster accessory pathway, resulting in fatal ventricular
dysrhythmias.
Medication
Adenosine: 6-mg rapid IV push; if ineffective, repeat with 12 mg; children: 0.1
mg/kg rapid IV push
Procainamide: 6–13 mg/kg IV at 0.2–0.5 mg/kg/min until arrhythmia controlled,
up to a total dose of 1,000 mg, then 2–6 mg/min (2)
Cather radiofrequency ablation (1):
Indications:
Symptomatic patients
All competitive athletes
Patients engaged in high-risk professions or recreational activities
Efficacy:
95%
Recurrent accessory pathway conduction is usually successfully ablated
during a 2nd session.
Complications (2–4%):
Complete heart block
Cardiac tamponade
Vascular access
Catheter manipulation
Unstable patients:
Synchronized cardioversion starting with 50 J/min
Increase incrementally until sinus rhythm is restored
Admission Criteria
Patients with signs of instability require admission to a monitored bed.
Failure of outpatient therapy for continuous pharmacologic control or ablation
Discharge Criteria
Most patients will be stable and can be discharged once converted to sinus
rhythm.
Follow-up should be arranged with a cardiologist.
Ongoing Care
Return-to-play guidelines:
3–6 mos after catheter ablation
Asymptomatic
Negative EPS(no inducible accessory pathway)
References
1. Tischenko A, Fox D, Yee R, et al. When should we recommend catheter ablation for
patients with the Wolff-Parkinson-White syndrome? Current Opinion in Cardiology.
2008;23:32–37.
2. Sethi KK, Dhall A, Chadha DS, et al. WPW and Preexcitation Syndromes. Supplement of
JAPI. 2007;55:10–15.
3. Heidbuchel H, Panhuyzen-Goedkoop N, Corrado D, et al. Recommendations for

participation in leisure-time physical activity and competitive sports in patients with
arrhythmias and potentially arrhythmogenic conditions, Part I: Supraventricular arrhythmias
and pacemakers. European Journal of Cardiovascular Prevention and Rehabilitation.
2006;13:475–484.
4. Lee KW, Badhwar N, Scheinman MM. Supraven-tricular tachycardia–part I. Curr Probl
Cardiol. 2008;33:467–546.
Additional Reading
Brembilla-Perrot, Beatrice. When and how to assess an asymptomatic ventricular pre-
excitation syndrome? Archives of Cardiovascular Disease. 2008;101:407–411.
Lee KW, Badhwar N, Scheinman MM. Supraven-tricular Tachycardia-Part II: History,

Presentation, Mechanism, and Treatment. Curr Probl Cardiol. 2008;33:557–622.
Saxena A, Chang C, Wang S. Wolff-Parkinson-White Syndrome in Athletes. Current Sports

Medicine Reports. 2006;5:254–257.
Shah CP, Thakur RK, Xie B, et al. Clinical approach to wide QRS complex tachycardias.
Emerg Med Clin North Am. 1998;16:331–360.
Surawicz B, Childers R, Deal B, et al. AHA/ACCF/HRS Recommendations for the

Standardization and Interpretation of the Electrocardiogram, Part III: Intraventricular
Conduction Disturbances. JACC. 2009;53:976–981.
Wolf-Parkinson-White (WPW) Syndrome, Atrioventricular Reentrant Tachycardia. Current

Problems in Cardiology. September 2008:504–522.
Xie B, Thakur RK, Shah C, et al. Emergency management of cardiac arrhythmias. Clinical
differentiation of narrow QRS complex tachycardias. Emerg Clin North Am 1998;16:295–
330.
Codes
ICD9
426.7 Anomalous atrioventricular excitation
Appendix A
Musculoskeletal Radiography
Tudor Hughes
When ordering radiographic studies, it is important to know which is the most appropriate study
to answer the questions at hand. To this end, it is necessary to know which images are
obtained when a certain series is requested, and the advantages of each series and projection.
Although all centers will have slightly different series, what follows is a general guideline.
As a general rule, CT is a useful adjunct for intraarticular fracture preoperative planning in
larger joints where the fractured bone is to be repaired rather than replaced, or complex areas
such as the carpal or tarsal regions. Although CT does involve a significant dose of ionizing
radiation, this is of most concern centrally rather than peripherally. A full x-ray series of the
pelvis or lumbar spine can give a higher radiation dose and less useful information than coned
down CT of the area of interest.
US is an ideal inexpensive way of assessing superficial soft tissues for both trauma and
masses. It has the distinct advantage of being dynamic, imaging the patient in real time as they
move, and also being interactive with the patient, assessing their points of pain.
MRI is a useful method for assessing the soft tissues for injury or mass, and the bones for
occult injuries and bone marrow changes.
Upper Extremities
Fingers
For 2nd–5th digits. Specifically to look at 1 finger for trauma, foreign body, or localized mass. A
marker should be applied, particularly on the lateral projection. Consider US for radiolucent
foreign body. Consider MRI or US for mass or tendon lesion/injury.
Figure 1 (A) PA hand. (B) Oblique of fingers. (C, D) Lateral of fingers.
Thumb
Specifically to look at the thumb for trauma, foreign body or localized mass. Good for ulnar
collateral ligament avulsion. A marker should be applied. Consider US for radiolucent foreign
body. Consider MRI or US for mass, UCL injury (without or with Stener lesion) or tendon
lesion/injury. Stress views are no longer encouraged for acute UCL injury for fear of converting
to a Stener lesion but maybe useful later on to assess stability.
Musculoskeletal Radiography
Figure 2 (A) PA hand. (B) PA thumb. (C) Lateral thumb.

Hand
Routine
This includes an off axis view of the wrist but should not be used to assess wrist alignment.
Good overview for hand pain. May need additional wrist views if pain is proximal or difficult to
localize. Important to have fingers spread on lateral view so that all volar plates are well
visualized. MRI or US may be useful adjuncts to look at adjacent soft tissues.
Figure 3 (A) PA of hand. (B) Oblique of hand. (C) Lateral of hand.
Hand
Arthritis Survey
Some centers prefer pronated obliques over supinated ball catcher (Norgaard) obliques. Both
of these are good for overall assessment of arthritis, individual erosions, soft tissue swelling,
and distribution. MRI or US are useful adjuncts to assess the soft tissues, for synovitis joint fluid
and are said to be more sensitive for erosions.
Figure 4 (A, B) PA of each hand. (C) AP Norgaard projection (Ball catcher's position).
Wrist
Nontrauma, Infection
For typical wrist pain evaluations including arthritis or mass. Good for carpal alignment. US:
good for soft tissue masses, tendon pathology. CT scan may be a useful adjunct to assess for
occult scaphoid fractures and for healing, as well as other occult injuries such as hook of
hamate fracture. CT is often used in the preoperative workup of intraarticular distal radial
fractures. MRI is good for occult fractures, Kienböck's, AVN of lunate or scaphoid, triangular
fibrocartilage tears, or intercarpal ligament injuries.
Figure 5 (A) PA wrist. (B) Ulnar oblique wrist. (C) Lateral wrist.
Trauma
Additional scaphoid views include oblique and ulnar deviation with cranial angulation. These are
good to assess for most aspects of trauma including fracture, subluxation, or dislocation. Of
note, the lateral view can only be used to assess alignment when the volar aspect of the
pisiform projects between the scaphoid and capitate. MRI is a useful adjunct to assess for
occult injury, intercarpal ligament injury, triangular fibrocartilage complex injury, mass, or
synovitis.
Figure 6 (A) PA wrist. (B) Ulnar oblique wrist. (C) Radial oblique wrist. (D) Lateral wrist.
(E) Navicular view.
Additional Views
Clenched fist views taken AP are useful for occult cases of scapholunate ligament disruption.
Clenching the fist pushes the carpal bones apart. Carpal tunnel view is good for looking for
hook of hamate, trapezial ridge fractures, or carpal tunnel syndrome posttrauma/wrist fracture.
CT is another good way to assess for occult carpal fractures. MRI without or with intraarticular
dilute Gadolinium is good to assess for internal derangement.
Figure 7 (A) Clenched fist. (B) Carpal tunnel views.
Forearm
Good for trauma, mass, foreign body, cellulitis/osteomyelitis, or abscess. It is important that
the elbow rotates through 90 degrees between the AP and lateral so that 2 identical views of
the ulna are not obtained. Consider US or MRI to assess for mass or soft tissue injury.
Figure 8 (A) AP forearm. (B) Lateral forearm.
Elbow
Nontrauma
Chronic injuries, arthritis, foreign bodies, and infection. Lateral is good for effusion and
olecranon bursitis. AP is good for epicondylar enthesopathy and osteophytes. Consider US or
MRI for soft tissue mass.
Figure 9 (A) AP elbow. (B) Lateral elbow.
Trauma
Good to assess for otherwise occult radial head fractures. Often AP, lateral, and radial head
are enough for trauma. US or MRI can assess for ligamentous or tendon injuries.
Figure 10 (A) AP. (B) Lateral. (C) Lateral (external or radial) oblique. (D) Medial (internal
or ulnar) oblique. (E) Radial head view.
Additional Views
Good to assess for radio opaque causes of cubital tunnel syndrome, such as osteophytes.
Consider US or MRI for further assessment of cubital tunnel.
Figure 11 Cubital tunnel view.
Humerus
To assess for trauma, infection, mass, or foreign body. Both the shoulder and elbow should be
included on the study in both projections, but they should not be over interpreted on such limited
views.
Figure 12 (A) AP to include shoulder joint. (B) Lateral to include shoulder joint. (C) AP to
include elbow joint. (D) Lateral to include elbow joint.
Shoulder
Nontrauma, Chronic Pain
Shoulder series vary widely between institutions. Good to assess for location of hydroxyapatite,
osteoarthrosis, and other degenerative changes. US or MRI is best to assess for rotator cuff
tears. If a rotator cuff tear is seen on plain films by reduced acromiohumeral distance, then
MRI is better than US to show the degree of retraction and atrophy, if the patient is a candidate
for repair. MRI is best for glenoid labral pathology for which an MRI arthrogram will give
additional information. CT is useful in the preoperative planning of shoulder arthroplasty to
assess for bone stock and any intra-articular glenoid fracture.
Figure 13 (A) AP neutral. (B) AP internal rotation. (C) AP external rotation.
Trauma, Acute Injuries

To evaluate for humeral neck/tuberosity fractures and shoulder dislocations. CT is useful to
assess for Hill Sachs lesions and bony Bankart. MRI can be difficult to interpret acutely due to
blood tracking into the rotator cuff from tuberosity fractures. Subacutely, MRI may be useful to
assess for accompanying internal derangement.
Figure 14 (A) AP scapula,- neutral rotation. (B) Lateral “Y” view. (C) Axillary view, as
tolerated by patient.
Additional Views
Outlet view is good to look at subacromial space to assess for causes of external shoulder
subacromial impingement. It can also be used to localize calcium in the rotator cuff. Stryker
notch view is good for Hill Sachs lesions, but most are seen on neutral rotation AP shoulder.
Westpoint view is good for detecting bony Bankart lesions, but consider CT. Velpeau view can
be a useful adjunct to assess for dislocation in a patient who cannot raise their arm.
Figure 15 (A) Supraspinatus view (outlet, Bigliani method). (B) Westpoint. (C) Stryker. (D)
Velpeau.
Scapula
Good for trauma, scapulothoracic syndrome. Consider CT for trauma workup to assess for
glenoid involvement. MRI can assess for scapulothoracic friction syndromes.
Figure 16 (A) AP scapula. (B) Lateral scapula.
Acromioclavicular Joints
These are routinely assessed on AP shoulder views. Views without and with weights to look for
occult type 1 separations usually do not alter management but can make the diagnosis. May be
useful in legal cases. Consider MRI to assess for deltotrapezial disruption in type 3 or higher
injuries.
Figure 17 (A) AP without weights. (B) AP with weights.
Clavicles
Good for clavicle fractures. Medial clavicle fractures can be difficult to see. Consider CT for
possible medial clavicle fractures.
Figure 18 (A) AP, 0-degree tube angle. (B) AP, 10-degree cephalad angle.
Lower Extremities
Toes
For 1st–5th digits. Specifically to look at 1 toe for trauma, foreign body or localized mass.
Socks off. A marker should be applied. The lateral view should have the affected toe lifted or
depressed clear of the others. Consider US for radiolucent foreign body. Consider MRI or US
for mass or tendon lesion/injury.
Figure 19 (A) AP foot. (B) Medial oblique of affected toe(s). (C) Lateral of toe(s).
Foot
Perform all 3 views for trauma and nontrauma cases. A limited 2-view foot is discouraged.
Weight-bearing to assess foot alignment. Non–weight-bearing if painful to stand or looking for a
foreign body or mass. Non–weight-bearing if ulcer and looking for osteomyelitis. Always
remove socks!
Consider US for Morton's neuroma or plantar fasciitis, or superficial mass. CT is good for full
assessment of Lisfranc injuries. MRI good for occult fracture or mass.
Figure 20 (A) AP (dorsoplantar). (B) Medial oblique. (C) Lateral (mediolateral projection).
Sesamoid View
Good to look at sesamoid alignment with metatarsal head in hallux valgus, to assess metatarsal
sesamoid osteoarthrosis or to look for fracture of sesamoid.
Figure 21 Sesamoid projection.
OS Calcis
Weight-bearing for alignment or non–weight-bearing for mass or if too painful to stand. Good
for trauma and heel alignment. This should be the preferred study for heal pain rather than a
foot series. The posterior subtalar joint and middle subtalar facet are often well visualized on
the axial or Harris Beath view. Consider CT for full preoperative assessment of calcaneal
fractures.
Figure 22 (A) Lateral calcaneus mediolateral projection. (B) PA axial plantodorsal.
Ankle
Weight-bearing if alignment being assessed, or non–weight-bearing if trauma, or looking for
mass.
Ideal for all acute ankle injuries. The base of 5th metatarsal should be included in case the
ankle pain originates from here. For heel pain, use heel or calcaneal projections. US is useful to
assess tendon injuries. CT is good for complex hind foot fractures. MRI is good to assess the
tendons and ligaments for masses and occult fractures.
Figure 23 (A) AP ankle. (B) Mortise ankle. (C) Mediolateral lateral.
Posterior Subtalar Joint

The Broden view is a useful adjunct view to look at the posterior subtalar joint to assess for
intraarticular fractures and arthritis.
Figure 24 Broden view of posterior subtalar joint.
Weight-Bearing Views of the Ankle

Weight-bearing views are useful to eliminate the effects of a large joint effusion from widening
or straightening the ankle mortise.
Figure 25 (A) AP weight-bearing ankle. (B) Mortise weight-bearing ankle. (C) Mediolateral
lateral weight-bearing ankle.
Stress Views of the Ankle
These give more functional information than MRI about ligamentous laxity and are useful in
planning treatment for unstable ankles. It is important to have the other side for comparison.
Figure 26 AP ankle with varus stress.
Tibia/Fibula
This should include both the ankle and knee joints. The ankle and knee should not be over
interpreted on these off axis views. Good for trauma, foreign body, mass, cellulitis. For stress
fractures, consider MRI or bone scan.
Figure 27 (A) AP. (B) Mediolateral lateral.
Knee
Nontrauma, Chronic Injury
Good for initial arthritis assessment. MRI is useful to assess for internal derangement but is of
less value when there is obvious osteoarthrosis on radiographs.
Figure 28 (A) AP. (B) Mediolateral lateral.
Trauma, Acute Injury

Shoot through lateral added to assess for a lipohemarthrosis, if present a fracture must be
sought. CT is a useful adjunct to assess for occult tibial plateau fractures and to plan surgery
with fractures seen on radiographs. MRI being used increasingly to assess accompanying soft
tissue injuries in cases of tibial plateau fractures.
Figure 29 (A) AP. (B) Mediolateral lateral. (C) Lateromedial crosstable lateral.
Additional Views
Rosenberg view. This weight-bearing posteroanterior view with flexion is useful to show both
the intercondylar notch and the joint space formed by the more posterior femoral condyle.
Figure 30 Rosenberg view.
Oblique views. Traditionally used to assess for occult tibial plateau fractures, still useful but
now often replaced by CT or MRI.
Figure 31 (A) Medial oblique. (B) Lateral oblique.

Patella. Initially a routine knee is performed in cases of trauma.
Figure 32 (A) PA knee. (B) Mediolateral lateral.
Additional Views
Merchants view is good to assess patella alignment in cases of subluxation, dislocation, or
tracking problems. These are taken at 30 degrees of flexion, the angle at which the patella is
most unstable. It is taken caudal cranial and includes both knees. The Sunrise axial projection is
taken kneeling of just the affected the knee.
Figure 33 Merchants (bilateral patellar view).

Figure 34 Axial projection (unilateral sunrise method).
Femur
Acute Injury, Trauma
Views of the femur should include both the hip and knee. The trauma series has a crosstable
lateral of both the hip and knee so that the patient does not have to move.
Figure 35 (A) AP proximal. (B) AP distal. (C) X-table lateral femur to include knee joint.
(D) Inferosuperior lateral to include proximal femur and hip joint for unilateral injury.
Nonacute Injury
The views include both the hip and the knee, but the hip is a frog lateral and the knee a rolled
mediolateral. For soft tissue mass, consider MRI.
Figure 36 (A) AP to include hip and proximal femur. (B) AP to include knee and distal
femur. (C) Mediolateral lateral to include knee. (D) Lateral frog-leg hip.
Pelvis
Include Both Hips on Image
Good initial screening test for acute trauma. Good for ill defined pain or metastatic search.
Consider CT for full assessment of pelvic trauma.
Figure 37 AP pelvis.
Hips
Trauma, Acute Injury. AP pelvis and a crosstable lateral to assess for hip pain localized to the
1 side of the pelvis/hip.
Figure 38 (A) AP pelvis. (B) Inferosuperior lateral to include proximal femur and hip joint
for unilateral injury.
Nontrauma, Chronic Injury. The crosstable lateral is replaced by a frog lateral. The frog leg
can be bilateral or unilateral depending on the pain. MRI is an excellent way to assess hip pain
if the radiographs show only minimal abnormality. MRI arthrogram can give useful additional
information about the labrum.
Figure 39 (A) AP pelvis. (B) Bilateral frog leg. (C) or Frog-leg lateral of affected hip.
Sacroiliac Joints
Good initial screening test for sacroiliitis. MRI is more sensitive and saves radiation to the
gonads.
Figure 40 (A) AP pelvis. (B) AP oblique of right sacroiliac joint. (C) AP oblique of left
sacroiliac joint.
Acetabulum (Judet Views)

Good for assessing acetabular fractures, but now usually replaced by oblique images of whole
pelvis. Requires 4 images: 2 RPO and 2 LPO images, collimated to affected side only.
Figure 41 (A) AP pelvis. (B) Right posterior oblique (RPO) CR on up-side. (C) Right
posterior oblique (RPO) CR on down-side. (D) Left posterior oblique (LPO) CR on up-side.
(E) Left posterior oblique (LPO) CR on down-side.
Oblique Pelvis
Also good for assessing fractures about the acetabular. CT is good for the initial assessment,
but when there is a need to follow up fractures, oblique views are usually used.
Figure 42 (A) AP pelvis. (B) Right posterior oblique (RPO). (C) Left posterior oblique
(LPO).
Inlet/Outlet
Good to assess for pelvic fractures involving the pubic rami and sacrum. CT is good for the
initial assessment, but when there is a need to follow up fractures at these locations, inlet and
outlet views are usually used.
Figure 43 (A) AP pelvis. (B) AP axial outlet view. (C) AP axial inlet view.
Vertebral Column
Not used very often because most indications for a skull radiograph are better served by a CT.
Can still be used to assess shunt continuity.
Figure 44 (A) PA skull. (B) Lateral skull. (C) Townes view.
Face
Good initial screening test for facial trauma. If found, these will usually be followed up with CT
to show the full extent.
Figure 45 (A) Occipitofrontal. (B) Occipitomental. (C) Occipitomental with 30-degree

cranial angulation. (D) Lateral face.
Orbits
Useful to look for any destructive bony lesion about the orbit. Replaced by CT when available.
Figure 46 (A) Lateral face. (B) Occipitofacial. (C) Occipitomental.
Eyes
Only indication would be to look for foreign body within the eye, usually prior to MRI. By looking
up and down, it is possible to see if the body moves with the eye.
Figure 47 (A) Occipitofacial looking up. (B) Occipitofacial looking down.
Mandible
The 1st investigation to look for mandible trauma, but also used to look for disease related to
the teeth and their sockets. CT is a useful adjunct for mandibular trauma. The oblique views
show the labeled side as the inferiorly.
Figure 48 (A) Occipitofacial. (B) AP axial. (C) Left inferosuperior oblique. (D) Right
inferosuperior oblique.
Nasal Bone
Used to assess for nasal trauma. Can also be used to show the septum in cases of nasal
septal destruction, but would usually be replaced by CT for the latter. Many advocate not
radiographing the nose for 7–10 days until the swelling has subsided, and then only if the
patient is unhappy with the appearance. Bilateral lateral views are probably overdoing things.
Figure 49 (A) Coned down occipitofacial. (B) Left lateral soft tissue exposure. (C) Right
lateral soft tissue exposure.
Cervical Spine
Complete
Include a swimmer's view if C7–T1 junction is not well visualized on the lateral view, and a
Fuch's view if the odontoid is suboptimal. Such a full series is rarely used and would be
replaced by CT for acute trauma and CT or MRI for chronic pain/radiculopathy. Oblique views
such as these would be difficult in the trauma setting and would be done as trauma obliques
with the patient supine and the beam angled obliquely. They can be useful to show the posterior
elements, particularly at the cervicothoracic junction where it may otherwise be difficult.
Figure 50 (A) AP. (B) Lateral. (C) AP odontoid (open mouth). (D) Right anterior oblique
(wrongly labeled). (E) Left anterior oblique. (F) Swimmer's view to visualize C7–T1. (G)
Fuch's view.
Limited
A more reasonable series for acute trauma. Follow-up or chronic pain would usually emphasize
the area of interest.
Figure 51 (A) AP. (B) Lateral. (C) AP odontoid (open mouth). (D) Swimmer's view
Flex-ext Series
The best way to assess for cervical stability. They cannot be obtained acutely after trauma
when there will likely be spasm but should be delayed 10 days.
Figure 52 (A) Flexion lateral. (B) Extension lateral.
Thoracic Spine
Good initial assessment of pain and trauma. The lateral view may need to be augmented by a
swimmer's view to show the cervicothoracic junction.
Figure 53 (A) AP thoracic spine. (B) Lateral thoracic spine.
Additional Views
The lateral view may need to be augmented by a swimmer's view to show the cervicothoracic
junction. CT is used to characterize any fractures seen and MRI in cases of long tract signs.
Figure 54 Swimmer's view of cervicothoracic junction.
Lumbar Spine
Routine Imaging
The images vary from center to center. Some will include an AP pelvis, others just AP and
lateral lumbar spine. Good to assess for acute trauma, alignment, spondylolysis, and
spondylolisthesis. CT is usually performed if trauma is seen on the radiographs. MRI is useful in
cases of radiculopathy.
Figure 55 (A) AP pelvis. (B) AP lumbar spine. (C) Lateral lumbar spine.
Additional Views
For follow-up flex-ext exams, a neutral lateral is not needed. These extra images start to incur
a large radiation dose for little extra information and are not encouraged. Oblique views allow
visualization of the facet joints, and can show pars defects, although these are often better
seen on the lateral view. The flexion extension views are to look for instability in the
preoperative planning of possible spinal fusion, or the postoperative assessment of fusion. The
coned-down lateral view of the lumbosacral junction is useful since often this region is obliqued
on the lateral lumbar spine.
Figure 56 (A) Right posterior oblique lumbar spine. (B) Left posterior oblique lumbar spine.
(C) Flexion lateral lumbar spine. (D) Extension lateral lumbar spine. (E) L5–S1 lateral.
Sacrum
Often difficult to see even with good radiographs due to bowel gas and feces. Not usually
imaged separately from the pelvis in trauma. Can be used to look for lesions affecting the
sacral plexus.
Figure 57 (A) AP cranial. (B) Lateral. (C) AP caudal.
Coccyx
Used in cases of coccydynia. The coccyx has a wide variety of shapes and angles and is often
inconclusive for the radiation dose used.
Figure 58 (A) AP. (B) AP caudal. (C) Lateral.
Scoliosis Series
Used to measure the Cobb angle and look for progression. Also used to look for underlying
congenital vertebral anomaly.
Figure 59 (A) PA taken weight-bearing. (B) Lateral taken weight-bearing.

