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ADVANCED PAEDIATRIC LIFE SUPPORT

Fourth edition

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ADVANCEDPAEDIATRIC

LIFE SUPPORT

The Practical Approach

Fourth edition

Advanced Life Support Group

Edited byKevin Mackway-JonesElizabeth Molyneux

Barbara PhillipsSusan Wieteska

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c© 2005 by Blackwell Publishing LtdBMJ Books is an imprint of the BMJ Publishing Group Limited, used under licence

Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USABlackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK

Blackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia

The right of the Author to be identified as the Author of this Work has been asserted in accordance withthe Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system,or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording orotherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the

prior permission of the publisher.

First published in 1993 by the BMJ Publishing Group

Reprinted in 1994, 1995, 1996

Second edition 1997, reprinted 1998, reprinted with revisions 1998, 1999, 2000

Third edition 2001, second impression 2003, third impression 2003

Library of Congress Cataloging-in-Publication DataAdvanced paediatric life support : the practical approach / Advanced Life Support Group;

edited by Kevin Mackway-Jones . . . [et al.].– 4th ed.p.; cm.

Includes index.ISBN 0-7279-1847-8

1. Pediatric emergencies. 2. Pediatric intensive care. 3. Life support systems (Critical care)[DNLM: 1. Emergencies–Child. 2. Emergencies–Infant. 3. Critical Care–Child. 4. CriticalCare–Infant. 5. Wounds and Injuries–therapy–Child. 6. Wounds and Injuries–therapy–Infant.

WS 205 A244 2004] I. Mackway-Jones, Kevin. II. Advanced Life Support Group(Manchester, England)

RJ370.A326 2004618.92’0028–dc22

2004021823ISBN-13: 9780727918475

ISBN-10: 0727918478

Catalogue records for this title are available from the British Library and the Library of Congress

Set by Techbooks, New Delhi, IndiaPrinted and bound in Spain by GraphyCems, Navarra

Commissioning Editor: Mary BanksDevelopment Editor: Veronica Pock

Production Controller: Kate Charman

For further information on Blackwell Publishing, visit our website:http://www.blackwellpublishing.com

The publisher’s policy is to use permanent paper from mills that operate a sustainable forestry policy,and which has been manufactured from pulp processed using acid-free and elementary chlorine-free

practices. Furthermore, the publisher ensures that the text paper and cover board used have metacceptable environmental accreditation standards.

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CONTENTS

Working Group ix

Contributors xi

Preface to the Fourth Edition xiii

Preface to the First Edition xiv

Acknowledgements xv

Contact Details and Further Information xvii

PART I: INTRODUCTION

Chapter 1 Introduction 3Chapter 2 Why treat children differently? 7Chapter 3 Structured approach to emergency paediatrics 15

PART II: LIFE SUPPORT

Chapter 4 Basic life support 21Chapter 5 Advanced support of the airway and ventilation 37Chapter 6 The management of cardiac arrest 47

PART III: THE SERIOUSLY ILL CHILD

Chapter 7 The structured approach to the seriously ill child 59Chapter 8 The child with breathing difficulties 73Chapter 9 The child in shock 97Chapter 10 The child with an abnormal pulse rate or rhythm 115Chapter 11 The child with a decreased conscious level 125Chapter 12 The convulsing child 139

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CONTENTS

PART IV: THE SERIOUSLY INJURED CHILD

Chapter 13 The structured approach to the seriously injured child 151Chapter 14 The child with chest injury 167Chapter 15 The child with abdominal injury 175Chapter 16 The child with trauma to the head 179Chapter 17 The child with injuries to the extremities or the spine 189Chapter 18 The burned or scalded child 199Chapter 19 The child with an electrical injury or drowning 205

PART V: PRACTICAL PROCEDURES

Chapter 20 Practical procedures – airway and breathing 215Chapter 21 Practical procedures – circulation 231Chapter 22 Practical procedures – trauma 243Chapter 23 Interpreting trauma X-rays 253Chapter 24 Structured approach to stabilisation and transfer 265

PART VI: APPENDICES

Appendix A Acid–base balance 279Appendix B Fluid and electrolyte management 285Appendix C Child abuse 299Appendix D Prevention of injury in children 309Appendix E When a child dies 313Appendix F Management of pain in children 317Appendix G Triage 327Appendix H General approach to poisoning and envenomation 331Appendix I Resuscitation of the baby at birth 347Appendix J Formulary 361

Index 385

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ASSOCIATE EDITORS

P. Oakley Trauma Anaesthesia, Stoke on Trent

B. Phillips Paediatric Emergency Medicine, Liverpool

M. Samuels Paediatric ICU, Stoke on Trent

S. Young Paediatric Emergency Medicine, Melbourne

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WORKING GROUP

A. Argent Paediatric ICU, Cape Town

A. Charters Emergency Nursing, Portsmouth

E. Duval Paediatrics, Antwerp

C. Ewing Paediatrics, Manchester

M. Felix Paediatrics, Coimbra

G. Hughes Emergency Medicine, Wellington

F. Jewkes Pre-Hospital Paediatrics, Wiltshire

K. Katsanoulas Anaesthetics/ICU, Thessaloniki

J. Leigh Anaesthesia, Bristol

K. Mackway-Jones Emergency Medicine, Manchester

E. Molyneux Paediatric Emergency Medicine, Blantyre, Malawi

P. Oakley Anaesthesia/Trauma, Stoke on Trent

T. Rajka Paediatrics, Oslo


I. Sammy Paediatric Emergency Medicine, Trinidad


N. Turner Anaesthesia, Amsterdam

I. Vidmar Paediatrics, Ljubljana

J. Walker Paediatric Surgery, Sheffield

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WORKING GROUP

C. Whyte Paediatric ICU Nursing, Middlesbrough

S. Wieteska ALSG Group Manager, Manchester

K. Williams Paediatric Emergency Nursing, Liverpool

J. Wyllie Neonatology, Middlesbrough


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CONTRIBUTORS

R. Appleton Paediatric Neurology, Liverpool

A. Argent Paediatric ICU, Cape Town

C. Baillie Paediatric Surgery, Liverpool

P. Baines Paediatric Intensive Care, Liverpool

I. Barker Paediatric Anaesthesia, Sheffield

D. Bickerstaff Paediatric Orthopaedics, Sheffield

R. Bingham Paediatric Anaesthesia, London

P. Brennan Paediatric Emergency Medicine, Sheffield

J. Britto Paediatric Intensive Care, London

G. Browne Paediatric Emergency Medicine, Sydney

C. Cahill Emergency Medicine, Portsmouth

H. Carty Paediatric Radiology, Liverpool

A. Charters Emergency Nursing, Portsmouth

M. Clarke Paediatric Neurology, Manchester

J. Couriel Paediatric Respiratory Medicine, Liverpool

P. Driscoll Emergency Medicine, Manchester

J. Fothergill Emergency Medicine, London

P. Habibi Paediatric Intensive Care, London

D. Heaf Paediatric Respiratory Medicine, Liverpool

J. K. Heltne Anaesthesia, Haukeland

F. Jewkes Pre-Hospital Paediatrics, Wiltshire

E. Ladusans Paediatric Cardiology, Manchester

J. Leggatte Paediatric Neurosurgery, Manchester

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CONTRIBUTORS

J. Leigh Anaesthesia, Bristol

S. Levene Child Accident Prevention Trust, London

M. Lewis Paediatric Nephrology, Manchester

K. Mackway-Jones Emergency Medicine, Manchester

I. Maconochie Emergency Paediatrics, London

J. Madar Neonatology, Plymouth

T. Martland Paediatric Neurologist, Manchester

E. Molyneux Paediatric Emergency Medicine, Malawi

D. Nicholson Radiology, Manchester

A. Nunn Pharmacy, Liverpool

P. Oakley Anaesthesia, Stoke on Trent

R. Perkins Paediatric Anaesthesia, Manchester


T. Rajka Paediatrics, Oslo

J. Robson Paediatric Emergency Medicine, Liverpool

I. Sammy Paediatric Emergency Medicine, Trinidad


D. Sims Neonatology, Manchester

A. Sprigg Paediatric Radiology, Sheffield

B. Stewart Paediatric Emergency Medicine, Liverpool

J. Stuart Emergency Medicine, Manchester

L. Teebay Child Protection and Paediatric Emergency Medicine, Liverpool

J. Tibballs Paediatric Intensive Care, Melbourne

N. Turner Anaesthesia, Amsterdam

J. Walker Paediatric Surgery, Sheffield

W. Whitehouse Paediatric Neurologist, Nottingham

S. Wieteska ALSG Group Manager, Manchester

M. Williams Emergency Medicine, York

B. Wilson Paediatric Radiology, Manchester

J. Wyllie Neonatology, Middlesbrough


D. Zideman Anaesthesia, London

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PREFACE TO FOURTH EDITION

When we first published this book in 1993 our aim was to bring a structured approach and simple guidelines tothe emergency management of ill and injured children. The Advanced Paediatric Life Support (APLS) conceptand courses have gone a long way towards this.

