You are on page 1of 435

P E M C

Pediatric
IP : 196.52.84.10
Emergency
Medicine Course
The 60 seconds advantage to get sick kids
back on track... with a smile!

IP : 196.52.84.10
IP : 196.52.84.10

Disclaimer
Every effort has been made to ensure that the drug doses herein are accurate and in accordance
with the standards accepted at the time of publication. However, the user is advised to check
the doses carefully. The author shall not be responsible for any error in this publication.
Besides, as new research and experience broaden our knowledge, changes in treatment and
drug therapy occur. Therefore, the reader is advised to check the product information sheet
included in the package of every drug he/she plans to administer to be certain that changes have
not been made in the recommended dosage or in the contraindications. This is of particular
importance in regard to new or infrequently used drugs. In addition the protocols given in this
IP : 196.52.84.10
book are valid at the time of publication and are subject to constant review.

The ‘Pediatric Emergency Medicine Course’— ‘PEMC’. The name and the power point
presentations have been legally copyrighted to the Indian Society of Critical Care Medicine-
Chennai Chapter. The name of the course ‘Pediatric Emergency Medicine Course’ or ‘PEMC’
or its contents cannot be used by other individuals or societies in conducting courses of
this nature without the written consent of the ISCCM-Chennai Chapter. No unauthorized
copying/editing, etc. of the manual or power point presentations from the course material
are permitted. Use of the name or course content as mentioned above will imply violation of
copyright laws.
Pediatric
Emergency

P E M C
IP : 196.52.84.10

Medicine Course
The 60 seconds advantage to get sick kids
back on track... with a smile!
Second Edition
IP : 196.52.84.10

Editor
Indumathy Santhanam md dch
Professor and Head
Department of Pediatrics
Government Royapettah Hospital
Kilpauk Medical College
Chennai, Tamil Nadu, India

Jaypee Brothers Medical Publishers (P) Ltd


New Delhi • London • Philadelphia • Panama
®

Jaypee Brothers Medical Publishers (P) Ltd

IP : 196.52.84.10 Headquarters
Jaypee Brothers Medical Publishers (P) Ltd
4838/24, Ansari Road, Daryaganj
New Delhi 110 002, India
Phone: +91-11-43574357
Fax: +91-11-43574314
Email: jaypee@jaypeebrothers.com

Overseas Offices
J.P. Medical Ltd Jaypee-Highlights Medical Publishers Inc Jaypee Medical Inc
83 Victoria Street, London City of Knowledge, Bld. 237, Clayton The Bourse
SW1H 0HW (UK) Panama City, Panama 111 South Independence Mall East
Phone: +44-2031708910 Phone: + 507-301-0496 Suite 835, Philadelphia, PA 19106, USA
Fax: +02-03-0086180 Fax: + 507-301-0499 Phone: + 267-519-9789
IP : 196.52.84.10
Email: info@jpmedpub.com Email: cservice@jphmedical.com Email: joe.rusko@jaypeebrothers.com

Jaypee Brothers Medical Publishers (P) Ltd Jaypee Brothers Medical Publishers (P) Ltd
17/1-B Babar Road, Block-B, Shaymali Shorakhute, Kathmandu
Mohammadpur, Dhaka-1207 Nepal
Bangladesh Phone: +00977-9841528578
Mobile: +08801912003485 Email: jaypee.nepal@gmail.com
Email: jaypeedhaka@gmail.com

Website: www.jaypeebrothers.com
Website: www.jaypeedigital.com

© 2013, Jaypee Brothers Medical Publishers

All rights reserved. No part of this book may be reproduced in any form or by any means without the prior permission of the
publisher.
Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com
This book has been published in good faith that the contents provided by the contributors contained herein are original, and
is intended for educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the
editor specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the
contents of this work. If not specifically stated, all figures and tables are courtesy of the editor. Where appropriate, the readers
should consult with a specialist or contact the manufacturer of the drug or device.

Pediatric Emergency Medicine Course (PEMC)


First Edition: 2008
Reprint: 2011
Second Edition: 2013
ISBN 978-93-5090-694-1
Printed at
IP : 196.52.84.10

Dedicated to
IP : 196.52.84.10 The postgraduates and nurses of
Institute of Child Health, Madras Medical College, whose disciplined efforts,
skills and insights have helped establish the founding principles behind the
‘60 seconds advantage’ in saving lives.
IP : 196.52.84.10

∫ ∫
satyameva jayate nān™taˆ
satyena panthā vitato devayānaƒ |
yenākramanty™¢ayo hyāptakāmā
yatra tat satyasya paramaˆ nidhānam ||
IP : 196.52.84.10
Truth alone triumphs; not falsehood.
Through truth the divine path is spread out by which
the sages whose desires have been completely fulfilled,
reach where that supreme treasure of Truth resides.

Mundaka Upanishad
3.1.6
circa 2500 BCE
Contributors

IP : 196.52.84.10 Editor in Chief Associate Editor


Indumathy Santhanam md dch
Janani Shankar dnb phD
Professor and Head
Senior Consultant
Department of Pediatrics
Kanchi Kamakoti Childs Trust
Government Royapettah
Hospital
Hospital
Chennai, Tamil Nadu, India
Kilpauk Medical College
Chennai, Tamil Nadu, India Procedures
All topics except those from
contributors

Associate Editor Associate Editor


IP : 196.52.84.10 Jayanthi Ramesh dnb Radhika Raman dnb
Senior Consultant Senior Consultant
Kanchi Kamakoti Childs Trust Kanchi Kamakoti Childs Trust
Hospital Hospital
Chennai, Tamil Nadu, India Chennai, Tamil Nadu, India
Procedures Procedures

Associate Editor
Associate Editor
Shanthi Sangareddi md dch
Thangavelu S md mrcph
Associate Professor
Senior Consultant
Chinglepet Medical College
Mehtas’ Children’s Hospital
Chinglepet, Tamil Nadu, India
Chennai, Tamil Nadu, India
Hypertension
Interpretation of Chest
DKA
Radiographs
Dengue

Associate Editor
Associate Editor
Ramesh Babu B
Balaji J
Assistant Professor
Assistant Professor
Government Dharmapuri
Government Dharmapuri
Medical College
Medical College
Dharmapuri, Tamil Nadu, India
Dharmapuri, Tamil Nadu, India
Emergency Medications and
Snake Envenomation
Equipments
viii Pediatric Emergency Medicine Course (PEMC)

Guest Editors
Mahadevan md Suresh Gupta md dch
Professor and Head Consultant Pediatrician
Department of Pediatrics Pediatric Emergency
Jawaharlal Institute of Postgraduate Department
Medical Education and Research Sir Ganga Ram Hospital
IP : 196.52.84.10 Puducherry, India New Delhi, India
Envenomation Poisons

Contributors
Thanyanat Bunnag md Pradeep Padmanabhan md msc
Professor Assistant Professor
Queen Sirikit National Institute of Child Health Division of Pediatric Emergency Medicine
Bangkok, Thailand University of Louisville
Louisville, KY, USA
Pra-on Supradish md Pain and Sedation in the ED
Queen Sirikit National Institute of Child Health
Bangkok, Thailand Jayshree Muralidharan md
IP : 196.52.84.10
Additional Professor
Siripen Kalayanarooj md Department of Pediatric Intensive Care
Queen Sirikit National Institute of Child Health Advance Pediatric Center
Bangkok, Thailand Postgraduate Institute of Medical Education and Research
Dengue Chandigarh, India
Diabetic Ketoacidosis
Ramesh Menon P
Senior Lecturer Yuri Gilhotra
Department of Pediatrics Consultant
TD Medical College Division of Pediatric Emergency Medicine
Alappuzha, Kerala, India University of Brisbane
Australia
Rakesh Lodha
Assistant Professor Sonia Singh
All India Institute of Medical Sciences Consultant
New Delhi, India Division of Pediatric Emergency Medicine
Specific Poisons University of Pittsburgh
USA
Severe Traumatic Brain Injury
Contributors ix

Student Editorial Committee (Institute of Child Health, Madras Medical College)

IP : 196.52.84.10

Associate Editor Associate Editor Associate Editor


Editor in Chief
Padmavathy Sangeetha Yoganand Rajeshwari Sridharan
Gunda Srinivas dch (2007)
Venkatasubbu dch (2010) md dm (2005) md (2007)

IP : 196.52.84.10

Associate Editor Associate Editor Vishwanthan T md (2002) Prasanna dnb (2002)


Kumar N md (2005) Ramkumar md dm (2007)

Naushad Mallagi dnb Jyothsna S dch mrcph Jayaprakash mrcph Narmada dch dnb mrcph
(2002) (2003) (2003) (2003)

Sendhil Kumar KS md Shekhar md dch Padma dnb Priyavardhini md


(2003) (2004) (2004) (2005)
x Pediatric Emergency Medicine Course (PEMC)

IP : 196.52.84.10
Rajesh Balakrishnan dch Srinivas md Murali T md Sendhilnathan P dch
(2005) (2005) (2005) (2006)

IP : 196.52.84.10
Gowrishankar md Arun Kumar T md dch Kamalkanth dch Palani Rajan dch
(2006) (2006) (2007) (2007)

Arun Kumar dch Susheel Narain dch Sujatha md Nandini dch dnb
(2007) (2007) (2007) (2007)

Shanthakumar md Sendhil Kumar md dm Mullai Baalaaji md Vijaykumar dch


(2007) (2007) (2008) (2009)
Contributors xi

IP : 196.52.84.10
Rajitha K dch Sugavanesh dch Babu Balachandar dch Sangeetha dch
(2009) (2009) (2009) (2009)

IP : 196.52.84.10
Dhakshayini md Sasikala dch Jagadeesh A md Satya Priya dch
(2009) (2009) (2010) (2010)

Vidyasagar dch Shankar Srinivasan dch Jeyanthi md dch Gandhi dch


(2010) (2010) (2012) (2012)

Gopinath md (2002)
Rajendran md (2003)
Sivaraman md (2005)
Saravanan K dch (2005)
Ramachandran T dch (2007)
Capt. Murali md (2008)
Santhosh dch (2009)
Sweetlin dch (2009)
Gokul dch (2012) Punitha R md (2012) Uma md dch
IP : 196.52.84.10

IP : 196.52.84.10
Foreword

IP : 196.52.84.10In 2010 India recorded 1.3 million infant deaths—the highest for any country.1 Millennium
Development Goal 4 (MDG 4) requires a two-thirds reduction infant mortally rates (IMR)
from 1990 levels by 2015.2 It is predicted that, if current rates of decline in IMR continue,
India will achieve MDG4 by 2023-2024, however, if the pace slows, it may only be achieved
by 2033-2034.1
All too often medical, pediatric and emergency textbooks, courses and research are
targeted at developed countries. Unfortunately, those of us working in developing countries,
frequently struggle to translate the recommended best practice into our workplaces.
In the field of emergency pediatrics in the developing world, our patients are most likely
to present with neonatal emergencies or childhood infections2,3 (sometimes complicated by
malnutrition, lack of immunizations, Tuberculosis or HIV). Developing world emergency patients frequently present
late and in a critical condition. We often have to contend with woefully inadequate staffing, equipment and resources.
OurIPstaff
: 196.52.84.10
have rarely been trained in the assessment and management of pediatric and neonatal emergencies. In many
developing countries prehospital care, transport and emergency medical systems are underdeveloped or absent. For these
reasons many courses and much of the research published from developed countries is not directly relevant to the practice
of emergency care in poorer parts the world.
Therefore, it gives me great pleasure to endorse the second edition of this excellent pediatric emergency textbook
catering for the developing world emergency environment. Given that India accounts for 21% of worldwide under-5
deaths4 it is very encouraging to see experts from this country highlighting quality emergency care of children as a crucial
part of the solution.
The Pediatric Emergency Care Manual has been written by expert pediatric practitioners—who are clearly experienced
in high volume, high acuity, low-resource emergency settings. This book is first and foremost a practical manual of “How
to manage seriously ill children?” and this is explained in an easy-to-follow clear manner—often with the use of high
quality photographs to illustrate techniques. There are also lots of handy tips—my particular favorite being the ‘common
errors’ box included at the end of most chapters. These invariably contain the kinds of ‘pearls of wisdom’ only gained
through considerable experience and rarely passed on in textbooks.
I am especially impressed by the in-depth explanations of underlying mechanisms of disease and pathophysiology.
These help the reader to understand in a ‘back to basics’ way what is going on in a patient and help make differential
diagnoses. There is also considerable detail and up to date information on key drugs, emergency treatments and essential
equipment.
If ever there was a time for pediatric emergency knowledge, skills and expertise to be shared, particularly in India and
other developing countries, it is now. Books like this will hopefully form part of the armamentaria of practical help for
frontline emergency workers in the battle to reduce global child mortality.
xiv Pediatric Emergency Medicine Course (PEMC)

References
1. Reddy H, Pradhan MR, Ghosh R, Khan Ag. India’s progress towards the Millennium Development Goals 4 and 5 on infant and
maternal mortality. WHo South-East Asia Journal of Public Health. 2012;3:279-89.
2. Building a Future for Women and Children: The 2012 Report. Available: http://www.countdown2015mnch.org/reports-and-
articles/2012-report.
3. Lozano R, Wang H, Foreman KJ, Rajaratnam JK, Naghavi M, Marcus JR, et al. Progress towards Millennium Development
Goals 4 and 5 on maternal and child mortality: an updated systematic analysis. Lancet. 2011;378(9797):1139-65.
IP : 196.52.84.10 4. You D, Jones G, Hill K, Wardlaw T, Chopra M. Levels and trends in child mortality, 1990-2009. The Lancet. 2010;
379(9745):931-3.

Baljit Cheema mbbs mrcpch bsc dtm&h


Chair of Pediatric Emergency Care of South Africa (PECSA)
Sub-group of Emergency Medicine Society of South Africa (EMSSA)
Member and Lead for Standards of Emergency Care Document-Pediatric Emergency Medicine
Special Interest Group of the International Federation of Emergency Medicine (IFEM)
Pediatric Emergency Specialist, Khayelitsha Hospital, Cape Town and Emergency Medical Service, Western Cape
Honorary Senior Lecturer
Department of Health
IP : 196.52.84.10 Division of Emergency Medicine
University of Cape Town
South Africa
Preface to the Second Edition

IP : 196.52.84.10The long awaited second edition of the Pediatric Emergency Medicine Course (PEMC)
manual is here. A veritable atlas of resuscitation, it has the largest number of photographs
taken before, during and after resuscitation! It explains how the pediatric assessment triangle
has been modified to help take therapeutic decisions. Current evidence-based guidelines
have been incorporated such that safer and more effective treatments are employed during
resuscitation.
What’s more! For the first time evidence from our own patients has been used to teach how
to save life in the initial minutes.
Since 2008, the Pediatric Emergency Medicine Course (PEMC) has achieved several
milestones to its credit. In 2010, the Vice Chancellor, Dr Myilvahanan Natarajan ms mch phd
and the senate of the Tamil Nadu Dr MGR Medical University, Tamil Nadu, India, passed a resolution making PEMC
mandatory for interns (PEMC for house officers) passing out from all medical colleges in Tamil Nadu state. To ensure that
thisIPwas implemented, Dr Srilakshmi dch phd, Head, Curriculum Development, Tamil Nadu Dr MGR Medical University,
: 196.52.84.10
undertook the task of organizing the ‘train the trainers’ program for Professors and Assistant Professors from all its
medical colleges. Her concerted efforts made the PEMC for house officers a reality.
In 2011, at the executive committee meeting of the Society of Trauma and Emergency Pediatrics, decision was taken
to endorse the PEMC. Earlier in 2006, the PEMC had been copyrighted to the Indian Society of Critical Care Medicine—
Chennai Chapter. In 2011, on the eve of the National Assembly of Pediatric Emergency Medicine (NAPEM-2011), the
first PEMC-instructor course was conducted. Over 40 instructors from different parts of the country participated.
Meanwhile, the PEMC continued to gain in popularity and more than 100 courses were conducted in different parts of
the country viz Hyderabad, Kakinada, Thiruvananthapuram, Bengaluru, Agartala, Kolkata and Chennai. The PEMC also
went overseas and was conducted in Sydney as part of the Pediatric Critical Care—Pre-congress workshop in 2011.
In 2012, the Indian Academy of Pediatrics—Tamil Nadu State Branch under the Presidency of Dr Sivaprakasam,
resolved to conduct the course (PEMC for Practitioners) in every district.
In 2013, it was conducted as part of the pre-congress workshop of the national Indian Academy of Pediatrics (IAP)
Congress, PEDICON at Kolkata.
The lessons learnt have now become the core curriculum of the postdoctoral PEM fellowship conducted under the
auspices of the Tamil Nadu Dr MGR Medical University. Dr Jeyachandran md dch, Dr P Ramachandran md dch and
Dr M Kannaki md dch (Directors of the Institute of Child Health, Madras Medical College), facilitated establishing the
fellowship program at this hospital.

Indumathy Santhanam
IP : 196.52.84.10

IP : 196.52.84.10
Preface to the First Edition

IP : 196.52.84.10 “Excellence in specialized pediatric emergency care to get kids back on track”

Few situations in a pediatrician’s practice evoke the anxiety and panic which accompanies the management of an acutely
ill child. The Pediatric Emergency Medicine Course (PEMC) offers a structured approach to handle the crisis using a time
sensitive, goal directed approach during the initial “golden hour” of critical illness.
Conceived by Dr S Krishnan, a pilot course was conducted in 1999 with the collaboration of the emergency and
intensive care physicians of the Kanchi Kamakoti Childs Trust Hospital and the Institute of Child Health, Madras Medical
College, under the suspices of the Indian Society of Critical Care Medicine (ISCCM)—Chennai Chapter. Since then the
content of the course has undergone tremendous changes as international resuscitation guidelines evolved providing
better standards of care. In 2006, this course was formally copyrighted to the ISCCM, Chennai Chapter.
At the 5th National Pediatric Critical Care Conference, executive body meeting of the Indian Academy of Pediatrics,
Critical Care Chapter held at Surat in October 2003, it was suggested the PEMC manual be re-written with evidence-based
IP : 196.52.84.10
guidelines. This was not easy. Most resuscitation guidelines are based on work published in Western centers. Do these
protocols work for us? Evidence is sparse in the Indian context! Using international guidelines as a prototype, protocols
were modified to suit realities of a large volume Emergency Department of a public children’s hospital with little access
to resources and advanced technology. Surprisingly, implementation of these modified protocols over the last ten years
resulted in mortality rates to levels almost on par with developed nations in life-threatening pediatric emergencies.
This is of special relevance in our country, where the vast majority of critically ill children, do not have access to
appropriate prehospital emergency medical services, specialist retrieval teams and advanced intensive care facilities.
Where critical care often evokes thoughts of advanced technology involving expensive resources this message is of
paramount importance.
Emergency medicine also involves the ability to take quick and accurate decisions in life-threatening pediatric
emergencies. To assist novice residents to take acceptable lines of action quickly in critical illnesses, this manual elucidates
a structured method of fitting the findings of the cardiopulmonary assessment into the pediatric assessment triangle,
understanding the physiological status and making the optimal therapeutic decisions in the first hour of resuscitation in
the absence of biochemical or radiological support.
While academicians may feel that the methods published in this manual may not have been validated in other centers,
this approach has dramatically improved survival at the Emergency Department (ED) of the Institute of Child Health,
which receives and resuscitates the largest volume of pediatric emergencies in the planet!

Indumathy Santhanam
IP : 196.52.84.10

IP : 196.52.84.10
Acknowledgments

IP : 196.52.84.10Successful achievement of therapeutic goals in resuscitation is based on coordinated team efforts. Many of the milestones
of the Pediatric Emergency Medicine Course (PEMC) have been achieved by the combined effort of a hugely talented
team. Dr Jayanthi, convenor for the PEMC and south zone coordinator for the BLS, has been a bulwark of strength and
integrity on which this course has grown. Dr Shanthi, an active PEMC instructor and former south zone convenor for
the PALS, is known for her tremendous commitment for teaching pediatric emergency medicine to young doctors at
the bed side. Dr Janani, the former National convenor of the PALS and team leader par excellence is the dynamic force
behind this course. Dr Radhika, the South zone convenor of the PALS and coordinator for the BLS is also known for her
passion for training doctors in CPR. Under the banner of the Indian Academy of Paediatrics, Tamil Nadu State Branch,
Dr Thangavelu, Dr P Ramachandran and Dr Poovazhagi some of the finest intensive care teachers of Tamil Nadu state
have taken key messages of this course to the far nook and corners of every district.
I thank Dr Suresh Gupta, President and Founding Member of the Society of Trauma and Emergency Pediatrics, and
Dr Mahadevan, Professor and Head, Department of Pediatrics, Postgraduate Institute of Medical Education and Research
(PGIMER), Chandigarh, India for editing the section on poisons and envenomation. I also thank, Professor P Arasar
IP : 196.52.84.10
Seeralar, Dr Ramesh Babu, Dr J Balaji, Dr Gowrishankar, Dr Gandhi, Dr Punitha, Dr Vijaykumar, Dr Sasikala, Dr Uma
and Dr Ashok of the Department of Pediatrics, Government Dharmapuri Medical College, Dharmapuri, Tamil Nadu,
India for adopting these methods in their practice. By enthusiastically implementing these protocols, they were able to
demonstrate ‘zero’ mortality during the dengue and scrub typhus epidemic in a rural district known for female infanticide
and high infant mortality rates.
The concepts that have been taught over many years at the PED of the Institute of Child Health, Madras Medical
College were translated on to paper by the creative efforts of Dr Gunda Srinivas. His generosity in sharing his collection
of photos and films have greatly enhanced the quality of this manual. Special thanks to Dr Padmavathy, Dr Sangeetha
and Dr Rajeshwari for their amazing editorial inputs! I also thank Dr S Thangavelu, Former Professor In-Charge of the
Pediatric Intensive Care Unit at ICH, for promptly sending his entire database of valuable clinical material.
I am grateful to Dr Bunnag and his team, Dr Padmanaban, Dr Yuri, Dr Sonia, Dr Rakesh Lodha, Dr Ramesh Menon,
Dr Jayshree Muralidaran, Dr Balaji and Dr Ramesh Babu for their contributions.
It was providence that came to our aid when Dr Marianne Gausche Hill, [the force behind the Advanced Pediatric Life
Support (APLS) course] offered to write the prologue and Dr Baljit Cheema, member of the International Federation of
Emergency Medicine, the foreword for this manual. I am deeply indebted to them.
Words cannot express how grateful I am to all the parents who entrusted their most precious possession to our care and
who stood by us as we resuscitated, taught and documented the treatment given to their children. I thank all these parents
for permitting us to use photographs taken during resuscitation for educational purposes.
I am grateful to my teachers, Dr Elizabeth John md, Dr L Subramanium md and Dr Muralinath md for teaching us the
principles of interpreting radiographs in acutely ill children. Many key points have been expounded in this manual.
I remember with gratitude Dr Suchitra Ranjith, Dr Soonu Udani, Dr B Ramachandran, Dr P Ramachandran and
Dr Indira Jayakumar who made the first edition a great success with their contributions.
xx Pediatric Emergency Medicine Course (PEMC)

This course owes a great deal to the management of the Kanchi Kamakoti Childs Trust Hospital for providing us with
their hospitality and venue to conduct this course.
My special thanks to my family. I would not have come this far without the support and encouragement of my
husband, Dr Ramesh Dorairajan, my daughter Dr Varshini Ramesh, my parents, Subhashini, Selvan JP and Kicchamma.
I would like to thank for the support extended by Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing
Director) and Mr Tarun Duneja (Director-Publishing) and his associates, Ms Seema Dogra (Cover Designer) of
M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, and I also thank Mr Jayanandan, Mr Mukherjee and
IP : 196.52.84.10 Ms Sajini (Bengaluru Branch) and her team, for their tireless efforts in making this edition a unique one.

IP : 196.52.84.10
Contents

IP : 196.52.84.10 Section I Recognition of Critical Illness

1. Recognition of Early Signs of Critical Illness in the Outpatient Department ----------------- 3

Section II Airway

2. Basic Airway Management ---------------- 25


3. Pharmacologically Assisted Intubation (PAI) in the PED ---------------- 30
4. Assessment and Management of the Difficult Airway ---------------- 44
5. Flow Inflating Ventilation Device: Non-invasive CPAP in Settings without Immediate
Access to Mechanical Ventilation ---------------- 53

IP : 196.52.84.10
Section III Approach to Stridor

6. Stridor ---------------- 61

Section IV Breathing

7. Approach to Respiratory Distress ---------------- 77


8. Management of an Asthmatic Exacerbation ---------------- 84
9. Pulse Oximeter ---------------- 95

Section V Circulation

10. General Approach to the Management of Shock -------------- 101


11. Intraosseous Access ---------------114
12. Vasoactive Drugs in the ED ---------------119
13. Approach to Acute Diarrhea and Shock in the ED -------------- 129
14. Cardiogenic Shock -------------- 134
15. Septic Shock -------------- 143
16. Approach to Recognition and Management of Dengue in the ED -------------- 158
17. Anaphylaxis -------------- 170
18. Cyanotic Spell -------------- 174
19. Hypertensive Emergencies -------------- 179

Section VI Disability

20. Approach to Decreased Level of Consciousness -------------- 187


21. Status Epilepticus -------------- 198
xxii Pediatric Emergency Medicine Course (PEMC)

Section VII Envenomation

22. Scorpion Sting -------------- 217


23. Snake Bite Envenomation -------------- 225

Section VIII Poisoning


IP : 196.52.84.10
24. Poisoning: General Approach -------------- 239
25. Specific Poisons -------------- 247

Section IX Trauma

26. Approach to Traumatic Brain Injury (TBI) -------------- 265


27. Approach to Polytrauma -------------- 281

Section X Environmental Injury

28. Burns
IP : 196.52.84.10 -------------- 291
29. Electrical Injury -------------- 296
30. Submersion Injury -------------- 299

Section XI Special Topics

31. Gastrointestinal Bleeding -------------- 305


32. Interpretation of Chest X-rays in Critically Ill Children -------------- 312
33. Procedural Sedation and Management of Pain in Children -------------- 335
34. Diabetic Ketoacidosis -------------- 344
35. Setting up Pediatric Resuscitation and Emergency Services -------------- 355

Section XII Procedures

36. Nebulizer Therapy -------------- 367


37. Needle Thoracocentesis and Thoracostomy -------------- 370
38. Pericardiocentesis -------------- 375
39. Cannulation of External Jugular Vein -------------- 378
40. Foley Catheter Insertion -------------- 380
41. Spinal Stabilization -------------- 382

Appendices

Appendices 1 to 13 389-405

Epilogue 407
Index 409
Abbreviations

IP : 196.52.84.10ALI - Acute lung injury MV - Minute volume


ALOC - Altered level of consciousness NAC - N-acetyl cysteine
ALTB - Acute laryngotracheobronchitis NCSE - Nonconvulsive status epilepticus
APLS - Advanced pediatric life support NE - Norepinephrine
ARDS - Acute respiratory distress syndrome NGT - Nasogastric tube
BBB - Blood brain barrier NIPPV - Noninvasive positive pressure
BURP - Backwards, upwards, rightward cricoid ventilation
pressure NMB - Neuromuscular blocking agent
BVM - Bag valve mask OPC - Or­ganophosphorus compound
CBF - Cerebral blood flow OPD - Outpatient Department
CICV - Cannot intubate cannot ventilate OR - Operating room
CPAP - Continuous positive airway pressure PAI - Pharmacologically assisted intubation
CPP - Cerebral perfusion pressure PALS - Pediatric advanced life support
IP : 196.52.84.10
CPR - Cardiopulmonary resuscitation PAM - Pralidoxime
CRT - Capillary refilling time PAT - Pediatric assessment triangle
CSE - Convulsive status epilepticus PBF - Pulmonary blood flow
DEM - Dolls eye movement PCR - Polymerase chain reaction
DHF - Dengue hemorrhagic fever PED - Pediatric emergency department
DIC - Disseminated intravascular coagulation
PE - Pulmonary edema
DKA - Diabetic ketoacidosis
PEEP - Positive end expiratory pressure
DOPE - Displacement obstruction
PEFR - Peak expiratory flow rate
pneumothorax equipment failure
PEGLEC - Polyethylene glycol with electrolytes
DSS - Dengue shock syndrome
PERL - Pupils equal and reactive to light
EOM - External ocular movement
PRES - Posterior reversible encephalopathic
ETCO2 - End tidal carbon dioxide
syndrome
ET - Endotracheal tube
RPA - Retropharyngeal abscess
FAST - Focused abdominal sonogram for
RSI - Rapid sequence intubation
trauma
FB - Foreign body PT - Prothrombin time
FRC - Functional residual capacity SABA - Short acting beta agonist
GCS - Glasgow coma score SCIWORA - Spinal cord injury without radiological
GERD - Gastroesophageal reflux disease abnormality
GNS - Glucose normal saline SE - Status epilepticus
GTCs - Generalized tonic-clonic convulsions SIRS - Systemic inflammatory response
ICP - Intracranial pressure syndrome
JR - Jackson-Rees SVR - Systemic vascular resistance
LOC - Loss of consciousness TBI - Traumatic brain injury
LMA - Laryngeal mask airway TV - Tidal volume
MAP - Mean arterial pressure WBCT - Whole blood clotting time
MDI - Metered dose inhaler WBI - Whole bowel irrigation
MODS - Multiorgan dysfunction syndrome WHO - World Health Organization
MVA - Motor vehicle accidents WOB - Work of breathing
IP : 196.52.84.10

IP : 196.52.84.10
Prologue

IP : 196.52.84.10

April 19, 2013


To,

Indumathi Santhanam md
IP : 196.52.84.10
Professor and Head
Department of Pediatrics
Government Royapettah Hospital
Kilpauk Medical College
Chennai, Tamil Nadu, India

Dear Dr Santhanam

I want to congratulate you, as editor, your contributors and publisher M/s Jaypee Brothers Medical Publishers (P) Ltd,
New Delhi, India for the production of the Second Edition of the Pediatric Emergency Medicine Course (PEMC) manual.
It is designed and was first published in 2008, to be a manual for an educational course bearing its name and implemented
throughout India since 1999; yet its scope goes beyond a course manual. This comprehensive and well-illustrated manual
covers information vital to the care of critically ill and injured children and includes chapters on the following topic areas:
Recognition of Critical Illness, Management of the Airway, Approach to Stridor, Respiratory Distress and Respiratory
Failure, Shock, Diarrhea and Dehydration, Alteration of Mental Status, Envenomation, Poisonings, Traumatic Injury
including Severe Traumatic Brain Injury, Orthopedic Trauma, and Environmental Emergencies. It also has a chapter
dedicated to Radiology in the Emergency Department (ED), Pain and Sedation, Setting up Pediatric Emergency Medical
Services in Rural Hospitals, and a section on Critical Procedures in Pediatric Emergency Care. It is a perfect reference for
pediatric residents, pediatricians, and other medical care providers caring for children in emergency settings.
This manual is based on the experiences of a physician practicing at a large volume pediatric emergency department
at The Institute of Child Health, Madras Medical College, Chennai, Tamil Nadu, India, who resuscitate nearly 13,000
seriously ill children and neonates every year, and see nearly 750,000 pediatric outpatient visits. This manual provides
sorely needed education for physicians caring for children in rural and resource poor environments, as well as physicians
with access to more sophisticated medical resources.
This is an amazing manual—I reviewed the Pediatric Assessment Triangle (PAT) and I think your modification is
brilliant—the original PAT may be too simplistic but there is something to be said for simplicity—I love all your features
and the algorithms at the end.
xxvi Pediatric Emergency Medicine Course (PEMC)

The manual incorporates a number of special features that provides the learner with tools to rapidly assess and treat
critically ill and injured children. Each chapter presents case scenario pertinent to the topic area, such as a child in
respiratory distress, then proceeds through a systematic discussion of the rapid assessment of that patient using a tool based
on a similar tool used in the United States for the rapid assessment of children, the Pediatric Assessment Triangle (PAT).
The method described includes evaluation of appearance, airway and breathing, and circulation, which when combined
together can create a picture of the physiologic status of the child and will drive management priorities including the rapid
initiation of life-saving treatment. Besides Case Scenarios and use of a Rapid Assessment Tool, other features include
IP : 196.52.84.10 Call Outs that provide key clinical pearls for the learner to better understand either the pathophysiology or the treatment
plan. At the end of each chapter are Key Points which emphasizes important concepts that should not be forgotten in the
care of children in emergency settings, Common Errors that describe important pitfalls to avoid in the care of children
with a particular life-threatening condition highlighted in the chapter, and finally a Protocol is provided at the end of
the chapter to serve as a quick reference guide which could be posted for pediatric emergency care providers to manage
children with potentially life-threatening conditions.
This manual appropriately highlights some of the serious illnesses occurring in children in the subcontinent of India,
including acute diarrheal illness and hypovolemic shock. Given that there are over 450,000 cases of diarrheal disease
worldwide and that 22% of deaths due to this disease occur in India, it is critical that emergency care providers recognize
early signs of dehydration and hypovolemic shock and have a management plan to rapidly treat these infants and children.
Recognition and management of septic shock, dengue shock syndrome and specific poisons and envenomations that are
endemic in India are also discussed. Finally the manual highlights the assessment and treatment of the mortal conditions
that affect children worldwide including respiratory failure, status epilepticus, burns, submersion injury, and traumatic
IP : 196.52.84.10
brain injury.
This comprehensive manual is a must read for any physician caring for children worldwide. With many physicians
and nongovernmental organizations reaching out to provide medical care all over the world, it can be a valuable resource
for these providers caring for children in many parts of the world. As the world of medicine continues to ‘go global’ this
manual can serve as an important reference for physicians who may not frequently encounter some of these conditions
in their home country.
I applaud your efforts in educating emergency caregivers in the rapid assessment and resuscitation of children in India.
This manual could be used by emergency care providers worldwide for improving the education of the physicians who
are caring for critically ill and injured children in emergency settings. In summary, the Pediatric Emergency Medicine
Course (PEMC) manual is comprehensive, easy-to-read, full of vital clinical information and pearls and, probably most
importantly, it provides an organized approach for the pediatric emergency care provider from assessment through
management. With algorithms for care at the end, it provides a means for rapid review of important concepts in the
management of critically ill and injured children.
Bravo, Dr Santhanam and best wishes with this important publication.

Marianne Gausche-Hill md facep faap


Professor of Clinical Medicine, David Geffen School of Medicine at UCLA
Vice Chair and Chief of the Division of Pediatric Emergency Medicine
Director of EMS and Pediatric Emergency Medicine Fellowships
Harbor-UCLA Medical Center, Department of Emergency Medicine
Torrance, California, USA
Recognition of
IP : 196.52.84.10

Section I
Critical Illness
IP : 196.52.84.10
1
Recognition of Early Signs
IP : 196.52.84.10
of Critical Illness in the
Out Patient Department

Figure 1.1: Long queues waiting at the OPD of a medical college affiliated, public children’s hospital in Southern India

Learning Objectives
1. Triage questions that help recognize early hypoxia, 3. The modified cardiopulmonary cerebral assessment
shock and myocardial dysfunction in children pre- and pediatric assessment triangle.
senting with ‘minor symptoms’ to the out patient 4. Using the modified pediatric assessment triangle to
department (OPD). recognize cardiogenic shock, non-convulsive status
2. Differentiate seizures from posturing secondary to epilepticus or raised intracranial pressure (ICP) in
hypoxia and shock. addition to respiratory failure and shock within the
first minute of arrival.

Early recognition of critical illness, is perhaps the most im- ASSESSMENT OF APpEARANCE BASED
portant link in the chain of survival. Delayed recognition, ON THE AVPU SCALE
late referral and failure to provide effective prehospital re-
suscitation were some of the reasons for children reaching An acute fall in mental status is one of the earliest symp-
our hospital with respiratory failure and shock.1 toms of hypoxia and shock. The severity of altered level of
consciousness (ALOC) or ‘appearance’ may be evaluated
This is highlighted by the fact that children who pre- rapidly using the alert, voice responsive, pain responsive,
sented late to the emergency service with respiratory unresponsive (AVPU) scale.3
failure and shock had increased risk of mortality.1 More
recently features of pulmo­nary edema, myocardial dys- Ù
function and non-convulsive status epilepticus2 were also In a large volume pediatric emergency department
(PED), symptoms of ALOC such as incessant cry,
associated with increased risk of hospital mortality.
lethargy, excessive sleepiness have been useful in
This chapter discusses, how to pick up early signs of recognizing hypoxia and shock.4
serious illness in a large volume PED (Figure 1.1) and
avoid the consequences of prolonged hypoxia and shock ●● Incessant cry, a seemingly innocuous symptom emerged
as the most ominous of all the presenting symptoms in
on the heart, lung and brain.
a cohort of shocked children.5
4 Section I n Recognition of Critical Illness

●● ‘Drowsiness’ in the background of fever, diarrhea or Alert (A)


breathlessness may be missed by the physician, since
a drowsy child could briefly wake up and appear alert,
IP : 196.52.84.10
while he is being assessed.
●● Unresponsiveness can be considered as ‘sleeping’ by
parents and not brought to the attention of the ED per-
sonnel in a busy OPD.
Ù
Caveat: An early sign of critical illness, incessant cry is
often dismissed as normal. Since crying is precipitated
by either undressing or stranger distress, it should be
identified even as the child is waiting in queue.
History of incessant crying must be confirmed by the
mother.
The best opportunity to recognize critical illness is to Figure 1.3: This infant was brought by his mother for diarrhea
observe ‘appearance’ before being formally evaluated and fever. Since he was alert and playing he was triaged as
or touched by the physician. normal and referred to the oral rehydration therapy (ORT) cell.
As seen in Figure 1.2, alteration in mental status is
ideally evaluated, whilst children wait in queue. Alertness is evaluated based on age appropriate interaction
of a child with his parents and environment (Figure 1.3).

Responsive to Voice (V)


Recognition of drop in mental status to ‘responsive to
voice’ is a challenge in all age groups.
Most infants will initiate crying when put down and
will stop crying immediately when picked up and held.
Crying has frequently been thought of as attachment
behavior caused by an infant’s need to cling to its care-
giver. If an infant with ‘minor symptoms’, continues to
cry despite being carried and cuddled, evaluate and treat
fever, pain, dehydration, wet nappy, etc. If crying does not
Figure 1.2: This figure shows a healthcare worker scanning resolve, categorize as responsive to voice and perform the
children as they wait in queue rapid cardiopulmonary cerebral assessment.
All too often, the physician seated in a busy OPD, can
miss early fall in mental status. Responsive to Painful Stimulus (P)
It is worthwhile to remember that a mother knows her Acute onset of posturing or failure to respond to the mother
child best. is alarming. Such children must be rushed directly into the
If she reports that her child is ‘not as usual’ then it is ED. Sudden flexor or extensor stiffening associated with
best to triage her child as hypoxic or shocked even if her an upward gaze or hypotonia in a neurologically normal
child appears to be alert. child may be secondary to respiratory failure and shock
due to sepsis, hypovolemia, near fatal asthma, etc.
Ù Refer Protocol 1.1: PEMC approach: Recognition of
Perform a detailed cardiopulmonary cerebral assessment
for any child who’s mother reports ‘not as usual’, ‘more relative bradypnea and relative bradycardia; Protocol 1.2:
PEMC approach: Recognition of severity of illness on ar-
sleepy’, even, if he looks ‘normal’.
rival to the ED, and also Figures 1.4 to 1.7.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 5

IP : 196.52.84.10

Figure 1.4: A 3-year-old asthmatic girl was brought to the


Figure 1.6: This infant also presented with odd squirming,
OPD with history of increasing breathlessness and incessant
wriggling movements of the limbs, which vary from the classical
cry since early morning. She was triaged as having a near
tonic-clonic components of status epilepticus. Features of severe
fatal attack of asthma, since she was sleepy with features
of respiratory failure. Note her tone and posture as she lies cardiopulmonary failure help differentiate convulsive status
floppily on her mother’s lap. epilepticus from posturing secondary to hypoxia and shock.

A weak cry and loss of eye contact in infants more than Febrile infants who present with squirming move-
2 months of age are early ominous signs of cerebral hypop- ments and upward gaze are often inappropriately referred
erfusion. In older children lethargy, inability to sit, stand or treated as atypical febrile fits.
or walk, agitation, fighting the oxygen mask and confusion
alternating with drowsiness herald brain hypoperfusion.
Ù
Control the urge to administer anticonvulsants.
Ù
Inability to recognize the mother or a vacant look is an
ominous sign.

Figure 1.7: Hypoxia, shock and myocardial function


improved following fluids, inotropes and elective intubation.
Administration of anticonvulsants would have aggravated
Figure 1.5: A 11-month baby was brought to the OPD for cardiorespiratory failure precipitating cardiac arrest.
acute onset of respiratory distress and fever. Since the morning
he had been crying incessantly and was not recognizing his 1. Confirm history to find out whether the child is having
mother. Enroute to the hospital he developed posturing. This
a tonic-clonic movement or posturing.
baby presented with airway instability, RR > 80/min, grunt,
abdominal respiration, tachycardia, muffled heart sounds, de- 2. Ask targeted questions to find out whether the child
compensated shock and increased liver span. Note the vacant had fall in mental status such as lethargy or incessant
upward gaze of the infant. His saturation was < 92%. crying prior to the onset of abnormal movements.
6 Section I n Recognition of Critical Illness

3. Perform the rapid cardiopulmonary cerebral assess-


ment.
4. Correct hypoxia and
IPshock. Reassess; a clearer picture
: 196.52.84.10
may emerge to guide therapy.
A neurologically normal child developing difficulty in
sitting or standing without support or being carried into
the hospital, is indicative of critical illness (Figures 1.7 to
1.10).
Children who are normal will not voluntarily lie un-
attended (when parents leave their line of vision). Hence,
older children with fever, vomiting, etc. who lie quietly (do
not protest) in their parents absence should also be sub-
jected to a more detailed assessment (Figure 1.8). Figure 1.9: Fluids were interrupted, inotrope initiated and
intubation was performed using ketamine, atropine and
suxamethonium. Crepitations resolved, saturations improved
to 100% and the hepatomegaly resolved. Further fluid boluses
were continued till therapeutic goals of shock were achieved.
Thirst for water is another ominous symptom in older children
presenting with respiratory distress and shock. Failure to
recognize this ‘red flag’ symptom and aggressively resuscitate
has often resulted in cardiac arrest!

Figure 1.8: A 6-year-old girl, with fever and first episode of


acute respiratory distress was carried into the OPD. Since
she was unable to maintain her usual tone and posture, she
was triaged into the PED. She presented with impending
respiratory failure and shock. At 40 mL/kg, she developed
grunt, abdominal respiration, SaO2 of 90% and hepatomegaly,
but shock persisted.

Ù Figure 1.10: Note the alert, smiling child in comparison with


herself in Figure 1.8. Early recognition of ALOC secondary to
Febrile children who are abusive or are inappropriately
hypoxia and shock and early goal-directed management were
rude to the physician or their parents should also be
responsible for her neurologically intact survival.
assessed in greater detail.

Thirst for water is another ominous symptom in older


Ù
Restlessness and talking unintelligibly at any age
children presenting with respiratory distress and shock.
is indicative of severe hypoxia or shock.6
Failure to recognize this ‘red flag’ symptom and aggres-
sively resuscitate has often resulted in cardiac arrest! • The verbal score is 2 (GCS).
• Consider deep unconsciousness.
Acute onset of altered behavior, incoherent speech, • Failure to aggressively resuscitate these kids could
agitation or fighting the mask in older children with ad- result in rapid deterioration and cardiac arrest!
ditional history of fever, trauma, diarrhea, etc. may also
suggest a serious drop in mental status.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 7

●● Occasionally, acute posturing and abnormal eye move-


ments (oculogyric crisis) occur due to an over dose of
IP : 196.52.84.10 phenothiazine group of drugs. Negative ‘triage ques-
tions’ and normal ABCs in an alert child are diagnostic
of acute phenothiazine toxicity.
●● History of fever, breathlessness (due to varied etiolo-
gies), acute watery diarrhea, etc. followed by progres-
sive LOC and posturing is suggestive of very severe
hypoxia and shock.

Breathlessness
Breathlessness is the commonest symptom for which an
acutely ill child is brought to the PED (Figure 1.12).
Figure 1.11: This picture shows a 7-year-old child with shock
fighting the oxygen mask. It is an ominous sign indicative of
severe hypoxia especially in older children, who are aware that
an oxygen mask is not a noxious intervention. Fighting the
mask, however is normal in infants and toddlers if the other
parts of the pediatric assessment triangle are normal.

Unresponsiveness (U)
Unresponsiveness, whilst not difficult to triage, is often a
diagnostic challenge to novice pediatricians manning the
ED.
●● Sudden unresponsiveness in the absence of precipitat-
ing events in a previously normal child or a child with
seizure disorder is suggestive of non-convulsive status
epilepticus (NCSE).
●● Failure to regain baseline consciousness after a brief
generalized tonic-clonic seizure is also suggestive of
NCSE.
Figure 1.12: This figure shows why children presenting with
Ù severe shock may also have respiratory distress.
All abnormal movements in unresponsive children are
not seizures. Upward gaze with extensor stiffening or Bronchiolitis, pneumonia and asthma are well known eti-
flexor spasm of limbs can occur due to hypoxia and ologies of acute respiratory distress. However, a significant
number of shocked children who present to the ED, have
shock. This clinical presentation must be differentiated
breathlessness due to pulmonary edema2 (Figure 1.11).
from convulsive status epilepticus. A targeted history and
rapid cardiopulmonary cerebral assessment (protocol I) Severe insults such as sepsis, anaphylaxis, status epi-
are essential to guide management. lepticus, scorpion sting, submersion injury, perinatal de-
Inadvertent administration of anticonvulsant drugs pression can directly affect the heart, systemic and pulmo-
for posturing secondary to severe hypoxia or/and nary vasculature.
shock can be lethal. On the contrary, administration of ●● Vasodilation and capillary leak leads to loss of fluids.
anticonvulsant drugs is life saving in NCSE. Loss exceeding 25% of effective circulating volume,
results in shock.
8 Section I n Recognition of Critical Illness

●● Capillary leak also occurs in the pulmonary capil- tone of these muscles in unresponsive victims result in air-
laries. Increased pulmonary vascular permeability way obstruction.
leads to pulmonaryIPedema, also known as acute lung
: 196.52.84.10 ●● Neurogenic or functional stridor should be recognized
injury (ALI). early. The airway is positioned using the head tilt- chin
●● Severe insults (hypoxia, prolonged shock, venom, etc.) lift maneuver.
can lead to acute myocardial dysfunction. The resultant ●● If trauma is suspected in the unresponsive child, jaw
hydrostatic pulmonary edema can present as respira- thrust maneuver must be employed to open the air-
tory distress. way.
●● Crying children or children with suspected ‘structural’
Ù Triage Questions airway compromise should be evaluated in their par-
1. Mother can provide information of early hypoxia and ent’s lap.
shock for children presenting with fever, acute diar-
rhea, asthmatic exacerbations or focus of infection. Assessment of Breathing
• Is the child more tired, sleepy than usual? Oxygen must be administered simultaneously as the as-
• Is he as usual or not? sessment is being performed.
• Does the child cry inconsolably (in younger in-
●● Use a flow-inflating ventilation device (refer Chapter
fants)?
5), if respiratory distress is identified (with the excep-
2. Mother can also help us find out whether her child tion of asthma).
with sepsis, diarrhea, scorpion envenomation, sei- ●● Use non-rebreathing mask, if effortless tachypnea is
zures, etc. has developed features of pulmonary ede- noted.
ma. ●● Simultaneously, place the hand on the chest and count
• Has the child developed respiratory distress? respiratory rate for 6 seconds and multiply by 10.
• Is it the first episode (not since birth or episodic)? ●● Check the vital signs chart for age-related ranges.
●● Note whether respiratory rates for age are increased,
Ù decreased or normal.
The three components of the PAT, appearance, breathing Vital signs for each age group must be displayed in the
(evaluation of the airway is included in breathing) and ED. Refer protocol 1.1.
circulation is depicted as 3 separate colored triangles.
The arrows within the 3 triangles indicate the need to Ù
reassess systematically the response of interventions on • If respiratory rates appear to fall within the normal
range for age, but is associated with an unstable airway,
the ABCs. Each assessment is ideally performed in less
shock and unresponsiveness, recognize respiratory
than 60 seconds (Figure 1.24).
failure. Initiate bag-valve-mask ventilation, whilst,
the next responder continues to perform the remaining
Assessment of airway part of the cardiopulmonary cerebral assessment.
• As the respiratory rate is being counted, look for
Crying or vocalization indicates that the airway is patent. grunt, retractions and whether respiration is thoracic
Harsh inspiratory sounds suggests stridor secondary to or abdominothoracic.
structural airway obstruction. ‘Snoring’ in an unresponsive • Grunt and abdominothoracic respiration are ominous
child indicates that the airway is obstructed by secretions signs of impending respiratory failure.3
or falling back of tongue. Unresponsive children presenting
with stridor must be evaluated on the resuscitation trolley.7 Respiratory effort offers information, as to whether the
Ù
Presume that the airway is unmaintainable in children
child has respiratory distress or respiratory failure.
●● Auscultate infra-axillary regions on both sides.
who are unconscious or posturing. ●● Listen for air entry, wheeze and crepitations.
The patency of the airway is maintained by the normal ●● Evaluate color by comparing the palm of the physician
tone of the palatopharyngeal muscles and tongue. Loss of with that of the child’s sole (Figure 1.13).
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 9

●● Pallor, dusky hue, ashen, mottling is documented as ●● However, tachycardia may persist when atropine is
abnormal. used for intubating children in shock.5
●● Other causes of persistent tachycardia are fever, anxi-
IP : 196.52.84.10
ety, pain and systemic inflammatory response syn-
drome (SIRS).3,9
●● In addition, tachycardia may be the only sign of ongo-
ing seizure activity in a paralyzed and sedated child
with shock.
●● Heart rates greater than 220 beats/minute in infants and
180 beats/minute in children warrant urgent evaluation
and treatment.3 An electrocardiography (ECG) may be
necessary, because the pulse oximeter may be unreli-
able in identifying supraventricular tachycardia.
Ù
A heart rate that is relatively normal for age despite
the presence of severe respiratory distress or failure
Figure 1.13: It is not uncommon for the color to be noted as and shock (relative bradycardia) is an ominous sign.
normal in shocked children. The difference may be apparent These children have exhausted their physiological
only when comparing with the ‘normal’ color of the physician. compensatory mechanisms and are at risk for abrupt
deterioration and arrest.
Assessment of circulation
●● Other causes of relative bradycardia in children pre-
Heart Rate senting with shock are raised intracranial pressure,10,11
hypothermia, hypokalemia (often noted in diarrheal
Assess heart rate for 6 seconds and multiply by 10. Simul- dehydration and severe malnutrition complicating sep-
taneously, check the vital signs chart to determine whether tic shock), dengue shock syndrome12 and drugs such as
tachycardic, bradycardic or normal for age (Figure 1.14). digoxin and beta blockers.

Perfusion
Comparison of Pulses
Central pulse (femoral) is felt by placing the index finger
of one hand snugly into the inguinal region. It is compared
with the dorsalis pedis, which is felt by simultaneously
placing three fingers perpendicularly on the dorsum of the
foot.
●● Weak or absent distal pulses is caused by peripheral
vasoconstriction, while absent distal pulses suggest
decompensated shock.
●● Loss of central pulses is a premorbid sign requiring
Figure 1.14: Assessment of heart rate. Note that the physician very rapid intervention.7
is holding the airway as he evaluates the heart rate. ●● Bounding central and distal pulses in association with
tachypnea, tachycardia and altered mental status sug-
●● Tachycardia is the earliest compensatory response to gest the presence of a hyperdynamic circulation with
decreased stroke volume or hypoxemia. low systemic vascular resistance.
●● Young infants and neonates, however, may respond ●● Vasodilatory shock is identified when diastolic pres-
with paradoxical bradycardia.3 sure is lower than 50% of systolic blood pressure.15
●● Normalization of heart rate is one of the most reliable ●● If dorsalis is not felt, do not report as ‘normal’ periph-
signs of shock resolution.8 eral pulse based on the posterior tibial (Figure 1.15).
10 Section I n Recognition of Critical Illness

Core-peripheral Temperature Gap


Assess core-peripheral temperature gap by comparing si-
IP : 196.52.84.10 multaneously, the temperature of the trunk with that of pe-
ripheries using the dorsal surface of both hands (gloves need
not be removed to evaluate this variable) (Figure 1.16).

Figure 1.15: Comparison of central and peripheral pulses is


shown in this picture. Since interpretation of this sign is not
easy, it needs experience to feel and compare the femoral and
dorsalis pedis in infants. Occasionally, difficult to feel central
pulses with palpable dorsalis pedis in a neonate presenting
with cardiogenic shock harbingers coarctation of aorta with a
patent ductus arteriosus. Figure 1.16: Note that the dorsal surface of one hand is placed
over the trunk of the infant, while the dorsal surface of the
Reassuring one’s self that the child is not shocked based other hand slides over the thigh, leg and foot to compare the
on the presence of the posterior tibial pulse in the absence difference in temperature between the center and peripheries.
of the dorsalis pedis has often resulted in failing to pick If warm or cool throughout, it could signal warm or cold shock
in children when other parts of the PAT are abnormal.
up hypotensive shock. [Caution: The dorsalis pedis artery
may be absent in 12% of normal individuals (Sarrafian’s
●● When cardiac output falls, cooling of the skin begins
anatomy of the foot and ankle by Armen S Kelikian)].
peripherally in the fingers and toes and extends proxi-
Ù mally towards the trunk. A core/toe temperature differ-
History of early LOC, abnormal cardiopulmonary ence of more than 2ºC is a sign of poor perfusion.
cerebral assessment, palpable posterior tibial with
difficult to feel dorsalis pedis: Recognize shock. Capillary Refill Time (CRT)
Table 1.1: Comparison of femorals and dorsalis pedis It is well known that poor peripheral perfusion may result
from cool environmental temperatures in very young in-
Dorsalis fants3 and hence, in very young age groups, this sign may
Femorals Pulse pressure Inference
pedis have limited utility for both the recognition of shock and
+++1 ++3 30–40 mm Hg Normal monitoring response to therapy. Other therapeutic goals
+++1 +++4 > 40 mm Hg Bounding such as normalization of mental status, respiratory rates
(vasodilation) and heart rates for age may be more reliable when evalu-
+++1 +5 < 40 mm Hg Shock
ating for shock resolution in this age group. Conversely,
++ 2
0 6
Not recordable Hypotension early alterations in extremity perfusion are more reliable
1: Easy to feel femorals. in older children, where the baseline mental status may
appear to be relatively well preserved despite circulatory
2: Difficult to feel femorals.
compromise.
3: Easy to feel dorsalis pedis.
4: Dorsalis pedis as well felt as femoral pulse.
Ù
Avoid diagnosing shock based on prolongation of CRT
5: Dorsalis pedis just felt. in the absence of significant history and other features
6: Dorsalis pedis not felt. of shock.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 11

ic anemia and congenital heart diseases with shunt lesions.


Accurate blood pressure measurement requires the use of
IP : 196.52.84.10 an appropriate sized cuff covering at least 75%–80% of
the upper arm. Normal blood pressure readings should be
displayed in the ED. Age-associated blood pressure cuffs
should be used to record this vital sign (Figure 1.18).
Table 1.2: Hypotension based on Emergency Cardiovascular
Care Guidelines 2000 is characterized by the following limits of
systolic blood pressure (SBP)

Age SBP
Term newborn (0–28 days) < 60 mm Hg
For infant < 12 months < 70 mm Hg
1–10 years < 70 + (2 × age)
> 10 years < 90 mm Hg

Figures 1.17A and B: The capillary refill time (CRT) is assessed


by lifting the extremity slightly above the level of the heart
and applying enough pressure to blanch the skin. Normal
time taken for refilling of the blanched area is 2 seconds or
less. A prolonged CRT may be seen in shock, rising fever and
cold ambient temperature. It is also influenced by lighting and
age.3 Figure 1.18: Different sizes of BP cuffs used in children. Use
of inappropriate large cuffs in small children will result in the
Blood Pressure recording low BP and vice versa.

Blood pressure (Table 1.2) may be preserved in early shock Systolic blood pressure: Interpretation of systolic blood
due to the compensatory increase in systemic vascular resis- pressure in children with shock:
tance (SVR). In young children, increase in vasomotor tone
results in BP that is in the higher range for age. Under these ●● High in shock (normal response).
circumstances, as therapeutic goals of shock are achieved, ●● Normal range (relative hypotension).
blood pressures may decrease to the normal range for age. ●● Hypotension (can progress to imminent arrest in min-
utes).
In vasodilatory shock states, low SVR results in widen- Diastolic blood pressure13: As mentioned earlier, diastolic
ing of pulse pressure. This is characterized by a diastolic pressures less than 50% of systolic pressure harbinger va-
BP that is less than or equal to half of the systolic BP. In sodilatory shock when associated with altered mental sta-
these children, pulse pressure narrows with resolution of tus, abnormal respiratory rates, work of breathing, tachy-
shock. Wide pulse pressures may also be noted in children cardia, warm, pink peripheries, bounding pulses and rapid
with neurogenic and anaphylactic shock, as well as chron- CRT.
12 Section I n Recognition of Critical Illness

●● Mean arterial pressure (MAP) is calculated as the sum ●● If the liver span is increased in children presenting with
of the diastolic pressure and one-third pulse pressure. A respiratory distress, it is probable that myocardial dys-
value less than 65 mmIP Hg is considered as hypotension.
: 196.52.84.10 function is the causative factor.
●● Conventionally, documentation of systolic pressure is ●● A normal liver span on the other hand points to primary
given importance. Early warm shock could be missed, lung pathology as causative of respiratory distress.
if diastolic pressure and MAP are not noted.
Ù
Alteration in liver span following each bolus of fluid,
Liver Span intubation or inotrope infusion helps to decide whether
Measure liver span during the assessment of circulation. myocardial dysfunction is improving or not. Thus
It is helpful in assessing and monitoring the severity of assessment of liver span is a simple method of assessing
myocardial dysfunction.5 myocardial dysfunction in settings without access to
invasive monitoring.

Disability Assessment
Neurological assessment is an integral part of evaluation
of a child with hypoxia, shock and seizure activity and
may provide clues to the underlying etiology and response
to therapy.
When examining for pupillary response, simultaneous-
ly, look at the position of eyes. Is it conjugating or mid-po-
sition? Note for presence of abnormal ocular movements.
Abnormal ocular movements in a child presenting with
an exacerbation of asthma is suggestive of a near fatal at-
tack. Identification of this sign in a child with respiratory
failure and shock due to bronchiolitis suggests the need to
aggressively resuscitate hypoxia.
Indeed, eye signs in children presenting with severe
cardiopulmonary failure in the absence of seizure history,
has been associated with increased risk of mortality.14
●● Conjugate eye deviation, nystagmus or eyelid twitch
indicate presence of NCSE or severe hypoxic ischemic
insult to the brain (Figures 1.20A to C). Other gaze ab-
normalities, which may mimic non-convulsive status
Figures 1.19A and B: A. Marking lower border of liver; B. epilepticus are upward gaze and roving nystagmus.
Measuring the liver span. Assessment of liver span helps in the
Continuous epileptiform electroencephalogram (EEG)
evaluation of myocardial dysfunction in critical illness.
abnormalities have been noted in comatose adults with
severe metabolic or anoxic encephalopathies.15
●● The upper border is identified by percussion and the
lower border by palpation (Figures 1.19A and B). Us- ●● Avoid rushing to administer anticonvulsants.
ing a pen, both borders are marked and the total span is ●● The importance of early recognition and simultaneous
measured and documented. management of status epilepticus (convulsive and non-
●● These measurements are compared with normal values convulsive) is important in ensuring successful out-
displayed in the ED. comes in shock.8
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 13

Ù
Management of eye signs of non-convulsive status
IP : 196.52.84.10 epilepticus (NCSE) is based on the history. If history
is suggestive of GTCS, the NCSE is probably due to
ongoing seizure activity, administer anticonvulsants.
If on the contrary, altered mental status follows acute
diarrhea, fever, breathlessness, scorpion sting, etc. the
eye signs denote the severity of the shock and hypoxia.

Pupillary Examination (Figures 1.21 and 1.22)

Figure 1.21: Pupillary examination is also performed to


assess briskness of response and inequality

Unequal pupils may often be noted from increased intrac-


ranial pressure or non-convulsive status. Pupils provide
important information regarding response to therapy and
normalization of abnormal pupillary size, reaction or sym-
metry indicates resolution of cerebral hypoxia-ischemia.

Figures 1.20A to C: Conjugate deviation in a child presenting


with profound shock and posturing. The dolls eye movement is
being performed in the figures. Usually, the deviation persists
during the side-to-side movement performed for eliciting the
DEM (Courtesy: Dr Gunda Srinivas).

Ù
Do not forget to look at eye position and eye movements Figure 1.22: Unequal pupils. Examination of the pupils can
help pick up a wide variety of other unexpected conditions
during rapid cardiopulmonary cerebral assessment.
such as coloboma, xerophthalmia, etc. in seriously ill children
(Courtesy: Dr Gunda Srinivas).
14 Section I n Recognition of Critical Illness

●● Resuscitation from shock due to intracranial infections Airway


or head trauma will be incomplete if intracranial hyper-
tension is not simultaneously identified and treated. ●● If stable or obstructed: No positioning is needed.
IP : 196.52.84.10 ●● If airway is unstable or unmaintainable: Open the air-
way using the head tilt-chin lift maneuver (jaw thrust if
Interpretation of PAT
head trauma is suspected).
●● As the rapid cardiopulmonary cerebral assessment is
being performed, simultaneously the heart rates, respi- Breathing
ratory rates, BP and liver span should be verified with
the normal values for age. ●● If effortless tachypnea: Provide O2 via the non-re-
●● The variables are interpreted as normal for age, in- breathing mask.
creased or decreased based on the other parts of the ●● If respiratory distress or impending respiratory failure:
PAT.16 This helps to determine the physiological status Provide O2 using the Jackson-Rees circuit.
and guide therapy. ●● If apnea: Suction oropharynx, decompress stomach
●● No single variable should be taken in isolation. All with appropriate sized nasogastric tube and initiate
sides of the PAT16 should be compromised to recognize bag-valve-mask ventilation.
respiratory failure or shock.
●● Decreased mental status, respiratory compromise, al- Circulation
teration in heart rates and alteration in skin perfusion
●● If bradycardia: Initiate chest compressions.
suggestive of warm or cold shock with or without fall
in blood pressure should be taken together in the recog- ●● If tachypneic, tachycardic and shocked, without he-
nition of critical illness. patomegaly: Administer 20 mL/kg over 20 minutes.
●● If respiratory distress, tachycardia, shocked with or
PHYSIOLOGICAL STATUS and without hepatomegaly: Administer smaller boluses of
5–10 mL/kg over 5–10 minutes.
appropriate interventions
●● If BP low: Use pull-push method for administering flu-
Determine physiological status as Airway/Breathing/Cir- ids until BP normalizes (Plan intubation and epineph-
culation/Disability: Separate therapeutic interventions are rine infusion).
necessary for each of the parameters (Figure 1.24).
●● If pulse pressure wide, MAP < 65 mm Hg: Plan large
volumes of fluids.

Disability
●● If child having altered level of consciousness: Correct
hypoxia and shock and then reassess.
●● If NCSE/CSE: Treat seizure activity as discussed in
Chapter 21.
●● If raised ICP: Treat ICP as discussed in Chapter 20.
Ù
Repeat cardiopulmonary cerebral assessment after
administration of fluid bolus, anticonvulsant, intubation,
etc. and determine the new physiological status.
Figure 1.23: The Broselow tape
Intervene appropriately for each of the parameters viz
Often children who are critically ill cannot be weighed
ABCDs (Figure 1.24).
conventionally, for such children Broselow tape is useful
to calculate approximate weight based on length of the Uncompromising standards are needed in terms of accu-
child (Figure 1.23). racy, speed and skill in performing rapid cardiopulmonary
IP : 196.52.84.10
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
15

Figure 1.24: Pediatric Assessment Triangle (PAT) to enable recognition of severity and decision making in seriously ill children in the emergency setting
(Modified from Dieckmann RA, Brownstein D, Gausche-Hill M. The Pediatric Assessment Triangle–a novel approach for the rapid evaluation of children. Pediatr Emerg Care. 2010 Apr;26(4):312-15)
16 Section I n Recognition of Critical Illness

cerebral assessment and its interpretation in critical illness.


Refer Figure 1.25. Key Points
ü
Accurate documentation of clinical findings is crucial
IP : 196.52.84.10 1. The two steps for early recognition of serious illness
following each intervention (Table 1.1 and 1.2). Refer Fig- in children presenting with ‘minor’ symptoms are:
ure 1.26A and B. a. Asking the 2 triage questions and
b. Performing a meticulous rapid cardiopulmonary
Stringent precautions need to be taken since error or neg- cerebral assessment.
ligence on the part of the physician could be fatal to children 2. Recognition based on OBVIOUS drop in
whose care depends so heavily on clinical assessment.
consciousness can result in poor outcomes.
3. Consider the possibility of pulmonary edema when
children in shock present with respiratory distress
due to non-lung etiologies.

common errors
1. Recognizing serious illness only when the
û
‘consciousness’ drops profoundly.
2. Referring the febrile child with acute onset posturing
to the neurologist or to the psychiatrist for agitated
behavior.
3. Administration of higher antibiotics for a febrile
child with altered mental status without evaluating
or managing coexisting shock.
Figure 1.25: This picture shows a very young infant making 4. Administration of sedatives for infants with incessant
eye contact with his happy mother following successful
cry without ruling out hypoxia and shock.
shock resuscitation. His response to his mother, suggests
neurologically intact survival.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 17

IP : 196.52.84.10

Figure 1.26A: Pediatric emergency case record: front page (assessment part)
18 Section I n Recognition of Critical Illness

IP : 196.52.84.10

Figure 1.26B: Pediatric emergency case record: back page (monitoring and reassessment part)

Note: Refer appendix for sample documentation of Pediatric Emergency Case Record
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 19

Protocol 1.1: PEMC approach: Recognition of relative bradypnea and relative bradycardia
IP : 196.52.84.10
20 Section I n Recognition of Critical Illness

Protocol 1.2: PEMC approach: Recognition of severity of illness on arrival to the ED


IP : 196.52.84.10
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 21

References ment of severe sepsis and septic shock. Crit Care Med.
2008;36(1):296-327.
1. Santhanam Indumathy, Pai M, Kasthuri KR, et al. Mortal-
IPthe
: 196.52.84.10 9. Goldstein B, Giroir B, Randolph A. International pediat-
ity after admission in pediatric emergency department:
A prospective study from a referral children’s hospital in ric sepsis consensus conference: definitions for sepsis and
Southern India. Pediatr Crit Care Med. 2002;3:358-363. organ dysfunction in pediatrics. Pediatr Crit Care Med.
2005;6:02-08.
2. Santhanam I, et al. Implementation of Pediatric Emergency
Medicine Course Guidelines (PEMC). Impact on mortality 10. Pollard AJ, Britto J, Nadel S, et al. Emergency management
in critically ill children presenting to a large volume PED of meningococcal disease. Arch Dis Child. 1999;80:290-
of an academic children’s hospital in India. Pediatr Crit 96.
Care Med. 2011;(12):3. 11. Pollard AJ, Nadel S, Ninis N, et al. Emergency manage-
3. Zaritsky AL, Nadkarni VM, Hickey RW, et al. Recognition ment of meningococcal disease: eight years on. Arch Dis
of respiratory failure and shock. Textbook of Pediatric Ad- Child. 2007;92:283-86.
vanced Life Support. Dallas TX: American Heart Associa- 12. Ranjit S, Kissoon N, Ghandhi D, et al. Early differentia-
tion; 2002. 36:97-98. tion between dengue and septic shock by comparison of
4. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- admission hemodynamic, clinical and laboratory variables:
spective randomized controlled study of two fluid regimens a pilot study. Pediatr Emerg Care. 2006;23:368-75.
in the initial management of septic shock in the emergency
13. L. Chameides, R. Samson, Schexnayder SM, et al. Pedi-
department. Pediatr Emerg Care. 2008;24:647-55.
atric Advanced Life Support. American Heart Association;
5. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- 2011. pp. 72.
spective randomized controlled study of two fluid regimens
in the initial management of septic shock in the emergency 14. Santhanam I, Padma V, Murali T, et al. Predictors of mor-
department. Pediatr Crit Care Med. 2007;Suppl Vol 8, No tality of serious sepsis. Proceedings of the 1st European
3:A17. (Paper presented at the 5th Pediatric Critical Care congress on Pediatric Resuscitation and Emergency Medi-
Congress June 24th 2007, Geneva). cine (PREM). May 2nd, 3rd 2013:Ghent, Belgium.
6. Kirkham FJ, Newton CR, Whitehouse W. Paediatric coma 15. Jordan KG. Non-convulsive status epilepticus in acute
scales. Dev Med Child Neuro. 2008;50:267-74. brain injury. J Clin Neurophysiol. 1999;16:332-40.
7. Santhanam I, Ranjit S, Kissoon N. Management of shock in 16. Dieckmann RA, Brownstein D, Gausche-Hill M. The
the emergency department. Minerva Pediatr. 2009;61:01-15. Pediatric Assessment Triangle–a novel approach for the
8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving rapid evaluation of children. Pediatr Emerg Care. 2010
Sepsis Campaign: International guidelines for manage- Apr;26(4):312-15).
Airway

Section II
IP : 196.52.84.10
IP : 196.52.84.10
2
IP : 196.52.84.10

Basic Airway Management

Figure 2.1: Effective bag-valve-mask ventilation technique is key to successful resuscitation (Courtesy: Dr Gunda Srinivas).

Learning Objectives
1. Why the emergency physician must master the 3. EC-clamp: Pearls and pitfalls.
skills of bag-valve-mask ventilation? 4. Precautions taken during bag-valve-mask ventila-
2. Selection of the appropriate sized self-inflating tion.
bag-valve-mask device for resuscitation.

INTRODUCTION a child difficult. In fact, level I evidence supports the use


of bag-valve-mask versus tracheal intubation in the pre-
Expertise in basic airway maneuvers initially, followed
hospital setting.
by pharmacologically assisted tracheal intubation are core
skills essential in resuscitation care. Survival and neurological outcomes were same, wheth-
er intubation was performed or mask ventilation was pro-
The pediatric airway differs in many ways from the
adult airway. A relatively large tongue, makes visualization vided before reaching the PED.1
of the larynx difficult, with little space for maneuvering the
laryngoscope and even less space for passage of the tube.
Ù
Bag-valve-mask ventilation is recommended over tra-
Reduced tone of the pharyngeal muscles can also predis- cheal intubation for ventilatory support in the out-of
pose to airway obstruction. The small, narrow, fragile and hospital setting.1
horizontally placed epiglottis makes visualization of the
vocal cords difficult. The anterior placement of the larynx This is also true in PEDs manned by novice physicians
aggravates the difficulty in visualization. The short trachea where intubation skills may not be available 24 × 7.
predisposes to intubation of the right main bronchus. The
cricoid ring (the narrowest portion of the airway), is at in-
creased risk of trauma during tube insertion. Bag-valve-mask Ventilation
For all the reasons mentioned above, the first responder Self-inflating bag-valve-mask devices are used to initiate
in the PED, (usually a novice resident) may find intubating respiratory support in apneic children. It is designed to de-
26 Section II n Airway

liver positive pressure breaths when compressed. Key to


tion of critically ill children on arrival into the ED.
successful bag-valve-mask ventilation is the technique of
Use the largest sized bags in any child beyond the new-
applying an airtight sealIP(Figure 2.1).
: 196.52.84.10 born period. “Regardless of the size of the bag, cau-
●● Selection of the appropriate sized bag is the first step to tion should be taken to use the force and tidal volume to
successful resuscitation. make the chest just visibly rise.”3
●● A mask that extends from bridge of nose to chin must
be selected. The correct fitting mask is crucial for a
tight seal.
●● Insert NGT and decompress stomach contents prior to
initiating bag-valve-mask ventilation.
●● The self-inflating bag-valve-mask device cannot be
used to deliver oxygen to the spontaneously breathing
child.2

Figure 2.3: This neonate who presented with respiratory


failure to the ED had severe pulmonary edema and shock due
to sepsis. He needed a 1 liter bag and minimal hyperextention
at neck to ensure adequate chest rise and improvement in
Figure 2.2: Which sized bag would you choose, when a oxygen saturation.
3-month-old infant presents with respiratory failure due to
probable pneumonia? ●● Prior to initiating BVM ventilation, suction the orophar-
Answer: The largest size bag in this picture. The 250 mL bag is ynx using a large bore Yankauer suction catheter.
used for preterm neonates. 450–750 mL bag is recommended
●● The Yankauer catheter has a wide bore tip that aids
for resuscitating the term neonate in labor ward settings (lung
in clearing large volume vomitus and food particles
parenchyma may not have sustained damage immediately
rapidly.
after birth).
●● Avoid stimulation of the posterior pharynx during suc-
tioning by turning the head to one side. This simple
Age appropriate sizes of bags are available for the dif- maneuver prevents vagal-induced bradycardia.
ferent age groups (Figure 2.2). 450–750 mL bags are rec- ●● Simultaneously, empty stomach contents.
ommended for resuscitating term newborns and infants. ●● Rapidly introduce a large bore nasogastric tube and
Conventionally, larger bags (1–1.5 liters) are recommend- decompress the stomach by connecting the tip to the
ed exclusively for adults. In reality, however, 450–750 mL suction apparatus (Figure 2.4).
bag-valve-mask devices are often insufficient in ventilat-
ing young infants presenting with respiratory failure.

Ù
Most infants and children who require respiratory sup-
port on arrival in to the ED, have abnormal lung paren-
chyma. Chest compliance is poor and immense effort is
often needed to provide effective ventilation and normal-
ize oxygen saturation (Figure 2.3). The largest bags (at
least 1 liter) are needed to provide effective chest rise.
Smaller bags or ‘pediatric bags’, i.e. 450–750 mL are not
sufficient for providing bag-valve-mask (BVM) ventila-
Figure 2.4: Gastric decompression via NGT
Chapter 2 n Basic Airway Management 27

●● In small infants neonates, the nasogastric tube should


be aspirated using a syringe.
Ù IP : 196.52.84.10
Suctioning pressure should not exceed 100 mm Hg in
young infants and 300 mm Hg in older children.

●● Avoid suction, if the child is having active gastrointes-


tinal bleed.
●● Tie a collection bag to the nasogastric tube to avoid
spillage of gastric contents.
Ù
Vomiting of gastric contents secondary to gastric disten-
sion during bag-valve-mask ventilation, could result in Figure 2.6 Inappropriate EC-clamp: Avoid encircling the
disastrous consequences during resuscitation. top of the mask and pressing it down. Airtight seal will not be
One nurse should be assigned to the left of the airway possible and BVM ventilation may be ineffective.
manager exclusively for suctioning (Figure 2.5).

Figure 2.7 Inappropriate EC-clamp: Avoid standing and


bagging, failure to support one’s elbows can kink the neck and
Figure 2.5: Additional precautions during bag-valve-mask obstruct the airway. Standing can also strain the back of the
ventilation—nasogastric tube should be inserted prior to airway manager.
initiating BVM ventilation. Oropharyngeal secretions should
also be suctioned simultaneously. One nurse should be
assigned exclusively for suctioning since frequent suctioning
may be needed. Suctioning is performed by turning the child’s
head to one side to avoid stimulation of the posterior pharynx
and causing vagal-induced bradycardia.

Effective BVM technique may look apparently easy.


However, several potentially difficult steps are needed to
provide adequate ventilation.
Separate and position the individual digits (index, mid-
dle and ring finger) over the bony part of the mentum, ra-
mus and angle of mandible respectively. Avoid compress-
ing the soft tissues in the midline. Care is taken to ensure
that the fingers providing the E-clamp are as far away from Figure 2.8 Inappropriate EC-clamp: Avoid bunching the
the midline as possible. fingers used for provision of C-clamp.
28 Section II n Airway

IP : 196.52.84.10

Figure 2.9 Double EC-clamp: Often provision of effective BVM Figure 2.10 Appropriate EC-clamp: The airway manager
ventilation may need two persons. One person provides the should sit and support his elbows, while performing BVM
double EC-clamp. The second person pumps the bag, while ventilation. Fingers providing C-clamp should encircle the rim
giving additional pressure on the mask to prevent air leak. of the mask. Effort is taken to prevent air leak at the site of exit
of the NGT. Fingers providing E-clamp should be flexed at the
The commonest cause for ineffective BVM technique MP joints to hook and lift the jaw. The middle fingers is at the
stems from failure to provide an airtight seal of the mask. mentum, the ring finger at the ramus and the little finger at the
angle of the jaw.
The nasogastric tube emerging from the rim can thwart
attempts to make the seal airtight.

Ù
The correct EC-clamp technique (not easy) is the impor-
tant first step (Figures 2.5–2.11).
The E-clamp is provided using the middle, ring and lit-
tle fingers each of which are positioned on the mentum,
ramus and the angle of the mandible. The tip of these
fingers should indent the soft tissue along the bony rim
of the mandible. The E-clamp acts as a bucket handle
to lift the jaw to meet the C-clamp such that the seal is
airtight.
The C-clamp is provided using the thumb and index fin- Figure 2.11 Inappropriate technique: Mask ventilating
ger to encircle the mask along its rim. children presenting with respiratory failure, needs immense
effort to move the chest. Avoid pumping the bag from below.
The elbow of the hand holding the EC-clamp should be
placed on the resuscitation trolley. The ‘V’ position of the
Ù
Ability to bag-valve-mask effectively is the foundation
elbow automatically ensures that airway patency is main- for advanced airway skills.4
tained (‘head tilt, chin lift’).
The EC-clamp will be effective if the following precau-
Ù
Ensure that the elbow is at a lower level than the EC-
tions are taken:
clamp to avoid compromise of the airway. ●● Fingers (E-clamp) should not be bunched together.
●● Fingers providing the E-clamp should be flexed at
Avoid standing and bagging when the elbow gets posi- both the metacarpal joints thus avoiding soft tissue
tioned above the EC-clamp (refer Figure 2.7). obstruction.
Chapter 2 n Basic Airway Management 29

●● Elbows must be supported on the resuscitation trolley


whilst the thenar eminence is used to tilt the fore head
ensuring the head tilt maneuver.
common errors
û
1. Rushing to intubate before preoxygenating (mask
IP : 196.52.84.10
●● Standing may lead to improper positioning and kinking ventilation).
of the neck. 2. Selection of smaller sized bags.
●● Avoid using bag-valve-masks without the reservoir. 3. Standing and bending, while initiating mask ventila-
●● Lack of oxygen reservoir or a leaking reservoir, will tion.
prevent the provision of 100% oxygen to the child
4. Not decompressing the stomach prior to mask venti-
with apnea.
lation.
The brain suffers hypoxic injury when oxygen depriva- 5. Failure to recognize the sound of air leak during
tion lasts for more than 5 minutes. Hypoxic encephalopathy, mask ventilation.
can result in permanent crippling neurological handicap. 6. Failure to recognize that the reservoir is not distend-
Preventing hypoxia-induced brain damage is one of the ed (oxygen tube is not connected to the bag).
prime responsibilities of the ED physician. Recognizing 7. Failure to use a bag-valve-mask device with the ox-
respiratory failure and initiating effective bag-valve-mask ygen reservoir. Lack of the latter can reduce oxygen
ventilation can not only improve survival, but also ensure delivery up to 40% to the apneic child.
neurologically intact survival. 8. Failure to occlude the pop-off valve in the older
Anticipation of respiratory arrest is key to successful child.
resuscitation. Flying, to the airway end of the resuscitation
trolley when, an unresponsive child is being rushed gives References
a 2 second advantage in initiating bag-valve-mask ventila- 1. M Gausche, MD Roger J. Lewis, et al. Effect of Out-of-
tion. Recognizing apnea and initiating effective bag-valve- Hospital Pediatric Endotracheal Intubation on Survival and
mask ventilation early can not only reduce mortality, but Neurological Outcome A Controlled. Clinical Trial JAMA.
also ensure neurologically intact survival. 2000;283(6):783-90.doi:10.1001/jama.283.6.783.
Key Points
ü 2. Carter BG, Fairbank B, Tibbals J, et al. Oxygen delivery
using self-inflating resuscitation bags. Pediatr Crit Care
1. Recognizing respiratory failure and providing ef- Med. 2005;6:125-28.
fective bag-valve-mask ventilation is the most im-
3. Ralston M, Hazinski MF, Zaritsky AL, et al. Textbook of
portant responsibility of the emergency physician or
Pediatric Advanced Life Support, American Heart Associa-
nurse.
tion. 2006-2007.
2. Initiation of bag-valve-mask ventilation is the ap-
propriate first maneuver for a child presenting with 4. Benger J, Nolan J, Clancy M. Basic airway management
techniques. Emergency Airway Management. Cambridge:
respiratory arrest.
Cambridge University Press; 2008. pp. 27-40.
Pharmacologically Assisted
3
IP : 196.52.84.10

Intubation (PAI) in the PED

Figure 3.1: Sequential steps of PAI

Learning Objectives
1. Anatomy of “why intubation is challenging in 3. Hazards of intubating children without using drugs
children?” for sedation or paralysis.
2. Case scenarios illustrating indications for intubation 4. Pharmacologically assisted intubation (PAI): Protocol
using the pediatric assessment triangle. used in a large volume PED.

INTRODUCTION rib cage and poorly maintained negative intrathoracic pres-


sure result in lower functional residual capacity (FRC) in
More than a decade ago, virtually all ‘outside the operation
infants. In addition to the lower FRC (due to causes men-
room’ intubations were performed when children presented
tioned above), higher BMR, higher O2 consumption and
with imminent arrest. Currently however, anesthetic drugs
have enabled elective intubation in spontaneously breath- greater CO2 production make infants more prone to desatu-
ing critically ill children. Profoundly deranged physiol- ration when they slip into respiratory failure.
ogy, severe metabolic dysfunction, absence of nil per oral Upper airway muscles are also more sensitive to the
precautions, incomplete information from parents, unan- effects of anesthetic agents with a greater predisposition
ticipated difficult airway situations, presence of distraught to collapse.
parents and the responsibility of concurrently resuscitating
other sicker babies can often make intubation a challenge Controversy exists in several areas of RSI1, including
in the ED setting (Figure 3.1). use of atropine as an adjunct for children, the role of Li-
docaine as premedication, the role of a ‘de-fasciculating’
Smaller-sized vocal cords, positioning of glottis at dose of a non-depolarizing paralytic agent, relative con-
C1-4, leafy shaped, floppy epiglottis and a large occiput traindications for the use of succinylcholine, methods of
make intubation difficult in young children.
preoxygenation and the need to use cricoid pressure. How-
Infants also have a very compliant rib cage, where the ever, this chapter is based on the experience of a large vol-
inward recoil is greater than the outward recoil. The soft ume PED.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 31

Indications for Intubation citation for respiratory failure due to severe parenchymal
lung disease (Figure 3.3).
A 6-month-old infant has been having acute watery di-
arrhea and vomiting IP for: the
196.52.84.10
past 2 days. He had not A 9-year-old boy is referred for snake envenomation.
been responsive to his mother since the evening. For the Even as he is being evaluated, he develops bilateral pto-
past ½ hour he had been ‘mouth breathing’. sis and apnea.

Figure 3.2 Physiological status: Imminent arrest Figure 3.4 Physiological status: Respiratory failure due to
respiratory muscle paralysis
Imminent arrest is the most well-known indication for
urgent intubation. Airway protective reflexes are absent After provision of basic airway management, he needs
and vocal cords are not responsive. In these situations, to be intubated and ventilated for respiratory failure sec-
BVM is initiated and intubation performed without resort- ondary to neuromuscular paralysis (Figure 3.4).
ing to anesthetic drugs (Figure 3.2).
A 5-year-old child is being provided BVM ventilation
A 1-year-old child is being treated for cellulitis over for respiratory arrest secondary to convulsive status
the right upper limb. She has been crying inconsolably epilepticus. She continues to convulse despite 2 doses
since the morning. of Lorazepam and loading dose of Phenytoin. Is there a
need to intubate this child (Figure 3.5)?

Figure 3.3 Physiological status: Sepsis with Figure 3.5 Physiological status: Refractory status
cardiogenic shock epilepticus

This child has presented with respiratory failure either Provision of prolonged mask ventilation cannot be sus-
due to, cardiogenic or non-cardiogenic pulmonary edema. tained. This child’s seizures have been refractory to the ini-
In addition, she also has vasodilatory shock with low mean tial drugs. Administration of further anticonvulsant drugs
arterial pressure secondary to severe sepsis. She will even- is an indication for elective intubation using anesthetic
tually need elective intubation after the initial fluid resus- agents (Figure 3.5).
32 Section II n Airway

A 2-year-old child is rushed into the ED after he devel- lent intubating conditions 60 seconds after administration
ops stridor, respiratory distress following intravenous of anesthetic drugs.
contrast administrationIP in the radiology department.
: 196.52.84.10 Excellent intubating conditions are defined as com-
plete jaw relaxation, open immobile vocal cords with ab-
sence of coughing, bucking and diaphragmatic movement
in response to intubation. It is implemented in a logical
sequence and comprises of several coordinated steps.
The pharmacologically assisted intubation (PAI) de-
scribed in this manual deviates from the classical RSI.

Pharmacologically Assisted Intubation


Unlike, pharmacologically facilitated intubation2, which is
described as ‘sedation only protocol’, we made the follow-
ing modifications:
Figure 3.6 Physiological status: Obstructed airway and 1. Sedative and paralytic agents were used to assist
hypotensive shock secondary to anaphylaxis intubation.
Obstruction to the airway secondary to anaphylaxis fa­ 2. To avoid aspiration of stomach contents during
cial trauma, epiglottitis, can often worsen. In these clinical intubation, the stomach was decompressed.
scenarios elective intubation is advisable (Figure 3.6). 3. Children were preoxygenated using the bag-valve-
mask technique after paralysis, until saturations were
maintained at 100%.
HAZARDS OF INTUBATION
Direct laryngoscopy activates airway protective responses Steps 2 and 3 were deemed mandatory to avoid cardiac
by stimulating the glossopharyngeal nerve above the epi- arrest from occurring in children presenting with profound
glottis and the vagus nerve below it. Gagging, coughing, hypoxia and shock.
apnea, laryngospasm and bronchospasm are some of the Cricoid pressure was applied during intubation not to
noxious respiratory responses. Hypertension and tachycar- prevent regurgitation, but to en­able visualization of the vo-
dia in older children and bradycardia in children less than cal cords.
5 years occur due to stimulation of the sympathetic and
parasympathetic nervous system. Furthermore, difficulty Ù
Nasotracheal Intubation (NTI)
in visualizing the glottis, often results in prolonged ma-
nipulation of the airway resulting in worsening of hypoxia Securing the airway via the the orotracheal route is
and hypercapnia. This in turn could trigger cardiac arrest faster and is therefore preferred in ED settings.
in the seriously ill child. Airway trauma, breakage of teeth
and bleeding are other hazards when electively intubating 1. History and evaluation of the patient.
a struggling child. 2. Preparation:
a. Gastric decompression.
RSI facilitates airway visualization with the use of
b. Preoxygenation of patient: 3–5 minutes.
drugs that cause muscle relaxation, control agitation, con-
c. Equipment and staff.
trol seizures and blunt the gag and cough reflexes. Use of
d. Medications.
premedications minimizes the risk of autonomic-induced
3. Administration of premedication.
cardiovascular complications such as bradycardia during
4. Administration of sedation.
emergency intubation.
5. Cricoid pressure and ventilation.
RSI is defined as “the simultaneous administration of 6. Administration of neuromuscular blockage.
a sedative (induction agent) and a neuromuscular blocking 7. Postintubation documentation and monitoring.
agent for the purpose of intubation”. RSI produces excel- 8. Continuous sedation and paralysis.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 33

HISTORY AND EVALUATION OF PATIENT ●● Evidence of facial and neck trauma.


●● Micrognathia or mandibular hypoplasia.
Coordinated preparation is essential for success in per- ●● Low-set ears.
forming pharmacologicallyIP : 196.52.84.10
assisted intubation. Rigorous ●● Dysmorphic facial features.
assessment of the airway before administration of paralytic ●● Limited mouth opening, small mouth.
agents is an essential first step. ●● High-arched palate.
●● Large tongue.
●● Loose teeth, prominent upper incisors with overriding
HAZARDS OF ANESTHETIC maxilla.
DRUGS IN THE PED ●● Stridor due to structural abnormality of the airway.
Use of paralytic drugs, in children who are difficult to in- ●● Mallampati class III and IV (rarely assessed in the
tubate could result in tragic outcomes. In these children emergency setting).
whose respiratory efforts have been eliminated, gas ex-
change will not occur when intubation fails. Bag-valve- AMPLE History is Obtained Before Intubation
mask ventilation may also become impossible, since tone History should be brief objective and cover the following
of the oropharyngeal muscles and ligaments are lost. The issues represented by the acronym AMPLE, a mnemonic
ED physicians nightmare of ‘cannot intubate, cannot ven- to facilitate intubation:
tilate’ can occur.
●● A = Allergies.
Problems in Intubation ●● M = Medications.
●● P = Past history.
Characteristics that contribute to causing difficulty in visu- ●● L = Liquids and last meal.
alizing the glottis or introducing the tracheal tube are: ●● E = Events leading to the need for intubation.
Table 3.1: Airway equipment to be prepared prior to intubation (SOAPME)

Suction Yankauer suction catheter


Oxygen source ●● Cylinder or central oxygen should be connected to the bag-valve-mask device
●● Sufficiency of oxygen verified by demonstration of filling up of the O2 reservoir of the
bag-valve-mask device
Airway equipment
●● Bag-valve-mask device ●● 750 mL, 1,000 mL
●● Non-rebreathing mask
●● Jackson-Rees circuit, Bain circuit
Age appropriate endotracheal tubes ●● Uncuffed tube: 4+ (age in years/4)
●● Cuffed tube: 3+ (age in years/4)
●● Prepare 1/2 size smaller and larger
Appropriate sized laryngoscope ●● Up to 2 years: Straight blade
●● 2 years to adolescence: Curved blade (Size of curved blade: Measure from mouth to
thyroid prominence (refer Figure 3.11)
Appropriate sized oral airway ●● Flange to tip is measured from angle of jaw to angle of lip
Tincture benzoin soaked cotton ●● Adhesive applied above the upper and below the lower lip prior to sticking plaster
Plaster for securing tube ●● Cut as ‘trouser legs’ (refer Figure 3.10)
Pharmacology Drugs must be constituted and labeled before use
●● Premedication agents: Atropine, Lidocaine
●● Induction agents: Thiopental, Ketamine
●● Neuromuscular blocking agents: Suxamethonium, Vecuronium, Rocuronium
Monitoring Equipment ●● Pulse oximeter
●● Cardiorespiratory monitor
●● ETCO2 monitor
34 Section II n Airway

Preparation of Patient Preoxygenate for 3–5 minutes using a non-rebreathing


mask or flow inflating ventilation device (refer Chapter 5).
Refer Table (SOAPME) 3.1.
IP : 196.52.84.10 This ensures that alveolar nitrogen is replaced by oxy-
Nasogastric Tube Insertion gen. Children need this additional oxygen to remain satu-
If the child presents with respiratory failure, a nasogastric rated for the 2–3 minutes of pharmacologically induced
tube (NGT) is introduced and stomach contents are rap- apnea prior to intubation.
idly decompressed by connecting the NGT to the suction
apparatus. Simultaneously, bag-valve-mask ventilation is
initiated as shown in this picture (Figure 3.8).
Due to the inherent risk of regurgitation of stomach
contents, the NGT is not introduced prior to intubation in
the classical RSI technique.
In the PAI, the NGT must be introduced as soon as the
decision to intubate is taken since children presenting to
the ED seldom present with empty stomach.
Ù
Failure to decompress stomach contents prior to bag-
valve-mask ventilation can irrevocably damage lung
parenchyma by aspiration of stomach contents and
worsens hypoxia precipitating CARDIAC ARREST.

If the child struggles or gags, introduce the NGT after


a sedative agent has been given.
Preoxygenation of Patient
Ù
The spontaneously breathing patient should be pre- Figure 3.8: A modification of the classical RSI, introduction
oxygenated with supplemental oxygen (Figures 3.7 and of the NGT and decompression has been safely employed to
3.8). prevent aspiration during mask ventilation in a large number
of pharmacologically assisted intubations in a busy PED.3
This picture also shows two lines secured prior to RSI: An
intraosseous line (secured on arrival in view of severe shock) for
inotrope infusion and one intravenous lines for administration
of anesthetic drugs, fluids, etc.

Ù
Secure 2 intravenous lines prior to intubation
One line is dedicated for inotrope infusion
Most critically ill children requiring intubation in
ED settings have shock. Since sedatives tend to lower
systemic vascular resistance and the application of
positive pressure concurrently decreases preload, shock
could worsen immediately after intubation and assisted
ventilation. An additional bolus, is recommended post-
intubation.
Figure 3.7: The airway being positioned and oxygen is The second line is dedicated for administration for
provided using a Jackson-Rees circuit. Note that the NGT has anesthetic drugs.
been inserted prior to administration of anesthetic agents.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 35

●● The right-sided nurse assists the airway manager by


Avoid having a single intravenous line during PAI.
handing her the laryngoscope, tracheal tube and helps
Dependence on a single line with its risk of ‘getting
IP :be196.52.84.10 to secure the tube.
blocked or bulged’ could dangerous when anesthetic
●● The nurse to the left of the airway manager is respon-
drugs are being administered in the hypoxic or shocked
sible for suctioning. She operates the electrical and
child!
vacuum suction simultaneously.

Positioning Preparation of Airway Tray (Figures 3.10, 3.11)


The external auditory meatus is aligned with the anterior
border of the shoulder such that the oropharynx is in line
with the laryngopharynx. This is accomplished by placing
a towel or folded cloth under the shoulder. In older children
where occiput is not as prominent as in infants, the cloth is
placed under the head to ensure alignment (Figure 3.9).

Figure 3.10: 1. Appropriate sized oropharyngeal airways.


2. Anesthetic drugs; 3. Tra­cheal tubes (calculated size for age
as per the PALS guidelines, with half size greater and half size
less for age); 4. Appropriate sized bag-valve-mask device;
Figure 3.9: Positioning of airway 5. Elastoplast (cut up to one third like trouser legs); 6. Cotton
with tincture benzoin; 7. Age appropriate laryngoscopes;
Ù 8. Towels for positioning the airway; 9. O2 tubings.
Proper positioning is one of the most crucial aspects of
visualizing the glottis. A few moments spent in confirming
alignment can mean a difference between success and
failure in intubation.

Preparation of Staff
Ideally, securing the airway using neuromuscular block-
ade agents in critically ill children, requires a trained team
comprising of at least two physicians and three nurses.
●● The airway manager (team leader) calls out instruc-
tions and should be the only voice heard.
●● A trained nurse is dedicated for application of cricoid
pressure in the older child. Figure 3.11: The appropriate sized laryngoscopic blade is
●● The second physician is assigned the responsibility of selected by matching the blade with the distance between
performing the cardiopulmonary assessment following angle of mouth and thyroid prominence as shown in this
intubation. picture (Courtesy: Dr Mullai Baalaaji).
36 Section II n Airway

Medications: Choice of Drugs


Table 3.2: Anesthetic agents of choice
IP : 196.52.84.10
Physiological status Anesthetic agents
Shock without raised Atropine, Ketamine and
intracranial pressure Succinylcholine
Shock with raised intracranial Lidocaine, with or without
pressure Atropine, Thiopental 2 mg/kg,
Vecuronium
Raised intracranial pressure Lidocaine, Atropine,
without shock Thiopental 5 mg/kg and
Vecuronium
The drug names are called out immediately after being
administrated to avoid confusion, e.g. ‘ketamine given!’
‘vecoronium given!’ Figure 3.12: Majority of children requiring intubation in the ED
are hypoxic on arrival. After administration of premedication
Sequence of Intubation (Figures 3.12 to 3.18) and sedative agent as shown in this figure, cricoid pressure is
applied. Neuromuscular blocking (NMB) agent is administered
The following intubation sequence (steps 3, 4, 5, 6) from and bag-valve-mask is initiated to improve oxygen
start to finish has been captured over a period of 5 minutes. saturation. Failure to provide bag-valve-mask ventilation
after administration of NMB agent, could result in worsening
Sellick’s Maneuver4 of hypoxia leading to cardiac arrest in children presenting to
the emergency department with profound hypoxia and shock
Though not recommended, after administration of induc- (Note the timings on photos).
tion agent, cricoid pressure may be applied to enable vi-
sualization of the glottis. Since the breadth of the crico-
thyroid membrane admits tip of nail in young children, the
finger providing Sellick’s pressure should be held perpen-
dicular to the surface of the neck.
Ù
Caution: The routine use of cricoid pressure application
to prevent aspiration during endotracheal intubation
in children is no longer recommended. If the cricoid
pressure interferes with ventilation or the speed or ease
of intubation, it should be discontinued.

In small infants and neonates, the intubator can apply


pressure over the cricoid to help visualize the glottis using
the tip of his/her little finger. The hand holding the laryn- Figure 3.13: Tube insertion: When the drugs have been given
goscope can be used for this purpose. and the child’s saturations are optimal, the mouth is opened
Ù
Excessive cricoid pressure can distort the airway
and the laryngoscope is introduced. The blade is used to push
the tongue to the left side. Simultaneously, the tip is placed in
preventing visualization of the glottis. the vallecula (curved Macintosh blade) or tip of epiglottis (if
straight Miller blade) is used. The tracheal tube is introduced

Ù
Vomiting during intubation is one of the dreaded com­
into the glottis under vision.
The airway physician, receives the larygnoscope handle
plications. Quickly release cricoid pressure, turn the head in his left hand, with the blade pointing down. The blade
to one side and rapidly suction and clear the airway. is inserted from the right side of the mouth and is used to
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 37

move the tongue to the left. The tip of the laryngoscope is


used to hold the tip of the epiglottis.
The tube is held in IP
the :right
196.52.84.10
hand and inserted into the
glottis up to the vocal cord mark using the right hand.

Ù
Caution: Introduction of the blade beyond the base
of the tongue is the commonest error made by novice
physicians resulting in esophageal intubation.

Postintubation Management
Ù
A common misconception amongst novice airway
managers is that the ‘job is done after intubation’.
Fixing the tube is as important as intubation!

Confirmation of Tube Position


Figure 3.14: Postintubation management: Confirmation of
Tube position is usually confirmed by auscultating over tube position prior to fixation of tube: This picture shows how
the right and left infraclavicular areas, right and left infra- the tracheal tube is held steady by the airway manager soon
axillary areas and over the stomach. after intubation. It is held at the corner of the mouth using
the thumb and the index finger between the inner and outer
Ù aspect of the cheek. Note that tube position is being confirmed
It is mandatory to verify whether the tube is in the trachea by the 5-point auscultation.
and not in the stomach or in the right main bronchus.

Auscultation for air-entry and normal pulse oximetry


readings are insufficient to confirm tube place­ment.
Air-entry may be reported as ‘equally heard’ even if the
tube had been wrongly placed in the esophagus.
In these patients, saturations can remain 100% second-
ary to effective preoxygenation.
Failure in heart rate improvement, persistence of cy-
anosis, hepatomegaly, fall in BP, etc. can herald a wrongly
placed tube.

Ù Figure 3.15: This picture shows how auscultation over the


To confirm tube position, perform the complete stomach is being performed during the 5-point auscultation
cardiopulmonary cerebral assessment. Check pulse as the tracheal tube is being secured
oximetry and ETCO2 if available.
Condensation of vapor in the tube, bilateral chest rise,
Shock can worsen following intubation and positive improvement in heart rate if bradycardic, improvement
pressure ventilation. Venous return falls, leading to fall in color, stabilization of BP, normalization of saturations
in cardiac output. The rapid cardiopulmonary cerebral as- to 100%, briskly responding pupils suggest that the intu-
sessment helps to recognize whether shock is persistent or bation process was successful. Liver span normalizes as
worsening. myocardial function improves.
38 Section II n Airway

If breath sounds are absent on the left side, the tube is


most likely inserted into the right main bronchus. The tube
is repositioned by pullingIP the tube and fixing at the appro-
: 196.52.84.10
priate length. The depth of the tube can be estimated by
multiplying the tube size into three. The tip of the tube ide-
ally must lie at the carina. When the tube is in position, care
must be taken to fix it securely such that it does not slip.

Figure 3.18: Endotracheal tube is fixed securely and the child


is being ventilated with self-inflating BVM device bag

DOCUMENTATION AND MONITORING


AFTER INTUBATION
Drugs, their dosages, size of the tube, length at which it
was fixed, cardiopulmonary response of the patient to in-
tubation and complications which occurred during the pro-
cedure should be documented (Table 3.3).
Figure 3.16: Method of fixation of tracheal tube: Tube is fixed The following monitoring equipment and personnel
as shown in the figure, after applying tincture benzoin as must be available during intubation.
adhesive using 2 bits of plaster cut into ‘trouser legs’. One half
of the trouser leg is fixed along the lower lip and the other strip ●● Pulse oximeter.
is coiled around the tube. ●● ECG monitor.
●● Non-invasive BP monitor.
●● End tidal carbon dioxide monitor.
Delegate one team member to assess tube position, he-
modynamic status and monitor the monitors.

INTUBATION IN ED
SETTINGS: CHALLENGES
Pharmacologically assisted intubation involves use of
anesthetic drugs commonly used in the OR. Children for
whom elective intubation is planned, are advised ‘nil per
oral’ 6 hours prior to surgery. Surgery is often canceled if
minor illnesses are identified during evaluation for anes-
thetic fitness. Besides, if intubation is difficult following
Figure 3.17: This is repeated for the second piece of plaster
after induction, the anesthetist has the option of postpon-
on the upper lip as shown in the next picture
ing surgery to another day.
Following intubation, the 5-point auscultation, is used ●● On the contrary, critically ill children are presumed to
to check tube position. Auscultation is performed over the have ‘full stomach’.
right infraclavicular region, then over the left infraclavicu- ●● They are being intubated for severe hemodynamic in-
lar, right infra-axillary, left infra-axillary areas and over stability.
the stomach. Next, HR, color, CRT, pulses, core-peripheral ●● Unlike, intubations performed in the OT, emergency
temperature gap, BP, liver span and pupils are examined intubations are performed in full view of anxious and
sequentially. often grief stricken parents.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 39

●● ‘Need to ventilate cannot intubate’ after neuromuscular a minimum dose of 0.1 mg (lesser dose causes paradoxical
blockade is perhaps the most anxiety provoking situa- bradycardia). Atropine also blocks secretions induced by
tion for the ED physician. succinylcholine and ketamine.
IP : 196.52.84.10
●● Postponing intubation to a later date is not an option
in the ED. Studies have shown that use of atropine is unneces-
sary when performing RSI in pediatric patients in the ED.
Caution However, this evidence lacks statistical power and further
studies are needed.6
Intubation using anesthetic drugs is hazardous when un-
dertaken by physicians who are not trained in the OT under
the guidance of anesthetists. The key to successful intuba- Lidocaine7,8
tion is the ability to perform effective bag-valve-mask ven- Lidocaine is advocated as pretreatment in the manage-
tilation, have thorough knowledge of anesthetic drugs and ment of children with risk of raised intracranial pressure.
should have performed several intubations using ‘sedation It is useful in attenuating the rise in ICP caused by reflex
only’ protocol. sympathetic response to laryngoscopy. It is administered
Intubation using paralytic agents in the ED requires prior to succinylcholine (1.5 mg/kg intravenously) to
enormous dedication, expertise and team work for suc- avoid drug-induced rise in ICP. Use of lidocaine should be
cessful outcomes. Drawing up appropriate medications avoided in patients with bradyarrhythmia, hypotension and
and assigning tasks to all personnel assisting in the proce- in those allergic to amides.
dure should be seamlessly performed. RSI medications, are divided into induction and para-
Ù lytic agents. Development of pulmonary edema, hypoten-
In the Indian context, majority of children reaching the ED sion, imminent arrest, raised ICP, respiratory failure and
are in respiratory failure with severe hypoxia on arrival. refractory status epilepticus are the commonest indications
Under these circumstances, preoxygenation with non- for intubation in the ED.
rebreathing mask prior to intubation seems in-sufficient
to improve oxygen reserves. It appears safer to provide
positive pressure ventilation after administration
Induction Agents
of neuromuscular blockade. This practice, prevents Induction agents are primarily administered to sedate prior
deterioration to cardiac arrest during during intubation to paralyzing. Commonly used induction agents are:
in the hemodynamically compromised child. To avoid,
Midazolam, Thiopental, Ketamine, Fentanyl, Etomidate
gastric distension and aspiration, a nasogastric tube is
introduced to rapidly remove gastric contents.
Midazolam
This modified technique employing preoxygenation
Midazolam, a sedative and hypnotic agent, is also useful
using bag-valve-mask after paralysis and NGT decom­
in controlling convulsions. A frequently used induction
pression has not resulted in mishaps in a large volume agent, it causes respiratory depression and hypotension.
PED. No child desaturated during intubation attempts.4
Ù
Midazolam should be avoided in children presenting
Medications with hypotensive shock.
Atropine
Pediatric Emergency Medicine Committee of the Ameri- Thiopental
can College of Emergency Physicians5 recommends at- Thiopental an ultrashort acting barbiturate, acts by inhibit-
ropine for RSI in children younger than 1 year, for older ing the GABA receptor complex. It causes a dose-depen-
children (1–5 years) receiving succinylcholine and ado- dent decrease in cerebral metabolic oxygen consumption,
lescents receiving a second dose of succinylcholine. The cerebral blood flow and ICP. It also maintains cerebral per-
recommended atropine dose is 0.02 mg/kg in children with fusion pressure. Thus, its cerebroprotective effect is useful
40 Section II n Airway

in clinical scenarios complicated by cerebral edema and Fentanyl


status epilepticus. Unfortunately, its myocardial depres-
sant effect results in hypotension. It is therefore the drug Fentanyl, an opioid agent, reduces the cardiovascular side
IP : 196.52.84.10 effects of laryngoscopy and intubation. It is 100 times
of choice in head trauma and central nervous system infec-
tions and contraindicated in hypotensive shock. more potent than morphine in its analgesic effect and helps
to attenuate the hypertensive effects of intubation render-
ing it useful in raised ICP. Since, its sedative effect is not
Ketamine adequate, it is often combined with a benzodiazepine. The
combination however, could cause profound cardiovascu-
Ketamine is a dissociative amnestic agent, which causes lar compromise and troublesome apnea.
the peculiar sensation of the mind being separated from the
body. It belongs to the phencyclidine group of drugs. Ket- Ù
Chest wall rigidity and bradycardia are precipitated
amine stimulates norepinephrine release in those patients
with adequate presynaptic stores and is associated with less when fentanyl is administered rapidly.
cardiovascular depression than barbiturates or Benzodiaz-
epines. Hence, it is useful in maintaining blood pressure in
shocked children and has been recommended as an induc-
Etomidate
tion agent for children with septic shock.7 Infants and the Etomidate is an imidazole hypnotic agent, which does not
chronically ill may have inadequate norepinephrine stores; cause either hypotension or raised intracranial tension. It
in this setting ketamine’s direct myocardial depressant causes adrenal suppression and therefore is avoided in sep-
action may become apparent. Low-dose fentanyl may be tic shock (relative adrenal insufficiency). At the time of
considered for the induction of hemodynamically unstable writing this manual it is not currently available for wide
septic patients. It also causes tachycardia, which helps to spread use in our country.
block the bradycardia caused by laryngoscopic manipu-
lation of the upper airway. Bronchodilation secondary to
beta 2 adrenergic stimulation is another beneficial effect, Neuromuscular Blockade Agents
making ketamine the induction agent of choice in asthma. Succinylcholine
Ketamine increases intracranial and intraocular pres- Succinylcholine remains the most preferred neuromuscular
sure. Consequently, it is contraindicated in head injury, blocking agent for RSI in the ED. It owes its popularity to
meningoencephalitis and glaucoma. It also increases sali- its rapid onset of action with shortest duration of paralysis.
vation and emergence reactions consisting of visual and Despite its long list of complications, it creates excellent
auditory hallucinations. Atropine, counteracts salivation intubating conditions more reliable than Rocuronium.10
and midazolam lessens hallucinations when ketamine9 is
used as an induction agent. Laryngospasm, another side It is available as a 20 mg/mL solution. It rapidly loses
effect of ketamine is countered by the use of a neuromus- potency after one month if stored in room temperature.
cular blockade agent given sequentially after ketamine. The dose requirement is increased by 50% if defasciculat-
Ù ing doses are used. When given through the intramuscular
route, onset is delayed and the duration of action is ap-
Caution:
proximately 20 minutes.
• Ketamine could worsen hypotension and
precipitate cardiac arrest in children presenting Transient increase in heart rate is often noted. Brady-
with decompensated shock secondary to chronic cardia can also occur, but is countered by atropine (pre-
myocardial dysfunction. Avoid ketamine in children medication agent). The most devastating arrhythmias are
presenting with severe congestive heart failure and caused by hyperkalemia, which can lead to cardiac arrest.
shock. Conditions, which predispose to hyperkalemia are exten-
sive burns, severe trauma, myopathies and muscle necrosis.
• In children being intubated for upper airway The period of greatest risk of hypokalemia varies between
obstruction (where paralytic agents are 2 days and 6 months after the onset of these comorbidities.
contraindicated), ketamine may be contraindicated If ECG changes of hyperkalemia are noted, NMB should
due to its inherent risk of laryngospasm. be avoided. Rise in intracranial pressure and intraocular
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 41

pressure has been attributed to the use of succinylcholine. cally difficult and intellectually challenging procedure
Hence this drug is withheld in children with risk of ICP performed on critically ill children in ED settings. If per-
and glaucoma. In general,
IP fasciculations
: 196.52.84.10are less intense in formed successfully, the outcomes can be extraordinarily
children than in adults. The routine use of defasciculation gratifying.
doses of succinylcholine in the ED is controversial.8
Key Points11
ü
Vecuronium, Pancuronium and Rocuronium 1. Preoxygenate on arrival and insert NGT.
2. Initiate inotrope.
Vecuronium, pancuronium and rocuronium are the com- 3. Preparation—O2, suction, IV access, tubes, tapes,
monly used non-depolarizing agents. These drugs act by
drugs, equipment.
binding to the neuromuscular receptor causing blockade,
4. Premedicate.
but no depolarization. All act less quickly and last much
longer than succinylcholine. 5. Put to sleep.
6. Position the patient.
Amongst these drugs, rocuronium has the fastest onset 7. Pressure on cricoid.
of action (60–90 seconds) with duration of action of ap- 8. Paralysis.
proximately 30–40 minutes. Pancuronium has the slowest 9. Preoxygenate using bag-valve-mask device.
onset and longest duration of action lasting up to 60–90
10. Place the tube and check position.
minutes. Though the side effects described for succinyl-
11. Prevent dislodgement during transport.
choline do not exist in this group of drugs, the longer dura-
tion of action delays recovery. Difficulty in securing the
airway would be hazardous under these circumstances. common errors
1. Failure to adequately preoxygenate prior to
û
Failed Intubation intubation.
●● Intubate within the time taken for you to breathe out! 2. Failure to position the child such that the oropharynx
(20–30 seconds). and laryngopharynx are not in the same straight
●● Avoid making more than 2 attempts if unsuccessful on line.
the first attempt. 3. Inserting the laryngoscope into the esophagus.
When patient is paralyzed and the ET tube cannot be 4. Failure to confirm tube position by performing the
placed, the first option is to ventilate the child using a bag- complete cardiopulmonary cerebral assessment.
valve-mask device until the return of spontaneous respira-
5. Failure to initiate an inotrope prior to administration
tion. This technique can be employed until expert help ar-
of anesthetic agents.
rives (Refer to Chapter 4 on Assessment and Management
of the Difficult Airway). 6. Failure to hold the ET tube, until it is secured.
7. Failure to anticipate that shock can worsen after
Pharmacologically assisted intubation, in the hemo- intubation.
dynamically unstable child, is perhaps the most techni-
42 Section II n Airway

Table 3.3: Drugs for rapid sequence induction

Drugs Dose Route Duration Side Effects Comments


Premedications
IP : 196.52.84.10
Atropine 0.01 IV > 30 min Paradoxical bradycardia a. Inhibits bradycardic response to hypoxia
mg–0.02 IM can occur with doses < b. Dilates the pupil but will not fix it
mg/kg 0.1 mg c. Recommended when ketamine and/or
Min: 0.1 mg succinylcholine is being used
Max: 1 mg d. Used for intubating children < 4 years
IM dose: e. Used in intubating children with bradycardia
0.02 mg/kg
Glycopyrrolate 0.005–0.01 IV > 30 min Tachycardia a. Inhibits bradycardic response to hypoxia
mg/kg Dry Mouth b. Dilates the pupil, but will not fix it
Max: 0.2 mg c. Has less tachycardia compared to atropine
Narcotic agents
Fentanyl citrate 2–4 ug/kg IV, IM 1–2 h Respiratory depression, a. Less histamine release associated hypotension
hypotension, chest wall than with other opioids
rigidity and bradycardia b. May elevate ICP
can occur when given c. Movement disorders can occur with prolonged
rapidly use
Sedative hypnotics agents
Midazolam 0.1–0.2 IV, IM 30–60 min Respiratory depression a. Potentiates respiratory depressive effects of
mg/kg and hypotension narcotics and barbiturates
Max: 4 mg
Diazepam 0.1–0.2 IV 30–90 min Hypotension b. No analgesic properties
mg/kg
Max: 4 mg
Thiopentone 2–4 mg/kg IV 5–10 min Negative inotropic a. Ultrashort-acting barbiturate
effects hypotension b. Decreases cerebral metabolic rate and ICP
c. Potentiates respiratory depressive effects of
narcotics and benzodiazepines
d. No analgesic properties
Propofol 2 mg/kg (up IV 3–5 min Hypotension in a. On prolonged infusion can caused propofol
to 3 mg/kg children with relative infusion syndrome
in young hypovolemia, pain on b. Potentiates respiratory depression
children) injection c. No analgesic properties
d. Highly lipid soluble with short duration of
action
e. Less likely to increase airway reactivity
Anesthetic agents
Lidocaine 1–2 mg/kg IV = 30 min Myocardial and CNS Decreases ICP
depression with high Hypotension less common
doses. Seizures can
occur with repeated
doses
Ketamine 1–4 mg/kg IV, IM 30–60 min Increased ICP and BP Dissociative anesthetic agents No to limited
increased secretions respiratory depression, bronchodilator
and laryngospasm
hallucinations and
emergence reactions
Contd...
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 43

Contd...

