Professional Documents
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Pediatric
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Emergency
Medicine Course
The 60 seconds advantage to get sick kids
back on track... with a smile!
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Disclaimer
Every effort has been made to ensure that the drug doses herein are accurate and in accordance
with the standards accepted at the time of publication. However, the user is advised to check
the doses carefully. The author shall not be responsible for any error in this publication.
Besides, as new research and experience broaden our knowledge, changes in treatment and
drug therapy occur. Therefore, the reader is advised to check the product information sheet
included in the package of every drug he/she plans to administer to be certain that changes have
not been made in the recommended dosage or in the contraindications. This is of particular
importance in regard to new or infrequently used drugs. In addition the protocols given in this
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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.
Pediatric
Emergency
P E M C
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Medicine Course
The 60 seconds advantage to get sick kids
back on track... with a smile!
Second Edition
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Editor
Indumathy Santhanam md dch
Professor and Head
Department of Pediatrics
Government Royapettah Hospital
Kilpauk Medical College
Chennai, Tamil Nadu, India
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Dedicated to
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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 ||
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Truth alone triumphs; not falsehood.
Through truth the divine path is spread out by which
the sages whose desires have been completely fulfilled,
reach where that supreme treasure of Truth resides.
Mundaka Upanishad
3.1.6
circa 2500 BCE
Contributors
Associate Editor
Associate Editor
Shanthi Sangareddi md dch
Thangavelu S md mrcph
Associate Professor
Senior Consultant
Chinglepet Medical College
Mehtas’ Children’s Hospital
Chinglepet, Tamil Nadu, India
Chennai, Tamil Nadu, India
Hypertension
Interpretation of Chest
DKA
Radiographs
Dengue
Associate Editor
Associate Editor
Ramesh Babu B
Balaji J
Assistant Professor
Assistant Professor
Government Dharmapuri
Government Dharmapuri
Medical College
Medical College
Dharmapuri, Tamil Nadu, India
Dharmapuri, Tamil Nadu, India
Emergency Medications and
Snake Envenomation
Equipments
viii Pediatric Emergency Medicine Course (PEMC)
Guest Editors
Mahadevan md Suresh Gupta md dch
Professor and Head Consultant Pediatrician
Department of Pediatrics Pediatric Emergency
Jawaharlal Institute of Postgraduate Department
Medical Education and Research Sir Ganga Ram Hospital
IP : 196.52.84.10 Puducherry, India New Delhi, India
Envenomation Poisons
Contributors
Thanyanat Bunnag md Pradeep Padmanabhan md msc
Professor Assistant Professor
Queen Sirikit National Institute of Child Health Division of Pediatric Emergency Medicine
Bangkok, Thailand University of Louisville
Louisville, KY, USA
Pra-on Supradish md Pain and Sedation in the ED
Queen Sirikit National Institute of Child Health
Bangkok, Thailand Jayshree Muralidharan md
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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
Australia
Rakesh Lodha
Assistant Professor Sonia Singh
All India Institute of Medical Sciences Consultant
New Delhi, India Division of Pediatric Emergency Medicine
Specific Poisons University of Pittsburgh
USA
Severe Traumatic Brain Injury
Contributors ix
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Naushad Mallagi dnb Jyothsna S dch mrcph Jayaprakash mrcph Narmada dch dnb mrcph
(2002) (2003) (2003) (2003)
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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)
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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)
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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Foreword
IP : 196.52.84.10In 2010 India recorded 1.3 million infant deaths—the highest for any country.1 Millennium
Development Goal 4 (MDG 4) requires a two-thirds reduction infant mortally rates (IMR)
from 1990 levels by 2015.2 It is predicted that, if current rates of decline in IMR continue,
India will achieve MDG4 by 2023-2024, however, if the pace slows, it may only be achieved
by 2033-2034.1
All too often medical, pediatric and emergency textbooks, courses and research are
targeted at developed countries. Unfortunately, those of us working in developing countries,
frequently struggle to translate the recommended best practice into our workplaces.
In the field of emergency pediatrics in the developing world, our patients are most likely
to present with neonatal emergencies or childhood infections2,3 (sometimes complicated by
malnutrition, lack of immunizations, Tuberculosis or HIV). Developing world emergency patients frequently present
late and in a critical condition. We often have to contend with woefully inadequate staffing, equipment and resources.
OurIPstaff
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have rarely been trained in the assessment and management of pediatric and neonatal emergencies. In many
developing countries prehospital care, transport and emergency medical systems are underdeveloped or absent. For these
reasons many courses and much of the research published from developed countries is not directly relevant to the practice
of emergency care in poorer parts the world.
Therefore, it gives me great pleasure to endorse the second edition of this excellent pediatric emergency textbook
catering for the developing world emergency environment. Given that India accounts for 21% of worldwide under-5
deaths4 it is very encouraging to see experts from this country highlighting quality emergency care of children as a crucial
part of the solution.
The Pediatric Emergency Care Manual has been written by expert pediatric practitioners—who are clearly experienced
in high volume, high acuity, low-resource emergency settings. This book is first and foremost a practical manual of “How
to manage seriously ill children?” and this is explained in an easy-to-follow clear manner—often with the use of high
quality photographs to illustrate techniques. There are also lots of handy tips—my particular favorite being the ‘common
errors’ box included at the end of most chapters. These invariably contain the kinds of ‘pearls of wisdom’ only gained
through considerable experience and rarely passed on in textbooks.
I am especially impressed by the in-depth explanations of underlying mechanisms of disease and pathophysiology.
These help the reader to understand in a ‘back to basics’ way what is going on in a patient and help make differential
diagnoses. There is also considerable detail and up to date information on key drugs, emergency treatments and essential
equipment.
If ever there was a time for pediatric emergency knowledge, skills and expertise to be shared, particularly in India and
other developing countries, it is now. Books like this will hopefully form part of the armamentaria of practical help for
frontline emergency workers in the battle to reduce global child mortality.
xiv Pediatric Emergency Medicine Course (PEMC)
References
1. Reddy H, Pradhan MR, Ghosh R, Khan Ag. India’s progress towards the Millennium Development Goals 4 and 5 on infant and
maternal mortality. WHo South-East Asia Journal of Public Health. 2012;3:279-89.
2. Building a Future for Women and Children: The 2012 Report. Available: http://www.countdown2015mnch.org/reports-and-
articles/2012-report.
3. Lozano R, Wang H, Foreman KJ, Rajaratnam JK, Naghavi M, Marcus JR, et al. Progress towards Millennium Development
Goals 4 and 5 on maternal and child mortality: an updated systematic analysis. Lancet. 2011;378(9797):1139-65.
IP : 196.52.84.10 4. You D, Jones G, Hill K, Wardlaw T, Chopra M. Levels and trends in child mortality, 1990-2009. The Lancet. 2010;
379(9745):931-3.
IP : 196.52.84.10The long awaited second edition of the Pediatric Emergency Medicine Course (PEMC)
manual is here. A veritable atlas of resuscitation, it has the largest number of photographs
taken before, during and after resuscitation! It explains how the pediatric assessment triangle
has been modified to help take therapeutic decisions. Current evidence-based guidelines
have been incorporated such that safer and more effective treatments are employed during
resuscitation.
What’s more! For the first time evidence from our own patients has been used to teach how
to save life in the initial minutes.
Since 2008, the Pediatric Emergency Medicine Course (PEMC) has achieved several
milestones to its credit. In 2010, the Vice Chancellor, Dr Myilvahanan Natarajan ms mch phd
and the senate of the Tamil Nadu Dr MGR Medical University, Tamil Nadu, India, passed a resolution making PEMC
mandatory for interns (PEMC for house officers) passing out from all medical colleges in Tamil Nadu state. To ensure that
thisIPwas implemented, Dr Srilakshmi dch phd, Head, Curriculum Development, Tamil Nadu Dr MGR Medical University,
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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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Preface to the First Edition
IP : 196.52.84.10 “Excellence in specialized pediatric emergency care to get kids back on track”
Few situations in a pediatrician’s practice evoke the anxiety and panic which accompanies the management of an acutely
ill child. The Pediatric Emergency Medicine Course (PEMC) offers a structured approach to handle the crisis using a time
sensitive, goal directed approach during the initial “golden hour” of critical illness.
Conceived by Dr S Krishnan, a pilot course was conducted in 1999 with the collaboration of the emergency and
intensive care physicians of the Kanchi Kamakoti Childs Trust Hospital and the Institute of Child Health, Madras Medical
College, under the suspices of the Indian Society of Critical Care Medicine (ISCCM)—Chennai Chapter. Since then the
content of the course has undergone tremendous changes as international resuscitation guidelines evolved providing
better standards of care. In 2006, this course was formally copyrighted to the ISCCM, Chennai Chapter.
At the 5th National Pediatric Critical Care Conference, executive body meeting of the Indian Academy of Pediatrics,
Critical Care Chapter held at Surat in October 2003, it was suggested the PEMC manual be re-written with evidence-based
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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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Acknowledgments
IP : 196.52.84.10Successful achievement of therapeutic goals in resuscitation is based on coordinated team efforts. Many of the milestones
of the Pediatric Emergency Medicine Course (PEMC) have been achieved by the combined effort of a hugely talented
team. Dr Jayanthi, convenor for the PEMC and south zone coordinator for the BLS, has been a bulwark of strength and
integrity on which this course has grown. Dr Shanthi, an active PEMC instructor and former south zone convenor for
the PALS, is known for her tremendous commitment for teaching pediatric emergency medicine to young doctors at
the bed side. Dr Janani, the former National convenor of the PALS and team leader par excellence is the dynamic force
behind this course. Dr Radhika, the South zone convenor of the PALS and coordinator for the BLS is also known for her
passion for training doctors in CPR. Under the banner of the Indian Academy of Paediatrics, Tamil Nadu State Branch,
Dr Thangavelu, Dr P Ramachandran and Dr Poovazhagi some of the finest intensive care teachers of Tamil Nadu state
have taken key messages of this course to the far nook and corners of every district.
I thank Dr Suresh Gupta, President and Founding Member of the Society of Trauma and Emergency Pediatrics, and
Dr Mahadevan, Professor and Head, Department of Pediatrics, Postgraduate Institute of Medical Education and Research
(PGIMER), Chandigarh, India for editing the section on poisons and envenomation. I also thank, Professor P Arasar
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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 : 196.52.84.10 Ms Sajini (Bengaluru Branch) and her team, for their tireless efforts in making this edition a unique one.
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Contents
Section II Airway
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Section III Approach to Stridor
6. Stridor ---------------- 61
Section IV Breathing
Section V Circulation
Section VI Disability
Section IX Trauma
28. Burns
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29. Electrical Injury -------------- 296
30. Submersion Injury -------------- 299
Appendices
Appendices 1 to 13 389-405
Epilogue 407
Index 409
Abbreviations
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Prologue
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Indumathi Santhanam md
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Professor and Head
Department of Pediatrics
Government Royapettah Hospital
Kilpauk Medical College
Chennai, Tamil Nadu, India
Dear Dr Santhanam
I want to congratulate you, as editor, your contributors and publisher M/s Jaypee Brothers Medical Publishers (P) Ltd,
New Delhi, India for the production of the Second Edition of the Pediatric Emergency Medicine Course (PEMC) manual.
It is designed and was first published in 2008, to be a manual for an educational course bearing its name and implemented
throughout India since 1999; yet its scope goes beyond a course manual. This comprehensive and well-illustrated manual
covers information vital to the care of critically ill and injured children and includes chapters on the following topic areas:
Recognition of Critical Illness, Management of the Airway, Approach to Stridor, Respiratory Distress and Respiratory
Failure, Shock, Diarrhea and Dehydration, Alteration of Mental Status, Envenomation, Poisonings, Traumatic Injury
including Severe Traumatic Brain Injury, Orthopedic Trauma, and Environmental Emergencies. It also has a chapter
dedicated to Radiology in the Emergency Department (ED), Pain and Sedation, Setting up Pediatric Emergency Medical
Services in Rural Hospitals, and a section on Critical Procedures in Pediatric Emergency Care. It is a perfect reference for
pediatric residents, pediatricians, and other medical care providers caring for children in emergency settings.
This manual is based on the experiences of a physician practicing at a large volume pediatric emergency department
at The Institute of Child Health, Madras Medical College, Chennai, Tamil Nadu, India, who resuscitate nearly 13,000
seriously ill children and neonates every year, and see nearly 750,000 pediatric outpatient visits. This manual provides
sorely needed education for physicians caring for children in rural and resource poor environments, as well as physicians
with access to more sophisticated medical resources.
This is an amazing manual—I reviewed the Pediatric Assessment Triangle (PAT) and I think your modification is
brilliant—the original PAT may be too simplistic but there is something to be said for simplicity—I love all your features
and the algorithms at the end.
xxvi Pediatric Emergency Medicine Course (PEMC)
The manual incorporates a number of special features that provides the learner with tools to rapidly assess and treat
critically ill and injured children. Each chapter presents case scenario pertinent to the topic area, such as a child in
respiratory distress, then proceeds through a systematic discussion of the rapid assessment of that patient using a tool based
on a similar tool used in the United States for the rapid assessment of children, the Pediatric Assessment Triangle (PAT).
The method described includes evaluation of appearance, airway and breathing, and circulation, which when combined
together can create a picture of the physiologic status of the child and will drive management priorities including the rapid
initiation of life-saving treatment. Besides Case Scenarios and use of a Rapid Assessment Tool, other features include
IP : 196.52.84.10 Call Outs that provide key clinical pearls for the learner to better understand either the pathophysiology or the treatment
plan. At the end of each chapter are Key Points which emphasizes important concepts that should not be forgotten in the
care of children in emergency settings, Common Errors that describe important pitfalls to avoid in the care of children
with a particular life-threatening condition highlighted in the chapter, and finally a Protocol is provided at the end of
the chapter to serve as a quick reference guide which could be posted for pediatric emergency care providers to manage
children with potentially life-threatening conditions.
This manual appropriately highlights some of the serious illnesses occurring in children in the subcontinent of India,
including acute diarrheal illness and hypovolemic shock. Given that there are over 450,000 cases of diarrheal disease
worldwide and that 22% of deaths due to this disease occur in India, it is critical that emergency care providers recognize
early signs of dehydration and hypovolemic shock and have a management plan to rapidly treat these infants and children.
Recognition and management of septic shock, dengue shock syndrome and specific poisons and envenomations that are
endemic in India are also discussed. Finally the manual highlights the assessment and treatment of the mortal conditions
that affect children worldwide including respiratory failure, status epilepticus, burns, submersion injury, and traumatic
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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.
Section I
Critical Illness
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1
Recognition of Early Signs
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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
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A weak cry and loss of eye contact in infants more than Febrile infants who present with squirming move-
2 months of age are early ominous signs of cerebral hypop- ments and upward gaze are often inappropriately referred
erfusion. In older children lethargy, inability to sit, stand or treated as atypical febrile fits.
or walk, agitation, fighting the oxygen mask and confusion
alternating with drowsiness herald brain hypoperfusion.
Ù
Control the urge to administer anticonvulsants.
Ù
Inability to recognize the mother or a vacant look is an
ominous sign.
Breathlessness
Breathlessness is the commonest symptom for which an
acutely ill child is brought to the PED (Figure 1.12).
Figure 1.11: This picture shows a 7-year-old child with shock
fighting the oxygen mask. It is an ominous sign indicative of
severe hypoxia especially in older children, who are aware that
an oxygen mask is not a noxious intervention. Fighting the
mask, however is normal in infants and toddlers if the other
parts of the pediatric assessment triangle are normal.
Unresponsiveness (U)
Unresponsiveness, whilst not difficult to triage, is often a
diagnostic challenge to novice pediatricians manning the
ED.
●● Sudden unresponsiveness in the absence of precipitat-
ing events in a previously normal child or a child with
seizure disorder is suggestive of non-convulsive status
epilepticus (NCSE).
●● Failure to regain baseline consciousness after a brief
generalized tonic-clonic seizure is also suggestive of
NCSE.
Figure 1.12: This figure shows why children presenting with
Ù severe shock may also have respiratory distress.
All abnormal movements in unresponsive children are
not seizures. Upward gaze with extensor stiffening or Bronchiolitis, pneumonia and asthma are well known eti-
flexor spasm of limbs can occur due to hypoxia and ologies of acute respiratory distress. However, a significant
number of shocked children who present to the ED, have
shock. This clinical presentation must be differentiated
breathlessness due to pulmonary edema2 (Figure 1.11).
from convulsive status epilepticus. A targeted history and
rapid cardiopulmonary cerebral assessment (protocol I) Severe insults such as sepsis, anaphylaxis, status epi-
are essential to guide management. lepticus, scorpion sting, submersion injury, perinatal de-
Inadvertent administration of anticonvulsant drugs pression can directly affect the heart, systemic and pulmo-
for posturing secondary to severe hypoxia or/and nary vasculature.
shock can be lethal. On the contrary, administration of ●● Vasodilation and capillary leak leads to loss of fluids.
anticonvulsant drugs is life saving in NCSE. Loss exceeding 25% of effective circulating volume,
results in shock.
8 Section I n Recognition of Critical Illness
●● Capillary leak also occurs in the pulmonary capil- tone of these muscles in unresponsive victims result in air-
laries. Increased pulmonary vascular permeability way obstruction.
leads to pulmonaryIPedema, also known as acute lung
: 196.52.84.10 ●● Neurogenic or functional stridor should be recognized
injury (ALI). early. The airway is positioned using the head tilt- chin
●● Severe insults (hypoxia, prolonged shock, venom, etc.) lift maneuver.
can lead to acute myocardial dysfunction. The resultant ●● If trauma is suspected in the unresponsive child, jaw
hydrostatic pulmonary edema can present as respira- thrust maneuver must be employed to open the air-
tory distress. way.
●● Crying children or children with suspected ‘structural’
Ù Triage Questions airway compromise should be evaluated in their par-
1. Mother can provide information of early hypoxia and ent’s lap.
shock for children presenting with fever, acute diar-
rhea, asthmatic exacerbations or focus of infection. Assessment of Breathing
• Is the child more tired, sleepy than usual? Oxygen must be administered simultaneously as the as-
• Is he as usual or not? sessment is being performed.
• Does the child cry inconsolably (in younger in-
●● Use a flow-inflating ventilation device (refer Chapter
fants)?
5), if respiratory distress is identified (with the excep-
2. Mother can also help us find out whether her child tion of asthma).
with sepsis, diarrhea, scorpion envenomation, sei- ●● Use non-rebreathing mask, if effortless tachypnea is
zures, etc. has developed features of pulmonary ede- noted.
ma. ●● Simultaneously, place the hand on the chest and count
• Has the child developed respiratory distress? respiratory rate for 6 seconds and multiply by 10.
• Is it the first episode (not since birth or episodic)? ●● Check the vital signs chart for age-related ranges.
●● Note whether respiratory rates for age are increased,
Ù decreased or normal.
The three components of the PAT, appearance, breathing Vital signs for each age group must be displayed in the
(evaluation of the airway is included in breathing) and ED. Refer protocol 1.1.
circulation is depicted as 3 separate colored triangles.
The arrows within the 3 triangles indicate the need to Ù
reassess systematically the response of interventions on • If respiratory rates appear to fall within the normal
range for age, but is associated with an unstable airway,
the ABCs. Each assessment is ideally performed in less
shock and unresponsiveness, recognize respiratory
than 60 seconds (Figure 1.24).
failure. Initiate bag-valve-mask ventilation, whilst,
the next responder continues to perform the remaining
Assessment of airway part of the cardiopulmonary cerebral assessment.
• As the respiratory rate is being counted, look for
Crying or vocalization indicates that the airway is patent. grunt, retractions and whether respiration is thoracic
Harsh inspiratory sounds suggests stridor secondary to or abdominothoracic.
structural airway obstruction. ‘Snoring’ in an unresponsive • Grunt and abdominothoracic respiration are ominous
child indicates that the airway is obstructed by secretions signs of impending respiratory failure.3
or falling back of tongue. Unresponsive children presenting
with stridor must be evaluated on the resuscitation trolley.7 Respiratory effort offers information, as to whether the
Ù
Presume that the airway is unmaintainable in children
child has respiratory distress or respiratory failure.
●● Auscultate infra-axillary regions on both sides.
who are unconscious or posturing. ●● Listen for air entry, wheeze and crepitations.
The patency of the airway is maintained by the normal ●● Evaluate color by comparing the palm of the physician
tone of the palatopharyngeal muscles and tongue. Loss of with that of the child’s sole (Figure 1.13).
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 9
●● Pallor, dusky hue, ashen, mottling is documented as ●● However, tachycardia may persist when atropine is
abnormal. used for intubating children in shock.5
●● Other causes of persistent tachycardia are fever, anxi-
IP : 196.52.84.10
ety, pain and systemic inflammatory response syn-
drome (SIRS).3,9
●● In addition, tachycardia may be the only sign of ongo-
ing seizure activity in a paralyzed and sedated child
with shock.
●● Heart rates greater than 220 beats/minute in infants and
180 beats/minute in children warrant urgent evaluation
and treatment.3 An electrocardiography (ECG) may be
necessary, because the pulse oximeter may be unreli-
able in identifying supraventricular tachycardia.
Ù
A heart rate that is relatively normal for age despite
the presence of severe respiratory distress or failure
Figure 1.13: It is not uncommon for the color to be noted as and shock (relative bradycardia) is an ominous sign.
normal in shocked children. The difference may be apparent These children have exhausted their physiological
only when comparing with the ‘normal’ color of the physician. compensatory mechanisms and are at risk for abrupt
deterioration and arrest.
Assessment of circulation
●● Other causes of relative bradycardia in children pre-
Heart Rate senting with shock are raised intracranial pressure,10,11
hypothermia, hypokalemia (often noted in diarrheal
Assess heart rate for 6 seconds and multiply by 10. Simul- dehydration and severe malnutrition complicating sep-
taneously, check the vital signs chart to determine whether tic shock), dengue shock syndrome12 and drugs such as
tachycardic, bradycardic or normal for age (Figure 1.14). digoxin and beta blockers.
Perfusion
Comparison of Pulses
Central pulse (femoral) is felt by placing the index finger
of one hand snugly into the inguinal region. It is compared
with the dorsalis pedis, which is felt by simultaneously
placing three fingers perpendicularly on the dorsum of the
foot.
●● Weak or absent distal pulses is caused by peripheral
vasoconstriction, while absent distal pulses suggest
decompensated shock.
●● Loss of central pulses is a premorbid sign requiring
Figure 1.14: Assessment of heart rate. Note that the physician very rapid intervention.7
is holding the airway as he evaluates the heart rate. ●● Bounding central and distal pulses in association with
tachypnea, tachycardia and altered mental status sug-
●● Tachycardia is the earliest compensatory response to gest the presence of a hyperdynamic circulation with
decreased stroke volume or hypoxemia. low systemic vascular resistance.
●● Young infants and neonates, however, may respond ●● Vasodilatory shock is identified when diastolic pres-
with paradoxical bradycardia.3 sure is lower than 50% of systolic blood pressure.15
●● Normalization of heart rate is one of the most reliable ●● If dorsalis is not felt, do not report as ‘normal’ periph-
signs of shock resolution.8 eral pulse based on the posterior tibial (Figure 1.15).
10 Section I n Recognition of Critical Illness
Age SBP
Term newborn (0–28 days) < 60 mm Hg
For infant < 12 months < 70 mm Hg
1–10 years < 70 + (2 × age)
> 10 years < 90 mm Hg
Blood pressure (Table 1.2) may be preserved in early shock Systolic blood pressure: Interpretation of systolic blood
due to the compensatory increase in systemic vascular resis- pressure in children with shock:
tance (SVR). In young children, increase in vasomotor tone
results in BP that is in the higher range for age. Under these ●● High in shock (normal response).
circumstances, as therapeutic goals of shock are achieved, ●● Normal range (relative hypotension).
blood pressures may decrease to the normal range for age. ●● Hypotension (can progress to imminent arrest in min-
utes).
In vasodilatory shock states, low SVR results in widen- Diastolic blood pressure13: As mentioned earlier, diastolic
ing of pulse pressure. This is characterized by a diastolic pressures less than 50% of systolic pressure harbinger va-
BP that is less than or equal to half of the systolic BP. In sodilatory shock when associated with altered mental sta-
these children, pulse pressure narrows with resolution of tus, abnormal respiratory rates, work of breathing, tachy-
shock. Wide pulse pressures may also be noted in children cardia, warm, pink peripheries, bounding pulses and rapid
with neurogenic and anaphylactic shock, as well as chron- CRT.
12 Section I n Recognition of Critical Illness
●● Mean arterial pressure (MAP) is calculated as the sum ●● If the liver span is increased in children presenting with
of the diastolic pressure and one-third pulse pressure. A respiratory distress, it is probable that myocardial dys-
value less than 65 mmIP Hg is considered as hypotension.
: 196.52.84.10 function is the causative factor.
●● Conventionally, documentation of systolic pressure is ●● A normal liver span on the other hand points to primary
given importance. Early warm shock could be missed, lung pathology as causative of respiratory distress.
if diastolic pressure and MAP are not noted.
Ù
Alteration in liver span following each bolus of fluid,
Liver Span intubation or inotrope infusion helps to decide whether
Measure liver span during the assessment of circulation. myocardial dysfunction is improving or not. Thus
It is helpful in assessing and monitoring the severity of assessment of liver span is a simple method of assessing
myocardial dysfunction.5 myocardial dysfunction in settings without access to
invasive monitoring.
Disability Assessment
Neurological assessment is an integral part of evaluation
of a child with hypoxia, shock and seizure activity and
may provide clues to the underlying etiology and response
to therapy.
When examining for pupillary response, simultaneous-
ly, look at the position of eyes. Is it conjugating or mid-po-
sition? Note for presence of abnormal ocular movements.
Abnormal ocular movements in a child presenting with
an exacerbation of asthma is suggestive of a near fatal at-
tack. Identification of this sign in a child with respiratory
failure and shock due to bronchiolitis suggests the need to
aggressively resuscitate hypoxia.
Indeed, eye signs in children presenting with severe
cardiopulmonary failure in the absence of seizure history,
has been associated with increased risk of mortality.14
●● Conjugate eye deviation, nystagmus or eyelid twitch
indicate presence of NCSE or severe hypoxic ischemic
insult to the brain (Figures 1.20A to C). Other gaze ab-
normalities, which may mimic non-convulsive status
Figures 1.19A and B: A. Marking lower border of liver; B. epilepticus are upward gaze and roving nystagmus.
Measuring the liver span. Assessment of liver span helps in the
Continuous epileptiform electroencephalogram (EEG)
evaluation of myocardial dysfunction in critical illness.
abnormalities have been noted in comatose adults with
severe metabolic or anoxic encephalopathies.15
●● The upper border is identified by percussion and the
lower border by palpation (Figures 1.19A and B). Us- ●● Avoid rushing to administer anticonvulsants.
ing a pen, both borders are marked and the total span is ●● The importance of early recognition and simultaneous
measured and documented. management of status epilepticus (convulsive and non-
●● These measurements are compared with normal values convulsive) is important in ensuring successful out-
displayed in the ED. comes in shock.8
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 13
Ù
Management of eye signs of non-convulsive status
IP : 196.52.84.10 epilepticus (NCSE) is based on the history. If history
is suggestive of GTCS, the NCSE is probably due to
ongoing seizure activity, administer anticonvulsants.
If on the contrary, altered mental status follows acute
diarrhea, fever, breathlessness, scorpion sting, etc. the
eye signs denote the severity of the shock and hypoxia.
Ù
Do not forget to look at eye position and eye movements Figure 1.22: Unequal pupils. Examination of the pupils can
help pick up a wide variety of other unexpected conditions
during rapid cardiopulmonary cerebral assessment.
such as coloboma, xerophthalmia, etc. in seriously ill children
(Courtesy: Dr Gunda Srinivas).
14 Section I n Recognition of Critical Illness
Disability
●● If child having altered level of consciousness: Correct
hypoxia and shock and then reassess.
●● If NCSE/CSE: Treat seizure activity as discussed in
Chapter 21.
●● If raised ICP: Treat ICP as discussed in Chapter 20.
Ù
Repeat cardiopulmonary cerebral assessment after
administration of fluid bolus, anticonvulsant, intubation,
etc. and determine the new physiological status.
Figure 1.23: The Broselow tape
Intervene appropriately for each of the parameters viz
Often children who are critically ill cannot be weighed
ABCDs (Figure 1.24).
conventionally, for such children Broselow tape is useful
to calculate approximate weight based on length of the Uncompromising standards are needed in terms of accu-
child (Figure 1.23). racy, speed and skill in performing rapid cardiopulmonary
IP : 196.52.84.10
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department
15
Figure 1.24: Pediatric Assessment Triangle (PAT) to enable recognition of severity and decision making in seriously ill children in the emergency setting
(Modified from Dieckmann RA, Brownstein D, Gausche-Hill M. The Pediatric Assessment Triangle–a novel approach for the rapid evaluation of children. Pediatr Emerg Care. 2010 Apr;26(4):312-15)
16 Section I n Recognition of Critical Illness
common errors
1. Recognizing serious illness only when the
û
‘consciousness’ drops profoundly.
2. Referring the febrile child with acute onset posturing
to the neurologist or to the psychiatrist for agitated
behavior.
3. Administration of higher antibiotics for a febrile
child with altered mental status without evaluating
or managing coexisting shock.
Figure 1.25: This picture shows a very young infant making 4. Administration of sedatives for infants with incessant
eye contact with his happy mother following successful
cry without ruling out hypoxia and shock.
shock resuscitation. His response to his mother, suggests
neurologically intact survival.
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 17
IP : 196.52.84.10
Figure 1.26A: Pediatric emergency case record: front page (assessment part)
18 Section I n Recognition of Critical Illness
IP : 196.52.84.10
Figure 1.26B: Pediatric emergency case record: back page (monitoring and reassessment part)
Note: Refer appendix for sample documentation of Pediatric Emergency Case Record
Chapter 1 n Recognition of Early Signs of Critical Illness in the Out Patient Department 19
Protocol 1.1: PEMC approach: Recognition of relative bradypnea and relative bradycardia
IP : 196.52.84.10
20 Section I n Recognition of Critical Illness
References ment of severe sepsis and septic shock. Crit Care Med.
2008;36(1):296-327.
1. Santhanam Indumathy, Pai M, Kasthuri KR, et al. Mortal-
IPthe
: 196.52.84.10 9. Goldstein B, Giroir B, Randolph A. International pediat-
ity after admission in pediatric emergency department:
A prospective study from a referral children’s hospital in ric sepsis consensus conference: definitions for sepsis and
Southern India. Pediatr Crit Care Med. 2002;3:358-363. organ dysfunction in pediatrics. Pediatr Crit Care Med.
2005;6:02-08.
2. Santhanam I, et al. Implementation of Pediatric Emergency
Medicine Course Guidelines (PEMC). Impact on mortality 10. Pollard AJ, Britto J, Nadel S, et al. Emergency management
in critically ill children presenting to a large volume PED of meningococcal disease. Arch Dis Child. 1999;80:290-
of an academic children’s hospital in India. Pediatr Crit 96.
Care Med. 2011;(12):3. 11. Pollard AJ, Nadel S, Ninis N, et al. Emergency manage-
3. Zaritsky AL, Nadkarni VM, Hickey RW, et al. Recognition ment of meningococcal disease: eight years on. Arch Dis
of respiratory failure and shock. Textbook of Pediatric Ad- Child. 2007;92:283-86.
vanced Life Support. Dallas TX: American Heart Associa- 12. Ranjit S, Kissoon N, Ghandhi D, et al. Early differentia-
tion; 2002. 36:97-98. tion between dengue and septic shock by comparison of
4. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- admission hemodynamic, clinical and laboratory variables:
spective randomized controlled study of two fluid regimens a pilot study. Pediatr Emerg Care. 2006;23:368-75.
in the initial management of septic shock in the emergency
13. L. Chameides, R. Samson, Schexnayder SM, et al. Pedi-
department. Pediatr Emerg Care. 2008;24:647-55.
atric Advanced Life Support. American Heart Association;
5. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- 2011. pp. 72.
spective randomized controlled study of two fluid regimens
in the initial management of septic shock in the emergency 14. Santhanam I, Padma V, Murali T, et al. Predictors of mor-
department. Pediatr Crit Care Med. 2007;Suppl Vol 8, No tality of serious sepsis. Proceedings of the 1st European
3:A17. (Paper presented at the 5th Pediatric Critical Care congress on Pediatric Resuscitation and Emergency Medi-
Congress June 24th 2007, Geneva). cine (PREM). May 2nd, 3rd 2013:Ghent, Belgium.
6. Kirkham FJ, Newton CR, Whitehouse W. Paediatric coma 15. Jordan KG. Non-convulsive status epilepticus in acute
scales. Dev Med Child Neuro. 2008;50:267-74. brain injury. J Clin Neurophysiol. 1999;16:332-40.
7. Santhanam I, Ranjit S, Kissoon N. Management of shock in 16. Dieckmann RA, Brownstein D, Gausche-Hill M. The
the emergency department. Minerva Pediatr. 2009;61:01-15. Pediatric Assessment Triangle–a novel approach for the
8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving rapid evaluation of children. Pediatr Emerg Care. 2010
Sepsis Campaign: International guidelines for manage- Apr;26(4):312-15).
Airway
Section II
IP : 196.52.84.10
IP : 196.52.84.10
2
IP : 196.52.84.10
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.
Ù
Most infants and children who require respiratory sup-
port on arrival in to the ED, have abnormal lung paren-
chyma. Chest compliance is poor and immense effort is
often needed to provide effective ventilation and normal-
ize oxygen saturation (Figure 2.3). The largest bags (at
least 1 liter) are needed to provide effective chest rise.
Smaller bags or ‘pediatric bags’, i.e. 450–750 mL are not
sufficient for providing bag-valve-mask (BVM) ventila-
Figure 2.4: Gastric decompression via NGT
Chapter 2 n Basic Airway Management 27
IP : 196.52.84.10
Figure 2.9 Double EC-clamp: Often provision of effective BVM Figure 2.10 Appropriate EC-clamp: The airway manager
ventilation may need two persons. One person provides the should sit and support his elbows, while performing BVM
double EC-clamp. The second person pumps the bag, while ventilation. Fingers providing C-clamp should encircle the rim
giving additional pressure on the mask to prevent air leak. of the mask. Effort is taken to prevent air leak at the site of exit
of the NGT. Fingers providing E-clamp should be flexed at the
The commonest cause for ineffective BVM technique MP joints to hook and lift the jaw. The middle fingers is at the
stems from failure to provide an airtight seal of the mask. mentum, the ring finger at the ramus and the little finger at the
angle of the jaw.
The nasogastric tube emerging from the rim can thwart
attempts to make the seal airtight.
Ù
The correct EC-clamp technique (not easy) is the impor-
tant first step (Figures 2.5–2.11).
The E-clamp is provided using the middle, ring and lit-
tle fingers each of which are positioned on the mentum,
ramus and the angle of the mandible. The tip of these
fingers should indent the soft tissue along the bony rim
of the mandible. The E-clamp acts as a bucket handle
to lift the jaw to meet the C-clamp such that the seal is
airtight.
The C-clamp is provided using the thumb and index fin- Figure 2.11 Inappropriate technique: Mask ventilating
ger to encircle the mask along its rim. children presenting with respiratory failure, needs immense
effort to move the chest. Avoid pumping the bag from below.
The elbow of the hand holding the EC-clamp should be
placed on the resuscitation trolley. The ‘V’ position of the
Ù
Ability to bag-valve-mask effectively is the foundation
elbow automatically ensures that airway patency is main- for advanced airway skills.4
tained (‘head tilt, chin lift’).
The EC-clamp will be effective if the following precau-
Ù
Ensure that the elbow is at a lower level than the EC-
tions are taken:
clamp to avoid compromise of the airway. ●● Fingers (E-clamp) should not be bunched together.
●● Fingers providing the E-clamp should be flexed at
Avoid standing and bagging when the elbow gets posi- both the metacarpal joints thus avoiding soft tissue
tioned above the EC-clamp (refer Figure 2.7). obstruction.
Chapter 2 n Basic Airway Management 29
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.
Indications for Intubation citation for respiratory failure due to severe parenchymal
lung disease (Figure 3.3).
A 6-month-old infant has been having acute watery di-
arrhea and vomiting IP for: the
196.52.84.10
past 2 days. He had not A 9-year-old boy is referred for snake envenomation.
been responsive to his mother since the evening. For the Even as he is being evaluated, he develops bilateral pto-
past ½ hour he had been ‘mouth breathing’. sis and apnea.
Figure 3.2 Physiological status: Imminent arrest Figure 3.4 Physiological status: Respiratory failure due to
respiratory muscle paralysis
Imminent arrest is the most well-known indication for
urgent intubation. Airway protective reflexes are absent After provision of basic airway management, he needs
and vocal cords are not responsive. In these situations, to be intubated and ventilated for respiratory failure sec-
BVM is initiated and intubation performed without resort- ondary to neuromuscular paralysis (Figure 3.4).
ing to anesthetic drugs (Figure 3.2).
A 5-year-old child is being provided BVM ventilation
A 1-year-old child is being treated for cellulitis over for respiratory arrest secondary to convulsive status
the right upper limb. She has been crying inconsolably epilepticus. She continues to convulse despite 2 doses
since the morning. of Lorazepam and loading dose of Phenytoin. Is there a
need to intubate this child (Figure 3.5)?
Figure 3.3 Physiological status: Sepsis with Figure 3.5 Physiological status: Refractory status
cardiogenic shock epilepticus
This child has presented with respiratory failure either Provision of prolonged mask ventilation cannot be sus-
due to, cardiogenic or non-cardiogenic pulmonary edema. tained. This child’s seizures have been refractory to the ini-
In addition, she also has vasodilatory shock with low mean tial drugs. Administration of further anticonvulsant drugs
arterial pressure secondary to severe sepsis. She will even- is an indication for elective intubation using anesthetic
tually need elective intubation after the initial fluid resus- agents (Figure 3.5).
32 Section II n Airway
A 2-year-old child is rushed into the ED after he devel- lent intubating conditions 60 seconds after administration
ops stridor, respiratory distress following intravenous of anesthetic drugs.
contrast administrationIP in the radiology department.
: 196.52.84.10 Excellent intubating conditions are defined as com-
plete jaw relaxation, open immobile vocal cords with ab-
sence of coughing, bucking and diaphragmatic movement
in response to intubation. It is implemented in a logical
sequence and comprises of several coordinated steps.
The pharmacologically assisted intubation (PAI) de-
scribed in this manual deviates from the classical RSI.
Ù
Secure 2 intravenous lines prior to intubation
One line is dedicated for inotrope infusion
Most critically ill children requiring intubation in
ED settings have shock. Since sedatives tend to lower
systemic vascular resistance and the application of
positive pressure concurrently decreases preload, shock
could worsen immediately after intubation and assisted
ventilation. An additional bolus, is recommended post-
intubation.
Figure 3.7: The airway being positioned and oxygen is The second line is dedicated for administration for
provided using a Jackson-Rees circuit. Note that the NGT has anesthetic drugs.
been inserted prior to administration of anesthetic agents.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 35
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
Ù
Vomiting during intubation is one of the dreaded com
into the glottis under vision.
The airway physician, receives the larygnoscope handle
plications. Quickly release cricoid pressure, turn the head in his left hand, with the blade pointing down. The blade
to one side and rapidly suction and clear the airway. is inserted from the right side of the mouth and is used to
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 37
Ù
Caution: Introduction of the blade beyond the base
of the tongue is the commonest error made by novice
physicians resulting in esophageal intubation.
Postintubation Management
Ù
A common misconception amongst novice airway
managers is that the ‘job is done after intubation’.
Fixing the tube is as important as intubation!
INTUBATION IN ED
SETTINGS: CHALLENGES
Pharmacologically assisted intubation involves use of
anesthetic drugs commonly used in the OR. Children for
whom elective intubation is planned, are advised ‘nil per
oral’ 6 hours prior to surgery. Surgery is often canceled if
minor illnesses are identified during evaluation for anes-
thetic fitness. Besides, if intubation is difficult following
Figure 3.17: This is repeated for the second piece of plaster
after induction, the anesthetist has the option of postpon-
on the upper lip as shown in the next picture
ing surgery to another day.
Following intubation, the 5-point auscultation, is used ●● On the contrary, critically ill children are presumed to
to check tube position. Auscultation is performed over the have ‘full stomach’.
right infraclavicular region, then over the left infraclavicu- ●● They are being intubated for severe hemodynamic in-
lar, right infra-axillary, left infra-axillary areas and over stability.
the stomach. Next, HR, color, CRT, pulses, core-peripheral ●● Unlike, intubations performed in the OT, emergency
temperature gap, BP, liver span and pupils are examined intubations are performed in full view of anxious and
sequentially. often grief stricken parents.
Chapter 3 n Pharmacologically Assisted Intubation (PAI) in the PED 39
●● ‘Need to ventilate cannot intubate’ after neuromuscular a minimum dose of 0.1 mg (lesser dose causes paradoxical
blockade is perhaps the most anxiety provoking situa- bradycardia). Atropine also blocks secretions induced by
tion for the ED physician. succinylcholine and ketamine.
IP : 196.52.84.10
●● Postponing intubation to a later date is not an option
in the ED. Studies have shown that use of atropine is unneces-
sary when performing RSI in pediatric patients in the ED.
Caution However, this evidence lacks statistical power and further
studies are needed.6
Intubation using anesthetic drugs is hazardous when un-
dertaken by physicians who are not trained in the OT under
the guidance of anesthetists. The key to successful intuba- Lidocaine7,8
tion is the ability to perform effective bag-valve-mask ven- Lidocaine is advocated as pretreatment in the manage-
tilation, have thorough knowledge of anesthetic drugs and ment of children with risk of raised intracranial pressure.
should have performed several intubations using ‘sedation It is useful in attenuating the rise in ICP caused by reflex
only’ protocol. sympathetic response to laryngoscopy. It is administered
Intubation using paralytic agents in the ED requires prior to succinylcholine (1.5 mg/kg intravenously) to
enormous dedication, expertise and team work for suc- avoid drug-induced rise in ICP. Use of lidocaine should be
cessful outcomes. Drawing up appropriate medications avoided in patients with bradyarrhythmia, hypotension and
and assigning tasks to all personnel assisting in the proce- in those allergic to amides.
dure should be seamlessly performed. RSI medications, are divided into induction and para-
Ù lytic agents. Development of pulmonary edema, hypoten-
In the Indian context, majority of children reaching the ED sion, imminent arrest, raised ICP, respiratory failure and
are in respiratory failure with severe hypoxia on arrival. refractory status epilepticus are the commonest indications
Under these circumstances, preoxygenation with non- for intubation in the ED.
rebreathing mask prior to intubation seems in-sufficient
to improve oxygen reserves. It appears safer to provide
positive pressure ventilation after administration
Induction Agents
of neuromuscular blockade. This practice, prevents Induction agents are primarily administered to sedate prior
deterioration to cardiac arrest during during intubation to paralyzing. Commonly used induction agents are:
in the hemodynamically compromised child. To avoid,
Midazolam, Thiopental, Ketamine, Fentanyl, Etomidate
gastric distension and aspiration, a nasogastric tube is
introduced to rapidly remove gastric contents.
Midazolam
This modified technique employing preoxygenation
Midazolam, a sedative and hypnotic agent, is also useful
using bag-valve-mask after paralysis and NGT decom
in controlling convulsions. A frequently used induction
pression has not resulted in mishaps in a large volume agent, it causes respiratory depression and hypotension.
PED. No child desaturated during intubation attempts.4
Ù
Midazolam should be avoided in children presenting
Medications with hypotensive shock.
Atropine
Pediatric Emergency Medicine Committee of the Ameri- Thiopental
can College of Emergency Physicians5 recommends at- Thiopental an ultrashort acting barbiturate, acts by inhibit-
ropine for RSI in children younger than 1 year, for older ing the GABA receptor complex. It causes a dose-depen-
children (1–5 years) receiving succinylcholine and ado- dent decrease in cerebral metabolic oxygen consumption,
lescents receiving a second dose of succinylcholine. The cerebral blood flow and ICP. It also maintains cerebral per-
recommended atropine dose is 0.02 mg/kg in children with fusion pressure. Thus, its cerebroprotective effect is useful
40 Section II n Airway
pressure has been attributed to the use of succinylcholine. cally difficult and intellectually challenging procedure
Hence this drug is withheld in children with risk of ICP performed on critically ill children in ED settings. If per-
and glaucoma. In general,
IP fasciculations
: 196.52.84.10are less intense in formed successfully, the outcomes can be extraordinarily
children than in adults. The routine use of defasciculation gratifying.
doses of succinylcholine in the ED is controversial.8
Key Points11
ü
Vecuronium, Pancuronium and Rocuronium 1. Preoxygenate on arrival and insert NGT.
2. Initiate inotrope.
Vecuronium, pancuronium and rocuronium are the com- 3. Preparation—O2, suction, IV access, tubes, tapes,
monly used non-depolarizing agents. These drugs act by
drugs, equipment.
binding to the neuromuscular receptor causing blockade,
4. Premedicate.
but no depolarization. All act less quickly and last much
longer than succinylcholine. 5. Put to sleep.
6. Position the patient.
Amongst these drugs, rocuronium has the fastest onset 7. Pressure on cricoid.
of action (60–90 seconds) with duration of action of ap- 8. Paralysis.
proximately 30–40 minutes. Pancuronium has the slowest 9. Preoxygenate using bag-valve-mask device.
onset and longest duration of action lasting up to 60–90
10. Place the tube and check position.
minutes. Though the side effects described for succinyl-
11. Prevent dislodgement during transport.
choline do not exist in this group of drugs, the longer dura-
tion of action delays recovery. Difficulty in securing the
airway would be hazardous under these circumstances. common errors
1. Failure to adequately preoxygenate prior to
û
Failed Intubation intubation.
●● Intubate within the time taken for you to breathe out! 2. Failure to position the child such that the oropharynx
(20–30 seconds). and laryngopharynx are not in the same straight
●● Avoid making more than 2 attempts if unsuccessful on line.
the first attempt. 3. Inserting the laryngoscope into the esophagus.
When patient is paralyzed and the ET tube cannot be 4. Failure to confirm tube position by performing the
placed, the first option is to ventilate the child using a bag- complete cardiopulmonary cerebral assessment.
valve-mask device until the return of spontaneous respira-
5. Failure to initiate an inotrope prior to administration
tion. This technique can be employed until expert help ar-
of anesthetic agents.
rives (Refer to Chapter 4 on Assessment and Management
of the Difficult Airway). 6. Failure to hold the ET tube, until it is secured.
7. Failure to anticipate that shock can worsen after
Pharmacologically assisted intubation, in the hemo- intubation.
dynamically unstable child, is perhaps the most techni-
42 Section II n Airway
Contd...
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.
Step 2: Ensure Oxygenation ●● Avoid manipulation of the airway if more than two
attempts had been made and earlier attempts had
1. Provide high concentration oxygen using a flow inflat-
IP :(refer
196.52.84.10 failed.
ing ventilation device Chapter 5) in a spontane-
ously breathing child with airway obstruction. ●● If saturations cannot be maintained despite effec-
tive bag-valve-mask ventilation, plan to insert the
2. Initiate bag-valve-mask ventilation, if the child pres-
ents with respiratory failure or has not recovered from laryngeal-mark airway (LMA).
paralysis. Oxygen flow should be enough to keep the
reservoir inflated throughout the respiratory cycle.
Ù Patients need oxygen not tube.5
3. Constantly, ensure that the oxygen saturation is great-
er than 95% (one member in team should be delegated Difficult tracheal intubation can be divided into problems
the responsibility of informing the airway manager with laryngoscopy and problems with intubation.
when the saturations drop to 92%).
Ù Step 3: Laryngoscopy and Intubation
Bag-valve-mask ventilation could be difficult when oral
or posterior pharyngeal structures crowd the airway. Ù
Difficult laryngoscopy most commonly results from
Large tongue, tonsils, or adenoids, or a ‘floppy’ larynx
can all obstruct the airway. improper head positioning along the frontal plane.
●● Use sedatives with caution, since these drugs can 5. Change the airway manager
cause hypotension and can convert a difficult air- If the airway manager, is unable to intubate after 2 at-
way into an obstructed airway. tempts, ideally, assistance must be sought from a more
IP : 196.52.84.10
●● Give half the dose initially followed by another skilled person (Figures 4.2 to 4.5).
half dose if airway and breathing can be supported
by bag-valve-mask ventilation. Continue to initiate bag-valve-mask ventilation and
●● Consider use of atropine to avoid vagal-induced wait until a more experienced airway physician arrives.
bradycardia during laryngoscopy, though evi- This could be an anesthetist, ENT surgeon’s or ED or in-
dence for this practice is equivocal.6 tensive care physician.
●● Use muscle relaxants judiciously in upper airway
obstruction. Ù
Patients do not die from failure to intubate. They die
●● Avoid muscle relaxant, if bag-mask-valve ventila- from failure to STOP trying to intubate.5
tion is ineffective.
●● Rapidly transport to the operating room for inha-
lational induction, if child presents with stridor
and respiratory failure to the ED.
4. Intubation.
Difficult tracheal intubation could result from several
problems.
Small endotracheal tubes are compliant leading to diffi-
culty in negotiating the acute angle of an anteriorly placed
pediatric larynx.
Ù
Use an introducer, bent into a ‘hockey-stick’ . Figure 4.3: Note the abscess on the back can prevent
visualization of the glottis. Though the neck appears
The small size of the newborn’s mouth causes diffi- hyperextended, optimal airway alignment was possible
culty in visualizing the vocal cords, when introducing the based on the position, which ensured maximum chest rise,
endotracheal tube (mentioned earlier). improvement in heart rate, perfusion and SaO2.
Ù
Insert the endotracheal tube from the right-hand corner
of the mouth with the plane of insertion at 90° from the
plane of the cord visualizing.
Ù
If despite all the maneuvers mentioned above, intubation
has failed and saturations are dropping, resort to LMA.
Laryngeal mask airway is a rescue device in a ‘cannot Figure 4.7: Technique of insertion
intubate cannot ventilate’ (CICV) situation. 4. Place the head and neck in the sniffing position. Open
the mouth, while lifting the chin forward (Figure 4.8).
Figure 4.6: Parts of laryngeal mask airway (LMA). Figure 4.8: Technique of insertion (Contd...)
Chapter 4 n Assessment and Management of the Difficult Airway 49
9. Inflate the cuff using an air filled syringe until the pi-
lot balloon gets filled up. The laryngeal mask may be
observed to ‘rise up' slightly out of the oropharynx
(Figure 4.13).
10. Fix the LMA in the midline with dynaplast tape around
the tube. Also insert a roll of gauze on either side of
Figure 4.10: Technique of insertion (Contd...) the LMA to avoid biting the tube.
The laryngeal mask does not prevent reflux and aspi-
7. Maintaining pressure with the finger on the tube in the
ration of gastric contents. It is not helpful with glottic or
cranial direction, advance the mask until definite re-
subglottic pathology and cannot be used to deliver high
sistance is felt at the base of the hypopharynx. Note
pressure ventilation (laryngeal mask seal pressure is ~25
the flexion of the wrist (Figure 4.11).
mm H2O).
50 Section II n Airway
IP : 196.52.84.10
5
IP : 196.52.84.10
Non-invasive CPAP in Settings
Without Immediate Access to
Mechanical Ventilation
Figure 5.1: Flow inflating ventilation device, a boon in the ED management of acute pulmonary edema and shock
Learning Objectives
1. CPAP and its benefits in the management of acute 3. Pearls and pitfalls when using this device.
pulmonary edema during shock resuscitation. 4. Evidence supporting the use of non-invasive posi-
2. Parts of the flow inflation ventilation device (Jack- tive pressure ventilation (NIPPV).
son-Rees/Pediatric Bain circuit).