APLS is now well established in the United Kingdom, Australasia, the Caribbean, mainland Europe, theMiddle East, Scandanavia and South Africa. Modified versions of the course are being taught in countrieswhich are developing, have a poorer health infrastructure and have specific serious health problems. Theseinclude Africa and parts of Asia and South America. In this work the Advanced Life Support Group (ALSG) arecollaborating with many other agencies: more information on these developments can be found on the ALSGWeb site.

A small “family” of courses have developed from APLS in response to different training needs. One is thePaediatric Life Support (PLS) course, a 1-day, locally delivered course for health professionals who have asubsidiary responsibility for the emergency care of children, and the other is the Pre-Hospital Paediatric LifeSupport (PHPLS) course, which has its own textbook and is for the pre-hospital provider.

In the original APLS course the aim was to manage the critically ill or injured child for the first hour. Asthe course has developed, there has been gradual extension of its scope and the inclusion of more material andtraining so as to provide the emergency team with the knowledge and skills to manage the seriously ill or injuredchild to stabilisation and transfer. The presentation of the fourth edition reflects the pace of change of medicalscience and the international nature of APLS. The text is now presented in a loose leaf format. When thereare evidence-based changes to practice that can benefit children in the emergency situation, a new page will beavailable to be downloaded from the ALSG Web site and inserted in the current text. In late 2005, for example,new International Liaison Committee on Resuscitation (ILCOR) guidelines for resuscitation from cardiac arrestwill be published and ALSG will publish an update to the chapter on our Web site. The basic text reflects UKpractice as this country is still the largest user of courses. However, for areas of the world where practice isdifferent there is a facility for pages to be printed from the ALSG Web site and substituted in the text. See the“Contact Details and Further Information” page for details.

A further presentational change is the inclusion of marginal indicators to show where BestBETs and otherWeb-based references can be found. A list of references becomes obsolete no sooner than it is printed, so we haveengaged the power of the World Wide Web to keep our readers up to date with the evidence. See the “ContactDetails and Further Information” page for details.

The days spent on courses are just part of a learning process; both skills and knowledge need continualreinforcement. At the end of your APLS course you will receive a CD-ROM and a logbook for you to use back atyour place of work. We hope that this will contribute to the development of your emergency paediatric practice.

Over the years an increasing number of experts have contributed to the work and we extend our thanks bothto them and to our instructors, who unceasingly provide helpful feedback. Consultation with instructors hasgreatly contributed to this new edition and to the revised course.

KMJEMBPSW

Manchester 2005

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PREFACE TO THE FIRST EDITION

Advanced Paediatric Life Support: The Practical Approach was written to improve the emer-gency care of children, and has been developed by a number of paediatricians, paediatricsurgeons, emergency physicians and anaesthetists from several UK centres. It is the coretext for the APLS (UK) course, and will also be of value to medical and allied personnelunable to attend the course. It is designed to include all the common emergencies, andalso covers a number of less common diagnoses that are amenable to good initial treat-ment. The remit is the first hour of care, because it is during this time that the subsequentcourse of the child is set.

The book is divided into six parts. Part I introduces the subject by discussing the causesof childhood emergencies, the reasons why children need to be treated differently andthe ways in which a seriously ill child can be recognised quickly. Part II deals with thetechniques of life support. Both basic and advanced techniques are covered, and there is aseparate section on resuscitation of the newborn. Part III deals with children who presentwith serious illness. Shock is dealt with in detail, because recognition and treatment canbe particularly difficult. Cardiac and respiratory emergencies, and coma and convulsions,are also discussed. Part IV concentrates on the child who has been seriously injured. Injuryis the most common cause of death in the 1–14-year age group and the importance ofthis topic cannot be overemphasised. Part V gives practical guidance on performing theprocedures mentioned elsewhere in the text. Finally, Part VI (the appendices) deals withother areas of importance.

Emergencies in children generate a great deal of anxiety – in the child, the parents andin the medical and nursing staff who deal with them. We hope that this book will shedsome light on the subject of paediatric emergency care, and that it will raise the standardof paediatric life support. An understanding of the contents will allow doctors, nursesand paramedics dealing with seriously ill and injured children to approach their care withconfidence.

Kevin Mackway-JonesElizabeth Molyneux

Barbara PhillipsSusan Wieteska

(Editorial Board)

1993

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ACKNOWLEDGEMENTS

A great many people have put a lot of hard work into the production of this book, andthe accompanying advanced life support course. The editors would like to thank all thecontributors for their efforts and all the APLS instructors who took the time to send ustheir comments on the earlier editions.

We are greatly indebted to Helen Carruthers, MMAA, Mary Harrison, MMAA, andKate Wieteska for producing the excellent line drawings that illustrate the text. Thanksto the Status Epilepticus Working Party for the status epilecticus protocol and the Child’sGlasgow Coma Scale. The information in Table 9.1 is taken from Lessons from Researchfor Doctors in Training produced by the Meningitis Research Foundation.

We are also grateful to Dr Ros Roden, from the ATLS subcommittee who advised onconsistency issues between ATLS and APLS trauma.

ALSG gratefully acknowledge the support of the Royal College of Paediatrics and ChildHealth (UK). The Specialist Groups of the RCPCH have agreed to advise on the clinicalcontent of chapters relevant to their specialism. ALSG wish to thank the following:

British Society for Paediatric Endocrinology Dr G Butler, Paediatric & AdolescentEndocrinology, Leeds

Dr J Edge, Paediatrics, Oxford

British Paediatric Cardiac Association Dr B Craig, Paediatric Cardiology,Belfast

British Association for Paediatric Nephrology Dr J Evans, Paediatric Nephrology,Nottingham

British Association of Community Child Health Dr T Hutchison, CommunityPaediatrics, Bath

Dr J Mok, Community Paediatrics,Edinburgh

British Paediatric Haematology Forum Dr S Kinsey, Paediatric Haematology, Leeds

British Paediatric Intensive Care Group Dr P Habibi, Paediatric Intensive Care,London

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ACKNOWLEDGEMENTS

British Paediatric Immunology and Infectious Dr H Lyall, Paediatric InfectiousDiseases, LondonDiseases Group

British Inherited Metabolic Disease Group Dr G Shortland, Paediatrics, Cardiff

Dr Hall, Paediatrics, Sheffield

Dr R Bowker, Paediatrics, Nottingham

British Paediatric Radiology and Dr A Sprigg, SheffieldImaging Group

British Paediatric Respiratory Society Dr J Couriel, Respiratory Paediatrics,Liverpool

Finally, we would like to thank, in advance, those of you who will attend the AdvancedPaediatric Life Support course and other courses using this text; no doubt, you will havemuch constructive criticism to offer.

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CONTACT DETAILS AND FURTHER INFORMATION

ALSG: www.alsg.orgBestBETS: www.bestbets.org

For details on ALSG courses visit the Web site or contact:

Advanced Life Support GroupALSG Centre for Training & Development29-31 Ellesmere StreetSwinton, ManchesterM27 0LA

Tel: +44 (0)161 794 1999Fax: +44 (0)161 794 9111Email: [email protected]

Clinicians practising in tropical and under-resourced health care systems are advised toread A Manual for International Child Health Care (0 7279 1476 6) published by Blackwell,which gives details of additional relevant illnesses not included in this text.

NOTE

Sections with the grey marginal tint are relevant for the Paediatric Life Support (PLS)course.

UPDATES

The material contained within this book is updated on a 4-yearly cycle. However, practicemay change in the interim period. For example, it is anticipated that there will be minorchanges made following the publication of the updated ILCOR guidelines at the end of2005.

We will post any changes on the ALSG Web site, so we advise that you visit the Web siteregularly to check for updates (url: www.alsg.org/updates). The Web site will provide youwith a new page to download and replace the existing page in your book.

REFERENCES

Throughout the text, you will see one of two logos indicating that evidence/referencesare available via the Web:

To access the evidence, visit the BestBETs Web site www.bestbets.org (thenumber next to the logo indicates the BestBET reference number. To find aspecific BET click on “Databases”, “Search” and type in the BET numberunder “Terms”, then click “Search”.

To access the references visit the ALSG Web site www.alsg.org/references

ON-LINE FEEDBACK

It is important to ALSG that the contact with our providers continues after a course iscompleted. We now contact everyone 6 months after their course has taken place askingfor on-line feedback on the course. This information is then used whenever the course isupdated to ensure that the course provides optimum training to its participants.

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PART

IINTRODUCTION

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CHAPTER

1Introduction

1.1 INTRODUCTION

Each year many millions of children around the world die from potentially preventableand treatable causes. Whilst the majority of these deaths would be prevented by atten-tion to living conditions and public health measures, an improvement in the recogni-tion of serious illness and delivery of initial medical treatment would undoubtedly savelives.

The training of health care practitioners and the resources available for health care de-livery varies enormously among countries. It is possible however to improve the outcomeof serious illness and injury in children with modest resources if the basic principles ofresuscitation are adhered to. The structured sequential approach to the recognition andtreatment of the seriously ill and injured child followed in this manual is applicable inmany situations and circumstances.

