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Medicine Course
The 60 seconds advantage to get sick kids
back on track... with a smile!

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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
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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.

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

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

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Pediatric Emergency Medicine Course (PEMC)

First Edition: 2008
Reprint: 2011
Second Edition: 2013
ISBN 978-93-5090-694-1
Printed at
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Dedicated to
IP : 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.
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∫ ∫
satyameva jayate nān™taˆ
satyena panthā vitato devayānaƒ |
yenākramanty™¢ayo hyāptakāmā
yatra tat satyasya paramaˆ nidhānam ||
IP :
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
circa 2500 BCE

IP : 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
Chennai, Tamil Nadu, India
Kilpauk Medical College
Chennai, Tamil Nadu, India Procedures
All topics except those from

Associate Editor Associate Editor

IP : 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
Interpretation of Chest

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
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 : Puducherry, India New Delhi, India
Envenomation Poisons

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
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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
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
Severe Traumatic Brain Injury
Contributors ix

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

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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)

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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)

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

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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

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Rajitha K dch Sugavanesh dch Babu Balachandar dch Sangeetha dch
(2009) (2009) (2009) (2009)

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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
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IP : 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.
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
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)

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:
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 : 4. You D, Jones G, Hill K, Wardlaw T, Chopra M. Levels and trends in child mortality, 1990-2009. The Lancet. 2010;

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 : Division of Emergency Medicine
University of Cape Town
South Africa
Preface to the Second Edition

IP : 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
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,
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
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IP :
Preface to the First Edition

IP : “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
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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
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IP :

IP : 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
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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 : Ms Sajini (Bengaluru Branch) and her team, for their tireless efforts in making this edition a unique one.

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IP : 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

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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

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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
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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 1 to 13 389-405

Epilogue 407
Index 409

IP : - 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
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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
ET - Endotracheal tube
RPA - Retropharyngeal abscess
FAST - Focused abdominal sonogram for
RSI - Rapid sequence intubation
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 :

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IP :

April 19, 2013


Indumathi Santhanam md
IP :
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 : 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 :
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 :

Section I
Critical Illness
IP :
Recognition of Early Signs
IP :
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 :
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.
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
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 :

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.
Control the urge to administer anticonvulsants.
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-

4. Correct hypoxia and
IPshock. Reassess; a clearer picture
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
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

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 : 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 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
●● 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
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
: ●● 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
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
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 :
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.
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.

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
●● 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 : 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.
3: Easy to feel dorsalis pedis.
4: Dorsalis pedis as well felt as femoral pulse.
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 : 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)

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-
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.
: 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.
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

Management of eye signs of non-convulsive status
IP : 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).

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 : ●● 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.

●● 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.
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 :
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department

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
Accurate documentation of clinical findings is crucial
IP : 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
‘consciousness’ drops profoundly.
2. Referring the febrile child with acute onset posturing
to the neurologist or to the psychiatrist for agitated
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 :

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

IP :

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 :
20 Section I n Recognition of Critical Illness

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

IP :
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.
1. Santhanam Indumathy, Pai M, Kasthuri KR, et al. Mortal-
: 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.
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).

Section II
IP :
IP :
IP :

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.
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).
: 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

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
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.

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 :
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.
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 :

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.

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
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
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-
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
1. Rushing to intubate before preoxygenating (mask
IP :
●● 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.
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-
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
IP :

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
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.
: 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%.
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 :
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
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 : 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.
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
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.

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-
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
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 :
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,
Raised intracranial pressure Lidocaine, Atropine,
without shock Thiopental 5 mg/kg and
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.
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
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

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
hand and inserted into the
glottis up to the vocal cord mark using the right hand.

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
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-
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


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.