IP : 196.52.84.10
Figure 5.2: Parts of the flow inflating ventilation device (Jackson-Rees circuit)
7. Avoid using the JR circuit in an apneic child 3. Nava S, Carbone G, Di Battista N, et al. Noninvasive venti-
Assisted ventilation for the non-intubated child, is best lation in cardiogenic pulmonary edema. A multicenter, ran-
provided using theIPself-inflating bag-valve-mask de- domized trial. Am J Respir Crit Care Med. 2003;168:1-6.
: 196.52.84.10 4. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe
vice.
8. Use age appropriate reservoirs cardiogenic pulmonary edema with continuous positive
airway pressure delivered by face mask. N Engl J Med.
When smaller reservoirs are used in older children, hy- 1991;325:1825-830.
poxia can worsen or not improve. Use of larger reser-
5. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continu-
voirs and circuits increase dead space ventilation and ous positive airway pressure therapy in acute cardiogenic
predispose to respiratory fatigue in young infants. pulmonary edema: short-term results and long-term fol-
9. Continue to use the flow inflating ventilation de- low-up. Chest. 1995;107:1379-386.
vice, until respiratory distress and shock resolves. 6. Pang D, Keenan SP, Cook DJ, et al. The effect of positive
Parents and attendants must be taught to hold the mask airway pressure on mortality and the need for intubation
under supervision in centers where healthcare provid- in cardiogenic pulmonary edema. Chest. 1998;114:1185-
ers are not available round the clock. 192.
10. JR circuit is contraindicated if level of consciousness 7. Park M, Sangean MC, Volpe Mde S, et al. Randomized,
prospective trial of oxygen, continuous positive airway
drops profoundly.
pressure, and bilevel positive airway Pressure by face mask
Development of hypotonia or posturing or seizure ac- in acute cardiogenic pulmonary edema. Crit Care Med.
tivity are indications for intubation. 2004;32:2407-415.
11. Worsening of irritability, inconsolable cry and postur- 8. Crane SD, Elliott MW, Gilligan P, et al. Randomised con-
ing may be noted in some children when applying the trolled comparison of continuous positive airways pressure,
Jackson-Rees circuit. As respiratory distress and shock bilevel non-invasive ventilation, and standard treatment in
resolve, tolerance improves. emergency department patients with acute cardiogenic pul-
monary oedema. Emerg Med J. 2004;21:155-61.
Key Points
ü 9. Bellone A, Monari A, Cortellaro F, et al. Myocardial in-
farction rate in acute pulmonary edema: noninvasive pres-
1. Use the flow inflating ventilation device to provide
sure support ventilation versus continuous positive airway
O2 to all critically ill children presenting with respi- pressure. Crit Care Med. 2004;32:1860-865.
ratory distress and shock. 10. Bellone A, Vettorello M, Monari A, et al. Non-invasive
2. Flow inflating ventilation device is useful to provide pressure support ventilation versus continuous positive
O2 for children presenting with acute cardiogenic airway pressure in acute hypercapnic pulmonary edema.
shock due to various etiologies such as scorpion Intensive Care Med. 2005;31:807-11.
sting, sepsis, submersion injury, etc. 11. Giacomini M, Iapichino G, Cigada M, et al. Short-term
noninvasive pressure support ventilation prevents ICU
admittance in patients with acute cardiogenic pulmonary
common errors
û
1. Use of flow inflating device in apneic children (bag-
edema. Chest. 2003;123:2057-061.
12. Masip J, Roque M, Sanchez B, et al. Noninvasive venti-
valve-mask preferred). lation in acute cardiogenic pulmonary edema. Systematic
2. Inappropriate sized reservoir. review and meta-analysis. JAMA. 2005;294:3124-130.
3. Complete closure of pressure release valve. 13. Ho KM, Wong K. A comparison of continuous and bilevel
positive airway pressure non-invasive ventilation in-pa-
tients with acute cardiogenic pulmonary edema: a meta-
REFERENCES analysis. Crit Care. 2006;10:R49.
1. Shah PS, Ohlsson A, Shah JP. Continuous negative extra- 14. Collins SP, MielniczukLM, Whittingham HA, et al. The
thoracic pressure or continuous positive airway pressure use of noninvasive ventilation in emergency department
for acute hypoxemic respiratory failure in children. Co- patients with acute cardiogenic pulmonary edema: a sys-
chrane Database Syst Rev. 2008;1:CD003699. tematic review. Ann Emerg Med. 2006;48:260-69.
2. Mehta S, Jay GD, Woolard RH, et al. Randomized pro- 15. Winck JC, Azevedo LF, Costa-Pereira A, et al. Efficacy and
spective trial of bilevel versus continuous positive air- safety of non-invasive ventilation in the treatment of acute
way pressure in acute pulmonary edema. Crit Care Med. cardiogenic pulmonary edema: a systematic review and
1997;25:620-28. meta-analysis. Crit Care. 2006;10:R69.
Chapter 5 n Flow Inflating Ventilation Device: Non-invasive CPAP in Settings Without Immediate Access to
Mechanical Ventilation 57
16. Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of non- tive airway pressure versus non-invasive positive pressure
invasive positive pressure ventilation (NIPPV) on mortal- ventilation. Chest. 2007;132:1804-809.
ity in patients with acute cardiogenic pulmonary edema: a 18. Santhanam I, Padma V, Murali T, et al. Predictors of mor-
IP 2006;367:1155-163.
meta-analysis. Lancet. : 196.52.84.10 tality of children presenting with severe sepsis. Proceed-
17. Ferrari G, Olliveri F, De Filippi G, et al. Non-invasive ings from the first European congress on Pediatric resusci-
positive airway pressare and risk of myocardial infarctio tation and emergency medicine, Ghent. May 2013.
in acute cardiogenic pulmonary edema: continuous posi-
Section III
Approach to
IP : 196.52.84.10
Stridor
IP : 196.52.84.10
6
IP : 196.52.84.10
Stridor
Figure 6.1: A child being resuscitated for acute laryngotracheobronchitis in the PED (Courtesy: Dr Gunda Srinivas)
Learning Objectives
1. Highlight the importance of recognizing supraglot- 4. Evidence and treatment is based on etiology.
tic stridor. 5. Establish severity using the rapid cardiopulmonary
2. Precautions taken during assessment and manage- cerebral assessment and pediatric assessment tri-
ment. angle.
3. Establish etiology. 6. Management based on severity and etiology.
Even minimal mucosal edema can significantly reduce lapsible due to lack of cartilaginous support. The presence
the diameter of the pediatric airway and increase resistance of multiple tissue planes in this region encourages rapid
to airflow and work of breathing. spread of infection especially in infancy. In addition, in
IP : 196.52.84.10
Ù
Crying can aggravate hypoxia by increasing air
children less than 2 years of age, the retropharyngeal space
contains lymph nodes that serve as a nidus for the forma-
turbulence in the obstructed airway. tion of abscess. As the nodes atrophy, the risk of abscess
All precautions should be taken to prevent a child with formation becomes much less.
stridor from crying. Obstruction at the supraglottis, i.e. above the level of
the esophagus, as in epiglottitis or retropharyngeal abscess
GENERAL APPROACH causes pooling of saliva. The latter leads to:
1. Avoid the following maneuvers in children present- 1. Soft stridor (may not be reported by the mother, but
ing with stridor. identified by the ER physician).
●● Do not separate the child from his mother. 2. Drooling and dysphagia.
Examine and manage the child on his mother’s lap. 3. Muffling of voice (‘hot potato voice’).
●● Avoid changing the position of comfort, which 4. Ineffective cough.
the child has adopted.
Do not make an alert or agitated child with stridor, Glottis
lie down on the resuscitation trolley or bed. It could
precipitate complete airway obstruction. The glottic and subglottic region extends from the vo-
●● Avoid forcing an oxygen mask on a screaming cal cords to the trachea before entering the thoracic cage.
child. Since the cricoid cartilage and tracheal cartilaginous rings
Without separating the child from his mother, help surround majority of its length, this section of the airway
the mother to administer oxygen in a non-threaten- is not as collapsible as the supraglottis. The commonest
ing manner. causes of obstruction at this site are inflammation and ede-
ma due to acute laryngotracheobronchitis (ALTB).
2. Ascertain the severity of the lesion based on the
physiological status. 1. Hoarse voice.
●● Perform the rapid cardiopulmonary cerebral assess- 2. The harsh stridor may occur in either the inspiratory or
ment. expiratory phase or occasionally both phases of respi-
It helps to quickly determine whether the airway ration (biphasic). The latter is due to minimal altera-
obstruction can be handled in the ED or in the OT. tions in the size and shape of the airway obstruction
during both phases of respiration.
3. Simultaneously, obtain a focused history to estab-
lish the anatomical site of obstruction. The ‘5A’s 3. Brassy cough.
approach helps to identify the level of lesion. 4. Drooling and dysphagia are not characteristic features
●● Age: What is the age of the child? of glottic obstruction unless the obstruction is large
●● Acuity: Is the presentation, hyperacute, acute, enough to compress the esophagus.
chronic or acute on chronic?
●● Acoustics: Is the stridor harsh or soft. Intrathoracic
●● Associated symptoms: Is stridor associated with fe-
ver, dysphagia or drooling? The intrathoracic airway comprises of the trachea and
●● What is the quality of voice (hoarse or muffled)? the main stem bronchus. Intrathoracic airway obstruction
●● Aggravating factors? causes stridor that is loudest during expiration. Increase in
intrathoracic pressure during expiration, causes collapse of
SITE OF OBSTRUCTION the airway. During inspiration, the intrathoracic pressure
falls. As a result, the obstructed thoracic airway expands
Supraglottis leading to a quieter sound.
The supraglottis extends between the nose and the vocal Congenital malformations of the airway are the com-
cords. As mentioned earlier, it is easily distensible and col- monest causes of obstruction within the thorax.
Chapter 6 n Stridor 63
Case Scenario 1
A toddler presented with 1 day history of fever, stridor
IP : 196.52.84.10
and swelling in front of the neck (Figures 6.2 to 6.8).
Intervention
Figure 6.3 Physiological status: Structural stridor with ●● A: Airway was positioned using the head tilt-chin lift
impending respiratory failure, compensated shock and altered maneuver (Figure 6.4).
mental status ●● B: Oxygen was given via the Jackson-Rees Circuit.
●● C: Dopamine was initiated at 10 μg/kg/minute.
Intervention ●● The surgeon performed diagnostic aspiration (thick pus
was aspirated).
●● A: Child was seated in his mother’s lap. ●● Airway tray was ordered.
●● B: Oxygen was given by his mother in a non-threaten- ●● Fentanyl and atropine were ordered
ing manner. ●● Ketamine was avoided for its risk of laryngospasm.
●● C: Vascular access was secured and 10 mL/kg of NS ●● Succinylcholine, was also avoided since paralysis
was started over 20 minutes. would have deprived the child of his respiratory effort
●● ENT specialist and the pediatric surgeon were called where difficulty was anticipated during intubation.
for help immediately.
Chapter 6 n Stridor 65
IP : 196.52.84.10
Infectious
1. ALTB (classical croup)
2. Acute epiglottitis
3. Bacterial tracheitis
4. Retropharyngeal abscess
Non-infectious
1. Congenital malformations obstructing the airway
2. Spasmodic croup
3. Foreign body obstruction
4. Angioedema
Figure 6.7 Physiological status: Airway intubated, assisted
5. Laryngomalacia
ventilation, hypotensive shock with low MAP.
6. Laryngeal papilloma
7. Hypocalcemia
8. Vocal cord paralysis
Intervention
●● A: Laryngoscopic evaluation showed a smooth globu-
lar swelling with no anatomical landmarks to guide in-
Acute Laryngotracheal Bronchitis (Box 6.1)
tubation. Viz: epiglottis, arytenoid folds or vocal cords A careful history and physical exam is mandatory to con-
were not visible. firm diagnosis and simultaneously, rule out FB aspiration
●● B: Bag-valve-mask ventilation was initiated. Chest rise or epiglottitis.
was adequate and saturation improved to 100%.
Most children present with acute onset barking cough,
●● Successfully intubated on the 6th attempt using a 3.5
stridor and chest wall in drawing.3,4 It is preceded by a
mm tube. Each attempt was preceded by preoxygen-
prodrome of cough, cold and low-grade fever. Typically,
ating with bag-valve-mask ventilation, such that SaO2 the illness lasts for 3–7 days. As the obstruction worsens,
was > 95%. the child becomes increasingly tachypneic with distress
●● C: 80 mL/kg NS, dopamine and norepinephrine infu- of variable severity. Tachycardia is noted when the child
sions were needed to resolve warm shock with low becomes hypoxia. Severe airway obstruction is associated
MAP. with pulsus paradoxus. Rarely, progressive increase in the
●● The first dose of antibiotic was also administered. work of breathing leads to respiratory failure, character-
●● Hypoglycemia was ruled out. GNS with KCl was initi- ized by severe chest retractions, decrease in breath sounds
ated at maintenance rates. and oxygen saturation. Increasing cyanosis along with
66 Section III n Approach to Stridor
change in mental status indicate need for intubation. Some Epinephrine is the drug of choice. Due to its non-se-
children with ALTB may develop secondary bacterial tra- lective α-adrenergic and β-agonistic action, it relieves mu-
cheitis. IP : 196.52.84.10 cosal edema and improves breathing mechanics. In most
Ù children, one dose is adequate, although it may be repeated
after 4–6 hours.
Tachycardia indicates hypoxia. Peripheral perfusion
is usually normal, but can be compromised in severe The Cochrane review5 concluded that nebulized epi-
hypoxia.
nephrine, both racemic and L-isomeric preparation caused
reduction of croup symptoms within 30 minutes after treat-
CASE SCENARIO 2 ment and improved stridor related respiratory distress. Ide-
A 1-year-old child presents with barking cough and in- ally, both pulse oximetry and ECG monitoring should be
spiratory stridor. His mother reports that her son has available during epinephrine nebulization.
been coughing for a week (Figure 6.9).
Glucocorticoids6-15
Glucocorticoids reduce upper airway swelling leading to
significant improvement in croup symptoms. Their onset
of action occurs within 1 hour after administration. Action
is delayed when compared with inhaled epinephrine. Peak
effect is noted, 6–12 hours after administration. A recent
cochrane review further confirmed that, glucocorticoids
are effective in improving severity of croup, decreasing the
number of return visits, readmissions and length of stay in
hospital.
Dexamethasone rapidly improves stridor, decreases
hospital stay and reduces the need for intubation.
Figure 6.9 Physiological status: Stridor due to glottic edema ●● Administer 0.6 mg/kg/dose IM, IV or oral (maximum
with respiratory distress and tachycardia. Perfusion, BP and mental
status is normal.
10 mg). An oral dose of 0.15 mg/kg is also effective.
Onset of action occurs within 1–2 hours.
The history is suggestive of croup. ●● A single dose is generally sufficient in most children
for prompt and sustained improvement. If necessary,
Treatment the steroid dose may be repeated after 12–24 hours.
●● No significant differences have been noted between the
●● Administer ‘blow-by’ oxygen through a plastic hose
use of prednisolone (1 mg/kg/dose) and dexametha-
with its end held within a few centimeters of the child’s
nose and mouth. sone (dose at either 0.15 or 0.6 mg/kg) in the treatment
of children with mild to moderate croup.
Epinephrine
Budesonide
●● Add, 0.5 mg/kg up to a maximum of 5 mg epinephrine
(1:1,000) to 2–3 mL of NS into the nebulizing cham- Nebulized budesonide has a rapid effect. High-dose nebu-
ber. Nebulize through oxygen. lized budesonide seems as effective as either oral or intra-
●● Observe the child for recurrence for at least 2 hours muscular dexamethasone in the treatment of mild to mod-
after nebulization. erate croup.
●● Less than 4 years—2.5 mL.
●● Dose: Nebulized budesonide 2–4 mg irrespective of age.
●● More than 4 years—5 mL.
Chapter 6 n Stridor 67
●● Acute epiglottitis occurs due to bacterial cellulitis of the Diagnosis is made by direct laryngoscopic visualiza
supraglottic structures, notably epiglottis and aryepi- tion. Epiglottitis is diagnosed when a large, swollen, cher-
glottic folds. Rapid inflammatory swelling of these ry like epiglottis is found with erythema and swelling of
tissues can obstruct the airway. Almost 80%–90% of the arytenoids and aryepiglottic folds. The examination
affected children will require early and elective intuba- should be done in the OT with experienced personnel. If
tion. Haemophilus influenzae type b is the most com- epiglottitis is suspected, culture of the epiglottic surface is
mon causative organism. taken and the child intubated with a tracheal tube one size
smaller than calculated for the age. Blood culture is taken
and appropriate IV antibiotic (ceftriaxone, cefotaxime or
68 Section III n Approach to Stridor
amoxiclav) is started. The tracheal tube should remain in ●● Most use eye movements to look up. The head is main-
situ for 48–72 hours. tained in the stationary position.
Ù IP : 196.52.84.10 ●● Some children present with torticollis.
●● Examination of the oropharynx reveals a bulging of
Avoid direct laryngoscopic examination in the ED.
both posterior pharyngeal wall and soft palate.
Laryngoscopic evaluation of an obstructed airway in
A lateral X-ray pharynx shows, soft tissue swelling,
an alert child could convert a difficult airway into an
which is more than half the width of the adjacent ver-
impossible one!
tebral body. Occasionally an air fluid level may be
seen.
Bacterial Tracheitis CT scan is useful to distinguish patients with RPA
from those with retropharyngeal cellulitis.
Usually follows viral ALTB and is caused by Staphylococ-
cus aureus; rarely by H. influenza and Group A, B hemo-
lytic Streptococcus. Treatment
Age: 6 months to 8 years. Most patients with retropharyngeal cellulitis and some
with RPA can be treated successfully without surgery. If
The initial croup-like symptoms are associated with high surgical drainage of the abscess is planned, intubation is
fever, toxic appearance and increasing respiratory distress. needed to avoid aspiration of pus in the OR.
Difficulty in swallowing and drooling is not common.
●● Administer intravenous antibiotics (penicillinase-resis
Direct laryngoscopy reveals pus in the glottic region. tant penicillins, amoxiclav).
Bronchoscopy may also reveal the presence of pus, slough- ●● Monitor closely if surgical drainage and intubation
ing of tracheal mucosa and a pseudomembrane formation have been performed.
in the subglottic region.
Ù
Bacterial tracheitis is suspected when croup does not
Spasmodic Croup
Acute attacks of stridor occurring at nights and subsiding
subside and child becomes febrile, ill and toxic. in a short time characterize spasmodic croup. It tends to
recur in subsequent nights.
Treatment Age: 1–3 years.
●● Shift to OT for early intubation. Symptoms are similar to croup, but features of infection
●● Plan for frequent and meticulous suctioning. (URI or fever) are absent. The child is usually awakened
●● Administer appropriate antistaphylococcal antibiotics. from sleep with a stridor and onset of a harsh, barking, me-
tallic cough. Acute vocal cord abductor spasm triggered by
Retropharyngeal Abscess viral, allergy, gastroesphageal reflux or psychogenic fac-
tors have been postulated as causative.
Retropharyngeal abscess (RPA) is a potentially, serious
deep space neck infection. Complications include, airway Treatment: Taking the child into the cool night air may
compromise, invasion of contiguous structures and sepsis. stop the stridor. If the stridor persists,
Suppuration, occurs in the potential space between the pos
●● Humidified air through nebulizer.
terior pharyngeal wall and prevertebral fascia. Causative
●● Nebulized epinephrine.
organisms: Group A, B-hemolytic Streptococcus, oral an
aerobes, Staphylococcus aureus.
Foreign Body (FB) Obstruction
Sudden attack of respiratory symptoms, such as cough,
Clinical Features16 choking, gagging or cyanosis in a previously normal child
Fever, dysphagia, drooling, muffled voice, noisy breathing, should arouse suspicion of FB aspiration. Symptoms de-
respiratory distress, toxic appearance and neck stiffness. pend on the location of the FB. Laryngeal/tracheal FB may
present with croupy cough resembling ALTB. Varying de-
●● Children prefer to keep their neck in the neutral posi- grees of stridor, wheeze, chest retraction, hypoxia and cy-
tion with limitation of neck extension and flexion. anosis may also be seen. The clinical features may change
Chapter 6 n Stridor 69
Ù
Examination of the throat in an alert child to remove
Figures 6.10A and B: Heimlich maneuver to dislodge foreign body
in infants. Remove FB, if visualized. Avoid blind finger sweep.
the FB causing stridor in the ER can precipitate cardiac
arrest.
●● Children > 1 year: Repetitive abdominal thrusts or
Heimlich maneuver.
70 Section III n Approach to Stridor
Hypocalcemia
Hypocalcemia presents with intermittent stridor, hypocal-
cemic tetany, seizures and cardiac failure. The child appears
normal between the episodes of stridor. Serum calcium < 7
Figure 6.13 Physiological status: Airway un-maintainable and mg/dL or ionized calcium < 1 mmol/dL is diagnostic. CXR
obstructed, respiratory failure, bradycardia, hypotensive shock may show signs of rickets, cardiomegaly and pulmonary
with altered mental status. congestion.
●● Initiate bag-valve-mask ventilation, chest compres-
Treatment
sions, injection epinephrine 1.2 mL (1:10,000) IV.
●● Urgently call for ENT assistance. ●● Maintain airway patency.
Dose: IV calcium gluconate at 0.5 mL/kg slowly fol-
Ù
An unstable airway, bradypnea, tachycardia or
lowed by a maintenance dose are therapeutic.
bradycardia, cyanosis and deteriorating mental status Rate of administration: 0.5–1 mL/kg not exceeding 0.1
are indicative that urgent resuscitative efforts are needed mL/kg/minute.
in the ER.
Vocal Cord Paralysis
●● Preoxygenate prior to intubation attempts.
Bilateral abductor palsy occurs due to the abnormal medial
●● Avoid paralytic agents during intubation.
position of the vocal cords. It results in severe stridor and
●● Removal of foreign body may be attempted after intu-
respiratory distress. Bilateral abductor palsy causes apho
bation.
nia with little respiratory distress.
●● During the process of intubation, if it is not possible to
remove the FB in the ER, attempt to dislodge it into the
main stem bronchus. Diagnosis
●● Long duration of stridor, older children, (not within the
This will at least ensure that half of respiratory tree is
age group for developing ALTB), absence of fever, poor
freed for ventilation. Follow-up bronchoscopy may be per-
response to nebulized epinephrine and persistence of
formed later for removal of FB.
stridor are clues to recognition of vocal cord paralysis.
●● Laryngoscopy is confirmatory.
Laryngomalacia (Congenital
Laryngeal Stridor) Treatment
Intermittent stridor and chest retractions occur from 2–6 ●● Supportive.
weeks of age. Symptoms peak at 3–5 months, but most ●● Temporary intubation.
resolve spontaneously by 10 months. ●● Rarely surgery.
Chapter 6 n Stridor 71
72
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Section III n Approach to Stridor
Chapter 6 n Stridor 73
REFERENCES and placebo for moderately severe croup.” The New Eng-
land Journal of Medicine. 1998;339(8):498-503.
1. Geelhoed GC. Croup. Pediatr Pulmonol. 1997;23 (5):70-
374. IP : 196.52.84.10 10. Klassen TP, Craig WR, Moher D, et al. “Nebulized budes-
onide and oral dexamethasone for treatment of croup: a
2. Cordle RJ, Relich NC. Pediatrics: Upper respiratory emer-
randomized controlled trial.” Journal of the American
gencies. In: Tintinalli JE, Kelen GD, Stapczynski JS (Eds).
Emergency Medicine: A Comprehensive Study Guide. 5th Medical Association. 1998;279(20):1629-632.
edition. New York, NY: McGraw-Hill Health Professions 11. Klassen TP, Watters LK, Feldman ME, et al. “The efficacy
Division; 2000. pp. 384-91.doi:10.1056/NEJMep072022. of nebulized budesonide in dexamethasone-treated outpa-
3. Bjornson CL, Johnson DW. ‘Croup’. The Lancet. 2008; tients with croup.” Pediatrics. 1996;97(4):463-66.
(371)329-339, DOI:10. 1016/S0140-6736(08)60170-1. 12. Geelhoed GC. “Budesonide offers no advantage when
4. Cherry JD. Clinical Practice. Croup. N Engl J Med. added to oral dexamethasone in the treatment of croup.”
2008;358:384-391. Pediatric Emergency Care. 2005;21(6):359-62.
5. Bjornson C, Durec T, Vandermeer B, et al. “Nebulized 13. Chub-Uppakarn S, Sangsupawanich P. “A randomized
epinephrine for croup in children,” Cochrane Database of comparison of dexamethasone 0.15 mg/kg versus 0.6 mg/
Systematic Reviews, no. 3, Article ID CD006619, 2007. kg for the treatment of moderate to severe croup.” In-
6. Luria JW, Gonzalez-Del-Rey JA, DiGiulio GA, et al. “Ef- ternational Journal of Pediatric Otorhinolaryngology.
fectiveness of oral or nebulized dexamethasone for chil- 2007;71(3)473-77.
dren with mild croup,” Archives of Pediatrics and Adoles-
14. Geelhoed GC, Macdonald WB. “Oral dexamethasone in
cent Medicine. 2001;155(12):1340-345.
the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus
7. Rittichier KK, Ledwith CA. “Out-patient treatment of
0.6 mg/kg.” Pediatric Pulmonology. 1995;20(6):362-68.
moderate croup with dexamethasone: intramuscular versus
oral dosing.” Pediatrics. 2000;106(6)1344-348. 15. Fifoot AA, Ting JYS. “Comparison between single-dose
8. Cetinkaya F, Tufekci BS, Kutluk G. “A comparison of neb- oral prednisolone and oral dexamethasone in the treatment
ulized budesonide, intramuscular and oral dexamethasone of croup: a randomized, double-blinded clinical trial.”
for treatment of croup.” International Journal of Pediatric Emergency Medicine Australasia. 2007;19(1)51-8.
Otorhinolaryngology. 2004;68(4): 453-56. 16. Craig FW Schunk JE. Retropharyngeal abscess in children:
9. Johnson DW, Jacobson S, Edney PC, et al. “A comparison clinical presentation, utility of Imaging and current man-
of nebulized budesonide, intramuscular dexamethasone, agement. Pediatrics. 2003;111:1394-398.
Section IV
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Breathing
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7
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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.
CLASSIFICATION OF ABNORMAL
RESPIRATION
●● Effortless tachypnea.
●● Respiratory distress.
●● Respiratory distress with features of respiratory failure.
●● Relative bradypnea.
●● Apnea.
Effortless Tachypnea
Figure 7.3 Physiological status: Life-threatening asthma Tachypnea occurs due to a variety of causes: Hypoxia,
with shock. hypercarbia, shock, metabolic acidosis, pain, anxiety and
Ù
To avoid precipitating hypoxia consequent to crying
central nervous system pathologies in comatose children.
●● Effortless tachypnea or quiet tachypnea is defined as
or agitation, children with respiratory distress or increased respiratory rates without increased work of
impending respiratory failure should not be separated breathing.
from their mother. ●● Hypoxia and shock due to various etiologies result in
decreased availability of oxygen at the cellular level.
●● It is preferable, that on arrival and during subsequent Anerobic metabolism supervenes, leading to lactic aci-
management, children with respiratory distress remain dosis. The latter triggers the respiratory centers. Respi-
seated in their mother’s lap. ratory rates increase in an attempt to maintain a normal
●● The mother should be taught to administer oxygen by pH.
holding the rebreathing mask or flow inflating ventila-
tion device in a non-threatening manner. Ù
Lung parenchyma is normal in children presenting with
●● Infants who cry and resist the mask can be adminis
effortless tachypnea.
tered oxygen via a tube held close to the nose.
Chapter 7 n Approach to Respiratory Distress 79
Abdominal Respiration
Respiratory Failure
The ribs and the costal cartilage in the infant are soft and
It is characterized by inadequate oxygenation, ventilation or
both. It may be functionally defined as a clinical state that re- compliant resulting in failure to support the lungs or keep
quires intervention to prevent respiratory or cardiac arrest. them adequately expanded. Hence, when the airways be-
come obstructed, active inspiration causes paradoxical in-
●● Recognition of respiratory failure is based on the clini- tercostal retractions rather than chest and lung expansion.
cal features (discussed below) and not on blood gas The tidal volume becomes dependent on the movement of
analysis. the diaphragm and functional residual capacity falls. When
Deterioration in respiratory function or imminent re- diaphragmatic movement is impeded by gastric distension
spiratory arrest should be anticipated in infants or children or increased intrathoracic pressure such as asthma or bron-
who demonstrate any of the following signs: chiolitis, respiration can become further compromised.
●● Inadequate respiratory rate or gasping respiration. Fatigued intercostal muscles also lead to abdominal res-
●● Inadequate effort or chest excursion with diminished piration.
peripheral breath sounds.
●● Grunting respirations.
Ù
See-saw or abdominal respiration indicate respiratory
●● Abdominal or see-saw respiration. muscle fatigue and impending respiratory failure.
●● Decreased level of consciousness or response to pain;
poor skeletal muscle tone or cyanosis.
Grunting
Ù
Due to high metabolic rates, the child has a higher An ominous sign, grunt is indicative of impending respi-
oxygen demand than the adult. Oxygen consumption is ratory failure. It is produced by premature closure of the
6–8 mL/kg in children as compared to 3–4 mL/kg in the glottis at the end of expiration in order to generate positive
adults. Consequently, when a child develops alveolar end-expiratory pressure in an effort to improve the FiO2.
hypoventilation or apnea, hypoxemia develops more Grunting helps to keep the alveoli patent and improve the
rapidly. functional residual capacity.
80 Section IV n Breathing
●● 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
Key Points
1. Avoid separating mother
ü
and child during assessment
common errors
û
1. Diagnosing asthma in all children presenting with
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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
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PE, pulmonary edema; CLD, chronic lung disease; CHD, congenital heart disease; DCM, dilated cardiomyopathy; CCF, congestive cardiac failure.
Chapter 7 n Approach to Respiratory Distress
83
Management of an
8
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Asthmatic Exacerbation
Figure 8.1: Systematic approach, repeated rapid cardiopulmonary assessments lead to dramatic improvement in acutely ill
asthmatic kids. A child with near fatal attack of asthma being successfully resuscitated with subcutaneous epinephrine.
Learning Objectives
1. Using the rapid cardiopulmonary cerebral 2. Pearls and pitfalls in salbutamol nebulization.
assessment and PAT to identify severity and 3. Evidence-based management of acute exacerbation
response to therapy. of asthma.
INTRODUCTION Appearance
The management of acute exacerbation of asthma in the ●● Obtundation, impaired alertness, incessant cry, exhaus-
ED, has been based on the recommendations of the National tion, diaphoresis, agitation, not tolerating the oxygen
Asthma Education and Prevention Program. Expert Panel mask, confusion or combativeness are signs sugges-
Report 3: Guidelines for the Diagnosis and Management of tive of profound hypoxia viz near fatal exacerbation of
Asthma (Summary Report 2007) and the British Thoracic asthma.
Society, Scottish Intercollegiate Guidelines Network: Brit- ●● Floppiness and inability to maintain posture correlate
ish Guideline on the Management of Asthma, June 2009. clinically with hypercarbia.1
are more ominous and indicate impending respiratory pneumonia, bronchiolitis, tracheobronchomalacia, cystic
failure. fibrosis and congenital anomalies could present with re-
●● Other signs of a near
IP :fatal attack include diminished
196.52.84.10 current wheeze and respiratory distress.
air-entry, absence of wheeze due to severe bronchos
Response to short-acting bronchodilator agent (SABA)
pasm (silent chest) and or saturation < 92% in room air.
is often inconsistent in these children
Serial pulse oximetry measurements have been found
useful in assessing the severity of exacerbation and evalu-
ating improvement with treatment (Evidence B). Investigations: Role in Resuscitation
of Asthmatic Exacerbations
Ù ●● Chest radiographs are not routinely indicated in an
Though low oxygen saturation is helpful in recognizing
severity, normal oxygen saturations does not rule out a asthmatic child. They are ordered if there is failure to
severe asthmatic exacerbation.3 improve or deterioration occurs during the manage-
ment of life-threatening or near fatal asthmatic exac-
Circulation erbation.
ASTHMA MIMICS Ù
Assessment of severity is the first step in the management
It is not uncommon for central airway obstruction to be of acute asthma.
misdiagnosed as asthma. Upper airway foreign bodies,
epiglottitis, structural diseases of the larynx, vocal cord The exacerbation is classified as moderate, acute se-
dysfunction and tracheal narrowing could mimic asthma. vere, life-threatening or near fatal attack. Based on the se-
Dysphonia, inspiratory stridor, wheezing loudest over the verity of the attack, the appropriate bronchodilatory thera-
central airway are some of the clues, which help differenti- py is initiated (Protocol 8.1).
ate these causes from asthma.
Diagnosis of asthma in toddlers and infants is unusual.
Ù
Repeated assessment is recommended after each
Intermittent wheezing attacks may be due to recurrent vi- intervention (bronchodilator) (Evidence A).
ral infections. Recurrent aspiration leading to pneumonitis,
86 Section IV n Breathing
Ipratropium Bromide
Ipratropium bromide (IB), an anticholinergic derivative
competes with the acetylcholinesterase at the M3 musca
rinic receptor attenuating the neural signal for broncho-
constriction, thus leading to relaxation of airway smooth
muscle. It also relieves mucosal edema and secretions.
Figure 8.7: This picture shows her following emergency
intubation and ventilation after deterioration during her Contractility of the smooth muscle lining the large and
nebulization. This particular episode of respiratory distress was medium sized airways is under parasympathetic neural
secondary to pneumonia and not due to asthma. Hence, for control and is activated by acetylcholine (ACh) release.
sudden deterioration during salbutamol even in asthma stop
nebulization, reconsider etiology. ●● The larger airways are constricted in life-threatening
asthma resulting in greater benefits with the use of IB.
●● Respiratory viruses trigger asthmatic exacerbations by
Intermittent Versus Continuous increasing parasympathetic activity of the airways viz
Nebulization with Salbutamol bronchospasm and airway secretions. Inhaled IB has
●● 2.5–5 mg of salbutamol nebulization is repeated every been found to be more beneficial in pediatric asthma
triggered by viral upper respiratory tract infection
20–30 minutes.
(URTI).
●● Continuous nebulization entails that 10–20 mg is added
●● High doses of racemic SABA contain an S-isomer,
to the chamber and administered over 1 hour.
which increases intracellular concentration of free cal-
The onset of action for SABAs is less than 5 minutes; cium in the smooth muscles of the airways. The latter
repetitive administration produces incremental bronchodi- provokes bronchoconstriction. Concomitant use of IB,
lation. Continuous administration of SABA may be more when high doses of salbutamol are being used abol-
effective in more severely obstructed patients. However, ishes this response.
this should be performed under very close supervision. ●● A multidose regimen showed statistically significant
improvement in lung function and clinical asthma
score.
Chapter 8 n Management of an Asthmatic Exacerbation 89
Conversely, the British Thoracic Guidelines suggest ●● However, it is not uncommon for young children with
that aminophylline may be useful in near fatal asthma not life-threatening asthma to present with shock.
responding to maximalIPdoses of bronchodilators and ste
: 196.52.84.10 These children often require large volumes in our set-
roids. In settings, where access to mechanical ventilation is
ting to attain therapeutic goals of hypoxia and shock reso-
limited, this drug has been useful in reducing ICU admis
lution. Perhaps, the increased fluid requirement, may be
sion and fatality in asthma-induced respiratory failure.
secondary to late referral, refusal of feeds, vomiting and
Ù
Aminophylline is not recommended in mild and moderate
coexisting sepsis or dengue.
asthma. Its troublesome side effects far outweigh its There may be a drop in serum potassium levels sec-
bronchodilatory effects. ondary to use of SABA, theophylline, steroids and epi-
nephrine. Consequently, potassium should be monitored
●● 5 mg/kg loading dose is given as an infusion over 20 closely in children with refractory asthma.
minutes followed by a continuous infusion at 1mg/
kg/h.
PEF Monitoring9
●● The loading dose is avoided in children, who have been
on chronic theophylline therapy or have received a pre- ●● If peak expiratory flow rate (PEFR) is less than 33%, it
hospital intramuscular dose of deriphyllin. is suggestive of acute severe asthma.
●● ECG monitoring is recommended during aminophyl- ●● PEFR less than 60% of the child’s best or predicted
line infusion. values, is indicative of life-threatening asthma.
Monitoring asthma based on PEFR is useful for chil-
Intravenous Salbutamol dren older than 5 years of age. In children less than 5 years,
●● Intravenous (IV) salbutamol (15 mg/kg) is reserved for this maneuver can aggravate hypoxia by causing dynamic
those children for whom the drug cannot be reliably airway collapse. Unfortunately, this may not always be
administered through the nebulizer unit. possible in busy ED, which prevents its wide spread use in
●● Continuous IV infusion of beta 2 agonist is not superior the Indian scenario.
to maximal inhaled dose.
●● Hypoxia occurring due to the salbutamol-induced V/Q
Ù
The expert panel report 3 has given recommendations
mismatch is more severe with IV beta-2 agonist infu- for the following interventions in the management of
sion than the inhaled route. acute asthma in the ED.
●● In addition, there is a greater risk of arrhythmias mak-
ing ECG monitoring mandatory during therapy. Any ●● Antibiotics are not recommended during the ED treat-
intravenous therapy in asthma requires continuous ment of acute asthma exacerbations (Evidence B) un-
ECG monitoring. less evidence of bacterial sepsis is available.
●● Mucolytics are not recommended (Evidence C).
Other Therapies ●● Sedation: Anxiolytic and hypnotic drugs are contrain-
dicated in severely ill asthma patients, because of their
Intravenous Fluids respiratory depressant effect (Evidence D).
Aggressive hydration is not recommended for old- Indications for intubation is based on clinical judgment
er children, but may be indicated for young children (Evidence D). Absolute indications for intubation and me-
(Evidence D). chanical ventilation are minimal and include:
●● Correct dehydration since it could cause reduction in ●● Apnea and coma.
ciliary activity and mucus plugging. ●● Fatigue, with poor respiratory effort.
●● In the absence of dehydration, fluids are administered ●● Imminent arrest and arrhythmias.
cautiously at two-thirds maintenance due to the risk of Since intubation is difficult in patients who have asthma,
SIADH induced by pulmonary edema.
it should be performed by a physician, who has extensive
Chapter 8 n Management of an Asthmatic Exacerbation 91
experience in intubation and airway management in the ●● The spacer should be washed periodically with deter-
ED. Ketamine usage for premedication prior to intubation, gent to reduce the electrostatic and enhance delivery.
have not shown clinical IPbenefit. Ideally, even without in-
: 196.52.84.10 Refer Table 8.1.
tubation, patients who have not been improving satisfac-
torily or deteriorating despite aggressive bronchodilatory Discharge
therapy in the ED should be transferred into the ICU.
An asthmatic exacerbation is considered a failure of pre-
ventive therapy and discharge plans should take into ac-
count the following:
●● Motivate the parents and the child to take regular in-
haler therapy.
●● Consider use of steroid inhalers.
●● Explain the use of these devices with a detailed written
asthma plan and the need for regular follow-up.
●● Advise regarding the need to seek urgent help, if there
is exacerbation of asthma.
●● Arrange for care in the asthma clinic.
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Chapter 8 n Management of an Asthmatic Exacerbation
93
94 Section IV n Breathing
Pulse Oximeter
Figure 9.1: Different equipments used for pulse oximetry and cardiorespiratory monitoring
Learning Objectives
1. How does the pulse oximeter work? 2. Pearls and pitfalls in pulse oximetry.
INTRODUCTION
Considered as the ‘5th vital parameter’, the pulse oxime-
ter helps to determine the oxygen content of hemoglobin
(SpO2) using a finger probe (Figure 9.1). It works by utiliz-
ing selective wavelengths of light. Having understood the
significance of pulse oximetry as a component of clinical
assessment and decision-making in young infants and chil-
dren, pulse oximeters have been made available even in
the Primary Health Centers.
Figure 9.2: Photodetector picks up R/IR light source.
Principle The pulse oximeter probe, emits both red and infra-
Oxygenated hemoglobin absorbs infrared light and al- red light using LED technology. The light shines through
lows red light to pass through. Deoxygenated (or reduced) a site with good blood flow. Typical adult/pediatric sites
hemoglobin absorbs red light and allows infrared light to with good blood flow are the finger, toe, pinna (top) or lobe
pass through. of the ear. Infant sites are the foot, palm, hand, big toe or
thumb.
Red light is within the 600–750 nm wavelength light
band, (Figure 9.2) while the infrared band lies within the Opposite the emitter is a photodetector that receives
850–1,000 nm wavelength band (Figure 9.3). the light passing through the measuring site.
96 Section IV n Breathing
●● The LED emits red light alternatively at two different LIMITATIONS OF PULSE OXIMETER
wavelengths, visible and infrared regions of the elec-
tromagnetic spectrum. 1. The pulse oximeter picks up late and severe hypox-
IP : 196.52.84.10 emia. It fails to pick up early, minimal fall in oxygen
levels.
Ù
An oxygen saturation of 90% in the pulse oximeter
equates to a blood gas of 60 mm Hg!
The arteriolar bed pulsates and absorbs variable Tips for Use
amounts of light during systole (peak) and diastole
(trough), as blood volume increases and decreases. The 1. Ensure that the optical components of the sensor are
ratio of light absorbed at the peak and trough is translated properly aligned.
into oxygen saturation measurements. Since peaks occur 2. Check adhesive sensor sites every 8 hours and move it
with each heartbeat or pulse, the term ‘pulse oximetry’ was to a new site if necessary.
coined (Figure 9.4). 3. Change the site of sensors to a new site at least every
4 hours.
4. Adhesive digit sensors may be reused on the same pa-
tient if the adhesive tape attaches without slipping.
5. Replace the sensor whenever the adhesive quality is
depleted.
6. Fix the probe in an extremity free of an arterial cath-
eter, blood pressure cuff intravascular infusion line.
7. Clean reusable sensors between patients.
8. Document SpO2 results in the patient's medical record.
It should detail the conditions under which readings
Figure 9.4: Variable absorption of light.
were obtained viz date, time of measurement, concen-
●● The pulse oximeter provides continuous non-invasive tration of inspired oxygen concentration and type of
monitoring of oxygenation at the tissue level. oxygen delivery device being used.
●● Monitoring of oxygen is not affected by skin pigmenta- 9. Cardiopulmonary assessment must be documented
tion. along with pulse oximeter reading.
Chapter 9 n Pulse Oximeter 97
Section V
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General Approach to the
10
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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’.
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Figure 10.2: Rapid compensatory mechanism in shock (Boxed entities are the manifested symptoms clinically).
GFR, glomerular filtration rate; RAS, reticular activating system; SVR, systemic vascular resistance; BP, blood pressure.
3. Neurohormonal responses are activated early to resistance to ventricular ejection (afterload) and myo-
preserve adequate tissue perfusion and maintain vital cardial contractility. Autoaugmentation of preload de-
organ function6 (Figure 10.2). However, with further pends on the two-thirds of the total circulating blood
deterioration, these mechanisms can no longer com- volume, which is contained in the small veins. When
pensate and hypotension, a late sign of shock ensues. shock occurs, one of the earliest responses is alpha-
4. Cardiovascular response to shock: Attempts to in- adrenergic mediated vasoconstriction that diverts this
crease cardiac output is dependent on increase of heart reservoir of blood centrally to improve venous return
rate and augmentation of stroke volume. Stroke vol- and ventricular filling. In septic and neurogenic shock
ume has three determinants—the volume of blood venous dilatation rather than vasoconstriction occurs,
present in the ventricle before contraction (preload), further accentuating preload deficits and myocardial
Chapter 10 n General Approach to the Management of Shock 103
dysfunction. Reduction in stroke volume for a given is about 25%. In shock, low SvO2 in the face of normal
ventricular end-diastolic volume leads to an increase arterial oxygen saturation indicates that the tissues are ex-
in systemic vascular IP resistance (SVR), a compensa-
: 196.52.84.10 tracting greater than 25% of oxygen from the arterial blood
tory mechanism to augment blood pressure. While an in order to maintain adequate tissue oxygenation because
increased SVR is an important compensatory mecha- of decreased cardiac output. Ideally, therapy should be tar-
nism that helps preserve vital organ perfusion, patho- geted towards normalization of SvO2.7 Since monitoring
logic increases in afterload can occur in patients with of SvO2 requires intensive care expertise, which is not usu-
cardiac tamponade, tension pneumothorax and dia- ally available to staff in the ED, management in the ED
phragmatic hernia. should be targeted towards normalization of clinical goals
Normally, an increase in SVR is an important of shock resolution.8
compensatory mechanism that helps preserve vital or-
gan perfusion. Excessive increase in (SVR) afterload The commonest causes of shock are shown in Box 10.1.
can obstruct cardiac output thereby worsening shock Box 10.1: Types of shock
(Refer Chapter on Cardiogenic Shock). Structural
obstruction to cardiac output occurs due to cardiac Hypovolemic shock (decreased blood volume)
tamponade, tension pneumothorax and diaphragmatic Hemorrhage
hernia. These conditions can cause profound shock Trauma
Surgery
that is refractory to fluids and inotropes.
Burns
5. Pulmonary response: Initially, metabolic acidosis Vomiting and diarrhea
induces effortless tachypnea. As the SVR increases, Severe sepsis
pulmonary vascular resistance also increases resulting Distributive shock (marked vasodilation; also called
in increased minute ventilation. Uncorrected shock vasogenic or low resistance shock)
can lead to capillary leak and vasodilation in the pul- Anaphylaxis
monary circulation resulting in acute lung injury and Severe sepsis
acute respiratory distress syndrome (non-cardiogenic Cardiogenic shock (inadequate output due to cardiac
dysfunction)
pulmonary edema), which manifests clinically as in-
Congestive heart failure
creased work of breathing. Myocardial dysfunction, a Myocardial dysfunction
precursor or the end result of shock due to a variety Arrhythmias
of etiologies can also cause respiratory distress due to Severe sepsis
cardiogenic pulmonary edema. Obstructive shock (obstruction to blood flow)
6. Renal response: Prolonged renal hypoperfusion may Tension pneumothorax
result in pre-renal and ultimately acute renal failure. Diaphragmatic hernia
Pulmonary embolism
In compensated shock, blood flow is redistributed to Cardiac tamponade
the vital organs and oxygen consumption is maintained by Severe sepsis
an increased extraction of oxygen leading to lower oxygen Dissociative shock
saturation in venous blood. Methemoglobinemia
Carbon monoxide poisoning
Oxygen delivery can be calculated by the following
formula: Oxygen delivery (DaO2) = Cardiac output (CO) ×
Arterial Oxygen content (CaO2). CaO2 is the product of the Recognition
hemoglobin concentration and arterial oxygen concentra-
tion. It is calculated by the formula: CaO2 = Hb (g/dL) × Early signs of hypoxia or shock are subtle and identifying
1.39 × SaO2. The normal O2 content of arterial blood is 18– at risk patients may be challenging.2,9,10 Late shock is easy
20 mL/dL and mixed venous blood is 75% saturated. The to recognize, but resuscitation may be futile. Consequently
normal tissue extraction ratio for oxygen is measured with emergency department (ED) staff must be sensitized to
the following formula: Extraction ratio = (CaO2- CvO2)/ situations in which shock may occur.
CaO2. Oxygen saturation is used as a surrogate to calculate Triage questions, which help recognize shock have al-
the extraction ratio viz SaO2-SvO2/SaO2. The normal value ready been discussed in Chapter 1.
104 Section V n Circulation
Airway
Ù ●● Airway is patent or maintainable or clear if the infant is
If the clinical setting suggests the possibility of shock,
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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.
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Figure 10.6: This picture shows a toddler receiving O2 via a Figure 10.7: Insert two large bore short-length intravascular
flow inflating ventilation device (Jackson-Rees circuit) during catheters. One line is used for fluid resuscitation and
fluid resuscitation for shock with respiratory distress. medications. The second line is dedicated for inotrope
infusion.
●● Consider early intubation in an apneic child with shock,
using ketamine, suxamethonium and atropine. Ù
●● If the child is apneic and bradycardic, intubation can be During fluid therapy, watch out for signs of pulmonary
performed without drugs. edema!
Use a CPAP device to reduce risk of intubation in settings
Ù with limited access to mechanical ventilators.
Waiting for confirmatory blood gas analysis to intubate Initiate inotrope infusion if signs of PE are noted.
is not recommended when the child presents with Continuation of fluids without provision of PEEP or
respiratory failure. inotropes when signs of PE are noted can result in
cardiac arrest.
Ketamine11 is the induction agent and atropine the pre-
medication agent of choice. However, in a hypotensive
child with chronic congestive cardiac failure ketamine,
may worsen cardiac function. A short acting neuromuscu-
lar blocker may be used to facilitate intubation.
Ù
Induction agents such as midazolam can worsen hy
potension. Avoid midazolam for intubation in hypotensive
shock.
Circulation
Fluids are the cornerstone of shock therapy. As fluids are
being administered to correct hypoperfusion, fluid can leak Figure 10.8: Intraosseous access is life saving in shock
out of leaky pulmonary capillaries resulting in pulmonary management. After infusing the first 20–40 mL/kg, intravenous
edema. PEEP must be provided during fluid therapy for access becomes easier. Avoid damage to peripheral veins in
the attempt to secure peripheral access in the shocked child.
shocks of all etiologies except hypovolemia.
Ù ●● After securing intravenous or intraosseous access,
Do not forget to position the airway and provide oxygen check dextrostix (refer Figures 10.7 to 10.9).
throughout fluid resuscitation.
106 Section V n Circulation
Figure 10.9: After addressing the ABCs, DEFG: “Do not ever
forget glucose”! Correct documented hypoglycemia with 25%
dextrose: 2 mL/kg bolus.
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Ù Ù
Non-convulsive status epilepticus (NCSE) signals severe If eye signs are ignored or not recognized generalized
hypoxia and shock: IP : 196.52.84.10 tonic-clonic fits supervenes as a preterminal event.
●● On arrival and during every step in the management of How do I ensure a stable metabolic profile during shock
shock, examine the eyes for position and movements. resuscitation?
Conjugate deviation, nystagmus and eyelid twitch sig
●● Initiate GNS with KCl and administer at maintenance
nal the coexistence of severe hypoxia and shock.17
rates for age. Example, 4 mL/kg/hour in infants less
If the child presented to the PED, with the history of than 10 kg. Ensure that the child has voided urine prior
generalized tonic-clonic activity, eye signs suggest pri- to addition of potassium (Figure 10.16).
mary seizure activity needing immediate anticonvulsant Do not forget to simultaneously treat etiology of
drugs. If however, the presenting history was acute diar- shock!
rhea, fever, breathlessness, submersion, envenomation, etc.
and any one sign of NCSE is noted anytime during shock ●● Simultaneously, provide appropriate treatment for the
resuscitation, it signals severe cerebral hypoperfusion. It is etiology of shock (Table 10.2).
not uncommon to note these findings during resuscitation
of hypotensive shock or cardiac arrest.
Ù
The physiological responses of individual children to
●● Initiate an inotrope. shock resuscitation are often variable and unpredictable.