1.2 MORTALITY RATES IN CHILDHOOD

Worldwide mortality rates in children have fallen substantially and consistently overthe last 100 years. The World Health Organisation has estimated that the global infantmortality rate has fallen from 180 in 1950 to 67 in 2000. In some developed countriesthe fall has been even more dramatic. For example in Australia the infant mortality ratein 1902 was 107: one hundred years later in 2002 the figure had reduced to 5.0. Evenwith figures at such low levels, the rates in developed countries have recently continuedto fall. In England and Wales the infant mortality rates have halved in the last 18 years,falling from 10.8 in 1983 to 5.1 in 2001.

These dramatic improvements in infant mortality are due largely to improvements inliving conditions such as sanitation, shelter, quality of drinking water and better nutri-tion. Some medical measures such as better obstetric and neonatal care and the ad-vent of mass vaccination have also played substantial roles. The delivery of better acutecare for seriously ill and injured children is likely to assist in reducing mortality ratesfurther.

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INTRODUCTION

The infant mortality rate is defined as the number of deaths of children under 1 year ofage in one calendar year per 1000 live births in the same calendar year.

The mortality rate decreases significantly with the increasing age of the child, with thehighest death rate occurring in the first 28 days, and indeed most deaths occur on thefirst day of life. Male children are more likely to die than females in all age groups, atrend which is not reversed until much later in life.

Table 1.1. Number of deaths and death rate by age group

England and Wales 2001 Australia 2000 Holland 2001

Age group Number Rate per 1000 Number Rate per 1000 Number Rate per 1000

0–28 days 2137 3.6 858 3.4 3.94–52 weeks 1103 1.9 406 1.6 1.51–4 years 588 0.24 260 0.2 210 0.45–14 years 832 0.12 432 0.1 280 0.11–14 years 1420 0.15 692 0.1 490

Source: England and Wales – Office of National Statistics 2003Australia – Australian Bureau of Statistics 2003Holland – Centraal Bureau voor de Statistiek

1.3 CAUSES OF DEATH IN CHILDHOOD

The causes of death vary with age as shown in Table 1.2. In the newborn period the mostcommon causes are congenital abnormalities and factors associated with prematurity,such as respiratory immaturity, cerebral haemorrhage and infection due to immaturityof the immune response.

From 1 month to 1 year of age sudden infant death syndrome (SIDS) is the mostcommon cause of death in developed countries. In many of these countries there hasbeen a striking reduction in the incidence of SIDS over the last few years. In Englandand Wales, for example, the number of deaths has decreased from 1597 in 1988 to 164 in2002. This reduction has followed national campaigns to inform parents of risk factorssuch as the prone sleeping position in the infant and parental smoking.

Congenital abnormalities contribute significantly to mortality rates during all stagesof childhood. Complex congenital heart disease, central nervous system malformations,metabolic disorders and chromosomal anomalies are the commonest lethal disorders.

Table 1.2. Common causes of death by age group, England and Wales, 2002

4–52 weeks 1–4 years 5–14 years

Cause Number Percent Number Percent Number Percent

Sudden infant death syndrome 164 13 0 0 0 0Congenital abnormality 205 20 97 18 64 8Infection 65 6 52 10 27 3Trauma 53 5 90 16 197 24Neoplasms 15 1 89 16 218 26

Source: England and Wales – Office of National Statistics 2004

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INTRODUCTION

After 1 year of age trauma is a frequent cause of death in the UK, and remains sountil well into adult life. Deaths from trauma have been described as falling into threegroups. In the first group there is overwhelming damage at the time of trauma, andthe injury caused is incompatible with life; children with such massive injuries will diewithin minutes whatever is done. Those in the second group die because of progressiverespiratory failure, circulatory insufficiency, or raised intracranial pressure secondary tothe effects of injury; death occurs within a few hours if no treatment is administered,but may be avoided if treatment is prompt and effective. The final group consists of latedeaths due to raised intracranial pressure, infection or multiple organ failure. Appropriatemanagement in the first few hours will decrease mortality in this group also.

In developing countries infectious diseases are still major causes of death. Seven outof 10 childhood deaths can be attributed to just five main causes: pneumonia, diarrhoea,measles, malaria and malnutrition. Three out of every four children seen by health ser-vices are suffering from at least one of these conditions. HIV/AIDS has contributed tothis and also been associated with increasing deaths from tuberculosis in countries af-fected. As these societies become more urbanised the mortality from trauma, especiallyfrom motor vehicle accidents, increases. In South Africa, a country which, althoughdeveloping rapidly, has large areas of severe poverty, the under-5’s mortality rate has re-cently been shown to include 40% (42,749) deaths from HIV/AIDS, 11% (11,876) fromlow birth weight, 21% (22,680) from infections and 3% (3506) from trauma. In olderSouth African children, trauma, especially road traffic accidents, homicide and suicideare leading causes of death. In Trinidad, children under 1 year of age accounted for 4%of deaths in 1997, with infant mortality at 17 per 1000 live births. In Trinidadian schoolchildren, the foremost cause of death was injury, with infections causing one fifth ofdeaths.

In developed countries, many children with diseases that were once invariably fatal,such as complex congenital heart disease, inborn errors of metabolism, haematologicalmalignancies or cystic fibrosis, are now treated or “cured” by drugs, operation, diet,transplant or, soon, even gene therapy. In these children, common acute illnesses suchas varicella or chest infections have potentially lethal consequences. They require a lowthreshold for rapid aggressive treatment delivered by a team with an understanding oftheir underlying disease.

Only a minority of childhood deaths, such as those due to end-stage neoplastic disease,are expected and “managed”. There should be timely discussions among child, familyand health carers to identify whether and in what manner resuscitation should be carriedout to prevent unwanted and inappropriate resuscitation and interventions.

1.4 PATHWAYS LEADING TO CARDIORESPIRATORYARREST

As the outcome from cardiorespiratory arrest in children is poor the only effective wayto prevent death and permanent disability is to understand its antecedent events, and beable to recognise and treat them vigorously.

Cardiac arrest in children is rarely due to primary cardiac disease. This differs fromthe situation in an adult where the primary arrest is often cardiac, and circulatory andrespiratory function may remain near-normal until the moment of arrest.

In children, most cardiorespiratory arrests are secondary to hypoxia caused by respi-ratory pathology, including birth asphyxia, inhalation of foreign body, bronchiolitis andasthma. Respiratory arrest also occurs secondary to neurological dysfunction caused bysuch events as a convulsion or poisoning. Raised intracranial pressure (ICP) due to head

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INTRODUCTION

injury or acute encephalopathy eventually leads to respiratory arrest, but severe neuronaldamage has already been sustained before the arrest occurs.

Whatever the cause, by the time of cardiac arrest the child has had a period of respiratoryinsufficiency, which will have caused hypoxia and respiratory acidosis. The combinationof hypoxia and acidosis causes cell damage and death (particularly in more sensitiveorgans such as the brain, liver and kidney), before myocardial damage is severe enoughto cause cardiac arrest.

Most other cardiac arrests in children are secondary to circulatory failure. This willhave resulted often from fluid or blood loss, or from fluid maldistribution within thecirculatory system. The former may be due to gastroenteritis, burns or trauma, whilstthe latter is often caused by sepsis or anaphylaxis. Because all organs are deprived ofessential nutrients and oxygen as shock progresses to cardiac arrest, circulatory failure,like respiratory failure, causes tissue hypoxia and acidosis. In fact, both pathways mayoccur in the same condition. The pathways leading to cardiac arrest in children aresummarised in Figure 1.1.

Figure 1.1. Pathways leading to cardiac arrest in childhood (with examples of underlying causes)

1.5 OUTCOME FROM CARDIAC ARREST IN CHILDREN

The outcome of cardiac arrest in children is invariably poor. Of those few who survive,many are left with permanent neurological deficits. The worst outcome is in children whohave had an out-of-hospital arrest and who arrive at hospital apnoeic and pulseless. Thesechildren have almost no chance of intact neurological survival, especially if cardiopul-monary resuscitation has been going on for 20 minutes or longer. There has often been aprolonged period of hypoxia and ischaemia before the start of adequate cardiopulmonaryresuscitation.

Earlier recognition of seriously ill children and paediatric cardiopulmonary resuscita-tion training for the public could improve the outcome for these children.

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CHAPTER

2Why treat children differently?

2.1 INTRODUCTION

Children are a diverse group of people. They vary enormously in weight, size, shape,intellectual ability and emotional responses. At birth a child is, on average, a 3·5-kg,50-cm-long individual with small respiratory and cardiovascular reserves and an imma-ture immune system. They are capable of limited movement, exhibit limited emotionalresponses and are dependent upon adults for all their needs. Fourteen or more years laterat the other end of childhood, the adolescent is a 50-kg, 160-cm-tall person who lookslike an adult.

Competent management of a seriously ill or injured child who may fall anywherebetween these two extremes requires a knowledge of these anatomical, physiological andemotional differences and a strategy of how to deal with them.

The key differences to consider in children are:

1. Weight2. Anatomical – size and shape3. Physiological – cardiovascular, respiratory, immune function4. Psychological – intellectual ability and emotional response

2.2 WEIGHT

The most rapid changes in weight occur during the first year of life. An averagebirth weight of 3·5 kg would have increased to 10·3 kg by the age of 1 year. Afterthat time weight increases more slowly until the pubertal growth spurt. This isillustrated in the weight chart for boys shown in Figure 2.1.