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 :
●● 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.
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
Midazolam should be avoided in children presenting
Medications with hypotensive shock.
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 : 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-
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-
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
: 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
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
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

IP :
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
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
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
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
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 43


Drugs Dose Route Duration Side Effects Comments

IP :
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. (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. page /symposium/2010.
emj.2007.048512. Presentations/PREP-1013. PDF.
Assessment and Management
IP :

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
specialized airway equipment (Box 4.1).
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
●● 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
5. Introduce oropharyngeal/nasopharyngeal airway
●● 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
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.
‘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 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:
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 :
●● 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
Small endotracheal tubes are compliant leading to diffi-
culty in negotiating the acute angle of an anteriorly placed
pediatric larynx.
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.

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.
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 : 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).

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 :
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 :

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 :
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
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
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 :
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.
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:

IP :
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
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 :

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
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 : 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.
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.
: 4. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe
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
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. : 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 :

IP :
IP :


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
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,
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 :
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

1. Age at which stridor presents helps in recognizing
IP : 4. Associated symptoms.
●● 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.
64 Section III n Approach to Stridor

Case Scenario 1
A toddler presented with 1 day history of fever, stridor
IP :
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.

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 :

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

1. ALTB (classical croup)
2. Acute epiglottitis
3. Bacterial tracheitis
4. Retropharyngeal abscess
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
●● 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 : 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-
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).
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
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.
●● 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 : 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.
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 : ●● 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
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.
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 :
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

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.

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
●● 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 :
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 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-
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-
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
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.
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

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


IP :
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 : 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 :

IP :
IP :

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 : 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.
Roughly, doubling of normal (low normal range)
respiratory rates for age should be interpreted as
respiratory failure.

●● 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
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.
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.
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.
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.
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 : 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
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.
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

Muffled heart sounds, IP :gallop, relative bradycardia,
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
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.
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
and child during assessment
common errors
1. Diagnosing asthma in all children presenting with
IP :
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 :

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
Management of an
IP :

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.

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 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

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.
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
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
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

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
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 :
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
to ventilation perfusion mismatch and can precipitate cardiac
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 :
●● If deterioration is profound, stop nebulization and re-
consider the diagnosis. All that wheezes is not asthma!
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.
●● 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
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
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-
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.
●● 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
: 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
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/
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
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-
: 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
1. Recognize asthma since “all that wheezes is not
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
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
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
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
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
Protocol 8.1: PEMC approach: Management of acute exacerbation of asthma

IP :
Chapter 8 n Management of an Asthmatic Exacerbation
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
(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.
IP :

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.

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
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 : emia. It fails to pick up early, minimal fall in oxygen
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-
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
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
1. Failure to immediately respond to a fall in SaO2 <
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.

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

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
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 :

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-
: 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
that is refractory to fluids and inotropes.
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
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

Ù ●● Airway is patent or maintainable or clear if the infant is
If the clinical setting suggests the possibility of shock,
IP :
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 :

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
●● 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.

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

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 : ●● 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
●● 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 :

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 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 :
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
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

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
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
Norepinephrine Low BP with low SVR Tachy, brady 0.05–1.0 µg/kg/min
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
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

Non-convulsive status epilepticus (NCSE) signals severe If eye signs are ignored or not recognized generalized
hypoxia and shock: IP : 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.
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
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.

Anticonvulsant medications may be hazardous in this
●● 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 :
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,
Trauma Control bleed
Seizures Anticonvulsant therapy

suscitation is likely to yield the most favorable outcomes.

Isotonic fluids form the cornerstone of treatment and the
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.
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.
1. Avoiding administration of fluids for fear of
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
Refer Protocol 10.1.
112 Section V n Circulation

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

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
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.
IP :

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.
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 : 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
●● 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
●● 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 :

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 : 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

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
1. Using the blood set needle (which does not have a
IP :
2. Preferring to obtain access using ‘cut down’
3. Failing to fix during bolus therapy resulting in
slippage of the IO needle.
4. Not using screwing movements to enter the marrow
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.
IP :

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.

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

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 : 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.
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 : 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
●● 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.

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,
An increase in heart rate without improvement in shock
should prompt a reduction in the rate of infusion.