Drugs Dose Route Duration Side Effects Comments


IP : 196.52.84.10
Neuromuscular blocking agents
Succinylcholine IV: 1–1.5 IV, IM 3–5 min Muscle fasiculations, rise Depolarizing muscle relaxant with rapid onset
mg/kg for in intraocular, and short duration of action; Avoid in renal failure,
children intracranial burns or hyperkalemic states; Consider non-
IV: 2 mg/kg intragastric pressure, depolarizing agent in children < 5 years of age
for infants life-threatening Do not use for maintenance of paralysis
IM: Double hyperkalemia,
the dose hypertension
for IV
Vecuronium 0.1–0.2 IV, IM 30–90 min Minimal cardiovascular Non-depolarizing agent acting within 2–3
mg/kg side effects minutes and having longer duration of respiratory
paralysis compared to succinylcholine (caution if
intubation is difficult in the ED)
Rocuronium 0.6–1.2 IV 30–60 min Minimal cardiovascular Non-depolarizing agent that has a rapid onset of
mg/kg side effects action equaling succinyl choline

REFERENCES 7. Salhi B, Stettner E. In defense of the use of lidocaine in


rapid sequence intubation. Mower III WR, Knopp RK,
1. Audrey Zelicof-Paul, et al. Controversies in rapid sequence (Ed). Clinical controversies: lidocaine administration
intubation in children. Curr Opin Pediatr. 2005;17:355-62. before rapid sequence intubation in patients with traumatic
2. SE Mace. Challenges and Advances in Intubation: Rapid brain injuries. Ann Emerg Med. 2007;49(1):84-86.
Sequence Intubation Emerg Med Clin N Am; 2008 1043– 8. Vaillancourt C. Kapur AK. Opposition to the use of lidocaine
1068 doi:10.1016/j.emc.2008.10.002. in rapid sequence intubation. Mower III WR, Knopp RK,
3. Preethi V, Venkatesh P, I Santhanam, P Jeyachandran, Profile Ed. Clinical controversies lidocaine administration before
of rapid sequence intubation in the PED of an academic rapid sequence intubation in patients with traumatic brain
children’s hospital in S.India- A pilot study. Proceedings of injuries. Ann Emerg Med. 2007;(1):86-87.
the National Assembly on Pediatric Emergency Medicine,
2012. 9. Wathen JE, Roback MG, Mackenzie T, et al. Does
midazolam alter the clinical effects of intravenous ketamine
4. Ellis DY, Harris T, Zideman D.H.Cricoid pressure in
sedation in children? A double-blind, randomized,
emergency department rapid sequence tracheal intubations:
a risk-benefit analysis. Ann Emerg Med. 2007;50(6):653- controlled, emergency department trial. Ann Emerg Med.
65. 2000;36:579-88.
5. ACEP Policy Statement. Rapid-sequence intubation. 10. Perry J, Lee J, Sillberg VAH, et al. Rocuronium versus
Approved by ACEP Board of Directors – 2006, www. succinylcholine for rapid sequence induction intubation.
ACEP.org. (database online) Cochrane Database Syst Rev. (2):
6. A. Bean. Atropine. Re-evaluating its use during pediatric 2008;CD002788.
RSI. Emerg Med J. 2007;24(5):361-62. doi: 10.1136/ 11. www.vdh.virginia.gov/OEMS/files page /symposium/2010.
emj.2007.048512. Presentations/PREP-1013. PDF.
Assessment and Management
4
IP : 196.52.84.10

of the Difficult Airway

Figure 4.1: Spectrum of difficult airway (Courtesy: Dr Thangavelu S and Dr Gunda Srinivas).

Learning Objectives
1. Defining a ‘Difficult airway’. 3. A modified ‘Difficult airway protocol’.
2. How do we recognize the red flag signs of airway 4. Laryngeal mask airway (LMA).
difficulty? 5. Difficult airway equipment.

Introduction In many instances, difficult bag-valve-mask ventilation


or intubation can be predicted.
Being confronted with a need to intubate a child presenting
with respiratory failure and not being able to do so is every Ability to recognize a difficult airway, helps to plan on
ED physician’s nightmare (Figure 4.1). an alternative method if one technique fails. To avoid a po-
tentially life-threatening ‘cannot ventilate, cannot intubate’
situation, a ‘difficult airway’ algorithm must be available.
Difficult airway
In most instances, securing the airway of a child, will be Preparation
straightforward if the clinician is skilled and the airway
anatomy is normal. ●● If a difficult airway is suspected following focussed
history and physical examination and the child is not
A difficult airway can result from a variety of anatomi- in cardiopulmonary failure, notify subspecialty teams
cal or clinical conditions. from critical care, otolaryngology or pulmonology who
are skilled in flexible or rigid bronchoscopy.
Difficult airway can be recognized:
1. On arrival—when the child reaches may have Ù
Do not meddle with a difficult airway. Call for ENT
spontaneous breathing or in respiratory arrest. physician’s or anesthesiologist’s help.
2. During BVM ventilation—before or after a paralyzing
agent has been administered. ●● Difficult intubation equipment should ideally be read-
3. During laryngoscopy. ily available in one location in addition to standard in-
4. During tracheal intubation. tubation equipment.
Chapter 4 n Assessment and Management of the Difficult Airway 45

It is very rare that a surgical cricothyrotomy will be STEP 1


needed to perform in children and it should be avoided at Recognize ‘Red flag’ signs during Airway assessment
all costs in the ED. TheIPintubator should be familiar with
: 196.52.84.10
specialized airway equipment (Box 4.1).
STEP 2
Box 4.1: Difficult airway kit3 Ensure oxygenation
Position the airway
●● Bag-valve-mask (various sizes)
●● Guedel airways (various sizes) Open the airway
●● Nasopharyngeal airways (various sizes) Suction
●● Laryngeal mask airways (various sizes) Flow inflating device if spontaneously breathing, or
●● Laryngoscope blades (straight, curved, McKoy) Magill BVM ventilation in respiratory failure
forceps
●● Gum elastic bougie If BVM is difficult,
●● Needle cricothyrotomy set (14G cannula, 5 mL syringe, 3.0 1. Reposition
ETT adapter) 2. Consider airway obstruction such as FB
●● Surgical cricothyrotomy set 3. Jaw thrust
●● Jet ventilation set (high pressure oxygen tubing, 3-way 4. Two-person technique
tap)
5. Introduce oropharyngeal/nasopharyngeal airway
Optional:
●● Intubating laryngeal mask
●● Light wand STEP 3
●● Fiberoptic laryngoscope bronchoscope Laryngoscopy and Intubation
●● Video laryngoscope
Difficult laryngoscopy
More specialized equipments such as intubating la- 1. Reposition
ryngeal mask, light wand or fiberoptic intubating laryngo-
2. Change blade
scope may be helpful only if the intubator be familiar with
3. Cricoid pressure
their use.4
4. BURP
5. Bimanual laryngoscopy
Step 1: Recognize ‘Red Flag’ Signs During
Difficult tracheal intubation
Airway Assessment
1. Change ETT (0.5 mm smaller, cuffed over un-
Emergent airway management often includes the ability cuffed when choosing a smaller size (ETT)
to take a comprehensive history and perform a thorough 2. Laryngospasm
physical exam. Clinical examination, provides clues that
can predict potentially ‘difficult to intubate’ airway.
STEP 4
‘Red flags’ for a potentially difficult airway include: Supraglottic airway devices/difficult airway adjuncts—
Laryngeal Mask Airway
●● Young age (infant or neonate).
●● History of trauma (including facial, laryngeal or tra-
cheal trauma or trauma with possible cervical spine STEP 5
involvement). Equipments used to intubate difficult airways like Bougie,
●● Inhalational injury. videoscopy, etc. by airway experts (ENT or anesthetists).
●● Acute infectious disease such as epiglottitis.
●● History consistent with foreign body aspiration.
●● Known difficult airway from prior intubation. STEP 6
Surgical airway
●● Congenital craniofacial abnormalities:
– Micrognathia, large tongue and short neck. Cricothyrotomy
●● Stridor. Figure 4.2: Difficult airway algorithm
●● Drooling. Recommendations for the management of the difficult
●● Obesity. pediatric airway have been proposed, but the technique
●● Significant scoliosis.2 used depends on the skill of the intubator.5
46 Section II n Airway

Step 2: Ensure Oxygenation ●● Avoid manipulation of the airway if more than two
attempts had been made and earlier attempts had
1. Provide high concentration oxygen using a flow inflat-
IP :(refer
196.52.84.10 failed.
ing ventilation device Chapter 5) in a spontane-
ously breathing child with airway obstruction. ●● If saturations cannot be maintained despite effec-
tive bag-valve-mask ventilation, plan to insert the
2. Initiate bag-valve-mask ventilation, if the child pres-
ents with respiratory failure or has not recovered from laryngeal-mark airway (LMA).
paralysis. Oxygen flow should be enough to keep the
reservoir inflated throughout the respiratory cycle.
Ù Patients need oxygen not tube.5
3. Constantly, ensure that the oxygen saturation is great-
er than 95% (one member in team should be delegated Difficult tracheal intubation can be divided into problems
the responsibility of informing the airway manager with laryngoscopy and problems with intubation.
when the saturations drop to 92%).
Ù Step 3: Laryngoscopy and Intubation
Bag-valve-mask ventilation could be difficult when oral
or posterior pharyngeal structures crowd the airway. Ù
Difficult laryngoscopy most commonly results from
Large tongue, tonsils, or adenoids, or a ‘floppy’ larynx
can all obstruct the airway. improper head positioning along the frontal plane.

If bag-valve-mask ventilation is difficult: 1. Reposition.


●● Reposition the airway by manipulating—head tilt-chin
●● Reposition airway, such that the external auditory
lift maneuver/jaw thrust technique.
meatus and anterior edge of the shoulder are in the
●● Release cricoid pressure, if ventilation is difficult in
paralysed child.5 same straight line or position where chest rise is
●● Use nasopharyngeal or oropharyngeal airways to im- maximal during bag-valve-mask ventilation.
prove airway patency. ●● Extend or flex the neck to improve the intubator’s
view of the vocal cords.
Measure the distance between tip of nose and tragus and
cut a 3.5 sized endotracheal (ET) tube to fashion a na- ●● Place a towel under the shoulder blades of infants
sopharyngeal airway. Attach an adaptor to the cut end of or neonates. This allows for better alignment of
tube (to avoid slippage into the air passage). the oral/pharyngeal/and laryngeal axes.
●● Place a towel under the head for adolescents to
●● Two persons can be delegated to ventilate, one to hold
the mask using both hands and the other to pump the achieve the same.
bag. This technique will be needed in high-pressure ●● Apply backwards, upwards, rightward cricoid
bag-valve-mask ventilation in obese patients or in pa- pressure (‘BURP’). The anteriorly placed infant
tients with low chest wall compliance (refer Figure larynx may be better visualized with external la-
21.1, Chapter on status epilepticus). ryngeal manipulation.
Adequacy of bag-valve-mask ventilation is assessed by 2. Change the technique of inserting the laryngo-
following methods:
scope.
1. Degree of chest rise and fall.
●● Insert the laryngoscope into the right side of the
2. Improvement of heart rate if bradycardic, color and
mouth and actively ‘sweep' the tongue out of the
oxygen saturation.
intubator's line of vision.
●● If oxygenation and ventilation can be provided, by
effective bag-valve-mask ventilation, continue to Oropharyngeal crowding is normal in neonates
do so until help arrives. due to their relatively large tongue.
●● If effective bag-valve-mask ventilation is possible, 3. Intubating medications.
intubation may not be so difficult. ●● Use lower doses of intubating medications, if dif-
●● Call for expert help to intubate (ENT physicians or ficulty is anticipated.
anesthetists) at the earliest.
Chapter 4 n Assessment and Management of the Difficult Airway 47

●● Use sedatives with caution, since these drugs can 5. Change the airway manager
cause hypotension and can convert a difficult air- If the airway manager, is unable to intubate after 2 at-
way into an obstructed airway. tempts, ideally, assistance must be sought from a more
IP : 196.52.84.10
●● Give half the dose initially followed by another skilled person (Figures 4.2 to 4.5).
half dose if airway and breathing can be supported
by bag-valve-mask ventilation. Continue to initiate bag-valve-mask ventilation and
●● Consider use of atropine to avoid vagal-induced wait until a more experienced airway physician arrives.
bradycardia during laryngoscopy, though evi- This could be an anesthetist, ENT surgeon’s or ED or in-
dence for this practice is equivocal.6 tensive care physician.
●● Use muscle relaxants judiciously in upper airway
obstruction. Ù
Patients do not die from failure to intubate. They die
●● Avoid muscle relaxant, if bag-mask-valve ventila- from failure to STOP trying to intubate.5
tion is ineffective.
●● Rapidly transport to the operating room for inha-
lational induction, if child presents with stridor
and respiratory failure to the ED.
4. Intubation.
Difficult tracheal intubation could result from several
problems.
Small endotracheal tubes are compliant leading to diffi-
culty in negotiating the acute angle of an anteriorly placed
pediatric larynx.
Ù
Use an introducer, bent into a ‘hockey-stick’ . Figure 4.3: Note the abscess on the back can prevent
visualization of the glottis. Though the neck appears
The small size of the newborn’s mouth causes diffi- hyperextended, optimal airway alignment was possible
culty in visualizing the vocal cords, when introducing the based on the position, which ensured maximum chest rise,
endotracheal tube (mentioned earlier). improvement in heart rate, perfusion and SaO2.

Ù
Insert the endotracheal tube from the right-hand corner
of the mouth with the plane of insertion at 90° from the
plane of the cord visualizing.

Difficulty may be encountered, when advancing the en-


dotracheal tube beyond the vocal cords. This results from
the narrowing of the pediatric airway at the cricoid ring or
could be the result of a pathological subglottic process.
Ù
Use 0.5 mm smaller internal diameter of the endotracheal
tube appropriate for the age. Cuffed tubes may be
Figure 4.4: Note the airway manager manipulating the airway
preferred over uncuffed, while using ET tubes smaller
using the little finger. Also note the airway nurse on the right
than appropriate for age to avoid air leak for effective hand side of the intubator providing lip retraction whilst the
ventilation. airway nurse on the left side is poised with a suction catheter.
Ability to anticipate the needs of the airway manager and
●● Stop intubation attempts and reoxygenate (continue assist in the intubation process, is one of the most important
bag-valve-mask ventilation) if saturations drop. skills of the airway nurse.
48 Section II n Airway

Choice of appropriate LMA is based on the patient's weight


are listed in Table 4.1.7
IP : 196.52.84.10 Table 4.1: Selection of LMA

LMA size Patient size Max cuff volume (mL)


1 < 5 kg 4
1.5 5–10 kg 7
2 10–20 kg 10
2.5 20–30 kg 14
3 30–50 kg 20

Figure 4.5: The airway manager is holding the tube against
1. Lubricate the posterior surface of the LMA with a wa-
the inner aspect of the cheek, while tube position is being ter soluble lubricant.
checked prior to fixing the tube. 2. Place an inflation syringe in the cuff valve and deflate
the cuff completely for insertion, making sure that the
leading tip is not folded backwards.
Step 4: Failed Intubation
3. Hold the LMA close to the cuff using a pencil grip
Laryngeal Mask Airway (LMA) (Figure 4.7).
The LMA is a small inflatable mask, attached to tubing with
an universal adapter. It is designed to sit in the oropharynx
with the tip in the hypopharynx and the base at the epiglot-
tis. With the cuff inflated, the laryngeal mask creates a seal
around the supraglottic area, allowing air flow between the
tubing and trachea (Figure 4.6).

Ù
If despite all the maneuvers mentioned above, intubation
has failed and saturations are dropping, resort to LMA.
Laryngeal mask airway is a rescue device in a ‘cannot Figure 4.7: Technique of insertion
intubate cannot ventilate’ (CICV) situation. 4. Place the head and neck in the sniffing position. Open
the mouth, while lifting the chin forward (Figure 4.8).

Figure 4.6: Parts of laryngeal mask airway (LMA). Figure 4.8: Technique of insertion (Contd...)
Chapter 4 n Assessment and Management of the Difficult Airway 49

5. To facilitate LMA introduction into the oral cavity,


gently press the middle finger down on the jaw (Fig-
ure 4.8). IP : 196.52.84.10
6. Simultaneously, press the LMA against the hard palate
and guide it along the posterior oropharynx until the
operator feels firm resistance. The opening of the cuff
faces towards the tongue. This method prevents fold-
ing up of the epiglottis (Figures 4.9 and 4.10).
Ensure that the patient is fully unconscious when
inserting the LMA. Often, the partially conscious
victim may inadvertently bite the finger of the rescuer
as he inserts it in this manner.

Figure 4.11: LMA inserted.


8. Gently maintain cranial pressure with the non-dominant
hand, while removing the index finger (Figure 4.12).

Figure 4.9: Technique of insertion (Contd...)

Figure 4.12: Stabilization of LMA.

9. Inflate the cuff using an air filled syringe until the pi-
lot balloon gets filled up. The laryngeal mask may be
observed to ‘rise up' slightly out of the oropharynx
(Figure 4.13).
10. Fix the LMA in the midline with dynaplast tape around
the tube. Also insert a roll of gauze on either side of
Figure 4.10: Technique of insertion (Contd...) the LMA to avoid biting the tube.
The laryngeal mask does not prevent reflux and aspi-
7. Maintaining pressure with the finger on the tube in the
ration of gastric contents. It is not helpful with glottic or
cranial direction, advance the mask until definite re-
subglottic pathology and cannot be used to deliver high
sistance is felt at the base of the hypopharynx. Note
pressure ventilation (laryngeal mask seal pressure is ~25
the flexion of the wrist (Figure 4.11).
mm H2O).
50 Section II n Airway

IP : 196.52.84.10

Figure 4.14: Bougie


Figure 4.13: Cuff being inflated.
Complications of LMA insertion:
●● Partial airway obstruction by the epiglottis.
●● Loss of adequate seal with patient movement.
●● Air leak during positive pressure ventilation.
●● Poor tolerance of the LMA, if airway protective reflex-
es are intact or recovering.

Step 5: Airway Experts


Bougie8 (Figure 4.14)
●● The Bougie is a straight, semirigid stylet-like device
with a bent tip that can be used when intubation is (or Figure. 4.15: Endotracheal tube introduced over bougie.
is predicted to be) difficult. Fiberoptic scopes may be broadly classified into two
●● When vocal cords cannot be visualized due to extreme groups:
anterior positioning, the bougie can be inserted blindly
above the epiglottis. 1. Flexible devices.
●● Confirmation of insertion into the trachea occurs, when 2. Rigid and semirigid devices. This device permits in-
the bougie can be felt to ‘hop' along the tracheal rings direct visualization of the glottis through an image
as it is advanced. transmitted via fiberoptic bundles. The fiberoptic bun-
●● Introduce an endotracheal tube over the bougie into the dles are aligned with a non-malleable blade or stylet
trachea and remove the bougie (Figure 4.15). with a J-shape or L-shape, allowing the physician to
●● The Bougie is an important part of the armamentarium see around the corner.
of the anesthetist. If in need, do not hesitate to call for
Examples of rigid devices include the bullard laryn-
expert help.
goscope (ACMI Corp, Southborough, Mass); the Upshers
cope F2 (Mercury Medical, Clearwater, Fla) and the Wu-
Videoscopic Techniques8 Scope (mercury medical).
A variety of fiberoptic and videoscopic devices facilitate
Readers should familiarize themselves with the advan-
intubation in difficult airway scenarios, where direct lar-
yngoscopic visualization of the laryngeal opening is not tages and disadvantages of each of these instruments and
possible. Practice and familiarity are needed to make use techniques.8 The use of these devices however, is beyond
of these devices. the scope of this manual.
Chapter 4 n Assessment and Management of the Difficult Airway 51

Step 6: Surgical Airway—Cricothyrotomy


(Rarely Needed)
IP : 196.52.84.10
This method should be reserved as a last resort. A hazard-
ous procedure, needle cricothyroidectomy should not be
undertaken lightly.
Consider needle cricothyrotomy, if upper airway ob-
struction is proximal to the glottic opening and other mea-
sures of securing the airway have failed.
1. Equipment necessary for the procedure includes:
• 14 gauge intravenous cannula.
• 3.0 size endotracheal tube adapter.
• 5 mL syringe. Figure 4.16: The happy mother and her newborn 4 days
2. Position child supine by extending the head and plac- following resuscitation (same new born managed in 4.3–4.5).
ing a towel under the shoulders.
3. If cricothyroid membrane is palpable, cannula should
be inserted at this point.
Key Points
ü
1. Practice of protocols for the management of the
4. If cricothyroid membrane is not palpable as in young difficult airway is necessary.
infants, palpate and immobilize the trachea. 2. Effective bag-valve-mask ventilation is the most
5. Advance cannula to which syringe is attached into important technique in the management of the
the tracheal lumen at a 30° angle until air is aspirated. difficult pediatric airway.
6. Fix the 3.0 endotracheal tube adapter to the hub of the 3. Repositioning is the most effective means of
cannula and initiate bag ventilation. providing adequate bag-valve-mask ventilation.
7. Transtracheal jet ventilation should be used with ex- 4. The laryngeal mask may be a life-saving device in
treme caution. It should only be used when a pressure event of failed intubation, desaturation and inability
release valve is attached to the system (such as a 3-way to bag-valve-mask ventilate.
tap) to prevent excessive air flow and barotrauma. 5. Fiberoptic techniques are useful for visualization
Complications include bleeding, subcutaneous emphy- and should also be practiced.
sema and failure to adequately oxygenate. 6. Surgical techniques such as needle cricothyrotomy
Ù are rarely necessary.
Surgical cricothyrotomy is discouraged in young children
(< 10 years) due to the low likelihood of success and
high complication rate in the emergency setting.6
common errors
û
1. Failure to recognize ‘red flag’ signs of difficult
Documentation should focus on the following: airway.
i. Difficulties encountered during intubation. 2. Failure to call for expert help.
ii. Methods used to secure the airway. 3. Making multiple attempts despite repeated failure.
The sight of recovered child with their parents after 4. Failure to oxygenate between attempts.
successful resuscitation in the ER is always a satisfying 5. Failure to respond urgently to fall in saturations to
experience. Refer Figure 4.16 92%.
52 Section II n Airway

References 5. Benger J. Nolan J, Clancy M. Emergency Airway Manage-


ment. London: Cambridge University Press; 2009: pg 81.
1. The American Society of Anesthesiologists Task Force: 6. Weiss M, Dullenkopf A, Fischer JE, et al. European Pae-
Practice guidelines IP : 196.52.84.10
for management of the difficult airway. diatric Endotracheal Intubation Study Group. Prospective
Anesthesiology. 2003;98:1267-277. randomized controlled multi-centre trial of cuffed or un-
2. Murphy MF, Walls RM. Identification of the difficult and cuffed endotracheal tubes in small children. Br J Anaes.
failed airway. In: Walls RM, Murphy M, Luten RC (Eds). 2009;103(6):867-73.
Manual of Emergency Airway Management. Philadelphia. 7. http://www.lmana.com/faqs.php#faq03
PP. P. Lippincott Williams and Wilkins; 2008;82. 8. Levin R, Kissoon N, Froese N. Fibreoptic and videoscopic
indirect intubation techniques for intubation in children.
3. Preece R. Guidelines for difficult airway equipment in
Pediatr Emerg Care. 2009;25(7):479.
emergency departments. Emerg Med J. 2006;3:230.
9. Cote C, C Hartnick. Pediatric trans-tracheal and cricothy-
4. Walker R, Ellwood J. The Management of difficult intuba- rotomy devices for emergency use: which are appropriate
tion in children. Pediatr Anes th. 2009;19:77-87. for infants and children? Pediatr Anaes th. 2009;19:66-76.
Flow Inflating Ventilation Device:

5
IP : 196.52.84.10
Non-invasive CPAP in Settings
Without Immediate Access to
Mechanical Ventilation

Figure 5.1: Flow inflating ventilation device, a boon in the ED management of acute pulmonary edema and shock

Learning Objectives
1. CPAP and its benefits in the management of acute 3. Pearls and pitfalls when using this device.
pulmonary edema during shock resuscitation. 4. Evidence supporting the use of non-invasive posi-
2. Parts of the flow inflation ventilation device (Jack- tive pressure ventilation (NIPPV).
son-Rees/Pediatric Bain circuit).

INTRODUCTION trolled studies to support the use of non-invasive respira-


tory support in children.1
A large number of seriously ill children reach our hospitals
with respiratory distress or failure, have features of acute
pulmonary edema or cardiac dysfunction (Figure 5.1). PHYSIOLOGY
Ù
Hypoxic and shocked children due to various etiologies
Functional residual capacity (FRC) is the volume of gas
remaining in the lungs during normal expiration. Diseased
often present with pulmonary edema due to cardiac lungs with atelectasis have reduced FRC. Consequently,
dysfunction or acute lung injury. blood is shunted to the heart without oxygenation (intra-
pulmonary shunting). Lung compliance decreases, while
Under these circumstances, the flow inflating ventila-
airway resistance increases. A combination of these factors
tion device, which provides continuous positive airway
result in increased work of breathing.
pressure in spontaneously breathing patients, appears to be
a boon in the initial management of these children in set- Application of continuous positive airway pressure
tings without immediate access to mechanical ventilation. (CPAP) improves FRC, thereby alleviating intrapulmo-
However, the use of NIPPV for pediatric patients in nary shunting and increasing oxygenation. Lung compli-
emergency situations is not well established and a recent ance becomes better, airway resistance falls and work of
Cochrane review notes the lack of well-designed and con- breathing is reduced (Figures 5.2 to 5.5).
54 Section II n Airway

IP : 196.52.84.10

Figure 5.2: Parts of the flow inflating ventilation device (Jackson-Rees circuit)

Under-ventilated alveoli open up (recruitment) as FRC


improves. Perfusion to the newly recruited alveoli takes
place, thereby improving oxygenation.
In acute cardiogenic PE, CPAP reduces left ventricular
transmural pressure. This is the main mechanism by which
CPAP improves oxygenation in cardiogenic PE. CPAP in-
creases intrathoracic pressure. Consequently, preload and
afterload falls leading to improvement in cardiac output
and PE.

Figure 5.3: This infant is being manually ventilated in the ED


following intubation using the flow inflating ventilation device.
Inotrope and catecholamine infusions are on flow during fluid
resuscitation of myocardial dysfunction and shock.
Figure 5.4: Parts of the flow inflating ventilation device
continued...
Chapter 5 n Flow Inflating Ventilation Device: Non-invasive CPAP in Settings Without Immediate Access to
Mechanical Ventilation 55

analysis12-16 in adult patients. Compared to administra-


tion of oxygen alone, application of CPAP reduces the
IP : 196.52.84.10 need for intubation, as well as risk of mortality.
●● Non-invasive application of continuous positive airway
pressure, using the flow inflation ventilation device
during fluid resuscitation of septic shock has shown a
significant drop in hospital mortality.17

Technique: How to Use the


Jackson-Rees Circuit?
1. Ensure that airway is spontaneously maintainable and
apply the face mask, such that it fits with an airtight
Figure 5.5: Note that the child is being given an inotrope seal (Figure 5.4).
infusion and is being monitored with a pulse oximeter. The 2. The person holding the mask should ensure that the
bag- valve-mask is available close at hand.
reservoir remains inflated at all times.
3. A severely hypoxic child will tend to fight the mask.
Children presenting with respiratory distress often, also
Hold the mask firmly in position. Tolerance improves
have auto-PEEP or dynamic hyperinflation. Normally, up-
as hypoxia resolves. Until then, the child may need to
per airway pressure is higher than the positive end expira-
be restrained or cajoled by his mother.
tory pressure at the alveoli for inspiratory gas flow to occur.
4. Monitor using a pulse oximeter and cardiac monitor.
Inspiratory muscles, have to work harder to drop alveolar
pressure from its baseline positive end expiratory value to 5. Avoid closing the expiratory pressure valve.
less than upper airway pressure (normally 0) before inspira- Insufficient venting of exhaled gas will cause both
tory gas flow occurs. This is termed ‘threshold work’. By volume and pressure to increase within the system.
increasing airway pressure, CPAP reduces the work re- This would prevent expiration and increase intratho-
quired to initiate inspiratory flow. The beneficial effects of racic pressure. The latter, may lead to barotrauma or
reducing the work of breathing are improvement in respira- aggravate ICP in children with cerebral edema.
tory rates and a fall in PaCO2. For this reason, provision of The latter may lead to barotrauma in the lung and ag-
CPAP is considered to provide ventilatory support. Refer gravate ICP in children with cerebral edema.
Figure 5.6 for mechanism of working of JR circuit. 6. Inadequate oxygen flow
Inadequate flow of O2 results in failure to flush out
Ù CO2. The resultant rebreathing leads to hypercarbia.
The flow inflating ventilation device has dual benefits;
The latter can cause increase in cerebral blood flow,
delivery of 100% oxygen with the benefits of continuous
ICP and predisposition to cardiac arrhythmias.
positive airway pressure.
Ù
If the reservoir over-distends, check whether the pressure
●● Use of non-invasive positive pressure ventilation in
acute cardiogenic pulmonary edema has been support- release valve is closed or the flow of gas has become
ed by randomized controlled trials (RCTs)2-11 and meta- excessive.

Figure 5.6: Mechanism of working of Jackson-Rees circuit


56 Section II n Airway

7. Avoid using the JR circuit in an apneic child 3. Nava S, Carbone G, Di Battista N, et al. Noninvasive venti-
Assisted ventilation for the non-intubated child, is best lation in cardiogenic pulmonary edema. A multicenter, ran-
provided using theIPself-inflating bag-valve-mask de- domized trial. Am J Respir Crit Care Med. 2003;168:1-6.
: 196.52.84.10 4. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe
vice.
8. Use age appropriate reservoirs cardiogenic pulmonary edema with continuous positive
airway pressure delivered by face mask. N Engl J Med.
When smaller reservoirs are used in older children, hy- 1991;325:1825-830.
poxia can worsen or not improve. Use of larger reser-
5. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continu-
voirs and circuits increase dead space ventilation and ous positive airway pressure therapy in acute cardiogenic
predispose to respiratory fatigue in young infants. pulmonary edema: short-term results and long-term fol-
9. Continue to use the flow inflating ventilation de- low-up. Chest. 1995;107:1379-386.
vice, until respiratory distress and shock resolves. 6. Pang D, Keenan SP, Cook DJ, et al. The effect of positive
Parents and attendants must be taught to hold the mask airway pressure on mortality and the need for intubation
under supervision in centers where healthcare provid- in cardiogenic pulmonary edema. Chest. 1998;114:1185-
ers are not available round the clock. 192.
10. JR circuit is contraindicated if level of consciousness 7. Park M, Sangean MC, Volpe Mde S, et al. Randomized,
prospective trial of oxygen, continuous positive airway
drops profoundly.
pressure, and bilevel positive airway Pressure by face mask
Development of hypotonia or posturing or seizure ac- in acute cardiogenic pulmonary edema. Crit Care Med.
tivity are indications for intubation. 2004;32:2407-415.
11. Worsening of irritability, inconsolable cry and postur- 8. Crane SD, Elliott MW, Gilligan P, et al. Randomised con-
ing may be noted in some children when applying the trolled comparison of continuous positive airways pressure,
Jackson-Rees circuit. As respiratory distress and shock bilevel non-invasive ventilation, and standard treatment in
resolve, tolerance improves. emergency department patients with acute cardiogenic pul-
monary oedema. Emerg Med J. 2004;21:155-61.
Key Points
ü 9. Bellone A, Monari A, Cortellaro F, et al. Myocardial in-
farction rate in acute pulmonary edema: noninvasive pres-
1. Use the flow inflating ventilation device to provide
sure support ventilation versus continuous positive airway
O2 to all critically ill children presenting with respi- pressure. Crit Care Med. 2004;32:1860-865.
ratory distress and shock. 10. Bellone A, Vettorello M, Monari A, et al. Non-invasive
2. Flow inflating ventilation device is useful to provide pressure support ventilation versus continuous positive
O2 for children presenting with acute cardiogenic airway pressure in acute hypercapnic pulmonary edema.
shock due to various etiologies such as scorpion Intensive Care Med. 2005;31:807-11.
sting, sepsis, submersion injury, etc. 11. Giacomini M, Iapichino G, Cigada M, et al. Short-term
noninvasive pressure support ventilation prevents ICU
admittance in patients with acute cardiogenic pulmonary
common errors
û
1. Use of flow inflating device in apneic children (bag-
edema. Chest. 2003;123:2057-061.
12. Masip J, Roque M, Sanchez B, et al. Noninvasive venti-
valve-mask preferred). lation in acute cardiogenic pulmonary edema. Systematic
2. Inappropriate sized reservoir. review and meta-analysis. JAMA. 2005;294:3124-130.
3. Complete closure of pressure release valve. 13. Ho KM, Wong K. A comparison of continuous and bilevel
positive airway pressure non-invasive ventilation in-pa-
tients with acute cardiogenic pulmonary edema: a meta-
REFERENCES analysis. Crit Care. 2006;10:R49.
1. Shah PS, Ohlsson A, Shah JP. Continuous negative extra- 14. Collins SP, MielniczukLM, Whittingham HA, et al. The
thoracic pressure or continuous positive airway pressure use of noninvasive ventilation in emergency department
for acute hypoxemic respiratory failure in children. Co- patients with acute cardiogenic pulmonary edema: a sys-
chrane Database Syst Rev. 2008;1:CD003699. tematic review. Ann Emerg Med. 2006;48:260-69.
2. Mehta S, Jay GD, Woolard RH, et al. Randomized pro- 15. Winck JC, Azevedo LF, Costa-Pereira A, et al. Efficacy and
spective trial of bilevel versus continuous positive air- safety of non-invasive ventilation in the treatment of acute
way pressure in acute pulmonary edema. Crit Care Med. cardiogenic pulmonary edema: a systematic review and
1997;25:620-28. meta-analysis. Crit Care. 2006;10:R69.
Chapter 5 n Flow Inflating Ventilation Device: Non-invasive CPAP in Settings Without Immediate Access to
Mechanical Ventilation 57

16. Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of non- tive airway pressure versus non-invasive positive pressure
invasive positive pressure ventilation (NIPPV) on mortal- ventilation. Chest. 2007;132:1804-809.
ity in patients with acute cardiogenic pulmonary edema: a 18. Santhanam I, Padma V, Murali T, et al. Predictors of mor-
IP 2006;367:1155-163.
meta-analysis. Lancet. : 196.52.84.10 tality of children presenting with severe sepsis. Proceed-
17. Ferrari G, Olliveri F, De Filippi G, et al. Non-invasive ings from the first European congress on Pediatric resusci-
positive airway pressare and risk of myocardial infarctio tation and emergency medicine, Ghent. May 2013.
in acute cardiogenic pulmonary edema: continuous posi-
Section III
Approach to
IP : 196.52.84.10

Stridor
IP : 196.52.84.10
6
IP : 196.52.84.10

Stridor

Figure 6.1: A child being resuscitated for acute laryngotracheobronchitis in the PED (Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Highlight the importance of recognizing supraglot- 4. Evidence and treatment is based on etiology.
tic stridor. 5. Establish severity using the rapid cardiopulmonary
2. Precautions taken during assessment and manage- cerebral assessment and pediatric assessment tri-
ment. angle.
3. Establish etiology. 6. Management based on severity and etiology.

INTRODUCTION Different parts of the airway are more collapsible than


others. Anatomically, the upper airway is divided into su-
The presentation of stridor with impending respiratory fail-
praglottic, glottic and subglottic regions. The vocal cords,
ure, is an ED physician’s nightmare (Figure 6.1). To avoid
the dreaded complication of complete airway obstruction, glottis or trachea (good cartilaginous support) are less col-
a swift, systemic, protocol based approach is mandatory. lapsible than the supraglottis region. The lack of cartilagi-
nous support, enhances the tendency for complete collapse
PATHOPHYSIOLOGY when airway obstruction occurs due to supraglottic pa-
thologies. This risk is aggravated in young children where
The upper airway begins at the nose and extends up to the the subglottic airway is smaller and even more compliant
main bronchi. Stridor, a high pitched sound of respiration is (supporting cartilage less developed than in the adult).
a sign of partial obstruction of any part of the upper airway.
The effect of upper airway obstruction can be explained by
the ‘venturi effect’. Pressure exerted on a partially closed
Ù
Supraglottis can easily become obstructed by mucus,
tube of gas, is equal in all directions except during linear blood, pus, edema, active constriction, external
movement of air. The linear flow of air creates an addi- compression or pressure differences created during
tional pressure in the forward direction within the tube,
spontaneous respiratory effort in the presence of airway
resulting in a fall in pressure along the lateral wall. Hence,
obstruction.
during inspiration, the airway has a tendency to collapse.
62 Section III n Approach to Stridor

Even minimal mucosal edema can significantly reduce lapsible due to lack of cartilaginous support. The presence
the diameter of the pediatric airway and increase resistance of multiple tissue planes in this region encourages rapid
to airflow and work of breathing. spread of infection especially in infancy. In addition, in
IP : 196.52.84.10
Ù
Crying can aggravate hypoxia by increasing air
children less than 2 years of age, the retropharyngeal space
contains lymph nodes that serve as a nidus for the forma-
turbulence in the obstructed airway. tion of abscess. As the nodes atrophy, the risk of abscess
All precautions should be taken to prevent a child with formation becomes much less.
stridor from crying. Obstruction at the supraglottis, i.e. above the level of
the esophagus, as in epiglottitis or retropharyngeal abscess
GENERAL APPROACH causes pooling of saliva. The latter leads to:
1. Avoid the following maneuvers in children present- 1. Soft stridor (may not be reported by the mother, but
ing with stridor. identified by the ER physician).
●● Do not separate the child from his mother. 2. Drooling and dysphagia.
Examine and manage the child on his mother’s lap. 3. Muffling of voice (‘hot potato voice’).
●● Avoid changing the position of comfort, which 4. Ineffective cough.
the child has adopted.
Do not make an alert or agitated child with stridor, Glottis
lie down on the resuscitation trolley or bed. It could
pre­cipitate complete airway obstruction. The glottic and subglottic region extends from the vo-
●● Avoid forcing an oxygen mask on a screaming cal cords to the trachea before entering the thoracic cage.
child. Since the cricoid cartilage and tracheal cartilaginous rings
Without separating the child from his mother, help surround majority of its length, this section of the airway
the mother to administer oxygen in a non-threaten- is not as collapsible as the supraglottis. The commonest
ing manner. causes of obstruction at this site are inflammation and ede-
ma due to acute laryngotracheobronchitis (ALTB).
2. Ascertain the severity of the lesion based on the
physiological status. 1. Hoarse voice.
●● Perform the rapid cardiopulmonary cerebral assess- 2. The harsh stridor may occur in either the inspiratory or
ment. expiratory phase or occasionally both phases of respi-
It helps to quickly determine whether the air­way ration (biphasic). The latter is due to minimal altera-
obstruction can be handled in the ED or in the OT. tions in the size and shape of the airway obstruction
during both phases of respiration.
3. Simultaneously, obtain a focused history to estab-
lish the anatomical site of obstruction. The ‘5A’s 3. Brassy cough.
approach helps to identify the level of lesion. 4. Drooling and dysphagia are not characteristic features
●● Age: What is the age of the child? of glottic obstruction unless the obstruction is large
●● Acuity: Is the presentation, hyperacute, acute, enough to compress the esophagus.
chronic or acute on chronic?
●● Acoustics: Is the stridor harsh or soft. Intrathoracic
●● Associated symptoms: Is stridor associated with fe-
ver, dysphagia or drooling? The intrathoracic airway comprises of the trachea and
●● What is the quality of voice (hoarse or muffled)? the main stem bronchus. Intrathoracic airway obstruction
●● Aggravating factors? causes stridor that is loudest during expiration. Increase in
intrathoracic pressure during expiration, causes collapse of
SITE OF OBSTRUCTION the airway. During inspiration, the intrathoracic pressure
falls. As a result, the obstructed thoracic airway expands
Supraglottis leading to a quieter sound.
The supraglottis extends between the nose and the vocal Congenital malformations of the airway are the com-
cords. As mentioned earlier, it is easily distensible and col- monest causes of obstruction within the thorax.
Chapter 6 n Stridor 63

ETIOLOGY OF OBSTRUCTION ●● Epiglottitis develops over a few hours after onset of


symptoms.
1. Age at which stridor presents helps in recognizing
IP : 196.52.84.10 4. Associated symptoms.
etiology.
●● High grade fever indicates bacterial etiology, e.g.
●● Stridor in young infants is more likely due to a con-
epiglottitis, retropharyngeal abscess or tracheitis.
genital problem. Older children (1–4 year) are more
●● Low-grade fever could be associated with ALTB
likely to have an infectious etiology or foreign body (Box 6.1).
aspiration. ●● Non-infectious causes such as FB aspiration or con-
●● Unusual in infants younger than 6 months, croup genital causes are characterized by absence of fever.
reaches its peak incidence during the second year ●● Drooling, dysphagia and a ‘hot potato voice’ indi-
of life.1 Around 6 years of age, a child's airway is cate that the obstruction is at the level of the supra-
similar to that of an adult and the effect of mucosal glottis.
edema becomes minimal. ●● Barking cough, brassy voice along with stridor is
●● Epiglottitis, historically peaks at 3 years of age. commonly due to croup.
More recently, its presentation has shifted to older ●● Restriction of neck movements is diagnostic of ret-
children and adults.2 ropharyngeal abscess.
●● Retropharyngeal abscess is most commonly seen in ●● Children with stridor due to epiglottitis, diphtheria,
infants and children up to age 4 years.2 Infections retropharyngeal abscess appear toxic, hyperalert
of the nasopharynx, paranasal sinuses or middle ear and maintain a tripod position.
can extend up to lymph nodes located in the space ●● A weak cry is associated with laryngeal anomaly or
between the posterior pharyngeal wall and the pre- neuromuscular disorders.
vertebral fascia. Since these retropharyngeal nodes ●● Hemangiomas elsewhere in the body of a child with
atrophy beyond 4 years of age, retropharyngeal ab- stridor, suggest that the obstruction to the airway, is
due to a hemangioma in the subglottic region.
scesses are common under this age.
●● Respiratory rates are usually normal or mildly el-
●● From 6 months to 6 years of age, children tend to
evated. Head bobbing, retractions and use of acces-
explore their environment, increasing the risk of
sory muscles indicate impending respiratory fail-
foreign body aspiration. Stridor due to aspiration of ure.
a foreign body is most common in children aged be- ●● Sternal retractions in the young infant or neonate
tween 1 and 3 years. suggest the presence of an airway obstruction, even,
●● The incidence of peritonsillar abscess peaks at 10 if the stridor is not clearly audible.
years. ●● Acute viral croup, follows a protracted prodromal
●● Past history of intubation or birth injury suggest vo- period of cough and rhinorrhea.
cal cord paralysis or laryngotracheal stenosis. ●● Bacterial tracheitis and retropharyngeal abscess may
2. Acoustics of the stridor often help in identification be preceded by a viral upper respiratory infection.
of the level of airway obstruction. 5. Factors which aggravate or make the stridor louder!
●● An inspiratory soft stridor suggests supraglottic pa- ●● Crying: Laryngomalacia, subglottic hemangioma.
thology. ●● Choking: Tracheoesophageal fistula, FB.
●● A harsh inspiratory or a biphasic stridor is sugges- ●● Supine position: Laryngomalacia, macroglossia,
tive of either a glottic or subglottic lesion. micrognathia.
●● Expiratory stridor is more in favor of an intratho- ●● Virtually all children presenting with acute stridor
racic lesion. and respiratory distress, (except ALTB and angioe-
3. Acuity or rapidity of onset. dema) should be evaluated and managed in the OT
●● Hyperacute onset of stridor should arouse suspicion by ENT specialists or anesthetists.
of FB aspiration.
●● Children with an anaphylactic response will pres- Ù
If airway obstruction is associated with respiratory
ent with acute stridor, wheeze, hypotensive shock
failure, call for ENT help. Urgent intubation must be
and rashes within 5 minutes of contact with the al-
performed in the ED by airway experts.
lergen.
64 Section III n Approach to Stridor

Case Scenario 1
A toddler presented with 1 day history of fever, stridor
IP : 196.52.84.10
and swelling in front of the neck (Figures 6.2 to 6.8).

Figure 6.4: Case progression: As oxygen and fluids were being


given, the child’s mental status deteriorated. His assessment was
as follows:

Figure 6.2: Swelling in front of the neck

Figure 6.5 Physiological status: Unmaintainable airway with


respiratory failure, compensated shock and coma.

Intervention
Figure 6.3 Physiological status: Structural stridor with ●● A: Airway was positioned using the head tilt-chin lift
impending respiratory failure, compensated shock and altered maneuver (Figure 6.4).
mental status ●● B: Oxygen was given via the Jackson-Rees Circuit.
●● C: Dopamine was initiated at 10 μg/kg/minute.
Intervention ●● The surgeon performed diagnostic aspiration (thick pus
was aspirated).
●● A: Child was seated in his mother’s lap. ●● Airway tray was ordered.
●● B: Oxygen was given by his mother in a non-threaten- ●● Fentanyl and atropine were ordered
ing manner. ●● Ketamine was avoided for its risk of laryngospasm.
●● C: Vascular access was secured and 10 mL/kg of NS ●● Succinylcholine, was also avoided since paralysis
was started over 20 minutes. would have deprived the child of his respiratory effort
●● ENT specialist and the pediatric surgeon were called where difficulty was anticipated during intubation.
for help immediately.
Chapter 6 n Stridor 65

IP : 196.52.84.10

Figure 6.6: The child continued to worsen and developed apnea.


Figure 6.8: This picture shows a neurologically normal child who
was briefly ventilated. Complete drainage of the abscess was
performed in the intensive care unit.
Box 6.1: Etiology of stridor

Infectious
1. ALTB (classical croup)
2. Acute epiglottitis
3. Bacterial tracheitis
4. Retropharyngeal abscess
Non-infectious
1. Congenital malformations obstructing the airway
2. Spasmodic croup
3. Foreign body obstruction
4. Angioedema
Figure 6.7 Physiological status: Airway intubated, assisted
5. Laryngomalacia
ventilation, hypotensive shock with low MAP.
6. Laryngeal papilloma
7. Hypocalcemia
8. Vocal cord paralysis
Intervention
●● A: Laryngoscopic evaluation showed a smooth globu-
lar swelling with no anatomical landmarks to guide in-
Acute Laryngotracheal Bronchitis (Box 6.1)
tubation. Viz: epiglottis, arytenoid folds or vocal cords A careful history and physical exam is mandatory to con-
were not visible. firm diagnosis and simultaneously, rule out FB aspiration
●● B: Bag-valve-mask ventilation was initiated. Chest rise or epiglottitis.
was adequate and saturation improved to 100%.
Most children present with acute onset barking cough,
●● Successfully intubated on the 6th attempt using a 3.5
stridor and chest wall in drawing.3,4 It is preceded by a
mm tube. Each attempt was preceded by preoxygen-
prodrome of cough, cold and low-grade fever. Typically,
ating with bag-valve-mask ventilation, such that SaO2 the illness lasts for 3–7 days. As the obstruction worsens,
was > 95%. the child becomes increasingly tachypneic with distress
●● C: 80 mL/kg NS, dopamine and norepinephrine infu- of variable severity. Tachycardia is noted when the child
sions were needed to resolve warm shock with low becomes hypoxia. Severe airway obstruction is associated
MAP. with pulsus paradoxus. Rarely, progressive increase in the
●● The first dose of antibiotic was also administered. work of breathing leads to respiratory failure, character-
●● Hypoglycemia was ruled out. GNS with KCl was initi- ized by severe chest retractions, decrease in breath sounds
ated at maintenance rates. and oxygen saturation. Increasing cyanosis along with
66 Section III n Approach to Stridor

change in mental status indicate need for intubation. Some Epinephrine is the drug of choice. Due to its non-se-
children with ALTB may develop secondary bacterial tra- lective α-adrenergic and β-agonistic action, it relieves mu-
cheitis. IP : 196.52.84.10 cosal edema and improves breathing mechanics. In most
Ù children, one dose is adequate, although it may be repeated
after 4–6 hours.
Tachycardia indicates hypoxia. Peripheral perfusion
is usually normal, but can be compromised in severe The Cochrane review5 concluded that nebulized epi-
hypoxia.
nephrine, both racemic and L-isomeric preparation caused
reduction of croup symptoms within 30 minutes after treat-
CASE SCENARIO 2 ment and improved stridor related respiratory distress. Ide-
A 1-year-old child presents with barking cough and in- ally, both pulse oximetry and ECG monitoring should be
spiratory stridor. His mother reports that her son has available during epinephrine nebulization.
been coughing for a week (Figure 6.9).
Glucocorticoids6-15
Glucocorticoids reduce upper airway swelling leading to
significant improvement in croup symptoms. Their onset
of action occurs within 1 hour after administration. Action
is delayed when compared with inhaled epinephrine. Peak
effect is noted, 6–12 hours after administration. A recent
cochrane review further confirmed that, glucocorticoids
are effective in improving severity of croup, decreasing the
number of return visits, readmissions and length of stay in
hospital.
Dexamethasone rapidly improves stridor, decreases
hospital stay and reduces the need for intubation.
Figure 6.9 Physiological status: Stridor due to glottic edema ●● Administer 0.6 mg/kg/dose IM, IV or oral (maximum
with respiratory distress and tachycardia. Perfusion, BP and mental
status is normal.
10 mg). An oral dose of 0.15 mg/kg is also effective.
Onset of action occurs within 1–2 hours.
The history is suggestive of croup. ●● A single dose is generally sufficient in most children
for prompt and sustained improvement. If necessary,
Treatment the steroid dose may be repeated after 12–24 hours.
●● No significant differences have been noted between the
●● Administer ‘blow-by’ oxygen through a plastic hose
use of prednisolone (1 mg/kg/dose) and dexametha-
with its end held within a few centimeters of the child’s
nose and mouth. sone (dose at either 0.15 or 0.6 mg/kg) in the treatment
of chil­dren with mild to moderate croup.
Epinephrine
Budesonide
●● Add, 0.5 mg/kg up to a maximum of 5 mg epinephrine
(1:1,000) to 2–3 mL of NS into the nebulizing cham- Nebulized budesonide has a rapid effect. High-dose nebu-
ber. Nebulize through oxygen. lized budesonide seems as effective as either oral or intra-
●● Observe the child for recurrence for at least 2 hours muscular dexamethasone in the treatment of mild to mod-
after nebulization. erate croup.
●● Less than 4 years—2.5 mL.
●● Dose: Nebulized budesonide 2–4 mg irrespective of age.
●● More than 4 years—5 mL.
Chapter 6 n Stridor 67

Analgesics Clinical Features


Analgesics provide some degree of comfort by reducing It presents with an acute onset of fever, irritability, throat
IP : 196.52.84.10 pain, difficulty in swallowing and drooling of saliva. Respi-
fever and pain.
ratory failure may follow rapidly (progression is in hours).
Antitussives and Decongestants The child has a toxic appearance and adopts position
of comfort by sitting with chin up, mouth open and tongue
No experimental studies have been published regarding
hanging out. Due to inability to swallow saliva, voice be-
the potential benefit of antitussives or decongestants in comes muffled viz ‘hot potato voice’. Supraglottic stridor is
children with croup. There is no rational basis for their use. soft and needs a high index of suspicion to identify.

Antibiotics When epiglottitis is suspected


No role for antibiotics in the management of croup. Rarely, ●● Avoid examining the oropharynx in the ED.
it may be used when bacterial superinfection is suspected. ●● Avoid separating the child from his parents.
●● Avoid forcing him to lie down for examination, X-ray
Heliox or during shift to the OT.
●● Allow him to assume ‘position of comfort’.
Helium-oxygen mixture 60:40 or 70:30 acts by promoting
laminar gas flow in the obstructed airway. This therapeutic Stridor with Respiratory Distress
modality is not yet widely available in our country.
●● Instruct parents to carry their child in the sitting posi-
Diagnosis tion to the OT.
●● Organize a physician who can effectively bag-valve-
●● Croup is diagnosed clinically. CXR is not useful in the mask ventilate the child, if he deteriorates during trans-
diagnosis of croup. X-rays are ordered only if other fer.
causes are being consid­ered. Lateral neck films may be ●● Airway should be secured in the OT by pediatric anes-
indicated, if retropharyngeal abscess is a possibility. A thesiologist and otolaryngologist in attendance.
chest film is helpful to rule out pneumonia or aspiration
of a radiopaque foreign body.
Ù
Making a child with stridor, lie down is dangerous. It can
●● The classic radiographic ‘steeple sign’ or ‘pencil point’ convert a partial obstruction to complete obstruction.
sign (narrowing of the tracheal shadow) may be unreli-
able for diag­nosing or excluding croup. An X-ray neck is not usually informative. A thick,
●● There is no role for routine blood tests.
thumb like epiglottis is suggestive of epiglottitis.
●● The need for tracheal intubation in ALTB is extremely
rare and is indicated only when the obstruction is wors­
ens and respiratory failure is imminent. Stridor with Respiratory Failure
●● A smaller sized tracheal tube should be used and needs
to be retained in situ for 3–5 days. ●● Bag-valve-mask ventilation till help arrives.
●● Prepare for emergency airway management.
Acute Epiglottitis ●● Call for help (anesthetist and otolaryngologist).

●● Acute epiglottitis occurs due to bacterial cellulitis of the Diagnosis is made by direct laryngoscopic visualiza­
supraglottic structures, notably epiglottis and aryepi- tion. Epiglottitis is diagnosed when a large, swollen, cher-
glottic folds. Rapid inflammatory swelling of these ry like epiglottis is found with erythe­ma and swelling of
tissues can obstruct the airway. Almost 80%–90% of the arytenoids and aryepiglottic folds. The examination
affected children will require early and elective intuba- should be done in the OT with experienced personnel. If
tion. Haemophilus influenzae type b is the most com- epiglottitis is suspected, culture of the epiglottic surface is
mon causative organism. taken and the child intubated with a tracheal tube one size
smaller than calculated for the age. Blood culture is taken
and appropriate IV antibiotic (ceftriaxone, cefotaxime or
68 Section III n Approach to Stridor

amoxiclav) is started. The tracheal tube should remain in ●● Most use eye movements to look up. The head is main-
situ for 48–72 hours. tained in the stationary position.
Ù IP : 196.52.84.10 ●● Some children present with torticollis.
●● Examination of the oropharynx reveals a bulging of
Avoid direct laryngoscopic examination in the ED.
both pos­terior pharyngeal wall and soft palate.
Laryngoscopic evaluation of an obstructed airway in
A lateral X-ray pharynx shows, soft tissue swelling,
an alert child could convert a difficult airway into an
which is more than half the width of the adjacent ver-
impossible one!
tebral body. Occasionally an air fluid level may be
seen.
Bacterial Tracheitis CT scan is useful to distinguish patients with RPA
from those with retropharyngeal cellulitis.
Usually follows viral ALTB and is caused by Staphylococ-
cus aureus; rarely by H. influenza and Group A, B hemo-
lytic Streptococcus. Treatment
Age: 6 months to 8 years. Most patients with retropharyngeal cellulitis and some
with RPA can be treated successfully without surgery. If
The initial croup-like symptoms are associated with high surgical drainage of the abscess is planned, intubation is
fever, toxic appearance and increasing respiratory distress. needed to avoid aspiration of pus in the OR.
Difficulty in swallowing and drooling is not common.
●● Administer intravenous antibiotics (penicillinase-resis­
Direct laryngoscopy reveals pus in the glottic region. tant penicillins, amoxiclav).
Bronchoscopy may also reveal the presence of pus, slough- ●● Monitor closely if surgical drainage and intubation
ing of tracheal mucosa and a pseudomembrane formation have been performed.
in the subglottic region.
Ù
Bacterial tracheitis is suspected when croup does not
Spasmodic Croup
Acute attacks of stridor occurring at nights and subsiding
subside and child becomes febrile, ill and toxic. in a short time characterize spasmodic croup. It tends to
recur in subsequent nights.
Treatment Age: 1–3 years.
●● Shift to OT for early intubation. Symptoms are similar to croup, but features of infection
●● Plan for frequent and meticulous suctioning. (URI or fever) are absent. The child is usually awakened
●● Administer appropriate antistaphylococcal antibiotics. from sleep with a stridor and onset of a harsh, barking, me-
tallic cough. Acute vocal cord abductor spasm triggered by
Retropharyngeal Abscess viral, allergy, gastroesphageal reflux or psychogenic fac-
tors have been postulated as causative.
Retropharyngeal abscess (RPA) is a potentially, serious
deep space neck infection. Complications include, airway Treatment: Taking the child into the cool night air may
compromise, invasion of contiguous structures and sepsis. stop the stridor. If the stridor persists,
Suppuration, occurs in the potential space between the pos­
●● Humidified air through nebulizer.
terior pharyngeal wall and prevertebral fascia. Causative
●● Nebulized epinephrine.
organisms: Group A, B-hemolytic Streptococcus, oral an­
aerobes, Staphylococcus aureus.
Foreign Body (FB) Obstruction
Sudden attack of respiratory symptoms, such as cough,
Clinical Features16 choking, gagging or cyanosis in a previously normal child
Fever, dysphagia, drooling, muffled voice, noisy breathing, should arouse suspicion of FB aspiration. Symptoms de-
respiratory distress, toxic appearance and neck stiffness. pend on the location of the FB. Laryngeal/tracheal FB may
present with croupy cough resembling ALTB. Varying de-
●● Children prefer to keep their neck in the neutral posi- grees of stridor, wheeze, chest retraction, hypoxia and cy-
tion with limitation of neck extension and flexion. anosis may also be seen. The clinical features may change
Chapter 6 n Stridor 69

if the FB migrates. An esophageal FB can compromise the FB Obstruction in the ED


airway if it is impacted high up or has been retained for a
long time. CASE SCENARIO 3
IP : 196.52.84.10
Diagnosis is based on a high index of suspicion, his- A 1-year-old male child was rushed by his mother for
tory, neck X-ray and flexible fiber optic bronchoscopy. aspirating a fish. He had been splashing water in the
bucket of water freshly drawn from the well by his
Treatment mother (Figures 6.11 and 6.12).
●● Provide supplemental oxygen, while allowing the child
to maintain position of comfort in the mother's lap,
●● Avoid noxious stimuli.
●● Plan elective airway evaluation and removal using rig-
id, open tube bronchoscopy in the OT.

Acute FB Obstruction in the


Prehospital Setting (Figures 6.10A and B)
●● Children < 1 year: 5 back blows followed by 5 chest
thrusts.

Figure 6.11: Fish which was removed later in the hospital

Figure 6.12 Physiological status: Alert child with stridor and


respiratory distress. The normal heart rate suggests, that this child
is not hypoxic.

●● Call ENT specialists and transfer to the OT for removal


of FB.

Ù
Examination of the throat in an alert child to remove
Figures 6.10A and B: Heimlich maneuver to dislodge foreign body
in infants. Remove FB, if visualized. Avoid blind finger sweep.
the FB causing stridor in the ER can precipitate cardiac
arrest.
●● Children > 1 year: Repetitive abdominal thrusts or
Heimlich maneuver.
70 Section III n Approach to Stridor

CASE SCENARIO 4 No specific treatment is required. Super added viral


infec­tion could worsen obstruction resulting in the need
A 2-year-old male child was rushed into ER by the par- for in­tubation.
IP : 196.52.84.10
ents who found him unresponsive while playing. Some
parts of a toy were found missing (Figure 6.13).
Laryngeal Papilloma
This is the commonest benign tumor of the larynx occur-
ring in childhood. It causes an acute onset of stridor and
dysphonia. Recurrent episodes are common and lethal air-
way obstruction resulting in death is not uncommon.
Treatment: surgical removal.

Hypocalcemia
Hypocalcemia presents with intermittent stridor, hypocal-
cemic tetany, seizures and cardiac failure. The child appears
normal between the episodes of stridor. Serum calcium < 7
Figure 6.13 Physiological status: Airway un-maintainable and mg/dL or ionized calcium < 1 mmol/dL is diagnostic. CXR
obstructed, respiratory failure, bradycardia, hypotensive shock may show signs of rickets, cardiomegaly and pulmonary
with altered mental status. congestion.
●● Initiate bag-valve-mask ventilation, chest compres-
Treatment
sions, injection epinephrine 1.2 mL (1:10,000) IV.
●● Urgently call for ENT assistance. ●● Maintain airway patency.
Dose: IV calcium gluconate at 0.5 mL/kg slowly fol-
Ù
An unstable airway, bradypnea, tachycardia or
lowed by a maintenance dose are therapeutic.
bradycardia, cyanosis and deteriorating mental status Rate of administration: 0.5–1 mL/kg not exceeding 0.1
are indicative that urgent resuscitative efforts are needed mL/kg/minute.
in the ER.
Vocal Cord Paralysis
●● Preoxygenate prior to intubation attempts.
Bilateral abductor palsy occurs due to the abnormal medial
●● Avoid paralytic agents during intubation.
position of the vocal cords. It results in severe stridor and
●● Removal of foreign body may be attempted after intu-
respiratory distress. Bilateral abductor palsy causes apho­
bation.
nia with little respiratory distress.
●● During the process of intubation, if it is not possible to
remove the FB in the ER, attempt to dislodge it into the
main stem bronchus. Diagnosis
●● Long duration of stridor, older children, (not within the
This will at least ensure that half of respiratory tree is
age group for developing ALTB), absence of fever, poor
freed for ventilation. Follow-up bronchoscopy may be per-
response to nebulized epinephrine and persistence of
formed later for removal of FB.
stridor are clues to recognition of vocal cord paralysis.
●● Laryngoscopy is confirmatory.
Laryngomalacia (Congenital
Laryngeal Stridor) Treatment
Intermittent stridor and chest retractions occur from 2–6 ●● Supportive.
weeks of age. Symptoms peak at 3–5 months, but most ●● Temporary intubation.
resolve spontaneously by 10 months. ●● Rarely surgery.
Chapter 6 n Stridor 71

Neurogenic Stridor 4. If stridor with respiratory failure is recognized in the


The child is brought with the history of profound fall in ED, initiate bag-mask ventilation and call for urgent
mental status, seizuresIPor: posturing.
196.52.84.10
Noisy breathing of ENT help.
stridor is not the reason for bringing the child to the ED.
5. Avoid paralytic agents while attempting to intubate
In the critically ill unresponsive child, the airway is a child with structural obstruction.
unmaintainable. Airway protective reflexes are absent and 6. Intubation in the ED is mandatory in the manage-
the tongue falls back obstructing the airway. ment of neurogenic stridor.
●● Intubation is recommended using ICP precautions in 7. Etiology of stridor is made from history and not
the ED. from radiographs.

Refer Protocol 6.1. common errors


û
Key Points
ü 1. Attempting to perform laryngoscopic examination
in an alert child with stridor in the ED.
1. Determining anatomic level of obstruction enables 2. Separating the stridorous child and his mother and
appropriate management. placing him on the couch for examination.
2. Assessment of severity helps decide whether the 3. Administering nebulized epinephrine for all etiolo-
child needs respiratory support in the ED or can wait gies of stridor.
to be shifted to the OT for definitive care. 4. Not taking a focussed history and not performing a
3. Use of pulse oximeter to diagnose respiratory fail- rapid clinical exam to establish etiology.
ure not reliable.
Protocol 6.1: PEMC approach: Management of stridor in the emergency department

72

IP : 196.52.84.10
Section III n Approach to Stridor
Chapter 6 n Stridor 73

REFERENCES and placebo for moderately severe croup.” The New Eng-
land Journal of Medicine. 1998;339(8):498-503.
1. Geelhoed GC. Croup. Pediatr Pulmonol. 1997;23 (5):70-
374. IP : 196.52.84.10 10. Klassen TP, Craig WR, Moher D, et al. “Nebulized budes-
onide and oral dexamethasone for treatment of croup: a
2. Cordle RJ, Relich NC. Pediatrics: Upper respiratory emer-
randomized controlled trial.” Journal of the American
gencies. In: Tintinalli JE, Kelen GD, Stapczynski JS (Eds).
Emergency Medicine: A Comprehensive Study Guide. 5th Medical Association. 1998;279(20):1629-632.
edition. New York, NY: McGraw-Hill Health Professions 11. Klassen TP, Watters LK, Feldman ME, et al. “The efficacy
Division; 2000. pp. 384-91.doi:10.1056/NEJMep072022. of nebulized budesonide in dexamethasone-treated outpa-
3. Bjornson CL, Johnson DW. ‘Croup’. The Lancet. 2008; tients with croup.” Pediatrics. 1996;97(4):463-66.
(371)329-339, DOI:10. 1016/S0140-6736(08)60170-1. 12. Geelhoed GC. “Budesonide offers no advantage when
4. Cherry JD. Clinical Practice. Croup. N Engl J Med. added to oral dexamethasone in the treatment of croup.”
2008;358:384-391. Pediatric Emergency Care. 2005;21(6):359-62.
5. Bjornson C, Durec T, Vandermeer B, et al. “Nebulized 13. Chub-Uppakarn S, Sangsupawanich P. “A randomized
epinephrine for croup in children,” Cochrane Database of comparison of dexamethasone 0.15 mg/kg versus 0.6 mg/
Systematic Reviews, no. 3, Article ID CD006619, 2007. kg for the treatment of moderate to severe croup.” In-
6. Luria JW, Gonzalez-Del-Rey JA, DiGiulio GA, et al. “Ef- ternational Journal of Pediatric Otorhinolaryngology.
fectiveness of oral or nebulized dexamethasone for chil- 2007;71(3)473-77.
dren with mild croup,” Archives of Pediatrics and Adoles-
14. Geelhoed GC, Macdonald WB. “Oral dexamethasone in
cent Medicine. 2001;155(12):1340-345.
the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus
7. Rittichier KK, Ledwith CA. “Out-patient treatment of
0.6 mg/kg.” Pediatric Pulmonology. 1995;20(6):362-68.
moderate croup with dexamethasone: intramuscular versus
oral dosing.” Pediatrics. 2000;106(6)1344-348. 15. Fifoot AA, Ting JYS. “Comparison between single-dose
8. Cetinkaya F, Tufekci BS, Kutluk G. “A comparison of neb- oral prednisolone and oral dexamethasone in the treatment
ulized budesonide, intramuscular and oral dexamethasone of croup: a randomized, double-blinded clinical trial.”
for treatment of croup.” International Journal of Pediatric Emergency Medicine Australasia. 2007;19(1)51-8.
Otorhinolaryngology. 2004;68(4): 453-56. 16. Craig FW Schunk JE. Retropharyngeal abscess in children:
9. Johnson DW, Jacobson S, Edney PC, et al. “A comparison clinical presentation, utility of Imaging and current man-
of nebulized budesonide, intramuscular dexamethasone, agement. Pediatrics. 2003;111:1394-398.
Section IV
IP : 196.52.84.10

Breathing
IP : 196.52.84.10
7
IP : 196.52.84.10

Approach to Respiratory Distress

Figure 7.1: Most commonly seen condition in children viz respiratory distress can have varying etiologies, systematic approach
often reveals the etiology (Courtesy: Dr Thangavelu S, Dr Gunda Srinivas).

Learning Objectives
1. Approach to respiratory distress using a stepwise 3. Classification of breathing patterns to determine
structured history. the physiological status.
2. Using the modified rapid cardiopulmonary cerebral
assessment and the pediatric assessment triangle to
recognize severity of respiratory distress.

INTRODUCTION counter airway resistance, increases turbulence of air


flow further worsening hypoxia.
Breathlessness is the commonest cause for referral to the ●● Crying or agitation can also aggravate hypoxia.
PED. This chapter will discuss a simple approach to recog-
nition and management of a very common pediatric emer- Ù
Maneuvers such as provision of oxygen, performance of
gency. Refer Figure 7.1.
rapid cardiopulmonary cerebral assessment, connecting
PATHOPHYSIOLOGY to the pulse oximeter or securing an IV access may
aggravate the hypoxia in the sick child.
The unique anatomic and physiologic characteristics of the
respiratory tract in children and infants make them vulner-
able to respiratory failure and hypoxia. CASE SCENARIO
●● The pediatric airway is narrower than the adult. Con- A 4-year-old boy with episodic breathlessness is brought
sequently, pathological processes that cause narrowing into the PED, with an acute exacerbation of asthma. He
of the airway could result in an exponential increase in has no fever, but has become too dyspneic to speak or
airway resistance increasing the risk of hypoxia (Fig- feed. He has also become lethargic and unable to walk
ure 7.2). In addition, respiratory efforts generated to into the hospital (Figure 7.3).
78 Section IV n Breathing

Evaluation of the respiratory rate


and work of breathing
IP : 196.52.84.10 Normal breathing is quiet and is accomplished with mini­
mal work of the respiratory muscles. The normal respira-
tory rate in the neonate is rapid. As the child grows older,
the respiratory rates fall. However, tidal volume or the vol­
ume of each breath per kilogram of body weight remains
fairly constant throughout life. Adequacy of tidal volume
is clinically evaluated by observing chest wall excursion
and auscultating the lung fields.
Parenchymal lung diseases or shock lead to an increase
in minute ventilation (MV = TV × RR). As respiratory
rates increase, the tidal volume falls, i.e. each breath be-
Figure 7.2: Note that this boy with respiratory distress is comes shallow.
looking sleepy and is not able to maintain an upright posture.
He is profoundly hypoxic.
Ù
Roughly, doubling of normal (low normal range)
respiratory rates for age should be interpreted as
respiratory failure.

CLASSIFICATION OF ABNORMAL
RESPIRATION
●● Effortless tachypnea.
●● Respiratory distress.
●● Respiratory distress with features of respiratory failure.
●● Relative bradypnea.
●● Apnea.

Effortless Tachypnea
Figure 7.3 Physiological status: Life-threatening asthma Tachypnea occurs due to a variety of causes: Hypoxia,
with shock. hypercarbia, shock, metabolic acidosis, pain, anxiety and
Ù
To avoid precipitating hypoxia consequent to crying
central nervous system pathologies in comatose children.
●● Effortless tachypnea or quiet tachypnea is defined as
or agitation, children with respiratory distress or increased respiratory rates without increased work of
impending respiratory failure should not be separated breathing.
from their mother. ●● Hypoxia and shock due to various etiologies result in
decreased availability of oxygen at the cellular level.
●● It is preferable, that on arrival and during subsequent Anerobic metabolism supervenes, leading to lactic aci-
management, children with respiratory distress re­main dosis. The latter triggers the respiratory centers. Respi-
seated in their mother’s lap. ratory rates increase in an attempt to maintain a normal
●● The mother should be taught to administer oxygen by pH.
holding the rebreathing mask or flow inflating ventila-
tion device in a non-threatening manner. Ù
Lung parenchyma is normal in children presenting with
●● Infants who cry and resist the mask can be adminis­
effortless tachypnea.
tered oxygen via a tube held close to the nose.
Chapter 7 n Approach to Respiratory Distress 79

Respiratory Distress Relative Bradypnea


Respiratory distress is characterized by tachypnea and in- Slowing of respiratory rates indicate respiratory muscle
IP :Increased
creased work of breathing. 196.52.84.10
airway resistance and fatigue. Inability of young infants to sustain prolonged
decreased chest and lung compliances in pathological con- respiratory distress, result in early fatigue and respiratory
ditions would require a greater pressure to inflate the lung failure.
to the same lung volume. This imposes a greater workload
Slowing of respiratory rates with reduced work of
on the respiratory muscles and increases the oxygen cost
breathing is not as easy to identify as respiratory distress.
of breathing. When the oxygen supply-demand balance
The profound fall in mental status, hypotonia and poor
to the respiratory muscles is disturbed, respiratory failure
color suggest that the child is slipping into respiratory fail-
may ensue because of muscle fatigue.
ure.
Ù Ù
Abnormal lungs due to alveo­lar edema, pneumonia,
The ‘normal respiratory rate for age', in association with
bronchospasm, bronchiolitis, etc. result in recruitment
profound alteration of mental status, grunt, abdominal
of the accessory muscles of respiration. Re­tractions of
respirations, cyanosis, tachycardia, bradycardia and
the intercostal, subcostal, sternal and supra­clavicular
shock indicate that respiration is failing. Unless
muscles indicate that the underlying lung is diseased. In
recognized and managed in the ED, respiratory arrest
young infants, severe respiratory compromise can result
may supervene.
in nasal flare and head bobbing with each breath.

Abdominal Respiration
Respiratory Failure
The ribs and the costal cartilage in the infant are soft and
It is characterized by inadequate oxygenation, ventilation or
both. It may be functionally defined as a clinical state that re- compliant resulting in failure to support the lungs or keep
quires intervention to prevent respiratory or cardiac arrest. them adequately expanded. Hence, when the airways be-
come obstructed, active inspiration causes paradoxical in-
●● Recognition of respiratory failure is based on the clini- tercostal retractions rather than chest and lung expansion.
cal features (discussed below) and not on blood gas The tidal volume becomes dependent on the movement of
analysis. the diaphragm and functional residual capacity falls. When
Deterioration in respiratory function or imminent re- diaphragmatic movement is impeded by gastric distension
spiratory arrest should be anticipated in infants or children or increased intrathoracic pressure such as asthma or bron-
who demonstrate any of the following signs: chiolitis, respiration can become further compromised.
●● Inadequate respiratory rate or gasping respiration. Fatigued intercostal muscles also lead to abdominal res-
●● Inadequate effort or chest excursion with diminished piration.
peripheral breath sounds.
●● Grunting respirations.
Ù
See-saw or abdominal respiration indicate respiratory
●● Abdominal or see-saw respiration. muscle fatigue and impending respiratory failure.
●● Decreased level of consciousness or response to pain;
poor skeletal muscle tone or cyanosis.
Grunting
Ù
Due to high metabolic rates, the child has a higher An ominous sign, grunt is indicative of impending respi-
oxygen demand than the adult. Oxygen consumption is ratory failure. It is produced by premature closure of the
6–8 mL/kg in children as compared to 3–4 mL/kg in the glottis at the end of expiration in order to generate positive
adults. Consequently, when a child develops alveolar end-expiratory pressure in an effort to improve the FiO2.
hypoventilation or apnea, hypoxemia develops more Grunting helps to keep the alveoli patent and improve the
rapidly. functional residual capacity.
80 Section IV n Breathing

Cyanosis ●● Acute first episode of respiratory distress, associated


with history of fever and non-lung foci of sepsis suggests
Is a late and ominous sign, representing inadequate oxy-
IP : 196.52.84.10 the possibility of acute cardiogenic pulmonary edema.
genation within the pulmonary bed or poor oxygen deliv-
ery by the cardiovascular system.
Step 2
Targeted history to identify hypoxia or shock.
Alteration in Mental Status
●● Ask mother, for history suggestive of altered mental
Incessant, inconsolable cry, failure to recognize the mother, status in any child presenting with respiratory distress.
sleepiness or posturing in the young infant with respiratory If she denies fall in mental status, the child is unlikely
distress, indicate varying severity of hypoxia. Fighting the to have respiratory failure.
oxygen mask, combativeness and diaphoresis also suggest ●● History of talking or taking feeds could be mislead-
severe hypoxia and imminent respiratory failure. ing. Mother is the best judge. If she reports: ‘Not as
Somnolence and obtundation occurs as hypercarbia su- usual’, lethargic, ‘sleepier than usual’, recognize early
pervenes. hypoxia or shock.
Tachycardia is an early sign of hypoxia in a child with
respiratory distress. A fall in the heart rate to the ‘normal Step 3
range’ or ‘relative bradycardia’ is ominous indicating that Targeted history of fever suggests infective causes for
respiratory failure is imminent. Relative bradycardia can respiratory distress.
be recognized when associated with signs of poor perfu-
sion with profound alteration in mental status and abnor- Example: Pneumonia, bronchiolitis.
mality in tone and posture.
Step 4
Ù
Avoid rushing to take an X-ray as the first intervention in Perform the rapid cardiopulmonary cerebral assess-
a child presenting with respiratory distress or respiratory ment.
failure.
a. Does this child have respiratory distress or respira-
tory failure?
Step 1 Ù
Targeted history to identify etiology. Classifying whether respiratory distress or respiratory
failure whilst taking history on arrival helps initiate bag-
Ù valve-mask ventilation if needed. If ‘BRADYPNEIC’,
Duration of respiratory distress offers many clues to the further assessment, should be continued by the next
possible etiology. responder.

●● Hours (hyperacute) suggests that aspiration could be b. Does this child have shock or not?
the cause of respiratory distress.
●● Days (acute) indicates that the presence of an infective Ù
It is not uncommon for shock to coexist in hypoxic
lung disease, e.g. pneumonia, empyema, bronchilitis, children. Early and aggressive fluid resuscitation of
etc. shock is mandatory for early resolution of hypoxia.
●● Respiratory distress in months or since birth (chron- Respiratory distress and shock viz cardiogenic shock
ic) implies that the possible etiology is cardiac or less may mimic asthma or bronchiolitis!
commonly chronic lung disease. When respiratory distress and shock are noted in
●● Episodic breathlessness with symptom-free periods, children presenting with ‘non-lung etiologies’ such as
points towards asthma. Rarely, recurrent aspiration scorpion sting, septic foci, acute diarrhea, submersion
syndromes can present with episodic respiratory dis- injury, hypoxic ischemic encephalopathies, etc. suspect
tress. Unlike asthmatic children, the latter is often as- the presence of pulmonary edema due to cardiac
sociated with failure to thrive or developmental delay. dysfunction or acute lung injury.
Chapter 7 n Approach to Respiratory Distress 81

c. Does this child have cardiogenic shock or not? Bronchiolitis


Ù
Muffled heart sounds, IP :gallop, relative bradycardia,
196.52.84.10
Acute first episode breathlessness with wheeze in young
healthy infants, presenting with low-grade fever and pro-
low BP, low MAP are signs of myocardial dysfunction. drome is suggestive of bronchiolitis.
Examination of the liver span in a child with respiratory
distress often provides valuable information on cardiac ●● Provide O2 using the JR circuit.
function. Since a pushed down liver could erroneously ●● Correct shock if identified (usually 20–30 mL/kg may
suggest hepatomegaly, emphasis is laid in assessment be needed unless the infant shows signs of SIRS with
of the span. Assessment of the liver span during the septic shock).
cardiopulmonary assessment helps to find out whether ●● Nebulize with hypertonic saline.
respiratory distress is due to respiratory or cardiac ●● Epinephrine nebulization 0.1 mL/kg (1:1,000) in 4 mL
causes. of normal saline has also been recommended. Monitor
Chronic respiratory distress associated with increased ECG for cardiac arrhythmias.
liver span, points towards a structural heart disease
with cardiac failure. Septic Cardiogenic Shock
Acute respiratory distress with increased liver span
First episode respiratory distress with or without hepato-
could occur due to cardiac failure or cardiogenic shock
megaly due to acute pulmonary edema (refer Chapter 15).
secondary to myocarditis or severe sepsis.
●● Provide oxygen through flow inflating ventilation
d. Does this child have severe hypoxia or shock as evi- de­vice.
denced by features of non-convulsive status epilep- ●● Administer smaller aliquots of fluids.
ticus? ●● Initiate early inotrope infusion and perform early intu­
Ù
Nystagmus, conjugate deviation or eyelid twitch or a
bation if needed.
●● Administer 1st dose of antibiotic.
combination of signs, which signal severe hypoxia in
young children and infants with respiratory distress Asthma
indicate NCSE (avoid treating with anticonvulsants). Ù
Episodic breathlessness in healthy children more than 2
●● Increased respiratory rates without increased work of years of age is probably asthma.
breathing (quiet tachypnea), point towards a non-car­
diorespiratory etiologies such as acidosis secondary to ●● Grade severity and implement treatment as per asthma
DKA, hypovolemic shock, etc. management guidelines (refer Chapter 8).
●● Comatose children present with altered breathing pat-
terns secondary to neurogenic etiologies. Ù
Caution: Avoid treating all children with respiratory
MANAGEMENT BASED ON ETIOLOGY distress and wheeze as asthma. Acute cardiogenic or non-
cardiogenic pulmonary edema could mimic asthma.
Aspiration Avoid rushing to diagnose asthma in infants less than 2
Hyperacute respiratory distress: Treatment is focused on years of age. Other causes of acute or chronic respiratory
correction of hypoxia and shock (refer Chapter 6). distress, which mimic asthma such as congenital heart
diseases , cystic fibrosis, etc. should not be misdiagnosed
as asthma.
Pneumonia
Acute first episode of breathlessness with high grade: A suggested approach to child more than 1 month pre-
Whilst correcting hypoxia and shock, administer the first senting with respiratory distress in the ED is shown in Pro-
dose of antibiotic in the ED. tocol 7.1.
82 Section IV n Breathing

Key Points
1. Avoid separating mother
ü
and child during assessment
common errors
û
1. Diagnosing asthma in all children presenting with
IP : 196.52.84.10
of a child presenting with respiratory distress. the respiratory distress and wheeze.
2. Teach mother to hold the oxygen mask in a non- 2. Nebulization of all children and infants presenting
threatening manner. with respiratory distress without considering
3. Focused history with emphasis on duration provides etiology.
clues to the possible etiology. 3. Failure to recognize the need to assess liver span in
4. A focused history also helps recognize early signs children presenting with respiratory distress.
of hypoxia in a child presenting with respiratory 4. Failure to anticipate that acute pulmonary edema due
distress. to acute lung injury or acute myocardial dysfunction
5. Recognize myocardial dysfunction or acute lung
could present as respiratory distress secondary to
injury when respiratory distress occurs in children
severe hypoxic insults.
presenting with ‘non-lung’ etiologies.
5. Failure to provide CPAP for children presenting
6. Rapid cardiopulmonary assessment, which incor­
porates assessment of liver span helps to recognize with pulmonary edema and shock.
whether respiratory distress is due to respiratory or 6. Believing that diagnosis of respiratory failure is
cardiac causes. dependent on laboratory investigations and not on
clinical features on arrival into the ED.
Protocol 7.1: PEMC approach: Respiratory distress

IP : 196.52.84.10

PE, pulmonary edema; CLD, chronic lung disease; CHD, congenital heart disease; DCM, dilated cardiomyopathy; CCF, congestive cardiac failure.
Chapter 7 n Approach to Respiratory Distress
83
Management of an
8
IP : 196.52.84.10

Asthmatic Exacerbation

Figure 8.1: Systematic approach, repeated rapid cardiopulmonary assessments lead to dramatic improvement in acutely ill
asthmatic kids. A child with near fatal attack of asthma being successfully resuscitated with subcutaneous epinephrine.

Learning Objectives

1. Using the rapid cardiopulmonary cerebral 2. Pearls and pitfalls in salbutamol nebulization.
assessment and PAT to identify severity and 3. Evidence-based management of acute exacerbation
response to therapy. of asthma.

INTRODUCTION Appearance
The management of acute exacerbation of asthma in the ●● Obtundation, impaired alertness, incessant cry, exhaus-
ED, has been based on the recommendations of the National tion, diaphoresis, agitation, not tolerating the oxygen
Asthma Education and Prevention Program. Ex­pert Panel mask, confusion or combativeness are signs sugges-
Report 3: Guidelines for the Diagnosis and Man­agement of tive of profound hypoxia viz near fatal exacerbation of
Asthma (Summary Report 2007) and the British Thoracic asthma.
Society, Scottish Intercollegiate Guide­lines Network: Brit- ●● Floppiness and inability to maintain posture correlate
ish Guideline on the Management of Asthma, June 2009. clinically with hypercarbia.1

The PEMC approach, employs the rapid cardiopulmo-


nary cerebral assessment and the pediatric assessment tri- Breathing
angle to recognize severity of the asthmatic exacerbation Respiratory rates:
and use these guidelines to manage appropriately (refer
Figure 8.1). ●● > 30/min in children more than 5 years.
●● > 50/min in children between 2 and 5 years.
Severity is scored as follows: Refer Protocol 8.1. ●● > 60/min in 2 years in an asthmatic child suggest acute
●● Moderate asthma. ex­acerbation of asthma.2
●● Acute severe asthma. ●● Reduced respiratory rate for age (bradypnea), grunt,
●● Life-threatening asthma. head bobbing, nasal flare, use of accessory muscles
●● Near fatal asthma. and abdominal or paradoxical chest wall movements
Chapter 8 n Management of an Asthmatic Exacerbation 85

are more ominous and indicate impending respiratory pneumonia, bronchiolitis, tracheobroncho­malacia, cystic
failure. fibrosis and congenital anomalies could present with re-
●● Other signs of a near
IP :fatal attack include diminished
196.52.84.10 current wheeze and respiratory distress.
air-entry, absence of wheeze due to severe bronchos­
Response to short-acting bronchodilator agent (SABA)
pasm (silent chest) and or saturation < 92% in room air.
is often inconsistent in these children
Serial pulse oximetry measurements have been found
useful in assessing the severity of exacerbation and evalu-
ating improvement with treatment (Evidence B). Investigations: Role in Resuscitation
of Asthmatic Exacerbations
Ù ●● Chest radiographs are not routinely indicated in an
Though low oxygen saturation is helpful in recognizing
severity, normal oxygen saturations does not rule out a asthmatic child. They are ordered if there is failure to
severe asthmatic exacerbation.3 improve or deterioration occurs during the manage-
ment of life-threatening or near fatal asthmatic exac-
Circulation erbation.

●● Tachycardia denotes early hypoxia. Ù


●● Relative bradycardia is suggestive of very severe When deterioration occurs during salbutamol nebuliza­
hypoxia. tion, the respiratory distress and wheeze is more likely
●● Very high heart rates should prompt evaluation for the due to non-asthmatic causes.
presence of coexisting shock.
●● Arterial blood gas (ABG) measurements are also not
Normalization of heart rate during bronchodilatory routinely indicated and do not give additional useful
intervention is a reassuring sign of improvement. On the information.
other hand, increasing heart rates during inhalation therapy ●● In the early phase of an asthmatic exacerbation, the
indicate the presence of other causes of respiratory distress partial­pressure of carbon dioxide (PaCO2) is low.
mimicking asthma.
●● A normal PaCO2 is indicative of severe respiratory dis-
Ù tress and a rise in PaCO2 is a sign that respiratory col-
Cyanosis is a late sign of severe exacerbation. lapse is imminent.

Shock often complicates near fatal attacks of asthma. Ù


Severe hypoxia, insensible water loss due to re­spiratory “Treat the patient and not the numbers”.1
distress, vomiting, refusal of feeds during the exacerbation
Blood gas analysis may be performed only when the
and coexisting sepsis may increase the need for fluids dur-
ing resuscitation. child has respiratory failure requiring intubation despite
initial management in the emergency department.1

ASTHMA MIMICS Ù
Assessment of severity is the first step in the management
It is not uncommon for central airway obstruction to be of acute asthma.
misdiagnosed as asthma. Upper airway foreign bodies,
epiglottitis, structural diseases of the larynx, vocal cord The exacerbation is classified as moderate, acute se-
dysfunction and tracheal narrowing could mimic asthma. vere, life-threatening or near fatal attack. Based on the se-
Dysphonia, inspiratory stridor, wheezing loudest over the verity of the attack, the appropriate bronchodilatory thera-
central airway are some of the clues, which help differenti- py is initiated (Protocol 8.1).
ate these causes from asthma.
Diagnosis of asthma in toddlers and infants is unusual.
Ù
Repeated assessment is recommended after each
Intermittent wheezing attacks may be due to recurrent vi- intervention (bronchodilator) (Evidence A).
ral infections. Recurrent aspiration leading to pneumonitis,
86 Section IV n Breathing

●● Each therapeutic intervention should be followed by


the rapid cardiopulmonary cerebral assessment to de-
termine wheth­er theIPchild had improved, deteriorated
: 196.52.84.10
or remained status quo.
●● This helps to decide the next step in the treatment.
●● If oxygen, fluids, the first inhalational dose of salbu-
tamol/ipratropium and subcutaneous epinephrine have
resulted in improvement in a child presenting with near
fatal asthma, the subsequent dose of epinephrine may
be withheld. However, if he remains in the same physi-
ological status, epinephrine may be repeated along
with the next inhalation of salbutamol and ipratropium
bromide.
Ù
A structured approach using a proforma is the most Figure 8.3 Near fatal asthma: Child in respiratory distress
important determinant of a successful outcome in the with grunting, progressive fall in mental status, loss of tone,
ED. evidence of shock, agitation, fighting the mask, cyanosis
diaphoresis.

Case scenario ●● Supplemental oxygen through a tight fitting face mask


or a non-rebreathing bag or a nasal cannulae at flow
A 3-year-old asthmatic child is brought to the ED after rates sufficient to maintain saturations > 92% should be
his usual home treatment failed to give relief. He is too
dyspneic to speak or feed. He has diaphoresis his as- provided (Class A evidence).
sessment is as follows (Figures 8.2 and 8.3). ●● Oxygen and inhalational therapy should be provided in
a non-threatening manner with the child seated com-
fortably on the mother’s lap.
●● Separation of child from his mother is contrain­dicated,
since agitation and crying could worsen hypoxia.
●● Besides, mother’s help is crucial for holding the nebu-
lizer mask. She is the most sensitive ‘monitor’ during
nebulization of a hypoxic child and is the first to alert
emergency personnel if sudden deterioration occurs
during nebulization.
While assessment is being performed, a brief, focused
history is taken. A more detailed history, complete physi-
cal examination and laboratory studies should be performed
only after initial therapy has been completed (Evidence D).
Figure 8.2: Note the diaphoresis, loss of tone and failure of
the pulse oximeter to pick up oxygen saturation in this child
Ù
Short-acting beta 2-agonist treatment is recommended
with a near fatal attack of asthma. Children, often resent the
face mask. The apparent tolerance to the nebulizer mask
for all patients (Evidence A).1,2,3,4,5
suggests significant drop in level of consciousness due to
severe hypoxia. Also, note that this child with an asthmatic
exacerbation appears well nourished. For less known reasons, Nebulizer Therapy
asthma does not seem common in malnourished kids.
●● Administer salbutamol by nebulizer, driven by oxygen
if the asthmatic exacerbation is severe.
Chapter 8 n Management of an Asthmatic Exacerbation 87

●● 2.5 mg of salbutamol (nebulizer solution) is diluted in Caution


3–4 mL of normal saline. It should not be diluted using
distilled water. IP : 196.52.84.10
It would seem intuitive to dose salbutamol, based
on the child’s weight. However, a fixed amount of drug
is added to the nebulizing chamber (independent of
the child’s age or weight). The patient’s minute ventila-
tion regulates the amount deposited in the lungs. Thus, Figure 8.4 Hazards of salbutamol nebulization: In asthma,
a 12-year-old child (due to the greater minute ventila- bronchospasm causes reduction in oxygen within the alveoli.
tion) will deposit a larger amount of drug in the lungs, This leads to hypoxia-induced pulmonary vasoconstriction
than a 12-month-old infant. Other factors which limit diverting blood to the better ventilated alveoli. In
drug delivery in the young child are smaller airways, hypoxic asthmatics, salbutamol inhibits hypoxia-induced
shorter inspiratory times and lack of cooperation. Fur- vasoconstriction resulting in pulmonary vasodilation, which
thermore 90% of the drug is wasted to the atmosphere. further aggravates hypoxia!

In the small volume nebulizer, drug delivery is maximal


when the volume of solution is 3–4 mL and the flow rates
are set at 6–8 mL/min. The nebulizer with a mouth piece is
superior to face mask since nasal deposition is minimized.
Children with severe asthma who do not respond to the
initial salbutamol dose should be treated aggressively with
higher and more frequent doses. Drug dosing is individu- Figure 8.5 Hazards of salbutamol nebulization: In children,
presenting with respiratory distress and wheeze due to alveolar
alized according to severity and the subsequent doses are
causes, salbutamol has no beneficial effects. In hypoxic children,
based on the patient's response. salbutamol, will inhibit the reflex pulmonary vasoconstriction
causing pulmonary vasodialation and increase blood supply
to the hypoxic alveoli. The latter could aggravate hypoxia due
ADVERSE EFFECTS OF NEBULIZED
to ventilation perfusion mismatch and can precipitate cardiac
SALBUTAMOL IN HYPOXIC CHILDREN arrest!
Brochospasm causes alveolar hypoxia which results in Alveolar pathologies can also present with respiratory
pulmonary vasoconstriction. This protective reflex phe- distress and wheeze, e.g. pneumonia, pulmonary edema.
nomenon, diverts blood to better ventilated parts of the
lung thus maintaining the ventilation perfusion ratio.
Salbutamol prevents this beneficial reflex phenomena by
inhibiting the hypoxia-induced pulmonary vasoconstric-
tion resulting in pulmonary vasodilation. The latter leads
to increased blood flow to the hypoxic alveolus aggravat-
ing the ventilation-perfusion mismatch worsening hypoxia
in the already compromised child. It is not uncommon for
a hypoxic child to deteriorate during salbutamol nebulizer
therapy (refer Figures 8.4 to 8.8).
Close physician monitoring is essential during nebu-
lization. Nebulization of salbutamol should be performed
through high flow oxygen. Pulse oximetry and resuscita-
tion equipment should also be close at hand when nebuliz-
ing a child with life-threatening or near fatal asthma.
Figure 8.6: This asthmatic child, referred from the asthma
Prefilled epinephrine syringe (0.1 mL/kg of 1:10,000) clinic for a near fatal attack of asthma was being nebulized.
must also be available close at hand. During her third nebulization, she suddenly deteriorated and
progressed to severe respiratory failure needing ventilation.
88 Section IV n Breathing

●● Salbutamol nebulization unmasks or worsens hypoxia


in hypoxic asthmatics and can even precipitate cardiac
arrest (Figure 8.6)!4IP : 196.52.84.10
●● If deterioration is profound, stop nebulization and re-
consider the diagnosis. All that wheezes is not asthma!
Ù
Nebulization of salbutamol is one of the commonest
interventions in seriously ill children presenting with
respiratory distress. It is also one of the most hazardous
interventions in hypoxic children presenting with
respiratory distress (Figure 8.8).

Figure 8.8: A well-child and happy mother. Though asthmatic,


this episode of respiratory distress was secondary to
pneumonia. The catastrophic deterioration during nebulization
was a complication of salbutamol nebulization. Consider non-
asthmatic cause of respiratory distress, if sudden worsening
occurs during nebulization.

Ipratropium Bromide
Ipratropium bromide (IB), an anticholinergic derivative
competes with the acetylcholinesterase at the M3 musca­
rinic receptor attenuating the neural signal for broncho-
constriction, thus leading to relaxation of airway smooth
muscle. It also relieves mucosal edema and secretions.
Figure 8.7: This picture shows her following emergency
intubation and ventilation after deterioration during her Contractility of the smooth muscle lining the large and
nebulization. This particular episode of respiratory distress was medium sized airways is under parasympathetic neural
secondary to pneumonia and not due to asthma. Hence, for control and is activated by acetylcholine (ACh) release.
sudden deterioration during salbutamol even in asthma stop
nebulization, reconsider etiology. ●● The larger airways are constricted in life-threatening
asthma resulting in greater benefits with the use of IB.
●● Respiratory viruses trigger asthmatic exacerbations by
Intermittent Versus Continuous increasing parasympathetic activity of the airways viz
Nebulization with Salbutamol bronchospasm and airway secretions. Inhaled IB has
●● 2.5–5 mg of salbutamol nebulization is repeated every been found to be more beneficial in pediatric asthma
triggered by viral upper respiratory tract infection
20–30 minutes.
(URTI).
●● Continuous nebulization entails that 10–20 mg is added
●● High doses of racemic SABA contain an S-isomer,
to the chamber and administered over 1 hour.
which increases intracellular concentration of free cal-
The onset of action for SABAs is less than 5 minutes; cium in the smooth muscles of the airways. The latter
repetitive administration produces incremental bronchodi- provokes bronchoconstriction. Concomitant use of IB,
lation. Continuous administration of SABA may be more when high doses of salbutamol are being used abol-
effective in more severely obstructed patients. However, ishes this response.
this should be performed under very close supervision. ●● A multidose regimen showed statistically significant
improvement in lung function and clinical asthma
score.
Chapter 8 n Management of an Asthmatic Exacerbation 89

The quaternary ammonium compound, which forms


part of this drug makes it lipid insoluble preventing its sys- Ù
temic absorption. LessIP than 1% is systemically absorbed, Parenteral steroids are recommended in the management
: 196.52.84.10
making it one of the safest bronchodilator drugs used in the of asthma exacerbations (Evidence A).
management of acute asthma. Therapeutic response occurs
within 3–30 minutes after being given. The peak effect oc- Subcutaneous Adrenaline
curs at around 90 minutes and remains effective up to 6
●● Severely ill children have poor inspiratory flow due to
hours after nebulization. decreased tidal volume. Low tidal volume limits deliv-
●● Administer 250–500 µg via nebulizer through oxygen. ery of in­haled salbutamol to the terminal airways. This
●● Repeat every 20–30 min for 3 doses (maximum of subset of children benefit from urgent subcutaneous
1,500 µg) in the first hour along with intermittent aero- adminis­tration of beta-2 agonists.
solized SABA. ●● The ILCOR guidelines 2005 suggested that in near fa-
tal attacks of asthma, where tidal volume is reduced,
●● Repeat as needed up to the first 3 hours during the ini-
bolus doses of epinephrine or terbutaline may be used
tial management of severe exacerbations. as an initial therapy and re­peated every 20 minutes up
Ù to a maximum of 3 doses based on the response of the
patient in life-threatening asthma.
Inhaled ipratropium bromide is recommended for ED
management of life-threatening or near fatal asthma. ●● Dilute 1 mL adrenaline in 9 mL of NS (1:10,000).
(Evidence A).6 ●● Administer 0.1 mL/kg of 1:10,000 solution subcutane-
ously.
Corticosteroids Widely available, subcutaneous adrenaline has been
safe in children and does have a role in near fatal asthma
The early use of steroids, speed the resolution of airflow not responding to more conventional therapies. However,
obstruction, reduces need for hospitalization and prevents it is a non-selective adrenergic drug with side effects such
relapse of the asthma exacerbation. All steroid prepara- as tachycardia, arrhythmias, hypertension, etc.
tions are equally efficacious in so far as anti-inflammatory
effects are concerned. Magnesium Sulfate7,8
●● Intravenous hydrocortisone (4 mg/kg and repeated 4th Many patients, who present for assessment and treatment
hourly) is administered only when oral medications are to the ED with an asthmatic exacerbation may not benefit
not tolerated. from early treatment with magnesium sulfate.
Ù The NHLBI guidelines recommend that for severe ex­
acerbations, unresponsive to the initial treatments listed
Oral prednisolone is given at the dose of:
– 10 mg in infants < 2 years above, a single dose of intravenous magnesium may be
– 20 mg stat in children between 2 and 5 years considered (Evidence B). In patients with severe acute
– 30–40 mg > 5 years early in the management of asthma, magnesium sulfate appears to improve pulmonary
function and reduce hospital admissions.
asthma.
●● Magnesium sulfate is infused slowly in the dose of 25–
The dose is repeated if the child vomits the medication. 100 mg/kg/dose (maximum of 2 g) as a single dose.
Steroids may be given for 3–5 days and tapered depending A relatively safe drug, it is useful in children presenting
on the response to treatment. Currently, there is insuffi- with severe tachycardia complicating life-threatening asth-
cient evidence to support the use of inhaled corticosteroids ma. It is also believed to decrease the need for intubation.
in the management of acute asthma exacerbation in the
ED. Hence, inhaled steroids are not initiated in preference Aminophylline
to oral steroids (Evidence B). Steroids may be given 5–10
days following discharge to prevent early relapse. Ù
The NHLBI guidelines do not recommend the use of
methylxanthines (Evidence A).
90 Section IV n Breathing

Conversely, the British Thoracic Guidelines suggest ●● However, it is not uncommon for young children with
that aminophylline may be useful in near fatal asthma not life-threatening asthma to present with shock.
re­sponding to maximalIPdoses of bronchodilators and ste­
: 196.52.84.10 These children often require large volumes in our set-
roids. In settings, where access to mechanical ventilation is
ting to attain therapeutic goals of hypoxia and shock reso-
limited, this drug has been useful in reducing ICU admis­
lution. Perhaps, the increased fluid requirement, may be
sion and fatality in asthma-induced respiratory failure.
secondary to late referral, refusal of feeds, vomiting and
Ù
Aminophylline is not recommended in mild and moderate
coexisting sepsis or dengue.

asthma. Its troublesome side effects far outweigh its There may be a drop in serum potassium levels sec-
bronchodila­tory effects. ondary to use of SABA, theophylline, steroids and epi-
nephrine. Consequently, potassium should be monitored
●● 5 mg/kg loading dose is given as an infusion over 20 closely in children with refractory asthma.
minutes followed by a continuous infusion at 1mg/
kg/h.
PEF Monitoring9
●● The loading dose is avoided in children, who have been
on chronic theophylline therapy or have received a pre- ●● If peak expiratory flow rate (PEFR) is less than 33%, it
hospital intramuscular dose of deriphyllin. is suggestive of acute severe asthma.
●● ECG monitoring is recommended during aminophyl- ●● PEFR less than 60% of the child’s best or predicted
line infusion. values, is indicative of life-threatening asthma.
Monitoring asthma based on PEFR is useful for chil-
Intravenous Salbutamol dren older than 5 years of age. In children less than 5 years,
●● Intravenous (IV) salbutamol (15 mg/kg) is reserved for this maneuver can aggravate hypoxia by causing dynamic
those children for whom the drug cannot be reliably airway collapse. Unfortunately, this may not always be
administered through the nebulizer unit. possible in busy ED, which prevents its wide spread use in
●● Continuous IV infusion of beta 2 agonist is not superior the Indian scenario.
to maximal inhaled dose.
●● Hypoxia occurring due to the salbutamol-induced V/Q
Ù
The expert panel report 3 has given recommendations
mismatch is more severe with IV beta-2 agonist infu- for the following interventions in the management of
sion than the inhaled route. acute asthma in the ED.
●● In addition, there is a greater risk of arrhythmias mak-
ing ECG monitoring mandatory during therapy. Any ●● Antibiotics are not recommended during the ED treat-
intravenous therapy in asthma requires continuous ment of acute asthma exacerbations (Evidence B) un-
ECG monitoring. less evidence of bacterial sepsis is available.
●● Mucolytics are not recommended (Evidence C).
Other Therapies ●● Sedation: Anxiolytic and hypnotic drugs are contrain-
dicated in severely ill asthma patients, because of their
Intravenous Fluids respiratory depressant effect (Evidence D).
Aggressive hydration is not recommended for old- Indications for intubation is based on clinical judgment
er children, but may be indicated for young children (Evidence D). Absolute indications for intubation and me-
(Evidence D). chanical ventilation are minimal and include:
●● Correct dehydration since it could cause reduction in ●● Apnea and coma.
ciliary activity and mucus plugging. ●● Fatigue, with poor respiratory effort.
●● In the absence of dehydration, fluids are administered ●● Imminent arrest and arrhythmias.
cautiously at two-thirds maintenance due to the risk of Since intubation is difficult in patients who have asthma,
SIADH induced by pulmonary edema.
it should be performed by a physician, who has extensive
Chapter 8 n Management of an Asthmatic Exacerbation 91

experience in intubation and airway management in the ●● The spacer should be washed periodically with deter-
ED. Ketamine usage for premedication prior to intubation, gent to reduce the electrostatic and enhance delivery.
have not shown clinical IPbenefit. Ideally, even without in-
: 196.52.84.10 Refer Table 8.1.
tubation, patients who have not been improving satisfac-
torily or deteriorating despite aggressive bronchodilatory Discharge
therapy in the ED should be transferred into the ICU.
An asthmatic exacerbation is considered a failure of pre-
ventive therapy and discharge plans should take into ac-
count the following:
●● Motivate the parents and the child to take regular in-
haler therapy.
●● Consider use of steroid inhalers.
●● Explain the use of these devices with a detailed written
asthma plan and the need for regular follow-up.
●● Advise regarding the need to seek urgent help, if there
is exacerbation of asthma.
●● Arrange for care in the asthma clinic.

Figure 8.9: Child using MDI with spacer and mask


Key Points
ü
1. Recognize asthma since “all that wheezes is not
asthma”.
METERED DOSE INHALER AND SPACER
2. Salbutamol can precipitate cardiac arrest in hypoxic
●● Inhaled salbutamol provides the most rapid relief and children with respiratory distress and wheeze
is the initial bronchodilator of choice. It may be ad- secondary to non-asthmatic etiologies.
ministered through metered dose inhal­ers (MDI) with 3. Determine severity of the asthmatic exacerbation on
spacers or small volume nebulizers. MDI + spacer are arrival.
the preferred option in mild to moderate asthmatic ex- 4. Salbutamol can worsen hypoxia in near fatal attacks
acerbation associated with nor­mal tidal breathing. of asthma.
5. Every intervention should be followed by a rapid
●● The spacer, acts as a reservoir for the aerosol, resulting cardiopulmonary assessment to determine the next
in greater drug delivery to the airways and less wastage step in the protocol.
to the atmosphere. Since this MDI with spacer, also re-
duces the amount of drug deposited in the oropharynx,
it reduces systemic absorption and unwanted side ef-
fects such as tachycardia and hypoxia (Figure 8.9).
common errors
û
1. Nebulization using the electrical nebulizer and not
●● 6–8 puffs of B2 agonist using MDI and spacer can pro-
vide a dose of 2.5 mg. A reasonable starting dose may through high flow oxygen.
be one half puff/kg with a maximum of 10 puffs (OR). 2. Nebulization of child with respiratory distress due to
●● 2.5 mg of salbutamol via small volume nebulizer. pneumonia or cardiac failure.
●● Mild attacks: 2–4 puffs may be sufficient, while in se- 3. Continuing to treat based on initial assessment of
vere attacks 10 puffs may be needed. severity, without reassessment.
●● In children less than 4 years of age, face masks con- 4. Failure to recognize shock and manage
nected to the mouth piece of the spac­er are necessary. appropriately.
●● In children older than 4 years of age, mouth pieces con- 5. Failure to monitor and document during resuscitation
nected directly to the spacer are preferable. of hypoxic asthma.
●● Eight breaths are needed per actuation to completely 6. Failure to treat until resolution of therapeutic goals
empty the spacer. of hypoxia, bronchospasm and shock in the ED.
92 Section IV n Breathing

Table 8.1: Drugs used for asthmatic exacerbation in the ED

Drugs Route Dose Side effects Remarks


1. Salbutamol
IP Nebulized
: 196.52.84.10
0.05–0.1 mg/kg for three Tremors, nausea, Hypokalemia occurs with
doses. Continuous dose: tachycardia, blood continuous nebulization.
0.15–0.45 mg/kg/h pressure instability, Prolongation of QTc interval.
Max: 20 mg/h cardiac arrhythmias, Unmasks or worsens hypoxia in
myocardial instability hypoxic asthmatics.
2. Ipratropium bromide Nebulized 250–500 µg Rarely mydriasis and Peak response develops after 30–90
Q4–6 hourly blurred vision min.

3. Hydrocortisone IV 2–4 mg/kg Q6 hourly Hypertension, Always give H2 receptor blocker as


hyperglycemia, mood prophylaxis against gastritis and
disorders, gastritis perforation. Short course for 5–7
day. After the acute course is over,
can be changed to oral.
4. Methylprednisolone IV 0.5–1 mg/kg/dose Q6 Hypertension, Always give H2 blocker as
hourly hyperglycemia, mood prophylaxis for gastritis and to
disorders, gastritis prevent perforation. Short course
for 5–7 day. After the acute course is
over can be changed to oral.
5. Adrenaline SC 0.1 mL/kg (1:10,000) Tachycardia, Administered in near fatal asthma
hypertension
6. Terbutaline IV Loading dose: 10 µg/kg Same as salbutamol but Subcutaneous doses can be tried
over 10 min more pronounced before giving IV infusion. Adrenaline
Infusion: 0.1 µg/kg/min can be used as the other alternative.
0.01 mg/kg dose for 3
SC doses q20 min
7. Aminophyline IV Loading dose: 5 mg/kg/ Nausea, vomiting, fever, Extremely narrow therapeutic
dose dyskinesia, seizures and index. Decrease dose in patients
Over 20 min death with hepatic and cardiovascular
< 6 month: 0.5 mg/kg/h dysfunction.
6–1 year: 0.85–1 mg/kg/h
1–9 year: 1 mg/kg/h
> 9 year: 0.75 mg/kg/h
8. Magnesium sulfate IV 25–50 mg/kg/dose over Hypotension, nausea, No role for repeat doses or
20–30 min flushing arrhythmias, continuous infusion.
muscle weakness,
areflexia and respiratory
depression
9. Ketamine IV, IM Loading dose: 2 mg/kg Sialorrhea and increased Used as an adjunct for intubating
Infusion: 1–2 mg/kg/h airway secretions (can patients with asthma. Monitor for
be offset with atropine) increase in ICP, metabolic rate, BP
Dissociative anesthesia and heart rate.
(can be offset with
sedative)
Protocol 8.1: PEMC approach: Management of acute exacerbation of asthma

IP : 196.52.84.10
Chapter 8 n Management of an Asthmatic Exacerbation
93
94 Section IV n Breathing

References 5. Scarfone, et al. Beta-2 agonists in acute asthma: The evolv-


ing state of the art. Ped Emer Care. Dec 2002;18:442-48.
1. Circulation: Journal of the American Heart Association 6. Dotson K, Dallman M, Bowman M, Titus. MO Ipratropi-
2005; Vol 102. No 8.IPAugust
: 196.52.84.10
(Part 8.) um Bromide for acute asthma exacerbation Ped Emer Care.
2. Thorax: Journal of the British Thoracic Society 2003:58 2009;25(10)687-92.
(suppl I Annex 6.) 7. Cheuk D K L, Chau T C H, Lee S L A meta analysis on
3. National Asthma Education and Prevention Program. intra venous magnesium sulphate for treating acute asthma
Expert Panel Report 3: Guidelines for the Diagnosis and Arch Dis Child. 2005;90:74-77.
Management of Asthma (Summary Report 2007) In: 8. Rowe BH, Bretzlaff J, Bourdon C, Bota G, Blitz S, Cama-
Busse W, ed. J Allergy Immunol. 2007; 120 (5): S 94-138. rgo CA. Magnesium sulfate for treating exacerbations of
National Institute of Health ----National Heart Lung and acute asthma in the emergency department (Review). The
Blood Institute. Cochrane Library 2009.
4. British Thoracic Society, Scottish Intercollegiate Guide- 9. Gorelick M.H et al, Difficulty in obtaining Peak Expiratory
lines Network: British Guideline on the Management of Flow Measurements in Children with Acute Asthma. Ped
Asthma- June 2009. Emerg Care. Jan 2004:20(1):22-26.
9
IP : 196.52.84.10

Pulse Oximeter

Figure 9.1: Different equipments used for pulse oximetry and cardiorespiratory monitoring

Learning Objectives
1. How does the pulse oximeter work? 2. Pearls and pitfalls in pulse oximetry.

INTRODUCTION
Considered as the ‘5th vital parameter’, the pulse oxime-
ter helps to determine the oxygen content of hemoglobin
(SpO2) using a finger probe (Figure 9.1). It works by utiliz-
ing selective wavelengths of light. Having understood the
significance of pulse oximetry as a component of clinical
assessment and decision-making in young infants and chil-
dren, pulse oximeters have been made available even in
the Primary Health Centers.
Figure 9.2: Photodetector picks up R/IR light source.