As most drugs and fluids are given as the dose per kilogram of body weight, it isimportant to determine a child’s weight as soon as possible. The most accurate methodfor achieving this is to weigh the child on scales; however in an emergency this may be

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WHY TREAT CHILDREN DIFFERENTLY?

Figure 2.1. Centile chart for weight in boys

Figure 2.2. Body surface area (percent). (Reproduced courtesy of Smith & NephewPharmaceuticals Ltd.)

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impracticable. In this situation the child’s weight may be estimated by one of a numberof methods.

The Broselow tape uses the height (or length) of the child to estimate weight. The tapeis laid alongside the child and the estimated weight read from the calibrations on the tape.This is a quick, easy and relatively accurate method.

If a child’s age is known and it is between 1 and 10 years, the following formula maybe useful:

Weight (in kg) = 2 (age in years + 4)

The formula method has the added advantage of allowing an estimationof the weight to be made before the child arrives in hospital so that the appro-priate equipment and drugs may be arranged for. Whatever the method, it isessential that the carer is sufficiently familiar with it to be able to use it quickly 64and accurately under pressure.

2.3 ANATOMICAL

As the child’s weight increases with age the size, shape and proportions of variousorgans also change. Particular anatomical changes are relevant to emergency care.

Airway

The airway is influenced by anatomical changes in the tissues of the mouth and neck.In a young child the head is large and the neck short, tending to cause neck flexion andairway narrowing. The face and mandible are small, and teeth or orthodontic appliancesmay be loose. The tongue is relatively large and not only tends to obstruct the airway inan unconscious child, but may also impede the view at laryngoscopy. Finally, the floorof the mouth is easily compressible, requiring care in the positioning of fingers whenholding the jaw for airway positioning. These features are summarised in Figure 2.3.

Figure 2.3. Summary of significant upper airway anatomy

The anatomy of the airway itself changes with age, and consequently different problemsaffect different age groups. Infants less than 6 months old are obligate nasal breathers.As the narrow nasal passages are easily obstructed by mucous secretions, and as upperrespiratory tract infections are common in this age group, these children are at particularrisk of airway compromise. In 3- to 8-year-olds, adenotonsillar hypertrophy may be aproblem. This not only tends to cause obstruction, but also causes difficulty when thenasal route is used to pass pharyngeal, gastric or tracheal tubes.

In all young children the epiglottis is horseshoe-shaped, and projects posteriorly at 45◦,making tracheal intubation more difficult. This, together with the fact that the larynx is

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high and anterior (at the level of the second and third cervical vertebrae in the infant,compared with the fifth and sixth vertebrae in the adult), means that it is easier to intubatean infant using a straight-blade laryngoscope. The cricoid ring is the narrowest part of theupper airway (as opposed to the larynx in an adult). The narrow cross-sectional area atthis point, together with the fact that the cricoid ring is lined by pseudo-stratified ciliatedepithelium loosely bound to areolar tissue, makes it particularly susceptible to oedema.As tracheal tube cuffs tend to lie at this level, uncuffed tubes are preferred in pre-pubertalchildren.

The trachea is short and soft. Overextension of the neck as well as flexion may thereforecause tracheal compression. The short trachea and the symmetry of the carinal anglesmean that not only is tube displacement more likely, but a tube or a foreign body is alsojust as likely to be displaced into the left as the right main-stem bronchus.

Breathing

The lungs are relatively immature at birth. The air–tissue interface has a relatively smalltotal surface area in the infant (less than 3 m2). In addition, there is a 10-fold increase inthe number of small airways from birth to adulthood.

Both the upper and lower airways are relatively small, and are consequently more easilyobstructed. As resistance to flow is inversely proportional to the fourth power of the airwayradius (halving the radius increases the resistance 16-fold), seemingly small obstructionscan have significant effects on air entry in children.

Infants rely mainly on diaphragmatic breathing. Their muscles are more likely to fa-tigue, as they have fewer type I (slow-twitch, highly oxidative, fatigue-resistant) fibrescompared with adults. Pre-term infants’ muscles have even less type I fibres. These chil-dren are consequently more prone to respiratory failure.

The ribs lie more horizontally in infants, and therefore contribute less to chest ex-pansion. In the injured child, the compliant chest wall may allow serious parenchymalinjuries to occur without necessarily incurring rib fractures. For multiple rib fractures tooccur the force must be very large; the parenchymal injury that results is consequentlyvery severe and flail chest is tolerated badly.

Circulation

At birth the two cardiac ventricles are of similar weight; by 2 months of age the RV/LVweight ratio is 0·5. These changes are reflected in the infant’s ECG. During the firstmonths of life the right ventricle (RV) dominance is apparent, but by 4–6 months of agethe left ventricle (LV) is dominant. As the heart develops during childhood, the sizes ofthe P wave and QRS complex increase, and the P–R interval and QRS duration becomelonger.

The child’s circulating blood volume per kilogram of body weight (70–80 ml/kg) ishigher than that of an adult, but the actual volume is small. This means that in infants andsmall children, relatively small absolute amounts of blood loss can be critically important.

Body surface area

The body surface area (BSA) to weight ratio decreases with increasing age. Smallchildren, with a high ratio, lose heat more rapidly and consequently are relatively moreprone to hypothermia. At birth the head accounts for 19% of BSA; this falls to 9% bythe age of 15 years. Figure 2.2 shows these changes.

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2.4 PHYSIOLOGICAL

Respiratory

The infant has a relatively greater metabolic rate and oxygen consumption. This is onereason for an increased respiratory rate. However, the tidal volume remains relativelyconstant in relation to body weight (5–7 ml/kg) through to adulthood. The work ofbreathing is also relatively unchanged at about 1% of the metabolic rate, although it isincreased in the pre-term infant.

Table 2.1. Respiratory rate by age at rest

Age (years) Respiratory rate (breaths per minute)

<1 30–401–2 25–352–5 25–305–12 20–25>12 15–20

In the adult, the lung and chest wall contribute equally to the total compliance. Inthe newborn, most of the impedance to expansion is due to the lung, and is criticallydependent on the surfactant. The lung compliance increases over the first week of life asfluid is removed from the lung. The child’s compliant chest wall leads to prominent sternalrecession and rib space indrawing when the airway is obstructed or lung compliancedecreases. It also allows the intrathoracic pressure to be less “negative”. This reducessmall-airway patency. As a result, the lung volume at the end of expiration is similar tothe closing volume (the volume at which small-airway closure starts to take place).

At birth, the oxygen dissociation curve is shifted to the left and P50 (P2 at 50% oxygensaturation) is greatly reduced. This is due to the fact that 70% of the haemoglobin is inthe form of HbF; this gradually declines to negligible amounts by the age of 6 months.

The immature infant lung is also more vulnerable to insult. Following prolonged venti-lation of a pre-term infant, bronchopulmonary dysplasia may cause oxygen dependencefor up to a year. Many infants who have suffered from bronchiolitis remain “chesty” fora year or more.

Cardiovascular

The infant has a relatively small stroke volume (1·5 ml/kg at birth) but has the highestcardiac index seen at any stage of life (300 ml/min/kg). Cardiac index decreases with ageand is 100 ml/min/kg in adolescence and 70–80 ml/min/kg in the adult. At the same timethe stroke volume increases as the heart gets bigger. As cardiac output is the product ofstroke volume and heart rate, these changes underlie the heart rate changes seen duringchildhood (shown in Table 2.2).

Table 2.2. Heart rate by age

Age (years) Heart rate (beats per minute)

<1 110–1601–2 100–1502–5 95–1405–12 80–120>12 60–100

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As the stroke volume is small and relatively fixed in infants, cardiac output is directlyrelated to heart rate. The practical importance of this is that the response to volumetherapy is blunted because stroke volume cannot increase greatly to improve cardiacoutput. By the age of 2 years myocardial function and response to fluid are similar tothose of an adult.

Systemic vascular resistance rises after birth and continues to do so until adulthood isreached. This is reflected in the changes seen in blood pressure – shown in Table 2.3.

Table 2.3. Systolic blood pressure by age

Age (years) Systolic blood pressure (mmHg)

<1 70–901–2 80–952–5 80–1005–12 90–110>12 100–120

Immune function

At birth the immune system is immature and consequently babies are moresusceptible than older children to many infections such as bronchiolitis, sep-ticaemia, meningitis and urinary tract infections. Maternal antibodies acqui-red across the placenta provide some early protection but these progressivelydecline during the first 6 months. These are replaced slowly by the infant’s as

756

he or she grows older. Breastfeeding provides some protection against respiratory andgastrointestinal infections.

2.5 PSYCHOLOGICAL

Children vary enormously in their intellectual ability and their emotional response. Aknowledge of child development assists in understanding a child’s behaviour and formu-lating an appropriate management strategy. Particular challenges exist in communicatingwith children and as far as possible easing their fear of the circumstances they find them-selves in.

Communication

Infants and young children either have no language ability or are still developing theirspeech. This causes difficulty when symptoms such as pain need to be described. Evenchildren who are usually fluent may remain silent. Information has to be gleaned fromthe limited verbal communication, and from the many non-verbal cues (such as facialexpression and posture) that are available. Older children are more likely to understandaspects of their illness and treatment and so be reassured by adequate age-appropriatecommunication.