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 :
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
●● 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 : ation of infusion.

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?

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
Placement of an arterial catheter for intra-arterial
IP :
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
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
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
3. Epinephrine is the only agent, which can be initiated
simultaneously with fluids even before establishing
euvolemia in hypotensive shock.

common errors
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
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
(add to 100 mL) Rule of 3 (add to 50 mL) Dose
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,
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
Norepinephrine Low BP with low SVR Tachy, brady 0.05–1.0 µg/kg/min
Milrinone Cardiogenic shock with high SVR Hypotension 50–75 µg/kg over 10–60 minute
followed by infusion 0.5–0.75
SVR, systemic vascular resistance; †CVS, cardiovascular; ‡ SVT, supraventricular tachycardia; §VPC, ventricular premature contractions.

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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
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 :
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
IP :

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.


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 :

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.
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.
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 :
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.


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

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


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.

●● Signs of shock.
●● Ileus or intestinal obstruction (proven or suspected).
●● Comatose or unconscious.
●● Unable to tolerate oral/NGT rehydration (persistent
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.

common errors
1. Failure to recognize shock and treat as severe
Correct shock and re-evaluate renal parameters in
IP :
previously normal children.
2. Failure to anticipate that hypovolemic shock may
co­exist with septic shock secondary to GI sepsis.
Key Points
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 :
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED
IP :

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.

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 :
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

Supraventricular tachycardia
Ventricular dysrhythmias
The failing heart has to work harder against more
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
7. Metabolic
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


A previously healthy, 65-day-old baby, is brought with Goals
IP :
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
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.
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
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.
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 :
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.
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

Following intubation, if features of pulmonary edema Ionized calcium level less than 0.9 mmol/L.
IP : 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.
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
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
without history of seizures or stridor.
Chapter 14 n Cardiogenic Shock 139

Ù Perform the rapid cardiopulmonary cerebral assess­
Initiate the following inotropes if signs of pulmonary
edema are noted duringIP fluid
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
●● 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
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
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
1. High index of suspicion needed to recognize acute
IP : 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

Protocal 14.1: PEMC approach: Recognition and management of cardiogenic shock
History of respiratory
IPdistress following submersion, perinatal depression, envenomation, severe sepsis, prolonged
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 :
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.
IP :

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.

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 :
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
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-

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
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 : dominal distension and vomiting for 1 day. She had
●● 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
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
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 :
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

●● 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-
●● Intubation should not be delayed till the child is mori-
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.
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 :

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
●● 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.
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
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
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
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.
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-
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 :

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 : 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).

Normalization of respiratory rates to age appropriate
●● 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.
●● 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
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

Avoid stopping resuscitation when peripheries become
IP :
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.
●● 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
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

Stomach contents should be emptied rapidly, if intubation
IP :
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-
●● 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
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.
Development of pulmonary edema makes intubation
a challenge. Froth, that is noted during the fluid
resuscitation (Figure 15.9) predicts increased risk of

Figure 15.18: Signs of pulmonary edema and cardiac


●● 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.
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
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 : 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
1. Recognize septic shock by looking for evidence of
IPin: the
Drugs to be avoided
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
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 :
Chapter 15 n Septic Shock
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
• 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 :
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
IP :

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

Hematocrit is a simple bed-side tool to identify severity
IP : 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
Dengue is classified based on severity (Table 16.1)
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).

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
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 : 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
●● 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.
●● 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
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
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

No shock and HCT is high: The patient should be closely monitored. The rapid
IP :
• 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 :
in patients with intractable shock.6,7,8
●● Call for inotrope infusion.
●● Dopamine if BP is low nor­mal. Epinephrine if severely
●● Catheterize and monitor urine output.
●● Check hematocrit before and after every fluid bolus.
●● Collect blood for grouping, crossmatching and lab in-
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
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 :

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
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
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 :
●● 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.