Principle The pulse oximeter probe, emits both red and infra-
Oxygenated hemoglobin absorbs infrared light and al- red light using LED technology. The light shines through
lows red light to pass through. Deoxygenated (or reduced) a site with good blood flow. Typical adult/pediatric sites
hemoglobin absorbs red light and allows infrared light to with good blood flow are the finger, toe, pinna (top) or lobe
pass through. of the ear. Infant sites are the foot, palm, hand, big toe or
thumb.
Red light is within the 600–750 nm wavelength light
band, (Figure 9.2) while the infrared band lies within the Opposite the emitter is a photodetector that receives
850–1,000 nm wavelength band (Figure 9.3). the light passing through the measuring site.
96 Section IV n Breathing

●● The LED emits red light alternatively at two different LIMITATIONS OF PULSE OXIMETER
wavelengths, visible and infrared regions of the elec-
tromagnetic spectrum. 1. The pulse oximeter picks up late and severe hypox-
IP : 196.52.84.10 emia. It fails to pick up early, minimal fall in oxygen
levels.
Ù
An oxygen saturation of 90% in the pulse oximeter
equates to a blood gas of 60 mm Hg!

2. Fails to detect signals in severe shock. Intense vaso-


constriction reduces pulsatile signals to the probe.
3. Does not provide any information on PaCO2: The
child may have severe hypercapnea due to al­veolar
hypoventilation or respiratory failure. If the child is re-
ceiving a high concentration of inspired O2, the pulse
oximeter will continue to show normal oxygen satura-
tions.
4. Will not show correct values in children with abnor-
mal hemoglobinopathies.
5. Progressively under-reads the saturation as the hemo-
globin decreases. However, it is not affected by poly-
Figure 9.3: Wavelength spectrum. cythemia.
●● These are transmitted through the tissues and adsorbed 6. Unreliable when child has excessive movements such
to different degrees by oxyhemoglobin and deoxyhe- as status epilepticus.
moglobin. 7. May not be accurate in bright extraneous light.

The arteriolar bed pul­sates and absorbs variable Tips for Use
amounts of light during systole (peak) and diastole
(trough), as blood volume increases and decreases. The 1. Ensure that the optical components of the sensor are
ratio of light absorbed at the peak and trough is translated properly aligned.
into oxygen saturation measure­ments. Since peaks occur 2. Check adhesive sensor sites every 8 hours and move it
with each heartbeat or pulse, the term ‘pulse oximetry’ was to a new site if necessary.
coined (Figure 9.4). 3. Change the site of sensors to a new site at least every
4 hours.
4. Adhesive digit sensors may be reused on the same pa-
tient if the adhesive tape attaches without slipping.
5. Replace the sensor whenever the adhesive quality is
depleted.
6. Fix the probe in an extremity free of an arterial cath-
eter, blood pressure cuff intravascular infusion line.
7. Clean reusable sensors between patients.
8. Document SpO2 results in the patient's medical record.
It should detail the conditions under which readings
Figure 9.4: Variable absorption of light.
were obtained viz date, time of measurement, concen-
●● The pulse oximeter provides continuous non-invasive tration of inspired oxygen concentration and type of
monitoring of oxygenation at the tissue level. oxygen delivery device being used.
●● Monitoring of oxygen is not affected by skin pigmenta- 9. Cardiopulmonary assessment must be documented
tion. along with pulse oximeter reading.
Chapter 9 n Pulse Oximeter 97

10. The external portion of the monitor should be cleaned


according to manufacturer's recommendations. When
soiled, it can be a IP
source of potentially transmissible
common errors
û
1. Failure to immediately respond to a fall in SaO2 <
: 196.52.84.10
organisms. 92% in an intubated child can result in cardiac arrest
in minutes.
Key Points
ü 2. Using the pulse oximeter as the sole method to
1. SaO2 of < 92% in room air or with supplemental recognize critical illness!
oxygen, for a child presenting with respiratory 3. Failing to provide supplemental oxygen to a shocked
distress is suggestive of severe hypoxia. child because the pulse oximeter is showing normal
2. SaO2 < 92% in an intubated child suggests that the saturations.
oxygen levels in the blood have fallen to 60 mm 4. Considering that a normal pulse oximeter reading is
Hg. the only criteria for intubation.
Circulation

Section V
IP : 196.52.84.10
IP : 196.52.84.10
General Approach to the
10
IP : 196.52.84.10

Management of Shock

Figure 10.1: Pull push technique used to administer fluids in a child presenting with respiratory failure and hypotensive shock.
Time-sensitive goal-directed therapy results in successful outcomes.

Learning Objectives
1. Pathophysiology of shock. 3. Pearls and pitfalls in shock management.
2. Risks of fluid therapy during shock resuscitation. 4. A modified shock protocol based on ‘small volume
or large volume etiologies’.

INTRODUCTION to pyruvate and lactate. This represents an inefficient


utilization of substrate with minimal energy production.
Early recognition of shock is key to successful resuscita-
Although this early injury is often reversible, persistent
tion in critically ill children.1,2 Often, shock results in or
hypoperfusion leads to cellular injury, which further ex-
coexists with myocardial dysfunction or acute lung injury.
acerbates the microcirculatory derangements and mald-
Recognition and resuscitation should be directed to resto-
istribution of blood flow that can further impair perfu-
ration of tissue perfusion, normalization of cardiac func-
sion and eventually cause irreversible tissue damage.4
tion and resolution of pulmonary edema. Underlying cause
of shock should also be addressed urgently3 (Figure 10.1). 2. Inflammatory mediators: Tissue hypoperfusion ac-
tivates multiple humoral mediators along with the
complement cascade. Activation of the complement
PATHOPHYSIOLOGY
cascade results in widespread endothelial injury, sys-
Shock results from inadequate delivery of oxygen and nu- temic leukocyte adhesion, pulmonary alveolar capillary
trients to tissues relative to their metabolic demand. The damage, acute respiratory distress syndrome (ARDS)
impaired tissue perfusion and consequent cellular hypoxia and activation of the coagulation system culminating
results in cellular injury, which in turn causes metabolic in disseminated intravascular coagulation and multio-
derangements and the release of inflammatory mediators. rgan failure.4,5 Signs of acute lung injury (respiratory
1. Metabolic derangements: The reduced availability distress) is often an early sign of organ dysfunction in
of oxygen also results in glucose being metabolized a shocked child compared to DIC, which occurs later.
102 Section V n Circulation

IP : 196.52.84.10

Figure 10.2: Rapid compensatory mechanism in shock (Boxed entities are the manifested symptoms clinically).
GFR, glomerular filtration rate; RAS, reticular activating system; SVR, systemic vascular resistance; BP, blood pressure.

3. Neurohormonal responses are activated early to resistance to ventricular ejection (afterload) and myo-
preserve adequate tissue perfusion and maintain vital cardial contractility. Autoaugmentation of preload de-
organ function6 (Figure 10.2). However, with further pends on the two-thirds of the total circulating blood
deterioration, these mechanisms can no longer com- volume, which is contained in the small veins. When
pensate and hypotension, a late sign of shock ensues. shock occurs, one of the earliest responses is alpha-
4. Cardiovascular response to shock: Attempts to in- adrenergic mediated vasoconstriction that diverts this
crease cardiac output is dependent on increase of heart reservoir of blood centrally to improve venous return
rate and augmentation of stroke volume. Stroke vol- and ventricular filling. In septic and neurogenic shock
ume has three determinants—the volume of blood venous dilatation rather than vasoconstriction occurs,
present in the ventricle before contraction (preload), further accentuating preload deficits and myocardial
Chapter 10 n General Approach to the Management of Shock 103

dysfunction. Reduction in stroke volume for a given is about 25%. In shock, low SvO2 in the face of normal
ventricular end-diastolic volume leads to an increase arterial oxygen saturation indicates that the tissues are ex-
in systemic vascular IP resistance (SVR), a compensa-
: 196.52.84.10 tracting greater than 25% of oxygen from the arterial blood
tory mechanism to augment blood pressure. While an in order to maintain adequate tissue oxygenation because
increased SVR is an important compensatory mecha- of decreased cardiac output. Ideally, therapy should be tar-
nism that helps preserve vital organ perfusion, patho- geted towards normalization of SvO2.7 Since monitoring
logic increases in afterload can occur in patients with of SvO2 requires intensive care expertise, which is not usu-
cardiac tamponade, tension pneumothorax and dia- ally available to staff in the ED, management in the ED
phragmatic hernia. should be targeted towards normalization of clinical goals
Normally, an increase in SVR is an important of shock resolution.8
compensatory mechanism that helps preserve vital or-
gan perfusion. Excessive increase in (SVR) afterload The commonest causes of shock are shown in Box 10.1.
can obstruct cardiac output thereby worsening shock Box 10.1: Types of shock
(Refer Chapter on Cardiogenic Shock). Structural
obstruction to cardiac output occurs due to cardiac Hypovolemic shock (decreased blood volume)
tamponade, tension pneumothorax and diaphragmatic Hemorrhage
hernia. These conditions can cause profound shock Trauma
Surgery
that is refractory to fluids and inotropes.
Burns
5. Pulmonary response: Initially, metabolic acidosis Vomiting and diarrhea
induces effortless tachypnea. As the SVR increases, Severe sepsis
pulmonary vascular resistance also increases resulting Distributive shock (marked vasodilation; also called
in increased minute ventilation. Uncorrected shock vasogenic or low resistance shock)
can lead to capillary leak and vasodilation in the pul- Anaphylaxis
monary circulation resulting in acute lung injury and Severe sepsis
acute re­spiratory distress syndrome (non-cardiogenic Cardiogenic shock (inadequate output due to cardiac
dysfunction)
pulmo­nary edema), which manifests clinically as in-
Congestive heart failure
creased work of breathing. Myocardial dysfunction, a Myocardial dysfunction
precursor or the end result of shock due to a variety Arrhythmias
of etiologies can also cause respiratory distress due to Severe sepsis
cardiogenic pulmonary edema. Obstructive shock (obstruction to blood flow)
6. Renal response: Prolonged renal hypoperfusion may Tension pneumothorax
result in pre-renal and ultimately acute renal failure. Diaphragmatic hernia
Pulmonary embolism
In compensated shock, blood flow is redistributed to Cardiac tamponade
the vital organs and oxygen consumption is maintained by Severe sepsis
an increased extraction of oxygen leading to lower oxygen Dissociative shock
saturation in venous blood. Methemoglobinemia
Carbon monoxide poisoning
Oxygen delivery can be calcu­lated by the following
formula: Oxygen delivery (DaO2) = Cardiac output (CO) ×
Arterial Oxygen content (CaO2). CaO2 is the product of the Recognition
hemoglobin concentra­tion and arterial oxygen concentra-
tion. It is calculated by the formula: CaO2 = Hb (g/dL) × Early signs of hypoxia or shock are subtle and identifying
1.39 × SaO2. The nor­mal O2 content of arterial blood is 18– at risk patients may be challenging.2,9,10 Late shock is easy
20 mL/dL and mixed venous blood is 75% saturated. The to recognize, but resuscitation may be futile. Consequently
normal tissue extraction ratio for oxygen is measured with emergency department (ED) staff must be sensitized to
the following formula: Extraction ratio = (CaO2- CvO2)/ situations in which shock may occur.
CaO2. Oxygen saturation is used as a surrogate to calculate Triage questions, which help recognize shock have al-
the extraction ratio viz SaO2-SvO2/SaO2. The normal value ready been discussed in Chapter 1.
104 Section V n Circulation

Airway
Ù ●● Airway is patent or maintainable or clear if the infant is
If the clinical setting suggests the possibility of shock,
IP : 196.52.84.10
then it is best to treat early when signs are subtle rather crying or vocalizing.
than waiting for overt signs to develop.9 If airway is clear:
●● Perform assessment and shock resuscitation, whilst
This is of special relevance in children who may pres-
oxygen is being administered.
ent with non-specific symptoms such as breathlessness, di-
arrhea and fever, where symptoms may be misinterpreted Airway positioning is warranted:
as benign and their significance dismissed.3 Early recogni- ●● If the child is carried into the ED, ‘responsive to pain’,
tion of shock has been discussed in Chapter 1. unresponsive or convulsing.
●● Place the child on the resuscitation trolley and open the
CASE SCENARIO airway as shown in Figure 10.5.

A neonate was brought into the ED, 3 hours after birth, Breathing
for the bullous lesions on the skin (Figures 10.3 and 10.4).
●● Provide oxygen through non-rebreathing mask in older
children and oxyhood in young infants presenting with
effortless tachypnea.

Figure 10.3: Anticipation that loss of fluids via the extensive


weeping exudative lesions can cause shock along with clinical
findings of shock is key to successful resuscitation.
Figure 10.5: Airway being opened using the head tilt-chin
lift maneuver in this unresponsive child with shock. Oxygen is
being provided using the non-rebreathing mask. Up to 80%–
90% O2 can be administered using this device in contrast to the
nasal cannula, which delivers a maximum of 40% O2 (Courtesy:
Dr Mullai Baalaaji).

●● Provide oxygen through flow inflating ventilation de-


vice (Jackson-Rees circuit) for children presenting
with respiratory distress and shock (Figure 10.6).
●● If apneic, initiate bag-valve-mask ventilation.
●● Call for the intubation tray.
Prepare age-appropriate laryngoscopes, tracheal tubes,
ties, plaster, tincture benzoin and drugs (Refer Chapter
3 on PAI).
●● However, avoid rushing to intubate.
Figure 10.4 Physiological status: Effortless tachypnea, ●● Effective bag-valve-mask ventilation should be contin-
tachycardia, shock with altered mental status. ued until IO or IV access is secured.
Chapter 10 n General Approach to the Management of Shock 105

IP : 196.52.84.10

Figure 10.6: This picture shows a toddler receiving O2 via a Figure 10.7: Insert two large bore short-length intravascular
flow inflating ventilation device (Jackson-Rees circuit) during catheters. One line is used for fluid resuscitation and
fluid resuscitation for shock with respiratory distress. medications. The second line is dedicated for inotrope
infusion.
●● Consider early intubation in an apneic child with shock,
using ketamine, suxamethonium and atropine. Ù
●● If the child is apneic and bradycardic, intubation can be During fluid therapy, watch out for signs of pulmonary
performed without drugs. edema!
Use a CPAP device to reduce risk of intubation in settings
Ù with limited access to mechanical ventilators.
Waiting for confirmatory blood gas analysis to intubate Initiate inotrope infusion if signs of PE are noted.
is not recommended when the child presents with Continuation of fluids without provision of PEEP or
respiratory failure. inotropes when signs of PE are noted can result in
cardiac arrest.
Ketamine11 is the induction agent and atropine the pre-
medication agent of choice. However, in a hypotensive
child with chronic congestive cardiac failure ketamine,
may worsen cardiac function. A short acting neuromuscu-
lar blocker may be used to facilitate intubation.

Ù
Induction agents such as midazolam can worsen hy­
potension. Avoid midazolam for intubation in hypotensive
shock.

Circulation
Fluids are the cornerstone of shock therapy. As fluids are
being administered to correct hypoperfusion, fluid can leak Figure 10.8: Intraosseous access is life saving in shock
out of leaky pulmonary capillaries resulting in pulmonary management. After infusing the first 20–40 mL/kg, intravenous
edema. PEEP must be provided during fluid therapy for access becomes easier. Avoid damage to peripheral veins in
the attempt to secure peripheral access in the shocked child.
shocks of all etiologies except hypovolemia.
Ù ●● After securing intravenous or intraosseous access,
Do not forget to position the airway and provide oxygen check dextrostix (refer Figures 10.7 to 10.9).
throughout fluid resuscitation.
106 Section V n Circulation

Speed of Fluid Administration


Normotensive Shock
IP : 196.52.84.10 ●● Infuse 20 mL/kg at the rate of 20 minutes (by gravity)8
if the shocked child presents with effortless tachypnea.
●● Infuse 5–10 mL/kg at 5–10 minutes if he has respira-
tory distress and shock (pulmonary edema and shock).
●● Hypotensive shock: Use a pull push technique, using a
3-way stopcock and reservoir, if the child presents with
hypotensive shock (Figure 10.10).

Figure 10.9: After addressing the ABCs, DEFG: “Do not ever
forget glucose”! Correct documented hypoglycemia with 25%
dextrose: 2 mL/kg bolus.

What is the best fluid to correct shock?


●● Administer 20 mL/kg Ringer’s lactate or 0.9% normal
saline.
●● Isotonic fluids are given to establish euvolemia. RL is
preferred for diarrheal losses. NS is preferred in shock Figure 10.10: This picture shows the fluid bolus therapy
due to DKA and severe traumatic brain injury. being initiated using a pull push technique in this infant with
hypotension due to hypovolemia complicated by marasmus
●● Avoid dextrose containing fluids to resolve shock. Ad-
and severe sepsis. One team member is poised with her hand
ministration of glucose containing fluids cause cellu- around the chest to initiate cardiac massage if the need arises.
lar dehydration and osmotic diuresis, thus worsening
shock. Hypotension is suggestive of severe myocardial dysfunc-
●● Theoretically, crystalloids are redistributed into the ex- tion and imminent arrest indicating need for early epineph-
tracellular compartment resulting in an increased risk rine infusion, intubation and ventilation (Figure 10.11).
of tissue edema. It also reduces serum protein concen-
trations and packed red cell volume.12 Besides, large Ù
volumes of normal saline may result in hyperchloremic If the child is maintaining his airway and has spontaneous
metabolic acidosis. Alteration in bicarbonate levels breathing, fluid boluses are enough to correct shock
may also alter renal function, this being one of the de- due to hypovolemia (acute diarrhea). Intubation and
terminants of normal renal blood flow.13,14 epinephrine infusion are rarely needed in hypotensive
●● In reality, 100–120 mL/kg of NS or RL can be admin- shock due to hypovolemia.
istered in the initial hours of resuscitation without dan-
gerous metabolic consequences. Level 1 evidence8 suggests that pushing large volume
●● Besides, crystalloids are inexpensive, readily available, fluids in a short span of time (15 minutes to 1 hours) in
can be stored conveniently and are unlikely to transmit normotensive shock could precipitate volume overload.
infectious agents. The inherent risk of pulmonary edema in the back
Ù ground of acute lung injury and the failing heart must al-
ways be taken into consideration.
Colloids such as albumin are expensive, not readily avail­
able and have not been found beneficial in comparison Fluids infused by gravity can safely resolve shock
with isotonic crystalloids.15 without increasing risk of PE or hepatomegaly.
Chapter 10 n General Approach to the Management of Shock 107

IP : 196.52.84.10

Figure 10.11: Hypovolemic shock due to loss of fluid from


the exposed bowel and viscera Figure 10.12: This emergency case record shows how this
infant was monitored by performing the rapid cardiopulmonary
Despite the need for fluids to resolve severe shock, assessment at the end of each fluid bolus until he achieved
some children may progress to cardiac arrest during fluid all therapeutic goals of shock resolution (refer appendix for
administration. Preload unresponsiveness, suggests severe sample documented case record in a child with septic shock).
myocardial dysfunction. Underlying comorbidities such as
se­vere malnutrition, anemia, electrolyte disorders can also ●● If the answer to all three of these questions is nega-
contribute to the deleterious effects of fluids on a failing tive, then the total volume of fluids needed to re-
heart. solve shock in the ‘Golden hour’ is probably less
than 20–30 mL/kg. Etiologies such as, congenital
How much fluids needed to correct shock? More than heart diseases, myocarditis, arrhythmias, near fatal
60 mL/kg or less than 20–30 mL/kg? asthma, status epilepticus, envenomation, submer-
Ù sion injury, toxins, DKA, trauma, severe traumatic
brain injury, etc. need less than 20–30 mL/kg unless
As the initial resuscitative steps are being performed,
simultaneously evaluate for etiology of shock: Is the these etiologies are complicated by fluid loss, sepsis
shock due to sepsis, hypovolemia or anaphylaxis. or anaphylaxis.
What do I look for after each bolus?
Ask for history of:
Perform the rapid cardiopulmonary cerebral assessment
1. Fever with or without infective focus? and find out whether the child has:
2. Vomiting, diarrhea, abdominal distension, trauma,
bleed? ●● Achieved therapeutic goals (signs of shock resolution:
3. Allergen, drugs? Box 10.2).
●● Remained status quo (shock persists but no signs of
●● If the answer to any of these questions is ‘Yes’ viz PE).
sepsis, vomiting, diarrhea, intussusception, perito- ●● Deteriorated (shock persists, but signs of pulmonary
nitis, burns and polyuria, plan to administer large edema: Box 10.3).
volumes (Figures 10.11 and 10.12).
Ù
Ù Caution: Watch out for signs of pulmonary edema and
Large volume fluids (up to 120 mL/kg in the initial hours preload unresponsiveness.
of resuscitation) may be needed to resolve shock due
to gastrointestinal losses, abdominal sepsis and warm ●● If signs of PE are not noted, but therapeutic goals have
shock due to severe sepsis. not been attained continue fluid therapy.
108 Section V n Circulation

Box 10.2: Therapeutic goals of shock resolution in fluid


responsive shock.
IP : 196.52.84.10
Airway: Maintainable airway.
Breathing: Normal respiratory rate for age, normal work
of breathing, absence of grunt, retractions, abdominal
respirations (in the absence of pneumonia, empyema or other
foci of sepsis in the lung).
Circulation: Normal heart rate for age, easy to feel dorsalis
pedis, warm, pink peripheries, CRT < 2 sec, normal range of
systolic BP for age with a normal pulse pressure. In vasodilatory
or warm shock, wide pulse pressure due to low systemic
vascular resistance may be characterized by diastolic BP that
is less than or equal to half of the systolic BP. In these children,
narrowing of pulse pressure is an additional therapeutic goal.
Normal liver span
Urine output > 1 mL/kg/h
Figure 10.13: This picture shows a young infant with
Disability: Return to baseline mental status in the AVPU scale.
cardiogenic septic shock developing froth during fluid
Eyes mid position with normal extraocular movements in older
therapy.
children or dolls eye movement in very young infants.
Pupils, which are equal and are briskly responsive to light. The 3. Provide CPAP using the Jackson-Rees circuit (if not
brisk response to light may be the only indicator of resolution using already) or intubate.8
of cerebral hypoxia, hypoperfusion, seizure activity or ICP in a
sedated and paralyzed child. Ù
When giving the shocked child a sedative or anesthetic
Box 10.3: Signs of pulmonary edema8 agent for intubation, the sympathetic response to stress
is removed. It is this response that has been maintaining
Airway: Airway instability, froth, new onset cough. the heart rate and BP. If the sympathetic drive is
Breathing: Decreased or increased respiratory rates requiring removed, HR and BP would drop dangerously leading
respiratory support in the absence of neuromuscular diseases. sudden cardiac arrest during the procedure.
Onset of grunt, retractions, abdominal respirations, new rales
Hence, initiation of an appropriate inotrope infusion is
or wheeze, drop in saturations < 92%.
MANDATORY to ensure hemodynamic stability during
Circulation: Bradycardia for age, gallop, hypotension, increase
in liver span from baseline, shock not resolving with 60 mL/kg. intubation.
Disability: Agitation, fighting the mask, combativeness, thirst.
If features of pulmonary edema and/or hepatomegaly
resolve, but shock per­sists after application of flow inflat-
Ù ing ventilation device and initiating the appropriate ino-
Achievement of all therapeutic goals of shock is trope, continue administering small boluses of fluids until
necessary for successful resuscitation of shock.8 shock resolves. Refer Figure 10.13.
What if signs of PE are identified, but shock persists? Ù
If shock is due to ‘large volume etiologies’ such as
1. Interrupt further fluids.
sepsis, further fluid in aliquots (up to a maximum of
2. Initiate an appropriate inotrope8 (Table 10.1).
100–120 mL/kg) may be given in the initial hours until
a. Dopamine, if BP is low normal with warm shock.
shock resolves.
b. Dobutamine, if BP is high with cool shock.
Caveat: ‘Small volume etiologies’ causing shock could be
c. Epinephrine, if BP is low.
complicated by hypovolemia, sepsis or anaphylaxis such
d. Norepinephrine, if systolic BP is in the hypotensive
as severe diaphoresis in scorpion sting, anaphylactic
range and diastolic pressure is less than 50% of sys-
shock during administration of antisnake venom or
tolic pressure.
acute watery diarrhea in a child presenting with near
fatal asthma.
Chapter 10 n General Approach to the Management of Shock 109

Table 10.1: Indications for initiating inotropes, vasopressors and inodilators

Drug Indication Adverse CVS† effects Dose


Dopamine
IPShock
: 196.52.84.10
with normal BP and low SVR* SVT , VPC , VT,
‡ §
10 µg/kg/min
Cardiogenic shock Hypertension
Distributive shock
Epinephrine Severe bradycardia with shock SVT, VPC, VT, ST 0.05–1.0 µg/kg/min
elevation, post
resuscitation
myocardial dysfunction
Pulse-less electrical activity
Post cardiopulmonary arrest stabilization,
toxic doses of calcium channel antagonists,
β-blocking drugs
Hypotensive shock of all etiologies Hypertension
Anaphylactic shock 1–4 µg/kg/min
Dobutamine Cardiogenic shock with high SVR, cardiac 5–20 µg/kg/min
failure
Norepinephrine Low BP with low SVR Tachy, brady 0.05–1.0 µg/kg/min
arrhythmias,
hypertension
Milrinone Cardiogenic shock with high SVR Hypotension 50–75 µg/kg over 10–60 minute
followed by infusion
0.5–0.75 µg/kg/min
*
SVR, systemic vascular resistance; †CVS, cardiovascular; ‡ SVT, supraventricular tachycardia; §VPC, ventricular premature contractions.

OBSTRUCTIVE SHOCK ●● Catheterize to monitor urine output during shock man-


agement (Figure 10.15).
Tension pneumothorax, massive empyema, cardiac tam-
ponade are some of the causes of obstruction to cardiac
output.
Needle thoracocentesis or pericardiocentesis should be
performed to relieve shock (Figure 10.14).

Figure 10.15: Urine output is decreased or absent in shock


and catheterization is recommended for monitoring urine
output during resuscitation. Urine output of > 1–2 mL/
Figure 10.14: Needle thoracocentesis to relieve massive
kg/h is a reassuring sign of normal renal perfusion in shock
empyema that was obstructing cardic output during shock
in children beyond 1 year of age. Polyuria or anuria may
resuscitation in the PED. Note the large volume purulent
occur as complications of renal impairment in septic shock.
material that is being aspirated in the syringe. Obstructive
Inappropriate polyuria has been noted in patients with severe
shock will not resolve with fluids, inotropes and intubation.
sepsis and normal baseline renal function.16
110 Section V n Circulation

Ù Ù
Non-convulsive status epilepticus (NCSE) signals severe If eye signs are ignored or not recognized generalized
hypoxia and shock: IP : 196.52.84.10 tonic-clonic fits supervenes as a preterminal event.

●● On arrival and during every step in the management of How do I ensure a stable metabolic profile during shock
shock, examine the eyes for position and movements. resuscitation?
Conjugate deviation, nystagmus and eyelid twitch sig­
●● Initiate GNS with KCl and administer at maintenance
nal the coexistence of severe hypoxia and shock.17
rates for age. Example, 4 mL/kg/hour in infants less
If the child presented to the PED, with the history of than 10 kg. Ensure that the child has voided urine prior
generalized tonic-clonic activity, eye signs suggest pri- to addition of potassium (Figure 10.16).
mary seizure activity needing immediate anticonvulsant Do not forget to simultaneously treat etiology of
drugs. If however, the presenting history was acute diar- shock!
rhea, fever, breathlessness, submersion, envenomation, etc.
and any one sign of NCSE is noted anytime during shock ●● Simultaneously, provide appropriate treatment for the
resuscitation, it signals severe cerebral hypoperfusion. It is etiology of shock (Table 10.2).
not uncommon to note these findings during resuscitation
of hypotensive shock or cardiac arrest.
Ù
The physiological responses of individual children to
●● Initiate an inotrope. shock resuscitation are often variable and unpredictable.
●● Intubate and ventilate. Therefore, repeated assessments with continuous, non-
invasive monitoring are needed for taking appropriate
Ù
Signs of NCSE in a shocked child denote very poor
decisions in the ED. While the protocol for shock
management is based on broad guidelines, the treatment
prognosis. often needs to be individualized.

Anticonvulsants
Anticonvulsant medications may be hazardous in this
situation.
●● During every reassessment do not forget to look for eye
signs of NCSE.
NCSE is an indication that aggressive management of
hypoxia and shock are needed. Resolution of NCSE oc-
curs if hypoxia and shock are corrected. If however, these
signs persist, anti­convulsant drugs may be administered
very cautiously.
●● Avoid phenytoin, if seizure activity is noted in a child
with shock and myocardial dysfunction.
Phenytoin has been noted to be hazardous in emergen- Figure 10.16: This 36-day-old infant is being managed with the
cy settings, where seizure activity complicates shock and NS boluses, JR circuit, inotrope infusions to combat pulmonary
myocardial depression. edema and shock in the PED. Maintenance (GNS with KCl)
fluids are also being infused at 4 mL/kg/hour throughout
●● If eye signs are not apparent in paralyzed children, resuscitation.
tachycardia, not explained by shock or pain relief sug-
gests the coexistence of NCSE. Shock may be precipitated in children by a variety of
causes. Early recognition of shock and aggressive early re-
Chapter 10 n General Approach to the Management of Shock 111

Table 10.2: Etiologies of shock

Etiology Specific management


IP : 196.52.84.10
Acute laryngotracheobronchitis upper airway obstruction Epinephrine, steroids, call for ENT, anesthetist assistance for
securing the airway
Asthma Bronchodilator therapy, steroids
Anaphylaxis Early intubation if airway obstruction is anticipated or CPR,
epinephrine, steroids, antihistamines, antacids
Sepsis Antibiotics, source control
Poisons Elimination, decontamination, antidotes
Envenomation Antivenom serum
SVT, Arrhythmias Adenosine, cardioversion
Cardiac tamponade, pneumothorax Pericardiocentesis,
thoracocentesis
Trauma Control bleed
Seizures Anticonvulsant therapy

suscitation is likely to yield the most favorable outcomes.


Isotonic fluids form the cornerstone of treatment and the
KEY POINTS
ü
amount required for resuscitation is based on etiologies 1. Anticipate shock in the appropriate clinical
and therapeutic response. After resuscitation has been scenario.
initiated, targeted history and clinical evaluation must be 2. Glucose normal saline infusions can worsen shock
performed to ascertain the cause of shock. Management by causing osmotic diuresis.
of comorbidities such as asthma and seizures should be 3. Volumes greater than 20 mL/kg are needed to correct
implemented simultaneously. Inotropes, respiratory sup- shock due to hypovolemia, anaphylaxis and sepsis.
port, antibiotics and steroids may also be needed during 4. Avoid volumes greater than 20 mL/kg in shock due
the management of shock. While the management of to scorpion sting, submersion injury, isolated severe
shock can be protocol based, the treatment needs to be traumatic head injury, asthma, status epilepticus, etc.
5. Reassess at the end of every bolus.
individualized depending on the suspected etiology and
6. Treat until all therapeutic goals of shock are
therapeutic response.
achieved.
Management of shock is one of the most labor inten­
sive protocols. Anticipation of potential side effects of flu-
ids based on the pathophysiology is key to survival.
COMMON ERRORS
1. Avoiding administration of fluids for fear of
û
Repeated rapid cardiopulmonary cerebral assessment precipitating pulmonary edema.
provides a 60 second advantage in deciding whether to 2. Failure to anticipate that pulmonary edema could
continue the same intervention, stopping or changing tac- occur due to coexisting cardiac dysfunction or leaky
tics. Indeed, “repeated cardiopulmonary assessment of the pulmonary capillaries.
patient in shock, by a competent observer remains the most 3. Failure to initiate inotrope and intubate when features
effective and sensitive physiologic monitor in the manage- of pulmonary edema are noted.
ment of shock” (Zimmerman-1999). 4. Failure to treat until all therapeutic goals of shock are
resolved.
Refer Protocol 10.1.
112 Section V n Circulation

Protocol 10.1: PEMC approach: Management of shock with or without myocardial dysfunction
IP : 196.52.84.10

Airway and Breathing:


1. Effortless tachypnea and shock: O2 through non-rebreathing mask.
2. Grunt, retractions, abdominal respiration and shock (cardiogenic shock): O2(Jackson-Rees circuit).
3. Bradypnea* and shock (cardiogenic shock)*: Initiate bag-valve-mask ventilation (*plan intubation).
Circulation: Secure 2 peripheral IV access,
1. a. Normal BP: Shock with effortless tachypnea: NS/RL 20 mL/kg @ 20 minutes.
b. Shock with respiratory distress: 5–10 mL/kg @ 5–10 minutes.
2. Hypotensive/(NCSE signals severe hypoxia/shock): Pull push 20 mL/kg through IV/IO until BP normalizes. Call for epinephrine infusion
@ 0.3 µg/kg/min (at any step in protocol) and urgent intubation
Disability: GTCS: lorazepam 0.1 mg/kg × 2, levetiracetam 20–30 mg/kg IV (avoid phenytoin in cardiogenic shock)
Avoid treating extensor or flexor posturing due to hypoxia/shock/raised ICP as fits
Dextrostix: Correct documented hypoglycemia; infuse GNS + KCl at maintenance rate for age.
Chapter 10 n General Approach to the Management of Shock 113

REFERENCES 9. Seear MD, Shock A, Macnab D, et al. Henning (Eds). Care


of the Critically ill Child, London, UK 1999; Churchill
1. Han YY, Carcillo JA, et al. Early reversal of pediatric-neo- Livingstone: 1999. pp. 60-67.
natal septic shock byIPcommunity
: 196.52.84.10
physicians is associated
10. McQuillan P, Pilkington S, et al. Confidential enquiry into
with improved outcome. Pediatrics. 2003;112(4):793-99.
quality of care before admission to intensive care. BMJ.
2. Ninis N, Phillips C, Bailey L, et al. The role of healthcare 1998;20;316(7148):1853-58.
delivery on outcome of meningococcal disease in chil-
11. Reynolds SF, Heffner J, Airway management of the criti-
dren: case-control study of fatal and non-fatal cases. BMJ.
2005;330(7505):1475. cally Ill patient:*rapid-sequence intubation. Chest. 2005;1
27;1397-412 DOI 10.1378/chest.127.4.1397.
3. Santhanam I, Ranjit S, Kissoon N: Management of shock in
the Emergency Department. Minerva Pediatr. 2009;61:1-15. 12. Martin GS, Lewis CA. Fluid management in shock. Semin
Respir Crit Care Med. 2004;25:683-694.
4. Deitch EA. Multiple organ failure: Pathophysiology and po-
tential future therapy. Ann Surg. 1992 Aug;216(2):117-34. 13. Wilcox CS. Regulation of renal blood flow by plasma chlo-
ride. J Clin Invest. 1983;71:726-35.
5. Maier RV. Approach to a patient in shock Fauci, In Braun-
wald , Kasper , Hauser, Longo, Jameson, Loscalzo (Eds). 14. Williams EL, Hildebrand KL, McCormick SA, et al. The
Harrisons’ s Principles of Internal Medicine, United States effect of intravenous lactated Ringer’s solution versus
of America: McGraw Hill; pp. 1689-702. 0.9% sodium chloride solution on serum osmolality in hu-
6. Ganong WF. Shock Review of Medical Physiology. Bos- man volunteers. Anesth Anal. 1999;88:999-1003.
ton: McGraw-Hill; 2005. pp. 636-40. 15. Finfer S, Bellomo R, Boyce N. SAFE Study Investigators.
7. Nadel S, Ranjith S, Kissoon N. Recognition and initial A comparison of Albumin and Saline for fluid resuscitation
management of shock. Philadelphia Walter Roger’s Text- in the intensive care unit. NEJM. 2004;350:2247-256.
book of Pediatric Intensive Care. DA Nichols 4th edition 16. Cortez A, Zito J, Lucas CE, et al. Mechanism of inappropri-
(Eds) . Kluwer /Lippincott Williams and Wilkins; 2008. pp. ate polyuria in septic patients. Arch Surg. 1977;112:471-76.
372-83. 17. Santhanam I, Padma V, Murali T, et al. Predictors of mor-
8. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- tality of children presenting with severe sepsis to the PED.
spective randomized controlled study of two fluid regimens Proceedings of the 1st European Congress of Pediatric Re-
in the initial management of septic shock in the emergency suscitation and Emergency Medicine (PREM), May 2nd,
department. Pediatr Emerg Care. 2008;24:647-655. 3rd 2013:Ghent, Belgium.
11
IP : 196.52.84.10

Intraosseous Access

Figure 11.1: Intraosseous access is a life-saving procedure in shock when peripheral IV access is difficult.

Learning Objectives
1. How to organize an intraosseous tray? 3. Pearls and pitfalls in IO access.
2. How to secure an IO access? 4. Evidence supporting intraosseous access in
emergency settings.

Introduction ●● Betadine, sterile gloves, masks, surgical gowns.


●● Small stainless steel cups.
American Heart Association’s resuscitation guidelines
●● Draping site of insertion.
state that the intraosseous (IO) route should be the first al-
ternative to difficult or delayed intravenous access.1 This ●● Bone marrow needle (16G, 18G): Easily available
chapter will discuss the preparation of an intraosseous and inexpensive, this needle can be safely used to se-
access tray and the method of performing this procedure cure IO access.
(Figure 11.1). ●● 10 or 20 mL syringes: Ensure that both syringes are
When used in severely shocked kids, IO access is faster filled with NS or RL prior to insertion. Avoid, waiting
and more easily obtained than other access. Complications to fill the syringe after entry. Delay can cause clogging
are not more than other venous access methods. However, of the needle.
IO access is still under utilized because of lack of aware- ●● Dynaplast: To fix the IO needle.
ness, proper training and lack of appropriate equipment.2 ●● IV infusion set.
The last statement appears to be true in the Indian context ●● Normal saline or Ringer’s lactate bottles.
as well. ●● 3-way stopcock.
●● Medications.
Preparation of an Intraosseous Tray ●● Infusion pumps.
(Figure 11.2)
●● Sand bag: Used for positioning the limb.
Ù
Use universal aseptic precautions.
●● Gauze.
Chapter 11 n Intraosseous Access 115

How To Secure Intraosseous Access?


Figure 11.3 shows the intraosseous access in a secured
IP : 196.52.84.10 way.
●● Place a sand bag under the knee (refer Figure 11.4).
●● Slightly abduct and rotate the knee externally.
●● Clean the site of insertion with Betadine-soaked
gauze.
●● Identify the tibial tubercle.
●● Then introduce the bone marrow needle with trocar 1
cm below and medial to this anatomic landmark.

Figure 11.2: Organization of the intraosseous tray. 1. Towel


roll for support; 2. Stainless steel tray; 3. Tincture Benzoin; 4.
Bone marrow needle (16G, 18G) with trocar; 5. Betadine; 6. 2 cups
with gauze; 7. Dynaplast (cut to fix the needle); 8. 3-way adapter;
9. Disposable sterile gloves; 10. Saline bottle; 11. 10 mL syringes;
12. Drape; 13. Infusion set. Both items 1 and 2 must be
autoclaved and ready for use.

Figure 11.4: Positioning and method of insertion of IO needle

●● The patented intraosseous needle is expensive and not


widely available in India.
●● The bone marrow needle on the other hand, is an easily
available alternative.
●● Unfortunately, it is not sturdy enough for use in older
children.
●● Currently, intraosseous guns are available.
– This device has been used in adults and can effort-
lessly and painlessly penetrate hard bone and enter
the marrow space.
●● Ideally, the intraosseous route should NOT be used be-
Figure 11.3: Intraosseous (IO) access is a rapid, safe and yond 24 hours.
effective route for administration of fluids, epinephrine, ●● It is retained until an intravenous access has been se-
anticonvulsants, blood products and inotropes. Onset of action cured.
and drug levels reached in the circulation were comparable ●● Other locations for introduction of IO needle:
to venous administration. Administration of a drug should – Proximal tibia in infants.
be followed by a 5 mL saline flush to promote entry into the – Proximal tibia and distal femur in adolescents.
central circulation.
– Iliac crest and distal tibia (when conventional sites
are unavailable).
Note that in this picture, the airway has been positioned
●● Technique used in infants is described below:
and bag-valve-mask ventilation is in progress even prior
to securing IO access. Oxygen saturation has normalized. The thumb of the left hand is used to fix the tibial tuber-
Tachycardia is due to shock. osity to guide insertion of the bone marrow needle.
116 Section V n Circulation

Method of Insertion After Insertion


(Figures 11.5A and B) (Figures 11.6A and B)
IP : 196.52.84.10

Figures 11.5A and B: The left hand is used to palpate the tibial Figures 11.6A and B: Introduce the BM needle until a ‘give’ is
tubercle and guide insertion of the bone marrow needle 1 cm felt. The needle will stand proud. The trocar is removed. Prior
below and medial to it. to insertion of bone marrow needle, prefilled syringes should
be available. Waiting to fill the syringe after entry will delay
●● Use screwing movements to introduce the bone mar- infusion and result in clogging of the needle with marrow.
row needle into the tibia. Connect the syringe to the bone marrow needle and manually
push fluid.
●● Enter the tibia perpendicular to its shaft. Continue to
fix the knee with the left hand.
●● Avoid using the same site during second time.
●● Point away from the growth cartilage
●● Introduce the BM needle until a ‘give’ is felt. The nee-
●● Other sites of insertion are lower end of tibia at the
dle will stand proud.
malleolus, lower end of femur and ischiorectal spine. ●● Remove the trocar and connect the fluid filled syringe.
●● Avoid IO access, if the bone above the site of insertion Prior to insertion of bone marrow needle, prefilled sy-
is fractured, infected or the child has osteogenesis im- ringes should be available. Waiting to fill the syringe
perfecta. The commonest contraindication is however after entry, will delay infusion and result in clogging of
failed IO access. the needle with marrow.
●● If intraosseous access had been unsuccessful in one ●● Connect the syringe to the bone marrow needle and
limb, make an attempt on the other limb. manually push fluid.
Chapter 11 n Intraosseous Access 117

Pushing Fluids via IO Route ●● Ceftriaxone, chloramphenicol, phenytoin, tobramycin


(Figure 11.7) and vancomycin may result in lower peak serum con-
IP : 196.52.84.10 centrations.
●● Fix the needle with the other hand. ●● The most common adverse effect seen with IO use, ex-
Often, displacement can occur as the syringe is travasation2, compartment syndrome, osteomyelitis and
withdrawn. A great deal of effort is needed to push the tibial fracture. These are rare, but have been reported.3
fluid into the marrow space.
●● Apply tincture benzoin around the site of entry of the
IO needle. Encircle the needle with gauze and fix with
dynaplast.

Figure 11.9: IO access may be removed once a peripheral


venous access is obtained. In the management of severe shock
IO is retained even if a peripheral IV line is obtained later.
While, the peripheral IV access is useful for administration of
fluid boluses, anesthetic medications, dextrose, etc. during
Figure 11.7: During bolus therapy, dislodgement can occur resuscitation, the IO line may be used exclusively for inotrope
resulting in extravasation. To avoid this complication, fix the infusion.
needle with gauze and dynaplast.
Airway Manager
●● Throughout the procedure, ensure that the airway is
opened as shown in the picture and oxygen should be
provided (refer Figure 11.9).
●● The bag-valve-mask must be available close at hand.
●● Failure to obtain IV access and need for IO access sug-
gests that the child is in severe shock. Hence, fluid re-
suscitation can precipitate features of pulmonary ede-
ma in the failing heart.
●● The airway manager must watch out for signs of pul-
monary edema such as froth, signs of respiratory dis-
tress or respiratory failure.
Figure 11.8: A second peripheral IV line is obtained after the ●● Consider the need for intubation and call for an airway
first bolus through the IO line tray.
●● Repeat the rapid cardiopulmonary cerebral assessment
●● Use an infusion pump to continue fluids or infusions. after every fluid bolus.
Fluids will not run freely from the intravenous bottle. ●● Depute one team member to keep track of the number
●● Attempt to secure IV access after pushing 20–40 mL/kg of fluid boluses.
of fluids. Usually, a second peripheral IV line is obtained ●● When disconnecting the syringe from the IO needle, care
after first bolus through the IO line (Figure 11.8). must be taken to avoid dislodgement of the needle.
●● All resuscitation drugs can reach therapeutic levels in ●● Look carefully for signs of extravasation.
blood. Figure 11.10 shows recovered child after resuscitation.
118 Section V n Circulation

common errors
û
1. Using the blood set needle (which does not have a
IP : 196.52.84.10
trocar).
2. Preferring to obtain access using ‘cut down’
technique.
3. Failing to fix during bolus therapy resulting in
slippage of the IO needle.
4. Not using screwing movements to enter the marrow
space.
5. Connecting the IV bottle directly to the IO needle
and expecting it to run as in IV access.
Figure 11.10: Intraosseous access is a life-saving intervention. 6. Not fixing the IO needle effectively after entering
This infant with hydronephrosis and urosepsis presented to the marrow space.
the ED with hypotensive shock. He required 120 mL/kg fluid
in the initial hours of resuscitation to resolve shock. In this REFERENCEs
picture, he is responding to the mother after correction of
shock (therapeutic goal). 1. R Fowler, JV Gallagher, SM Isaacs, et al. The Role of In-
traosseous Vascular Access in the Out-of-Hospital Environ-
Key Points
ü ment (Resource Document to NAEMSP Position Statement)
2007, (11) 1 , 63-66 (doi:1. 1080/10903120601021036).
1. Prefer to use IO access. Avoid damaging veins, if IV 2. ML Buck, BS Wiggins, JM Sesler. Intra-osseous drug ad-
access is not easily available. ministration in children and adults during cardiopulmonary
2. Follow all drugs with 5–10 mL of NS flush. resuscitation. Ann Pharmacother. 2007 Oct;41(10):1679-86.
3. Early use of IO access prevents damage to the veins. 3. Voigt J, Waltzman M, Lottenberg L. Intraosseous vas-
After bolusing 20–40 mL/kg, IV access is easier. cular access for in-hospital emergency use: a system-
atic clinical review of the literature and analysis. Pe-
4. Ideally, if 2 separate secure IV access had been
diatr Emerg Care. 2012 Feb;28(2):185-99. doi: 10.1097/
obtained, the IO needle should be removed. PEC.0b013e3182449edc.
12
IP : 196.52.84.10

Vasoactive Drugs in the ED

Figure 12.1: Vasoactive medications: The magic drugs to restore hemodynamics

Learning Objectives
1. Case scenarios illustrating the choice of inotropes. 3. Evidence-based approach for the use of vasoactive
2. Pharmacology of the vasoactive medications. medications in ED settings.

INTRODUCTION
This chapter will discuss an overview of inotropes and cat-
echolamines in ED settings1 (Figure 12.1).

CASE SCENARIO 1
A febrile 32-day-old infant presented with history of
breathlessness and not behaving ‘as usual’. He had an
abscess in his arm (Figures 12.2 to 12.4).
The rapid cardiopulmonary cerebral assessment re-
veals. RR: 70/minute, minimal retractions, HR: 200/min-
ute, warm, pink peripheries, well felt peripheral pulses,
rapid CRT and normal liver span. His suck and moro are Figure 12.2: Triaged as respiratory distress and shock due to
sluggish, eyes are mid-position, DEM is normal. His tem- severe sepsis, he receives O2 through the oxyhood and 35 mL
perature is 38.5ºC and his capillary blood glucose is 72 of NS (10 mL/kg) as the initial fluid bolus for shock (Note the
mg/dL. He had a large abscess over his left shoulder. huge abscess over the left arm). Reassessment is as follows:
120 Section V n Circulation

These effects mentioned above are dose-dependent.


Hemodynamic response to dopamine varies from patient-
IP : 196.52.84.10 to-patient.2–4 While dopamine is the commonest initial
drug of choice, age-specific insensitivity to dopamine is a
concern in infants less than 6 months.5,6

Figure 12.3 Physiological status: Respiratory failure, wide


pulse pressure (warm cardiogenic) shock.

You are planning to intubate. Which vasoactive medica-


tion would be appropriate?
Figure 12.4: This picture shows the same baby being fluid
resuscitated after intubation. Dopamine and norepinephrine
Dopamine infusion are on flow and abscess has been drained.
Dopamine hydrochloride is an endogenous catecholamine
and a chemical precursor of norepinephrine (NE). It has ●● Dopamine is initiated and maintained at the rate of 10
both α- and β-receptor stimulating actions. In addition, μg/kg/minute. Increasing rates of infusion will increase
it also has receptors unique to this group of drugs (DA1, risk of tachyarrhythmias, peripheral vasoconstriction
DA2, i.e. dopaminergic receptors). and ischemia.7
●● Frequent monitoring of the cardio­pulmonary response
●● At low infusion rates (5 µg/kg/min), activation of the to dopamine infusion is advisable.
DA1, DA2 receptors cause relaxation of vascular tone ●● The onset of action is within 2 minutes, peak 10 minutes
and increase blood flow to the renal, splanchnic, cere- and its effects wane within 10 minutes of stopping the
bral and coronary vascular beds. infusion. Tapering or stopping dopamine prematurely
●● At higher infusion rates (10–15 µg/kg/min), Dopamine viz as soon as the child’s cardiopulmonary parameters
stimulates the heart, directly through β-adrenergic re- have stabi­lized is a common error in the postresuscita-
ceptors and indirectly through release of stored NE tive period.
from the nerve endings.
●● At higher rates (> 15 µg/kg/min), dop­amine infusion, Clinical Role
causes vasoconstriction through two pathways. Direct
stimulation of α-receptors and indi­rect stimulation Ù
Prior to initiating dopamine, volume repletion is
through release of stored NE from the nerve endings.
mandatory and cardiac rhythm should be normal.
In shock secondary to myocardial dysfunction, dop-
In chronic congestive heart failure, depletion of stored
amine improves myocardial contractility. Improved con-
NE occurs, resulting in resistance to the effects of
tractility, causes reduc­tion in both preload and afterload.
dopamine.7
These factors, further increase cardiac output. Coronary
perfusion pressure also improves (increasing oxygen sup-
ply). In addition, the re­duction in heart rate, enhances Indications
diastolic coronary perfu­sion. The increase in oxygen con- ●● Cardiogenic shock secondary to scorpion sting, status
sumption is countered by the improvement in coronary epilepticus, heart disease, perinatal depression, hyaline
blood flow. The net effect on oxygen delivery is beneficial. membrane disease.8
Chapter 12 n Vasoactive Drugs in the ED 121

●● Cardiogenic shock with vasodilation (warm septic Preparation and Administration


shock), characterized by elevated cardiac output, low
systemic vascular resistance and normotension.8 Ideally dopamine should be administered through a cen-
IP : 196.52.84.10 tral line. However in the ED, it can be initiated through a
secure peripheral IV line or intraosseous route18,19 using an
Not Useful
infu­sion pump. Mixing with sodium bicarbonate solutions
●● Hypotensive shock of any etiology where epinephrine is avoided.
is more appropriate.
●● Primary myocardial disease presenting with hypoten- CASE SCENARIO 2
sive cardiogenic shock. Dopamine is not preferred,
since it aggravates tachyarrhythmias and increases A 6-week-old baby, being evaluated for congenital
myocardial oxygen consumption thereby worsening of heart disease, has had worsening of breathlessness. He
cardiac dysfunction. Dobutamine is the preferred drug has not been able to take his usual feeds at breast since
the morning (Figure 12.5).
in this scenario.

Adverse Effects
●● Tachycardia, dysrhythmias and hypertension could
occur as a result of dopamine infusion. Tachycardia,
increases oxygen consumption and shortens diastole
(reducing coronary perfusion during diastole). The
deleterious effects of dopamine on myocardial oxygen
consumption is less than epinephrine, but greater than
Dobutamine, Amrinone and Milrinone.9
●● Dobutamine has also been shown to depress minute
ventilation10,11 in response to hypoxia and hypercarbia
by as much as 60%. Within the lung, it increases blood
flow to the hypoventilated areas worsening hypoxia. Figure 12.5 Physiological status: Cardiogenic shock due to
CHD.
●● Low dose of dopamine does not improve glomerular
filtration rate and is not protective to the kidney.12,13
Oxygen is provided through JR circuit and 5 mL/kg of
●● It increases splanchnic oxygen consumption15, adverse-
NS is administered over 20 minutes. Reas­sessment after
ly affects gastrointestinal motility14,15 with varying ef- the bolus shows that BP had improved to 90/60 mm Hg,
fects on the splanchnic circulation16-18. but the liver span had increased to 8 cm.
Ù The intubation tray is being prepared. What inotrope
Extravasation of dopamine can cause limb ischemia infusion would you order?
resulting in gangrene of limbs and extensive skin
necrosis. Infusion rates as low as 1.5 µg/kg/minute have
been known to be associated with limb loss! Dobutamine21-23
A selective beta-1 adrenergic agent, Dobutamine increases
●● To prevent this dreaded complication, tight strapping heart rate by stimulating the SA node. It also increases auto-
the entire limb must be avoided. maticity, conduction velocity and myocardial contractility.
●● The IV line should be checked for free flow. Tachycardia and vasodilation also occurs due to its action on
●● Flushing the inotrope line must be avoided. the Beta-2 receptors. Due to its alpha-adrenergic blocking
●● Extravasation, should be treated with local infiltration activity it can cause cause severe vasodilation (especially in
with a solution of phentolamine (5 mg in 15 mL of nor- septic shock) and precipitate hypotension. In addition dobu-
mal sa­line) using a fine hypodermic needle. tamine also causes pulmonary vasodilation.
122 Section V n Circulation

Clinical Role
●● Normotensive cardiogenic shock due to primary myo-
IP :as196.52.84.10
cardial pathology such myocarditis, rheumatic, con-
genital heart disease, Kawasaki’s disease, etc.
●● Fluid refractory septic shock when the blood pressure
is normal or high.
●● Cardiogenic shock due to severe hypoxia-ischemia of
any etilogy.

Administration
Therapy is started at the rate of 5–10 µg/kg/minute and
titrated based on clinical response of the child. Mixing
Figure 12.6: He is bag ventilated and cardiac compressions
with sodium bicarbonate solutions should be avoided. The are initiated. Epinephrine 1.2 mL of 1:10,000 dilution is
onset of action, duration, peak action and precautions tak- administered through the intravenous catheter, which had
en for infusion are similar to dopamine. been placed for administration of contrast.
Repeat cardiopulmonary assessment after CPR as
Adverse Effects shown in Figure 12.6.
●● Dobutamine increases myocardial oxygen demand.
However, improved cardiac contractility in children
with cardiac dysfunction results in enhanced oxygen
supply to the heart.
●● Hypotension, hypertension, tachyarrhythmias, VPCs,
angina.
Ù
An increase in heart rate without improvement in shock
should prompt a reduction in the rate of infusion.

CASE SCENARIO 3
A 2-year-old child was being given contrast intrave- Figure 12.7: Cardiac compressions are stopped. 240 mL
nously in the radiology department to evaluate a void- saline is being pushed with a 3-way stopcock.
ing cystourethrogram. He vomits, postures and be-
comes unresponsive. As he was being rushed into the Reassessment
PED, he developed swelling around the eyes, lips and Physiological status: Assisted ventilation, relative brady-
face. Generalized rashes were also noted. cardia with hypotensive shock (Figure 12.7).
On arrival into the PED, his airway is opened using Cardiac compressions were stopped. 240 mL saline is
the head tilt-chin lift maneuver. The airway nurse suctions being pushed with a 3-way stopcock. Which vasoactive
oropharyngeal secretions, inserts a nasogastric tube (10F) medication would you start after CPR when heart rate has
and decompresses stomach by connecting the NGT to a been established?
suction apparatus. Simultaneously, the airway manager
recognizes that the child is not breathing and initiates bag-
valve-mask ventilation. The team member who is assess- Epinephrine
ing HR, starts initiating chest compression. A 3rd team A stress hormone, epinephrine has affinity for β-1, 2 and
continues assessment... α-receptors (present in both cardiac and vascular smooth
muscle). β-adrenergic effects are more pronounced at lower
Chapter 12 n Vasoactive Drugs in the ED 123

doses, whilst, α-1 adrenergic effects manifest at higher ●● If hypotension persists despite epinephrine bolus in-
dos­es.24 jections and fluid administration, initiate epinephrine
infusion at the rate of 0.1–1 µg/kg/minute.
Beta-1 adrenergic receptor stimulation increases heart
IP : 196.52.84.10
rate, myocardial contractility, automaticity and conduction
velocity. Administration
Beta-2 adrenergic receptors stimulation occurs at lower It can be safely administered through an intraosseous or
doses resulting in effects similar to β-1 activity. The other peripheral intravenous route using an infusion pump.
effects of β-2 activity are bronchodilation and dilation of
the arterioles by decreasing the diastolic BP. SVR decreas- Adverse Effects
es and diastolic pressure falls. There is a slight increase ●● Tachyarrhythmias, such as atrial and ventricular extra-
in heart rate, cardiac output and systolic BP. The force of systoles, tachycardias and fibrillation.
contraction also increases. However, the myocardial oxy- ●● Hypertension and ischemic changes in the ECG are
gen consumption is disproportionate to the improvement other dangerous side effects of this drug.
in myocardial contractility.
Prolonged infusions of high doses can be cardiotoxic Metabolic Effects
and lead to apoptosis.
●● Hypokalemia occurs due to β-2 adrenergic receptor
Epinephrine has been shown to reduce splanch­nic stimulation.
blood flow, increase carbon dioxide production in the gas- ●● Hyperglycemia results from α-adrenergic mediated
tric mucosa and lactate production in the regional and sys- suppression of insulin release.
temic circulation.25,26 ●● Infiltration into skin and tissues can produce severe va-
sospasm and tissue injury.
Clinical Role
CASE SCENARIO 4
●● Anaphylactic shock.
An 8-month-old is being treated for septic shock in the
●● Hypotensive shock of any etiology. ED. She had received 100 mL/kg isotonic saline and
●● Fluid unresponsive, dopamine refractory, hypotensive had been intubated. Dopamine had been initiated when
septic shock.27,28,29 her shock was refractory to 60 mL/kg.
●● Drug of choice in CPR and postcardiac arrest shock.
Her assessment was as follows (Figures 12.8, 12.9 and
Dose 12.11).
Anaphylaxis: DEEP IM (avoid subcutaneous route,
since it may delay absorption): 0.01 mg/kg (0.1 mL/kg of
1:10,000) every 15 minutes PRN (maximum dose 0.3 mg).
IV/IO route: 0.01 mg/kg (0.1 mL/kg of 1:10,000) every
3–5 minutes up to a maximum dose 1 mg, if hypotension
is noted. Each bolus of epinephrine must be followed by a
saline flush (5 mL of NS), if the drug is administered via
the IO route.
Cardiac arrest: 0.01 mg/kg (0.1 mL/kg of 1:10,000) via
the IO/IV route every 3–5 minutes for a maximum of 1
mg. If heart rate is established, but hypotensive shock is
noted initiate epinephrine infusion at the rate of 0.1–1 µg/
kg/minute via a secure peripheral or IO line. Figure 12.8: Note the flushed, bright pink palms and soles of
this infant who has received 100 mL/kg fluids and dopamine.
●● If IV/IO access is not immediately available, 10 times These findings should not be misconstrued as normalization
the calculated dose for weight may be adminis­tered of shock. Check her BP with special emphasis on the point of
into the endotracheal tube. disappearance of the Korotkoff sounds (for diastolic BP).
124 Section V n Circulation

kaline solutions. Watch closely for extravasation. The


drug effects will cease within 10 minutes of discontinu-
IP : 196.52.84.10 ation of infusion.

CASE SCENARIO 5
A 9-month-old infant presenting with acute cardiogenic
shock and a possible diagnosis of myocarditis has been
fluid resuscitated, intubated and is having dobutamine
administered at the rate of 10 µg/kg/min. The current car-
diopulmonary status shows the following (Figure 12.10)

Figure 12.9 Physiological status: Fluid unresponsive,


dopamine refractory hypotensive va­sodilatory shock with low
mean arterial pressure of 40 mm Hg.

Which vasoactive medication should be initiated now?

Norepinephrine32-37
This endogenous catecholamine is a potent alpha-1 adren­
ergic receptor agonist with some β agonist activity. Pre-
dominantly a vasoconstrictor, it increases systolic, dia- Figure 12.10 Physiological status: Refractory cardiogenic
stolic and pulse pressures with minimal effects on cardiac shock with high BP.
out­put and heart rate. This latter effect makes it a useful
cat­echolamine in children with tachycardia. Improvement What would be the appropriate drug in this setting?
in cardiac output has been attributed to better coronary per-
fusion pressures. Several studies have demonstrated that Bipyridines
norepinephrine normalized hemodynamic parameters, re-
These agents increase the levels of cAMP by inhibiting its
established urine output, decreased serum creatinine and
breakdown in the cardiac myocyte and vascular smooth
increased creatinine clearance in high output, low systemic
muscle.39 These properties result in increased myocardial
vascular resistance septic shock.
contractility and vasodilatation. In addition, it also im-
proves diastolic relaxation (lusitropy), thus reducing pre-
Clinical Role load, after load and systemic vascular resistance. PDI have
long half-lives ranging from 0.5 hour i.e Milrinone and 4
●● Hypotensive warm shock not responding to intravas- hours viz Amrinone. Unlike catecholamines, PDI are rec­
cular volume repletion and dopamine infusion. In this ommended for cold shock with normal or high MAP40,41
scenario, NE infusion increases SVR, BP and urine a clinical scenario often encountered in catecholamine re-
output without significantly elevating the heart rate.16 fractory low cardiac output and high vascular resistance
●● Other indications for NE are vasodilator ingestion and states and after initiation of epinephrine, where blood pres-
CNS de­pressant intoxication where shock is character- sure is increased, but the other therapeutic goals of shock
ized by low SVR and hypotension. are not achieved.
●● Adverse effects are similar to other vasoactive medica- The main concerns of the PDI are related to their pro-
tions. However, bradycardia is an unusual complica- pensity to cause hypotension in volume depleted patients,
tion of norepinephrine infusion. accumulation in renal failure and occurrence of thrombo-
●● Dose: 0.1–2 µg/kg/minute (titrate based on repeated cytopenia with prolonged infusions.
cardiopulmonary assessment. Avoid mixing with al-
Chapter 12 n Vasoactive Drugs in the ED 125

Clinical Role
●● Catecholamine resistant cold septic shock with normal
Ù
Placement of an arterial catheter for intra-arterial
IP : 196.52.84.10
or increased blood pressure. pressure monitoring is mandatory during administration
●● Catecholamine resistant shock complicated by severe of this drug. Since invasive monitoring is fraught with
tachyarrhythmias. complications in shocky children, its use in the ED is
limited.
Adverse Effects Vasopressin
Amrinone can aggravate myocardial ischemia and cause Vasopressin is released in response to increased plasma os-
supraventricular and ventricular ectopy. Rapid infusions molality, hypoxia or shock. It acts on the V1 receptor in the
of amrinone and milrinone during loading may produce vascular smooth muscle to produce vasoconstriction and
hypotension, which is aggravated by volume depletion. the V2 receptors, which mediate water reabsorption in the
Amrinone also produces reversible dose-dependent throm- renal collecting ducts. A few case studies have shown its
bocytopenia. usefulness in norepinephrine unresponsive warm shock.41
However, data is limited in the use of vasopressin in chil-
Administration dren42 and there is little evidence to support its use as res-
cue therapy in catecholamine resistant shock.43 Besides,
Amrinone and milrinone are formulated in a manner simi- children with septic shock have been shown to have high
lar to dopamine and dobutamine. Amrinone is not compat- levels of vasopressin.44,45
ible with dextrose containing solutions unlike milrinone,
which is compatible with dextrose containing solutions. Indications
●● Amrinone is administered as a loading dose of 1–2 mg/ ●● Hypotensive, warm septic shock refractory to fluid,
kg over 30–60 minutes. The infusion ranges from 5–10 Dopamine and norepinephrine infusion.
µg/kg/minute. Caution should be taken to correct in-
travascular volume depletion, since this group of drugs
can cause profound hypotension. Dose adjust­ment
Key Points
ü
needs to be made in children with renal failure. 1. Initiate the appropriate inotrope when signs of
pulmonary edema are noted or when shock is
refractory to fluids.
2. Choose the appropriate inotrope based on blood
pressure.
3. Epinephrine is the only agent, which can be initiated
simultaneously with fluids even before establishing
euvolemia in hypotensive shock.

common errors
û
1. Stepping up the dopamine infusion from 10 µg/kg/
min to 20 µg/kg/min in refractory shock.
2. Combining dopamine and dobutamine in the same
syringe.
Figure 12.11: Neurologically intact survival of a child with 3. Initiating inotropic agents prior to correction of
septic shock. Timing and use of the ‘best’ vasoactive medication hypovolemia.
is crucial for successful outcomes (Same child as managed in
4. Failing to initiate an appropriate inotrope.
Figure 12.8).
126 Section V n Circulation

Table 12.1: Preparation and infusion rates of commonly used vasoactive agents in the ED

Rate of administration: 10
Name of drug Rule
IPof:6196.52.84.10
(add to 100 mL) Rule of 3 (add to 50 mL) Dose
mL/h
Epinephrine 0.6 × body weight mg 0.3 × body weight mg 1 µg/kg/min 0.1–1.0 µg/kg/min

Norepinephrine 0.6 × body weight mg 0.3 × body weight mg 1 µg/kg/min 0.1–1.0 µg/kg/min
Dopamine 6 × body weight mg 3 × body weight mg 10 µg/kg/min 5–10 µg/kg/min
Dobutamine 6 × body weight mg 3 × body weight mg 10 µg/kg/min 5–10 µg/kg/min

Table 12.2: Indications for initiating inotropes, vasopressors and inodilators

Drug Indication Adverse CVS† effects Dose


Dopamine Shock with normal BP and low SVR* SVT ‡,VPC§, VT, 10 µg/kg/min
Cardiogenic shock Hypertension
Distributive shock
Epinephrine Severe bradycardia with shock SVT,VPC, VT, 0.05–1.0 µg/kg/min
ST elevation,
postresuscitation
myocardial dysfunction
Pulseless electrical activity
Postcardiopulmonary arrest stabilization,
toxic doses of calcium channel antagonists,
β-blocking drugs
Hypotensive shock of all etiologies Hypertension
Anaphylactic shock 1–4 µg/kg/min
Dobutamine Cardiogenic shock with high SVR, cardiac 5–20 µg/kg/min
failure
Norepinephrine Low BP with low SVR Tachy, brady 0.05–1.0 µg/kg/min
arrhythmias,
hypertension
Milrinone Cardiogenic shock with high SVR Hypotension 50–75 µg/kg over 10–60 minute
followed by infusion 0.5–0.75
µg/kg/min
*
SVR, systemic vascular resistance; †CVS, cardiovascular; ‡ SVT, supraventricular tachycardia; §VPC, ventricular premature contractions.

References 4. Zaritsky A, Lotze A, Stull R, et al. Steady state dopamine


clearance in critically ill infants and children. Crit Care
1. Overgaard CB, Davik V. Ionotropes and Vasopessors. Re- Med. 1988;16:217-90.
view of physiology and clinical use in cardiovascular dis- 5. Padbury JF, Agata Y, Baylen BG, et al. Dopamine phar-
ease. Circulation. 2008;118:1047-56. macokinetics in critically ill newborn infants. J Pediatr.
2. Allen E, et al. Alterations in dopamine clearance and cate- 1987;110:293-98.
chol O- methyl- transferase activity by dopamine infusions 6. Padbury JF, Agata Y, Baylen BG, et al. Pharmacokinetics of
in children. Crit Care Med. 1997;25. dopamine in critically ill newborn infant. J Pediatric.1990;
3. Notterman DA, et al. Dopamine clearance in critically ill 117:472-76.
infants and children effects of age and organ system dys- 7. Ralston M, Hazinski MF, Zaritsky AL, et al. Textbook of
function. Clin Pharmacol Ther. 1990;48:138. Pediatric Advanced Life Support, American Heart Associa-
tion. 2007.
Chapter 12 n Vasoactive Drugs in the ED 127

8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving 21. Sharanz D, Stopfkuchen H, Jungst BK, et al. Hemodynam-
Sepsis Campaign: International guidelines for manage- ic effects of Dobutamine in children with cardiac failure.
ment of severe sepsis and septic shock. Crit Care Med. Eur J Pediatr. 1982;139:4-7.
2008;36(1):296-327. IP : 196.52.84.10
22. Majerus TC, et al. Dobutamine: Ten years later, Pharmaco-
9. Regnier B, Safran D, Carlet J, et al. Comparative hemo- therapy. 1989;9:245.
dynamics of dopamine and dobutamine in septic shock. 23. Berg RA, et al. Dobutamine pharmacokinetics and phar-
Intensive Care Med. 1979;5:115-20. macodynamics in normal children and adolescents. J Phar-
10. Jardin F, Gurdjian F, Desfonds P, et al. Effects of dopamine macol Exp Ther. 1993;265:1232.
on intra-pulmonary shunt fraction and oxygen transport in
24. Habib DM, et al. Dobutamine pharmacokinetics and phar-
severe sepsis with circulatory and respiratory failure. Crit
macodynamics in pediatric intensive care patients. Crit
Care Med. 1979;7:273-77.
Care Med. 1992;20:601.
11. Vane de Borne P, Oren R, Somers V. Dopamine depresses
25. Fisher DG, Shwartz PH, Davis AL. Pharmacokinetics of
minute ventilation in patients with heart failure. Circula-
tion. 1998;98:126-31. exogenous epinephrine in critically ill children. Crit Care
Med. 1993;21:111
12. Denton MD, Chertow GM, Brady HR. Renal –dose Do-
pamine for the treatment of acute renal failure: scientific 26. Meier-Hellman A, Reinhart K, Bredle DC. Epinephrine
rationale, experimental studies and clinical trials. Kidney impairs splanchnic perfusion in septic shock. Crit Care
Int. 1996;50:4-14. Med. 1997;25:399-404.
13. Bellomo R, Chapman M, Finfer S, et al. Low dose dop- 27. Levy B, Bollaert FE, Charpentier C, et al. Comparison of
amine in patients with early renal dysfunction: A placebo nor-epinephrine and dobutamine to epinephrine for hemo-
controlled randomized trial. Australian and New Zealand dynamics, lactate metabolism, and gastric tonometric vari-
Intensive Care Society (ANZICS) Clinical trial group. ables in septic shock. Intensive Care Med. 1997;23:282-
Lancet 2000;356:2139-43. 287.
14. Jakob SM, Ruokonen E, Takala J. Effects of dopamine on 28. Bollaert FE, Baeur P, Audibert, et al. Effects of epinephrine
systemic and regional blood flow and metabolism in septic on hemodynamics and oxygen metabolism in dopamine re-
and cardiac surgery patients. Shock. 2002;18:8-13. sistant shock. Chest. 1990;98:949-53.
15. Meier-Hellman A, Bredle DL, et al. The effect of low dose 29. Wilson W, Lipman J, Scribante J, et al. Septic shock: Does
dopamine on splanchnic blood flow and oxygen uptake in adrenaline have a role as a frontline inotropic agent in sep-
patients with septic shock. Intensive Care Med. 1997;23:31- tic shock? Anaesth Intensive Care. 1992;21:70-77.
37. 30. Moran JL, et al. Epinephrine as an inotropic agent in
16. De Backer D, Creteur J, Silva E, et al. Effects of dop- septic shock: a dose profile analysis, Crit Care Med.
amine, norepinephrine and epinephrine on the splanch- 1993;21(1):70.
nic circulation in septic shock: which is best? Crit Care
31. Brown C, et al. A comparison of standard-dose and high
Med.2003;31:1659-667.
dose epinephrine in cardiac arrest outside the hospital. N
17. Ruokonen E, Takala J, Kari A, et al. Regional blood flow
Engl J Med. 1992;327(15):1051.
and oxygen transport in septic shock. Crit Care Med.
1993;21:1296-1303. 32. Dieckman R, Vardis R. High dose epinephrine in pediatric
out of- hospital cardiopulmonary arrest. Pediatrics. 1995;
18. Neviere R, Mathieu D, Chagnon JL, et al. The contrasting
effects of dobutamine and dopamine on gastric mucosal 95:901.
perfusion in septic patients. Am J Respir. Crit Care Med. 33. Desjars P, Pinaud M, Potel G, et al. A re-appraisal of nor-
1996;154:1684-88. epinephrine therapy in human septic shock. Crit Care Med.
19. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- 1987;15:134-37.
spective randomized controlled study of two fluid regimens 34. Desjars P, Pinaud M, Bugnon D, et al. Nor-epinephrine
in the initial management of septic shock in the emergency therapy has no deleterious renal effects in human septic
department. Pediatr Emerg Care. 2008;24:647-55. shock. Crit Care Med 1989;17:426-29.
20. Orlowski JP, Porembka DT, Gallagher JM. Comparison 35. Hesselvik JF, Brodin B. Low dose norepinephrine in pa-
study of intra-osseous, central intravenous and peripheral tients with septic shock and oliguria: Effects of after load,
intravenous infusions of emergency drugs. Am J Dis Child. urine flow and oxygen transport. Crit Care Med. 1989;17:
1990;144:112. 179.
128 Section V n Circulation

36. Martin C, et al. Renal effects of nor-epinephrine used to 41. Choong K, Kissoon N. Vasopressin in pediatric shock and
treat septic shock patients. Crit Care Med. 1990;18:282. cardiac arrest. Ped Crit Med. 2008;9:372-379
37. Martin C, Papazian L, Perrin G, et al. Nor-epinephrine or 42. Mayer S, Gortner L, McGuire W, et al. Vasopressin in
IP : 196.52.84.10
dopamine for the treatment of hyper-dynamic septic shock? catecholamine refractory shock in children. Anesthesia.
Chest. 1993;103:1826-31. 2008;63:228-234.
38. Martin C, et al. Effects of norepinephrine on right ventricu- 43. Leclerc F, Walter-Nicolet E, Leteurtre S, et al. Admission
lar function in septic shock patients. Intensive Care Med. plasma vasopressin levels in children with meningococcal
1994;20:444. septic shock. Intensive Care Med. 2003;29:1339-44.
39. Richard J Beale, Steven M Hollenberg, Jean Louis Vincent, 44. Lodha R, Vivekanandhan S, Sarthi M. Serial circulating
et al. “Vasopressor and inotropic support in septic shock: vasopressin levels in children with septic shock. Pediatr
An evidence based review”. Surviving Sepsis Campaign
Crit Care Med. 2006;7:220-224.
Guidelines. Crit Care Med. 2004;Vol 32: No.11 (Suppl).
45. Vasudevan A, Lodha R, Kabra SK. Vasopressin infusion
40. Barton P, Garcia J, Kouat HA, et al. Hemodynamic effects
in children with catecholamine-resistant septic shock. Acta
of IV milrinone lactate in pediatric patients with septic
shock. Chest. 1996;109:1302-12. Pediatrica. 2005;94:380-83(d).
Approach to Acute Diarrhea
13
IP : 196.52.84.10

and Shock in the ED

Figure 13.1: Severe dehydration responds dramatically to IV fluid therapy (Courtesy: Dr Mullai Baalaaji and Dr Gunda Srinivas)

Learning Objectives
1. Recognition of severity of dehydration and shock 2. How fluids are administered using the pull push
using the modified rapid cardiopulmonary cerebral technique?
assessment and the pediatric assessment triangle. 3. Recognition of coexisting septic shock in a child
presenting with diarrhea and hypovolemic shock.

INTRODUCTION CASE SCENARIO


Acute diarrhea with or without shock is the commonest A 10-year-old girl is rushed into the ED following sev-
emergency encountered in day to day practice (Figure 13.1). eral episodes of diarrhea and vomiting. She is drowsy.
This chapter is predominantly based on the WHO recom-
mendations—20051 for the management of acute diarrhea.
The PEMC approach helps the novice physician to
identify the severity of fluid loss using the rapid cardiopul-
monary cerebral assessment and the pediatric assessment
triangle and match fluid resuscitation.
This approach also emphasizes that altered mental sta-
tus (lethargy), in the background of severe dehydration
may be secondary to hypovolemic shock.
This observation is based on the fact that loss exceed-
ing 25% of effective circulating volume leads to decreased
cerebral perfusion and fall in level of consciousness. Se- Figure 13.2: Note the sunken eyes in this child, who presented
vere dehydration is attributed to loss of 10% circulating with hypovolemic shock. Two intravenous lines have been
volume. However, altered mental status in children with secured. Pull push technique is being used to administer RL
severe dehydration may also result from dyselectrolytemia boluses (Note O2 being given through NRM and BP cuff tied for
or hypoglycemia. BP monitoring) (Courtesy: Dr Gunda Srinivas).
130 Section V n Circulation

IP : 196.52.84.10

Figure 13.4: The 3-way stopcock is turned to close the patient


end and facilitate withdrawal of fluid from the reservoir
Figure 13.3 Physiological status: Airway stable/effortless (Courtesy: Dr Gunda Srinivas).
tachypnea/hypotensive shock/with altered mental status and
severe dehydration.

Management (Figure 13.2 to 13.8)


●● Provide oxygen using the non-rebreathing mask.
●● Secure 2 IV lines and infuse RL 20 mL/kg using push-
pull technique.
●● Until BP normalizes for age.
●● Remember systolic BP less than or equal to 90 mm Hg
should be considered as hypotension in children aged
10 years or more.
●● Check Dextrostix and correct documented hypoglyce­mia.
●● Repeat rapid cardiopulmonary cerebral assessment af- .
ter every fluid bolus. Figure 13.5: The 3-way stopcock is now turned such that fluids
●● Send blood for electrolytes, urea, creatinine. can be pushed into the intravenous line (Courtesy: Dr Gunda
●● Avoid antibiotics, since most diarrheal episodes are Srinivas).
secondary to viral infections.
●● If acute gastroenteritis is due to giardiasis or the child is The pull push method described above is one of the
having dysentery or less than 6 months of age or has sys- fastest methods of administering large volumes of fluids in
temic illness or has proven or sus­picion of shigellosis. the shortest period of time.
Ù
Cholera: Oral Doxycycline
Dedicate one team member to:

Dose: 4–5 years 100 mg stat, ●● Keep track of the number of boluses that are being ad-
2–4 years: 50 mg stat single dose. ministered.
●● Perform the rapid cardiopulmonary cerebral assess-
Shigellosis: Ciprofloxacin
ment after each intervention.
Dose: 1 month to 18 years 20 mg/kg (max 750 mg) twice ●● Document the findings and response to treatment.
daily.
Giardiasis: Oral Metronidazole Ù
Do not stop fluid boluses on the basis of normalization
1–3 years : 500 mg OD for 3 days of BP. All the therapeutic goals should be achieved. If
3–7 years : 600–800 mg OD for 3 days shock persists, plan to continue fluid therapy.
Child 7–10 years : 1 g OD for 3 days Dehydration may persist after shock correction.
10–18 years : 2 g OD for 3 days.
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED 131

CASE SCENARIO CONTINUED ●● Discontinue oxygen therapy.


●● If the patient can drink, begin giving oral rehydration
Following three rapid boluses of 20 mL/kg, her repeat salts (ORS) solution by mouth.
IP : 196.52.84.10
assessment was as follows:
Children > 1 year
●● 30 mL/kg as rapidly as possible (within 30 minutes);
then 70 mL/kg in the next 2 hours.
Children < 1 year
●● 30 mL/kg in the 1st hour; then.
●● 70 mL/kg in the next 5 hours.

CASE SCENARIO CONTINUED


Following RL 100 mL/kg over 6 hours, her repeat assess­
ment revealed.

Figure 13.6 Physiological status: Airway stable/tachypnea/


tachycardia with normotensive shock with severe
dehydration.

Management
●● Continue O2 administration using the non-rebreathing
mask.
●● Infuse RL 20 mL/kg over 20 minutes.

CASE SCENARIO CONTINUED


Following the 4th bolus of 20 mL/kg, her repeat as­ Figure 13.8 Physiological status: Cardiopulmonary cerebral
sessment revealed. status is normal, tachycardia has also resolved. She has features
of ‘some dehydration’.

●● Advice ORS 75 mL/kg for 4 hours and review.


●● ORS ad lib in the older child.
●● When hydration becomes normal: Advice ORS 10 mL/
kg for every loose stool.

CONTRAINDICATIONS
TO ORAL REHYDRATION
●● Signs of shock.
●● Ileus or intestinal obstruction (proven or suspected).
●● Comatose or unconscious.
●● Unable to tolerate oral/NGT rehydration (persistent
vomiting).
Figure 13.7 Physiological status: Airway stable/breathing ●● Often, children presenting with hypovolemic shock
normal/shock has resolved, but she has dehydration as have elevated renal parameters due to prerenal failure.
evidenced by sunken eyes and loss of skin turgor. Persistent Decision to withhold fluids will have disastrous con-
tachycardia is a sign of dehydration, since shock as resolved. sequences.
132 Section V n Circulation

Refer Protocol 13.1.


Ù
common errors
û
1. Failure to recognize shock and treat as severe
Correct shock and re-evaluate renal parameters in
IP : 196.52.84.10
dehydration!
previously normal children.
2. Failure to anticipate that hypovolemic shock may
co­exist with septic shock secondary to GI sepsis.
Key Points
ü
1. Repeat cardiopulmonary cerebral assessment after
3. Initiating dopamine for shock persisting after
adminis­tration of 60 mL/kg of fluids.
every fluid order. Recurrence of diarrheal episodes 4. Using GNS or other glucose containing fluids to
and vomiting can alter the physiological status. cor­rect shock.
2. Attempt to shift the pediatric assessment triangle 5. Withholding fluids in shocked children in view of
from hypotensive shock to the normal triangle. elevated urea and creatinine.
3. Inotropes and intubation are rarely needed in the 6. Failure to correct metabolic abnormalities after
management of uncomplicated hypovolemic shock. resolving shock and dehydration.
4. Evidence of warm shock (wide pulse pressure), 7. Failure to anticipate that failure in improvement in
tachy­cardia and tachypnea fulfilling the SIRS tone and posture after correction of shock could be
criteria, in a dehydrated child should alert the to due to persistent hypokalemia.
the possibility of coexisting GI sepsis. Evidence of
respiratory distress in a shocked child with diarrhea,
but without respiratory symptoms is hallmark of REFERENCE
cardiogenic or non-cardiogenic pulmonary edema 1. “The Treatment Of Diarrhea, A manual for physicians and
in GI sepsis. other senior health workers”: WHO-2005.
Protocol 13.1: PEMC approach: Recognition of the severity of dehydration and presence of septic shock in children
presenting with diarrhea

IP : 196.52.84.10
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED
133
14
IP : 196.52.84.10

Cardiogenic Shock

Figure 14.1: Rapid IV adenosine can reverse certain arrhythmias in seconds (Courtesy: Dr Gunda Srinivas, Dr Bhushan Chavan).

Learning Objectives
1. Using the pediatric assessment triangle to recognize 2. Management of cardiogenic shock in the ED.
cardiogenic shock.

Introduction PATHOPHYSIOLOGY
Cardiogenic shock is a hemodynamic state wherein, prima­ Depressed myocardial contractility causes a reduction in
ry myocardial dysfunction is responsible for the failure of stroke volume and cardiac output leading to tissue hypo-
the cardiovascular system to meet metabolic demands of perfusion. The ensuing metabolic acidosis further impairs
tissues. myocardial function. Other causative factors of myocar­
dial dysfunction are myocardial depressant factor (found
Structural heart disease, arrhythmias or myocarditis are in severe sepsis), myocardial edema, adrenergic receptor
well known causes of cardiogenic shock (Figure 14.1). dysfunction, impaired sarcolemmic calcium flux and re­
duced coronary blood flow.2
Ù Myocardial dysfunction may be systolic or diastolic.
Surprisingly, cardiogenic shock has been more
commonly noted in children presenting with shock due Diastolic dysfunction occurs due to inadequate myocar­
to severe sepsis, scorpion envenomation, established dial relaxation. The latter results in increased end diastolic
status epilepticus, submersion injury, etc. pressure for a given end diastolic volume.3 The increased
Probably, failure to provide appropriate prehospital left ventricular pressure is transmitted to the lungs causing
pulmonary edema.
resuscitation and delay in recognition of early signs of
hypoxia and shock are the other causes contributing to Similarly, systolic dysfunction causes an increase in
cardiogenic shock in our setting.1 end systolic volume for a given pressure leading to a fall
in the stroke volume.
Chapter 14 n Cardiogenic Shock 135

In the failing heart, however, both systolic and dia­stolic


dysfunction, coexist. Consequently, cardiac output falls
and pulmonary congestion occurs. At the cellular level,
IP : 196.52.84.10
lactate levels increases and central venous (superior vena
cava) oxygen saturation (SvcO2) falls. SvcO2 saturations
could fall to less than 20% of the arterial oxygen satura­
tion. Ideally, management is aimed at maintaining SvcO2
above 70%.4
In cardiogenic shock, as in other types of shock, com­
pensatory neurohormonal responses increase systemic
vascular resistance. Activation of adrenergic receptors,
heightened renin-angiotension response, increased stimu­
lation of endothelin are some of the factors that increase
systemic vascular resistance.
As opposed to hypovolemic shock, these compensa­
Figure 14.3: Increase in systemic vascular resistance (a
tory responses have a deleterious effect on the failing heart
physiological response) can be counterproductive in a child with
(Figures 14.2 and 14.3).
myocardial dysfunction resulting in a further fall in cardiac output.
As cardiac output (COP) decreases, systemic vascular Box 14.1: Common causes of cardiogenic shock in children2
resistance (SVR) progressively increases, increasing the
afterload effect on the heart. 1. Heart rate abnormalities
Ù

Supraventricular tachycardia
Ventricular dysrhythmias
The failing heart has to work harder against more
Bradycardia
pressure. 2. Congenital heart disease
3. Cardiomyopathy
4. Myocarditis
5. Hypoxic ischemic events
Cardiac arrest
Prolonged hypoxia and shock due to various etiologies
Anomalous left coronary artery from the pulmonary
artery (ALCAPA)
Kawasaki’s disease
Excessive catecholamine state
Cardiopulmonary bypass
6. Sepsis
Viral
Bacterial
7. Metabolic
Hypoglycemia
Figure 14.2: This picture shows the physiological mechanisms Acidosis
that help to maintain cardiac output when myocardial Hypocalcemia
contractility fails. Hypothermia
Worsening myocardial pump failure, decreasing stroke 8. Mechanical
Cardiac tamponade
volume and increasing afterload leads to a vicious cycle. 9. Others
Whilst, in cardio­genic shock secondary to myocarditis or Burns
structural heart disease, the preload may be adequate or Anaphylaxis
increased. Cardio­genic shock due to sepsis is characterized Envenomations
by massive defi­cits in circulating blood volume. Causes of Toxic reactions (penicillins, anthracyclines)
cardiogenic shock are shown in Box 14.1. Submersion injury
136 Section V n Circulation

case SCENARIO INTERVENTIONS IN THE ED


A previously healthy, 65-day-old baby, is brought with Goals
IP : 196.52.84.10
history of breathlessness for a week. He has had no
1. Minimize myocardial oxygen demand.
fever or cough. He was not responding to his mother. 2. Maximise myocardial performance.
Temperature is 38.5°C. SaO2: 92%, ECG monitor 3. Correct metabolic abnormalities.
shows ST segment depression with ventricular prema-
ture contractions (Figures 14.4 and 14.5). Minimize Myocardial Oxygen Demand
Airway
Provide oxygen using the flow inflating ventilation de­vice.
Continuous positive airway pressure ventilation using a
flow inflating ventilation device improves outcomes in
acute cardiogenic pulmonary edema.
Ù
If signs of PE and hepatomegaly do not resolve with
application of CPAP and inotropes, plan elective
intubation and ventilation.

Elective, early intubation and mechanical ventilation


will decrease the oxygen consumption of the respiratory
Figure 14.4: Froth in the mouth and in the nasogastric tube muscles, thus diverting blood supply to the vital organs.
(Courtesy: Dr Gunda Srinivas).
Mechanical ventilation also improves the FRC thereby
decreasing intrapulmonary shunting and improving oxy­
genation. As hypoxia within the alveoli improves, pul­
monary vascular resistance (PVR) falls. As a result, right
ventricular (RV) performance improves.
Ventilation also decreases the afterload on the failing
heart (remember increased afterload acts as a villain to the
failing heart), thus improving cardiac output.5
Ù
Caution During Intubation
Use sedating and muscle relaxing agents that do not
aggravate shock.

Figure 14.5 Physiological status: Impending respiratory Ketamine is the ideal drug for intubating a child presenting
failure with hypotensive cardiogenic shock and non-convulsive with acute cardiogenic shock in the ED. Avoid ketamine
status epilepticus (secondary to severe hypoxia and shock). in cardiogenic shock due to chron­ic heart failure. Its nega­
tive inotropic effect could precipitate cardiac arrest during
Ù intubation.
Consider early cardiogenic shock whenever a child with
shock presents with respiratory distress or respiratory Ù
Whenever sedative drugs are being considered for
failure. Bradycardia, muffled heart sounds, gallop,
intubating a child with acute cardiogenic shock, an
hepatomegaly and hypotension are late signs of cardiac
inotrope infusion must be initiated prior to intubation.
dysfunction.
Chapter 14 n Cardiogenic Shock 137

Table 14.1: Maintenance of fluid requirements (Holliday and Segar, 1957)

Body weight Volume/amount in 24 hour Volume per hour


< 10 kg
IP : 196.52.84.10
100 mL/kg 4 mL/kg/h
11–20 kg 1,000 mL + 50 mL/kg for each kg >10 kg 40 mL/h + 2 mL/kg/h for each kg >10 kg
> 20 kg 1,500 mL + 20 mL/kg for each kg > 20 kg 60 mL/h + 1 mL/kg/h for each kg > 20 kg
Note: Maximum fluid rate 100 mL/h. Reduce maintenance fluids to two third, if history of structural heart disease, arrhythmias, cardiomyopathies, etc.

Intubation for child with cardiogenic shock without the Maximize Myocardial Performance
aid of inotropes or anesthetic drugs could precipitate car­
diac arrest Refer Table 14.1 for fluid requirement. Optimize Preload
Precautions taken during intubation of a hypoten- Administer 5–10 mL/kg of normal saline (NS) or Ring-
sive child with cardiogenic shock. er’s lactate (RL) up to a maximum of 20 mL/kg in car-
diogenic shock due to non-sepsis etiologies.
●● Order an Epinephrine infusion prior to intubation.
●● Dedicate one team member to initiate chest compres­ Intravascular volume is characteristically normal or in­
sion if heart rate begins to fall. creased in cardiogenic shock due to many etiologies.
●● Initiate chest compressions when there is a significant
fall of heart rate from baseline (e.g. fall from baseline Ù
HR of 170/min–100/min). Do not wait for heart rate to Administer 5–10 mL/kg aliquots up to a maximum of
fall to less than 60/min. 60–120 mL/kg in cardiogenic shock due to sepsis.

Maintain Normal Temperature In cardiogenic shock due to sepsis, intravascular vol­


ume (preload) is sig­nificantly reduced. Large volume flu­
Resuscitate young infants under a warmer. ids are needed to optimize preload and im­prove myocar­
●● Hypothermia increases vasoconstriction and worsens dial dysfunction.
the afterload effect on the heart.
1. Hypovolemia could complicate cardiogenic shock of
●● Use Paracetamol suppository to reduce temperature
all etiologies.
(15 mg/kg every 6 hourly).
2. Check history of vomiting, poor intake, severe diapho­
●● Hyperthermia increases metabolic demand and oxygen
consumption. resis, sepsis and anaphylaxis in all children presenting
with shock.
Sedation Ù
Administer morphine 0.1 mg/kg and midazolam 0.1 Caution: Fluids can be dangerous if child has
mg/kg (slow IV), if the child has been intubated. undiagnosed or untreated structural heart disease. To
avoid fatal errors ask whether history of respiratory
Agitation and restlessness will increase oxygen demand distress is truly acute or ‘acute on chronic’.
and systemic vascular resistance. Both factors could stress
the failing heart. During fluid therapy, if signs of pulmonary edema (intuba­
Ù tion triggers) are noted:
Avoid sedative drugs in restless, agitated children with ●● Stop bolus therapy.
cardiogenic shock who have not been intubated. ●● Initiate inotrope infusion.
●● Perform intubation.
Maintain Hematocrit Diuretics are contraindicated in the presence of shock.
Transfuse 5–10 mL/kg of fresh PRBCs if hemoglobin is
less than 10 g/dL.
Ù
Cautious diuresis may be implemented in the intensive
The oxygen carrying capacity of blood should be opti­ care unit (ICU) after correction of shock.
mized by maintaining the hematocrit at 35%–40%.6
138 Section V n Circulation

Ù Ù
Following intubation, if features of pulmonary edema Ionized calcium level less than 0.9 mmol/L.
IP : 196.52.84.10 Ad­minister calcium gluconate (9 mg elemental calcium
and hepatomegaly resolve, but shock persists, ask three
questions. per mL).
• Is the cardiogenic shock due to sepsis, anaphylaxis Dose: 1 mL/kg (100 mg/kg) diluted 1:1 with normal
or hypovolemia? saline over 10 minutes.
• If yes to any of the three questions, continue Rate of administration: 1 mL/minute, slow IV bolus
smaller al­iqouts, until therapeutic goals of shock under cardiac monitoring.
are achieved. Follow-up with 150–200 mg/kg/24 hour of calcium to
• If pulmonary edema or hepatomegaly worsen, maintain ionized calcium > 0.9 mmol/L.
further fluid therapy is contraindicated even if
shock persists.
Hypokalemia
Afterload Reduction Suspect hypokalemia if large volume gastrointestinal (GI)
Clinically, if cardiogenic shock persists despite establish­ losses complicate cardiogenic shock.
ing euvolemia and inotropes, management should focus on Clinically hypokalemia may be suspected when brady­
reducing after load. cardia is not associated with other features of imminent ar­
Sedation and pain relief (discussed earlier). rest. Other clues include, persistence of hypotonia despite
Improve Myocardial Contractility correction of shock.

1. Correct rhythm disturbances (refer Pediatric Advanced 1 mL of KCl = 2 mEq/mL of potassium


Life Support PALS algorithm). Up to a maximum of 40 mEq/L can be added to the
2. Initiate inotropes (discussed in the Chapter on Vasoac­ maintenance fluid and infused via the peripheral IV line.
tive Medications).
3. Correct metabolic disturbances such as hypoglycemia, Ù
If higher concentrations of KCl need to be infused, central
hypocalcemia, acidosis, hypokalemia.
venous access should be the route of administration.
Correct Metabolic Abnormalities
Maintain Euglycemia Metabolic Acidosis

Correct documented hypoglycemia with 2 mL/kg of Correction of acidosis improves myocardial performance,
25% dextrose. decreases systemic and pulmonary vascular resistance and
decreases the need for increased respiratory effort. A base
Ù
Initiate GNS infusion to which potassium chloride (KCl)
deficit of > 10 mEq in cardiogenic shock is associated with
poor outcome.
has been added at recommended maintenance rates
after establishing urine output. Initiate maintenance ●● After intubation and ventilation, if pH < 7.2 or a base
fluids at two third of calculated volumes, if the etiology deficit of more than 6 mEq administer sodium bicar­
of cardiogenic shock is CHD, RHD, myocarditis or bonate IV bolus at 1–2 mEq/kg body weight (dilute in
cardiomyopathy. equal amount of 5% D and infuse over 30 minutes.
●● Monitor for hypernatremia and hyperosmolality.

Hypocalcemia Drug Therapy


Suspect hypocalcemia if cardiogenic shock is associ­ated Refer to Chapter 12 on Vasoactive Medications.
with rachitic rosary, wide open anterior fontanel (AF), poor
The effects of inotropes vary from patient-to-patient and
dentition, widening of malleolus, Harrison sulcus with or
hour-to-hour.
without history of seizures or stridor.
Chapter 14 n Cardiogenic Shock 139

Monitoring
Ù Perform the rapid cardiopulmonary cerebral assess­
Initiate the following inotropes if signs of pulmonary
edema are noted duringIP fluid
: 196.52.84.10
resuscitation of shock. ment frequently during vasoactive drug therapy.
1. Dobutamine when blood pressure is normal or
high with cool shock. Bedside limited echocardiography by the emergency
2. Epinephrine preferred in cardiogenic shock physician (BLEEP) accurately determines diminished car­
presenting with hypotension, muffling of heart diac function, mechanical compromise of the heart and
sounds, gallop or chronic heart failure due to hypovolemia in the shocked patient7 (Table 14.2). It helps
structural heart disease. to assess systolic and diastolic function, cardiac output, in­
ferior vena cava diameter in relation with respiration8,9 and
Therapy must be continuously tailored to patient’s re­ volume status.
sponse. Inotropes initiated at rates greater than 10 µg/kg/ Table14.2: ECHO findings in shock
minute increases both myocardial oxygen consumption
and systemic vascular resistance. End-systolic End-diastolic Fractional Shock
volume volume shortening
When cardiogenic shock does not respond to inotropes, or ejection
afterload reducing agents will improve myocardial perfor­ fraction
mance. Refer Chapter on Vasoactive Medications. Very low Low High Hypovolemic
shock
●● Vasodilators may be safely used with invasive moni­
High High Low Cardiogenic
toring. Hence, they are not employed in ED settings. shock
●● Combination of vasodilators and inotropes often bring
Very low Normal or High Distributive
about an improvement in hemodynamic status not high shock
achieved by either drug alone.
●● The vasodilators commonly used in cardiogenic shock
are phosphodiesterase (PDE) III inhibitors, sodium ni­
Ù
Plan surgery for surgically correctable lesions.
troprusside and nitroglycerine. These drugs should not
be used as first-line therapy to reverse shock.
Factors that increase SVR such as hypothermia, acido­
sis, hypoxia, pain and anxiety should also be treated simul­
INVESTIGATIONS
taneously. Refer Protocol 14.1. 1. Chest X-ray usually reveals cardiomegaly and pulmo­
nary congestion.
Antibiotics 2. Serum electrolytes, calcium, arterial blood gases (ABG),
If sepsis is suspected administer 3rd generation Cepha- renal function test (RFT), liver function test (LFT).
losporins (Ceftriaxone 100 mg/kg) empirically, after col- 3. ECG helps to recognize dysrhythmias.
lecting blood and body fluids for culture. 4. Complete blood count, sepsis screen and serology for
dengue, rickettsia, leptospirosis, typhoid etc. Body
●● If focus of sepsis is obvious, administer the first dose fluids and urine for culture.
of appropriate antibiotics (e.g. Azithromycin, Doxycy­
5. Evaluate hormonal levels such as TSH, ACTH, PTH if
cline for rickettsia).
deficiency is suspected.
140 Section V n Circulation

Key Points
ü common errors
û
1. High index of suspicion needed to recognize acute
IP : 196.52.84.10 1. Failing to identify acute cardiogenic shock, in
cardiogenic shock following a wide variety of hypoxic shocked chil­dren presenting with respiratory distress
insults. or failure.
2. Check list history of chronic respiratory distress to 2. Not check-listing for coexisting cardiac disease.
identify underlying structural heart disease. 3. Mistaking acute cardiogenic shock for an asthmatic
3. Position airway and provide 100% oxygen using exacerbation and nebulizing with salbutamol.
the flow inflating ventilation device throughout 4. Failure to use afterload reducing agents after
resuscitation of acute cardiogenic shock. stabilizing BP.
4. Rule out history of chronic respiratory distress to 5. Using furosemide in the ED to treat pulmonary
check for underlying structural heart disease. edema in children with cardiogenic shock.
5. Maintain airway and provide highest concentration 6. Withholding fluids in cardiogenic shock due to
of oxygen using the flow inflating ventilation sepsis.
device. 7. Failing to establish euvolemia prior to initiating
6. Perform early intubation using RSI and guarantee dopamine or dobutamine.
ventilatory support. 8. Failing to correct rhythm disturbances.
7. Dobutamine is the inotrope of choice in normotensive 9. Not monitoring and managing serum potassium and
cardiogenic shock. calcium deficits.
Chapter 14 n Cardiogenic Shock 141

Protocol
Protocal 14.1: PEMC approach: Recognition and management of cardiogenic shock
History of respiratory
IPdistress following submersion, perinatal depression, envenomation, severe sepsis, prolonged
: 196.52.84.10
seizures, airway obstruction, toxins, cardiac diseases, etc.
142 Section V n Circulation

References 5. Fuhrman and Zimmerman. Pediatric Critical Care, 3rd


edition. Lincoln Smith, Lynn Hernan Chapter 27; Shock
1. Santhanam I, et al. Implementation of Pediatric Emergency states.
IP : 196.52.84.10
Medicine Course Guidelines (PEMC). Impact on mortal­
ity in critically ill children presenting to a large volume 6. Nelson. Textbook of Pediatrics, 19th edition; Chapter 462
PED of an academic children’s hospital in India. Pediat Red blood cell transfusions and erythropoietin therapy.
Crit Care Med. 2011.(12):3 (Paper presented at the 6th 7. Field LC, Guldan GJ III and Finley AC, et al. Echocardiog­
Pediatric Critical Care Congress March 13th–17th 2011, raphy in the intensive care unit. Semin Cardiothorac Vasc
Sydney. Anesth. 2011;15:25.
2. Califf RM, Bengtson JR. Cardiogenic shock. N Engl J 8. Charron C, Caille V, Jardin F, et al. Echocardiographic
Med. 1994;330:1724-730. measurement of fluid responsiveness. Curr Opin Crit Care.
3. Arques S, Ambrosi P, Gelisse R, et al. Prevalence of angio­ 2006 Jun;12(3):249-54.
graphic coronary artery disease in patients hospitalized for 9. Feissel M, Michard F, Faller JP, et al. The respiratory varia­
acute diastolic heart failure without clinical and electrocar­ tion in inferior vena cava diameter as a guide to fluid ther­
diographic evidence of myocardial ischemia on admission. apy. Intensive Care Med. 2004 Sep;30(9):1834-837. Epub
Am J Cardiol. 2004;94:133-35. 2004 Mar 25.
4. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed
therapy in the treatment of severe sepsis and septic shock.
N Engl J Med. 2001;345:1368-377.
15
IP : 196.52.84.10

Septic Shock

Figure 15.1: Focus of infection must be detected and treated along with hemodynamic interventions for complete recovery

Learning Objectives
1. Recognition of shock, pulmonary edema and 2. Fluid resuscitation of septic shock until clinical
cardiovascular dysfunction and non-convulsive therapeutic goals of shock resolution are attained
status epilepticus in febrile children using the in a time sensitive manner.
pediatric assessment triangle and the rapid 3. Recognition and management of pulmonary edema
cardiopulmonary cerebral assessment. during fluid resuscitation.
4. Modified septic shock protocol for settings with
limited access to mechanical ventilation.

INTRODUCTION PATHoPHYSIOLOGY
In India, fever and infections are the leading cause for vis- Local and systemic inflammatory response occurs when
its to the OPD, whilst, the commonest cause of hospital mi­crobes traverse the epithelial and tissue barriers. This
mortality is serious sepsis (Figure 15.1). response to microbial invasion is known as ‘systemic in-
flammatory response syndrome’ (SIRS).
Fifty percent of deaths due to serious sepsis in develop-
ing countries occurred within the first 24 hours and these Fever (> 38.5ºC) or hypothermia (< 36.5ºC), tachypnea
deaths were a result of shock.1 This chapter describes an (respiratory rates > 2 SD above normal) and tachycardia
ED protocol that made a dramatic impact on hospital mor- (heart rate > 2 SD above normal) are the cardinal clinical
tality in severe sepsis. Developed from the findings of a signs of SIRS. Leukocytosis, leuko­penia and band count
prospective randomized controlled study on fluid resusci- more than 10% are the other features of SIRS.3,4
tation of septic shock, it teaches how to resuscitate shocked Sepsis is diagnosed when SIRS occurs in association
children prone for pulmonary edema.2 with suspected, proven or obvious infection.
It also teaches how the pediatric assessment triangle Severe sepsis is diagnosed, when sepsis is associated with
can be used to recognize severe sepsis. dysfunction of organs distant from the site of infection.5
144 Section V n Circulation

It is interesting to note that microbial invasion from the


site of infection into the blood stream does not cause dys- Ù
function of distant organs. On the contrary, microbes cause Respiratory distress due to ALI is characterized by
IP : 196.52.84.10
organ damage by stimulating the inflammatory cascade, features of severe sepsis and shock.5
leading to excessive release of inflammatory mediators in If triage questions are positive, perform the rapid
susceptible individuals. The latter causes acute lung injury cardiopulmonary cerebral assessment to ascertain
in addition to dysfunction of other organs (MODS).5 whether the child is presenting with SIRS, sepsis, or
Kids presenting with septic shock are very likely to have serious sepsis within the 1st minute of arrival (Figure
features of ALI and MODS. 15.2).
The International Sepsis Definitions Conference de-
fined organ dysfunction based on the laboratory variables The pediatric assessment triangle is used to diagnose
shown in the Table 15.1. In many low and middle income serious sepsis in children presenting with temperature >
countries, laboratory facilities may not be available at the 38°C or < 36°C, suspected, proven or visually seen focus
time of entry into the hospital, thereby delaying recogni- of infection (Figure 15.2).
tion and resuscitation.
This chapter discusses a modified guidelines to recognize
severe sepsis in children presenting with fever and foci.

Ù Triage Questions
Ask the following triage questions to mothers bringing
children to the OPD with fever with or without focus of
infec­tion.
1. History of incessant cry, lethargy, more sleepy than
usual, ‘not as usual’ or posturing? Which help to
detect abrupt changes in mental status.
2. History of breathlessness in children presenting
with altered mental status and perfusion defects?
Which help to recognize pulmonary edema. Foci of Figure 15.2 Physiological status: Respiratory distress or failure
sepsis outside the lung such as diarrhea, urinary with tachycardia, shock with or without myocardial dysfunction,
tract infections, malaria in shocked children are ALOC with or without NCSE.
clues to recognizing acute lung injury or cardiac
dysfunction. The pathophysiology of shock in severe sepsis is mul-
tifactorial.6

Table 15.1: Definitions of SIRS and different degrees of severity of sepsis3,4

Condition Description
SIRS Two or more of the following conditions: temperature > 38.5°C or < 35.0°C; heart rate of > 90 beats/min;
respiratory rate of > 20 breaths/min or PaCO2 of < 32 mm Hg and WBC count of > 12,000 cells/mL, < 4,000 cells/
mL or > 10% immature (band) forms
Sepsis SIRS in response to documented infection (culture or gram stain of blood, sputum, urine, or normally sterile
body fluid positive for pathogenic microorganism or focus of infection identified by visual inspection, e.g.
ruptured bowel with free air or bowel contents found in abdomen at surgery, wound with purulent discharge)
Severe sepsis Sepsis and at least one of the following signs of organ hypoperfusion or organ dysfunction: areas of mottled
skin; capillary refilling of ≥ 3 s; urinary output of < 0.5 mL/kg for at least 1 hour or renal replacement therapy;
lactate > 2 mmol/L; abrupt change in mental status or abnormal EEG findings; platelet count of < 100,000
cells/mL or disseminated intravascular coagulation; acute lung injury/ARDS and cardiac dysfunction
(echocardiography)
Chapter 15 n Septic Shock 145

●● Hypovolemia : Venodilation, capillary leak. Case scenario


●● Cardiogenic : Decreased myocardial contractility.
●● Obstructive : Increased pulmonary vascular resis- A 1 month infant presented with history of fe­ver, ab-
IP : 196.52.84.10 dominal distension and vomiting for 1 day. She had
tance.
●● Distributive : Maldistribution, hypoperfusion. been grunting since morn­ing (Figures 15.3–15.21).
●● Cytotoxic : Cellular inability to utilize oxygen de-
spite adequate supply.
Principles which assist in the management
Septic shock is characterized by decreased systemic vascu­
lar resistance (vasodilation) and increased cardiac index.7
Transient intrinsic depression of left ventricular perfor­
mance is also a feature of severe sepsis (cardiac func-
tion normalizes within 10 days after the onset of septic
shock).7
In addition, several studies have shown clear evidence
of transient intrinsic depression of left ventricular perfor-
mance (cardiac function normalizes within 10 days after Figure 15.3: Note the tense abdominal distension and bilious
the onset of septic shock).8 aspirate in this infant with shock. He is being given boluses for
correction of shock on arrival into the ED, while awaiting surgical
Pulmonary hydrostatic pressure secondary to sepsis-in- opinion.
duced cardiac dysfunction rises, driving the plasma ultra-
filtrate to cross the pulmonary capillary mem­brane into the
interstitium. Simultaneously, permeability changes in the
pulmonary capillary membrane8 lead to non-cardiogenic
pulmonary edema or ALI.8
Large volumes of fluids are needed to resuscitate chil­
dren with septic shock. Elevation in circulating blood vol­
ume and subsequent increase in intravascular pressure can
worsen alveolar fluid collection and deoxygenation.9
Ù
Pulmonary edema (PE) is an inherent complication
of severe sepsis. Therapy to correct shock can also
aggravate PE. Despite the risk of PE, it is important
to fluid resuscitate shock, in order to maximize patient Figure 15.4 Physiological status: Maintainable airway with
outcomes. effortless tachypnea, cardiogenic shock (warm shock), low mean
arterial pressure (MAP: 40 mm Hg) with non-convulsive status
Positive end-expiratory pressure (PEEP), an im­portant epilepticus.
strategy in the management of acute PE, improves oxygen-
ation by increasing mean alveolar pressure, opening col-
Airway and Breathing
lapsed alveoli and reducing repetitive opening and closure
of alveoli during the respiratory cycle. ●● Provide oxygen through the non-rebreathing mask or
hood if the child with shock has effortless tachypnea.
Providing PEEP however, is a challenge in settings
with limited access to mechanical ventilation.2 Restriction ●● Even if the airway appears maintainable on arrival,
of fluids to avoid the risk of PE is lethal.10 Administration watch out for signs of deterioration. Neonates and
of fluids without provision of PEEP can also increase the young infants can quietly slip into apnea as shock is
risk of mortality in resource limited settings.11 being resuscitated.
146 Section V n Circulation

●● Initiate bag-valve-mask ventilation if child presents


with bradypnea.
●● During shock resucitation, consider intubation if the
IP : 196.52.84.10
airway becomes unmaintainable or signs of respiratory
failure, bradycardia, hypotension, unresponsiveness or
signs of non-convulsive or convulsive status epilepti-
cus are noted (Figure 15.6).

Figure 15.5: The airway is being positioned as oxygen is being


provided using the non-rebreathing mask. Note that the bag-
valve-mask device is available at the head end of the infant (for
immediate access) in anticipation of the adverse effects of fluid
administration.

●● Administer oxygen through flow inflating ventilation


device (Jackson-Rees circuit), if the child has respira­
tory distress and shock (Figure 15.5).
Figure 15.7: This infant with cellulitis was presented with
bradypnea and shock. On arrival he was ventilated using bag-
valve-mask device as vascular access was being obtained.

Respiratory distress leads to a 10 fold increase in blood


supply to the diaphragm.12 Diversion of blood supply away
from the muscles of respiration to the vital regions could
be enhanced by paralysis, sedation and mechanical venti-
lation.
●● Intubation should not be delayed till the child is mori-
bund.12
Ù
Despite lack of postresuscitation mechanical ventilatory
facilities, intubation and manual ventilation offers a
Figure 15.6: This child presented with unmaintainable airway, 50% chance of survival to children who need it, while
respiratory failure, tachycardia, shock and unresponsiveness. failure to intubate would mean certain death.2
The airway being positioned and provision of oxygen using the
Jackson-Rees circuit. Note the lines drawn to mark the liver span.
Circulation
Ù
When respiratory distress or failure due to acute
Secure two intravenous lines simultaneously on arrival.
cardiogenic shock is anticipated or being treated, the ●● If IV access is not immediately available, intraosseous
flow-inflating ventilation bag may be a more appropriate (IO) line should be urgently secured.
device to deliver oxygen. ●● Obtaining intravenous access is key to survival.
The Jackson-Rees or pediatric Bain circuit can be used ●● Remember every device you insert will breach the nat-
to tide over acute pulmonary edema during fluid therapy ural body defences your patient has against infection.
in settings without immediate access to mechanical ●● Protect your patient: Use skin prep and aseptic tech-
ventilation. nique.
●● Protect yourself: Adopt universal precautions.
Chapter 15 n Septic Shock 147

IP : 196.52.84.10

Figure 15.8: Throughout fluid resuscitation, ensure that the


airway is positioned and oxygen is provided. The airway manager
Figure 15.9: Pull push technique needs a 3-way stopcock to
must be alert to the possibility of developing respiratory distress
help draw fluids from the reservoir and push into the patient.
or failure secondary to pulmonary edema.
Coordination is needed to close the reservoir line, while pushing
fluids into the patient’s line.
Occasionally, during ongoing resuscitation, with se-
cure IV lines, sudden cardiovascular collapse can occur. ●● Administer small boluses of 5–10 mL/kg cautiously,
The previously functioning IV lines tend to ‘back up’. In with frequent assessments.
these children, urgent intraosseous access during resuscita-
tion is life saving. Ù
Fluids could precipitate or worsen bradycardia in the
failing heart.
Hypotensive shock
●● Assign one responder to initiate chest compressions
Hypotensive shock suggests the presence of significant
during fluid resuscitation, especially when intubation
myocardial dysfunction. It can progress to cardiac ar-
rest within minutes! is in progress (Figure 15.9).
●● Order for epinephrine infusion simultaneously and ini-
The following unique steps are taken during resuscita- tiate at 0.3–1 µg/kg/minute.
tion of hypotensive shock: ●● Ensure that age appropriate bolus doses of epinephrine
●● Assign one physician exclusively for managing the (0.1 mL/kg of 1:10,000) are available close at hand.
airway, even if breathing or oxygen saturations look
normal.
●● He should be prepared to initiate bag-mask ventilation.
Due to the propensity for the child to develop cardiac
arrest, the airway manager should be prepared to initi-
ate bag-mask ventilation.
●● Call for airway tray.
●● If IV access is not available, double the dose of ket-
amine, atropine and succinylcholine can be adminis-
tered through the intramuscular route.
●● Secure intravenous or intraosseous access urgently.
●● Administer 1st bolus using pull push technique till the
blood pressure improves to the normal range.
Ù
Resuscitation of hypotensive shock needs a large team
Figure 15.10: This infant presented with respiratory failure
and hypotensive shock. The airway manager is bagging, the
of trained rescuers. bolus is being given. One rescuer is poised for initiating chest
compression.
148 Section V n Circulation

Unlike Dopamine, Dobutamine, etc. which should be ●● If initial assessment suggests effortless tachypnea with
initiated after establishing euvolemia, epinephrine infu- shock, viz the increased respiratory rate is secondary
sion may be started along
IP with fluids. It should be on flow
: 196.52.84.10
to metabolic acidosis and lung parenchyma is normal,
during both fluid resuscitation and intubation. administer 20 mL/kg over 20 minutes.2

Even if BP normalizes, epinephrine should not be dis- Ù


continued. Fluid boluses should be directed towards achievement
of clinical therapeutic goals of shock resolution.
●● If BP increases to higher than normal range, with tachy- Discontinuing fluid therapy based on achievement of
cardia, taper adrenaline infusion to minimal rates. some and not all the goals could result in inadequate
●● Do not stop adrenaline despite high normal range of resuscitation.9
BP in the initial hours of resuscitation of hypotensive
shock.
Following each bolus

Figure 15.11: BP normalized in this hypotensive infant.