Additional Views
Views taken erect, leaning to the left and to the right are useful to look for mobile and fixed
segments of scoliosis in planning surgery.
Figure 60 (A) AP best bend right. (B) AP erect. (C) AP best bend left.
Miscellaneous Bone Studies

Used to measure leg length. Coned-down views are taken of the iliac crests, hips, knees, and
ankles with a ruler behind the patient. The beam being centered on each area of interest will
reduce artifact due to parallax.
Figure 61 (A) AP wing of pelvis. (B) AP hip joint.
Leg Alignment—Include Joints from Hip to Ankle

Patient upright, equal weight in each foot. Both leg alignment and leg length can be assessed
on this study if weight-bearing. The weight-bearing line passes from the middle of the femoral
head to the middle to the tibial plafond and should pass between the tibial eminences. This
determines varus or valgus deformity at the knees. Used for pre- and postoperative
assessment of total knee arthroplasty.
Figure 62 AP both legs.
Arthritis Joint Survey

This could include up to; AP/lateral C-spine, AP/lateral T-spine, AP/lateral L-spine, AP bilateral
shoulders, AP/lateral bilateral Knees, AP pelvis, AP, oblique and lateral bilateral hands (to
include wrists), AP/lateral bilateral ankles (include heel on lateral views), AP/oblique bilateral
feet. Since this would be a large radiation dose, it is often better to tailor this to the regions of
pain.
Metastatic Bone Survey

This varies from one center to another and could include from 5–30 images. The most
important areas to image are the axial skeleton and the proximal appendicular skeleton. A full
survey would include: left lateral skull, AP/lateral, C-spine, AP/lateral L-spine, AP/lateral
bilateral humerus (to include shoulders), AP/lateral bilateral forearms, AP ribs, bilaterally, A
AP/lateral T-spine, AP pelvis, AP/lateral bilateral femurs, AP/lateral bilateral tibia/fibulas.
Bony Thorax
For most acute rib injuries, the protocol is a PA erect chest exam to evaluate for pneumothorax.
Only patients with pathological fractures or patients who have undergone a bone scan should
be imaged for rib fractures. Legal cases may also require documentation of fracture. It is
important to have a “bb” at the site of pain and for the technologist to annotate if the bb is
anterior or posterior.
Figure 63 PA chest only. If history is acute rib injury.
Figure 64 Post bone scan or pathological fractures. (A) AP or PA ribs—dependent on site

of injury. (B, C) Affected side closest to Bucky oblique ribs.
Sternum
Even on good radiographs, visualization of the sternum is limited. The study of choice is CT.
Figure 65 (A) Lateral. (B) Right anterior oblique.
Sternoclavicular Joints
Study of choice is CT. These are very poorly visualized radiographically. A useful sign is a
difference in height of the anterior ends of the ribs.
Figure 66 (A) PA. (B) AP axial. (C) Coned down PA.

Figure 67 PA and obliques.
Appendix B: Office Rehabilitation

Sean McKeowen
The home exercise programs included within this text have been designed to allow the
practitioner a means to enable a patient to begin a basic exercise program. The programs
consist of a brief introduction of the condition, common causes, signs and symptoms,
treatment, and a stretching and strengthening exercise routine with progression. The programs
are intended for those patients whose conditions could be managed in this way. For moderate
to severe cases, as well as chronic conditions, a referral to a physical therapist is warranted.
Hamstring Strain
What are Hamstring Strains?
A hamstring strain is an injury to the muscles located in the back of the thigh. The injury can
consist of a slight tearing of the muscle fibers (1st degree) or a moderate tearing (2nd degree),
or be serious enough to cause a complete tear of the muscle (3rd degree).
Common Causes
Many factors can cause this type of injury: Lack of flexibility, lack of appropriate warm-up and
stretching, jumping, fatigue, running mechanics (overstriding, missed step, quick moves),
imbalances between the quadriceps and hamstring muscle groups, and/or inadequate
rehabilitation following previous injury to this muscle group, causing repetitive trauma.
Signs and Symptoms

Pain and tenderness are felt most commonly in the mid-belly of the muscle. Minor tears involve
a smaller area; larger tears would be more widespread. Bruising and swelling at the site of the
injury, as well as down the leg even days afterward, can occur. Stiffness with inability to fully
extend the knee is associated with the injury. There is weakness of the leg, and walking may be
difficult.
Treatment
Initially, rest, ice, compression, and elevation above the heart (RICE) treatment is
applied for 2–3 days following the injury. Icing is performed for 15–20 min, 2–3
times during the day. For moderate to severe strains, your physician may
prescribe physical therapy for modalities (US, soft tissue massage, electrical
stimulation), evaluation of weakened/tight muscles, gait analysis, and exercise
progression. Crutches should be used if walking is painful. Once walking can be
performed without a limp, crutches should be discontinued. Stretching and
strengthening exercises, used to promote range of motion and strength, are
initiated progressively within 3–4 days following injury. Elastic thigh wraps or
sleeves can be used for extra support and warmth to the muscles upon returning
to sport participation.
Stretching
Guidelines for performance and progression of stretching exercises are as follows and/or as
prescribed by your physician:
Keep the stretch to a comfortable level. (Do not force the stretch or cause excessive pain.)
Do not hold your breath while stretching.
Strengthening
Guidelines for performance and progression of strengthening exercises are as follows and/or
as prescribed by your physician:
Do not hold your breath while you lift.
Stay below the level of pain.
Do 2–3 sets of 10–15 repetitions 2–4 times a week. Once you can complete 3 sets of 15
repetitions easily, increase the weight, reduce the repetitions to 10, and build back up to 15.
Home Exercise Program

This program is designed to allow you to start with basic exercises. If you should have any
questions or difficulties, refer back to your physician.
Stretching Exercises
Guidelines: Stretch 3–6 times, holding 30 sec.
A variety of hamstring stretches are given. Not all have to be performed.
Seated Hamstring Stretch

While seated on the floor or table, extend the injured leg straightforward and bend the opposite
leg at the knee into a figure “4” position. Bend forward from the hip over the extended leg with
head up. Keep the back and the knee of the injured leg straight. Do not round your back.
Hamstring Doorway Stretch

Lying on the ground, raise the heel of the injured leg onto the doorframe or wall and extend the
opposite leg through the doorway. Keep the back and the knee of the injured leg straight. Move
closer to the wall to help increase the stretch. Hands can be used to help keep the knee from
bending. Keep the upper body and neck relaxed.
Standing Hamstring Stretch
Place the heel of the injured leg on a bench or stool. Lean forward from the hip over the
extended leg. Keep the back and knee of the injured leg straight. Do not round your back
Achilles Stretch
Stand, leaning onto a wall in a lunge position with the injured leg placed further back than the
opposite leg. Lunge forward onto the opposite leg while keeping the knee of the injured leg
straight and the heel on the ground. Stretch is felt in the calf.
Strengthening Exercises
Guidelines: Start with 3 sets of 10 repetitions, if able (fewer, if unable); progress to 3 sets of
15 repetitions. Once this is accomplished easily, reduce the repetitions to 3 sets of 10 and
increase the weight intensity.
Standing Hamstring Curls

Support yourself with a chair or counter in front of you. Bend the injured leg at the knee while
keeping the thigh pointed straight down. You can begin with no weight and then progress to
ankle weights.
Prone Hamstring Curls

Lying on your stomach, bend the knee of the injured leg toward your buttocks. You can begin
with no weight and then progress to ankle weights.
Clam Shell Exercises
Lie on side with knees bent, feet together. Lift knee upward. Lower and repeat. Exercise lying
one side. Keep your back straight and hips slightly rotated forward.
Special instructions: Make sure you keep your hips rolled forward. Lift knee upward. Progress
2..3..4..5 sec as tolerated. Perform 1 set of 20 repetitions, 1 a day. Hold exercise for 1 sec.
Bilateral Heel Raises

Stand with your feet shoulder-width apart. Raise the heels off the ground onto the balls of the
feet. Fingertips can be placed on a counter for light balance.
Single Heel Raise
Same as for bilateral heel raises, but using the injured leg only.
Bicycling
Begin cycling at an easy pace, with progression of speed, resistance, and time.
Jogging, Running, Sprinting (Straight Lines)

Start easy jogging in straight lines first. Progress speed and distances gradually as tolerated.
Jogging, Running, Sprinting (Figure 8s and Zig-Zag Patterns)

Jog slowly, making a pattern of large figure 8s, and progress to smaller and smaller patterns
with increasing speed. Jog in zig-zag patterns with large cuts 1st and then progress to sharper
cuts with increasing speed as tolerated.
Hopping/Jumping (Front, Back, Side to Side)
Begin by hopping with both feet up and down and progress to front, back, and side-to-side
movements. Further progression is achieved by hopping in these same patterns with the
affected leg only. Advance to jumping with these same criteria.
Patella Femoral Pain Syndrome

What is Patella Femoral Pain Syndrome?
Patella femoral pain syndrome is pain localized to the kneecap (patella). The patella is encased
within the quadriceps tendon, which is attached to the tibia (shin bone) by way of the patellar
tendon. The patella slides back and forth in between grooves located at the end of the femur
(thigh bone). Normally, there is a relatively small angle created by the line of the quadriceps
muscle pull from the hip, the center of the kneecap, and the insertion of the tendon into the shin
bone. If there is malalignment present and repeated motion in this area, the undersurface of the
kneecap can become irritated and inflamed and, eventually, can wear out (chondromalacia).
Weakness of the hip muscles can contribute to altered mechanics of the knee especially if a
malalignment is present. The important factor with this condition is to determine the cause.
Common Causes
Many causes have been attributed to this condition:
Pronation of the feet (a rolling inward of the feet, with a flattening of the arch), which causes
the knees to bend inward (knock-knee)
Anatomic variance such as wide hips, knock-knees, and/or a lateral placement of the
insertion of the patellar tendon onto the shin bone, which increases the angle of muscle pull
and then draws the patella toward the outside of the knee
Anatomic variance in the size and shape of the patella and/or femoral grooves
Weakness or fatigue of the quadriceps and hamstrings
Poor mechanics
Decreased flexibility
Overuse in activities such as running, jumping, cycling, and walking
Tightness in the lateral knee structures
Weakness of hip muscles (primarily gluteus maximus and gluteus medius) which may change
forces on the knee
Assessment of hip muscles is important (glut max, glut medius)
Quadricep dominant squatting
Signs and Symptoms

There is pain about the patella, with possible swelling, depending on how much the knee is
used. Grinding may be felt or heard with knee movements. Pain occurs with walking, running,
and prolonged sitting. Eccentric contractions, such as squatting and walking down stairs or hills,
are usually aggravating factors.
Treatment
Initially helpful is rest and ice 2–3 times per day for 15–20 min. Wait 60 min
between icing. Icing is beneficial as long as the inflammatory condition continues.
Ice can be applied after activity and/or rehabilitation to help decrease pain and
muscle spasm. Anti-inflammatory drugs are sometimes prescribed. Stretching
and strengthening exercises, used to promote range of motion and strength, are
initiated when pain is decreased. Physical therapy can be prescribed by your
physician to help with evaluation of weakened and/or tight muscles, gait analysis,
application of modalities in moderate to severe cases (US and electrical
stimulation), and overall progression of exercises. Knee bracing or patellar taping
can be beneficial when attempting to strengthen the knee. If the condition has
progressed to severe chondromalacia, surgery may be necessary. Surgical
anatomic correction is sometimes performed as well.
Stretching
Guidelines for performance or progression of stretching exercises are as follows and/or as
Strengthening
Guidelines for performance or progression of strengthening exercises are as follows and/or as

Seated Hamstring Stretch

While seated on the floor or table, extend the injured leg straight forward and bend the opposite
leg at the knee into a figure “4” position. Bend forward from the hip over the extended leg, with
your head up. Keep the back and the knee of the injured leg straight. Do not round back
Iliotibial Band Stretch

Stand with the involved leg crossed in back of the opposite leg. Slowly lean upper body toward
the “good” leg by bending at the waist. You can lean into a wall or balance by lightly touching a
chair. Stretch should be felt at the side of the hip facing the wall and down the outer thigh.
Quadriceps Stretch
Stand in back of a chair for assistance with balance. Hold the top of the foot of the involved leg
with the hand of the same side. Slowly bend the knee backward toward the buttocks.
Hip Flexor Stretch

Kneeling on involved knee, slowly push pelvis down while arching back until stretch is felt in
front of hip. Hold 10 sec, repeat 5–10 times per set. Do 1 set per session. Do 1–2 sessions
per day.
Achilles Stretch
Stand, leaning onto a wall in a lunge position with injured leg placed further back then opposite
leg. Lunge forward by bending the good leg while keeping the knee of the injured leg straight
and the heel on the ground. Stretch is felt in the calf.
Guidelines: Start with 3 sets of 10 repetitions if able (less if unable); progress to 3 sets of 15.
Once this is accomplished easily, reduce repetitions to 3 sets of 10 and increase the weight
intensity.
Quadriceps Set (Quad Set)

Place a small, rolled-up towel under the involved knee. Slowly tighten the top thigh muscle while
pushing the back of the knee into the towel. The kneecap can be seen to move upward. Stay
within pain-free range as you attempt to progress to a full contraction with a fully extended leg.
Hold the contraction 6–8 sec and repeat 10 times.
Towel Squeeze
Long sit on a table, with legs extended and a towel roll placed above the knees and between
the thighs. Squeeze the towel roll by bringing your thighs together and digging your heels into
the table. The feet are in a V position. Hold the contraction for 6–8 sec and repeat 10 times.
Straight-Leg Raises
Straight-leg raises can be performed once you can maintain a quad set with little to no
discomfort.
Hip Flexion: Lying on your back, bend the uninvolved knee so that the foot is on the table.
Perform a quad set with the injured leg, and then lift the leg up to the level of the opposite
knee.
Hip Abduction: Lying on the uninvolved side, perform a quad set and then raise the leg to a
30-degree angle. You can bend the bottom knee for balance (not shown in illustration).
Clam Shell Exercises

Lie on side with knees bent, feet together. Lift knee upward. Lower and repeat. Exercise lying
one side. Keep your back straight and hips slightly rotated forward.
Special instructions: Make sure you keep your hips rolled forward. Lift knee upward. Progress
2..3..4..5 sec as tolerated. Perform 1 set of 20 repetitions, once a day. Hold exercise for 1
sec.
Prone Leg Extension
Lift leg 6–8 inches from the floor, keeping knee locked. Lower and the repeat with left leg,
Continue alternating legs. Repeat 10–20 times per set. Do 1 set per session. Do 1 session per
day.
Proprioceptive Training
Assume a standing position, with feet a shoulder-width apart. Stand on the affected ankle, as
tolerated, working up to 30 sec with your eyes open. Progress to balancing for 30 sec with
your eyes closed. Repeat 3–5 times. Can be done 2–3 times per day. Have stance knee
slightly bent.
Donkey Kick
Lean over table, bending at hips, stand on uninvolved leg with knee slightly bent. Bend knee on
non–stance leg, Lift leg up and backward as shown. Return to start and repeat. Repeat
opposite side. Perform 1 set of 20 repetitions, once a day. Hold for 2 sec.
Hip Adduction
Lying on the involved side, take the opposite leg, bend the knee, and place the foot on the table
in front of you. With the involved leg straight, perform a quad set and lift the leg 4–6 inches.
Hip Extension
Lying flat on your stomach, with both legs straight, perform a quad set with the involved leg and
lift the leg 4–6 inches. The back should not arch or rotate with this exercise. A small, rolled-up
towel could be used under the involved thigh to help prevent compression of the kneecap on the
table.
Short-Arc Knee Extension
Long sit on a table. Place a rolled-up towel under the involved Leg, allowing the knee to flex to
15 degrees (small bend). Slowly straighten the knee toward full knee extension. Progress to a
larger towel roll by increasing the angle of knee bend.
Prone Hamstring Curls

Lying on your stomach, bend the knee of the injured leg toward your buttocks. You can begin
with no weight and then progress to ankle weights.
Step Ups
Begin with a 2-inch step. Step up with the involved leg, followed by the good leg. Step down
with the good leg, followed by the injured leg. Progress to larger steps, such as 4 inches and
then 6 inches. Progression is made only as symptoms allow. No pain should be felt when
performing this exercise. Perform 1 set of 10 repetitions (or fewer, if unable). Progress to 3
sets of 10, followed by an increase in the height of the step, whereby repetitions are again
decreased to one set.
Lateral Step Up
This is a progression of the forward step up. Place the involved leg laterally on a 2-inch step
and the uninjured leg on the floor beside it. Raise the toes of the uninjured leg so that the heel
of this leg is its only contact with the floor. Raise your body to the level of the step by extending
the involved leg. Slowly lower your body by bending the knee of the involved leg so that the heel
of the good leg contacts the floor once again. Do not allow the hip to drop to reach the floor.
Progress to larger steps, such as 4 inches and then 6 inches. No pain should be allowed with
this exercise. Perform 1 set of 10 repetitions (or fewer, if unable). Progress to 3 sets of 10,
followed by an increase in the height of the step, whereby repetitions are again decreased to
one set. Do not let the knee go past the toes.
Wall Slides
Stand with your back against a wall and your feet a shoulder-width apart. Slowly squat by
sliding down the wall. Progress the squat from ¼–1/2 as symptoms allow Perform 1 set of 10
repetitions, progressing to 3 sets of 10–15 repetitions. Further strength progression can be
achieved by holding progressive weights in your hands. Make sure the knees do not go past the
toes.
Placing elastic band around your knees and keeping knees apart during the squat exercise can
enhance this exercise
Leg Press
Leg press machines can be utilized, limiting the amount of knee motion to pain-free ranges and
then progressing to the full range.
Lunges
Start with a step forward with the involved leg and slowly bend at the knee to a minimal degree,
then return to a standing position. Progress this exercise by increasing the degree of knee bend
and by utilizing progressive hand weights or bars. Perform 1 set of 10 repetitions, progressing
to 3 sets of 10–15. Be sure the knee does not pass front of toes.
Stand with your feet a shoulder-width apart. Raise your heels off the ground and roll your
weight onto the balls of your feet. Fingertips can be placed on a counter for light balance. To
continue to improve strength, progress to standing heel raises on weight machines.
Single-Heel Raise
Same as for bilateral heel raises, but using the injured leg only.
Bicycling
Begin cycling at an easy pace, with progression of speed, resistance, and time.

Start with a walk/jog walk pattern to gradually increase force. Start easy jogging in straight
lines first. Progress speed and distances gradually.

with increasing speed. Jog in zig-zag patterns with large cuts first and then progress to sharper
cuts with increasing speed.
Hopping/Jumping (Front, Back, Side to Side)
affected leg only. Advance to jumping with these same criteria.
Ankle Sprains
What is an Ankle Sprain?
An ankle sprain is a tear of the ligaments that help to support the ankle joint. The injury can be
minimal, involving microscopic tears, or can completely rupture the supporting structures. The
most common type of ankle sprain is termed inversion and involves the ligaments on the
outside of the joint.
Common Causes
An ankle sprain occurs when the foot is taken beyond its normal range of motion. This can
happen when the foot lands on an uneven surface and the pressure of a person's body weight
is forced onto the outside of the foot. An inversion sprain involves the foot turning inward. The
foot also can turn outwardly and injure the inside of the ankle, causing an eversion type of
sprain.
Signs and Symptoms

Pain, swelling, and/or bruising along either the inside or the outside of the ankle joint
Treatment
Initially, rest, ice, compression, and elevation above the heart (RICE) treatment is
used for 2–3 days following the injury. Icing is performed for 15–20 min 2–3
times during the day. One hour breaks between icing if done more often. Anti-
inflammatory medications may be used to help decrease pain and swelling. Early
weight bearing to pain tolerance should be conducted and can be assisted by the
use of crutches. When walking can be performed without a limp, use of crutches
should be discontinued. Stretching and strengthening exercises, used to promote
range of motion and strength, are then initiated. Physical therapy may be
prescribed by your physician to help with application of modalities (whirlpool, US,
electrical stimulation, soft tissue massage), gait analysis, retaining balance
abilities, evaluation of ankle range of motion, along with assessment of weak
muscles and overall exercise progression. Ankle taping or braces could be used
to help with prevention of further episodes but should not be used as a substitute
for exercises.
Stretching
Guidelines for performance and progression of stretching exercises are as follows and/or as
Strengthening
Guidelines for performance and progression of strengthening exercises are as follows and/or
as prescribed by your physician:
Do 2–3 sets of 10–15 repetitions 2–4 times a week. Once you can easily complete 3 sets of
15 repetitions, increase the weight, reduce the repetitions to 10, and build back up to 15.

Ankle Pumps (To Reduce Swelling)

Elevate your foot higher than heart level. Move the ankle up and down 30 times. Rest a minute
and then repeat 4–5 times. Ice the ankle at the same time.
Towel Stretch (Achilles)

Assume a seated position, with legs extended. Place a towel around your foot and hold the
ends with both hands. Pull back on the towel, bringing your foot toward you.
Achilles Stretch
Stand, leaning onto a wall, with the involved foot placed further back than the other foot. Lunge
forward onto your uninjured foot while keeping the knee straight and the heel of involved leg on
the ground. Stretch is felt in calf. Stretches gastrocnemius muscle.
Bent-Knee Stretch
Same as for the Achilles stretch, but the involved leg is bent at the knee. Stretch is felt in the
calf. Stretches the soleus and other deep calf muscles.
Squats
With your feet shoulder-width apart and your heels remaining on ground, bend your knees until
stretch is felt in the calf and ankles. Do not let the knees pass in front of the toes.
Strengthening Exercises–Beginning Phase

15. When this is accomplished easily, reduce the repetitions to 3 sets of 10 and increase the
weight.
Towel Crunches
Assume a seated position. Place a towel on the floor (not on a carpet). Place the involved foot
on top of the towel and curl your toes, gathering the towel underneath and toward you. Repeat
10 times, advance to 3 sets of 10–15 repetitions, and then add weight to the towel. Begin again
with fewer repetitions, advancing to 3 sets of 10–15 repetitions.
Ankle Alphabet
Using involved ankle and foot only, trace the letters of the alphabet. Perform from A to Z.
Repeat 1–2 times per set. Do 1 set per session
Isometric Inversion/Eversion
Assume a seated position. Place the inside of your foot against an immovable object (eg, a
table leg) and push against it. Then repeat the same exercise with the outside of your foot
against the object. Hold the contraction for 6–8 sec and repeat 10 times.
Marble Pick-Up
Assume a seated position. Place several marbles on the floor and attempt to pick them up by
curling your toes around them. Once a marble is lifted, turn the foot and place the marble back
down on the floor a foot or so away. Repeat for total of 30 repetitions.
Weight Shifts
Stand with your feet a shoulder-width apart. Your hands are placed on a counter or table to
help support the weight of your body. Lean your body weight over to the affected ankle and
shift your weight back and forth between the 2 legs. Progress until full weight is placed on the
affected ankle. Hold for 10–30 sec; repeat 3–6 times.
Strengthening Exercises–Middle Phase

Single-Leg Balance (Eyes Open/Closed)
Assume a standing position, with feet a shoulder-width apart. Stand on the affected ankle, as
tolerated, working up to 30 sec with your eyes open. Progress to balancing for 30 sec with
your eyes closed. Repeat 3–5 times. Can be done 2–3 times per day. Have stance knee
slightly bent
Thera-Band Exercises
With the use of a Thera-Band, wrap one end of the band onto an immovable object and the
other end around the mid-foot. Avoid hip movement.
Ankle movement is toward you.
Ankle movement is toward the little toe side.
Ankle movement is toward the big toe side.
Start with 1 set of 10 repetitions, progressing to 3 sets of 10–15 repetitions. When you can
achieve this easily, advance the color of the Thera-Band and begin again with 3 sets of 10–15
repetitions.

Stand with your feet a shoulder-width apart. Raise your heels off the ground onto the balls of
your feet. Fingertips can be placed on a counter for light balance. You can progress to weight
machines, performing same action with increasing weight intensity.
Strengthening Exercises–Final Phase
Heel Raise (Single Leg)
Raise the heel of the affected ankle up and down. Fingertips can be placed on a counter for
light balance. You can progress to weight machines, performing the same actions with added
weight intensity.
Single Leg Stance with Clock Reach

Stand on leg, bending opposite leg as shown. Visualize a clock where 12:00 is in front of you.
With the right arm reach to 12:00. Then reach to 3:00, 6:00, and 9:00. Maintain balance
throughout the activity. Repeat sets standing on opposite leg and reaching with left arm,
Perform 1 set of 5 min, once a day. Hold exercise for 30 sec.
Hopping (Front, Back, Side to Side)

affected ankle only. Work on soft landing and good shock absorption.