●● Intubate and ventilate. Therefore, repeated assessments with continuous, non-
invasive monitoring are needed for taking appropriate
Ù
Signs of NCSE in a shocked child denote very poor
decisions in the ED. While the protocol for shock
management is based on broad guidelines, the treatment
prognosis. often needs to be individualized.
Anticonvulsants
Anticonvulsant medications may be hazardous in this
situation.
●● During every reassessment do not forget to look for eye
signs of NCSE.
NCSE is an indication that aggressive management of
hypoxia and shock are needed. Resolution of NCSE oc-
curs if hypoxia and shock are corrected. If however, these
signs persist, anticonvulsant drugs may be administered
very cautiously.
●● Avoid phenytoin, if seizure activity is noted in a child
with shock and myocardial dysfunction.
Phenytoin has been noted to be hazardous in emergen- Figure 10.16: This 36-day-old infant is being managed with the
cy settings, where seizure activity complicates shock and NS boluses, JR circuit, inotrope infusions to combat pulmonary
myocardial depression. edema and shock in the PED. Maintenance (GNS with KCl)
fluids are also being infused at 4 mL/kg/hour throughout
●● If eye signs are not apparent in paralyzed children, resuscitation.
tachycardia, not explained by shock or pain relief sug-
gests the coexistence of NCSE. Shock may be precipitated in children by a variety of
causes. Early recognition of shock and aggressive early re-
Chapter 10 n General Approach to the Management of Shock 111
Protocol 10.1: PEMC approach: Management of shock with or without myocardial dysfunction
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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.
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
common errors
û
1. Using the blood set needle (which does not have a
IP : 196.52.84.10
trocar).
2. Preferring to obtain access using ‘cut down’
technique.
3. Failing to fix during bolus therapy resulting in
slippage of the IO needle.
4. Not using screwing movements to enter the marrow
space.
5. Connecting the IV bottle directly to the IO needle
and expecting it to run as in IV access.
Figure 11.10: Intraosseous access is a life-saving intervention. 6. Not fixing the IO needle effectively after entering
This infant with hydronephrosis and urosepsis presented to the marrow space.
the ED with hypotensive shock. He required 120 mL/kg fluid
in the initial hours of resuscitation to resolve shock. In this REFERENCEs
picture, he is responding to the mother after correction of
shock (therapeutic goal). 1. R Fowler, JV Gallagher, SM Isaacs, et al. The Role of In-
traosseous Vascular Access in the Out-of-Hospital Environ-
Key Points
ü ment (Resource Document to NAEMSP Position Statement)
2007, (11) 1 , 63-66 (doi:1. 1080/10903120601021036).
1. Prefer to use IO access. Avoid damaging veins, if IV 2. ML Buck, BS Wiggins, JM Sesler. Intra-osseous drug ad-
access is not easily available. ministration in children and adults during cardiopulmonary
2. Follow all drugs with 5–10 mL of NS flush. resuscitation. Ann Pharmacother. 2007 Oct;41(10):1679-86.
3. Early use of IO access prevents damage to the veins. 3. Voigt J, Waltzman M, Lottenberg L. Intraosseous vas-
After bolusing 20–40 mL/kg, IV access is easier. cular access for in-hospital emergency use: a system-
atic clinical review of the literature and analysis. Pe-
4. Ideally, if 2 separate secure IV access had been
diatr Emerg Care. 2012 Feb;28(2):185-99. doi: 10.1097/
obtained, the IO needle should be removed. PEC.0b013e3182449edc.
12
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Learning Objectives
1. Case scenarios illustrating the choice of inotropes. 3. Evidence-based approach for the use of vasoactive
2. Pharmacology of the vasoactive medications. medications in ED settings.
INTRODUCTION
This chapter will discuss an overview of inotropes and cat-
echolamines in ED settings1 (Figure 12.1).
CASE SCENARIO 1
A febrile 32-day-old infant presented with history of
breathlessness and not behaving ‘as usual’. He had an
abscess in his arm (Figures 12.2 to 12.4).
The rapid cardiopulmonary cerebral assessment re-
veals. RR: 70/minute, minimal retractions, HR: 200/min-
ute, warm, pink peripheries, well felt peripheral pulses,
rapid CRT and normal liver span. His suck and moro are Figure 12.2: Triaged as respiratory distress and shock due to
sluggish, eyes are mid-position, DEM is normal. His tem- severe sepsis, he receives O2 through the oxyhood and 35 mL
perature is 38.5ºC and his capillary blood glucose is 72 of NS (10 mL/kg) as the initial fluid bolus for shock (Note the
mg/dL. He had a large abscess over his left shoulder. huge abscess over the left arm). Reassessment is as follows:
120 Section V n Circulation
Adverse Effects
●● Tachycardia, dysrhythmias and hypertension could
occur as a result of dopamine infusion. Tachycardia,
increases oxygen consumption and shortens diastole
(reducing coronary perfusion during diastole). The
deleterious effects of dopamine on myocardial oxygen
consumption is less than epinephrine, but greater than
Dobutamine, Amrinone and Milrinone.9
●● Dobutamine has also been shown to depress minute
ventilation10,11 in response to hypoxia and hypercarbia
by as much as 60%. Within the lung, it increases blood
flow to the hypoventilated areas worsening hypoxia. Figure 12.5 Physiological status: Cardiogenic shock due to
CHD.
●● Low dose of dopamine does not improve glomerular
filtration rate and is not protective to the kidney.12,13
Oxygen is provided through JR circuit and 5 mL/kg of
●● It increases splanchnic oxygen consumption15, adverse-
NS is administered over 20 minutes. Reassessment after
ly affects gastrointestinal motility14,15 with varying ef- the bolus shows that BP had improved to 90/60 mm Hg,
fects on the splanchnic circulation16-18. but the liver span had increased to 8 cm.
Ù The intubation tray is being prepared. What inotrope
Extravasation of dopamine can cause limb ischemia infusion would you order?
resulting in gangrene of limbs and extensive skin
necrosis. Infusion rates as low as 1.5 µg/kg/minute have
been known to be associated with limb loss! Dobutamine21-23
A selective beta-1 adrenergic agent, Dobutamine increases
●● To prevent this dreaded complication, tight strapping heart rate by stimulating the SA node. It also increases auto-
the entire limb must be avoided. maticity, conduction velocity and myocardial contractility.
●● The IV line should be checked for free flow. Tachycardia and vasodilation also occurs due to its action on
●● Flushing the inotrope line must be avoided. the Beta-2 receptors. Due to its alpha-adrenergic blocking
●● Extravasation, should be treated with local infiltration activity it can cause cause severe vasodilation (especially in
with a solution of phentolamine (5 mg in 15 mL of nor- septic shock) and precipitate hypotension. In addition dobu-
mal saline) using a fine hypodermic needle. tamine also causes pulmonary vasodilation.
122 Section V n Circulation
Clinical Role
●● Normotensive cardiogenic shock due to primary myo-
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cardial pathology such myocarditis, rheumatic, con-
genital heart disease, Kawasaki’s disease, etc.
●● Fluid refractory septic shock when the blood pressure
is normal or high.
●● Cardiogenic shock due to severe hypoxia-ischemia of
any etilogy.
Administration
Therapy is started at the rate of 5–10 µg/kg/minute and
titrated based on clinical response of the child. Mixing
Figure 12.6: He is bag ventilated and cardiac compressions
with sodium bicarbonate solutions should be avoided. The are initiated. Epinephrine 1.2 mL of 1:10,000 dilution is
onset of action, duration, peak action and precautions tak- administered through the intravenous catheter, which had
en for infusion are similar to dopamine. been placed for administration of contrast.
Repeat cardiopulmonary assessment after CPR as
Adverse Effects shown in Figure 12.6.
●● Dobutamine increases myocardial oxygen demand.
However, improved cardiac contractility in children
with cardiac dysfunction results in enhanced oxygen
supply to the heart.
●● Hypotension, hypertension, tachyarrhythmias, VPCs,
angina.
Ù
An increase in heart rate without improvement in shock
should prompt a reduction in the rate of infusion.
CASE SCENARIO 3
A 2-year-old child was being given contrast intrave- Figure 12.7: Cardiac compressions are stopped. 240 mL
nously in the radiology department to evaluate a void- saline is being pushed with a 3-way stopcock.
ing cystourethrogram. He vomits, postures and be-
comes unresponsive. As he was being rushed into the Reassessment
PED, he developed swelling around the eyes, lips and Physiological status: Assisted ventilation, relative brady-
face. Generalized rashes were also noted. cardia with hypotensive shock (Figure 12.7).
On arrival into the PED, his airway is opened using Cardiac compressions were stopped. 240 mL saline is
the head tilt-chin lift maneuver. The airway nurse suctions being pushed with a 3-way stopcock. Which vasoactive
oropharyngeal secretions, inserts a nasogastric tube (10F) medication would you start after CPR when heart rate has
and decompresses stomach by connecting the NGT to a been established?
suction apparatus. Simultaneously, the airway manager
recognizes that the child is not breathing and initiates bag-
valve-mask ventilation. The team member who is assess- Epinephrine
ing HR, starts initiating chest compression. A 3rd team A stress hormone, epinephrine has affinity for β-1, 2 and
continues assessment... α-receptors (present in both cardiac and vascular smooth
muscle). β-adrenergic effects are more pronounced at lower
Chapter 12 n Vasoactive Drugs in the ED 123
doses, whilst, α-1 adrenergic effects manifest at higher ●● If hypotension persists despite epinephrine bolus in-
doses.24 jections and fluid administration, initiate epinephrine
infusion at the rate of 0.1–1 µg/kg/minute.
Beta-1 adrenergic receptor stimulation increases heart
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rate, myocardial contractility, automaticity and conduction
velocity. Administration
Beta-2 adrenergic receptors stimulation occurs at lower It can be safely administered through an intraosseous or
doses resulting in effects similar to β-1 activity. The other peripheral intravenous route using an infusion pump.
effects of β-2 activity are bronchodilation and dilation of
the arterioles by decreasing the diastolic BP. SVR decreas- Adverse Effects
es and diastolic pressure falls. There is a slight increase ●● Tachyarrhythmias, such as atrial and ventricular extra-
in heart rate, cardiac output and systolic BP. The force of systoles, tachycardias and fibrillation.
contraction also increases. However, the myocardial oxy- ●● Hypertension and ischemic changes in the ECG are
gen consumption is disproportionate to the improvement other dangerous side effects of this drug.
in myocardial contractility.
Prolonged infusions of high doses can be cardiotoxic Metabolic Effects
and lead to apoptosis.
●● Hypokalemia occurs due to β-2 adrenergic receptor
Epinephrine has been shown to reduce splanchnic stimulation.
blood flow, increase carbon dioxide production in the gas- ●● Hyperglycemia results from α-adrenergic mediated
tric mucosa and lactate production in the regional and sys- suppression of insulin release.
temic circulation.25,26 ●● Infiltration into skin and tissues can produce severe va-
sospasm and tissue injury.
Clinical Role
CASE SCENARIO 4
●● Anaphylactic shock.
An 8-month-old is being treated for septic shock in the
●● Hypotensive shock of any etiology. ED. She had received 100 mL/kg isotonic saline and
●● Fluid unresponsive, dopamine refractory, hypotensive had been intubated. Dopamine had been initiated when
septic shock.27,28,29 her shock was refractory to 60 mL/kg.
●● Drug of choice in CPR and postcardiac arrest shock.
Her assessment was as follows (Figures 12.8, 12.9 and
Dose 12.11).
Anaphylaxis: DEEP IM (avoid subcutaneous route,
since it may delay absorption): 0.01 mg/kg (0.1 mL/kg of
1:10,000) every 15 minutes PRN (maximum dose 0.3 mg).
IV/IO route: 0.01 mg/kg (0.1 mL/kg of 1:10,000) every
3–5 minutes up to a maximum dose 1 mg, if hypotension
is noted. Each bolus of epinephrine must be followed by a
saline flush (5 mL of NS), if the drug is administered via
the IO route.
Cardiac arrest: 0.01 mg/kg (0.1 mL/kg of 1:10,000) via
the IO/IV route every 3–5 minutes for a maximum of 1
mg. If heart rate is established, but hypotensive shock is
noted initiate epinephrine infusion at the rate of 0.1–1 µg/
kg/minute via a secure peripheral or IO line. Figure 12.8: Note the flushed, bright pink palms and soles of
this infant who has received 100 mL/kg fluids and dopamine.
●● If IV/IO access is not immediately available, 10 times These findings should not be misconstrued as normalization
the calculated dose for weight may be administered of shock. Check her BP with special emphasis on the point of
into the endotracheal tube. disappearance of the Korotkoff sounds (for diastolic BP).
124 Section V n Circulation
CASE SCENARIO 5
A 9-month-old infant presenting with acute cardiogenic
shock and a possible diagnosis of myocarditis has been
fluid resuscitated, intubated and is having dobutamine
administered at the rate of 10 µg/kg/min. The current car-
diopulmonary status shows the following (Figure 12.10)
Norepinephrine32-37
This endogenous catecholamine is a potent alpha-1 adren
ergic receptor agonist with some β agonist activity. Pre-
dominantly a vasoconstrictor, it increases systolic, dia- Figure 12.10 Physiological status: Refractory cardiogenic
stolic and pulse pressures with minimal effects on cardiac shock with high BP.
output and heart rate. This latter effect makes it a useful
catecholamine in children with tachycardia. Improvement What would be the appropriate drug in this setting?
in cardiac output has been attributed to better coronary per-
fusion pressures. Several studies have demonstrated that Bipyridines
norepinephrine normalized hemodynamic parameters, re-
These agents increase the levels of cAMP by inhibiting its
established urine output, decreased serum creatinine and
breakdown in the cardiac myocyte and vascular smooth
increased creatinine clearance in high output, low systemic
muscle.39 These properties result in increased myocardial
vascular resistance septic shock.
contractility and vasodilatation. In addition, it also im-
proves diastolic relaxation (lusitropy), thus reducing pre-
Clinical Role load, after load and systemic vascular resistance. PDI have
long half-lives ranging from 0.5 hour i.e Milrinone and 4
●● Hypotensive warm shock not responding to intravas- hours viz Amrinone. Unlike catecholamines, PDI are rec
cular volume repletion and dopamine infusion. In this ommended for cold shock with normal or high MAP40,41
scenario, NE infusion increases SVR, BP and urine a clinical scenario often encountered in catecholamine re-
output without significantly elevating the heart rate.16 fractory low cardiac output and high vascular resistance
●● Other indications for NE are vasodilator ingestion and states and after initiation of epinephrine, where blood pres-
CNS depressant intoxication where shock is character- sure is increased, but the other therapeutic goals of shock
ized by low SVR and hypotension. are not achieved.
●● Adverse effects are similar to other vasoactive medica- The main concerns of the PDI are related to their pro-
tions. However, bradycardia is an unusual complica- pensity to cause hypotension in volume depleted patients,
tion of norepinephrine infusion. accumulation in renal failure and occurrence of thrombo-
●● Dose: 0.1–2 µg/kg/minute (titrate based on repeated cytopenia with prolonged infusions.
cardiopulmonary assessment. Avoid mixing with al-
Chapter 12 n Vasoactive Drugs in the ED 125
Clinical Role
●● Catecholamine resistant cold septic shock with normal
Ù
Placement of an arterial catheter for intra-arterial
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or increased blood pressure. pressure monitoring is mandatory during administration
●● Catecholamine resistant shock complicated by severe of this drug. Since invasive monitoring is fraught with
tachyarrhythmias. complications in shocky children, its use in the ED is
limited.
Adverse Effects Vasopressin
Amrinone can aggravate myocardial ischemia and cause Vasopressin is released in response to increased plasma os-
supraventricular and ventricular ectopy. Rapid infusions molality, hypoxia or shock. It acts on the V1 receptor in the
of amrinone and milrinone during loading may produce vascular smooth muscle to produce vasoconstriction and
hypotension, which is aggravated by volume depletion. the V2 receptors, which mediate water reabsorption in the
Amrinone also produces reversible dose-dependent throm- renal collecting ducts. A few case studies have shown its
bocytopenia. usefulness in norepinephrine unresponsive warm shock.41
However, data is limited in the use of vasopressin in chil-
Administration dren42 and there is little evidence to support its use as res-
cue therapy in catecholamine resistant shock.43 Besides,
Amrinone and milrinone are formulated in a manner simi- children with septic shock have been shown to have high
lar to dopamine and dobutamine. Amrinone is not compat- levels of vasopressin.44,45
ible with dextrose containing solutions unlike milrinone,
which is compatible with dextrose containing solutions. Indications
●● Amrinone is administered as a loading dose of 1–2 mg/ ●● Hypotensive, warm septic shock refractory to fluid,
kg over 30–60 minutes. The infusion ranges from 5–10 Dopamine and norepinephrine infusion.
µg/kg/minute. Caution should be taken to correct in-
travascular volume depletion, since this group of drugs
can cause profound hypotension. Dose adjustment
Key Points
ü
needs to be made in children with renal failure. 1. Initiate the appropriate inotrope when signs of
pulmonary edema are noted or when shock is
refractory to fluids.
2. Choose the appropriate inotrope based on blood
pressure.
3. Epinephrine is the only agent, which can be initiated
simultaneously with fluids even before establishing
euvolemia in hypotensive shock.
common errors
û
1. Stepping up the dopamine infusion from 10 µg/kg/
min to 20 µg/kg/min in refractory shock.
2. Combining dopamine and dobutamine in the same
syringe.
Figure 12.11: Neurologically intact survival of a child with 3. Initiating inotropic agents prior to correction of
septic shock. Timing and use of the ‘best’ vasoactive medication hypovolemia.
is crucial for successful outcomes (Same child as managed in
4. Failing to initiate an appropriate inotrope.
Figure 12.8).
126 Section V n Circulation
Table 12.1: Preparation and infusion rates of commonly used vasoactive agents in the ED
Rate of administration: 10
Name of drug Rule
IPof:6196.52.84.10
(add to 100 mL) Rule of 3 (add to 50 mL) Dose
mL/h
Epinephrine 0.6 × body weight mg 0.3 × body weight mg 1 µg/kg/min 0.1–1.0 µg/kg/min
Norepinephrine 0.6 × body weight mg 0.3 × body weight mg 1 µg/kg/min 0.1–1.0 µg/kg/min
Dopamine 6 × body weight mg 3 × body weight mg 10 µg/kg/min 5–10 µg/kg/min
Dobutamine 6 × body weight mg 3 × body weight mg 10 µg/kg/min 5–10 µg/kg/min
8. Dellinger RP, Mitchell M, Carlet JM, et al. Surviving 21. Sharanz D, Stopfkuchen H, Jungst BK, et al. Hemodynam-
Sepsis Campaign: International guidelines for manage- ic effects of Dobutamine in children with cardiac failure.
ment of severe sepsis and septic shock. Crit Care Med. Eur J Pediatr. 1982;139:4-7.
2008;36(1):296-327. IP : 196.52.84.10
22. Majerus TC, et al. Dobutamine: Ten years later, Pharmaco-
9. Regnier B, Safran D, Carlet J, et al. Comparative hemo- therapy. 1989;9:245.
dynamics of dopamine and dobutamine in septic shock. 23. Berg RA, et al. Dobutamine pharmacokinetics and phar-
Intensive Care Med. 1979;5:115-20. macodynamics in normal children and adolescents. J Phar-
10. Jardin F, Gurdjian F, Desfonds P, et al. Effects of dopamine macol Exp Ther. 1993;265:1232.
on intra-pulmonary shunt fraction and oxygen transport in
24. Habib DM, et al. Dobutamine pharmacokinetics and phar-
severe sepsis with circulatory and respiratory failure. Crit
macodynamics in pediatric intensive care patients. Crit
Care Med. 1979;7:273-77.
Care Med. 1992;20:601.
11. Vane de Borne P, Oren R, Somers V. Dopamine depresses
25. Fisher DG, Shwartz PH, Davis AL. Pharmacokinetics of
minute ventilation in patients with heart failure. Circula-
tion. 1998;98:126-31. exogenous epinephrine in critically ill children. Crit Care
Med. 1993;21:111
12. Denton MD, Chertow GM, Brady HR. Renal –dose Do-
pamine for the treatment of acute renal failure: scientific 26. Meier-Hellman A, Reinhart K, Bredle DC. Epinephrine
rationale, experimental studies and clinical trials. Kidney impairs splanchnic perfusion in septic shock. Crit Care
Int. 1996;50:4-14. Med. 1997;25:399-404.
13. Bellomo R, Chapman M, Finfer S, et al. Low dose dop- 27. Levy B, Bollaert FE, Charpentier C, et al. Comparison of
amine in patients with early renal dysfunction: A placebo nor-epinephrine and dobutamine to epinephrine for hemo-
controlled randomized trial. Australian and New Zealand dynamics, lactate metabolism, and gastric tonometric vari-
Intensive Care Society (ANZICS) Clinical trial group. ables in septic shock. Intensive Care Med. 1997;23:282-
Lancet 2000;356:2139-43. 287.
14. Jakob SM, Ruokonen E, Takala J. Effects of dopamine on 28. Bollaert FE, Baeur P, Audibert, et al. Effects of epinephrine
systemic and regional blood flow and metabolism in septic on hemodynamics and oxygen metabolism in dopamine re-
and cardiac surgery patients. Shock. 2002;18:8-13. sistant shock. Chest. 1990;98:949-53.
15. Meier-Hellman A, Bredle DL, et al. The effect of low dose 29. Wilson W, Lipman J, Scribante J, et al. Septic shock: Does
dopamine on splanchnic blood flow and oxygen uptake in adrenaline have a role as a frontline inotropic agent in sep-
patients with septic shock. Intensive Care Med. 1997;23:31- tic shock? Anaesth Intensive Care. 1992;21:70-77.
37. 30. Moran JL, et al. Epinephrine as an inotropic agent in
16. De Backer D, Creteur J, Silva E, et al. Effects of dop- septic shock: a dose profile analysis, Crit Care Med.
amine, norepinephrine and epinephrine on the splanch- 1993;21(1):70.
nic circulation in septic shock: which is best? Crit Care
31. Brown C, et al. A comparison of standard-dose and high
Med.2003;31:1659-667.
dose epinephrine in cardiac arrest outside the hospital. N
17. Ruokonen E, Takala J, Kari A, et al. Regional blood flow
Engl J Med. 1992;327(15):1051.
and oxygen transport in septic shock. Crit Care Med.
1993;21:1296-1303. 32. Dieckman R, Vardis R. High dose epinephrine in pediatric
out of- hospital cardiopulmonary arrest. Pediatrics. 1995;
18. Neviere R, Mathieu D, Chagnon JL, et al. The contrasting
effects of dobutamine and dopamine on gastric mucosal 95:901.
perfusion in septic patients. Am J Respir. Crit Care Med. 33. Desjars P, Pinaud M, Potel G, et al. A re-appraisal of nor-
1996;154:1684-88. epinephrine therapy in human septic shock. Crit Care Med.
19. Santhanam I, Sangareddi S, Venkataraman S, et al. A pro- 1987;15:134-37.
spective randomized controlled study of two fluid regimens 34. Desjars P, Pinaud M, Bugnon D, et al. Nor-epinephrine
in the initial management of septic shock in the emergency therapy has no deleterious renal effects in human septic
department. Pediatr Emerg Care. 2008;24:647-55. shock. Crit Care Med 1989;17:426-29.
20. Orlowski JP, Porembka DT, Gallagher JM. Comparison 35. Hesselvik JF, Brodin B. Low dose norepinephrine in pa-
study of intra-osseous, central intravenous and peripheral tients with septic shock and oliguria: Effects of after load,
intravenous infusions of emergency drugs. Am J Dis Child. urine flow and oxygen transport. Crit Care Med. 1989;17:
1990;144:112. 179.
128 Section V n Circulation
36. Martin C, et al. Renal effects of nor-epinephrine used to 41. Choong K, Kissoon N. Vasopressin in pediatric shock and
treat septic shock patients. Crit Care Med. 1990;18:282. cardiac arrest. Ped Crit Med. 2008;9:372-379
37. Martin C, Papazian L, Perrin G, et al. Nor-epinephrine or 42. Mayer S, Gortner L, McGuire W, et al. Vasopressin in
IP : 196.52.84.10
dopamine for the treatment of hyper-dynamic septic shock? catecholamine refractory shock in children. Anesthesia.
Chest. 1993;103:1826-31. 2008;63:228-234.
38. Martin C, et al. Effects of norepinephrine on right ventricu- 43. Leclerc F, Walter-Nicolet E, Leteurtre S, et al. Admission
lar function in septic shock patients. Intensive Care Med. plasma vasopressin levels in children with meningococcal
1994;20:444. septic shock. Intensive Care Med. 2003;29:1339-44.
39. Richard J Beale, Steven M Hollenberg, Jean Louis Vincent, 44. Lodha R, Vivekanandhan S, Sarthi M. Serial circulating
et al. “Vasopressor and inotropic support in septic shock: vasopressin levels in children with septic shock. Pediatr
An evidence based review”. Surviving Sepsis Campaign
Crit Care Med. 2006;7:220-224.
Guidelines. Crit Care Med. 2004;Vol 32: No.11 (Suppl).
45. Vasudevan A, Lodha R, Kabra SK. Vasopressin infusion
40. Barton P, Garcia J, Kouat HA, et al. Hemodynamic effects
in children with catecholamine-resistant septic shock. Acta
of IV milrinone lactate in pediatric patients with septic
shock. Chest. 1996;109:1302-12. Pediatrica. 2005;94:380-83(d).
Approach to Acute Diarrhea
13
IP : 196.52.84.10
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.
IP : 196.52.84.10
Dose: 4–5 years 100 mg stat, ●● Keep track of the number of boluses that are being ad-
2–4 years: 50 mg stat single dose. ministered.
●● Perform the rapid cardiopulmonary cerebral assess-
Shigellosis: Ciprofloxacin
ment after each intervention.
Dose: 1 month to 18 years 20 mg/kg (max 750 mg) twice ●● Document the findings and response to treatment.
daily.
Giardiasis: Oral Metronidazole Ù
Do not stop fluid boluses on the basis of normalization
1–3 years : 500 mg OD for 3 days of BP. All the therapeutic goals should be achieved. If
3–7 years : 600–800 mg OD for 3 days shock persists, plan to continue fluid therapy.
Child 7–10 years : 1 g OD for 3 days Dehydration may persist after shock correction.
10–18 years : 2 g OD for 3 days.
Chapter 13 n Approach to Acute Diarrhea and Shock in the ED 131
Management
●● Continue O2 administration using the non-rebreathing
mask.
●● Infuse RL 20 mL/kg over 20 minutes.
CONTRAINDICATIONS
TO ORAL REHYDRATION
●● Signs of shock.
●● Ileus or intestinal obstruction (proven or suspected).
●● Comatose or unconscious.
●● Unable to tolerate oral/NGT rehydration (persistent
vomiting).
Figure 13.7 Physiological status: Airway stable/breathing ●● Often, children presenting with hypovolemic shock
normal/shock has resolved, but she has dehydration as have elevated renal parameters due to prerenal failure.
evidenced by sunken eyes and loss of skin turgor. Persistent Decision to withhold fluids will have disastrous con-
tachycardia is a sign of dehydration, since shock as resolved. sequences.
132 Section V n Circulation
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Chapter 13 n Approach to Acute Diarrhea and Shock in the ED
133
14
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Cardiogenic Shock
Figure 14.1: Rapid IV adenosine can reverse certain arrhythmias in seconds (Courtesy: Dr Gunda Srinivas, Dr Bhushan Chavan).
Learning Objectives
1. Using the pediatric assessment triangle to recognize 2. Management of cardiogenic shock in the ED.
cardiogenic shock.
Introduction PATHOPHYSIOLOGY
Cardiogenic shock is a hemodynamic state wherein, prima Depressed myocardial contractility causes a reduction in
ry myocardial dysfunction is responsible for the failure of stroke volume and cardiac output leading to tissue hypo-
the cardiovascular system to meet metabolic demands of perfusion. The ensuing metabolic acidosis further impairs
tissues. myocardial function. Other causative factors of myocar
dial dysfunction are myocardial depressant factor (found
Structural heart disease, arrhythmias or myocarditis are in severe sepsis), myocardial edema, adrenergic receptor
well known causes of cardiogenic shock (Figure 14.1). dysfunction, impaired sarcolemmic calcium flux and re
duced coronary blood flow.2
Ù Myocardial dysfunction may be systolic or diastolic.
Surprisingly, cardiogenic shock has been more
commonly noted in children presenting with shock due Diastolic dysfunction occurs due to inadequate myocar
to severe sepsis, scorpion envenomation, established dial relaxation. The latter results in increased end diastolic
status epilepticus, submersion injury, etc. pressure for a given end diastolic volume.3 The increased
Probably, failure to provide appropriate prehospital left ventricular pressure is transmitted to the lungs causing
pulmonary edema.
resuscitation and delay in recognition of early signs of
hypoxia and shock are the other causes contributing to Similarly, systolic dysfunction causes an increase in
cardiogenic shock in our setting.1 end systolic volume for a given pressure leading to a fall
in the stroke volume.
Chapter 14 n Cardiogenic Shock 135
Figure 14.5 Physiological status: Impending respiratory Ketamine is the ideal drug for intubating a child presenting
failure with hypotensive cardiogenic shock and non-convulsive with acute cardiogenic shock in the ED. Avoid ketamine
status epilepticus (secondary to severe hypoxia and shock). in cardiogenic shock due to chronic heart failure. Its nega
tive inotropic effect could precipitate cardiac arrest during
Ù intubation.
Consider early cardiogenic shock whenever a child with
shock presents with respiratory distress or respiratory Ù
Whenever sedative drugs are being considered for
failure. Bradycardia, muffled heart sounds, gallop,
intubating a child with acute cardiogenic shock, an
hepatomegaly and hypotension are late signs of cardiac
inotrope infusion must be initiated prior to intubation.
dysfunction.
Chapter 14 n Cardiogenic Shock 137
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.
Ù Ù
Following intubation, if features of pulmonary edema Ionized calcium level less than 0.9 mmol/L.
IP : 196.52.84.10 Administer calcium gluconate (9 mg elemental calcium
and hepatomegaly resolve, but shock persists, ask three
questions. per mL).
• Is the cardiogenic shock due to sepsis, anaphylaxis Dose: 1 mL/kg (100 mg/kg) diluted 1:1 with normal
or hypovolemia? saline over 10 minutes.
• If yes to any of the three questions, continue Rate of administration: 1 mL/minute, slow IV bolus
smaller aliqouts, until therapeutic goals of shock under cardiac monitoring.
are achieved. Follow-up with 150–200 mg/kg/24 hour of calcium to
• If pulmonary edema or hepatomegaly worsen, maintain ionized calcium > 0.9 mmol/L.
further fluid therapy is contraindicated even if
shock persists.
Hypokalemia
Afterload Reduction Suspect hypokalemia if large volume gastrointestinal (GI)
Clinically, if cardiogenic shock persists despite establish losses complicate cardiogenic shock.
ing euvolemia and inotropes, management should focus on Clinically hypokalemia may be suspected when brady
reducing after load. cardia is not associated with other features of imminent ar
Sedation and pain relief (discussed earlier). rest. Other clues include, persistence of hypotonia despite
Improve Myocardial Contractility correction of shock.
Correct documented hypoglycemia with 2 mL/kg of Correction of acidosis improves myocardial performance,
25% dextrose. decreases systemic and pulmonary vascular resistance and
decreases the need for increased respiratory effort. A base
Ù
Initiate GNS infusion to which potassium chloride (KCl)
deficit of > 10 mEq in cardiogenic shock is associated with
poor outcome.
has been added at recommended maintenance rates
after establishing urine output. Initiate maintenance ●● After intubation and ventilation, if pH < 7.2 or a base
fluids at two third of calculated volumes, if the etiology deficit of more than 6 mEq administer sodium bicar
of cardiogenic shock is CHD, RHD, myocarditis or bonate IV bolus at 1–2 mEq/kg body weight (dilute in
cardiomyopathy. equal amount of 5% D and infuse over 30 minutes.
●● Monitor for hypernatremia and hyperosmolality.
Monitoring
Ù Perform the rapid cardiopulmonary cerebral assess
Initiate the following inotropes if signs of pulmonary
edema are noted duringIP fluid
: 196.52.84.10
resuscitation of shock. ment frequently during vasoactive drug therapy.
1. Dobutamine when blood pressure is normal or
high with cool shock. Bedside limited echocardiography by the emergency
2. Epinephrine preferred in cardiogenic shock physician (BLEEP) accurately determines diminished car
presenting with hypotension, muffling of heart diac function, mechanical compromise of the heart and
sounds, gallop or chronic heart failure due to hypovolemia in the shocked patient7 (Table 14.2). It helps
structural heart disease. to assess systolic and diastolic function, cardiac output, in
ferior vena cava diameter in relation with respiration8,9 and
Therapy must be continuously tailored to patient’s re volume status.
sponse. Inotropes initiated at rates greater than 10 µg/kg/ Table14.2: ECHO findings in shock
minute increases both myocardial oxygen consumption
and systemic vascular resistance. End-systolic End-diastolic Fractional Shock
volume volume shortening
When cardiogenic shock does not respond to inotropes, or ejection
afterload reducing agents will improve myocardial perfor fraction
mance. Refer Chapter on Vasoactive Medications. Very low Low High Hypovolemic
shock
●● Vasodilators may be safely used with invasive moni
High High Low Cardiogenic
toring. Hence, they are not employed in ED settings. shock
●● Combination of vasodilators and inotropes often bring
Very low Normal or High Distributive
about an improvement in hemodynamic status not high shock
achieved by either drug alone.
●● The vasodilators commonly used in cardiogenic shock
are phosphodiesterase (PDE) III inhibitors, sodium ni
Ù
Plan surgery for surgically correctable lesions.
troprusside and nitroglycerine. These drugs should not
be used as first-line therapy to reverse shock.
Factors that increase SVR such as hypothermia, acido
sis, hypoxia, pain and anxiety should also be treated simul
INVESTIGATIONS
taneously. Refer Protocol 14.1. 1. Chest X-ray usually reveals cardiomegaly and pulmo
nary congestion.
Antibiotics 2. Serum electrolytes, calcium, arterial blood gases (ABG),
If sepsis is suspected administer 3rd generation Cepha- renal function test (RFT), liver function test (LFT).
losporins (Ceftriaxone 100 mg/kg) empirically, after col- 3. ECG helps to recognize dysrhythmias.
lecting blood and body fluids for culture. 4. Complete blood count, sepsis screen and serology for
dengue, rickettsia, leptospirosis, typhoid etc. Body
●● If focus of sepsis is obvious, administer the first dose fluids and urine for culture.
of appropriate antibiotics (e.g. Azithromycin, Doxycy
5. Evaluate hormonal levels such as TSH, ACTH, PTH if
cline for rickettsia).
deficiency is suspected.
140 Section V n Circulation
Key Points
ü common errors
û
1. High index of suspicion needed to recognize acute
IP : 196.52.84.10 1. Failing to identify acute cardiogenic shock, in
cardiogenic shock following a wide variety of hypoxic shocked children presenting with respiratory distress
insults. or failure.
2. Check list history of chronic respiratory distress to 2. Not check-listing for coexisting cardiac disease.
identify underlying structural heart disease. 3. Mistaking acute cardiogenic shock for an asthmatic
3. Position airway and provide 100% oxygen using exacerbation and nebulizing with salbutamol.
the flow inflating ventilation device throughout 4. Failure to use afterload reducing agents after
resuscitation of acute cardiogenic shock. stabilizing BP.
4. Rule out history of chronic respiratory distress to 5. Using furosemide in the ED to treat pulmonary
check for underlying structural heart disease. edema in children with cardiogenic shock.
5. Maintain airway and provide highest concentration 6. Withholding fluids in cardiogenic shock due to
of oxygen using the flow inflating ventilation sepsis.
device. 7. Failing to establish euvolemia prior to initiating
6. Perform early intubation using RSI and guarantee dopamine or dobutamine.
ventilatory support. 8. Failing to correct rhythm disturbances.
7. Dobutamine is the inotrope of choice in normotensive 9. Not monitoring and managing serum potassium and
cardiogenic shock. calcium deficits.
Chapter 14 n Cardiogenic Shock 141
Protocol
Protocal 14.1: PEMC approach: Recognition and management of cardiogenic shock
History of respiratory
IPdistress following submersion, perinatal depression, envenomation, severe sepsis, prolonged
: 196.52.84.10
seizures, airway obstruction, toxins, cardiac diseases, etc.
142 Section V n Circulation
Septic Shock
Figure 15.1: Focus of infection must be detected and treated along with hemodynamic interventions for complete recovery
Learning Objectives
1. Recognition of shock, pulmonary edema and 2. Fluid resuscitation of septic shock until clinical
cardiovascular dysfunction and non-convulsive therapeutic goals of shock resolution are attained
status epilepticus in febrile children using the in a time sensitive manner.
pediatric assessment triangle and the rapid 3. Recognition and management of pulmonary edema
cardiopulmonary cerebral assessment. during fluid resuscitation.
4. Modified septic shock protocol for settings with
limited access to mechanical ventilation.
INTRODUCTION PATHoPHYSIOLOGY
In India, fever and infections are the leading cause for vis- Local and systemic inflammatory response occurs when
its to the OPD, whilst, the commonest cause of hospital microbes traverse the epithelial and tissue barriers. This
mortality is serious sepsis (Figure 15.1). response to microbial invasion is known as ‘systemic in-
flammatory response syndrome’ (SIRS).
Fifty percent of deaths due to serious sepsis in develop-
ing countries occurred within the first 24 hours and these Fever (> 38.5ºC) or hypothermia (< 36.5ºC), tachypnea
deaths were a result of shock.1 This chapter describes an (respiratory rates > 2 SD above normal) and tachycardia
ED protocol that made a dramatic impact on hospital mor- (heart rate > 2 SD above normal) are the cardinal clinical
tality in severe sepsis. Developed from the findings of a signs of SIRS. Leukocytosis, leukopenia and band count
prospective randomized controlled study on fluid resusci- more than 10% are the other features of SIRS.3,4
tation of septic shock, it teaches how to resuscitate shocked Sepsis is diagnosed when SIRS occurs in association
children prone for pulmonary edema.2 with suspected, proven or obvious infection.
It also teaches how the pediatric assessment triangle Severe sepsis is diagnosed, when sepsis is associated with
can be used to recognize severe sepsis. dysfunction of organs distant from the site of infection.5
144 Section V n Circulation
Ù Triage Questions
Ask the following triage questions to mothers bringing
children to the OPD with fever with or without focus of
infection.
1. History of incessant cry, lethargy, more sleepy than
usual, ‘not as usual’ or posturing? Which help to
detect abrupt changes in mental status.
2. History of breathlessness in children presenting
with altered mental status and perfusion defects?
Which help to recognize pulmonary edema. Foci of Figure 15.2 Physiological status: Respiratory distress or failure
sepsis outside the lung such as diarrhea, urinary with tachycardia, shock with or without myocardial dysfunction,
tract infections, malaria in shocked children are ALOC with or without NCSE.
clues to recognizing acute lung injury or cardiac
dysfunction. The pathophysiology of shock in severe sepsis is mul-
tifactorial.6
Condition Description
SIRS Two or more of the following conditions: temperature > 38.5°C or < 35.0°C; heart rate of > 90 beats/min;
respiratory rate of > 20 breaths/min or PaCO2 of < 32 mm Hg and WBC count of > 12,000 cells/mL, < 4,000 cells/
mL or > 10% immature (band) forms
Sepsis SIRS in response to documented infection (culture or gram stain of blood, sputum, urine, or normally sterile
body fluid positive for pathogenic microorganism or focus of infection identified by visual inspection, e.g.
ruptured bowel with free air or bowel contents found in abdomen at surgery, wound with purulent discharge)
Severe sepsis Sepsis and at least one of the following signs of organ hypoperfusion or organ dysfunction: areas of mottled
skin; capillary refilling of ≥ 3 s; urinary output of < 0.5 mL/kg for at least 1 hour or renal replacement therapy;
lactate > 2 mmol/L; abrupt change in mental status or abnormal EEG findings; platelet count of < 100,000
cells/mL or disseminated intravascular coagulation; acute lung injury/ARDS and cardiac dysfunction
(echocardiography)
Chapter 15 n Septic Shock 145
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Unlike Dopamine, Dobutamine, etc. which should be ●● If initial assessment suggests effortless tachypnea with
initiated after establishing euvolemia, epinephrine infu- shock, viz the increased respiratory rate is secondary
sion may be started along
IP with fluids. It should be on flow
: 196.52.84.10
to metabolic acidosis and lung parenchyma is normal,
during both fluid resuscitation and intubation. administer 20 mL/kg over 20 minutes.2
IP : 196.52.84.10
Figure 15.13: This picture shows the airway being positioned Figure 15.14: This picture shows the child being reassessed
and oxygen being provided using the JR circuit. The assessor is after intubation.
evaluating the pulses after the heart rate.
Step 7
ii. Count heart rate for 6 seconds and multiply by 10. As-
Check whether each individual components of the airway,
sess, whether the heart rate is increased, decreased or
normal for age. While counting, evaluate for presence breathing, circulation and disability have improved, dete-
of gallop or whether the heart sounds are muffled (dif- riorated or remained status quo. Re-evaluate the cardio-
ficult to hear). pulmonary cerebral assessment and re-establish the physi-
ological status.
●● If bradycardic, the second responder initiates chest
compression. Step 8
●● If not, continue to evaluate the peripheral perfusion, Initiate the next therapeutic intervention until therapeutic
liver span and the BP. goals of shock, pulmonary edema, cardiac dysfunction and
●● Check whether the BP is normal or decreased seizures are achieved.
for age.
●● Check whether the liver span has regressed to nor-
mal for age or increased. therapeutic goals of
iii. Look at eye position, check for abnormal movements shock resolution (Table 15.2)
and evaluate the pupils for response to light.
Table 15.2: Therapeutic goals of shock resolution2
Step 3
Goals Features
Document the clinical variables immediately.
Airway Crying, verbalization in children, who have
Step 4 not been intubated
Interpret the physiological status after verifying normal Breathing RR (normal for age), absence of grunt,
values for age. retractions, normal thoracic respirations,
no added sounds
Step 5 Circulation HR (normal for age), pulses +++/++, CRT
Initiate appropriate intervention to the individual compo- < 2, warm peripheries, pink, liver span
(normal for age), BP: normal for age, with
nents of the ABCDs simultaneously.
normal pulse pressure, urine output >
Step 6 1mL/kg/h
Repeat this assessment either as soon as the therapeutic Disability Alert, normal tone and posture, eyes mid-
position, normal extraocular movements
intervention is completed or after allowing time for drug to in children, who were not intubated. Pupils
act (e.g. fluid bolus, intubation, initiating inotrope therapy are equal and reacting to light
or administration of an anticonvulsant).
150 Section V n Circulation
Breathing
Normalization of respiratory rates to age appropriate
ranges.
●● Restoration of normal perfusion results in resolution of
metabolic acidosis and reduction of respiratory rates to
the normal range.
Normalization of work of breathing
●● Fluid bolus therapy can resolve grunt, retractions, ab- Figure 15.15: The flushed bright pink color is commonly construed
dominal respiration and crepitations. as normalization of circulation. If this finding is associated with
●● Fluid therapy not only improves perfusion, but also respiratory distress, tachycardia, wide pulse pressure and altered
mental status as in this child, consider progression from cool shock
corrects myocardial dysfunction secondary to preload to warm septic shock during fluid resuscitation.
deficits.
●● Resolution of acute cardiogenic pulmonary edema re- ●● When these parameters are noted, counter check BP
sults in normalization of the work of breathing. and find out whether the pulse pressure is normal or
wide (diastole < 50% of systole is clue to the diagnosis
Circulation of vasodilatory shock).
relief, abscess drainage and mother’s close proximity Normalization of blood pressure with normal pulse
can often help in achievement of normal range of heart pressure.
rate in the appropriate clinical scenarios.
●● Blood pressure in young children and infants with
●● Heart rate, which falls within the normal range for age, shock is often higher than normal. As shock begins to
in children with respiratory distress or impending re- respond to therapy, the blood pressures drops to the
spiratory failure and shock is an ominous sign. These normal range for age.
children are at risk of profound deterioration (immi- ●● Whilst the resolution of hypotensive shock is based
nent arrest). on improvement in systolic blood pressure for age,
●● Muffling should disappear and the heart sounds should diastolic pressure should also improve such that it is
be well heard. Gallop should also resolve. greater than 50% of systolic pressure.
Chapter 15 n Septic Shock 151
Disability
Ù
Avoid stopping resuscitation when peripheries become
IP : 196.52.84.10
Ù
Normalization of mental status to base line is one of the
warm and pink, pulses become well felt and CRT < 2
seconds. Check the other parts of the pediatric assessment most important goals of shock resolution.
triangle. If child remains in altered mental status, has
●● Fluid responsive shock is characterized by resolution
respiratory distress, with or without hepatomegaly and
of incessant cry, lethargy and posturing resulting in
BP is associated with wide pulse pressure, continue fluid
consolable cry, playfulness and normal sleep.
resuscitation.
●● Consolable cry as a therapeutic goal of fluid responsive
shock is recognized when fluid therapy and monitoring
Resolution of Hepatomegaly is performed with the child in his mother’s arms.
●● Normalization of liver span for age is suggestive of Resolution of eye signs of non-convulsive status epilep-
resolution of myocardial dysfunction. ticus.
●● It is not uncommon to encounter eye signs of non-con-
Regression of liver span is often noted during bolus
vulsive status epilepticus on arrival or during resuscita-
therapy, inotrope infusion and following intubation.
tion of hypoxia or shock due to severe sepsis.
●● Successful resuscitation of fluid responsive shock is as-
Urine Output sociated with return of eyes to mid position and normal
extraocular movements.
●● Urine output greater than 1 mL/kg/h in children beyond ●● Examine eyes for lateral conjugate deviation, eyelid
1 year of age and greater than 1.5 mL/kg/h in infants twitch and/or nystagmus following each intervention
suggests normal renal perfusion. during resuscitation.
●● Urine output of less than 1 mL/kg/h during resuscita
tion is an ominous sign of refractory shock. Ù
The importance of early recognition and simultaneous
●● However, it may fail to provide information, when
management of convulsive and non-convulsive status
polyuria or anuria occurs as complications of renal dis
epilepticus cannot be understated in ensuring successful
eases with septic shock.
outcomes in septic shock.
Ù
Stomach contents should be emptied rapidly, if intubation
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is being considered.
Source Control
Ù ●● Obvious foci of sepsis should be drained even as resus-
Following intubation if oxygen saturations drop below
IP : 196.52.84.10 citation is in progress. If focus of sepsis is inaccessible,
92%, ‘DOPE’ should be ruled out to avoid lethal
consequences. the child is shifted to the OR at the earliest after stabi-
lization. Avoid transferring to the ICU or ward without
In vasodilatory shock in severe sepsis, it is not uncommon draining the focus of sepsis.
for recurrence of pulmonary edema.
●● Development of froth, crepts, desaturation, gallop,
muffling of heart sound, fall in mean arterial pressure,
increase in liver span, suggests the development of flu-
id refractory, dopamine unresponsive shock.
●● Add norepinephrine infusion at the rate of 0.3 µg/kg/
minute and titrate up to 0.5 µg/kg/minute.
●● Continue smaller and slower fluid boluses until signs
of shock and pulmonary edema have resolved.
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Chapter 15 n Septic Shock
155
156 Section V n Circulation
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
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).
Ù
Hematocrit is a simple bed-side tool to identify severity
IP : 196.52.84.10 of capillary leak. Serial evaluation of hematocrit is more
informative during resuscitation than serology test that
confirm dengue infection. Indian children with DHF
have a lower than expected rise in hematocrit during
the period of leakage of plasma. This phenomena has
been attributed to the high prevalence of iron deficiency
anemia in the general population. Normal HCT in healthy
Indian children is, 32% ± 3%. It has been proposed that
the cutoff for elevated HCT is 36.3%. This value seems
to identify > 80% of children with DSS in India.4
Case scenario 1
Figure 16.2: Time line for the dengue infection
A 3-year-old girl had fever for 5 days. On the 6th
Ù
Dengue is classified based on severity (Table 16.1)
2
day, she developed erythematous rashes all over
body with flushing of palms. Since morning she has
● Probable dengue. been afebrile. She has no abdominal pain or vomit-
● Dengue with or without warning signs. ing. There is no evidence of hepatomegaly, splenom-
● Severe dengue. egaly, ascites, bleed, edema or puffiness (Figures 16.3
and 16.4).
Recognition of Probable Dengue
Clinical clues that distinguish dengue from other fevers in
febrile phase are:
●● Fever without a source.
●● Flushed face.
●● History of living in a dengue-endemic area.
Two helpful clinical tools which help in the early diag-
nosis of dengue in the febrile stage:
1. Positive tourniquet test.
Figure 16.3: Tourniquet test shows multiple petechiae
2. Leukopenia: Total white blood cell count < 5,000 cell/ (Courtesy: Dr Thangavelu S).
mm3.
Confirmatory Tests
NS1 antigen (positive in the first 5–7 days) and dengue
IgM identified after 5–7 days are useful to confirm dengue.
Viral cultures and PCR are commonly used for research
purposes.
Whilst their application in clinical practice is limited,
the rapid NS1 antigen lab kit is currently being used for
early detection in the OPD setting.
High titres of NS1 antigen have been noted in the early
clinical phase. By day 5, it drops to 56.5%. Possibility of Figure 16.4 Physiological status: Her cardiopulmonary cerebral
diagnosis is enhanced when IgM antibody is also positive. status is normal. She has probable dengue.
160 Section V n Circulation
Probable dengue Dengue with warning signs* Criteria for severe dengue (one or more
IP : 196.52.84.10 of the following signs)
Live in/travel to dengue-endemic area ●● Abdominal pain or tenderness Severe plasma leakage leading to:
●● Fever and two of the following criteria: ●● Persistent vomiting ●● Shock (DSS)
– Nausea/vomiting ●● Clinical fluid accumulation ●● Fluid accumulation with or without
– Rash ●● Mucosal bleed respiratory distress
– Aches and pains ●● Lethargy ●● Severe bleeding
– Tourniquet test positive ●● Restlessness ●● Severe organ impairment
– Leukopenia ●● Liver enlargement > 2 cm ●● Liver AST or ALT >1,000
– Any warning sign ●● Lab: Increase in HCT ●● CNS-impaired consciousness
Laboratory confirmed dengue ●● Rapid decrease in platelet count ●● Heart and other organs
(important when no signs of plasma *Requiring strict observation and medical
leakage) intervention
Triage: ER physician should categorize based on severity and treat appropriately.
A 10-year-old girl presented with fever for 4 days. Since ●● If hematocrit is reduced in a shocked child, consider
the morning fever has settled, but she has developed blood transfusion.
abdominal pain. She is lethargic, does not wish to stand ●● If severe overt bleeding occurs, transfuse PRBC or
up or walk. She has no bleeding tendency. WBC: 4,000/ fresh whole blood.
mm3, HCT 43%, platelet count: 34,000/mm3. ●● If overt bleeding is not noted, infuse colloid.
●● If no improvement after colloid, consider blood or
PRBC transfusion.
162 Section V n Circulation
Ù Ù
No shock and HCT is high: The patient should be closely monitored. The rapid
IP : 196.52.84.10
• Isotonic fluids should be gradually reduced to cardiopulmonary assessment should be performed every
5–7 mL/kg for 1–2 hours, then to 3–5 mL/kg for 15–30 minutes till shock is corrected and then hourly
2–4 hours and then to 2–3 mL/kg/h. Further fluid till the critical phase is over. Fluids may have to be
administration is based on clinical response. Fluids continued for 24–48 hours. Child may go in and out of
should be maintained for a maximum of 24–48 shock during the critical phase. Judicious administration
hours. of fluid is essential to prevent fluid overload.