Epinephrine was tapered and continued in lower doses. Dopamine
had also been initiated once BP had stabilized.
Figure 15.12: Assessment of heart rate for 6 seconds.
Ù
Recent hypotension suggests severe myocardial dys­
Step 1
function and response to therapy does not mean that it Open the airway using the head tilt-chin lift maneuver in
has resolved completely. children, who are responsive to pain or unresponsive si-
multaneously.
Management of hypotensive shock is one of the most
challenging situations in the ED. Survival in hypotensive Step 2
shock could be greatly improved with availability of ad- Count respiratory rates for 6 seconds and multiply by 10.
vanced postresuscitative intensive care.
i. Assess whether the respiratory rate is increased, de-
creased or normal for age.
Normotensive shock2
●● If apnea or bradypnea is identified, rapidly initiate
Speed of Fluid Administration bag-valve-mask ventilation and the next responder
assesses the heart rate.
Fluids should be administered in aliquots of 20 mL/kg
over 20 minutes (Level I). ●● If not apneic, check for grunt, retractions and pat-
tern of breathing whilst evaluating the respiratory
Administration of large volumes (60 mL/kg over 15 rate.
min)13 can result in life-threaten­ing pulmonary edema with ●● Auscultate the infra-axillary areas and listen for
increased need for intubation.
added sounds.
If the initial assessment suggests pulmonary edema or ●● All three lobes of the lung are represented in the
respiratory distress and shock, plan to administer small ali- infra-axillary region, which makes it an ideal point
quots of fluid 5–10 mL/kg over 5–10 minutes. for rapid auscultation.
Chapter 15 n Septic Shock 149

IP : 196.52.84.10

Figure 15.13: This picture shows the airway being positioned Figure 15.14: This picture shows the child being reassessed
and oxygen being provided using the JR circuit. The assessor is after intubation.
evaluating the pulses after the heart rate.
Step 7
ii. Count heart rate for 6 seconds and multiply by 10. As-
Check whether each individual components of the airway,
sess, whether the heart rate is increased, decreased or
normal for age. While counting, evaluate for presence breathing, circulation and disability have improved, dete-
of gallop or whether the heart sounds are muffled (dif- riorated or remained status quo. Re-evaluate the cardio-
ficult to hear). pulmonary cerebral assessment and re-establish the physi-
ological status.
●● If bradycardic, the second responder initiates chest
compression. Step 8
●● If not, continue to evaluate the peripheral perfusion, Initiate the next therapeutic intervention until therapeutic
liver span and the BP. goals of shock, pulmonary edema, cardiac dysfunction and
●● Check whether the BP is normal or decreased seizures are achieved.
for age.
●● Check whether the liver span has regressed to nor-
mal for age or increased. therapeutic goals of
iii. Look at eye position, check for abnormal movements shock resolution (Table 15.2)
and evaluate the pupils for response to light.
Table 15.2: Therapeutic goals of shock resolution2
Step 3
Goals Features
Document the clinical variables immediately.
Airway Crying, verbalization in children, who have
Step 4 not been intubated
Interpret the physiological status after verifying normal Breathing RR (normal for age), absence of grunt,
values for age. retractions, normal thoracic respirations,
no added sounds
Step 5 Circulation HR (normal for age), pulses +++/++, CRT
Initiate appropriate intervention to the individual compo- < 2, warm peripheries, pink, liver span
(normal for age), BP: normal for age, with
nents of the ABCDs simultaneously.
normal pulse pressure, urine output >
Step 6 1mL/kg/h

Repeat this assessment either as soon as the therapeutic Disability Alert, normal tone and posture, eyes mid-
position, normal extraocular movements
intervention is completed or after allowing time for drug to in children, who were not intubated. Pupils
act (e.g. fluid bolus, intubation, initiating inotrope therapy are equal and reacting to light
or administration of an anticonvulsant).
150 Section V n Circulation

Airway Peripheral Perfusion


Crying or vocalalization suggests a maintainable air- ●● Normalization of peripheral pulses, color, capillary re­
way. IP : 196.52.84.10 fill time and core peripheral temperature gap.
●● As hypoxia and shock resolve, improvement in the ce- During fluid resuscitation, cool septic shock often
rebral perfusion results in return of mental status and changes to warm septic shock before complete resolution.
stabilization of the airway. This change is heralded by warm, pink peripheries with
●● Development of new cough, froth or stridor during well felt pulses and rapid capillary refill time (all signs
fluid resuscitation indicates the development of pulmo- mimic return of normal perfusion).
nary edema (see the end of Chapter for protocol when
intubation triggers are noted).

Breathing
Normalization of respiratory rates to age appropriate
ranges.
●● Restoration of normal perfusion results in resolution of
metabolic acidosis and reduction of respiratory rates to
the normal range.
Normalization of work of breathing
●● Fluid bolus therapy can resolve grunt, retractions, ab- Figure 15.15: The flushed bright pink color is commonly construed
dominal respiration and crepitations. as normalization of circulation. If this finding is associated with
●● Fluid therapy not only improves perfusion, but also respiratory distress, tachycardia, wide pulse pressure and altered
mental status as in this child, consider progression from cool shock
corrects myocardial dysfunction secondary to preload to warm septic shock during fluid resuscitation.
deficits.
●● Resolution of acute cardiogenic pulmo­nary edema re- ●● When these parameters are noted, counter check BP
sults in normalization of the work of breathing. and find out whether the pulse pressure is normal or
wide (diastole < 50% of systole is clue to the diagnosis
Circulation of vasodilatory shock).

Normalization of heart rate is one of the most reliable Ù


Wide pulse pressure, in association with respiratory
signs of shock resolution.13
distress and altered mental status is suggestive of
Ù
Antipyretic measures, antiseizure medications, pain
vasodilatory shock.

relief, abscess drainage and mother’s close proximity Normalization of blood pressure with normal pulse
can often help in achievement of normal range of heart pressure.
rate in the appropriate clinical scenarios.
●● Blood pressure in young children and infants with
●● Heart rate, which falls within the normal range for age, shock is often higher than normal. As shock begins to
in children with respiratory distress or impending re- respond to therapy, the blood pressures drops to the
spiratory failure and shock is an ominous sign. These normal range for age.
children are at risk of profound deterioration (immi- ●● Whilst the resolution of hypotensive shock is based
nent arrest). on improvement in systolic blood pressure for age,
●● Muffling should disappear and the heart sounds should diastolic pressure should also improve such that it is
be well heard. Gallop should also resolve. greater than 50% of systolic pressure.
Chapter 15 n Septic Shock 151

Disability
Ù
Avoid stopping resuscitation when peripheries become
IP : 196.52.84.10
Ù
Normalization of mental status to base line is one of the
warm and pink, pulses become well felt and CRT < 2
seconds. Check the other parts of the pediatric assessment most important goals of shock resolution.
triangle. If child remains in altered mental status, has
●● Fluid responsive shock is characterized by resolution
respiratory distress, with or without hepatomegaly and
of incessant cry, lethargy and posturing resulting in
BP is associated with wide pulse pressure, continue fluid
consolable cry, playfulness and normal sleep.
resuscitation.
●● Consolable cry as a therapeutic goal of fluid responsive
shock is recognized when fluid therapy and monitoring
Resolution of Hepatomegaly is performed with the child in his mother’s arms.

●● Normalization of liver span for age is suggestive of Resolution of eye signs of non-convulsive status epilep-
resolution of myocardial dysfunction. ticus.
●● It is not uncommon to encounter eye signs of non-con-
Regression of liver span is often noted during bolus
vulsive status epilepticus on arrival or during resuscita-
therapy, inotrope infusion and following intubation.
tion of hypoxia or shock due to severe sepsis.
●● Successful resuscitation of fluid responsive shock is as-
Urine Output sociated with return of eyes to mid position and normal
extraocular movements.
●● Urine output greater than 1 mL/kg/h in chil­dren beyond ●● Examine eyes for lateral conjugate deviation, eyelid
1 year of age and greater than 1.5 mL/kg/h in infants twitch and/or nystagmus following each intervention
suggests normal renal perfusion. during resuscitation.
●● Urine output of less than 1 mL/kg/h during resuscita­
tion is an ominous sign of refractory shock. Ù
The importance of early recognition and simultaneous
●● However, it may fail to provide information, when
management of convulsive and non-convulsive status
polyuria or anuria occurs as complications of renal dis­
epilepticus cannot be understated in ensuring successful
eases with septic shock.
outcomes in septic shock.

●● Persistence of posturing after achieving therapeutic


goals of shock resolution associated with abnormal
patterns of respiration, bradycardia, high BP, abnormal
pupillary response and defective doll’s eye movement
suggest the presence of raised intracranial pressure
(ICP).
Ù
Resuscitation of shock due to intracranial infections
would be incomplete, if raised ICP is not simultaneously
identified and treated in the initial hours of management.

●● Clinical signs suggestive of myocardial dysfunction or


Figure 15.16: This picture shows catheterization for monitoring pulmonary edema on arrival or its development during
urine output in fluid unresponsive, inotrope responsive shock in fluid therapy should be anticipated.
settings without access to central venous pressure monitoring.
This variable can occasionally be inaccurate in assessing renal If signs of pulmonary edema (intubation triggers) (Fig-
perfusion pressure, when underlying renal disease exists as in this ure 15.6) are noted during fluid therapy, further fluid ad-
child with hematuria and pyuria. ministration is interrupted briefly.
152 Section V n Circulation

Ù
Stomach contents should be emptied rapidly, if intubation
IP : 196.52.84.10
is being considered.

3. Initiate an appropriate inotrope.


4. Consider intubation.
●● Provide O2 using the flow inflating ventilation device if
not being used already. If the child is unable to protect
the airway, unresponsive, having evidence of NSCE or
convulsive SE or signs of imminent arrest consider in-
tubation.
●● After initiating inotrope and CPAP, or inotrope and in-
Figure 15.17: Note the froth within the mask. On identification of tubation, perform the rapid cardiopulmonary cerebral
this sign of PE, further fluids were interrupted, inotrope initiated
assessment.
and CPAP device was used to provide O2.
If signs of PE and hepatomegaly have resolved and
Inotrope/CPAP/Intubation Triggers 2 shock persists:
●● Continue to provide CPAP via mask (non-invasive-
ly) or after intubation using the Jackson-Rees circuit
throughout fluid therapy.
Ù ●● Ensure that an inotrope infusion is also on flow through-
out fluid therapy.
Ù
Development of pulmonary edema makes intubation
a challenge. Froth, that is noted during the fluid
resuscitation (Figure 15.9) predicts increased risk of
mortality.

Figure 15.18: Signs of pulmonary edema and cardiac


dysfunction.

●● Other intubation triggers: seizures not resolving with 2


doses of Benzodiazepine, features of raised ICP.
During bolus therapy, if any one or a cluster of signs of
deterioration, viz pulmonary edema are identified:
1. Interrupt fluid boluses briefly.
Ù
Continuation of fluid therapy when signs of PE have
developed suggests the need for inotropes and provision
of PEEP. Failure to do so could precipitate cardiac Figure 15.19: Note the development of froth during fluid therapy
arrest. both in the mouth and in the nasogastric tube (Courtesy: Dr Gunda
Srinivas).
2. Insert a nasogastric tube and decompress stomach ●● Continue smaller and slower fluid boluses until signs
contents. of shock and pulmonary edema have resolved.
Chapter 15 n Septic Shock 153

Source Control
Ù ●● Obvious foci of sepsis should be drained even as resus-
Following intubation if oxygen saturations drop below
IP : 196.52.84.10 citation is in progress. If focus of sepsis is inaccessible,
92%, ‘DOPE’ should be ruled out to avoid lethal
consequences. the child is shifted to the OR at the earliest after stabi-
lization. Avoid transferring to the ICU or ward without
In vasodilatory shock in severe sepsis, it is not uncommon draining the focus of sepsis.
for recurrence of pulmonary edema.
●● Development of froth, crepts, desaturation, gallop,
muffling of heart sound, fall in mean arterial pressure,
increase in liver span, suggests the development of flu-
id refractory, dopamine unresponsive shock.
●● Add norepinephrine infusion at the rate of 0.3 µg/kg/
minute and titrate up to 0.5 µg/kg/minute.
●● Continue smaller and slower fluid boluses until signs
of shock and pulmonary edema have resolved.

Figure 15.20: Crossing limits to save lives: This infant shown


above received up to 250 mL/kg during the initial 24 hours to
attain therapeutic goals of shock resolution. He developed PE and
cardiac dysfunction, was intubated and needed dopamine and Figures 15.21A and B: These two pictures show incision and
norepinephrine before he achieved all therapeutic goals (Courtesy: drainage of an abscess in progress in an infant, who has been
Dr Gunda Srinivas). intubated and ventilated using the pediatric Jackson-Rees circuit.
He is receiving his fluids while inotrope is being infused.
Treatment and Prevention
of Hypoglycemia Blood Transfusion
●● Correct documented hypoglycemia with 2 mL/kg of Blood transfusion is planned in a semielective manner. If
25% dextrose. hemoglobin is less than 10 g/dL, transfusion can be con-
●● Throughout resuscitation, glucose normal saline (GNS) sidered after correction of shock. Septic shock complicated
to which potassium has been added should be infused by other important indicators for transfusion. Fluids, ino-
at maintenance rates for age. tropes or intubation should not be delayed, while waiting
for blood.
Simultaneously Evaluate for
Focus of Sepsis Steroids
●● Blood and body fluids are collected for culture and a Hydrocortisone (2 mg/kg) is administered intravenously
third generation cephalosporin is administered in the for children who have been on steroid therapy in the recent
initial hours of resuscitation.
154 Section V n Circulation

past. It is also indicated when hypotensive shock is refrac-


tory to catecholamine infusion.
Key Points
ü
1. Recognize septic shock by looking for evidence of
IPin: the
Drugs to be avoided 196.52.84.10
management of septic car-
decreased mental status and peripheral perfusion in
diogenic shock: any ill looking child with fever.
●● Fursemide, mannitol can worsen shock and precipitate 2. Altered level of consciousness in a febrile child
cardiac arrest. could be due to septic shock. Correction of the
●● Nebulized salbutamol to relieve wheeze, due to PE, hypoxia and shock often improves mental status in
can worsen hypoxia and precipitate cardiac arrest. the ED.
3. Resuscitation should be continued till all therapeutic
The protocol for septic shock provides a broad guide- goals of shock and pulmonary edema are resolved.
line. Treatment should be individualized for the patient at
hand. Refer Protocol 15.1 and 15.2.
The physiological response of every critically ill child
common errors
1. Mistaking the flushed warm peripheries in the
û
to resuscitative interventions is variable, unpredictable
presence of abnormal mental status, tachypnea and
and occasionally anxiety provoking. In the initial hours of
tachycardia in a febrile child as normal. Recognize
resuscitation in the ED, where radiological, biochemical
warm septic shock.
evaluation and invasive monitoring are unavailable, it is
2. Failing to note diastolic pressure. A diastolic pressure
imperative for the treating physician to stand by the bed­
less than 50% of systole will help to recognize
side and repeatedly perform the cardiopulmonary assess­ vasodilatory (warm) shock.
ment to accurately assess trends in patient’s response and 3. Diagnosing fever with altered mental status as
intervene appropriately. central nervous system infection, atypical febrile fits
The rapid clinical assessment and intimate awareness, or febrile encephalopathy.
of the risk of PE, provides the ED physician with a 60 sec- 4. Stopping fluids, if signs of pulmonary edema are
ond advantage to change track and save life. identified.
Protocol 15.1: PEMC approach: Early recognition of septic shock in the out patient department

IP : 196.52.84.10
Chapter 15 n Septic Shock
155
156 Section V n Circulation

Protocol 15.2: PEMC approach: Management of septic shock


Airway and Breathing Inotrope/CPAP/Intubation triggers
IP : O196.52.84.10
Effortless tachypnea: Provide 2
via non-rebreathing mask Airway: Instability
Respiratory distress: Provide O2 via Jackson-Rees circuit • New cough
Apnea: Provide O2 via bag-valve-mask ventilation (plan early intubation using RSI*) • Pink froth
Breathing: Bradypnea
Circulation
• RR > 80/min
Establish venous access: If IV access not available → intraosseous access
• Grunt
BP (N): Effortless tachypnea: 20 @ 20 minute from reservoir
• New chest retractions
Respiratory distress: 5–10 mL/kg boluses @ 5–10 minute
• New onset abdominal respiration
Low BP: Pull push 5–10 mL/kg boluses of NS/RL until BP normalizes
• New rales/wheeze
Low BP on arrival or any step in protocol: Call for epinephrine infusion and plan early intubation
Circulation: Bradycardia, gallop
Reassess for response or deterioration following each bolus (5, 10, 20 mL/kg)
• Muffling of heart sounds
Broad spectrum antibiotic, collect body fluids for cultures
• Fall in BP, low MAP
Perform incision and drainage for source control. If focus inaccessible: Shift to OT after resuscitation
• Liver span↑
Correct documented hypoglycemia: 25% dextrose 2–4 mL/kg bolus followed by GNS + KCl age-
Disability: Agitation, GCS < 8
dependent maintenance rates
• Fighting mask
After each 5 mL/kg, 10 mL/kg, 20 mL/kg perform the rapid cardiopulmonary cerebral assessment
• SpO2 < 92%
immediately in 1 minute • Asking for water
• ICP, refractory SE

Caution: Children with septic shock have coexisting acute lung injury and myocardial dysfunction. Fluid administration without initiation of
inotrope and/or intubation when “intubation triggers are identified could be dangerous leading to cardiac arrest’’.

Santhanam I, Sangareddi S, Venkataraman S, et al. A prospective randomized controlled study of two fluid regimens in the initial
management of septic shock in the ED. Pediatr Emerg Care. 2008;24: 647-655.
Chapter 15 n Septic Shock 157

References 7. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound


but reversible myocardial depression in patients with septic
1. Robertson MA, Molyneux EM. Description of serious ill- shock. Ann Intern Med. 1984;100:483-90.
ness and outcome inIP : 196.52.84.10
patients identified using ETAT guide-
8. Tranbaugh, et al. Lung water changes after thermal injury
lines in urban, Malawi. Arch Dis Child. 2001;85:214-17.
the effects of crystalloid resuscitation and sepsis. Ann:
2. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- Surg; 1980.
spective randomized controlled study of two fluid regimens
9. DG Perina. Non-cardiogenic pulmonary edema. Emerg
in the initial management of septic shock in the emergency
Med Clin N Am. 2003(21):385-93.
de­partment. Pediatr Emerg Care. 2008;24:647-55.
3. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ 10. Oliviera CF, et al. Time and fluid sensitive resuscitation for
ESICM/ACCP/ATS/SIS International Sepsis Definitions hemodynamic support of children with septic shock. Bar-
Conference. Crit Care Med. 2003;31:1250-256. riers to the implementation of the ACCM/PALS guidelines
in a pediatric intensive care unit in the developing world.
4. Micha Maeder, Thomas Fehr Hans Rickli, Peter Ammann
Sepsis-Associated Myocardial Dysfunction: Diagnostic Pediatr Emerg Care. 2008;24:810-15.
and Prognostic Impact of Cardiac Troponins and Natriuret­ 11. Maitland K, et al. Mortality after Fluid Bolus in Af-
ic Peptides CHEST. 2006;129(5):1349. 1366. doi:10.1378/ rican Children with Severe Infection. N Engl J Med.
chest.129.5.1349. 2011;364(26):2483-495.
5. Michael A Matt Hay. Future Research Directions in Acute 12. Russel RR, Day T, Faizal MA, et al. Tracheal intubation in
Lung Injury Summary of a National Heart, Lung and Blood meningococcal disease and septic shock. Arch Dis Child.
Institute Working Group. Am J Respir Crit Care Med. 2007;92:827.
2003(167);1027-035. DOI: 10.1164/rccm.200208-966WS. 13. Dellinger RP, Mitchell M, Carlet JM, et al. “Surviving
6. Phillip D. Cardiovascular management of septic shock. Sepsis Guide­lines Campaign: International guidelines for
Critical Care Medicine. 2003;(31)3:946-55 doi: 10.1097/01. management of severe sepsis and septic shock: 2008”. Crit
CCM.0000057403.73299.A6. Care Med. 2008;36(1):297-320.
Approach to Recognition and
16
IP : 196.52.84.10

Management of Dengue in the ED

Figure 16.1: Management of severe dengue involves recognition of appropriate phase of illness, shock correction and meticulous
monitoring for successful outcomes (Courtesy: Dr Thangavelu S and Dr Gunda Srinivas).

Learning Objectives
1. Method of implementation of the WHO-Dengue 2. Highlight use of the Jackson-Rees circuit in
Guidelines: 2012 using the rapid cardiopulmonary children with dengue presenting with respiratory
cerebral assessment and Pediatric Assessment distress.
Triangle (PAT).

Introduction triggers an overwhelming host production of inflammatory


mediators, cytokines and chemokines. The resulting vas-
Dengue is an important cause of mortality in children. cular endothelial cell dysfunction and derangement of the
Epidemic in many parts of India, this disease is typically hemocoagulation system lead to plasma leakage, shock
unpredictable in its course and progression. Key to suc- and bleeding.
cessful management is the early recognition and early
management of severe dengue (Figure 16.1). 1. Leakage of plasma from the vascular compartment
into interstitial compartment and third space results
Dengue is caused by four serotypes of Dengue virus in hemoconcentration, hypovolemic shock and fluid
DEN-1, 2, 3, 4. The infection caused by one serotype re- overload.
sults in serotype-specific immunity along with transient 2. Bleeding tendencies are secondary to many
cross immunity against the other three serotypes. Follow- abnormalities in hemostasis. Hypoxia, acidosis, shock,
ing the bite of the mosquito infected with Dengue virus, low platelet count, platelet dysfunction, coagulopathy,
clinical features appear after an incubation period of 7–10 vasculopathy and disseminated intravascular coagula­
days. Majority of infected children however, do not de- tion are some of the many causes.
velop symptoms and severe dengue occurs only in a small
proportion. Clinical Presentation
Secondary infection, causes an antibody-dependent en- Dengue infection is classified into three clinically recog-
hancement, wherein the pre-existing antibody to the previ- nizable phases (over 4–10 days) namely Febrile phase,
ous serotype paradoxically enhances viral replication. This Critical phase and Recovery phase (Figure 16.2).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 159

Ù
Hematocrit is a simple bed-side tool to identify severity
IP : 196.52.84.10 of capillary leak. Serial evaluation of hematocrit is more
informative during resuscitation than serology test that
confirm dengue infection. Indian children with DHF
have a lower than expected rise in hematocrit during
the period of leakage of plasma. This phenomena has
been attributed to the high prevalence of iron deficiency
anemia in the general population. Normal HCT in healthy
Indian children is, 32% ± 3%. It has been proposed that
the cutoff for elevated HCT is 36.3%. This value seems
to identify > 80% of children with DSS in India.4

Case scenario 1
Figure 16.2: Time line for the dengue infection
A 3-year-old girl had fever for 5 days. On the 6th
Ù
Dengue is classified based on severity (Table 16.1)
2
day, she developed erythematous rashes all over
body with flushing of palms. Since morning she has
● Probable dengue. been afebrile. She has no abdominal pain or vomit-
● Dengue with or without warning signs. ing. There is no evidence of hepatomegaly, splenom-
● Severe dengue. egaly, ascites, bleed, edema or puffiness (Figures 16.3
and 16.4).
Recognition of Probable Dengue
Clinical clues that distinguish dengue from other fevers in
febrile phase are:
●● Fever without a source.
●● Flushed face.
●● History of living in a dengue-endemic area.
Two helpful clinical tools which help in the early diag-
nosis of dengue in the febrile stage:
1. Positive tourniquet test.
Figure 16.3: Tourniquet test shows multiple petechiae
2. Leukopenia: Total white blood cell count < 5,000 cell/ (Courtesy: Dr Thangavelu S).
mm3.

Confirmatory Tests
NS1 antigen (positive in the first 5–7 days) and dengue
IgM identified after 5–7 days are useful to confirm dengue.
Viral cultures and PCR are commonly used for research
purpos­es.
Whilst their application in clinical practice is limited,
the rapid NS1 antigen lab kit is currently being used for
early detection in the OPD setting.
High titres of NS1 antigen have been noted in the early
clinical phase. By day 5, it drops to 56.5%. Possibility of Figure 16.4 Physiological status: Her cardiopulmonary cerebral
diagnosis is enhanced when IgM antibody is also positive. status is normal. She has probable dengue.
160 Section V n Circulation

Table 16.1: Classification of dengue severity

Probable dengue Dengue with warning signs* Criteria for severe dengue (one or more
IP : 196.52.84.10 of the following signs)
Live in/travel to dengue-endemic area ●● Abdominal pain or tenderness Severe plasma leakage leading to:
●● Fever and two of the following criteria: ●● Persistent vomiting ●● Shock (DSS)
– Nausea/vomiting ●● Clinical fluid accumulation ●● Fluid accumulation with or without
– Rash ●● Mucosal bleed respiratory distress
– Aches and pains ●● Lethargy ●● Severe bleeding
– Tourniquet test positive ●● Restlessness ●● Severe organ impairment
– Leukopenia ●● Liver enlargement > 2 cm ●● Liver AST or ALT >1,000
– Any warning sign ●● Lab: Increase in HCT ●● CNS-impaired consciousness
Laboratory confirmed dengue ●● Rapid decrease in platelet count ●● Heart and other organs
(important when no signs of plasma *Requiring strict observation and medical
leakage) intervention
Triage: ER physician should categorize based on severity and treat appropriately.

●● This child can be managed at home.


●● Educate her parents about early warning signs and ask
them to report immediately if these signs develop (Ta-
ble 16.1).
●● Mother can be taught to monitor her urine output at
home.
●● Administer ORS as shown in Table 16.2.
●● Avoid NSAIDs.
●● Treat fever with Paracetamol (dose 10 mg/kg).
Table 16.25: ORS administration with body weight

Body weight in kg ORS (mL/kg/day)


3–10 100 Figure 16.5 Physiological status: Cardiopulmonary cerebral
10–20 75 status is normal. Since his HCT is increased and platelets are low
20–30 50–60 he has dengue with warning signs.

30–60 50–60 ●● Repeat the rapid cardiopulmonary cerebral assessment


every hour during the critical phase.
Ù ●● Monitor urine output 4–6 hourly.
●● Repeat hematocrit after fluid therapy and 6–12 hourly
Parents should be instructed to identify early warning
signs during defervescence (See Table 16.1). thereafter.
Mothers should also be taught to meticulously monitor
urine output. Fluid Therapy
●● 1–2 hours: Initiate isotonic infusion (NS or RL) at the
rate of 5–7 mL/kg/h.
Management of Dengue ●● 2–4 hours: Reduce rate of flow to 3–5 mL/kg/h.
with warning signs ●● Beyond 4 hours: Reduce rate of flow to 2–3 mL/kg/h
Case scenario 2 based on the clinical response and the hematocrit.

A 10-year-old child has been brought with the history Monitoring


of abdominal pain since morning. He has been hav­ing
fever for the past 5 days but now the fever had settled. ●● Monitor urine output every hour.
He has been vomiting since the morning. He had voided ●● Catheterize to ensure continuous monitoring.
urine 4 hours ago. His platelet count: 70,000/mm3 and ●● Discard the first urine volume after bladder catheteriza-
hematocrit 40% (Figure 16.5). tion since the duration within the bladder is unknown.
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 161

●● Ensure that urine output is about 0.5 mL/kg/hour.


●● Monitor hematocrit before and after every fluid bolus
until stable and thenIPevery 4−6 hours.
: 196.52.84.10
●● The interpretation will be meaningful only if the cor-
responding hemodynamic state and response to fluid
therapy is evaluated simultaneously.
●● Random HCT in the absence of information about the
hemodynamic status or response to fluids is unlikely to
be useful.
●● Check dextrostix for blood glucose (before fluid resus-
citation and repeat as indicated). Figure 16.6: Respiratory distress with compensated shock. She
Ù
If hematocrit remains the same or increases minimally
also has right sided pleural effusion (Courtesy: Dr Thangavelu S).

and cardiopulmonary assessment is stable:


• Continue NS at the rate of 2–3 mL/kg/h for another
2–4 hours.
• Change to oral fluids once the patient tolerates oral
feeds.
If hematocrit increases rapidly and the cardiopul­
monary assessment suggests deterioration:
• Increase fluids to 5–10 mL/kg/h for 1–2 hours.
• Further fluid administration is based on the clinical
condition and repeat hematocrit values.

●● Titrate fluids to maintain normal perfusion and urine


output of 0.5 mL/kg/hour. Figure 16.7: Respiratory distress with compensated shock. She
●● Fluids should not exceed 1.5 times maintenance. also has right sided pleural effusion. Severe dengue.

Ù Fluid Management in Severe Dengue with


Ideal body weight is used for calculation of fluid infusion
in obese children. Compensated Shock (Figures 16.6 to 16.8)
●● Administer supplemental oxygen through the Jackson-
●● Intravenous fluids are required for 24–48 hours. Rees circuit are non-re­breathing mask.
●● When the peripheral pulses are felt better and urine ●● Initiate 0.9 NS 10 mL/kg over 1 hour.
output is more than 0.5 mL/kg/h, intravenous fluids ●● Insert urinary catheter to monitor hourly urine output.
should be stopped. Administration of IV fluids for a ●● Repeat cardiopulmonary cerebral assessment.
longer period of time (especially when not needed) can ●● Check hematocrit.
precipitate fluid overload.
Repeat cardiopulmonary cerebral assessment and he-
matocrit helps guide further fluid therapy. If shock is re-
Severe Dengue: Compensated shock solved fluid can be tapered. If not a repeat bolus may be
Case scenario 3 needed if hematocrit is increased.

A 10-year-old girl presented with fever for 4 days. Since ●● If hematocrit is reduced in a shocked child, consider
the morning fever has settled, but she has developed blood transfusion.
ab­dominal pain. She is lethargic, does not wish to stand ●● If severe overt bleeding occurs, transfuse PRBC or
up or walk. She has no bleeding tendency. WBC: 4,000/ fresh whole blood.
mm3, HCT 43%, platelet count: 34,000/mm3. ●● If overt bleeding is not noted, infuse colloid.
●● If no improvement after colloid, consider blood or
PRBC transfusion.
162 Section V n Circulation

Ù Ù
No shock and HCT is high: The patient should be closely monitored. The rapid
IP : 196.52.84.10
• Isotonic fluids should be gradually reduced to cardiopulmonary assessment should be performed every
5–7 mL/kg for 1–2 hours, then to 3–5 mL/kg for 15–30 minutes till shock is corrected and then hourly
2–4 hours and then to 2–3 mL/kg/h. Further fluid till the critical phase is over. Fluids may have to be
administration is based on clinical response. Fluids continued for 24–48 hours. Child may go in and out of
should be maintained for a maximum of 24–48 shock during the critical phase. Judicious administration
hours. of fluid is essential to prevent fluid overload.
Shock persists: Caution: Restrict fluids such that the urine output is 0.5
• Check hematocrit after the first bolus. mL/kg/hour. If urine output exceeds 1–2 mL/kg/hour, it
Hematocrit is still increased: indicates excessive fluid administration.
• Repeat a second bolus of 10–20 mL/kg/hour
• If shock has resolved, reduce the rate of fluids to
7–10 mL/kg/h for 1–2 hours and then reduce further
Severe Dengue: Hypotensive shock
as mentioned above. Case scenario 4
Hematocrit is reduced (suggests bleeding):
A 10-year-old child is rushed into the ER following fever
• Transfuse 5–10 mL/kg of packed red cells or 10–20
for one week. The fever had settled, but since morning
mL/kg of fresh whole blood. she had been vomiting several times and has become

Figure 16.8: Management of severe dengue with compensated shock (Source: WHO Handbook for clinical management of dengue, 2012).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 163

progressively lethargic. She has edema and ascites as Though there is no clear advantage of colloids over crys-
shown in Figure 16.9. She has bleeding from intrave- talloids. Colloids have been shown to restore the cardiac
nous (IV) sites. Hematocrit is 45%. index and reduce the level of HCT faster than crystalloids
IP : 196.52.84.10
in patients with intractable shock.6,7,8
●● Call for inotrope infusion.
●● Dopamine if BP is low nor­mal. Epinephrine if severely
hypotensive.
●● Catheterize and monitor urine output.
●● Check hematocrit before and after every fluid bolus.
●● Collect blood for grouping, crossmatching and lab in-
vestigations.
Repeat rapid cardiopulmonary cerebral assessment
Shock with normal blood pressure:
Figure 16.9: Note the facial ecchymoses, fresh bleed in the ●● Repeat a second bolus of crystalloid or colloid 10 mL/
nasogastric tube and abdominal distension due to ascites kg over 1 hour.
(Courtesy: Dr Thangavelu S). ●● Gradually reduce to 5–7 mL/kg/hour for 1–2 hours,
Many severe dengue children especially the older ones 3–5 mL/kg/h for 2–4 hours and then to 2–3 mL/kg/h
with hypotension may deceptively remain alert and may be or less.
ambulant. Shock may not be suspected in these children ●● Maintain 2–3 mL/kg/h for 24–48 hours.
unless they are touched. The cold extremities can then be Hypotension not resolved:
identified. A rapid cardiopulmonary cerebral assessment is
mandatory in these children to detect shock (Figure 16.10). Check hematocrit.
If HCT remains high after the 1st bolus:
●● Repeat another 10 mL/kg of colloid over 30 min­utes to
1 hour and reassess.
●● If cardiopulmonary cerebral reassessment reveals that
there is improvement, continue colloid at 7–10 mL/kg
for 1–2 hours.
●● Reassess: If improvement persists, change to crystal-
loid infusion and gradually reduce it as mentioned
above.
If the HCT still remains high after the 2nd bolus and
shock persists:
●● Repeat 3rd bolus of 10 mL/kg of colloid over 1 hour.
Figure 16.10 Physiological status: Respiratory distress with ●● Repeat the cardiopulmonary cerebral assessment.
hypotensive shock and altered mental status.
●● If there is improvement, taper as mentioned above.

Fluid Management in Severe Dengue If resuscitation is effective, the hematocrit level will
with Hypotensive Shock (Figure 16.11) gradually decline by approximately 10% after each dose
of colloidal solution with improvement in the cardiopul-
●● Provide O2 through the Jackson-Rees circuit. monary status.
●● Initiate 0.9% NS or colloid solution 20 mL/kg, IV bo-
lus over 15 minutes. ●● If the hematocrit level declines with no sign of im­
●● Colloids are preferred, if BP has to be restored urgent- provement, after the 1st, 2nd or 3rd bolus, it is likely
ly.2 that there may be concealed or internal bleeding.
164 Section V n Circulation

IP : 196.52.84.10

Figure 16.11: Management of severe dengue with hypotensive shock (Source: WHO Handbook for Clinical Management of Dengue, 2012)

●● Transfuse fresh packed red cell (5–10 mL/kg/) or whole It is important to understand that the outcome in severe DSS
blood (10–20 mL/kg) without delay. is very poor despite heroic measures undertaken at a ter-
●● If signs of pulmonary edema or worsening hepatomeg­ tiary care center. Hence the goal is to identify the children
aly is identified during fluid therapy, initiate inotropes. with dengue early, when they present with warning signs.
●● If overt bleed, hypotension persists and HCT is low,
start colloid 10–20 mL/kg/h. If HCT remains low, and
Ù
In India DSS often coexists with shock due to sepsis
hypotension persists consider fresh blood transfusion.
of other etiologies (e.g. UTI, malaria, typhoid, scrub
●● Continuous monitoring of these patients and careful
typhus, etc.). Differentiation between DSS and septic
titration of fluids based on frequent CPA improves
shock (see Protocol 16.1). Hence, larger volumes may
survival.­
be needed to correct shock in our setting.
●● Children presenting with severe dengue may have as-
sociated metabolic abnormalities such as hypoglyce- ●● Perform sepsis screen and prescribe appropriate anti-
mia, hyponatremia, hypocalcemia and acidosis. These microbial therapy.
conditions should be identified early and treated appro-
priately. Note: Agitation may be a sign of shock, hepatic failure,
●● Monitor blood sugar frequently since glucose free flu- metabolic derangement, encephalopathy or cerebral ede-
ids are being infused. ma. Sedation without correction of the underlying prob-
●● If facilities to monitor glucose are unavailable and the lems may prevent recognition of alteration in mental status
child is young, infuse DNS after correction of shock. (an important sign of critical illness).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 165

Complications (Figure 16.12) ●● Children with impaired hepatic function are at in-
creased risk of bleeding.
●● Avoid intramuscular injections.
IP : 196.52.84.10
●● Avoid non-steroidal anti-inflammatory agents.
Management when internal bleeding is suspected:
●● Send blood for cross matching if epistaxis, hematem-
esis or melena is noted.
●● Do not wait until the hematocrit drops to 30% (cut-off
for transfusion in children with septic shock). Higher
hematocrits are expected in children with DSS.
●● Do not hesitate to provide fresh blood transfusion when
there is worsening of clinical signs and symp­toms and
fall in hemotocrit level during the critical stage.
Figure 16.12: The chest X-ray of the child shown in the figure
shows right pleural effusion. Note the ET tube positioned at T-4 Ù
(Courtesy: Dr Thangavelu S). It is well documented that adequate shock cor­rection is
the best way to prevent hemorrhage.
The four most common causes of death among DSS patients:
●● Administer vitamin K.
●● Prolonged shock.
●● Do not call for platelet concentrate infusion.
●● Massive bleeding.
●● Fluid overload. ●● Transfuse 10–20 mL/kg of fresh whole blood. Fresh
●● Organ disturbance: Acute encephalopathy, hepatic fail- blood is rich in 2,3 DPG that will correct hypoxia and
ure. acidosis.

Ù Ù
As first responders, it is possible that the ED physicians Persistent hypoxia and shock are believed to be the
can play a critical role to prevent occurrence of these cause for bleeding.
seri­ous complications.
●● Avoid platelet concentrates to treat thrombocy­topenia.
●● Prophylactic platelet transfusions for severe thrombocy­
Prevent patient slipping into shock by:
topenia in hemodynamically stable patients are not
1. Early recognition of dengue in the febrile stage. effec­tive and are not indicated.10
●● Leukopenia (WBC < 5,000) ●● Platelets have a short half-life and are at increased risk
●● Positive tourniquet test.9 of destruction during dengue infection.
2. Early detection of critical stage. ●● Avoid routine administration of fresh frozen plasma.
●● Rising hematocrit and decreasing platelet < These blood products may contribute to fluid overload.
100,000.
●● Close monitoring and adjustment of fluid rate. Fluid Overload (Figures 16.13 to 16.15)
●● Avoid delay in switching from crystalloid to colloid
ED physicians must be aware of common pitfalls dur-
solution when indicated.
ing management that may lead to fluid overload: Lead-
Consider occult bleeding in the following situations ing cause of death in children with severe dengue is fluid
●● Prolonged shock that fails to respond to 40–60 mL/kg. overload. This may result in pulmonary edema, chest wall
●● Persistent shock despite reduction of hematocrit level. edema and abdominal compartment syndrome. All these
●● Unexplained tachycardia. conditions can lead to respiratory embarrassment and he-
●● Decline in hematrocrit is greater than expected. modynamic instability.
●● Hypotensive shock with low/normal HCT before fluid Fluid overload can occur in both the critical and recov-
resuscitation. ery phase leading to therapeutic dilemmas viz respiratory
●● Persistent or worsening metabolic acidosis in children distress and shock. In this scenario, management of one
with severe abdominal tenderness and distension. problem can worsen the other.
166 Section V n Circulation

●● Large pleural effusions and tense ascites.


●● Chest X-ray and USG abdomen in the ER will supple-
IP : 196.52.84.10 ment the clinical impression.

Figure 16.13: Purpura due to severe dengue (Courtesy: Dr


Thangavelu S).

●● Prolonged administration of IV fluid administration (>


48 hour).
●● Higher rate of IV fluid than those recommended in the
guidelines. Figure 16.14: Chest X-ray taken prior to fluid therapy in a child
●● Use of hypotonic solutions. who presented in shock (Courtesy: Dr Thangavelu S).
●● Inappropriate timing of IV fluid administration, e.g.
starting IV fluid too early during the febrile stage be­
fore plasma leakage occurs.
●● Delay in the use of colloids when indicated.
●● Using actual weight when calculating the total fluid
rather than ideal body weight for obese children.
●● Not accounting for IV fluid received as prehospital
therapy.

Ù
Management of DSS is based on correct replacement of
fluid loss occurring due to capillary leak. Too much fluids
will lead to fluid overload and too little will not improve
shock. Besides, the quantity of leak can change every Figure 16.15: Chest X-ray taken the following day shows signs of
hour during the critical phase. Repeated assessment of fluid overload (Courtesy: Dr Thangavelu S).
perfusion and urine output with replacement of fluids is
key to survival. Paramedics and nurses must be trained Management of Fluid Overload
to collect data on input/output to guide therapy.
The management varies based on the phase of illness and
the child’s hemodynamic status.
Clinical Clues to Detect Fluid Overload
●● Recovery phase and cardiopulmonary status stable:
It may be difficult to differentiate ‘fluid overload’ and – Stop intravenous fluids: Most children will void and
‘shock’ in critically ill patients who have been referred improve spontaneously.
from other hospitals after fluid therapy. The following – Provide O2 and CPAP using the Jackson-Rees cir-
clinical clues may be helpful to the ED physicians to de- cuit: CPAP helps to resolve respiratory distress due
tect fluid overload: to pulmonary congestion.
– Oral or IV furosemide 0.5–1.0 mg/kg/dose once or
●● > 2 mL/kg/hour urine output in the absence of glycosu- twice daily or a continuous infusion of furosemide
ria or furosemide. at 0.1 mg/kg/h: Prior to diuretics ensure that there
●● Weight gain, raising respiratory rate, respiratory dis- had been no shock in the preceding 12–24 hours.
tress with falling SpO2 requiring oxygen to maintain – Monitor serum potassium.
saturation.
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 167

●● Critical phase but not in shock Other Complications


– Provide O2 and CPAP using the Jackson-Rees cir- ●● Hyperglycemia and hypoglycemia.
cuit to resolve pulmonary congestion.
IP : 196.52.84.10 ●● Electrolyte disturbances such as hyponatremia, hy-
– Reduce the IV fluids accordingly.
pokalemia, hyperkalemia, hypocalcemia and metabolic
– Monitor closely using the rapid cardiopulmonary
acidosis.
cerebral assessment and urine output.
●● Malaria, leptospirosis, enteric fever or scrub typhus can
– Avoid furosemide in the plasma leakage phase since
complicate the clinical presentation and management.
it may lead to intravascular volume depletion.
Severe dengue patients may have severe organ impair-
●● Critical phase and shock
ment such as acute liver failure, encephalopathy, renal failure.
– It is very difficult to balance the IV fluid treatment Cardiomyopathy, myocarditis and dengue encephalitis have
in DSS patients who are still in shock with fluid
also been reported. Other atypical manifestations in dengue
overload. If the amount of fluid administered is
are acalculous cholecystitis, acute pancreatitis, hemolytic
not adequate, the patient will experience prolonged
uremic syndrome, ARDS, myositis with raised serum cre-
shock, if the amount of fluid is too much, the patient
atine phosphokinase, rhabdomyolysis, infection associated
can develop pulmonary edema.
hemophagocytic syndrome and macular hemorrhage.11
– Provide O2 and CPAP using the Jackson-Rees cir-
cuit to resolve pulmonary congestion. Criteria for discharge: All of the following must be present2
– The following IV fluid management techniques
Clinical:
may be helpful in the ER.
●● No fever for 48 hours.
●● Low or normal HCT with signs of fluid overload
and shock Improvement in clinical status:
– Provide Oxygen via the Jackson-Rees circuit. ●● General well-being.
– Transfuse fresh whole blood for occult hemor- ●● Good appetite.
rhage. ●● No respiratory distress.
●● High HCT with signs of fluid overload and shock ●● Normal hemodynamic status.
– Provide oxygen via the Jackson-Rees circuit. ●● Normal urine output.
– Administer small boluses of colloids. Laboratory:
Ù ●● Increasing trend of platelets.
Avoid furosemide in children with shock and pulmonary ●● Normal hematocrit.
edema.
168 Section V n Circulation

Key Points
1. Repeated rapid IP cardiopulmonary
ü
and cerebral
common errors
û
1. Not reducing the rate of fluid administration after
: 196.52.84.10
assessment in conjunction with hematological and shock correction leads to increase in ascites, pleural
urine output monitoring during defervescence helps effusion and pulmonary edema.
identify the critical phase. 2. Giving furosemide to a child who is hemodynamically
2. Early diagnosis of dengue with warning signs and unstable can be catastrophic.
ap­propriate fluid administration at this stage prevents 3. Not changing the fluid to colloids, when there is
the child from developing shock. no response to initial crystalloid boluses and the
3. Fluid administration is only needed for 24–48 hours hematocrit remains high.
in the leak phase. 4. Not giving fresh blood to a child, who remains hemo­
4. Judicious fluid therapy prevents fluid overload, dynamically unstable with a normal hematocrit.
(dreaded complication). 5. Blood transfusion in the convalescent phase for low
5. Adequate shock correction is the best method to hematocrit (dilutional).
prevent bleeding
6. Under estimating shock based on normal conscious
6. Prophylactic platelet transfusion has very little role
level, systolic BP and pulse oximetry (SpO2 95%–
in the management of hemodynamically stable
100%).
dengue patients.

Protocol 16.1: Differentiation of dengue shock and septic shock

* Usually occurs in defervescence period, hence probe for h/o fever in the recent past .
* Shock can recur after correction in the ER, hence warrants close monitoring in wards.

“Men and microbes fight each other for supremacy and survival. Microbes were in existence even before the human
race. They may survive even beyond...”
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 169

References of four intravenous fluid regimens. Clinical Infectious


Diseases.1999;29:787-94.
1. WHO, dengue hemorrhagic fever: Diagnosis, treatment
IP :2nd
196.52.84.10 7. Nhan NT, Phuong CXT, Kneen R, et al. Acute manage-
prevention and control. edition. Geneva:World Health
Organization;1997. ment of dengue shock syndrome a randomized double-
blind comparison of 4 intravenous fluid regimens in the
2. World Health Organizationand the Special Programme for
Research and Training in Tropical Diseases.Dengue guide- first hour. Clinical Infectious Diseases.2001;32:204-13.
line for diagnosis, treatment, prevention and control. New 8. Wills BA, Dung NM, Loan HT, et al. Comparison of three
edition 2009. fluid regimens for resuscitation in dengue shock syndrome.
3. Kalayanarooj S, et al. Early clinical and laboratory indica- N Eng J Med. 2005;353:877-99.
tion of acute dengue illness. Journal of infectious disease. 9. Bunnag T. Accuracy in diagnosis of DHF at observation
1997;176:313-21. room, dengue corner. Thai pediatric journal. 2001:8(2).
4. Gomber S, Ramachandran VG, Satish Kumar, et al. He- 10. Lum L, et al. Preventive transfusion in dengue shock syn-
matological observations as diagnostic markers in den- drome-is it necessary? Journal of Pediatrics. 2003;143:682-
gue hemorhagic fever-a reappraisal. Indian Pediatrics. 84.
2001;38(5):477-81.
11. Gulati S, Maheswari A. Atypical manifestations of dengue.
5. 2010 interim guidelines on fluid management of dengue
Trop Med Int Health. 2007;12(9):1087-095.
Fever and Dengue Hemorrhagic Fever.
12. Handbook for clinical management of dengue-WHO
6. Dung NM, Day NP, Tam DT. Fluid replacement in dengue
shock syndrome: a randomized double-blind comparison 2012.
17
IP : 196.52.84.10

Anaphylaxis

Figure 17.1: Rapid deterioration can occur in minutes if intervention is not immediate (Courtesy: Dr Radhika, Dr Gunda Srinivas).

Learning Objectives
1. Defining anaphylactic shock. 3. Using the pediatric assessment triangle to recognize
2. Pathophysiology of anaphylaxis. anaphylactic shock.
4. Evidence-based management of anaphylactic
shock.

Introduction 1. Sudden and severe vasodilation contributes to relative


hypovolemia, whereas increased vascular permeability
Anaphylaxis is an acute clinical syndrome caused by ex-
results in absolute hypovolemia. The resultant profound
posure to a foreign substance to which the patient has been
loss of effective circulating volume leads to sudden cir-
previously sensitized.1 It is defined as a severe, life-threat-
culatory failure and hypotension. Cardiovascular col-
ening, generalized or systemic hypersensitivity reaction.2
lapse is the commonest prearrest manifestation.
2. Edema of the airway results in lethal airway obstruc-
PATHOPHYSIOLOGY tion (stridor) and bronchospasm (respiratory distress
with wheeze).
Anaphylaxis is a type 1 hypersensitivity reaction mediated
3. Other symptoms include itching, urticaria, sneezing,
by immunoglobulin E (IgE) and IgG4 subclass of antibodies.
conjunctivitis, abdominal pain, vomiting and diarrhea.
A complement-mediated hypersensitivity reaction occurs in
Angioedema manifests as edema of the face, eyes,
allergic response to blood products. Anaphylaxis occurs sec­
tongue and larynx.
ondary to release of chemical mediators from the mast cells.
The exogenous antigen binds to the immunoglobulin located The commonest triggers are, nuts, paralytic agents
on the mast cell. This results in degranulation and release (suxamethonium, vecuronium and atracurium), antibiotics
of mediators such as histamines, bradykinin, leukotrienes, (commonest being, penicillin, cephalosporin, amphoteri­
prostaglandins and thromboxanes. The latter cause various cin, ciprofloxacin and vancomycin), non-steroidal anti-
effects on the skin, mucosa, lining of the respiratory tract, inflammatory drugs (NSAIDs) and Aspirin. Other culprits
blood vessels and the heart. Refer Figure 17.1. are insect stings, contrast media, blood and blood products,
Chapter 17 n Anaphylaxis 171

vaccines, food additives and latex. Exercise, especially af-


ter ingestion of certain foods has also been known to cause Ù
Less severe systemic allergic reactions such as urticaria,
anaphylactic reactions.IP : 196.52.84.10
angioedema or rhinitis should not be described as an
anaphylactic reaction, when compromise of the ABCs
CASE SCENARIO leading to life-threatening complications are not
A 2-year-old child was rushed into the ED, after he de- present.
veloped sudden unresponsiveness. He had been given
Brufen syrup by a practitioner in a nearby clinic for Time of Onset of Anaphylactic Reactions
fever (Figure 17.2).
●● Fatal food reactions cause respiratory arrest after 30–
35 minutes.
●● Insect stings cause collapse from shock in 10–15 min-
utes.
●● Death caused by intravenous medication occur within
5 minutes.
Note: Death has not been documented beyond 6 hours af-
ter contact with the trigger.3

Airway and Breathing


●● Provide oxygen using a non-rebreathing mask.
●● Intubate if labial, lingual swelling, hoarseness or stri-
dor is noted.
Intubation is performed early (rapid, progressive edema
Figure 17.2 Physiological status: Angioedema of the upper can obscure all landmarks, making even bag-valve-mask
airway, respiratory distress with bronchospasm, bradycardia,
hypotensive shock.
ventilation difficult).1 Urgent PAI technique is the method
of choice for securing the airway.
Ù Ù
Anaphylaxis is likely when all of the following three Complete airway obstruction with distortion of anato-
criteria are met2: mical landmarks is the worst scenario encountered by
• Sudden onset and rapid progression of symptoms. the airway manager in the ED.
• Life-threatening airway and/or breathing and/or
circulation (ABC) problems. ●● Paralytic agents should be avoided.1 This precaution is
• Skin and/or mucosal changes (flushing, urticaria, taken to permit spontaneous breathing efforts to ensure
angioedema). ventilation, lest intubation is impossible due to inabil-
ity to intubate.
Exposure to a known allergen for the patient supports ●● Tracheal tubes smaller than calculated for age should
the diagnosis. also be available.
Fiberoptic intubation, blind digital tracheal intubation,
Skin or mucosal changes alone do not constitute as sign needle cricothyrotomy followed by transtracheal ventila-
of an anaphylactic reaction. Sometimes, skin and mucosal tion have been described in securing the airway when con-
changes can be subtle or even absent in up to 20% of re- ventional methods have failed.
actions, where isolated hypotension may be the sole sign
of anaphylaxis. Occasionally, gastrointestinal symptoms
Circulation
such as vomiting, abdominal pain, incontinence have also
been noted.2 1. Secure vascular access and administer isotonic fluid
boluses as much as 60–200 mL/kg of isotonic fluids
172 Section V n Circulation

may be needed to restore peripheral perfusion and Administer chlorpheniramine maleate intramuscularly
blood pressure. or slowly through the intravenous route.
2. Perform the rapidIP cardiopulmonary cerebral assess-
: 196.52.84.10
ment following each bolus to determine, whether the
Ù
Dose of Chlorpheniramine maleate:
child is showing signs of improvement, deterioration > 12 years and adults: 10 mg IM or IV slowly.
or is remaining status quo. 6–12 years: 5 mg IM or IV slowly.
6 months–6 years: 2.5 mg IM or IV slowly.
Epinephrine < 6 months: 250 µg/kg IM or IV slowly.
Administer Epinephrine
Adrenaline is the drug of choice in anaphylaxis. An
Steroids2
α-receptor agonist, it reverses peripheral vasodilation and Steroids may reduce the duration of illness. Little evi-
reduces edema. Its β-receptor activity dilates the bronchial dence is available on the optimal dosing for corticoster-
airways, increases the force of myocardial contraction and oids. The resuscitation council of UK suggest the follow-
suppresses histamine and leukotriene release. Adrenaline ing dosing schedule:
also acts on the β2-adrenergic receptors on mast cells4 and
inhibit ac­tivation.5 Hence, early use of adrenaline attenuates Ù
the severity of IgE-mediated allergic reactions. Adrenaline Dose of hydrocortisone:
seems to work best when given early after the onset of the > 12 years and adults: 200 mg IM or IV slowly.
reaction.6 6–12 years: 100 mg IM or IV slowly.
6 months–6 years: 50 mg IM or IV slowly.
Administer epinephrine deep IM or IV (if intravenous ac­ < 6 months: 25 mg IM or IV slowly.
cess is available): Epinephrine is administered at 0.1 mg/
kg per dose (1:1,000) intramuscularly at 5 minute intervals There is no data to support the use of H2 receptor block-
based on patient’s response. er in the acute resuscitation of a child with anaphy­lactic
Ù
Dose of epinephrine:
shock.11

12 years: 500 µg IM (0.5 mL), i.e. same as adult dose. Ù


Prolonged CPR is advised in anaphylactic cardiac ar­
If child is small or prepubertal: 300 µg (0.3 mL).
6–12 years: 300 µg IM (0.3 mL). rest since the underlying heart and lungs are normal.
6 months–6 years: 150 µg IM (0.15 mL).
< 6 months: 150 µg IM (0.15 mL). PREHOSPITAL CARE
●● Subcutaneous or inhaled routes for adrenaline are not 1. Advice patients with airway obstruction or respiratory
recommended for the treatment of an anaphylactic re­ distress to adopt a position of airway comfort.
action because absorption is inadequate.7,8,9 2. If the victim is feeling faint or unable to sit or stand,
●● Stridor or airway swelling, respiratory distress and or advise him to lie down.
shock: Administer epinephrine intravenously. The rec- 3. Hypotensive patients could rapidly progress to car­diac
ommended IV dose is 0.5 mL/kg (1:10,000 dilution). arrest, if they are in the upright position.12
●● The strength of 1:1000, should not be administered in- 4. Place unresponsive children, who are breathing in the
travenously without dilution. recovery position on their side.
●● If bradycardia or hypotensive shock occurs, initiate
epinephrine infusion at 1–4 µg/kg/minute. ELIMINATION OF TRIGGER
Though arrhythmias are uncommon in children with 1. Discontinuation of drug suspected of causing an ana-
anaphylaxis, cardiac rhythm should be monitored. phylactic reaction (e.g. stop intravenous infusion of a
gelatin solution or antibiotic).
Antihistamines10 2. Early removal of stinger after a bee sting13 and appli-
H1-antihistamine helps to counter histamine-mediated va- cation of ice at the site of sting may slow antigen ab-
sodilation and bronchoconstriction. sorption.
Chapter 17 n Anaphylaxis 173

3. After food-induced anaphylaxis, attempts to make 3. Pumphrey RS. Lessons for management of anaphy-
the patient vomit are not useful and hence not recom- laxis from a study of fatal reactions. Clin Exp Allergy.
mended. 2000;30(8):1144-50.
IP : 196.52.84.10 4. Kay LJ, Peachell PT. Mast cell beta2-adrenoceptors. Chem
4. Observation for 24 hours is recommended, since
Immunol Allergy. 005;87:145-53.
symptoms could recur within 1–8 hours in 20% of pa-
5. Chong LK, Morice AH, Yeo WW, et al. Functional desensi-
tients.
tization of beta agonist responses in human lung mast cells.
Am J Respir Cell Mol Biol. 1995;13(5):540-46.
Key Points
ü 6. Bautista E, Simons FE, Simons KJ, et al. Epinephrine
fails to hasten hemodynamic recovery in fully developed
1. Early recognition and anticipation of deterioration
canine anaphylactic shock. Int Arch Allergy Immunol.
in anaphylaxis crucial to survival. 2002;128(2):151-64.
2. IM epinephrine is life saving. 7. Simons FE, Gu X, Simons KJ. Epinephrine absorption in
3. Early intubation, aggressive fluid resuscitation adults: intramuscular versus subcutaneous injection. J Al-
and epinephrine in appropriate doses and lergy Clin Immunol. 2001;108(5):871-73.
routes mandatory in hypotensive shock due to 8. Song TT, Nelson MR, Chang JH. Adequacy of the epineph-
anaphylaxis. rine autoinjector needle length in delivering epinephrine to
4. Aggressive CPR recommended even if cardiac arrest the intramuscular tissues. Ann Allergy Asthma Immunol.
supervenes. 2005;94(5):539-42.
9. Simons FE, Roberts JR, Gu X, et al. Epinephrine absorp-
tion in children with a history of anaphylaxis. J Allergy
common errors
1. Delayed administration of epinephrine.
û Clin Immunol. 1998;101(1 1):33-37.
10. Simons FE, Gu X, Johnston LM, et al. Can epinephrine
inhalations be substituted for epinephrine injection in
2. Failure to give deep IM epinephrine. children at risk for systemic anaphylaxis? Pediatrics.
3. Initiating dopamine for anaphylactic shock. 2000;106(5):1040-44.
11. Sheikh A, Ten Broek V, Brown SG, et al. H(1)-antihista-
REFERENCES mines for the treatment of anaphylaxis: Cochrane system-
atic review. Allergy. 2007;62(8):830-37.
1. Anaphylaxis, Circulation, Journal of the American Heart 12. Lin RY, Curry A, Pesola GR, et al. Improved outcomes
Association. 2005;IV 143-IV 145. in patients with acute allergic syndromes who are treated
2. Johansson SG, Bieber T, Dahl R, et al. Revised nomencla- with combined H1 and H2 antagonists. Ann Emerg Med.
ture for allergy for global use: Report of the Nomenclature 2000;36(5):462-8.
Review Committee of the World Allergy Organization, Oc- 13. Visscher PK, Vetter RS, Camazine S. Removing bee stings.
tober 2003. J Allergy Clin Immunol. 2004;113(5):832-36. Lancet. 1996;348(9023):301-02.
18
IP : 196.52.84.10

Cyanotic Spell

Figure 18.1: Simple knee-chest position plays an important role in the management of cyanotic spell

Learning Objectives
1. Pathophysiology of cyanotic spell. 3. Management of cyanotic spell in the ED.
2. Using the rapid cardiopulmonary assessment
and the pediatric assessment triangle to identify
severity of spell.

INTRODUCTION out flow obstruction is absent during the spell due to reduced
antegrade flow across the muscular obstruction. Children
Cyanotic spell is also known as hypercyanotic spell, ‘TET’ become severely cyanotic, tachypneic and lethargic. With
spell, hypoxic spell, paroxysmal hyperpnea, anoxic spell the development of meta­bolic acidosis, pulmonary vascular
and blue spell. Approximately, one fourth of children with resistance increases and systemic vascular resistance falls.
cyanotic congenital heart diseases develop this medical Cardiac output becomes compromised due to myocardial
emergency (Figure 18.1). Though common in tetralogy ischemia. Impending collapse and death can ensue. Children
of fallot (TOF), it is also encountered in other cyanotic with iron deficiency anemia have a pre­disposition to the oc­
congenital heart diseases with decreased pulmonary blood currence of cyanotic spells.
flow (PBF) such as tricuspid atresia with restrictive VSD
and VSD with severe valvular pulmonic stenosis.

PATHOPHYSIOLOGY
The hypercyanotic spell1,2 is characterized by a sudden and
striking decrease in the oxygen saturation (Figures 18.2 and
18.3) due to acute and complete or near complete obstruction
of the subpulmonary outflow tract. Agitation and decreased
hydration can exacerbate dynamic infundibular obstruction.
Ejection systolic murmur produced by the right ventricular Figure 18.2: Pathophysiology of cyanotic spell
Chapter 18 n Cyanotic Spell 175

CASE SCENARIO 1
A 3-month-old infant is brought with history of inces-
IP : 196.52.84.10 sant cry, breathlessness and increasing cyanosis. He is
being evaluated for cyanotic congenital heart disease at
the cardiology department (Figures 18.4 and 18.5).

Figure 18.3: Note the severe cyanosis in this infant who is receiving
100% oxygen via the flow inflating bag. The knee-chest position is
being maintained throughout resuscitation.

Clinical Features
Cyanotic spells typically occur in the morning, follow­ing Figure 18.4: Note that one team member is dedicated to holding
the knee-chest position during resuscitation of cyanotic spell.
crying, feeding and defecation (Box 18.1).
Also note that the airway is kept open and oxygen is being
Spells are characterized by paroxysm of: administered.

●● Hyperpnea (rapid and deep respiration), irritability,


prolonged or inconsolable crying.
●● Diaphoresis.
●● Increasing cyanosis.
●● Decreasing intensity or disappearance of the heart
murmur.
●● A severe spell may lead to syncope, limpness, convul­
sions, cerebrovascular accidents and even death.
●● In the early stages, an older child may spontaneously
assume the squatting (or knee-chest) position in order
to alleviate symptoms.
Box 18.1: Precipitating factors of cyanotic spell
Figure 18.5 Physiological status: Maintainable airway, effortless
Crying tachypnea, normotensive shock with no evidence of cardiac
Defecation failure, with altered mental status.
Increased physical activity
Dehydration
Anemia
Management
Anxiety Treatment is focused on decreasing pulmonary resistance
Fever and in­creasing systemic vascular resistance. This would
Pain promote left to right flow across the ventricular septal de­
fect and subsequently into the subpulmonary outlet.
Age
Prehospital Management3
●● 1 month–12 years (peaking between 2–4 months).
Ù
Teach parents with a child prone to cyanotic spells to
Duration of the Spell
place him in knee-chest position.
●● This may vary from minutes to several hours.
176 Section V n Circulation

This maneuver increases systemic vascular resis­ Its mechanism of action is not clear. It probably acts by
tance and promotes systemic venous return to the right reducing spasm of the right ventricular outflow tract and
heart. This will theoretically increase intracardiac shunt­
IP : 196.52.84.10 slowing the heart rate.
ing from left-to-right across the interventricular com­
Esmolol, an ultrashort acting beta blocker is an alter­
munication, as well as increase the preload of the right
native to propranolol. This is administered as a bolus of
ventricle.
0.5–1.0 mg/kg IV, followed by an infusion of 100–300 µg/
●● Stabilize the airway with the head tilt-chin lift maneu­ kg/min.
ver. Provide oxygen using the flow inflating ventilation
device (reduce risk of pulmonary edema during shock
Vasoconstrictors
correction).
●● Oxygen decreases peripheral pulmonary vasoconstric­ Phenylephrine infusion increases SVR, thereby reducing
tion and improves oxygenation once flow of blood to the right-to-left shunt.
the lungs is re-established. Dose: 3 mg/kg is diluted in 50 mL NS and infused
●● Intubation may be needed, if the cyanotic spell is re­ at 1 mL/kg/h to provide 1 μg/kg/min. The infusion may
fractory to management. be increased up to 5 μg/kg/min until oxygen saturations
●● Place the child in a knee-chest position throughout re­ improve.
suscitation in order to trap venous return in the legs Emergency surgery to repair the defect or to establish
thus increasing the SVR (Figure 18.4). systemic to pulmonary artery anastomosis should be con­
●● Secure intravenous access to administer fluids. sidered in refractory spells.
●● Fluids will improve right ventricular preload.
●● If shock is noted, administer 2.5–5 mL/kg NS up to
Ù
Avoid the use of digoxin and epinephrine as these drugs
a maximum of 20 mL/kg at the rate of 1 mL/kg/min­ may exacerbate the obstruction to right ventricular
ute, whilst monitoring for signs of PE as per the PEMC outflow and cause further deterioration.
guidelines.
●● Administer Morphine at a dose of 0.1–0.2 mg/kg/dose
intravenously or subcutaneously. It decreases release of Prevention
catecholamines. It also increases the time for right ven­ ●● Chronic oral therapy with propranolol 1–2 mg/kg/dose
tricular filling by de­creasing the heart rate and promoting q 6 h has been shown to decrease the frequency of the
relaxation of infundibular spasm. paroxysm. Propranolol stabilizes vascular reactivity
●● Administer sodium bicarbonate 1 mEq/kg IV slowly
of the systemic arteries thereby preventing a sudden
after dilution (1:1) at the rate of 1 mL/kg/minute. Sub­
decrease in SVR. However, this is discouraged in the
sequent doses are infused based on pH.
newborn, since it may cause severe cardiac depression.
Ù
Ensure adequate oxygenation and ventilation before
●● Prophylactic iron therapy is useful to prevent recur­
rence of cyanotic spell.
administering sodium bicarbonate. ●● Palliative shunt procedure is performed in children
with severe TOF for whom total correction may not
Most of the cyanotic spells respond to the above mea­ be possible.
sures. If not, the following medications are given: ●● Refer for early corrective surgery. Early identification
has become possible due to wide spread availability of
Beta Blockers pediatric cardiothoracic surgical facilities.

Propranolol is infused in a dose of 0.05–0.2 mg/kg/dose IV CYANOTIC SPELL WITH


over 4–5 minutes.
CARDIOGENIC SHOCK
Ù
It is not given in the neonate since it may cause severe It is not uncommon for very young infants with com­
cardiac depression. plex cyanotic heart diseases to have increased pulmonary
blood flow. These infants present with cyanotic spell with
Chapter 18 n Cyanotic Spell 177

cardiogenic shock. Recognition of this condition is im­


portant since the outcomes may not be as favorable as in
simple ‘tet spell’. Increased
Key Points
1. Maintenance of knee-chest position throughout
ü
IP : pulmonary blood flow can pre­
196.52.84.10
cipitate cardiac failure. The latter manifests as increasing resuscitation is key to successful outcome.
cyanosis, respiratory distress, shock with hepatomegaly. 2. Baseline pulse oximeter readings will suggest severe
Bedside echocardiography will help in finding out the ex­ hypoxia.
act cardiac malformation. 3. Cyanotic spell secondary to uncomplicated TOF
usually resolves with emergency resuscitation.
4. Cyanotic spell due to complex cyanotic heart disease
TREATMENT coexists with cardiac failure.
Management is similar to cyanotic spell. However, smaller
aliquots of fluid should be administered due to enhanced
risk of pulmonary edema (unlike TOF). Jackson-Rees cir­
common errors
1. Administration of digoxin.
û
cuit is very helpful in the management of such children
with associated pulmonary edema as explained in Chapter 2. Expecting normalization of saturations.
3. Failure to resuscitate severe cyanotic spell presenting
5. Inotropes and early intubation can tide over the crisis,
in cardiac arrest aggressively. Many will respond
but immediate surgical palliation will be needed for suc­
very well to resuscitation.
cessful outcomes. Refer Protocol 18.1.
178 Section V n Circulation

References
1. Roekens CN, Zuckerber AL. Emergency management
IP : 196.52.84.10 of hypercyanotic crises in tetralogy of Fallot. Annals of
Emergency Medicine. 1995;25(2):256-58.
2. Kothari SS. Mechanism of cyanotic spells in tetralogy
of Fallot-the missing link? International Journal of Car­
diology. 1992;37(1):1-5.
3. Bailliard F, Anderson RH. Review Tetralogy of
Fallot Orphanet Journal of Rare Diseases 2009, 4:2
doi:10.1186/1750-1172-4-2.
Protocol 18.1: PEMC approach: Cyanotic congenital heart disease
19
IP : 196.52.84.10

Hypertensive Emergencies

Figure 19.1: Hypertension in children can present as an emergency with significant morbidity (Courtesy: Dr Radhika R; Dr Devi R)

Learning Objectives
1. Defining hypertensive emergency and urgency. 3. Antihypertensive drugs used in the management of
2. Using the pediatric assessment triangle to hypertensive emergency.
identify severity of illness in a child with severe
hypertension.

INTRODUCTION Table 19.1: Cut off levels for hypertension by age1

High blood pressure is often noted in seriously ill children Age Severe hypertension Hypertensive crisis
on arrival into the ED. It occurs as a compensatory re­ Neonate
sponse to shock. Occasionally, hypertension is responsible 1 week SBP > 106 mm Hg
for cardiac failure, seizures and visual loss! 2–4 week SBP > 110 mm Hg
Infant
Drugs to reduce BP in shocked children can kill. On
the contrary, failure to reduce BP in primary hypertension < 2 year > 118/82 145/95
could also be dangerous (Figure 19.1). 3–5 year > 124/84 150/95
6–9 year > 130/86 160/100
Recognition and appropriate approach is essential to
10–12 year > 134/90 165/105
tide over the crisis of hypertension.
13–15 year > 144/92 175/110
Literature suggests that the prevalence of hypertension 16–18 year > 150/98 185/120
in the pediatric population is estimated at 1%–2%. Though (Data from report of the 2nd Task Force on BP Control in Children – 1987-
uncommon in children, the emergency physician may en­ Pediatrics 1987;79:1-25 and Burg Fb, Ingelfinger JR, Wald ER. Current
counter hypertensive emergencies in the ED. Pediatric Therapy. Philadelphia: WB Saunders. 1993;14:158-64)

The second task force on BP control in children defined Severe Hypertension


hypertension as systolic and or diastolic BP persistently
above the 95th percentile (Table 19.1). BP above the 99th percentile for age and sex.
180 Section V n Circulation

Hypertensive Emergency In the ED, an abnormally high BP should be confirmed


after reassessment, when the child is quiet. A patient with
It describes a situation in which, elevated BP is associated blood pressure levels greater than the 95th percentile in a
IP : 196.52.84.10
with evidence of secondary organ damage such as hyper­ physician’s office or clinic who is normotensive outside a
tensive encephalopathy or acute left ventricular failure. clinical setting has ‘white coat hypertension’. Ambulatory
blood pressure monitoring (ABPM) is usually required to
Hypertensive Urgency make the diagnosis.5
The elevated BP is potentially harm­ful, but lacks evidence A focused history, rapid cardiopulmonary assessment
of end-organ damage or dys­function. and a thorough physical examination to identify signs sug­
gestive of causes of hypertension is essential in the evalu­
ation (Refer Table 12.2).
Malignant Hypertension
Malignant hypertension is characterized by marked eleva­ CASE SCENARIO
tion in systolic and/or diastolic BP.
A 10-year-old child is being evaluated for periorbital
●● ≥ 160/ ≥ 105 in children < 10 years. puffiness and cola-colored urine. He is rushed into the
●● ≥ 170/ ≥ 110 in children > 10 years. ED with history of sudden onset of severe headache and
loss of bilateral vision. Even as the ophthalmologist is
It is often associated with spasm and tortuosity of the
evaluating his fundus, he has a brief generalized tonic-
retinal arteries, papilledema, hemorrhages and exu­dates.
clonic convulsion (Figures 19.2 and 19.3).
Some patients may have an acute onset and severe el­
evation of BP. They experience severe headache, altered
sensorium, seizures and visual disturbances. MRI and CT
shows evidence of vasogenic cerebral edema in the occipi­
tal and parietal regions. This combination of symptoms is
known as ‘Posterior reversible encephalopathic syndrome
(PRES)’.
Such patients are judged to be in imminent hy­pertensive
crisis and are treated as true emergencies.2
For purposes of evaluation and treatment, BP measure­
ments at or above ‘severe’ levels (above the 99th percentile
for age and sex) should be considered as hypertensive ur­
gency even in the absence of symptoms.
The 2004 report on high BP in children and adoles­
cents reiterates these definitions, but states that children Figure 19.2 Physiological status: Neurogenic stridor, cardiac
with blood pressures greater than 5 mm Hg above the 99th failure, hypertension, status epilepticus with cortical blindness
percentile require prompt treatment.3
History
Ù
Accurate BP measurement requires the use of the ap­ Ask for:
propriate sized cuff and equipment and the proper tech­ ●● Symptoms referable to the renal system. (kid­neys are
nique. The width of the inflatable bladder should be at the commonest cause of hypertension in pediatric age
least 40% of the arm circumference at a point midway group).
between the acromion process and the olecranon ●● Flushing, sweating, palpitations, fever and weight loss
process. For such a cuff to be optimal for an arm, the may indicate presence of pheochromocytoma.
cuff bladder length should cover 80%–100% of the ●● Significant family history of hypertension points to es­
circumference of the arm.4 sential hypertension as etiology. Ingestion of certain
drugs could increase BP.
Chapter 19 n Hypertensive Emergencies 181

●● Acute onset breathlessness suggest cardiovascular abdominal bruit or mass, differential pulses and BP record­
compromise. ing in all four limbs help to identify etiology of hyperten­
●● Visual changes, seizures, headache and vomiting sug­
IP : 196.52.84.10 sion. Fundoscopy should be performed looking for hemor­
gest disturbance to the central nervous system (Box rhage, papilledema or infarcts.
19.1).
Any increase in blood pressure that is sufficiently acute
Box 19.1: Hypertensive emergencies that need
immediate treatment or elevated to cause symptoms should be considered life-
threatening.
●● Hypertensive encephalopathy
●● Hypertension associated with acute heart failure or Laboratory Studies
pulmonary edema
●● Acute renal failure Complete blood count (CBC), electrolytes, blood urea ni­
●● Stroke trogen (BUN), creatinine, uric acid, urinalysis, urine cul­
●● Adrenergic crisis (pheochromocytoma)
ture, chest X-ray (CXR), ultrasonogram (USG) abdomen,
●● Hypertension with intracranial bleed
●● Hypertension-induced blindness electrocordiagram (ECG) and ECHO are needed in all
●● Myocardial infarction (rare in children) children. Further studies should be individualized and may
be done once the BP is controlled.

Physical Examination Management of Hypertensive Emergency


A rapid cardiopulmonary and cerebral assessment will help Principles
to recognize features of cardiac failure with or without fea­
tures of encephalopathy. ●● Provide oxygen via the flow inflating ventilation de­
vice.
A more profound fall in mental status or seizures might ●● Secure vascular access. Administer furosemide 1–2 mg/
point towards hypertensive encephalopathy. Evidence of kg intravenously (slowly), if cardiac failure is noted.
retinopathy, neurocutaneous markers, cushingoid facies,

Figure 19.3: Summary of the approach to a child with severe hypertension in the ED
182 Section V n Circulation

●● If systolic blood pressure has not responded to furo­ Table 19.3: Life-threatening causes of hypertension
semide, consider Labetalol.
Infancy Coarctation of the aorta, valvular insufficiency,
●● If hypertension does
IP :not resolve despite Labetalol,
196.52.84.10 congenital adrenal hyperplasia, renal vascular
consider drugs mentioned in Figure 19.3.
disease, renal parenchymal disease
Treatment must be rapid, but cautious. High BP must Childhood Renal parenchymal disease, renal vascular
be reduced gradually. The goal in management is the re­ disease, coarctation of the aorta,
duction of 10%–25% of the initial BP in the first 1–2 hours pheochromocytoma, increased intracranial
of therapy. A rapid fall in BP could cause hypoperfusion pressure, bacterial endocarditis, drug-induced/
of vital organs resulting in iatrogenic morbidity. Long- toxicologic
standing hypertension is often compensated by altering Adolescence Renal parenchymal disease, pheochro-
cerebral vascular autoregulatory mechanisms. When BP mocytoma, toxemia of pregnancy, drug-
is suddenly dropped iatrogenically, these compensatory induced/toxicologic
mechanisms are overwhelmed, the consequences being
deleterious to the patient. Hence, in order to reduce BP Nitroprusside
gradually, intravenous hypertensive drugs need to be ad­
ministered (Figure 19.1). Nitroprusside is the drug of choice in hypertensive crisis.
It has a rapid onset of action and lasts only as long as the
●● Standard protocol for status epilepticus. infusion is continued, enabling precise control of BP. A
●● Consider early use of Aspirin, if acute visual loss oc­ vasodilator of both venous and arterial vasculature, an ar­
curs in the hypertensive child (after ruling out magnetic
terial line is needed for its monitoring, the drug is prefer­
resonance imaging (MRI) proven intracranial bleed).
ably ad­ministered through a central line using an infusion
●● CT using contrast may be more easily available. How­
pump. The bottle and intravenous tubing should be cov­
ever, it should be avoided if child has elevated urea or
ered by a black sheet to protect from light. The solution
creatinine.
should be changed every 24 hours. Since its use requires
●● Monitor BP and urine output from the out s­ et.
intra-arterial monitoring it is not a drug recommended for
●● Insert an arterial line for monitoring intra-arterial pres­
use in the ED.
sure if nitroprusside, diazoxide or nicardipine are being
used. Dose: 0.3–8 µg/kg/min (Table 19.2).
Blood thiocyanate levels should be monitored if the
Pharmacotherapy of infusion lasts for more than 24 hours. The rate of infusion
Hypertensive Emergencies is maintained at 10 µg/kg/min for a duration longer than 6
The choice of drug depends on the severity of the patient’s hours. It is discontinued, if thiocyanate levels exceed 10
hypertension, current medications, the suspected cause of mg/dL. If toxic levels are noted, thiosulfate is the antidote
hypertension and the organs involved (Table 19.3). of choice.

Table 19.2: Drugs used for the treatment of hypertensive emergencies

Drug Dose Onset Peak Duration


Sodium 0.3–8 µg/kg/min Within second 1–2 minute During
nitroprusside IV infusion only
Esmolol IV 100–500 µg/kg bolus over 1–3 min then 50–300 µg/kg/min Immediate 1–2 minute 10–30 minute
Labetalol IV 0.2–1 mg/kg bolus followed by 0.25–1.5 mg/kg/h 2–5 minute 20–30 minute 2–6 hour
Diazoxide IV 1–5 mg/kg/dose max of 150 mg 1–5 minute 2–4 minute 4–12 hour
Hydralazine IV 0.1–0.5 mg/kg/dose maximum 20 mg 5–30 minute 20–40 minute 4–12 hour
Enalaprilat IV 5–10 µg/kg/dose Up to 60 minute 3–4 hour 4–6 hour
Nifedipine (Oral) 0.25–0.5 mg/kg/dose 5–15 minute 30–60 minute 3–6 hour
Chapter 19 n Hypertensive Emergencies 183

Labetalol Hydralazine
Labetalol has α and β blocking effects. The β-adrenergic Hydralazine causes relaxation of smooth muscle of both
IP : potent.
blockade activ­ity is more 196.52.84.10
Dosing is not affected the ar­teries and veins. It is less potent than other agents.
by poor renal function. It has been reported to be effec­ Dose: 0.1–0.5 mg/kg/dose.
tive in the management of severe hy­pertension that results
from pheochromocytoma and co­arctation of the aorta. It is
Esmolol
also used in the treatment of hypertensive crises in patients
with end-stage renal disease. Both intravenous and oral Esmolol is given as a loading dose of 100–500 µg/kg IV
preparations are available. over 1–2 minutes, followed by an infusion of 50–300 µg/
kg/minute. It is useful in hypertensive crisis following sur­
Dose: 0.2–1.0 mg/kg/dose intravenously followed by an gery for coarctation of aorta.
infusion of 0.25–1.5 mg/kg/h.
Side effects are dizziness, gastrointestinal upset, head­ Diazoxide
ache, urinary retention, bradycardia and bronchospasm in Diazoxide is given as a bolus of 1–3 mg/kg. It is very ef­
asthmatics. It is therefore contraindicated in asthmatic pa­ fective in rapidly lowering the blood pressure. However, it
tients. can cause precipitous hypotension and repeated boluses of
1 mg/kg may be preferable to a higher initial dose.
Nicardipine
Phentolamine
Nicardipine is a calcium channel blocker that can be ad­
ministered intravenously. It acts by causing vasodilata­ Phentolamine with its rapid onset of action and alpha
tion. blocking effect is useful in pheochromocytoma. The high
risk of hypotension after the primary lesion (e.g. pheochro­
Dose: Infusion at the rate of 0.5–3 µg/kg/min. mocytoma) is excised, which should not be forgotten. Care
Side effects are headache, tachycardia, dizziness, nau­ should be exercised and the surgeons should be alerted to
sea and vomiting. It is contraindicated in in­tracranial hem­ this possibility.
orrhage (ICH) as it increases cerebral blood flow. Dose: 0.1 mg/kg/dose IV (max 5 mg).

Nifedipine Enalaprilat
It is a calcium channel blocker with powerful vasodila­ Enalaprilat (intravenous form of enalapril) has been ad­
tor activity resulting in a decrease in peripheral vascular ministered as 5–10 µg/kg/dose. It has been used in adult
resistance. Route of administration is oral (bite and swal­ hypertensive emergencies with good results. However,
low). The effectiveness of the drug is due to its absorp­ studies of its use in children are limited. Little is known of
tion from the gastrointestinal tract. An exact dose may its side effects in children.
be difficult to administer especially when given by the
sublingual route. Fenoldopam
Dose: 0.25–0.5 mg/kg/dose, (max 10 mg). Fenoldopam is a selective dopamine agonist, causing va­
sodilation of the renal, cerebral, coronary and splanchnic
It is contraindicated when the child has an intracranial
vasculature. Infusion rates of 0.1–0.2 µg/kg/min have been
bleed.
used in children. Side effects include reflex tachy­cardia,
Ù raised intracranial pressure (ICP) and increased intra-ocu­
Ideally, Sodium Nitroprusside should be used to lar pressure. Experience in children is limited.
gradually reduce high blood pressure. This drug
mandates intra-arterial monitoring. Hence, Nifedipine Hypertensive Urgency6
is used as an alternate agent in settings without access
to intra-arterial monitoring. Administer oral antihypertensive agents to resolve high BP
presenting as hypertensive urgency.
184 Section V n Circulation

Ensure that one third of the total planned blood pres­


3. Hypertensive urgency is severe hypertension without
sure reduction is done during the first 6 hours, another third
end-organ damage.
during the next 24–36 IPhours and the final third during the
: 196.52.84.10 4. Treatment goals are to lower BP gradually in a safe
next 24–96 hours or even longer.
and effective manner.
After administration of the anti­hypertensive agent, ob­ 5. The choice of medication depends on the side effect
servation for adverse effects such as orthostasis is essential profile and physician’s familiarity with the drug.
for at least 4–6 hours.
Discharge with the same medications that were used to
treat hypertension in the ED.
common errors
û
1. Failure to realize that most children with early
Although, high BP is an emergency, avoid treating it compensated shock have elevated BP.
immediately. Often high BP in critically ill children is a 2. Rushing to administer furosemide or nifedipine in
compensatory response. children with increased BP and shock can precipitate
cardiac arrest.
●● Children presenting with septic shock or shock second­
ary to scorpion sting, etc. often have high systolic blood
pressure. As shock is resuscitated, BP normalizes. References
●● High BP in children presenting with non-traumat­ic 1. Julie R Ingelfinger. Evaluation and treatment of hyperten­
coma or head injury indicates presence of raised ICP. sion in children. In: Thomas W Smith (Ed). Cardiovascular
Treatment should be focused on providing controlled therapeutics a companion to Braunwald’s heart disease.
WB Saunders. Company; 1996. pp. 515-26.
ventilation.
●● High blood pressure may be noted in the initial half 2. Hypertensive crises. In Textbook of Paediatric Intensive
Care, 4th edition. Rogers MC (Ed): Baltimore, Williams
hour of status epilepticus. As SE resolves, BP normal­
and Wilkins. 2009.
izes.
3. Erika Constantine, James Linakis. The assessment and
Drug therapies to bring down blood pressure in these management of hypertensive emergencies and urgencies in
situations can have lethal consequences. Avoid rushing to children. Pediatic Emergency Care. 2005;21(6):391-96.
administer antihypertensive drug in the ED. High blood 4. Gomez-Marin O, Prineas RJ, Rastam L. Cuff bladder width
pressure is more commonly the result and not the cause of and blood pressure measurement in children and adoles­
cents. J Hypertens. 1992;10:1235-41.
the emergency in the critically ill child.
5. National High Blood Pressure Education Working Group
Key Points
ü on High Blood Pressure in Children and Adolescents. The
Fourth Report on the Diagnosis, Evaluation, and Treatment
1. Persistence of high BP after correction of hypoxia of High Blood Pressure in Children and Adolescents. Pedi­
and shock should be evaluated for hypertension. atrics. 2004;114;555-76.
2. Hypertensive emergency is characterized by severe 6. Srinivasan Suresh, Prashant Mahajan, Deepak Kamat.
hypertension with end-organ injury. Emergency management of pediatric hypertension. Clin
Pediatr (Phila): 2005;44;739.
Section VI
IP : 196.52.84.10

Disability
IP : 196.52.84.10
Approach to Decreased Level
20
IP : 196.52.84.10

of Consciousness

Figure 20.1: Child presenting with cardiogenic shock, coma with raised ICP and uncal herniation being successfully resuscitated

Learning Objectives
1. The risk of failing to recognize early decrease in 3. Step-wise approach to evaluate decreased level of
level of consciousness. consciousness in children.
2. Case-based management of non-traumatic coma. 4. Need to correct shock in the presence of raised
ICP.
5. Investigations in management of coma.

INTRODUCTION
Many acutely ill children are not fully conscious. Most
Ù
Based on evidence that even early decrease in the level
make a full neurological recovery as the underlying cause is of consciousness may be catastrophic if not recognized,
treated, but considerable skill is required to distinguish the this group advocated that evaluation and management
group at high-risk of further deterioration, leading either to should be initiated when the GCS dropped to less than
death or to severe handicap1 (Figures 20.1 and 20.2). 15 or ‘Responsive to voice’ in the AVPU scale.
Ù Recognition of early fall in mental status viz ‘Responsive
The Pediatric Accident and Emergency Group in the
United Kingdom reported that if the Glasgow Coma Scale to voice’ poses a challenge in all ages. In precommunicative
(GCS) was less than 12 in children between 1 month and children, early fall in mental status is best confirmed by ask­
18 years of age for greater than 6 hours, mortality was ing the mother triage questions (See Chapter 1).
as high as 40%.2 This definition was not applicable for Children of any age who are restless and talking un-
children with learning disabilities whose usual GCS was intelligibly have a verbal score of 2 and are considered to
less than 15, critically ill neonates or children with a be deeply unconscious. These children are at high-risk of
known diagnosis or with a definite treatment plan. catastrophic deterioration.3
188 Section VI n Disability

IP : 196.52.84.10

Figure 20.2: A typical scene in a PED where most seriously ill


children present with decreased level of consciousness. The
etiologies for ALOC in this picture are; hypoxia, shock, myocardial Figure 20.4 Physiological status: Neurogenic stridor, respiratory
dysfunction and non-convulsive status epilepticus. Time sensitive, fail­ure, bradycardia, cardiogenic shock, hypertension with non-
goal-directed management of these factors could often result in convulsive status epilepticus, raised intracranial pres­sure and
neurologically intact survival. uncal herniation.

Ù Ù
At initial presentation, it is preferable to err on the side Children presenting with altered level of consciousness
of recording a lower score, as it is easier to withdraw have several simultaneously occurring problems that
treatment from a child who is improving than to need concurrent management!
resuscitate one who deteriorates. • Hypoxia
• Shock
If altered mental status is doubtful, it is best to treat • Myocardial dysfunction
than to wait for overt clinical signs to develop. Provide • Prolonged convulsion, postconvulsive state
oxygen, administer the first bolus and correct documented • Sepsis, intracranial infection
hypoglycemia. A clearer picture will emerge, providing • Raised ICP
clues towards identifying the etiology of decreased level • Metabolic illness (dyselectrolytemia), hypoglycemia,
of consciousness. ketosis, etc.
• Trauma
CASE SCENARIO • Hypertension
• Cause unknown—toxins.
A 5-year-old boy was brought with history of fever, pro-
gressive lethargy and posturing for 3 days. He had been
vomiting several times since the morning. His tempera- Ù
ture was 40°C (Figures 20.3 and 20.4). A simple focused history should be obtained
simultaneously as assessment and resuscitation are in
progress.

●● Convulsions or posturing?
●● Progressive drop in consciousness such as incessant
cry, lethargy, more sleepy than usual?
●● Fever?
●● Breathlessness?
●● Vomiting?
●● Headache?
●● Length of symptoms?
●● Previous infant death in the family?
Figure 20.3: Note posturing in this unresponsive boy ●● Ingestion or availability of drugs at home?
Chapter 20 n Approach to Decreased Level of Consciousness 189

Box 20.1: Monitor during resuscitation ●● Thiopental is cerebroprotective and consequently the
induction agent of choice.
●● Airway
●● Vecuronium is the paralytic agent of choice, since suc-
●● Respiratory rate, workIPof :breathing
196.52.84.10
(WOB)
cinylcholine is known to worsen ICP.
●● Heart rate, perfusion, BP, liver span
●● Even if a comatose child appears to be breathing, con-
●● AVPU assessment every 15 minute
●● Eye position, eye movement, pupils
trolled mechanical ventilation should be instituted ear-
●● Monitor urine output
ly to avoid washing out of CO2. While oxygenation is
●● Temperature maintained at normal levels, PaCO2 is maintained in the
●● O2 saturations low 30s. Pulse oximeter and end tidal CO2 monitoring
●● Electrocardiography (ECG) enable non-invasive monitoring of gases in the PED.
●● BP
●● End tidal CO2 Indications for intubation
in comatose children
Initial management priorities ●● The Glasgow Coma Scale (GCS) is 12.
●● Deterioration in the GCS.
Airway and Breathing
●● Unstable airway (intubation mandatory, even if the
In the unresponsive child, loss of tone of the oropharyn­ GCS is higher).
geal muscles causes falling back of the tongue resulting ●● Respiratory depression (respiratory drive may be com-
in airway obstruction. Furthermore, loss of airway protec- promised in raised ICP).
tive reflexes lead to pooling of secretions. An unprotected ●● Neurogenic hyperventilation (hyperventilation may be
airway itself could worsen underlying hypoxia, shock, car- a sign of midbrain involvement).
diac failure, status epilepticus and raised ICP (Box 20.1). ●● Asymmetric or dilated pupils.
●● Evidence of herniation.
Clinically, airway obstruction manifests as stridor viz
neurogenic stridor, which is relieved by the following ma-
Circulation
neuvers:
Correct shock with NS (fluid of choice). If respiratory dis-
●● Open airway by head tilt-chin lift maneuver. tress or failure with or without signs of cardiac dysfunction
●● Use large bore suction cannula to rapidly clear oropha- are identified on arrival, the smaller boluses (5–10 mL/kg)
ryngeal secretions. are administered.
●● Provide oxygen using the CPAP device.
●● Call for intubation tray using SOAPME protocol. If septic shock is recognized (e.g. meningitis or en-
●● Intubate using ICP precautions. cephalitis) in the comatose child, larger vol­umes (60–80
mL/kg) may be warranted to correct shock. Close moni-
Ù toring for pulmonary edema and hepato­megaly is neces-
Raised ICP may be aggravated by painful or noxious sary during fluid resuscitation shock due to sepsis. If coma
interventions even though the child appears deeply was due to DKA or isolated head trauma, smaller volumes
comatose. Since the process of intubation can stimulate (10–30 mL/kg) may be warranted to resolve shock.
the gag reflex and aggravate ICP, drugs are used which Raised ICP is not a contraindication for shock correc-
blunt the deleterious effects of intubation. tion. Indeed, it signals the need for maintenance of high
mean arterial pressure (MAP).
Anesthetic drugs used for intubation for children at risk of
developing ICP are the following: Ù
Increased systemic BP is a physiological compensatory
●● Lidocaine is the premedication used to blunt­gag by acting response to maintain cerebral perfusion pressure when
on the sensory pathway of the glossopharyngeal nerve. ICP increases! BP is maintained at the 95th percentile
●● Atropine reduces vagal-induced bradycardia. Brady- for age/height in order to maintain cerebral perfusion
cardia in a shocked child provides clue that raised ICP pressure (CPP) in the face of an elevated ICP.
coexists.
190 Section VI n Disability

●● Antihypertensive drugs can kill, if used to reduce blood ●● Evaluation for pupillary inequality helps recognize
pressure in a child with ICP! herniation.
●● Infusing hypotonicIP fluids (5% or 10% dex­trose) can
: 196.52.84.10 ●● Examine the fundus for additional clues.
lead to cerebral edema in children presenting with ●● If seizures are refractory to anticonvulsants, evaluate
ICP. electrolytes and correct as shown in Table 20.3.
●● Documented hypoglycemia is corrected with a bolus ●● Coma not explained by the presence of seizure activity
dose of dextrose. If age is greater than 4 weeks, ad­ needs to be evaluated as discussed below.
minister 5 mL/kg IV of 10% dextrose as bolus. If age
of the child is less than 4 weeks, administer 2 mL/kg IV Recognizing Depth of Coma4
10% dextrose bolus.
The Glasgow Coma Scale (Table 20.1) was designed to as-
●● The presence of a very high glucose level may point to
sess the depth of post-traumatic brain injury coma in adults
a diabetic ketoacidosis (refer to Chapter 34 on DKA).
and children beyond the age of 5 years. However, for chil-
dren be­tween 9 months and 5 years of age, a modified mo­
Disability tor and eye opening scales has been recommended.
Clinical Seizures Motor response is elicited by applying supraocular
Eye deviation, nystagmus and eyelid twitching, character- pressure (and looked for flexion and extension).
istic of non-convulsive status epilepticus, pinpoint a treat- It may also be assessed by applying pressure over the
able etiology of coma. Unrecognized seizure activity in- nail bed using a pencil. Motor response is M5 if the infant
crease ICP and could precipitate cerebral herniation. They responds by withdrawing. There may be need for flexibil­
may be due to the excitatory toxic and ischemic mecha- ity due to overlap between the age groups. This method is
nisms of secondary brain damage. discussed below:

Table 20.1: Modified Glasgow Coma Score

Modified Glasgow Coma Score


Score Infant < 2 year Child 2–5 year 6 year–adult
Eyes
4 Open Open Open
3 To voice To voice To voice
2 To pain To pain To pain
1 No response No response No response
Verbal
5 Coos, babbles Appropriate words Oriented and alert
4 Irritable cry, consolable Inappropriate words Disoriented
3 Cries persistently to pain Cries/screams Inappropriate words
2 Moans Grunts Incomprehensible sounds
1 No response No response No response
Motor
6 Spontaneous movement Spontaneous movement Follows commands
5 Withdraws to touch Localizes to pain Localizes to pain
4 Withdraws to pain Withdraws to pain Withdraws to pain
3 Decorticate flexion Decorticate flexion Decorticate flexion
2 Decerebrate extension Decerebrate extension Decerebrate extension
1 No response No response No response
Chapter 20 n Approach to Decreased Level of Consciousness 191

Step 1: If eyes are open (E-4) request the mother to talk Recognizing Presence of Raised
to her child. Intracranial Pressure
●● Babbling: < 9 months.
IP : 196.52.84.10 Raised ICP exists in varying degrees of severity in all en-
●● Waving bye-bye: 9–10 months. cephalopathies of non-traumatic etiologies (infectious and
●● Words: 1 year. non-infectious causes).
●● Pointing body parts: 15–24 months.
●● Sentences: 2 years. Concurrent and early manage­ment of intracranial hy-
●● Orientation in place and time from 5 years. pertension in the ED is not only life-saving, but also en-
sures neurologically intact survival.
Ù
‘Raised intracranial pressure’ must be presumed in all
Step 2: If no eye opening or spontaneous speech
comatose children. Failure to recognize and manage
●● Ask child to obey simple command such as squeezing ICP in the ED could lead to death or neurological
finger or eyes (M6). handicap.

How is raised intracranial pressure recognized within


the first hour of arrival?
Step 3: If no response, press firmly on supraorbital notch
(beneath medial end of eyebrow) with your thumb and ob- Hypoxia, shock and myocardial dysfunction have been
serve whether corrected, but these clinical features are noted:

●● Eyes open. ●● Level of consciousness continues to worsen.


●● Moans. ●● Abnormal posturing persists.
●● Moves arms: ●● Abnormal breathing pattern persists.
1. Above the clavicle (M5). ●● Abnormal oculocephalic (Doll’s eye) or oculovestibu­
2. Below clavicle while flexing elbow (M3). lar reflex.
3. Below clavicle without flexion and with rotation of ●● Abnormal pupillary response is noted.
shoulder (M2). Ù
Cushing’s triad (apnea, bradycardia, hypertension)
is a late manifestation of raised ICP. It is advisable to
identify earlier signs.
Step 4: No movement, exert maximal pressure and ob-
serve for facial grimace or movement of any body part.
Careful examination of the fundi is mandatory.

Ù
• Acute elevation of ICP will not cause papilledema
Step 5: If child flexes, but does not localize, apply nail bed immediately. Hence, its absence must not be taken as
pressure, using a pencil. a reassuring sign. Neither, is it safe to entirely rely
●● If finger is withdrawn (M4). on the computed tomographic images to diagnose
●● If child moves limb across the body to dislodge the raised ICP. ICP is often a clinical diagnosis in the
painful stimulus (M5). acutely ill child!
• If papilledema is noted in association with
hypertension (systolic BP greater than 2 SD),
reevaluate
Step 6: Look for asymmetry of movement in any of the – BP in all the four limbs.
steps (Uncal herniation). – Send blood for urea and creatinine.
Algorithm: Modified from Kirkham FJ et al. Pediatric – Admit into the ICU.
coma scales. Devel­opment Medicine & Child Neurology. – Refer to the nephrologist.
2008;50:267-74.
192 Section VI n Disability

Variations in CPP, both decreased CPP (when raised The pattern of clinical findings to help in recognition of
ICP is associated with uncorrected shock) and increased the level of herniation is shown in Table 20.2.
CPP associated with raised ICP is thought to cause brain
IP : 196.52.84.10 Table 20.2: Herniation syndromes
damage by following two mech­anisms:
Uncal Diencephalic
• Hemiparesis • Flexor response to pain
• Minimal deviation of and or decorticate
eyes on oculocephalic/ posturing
oculovesti bular testing • Hypertonia/hyper-
• Unilateral ptosis reflexia with extensor
• Unilateral fixed dilated plantars
pupil • Cheyne-Stokes
breathing
Upper pontine
• Full deviation of eyes
• Extensor response to oculocephalic/
to pain and /or
oculovestibular testing
decerebrate posturing
• Small midpoint pupils
• Hyperventilation reactive to light
• Minimal deviation of
eyes on oculocephalic/ Lower pontine
Figure 20.5: Unequal pupils in a child with raised ICP and uncal oculovestibular testing • No response to pain or
herniation (Courtesy: Dr Arun Annamalai). • Midpoint pupils fixed to flexion of legs only
light • Flaccidity with extensor
Decreased Cerebral Perfusion Pressure Medullary
plantars
• Ataxic or shallow
Cerebral perfusion pressure is the difference between the • Slow irregular gasping respiration
respiration/respiratory
mean arterial pressure and the intracranial pressure, i.e. • No deviation of eyes
arrest with adequate
(CPP = MAP – ICP). When intracranial pressure is elevat- on oculocephalic/
cardiac output
oculovestibular testing
ed and coexisting shock is not resolved, cerebral perfusion • Pupils dilated and fixed • Midpoint pupils fixed to
pressure falls causing cerebral ischemia. Ischemia in the to light
light
border zones between the main arterial territories, cause
clinically silent brain damage. It rarely may be associated
with seizures or hypertensive encephalopathy.

Herniation Syndromes
Untreated, raised ICP leads to herniation syndromes. Dif-
ferences in pressure between the forebrain compart­ment
and the posterior fossa, may cause uncal (Figure 20.5),
diencephalic or midbrain/upper pontine herniation. The
temporal lobes herniate through the tentorium. Similarly,
a pressure differential between the posterior fossa and the
spinal canal can lead to herniation of the brain through the
foramen magnum (Figure 20.6). The resulting lower pon- Figure 20.6: Lesions in various sites in the brain causing
herniation syndromes
tine and medullary hernia­tion syndromes can be lethal.
Brain herniation causes direct mechanical damage in ●● Memorize stages of progressive herniation that are
addition to ischemia and hemorrhage secondary to vascular compatible with intact survival.
distortion. Central or uncal herniation through the tentorium ●● Learn to serially examine the child’s level of conscious-
is compatible with intact survival; on the contrary, hernia- ness (Table 20.1) and the brainstem reflexes such that
tion through the foramen magnum is not. Changes from one progression is recognized immediately and appropriate
syndrome to the next signifies progressive worsening. action is taken swiftly.
Chapter 20 n Approach to Decreased Level of Consciousness 193

●● Drugs, toxins, metabolic abnormalities and the pos- ●● Blood ammonia: Reye’s syndrome, hyperammonemia.
tictal patient may mimic imminent herniation. Once ●● Blood lactate: Severe illness, inborn errors of metabo-
again, it is best to err lism (IEM).
IP on the side of treatment than to
: 196.52.84.10
await for the whole picture to unfold. ●● Call for metabolic specialist, if metabolic profile is ab-
normal.
First Tier Treatment of ●● Ketoacids: If finger stick glucose is high.
●● Serum sodium, calcium, magnesium (Table 20.3).
Intracranial Pressure ●● Blood urea, creatinine.
●● Nurse the child in the 30° head up position. ●● Peripheral smear: Malaria, hemolytic-uremic syndrome.
●● Keep head in neutral position to avoid kinking of the ●● Erythrocyte sedimentation rate (ESR), complete blood
neck. count (CBC).
●● Avoid noxious stimuli. Take efforts to provide pain re- ●● Coagulation profile: If platelets are low or bleeding occurs.
lief and sedation during painful procedures, since these
maneuvers could increase ICP. Blood Culture
●● Maintain euglycemia.
●● Control fever aggressively. ●● Stool culture: Shigella, Enteroviruses.
●● Treat seizures. ●● Mycoplasma IgG, IgM (unless cause known).
●● Severe sepsis with or without pyogenic meningitis may ●● Viral titers of blood and cerebrospinal fluid (CSF)
also present with varying degrees of coma. Administer (stored samples useful).
an antibiotic (Ceftriaxone) empirically, while awaiting – Elisa for Rickettsia, human immunodeficiency vi-
investigation. rus (HIV).
●● Hyperosmolar therapy: Infuse hypertonic saline (5 mL/ ●● Mantoux.
Kg) followed by continuous infusion between 0.1 and ●● Resting gastric juice for acid-fast bacilli.
1.0 mL/kg/h.
●● 3% NS has anti-inflammatory effects, increases intra- Lumbar Puncture
vascular volume and can be used in hy­potensive pa- LP may be performed when the child becomes hemody-
tients who have elevated ICP. A safe intervention, few namically stable with no clinical or radiological evidence
adverse effects have been noted with sodium levels as of raised ICP.
high as 160 mmol/L.
●● Ventilate to maintain eucapnia (PaCO2: 35–40 mm CSF may be sent for polymerase chain reaction (PCR)
Hg). for viruses, tu­berculosis (TB) antibodies, e.g. herpes sim-
●● Mannitol role has become limited. Since most children plex.
presenting with ICP also have shock or a propensity
to develop dehydration in the initial hours of manage-
Ù
Avoid LP if abnormal breathing patterns, shock,
ment, it is less often used in the ED setting. bradycardia, hypertension, GCS < 8, convulsive or
non-convulsive status epilepticus, abnormal dolls eye
Evaluate for Cause of Coma movement, dilated pupils, abnormal posture and ICP
After the ABCs are stabilized and ICP issues have been are noted.
addressed to prevent herniation, the patient may be trans- Delay LP and treat empirically when in doubt.
ported for imaging.
Ù Electroencephalography
Do not postpone stabilization while waiting for etiology EEG helps to confirm the diagnosis of seizure activity,5
to be identified. even if no clinical seizures (NCSE).

Investigations Less Common Investigations


●● Dextrostix. ●● Autoimmune screen for vasculitis.
●● Liver function tests even if primary liver cell failure is ●● Thyroid function test for encephalopathy associated
unlikely. with Hashimoto thyroiditis (Hashimoto encephalitis).
194 Section VI n Disability

While the list appears long, a protocol driven approach ness and neurological handicap. Although this data is
may help prevent repeated blood collections. It is good relevant for Haemophilus influenzae meningitis, the
practice to draw extra blood and store for future investiga-
IP : 196.52.84.10 benefit appear less certain for meningitis due to pneu-
tions. Investigations are requested in a stepwise manner, mococcus and other organisms.
especially if the etiology remains unclear. ●● If there is any suspicion of tuberculous meningitis or
if hydrocephalus is identified by CT scan, ATT should
Imaging be considered.
●● Empiric antimalarial treatment is also initiated.
If the child is deeply unconscious, afebrile or has focal ●● Empirical treatment of rickett­sia may be wise in epi-
signs, CT/MRI scan is the initial investigation of choice demic situations. It is best to treat with erythromycin
(even in infants with an open fontanelle). and doxycycline than to wait.
It helps to rule out intracerebral hemorrhage, ischemic When confronted with a child at high-risk of death or
stroke, hydrocephalus and space occupying lesion (SOL). disability, it would not be inappropriate to administer sev-
However, a nor­mal CT does not rule out the diagnosis of raised eral therapies on arrival. As the etiology of coma is con-
ICP. Thus, clinical signs of raised ICT are more important firmed, therapy is withdrawn, e.g. acyclovir acts best when
than a nor­mal CT scan. During transfer for investi­gations,
started early. However, if the results of the MRI, EEG and
ventilation, sedation and osmotic therapy must be continued.
PCR are all negative, therapy may be withdrawn.
If a surgically correctable cause is identified, call for
After the initial period of stabilization, the child must
neurosurgical consultation.
be transported to the PICU. Ideally an afebrile comatose
child should be transferred to a pediatric neurosurgical
Toxin Screen
unit. This should be done in the same manner as for im-
If etiology of coma has not been identified, consider the aging. Full sedation, controlled ventilation and minimal
possibility of toxins or drugs ingestions. handling with the bed/stretcher at a 30° head up angle
Ideally urine and blood should be collected and stored throughout transport is advised. The prognosis depends on
for evaluation of toxins/drugs early in the management of the etiology. Refer Protocol 20.1.
these children. Often, lack of laboratory support to establish diagnosis
of viral and metabolic disorders results in empirical treat-
Immediate Antimicrobial Coverage ment. However, effective supportive management of the
●● A third generation cephalosporin and Acyclovir is ABCs, maintenance of cerebral perfusion pressure and
empirically administered to cover the possibility of prevention of further damage often keeps the patient alive
infection. Acyclovir is therapeutic for herpes simplex till the primary problem resolves.
encephalitis. A positive MRI scan and electroencepha-
lography (EEG) have 95% sensitivity in the diagnosis
Key Points
ü
of herpes encephalitis. If the diagnosis is confirmed, the 1. Recognize potential risk of raised ICP and take im-
drug should be continued at a high dose for 2 weeks. mediate action to stabilize ABC.
●● Dexamethasone is given prior to the antibiotic, since 2. Secure airway using ICP precautions.
evidence suggests that it reduces the incidence of deaf- 3. Assess possibility of raised ICP.

Table 20.3: Corrections in electrolyte disturbances

Electrolyte Value Dose Rate of infusion


Sodium 115 mmol/L 5 mL/kg 3% NS 5–10 minutes
Calcium < 0.75 mmol/L 0.3 mL/kg calcium gluconate 5 minutes
Magnesium 0.65 mmol/L 50 mg/kg iv over 1 hour
Chapter 20 n Approach to Decreased Level of Consciousness 195

4.
5.
Check blood sugar.
Check for NCSE and treat.
common errors
û
1. Administration of Mannitol without ruling out shock
6. Lower temperature, IPif: more
196.52.84.10
than 38°C.
or monitoring hydration status.
7. Nurse in 30° head up positions. 2. Dextrose infusions in the absence of hypoglycemia.
8. Insert lines, urinary catheters, etc. under analgesia. 3. Failing to recognize non-convulsive status epilepticus.
9. Place on continuous monitoring. 4. Shifting for imaging without stabilization.
10. Administer broad spectrum antibiotic, antimalarial, 5. Administration of Diazepam for posturing move-
antiviral, erythrocin and doxycyclin for rickettsial ments in a comatose child.
infections and ATT for febrile children with coma. 6. Failure to ensure euglycemia and correct dyselectro-
11. If papilledema is identified in association with hy- lytemia.
pertension (systolic BP greater than 2 SD), call for 7. Failure to protect airway and ventilate the comatose
nephrology consultation. child.
Protocol 20.1: PEMC approach: Altered mental status and abnormal movements in a critically ill child
196
Section VI n Disability

IP : 196.52.84.10
Chapter 20 n Approach to Decreased Level of Consciousness 197

References 3. Santhanam Indumathy, Sangareddi S, Venkataraman, et


al. A prospective randomized controlled study of two fluid
1. Kirkham FJ. Non-traumatic coma in children. Arch Dis regimens in the initial management of septic shock in the
IP : 196.52.84.10
Child. 2001;85:303-12. emergency department. Pediatr Emerg Care. 2008;24:647-55.
2. Pediatric Accident and Emergency Group. ‘Evidence 4. Kirkham FJ. Newton CR, Whitehouse W. Pediatric coma
based guideline for the management of decreased level scales. Development Med Child Neurology. 2008;50:267-74.
of consciousness’. Arch Dis Childhood Edu and Practice.
5. Bauer, Trinka. Non-convulsive status epilepticus and coma.
2006;91.ep115-ep22.
Epilepsia. 2010;51(2):177-90.
21
IP : 196.52.84.10

Status Epilepticus

Figure 21.1: Airway management is as critical as anticonvulsants in the management of status epilepticus (Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Need for early initiation of bag-valve-mask venti­ 3. Evidence-based drug protocol in the management
lation in convulsive status epilepticus seizures last­ of status epilepticus.
ing for more than 5 minutes. 4. Differentiation between non-convulsive status epi­
2. Emphasize the need to recognize coexisting pul­ lepticus from postictal states.
monary edema that can worsen during phenytoin 5. Emphasize the importance of treating until all parts
administration and fluid therapy of shock. of the PAT have normalized.