Fear

All emergency situations, and many other situations that adults would not classify asemergencies, engender fear in children. This causes additional distress to the child and

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adds to parental anxiety. Physiological parameters, such as pulse rate and respiratory rate,are altered because of it, and this in turn makes clinical assessment more difficult.

Fear is a particular problem in the pre-school child who often has a “magical” conceptof illness and injury. This means that the child may think that the problem has been causedby some bad wish or thought that he or she has had. School-age children and adolescentsmay have fearsome concepts of what might happen to them in hospital because of ideasthey have picked up from adult conversation, films and television.

Knowledge allays fear and it is therefore important to explain things as clearly aspossible to the child. Explanations must be phrased in a way that the child can understand.Play can be used to do this (e.g. applying a bandage to a teddy first), and also helps tomaintain some semblance of normality in a strange and stressful situation. Finally, parentsmust be allowed to stay with the child at all times; their absence from the child’s bedsidewill only add further fears, both to the child and to the parents themselves.

2.6 SUMMARY

• Absolute size and relative body proportions change with age.• Observations on children must be related to their age.• Therapy in children must be related to their age and weight.• The special psychological needs of children must be considered.

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14



CHAPTER

3Structured approach toemergency paediatrics

3.1 INTRODUCTION

The reception of a child with a life-threatening condition or the collapse of a child on theward presents a major challenge to staff. The infrequency and, often unforeseen, natureof the events adds to the anxiety for all, including parents. The structured approach willenable the clinician to manage emergencies.

This approach will initially focus on identifying and treating the immediate threats to life,that is a closed or obstructed airway, absent or distressed respiration, or pulselessness orshock. These first interventions comprise resuscitation.

The next step is to identify the key features that in any serious illness or injury givethe clinician a signpost to the likeliest working diagnosis. From this, the best emergencytreatment can be identified to start to treat the child’s illness or injury.

The final phase of the structured approach is to stabilise the child, focussing on achievinghomoeostasis and system control and leading onto transfer to a definitive care environ-ment, which will often be the paediatric intensive care unit.

Figure 3.1 shows the structured approach in diagrammatic form. Throughout this textthe same structure will be used so the clinician will become familiar with the approachand be able to apply it to any clinical emergency situation.

3.2 PREPARATION

If warning has been received of the child’s arrival then preparations can be made:

• Ensure that appropriate help is available: critical illness and injury need a team ap-proach.

• Work out the likely drug, fluid and equipment needs.

For unexpected emergencies, ensure that all areas where children may be treated arestocked with the drugs, fluid and equipment needed for any childhood emergencies.

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STRUCTURED APPROACH TO EMERGENCY PAEDIATRICS

Figure 3.1. Structured approach to emergency paediatrics

3.3 TEAMWORK

Nowhere is a well-functioning team more vital than in the emergency situation. Successdepends on each team member’s carrying out his or her own tasks and being aware of thetasks and the skills of other team members. The whole must be under the direction of ateam leader. Scenario practice by teams who work together is an excellent way to keepup skills, knowledge and team co-ordination in preparation for the “real thing”.

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STRUCTURED APPROACH TO EMERGENCY PAEDIATRICS

3.4 COMMUNICATION

In the previous chapter, issues about communication with the ill or injured child werehighlighted. Communication is no less important with families and with clinical col-leagues. When things have gone wrong a fault in communication has often been involved.Contemporaneous recording of clinical findings, of the child’s history and of test resultsand management plans seems obvious but in the emergency situation can be overlooked.A template for note keeping is to be found in Chapter 13.

3.5 CONSENT

Consent legislation and practice are complex areas: different jurisdictions have differentrulings. The general approach is that in an emergency where you consider that it is inthe child’s best interests to proceed, you may treat the child, provided it is limited to thattreatment which is reasonably required in that emergency.

In the UK the General Medical Council provides guidance for doctors, and hospitalswill have internal policies with which you should be familiar.

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18



PART

IILIFE SUPPORT

19



20



CHAPTER

4Basic life support

LEARNING OBJECTIVES

In this chapter, you will learn:

• how to assess the collapsed patient and perform basic life support

4.1 INTRODUCTION

Paediatric basic life support (BLS) is not simply a scaled-down version of that providedfor adults. Although the general principles are the same, specific techniques are requiredif optimum support is to be given. The exact techniques employed need to be variedaccording to the size of the child. A somewhat artificial line is generally drawn betweeninfants (less than 1 year old) and small children (less than 8 years old), and this chapterfollows that approach. The preponderance of hypoxic causes of paediatric cardiorespi-ratory arrest means that oxygen delivery rather than defibrillation is the critical step inchildren. This underlines the major differences with the adult algorithm.

By applying the basic techniques described, a single rescuer can support the vitalrespiratory and circulatory functions of a collapsed child with no equipment.

Basic life support is the foundation on which advanced life support is built. Thereforeit is essential that all advanced life support providers are proficient at basic techniques,and that they are capable of ensuring that basic support is provided continuously andwell during resuscitation.

4.2 PRIMARY ASSESSMENT AND RESUSCITATION

Once the child has been approached correctly and a simple test for unresponsivenesshas been carried out, assessment and treatment follow the familiar ABC pattern. Theoverall sequence of basic life support in paediatric cardiopulmonary arrest is summarisedin Figure 4.1.

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BASIC LIFE SUPPORT

Figure 4.1. The overall sequence of basic life support in cardiopulmonary arrest(CPR = cardiopulmonary resuscitation)

The SAFE approach

Additional help should be summoned rapidly. Furthermore, it is essential that therescuer does not become a second victim, and that the child is removed from continuingdanger as quickly as possible. These considerations should precede the initial airwayassessment. They are summarised in Figure 4.2.

Figure 4.2. The SAFE approach

When more than one rescuer is present one starts BLS while another activates theEmergency Medical Services (EMS) system then returns to assist in the BLS effort. If

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BASIC LIFE SUPPORT

there is only one rescuer and no help has arrived after 1 minute of CPR then the rescuermust activate the EMS system himself or herself. In the case of a baby or small childthe rescuer will probably be able to take the victim with him or her to a telephone whilstattempting to continue CPR on the way.

In a few instances the sequence in the above paragraph is reversed. As previouslydescribed, in children, respiratory and circulatory causes of cardiac arrest predominate,and immediate respiratory and circulatory support as provided by the breaths and chestcompressions of BLS can be life saving. However, there are circumstances in whichearly defibrillation may be life saving, i.e. cardiac arrests caused by arrhythmia. On theseoccasions, where there is more than one rescuer, one may start BLS and another summonthe EMS as above. But if there is a lone rescuer then he or she should activate the EMSsystem first and then start BLS afterwards.

The clinical indication for EMS activation before BLS by a lone rescuer include:

• witnessed sudden collapse with no apparent preceding morbidity• witnessed sudden collapse in a child with a known cardiac condition and in the

absence of a known or suspected respiratory or circulatory cause of arrest.

Public access AEDs may result in a better outcome for this small group when guide-lines for trained lay persons in the use of AEDs for children have been agreed. (seesection 4.3)

Are you alright?

The initial simple assessment of responsiveness consists of asking the child “Are youalright?” and gently applying painful stimulus to the child. Infants and very small chil-dren who cannot talk yet, and older children who are very scared, are unlikely to replymeaningfully, but may make some sound or open their eyes to the rescuer’s voice ortouch.

In cases associated with trauma, the neck and spine should be immobilised during thisassessment. This can be achieved by a lone rescuer by placing one hand firmly on thehead.

Airway (A)

An obstructed airway may be the primary problem, and correction of the obstructioncan result in recovery without further intervention.

If a child is having difficulty breathing, but is conscious, then transport to hospitalshould be arranged as quickly as possible. A child will often find the best position tomaintain his or her own airway, and should not be forced to adopt a position that may beless comfortable. Attempts to improve a partially maintained airway in an environmentwhere immediate advanced support is not available can be dangerous, because totalobstruction may occur.

If the child is not breathing it may be because the airway has been blocked by thetongue’s falling back and obstructing the pharynx. An attempt to open the airway shouldbe made using the head tilt/chin lift manoeuvre. The rescuer places the hand nearest tothe child’s head on the forehead and applies pressure to tilt the head back gently. Thedesirable degrees of tilt are neutral, in the infant, and sniffing, in the child.

These are shown in Figures 4.3 and 4.4.

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BASIC LIFE SUPPORT

Figure 4.3. Chin lift in infants

Figure 4.4. Chin lift in children

The fingers of the other hand should then be placed under the chin and the chin shouldbe lifted upwards. Care should be taken not to injure the soft tissue by gripping too hard.As this action can close the child’s mouth, it may be necessary to use the thumb of thesame hand to part the lips slightly.

The patency of the airway should then be assessed. This is done by:

LOOKing for chest and/or abdominal movement,LISTENing for breath sounds andFEELing for breath,

and is best achieved by the rescuer placing his or her face above the child’s, with the earover the nose, the cheek over the mouth and the eyes looking along the line of the chestfor up to 10 seconds.