Shock persists: Caution: Restrict fluids such that the urine output is 0.5
• Check hematocrit after the first bolus. mL/kg/hour. If urine output exceeds 1–2 mL/kg/hour, it
Hematocrit is still increased: indicates excessive fluid administration.
• Repeat a second bolus of 10–20 mL/kg/hour
• If shock has resolved, reduce the rate of fluids to
7–10 mL/kg/h for 1–2 hours and then reduce further
Severe Dengue: Hypotensive shock
as mentioned above. Case scenario 4
Hematocrit is reduced (suggests bleeding):
A 10-year-old child is rushed into the ER following fever
• Transfuse 5–10 mL/kg of packed red cells or 10–20
for one week. The fever had settled, but since morning
mL/kg of fresh whole blood. she had been vomiting several times and has become
Figure 16.8: Management of severe dengue with compensated shock (Source: WHO Handbook for clinical management of dengue, 2012).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 163
progressively lethargic. She has edema and ascites as Though there is no clear advantage of colloids over crys-
shown in Figure 16.9. She has bleeding from intrave- talloids. Colloids have been shown to restore the cardiac
nous (IV) sites. Hematocrit is 45%. index and reduce the level of HCT faster than crystalloids
IP : 196.52.84.10
in patients with intractable shock.6,7,8
●● Call for inotrope infusion.
●● Dopamine if BP is low normal. Epinephrine if severely
hypotensive.
●● Catheterize and monitor urine output.
●● Check hematocrit before and after every fluid bolus.
●● Collect blood for grouping, crossmatching and lab in-
vestigations.
Repeat rapid cardiopulmonary cerebral assessment
Shock with normal blood pressure:
Figure 16.9: Note the facial ecchymoses, fresh bleed in the ●● Repeat a second bolus of crystalloid or colloid 10 mL/
nasogastric tube and abdominal distension due to ascites kg over 1 hour.
(Courtesy: Dr Thangavelu S). ●● Gradually reduce to 5–7 mL/kg/hour for 1–2 hours,
Many severe dengue children especially the older ones 3–5 mL/kg/h for 2–4 hours and then to 2–3 mL/kg/h
with hypotension may deceptively remain alert and may be or less.
ambulant. Shock may not be suspected in these children ●● Maintain 2–3 mL/kg/h for 24–48 hours.
unless they are touched. The cold extremities can then be Hypotension not resolved:
identified. A rapid cardiopulmonary cerebral assessment is
mandatory in these children to detect shock (Figure 16.10). Check hematocrit.
If HCT remains high after the 1st bolus:
●● Repeat another 10 mL/kg of colloid over 30 minutes to
1 hour and reassess.
●● If cardiopulmonary cerebral reassessment reveals that
there is improvement, continue colloid at 7–10 mL/kg
for 1–2 hours.
●● Reassess: If improvement persists, change to crystal-
loid infusion and gradually reduce it as mentioned
above.
If the HCT still remains high after the 2nd bolus and
shock persists:
●● Repeat 3rd bolus of 10 mL/kg of colloid over 1 hour.
Figure 16.10 Physiological status: Respiratory distress with ●● Repeat the cardiopulmonary cerebral assessment.
hypotensive shock and altered mental status.
●● If there is improvement, taper as mentioned above.
Fluid Management in Severe Dengue If resuscitation is effective, the hematocrit level will
with Hypotensive Shock (Figure 16.11) gradually decline by approximately 10% after each dose
of colloidal solution with improvement in the cardiopul-
●● Provide O2 through the Jackson-Rees circuit. monary status.
●● Initiate 0.9% NS or colloid solution 20 mL/kg, IV bo-
lus over 15 minutes. ●● If the hematocrit level declines with no sign of im
●● Colloids are preferred, if BP has to be restored urgent- provement, after the 1st, 2nd or 3rd bolus, it is likely
ly.2 that there may be concealed or internal bleeding.
164 Section V n Circulation
IP : 196.52.84.10
Figure 16.11: Management of severe dengue with hypotensive shock (Source: WHO Handbook for Clinical Management of Dengue, 2012)
●● Transfuse fresh packed red cell (5–10 mL/kg/) or whole It is important to understand that the outcome in severe DSS
blood (10–20 mL/kg) without delay. is very poor despite heroic measures undertaken at a ter-
●● If signs of pulmonary edema or worsening hepatomeg tiary care center. Hence the goal is to identify the children
aly is identified during fluid therapy, initiate inotropes. with dengue early, when they present with warning signs.
●● If overt bleed, hypotension persists and HCT is low,
start colloid 10–20 mL/kg/h. If HCT remains low, and
Ù
In India DSS often coexists with shock due to sepsis
hypotension persists consider fresh blood transfusion.
of other etiologies (e.g. UTI, malaria, typhoid, scrub
●● Continuous monitoring of these patients and careful
typhus, etc.). Differentiation between DSS and septic
titration of fluids based on frequent CPA improves
shock (see Protocol 16.1). Hence, larger volumes may
survival.
be needed to correct shock in our setting.
●● Children presenting with severe dengue may have as-
sociated metabolic abnormalities such as hypoglyce- ●● Perform sepsis screen and prescribe appropriate anti-
mia, hyponatremia, hypocalcemia and acidosis. These microbial therapy.
conditions should be identified early and treated appro-
priately. Note: Agitation may be a sign of shock, hepatic failure,
●● Monitor blood sugar frequently since glucose free flu- metabolic derangement, encephalopathy or cerebral ede-
ids are being infused. ma. Sedation without correction of the underlying prob-
●● If facilities to monitor glucose are unavailable and the lems may prevent recognition of alteration in mental status
child is young, infuse DNS after correction of shock. (an important sign of critical illness).
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 165
Complications (Figure 16.12) ●● Children with impaired hepatic function are at in-
creased risk of bleeding.
●● Avoid intramuscular injections.
IP : 196.52.84.10
●● Avoid non-steroidal anti-inflammatory agents.
Management when internal bleeding is suspected:
●● Send blood for cross matching if epistaxis, hematem-
esis or melena is noted.
●● Do not wait until the hematocrit drops to 30% (cut-off
for transfusion in children with septic shock). Higher
hematocrits are expected in children with DSS.
●● Do not hesitate to provide fresh blood transfusion when
there is worsening of clinical signs and symptoms and
fall in hemotocrit level during the critical stage.
Figure 16.12: The chest X-ray of the child shown in the figure
shows right pleural effusion. Note the ET tube positioned at T-4 Ù
(Courtesy: Dr Thangavelu S). It is well documented that adequate shock correction is
the best way to prevent hemorrhage.
The four most common causes of death among DSS patients:
●● Administer vitamin K.
●● Prolonged shock.
●● Do not call for platelet concentrate infusion.
●● Massive bleeding.
●● Fluid overload. ●● Transfuse 10–20 mL/kg of fresh whole blood. Fresh
●● Organ disturbance: Acute encephalopathy, hepatic fail- blood is rich in 2,3 DPG that will correct hypoxia and
ure. acidosis.
Ù Ù
As first responders, it is possible that the ED physicians Persistent hypoxia and shock are believed to be the
can play a critical role to prevent occurrence of these cause for bleeding.
serious complications.
●● Avoid platelet concentrates to treat thrombocytopenia.
●● Prophylactic platelet transfusions for severe thrombocy
Prevent patient slipping into shock by:
topenia in hemodynamically stable patients are not
1. Early recognition of dengue in the febrile stage. effective and are not indicated.10
●● Leukopenia (WBC < 5,000) ●● Platelets have a short half-life and are at increased risk
●● Positive tourniquet test.9 of destruction during dengue infection.
2. Early detection of critical stage. ●● Avoid routine administration of fresh frozen plasma.
●● Rising hematocrit and decreasing platelet < These blood products may contribute to fluid overload.
100,000.
●● Close monitoring and adjustment of fluid rate. Fluid Overload (Figures 16.13 to 16.15)
●● Avoid delay in switching from crystalloid to colloid
ED physicians must be aware of common pitfalls dur-
solution when indicated.
ing management that may lead to fluid overload: Lead-
Consider occult bleeding in the following situations ing cause of death in children with severe dengue is fluid
●● Prolonged shock that fails to respond to 40–60 mL/kg. overload. This may result in pulmonary edema, chest wall
●● Persistent shock despite reduction of hematocrit level. edema and abdominal compartment syndrome. All these
●● Unexplained tachycardia. conditions can lead to respiratory embarrassment and he-
●● Decline in hematrocrit is greater than expected. modynamic instability.
●● Hypotensive shock with low/normal HCT before fluid Fluid overload can occur in both the critical and recov-
resuscitation. ery phase leading to therapeutic dilemmas viz respiratory
●● Persistent or worsening metabolic acidosis in children distress and shock. In this scenario, management of one
with severe abdominal tenderness and distension. problem can worsen the other.
166 Section V n Circulation
Ù
Management of DSS is based on correct replacement of
fluid loss occurring due to capillary leak. Too much fluids
will lead to fluid overload and too little will not improve
shock. Besides, the quantity of leak can change every Figure 16.15: Chest X-ray taken the following day shows signs of
hour during the critical phase. Repeated assessment of fluid overload (Courtesy: Dr Thangavelu S).
perfusion and urine output with replacement of fluids is
key to survival. Paramedics and nurses must be trained Management of Fluid Overload
to collect data on input/output to guide therapy.
The management varies based on the phase of illness and
the child’s hemodynamic status.
Clinical Clues to Detect Fluid Overload
●● Recovery phase and cardiopulmonary status stable:
It may be difficult to differentiate ‘fluid overload’ and – Stop intravenous fluids: Most children will void and
‘shock’ in critically ill patients who have been referred improve spontaneously.
from other hospitals after fluid therapy. The following – Provide O2 and CPAP using the Jackson-Rees cir-
clinical clues may be helpful to the ED physicians to de- cuit: CPAP helps to resolve respiratory distress due
tect fluid overload: to pulmonary congestion.
– Oral or IV furosemide 0.5–1.0 mg/kg/dose once or
●● > 2 mL/kg/hour urine output in the absence of glycosu- twice daily or a continuous infusion of furosemide
ria or furosemide. at 0.1 mg/kg/h: Prior to diuretics ensure that there
●● Weight gain, raising respiratory rate, respiratory dis- had been no shock in the preceding 12–24 hours.
tress with falling SpO2 requiring oxygen to maintain – Monitor serum potassium.
saturation.
Chapter 16 n Approach to Recognition and Management of Dengue in the ED 167
Key Points
1. Repeated rapid IP cardiopulmonary
ü
and cerebral
common errors
û
1. Not reducing the rate of fluid administration after
: 196.52.84.10
assessment in conjunction with hematological and shock correction leads to increase in ascites, pleural
urine output monitoring during defervescence helps effusion and pulmonary edema.
identify the critical phase. 2. Giving furosemide to a child who is hemodynamically
2. Early diagnosis of dengue with warning signs and unstable can be catastrophic.
appropriate fluid administration at this stage prevents 3. Not changing the fluid to colloids, when there is
the child from developing shock. no response to initial crystalloid boluses and the
3. Fluid administration is only needed for 24–48 hours hematocrit remains high.
in the leak phase. 4. Not giving fresh blood to a child, who remains hemo
4. Judicious fluid therapy prevents fluid overload, dynamically unstable with a normal hematocrit.
(dreaded complication). 5. Blood transfusion in the convalescent phase for low
5. Adequate shock correction is the best method to hematocrit (dilutional).
prevent bleeding
6. Under estimating shock based on normal conscious
6. Prophylactic platelet transfusion has very little role
level, systolic BP and pulse oximetry (SpO2 95%–
in the management of hemodynamically stable
100%).
dengue patients.
* 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
Anaphylaxis
Figure 17.1: Rapid deterioration can occur in minutes if intervention is not immediate (Courtesy: Dr Radhika, Dr Gunda Srinivas).
Learning Objectives
1. Defining anaphylactic shock. 3. Using the pediatric assessment triangle to recognize
2. Pathophysiology of anaphylaxis. anaphylactic shock.
4. Evidence-based management of anaphylactic
shock.
may be needed to restore peripheral perfusion and Administer chlorpheniramine maleate intramuscularly
blood pressure. or slowly through the intravenous route.
2. Perform the rapidIP cardiopulmonary cerebral assess-
: 196.52.84.10
ment following each bolus to determine, whether the
Ù
Dose of Chlorpheniramine maleate:
child is showing signs of improvement, deterioration > 12 years and adults: 10 mg IM or IV slowly.
or is remaining status quo. 6–12 years: 5 mg IM or IV slowly.
6 months–6 years: 2.5 mg IM or IV slowly.
Epinephrine < 6 months: 250 µg/kg IM or IV slowly.
Administer Epinephrine
Adrenaline is the drug of choice in anaphylaxis. An
Steroids2
α-receptor agonist, it reverses peripheral vasodilation and Steroids may reduce the duration of illness. Little evi-
reduces edema. Its β-receptor activity dilates the bronchial dence is available on the optimal dosing for corticoster-
airways, increases the force of myocardial contraction and oids. The resuscitation council of UK suggest the follow-
suppresses histamine and leukotriene release. Adrenaline ing dosing schedule:
also acts on the β2-adrenergic receptors on mast cells4 and
inhibit activation.5 Hence, early use of adrenaline attenuates Ù
the severity of IgE-mediated allergic reactions. Adrenaline Dose of hydrocortisone:
seems to work best when given early after the onset of the > 12 years and adults: 200 mg IM or IV slowly.
reaction.6 6–12 years: 100 mg IM or IV slowly.
6 months–6 years: 50 mg IM or IV slowly.
Administer epinephrine deep IM or IV (if intravenous ac < 6 months: 25 mg IM or IV slowly.
cess is available): Epinephrine is administered at 0.1 mg/
kg per dose (1:1,000) intramuscularly at 5 minute intervals There is no data to support the use of H2 receptor block-
based on patient’s response. er in the acute resuscitation of a child with anaphylactic
Ù
Dose of epinephrine:
shock.11
3. After food-induced anaphylaxis, attempts to make 3. Pumphrey RS. Lessons for management of anaphy-
the patient vomit are not useful and hence not recom- laxis from a study of fatal reactions. Clin Exp Allergy.
mended. 2000;30(8):1144-50.
IP : 196.52.84.10 4. Kay LJ, Peachell PT. Mast cell beta2-adrenoceptors. Chem
4. Observation for 24 hours is recommended, since
Immunol Allergy. 005;87:145-53.
symptoms could recur within 1–8 hours in 20% of pa-
5. Chong LK, Morice AH, Yeo WW, et al. Functional desensi-
tients.
tization of beta agonist responses in human lung mast cells.
Am J Respir Cell Mol Biol. 1995;13(5):540-46.
Key Points
ü 6. Bautista E, Simons FE, Simons KJ, et al. Epinephrine
fails to hasten hemodynamic recovery in fully developed
1. Early recognition and anticipation of deterioration
canine anaphylactic shock. Int Arch Allergy Immunol.
in anaphylaxis crucial to survival. 2002;128(2):151-64.
2. IM epinephrine is life saving. 7. Simons FE, Gu X, Simons KJ. Epinephrine absorption in
3. Early intubation, aggressive fluid resuscitation adults: intramuscular versus subcutaneous injection. J Al-
and epinephrine in appropriate doses and lergy Clin Immunol. 2001;108(5):871-73.
routes mandatory in hypotensive shock due to 8. Song TT, Nelson MR, Chang JH. Adequacy of the epineph-
anaphylaxis. rine autoinjector needle length in delivering epinephrine to
4. Aggressive CPR recommended even if cardiac arrest the intramuscular tissues. Ann Allergy Asthma Immunol.
supervenes. 2005;94(5):539-42.
9. Simons FE, Roberts JR, Gu X, et al. Epinephrine absorp-
tion in children with a history of anaphylaxis. J Allergy
common errors
1. Delayed administration of epinephrine.
û Clin Immunol. 1998;101(1 1):33-37.
10. Simons FE, Gu X, Johnston LM, et al. Can epinephrine
inhalations be substituted for epinephrine injection in
2. Failure to give deep IM epinephrine. children at risk for systemic anaphylaxis? Pediatrics.
3. Initiating dopamine for anaphylactic shock. 2000;106(5):1040-44.
11. Sheikh A, Ten Broek V, Brown SG, et al. H(1)-antihista-
REFERENCES mines for the treatment of anaphylaxis: Cochrane system-
atic review. Allergy. 2007;62(8):830-37.
1. Anaphylaxis, Circulation, Journal of the American Heart 12. Lin RY, Curry A, Pesola GR, et al. Improved outcomes
Association. 2005;IV 143-IV 145. in patients with acute allergic syndromes who are treated
2. Johansson SG, Bieber T, Dahl R, et al. Revised nomencla- with combined H1 and H2 antagonists. Ann Emerg Med.
ture for allergy for global use: Report of the Nomenclature 2000;36(5):462-8.
Review Committee of the World Allergy Organization, Oc- 13. Visscher PK, Vetter RS, Camazine S. Removing bee stings.
tober 2003. J Allergy Clin Immunol. 2004;113(5):832-36. Lancet. 1996;348(9023):301-02.
18
IP : 196.52.84.10
Cyanotic Spell
Figure 18.1: Simple knee-chest position plays an important role in the management of cyanotic spell
Learning Objectives
1. Pathophysiology of cyanotic spell. 3. Management of cyanotic spell in the ED.
2. Using the rapid cardiopulmonary assessment
and the pediatric assessment triangle to identify
severity of spell.
INTRODUCTION out flow obstruction is absent during the spell due to reduced
antegrade flow across the muscular obstruction. Children
Cyanotic spell is also known as hypercyanotic spell, ‘TET’ become severely cyanotic, tachypneic and lethargic. With
spell, hypoxic spell, paroxysmal hyperpnea, anoxic spell the development of metabolic acidosis, pulmonary vascular
and blue spell. Approximately, one fourth of children with resistance increases and systemic vascular resistance falls.
cyanotic congenital heart diseases develop this medical Cardiac output becomes compromised due to myocardial
emergency (Figure 18.1). Though common in tetralogy ischemia. Impending collapse and death can ensue. Children
of fallot (TOF), it is also encountered in other cyanotic with iron deficiency anemia have a predisposition to the oc
congenital heart diseases with decreased pulmonary blood currence of cyanotic spells.
flow (PBF) such as tricuspid atresia with restrictive VSD
and VSD with severe valvular pulmonic stenosis.
PATHOPHYSIOLOGY
The hypercyanotic spell1,2 is characterized by a sudden and
striking decrease in the oxygen saturation (Figures 18.2 and
18.3) due to acute and complete or near complete obstruction
of the subpulmonary outflow tract. Agitation and decreased
hydration can exacerbate dynamic infundibular obstruction.
Ejection systolic murmur produced by the right ventricular Figure 18.2: Pathophysiology of cyanotic spell
Chapter 18 n Cyanotic Spell 175
CASE SCENARIO 1
A 3-month-old infant is brought with history of inces-
IP : 196.52.84.10 sant cry, breathlessness and increasing cyanosis. He is
being evaluated for cyanotic congenital heart disease at
the cardiology department (Figures 18.4 and 18.5).
Figure 18.3: Note the severe cyanosis in this infant who is receiving
100% oxygen via the flow inflating bag. The knee-chest position is
being maintained throughout resuscitation.
Clinical Features
Cyanotic spells typically occur in the morning, following Figure 18.4: Note that one team member is dedicated to holding
the knee-chest position during resuscitation of cyanotic spell.
crying, feeding and defecation (Box 18.1).
Also note that the airway is kept open and oxygen is being
Spells are characterized by paroxysm of: administered.
This maneuver increases systemic vascular resis Its mechanism of action is not clear. It probably acts by
tance and promotes systemic venous return to the right reducing spasm of the right ventricular outflow tract and
heart. This will theoretically increase intracardiac shunt
IP : 196.52.84.10 slowing the heart rate.
ing from left-to-right across the interventricular com
Esmolol, an ultrashort acting beta blocker is an alter
munication, as well as increase the preload of the right
native to propranolol. This is administered as a bolus of
ventricle.
0.5–1.0 mg/kg IV, followed by an infusion of 100–300 µg/
●● Stabilize the airway with the head tilt-chin lift maneu kg/min.
ver. Provide oxygen using the flow inflating ventilation
device (reduce risk of pulmonary edema during shock
Vasoconstrictors
correction).
●● Oxygen decreases peripheral pulmonary vasoconstric Phenylephrine infusion increases SVR, thereby reducing
tion and improves oxygenation once flow of blood to the right-to-left shunt.
the lungs is re-established. Dose: 3 mg/kg is diluted in 50 mL NS and infused
●● Intubation may be needed, if the cyanotic spell is re at 1 mL/kg/h to provide 1 μg/kg/min. The infusion may
fractory to management. be increased up to 5 μg/kg/min until oxygen saturations
●● Place the child in a knee-chest position throughout re improve.
suscitation in order to trap venous return in the legs Emergency surgery to repair the defect or to establish
thus increasing the SVR (Figure 18.4). systemic to pulmonary artery anastomosis should be con
●● Secure intravenous access to administer fluids. sidered in refractory spells.
●● Fluids will improve right ventricular preload.
●● If shock is noted, administer 2.5–5 mL/kg NS up to
Ù
Avoid the use of digoxin and epinephrine as these drugs
a maximum of 20 mL/kg at the rate of 1 mL/kg/min may exacerbate the obstruction to right ventricular
ute, whilst monitoring for signs of PE as per the PEMC outflow and cause further deterioration.
guidelines.
●● Administer Morphine at a dose of 0.1–0.2 mg/kg/dose
intravenously or subcutaneously. It decreases release of Prevention
catecholamines. It also increases the time for right ven ●● Chronic oral therapy with propranolol 1–2 mg/kg/dose
tricular filling by decreasing the heart rate and promoting q 6 h has been shown to decrease the frequency of the
relaxation of infundibular spasm. paroxysm. Propranolol stabilizes vascular reactivity
●● Administer sodium bicarbonate 1 mEq/kg IV slowly
of the systemic arteries thereby preventing a sudden
after dilution (1:1) at the rate of 1 mL/kg/minute. Sub
decrease in SVR. However, this is discouraged in the
sequent doses are infused based on pH.
newborn, since it may cause severe cardiac depression.
Ù
Ensure adequate oxygenation and ventilation before
●● Prophylactic iron therapy is useful to prevent recur
rence of cyanotic spell.
administering sodium bicarbonate. ●● Palliative shunt procedure is performed in children
with severe TOF for whom total correction may not
Most of the cyanotic spells respond to the above mea be possible.
sures. If not, the following medications are given: ●● Refer for early corrective surgery. Early identification
has become possible due to wide spread availability of
Beta Blockers pediatric cardiothoracic surgical facilities.
References
1. Roekens CN, Zuckerber AL. Emergency management
IP : 196.52.84.10 of hypercyanotic crises in tetralogy of Fallot. Annals of
Emergency Medicine. 1995;25(2):256-58.
2. Kothari SS. Mechanism of cyanotic spells in tetralogy
of Fallot-the missing link? International Journal of Car
diology. 1992;37(1):1-5.
3. Bailliard F, Anderson RH. Review Tetralogy of
Fallot Orphanet Journal of Rare Diseases 2009, 4:2
doi:10.1186/1750-1172-4-2.
Protocol 18.1: PEMC approach: Cyanotic congenital heart disease
19
IP : 196.52.84.10
Hypertensive Emergencies
Figure 19.1: Hypertension in children can present as an emergency with significant morbidity (Courtesy: Dr Radhika R; Dr Devi R)
Learning Objectives
1. Defining hypertensive emergency and urgency. 3. Antihypertensive drugs used in the management of
2. Using the pediatric assessment triangle to hypertensive emergency.
identify severity of illness in a child with severe
hypertension.
High blood pressure is often noted in seriously ill children Age Severe hypertension Hypertensive crisis
on arrival into the ED. It occurs as a compensatory re Neonate
sponse to shock. Occasionally, hypertension is responsible 1 week SBP > 106 mm Hg
for cardiac failure, seizures and visual loss! 2–4 week SBP > 110 mm Hg
Infant
Drugs to reduce BP in shocked children can kill. On
the contrary, failure to reduce BP in primary hypertension < 2 year > 118/82 145/95
could also be dangerous (Figure 19.1). 3–5 year > 124/84 150/95
6–9 year > 130/86 160/100
Recognition and appropriate approach is essential to
10–12 year > 134/90 165/105
tide over the crisis of hypertension.
13–15 year > 144/92 175/110
Literature suggests that the prevalence of hypertension 16–18 year > 150/98 185/120
in the pediatric population is estimated at 1%–2%. Though (Data from report of the 2nd Task Force on BP Control in Children – 1987-
uncommon in children, the emergency physician may en Pediatrics 1987;79:1-25 and Burg Fb, Ingelfinger JR, Wald ER. Current
counter hypertensive emergencies in the ED. Pediatric Therapy. Philadelphia: WB Saunders. 1993;14:158-64)
●● Acute onset breathlessness suggest cardiovascular abdominal bruit or mass, differential pulses and BP record
compromise. ing in all four limbs help to identify etiology of hyperten
●● Visual changes, seizures, headache and vomiting sug
IP : 196.52.84.10 sion. Fundoscopy should be performed looking for hemor
gest disturbance to the central nervous system (Box rhage, papilledema or infarcts.
19.1).
Any increase in blood pressure that is sufficiently acute
Box 19.1: Hypertensive emergencies that need
immediate treatment or elevated to cause symptoms should be considered life-
threatening.
●● Hypertensive encephalopathy
●● Hypertension associated with acute heart failure or Laboratory Studies
pulmonary edema
●● Acute renal failure Complete blood count (CBC), electrolytes, blood urea ni
●● Stroke trogen (BUN), creatinine, uric acid, urinalysis, urine cul
●● Adrenergic crisis (pheochromocytoma)
ture, chest X-ray (CXR), ultrasonogram (USG) abdomen,
●● Hypertension with intracranial bleed
●● Hypertension-induced blindness electrocordiagram (ECG) and ECHO are needed in all
●● Myocardial infarction (rare in children) children. Further studies should be individualized and may
be done once the BP is controlled.
Figure 19.3: Summary of the approach to a child with severe hypertension in the ED
182 Section V n Circulation
●● If systolic blood pressure has not responded to furo Table 19.3: Life-threatening causes of hypertension
semide, consider Labetalol.
Infancy Coarctation of the aorta, valvular insufficiency,
●● If hypertension does
IP :not resolve despite Labetalol,
196.52.84.10 congenital adrenal hyperplasia, renal vascular
consider drugs mentioned in Figure 19.3.
disease, renal parenchymal disease
Treatment must be rapid, but cautious. High BP must Childhood Renal parenchymal disease, renal vascular
be reduced gradually. The goal in management is the re disease, coarctation of the aorta,
duction of 10%–25% of the initial BP in the first 1–2 hours pheochromocytoma, increased intracranial
of therapy. A rapid fall in BP could cause hypoperfusion pressure, bacterial endocarditis, drug-induced/
of vital organs resulting in iatrogenic morbidity. Long- toxicologic
standing hypertension is often compensated by altering Adolescence Renal parenchymal disease, pheochro-
cerebral vascular autoregulatory mechanisms. When BP mocytoma, toxemia of pregnancy, drug-
is suddenly dropped iatrogenically, these compensatory induced/toxicologic
mechanisms are overwhelmed, the consequences being
deleterious to the patient. Hence, in order to reduce BP Nitroprusside
gradually, intravenous hypertensive drugs need to be ad
ministered (Figure 19.1). Nitroprusside is the drug of choice in hypertensive crisis.
It has a rapid onset of action and lasts only as long as the
●● Standard protocol for status epilepticus. infusion is continued, enabling precise control of BP. A
●● Consider early use of Aspirin, if acute visual loss oc vasodilator of both venous and arterial vasculature, an ar
curs in the hypertensive child (after ruling out magnetic
terial line is needed for its monitoring, the drug is prefer
resonance imaging (MRI) proven intracranial bleed).
ably administered through a central line using an infusion
●● CT using contrast may be more easily available. How
pump. The bottle and intravenous tubing should be cov
ever, it should be avoided if child has elevated urea or
ered by a black sheet to protect from light. The solution
creatinine.
should be changed every 24 hours. Since its use requires
●● Monitor BP and urine output from the out s et.
intra-arterial monitoring it is not a drug recommended for
●● Insert an arterial line for monitoring intra-arterial pres
use in the ED.
sure if nitroprusside, diazoxide or nicardipine are being
used. Dose: 0.3–8 µg/kg/min (Table 19.2).
Blood thiocyanate levels should be monitored if the
Pharmacotherapy of infusion lasts for more than 24 hours. The rate of infusion
Hypertensive Emergencies is maintained at 10 µg/kg/min for a duration longer than 6
The choice of drug depends on the severity of the patient’s hours. It is discontinued, if thiocyanate levels exceed 10
hypertension, current medications, the suspected cause of mg/dL. If toxic levels are noted, thiosulfate is the antidote
hypertension and the organs involved (Table 19.3). of choice.
Labetalol Hydralazine
Labetalol has α and β blocking effects. The β-adrenergic Hydralazine causes relaxation of smooth muscle of both
IP : potent.
blockade activity is more 196.52.84.10
Dosing is not affected the arteries and veins. It is less potent than other agents.
by poor renal function. It has been reported to be effec Dose: 0.1–0.5 mg/kg/dose.
tive in the management of severe hypertension that results
from pheochromocytoma and coarctation of the aorta. It is
Esmolol
also used in the treatment of hypertensive crises in patients
with end-stage renal disease. Both intravenous and oral Esmolol is given as a loading dose of 100–500 µg/kg IV
preparations are available. over 1–2 minutes, followed by an infusion of 50–300 µg/
kg/minute. It is useful in hypertensive crisis following sur
Dose: 0.2–1.0 mg/kg/dose intravenously followed by an gery for coarctation of aorta.
infusion of 0.25–1.5 mg/kg/h.
Side effects are dizziness, gastrointestinal upset, head Diazoxide
ache, urinary retention, bradycardia and bronchospasm in Diazoxide is given as a bolus of 1–3 mg/kg. It is very ef
asthmatics. It is therefore contraindicated in asthmatic pa fective in rapidly lowering the blood pressure. However, it
tients. can cause precipitous hypotension and repeated boluses of
1 mg/kg may be preferable to a higher initial dose.
Nicardipine
Phentolamine
Nicardipine is a calcium channel blocker that can be ad
ministered intravenously. It acts by causing vasodilata Phentolamine with its rapid onset of action and alpha
tion. blocking effect is useful in pheochromocytoma. The high
risk of hypotension after the primary lesion (e.g. pheochro
Dose: Infusion at the rate of 0.5–3 µg/kg/min. mocytoma) is excised, which should not be forgotten. Care
Side effects are headache, tachycardia, dizziness, nau should be exercised and the surgeons should be alerted to
sea and vomiting. It is contraindicated in intracranial hem this possibility.
orrhage (ICH) as it increases cerebral blood flow. Dose: 0.1 mg/kg/dose IV (max 5 mg).
Nifedipine Enalaprilat
It is a calcium channel blocker with powerful vasodila Enalaprilat (intravenous form of enalapril) has been ad
tor activity resulting in a decrease in peripheral vascular ministered as 5–10 µg/kg/dose. It has been used in adult
resistance. Route of administration is oral (bite and swal hypertensive emergencies with good results. However,
low). The effectiveness of the drug is due to its absorp studies of its use in children are limited. Little is known of
tion from the gastrointestinal tract. An exact dose may its side effects in children.
be difficult to administer especially when given by the
sublingual route. Fenoldopam
Dose: 0.25–0.5 mg/kg/dose, (max 10 mg). Fenoldopam is a selective dopamine agonist, causing va
sodilation of the renal, cerebral, coronary and splanchnic
It is contraindicated when the child has an intracranial
vasculature. Infusion rates of 0.1–0.2 µg/kg/min have been
bleed.
used in children. Side effects include reflex tachycardia,
Ù raised intracranial pressure (ICP) and increased intra-ocu
Ideally, Sodium Nitroprusside should be used to lar pressure. Experience in children is limited.
gradually reduce high blood pressure. This drug
mandates intra-arterial monitoring. Hence, Nifedipine Hypertensive Urgency6
is used as an alternate agent in settings without access
to intra-arterial monitoring. Administer oral antihypertensive agents to resolve high BP
presenting as hypertensive urgency.
184 Section V n Circulation
Disability
IP : 196.52.84.10
Approach to Decreased Level
20
IP : 196.52.84.10
of Consciousness
Figure 20.1: Child presenting with cardiogenic shock, coma with raised ICP and uncal herniation being successfully resuscitated
Learning Objectives
1. The risk of failing to recognize early decrease in 3. Step-wise approach to evaluate decreased level of
level of consciousness. consciousness in children.
2. Case-based management of non-traumatic coma. 4. Need to correct shock in the presence of raised
ICP.
5. Investigations in management of coma.
INTRODUCTION
Many acutely ill children are not fully conscious. Most
Ù
Based on evidence that even early decrease in the level
make a full neurological recovery as the underlying cause is of consciousness may be catastrophic if not recognized,
treated, but considerable skill is required to distinguish the this group advocated that evaluation and management
group at high-risk of further deterioration, leading either to should be initiated when the GCS dropped to less than
death or to severe handicap1 (Figures 20.1 and 20.2). 15 or ‘Responsive to voice’ in the AVPU scale.
Ù Recognition of early fall in mental status viz ‘Responsive
The Pediatric Accident and Emergency Group in the
United Kingdom reported that if the Glasgow Coma Scale to voice’ poses a challenge in all ages. In precommunicative
(GCS) was less than 12 in children between 1 month and children, early fall in mental status is best confirmed by ask
18 years of age for greater than 6 hours, mortality was ing the mother triage questions (See Chapter 1).
as high as 40%.2 This definition was not applicable for Children of any age who are restless and talking un-
children with learning disabilities whose usual GCS was intelligibly have a verbal score of 2 and are considered to
less than 15, critically ill neonates or children with a be deeply unconscious. These children are at high-risk of
known diagnosis or with a definite treatment plan. catastrophic deterioration.3
188 Section VI n Disability
IP : 196.52.84.10
Ù Ù
At initial presentation, it is preferable to err on the side Children presenting with altered level of consciousness
of recording a lower score, as it is easier to withdraw have several simultaneously occurring problems that
treatment from a child who is improving than to need concurrent management!
resuscitate one who deteriorates. • Hypoxia
• Shock
If altered mental status is doubtful, it is best to treat • Myocardial dysfunction
than to wait for overt clinical signs to develop. Provide • Prolonged convulsion, postconvulsive state
oxygen, administer the first bolus and correct documented • Sepsis, intracranial infection
hypoglycemia. A clearer picture will emerge, providing • Raised ICP
clues towards identifying the etiology of decreased level • Metabolic illness (dyselectrolytemia), hypoglycemia,
of consciousness. ketosis, etc.
• Trauma
CASE SCENARIO • Hypertension
• Cause unknown—toxins.
A 5-year-old boy was brought with history of fever, pro-
gressive lethargy and posturing for 3 days. He had been
vomiting several times since the morning. His tempera- Ù
ture was 40°C (Figures 20.3 and 20.4). A simple focused history should be obtained
simultaneously as assessment and resuscitation are in
progress.
●● Convulsions or posturing?
●● Progressive drop in consciousness such as incessant
cry, lethargy, more sleepy than usual?
●● Fever?
●● Breathlessness?
●● Vomiting?
●● Headache?
●● Length of symptoms?
●● Previous infant death in the family?
Figure 20.3: Note posturing in this unresponsive boy ●● Ingestion or availability of drugs at home?
Chapter 20 n Approach to Decreased Level of Consciousness 189
Box 20.1: Monitor during resuscitation ●● Thiopental is cerebroprotective and consequently the
induction agent of choice.
●● Airway
●● Vecuronium is the paralytic agent of choice, since suc-
●● Respiratory rate, workIPof :breathing
196.52.84.10
(WOB)
cinylcholine is known to worsen ICP.
●● Heart rate, perfusion, BP, liver span
●● Even if a comatose child appears to be breathing, con-
●● AVPU assessment every 15 minute
●● Eye position, eye movement, pupils
trolled mechanical ventilation should be instituted ear-
●● Monitor urine output
ly to avoid washing out of CO2. While oxygenation is
●● Temperature maintained at normal levels, PaCO2 is maintained in the
●● O2 saturations low 30s. Pulse oximeter and end tidal CO2 monitoring
●● Electrocardiography (ECG) enable non-invasive monitoring of gases in the PED.
●● BP
●● End tidal CO2 Indications for intubation
in comatose children
Initial management priorities ●● The Glasgow Coma Scale (GCS) is 12.
●● Deterioration in the GCS.
Airway and Breathing
●● Unstable airway (intubation mandatory, even if the
In the unresponsive child, loss of tone of the oropharyn GCS is higher).
geal muscles causes falling back of the tongue resulting ●● Respiratory depression (respiratory drive may be com-
in airway obstruction. Furthermore, loss of airway protec- promised in raised ICP).
tive reflexes lead to pooling of secretions. An unprotected ●● Neurogenic hyperventilation (hyperventilation may be
airway itself could worsen underlying hypoxia, shock, car- a sign of midbrain involvement).
diac failure, status epilepticus and raised ICP (Box 20.1). ●● Asymmetric or dilated pupils.
●● Evidence of herniation.
Clinically, airway obstruction manifests as stridor viz
neurogenic stridor, which is relieved by the following ma-
Circulation
neuvers:
Correct shock with NS (fluid of choice). If respiratory dis-
●● Open airway by head tilt-chin lift maneuver. tress or failure with or without signs of cardiac dysfunction
●● Use large bore suction cannula to rapidly clear oropha- are identified on arrival, the smaller boluses (5–10 mL/kg)
ryngeal secretions. are administered.
●● Provide oxygen using the CPAP device.
●● Call for intubation tray using SOAPME protocol. If septic shock is recognized (e.g. meningitis or en-
●● Intubate using ICP precautions. cephalitis) in the comatose child, larger volumes (60–80
mL/kg) may be warranted to correct shock. Close moni-
Ù toring for pulmonary edema and hepatomegaly is neces-
Raised ICP may be aggravated by painful or noxious sary during fluid resuscitation shock due to sepsis. If coma
interventions even though the child appears deeply was due to DKA or isolated head trauma, smaller volumes
comatose. Since the process of intubation can stimulate (10–30 mL/kg) may be warranted to resolve shock.
the gag reflex and aggravate ICP, drugs are used which Raised ICP is not a contraindication for shock correc-
blunt the deleterious effects of intubation. tion. Indeed, it signals the need for maintenance of high
mean arterial pressure (MAP).
Anesthetic drugs used for intubation for children at risk of
developing ICP are the following: Ù
Increased systemic BP is a physiological compensatory
●● Lidocaine is the premedication used to bluntgag by acting response to maintain cerebral perfusion pressure when
on the sensory pathway of the glossopharyngeal nerve. ICP increases! BP is maintained at the 95th percentile
●● Atropine reduces vagal-induced bradycardia. Brady- for age/height in order to maintain cerebral perfusion
cardia in a shocked child provides clue that raised ICP pressure (CPP) in the face of an elevated ICP.
coexists.
190 Section VI n Disability
●● Antihypertensive drugs can kill, if used to reduce blood ●● Evaluation for pupillary inequality helps recognize
pressure in a child with ICP! herniation.
●● Infusing hypotonicIP fluids (5% or 10% dextrose) can
: 196.52.84.10 ●● Examine the fundus for additional clues.
lead to cerebral edema in children presenting with ●● If seizures are refractory to anticonvulsants, evaluate
ICP. electrolytes and correct as shown in Table 20.3.
●● Documented hypoglycemia is corrected with a bolus ●● Coma not explained by the presence of seizure activity
dose of dextrose. If age is greater than 4 weeks, ad needs to be evaluated as discussed below.
minister 5 mL/kg IV of 10% dextrose as bolus. If age
of the child is less than 4 weeks, administer 2 mL/kg IV Recognizing Depth of Coma4
10% dextrose bolus.
The Glasgow Coma Scale (Table 20.1) was designed to as-
●● The presence of a very high glucose level may point to
sess the depth of post-traumatic brain injury coma in adults
a diabetic ketoacidosis (refer to Chapter 34 on DKA).
and children beyond the age of 5 years. However, for chil-
dren between 9 months and 5 years of age, a modified mo
Disability tor and eye opening scales has been recommended.
Clinical Seizures Motor response is elicited by applying supraocular
Eye deviation, nystagmus and eyelid twitching, character- pressure (and looked for flexion and extension).
istic of non-convulsive status epilepticus, pinpoint a treat- It may also be assessed by applying pressure over the
able etiology of coma. Unrecognized seizure activity in- nail bed using a pencil. Motor response is M5 if the infant
crease ICP and could precipitate cerebral herniation. They responds by withdrawing. There may be need for flexibil
may be due to the excitatory toxic and ischemic mecha- ity due to overlap between the age groups. This method is
nisms of secondary brain damage. discussed below:
Step 1: If eyes are open (E-4) request the mother to talk Recognizing Presence of Raised
to her child. Intracranial Pressure
●● Babbling: < 9 months.
IP : 196.52.84.10 Raised ICP exists in varying degrees of severity in all en-
●● Waving bye-bye: 9–10 months. cephalopathies of non-traumatic etiologies (infectious and
●● Words: 1 year. non-infectious causes).
●● Pointing body parts: 15–24 months.
●● Sentences: 2 years. Concurrent and early management of intracranial hy-
●● Orientation in place and time from 5 years. pertension in the ED is not only life-saving, but also en-
sures neurologically intact survival.
Ù
‘Raised intracranial pressure’ must be presumed in all
Step 2: If no eye opening or spontaneous speech
comatose children. Failure to recognize and manage
●● Ask child to obey simple command such as squeezing ICP in the ED could lead to death or neurological
finger or eyes (M6). handicap.
Ù
• Acute elevation of ICP will not cause papilledema
Step 5: If child flexes, but does not localize, apply nail bed immediately. Hence, its absence must not be taken as
pressure, using a pencil. a reassuring sign. Neither, is it safe to entirely rely
●● If finger is withdrawn (M4). on the computed tomographic images to diagnose
●● If child moves limb across the body to dislodge the raised ICP. ICP is often a clinical diagnosis in the
painful stimulus (M5). acutely ill child!
• If papilledema is noted in association with
hypertension (systolic BP greater than 2 SD),
reevaluate
Step 6: Look for asymmetry of movement in any of the – BP in all the four limbs.
steps (Uncal herniation). – Send blood for urea and creatinine.
Algorithm: Modified from Kirkham FJ et al. Pediatric – Admit into the ICU.
coma scales. Development Medicine & Child Neurology. – Refer to the nephrologist.
2008;50:267-74.
192 Section VI n Disability
Variations in CPP, both decreased CPP (when raised The pattern of clinical findings to help in recognition of
ICP is associated with uncorrected shock) and increased the level of herniation is shown in Table 20.2.
CPP associated with raised ICP is thought to cause brain
IP : 196.52.84.10 Table 20.2: Herniation syndromes
damage by following two mechanisms:
Uncal Diencephalic
• Hemiparesis • Flexor response to pain
• Minimal deviation of and or decorticate
eyes on oculocephalic/ posturing
oculovesti bular testing • Hypertonia/hyper-
• Unilateral ptosis reflexia with extensor
• Unilateral fixed dilated plantars
pupil • Cheyne-Stokes
breathing
Upper pontine
• Full deviation of eyes
• Extensor response to oculocephalic/
to pain and /or
oculovestibular testing
decerebrate posturing
• Small midpoint pupils
• Hyperventilation reactive to light
• Minimal deviation of
eyes on oculocephalic/ Lower pontine
Figure 20.5: Unequal pupils in a child with raised ICP and uncal oculovestibular testing • No response to pain or
herniation (Courtesy: Dr Arun Annamalai). • Midpoint pupils fixed to flexion of legs only
light • Flaccidity with extensor
Decreased Cerebral Perfusion Pressure Medullary
plantars
• Ataxic or shallow
Cerebral perfusion pressure is the difference between the • Slow irregular gasping respiration
respiration/respiratory
mean arterial pressure and the intracranial pressure, i.e. • No deviation of eyes
arrest with adequate
(CPP = MAP – ICP). When intracranial pressure is elevat- on oculocephalic/
cardiac output
oculovestibular testing
ed and coexisting shock is not resolved, cerebral perfusion • Pupils dilated and fixed • Midpoint pupils fixed to
pressure falls causing cerebral ischemia. Ischemia in the to light
light
border zones between the main arterial territories, cause
clinically silent brain damage. It rarely may be associated
with seizures or hypertensive encephalopathy.
Herniation Syndromes
Untreated, raised ICP leads to herniation syndromes. Dif-
ferences in pressure between the forebrain compartment
and the posterior fossa, may cause uncal (Figure 20.5),
diencephalic or midbrain/upper pontine herniation. The
temporal lobes herniate through the tentorium. Similarly,
a pressure differential between the posterior fossa and the
spinal canal can lead to herniation of the brain through the
foramen magnum (Figure 20.6). The resulting lower pon- Figure 20.6: Lesions in various sites in the brain causing
herniation syndromes
tine and medullary herniation syndromes can be lethal.
Brain herniation causes direct mechanical damage in ●● Memorize stages of progressive herniation that are
addition to ischemia and hemorrhage secondary to vascular compatible with intact survival.
distortion. Central or uncal herniation through the tentorium ●● Learn to serially examine the child’s level of conscious-
is compatible with intact survival; on the contrary, hernia- ness (Table 20.1) and the brainstem reflexes such that
tion through the foramen magnum is not. Changes from one progression is recognized immediately and appropriate
syndrome to the next signifies progressive worsening. action is taken swiftly.
Chapter 20 n Approach to Decreased Level of Consciousness 193
●● Drugs, toxins, metabolic abnormalities and the pos- ●● Blood ammonia: Reye’s syndrome, hyperammonemia.
tictal patient may mimic imminent herniation. Once ●● Blood lactate: Severe illness, inborn errors of metabo-
again, it is best to err lism (IEM).
IP on the side of treatment than to
: 196.52.84.10
await for the whole picture to unfold. ●● Call for metabolic specialist, if metabolic profile is ab-
normal.
First Tier Treatment of ●● Ketoacids: If finger stick glucose is high.
●● Serum sodium, calcium, magnesium (Table 20.3).
Intracranial Pressure ●● Blood urea, creatinine.
●● Nurse the child in the 30° head up position. ●● Peripheral smear: Malaria, hemolytic-uremic syndrome.
●● Keep head in neutral position to avoid kinking of the ●● Erythrocyte sedimentation rate (ESR), complete blood
neck. count (CBC).
●● Avoid noxious stimuli. Take efforts to provide pain re- ●● Coagulation profile: If platelets are low or bleeding occurs.
lief and sedation during painful procedures, since these
maneuvers could increase ICP. Blood Culture
●● Maintain euglycemia.
●● Control fever aggressively. ●● Stool culture: Shigella, Enteroviruses.
●● Treat seizures. ●● Mycoplasma IgG, IgM (unless cause known).
●● Severe sepsis with or without pyogenic meningitis may ●● Viral titers of blood and cerebrospinal fluid (CSF)
also present with varying degrees of coma. Administer (stored samples useful).
an antibiotic (Ceftriaxone) empirically, while awaiting – Elisa for Rickettsia, human immunodeficiency vi-
investigation. rus (HIV).
●● Hyperosmolar therapy: Infuse hypertonic saline (5 mL/ ●● Mantoux.
Kg) followed by continuous infusion between 0.1 and ●● Resting gastric juice for acid-fast bacilli.
1.0 mL/kg/h.
●● 3% NS has anti-inflammatory effects, increases intra- Lumbar Puncture
vascular volume and can be used in hypotensive pa- LP may be performed when the child becomes hemody-
tients who have elevated ICP. A safe intervention, few namically stable with no clinical or radiological evidence
adverse effects have been noted with sodium levels as of raised ICP.
high as 160 mmol/L.
●● Ventilate to maintain eucapnia (PaCO2: 35–40 mm CSF may be sent for polymerase chain reaction (PCR)
Hg). for viruses, tuberculosis (TB) antibodies, e.g. herpes sim-
●● Mannitol role has become limited. Since most children plex.
presenting with ICP also have shock or a propensity
to develop dehydration in the initial hours of manage-
Ù
Avoid LP if abnormal breathing patterns, shock,
ment, it is less often used in the ED setting. bradycardia, hypertension, GCS < 8, convulsive or
non-convulsive status epilepticus, abnormal dolls eye
Evaluate for Cause of Coma movement, dilated pupils, abnormal posture and ICP
After the ABCs are stabilized and ICP issues have been are noted.
addressed to prevent herniation, the patient may be trans- Delay LP and treat empirically when in doubt.
ported for imaging.
Ù Electroencephalography
Do not postpone stabilization while waiting for etiology EEG helps to confirm the diagnosis of seizure activity,5
to be identified. even if no clinical seizures (NCSE).
While the list appears long, a protocol driven approach ness and neurological handicap. Although this data is
may help prevent repeated blood collections. It is good relevant for Haemophilus influenzae meningitis, the
practice to draw extra blood and store for future investiga-
IP : 196.52.84.10 benefit appear less certain for meningitis due to pneu-
tions. Investigations are requested in a stepwise manner, mococcus and other organisms.
especially if the etiology remains unclear. ●● If there is any suspicion of tuberculous meningitis or
if hydrocephalus is identified by CT scan, ATT should
Imaging be considered.
●● Empiric antimalarial treatment is also initiated.
If the child is deeply unconscious, afebrile or has focal ●● Empirical treatment of rickettsia may be wise in epi-
signs, CT/MRI scan is the initial investigation of choice demic situations. It is best to treat with erythromycin
(even in infants with an open fontanelle). and doxycycline than to wait.
It helps to rule out intracerebral hemorrhage, ischemic When confronted with a child at high-risk of death or
stroke, hydrocephalus and space occupying lesion (SOL). disability, it would not be inappropriate to administer sev-
However, a normal CT does not rule out the diagnosis of raised eral therapies on arrival. As the etiology of coma is con-
ICP. Thus, clinical signs of raised ICT are more important firmed, therapy is withdrawn, e.g. acyclovir acts best when
than a normal CT scan. During transfer for investigations,
started early. However, if the results of the MRI, EEG and
ventilation, sedation and osmotic therapy must be continued.
PCR are all negative, therapy may be withdrawn.
If a surgically correctable cause is identified, call for
After the initial period of stabilization, the child must
neurosurgical consultation.
be transported to the PICU. Ideally an afebrile comatose
child should be transferred to a pediatric neurosurgical
Toxin Screen
unit. This should be done in the same manner as for im-
If etiology of coma has not been identified, consider the aging. Full sedation, controlled ventilation and minimal
possibility of toxins or drugs ingestions. handling with the bed/stretcher at a 30° head up angle
Ideally urine and blood should be collected and stored throughout transport is advised. The prognosis depends on
for evaluation of toxins/drugs early in the management of the etiology. Refer Protocol 20.1.
these children. Often, lack of laboratory support to establish diagnosis
of viral and metabolic disorders results in empirical treat-
Immediate Antimicrobial Coverage ment. However, effective supportive management of the
●● A third generation cephalosporin and Acyclovir is ABCs, maintenance of cerebral perfusion pressure and
empirically administered to cover the possibility of prevention of further damage often keeps the patient alive
infection. Acyclovir is therapeutic for herpes simplex till the primary problem resolves.
encephalitis. A positive MRI scan and electroencepha-
lography (EEG) have 95% sensitivity in the diagnosis
Key Points
ü
of herpes encephalitis. If the diagnosis is confirmed, the 1. Recognize potential risk of raised ICP and take im-
drug should be continued at a high dose for 2 weeks. mediate action to stabilize ABC.