INTRODUCTION Progression of Status Epilepticus4


Status epilepticus (SE) is defined as seizures persisting for Overt generalized status epilepticus, if left untreated will
more than 5 minutes in children > 5 years of age or two evolve into non-convulsive status epilepticus.
or more seizures occurring consecutively without an in­
tervening period of full recovery of consciousness.1 More
recently,2 a time sensitive classification has been proposed. PATHoPHYSIOLOGY
●● Early or impending SE: 5–30 minutes. The deleterious cerebral, metabolic and physiological
●● Established SE: 30–60 minutes. changes that occur as the duration of seizures increase is
●● Refractory SE: Seizures persisting after treatment with shown in Box 21.1. Also refer Table 21.1.
adequate doses of 2 or 3 initial antiepileptic medica­
tions. Anticonvulsants act by altering the neuro­peptide activ­
Seizures that do not cease in 5 minutes are less likely ity within the brain. Most seizures terminate spontaneous­
to terminate without intervention.3 Hence, a child who is ly within 2 minutes. Spontaneous resolution, is the result
convulsing on arrival into the ED is more likely to contin­ of γ-aminobutyric acid-mediated inhibition that occurs in
ue to convulse and cause respiratory insufficiency unless response to seizures.
actively treated (Refer Figure 21.1).
Chapter 21 n Status Epilepticus 199

Box 21.1: Medical complications of status epilepticus result in decreased inhibitory control and increased ex­
Cerebral citation leading to continuation of status epilepticus.
– Interictal coma IP : 196.52.84.10 ●● Benzodiazepines bind to GABA-A5 receptors and pro­
– Cumulative anoxia mote neuronal inhibition.
– Altered autoregulation ●● Since the number of active GABA-A receptors de­
– Increased cerebral blood flow creases as an episode of SE progresses,6 the first dose
– Cardiac arrest
of benzodiazepines should be given as early as possible
– Hypertension
– Cardiac failure, hypotension for seizure termination.
– Cardiogenic shock
●● Respiratory system failure CASE SCENARIO 1
– Apnea
– Cheyne-Stokes breathing An 8-month-old girl is brought with history of seizures
– Tachypnea lasting for 20 minutes. She had been having fever for 1
– Neurogenic pulmonary edema day (Figures 21.2 and 21.3).
– Aspiration, pneumonia
– Respiratory acidosis
– Cyanosis
●● Renal failure
– Oliguria, uremia
– Acute tubular necrosis
– Rhabdomyolysis
– Lower nephron necrosis
●● Autonomic system disturbance
– Hyperpyrexia
– Excessive sweating, vomiting
– Hypersecretion (salivary, tracheobronchial)
– Airway obstruction
●● Metabolic and biochemical abnormalities
– Acidosis (metabolic acidosis)
Figure 21.2: Active convulsions can make effective bag-valve-
– Anoxemia
mask ventilation a challenge. Hence double EC-clamp technique
– Hypernatremia, hyponatremia
of BVM ventilation is employed.
– Hypoglycemia
– Hepatic failure
– Dehydration
●● Infection
– Pulmonary
– Bladder
– Skin
●● Others
– Altered autoregulation
– Cerebral metabolic rate for oxygen (CMRO2)
– Disseminated intravascular coagulation
– Multiple organ dysfunction
– Fractures, thrombophlebitis

●● Loss of the GABA5-mediated protective effect leads to


ongoing seizure activity. The GABA recep­tors on the
cell membrane are either destroyed or recycled. At the Figure 21.3 Physiological status: Unmaintainable airway,
same time, continued seizure activ­ity results in mobili­ respiratory failure, tachycardia, shock with high normal blood
pressure with convulsive status epilepticus.
zation of excitatory N-methyl-D-aspartate receptors.
●● The reduced activity of GABA (seizure control neu­
ropeptides) and increased activity of N-methyl-D- Prehospital Therapy
aspartate receptors (seizure provoking neuropeptides) ●● Place the convulsing child in the recovery position to
enable drainage of secretions.
200 Section VI n Disability

Table 21.1: Cerebral, metabolic and physiological derangements during prolonged seizures

Parameter Duration of seizure < 30 min (phase I) Duration of seizure < 30 min (phase II) Hours (refractory)
Blood pressure
IP : 196.52.84.10
Increased Decreased Hypotension
Arterial oxygen Decreased Decreased Decreased
Arterial carbon dioxide Increased Variable Hypercapnia
Lung fluid Increased Increased Pulmonary edema
Autonomic activity Increased Increased Arrhythmias
Temperature Increased 1ºC Increased 2ºC Fever—hyperpyrexia
Serum pH Decreased Variable Acidosis
Lactate Increased Increased Lactic acidosis
Glucose Increased Normal or raised Hypoglycemia
Serum potassium Increased or normal Increased Hyperkalemia
Cerebral blood flow Increased 900% Increased 200% Cerebral edema
Cerebral oxygen Compensated Failed Deficit—ischemia
consumption

●● Open airway using the head-tilt chin-lift maneuver 3. Use a large bore rigid suction catheter to suction
(while maintaining the recovery position). oropharyngeal secretions.
●● Suction oropharyngeal secretions without stimulating 4. Rapidly decompress stomach with a nasogastric tube
the posterior pharyngeal wall. to prevent vomiting and pulmonary aspiration.
●● Provide oxygen using a non-rebreathing mask. 5. Introduce an appropriate sized oropharyngeal airway,
●● Administer midazolam (0.2 mg/kg) via the intra- if feasible.
muscu­lar or intrabuccal or intranasal route.7
●● Fever a common cause of seizures in children should
Ù
Avoid forcible opening of clenched jaws during a
be controlled rapidly by tepid sponging and placing a convulsive episode.
rectal suppository of paracetamol.
●● Unresponsiveness due to seizure activity results in the
Management of SE in the ED (Protocol 21.1) falling back of tongue.
The median duration of convulsions prior to reaching the ●● Loss of airway protective reflexes leads to failure in
PED of an academic children’s hospital in Southern India, handling the tracheobronchial secretions.
was 1 hour.8 ●● Glottic spasm also contributes to airway obstruction
during seizure activ­ity.
Most presented with features of pulmonary edema with or
without cardiac dysfunction. The modified SE protocol de­ Breathing
scribed in this manual is based on this ex­perience.
Ineffective respiration is almost always noted during con­
vulsive status epilepticus.
Airway
Tonic-clonic activity of the intercostal muscles inhibit
At least two members (one doctor and one nurse) must be the normal inspiratory/expiratory movements of respira­
dedicated for airway management. The maneuvers men­ tion.
tioned below should be implemented simultaneously.
●● Jerky respirations are probably due to contraction of
1. Open the airway using the head-tilt and chin-lift ma­ involuntary muscles of diaphragm.
neuver. ●● Drugs used in the management of status epilepticus can
2. C-spine precautions are taken if trauma is suspected. also lead to respiratory failure.
Chapter 21 n Status Epilepticus 201

Ù
An unstable and obstructed airway in combination with
Ù
Opening the airway and provision of oxygen without
ineffective ventilationIPfor: 196.52.84.10
greater than 5 minutes can initiating bag-valve-mask ventilation is not enough to
cause: correct hypoxia in actively convulsing children in the
• Severe hypoxia. emergency setting.
• Shock.
• Myocardial dysfunction. ●● Whilst, the airway is being cleared by the airway nurse,
• Increased risk of prolonged seizure activity. initiate bag-valve-mask ventilation using the largest
sized bag.
Emergency medical response systems reach a convuls­ Almost 50% of children presenting with convulsive SE
ing child within 5 minutes after activating the EMS. Pre­ can be mask ventilated without being intubated.8
hospital protocol-based management is rapidly initiated
in western countries. Decision to intubate is taken within ●● If spontaneously breathing, provide O2 using the flow-
20–30 minutes after onset of convulsions9 in the prehospi­ inflating ventilation device.
tal setting. ●● Oxygen saturations are monitored using pulse oximeter.

Ù
Since early and structured prehospital care by EMS
Note: Antiseizure drugs inherently depress respiration and
may aggravate the underlying hypoxia in SE. Adminis­
is unavailable in many parts of our country, it is tration of anticonvulsant without addressing the ABCs (a
recommended that primary care physicians to whom the common error) could result in lethal complications.
child is brought, administer early and aggressive airway
management to avoid the deleterious effects of hypoxia
in convulsing children.

Figure 21.5: The tube position being verified before fixing


the tube

Indications for Intubation in SE (Figure 21.5)


Figure 21.4: A third physician formulates the initial dose of ●● Failure to maintain optimal saturations despite effec­
lorazepam and administers it over 1–2 minutes, whilst two
tive bag-valve-mask technique.
responders are managing the airway and breathing on arrival.
Pulse oximeter is connected for monitoring during resuscitation. ●● Features of pulmonary edema or cardiac dysfunction
noted at any step in the protocol.
Failure to provide effective ventilatory support during ●● Hypotensive shock associated with SE.
the emergency management of SE contributes to signifi­ ●● Prior to starting phenobarbitone or midazolam infusion
cant morbidity and mortality in our country. On the con­ for SE not responding to benzodiazepines and phenytoin.
trary, effective respi­ratory support along with appropriate ●● Severe traumatic brain injury, where there is a need to
anticonvulsants can of­ten resolve seizure, whilst simulta­ provide controlled ventilation.
neously establishing breathing (Figures 21.4). ●● Raised intracranial pressure.
202 Section VI n Disability

IP : 196.52.84.10

Figure 21.6: This picture shows capillary blood glucose being Figure 21.7: This picture shows a convulsing child being mask
evaluated during resuscitation ventilated on arrival using the two person technique. Bag-valve-
mask ventilation of the older child is not easy. The respiratory
arrest secondary to involvement of the intercostal muscles during
Glucose active convulsions can make effective bagging very difficult. The
Hypoglycemia can severely disrupt cerebral blood flow airway nurse is suctioning. Two nurses are assigned to secure
autoregula­tion leading, to adverse neurological outcomes. intravascular access. One more member of the emergency team
Refer Figure 21.6. formulates the initial dose of lorazepam and administers it over
1–2 minutes.
●● Dextrostix should be used to measure sugar levels early
in the management of SE. Circulation
●● Documented hypoglycemia is corrected with an intra­
venous bolus of 2 mL/kg of 25% dextrose solution. Shock could occur due to a wide variety of causes in con­
●● If dextrostix is not immediately available, to avoid the vulsing children.
dangerous effects of unrecognized hypoglycemia, 25% ●● Neurogenic: Distributive shock.
dextrose may be administered emperically. ●● Hypoxia: Distributive shock with or without myocar­
●● Prolonged status epilepticus can cause hypoglycemia. dial dysfunction.
Hypoglycemia can precipitate status epilepticus. Of­
●● Coexisting sepsis.
ten, hypoglycemia can recur after correction. Hence,
●● Coexisting hypovolemia.
throughout resuscitation, a maintenance fluid should be
infused as per the Holliday-Segar formula. During SE, cerebrovascular resistance falls due to
●● Infuse GNS to which KCl and calcium have been hypox­ia, resulting in severe derangement of cerebral auto-
added. regulation.
Ù
Glucagon is indicated for treating hypoglycemia and
Cerebral perfusion becomes directly dependent on sys­
temic blood pressure. Within the first ½ hour of SE, blood
seizure in insulin-dependent diabetes mellitus. pressure rises. Later blood pressure either becomes normal
or hypotensive.
Dose: 1–2 years: 500 µg stat
●● Secure intravenous access on arrival and provide non-glu­
2–18 years: < 25 kg: 500 µg cose containing isotonic fluids. At least two nurses may
> 25 kg: 1 mg be needed to secure intravenous access (Figure 21.7).
Route of administration in IDDM: Subcutaneous, ●● If IV access is unavailable, intraosseous access must be
intramuscular or intravenous. secured. If shock is identified the first bolus of 20 mL/
kg is administered.
●● Monitor serum sodium, calcium and magnesium. ●● If euvolemic restrict fluids to 2–3 mL/kg/h.
●● Refractory status epilepticus can often be corrected by ●● Shock secondary to idiopathic SE will resolve follow­
resolving metabolic abnormalities. ing administration of 20–30 mL/kg of fluids.
Chapter 21 n Status Epilepticus 203

●● Shock complicated by diarrhea or sepsis will require Metabolic disorders were reported in an average of 6%
large volumes to attain therapeutic goals. (range 1%–16%) of children with SE9.
●● Caution: Fluid therapy
IP :or196.52.84.10
phenytoin administration can
unmask underlying myocardial dysfunction.

Myocardial Dysfunction and


Pulmonary Edema
Status epilepticus can precipitate acute lung injury. Severe
sepsis can also have the same impact on the alveolar cap­
illary membrane. Myocardial dysfunction can also occur
in children with prolonged SE. Drugs and fluid therapy
can unmask PE during management. If signs of PE are not
recognized during resuscitation of SE, cardiac arrest can
supervene.
Repeated cardiopulmonary cerebral assessments are
Figure 21.8: This picture shows the management of convulsive
crucial for recognizing these dreaded complications. SE on arrival: The first responder opens the airway using the head-
●● If signs of pulmonary edema or myocardial dysfunc­ tilt, chin-lift maneuver and initiates bag-valve-mask ventilation.
The airway nurse simultaneously suctions the oropharynx
tion are identified during fluid administration:
inserts an age appropriate nasogastric tube and decompresses
– Interrupt fluids. stomach contents. Whilst airway management is in progress, the
– Initiate an inotrope. second physician performs the rapid cardiopulmonary cerebral
– Intubate using ICP precautions. assessment. The pulse oximeter is showing 91% saturation. The
●● After intubation, if features of PE and hepatomegaly third physician or nurse secures vascular access and administers
resolve, further fluids are administered if shock persists drugs and fluids, etc.
secondary to sepsis or hypovolemia.
●● If child is receiving phenytoin when signs of PE are Drug Therapy
identified (stop the drug) or avoid phenytoin if not al­
The goal of drug therapy is the rapid control of convul­
ready started.
sions. The longer the duration of convulsion, the greater
Ù
Aggressive management of shock based on etiology is
the risk of complications. Hence, it seems mandatory to
follow a clear drug protocol, which is understood by all
mandatory for intact neurological survival. personnel. Continuous monitoring and skilled care is es­
sential during administration of drugs due to the grave risk
Resuscitation of SE requires team effort and coordination of hypoventilation and hypotension during resuscitation.
in a time sensitive manner (Figure 21.8).
1. Benzodiazepines10,11 are the most potent and effective
●● One emergency physician and nurse manages the air­ first-line drugs in the management of SE. Presence
way and breathing on arrival (the airway nurse assists of apnea is not a contraindication to the administra­
in suctioning). tion of benzodiazepines. The rapid onset of action of
●● The second physician performs the rapid cardiorespira­ benzodiazepines is often useful in resolving seizure-
tory assessment and documents the clinical findings. induced apnea. Due to the risk of respiratory depres­
●● Two nurses are needed to secure IV access, ad­minister sion, ability to support ventilation is a prerequisite
fluids, dextrose and the first dose of anticonvulsant. during administration of any of the benzodiazepines.
●● The airway manager should also attempt to obtain a ●● Lorazepam controls seizures within 3 minutes in
focussed history, confirm eye signs, ensure that a 50% of patients. Despite being comparable in po­
thermometer, pulse oximeter and cardiac monitor are tency and efficacy to diazepam, lorazepam has a
placed to monitor the child. longer duration of antiseizure effect (12–24 hours).
●● Collect blood for Na, K, Ca, Mg, urea and creatinine. Reduced risk of recurrence has made lorazepam the
204 Section VI n Disability

preferred first-line benzodi­azepines in the treatment with prolonged uncorrected SE or SE complicating


of SE. Besides, lorazepam has less respiratory de­ serious sepsis or SE in children with evidence of
pression than diazepam. However, lorazepam needs
IP : 196.52.84.10 cardiac dysfunction should be viewed with cau­
to be refrigerated and should be diluted and admin­ tion.
istered as a bolus over 1 minute.
●● The anticonvulsant effect of diazepam lasts for 30 Ù
Phenytoin is potentially cardiotoxic.16,17
minutes resulting in a high risk of recurrence of SE if
this drug is used alone. It is therefore recommended To avoid the worsening of myocardial dysfunction in chil­
that, even if diazepam has stopped a convulsive SE, dren presenting with SE in our setting the following pre­
phenytoin should be given to prevent recurrence of cautions are taken in planning the drug protocol (Figure
seizures. Even if the fit appears to have been con­ 21.9):
trolled during administration of benzodiazepines,
the full dose should be given in order to avoid con­
verting a convulsive SE to non-convulsive SE.
●● Midazolam11,12 has no advantage over diazepam or
lorazepam. It is advantageous, since it is the only
benzodiazepine that can be administered via the in­
tramuscular route when other routes are not avail­
able. It has a rapid onset of action and controls sei­
zures in 90% of patients. Its shorter half-life and
resultant increased risk of recurrence makes it a less
preferred drug to lorazepam in the initial manage­
ment of SE in the ED. Midazolam also has an added
risk of hypotension, a dreaded complication in SE
resuscitation. Figure 21.9: History that aids in anticipation of pulmonary
●● A second dose of lorazepam or diazepam may be edema and hence phenytoin is unsafe
repeated in 5 minutes, if seizures are not controlled
with the first dose. 1. Check history to find out whether abnormal move­
2. Phenytoin13,14,15 is the second-line drug in patients not ments were truly:
responding to the initial two doses of benzodiazepines. a. Tonic-clonic? or
Since it is poorly soluble in water and precipitates in b. Stiffening, upward gaze, squirming movements?
dextrose containing solutions. It is infused in normal etc.
saline (dose of 15–20 mg/kg) at the rate of 1 mg/kg/ c. The caretaker who rushed the child must demon­
min with maximum rate of 50 mg/min. Anti-seizure strate whether the movements were indeed convul­
threshold in the brain is reached within 10–30 minutes sions not posturing.
after infusion. If convulsions are not controlled, 5 mg/ 2. Were the movements preceded by precipitating events
kg increments can be administered up to a maximum such as fever, breathlessness or diarrhea.
loading dose of 30 mg/kg.
a. History of altered mental status such as incessant
●● Phenytoin decreases automaticity of cardiac tissue crying, lethargy, increased sleepiness, posturing or
by pro­longing the effective refractory period. stiffening, between precipitating event or not?
●● Phenytoin decreases the force of cardiac contrac­ b. Were the movements not preceded by altered men­
tion leading to hypotension following rapid IV ad­ tal status: Child was playing, performing routine
ministration. activities?
●● Severe cardiotoxic reactions and fatalities have
been reported with atrial and ventricular conduc­tion
Ù
depression and ventricular fibrillation. Phenytoin If GTCs was preceded by altered mental status, consider
can be safely used in children who come early in the possibility of hypoxia or shock complicating SE.
the course of seizures. Its use in children presenting Avoid phenytoin.
Chapter 21 n Status Epilepticus 205

Pyridoxine
When seizures are not responsive to phenytoin, pyridox­
IP : 196.52.84.10 ine (50–100 mg) and the convulsing infant is less than 18
months, pyridoxine should be administered. Watch out for
apnea.

Valproic Acid
Valproic acid19–23 a broad-spectrum anticonvulsant acts by
modulating sodium and calcium channels and in­hibiting
aminobutyric acid transmission.
●● Sodium valproate is given as initially as a bolus: 25
Figure 21.10: History that rules out of pulmonary edema and mg/kg bolus (max 40 mg/kg), followed by an infusion
hence phenytoin is safe of 5 mg/kg/hour.
●● Sodium valproate has less sedation, good cardio­
3. During phenytoin infusion, if the following signs of vascular profile and lower risk of respiratory failure
cardiac dysfunction or pulmonary edema are noted, compared to other anticonvulsants.
stop phenytoin infusion. ●● Sodium valproate should be avoided, if child has evi­
dence of liver disease or metabolic disease or hemo­
a. Pink froth. static abnormalities.
●● It may be difficult to differentiate froth from
oropharyngeal secretions due to GTCs. Onset of Levetiracetam24-28
froth in a child whose airway was initially clear,
may be the first clue that PE is developing in a Levetiracetam acts through calcium channels, glutamate
fitting child. Refer Figure 21.10. receptors and g-aminobutyric acid modulation (synap­
tic vesicle 2A ligand). Intravenous Levetiracetam is not
b. Retractions, grunting.
metabo­lized by the liver, has little affinity to protein, is
c. Gallop, muffling of heart sounds, bradycardia, hy­
ex­creted via renal pathway and has minimal drug-drug in­
potension, widening of pulse pressure with low teractions.
mean arterial pressures, increasing liver span or
drop in oxygen saturations. ●● It is administered as a bolus of 20–30 mg/kg IV at 5
mg/kg/min (max 3 g).
Ù ●● When SE is complicated by pulmonary edema, myo­
If pulmonary edema or myocardial dysfunction is cardial dysfunction coagulopathy, liver failure or hy­
anticipated or occurs during phenytoin infusion, consider potension, Levetiracetam is an excellent alternative
initiating levetiracetam or/and sodium valproate after antiseizure agent.
the initial doses of benzodiazepines. ●● In some children it may cause reversible behavioral
changes.
Fosphenytoin, a water-soluble phosphoester of pheny­
toin has been considered less cardiotoxic effects than phe­ Alternative Routes of Drug Administration
nytoin and may be safer. However, cardiac dysrrythmias
When intravenous access is not available, midazolam (0.2
have been reported even with the use of fosphenytoin.18 mg/kg) can be given intramuscularly, rectally or into the
This drug can be given/administered through the intramus­ buccal space.
cular route if intravenous (IV) access is not available.
●● All anticonvulsant drugs except phenytoin have
The APLS recommends that, the loading dose of phe­ achieved therapeutic levels in the blood when ad­
nytoin should be avoided for children taking chronic phe­ ministered via the intraosseous route. The doses of
nytoin therapy. these drugs are the same as for the IV route.
206 Section VI n Disability

case scenario 2 Continuation of the aggressive management of the air­


way, breathing and circulation with the same drug protocol
An 8-years-old girl was rushed into the ER after being
as for CSE until all therapeutic goals are achieved is rec­
found unresponsive inIPthe
: 196.52.84.10
bathroom. She has been on
treatment for seizures for the past 5 years, but missed ommended (Figure 21.13).
her medication for the last 2 days.

Figure 21.13: Therapeutic goals of seizure control—Normal


cardiorespiratory cerebral assessment

Figure 21.11: Conjugate deviation of eyes


The management of NCSE is similar to CSE. Continue
therapy until all therapeutic goals of shock and seizure ac­
tivity has resolved.

Ù
A good indicator of seizure control is return of baseline
sensorium.

●● Failure to regain baseline consciousness following a con­


vulsion often indicates the presence of ongoing NCSE.
Cessation of overt motor movements alone should not
be considered as achievement of complete seizure control.
Careful monitoring and management should continue until
all therapeutic goals (seizure, hypoxia, shock and cardiac
Figure 21.12 Physiological status: Airway obstructed, effortless
dysfunction are achieved).
tachypnea, tachycardia, normotensive shock, NCSE. Ù
Persistence of altered level of consciousness:
Non-convulsive Status Epilepticus (NCSE) ‘Responsive to pain or unresponsive’ is often mistaken
as ‘postictal state’. A high index of suspicion is needed
Conjugate deviation of eyelid twitch, nystag­mus or unilat­
to identify NCSE or shock in children presenting with
eral clonus in an unresponsive child helps to recognize this
condition (Figures 21.11 and 21.12). seizure activity.

●● Anticipate non-convulsive SE in children who pres­


ent with sud­den unresponsiveness or who have been Refractory Status Epilepticus
having seizures, but who have not regained baseline Definitions of refractory status epilepticus (RSE) vary.
consciousness. Since, majority of children have been convulsing for > 1
●● More commonly, convulsive status epilepticus (CSE) hour and have not received prehospital respiratory support
evolves into subtle SE during resuscitation. Active
during the management of seizures, we define this entity
convulsions disappear, but the child remains apneic or
as SE not controlled with the initial two adequate doses of
tachypneic, shocky and unresponsive. The eye signs
indicate persistence of ongoing seizure activity. benzodiazepines and phenytoin.
Chapter 21 n Status Epilepticus 207

Midazolam Targeted History


Midazolam 29-35
a water-soluble benzodiazepine, rapid­ Often panic-stricken parents will be unable to provide a
IP : 196.52.84.10
ly penetrates the blood-brain barrier and exerts its anti- coherent history on reaching the ED with a convulsing
convulsive effect for a short duration. It suppresses neu­ child. Nowhere, is a correct history more important than
ronal excitability by modulating the γ-aminobutyric acid in management of SE. Hence, a short targeted history is
receptors. Mi­dazolam is hydroxylated in the liver and the essential to ensurse appropriate therapy.
metabolite is excreted by the kidneys. Hence midazolam
should be used with caution in children with underlying Ù
1. Are the movements tonic-clonic or posturing
he­patic or renal dysfunction.
(stiffening, upward gaze, flexor or extensor posturing,
●● Midazolam a good choice for the initial treatment of squirming movements, etc.).
RSE, is given as 0.2 mg/kg IV bolus. To avoid hypoten­ Since, all abnormal movements should not be treated as
sion, midazolam is given slowly over 1–3 minutes. CSE, it is worthwhile requesting parents who accompany
●● A continuous infusion of 1 µg/kg/min of midazolam the child to enact the abnormal movements.
with increments of 1 µg/kg/min every 15 minutes is 2. Time of onset.
recommended until the seizures are controlled. The 3. Place of onset helps to determine the approximate
maximum rate of infusion is 50 µg/kg/min. time taken to reach your hospital (duration of
●● Though higher boluses and more rapid escalation may convulsive event).
be associated with more prompt seizure control, hy­ 4. Number of episodes.
potension following use of midazolam remains a seri­ 5. Did the mental status revert to normal (alert, playing)
ous concern. after the convulsion?
●● Midazolam infusion requires the use of infusion pumps 6. History of precipitating event such as fever, diarrhea,
to ensure precise titration. vomiting, toxin, trauma?
7. History of altered level of consciousness between
Phenobarbital36 fever or diarrhea (precipitating event) and fit (as
discussed earlier).
Indicated in RSE and neonatal SE. It depresses neuronal
– A systematic history helps in determining two
excitability by enhancing the g-aminobutyric acid recep­
important issues, which help in the management:
tor response. Depression of men­tal status and respiratory
whether the con­vulsion was a primary event or
failure are common side effects. Intubation is mandatory
whether it was precipitated by hypoxia or shock.
if Phenobarbital is administered after benzodizepines. Be­
– The latter suggests a more critically ill child who
sides, the drug must be administered slowly to avoid hy­
would need greater aggression in the management
potension.
of underlying hemodynamic compromise. In these
●● The recommended dose is 20 mg/kg up to a maximum children use of phenytoin should be avoided,
of 30 mg/kg and the rate of infusion is 1–2 mg/kg/min. since it worsens the underlying myocardial
The antiseizure effect occurs within 10–20 minutes. dysfunction.
Unlike phenytoin, Phenobarbital can be safely used in
8. Was the child developmentally normal or abnormal?
patients already maintained on this drug.
9. Did the child have seizures or any other comorbidity
in the past?
Thiopental37 10. Was he on antiepileptic drugs? How was his drug
The loading dose of thiopentone sodium is 3–5 mg/kg. It compliance?
is followed by an infusion. Severe hypotension requiring 11. What was the nature of prehospital care? Use of
vasopressor therapy and prolonged postinfusion weakness benzodiazepines or intravenous phenytoin in pre-
and delaying weaning make it a less commonly used drug hospital settings could help to titrate the loading
in RSE. dose of these drugs.
208 Section VI n Disability

Emergency Investigations The presence of strict treatment protocols for SE made


readily available for the treating staff could potentially im­
Blood is collected for glucose, renal and liver functions, prove the outcome of patients.
IP : 196.52.84.10
cal­cium, magnesium, complete blood count (CBC), cul­
tures, prothrombin time (PT), prothromboplastin time
(PTT) and blood gases. As per the recommendations of
Key Points
ü
American Academy of Neurology,38 the following have 1. Differentiation of convulsion from hypoxic postur­
ing.
been suggested:
2. Differentiation of postictal state from persistence of
●● There is insufficient data to support or refute the altered level of consciousness secondary to ongoing
recommenda­tions for taking blood or CSF for culture NCSE or hemodynamic compromise.
on a routine basis (no clinical suspicion of systemic or 3. Failure to initiate bag-valve-mask and correction
CNS in­fection) (Level U). of shock during management of status epilepticus
●● Anticonvulsant levels should be considered when a could be lethal.
child with treated epilepsy develops SE (Level B). 4. Administration of IM diazepam will worsen seda­
●● Toxicology studies and metabolic studies for inborn er­ tion and respiratory failure without resolving seizure
rors of metabolism may be considered in children with activity.
SE when there are clinical indicators for concern or when 5. Phenytoin administration could be dangerous in
the initial evaluation reveals no etiology (Level C). children who develop signs of pulmonary edema
●● An EEG may be considered in a child with SE as it and myocardial dysfunction during management of
may be helpful in determining, whether there are fo­ status epilepticus.
cal or generalized epileptiform abnormalities that may 6. Rapid IV administration of midazolam could result
guide further testing for the etiology of SE, when there in hypotension.
is suspicion of pseudostatus epilepticus (non-epileptic
SE) or non-convulsive SE (Level C).
●● Neuroimaging may be considered after the child with
SE has been stabilized, if there are clinical indications
common errors
û
1. Oxygen via non-rebreathing mask is sufficient to
or if the etiology is unknown (Level C). There is insuf­ correct hypoxia in a child convulsing for more than
ficient evidence to support or refute routine neuroimag­ 5 minutes.
ing in a child presenting with SE (Level U). 2. All abnormal movements are convulsions.
3. Unaware that use of anticonvulsants in hypoxic pos­
Treatment of Specific Causes of SE turing could precipitate cardiac respiratory arrest.
4. Failure to remember that the longer duration of ac­
Central nervous system infections, head trauma, cerebral tion of lorazepam helps to prevent recurrence.
edema, space occupying lesion, hemorrhage, poisons, hy­ 5. Failure to realize that rapid administration of mi­
poglycemia, hypoxia, hypertensive encephalopathy, elec­ dazolam or phenobarbital can precipitate hypoten­
trolyte imbalances and drug toxicity can all produce sei­ sion.
zures that are difficult to control. Assessment of patient for 6. Failure to continue treatment after active convulsion
possible etiology is performed after controlling the seizures. has stopped in a child who remains hemodynami­
Refer Table 21.2 for drugs used. cally compromised with NCSE.
Chapter 21 n Status Epilepticus 209

Table 21.2: Drugs used in emergency room for management of status epilepticus

Drug Initial dose Route IV administration Onset of Half-life Adverse effects


IP : 196.52.84.10 action
Lorazepam 0.05 mg IV IV 0.5 mg/kg 1–3 minute Neonates: 40 Sedation, hypotension,
0.1 mg/kg Infusion: 0.01-0.1 hour bradycardia, respiratory
Max: 4 mg mg/kg/h Children: 10 depression, hyperactivity.
hour
Diazepam 0.05–0.3 mg/kg IV 0.1 mg/kg/min 1–3 minute Neonates: Sedation, hypotension,
Max: < 5 y–5 PR 50.95 h. bradycardia, respiratory
mg > 5 y–10 Infants: 40–50 depression, hyperactivity
mg hour thrombophlebitis.
PR dose–0.5 Children:
mg/kg 15–20 hour
Midazolam 0.1–0.15 mg/kg IV Infusion: 1 mg/kg/ 1–5 minute Neonates: Sedation, hypotension,
Max: 0.15 mg/ PR min - to max of 24 4–12 hour bradycardia,(if hypotensive or
kg mg/kg/min Children: 3–4 h bradycardic avoid midazolam)
respiratory depression, apnea,
laryngospasm, hyperactivity.
Phenytoin 15–20 mg/kg IV Slow IV over a 10 minute 7–24 hour (first Tachyarrhythmia commonly
Max: 1 g period of 20 minute after the order kinetics seen during administration.
@ 1 mg/kg/min to infusion is do not apply) Decreased infusion rate. Brady-
max of 50 mg/kg/ over arrhythmia, gallop, pulmonary
min. Monitor heart edema, hypotension noted
rate and BP during during infusion is suggestive
administration. of underlying myocardial
Infusion may be depression due to RSE, severe
titrated to maintain sepsis, etc.
base line heart rate. Stop PHT and consider
alternative.
Dysarthria, ataxia, sedation,
thrombophlebitis, purple glove
syndrome.
Fosphenytoin 15–20 mg PE/ IV 3 mg PE/kg/min to 7 minute 12–29 h (first Dysarthria, ataxia, sedation,
kg IM max 150 mg PE/ 5/12 to order kinetics hypotension, arrhythmia.
min convert to do not apply)
phenytoin
Valproic acid 15–20 mg/kg IV 5 mg/kg/min > 2 month 7–13 Hypotension, arrhythmia,
Max: 25 mg/kg Infusion: 1–4 mg/ hour hepatitis, pancreatitis.
kg/h 2–14 year
40–20 hour
Paraldehyde 200–400 mg/kg PR n/a 4–10 hour Rectal irritation, lung toxicity.
Max: 10 g PR
Levetiracetam Bolus of 20–30 IV 5 mg/kg/min (max 1 hour 6-8 hour Behavioral changes
mg/kg 3 g)
Phenobarbitone 15–20 mg/kg IV 1 mg/kg/min up to 5 minute Neonates: Respiratory depression,
up to max 1 g/ max of 60 mg/min 45–200 hour prolonged sedation,
dose Infants: hypotension
20–133 hour immunosuppression.
Children: Intubate, if used following
33–73 hour benzodiazepines.
Contd...
210 Section VI n Disability

Contd...

Drug Initial dose Route IV administration Onset of Half-life Adverse effects


IP : 196.52.84.10 action
Thiopentone 2–4 mg/kg IV 1–6 mg/kg/h 30–60 14–34 hour Sedation, hypotension,
second respiratory depression,
accumulation due to lipid
solubility, extravasation can
cause skin necrosis due to pH
of 10.6.
Lidocaine 2–3 mg/kg IV 3–10 mg/kg/h 50 mg/min 1.5–2 hour in Sedation
(Max: 200–300 adults
mg)
Chapter 21 n Status Epilepticus 211

Protocol 21.1: PEMC approach: Recognition and management of convulsive and non-convulsive
status epilepticus in ED
IP : 196.52.84.10
212 Section VI n Disability

REFERENCES 17. JG Boggs, et al. Analysis of electrocardiographic changes


in status epilepticus. Epilepsy Research. 1993;(14):187-94.
1. Lowenstein DH, Bleck T, Macdonald RL. It’s time to
18. BD Adams. Fos-phenytoin may cause hemodynamically
revise the definitionIP :of196.52.84.10
status epilepticus. Epilepsia
1999;40:120-22. unstable bradydysrhythmias. Presented at the Southern
Medical Association Annual Scientific Assembly. Wash­
2. Nicholas S, Abend, MD, et al. Medical treatment of pediatric
status epilepticus. Semin Pediatr Neurol. 2000;17:169-75. ington, DC: November 2002;13-16.
3. Shinnar S, Berg AT, Moshe SL, et al. How long do new-on­ 19. Limdi NA, Knowlton RK, Cofield SS, et al. Safety of rapid in­
set seizures in children last? Ann Neurol. 2001;49:659-64. tra-venous loading of valproate. Epilepsia. 2007;48:478-83.
4. Wasterlain CG, Chen JW. Definition and classification of 20. Yu KT, Mills S, Thompson N, et al. Safety and efficacy
status epilepticus. In: Wasterlain CG, Treiman DM (Eds). of intravenous valproate in pediatric status epilepticus and
Status Epilepticus. Cambridge MA: MIT Press;2006.11-16. acute repetitive seizures. Epilepsia. 2003;44:724-26.
5. Sperk G. Changes in GABA-A receptors in status epilepti­ 21. Uberall MA, Trollmann R, Wunsiedler U, et al. Intrave­
cus. Epilepsia. 2007;48(Suppl 8):11-13. nous valproate in pediatric epilepsy patients with refrac­
6. Loscher W. Mechanisms of drug resistance in status epilep­ tory status epilepticus. Neurology. 2000;54:2188-189.
ticus. Epilepsia. 2007;48(Suppl. 8):74-77. 22. White JR, Santos CS. Intravenous valproate associated
7. McIntyre J, Robertson S, Norris E, et al. Safety and ef­ with significant hypotension in the treatment of status epi­
ficacy of buccal midazolam versus rectal diazepam for lepticus. J Child Neurol. 1999;14:822-23.
emergency treatment of seizures in children: A randomized
controlled trial. Lancet. 2005;366:205-10. 23. Mehta V, Singhi P, Singhi S. Intravenous sodium valproate
ver-sus diazepam infusion for the control of refractory sta­
8. M Ballaaji, I Santhanam, P Venkatesh, et al. Clinical profile
and risk factors for intubation in children presenting with tus epilep-ticus in children: a randomized controlled trial. J
status epilepticus to the pediatric emergency department. Child Neurol. 2007;22:1191-197.
Proceedings of National Assembly on Pediatric Emergency 24. Szaflarski JP, Meckler JM, Szaflarski M, et al. Leve­
Medicine. 2011. p. 189. tiracetam use in critically ill patients. Neurocrit Care.
9. KD Statler, CB Van Orman. Status Epilepticus Roger’s 2007;7:140-47.
Handbook of Pediatric Intensive Care, 4th edition. 2009. 25. Ramael S, Daoust A, Otou C, et al. Levetiracetam intra­
10. Riviello JJ Jr, Ashwal S, Hirtz D, et al. Practice parameter: venous infusion: A randomized, placebo-controlled safety
diagnostic assessment of the child with status epilepticus and pharmacokinetic study. Epilepsia. 2006;47:1128-135.
(an evidence-based review): report of the Quality Stan­ 26. Patel NC, Landan IR, Levin J, et al. The use of levetiracetam
dards Subcommittee of the American Academy of Neurol­
in refractory status epilepticus. Seizure. 2006;15:137-41.
ogy and the Practice Committee of the Child Neurology
Society. Neurol. 2006;67(9):1542-550. 27. Nicholas S, Abend MD, et al. Intravenous levetiracetam in
11. Appleton R, Macleod S, Martland T. Cochrane review critically ill children with status epilepticus or acute repeti­
2009: Drug management for acute tonic-clonic convul­ tive seizures. Pediatr Crit Care Med. 2009;10(4):505-10.
sions including convulsive status epilepticus in children. 28. Levetiracetam in children with refractory status epilepti­
12. McMullan, et al. Midazolam versus Diazepam for the cus. Epilepsy Behav. 2009;14(1):215-18.
treatment of status epilepticus in children and young 29. Koul RL, Raj Aithala G, Chacko A, et al. Continuous mida­
adults: A Meta-analysis. Academic Emergency Medicine. zolam infusion as treatment of status epilepticus. Arch Dis
2010;17:575-82. Child. 1997;76:445-48.
13. Rivera R, Segnini M, Baltodano A, et al. Midazolam in the 30. Igartua J, Silver P, Maytal J, et al. Midazolam coma for
treatment of status epilepticus in children. Crit Care Med.
refractory status epilepticus in children. Crit Care Med.
1993;21:991-94.
1999;27:1982-985.
14. Brevoord JC, Joosten KF, Arts WF, et al. Status epilepticus:
Clinical analysis of a treatment protocol based on midazo­ 31. Ozdemir D, Gulez P, Uran N, et al. Efficacy of continu­
lam and phenytoin. J Child Neurol. 2005;20:476-81. ous midazolam infusion and mortality in childhood refrac­
15. Lewena S, Young S. When benzodiazepines fail: How ef­ tory generalized convulsive status epilepticus. Seizure.
fective is second line therapy for status epilepticus in chil­ 2005;14:129-32.
dren? Emerg Med Australas. 2006;18:45-50. 32. Gilbert DL, Gartside PS, Glauser TA. Efficacy and mortal­
16. York RC, Coleridge ST. Cardiopulmonary arrest following ity in treatment of refractory generalized convulsive status
intravenous phenytoin loading. Acta Neurologica Scandi­ epilepticus in children: A meta-analysis. J Child Neurol.
navica. 1992;3(85):174-76. 1999;14:602-09.
Chapter 21 n Status Epilepticus 213

33. Morrison G, Gibbons E, Whitehouse WP. High-dose mida­ 36. Lee WK, Liu KT, Young BW. Very-high-dose phenobarbi­
zolam therapy for refractory status epilepticus in children. tal for childhood refractory status epilepticus. Pediatr Neu­
Intensive Care Med. 2006;32:2070-076. rol. 2006;34:63-65.
IP : 196.52.84.10
34. Koul R, Chacko A, Javed H, et al. Eight-year study of 37. Andrea O Rossetti. Which anesthetic should be used in
childhood status epilepticus: Midazolam infusion in man­ the treatment of refractory status epilepticus? Epilepsia.
agement and outcome. J Child Neurol. 2002;17:908-10. 2007;48(Suppl. 8):52-55.
35. Hayashi K, Osawa M, Aihara M, et al. Efficacy of intrave­ 38. Riviello JJ, Ashwal S, Hirtz D, et al. Practice parameter: Di­
nous midazolam for status epilepticus in childhood. Pediatr agnostic assessment of the child with status epilepticus (an
Neurol 2007;36:366-72. evidence based review). Neurology. 2006;67:1542-550.
Section VII
IP : 196.52.84.10

Envenomation
IP : 196.52.84.10
22
IP : 196.52.84.10

Scorpion Sting

Figure 22.1: Appropriate knowledge of the pathophysiology is essential to manage children with scorpion bite successfully
(Courtesy: Dr Thangavelu S).

Learning Objectives
1. Newer concepts on how the venom affects the au- 3. Evidence-based drug protocol.
tonomic system, heart and lungs. 4. Case scenarios illustrating how the PAT can be
2. To assess the severity of scorpion envenomation used to decide management.
using the rapid cardiopulmonary cerebral assess-
ment and the pediatric assessment triangle.

Introduction tributed to excessive catecholamine release.7,8,9 The venom


induces excessive catecholamine release or an autonomic
Scorpion stings are common in rural areas. Although 99 storm which activates the α-receptors, leading to the ef-
species of scorpion have been identified in India, only two, fects mentioned above viz. pulmonary edema, myocardial
Mesobuthus tamulus (the common red scorpion) (Figure dysfunction, tachycardia, shock, hypertension and exces-
22.1) and Palamnaeus swammerdami are poisonous.1 Car- sive sweating.
diac mani­festations, are common in Indian red scorpion
envenoma­tion. If not treated, death can occur in up to 25%
of children below the age of 5 years. Clinical Features
Clinical manifestations may be local or systemic. The
Pathophysiology symptoms may progress to maximal severity in 3–5 hours
and subside within 1–2 days.
Pulmonary edema (PE) is the most common cause of death
in scorpion envenomation.2 Cardiac dysfunction is the ●● The local manifestations include intense pain at the site
commonest cause of this dreaded complication.3,4 In addi- of sting, swelling and ecchymosis. It has also been ob-
tion, acute lung injury due to increased alveolar capillary served that if the pain is severe, there is less propensity
membrane permeability (non-cardiogenic pulmonary ede­ for progression to the more severe manifestations.
ma) has also has been noted.3,5,6 Pathogenesis of myocar- ●● The initial cholinergic stimulation causes vomiting,
dial dysfunction and increased blood pressure has been at- salivation, sweating, cold extremities, priapism and
218 Section VII n Envenomation

bradycardia. Sweating and salivation may persist for


6–13 hours. Occurrence of priapism, a poor prognostic
sign seems to be associated with myocardial dysfunc-
IP : 196.52.84.10
tion.
●● Stimulation of the sympathetic system leads to tac-
hypnea, pulmonary edema, tachycardia, arrhythmias,
hypertension, peripheral vasoconstriction, shock and
myocardial dysfunction. Hypertension usually lasts for
4–8 hours.
●● Hypotension which occurs in the early cholinergic
phase (1–2 hours) secondary to bradycardia indicates
a poor prognosis. It has also been noted at 4–48 hours
when it has been attributed to severe left ventricular Figure 22.3 Physiological status: Impending respi­ratory
dysfunction. Hypotension can also manifest 48–72 failure with hypotensive cardiogenic shock.
hours secondary to depletion of stored catecholamine.
●● Pulmonary edema, either cardiogenic or non-cardio-
genic can occur as early as 30 minutes after the scor- Interventions
pion sting. ●● Position airway and suction.
●● Neurotoxicity secondary to scorpion envenomation ●● Provide O2 via the JR circuit.
though uncommon is reported in India.10 The signs in- ●● 5–10 mL/kg NS bolus (pull push technique).
clude uncoordinated neuromotor hyperactivity, oculo- ●● Watch for signs of improvement or deterioration (evi-
motor and visual abnormalities, restlessness, agitation, dence of PE).
abnormal behavior, altered sensorium, convulsions, ●● Withhold Prazosin till BP normalizes.
hemiplegia and cerebral thrombosis.11,12 ●● After 10 mL/kg, the assessment was repeated.
●● Other rare, but fatal complications include DIC, hemo-
lysis, and pancreatitis.

Case scenario 1
A 10-year-old child is rushed into the ED with a history
of having been stung by a scorpion 3 hours ago. He has
increased salivation and has vomited twice. He also has
severe diaphoresis (Figures 22.2 to 22.4).

Figure 22.4 Physiological status: Worsening of pulmonary


edema, but his heart rate and BP have improved.

●● Initiate Dobutamine infusion at 10 µg/kg/min.


●● Intubate using PAI.

CASE SCENARIO 2
Figure 22.2: Sweating and salivation may persist for 6–13
hours (Courtesy: Dr Bawaskar HS). A 3-year-old girl had been rushed to the ED as soon as
she was bitten by a scorpion an hour ago at her home.
Chapter 22 n Scorpion Sting 219

She was crying due to severe pain over right foot. She Prazosin is available as 1 mg (scored) tablet. Sustained
was also having increased salivation and was profusely release tablets are not advised in this condition. The rec-
sweating (Figure 22.5). ommended dose is 30 µg/ kg/dose.
IP : 196.52.84.10
Administration of Prazosin in the prehospital setting
is one of the most useful strategies to reduce mortality in
scorpion envenomation.
Ù
Indeed, Prazosin must be stocked in every primary
health center and administered when signs of ‘autonom-
ic storm’ are identified.

Prazosin is administered only when features of auto-


nomic storm are identified. In hemodynamically unstable
patients, the priority remains in stabilization of the airway,
breathing and circulation. If shocked and hypotensive, it
Figure 22.5 Physiological status: Her cardiopulmonary and seems intuitive to correct shock and BP prior to adminis-
cerebral assessment was normal. However, she is showing tration of Prazosin. This drug should not be given prophy-
signs of autonomic storm and has higher than normal blood lactically in the absence of the ‘autonomic storm’. If the
pressure with peripheral vasoconstriction. child is unable to swallow, it may be administered through
a nasogastric tube. The mother should be instructed to
Management of Local and Systemic Effects keep the child in the supine position to avoid ‘first dose
hypotension’ due to Prazosin.
●● Local pain is managed with ice compression, oral par-
acetamol and regional nerve block using low concen- The rapid cardiopulmonary assessment should be per-
formed every 30 minutes for 3 hours, every hour for next
tration of lidocaine (without epinephrine).
6 hours and later every 4 hours till improvement. Prazosin
●● Antiemetics may be needed if vomiting is severe.
is repeated in the same dose at the end of 3 hours and later
●● Seizures are managed with benzodiazepines.
every 6 hours till extremities are warm and dry. Not more
●● Tetanus toxoid should be given intramuscularly.
than 4 doses are usually required in children.
●● Routine antimicrobials are not needed.13
●● Profuse diaphoresis and vomiting can cause fluid loss.
CASE SCENARIO 3
If the cardiopulmonary assessment suggests that the
child is stable but dehydrated, the hydration status is A 2-year-old boy was rushed into the ED with history of
corrected by fluid replacement. unknown insect bite over his right elbow. He had vom-
●● Prazosin is administered orally in the prescribed dose. ited twice and had profuse sweating. He had been taken
to the nearest PHC prior to referral and had reached
Prazosin the ED 6 hours after the bite (Figures 22.6 and 22.7).

Mechanism of action
Prazosin suppresses the sympathetic outflow and acti-
vates venom inhibited potassium channels. It blocks the
postsynaptic α-1 receptors and also prevents prostaglan-
din production. It reduces cardiac preload, afterload, BP
and CNS sympathetic stimulation without increasing the
heart rate or cardiac output (cardioprotective effect). Thus,
it prevents the hypertensive stress on the myocardium. Its
mechanism of action seems to counter the activity of the
scorpion venom. Oral Prazosin is fast acting, easily avail- Figure 22.6: Priapism, a poor prognostic sign seems to
able, relatively cheap, free from any anaphylaxis and high- be associat­ed with myocardial dysfunction (Courtesy: Dr
ly effective. Thangavelu S).
220 Section VII n Envenomation

IP : 196.52.84.10

Figure 22.7 Physiological status: Respiratory distress Figure 22.8: This picture shows pink froth which should be
probably due to cardiogenic or non-cardiogenic pulmonary differentiated from salivation (Courtesy: Dr Thangavelu S).
edema with normotensive shock.

Ù
Autonomic storm or pulmonary edema or priapism con-
firm the diagnosis of scorpion sting.

●● Provide O2 using a JR circuit.


●● Secure vascular access.
●● Administer 10 mL/kg of NS or RL; Prescribe oral Pra-
zosin (via NGT if he is unable to tolerate orally or is
vomiting).
●● Advice mother to keep her child supine to avoid drug-
induced hypoten­sion.
●● Repeat cardiopulmonary cerebral assessment. Figure 22.9 Physiological status: Respiratory failure,
●● If therapeutic goals of shock have not resolved and no bradycardia, hypotensive cardiogenic shock with altered
signs of pulmonary edema are noted, administer 5–10 mental status.
mL/kg of fluids (maximum of 20 mL/kg) until shock
resolves.
Management of Complications
●● Administer Prazosin 4th hourly as needed.
●● If shock has not resolved at 20 mL/kg or signs of pul- Airway and Breathing (Refer Protocol 22.1)
monary edema are noted at 5 or 10 or 15 or 20 mL/kg,
Since the risk of pulmonary edema is great in scorpion en-
initiate Dobutamine if BP is high3,8,9,10 and plan intuba-
venomation, oxygen is administered using the JR circuit.
tion.
This device, helps to provide CPAP in addition to oxygen
during resuscitation in the ED.
CASE SCENARIO 4
A 6-year-old girl was rushed into the ED for having been
stung by a scorpion the previous night. The nurse in the
Circulation
PHC where she had been taken, had injected her with Likewise, since the risk of myocardial dysfunction and
Decadron, Avil and Paracetamol and adviced to return pulmonary edema exists in children presenting with shock,
home. Next day she was found to be drowsy, breath- it would be wise to administer smaller boluses of 5 mL/kg
less with profuse sweating, vomiting. She was coughing up to a maximum of 20 mL/kg.
pink, frothy sputum (Figures 22.8 to 22.10).
●● If shock improves, further fluids may be stopped.
Chapter 22 n Scorpion Sting 221

●● If shock does not improve after the initial 20 mL/kg,


check for history of hypovolemia such as vomiting or Ù
diaphoresis. If yes, IP
smaller boluses may be considered. Children who received steroid and antihistaminics
: 196.52.84.10 either with or without Prazosin had a significantly
If not, consider initiating an inotrope infusion.
●● If during fluid therapy, signs of pulmonary edema or higher mortality than those who did not receive any
hepatomegaly are noted, stop fluids, initiate inotrope treatment.3
and plan intubation.
●● Dobutamine may be used if BP is high or normal. Recovery
●● Severe myocardial dysfunction manifested by hypoten-
sion may be treated with epinephrine infusion.
●● Arrhythmias should be managed as per PALS guide-
lines.
Ù
Vomiting, salivation, sweating contribute to dehydra-
tion. Correction of hypovolemia is a priority.

Investigations
●● Monitor sugar, urea, creatinine and liver enzymes.
●● ECG is useful in identifying ST depression, inverted T
waves, deep Q-waves in lead I and AVL, various de-
grees of heart block and arrhythmias. Figure 22.10 Physiological status: Alertness, normalization of
●● Echocardiogram may reveal systolic LV dysfunction. respiratory rates, work of breathing, heart rates with warm dry
normal peripheries, normal BP and liver span are suggestive
of recovery.
Scorpion Antivenom
Though considered as the specific treatment for scorpion
Prognosis
envenomation, it must be administered within 30 min­utes
of sting.18 Scorpion antivenom has not been found to be
more effective in reversing the cardiovascular toxic effects
Ù
Pain and age greater than 6 years are good prognostic
of the venom. Indeed, Prazosin has been found to prevent signs.
and relieve the cardiovascular manifestations in severe Delay in initiation of Prazosin therapy, pulmonary ede-
scorpion envenomation. ma, arrhythmias, encephalopathy and age less than 6
Avoid following drugs in the emergency management years, indicate a poor prognosis.
of cardiogenic shock due to scorpion sting.
Children presenting with scor­pion sting envenomation
●● Lytic cocktail. should be observed for at least 24 hours even if asymp-
●● Morphine. tomatic. Outcomes have improved with early identification
●● Steroids. and management of pulmonary edema and shock in the
●● Antihistamines ED. The early use of Prazosin also seems to have improved
●● Digoxin. the speed of recovery.
●● Diuretics.
222 Section VII n Envenomation

Key Points
1. Prehospital Prazosin
ü common errors
û
IP therapy improves outcome and
: 196.52.84.10 1. Restriction of fluid due to fear of pulmonary
prevents complications. edema.
2. Keep the patient in lying posture for about 3 hours 2. Failure to administer Prazosin to a stable child with
(even while examining the case) in order to prevent features of autonomic storm.
‘first dose phenomenon’ (hypotension). 3. Administration of Prazosin in a shocked child
3. Recognize pulmonary edema and shock since without attempting to resolve shock.
cardiac manifestations are common in Indian red 4. Administration of large volume of fluids (40–60
scorpion envenomation. mL/kg) in the absence of history suggestive of
4. Use JR circuit to provide oxygen if child has hypovolemia.
respiratory distress. 5. Failure to recognize development of pulmonary
5. Administer small aliquots of fluids to resolve edema during fluid therapy.
shock. 6. Failure to use JR circuit to provide oxygen in
6. Initiate inotrope and perform early intubation if respiratory distress.
signs of pulmonary edema are noted during shock 7. Use of morphine, digoxin, atropine, antihistamine
management. or furosemide for pulmonary edema.
Protocol 22.1: PEMC approach: Management of scorpion sting in the ED

IP : 196.52.84.10

Caution:
●● Risk of cardiogenic or non-cardiogenic pulmonary edema complicates shock management due to scorpion envenomation.
Chapter 22 n Scorpion Sting

●● During fluid therapy, monitor for airway instability, pink froth, increase or decrease in respiratory rates, grunt, retractions, abdominal respiration, fresh rales,
gallop, increasing liver span, agitation, fighting the mask and drop in oxygen saturations (i.e. signs of pulmonary edema). If any one or a cluster of signs
develop, stop further fluid, initiate inotropes and prepare to intubate.
223
224 Section VII n Envenomation

References 7. Peker E, Oktar S, Dogan M, et al. Prazosin treatment in the


management of scorpion envenomation. Hum Exp Toxicol.
1. Utpal Kant Singh, Layland FC, Sanjay, et al. Animal poi- 2010 Jan 12 [Epub ahead of print].
IP :in196.52.84.10
soning. In: Poisoning children, 2nd edition. Jaypee 8. Gupta BD, Parakh M, Purohit A. Management of Scorpion
Brothers Medical Publishers (P) Ltd. 68-74. Sting: Prazosin or Dobutamine. J Trop Pediatr. 2009 Aug
2. Mahadevan S. Scorpion sting. Indian Pediatrics. 26 [Epub ahead of print].
2000;37:504-14. 9. Patil SN. A retrospective analysis of a rural set up experi-
3. Biswal N, Bashir RA, Murmu UC, et al. Outcome of scor- ence with special reference to dobutamine in prazosin-re-
pion sting envenomation after a protocol guided therapy. sistant scorpion sting cases. J Assoc Physicians India. 2009
Indian J Pediatr. 2006 Jul;73(7):577-82. Apr;57:301-04.
4. Boyer LV, Theodorou AA, Berg RA, et al. Arizona Enveno- 10. Bawaskar HS, Bawaskar PH. Clinical profile of severe
scorpion envenomation in children at rural setting. Indian
mation Investigators, Chávez-Méndez A, García-Ubbeloh-
Pediatr. 2003 Nov;40(11):1072-075.
de W, Hardiman S, Alagón A. Antivenom for critically ill
children with neurotoxicity from scorpion sting. N ENGL J 11. Bawaskar HS, Bawaskar PH. Efficacy and safety of scorpi-
on antivenom plus prazosin compared with prazosin alone
MED. 2009 May 14;360(20):2090-098.
for venomous scorpion sting(mesbuthus tamulus): Ran-
5. Bahloul M, Rekik N, Chabchoub I, et al. Neurological domised open label clinical trial. BMJ. 2010:341 C7136
complications secondary to severe scorpion envenomation. 12. Deshpande SB. Antiscorpion venom scores over other
Med Sci Monit. 2005 Apr;11(4):CR196-202. Epub 2005 strategies in the treatment of scorpion envenomation. J
Mar 24. Postgrad Med. 2010;56:253-54.
6. Handbook on treatment guidelines for snake bite and scor- 13. Boyer LV, Theodorou AA, Berg RA, et al. Arizona Enveno-
pion sting. Tamil Nadu Health Systems Project, Health and mation Investigators. Chαvez-Mιndez A, et al. Antivenom
Family Welfare Department, Government of Tamil Nadu, for critically ill children with neurotoxicity from scorpion
Chennai. 2008. stings. N Engl J Med. 2009;360:2090-098.
23
IP : 196.52.84.10

Snake Bite Envenomation

Figure 23.1: Evidence-based resuscitation of snake envenomation leads to successful outcomes


(Courtesy: Dr Balaji J and Dr Gunda Srinivas)

Learning Objectives
1. Evidence-based prehospital care. ment and incorporating it into the pediatric assess-
2. Recognition of symptoms and signs of envenoma- ment triangle.
tion. 4. Evidence-based management of snake envenoma-
3. Management of snake envenomation using the tion.
modified rapid cardiopulmonary cerebral assess-

INTRODUCTION First Aid


Three hundred and thirty species of snakes are found in In- Prehospital care should focus on stabilization and rap-
dia, of which 70 species are poisonous. 70% of snake bites id transport to a health care facility where antivenom is
are ‘dry’ bites and do not result in envenomation. The ma- available.6
jority of bites occur in rural areas between April and Octo-
ber. Most significant envenomations in India are caused by Do it ‘RIGHT’
the common krait (Bungarus caeruleus) and Indian cobra
(Naja naja), which are neurotoxic and the saw-scaled vi- ●● R: Reassure the patient. 70% of all snake bites are
per (Echis carinatus) and Russell’s viper (Daboia russelii) by non-poisonous species.
both of which are hemotoxic1,2,3 (Figure 23.1). ●● I: Immobilize the bitten limb in a manner similar to
a frac­tured limb.
Use bandages or cloth to hold the splints.
PATHOPHYSIOLOGY OF SNAKE VENOM Do not block blood supply or apply pressure.
Snake venom is a complex mixture of enzymatic compounds Do not tie tight ligatures.6,7,8,9,10
(Table 23.1) (Phospholipases A2, D hydrolases, proteases,
hyaluronidase, nucleotidase and ATPases) and non-enzy-
Ù
Tight ligatures are dangerous.
matic compounds such as neuro and hemotoxins.4,5
226 Section VII n Envenomation

Table 23.1: Pathophysiology of snake venom

Snake Type of venom General site of action Type of venom component Clinical effects
IP :action
196.52.84.10
Viper, cobra Local toxins Bite site and bitten Neurotoxins, cytotoxin Local—pain, swelling,
limb blistering, bruising, necrosis
Cobra, krait, coral Neurotoxins Neuromuscular Neurotoxins (presynaptic, Progressive flaccid paralysis of
snake junction postsynaptic), dendrotoxins, skeletal muscle and diaphragm
fasciculins
Sea snakes Myolytic toxins Skeletal muscle Myotoxins Destruction of skeletal muscle
Viper Hematologic toxins Effect hemostasis— Procoagulants, fibrinolytics, Consumptive coagulopathy,
damage vessel walls, anticoagulants, hemorrhagin complete defibrination,
promote bleeding hemorrhage, thrombosis,
infarction, embolism
Viper Nephrotoxic toxins Kidneys Nephrotoxins Renal damage, failure, necrosis
Viper Cardiotoxic toxins Heart Cardiotoxins Cardiac arrhythmias, failure,
arrest

●● G, H: Get to the Hospital immediately.11


Ù Ù
Suction does not reduce the amount of circulating ven-
Do not waste time in traditional remedies which have om. It may in fact increase envenomation and also in-
NO PROVEN benefit. crease the risk of necrosis at the site of bite.
●● T: Tell the doctor of any systemic symptoms such as ●● Do not apply electric shock or cryotherapy to the
ptosis that manifest on the way to hospital. wound.

Indian National Snakebite Protocol 20077 Ù


Both measures have no benefit, but enhance the necrotic
The following traditional methods are not recommended: effect of the venom.
●● Do not wash the wound.
●● Avoid pressure immobilization.14
Ù Ù
Washing the wound increases the flow of venom into the
system by stimulating the lymphatic system. Pressure immobilization widely recommended in other
countries is not applicable in the Indian setting. Ban-
●● Do not apply tourniquets. dages increase the risk of local necrosis.

Ù
Tourniquet made of rope, string, belt and cloth increase Approach to an Individual
the risk of ischemia, necrosis and limb loss. When tour- Allegedly Bitten by a Snake
niquet is removed, there is risk of massive neu­rotoxin
●● Determine whether the patient has been bitten by a poi­
release or occurrence of embolism.
sonous snake.
●● Do not incise the wound.
Look for Fang Marks
Ù ●● The depth of the bite varies anywhere from 1 to 8 mm.
Incision of the wound due to hemotoxic bite increases
the risk of severe bleeding. ●● In some cases, there may be no external evidence of
snake bite.
●● Do not apply suction to the wound.12,13 ●● Absence of fang marks do not rule out snake bite in
agricultural areas.
Chapter 23 n Snake Bite Envenomation 227

Table 23.2: Summary of manifestations of bites from various species of snakes

Feature Cobras Kraits Russell’s viper Saw-scaled viper Hump-nosed viper


IP : 196.52.84.10
Local pain/tissue damage Yes No Yes Yes Yes
Ptosis/neurological signs Yes Yes Yes No No
Hemostatic abnormalities No No Yes Yes Yes
Renal complications No No Yes No Yes
Response to neostigmine Yes No? No? NA NA
Response to ASV Yes Yes Yes Yes No

Note Time of Bite


●● Time of onset of poisoning may be as early as 5 min-
Ù
Ptosis is an early sign of kraits and cobra bites.
utes or as late as 10 hours as in cobra bites. In viper
bites, the mean duration of onset of symptoms may be ●● Bleeding occurs at the site of bite, skin, gas­trointestinal
20 minutes, while in sea snake bites, myotoxic features tract, urinary tract and within the brain. Prolongation of
may occur within 2 hours. clotting time can occur in asymptomatic victims.
Ù Ù
In regions where snake bites are common, a high index Hemostatic abnormalities are the hallmark of viper
of suspicion based on symptoms and signs is needed to bites.
initiate therapy.
●● Cardiotoxicity manifests as tachycardia, hypotension,
myocardial infarction and cardiac arrest.
Local Manifestations
●● Hypotension and shock occur due to hemorrhage, va-
●● Local pain, tenderness, edema, erythema or discolor- sodilation, increased capillary permeability, acute pitu-
ation occur within 6–30 minutes (Table 23.2). itary, adrenal insufficiency (Russell’s viper bites) and
●● Tingling and numbness over the tongue, mouth and anaphylaxis due to ASV.
scalp are common in viper bites. ●● Acute renal failure (oliguria) is a complication of viper
●● Local bleeding including petechial and purpuric rash bite-induced muscle necrosis and myoglobinuria.16
are common in viper bites. ●● Ongoing absorption of the venom from blood (half-life
●● Wet gangrenous lesions and compartment syndrome of venom is between 26 and 96 hours) can lead to re-
are common in cobra bites. currence of symptoms.
●● Regional lymphadenopathy has been reported as an ●● Frequent evaluation of the patients is essential for 3–4
early and reliable sign of systemic poisoning.15 days.
●● Delayed manifestations in the initially stabilized pa-
Systemic Manifestation tients may occur even after 3 weeks. Venom released
●● Severe vomiting, headache, myalgia, vertigo and hy­ from local blebs (venom depots, not accessible to anti-
persalivation are common. venom) may be the cause of this phenomenon.

Neurological Symptoms Late-onset Envenomation


●● Ptosis, external ophthalmoplegia, hyperacusis and ●● Closely observe patients for at least 24 hours.
weakness of muscles of palate, jaw, tongue, larynx, ●● Krait and the hump-nosed pit viper poisoning can man-
neck and muscles of deglutition have been noted. Cra- ifest as late as 6–12 hours after the bite. At the start of
nial nerve involvement, drowsiness, coma and respira- the rainy season, juvenile snakes tend to bite the victim
tory muscle paralysis are other signs of severe enveno- in the hard tissue of the foot resulting in late signs of
mation. The diaphragm is the last to be affected.15,16 envenomation.
228 Section VII n Envenomation

CASE SCENARIO 1
A 10-year-old boy was brought to the ED with history of
IPthumb.
snake bite over the right : 196.52.84.10
He had severe pain over
bite site with progressive swelling (Figures 23.2 and 23.3).

Figure 23.4: Progression of edema (after 19 hours).

Figure 23.2: This child was rushed within an hour after snake
bite. His mother had immediately tied a tight tourniquet above
the forearm. On arrival he received 8 vials of ASV. Subsequently,
he received up to 30 vials based on rapidly progressing
cellulitis. This picture showing fang marks with bleb was taken
19 hours after the bite.

Figure 23.5: Note the rapidity of progression in 24 hours. Wound


was exposed for re-examination (note the date on photograph).

APPROACH TO ENVENOMATION IN THE ED


Investigations (Figures 23.6A and B)
20 minute whole blood clotting test (20 WBCT).

Figure 23.3 Physiological status: Cardiopulmonary cerebral


assessment is normal with signs of severe envenomation

At 19 hours after the bite, the swelling had extended al-


most to the axilla (Figure 23.4). Note the mark made by the
physician on the forearm, showing the extent of the edema.
This child was referred to the surgeon for rapid progressive
formation of gangrene on the same day. Within the next
12 hours, unfortunately, the surgeon who had taken up the
child for debridement had to disarticulate the thumb due to
gangrene of the joint (Figure 23.5). Figure 23.6A: Sample for whole blood clotting time collected
at 11:00 AM. C, Control; T, Test.
Chapter 23 n Snake Bite Envenomation 229

●● Take a 1–2 mL of fresh venous blood in a new, clean, ●● Urine analysis: Hematuria, proteinuria, hemoglobinu-
dry test tube and leave it undisturbed for 20 minutes. ria or myoglobinuria.
●● Gently tilt the tube without shaking. If the blood is still
IP : 196.52.84.10 ●● Blood group type and crossmatch.
liquid, then the patient has incoagulable blood. ●● ECG: Changes are usually non-specific and include
bradycardia, AV block with ST segment elevation or
depression. The ECG may also show features of hyper-
kalemia with peaked T waves.

Local Wound Management


●● Cleanse the wound and leave it open.
●● Mark with ink the proximal edge of the swelling or
where tenderness is noted. Note the time, such that
progression may be easily monitored.
●● If swelling is noted, elevate the affected limb using a
pillow.
●● Measure the circumference of the injured extremity ev-
Figure 23.6B: WBCT sample at 11:20 AM. C, Control; T, Test.
ery hour to monitor the level of edema.
●● If the 20 WBCT is normal, repeat the test every 30 min- ●● Elevate limb in the initial stages to reduc­e ede-
utes for 3 hours and then hourly thereafter for at least ma. However, there is no evidence to support its
24 hours to avoid missing late-onset envenomation. effectiveness.6,7
●● If 20 WBCT is abnormal, repeat 6th hourly (the liver
takes 6 hours to replace the clotting factors). Indication for Surgical Call Over
●● Although coagulation parameters such as prothrombin ●● Ulcer at the site of fang marks.
time, partial thromboplastin time and thrombin time ●● Necrosis of the skin and underlying tissues.
may be prolonged, these tests are not immediately ●● Gangrene of the toes and fingers.
needed during resuscitation in the emergency service. ●● Debridement of necrotic tissue.
●● Compartment syndrome.
Ù
20 minutes WBCT is a reliable test of coagulation, can Ù
be carried out at the bedside without specialist training Consider compartment syndrome if any of the following
in the most basic settings.6,7 6 Ps are noted:
Pain on passive stretching
Other laboratory tests which are useful for monitoring, Pain (out of proportion)
prognosticating and determining the stages of intervention Pulselessness
include: Pallor
Paresthesia
●● CBC: Anemia, leukocytosis and thrombocytopenia.
Paralysis.
●● Peripheral smear may provide evidence of hemolysis
and DIC especially in viperine bites.
●● Coagulation profile: PT, PTT, fibrinogen, FDP, clotting Care of the Wound
time and clot lysis time provide objective information
●● Minimize unnecessary blood loss.
regarding DIC. The quality of clot formed may be a
●● Remove debris and necrotic tissue by gently irrigating
better indicator of coagulation capability than the ac- with normal saline.
tual time required for formation. Clot lysis has been ●● Expose viable tissues and excise eschar after control-
observed in several patients who have a normal clot- ling the hemotoxic complications.
ting time. ●● Apply topical agents and non­-adherent dressing. This
●● BUN, creatinine, electrolytes, azotemia and hyper- will ensure epithelialization and prevent contamination
kalemia. of the wound.
230 Section VII n Envenomation

●● Perform surgical debridement, if needed.


●● Prepare for skin grafting if required.6
IP : 196.52.84.10
Fasciotomy
●● Prophylactic fasciotomy does not remove or reduce en-
venomation.
●● Visual impression is an unrealistic guide of intracom-
partmental pressure.
●● Tissue injury after compartment syndrome may be dis­
proportionate to the clinical status.
Ù
Fasciotomy is not required for every case (there is lit­tle
evidence that intracompartmental pressure) increases to Figure 23.7 Physiological status: Respiratory distress,
such an extent that fasciotomy is warranted.6,7 hypotensive shock with altered mental status and non-
convulsive status epilepticus.
●● If fasciotomy is required for compartmental syndrome
the wound needs to be taken care to prevent secondary Resuscitation
bacterial infection.
●● Provide oxygen through the Jackson-Rees circuit. Plan
intubation.
Criteria for fasciotomy ●● NS boluses of 5–10 mL/kg up to 20 mL/kg. If shock per-
1. Hemostatic abnormalities should have been corrected. sists after 20 mL/kg and significant bleed is not­ed more
2. Clinical evidence of compartmental syndrome. fluids may be warranted. Call for epinephrine infusion.
3. Intracompartmental pressure exceeds 30–40 mm of ●● Specific management: ASV: 8–10 vials.
Hg (normal < 20 mm Hg, measured using Stryker ●● Repeat WBCT every 6 hours.
pressure monitor or saline monitor).6,7,10 ●● If WBCT is abnormal, repeat 5–10 vials of ASV up to
a maximum of 30 vials.
Ù ●● If bleeding persists consider FFP, cryoprecipitate, fibrin-
Early treatment with adequate antivenom remains the ogen, factor VIII, fresh whole blood and platelets.
best way of preventing irreversible muscle damage.10
CASE SCENARIO 3
Medications A 10-year-old boy was rushed into the ED with history of
●● Administer tetanus toxoid. snakebite on his right forearm, whilst playing in the gar­
●● Administer antibiotic. den. He complained of pain at the site of bite. Fang marks
●● Mix 8–10 vials of ASV in NS or GNS and administer were noted. His 20 WBCT was normal (Figure 23.8).
over 1 hour.
●● Re-evaluate WBCT every 6 hours.

CASE SCENARIO 2
A 10-year-old girl was rushed into the ED following
snake bite over her right foot during the night, while
she was sleeping in the open field.
She was lethargic and breathless with swelling of the
right foot. Bleeding was noted from the bite site. She was
also passing red colored urine. Refer Figure 23.7.
She did not have ptosis, but had conjugate gaze to the
right. Whole blood clotting time prior to transfer to the Figure 23.8: Hemodynamically stable child with snake bite.
hospital was more than 20 minutes.
Chapter 23 n Snake Bite Envenomation 231

3. Swelling extending:
a. 15 cm or more within 1 hour.
b. Swelling reaching the knee or elbow < 4 hours after
IP : 196.52.84.10
bite involving the limbs.
c. Swelling involving the whole limb within 8 hours.
d. Extension to the trunk.
e. Swelling causing airway compromise or shortness
of breath.
f. Compartment syndrome or major vessel entrap-
ment.
Ù
Painful swelling that is both progressive and severe is a
definitive indication for ASV.
Figure 23.9 Physiological status: Cardiopulmonary cerebral
assessment normal 4. Cardiovascular abnormalities: hypotension, shock,
cardiac arrhythmias, abnormal ECG patterns.
Ù 5. Persistent and severe vomiting or abdominal pain.6
Swelling confined to the site of bite or fang mark from
an apparently venomous snake are not grounds for ad­ ASV Dose
ministration of ASV. Refer Figure 23.9. ●● 8–10 vials of ASV should be adminis­tered over 1 hour
(Figures 23.10A and B).
Specific Therapy: AntiSnake Venom It is given to neutralize the venom. There is no ben-
efit in administering it over longer periods and prolonging
Antisnake venom (ASV) a polyvalent venom, is effective
the time to neutralize. Snakes inject the same amount of
against all four common species such as Russell’s viper,
venom into adults as in children. Hence it is intuitive that
common cobra, common krait and saw-scaled viper. It is children receive the same ASV dosage as adults. The rec-
available in both liquid and lyophilized forms. Liquid ASV ommended dosage level has been based on published re-
has a 2-year shelf life, requires refrigeration and a reliable search that Russell’s viper injects around 63 mg of venom
cold chain during transportation. Lyophilized ASV in pow- (range 5–147 mg).17 One vial of ASV neutralises 6 mg of
der form does not need refrigeration for storage. This is Russell’s viper venom. Hence the requirement ranges from
par­ticularly useful in remote areas where power supply is 8–25 vials. The approximate requirement ranges from
inconsistent.6,7 8–25 vials.
ASV is a scarce and costly commodity. Every snake The dose of antisnake venom is determined by the
bite, even if poisonous, does not warrant snake antivenom. amount of venom that is injected.
The prophylactic use of antivenom should be avoided due
In fact, the amount of venom per square body surface
to the inherent risk of hypersensitivity reactions. Antiven-
may be more for children and young infants than adults.
om is indicated only if there are signs of systemic enveno-
mation or severe local swelling. Ù
Avoid using smaller doses for young infants and chil-
Refer Protocol 23.1. dren.
Administer 8–25 vials for all ages if signs of envenvo-
Indications for Administration of ASV mation are noted.
1. Evidence of coagulopathy: Whole blood clotting time The patient must be closely monitored for reactions to
exceeds 20 minutes or signs of spontaneous bleeding ASV for a minimum of 2 hours.
are noted.
2. Evidence of neurotoxicity: Ptosis, inability to lift the The lyophilized form is diluted in 10 mL of water and
head, diplopia, stridor, respiratory distress, neuropa- rolled between the palms. Shaking is not advisable since,
ralysis or coma. it could cause denaturation of the protein.
232 Section VII n Envenomation

●● Interrupt ASV infusion.


●● Administer 0.1 mL/kg of 1:10,000 adrenaline IV (since
IP : 196.52.84.10 IV access is already available during ASV administra-
tion).
●● Administer 2–6 mg/kg hydrocortisone IV.
●● Administer Antihistamine.
●● If any one sign is noted along with abnormal cardio-
respiratory status:
– Respiratory arrest: Initiate bag-valve-mask ventila-
tion and plan early intubation.
– Respiratory distress with shock: Provide oxygen
through non-rebreathing mask and nebulize.
– Nebulize with Salbutamol and Adrenaline for bron-
chospasm and laryngeal edema respectively.
– Initiate epinephrine infusion at the rate of 0.1–0.4
µg/kg/minute if hypotensive or bradycardic.
– Administer 20 mL/kg of NS boluses until shock
resolves (60–200 mL/kg may be needed to resolve
shock).
●● Antihistamine is controversial and is contraindicated in
the setting of hypotensive shock.
●● Continue ASV infusion at slower rates for 10–15 min­
utes keeping the patient under close observation. The
normal drip rate may be resumed. Monitor cardiopul-
Figure 23.10A and B: Method of administration of ASV. monary status and provide supportive mea­sures.6

●● IV infusion: Reconstituted ASV is diluted in 5–10 mL/


CASE SCENARIO 4
kg body weight of NS or GNS and infused in 1 hour at
a constant speed and closely monitored for 2 hours. A 1-year-old boy was rushed into the ED with history of
snakebite on his right leg whilst playing in the gar­den.
Ù He complained of pain and swelling at the site of bite.
Avoid administering ASV into the bite site. It is ineffec-
Fang marks and swelling of the right leg were noted.
tive, painful and raises the intracompartmental pres-
He also had ptosis (Figures 23.11 and 23.12).
sure, particularly in the digits.

Precautions Taken During


ASV Administration
●● Do not administer test dose.
A test dose does not predict occurrence of anaphylac-
toid or late serum reactions. These reactions may sensitize
thereby creating a greater risk of ana­phylaxis.
●● Monitor for anaphylaxis.

Anaphylaxis During ASV Administration


(Refer Figure 17.1, right extreme photograph)
If any one sign is noted, but rapid cardiopulmonary status Figure 23.11: Note the ptosis in this child brought with
is normal: history of envenomation (Courtesy: Dr Balaji J).
Chapter 23 n Snake Bite Envenomation 233

IP : 196.52.84.10

Figure 23.12 Physiological status: Cardiorespiratory


cerebral assessment is normal with ptosis.
Figure 23.13 Physiological status: Imminent
cardiorespiratory arrest.
Specific Management of
Neurotoxic Envenomation Resuscitation
●● Initiate bag-valve-mask ventilation followed by intu-
Neostigmine
bation and ventilation.
An anticholinesterase, Neostigmine prolongs the effect ●● Chest compression, if bradycardic.
of acetylcholine thereby reversing respiratory failure and ●● Epinephrine: 0.1 mL/kg (1:10,000) up to a maximum
other neurotoxic symptoms. It is particularly helpful in re- of 3 doses until heart rate improves to > 100/minute.
solving postsynaptic neurotoxins (Cobra). There is some ●● Administer NS bolus: 20 mL/kg (maximum 30 mL/kg
doubt over its usefulness against the presynaptic neurotox- unless anaphylaxis occurs or hypovolemia is noted in
ins secreted by Krait and Russell’s viper. However it is history).
worth trying in these cases.7 ●● Initiate epinephrine, if hypotensive or dopamine if nor-
motensive.
Neostigmine test
●● Administer 0.04 mg/kg of neostigmine IM along with
Specific Management
0.05mg/kg of atropine. ●● 8–10 vials of ASV mixed with 100 mL of GNS and
●● If the victim responds to the neostigmine test, then administered over 1 hour.
continue with 0.04 mg of neostigmine IM half hourly ●● Atropine: 0.02–0.05 mg/kg intravenously every 30
plus 0.05 mg of atropine IV half hourly until neuro- minutes.
logical recovery. Continuous infusion over 8 hours has ●● Neostigmine: 0.04–0.1 mg/kg every 30 minutes.
been advised in adults. If there has been no improve-
ment in symptoms after one hour, neostigmine should
Repeated ASV Doses
be stopped.7
Hemostatic bites:
CASE SCENARIO 5 ●● After the initial dose has been administered, no further
A 7-year-old boy was rushed into the ED. He was found ASV is given for six hours.
to be gasping for breath and unconscious since morning. ●● Repeat whole blood clotting time. If it exceeds 20 min-
He had been normal when he had gone to sleep the pre- utes (performed every 6 hours) it will help determine
vious night . There was no history of trauma or poison- whether additional ASV is required (max 30 vials).6
ing. A swelling was noted over the right elbow (Figure Neurotoxic bites:
23.13).
●● If 2 hours after the first dose of ASV and neostigmine,
Suspect snake envenomation in rural areas when sud- the victim has not improved or has worsened or has
den deterioration of hemodynamic status occurs in a previ- developed respiratory failure a second and final dose
ously normal child. Unprovoked bites usually occur due should be given.
to Krait.
234 Section VII n Envenomation

●● Administer the second dose of 10 vials over 1 hour. stabilize airway breathing and circulatory problems and
Maximum dose of ASV is 20 vials.6 consider early antivenom administration.
IP : 196.52.84.10
Recovery Phase Key Points
ü
If an adequate dose of appropriate antivenom has been ad- 1. Relieve anxiety and reassure victims that fatality is
ministered, the following responses may be seen: minimal. Most will recover.
2. Cellulitis and hemostatic abnormalities are the hall­
●● Spontaneous systemic bleeding such as gum bleeding
mark of Viperine envenomation.
usually stops within 15–30 minutes.
3. Ptosis is an early sign of krait and cobra (elapid
●● Blood coagulability is usually restored in 6 hours.
●● Postsynaptic neurotoxic envenoming (Cobra) may be- envenomation).
gin to improve as early as 30 minutes after antivenom, 4. 20 minutes WBCT test is the most useful bedside
but can take several hours. test to detect hemostatic abnormalities.
●● Presynaptic neurotoxic envenoming (Krait), usually 5. Children should receive the same ASV dosage
takes a considerable time to improve reflecting the need as adults, since snakes inject the same amount of
for the body to generate new acetylcholine emitters. venom into adults and children.
●● Active hemolysis and rhabdomyolysis may cease with- 6. ASV neutralizes the unbound venom and must be
in a few hours and the urine returns to its normal color. given as early as possible.
●● In hypotensive patients, blood pressure may increase 7. ASV is required only to those who show definite
after 30 minutes. signs and symptoms of envenomation.
What ASV cannot do? 8. Anaphylaxis or late serum sickness cannot be
determined or prevented by test dose.
1. Prevent or reverse necrotic action of the venom on tis- 9. Even if the patient develops reaction(s), the total
sue.
dose required should be administered slowly after
2. Prevent or reverse local swelling.
the patient recovers from the reaction(s).
3. Reverse coagulopathy (Liver regenerates clotting fac-
tors).
4. Reverse presynaptic envenomation. Nerve damage is
structural and large quantities of ASV are ineffective.
common errors
û
1. Resorting to traditional treatment rather than rushing
Body must regenerate synaptic vesicles.
to the hospital immediately.
5. Reverse acute kidney injury.
2. Incision (cutting) of the site of bite and suctioning
the incoagulable blood.
Renal Failure
3. Applying tight tourniquets over the bite site.
Acute kidney injury (AKI) a potentially lethal complica- 4. Local administration of ASV is ineffective, painful
tion, can occur even if WBCT has normalized. Overt clini- and raises intracompartmental pressure.
cal features of AKI are seen 5–12 days after the bite. 5. Using wet (not properly dried) test tube for the 20
●● Recognize and refer for hemodialysis. minutes WBCT test.
6. Washing the test tube with detergent (inhibit the
conclusion contact element of the clotting mechanism).
7. Administration of ASV without adequate agents for
The ability to identify poisonous from non-poisonous managing anaphylaxis.
snakes may help mitigate fear, facilitate effective treat- 8. Administration of ASV as IV bolus or IM directly.
ment strategies and reduce mortality. Most snakebites are 9. Discontinuation of ASV after mild reactions.
due to non-venomous snakes. A large number of snake- 10. Failure to treat shock and failure to provide early
bites by poisonous snakes are also asymptomatic. Reas-
ventilatory support in neuropoisonous snakebite.
surance, allaying of anxiety, rapid shift to the hospital and
11. Proceed to surgical management before coagulation
hospitalization for 24–48 hours are all that is required for
resolves.
the majority of cases. If signs of envenomation develop,
Chapter 23 n Snake Bite Envenomation 235

Protocol 23.1: PEMC approach to the management of snake bite in the ED


IP : 196.52.84.10
236 Section VII n Envenomation

References 10. Warrell DA. WHO/SEARO Guidelines for the clinical


management of snake bites in the Southeast Asian region.
1. Chippaux JP. Snake bites: Appraisal of the global situation. Southeast Asian J Trop Med Public Health. 1999;30 (Suppl
Bull World Health Organ. 1998;76(5):515-24.
IP : 196.52.84.10 1):1-85.
2. Gaitonde BB, Bhattacharya S. An epidemiological survey 11. McKinney PE. Out-of-Hospital and interhospital man-
of snake-bite cases in India. Snake. 1980;12:129-33. agement of crotaline snake bite. Ann Emerg Med.
3. Whitaker R. Common Indian Snakes-A Field Guide. Delhi: 2001;37(2):168-74.
MacMillan India Ltd; 1978. pp. 1-154. 12. Alberts MB, Shalit M, Logalbo F. Suction for venomous
4. Philip E. Snake bite and scorpion sting. In: Srivatava RN snakebite: a study of “mock venom in a human model”.
(Ed). Paediatric and Neonatal Emergency Care. New Del- Ann Emerg Med. 2004 Feb;43(2):181-86.
hi: Jaypee Brothers Medical Publishers (P) Ltd. 1994. pp. 13. Bush SP. Snakebite suction devices don’t remove venom:
227-34. they just suck. Ann Emerg Med. 2004;43(2):187-88.
5. Pillay VV. Comprehensive Medical Toxicology, 1st edi- 14. Gray S. Pressure Immobilization of Snakebite. Wilderness
tion, Hyderabad: Paras Medical Publishers; 2003. and Environmental Medicine. 2003;14(1):73.
6. Handbook on Treatment Guidelines for Snake Bite and 15. Wallace JF. Disorders caused by venoms, bites and stings.
Scorpion Sting. Tamil Nadu Health Systems Project, Health In: Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf
and Family Welfare Department, Chennai: Government of RG, Martin JB, Fauci AS, Root RK (Eds). Harrison’s Prin-
Tamil Nadu, 2008. ciple of Internal Medicine. Volume 2. 12th Edition. New
7. Indian National Snakebite protocols 2007, Indian National York: McGraw-Hill. 1991:2187-194.
snakebite protocol consultation meeting 2nd August 2007, 16. Theakston RDG, Phillips RE, Warrell DA, et al. Envenom-
Delhi. ing by the Common Krait (Bungarus caeruleus) and Sri
8. Simpson ID. The paediatric management of snake bite: Lankan Cobra (Naja naja) efficacy and complications of
The National Protocol. Indian Pediatrics. 2007;44:173-76. therapy with Halfkein antivenom. Transactions of the Royal
9. Simpson ID. Snakebite: Recent Advances 2006 in Medi- Society of Tropical Medicine and Hygiene 1990;84:301-08.
cine Update 2006 Ed Sahay BK The Association of Physi- 17. Tun P, Khin AC. Amount of venom injected by Russell’s
cians of India. 639-643. Viper (Vipera russelli): Toxicon. 1986;24:730-33.
Section VIII
IP : 196.52.84.10

Poisoning
IP : 196.52.84.10
24
IP : 196.52.84.10

Poisoning: General Approach

Figure 24.1: Children with poisoning need to be managed appropriately as fast as possible

Learning Objectives
1. Principles of management specific for the poisoned 3. Evidence-based approach for prevention of absorp-
child. tion of toxins.
2. Toxidromes which help recognize seriously ill poi- 4. Methods available for enhancement of excretion.
soned children.

Ingestion of a harmful substance is among the most com- evidence such as an empty bottle, presence of tablets or
mon causes of injury to children less than 6 years of age. spillage of house hold chemicals near a child.
Fortunately, in most cases the ingested agent has minimal ●● Evaluate constituents of the ingested substance and
or no clinically important toxic effects. Rarely, the ingest- calculate its per kilogram body weight.
ed amount is life-threatening resulting in death. Some of
●● In young infants, presume that maximum amount has
the commonest toxin-induced injuries encountered in our
country are following ingestion of kerosene, herbal medi- been ingested by comparing the volume of liquid or
cines such as vasambu (Acorus calamus or commonly number of the tablets remaining in the container. Take
called Sweet Flag), camphor, neem oil, insecticides and spillage into account.1
corrosives. Commonest drugs ingested by children are
dapsone, iron preparations, oral hypoglycemics and anti- Management
hypertensives (Figure 24.1).
1. Cardiopulmonary cerebral assessment and resuscitation.
2. Prevention or reduction of absorption.
Identification of Poison 3. Enhancement of excretion.
A high index of suspicion is needed to recognize poisoning 4. Administration of antidotes.
if history is unavailable.
Ù
Early aggressive efforts to eliminate the toxin is the best
●● Suspect poisoning if an apparently normal child devel­
ops symptoms of organ dysfunction with circumstan­tial guarantor for successful outcomes.
240 Section VIII n Poisoning

Cardiopulmonary Cerebral ●● Perform dextrostix and correct documented hypogly­


Assessment and Resuscitation1 cemia with boluses of 5 mL/kg of 10% dextrose. Initi-
ate intravenous fluids at maintenance rates if the victim
Ù IP : 196.52.84.10
“Treat the patient not the poison.”
presents with nausea and vomiting in the absence of
shock.
●● Avoid treating mild metabolic acidosis, since it is often
●● Plan early intubation, if victim presents with an unmain­ encountered, but does not require specific therapy.
tainable airway or/and respiratory failure. ●● Treat convulsions using the standard protocol for status
●● Profound depression of mental status can result in air- epilepticus.
way com­promise and respiratory failure. ●● Monitor hepatic and renal function.
●● Correct shock with 10–20 mL/kg isotonic fluids. Shock
may occur due to vomiting and diarrhea.
Management of Arrhythmias
●● If cardiogenic shock is noted initiate appropriate iono­
trope infusion based on blood pressure (BP) (Establish ●● Treat hypoxia and hypercarbia.
euvolemia prior to starting intrope). ●● Correct dyselectrolytemia and acid-base abnormalities.

Table 24.1: Toxidromes

Toxidromes Associated signs Possible toxin


Anticholinergic activity 1. Hot as a hare: Hyperthermia Atropine
2. Dry as a bone: Dry mucosa and skin Antihistamine
3. Red as a beet: Flushing Antispasmodics
4. Mad as a hatter: Delirum Phenothiazines
5. Blind as a bat: Mydriasis Tricyclic antidepressants
6. Tachycardia Mushroom poisoning
7. Urinary retention Antiparkinsonian drugs
Cholinergic activity
Muscarinic effect 1. Salivation Organophosphorus toxins (insecticides)
2. Lacrimation
3. Urination
4. Defecation
5. Gastrointestinal cramping
6. Emesis
7. Miosis
Nicotinic effect
Stimulation followed by paralysis of Fasciculations, weakness, paralysis Organophosphorus poisons
preganglionic and somatic nerve fibers,
excessive cholinergic stimulation of the
motor end plate
Sympathetic nervous system activity Fever, flushing, tachycardia, hypertension, Cough and decongestants, theophylline
miosis, sweating
Methemoglobinemia Cyanosis resistant to oxygen Alamine dyes, nitrates, benzocaine,
phenacetin, nitrobenzene, chlorates
Acute ataxia and nystagmus Antihistamines, alcohol, anticonvulsants,
bromides, organic solvents
Metabolic acidosis Effortless tachypnea Ethanol, carbon monoxide, iron, diabetic
medications, salicylates, tricyclic
antidepressants
Renal failure Oliguria, anuria, hematuria, myoglobinuria Carbon tetrachloride, ethylene glycol,
methanol, mushrooms, oxalates
Chapter 24 n Poisoning: General Approach 241

Ù Ù
Arrhythmias are usually rare, but if present, treatment of Gastric lavage, can be considered, when a potentially
IP : 196.52.84.10 life-threatening amount of a poison has been ingested.
hypoxia, hypercarbia, dyselectrolytemia and acid-base
abnormalities are usually sufficient to correct them.

●● Consider specific therapy, if supportive measures are


not adequate to correct arrhythmias.

Poison Syndromes2 (Toxidromes)


Toxins can result in a cluster of signs, which help to recog-
nize the specific agent (Table 24.1).
Perform a complete neurological assessment, while
resuscitation is in progress. It could reveal clues, which
point towards the specific toxin especially when history is
unavailable.
Figure 24.2: Activated charcoal is being administered as a
slurry through the nasogastric tube
Laboratory Investigations
●● Unless intubated, gastric lavage is con­traindicated, if
Laboratory analysis of serum or urine should be guided by
the substance ingested, its anticipated degree of toxic­ity children whose airway protective reflexes are lost.
and the value of measuring these concentrations. The need ●● Gastric lavage is contraindicated, if a hydrocarbon with
for toxicologic screening tests in children is rare, since the high aspiration potential has been ingested.
ingested substance is usually known. ●● Gastric lavage is also contraindicated, if a corrosive
substance has been ingested.
Prevention or Reduction of Absorption Ù
Patients, who are more like­ly to benefit from aggressive
The term ‘gastrointestinal decontamination’ includes in- gastrointestinal decontamination.7
terventions that are used to prevent the absorption of an • Obtunded patients presenting very soon after in-
ingested toxin (Figure 24.2). gestion.
Ù
Routine induction of emesis is not recommended in the
• Ingestion of a life-threatening or massive amount.
• Drugs that could delay gastric emptying.
management of toxin ingestion. • Ingestion of sustained release tablets.

Method
Syrup Ipecac3
Ipecac has no role in the routine management of acutely 1. Competence of the gag reflex should first be con­
poisoned patients. firmed.
2. Once properly restrained, the child should be placed in
a left lateral decubitus (Trendelenburg position) in or­der
Gastric Lavage4,5,6 to limit the movement of the gastric contents into the
Ù
Gastric lavage should not be employed routinely, if ever,
duodenum and minimize the risk of aspiration.
3. A large bore, single lumen tube should be placed by an
in the management of poisoned patients. orogastric route.
4. The proper placement of the tube is confirmed by the
American Academy of Clinical Toxicology; European As- spontaneous or aspirated return of gastric contents or
sociation of Poisons Centers and Clinical Toxicologists by auscultation of insufflated air when a stethoscope is
recommend the following: placed over the stomach after placement of the tube.
242 Section VIII n Poisoning

5. NS in aliquots of 10–15 mL/kg of body weight are creased systemic absorption of the ingested toxins when
instilled through the tube and then aspirated. This pro- compared with standard activated charcoal.12,13 They are
cess is continued until
IP :the aspirated contents are clear.
196.52.84.10 also more palatable than standard charcoal products.
Volumes as large as several liters may be necessary to When administered within 1 hour after ingestion, acti-
produce a clear aspirate. vated charcoal can reduce the absorption of toxins by up to
When performed 1 hour after the ingestion of a toxic 75%. Optimal adsorption occurs when the ratio of charcoal
substance, lavage retrieves less than 30% of the toxin. to toxin is 10:1 or higher.14
Hence, its use beyond the 1st hour is questionable. If not
●● Recommended dose is 1 g/kg body weight.
properly performed, gastric lavage has the potential com­
plication of propelling toxins into the duodenum, thereby
increasing the likelihood of absorption.8 Method of Administration
Ù Normal mental status:
The greatest risks associated with gastric lavage are: ●● Mix activated charcoal in fruit juice or bottled drinks as
• Inadvertent placement of the tube into the trachea a slurry for children.
or a main stem bronchus. ●● Additives, such as bottled drinks or fruit juices, make
• Esophageal injury. charcoal more palatable without reducing its effica-
• Hypothermia. cy.13
• Hyponatremia. ●● Young children will not voluntarily drink activated
• Water intoxication. charcoal quickly enough for it to work optimally.
Avoid gastric lavage if: ●● Introduce a nasogastric tube in young children to en-
• Mental status is depressed and airway protective sure prompt administration.
reflexes are lost.
• Kerosene ingestion (low-viscosity hydrocarbon). Depressed mental status or respiratory failure:
• Corrosive agent ingestion. ●● Intubate (for airway protection) and use nasogastric
tube for administration.
Nasogastric aspiration is performed by placing a naso-
gastric tube (smaller than a orogastric tube) and aspirating ●● Elevate head end by 45°.
gastric contents without instilling water.
Complications
Nasogastric aspiration may be effective in cases of liq-
uid poison ingestion,9 but it is not adequate for ingestion The main hazards associated with the administration of
of pills. activated charcoal are vomiting and aspiration.15,16,17,18 Al-
though activated charcoal is often described as inert, data
Activated Charcoal from experimental studies indicate that aspirated charcoal
can produce pulmonary parenchymal injury or bronchioli­
Ù tis obliterans. The installation of charcoal into the lungs
Activated charcoal should be administered within 1 hour through the inadvertent placement of an orogastric or na­
of ingestion of toxin.10 sogastric tube into the trachea has had disastrous results
including, death. Bowel sounds should be monitored, since
Activated charcoal ‘adsorbs’ poisons dissolved in the
constipation and rarely intestinal obstruction have been re-
intestine such that the poison remains in the gut rather than
ported.
being absorbed into circulation. It limits the systemic ab-
sorption of many drugs in a time-dependent manner and
may decrease the need for antidotal therapy for patients Indications for Activated Charcoal
who present within 2 hours of acetaminophen ingestion.11
Medications that are well bound by charcoal are drugs that
However, activated charcoal has not been shown to im- undergo enterohepatic or enteroenteric circulation such as:
prove the outcomes of non-selected poisoning patients.
●● Salicylates.
Currently superactivated charcoal products with in­
●● Phenobarbital.
creased surface area are available. These products de­
Chapter 24 n Poisoning: General Approach 243

●● Carbamazepine. ●● Administer Metoclopramide (antiemetic), since it in­


●● Digoxin. creases GI motility.
●● Theophylline. ●● Provide a bedside commode for patients who are
IP : 196.52.84.10
awake.
Substances which are not adsorbed by activated char-
coal are remembered by the mnemonic PHAILS: Whole bowel irrigation is safe in children, volumes as
large as 44 L have been administered without ill effects.
●● P: Pesticides. Typical rates of administration are 500–1,000 mL/h, orally
●● H: Hydrocarbons. or by nasogastric tube. The adverse effects associated with
●● A: Acids, alkalis, alcohols. this procedure consist of vomiting, abdominal cramps and
●● I: Iron. bloating.
●● L: Lithium.
●● S: Solvents. Patients with trivial ingestion do well without treat-
ment and their greatest risk is an iatrogenic complication.
Even patients with more serious ingestions usually have
Catharsis good outcomes with supportive care alone. It is no longer
Cathartic agents have been advocated in poisoned victims sufficient to justify gastric lavage or forced administra-
to increase gastrointestinal motility and hasten expulsion tion of activated charcoal with the supposition that “the
of the toxin or the toxin-adsorbent complex.19 patient could have taken something bad”. However, there
are some overdoses, where limiting the systemic absorp-
Commonly used osmotic agents are magnesium citrate tion of the poison may limit the toxic effects and prevent
and sorbitol. These agents promote retention of colonic serious toxicity. After careful consideration of the risks, GI
fluid and stimu­late gastrointestinal motility. decontamination should be targeted at patients who, in the
opinion of the treating physician, have a potentially life-
Ù
Currently, cathartic agents are contraindicated. The threatening exposure.3
risk of hypernatremic dehydration and cardiovascular
collapse is high with sorbitol, while hypermagnesemia Enhancement of Excretion: Ion Trapping
is a hazard in children with renal disease.
Urine Alkalinization
Whole Bowel Irrigation (WBI)20,21,22 Urine alkalinization23 is a treatment regimen that increases
elimination of poison by the administration of intravenous
In this procedure, large volumes of solution are adminis- sodium bicarbonate to produce urine with a pH of 7.5. The
tered enterally until the rectal effluent is clear. Polyethyl- term urine alkalinization emphasizes that urine pH ma-
ene glycol-electrolyte (PEGLEC) lavage solution has been nipulation rather than a diuresis as the prime objective of
formulated to prevent extensive absorption or secretion of treatment.
fluid across the gastrointestinal mucosa (Table 24.2).
●● Consider urine alkalinization as first line treatment for
●● Elevate head end of bed to at least 45° to prevent as- patients who have moderately severe salicylate poison-
piration. ing and who do not meet the criteria for hemodialysis.
●● Discontinue the infusion for 30 minutes, if emesis oc-
●● Urine alkalinization cannot be recommended as first
curs and restart at half the previous rate.
●● Increase the rate as tolerated. line treatment in cases of phenobarbital poisoning as
multiple-dose activated charcoal is superior.
Table 24.2: Whole bowel irrigation

Route Nasogastric tube


Indication Iron tablets, slow release drugs, lithium21,22
Dose 30 mL/kg /h
End point Clear effluent after several hours
Contraindication GI bleed, bowel obstruction
244 Section VIII n Poisoning

Table 24.3: Commonly available specific antidotes

Poison Antidote and dose


Anticholinergics
IP : 196.52.84.10 Physostigmine [0.5 mg, slow IV over 5 (atropine group) minute; repeated
every l0 minute till a maximum of 2 mg].
Arsenic, mercury Dimercaprol
β-blockers Glucagon
Benzodiazepines Flumazenil
Calcium channel blockers, hydrogen fluoride Calcium
Carbon monoxide Pure oxygen
Copper Penicillamine
Cyanide Sodium nitrite 3% solution, 0.2 mL/kg, IV over 2 minute followed by sodium
thiosulphate (25% solution, 1 mL/kg, IV, over l0–20 minute)
Digoxin Digoxin-specific FAB fragments

Ethylene glycol and Methanol (used in antifreeze, Fomepizole


heating fuel, wind screen wiper and deicing products)
Heparin Protamine

Iron Desferrioxamine l5 mg/kg/h IV in 100–200 mL 5% glucose solution


(maximum of 6 g)
Isoniazid, ethylene glycol Pyridoxine

Lead Sodium calcium edetate

Methemoglobinemia Methylene blue

Narcotics (opium) Naloxone—0.l mg/kg, IV or intratracheal, morphine from birth up to 5 year


or 20 kg of weight, at which time a minimum of 2 mg is used
Nitrate and nitrites If methemoglobinemia, treat with methylene blue
Opioids Naloxone, Nalmefene
Organophosphates Atropine—0.05 mg/kg IV, every 10 minute until signs of atropinization.
PAM 25–50 mg/kg IV, in older children and 250 mg IV in infants over 5–10
minute, 8 hourly up to 36 hour
Paracetamol N-acetylcysteine; Oral—intially 140 mg/kg, then 4 hourly, up to 72 hour.
IV—150 mg/kg by infusion
Over 15 minute followed by 50 mg/kg 4 hourly for 72 hour
Phenothiazine Benadryl (diphenhydramine) 1–2 mg/kg (promethazine)
Sulfonylurea class of oral hypoglycemic drugs Octreotide
Warfarin Vitamin K
Chapter 24 n Poisoning: General Approach 245

●● Urine alkalinization and high urine flow (approxi­ removal of toxins than from advanced intensive care after
mately 600 mL/h) increases urine elimination of 2,4- entry of toxins into the human circulation.
dichlorophenoxyacetic
IP :acid and mecoprop poisoning.
Ù
196.52.84.10 Key Points
ü
Hypokalemia is the most common complication, but can 1. Energetic emergency care and elimination of toxin
be corrected by giving potassium supplements. Alkalotic is key to survival in the poisoned victim.
tetany occurs occasionally, but hypocalcemia is rare. 2. Emesis has been replaced by activated charcoal and
There is no evidence to suggest that relatively short-du- whole bowel irrigation.
ration alkalemia (more than a few hours) poses a risk to 3. Gastric lavage should not be performed routinely in
life in normal individuals. all children with toxin ingestion.

Forced Neutral Diuresis common errors


1. Failing to consider poisoning in an apparently
û
This is a method of flushing the toxin out of the system by
increasing the ad­ministration of fluids. normal child with profound fall in mental status.
2. Performing gastric lavage for minimal ingestion.
Increase urinary flow by infusion of large volume of 3. Not using activated charcoal or whole bowel
intravenous crystalloid. irrigation for the appropriate toxins.
1. Indications: Lithium, bromide ingestion.
2. Contraindications: Pulmonary edema, cerebral edema REFERENCES
and renal failure. 1. M Riordan, G Rylance, K Berry, et al. Poisoning in chil-
Ù dren 3: Common medicines. Arch Dis Childhood. 2002
87:400-402 doi:10.1136/adc.87.5.400.
Forced neutral diuresis has limited clinical value.
2. Diane P Callelo, et al. New and novel antidotes in pediat-
rics. Pediatr Emerg Care. 2006;22(7).
Hemodialysis 3. K. Heard, Gastric Decontamination. Med Clin N Am 89.
2005:1067-078.
An invasive procedure, hemodialysis is reserved for spe­cific
4. Vale JA. Position statement: gastric lavage. American
life-threatening toxins in the intensive care setting.
Academy of Clinical Toxicology; European Association of
Poisons Centres and Clinical Toxicologists. J Toxicol Clin
Indications Toxicol. 1997;35:711–19.
Methanol, ethylene glycol, salicylate, phenobarbital, theo- 5. Vale JA, Kulig K; American Academy of Clinical Toxicol-
phylline, lithium. ogy; European Association of Poisons Centres and Clinical
Toxicologists. J Toxicol Clin Toxicol. Position paper: Gas-
tric lavage 2004;42(7):933-43.
Antidotes 6. Tucker, Jeffrey R. Indications for techniques of complica-
(Table 24.3) tions of and efficacy of gastric lavage in the treatment of
Rarely, emergency management involves the administra- the poisoned child. Current Opinion in Pediatrics. 2000;
tion of an antidote such as Naloxone after an over dose of (12). pp. 163-65.
an opioid drug. 7. Bond GR. The role of activated charcoal and gastric emp-
tying in gastrointestinal decontamination: a state-of-the-art
Despite the vast number of toxins and drugs that are review. Ann Emerg Med. 2002;39:273-86.
ingested, only a few antidotes are available.
8. Grierson R, Green R, Sitar DS, et al. Gastric lavage for
Ù
Medicolegal entries should be made by physicians not
liquid poisons. Ann Emerg Med. 2000;35:435-39.
9. Saetta JP, March S, Gaunt ME, et al. Gastric emptying pro-
involved in resuscitation. cedures in the self-poisoned patient: are we forcing con-
tents beyond the pylorus? J R Soc Med. 1991;84:274-76.
In summary, poisoned children derive more benefit 10. Chyka PA, Seger D. Position statement: single-dose acti-
from early and aggressive resuscitation of the ABCs and vated charcoal. American Academy of Clinical Toxicol-
246 Section VIII n Poisoning

ogy; European Association of Poisons Centres and Clinical 17. Liisanantti J, Kaukoranta P, Martikainen M, et al. Aspira-
Toxicologists. J Toxicol Clin Toxicol. 1997;35:721-41. tion pneumonia following severe self-poisoning. Resusci-
11. Buckley NA, Whyte IM, O’Connell DL, et al. Activated tation. 2003;56:49-53.
IP : 196.52.84.10
charcoal reduces the need for N-acetylcysteine treatment 18. Pollack MM, Dunbar BS, Holbrook PR, et al. Aspiration of
after acetaminophen (Paracetamol) overdose. J Toxicol activated charcoal and gastric contents. Ann Emerg Med.
Clin Toxicol. 1999;37:753-57. 1981;10:528-29.
12. Roberts JR, Gracely EJ, Schoffstall JM. Advantage of high- 19. Barceloux D, McGuigan M, Hartigan-Go K. Position state-
surface-area charcoal for gastrointestinal decontamination ment: cathartics. American Academy of Clinical Toxicol-
in a human acetaminophen ingestion model. Acad Emerg
ogy; European Association of Poisons Centers and Clinical
Med. 1997;4:167-74.
Toxicologists. J Toxicol Clin Toxicol. 1997;35:743-52.
13. Krenzelok EP, Heller MB. Effectiveness of commercially
20. Anonymous. Position paper: whole bowel irrigation. J
available aqueous activated charcoal products. Ann Emerg
Toxicol Clin Toxicol. 2004;42:844-54.
Med. 1987;16:1340-43.
14. Osterhoudt, Kevin C, Alpern, et al. Activated Charcoal Ad- 21. Tenenbein M. Whole bowel irrigation as a gastrointestinal
ministration in a Pediatric Emergency. Department Pediat- decontamination procedure after acute poisoning. Med
ric Emergency Care; 2004(20)8. pp. 493-98. Toxicol. 1988;3:77-84.
15. Arnold TC, Willis BH, Xiao F, et al. Aspiration of activated 22. Buckley N, Dawson AH, Howarth D, et al. Slow-re-
charcoal elicits an increase in lung microvascular perme- lease verapimil poisoning. Use of polyethylene glycol
ability. J Toxicol Clin Toxicol. 1999;37:9-16. whole-bowel lavage and high-dose calcium. Med J Aust.
16. Moll J, Kerns W II, Tomaszewski C, et al. Incidence of 1993;158:202-04.
aspiration pneumonia in intubated patients receiving acti- 23. Proudfoot AT, Krenzelok EP, Vale JA, et al. Position Paper
vated charcoal. J Emerg Med. 1999;17:279-83. on Urine Alkalinization. 2004;(42):1-26.
25
IP : 196.52.84.10

Specific Poisons

Figure 25.1: Common household products that carry potential risk of poisoning in young children

Learning Objectives
1. Approach to management of poisoning in 2. Management of organophosphorus poisoning
children using the rapid cardiopulmonary cerebral based on the Cochrane 2012 guidelines.
assessment and the pediatric assessment triangle. 3. Approach to kerosene, opioids, barbiturates, iron,
paracetamol and button battery ingestion.

Specific poisons (HETP), Diazinon, Tik-20, Methyl Parathion, Metacide


and TEPP:
The common household products, which are easily acces­sible
to children is shown in the Figure 25.1. These have potential ● ● HETP is the least toxic.
to cause poisoning when consumed in large quantities. Kero­ ● ● TEPP is the most toxic and fastest acting OP com­
sene, organophosphorus compounds (OPC) and carbamates pound.
are the other most commonly consumed poisons. Used as fuel ●● The noxious odor and taste of OP ensures that accidental
and pesticides in agri­cultural households, accidental poison­ ingestion is minimal and therefore non-lethal. On the con­
ing can occur from inhalation of spray, ingestion and absorp­ trary, homicidal administration is usually lethal.
tion through the skin and mucosa. Fatal poisoning from OPC
can re­sult from contamination of clothing and food articles. Pathophysiology
The worst affected are farm workers and their children.1 Ado­ OPC binds irreversibly to enzyme acetylcholinest­erase,
lescents consume OPC with suicidal intent. preventing the breakdown of acetylcholine. Acetylcho­
line accumulates resulting in muscarinic, nicotinic and
ORGANOPHOSPHATE INSECTICIDES parasympathetic stimulation of the central nervous system
(Figure 25.2).
Common Agents
Respiratory route of absorption leads to the fastest onset
Malathion, Parathion (fatal dose 0.l mg/kg), Octam­ethyl
of action. Clinical features appear when cholinesterase ac­
pyrophosphoramide (OMPA), Hexaethyltetra­phosphate
tivity falls to 25%–30% of normal.
248 Section VIII n Poisons

IP : 196.52.84.10

Figure 25.2: The sites of nicotinic and muscarinic acetylcholine re­ceptors.


(ACh, acetylcholine; N, nicotinic; NE, norepineph­rine; NT, neurotransmitter).

Clinical Picture
Ù Table 25.1: Clinical manifestations of organophosphates
Muscarinic effects of acetylcholine is represented by the
poisoning (OPP)
two mnemonics: (seen more commonly in adults)
SLUDGE—Salivation, Lacrimation, Urination, RS Rhinorrhea, bronchorrhea, bronchoconstriction,
Defecation, Gastrointestinal cramping and Emesis. wheezing, dyspnea, pulmonary edema, respiratory
DUMBBELS—Diarrhea, Urinary incontinence, Miosis, arrest within 72 hours
Muscle fasciculation, Bronchorrhea, Bronchospasm, CVS Bradycardia, heart block, cardiac arrest
Bradycardia, Emesis, Lacrimation, Salivation. CNS ÙHeadache,
common)
giddiness, coma, convulsions (most

●● Nicotinic effect initially results in stimulation followed GIT Nausea, vomiting, diarrhea, abdominal cramps
by paralysis of the preganglionic and somatic nerve fi­ Eye Miosis, blurred vision, lacrimation (red tears due
bers leading to twitching of eyelids, tongue and facial to porphyrin accumulation in lacrimal glands),
muscles. This is followed by neuromuscular blockade papilledema
and paralysis. Skin Sweating, dermatitis
●● Preganglionic sympathetic stimulation may lead to tach­ Others Fasciculation, flaccidity, salivation, delirium, psychosis
yarrhythmias, hypertension and cardiorespiratory arrest. likely to produce tachycardia.
●● Acetylcholine also causes initial stimulation followed
by depression of the CNS. The clinical manifestations appear within 30 minutes
●● One of the commonest effects of OPP is respiratory to 1 hour and reach the peak in 2–8 hours.
failure (Table 25.1). The latter is aggravated by secre­
tions that flood the airway and the lungs.
Ù
Secretions, altered mental status and miosis are the
●● The usual cause of death is respiratory failure. commonest presentations in children.2,3
Chapter 25 n Specific Poisons 249

Clinical scenario 1 (Figure 25.3) ●● 2 mg in children > 12 years and adults


This dose will relieve symptoms in a child with
2-year-old boy rushed to the ED when he was found un- OPP, but cause the side effects of atro­pinization in a
IP : 196.52.84.10
responsive after accidently consum­ing an insecticide. normal child.

Airway and Breathing


Profuse secretions and respiratory failure could occur due
to overwhelming bronchorrhea. Mechanical ventilation
may be required in up to 25% of patients.
Ù
Correction of hypoxia is mandatory prior to atropiniza-
tion to avoid the risk of ventricular fibrillation.