If the head tilt/chin lift manoeuvre is not possible or is contraindicated because ofsuspected neck injury, then the jaw thrust manoeuvre can be performed. This is achievedby placing two or three fingers under the angle of the mandible bilaterally and lifting thejaw upwards. This technique may be easier if the rescuer’s elbows are resting on the samesurface as the child is lying on. A small degree of head tilt may also be applied if there isno concern about neck injury. This is shown in Figure 4.5.

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BASIC LIFE SUPPORT

Figure 4.5. Jaw thrust

As before, the success or failure of the intervention is assessed using the techniquedescribed above.

LOOKLISTEN

FEEL

It should be noted that, if there is a history of trauma, then the head tilt/chin liftmanoeuvre may exacerbate cervical spine injury. The safest airway intervention in thesecircumstances is jaw thrust without head tilt. Proper cervical spine control can onlybe achieved in such cases by a second rescuer maintaining in-line cervical stabilisationthroughout.

The finger sweep technique often recommended in adults should not be used in chil-dren. The child’s soft palate is easily damaged, and bleeding from within the mouthcan worsen the situation. Furthermore, foreign bodies may be forced further down theairway; they can become lodged below the vocal cords (vocal folds) and be even moredifficult to remove.

If a foreign body is not obvious but is highly suspected and sufficient ventilation isoccurring, inspection should be done under direct vision with a laryngoscope in hospitaland, if appropriate, removal should be attempted using Magill’s forceps. For interventionin the absence of effective ventilation see section 4.5.

In the child with a tracheostomy, additional procedures may be necessary. (see Chap-ter 20, section on management of a blocked tracheostomy)

Breathing (B)

If the airway-opening techniques described above do not result in the resumption of ad-equate breathing within 10 seconds, exhaled air resuscitation should be commenced. Therescuer should distinguish between adequate and ineffective, and gasping or obstructedbreathing. If in doubt, attempt rescue breathing.

Up to five initial rescue breaths should be givento achieve two effective breaths.

While the airway is kept open as described above, the rescuer breathes in and seals hisor her mouth around the victim’s mouth, or mouth and nose as shown in Figure 4.6. Ifthe mouth alone is used then the nose should be pinched closed using the thumb andindex fingers of the hand that is maintaining head tilt. Slow exhalation (1–1.5 seconds) bythe rescuer should make the victim’s chest rise. The rescuer should take a breath betweenrescue breaths to maximise oxygenation of the victim.

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BASIC LIFE SUPPORT

Figure 4.6. Mouth-to-mouth-and-nose in an infant

If the rescuer is unable to cover the mouth and nose in an infant he or she may attemptto seal only the infant’s nose or mouth with his or her mouth and should close the infant’slips or pinch the nose to prevent air escape.

As children vary in size only general guidance can be given regarding the volume andpressure of inflation (see the box).

General guidance for exhaled air resuscitation

• The chest should be seen to rise• Inflation pressure may be higher because the airway is small• Slow breaths at the lowest pressure reduce gastric distension• Firm, gentle pressure on the cricoid cartilage may reduce gastric insufflation

If the chest does not rise then the airway is not clear. The usual cause is failure toapply correctly the airway-opening techniques discussed above. Thus, the first thing todo is to readjust the head tilt/chin lift position, and try again. If this does not work jawthrust should be tried. It is quite possible for a single rescuer to open the airway usingthis technique and perform exhaled air resuscitation; however, if two rescuers are presentone should maintain the airway whilst the other breathes for the child. Up to five rescuebreaths may be attempted so that for the inexperienced rescuer at least two are effective.

Failure of both head tilt/chin lift and jaw thrust should lead to the suspicion that aforeign body is causing the obstruction, and appropriate action should be taken. (see“Choking Child”, section 4.5)

Circulation (C)

Once the rescue breaths have been given as above, attention should be turned to thecirculation.

AssessmentInadequacy of the circulation is recognised by the absence of a central pulse for up

to 10 seconds, by the presence of a pulse at an insufficient rate and by the absence ofother signs of circulation, i.e. no breaths or cough in response to rescue breaths and nospontaneous movement. In children, as in adults, the carotid artery in the neck can bepalpated.

In infants the neck is generally short and fat, and the carotid artery may be difficultto identify. Therefore the brachial artery in the medial aspect of the antecubital fossa(Figure 4.7), or the femoral artery in the groin, should be felt.

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BASIC LIFE SUPPORT

Figure 4.7. Feeling for the brachial pulse

Start chest compressions if

• no pulse• slow pulse• no signs of circulation

“Unnecessary” chest compressions are almost never damaging.If the pulse is absent for up to 10 seconds or is inadequate (less than 60 beats per

minute, with signs of poor perfusion) and/or there are no other signs of circulation,then cardiac compression is required. If the pulse is present – and has an adequate rate,with good perfusion – but apnoea persists, exhaled air resuscitation must be continueduntil spontaneous breathing resumes. Signs of poor perfusion include pallor, lack ofresponsiveness and poor muscle tone.

Cardiac compressionFor the best output the child must be placed lying flat on his or her back, on a hard

surface. In infants it is said that the palm of the rescuer’s hand can be used for thispurpose, but this may prove difficult in practice.

Children vary in size, and the exact nature of the compressions given should reflect this.In general, infants (less than 1 year) require a technique different from small children. Inchildren over 8 years of age, the method used in adults can be applied with appropriatemodifications for their size. Compressions should be approximately one third to one halfof the depth of the child’s or infant’s chest.

Infants As the infant heart is lower with relation to external landmarks when comparedto older children and adults, the area of compression is found by imagining a line betweenthe nipples and compressing over the sternum one finger-breadth below this line. Twofingers are used to compress the chest. This is shown in Figure 4.8. There is someevidence that infant cardiac compression can be more effectively achieved using thehand-encircling technique: the infant is held with both the rescuer’s hands encirclingor partially encircling the chest. The thumbs are placed over the correct part of thesternum (as detailed above) and compression carried out, as shown in Figure 4.9. Thismethod is only possible when there are two rescuers, as the time needed to repositionthe airway precludes its use by a single rescuer if the recommended rates of compressionand ventilation are to be achieved. The single rescuer should use the two-finger method,employing the other hand to maintain the airway position as shown in Figure 4.8.

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BASIC LIFE SUPPORT

Figure 4.8. Infant chest compression: two-finger technique

Figure 4.9. Infant chest compression: hand-encircling technique

Small children The area of compression is one finger-breadth above the xiphisternum.The heel of one hand is used to depress the sternum (Figure 4.10).

Figure 4.10. Chest compression in small children

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BASIC LIFE SUPPORT

Larger children (in general those of 8 years and older) The area of compression is twofinger-breadths above the xiphisternum. The heels of both hands are used to depress thesternum (Figure 4.11).

Figure 4.11. Chest compression in older children

Once the correct technique has been chosen and the area for compression identified,five compressions should be given, in older children (8 years and above) the number ofcompressions is 15.

Continuing cardiopulmonary resuscitation

The compression rate at all ages is 100 per minute. A ratio of five compressions to oneventilation is maintained whatever the number of rescuers, except in older children (8years and above) who should receive a ratio of 15 compressions to 2 ventilations with anynumber of rescuers. If no help has arrived the emergency services must be contacted after1 minute of cardiopulmonary resuscitation. With pauses for ventilation there will be lessthan 100 compressions per minute although the rate is 100 per minute. Compressionscan be recommenced at the end of inspiration and may augment exhalation. Apart fromthis interruption to summon help, basic life support must not be interrupted unless the child movesor takes a breath.

Any time spent readjusting the airway or re-establishing the correct position for com-pressions will seriously decrease the number of cycles given per minute. This can bea very real problem for the solo rescuer, and there is no easy solution. In the infantand small child, the free hand can maintain the head position. The correct position forcompressions does not need to be remeasured after each ventilation.

The cardiopulmonary resuscitation manoeuvres recommended for infants and childrenare summarised in Table 4.1.

Mechanical adjuncts for chest compression

Mechanical devices to compress the sternum are currently not recommended for paedi-atric patients. They were designed and tested for use in adults and there is no informationon safety and efficacy in childhood.

Similarly, active compression–decompression CPR, considered an optional techniquein adults, has not been studied and is therefore not recommended in children.

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BASIC LIFE SUPPORT

Table 4.1. Summary of basic life support techniques in infants and children

Infant (<1yr) Small child (1–7) Larger child (8+)

AirwayHead-tilt position Neutral Sniffing Sniffing

BreathingInitial slow breaths Two effective Two effective Two effective

CirculationPulse check Brachial or femoral Carotid CarotidLandmark One finger-breadth

below nipple lineOne finger-breadth

above xiphisternumTwo finger-breadths

above xiphisternumTechnique Two fingers or two

thumbsOne hand Two hands

Cardiopulmonaryresuscitation ratio

5:1 5:1 15:2

Automatic external defibrillators (AEDs) in children

The use of the AED is now included in basic life support teaching for adults becauseearly defibrillation is the most effective intervention for the large majority of unpredictedcardiac arrests in adults. As has been stated, in children and young people circulatoryor respiratory causes of cardiac arrest predominate. However, in certain circumstances(described in section 4.2) children may suffer a primary cardiac cause for cardiac arrest,and the use of an AED may be life saving. Recently there has been a large increase inthe number of AEDs, together with trained operators, made available in public placessuch as airports, places of entertainment and shops, so the opportunity for their use willcorrespondingly increase. Public access AEDs may result in a better outcome for thissmall group when guidelines for use by trained lay people in under-8-year-olds have beenagreed.