●● Dexamethasone is given prior to the antibiotic, since 2. Secure airway using ICP precautions.
evidence suggests that it reduces the incidence of deaf- 3. Assess possibility of raised ICP.
4.
5.
Check blood sugar.
Check for NCSE and treat.
common errors
û
1. Administration of Mannitol without ruling out shock
6. Lower temperature, IPif: more
196.52.84.10
than 38°C.
or monitoring hydration status.
7. Nurse in 30° head up positions. 2. Dextrose infusions in the absence of hypoglycemia.
8. Insert lines, urinary catheters, etc. under analgesia. 3. Failing to recognize non-convulsive status epilepticus.
9. Place on continuous monitoring. 4. Shifting for imaging without stabilization.
10. Administer broad spectrum antibiotic, antimalarial, 5. Administration of Diazepam for posturing move-
antiviral, erythrocin and doxycyclin for rickettsial ments in a comatose child.
infections and ATT for febrile children with coma. 6. Failure to ensure euglycemia and correct dyselectro-
11. If papilledema is identified in association with hy- lytemia.
pertension (systolic BP greater than 2 SD), call for 7. Failure to protect airway and ventilate the comatose
nephrology consultation. child.
Protocol 20.1: PEMC approach: Altered mental status and abnormal movements in a critically ill child
196
Section VI n Disability
IP : 196.52.84.10
Chapter 20 n Approach to Decreased Level of Consciousness 197
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.
Box 21.1: Medical complications of status epilepticus result in decreased inhibitory control and increased ex
Cerebral citation leading to continuation of status epilepticus.
– Interictal coma IP : 196.52.84.10 ●● Benzodiazepines bind to GABA-A5 receptors and pro
– Cumulative anoxia mote neuronal inhibition.
– Altered autoregulation ●● Since the number of active GABA-A receptors de
– Increased cerebral blood flow creases as an episode of SE progresses,6 the first dose
– Cardiac arrest
of benzodiazepines should be given as early as possible
– Hypertension
– Cardiac failure, hypotension for seizure termination.
– Cardiogenic shock
●● Respiratory system failure CASE SCENARIO 1
– Apnea
– Cheyne-Stokes breathing An 8-month-old girl is brought with history of seizures
– Tachypnea lasting for 20 minutes. She had been having fever for 1
– Neurogenic pulmonary edema day (Figures 21.2 and 21.3).
– Aspiration, pneumonia
– Respiratory acidosis
– Cyanosis
●● Renal failure
– Oliguria, uremia
– Acute tubular necrosis
– Rhabdomyolysis
– Lower nephron necrosis
●● Autonomic system disturbance
– Hyperpyrexia
– Excessive sweating, vomiting
– Hypersecretion (salivary, tracheobronchial)
– Airway obstruction
●● Metabolic and biochemical abnormalities
– Acidosis (metabolic acidosis)
Figure 21.2: Active convulsions can make effective bag-valve-
– Anoxemia
mask ventilation a challenge. Hence double EC-clamp technique
– Hypernatremia, hyponatremia
of BVM ventilation is employed.
– Hypoglycemia
– Hepatic failure
– Dehydration
●● Infection
– Pulmonary
– Bladder
– Skin
●● Others
– Altered autoregulation
– Cerebral metabolic rate for oxygen (CMRO2)
– Disseminated intravascular coagulation
– Multiple organ dysfunction
– Fractures, thrombophlebitis
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
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Increased Decreased Hypotension
Arterial oxygen Decreased Decreased Decreased
Arterial carbon dioxide Increased Variable Hypercapnia
Lung fluid Increased Increased Pulmonary edema
Autonomic activity Increased Increased Arrhythmias
Temperature Increased 1ºC Increased 2ºC Fever—hyperpyrexia
Serum pH Decreased Variable Acidosis
Lactate Increased Increased Lactic acidosis
Glucose Increased Normal or raised Hypoglycemia
Serum potassium Increased or normal Increased Hyperkalemia
Cerebral blood flow Increased 900% Increased 200% Cerebral edema
Cerebral oxygen Compensated Failed Deficit—ischemia
consumption
●● Open airway using the head-tilt chin-lift maneuver 3. Use a large bore rigid suction catheter to suction
(while maintaining the recovery position). oropharyngeal secretions.
●● Suction oropharyngeal secretions without stimulating 4. Rapidly decompress stomach with a nasogastric tube
the posterior pharyngeal wall. to prevent vomiting and pulmonary aspiration.
●● Provide oxygen using a non-rebreathing mask. 5. Introduce an appropriate sized oropharyngeal airway,
●● Administer midazolam (0.2 mg/kg) via the intra- if feasible.
muscular or intrabuccal or intranasal route.7
●● Fever a common cause of seizures in children should
Ù
Avoid forcible opening of clenched jaws during a
be controlled rapidly by tepid sponging and placing a convulsive episode.
rectal suppository of paracetamol.
●● Unresponsiveness due to seizure activity results in the
Management of SE in the ED (Protocol 21.1) falling back of tongue.
The median duration of convulsions prior to reaching the ●● Loss of airway protective reflexes leads to failure in
PED of an academic children’s hospital in Southern India, handling the tracheobronchial secretions.
was 1 hour.8 ●● Glottic spasm also contributes to airway obstruction
during seizure activity.
Most presented with features of pulmonary edema with or
without cardiac dysfunction. The modified SE protocol de Breathing
scribed in this manual is based on this experience.
Ineffective respiration is almost always noted during con
vulsive status epilepticus.
Airway
Tonic-clonic activity of the intercostal muscles inhibit
At least two members (one doctor and one nurse) must be the normal inspiratory/expiratory movements of respira
dedicated for airway management. The maneuvers men tion.
tioned below should be implemented simultaneously.
●● Jerky respirations are probably due to contraction of
1. Open the airway using the head-tilt and chin-lift ma involuntary muscles of diaphragm.
neuver. ●● Drugs used in the management of status epilepticus can
2. C-spine precautions are taken if trauma is suspected. also lead to respiratory failure.
Chapter 21 n Status Epilepticus 201
Ù
An unstable and obstructed airway in combination with
Ù
Opening the airway and provision of oxygen without
ineffective ventilationIPfor: 196.52.84.10
greater than 5 minutes can initiating bag-valve-mask ventilation is not enough to
cause: correct hypoxia in actively convulsing children in the
• Severe hypoxia. emergency setting.
• Shock.
• Myocardial dysfunction. ●● Whilst, the airway is being cleared by the airway nurse,
• Increased risk of prolonged seizure activity. initiate bag-valve-mask ventilation using the largest
sized bag.
Emergency medical response systems reach a convuls Almost 50% of children presenting with convulsive SE
ing child within 5 minutes after activating the EMS. Pre can be mask ventilated without being intubated.8
hospital protocol-based management is rapidly initiated
in western countries. Decision to intubate is taken within ●● If spontaneously breathing, provide O2 using the flow-
20–30 minutes after onset of convulsions9 in the prehospi inflating ventilation device.
tal setting. ●● Oxygen saturations are monitored using pulse oximeter.
Ù
Since early and structured prehospital care by EMS
Note: Antiseizure drugs inherently depress respiration and
may aggravate the underlying hypoxia in SE. Adminis
is unavailable in many parts of our country, it is tration of anticonvulsant without addressing the ABCs (a
recommended that primary care physicians to whom the common error) could result in lethal complications.
child is brought, administer early and aggressive airway
management to avoid the deleterious effects of hypoxia
in convulsing children.
IP : 196.52.84.10
Figure 21.6: This picture shows capillary blood glucose being Figure 21.7: This picture shows a convulsing child being mask
evaluated during resuscitation ventilated on arrival using the two person technique. Bag-valve-
mask ventilation of the older child is not easy. The respiratory
arrest secondary to involvement of the intercostal muscles during
Glucose active convulsions can make effective bagging very difficult. The
Hypoglycemia can severely disrupt cerebral blood flow airway nurse is suctioning. Two nurses are assigned to secure
autoregulation leading, to adverse neurological outcomes. intravascular access. One more member of the emergency team
Refer Figure 21.6. formulates the initial dose of lorazepam and administers it over
1–2 minutes.
●● Dextrostix should be used to measure sugar levels early
in the management of SE. Circulation
●● Documented hypoglycemia is corrected with an intra
venous bolus of 2 mL/kg of 25% dextrose solution. Shock could occur due to a wide variety of causes in con
●● If dextrostix is not immediately available, to avoid the vulsing children.
dangerous effects of unrecognized hypoglycemia, 25% ●● Neurogenic: Distributive shock.
dextrose may be administered emperically. ●● Hypoxia: Distributive shock with or without myocar
●● Prolonged status epilepticus can cause hypoglycemia. dial dysfunction.
Hypoglycemia can precipitate status epilepticus. Of
●● Coexisting sepsis.
ten, hypoglycemia can recur after correction. Hence,
●● Coexisting hypovolemia.
throughout resuscitation, a maintenance fluid should be
infused as per the Holliday-Segar formula. During SE, cerebrovascular resistance falls due to
●● Infuse GNS to which KCl and calcium have been hypoxia, resulting in severe derangement of cerebral auto-
added. regulation.
Ù
Glucagon is indicated for treating hypoglycemia and
Cerebral perfusion becomes directly dependent on sys
temic blood pressure. Within the first ½ hour of SE, blood
seizure in insulin-dependent diabetes mellitus. pressure rises. Later blood pressure either becomes normal
or hypotensive.
Dose: 1–2 years: 500 µg stat
●● Secure intravenous access on arrival and provide non-glu
2–18 years: < 25 kg: 500 µg cose containing isotonic fluids. At least two nurses may
> 25 kg: 1 mg be needed to secure intravenous access (Figure 21.7).
Route of administration in IDDM: Subcutaneous, ●● If IV access is unavailable, intraosseous access must be
intramuscular or intravenous. secured. If shock is identified the first bolus of 20 mL/
kg is administered.
●● Monitor serum sodium, calcium and magnesium. ●● If euvolemic restrict fluids to 2–3 mL/kg/h.
●● Refractory status epilepticus can often be corrected by ●● Shock secondary to idiopathic SE will resolve follow
resolving metabolic abnormalities. ing administration of 20–30 mL/kg of fluids.
Chapter 21 n Status Epilepticus 203
●● Shock complicated by diarrhea or sepsis will require Metabolic disorders were reported in an average of 6%
large volumes to attain therapeutic goals. (range 1%–16%) of children with SE9.
●● Caution: Fluid therapy
IP :or196.52.84.10
phenytoin administration can
unmask underlying myocardial dysfunction.
Pyridoxine
When seizures are not responsive to phenytoin, pyridox
IP : 196.52.84.10 ine (50–100 mg) and the convulsing infant is less than 18
months, pyridoxine should be administered. Watch out for
apnea.
Valproic Acid
Valproic acid19–23 a broad-spectrum anticonvulsant acts by
modulating sodium and calcium channels and inhibiting
aminobutyric acid transmission.
●● Sodium valproate is given as initially as a bolus: 25
Figure 21.10: History that rules out of pulmonary edema and mg/kg bolus (max 40 mg/kg), followed by an infusion
hence phenytoin is safe of 5 mg/kg/hour.
●● Sodium valproate has less sedation, good cardio
3. During phenytoin infusion, if the following signs of vascular profile and lower risk of respiratory failure
cardiac dysfunction or pulmonary edema are noted, compared to other anticonvulsants.
stop phenytoin infusion. ●● Sodium valproate should be avoided, if child has evi
dence of liver disease or metabolic disease or hemo
a. Pink froth. static abnormalities.
●● It may be difficult to differentiate froth from
oropharyngeal secretions due to GTCs. Onset of Levetiracetam24-28
froth in a child whose airway was initially clear,
may be the first clue that PE is developing in a Levetiracetam acts through calcium channels, glutamate
fitting child. Refer Figure 21.10. receptors and g-aminobutyric acid modulation (synap
tic vesicle 2A ligand). Intravenous Levetiracetam is not
b. Retractions, grunting.
metabolized by the liver, has little affinity to protein, is
c. Gallop, muffling of heart sounds, bradycardia, hy
excreted via renal pathway and has minimal drug-drug in
potension, widening of pulse pressure with low teractions.
mean arterial pressures, increasing liver span or
drop in oxygen saturations. ●● It is administered as a bolus of 20–30 mg/kg IV at 5
mg/kg/min (max 3 g).
Ù ●● When SE is complicated by pulmonary edema, myo
If pulmonary edema or myocardial dysfunction is cardial dysfunction coagulopathy, liver failure or hy
anticipated or occurs during phenytoin infusion, consider potension, Levetiracetam is an excellent alternative
initiating levetiracetam or/and sodium valproate after antiseizure agent.
the initial doses of benzodiazepines. ●● In some children it may cause reversible behavioral
changes.
Fosphenytoin, a water-soluble phosphoester of pheny
toin has been considered less cardiotoxic effects than phe Alternative Routes of Drug Administration
nytoin and may be safer. However, cardiac dysrrythmias
When intravenous access is not available, midazolam (0.2
have been reported even with the use of fosphenytoin.18 mg/kg) can be given intramuscularly, rectally or into the
This drug can be given/administered through the intramus buccal space.
cular route if intravenous (IV) access is not available.
●● All anticonvulsant drugs except phenytoin have
The APLS recommends that, the loading dose of phe achieved therapeutic levels in the blood when ad
nytoin should be avoided for children taking chronic phe ministered via the intraosseous route. The doses of
nytoin therapy. these drugs are the same as for the IV route.
206 Section VI n Disability
Ù
A good indicator of seizure control is return of baseline
sensorium.
Table 21.2: Drugs used in emergency room for management of status epilepticus
Contd...
Protocol 21.1: PEMC approach: Recognition and management of convulsive and non-convulsive
status epilepticus in ED
IP : 196.52.84.10
212 Section VI n Disability
33. Morrison G, Gibbons E, Whitehouse WP. High-dose mida 36. Lee WK, Liu KT, Young BW. Very-high-dose phenobarbi
zolam therapy for refractory status epilepticus in children. tal for childhood refractory status epilepticus. Pediatr Neu
Intensive Care Med. 2006;32:2070-076. rol. 2006;34:63-65.
IP : 196.52.84.10
34. Koul R, Chacko A, Javed H, et al. Eight-year study of 37. Andrea O Rossetti. Which anesthetic should be used in
childhood status epilepticus: Midazolam infusion in man the treatment of refractory status epilepticus? Epilepsia.
agement and outcome. J Child Neurol. 2002;17:908-10. 2007;48(Suppl. 8):52-55.
35. Hayashi K, Osawa M, Aihara M, et al. Efficacy of intrave 38. Riviello JJ, Ashwal S, Hirtz D, et al. Practice parameter: Di
nous midazolam for status epilepticus in childhood. Pediatr agnostic assessment of the child with status epilepticus (an
Neurol 2007;36:366-72. evidence based review). Neurology. 2006;67:1542-550.
Section VII
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Envenomation
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22
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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.
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).
CASE SCENARIO 2
Figure 22.2: Sweating and salivation may persist for 6–13
hours (Courtesy: Dr Bawaskar HS). A 3-year-old girl had been rushed to the ED as soon as
she was bitten by a scorpion an hour ago at her home.
Chapter 22 n Scorpion Sting 219
She was crying due to severe pain over right foot. She Prazosin is available as 1 mg (scored) tablet. Sustained
was also having increased salivation and was profusely release tablets are not advised in this condition. The rec-
sweating (Figure 22.5). ommended dose is 30 µg/ kg/dose.
IP : 196.52.84.10
Administration of Prazosin in the prehospital setting
is one of the most useful strategies to reduce mortality in
scorpion envenomation.
Ù
Indeed, Prazosin must be stocked in every primary
health center and administered when signs of ‘autonom-
ic storm’ are identified.
Mechanism of action
Prazosin suppresses the sympathetic outflow and acti-
vates venom inhibited potassium channels. It blocks the
postsynaptic α-1 receptors and also prevents prostaglan-
din production. It reduces cardiac preload, afterload, BP
and CNS sympathetic stimulation without increasing the
heart rate or cardiac output (cardioprotective effect). Thus,
it prevents the hypertensive stress on the myocardium. Its
mechanism of action seems to counter the activity of the
scorpion venom. Oral Prazosin is fast acting, easily avail- Figure 22.6: Priapism, a poor prognostic sign seems to
able, relatively cheap, free from any anaphylaxis and high- be associated with myocardial dysfunction (Courtesy: Dr
ly effective. Thangavelu S).
220 Section VII n Envenomation
IP : 196.52.84.10
Figure 22.7 Physiological status: Respiratory distress Figure 22.8: This picture shows pink froth which should be
probably due to cardiogenic or non-cardiogenic pulmonary differentiated from salivation (Courtesy: Dr Thangavelu S).
edema with normotensive shock.
Ù
Autonomic storm or pulmonary edema or priapism con-
firm the diagnosis of scorpion sting.
Investigations
●● Monitor sugar, urea, creatinine and liver enzymes.
●● ECG is useful in identifying ST depression, inverted T
waves, deep Q-waves in lead I and AVL, various de-
grees of heart block and arrhythmias. Figure 22.10 Physiological status: Alertness, normalization of
●● Echocardiogram may reveal systolic LV dysfunction. respiratory rates, work of breathing, heart rates with warm dry
normal peripheries, normal BP and liver span are suggestive
of recovery.
Scorpion Antivenom
Though considered as the specific treatment for scorpion
Prognosis
envenomation, it must be administered within 30 minutes
of sting.18 Scorpion antivenom has not been found to be
more effective in reversing the cardiovascular toxic effects
Ù
Pain and age greater than 6 years are good prognostic
of the venom. Indeed, Prazosin has been found to prevent signs.
and relieve the cardiovascular manifestations in severe Delay in initiation of Prazosin therapy, pulmonary ede-
scorpion envenomation. ma, arrhythmias, encephalopathy and age less than 6
Avoid following drugs in the emergency management years, indicate a poor prognosis.
of cardiogenic shock due to scorpion sting.
Children presenting with scorpion sting envenomation
●● Lytic cocktail. should be observed for at least 24 hours even if asymp-
●● Morphine. tomatic. Outcomes have improved with early identification
●● Steroids. and management of pulmonary edema and shock in the
●● Antihistamines ED. The early use of Prazosin also seems to have improved
●● Digoxin. the speed of recovery.
●● Diuretics.
222 Section VII n Envenomation
Key Points
1. Prehospital Prazosin
ü common errors
û
IP therapy improves outcome and
: 196.52.84.10 1. Restriction of fluid due to fear of pulmonary
prevents complications. edema.
2. Keep the patient in lying posture for about 3 hours 2. Failure to administer Prazosin to a stable child with
(even while examining the case) in order to prevent features of autonomic storm.
‘first dose phenomenon’ (hypotension). 3. Administration of Prazosin in a shocked child
3. Recognize pulmonary edema and shock since without attempting to resolve shock.
cardiac manifestations are common in Indian red 4. Administration of large volume of fluids (40–60
scorpion envenomation. mL/kg) in the absence of history suggestive of
4. Use JR circuit to provide oxygen if child has hypovolemia.
respiratory distress. 5. Failure to recognize development of pulmonary
5. Administer small aliquots of fluids to resolve edema during fluid therapy.
shock. 6. Failure to use JR circuit to provide oxygen in
6. Initiate inotrope and perform early intubation if respiratory distress.
signs of pulmonary edema are noted during shock 7. Use of morphine, digoxin, atropine, antihistamine
management. or furosemide for pulmonary edema.
Protocol 22.1: PEMC approach: Management of scorpion sting in the ED
IP : 196.52.84.10
Caution:
●● Risk of cardiogenic or non-cardiogenic pulmonary edema complicates shock management due to scorpion envenomation.
Chapter 22 n Scorpion Sting
●● During fluid therapy, monitor for airway instability, pink froth, increase or decrease in respiratory rates, grunt, retractions, abdominal respiration, fresh rales,
gallop, increasing liver span, agitation, fighting the mask and drop in oxygen saturations (i.e. signs of pulmonary edema). If any one or a cluster of signs
develop, stop further fluid, initiate inotropes and prepare to intubate.
223
224 Section VII n Envenomation
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-
Snake Type of venom General site of action Type of venom component Clinical effects
IP :action
196.52.84.10
Viper, cobra Local toxins Bite site and bitten Neurotoxins, cytotoxin Local—pain, swelling,
limb blistering, bruising, necrosis
Cobra, krait, coral Neurotoxins Neuromuscular Neurotoxins (presynaptic, Progressive flaccid paralysis of
snake junction postsynaptic), dendrotoxins, skeletal muscle and diaphragm
fasciculins
Sea snakes Myolytic toxins Skeletal muscle Myotoxins Destruction of skeletal muscle
Viper Hematologic toxins Effect hemostasis— Procoagulants, fibrinolytics, Consumptive coagulopathy,
damage vessel walls, anticoagulants, hemorrhagin complete defibrination,
promote bleeding hemorrhage, thrombosis,
infarction, embolism
Viper Nephrotoxic toxins Kidneys Nephrotoxins Renal damage, failure, necrosis
Viper Cardiotoxic toxins Heart Cardiotoxins Cardiac arrhythmias, failure,
arrest
Ù
Tourniquet made of rope, string, belt and cloth increase Approach to an Individual
the risk of ischemia, necrosis and limb loss. When tour- Allegedly Bitten by a Snake
niquet is removed, there is risk of massive neurotoxin
●● Determine whether the patient has been bitten by a poi
release or occurrence of embolism.
sonous snake.
●● Do not incise the wound.
Look for Fang Marks
Ù ●● The depth of the bite varies anywhere from 1 to 8 mm.
Incision of the wound due to hemotoxic bite increases
the risk of severe bleeding. ●● In some cases, there may be no external evidence of
snake bite.
●● Do not apply suction to the wound.12,13 ●● Absence of fang marks do not rule out snake bite in
agricultural areas.
Chapter 23 n Snake Bite Envenomation 227
CASE SCENARIO 1
A 10-year-old boy was brought to the ED with history of
IPthumb.
snake bite over the right : 196.52.84.10
He had severe pain over
bite site with progressive swelling (Figures 23.2 and 23.3).
Figure 23.2: This child was rushed within an hour after snake
bite. His mother had immediately tied a tight tourniquet above
the forearm. On arrival he received 8 vials of ASV. Subsequently,
he received up to 30 vials based on rapidly progressing
cellulitis. This picture showing fang marks with bleb was taken
19 hours after the bite.
●● Take a 1–2 mL of fresh venous blood in a new, clean, ●● Urine analysis: Hematuria, proteinuria, hemoglobinu-
dry test tube and leave it undisturbed for 20 minutes. ria or myoglobinuria.
●● Gently tilt the tube without shaking. If the blood is still
IP : 196.52.84.10 ●● Blood group type and crossmatch.
liquid, then the patient has incoagulable blood. ●● ECG: Changes are usually non-specific and include
bradycardia, AV block with ST segment elevation or
depression. The ECG may also show features of hyper-
kalemia with peaked T waves.
CASE SCENARIO 2
A 10-year-old girl was rushed into the ED following
snake bite over her right foot during the night, while
she was sleeping in the open field.
She was lethargic and breathless with swelling of the
right foot. Bleeding was noted from the bite site. She was
also passing red colored urine. Refer Figure 23.7.
She did not have ptosis, but had conjugate gaze to the
right. Whole blood clotting time prior to transfer to the Figure 23.8: Hemodynamically stable child with snake bite.
hospital was more than 20 minutes.
Chapter 23 n Snake Bite Envenomation 231
3. Swelling extending:
a. 15 cm or more within 1 hour.
b. Swelling reaching the knee or elbow < 4 hours after
IP : 196.52.84.10
bite involving the limbs.
c. Swelling involving the whole limb within 8 hours.
d. Extension to the trunk.
e. Swelling causing airway compromise or shortness
of breath.
f. Compartment syndrome or major vessel entrap-
ment.
Ù
Painful swelling that is both progressive and severe is a
definitive indication for ASV.
Figure 23.9 Physiological status: Cardiopulmonary cerebral
assessment normal 4. Cardiovascular abnormalities: hypotension, shock,
cardiac arrhythmias, abnormal ECG patterns.
Ù 5. Persistent and severe vomiting or abdominal pain.6
Swelling confined to the site of bite or fang mark from
an apparently venomous snake are not grounds for ad ASV Dose
ministration of ASV. Refer Figure 23.9. ●● 8–10 vials of ASV should be administered over 1 hour
(Figures 23.10A and B).
Specific Therapy: AntiSnake Venom It is given to neutralize the venom. There is no ben-
efit in administering it over longer periods and prolonging
Antisnake venom (ASV) a polyvalent venom, is effective
the time to neutralize. Snakes inject the same amount of
against all four common species such as Russell’s viper,
venom into adults as in children. Hence it is intuitive that
common cobra, common krait and saw-scaled viper. It is children receive the same ASV dosage as adults. The rec-
available in both liquid and lyophilized forms. Liquid ASV ommended dosage level has been based on published re-
has a 2-year shelf life, requires refrigeration and a reliable search that Russell’s viper injects around 63 mg of venom
cold chain during transportation. Lyophilized ASV in pow- (range 5–147 mg).17 One vial of ASV neutralises 6 mg of
der form does not need refrigeration for storage. This is Russell’s viper venom. Hence the requirement ranges from
particularly useful in remote areas where power supply is 8–25 vials. The approximate requirement ranges from
inconsistent.6,7 8–25 vials.
ASV is a scarce and costly commodity. Every snake The dose of antisnake venom is determined by the
bite, even if poisonous, does not warrant snake antivenom. amount of venom that is injected.
The prophylactic use of antivenom should be avoided due
In fact, the amount of venom per square body surface
to the inherent risk of hypersensitivity reactions. Antiven-
may be more for children and young infants than adults.
om is indicated only if there are signs of systemic enveno-
mation or severe local swelling. Ù
Avoid using smaller doses for young infants and chil-
Refer Protocol 23.1. dren.
Administer 8–25 vials for all ages if signs of envenvo-
Indications for Administration of ASV mation are noted.
1. Evidence of coagulopathy: Whole blood clotting time The patient must be closely monitored for reactions to
exceeds 20 minutes or signs of spontaneous bleeding ASV for a minimum of 2 hours.
are noted.
2. Evidence of neurotoxicity: Ptosis, inability to lift the The lyophilized form is diluted in 10 mL of water and
head, diplopia, stridor, respiratory distress, neuropa- rolled between the palms. Shaking is not advisable since,
ralysis or coma. it could cause denaturation of the protein.
232 Section VII n Envenomation
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●● Administer the second dose of 10 vials over 1 hour. stabilize airway breathing and circulatory problems and
Maximum dose of ASV is 20 vials.6 consider early antivenom administration.
IP : 196.52.84.10
Recovery Phase Key Points
ü
If an adequate dose of appropriate antivenom has been ad- 1. Relieve anxiety and reassure victims that fatality is
ministered, the following responses may be seen: minimal. Most will recover.
2. Cellulitis and hemostatic abnormalities are the hall
●● Spontaneous systemic bleeding such as gum bleeding
mark of Viperine envenomation.
usually stops within 15–30 minutes.
3. Ptosis is an early sign of krait and cobra (elapid
●● Blood coagulability is usually restored in 6 hours.
●● Postsynaptic neurotoxic envenoming (Cobra) may be- envenomation).
gin to improve as early as 30 minutes after antivenom, 4. 20 minutes WBCT test is the most useful bedside
but can take several hours. test to detect hemostatic abnormalities.
●● Presynaptic neurotoxic envenoming (Krait), usually 5. Children should receive the same ASV dosage
takes a considerable time to improve reflecting the need as adults, since snakes inject the same amount of
for the body to generate new acetylcholine emitters. venom into adults and children.
●● Active hemolysis and rhabdomyolysis may cease with- 6. ASV neutralizes the unbound venom and must be
in a few hours and the urine returns to its normal color. given as early as possible.
●● In hypotensive patients, blood pressure may increase 7. ASV is required only to those who show definite
after 30 minutes. signs and symptoms of envenomation.
What ASV cannot do? 8. Anaphylaxis or late serum sickness cannot be
determined or prevented by test dose.
1. Prevent or reverse necrotic action of the venom on tis- 9. Even if the patient develops reaction(s), the total
sue.
dose required should be administered slowly after
2. Prevent or reverse local swelling.
the patient recovers from the reaction(s).
3. Reverse coagulopathy (Liver regenerates clotting fac-
tors).
4. Reverse presynaptic envenomation. Nerve damage is
structural and large quantities of ASV are ineffective.
common errors
û
1. Resorting to traditional treatment rather than rushing
Body must regenerate synaptic vesicles.
to the hospital immediately.
5. Reverse acute kidney injury.
2. Incision (cutting) of the site of bite and suctioning
the incoagulable blood.
Renal Failure
3. Applying tight tourniquets over the bite site.
Acute kidney injury (AKI) a potentially lethal complica- 4. Local administration of ASV is ineffective, painful
tion, can occur even if WBCT has normalized. Overt clini- and raises intracompartmental pressure.
cal features of AKI are seen 5–12 days after the bite. 5. Using wet (not properly dried) test tube for the 20
●● Recognize and refer for hemodialysis. minutes WBCT test.
6. Washing the test tube with detergent (inhibit the
conclusion contact element of the clotting mechanism).
7. Administration of ASV without adequate agents for
The ability to identify poisonous from non-poisonous managing anaphylaxis.
snakes may help mitigate fear, facilitate effective treat- 8. Administration of ASV as IV bolus or IM directly.
ment strategies and reduce mortality. Most snakebites are 9. Discontinuation of ASV after mild reactions.
due to non-venomous snakes. A large number of snake- 10. Failure to treat shock and failure to provide early
bites by poisonous snakes are also asymptomatic. Reas-
ventilatory support in neuropoisonous snakebite.
surance, allaying of anxiety, rapid shift to the hospital and
11. Proceed to surgical management before coagulation
hospitalization for 24–48 hours are all that is required for
resolves.
the majority of cases. If signs of envenomation develop,
Chapter 23 n Snake Bite Envenomation 235
Poisoning
IP : 196.52.84.10
24
IP : 196.52.84.10
Figure 24.1: Children with poisoning need to be managed appropriately as fast as possible
Learning Objectives
1. Principles of management specific for the poisoned 3. Evidence-based approach for prevention of absorp-
child. tion of toxins.
2. Toxidromes which help recognize seriously ill poi- 4. Methods available for enhancement of excretion.
soned children.
Ingestion of a harmful substance is among the most com- evidence such as an empty bottle, presence of tablets or
mon causes of injury to children less than 6 years of age. spillage of house hold chemicals near a child.
Fortunately, in most cases the ingested agent has minimal ●● Evaluate constituents of the ingested substance and
or no clinically important toxic effects. Rarely, the ingest- calculate its per kilogram body weight.
ed amount is life-threatening resulting in death. Some of
●● In young infants, presume that maximum amount has
the commonest toxin-induced injuries encountered in our
country are following ingestion of kerosene, herbal medi- been ingested by comparing the volume of liquid or
cines such as vasambu (Acorus calamus or commonly number of the tablets remaining in the container. Take
called Sweet Flag), camphor, neem oil, insecticides and spillage into account.1
corrosives. Commonest drugs ingested by children are
dapsone, iron preparations, oral hypoglycemics and anti- Management
hypertensives (Figure 24.1).
1. Cardiopulmonary cerebral assessment and resuscitation.
2. Prevention or reduction of absorption.
Identification of Poison 3. Enhancement of excretion.
A high index of suspicion is needed to recognize poisoning 4. Administration of antidotes.
if history is unavailable.
Ù
Early aggressive efforts to eliminate the toxin is the best
●● Suspect poisoning if an apparently normal child devel
ops symptoms of organ dysfunction with circumstantial guarantor for successful outcomes.
240 Section VIII n Poisoning
Ù Ù
Arrhythmias are usually rare, but if present, treatment of Gastric lavage, can be considered, when a potentially
IP : 196.52.84.10 life-threatening amount of a poison has been ingested.
hypoxia, hypercarbia, dyselectrolytemia and acid-base
abnormalities are usually sufficient to correct them.
Method
Syrup Ipecac3
Ipecac has no role in the routine management of acutely 1. Competence of the gag reflex should first be con
poisoned patients. firmed.
2. Once properly restrained, the child should be placed in
a left lateral decubitus (Trendelenburg position) in order
Gastric Lavage4,5,6 to limit the movement of the gastric contents into the
Ù
Gastric lavage should not be employed routinely, if ever,
duodenum and minimize the risk of aspiration.
3. A large bore, single lumen tube should be placed by an
in the management of poisoned patients. orogastric route.
4. The proper placement of the tube is confirmed by the
American Academy of Clinical Toxicology; European As- spontaneous or aspirated return of gastric contents or
sociation of Poisons Centers and Clinical Toxicologists by auscultation of insufflated air when a stethoscope is
recommend the following: placed over the stomach after placement of the tube.
242 Section VIII n Poisoning
5. NS in aliquots of 10–15 mL/kg of body weight are creased systemic absorption of the ingested toxins when
instilled through the tube and then aspirated. This pro- compared with standard activated charcoal.12,13 They are
cess is continued until
IP :the aspirated contents are clear.
196.52.84.10 also more palatable than standard charcoal products.
Volumes as large as several liters may be necessary to When administered within 1 hour after ingestion, acti-
produce a clear aspirate. vated charcoal can reduce the absorption of toxins by up to
When performed 1 hour after the ingestion of a toxic 75%. Optimal adsorption occurs when the ratio of charcoal
substance, lavage retrieves less than 30% of the toxin. to toxin is 10:1 or higher.14
Hence, its use beyond the 1st hour is questionable. If not
●● Recommended dose is 1 g/kg body weight.
properly performed, gastric lavage has the potential com
plication of propelling toxins into the duodenum, thereby
increasing the likelihood of absorption.8 Method of Administration
Ù Normal mental status:
The greatest risks associated with gastric lavage are: ●● Mix activated charcoal in fruit juice or bottled drinks as
• Inadvertent placement of the tube into the trachea a slurry for children.
or a main stem bronchus. ●● Additives, such as bottled drinks or fruit juices, make
• Esophageal injury. charcoal more palatable without reducing its effica-
• Hypothermia. cy.13
• Hyponatremia. ●● Young children will not voluntarily drink activated
• Water intoxication. charcoal quickly enough for it to work optimally.
Avoid gastric lavage if: ●● Introduce a nasogastric tube in young children to en-
• Mental status is depressed and airway protective sure prompt administration.
reflexes are lost.
• Kerosene ingestion (low-viscosity hydrocarbon). Depressed mental status or respiratory failure:
• Corrosive agent ingestion. ●● Intubate (for airway protection) and use nasogastric
tube for administration.
Nasogastric aspiration is performed by placing a naso-
gastric tube (smaller than a orogastric tube) and aspirating ●● Elevate head end by 45°.
gastric contents without instilling water.
Complications
Nasogastric aspiration may be effective in cases of liq-
uid poison ingestion,9 but it is not adequate for ingestion The main hazards associated with the administration of
of pills. activated charcoal are vomiting and aspiration.15,16,17,18 Al-
though activated charcoal is often described as inert, data
Activated Charcoal from experimental studies indicate that aspirated charcoal
can produce pulmonary parenchymal injury or bronchioli
Ù tis obliterans. The installation of charcoal into the lungs
Activated charcoal should be administered within 1 hour through the inadvertent placement of an orogastric or na
of ingestion of toxin.10 sogastric tube into the trachea has had disastrous results
including, death. Bowel sounds should be monitored, since
Activated charcoal ‘adsorbs’ poisons dissolved in the
constipation and rarely intestinal obstruction have been re-
intestine such that the poison remains in the gut rather than
ported.
being absorbed into circulation. It limits the systemic ab-
sorption of many drugs in a time-dependent manner and
may decrease the need for antidotal therapy for patients Indications for Activated Charcoal
who present within 2 hours of acetaminophen ingestion.11
Medications that are well bound by charcoal are drugs that
However, activated charcoal has not been shown to im- undergo enterohepatic or enteroenteric circulation such as:
prove the outcomes of non-selected poisoning patients.
●● Salicylates.
Currently superactivated charcoal products with in
●● Phenobarbital.
creased surface area are available. These products de
Chapter 24 n Poisoning: General Approach 243
●● Urine alkalinization and high urine flow (approxi removal of toxins than from advanced intensive care after
mately 600 mL/h) increases urine elimination of 2,4- entry of toxins into the human circulation.
dichlorophenoxyacetic
IP :acid and mecoprop poisoning.
Ù
196.52.84.10 Key Points
ü
Hypokalemia is the most common complication, but can 1. Energetic emergency care and elimination of toxin
be corrected by giving potassium supplements. Alkalotic is key to survival in the poisoned victim.
tetany occurs occasionally, but hypocalcemia is rare. 2. Emesis has been replaced by activated charcoal and
There is no evidence to suggest that relatively short-du- whole bowel irrigation.
ration alkalemia (more than a few hours) poses a risk to 3. Gastric lavage should not be performed routinely in
life in normal individuals. all children with toxin ingestion.
ogy; European Association of Poisons Centres and Clinical 17. Liisanantti J, Kaukoranta P, Martikainen M, et al. Aspira-
Toxicologists. J Toxicol Clin Toxicol. 1997;35:721-41. tion pneumonia following severe self-poisoning. Resusci-
11. Buckley NA, Whyte IM, O’Connell DL, et al. Activated tation. 2003;56:49-53.
IP : 196.52.84.10
charcoal reduces the need for N-acetylcysteine treatment 18. Pollack MM, Dunbar BS, Holbrook PR, et al. Aspiration of
after acetaminophen (Paracetamol) overdose. J Toxicol activated charcoal and gastric contents. Ann Emerg Med.
Clin Toxicol. 1999;37:753-57. 1981;10:528-29.
12. Roberts JR, Gracely EJ, Schoffstall JM. Advantage of high- 19. Barceloux D, McGuigan M, Hartigan-Go K. Position state-
surface-area charcoal for gastrointestinal decontamination ment: cathartics. American Academy of Clinical Toxicol-
in a human acetaminophen ingestion model. Acad Emerg
ogy; European Association of Poisons Centers and Clinical
Med. 1997;4:167-74.
Toxicologists. J Toxicol Clin Toxicol. 1997;35:743-52.
13. Krenzelok EP, Heller MB. Effectiveness of commercially
20. Anonymous. Position paper: whole bowel irrigation. J
available aqueous activated charcoal products. Ann Emerg
Toxicol Clin Toxicol. 2004;42:844-54.
Med. 1987;16:1340-43.
14. Osterhoudt, Kevin C, Alpern, et al. Activated Charcoal Ad- 21. Tenenbein M. Whole bowel irrigation as a gastrointestinal
ministration in a Pediatric Emergency. Department Pediat- decontamination procedure after acute poisoning. Med
ric Emergency Care; 2004(20)8. pp. 493-98. Toxicol. 1988;3:77-84.
15. Arnold TC, Willis BH, Xiao F, et al. Aspiration of activated 22. Buckley N, Dawson AH, Howarth D, et al. Slow-re-
charcoal elicits an increase in lung microvascular perme- lease verapimil poisoning. Use of polyethylene glycol
ability. J Toxicol Clin Toxicol. 1999;37:9-16. whole-bowel lavage and high-dose calcium. Med J Aust.
16. Moll J, Kerns W II, Tomaszewski C, et al. Incidence of 1993;158:202-04.
aspiration pneumonia in intubated patients receiving acti- 23. Proudfoot AT, Krenzelok EP, Vale JA, et al. Position Paper
vated charcoal. J Emerg Med. 1999;17:279-83. on Urine Alkalinization. 2004;(42):1-26.
25
IP : 196.52.84.10
Specific Poisons
Figure 25.1: Common household products that carry potential risk of poisoning in young children
Learning Objectives
1. Approach to management of poisoning in 2. Management of organophosphorus poisoning
children using the rapid cardiopulmonary cerebral based on the Cochrane 2012 guidelines.
assessment and the pediatric assessment triangle. 3. Approach to kerosene, opioids, barbiturates, iron,
paracetamol and button battery ingestion.
IP : 196.52.84.10
Clinical Picture
Ù Table 25.1: Clinical manifestations of organophosphates
Muscarinic effects of acetylcholine is represented by the
poisoning (OPP)
two mnemonics: (seen more commonly in adults)
SLUDGE—Salivation, Lacrimation, Urination, RS Rhinorrhea, bronchorrhea, bronchoconstriction,
Defecation, Gastrointestinal cramping and Emesis. wheezing, dyspnea, pulmonary edema, respiratory
DUMBBELS—Diarrhea, Urinary incontinence, Miosis, arrest within 72 hours
Muscle fasciculation, Bronchorrhea, Bronchospasm, CVS Bradycardia, heart block, cardiac arrest
Bradycardia, Emesis, Lacrimation, Salivation. CNS ÙHeadache,
common)
giddiness, coma, convulsions (most
●● Nicotinic effect initially results in stimulation followed GIT Nausea, vomiting, diarrhea, abdominal cramps
by paralysis of the preganglionic and somatic nerve fi Eye Miosis, blurred vision, lacrimation (red tears due
bers leading to twitching of eyelids, tongue and facial to porphyrin accumulation in lacrimal glands),
muscles. This is followed by neuromuscular blockade papilledema
and paralysis. Skin Sweating, dermatitis
●● Preganglionic sympathetic stimulation may lead to tach Others Fasciculation, flaccidity, salivation, delirium, psychosis
yarrhythmias, hypertension and cardiorespiratory arrest. likely to produce tachycardia.
●● Acetylcholine also causes initial stimulation followed
by depression of the CNS. The clinical manifestations appear within 30 minutes
●● One of the commonest effects of OPP is respiratory to 1 hour and reach the peak in 2–8 hours.
failure (Table 25.1). The latter is aggravated by secre
tions that flood the airway and the lungs.
Ù
Secretions, altered mental status and miosis are the
●● The usual cause of death is respiratory failure. commonest presentations in children.2,3
Chapter 25 n Specific Poisons 249
●● Oropharyngeal suctioning.
●● Provide oxygen using a JR circuit..
Figure 25.3 Physiological status: Airway is obstructed with ●● Intubate using the pharmacologically assisted intuba
secretions, respiratory distress, bradycardia with hypotensive
shock, coma with miosis.
tion (PAI) technique.
Ù
Avoid Succinylcholine since it increases secretions and
Prehospital Therapy
can prolong muscle paralysis in OPP.
●● Remove patient from source of exposure.
●● Remove clothing rapidly.
●● Decontaminate skin by washing with copious amounts Circulation
of water and soap. ●● Administer NS 10 mL/kg (max 20–30 mL/kg may be
●● If a large quantity of poison has been ingested and the needed to correct shock).
child has been brought within 1 hour of ingestion gas ●● Inotrope may be needed if hypotensive or hypoxia has
tric lavage may be helpful. caused cardiogenic shock.
Ù Disability
The Cochrane group suggests that gastric lavage is an
easily performed and cheap intervention. It could be
Manage convulsions using the standard protocol for status
used as an adjunct in the treatment of OP poisoning.4
epilepticus.
●● Irrigate eyes with normal saline, if contamination is
suspected. Specific Treatment4
Atropine neutralizes the muscarinic effects of acetyl
Clinical Diagnosis in the ED choline by competitive antagonism at postsynaptic mus
1. A high index of suspicion is needed to consider OP carinic receptors.
poisoning, when a child is brought in profound altered
Dose: Children < 12 years with signs of moderate to severe
mental status and history of exposure is not forthcom
toxicity:
ing. The clinical features described in (Table 25.1) will
help in the diagnosis. ●● Administer 0.05 to 0.1 mg/kg of atropine.
2. In case of doubt, a therapeutic challenge of atropine ●● In children > 12 years and adults with signs of moder
may be attempted: ate to severe toxicity: Administer 2 to 4 mg.
●● Administer 0.01 mg/kg Atropine in children < 12 ●● Double the previous dose after every 5 minutes in
year (minimum dose of 0.1 mg). terval, until secretions resolve (dry mouth), crepita
250 Section VIII n Poisons
Prevention
●● Counsel parents about the hazards of storing kerosene
in familiar beverage or household containers.
●● Teach them to avoid placing these containers on the
floor (within easy reach of infants and toddlers).
Figure 25.5 Physiological status: Unmaintainable airway,
●● Avoid using palm oil as a household remedy.
respiratory failure, normotensive shock with altered mental
status. Barbiturates
Ù
Do not induce emesis.
Barbiturate poisoning in children is usually due to acci
dental ingestion. Mental confusion resulting in repeated
Do not perform gastric lavage. dosages have been reported in adults and is also known as
Both procedures can enhance risk of aspiration. ‘involuntary suicide’ or ‘barbiturate automatism’.
Toxic ingestion of barbiturate can cause global de
Resuscitation pression or neuronal excitability. Large doses depress both
the respiratory and vasomotor centers. Renal function may
●● Administer oxygen via the JR circuit, since this child be compromised secondary to drug-induced hypotension.
has presented with impending respiratory failure.
●● Initiate bag-valve-mask ventilation and proceed to in Box 25.1: Common household things of low toxicity
tubate using PAI technique, if he had presented with No treatment required
respiratory arrest. Bar soap, lipstick, dry cells, newspaper, candles, pencil,
●● Treat shock with 10 mL/kg boluses of NS (up to a chalk, shampoo, clay (modeling), shaving cream and lotions,
maximum of 20 mL/kg). Consider more, only if hypo crayons, shoe polish, dehumidifying packets, striking surface
of matches, detergents, sweetening agents, hand lotion and
volemic due to persistant vomiting. If shock persists,
creams, thermometer, ink, toothpaste.
initiate appropriate inotrope. Removal necessary only, if large amounts ingested
●● Prophylactic antibiotics are not indicated. After shave lotion, body conditioners, colognes, deodorants,
●● Avoid corticosteroids (may be harmful). fabric softners, hair dyes, hair tonic, marker ink, match stick >
20, oral contraceptive, perfumes, toilet cleaner.
252 Section VIII n Poisons
Case Scenario 3 ●● Correct shock. Not more than 20 mL/kg may be need
ed. Epinephrine is indicated, if hypotension persists
A 5-year-old child could not be woken up. An open bot- after fluid bolus. If blood pressure stabilizes, dopamine
IP for
tle of tablets prescribed : 196.52.84.10
his brother’s seizure disor- is indicated.
der was found half empty near him. His temperature:
96.5°F (Figure 25.6).
Decontamination
Severe Poisoning
●● Perform gastric lavage, if a large quantity has been in
gested and the child has been brought within 1 hour of
ingestion.
●● Insert nasogastric tube and administer 1 g/kg of acti
vated charcoal prepared with aerated drink as a slurry
(refer Chapter 24 on Poisoning: General Approach).
Resuscitation
Resuscitation
●● Stabilize the airway, breathing, circulation.
●● Stabilize airway, breathing and circulation.
●● Administer naloxone (specific antidote) immediately
in the dose of 0.01 mg/kg IV or IM.
Decontamination
●● Repeat the dose of naloxone in 3–10 minutes if no re ●● Administer activated charcoal 1 g/kg .
sponse is noted. ●● Gastric lavage, if large life-threatening amount has
been ingested and the child reaches within the first
Ù
Response is evident when the depth and rate of hour of ingestion.
respiration improve. Pupils do not dilate and are not the
end point of therapy. Antidote
Specific antidotes are used in the presence of seizures, hal
●● Gastric lavage is useful only if a large life-threaten lucinations and arrhythmias.
ing amount has been ingested and the child has been
brought within 1 hour of ingestion. ●● Neostigmine methyl sulfate (dose: 0.5–2.5 mg IM at
●● Use activated charcoal. frequent intervals).
●● Administer via nasogastric tube as a slurry (1 g/kg). ●● Physostigmine: Dose: 0.5 mg slowly IV/IM (repeat ev
●● Intubate to protect the airway, if the child’s mental sta ery 5 minutes up to a maximum of 2 mg). Note: This
tus has dropped significantly. drug crosses the blood brain barrier.
254 Section VIII n Poisons
Figure 25.8: Time course of rise, peak and fall of laboratory values
in patients with paracetamol poisoning who survive. Peaks are not Table 25.4: Common iron preparations
proportional. Significant individual variations may occur.
Compound Elemental iron %
Ferrous sulfate 20
N-acetylcysteine
Ferrous fumarate 33
●● 150 mg/kg in 5% D over 1 hour.
●● 10 mg/kg/hour for 20 hours (delay < 10 hours). Ferrous gluconate 12
●● 32 hours (delay 10–16 hour). Ferric pyrophosphate 30
●● 72 hours (delay > 16 hour) and longer, if encephalo Ferrocholinate 14
pathic.
●● Monitor potassium levels. Ferroglycine sulfate 16
Ferrous sulfate, dried 33
Oral Methionine is an alternative drug.
Ferrous carbonate, anhydrous 38
Dose: 2.5 g stat followed by 2.5 g 4 hourly up to a total of
Carbonyl iron 99
l0 g over 12 hours (it is not as reliable as NAC).
The antenatal mother is the commonest source of iron
Supportive Treatment tablets. Prescribed for a period of a month and attractively
packaged, hence these tablets are easily accessible by curi
●● Maintain electrolyte balance.
ous young children.
●● Treat coagulopathy.
256 Section VIII n Poisons
Table 25.5: Toxicity of iron by amount ingested and ●● Iron levels, less than 350 µg/dL, when drawn
peak serum levels 2–6 hours after ingestion, predict an asymptom
IP : serum
196.52.84.10 atic course.
Elemental iron Peak iron
(mg/kg) (μg/DL)
Toxicity ●● Iron levels greater than 500 µg/dL suggest signifi
cant risk for phase III manifestations.
< 20 50–150 None In absence of serum iron levels, early clinical assess
20–40 150–300 Mild ment and several simple laboratory tests may be used to
40–60 300–500 Moderate predict approximate iron levels.
> 60 > 500 Severe
Ù
Vomiting, diarrhea, S. glucose > l50 mg/dL, WBC >
Pathophysiology l5,000/mm3 and radiopaque material on abdominal
radiograph correlate with an elevated serum iron level
●● Iron directly damages the GI mucosa resulting in mas greater than 300 µg/dL.
sive fluid loss and hemorrhage (Table 25.5).
●● Vasodilation, occurs secondary to ferritin and other
iron metabolites in the liver. Case scenario 6
●● Both factors predispose to the development of shock 4-year-old child was brought to the ED after he was
due to absolute or relative hypovolemia. found to have eaten up most of his mother’s monthly
●● Acidosis occurs due to the action of iron on oxidative prescription of iron tablets for pregnancy (Figure 25.9).
metabolism.
●● Coagulopathy and the resultant bleeding predispose to
circulatory failure.
●● The absorbed iron causes direct damage to the liver
parenchymal cells leading to massive hepatic necrosis
and liver failure.
Clinical Course
l. Gastrointestinal stage: The early symptoms include
vomiting, rapid onset of diarrhea, colicky abdominal
pain and GI hemorrhage.
2. Relatively stable stage: Reports have suggested that
there is a period of relative stability, which begins
Figure 25.9 Physiological status: Normal
3–4 hours after ingestion and lasts for as long as 48
hours. Subtle signs, such as mild GI bleeding, hyper
ventilation and poor capillary refill may exist during Resuscitation
this stage and may go unrecognized.