●● Oropharyngeal suctioning.
●● Provide oxygen using a JR circuit..
Figure 25.3 Physiological status: Airway is obstructed with ●● Intubate using the pharmacologically assisted intuba­
secretions, respiratory distress, bradycardia with hypotensive
shock, coma with miosis.
tion (PAI) technique.
Ù
Avoid Succinylcholine since it increases secretions and
Prehospital Therapy
can prolong muscle paralysis in OPP.
●● Remove patient from source of exposure.
●● Remove clothing rapidly.
●● Decontaminate skin by washing with copious amounts Circulation
of water and soap. ●● Administer NS 10 mL/kg (max 20–30 mL/kg may be
●● If a large quantity of poison has been ingested and the needed to correct shock).
child has been brought within 1 hour of ingestion gas­ ●● Inotrope may be needed if hypotensive or hypoxia has
tric lavage may be helpful. caused cardiogenic shock.
Ù Disability
The Cochrane group suggests that gastric lavage is an
easily performed and cheap intervention. It could be
Manage convulsions using the standard protocol for status
used as an adjunct in the treatment of OP poisoning.4
epilepticus.
●● Irrigate eyes with normal saline, if contamination is
suspected. Specific Treatment4
Atropine neutralizes the muscarinic effects of acetyl­
Clinical Diagnosis in the ED choline by competitive antagonism at postsynaptic mus­
1. A high index of suspicion is needed to consider OP carinic receptors.
poisoning, when a child is brought in profound altered
Dose: Children < 12 years with signs of moderate to severe
mental status and history of exposure is not forthcom­
toxicity:
ing. The clinical features described in (Table 25.1) will
help in the diagnosis. ●● Administer 0.05 to 0.1 mg/kg of atropine.
2. In case of doubt, a therapeutic challenge of atropine ●● In children > 12 years and adults with signs of moder­
may be attempted: ate to severe toxicity: Administer 2 to 4 mg.
●● Administer 0.01 mg/kg Atropine in children < 12 ●● Double the previous dose after every 5 minutes in­
year (mini­mum dose of 0.1 mg). terval, until secretions resolve (dry mouth), crepita­
250 Section VIII n Poisons

tions disappear, oxygenation improves and tachy­cardia CARBAMATES


> 140/minute occurs.
Carbofuran (Furadan), propoxur (Baygon), Bufencarb
●● Repeat doses, based IPon recurrence of symptoms for
: 196.52.84.10 (Bux) are carbamate insecticides. Non-toxic com­pounds
2–12 hours.
such as Sevin (of carbaryl group) are also included in the
Ù group. Their mode of action is similar to OP, though they
Atropine should be used for at least 24 hours to reverse are less toxic. The latter is due to the fact that they do not
the cholinergic signs, while the organophosphate is penetrate into the CNS and reversibly carbamy­late the es­
metabolized. ter site of the cholinesterase (ChE) enzyme. Their dura­
tion of action is also short. Hemolytic anemia has been
●● Dosing can be decreased when symptoms do not recur reported, but no intermediate or chronic effects has been
for 6 hours. described.
Ù ●● Management of carbamate toxicity is similar to that of
The Cochrane group recommends incremental dose OP poisoning.
administration of atropine as the standard of care. The ●● Oximes are not recommended.
role of glycopyrrolate alone or in combination with
atropine is not clear.4 Kerosene
Acute accidental ingestion of kerosene is common in lower
●● Pralidoxime (2-PAM) is a cholinesterase reactivator and
socioeco­nomic groups.
counteracts the nicotinic effects. It is useful when the
vic­tim has respiratory muscle weakness (Figure 25.4). Due to its low surface tension, kerosene tends to get
●● Administer 2-PAM, as an IV infusion after the loading aspirated into the lungs during ingestion, vomiting and in­
dose, until signs of weak­ness improve. halation of vapors. Kerosene toxicity has also been noted
●● Dose: 30 mg/kg (5% solution) in isotonic saline over following application of kerosene on the skin of neonates,
5–10 minutes as early as possible followed by a con­ indicating that transdermal absorption can also result in
tinuous infusion of 8 mg/kg/hour. toxic effects.
●● The drug is probably not useful 36 hours after expo­
sure.
Ù
Ingestion of 30 mL is lethal.
Ù
The Cochrane group (2012) reports that the current Pathophysiology
evi­dence is insufficient to indicate whether oximes are
harm­ful or beneficial.4 Aspiration of kerosene causes chemical pneumonitis,
which may progress to atelectasis, pneumatoceles or pneu­
mothorax. Hyperemia, edema, small airway obstruction,
inflammation, diffuse hemorrhages and cellular infiltra­
tion of the lungs are the various conditions which interfere
with gas exchange resulting in hypoxia. The latter leads
to alteration in mental status. Liver damage, cardiomyo­
pathy, renal toxicity and gastrointestinal (GI) involvement
have been reported. Temperature regulation may also be
impaired due to its direct effect on the CNS.
●● Cough and breath­lessness due to aspiration pneumonia,
may appear as early as l5 minutes or as late as 24 hours
after kerosene ingestion. Hemoptysis, has been reported
in very severe toxicity.
Figure 25.4: Pralidoxime and atropine used in ●● Fever occurs later and may persist for as long as 10 days
organophosphorous poisoning. after kerosene ingestion.
Chapter 25 n Specific Poisons 251

●● Primary CNS toxicity can present with lethargy, dizzi­


ness, headache, visual disturbances, seizures and hyper­ Ù
pyrexia. Coma and respiratory paralysis lead to death. If the child is asymptomatic it is unlikely that significant
IP : 196.52.84.10
●● Leukocytosis is often noted, though bacteria are not the problems will occur.
cause of aspiration pneumonia.
●● Hyperexpansion of the chest is occasionally seen. ●● Observe asymptomatic children for at least 24 hours,
●● Most children, however recover and symptoms resolve since symptoms may appear late.
between the 2nd and 5th day.
Radiographic Findings
Case Scenario 2 ●● Chest X-ray helps to identify pulmonary involvement
(60% are not appreciable by auscultation).
A 2-year-old child is rushed into the ED, after he was ●● Chest X-ray may be normal for as long as 6–8 hours
found vomiting and drowsy near an overturned bottle after ingestion.
of kerosene. He is smelling of kerosene (Figure 25.5). ●● Chest X-ray may reveal perihilar mottling, consolida­
tion, areas of collapse or pulmonary edema. Pneumoni­
tis commonly involves both lower lobes. There may be
evidence of pleural effusion, cysts and pneumothorax.
Pneumatoceles, may appear 2–3 weeks after clinical
resolution.

Prevention
●● Counsel parents about the hazards of storing kerosene
in familiar beverage or household containers.
●● Teach them to avoid placing these containers on the
floor (within easy reach of infants and toddlers).
Figure 25.5 Physiological status: Unmaintainable airway,
●● Avoid using palm oil as a household remedy.
respiratory failure, normotensive shock with altered mental
status. Barbiturates
Ù
Do not induce emesis.
Barbiturate poisoning in children is usually due to acci­
dental ingestion. Mental confusion resulting in repeated
Do not perform gastric lavage. dosages have been reported in adults and is also known as
Both procedures can enhance risk of aspiration. ‘involuntary suicide’ or ‘bar­biturate automatism’.
Toxic ingestion of barbiturate can cause global de­
Resuscitation pression or neuronal excitability. Large doses depress both
the respiratory and vasomotor centers. Renal function may
●● Administer oxygen via the JR circuit, since this child be compromised secondary to drug-induced hypotension.
has presented with im­pending respiratory failure.
●● Initiate bag-valve-mask ventilation and proceed to in­ Box 25.1: Common household things of low toxicity
tubate using PAI technique, if he had presented with No treatment required
respiratory arrest. Bar soap, lipstick, dry cells, newspaper, candles, pencil,
●● Treat shock with 10 mL/kg boluses of NS (up to a chalk, shampoo, clay (modeling), shaving cream and lotions,
maximum of 20 mL/kg). Consider more, only if hypo­ crayons, shoe polish, dehumidifying packets, striking surface
of matches, detergents, sweetening agents, hand lotion and
volemic due to persistant vomiting. If shock persists,
creams, thermometer, ink, toothpaste.
initiate appropriate inotrope. Removal necessary only, if large amounts ingested
●● Prophylactic antibiotics are not indicated. After shave lotion, body conditioners, colognes, deodorants,
●● Avoid corticosteroids (may be harmful). fabric softners, hair dyes, hair tonic, marker ink, match stick >
20, oral contraceptive, perfumes, toilet cleaner.
252 Section VIII n Poisons

Case Scenario 3 ●● Correct shock. Not more than 20 mL/kg may be need­
ed. Epinephrine is indicated, if hypotension persists
A 5-year-old child could not be woken up. An open bot- after fluid bolus. If blood pressure stabilizes, dopamine
IP for
tle of tablets prescribed : 196.52.84.10
his brother’s seizure disor- is indicated.
der was found half empty near him. His temperature:
96.5°F (Figure 25.6).
Decontamination
Severe Poisoning
●● Perform gastric lavage, if a large quantity has been in­
gested and the child has been brought within 1 hour of
ingestion.
●● Insert nasogastric tube and administer 1 g/kg of acti­
vated charcoal prepared with aerated drink as a slurry
(refer Chapter 24 on Poisoning: General Approach).

Mild to Moderate Poisoning


Admit for observation. They require no vigorous treatment.
Figure 25.6 Physiological status: Airway is unmaintainable, If gag is intact, make the child drink a 1 g/kg of slurry of
respiratory failure, hypotensive shock with altered mental status. activated charcoal mixed with aerated drinks. Urine alka­
Diagnosis is based on the history, clinical features and linization is no more recommended as first line treatment
circumstantial evidence. Serum levels of barbiturate > l0 in cases of phenobarbital poisoning as multiple-dose acti­
mg/dL reflect the severity of intoxication. An EEG pro­ vated charcoal is superior.5
vides useful evidence of poisoning. Differential diagnosis
includes other causes of non-traumatic coma. OPIUM AND ITS DERIVATIVES
Morphine, Codeine, Pethidine, Heroin, Propoxyphene, etc
Resuscitation (Box 25.1 and Table 25.2).
●● Initiate bag-valve-mask ventilation and plan early intu­ ●● These toxins are easily absorbed from the GIT, muscle
bation for respiratory failure and coma. and lungs. Opioid overdose can occur in adolescents.

Table 25.2: Clinical findings of sedative-hypnotic overdose

Clinical signs Sedative-hypnotics


Hypothermia Barbiturates, bromides, ethchlorvynol
Unique odors Chloral hydrate (pear), ethchlorvynol (new vinyl shower curtain)
Cardiotoxicity
• Myocardial depression • Meprobamate
• Dysrhythmias • Chloral hydrate
Muscular twitching GHB, methaqualone, propofol, etomidate
Acneiform rash Bromides
Fluctuating coma Glutethimide, meprobamate
GI hemorrhage Chloral hydrate, methaqualone
Discolored urine Propofol (green/pink)
Anticholinergic signs Glutethimide
Chapter 25 n Specific Poisons 253

Acciden­tal overdose have been documented in infants Belladonna Alkaloids, Datura


following its use for diarrhea and sedation. (Atropine Group)
●● Fatal dose: oral > 0.3
IPg: parenteral > 0.l g.
196.52.84.10 The toxic effects are due to parasympathetic blockade (an­
CASE SCENARIO 4 ticholinergic effect) at the muscarinic receptors. The nico­
tinic receptors at neuromuscular junctions are unaffected
4-month-old infant was treated with 2 teaspoons of co- in datura poisoning.
deine syrup for coughing and crying in the night. He
was not arousable in the morning (Figure 25.7).
CASE SCENARIO 5
2-year-old toddler was found chewing a green fleshy
pod. On arrival he was agitated. His cardiopulmonary
cerebral assessment was stable except for widely di-
alated pupils. His temperature was 38.5°C. He was also
looking flushed and his mucosa was dry.
●● Mild poisoning results in dryness of the mouth, hyper­
pyrexia and widely dilated pupils.
●● Higher doses cause tachycardia, flushing of face (red,
hot, dry face), hyperpyrexia, mental disturbances
(‘muttering’ delirium, hallucinations and excitation)
and cardiac rhythm disturbances.
Figure 25.7 Physiological status: Airway unmaintainable, ●● If left untreated, seizures, coma and death can occur.
respiratory failure, bradycardia, shock, BP: Normal, coma with
miotic pupils. Diagnosis: Datura poisoning.
He had bladder distension and his temperature was 35.4°. Differential diagnosis: Encephalitis, cerebral malaria,
acute meningitis, intracranial bleed, over dose of antihista­
Diagnosis: It is evident by the history of ingestion and
mines and tricyclic antidepressants.
typical clinical picture.

Resuscitation
Resuscitation
●● Stabilize the airway, breathing, circulation.
●● Stabilize airway, breathing and circulation.
●● Administer naloxone (specific antidote) immediately
in the dose of 0.01 mg/kg IV or IM.
Decontamination
●● Repeat the dose of naloxone in 3–10 minutes if no re­ ●● Administer activated charcoal 1 g/kg .
sponse is noted. ●● Gastric lavage, if large life-threatening amount has
been ingested and the child reaches within the first
Ù
Response is evident when the depth and rate of hour of ingestion.
respiration improve. Pupils do not dilate and are not the
end point of therapy. Antidote
Specific antidotes are used in the presence of seizures, hal­
●● Gastric lavage is useful only if a large life-threaten­ lucinations and arrhythmias.
ing amount has been ingested and the child has been
brought within 1 hour of ingestion. ●● Neostigmine methyl sulfate (dose: 0.5–2.5 mg IM at
●● Use activated charcoal. frequent intervals).
●● Administer via nasogastric tube as a slurry (1 g/kg). ●● Physostigmine: Dose: 0.5 mg slowly IV/IM (repeat ev­
●● Intubate to protect the airway, if the child’s mental sta­ ery 5 minutes up to a maximum of 2 mg). Note: This
tus has dropped significantly. drug crosses the blood brain barrier.
254 Section VIII n Poisons

●● If the patient is excited and restless, phenobarbitone


l00 mg or diazepam 0.2–0.3 mg/kg/24 hours is admin­ Ù
istered once in 6 hours. Stage 1: Symptoms appear within an average of 6
IP : 196.52.84.10 hours after ingestion
●● Correction of fluid and electrolyte imbalance.
• Dia­phoresis, though children less than 6 years of
Paracetamol (Acetaminophen)6 age do not have this symptom.
• Vomiting is more common.
Inadvertent ingestion of pain killers and antipyretics are
some of the commonest reasons, why parents rush to the Stage 2: Symptoms become less
ED. Parents must be educated about the hazards of par­ • Biochemical evidence of liver damage becomes
acetamol and taught that the maximum permissible dose apparent.
of paracetamol is 60 mg/kg per day (15 mg/kg/dose q 6th Stage 3: (48–96 hour after ingestion)
hourly). Fortunately, paracetamol-induced liver damage in
• Less than 1% of patients develop fulminant hepatic
children is less common than in adults.
failure on the 3rd to 6th days.
Ù
Paracetamol dose less than 150 mg/kg does not warrant
• Serum glutamic-oxaloacetic transaminase (SGOT)
levels may be as high as 20,000 or 30,000 IU/L.
further action. • Death may occur. Histopathology reveals centri­
loblar necrosis with periportal sparing.
The drug is rapidly absorbed and metabolized in the Stage 4: High liver enzyme levels persist in a few
liver to metabolically inert excretory products. Up to patients.
2%–4% is metabolized by the cytochrome P450 mixed
function oxidase system with glutathione to form a non-
toxic product (mercapturic acid). With paracetamol over­ Diagnosis
dose, hepatic stores of glutathione are depleted to less than i. History of ingestion.
70% of normal, resulting in the formation of highly reac­ ii. Clinical features.
tive interme­diate metabolites that bind to hepatic macro­ iii. Plasma acetaminophen levels.
molecules resulting in damage to the hepatocytes. Besides
●● Once the plasma level has been determined, plot it on
hepatocellular damage, they also cause renal tu­bular dam­
the Matthews-Rumack nomogram. This will help to de­
age and hypoglycemic coma. Enzyme inducers (e.g. an­
termine whether the level in relation to time is toxic.
ticonvulsants, antitubercular drugs) worsen hepatocellular
damage by promoting cytochrome P450 metabolism. Alternatively, draw a line on semilogarithmic graph
joining 200 µg/mL at 4 hours and 50 µg/mL at l2 hours
The clinical course comprises of four stages (Table
after ingestion. With values above this line there is a 60%
25.3).
chance of severe liver damage (Figure 25.8).
Table 25.3: Time course and clinical stages of acetaminophen toxicity

Stage Time course Name Symptoms Signs


1 0–12 (up to 24–36) Preinjury Nausea, vomiting, anorexia, Elevated serum acetaminophen
hour malaise, diaphoresis concentration, PT normal
2 8–36 hour Liver injury Nausea, vomiting, Transaminitis (AST begins to rise 8–36 h
right upper quadrant after ingestion), mild jaundice
abdominal tenderness, mild
hepatomegaly
3 2–4 day Maximum liver injury Liver failure (encephalopathy, Hemorrhage, ARDS, sepsis/SIRS,
coagulopathy, hemorrhage, multiorgan failure, cerebral edema
acidosis)
4 > 4 day–2 week Recovery None Complete hepatic histologic recovery
Chapter 25 n Specific Poisons 255

●● Monitor liver function tests frequently.


Ù ●● Most patients (99%) will recover within a week.
Activated charcoal or alkalinization of urine is of no
value in paracetamol IP : 196.52.84.10
toxicity. Ù
NSAID group of drugs8 cause little toxicity and ingestion
is considered life-threatening only, if the amount
Antidote consumed is:
●● N-acetylcysteine, the drug of choice is more effective 1. > 100 mg/kg of brufen.
when given orally, preferably within 10 hours (even if 2. > 25 mg/kg mefenamic acid.
the drug level cannot be determined in time).
Treat vomiting-induced dehydration.
Dose: The oral loading dose is 140 mg/kg followed by
70 mg/kg every 4 hours for 3 days up to a total of 17 doses.
IRON9
Since it has an unpleasant smell of sulfur that makes it un­
palatable, the concentrate is diluted by mixing one part with Iron ingestion is common in children under 5 years of age.
three parts of any carbonated beverage or (orange) juice. It can be fatal, if not managed appropriately (Table 25.4).
Ù
The lethal oral dose is between 200 and 500 mg/kg el­
emental iron.

●● GI symptoms can be seen at doses of l5–30 mg/kg.


Ù
Significant toxicity is uncommon at amounts less than 50
mg/kg. The toxic dose is not absolute and fatal reactions
have been reported even with small amounts.
All ingestions should therefore be considered potentially
dangerous.

Figure 25.8: Time course of rise, peak and fall of laboratory values
in patients with paracetamol poisoning who survive. Peaks are not Table 25.4: Common iron preparations
proportional. Significant individual variations may occur.
Compound Elemental iron %
Ferrous sulfate 20
N-acetylcysteine
Ferrous fumarate 33
●● 150 mg/kg in 5% D over 1 hour.
●● 10 mg/kg/hour for 20 hours (delay < 10 hours). Ferrous gluconate 12
●● 32 hours (delay 10–16 hour). Ferric pyrophosphate 30
●● 72 hours (delay > 16 hour) and longer, if encephalo­ Ferrocholinate 14
pathic.
●● Monitor potassium levels. Ferroglycine sulfate 16
Ferrous sulfate, dried 33
Oral Methionine is an alternative drug.
Ferrous carbonate, anhydrous 38
Dose: 2.5 g stat followed by 2.5 g 4 hourly up to a total of
Carbonyl iron 99
l0 g over 12 hours (it is not as reliable as NAC).
The antenatal mother is the commonest source of iron
Supportive Treatment tablets. Prescribed for a period of a month and attractively
packaged, hence these tablets are easily accessible by curi­
●● Maintain electrolyte balance.
ous young children.
●● Treat coagulopathy.
256 Section VIII n Poisons

Table 25.5: Toxicity of iron by amount ingested and ●● Iron levels, less than 350 µg/dL, when drawn
peak serum levels 2–6 hours after ingestion, predict an asymptom­
IP : serum
196.52.84.10 atic course.
Elemental iron Peak iron
(mg/kg) (μg/DL)
Toxicity ●● Iron levels greater than 500 µg/dL suggest signifi­
cant risk for phase III manifestations.
< 20 50–150 None In absence of serum iron levels, early clinical assess­
20–40 150–300 Mild ment and several simple laboratory tests may be used to
40–60 300–500 Moderate predict approximate iron levels.
> 60 > 500 Severe
Ù
Vomiting, diarrhea, S. glucose > l50 mg/dL, WBC >
Pathophysiology l5,000/mm3 and radiopaque material on abdominal
radiograph correlate with an elevated serum iron level
●● Iron directly damages the GI mucosa resulting in mas­ greater than 300 µg/dL.
sive fluid loss and hemorrhage (Table 25.5).
●● Vasodila­tion, occurs secondary to ferritin and other
iron metabolites in the liver. Case scenario 6
●● Both factors predispose to the development of shock 4-year-old child was brought to the ED af­ter he was
due to absolute or relative hypovolemia. found to have eaten up most of his mother’s monthly
●● Acidosis occurs due to the action of iron on oxidative prescription of iron tablets for pregnancy (Figure 25.9).
metabolism.
●● Coagulopathy and the resultant bleeding pre­dispose to
circulatory failure.
●● The absorbed iron causes di­rect damage to the liver
parenchymal cells leading to mas­sive hepatic necrosis
and liver failure.

Clinical Course
l. Gastrointestinal stage: The early symptoms include
vomiting, rapid onset of diarrhea, colicky abdominal
pain and GI hemorrhage.
2. Relatively stable stage: Reports have suggested that
there is a period of relative stability, which begins
Figure 25.9 Physiological status: Normal
3–4 hours after ingestion and lasts for as long as 48
hours. Subtle signs, such as mild GI bleeding, hyper­
ventilation and poor capillary refill may exist during Resuscitation
this stage and may go unrecognized.
1. Care of the airway, breathing is the priority in manage­
3. Shock stage: The third stage is characterized by circula­
ment, if the patient has altered level of consciousness.
tory failure and profound shock, which may be fatal.
2. Correct shock if identified.
4. Hepatotoxicity stage: Hepatotoxicity occurs within
the first 48 hours. This is the second most common Since this 4-year-old child is stable, plan to decontami­
cause of death. nate.
5. Gastric scarring is a late manifestation occurring 2–6
weeks after ingestion and is manifested by obstruction
of the gastric outlet and portions of the small intestine.
Decontamination
The amount of iron ingested often is hard to quantify ●● Perform gastric lavage for large life-threatening inges­
clinically. Serum iron levels, if obtained promptly, tion, if the child presented within the first few hours of
have been shown to correlate with the symptoms: ingestion.
Chapter 25 n Specific Poisons 257

●● Whole bowel irrigation is considered as the technique ●● Chelation is continued until the urine color and serum
of choice. iron level return to normal or the maximum daily dose
●● Mix PEGLEG in a IP carbonated drink and administer it
: 196.52.84.10 has been reached.
in the dose of: ●● Patients with mild symptoms or those who are asymp­
– 6–12 years: 1,000 mL/hour. tomatic, but have high serum iron or a positive chal­
– 9 months to 12 years: 500 mL/hour. lenge test, should receive:
– > 12 years 1,500–2,000 mL/hour. – 20–40 mg/kg of desferrioxamine infused over 4
hours or 20 mg/kg IM, 4–8 hourly.
Ù
Avoid PEGLEG, if airway is unprotected, shock, in­tractable
vomiting, GI bleed, perforation, ileus or obstruction.10 Supportive Treatment
●● Blood transfusion should be considered in severe
● ● Gastrostomy should be considered in massive hemorrhage.
overdoses. ●● Persistent metabolic acidosis may require treatment
Ù with sodium bicarbonate.
●● Dyselectrolytemia and hyperglycemia should be man­
Activated charcoal is not effective in binding iron salts.
Ipecac-induced emesis is not found to be beneficial. aged appropriately.
●● Liver and renal failure are treated symptomatically.

CORROSIVES
The most frequently ingested alkalis are button batteries,
dishwashing powder, disinfectants and caustic soda used
for cleaning ovens and degreasers. These may produce ir­
reversible damage at the site of contact.
Absence of antidotes or definitive treatment modalities
makes this toxin particularly dangerous. In addition, it can
cause permanent damage to the gut resulting in strictures.

Ù
Prevention is better than cure.
Parents must be taught to store house hold disinfectants
Figure 25.10: Desferrioxamine administration in iron toxicity and cleaning agents away from children.
results in excretion of vin rose color urine (Courtesy: Dr S
Thangavelu).

●● Blood should be drawn for complete blood cell count, Pathophysiology


blood glucose, electrolytes, BUN, liver function tests,
Patients with significant ingestion may have vomiting,
serum iron, total iron binding capacity, typing and cross
drooling, stridor, dyspnea, hematemesis, fever and oral
matching.
burns (Figure 25.11).
Antidote Presence of two or more symptoms namely vom­iting,
drooling or stridor correlates well with esopha­geal and la­
●● Initiate desferrioxamine infusion at a dose of l5 mg/
ryngeal injury. This may be accompanied by clinical signs
kg/h (max 6 g/day). Higher infusion rates associated
of lip swelling, tongue erythema, leu­koplakia or oral ulcer­
with risk of hypoten­sion.
ation. Substernal chest pain, ab­dominal pain and rigidity
●● The appearance of a pinkish (Vin rose) urine indicates
the presence of iron desferrioxamine complexes. Refer suggest profound injury and perforation of the esophagus
Figure 25.10. or stomach.11
258 Section VIII n Poisons

Specific Management
●● Immediate dilution and irrigation with clean water for
IP : 196.52.84.10 30 minutes.
Ù
Neutralization agents, such as vinegar is contraindicated
as it is thought that an exothermic reaction will occur,
further injuring the tissue .12
Emesis, lavage, charcoal and cathartics are contrain-
dicated in corrosive poisoning.

●● Order lateral neck and chest X-rays as part of the initial


assessment to corroborate any underlying suspicion of
perforation.
Figure 25.11: The infant presented with stridor and respiratory
●● Do not order barium swallow. This of little use in the
distress with impending failure. He was intubated in the ED.
Examination of the oral cavity shows leukoplakia and ulceration acute phase, since it delays endoscopy and will not re­
(Courtesy: Dr P Ramachandran). veal first or second de­gree mucosal injuries.13
●● Plan to perform esophagoscopy within 48 hours after
the inciting event.
CASE SCENARIO 7 ●● During this time period, the effects of the injury would
have demarcated itself, enabling grading of severity.
2-month-old infant was fed floor cleaner by his grand-
Prior to this time pe­riod, one may underestimate the
mother by mistake (Figure 25.12).
severity of injury, since erythema may be seen in the
early phases of even grade 2 and 3 injuries.
●● Endoscopy after 72 hours, increases the chance of iat­
rogenic perforation.13
●● Avoid steroids. Multiple trials and reviews have
shown little or no measurable benefit from varying
doses of steroids in their ability to reduce the rate of
stricture formation. 14,15,16
●● Prescribe Omeprazole, Pantoprazole, for 6 weeks.17,18,19
Antireflux therapy prevents reflux asso­ciated esopha­
geal injury, which could further aggravate the already
damaged area.
●● Prescribe third generation cephalosporin and if oral in­
take is tolerated change over to clindamycin for 1 week
Figure 25.12 Physiological status: Obstructed airway, respiratory to ensure a broad spectrum cover.14
distress, tachycardia, normotensive shock with altered mental
●● Introduce nasogastric tube only during endoscopy. It
status.
can be used for enteral feeding during the period when
the patient is kept without oral feeding. It also keeps
Resuscitation the esophageal lumen patent, so that adherence and
obliteration of the lumen does not occur. The nasogas­
●● Plan intubation. Call for ENT/anesthetist to help secure tric tube may be removed at 1 week and normal oral
the airway. Plan for cricothyrotomy or tracheostomy feeding commenced as tolerated by the child.14
depending upon the se­verity of damage.
●● Anticipate a difficult airway and call for help. Button Battery Ingestion20
●● Positive pressure ventilation may be required in pa­
tients who develop pulmonary edema. ●● NPO instructions should be followed until the posi­
●● Correct shock with 20 mL/kg of NS. tion of the esophageal battery is confirmed by CXR.
Chapter 25 n Specific Poisons 259

●● Anesthesia may be required for removal. Do not in­ layed for up to 27 days postremoval. Esopha­geal strictures
duce vomiting. may not manifest for weeks to months postingestion.
●● If the patient is asymptomatic, determine the diameter
IP : 196.52.84.10
based on the size of a comparable battery. Ù
Retrieve batteries, endoscopically if possible from the
●● If the patient is ≤ 12 years, immediately obtain an X-ray
to locate the battery. Batteries lodged in the esophagus stomach or beyond if:
may cause serious burns in as little as 2 hours. Do not • A magnet is ingested and the patient develops signs
or symptoms that are likely related to the battery
wait for symptoms to develop. Patients with a battery
ingestion.
in the esophagus may be asymptomatic initially.
●● If the patient is > 12 years and the battery diameter is
• A large battery (≥ 15 mm diameter), ingested by a
child younger than 6 years, remains in the stomach
> 12 mm or unknown, immediately obtain an X-ray to
for 4 days or longer.
locate the battery.
• If battery diameter is unknown, estimate it from the
Ù
If the patient is > 12 years and the ingested battery is ≤
X-ray, factoring out magnification (which tends to
overestimate battery diameter).
12 mm, no X-ray to locate the battery is required, if all
of the following conditions are met: ●● Allow batteries to pass spontaneously, if they have
• The patient is entirely asymptomatic and has been passed beyond the esophagus and no clinical indication
as­ymptomatic, since the battery was ingested. of GI injury is evident. Avoid unnecessary endoscopic
• Only one battery was ingested. or surgical removal in asymptomatic patients.
• A magnet was ingested. ●● Promptly re-evaluate all patients who develop signs or
• The battery has been reliably identified and size symptoms possibly related to the battery. Endoscopic
con­firmed as less than < 12 mm. removal of batteries still in the stomach should be pur­
• There is no history of pre-existing esophageal dis­ sued for even minor symptoms. For batteries beyond
ease. the reach of the endoscope, surgical battery removal
may be required in the unusual patients with evidence
●● Order X-rays of entire esophagus, neck and abdomen. of occult or visible bleeding, abdominal pain, pro­
Obtain both AP and lateral X-rays for batteries in the foundly decreased appetite, vomiting, signs of an acute
esophagus to determine orientation of the positive and abdomen and/or fever, unless these clinical manifesta­
negative poles. tions are clearly unrelated to the battery.
●● Confirm battery passage by inspecting stools. Con­
On the lateral film, if the step-off is on the negative sider repeat radiographs to confirm passage if passage
side of the battery (the negative pole has a slightly smaller not observed in 10–14 days. Confirming passage may
diameter). Anticipate complications based on battery posi­ avoid urgent diagnostic intervention for minor symp­
tion and orientation. Damage will be more severe in tissue toms developing later.
adjacent to the negative pole. ●● Manage ingestion of a hearing aid containing a battery
Immediately remove batteries lodged in the esophagus. as an ingestion of a small battery (≤ 12 mm).
Serious burns can occur in 2 hours. Do not delay re­moval,
even if the child has eaten recently. The esophageal bat­
Ù
Avoid these ineffective, unnecessary or unproven thera­
tery should not be pushed into the stom­ach as the risk of peutic interventions:
esophageal perforation may increase. • Ipecac administration (ineffective).
After removing a battery from the esophagus, the child • Laxatives (ineffective).
should be observed for delayed complications, such as • PEGLEC solution (unproven effectiveness and not
tracheoesophageal fistula, esophageal perforation, medi­ known, if solution enhances electrolysis).
astinitis, vocal cord paralysis, tracheal stenosis or trache­
omalacia, aspiration pneumonia, empyema, lung abscess, NEEM OIL INGESTION
pneumothorax, spondylodiscitis or exsanguination from
perforation into a large vessel. Esophageal perforations and This is the commonest cause of refractory seizures. Symp­
fistulas involving the trachea or major vessels may be de­ toms may start as early as 10 minutes. The active ingredient,
260 Section VIII n Poisons

which causes the toxicity is not known. Treatment is simi­ ●● Other neurologic symptoms include confusion, verti­
lar to the management of status epilepticus. go, restlessness, delirium and hallucinations. Increased
IP : 196.52.84.10 muscular activity, tremors and jerky movements, which
can often progress to epileptiform convulsions.-
CAMPHOR POISONING21
●● GI symptoms consist of oral and intestinal burning,
●● Camphor poisoning is a common ingredient in many nausea and vomiting.
cam­phorated oils, ointments and inhalants for the home ●● Tachycardia, mydriasis, visual disturbances, urinary
treat­ment of colds. It is also used for pooja. Children retention can also occur.
are at­tracted by the smell, texture and feel. ●● Albuminuria, mild transient elevations of the aspartate
●● Camphor is rapidly absorbed when taken orally, but a dehydrogenase and lactic dehydrogenase concentra­
considerable amount can also be absorbed via inhala­ tions and rarely, hepatic failure have been noted.
tion or through intact skin. Typically, symptoms begin
5–90 minutes after ingestion of a toxic dose. Although a variety of other conditions or intoxica­
●● Seizures may occur as soon as 4 minutes after inges­ tions can exhibit similar symptoms, a strong odor of
tion of 28 g of camphorated oil. Death may result from camphor on the breath or a history of recent treatments
respi­ratory depression or complications of status epi­ with camphor-containing agents will strongly suggest
lepticus. camphor intoxication.

Table 25.6: Common herbal medications and adverse/toxic effects

Herbal name Botanical name Uses Adverse effects


Betel nut Areca catechu Stimulant Bronchospasm
Cantharidin (blister beetle) Cantharis Aphrodisiac Priapism, dermatitis, renal
Ephedra Ephedra sinica Stimulant, asthma Hypertension, tachycardia, CNS, MI
(ma huang, chinese)
Fenugreek (methi) Trigonella foenum-graecum Expectorant, anti-inflammatory None reported
Feverfew Chrysanthemum parthenium Migraines, antipyretic Postfeverfew syndrome, rebound
(parthenium) migraine

Garlic (lasoon) Allium sativum Infection, CAD, hypertension Dermatitis, GI


Ginger (adrak) Zingiber officinale Motion sickness, GI illness None reported
Henbane (stinking Hyoscyamus niger Sedative, GI discomfort Anticholinergic toxicity
nightshade)
Jimson weed Datura stramonium Asthma Anticholinergic toxicity
Kava kava Piper methysticum Sedative, aphrodisiac Euphoria, CNS
Licorice Glycyrrhiza glabra Cough, GI illnesses Hypokalemia, drug interactions
Mistletoe Viscum album GI illness, cancer, HIV GI, bradycardia, CNS
Nutmeg Myristica fragrans Aphrodisiac, hallucinogen CNS, GI
St John’s wort Hypericum perforatum Depression, anxiety Drug interactions
Sassafras Sassafras albidum GI stimulant (root beer), Hepatotoxicity, carcinogen
anticoagulant, syphilis
Soy Glycine max Menopause, CAD Carcinogen
Himalayan Yew (paclitaxel) Taxus baccata GI illness, cancer Dizziness, bradycardia
Yohimbine Pausinystalia yohimbe Sexual disorders, aphrodisiac Hypertension, agitation,
CNS effects
Chapter 25 n Specific Poisons 261

Supportive Treatment Table 25.7: Drug interactions with herbal products

●● Decontamination of gut or skin by gastric lavage. Herbal product Interacting drugs


IP epilepticus.
●● Management of status : 196.52.84.10 Ginkgo biloba Aspirin, warfarin (Coumadin),
ticlopidine (Ticlid), clopidogrel
Pyrethroids (Plavix), dipyridamole (Persantine)
Ephedra Caffeine, decongestants, stimulants
Pyrethroids (mosquito repellents) are non-toxic to humans.
Pyrethrins from chrysanthemum flowers are neurotoxic to Ginestra Warfarin
insects. In sensitive individuals it may cause skin manifes­ Kava Sedatives, sleeping pills,
tations and rarely neurological manifestations. Betel nut antipsychotics, alcohol
Ephedra, Fenugreek Prednisone, salbutamol,
Ginseng MAO inhibitors
Methemoglobinemia Licorice Warfarin
Blood sample from a child who had accidentally ingested Soy Ethanol,Warfarin
dapsone has turned chocolate brown (Figure 25.13). The Yohimbine Prednisolone,
Antihypertensives
control sample on the right is normal. Warfarin
Tricyclic antidepressants
St John’s SSRI (serotonin
wort syndrome)
Theophylline
Digoxin
Cyclosporine
Indinavir Decreased drug
Irinotecan concentration
Nevirapine
Simvastatin

Box 25.2: Sedative hypnotic poisonings

Figure 25.13: Methemoglobin formation due to Dapsone Barbiturates


ingestion (sample on left) (Courtesy: Dr Shankar Srinivasan). Ultrashort acting—Methohexital
Short and intermediate acting—Pentobarbital
MISCELLANEOUS22, 23
Long acting—Phenobarbital
A growing number of people, especially in our coun­ Non-barbiturates
try, still use herbal products for preventive and thera­
Benzodiazepines
peutic purposes. The manufacturers of these products,
both indigenous practitioners and commercial ventures, Carbamates—Meprobamate
are not required to submit proof of safety and efficacy Chloral derivatives—Chloral hydrate
to regulatory agencies before marketing. For this rea­ Ethchlorvynol
son, the adverse effects (Table 25.6) and drug interac­
Piperidines—Glutethimide
tions (Table 25.7) associated with herbal remedies are
largely unknown. For example, Ginkgo biloba extract, Quinazolinone—Methaqualone
advertised as improving cognitive functioning, has been Imidazopyridine—Zolpidem
reported to cause spontaneous bleeding and it may in­ Antihistamines—Diphenhydramine and doxylamine
teract with anticoagulants and antiplatelet agents. Seeds
of stone fruits like cherry, plum, peach, apricot, bitter GHB—Gamma-hydroxybutyrate
almond, roots of cassava contain amygdalin, which on
ingestion release cyanide.
crossfire of biological warfare and military repression may
Laboratory personnel, children inhabiting colonies be exposed to inhaled pollutants/toxins with adverse ef­
around factories/chemical plants and those caught in the fects on growth and development.
262 Section VIII n Poisons

Many household things kept within reach of the chil­ 7. Frank Shann Drug Doses Intensive Care Unit, Royal Chil­
dren are often ingested by them due to their curiosity to dren’s hospital Austrailia, 15th Edn 2010.
explore nature. A list ofIPthings which are innocuous or of 8. Riordan M, Rylance G, Berry K. Poisoning in children1:
: 196.52.84.10 General management. Arch Dis Child. 2002 ;87:392-396.
low toxicity are given in Box 25.1. Reassurance of the par­
ents is all that is needed. 9. Salgia AD, Kosnik SD. When acetaminophen use becomes
toxic. Treating acute accidental and intentional overdose.
Key Points
1. Organophosphorus compounds are the commonest
ü Postgrad Med. 1999;105:81-4, 87, 90.
10. Singhi SC, Baranwal AK, M J. Acute iron poisoning:clinical
picture, intensive care needs and Outcome. Indian Pediatr.
toxin ingested in the rural agricultural areas. 2003; 40:1177-182.
2. Atropine usage is based on the recommendations of 11. GP Cantwell, RS Weisman. Poisoning Roger’s Handbook
the Cochrane data base 2012. of Pediatric Intensive Care 2009; 4th edition, N. Delhi Wil­
3. Ingestion of corrosives and button batteries are liams and Wilkins.
hazardous and should be handled using a protocol 12. F Riffat, A Cheng. Pediatric caustic ingestion: 50 consecu­
based approach. tive cases and a review of the literature Diseases of the
4. Usually common house hold products are safe unless Esophagus. 2009(22), 89-94DOI: 10.1111/j.1442-2050.
2008.00867.
large quantities are ingested.
13. Millar A, Numanoglu A, Rode H. Caustic strictures of the
5. Always resuscitate ABCs in addition to poison
esophagus. In: Grosfeld J, O’Neill J, Coran A, Fonkalsrud
elimination or treatment. E (eds). Grosfeld: Pediatric Surgery, Chapter 68. St. Louis,
MO: Mosby. 2006; 969-79.
common errors
û
1. Performing gastric lavage for kerosene and caustic
14. Friedman EM. Caustic ingestions and foreign bodies in
the aero digestive tract of children. Pediatr Clin North Am.
1989; 6: 1403-410.
ingestion. 15. Ulman I, Mutaf O. A critique of systemic steroids in the
2. Failing to ventilate for severe OP poisoning. management of esophageal burns in children. Eur J Pediatr
3. Not considering the potential for oesophageal Surg. 1998;8:71.
damage following battery ingestion. 16. Anderson KD, Rouse TM, Randolph JG. A controlled trial
of corticosteroids in children with corrosive injury of the
4. Failure to seek assistance from regional poison
esophagus. N Engl J Med. 1990;323:637.
center.
17. Poley J, Steyerberg E, Kuipers E, et al. Ingestion of acid
and alkaline agents: outcome and prognostic value of early
References endoscopy. Gastrointest Endosc 2004;60(3):372-7.
1. Srivastava A, Peshin SS, Kaleekal T, et al. An epidemio­ 18. Rothstein FC. Caustic injuries to the esophagus in chil­
dren. Pediatr Toxicol Pediatr. Clin North Am. 1986;33(3):
logical study of poisoning cases reported to the National
665-74.
Poisons Information Centre. All India Institute of Medi­
19. Pintus C et al. Caustic ingestion in childhood: current treat­
cal Sciences, New Delhi. Human Experimental Toxicol.
ment possibilities and their complications. Pediatr Surg Int
2005;24:279-85. 1993; 8: 109.
2. van Heel W, Hachimi-Idrissi S. Accidental organophos­ 20. Litovitz T, Whitaker N, Clark L, et al. Emerging bat­
phate insecticide intoxication in children: a reminder. Int J tery ingestion hazard: Clinical implications. Pediatrics
Emerg Med. Jun 15 2011;4(1):32. 2010;125(6): 1168-1177. epub 24 May 2010. Guideline
3. Kozer E, Mordel A, Haim SB, et al. Pediatric poisoning from the National Battery Ingestion Hotline at the National
from trimedoxime (TMB4) and atropine automatic injec­ Capital Poison Center ©National Capital Poison Center,
tors. J Pediatr. Jan 2005;146(1):41-44. 2009.
4. Interventions for acute Organophophate poison South 21. Theis JGW, Koren G.Camphorated oil: Still endanger­
ing the lives of Canadian children.Can Med Assoc J.
Asian Cochrane Network and Centre (SASIANCC) 2012.
1995;152:1821-824.
5. Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on 22. Cupp MJ. Herbal Remedies: Adverse Effects and Drug In­
Urine alkalinization Journal of Toxicology Clinical Toxi­ teractions.1999; Accessed from www.aafp.org (59)-5.
cology. 2004;42(1):1-26. 23. Fugh-Berman A, Ernst E. Herb±drug interactions: Review
6. Hanhan UA. The poisoned child in the pediatric intensive and assessment of report reliability Br J Clin Pharmacol.
care unit. Pediatr Clin N Am. 2008; 55: 669-86. 52:587-95.
Section IX
IP : 196.52.84.10

Trauma
IP : 196.52.84.10
Approach to
26
IP : 196.52.84.10

Traumatic Brain Injury (TBI)

Figure 26.1: Head injuries are very scary and can prove fatal if not managed appropriately (Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Pathophysiology of severe traumatic brain injury. 3. Case scenario-based management.
2. Spectrum of head injuries. 4. Pearls and pitfalls in management.

Introduction
Over 1.5 million pediatric head injuries are reported each
year1. Motor Vehicle Accidents (MVA) associated head
trauma have the highest morbidity and mortality in all age
groups (Figure 26.1). Mild traumatic brain injury (TBI)
appears to be the most common injury but generally has
good outcomes. In India, severe traumatic brain injury oc­
curs most commonly following falls from upper stories of
buildings with unbarred windows and verandahs refer Fig­
ure 27.1 Chapter of Polytrauma. Child abuse should also
be considered when children present with unexplained
head trauma or when there has been delay in seeking care.

Closed Head Trauma


Figure 26.2: Primary injury leads to secondary injury.
Pathophysiology CBF, cerebral blood flow; BBB, blood-brain barrier.
Closed head trauma implies that an injury has not pen­ ●● Primary injury results from the direct force of impact.
etrated the covering of the brain. Concussion results in ●● Unlike adults, increased head to torso ratio and in­
dysauto­regulation of cerebral blood flow (CBF). creased brain water content are some of the factors
●● Brain injury can be primary and secondary (Figure 26.2). responsible for the diffused injury noted in children.
266 Section IX n Trauma

●● Secondary brain injury may develop acutely or sub­- Intracranial Pressure


acutely following primary brain injury. Neurochemi­
cally mediated vasospasm and astrocytic swelling com­ Normal intracranial pressure is maintained by its contents;
IP : 196.52.84.10 brain, CSF and blood.
presses the microcirculation within the first 24 hours of
injury. This reduces cerebral blood flow. Disruption of The Monroe-Kellie doctrine states that in order to main­
the blood-brain barrier (BBB) and alteration in cere­ tain intracranial pressure in the normal range, an increase
bral autoregulation also play a significant role. Release in intrac­ranial volume of one compartment is counter bal­
of excitotoxic neurotransmitters, elevated intracellular anced by reduction in volume in the other compartment.
calcium and potassium concentrations, formation of Critical increase in volume of any one com­partment results
free radicals and apoptosis additionally contribute to in increased ICP (Figures 26.4–26.5).
secondary injury.
The brain maintains a constant blood flow by a mecha­
Ù
Anticipate raised ICP in every child with TBI. Initiate
nism known as autoregulation (Figure 26.3). Autoregula­ measures to prevent and treat raised ICP in every step
tion of cerebral blood flow occurs over a wide range of of resuscitation.
blood pressures by a process of changing cerebral resis­
tance in response to fluctuations in mean arterial pres­sure. Maintenance of normal cerebral perfusion pressure and
Under normal circumstances, CBF is maintained at a con­ cerebral blood flow are crucial for intact survival.
stant between a MAP of 60–150 mm Hg. At 60 mm Hg, ce­
rebral vasculature is maximally di­lated and at 150 mm Hg, Resolution of shock takes precedence over raised ICP,
it is maximally constricted. Fluc­tuations of MAP beyond since, Cerebral perfusion pressure = Mean arterial pres­
either end of this range lead to alterations in CBF, which sure – Intracranial pressure. CPP is a critical determinant
can either cause ischemia or disruption of the blood-brain of cerebral blood flow. Unresolved shock with raised ICP
barrier. CBF can also be altered by changes in partial pres­ could compromise cerebral perfusion pressure result­ing in
sure of oxygen or carbon dioxide. cerebral ischemia.
Hypoxia causes vasodilatation with significant in­
crease in CBF. On the contrary, increases in oxygen pres­ Ù
sure causes vasoconstriction. Hypercarbia increases CBF, Raised ICP is not a contraindication to correct shock.
up to 350% of normal whereas, hypocapnia produces a Correction of shock and maintenance of BP can help
decrease in CBF. This mechanism is preserved even when maintain normal cerebral pressure.
auto­regulation is lost.

Figure 26.3: Mean arterial pressure – intracranial pressure =


cerebral perfusion pressure

Ù
CBF remains constant over a wide range of cerebral per- Figure 26.4: Relation between intracranial pressure and
fusion pressures. intracranial volume
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 267

IP : 196.52.84.10

Figure 26.5: Monroe-Kellie doctrine

Simultaneously, steps must be taken to lower ICP to a ●● Alert the parents/caretakers for the possibility of a
level that is ad­equate to increase cerebral perfusion pres­ postconcussive syndrome.
sure (CPP). This important step is key to improving cere­
bral oxygenation and preventing cerebral ischemia. In this Ù
context, Mannitol, a drug that acts by causing diuresis is Children under 2 years of age with normal mental sta-
not preferred. It reduces ICP, but worsens shock thereby tus, no scalp hematoma (except frontal), no loss of con-
reducing CPP. Efforts must also be focussed on early de­ sciousness (LOC) or brief loss of consciousness < 5 sec,
tection of cerebral her­niation. non-severe mechanism, no palpable skull fracture and
behaving normally as reported by the parents are less
likely to have a severe traumatic brain injury.2
MINOR HEAD TRAUMA
Head trauma associated with a GCS > 13.
●● Loss of consciousness (< 1 minute).
Ù
Children over 2 years of age were at low-risk if men-
●● Seizure, vomiting, confusion, headache or lethargy. tal status was normal, there had been no loss of con­
●● Normal mental status at time of exam. sciousness, no vomiting, non-severe injury mechanism,
●● Normal physical exam (including fundus). no signs of basilar skull fracture and absence of a head-
●● No evidence of skull fracture (hemotympanum, Bat­ ache.2
tle’s sign or palpable bone depression).
●● CT brain is recommended.
Scalp Lacerations
●● Skull radiographs are recommended only if, CT scan is
unavailable, or for children less than 2 years. The scalp is a very vascular structure made up of five lay­
●● If child abuse is suspected. ers that include: skin, subcutaneous tissue, galea aponeu­
rosis, loose areolar tissue and the pericranium (SCALP).
●● Infants younger than 2 years.
The large vessels that supply the scalp run just above the
galea aponeurosis and injury to this layer may result in sig­
Management nificant blood loss (Figure 26.6).
●● Reassure. Debris from the accident site, as well as hair or clothing,
●● Advice rest and follow-up. may become entangled in the wound.
268 Section IX n Trauma

IP : 196.52.84.10

Figure 26.6: Bleeding from scalp lacerations can result in


Figure 26.7: Skull radiograph of a simple linear skull fracture
hemorrhagic shock

Ù
Clean wound meticulously prior to wound closure.
Explore all scalp lacerations to rule out a skull fracture
prior to closure.

In rare instances, an injury to the scalp may lead to bleed­


ing into the subgaleal space. The degree of trauma may be
very minor or completely unrecognized by the patient. The
area of swelling associated with the subgaleal hematoma may
be variable and is frequently associated with headache.
Subgaleal hematomas cross the suture lines and can
lead to significant blood accumulation and hypov­olemia. Figure 26.8: Compound depressed skull fracture caused by a
In general, these hematomas will resolve spontaneously. hammer blow

Ù In almost all cases, a simple fracture of the skull will


Do not attempt to tap the fluid since they frequently heal with time. The edges of the fracture are fixed into rig­
reaccumulate. id approximation of the skull itself enabling spontaneous
healing.

SEVERE TRAUMATIC brain INJURY In skull fractures, the dura, which is closely approxi­
mated to the inner table of the skull, may be lacerated. In
Skull Fracture children under the age of two, a dural laceration may re­
Children often present with linear, depressed or basilar skull sult in herniation of the leptomeninges into the bony cleft.
fractures. About 75% of skull fractures are linear, with the At this age, as the brain is growing at a very rapid rate,
parietal bone being the most common site. The significance the bony edges may not have time to heal completely. The
of a skull fracture is that it indicates the amount of energy growth and pulsation of the brain may lead to a growing
that was applied to the patient’s head. A large amount of skull fracture or leptomeningeal cyst. Repair of these cysts
concentrated force is necessary to crack both tables of the can be very difficult if they are left untreated.
skull. The amount of energy that is trans­mitted to the un­
derlying structures is therefore of concern. Hence, presence
Ù
Children who sustain skull fractures under the age of
of a fracture denotes that a more severe injury to the brain two should have neurosurgical follow-up to ensure that
exists. Ap­proximately, 48% of patients have associated in­ the fracture closes and does not grow into a large cyst.
tracranial lesions (Figures 26.7 to 26.8 and Table 26.1).
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 269

Depressed Skull Fracture ●● A fracture through the anterior cranial fossa with injury
to the olfactory apparatus will result in loss of the sense
Depressed skull fractures (Figure 26. 8) result from forces
IP : 196.52.84.10 of smell.
applied to a small cross-sectional area and often require
●● Anterior fossa fractures can also lead to injury of the
surgical repair.
optic or oculomotor nerves passing through the supe­
The skin over the injury site may be open, closed, con­ rior orbital fissure.
tused or absent. Brain may be present in the wound or on ●● The most commonly injured cranial nerves are the VII
rare occasions, severe cortical bleeding from a lacerated and VIII, leading to a facial paralysis and sensorineural
artery or vein may also be present. hearing loss. Sometimes, the VII nerve damage may
●● Complicated injuries require vigorous debridement manifest later. Therefore, it is crucial to examine and
and closure. document severity of loss of facial movements. Injury
●● If brain matter is exposed, the wound should be cov­ to the lower cranial nerves passing through the jugular
ered with saline-soaked gauze to prevent drying of the or hypoglossal foramen is relatively uncommon.
brain prior to surgical repair. ●● Basilar skull fractures are often associated with venous
●● Children with depressed skull fractures are at higher bleeding in soft tissues behind the ear.
risk for developing seizures and need prophylactic an­
ticonvulsants. Ù
Bleed behind the ear is called the ‘battle sign’ and an
Ù accumulation of blood in the pe­riorbital region is known
All depressed skull fractures should be evaluated by a as the ‘raccoon sign’.
neurosurgical specialist to determine the appropriate-
ness of surgical decompression and repair. Either of these signs should alert the clinician to the
possi­bility of a basilar fracture and a computerized tomog­
raphy (CT) scan should be ordered.
Basilar Skull Fracture
Fractures of base of skull are not seen well on plain X- Cerebrospinal Fluid Leak
ray films, but should always be considered in patients with
head trauma. In these patients, the fracture almost always At the base of the skull, the dura is tightly adherent to the
heals without surgical intervention except in the most se­ bony structure in a number of places. Should a fracture oc­
vere cases. The factor that differentiates the basilar skull cur, the meninges is at risk of tearing leading to CSF leak
fracture from a fracture over the convexity of the brain is through the fracture.
the associated structures that run through the base of the ●● The CSF may leak into the air-filled sinuses and na­
skull. Injury to the cranial nerves, vascu­lar structures or sopharynx, resulting in CSF rhinorrhea.
basilar dura may be disabling or in some cases fatal.
●● CSF can also leak through the mastoid or floor of the
The carotid artery enters the base of the skull deep to middle fossa into the middle ear, where it may pass
the temporomandibular joint. through a ruptured tympanic membrane, producing
●● Injury to the carotid vessels in basilar skull fracture otorrhea or through the eustachian tube into the na­
causes either a vascular thrombosis or bleeding into the sopharynx.
middle ear with a resultant hemotympanum or blood in In most cases, a CSF leak will stop within two weeks.
the external auditory canal. The use of prophylactic anti­biotics for this type of injury is
Ù
All cranial nerves passing through the base of skull are
controversial. Some suggest that bacterial flora is reduced
by the use of antibiotics and therefore the risk of infection
at risk for injury from basilar skull fractures. The anato- is reduced. Others suggest that antibiotic usage encourages
my of injured region determines the frequency of cranial resistance without protec­tion and if meningitis were to re­
nerve deficits. sult from a CSF leak, the organism would be more difficult
to treat.
270 Section IX n Trauma

Table 26.1: Localization of head injury


Site examined Findings Interpretation
Small pupil IP : 196.52.84.10
Unilateral or Horner’s syndrome Sympathetic chain disruption, common carotid
injury, arterial dissection in neck or skull base (may
progress to stroke)
Ocular movements Conjugate tonic eye movement Ipsilateral frontal lobe injury or contralateral seizure
activity
Ipsilateral conjugate lateral gaze palsy Dysfunction of parapontine reticular formation
V CN Corneal reflex absent Pontine dysfunction
VII CN Unilateral LMN Nerve injury from basilar skull fracture
VIII CN Absent [normally cold-opposite, warm-same side Brain stem dysfuntion between pontine vestibular
Vestibular calorics (COWS)] nuclei and oculomotor nucleus in midbrain
IX and X Gag and cough reflexes Test integrity of medullary centers
Breathing Periodic or Cheyne-Stokes Bilateral hemispheric or upper pontine injury
Apneustic Mid-caudal pontine injury
Ataxic Medullary respiratory centers site examined
Scalp, skull Contusions, lacerations, depression of skull Underlying brain injury
Face Periorbital, retroauricular bruising (blue discoloration Basilar skull fracture
will occur the following day)
Ear and nose Hemotympanum, rhinorrhea, otorrhea Basilar skull fracture
Fundus Petechial hemorrhages Shaken baby syndrome
Papilledema (Not to be expected in acute phase) Raised ICP
Neurological examination In addition to the GCS, which must be done at
(secondary survey) regular intervals
Transient LOC Concussion
Dilated pupils Unilateral fixed dilated +/- contralateral hemiparesis Transtentorial herniation
Enlarged non-reactive (mydriasis) Midbrain, third nerve or direct orbital trauma
Bilateral or fluctuating mydriasis Ictal or postictal phenomena
Bilateral Drugs used in CPR

An epidural hematoma (Figure 26.9) results from


Ù blood accumulating between the dura and the skull. The
The child with CSF leakage should be evaluated by a clinical presentation, characterized by a period of lucency
neurosurgeon, who may either drain the CSF with a followed by rapid deterioration of consciousness, is rare
lumbar catheter or surgically repair the site of leakage. in children. Epidural hematomas in this population occur
from bleeding of the diploic veins.
Intracranial Lesions The more characteristic source of blood causing the
epidural hematoma is arterial. The middle meningeal ar­
The cranium is a closed space within which only a limited
tery runs within the structure of the temporal bone and in
amount of volume can accumulate. The layers of the skull the first part of its course may be completely surrounded
above the brain are the arachnoid, which contains the CSF, by bony investiture. Fracture of the bone across this bony
the dura and the skull. Blood may accumulate in any of canal will commonly lacerate the artery and cause a hema­
these areas, producing distinctive radiological and clinical toma under pressure. This rapid accumulation of blood is
syndromes. the reason for the classical lucent period following head
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 271

trauma prior to the onset of unconsciousness. In general, one area ‘coup injury’ of the brain with a similar injury direct­
the relatively focal nature of the epidural hematoma and ly across the head called a ‘contra coup’ injury. Parenchymal
mechanism of injury leading to less diffuse brain trauma
IP : 196.52.84.10 bleeding may extend into the subarachnoid space or into the
herald a better outcome than would be expected with other ventri­cles and may occasionally lead to acute hydrocephalus.
sites of hematoma accumulation.

Figure 26.9: Hematoma causes mass effect. This radiograph


shows an epidural (extradural) hematoma viz collection of
blood between duramater and skull (It can also occur in the
spinal cord). Build up of epidural hematoma can rapidly result in
compression of the underlying brain and spinal cord leading to Figures 26.10A and B: This child presented with profuse
severe neurological dysfunction. Most epidural hematomas are bleeding from a scalp injury following MVA. On arrival he was
due to injury to the artery. An epidural hematoma is potentially unresponsive and apneic. His HR was 60/minute and his blood
fatal but complete recovery is possible if detected early. pressure was 160/120 mm Hg. The airway physician initiated
bag-valve-mask ventilation. One member was dedicated to
If the small bridging vessels of the subdural space are manually stabilize the C-spine and perform the jaw thrust
torn, a subdural hematoma results. The plane of dissection maneuver. As the airway tray was being prepared, his blood
pressure dropped to 60/?. 40 mL/kg NS was rushed using pull
for blood is along a path of much less re­sistance than that
-push technique. Epinephrine infusion was initiated, blood was
for the epidural hematoma and leads to the characteristic transfused and the bleed ligated. He was intubated using ICP
crescent shape seen on the CT scan. In general, the out­ precautions and loaded with phenytoin prior to shifting for CT
come from a subdural hematoma is worse, perhaps because (26.9A). The CT scan shows evidence of ICH. This case illustrates
of associated brain trauma. The bleeding source, like in the the importance of correcting shock in the background of ICP.
epidural hematoma, may be either ve­nous or arterial and
the clinical course will vary depending on the rapidity of Ù
Fluid resuscitation of shock in severe traumatic brain
accumulation and mass effect. injury:
Bleeding may also occur within the parenchyma of the Isolated head trauma with no external evidence of in-
brain as seen in Figures 26.10A and B. The common areas for jury: Plan 20–30 mL/kg NS
intra­parenchymal bleeds are the frontal and temporal lobes. It Severe TBI with fractures, intra-abdominal trauma, cer-
is not uncommon in the traumatized brain to identify injury in vical transection scalp laceration: > 30–50 mL/kg.
272 Section IX n Trauma

Case scenario 1
7-year-old boy was rushed into the ED after fall from
IP : to
first floor (Figures 26.11 196.52.84.10
26.14).

Figure 26.13: This CT with contrast taken just after resuscitation


shows a large lesion in the right parietal cortex with a
hypodense center with surrounding darker zone suggestive of
fluid collection. There is a midline shift to the left. This picture is
suggestive of intraparenchymal hemorrhage and edema.

Figure 26.11 Physiological status: Airway unmaintainable


and obstructed, bradypnea, bradycardia, shock, hypertension,
no features of myocardial dysfunction with evidence of ICP,
herniation and non-convulsive status epilepticus.

Figure 26.14: A happy mother with her son after successful


resuscitation. He was attending the rehabilitation department
for hemiparesis and dysphasia. First-tier management of shock,
hypoxia and raised ICP in the ED appears to have been crucial
for survival in this child with severe traumatic brain injury.

Therapeutic Goals of
Figure 26.12: The airway was stabilized using the jaw thrust Traumatic Brain Injury in the ED
maneuver, cervical collar was applied and he was immobilized
on a spinal board. Orogastric tube was used to decompress Ù
the stomach. Orotracheal intubation was performed us­ing Maximize oxygen delivery to the brain
ICP precautions. During intubation, care was taken to avoid C-spine precautions
flexing or extending the neck using in-line manual cervical Correct shock
stabilization. Shock was corrected with one bolus of NS. He was Maximize cerebral perfusion pressure
catheterized, given pain and sedation drugs to avoid further Lower intracranial pressures
increase in ICP during transfer for CT scan and neurosurgeon’s
Maintain eucapnia.
opinion. His head end was elevated and 3% NS was initiated at
the rate of 1 mL/kg.
Primary survey is performed even as a focused history is
Secondary survey revealed no obvious evidence of ex­ being obtained in the ED.
ternal injuries or bleeds. His fundus was normal.
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 273

Airway: Is the airway unstable or obstructed?


C-spine injury is presumed in all children with TBI since
Ù IPfacial,
: 196.52.84.10
it is difficult to rule out spinal cord injury on arrival.
Look for bleed­ing from mandibular injury, laryn- Furthermore, children are prone to have spinal cord in-
geal and tra­cheal injury, broken teeth, bone fragments, jury without radiological abnormality (SCIWORA). It is
any other foreign bodies. therefore advisable to plan on removal of cervical collar
and spinal immobilization device only after ruling out
Breathing: Bradypnea or respiratory distress spinal cord injury by CT scan, X-ray spine and neurolo-

Ù gist’s opinion.

Look for tension pneumothorax, flail chest, hemothorax


Box 26.1: Classification of severity of intracranial injury based
or pneumotho­rax.
on signs and symptoms as per the CHALICE guidelines3
Circulation: Bradycardia, shock, hypertension. ●● Mild

Ù Asymptomatic
Mild headache
Look for bleeding injuries. Three or fewer episodes of vomiting
Glasgow Coma Scale score of 14–15
Disability: Raised intracranial pressure, non-convul­sive Loss of consciousness for less than 5 minute
status epilepticus. ●● Moderate
Loss of consciousness for 5 min or more
Following resuscitation of the ABCs the secondary Progressive lethargy
survey is performed to in­clude a formal assessment of the Progressive headache
level of consciousness using the Glasgow Coma Scale Protracted vomiting (more than three times) or associated with
(GCS). other symptoms
Post-traumatic amnesia
●● Patients are described as having: Severe head injury if Post-traumatic seizure
the GCS is 8 or less. Multiple trauma
●● Moderate head injury is considered when the GCS Serious facial injury
Signs of basal skull fracture
is 9–12. Possible penetrating injury or depressed skull fracture
● ● Minor head injury correlates with a GCS of 13– Suspected child abuse
15. Glasgow Coma Scale score of 11–13
These classifications guide therapy as well as progno­ ●● Severe
sis. Severity of intracranial injury may also be classified as Glasgow Coma Scale score of 10 or less, or decrease of 2 points
mild, moderate and severe based on clinical examination or more not clearly caused by seizures, drugs, decreased
(Box 26.1). cerebral perfusion or metabolic factors
Focal neurologic signs
Penetrating skull injury
MANAGEMENT 5,6,7,8 Palpable depressed skull fracture
Compound skull fracture
Airway
●● Open airway using the jaw thrust maneuver. Other Airway Precautions
●● Head tilt-chin lift maneuvers should be avoided. ●● Prepare to suction large volume particulate material.
●● Manually hold the C-spine in-line until an age appro­
priate collar can be placed along with the spinal im­
mobilization.
Ù
Both central and electrical suction with Yankauer suc-
Ù tion tip should be available.
Manual in-line cervical immobilization throughout in-
tubation, which helps to prevent neck movement and the ●● Introduce orogastric tube.
dreaded risk of quadriplegia. ●● Intubate using orotracheal route (Figure 26.15).
274 Section IX n Trauma

Box 26.2: Drugs used to reduce the risk of increasing ICP


Ù during intubation in TBI
Nasogastric/orotracheal tube may enter the base of skull
IP : 196.52.84.10 ●● Atropine: Prevents bradycardia
in unsuspected basilar fracture.
●● Lidocaine: Anesthetizes glossopharyngeal nerve
●● Thiopental: Cerebroprotective, anticonvulsant
●● Rocuronium, vecuronium: Does not worsen ICP unlike
succinylcholine

Prevention of hypoxia and hypercapnia are vital in


improv­ing outcomes in severe traumatic brain injury. One
of the most important therapeutic interventions therefore is
provision of assisted ventilation for which early and elective
intubation is necessary in the PED. The other indications
for intubation in severe traumatic brain injury are given in
Box 26.3.

Box 26.3: Indications for intubation in traumatic brain injury


Figure 26.15: Orogastric tube inserted and orotracheal
intubation performed in child presenting with TBI to the ED ●● Unstable airway
(Courtesy: Dr Gunda Srinivas). ●● Facial, neck trauma
●● Respiratory compromise, hypoxia
●● Decompensated shock
Breathing ●● Decreased level of consciousness ‘P’, ‘U’
●● Seizures
●● Provide oxygen via a non-rebreathing mask. ●● Raised ICP
●● If the child is bradypneic initiate bag-valve-mask ven­ ●● Other major injuries
tilation whilst one more team member keeps the airway
Securing the airway in child presenting with TBI is
manually open using the jaw thrust maneuver until in­
fraught with risk due to the following reasons:
tubation is accomplished.
1. Difficulty in visualizing airway.
Ù a. Secondary to a distorted airway.
Intubate using pharmcologically assisted intubation (PAI) b. Airway bleed.
technique with ICP precautions (see Chapter PAI). c. Cervical immobilization during ET.
2. Risk of precipitating quadriplegia if associated spinal
●● Lidocaine (1–2 mg/kg) should be administered 2–5 trauma.
minutes before laryngoscopy. 3. Aggravation of ICP.
●● Sodium thiopental, etomidate or propofol can be used
as sedative agents for their cerebroprotective effect.
●● Midazolam, may be used but is contraindicated if hy­
Ù
Manual in-line cervical immobilization throughout in-
potension complicates head trauma. tubation process IS NECESSARY to avoid aggravating
●● Ketamine was thought to be contraindicated in head SPINAL CORD INJURY due to neck movements with its
injury, but recent studies have shown that not only is risk of quadriplegia
ketamine safe in this setting, it may be neuroprotective.
In the setting of hypotension, ketamine is the induction
agent of choice.4 Ù
Many team members are needed during the process of
●● Use non-depolarizing agents such as rocuronium (0.6–
intubation in severe traumatic brain injury.
1.2 mg/kg) for paralysis (Box 26.2).
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 275

1. Airway physician: Responsible for intubation (Team


leader: The only voice to be heard). Ù
2. Nurse or physician to Optimization of mean arterial pressure (MAP) with
IPhold the neck manually in-line dur­
: 196.52.84.10 fluid therapy and vasoactive drugs is crucial for main-
ing intubation (to prevent excessive extension). Should
be prepared to perform BURP/Sellick if needed). taining CPP.
3. Physician who assesses following intubation and
keeps track of the the monitors and saturations. ●● If the hemoglobin is less than 10 mg/dL consider blood
4. Nurse for suctioning the airway (positioned on the left transfusion using warmed blood.
of the airway manager).
5. Airway nurse for handing the laryngoscope, tube, fixing
Ù
Dextrose containing fluids are contraindicated during
tube, etc. (posi­tioned on the right of the airway manager). the initial resuscitation of TBI. It can aggravate cerebral
edema.
Circulation
●● If shock is not due to the three causes mentioned above,
Secure IV/IO access and correct shock with 20 mL/kg of NS. perform needle thoracocentesis to rule out obstructive
Hypovolemia is a common problem noted in pediatric shock due to pneumothorax.
trauma victims. Signs of hypoperfusion include increased ●● A minimal cerebral perfusion pressure of 40 mm Hg
heart rate, loss of peripheral pulses, peripheral coolness for infants and 50 mm Hg for adolescents is consid­
and prolonged capillary refill. ered optimal.

Ù Disability
Bradycardia and high blood pressure secondary to ICP
●● Head injury patients are prone to develop raised ICP
may mask features of shock in TBI. In addition, children
which can potentiate secondary injury. Careful neuro­
often maintain systolic blood pressure despite significant
logical monitoring helps in early detection of cerebral
blood loss until they develop acute hypotension. Pulse herniation.
pressure is usually narrow in hemorrhagic shock. How- ●● The goal of treatment is to lower the ICP to a level
ever if the diastolic pressure is less than 50% systolic, that is adequate to increase cerebral perfusion pressure
then the possibility of vasodilatory neurogenic shock (CPP) as this is key to improve cerebral oxygenation
should be considered secondary to severe CNS injury. and prevent cerebral ischemia.

Blood loss inside cranium (closed head injury with­ Note: Risk of raised ICP exists even in infants despite
out multisystem trauma) is not sufficient to cause hy­ open AF or sutures.
povolemic shock. Hence, not more than 20–30 mL/kg
of fluids may be needed to resolve shock in isolated
Management of Raised
head injury.
Intracranial Pressure (Box 26.4)
If shock persists after administering 20 mL/kg in TBI,
Box 26.4: Management of raised intracranial pressure
consider the following possibilities.
●● Scalp injuries can cause significant blood loss in young Measures to improve jugular venous flow from brain
children. ●● Place head and neck in midline
●● Elevate head end of the bed not more than 30°
●● Fracture of long bones with or without intra-ab­dominal
( if elevated less than 30° CPP could fall)
injury. ●● Avoid tight ties for the ET tube
●● Vasodilatory shock due to spinal cord transection. ●● Minimize stimulation (suctioning and movement)
●● More volume will be needed to resolve shock for the Other measures
first three conditions. Isotonic normal saline is pre­ ●● Provide Morphine 0.1 mg/kg and lorazepam 0.1 mg/kg
ferred to lac­tated Ringer solution, since the former is ●● Adequate sedation and analgesia should be maintained
isonatremic compared to RL. with opioids and benzodiazepines to avoid anxiety and
●● Persistent hypotension refractory to volume resuscita­ pain, which may cause spikes in intracranial pressure
tion should be treated with dopamine or epinephrine to ●● Propofol as a sedative, is avoided owing to the risk of
metabolic acidosis
ensure adequate cerebral perfusion. Contd...
276 Section IX n Trauma

Contd... Surgery: Surgery is not a first-line treatment except to


●● Prescribe Paracetamol suppository: 10 mg/kg evacuate compressive subdural or epidural hematomas.
●● Maintain normothermia Refractory intracranial hypertension can be treated with
●● Maintain normoxia andIP normocarbia
: 196.52.84.10
(PaCO2 = 35 mm Hg)
●● Administer hypertonic saline (3% saline 0.1 mL/kg – 1 mL/ decompressive craniectomy. Children likely to benefit
kg) on a sliding scale11 from surgery are those with diffuse cerebral swelling,
●● Avoid prophylactic hyperventilation11 within 48 h of injury, no episodes of sustained ICP > 40
●● Administer prophylactic phenytoin for seizure control mm Hg, secondary clinical deterioration, evolving cere­
bral herniation syndrome (Table 26.2).
Osmotic therapy9,10: There is increasing evidence for
the use of hypertonic saline (HS) in children. It has been Routine antibiotics are not warranted. However, they may
shown that an increase in serum sodium concentration sig­ be indicated if the child has sustained a penetrating injury.
nificantly decreases ICP and increases CPP in severe TBI. Steroids have no role in the management of TBI.
Sustained hypernatremia and hyperosmolarity is safely
tolerated in these patients. While resuscitation is in progress, one physician who is
not part of the resuscitation team should elicit history.
Avoid prophylactic hyperventilation11
Mechanical ventilation should provide adequate oxygen­ History should focus on the following:
ation (oxygen saturation > 90%) and avoid hypercarbia ●● Mechanism of injury.
(PaCO2 > 38 mm Hg). In children, hypocarbia (paCO2< 35 ●● Severity of altered mental status.
mm Hg) decreases cerebral blood flow and can induce ce­
●● Posturing.
rebral ischemia hence hyperventilation should be avoided.
●● Seizures.
Administer prophylactic phenytoin for seizure control ●● Vomiting at the scene of injury or during transport.
if CT scan shows parenchymal damage
If the patient was confused at the scene and is now
Continuous EEG (if possible) is helpful to detect subclini­ normal, there is less reason for concern. However, the
cal/subtle seizures especially in sedated patients so that contrary scenario is more worrisome. Besides, a detailed
adequate anticonvulsants can be given. medical history is frequently unavailable during the ini­
CSF drainage: CSF drainage provides immediate but tial assessment of the patient and associated medical
transient effect and is especially indicated in situations conditions such as insulin-dependent diabetes may not
where the raised ICP is secondary to hydrocephalus. How­ be known.
ever, diffuse brain swelling as in TBI may cause chinked
ventricles making CSF drainage difficult.
Table 26.2: Surgical interventions in STBI

Injury Features Treatment


Subgaleal hematomas Collection of blood above periosteum No needling; Watch hematocrit

Cephalhematoma Subperiosteal; limited by suture line No treatment required


Skull fractures Linear, diastatic or depressed Depressed fractures may require urgent elevation
Basilar skull fractures CSF otorrhea or rhinorrhea β2 transferrin Expectant management; no packing of ear, no
distinguishes CSF or not prophylactic antibiotics; 85% spontaneously seal;
4% meningitis; if leak persists ENT repair
Epidural hematoma Lucid interval Urgent evacuation if mass effect
Subdural hematoma Underlying brain injury common, cortical bridging Evacuate if large and causing mass effect
veins tear; if chronic, think of child abuse
Intraparenchymal injury Fatal contusions, diffuse axonal injury, hematomas Neurosurgical intervention is usually not helpful,
decompressive craniotomy with or without
lesionectomy
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 277

LABORATORY AND RADIOLOGY


Ù Blood counts and chemistries, arterial blood gases and se­
Resuscitation of TBI in the ED is perhaps the most
IP : 196.52.84.10 rum alcohol levels, routine clotting studies [PT (prothrom­
complex of all resuscitations requiring a larger team
bin time) and PTT (partial thromboplastin time)] should
performing many tasks simultaneously. A separate phy-
be performed. When severe injury to the brain occurs, fac­
sician (Casualty Medical Officer) not involved in the re- tors released into the blood can lead to a fulminant dis­
suscitation should be responsible for obtaining history seminated intravascular coagulopathy. This complication
and documenting medicolegal entries. is a hallmark of a bad outcome and indicates the degree of
brain injury that may be present.
Case scenario 2
A 6-year-old girl falls from a construction site of the Computerized Axial Tomography (CAT or CT)
2nd floor (Figure 26.17 and 26.18). (CHALICE Guidelines)12
CT of the brain will help determine the presence of
a surgically removable mass lesion or identify a pa­
tient with an injury more severe than clinical exami­
nation indicated and will require expectant observa­
tion (Box 26.5).
Box 26.5: A head CT is required if any of the following are
present12

History
●● Witnessed LOC > 5 min
●● Abnormal drowsiness
●● Vomiting ≥ 3 episodes
Figure 26.16: She is intubated with ICP precautions and C- ●● Suspicion of non-accidental trauma
spine precautions. One bolus of 20 mL/kg of NS is administered. ●● Seizure in a patient who has no history of seizures
Following intubation her HR: 160/minute, but her BP is un- Examination
●● GCS < 14 or GCS < 15 if less than 1-year-old
recordable. A quick secondary survey reveals no injury to the
●● Suspicion of penetrating or depressed skull injury or
long bones or scalp. Her abdomen is scaphoid and soft. A
tense fontanelle
needle thoracocentesis in the right midclavicular line releases
●● Signs of basal skull fracture
a gush of air due to a pneumothorax. ●● Focal neurological deficit (motor, sensory, coordination
or reflexes)
●● Bruise, swelling or laceration > 5 cm if less than 1-year-old
Mechanism
●● High speed traffic accident (> 64 km/h)
●● Fall > 3 m in height
●● High speed injury from a projectile or an object
High-risk factors
●● GCS < 15 at 2 hour after injury
●● Suspected open or depressed skull fracture
●● History of worsening headache
●● Irritability on examination
This would require 30% of patients to get a head CT.
Medium-risk factors
●● Any sign of basal skull fracture
●● Large boggy hematoma of the scalp
Figure 26.17: In this picture taken 24 hours later, her
●● Dangerous mechanism of injury (MVA, fall from height >
cardiopulmonary assessment is apparently normal. Obstructive 0.9 m or 5 stairs, fall from a bicycle with no helmet
shock (due to tension pneumothorax in this child) had
complicated severe traumatic brain injury.
278 Section IX n Trauma

There is no role for contrast enhanced head CT in the nitive outcome and fewer developmental and behavioral
acutely injured child, unless an angiogram is being per­ sequelae.13
formed to evaluate for IP concomitant vessel injury. CT scan
: 196.52.84.10 Head injury education and prevention, i.e. car seats,
is a safe and accurate investigation for older chil­dren who
seat belts and helmets help reduce the incidence and se­
are able to lie still for the procedure. In younger children,
verity of head injury. Children who have suffered mild-
particularly those under 5 years, general anesthe­sia or pro­
moderate concussions should not return to contact sports
cedural sedation may be required to achieve CT scanning.
until they are completely symptom free, both at rest and
In addition, the risks of cranial irradiation need to be con­
with exer­tion. Any child with symptoms persisting greater
sidered. Therefore, particularly in younger chil­dren, the
than a week after a head trauma should be referred for neu­
risk of CT should be balanced against the risk of delayed
rocognitive evaluation.
diagnosis (Refer Protocol 26.1).

X-rays in Severe Traumatic Brain Injury Key Points


ü
There is some controversy over the usefulness of plain 1. C-spine immobilization should be performed along
skull X-rays. For almost all types of head trauma, the CT with airway opening maneuvers. Protect C-spine
scan provides more information than plain skull films. In until it is cleared.
limited instances (associated mandible or facial fractures) 2. Resuscitation should not be delayed while awaiting
skull X-rays, are indicated in addition to CT scan. Many neurosurgical opinion or CT scan.
studies have illustrated that the presence of a skull fracture 3. Once ABCDEs are stabilized management focused
significantly increases the risk of intracranial in­jury. on cerebroprotective measures.
4. Refractory shock in apparently isolated TBI, con­
The patient with serious head trauma should also have rou­
sider cord transection, internal bleed, pneumothorax
tine cervical spine X-rays to rule out an associated injury. Cervi­
cal injury must be anticipated in young infants, where the head and cardiac tamponade.
mass is disproportionately large compared to the cervical spine. 5. Mannitol could aggravate shock in the ED.
6. Hypertonic saline more useful in ICP and shock due
Indications for Skull Radiography to TBI.
7. Avoid hypoxia.
●● Possible penetration. 8. Avoid hypotension.
●● Possible depressed fracture. 9. Avoid hyperventilation.
●● Compound fracture. 10. Avoid hypoglycemia.
●● Previous craniotomy with indwelling shunt. 11. Avoid hyperglycemia.
●● Child less than 2 years of age with ‘boggy’ scalp he­ 12. Avoid hypothermia.
matoma.
●● Suspected non-accidental trauma.

Conclusion
common errors
û
1. Shifting the child for CT scan without stabilization.
The long-term neurocognitive and behavioral consequenc­ 2. Waiting for neurosurgeon opinion without correct­
es of head trauma can vary widely, based on the extent ing hypoxia and shock.
of injury. Overall, children have a better prognosis and 3. Failure to maintain C-spine precautions and spinal
improvement in function may continue for years after in­ immobilization until clearance of spine.
jury. Those pa­tients with a GCS score less than three have 4. Focusing on the medicolegal entries prior to stabili­
a high mortal­ity and morbidity. Children with coma that zation
lasts less than 2 weeks, have considerable better neurocog­ 5. Steroid therapy.
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 279

Protocol 26.1: Indications for CT brain

IP : 196.52.84.10
280 Section IX n Trauma

REFERENCES 8. Orliaget GA, Meyer PG, Baugnon T. Management of criti­


cally ill children with traumatic brain injury. Pediatric An­
1. Canadian Paediatric Society (CPS) Management of chil­ esthesia. 2008;18:455-46.
IP :CMAJ.
dren with head trauma. 196.52.84.10
1990;142(9):949-52.
9. Wakai A, Roberts IG, Schierhout G. Mannitol for acute
2. Filanovsky Y, Miller P, Kao J Myth. Ketamine should not traumatic brain injury Cochrane Database of System­
be used as an induction agent for intubation in patients with atic Reviews 2007, Issue 1. Art. No: CD001049. DOI:
head injury. CJEM. 2010;12(2):154-57. 10.1002/14651858.CD001049.
3. Greenes DS, Schutzman SA. Clinical indicators of head in­ 10. Upadhyay P, Tripathi VN, et al. Role of hypertonic saline
jury in head injured children. Pediatrics. 1999;104:861-67. and mannitol in the management of raised intracranial
4. Kupperman N, Holmes JF, et al. Identification of children pressure in children: A randomized comparative study. J
at very low risk of clinically important brain injuries after Pediatr Neurosci. 2010;5:18-21.
head trauma: a prospective cohort study. PECARN. Lancet 11. Kohanek P, et al. Guidelines for acute medical manage­
2009;374:1160-170. ment of severe traumatic brain injury in infants, children
5. Mazzoa CA, Adelson PD. Critical care management and adolescents. Pediatr Crit Care Med. 2012;(13)1S
of head trauma in children. Crit Care Med. 2002;30(11 1-16.
Suppl):S393-401. 12. Osmod MH, Klassen TP, et al. CATCH: a clinical de­
6. Meyer PG, Ducrocq S, Carli P. Pediatric neurologic emer­ cision rule for the use of computed tomography
gencies. Curr Opin Crit Care. 2001;7(2):81-87. in children with minor head injury. PERC. CMAJ.
7. Nationl Collaborating Centre for Acute Care. Head injury. 2010;182(4):341-48.
Triage, assessment, investigation and early management of 13. Dunning J, Daly JP, et al. Derivation of the children’s head.
head injury in infants, children and adults. London (UK): injury algorithm for the prediction of important clinical
National Institute for Health and Clinical Excellence events decision rule for head injury in children. CHALICE.
(NICE);2007 Sep. 54 p. (Clinical guideline; no.56). Arch Dis Child. 2006;91:885-91.
27
IP : 196.52.84.10

Approach to Polytrauma

Figure 27.1: Common hazards: Lack of balcony railings, walkers, unsupported TVs and lack of supervision in construction sites
(Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Principles of primary and secondary survey. 3. Recognition of abdominal trauma.
2. Management of orthopedic trauma. 4. Recognition of trauma to nerves and vessels.

INTRODUCTION ●● Introduce orogastric tube if altered mental status is


noted or abdominal trauma is suspected.
Major trauma is not as common as medical emergencies.
Children are exposed to potential environmental hazards as ●● Stabilize the C-spine, using age-appropriate cervical
shown in Figure 27.1. In addition, at the time this manual collars for children beyond infancy, towels and tape for
has been written, the initial assessment of trauma victims infants.
is being performed on arrival into the ED and not at the ●● Intubate early using PAI tech­nique (refer Chapter 3) if
site of accident. the victim is:
The rapid cardiopulmonary cerebral assessment must be – Responsive to pain or unresponsive.
per­formed, while evaluating for life-threatening injuries. Si- – Craniofacial injuries.
multaneously, aggres­sive resuscitative measures must also – Inhalational injuries due to burns.
be undertaken. ●● Talking or crying suggests that the airway is pat­ent and
Assessment of injuries involves primary survey and breathing is spontaneous. For spinal immobilization re-
secondary survey. fer to Chapter 41.

PRIMARY SURVEY Breathing


Airway with Cervical Spine Protection ●● Provide oxygen using the non-rebreathing mask if
spontaneously breathing.
●● Open the airway using the jaw thrust maneuver. ●● Check respiratory rate, work of breathing, air-entry and
●● Suction if secretions are seen. pulse oximetry.
282 Section IX n Trauma

●● If not breathing adequately, initiate bag-valve-mask Secondary Survey


ventilation and plan early intubation.
Secondary survey is a more detailed evaluation for injuries
●● In the absence of obvious external injury or cervical
IP : 196.52.84.10 prior to transfer for definitive care.
cord transection, if the child has unexplained hypoten-
sive shock despite initial fluid bolus, suspect tension 1. Head and skull
pneumothorax. Perform needle thoracocentesis to rule ●● Scalp lacerations are major cause of loss of blood
out this life-threatening emergency. resulting in shock in young children. Saline irriga-
tion, debridement and suturing should be performed
Ù at the earliest.
Do not delay needle thoracocentesis in order to take a ●● Bulging anterior fontanels suggest intracranial injury.
chest X-ray if tension pneumothorax is suspected. ●● Depressed fontanels suggest hypovolemia.
2. Maxillofacial and intraoral trauma
Circulation ●● Check nasal and oral patency. Edema could develop
during fluid resuscitation in children with craniofa-
●● If shock is noted, 20 mL/kg of normal saline is admin­ cial trauma.
istered up to a maximum of 50 mL/kg, if shock per- ●● Intubate early for significant maxillofacial trauma.
sists, plan blood transfusion. ●● Blood in oral cavity should be checked for basal
●● Blood is collected for grouping and crossmatching. skull fracture, nasal or oral trauma, tongue lacera-
Fresh whole blood preferable tion or/and injury or avulsion of teeth.
●● If hypotensive and intra-abdominal injury is suspect­ ●● Thorough irrigation with saline and antibiotics may
ed, the bolus must be administered cautiously to avoid be warranted.
dislodging clots (permissive hypotension). ●● Loose tooth should be preserved for reimplantation.
●● Call for urgent ophthalmologic and plastic surgeon
●● Apply direct pressure if obvious bleeding is noted.
for their assessment of injuries.
●● Splint bones if obviously fractured.
●● Wrap and splint pelvis to reduce bleeding into pelvic or 3. Neck
retroperitoneal space due to pelvic fractures. ●● Since the short neck of infants are difficult to assess,
we can safely presume that an active child moving all
Ù four limbs is unlikely to have cervical cord injury.
●● Maintain C-spine precaution in the unresponsive
Rapid shift to OR is planned if hypotension is noted.
child or infant.
4. Chest
Disability ●● Fracture of ribs and therefore, flail chest is not com-
●● Mental status is evaluated in the AVPU scale. mon in young children.
●● Check pupils for reaction and size along with eye po­ ●● Initial chest X-ray may not show evidence of lung
sition and movements for non-convulsive status epi- contusion.
lepticus in unresponsive children. 5. Abdomen
●● Evaluate for spontaneous movement. Note presence of ●● Spleen and liver—Refer to section on Ab­dominal
posturing or seizure activity. and Pelvic trauma.
●● Assess for pain and sensation. 6. Perineum/rectum/vagina
●● Look for obvious limb deformities. ●● Inspection of the perineum and the orifices give in-
formation on pelvic trauma (more common in chil-
Exposure dren than in adults).
●● Remove clothing and diaper for complete secondary ●● Blood in the vagina or rectum warrants examination
survey. under anesthesia.
●● Burns are calculated using the patient’s palmar surface ●● Unless blood is seen in the orifices, speculum ex-
as 1% (refer Chapter 28). amination need not be routinely performed in the
●● If burns are noted, the affected surface is covered by prepubertal girl.
moist saline dressings. 7. Musculoskeletal (refer to section on Orthopedic trauma).
Chapter 27 n Approach to Polytrauma 283

8. Neurological evaluation Primary Survey and Initial Management


●● Altered mental status due to hypoxia and shock may
prevent accurate IP
evaluation of the neurological status. Cervical spine stabilization in the neutral position should
: 196.52.84.10 be maintained not only throughout resuscitation but also
●● Emesis may suggest presence of raised intracranial
pressure. during transport for im­aging. These precautions are taken
●● Loss of tone, flaccidity and loss of sensation war- until bony or ligamentous injuries have been ex­cluded.
rant neurosurgical consultation. This is done by employing the following methods:
●● However, lower spinal injuries are uncommon in
●● Use appropriate sized collar.
children.
●● If immobilization device is not available use rolled
tow­els (thick) or sand bags secured against the side of
Interventions During the neck.
Secondary Survey
●● Antibiotics are administered for fractures, craniofacial
Ù
The larger head in infants and children less than 4 years,
injuries and abdominal trauma.
results in flexion of the neck when placed supine on flat
●● Tetanus prophylaxis.
surfaces.
●● Analgesia:
– Morphine (0.1 mg/kg/dose).
●● Use a spinal board with hollow beneath the head.
– Fentanyl (1 μg/kg/dose).
●● Place folded towel under the shoulders.
– Paracetamol (15 mg/kg/dose PO/PR/NG).
●● Steroids:
Steroids not warranted for suspected spinal cord injury.
Ù
Children presenting with head trauma, neck pain follow-
Ù ing trauma or any neurological deficit are considered at
greater risk of cervical cord injury.
If a child fails to stabilize with aggressive resuscitation
or has blood detected within the chest or abdomen, ur-
gent operative intervention must be undertaken. Circulation
●● Apply direct pressure over open wounds.
ORTHOPEDIC TRAUMA ●● Simultaneously, realign the injured limb or limbs in the
Pathophysiology near anatomic position.
●● Splint injured limbs.
Fractures can occur in the diaphysis (shaft), metaphysis
(flare), physis ( growth plate) or epiphysis (secondary cen- Ù
ters of ossification). Cartilaginous growth plates, which Realignment and splinting can significantly improve cir-
persist at the end of growing bones, are responsible for culation.
the longitudinal growth of bones. These growth plates are Femoral fractures can result in loss of 20% of blood re-
weaker than the nearby bone making them prone for frac- sulting in shock.
tures. Fortunately, most growth plate injuries heal read-
ily with simple or no treatment. Indeed, growth plate and
metaphyseal fractures heal in half the time taken for dia- Disability
physeal fractures. ●● Assess gross motor function and circulation of each
Trauma occurring as a result of traveling in motor ve- limb during the primary survey.
hicles, cyclist or pedestrian being hit by a moving motor
vehicle, fall from twice the height of the child result in Secondary Survey
high-energy fractures. Play-ground injuries and falls from
lesser heights usually result in low-energy fractures. High- Comfort
energy mechanism is associated with injuries to nerves, If airway, breathing and circulation are stable, ensure that
vessels, open fractures, swelling or compartment syn- the child is as comfortable as possible:
dromes, growth plate damage and systemic injuries.
284 Section IX n Trauma

●● Move the deformed limb as little as possible. Spinal Injury


●● Early splinting is the best analgesic.
●● Avoid eliciting fracture Palpate cervical spine for tenderness.
IP : crepitus.
196.52.84.10
●● Remove the spinal board after spinal injuries have been ●● A fully conscious child, who is cooperative can be re-
ruled out by thorough neurological, radiological and quested to turn his head in all directions after removing
magnetic resonance imaging (MRI) assessment. the collar.
●● Log roll the child and inspect and palpate the thoracic
Look, Feel, Move and lumbar spine up to the sacrum. Signs of injury
include:
Use your fingers to look, feel and move:
– Tenderness.
●● From sternum and scapula to finger tips.
– Bruising.
●● From anterior superior iliac spine to toes. – Swelling.
●● Examine pelvis for shape, tenderness, horizontal and – Deformity.
vertical stability.
●● Horizontal stability assessed by medial followed by Ù
Boggy swelling over the lumbar spinous process or seat
lateral pressure on both anterior superior iliac spines.
●● Vertical stability assessed by traction on one leg at a belt bruise denotes seat belt injury to spine.
time, while stabilizing the pelvis.
However, multiple injuries may be difficult to diagnose
Ù when the child is not alert or in pain. On the contrary, after
Pelvic fractures can cause exsanguinating bleed. a careful initial examination, a repeat physical examina-
tion at 24 hours or when the child becomes alert minimizes
●● Bind the pelvis circumferentially with a sheet to de- chances of missing injuries. Commonly missed injuries in
crease its internal volume. motor vehicle accidents are fractures of metatarsal, tarsal,
●● Refer early for orthopedic intervention. metacarpal and carpal bones.
●● Pelvic injury often associated with abdominal trauma.
Laparotomy may be needed and may be performed
Vascular Examination
along with pelvic stabilization (Figure 27.2).

Ù Ù
Integrity of circulation should be evaluated early in the
Examine an unstable pelvis only once. Repeated assess-
management of a critically injured child.
ments could disrupt a clot and lead to blood loss. Bind the
pelvis with a cloth/sheet to reduce volume and mo­tion. ●● Examine and document presence or absence of radial,
ulnar, dorsalis pedis and posterior tibial pulses in all
four limbs whether the limb appears injured or not.
●● Document color, temperature and motor function of all
four limbs.

Neurological Examination
Evaluation of the power of each muscle according to the
Medical Research Council (MRC) classification establish-
es, whether the nerve is intact along its course. Younger
children may be examined by observation using toys.
0 = No movement
1 = Flicker
Figure 27.2: Child with polytrauma
(Courtesy: Dr Gunda Srinivas). 2 = Moves without gravity (gravity eliminated)
Chapter 27 n Approach to Polytrauma 285

3 = Moves with gravity (against gravity) Imaging


4 = Weaker than full strength Plain X-rays ordered for initial trauma survey are:
IP : 196.52.84.10
5 = Full strength ●● Lateral C-spine.
Sensory examination along with motor examination is ●● Chest.
●● Pelvis.
shown in the Table 27.1.
●● Two views at 90° for injured limb segments and
Table 27.1: Neurological examination spine.
●● Include the joint above and below the injured segment.
Nerve Sensory Motor
Table 27.2: The Gustilo classification of open fractures to
Radial nerve First dorsal web Thumb extension,
decide on antibiotic prophylaxis
space extension across
MCP joints Gustilo grade Soft tissue injury Antibiotic prophylaxis
Median nerve Ulnar border of the Thumb opposition I Small laceration Cefazolin 40 mg/kg
index finger < 1 cm
Ulnar nerve Tip of small finger Abduction of index II Laceration 1–10 If pencillin/ cef allergy:
finger cm, graft or flaps clindamycin 10 mg/kg
Anterior N/A Flexion of DIP joint needed to cover
interosseous nerve of index finger and III a Large laceration > Cefazolin 40 mg/kg IV
thumb 10 cm, extensive with gentamicin 2.5 mg/
Peroneal nerve Deep branch—first Great toe degloving injury, kg IV with metronidazole
dorsal web space dorsiflexion but bone can be 10 mg/kg if grossly
Tibial nerve Sole of foot at Ankle and toe covered contaminated (fecal, soil)
metatarsal heads plantar flexion or devitalized tissue
III b Large laceration, 10 mg/kg clindamycin if
bone cannot pen/cef allergy
Open Wounds with or
be covered,
without Open Fractures often extensive
contamination
●● Surface irrigation with saline.
III c Open fracture 10 mg/kg clindamycin if
●● Apply sterile dressing.
with arterial pen/cef allergy
●● Administer antibiotics (Table 27.2) and tetanus toxoid injury in same
where needed. limb
●● Tetanus prophylaxis. pen, pencillin; cef, cefazolin.

Tetanus toxoid is administered, if the child has not be im-


CT Scan
munized as per the national immunization schedule or if he is
older than 5 years (booster dose would have been given). ●● Useful if complex flat bone trauma such as pelvis, spi-
nal injuries are suspected.

Risk Factors for Infection MRI


Based on whether:
●● Does not play a major role in management of orthope-
●● Injury is due to high-energy trauma. dic injuries.
●● Extensive soft tissue damage. ●● Indicated if clinical signs of spinal cord injury are noted.
●● Contamination.
●● Circulatory impairment. ABDOMINAL AND PELVIC TRAUMA
Ù Pathophysiology
Transfer for imaging ONLY after stabilization. Since children are small, they are more susceptible to the
transmission of kinetic energy over a smaller area. The ribs
286 Section IX n Trauma

are soft and more compliant resulting in more force be- ●● Blood.
ing transmitted to thoracic and upper abdominal organs. ●● Palpable bony fragments.
Thinner abdominal wall IP musculature offers less protec-
: 196.52.84.10 ●● Linear ecchymosis ‘seat belt injury’ is often associated
tion to intra-abdominal organs. Close proximity of all the with intra-abdominal injury.
intra-abdominal organs also predisposes to a greater risk of
Whilst abdominal X-ray is not useful in evaluation of
trauma to the solid organs within the abdomen.
intra-abdominal injury, radiographic evidence of gas in
In India, common causes of abdominal trauma are mo­tor soft tissue (taken after stabilization) may provide some
vehicle accidents, fall from heights and bull gore injuries. clues suggestive of bowel injury.
Suspect abdominal injury if secondary survey reveals
the following (Refer Figure 27.3 for hemothorax):
Splenic Injury
●● Abdominal distension.
●● Left shoulder pain (Kehr’s sign).
●● Abdominal tenderness.
●● Abrasions and tenderness in left upper quadrant.
●● Abrasions.
●● Abdominal distension.
●● Ecchymosis.
●● Associated with shock.
Ù Hepatic Injury
• Suspect serious abdominal trauma if infants are hav-
ing predominantly chest breathing or the older child is ●● Abdominal distension.
lying still and whimpering or has referred pain to the ●● Right shoulder pain.
shoulder. Trauma to the lower six ribs or abdominal ●● Abrasions and tenderness in right side of abdomen.
distension in a hemodynamically unstable child is also ●● Hypotensive shock.
associated with serious intra-abdominal injury. ●● Injuries to the ribs are common.
• Gastric distension due to aerophagia in young infants
may be misinterpreted as abdominal distension. An
Urological Injury
orogastric tube should be placed early in the evalua-
tion to avoid misdiagnosis. ●● Blood at penile meatus.
●● Perineal bruising or swelling.
●● High riding prostate.

Ù
If any of these signs are present, DO NOT insert a Foley
catheter. Diagnosis is confirmed by performing a retro-
grade urethrogram.

Imaging
Ù
Whilst routine X-rays for lateral spine, pelvis and chest
are obtained, plain abdominal films are not useful in
evaluation of acutely injured children.
Figure 27.3: This child was nearly run over by a vehicle.
Note the tyre markings on the lateral chest. He developed a
1. Focused abdominal sonogram for trauma (FAST).
hemothorax that was relieved by a thoracostomy.
●● FAST is a focused goal-directed sonographic ex-
amination of the abdomen used to rapidly assess
Bowel Injury
for free fluid (bleed in peritoneal space, abdomen,
Suspect injury to the gut if digital rectal examination re- pleural space and pericardial sac).
veals evidence of:
Chapter 27 n Approach to Polytrauma 287

●● FAST has replaced diagnostic peritoneal lavage ●● Use small volumes of 3% saline for resuscitation to
(DPL) to identify intra-abdominal bleed. treat life-threatening hypotension.
●● Helps in triaging for the need to perform abdomen ●● Consider vasopressin infusion to maintain blood
IP : 196.52.84.10
computerized tomography (CT) scan. pressure at minimally acceptable ranges.
●● Recently eFAST (extended focused assessment
with sonography for trauma) has been used, which Ù
allows an emergency physician to detect whether Major exsanguinating trauma: Urgently shift to OT for
a patient has pneumothorax, hemothorax, pleural damage control surgery and resuscitation.
effusion, mass/tumor or a large foreign body. This
examination allows for visualization of the echo- 3. Damage control surgery.
genic tissue, ribs and lung tissue using few radio-
●● Traditional surgery is not performed until the victim
graphic signs.
has been stabilized.
2. Intravenous contrast enhanced CT abdomen is the di- ●● Surgical strategies are focused to control bleeding
agnostic modality of choice to identify intra-abdomi- and reduce wound contamination.
nal injuries.
3. Magnetic resonance imaging not needed for evalua-
tion of abdominal or pelvic trauma.
Key Points
ü
Acute coagulopathy, hypothermia and acidosis also 1. Avoid rushing to evaluate obvious injuries and fail
known as the ‘lethal triad’ can occur following severe ex- to stabilize the ABCs.
sanguinating trauma. To avoid these dangerous complica- 2. Stabilization and immobilization of the spine is a
tions, resuscitation is focused towards damage control. priority in trauma victims.
3. Rule out hemo/pneumothorax and control bleeding
1. Permissive hypotension in addition to stabilization of the ABCs.
●● Replacement of large volume normal saline in ma- 4. Ensure comfort for children who do not have life-
jor exsanguinating trauma can result in clot dis-
threatening injuries.
lodgement, rebleeding, hyperchloremic acidosis
5. MRI is not a useful modality in orthopedic trauma.
and dilutional coagulopathy.
●● Give just enough fluids to maintain 70–80 systolic 6. FAST mandatory in ruling out intra-abdominal
blood pressure. bleed.

Ù
This strategy works only when time between inciting trau-
ma and shifting to the OT is less than 30–40 minutes.
common errors
û
Permissive hypotension SHOULD BE AVOIDED when 1. Failure to manually immobilize C-spine until the
head injury coexists. Cerebral perfusion pressure must cervical collar and spinal board have been applied.
not be compromised. 2. Failure to shift to OT when shock is refractory to
fluid therapy.
2. Hemostatic resuscitation 3. Transferring trauma victim for imaging without sta-
●● Infuse whole blood as initial resuscitation fluid. bilization.
– This strategy helps to treat intrinsic acute trau- 4. Not infusing whole blood early in the management
matic coagulopathy and prevent dilutional co- of exsanguinating bleed due to trauma.
agulopathy.
Environmental

Section X
IP : 196.52.84.10

Injury
IP : 196.52.84.10
28
IP : 196.52.84.10

Burns

Figure 28.1: Adequate supervision is needed to prevent burns in children

Learning Objectives
1. Pathophysiology of burns. 3. Management of the ABCs specific for burns.
2. Calculation of percentage of burns. 4. Care of the burned area.

INTRODUCTION BURN CLASSIFICATION


Scalds are perhaps the commonest type of burn injury that Burn classification is based on depth, extent and
are encountered in our setting (accidental spillage of hot involve­ment of hands or face or perineum.
rasam, sambar, water in the kitchen). Severe burns involves
1. First degree/superficial
rapid assessment of degree of burns, aggressive resusci­
tation and early referral to a burn center (Figure 28.1).1 ●● Red, dry painful.
●● Will heal after a few days with no scar.
PATHoPHYSIOLOGY 2. Second degree/partial thickness
Loss of cutaneous barrier results in insensible fluid loss. ●● Wet, red, very painful.
Increased capillary permeability also causes loss of flu­ ●● Superficial or deep partial thickness.
ids. Locally, fluid shift into the burn wound leads to burn ●● Will heal by scar (may require skin graft).
wound edema. Systemic capillary leak in burns greater ●● Needs wound care and possible debridement, but
than 25% of body surface area (BSA) could result in hy­ will heal after weeks.
povolemia. Hypoproteinemia, systemic inflammatory re­
3. Third degree/full thickness
sponse sysdrome (SIRS) and hormone derangements are
other contributing factors to loss of fluids in severe burns. ●● Leathery, dry, loss of sensation, waxy.
Circumferential burns can lead to formation of eschars ●● Will heal with excision and grafting.
which can cause vascular insufficiency by pressure effect.
4. Fourth degree
Hence, these need to be removed to prevent the same dur­
ing healing. ●● Involves subcutaneous tissue, tendon and bone.
292 Section X n Environmental Injury

Total Burn Surface Area


●● Calculate using rule of nine (Figure 28.2).
Ù
Consider early intubation, if the following signs are noted:
●● Exclude first degreeIPburns
: 196.52.84.10
when calculating total burn
surface area (TBSA) (Table 28.1). • Singed nasal hairs and eyebrows.
• Carbonaceous deposits in oropharynx and face.
MAJOR BURNS • Oropharyngeal edema.
• Hoarseness, persistent coughing, stridor.
●● Burns involving the hands, face, feet or perineum. • Face, neck, upper torso burns.
●● Burns that cross major joints.
• Aspiration of hot liquids can also cause airway
●● Circumferential burns to any extremity.
●● Burns associated with inhalational injury. com­promise.
●● Electrical burns. • Anticipate a difficult airway and call for ENT or
●● Burns associated with fractures or other trauma. anesthesiologist help and use a smaller size ET tube.
●● Burns in infants.

Prehospital Care
1. Do not remove burned clothing.
Make sure the victim is no longer in contact with hot
or burning material or exposed to smoke or heat.
2. Cool the area within 30 minutes of the burn with
cool water. This intervention reduces the depth of
burnt area and pain.

Ù
Do not put ice on the burn.

3. Do not immerse large severe burns in ice cold water.


Doing so could cause a drop in body temperature (hy­
pothermia) and deterioration of blood pressure and
circulation (shock).
4. Cover the area of the burn. Use a cool, moist, sterile
bandage; clean, moist cloth; or moist cloth towels.
Figure 28.2: Calculation of burns percentage based on parts
Management of body involved
●● Elevate the burned body part or parts above heart level,
when possible. Circulation
●● Two large peripheral intravenous lines should be obtained.
Airway and Breathing ●● Correct shock with normal saline (NS) boluses.
●● If the child has suffered inhalation injuries along with
●● If there is no breathing or other sign of circulation, be­
skin burns, 40%–50% more fluid may be warranted.
gin CPR.
●● Airway is most commonly affected by smoke or steam and Ù
Burns GREATER THAN 15% BSA are associated with
could be compromised even in the absence of skin burns.
●● Respiratory failure could result from loss of airway significant fluid loss, which should be aggressively
patency, pulmonary edema, bronchospasm, diminished corrected.
lung compliance and small airway occlusion. Burns LESS THAN 15% BSA are not associated with
●● Consider the potential for carbon monoxide poisoning. significant capillary leak.
Chapter 28 n Burns 293

●● In burns < 15% encourage oral intake of fluids. Facial Burns


●● Monitor urine output and maintain 1–2 mL/kg/h output.
●● Rule out corneal injury.
IP : 196.52.84.10 ●● Lubricate, if eyelids are swollen.
SPECIFIC INJURIES ●● Secure endotracheal (ET) tube with wire, if the face is
Scalds extensively involved.
●● Scald burns do not require surgery, if daily wound ●● Avoid using adhesive tapes.
cleansing and dressing changes are done (Figure 28.3). Scalp Burns
●● Provide adequate analgesia.
●● Shave hair to assess extent of burns.
●● Keep wound clean.
Hand Burns
●● Meticulous wound cleaning and dressing.
●● Plastic surgery follow-up to avoid contractures.
Commissure Burns (Burns Around Mouth)
●● Warn parents about the risk for late bleeding (The la­
Figure 28.3: This picture shows a child, who is being ventilated bial ar­tery can get exposed when the eschar separates
for cardiorespiratory failure due to scalds secondary to spillage after 5–10 days).
of hot sambar while being cooked (Courtesy: Dr Thangavelu S).

Table 28.1: Calculation of burns percentage

Birth–1 year 1–4 year 5–9 year 10–14 year 15 year Adult Burn size estimate
Head 19 17 13 11 9 7
Neck 2 2 2 2 2 2
Anterior trunk 13 13 13 13 13 13
Posterior trunk 13 13 13 13 13 13
Right buttock 2.5 2.5 2.5 2.5 2.5 2.5
Left buttock 2.5 2.5 2.5 2.5 2.5 2.5
Genitalia 1 1 1 1 1 1
Right upper arm 4 4 4 4 4 4
Left upper arm 4 4 4 4 4 4
Right lower arm 3 3 3 3 3 3
Left lower arm 3 3 3 3 3 3
Right hand 2.5 2.5 2.5 2.5 2.5 2.5
Left hand 2.5 2.5 2.25 2.5 2.5 2.5
Right thigh 5.5 6.5 8 8.5 9 9.5
Left thigh 5.5 6.5 8 8.5 9 9.5
Right leg 5 5 5.5 6 6.5 7
Left leg 5 5 5.5 6 6.5 7
Right foot 3.5 3.5 3.5 3.5 3.5 3.5
Left foot 3.5 3.5 3.5 3.5 3.5 3.5
Total TBSA
294 Section X n Environmental Injury

Parkland Resuscitation Formula2 wound. Wrap the gauze loosely to avoid applying
pressure on burned skin. Bandaging keeps air off the
Ù IP : 196.52.84.10 burn, reduces pain and protects blistered skin.
4 mL/kg of fluids/% total burn surface area. 3. Prescribe paracetamol: 10 mg/kg/dose.

● ● Time zero for fluid resuscitation = Time of burn Management


injury.
●● Total fluids to be given for first 24 hours = Normal main­ ●● Call the surgeon for debridement cleaning and dressing.
tenance for age + 4 mL/kg/% total body surface area. ●● Silver sulfadiazine is not recommended, since it pro­
●● Give half of calculated fluids over first 8 hours from longs healing time.4
time of injury. ●● Apply biosynthetic dressing.5 Evidence supports the
●● Give remaining half of calculated volume over the fol­ fact that this may speed healing.
lowing 16 hours.
●● Do not forget on-going losses such as vomiting. HISTORY
●● Adjust fluids to maintain output of 1–2 mL/kg/hour. ●● Where, when and how did the burn injury occur?
●● Loss of albumin in open wounds could result in hy­ ●● Petroleum, kerosene, or steam, hot water?
poalbuminemia. However, during resuscitation, albu­ ●● Pain related to burns.
min is not advised. ●● Breathlessness.
Refer Figure 28.4 showing recovered child. ●● Cough.
●● Loss of consciousness.
Do not Forget ●● Past history.
●● Tetanus prophylaxis.
●● Avoid prophylactic antibiotics. BURN-SPECIFIC SECONDARY SURVEY
●● Provide pain relief. ●● Rule out intracranial trauma.
●● Intravenous antibiotics are recommended only in those ●● Corneal fluorescein exam for corneal injury.
with large and severe burns.3 ●● Assess for burns and exposed cartilage.
●● Circumferential burns around chest may warrant es­
Minor burns charotomy.
For minor burns, including first-degree burns and second- ●● If the limb has been exposed to circumferential burns,
degree burns limited to an area no larger than 7.5 centime­ elevate it above the level of the heart to reduce edema.
ters in diameter, take the following action. ●● Abdominal compartment syndrome could occur.
●● Check foreskin for genitourinary injury.
Prehospital Care ●● Pain during passive/voluntary movements (consider
escharotomy, if circumferential burns).
1. Cool the burn: Hold the burned area under cool (not
cold) running water for 10–15 minutes or until the
pain subsides. If this is impractical, immerse the burn INVESTIGATIONS
in cool water or cool it with cold compress. Cooling ●● Complete blood count (CBC)
the burn reduces swelling by conducting heat away ●● Serum electrolytes.
from the skin. ●● Serum albumin.
●● Renal function.
2. Cover the burned area with a sterile gauze bandage.
●● Chest X-ray.
Avoid fluffy cotton, or materials that may get into the
Chapter 28 n Burns 295

1.
common errors
Failure to provide pain relief.
û
IP : 196.52.84.10
2. Application of native medications.
3. Covering the child with warm clothes during transport.
4. Breaking blebs.

REFERENCES
1. Bhattacharya S. Principles and practice of burn Care. In­
dian J Plast Surg.2009;42:282-83.
2. Tintinalli, Judith E. Emergency Medicine: A Compre­
Figure 28.4: Child seen in Figure 28.3 recovered after hensive Study Guide [Emergency Medicine (Tintinalli)].
ventilatory and wound care. Note his tracheostomy. The New York: McGraw-Hill Companies 2010. ISBN 0-07-
airway had been compromised due to edema following 148480-9.
inhalational burns (Courtesy: Dr Thangavelu S). 3. Avni T, Levcovich A, Ad-El DD, et al. “Prophylactic an­
tibiotics for burns patients: systematic review and meta-
Key Points
ü analysis”. BMJ 2010;340:c241. doi:10.1136/bmj.c241.
PMC 2822136. PMID 20156911.
1. Wash burned areas with tap water in the prehospital
4. Storm-Versloot MN, Vos CG, Ubbink DT, et al. In: Storm-
setting. Versloot Marja N. (Ed)2010 Mar 17. “Topical silver for pre­
2. Anticipating need for early intubation, if airway is venting wound infection”. Cochrane database of systematic
involved. reviews (Online) (3): CD006478. doi:10.1002/14651858.
3. Estimation of burned surface and calculating the CD006478.pub2. PMID 20238345.
appropriate fluids. 5. Hubley P. “Review: evidence on dressings for superficial
4. Removal of eschars in circumferential burns to burns is of poor quality”. Evid Based Nurs” 2009 (3): 78.
prevent vascular insufficiency. doi:10.1136/ebn.12.3.78. PMID 19553415.
29
IP : 196.52.84.10

Electrical Injury

Figure 29.1: Few seconds of negligence can cause severe and occasionally fatal electrical burn injuries
(Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Pathophysiology of electrical injury. 3. Resuscitation and investigations following electric
2. Assessment of severity of injury based on injury.
cardiopulmonary cerebral assessment and the
pediatric assessment triangle.