Start with walk/jog/walk pattern and gradually increase force. Start easy jogging in straight
lines first. Progress speed and distances gradually.

Shin Splints (Medial Tibial Stress Syndrome)
What are Shin Splints?
The term shin splints has been a “wastebasket” term used to describe pain about the lower
leg. More recently, it has been used to identify pain occurring about the front or medial side of
the lower leg. The term medial tibial stress syndrome, or MTSS, is now being used frequently.
The condition itself may be an inflammation of either muscle or bone involving the tibia or
shinbone. The involved muscles include the posterior tibialis, flexor hallucis longus, and flexor
digitorum longus. Your physician must differentiate this condition from stress fractures or
compartment syndromes.
Common Causes
Overuse, especially at the start of sport seasons, from excessive running or jumping
Pronated feet (an inward turning of the foot, which causes stretching of the involved muscles)
Fallen arches
Types of training surfaces (softer ground may allow for increased foot pronation)
Shoes with broken-down medial borders
Running on slanted surfaces along roads
Weakness in the involved muscle groups
Signs and Symptoms
Pain can be felt when touching the area just behind the shinbone from above the medial ankle
bone and extending upward by more than half way. Pain can be produced with walking and/or
running.
Treatment
Initially, rest and ice 2–3 time per day for 15–20 min is helpful. Icing is beneficial
as long as the inflammatory condition continues. Ice can be applied after activity
and/or rehabilitation to help decrease pain and muscle spasm. Anti-inflammatory
medications are used to help decrease pain and swelling. Crutches may need to
be used if walking causes pain. Training can continue in the pool or by cycling as
long as no pain is felt. Orthotics (a shoe inset used to help correct foot
malalignments) may be prescribed if pronation cannot be corrected with
strengthening. Supportive taping of the lower leg is of benefit. Physical therapy
may be prescribed by your physician to help with application of modalities (US
and/or electrical stimulation), gait analysis, evaluation of weak or tight muscles,
and overall exercise progression in moderate to severe cases.
Stretching
Strenghtening
Do 2–3 sets of 10–15 repetitions 2–4 times a week. When you can complete 3 sets of 15

Guidelines: Stretch 3–6 times, holding for 30 sec.
Achilles Stretch
Stand, leaning onto a wall, with involved foot placed further back than the other foot. Lunge
forward onto the uninjured foot while keeping the knee straight and the heel of the involved leg
on the ground. Stretch is felt in calf. Stretches the gastrocnemius muscle.
Bent-Knee Stretch
Same as for the Achilles stretch, but the involved leg is bent at the knee. Stretch is felt in the
calf. Stretches the soleus and deep flexor muscles.
Pointed-Toe Stretch
While seated, with the involved leg bent into a figure 4 position, grasp the top of the foot and
stretch the foot downward into a pointed position. Stretch is felt in the top of the foot.
Guidelines: Start with 3 sets of 10, if able (fewer, if unable); progress to 3 sets of 15
repetitions. When this is accomplished easily, reduce the repetitions to 3 sets of 10 and
increase the weight.
Towel Crunches
Assume a seated position. Place a towel on the floor (not on a carpet). Place your foot on top
of the towel and curl your toes, gathering the towel underneath and toward you.
Marble Pick-Up
Assume a seated position. Place several marbles on the floor and attempt to pick up them up
by curling your toes around them. Once a marble is lifted, turn your foot and place back down
on the floor a foot or so away. Repeat for a total of 30 repetitions.
Heel Walking
Walk on your heels, starting with short distances, such as 10–15 feet, progressing to 50 feet.
With the use of Thera-Band, wrap one end of the band onto an immovable object and the other
end around your mid-foot. Avoid hip movement.

Start with 1 set of 10 repetitions, progressing to 3 sets of 10–15 repetitions. Once you can
achieve this, advance the color of the Thera-Band and begin again toward 3 sets of 10–15
repetitions.

Stand with your feet shoulder-width apart. Raise your heels off the ground and roll your weight
onto the balls of your feet. Fingertips can be placed on a counter for light balance. You can
progress to weight machines, performing same action, with increasing weight intensity.
light balance. You can progress to weight machines, performing the same actions for added
weight intensity.

movements. Further progression is achieved by hopping in same patterns with the affected
ankle only.
Start with walk/jog/walk pattern. Start easy jogging in straight lines first. Progress speed and
distances gradually.

Plantar Fasciitis (Heel Spur Syndrome)

What is Plantar Fasciitis?
The plantar fascia is a broad band of connective tissue that runs from the calcaneus (heel
bone) to the heads of the metatarsal bones in the foot. Its purpose is to provide arch support.
This tissue can become inflamed, causing pain to this area.
Common Causes
Tight Achilles tendon
Overuse, especially at the start of sport seasons, from excessive running or jumping
Pronated feet (an inward turning of the foot, which causes stretching of the involved muscles
Fallen arches
Types of training surfaces (softer ground may allow for increased foot pronation)
Shoes with broken-down medial borders
Weakness in the involved muscle groups
Signs and Symptoms

Pain is primarily located along the front part of the heel where the connective tissue becomes
narrow. Touching this area may produce pain, and it could extend along the tissue into the arch.
Upon awakening, the 1st steps may be very painful to perform due to the stretch being placed
on the tissue. Extending the toes upward also causes pain in this area.
Treatment
Initially, rest, medication, and ice 2–3 times per day for 15–20 min are helpful.
Icing is beneficial as long as the inflammatory condition continues. Ice massage
to this area is very beneficial. It can be applied after activity and/or rehabilitation
to help decrease pain. Anti-inflammatory medications are used to help decrease
pain and swelling. Sometimes, cortisone injections are administered. Stretching
and strengthening exercises, used to promote range of motion and strength, are
initiated when pain is decreased. Taping the arch is helpful. Proper footwear is a
necessity, and the use of orthotics (a shoe insert used to correct foot
malalignments) may be necessary. Physical therapy may be prescribed by your
physician to help with evaluation of weakened and/or tight muscles, gait analysis,
application of modalities in moderate to severe cases (US, soft tissue massage,
and electrical stimulation), and overall progression of exercises.
Stretching
Strengthening

difficulties, refer back to your physician.
Achilles Stretch
Stand, leaning onto a wall with the involved foot placed further back than the other foot. Lunge
forward onto the good foot while keeping the knee straight and the heel of the involved leg on
the ground. Stretch is felt in the calf.
Bent-Knee Stretch
Same as for Achilles stretch, but the involved leg is bent at the knee. Stretch is felt in the calf.
Pointed-Toe Stretch
While seated, with the involved leg bent into a figure 4 position, grasp the top of the foot and
stretch the foot downward into a pointed position. Stretch is felt in the top of the foot
15. Once this is accomplished easily, reduce the repetitions to 3 sets of 10 and increase the
weight intensity.
Towel Crunches
Assume a seated position. Place a towel on the floor (not on a carpet). Place your foot on top
of the towel and curl your toes, gathering the towel underneath and toward you.
Marble Pick-Up
Assume a seated position. Place several marbles on the floor and attempt to pick them up by
curling your toes around them. Once a marble is lifted, turn your foot and place the marble back
down on the floor a foot or so away. Repeat for total of 30 repetitions.
With the use of Thera-Band, wrap one end of the band onto an immovable object and the other
end around your mid-foot. Avoid hip movement.

Start with 1 set of 10 repetitions, progressing to 3 sets of 10–15. Once you can achieve this,
advance the color of the Thera-Band and begin again toward 3 sets of 10–15 repetitions.

Stand with your feet shoulder-width apart. Raise your heels off the ground and roll your weight
onto the balls of your feet. Fingertips can be placed on a counter for light balance. You can
progress to weight machines, performing same action with increasing weight intensity.
light balance. You can progress to weight machines, performing same actions for added weight
intensity.

movements. Further progression is achieved by hopping in same patterns with the affected
ankle only.
Start with walk/jog/walk pattern. Start easy jogging in straight lines first. Progress speed and
distances gradually.

Jog slowly, making a pattern of large figure 8s, and then progress to smaller and smaller
patterns with increasing speed. Jog in zig-zag patterns with large cuts first and then progress
to sharper cuts with increasing speed.
Rotator Cuff Tendinitis

What is Rotator Cuff Tendinitis?
The rotator cuff is comprised of a group of 4 muscles that surround the front, top, and back of
the shoulder. The purpose of these muscles is to rotate the shoulder inward or outward. During
elevation of the shoulder, these muscles help to keep the major shoulder bone, the humerus, in
the socket. Directly above the superior rotator cuff muscle is a sac called a bursa, which
contains a fluid substance, used to decrease friction
between this muscle and the end of the collarbone. Rotator cuff tendinitis is an inflammation of
the tendons, which occurs most commonly to the superior tendon, called the supraspinous. An
inflammation of the bursa (bursitis) can occur as well.
Common Causes
The following are common causes of tendinitis:
Overuse (excessive overhead activities)
Weakness or fatigue of the rotator cuff muscles
Improper mechanics (throwing, swimming, serving)
Lack of flexibility
Poor posture, usually consisting of rounded shoulders
Signs and Symptoms

Pain or aching about the front and side of the shoulder. The pain can extend down the outside
of the shoulder midway to the elbow. Pain usually increases as one elevates the shoulder into
overhead positions.
Treatment
Icing is beneficial as long as the inflammatory condition continues. It can be
applied after activity and/or rehabilitation to help decrease pain and muscle
spasm. Anti-inflammatory medications are used to help decrease pain and
swelling. Sometimes, cortisone injections are administered. Stretching and
strengthening exercises, used to promote range of motion and strength, are then
initiated when pain is decreased. For moderate to severe cases, your physician
may prescribe physical therapy for modalities (US, iontophoresis, soft tissue
massage, electrical stimulation), evaluation of weak/tight muscles, posture
analysis, and exercise progression.
Stretching
Repeat 2–3 times per day.
Strengthening

Posterior Capsule Stretch

Pull the involved arm across your chest, positioning your hand under the opposite shoulder.
Towel Stretch (Internal Rotation)

This is performed with a towel. Place the uninvolved hand behind your head and the involved
hand behind your back while grasping a towel with both hands. Gently pull the towel up toward
the ceiling.
Shoulder External Rotation

Lie on back with elbows bent to 90 degrees, holding stick in front of you. Using a stick for
assistance, rotate your _____ hand and forearm out away from your body. Do not allow your
upper arm to move away from your body. Hold 10 sec. Do 10 repetitions, 1–3 times per day.
Flexion Stretch
While on your back, clasp your hands together, straighten your elbows, and raise your arms up
and over your head.
Wand Stretch
Lie on back holding wand. Raise arm over head. Hold 10 sec. Repeat 10 times per set. Do 1
set per session. Do 1–3 sessions per day.
Extension Stretch
When standing, clasp your hands behind your back and gently raise your arms up toward the
ceiling.
Pectoralis Stretch
Standing in a corner or in a doorway, raise your elbows to shoulder level while supporting your
forearms on the doorframe or wall. Place 1 leg in front of the other and gently lunge forward by
bending the forward knee. Keep your back straight during the stretch.
increase the weight intensity. Use slow controlled movements.
External Rotation
Lie on the uninvolved side, with involved elbow flexed and held against the side of the body.
Bring your hand up toward the ceiling. Hand should only raise a little above the horizontal. Add
hand weights to progress the exercise.
Empty Can
While standing, with your arm extended and the thumb pointed down toward the floor, bring
your arm up to 90 degrees or below the pain level. The arm is positioned at a 30-degree angle
from the side of the body. Progress up to a 5-lb limit with this exercise. Make sure your hand
does not go higher than your shoulder.
Shoulder Flexion
While standing, raise the involved hand, with the elbow straight toward the ceiling, to shoulder
level. Your thumb should be pointed toward the ceiling.
Shoulder Abduction
While standing, raise the involved hand, with the elbow straight out away from the body, to just
below shoulder level.
Single Row
Lean forward, bending from the trunk, and support your body with the uninvolved hand on a
surface (desk, table). Pull the arm up by bending the elbow toward the ceiling until motion is
stopped.
Isometric External Rotation

Using wall to provide resistance and keeping art at side, press back of hand into pillow using
light to moderate pressure. Hold 1–3 sec. Repeat 15–20 times per set. Do 1 set per session.
Do 1–2 sessions per day.
Isometric Internal Rotation
Using door frame for resistance, press palm of hand into pillow with mild-moderate pressure.
Keep elbows at side. Hold 1–3 sec. Repeat 15–20 times per set. Do 1 set per session. Do 1–2
sessions per day.
Epicondylitis
What is Epicondylitis?
Epicondylitis is an inflammatory condition involving the tendons and muscles where they
originate along the inside and outside of the elbow. Tennis elbow is a term commonly referred
to when the condition occurs on the outside or lateral aspect of the elbow. Lateral epicondylitis
occurs more frequently than medial epicondylitis.
Common Causes
Activities that involve forceful and/or continuous wrist motions or a large amount of stabilization
applied by the wrist such as playing racquet sports, swimming, swinging a golf club, throwing,
playing tennis, using a computer keyboard, or playing piano.
Signs and Symptoms

Pain and tenderness along either the inside or the outside of the elbow, extending into the
same side of the forearm.
Difficulty gripping without pain; decreased wrist strength
Tightness/stiffness when stretching elbow and wrist
Treatment
Icing is beneficial as long as the inflammatory condition continues. Ice can be
applied after activity and/or rehabilitation to help decrease pain and muscle
spasm. Anti-inflammatory medications are used to help decrease pain and
swelling. Sometimes, cortisone injections are administered. Stretching and
strengthening exercises, used to promote range of motion and strength, are
initiated when pain is decreased. A brace worn just below the elbow joint also can
be helpful. Your physician may prescribe physical therapy for modalities (US,
iontophoresis, soft tissue massage, electrical stimulation), evaluation of weak or
tight muscles, posture analysis, and exercise progression.
Stretching

Strengthening

Wrist Flexion Stretch

Bend the involved wrist down gently by grasping it with the other hand until a pulling sensation is
felt. Keep your elbow straight.
Wrist Flexion Stretch (Advanced)

Same as for the wrist flexion stretch, but with the addition of wrist movement toward the side of
the little finger.
Wrist Extension Stretch

Bend the involved wrist up gently by grasping it with the opposite hand until a pulling sensation
is felt. Keep your elbow straight.
Pronator Teres Stretch
Bend elbow and grasp fingers with opposite hand. Bend wrist backward, keeping fingers
straight. Mild stretch. Slowly straighten arm while keeping fingers straight. Next, pull fingers
inward and cold. Perform 1 set of 10 repetitions, twice a day.
Do exercises as described unless they cause increased pain during or after the exercise lasting
longer than 10–15 min. Use heat for stiffness/ache and ice for pain or swelling for at least 10
min but not longer than 20 min.
Triceps Stretch
Begin with arm at side. Bend elbow if involved arm. With other arm slowly list arm overhead,
keeping elbow bent. Relax and repeat. Perform 1 set of 10 repetitions, twice a day. Hold
exercise for 5 sec.
Do exercises as described unless they cause increased pain during or after the exercise lasting
longer than 10–15 min. Use heat for stiffness/ache and ice for pain or swelling for at least 10
min but not longer than 20 min.
increase the weight intensity.
Wrist Extension Curls

With your forearm supported by your leg or a table and your palm facing downward, lift and
lower the weight.
Wrist Flexion Curls

With your forearm supported by your leg or a table and your palm facing upward, lift and lower
the weight.
Forearm Pronation/Supination
With your forearm supported by your leg or a table, turn your palm up and then down while
holding onto a weight.
Neutral Gripping
With forearm resting on surface, gently squeeze towel. Repeat 15–20 times per set. Do 1 set
per session. Do 12 sessions per day.
Gripping
To start, gently grip a rubber ball, a towel, or putty and then advance to items with more
resistance. Perform 10–30 repetitions, increasing in intensity once you are able to perform 30
repetitions.
Finger Extension
Wrap a rubber band around the outside of all your fingers and thumb, gently extend the hand by
opening the fingers, and then close the fingers. Perform 10–30 repetitions.
Appendix C: Joint and Soft Tissue Injection

Kalli Sanchez
Anna P. Quan
Introduction
Joint and soft tissue injections are valuable tools in the treatment of common musculoskeletal
conditions. When other modalities fail, such as NSAIDs, activity modification, splinting, ice, heat,
and physical therapy, corticosteroid injections can be used to provide temporary pain relief.
Indications
Diagnostic:
Local anesthetic provides pain relief to allow a more thorough physical exam
(eg, rule out rotator cuff tear versus weakness secondary to pain)
Exam of fluids for the diagnosis of gout/pseudogout (crystal analysis), septic
arthritis (elevated WBC and/or positive gram stain and culture), or trauma
(hemarthrosis)
Therapeutic:
Decrease pain
Increase range of motion
Improve quality of life
Conditions:
Crystalline arthropathies
Osteoarthritis
Inflammatory arthritis
Bursitis
Tendonitis
Ganglion cysts
Trigger points
Nerve entrapments
Fasciitis
Contraindications
Absolute:
Infection (overlying cellulitis)
Lack of informed consent
Allergy to injection medications or history of steroid flare
Injection into weight bearing tendons such as Achilles and patella due to high risk of rupture
Relative:
Brittle or out of control diabetes
Coagulopathy (safe in patients with INR <3.5)
Previous joint replacement
History of avascular necrosis
Supplies
Nonsterile gloves
Syringe: 3–5 cc, larger for aspiration (10, 20, 60 cc)
Needle:
20 g for drawing up fluid
18 g for aspiration
Depending on site of injection: 22 g 1.5-in, 25 g 1.5-in, 25 g 5/8- or 1-in 22-gauge 3.5-in
spinal needles occasionally for trochanteric bursa injection
Betadine swabs
Alcohol swabs
Gauze
Band-Aids
Topical vapocoolant spray such as ethyl chloride
Hemostat clamp
Topical Anesthetic
Topical anesthetic can be used to aid in diagnosis or for temporary pain relief.
The choice of anesthetic depends on formulary availability and desired duration of action.
In general, lidocaine has a quick onset of 3–5 min with 1–2 hrs duration, and bupivacaine has
a 15–20 min onset with 3–4 hrs duration.
Bupivacaine or lidocaine with epinephrine can be used in certain areas for possible prolonged
benefit of the injection but should not be used when injecting digits or smaller joints.
Corticosteroid
Decrease inflammation resulting in decreased pain and swelling
Lower soluble steroids have longer duration of action
To avoid suppression of hypothalamic-pituitary-adrenal axis, limit to 3–4 injections per year
Table 1 Properties of Injectable Corticosteroids
Relative Antiinflammatory Biological

Corticosteroid Solubility
Potency Half-life
Hydrocortisone 1 High 8–12 hr
12–36
Triamcinolone (Kenalog) 5 Intermediate
hr
Methylprednisolone (Depo– 12–36

5 Intermediate
Medrol) hr
Betamethasone (Celestone 26–54

20–30 Low
Soluspan) hr
Dexamethasone (Decadron LA) 20–30 Low 26–54
From McNabb, James W. A Practical Guide to Joint and Soft Tissue Injection and
Aspiration. 1st ed. Philadelphia: Lippincott Williams & Wilkins, 2005.
Table 2 Equivalent Dosages of Injectable Corticosteroids
Corticosteroid Preparation Equivalent Dose/Volume
Kenalog 40 mg/mL
Depo-Medrol 40 mg/mL
Celestone Soluspan 6 mg/mL
Decadron LA 4 mg/mL
From McNabb, James W. A Practical Guide to Joint and Soft Tissue Injection and
Aspiration. 1st ed. Philadelphia: Lippincott Williams & Wilkins, 2005.
Viscosupplementation
Sodium hyaluronate is a glycosaminoglycan found in normal joint fluid.
In osteoarthritis, the concentration of sodium hyaluronate is lower.
Synthetic formulations of sodium hyaluronate are derived from rooster combes.
Available products:
Hyalgan (Sanofi-Synthelabo)—5 weekly
Supartz (Smith and Nephew)—5 weekly
Synvisc (Genzyme)—3 weekly
Lack of good evidence showing efficacy
Used for patients failing conservative therapy or when corticosteroids are contraindicated
Contraindicated in patients with allergies to avian proteins or eggs
Technique
The specific techniques for each joint will be discussed in each joint section.
In general, the following techniques should be followed.
Identify the anatomic landmarks and mark the entry site with the cap of the needle.
Cleanse the area with Betadine and alcohol.
Spray ethyl chloride if available to anesthetize the skin for needle entry.
Insert the needle to the proper depth for the particular injection.
Inject the steroid/analgesic mixture. There should be free flow (without resistance) of the
medication.
Remove the needle and apply pressure with gauze.
Apply a Band-Aid.
Complications
Major risks of corticosteroid injections include bleeding, infection, tendon
rupture, steroid flare, fat pad or soft tissue atrophy, and skin depigmentation.
Steroid flare (crystal synovitis) is treated with rest, ice, NSAIDs and usually
resolves spontaneously after 24–36 hrs.
The estimated risk of causing septic arthritis is rare, on the order of 0.01%.
Aftercare
While the anesthetic is in effect, the patient will not feel an injury to the joint; therefore, it is
recommended to rest the injected joint for several hours.
The patient is educated to monitor for signs or symptoms of infection including fever,
erythema, warmth, or increasing pain.
Ice is an effective modality for pain control following an injection.
Activities can generally be resumed after 3–5 days when the cortisone has had a chance to
take effect.
Informed Consent
Every invasive procedure (including joint aspirations or injections) should include a detailed
informed consent.
Lawsuits have occurred over complications to joint injections and, in these situations, having
an informed consent signed and kept with the patient's medical record is of utmost
importance.
The informed consent includes documentation that the patient is competent to make
decisions, and that a discussion of the risks and benefits of a corticosteroid injection have
been reviewed.
Billing/Coding
Current Procedural Terminology (CPT) 2009 Codes should be used to accurately assign the
proper codes for the procedures performed.
ICD9 codes and CPT codes will be listed with each joint or soft tissue injection discussed.
Bibliography
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Wilkins, 2009.
Blair B, Rokito AS, Cuomo F, et al. Efficacy of injections of corticosteroids for subacromial
impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685–1689.
Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane
Database Syst Rev. 2003;(1): CD004016.
Cardone DA, Tallia AF. Diagnostic and therapeutic injection of the elbow region. Am Fam
Physician. 2002;66(11):2097–2100.
Cardone D, Tallia A. Joint and soft tissue injection. Am Fam Physician 2002;66:283–288,
290.
Cardone D, Tallia A. Diagnostic and therapeutic injection of the hip and knee. Am Fam
Physician. 2003;67:2147–2152.
Esenyel C, Demirhan M, et al. Comparison of four different intra-articular injection sites in the
knee: a cadaver study. Knee Surg Sports Trauma Arthrosc. 2007;15(5):573–577.
Griffin, Letha Yurko, ed. Essentials of Musculoskeletal Care, 3rd ed. American Academy of
Orthopaedic Surgeons, 2005.
http://www.orthogastonia.com
Jackson DW, Evans N, Thomas B. Accuracy of needle placement into the intra-articular
space of the knee. J Bone Joint Surgery Am. 2002;84:1522–1527.
Kang MN, Rizio L, Prybicien M, et al. The accuracy of subacromial corticosteroid injections: a
comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(1 Suppl):61S–66S.
Lievense A, Bierma-Zeinstra S, Schouten B, et al. Prognosis of trochanteric pain in primary
care. Br J Gen Pract. 2005;55(512):199–204.
Luc M, Pham T, Chagnaud C, et al. Placement of intra-articular injection verified by the
backflow technique. Osteoarthritis Cartilage. 2006;14(7):714–716.
McNabb JW. A Practical Guide to Joint and Soft Tissue Injection and Aspiration.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Safran MR, McKeag DB, Van Camp SP. Manual of Sports Medicine. Philadelphia: Lippincott-
Raven Publishers; 1998.
Saunders S. Injection Techniques in Orthopaedic and Sports Medicine, 2nd ed. Philadelphia:
WB Saunders; 2002.
Shbeeb MI, O'Duffy JD, Michet CJ, et al. Evaluation of glucocorticosteroid injection for the
treatment of trochanteric bursitis. J Rheumatol. 1996;23(12):2104–2106.
Smidt N, vad der Windt DA, Assendelft WJ, et al. Corticosteroid injections, physiotherapy, or
a wait-and-see policy for lateral epicondylitis: a randomized controlled trial. Lancet.
2002;359(9307):657–662.
Stephens, Mark B. Beutler, Anthony I. O'Connor. Musculoskeletal Injections: A Review of the
Evidence. Am Fam Physician. 2008;78(8):971–976.
Tallia A, Cardone D. Diagnostic and therapeutic injection of the wrist and hand region. Am
Fam Physician. 2003;67:745–750.
Tallia AF, Cardone DA. Diagnostic and therapeutic injection of the shoulder region. Am Fam
Physician. 2003;67(6):1271–1278.
Tallia A, Cardone D. Diagnostic and therapeutic injection of the ankle and foot. Am Fam
Physician. 2003;68:1356–1362.
Zuber T. Knee joint aspiration and injection. Am Fam Physician. 2002;66:1497–1500, 1503–
1504, 1507, 1511–1512.
Credits: Images from Griffin, Letha Yurko, ed. Essentials of Musculoskeletal Care 3rd Edition.
American Academy of Orthopaedic Surgeons, 2005. McNabb, James W. A Practical Guide to
Joint and Soft Tissue Injection and Aspiration. 1st ed. Philadelphia: Lippincott Williams &
Wilkins, 2005. Agur AM, Dalley AF. Grants Atlas of Anatomy, 12th ed. Philadelphia: Lippincott
Williams & Wilkins, 2009.
Trigger Point Injection