1. Care of the airway, breathing is the priority in manage
3. Shock stage: The third stage is characterized by circula
ment, if the patient has altered level of consciousness.
tory failure and profound shock, which may be fatal.
2. Correct shock if identified.
4. Hepatotoxicity stage: Hepatotoxicity occurs within
the first 48 hours. This is the second most common Since this 4-year-old child is stable, plan to decontami
cause of death. nate.
5. Gastric scarring is a late manifestation occurring 2–6
weeks after ingestion and is manifested by obstruction
of the gastric outlet and portions of the small intestine.
Decontamination
The amount of iron ingested often is hard to quantify ●● Perform gastric lavage for large life-threatening inges
clinically. Serum iron levels, if obtained promptly, tion, if the child presented within the first few hours of
have been shown to correlate with the symptoms: ingestion.
Chapter 25 n Specific Poisons 257
●● Whole bowel irrigation is considered as the technique ●● Chelation is continued until the urine color and serum
of choice. iron level return to normal or the maximum daily dose
●● Mix PEGLEG in a IP carbonated drink and administer it
: 196.52.84.10 has been reached.
in the dose of: ●● Patients with mild symptoms or those who are asymp
– 6–12 years: 1,000 mL/hour. tomatic, but have high serum iron or a positive chal
– 9 months to 12 years: 500 mL/hour. lenge test, should receive:
– > 12 years 1,500–2,000 mL/hour. – 20–40 mg/kg of desferrioxamine infused over 4
hours or 20 mg/kg IM, 4–8 hourly.
Ù
Avoid PEGLEG, if airway is unprotected, shock, intractable
vomiting, GI bleed, perforation, ileus or obstruction.10 Supportive Treatment
●● Blood transfusion should be considered in severe
● ● Gastrostomy should be considered in massive hemorrhage.
overdoses. ●● Persistent metabolic acidosis may require treatment
Ù with sodium bicarbonate.
●● Dyselectrolytemia and hyperglycemia should be man
Activated charcoal is not effective in binding iron salts.
Ipecac-induced emesis is not found to be beneficial. aged appropriately.
●● Liver and renal failure are treated symptomatically.
CORROSIVES
The most frequently ingested alkalis are button batteries,
dishwashing powder, disinfectants and caustic soda used
for cleaning ovens and degreasers. These may produce ir
reversible damage at the site of contact.
Absence of antidotes or definitive treatment modalities
makes this toxin particularly dangerous. In addition, it can
cause permanent damage to the gut resulting in strictures.
Ù
Prevention is better than cure.
Parents must be taught to store house hold disinfectants
Figure 25.10: Desferrioxamine administration in iron toxicity and cleaning agents away from children.
results in excretion of vin rose color urine (Courtesy: Dr S
Thangavelu).
Specific Management
●● Immediate dilution and irrigation with clean water for
IP : 196.52.84.10 30 minutes.
Ù
Neutralization agents, such as vinegar is contraindicated
as it is thought that an exothermic reaction will occur,
further injuring the tissue .12
Emesis, lavage, charcoal and cathartics are contrain-
dicated in corrosive poisoning.
●● Anesthesia may be required for removal. Do not in layed for up to 27 days postremoval. Esophageal strictures
duce vomiting. may not manifest for weeks to months postingestion.
●● If the patient is asymptomatic, determine the diameter
IP : 196.52.84.10
based on the size of a comparable battery. Ù
Retrieve batteries, endoscopically if possible from the
●● If the patient is ≤ 12 years, immediately obtain an X-ray
to locate the battery. Batteries lodged in the esophagus stomach or beyond if:
may cause serious burns in as little as 2 hours. Do not • A magnet is ingested and the patient develops signs
or symptoms that are likely related to the battery
wait for symptoms to develop. Patients with a battery
ingestion.
in the esophagus may be asymptomatic initially.
●● If the patient is > 12 years and the battery diameter is
• A large battery (≥ 15 mm diameter), ingested by a
child younger than 6 years, remains in the stomach
> 12 mm or unknown, immediately obtain an X-ray to
for 4 days or longer.
locate the battery.
• If battery diameter is unknown, estimate it from the
Ù
If the patient is > 12 years and the ingested battery is ≤
X-ray, factoring out magnification (which tends to
overestimate battery diameter).
12 mm, no X-ray to locate the battery is required, if all
of the following conditions are met: ●● Allow batteries to pass spontaneously, if they have
• The patient is entirely asymptomatic and has been passed beyond the esophagus and no clinical indication
asymptomatic, since the battery was ingested. of GI injury is evident. Avoid unnecessary endoscopic
• Only one battery was ingested. or surgical removal in asymptomatic patients.
• A magnet was ingested. ●● Promptly re-evaluate all patients who develop signs or
• The battery has been reliably identified and size symptoms possibly related to the battery. Endoscopic
confirmed as less than < 12 mm. removal of batteries still in the stomach should be pur
• There is no history of pre-existing esophageal dis sued for even minor symptoms. For batteries beyond
ease. the reach of the endoscope, surgical battery removal
may be required in the unusual patients with evidence
●● Order X-rays of entire esophagus, neck and abdomen. of occult or visible bleeding, abdominal pain, pro
Obtain both AP and lateral X-rays for batteries in the foundly decreased appetite, vomiting, signs of an acute
esophagus to determine orientation of the positive and abdomen and/or fever, unless these clinical manifesta
negative poles. tions are clearly unrelated to the battery.
●● Confirm battery passage by inspecting stools. Con
On the lateral film, if the step-off is on the negative sider repeat radiographs to confirm passage if passage
side of the battery (the negative pole has a slightly smaller not observed in 10–14 days. Confirming passage may
diameter). Anticipate complications based on battery posi avoid urgent diagnostic intervention for minor symp
tion and orientation. Damage will be more severe in tissue toms developing later.
adjacent to the negative pole. ●● Manage ingestion of a hearing aid containing a battery
Immediately remove batteries lodged in the esophagus. as an ingestion of a small battery (≤ 12 mm).
Serious burns can occur in 2 hours. Do not delay removal,
even if the child has eaten recently. The esophageal bat
Ù
Avoid these ineffective, unnecessary or unproven thera
tery should not be pushed into the stomach as the risk of peutic interventions:
esophageal perforation may increase. • Ipecac administration (ineffective).
After removing a battery from the esophagus, the child • Laxatives (ineffective).
should be observed for delayed complications, such as • PEGLEC solution (unproven effectiveness and not
tracheoesophageal fistula, esophageal perforation, medi known, if solution enhances electrolysis).
astinitis, vocal cord paralysis, tracheal stenosis or trache
omalacia, aspiration pneumonia, empyema, lung abscess, NEEM OIL INGESTION
pneumothorax, spondylodiscitis or exsanguination from
perforation into a large vessel. Esophageal perforations and This is the commonest cause of refractory seizures. Symp
fistulas involving the trachea or major vessels may be de toms may start as early as 10 minutes. The active ingredient,
260 Section VIII n Poisons
which causes the toxicity is not known. Treatment is simi ●● Other neurologic symptoms include confusion, verti
lar to the management of status epilepticus. go, restlessness, delirium and hallucinations. Increased
IP : 196.52.84.10 muscular activity, tremors and jerky movements, which
can often progress to epileptiform convulsions.-
CAMPHOR POISONING21
●● GI symptoms consist of oral and intestinal burning,
●● Camphor poisoning is a common ingredient in many nausea and vomiting.
camphorated oils, ointments and inhalants for the home ●● Tachycardia, mydriasis, visual disturbances, urinary
treatment of colds. It is also used for pooja. Children retention can also occur.
are attracted by the smell, texture and feel. ●● Albuminuria, mild transient elevations of the aspartate
●● Camphor is rapidly absorbed when taken orally, but a dehydrogenase and lactic dehydrogenase concentra
considerable amount can also be absorbed via inhala tions and rarely, hepatic failure have been noted.
tion or through intact skin. Typically, symptoms begin
5–90 minutes after ingestion of a toxic dose. Although a variety of other conditions or intoxica
●● Seizures may occur as soon as 4 minutes after inges tions can exhibit similar symptoms, a strong odor of
tion of 28 g of camphorated oil. Death may result from camphor on the breath or a history of recent treatments
respiratory depression or complications of status epi with camphor-containing agents will strongly suggest
lepticus. camphor intoxication.
Many household things kept within reach of the chil 7. Frank Shann Drug Doses Intensive Care Unit, Royal Chil
dren are often ingested by them due to their curiosity to dren’s hospital Austrailia, 15th Edn 2010.
explore nature. A list ofIPthings which are innocuous or of 8. Riordan M, Rylance G, Berry K. Poisoning in children1:
: 196.52.84.10 General management. Arch Dis Child. 2002 ;87:392-396.
low toxicity are given in Box 25.1. Reassurance of the par
ents is all that is needed. 9. Salgia AD, Kosnik SD. When acetaminophen use becomes
toxic. Treating acute accidental and intentional overdose.
Key Points
1. Organophosphorus compounds are the commonest
ü Postgrad Med. 1999;105:81-4, 87, 90.
10. Singhi SC, Baranwal AK, M J. Acute iron poisoning:clinical
picture, intensive care needs and Outcome. Indian Pediatr.
toxin ingested in the rural agricultural areas. 2003; 40:1177-182.
2. Atropine usage is based on the recommendations of 11. GP Cantwell, RS Weisman. Poisoning Roger’s Handbook
the Cochrane data base 2012. of Pediatric Intensive Care 2009; 4th edition, N. Delhi Wil
3. Ingestion of corrosives and button batteries are liams and Wilkins.
hazardous and should be handled using a protocol 12. F Riffat, A Cheng. Pediatric caustic ingestion: 50 consecu
based approach. tive cases and a review of the literature Diseases of the
4. Usually common house hold products are safe unless Esophagus. 2009(22), 89-94DOI: 10.1111/j.1442-2050.
2008.00867.
large quantities are ingested.
13. Millar A, Numanoglu A, Rode H. Caustic strictures of the
5. Always resuscitate ABCs in addition to poison
esophagus. In: Grosfeld J, O’Neill J, Coran A, Fonkalsrud
elimination or treatment. E (eds). Grosfeld: Pediatric Surgery, Chapter 68. St. Louis,
MO: Mosby. 2006; 969-79.
common errors
û
1. Performing gastric lavage for kerosene and caustic
14. Friedman EM. Caustic ingestions and foreign bodies in
the aero digestive tract of children. Pediatr Clin North Am.
1989; 6: 1403-410.
ingestion. 15. Ulman I, Mutaf O. A critique of systemic steroids in the
2. Failing to ventilate for severe OP poisoning. management of esophageal burns in children. Eur J Pediatr
3. Not considering the potential for oesophageal Surg. 1998;8:71.
damage following battery ingestion. 16. Anderson KD, Rouse TM, Randolph JG. A controlled trial
of corticosteroids in children with corrosive injury of the
4. Failure to seek assistance from regional poison
esophagus. N Engl J Med. 1990;323:637.
center.
17. Poley J, Steyerberg E, Kuipers E, et al. Ingestion of acid
and alkaline agents: outcome and prognostic value of early
References endoscopy. Gastrointest Endosc 2004;60(3):372-7.
1. Srivastava A, Peshin SS, Kaleekal T, et al. An epidemio 18. Rothstein FC. Caustic injuries to the esophagus in chil
dren. Pediatr Toxicol Pediatr. Clin North Am. 1986;33(3):
logical study of poisoning cases reported to the National
665-74.
Poisons Information Centre. All India Institute of Medi
19. Pintus C et al. Caustic ingestion in childhood: current treat
cal Sciences, New Delhi. Human Experimental Toxicol.
ment possibilities and their complications. Pediatr Surg Int
2005;24:279-85. 1993; 8: 109.
2. van Heel W, Hachimi-Idrissi S. Accidental organophos 20. Litovitz T, Whitaker N, Clark L, et al. Emerging bat
phate insecticide intoxication in children: a reminder. Int J tery ingestion hazard: Clinical implications. Pediatrics
Emerg Med. Jun 15 2011;4(1):32. 2010;125(6): 1168-1177. epub 24 May 2010. Guideline
3. Kozer E, Mordel A, Haim SB, et al. Pediatric poisoning from the National Battery Ingestion Hotline at the National
from trimedoxime (TMB4) and atropine automatic injec Capital Poison Center ©National Capital Poison Center,
tors. J Pediatr. Jan 2005;146(1):41-44. 2009.
4. Interventions for acute Organophophate poison South 21. Theis JGW, Koren G.Camphorated oil: Still endanger
ing the lives of Canadian children.Can Med Assoc J.
Asian Cochrane Network and Centre (SASIANCC) 2012.
1995;152:1821-824.
5. Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on 22. Cupp MJ. Herbal Remedies: Adverse Effects and Drug In
Urine alkalinization Journal of Toxicology Clinical Toxi teractions.1999; Accessed from www.aafp.org (59)-5.
cology. 2004;42(1):1-26. 23. Fugh-Berman A, Ernst E. Herb±drug interactions: Review
6. Hanhan UA. The poisoned child in the pediatric intensive and assessment of report reliability Br J Clin Pharmacol.
care unit. Pediatr Clin N Am. 2008; 55: 669-86. 52:587-95.
Section IX
IP : 196.52.84.10
Trauma
IP : 196.52.84.10
Approach to
26
IP : 196.52.84.10
Figure 26.1: Head injuries are very scary and can prove fatal if not managed appropriately (Courtesy: Dr Gunda Srinivas)
Learning Objectives
1. Pathophysiology of severe traumatic brain injury. 3. Case scenario-based management.
2. Spectrum of head injuries. 4. Pearls and pitfalls in management.
Introduction
Over 1.5 million pediatric head injuries are reported each
year1. Motor Vehicle Accidents (MVA) associated head
trauma have the highest morbidity and mortality in all age
groups (Figure 26.1). Mild traumatic brain injury (TBI)
appears to be the most common injury but generally has
good outcomes. In India, severe traumatic brain injury oc
curs most commonly following falls from upper stories of
buildings with unbarred windows and verandahs refer Fig
ure 27.1 Chapter of Polytrauma. Child abuse should also
be considered when children present with unexplained
head trauma or when there has been delay in seeking care.
Ù
CBF remains constant over a wide range of cerebral per- Figure 26.4: Relation between intracranial pressure and
fusion pressures. intracranial volume
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 267
IP : 196.52.84.10
Simultaneously, steps must be taken to lower ICP to a ●● Alert the parents/caretakers for the possibility of a
level that is adequate to increase cerebral perfusion pres postconcussive syndrome.
sure (CPP). This important step is key to improving cere
bral oxygenation and preventing cerebral ischemia. In this Ù
context, Mannitol, a drug that acts by causing diuresis is Children under 2 years of age with normal mental sta-
not preferred. It reduces ICP, but worsens shock thereby tus, no scalp hematoma (except frontal), no loss of con-
reducing CPP. Efforts must also be focussed on early de sciousness (LOC) or brief loss of consciousness < 5 sec,
tection of cerebral herniation. non-severe mechanism, no palpable skull fracture and
behaving normally as reported by the parents are less
likely to have a severe traumatic brain injury.2
MINOR HEAD TRAUMA
Head trauma associated with a GCS > 13.
●● Loss of consciousness (< 1 minute).
Ù
Children over 2 years of age were at low-risk if men-
●● Seizure, vomiting, confusion, headache or lethargy. tal status was normal, there had been no loss of con
●● Normal mental status at time of exam. sciousness, no vomiting, non-severe injury mechanism,
●● Normal physical exam (including fundus). no signs of basilar skull fracture and absence of a head-
●● No evidence of skull fracture (hemotympanum, Bat ache.2
tle’s sign or palpable bone depression).
●● CT brain is recommended.
Scalp Lacerations
●● Skull radiographs are recommended only if, CT scan is
unavailable, or for children less than 2 years. The scalp is a very vascular structure made up of five lay
●● If child abuse is suspected. ers that include: skin, subcutaneous tissue, galea aponeu
rosis, loose areolar tissue and the pericranium (SCALP).
●● Infants younger than 2 years.
The large vessels that supply the scalp run just above the
galea aponeurosis and injury to this layer may result in sig
Management nificant blood loss (Figure 26.6).
●● Reassure. Debris from the accident site, as well as hair or clothing,
●● Advice rest and follow-up. may become entangled in the wound.
268 Section IX n Trauma
IP : 196.52.84.10
Ù
Clean wound meticulously prior to wound closure.
Explore all scalp lacerations to rule out a skull fracture
prior to closure.
SEVERE TRAUMATIC brain INJURY In skull fractures, the dura, which is closely approxi
mated to the inner table of the skull, may be lacerated. In
Skull Fracture children under the age of two, a dural laceration may re
Children often present with linear, depressed or basilar skull sult in herniation of the leptomeninges into the bony cleft.
fractures. About 75% of skull fractures are linear, with the At this age, as the brain is growing at a very rapid rate,
parietal bone being the most common site. The significance the bony edges may not have time to heal completely. The
of a skull fracture is that it indicates the amount of energy growth and pulsation of the brain may lead to a growing
that was applied to the patient’s head. A large amount of skull fracture or leptomeningeal cyst. Repair of these cysts
concentrated force is necessary to crack both tables of the can be very difficult if they are left untreated.
skull. The amount of energy that is transmitted to the un
derlying structures is therefore of concern. Hence, presence
Ù
Children who sustain skull fractures under the age of
of a fracture denotes that a more severe injury to the brain two should have neurosurgical follow-up to ensure that
exists. Approximately, 48% of patients have associated in the fracture closes and does not grow into a large cyst.
tracranial lesions (Figures 26.7 to 26.8 and Table 26.1).
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 269
Depressed Skull Fracture ●● A fracture through the anterior cranial fossa with injury
to the olfactory apparatus will result in loss of the sense
Depressed skull fractures (Figure 26. 8) result from forces
IP : 196.52.84.10 of smell.
applied to a small cross-sectional area and often require
●● Anterior fossa fractures can also lead to injury of the
surgical repair.
optic or oculomotor nerves passing through the supe
The skin over the injury site may be open, closed, con rior orbital fissure.
tused or absent. Brain may be present in the wound or on ●● The most commonly injured cranial nerves are the VII
rare occasions, severe cortical bleeding from a lacerated and VIII, leading to a facial paralysis and sensorineural
artery or vein may also be present. hearing loss. Sometimes, the VII nerve damage may
●● Complicated injuries require vigorous debridement manifest later. Therefore, it is crucial to examine and
and closure. document severity of loss of facial movements. Injury
●● If brain matter is exposed, the wound should be cov to the lower cranial nerves passing through the jugular
ered with saline-soaked gauze to prevent drying of the or hypoglossal foramen is relatively uncommon.
brain prior to surgical repair. ●● Basilar skull fractures are often associated with venous
●● Children with depressed skull fractures are at higher bleeding in soft tissues behind the ear.
risk for developing seizures and need prophylactic an
ticonvulsants. Ù
Bleed behind the ear is called the ‘battle sign’ and an
Ù accumulation of blood in the periorbital region is known
All depressed skull fractures should be evaluated by a as the ‘raccoon sign’.
neurosurgical specialist to determine the appropriate-
ness of surgical decompression and repair. Either of these signs should alert the clinician to the
possibility of a basilar fracture and a computerized tomog
raphy (CT) scan should be ordered.
Basilar Skull Fracture
Fractures of base of skull are not seen well on plain X- Cerebrospinal Fluid Leak
ray films, but should always be considered in patients with
head trauma. In these patients, the fracture almost always At the base of the skull, the dura is tightly adherent to the
heals without surgical intervention except in the most se bony structure in a number of places. Should a fracture oc
vere cases. The factor that differentiates the basilar skull cur, the meninges is at risk of tearing leading to CSF leak
fracture from a fracture over the convexity of the brain is through the fracture.
the associated structures that run through the base of the ●● The CSF may leak into the air-filled sinuses and na
skull. Injury to the cranial nerves, vascular structures or sopharynx, resulting in CSF rhinorrhea.
basilar dura may be disabling or in some cases fatal.
●● CSF can also leak through the mastoid or floor of the
The carotid artery enters the base of the skull deep to middle fossa into the middle ear, where it may pass
the temporomandibular joint. through a ruptured tympanic membrane, producing
●● Injury to the carotid vessels in basilar skull fracture otorrhea or through the eustachian tube into the na
causes either a vascular thrombosis or bleeding into the sopharynx.
middle ear with a resultant hemotympanum or blood in In most cases, a CSF leak will stop within two weeks.
the external auditory canal. The use of prophylactic antibiotics for this type of injury is
Ù
All cranial nerves passing through the base of skull are
controversial. Some suggest that bacterial flora is reduced
by the use of antibiotics and therefore the risk of infection
at risk for injury from basilar skull fractures. The anato- is reduced. Others suggest that antibiotic usage encourages
my of injured region determines the frequency of cranial resistance without protection and if meningitis were to re
nerve deficits. sult from a CSF leak, the organism would be more difficult
to treat.
270 Section IX n Trauma
trauma prior to the onset of unconsciousness. In general, one area ‘coup injury’ of the brain with a similar injury direct
the relatively focal nature of the epidural hematoma and ly across the head called a ‘contra coup’ injury. Parenchymal
mechanism of injury leading to less diffuse brain trauma
IP : 196.52.84.10 bleeding may extend into the subarachnoid space or into the
herald a better outcome than would be expected with other ventricles and may occasionally lead to acute hydrocephalus.
sites of hematoma accumulation.
Case scenario 1
7-year-old boy was rushed into the ED after fall from
IP : to
first floor (Figures 26.11 196.52.84.10
26.14).
Therapeutic Goals of
Figure 26.12: The airway was stabilized using the jaw thrust Traumatic Brain Injury in the ED
maneuver, cervical collar was applied and he was immobilized
on a spinal board. Orogastric tube was used to decompress Ù
the stomach. Orotracheal intubation was performed using Maximize oxygen delivery to the brain
ICP precautions. During intubation, care was taken to avoid C-spine precautions
flexing or extending the neck using in-line manual cervical Correct shock
stabilization. Shock was corrected with one bolus of NS. He was Maximize cerebral perfusion pressure
catheterized, given pain and sedation drugs to avoid further Lower intracranial pressures
increase in ICP during transfer for CT scan and neurosurgeon’s
Maintain eucapnia.
opinion. His head end was elevated and 3% NS was initiated at
the rate of 1 mL/kg.
Primary survey is performed even as a focused history is
Secondary survey revealed no obvious evidence of ex being obtained in the ED.
ternal injuries or bleeds. His fundus was normal.
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 273
Ù gist’s opinion.
Ù Asymptomatic
Mild headache
Look for bleeding injuries. Three or fewer episodes of vomiting
Glasgow Coma Scale score of 14–15
Disability: Raised intracranial pressure, non-convulsive Loss of consciousness for less than 5 minute
status epilepticus. ●● Moderate
Loss of consciousness for 5 min or more
Following resuscitation of the ABCs the secondary Progressive lethargy
survey is performed to include a formal assessment of the Progressive headache
level of consciousness using the Glasgow Coma Scale Protracted vomiting (more than three times) or associated with
(GCS). other symptoms
Post-traumatic amnesia
●● Patients are described as having: Severe head injury if Post-traumatic seizure
the GCS is 8 or less. Multiple trauma
●● Moderate head injury is considered when the GCS Serious facial injury
Signs of basal skull fracture
is 9–12. Possible penetrating injury or depressed skull fracture
● ● Minor head injury correlates with a GCS of 13– Suspected child abuse
15. Glasgow Coma Scale score of 11–13
These classifications guide therapy as well as progno ●● Severe
sis. Severity of intracranial injury may also be classified as Glasgow Coma Scale score of 10 or less, or decrease of 2 points
mild, moderate and severe based on clinical examination or more not clearly caused by seizures, drugs, decreased
(Box 26.1). cerebral perfusion or metabolic factors
Focal neurologic signs
Penetrating skull injury
MANAGEMENT 5,6,7,8 Palpable depressed skull fracture
Compound skull fracture
Airway
●● Open airway using the jaw thrust maneuver. Other Airway Precautions
●● Head tilt-chin lift maneuvers should be avoided. ●● Prepare to suction large volume particulate material.
●● Manually hold the C-spine in-line until an age appro
priate collar can be placed along with the spinal im
mobilization.
Ù
Both central and electrical suction with Yankauer suc-
Ù tion tip should be available.
Manual in-line cervical immobilization throughout in-
tubation, which helps to prevent neck movement and the ●● Introduce orogastric tube.
dreaded risk of quadriplegia. ●● Intubate using orotracheal route (Figure 26.15).
274 Section IX n Trauma
Ù Disability
Bradycardia and high blood pressure secondary to ICP
●● Head injury patients are prone to develop raised ICP
may mask features of shock in TBI. In addition, children
which can potentiate secondary injury. Careful neuro
often maintain systolic blood pressure despite significant
logical monitoring helps in early detection of cerebral
blood loss until they develop acute hypotension. Pulse herniation.
pressure is usually narrow in hemorrhagic shock. How- ●● The goal of treatment is to lower the ICP to a level
ever if the diastolic pressure is less than 50% systolic, that is adequate to increase cerebral perfusion pressure
then the possibility of vasodilatory neurogenic shock (CPP) as this is key to improve cerebral oxygenation
should be considered secondary to severe CNS injury. and prevent cerebral ischemia.
Blood loss inside cranium (closed head injury with Note: Risk of raised ICP exists even in infants despite
out multisystem trauma) is not sufficient to cause hy open AF or sutures.
povolemic shock. Hence, not more than 20–30 mL/kg
of fluids may be needed to resolve shock in isolated
Management of Raised
head injury.
Intracranial Pressure (Box 26.4)
If shock persists after administering 20 mL/kg in TBI,
Box 26.4: Management of raised intracranial pressure
consider the following possibilities.
●● Scalp injuries can cause significant blood loss in young Measures to improve jugular venous flow from brain
children. ●● Place head and neck in midline
●● Elevate head end of the bed not more than 30°
●● Fracture of long bones with or without intra-abdominal
( if elevated less than 30° CPP could fall)
injury. ●● Avoid tight ties for the ET tube
●● Vasodilatory shock due to spinal cord transection. ●● Minimize stimulation (suctioning and movement)
●● More volume will be needed to resolve shock for the Other measures
first three conditions. Isotonic normal saline is pre ●● Provide Morphine 0.1 mg/kg and lorazepam 0.1 mg/kg
ferred to lactated Ringer solution, since the former is ●● Adequate sedation and analgesia should be maintained
isonatremic compared to RL. with opioids and benzodiazepines to avoid anxiety and
●● Persistent hypotension refractory to volume resuscita pain, which may cause spikes in intracranial pressure
tion should be treated with dopamine or epinephrine to ●● Propofol as a sedative, is avoided owing to the risk of
metabolic acidosis
ensure adequate cerebral perfusion. Contd...
276 Section IX n Trauma
History
●● Witnessed LOC > 5 min
●● Abnormal drowsiness
●● Vomiting ≥ 3 episodes
Figure 26.16: She is intubated with ICP precautions and C- ●● Suspicion of non-accidental trauma
spine precautions. One bolus of 20 mL/kg of NS is administered. ●● Seizure in a patient who has no history of seizures
Following intubation her HR: 160/minute, but her BP is un- Examination
●● GCS < 14 or GCS < 15 if less than 1-year-old
recordable. A quick secondary survey reveals no injury to the
●● Suspicion of penetrating or depressed skull injury or
long bones or scalp. Her abdomen is scaphoid and soft. A
tense fontanelle
needle thoracocentesis in the right midclavicular line releases
●● Signs of basal skull fracture
a gush of air due to a pneumothorax. ●● Focal neurological deficit (motor, sensory, coordination
or reflexes)
●● Bruise, swelling or laceration > 5 cm if less than 1-year-old
Mechanism
●● High speed traffic accident (> 64 km/h)
●● Fall > 3 m in height
●● High speed injury from a projectile or an object
High-risk factors
●● GCS < 15 at 2 hour after injury
●● Suspected open or depressed skull fracture
●● History of worsening headache
●● Irritability on examination
This would require 30% of patients to get a head CT.
Medium-risk factors
●● Any sign of basal skull fracture
●● Large boggy hematoma of the scalp
Figure 26.17: In this picture taken 24 hours later, her
●● Dangerous mechanism of injury (MVA, fall from height >
cardiopulmonary assessment is apparently normal. Obstructive 0.9 m or 5 stairs, fall from a bicycle with no helmet
shock (due to tension pneumothorax in this child) had
complicated severe traumatic brain injury.
278 Section IX n Trauma
There is no role for contrast enhanced head CT in the nitive outcome and fewer developmental and behavioral
acutely injured child, unless an angiogram is being per sequelae.13
formed to evaluate for IP concomitant vessel injury. CT scan
: 196.52.84.10 Head injury education and prevention, i.e. car seats,
is a safe and accurate investigation for older children who
seat belts and helmets help reduce the incidence and se
are able to lie still for the procedure. In younger children,
verity of head injury. Children who have suffered mild-
particularly those under 5 years, general anesthesia or pro
moderate concussions should not return to contact sports
cedural sedation may be required to achieve CT scanning.
until they are completely symptom free, both at rest and
In addition, the risks of cranial irradiation need to be con
with exertion. Any child with symptoms persisting greater
sidered. Therefore, particularly in younger children, the
than a week after a head trauma should be referred for neu
risk of CT should be balanced against the risk of delayed
rocognitive evaluation.
diagnosis (Refer Protocol 26.1).
Conclusion
common errors
û
1. Shifting the child for CT scan without stabilization.
The long-term neurocognitive and behavioral consequenc 2. Waiting for neurosurgeon opinion without correct
es of head trauma can vary widely, based on the extent ing hypoxia and shock.
of injury. Overall, children have a better prognosis and 3. Failure to maintain C-spine precautions and spinal
improvement in function may continue for years after in immobilization until clearance of spine.
jury. Those patients with a GCS score less than three have 4. Focusing on the medicolegal entries prior to stabili
a high mortality and morbidity. Children with coma that zation
lasts less than 2 weeks, have considerable better neurocog 5. Steroid therapy.
Chapter 26 n Approach to Traumatic Brain Injury (TBI) 279
IP : 196.52.84.10
280 Section IX n Trauma
Approach to Polytrauma
Figure 27.1: Common hazards: Lack of balcony railings, walkers, unsupported TVs and lack of supervision in construction sites
(Courtesy: Dr Gunda Srinivas)
Learning Objectives
1. Principles of primary and secondary survey. 3. Recognition of abdominal trauma.
2. Management of orthopedic trauma. 4. Recognition of trauma to nerves and vessels.
Ù Ù
Integrity of circulation should be evaluated early in the
Examine an unstable pelvis only once. Repeated assess-
management of a critically injured child.
ments could disrupt a clot and lead to blood loss. Bind the
pelvis with a cloth/sheet to reduce volume and motion. ●● Examine and document presence or absence of radial,
ulnar, dorsalis pedis and posterior tibial pulses in all
four limbs whether the limb appears injured or not.
●● Document color, temperature and motor function of all
four limbs.
Neurological Examination
Evaluation of the power of each muscle according to the
Medical Research Council (MRC) classification establish-
es, whether the nerve is intact along its course. Younger
children may be examined by observation using toys.
0 = No movement
1 = Flicker
Figure 27.2: Child with polytrauma
(Courtesy: Dr Gunda Srinivas). 2 = Moves without gravity (gravity eliminated)
Chapter 27 n Approach to Polytrauma 285
are soft and more compliant resulting in more force be- ●● Blood.
ing transmitted to thoracic and upper abdominal organs. ●● Palpable bony fragments.
Thinner abdominal wall IP musculature offers less protec-
: 196.52.84.10 ●● Linear ecchymosis ‘seat belt injury’ is often associated
tion to intra-abdominal organs. Close proximity of all the with intra-abdominal injury.
intra-abdominal organs also predisposes to a greater risk of
Whilst abdominal X-ray is not useful in evaluation of
trauma to the solid organs within the abdomen.
intra-abdominal injury, radiographic evidence of gas in
In India, common causes of abdominal trauma are motor soft tissue (taken after stabilization) may provide some
vehicle accidents, fall from heights and bull gore injuries. clues suggestive of bowel injury.
Suspect abdominal injury if secondary survey reveals
the following (Refer Figure 27.3 for hemothorax):
Splenic Injury
●● Abdominal distension.
●● Left shoulder pain (Kehr’s sign).
●● Abdominal tenderness.
●● Abrasions and tenderness in left upper quadrant.
●● Abrasions.
●● Abdominal distension.
●● Ecchymosis.
●● Associated with shock.
Ù Hepatic Injury
• Suspect serious abdominal trauma if infants are hav-
ing predominantly chest breathing or the older child is ●● Abdominal distension.
lying still and whimpering or has referred pain to the ●● Right shoulder pain.
shoulder. Trauma to the lower six ribs or abdominal ●● Abrasions and tenderness in right side of abdomen.
distension in a hemodynamically unstable child is also ●● Hypotensive shock.
associated with serious intra-abdominal injury. ●● Injuries to the ribs are common.
• Gastric distension due to aerophagia in young infants
may be misinterpreted as abdominal distension. An
Urological Injury
orogastric tube should be placed early in the evalua-
tion to avoid misdiagnosis. ●● Blood at penile meatus.
●● Perineal bruising or swelling.
●● High riding prostate.
Ù
If any of these signs are present, DO NOT insert a Foley
catheter. Diagnosis is confirmed by performing a retro-
grade urethrogram.
Imaging
Ù
Whilst routine X-rays for lateral spine, pelvis and chest
are obtained, plain abdominal films are not useful in
evaluation of acutely injured children.
Figure 27.3: This child was nearly run over by a vehicle.
Note the tyre markings on the lateral chest. He developed a
1. Focused abdominal sonogram for trauma (FAST).
hemothorax that was relieved by a thoracostomy.
●● FAST is a focused goal-directed sonographic ex-
amination of the abdomen used to rapidly assess
Bowel Injury
for free fluid (bleed in peritoneal space, abdomen,
Suspect injury to the gut if digital rectal examination re- pleural space and pericardial sac).
veals evidence of:
Chapter 27 n Approach to Polytrauma 287
●● FAST has replaced diagnostic peritoneal lavage ●● Use small volumes of 3% saline for resuscitation to
(DPL) to identify intra-abdominal bleed. treat life-threatening hypotension.
●● Helps in triaging for the need to perform abdomen ●● Consider vasopressin infusion to maintain blood
IP : 196.52.84.10
computerized tomography (CT) scan. pressure at minimally acceptable ranges.
●● Recently eFAST (extended focused assessment
with sonography for trauma) has been used, which Ù
allows an emergency physician to detect whether Major exsanguinating trauma: Urgently shift to OT for
a patient has pneumothorax, hemothorax, pleural damage control surgery and resuscitation.
effusion, mass/tumor or a large foreign body. This
examination allows for visualization of the echo- 3. Damage control surgery.
genic tissue, ribs and lung tissue using few radio-
●● Traditional surgery is not performed until the victim
graphic signs.
has been stabilized.
2. Intravenous contrast enhanced CT abdomen is the di- ●● Surgical strategies are focused to control bleeding
agnostic modality of choice to identify intra-abdomi- and reduce wound contamination.
nal injuries.
3. Magnetic resonance imaging not needed for evalua-
tion of abdominal or pelvic trauma.
Key Points
ü
Acute coagulopathy, hypothermia and acidosis also 1. Avoid rushing to evaluate obvious injuries and fail
known as the ‘lethal triad’ can occur following severe ex- to stabilize the ABCs.
sanguinating trauma. To avoid these dangerous complica- 2. Stabilization and immobilization of the spine is a
tions, resuscitation is focused towards damage control. priority in trauma victims.
3. Rule out hemo/pneumothorax and control bleeding
1. Permissive hypotension in addition to stabilization of the ABCs.
●● Replacement of large volume normal saline in ma- 4. Ensure comfort for children who do not have life-
jor exsanguinating trauma can result in clot dis-
threatening injuries.
lodgement, rebleeding, hyperchloremic acidosis
5. MRI is not a useful modality in orthopedic trauma.
and dilutional coagulopathy.
●● Give just enough fluids to maintain 70–80 systolic 6. FAST mandatory in ruling out intra-abdominal
blood pressure. bleed.
Ù
This strategy works only when time between inciting trau-
ma and shifting to the OT is less than 30–40 minutes.
common errors
û
Permissive hypotension SHOULD BE AVOIDED when 1. Failure to manually immobilize C-spine until the
head injury coexists. Cerebral perfusion pressure must cervical collar and spinal board have been applied.
not be compromised. 2. Failure to shift to OT when shock is refractory to
fluid therapy.
2. Hemostatic resuscitation 3. Transferring trauma victim for imaging without sta-
●● Infuse whole blood as initial resuscitation fluid. bilization.
– This strategy helps to treat intrinsic acute trau- 4. Not infusing whole blood early in the management
matic coagulopathy and prevent dilutional co- of exsanguinating bleed due to trauma.
agulopathy.
Environmental
Section X
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Injury
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28
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Burns
Learning Objectives
1. Pathophysiology of burns. 3. Management of the ABCs specific for burns.
2. Calculation of percentage of burns. 4. Care of the burned area.
Prehospital Care
1. Do not remove burned clothing.
Make sure the victim is no longer in contact with hot
or burning material or exposed to smoke or heat.
2. Cool the area within 30 minutes of the burn with
cool water. This intervention reduces the depth of
burnt area and pain.
Ù
Do not put ice on the burn.
Birth–1 year 1–4 year 5–9 year 10–14 year 15 year Adult Burn size estimate
Head 19 17 13 11 9 7
Neck 2 2 2 2 2 2
Anterior trunk 13 13 13 13 13 13
Posterior trunk 13 13 13 13 13 13
Right buttock 2.5 2.5 2.5 2.5 2.5 2.5
Left buttock 2.5 2.5 2.5 2.5 2.5 2.5
Genitalia 1 1 1 1 1 1
Right upper arm 4 4 4 4 4 4
Left upper arm 4 4 4 4 4 4
Right lower arm 3 3 3 3 3 3
Left lower arm 3 3 3 3 3 3
Right hand 2.5 2.5 2.5 2.5 2.5 2.5
Left hand 2.5 2.5 2.25 2.5 2.5 2.5
Right thigh 5.5 6.5 8 8.5 9 9.5
Left thigh 5.5 6.5 8 8.5 9 9.5
Right leg 5 5 5.5 6 6.5 7
Left leg 5 5 5.5 6 6.5 7
Right foot 3.5 3.5 3.5 3.5 3.5 3.5
Left foot 3.5 3.5 3.5 3.5 3.5 3.5
Total TBSA
294 Section X n Environmental Injury
Parkland Resuscitation Formula2 wound. Wrap the gauze loosely to avoid applying
pressure on burned skin. Bandaging keeps air off the
Ù IP : 196.52.84.10 burn, reduces pain and protects blistered skin.
4 mL/kg of fluids/% total burn surface area. 3. Prescribe paracetamol: 10 mg/kg/dose.
1.
common errors
Failure to provide pain relief.
û
IP : 196.52.84.10
2. Application of native medications.
3. Covering the child with warm clothes during transport.
4. Breaking blebs.
REFERENCES
1. Bhattacharya S. Principles and practice of burn Care. In
dian J Plast Surg.2009;42:282-83.
2. Tintinalli, Judith E. Emergency Medicine: A Compre
Figure 28.4: Child seen in Figure 28.3 recovered after hensive Study Guide [Emergency Medicine (Tintinalli)].
ventilatory and wound care. Note his tracheostomy. The New York: McGraw-Hill Companies 2010. ISBN 0-07-
airway had been compromised due to edema following 148480-9.
inhalational burns (Courtesy: Dr Thangavelu S). 3. Avni T, Levcovich A, Ad-El DD, et al. “Prophylactic an
tibiotics for burns patients: systematic review and meta-
Key Points
ü analysis”. BMJ 2010;340:c241. doi:10.1136/bmj.c241.
PMC 2822136. PMID 20156911.
1. Wash burned areas with tap water in the prehospital
4. Storm-Versloot MN, Vos CG, Ubbink DT, et al. In: Storm-
setting. Versloot Marja N. (Ed)2010 Mar 17. “Topical silver for pre
2. Anticipating need for early intubation, if airway is venting wound infection”. Cochrane database of systematic
involved. reviews (Online) (3): CD006478. doi:10.1002/14651858.
3. Estimation of burned surface and calculating the CD006478.pub2. PMID 20238345.
appropriate fluids. 5. Hubley P. “Review: evidence on dressings for superficial
4. Removal of eschars in circumferential burns to burns is of poor quality”. Evid Based Nurs” 2009 (3): 78.
prevent vascular insufficiency. doi:10.1136/ebn.12.3.78. PMID 19553415.
29
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Electrical Injury
Figure 29.1: Few seconds of negligence can cause severe and occasionally fatal electrical burn injuries
(Courtesy: Dr Gunda Srinivas)
Learning Objectives
1. Pathophysiology of electrical injury. 3. Resuscitation and investigations following electric
2. Assessment of severity of injury based on injury.
cardiopulmonary cerebral assessment and the
pediatric assessment triangle.
INTRODUCTION PATHOPHYSIOLOGY
Young children are usually referred to the ED with low volt- Electricity passes between two points through the path
age injuries. Electrical burns can occur due to exposure to of least resistance. The most dangerous pathway for the
electrical appliances and electrical wall outlets (Figure 29.1). current is along the vertical axis of the body as it passes
Ù through all vital organs. Hand to hand flow will involve the
heart, respiratory muscles and spinal cord.
High voltage injuries could lead to death.
Low voltage current can cause tetanic contraction of
CLASSIFICATION the respiratory muscles and ventricular fibrillation. High
voltage current can throw the victim and cause trauma in
Of the two types of current viz alternating current (AC) addition to the effects mentioned above.
and direct current (DC), the former is more dangerous. Te-
tanic muscle contractions occur as a result of prolonged
contact. AC is used for domestic purposes and DC is used CASE SCENARIO 1
in batteries, defibrillators and pacemakers. A 10-year-old boy is rushed into the ED after being
●● Low voltage: < 600 V. found unconscious near a high tension wire. Thinking
●● High voltage: > 1,000 V. the wire as a rope, boy had tried swinging while holding
●● Lightning: > 30 × 106 V.
Chapter
Chapter 3 n Modified 29 nSequence
Rapid ElectricalIntubation
Injury 297297
the wire. Skin wound was not bleeding. Edges showed ●● Circulation: Low voltage causes ventricular fibrilla-
signs of coagulation (Figures 29.2 to 29.5). tion, heart block, bundle branch block, supraventricu-
IP : 196.52.84.10 lar tachycardia, ST changes, atrial fibrillations. Car-
diogenic shock can supervene. High voltage can cause
asystole.
●● Disability: Evaluate for altered mental status, seizures,
visual and auditory disturbances, quadriplegia (ver-
tebral fractures) and cranial nerve deficits (rupture of
tympanic membrane).
●● Obtain targeted history:
a. High voltage or low voltage.
b. Loss of consciousness.
Figure 29.2: Charred wound at the site of contact with wire
c. Duration of contact.
d. Thrown from site or not.
●● Assess for entry and exit wounds.
●● Even if wound looks small, there may be severe un-
derlying injury. Cutaneous injuries may extend from
erythema to full thickness burns. Coagulation and ne-
crosis of deep muscles can occur, while sparing the
skin. Delayed bleeding is possible after the eschar
falls off.
●● Electrocardiography (ECG), computed tomography
(CT) of head for altered mental status, X-rays for mus-
culoskeletal injuries.
●● Complete blood count (CBC), electrolytes, renal func-
tion, cardiac enzymes, blood group and crossmatch.
PREHOSPITAL CARE
At site
●● Turn off current source, prior to accessing the victim.
●● Assess whether pulseless and initiate cardiopulmonary
resuscitation (CPR) as per pediatric advanced life sup-
port (PALS) guidelines.
●● Airway and breathing: Direct injury to the respira- Figure 29.4: This boy was referred to the ED with loss of
consciousness following swinging on a high tension wire. The
tory control center can cause apnea. Tetanic contrac-
skin wound was not bleeding with the edges showing signs of
tions of the respiratory muscles (especially diaphragm) coagulation. He was intubated, after administration of 5 mL/kg
can also cause respiratory arrest. of fluids and Dobutamine for cardiogenic shock.
298298 Section X nIIEnvironmental
Section n Airway Injury
IP : 196.52.84.10
Key Points
ü
1. Arrhythmias are common, leading to cardiac arrest
or cardiogenic shock. Obtain ECG to evaluate for
myocardial damage.
2. CT head to evaluate central nervous system (CNS)
in high voltage injuries.
3. Orofacial injuries could bleed later and should be
advised follow-up.
common errors
û
1. Assuming that tissue and vessels are viable
immediately after injury following high voltage
exposure.
Figures 29.6A and B: Entry wound in the forearm, and exit 2. Assuming that the small size of the external wound
wound on the soles, where the tissues have become charred. determines extent of internal damage.
This boy was accidentally holding a high tension wire while
standing on iron rod (Courtesy: Dr Gunda Srinivas).
30
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Submersion Injury
Figure 30.1: Children’s natural attraction to water enhances their risk of drowning in water bodies (Courtesy: Dr Gunda Srinivas)
Learning Objectives
1. Pathphysiology following submersion injury. 3. Using the PAT to assess a drowning victim.
2. Principles of prehospital care. 4. Steps in management of a drowning victim.
INTRODUCTION PATHOPHYSIOLOGY
Drowning is the leading cause of accidental death of children Submersion results in loss of normal breathing patterns,
in industrialized countries.1 In these countries, it has been panic and laryngospasm. Apnea and pulmonary aspiration,
noted that the site of drowning was bathtubs for infants, swim- which follow, lead to hypoxemia.6 The resultant hypercar
ming pools for children between 1 and 4 years of age, and bia, hypoxia and acidosis lead to circulatory arrest and
natural collection of water in older children (Figure 30.1).2 multiorgan failure.
Drowning is the result of respiratory impairment from Loss of surfactant, atelectasis, acute lung injury, pulmo-
submersion or immersion in a liquid.3,4 The presence of nary edema, intrapulmonary shunting and ventilation perfu-
liquid/air interface at the entrance of the airway prevents sion mismatch are some of the causes of respiratory failure.
the victim from breathing air. The victim may live or die Prolonged hypoxia, severe peripheral vasoconstriction,
after this event. Despite the outcome, he is defined as be- intravascular fluid loss, extravascular fluid shifts, brady-
ing involved in a drowning incident. The Utstein statement cardia and ventricular fibrillation are perhaps the common-
recommended that the term near-drowning should not be est causes of cardiac arrest.7,8
used.4 It has also de-emphasized the classification based on
the nature of submersion fluid viz salt water versus fresh
water.4 Although there are differences that have been re- Prehospital Management
ported in laboratory conditions, they have not been found Though there are no modifications to the standard ba-
clinically significant. sic life support maneuvers, some precautions have been
300 Section X n Environmental
Section II n Airway Injury
considered appropriate for cardiopulmonary resuscitation ●● If airway is maintainable and the child has respira-
(CPR) in drowning victims.9 tory distress, provide supplemental oxygen using the
Bain circuit.
IP : 196.52.84.10
Recovery from Water ●● Early use of continuous positive airway pressure
(CPAP) is helpful in reversing hypoxia secondary to
●● Remove from water immediately. the capillary leak in the alveoli.
When rescuing the victim, the rescuer should reach the ●● If the airway is not maintainable and breathing is inad
victim at the earliest, while being fully aware of per- equate, initiate bag-valve-mask ventilation.
sonal safety.
Plan early intubation using ICP precautions, if airway
●● Routine spinal stabilization is not recommended, un- is unprotected, respiratory failure, cardiogenic shock or
less spinal injury is suspected.10 hypotension is identified.
History of diving, use of water slide, signs of injury
or alcohol intoxication suggest the need for spinal im-
Circulation
mobilization.
Ù
Plan smaller aliquots of NS (5–10 mL/kg).
Provide Cardiopulmonary Resuscitation
Treatment should be based on the guidelines provided by ●● Due to the risk of pulmonary edema secondary to acute
the pediatric advanced life support (PALS) and the ad- lung injury or myocardial dysfunction, avoid adminis-
vanced cardiac life support (ACLS) algorithms.9 tering more than 20 mL/kg.
●● At any point during bolus therapy, if signs of pulmo
Ù
Attempts to remove water from the air passages by
nary edema develop or worsen, initiate an appropriate
inotropic agent and plan intubation.
abdominal thrusts or Heimlich maneuver are potentially
dangerous and are contraindicated.11,12 Ù
If shock persists after intubation, AVOID further
fluids unless history is suggestive of hypovolemia.
CASE SCENARIO 1 Occasionally, torrential bleeding from a scalp injury
can lead to hypovolemic shock.
1-year-old infant, was found unresponsive after acci-
dentally falling into a bucket of water (Figure 30.2).
Disability
●● Treat GTC seizures, if identified.
●● Eye signs of non-convulsive status epilepticus if noted,
suggest severe shock or hypoxia. Treatment should be
targeted towards early intubation and shock correction.
If eye signs persist, the SE protocol may be implement-
ed cautiously.
●● Take ICP precautions when intubating a drowning vic-
tim. Drowning victims have features of hypoxic isch-
emic encephalopathy.13
A secondary survey, is performed for other injuries
such as head trauma, abrasions, lacerations or contusions.
Submersion in a bathtub should raise a suspicion of
child abuse. Teenage drowning is frequently associated
Figure 30.2 Physiological status: Stridor with respiratory with illicit drug or alcohol abuse14 and appropriate toxicol
distress, pulmonary edema and shock. ogy tests may be warranted.
ChapterRapid
Chapter 3 n Modified 30 n Submersion Injury
Sequence Intubation 301 301
●● All victims of submersion should be observed for at 2. Karch SB. Pathology of lung in near-drowning. Am J
least 4–6 hours even if they do appear hemodynami- Emerg Med. 1986;4:4.
cally stable on arrival. 3. Karpovich PV. Water in the lungs of drowned animals.
IP : 196.52.84.10 Arch Pathol Lab Med. 1933;15:828.
●● Electrocardiography (ECG) and blood gas determina
tion should be performed as soon as possible. 4. Idris AH, Berg RA, Bierens J, et al. Recommended
●● Victims with respiratory and other organ dysfunction guidelines for uniform reporting of data from drowning:
the “Utstein style” Resuscitation. 2003;59:45-57.
symptoms, decreased oxygen saturation and altered
5. Hoff BH. Multisystem failure: a review with special
sensorium, require monitoring in the intensive care
reference to drowning. Crit Care Med. 1979;7:310.
unit (ICU).
6. Karch SB. Pathology of heart in near-drowning. Am J
Severe bradycardia and intense vasoconstriction as Emerg Med. 1985;109:76.
sociated with marked hypothermia may make victims 7. Lunt DW, Rose AG. Pathology of human heart in drowning.
appear dead, but resuscitative attempts should not be Arch Pathol Lab Med. 1987;111:939.
abandoned.13,15,16 8. American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. IV-133-135. Part 10.3: Drowning.
Key Points
ü
1. Prevention can reduce the incidence of drowning.17
Circulation. 2005;112:24.
9. Watson RS, Cummings P, Quan L, et al. Cervical spine
2. Immediate and appropriate bystander CPR and injuries among submersion injury. Pediatrics.1994;94:137-42.
early basic life support (BLS) care can improve 10. Rosen P, Stoto M, Harley J. The use of the Heimlich
survival.19,20 maneuver in near drowning. Institute of Medicine Report.