INTRODUCTION PATHOPHYSIOLOGY
Young children are usually referred to the ED with low volt- Electricity passes between two points through the path
age injuries. Electrical burns can occur due to exposure to of least resistance. The most dangerous pathway for the
electrical appliances and electrical wall outlets (Figure 29.1). current is along the vertical axis of the body as it passes
Ù through all vital organs. Hand to hand flow will involve the
heart, respiratory muscles and spinal cord.
High voltage injuries could lead to death.
Low voltage current can cause tetanic contraction of
CLASSIFICATION the respiratory muscles and ventricular fibrillation. High
voltage current can throw the victim and cause trauma in
Of the two types of current viz alternating current (AC) addition to the effects mentioned above.
and direct current (DC), the former is more dangerous. Te-
tanic muscle contractions occur as a result of prolonged
contact. AC is used for domestic purposes and DC is used CASE SCENARIO 1
in batteries, defibrillators and pace­makers. A 10-year-old boy is rushed into the ED after being
●● Low voltage: < 600 V. found unconscious near a high tension wire. Thinking
●● High voltage: > 1,000 V. the wire as a rope, boy had tried swinging while holding
●● Lightning: > 30 × 106 V.
Chapter
Chapter 3 n Modified 29 nSequence
Rapid ElectricalIntubation
Injury 297297

the wire. Skin wound was not bleeding. Edges showed ●● Circulation: Low voltage causes ventricular fibrilla-
signs of coagulation (Figures 29.2 to 29.5). tion, heart block, bundle branch block, supraventricu-
IP : 196.52.84.10 lar tachycardia, ST changes, atrial fibrillations. Car-
diogenic shock can supervene. High voltage can cause
asystole.
●● Disability: Evaluate for altered mental status, seizures,
visual and auditory disturbances, quadriplegia (ver-
tebral fractures) and cranial nerve deficits (rupture of
tympanic membrane).
●● Obtain targeted history:
a. High voltage or low voltage.
b. Loss of consciousness.
Figure 29.2: Charred wound at the site of contact with wire
c. Duration of contact.
d. Thrown from site or not.
●● Assess for entry and exit wounds.
●● Even if wound looks small, there may be severe un-
derlying injury. Cutaneous injuries may extend from
erythema to full thickness burns. Coagulation and ne-
crosis of deep muscles can occur, while sparing the
skin. Delayed bleeding is possible after the eschar
falls off.
●● Electrocardiography (ECG), computed tomography
(CT) of head for altered mental status, X-rays for mus-
culoskeletal injuries.
●● Complete blood count (CBC), electrolytes, renal func-
tion, cardiac enzymes, blood group and crossmatch.

Figure 29.3 Physiological status: Airway not maintainable,


cardiogenic shock, altered level of consciousness with non-
convulsive status epilepticus.

PREHOSPITAL CARE
At site
●● Turn off current source, prior to accessing the victim.
●● Assess whether pulseless and initiate cardiopulmonary
resuscitation (CPR) as per pediatric advanced life sup-
port (PALS) guidelines.
●● Airway and breathing: Direct injury to the respira- Figure 29.4: This boy was referred to the ED with loss of
consciousness following swinging on a high tension wire. The
tory control center can cause apnea. Tetanic contrac-
skin wound was not bleeding with the edges showing signs of
tions of the respiratory muscles (especially diaphragm) coagulation. He was intubated, after administration of 5 mL/kg
can also cause respiratory arrest. of fluids and Dobutamine for cardiogenic shock.
298298 Section X nIIEnvironmental
Section n Airway Injury

IP : 196.52.84.10

Figure 29.5: This picture shows the child following recovery


with his relieved parents after successful resuscitation.
Fortunately no major vessels or nerves had been injured.

Figure 29.7 Physiological status: Cardiopulmonary cerebral


CASE SCENARIO 2 (Figures 29.6A and B, 29.7) status nor­mal. Extensive skin burns with exit wounds on his
A 12-year-old boy was accidentally holding an high ten- soles.
sion wire and standing on iron rod in a terrace.
INTERVENTIONS
●● Since his ABCs were stable monitor for cardiac ar-
rhythmias.
●● Skin care for burns. Refer Chapter 28.
●● Look for compartment syndrome.
●● Complete blood count (CBC), electrolytes, renal func-
tion, cardiac enzymes, blood group and crossmatch.

Key Points
ü
1. Arrhythmias are common, leading to cardiac arrest
or cardiogenic shock. Obtain ECG to evaluate for
myocardial damage.
2. CT head to evaluate central nervous system (CNS)
in high voltage injuries.
3. Orofacial injuries could bleed later and should be
advised follow-up.

common errors
û
1. Assuming that tissue and vessels are viable
immediately after injury following high voltage
exposure.
Figures 29.6A and B: Entry wound in the forearm, and exit 2. Assuming that the small size of the external wound
wound on the soles, where the tissues have become charred. determines extent of internal damage.
This boy was accidentally holding a high tension wire while
standing on iron rod (Courtesy: Dr Gunda Srinivas).
30
IP : 196.52.84.10

Submersion Injury

Figure 30.1: Children’s natural attraction to water enhances their risk of drowning in water bodies (Courtesy: Dr Gunda Srinivas)

Learning Objectives
1. Pathphysiology following submersion injury. 3. Using the PAT to assess a drowning victim.
2. Principles of prehospital care. 4. Steps in management of a drowning victim.

INTRODUCTION PATHOPHYSIOLOGY
Drowning is the leading cause of accidental death of children Submersion results in loss of normal breathing patterns,
in industrialized countries.1 In these countries, it has been panic and laryngospasm. Apnea and pulmonary aspiration,
noted that the site of drowning was bathtubs for infants, swim- which follow, lead to hypoxemia.6 The resultant hypercar­
ming pools for children between 1 and 4 years of age, and bia, hypoxia and acidosis lead to circulatory arrest and
natural collection of water in older children (Figure 30.1).2 multiorgan failure.
Drowning is the result of respiratory impairment from Loss of surfactant, atelectasis, acute lung injury, pulmo-
submersion or immersion in a liquid.3,4 The presence of nary edema, intrapulmonary shunting and ventilation perfu-
liquid/air interface at the entrance of the airway prevents sion mismatch are some of the causes of respiratory failure.
the victim from breathing air. The victim may live or die Prolonged hypoxia, severe peripheral vasoconstriction,
after this event. Despite the outcome, he is defined as be- intravascular fluid loss, extravascular fluid shifts, brady-
ing involved in a drowning incident. The Utstein statement cardia and ventricular fibrillation are perhaps the common-
recommended that the term near-drowning should not be est causes of cardiac arrest.7,8
used.4 It has also de-emphasized the classification based on
the nature of submersion fluid viz salt water versus fresh
water.4 Although there are differences that have been re- Prehospital Management
ported in laboratory conditions, they have not been found Though there are no modifications to the standard ba-
clinically significant. sic life support maneuvers, some precautions have been
300 Section X n Environmental
Section II n Airway Injury

considered appropriate for cardiopulmonary resuscitation ●● If airway is maintainable and the child has respira-
(CPR) in drowning victims.9 tory distress, provide supplemental oxygen using the
Bain circuit.
IP : 196.52.84.10
Recovery from Water ●● Early use of continuous positive airway pressure
(CPAP) is helpful in reversing hypoxia secondary to
●● Remove from water immediately. the capillary leak in the alveoli.
When rescuing the victim, the rescuer should reach the ●● If the airway is not maintainable and breathing is inad­
victim at the earliest, while being fully aware of per- equate, initiate bag-valve-mask ventilation.
sonal safety.
Plan early intubation using ICP pre­cautions, if airway
●● Routine spinal stabilization is not recommended, un- is unprotected, respiratory failure, cardiogenic shock or
less spinal injury is suspected.10 hypotension is identified.
History of diving, use of water slide, signs of in­jury
or alcohol intoxication suggest the need for spinal im-
Circulation
mobilization.
Ù
Plan smaller aliquots of NS (5–10 mL/kg).
Provide Cardiopulmonary Resuscitation
Treatment should be based on the guidelines provided by ●● Due to the risk of pulmonary edema secondary to acute
the pediatric advanced life support (PALS) and the ad- lung injury or myocardial dysfunction, avoid adminis-
vanced cardiac life support (ACLS) algorithms.9 tering more than 20 mL/kg.
●● At any point during bolus therapy, if signs of pulmo­
Ù
Attempts to remove water from the air passages by
nary edema develop or worsen, initiate an appropriate
inotropic agent and plan intubation.
abdominal thrusts or Heimlich maneuver are potentially
dangerous and are contraindicated.11,12 Ù
If shock persists after intubation, AVOID further
fluids unless history is suggestive of hypovolemia.
CASE SCENARIO 1 Occasionally, torrential bleeding from a scalp injury
can lead to hypovolemic shock.
1-year-old infant, was found unresponsive after acci-
dentally falling into a bucket of water (Figure 30.2).
Disability
●● Treat GTC seizures, if identified.
●● Eye signs of non-convulsive status epilepticus if noted,
suggest severe shock or hypoxia. Treatment should be
targeted towards early intubation and shock cor­rection.
If eye signs persist, the SE protocol may be implement-
ed cautiously.
●● Take ICP precautions when intubating a drowning vic-
tim. Drowning victims have features of hypoxic isch-
emic encephalopathy.13
A secondary survey, is performed for other injuries
such as head trauma, abrasions, lacerations or contusions.
Submersion in a bathtub should raise a suspicion of
child abuse. Teenage drowning is frequently associated
Figure 30.2 Physiological status: Stridor with respiratory with illicit drug or alcohol abuse14 and appropriate toxicol­
distress, pulmonary edema and shock. ogy tests may be warranted.
ChapterRapid
Chapter 3 n Modified 30 n Submersion Injury
Sequence Intubation 301 301

●● All victims of submersion should be observed for at 2. Karch SB. Pathology of lung in near-drowning. Am J
least 4–6 hours even if they do appear hemodynami- Emerg Med. 1986;4:4.
cally stable on arrival. 3. Karpovich PV. Water in the lungs of drowned animals.
IP : 196.52.84.10 Arch Pathol Lab Med. 1933;15:828.
●● Electrocardiography (ECG) and blood gas determina­
tion should be performed as soon as possible. 4. Idris AH, Berg RA, Bierens J, et al. Recommended
●● Victims with respiratory and other organ dysfunction guidelines for uniform reporting of data from drowning:
the “Utstein style” Resuscitation. 2003;59:45-57.
symptoms, decreased oxygen saturation and altered
5. Hoff BH. Multisystem failure: a review with special
sensorium, require monitoring in the intensive care
reference to drowning. Crit Care Med. 1979;7:310.
unit (ICU).
6. Karch SB. Pathology of heart in near-drowning. Am J
Severe bradycardia and intense vasoconstriction as­ Emerg Med. 1985;109:76.
sociated with marked hypothermia may make victims 7. Lunt DW, Rose AG. Pathology of human heart in drowning.
appear dead, but resuscitative attempts should not be Arch Pathol Lab Med. 1987;111:939.
abandoned.13,15,16 8. American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. IV-133-135. Part 10.3: Drowning.
Key Points
ü
1. Prevention can reduce the incidence of drowning.17
Circulation. 2005;112:24.
9. Watson RS, Cummings P, Quan L, et al. Cervical spine
2. Immediate and appropriate bystander CPR and injuries among submersion injury. Pediatrics.1994;94:137-42.
early basic life support (BLS) care can improve 10. Rosen P, Stoto M, Harley J. The use of the Heimlich
survival.19,20 maneuver in near drowning. Institute of Medicine Report.
3. Improved outcomes, if rescue breathing is provided J Emerg Med. 1995;13:397-405.
even before the victim is pulled out of water. 11. Sarnaik AP, Preston G, Lieh-Lai M, et al. Intracranial
4. Routine cervical spine stabilization is not pressure and cerebral perfusion pressure in near-drowning.
Crit Care Med. 1985;13:224.
necessary.
12. Howland J, Hingson R. Alcohol as a risk factor for
drowning A review of literature (1950-1985). Accid Anal
common errors
û
1. Attempts to remove water from the air passages
Prev. 1988;20:19.
13. Kyriacou DN, Arcinue EL, Peek C, et al. Effect of
immediate resuscitation on children with submersion
by abdominal thrusts or Heimlich maneuver are injury. Pediatrics. 1994;94:137-42.
potentially dangerous and are contraindicated. 14. Siebke H, Rod T, Breivik H, et al. Survival after 40
2. Failure to provide oxygen with a flow inflating minutes; submersion without cerebral sequeae. Lancet.
ventilation device. 1975;1(7919)1275-77.
3. Failure to recognize that respiratory distress could 15. Southwick FS, Dalglish PH Jr. Recovery after prolonged
be due to cardiogenic or non-cardiogenic pulmonary asystolic cardiac arrest in profound hypothermia. A case
edema. report and literature review. JAMA. 1980;243:1250-53.
16. Thompson DC, Rivara FP. Pool fencing for preventing
drowning in children. Cochrane Database Syst Rev
REFERENCES 2000;(2):CD001047.
1. Rowe MI, Arango A, Allington G. Profile of pediatric 17. Quan L, Wentz KR, Gore EJ, et al. Outcome and predictors
drowning victims in a water-oriented society. J Trauma. of pediatric submersion victims receiving prehospital care
1977;17:587. in King County, Washington. Pediatrics. 1990;86:586-93.
Section XI
IP : 196.52.84.10

Special Topics
IP : 196.52.84.10
31
IP : 196.52.84.10

Gastrointestinal Bleeding

Figure 31.1: Spectrum of gastrointestinal bleeding (Courtesy: Dr Thangavelu S, Dr Gunda Srinivas)

Learning Objectives
1. Approach to gastrointestinal bleed. 3. Evidence-based approach to therapeutic
2. Cases illustrating common presentations interventions.
of gastrointestinal bleeds.

Introduction acute rheumatic fever for which he had been pre-


scribed aspirin (Figure 31.2).
Approach to gastrointestinal (GI) bleeding in children var-
ies based on etiology, age and site of bleeding1-5 (Figure
31.1).
Ù
Identify whether bleeding is localized or systemic.

History of retching and vomiting suggest Mallory-Weiss


syndrome. NSAIDS intake point towards drug-induced
gastritis. Stigmata of liver disease are clues to diagnose
portal hypertension. Fever, sepsis or capillary leak suggest
severe sepsis or Dengue. Presence of hepato splenomega­
ly, lymphadenopathy and mucosal bleeds are indicative of
malignancies.

Figure 31.2 Physiological status: Airway stable/Tachypnea/


Case Scenario 1 Tachycardia with shock (no features of myocardial dysfunction or
A 7-year-old male child with hematemesis is rushed pulmonary edema). GI bleed due to drug-induced gastritis.
into the ED. He had been recently diagnosed ashaving
306 Section XI n Special Topics

APPROACH TO GI BLEEDING IN THE ED ●● Ranitidine: IV—1 mg/kg/dose (max 50 mg) 6–8 hourly
Oral 2–4 mg/kg/dose (max 150 mg) 8–12 hourly.
Airway and Breathing ●● Omeprazole: IV— 2 mg/kg/dose (max 80 mg) stat for-
IP : 196.52.84.10
●● Provide supplemental oxygen us­ing non-rebreath- ward by 1 mg/kg (max 40 mg) 8–12 hourly.
ing mask. Oral: < 3 year: 10 mg 12 hourly, > 3 years: 20 mg 12
●● Insert nasogastric tube. hourly. Sucralfate: 500 mg 6 hourly.
●● Plan to intubate if airway is compromised. Sucralfate:
●● 1 month–2 years: 250 mg Q 4–6 hourly.
Circulation
●● 2–12 years: 500 mg Q 4–6 hourly.
Simultaneously secure 2 vascular lines, col­lect blood for ●● 12–15 years: 1 g Q 4–6 hourly.
grouping and cross matching, Hb, CBC, co­agulation pro- ●● Somatostatin and octreotide are not routinely recom-
file and LFT. mended for patients with acute ulcer bleeding7.
●● Perform the rapid cardiopulmonary ce­rebral assessment. ●● Order chest X-ray (CXR), ultrasonogram.
●● Connect pulse oximeter and cardiac monitors. ●● Request for an emergency endoscopy after stabilization.
●● Infuse first bolus of RL/NS (20 mL/kg). Continue fluid
bolus until therapeutic goals of shock are resolved. Case Scenario 2
●● Establish etiology by careful history, physical exami- A 4-year-old girl with fever for 5 days has been afe-
nation (in this child, look carefully for signs of cardiac brile since morning. She has vomited several times and
failure, infective endocarditis). Monitor carefully for the last 2 episodes were coffee ground in color. She has
signs of pulmonary edema and myocardial dysfunction been complaining of severe abdominal pain. While she
secondary to fluid therapy since this child has RHD. was being transferred she had become lethargic.
●● Catheterize and monitor urine output.
●● Monitor hematocrit every 2–3 hour, until bleeding stops
and later 4–6 hourly (maintain hematocrit at 30%).
●● Arrange for blood transfusion if hemoglobin (Hb) <
7–8 g/dL.
●● If 1 unit of blood is needed every 2 hours, massive
transfusion protocol is implemented to avoid coagu-
lopathies.
Ù
Massive transfusion protocol
• For every 3 units of RBC, 2 units of FFP are trans­
fused.
• For every 5 units of RBC, 1 unit of platelets is
trans­fused. Figure 31.3 Physiological status: Airway maintainable,
• Goal of blood transfusion: HCT of 21–24 or Hb effortless tachypnea/shock/altered mental status (probable
of 7–8 g/dL. etiology: severe dengue).
• Transfuse whole blood based on the presence of
continued bleed. Once bleeding stops, transfuse Resuscitation and specific management (See Chapter on
packed cells. Dengue) (Figure 31.3).

Pharmacologic Management of Case Scenario 3


Drug-Induced Gastritis6 A 10-year-old boy was rushed to the ED with com-
●● Omit offending drug. plaints of two episodes of hematemesis and one episode
●● Antacids: 0.5 mL/kg (Not to exceed 30 mL/dose) every of black tarry stools. His mother denied history of fe-
1–2 hours. ver or drug intake. He had been apparently normal
Chapter 31 n Gastrointestinal Bleeding 307

till date, except for admission in the newborn period Gastric Lavage
for jaundice. He had received an exchange transfusion
during his stay in the IP
NICU (Figure 31.4). Use normal saline (room temperature) if needed. Chilled
: 196.52.84.10 or ‘iced’ saline does not stop bleeding and may cause cen-
tral hypo­thermia, particularly in young infants.

Pharmacologic Management of
Portal Hypertension
Pharmacologic therapy10 to decrease portal pressure may
be considered in patients with continued bleeding.
Vasopressin and its analogues act by increas­ing
splanchnic vascular tone thereby decreasing portal blood
flow.
1. Terlipressin:11
Dose: Administer 0.04 mg/kg IV (bolus) followed by
Figure 31.4 Physiological status: Airway stable/Tachypnea/ 0.02-0.04 mg/kg, every 4–6 hours till a bleeding free
Tachy­cardia with hypotensive shock. (probable etiology: ex­tra
interval of 24–72 hours is achieved.
hepatic portal hypertension with variceal bleed8).
It is less cardiotoxic than vasopressin and is the
●● Take care of the ABCs. drug of choice in variceal bleed. It is more effective
●● CBC, Hb, grouping, cross matching, Dengue serology, than endoscopic injection sclero­therapy (EIS), safer
electrolytes, sugar, urea and creatinine. than vasopressin in combination with nitroglycerin
●● Coagulation profile: and EIS. It also improves survival. However, continu-
– Elevated PT indicates coagulopathy (i.e. dissemi- ous infusion can cause necrosis.
nated intravascular coagulation) or profound impair- 2. Octreotide11,12 (Synthetic analogue of somatostatin)
ment of liver synthetic function. Dose: Loading dose of 1 μg/kg IV over 30 minutes,
– Prolonged aPTT indicates hemophilia or coagulopathy. followed by 0.5 μg/kg/h. Its high cost, propensity to
●● Order LFT. cause nausea, flatulence, malabsorption and bowel
– Increased aspartate aminotransferase and alanine ischemia should be taken to consideration.
aminotransferase enzyme levels are suggestive of 3. Vasopressin11
portal hypertension with liver disease.
Dose: 6 U/kg in 50 mL at 1-5 mL/h. The drug has a
half-life of approximately 30 minutes (Va­sopressin 1
Fluid Therapy mL = 20U).
In most children with extrahepatic portal hypertension and Its use is limited by side effects such as vasoconstric­
normal hepatic synthetic function, bleeding stops sponta- tion, impairment of cardiac function and perfusion
neously.9 to the heart, bowel and kidneys. It also exacerbates
Caution: Aggressive fluid resuscitation can increase risk of fluid retention.
rebleed due to high venous pressure.
Endoscopy
Introduce a Nasogastric Tube ●● The site of upper GI bleeding can be identified in
90% of cases, when endoscopy is performed within
Placement of a nasogastric tube (NGT) helps to remove 24 hours. Emergency sclerotherapy can also be per-
blood from the stomach. It prevents development of en- formed if needed. However, it should be undertaken
cephalopathy in cirrhosis and also helps to monitor recur- after correction of coagulation disorders and hemody-
rence of bleed. namic instability.
308 Section XI n Special Topics

●● Endoscopic variceal ligation is currently considered a ●● Order cryoprecipitate if plasma fibrinogen is less than
superior option to endoscopic sclerosis since, compli- 1 g/L, although there is no clear threshold for clinically
cations are rarer with the former modality. significant hypofibrinogenemia.
IP : 196.52.84.10
●● In patients who continue to bleed despite pharmacologic ●● Uncontrolled massive bleeding, unresponsive to con-
and endoscopic methods to control hemorrhage, a Seng- ventional blood component therapy: Consider rFVIIa,
staken-Blake more tube may be placed to stop hemorrhage (dose: 100 μg/kg). A repeat dose may be given after an
by mechanically compressing esophageal and gastric va- interval of 30 minutes to 1 hour. The same dose may be
rices (mechanical tamponade). It poses a particularly high repeated at an interval of 1–4 hours until cessation of
risk for pulmonary aspiration and the tube is not well tol- bleeding has been achieved.14
erated in children without significant sedation. ●● Simultaneously treat underlying cause.
The etiological factors associated with upper gastroin­
Surgical Procedures that Divert Portal Blood testinal bleeding vary with age.15,16
Flow and Decrease Portal Pressure
●● A transjugular intrahepatic portosystemic shunt (TIPS) Infancy–1 Year
is a method by which a stent is placed by an interven- 1. Esophagitis, gastritis.
tional radiologist between the right hepatic vein and the 2. Severe dengue (see Chapter on Dengue).
right or left branch of the portal vein. It aids providing 3. Stress ulcer: GI bleeds in infants admitted for burns,
temporary relief in children with portal hypertension. It sepsis, raised ICP, head injury, encephalitis and gas-
is particularly useful in children needing liver transplan- troesophageal reflux disease (GERD).
tation. However, the TIPS procedure may precipitate 4. Mallory-Weiss tear: Fresh bleed following repeated
hepatic encephalopathy and is prone to thrombosis. retching is suggestive of esophageal tear (Mallory-
●● Recent studies indicate that a combination of endo- Weiss syndrome).
scopic sclerotherapy with β-blockers is far superior 5. Vascular malformation.
than any other form of treatment for the prevention of 6. GIT duplication.
recurrence of UGI bleeding. 7. Malrotation.
Coagulopathy 1–12 Year
IV Vitamin K, cryoprecipitate, FFP, recombinant fac-
1. Severe dengue (see Chapter on dengue).
tor VIIa and platelet transfusions are some of the in-
2. Esophageal varices due to extrahepatic portal hyper-
terventions, which are useful in controlling bleeds due
tension or cirrhosis with portal hypertension.7
to coagulopathy secondary to hepatic dysfunction and
thrombocytopenia.13,14 a. Liver disease (hepatic cause for portal hyperten-
sion like cirrhosis).
●● Prolonged PT–INR is diagnostic of vitamin K defi- b. Neonatal umbilical sepsis or umbilical vein cath-
ciency. eterization (extrahepatic portal hypertension).
●● Administer vitamin K: 0.3 mg/kg IV over 1 hour (max 3. Esophagitis, gastritis, peptic ulcer disease.17 Recur-
10 mg). rent abdominal pain is suggestive of peptic ulcer.
●● Infuse 10 mL/kg of FFP.
4. Stress ulcer: Stress related GI bleed in critically ill
●● Administer Ranitidine (2 mg/kg/dose) intravenously to
children being managed in the ED.
reduce risk of bleeding from gastric erosions.
5. Mallory-Weiss tear (see above).
Disseminated Intravascular Coagulation 6. Drug intake: non-steroidal anti-inflammatory drugs
(NSAIDS) and steroids are the commonest drugs
The British Committee for Standards in Haematology, causing gastritis.
Blood Transfusion Task Force Guidelines for the use of 7. Bleeding tendency: DIC manifests as GI bleed, bleeds
fresh frozen plasma, cryoprecipitate and cryosupernatant- from IV site, skin, hemarthrosis, etc. in seriously ill
2004 suggest that fresh frozen plasma and platelets are in- children.
dicated when there are demonstrable multifactor deficien-
8. Family history of bleeding disorder: Von Willebrand’s
cies associated with severe bleeding and/or DIC.
disease, hemophilia.
Chapter 31 n Gastrointestinal Bleeding 309

9. Odynophagia with oral candidiasis is suggestive of for less than 24 hour. Barium study is contraindicated
candidal esophagitis ( HIV). if perforation is suspected. Air contrast enemas have
IP : 196.52.84.10 also been used with similar success rates, with air en-
Case Scenario 4 emas requiring less radiographic exposure, but having
slightly higher perforation rates. Enemas with saline
A 6 month infant is rushed to the ED with incessant
contrast require experienced sonographers.
cry accompanied by episodes of straining. He has
vomited his feeds and is passing blood and mucus Evaluate for other etiologies of lower GI bleed
along with stools (Figure 31.5).
1. Infants
●● Anal fissure—presents with constipation and pain-
ful defecation.
●● Intussusception.
●● Infective colitis—passing small quantities of blood
and mucus in the stool, crampy lower abdominal
pain and tenesmus.
●● Midgut volvulus.
●● Meckel’s diverticulum.
●● Vascular malformations.
●● Coagulation disorders.
2. Older children
●● Anal fissure: Pain during defecation with blood-
streaked stools.
●● Rectal prolapse: Associated with mass seen per
Figure 31.5 Physiological status: Airway stable/Tachypnea/
Tachycardia and shock (possible etiology: intussusception).
rectum.
●● Bacterial enteritis: Dysentry, fever and crampy low-
er abdominal pain.
Management ●● Polyps—painless rectal bleeding with a large amount
of bleed per rectum.
●● Provide O2 using a non-rebreathing mask.
●● Gangrenous bowel due to volvulus is character-
●● Introduce NGT.
ized by bilious vomiting, abdominal distension and
●● Secure two lines and administer RL (20 mL/kg) bo-
bleeding per rectum.
lus. Repeat cardiopulmonary cerebral assessment and
●● Meckel’s diverticulum: Intermittent, painless hema-
continue boluses until therapeutic goals of shock are tochezia.
resolved. ●● Vascular malformations: Painless, massive bleed.
●● Since, the etiology of shock is hypovolemia due to GI ●● Bleeding disorder: GI bleed will be associated with
loss up to 120 mL/kg may be needed in the initial hours bleeds from other sites.
of resuscitation. ●● Inflammatory bowel disease: Associated with chron-
●● Collect blood for grouping crossmatching, RFT, LFT, ic diarrhea and failure to thrive.
coagulation profile, CBC and sepsis screen.
Physical examination in acute GI bleed, which can sug-
●● Arrange for blood.
gest the etiology
●● X-ray abdomen can help identify intestinal obstruction
●● Request for color Doppler ultrasonography. It helps to ●● Examine ears, eyes, nose and throat: Look for epistaxis,
diagnose intussusception. nasal polyps and oropharyngeal erosions from caustics
●● Involve pediatric surgeon and radiologist urgently and other ingestions.
●● Order enema studies.18 ●● Look for abdominal surgical scars and elicit the indica-
Barium enema reduction have traditionally been used tion for surgery.
with success rates of 50% –90%. Rate of detection of ●● Abdominal tenderness with or without a mass, raises
intussusception is more when symptoms are present the suspicion of intussusception or ischemia.
310 Section XI n Special Topics

●● Hepatomegaly, splenomegaly, jaundice or caput medu- longer; the most common etiologies are juvenile colo-
sae suggests liver disease and subsequent portal hyper- rectal polyps and non-specific proctitis.
tension. IP : 196.52.84.10
●● Splenomegaly is suggestive of portal hypertension; but
following a massive bleed, the spleen may contract and
hence may be impalpable. (Smith-Howard syndrome).
Key Points
ü
1. Find out whether GI bleed is localized or systemic.
●● Inspect perianal area: Look for fissures, fistulas, skin 2. Identify whether the bleed is secondary to varices or
breakdown or evidence of trauma. clotting defects.
●● Look for evidence of child abuse, such as perianal tear- 3. Control bleed based on etiology.
ing, tags or irregularities in anal tone and contor. 4. Transfuse appropriately.
●● Specifically include bowel sound frequency in the ab- 5. Treat coagulation defects.
dominal examination. Hyperactive bowel sounds are
more common in upper GI bleeding.
●● Examine skin for evidence of systemic disorders, such
as inflammatory bowel disease: intermittent maculo-
common errors
û
1. Children with epistaxis or oropharyngeal bleeding
papular rash. or hemoptysis often vomit bright red blood.
●● Henoch-Schönlein purpura: palpable purpura in both 2. Failure to recognize intussusception leading to late
lower limbs and Peutz-Jeghers polyposis. referral to the surgeon.
●● Digital rectal exam should be performed in the OT 3. Delay in resuscitation in an effort to search for the
under sedation. It may reveal polyps, masses or oc- etiology.
cult blood.
References
Workup
1. Arain Z, Rossi TM. Gastrointestinal bleeding in children:
Laboratory Studies An overview of conditions requiring non-operative man-
agement. Semin Pediatr Surg. 1999; 8 (4):172-80.
●● Confirm presence of blood by requesting for perox- 2. Erlich F. Gastrointestinal bleeding. In:Fleisher GR, Lud-
ide based tests such as the hemoccult or hematest to wig S, (Eds). Synopsis of Pediatric Emergency Medicine.
identify lower GI bleeding and gastroccult for upper Baltimore: MD Lippincott Williams and Wikins; 1996. pp.
GI bleeding. 100-05.
●● Red meat, iron and peroxidase containing vegetables 3. Arora NK, Ganguly, S Mathur P, et al. A Upper gastroin-
testional bleeding: Etiology and Management. Ind JI Pedi-
(e.g. turnips, horseradish, broccoli, cauliflower and
atrics. 2002;69 (2):155-68
cantaloupe) can give false-positive results.
4. Berkowitz C. Gastrointestinal bleeding. In: Pedaitrics:
A Primary Care Approach. Philadelphia, PA: WB Saun-
Imaging Studies ders; 1996.
●● Meckel scan, using technetium-99m pertechnetate 5. Peters JM. Management of Gastrointestinal Bleeding in Chil-
helps to identify ectopic gastric mucosa. dren. Curr Treat Options Gastroenterol. 2002;5(5):399-413.
●● Push enteroscopy is a long endoscope that is placed 6. Thapa BR, Bansal D.Management of upper Gastrointes-
through the mouth into the jejunum. It can reach about tinal bleeding in children.Ind JI Practical Pediatrics. 200;
4:398-416.
160 cm beyond the ligament of Treitz. One study has
shown that push enteroscopy identified a large num- 7. Alan N Barkun, Marc Bardou, Ernst J, Kuipers, et al.
ber of mucosal lesions that could not be identified by a International Consensus Upper Gastrointestinal Bleed-
standard endoscope. ing Conference Group. International Consensus Rec-
ommendations on the Management of Patients With
●● Colonoscopy should be performed only when the pa-
Nonvariceal Upper Gastrointestinal Bleeding. Ann In-
tient is stable and when blood and feces will not con-
tern Med. 2010;152 (2):101-13.
ceal proper visualization.
●● Sigmoidoscopy19 is indicated in children who have 8. Molleston JP. Variceal bleeding in children. J Pediatr Gas-
troenterol Nutr. 2003;37(5):538-45.
symptoms of chronic lower GI bleeding for 1 year or
Chapter 31 n Gastrointestinal Bleeding 311

9. Comar Kevin M,Sanyal AJ. Portal hypertensive bleeding pediatric patients. Blood coagulation and Fibrinolysis.
Gastroentrol Clin North Am. 2003;32(4):1079-105. 2010;21:354-362.
10. Tatro DS, Borgsdorf 15. Huang CS. Lichtenstein DR. Non-variceal upper gastro-
IPLR, Lopez JR, et al. A to Z Drug
: 196.52.84.10 intestinal bleeding. Gastroentrol Clin North Am. 2003;32
facts. 5th edition. St Louis,MO: Facts and Comparisons;
2005. (4):1053-78.
16. Fox VL. Gastrointestinal bleeding in infancy and child-
11. Frank Shann. Drug Doses; 15th edition, Victoria Austrail-
hood. Gastroentrol Clin North Am. 2000;29(1):37-66.
ia. 2010.
17. Johnson D, L’Heureux P, Thompson T. Peptic ulcer disease
12. Ioannou GN, Doust J, Rockey DC. Systematic review: Ter- in early infancy: Clinical presentation and roentgenograph-
lipressin in acute oesophageal variceal haemorrhage. Ali- ic features. Acta Paediatr Scand. 1980;69(6):753-60.
ment Pharmacol Ther. 2003;17(1):53–64. 18. Henikson S, Blane CE, Koujok K, et al. The effect of
13. E Mileti, P Rosenthal. Management of Portal Hyperten- screening sonography on the positive rate of Enemas for
sion in Children. Curr Gastroenterol Rep (2011); 13(1):10– intussusception. Pediatr Radiol. 2003;33(3):190-93.
16 DOI 10.1007/s11894-010-0151-y.” 19. Mandhan P. Sigmoidoscopy in children with chronic
14. Ampaiwan C, et al. Recombinant-activated factor VII for lower gastrointestinal bleeding. J Paediatr Child Health.
control and prevention of hemorrhage in non-hemophilic 2004;40(7):365-68.
Interpretation of Chest X-rays in
32
IP : 196.52.84.10

Critically Ill Children

Figure 32.1: Interpretation of X-rays in critically ill children is a skill adjunct to clinical acumen and guide therapeutic decisions
(Courtesy: Dr Thangavelu S, Dr Gunda Srinivas)

Learning Objectives
1. Systematic approach to reading an chest X-ray 3. Pearls and pitfalls in interpretation of chest radio­
(CXR) in the ED. graphs.
2. Case scenarios illustrating various respiratory
emergencies.

On most occasions, the first responder in the ED who 4. Date and time of taking the X-ray.
is confronted with the need to take life saving decisions 5. Whether right and left side have been documented
based on a chest X-ray is also the least experienced. This correctly.
chapter teaches a structured approach to the interpretation 6. Whether, the X-ray was taken in the anteroposterior
of a chest radiograph in emergency settings (Figure 32.1). or posteroanterior view.
●● The physician who ordered the chest X-ray must see
the film within 5–10 minutes.
Ù
Anteroposterior view:
●● Occasionally, even a delay of 5 minutes would be le- a. A notch in the middle of the clavicle.
thal in scenarios such as pneumothorax, or a displaced b. Lung tissue not seen above the clavicle.
endotracheal tube. In these situations, rapid clinical Posteroanterior view:
assessment and intervention is life saving rather than a. Clavicle will appear straight.
waiting for chest film interpretation. b. Lung tissue will be seen above the clavicle.

Stepwise assessment 7. Whether the film has been centered or rotated.

General Data: Check Ù


Symmetry of both medial ends of clavicle indicate that
1. Name. the CXR is not rotated.
2. Age.
3. Gender. 8. Phase of respiration in which the X-ray is taken.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 313

Ù
The middle of the diaphragm should correspond to the
IP : 196.52.84.10
anterior end of 5th to the 7th ribs. Anterior end stops short
and the posterior end joins the vertebral column.

Figure 32.3: Normal CXR of an infant showing normal thymus


(sail-shaped).

9. In a well-penetrated chest film, the vertebral bodies


and intervertebral discs will be noticeable (but not
very clear) behind the heart. In an under-penetrated
Figure 32.2A: Normal AP view film, the lungs will be diffusely white and the verte-
bral bodies will not be visible.
10. In the over-penetrated film, the lungs are diffusely
dark with poorly differentiated lung markings and the
vertebral bodies will be seen very clearly.

Specific Data
1. Tubes: endotracheal tube, tracheostomy tube, chest
tube or rarely pig tail catheter left in pericardial cavity.
2. Lines: external jugular (EJV), internal jugular (IJV),
subclavian lines, PORT-A-CATH (subcutaneously
implantable venous access system) or tunneled lines.
3. Above the diaphragm.
Scan from periphery to center.
– Soft tissue.
Figure 32.2B: Normal PA view – Chest wall.
– Costophrenic angle.
Normal X-ray: In the AP view, there will be a notch in
the middle of the clavicle (Figure 32.2A). No lung tissue – Mediastinum and normal thymus (Figure 32.3).
will be seen above clavicle. When the X-ray is taken in – Cardiophrenic angle.
the inspiratory phase, the anterior end of the 5th rib cor- – Lung tissue.
responds to middle of the dome of diaphragm (marked by – Heart.
horizontal arrow in Figure 32. 2B) (the posterior end of rib 4. Below the diaphragm.
is marked by the vertical arrow). The two vertical yellow – Look for air under the diaphragm
lines indicate the medial end of clavicle and lateral margin – Air fluid levels suggestive of intestinal obstruction.
of vertebrae. If the lines are equidistant on both sides of the – Bowel shadows crowded in the center is indica-
vertebra, it implies that the film has been centered without
tive of ascites.
rotation.
314 Section XI n Special Topics

Lung Parenchyma Air Bronchogram


Compare both hemithoraces. These are luminal, linear branching gas shadows in the
IP : 196.52.84.10 background of parenchymal opacities such as pneumonia,
●● Size of the hemithorax.
collapse and ARDS. Air bronchograms are not seen in the
●● Color or lucency. presence of pleural fluid or pulmonary edema.
– Black shadows and air bronchogram.
●● Costophrenic angle: intact or obliterated.
●● Mediastinal shift.
Costophrenic Angle
Obliteration of costophrenic angle suggests presence of
Size of Hemithorax pleural fluid.
a. Increase in size of hemithorax compared with the oppo-
site side may be due to pneumothorax or emphysema. Mediastinal Shift
b. Decrease in size, may be due to collapse or fibrosis.
a. Shift to the same side occurs in collapse or fibrosis.
b. Shift to the opposite side occurs in pleural effusion or
Compare the Color and Lucency pneumothorax.
a. Darker hemithorax indicates presence of abnormal air
(pneumothorax or emphysema). Ù
b. Opacity indicates any one of the causes mentioned in Note: Usually one finger breadth or 1/4th of the heart
Table 32.1. shadow will be seen on the right side.
Table 32.1: Types of opacity and its diagnosis

Type of opacity Diagnosis


Heart
Linear and branching Normal bronchovascular Cardiomegaly
markings
a. Cardiothoracic ratio > 0.6.
Patchy Bronchopneumonia or
b. Normal shaped heart.
subsegmental collapse
c. Acute cardiophrenic angle.
Homogeneous Consolidation
d. Pulmonary plethora.
Presence of air bronchogram Consolidation
Absence of air bronchogram Pleural fluid or tumor Pericardial Effusion
Bilateral ARDS, pulmonary edema,
a. Loss of normal shape of the heart.
extensive bronchopneumonia
b. Obtuse cardiophrenic angle.
Lung volume decreased Collapse or fibrosis
c. Absence of pulmonary plethora.
Uniform density, costophrenic Pleural fluid
angle lost
Varying density, air Pneumonia Tubes and Lines
bronchogram
Tubes and lines are important artificial structures to be
Uniform density, decreased Collapse identified in addition to the natural structures in a critically
volume, mediastinal shift,
ill child. Tubes introduced for various purposes can be the
rapid change
cause of many life-threatening complications in critically
Triangular, uniform density Segmental collapse ill children. Check for position of the endotracheal tube,
tracheostomy tube, chest tube or rarely pig tail catheter
Black Shadows within the pericardial cavity.
Normal appearance of the lung is gray color interspersed Lines may have been inserted into the external jugular,
with bronchovascular markings. Presence of air will make internal jugular or subclavian veins. Check for placement
it darker than normal. and position.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 315

Interpretation of CXR with Case scenario 2 (Figure 32.5)


case scenarios This child with DSS, was referred after fluid therapy.
IP : 196.52.84.10
Case scenario 1 (Figure 32.4)
A 3-week-old infant brought for cough and fever.

Figure 32.5

Your Observations
Figure 32.4

Your Observations

Diagnosis: Normal lung fields. Fracture clavicle with cal-


lus formation.
Though, this CXR shows no evidence to support the
history of a respiratory infection, verification of the chest
wall for soft tissue and bones reveals fracture clavicle with
callus formation . The 3 bones that can be evaluated in a
CXR are clavicle, ribs and humerus.
Finding: Fracture clavicle with callus formation.
The clavicle, ribs and humerus also help in recognizing im-
portant bone disorders.
●● Absent clavicle is characteristic of cleidocranial dys-
ostosis.
●● Widening of the anterior ends of ribs, cupping and fray-
ing of the upper end of humerus are features of vitamin
D deficiency. This is particularly useful when a child Finding: Chest wall edema probably due to capillary leak
presents with seizures. due to volume overload in dengue shock syndrome.
316 Section XI n Special Topics

Case scenario 3 (Figure 32.6) Case scenario 4 (Figures 32.7A and B)


History of fever and respiratory distress for 3 days. A 7-year-old girl, presents with fever, respiratory dis-
IP : 196.52.84.10 tress and oral thrush.

Figure 32.6
Figure 32.7A: Oral thrush
Your Observations

Figure 32.7B
CXR: Bilateral extensive opacities.
Diagnosis: This picture can occur in three conditions.
●● Extensive bronchopneumonia.
●● ARDS.
●● Pulmonary edema.
Diagnosis is made based on clinical findings. Picture
shows oral thrush, hence the diagnosis is extensive broncho-
pneumonia with probable immune deficiency. Radiographs,
Both hemithoraces are of the same size. The opacity is ho-
such as the one above, can reveal opacities in the lung. How-
mogeneous with no mediastinal shift.
ever, it cannot pin-point etiology. As in this case, the diagno-
Diagnosis: Consolidation. sis becomes apparent only from clinical history.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 317

Case scenario 5 (Figure 32.8) Case scenario 6 (Figure 32.9)


A 2-year-old boy presented with fever and respiratory A 3-year-old child presented to emergency 1 hour after
distress for 3 days. He IP
had: been
196.52.84.10
grunting since morning. consumption of kerosene. She was in respiratory fail-
ure and hypotensive. She needed urgent intubation and
ventilation in the ED.

Figure 32.8

Your Observations
Figure 32.9

Your Observations

Homogeneous density on the whole of left side with no


air bronchogram. Costophrenic angle is obliterated. Medi-
astinal shift is absent. In acute collection of fluid, mediasti-
nal shift may be absent. CXR: Completely whitened lung.

Diagnosis: Left-sided pleural fluid. Diagnosis: ARDS.


318 Section XI n Special Topics

Case scenario 7 (Figures 32.10A and B) Case scenario 8 (Figures 32.11A to C)


A 6-year-old girl presented with severe respiratory dis- A 2-year-old child presents with brief history of fever
IP : 196.52.84.10
tress, 8 hours after scorpion sting. She developed ven- and breathlessness.
tricular tachycardia followed by fibrillation and could
not be revived. The ET tube was flooded with pink,
frothy secretions due to pulmonary edema.

Figure 32.11A
Figure 32.10A: Froth oozing out from ET tube due to
pulmonary edema
Your Observations

Patchy opacity on the right side with pneumatocele.


Note the air bronchogram.

Figure 32.10B: The bilateral butterfly-shaped opacities is


sugges­tive of pulmonary edema

Your Observations
Figure 32.11B

Your Observations
Presence of bilateral hilar opacities, in the background of
scorpion sting confirm the diagnosis as pulmonary edema.
But this classical picture may not be seen in all situations. Since the child developed respiratory failure, she was
ventilated. The pneumatocele increased in size.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 319

Case scenario 9 (Figure 32.12)


A 5-year-old child admitted for breathlessness.
IP : 196.52.84.10

Figure 32.11C

Your Observations
Figure 32.12

Your Observations

Note the homogeneous opacity on the right, oblitera-


The right hemithorax is larger than the left. It is more tion of the costophrenic angle and mediastinal shift to the
lucent without vascular markings and the mediastinum has opposite side. A chest tube was introduced after suspecting
shifted to the left suggesting the presence of a right-sided empyema. Since there was no relief, the possibility of tu-
pneumothorax. mor was considered. CT revealed a mediastinal tumor.
320 Section XI n Special Topics

Case scenario 10 (Figure 32.13) Case scenario 11 (Figures 32.14A and B)


Following measles, a 7-year-old boy developed high- A toddler was rushed into the ED for sudden onset of
IP : 196.52.84.10
grade fever and breathlessness. breathlessness. His elder brother, who was playing near
by was eating peanuts. Breath sounds were diminished
on the left side.

Figure 32.13
Homogeneous opacity in the right base with obliteration
of the costophrenic and cardiophrenic angles. Presence of air
fluid level on the right side suggests the diagnosis of pyo- Figure 32.14A
pneumothorax. Mediastinal shift is not apparent, probably The left hemithorax appears bigger and has greater
due to the thoracostomy. Note the presence of the chest tube. radiolucency (appears more black) compared to the right.
In the background of measles and respiratory distress, Presence of bronchovascular markings and absence of col-
one may anticipate pneumonia or empyema. Training one’s lapsed lung margins favor the diagnosis of obstructive em-
eyes to see what is expected in the clinical backdrop can physema on the left side.
often clinch the diagnosis (Table 32.2).
Table 32.2: X-ray clues to diagnosis

Description Diagnosis
Circular air collection in the Pneumatocele
background of white opacities
Bigger and darker hemithorax Obstructive/compensatory
with bronchovascular emphysema (here opposite
markings lung will be abnormal)
Confined to one lobe with Congenital lobar emphysema
herniation to opposite side
and collapse of the adjacent
lobe
Bigger and darker hemithorax, Pneumothorax
no bronchovascular markings,
collapsed lung margins are
seen Figure 32.14B
Continuous diaphragm sign, Pneumomediastinum This chest X-rays of a different child with similar his-
lifting of the thymic shadow
tory shows similar findings though very subtle.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 321

Case scenario 12 (Figures 32.15A and B) Case scenario 13 (Figures 32.16A to D)


A young infant presented with breathlessness of 1 History of aspiration of a nail.
month duration. IP : 196.52.84.10

Figure 32.16A
Figure 32.15A

Figure 32.16B
Figure 32.15 B
Your Observations
Your Observations

The volume of the left lung is more than the right (em-
physematous). The left lower lobe is collapsed with a sharp
margin with herniation of the upper lobe to the right side.
Note the mediastinal shift to the right. The bronchovascu-
Nail in the right lower lobe with segmental collapse of
lar markings in the emphysematous left lung differentiates
the lower lobe.
it from a pneumothorax.
Bronchoscopic removal failed and child developed
Diagnosis: Congenital lobar emphysema of the left upper lobe.
pneumothorax.
322 Section XI n Special Topics

Case scenario 14 (Figure 32.17)


A 3-day-old neonate was referred to the ED with
IP : 196.52.84.10 breathlessness, cyanosis, dextrocardia and a scaphoid
abdomen.

Figure 32.16C
Chest tube was inserted and pneumothorax drained.

Figure 32.17

Your Observations

Figure 32.16D Compare the size, lucency, color, CP angles of both the
hemithoraces. Then look at the mediastinum.
Your Observations Size: The left sided hemithorax appears larger than the
right side.
Color or lucency: Left hemithorax is filled with cyst like
structures (bowel shadows).
Costophrenic (CP) angle: The CP angle on the right is
free, but obliterated on the left.
Mediastinal shift: The mediastinum is shifted to the right.
Other findings: Absence of abdominal gas shadows. The
diaphragm is not visible. Note presence of umbilical artery
and umbilical vein catheters.
Nail removed and pneumothorax resolved. Normal X-ray. Diagnosis: Diaphragmatic hernia.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 323

Case scenario 15 (Figure 32.18) Case scenario 16 (Figure 32.19)


A 6-month-old presented with cough, fever and respi- Another 8 month infant presented with the history of
IP duration.
ratory distress of 4 days : 196.52.84.10 cough, fever and acute onset breathlessness.

Figure 32.18
Figure 32.19

Your Observations
Your Observations

There is less lung volume on the right than the left. A


homogeneous opacity is also seen on the right upper lobe.
It has a sharp margin suggesting the presence of right up-
per lobe segmental collapse.

Reminder
When evaluating lung fields, four aspects need to be
compared. Both hemithoracis have similar volume. There is no
significant mediastinal shift.
●● Volume of hemithorax.
●● Color or lucency. A homogeneous triangular opacity is seen on both sides
●● Costophrenic angles. with sharp margins suggesting the diagnosis of bilateral
●● Mediastinal shift. lower lobe segmental collapse.
324 Section XI n Special Topics

Case scenario 17 (Figure 32.20) Case scenario 18 (Figures 32.21A and B)


A 5-year-old child with history of recurrent wheezing, A 3-year-old child had been intubated in a peripheral
IP : 196.52.84.10
presented with distressing cough and breathlessness. hospital for respiratory failure. On arrival, his air-en-
try was reduced on the left and his SpO2 was 88%.

Figure 32.20
Figure 32.21A
Your Observations
Your Observations

The endotracheal tube has slipped into the right main


bronchus resulting in the collapse of the left lung. The tip
1. Usually the cardiac silhouette and the thymic silhou- of the ET is almost at the level of T5 vertebra. Normally,
ette are merged and seen as single cardiothymic shad- it should be positioned at the level of T2-T3.
ow. In this CXR the thymic shadow is separated from
1. The volume of the left lung is less than the right lung.
cardiac shadow (see the upward arrows).
The ribs on the left side appear to be crowded in com-
2. The shadow of diaphragmatic domes also merge with
parison to the right. There is a homogeneous opacity
the cardiac shadow. Here, in this picture, a dark line
of the left side with mediastinal shift.
of air separates the diaphragm from the lower border
2. The left costophrenic angle appears to be obliterated.
of the heart. ‘Continuous diaphragm sign’ (double
headed horizontal arrow): Also has subcutaneous em- The tube was repositioned and fixed. Air-entry im-
physema on the right side. proved on both sides and SpO2 normalized. Repeat CXR
Both signs are diagnostic of pneumomediastinum. after repositioning of ETT.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 325

Case scenario 19 (Figure 32.22)


A 5-year-old boy was intubated following submersion
IP : 196.52.84.10 injury and referred to the PED.
He suddenly desaturated, developed hypotension and
bradycardia.
Consider ‘DOPE’
Air-entry on both sides were equal confirming the tube
position. No air was heard over the epigastric region. Suc-
tioning the tube yielded nothing ruling out obstruction.
Equipment failure was ruled out. The last possibility was
pneumothorax. A bed X-ray taken just prior to needle tho-
racocentesis showed the following.

Figure 32.21B

Your Observations

Figure 32.22

Reminder
●● Displacement: Clinical finding that is diagnostic is the
absence of breath sounds on the left side.
●● The radiograph will show collapse of the left lung.
●● Obstruction: Is characterized by resistance, while
ventilating with bag. The radiograph will not show
any change.
●● Pneumothorax is characterized by absent breath sounds
with resonance on percussion on the side of the pathol-
ogy viz pneumothorax.
Repeat CXR after repositioning of ETT. ●● The right hemithorax is bigger and darker than the left.
● ● No bronchovascular markings are seen on the
●● The left lung has expanded. The volume of both lung right side.
fields are normal. The mediastinum is in the midline. ●● Also note the collapsed lung on the right side.
●● There is minimal pleural fluid on the left side. Diagnosis: Right-sided pneumothorax.
●● The ET is now at T4. Still needs to be pulled out.
326 Section XI n Special Topics

Case scenario 20 (Figures 32.23A and B) Case scenario 21 (Figures 32.24A and B)
A 12-year-girl presented with history of fever, hemopt- A 4-year-old boy presented with failure to thrive, breath-
ysis and expectorationIPof:foul
196.52.84.10
smelling yellow sputum. lessness and oxygen dependency since infancy. Two sib-
lings had died earlier with similar history. This child
developed respiratory failure requiring ventilation.

Figure 32.23A

Figure 32.24A

Figure 32.23B

Your Observations

Figure 32.24B
The 2nd chest radiograph shows the development of a
small pocket of air in the right upper and lower zone.
Compare the contour of the diaphragm on both sides.
On the side of the pneumothorax the usual contour is lost.
1. Homogeneous opacity with air fluid level in the right a. The reticulogranular pattern of opacity on both side
lower lobe. suggests the diagnosis of interstitial pneumonia.
2. Also has scoliosis. CT chest confirms lung abscess b. This CXR shows pneumothorax that occurred during
with air fluid level. mechanical ventilation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 327

Case scenario 22 (Figure 32.25) Case scenario 23 (Figure 32.26)


This child presented with respiratory distress. He had A 2-year-old girl presented with respiratory distress
IP : 196.52.84.10
diminished breath sounds on the left side. since birth. She had tachycardia, gallop and hepato-
megaly.

Figure 32.25
Figure 32.26
Your Observations
Your Observations

1. The left hemithorax is smaller since the left dome of


diaphragm is at a higher level than the right.
2. The mediastinum is shifted to the right. 1. Cardiothoracic ratio is > 0.6 (increased).
3. The fundus of the stomach lies just below the left 2. Cardiophrenic angle is acute.
dome of diaphragm (gastric bubble is always below 3. Pulmonary congestion suggestive of pulmonary
the diaphragm). edema.
Diagnosis: Eventration of diaphragm. Diagnosis: Cardiomegaly.
328 Section XI n Special Topics

Case scenario 24 (Figures 32.27A and B)


A 14-month-old infant presented with fever, breathless-
IP : 196.52.84.10
ness, tachycardia, hepatomegaly and seizures.

Figure 32.27B

Your Observations
Figure 32.27A

Your Observations

Wrist X-ray shows classical features of rickets.

1. The cardiothoracic ratio is greater than 0.6 is In lead poisoning, a dense band will be noted in the
suggestive of cardiomegaly. metaphyseal end (lead deposits).
2. The associ­ated pulmonary plethora is diagnostic of The ECHO of this child revealed a low ejection frac­
congestive cardiac failure. tion without evidence of anatomical abnormalities. Serum
3. The upper end of humerus, shows cupping, fraying of ionized calcium was 0.7 (low). Serum 25-hydroxyvitamin
metaphyseal ends and widening of physis suggestive D level was low.
of rickets.
Note: When a child presents with seizures, X-ray Diagnosis: Vitamin D deficiency rickets, cardiomegaly
chest can give clues to the etiology of seizures such as and cardiac failure. Treatment with vitamin D and calcium
rickets or lead poisoning. was curative.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 329

Case scenario 25 (Figures 32.28A to C)

IP : 196.52.84.10

Figure 32.28C
Figure 32.28A
Your Observations
Figure A: The normal shape of the heart is preserved, the
cardiophrenic angle is acute with increased pulmonary
congestion.
Whenever CXR shows cardiomegaly, always look
again to see the signs of pericardial effusion as it can be
relieved only by pericardiocentesis.
Diagnosis: Cardiomegaly with CCF.

Figure 32.28B
CXR after pericardial tap. Note the presence of pig tail
The normal shape of the heart is not seen, the cardio-
catheter, which was kept in situ. Also note the change in
phrenic angle is obtuse and pulmonary plethora is not seen.
the shape of the heart and the cardiophrenic angle.
Diagnosis: Pericardial effusion.
Diagnosis: After pericardiocentesis.
330 Section XI n Special Topics

Case scenario 26 (Figures 32.29A to C)


A 5-year-old playing boy was referred with history of
IP : 196.52.84.10
breathlessness while playing with a top.

Figure 32.29B

Your Observations
Figure 32.29A

Your Observations

Lateral view shows the top’s metallic axis penetrating


the posterior wall of trachea causing air leak.

Figure 32.29C: The FB after it was retrieved


Order a lateral view to visualize the nature of the for-
eign body.
The shadow, which appeared as a circular shadow
Coin shadow seen in the neck. If the FB is seen in the characteristic of a coin in the AP view, was a top. This was
apparent in the lateral view.
sagittal plane, it is caught up in the trachea. If it is placed in
the coronal plane, the object is in the cricopharynx.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 331

Case scenario 27 (Figures 32.30A to D)


2-year-old child with Down syndrome was brought
with stridor. IP : 196.52.84.10
X-ray showed a coin shadow in the neck. Despite re-
moval of FB, he deteriorated and developed respiratory
distress. Child developed bilateral pneumothorax and was
treat­ed with chest tube insertion and ventilatory support.

Figure 32.30C
Right hemithorax is wide, more black with collapsed
lung margin suggestive of right pneumothorax. Subcutane-
ous emphysema is also seen in the neck as verti­cal trans-
lucencies in the neck. Continuous diaphragm sign: pneu-
Figure 32.30A: Child ventilated with bilateral ICD momediastinum.

Figure 32.30D
Figure 32.30B: Coin shadow in the neck with heart and lungs
being normal.
Your Observations
Your Observations

The foreign body was cleaned and re-examined. It was


a button battery and not a coin. The deterioration was due
to corrosive necrosis, which can occur as early as 4 hours
after ingestion.
332 Section XI n Special Topics

Case scenario 28 (Figure 32.31) Case scenario 29 (Figures 32.32A and B)


A 8-year-old boy presented with fever, biphasic stridor A girl with T-cell lymphoma, developed fever, abdomi-
IP : 196.52.84.10
and hepatosplenomegaly. nal pain and shock.

Figure 32.31 Figure 32.32A

Your Observations Your Observations

Figure 32.32B

Your Observations

Mediastainal node is seen (arrow). It is probably causing Haziness suggestive of peritonitis, multiple fluid levels
intrathoracic airway obstruction. with air under diaphragm.
Diagnosis: Lymphoma. Diagnosis: Pneumoperitoneum secondary to perforation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 333

Case scenario 30 (Figure 32.33) Case scenario 31 (Figures 32.34A to D)


A 2-year-old boy presented with fever, acute diarrhea A 10-year-old girl fell down from a cycle and appeared
IP He
and vomiting for 3 days. : 196.52.84.10
developed tense abdominal bloated. Cycle tube nozzle injury caused injury to the heel
distension. causing extensive air leakage and subcutaneous emphy-
sema over the face, submandibular region and chest wall.

Figure 32.34A: Site of nozzle injury

Figure 32.33

Your Observations

Figure 32.34B

This intubated infant has chest wall and abdominal wall


edema. She also has air under the diaphragm. Bowel loops
are dilated with air fluid levels.
Diagnosis: Pneumoperitoneum. Figure 32.34C: Subcutaneous emphysema of face and chest wall
334 Section XI n Special Topics

Key Points
ü
IP : 196.52.84.10 1. Clinical background should be taken into
consideration, before interpreting X-rays.
2. Stepwise evaluation is mandatory to avoid missing
subtle findings.
3. Scan the X-ray from periphery to center and from
less obvious to obvious radiological finding.
4. Familiarity with normal X-ray films will aid in
recognizing abnormalities.
5. If clinical background and X-ray findings grossly
disagree, repeat the film to avoid simple errors
leading to serious consequences.

Figure 32.34D common errors


û
1. Pneumothorax is one of the most serious conditions
Your Observations
that could be missed in a X-ray film in a rapidly
deteriorating child. In a rapidly deteriorating child
if a CXR has been taken recently, it is wise to give a
closer look for pneumothorax. Change in the contour
of diaphragm may be a clue. Avoid mistaking a
skin fold or emphysematous change in the lung as
pneumothorax.
2. Missing findings such as pneumoperitoneum in a
child with suspected air leak.
3. Whenever endotracheal tube depth is assessed,
consider the neck position also. A flexed neck will
push the tube deeper and extended neck will pull
out higher.
4. Failing to identify features of pericardial effusion
in a child presenting with cardiomegaly. Remember
pericardiocentesis is life saving.
1. Subcutaneous emphysema in chest wall. 5. Missing basic data such as name, date, time and
2. Pneumomediastinum. side mark may lead to disastrous outcome, if
3. Air under diaphragm. wrongly judged.
4. Perinephric air.
Procedural Sedation and
33
IP : 196.52.84.10

Management of Pain in Children

Figure 33.1: Pain management in children helps in smooth performance of procedures

Learning Objectives
1. Defining procedural sedation. 3. Pearls and pitfalls in the use of sedative and
2. Steps taken to administer sedation for procedures analgesic drugs.
in the ED. 4. Discharge criteria.

Introduction Procedural sedation


Sedation reduces anxiety and minimizes pain and Procedural sedation (conscious sedation) is the technique
discomfort.1,2 The availability of safer drugs with precise, of administering sedatives or dissociative agents with or
short duration of action, a clear knowledge of adverse without analgesics, to induce a state or a level of conscious-
events and improved non-invasive monitoring have made ness that allows the child to tolerate procedures, while be-
procedural sedation a safe and valuable tool in the man- ing able to maintain cardiorespiratory function and airway
agement of painful and anxiety provoking procedures.3 without assistance.2 Procedural sedation is also essential
for the comfort of children and improves their overall ex-
perience during the procedure.4
A list of procedures requiring sedation is provided in
Table 33.1. Also refer Figures 33.1 and 33.2.

Steps of Procedural Sedation


Step 1: Presedation Assessment
History

Figure 33.2: Wong-Baker faces pain scale (WPFPS) and faces 1. Obtain history on the present health status, associated
pain scale-revised (FPSR). comorbid conditions, weight, allergies, prior medical
336 Section XI n Special Topics

Table 33.1: Procedures requiring sedation

Painful procedures Imaging Miscellaneous


Laceration repair
IP : 196.52.84.10
Magnetic resonance imaging (MRI) Electroencephalography (EEG)
Vascular access (central line placements) Nuclear scans (e.g. bone scans) Audiology (brainstem evoked response studies)
Fracture reduction Computerized tomography (CT) scans Biopsy
with contrast
Chest tube placement Fluoroscopy (e.g. nasogastric tube Foreign body removal
placement)
Lumbar puncture (chemotherapy)
Bone marrow aspiration

history, pertinent past anesthesia/sedation experience,


current medications and last meal/drink. Ù
2. Categorize risk based on the guidelines of the The Mallampati classification can be performed only
American Society of Anesthesiologists (ASA) 5,6 in the older child who can cooperate and open his/her
(Table 33.2). mouth when requested.
3. Call for help from anesthetists for class III/IV.
Procedural sedation by non-anesthesiologists may be
risky in class III/IV.
Table 33.2: American Association of Anesthesiologists (ASA)
classification
Class Description
I No underlying problems
II Mild systemic illness
III Severe systemic illness
IV Severe illness that is a constant threat to life
V Patient unlikely to survive beyond 24 hour
(Courtesy: American Society of Anesthesiologists)

Physical examination
Airway assessment includes:
1. Neck mobility and length.
2. Ability to open mouth widely.
3. Size of oral cavity.
4. Anatomical jaw abnormalities (e.g. Pierre-Robin syn-
drome, macroglossia).
Figure 33.3: Mallampati classification
5. Ability to protrude the jaw.
6. Keep mouth wide open and evaluate the airway for Table 33.3: Fasting guidelines
ease of assisted ventilation.
Clear Solids/breast
Mallampati classification is useful in predicting dif- Age Non-clear fluids
liquids milk
ficult airways (class III/IV). It is based on whether
Infants 2 hour 4 hour 6 hour
the posterior pharynx can be visualized well or not
(Figure 33.3). Children 2–3 hour 6 hour 6 hour
Chapter 33 n Procedural Sedation and Management of Pain in Children 337

Both assisted ventilation and oxygenation can be dif- Step 3: Measures Which Ensures Safety
ficult in children who have difficult airways. During Sedation in the Emergency Room
Sedation should be IP
performed by anesthesiologists and
: 196.52.84.10 Personnel and Equipment
not by other caregivers for the following categories:
1. The physician who is administering procedural seda-
●● Children assigned a category three or above by ASA tion should be trained in the use of anesthetic drugs.
classification. He/she should be aware of the nature of drugs, ad-
●● Very young infants (less than 6 month). verse events, timing, etc. of the sedative agents.
●● Children with airway abnormalities. 2. The physician must have expertise in recognition
(e.g. chest wall rigidity) and management of adverse
Step 2: Presedation Preparation events dur­ing sedation. He/she should also have skills
Fasting in managing the airway.
3. A nurse or physician (not performing the procedure)
The nil per oral (NPO) guidelines have been recommended should be present throughout sedation to observe the
by the ASA to prevent aspiration in the event of loss of child for adverse events until return to baseline status.
protective airway reflexes (Table 33.3). 4. Lighting, oxygen source, suction apparatus and air-
Table 33.4: University of Michigan Sedation Scale (UMSS) way equipment (nasal cannulas, nasal/oral airways,
bag/mask devices, laryngoscope blades, endotracheal
Score Level of sedation tubes) must be available.
0 Awake and alert 5. The heart rate, blood pressure, pulse oximeter and
I Minimally sedated: Tired/sleepy, appropriate preferably capnography to monitor nasal end tidal car-
response to verbal conversation and/or sound bon dioxide should be connected to patient through-
II Moderately sedated: Somnolent/sleeping, easily out the procedure.
aroused with light touch or a simple verbal 6. Emergency resuscitation drugs (e.g. epinephrine), iso-
command tonic intravenous fluids (normal saline) and reversal
III Deeply sedated: Deep sleep, arousable only with agents (naloxone, flumazenil) should also be readily
significant physical stimulation available.
IV Unarousable
Monitoring
1. Avoid solids for 6 hours and clear fluids for 2 hours in 1. All children undergoing procedural sedation should
healthy patients undergoing elective surgery. be closely monitored till they return to baseline alert-
2. Carbohydrate containing fluids may safely be given, ness and level of functioning according to established
up to 2 hours prior to sedation for malnourished chil- guidelines.13
dren with poor glycogen reserves.8 2. Monitoring should include frequent blood pressure,
Studies have noted that more than a third of chil- heart rate and respiratory rate measurements along
with continuous pulse oximetry.
dren who underwent sedation, fasted less than 4 hour,
3. The monitoring personnel should have complete ac-
for solids, but still had no higher incidence of ad-
cess and non-obstructed views of the child undergo-
verse effects or aspiration.9 The incidence of adverse
ing sedation.
events had not significantly increased when fasting 4. Pulse oximetry is useful in detecting hypoxia, but its
guidelines were not observed.10 Prolonged fasting (6 accuracy may be impeded by movement, decreased
hour, instead of 2 hours for liquids) offered no ad- circulation, temperature changes, etc. Since pulse
ditional benefit and did not reduce risk.11,12 An urgent oximeters do not detect very low saturations (less
procedure may override NPO guidelines for sedation than 75%), it may not be useful in children with cy-
provided, the airway is protected. Factors such as anotic heart disease. During respiratory depression,
gastroesophageal reflux, young infants (< 6 month), pulse oximetry may initially be normal, especially in
severe systemic illness and developmental delay may healthy adolescents as the respiratory reserve may be
increase risk of aspiration. adequate to meet the oxygen demands. Hypoventila-
338 Section XI n Special Topics

tion often precedes hypoxia in children undergoing Table 33.5: Specific indications for sedatives/analgesics
procedural sedation.
Indication Sedative/analgesic
5. Respiratory depression may be recognized by capnog-
IP : 196.52.84.10 Non-invasive painless procedures Chloral hydrate,
raphy earlier than pulse oximetry.14,15 Capnography
(imaging, EEG) midazolam, pentobarbital,
has also been noted to be superior to clinical observa- thiopental, propofol
tion in the detection of hypoventilation.16 Ultra short painful procedures Morphine*, fentanyl
6. Supplemental oxygen in the absence of oxygen re- (lumbar puncture, chest tube
quirement can be deleterious as it may prevent the insertion)
early detection of respiratory depression.17,18 There- Brief procedures (laceration Ketamine*, fentanyl
fore, routine supplemental oxygen is not recom- repair, fracture reduction, central
mended. venous line placement)
7. The depth of sedation could be assessed using sev- Dental procedures Nitrous oxide
eral sedation scales (Ramsay sedation scale, Uni- *Drugs often administered in combination with sedatives (e.g. midazolam)
versity of Michigan sedation scale) and the severity 3. Prior sedative experience of the child.
of pain from pain scales depending on age (Table 4. Required depth of sedation (Is there a need to be ab-
33.4).19 solutely still?).
5. Specific risk factors (ketamine contraindicated in head
8. Repeated assessment of sedation scores have been
found to be beneficial in reducing risks associated trauma).
with sedation.11 6. Experience and familiarity of the sedation provider
with the various drug options.
Step 4: Choice of Drugs Considerable differences may exist between individual
Description of sedatives/analgesics responses to various sedatives and the drug doses should
be titrated to effect.
A host of factors influence the decision making in drug
selection during procedural sedation. The choice of drugs 1. Painless procedures that do not require intravenous
is dependent upon: access, oral or intranasal routes may be utilized for
anxiolysis.
1. Age. 2. The specific indications for the various sedatives and
2. Type of procedure (painful vs painless, short vs long). the doses and in which these drugs are recommend-

Table 33.6: Sedatives and analgesics—pharmacodynamics

Drug Dose Route Onset Duration


Ketamine 1–2 mg/kg IV* PO† 1 minute 15–30 minute ( IV)
4–6 mg/kg IM‡ IV
10 mg/kg PO IM
Midazolam 0.05–0.1 mg/kg IV IV 1 minute 30–60 minute
0.5 mg/kg PO ( max 20 mg) PO
0.2 mg/kg IN( max 5 mg) IN§
Pentobarbital 2 mg/kg ( total 6 mg/kg) IV 3-5 minute 30–60 minute
Propofol 1.5–3 mg/kg IV < 1 minute 5–10 minute
Etomidate 0.3 mg/kg IV
Fentanyl 1–2 µg/kg (max 100 µg) IV rapid 30 minute
Morphine 0.1 mg/kg IV, SC ||
2–3 hour half-life
Chloral hydrate 30–100 mg/kg PO 25 minute 8–12 hour, up to 24 hour
Naloxone 0.1 mg/kg IV 1 minute 1 hour
IV, Intravenous route; PO, Oral route; IM, Intramuscular route; §IN, intranasal route; SC, subcutaneous route.
* † ‡ ||
Chapter 33 n Procedural Sedation and Management of Pain in Children 339

ed have been highlighted (Tables 33.4 to 33.6). The Chloral Hydrate: 30–100 mg/kg/dose (max dose 2 g).
doses have been adopted the consensus guidelines on
sedation and analgesia
IP : in critically ill children.20
196.52.84.10 Midazolam
Even though all benzodiazepines are useful, diazepam and
Sedatives lorazepam are longer acting than midazolam (preferred
Chloral Hydrate benzodiazepine for procedural sedation).

Chloral hydrate (active ingredient trichloroethanol) can be Midazolam acts through GABA and produces hypnosis
given both orally and rectally. It is rapidly absorbed from and anxiolysis. The advantages of midazolam include its
gastrointestinal tract (almost 100%). Its sedative effect short duration and the convenience of administration by
which occurs within 25 minutes, lasts for 8–12 hours. additional routes. It can be repeated IV every 3 minutes.
It has a rapid onset of action, with duration of action up
Chloral hydrate can cause myocardial depression and to 30–60 minutes. Intranasal or sublingual midazolam is
arrhythmias (Table 33.7). usually given at a higher dose (0.2–0.4 mg/kg). Midazo-
Table 33.7: Adverse events of sedatives lam produces anxiolysis in 15–20 minutes orally and 5–10
minutes intranasally. Midazolam is unpleasant orally and
Sedative Adverse event causes burning sensation when given via nose (preserva-
Chloral hydrate Myocardial/respiratory depression (can be tive—benzyl alcohol).
delayed)
The side effects include paradoxical excitement,
Ketamine Apnea, delirium, increased secretions, hypotension or bradycardia, respiratory depression
laryngospasm, increased IOP/ICP
or apnea.
Midazolam Paradoxical excitement, hypotension,
bradycardia, respiratory depression Even though midazolam alone produces sufficient
Pentobarbital Respiratory depression, apnea and anxiolysis, other sedatives such as pentobarbital (imaging
hypotension with rapid administration studies) or ketamine (fracture reduction, laceration repair)
are usually given in addition.
Morphine Respiratory depression, vomiting
Fentanyl Hypotension, bradycardia, respiratory Intravenous midazolam in conjunction with ketamine
depression, rarely chest wall rigidity is the most common combination regimen utilized in the
Etomidate Local pain on injection, thrombophlebitis, United States for procedural sedation. Midazolam pro-
myoclonus vides no analgesia. Even though combination regimens are
Propofol Bradycardia, hypotension, dose- used frequently and have been found to be safe, additional
dependent respiratory depression and sedatives (e.g. narcotics) may increase the likelihood of
apnea respiratory depression/apnea.
Avoid chloral hydrate in children who are on tri­ Midazolam: 0.01–0.1 mg/kg IV (max dose 3 mg/dose).
cyclic antidepressants and phenothiazines (The combi-
nation has been noted to have a greater predisposition to
Barbiturates
ventricular dysrhythmias).
Higher doses may result in respiratory depression
Thiopental
or airway obstruction, which could be fatal.21 Thiopental has a short duration of action (5–10 minutes).
It is still widely used and could be dangerous owing Thiopental should not be given in volume depleted
to its long half-life and side effects occurring beyond the children. It can cause hypotension due to vasodilata­
period of observation. tion and negative inotropic effects on the heart.

When children are discharged after chloral hydrate, Rectal administration is effective, but the prolonged
parents should be advised to watch for possible delayed duration of action (up to 90 minutes) limits its use.
side effects, including respiratory depression. Thiopental: 25–50 mg/kg IV.
340 Section XI n Special Topics

Pentobarbital
Pentobarbital is a rapidly acting barbiturate with an onset
Ù
Side effects include bradycardia, hypotension, dose-
IP : 196.52.84.10
of action within 3–5 minutes and duration of action of 30– dependent respiratory depression and apnea. Pro­
60 minutes. longed use of propofol for more than 48 hours has been
It is widely used for imaging studies (e.g. MRI) since it associated with metabolic acidosis.
provides prolonged sedation with sufficient depth to allow
It is useful in ultra short painless procedures (e.g. spi-
the child to remain still for an extended period of time.
nal tap). Propofol is usually given with a narcotic for pain-
Ù
Major side effects include respiratory depression and
ful procedures. Even though it is gaining popularity, its use
is restricted to anesthesiologists in many medical facilities
hypotension. due to its cardiovascular side effects.

Pentobarbital: 2 mg/kg IV, (max 6 mg/kg). Propofol: 1.5–3 mg/kg IV bolus followed by 50–100
μg/kg maintenance.
Ketamine
Etomidate
The rapid onset (1 minute), short duration of action,
(15–30 minutes), the predictable excellent analgesia and Etomidate acts by altering chloride conductance on the
sedation and the ability to be administered through mul- GABA receptors. It can be administered intravenously and
is available as a mixture with propyl glycol. It is rapid in
tiple routes have made ketamine the most popular drug
onset and produces excellent sedation and amnesia. Etomi-
for painful procedures. Ketamine produces ‘dissociative
date is very safe with an excellent cardiovascular profile.
sedation,’ a cataleptic state characterized by significant
analgesia and amnesia. It is postulated to act on the thal-
amic/limbic systems in mechanisms not clearly under-
Ù
Side effects include pain at site, thrombophlebitis
stood. Ketamine offers an ‘all or none phenomena’ in and myoclonus. Suppression of endogenous steroid
terms of sedation and does not have a dose related esca- production has been noted with its use.
lating effect. As an effective bronchodilator, it is safe and
indicated in asthmatic children. Etomidate: 0.3 mg/kg IV.
Side effects include apnea if used in infants less
than 3 months, increased secretions, laryngospasm, Management of Pain
transient nystagmus, hallucinations during recovery Pain in children is often overlooked and frequently under-
and seizures in children at risk. Unlike other sedatives, treated. Adequate management of pain will improve com-
ketamine may increase heart rate and blood pressure pliance of children, enhance the quality of outcome of the
due to its effect on the sympathetic nervous system. procedure performed and improve parental satisfaction.
Avoid ketamine when raised intracranial or intraocu­ Opioids are the mainstay in the management of severe
lar pressure is suspected. pain in the emergency room. When dosed correctly with
Ketamine: 1–2 mg/kg IV. the understanding of duration, side effects and interactions
with other sedatives, they can be safe and effective in the
treatment of pain.
Propofol
Propofol, a GABA agonist, is a sedative and hypnotic. It Morphine
is rapidly effective and has an ultrashort duration of action
Morphine is the most commonly used narcotic due to
(5–10 minutes). It has antiemetic and antiepileptic prop-
its quick onset, predictable duration and adequate safety
erties. Since propofol can decrease intracranial pressure
profile. Its half-life is 2–3 hours. In children < 3 months,
(ICP) and cerebral metabolic rate, it is used in head trauma
morphine may not be cleared quickly as the neonatal liver
and in children with seizures.
Chapter 33 n Procedural Sedation and Management of Pain in Children 341

is immature to permit effective glucuronidation, the main as they can cause severe withdrawal syndrome or increased
pathway of morphine metabolism. Hence, repeat doses of seizure threshold.
morphine have to be administered with caution in infants
IP : 196.52.84.10
and in those with liver disease. Naloxone
Morphine: 0.1 mg/kg IV. Naloxone is an opioid antagonist neutralizing all the an-
algesic, sedative and side effects of narcotics by binding
Fentanyl to the μ receptor. The onset is within 1 minute and it has a
half-life of 1 hour though the duration may be prolonged
Fentanyl, a morphine analogue, is a pure analgesic and of-
in infants. Due to its low affinity, repeat doses may be
fers no sedation. It is rapid in onset and short in duration (30
required to reverse the side effects of long acting narcot-
minutes). Fentanyl is very effective (potency—100 × mor-
ics (e.g. meperidine) and in overdose situations. In young
phine) and is indicated in painful orthopedic procedures. infants born to narcotic addicted mothers and in chronic
Side effects of fentanyl include hypotension, bradycardia overdose situations, naloxone can precipitate withdrawal
and respiratory depression. Watch for chest wall rigidity, symptoms.
a unique life-threatening side effect of fentanyl associated
with rapid administration. Chest wall rigidity will require Naloxone: 0.1 mg/kg.
immediate reversal with the antidote, naloxone and if re-
quired, paralysis with succinyl choline. Caution should be Flumazenil
exercised in calculating the amount of fentanyl to be given Flumazenil is a benzodiazepine antagonist and is used
due to the high concentration in solution (available as a 50 when cardiovascular and respiratory depression occurs
μg/mL solution). Newer preparations such as remifentanyl with toxic dose of benzodiazepines.
are ultra short with recovery within 5–20 minutes.
Even though it fully reverses benzodiazepine-induced
Fentanyl: 1–2 μg/kg IV. sedation, its effect on respiratory depression is not as pro-
nounced. Hence, assisted respirations and supplemental
Mepiridine (Demerol) oxygen are necessary for successful recovery from seda-
tion-induced respiratory depression. It is contraindicated in
Even though it is an effective narcotic and offers pain con-
children on long term benzodiazepines as it may increase
trol lasting up to 4 hour, it is falling out of favor due to the
the likelihood of seizures. Adverse events include agitation,
increased incidence of CNS side effects (tremors, seizures)
headache and dizziness.
due to its metabolite, normeperidine, which can accumu-
late after repeated doses. Anticonvulsants can also increase Flumazenil: 5 µg/kg every 1 minute to max of 40 µg/kg
the production of normeperidine resulting in increased sei- (adult 2 mg), then 2–10 µg/kg/h IV.
zure activity.
Management of Adverse Events
Sucrose
The incidence of serious adverse events is low if proce-
Oral sucrose is easy to administer and effective in pain dural sedation is performed by well trained personnel.23,24
control in neonates during painful short procedures (vac- Lack of knowledge of the onset and duration of action, in-
cinations, lumbar punctures). Sucrose mediates release of adequate monitoring and discharging children when crite-
endogeneous opiates resulting in alleviation of pain.22 ria for discharge are not met can contribute to an increased
frequency of adverse events in sedation.25
Reversal Agents
●● Sedation drugs, should be used only by physicians
Reversal agents should always be available in the event of trained in its use.
serious cardiovascular or respiratory adverse event which Combinations of sedatives and narcotics can increase
does not improve immediately with simple supportive the incidence of respiratory depression. Studies have
measures (supplemental oxygen, assisted ventilations). noted that adverse events were higher when more than
However, administering reversal agents is not without risk three drugs were utilized for sedation.26
342 Section XI n Special Topics

●● Use only one appropriate drug. The parents should be informed about delayed adverse
●● Respiratory depression is the most common adverse effects, such as chloral hydrate. They should be provided
event apart from failed
IP :or196.52.84.10
inadequate sedation.27 contact telephone numbers, if the need arise.
●● Respiratory depression during sedation is often a result
of hypercarbia, hypoventilation or obstruction of the Box 33.1: Discharge criteria
airway.
Stable cardiorespiratory function
●● Open the airway with head tilt-chin lift maneuver and
provide supplemental oxygen. Patient is easily arousable and protective reflexes are intact
●● Assisted ventilation may be needed. Patient can talk or verbalize (age-appropriate verbal response)
●● If respiratory depression is protracted, not responding Child can sit up unaided (if appropriate for age and
development)
to simple measures or cardiac irregularities are noted,
Level of responsiveness is close to baseline
naloxone is warranted for a child receiving narcotics.
Child is adequately hydrated
●● Bradycardia during sedation occurs secondary to respi-
ratory depression. It improves with assisted ventilation
and oxygenation.
●● More adverse events were noted, when benzodiaz-
Key Points
ü
epines were used for sedation in children at high risk 1. Children should not be exposed to pain during
(ASA classification III, IV).28 elective procedures in the ED.
2. The health care provider must be well versed in
Sedation was associated with more adverse events recognizing and managing respiratory depression
when benzodiazepines alone were used for sedation and during administration of sedative drugs.
in those considered high risk by ASA classification.28 The 3. Two trained health care providers must be available.
incidence of respiratory depression/apnea has been report- One to perform the procedure and the second to
ed to be up to 20%–29% of patients receiving procedural monitor and resuscitate.
sedation even though large studies in children’s hospitals
have lower rates of 3%– 4%.23,28
The specific common adverse events of the sedatives
and analgesics are listed in Table 33.7.
common errors
1. Failure to provide adequate pain relief during
û
procedures such as lumbar puncture, bone marrow
Discharge Criteria aspiration, thoracostomy, etc.
2. Administration of sedation without adequate
Once the procedure is complete, monitor the child un- analgesia.
til the child becomes awake and returns to baseline 3. Lack of awareness of potential side effects.
mental status. 4. Premature discharge without ruling out whether the
Most complications have been noted in the initial 5 child has recovered.
minutes (induction phase) after administration of intrave-
nous sedatives. All serious complications were noted in the REFERENCES
first 30 minutes of sedation.29 It is important to note that
painful procedures such as fracture reduction may obscure 1. Dresser S. The effectiveness of conscious sedation on anxi-
ety, pain and procedural complications in young children.
the potential depth of sedation due to the pain associated
Pediatric Nursing. 2003;29:320-23.
with the procedure. Hence, respiratory depression may
2. Krauss B, Green SM. Procedural sedation and analgesia in
manifest after a painful procedure, well beyond the induc- children. In: Lancet: Lancet; 2006. pp. 766-80.
tion phase. If the child has symptoms such as vomiting 3. Green SM. Research advances in procedural sedation and
or emergence reactions, the child should be observed for analgesia. Ann Emerg Med. 2007;49:31-36.
a longer period of time. The criteria for discharge as rec- 4. Claar RL, Simons LE, Logan DE. Parental response to chil-
ommended by the American Academy of Pediatrics (AAP) dren’s pain: The moderating impact of children’s emotional
are provided in Box 33.1. distress on symptoms and disability. In: Pain (03043959);
2008. pp. 172-79.
Chapter 33 n Procedural Sedation and Management of Pain in Children 343

5. Burgoyne LL, Smeltzer MP, Pereiras LA, et al. How well do to current sedation monitoring practices? Acad Emerg
pediatric anesthesiologists agree when assigning ASA physi- Med. 2006;13:500-04.
cal status classifications to their patients? In: Pediatric Anes- 17. Keidan I, Gravenstein D, Berkenstadt H, et al. Supple-
IP : 196.52.84.10
thesia Blackwell Publishing Limited; 2007. pp. 956-62. mental oxygen compromises the use of pulse oximetry for
6. Ragheb J, Malviya S, Burke C, et al. An assessment of detection of apnea and hypoventilation during sedation in
interrater reliability of the ASA physical status classifica- simulated pediatric patients. Pediatrics 2008;122:293-98.
tion in pediatric surgical patients. In: Pediatric Anesthesia: 18. Fu ES, Downs JB, Schweiger JW, et al. Supplemental oxy-
Blackwell Publishing Limited; 2006. pp. 928-31. gen impairs detection of hypoventilation by pulse oxim-
7. Rosenstock C, Gillesberg I, Gatke MR, et al. Inter-observer etry. Chest 2004;126:1552-558.
agreement of tests used for prediction of difficult laryngos- 19. Crellin D, Sullivan TP, Babl FE, et al. Analysis of the valida-
copy/tracheal intubation. In: Acta Anaesthesiologica Scandi- tion of existing behavioral pain and distress scales for use in
navica: Blackwell Publishing Limited; 2005. pp. 1057-062. the procedural setting. Pediatric Anesthesia. 2007;720-33.
8. Sareide E, Eriksson LI, Hirlekar G, et al. Pre-operative 20. Playfor S, Jenkins I, Boyles C, et al. Consensus guidelines
fasting guidelines: an update. In: Acta Anaesthesiologica on sedation and analgesia in critically ill children. Inten-
Scandinavica: Blackwell Publishing Limited; 2005. pp. sive Care Medicine.2006;32:1125-136.
1041-047. 21. Cohen Mr. Chloral Hydrate Overdoses Implicated In
9. Roback MG, Bajaj L, Wathen JE, et al. Preprocedural fast- Deaths. Nursing. 1993;23:25.
ing and adverse events in procedural sedation and analge- 22. Gibbins S, Stevens B. Mechanisms of sucrose and non-nu-
sia in a pediatric emergency department: are they related? tritive sucking in procedural pain management in infants.
Ann Emerg Med. 2004;44:454-59. Pain Res Manag. 2001;6:21-28.
10. Bell A, Treston G, McNabb C, et al. Profiling adverse re- 23. Cravero JP, Blike GT, Beach M, et al. Incidence and na-
spiratory events and vomiting when using propofol for ture of adverse events during pediatric sedation/anesthe-
emergency department procedural sedation. Emergency sia for procedures outside the operating room: report from
Medicine Australasia. 2007;19:405-10. the Pediatric Sedation Research Consortium. Pediatrics;
11. Hoffman GM, Nowakowski R, Troshynski TJ, et al. Risk 2006;118:1087-096.
reduction in pediatric procedural sedation by application 24. Meyer S, Grundmann U, Gottschling S, et al. Sedation
of an American Academy of Pediatrics/American Soci- and analgesia for brief diagnostic and therapeutic pro-
ety of Anesthesiologists Process Model. Pediatrics;109 cedures in children. European Journal of Pediatrics:
2002:236-43. 2007;166:291-302.
12. Treston G. Prolonged pre-procedure fasting time is unnec- 25. Cote CJ, Notterman DA, Karl HW, et al. Adverse sedation
essary when using titrated intravenous ketamine for pae- events in pediatrics: a critical incident analysis of Contrib-
diatric procedural sedation. In: Emergency Medicine Aus- uting factors. Pediatrics. 2000;105:805.
tralasia: Blackwell Publishing Limited; 2004 pp.145-50.
26. Cote CJ, Karl HW, Notterman DA, et al. Adverse sedation
13. Cote CJ, Wilson S, Work Group on S. Guidelines for moni- events in pediatrics: analysis of medications used for seda-
toring and management of pediatric patients during and af- tion. Pediatrics. 2000;106:633-44.
ter sedation for diagnostic and therapeutic procedures: an
27. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of
update. Pediatrics. 2006;118:2587-602.
procedural sedation and analgesia by nonanesthesiologists
14. Miner JR, Heegaard W, Plummer D. End-tidal carbon di- in a pediatric emergency department. Arch Pediatr Adolesc
oxide monitoring during procedural sedation. Acad Emerg Med. 2003;157:1090-096.
Med. 2002;9:275-80.
28. Malviya S, Voepel-Lewis T, Eldevik OP, et al. Sedation and
15. Lightdale JR, Goldmann DA, Feldman HA, et al. Mi- general anaesthesia in children undergoing MRI and CT: ad-
crostream capnography improves patient monitoring dur- verse events and outcomes. Br J Anaesth. 2000;84:743-48.
ing moderate sedation: a randomized, controlled trial. Pe- 29. Newman DH, Azer MM, Pitetti RD, et al. When is a patient
diatrics. 2006;117:1170-178. safe for discharge after procedural sedation? The timing of
16. Burton JH, Harrah JD, Germann CA, et al. Does end-tidal adverse effect events in 1367 pediatric procedural seda-
carbon dioxide monitoring detect respiratory events prior tions. Ann Emerg Med. 2003;42:627-35.
34
IP : 196.52.84.10

Diabetic Ketoacidosis

Figure 34.1: Protocolised approach and intensive monitoring of children with diabetes improve their quality of life.

Learning Objectives
1. Pathophysiology of DKA. 2. Use of the rapid cardiopulmonary cerebral assess-
ment and the pediatric assessment triangle to im-
plement the ISPAD guidelines.

Introduction Excess CRH coupled with insulinopenia also stimu-


lates hepatic gluconeogenesis, hepatic and skeletal muscle
Diabetic ketoacidosis (DKA) a biochemical triad of hy-
glycogenolysis and decreased peripheral utilization of
perglycemia, ketonemia and acidemia is characterized by
glucose, culminating in severe hyperglycemia. The latter
metabolic acidosis (pH < 7.3), plasma bicarbonate < 15
causes osmotic diuresis, polydipsia and polyuria. Dehy-
mEq/L, plasma glucose > 200 mg% and urine ketostix re-
dration and electrolyte loss ensues, which in course of time
action 2+ or plasma ketostix > 1+.1 Refer Figure 34.1.
causes impaired renal perfusion. Renal glucose clearance
is reduced, further exacerbating hyperglycemia. Thus a vi-
Pathophysiology cious cycle occurs wherein, hyperglycemia begets hyper-
glycemia.
Insulin deficiency, leads to increased secretion of
counter-regulatory hormones (CRH). The imbalance Osmotic diuresis leads to loss of sodium, potassium
causes alterations in the metabolism of fat, protein and and magnesium. Sodium loss is aggravated by insulin de-
carbohydrate (Figure 34.2). Lipolysis increases and ficiency and glucagon excess. The dilutional hyponatremia
leads to elevated circulating levels of free fatty acids (low measured serum sodium) is caused by the osmotic
(FFA). The latter is esterified to triglycerides and oxi- shift of intracellular water to the extracellular compart-
dized to ketone bodies in the liver resulting in a wide ment due to hyperglycemia. A rise in blood glucose of 100
anion gap acidosis. mg/dL leads to a fall of 1.6 mEq/L of serum sodium.2
Chapter 34 n Diabetic Ketoacidosis 345

IP : 196.52.84.10

Figure 34.2: Flow chart showing the pathogenesis of DKA

Increased production of ketoanions exceed the capacity


Ù of existing buffer ions (HCO3–) to maintain physiologic pH.
Serum Sodium Correction As a result DKA is characterized by metabolic acidosis.
Add 1.6 mEq sodium for each 100 mg plasma glucose >
100 mg/dL to the measured serum sodium value.
Ù
Retention of ketoanions after buffering is the cause for
Corrected Na = Measured Na + 1.6 [(glucose – 100)/100] the increased anion gap acidosis.

The kaliuresis, which occurs in DKA is due to osmotic Hyperglycemia and ketoanions enhance the glomerular
diuresis secondary to hyperaldosteronism caused by so- filtration rate. Progressive volume depletion decreases GFR,
dium depletion and the presence of negatively charged ke- leading to worsening hyperglycemia and ketonemia.
toanions in tubular fluid.
Ù
Despite these losses, plasma potassium concentrations Simple rehydration itself can improve hyperglycemia,
are typically normal or elevated at the time of diagnosis of ketosis and anion gap acidosis.
DKA. This is a result of the shift of K+ from intracellular to
extracellular compartment secondary to acidosis, hyperos-
Signs and Symptoms
molarity, insulinopenia and intracellular lysis of proteins.
DKA can be easily missed in a child presenting with new
Ù onset diabetes.3
Normal or low serum potassium during initial evaluation
should alert the clinician towards severely depleted total Ù
To avoid missing DKA in the ED, routinely perform
potassium stores.
dextrostix in every critically ill child.
346 Section XI n Special Topics

Clinical signs and symptoms of DKA do not correlate ●● Measured hyponatremia is common in DKA.
with the severity of acidosis and dehydration. Classic signs Normal or high measured sodium in face of severe hy-
and symptoms of DKAIP include:
: 196.52.84.10 perglycemia indicates hyperosmolarity and dehydration.
●● Leukocytosis with a shift to the left is often seen in
●● Hyperglycemia: Polyuria, polydipsia, nocturia.
●● Acidosis: Hyperventilation, abdominal pain. DKA.
●● Abdominal pain mimicking an acute abdomen has been This may not be due to infection, but warrants work-up
described in approximately 46% of patients with DKA. if it fails to normalize after rehydration.
This symptom has been attributed to dehydration of ●● Majority of patients present with blood glucose lev-
muscle tissue, delayed gastric emptying and ileus sec- el greater than 300 mg/dL.
ondary to acidosis.4 Patients who have received insulin before presenta-
●● Dehydration. tion may have reduced levels.
●● A fruity odor of the breath, akin to the odor of nail var- ●● The diagnosis of DKA may be confounded by the
nish remover is a clinical clue in a previously undiag- coexistence of other acid base disturbances.
nosed patient presenting with acidosis and dehydration. Persistent vomiting and severe hypovolemia can some-
●● Hypotension is a late finding in DKA, often associated times give rise to metabolic alkalosis (Diabetic alka-
with sepsis. losis).
●● Fever is rare, though when present is usually indicative
of underlying infection.
Ù
Mixed acid base abnormalities in DKA offer a clue
Ù
Differential diagnosis of DKA include gastroenteritis
to coexistent problems, e.g. respiratory alkalosis is
suggestive of sepsis.
with dehydration and hypovolemic shock, stress-induced
hyperglycemia, bronchiolitis, asthma, pneumonia,
meningitis, UTI and an acute ‘surgical abdomen’. Management
Therapeutic goals of the specific management of DKA
Classification of DKA include:

DKA can be classified as mild, moderate or severe based 1. Correction of fluid and electrolyte deficits: Fluid therapy.
on the degree of acidosis. Table 34.1. 2. Decrement of blood glucose and the ongoing osmotic
diuresis: Hydration and insulin therapy.
Table 34.1: Classification of DKA
3. Halting of ketoacid production: Insulin therapy.
DKA Venous pH Serum bicarbonate 4. Assessment and treatment of precipitating cause (e.g.
Mild < 7.3 < 15 mEq/L infection).
Moderate < 7.2 < 10 mEq/L 5. Close monitoring for complications (e.g. cerebral
Severe < 7.1 < 5 mEq/L edema).

Laboratory Evaluation Fluid Therapy


In addition to hyperglycemia, metabolic acidosis, ketone- Volume depletion triggers release of CRH, which then
mia, ketonuria and an elevated anion gap, leukocytosis, activates the renin-angiotensin-aldosterone axis. The hor-
hyponatremia, hypophosphatemia and hyperosmolarity mones, whose combined actions are directed towards pre-
may also be identified. serving intravascular volume, also cause insulin resistance.

Ù
Elevation of ketone bodies is diagnostic of DKA. The
Fluid therapy, hence, results in significant improve-
ment of hyperglycemia, hypertonicity and acidemia.
sodium nitroprusside test, which identifies acetoacetate Euvolemia or hydration, causes a decline in the counter-
and acetone, does not recognize beta hydroxybutyrate regulatory hormones, enhances renal glucose clearance
making this a poor test for estimation of severity of (following improved renal perfusion) and improves sen-
ketonemia. sitivity to insulin.
Chapter 34 n Diabetic Ketoacidosis 347

Ù Ù
Hydration alone hasIPbeen shown to reduce glucose Repeat fluids based on reassessment. Do not exceed 30
: 196.52.84.10
concentration by 25–50 mg/h in the first 1 hour. mL/kg.5
Fluid therapy though very important in DKA Rehydration phase begins after shock is corrected.
management, large volumes over short period of time has
been found to be a probable factor in the development of Rehydration fluid:
overt cerebral edema. ●● Deficit correction + Maintenance fluids.
●● A standard water deficit of 100 mL/kg (10% dehydra-
tion) is assumed if the child presents with shock and a
CASE SCENARIO 1 (Figures 34.3 to 34.7) deficit of 85 mL/kg (8.5% dehydration) is assumed if
8-year-old child presents with progressive lethargy and the child presents with only dehydration and no shock.
breathlessness. He has been having increased thirst and ●● Maintenance fluid.
has been voiding urine excessively over the past 2 days. Ongoing losses—urinary losses are usually not replaced.
●● Assuming the patient’s weight as 20 kg in this case sce-
nario, fluids are calculated as follows:
Total fluid to be infused in 48 hours.
●● Shock correction: 200 mL (10 mL/kg NS) over 1 hour.
●● Maintenance fluid for 48 hours 1,500 × 2 = 3,000 mL.
●● Deficit: 100 mL/kg = 2,000 mL.

Ù
Total fluid to be infused in 48 hours (including shock
correction).
Deficit + maintenance fluid for 48 hours – fluid bolus
given for shock correction (during first hour).
3,000 + 2,000 – 200 = 4,800 mL (over 47 hours).
Figure 34.3 Physiological status: Airway stable, effortless
tachypnea, tachycardia, shock with altered mental status. ●● Plan to administer 100 mL/h of NS to which 40 mEq/L

Ù of potassium chloride is added.


Ketonemia itself can cause drying of oral mucosa and Ù
peripheral vasoconstriction mimicking dehydration and Due to the inherent risk of cerebral edema, the first 24
shock. hours total fluid intake is restricted to less than 4L/m2/24
h (1.5–2 times the maintenance fluid/day).5
Shock: 1–2 Hours Potassium is added to the maintenance fluid to counter
insulin mediated shift of potassium into the intracellular
●● Provide oxygen using the non-rebreathing mask. compartment.
●● Introduce NGT and decompress stomach. Ensure that the total fluid is administered over 48 hours.
Gastric atony and dilation of the stomach are common
in DKA. Nasogastric suction is important to prevent as- ●● Use an infusion pump to administer fluids. Precision
piration especially in obtunded patients. is necessary to ensure accuracy in the rate of fluid ad-
●● Catheterize the bladder if unresponsive or in young in- ministration.
fants and children.
●● Initiate 10–20 mL/kg of isotonic saline (0.9%) bolus Ù
When blood glucose level falls below 250 mg/dL,
over 1–2 hour.
●● If hypotensive shock: Administer 20 mL/kg using pull change from 0.9 NS to 0.45 NS with 5% dextrose to
push technique. which 40 mEq/L of KCl is added.
348 Section XI n Special Topics

●● Switch to oral hydration as soon as the clinical condi-


tion permits, to avoid overhydration.

Ù IP : 196.52.84.10
Hyperglycemia resolves faster than acidosis.
Administration of 10% or 12.5% dextrose is necessary to
prevent hypoglycemia during the management of DKA.

Insulin Therapy
Insulin reverses proteolysis, lipolysis, suppresses ketone
body and ketoacid formation. It also lowers blood glucose, Figure 34.5: Withdraw 40 units of plain insulin
by inhibiting glycogenolysis and gluconeogenesis and
stimulates cellular glucose uptake.

Preparation of Insulin Infusion


●● Add 50 units of plain insulin to 50 mL of normal saline,
such that each mL will contain 1 unit of insulin. Flush
IV tubing thoroughly with 25 mL of this insulin solu-
tion to saturate binding sites before administering to
the patient.
●● Insulin infusion is initiated at the rate of 0.1 U/kg/h
after correction of shock.
●● For example, for a child weighing 10 kg, 0.1 mL/kg/h of Figure 34.6: Add insulin to the 50 mL syringe filled with NS
this solution (1 mL/h) will deliver 0.1 U/kg/h.
●● Insulin should be delivered in a separate infusion and
not mixed with the rehydrating solution.

Figure 34.7: Insulin infusion line is primed by flushing. Insulin


can adhere to plastic material. Flush out 25 mL of the solution.
Initiate at the rate of 0.1mL/kg/h.

Figure 34.4: Equipment needed to prepare an insulin Ù


infusion. Error in insulin preparation is the commonest cause of
failure to respond.
●● If hyperglycemia or acidosis is not improving within
End point of insulin therapy is resolution of ketoacidosis
an hour of initiation of infusion, look for markers of
and not hyperglycemia.
sepsis, persistence of hypovolemia and review the dose
and rate of insulin infusion. Check IV patency, it is pos- ●● Decrease infusion rate to 0.05 U/kg/h as acidosis starts
sible that insulin has extravasated. to resolve and blood glucose declines to 250 mg/dL.
Chapter 34 n Diabetic Ketoacidosis 349

Case scenario 2 (Figures 34.8 to 34.9) ●● Initiate insulin therapy 1–2 hours after rehydration at
the dose of 0.1 U/kg/h.
5-year-old girl (weight:15 kg) is brought with a history ●● Change to subcutaneous insulin once acidosis resolves
IP : 196.52.84.10
of polyuria and polydipsia for 15 days. She has been and patient starts to take oral feeds.
having abdominal pain and several episodes of vomit­ ●● Continue intravenous insulin for 30 minutes (for rapid
ing since morning. Her capillary blood glucose is 400 acting insulin) and 1 hour (for regular insulin) after the
mg/dL and her urine is positive for ketones. administration of first dose of subcutaneous insulin.

Ù
This overlap is essential, since the half-life of IV insulin is
short (5–10 min). An abrupt discontinuation of IV insulin,
coupled with a delayed onset of subcutaneous insulin
regimen may lead to worsening of DKA.

Case scenario 3
6-year-old girl on treatment for insulin-dependent
diabetes mellitus, missed her usual dose. Her routine
capillary blood glucose (CBG) shows 510 mg/dL. Urine
ketostix is positive (Figure 34.10).
Figure 34.8 Physiological status: Moderate DKA with
severe dehydration

Fluid therapy: A standard water deficit of 8.5% is as-


sumed (only dehydration, no shock). Fluid is calculated
based on this.
●● No bolus therapy is given.
●● 48 hour maintenance = 1,250 × 2 = 2,500 mL.
●● Deficit = 85 mL/kg = 85 × 15 kg = 1,275 mL.
●● Total fluid to be given in 48 hour = 2,500 + 1,275=
3,775 mL or 79 mL/h.

Figure 34.10 Physiological status: Cardiopulmonary


cerebral assessment normal with mild or uncomplicated DKA.
●● Initiate 0.1 U/kg of short acting or rapid acting insulin
subcutaneous or IM every 1–2 hourly.5 Though the IS-
PAD guidelines suggest hourly or 2 hourly SC insulin,
most patients in our setting can be managed well with
1 U/kg/day plain insulin given subcutaneously in 3–4
divided doses half an hour before each meal.
●● Oral feeds are given ad lib.
Figure 34.9: Severely dehydrated child with DKA
Rationale for Potassium Replacement
●● Order 0.9 NS with 40 mEq/L of KCl at 79 mL/h for the
initial 4–6 hours. Hydration and insulin therapy induces a rapid decline in
●● Once the blood glucose falls to < 250 mg change to plasma potassium during the initial hours due to the intra-
0.45 NS with 5% dextrose. cellular shift.
350 Section XI n Special Topics

Serum potassium is a poor indicator of intracellular po- ●● Monitor serum calcium during phosphate adminis-
tassium status. Monitor potassium status indirectly using tration.10
the ECG monitor. IP : 196.52.84.10
Monitoring and Posthyperglycemic Care
Potassium Administration ●● Cardiopulmonary assessment.
●● Replace potassium only after correction of shock. Do
not correct potassium if documented hyperkalemia or
Ù
Assess level of consciousness and document every 2
renal insufficiency exists. hourly.
●● Add 40 mEq/L potassium chloride to the rehydrating
fluid. It can be increased up to a maximum of 60 mEq/L ●● Strict hourly input output chart.
based on serum potassium levels and electrocardio- ●● SaO2, ECG .
gram (ECG). ●● Random blood sugar.
●● Patients with ECG changes consistent with hypokalemia
should receive rapid potassium correction at the rate of
Ù
Monitor glucose every hour in the first 6 hours and
0.3–0.5 mEq/kg/h till the ECG normalizes.6 thereafter every 2–4 hours until the patient is taking oral
●● Use an infusion pump for potassium replacement under fluids.
close cardiac monitoring.
●● Electrolytes.
Rationale for Avoiding Bicarbonate Serum electrolytes should be measured every 2–6
hours with special emphasis on potassium, corrected
Acidosis can cause negative inotropy, central nervous
sodium and bicarbonate.
system (CNS) depression, insulin resistance and hyper-
●● VBG: 4, 6, 8 hourly.
kalemia. However, bicarbonate therapy can aggravate Venous pH can be used to monitor acidosis; pH may
hypokalemia, paradoxical CNS acidosis, hypernatremia, improve, even when bicarbonate is low.
rebound alkalosis and hypocalcemia. More recently, bicar- ●● Monitor urea and creatinine every 12 hours.
bonate therapy has been associated with increased risk of Measurement of blood or urinary ketones is not nec-
cerebral edema.7-9 essary either during treatment or during the recovery
phase. Conversion of β-hydroxybutyrate to acetoac-
etate increases with improvement in circulatory status
Guidelines for Administering Bicarbonate and hypoxia, giving rise to a paradoxical increase in
●● Administer Bicarbonate (1–2 mEq/kg) slowly over 1–2 ketones and may take 1 week to disappear in the post-
hours10 if child presents with severe acidosis and im- DKA period.
pending cardiovascular collapse or imminent arrest. ●● Search for hidden foci of infection.
– Empiric broad spectrum antibiotics should be con-
sidered in children who appear sick. Sepsis may be a
Phosphate triggering event.
Enhanced urinary excretion of phosphate in DKA, com- – End tidal carbon dioxide measurements or newer
monly leads to hypophosphatemia. home glucose meters with the ability to measure
blood β-hydroxybutyrate concentration have been
shown to be accurate and may be beneficial in guid-
Guidelines ing therapy in DKA.14,15
●● Do not routinely replace phosphate. ●● Encourage oral feeding as early as possible, once the
●● Replacement is indicated in those with anemia, cardiac ketoacidosis resolves.
dysfunction, respiratory depression or muscle weakness
or serum phosphate lower than 1–1.5 mg/dL. Criteria for DKA Resolution
●● Administer one third of calculated phosphate as potas- ●● Blood glucose < 200 mg/dL.
sium phosphate.11-13 ●● Serum bicarbonate level > 15 mEq/L.
Chapter 34 n Diabetic Ketoacidosis 351

●● Venous pH 7.3. time to get dissipated. During this period, rapid decrease
●● Calculated anion gap of 12 mEq/L. in extracellular osmolality draws fluid into the intracellular
Resolution of DKA IPwarrants switch to subcutaneous
: 196.52.84.10 compartment resulting in cerebral edema because of the
insulin therapy. following causes.

Indication for Change Iatrogenic Causes of Cerebral Edema


to Subcutaneous Insulin ●● Rapid reduction of blood glucose.
●● Alert, tolerating oral feeds. ●● Vigorous fluid replacement.
●● Resolution of acidosis. ●● Failure of corrected sodium to rise with therapy.
●● Initiate subcutaneous insulin just before a meal. ●● Bicarbonate use.
●● Continue intravenous insulin for 30 minutes (for rapid Recognition of cerebral edema, is based on a high in-
acting insulin) and 1 hour (for regular insulin) after the dex of clinical suspicion. Characterized by headache,
administration of first dose of subcutaneous insulin to behav­ioral changes and abrupt neurological deteriora-
prevent rebound hyperglycemia. tion 2–24 hours after starting therapy, it can rapidly
●● The dose of subcutaneous plain insulin is 1 U/kg/day progress to death.
in three divided doses administered half an hour prior ●● Impaired sensorium persisting despite improvement in
to meals. pH and blood glucose levels.
●● Continue for 2–3 days. ●● Early subtle neurological signs.
●● Once blood glucose levels stabilize around 150–200 ●● Fall in Glasgow coma scale (GCS).
mg, initiate insulin in 2 doses using a combination of ●● Perform frequent cardiopulmonary cerebral assessment
short acting and intermediate acting insulin. to detect early signs of cerebral edema.
●● 2/3rd of the total dose is given in the morning of which
2/3rd is intermediate acting insulin (Monotard) and Management of Cerebral Edema5,23
1/3rd is short acting insulin (Actrapid). ●● Avoid rapid fall in glucose. When cerebral edema is
●● Another 1/3rd of the total dose is given in the eve- suspected, the blood glucose decrements should be
ning, which again split into 2/3rd intermediate act- gradual in order to avoid aggravation of the osmotic
ing insulin (Monotard) and 1/3rd short acting insulin disequilibrium.
(Actrapid). ●● Intubate for controlled ventilation.
For example, for a child weighing 30 kg: ●● Elevate the head end of the bed (avoid elevation if hy-
potensive).
●● Morning: Total dose needed is 20 units: Lente (inter- ●● Restrict fluids to two-third maintenance.
mediate acting) 13 and plain (rapid acting) 7. ●● If not in shock, administer mannitol 0.25–1 g/kg IV
●● Evening: Total dose needed is 10 units; Lente (inter- over 20 minutes. A repeat dose may be given if no re-
mediate acting) 7 and plain (rapid acting) 3. sponse is noted within 30 minutes to 2 hours.
●● 3% saline may be used at a dose of 5 mL/kg over 30
Complications in DKA minutes and can be repeated 8th hourly as needed.
●● Order computed tomography (CT) brain after stabiliza-
Cerebral Edema15-22 tion to rule out thrombosis and intracranial hemorrhage.
Vasogenic cerebral edema has been noted even before ini-
tiation of therapy. It is caused by blood brain barrier en-
Acute Respiratory Distress Syndrome (ARDS)
dothelial injury due to hypoxia, ischemia, inflammation or Non-cardiogenic pulmonary edema is generated by reduction
metabolic stress. in colloid osmotic pressure in pulmonary capillaries by ex-
clusive crystalloid replacement in DKA. Hypoxemic patients
Cytotoxic cerebral edema is caused by brain swelling with a widened pulmonary alveolar arterial gradient (PAO2-
secondary to hyperosmolar state, which is largely related PaO2) should be suspected to have pulmonary edema.
to therapy. ‘Idiogenic osmoles’ in the brain cells are gener- ●● Avoid ARDS by judicious fluid replacement.
ated in the face of hypertonic plasma, to guard against in- ●● Use colloids to treat hypotension refractory to crystal-
tracellular dehydration and shrinkage. These osmoles take loid replacement.24
352 Section XI n Special Topics

Hyperchloremic Acidosis 2. Check sugar with dextrostix in order to identify


A normal anion gap metabolic acidosis resulting from rela- DKA early in the critically ill child.
tive anion clearance andIPloss
: 196.52.84.10
of potential bicar­bonate from 3. Fluid therapy should be given evenly over 48 hours.
the tubules, it can also be secondary to ex­cessive infusion Aggressive fluid correction may lead to cerebral
of sodium chloride. It can last for up to 24–48 hours and edema.
has no adverse clinical effects.25 4. Insulin infusion should be started only after shock
correction or at least 1–2 hours of fluid therapy in
the patient without shock.
Steps to Prevent DKA in Diabetic Children 5. Signs of cerebral edema should be closely watched
Teach parents and children ‘sick day’ management: for and managed aggressively if identified to prevent
mortality.
●● Do not stop insulin completely.
●● Monitor blood glucose and urine ketones more closely
during intercurrent illness.
common errors
û
1. The insulin dose and insulin infusion should be
●● Continue the usual carbohydrate intake.
●● Seek early medical help to avoid precipitating an attack counter checked by two personnel.
of DKA. 2. Check if the calculated fluid is within 1.5–2 times
daily maintenance.
Table 34.2 shows the DKA monitoring chart. 3. Do not exceed 30 mL/kg for shock correction. Give
boluses slowly over 1 hour in compensated shock.
Key Points
ü 4. Stopping insulin infusion before acidosis is fully
corrected.
1. 50% of DKA patients present with new onset dia-
betes. Hence a high index of suspicion is needed to 5. If glucose levels fall rapidly and acidosis persists,
diagnose DKA. increase glucose concentration to 10%–12.5% and
continue insulin infusion.