Indications
Trigger points occur due to focal areas of muscular ischemia, spasm, and
inflammation, usually involving the back muscles.
There is no evidence indicated injections are beneficial but some patients
respond to injections.
ICD-9 307.81 Tension headache
ICD-9 720.1 Spinal enthesopathy
ICD-9 723.1 Cervicalgia
ICD-9 729.0 Rheumatism unspecified and fibrositis
ICD-9 729.1 Fibromyalgia/fibromyositis and myalgia
ICD-9 729.2 Neuralgia, neuritis, and radiculitis
Anatomy
The anatomy depends on the location of the trigger point injection.
The injection is performed over the tender nodule, which is usually in the muscles surrounding
the scapula.
Supplies
Gloves
Betadine and alcohol swabs
3-mL syringe with 25-gauge 5/8–1-in needle
1 mL 1% lidocaine
1 mL (20 mg) Kenalog or equivalent (optional)
Ethyl chloride
Gauze
Band-Aid
Technique
Palpate the tender nodule and mark with needle cap.
Cleanse the skin with Betadine and alcohol.
Apply ethyl chloride until skin turns white.
Injection site is directly into the nodule
A fanning technique can be used to disperse the fluid in various directions, which can be
helpful in large nodules.
Remove needle and apply pressure with gauze, gently massaging material.
Apply Band-Aid
Aftercare
Instruct patient that the area may be numb for several hours after the procedure and that
pain may be present for several days.
Instruct patient that the cortisone usually takes effect within 72 hrs.
Instruct patient to return to your office if they develop redness, swelling, or increased pain at
the injection site.
CPT Code
20552 Injection(s) of trigger point(s) in 1–2 muscle groups
20553 Injection(s) of trigger point(s) in 3 or more muscle groups
Subacromial Injection
Indications
Subacromial injections are useful for diagnostic and therapeutic purposes.
Any condition along the spectrum of rotator cuff diseases that cause
subacromial bursitis may respond to corticosteroid injection.
Injections are indicated once conservative therapy (activity modification,
NSAIDS, physical therapy) has failed; however, in some cases, an injection
given prior to PT can allow patients to perform their therapy better and with less
pain.
Subacromial corticosteroid injection provides short-term pain relief that is
greater than placebo and at least equal to NSAID therapy – Evidence rating B
ICD-9:
726.10 Rotator cuff syndrome NOS
727.61 Nontraumatic complete rupture of rotator cuff
840.4 Rotator cuff sprain
Anatomy
The subacromial space is bordered superiorly by the coracoacromial ligament stretching
between the coracoid process and acromion.
The contents of the subacromial space include the subacromial bursa, supraspinatus tendon,
and tendon of the long head of the biceps.
Supplies
Gloves
5-mL syringe with 22- or 25-gauge 1½-in needle
4-mL anesthetic (can combine 2 mL 1% lidocaine and 2 mL 0.25% Marcaine)
1 mL (40 mg) Kenalog or equivalent
Ethyl chloride
Gauze
Band-Aid
Technique
There are 3 approaches to the subacromial injection: Anterior, lateral, and posterolateral.
Given the increased risk of pneumothorax with the anterior approach, we do not recommend
this approach.
Determine which approach you will use and mark the area with the needle cap.
Lateral approach: The lateral edge of the acromion is palpated.
Apply ethyl chloride until the skin turns white.
The needle is inserted at the midpoint of the acromion and angled slightly upwards under the
acromion to full length (up to hub of needle).
Posterolateral approach: The distal, lateral, and posterior edges of the acromion are
palpated and the soft spot 1 cm below the posterolateral corner is marked.
Cleanse the skin with Betadine and alcohol
The needle is inserted 1 cm inferior to the posterolateral edge of the acromion. The needle
is directed toward the opposite nipple (coracoid).
Never inject under pressure—steroid injected directly into a tendon may cause tendon
rupture.
Remove needle and apply pressure with gauze.
Apply Band-Aid.
Have patient perform Codman exercises or arm swings to disperse the fluid through the
bursa.
Aftercare
Instruct patient that the shoulder may be numb for several hours after the procedure and that
Instruct patient that the cortisone usually takes effect within 72 hr.
After 5–7 days, the patient can resume his regular activity and you should recommend
starting ROM and rotator cuff strengthening exercises.
the injection site.
CPT Code
20610 Arthrocentesis, aspiration and/or injection; major joint or bursa (eg, shoulder, hip, knee
joint, subacromial bursa)
Glenohumeral Joint Injection

Indications
Glenohumeral injections are useful for patients with shoulder pain secondary to
osteoarthritis or rheumatoid arthritis.
Glenohumeral injections can aid in improving range of motion with physical
therapy for patients with adhesive capsulitis or frozen shoulder.
NSAIDS, physical therapy) has failed.
ICD-9:
714.0 Rheumatoid arthritis
715.11 Primary osteoarthritis, shoulder
715.21 Secondary osteoarthritis, shoulder (rotator cuff arthropathy)
726.0 Shoulder adhesive capsulitis
Anatomy
The glenohumeral joint is a ball and socket joint composed of the clavicle, scapula, and
humerus.
The glenoid cavity is very shallow but contains a lip of fibrous tissue called the glenoid
labrum, which deepens the glenoid and increases shoulder joint stability.
Supplies
Gloves
3-mL syringe with 22- or 25-gauge 1½-in needle
1–2 mL anesthetic
Ethyl chloride
Gauze
Band-Aid
Technique
The glenohumeral joint can be approached from the anterior or posterior direction.
The posterior approach is preferable since both subacromial and glenohumeral injections can
be done through one needle stick.
Posterior Approach: The distal, lateral, and posterior edges of the acromion are palpated,
and the soft spot 1 cm below the posterolateral corner is marked with the needle cap,
If available, have an assistant distract (pull down) and externally rotate the arm.
The needle is inserted just inferior to the posterolateral edge of the acromion. The needle
is directed anteriorly and may need to be walked into the joint.
Anterior Approach: The head of the humerus is palpated and the joint space determined and
marked with the needle cap.
The needle should be placed just medial to the head of the humerus and 1 cm lateral to the
coracoid process. The needle is directed posteriorly and slightly superiorly and laterally. If
the needle hits against bone, it should be pulled back and redirected at a slightly different
angle.
rupture.
Apply Band-Aid.
Have patient perform Codman exercises or arm swings to disperse the fluid through the
glenohumeral joint.
Aftercare
After 5–7 days, the patient can resume his regular activity,
the injection site.
CPT Code
20610 Arthrocentesis, aspiration and/or injection; major joint or bursa (eg, shoulder, hip, knee
joint, subacromial bursa)
Acromioclavicular Joint Injection

Indications
AC joint injections are indicated for patients with shoulder pain due to pathology
of the AC joint.
NSAIDS) has failed.
ICD-9:
719.41 AC joint pain
716.91 AC joint arthritis
715.91 AC joint osteoarthrosis
Anatomy
The AC joint can be palpated as a narrow indentation at the distal end of the clavicle, about
one thumb's width medial to the lateral edge of the acromion.
The joint line runs obliquely medially at approximately a 20-degree angle.
Supplies
Gloves
0.5 mL 1% lidocaine
0.5 mL (20 mg) Kenalog or equivalent
Ethyl chloride
Gauze
Band-Aid
Technique
Palpate the depression of the AC joint at the distal clavicle and mark it with the needle cap.
Insert the needle at a 15–20-degree angle (needle pointed more medially).
Viewing the x-rays prior to injection can help determine the exact angle of the AC joint.
Inject the fluid into the joint.
Apply Band-Aid.
Aftercare
the injection site.
Avoid repetitive or heavy overhead lifting.
CPT Code
20600 Arthrocentesis, aspiration and/or injection; small joint or bursa
Elbow Joint Injection

Indications
Elbow injections are useful for the treatment of elbow pain due to arthritis either
from trauma, osteoarthritis, or rheumatoid arthritis.
ICD-9:
729.5 Elbow pain
716.92 Elbow arthritis
Anatomy
The elbow joint is composed of the ulnohumeral, radiocapitellar, and proximal radioulnar
joints.
The elbow joint can be approached via the triangle formed by the lateral olecranon, head of
the radius, and lateral epicondyle.
Supplies
Gloves
3-mL syringe with 25-gauge 1-in needle
10–20 mL syringe with 20- or 22-gauge needle if aspirating
1 mL 1% lidocaine without epinephrine
Ethyl chloride
Gauze
Band-Aid
Technique
Place the patient's arm on the table at a 45-degree angle.
Mark the soft depression in the center of the triangle formed by the lateral olecranon, head of
the radius, and lateral epicondyle with the needle cap.
The needle is inserted into the elbow joint between the lateral epicondyle and the radial head.
If aspirating, remove as much fluid as possible then stabilize the needle in the joint, twist off
the 10-mL syringe, and place the 3-mL syringe containing cortisone mixture on the needle.
Apply Band-Aid.
Instruct the patient to perform flexion/extension range of motion exercises to disperse the
fluid within the joint.
Aftercare
Instruct patient that the elbow may be numb for several hours after the procedure and that
After 3–5 days, the patient can resume his regular activity.
the injection site.
CPT Code
20605 Arthrocentesis, aspiration and/or injection; intermediate joint or bursa
Epicondylitis Injection
Indications
Epicondylitis injections are indicated for the treatment of lateral (tennis elbow)
or medial (golfer's elbow) epicondylitis.
Lateral epicondylitis injections are very common in primary care.
P.
Corticosteroid injection reduces short-term (<6 wks) symptoms from lateral
epicondylitis, but physical therapy is superior to steroid injection after six weeks
– Evidence rating A
ICD-9:
726.32 Lateral epicondylitis
Anatomy
The origin of the common extensor tendon is at the lateral epicondyle.
The origin of the common flexor tendon is at the medial epicondyle.
The epicondyles are very superficial, which increases the risk of skin depigmentation and
atrophy with cortisone injections.
Supplies
Gloves
3-mL syringe with 25-gauge 5/8- or 1-in needle
0.5 mL 1% lidocaine without epinephrine

Ethyl chloride
Gauze
Band-Aid
Technique
Lateral Epicondyle: Place the patient's arm on the table at a 45-degree angle with the lateral
elbow facing up:
Palpate the area of most tenderness over the epicondyle and mark this with the cap of the
needle.
The needle is inserted down to the bone of the lateral epicondyle.
Inject the fluid into the area. If there is resistance of flow, then back the needle slightly out
so the hub of the needle is not against bone and then inject.
Take care not to inject cortisone while withdrawing the needle, as this superficial tracking
of cortisone can increase the risk of skin atrophy and depigmentation.
Apply Band-Aid
Medial epicondyle: Place the patient's arm on the table at a 45-degree angle with the medial
elbow facing up:
Palpate the area of most tenderness over the epicondyle and mark this with the cap of the
needle.
The needle is inserted down to the bone of the medial epicondyle.
Take care not to inject the ulnar nerve as it traverses posterior to the medial epicondyle in
the cubital tunnel. If the patient experiences pain or numbness in the ulnar nerve distribution
while the needle is inserted, then back out and reposition the needle more anteriorly before
injecting cortisone.
Inject the fluid into the area. If there is resistance of flow, then back the needle slightly out
so the hub of the needle is not against bone and then inject.
Take care not to inject cortisone while withdrawing the needle, as this superficial tracking
of cortisone can increase the risk of skin atrophy and depig-mentation
Apply Band-Aid.
Aftercare
Instruct patient that the elbow may be numb for several hours after the procedure and that
In addition, anesthetic spreading from the injection posteriorly may affect the ulnar nerve, and
transient ring and pinky finger numbness may occur.
NSAIDS and ice can be used to control postprocedure pain.
Consider an elbow extension splint to rest the elbow and/or wrist splint to avoid wrist
flexion/extension for 1–2 wks to allow the injection to take effect.
The patient should avoid repetitive wrist extension or flexion.
the injection site.
CPT Code
20551 Injection(s) of single tendon origin or insertion
Wrist Injection
Indications
Wrist injections are useful for the treatment of wrist pain due to arthritis either
from trauma, osteoarthritis, or rheumatoid arthritis.
ICD-9:
719.43 Wrist pain
716.94 Wrist arthritis
715.94 Wrist osteoarthrosis
Anatomy
The wrist joint capsule is not continuous but has septa, which makes the wrist injection
sometimes difficult.
The radiocarpal joint can be palpated just distal to the distal radius in a depression near the
scapholunate articulation.
Supplies
Gloves
10–20 mL syringe with 20- or 22-gauge 5/8- or 1-in needle for aspiration
½ mL 1% lidocaine without epinephrine
½ mL (20 mg) Kenalog or equivalent
Ethyl chloride
Gauze
Band-Aid
Technique
Palpate the depression distal to the distal radius near the scapholunate articulation.
Mark this area with the cap of the needle.
The needle is inserted into the wrist joint.
If aspirating, withdraw fluid with 10–20 mL syringe, then stabilize needle and exchange 3-mL
syringe containing steroid mixture and inject
If injecting, use 3-mL syringe with 25-gauge 1-in needle and inject fluid into joint.
The fluid should flow easily without resistance. If there is resistance, reposition the needle by
either advancing or withdrawing the needle until the flow of fluid is smooth.
Apply Band-Aid.
Have patient perform wrist flexion and extension exercises to disperse the fluid through the
wrist joint.
Aftercare
Instruct patient that the wrist may be numb for several hours after the procedure and that
After 3 days, the patient can resume his regular activity.
Consider use of wrist splint for 1–2 wks after injection.
the injection site.
CPT Code
De Quervain's Tenosynovitis Injection

Indications
de Quervain's tenosynovitis injections are indicated for the treatment of
tenosynovitis over the radial aspect of the wrist.
These injections are very common in primary care.
NSAIDS, occupational therapy, splinting) has failed.
ICD-9:
727.04 de Quervain's tenosynovitis
Anatomy
The dorsal wrist has 6 compartments containing tendons.
The 1st dorsal compartment contains the abductor pollicis longus and the extensor pollicis
brevis tendons.
de Quervain's tenosynovitis occurs when the tendon sheath becomes inflamed and thickened,
causing pain, swelling, and occasional triggering.
Supplies
Gloves
Ethyl chloride
Gauze
Band-Aid
Technique
Palpate the area of most tenderness over the 1st dorsal compartment and mark this with the
needle cap.
The needle is inserted into the tendon sheath between the abductor pollicis longus and
extensor pollicis brevis tendons at approximately a 30-degree angle.
Inject the fluid into the sheath. If there is resistance to flow, then the needle is likely in a
tendon and should be backed slightly out until free flow is obtained.
An elliptical shaped bulge occurs with the injection of the bolus of fluid into the sheath.
Take care not to inject cortisone while withdrawing the needle, since this superficial tracking
of cortisone can increase the risk of skin atrophy and depig-mentation.
Gently massage the fluid up and down along the tendon sheath.
Apply Band-Aid.
Aftercare
NSAIDS and ice can be used to control postprocedure pain.
Consider a thumb spica wrist splint to rest the tendons for 1–2 wk to allow the injection to
take effect.
The patient should avoid repetitive thumb abduction and/or extension.
the injection site.
CPT Code
20500 Injection(s); single tendon sheath, or ligament, aponeurosis
1st CMC Joint Injection

Indications
1st CMC (thumb) injections are useful for the treatment of thumb pain due to
arthritis either from trauma, osteoarthritis, or rheumatoid arthritis
NSAIDS, thumb spica splinting) has failed,
ICD-9:
719.44 Pain of thumb CMC joint
716.94 Arthritis of thumb CMC joint
715.94 Osteoarthrosis of thumb CMC joint
Anatomy
The thumb CMC joint is composed of the saddle-shaped base of the 1st metacarpal as it
articulates with the trapezium
The thumb CMC joint can be approached on the extensor surface proximal to the 1st
metacarpal, taking care to avoid the radial artery and extensor pollicis tendons
Supplies
Gloves
Ethyl chloride
Gauze
Band-Aid
Technique
Place the patient's arm on the table palm down.
Mark the depression at the base of the 1st metacarpal with needle cap.
Cleanse the skin with Betadine ×3 and alcohol.
To avoid the radial artery, the needle should enter toward the ulnar side of the extensor
pollicis brevis tendon. Distraction of the thumb can increase the space to get the needle into
the joint.

Apply Band-Aid.
Aftercare
Instruct patient that the thumb may be numb for several hours after the procedure and that
Suggest the patient wear the thumb spica splint for the next 1–2 wks.
the injection site.
CPT Code
Carpal Tunnel Injection

Indications
Carpal tunnel injections are useful for the treatment of wrist pain due to median
nerve compression at the carpal tunnel either from trauma, overuse, or
rheumatoid arthritis.
NSAIDs, splinting, physical therapy) has failed.
Local corticosteroid injections for carpal tunnel syndrome provide greater
symptom relief for 1 mo after injection compared with placebo (NNT = 2) and
oral corticosteroids. However, significant symptom relief after 1 mo has not
been demonstrated following injection (Stephens MB, et al.).
ICD-9:
354.0 Carpal tunnel syndrome
Anatomy
The carpal tunnel is bounded by the carpal bones dorsally, and the transverse carpal
ligament (flexor retinaculum), ventrally.
The contents of the tunnel include the median nerve and flexor tendons of the hand.
Supplies
Gloves
3-mL syringe with 25-gauge 1.5-in needle
Ethyl chloride
Gauze
Band-Aid
Technique
Have the patient lay the hand palm up on the table and make a fist with slight wrist flexion.
Observe the tendons of the palmaris longus (10% of the population will not have one) and the
flexor carpi radialis.
Mark a spot with the needle cap 4 cm proximal to the distal palmar crease between the 2
tendons mentioned above.
With the fist clenched and the wrist slightly flexed the needle is inserted at a shallow angle
( 20 degrees) along the tendon sheath, aiming toward the ring finger. Have the patient slowly
extend the wrist and fingers noticing the needle advance toward the carpal tunnel. This
indicates proper needle placement.
Ask the patient if they feel any increased pain or numbness. If they do, remove the needle as
it may be in the median nerve.
DO NOT INJECT INTO THE MEDIAN NERVE.
The fluid should flow easily without resistance. If there is resistance, reposition the needle by
repeating the technique from the beginning.
Massage the fluid distally towards the carpal tunnel.
Apply Band-Aid.
Aftercare
After 3 days, the patient can resume his regular activity.
Recommend continued use of wrist splint for 1–2 weeks after injection.
the injection site.
CPT Code
20526 Injection, therapeutic, carpal tunnel
Trigger Finger Injection

Indications
Trigger fingers occur when a flexor tendon nodule repetitively gets stuck under
the annular pulley on the palmar aspect of the finger.
splinting, NSAIDs) has failed.
ICD-9 727.03
Anatomy
Nodule or thickening occurs in the flexor tendon, which catches on the A-1 proximal pulley
making finger extension difficult.
Supplies
Gloves
0.5 mL 1% lidocaine
Ethyl chloride
Gauze
Band-Aid
Technique
Palpate the tender nodule on the palm of the hand and mark with needle cap.
Injection site is either directly into the nodule or at the proximal interphalangeal digital crease.
Insert needle at a 45-degree angle—when you feel rubbery resistance, you are at the level of
the tendon. Back needle out slowly until it is no longer in tendon and the fluid flows easily
within the tendon sheath.
rupture.
Remove needle and apply pressure with gauze, gently massaging material along tendon.
Apply Band-Aid.
Aftercare
Instruct patient that the finger may be numb for several hours after the procedure and that
The use of a finger splint after an injection for 1–2 wks can increase the efficacy of the
injection.
After 3 days, start extension exercises—hold finger in extension 10 sec × 10 times for 1 set.
Complete 3 sets/day.
the injection site
Avoid repetitive gripping, or use padded gloves for any vibrating tools (ie, jackhammers).
CPT Code
20550 - Injection(s); single tendon sheath, or ligament, aponeurosis (eg, plantar “fascia”)
Ganglion Cyst Injection

Indications
Most ganglion cysts resolve spontaneously.
Aspiration and corticosteroid injection can be considered for ganglion cysts if
patients complain of symptoms such as pain, limited range of motion,
paresthesias, or aesthetic considerations.
P.
Aspiration and steroid injection is effective without recurrence in 27–67% of
cases
ICD-9:
727.41 Ganglion cyst of joint
727.42 Ganglion cyst of tendon sheath
727.43 Ganglion cyst, unspecified
Anatomy
Ganglion cysts are the most common soft tissue tumors of the hand and wrist, more
commonly in women (3:1).
These thick mucin filled cysts may arise from trauma or repetitive irritation
Ganglion cysts are often connected to an underlying ligament or joint, primarily at the
scapholunate joint (60–70%), and next most frequently at the volar wrist (20–25%), and
thirdly at the palmar flexor tendon sheath (10–12%).
Supplies
Gloves
5–10 mL syringe with 18–22-gauge 1-in needle if aspirating (thick fluid)
3-mL syringe with 22-gauge 1-in needle if injecting
0.5 mL 40 mg/mL (20 mg) Kenalog or equivalent
Ethyl chloride
Gauze
Band-Aid
Technique
Position the patient in sitting position with his/her arm on the table with the ganglion cyst
facing upward.
Clean the skin with Betadine × 3 and alcohol.
Aspirate using the 18-gauge needle—the thick mucoid cyst contents may be difficult to
aspirate, and may actually be more effectively milked out of the puncture site.
Aspirate 1st, then stabilize the needle position with a hemostat, change to the syringe with
the steroid/lidocaine mixture—then inject.
Band-Aid
Aftercare
Apply pressure dressing.
the injection site.
Ganglion cyst recurrence is common, and may indicate the need for surgical ganglionectomy
if symptoms are severe.
CPT Code
20612 Aspiration and/or injection of ganglion cyst(s) any location
Trochanteric Bursa Injection

Indications
Corticosteroid injection is an accepted treatment for acute or chronic
trochanteric bursitis caused by chronic pressure, limping, leg length
discrepancies, acute trauma, hip surgery, or repetitive trauma, such as from
iliotibial band friction.
Injections are indicated if pain persists despite conservative therapy, including
avoiding direct pressure and repetitive trauma, ice, NSAIDs, and stretching of
the iliotibial band, tensor fascia lata, external hip rotators, hip flexors, and
quadriceps.
A randomized controlled trial showed prolonged benefit from early
corticosteroid injection for trochanteric bursitis
Another RCT showed the relative risk of recovery at 5 yr was 2.7 for patients
with corticosteroid injection, with the conclusion that steroid injection may help
prevent chronic bursitis pain.
ICD-9:
726.5 Trochanteric bursitis
Anatomy
The trochanteric bursa lies superficial to the greater trochanter of the femur, between the
trochanteric process and the gluteus medius/iliotibial tract.
Tenderness to palpation over the trochanteric process is the classic finding for trochanteric
bursitis.
Supplies
Gloves
6 mL syringe with 22-gauge 1.5–2 in needle for thin patients
22-gauge 3.5-in spinal needle may be needed for heavier patients
5 mL 1% lidocaine without epinephrine or 0.25% Marcaine
1 mL 40 mg/mL (20 mg) Kenalog or equivalent
Ethyl chloride
Gauze
Band-Aid
Technique
Lay the patient in lateral recumbent position, with the affected side up.
Flex the patient's hip at 50 degrees, and flex the knees 60–90 degrees.
Palpate the greater trochanteric process and identify the point of maximal tenderness, which
usually corresponds well to the most superficial point of bony prominence. Mark this area
with the needle cap.
Aim the needle perpendicular to the skin directly down to the tender point on the trochanteric
bony prominence.
Advance the needle until the tip reaches bone level.
Withdraw the needle 2–3 mm to remain within the trochanteric bursa.
For acute bursitis, the 5–6 cc of corticosteroid and lidocaine can be directly injected into the
bursa.
For chronic bursitis, a clockwise peppering motion may help break up scar tissue—each
time, the needle should reach the level of bone, then withdraw 2–3 mm.
Crepitus can often be felt at the needle tip if chronic scarring/bursitis/tendonitis is present.
Band-Aid
Aftercare
Relief from steroid anti-inflammatory effect may take 2–3 days after injection.
Avoid direct pressure or trauma to the trochanteric bursa.
Rest 3 days, then restart stretches of the iliotibial band, hip flexors, and extensors.
the injection site.
Injection can be repeated in 6–12 wks if pain relief was <50%.
CPT Code
20610 Arthrocentesis, aspiration and/or injection; major joint or bursa
Olecranon Bursa Injection
Indications
Olecranon bursa aspiration is useful for the relief of swelling in acute bursitis
and for the diagnosis of gouty bursitis or infectious bursitis (most often
Staphylococcus aureus). Olecranon bursa steroid injections are useful for the
treatment of chronic bursitis.
Most acute traumatic olecranon bursitis episodes are self-limited.
P.
Injections are indicated once conservative therapy (rest, ice, compression with
elbow sleeve, elevation, avoidance of direct pressure, NSAIDs) has failed.
ICD-9:
729.5 Elbow pain
Anatomy
The olecranon bursa overlies the olecranon process at the proximal ulna.
Olecranon bursitis is visible as posterior elbow swelling, often described as a golf ball or
goose egg over the elbow tip.
Supplies
Gloves
3-mL syringe with 25-gauge 1-in needle if injecting
5–10 mL syringe with 18–22-gauge needle if aspirating (thick fluid)
Ethyl chloride
Gauze
Band-Aid
Technique
Place the patient's arm on the table at maximal elbow flexion to accentuate the swelling.
Palpate over the olecranon bursa for fluctuance.
Aim the needle directly at the olecranon bursa.
Aspirate bursal fluid until the bursa is flat.
If infection has been ruled out, inject steroid/lidocaine into bursa.