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.
●● 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 : 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

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.
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 : ●● Electrolyte disturbances such as hyponatremia, hy-
– Reduce the IV fluids accordingly.
pokalemia, hyperkalemia, hypocalcemia and metabolic
– Monitor closely using the rapid cardiopulmonary
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
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.
168 Section V n Circulation

Key Points
1. Repeated rapid IP cardiopulmonary
and cerebral
common errors
1. Not reducing the rate of fluid administration after
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
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

1. WHO, dengue hemorrhagic fever: Diagnosis, treatment
IP :2nd 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.
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.
IP :


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

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 :
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-
●● 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.
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
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-
ment following each bolus to determine, whether the
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
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
Dose of epinephrine:

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 : 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-
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.
IP :

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.

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

A 3-month-old infant is brought with history of inces-
IP : 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
●● 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
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.
Prehospital Management3
●● 1 month–12 years (peaking between 2–4 months).
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 : 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
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
●● 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
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.
●● 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.
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.
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
IP : pulmonary blood flow can pre­
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.
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

1. Roekens CN, Zuckerber AL. Emergency management
IP : 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
Protocol 18.1: PEMC approach: Cyanotic congenital heart disease
IP :

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

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
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 :
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
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
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 : sion. Fundoscopy should be performed looking for hemor­
gest disturbance to the central nervous system (Box rhage, papilledema or infarcts.
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-
●● 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
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, 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
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
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
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 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
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
: 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
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.
●● 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.
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 :

IP :
Approach to Decreased Level
IP :

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
5. Investigations in management of coma.

Many acutely ill children are not fully conscious. Most
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 :

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.

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

●● 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
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-
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.
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
: ●● 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
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
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
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 : 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.
‘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.

• 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),
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.
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 : 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
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
• Ataxic or shallow
Cerebral perfusion pressure is the difference between the • Slow irregular gasping respiration
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
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
await for the whole picture to unfold. ●● Call for metabolic specialist, if metabolic profile is ab-
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-
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 : 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
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

Check blood sugar.
Check for NCSE and treat.
common errors
1. Administration of Mannitol without ruling out shock
6. Lower temperature, IPif: more
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
Section VI n Disability

IP :
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 :
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.
Epilepsia. 2010;51(2):177-90.
IP :

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 : ●● 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 :
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

●● 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
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.
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

An unstable and obstructed airway in combination with
Opening the airway and provision of oxygen without
ineffective ventilationIPfor:
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.

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 :

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.
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
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
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 : 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
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

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

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
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
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.

A good indicator of seizure control is return of baseline

●● 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 :
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
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 :
cal­cium, magnesium, complete blood count (CBC), cul­
tures, prothrombin time (PT), prothromboplastin time
(PTT) and blood gases. As per the recommendations of
Key Points
American Academy of Neurology,38 the following have 1. Differentiation of convulsion from hypoxic postur­
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
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 : 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.
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
Dysarthria, ataxia, sedation,
thrombophlebitis, purple glove
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)
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.
210 Section VI n Disability


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

IP : 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
Chapter 21 n Status Epilepticus 211

Protocol 21.1: PEMC approach: Recognition and management of convulsive and non-convulsive
status epilepticus in ED
IP :
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.
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 :
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 :

IP :
IP :

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 :
●● 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.

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 :
Administration of Prazosin in the prehospital setting
is one of the most useful strategies to reduce mortality in
scorpion envenomation.
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.
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 :

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.

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
●● 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
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.
This device, helps to provide CPAP in addition to oxygen
during resuscitation in the ED.
A 6-year-old girl was rushed into the ED for having been
stung by a scorpion the previous night. The nurse in the
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
: 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-
Vomiting, salivation, sweating contribute to dehydra-
tion. Correction of hypovolemia is a priority.

●● 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
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
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
IP therapy improves outcome and
: 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 :

●● 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.
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.
IP :

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-


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-
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
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
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,

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

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
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.

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 :
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-
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.
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,