Table 34.2: DKA monitoring chart

Pulses/ Blood Remark/


Date and time HR RR BP GCS Corrected Na IVF rate Insulin rate
perfusion sugar intervention
Protocol 34.1: PEMC approach: Management of children with DKA

Complete initial cardiopulmonary assessment, if no shock, calculate fluid requirements and correct over 48 hour.

IP : 196.52.84.10
Chapter 34 n Diabetic Ketoacidosis
353
354 Section XI n Special Topics

References dosis and hyperosmolar coma. Diabetic ketoacidosis and


hyperosmolar coma. Diabetes. 1980;29:87-95.
1. ISPAD Clinical Practice Consensus Guidelines 2009 Com-
14. Fearon DM,Steele DW. End tidal carbondioxide predicts
IP : 196.52.84.10
pendium, Diabetic ketoacidosis in children and Adolescents
the presence and severity of acidosis in children with dia-
with diabetes. Pediatric Diabetes. 2009:10 (Suppl.12):118-33.
betes. Acad Emerg Med. 2002;9:1373-378.
2. Katz MA. Hyperglycemia induced hyponatremia: calcu- 15. Rewers A, McFann K, Chase HP. Bedside monitoring of
lation of expected serum sodium depression. N Engl J blood beta hydroxyl butyrate levels in management of
Med. 1973;289:843-44. DKA in children. Diab Technol Ther. 2006:8:671-76.
3. Jayashree M, Singhi S. Diabetic ketoacidosis: Predictors of 16. Duck SC, Wyatt DT. Factors associated with brain hernia-
outcome in a pediatric intensive care unit of a developing tion in the treatment of diabetic ketoacidosis. J Pediatr.
country. Pediatr Crit Care Med. 2004;5:427-33. 1988;113:10-14.
4. Umpierrez G, Freire AX. Abdominal pain in patients with 17. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cere-
hyperglycemic crises. J Crit Care. 2002;17:63-67. bral edema in children with diabetic ketoacidosis. N Engl J
5. Global IDF/ISPAD guideline for diabetes in childhood and Med. 2001;344:264-69.
adolescence, International diabetes federation. 2011. 18. Edge JA, Hawkins MM, Winter DL, et al. The risk and
6. Singhi S, Gautham KS, Lal A. Safety and efficacy of a con- outcome of cerebral edema developing during diabetic ke-
centrated potassium chloride solution infusion for rapid cor- toacidosis. Arch Dis Child. 2001;85:16-22.
rection of hypokalemia. Indian Pediatr. 1994;31:565-70. 19. Arief Al, Kleeman CR. Studies on mechanisms of cere-
7. Allain V, Zeni F, Lafond P, et al. Does bicarbonate therapy bral edema in diabetic come, effects of hyperglucemia and
improve the management of severe diabetic ketoacidosis? rapid lowering of plasma glucose in normal rabbits J Clin
Crit Care Med. 1999;27:2690-694. Invest. 1973;52:571-83.
8. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cere- 20. Marcin JP, Glacer N, Barnett P, et al. Factors associated
bral edema in children with diabetic ketoacidosis. N Engl J with adverse outcomes in children in diabetic ketoacidosis
Med. 2001;344:264-69. related cerebral edema. J Pediatr. 2002;145:793-97.
9. Green SM, Rothrock SG, Ho JD, et al: Failure of adjunc- 21. Roberts M, Slover R, Chase H. Diabetic Ketoacido-
tive bicarbonate to improve outcome in severe pediatric sis with intracerebral complication. Pediatr Diabetes.
diabetic ketoacidosis. Ann Emerg Med. 1998;31:41-48. 2001;2:103-14.
10. Stuart A Weinzimer, Michael F Canarie, Edward Vincent 22. Levin DL. Cerebral edema in diabetic Ketoacidosis. Pe-
S, et al. Disorders of glucose homeostasis. In: David G. diatr Crit Care Med. 2008;9:320-29.
Nicholas. Roger’s Textbook of Pediatric Intensive Care, 23. Dunger DB, Sperling MA, Acerini CL, et al. ESPE/LWEPS
4th edition, Lippincott Williams and Wilkins; 2008. pp. consensus statement on diabetic ketoacidosis in children
1599-602. and adolescents Arch Dis Child. 2004;89:188-94.
11. Fisher JN, Kitabchi AE. A randomized study of phosphate 24. Carrol P, Matz R. Adult respiratory distress syndrome com-
therapy in the treatment of diabetic ketoacidosis. J Clin En- plicating severly uncontrolled diabetes mellitus: Report
docrinol Metab. 1983;57:177-70. of nine cases and review of the literature. Diabetes Care.
12. Wilson HK, Keuer SP, Lea AS, et al. Phosphate therapy in 1982;5:574-80.
diabetic ketoacidosis. Arch Intern Med. 1982;142:517-20. 25. Oh MS, Banerji MA, Carrol HJ. The mechanism of hyper-
13. Keller U, Berger W. Prevention of hypophosphatemia by chloremic acidosis during the recovery phase of diabetic
phosphate infusion during treatment of diabetic ketoaci- ketoacidosis. Diabetes. 1981;30:310-13.
Setting up Pediatric Resuscitation
35
IP : 196.52.84.10

and Emergency Services

Figure 35.1: Organized pediatric emergency services can generate tremendous good will in the community

Learning Objectives
1. How to set up a pediatric resuscitation and 2. Organizing equipment for the emergency service.
emergency unit at the entrance of the hospital? 3. The need for trained nursing personnel in pediatric
emergency medicine.

There is a critical and growing need for emergency phy- Competence in basic emergency medicine should be an
sicians and emergency medicine resources worldwide. To outcome measure for all medical students and represent a
meet this need, emergency services must be established criteria for completion of degree.1
and physicians must be trained to deliver time-sensitive
Globally, the millennium goal for the year 2015 aims
interventions and life-saving emergency care.
at reducing under 5 mortality by one third. Mortality has
Society has a right to expect that at the completion of already fallen to 20%–30% in many states in India due to
their medical school training all pediatricians must possess interventions such as immunization, appropriate antenatal,
basic knowledge of emergency care and the skills to man- natal and postnatal care, breastfeeding, etc. to 25%–30%.
age common acute problems. Emergency medicine is a Mortality can be further reduced by appropriate manage-
core medical discipline and should be a required portion of ment of acutely ill children and neonates in the Golden
the curriculum for every medical school and every medical hour. This is especially important, where the small family
student in the world (Figure 35.1). norm is being advocated.
Every graduating pediatric medical student, should be For both the pediatricians and children, the first step
able to provide care in an emergency situation without any would be to establish pediatric emergency services in ev-
faults or lack of confidence and should be independent at ery district and medical college hospitals.
the site of the emergency.
●● Create dedicated space in the casualty or outpatient de-
Every physician should be able to manage clinical de- partment exclusively for a pediatric emergency care unit.
cision-making under pressure of time when it is essential ●● The pediatric emergency service should be used only for
to save lives. evaluation and management of children referred with
356 Section XI n Special Topics

‘bad’ histories suggestive such as breathlessness, convul-


sions, loss of consciousness, envenomation, trauma, etc. Ù
●● Avoid evaluation and IPtreatment of stable children in the
: 196.52.84.10
All sides of patient should be accessible for
emergency unit. These children must be referred to the resuscitation.
OPD. Failure to do so will interfere with management
of critically ill children in large volume hospitals. ●● Electrical points should be placed 3 feet above the
●● Round the clock availability of physician and nurse is a ground (Figure 35.3).
very important aspect of service provided by the emer­
gency unit.
●● Avoid leaving the emergency unit when patients are
not being treated. Acutely ill children may be rushed in
at any time and absence of physician or nurse can result
in serious medicolegal problems for the hospital.
●● On the contrary, presence of personnel and immediate
attention to a sick child earns a great deal of good will
for the hospital.
●● The casualty medical officer should be responsible for
documentation of medicolegal entries, whilst the emer-
gency physicians should be responsible for resuscita-
tion of injured and poisoned children. Figure 35.3: Plug points are needed for pulse oximeter, infusion
●● ‘Brought dead’ should be certified by the casualty med- pumps, suction apparatus, warmer, light source and monitors.
ical officers.
●● Emergency services require a great deal of support from Ù
This ensures that the wires connecting electrical devices
the hospital administration for its smooth running.
such as monitors and infusion pumps do not prevent
●● Trained nurses, paramedical staff, easy accessibility to access to the patient.
the radiology suite, blood bank and laboratory backup
are essential to provide effective services. ●● 6–8 plug points of 5 and 15 amperes should be avail-
able on either side of the resuscitation trolley.
Design and Floor Plan of the ●● Centralized oxygen supply is preferable, if not avail-
Resuscitation Unit able oxygen cylinders can be used, but have to be peri-
odically checked and replaced.
●● Place the resuscitation trolley perpendicularly to the ●● Install a suction apparatus at the head end of the resus-
wall and not alongside (Figure 35.2). citation trolley.
●● Attach a disposable Yankauer suction catheter to the
suction equipment.

Ù
Ideally, both electrical and vacuum suction should be
available. In case of power failure, presence of the
vacuum suction is lifesaving.

●● Place a bag-valve-mask at the head end of the resusci-


tation trolley at all times (Figure. 35.4).
●● Place a stool at the head end of the trolley.

Figure 35.2: The resuscitation cot, as shown in this picture


should not not have railings around its sides.
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services 357

●● Age-appropriate Guedel’s airway devices (Figure 35.5).


Ù
The airway stool is placed such that the airway manager
●● Nasopharyngeal airways should also be available
(Figure 35.6).
IP : 196.52.84.10
can sit as he initiates bag-valve-mask ventilation. ●● Age-appropriate disposable Jackson-Rees circuits
Effective bag-valve-mask ventilation can be continued (Figure 35.7) for children who present with re­spiratory
until other aspects of resuscitation such as intravenous distress or respiratory failure.
access, intubation tray, etc. can be prepared. ●● Three sizes of Jackson-Rees circuits are available in
the Indian market:
●● Place an intravenous stand at the head end of the trolley.
– Neonatal and infants < 1 year.
●● Ensure that a saline bottle into which an infusion set has
been inserted be available at all times. – 1 year to 5 years.
– Older than 5 years.

Figure 35.4: Place a self-inflating bag-valve-mask device at


the head end of the resuscitation trolley.
Figure 35.6: Nasopharyngeal airway
Ù
Struggling to open and prepare a saline bottle during an
emergency should be avoided.

●● Install a pulse oximeter near the head end of the resus-


citation trolley.

Airway Equipment (Figures 35.5 to 35.10)


●● Organize the following airway equipment for all age
groups.

Figure 35.7: Jackson-Rees circuit

Ù
Non-rebreathing masks help to administer up to 90%
of oxygen compared to the simple facemask, which
provides 40% of oxygen.

Figure 35.5: Oropharyngeal airways


358 Section XI n Special Topics

IP : 196.52.84.10

Figure 35.10: Stock, age-appropriate disposable masks, since


Figure 35.8: Disposable non-rebreathing masks these are as important as having the correct sized ET tubes

Ù Equipments Chart, Vital Signs Chart and


Respiratory or cardiopulmonary arrest is a catastrophic
emergency in children. The first responder may not have Protocols (Figures 35.11 to 35.13)
the expertise in intubation. The easy to use laryngeal mask
airway is an attractive alternative to endotracheal tube.
Laryngeal mask airways (LMA), as compared with
endotracheal tube (ETT), led to more rapid establishment
of effective ventilation and fewer complications, when
performed by prehospital providers.2

Figure 35.11: Display age-based equipment sizes near the


crash cart. Display charts, which help to choose age-appropriate
nasogastric tubes, ET tubes, urinary catheters, etc. Nurses and
doctors should have easy access to this information to ensure
that the right size is inserted during resuscitation.

Figure 35.9: Stock, weight appropriate laryngeal mask


airways

Ù
Straight blades < 2 year; Curved blades > 2 year;
ET tubes : 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5 (cuffed and
uncuffed tubes); Tincture benzoin for sticking the ET
tube; Dynaplast cut and available as ‘trouser legs’;
gloves, syringes and cotton; Anesthetic drugs for rapid
sequence intubation.
Figure 35.12: Display vital signs chart at head end of
resuscitation trolley
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services 359

IP : 196.52.84.10

Figure 35.13: Display protocols for all common emergencies Figure 35.16: Organize the intraosseous tray with the following:
Bone marrow needle, sand bag, gloves, hole towel, dynaplast,
tincture of benzoin, betadine, stainless steel cups, gauze. Prior
Procedure Trays (Figures 35.14 to 35.16) to insertion of needle, prepare 2 fluid-filled syringes (preferably
5 mL in small infants and 10 mL in older children).

Drugs and Dosages (Figures 35.17 to 35.19)

Figure 35.14: An intubation tray should be organized and


ready at all times.

Figure 35.17: Display drugs with labels for ease of retrieval dur-
ing resuscitation. Replenish after the resuscitation is complete.
Stock all resuscitation drugs. Organize drugs in an ‘easy to
retrieve’ method by labeling. Stock adequate quantity of drugs.

Figure 35.15: Organize the intravenous tray with age


-appropriate intravenous catheters, cotton balls, disinfectant,
adhesive tapes and gloves.

Figure 35.18: Display drug dosages and methods of


preparation close to the crash cart
360 Section XI n Special Topics

IP : 196.52.84.10

Figure 35.19: Prefilled epinephrine should be available at Figure 35.21: Ultrasonography machine is very useful to detect
all times fluid and blood (FAST—focussed abdominal sonography in
trauma) in children with trauma.
●● Use a 10 mL syringe for mixing 1 mL of 1:1000 adren-
aline in 9 mL of NS (1:10,000 dilution).
●● Discard unused epinephrine once in 24 hours.
●● Make note of date and time of reconstitution on the
syringe.
●● When administering a bolus dose of epinephrine to the
child, load in a separate 2 mL syringe, this ensures pre-
cise dosage.

Ù
Avoid administering epinephrine directly from the 10
mL syringe.

●● Direct administration from the 10 mL syringe can lead Figure 35.22: Equip the emergency service with cardiac
monitor, end tidal CO2 monitor and a pulse oximeter
to over dosage (lethal consequences).
Special equipment—spinal immobilization board and cer-
vical collar for management of head and spinal injuries.
Biomedical Equipment (Figures 35.20 to 35.22)
Refer Figure 35.23.

Figure 35.20: Equip the ED with syringe pumps. Ideally, 4


pumps are needed for every resuscitation trolley viz vasoactive Figure 35.23: Spinal immobilization board and cervical collar
medications, anticonvulsants, sedation and pain relief and are essential for managing head and spinal injuries
maintenance fluids.
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services 361

Time Sensitive, Goal-directed Management Biomedical Waste Disposal (Figure 35.27)


and Documentation (Figures 35.24 to 35.26)
IP : 196.52.84.10

Figure 35.27: Organize biomedical waste disposal as per national


guidelines. Wash area should also be available near emergency service.
Figure 35.24: Install a digital clock to ensure time sensitive
goal-directed management Education and Training of Paramedical
Personnel (Figures 35.28 to 35.31)

Figure 35.25: Perform the rapid cardiopulmonary cerebral


Figure 35.28: Train nurses in emergency resuscitation. They
assess­ment and documentation following every intervention
should be able to recognize respiratory failure and initiate bag-
during resuscitation
valve-mask ventilation, initiate age-appropriate cardiac massage,
quickly prepare drugs and infusions, and set up age-appropriate
airway tray within minutes.

Figure 35.26: Use the emergency case record for


documentation after every assessment. Maximum information
should be documented within a minimum time frame. The Figure 35.29: Emergency nurses should know how to perform
case record should be available at the foot end of every backward and upward, rightward cricoid pressure (BURP)
resuscitation trolley. technique, Sellick’s maneuver and to assist airway manager.
362 Section XI n Special Topics

●● Encourage friendly behavior amongst all members of


team (nurses, doctors, house officers, nursing atten-
IP : 196.52.84.10 dants between resuscitation).
●● Work in the ED can be very stressful and rapport amongst
all members is essential for good outcomes. Indeed, suc-
cessful resuscitation depends on TEAM WORK.
●● Appreciating team members for all the right things
done in right way and constructive criticism of their
mistakes and further training to avoid them in future,
will reinforce their confidence, help improve them-
selves and encourage them to perform even better.
Figure 35.30: Train nurses to prepare age-appropriate anti- ●● Team members should be periodically updated on new-
convulsant, inotrope infusions. Nurses should be aware of er developments in the standards of care.
proto­cols for all common emergencies.
●● Encourage, parents and children who had been success-
fully resuscitated to come back and meet the ER team
prior to discharge. This boosts morale and cultivates
good team dynamics.
●● Celebrate successful resuscitation in the emergency
room with parents, child and emergency team.

Figure 35.31: Ideally, nurses who are trained in resuscitation


should be retained in the ED
●● House officers and junior doctors should be aware of
resuscitation protocols modified for the Indian context.
●● Train medical officers and house officers to take cor-
rect therapeutic decisions during resuscitation in criti-
cal illness.
●● Train them to avoid errors, which precipitate cardiac Figure 35.33: Happy mothers with their infants post-
arrest during resuscitation. resuscitation

“Emergency departments are places within the hospital


where the greatest good can be done for the greatest num-
ber of people”—‘Foreword from the first edition of Pediat-
ric Emergency Medicine Course- 2008 N. Kissoon’.

Figure 35.32: Team effort—Many hands... One goal


IP : 196.52.84.10
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services

ER MOTTO: “Intelligence and capability are not enough... there must be the joy of doing something beautiful”
363

- Dr Govindappa Venkataswamy, Founder, Aravind Eye Hospitals, Tamil Nadu, India


364 Section XI n Special Topics

Key Points
1. Space for the ‘Pediatric
ü common errors
û
IP : Resuscitation
196.52.84.10 and Emergency 1. Referring to the emergency service as ‘Casualty’!
Services’ unit must be created inside the casualty. 2. Failure to implement current evidence-based
2. The emergency service provides specialized care to protocols.
get kids back on track. 3. Failure to identify early signs of critical illness.
3. Dedicated doctors and nurses are needed to man the 4. Failure to resuscitate until therapeutic goals of
emergency service. hypoxia, shock, myocardial dysfunction and seizures
4. Resuscitation equipment and drugs must be have resolved.
organized and replenished when used.
5. Training in the Pediatric Advanced Life Support, References
Basic Life Support are mandatory prior to working
1. WP Burdick, et al. SAEM Education Committee, under-
in this area. graduate subcommittee academic emergency medicine,
1998;(5):1105-110.
2. Chen L, Hsiao AL. Randomized trial of endotracheal tube
versus laryngeal mask airway in simulated pre-hospital
pediatric arrest. Pediatrics. 2008;122;e294; DOI: 10.1542/
peds.2008-0103.
Section XII
Procedures
IP : 196.52.84.10
IP : 196.52.84.10
36
IP : 196.52.84.10

Nebulizer Therapy

Introduction Check List for Nebulization


The nebulizer is used to deliver medications directly into
the lungs in the form of an aerosol mist. It ensures that the
therapeutic dose is delivered within a short span of time
right into the lungs via the mouthpiece or a face mask.

NEBULIZER: HOW IT WORKS?


The Bernoulli’s principle (Venturi effect) is used to oper-
ate the jet nebulizer. Oxygen or compressed air is driven
through a tube. This creates an area of subatmospheric
pressure around the jet, as it exits the tube. As a result,
the solution in the nebulizing chamber is sucked up and
dispersed in the form of an aerosol. The size of the droplets Figure 36.1: Nebulization tray
are characteristically 1–20 microns. Droplets less than 5 Nebulizing kit (Figure 36.1) with appropriate sized face
microns get deposited in the distal airways. The baffle pro- mask.
vided in the chamber ensures uniformity in the size of the
particles. Larger sized particles are returned to the cham- ●● Mask: Used in ill children, less than 5 years of age.
ber and aerosolized. ●● Mouthpiece: Used in older children and adolescents. It
increases drug deposition.
Ù
Avoid using nebulizers that are driven by electricity in
●● Oxygen source.
●● Medications.
the emergency setting. Jet nebulizer that is driven by ●● 2 mL syringe.
oxygen is the method of choice in hypoxic children. ●● Cardiac monitor and pulse oximeter.

nebulization How to Use a Nebulizer?


●● Assemble the tubing, nebulizer cup and mouthpiece (or
Medications
mask).
●● Beta-agonists and Ipratropium in severe asthmatic ex- ●● Load the prescribed drug in a syringe.
acerbation. ●● Fill the nebulizing chamber with the medication.
●● Epinephrine and steroids for acute stridor due to ●● Fill the chamber with 4–5 mL of normal saline. If less-
ALTB. er volume is used, nebulization may not be possible
●● 3% sodium chloride for bronchiolitis. (avoid distilled water) (Figure 36.2A to F).
368 Section XII n Procedures

IP : 196.52.84.10

Figures 36.2A to F: A. Draw 0.5 mL of Salbutamol in a syringe;


B. Empty the contents into the chamber; C. Draw 0.5–1 mL of
Ipratropium Bromide solution separately; D. Add this to the
chamber containing Salbutamol; E. Draw 4 mL normal saline and
add to the chamber containing Salbutamol and Ipratropium; F.
Avoid drawing all drugs and NS together in the same syringe.

Ù
The minimum volume needed for nebulization is 4 mL.
Lower fill volumes can cause suboptimal drug delivery.
The maximum volume that can be loaded is 10 mL. NS
(normal saline) is the recommended diluent. Plain water
can cause bronchospasm.

●● Connect the nebulizer chamber to the oxygen source


and initiate nebulization using a flow rate of 8 mL/min.
(NB: Domiciliary oxygen cylinders do not provide an
adequate flow rate).
●● Nebulization should be stopped and the chamber tapped
when spluttering occurs.
●● The delivery time should not exceed 10 minute.
●● Ensure that the child is seated comfortably on his
mother’s lap, in an upright sitting position.
●● Ensure that the mask fits well such that minimal mist
escapes.
Chapter 36 n Nebulizer Therapy 369

●● Monitor the patient throughout the nebulizer treat- ●● Replace nebulizers once every 3 months.
ment. ●● Ideally, each patient should have his own nebulizer.
●● Stop nebulization if child’s mental status worsens or
IP : 196.52.84.10
saturations fall.
●● Ensure that the nebulizer chamber remains upright at
1.
Key Points
Nebulizer should be driven using oxygen.
ü
all times.
2. Ensure a gas flow rate of 8 liter per minute.
3. Avoid use of plain water. NS is the ideal diluent.
Maintenance
4. The nebulizer must be rinsed after each use.
●● Disconnect the nebulizer cup from the plastic tubing,
wash with warm tap water, mild detergent and air dry.
●● Do not wash or rinse the plastic tubing.
●● Store the dry nebulizer cup and plastic tube in a plas-
common errors
û
1. Drawing salbutamol, ipratropium and normal saline
tic bag. all together in the same syringe.
●● Once a week, soak the nebulizer cup and mouthpiece 2. Administering nebulization for stable asthmatics
or face mask for 20 minutes, in a disinfecting solution. with minimal wheeze.
●● Run the nebulizer empty for a few seconds before use.
Needle Thoracocentesis
37
IP : 196.52.84.10

and Thoracostomy

Pleural aspiration describes a procedure whereby pleural Equipments


fluid or air may be aspirated via a needle or tube inserted
into the pleural space (Figure 37.1). ●● 16, 18, 20 gauge over the needle angiocatheter.

Ù
Avoid butterfly needle since the needle could lacerate
the expanding lung.

●● 10 cc syringe half-filled with NS (aids in visualizing air


bubbles, thus confirming underlying pneumothorax).
●● Betadine solution.
●● Sterile gloves.
●● Sterile intravenous set.
●● Saline bottle for underwater seal drainage.

Figure 37.1: Right sided pneumothorax. Technique (Refer Figure 26.16 in Chapter 26)
●● Identify the second intercostal space in the midclavicu-
indications lar line.
1. Trauma with possibility of chest injury. ●● Prepare skin with Betadine solution.
2. Severe pneumonia with pneumatocele. ●● Attach syringe filled with saline to the angiocath.
3. Desaturation in the intubated child: ●● Insert perpendicular to chest wall above the third rib in
Rule out ‘DOPE’. the midclavicular line.
Oxygen saturations not normalizing despite the fol- ●● Aspirate, as the needle is advanced.
lowing maneuvers: ●● A rush of air/bubbles in the syringe denotes entry into
a. Confirmation of tube position. pleural space.
b. Ruling out obstruction by checking for adequacy ●● Withdraw stillette of the angiocath and keep the hub
of chest rise, bilateral air entry and suctioning the closed with your thumb to prevent air entering the
ET. pleural space.
c. Ruling out faulty equipment. ●● Connect an intravenous tube to a saline bottle such that
4. Congenital cystic adenomatoid malformation. an underwater seal drainage is provided.
●● Improvement in saturations and air bubbles in the sa-
Needle Thoracocentesis line bottle are confirmatory of tension pneumothorax.
●● Monitor using a pulseoximeter and cardiac monitor. ●● Confirmatory CXR.
●● Ensure that emergency medications are close at hand. ●● Prepare for definitive tube thoracostomy.
Chapter 37 n Needle Thoracocentesis and Thoracostomy 371

●● If fluid in the chest is causing respiratory embarrass-


ment aspirate using the procedure mentioned above.
●● Use the 4th, 5th or 6th
IP :intercostal space in the midaxil-
196.52.84.10
lary line.

Postprocedure Care
Prepare for thoracostomy insertion soon after CXR in sus-
pected tension pneumothorax.
In the instances where CXR may not be readily avail-
able, a second physician prepares to insert a chest tube
while urgent needle thoracocentesis is being performed by
Figure 37.2: Thoracostomy kit
the first physician.
●● Scalpel with 11 size blade.
Ù ●● Curved artery forceps (for blunt dissection).
Tension pneumothorax is a clinical diagnosis and needs ●● Antiseptic solution povidone iodine 10% or chlorhexi-
urgent intervention. dine in alcohol.
●● Appropriate sized chest tube.
Continue to monitor and maintain the ABCs a. Newborn : 8–12 FG.
The commonest complications from pleural aspiration are b. Infant : 12–16 FG.
pneumothorax, procedure failure, pain and hemorrhage. c. Child : 16–24 FG.
The most serious complication is visceral injury. d. Adolescent : 20–32 FG.
●● Connecting tube.
●● Sterile dressing tray with Tegaderm.
thoracostomy ●● Suture material with needle (‘1’ silk).
A chest drain is a tube, which is placed in the pleural space ●● Closed drainage system (including sterile water if un-
to drain its contents (fluid or air) and remains in place until derwater seal is used) (Figure 37.2).
drainage is complete.
Technique of Chest Tube Insertion
Indications
●● Obtain written consent.
1. Postoperatively, e.g. cardiac surgery, thoracotomy. ●● Connect cardiac monitor and pulse oximeter.
2. Pneumothorax. ●● Administer ketamine 2 mg/kg and midazolam 0.2 mg/
3. Hemothorax. kg IV for adequate pain relief and sedation.
4. Chylothorax. ●● Confirm the site of insertion clinically (Figure 37.3).
5. Pleural effusions.
Empyema is a serious and avoidable complication of
pleural aspiration, the risk of which is greater with mul-
tiple attempts. It is recommended that strict asepsis should
be employed, especially when carrying out therapeutic as-
pirations.

Equipments
●● Sterile gloves and gown.
●● Drape.
●● 1% or 2% lignocaine. Figure 37.3: Selection of site for ICD insertion
●● Syringes with needle (21–25 gauge). (Courtesy: Dr Gunda Srinivas)
372 Section XII n Procedures

●● Take universal precautions. ●● Unclamp the forceps and insert the chest tube till all the
●● Infiltrate skin, underlying tissue up to the periosteum holes are inside the pleural cavity (Figure 37.6).
using lignocaine (Figure 37.4).
IP : 196.52.84.10

Figure 37.6: ICD inserted in 4th intercostal space


Figure 37.4: Local anesthetic administration around the site of (Courtesy: Dr Gunda Srinivas).
ICD insertion (Courtesy: Dr Gunda Srinivas).
●● Connect the other end of the tube to the underwater
●● Position the child in the supine position or affected side
seal sterile drainage system or suction pump (Figure
up with the arm above the head.
●● Choose the 4th, 5th or 6th intercostal space in the pos- 37.7).
terior or midaxillary line. ●● Suction is not always required, and may lead to tissue
●● Make a small incision parallel to intercostal space over trauma and prolongation of an air leak in some pa-
the skin above the desired insertion point. tients.
●● Insert an artery forceps through the tissues above the ●● Suction on the drainage unit should be set to the pre-
rib, taking care to avoid damaging the neurovascular scribed level.
bundle in the in­ferior aspect of the rib. – -5 cm H20 is commonly used for neonates.
●● Push the artery forceps (not > 1 cm) through the inter- – -10– -20 cm H20 is usually used by convention for
costal muscles and pleura applying steady pressure to
children.
the blades.
●● Forcefully spread the blades to enlarge the hole wide
enough to accommodate the chest tube.
●● Clamp the tip of the chest tube parallel to the blades of
the artery forceps.
●● Use your forceps, to guide insertion of the chest tube
through the dissected pathway, until it is safe inside the
pleural space (Figure 37.5).

Figure 37.7: Underwater seal with air column moving (arrow)


(Courtesy: Dr Gunda Srinivas).
Figure 37.5: Controlled pressure during ICD insertion
(Courtesy: Dr Gunda Srinivas).
Chapter 37 n Needle Thoracocentesis and Thoracostomy 373

IP : 196.52.84.10

Figures 37.8A and B: Sutures to fix ICD


(Courtesy: Dr Gunda Srinivas). Figures 37.9A to C: Fixing of ICD (Courtesy: Dr Gunda Srinivas)

●● Apply two sutures (Figures 37.8A and B). ●● Check for bubbling of air and movement of air column
(Figure 37.7).
●● The first suture is to close the skin (mattress suture) af-
ter drainage removal and second one is a stay suture.
Care After the Thoracostomy
●● To prevent the tube from slipping, an omental tag of
tape has been described, which allows tube to lie a little ●● Take a chest X-ray to confirm position of the tube and
away from chest wall to prevent kinking and tension at lung expansion after thoracostomy.
the insertion site. ●● Watch for complications such as bleeding from in-
●● Dress the site of insertion using sterile dressing or tercostal vessels causing subcutaneous hematoma or
hemothorax, subcutaneous emphysema, infection and
Tegaderm (Figures 37.9A to C).
puncture of lung, liver or spleen.
●● Monitor hemodynamic status.
●● Adequate pain relief.
●● Never lift drain above chest level.
●● The unit and all tubing should be below patient’s chest
level to facilitate drainage.
●● Tubing should have no kinks or obstructions that may
inhibit drainage.
●● Ensure all connections between chest tubes and drain-
age unit are tight and secure.
●● Connections should have cable ties in place.
●● Tubing should be anchored to the patient’s skin to pre-
vent pulling of the drain.
374 Section XII n Procedures

●● In PICU and NICU, the tubing should also be secured


to patient bed to prevent accidental displacement.
●● Ensure the unit is securely positioned on its stand or
Key Points
ü
IP : 196.52.84.10 1. Use the 2nd inter­costal space for needle thoracocen-
hanging on the bed. tesis.
●● Suction on the drainage unit should be set to the pre- 2. Needle thoracocentesis is performed when satura-
scribed level as mentioned earlier. tions fail to improve following less invasive maneu-
vers to rule out DOPE.
Removal of the Thoracostomy Tube 3. If saturations improve following needle thoracocen-
tesis, plan thoracostomy.
Indications
4. Perform thoracostomy only after adequate pain re-
1. Absence of an air leak (pneumothorax). lief and sedation.
2. Drainage diminishes to little or nothing. 5. Avoid injury to the neurovascular bundle.
3. No evidence of respiratory compromise.
4. Chest X-ray showing lung re-expansion.
By clamping the chest drain for several hours followed
by a chest X-ray, a recurrence of a pneumothorax may be
common errors
û
ruled out. 1. Using butterfly needle (scalp vein set), large bore IV
The clamped drain should be closely supervised by needles for thoracocentesis.
nursing staff who are familiar with the management of 2. Wasting valuable time for taking the chest X-ray to
chest drains and who should unclamp the chest drain in the con­firm pneumothorax in a ventilated child who is
event of any clinical deterioration. desaturating.
3. Not providing underwater seal.
CXR should be performed post drain removal
4. Not closing the hub after entry into the pleural
Clinical status is the best indicator of a reaccumulation of space.
air or fluid. CXR should be performed if patient deterio- 5. Failing to fix the tube securely after insertion.
rates. Remove sutures 5 days post drain removal.
38
IP : 196.52.84.10

Pericardiocentesis

Pericardiocentesis is a procedure by which pericardial 3. Gross ascites, massive hepatomegaly and elevated dia-
fluid is removed by needle from the pericardial cavity for phragm can alter landmarks for subxiphoid approach.
diagnostic or therapeutic purposes, also called as pericar-
dial paracentesis. Equipment
●● Antiseptic solution.
Indications ●● Sterile drapes, gown and mask.
●● Local anesthetic (lidocaine 1%).
●● Life-threatening hemodynamic changes in a patient ●● 5, 10 and 50 mL syringes.
with suspected pericardial effusion (Figure 38.1). ●● No. 11 blade.
●● Aspiration of pericardial fluid for diagnostic and thera- ●● Needles 18 gauge and 25 gauge.
peutic purposes (Figure 38.2). ●● Spinal needle 18 gauge.
●● Emergency resuscitation drugs and intubation trolley.
●● Ultrasound machine (if available) and sterile ultra-
sound probe cover.

Procedure
●● Obtain written consent.
●● Ensure secure airway and vascular access.
●● Attach the patient to the cardiac monitor and pulse oxi-
meter.
●● Ideally, use ultrasound to visualize the heart and peri-
cardial space.

Figure 38.1: Chest X-ray showing pericardial effusion


(Courtesy: Dr Gunda Srinivas)

CONTRAINDICATIONS
There are no absolute contraindications.
Relative contraindications:
1. Blood dyscrasias.
2. Cutaneous infection at the site most feasible for peri­ Figure 38.2: Echocardiogram showing fluid in pericardial space
cardiocentesis. (marked by star) (Courtesy: Dr Gunda Srinivas)
376 Section XII n Procedures

●● Position the patient in a semirecumbent position at a


30°–45° angle. This position ensures that the heart is
closer to the anterior chest wall.
IP : 196.52.84.10
●● Take universal precautions.
●● Clean the area with antiseptic solution (Figure 38.3).

Figure 38.5: Pericardial cavity entered by needle

●● Connect 20 mL or 50 mL syringe to needle and aspirate.


Slowly advance needle until a return of fluid is visualized
or you notice ECG changes (arrhythmia) (Figure 38.6).

Figure 38.3: Preparation of patient for pericardiocentesis

●● Infiltrate with local anesthetic solution at the site by


first creating a skin wheal and then infiltrating the sub-
cutaneous and deeper tissues.
●● Enter the skin 1 cm to the left and inferior to the xiphoid
process at 45° angle to the skin (Figure 38.4 and 38.5).

Figure 38.6: Pericardial fluid being aspirated

●● Withdraw as much fluid as possible attaching a 3-way


stopcock. When the syringe is filled, stabilize the
needle, remove the filled syringe and replace it with
another one (Figure 38.7).

Figure 38.4: Site of insertion of needle

If the subxiphoid approach might be difficult (due to an


unusually located heart or elevated diaphragm), consider Figure 38.7: Pericardial fluid being aspirated through catheter
preparing the left sternal border. under ECHO guidance (Courtesy: Dr Gunda Srinivas)
Chapter 38 n Pericardiocentesis 377

●● Remove the needle, when fluid can no longer be aspi-


rated (pericardial fluid does not clot).
Key Points
ü
●● Apply dressing overIPthe: 196.52.84.10
site. 1. Take care of the ABCs during the pericardiocente-
●● Continue monitoring hemodynamic status. sis.
2. Always connect the child to the ECG monitor to vi-
●● Confirm resolution of pericardial effusion by ultra-
sualize electrical changes during the procedure.
sonogram.
3. Provide adequate pain relief and sedation.
●● Send pericardial fluid aspirated for relevant investiga-
tions.

Complications
common errors
1. Improper position of patient.
û
●● Dysrhythmias. 2. Delaying pericardiocentesis can cause obstructive
●● Damage to vascular structures. shock, which will not improve with fluids or ino-
●● Hemothorax and pneumothorax. tropes.
●● Pneumopericardium. 3. Delay in relieving pericar­dial effusion urgently, can
●● Hepatic injury. often result in constrictive peri­carditis.
●● Reaccumulation of pericardial fluid.
39
IP : 196.52.84.10

Cannulation of External Jugular Vein

The external jugular vein, a large peripheral vein, offers Contraindications


quick access to the central circulation when other smaller
●● Infection over the insertion site.
veins have collapsed and central venous (internal jugular,
●● Lack of anatomic landmarks due to neck size, shape or
subclavian or femoral) access could not be obtained im- deformities.
mediately (Figure 39.1). ●● Suspected or proven fracture of the cervical spine.
●● Bleeding diathesis.
Indications ●● Unsuccessful attempt at insertion with resultant hema-
toma.
●● Venous access when other peripheral veins are col-
lapsed especially in a shocked child. equipments
●● Placement of a large-bore venous catheter (16–20
gauge) in an emergent situation to deliver fluid, blood ●● Universal precaution.
products and inotropes. ●● Tape and dressings.

Figure 39.1: Anatomical landmark of external jugular vein and cannulation; lower head position (by 10°–20°) than thorax by
placing a towel under the spine.
Chapter 39 n Cannulation of External Jugular Vein 379

●● Lidocaine (4%). the shoulder on the same side. Advance the cannula,
●● Syringe (5 cc) and 25 gauge needle. while simultaneously applying suction.
●● 10% betadine solution
IP :and chlorhexidine wipes or al-
196.52.84.10 ●● When a flash of blood returns, advance the catheter
cohol swab. over the needle and remove the needle.
●● Large bore IV catheter over needle (16–20 gauge). ●● Attach the IV tubing to the catheter and secure the
●● IV fluid and IV tubing. catheter to the neck with transparent dressing or dy-
naplast. Turn on the IV fluids to ascertain that there is
Procedure good flow.

●● Use universal precautions and sterile technique. Complications


●● Attach the IV tubing to the IV fluids and place at the
bedside on the IV pole. ●● Local hematoma.
●● Laceration of the deeper internal jugular vein.
●● Place the patient in a Trendelenburg position (10°–20°
●● Infection.
head down) to enable of neck vein and also to reduce
●● Air embolism: Place the patient in the left lateral decu-
risk of air embolism.
bitus in the head down position to minimize the chance
●● Place the roll along the axis of the spine such that the of an air embolism.
child’s neck is hyperextended.
●● Turn the patient’s head away from the side chosen for
insertion.
Key Points
ü
1. Position the head such that it is 10°–20° below the
●● Prepare and drape the entire side of the neck chosen. level of the chest.
●● Identify the vein. Usually, the vein can be visualized 2. Cover the hub of the angiocath to avoid air embo-
running from the angle of the mandible inferolaterally lism.
to the clavicle, crossing the sternocleidomastoid mus- 3. Stringent aseptic precautions need to be taken.
cle above the clavicle. 4. No blind sticks. If you cannot see it, do not stick it.
●● If not visualized, occlude the vein by placing the in-
dex finger of your left hand in the supraclavicular
space parallel to the long axis of the clavicle. This
will result in engorgement of the vein enabling better
visualization. 1.
common errors
Improper position of patient.
û
2. Improper selection of patient.
●● Simultaneously, stretch the overlying skin with the
thumb of the same hand. With the bevel of the needle 3. Inadequate fixation of the IV catheter.
facing upward, puncture the skin at an angle of 30°. 4. Use of local anesthetics, which may be harmful, if
injected into the superficially placed external jugu-
●● The needle-tip should enter midway between the clavi-
lar vein.
cle and angle of mandible and should be aimed towards
40
IP : 196.52.84.10

Foley Catheter Insertion

Indications ●● Generously coat the distal portion (2–5 cm) of the cath-
eter with lubricant.
●● Monitoring of urine output in a child with hemody-
namic compromise.
●● Acute urinary retention.

Equipments

Figure 40.2: Insertion of Foley catheter

●● If female, separate labia using non-dominant hand.


●● If male, hold the penis with the non-dominant hand.
Maintain hand position until preparing to inflate bal-
Figure 40.1: Bladder catheterization tray
loon. Lift the penis to a position perpendicular to pa-
●● Universal precautions. tient’s body and apply light upward traction (with non-
●● Sterile gloves. dominant hand).
●● Sterile drapes. ●● Using dominant hand to handle forceps, cleanse peri-
●● Cleansing solution, e.g. povidone iodine.
urethral mucosa with povidone iodine. Clean anterior
●● Cotton swab forceps.
to posterior, inner to outer, one swipe per swab, discard
●● Sterile water (usually 10 cc).
swab away from sterile field.
●● Foley catheter (according to age), syringe (usually 10 cc),
lubricant (lignocaine jelly). ●● Pickup catheter with gloved (and still sterile) dominant
●● Collection bag and tubing (Figure 40.1). hand. Hold end of catheter loosely coiled in palm of
dominant hand.
Procedure ●● Identify the urinary meatus and gently insert until 1–2
inch beyond where urine is noted.
●● Get written consent.
●● Strict aseptic precautions. ●● Inflate balloon, using correct amount of sterile liquid
●● Position the patient supine; males with legs extended (usually 10 cc, but check actual balloon size).
and females with frog-leg posture (Figure 40.2). ●● Gently pull catheter until inflation balloon is snug
●● Choose age-appropriate catheter. against bladder neck.
Chapter 40 n Foley Catheter Insertion 381

●● Connect catheter to drainage system.


●● Secure catheter to abdomen or thigh, without tension
Key Points
ü
on tubing. IP : 196.52.84.10 1. Choose size based on weight and age of the child as
●● Place drainage bag below the level of bladder. per the ready reckoner.
●● Evaluate catheter function and amount, color, odor and 2. Push the Foley until the bifurcation is reached and
quality of urine. inflate with distilled water. Pull gently such that the
●● Remove gloves, dispose of equipment appropriately, bulb is seated on the neck of the bladder.
wash hands. 3. If correctly placed, urine will start filling the uro
●● Document the size of catheter inserted, amount of wa- bag. Do check ultrasound, if the catheterization is
ter in balloon, patient’s response to procedure and as- dry.
sessment of urine. 4. Distal end should be strapped to the medial aspect of
the thigh.
Contraindications
●● Urethral trauma.
●● Urethral stricture. common errors
û
Complications 1. Failing to insert the Foley up to the bifurcation in
male children and prematurely inflating the balloon
●● Trauma and bleeding. can cause ureteral rupture.
●● Infection. 2. Confusion and erroneous passage of catheter into
●● Creating false track. vagina in the female child.
●● Renal inflammation. 3. Failing to retract prepuce and clean well with Beta-
●● Pyelonephritis (if left in for prolonged periods). dine in a male child.
Catheter not draining/patient oliguric 4. Using smaller tubes can cause urinary leak and am-
moniacal dermatitis.
●● Check catheter/tubing not kinked. 5. Using larger tubes can traumatize and lead to stric-
●● Check catheter is still secured to patient leg and has not ture urethra.
migrated out of bladder.
●● Checking patency by irrigating catheter with 2–3 mL
of sterile 0.9% normal saline. Do not use force to instill REFERENCES
fluid. This is an aseptic procedure.
1. Gary R Fleisher, Stephen Ludwig. Text Book of Pediatric
Catheter leaking Emergency Medicine. 6th edition. Lippincott Williams &
●● Remove catheter. If indication for bladder catheteriza- Wilkins.
tion remains, then follow insertion procedure with new 2. Christopher King. Text Book of Pediatric Emergency Pro-
cedures. 2nd edition. Lippincott Williams & Wilkins.
catheter.
41
IP : 196.52.84.10

Spinal Stabilization

Cervical spine injuries occur in about 2% of patients with Other situations that mandate cervical spine immobi-
polytrauma. Since the consequences of cervical cord in­ lization:
jury are devastating, stabilization of the cervical spine
●● Unconscious child with significant injury.
should be continued along with immobilization of the en­ ●● Any child who has suffered traumatic respiratory arrest.
tire spinal column, while attending to the ABCs of trauma ●● Preverbal children (should automatically be considered
resuscitation. While head and facial injuries (due to rela­ high risk).
tively large head) are common in children, soft tissue, neck ●● Trauma associated with abnormal neurological exami­
and airway injuries are thankfully uncommon due to the nation.
shorter, protected neck. ●● Alert child with neck pain/tenderness/restricted neck
All trauma patients with a cervical spinal column in­ movements.
jury or with a mechanism of injury having the potential to ●● Polytrauma with significant ‘distracting’ injury (anoth­
cause cervical spine injury should be immobilized at the er injury, which may ‘distract’ the patient from com­
scene, throughout extrication, transport and transfer. plaining about a possible spinal injury).

Manual Stabilization of the Cervical Spine


STEPS IN SPINAL STABILIZATION
●● Manually immobilize the head and neck in neutral po­
●● Manual stabilization of cervical spine. sition as the first step.
●● Cervical collar application.
●● Maintain a clear airway with jaw thrust or head tilt (if
●● Immobilizing the entire spine.
jaw thrust is not achievable) if patient is unconscious or
has breathing difficulties.
Cervical Spine Stabilization is
●● Limit side to side movement of the head.
Recommended in the Following Situations ●● Manually stabilize the cervical spine, whether the pa­
Dangerous mechanisms of injury: tient is lying/sitting/standing (Figures 41.1A and B).
●● Fall from a height of ≥ 1 meter or 5 stairs.
●● Axial load to head.
Ù
Even after application of cervical collar, maintain
●● Injury sustained in a high speed motor vehicle (crash/ manual stabilization until securing the victim to the
roll over/ejection). spinal board.
●● Injury sustained, while using motorized recreational
vehicles.
●● Bicycle collision.
Technique of Manual Stabilization
●● Struck by motor vehicle. ●● Spread your fingers across the side of the child’s head
●● Diving and submersion injuries. to obtain maximum contact.
●● Sports injuries. ●● Stabilize your hands by resting your elbows firmly on
●● Objects falling over head accidentally indoor/outdoor the ground (supine position) or by locking the elbows.
Chapter 41 n Spinal Stabilization 383

IP : 196.52.84.10

Figures 41.1A and B: Steps of manual cervical spine stabilization (Courtesy: Dr Radhika R)
●● Align the head in the neutral position and fit the cervi­ ●● If patient is seated, apply chin support first and then
cal collar (The external acoustic meatus must be in line fasten the collar.
with the anterior shoulder). ●● Maintain neutral position of head throughout the pro­
cedure.
Ù
Trapezius grip or Vice grip are the other techniques of
Immobilizing the Entire Spine
manual stabilization.
●● If the patient is prone, log roll patient to the supine po­
sition.
Selection and Fixing of Appropriate
Cervical Collar Log Rolling
1. Use spinal immobilization devices to achieve spinal
stability during extrication and transport.
2. Use a combination of:
●● Rigid cervical collar immobilization.
●● Supportive blocks on either side of the head.
●● Rigid back board with straps to secure the entire
body of the patient (Figure 41.3).

Figure 41.2: Applying cervical collar


●● Examine neck for hematomas/subcutaneous emphy­
sema/open wounds/tracheal shift.
●● Avoid flexion or hyperextension of neck.
●● Measure distance between top of shoulders and bottom
of chin.
●● Single or two piece hard collar can be used.
●● Tallest collar that does not hyperextend the neck is
most appropriate.
●● Assemble the collar and slide collar behind neck with
Velcro folded (to avoid Velcro attachment to child’s
clothing or hair) and fit the chin piece (Figure 41.2). Figure 41.3: Log rolling (Courtesy: Dr Radhika R)
384 Section XII n Procedures

All three methods in combination are needed to limit lowed out or a blanket is placed under the torso, there­
motion of the cervical spine effectively. by maintaining a neutral position of the head and neck
IP : 196.52.84.10 (Figures 41.5A and B).
Cervical Spine Immobilization
Ù
Cervical spine immobilization using sandbags and tape
alone is not recommended.

1. Secure the patient preferably in the supine position to


a long hard spine board by tape or straps across bony
points (Figure 41.4).
●● Forehead.
●● Chin.
●● Bony prominences of the shoulders, pelvis and ex­
tremities.
●● Chest straps.
Figures 41.5A and B: Spine board maintaining neutral position
●● Hip and leg straps. of head and neck (reproduced from Copley LA, Dorman’s
All are secured in that order to minimize cervical JP: Cervical spine disorders in infants and children Am Acad
spine mobility. Orthop Surg. 1998;6: 204-14).
2. Assess the straps periodically for adequate and safe
restraint.
3. In the event of that the child needs to vomit, the back­ Airway Management
board may be rapidly rotated 90°, while the patient Immobilization techniques may agitate and distress the
remains fully immobilized in a neutral position. child, thus increasing movement of the cervical spine. It
4. Provide analgesia, if patient has been lying on a hard is important to be gentle, but firm and institute manual re­
backboard for an extended period. straint first. The presence of parents and close relatives is
5. For victims in sitting or standing position, cervical vital to calm the child.
collar application and spine immobilization should be
done in the same position using techniques for manual If immobilization attempts appear to cause more move­
cervical spine stabilization and sliding the spine board. ment of the cervical spine, than if it is not applied, abandon
attempts.
1. While managing the airway in the setting of spinal
cord injury, maintain the cervical spine in neutral
alignment at all times.
2. Clear oral secretions and/or debris to maintain airway
patency and to prevent aspiration.
3. Use modified jaw thrust and insertion of an oral airway
or intubation, as required to maintain airway patency.
4. Failure to intubate when needed, due to the potential
risk of worsening cervical cord injury must be avoid­
ed.
5. Open cervical collar anteriorly and maintain manu­
al inline spinal stabilization to facilitate mandibular
Figure 41.4: Spine stabilization (Courtesy: Dr Radhika R) movement for intubation (Figures 41.6A and B).
6. Occiput in infants and toddlers is prominent. Hence, 6. Secure surgical airway through the opening in the an­
ensure that the head end of the spine board is hol­ terior part of the collar, if situation warrants.
Chapter 41 n Spinal Stabilization 385

3. Imaging the spine does not take precedence over life-


saving diagnostic and therapeutic procedures.
IP : 196.52.84.10 Box 41.1: Preconditions that rule out cervical spine injury

The following history rules out cervical cord injury:


• Fully alert and orientated
• No head injury
• No drugs or alcohol
• No neck pain
• No abnormal neurology
• No significant other ‘distracting’ injury (another injury,
which may ‘distract’ the patient from complaining
about a possible spinal injury)

If these preconditions are met, the neck may be exam­


ined (Box 41.1).
If there is no bruising, deformity or tenderness and a
pain free range of active movements, the cervical spine can
be cleared.
It is important to remember that children are at in­
creased risk for traumatic cervical instability with no os­
seous injury [Spinal cord injury without radiological ab­
normality (SCIWORA)].

Order Lateral Cervical Spine X-ray


The lateral cervical spine X-ray can be difficult to inter­
pret:
1. Alignment.
2. Bone.
Figures 41.6A and B: Manual stabilization of cervical spine 3. Cartilage and joints.
during intubation. 4. Soft tissue.

Problems During Cervical Pitfalls in Cervical Spine Radiology


Spine Immobilization 1. SCIWORA
●● Worsening of injury due to application of collar in a ●● Spinal cord injury without radiological abnormality
struggling child. may occur in 20%–30% of younger children due to
●● Worsening of injury due to incorrect size of collar. increased ligamentous laxity, relatively large head,
●● Limited access to internal/external jugular vein. poorly developed cervical musculature, anterior
●● Limited visualization of neck injury/hematoma/subcu­ wedging of vertebral bodies, vulnerable growth zones
taneous emphysema/distorted anatomy. at vertebral end-plates and shallow facet joints.
2. Physeal lines.
Spinal Clearance ●● Physeal lines may give the appearance of fractures.
3. Psuedosubluxation.
1. Spinal immobilization is a priority in multiple trauma. ●● C2/C3 and C3/C4.
2. The spine should be assessed and cleared after taking Cervical spinal immobilization devices should be re­
into account, the severity of injury, neurological defi­ moved as soon as definitive evaluation is accomplished
cits and physi­ological status of the ABCs. and/or definitive management is initiated.
386 Section XII n Procedures

son Textbook of Pediatrics, 19th edition. Chapter 66. USA:


Key Points
ü 4.
Saunders;10 Jun 2011 ISBN: 9781437707557.
Fred M Henretig, Christopher King. Textbook of Pediat­
1. Consider cervical IP
spine precautions and spinal im­
: 196.52.84.10
mobilization in trauma victims. ric Emergency Procedures. 2nd Revised edition. Wolters
2. 3–4 trained personnel are needed to perform these Kluwer/Lippincott Williams and Wilkins; United States:
2007.
maneuvers.
3. C-spine precautions may withdrawn only after com­ 5. Joseph JT, Mary EF, Thomas M. Trauma. APLS: The Pe­
diatric Emergency Medicine resource. American Academy
plete neurological and radiological clearance.
of Pediatrics. American College of Emergency Physicians.
4. The purpose of spinal immobilization is prevent Jones & Bartlett Learning; USA: 4th edition; 2007. pp.
secondary quadriplegia or paraplegia. 274-75.
6. Julie L, Jeffry RL, Gary RS, et al. Pediatric cervical spine
common errors
û
1. Trauma victims being carried into hospitals by par­
injry. Pediatric emergency medicine, 3rd edition. Section
iv . Chapter 30.USA: McGraw-Hill; 2011.
7. American association of neurological surgeons (Spine Uni­
ents. verse homepage). Management of Pediatric Cervical Spine
2. Lack of trained manpower results in panic and fail­ and Spinal Cord Injuries. The Spine Section of the AANS
ure to follow protocols. and CNS 2012. www.spineuniverse.com/professional/
3. Failing to provide spinal stabilization (starting at the acute-cervical-spine-injury-guide.
site of accident). 8. Gary RF, Stephen Ludwig. Textbook of Pediatric Emer­
gency Medicine, 6th edition. Philadelphia: Wolters Klu­
wer/Lippincott Williams & Wilkins; 2010. ISBN-13:978-
REFERENCES 1-6054-7159-4.
9. Initial assessment of spinal injury, Spinal injury assessment
1. Jeremy Dewall. The ABCs of TBI. Evidence-based guide­ and clearance, 2002. Trauma.org. (Internet) www.trauma.
lines for adult traumatic brain injury care. JEMS a journal org/archive/spine/spine-conscious.htm
of emergency medical services. 2010;35(4):54-61.
10. Christopher WR. Pediatric Spine Trauma. J Bone Joint
2. Hadley MN, Walters BC, Grabb PA, et al. Management of Surg Am. 2007; 89(suppl 1) :98-107 doi:10.2106/
pediatric cervical spine and spinal cord injuries, Neurosur­ JBJS.F.00244.
gery. 2002; 50:S85-99. 11. Australian Life Saving Academy. Australian lifesaving
3. Cindy GR, Peter SD, Bruce L, Klein. Acute care of the academy learners guide IRB crew certificate. SLSA Ver­
victim of multiple trauma.In: Robert M, Kliegman, Bonita, sion. 2011. Pg 11 www.tamaramaslsc.org/twiki/bin/view­
Stanton, Joseph SG, Nina Schor, Richard EB (Eds). Nel­ file/IrbTraining.guide.
Appendices
IP : 196.52.84.10
IP : 196.52.84.10
IP : 196.52.84.10
Appendices

Appendix 1: VITAL SIGNS AND EQUIPMENTS


Age (kg) Resp. Heart Systolic ET ET Laryngo- Suction NGT Foley Chest
rate rate BP tube size* tube scope catheter (Fr) (Fr) tube (Fr)
distance blade
at lip
Preemie (1–2) 30–60 90–180 50–70 2.5–3.0 8 0 5–6 5 5 8–10
New born (3.5) 30–60 90–180 50–70 3.0–3.5 8–9.5 1 6 8 5 8–10
6 month (7) 24–40 85–170 65–106 3.5–4 9.5–11 1 8 8 5 12–16
1 year (10 20–40 80–140 72–110 4.0–4.5 11–12.5 2 8 10 8 14–20
3 year (15) 20–30 70–120 78–114 4.5–5.0 12.5–14 2 8 10 10 18–22
6 year (20) 18–25 65–110 80–116 5.0–5.5 14–15.5 2 10 12 10 20–28
8 year (25) 18–25 70–110 84–122 6.0–6.5 (cuff ) 17–18.5 2 10 12 10 28–32
10 year (30) 16–20 65–110 90–130 6.5–7.0 (cuff ) 18.5–20 3 12 14 12 28–32
12 year ( 40) 14–20 60–110 94–136 7 (cuff ) 20 3 12 4 12 28–32
15 year (50) 12–20 55–100 100–142 7.0–7.5 (cuff ) 20–21.5 3 12 16 14 32
ET selected in Indian children should be 0.5 size lesser than that recommended by PALS guidelines
*

Appendix 2: EMERGENCY INFUSIONS TITRATED TO PATIENTS RESPONSE


Medication Preparation Dose
Epinephrine 0.6 × body weight (kg) 1 mL/h delivers 0.2 μg/kg/min
(1:1,000) equals mg to add to 50 mL D5W/NS (0.2–2 μg/kg/min IV Infusion)
Norepinephrine 0.6 × body weight (kg) 1 mL/h delivers 0.2 μg/kg/min
equals mg to add to 50 mL D5W/NS (0.2–2 μg/kg/min IV Infusion)
Dopamine 6 × body weight (kg) 1 mL/h delivers 2 μg/kg/min
Dobutamine equals mg to add to 50 mL D5W/NS (5–20 µg/kg/min infusion)
Lignocaine (1%) 60 mg × body weight (kg) 1 mL/h delivers 20 μg/kg/min
equals mg to add in 50 mL D5W (15–50 µg/kg/min)
Prostaglandin E1 (alprostadil) 1 vial (500 mg) added to 0.1 mL/kg/h delivers 0.01 µg/kg/min
99 mL D5W yielding 5 μg/mL (0.05–0.1 µg/kg/min)
390 Appendices

Appendix 3: ANESTHETIC AGENTS USED TO ASSIST INTUBATION


a. Hemodynamically stable*
IP : 196.52.84.10
Medication Dose Route Comments
Fentanyl 2–5 μg/kg IV Slow push over 3–5 minute, flush
well.
Midazolam 0.05–0.2 mg/kg IV Slow push, flush well.
Rocuronium 1 mg/kg IV Quick push. Ventilation must be
supported.
Vecuronium 0.1–0.2 mg/kg IV
Normal BP for age, normal mental status, good perfusion
*

b. Hemodynamically unstable*
Medication Dose Route Comments
Etomidate or Ketamine 0.3 mg/kg; 1–2 mg/kg IV Not with raised ICP.
Midazolam ( not needed if Etomidate is used) 0.1 mg/kg IV Slow push, flush well.
Rocuronium or Vecuronium 1 mg/kg; 0.1–0.2 mg/kg IV Quick push, ventilation must be supported.
Abnormal BP for age, abnormal mental status, poor perfusion
*

c. Hemodynamically stable, suspected increased ICP


Medication Dose Route Comments
Lidocaine 1 mg/kg IV
Thiopental or Etomidate 5 mg/kg; 0.3 mg/kg IV
Rocuronium or Vecuronium 1 mg/kg; 0.1–0.2 mg/kg IV Quick push, ventilation must be supported.

Appendix 4: SEIZURES
Medication Dose Route Comments
Diazepam 0.1–0.3 mg/kg IV, IO Max rate = 1 mg/min
(Valium) 0.5 mg/kg initial Rectal Push over 5 minute
0.25 mg/kg subsequent
Lorazepam (Activan) 0.05–0.1mg/kg IV Slow push over 2 minute
Phenobarbital 20 mg/kg IV Max dose = 500 mg/kg
Push over 5 minute
Phenytoin 15–20 mg/kg, slow over IV Max dose = 1 g
20–30 min Max rate = 1 mg/kg/min
Levetiracetam 20–30 mg/kg at 5 mg/kg/min IV Max dose = 3 g
Sodium valproate 15–20 mg/kg at 5 mg/kg/min IV Max dose = 40 mg/kg
Infusion = 1–4 mg/kg/h
Midazolam 0.1–0.2 mg/kg IV, PR Max dose = 0.15 mg/kg
Infusion = 1 μg/kg/min to max
30 μg/kg/min


Fluid Replacement, Electrical Intervention, Resuscitation Medications 391

Appendix 5: FLUID REPLACEMENT


Age Fluid bolus in shock Packed Red Blood Cells
IP : 196.52.84.10 NS/RL* (10 mL/kg)
(20 mL/kg)
Preemie 10–20 (10 mL/kg) 5–10 (mL/kg)
New born 35 (10 mL/kg) 17 (5 mL/kg)
6 month 140 70
1 year 200 100
3 year 300 150
6 year 400 200
8 year 500 250
10 year 500 300
12 year 500 400
15 year 500 500
5–10 mL/kg of fluid boluses can be given to titrate response
*

Appendix 6: ELECTRICAL INTERVENTION


Initial No response
Defibrillation 2.0 Joule/kg 4.0 Joule/kg
Cardioversion 0.5–1.0 Joule/kg 1.0–2.0 Joule/kg

Appendix 7: RECUSCITATION MEDICATIONS


Age (kg) Epinephrine Atropine Bicarbonate Glucose Lidocaine 2% Crystalloid
1:10,000 0.1 mg/mL (1meq/l) (0.5 mL/kg) Bolus

Preemie(1–2) 0.2 mL 1 mL 2 mL (4.2%) 5 mL (D10) 0.1 mL 20 mL


New born (3.5) 0.35 mL 1 mL 3.5 mL (4.2%) 10 mL (D10) 0.18 mL 35 mL
6 month (7) 0.7 mL 1.4 mL 7 mL 14 mL (D25) 0.35 mL 140 mL
1 year (10) 1 mL 2 mL 10 mL 20 mL (D25) 0.5 mL 200 mL
3 year (15) 1.5 mL 3 mL 15 mL 30 mL (D25) 0.75 mL 300 mL
6 year (20) 2 mL 4 mL 20 mL 40 mL (D25) 1 mL 400 mL
8 year (25) 2.5 mL 5 mL 25 mL 50 mL (D25) 1.25 mL 500 mL
10 year (30) 3 mL 6 mL 30 mL 30 mL (D50) 1.5 mL 500 mL
12 year (40) 4 mL 8 mL 40 mL 40 mL (D50) 2 mL 500 mL
15 year (50) 5 mL 10 mL 50 mL 50 mL (D50) 2.5 mL 500 mL
392 Appendices

Appendix 8: DRUGS AND DOSAGES

IP : 196.52.84.10
DRUGS USED IN PEDIATRIC EMERGENCIES
Activated charcoal 1–2 g/kg through NG tube
Adenosine SVT
0.1 mg/kg IV/IO rapid push (ma× 6 mg), 0.2 mg/kg IV/IO rapid push (max 12 mg)
Albumin Shock, Trauma, Burns
0.5–1 g/kg (10–20 mL/kg of 5% solution) IV/IO rapid infusion
Albuterol Asthma, Anaphylaxis (bronchospasm), Hyperkalemia
(Salbutamol) MDI : 4–8 puffs INH q 20 min PRN with spacer (OR ET if intubated)
Nebulizer: 2.5 mg/dose (weight < 20 kg) OR 5 mg/dose (weight > 20 kg) INH q 20 minute PRN
Continuous nebulizer: 0.5 mg/kg/h INH (max 20 mg/h)
Alprostadil (PGE1) Ductal-dependent Congenital Heart Diseases (all forms)
0.05–0.1 µg/kg/min IV/IO infusion initially, then 0.01–0.05 µg/kg/min IV/IO
Amiodarone SVT, VT ( with pulses)
5 mg/kg IV/IO load over 20–60 minute (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g)
Pulseless Arrest (i.e. VF/pulseless VT)
5 mg/kg IV/IO bolus (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g)
8–10 vials in 100 mL NS over 1–2 hour (max 20 vials)
Aminophylline Refractory Near Fatal asthma
5 mg/kg loading (1 mg/kg/h IV infusion)
Antisnake venom Snake bite with signs of envenomation
8–10 vials in 100 mL NS over 1-2 hour (maximum 20 vials)
Atropine sulfate Bradycardia (symptomatic)
0.02 mg/kg IV/IO (min dose 0.1 mg, max single dose child 0.5 mg, max single dose adolescent 1 mg),
may repeat dose once, max total dose child 1 mg, max total dose adolescent 2 mg
0.04–0.06 mg/kg ET
Toxin overdose (e.g. organophosphate, carbamate)
0.02–0.05 mg/kg (<12 year) OR 0.05 mg/kg (> 12 year) IV/IO initially, repeat q 20–30 minute until
atropine effect (dry mouth, tachycardia, mydriasis) is observed or symptoms reverse
Blood 10 mL/kg over 4 hour
Calcium gluconate Hypocalcemia, Hyperkalemia, Hypermagnesemia, Calcium Channel Blocker Overdose
10% 200 mg/kg (0.2 mL/kg) IV/IO slow push during arrest or if severe hypotension, repeat PRN
Dexamethasone Croup
0.6 mg/kg PO/IM/IV (max 16 mg)
Dextrose Hypoglycemia
(Glucose) 0.5–1 g/kg IV/IO (D25 W 2–4 mL/kg; D10 W 5–10 mL/kg)
Diazepam 0.05–0.3 mg/kg, (Max < 5 year: 5 mg; 5 year: 10 mg) PR: 0.5 mg/kg, Infusion: 0.1 mg/kg/min
Diphenhydramine Anaphylactic Shock
1–2 mg/kg IV/IO/IM q 4–6 hour (max 50 mg)
Congestive Heart Failure, Cardiogenic Shock
2–20 µg/kg/min IV/IO infusion; titrate to desired effect
Dopamine Cardiogenic Shock, Distributive Shock
5–20 µg/kg/min IV/IO infusion; titrate to desired effect

Contd...
Drugs Used in Pediatric Emergencies 393

Contd...
DRUGS USED IN PEDIATRIC EMERGENCIES
Epinephrine IPPulseless
: 196.52.84.10
Arrest, Bradycardia (symptomatic)
0.01 mg/kg (0.1 mL/kg) 1:10, 000 IV/IO q 3–5 minute (max 1 mg; 1 mL)
0.1 mg/kg (0.1 mL/kg) 1:1,000 ET q 3–5 minute
Hypotensive Shock
0.1–1 µg/kg/min IV/IO infusion (consider higher doses if needed)
Anaphylaxis
0.01 mg/kg (0.01 mL/kg) 1:1,000 IM in thigh q 15 minute PRN (max 0.5 mg) or
Auto-injector 0.3 mg (weight ≥ 30 kg) IM or Child Jr Auto-injector 0.15 mg (weight 10–30 kg) IM
0.01 mg/kg (0.1 mL/kg) 1:10,000 IV/IO q 3–5 minute (max 1 mg) if hypotension
0.1–1 µg/kg/min IV/IO infusion in hypotension despite fluids and IM injection
Asthma
0.01 mg/kg (0.01 mL/kg) 1:1,000 SQ q 15 minute (max 0.5 mg; 0.5 mL)
Croup
0.25–0.5 mL racemic solution (2.25%) mixed in 3 mL NS INH OR 3 mL 1:1,000 INH
Epinephrine Toxins/overdose (e.g. β- adrenergic blocker, calcium channel blocker)
(continued) 0.01 mg/kg (0.1 mL/kg) 1:10,000) IV/IO (max 1 mg); if no response consider higher doses up to 0.1 mg/
kg (0.1 mL/kg) 1: 10,000 IV/IO
0.1–1 µg/kg/min IV/IO infusion (consider higher doses)
Fos-phenytoin Status Epilepticus refractory to 2 doses of benzodiazepines
20–30 mg/kg, IV, IM, 5 mg/kg/min (Max: 225 mg/min), [7.5 mg of Fos-phenytoin ~ 5 mg of Phenytoin]
Furosemide Pulmonary Edema, Fluid Overload
1 mg/kg IV/IM (usual max 20 mg if not chronically on loop diuretic)
Hydrocortisone Adrenal Insufficiency
2 mg/kg IV bolus (max 100 mg)
Inamrinone Myocardial Dysfunction and Increased SVR/PVR
Loading dose: 0.75–1 mg/kg IV/IO slow bolus over 5 minute (may twice to max 3 mg/kg), then 5–10 µg/
kg/min IV/IO infusion
Ipratropium Life-threatening asthma
Bromide 250–500 µg INH q 20 minute PRN × 3
Labetolol 0.25–0.5 mg/kg IV over 2 minute, can be repeated every 10 minute if required
Lidocaine VF/Pulseless VT, Wide-Complex Tachycardia (with pulses)
1 mg/kg IV/IO bolus
Maintenance: 20–50 µg/kg/min IV/IO infusion (repeat bolus dose if infusion initiated > 15 minute after
initial bolus) 2–3 mg/kg ET
Levetiracetam Refractory Status epilepticus, SE complicated with cardiac dysfunction
20–30 mg/kg IV at 5 mg/kg/min (maximum, 3 g) Intravenous
NGT route if IV preparation not available
Lorazepam 0.05–0.1 mg/kg (Max: 4 mg) IV Infusion: 0.1–0.01 mg/kg/h
Magnesium sulfate Asthma (refractory status asthmaticus), Torsades de Pointes, Hypomagnesemia
25–50 mg/kg IV/IO bolus (pulse less VT) or over 10–20 minute (VT with pulses) OR slow infusion over
15–30 minute (status asthmaticus) (max 2g)

Contd...
394 Appendices

Contd...

DRUGS USED IN PEDIATRIC EMERGENCIES


IP : 196.52.84.10
Mannitol 20% 0.25–0.5 g/kg/dose (1.25–2.5 mL/kg/dose) IV every 8 hour

Methylprednisolone Asthma (Status asthmaticus), Anaphylactic Shock


Load: 2 mg/kg IV/IO/IM (Max 80 mg) use acetate salt
Maintenance: 0.5 mg/kg IV/IO q 6 hour (max 120 mg/d)
Midazolam Seizures (pre-hospital), initial management of status epilepticus, Refractory SE
0.1–0.2 mg/kg (Max: 0.15 mg/kg) IV, PR, infusion 1 μg/kg/min to max 30 μg/kg/min
Milrinone Myocardial Dysfunction and Increased SVR/PVR
Loading dose: 50–75 µg/kg IV/IO over 10–60 minute followed by 0.5–0.75 µg/kg/min IV/IO infusion
Morphine 0.1–0.2 mg/kg/dose IV
Naloxone Narcotic (opiate) Reversal
Total reversal required (for narcotic toxicity secondary to overdose): 0.1 mg/kg IV/IO/IM/SQ bolus q 2
minute PRN (max 2 mg)
Total reversal not required (e.g. for respiratory depression associated with therapeutic narcotic user):
1–5 µg/kg IV/IO/IM/SQ; titrate to desired effect
Maintain reversal: 0.002–0.16 mg/kg/h IV/IO infusion
Neostigmine 0.05 mg/kg/dose IV
Nitroglycerin Congestive Heart Failure, Cardiogenic Shock
0.25–0.5 µg/kg/min IV/IO infusion, may increase by 0.5–1 µg//kg/min q 3–5 minute PRN to 1–5 µg/kg/
min (max 10 µg/kg/min)
Adolescents: 10–20 µg/min, increase by 5–10 µg/min every 5–10 minute PRN to max 200 µg/min
Norepinephrine Vasodilatory shock refractory to fluids and dopamine
0.1–2 µg/kg/min IV/IO infusion; titrate to desired effect
Oxygen Hypoxia, Hypoxemia, Shock, Trauma, Cardiopulmonary Failure, Cardiac Arrest
Administer 100% O2 via high-flow O2 delivery system (if spontaneous ventilations) or ET (if intubated);
titrate to desired effect
Phenytoin Status Epilepticus refractory to 2 doses of benzodiazepines
15–20 mg/kg (Max: 1 g) Slow IV over 20–30 minute @ 1mg/kg/min Max : 50 mg/min
Phenobarbitone Refractory status epilepticus, Neonatal status epilepticus
15–20 mg/kg up to max 1 g/dose IV, 1 mg/kg/min up to a maximum of 60 mg/min
Procainamide SVT, Atrial Flutter, VT (with Pulses)
15 mg/kg IV/IO load over 30–60 minute (do not use routinely with amiodarone)
Pralidoxime 25–50 mg/kg/dose IV
Prazosin 30 μg/kg/dose PO
Sodium bicarbonate Metabolic Acidosis (servere), Hyperkalemia
1 mg/kg IV/IO slow bolus
Sodium Channel Blocker Overdose (e.g. tricyclic antidepressant)
1–2 mEq/kg IV/IO bolus until serum pH is > 7.45 (7.50–7.55 for severe overdose) followed by IV/IO
infusion of 150 mEq NaHCO3/L solution to maintain alkalosis
Sodium nitroprusside Cardiogenic Shock (i.e. associated with high SVR), Severe Hypertension
1–8 µg/kg/min (weight < 40 kg) OR 0.1–5 µg/kg/min (weight > 40 kg) Iv/IO infusion
Sodium valproate Refractory status epilepticus
15–20 mg/kg up to max 40 mg/kg IV 5 mg/kg/min infusion: 1–4 mg/kg/h
Terbutaline Asthma (status asthmaticus), Hyperkalemia
3–6 μg/kg/min over 1hour, then 0.4-1 μg/kg/min
Sample Case Record: Status Epilepticus 395

Appendix 9

IP : 196.52.84.10

Sample documented pediatric emergency case record of status epilepticus—assessment sheet


396 Appendices

IP : 196.52.84.10

Sample documented pediatric emergency case record of status epilepticus—monitoring sheet


Sample Case Record: Drowning 397

Appendix 10

IP : 196.52.84.10

Sample documented pediatric emergency case record of drowning victim—assessment sheet


398 Appendices

IP : 196.52.84.10

Sample documented pediatric emergency case record of drowning victim—monitoring sheet


Sample Case Record: Near Fatal Asthma 399

Appendix 11

IP : 196.52.84.10

Sample documented pediatric emergency case record of near fatal asthma—assessment sheet
400 Appendices

IP : 196.52.84.10

Sample documented pediatric emergency case record of near fatal asthma—monitoring sheet
Sample Case Record: Head Injury (Raised ICP) 401

Appendix 12

IP : 196.52.84.10

Sample documented pediatric emergency case record of raised ICP due to head injury—assessment sheet
402 Appendices

IP : 196.52.84.10

Sample documented pediatric emergency case record of raised ICP due to head injury—monitoring sheet
Sample Case Record: Septic Shock 403

Appendix 13

IP : 196.52.84.10

Sample documented pediatric emergency case record of septic shock—assessment sheet


404 Appendices

IP : 196.52.84.10

Sample documented pediatric emergency case record of septic shock—monitoring sheet


Sample Case Record: Septic Shock 405

IP : 196.52.84.10

Sample documented pediatric emergency case record of septic shock—monitoring sheet continued...
Epilogue

IP : 196.52.84.10

IP : 196.52.84.10

Way back in 1997, when I was invited to take charge of the Pediatric Emergency Room, little did I expect that this
would be the beginning of the most exciting chapter in the history of the institute. Seriously ill children and neonates
were flooding its gates. Brought late by their parents, these children had received little prehospital resuscitation, were
recognized late and were from the most under-privilaged sections of the population. This was compounded by the fact
that pediatric emergency medicine was relatively new and few doctors were formally trained in this sub-specialty during
their under-graduation.
A large proportion of severely hypoxic and shocked children were presenting with features of pulmonary edema,
cardiac dysfunction with eyes signs of non-convulsive status epilepticus. To our surprise, response to apparently innocuous
interventions such as fluids, brochodilators and anticonvulsants were often detrimental! Why was this happening? Little
published evidence supported these observations. Perhaps, children reaching western hospitals were not so sick?! Perhaps,
these children were intubated earlier, resulting in failure to develop these findings and hence never documented.
Protocols were modified to incorporate this information. Residents were drilled to perform the rapid assessment
within 60 seconds. Evaluation of liver span and eye movements was enforced in every assessment. Response to each
intervention was vigorously assessed for improvement and deterioration. Anticipation for the development of pulmonary
edema and cardiac dysfunction were built into protocols in order to avoid deterioration to cardiac arrest. The innovations
started paying rich dividends and hospital mortality dropped dramatically.
Pursuit to seek the truth never ends. Only history can truly judge the impact of these innovations in the care of the
seriously ill child during the initial minutes of resuscitation.

Indumathy Santhanam md dch


Index

IP : 196.52.84.10 A Adrenergic receptor dysfunction 134


Advanced cardiac life support 300
Anticholinergic
activity 240
Abdominal Aggravate hypoxia 62 derivative 88
distension 286 Aggravating signs 252
pelvic trauma 285 factors 62 Anticholinesterase 233
respiration 79 hydration 90 Anticipation 104
sonogram for trauma 286 Agitation 86 Anticonvulsant drugs 31, 110
tenderness 286 Air Antidote 253, 255, 257
Abnormal bronchogram 314 Antiemetics 219
cardiopulmonary cerebral assessment embolism 379 Antiepileptic drugs 207
10 Airway Antihistamines 172
movements 7 assessment 45 Antihypertensive drugs 179
respiratory rates 11 breathing 171, 189, 249, 292, 306 Antisnake venom 231
Abrasions 286 cervical spine protection 281 Antitussives and decongestants 67
Acetaminophen 254 equipment 33, 357 Antivenom
IP : 196.52.84.10
Acidosis 135, 199 experts 50 administration 234
Acneiform rash 252 management 384 serum 111
Acoustics of the stridor 63 manager manipulating 47 Apneustic breathing 270
Activated charcoal 242, 255 obstruction 63, 141 Approach to
Acute positioning is warranted 104 decreased level of consciousness 187
accidental ingestion of kerosene 250 stable 130 GI bleeding in the ED 306
ataxia and nystagmus 240 unmaintainable 253 kerosene 247
cardiogenic pulmonary edema 55, 80, Albuminuria 260 PEMC 112
81, 136, 150 Alkalinization of urine 255 respiratory distress 77
cardiogenic shock 124, 136, 140 Allergies 33 traumatic brain injury 265
clinical syndrome 170 Alpha-adrenergic 102 Appropriate sized
diarrhea 129 Alteration in mental status 80 laryngoscope 33
epiglottitis 65, 67 Altered oral airway 33
FB obstruction 69 autoregulation 199 Armamentarium 50
gastroenteritis 130 level of consciousness 3 Arrhythmias 111, 134
infectious disease 45 mental status 130 Arterial
laryngotracheal bronchitis 62, 65 Aminophylline 89, 90, 92 blood gas 85, 139
lung injury 82, 144, 299, 300 Ammoniacal dermatitis 381 carbon dioxide 200
respiratory distress syndrome Analgesics 67 catheter 125
respiratory distress syndrome (ARDS) Anaphylactic shock 123, 170 oxygen 200
101, 351 Anaphylaxis 111, 135, 138, 171, 232 bed pulsates 96
tubular necrosis 199 Anatomical landmark 378 Aseptic procedure 381
urinary retention 380 Anemia and congenital heart diseases 11 Aspiration of pericardial fluid 375
viral croup 63 Anesthetic agents of choice 36 Assessment of
Administration of heart rate 9, 148
Angioedema 65
anticonvulsant drugs 7 urine 381
Anomalous left coronary artery 135
digoxin 177 Assisted tracheal intubation 25
Anoxemia 199
neuromuscular blockage 32 Asthma
Anoxic spell and blue spell 174
Administration of acute severe 84
Anteriorly placed pediatric larynx 47 exacerbation 84
premedication 32 Anthracyclines 135
sedation 32 mimics 85
Antibiotic prophylaxis 285 moderate 84
Adrenaline 92 Antibiotics 67 near fatal 84
410 Pediatric Emergency Medicine Course (PEMC)

ASV Brochospasm 87 Cardiorespiratory


administration 232 Bronchilitis 7, 79, 80, 81 cerebral assessment 233
dose 231 Bronchodilator monitoring 33, 95
Ataxic 270 intervention 85 Cardiovascular
Atelectasis 299 therapy 111 dysfunction 143
Atropine 36 Bronchorrhea 248 response to shock 102
Autoaugmentation 102 Bronchospasm 248 Carotid artery 269
Autonomic Broselow tape 14 Cartilaginous support 61
IP : 196.52.84.10 activity 200 Budesonide 66 Case scenarios illustrating indications 30
system disturbance 199 Bullard laryngoscope 50 Catastrophic deterioration 187
Autoregulation of cerebral blood flow Bungarus caeruleus 225 Catecholamine release 217
266 Burns Catecholamine resistant cold septic shock
and polyuria 107 125
around mouth 293 Cathartic agents 243
B classification 291 Catheter leaking 381
facial 293 Causative factors of myocardial
Bacterial tracheitis 65, 68
hand 293 dysfunction 134
Bag-valve-mask ventilation 25, 26, 46, 198
minor 294 Causes of
Barbiturate poisoning 251
scal 293 cardiac arrest 299
Basic airway management 25, 31
specific secondary survey 294 cardiogenic shock 134
Basic life support 301
cardiogenic shock in children 135
Basilar skull fracture 269
coma 193
Belladonna alkaloids 253 C hospital mortality 143
IP : 196.52.84.10
Benzodiazepines 40, 199, 204, 219, 203
respiratory failure 299
Bernoulli’s principle 367 Calculation of burns percentage 292, 293 Caveat 4
Beta blockers 176 Camphor poisoning 260 Cellulitis and hemostatic abnormalities
Bilateral Cannulation of external jugular vein 378 234
abductor palsy 70 Capillary Central
chest rise 37 blood glucose 202 nervous system depression 350
leak 8, 145 pulse (femoral) 9
hilar opacities 318 Cerebral
Bimanual laryngoscopy 45 refill time 10, 11 blood flow 200, 265
Bipyridines 124 Carbamates 250 edema 351
Bladder catheterization 380, 381 Carbamazepine 243 metabolic rate for oxygen 199
Carbon monoxide poisoning 103 perfusion pressure 266
Bleeding Cerebrospinal fluid leak 269
diathesis 378 Cardiac
arrest 123, 135, 199 Cervical collar application 382
from scalp lacerations 268 Cervical spine
diseases 141
Blood immobilization 384
dysfunction or acute lung injury 80,
culture 193 injuries 382
144, 152
dyscrasias 375 precautions 386
failure 199
pressure 11, 200 stabilization 301, 382
function 145
transfusion 153 index 145 Check list for nebulization 367
Blood-brain barrier 265 rhythm 120 Chest
Body surface area 291 surgery 371 injury 370
Boggy swelling 284 tamponade 109, 111, 135 radiographs 85
Bolus therapy 117 Cardiogenic shock 31, 80, 81, 103, 120, wall rigidity 40
Bone marrow needle 114 121, 132, 134, 135, 187, 188 X-ray (CXR) in the ED 312
Boon in the ED management of acute Cardiomyopathy 135 Cheyne-Stokes breathing 199
pulmonary edema and Cardioprotective effect 219 Children with
shock 53 Cardiopulmonary airway abnormalities 337
Bougie 50 assessment 124 diarrhea 132
Bradycardia 9, 14, 19, 37, 40, 135, 275, 299 bypass surgery 135 iron deficiency anemia 174
Bradypnea 19 cerebral assessment 80, 129, 130, 132, polytrauma 284
Brassy cough 62 139, 143, 144, 231, 240
Chloral hydrate 339
Breathing airwary 14, 112, 104, 150 cerebral status 131, 298
Cholinergic activity 240
Breathlessness 7 resuscitation 297, 300
Index 411

Cholinesterase reactivator 250 Contrecoup injury 271 Derangement of the hemocoagulation


Chronic Convulsive status epilepticus 199, 206, 297 system 158
congestive heart failure 120 Cool the burn 294 Deterioration in respiratory function 79
heart failure 136 Corneal reflex absent 270 Determine physiological status 14
Chylothorax 371 Correct hypoxia and shock 6 Development of pulmonary edema 152
Classification of Correction of Dextrostix 112, 202
breathing patterns 77 hypovolemia 125 Diabetic ketoacidosis (DKA) 344
DKA 346 shock 137 Diaphoresis 86
IP : 196.52.84.10Clinical Corrosive agent ingestion 242 Diaphragmatic hernia 103
stages of acetaminophen toxicity 254 Corticosteroids 89 Diarrhea and hypovolemic shock 129
Costophrenic angle 314
therapeutic goals of shock resolution Diastolic
Cotton swab forceps 380
143 blood pressure 11
Counter-regulatory hormones (CRH) 344
Closed head trauma 265 dysfunction 134
Cranial nerves 269
Coagulopathy 308 Craniofacial Diazepam 209
Colonoscopy 310 injuries 281 Diazoxide 183
Coma with raised ICP 187 trauma 282 Difficult airway
Common Cricoid pressure 32, 45 algorithm 45
herbal medications and adverse/toxic Cricothyrotomy 45 equipment 44
effects 260 Crisis of hypertension 179 kit 45
household things of low toxicity 251 Criteria for DKA resolution 350 protocol 44
iron preparations 255 Critical illness 3 Digital rectal exam 310
Comparison of Crystalloids 106 Digoxin 221, 243
central and peripheral pulses 10
IP : 196.52.84.10 CSF drainage 276 Direct laryngoscopy 32
femorals and dorsalis pedis 10 Cuff being inflated 50 Disability 14, 112, 151
pulses 9 Cumulative anoxia 199 Disseminated intravascular coagulation
Compartment syndrome 298 Cut off levels for hypertension 179 101, 199, 308
Compensated shock 161 Cute cardiogenic pulmonary edema 55 Dissociative shock 103
Complete blood count 139, 181, 208 Cyanosis diaphoresis 86 Distal pulses 9
Completion of degree 355 Cyanotic
Distributive shock 103
Complication of congenital heart diseases 174
Divert portal blood flow 308
pleural aspiration 371 spell 174
spell with cardiogenic shock 176 Dobutamine 109, 121
severe sepsis 145 Dobutamine for cardiogenic shock 297
renal diseases 151 Cystic fibrosis 81, 85
Cytotoxic 145 Dopamine refractory hypotensive
Components of status epilepticus 5 vasodilatory shock 124
Congenital
Dorsum of the foot 9
anomalies 85 D Drooling and dysphagia 62
craniofacial abnormalities 45
Drowsiness 4
cystic adenomatoid malformation 370 Damage control surgery 287
Drugs
heart disease 81, 122, 135 Dangerous mechanisms of injury 382
lobar emphysema 321 Decreased induced gastritis 306
malformations obstructing the airway cerebral perfusion pressure 192 interactions with herbal products 261
65 myocardial contractility 145 therapy 203
malformations of the airway 62 portal pressure 308 used for asthmatic exacerbation in the
Congestive heart failure 103 De-fasciculating 30 ED 92
Conjugate Dehydration and electrolyte loss ensues used in emergency room for
deviation of eyes 206 344 management of status epilepticus
tonic eye movement 270 Delayed administration of epinephrine 209
Consumption of the respiratory muscles 173 Dynaplast 114
136 Dengue virus 158 Dyselectrolytemia 129
Continuous Dengue with or without warning signs Dysmorphic facial features 33
epileptiform electroencephalogram 12 159
Dysphagia 62, 68
positive airway pressure ventilation Depressed
Dysphonia 85
136 mental status or respiratory failure 242
sedation and paralysis 32 Dysrhythmias 377
skull fracture 269
412 Pediatric Emergency Medicine Course (PEMC)

E Failure with tachycardia 144 GIT duplication 308


Fasciculations 41 Glasgow coma scale (GCS) 187, 273
Ecchymosis 286 Fasciotomy 230 Glossopharyngeal nerve 32
EC-clamp: appropriate 28 Fatal attack of asthma 86 Glottic edema 66
EC-double clamp 28 FB obstruction in the ED 69 Glottic obstruction 62
EC-inappropriate clamp 27 Features of Glottis 62
Ectopic gastric mucosa 310 pulmonary edema 138 Glucocorticoids 66
Effortless tachypnea 130 severe sepsis 144 Glucose normal saline 153
IP : 196.52.84.10 Electrical injury 296 Febrile Grunting 79
Electrocardiography 301 children 6 Guedel airways 45
Electroencephalography 193 infants 5 Gum elastic bougie 45
Emergency Fenoldopam 183 Gustilo
medicine 355 Fentanyl and atropine 64 classification of open fractures 285
services 355 Fiberoptic grade 285
Emesis 248 intubating laryngoscope 45
laryngoscope bronchoscope 45
Empyema 80, 371
Enalapril 183 scopes 50 H
Endogenous catecholamine 124 Fibrinolytics 226
Hazards of
Endotracheal 46 Fighting the mask 86
intubation 32
Endotracheal tube (ETT) 47, 50, 334, 358 Fixation of tracheal tube 38
salbutamol nebulization 87
Ensure oxygenation 45, 46 Flexible devices 50
Head and skull 282
Entry wound in the forearm 298 Floor plan of the resuscitation unit 356
Head bobbing 84
Envenomation 111, 141
IP : 196.52.84.10 Flow inflating ventilation device 53, 55, 56
Heart disease 120
Enzyme acetylcholinesterase 247 Fluid
Heart rate abnormalities 135
Epidural hematoma 270 bolus therapy 150
Hemangiomas 63
Epiglottitis 45, 63, 85 correct shock 106
Hematemesis 305
Epilepticus 31, 120 management in severe dengue 161
Hematocrit 159
Epinephrine 66, 109, 111, 122, 172 resuscitation of septic shock 143
Hematoma
Episodes of diarrhea and vomiting 129 resuscitation of shock 139
accumulation 271
Esmolol 183 unresponsive 124
causes mass effect 271
Esophageal injury 242 Flumazenil 341
Hemodialysis 245
Esophagitis 308 Focus of
Hemodynamic interventions 143
Etiology of shock 110 infection 143
Hemostatic
Etomidate 39, 40, 340 sepsis 153
bites 233
Euvolemic restrict fluids 202 Foley catheter insertion 380
resuscitation 287
Evidence of Forced neutral diuresis 245
Hemothorax 371, 377
facial and neck trauma 33 Foreign body (FB) obstruction 65, 68
Henoch-Schönlein purpura 310
respiratory distress 132 Fosphenytoin 205, 209
Hepatic injury 286, 377
warm shock 132 Fracture of
Hepatomegaly resolved 6
Excessive cervical spine 378
Herniation syndromes 192
catecholamine state 135 ribs 282
Hexaethyltetraphosphate 247
cricoid pressure 36 Free fatty acids (FFA) 344
High tension wire 297
sweating 199 Fresh whole blood preferable 282
History of
Expiratory pressure valve 55 Functional residual capacity 30
breathlessness in children 144
External chronic respiratory distress 140
auditory meatus 35
portion 97
G diving 300
respiratory distress 137, 141
Extravascular fluid shifts 299 Gag and cough reflexes 270 Hoarse voice 62
Galea aponeurosis 267 Hyaline membrane disease 120
F Gastric decompression via NGT 26 Hydralazine 183
Gastric lavage 241, 253, 261, 307 Hydrocortisone 92
Faces pain scale-revised (FPSR) 335 Gastritis 308 Hyperacute respiratory distress 81
Failure of the cardiovascular system 134 Gastrointestinal Hyperchloremic acidosis 352
Failure to decompress stomach contents bleeding 305 Hypercyanotic spell 174
34 decontamination 241 Hyperdynamic circulation 9
Index 413

Hyperglycemia and ketoanions 345 Inhalational Investigations in management of coma


Hypernatremia 199 induction 47 187
Hyperpyrexia 199 injuries due to burns 281 Ipratropium bromide 86, 88, 92
Hypersecretion 199 Inhaled Ipsilateral conjugate lateral gaze palsy
Hypertension in children 179 ipratropium bromide 89 270
Hypertensive salbutamol 91
emergency 179 Initiate bag-valve-mask ventilation 46
encephalopathy 181 Inotrope initiated 6
J
IP : 196.52.84.10 urgency 180, 183 Inotrope infusion 55 Jackson-Rees circuit 34, 55, 104, 105, 357
Hypocalcemia 65, 70, 135, 138 Inserting the laryngoscope 46 Jerky respirations 200
Hypoglycemia 129, 135, 202 Insertion of Foley catheter 380
Inspiratory stridor 85 Jet ventilation set 45
Hypokalemia 9, 138 JR circuit in an apneic child 56
Insulin
Hypoperfusion 145 deficiency 344
Hypopharynx 48 infusion line 348
Hypotensive resistance and hyperkalemia 350 K
cardiogenic shock 136, 218 therapy 348
intra-abdominal injury 282 Interictal coma 199 Kawasaki’s disease 122, 135
septic shock 123 Internal jugular vein 379 Kehr’s sign 286
Interpretation of Kerosene ingestion 242
shock associated with SE 201 chest radiographs 312
warm shock 124 critical illness 16 Ketamine 36, 39, 40, 64, 91, 92, 340
Hypothermia 9, 135, 143, 242 Interrupt Ketonemia and acidemia 344
Hypotonia 4 ASV infusion 232
fluids 203
Hypovolemic shock 129, 132, 135, 300
IP : 196.52.84.10
Hypoxic asthmatics 87
Intestinal obstruction 131 L
Intra-abdominal
Hypoxic injury 29 injury 286 Labetalol 183
Hypoxic ischemic encephalopathies 80 organs 286 Laboratory analysis of serum 241
Intra-arterial pressure monitoring 125 Lacrimation 248
Intracellular concentration 88
I Intracompartmental pressure 230 Large volume pediatric emergency 3
Larygnoscope handle 36
Intracranial
Iatrogenic causes of cerebral edema 351 infections 14 Laryngeal
Immediate antimicrobial coverage 194 lesions 270 mask airway 44, 45, 48, 358
pressure 266 papilloma 65, 70
Immobilizing the entire spine 383 tension 40
Impending respiratory failure 61 stridor 70
Intramuscular route if intravenous 205
Inability to recognize 5 Intranasal route 200 Laryngomalacia 63, 65, 70
Inadequate oxygen flow 55 Intraosseous Laryngoscope blades 35, 45
Inappropriate technique 28 access 105, 114 Laryngoscopic examination 68
Increased route 205 Laryngoscopy and intubation 45, 46
tray 114 Laryngospasm 45
cerebral blood flow 199 Intraparenchymal
production of ketoanions 345 Leakage of plasma 158
bleeds 271
pulmonary blood flow 177 hemorrhage and edema 272 Lethal oral dose 255
pulmonary vascular resistance 145 Intrapulmonary shunting 299 Leukocytosis 143, 251
Indian National Snakebite Protocol (2007) Intrathoracic Level of consciousness 187
airway 62 Levetiracetam 205
226
pressure 79 Lidocaine 36, 39
Indications for
Intravascular Life-asthma threatening 84
activated charcoal 242
catheters 105 Life-saving emergency care 355
CT brain 279
fluid loss 299 Liver
initiating inotropes 109, 126
volume 137 function test 139
intubation in comatose children 189
Intravenous injury 254
intubation in SE 201
hydrocortisone 89 span 12
Induction agents 33, 39
lines prior to intubation 34 Localization of head injury 270
Ineffective cough 62 salbutamol 90 Lorazepam 201, 209
Infant or neonate 45 Intubating Lorazepam controls seizures 203
Inflammatory mediators 101 laryngeal mask 45 Loss of
Infra-auscultate axillary 8 medications 46 cutaneous barrier 291
Ingestion of corrosives 262 Intubation triggers 152 surfactant 299
414 Pediatric Emergency Medicine Course (PEMC)

Low systemic vascular resistance septic Mechanism of working of Jackson-Rees Myocarditis 81, 122, 134
shock 124 circuit 55 Myopathies and muscle necrosis 40
Lower GI bleed 309 Mecoprop poisoning 245 Myotoxins 226
Lower nephron necrosis 199 Mediastinal shift 314
Low-set ears 33 Medical complications of status
Lubricate the posterior surface 48 epilepticus 199 N
Lumbar puncture 193 Mental status in children 129
N-acetylcysteine 255
Lung fluid 200 Mepiridine (demerol) 341
IP : 196.52.84.10 Naloxone 341
Lung parenchyma 78, 314 Metabolic
Nasal flare 84
Lytic cocktail 221 abnormalities 136, 138
Nasogastric tube (NGT) 27, 34, 200, 242,
acidosis 138, 199, 240
307
biochemical abnormalities 199
M demands of tissues 134
Nasogastric tube emerging 28
Nasogastric tube insertion 34
derangements 101
Macroglossia 63 Nasopharyngeal airway 45, 357
disorders 203
Magic drugs 119 Nasopharynx 63
effects 123
Magnesium sulfate 89, 92 Nasotracheal intubation (NTI) 32
fat 344
Maintain Near fatal asthma 86
Metered dose inhalers 91
electrolyte balance 255 Nebulization 367
Methemoglobinemia 103, 240, 261
euglycemia 138 Nebulization tray 367
Method of administration of ASV 232
fluid requirements 137 Nebulizer therapy 86, 367
Methylprednisolone 92
hematocrit 137 Nebulizing kit 367
Microbial invasion 143
normal temperature 137 Neck of the bladder 381
Micrognathia 33, 45, 63
IP : 196.52.84.10
Major burns 292
Midazolam 39, 105, 207, 209, 339
Need to ventilate cannot intubate 39
Maldistribution 145 Needle
Middle finger down 49
Malignant hypertension 180 Mild traumatic brain injury 265 cricothyrotomy 45
Mallampati classification 336 Milrinone 109 thoracocentesis 109, 282, 370
Malrotation 308 Minimal mucosal edema 62 Needle thoracocentesis 374
Management of Minor head trauma 267 Neem oil ingestion 259
acute Minor symptoms 4 Neostigmine test 233
diarrhea 129 Miosis 248 Nephrotoxins 226
exacerbation of asthma 84 Monitor serum sodium 202 Neurogenic
adverse events 341 Monitoring equipment 33 etiologies 81
anaphylactic shock 170 Monitoring of urine output 380 functional stridor 8
cardiogenic shock 134, 141 Monroe-Kellie doctrine 267 pulmonary edema 199
cerebral edema 351 Morphine 221, 340 stridor 71, 188
dengue with warning signs 158, 160 Motor vehicle accidents 265 Neurohormonal responses 102
drowning victim 299 Mpending respiratory failure 218 Neurological
eye signs 13 Mucolytics 90 assessment 12
fluid overload 166 Muffling of voice 62 evaluation 283, 285
hypertensive Multidose regimen 88 Neuromuscular blockade agents 33, 36,
emergency 179, 181 Multiorgan failure 101 40
shock 148 Multiple organ dysfunction 199 Neuronal excitability 207
Muscarinic acetylcholine receptors 248
intracranial hypertension 191 Neuropeptide activity 198
Muscarinic effect 240
local and systemic effects 219 Neurotoxic bites 233
Muscarinic effects of acetylcholine 248
non-traumatic coma 187 Neurotoxicity secondary 218
Muscular twitching 252
pain in children 335 Mydriasis 270 Neurotoxins 226
raised intracranial pressure 275 Myocardial Neurovascular bundle 374
severe dengue 158 contractility 138 Nicardipine 183
status epilepticus 198 depressant factor 134 Nicotinic effect 240
Mandibular hypoplasia 33 disease 121 Nifedipine 183
Manual stabilization of cervical spine 382 dysfunction 134, 144, 147, 188, 203, 300 Nitroprusside 182
Massive empyema 109 edema 134 Non-cardiogenic pulmonary edema 31,
Match fluid resuscitation 129 function 5, 134 81, 217, 145, 301
Maxillofacial and intraoral trauma 282 ischemia 125 Non-convulsive status epilepticus 7, 110,
136, 143, 188, 206
Mean arterial pressure (MAP) 12, 266 oxygen demand 136 Non-invasive positive pressure ventilation
Mechanical ventilation 143 performance 136 55
Index 415

Non-steroidal anti-inflammatory drugs


(NSAIDs) 170
P Pharmacotherapy of hypertensive
emergencies 182
Norepinephrine 109, 120, 124 Phenobarbital 207
Normal Pain management in children 335
pulse pressure 150 Painful procedures 336 Phenothiazine group of drugs 7
respiratory rate for age 79 Palliative shunt procedure 176 Phentolamine 183
Normalization of Palpable bony fragments 286 Phenytoin 204, 209
blood 150 Phosphate 350
heart rate 150 Pancuronium 41
Papilledema 270 Photodetector picks up R/IR light source
IP : 196.52.84.10 liver span 151
mental status 151 Paradoxical chest wall movements 84 95
peripheral pulses 150 Paralytic drugs 33 Pitfalls in cervical spine radiology 385
respiratory rates 150 Paranasal sinuses 63 Plaster for securing tube 33
saturations 177 Platelet dysfunction 158
Normotensive shock 148 Parasympathetic blockade 253
Parenchymal bleeding 271 Pleural
Nystagmus 12, 81
Parkland resuscitation formula 294 aspiration 370
Paroxysmal hyperpnea 174 effusions 371
O Parts of laryngeal mask airway 48 space 370
Pasmodic croup 65 Pneumatocele 370
Obesity 45 Pathophysiology of Pneumonia and asthma 7
Obstructed airway and hypotensive shock anaphylaxis 170 Pneumopericardium 377
secondary to anaphylaxis 32 cyanotic spell 174 Pneumoperitoneum 334
Obstructive shock 103 DKA 344 Pneumothorax 111, 334, 370, 371, 377
Ocular movements 270 shock 101 Poison syndromes 241
Oculogyric crisis 7 snake venom 225, 226 Poisoning: general approach 239
IP : 196.52.84.10
Oculomotor 218 Patients with polytrauma 382 Poisons 111
Oliguria 199 Peak expiratory flow rate 90 Polydipsia and polyuria 344
Omeprazole 258 Pearls and pitfalls 25, 53 Polytrauma 281
Ominous sign 79 Pediatric
Polyuria and polydipsia 349
Opioids 247 accident and emergency group 187
Portal hypertension 307
Oral rehydration advanced life support 297, 300
Positioning of airway 35
assessment triangle (PAT) 129, 134, 143,
salts 131 Positive end-expiratory pressure 145
158
therapy 4 Posterior oropharynx 49
bain circuit 53
Organ dysfunction 144 Postintubation management 37
emergency medicine 39
Organization of the intraosseous tray 115 resuscitation and emergency services Postsynaptic neurotoxins 233
Organophosphates 248 364 Potassium administration 350
Organophosphorus PEMC approach: respiratory distress 83 Pralidoxime and atropine 250
poisoning 250 Penicillins 135 Prazosin 219, 220
compounds 247, 262 Pentobarbital 340 Prehospital
Orogastric tube 272 Pericardial management 299
Oropharyngeal cavity 375, 376 setting 69
airways 357 effusion 314, 334, 375 Premedication agents 33
bleeding 310 fluid 375, 376, 377 Premorbid sign 9
secretions 205 paracentesis 375 Preoxygenate on arrival 41
suctioning 249 Pericardiocentesis 109, 375 Preoxygenation of patient 34
Oropharynx 48 Perinatal depression 120, 141 Preoxygenation with non-rebreathing
ORS administration with body weight 160 Perineum 282 mask prior 39
Orthopedic trauma 283 Peripheral Preparation of
Osmotic diuresis 344 perfusion 150 airway tray 35
Osmotic therapy 276 utilization of glucose 344 insulin infusion 348
Oxygen vasoconstriction 9 Prevalence of hypertension 179
delivery 103 Permissive hypotension 287 Primary survey and initial management
inhalational therapy 86 Petechial hemorrhages 270 283
saturation 26 Pharmacologically assisted intubation 30, Principles of prehospital care 299
source 33 32 Probable dengue 159
416 Pediatric Emergency Medicine Course (PEMC)

Problems during cervical spine Recognize Sand bag 114


immobilization 385 cardiogenic shock 134 Scalp injuries 275
Procedural sedation 335 pulmonary edema 144 Scalp lacerations 267
Procedures requiring sedation 336 ‘red flag’ signs during 45 Scorpion
Procoagulants 226 Recovery from water 300 antivenom 221
Progression of Rectum 282 envenomation 218, 220
edema 228 Recurrence of pulmonary edema 153 sting envenomation 221
status epilepticus 198 Refractory Seat belt injury 286
IP : 196.52.84.10 Progressive fall in mental status 86 cardiogenic shock 124 Secondary brain injury 266
Prolonged status epilepticus 206 Sedative
hypoxia 135, 299 Rehydration fluid 347 analgesics 338
seizures 141 Renal hypnotic overdose 252
Propofol 340 failure 199 hypnotic poisonings 261
Pull push technique 129 function test 139 paralytic agents 32
Pulmonary glucose clearance 344 Seizure control neuropeptides 199
artery 135 inflammation 381 Selection and fixing of appropriate
blood flow (PBF) 174 response 103 cervical collar 383
edema 80, 143, 145, 217, 218, 299, 300, Resolution of Selection of LMA 48
318 hepatomegaly 151 Sellick’s
embolism 103 hypotensive shock 150 maneuver 36
hydrostatic pressure 145 ketoacidosis 348 pressure 36
response 103 myocardial dysfunction 151 Semirigid 50
IPvascular resistance 136 Respiratory
: 196.52.84.10 Septic
Pulse oximeter 33, 55, 95, 96 acidosis 199
distress 136, 144, 158, 177, 300 cardiogenic shock 81
Pulsus paradoxus 65 neurogenic shock 102
emergencies 312
Pupillary Sequence of intubation 36
failure 29, 79, 120, 136, 188, 252, 253
examination 13 rate and work of breathing 78 Sequential steps of PAI 30
response 12 system failure 199 Serious sepsis 143
Push enteroscopy 310 Responsive to Serology for dengue 139
Pyelonephritis 381 pain or unresponsive 281 Serum
Pyrethroids 261 painful stimulus 4 electrolytes 139
Pyridoxine 205 voice 4 potassium 200
Restoration of tissue perfusion 101
sodium correction 345
Resultant hematoma 378
Q Resuscitation in critically ill children 101 Severe
Resuscitation of acute cardiogenic shock bradycardia 301
Quiet tachypnea 81 140 cardiotoxic reactions 204
Retention of ketoanions 345 chest retractions 65
dehydration 129, 130, 132
R Retropharyngeal abscess 63, 65, 68
dengue 159, 308
Reversal agents 341
Rhabdomyolysis 199 hyperglycemia 344
Raised intracranial pressure 9, 36, 191, 188
Right infraclavicular region 38 hypertension 179
Randomized controlled trials 55
Right ventricular 136 parenchymal lung disease 31
Rapid cardiopulmonary
Risk of peripheral vasoconstriction 299
assessment 82
air embolism 379 pneumonia 370
cerebral assessment 14, 84
drowning in water bodies 299 sepsis 81, 103, 141
mechanism in shock 102
pulmonary edema 177, 300 trauma 40
Rationale for
tachyarrhythmias 120 traumatic brain injury 268
avoiding bicarbonate 350
Rocuronium 33, 40, 41 Shaken baby syndrome 270
potassium replacement 349
Rothromboplastin time 208 Shock
Recognition of
correction 158
abdominal trauma 281
persists 108
coexisting septic shock 129
early signs 3
S resolution 149
with normal blood pressure 163
septic shock 155 Salbutamol nebulization 84, 85, 88 Short trachea predisposes 25
shock 143 Salivation 248
Index 417

Signs of Structural Train nurses in emergency resuscitation


acute lung injury 101 diseases of the larynx 85 361
cardiac dysfunction 136 heart disease 135, 139, 140 Transjugular intrahepatic portosystemic
Subcutaneous
dehydration 131 adrenaline 89 shunt (TIPS) 308
hypoxia 134 insulin 351 Traumatic brain injury in the ED 272
pulmonary edema 108, 125, 137, 139, Subgaleal hematomas 268, 276 Treatment of intracranial pressure 193
151, 152, 300 Subglottic regions 61 Type of
refractory shock 151 Submersion injury 7, 135, 299 venom action 226
IP : 196.52.84.10 shock 131 Subpulmonary outflow tract 174 venom component 226
shock resolution 150 Succinylcholine 39, 40, 41, 64, 249 shock 103, 135
Simultaneous administration 32 Suction oropharyngeal secretions 200
Site of insertion of needle 376 Suctioning pressure 27
Size of hemithorax 314 Sudden unresponsiveness 7 U
Skeletal muscle glycogenolysis 344 Supine position 63
Uncal herniation 187, 188
Skull fractures 268 Supraglottic airway devices 45
Unequal pupils 13
Small Supraglottis 61, 62
Unilateral
endotracheal tubes 47 region 61
fixed dilated 270
infants neonates 27 Supraventricular tachycardia 126, 135
LMN 270
pupil 270 Surface irrigation with saline 285
Unique odors 252
volume etiologies 108 Suspicion of shigellosis 130
Unmaintainable airway 199
Snake Suxamethonium 6, 33
Unstable and obstructed airway 201
bite envenomation 225 Swelling in front of the neck 64
Upper
envenomation 31 Systemic
IP : 196.52.84.10 hypersensitivity reaction 170
abdominal organs 286
Soft
airway foreign bodies 85
stridor 62 inflammatory response syndrome 143,
airway obstruction 47
tissue injury 285 291
Ureteral
Somnolence and obtundation 80 vascular resistance 126, 135, 137, 139
rupture 381
Spasmodic croup 68 Systolic blood pressure 11
stricture 381
Spectrum of
difficult airway 44 trauma 381
gastrointestinal bleeding 305 T Urinary tract infections 144
Speed of fluid administration 106, 148 Urine
Spinal Tachycardia 9, 79, 132 alkalinization 243, 245
clearance 385 Tachypnea 8, 78, 132, 143, 199 output 109, 151
immobilization in trauma victims 386 Technique of chest tube insertion 371 Urological injury 286
injury 284
stabilization 382 manual stabilization 382 Use of
Spleen and liver 282 Tension pneumothorax 103, 109 Jackson-Rees circuit 158
Splenic injury 286 Tetanus prophylaxis 283 rapid cardiopulmonary cerebral
Stabilization of the cervical spine 382 Tetralogy of Fallot (TOF) 174 assessment 344
Stable cardiorespiratory function 342 Theophylline 243 sedative and analgesic drugs 335
Status epilepticus 7, 198 Therapeutic goals of shock resolution 108
Steps of
manual cervical spine stabilization 383
procedural sedation 335
Thiopental 36, 39, 207, 339
Thoracostomy kit 371
V
spinal stabilization 382 Time of onset of anaphylactic reactions Vagal-induced bradycardia during
Sterile 171
drapes 380 laryngoscopy 47
Tincture benzoin soaked cotton 33 Vallecula 36
gloves 380
technique 379 Tonic-clonic activity 200, 207 Valproic acid 205, 209
water 380 Tourniquet made of rope 226 Valvular pulmonic stenosis 174
Sternal retractions 63 Toxic reactions 135 Variable absorption of light 96
Steroids 153, 172 Toxicity of iron by amount ingested 256
Stimulation of the sympathetic system Vascular
Toxidromes 240, 241 access 64
218
Stricture urethra 381 Toxin screen 194 endothelial cell dysfunction 158
Stridor Tracheal narrowing 85 examination 284
due to structural abnormality of the Tracheobronchomalacia 85 malformation 308
airway 33 Tracheoesophageal fistula 63 structures 377
with respiratory distress 67
418 Pediatric Emergency Medicine Course (PEMC)

Vasoactive medications 119 Viral Whole bowel irrigation 243, 257


Vasoconstrictors 176 infections 130 Wide pulse pressure 132
Vasodilatory shock, diagnosis of 150 upper respiratory tract infection 88 Wong-Baker faces pain scale (WPFPS) 335
Vasopressin 125 Visual abnormalities 218 Worsening hypoxia 56, 87, 88
Vasopressors and inodilators 109 Vocal cord
Vecoronium 33, 36, 41 dysfunction 85
Venodilation 145 paralysis 65 X
Venous return falls 37 Vomiting
IP : 196.52.84.10 and diarrhea 103 X-ray
Ventilation
during intubation 36 clues to diagnosis 320
device 136
of gastric contents secondary 27 severe traumatic brain injury 278
perfusion 299
X-whilst abdominal ray 286
Ventricular
dysrhythmias 135 W
ectopy 125 Y
fibrillation 299 Waiting for confirmatory blood gas
premature contractions 126 analysis 105 Yankauer suction catheter 26
Venturi effect 61 Wavelength spectrum 96 Young infants 9
Video laryngoscope 45 Wheezing
Videoscopic techniques 50 attacks 85
Viperine envenomation 234 loudest 85

IP : 196.52.84.10

You might also like