Band-Aid
Aftercare
A compressive neoprene elbow sleeve may help prevent fluid reaccumulation.
Avoid direct pressure or trauma to the elbow.
For recalcitrant olecranon bursitis, consider a posterior splint or elbow pads for 1–2 wks
after the steroid injection.
the injection site.
CPT Code
Prepatellar Bursa Injection

Indications
Acute trauma, repetitive pressure, or rarely infection can cause inflammation
and swelling in the prepatellar bursa.
Prepatellar aspiration may be performed to relieve acute pressure and
swelling.
Corticosteroid injection is a second line therapy for chronic prepatellar bursitis
after the failure of conservative therapy, including avoidance of direct pressure,
rest, ice, and NSAIDs.
ICD-9:
726.65 Prepatellar bursitis
Anatomy
The prepatellar bursa lies between the patella and the overlying skin.
Prepatellar bursitis is visible as a well-circumscribed region of swelling over the patella.
Prepatellar bursitis should be differentiated from patellar fracture or intra-articular knee
effusion.
Supplies
Gloves
5 mL syringe with 22-gauge 1-in needle if injecting
5–10 mL syringe with 18–22-gauge 1-in needle if aspirating (thick fluid)
2 mL 1% lidocaine without epinephrine (optional)
0.5 mL 40 mg/mL (20 mg) Kenalog or equivalent (optional)
Ethyl chloride
Gauze
Band-Aid
Technique
Position the patient in supine position with the knee flexed at 30 degrees on a pillow.
Position the affected leg with patella facing upward.
The prepatellar bursitis should be clearly visible.
Aspirate by approaching from the side of the visible prepatellar swelling.
Aspirate 1st, then stabilize the needle position with a hemostat while changing to the syringe
with the steroid/lidocaine mixture—then inject.
Band-Aid
Aftercare
Rest 3 days.
Continue the RICE conservative therapy.
the injection site.
CPT Code
Pes Anserine Bursa Injection

Indications
Trauma or repetitive friction over the anserine bursa can cause inflammation
that worsens with knee flexion or rotation.
Corticosteroid injections may be considered early in the course of treatment
for anserine bursitis, along with the conservative therapy of NSAIDs, rest, ice,
and stretching
ICD-9:
726.61 Pes anserine bursitis
Anatomy
The pes anserine bursa lies between the conjoined tendon of the sartorius, gracilis, and
semitendinosus muscles and the tibial insertion of the medial collateral ligament.
Diagnosis is made by tenderness to palpation over the anserine bursa, 2 cm below the
medial joint line at the proximal medial tibia.
Swelling is not usually visible with anserine bursitis.
Supplies
Gloves
Ethyl chloride
Gauze
Band-Aid
Technique
Lay the patient in supine position.
Position the affected leg with the medial joint line accessible.
Identify the anserine bursa 1–2 cm below the middle of the medial joint line.
The point of maximal tenderness along the medial tibial plateau often serves to identify the
ideal injection site—mark this site with the needle cap.
Insert the needle perpendicular to the skin.
Advance the needle to the level of bone to find the bursal space between the conjoined
tendons and the tibia.
Withdraw 2–3 mm to inject the steroid/lidocaine mixture into the bursa.

Band-Aid
Aftercare
Rest 3 days, then resume stretching exercises.
A physical therapy referral to develop a stretching plan for the knee adductors and
quadriceps, especially the vastus medialis, may help prevent recurrence
Sleeping with a cushion between the knees may help decrease direct pressure on the
anserine bursa.
the injection site.
CPT Code
20551 Injection of a single tendon origin or insertion
Knee Joint Injection

Indications
Knee joint aspiration is useful for the diagnosis of knee effusions (ie, to
diagnose crystalline disease, hemarthrosis, or rule out infection) and for the
reduction of pain and pressure from effusions.
Corticosteroid injection to the knee is indicated for the treatment of
osteoarthritis, crystalline disease, or synovitis in rheumatoid arthritis.
Hyaluronic acid viscosupplementation injections are FDA approved for
osteoarthritis.
Injections are indicated for pain relief if pain continues despite conservative
therapy (activity modification, NSAIDs, physical therapy).
ICD-9:
719.46 Knee pain
716.96 Knee arthritis or arthropathy
715.16 Knee osteoarthrosis, primary
715.26 Knee osteoarthrosis, secondary
Anatomy
The knee joint consists of the femoral–tibial and femoral–patellar joints, with stabilization from
the anterior and posterior cruciate ligaments and the medial and lateral collateral ligaments.
Supplies
Gloves
20–60 mL syringe with 18–22-gauge 1.5-in needle for aspirating
10 mL syringe with 22-gauge 1.5-in needle for injecting
5–7 mL 1% lidocaine without epinephrine and or 0.25% Marcaine
Ethyl chloride
Gauze
Band-Aid
Technique
The knee joint can be aspirated or injected from multiple approaches, including the anterior
medial or lateral approach with the knee flexed to 90 degrees, or a superior or midpatellar
approach with the knee in extension.
For the anterior approach, the patient is seated with the knee flexed at 90 degrees. The
needle is inserted in the “soft spot” demarcated by the patella, patellar tendon, tibial plateau,
and distal femoral condyle. The needle angle is parallel to the floor and aimed slightly
posterior.
The anterior approach has the advantage of less bony discomfort but had a success rate of
70–75% in a trial comparing knee injection techniques
For the medial or lateral midpatellar approach, the patient is prone with the knee either in full
extension, which gives the most patellar mobility, or slightly flexed at 5 degrees with a rolled
towel supporting underneath. The needle is advanced parallel to the floor directed straight
towards the patellar midpole.
The lateral midpatellar approach had a higher success rate of 93% in the same study and
may be a more reliable access to the knee joint in larger patients.
For the superior approach, draw lines from the superior and lateral borders of the patella—at
the intersection of these lines, insert the needle at a 45-degree angle directed toward the
middle of the patella
Cleanse the skin with Betadine × 3 and alcohol.

Apply ethyl chloride for superficial numbing.
Inject the fluid into the joint—there should be minimal resistance.
Apply Band-Aid.
Aftercare
Lidocaine lasts 4–6 hrs; Marcaine can last up to 12 hrs.
However, steroid effect may take 2–3 days to decrease inflammation.
After 3–5 days, the patient can resume his regular activity and advance as tolerated.
the injection site.
Recommend continued isometric quadriceps strengthening, low-impact exercise, and weight
loss.
Repeat injection can be done after 3 mos if the steroid injection afforded adequate pain relief
—average duration of effect for joint steroid injections is 4 wks.
CPT Code
Ankle Joint Injection

Indications
Ankle aspiration is useful for the diagnosis of ankle effusions (ie, to diagnose
crystalline disease or rule out infection).
Corticosteroid injection to the ankle is indicated for the treatment of ankle
arthritis, crystalline disease, or synovitis in rheumatoid arthritis.
NSAIDs, physical therapy) has failed.
ICD-9:
719.47 Ankle pain
716.97 Ankle arthritis
715.97 Ankle osteoarthrosis
Anatomy
The ankle joint consists of the articulation of the talo-tibial and talo-fibular joints.
The ankle joint can be approached either medially or laterally.
Supplies
Gloves
10–20 mL syringe with 20 or 22-gauge 1.5-in needle for aspirating
5–10 mL syringe with 25-gauge 1.5-in needle for injecting
Ethyl chloride
Gauze
Band-Aid
Technique
The patient can be in a sitting or supine position.
Medial approach: Identify the soft spot between the anterior tip of the medial malleolus and
the medial edge of the tibialis anterior tendon:
Palpate down to feel the talo-tibial joint line—mark this site with the needle cap.
Advance the needle in a posterolateral direction and inject.

Having an assistant apply mild eversion/plantarflexion pressure may help to open the joint.
Apply Band-Aid.
Lateral approach: Identify the triangular depression between the lateral tibia, fibula, and the
talus:
Palpate down to feel the talo-tibial joint line—mark this site with the needle cap.
Advance the needle in a posteromedial direction and inject.
Apply Band-Aid.
If aspirating remove as much fluid as possible then stabilize the needle in the joint with a
hemostat, and change to the syringe containing the steroid/lidocaine mixture.
Aftercare
If pain is improved, start ankle rehabilitation with range of motion exercises, strengthening
band flexion/extension exercises.
the injection site.
CPT Code
Plantar Fasciitis Injection

Indications
Excessive stretching and repetitive trauma can lead to microtears of the
plantar fascia from its insertion on the calcaneous. These microtears can lead
to chronic inflammation and pain at the calcaneal insertion or along the entire
plantar fascia.
Conservative treatment includes stretching, arch-supporting orthotics, heel
pads, NSAIDs, and nighttime plantar fascia splints.
Corticosteroid injection is a 2nd-line therapy after the failure of conservative
therapy, given the higher risk of complications, including fat pad atrophy and
rupture of the plantar fascia.
ICD-9:
728.71 Plantar fasciitis
Anatomy
The plantar fascia supports the medial longitudinal arch of the foot and stretches between the
base of the phalanges and the medial tuberosity of the calcaneous.
The plantar fascia lies deep to the fat layer of the heel.
On physical exam, the plantar fascia insertion point on the calcaneous is usually markedly
tender to palpation.
Supplies
Gloves
3-mL syringe with 25-gauge 1.5-in needle for injection
Ethyl chloride
Gauze
Band-Aid
Technique
Position the patient in the lateral recumbent position with the painful side down.
Position the affected foot medial side up.
Palpate the maximal point of tenderness at the plantar fascia insertion on the calcaneus,
usually in the middle of the heel—this gives the injection target depth along the width of the
heel.
Find the medial edge of the calcaneous and mark with needle cap—this marks the injection
point along the length of the foot.
Inject 90 degrees perpendicular to the medial foot, aiming just below the calcaneal edge in
order to avoid the heel fat pad.
If the calcaneous is reached with the needle tip, walk the needle off the bony edge, then
down to the depth of the point of maximal tenderness.
Inject the steroid/lidocaine mixture.
Apply Band-Aid
Aftercare
Rest 3 days.
Continue the RICE conservative therapy and consistent plantar fascia stretching.
the injection site.
CPT Code
20550 Injection(s); single tendon sheath, or ligament, aponeurosis
Morton's Neuroma Injection

Indications
Morton's neuroma results from irritation of the interdigital nerve in the foot from
repetitive compressive trauma, such as compression from tight or high-heeled
shoes.
Injections are indicated once conservative therapy (shoes with a wider
metatarsal box, metatarsal pads, orthotic arch supports, NSAIDs) has failed.
ICD-9:
355.6 Morton's neuroma
Anatomy
Morton's neuroma usually develop between the 2nd and 3rd, or between the 3rd and 4th
metatarsal heads.
Tenderness to palpation between the metatarsal heads usually confirms the diagnosis
Supplies
Gloves
3-mL syringe with 25-gauge 1–1.5-in needle
Ethyl chloride
Gauze
Band-Aid
Technique
Lay the patient in a supine position with a bent knee and the foot flat upon the table.
Identify the point of maximal tenderness between the metatarsal heads on the dorsal foot—
mark entry site with needle cap.
Advance the needle at a 45-degree angle proximally towards the point of maximal tenderness
or nodule—aim toward the heel and stop at the level of the interdigital fullness.
Do not inject at the level of the plantar fat pad to avoid fat pad atrophy.
Apply Band-Aid.
Aftercare
Lidocaine lasts 4–6 hours; Marcaine can last up to 12 hrs.
Advise continued proper footwear, metatarsal pads, and orthotics.
the injection site.
CPT Code
64450 Injection, nerve block, therapeutic, other peripheral nerve or branch
1st MTP Injection