In this text the discussion of the use of AEDs with regard to children will be found inthe chapter on The Management of Cardiac Arrest (Chapter 6).

Recovery position

No specific recovery position has been identified for children. The child should beplaced in a position that ensures maintenance of an open airway, ability to monitor andgain access to the patient, security of the cervical spine and attention to pressure points.

Audio prompts

The use of audio prompts such as a metronome set at 100 beats per minute appearsto help in both training and performance of CPR to keep chest compressions at therecommended rate.

4.2 BASIC LIFE SUPPORT AND INFECTION RISK

There have been a few reports of transmission of infectious diseases from casualties torescuers during mouth-to-mouth resuscitation. The most serious concern in children ismeningococcus, and rescuers involved in the resuscitation of the airway in such patientsshould take standard prophylactic antibiotics (usually rifampicin).

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BASIC LIFE SUPPORT

There have been no reported cases of transmission of either hepatitis B or human im-munodeficiency virus (HIV) through mouth-to-mouth ventilation. Blood-to-blood con-tact is the single most important route of transmission of these viruses, and in non-traumaresuscitations the risks are negligible. Sputum, saliva, sweat, tears, urine and vomit arelow-risk fluids. Precautions should be taken, if possible, in cases where there might becontact with blood, semen, vaginal secretions, cerebrospinal fluid, pleural and peritonealfluids and amniotic fluid. Precautions are also recommended if any bodily secretion con-tains visible blood. Devices that prevent direct contact between the rescuer and the victim(such as resuscitation masks) can be used to lower risk; gauze swabs or any other porousmaterial placed over the victim’s mouth is of no benefit in this regard.

The number of children in the UK with AIDS or HIV-1 infection is less than thenumber of adults similarly affected. If transmission of HIV-1 does occur in the UK, it istherefore much more likely to be from adult rescuer to child rather than the other wayaround.

In countries where HIV/AIDS is more prevalent the risk to the rescuer will be greater.In South Africa, in a medical ward 25–40% of children may be HIV-positive but theprevalence is lower in trauma cases. In the Caribbean, HIV prevalence is second onlyto sub-Saharan Africa. The situation may change, as effective anti-retroviral agents aremade available to poor countries.

Although practice manikins have not been shown to be a source of infection, regularcleaning is recommended and should be carried out as shown in the manufacturer’sinstructions. Infection rates vary from country to country and rescuers must be aware ofthe local risk.

4.3 THE CHOKING CHILD

Introduction

The vast majority of deaths from foreign body aspiration occur in pre-school children.Virtually anything may be inhaled. The diagnosis is very rarely clear-cut, but should besuspected if the onset of respiratory compromise is sudden and is associated with cough-ing, gagging and stridor. Airway obstruction may also occur with infections such as acuteepiglottitis and croup. In such cases, attempts to relieve the obstruction using the meth-ods described below are dangerous. Children with known or suspected infectious causesof obstruction, and those who are still breathing and in whom the cause of obstructionis unclear, should be taken to hospital urgently. The treatment of these children is dealtwith in Chapter 8.

The physical methods of clearing the airway, described below, should therefore onlybe performed if:

1. The diagnosis of foreign body aspiration is clear-cut (witnessed or strongly suspected)and ineffective coughing and increasing dyspnoea, loss of consciousness or apnoeahave occurred.

2. Head tilt/chin lift and jaw thrust have failed to open the airway of an apnoeic child.(The sequence of instructions is shown in Figure 4.12.)

If the child is coughing he should be encouraged. No intervention should be madeunless the cough becomes ineffective (quieter) or the child loses consciousness. A spon-taneous cough is more effective than any externally imposed manoeuvre.

If a foreign body is easily visible and accessible in the mouth then remove it but whileattempting that, take great care not to push it further into the airway. Do not performblind finger sweeps of the mouth or upper airway as these may further impact a foreignbody and damage tissues without removing the object.

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BASIC LIFE SUPPORT

Figure 4.12. The sequence of actions in a choking child

Infants

Abdominal thrusts may cause intra-abdominal injury in infants. Therefore a combi-nation of back blows and chest thrusts is recommended for the relief of foreign bodyobstruction in this age group.

The baby is placed along one of the rescuer’s arms in a head-down position, with therescuers hand supporting the infant’s jaw in such a way as to keep it open, in the neutralposition. The rescuer then rests his or her arm along the thigh, and delivers five backblows with the heel of the free hand.

If the obstruction is not relieved the baby is turned over and laid along the rescuer’sthigh, still in a head-down position. Five chest thrusts are given – using the same land-marks as for cardiac compression but at a rate of one per second. If an infant is too largeto allow use of the single-arm technique described above, then the same manoeuvres canbe performed by laying the baby across the rescuer’s lap. These techniques are shown inFigures 4.13 and 4.14.

Figure 4.13. Back blows in an infant

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BASIC LIFE SUPPORT

Figure 4.14. Chest thrusts in an infant

Children

Back blows and chest thrusts can be used as in infants (Figure 4.15). In the child theHeimlich manoeuvre can also be used. This can be performed with the victim eitherstanding, sitting, kneeling or lying.

Figure 4.15. Back blows in a small child

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BASIC LIFE SUPPORT

If this is to be attempted with the child standing, kneeling or sitting, the rescuer movesbehind the victim and passes his or her arms around the victim’s body. Owing to the shortheight of children, it may be necessary for an adult to raise the child or kneel behind themto carry out the standing manoeuvre effectively. One hand is formed into a fist and placedagainst the child’s abdomen above the umbilicus and below the xiphisternum. The otherhand is placed over the fist, and both hands are thrust sharply upwards into the abdomen.This is repeated five times unless the object causing the obstruction is expelled beforethen. This technique is shown in Figure 4.16.

Figure 4.16. Heimlich manoeuvre in a standing child

To carry out the Heimlich manoeuvre in a supine child, the rescuer kneels at his orher feet (Figure 4.17). If the child is large it may be necessary to kneel astride him orher. The heel of one hand is placed against the child’s abdomen above the umbilicus andbelow the xiphisternum. The other hand is placed on top of the first, and both handsare thrust sharply upwards into the abdomen, with care being taken to direct the thrustin the midline. This is repeated five times unless the object causing the obstruction isexpelled before that.

Figure 4.17. Abdominal thrusts

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BASIC LIFE SUPPORT

Note that lay people are recommended to perform relief of choking manoeuvres onlyin conscious infants and children. If the victim is unresponsive and apnoeic, lay peopleare advised to attempt CPR and call the EMS.

Trained health care professionals may attempt foreign body removal by relief of chokingmanoeuvres in conscious and unresponsive, apnoeic victims where indicated.

4.4 SUMMARY

Figure 4.18. Overall sequence of basic life support in cardiac arrest

The teaching in this chapter is consistent with the ILCOR guidelines, Re-suscitation 2000, and there are an enormous number of references which haveinformed this process. These are available on the ALSG Web site. See detailson the “Contact Details and Further Information” page.

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36



CHAPTER

5Advanced support of the

airway and ventilation

LEARNING OBJECTIVES


• how to assess and manage the airway with adjuncts and equipment• how to support breathing with simple equipment• how to respond to an airway/breathing problem with a structured approach

5.1 INTRODUCTION

Management of airway and breathing has priority in the resuscitation of patients ofall ages; however, the rate at which respiratory function can deteriorate in children isparticularly high. Effective resuscitation techniques must be applied quickly and in orderof priority. The differences between adults and children must be realised and familiaritywith equipment assured. Techniques for obtaining a patent and protected airway, and forachieving adequate ventilation and oxygenation, must be learned and practised. Thesetechniques must be integrated into a prioritised system of care. It should be stressed thatbasic, simple techniques are often effective and life saving.

5.2 EQUIPMENT FOR MANAGING THE AIRWAY

Necessary airway equipmentFace masksAirways including laryngeal mask airways (LMAs)Self-inflating bag–valve–mask devicesTracheal tubes, introducers and connectorsSuction devicesCricothyroidotomy cannulae

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ADVANCED SUPPORT OF THE AIRWAY AND VENTILATION

The airway equipment indicated in the box should be available in all resuscitation areas.It is crucial that familiarity with it is gained before an emergency situation occurs.

Pharyngeal airways

There are two main types of pharyngeal airway:

1. Oropharyngeal2. Nasopharyngeal

1. The oropharyngeal or Guedel airway is used in the unconscious or obtunded patientto provide a patent airway channel between the tongue and the posterior pharyngealwall. It may also be used to stabilise the position of an oral endotracheal tube.

In the awake patient with an intact gag reflex, it may not be tolerated and mayinduce vomiting.

The oropharyngeal airway is available in a variety of sizes. A correctly sized airwaywhen placed with its flange at the centre of the incisors, then curved around the face,will reach the angle of the mandible. Too small an airway may be ineffective, too largean airway may cause laryngospasm. Either may cause mucosal trauma or may worsenairway obstruction. Reassessment following placement is therefore a vital part of safeinsertion of an airway device. Techniques for insertion are described in Chapter 20.