3. Improved outcomes, if rescue breathing is provided J Emerg Med. 1995;13:397-405.
even before the victim is pulled out of water. 11. Sarnaik AP, Preston G, Lieh-Lai M, et al. Intracranial
4. Routine cervical spine stabilization is not pressure and cerebral perfusion pressure in near-drowning.
Crit Care Med. 1985;13:224.
necessary.
12. Howland J, Hingson R. Alcohol as a risk factor for
drowning A review of literature (1950-1985). Accid Anal
common errors
û
1. Attempts to remove water from the air passages
Prev. 1988;20:19.
13. Kyriacou DN, Arcinue EL, Peek C, et al. Effect of
immediate resuscitation on children with submersion
by abdominal thrusts or Heimlich maneuver are injury. Pediatrics. 1994;94:137-42.
potentially dangerous and are contraindicated. 14. Siebke H, Rod T, Breivik H, et al. Survival after 40
2. Failure to provide oxygen with a flow inflating minutes; submersion without cerebral sequeae. Lancet.
ventilation device. 1975;1(7919)1275-77.
3. Failure to recognize that respiratory distress could 15. Southwick FS, Dalglish PH Jr. Recovery after prolonged
be due to cardiogenic or non-cardiogenic pulmonary asystolic cardiac arrest in profound hypothermia. A case
edema. report and literature review. JAMA. 1980;243:1250-53.
16. Thompson DC, Rivara FP. Pool fencing for preventing
drowning in children. Cochrane Database Syst Rev
REFERENCES 2000;(2):CD001047.
1. Rowe MI, Arango A, Allington G. Profile of pediatric 17. Quan L, Wentz KR, Gore EJ, et al. Outcome and predictors
drowning victims in a water-oriented society. J Trauma. of pediatric submersion victims receiving prehospital care
1977;17:587. in King County, Washington. Pediatrics. 1990;86:586-93.
Section XI
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Special Topics
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31
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Gastrointestinal Bleeding
Learning Objectives
1. Approach to gastrointestinal bleed. 3. Evidence-based approach to therapeutic
2. Cases illustrating common presentations interventions.
of gastrointestinal bleeds.
APPROACH TO GI BLEEDING IN THE ED ●● Ranitidine: IV—1 mg/kg/dose (max 50 mg) 6–8 hourly
Oral 2–4 mg/kg/dose (max 150 mg) 8–12 hourly.
Airway and Breathing ●● Omeprazole: IV— 2 mg/kg/dose (max 80 mg) stat for-
IP : 196.52.84.10
●● Provide supplemental oxygen using non-rebreath- ward by 1 mg/kg (max 40 mg) 8–12 hourly.
ing mask. Oral: < 3 year: 10 mg 12 hourly, > 3 years: 20 mg 12
●● Insert nasogastric tube. hourly. Sucralfate: 500 mg 6 hourly.
●● Plan to intubate if airway is compromised. Sucralfate:
●● 1 month–2 years: 250 mg Q 4–6 hourly.
Circulation
●● 2–12 years: 500 mg Q 4–6 hourly.
Simultaneously secure 2 vascular lines, collect blood for ●● 12–15 years: 1 g Q 4–6 hourly.
grouping and cross matching, Hb, CBC, coagulation pro- ●● Somatostatin and octreotide are not routinely recom-
file and LFT. mended for patients with acute ulcer bleeding7.
●● Perform the rapid cardiopulmonary cerebral assessment. ●● Order chest X-ray (CXR), ultrasonogram.
●● Connect pulse oximeter and cardiac monitors. ●● Request for an emergency endoscopy after stabilization.
●● Infuse first bolus of RL/NS (20 mL/kg). Continue fluid
bolus until therapeutic goals of shock are resolved. Case Scenario 2
●● Establish etiology by careful history, physical exami- A 4-year-old girl with fever for 5 days has been afe-
nation (in this child, look carefully for signs of cardiac brile since morning. She has vomited several times and
failure, infective endocarditis). Monitor carefully for the last 2 episodes were coffee ground in color. She has
signs of pulmonary edema and myocardial dysfunction been complaining of severe abdominal pain. While she
secondary to fluid therapy since this child has RHD. was being transferred she had become lethargic.
●● Catheterize and monitor urine output.
●● Monitor hematocrit every 2–3 hour, until bleeding stops
and later 4–6 hourly (maintain hematocrit at 30%).
●● Arrange for blood transfusion if hemoglobin (Hb) <
7–8 g/dL.
●● If 1 unit of blood is needed every 2 hours, massive
transfusion protocol is implemented to avoid coagu-
lopathies.
Ù
Massive transfusion protocol
• For every 3 units of RBC, 2 units of FFP are trans
fused.
• For every 5 units of RBC, 1 unit of platelets is
transfused. Figure 31.3 Physiological status: Airway maintainable,
• Goal of blood transfusion: HCT of 21–24 or Hb effortless tachypnea/shock/altered mental status (probable
of 7–8 g/dL. etiology: severe dengue).
• Transfuse whole blood based on the presence of
continued bleed. Once bleeding stops, transfuse Resuscitation and specific management (See Chapter on
packed cells. Dengue) (Figure 31.3).
till date, except for admission in the newborn period Gastric Lavage
for jaundice. He had received an exchange transfusion
during his stay in the IP
NICU (Figure 31.4). Use normal saline (room temperature) if needed. Chilled
: 196.52.84.10 or ‘iced’ saline does not stop bleeding and may cause cen-
tral hypothermia, particularly in young infants.
Pharmacologic Management of
Portal Hypertension
Pharmacologic therapy10 to decrease portal pressure may
be considered in patients with continued bleeding.
Vasopressin and its analogues act by increasing
splanchnic vascular tone thereby decreasing portal blood
flow.
1. Terlipressin:11
Dose: Administer 0.04 mg/kg IV (bolus) followed by
Figure 31.4 Physiological status: Airway stable/Tachypnea/ 0.02-0.04 mg/kg, every 4–6 hours till a bleeding free
Tachycardia with hypotensive shock. (probable etiology: extra
interval of 24–72 hours is achieved.
hepatic portal hypertension with variceal bleed8).
It is less cardiotoxic than vasopressin and is the
●● Take care of the ABCs. drug of choice in variceal bleed. It is more effective
●● CBC, Hb, grouping, cross matching, Dengue serology, than endoscopic injection sclerotherapy (EIS), safer
electrolytes, sugar, urea and creatinine. than vasopressin in combination with nitroglycerin
●● Coagulation profile: and EIS. It also improves survival. However, continu-
– Elevated PT indicates coagulopathy (i.e. dissemi- ous infusion can cause necrosis.
nated intravascular coagulation) or profound impair- 2. Octreotide11,12 (Synthetic analogue of somatostatin)
ment of liver synthetic function. Dose: Loading dose of 1 μg/kg IV over 30 minutes,
– Prolonged aPTT indicates hemophilia or coagulopathy. followed by 0.5 μg/kg/h. Its high cost, propensity to
●● Order LFT. cause nausea, flatulence, malabsorption and bowel
– Increased aspartate aminotransferase and alanine ischemia should be taken to consideration.
aminotransferase enzyme levels are suggestive of 3. Vasopressin11
portal hypertension with liver disease.
Dose: 6 U/kg in 50 mL at 1-5 mL/h. The drug has a
half-life of approximately 30 minutes (Vasopressin 1
Fluid Therapy mL = 20U).
In most children with extrahepatic portal hypertension and Its use is limited by side effects such as vasoconstric
normal hepatic synthetic function, bleeding stops sponta- tion, impairment of cardiac function and perfusion
neously.9 to the heart, bowel and kidneys. It also exacerbates
Caution: Aggressive fluid resuscitation can increase risk of fluid retention.
rebleed due to high venous pressure.
Endoscopy
Introduce a Nasogastric Tube ●● The site of upper GI bleeding can be identified in
90% of cases, when endoscopy is performed within
Placement of a nasogastric tube (NGT) helps to remove 24 hours. Emergency sclerotherapy can also be per-
blood from the stomach. It prevents development of en- formed if needed. However, it should be undertaken
cephalopathy in cirrhosis and also helps to monitor recur- after correction of coagulation disorders and hemody-
rence of bleed. namic instability.
308 Section XI n Special Topics
●● Endoscopic variceal ligation is currently considered a ●● Order cryoprecipitate if plasma fibrinogen is less than
superior option to endoscopic sclerosis since, compli- 1 g/L, although there is no clear threshold for clinically
cations are rarer with the former modality. significant hypofibrinogenemia.
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●● In patients who continue to bleed despite pharmacologic ●● Uncontrolled massive bleeding, unresponsive to con-
and endoscopic methods to control hemorrhage, a Seng- ventional blood component therapy: Consider rFVIIa,
staken-Blake more tube may be placed to stop hemorrhage (dose: 100 μg/kg). A repeat dose may be given after an
by mechanically compressing esophageal and gastric va- interval of 30 minutes to 1 hour. The same dose may be
rices (mechanical tamponade). It poses a particularly high repeated at an interval of 1–4 hours until cessation of
risk for pulmonary aspiration and the tube is not well tol- bleeding has been achieved.14
erated in children without significant sedation. ●● Simultaneously treat underlying cause.
The etiological factors associated with upper gastroin
Surgical Procedures that Divert Portal Blood testinal bleeding vary with age.15,16
Flow and Decrease Portal Pressure
●● A transjugular intrahepatic portosystemic shunt (TIPS) Infancy–1 Year
is a method by which a stent is placed by an interven- 1. Esophagitis, gastritis.
tional radiologist between the right hepatic vein and the 2. Severe dengue (see Chapter on Dengue).
right or left branch of the portal vein. It aids providing 3. Stress ulcer: GI bleeds in infants admitted for burns,
temporary relief in children with portal hypertension. It sepsis, raised ICP, head injury, encephalitis and gas-
is particularly useful in children needing liver transplan- troesophageal reflux disease (GERD).
tation. However, the TIPS procedure may precipitate 4. Mallory-Weiss tear: Fresh bleed following repeated
hepatic encephalopathy and is prone to thrombosis. retching is suggestive of esophageal tear (Mallory-
●● Recent studies indicate that a combination of endo- Weiss syndrome).
scopic sclerotherapy with β-blockers is far superior 5. Vascular malformation.
than any other form of treatment for the prevention of 6. GIT duplication.
recurrence of UGI bleeding. 7. Malrotation.
Coagulopathy 1–12 Year
IV Vitamin K, cryoprecipitate, FFP, recombinant fac-
1. Severe dengue (see Chapter on dengue).
tor VIIa and platelet transfusions are some of the in-
2. Esophageal varices due to extrahepatic portal hyper-
terventions, which are useful in controlling bleeds due
tension or cirrhosis with portal hypertension.7
to coagulopathy secondary to hepatic dysfunction and
thrombocytopenia.13,14 a. Liver disease (hepatic cause for portal hyperten-
sion like cirrhosis).
●● Prolonged PT–INR is diagnostic of vitamin K defi- b. Neonatal umbilical sepsis or umbilical vein cath-
ciency. eterization (extrahepatic portal hypertension).
●● Administer vitamin K: 0.3 mg/kg IV over 1 hour (max 3. Esophagitis, gastritis, peptic ulcer disease.17 Recur-
10 mg). rent abdominal pain is suggestive of peptic ulcer.
●● Infuse 10 mL/kg of FFP.
4. Stress ulcer: Stress related GI bleed in critically ill
●● Administer Ranitidine (2 mg/kg/dose) intravenously to
children being managed in the ED.
reduce risk of bleeding from gastric erosions.
5. Mallory-Weiss tear (see above).
Disseminated Intravascular Coagulation 6. Drug intake: non-steroidal anti-inflammatory drugs
(NSAIDS) and steroids are the commonest drugs
The British Committee for Standards in Haematology, causing gastritis.
Blood Transfusion Task Force Guidelines for the use of 7. Bleeding tendency: DIC manifests as GI bleed, bleeds
fresh frozen plasma, cryoprecipitate and cryosupernatant- from IV site, skin, hemarthrosis, etc. in seriously ill
2004 suggest that fresh frozen plasma and platelets are in- children.
dicated when there are demonstrable multifactor deficien-
8. Family history of bleeding disorder: Von Willebrand’s
cies associated with severe bleeding and/or DIC.
disease, hemophilia.
Chapter 31 n Gastrointestinal Bleeding 309
9. Odynophagia with oral candidiasis is suggestive of for less than 24 hour. Barium study is contraindicated
candidal esophagitis ( HIV). if perforation is suspected. Air contrast enemas have
IP : 196.52.84.10 also been used with similar success rates, with air en-
Case Scenario 4 emas requiring less radiographic exposure, but having
slightly higher perforation rates. Enemas with saline
A 6 month infant is rushed to the ED with incessant
contrast require experienced sonographers.
cry accompanied by episodes of straining. He has
vomited his feeds and is passing blood and mucus Evaluate for other etiologies of lower GI bleed
along with stools (Figure 31.5).
1. Infants
●● Anal fissure—presents with constipation and pain-
ful defecation.
●● Intussusception.
●● Infective colitis—passing small quantities of blood
and mucus in the stool, crampy lower abdominal
pain and tenesmus.
●● Midgut volvulus.
●● Meckel’s diverticulum.
●● Vascular malformations.
●● Coagulation disorders.
2. Older children
●● Anal fissure: Pain during defecation with blood-
streaked stools.
●● Rectal prolapse: Associated with mass seen per
Figure 31.5 Physiological status: Airway stable/Tachypnea/
Tachycardia and shock (possible etiology: intussusception).
rectum.
●● Bacterial enteritis: Dysentry, fever and crampy low-
er abdominal pain.
Management ●● Polyps—painless rectal bleeding with a large amount
of bleed per rectum.
●● Provide O2 using a non-rebreathing mask.
●● Gangrenous bowel due to volvulus is character-
●● Introduce NGT.
ized by bilious vomiting, abdominal distension and
●● Secure two lines and administer RL (20 mL/kg) bo-
bleeding per rectum.
lus. Repeat cardiopulmonary cerebral assessment and
●● Meckel’s diverticulum: Intermittent, painless hema-
continue boluses until therapeutic goals of shock are tochezia.
resolved. ●● Vascular malformations: Painless, massive bleed.
●● Since, the etiology of shock is hypovolemia due to GI ●● Bleeding disorder: GI bleed will be associated with
loss up to 120 mL/kg may be needed in the initial hours bleeds from other sites.
of resuscitation. ●● Inflammatory bowel disease: Associated with chron-
●● Collect blood for grouping crossmatching, RFT, LFT, ic diarrhea and failure to thrive.
coagulation profile, CBC and sepsis screen.
Physical examination in acute GI bleed, which can sug-
●● Arrange for blood.
gest the etiology
●● X-ray abdomen can help identify intestinal obstruction
●● Request for color Doppler ultrasonography. It helps to ●● Examine ears, eyes, nose and throat: Look for epistaxis,
diagnose intussusception. nasal polyps and oropharyngeal erosions from caustics
●● Involve pediatric surgeon and radiologist urgently and other ingestions.
●● Order enema studies.18 ●● Look for abdominal surgical scars and elicit the indica-
Barium enema reduction have traditionally been used tion for surgery.
with success rates of 50% –90%. Rate of detection of ●● Abdominal tenderness with or without a mass, raises
intussusception is more when symptoms are present the suspicion of intussusception or ischemia.
310 Section XI n Special Topics
●● Hepatomegaly, splenomegaly, jaundice or caput medu- longer; the most common etiologies are juvenile colo-
sae suggests liver disease and subsequent portal hyper- rectal polyps and non-specific proctitis.
tension. IP : 196.52.84.10
●● Splenomegaly is suggestive of portal hypertension; but
following a massive bleed, the spleen may contract and
hence may be impalpable. (Smith-Howard syndrome).
Key Points
ü
1. Find out whether GI bleed is localized or systemic.
●● Inspect perianal area: Look for fissures, fistulas, skin 2. Identify whether the bleed is secondary to varices or
breakdown or evidence of trauma. clotting defects.
●● Look for evidence of child abuse, such as perianal tear- 3. Control bleed based on etiology.
ing, tags or irregularities in anal tone and contor. 4. Transfuse appropriately.
●● Specifically include bowel sound frequency in the ab- 5. Treat coagulation defects.
dominal examination. Hyperactive bowel sounds are
more common in upper GI bleeding.
●● Examine skin for evidence of systemic disorders, such
as inflammatory bowel disease: intermittent maculo-
common errors
û
1. Children with epistaxis or oropharyngeal bleeding
papular rash. or hemoptysis often vomit bright red blood.
●● Henoch-Schönlein purpura: palpable purpura in both 2. Failure to recognize intussusception leading to late
lower limbs and Peutz-Jeghers polyposis. referral to the surgeon.
●● Digital rectal exam should be performed in the OT 3. Delay in resuscitation in an effort to search for the
under sedation. It may reveal polyps, masses or oc- etiology.
cult blood.
References
Workup
1. Arain Z, Rossi TM. Gastrointestinal bleeding in children:
Laboratory Studies An overview of conditions requiring non-operative man-
agement. Semin Pediatr Surg. 1999; 8 (4):172-80.
●● Confirm presence of blood by requesting for perox- 2. Erlich F. Gastrointestinal bleeding. In:Fleisher GR, Lud-
ide based tests such as the hemoccult or hematest to wig S, (Eds). Synopsis of Pediatric Emergency Medicine.
identify lower GI bleeding and gastroccult for upper Baltimore: MD Lippincott Williams and Wikins; 1996. pp.
GI bleeding. 100-05.
●● Red meat, iron and peroxidase containing vegetables 3. Arora NK, Ganguly, S Mathur P, et al. A Upper gastroin-
testional bleeding: Etiology and Management. Ind JI Pedi-
(e.g. turnips, horseradish, broccoli, cauliflower and
atrics. 2002;69 (2):155-68
cantaloupe) can give false-positive results.
4. Berkowitz C. Gastrointestinal bleeding. In: Pedaitrics:
A Primary Care Approach. Philadelphia, PA: WB Saun-
Imaging Studies ders; 1996.
●● Meckel scan, using technetium-99m pertechnetate 5. Peters JM. Management of Gastrointestinal Bleeding in Chil-
helps to identify ectopic gastric mucosa. dren. Curr Treat Options Gastroenterol. 2002;5(5):399-413.
●● Push enteroscopy is a long endoscope that is placed 6. Thapa BR, Bansal D.Management of upper Gastrointes-
through the mouth into the jejunum. It can reach about tinal bleeding in children.Ind JI Practical Pediatrics. 200;
4:398-416.
160 cm beyond the ligament of Treitz. One study has
shown that push enteroscopy identified a large num- 7. Alan N Barkun, Marc Bardou, Ernst J, Kuipers, et al.
ber of mucosal lesions that could not be identified by a International Consensus Upper Gastrointestinal Bleed-
standard endoscope. ing Conference Group. International Consensus Rec-
ommendations on the Management of Patients With
●● Colonoscopy should be performed only when the pa-
Nonvariceal Upper Gastrointestinal Bleeding. Ann In-
tient is stable and when blood and feces will not con-
tern Med. 2010;152 (2):101-13.
ceal proper visualization.
●● Sigmoidoscopy19 is indicated in children who have 8. Molleston JP. Variceal bleeding in children. J Pediatr Gas-
troenterol Nutr. 2003;37(5):538-45.
symptoms of chronic lower GI bleeding for 1 year or
Chapter 31 n Gastrointestinal Bleeding 311
9. Comar Kevin M,Sanyal AJ. Portal hypertensive bleeding pediatric patients. Blood coagulation and Fibrinolysis.
Gastroentrol Clin North Am. 2003;32(4):1079-105. 2010;21:354-362.
10. Tatro DS, Borgsdorf 15. Huang CS. Lichtenstein DR. Non-variceal upper gastro-
IPLR, Lopez JR, et al. A to Z Drug
: 196.52.84.10 intestinal bleeding. Gastroentrol Clin North Am. 2003;32
facts. 5th edition. St Louis,MO: Facts and Comparisons;
2005. (4):1053-78.
16. Fox VL. Gastrointestinal bleeding in infancy and child-
11. Frank Shann. Drug Doses; 15th edition, Victoria Austrail-
hood. Gastroentrol Clin North Am. 2000;29(1):37-66.
ia. 2010.
17. Johnson D, L’Heureux P, Thompson T. Peptic ulcer disease
12. Ioannou GN, Doust J, Rockey DC. Systematic review: Ter- in early infancy: Clinical presentation and roentgenograph-
lipressin in acute oesophageal variceal haemorrhage. Ali- ic features. Acta Paediatr Scand. 1980;69(6):753-60.
ment Pharmacol Ther. 2003;17(1):53–64. 18. Henikson S, Blane CE, Koujok K, et al. The effect of
13. E Mileti, P Rosenthal. Management of Portal Hyperten- screening sonography on the positive rate of Enemas for
sion in Children. Curr Gastroenterol Rep (2011); 13(1):10– intussusception. Pediatr Radiol. 2003;33(3):190-93.
16 DOI 10.1007/s11894-010-0151-y.” 19. Mandhan P. Sigmoidoscopy in children with chronic
14. Ampaiwan C, et al. Recombinant-activated factor VII for lower gastrointestinal bleeding. J Paediatr Child Health.
control and prevention of hemorrhage in non-hemophilic 2004;40(7):365-68.
Interpretation of Chest X-rays in
32
IP : 196.52.84.10
Figure 32.1: Interpretation of X-rays in critically ill children is a skill adjunct to clinical acumen and guide therapeutic decisions
(Courtesy: Dr Thangavelu S, Dr Gunda Srinivas)
Learning Objectives
1. Systematic approach to reading an chest X-ray 3. Pearls and pitfalls in interpretation of chest radio
(CXR) in the ED. graphs.
2. Case scenarios illustrating various respiratory
emergencies.
On most occasions, the first responder in the ED who 4. Date and time of taking the X-ray.
is confronted with the need to take life saving decisions 5. Whether right and left side have been documented
based on a chest X-ray is also the least experienced. This correctly.
chapter teaches a structured approach to the interpretation 6. Whether, the X-ray was taken in the anteroposterior
of a chest radiograph in emergency settings (Figure 32.1). or posteroanterior view.
●● The physician who ordered the chest X-ray must see
the film within 5–10 minutes.
Ù
Anteroposterior view:
●● Occasionally, even a delay of 5 minutes would be le- a. A notch in the middle of the clavicle.
thal in scenarios such as pneumothorax, or a displaced b. Lung tissue not seen above the clavicle.
endotracheal tube. In these situations, rapid clinical Posteroanterior view:
assessment and intervention is life saving rather than a. Clavicle will appear straight.
waiting for chest film interpretation. b. Lung tissue will be seen above the clavicle.
Ù
The middle of the diaphragm should correspond to the
IP : 196.52.84.10
anterior end of 5th to the 7th ribs. Anterior end stops short
and the posterior end joins the vertebral column.
Specific Data
1. Tubes: endotracheal tube, tracheostomy tube, chest
tube or rarely pig tail catheter left in pericardial cavity.
2. Lines: external jugular (EJV), internal jugular (IJV),
subclavian lines, PORT-A-CATH (subcutaneously
implantable venous access system) or tunneled lines.
3. Above the diaphragm.
Scan from periphery to center.
– Soft tissue.
Figure 32.2B: Normal PA view – Chest wall.
– Costophrenic angle.
Normal X-ray: In the AP view, there will be a notch in
the middle of the clavicle (Figure 32.2A). No lung tissue – Mediastinum and normal thymus (Figure 32.3).
will be seen above clavicle. When the X-ray is taken in – Cardiophrenic angle.
the inspiratory phase, the anterior end of the 5th rib cor- – Lung tissue.
responds to middle of the dome of diaphragm (marked by – Heart.
horizontal arrow in Figure 32. 2B) (the posterior end of rib 4. Below the diaphragm.
is marked by the vertical arrow). The two vertical yellow – Look for air under the diaphragm
lines indicate the medial end of clavicle and lateral margin – Air fluid levels suggestive of intestinal obstruction.
of vertebrae. If the lines are equidistant on both sides of the – Bowel shadows crowded in the center is indica-
vertebra, it implies that the film has been centered without
tive of ascites.
rotation.
314 Section XI n Special Topics
Figure 32.5
Your Observations
Figure 32.4
Your Observations
Figure 32.6
Figure 32.7A: Oral thrush
Your Observations
Figure 32.7B
CXR: Bilateral extensive opacities.
Diagnosis: This picture can occur in three conditions.
●● Extensive bronchopneumonia.
●● ARDS.
●● Pulmonary edema.
Diagnosis is made based on clinical findings. Picture
shows oral thrush, hence the diagnosis is extensive broncho-
pneumonia with probable immune deficiency. Radiographs,
Both hemithoraces are of the same size. The opacity is ho-
such as the one above, can reveal opacities in the lung. How-
mogeneous with no mediastinal shift.
ever, it cannot pin-point etiology. As in this case, the diagno-
Diagnosis: Consolidation. sis becomes apparent only from clinical history.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 317
Figure 32.8
Your Observations
Figure 32.9
Your Observations
Figure 32.11A
Figure 32.10A: Froth oozing out from ET tube due to
pulmonary edema
Your Observations
Your Observations
Figure 32.11B
Your Observations
Presence of bilateral hilar opacities, in the background of
scorpion sting confirm the diagnosis as pulmonary edema.
But this classical picture may not be seen in all situations. Since the child developed respiratory failure, she was
ventilated. The pneumatocele increased in size.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 319
Figure 32.11C
Your Observations
Figure 32.12
Your Observations
Figure 32.13
Homogeneous opacity in the right base with obliteration
of the costophrenic and cardiophrenic angles. Presence of air
fluid level on the right side suggests the diagnosis of pyo- Figure 32.14A
pneumothorax. Mediastinal shift is not apparent, probably The left hemithorax appears bigger and has greater
due to the thoracostomy. Note the presence of the chest tube. radiolucency (appears more black) compared to the right.
In the background of measles and respiratory distress, Presence of bronchovascular markings and absence of col-
one may anticipate pneumonia or empyema. Training one’s lapsed lung margins favor the diagnosis of obstructive em-
eyes to see what is expected in the clinical backdrop can physema on the left side.
often clinch the diagnosis (Table 32.2).
Table 32.2: X-ray clues to diagnosis
Description Diagnosis
Circular air collection in the Pneumatocele
background of white opacities
Bigger and darker hemithorax Obstructive/compensatory
with bronchovascular emphysema (here opposite
markings lung will be abnormal)
Confined to one lobe with Congenital lobar emphysema
herniation to opposite side
and collapse of the adjacent
lobe
Bigger and darker hemithorax, Pneumothorax
no bronchovascular markings,
collapsed lung margins are
seen Figure 32.14B
Continuous diaphragm sign, Pneumomediastinum This chest X-rays of a different child with similar his-
lifting of the thymic shadow
tory shows similar findings though very subtle.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 321
Figure 32.16A
Figure 32.15A
Figure 32.16B
Figure 32.15 B
Your Observations
Your Observations
The volume of the left lung is more than the right (em-
physematous). The left lower lobe is collapsed with a sharp
margin with herniation of the upper lobe to the right side.
Note the mediastinal shift to the right. The bronchovascu-
Nail in the right lower lobe with segmental collapse of
lar markings in the emphysematous left lung differentiates
the lower lobe.
it from a pneumothorax.
Bronchoscopic removal failed and child developed
Diagnosis: Congenital lobar emphysema of the left upper lobe.
pneumothorax.
322 Section XI n Special Topics
Figure 32.16C
Chest tube was inserted and pneumothorax drained.
Figure 32.17
Your Observations
Figure 32.16D Compare the size, lucency, color, CP angles of both the
hemithoraces. Then look at the mediastinum.
Your Observations Size: The left sided hemithorax appears larger than the
right side.
Color or lucency: Left hemithorax is filled with cyst like
structures (bowel shadows).
Costophrenic (CP) angle: The CP angle on the right is
free, but obliterated on the left.
Mediastinal shift: The mediastinum is shifted to the right.
Other findings: Absence of abdominal gas shadows. The
diaphragm is not visible. Note presence of umbilical artery
and umbilical vein catheters.
Nail removed and pneumothorax resolved. Normal X-ray. Diagnosis: Diaphragmatic hernia.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 323
Figure 32.18
Figure 32.19
Your Observations
Your Observations
Reminder
When evaluating lung fields, four aspects need to be
compared. Both hemithoracis have similar volume. There is no
significant mediastinal shift.
●● Volume of hemithorax.
●● Color or lucency. A homogeneous triangular opacity is seen on both sides
●● Costophrenic angles. with sharp margins suggesting the diagnosis of bilateral
●● Mediastinal shift. lower lobe segmental collapse.
324 Section XI n Special Topics
Figure 32.20
Figure 32.21A
Your Observations
Your Observations
Figure 32.21B
Your Observations
Figure 32.22
Reminder
●● Displacement: Clinical finding that is diagnostic is the
absence of breath sounds on the left side.
●● The radiograph will show collapse of the left lung.
●● Obstruction: Is characterized by resistance, while
ventilating with bag. The radiograph will not show
any change.
●● Pneumothorax is characterized by absent breath sounds
with resonance on percussion on the side of the pathol-
ogy viz pneumothorax.
Repeat CXR after repositioning of ETT. ●● The right hemithorax is bigger and darker than the left.
● ● No bronchovascular markings are seen on the
●● The left lung has expanded. The volume of both lung right side.
fields are normal. The mediastinum is in the midline. ●● Also note the collapsed lung on the right side.
●● There is minimal pleural fluid on the left side. Diagnosis: Right-sided pneumothorax.
●● The ET is now at T4. Still needs to be pulled out.
326 Section XI n Special Topics
Case scenario 20 (Figures 32.23A and B) Case scenario 21 (Figures 32.24A and B)
A 12-year-girl presented with history of fever, hemopt- A 4-year-old boy presented with failure to thrive, breath-
ysis and expectorationIPof:foul
196.52.84.10
smelling yellow sputum. lessness and oxygen dependency since infancy. Two sib-
lings had died earlier with similar history. This child
developed respiratory failure requiring ventilation.
Figure 32.23A
Figure 32.24A
Figure 32.23B
Your Observations
Figure 32.24B
The 2nd chest radiograph shows the development of a
small pocket of air in the right upper and lower zone.
Compare the contour of the diaphragm on both sides.
On the side of the pneumothorax the usual contour is lost.
1. Homogeneous opacity with air fluid level in the right a. The reticulogranular pattern of opacity on both side
lower lobe. suggests the diagnosis of interstitial pneumonia.
2. Also has scoliosis. CT chest confirms lung abscess b. This CXR shows pneumothorax that occurred during
with air fluid level. mechanical ventilation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 327
Figure 32.25
Figure 32.26
Your Observations
Your Observations
Figure 32.27B
Your Observations
Figure 32.27A
Your Observations
1. The cardiothoracic ratio is greater than 0.6 is In lead poisoning, a dense band will be noted in the
suggestive of cardiomegaly. metaphyseal end (lead deposits).
2. The associated pulmonary plethora is diagnostic of The ECHO of this child revealed a low ejection frac
congestive cardiac failure. tion without evidence of anatomical abnormalities. Serum
3. The upper end of humerus, shows cupping, fraying of ionized calcium was 0.7 (low). Serum 25-hydroxyvitamin
metaphyseal ends and widening of physis suggestive D level was low.
of rickets.
Note: When a child presents with seizures, X-ray Diagnosis: Vitamin D deficiency rickets, cardiomegaly
chest can give clues to the etiology of seizures such as and cardiac failure. Treatment with vitamin D and calcium
rickets or lead poisoning. was curative.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 329
IP : 196.52.84.10
Figure 32.28C
Figure 32.28A
Your Observations
Figure A: The normal shape of the heart is preserved, the
cardiophrenic angle is acute with increased pulmonary
congestion.
Whenever CXR shows cardiomegaly, always look
again to see the signs of pericardial effusion as it can be
relieved only by pericardiocentesis.
Diagnosis: Cardiomegaly with CCF.
Figure 32.28B
CXR after pericardial tap. Note the presence of pig tail
The normal shape of the heart is not seen, the cardio-
catheter, which was kept in situ. Also note the change in
phrenic angle is obtuse and pulmonary plethora is not seen.
the shape of the heart and the cardiophrenic angle.
Diagnosis: Pericardial effusion.
Diagnosis: After pericardiocentesis.
330 Section XI n Special Topics
Figure 32.29B
Your Observations
Figure 32.29A
Your Observations
Figure 32.30C
Right hemithorax is wide, more black with collapsed
lung margin suggestive of right pneumothorax. Subcutane-
ous emphysema is also seen in the neck as vertical trans-
lucencies in the neck. Continuous diaphragm sign: pneu-
Figure 32.30A: Child ventilated with bilateral ICD momediastinum.
Figure 32.30D
Figure 32.30B: Coin shadow in the neck with heart and lungs
being normal.
Your Observations
Your Observations
Figure 32.32B
Your Observations
Mediastainal node is seen (arrow). It is probably causing Haziness suggestive of peritonitis, multiple fluid levels
intrathoracic airway obstruction. with air under diaphragm.
Diagnosis: Lymphoma. Diagnosis: Pneumoperitoneum secondary to perforation.
Chapter 32 n Interpretation of Chest X-rays in Critically Ill Children 333
Figure 32.33
Your Observations
Figure 32.34B
Key Points
ü
IP : 196.52.84.10 1. Clinical background should be taken into
consideration, before interpreting X-rays.
2. Stepwise evaluation is mandatory to avoid missing
subtle findings.
3. Scan the X-ray from periphery to center and from
less obvious to obvious radiological finding.
4. Familiarity with normal X-ray films will aid in
recognizing abnormalities.
5. If clinical background and X-ray findings grossly
disagree, repeat the film to avoid simple errors
leading to serious consequences.
Learning Objectives
1. Defining procedural sedation. 3. Pearls and pitfalls in the use of sedative and
2. Steps taken to administer sedation for procedures analgesic drugs.
in the ED. 4. Discharge criteria.
Figure 33.2: Wong-Baker faces pain scale (WPFPS) and faces 1. Obtain history on the present health status, associated
pain scale-revised (FPSR). comorbid conditions, weight, allergies, prior medical
336 Section XI n Special Topics
Physical examination
Airway assessment includes:
1. Neck mobility and length.
2. Ability to open mouth widely.
3. Size of oral cavity.
4. Anatomical jaw abnormalities (e.g. Pierre-Robin syn-
drome, macroglossia).
Figure 33.3: Mallampati classification
5. Ability to protrude the jaw.
6. Keep mouth wide open and evaluate the airway for Table 33.3: Fasting guidelines
ease of assisted ventilation.
Clear Solids/breast
Mallampati classification is useful in predicting dif- Age Non-clear fluids
liquids milk
ficult airways (class III/IV). It is based on whether
Infants 2 hour 4 hour 6 hour
the posterior pharynx can be visualized well or not
(Figure 33.3). Children 2–3 hour 6 hour 6 hour
Chapter 33 n Procedural Sedation and Management of Pain in Children 337
Both assisted ventilation and oxygenation can be dif- Step 3: Measures Which Ensures Safety
ficult in children who have difficult airways. During Sedation in the Emergency Room
Sedation should be IP
performed by anesthesiologists and
: 196.52.84.10 Personnel and Equipment
not by other caregivers for the following categories:
1. The physician who is administering procedural seda-
●● Children assigned a category three or above by ASA tion should be trained in the use of anesthetic drugs.
classification. He/she should be aware of the nature of drugs, ad-
●● Very young infants (less than 6 month). verse events, timing, etc. of the sedative agents.
●● Children with airway abnormalities. 2. The physician must have expertise in recognition
(e.g. chest wall rigidity) and management of adverse
Step 2: Presedation Preparation events during sedation. He/she should also have skills
Fasting in managing the airway.
3. A nurse or physician (not performing the procedure)
The nil per oral (NPO) guidelines have been recommended should be present throughout sedation to observe the
by the ASA to prevent aspiration in the event of loss of child for adverse events until return to baseline status.
protective airway reflexes (Table 33.3). 4. Lighting, oxygen source, suction apparatus and air-
Table 33.4: University of Michigan Sedation Scale (UMSS) way equipment (nasal cannulas, nasal/oral airways,
bag/mask devices, laryngoscope blades, endotracheal
Score Level of sedation tubes) must be available.
0 Awake and alert 5. The heart rate, blood pressure, pulse oximeter and
I Minimally sedated: Tired/sleepy, appropriate preferably capnography to monitor nasal end tidal car-
response to verbal conversation and/or sound bon dioxide should be connected to patient through-
II Moderately sedated: Somnolent/sleeping, easily out the procedure.
aroused with light touch or a simple verbal 6. Emergency resuscitation drugs (e.g. epinephrine), iso-
command tonic intravenous fluids (normal saline) and reversal
III Deeply sedated: Deep sleep, arousable only with agents (naloxone, flumazenil) should also be readily
significant physical stimulation available.
IV Unarousable
Monitoring
1. Avoid solids for 6 hours and clear fluids for 2 hours in 1. All children undergoing procedural sedation should
healthy patients undergoing elective surgery. be closely monitored till they return to baseline alert-
2. Carbohydrate containing fluids may safely be given, ness and level of functioning according to established
up to 2 hours prior to sedation for malnourished chil- guidelines.13
dren with poor glycogen reserves.8 2. Monitoring should include frequent blood pressure,
Studies have noted that more than a third of chil- heart rate and respiratory rate measurements along
with continuous pulse oximetry.
dren who underwent sedation, fasted less than 4 hour,
3. The monitoring personnel should have complete ac-
for solids, but still had no higher incidence of ad-
cess and non-obstructed views of the child undergo-
verse effects or aspiration.9 The incidence of adverse
ing sedation.
events had not significantly increased when fasting 4. Pulse oximetry is useful in detecting hypoxia, but its
guidelines were not observed.10 Prolonged fasting (6 accuracy may be impeded by movement, decreased
hour, instead of 2 hours for liquids) offered no ad- circulation, temperature changes, etc. Since pulse
ditional benefit and did not reduce risk.11,12 An urgent oximeters do not detect very low saturations (less
procedure may override NPO guidelines for sedation than 75%), it may not be useful in children with cy-
provided, the airway is protected. Factors such as anotic heart disease. During respiratory depression,
gastroesophageal reflux, young infants (< 6 month), pulse oximetry may initially be normal, especially in
severe systemic illness and developmental delay may healthy adolescents as the respiratory reserve may be
increase risk of aspiration. adequate to meet the oxygen demands. Hypoventila-
338 Section XI n Special Topics
tion often precedes hypoxia in children undergoing Table 33.5: Specific indications for sedatives/analgesics
procedural sedation.
Indication Sedative/analgesic
5. Respiratory depression may be recognized by capnog-
IP : 196.52.84.10 Non-invasive painless procedures Chloral hydrate,
raphy earlier than pulse oximetry.14,15 Capnography
(imaging, EEG) midazolam, pentobarbital,
has also been noted to be superior to clinical observa- thiopental, propofol
tion in the detection of hypoventilation.16 Ultra short painful procedures Morphine*, fentanyl
6. Supplemental oxygen in the absence of oxygen re- (lumbar puncture, chest tube
quirement can be deleterious as it may prevent the insertion)
early detection of respiratory depression.17,18 There- Brief procedures (laceration Ketamine*, fentanyl
fore, routine supplemental oxygen is not recom- repair, fracture reduction, central
mended. venous line placement)
7. The depth of sedation could be assessed using sev- Dental procedures Nitrous oxide
eral sedation scales (Ramsay sedation scale, Uni- *Drugs often administered in combination with sedatives (e.g. midazolam)
versity of Michigan sedation scale) and the severity 3. Prior sedative experience of the child.
of pain from pain scales depending on age (Table 4. Required depth of sedation (Is there a need to be ab-
33.4).19 solutely still?).
5. Specific risk factors (ketamine contraindicated in head
8. Repeated assessment of sedation scores have been
found to be beneficial in reducing risks associated trauma).
with sedation.11 6. Experience and familiarity of the sedation provider
with the various drug options.
Step 4: Choice of Drugs Considerable differences may exist between individual
Description of sedatives/analgesics responses to various sedatives and the drug doses should
be titrated to effect.
A host of factors influence the decision making in drug
selection during procedural sedation. The choice of drugs 1. Painless procedures that do not require intravenous
is dependent upon: access, oral or intranasal routes may be utilized for
anxiolysis.
1. Age. 2. The specific indications for the various sedatives and
2. Type of procedure (painful vs painless, short vs long). the doses and in which these drugs are recommend-
ed have been highlighted (Tables 33.4 to 33.6). The Chloral Hydrate: 30–100 mg/kg/dose (max dose 2 g).
doses have been adopted the consensus guidelines on
sedation and analgesia
IP : in critically ill children.20
196.52.84.10 Midazolam
Even though all benzodiazepines are useful, diazepam and
Sedatives lorazepam are longer acting than midazolam (preferred
Chloral Hydrate benzodiazepine for procedural sedation).
Chloral hydrate (active ingredient trichloroethanol) can be Midazolam acts through GABA and produces hypnosis
given both orally and rectally. It is rapidly absorbed from and anxiolysis. The advantages of midazolam include its
gastrointestinal tract (almost 100%). Its sedative effect short duration and the convenience of administration by
which occurs within 25 minutes, lasts for 8–12 hours. additional routes. It can be repeated IV every 3 minutes.
It has a rapid onset of action, with duration of action up
Chloral hydrate can cause myocardial depression and to 30–60 minutes. Intranasal or sublingual midazolam is
arrhythmias (Table 33.7). usually given at a higher dose (0.2–0.4 mg/kg). Midazo-
Table 33.7: Adverse events of sedatives lam produces anxiolysis in 15–20 minutes orally and 5–10
minutes intranasally. Midazolam is unpleasant orally and
Sedative Adverse event causes burning sensation when given via nose (preserva-
Chloral hydrate Myocardial/respiratory depression (can be tive—benzyl alcohol).
delayed)
The side effects include paradoxical excitement,
Ketamine Apnea, delirium, increased secretions, hypotension or bradycardia, respiratory depression
laryngospasm, increased IOP/ICP
or apnea.
Midazolam Paradoxical excitement, hypotension,
bradycardia, respiratory depression Even though midazolam alone produces sufficient
Pentobarbital Respiratory depression, apnea and anxiolysis, other sedatives such as pentobarbital (imaging
hypotension with rapid administration studies) or ketamine (fracture reduction, laceration repair)
are usually given in addition.
Morphine Respiratory depression, vomiting
Fentanyl Hypotension, bradycardia, respiratory Intravenous midazolam in conjunction with ketamine
depression, rarely chest wall rigidity is the most common combination regimen utilized in the
Etomidate Local pain on injection, thrombophlebitis, United States for procedural sedation. Midazolam pro-
myoclonus vides no analgesia. Even though combination regimens are
Propofol Bradycardia, hypotension, dose- used frequently and have been found to be safe, additional
dependent respiratory depression and sedatives (e.g. narcotics) may increase the likelihood of
apnea respiratory depression/apnea.
Avoid chloral hydrate in children who are on tri Midazolam: 0.01–0.1 mg/kg IV (max dose 3 mg/dose).
cyclic antidepressants and phenothiazines (The combi-
nation has been noted to have a greater predisposition to
Barbiturates
ventricular dysrhythmias).
Higher doses may result in respiratory depression
Thiopental
or airway obstruction, which could be fatal.21 Thiopental has a short duration of action (5–10 minutes).
It is still widely used and could be dangerous owing Thiopental should not be given in volume depleted
to its long half-life and side effects occurring beyond the children. It can cause hypotension due to vasodilata
period of observation. tion and negative inotropic effects on the heart.
When children are discharged after chloral hydrate, Rectal administration is effective, but the prolonged
parents should be advised to watch for possible delayed duration of action (up to 90 minutes) limits its use.
side effects, including respiratory depression. Thiopental: 25–50 mg/kg IV.
340 Section XI n Special Topics
Pentobarbital
Pentobarbital is a rapidly acting barbiturate with an onset
Ù
Side effects include bradycardia, hypotension, dose-
IP : 196.52.84.10
of action within 3–5 minutes and duration of action of 30– dependent respiratory depression and apnea. Pro
60 minutes. longed use of propofol for more than 48 hours has been
It is widely used for imaging studies (e.g. MRI) since it associated with metabolic acidosis.
provides prolonged sedation with sufficient depth to allow
It is useful in ultra short painless procedures (e.g. spi-
the child to remain still for an extended period of time.
nal tap). Propofol is usually given with a narcotic for pain-
Ù
Major side effects include respiratory depression and
ful procedures. Even though it is gaining popularity, its use
is restricted to anesthesiologists in many medical facilities
hypotension. due to its cardiovascular side effects.
Pentobarbital: 2 mg/kg IV, (max 6 mg/kg). Propofol: 1.5–3 mg/kg IV bolus followed by 50–100
μg/kg maintenance.
Ketamine
Etomidate
The rapid onset (1 minute), short duration of action,
(15–30 minutes), the predictable excellent analgesia and Etomidate acts by altering chloride conductance on the
sedation and the ability to be administered through mul- GABA receptors. It can be administered intravenously and
is available as a mixture with propyl glycol. It is rapid in
tiple routes have made ketamine the most popular drug
onset and produces excellent sedation and amnesia. Etomi-
for painful procedures. Ketamine produces ‘dissociative
date is very safe with an excellent cardiovascular profile.
sedation,’ a cataleptic state characterized by significant
analgesia and amnesia. It is postulated to act on the thal-
amic/limbic systems in mechanisms not clearly under-
Ù
Side effects include pain at site, thrombophlebitis
stood. Ketamine offers an ‘all or none phenomena’ in and myoclonus. Suppression of endogenous steroid
terms of sedation and does not have a dose related esca- production has been noted with its use.
lating effect. As an effective bronchodilator, it is safe and
indicated in asthmatic children. Etomidate: 0.3 mg/kg IV.
Side effects include apnea if used in infants less
than 3 months, increased secretions, laryngospasm, Management of Pain
transient nystagmus, hallucinations during recovery Pain in children is often overlooked and frequently under-
and seizures in children at risk. Unlike other sedatives, treated. Adequate management of pain will improve com-
ketamine may increase heart rate and blood pressure pliance of children, enhance the quality of outcome of the
due to its effect on the sympathetic nervous system. procedure performed and improve parental satisfaction.
Avoid ketamine when raised intracranial or intraocu Opioids are the mainstay in the management of severe
lar pressure is suspected. pain in the emergency room. When dosed correctly with
Ketamine: 1–2 mg/kg IV. the understanding of duration, side effects and interactions
with other sedatives, they can be safe and effective in the
treatment of pain.
Propofol
Propofol, a GABA agonist, is a sedative and hypnotic. It Morphine
is rapidly effective and has an ultrashort duration of action
Morphine is the most commonly used narcotic due to
(5–10 minutes). It has antiemetic and antiepileptic prop-
its quick onset, predictable duration and adequate safety
erties. Since propofol can decrease intracranial pressure
profile. Its half-life is 2–3 hours. In children < 3 months,
(ICP) and cerebral metabolic rate, it is used in head trauma
morphine may not be cleared quickly as the neonatal liver
and in children with seizures.
Chapter 33 n Procedural Sedation and Management of Pain in Children 341
is immature to permit effective glucuronidation, the main as they can cause severe withdrawal syndrome or increased
pathway of morphine metabolism. Hence, repeat doses of seizure threshold.
morphine have to be administered with caution in infants
IP : 196.52.84.10
and in those with liver disease. Naloxone
Morphine: 0.1 mg/kg IV. Naloxone is an opioid antagonist neutralizing all the an-
algesic, sedative and side effects of narcotics by binding
Fentanyl to the μ receptor. The onset is within 1 minute and it has a
half-life of 1 hour though the duration may be prolonged
Fentanyl, a morphine analogue, is a pure analgesic and of-
in infants. Due to its low affinity, repeat doses may be
fers no sedation. It is rapid in onset and short in duration (30
required to reverse the side effects of long acting narcot-
minutes). Fentanyl is very effective (potency—100 × mor-
ics (e.g. meperidine) and in overdose situations. In young
phine) and is indicated in painful orthopedic procedures. infants born to narcotic addicted mothers and in chronic
Side effects of fentanyl include hypotension, bradycardia overdose situations, naloxone can precipitate withdrawal
and respiratory depression. Watch for chest wall rigidity, symptoms.
a unique life-threatening side effect of fentanyl associated
with rapid administration. Chest wall rigidity will require Naloxone: 0.1 mg/kg.
immediate reversal with the antidote, naloxone and if re-
quired, paralysis with succinyl choline. Caution should be Flumazenil
exercised in calculating the amount of fentanyl to be given Flumazenil is a benzodiazepine antagonist and is used
due to the high concentration in solution (available as a 50 when cardiovascular and respiratory depression occurs
μg/mL solution). Newer preparations such as remifentanyl with toxic dose of benzodiazepines.
are ultra short with recovery within 5–20 minutes.
Even though it fully reverses benzodiazepine-induced
Fentanyl: 1–2 μg/kg IV. sedation, its effect on respiratory depression is not as pro-
nounced. Hence, assisted respirations and supplemental
Mepiridine (Demerol) oxygen are necessary for successful recovery from seda-
tion-induced respiratory depression. It is contraindicated in
Even though it is an effective narcotic and offers pain con-
children on long term benzodiazepines as it may increase
trol lasting up to 4 hour, it is falling out of favor due to the
the likelihood of seizures. Adverse events include agitation,
increased incidence of CNS side effects (tremors, seizures)
headache and dizziness.
due to its metabolite, normeperidine, which can accumu-
late after repeated doses. Anticonvulsants can also increase Flumazenil: 5 µg/kg every 1 minute to max of 40 µg/kg
the production of normeperidine resulting in increased sei- (adult 2 mg), then 2–10 µg/kg/h IV.
zure activity.
Management of Adverse Events
Sucrose
The incidence of serious adverse events is low if proce-
Oral sucrose is easy to administer and effective in pain dural sedation is performed by well trained personnel.23,24
control in neonates during painful short procedures (vac- Lack of knowledge of the onset and duration of action, in-
cinations, lumbar punctures). Sucrose mediates release of adequate monitoring and discharging children when crite-
endogeneous opiates resulting in alleviation of pain.22 ria for discharge are not met can contribute to an increased
frequency of adverse events in sedation.25
Reversal Agents
●● Sedation drugs, should be used only by physicians
Reversal agents should always be available in the event of trained in its use.
serious cardiovascular or respiratory adverse event which Combinations of sedatives and narcotics can increase
does not improve immediately with simple supportive the incidence of respiratory depression. Studies have
measures (supplemental oxygen, assisted ventilations). noted that adverse events were higher when more than
However, administering reversal agents is not without risk three drugs were utilized for sedation.26
342 Section XI n Special Topics
●● Use only one appropriate drug. The parents should be informed about delayed adverse
●● Respiratory depression is the most common adverse effects, such as chloral hydrate. They should be provided
event apart from failed
IP :or196.52.84.10
inadequate sedation.27 contact telephone numbers, if the need arise.
●● Respiratory depression during sedation is often a result
of hypercarbia, hypoventilation or obstruction of the Box 33.1: Discharge criteria
airway.
Stable cardiorespiratory function
●● Open the airway with head tilt-chin lift maneuver and
provide supplemental oxygen. Patient is easily arousable and protective reflexes are intact
●● Assisted ventilation may be needed. Patient can talk or verbalize (age-appropriate verbal response)
●● If respiratory depression is protracted, not responding Child can sit up unaided (if appropriate for age and
development)
to simple measures or cardiac irregularities are noted,
Level of responsiveness is close to baseline
naloxone is warranted for a child receiving narcotics.