Indications
Aspiration of the 1st metatarsal phalangeal joint is useful in the diagnosis of
gout and pseudogout.
Therapeutic steroid injection can be a useful adjunct therapy for 1st MTP
osteoarthritis, rheumatoid arthritis, or crystal arthropathies.
ICD-9:
719.47 Pain of first MTP joint
716.97 Arthritis of first MTP joint
715.97 Osteoarthrosis of first MTP joint
274.0 Acute gouty arthritis
Anatomy
The metatarsophalangeal joint line is palpable on the dorsal surface of the foot.
Supplies
Gloves
Ethyl chloride
Gauze
Band-Aid
Technique
Lay the patient in a supine position with a bent knee and the foot flat upon the table.
Flex and extend the 1st MTP joint to identify the joint line and mark with needle cap.
Distal traction may help open the joint space.
Aim the needle distally toward the toe and enter at a 60-degree angle to match the joint
slope.
The joint lies fairly superficially, and the injection solution should flow freely within the joint.
Apply Band-Aid.
Aftercare
However, steroid effect may take 2–3 days to decrease inflammation
Advise continued proper footwear and arch supports for proper walking mechanics.
the injection site.
CPT Code
A
Abdominal muscle strains 2–3
Abdominal wall musculature 2
Abductor pollicis longus tendon 114
Abrasions 350–353
Abscess
Brodie 428–431
cellulitis from 66
external ear 152–153
Accessory navicular 166–167
Accessory scaphoid bone 166–167
Accessory tarsal scaphoid 166–167
Acclimatization response 306
Acephalgic migraine 388–391
Acetabular fracture, radiography of
Judet views in 647 647–648
oblique view in 648 648
Acetabulum dysplasia 116
Acetabulum radiography, Judet views in 647 647–648
Acetic acids 406
Achilles stretch
for ankle sprains 668
for hamstring strain 663
for patellofemoral pain syndrome 665
for plantar fasciitis 671
for shin splints 670
Achilles tear 6–7
Achilles tendinitis 4–5
Achilles tendinopathy 4–5
Achilles tendinosis 4–5
Achilles tendon 4 6
Achilles tendon rupture 6–7
ACL See Anterior cruciate ligament
Acromioclavicular dislocations 14–15
Acromioclavicular joint
anatomy of 686 686 687
injection of 686–688 686 687
radiography of 636 636
Acromioclavicular ligament 14
Acroparesthesia 64
Acroparesthesia, nocturnal 64
AC sprain 14–15
Acute compartment syndrome 88 498
Acute hemorrhagic conjunctivitis 556
Acute mountain sickness 306–307
Acute otitis media 434–435
Adam forward bending test
for kyphosis 348
for scoliosis 522
Adductor thigh strain 16–17
Adhesive capsulitis 18–19
Adhesives, skin 352
Adolescent idiopathic scoliosis 522–523
Adson maneuver 580
Adventitial bursa 322
Aerogastralgia 46–47
Air embolism 524–525
Air sickness 396–397
Allen test 319 580
Allergic contact dermatitis 100–103
Allis method, for dislocated hip reduction 127
Allografts, for ACL reconstruction 10
Altitude, height and sickness from 306
Altitude illness 306–307
Alveolar bone fracture 110–113
Amenorrhea
in athlete 386
in female athlete triad 158–159 386–387
Anaphylaxis 20–23
from bites and stings 52
exercise-induced 20–21 140–141 146–147
Anemia, sports 494–495
Anesthetic injection 678
Angle of Gissane 173 173
Ankle
anatomy of 713 714
injection of 713–716 714 715
Ankle alphabet 668
Ankle dorsiflexion, for sciatica 520
Ankle fracture 208–209 See Also specific types
Ankle isometric inversion/eversion 669
Ankle pumps 668
Ankle radiography 639 639
for acute injuries 639 639
of posterior subtalar joint 639 639
stress views in 640 640
weight-bearing views in 640 640
Ankles, unstable, radiography for 639 639
Ankle sprain
causes of 668
description of 668
grading of 24 25
high 24 570–571
lateral 24–25
medial 26–27
rehabilitation exercises for 668–670
signs and symptoms of 668
strengthening guidelines for 668
stretching guidelines for 668
treatment of 668
Ankylosing spondylitis 28–29 548–549
Anogenital warts 624–625
Anterior compartment 88
Anterior compartment syndrome 88–89
Anterior cruciate ligament 8
bracing of
for injury prevention 8 10
postsurgical 11
training for injury prevention in 8
Anterior cruciate ligament injuries 8–11
Anterior cruciate ligament tear, in skeletally immature 12–13
Anterior drawer test
for ACL injury 9 12
for lateral ankle sprain 24
Anterior glenohumeral dislocation 270–271
Anterior interosseous nerve 30
Anterior interosseous syndrome 30–31
Anterior metatarsalgia 32–33
Anterior shoulder instability 534–535
Anterior table fracture 198
Anterior talofibular ligament 24
Anterior talofibular ligament injury 24–25
Anterior tibia-fibula ligament avulsion 598–599
Anteroinferior iliac spine (AIIS) avulsion fracture 168–169
Anterosuperior iliac spine (ASIS) avulsion fracture 168–169
Ant stings 52–53
AO classification 203
A-1 proximal pulley 699 699
Aortic sclerosis 34–35
Aortic stenosis 34–35
Aortic valve, congenital bicuspid 34–35
Apophysis 466
Apophysitis
calcaneal 532–533
medial 360–361
traction
at 5th metatarsal base 166
of tibial tubercle 420–421
Appendix testis torsion 576
Apprehension test
for anterior shoulder instability 534
for multidirectional shoulder instability 536
Arc test 328
Arm fracture See specific types
Arrhythmias, cardiac 62–63
Arterial gas embolism 524–525
Arthritis
with inflammatory bowel disease 550–551
of hand, radiography for 630 630
pseudorheumatoid 58
psoriatic 550–551
radiographic joint survey for 659
reactive 550–551
rheumatoid, in sports 514–515
septic (infectious) 530–531
Arthropathy, pyrophosphate 58–59
Arthropod bites 52–53
Aseptic necrosis
of femoral head 42–43
of tarsal navicular 346–349
Aseptic thrombophlebitis 586–589
Asthma, exercise-induced 142–143
Asymmetric septal hypertrophy 312–313
Athlete's foot 600–601
Athlete's heart 36–37 62
Athletes' pseudoanemia 494–495
Athletic heart syndrome 36–37
Athletic pubalgia 422–423 552–553
Atlantoaxial instability (AAI) 38–39
Atlantoaxial subluxation 38–39
Atrial fibrillation 62–63
Atrial flutter 63
Auditory exostosis, external 566–567
Auricular hematomas 40–41
Autochthonous bubbles 524
Autoimmune diabetes 118–121
Avascular necrosis
of lunate 214–215
of proximal femoral epiphysis 42–43
AV block 62–63
Avulsion (avulsion fracture) 262 See Also Tear
central slip 68–69
dental 110–113
epicondylar, medial 360
extensor tendon, from distal phalanx 150–151
flexor tendon 162–163
iliac crest 168–169
iliac spine
anteroinferior 168–169
anterosuperior 168–169
ischial tuberosity 168–169
metatarsal base, fifth 196–197
olecranon 608–609
pelvic 236–237
tibia-fibula ligament, anterior 598–599
tibial spine 12 262–263
tibiofibular ligament, posterolateral 264–265
tooth 110–113
triceps tendon 608–609
Axial spondyloarthritis 28–29
Axillary artery injury, with humeral head fracture 203
Axillary nerve 44
Axillary nerve injury 44–45
B
Babinski sign
for cervical disk disease 70
for cervical strains 77
Back pain
inflammatory 28
low 364–365 520
Ball catcher's position, in radiography 630 630
Bankart lesion 270 274–275
radiography for 635 635
Barlow test 116
Barodontalgia 46–47
Barotitis media 46–47
Barotrauma 524
of descent 46
middle ear 46–47
Barton fracture 192–193
Baseballs, safety 560
Basilar migraine 388–391
Bee stings 52–53
Behnken's sign 524
“Bell ringer” 94–97
Bends, the 524–525
Benign episodic headache 388
Benign exertional headache 148–149
Bennett's fracture 218–219
Bent-knee stretch
for ankle sprain 668 670
Biceps tendinitis 48–49
Biceps tendinopathy 48
Biceps tendinopathy maneuver, in adhesive capsulitis 19
Biceps tendinosis 48
Biceps tendon rupture 50–51
Bicondylar fractures, tibial plateau 260–261
Bicuspid aortic valve, congenital 34–35
Bicycling
Bilateral patellar view 644 644
Binge-eating disorder 134–135
Bites 52–53
Bladder trauma 622–623
Blisters 350–353
Blowout fracture 170–171 230–233
Body fracture, hamate 200–201
Bohler's (tuber joint) angle 173 173
Boil 164–165
Bone marrow changes, MRI for 629
Bone metastases, radiographic survey for 659
Bony Bankart, radiography for 635 635
Bony orbit 230
Boutonniere deformity 68–69
Boxer's fracture 220–221
Boyle's law 46
Brachial plexus injuries 54–55
Bradyarrhythmias 62–63
Broden view, of posterior subtalar joint 639 639
Brodie abscess 428–431
Broken arse 180–181
Broken ribs 246–247
Broken tailbone 180–181
Bronchoconstriction, exercise-induced 142–143
Brugada syndrome 80–83
Bruised hip 308–309
Bruised lung 496–497
Buccal lacerations 418–419
Bug bites 52–53
Bulimia nervosa 134–135
Bullous impetigo 326–327
Bunions 284–285 322
Burners 54–55
Burning hands syndrome 182
Bursa 56 322
olecranon 705 705
pes anserine 708 709
prepatellar 706 707
trochanteric 703 703
Bursitis 56–57 322
calcaneal 56
definition of 612
iliopsoas 56 322–323
infectious 528–529
olecranon 412–413
pes anserine 460–461
prepatellar 56
septic (infectious) 528–529
subacromial 328–329
subcalcaneobursitis 292
subdeltoid 56
superficial septic 56–57
trochanter(ic) 56 612–613
C
Caisson disease 524–525
Calcaneal apophysitis 532–533
Calcaneal bursitis 56
Calcaneal cuboid fault syndrome 108–109
Calcaneal nerve, medial 572
Calcaneal neuritis 292
Calcaneodynia 292
Calcaneofibular ligament 24
Calcaneofibular ligament injury 24–25
Calcaneus fracture 172–175
Calcific aortic stenosis 34–35
Calcific tendonitis of shoulder 328–329
Calcium pyrophosphate deposition disease (CPPD) 58–59
Calcium pyrophosphate dihydrate crystal deposition 276–279
Calluses 60–61
Candidal onychomycosis 416–417
Capital femoral epiphysis of femoral head osteonecrosis 42–43
Capitate fracture 176–177
Capitellum, osteochondritis dissecans of 438–439
Carboxylic acids 406
Carbuncle 164–165
Cardiac arrhythmias 62–63
Cardiac hypertrophy, physiologic 36–37
Cardiac phenotype 80
Cardinal sign 272
Cardiomyopathy, hypertrophic 312–313
Carpal bones 176
fractures of 176–177
ligaments of 368
Carpal compression test 64
Carpal navicular fracture 250–251
Carpal tunnel
anatomy of 697 698
injection of 697–699 698 699
Carpal tunnel syndrome 64–65 490
Carpometacarpal joint, first
anatomy of 695 696
injection of 695–697 696 697
Car sickness 396–397
Cartilage tear, meniscal 384
Catecholaminergic polymorphic ventricular tachycardia 80–83
Caterpillars 52–53
Cauliflower ear 40 152
Causalgia 90
Cellulitis 66–67
orbital (postseptal) 456–458
periorbital (preseptal) 456–458
Centipedes 52–53
Central extensor slip 224
Central slip avulsion 68–69
Cerebral bends 524
Cervical cord neurapraxia 74–75
Cervical disease, congenital 98–99
Cervical disk disease 70–73
Cervical radiculopathy 70–73
Cervical spine injuries 182
Cervical spine radiography
complete 652 652–653
flex-ext series in 654 654
limited 653 653
swimmer's view in 652 653 654 655 655
Cervical spine rheumatoid arthritis 514
Cervical sprain 76–79
Cervical stenosis 74–75
Cervical strains 76–79
Cervical vertebrae fusion 340–341
Chaffing 350–353
Channelopathies 80–83
Charley horse 498–499
Cheiralgia paresthetica 562–563
Chemical trauma, corneal abrasions from 104–105
Chest protectors 560
Chin to chest, for sciatica 520
Chokes 524
Cholinergic urticaria, exercise-induced 140 146
Chondritis, external ear 152–153
Chondrocalcinosis 58–59
Chondrocytes 58
Chondromalacia patella 448–451
Chronic actinic dermatitis 464–465
Ciliary neuralgia 86–87
Clam shell exercises 664 666
Claudication 84–85
Clavicle 178
Clavicle fracture 178–179
Clavicular osteolysis, distal 130–131
Claw toe 286–287
Clay shoveler injuries 252–253
Clenched fist injury 290–291
Clenched fist view, radiographic 631 632
Cluster headache 86–87
Coaching 436
Cobb angle
in kyphosis 348
in scoliosis 524–525
Coccydynia, radiography of 657 657
Coccyx 180
Coccyx 180
Coccyx fracture 180–181
Cold-induced anaphylaxis 20–23
Cold urticaria 20
Collapsed lung 476–479
Collapse, exercise-related 568
Colles fracture 192–193
Collodion cast dressing 41
Common extensor tendon 690 690
Common flexor tendon 690 690
Common warts 624–625
Commotio cerebri 94–97
Commotio cordis 62 560–561
Compartment syndrome 88
acute 88
anterior 88–89
exercise-induced 88
Complex regional pain syndrome 90–93 193
Compression fracture 182–183
Computed tomography (CT), for intraarticular fractures 629
Concussion 94–97
Conduction 310
Condylar fracture 186–187
Condylomata acuminata 624–625
Congenital aortic stenosis 34–35
Congenital bicuspid aortic valve 34–35
Congenital cervical disease 98–99
Congenital scoliosis 522–523
Congenital spondylolisthesis 550–551
Conjunctival hemorrhage 556–557
Conjunctivitis, acute hemorrhagic 556
Constant bursa 322
Constrictive pericarditis 454–455
Contact dermatitis 100–103
Contact lens misuse, corneal abrasions from 104–105
Contracture, Dupuytren's 132–133
Convection 310
Convulsions 526–527
Coracoclavicular ligament 14
Corneal abrasions 104–105
Corneal foreign body 338–339
Corneal ulcer 104–105
Corns 60–61
Coronoid fracture 184–185
Coronoid process 184
Cotton test 570
Cough headache 148–149
COX-1 406
COX-2 406
COX-2 inhibitors 406
Crankshaft phenomenon 522
Creatine phosphokinase, in rhabdomyolysis 512
Cremasteric reflex 576
Cross-arm test 130
Cross-body adduction test 564
Crossed-legs test 570
Crossed straight-leg raise 520
Crossover syndrome 336–337
Crossover test 14
Crown fractures 110–113
Crucial angle of Gissane 173 173
Cubital tunnel 106
Cubital tunnel syndrome 106–107
Cuboid dislocation 108–109
Cuboid fracture 108–109
Cuboid subluxation 108–109
Cuboid syndrome 108–109
Cuff sign 572
Curls, wrist
extension 675
flexion 675
hamstring
prone 664 667
standing 664
Curvature of spine 348–349
Cutis marmorata 524
Cycling
Cyclooxygenase (COX) enzymes 406
D
Daily training logs 436
Dancer's fracture 196–197
Dead-arm syndrome 534–535
Dead leg 498–499
Decompression illness 524–525
Decompression sickness 524–525
Deep vein thrombosis (DVT) 590–591
Degenerative joint disease 424–425
Deltoid ligament complex injury 26
Deltoid ligament sprain 26–27
Deltotrapezial disruption, radiography of 636 636
Denis system 248
Dental avulsion 110–113
Dental extrusion 110–113
Dental intrusion 110–113
Dental luxation 110–113
Dentoalveolar trauma 110–113
de Quervain's tenosynovitis 114–115 488
injection for 694–695 694 695
Dermatitis
allergic contact 100–103
chronic actinic 464–465
contact 100–103
irritant contact 100–103
photodermatitis 464–465
Developmental dysplasia of the hip 116–117
Diabetes 118–121
Dial test 486
Diaphyseal stress fractures 196–197
Diarrhea, exercise-induced (runner's) 144–145
“Ding” 94–97
DIP dislocation 122–123
DIP join See Distal interphalangeal (DIP) joint
Discoid meniscus 124–125
Disk disease, cervical 70–73
Disk herniation
cervical radiculopathy from 70
lumbar 366–367
Diskogenic pain, thoracic 582–585
Dislocation
acromioclavicular 14–15
cuboid 108–109
distal interphalangeal joint 122–123
elbow 136–137
femoral head 116
finger 470–471
first interphalangeal joint 122–123
glenohumeral 534–535
anterior 270–271
posterior 272–273
hip
classification of 126
posterior 126–129
prosthetic hip 128
knee 342–345
lunate 368–369
metacarpophalangeal joint 374–375
patellar 234–235 442–443
perilunar 368–369
peroneal tendon 458–459
phalangeal 462–463
proximal interphalangeal joint 470–471
scapholunate 368–369 518–519
shoulder (acromioclavicular) 14–15
sternoclavicular 554–555
Disordered eating 386
Dissociation See Dislocation
Distal clavicular osteolysis 130–131
Distal femur fracture 186–187
Distal interphalangeal (DIP) joint
dislocation of 122–123
hyperextension deformity of 68–69
Distal phalanx, extensor tendon avulsion from 150–151
Distal phalanx fracture 188–191
Donkey kick 666
Dorsal intercalated segment instability (DISI) 368 518–519
Dorsal nose deformity 398
Dorsiflexion-eversion test 572
Double fractures of the chest 246–247
Dowager's hump 348–349
Drawer test 570
Dressing, wound 352
Drop arm test 328
Dropped cuboid 108–109
Drowning 400–403
Dupuytren's contracture 132–133
Dynamic posterior shift test 482
Dysplastic spondylolisthesis 550–551
E
Ear abscess, external 152–153
Ear barotrauma 46–47
external 46–47
inner 46–47
Ear bends 524
Ear, cauliflower 40 152
Ear chondritis, external 152–153
Ear injuries, inner 330–331
Eating disorder not specified 134–135
Eating disorders 134–135
in athlete 386
in female athlete triad 158–159
Eggshell fracture 268–269
Eichoff test 114
Elbow See Also specific disorders
anatomy of 688 688
floating 204–207
golfer's 378–379
injection of 688–689 688 689
Little Leaguer's 360–361
miner's 412–413
nursemaid's 408–409
pulled 408–409
student's 412–413
temper tantrum 408–409
tennis 356–357
ulnar collateral ligament injuries of 616–617
Elbow capitellum, osteochondritis dissecans of 438–439
Elbow dislocation 136–137
Elbow flexion test 106
Elbow radiography
for cubital tunnel causes 633 634
for nontraumatic disorders 632 633
for traumatic disorders 633 633
Elbow subluxation 136–137
Elbow tendinosis, lateral 356–357
Elevated arm stress test 580
Embedded toenail 414–415
Embolism
air 524–525
arterial gas 524–525
pulmonary 590
Empty can 674
Enamel fractures 110–113
Endonyx onychomycosis 416–417
Energy balance, negative, in female athlete triad 158–159
Enolic acids 406
Enthesopathy of plantar fascia 474–475
Epicondylar enthesopathy, radiography of 632 633
Epicondylar osteophytes, radiography of 632 633
Epicondyles 690 690
Epicondylitis
description and causes of 674
lateral 356–357
medial 360–361 378–379
rehabilitation exercises for 675–676
strengthening guidelines for 674–675
stretching guidelines for 674–675
treatment of 674
Epidural hematomas 294–297
Epidural hemorrhage 294–297
Epilepsy 526–527
Epinephrine, for anaphylaxis 20 22
Epiphyseal plate injuries, Salter-Harris classification of 466–467
Epiphysiolysis, proximal humeral 362–363
Epiphysis
femoral
proximal, avascular necrosis of 42–43
slipped capital 540–541
pressure 466
traction 466
types of 466
Epistaxis 138–139
Eponychia 440–441
Epstein-Barr virus (EBV) 394
Erythema, exercise-induced cutaneous 140
Erythromelalgia of the head 86–87
Erythropoietic protoporphyria 464–465
Erythroprosopalgia of Bing 86–87
Essex-Lopresti lesion 244
Ethmoid sinuses 198
Etodolac 406
Evaporation 310
Exercise challenge test 140
Exercise-induced anaphylaxis 20–21 140–141 146–147
Exercise-induced asthma 142–143
Exercise-induced bronchoconstriction 142–143
Exercise-induced compartment syndrome 88
Exercise-induced diarrhea 144–145
Exercise-induced hematuria 298–301
Exercise-induced proteinuria 492–493
Exercise-induced urticaria 146–147
Exercise-related collapse 568
Exercise-related syncope 568–569
Exertional headache 148–149
Exertional heat illness 310–311
Exertional presyncope 568–569
Exertional syncope 568–569
Exostosis
external auditory 566–567
subungual 558–559
Extension stretch 673
Extensor mechanism disruption 446–447
Extensor pollicis brevis tendon 114
Extensor tendon avulsion from distal phalanx 150–151
Extensor tendonitis 114–115
External auditory exostosis 566–567
External ear abscess 152–153
External ear barotrauma 46–47
External ear chondritis 152–153
External genital trauma 154–155
External oblique muscle strain 2–3
External rotation 673
External rotation recurvatum test 486
External rotation test
for medial ankle sprain 26
for syndesmodial injury of lower leg 570
Extradural hematoma 294–297
Extradural hemorrhage 294–297
Extremity radiography 629–645
lower 637–645 See Also Lower extremity radiography
upper 629–636 See Also Upper extremity radiography
Extrusion luxations (dental) 110–113
Exudative retinal detachment 510–511
Eye radiography 651 651
Eyewear, protective 105
F
Face masks 110
Face radiography 650 650
Facet syndrome 582–585
Familial catecholaminergic polymorphic ventricular tachycardia 80–83
Familial hemiplegic migraine 388–391
Fasciitis, plantar 474–475
FDP avulsion 162–163
Felon 156–157 290–291
Female athlete triad 158–159 386–387 596
Femoral epiphysis
proximal, avascular necrosis of 42–43
slipped capital 540–541
Femoral head
aseptic necrosis of 42–43
capital femoral epiphysis of, osteonecrosis of 42–43
Femoral head dislocation 116
Femoral head subluxation 116
Femoral head teratologic dislocation 116
Femoral stretch test 544
Femur fracture, distal 186–187
Femur radiography
for acute injury and trauma 644 645
for nonacute injury 645 645
Fenamates 406
Fender fracture 242–243
Fibrillation, atrial 62–63
Fibula diaphyseal fracture 194–195
Fibula fracture 194–195
Fibula radiography 641 641
Fibular translation test 570
Fibula shaft fracture 194–195
Fifth metacarpal neck fracture 220–221
Fifth metatarsal fracture 196–197
Finger
jammed 122–123 334–335
jersey 162–163 188–191
mallet 150–151
trigger 610–611
Finger dislocation 470–471
Finger extension 676
Finkelstein test 114
in de Quervain tenosynovitis 114
in superficial radial nerve 562
First carpometacarpal joint
anatomy of 695 696
injection of 695–697 696 697
First interphalangeal joint dislocation 122–123
First metacarpal joint
anatomy of 719 719
injection of 719–720 719 720
First metatarsophalangeal (MTP) joint subluxation 284–285
First-second metatarsal-cuneiform fracture 212–213
Fits 526–527
Flail chest
from rib fracture 246–247
from sternum fracture 254–255
Flat warts 624–625
Flea bites 52–53
Flexion-rotation drawer examination 9
Flexion stretch 673
Flexor carpi radialis tendon 160
Flexor carpi radialis tendonitis 160–161
Flexor carpi ulnaris tendon 160
Flexor carpi ulnaris tendonitis 160–161
Flexor digitorum profundus tendon avulsion 162–163
Flexor digitorum superficialis 224
Flexor hallucis brevis 530
Flexor tendon avulsion 162–163
Flexor tendon of finger 699 699
Flexor tenosynovitis 290–291 610–611
Flick sign 64
Floating elbow 204–207
Floating kidney 508–509
Floating shoulder 179
Fly bites 52–53
Folliculitis 164–165
Food-dependent exercise-induced anaphylaxis 20–21
Food-induced anaphylaxis 20–21
Foot 222
Foot radiography 637 637
of os calcis 638 638
sesamoid view in 638 638
Footballer's groin/hernia 552–553
Foot fracture See specific types
Foot osteochondroses 166–167
Forced duction test 171
Forearm
pronation/supination of 676
Forefoot 222
Foreign bodies, intraocular 338–339
Forward bending test, Adam
for curvature of spine 348
for scoliosis 522
Fracture See Also specific types
alveolar bone 110–113
ankle 208–209
anteroinferior iliac spine 168–169
anterosuperior iliac spine 168–169
avulsion 262 See Also Avulsion (avulsion fracture)
Barton 192–193
Bennett's 218–219
blowout 170–171 230–233
boxer's 220–221
calcaneus 172–175
carpal bone 176–177
carpal navicular 250–251
clavicle 178–179
coccyx 180–181
Colles 192–193
compression 182–183
coronoid 184–185
crown 110–113
cuboid (nutcracker) 108–109
dancer's 196–197
eggshell 268–269
enamel 110–113
femur, distal 186–187
fender 242–243
fibula 194–195
frontal sinus 198–199
greenstick 280–281
hamate 176–177 200–201
body 200–201
hook 200–201
humerus
head 202–203
proximal 202–203
shaft 204–207
Hutchinson 192–193
iliac crest 168–169
intercondylar eminence 262–263
intraarticular, CT for 629
ischial tuberosity 168–169
Jones 196–197
Kienböck disease 214–215
lateral process 258–259
Le Fort 210–211
Lisfranc 212–213
lunate 214–215
malleolus
lateral and medial 208–209
posterior 238–239
mallet 150 188–191
mandibular 216–217
maxillofacial 210–211
metacarpus
base 218–219
neck 220–221
shaft 218–219
metatarsal
fifth 196–197
general 222–223
metatarsal-cuneiform, first-second 212–213
nasal 226–227
olecranon 228–229
orbital 230–233
orbital floor 170–171
orbital wall 170–171
osteochondral 258–259
patella 234–235
pelvic 236–237
phalanx
distal 188–191
middle 224–225
proximal 240–241
radius
distal 192–193
head 244–245
reverse Barton 192–193
reverse mallet 188–191
rib 246–247
Rolando 218–219
root (dental) 110–113
sacral 248–249
Salter-Harris type I 202
scaphoid 250–251
sesamoiditis 530–531
Seymour 188–191
shepherd 258–259
Smith 192–193
spinous and transverse processes 252–253
sternum 254–255 See Also specific types
stress
diaphyseal 196–197
metatarsal 256–257
sesamoid 530–531
tarsal navicular 256–257
tibial 596–597
talus 258–259
tarsometatarsal 212–213
tennis 196–197
thoracic spine 582–585
tibia
distal, transitional fracture 598–599
proximal 242–243
tibial condylar 260–261
tibial eminence 262–263
tibial plateau 260–261
tibial spine avulsion 12 262–263
Tillaux 598–599
tooth 110–113
trapdoor 170
Tuft 188–191
Volkmann 264–265
wedge 182
wrist 176–177
zygoma 266–267
Fracture-dislocation, Galeazzi 192–193
Freiberg's disease 268–269
Freiberg's infraction 268–269
Frog-leg views, of hip 646 647
Froment sign 618
Frontal sinuses 198
Frontal sinus fracture 198–199
Frostbite 320–321
“Frozen shoulder” 18–19
Fuch's view, of cervical spine 652 652
Functional hypothalamic amenorrhea 158–159
Functional spinal stenosis 74
Furunculosis 164–165
G
Galeazzi fracture-dislocation 192–193
Galeazzi sign 116
Gamekeeper's thumb 372–373 592–593
Ganglion cyst
anatomy of 701 701
injection of 700–703 701 702
Garrick test 480
Gas embolism, arterial 524–525
Gastrocnemius injury, medial 380–381
Gastrocnemius rupture 6–7
Gastrointestinal barotrauma 46–47
Generalized seizures 526–527
Genital trauma, external 154–155
Ghrelin 410
Gilmore groin 552–553
Glandular fever 394
Glenohumeral dislocation 534–535
anterior 270–271
posterior 272–273
Glenohumeral instability 272–273
Glenohumeral joint 274
anatomy of 684 684
injection of 684–685 684 685
Glenohumeral joint restriction, painful 18–19
Glenohumeral subluxation 534–535
Glenoid cavity 684 684
Glenoid labral tears 274–275
Glenoid labrum 274
Golfer's elbow 378–379
Gout 276–279
Greater trochanteric pain syndrome 56 612–613
Greenstick fracture 280–281
Gripping 676
Gripping, neutral 676
Groin strain 16–17
Ground current 358–359
Group A beta-hemolytic streptococcus, impetigo from 326–327
Guyon's canal 618
Guyon's canal syndrome 618–619
H
Haglund's deformity 282–283
Haglund's disease 282–283
Haglund's syndrome 282–283
Hallux valgus 284–285
Hamate fracture 176–177 200–201
Hammer toe 286–287
Hamstring curls
prone
standing 664
Hamstring strain 288–289
causes of 663
description of 664
rehabilitation for 663–664
treatment of 663
Hamstring stretch
seated
standing 663
Hamstring tendon autograft 10
Handcuff disease 562–563
Hand fracture See specific types
Hand infection 290–291
Hand pain, radiography for 630 630
Hand radiography
arthritis survey 630 630
routine 630 630
Handlebar palsy 618–619
Hands, burning 182
Harris Beath view 638 638
“Hatchet strike” defect 6
Hawkins maneuver 19
Hawkin's test 328
Headache
benign episodic 388
benign exertional 148–149
cluster (Horton's) 86–87
cough 148–149
exertional 148–149
migraine 388–391
sexual 148–149
weightlifter's (cough) 148–149
Head gear 97
Head trauma See Also specific injuries
minor 94–97
Heart contusion, commotio cordis from 560–561
Heat cramps 310–311
Heat dissipation 310
Heat exhaustion 310–311
Heat illness 310–311
Heat stroke 310–311
Heel alignment, radiography for 638 638
Heel-cord rupture 6–7
Heel fat pad syndrome 292–293
Heel pain 292–293
Heel pain syndrome 292
Heel raises
bilateral
single
for hamstring sprain 664
single leg
Heel walking 670
Helmets 97
Hematoma 350–353
auricular 40–41
epidural 294–297
extradural 294–297
intracranial 294–297
nasal septal 398–399
quadriceps 498–499
subdural 294–297
subungual 558–559
Hematuria 298–301
Hemicrania periodica neuralgiformis 86–87
Hemoglobinopathies 302–303
Hemopneumothorax 476–479
Hemorrhage
conjunctival 556–557
orbital 556
subconjunctival 556–557
Hemorrhagic conjunctivitis, acute 556
Hemothorax 476–479
Hernia, sports 552–553
Herniation, lumbar disc 366–367
Herpes gladiatorum 304–305
Herpes simplex virus (HSV) 304–305
Herpetic whitlow 290–291
High-altitude cerebral edema 306–307
High-altitude illness 306–307
High-altitude pulmonary edema 306–307
High ankle sprain 570–571
Hill Sachs lesion 270
Hind-foot 222
Hind-foot fractures, radiography for 639 639
Hip
developmental dysplasia of 116–117
radiography of
for nontraumatic disorders and chronic injury 646 647
unstable 116
Hip adduction exercise 666
Hip bruise 308–309
Hip contusion 308–309
Hip dislocation
classification of 126
posterior 126–129
prosthetic hip 128
Hip extension exercise 666
Hip flexor stretch 665
Hip pocket neuropathy 472–473
Hip pointer 168–169 308–309
Histaminic cephalalgia 86–87
Hives, exercise-induced 146–147
HLA B27-related spondyloarthropathy 548–549
Hoffman sign
in deep venous thrombosis 590
Hook fracture, hamate 200–201
Hopping
Horner's syndrome 404
Horton's headache 86–87
“Hot tub” folliculitis 164–165
Hueston tabletop test 132
Human papillomavirus (HPV), warts from 624–625
Humeral tuberosity fracture, radiography of 635 635
Humerus fracture
head 202–203
neck, radiography of 635 635
proximal 202–203
shaft 204–207
Humerus head dislocation, anterior 270–271
Humerus radiography 634 634
Hunchback 348–349
Hutchinson fracture 192–193
Hypercoagulable states 586–589
Hyperkeratotic lesions 60–61
Hyperthermia 310–311
Hypertonic hyponatremia 316–317
Hypertrophic cardiomyopathy 312–313
Hypertrophic zone 466
Hyphema 314–315
Hypobaric hypoxia 306–307
Hyponatremia 316–317
Hypothenar hammer syndrome 318–319
Hypothermia 320–321
Hypotonic hyponatremia 316–317
Hypoxia, in drowning victims 400–403
I
Iatrogenic pneumothorax 476–479
Idiopathic scoliosis 522–523
Idiopathic subaortic stenosis 312–313
Iliac crest avulsion fracture 168–169
Iliac crest contusion 308–309
Iliopsoas bursa 322
Iliopsoas bursitis 56 322–323
Iliotibial band 324
Iliotibial band friction syndrome 324–325
Iliotibial band stretch, for patellofemoral pain syndrome 665
Iliotibial band tendonitis 324–325
Ilium fracture, closed 168–169
Impetiginous impetigo 326–327
Impetigo 326–327
Impingement maneuver 19
Impingement, shoulder 328–329
Impingement test 328
Infectious arthritis 528–529
Infectious bursitis 528–529
Infectious mononucleosis 394–395
Inflammatory back pain 28
Inflammatory bowel disease, arthritis with 548–549
Inflammatory spine disease 28–29
In-fleshed toenail 414–415
Informed consent, for joint and soft tissue injection 679
Infraorbital nerve 170
Infraspinatus tear 516–517
Infraspinatus test 328
Ingrown toenail 414–415
Inguinal ligament sprain 552–553
Injection, joint and soft tissue 677–720
acromioclavicular joint 686–688 686 687
aftercare for 679
of ankle joint 713–716 714 715
billing/coding for 679
of carpal tunnel 697–699 698 699
of carpometacarpal joint, first 695–697 696 697
complications of 679
contraindications for 677
with corticosteroids 678 678 679
for de Quervain's tenosynovitis 694–695 694 695
of elbow joint 688–689 688 689
for epicondylitis 689–692 690 691
for ganglion cyst 700–703 701 702
glenohumeral 684–685 684 685
indications for 677
informed consent for 679
of knee joint 710–713 711–713
of metacarpal joint, first 719–720 719 720
for Morton's neuroma 717–719 718 719
of olecranon bursa 704–706 705 706
of pes anserine bursa 708–710 709 710
for plantar fasciitis 716–717 716 717
of prepatellar bursa 706–708 707 708
subacromial 681–683 682 683
supplies for 678
techniques for 679
with topical anesthetics 678
for trigger finger 699–700 699 700
of trigger points 680–681 681
of trochanteric bursa 703–704 703 704
for viscosupplementation 679
of wrist 692–693 692 693
Inner ear barotrauma 46–47
Inner ear bends 524
Inner ear injuries 330–331
Insulin-dependent diabetes mellitus 118–121
Intercondylar eminence fracture 262–263
Intercondylar notch radiography 639 639
Intermetatarsal neuroma 332–333
Internal oblique muscle strain 2–3
Interosseous nerve, anterior 30
Interosseous syndrome, anterior 30–31
Interphalangeal collateral ligament sprain 334–335
Interphalangeal joint dislocation, first 122–123
Intersection syndrome 336–337
Intraarticular fractures, CT for 629
Intracondylar fracture 186–187
Intracranial hematoma 294–297
Intracranial hemorrhage 294–297
Intraocular foreign bodies 338–339
Intrusion luxations (dental) 110–113
Inversion tilt test 24
Irritant contact dermatitis 100–103
Ischial tuberosity avulsion fracture 168–169
Ischium fracture, closed 168–169
Iselin disease 166–167
Isometric external rotation 674
Isometric internal rotation 674
Isometric inversion/eversion, ankle 669
Itching, exercise-induced 140
J
Jammed finger 122–123 334–335
Jersey finger 162–163 188–191
Jervell and Lange-Nielsen syndrome 80
Jobe test 564
Jock itch 600–601
Jogger's toe 558–559
Jogging
for ankle sprains 669–670
Joint injection 677–720
acromioclavicular 686–688 686 687
aftercare for 679
of ankle 713–716 714 715
of carpometacarpal, first 695–697 696 697
of elbow 688–689 688 689
for epicondylitis 689–692 690 691
glenohumeral 684–685 684 685
indications for 677
of knee 710–713 711–713
of metacarpal joint, first 719–720 719 720
supplies for 678
techniques for 679
for viscosupplementation 679
of wrist 692–693 692 693
Jones fracture 196–197
“J” sign 442
Judet views 647 647–648
Jumper's knee 444–445
Jumping
Juvenile onset spondyloarthritis 548–549
Juvenile osteochondrosis of upper extremity 362–363
Juvenile Tillaux fractures 598–599
K
Keratitis, ultraviolet 620–621
Kick test 506
Kidney
floating 508–509
mobile 508–509
Kidney trauma 508–509
Kienböck disease, fracture 214–215
Kienböck disease radiography 631 631
Kissing disease 394–395
Klenböck disease 176
Klippel-Fiel syndrome 98–99 340–341
Knee
anatomy of 710 711
injection of 710–713 711–713
Knee arthroplasty, radiographic assessment for 659 659
Knee bracing, prophylactic
for ACL injury prevention 8 10
after ACL surgery 11
Knee dislocation 342–345
Knee injuries 482
Knee radiography
for lipohemarthrosis 639 639
Merchants (bilateral patellar) view in 644 644
oblique views in 643 643
patella in 643 643
Rosenberg view in 642 642
Knee, synovitis of 506–507
Köhler (Koehler) disease 166–167 346–349
Köhler second disease 268–269
Kyphoscoliosis 348
Kyphosis 348–349
Kyphosis, Scheurmann 582–585
L
Labral “clunk” test 274
Labral tear, glenoid 274–275
Labrum, glenoid 274
radiography of 634 635 646 647
Lacerations 350–353
Lacertus fibrosis syndrome 490–491
Lachman test
for ACL injury 9 12
for turf toe 614
Laryngeal injuries 604–605
Lateral ankle sprains 24–25
Lateral collateral ligament 480
Lateral collateral ligament tear 354–355
Lateral elbow tendinosis 356–357
Lateral epicondylitis 356–357
Lateral plantar nerve 292
Lateral plantar nerve entrapment 292–293
Lateral plantar neuritis 108–109
Lateral process fracture 258–259
Lateral step up 667
Lateral talar process fracture 258–259
Le Fort fracture 210–211
Leg alignment, radiography for 659 659
Leg balance, single-leg 669
Leg extension, prone 666
Leg fracture See specific types
Leg length, radiography for 658 658
Leg press 667
Legg-Calve-Perthes disease 42–43
Leptin 410
Lhermitte sign
L-H system 264
Lice 52–53
Lidocaine test, in superficial radial nerve 562
Lightning injuries 358–359
Limb bends 524
Lisfranc fracture
Little Leaguer's elbow 360–361
Little League shoulder 362–363
Load and shift test
Locked cuboid 108–109
Long QT syndrome 80–83
Lordosis 348
Low back pain 520
general discussion of 364–365
sciatica with 520–521
Low back syndrome 364–365
Lower cervical anomalies, congenital 98–99
Lower extremity radiography 637–645
of acetabulum, Judet views 647 647–648
of ankle
acute injuries of 639 639
posterior subtalar joint of 639 639
stress views in 640 640
weight-bearing views in 640 640
femur
nonacute injury of 645 645
of femur
of foot 637 637
os calcis of 638 638
sesamoid view in 638 638
of hips
of knee
Merchants (bilateral patellar) view of 644 644
oblique views in 643 643
patella of 643 643
Rosenberg view in 642 642
of pelvis
both hips in 645 646
inlet/outlet in 648 648–649
of sacroiliac joints 647 647
sunrise axial projection in 644 644
of tibia/fibula 641 641
of toes 637 637
Lower leg syndesmodial injury 570–571
Ludington test 50
Lumbago 364–365
Lumbar disc disease 366–367
Lumbar disc herniation 366–367
Lumbar spine radiography
flex-ext series follow-up in 656 656
neutral lateral view in 656
routine imaging in 655 655
Lumbar sprain 364–365
Lumbosacral radicular syndrome 520–521
Lunate avascular necrosis 214–215
Lunate dissociation 368–369
Lunate fracture 176–177 214–215
Lunate radiography 631 631
Lunatomalacia 214–215
Lung
bruised 496–497
collapsed 476–479
Lung bends 524
Lunges 667
Lunotriquetral interosseous ligament 368
Luxation, dental 110–113
M
Malakopathy 268–269
Malgaigne's injury 408–409
Malleolus fracture
lateral and medial 208–209
posterior 238–239
Mallet finger 150–151
Mallet fracture 150 188–191
Mallet toe 286–287
Mandible radiography 651 651
Mandibular fracture 216–217
Mandibular trauma, radiography for 651 651
Marble pick-up
for ankle sprain 669
Marfan's syndrome 370–371
Mason classification, modified 244–245
Maxillary sinuses 198
Maxillofacial fractures, in children 210–211
Mayo classification 228
MCL See Medial collateral ligament
MCP See Metacarpophalangeal
Medial ankle sprains 26–27
Medial apophysitis 360–361
Medial calcaneal nerve 572
Medial collateral ligament 376
Medial collateral ligament tear 376–377
Medial epicondylar fragmentation and avulsion 360
Medial epicondylitis 360–361 378–379
Medial gastrocnemius injury 380–381
Medial instability, patellar 442
Medial plantar nerve 572
Medial plateau fracture 260–261
Medial tibial stress syndrome 382–383 670–671
treatment of 670
Median nerve entrapment 64–65 490–491
Medication overuse migraine 388–391
Mediopatellar plica test 506
Meloxicam 406
Meniscal tears 384–385
Meniscus 124 384
Meniscus, discoid 124–125
Menstrual disorders in the athlete 386–387
Menstrual migraine 388–391
Meralgia paresthetica, in pregnancy 488
Merchants (bilateral patellar) view 644 644
Metabolic syndrome 410
Metacarpal base fracture 218–219
Metacarpal joint injection, first 719–720 719 720
Metacarpal neck fracture 220–221
Metacarpal shaft fracture 218–219
Metacarpophalangeal collateral ligament sprain 372–373
Metacarpophalangeal joint 240 374
Metacarpophalangeal joint dislocation 374–375
Metacarpophalangeal joint rheumatoid arthritis 514
Metastatic bone survey, radiography for 659
Metatarsal avulsion fracture, of base of fifth metatarsal 196–197
Metatarsal-cuneiform fracture, first-second 212–213
Metatarsal disease, peculiar 268–269
Metatarsal fracture 196–197 222–223
Metatarsalgia 32
anterior 32–33
Metatarsalgia, anterior 32–33
Metatarsal head osteonecrosis 268–269
Metatarsal heads 717 718
Metatarsal sesamoid osteoarthrosis, radiography for 638 638
Metatarsal stress fracture 256–257
Metatarso-cuneiform/cuboid injury 222
Metatarso-cuneiform fracture, first-second 212–213
Metatarsophalangeal joint 719 719
Metatarsophalangeal joint injury 222
Metatarsophalangeal joint rheumatoid arthritis 514
Metatarsophalangeal joint subluxation, first MTP joint 284–285
Metatarsus primus varus 284–285
Methicillin-resistant Staphylococcus aureus (MRSA) cellulitis 66
Microhematuria 298–301
Microhyphema 314–315
Microscopic hematuria 298–301
Middle ear barotrauma 46–47
Middle phalanx fracture 224–225
Mid-foot 222
Mid-tarsal joint injury 222
Migraine headache 388–391
Migrainous neuralgia 86–87
Mild traumatic brain injury 94–97
Milking maneuver 616
Miner's elbow 412–413
Minor head trauma 94–97
Minor spinal fracture 252–253
Miserable malalignment syndrome 448
Mites 52–53
Mobile kidney 508–509
Modified Mason classification 244–245
Modified Thompson test 608
Molluscum contagiosum 392–393
Mondor sign 172
Mono 394
Mononucleosis 394–395
Monosodium urate crystal deposition 276–279
Monteggia fractures, posterior 244
Mortise ankle, radiography of 639 639
Morton foot 472
Morton's neuroma 332–333
injection of 717–719 718 719
Mosquitoes 52–53
Motion sickness 396–397
Mouthguards 110
Moving valgus stress test 616
MTP See Metatarsophalangeal joint
Mueller-Weiss disease 166–167
Mulder's click 332
Multidirectional shoulder instability 536–537
Murmur, in aortic stenosis 34
Musculotendinous unit 288
Musculoskeletal radiography 629–662 See Also Radiography, musculoskeletal
Myofasciitis, tibialis posterior 382–383
Myositis ossificans traumatica 498
Myotome 70
N
Nail ringworm 416–417
Nasal bleeding 138–139
Nasal bone, radiography of 652 652
Nasal fracture 226–227
Nasal septal destruction, radiography for 652 652
Nasal septal hematomas 398–399
Navicular
accessory 166–167
development of 346
tarsal
stress fracture of 256–257
Navicular fracture
carpal 250–251
tarsal stress fracture 256–257
Navicular secundum 166–167
Near-drowning 400–403
Neck injuries, penetrating 404–405
Neck lacerations 404–405
Neck zones 404
Neer classification 203
Neer maneuver 19
Neer test 328
Negative energy balance, in female athlete triad 158–159
Nephritic trauma 508–509
Nephroptosis 508–509
Nerve compression syndromes, in pregnancy 488
Nerve root pain 520–521
Neurapraxia, cervical cord 74–75
Neuritis
calcaneal 292
lateral plantar 108–109
sciatic 472–473
wallet 472–473
Neuromuscular scoliosis 522–523
Neutral gripping 676
Night splints, in pregnancy 488
Noble's compression test 324
Nonbullous impetigo 326–327
Non–insulin-dependent diabetes mellitus 118–121
Nonspontaneous pneumothorax 476–479
Nonsteroidal anti-inflammatory drug poisoning 406–407
Nosebleed 138–139
Nose deformity, dorsal 398
Nose picking 138
Nursemaid's elbow 408–409
Nutcracker fracture 108–109
O
Oarsman's wrist 336–337
Ober test
for iliotibial band tendonitis 324
for trochanter bursitis 612
Obesity 410–411
Oblique muscle strain 2–3
O'Brien's active compression test 274
Occipitoatlantal fusion, congenital 98–99
Occipitoatlantal instability, congenital 98–99
Occipitocervical junctional anomalies, congenital 98–99
Occipitofacial view 651 651
Occipitofrontal view 650 650
Occipitomental view 650–651 650–651
Occult injuries, MRI for 629
Oculocardiac reflex 170
Odontoid view, of cervical spine 652–653 652–653
Olecranon 228
Olecranon apophysitis 360
Olecranon avulsion fracture 608–609
Olecranon bursa
anatomy of 705 705
injection of 704–706 705 706
Olecranon bursitis 56 412–413
Olecranon fracture 228–229
Onychocryptosis 414–415
Onychomycosis 416–417
Oral lacerations 418–419
Orbit 230
Orbital blowout fractures 170–171 230–233
Orbital cellulitis 456–458
Orbital floor 230
Orbital floor fracture 170–171
Orbital fracture 230–233
Orbital hemorrhage 556
Orbital rim fracture 230–233
Orbital roof 230
Orbital septum 456
Orbital wall fracture 170–171 230–233
Ortolani test 116
Os calcis radiography 638 638
Osgood-Schlatter disease 420–421
Os naviculare (secundarium) 166–167
Osteitis pubis 422–423
Osteoarthritis 424–425
Osteochondral fractures 258–259
Osteochondral fractures, patellar 234–235
Osteochondritis
of capitellum 360
of pubic symphysis 422–423
Osteochondritis deformans juvenilis 42–43
of elbow capitellum 438–439
general discussion of 426–427
Osteochondrosis 256
of capitellum 360 438–439
of tarsal navicular 256–257
of upper extremity, juvenile 362–363
Osteolysis, distal clavicular 130–131
Osteomyelitis 428–431
Osteonecrosis
of capital femoral epiphysis of femoral head 42–43
metatarsal head 268–269
Osteopenia 432
Osteoporosis 432–433
in athlete 386
in female athlete triad 158–159
of pregnancy, transient 488–489
Os tibiale (externum) 166–167
Otitis externa 434–435
Otitis media 434–435
Ottawa Ankle Rules 208
Outlet view, at subacromial space 635 635
Overreaching 436
Overtraining 436–437
Overweight 410
Overweight management 410
Oxicams 406
P
Pace sign 472
Paget-Schroetter syndrome 580
Palmar fascia contracture 132–133
Palmar space infection 290–291
Panner disease 360 438–439
Paranasal sinus barotrauma 46–47
Paratenon 6
Paronychia 290–291 440–441
Partial seizures 526–527
Parvus tardus 34
Patella fracture 234–235
Patella radiography 643 643
Patellar dislocation 234–235 442–443
Patellar instability 442–443
Patellar subluxation 234–235
Patellar tendinitis 444–445
Patellar tendon autograft 10
Patellar tendon rupture 446–447
Patellar view, bilateral 644 644
Patellofemoral pain syndrome 448–451 664–668
causes of 664–665
description of 664
rehabilitation for
strengthening exercises in 665–668
strengthening guidelines in 665
stretching exercises in 665
stretching guidelines in 665
treatment of 665
Patellofemoral syndrome 506–507
Patrick-FABERE 612
Paxinos test 130
PCL See Posterior cruciate ligament
Pectoralis major tendon 452
Pectoralis major tendon rupture 452–453
Pectoralis stretch 673
Peculiar metatarsal disease 268–269
Pelvic fracture 236–237
radiography of
inlet/outlet in 648 648–649
Judet view in 647 647
Pelvic inlet/outlet radiography 648 648–649
Pelvis radiography
of both hips 645 646
inlet/outlet view in 648 648–649
Penile trauma, external 154–155
Percussion sign, in tarsal tunnel syndrome 572
Pericarditis 454–455
Perilunar dislocation 368–369
Perilunar dissociation 368–369
Perilunate injuries 368–369
Perionychia 440–441
Periorbital cellulitis 456–458
Peripheral arterial disease 84
Peritendinitis 114–115
Peritendinitis crepitans 336–337
Peroneal nerve 342
Peroneal tendon dislocation 458–459
Peroneal tendon subluxation 458–459
Peroneus brevis tendon 458
Peroneus longus tendon 458
Perthes disease 42–43
Pes anserine bursa
anatomy of 708 709
injection of 708–710 709 710
Pes anserine bursitis 460–461
Pes anserine tendon 460
Petrosal neuralgia of Gardner 86–87
Phalangeal injuries 462–463
Phalanx, distal, extensor tendon avulsion from 150–151
Phalanx fracture
distal 188–191
middle 224–225
proximal 240–241
Phalen test 64
Phlebitis 586–589
Phlebothrombosis 586–589
Phlegmasia cerulean dolens 590
Photoaggravated conditions 464–465
Photoallergens 464
Photoallergic eruptions 464–465
Photodermatitis 464–465
Photokeratitis 620–621
Photosensitizers 464
Phototoxic reactions 464–465
Physeal injuries in children, Salter-Harris classification of 466–467
Physiologic cardiac hypertrophy 36–37
Physis 466
Phytophotosensitizing agents 464
Pigmented villonodular synovitis 468–469
Pinna abscess 152–153
Pinna chondritis 152–153
PIN syndrome 502–503
PIP joint See Proximal interphalangeal joint
Piriformis syndrome 472–473
Pisiform fracture 176–177
Pityriasis versicolor 602–603
Pityrosporum 602
Pivot-shift test 9 12
Plantar fascia 716 716 717 718
Plantar fasciitis 474–475
injection of 716–717 716 717
treatment of 671
Plantar fasciosis 474–475
Plantar nerve entrapment, lateral 292–293
Plantar nerve, medial 572
Plantar neuritis, lateral 108–109
Plantar warts 624–625
Plica 506
Plica, redundant 506–507
Pneumothorax 476–479
Pointed-toe stretch
Policeman's heel 292
Polyarthritis 514
Polymorphous light eruption 464–465
Popeye deformity/sign
in biceps tendinitis 48
in biceps tendon rupture 50
Popliteal artery 342
Popliteal tendonitis 480–481
Popliteofibular ligament 480
Popliteus muscle 480
Porphyria cutanea tarda 464–465
Posterior capsule stretch 673
Posterior cruciate ligament 480
Posterior cruciate ligament tear 482–483
Posterior drawer test 482
Posterior glenohumeral dislocation 272–273
Posterior interosseous nerve 484
Posterior interosseous nerve syndrome 484–485 502–503
Posterior malleolus fracture 238–239
Posterior sag test 482
Posterior shoulder dislocation 272–273
Posterior talofibular ligament 24
Posterior talofibular ligament injury 24–25
Posterior tibial nerve entrapment 572–573
Posterior tibial tendinitis 382–383 594–595
Posterior tibial tendon dysfunction 594–595
Posterior tibial tendinopathy 594–595
Posterior vitreous detachment 510–511
Posterolateral capsular tear 486–487
Posterolateral corner 486
Posterolateral drawer test 486
Posterolateral rotation test 486
Posterolateral tibiofibular ligament avulsion 264–265
Post partum period, exercise in 488–489
Postseptal cellulitis 456–458
Postural roundback 348–349
Pregnancy, exercise in 488–489
Prehn sign 576
Premature ventricular contractions 62–63
Prepatellar bursa
anatomy of 706 707
injection of 706–708 707 708
Prepatellar bursitis 56
Preseptal cellulitis 456–458
Pressure epiphysis 466
Presyncope, exertional 568–569
Prisoner's palsy 562–563
Pronator quadratus, clinical isolation of 30
Pronator teres syndrome 490–491
Pronator teres stretch 675
Pronator teres syndrome 490–491
Prone hamstring curls
Prone leg extension exercise 666
Propionic acids 406
Proprioceptive training, for patellofemoral pain syndrome 666
Proteinuria 492–493
Proximal femoral epiphysis, avascular necrosis of 42–43
Proximal humeral epiphysiolysis 362–363
Proximal interphalangeal (PIP) joint
dislocations of 470–471
flexion deformity of 68–69
rheumatoid arthritis of 514
Proximal phalanx fracture 240–241
Proximal tibia fracture 242–243
Pseudoanemia 494–495
Pseudoarthritis 58
Pseudoboutonniere deformities 68–69
Pseudoclaudication 84
Pseudogout 58–59 276–279
Pseudohyponatremia 316–317
Pseudorheumatoid arthritis 58
Psoriatic arthritis 548–549

Pubalgia, athletic 422–423
Pubic symphysis enthesopathy 422–423
Pubic symphysitis 422–423
Pulled elbow 408–409
Pulled groin 16–17
Pulmonary barotrauma 46–47 524
Pulmonary contusion 496–497
Pulmonary embolism 590
Pump bump 282–283
Push-off test 570
Pyogenic arthritis 528–529
Pyrazolones 406
Pyrophosphate arthropathy 58–59
Q
Quadriceps active test 482
Quadriceps contusion 498–499
Quadriceps hematoma 498–499
Quadriceps (quad) set 665
Quadriceps strains 500–501
Quadriceps stretch 665
Quadriceps tear 500–501
Quadriceps tendinitis 444–445
Quadriceps tendon rupture 446–447
Quadrilateral space 44
Quadrilateral space syndrome 44
R
Radial head fracture 244–245
Radial head subluxation 408–409
Radial nerve 562
Radial nerve injury, with humeral shaft fracture 207
Radial nerve, superficial 562–563
Radial sensory nerve entrapment 562–563
Radial tunnel syndrome 502–503
Radiation 310
Radiculopathy 520–521
Radiculopathy, cervical 70–73
Radiocapitellar subluxation 408–409
Radiocarpal joint 692 692
Radiography, musculoskeletal 629–662
arthritis joint survey in 659
for intraarticular fracture, CT in 629
for leg alignment 659 659
for leg length 658 658
of lower extremities 637–645 See Also Lower extremity radiography
metastatic bone survey in 659
of pelvis 645–646
scan-o-gram in 658 658
of soft tissues
MRI 629
ultrasound 629
of thorax, bony 660–662
ribs 660 660
sternoclavicular joints 661 661–662
sternum 661 661
of upper extremities 629–636 See Also Upper extremity radiography
of vertebral column 649–658 See Also Vertebral column radiography
Rami fracture
radiography of 648 648–649
Rami fracture, pelvic 236–237
Reactive arthritis 548–549
Rectus abdominus muscle strain 2–3
Rectus femoris 500
Recurrent otitis media 434–435
Red eye 504–505
Redundant plica 506–507
Rehabilitation, office 663–676 See Also specific disorders
for epicondylitis 674–676
for hamstring strain 663–664
for patellofemoral pain syndrome 664–668
for plantar fasciitis 671–672
for rotator cuff tendinitis 672–674
for shin splints (medial tibial stress syndrome) 670–671
Relocation test
Renal trauma 508–509
Retina 510
Retinal detachment 510–511
Retinal migraine 388–391
Retinal tear 510–511
Reverse Barton fracture 192–193
Reverse mallet fracture 188–191
Reverse pivot shift test 486
Rhabdomyolysis 512–513
Rhegmatous retinal detachment 510–511
seronegative 548–549
in sports 514–515
Rib fracture 246–247
RICE 606
Ringworm 600–601
Rinne test 330
Risser sign 523
Rolando fracture 218–219
Romano-Ward syndrome 80
Romberg test 544
Root fracture (dental) 110–113
Rosenberg view, of knee 642 642
Rotator cuff impingement 50
Rotator cuff muscles 516
Rotator cuff tears 270 516–517
Rotator cuff tendinitis 328–329
causes of 673
description of 672–673
treatment of 673
Rotator interval lesions 50
Roundback, postural 348–349
Row, single 674
Runner's diarrhea 144–145
Runner's heel 292
Runner's knee 448–451
Runner's trots 144–145
Running
Rupture
scleral 556
splenic 546–547
tendon See Tendon rupture
Russell sign, in eating disorders 135
S
Sacral fracture 248–249
Sacral plexus injuries, radiography of 656 656
Sacroiliac joint radiography 647 647
Sacrum radiography 656 656
Safety baseballs 560
Salicylates 406
Salter-Harris classification, of physeal injuries in children 466–467
Salter-Harris fractures 264
type I 188–191 202
type II 188–191
SCA 560–561
Scan-o-gram 658 658
Scaphoid bone, accessory 166–167
Scaphoid bone fracture 176–177 250–251
Scaphoid fracture
Scaphoid instability, dynamic or occult 518–519
Scaphoid radiography 631 631
Scapholunate advanced collapse (SLAC) 518–519
Scapholunate dislocation 368–369
Scapholunate dissociation 368–369 518–519
Scapholunate interosseous ligament 368
Scapula
snapping 542–543
winging 542–543
Scapulothoracic friction syndromes, radiography of 636 636
Scapulothoracic syndrome, radiography of 636 636
Scarf test 14
Schatzker classification 260
Scheuermann's juvenile kyphosis 348–349
Scheuermann kyphosis 582–585
Sciatica 472–473 520–521
Sciatic nerve pain 520
from lumbar disc herniation 366–367
in piriformis syndrome 472–473
Sciatic neuritis 472–473
Scleral rupture 556
Scoliometer
for kyphosis 348
for scoliosis 522
Scoliosis 348–349 522–523
radiography for
additional views in 658 658
series in 657 657
Scorpion bites 52–53
Scratch test 106
Scrotum
acute 576
external trauma to 154–155
Scrum strep 326–327
Scuba diving 524–525
Sea sickness 396–397
Seated hamstring stretch
Secretory otitis media 434–435
Seizures 526–527
Sentinel spinous process fractures 252–253
Septal hematoma, nasal 398–399
Septal hypertrophy, asymmetric 312–313
Septic arthritis 528–529
Septic bursitis 56–57 528–529
Septic thrombophlebitis 586–589
Septum, orbital 456
Seronegative rheumatoid arthritis 548–549
Seronegative spondyloarthropathy 548–549
Sesamoid bones 530
Sesamoid dysfunction 530–531
Sesamoid fracture, radiography for 638 638
Sesamoid osteoarthrosis, radiography for 638 638
Sesamoiditis 530–531
Sesamoiditis stress fracture 530–531
Sever disease 534–535
Sexual headache 148–149
Seymour fracture 188–191
Shepherd fracture 258–259
Shin splints 382–383
treatment of 670
Shoe-removal maneuver 480
Short-arc knee extension exercise 666
Shoulder
adhesive capsulitis of 18–19
calcific tendonitis of 328–329
floating 179
“frozen” 18–19
Little League 362–363
radiography of
for bony Bankart lesions 635 635
for dislocation without arm raise 635 635
for Hill Sachs lesions 635 635
for nontraumatic injury and chronic pain 634 635
for rotator cuff calcium 635 635
subacromial space in 635 635
Shoulder abduction 674
Shoulder dislocation 14–15
anterior 270–271
posterior 272–273
Shoulder external rotation 673
Shoulder flexion 674
Shoulder impingement syndrome 328–329
Shoulder instability 272–273
anterior 534–535
multidirectional 536–537
Shoulder separation 14–15
Shoulder sprain 14–15
Shunt continuity, radiography for 649 649
Sickle cell trait 302–303
Side flash 358–359
Sigmoid notch 184
Silver-fork deformity 192–193
Simmonds-Thompson test, negative 4
Single-leg balance 669
Single leg stance with clock reach 669
Single-limb heel-rise test 594
Single row, for rotator cuff tendinitis 674
Sinus arrhythmias 62–63
Sinus tarsi 538
Sinus tarsi syndrome 538–539
Sitting knee extension 520
Skier's thumb 372–373 592–593
Skin adhesives 352
Skin bends 524
Skin closure 352
Skull radiography 649 649
SLAP lesion 274–275
Sleeve fractures, pediatric patellar 234–235
Slipped capital femoral epiphysis 540–541
Sluder neuralgia 86–87
Smith fracture 192–193
Snapping hip syndrome 322–323
Snapping scapula syndrome 542–543
“Snowboarder's ankle” 258–259
Soft tissue
MRI for 629
ultrasound for 629
Soft tissue injection
aftercare for 679
for ganglion cyst 700–703 701 702
indications for 677
for Morton's neuroma 717–719 718 719
of olecranon bursa 704–706 705 706
of pes anserine bursa 708–710 709 710
for plantar fasciitis 716–717 716 717
of prepatellar bursa 706–708 707 708
supplies for 678
techniques for 679
for trigger finger 699–700 699 700
trigger point 680–681 681
of trochanteric bursa 703–704 703 704
of wrist 692–693 692 693
Soft tissue injuries 350–353
Solar urticaria 464–465
Soleus syndrome 382–383
Spear tackler spine 182
Speeds maneuver, in adhesive capsulitis 19
Speed test 328
for biceps tendinitis 48
for biceps tendon rupture 50
for SLAP lesion 274
Spells 526–527
Sphenopalatine neuralgia 86–87
Spider bites 52–53
Spinal compression fractures 182
Spinal cord bends 524
Spinal decompression sickness 524
Spinal fracture See Also specific types
minor 252–253
Spinal stenosis 544–545
Spinal stenosis, functional 74
Spinal tumors 582–585
Spine curvature 348–349
Spinner tests 490
Spinoglenoid ligament 564
Spinous process fracture 252–253
Splenic contusion 546–547
Splenic rupture 546–547
Spondyloarthritis
ankylosing spondylitis 28–29
subtypes of 28
Spondyloarthropathies 548–549
Spondylolisthesis 550–551
Spondylolysis 550–551
Spondylolytic spondylolisthesis 550–551
Spontaneous pneumothorax 476–479
Sporadic hemiplegic migraine 388–391
Sports anemia 494–495
Sports hernias 552–553
Sportsman's hernias 552–553
Sportsman's toe 558–559
Sprinting
Spurling foraminal compression test 74
Spurling maneuver
for axillary nerve injury 44
Spurling test, for cervical strains 77
Squats 668
Squeaker's wrist 336–337
Squeeze test
for medial ankle sprain 26
for syndesmodial injury of lower leg 570
Stabilization test 570
Stance, single leg, with clock reach 669
Standing hamstring curls 664
Standing hamstring stretch 663
Staggers 524
Staphylococcus aureus
cellulitis from 66
felon from 156
folliculitis from 164–165
impetigo from 326–327
Staples 352
Status epilepticus 526
Steering wheel injury 246–247
Stener lesion 372 592
Stenosing tendonitis 114–115
Stenosing tenovaginitis 114–115
Stenosis
aortic 34–35
cervical 74–75
spinal 544–545
spinal, functional 74
subaortic, idiopathic 312–313
Step ups 667
Sternoclavicular joint 554
Sternoclavicular joint injury 554–555
Sternum radiography 661 661
Sternum fracture 254–255
Stimson method 127