Child is adequately hydrated
●● Bradycardia during sedation occurs secondary to respi-
ratory depression. It improves with assisted ventilation
and oxygenation.
●● More adverse events were noted, when benzodiaz-
Key Points
ü
epines were used for sedation in children at high risk 1. Children should not be exposed to pain during
(ASA classification III, IV).28 elective procedures in the ED.
2. The health care provider must be well versed in
Sedation was associated with more adverse events recognizing and managing respiratory depression
when benzodiazepines alone were used for sedation and during administration of sedative drugs.
in those considered high risk by ASA classification.28 The 3. Two trained health care providers must be available.
incidence of respiratory depression/apnea has been report- One to perform the procedure and the second to
ed to be up to 20%–29% of patients receiving procedural monitor and resuscitate.
sedation even though large studies in children’s hospitals
have lower rates of 3%– 4%.23,28
The specific common adverse events of the sedatives
and analgesics are listed in Table 33.7.
common errors
1. Failure to provide adequate pain relief during
û
procedures such as lumbar puncture, bone marrow
Discharge Criteria aspiration, thoracostomy, etc.
2. Administration of sedation without adequate
Once the procedure is complete, monitor the child un- analgesia.
til the child becomes awake and returns to baseline 3. Lack of awareness of potential side effects.
mental status. 4. Premature discharge without ruling out whether the
Most complications have been noted in the initial 5 child has recovered.
minutes (induction phase) after administration of intrave-
nous sedatives. All serious complications were noted in the REFERENCES
first 30 minutes of sedation.29 It is important to note that
painful procedures such as fracture reduction may obscure 1. Dresser S. The effectiveness of conscious sedation on anxi-
ety, pain and procedural complications in young children.
the potential depth of sedation due to the pain associated
Pediatric Nursing. 2003;29:320-23.
with the procedure. Hence, respiratory depression may
2. Krauss B, Green SM. Procedural sedation and analgesia in
manifest after a painful procedure, well beyond the induc- children. In: Lancet: Lancet; 2006. pp. 766-80.
tion phase. If the child has symptoms such as vomiting 3. Green SM. Research advances in procedural sedation and
or emergence reactions, the child should be observed for analgesia. Ann Emerg Med. 2007;49:31-36.
a longer period of time. The criteria for discharge as rec- 4. Claar RL, Simons LE, Logan DE. Parental response to chil-
ommended by the American Academy of Pediatrics (AAP) dren’s pain: The moderating impact of children’s emotional
are provided in Box 33.1. distress on symptoms and disability. In: Pain (03043959);
2008. pp. 172-79.
Chapter 33 n Procedural Sedation and Management of Pain in Children 343
5. Burgoyne LL, Smeltzer MP, Pereiras LA, et al. How well do to current sedation monitoring practices? Acad Emerg
pediatric anesthesiologists agree when assigning ASA physi- Med. 2006;13:500-04.
cal status classifications to their patients? In: Pediatric Anes- 17. Keidan I, Gravenstein D, Berkenstadt H, et al. Supple-
IP : 196.52.84.10
thesia Blackwell Publishing Limited; 2007. pp. 956-62. mental oxygen compromises the use of pulse oximetry for
6. Ragheb J, Malviya S, Burke C, et al. An assessment of detection of apnea and hypoventilation during sedation in
interrater reliability of the ASA physical status classifica- simulated pediatric patients. Pediatrics 2008;122:293-98.
tion in pediatric surgical patients. In: Pediatric Anesthesia: 18. Fu ES, Downs JB, Schweiger JW, et al. Supplemental oxy-
Blackwell Publishing Limited; 2006. pp. 928-31. gen impairs detection of hypoventilation by pulse oxim-
7. Rosenstock C, Gillesberg I, Gatke MR, et al. Inter-observer etry. Chest 2004;126:1552-558.
agreement of tests used for prediction of difficult laryngos- 19. Crellin D, Sullivan TP, Babl FE, et al. Analysis of the valida-
copy/tracheal intubation. In: Acta Anaesthesiologica Scandi- tion of existing behavioral pain and distress scales for use in
navica: Blackwell Publishing Limited; 2005. pp. 1057-062. the procedural setting. Pediatric Anesthesia. 2007;720-33.
8. Sareide E, Eriksson LI, Hirlekar G, et al. Pre-operative 20. Playfor S, Jenkins I, Boyles C, et al. Consensus guidelines
fasting guidelines: an update. In: Acta Anaesthesiologica on sedation and analgesia in critically ill children. Inten-
Scandinavica: Blackwell Publishing Limited; 2005. pp. sive Care Medicine.2006;32:1125-136.
1041-047. 21. Cohen Mr. Chloral Hydrate Overdoses Implicated In
9. Roback MG, Bajaj L, Wathen JE, et al. Preprocedural fast- Deaths. Nursing. 1993;23:25.
ing and adverse events in procedural sedation and analge- 22. Gibbins S, Stevens B. Mechanisms of sucrose and non-nu-
sia in a pediatric emergency department: are they related? tritive sucking in procedural pain management in infants.
Ann Emerg Med. 2004;44:454-59. Pain Res Manag. 2001;6:21-28.
10. Bell A, Treston G, McNabb C, et al. Profiling adverse re- 23. Cravero JP, Blike GT, Beach M, et al. Incidence and na-
spiratory events and vomiting when using propofol for ture of adverse events during pediatric sedation/anesthe-
emergency department procedural sedation. Emergency sia for procedures outside the operating room: report from
Medicine Australasia. 2007;19:405-10. the Pediatric Sedation Research Consortium. Pediatrics;
11. Hoffman GM, Nowakowski R, Troshynski TJ, et al. Risk 2006;118:1087-096.
reduction in pediatric procedural sedation by application 24. Meyer S, Grundmann U, Gottschling S, et al. Sedation
of an American Academy of Pediatrics/American Soci- and analgesia for brief diagnostic and therapeutic pro-
ety of Anesthesiologists Process Model. Pediatrics;109 cedures in children. European Journal of Pediatrics:
2002:236-43. 2007;166:291-302.
12. Treston G. Prolonged pre-procedure fasting time is unnec- 25. Cote CJ, Notterman DA, Karl HW, et al. Adverse sedation
essary when using titrated intravenous ketamine for pae- events in pediatrics: a critical incident analysis of Contrib-
diatric procedural sedation. In: Emergency Medicine Aus- uting factors. Pediatrics. 2000;105:805.
tralasia: Blackwell Publishing Limited; 2004 pp.145-50.
26. Cote CJ, Karl HW, Notterman DA, et al. Adverse sedation
13. Cote CJ, Wilson S, Work Group on S. Guidelines for moni- events in pediatrics: analysis of medications used for seda-
toring and management of pediatric patients during and af- tion. Pediatrics. 2000;106:633-44.
ter sedation for diagnostic and therapeutic procedures: an
27. Pitetti RD, Singh S, Pierce MC. Safe and efficacious use of
update. Pediatrics. 2006;118:2587-602.
procedural sedation and analgesia by nonanesthesiologists
14. Miner JR, Heegaard W, Plummer D. End-tidal carbon di- in a pediatric emergency department. Arch Pediatr Adolesc
oxide monitoring during procedural sedation. Acad Emerg Med. 2003;157:1090-096.
Med. 2002;9:275-80.
28. Malviya S, Voepel-Lewis T, Eldevik OP, et al. Sedation and
15. Lightdale JR, Goldmann DA, Feldman HA, et al. Mi- general anaesthesia in children undergoing MRI and CT: ad-
crostream capnography improves patient monitoring dur- verse events and outcomes. Br J Anaesth. 2000;84:743-48.
ing moderate sedation: a randomized, controlled trial. Pe- 29. Newman DH, Azer MM, Pitetti RD, et al. When is a patient
diatrics. 2006;117:1170-178. safe for discharge after procedural sedation? The timing of
16. Burton JH, Harrah JD, Germann CA, et al. Does end-tidal adverse effect events in 1367 pediatric procedural seda-
carbon dioxide monitoring detect respiratory events prior tions. Ann Emerg Med. 2003;42:627-35.
34
IP : 196.52.84.10
Diabetic Ketoacidosis
Figure 34.1: Protocolised approach and intensive monitoring of children with diabetes improve their quality of life.
Learning Objectives
1. Pathophysiology of DKA. 2. Use of the rapid cardiopulmonary cerebral assess-
ment and the pediatric assessment triangle to im-
plement the ISPAD guidelines.
IP : 196.52.84.10
The kaliuresis, which occurs in DKA is due to osmotic Hyperglycemia and ketoanions enhance the glomerular
diuresis secondary to hyperaldosteronism caused by so- filtration rate. Progressive volume depletion decreases GFR,
dium depletion and the presence of negatively charged ke- leading to worsening hyperglycemia and ketonemia.
toanions in tubular fluid.
Ù
Despite these losses, plasma potassium concentrations Simple rehydration itself can improve hyperglycemia,
are typically normal or elevated at the time of diagnosis of ketosis and anion gap acidosis.
DKA. This is a result of the shift of K+ from intracellular to
extracellular compartment secondary to acidosis, hyperos-
Signs and Symptoms
molarity, insulinopenia and intracellular lysis of proteins.
DKA can be easily missed in a child presenting with new
Ù onset diabetes.3
Normal or low serum potassium during initial evaluation
should alert the clinician towards severely depleted total Ù
To avoid missing DKA in the ED, routinely perform
potassium stores.
dextrostix in every critically ill child.
346 Section XI n Special Topics
Clinical signs and symptoms of DKA do not correlate ●● Measured hyponatremia is common in DKA.
with the severity of acidosis and dehydration. Classic signs Normal or high measured sodium in face of severe hy-
and symptoms of DKAIP include:
: 196.52.84.10 perglycemia indicates hyperosmolarity and dehydration.
●● Leukocytosis with a shift to the left is often seen in
●● Hyperglycemia: Polyuria, polydipsia, nocturia.
●● Acidosis: Hyperventilation, abdominal pain. DKA.
●● Abdominal pain mimicking an acute abdomen has been This may not be due to infection, but warrants work-up
described in approximately 46% of patients with DKA. if it fails to normalize after rehydration.
This symptom has been attributed to dehydration of ●● Majority of patients present with blood glucose lev-
muscle tissue, delayed gastric emptying and ileus sec- el greater than 300 mg/dL.
ondary to acidosis.4 Patients who have received insulin before presenta-
●● Dehydration. tion may have reduced levels.
●● A fruity odor of the breath, akin to the odor of nail var- ●● The diagnosis of DKA may be confounded by the
nish remover is a clinical clue in a previously undiag- coexistence of other acid base disturbances.
nosed patient presenting with acidosis and dehydration. Persistent vomiting and severe hypovolemia can some-
●● Hypotension is a late finding in DKA, often associated times give rise to metabolic alkalosis (Diabetic alka-
with sepsis. losis).
●● Fever is rare, though when present is usually indicative
of underlying infection.
Ù
Mixed acid base abnormalities in DKA offer a clue
Ù
Differential diagnosis of DKA include gastroenteritis
to coexistent problems, e.g. respiratory alkalosis is
suggestive of sepsis.
with dehydration and hypovolemic shock, stress-induced
hyperglycemia, bronchiolitis, asthma, pneumonia,
meningitis, UTI and an acute ‘surgical abdomen’. Management
Therapeutic goals of the specific management of DKA
Classification of DKA include:
DKA can be classified as mild, moderate or severe based 1. Correction of fluid and electrolyte deficits: Fluid therapy.
on the degree of acidosis. Table 34.1. 2. Decrement of blood glucose and the ongoing osmotic
diuresis: Hydration and insulin therapy.
Table 34.1: Classification of DKA
3. Halting of ketoacid production: Insulin therapy.
DKA Venous pH Serum bicarbonate 4. Assessment and treatment of precipitating cause (e.g.
Mild < 7.3 < 15 mEq/L infection).
Moderate < 7.2 < 10 mEq/L 5. Close monitoring for complications (e.g. cerebral
Severe < 7.1 < 5 mEq/L edema).
Ù
Elevation of ketone bodies is diagnostic of DKA. The
Fluid therapy, hence, results in significant improve-
ment of hyperglycemia, hypertonicity and acidemia.
sodium nitroprusside test, which identifies acetoacetate Euvolemia or hydration, causes a decline in the counter-
and acetone, does not recognize beta hydroxybutyrate regulatory hormones, enhances renal glucose clearance
making this a poor test for estimation of severity of (following improved renal perfusion) and improves sen-
ketonemia. sitivity to insulin.
Chapter 34 n Diabetic Ketoacidosis 347
Ù Ù
Hydration alone hasIPbeen shown to reduce glucose Repeat fluids based on reassessment. Do not exceed 30
: 196.52.84.10
concentration by 25–50 mg/h in the first 1 hour. mL/kg.5
Fluid therapy though very important in DKA Rehydration phase begins after shock is corrected.
management, large volumes over short period of time has
been found to be a probable factor in the development of Rehydration fluid:
overt cerebral edema. ●● Deficit correction + Maintenance fluids.
●● A standard water deficit of 100 mL/kg (10% dehydra-
tion) is assumed if the child presents with shock and a
CASE SCENARIO 1 (Figures 34.3 to 34.7) deficit of 85 mL/kg (8.5% dehydration) is assumed if
8-year-old child presents with progressive lethargy and the child presents with only dehydration and no shock.
breathlessness. He has been having increased thirst and ●● Maintenance fluid.
has been voiding urine excessively over the past 2 days. Ongoing losses—urinary losses are usually not replaced.
●● Assuming the patient’s weight as 20 kg in this case sce-
nario, fluids are calculated as follows:
Total fluid to be infused in 48 hours.
●● Shock correction: 200 mL (10 mL/kg NS) over 1 hour.
●● Maintenance fluid for 48 hours 1,500 × 2 = 3,000 mL.
●● Deficit: 100 mL/kg = 2,000 mL.
Ù
Total fluid to be infused in 48 hours (including shock
correction).
Deficit + maintenance fluid for 48 hours – fluid bolus
given for shock correction (during first hour).
3,000 + 2,000 – 200 = 4,800 mL (over 47 hours).
Figure 34.3 Physiological status: Airway stable, effortless
tachypnea, tachycardia, shock with altered mental status. ●● Plan to administer 100 mL/h of NS to which 40 mEq/L
Ù IP : 196.52.84.10
Hyperglycemia resolves faster than acidosis.
Administration of 10% or 12.5% dextrose is necessary to
prevent hypoglycemia during the management of DKA.
Insulin Therapy
Insulin reverses proteolysis, lipolysis, suppresses ketone
body and ketoacid formation. It also lowers blood glucose, Figure 34.5: Withdraw 40 units of plain insulin
by inhibiting glycogenolysis and gluconeogenesis and
stimulates cellular glucose uptake.
Case scenario 2 (Figures 34.8 to 34.9) ●● Initiate insulin therapy 1–2 hours after rehydration at
the dose of 0.1 U/kg/h.
5-year-old girl (weight:15 kg) is brought with a history ●● Change to subcutaneous insulin once acidosis resolves
IP : 196.52.84.10
of polyuria and polydipsia for 15 days. She has been and patient starts to take oral feeds.
having abdominal pain and several episodes of vomit ●● Continue intravenous insulin for 30 minutes (for rapid
ing since morning. Her capillary blood glucose is 400 acting insulin) and 1 hour (for regular insulin) after the
mg/dL and her urine is positive for ketones. administration of first dose of subcutaneous insulin.
Ù
This overlap is essential, since the half-life of IV insulin is
short (5–10 min). An abrupt discontinuation of IV insulin,
coupled with a delayed onset of subcutaneous insulin
regimen may lead to worsening of DKA.
Case scenario 3
6-year-old girl on treatment for insulin-dependent
diabetes mellitus, missed her usual dose. Her routine
capillary blood glucose (CBG) shows 510 mg/dL. Urine
ketostix is positive (Figure 34.10).
Figure 34.8 Physiological status: Moderate DKA with
severe dehydration
Serum potassium is a poor indicator of intracellular po- ●● Monitor serum calcium during phosphate adminis-
tassium status. Monitor potassium status indirectly using tration.10
the ECG monitor. IP : 196.52.84.10
Monitoring and Posthyperglycemic Care
Potassium Administration ●● Cardiopulmonary assessment.
●● Replace potassium only after correction of shock. Do
not correct potassium if documented hyperkalemia or
Ù
Assess level of consciousness and document every 2
renal insufficiency exists. hourly.
●● Add 40 mEq/L potassium chloride to the rehydrating
fluid. It can be increased up to a maximum of 60 mEq/L ●● Strict hourly input output chart.
based on serum potassium levels and electrocardio- ●● SaO2, ECG .
gram (ECG). ●● Random blood sugar.
●● Patients with ECG changes consistent with hypokalemia
should receive rapid potassium correction at the rate of
Ù
Monitor glucose every hour in the first 6 hours and
0.3–0.5 mEq/kg/h till the ECG normalizes.6 thereafter every 2–4 hours until the patient is taking oral
●● Use an infusion pump for potassium replacement under fluids.
close cardiac monitoring.
●● Electrolytes.
Rationale for Avoiding Bicarbonate Serum electrolytes should be measured every 2–6
hours with special emphasis on potassium, corrected
Acidosis can cause negative inotropy, central nervous
sodium and bicarbonate.
system (CNS) depression, insulin resistance and hyper-
●● VBG: 4, 6, 8 hourly.
kalemia. However, bicarbonate therapy can aggravate Venous pH can be used to monitor acidosis; pH may
hypokalemia, paradoxical CNS acidosis, hypernatremia, improve, even when bicarbonate is low.
rebound alkalosis and hypocalcemia. More recently, bicar- ●● Monitor urea and creatinine every 12 hours.
bonate therapy has been associated with increased risk of Measurement of blood or urinary ketones is not nec-
cerebral edema.7-9 essary either during treatment or during the recovery
phase. Conversion of β-hydroxybutyrate to acetoac-
etate increases with improvement in circulatory status
Guidelines for Administering Bicarbonate and hypoxia, giving rise to a paradoxical increase in
●● Administer Bicarbonate (1–2 mEq/kg) slowly over 1–2 ketones and may take 1 week to disappear in the post-
hours10 if child presents with severe acidosis and im- DKA period.
pending cardiovascular collapse or imminent arrest. ●● Search for hidden foci of infection.
– Empiric broad spectrum antibiotics should be con-
sidered in children who appear sick. Sepsis may be a
Phosphate triggering event.
Enhanced urinary excretion of phosphate in DKA, com- – End tidal carbon dioxide measurements or newer
monly leads to hypophosphatemia. home glucose meters with the ability to measure
blood β-hydroxybutyrate concentration have been
shown to be accurate and may be beneficial in guid-
Guidelines ing therapy in DKA.14,15
●● Do not routinely replace phosphate. ●● Encourage oral feeding as early as possible, once the
●● Replacement is indicated in those with anemia, cardiac ketoacidosis resolves.
dysfunction, respiratory depression or muscle weakness
or serum phosphate lower than 1–1.5 mg/dL. Criteria for DKA Resolution
●● Administer one third of calculated phosphate as potas- ●● Blood glucose < 200 mg/dL.
sium phosphate.11-13 ●● Serum bicarbonate level > 15 mEq/L.
Chapter 34 n Diabetic Ketoacidosis 351
●● Venous pH 7.3. time to get dissipated. During this period, rapid decrease
●● Calculated anion gap of 12 mEq/L. in extracellular osmolality draws fluid into the intracellular
Resolution of DKA IPwarrants switch to subcutaneous
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insulin therapy. following causes.
Complete initial cardiopulmonary assessment, if no shock, calculate fluid requirements and correct over 48 hour.
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Chapter 34 n Diabetic Ketoacidosis
353
354 Section XI n Special Topics
Figure 35.1: Organized pediatric emergency services can generate tremendous good will in the community
Learning Objectives
1. How to set up a pediatric resuscitation and 2. Organizing equipment for the emergency service.
emergency unit at the entrance of the hospital? 3. The need for trained nursing personnel in pediatric
emergency medicine.
There is a critical and growing need for emergency phy- Competence in basic emergency medicine should be an
sicians and emergency medicine resources worldwide. To outcome measure for all medical students and represent a
meet this need, emergency services must be established criteria for completion of degree.1
and physicians must be trained to deliver time-sensitive
Globally, the millennium goal for the year 2015 aims
interventions and life-saving emergency care.
at reducing under 5 mortality by one third. Mortality has
Society has a right to expect that at the completion of already fallen to 20%–30% in many states in India due to
their medical school training all pediatricians must possess interventions such as immunization, appropriate antenatal,
basic knowledge of emergency care and the skills to man- natal and postnatal care, breastfeeding, etc. to 25%–30%.
age common acute problems. Emergency medicine is a Mortality can be further reduced by appropriate manage-
core medical discipline and should be a required portion of ment of acutely ill children and neonates in the Golden
the curriculum for every medical school and every medical hour. This is especially important, where the small family
student in the world (Figure 35.1). norm is being advocated.
Every graduating pediatric medical student, should be For both the pediatricians and children, the first step
able to provide care in an emergency situation without any would be to establish pediatric emergency services in ev-
faults or lack of confidence and should be independent at ery district and medical college hospitals.
the site of the emergency.
●● Create dedicated space in the casualty or outpatient de-
Every physician should be able to manage clinical de- partment exclusively for a pediatric emergency care unit.
cision-making under pressure of time when it is essential ●● The pediatric emergency service should be used only for
to save lives. evaluation and management of children referred with
356 Section XI n Special Topics
Ù
Ideally, both electrical and vacuum suction should be
available. In case of power failure, presence of the
vacuum suction is lifesaving.
Ù
Non-rebreathing masks help to administer up to 90%
of oxygen compared to the simple facemask, which
provides 40% of oxygen.
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Ù
Straight blades < 2 year; Curved blades > 2 year;
ET tubes : 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5 (cuffed and
uncuffed tubes); Tincture benzoin for sticking the ET
tube; Dynaplast cut and available as ‘trouser legs’;
gloves, syringes and cotton; Anesthetic drugs for rapid
sequence intubation.
Figure 35.12: Display vital signs chart at head end of
resuscitation trolley
Chapter 35 n Setting up Pediatric Resuscitation and Emergency Services 359
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Figure 35.13: Display protocols for all common emergencies Figure 35.16: Organize the intraosseous tray with the following:
Bone marrow needle, sand bag, gloves, hole towel, dynaplast,
tincture of benzoin, betadine, stainless steel cups, gauze. Prior
Procedure Trays (Figures 35.14 to 35.16) to insertion of needle, prepare 2 fluid-filled syringes (preferably
5 mL in small infants and 10 mL in older children).
Figure 35.17: Display drugs with labels for ease of retrieval dur-
ing resuscitation. Replenish after the resuscitation is complete.
Stock all resuscitation drugs. Organize drugs in an ‘easy to
retrieve’ method by labeling. Stock adequate quantity of drugs.
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Figure 35.19: Prefilled epinephrine should be available at Figure 35.21: Ultrasonography machine is very useful to detect
all times fluid and blood (FAST—focussed abdominal sonography in
trauma) in children with trauma.
●● Use a 10 mL syringe for mixing 1 mL of 1:1000 adren-
aline in 9 mL of NS (1:10,000 dilution).
●● Discard unused epinephrine once in 24 hours.
●● Make note of date and time of reconstitution on the
syringe.
●● When administering a bolus dose of epinephrine to the
child, load in a separate 2 mL syringe, this ensures pre-
cise dosage.
Ù
Avoid administering epinephrine directly from the 10
mL syringe.
●● Direct administration from the 10 mL syringe can lead Figure 35.22: Equip the emergency service with cardiac
monitor, end tidal CO2 monitor and a pulse oximeter
to over dosage (lethal consequences).
Special equipment—spinal immobilization board and cer-
vical collar for management of head and spinal injuries.
Biomedical Equipment (Figures 35.20 to 35.22)
Refer Figure 35.23.
ER MOTTO: “Intelligence and capability are not enough... there must be the joy of doing something beautiful”
363
Key Points
1. Space for the ‘Pediatric
ü common errors
û
IP : Resuscitation
196.52.84.10 and Emergency 1. Referring to the emergency service as ‘Casualty’!
Services’ unit must be created inside the casualty. 2. Failure to implement current evidence-based
2. The emergency service provides specialized care to protocols.
get kids back on track. 3. Failure to identify early signs of critical illness.
3. Dedicated doctors and nurses are needed to man the 4. Failure to resuscitate until therapeutic goals of
emergency service. hypoxia, shock, myocardial dysfunction and seizures
4. Resuscitation equipment and drugs must be have resolved.
organized and replenished when used.
5. Training in the Pediatric Advanced Life Support, References
Basic Life Support are mandatory prior to working
1. WP Burdick, et al. SAEM Education Committee, under-
in this area. graduate subcommittee academic emergency medicine,
1998;(5):1105-110.
2. Chen L, Hsiao AL. Randomized trial of endotracheal tube
versus laryngeal mask airway in simulated pre-hospital
pediatric arrest. Pediatrics. 2008;122;e294; DOI: 10.1542/
peds.2008-0103.
Section XII
Procedures
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36
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Nebulizer Therapy
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Ù
The minimum volume needed for nebulization is 4 mL.
Lower fill volumes can cause suboptimal drug delivery.
The maximum volume that can be loaded is 10 mL. NS
(normal saline) is the recommended diluent. Plain water
can cause bronchospasm.
●● Monitor the patient throughout the nebulizer treat- ●● Replace nebulizers once every 3 months.
ment. ●● Ideally, each patient should have his own nebulizer.
●● Stop nebulization if child’s mental status worsens or
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saturations fall.
●● Ensure that the nebulizer chamber remains upright at
1.
Key Points
Nebulizer should be driven using oxygen.
ü
all times.
2. Ensure a gas flow rate of 8 liter per minute.
3. Avoid use of plain water. NS is the ideal diluent.
Maintenance
4. The nebulizer must be rinsed after each use.
●● Disconnect the nebulizer cup from the plastic tubing,
wash with warm tap water, mild detergent and air dry.
●● Do not wash or rinse the plastic tubing.
●● Store the dry nebulizer cup and plastic tube in a plas-
common errors
û
1. Drawing salbutamol, ipratropium and normal saline
tic bag. all together in the same syringe.
●● Once a week, soak the nebulizer cup and mouthpiece 2. Administering nebulization for stable asthmatics
or face mask for 20 minutes, in a disinfecting solution. with minimal wheeze.
●● Run the nebulizer empty for a few seconds before use.
Needle Thoracocentesis
37
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and Thoracostomy
Ù
Avoid butterfly needle since the needle could lacerate
the expanding lung.
Figure 37.1: Right sided pneumothorax. Technique (Refer Figure 26.16 in Chapter 26)
●● Identify the second intercostal space in the midclavicu-
indications lar line.
1. Trauma with possibility of chest injury. ●● Prepare skin with Betadine solution.
2. Severe pneumonia with pneumatocele. ●● Attach syringe filled with saline to the angiocath.
3. Desaturation in the intubated child: ●● Insert perpendicular to chest wall above the third rib in
Rule out ‘DOPE’. the midclavicular line.
Oxygen saturations not normalizing despite the fol- ●● Aspirate, as the needle is advanced.
lowing maneuvers: ●● A rush of air/bubbles in the syringe denotes entry into
a. Confirmation of tube position. pleural space.
b. Ruling out obstruction by checking for adequacy ●● Withdraw stillette of the angiocath and keep the hub
of chest rise, bilateral air entry and suctioning the closed with your thumb to prevent air entering the
ET. pleural space.
c. Ruling out faulty equipment. ●● Connect an intravenous tube to a saline bottle such that
4. Congenital cystic adenomatoid malformation. an underwater seal drainage is provided.
●● Improvement in saturations and air bubbles in the sa-
Needle Thoracocentesis line bottle are confirmatory of tension pneumothorax.
●● Monitor using a pulseoximeter and cardiac monitor. ●● Confirmatory CXR.
●● Ensure that emergency medications are close at hand. ●● Prepare for definitive tube thoracostomy.
Chapter 37 n Needle Thoracocentesis and Thoracostomy 371
Postprocedure Care
Prepare for thoracostomy insertion soon after CXR in sus-
pected tension pneumothorax.
In the instances where CXR may not be readily avail-
able, a second physician prepares to insert a chest tube
while urgent needle thoracocentesis is being performed by
Figure 37.2: Thoracostomy kit
the first physician.
●● Scalpel with 11 size blade.
Ù ●● Curved artery forceps (for blunt dissection).
Tension pneumothorax is a clinical diagnosis and needs ●● Antiseptic solution povidone iodine 10% or chlorhexi-
urgent intervention. dine in alcohol.
●● Appropriate sized chest tube.
Continue to monitor and maintain the ABCs a. Newborn : 8–12 FG.
The commonest complications from pleural aspiration are b. Infant : 12–16 FG.
pneumothorax, procedure failure, pain and hemorrhage. c. Child : 16–24 FG.
The most serious complication is visceral injury. d. Adolescent : 20–32 FG.
●● Connecting tube.
●● Sterile dressing tray with Tegaderm.
thoracostomy ●● Suture material with needle (‘1’ silk).
A chest drain is a tube, which is placed in the pleural space ●● Closed drainage system (including sterile water if un-
to drain its contents (fluid or air) and remains in place until derwater seal is used) (Figure 37.2).
drainage is complete.
Technique of Chest Tube Insertion
Indications
●● Obtain written consent.
1. Postoperatively, e.g. cardiac surgery, thoracotomy. ●● Connect cardiac monitor and pulse oximeter.
2. Pneumothorax. ●● Administer ketamine 2 mg/kg and midazolam 0.2 mg/
3. Hemothorax. kg IV for adequate pain relief and sedation.
4. Chylothorax. ●● Confirm the site of insertion clinically (Figure 37.3).
5. Pleural effusions.
Empyema is a serious and avoidable complication of
pleural aspiration, the risk of which is greater with mul-
tiple attempts. It is recommended that strict asepsis should
be employed, especially when carrying out therapeutic as-
pirations.
Equipments
●● Sterile gloves and gown.
●● Drape.
●● 1% or 2% lignocaine. Figure 37.3: Selection of site for ICD insertion
●● Syringes with needle (21–25 gauge). (Courtesy: Dr Gunda Srinivas)
372 Section XII n Procedures
●● Take universal precautions. ●● Unclamp the forceps and insert the chest tube till all the
●● Infiltrate skin, underlying tissue up to the periosteum holes are inside the pleural cavity (Figure 37.6).
using lignocaine (Figure 37.4).
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●● Apply two sutures (Figures 37.8A and B). ●● Check for bubbling of air and movement of air column
(Figure 37.7).
●● The first suture is to close the skin (mattress suture) af-
ter drainage removal and second one is a stay suture.
Care After the Thoracostomy
●● To prevent the tube from slipping, an omental tag of
tape has been described, which allows tube to lie a little ●● Take a chest X-ray to confirm position of the tube and
away from chest wall to prevent kinking and tension at lung expansion after thoracostomy.
the insertion site. ●● Watch for complications such as bleeding from in-
●● Dress the site of insertion using sterile dressing or tercostal vessels causing subcutaneous hematoma or
hemothorax, subcutaneous emphysema, infection and
Tegaderm (Figures 37.9A to C).
puncture of lung, liver or spleen.
●● Monitor hemodynamic status.
●● Adequate pain relief.
●● Never lift drain above chest level.
●● The unit and all tubing should be below patient’s chest
level to facilitate drainage.
●● Tubing should have no kinks or obstructions that may
inhibit drainage.
●● Ensure all connections between chest tubes and drain-
age unit are tight and secure.
●● Connections should have cable ties in place.
●● Tubing should be anchored to the patient’s skin to pre-
vent pulling of the drain.
374 Section XII n Procedures
Pericardiocentesis
Pericardiocentesis is a procedure by which pericardial 3. Gross ascites, massive hepatomegaly and elevated dia-
fluid is removed by needle from the pericardial cavity for phragm can alter landmarks for subxiphoid approach.
diagnostic or therapeutic purposes, also called as pericar-
dial paracentesis. Equipment
●● Antiseptic solution.
Indications ●● Sterile drapes, gown and mask.
●● Local anesthetic (lidocaine 1%).
●● Life-threatening hemodynamic changes in a patient ●● 5, 10 and 50 mL syringes.
with suspected pericardial effusion (Figure 38.1). ●● No. 11 blade.
●● Aspiration of pericardial fluid for diagnostic and thera- ●● Needles 18 gauge and 25 gauge.
peutic purposes (Figure 38.2). ●● Spinal needle 18 gauge.
●● Emergency resuscitation drugs and intubation trolley.
●● Ultrasound machine (if available) and sterile ultra-
sound probe cover.
Procedure
●● Obtain written consent.
●● Ensure secure airway and vascular access.
●● Attach the patient to the cardiac monitor and pulse oxi-
meter.
●● Ideally, use ultrasound to visualize the heart and peri-
cardial space.
CONTRAINDICATIONS
There are no absolute contraindications.
Relative contraindications:
1. Blood dyscrasias.
2. Cutaneous infection at the site most feasible for peri Figure 38.2: Echocardiogram showing fluid in pericardial space
cardiocentesis. (marked by star) (Courtesy: Dr Gunda Srinivas)
376 Section XII n Procedures
Complications
common errors
1. Improper position of patient.
û
●● Dysrhythmias. 2. Delaying pericardiocentesis can cause obstructive
●● Damage to vascular structures. shock, which will not improve with fluids or ino-
●● Hemothorax and pneumothorax. tropes.
●● Pneumopericardium. 3. Delay in relieving pericardial effusion urgently, can
●● Hepatic injury. often result in constrictive pericarditis.
●● Reaccumulation of pericardial fluid.
39
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Figure 39.1: Anatomical landmark of external jugular vein and cannulation; lower head position (by 10°–20°) than thorax by
placing a towel under the spine.
Chapter 39 n Cannulation of External Jugular Vein 379
●● Lidocaine (4%). the shoulder on the same side. Advance the cannula,
●● Syringe (5 cc) and 25 gauge needle. while simultaneously applying suction.
●● 10% betadine solution
IP :and chlorhexidine wipes or al-
196.52.84.10 ●● When a flash of blood returns, advance the catheter
cohol swab. over the needle and remove the needle.
●● Large bore IV catheter over needle (16–20 gauge). ●● Attach the IV tubing to the catheter and secure the
●● IV fluid and IV tubing. catheter to the neck with transparent dressing or dy-
naplast. Turn on the IV fluids to ascertain that there is
Procedure good flow.
Indications ●● Generously coat the distal portion (2–5 cm) of the cath-
eter with lubricant.
●● Monitoring of urine output in a child with hemody-
namic compromise.
●● Acute urinary retention.
Equipments
Spinal Stabilization
Cervical spine injuries occur in about 2% of patients with Other situations that mandate cervical spine immobi-
polytrauma. Since the consequences of cervical cord in lization:
jury are devastating, stabilization of the cervical spine
●● Unconscious child with significant injury.
should be continued along with immobilization of the en ●● Any child who has suffered traumatic respiratory arrest.
tire spinal column, while attending to the ABCs of trauma ●● Preverbal children (should automatically be considered
resuscitation. While head and facial injuries (due to rela high risk).
tively large head) are common in children, soft tissue, neck ●● Trauma associated with abnormal neurological exami
and airway injuries are thankfully uncommon due to the nation.
shorter, protected neck. ●● Alert child with neck pain/tenderness/restricted neck
All trauma patients with a cervical spinal column in movements.
jury or with a mechanism of injury having the potential to ●● Polytrauma with significant ‘distracting’ injury (anoth
cause cervical spine injury should be immobilized at the er injury, which may ‘distract’ the patient from com
scene, throughout extrication, transport and transfer. plaining about a possible spinal injury).
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Figures 41.1A and B: Steps of manual cervical spine stabilization (Courtesy: Dr Radhika R)
●● Align the head in the neutral position and fit the cervi ●● If patient is seated, apply chin support first and then
cal collar (The external acoustic meatus must be in line fasten the collar.
with the anterior shoulder). ●● Maintain neutral position of head throughout the pro
cedure.
Ù
Trapezius grip or Vice grip are the other techniques of
Immobilizing the Entire Spine
manual stabilization.
●● If the patient is prone, log roll patient to the supine po
sition.
Selection and Fixing of Appropriate
Cervical Collar Log Rolling
1. Use spinal immobilization devices to achieve spinal
stability during extrication and transport.
2. Use a combination of:
●● Rigid cervical collar immobilization.
●● Supportive blocks on either side of the head.
●● Rigid back board with straps to secure the entire
body of the patient (Figure 41.3).
All three methods in combination are needed to limit lowed out or a blanket is placed under the torso, there
motion of the cervical spine effectively. by maintaining a neutral position of the head and neck
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Cervical Spine Immobilization
Ù
Cervical spine immobilization using sandbags and tape
alone is not recommended.
b. Hemodynamically unstable*
Medication Dose Route Comments
Etomidate or Ketamine 0.3 mg/kg; 1–2 mg/kg IV Not with raised ICP.
Midazolam ( not needed if Etomidate is used) 0.1 mg/kg IV Slow push, flush well.
Rocuronium or Vecuronium 1 mg/kg; 0.1–0.2 mg/kg IV Quick push, ventilation must be supported.
Abnormal BP for age, abnormal mental status, poor perfusion
*
Appendix 4: SEIZURES
Medication Dose Route Comments
Diazepam 0.1–0.3 mg/kg IV, IO Max rate = 1 mg/min
(Valium) 0.5 mg/kg initial Rectal Push over 5 minute
0.25 mg/kg subsequent
Lorazepam (Activan) 0.05–0.1mg/kg IV Slow push over 2 minute
Phenobarbital 20 mg/kg IV Max dose = 500 mg/kg
Push over 5 minute
Phenytoin 15–20 mg/kg, slow over IV Max dose = 1 g
20–30 min Max rate = 1 mg/kg/min
Levetiracetam 20–30 mg/kg at 5 mg/kg/min IV Max dose = 3 g
Sodium valproate 15–20 mg/kg at 5 mg/kg/min IV Max dose = 40 mg/kg
Infusion = 1–4 mg/kg/h
Midazolam 0.1–0.2 mg/kg IV, PR Max dose = 0.15 mg/kg
Infusion = 1 μg/kg/min to max
30 μg/kg/min
Fluid Replacement, Electrical Intervention, Resuscitation Medications 391
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DRUGS USED IN PEDIATRIC EMERGENCIES
Activated charcoal 1–2 g/kg through NG tube
Adenosine SVT
0.1 mg/kg IV/IO rapid push (ma× 6 mg), 0.2 mg/kg IV/IO rapid push (max 12 mg)
Albumin Shock, Trauma, Burns
0.5–1 g/kg (10–20 mL/kg of 5% solution) IV/IO rapid infusion
Albuterol Asthma, Anaphylaxis (bronchospasm), Hyperkalemia
(Salbutamol) MDI : 4–8 puffs INH q 20 min PRN with spacer (OR ET if intubated)
Nebulizer: 2.5 mg/dose (weight < 20 kg) OR 5 mg/dose (weight > 20 kg) INH q 20 minute PRN
Continuous nebulizer: 0.5 mg/kg/h INH (max 20 mg/h)
Alprostadil (PGE1) Ductal-dependent Congenital Heart Diseases (all forms)
0.05–0.1 µg/kg/min IV/IO infusion initially, then 0.01–0.05 µg/kg/min IV/IO
Amiodarone SVT, VT ( with pulses)
5 mg/kg IV/IO load over 20–60 minute (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g)
Pulseless Arrest (i.e. VF/pulseless VT)
5 mg/kg IV/IO bolus (max 300 mg), repeat to daily max 15 mg/kg (or 2.2 g)
8–10 vials in 100 mL NS over 1–2 hour (max 20 vials)
Aminophylline Refractory Near Fatal asthma
5 mg/kg loading (1 mg/kg/h IV infusion)
Antisnake venom Snake bite with signs of envenomation
8–10 vials in 100 mL NS over 1-2 hour (maximum 20 vials)
Atropine sulfate Bradycardia (symptomatic)
0.02 mg/kg IV/IO (min dose 0.1 mg, max single dose child 0.5 mg, max single dose adolescent 1 mg),
may repeat dose once, max total dose child 1 mg, max total dose adolescent 2 mg
0.04–0.06 mg/kg ET
Toxin overdose (e.g. organophosphate, carbamate)
0.02–0.05 mg/kg (<12 year) OR 0.05 mg/kg (> 12 year) IV/IO initially, repeat q 20–30 minute until
atropine effect (dry mouth, tachycardia, mydriasis) is observed or symptoms reverse
Blood 10 mL/kg over 4 hour
Calcium gluconate Hypocalcemia, Hyperkalemia, Hypermagnesemia, Calcium Channel Blocker Overdose
10% 200 mg/kg (0.2 mL/kg) IV/IO slow push during arrest or if severe hypotension, repeat PRN
Dexamethasone Croup
0.6 mg/kg PO/IM/IV (max 16 mg)
Dextrose Hypoglycemia
(Glucose) 0.5–1 g/kg IV/IO (D25 W 2–4 mL/kg; D10 W 5–10 mL/kg)
Diazepam 0.05–0.3 mg/kg, (Max < 5 year: 5 mg; 5 year: 10 mg) PR: 0.5 mg/kg, Infusion: 0.1 mg/kg/min
Diphenhydramine Anaphylactic Shock
1–2 mg/kg IV/IO/IM q 4–6 hour (max 50 mg)
Congestive Heart Failure, Cardiogenic Shock
2–20 µg/kg/min IV/IO infusion; titrate to desired effect
Dopamine Cardiogenic Shock, Distributive Shock
5–20 µg/kg/min IV/IO infusion; titrate to desired effect
Contd...
Drugs Used in Pediatric Emergencies 393
Contd...
DRUGS USED IN PEDIATRIC EMERGENCIES
Epinephrine IPPulseless
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Arrest, Bradycardia (symptomatic)
0.01 mg/kg (0.1 mL/kg) 1:10, 000 IV/IO q 3–5 minute (max 1 mg; 1 mL)
0.1 mg/kg (0.1 mL/kg) 1:1,000 ET q 3–5 minute
Hypotensive Shock
0.1–1 µg/kg/min IV/IO infusion (consider higher doses if needed)
Anaphylaxis
0.01 mg/kg (0.01 mL/kg) 1:1,000 IM in thigh q 15 minute PRN (max 0.5 mg) or
Auto-injector 0.3 mg (weight ≥ 30 kg) IM or Child Jr Auto-injector 0.15 mg (weight 10–30 kg) IM
0.01 mg/kg (0.1 mL/kg) 1:10,000 IV/IO q 3–5 minute (max 1 mg) if hypotension
0.1–1 µg/kg/min IV/IO infusion in hypotension despite fluids and IM injection
Asthma
0.01 mg/kg (0.01 mL/kg) 1:1,000 SQ q 15 minute (max 0.5 mg; 0.5 mL)
Croup
0.25–0.5 mL racemic solution (2.25%) mixed in 3 mL NS INH OR 3 mL 1:1,000 INH
Epinephrine Toxins/overdose (e.g. β- adrenergic blocker, calcium channel blocker)
(continued) 0.01 mg/kg (0.1 mL/kg) 1:10,000) IV/IO (max 1 mg); if no response consider higher doses up to 0.1 mg/
kg (0.1 mL/kg) 1: 10,000 IV/IO
0.1–1 µg/kg/min IV/IO infusion (consider higher doses)
Fos-phenytoin Status Epilepticus refractory to 2 doses of benzodiazepines
20–30 mg/kg, IV, IM, 5 mg/kg/min (Max: 225 mg/min), [7.5 mg of Fos-phenytoin ~ 5 mg of Phenytoin]
Furosemide Pulmonary Edema, Fluid Overload
1 mg/kg IV/IM (usual max 20 mg if not chronically on loop diuretic)
Hydrocortisone Adrenal Insufficiency
2 mg/kg IV bolus (max 100 mg)
Inamrinone Myocardial Dysfunction and Increased SVR/PVR
Loading dose: 0.75–1 mg/kg IV/IO slow bolus over 5 minute (may twice to max 3 mg/kg), then 5–10 µg/
kg/min IV/IO infusion
Ipratropium Life-threatening asthma
Bromide 250–500 µg INH q 20 minute PRN × 3
Labetolol 0.25–0.5 mg/kg IV over 2 minute, can be repeated every 10 minute if required
Lidocaine VF/Pulseless VT, Wide-Complex Tachycardia (with pulses)
1 mg/kg IV/IO bolus
Maintenance: 20–50 µg/kg/min IV/IO infusion (repeat bolus dose if infusion initiated > 15 minute after
initial bolus) 2–3 mg/kg ET
Levetiracetam Refractory Status epilepticus, SE complicated with cardiac dysfunction
20–30 mg/kg IV at 5 mg/kg/min (maximum, 3 g) Intravenous
NGT route if IV preparation not available
Lorazepam 0.05–0.1 mg/kg (Max: 4 mg) IV Infusion: 0.1–0.01 mg/kg/h
Magnesium sulfate Asthma (refractory status asthmaticus), Torsades de Pointes, Hypomagnesemia
25–50 mg/kg IV/IO bolus (pulse less VT) or over 10–20 minute (VT with pulses) OR slow infusion over
15–30 minute (status asthmaticus) (max 2g)
Contd...
394 Appendices
Contd...
Appendix 9
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Appendix 10
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Appendix 11
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Sample documented pediatric emergency case record of near fatal asthma—assessment sheet
400 Appendices
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Sample documented pediatric emergency case record of near fatal asthma—monitoring sheet
Sample Case Record: Head Injury (Raised ICP) 401
Appendix 12
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Sample documented pediatric emergency case record of raised ICP due to head injury—assessment sheet
402 Appendices
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Sample documented pediatric emergency case record of raised ICP due to head injury—monitoring sheet
Sample Case Record: Septic Shock 403
Appendix 13
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Sample documented pediatric emergency case record of septic shock—monitoring sheet continued...
Epilogue
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Way back in 1997, when I was invited to take charge of the Pediatric Emergency Room, little did I expect that this
would be the beginning of the most exciting chapter in the history of the institute. Seriously ill children and neonates
were flooding its gates. Brought late by their parents, these children had received little prehospital resuscitation, were
recognized late and were from the most under-privilaged sections of the population. This was compounded by the fact
that pediatric emergency medicine was relatively new and few doctors were formally trained in this sub-specialty during
their under-graduation.
A large proportion of severely hypoxic and shocked children were presenting with features of pulmonary edema,
cardiac dysfunction with eyes signs of non-convulsive status epilepticus. To our surprise, response to apparently innocuous
interventions such as fluids, brochodilators and anticonvulsants were often detrimental! Why was this happening? Little
published evidence supported these observations. Perhaps, children reaching western hospitals were not so sick?! Perhaps,
these children were intubated earlier, resulting in failure to develop these findings and hence never documented.
Protocols were modified to incorporate this information. Residents were drilled to perform the rapid assessment
within 60 seconds. Evaluation of liver span and eye movements was enforced in every assessment. Response to each
intervention was vigorously assessed for improvement and deterioration. Anticipation for the development of pulmonary
edema and cardiac dysfunction were built into protocols in order to avoid deterioration to cardiac arrest. The innovations
started paying rich dividends and hospital mortality dropped dramatically.
Pursuit to seek the truth never ends. Only history can truly judge the impact of these innovations in the care of the
seriously ill child during the initial minutes of resuscitation.
Low systemic vascular resistance septic Mechanism of working of Jackson-Rees Myocarditis 81, 122, 134
shock 124 circuit 55 Myopathies and muscle necrosis 40
Lower GI bleed 309 Mecoprop poisoning 245 Myotoxins 226
Lower nephron necrosis 199 Mediastinal shift 314
Low-set ears 33 Medical complications of status
Lubricate the posterior surface 48 epilepticus 199 N
Lumbar puncture 193 Mental status in children 129
N-acetylcysteine 255
Lung fluid 200 Mepiridine (demerol) 341
IP : 196.52.84.10 Naloxone 341
Lung parenchyma 78, 314 Metabolic
Nasal flare 84
Lytic cocktail 221 abnormalities 136, 138
Nasogastric tube (NGT) 27, 34, 200, 242,
acidosis 138, 199, 240
307
biochemical abnormalities 199
M demands of tissues 134
Nasogastric tube emerging 28
Nasogastric tube insertion 34
derangements 101
Macroglossia 63 Nasopharyngeal airway 45, 357
disorders 203
Magic drugs 119 Nasopharynx 63
effects 123
Magnesium sulfate 89, 92 Nasotracheal intubation (NTI) 32
fat 344
Maintain Near fatal asthma 86
Metered dose inhalers 91
electrolyte balance 255 Nebulization 367
Methemoglobinemia 103, 240, 261
euglycemia 138 Nebulization tray 367
Method of administration of ASV 232
fluid requirements 137 Nebulizer therapy 86, 367
Methylprednisolone 92
hematocrit 137 Nebulizing kit 367
Microbial invasion 143
normal temperature 137 Neck of the bladder 381
Micrognathia 33, 45, 63
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Major burns 292
Midazolam 39, 105, 207, 209, 339
Need to ventilate cannot intubate 39
Maldistribution 145 Needle
Middle finger down 49
Malignant hypertension 180 Mild traumatic brain injury 265 cricothyrotomy 45
Mallampati classification 336 Milrinone 109 thoracocentesis 109, 282, 370
Malrotation 308 Minimal mucosal edema 62 Needle thoracocentesis 374
Management of Minor head trauma 267 Neem oil ingestion 259
acute Minor symptoms 4 Neostigmine test 233
diarrhea 129 Miosis 248 Nephrotoxins 226
exacerbation of asthma 84 Monitor serum sodium 202 Neurogenic
adverse events 341 Monitoring equipment 33 etiologies 81
anaphylactic shock 170 Monitoring of urine output 380 functional stridor 8
cardiogenic shock 134, 141 Monroe-Kellie doctrine 267 pulmonary edema 199
cerebral edema 351 Morphine 221, 340 stridor 71, 188
dengue with warning signs 158, 160 Motor vehicle accidents 265 Neurohormonal responses 102
drowning victim 299 Mpending respiratory failure 218 Neurological
eye signs 13 Mucolytics 90 assessment 12
fluid overload 166 Muffling of voice 62 evaluation 283, 285
hypertensive Multidose regimen 88 Neuromuscular blockade agents 33, 36,
emergency 179, 181 Multiorgan failure 101 40
shock 148 Multiple organ dysfunction 199 Neuronal excitability 207
Muscarinic acetylcholine receptors 248
intracranial hypertension 191 Neuropeptide activity 198
Muscarinic effect 240
local and systemic effects 219 Neurotoxic bites 233
Muscarinic effects of acetylcholine 248
non-traumatic coma 187 Neurotoxicity secondary 218
Muscular twitching 252
pain in children 335 Mydriasis 270 Neurotoxins 226
raised intracranial pressure 275 Myocardial Neurovascular bundle 374
severe dengue 158 contractility 138 Nicardipine 183
status epilepticus 198 depressant factor 134 Nicotinic effect 240
Mandibular hypoplasia 33 disease 121 Nifedipine 183
Manual stabilization of cervical spine 382 dysfunction 134, 144, 147, 188, 203, 300 Nitroprusside 182
Massive empyema 109 edema 134 Non-cardiogenic pulmonary edema 31,
Match fluid resuscitation 129 function 5, 134 81, 217, 145, 301
Maxillofacial and intraoral trauma 282 ischemia 125 Non-convulsive status epilepticus 7, 110,
136, 143, 188, 206
Mean arterial pressure (MAP) 12, 266 oxygen demand 136 Non-invasive positive pressure ventilation
Mechanical ventilation 143 performance 136 55
Index 415
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