Stingers 54–55
Stings 52–53
Stone bruise 292
Stove-in chest 246–247
Straddle injuries 622
Straight-leg raise exercise 666
Straight-leg raise test, for sciatica 520
Straight-leg test, for spinal stenosis 544
Strains See specific types
Streptococcus, group A beta-hemolytic, impetigo from 326–327
Streptococcus pyogenes cellulitis 66
Stress fracture See Also specific types
diaphyseal 196–197
metatarsal 256–257
sesamoid 530–531
tarsal navicular 256–257
tibial 596–597
Stryker view, of shoulder 635 635
Student's elbow 412–413
Styloid tenovaginitis 114–115
Subacromial bursitis 56 328–329
Subacromial injection 681–683 682 683
Subacromial space 681 682
Subaortic stenosis, idiopathic 312–313
Subcalcaneobursitis 292
Subconjunctival hemorrhage 556–557
Subdeltoid bursitis 56
Subdural hematomas 294–297
Subdural hemorrhage 294–297
Sublimis bridge syndrome 490–491
Subluxation
atlantoaxial 38–39
cuboid 108–109
elbow 136–137
femoral head 116
glenohumeral 534–535
patellar 234–235
peroneal tendon 458–459
radial head 408–409
radiocapitellar 408–409
of radius by elongation 408–409
Submetatarsal head pain 32–33
Subscapularis partial rupture 50
Subscapularis rupture 50
Subscapularis tear 516–517
Subtalar facet, middle, radiography of 638 638
Subtalar joint
posterior, radiography of 639 639
Subungual exostosis 558–559
Subungual hematoma 558–559
Subungual onychomycosis 416–417
Sudden cardiac arrest, from commotio cordis 560–561
Sudden cardiac death, from channelopathies 80–83
Sulcus sign 270
Sulcus test 536
Sunrise axial projection 644 644
Sunscreens 464
Sun spots 602
Superficial radial nerve 562–563
Superficial septic bursitis 56–57
Superficial thrombophlebitis 586–589
Superficial venous thrombosis 586–589
Superior labrum anterior posterior (SLAP) lesion 50 274–275
Suppurative otitis media 434–435
Suppurative thrombophlebitis 586–589
Supracondylar fracture 186–187
Suprascapular nerve palsy 564–565
Supraspinatus tear 516–517
Supraventricular tachycardia 62–63
Surfer's ear 566–567
Surgical tape 352
Sutures 352
Swan-neck deformity 188–191
Swimmer's ear 434–435
Swimmer's view, of cervical spine 652 653 654 655 655
Symptomatic accessory tarsal navicular 166–167
Syncope 568–569
Syndesmodial injury of lower leg 570–571
Synovitis
of knee 506–507
pigmented villonodular 468–469
Synovitis joint fluid, in hand, radiography for 630 630
T
Table fracture, anterior 198
Tachyarrhythmias 62–63
Tailbone, broken 180–181
Talar head fracture 258–259
Talar neck fracture 258–259
Talocalcaneal interosseous ligament 538
Talofibular ligament, anterior 24
Talofibular ligament injury, anterior 24–25
Talus fracture 258–259
Tape, surgical 352
Tarsal navicular
symptomatic accessory 166–167
Tarsal navicular stress fracture 256–257
Tarsal scaphoid, accessory 166–167
Tarsal tunnel 572
Tarsal tunnel syndrome 572–573
Tarsometatarsal fracture 212–213
Tear See Also Tendon rupture
Achilles 6–7
anterior cruciate ligament 12–13
glenoid labral 274–275
infraspinatus 516–517
lateral collateral ligament 354–355
medial collateral ligament 376–377
meniscal 384–385
meniscal cartilage 384
posterior cruciate ligament 482–483
posterolateral capsular 486–487
retinal 510–511
rotator cuff 270 516–517
subscapularis 516–517
supraspinatus 516–517
teres minor 516–517
triangular fibrocartilage complex 578–579
triceps tendon 608–609
Teeth barotrauma 46–47
Teeth trauma 110–113
Temper tantrum elbow 408–409
Temporomandibular joint injury 574–575
Tendinitis (tendonitis)
Achilles' 4–5
biceps 48–49
etiology and pathology of 160
extensor 114–115
flexor carpi radialis 160–161
flexor carpi ulnaris 160–161
iliotibial band 324–325
patellar 444–445
peritendinitis 114–115
popliteal 480–481
rotator cuff 328–329
stenosing 114–115
tibialis posterior 382–383 594–595
triceps 606–607
Tendinopathy
Achilles 4–5
biceps 48
definition of 612
posterior tibial 594–595
Tendinosis 4 48 160
Achilles 4–5
definition of 612
elbow, lateral 356–357
Tendonitis See Tendinitis (tendonitis)
Tendonosynovitis, stenosing 114–115
Tendon rupture See Also Tear; specific types
Achilles' 6–7
biceps 50–51
gastrocnemius 6–7
heel-cord 6–7
patellar 446–447
pectoralis major 452–453
posterior cruciate ligament 482–483
subscapularis 50
triceps 608–609
Tendosynovitis 160
Tennis elbow 356–357
Tennis fracture 196–197
Tennis heel 292
Tennis leg 380–381
“Tennis player's thigh” 100
Tennis toe 558–559
Tenosynovitis 48
de Quervain 114–115 488
flexor 290–291 610–611
Tenovaginitis
stenosing 114–115
styloid 114–115
Tension pneumothorax 476–479
Teratologic dislocation, femoral head 116
Teres minor tear 516–517
Terrible triad 244
Testicular torsion 576–577
Testicular trauma, external 154–155
Tests See specific tests and disorders
Tetanus vaccine 353
TFCC tears 578–579
Thalassemia 302–303
Thalassemia minor 302
Thera-band exercises
for ankle sprain 669
for shin splints 670–671
Thigh bruise 498–499
Thigh strain, adductor muscle 16–17
30-30 rule 358 359
Thompson test
modified 608
positive 6
Thoracic diskogenic pain 582–585
Thoracic outlet syndrome 580–581
Thoracic spine fracture 582–585
Thoracic spine injury 582–585
Thoracic spine radiography 654 654
Thoracic trauma, blunt, pulmonary contusion from 496–497
Thoracolumbar spine 182
Thorax, bony, radiography of 660–662
ribs 660 660
sternoclavicular joints 661 661–662
sternum 661 661
Thrombophlebitis
aseptic 586–589
septic (suppurative) 586–589
superficial 586–589
Thrombosis, venous 590
deep 590–591
upper extremity 580
Thumb
CMC joint of
anatomy of 695 696
injection of 695–697 696 697
gamekeeper's 372–373 592–593
skier's 372–373 592–593
ulnar collateral ligament injuries of MCP joint of 372–373
Thumb ulnar collateral ligament sprain 592–593
Tibia-fibula ligament avulsion, anterior 598–599
Tibia fracture
distal, transitional fracture 598–599
proximal 242–243
stress 596–597
Tibia radiography 641 641
Tibial condylar fracture 260–261
Tibial eminence fracture 262–263
Tibial nerve 572
Tibial nerve entrapment, posterior 572–573
Tibial plateau fracture 242–243 260–261
Tibial spine avulsion fracture, in skeletally immature 12
Tibial stress syndrome, medial 382–383
Tibial tendonopathy, posterior 594–595
Tibial tubercle, traction apophysitis of 420–421
Tibialis posterior myofasciitis 382–383
Tibialis posterior tendonitis 382–383 594–595
Tibiofibular ligament avulsion, posterolateral 264–265
Tick bites 52–53
Tillaux fractures 598–599
Tinea capitis 600–601
Tinea corporis 600–601
Tinea cruris 600–601
Tinea gladiatorum 600–601
Tinea pedis 600–601
Tinea unguium 416–417
Tinea versicolor 602–603
Tinel sign
in carpal tunnel syndrome 64
in cubital tunnel syndrome 106
in superficial radial nerve 562
in tarsal tunnel syndrome 572
TMJ pain dysfunction syndrome 574–575
Toe
claw 286–287
hammer 286–287
jogger's 560–561
mallet 286–287
sportsman's 560–561
tennis 560–561
turf 614–615
Too many toes sign 594
Tooth avulsion 110–113
Tooth exarticulation 110–113
Tooth fractures 110–113
Tophaceous gout 276–279
Topical anesthetic injection 678
Torsion of appendix testis 576
Towel crunches
Towel squeeze 665
Towel stretch
Achilles, for ankle sprains 668
internal rotation, for rotator cuff tendinitis 673
Townes view, of skull 649 649
Tracheal injuries 604–605
Tractional retinal detachment 510–511
Traction apophysitis
at fifth metatarsal base 166
of tibial tubercle 420–421
Traction epiphysis 466
Training logs, daily 436
Training techniques, proper 436
Transient osteoporosis of pregnancy 488–489
Transitional fracture of distal tibia 598–599
Transverse abdominus muscle strain 2–3
Transverse process fracture 252–253
Trapdoor fracture 170
Trapezium fracture 176–177
Trapezoid fracture 176–177
Traumatic brain injury
epidural and subdural hematomas from 294–297
mild 94–97
Traumatic pneumothorax 476–479
Trendelenburg sign 612
Trephination 296
Triangular fibrocartilage complex tears 578–579
Triceps muscle tear 608–609
Triceps stretch 675
Triceps tendinitis 606–607
Triceps tendon rupture 608–609
Triceps tendon tear 608–609
Trigger finger 610–611
Trigger point injection 680–681 681
Triquetrum fracture 176–177
Trochanteric bursa
anatomy of 703 703
injection of 703–704 703 704
Trochanter(ic) bursitis 56 612–613
Tuber calcaneal pain 292
Tuberosity, avulsion fracture of 196–197
Tuft fracture 188–191
Turf toe 614–615
Tympanic membrane perforation 330–331
Type 1 diabetes 118–121
Type 2 diabetes 118–121
U
Ulna, hypertrophy of 360
Ulnar canal 618
Ulnar collateral ligament injuries
avulsion, radiography for 629 630
of elbow 616–617
of MCP joint of thumb 372–373 592–593
Ulnar collateral ligament sprain 372–373
Ulnar nerve compression, cubital tunnel syndrome from 106–108
Ulnar tunnel syndrome 106–108 618–619
Ultrasound, for soft tissue trauma and masses 629
Ultraviolet (UV) keratitis 620–621
Ultraviolet (UV) radiation 464
Undifferentiated spondyloarthropathy 550–551
Unguis incarnatus 414–415
Unstable hip 116
Upper cervical anomalies, congenital 98–99
Upper extremity radiography 629–636
of acromioclavicular joints 636 636
of clavicles 636 636
elbow
for nontraumatic disorders 632 633
for trauma 633 633
of elbow
for cubital tunnel causes 633 634
of fingers 629 629
of forearm 632 632
of hand
arthritis survey in 630 630
routine 630 630
of humerus 634 634
of scapula 636 636
of shoulder
for bony Bankart lesions 635 635
for dislocation without arm raise 635 635
for Hill Sachs lesions 635 635
for nontraumatic disorders and chronic pain 634 635
for rotator cuff calcium 635 635
of subacromial space 635 635
of thumb 629 630
of wrist
clenched fist views in 631 632
for nontraumatic disorders and infection 631 631
for trauma 631 631
Upper extremity venous thrombosis 580
Upper limb tension tests 580
Ureteral trauma 622–623
Urethral trauma
external 154–155
general 622–623
Urticaria
cholinergic, exercise-induced 140 146
cold 20
exercise-induced 140 146–147
solar 464–465
UVA 464
UVA filters 464
UVB 464
UVB filters 464
V
Vaccine, tetanus 353
Vaginal trauma, external 154–155
Valgus deformity 242
Valgus stress test 616
Valgus talar tilt test 26
Valsalva maneuver, headache from 148–149
Valvular heart disease, aortic stenosis 34–35
Varus deformity 242
Velpeau view, of shoulder 635 635
Venous thrombosis 590
deep 590–591
upper extremity 580
Ventricular fibrillation, in commotio cordis 518–519
Ventricular tachycardia
in commotio cordis 518–519
familial catecholaminergic polymorphic 80–83
Verruca plana 624–625
Verruca plantaris 624–625
Verruca vulgaris 624–625
Vertebral column radiography 649–658
of cervical spine
complete 652 652–653
flex-ext series in 654 654
limited 653 653
swimmer's view in 652 653 654 655 655
of coccyx 657 657
of eyes 651 651
of face 650 650
of lumbar spine
flex-ext series follow-up in 656 656
neutral lateral view in 656
routine imaging in 655 655
of mandible 651 651
of nasal bone 652 652
of orbits 651 651
of sacrum 656 656
for scoliosis
additional views in 658 658
series in 657 657
of skull 649 649
of thoracic spine 654 654
Virchow's triad 590
Viridian neuralgia 86–87
Viscosupplementation, injection for 679
Vitreous detachment, posterior 510–511
Volar plate 374
Volkmann fracture 264–265
W
Wall slides 667
Wallet neuritis 472–473
Wand stretch, for rotator cuff tendinitis 673
Wartenberg disease 562–563
Wartenberg sign 618
Wartenberg syndrome entrapment 562–563
Warts 624–625
Wasp stings 52–53
Watanabe classification, of discoid meniscus 124
Watson scaphoid shift test 520
Weber test 330
Wedge fracture 182
Weight gain 410
Weight shifts 669
Weightlifter's headache 148–149
Weight management 410–411
Westpoint view, of shoulder 635 635
Whiplash 76–79
Whiplash-associated disorders 76–79
Whistler method 127
White superficial onychomycosis 416–417
Winging scapula 544–545
Wolff-Parkinson-White (WPW) syndrome 62–63 626–627
Wounds
dressing of 352
open 350–353
Wright test 580
Wrisburg type discoid meniscus 124
Wrist extension curls 675
Wrist extension stretch 675
Wrist flexion curls 675
Wrist flexion stretch 675
Wrist fracture 176–177 See Also specific types
Wrist injection 692–693 692 693
Wrist joint capsule 692 692
Wrist radiography
clenched fist views in 631 632
for nontraumatic disorders and infection 631 631
for trauma 631 631
Y
Yergason test
for biceps tendinitis 48
for biceps tendon rupture 50
Young-Burgess system 236
Z
Zygoma fracture 266–267

The 5-Minute Sports Medicine Consult 2nd Edition 2011

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The 5-Minute Sports Medicine Consult 2nd Edition 2011

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2011

Lippincott Williams & Wilkins

Copyright 2011 by LIPPINCOTT WILLIAMS & WILKINS a WOLTERS KLUWER business

Andrea L. Pana MD, MPH

Delmas J. Bolin MD, PhD

Jeffrey R. Bytomski DO, FAOASM

James M. Daniels II MD, MPH, FAAFP, FACPM, FACOEM

Mark I. Ellen MD, FABPMR, CAQ-SM

Kim Fagan MD, FACP

George D. Harris MD, MS

Shawn F. Kane MD, LTC, MC, US Army

Chris Koutures MD, FAAP

Kim Edward LeBlanc MD, PhD, FAAFP, FACSM

Deepak S. Patel MD, FAAFP

George G.A. Pujalte MD, CAQSM

Margot Putukian MD, FACSM

Sam Rifat MD, FACSM

Brent S. E. Rich MD, ATC

Suraj A. Achar MD, FAAFP

Chad A. Asplund MD, FACSM

Robert J. Baker MD, PhD, ATC

Karrn Bales DO, CAQSM, Board Certified ABFM

Kenneth Barnes MD, MSc, CAQSM

David E. J. Bazzo MD, FAAFP

Holly J. Benjamin MD, FAAP, FACSM

W. Scott Black MD, MS

Delmas J. Bolin MD, PhD

James R. Borchers MD, MPH

William W. Briner Jr. MD, FACSM, FAAFP CAQ

Stacey L. Brown Brocklehurst MD

Jeffrey R. Bytomski DO, FAOASM

David Carfagno DO, CAQSM

Kyle J. Cassas MD, GHS

Julie J. Chuan MD, FAAFP

Kristen Samuhel Clarey MD

Rachel A. Coel MD, PhD

Kara D. Cox MD, FAAFP

Steven C. Cuff MD, FAAP

Claudia Dal Molin DO

Marjorie Delo MD, CAQSM

Rania L. Dempsey MD, MS

Kevin deWeber MD, FAAFP, LTC(P), Medical Corps, Army, USUHS

Kevin E. Elder MD, FAAFP

Ryan C. Fowler MD, LCDR, MC, USN

Rodney S. Gonzalez MD, FAAFP

Steven A. Greer MD, CAQ Sports Medicine

COL Mark D. Harris MD, MPH, Medical Corps, Army, USUHS

Michal “Kalli” Hose MD

Tudor Hesketh Hughes MD, FRCR

Arthur Islas MD, MPH, FAWM, CAQSM

Carrie A. Jaworski MD, FACSM, FAAFP

Sandeep Johar DO, MS

Scott Fister Johnson MD

Rahul Kapur MD, CAQSM

Robert B. Kiningham MD, FACSM

K. Michele Kirk MD, CAQ Sports Medicine

Jennifer Scott Koontz MD, MPH

Chris Koutures MD, FAAP

Jeffrey B. Kreher MD, FAAP

Geoffrey Kuhlman MD, CAQSM, FAAFP

Mark E. Lavallee MD, CSCS, FACSM

Lt Col (P) Jeffrey C. Leggit MD, CAQSM

Kelsey Logan MD, FAAP

James H. Lynch MD, MS

Navid Mahooti MD, MPH

Sean McKeown MS, PT, Cred MDT

Brent H. Messick MD, MS