2. The nasopharyngeal airway is often better tolerated than the Guedel airway. It is con-traindicated in fractures of the anterior base of the skull. It may also cause significanthaemorrhage from the vascular nasal mucosa. A suitable length can be estimatedby measuring from the tip of the nose to the tragus of the ear. An appropriate di-ameter is one that just fits into the nostril without causing sustained blanching ofthe alae nasi. As small-sized nasopharyngeal airways are not commercially available,shortened endotracheal tubes may be used.

The acid test of success, as in all therapeutic interventions, is that insertion of one orother of these devices should result in improvement in the patient’s condition. If it doesnot occur then a reappraisal of the choice or size of airway is urgently required.

Figure 5.1. Sizing an oropharyngeal airway

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Laryngoscopes

Two principal designs of laryngoscope for use in children exist: straight bladed andcurved bladed.

The straight-bladed laryngoscope is usually employed to directly lift the epiglottis,thereby uncovering the vocal folds. The advantage of this approach is that the epiglottisis moved sufficiently so that it does not obscure the cords. The disadvantage potentiallyis vagal stimulation causing laryngospasm or bradycardia.

The curved-bladed laryngoscope is designed to move the epiglottis forward by liftingit from in front. The tip of the blade is inserted into the mucosal pocket, known as thevallecula, anterior to the epiglottis and the epiglottis is then moved forward by pressurein the vallecula. This may be equally effective at obtaining a view of the cords and has theadvantage that less vagal stimulation ensues, as the mucosa of the vallecula is innervatedby the glossopharyngeal nerve.

A laryngoscope blade should be chosen appropriate for age. It is possible to intubatewith a blade which is too long but not one which is too short.

Laryngoscopes are notoriously unreliable pieces of equipment which may develop flatbatteries and unserviceable bulbs very quickly between uses. It is vital therefore, that aspare should be available at all times and that equipment should be regularly checked toensure it is in good working order.

Trachea

Laryngeal inlet

Figure 5.2. View of larynx using a straight-bladed laryngoscope

Tracheal tubes

Tracheal tubes come in a variety of designs, the most useful for resuscitation beingthe plain plastic tube. Uncuffed tubes are preferred up until approximately 8 to 10 yearsof age. Until this point, the larynx is circular in cross section and the narrowest part of

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Epiglottis

Trachea

Laryngeal inlet

Figure 5.3. View of larynx using a curved-bladed laryngoscope

it is at the cricoid ring, rather than the vocal cords. An appropriately sized tube shouldgive a relatively gas-tight fit in the larynx but should not be so tight that no leak isaudible when the bag is compressed. Failure to observe this condition may lead to dam-age to the mucosa at the level of the cricoid ring and to subsequent oedema followingextubation.

Estimating the appropriate size of a tracheal tube is carried out as follows:

Internal diameter (mm) = (Age/4) + 4Length (cm) = (Age/2) + 12 for an oral tubeLength (cm) = (Age/2) + 15 for nasal tube

These formulae are appropriate for ages over 1 year. Neonates usually require a tubeof internal diameter 3–3.5 mm, although pre-term infants may need one of diameter2.5 mm. Tracheal tubes are measured in sizes by their internal diameter in millimetres.They are provided in whole- and half-millimetre sizes. The clinician should select a tubeof appropriate size but also prepare one a size smaller and one a size larger.

Tracheal tube introducersIntubation can be facilitated by the use of a stylet or introducer, placed through the

lumen of the tracheal tube. There are two types: soft and flexible or firm and malleable.The former can be allowed to project out of the tip of the tube, as long as it is handledvery gently. The latter is used to alter the shape of the tube, but can easily damage thetissues if allowed to protrude from the end of the tracheal tube. Tracheal tube introducersshould not be used to force a tracheal tube into position.

Tracheal tube connectorsIn adults, the proximal end of the tube connectors is of standard size, based on the

15–22-mm system, ensuring that they can be connected to a standard self-inflating bag.

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The same standard Portex system exists for children, including neonates. Smaller con-nectors may be used later in ICUs (in infants) but should be avoided in the resuscitationsetting.

Magill’s forceps

Magill’s forceps are angled to allow a view around the forcep when in the mouth. Theymay be useful to help position a tube through the cords by lifting it anteriorly, or toremove pharyngeal or supraglottic foreign bodies.

Suction devices

In the resuscitation room, the usual suction device is the pipeline vacuum unit. Itconsists of a suction hose inserted into a wall terminal outlet, a controller (to adjust thevacuum pressure), a reservoir jar, suction tubing and a suitable sucker nozzle or catheter.In order to aspirate vomit effectively, it should be capable of producing a high negativepressure and a high flow rate, although these can be reduced in non-urgent situations, soas not to cause mucosal injury.

The most useful suction ending is the Yankauer sucker, which is available in both adultand paediatric sizes. It may have a side hole, which can be occluded by a finger, allowinggreater control over vacuum pressure. In small infants, a suction catheter and a Y-pieceare often preferred, but are less capable of removing vomit.

Portable suction devices are required for resuscitation in remote locations, and fortransport to and from the resuscitation room. These are usually battery powered.

Tracheal suction catheters

These may be required after intubation to remove bronchial secretions or aspiratedfluids. In general, the appropriate size in French gauge is numerically twice the internaldiameter in millimetres, e.g. for a 3-mm tube the correct suction catheter is a Frenchgauge 6.

Cricothyroidotomy cannulae and ventilation systems

Purpose-made cricothyroidotomy cannulae are available, usually in three sizes:12-gauge for an adult, 14-gauge for a child and 18-gauge for a baby. They are less liableto kinking than intravenous cannulae and have a flange for suturing or securing to theneck.

In an emergency, an intravenous cannula can be inserted through the cricothyroidmembrane and oxygen insufflated at 2 l/min to provide some oxygenation (but no ven-tilation). A side hole can be cut in the oxygen tubing or a Y-connector can be placedbetween the cannula and the oxygen supply, to allow intermittent occlusion and achievepartial ventilation as described in Chapter 20.

5.3 EQUIPMENT FOR PROVIDING OXYGEN ANDVENTILATION

The equipment for oxygenation and ventilation indicated in the box should be readilyavailable.

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Necessary equipment for oxygenation and ventilation

Oxygen source and masks for spontaneous breathingFace masks (for artificial ventilation)Self-inflating bagsT-piece and open-ended bagMechanical ventilatorsChest tubesGastric tubes

Oxygen source and masks for spontaneous breathing

A wall oxygen supply (at a pressure of 4 atmospheres, 400 kPa or 60 p.s.i.) is providedin most resuscitation rooms. A flowmeter capable of delivering at least 15 l/min shouldbe fitted.

A mask with a reservoir bag should be used in the first instance so that a high concen-tration of oxygen is delivered. A simple mask or other device such as a head box may beused later on if a high oxygen concentration is no longer required. Nasal prongs are oftenwell tolerated in the pre-school age, but they cause drying of the airway, may cause nasalobstruction in infants and provide an unreliable oxygen concentration.

Younger children are more susceptible to the drying effect of a non-humidified oxygensupply.

Although the pre-term infant is vulnerable to retrolental fibroplasia caused by high-concentration oxygen, high concentrations should never be withheld for immediate re-suscitation.

Face masks (for artificial ventilation)

Face masks for mouth-to-mouth or bag–valve–mask ventilation in infants are of twomain designs. Some masks conform to the anatomy of the child’s face and have a lowdeadspace. Circular soft plastic masks give an excellent seal and are preferred by many.Children’s masks should be clear to allow the child’s colour or the presence of vomit tobe seen.

The Laerdal pocket mask is a single-size clear plastic mask with an air-filled cushionrim designed for mouth-to-mask resuscitation. It can be supplied with a port for attachingto the oxygen supply and can be used in adults and children. By using it upside down itmay be used to ventilate an infant.

Self-inflating bags

Self-inflating bags come in three sizes: 250, 500 and 1500 ml. The smallest bag isineffective except in very small babies. The two smaller sizes usually have a pressure-limiting valve set at 4.5 kPa (45 cmH2O), which may (rarely) need to be overriddenfor high resistance/low compliance lungs, but which protects the normal lungs frominadvertent barotrauma. The patient end of the bag connects to a one-way valve of afish-mouth or leaf-flap design. The opposite end has a connection to the oxygen supplyand to a reservoir attachment. The reservoir enables high oxygen concentrations to bedelivered. Without a reservoir bag, it is difficult to supply more than 50% oxygen to thepatient whatever the fresh gas flow, whereas with one, an inspired oxygen concentrationof 98% can be achieved.

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T-piece and open-ended bag

This equipment should only be used in children up to about 20 kg. It is used frequentlyby anaesthetists, but is difficult to use for inexperienced hands and should not be used ina resuscitation environment. It is entirely ineffective unless a pressurised supply of freshgas is available.

Mechanical ventilators

A detailed discussion of individual mechanical ventilators is beyond the scope of thisbook. If a ventilator is used, continual re-evaluation with monitoring of expired CO2 ismandatory, as is measurement of arterial blood gases.

Chest drain

These are included because haemothorax or pneumothorax may severely limit venti-lation. They are described elsewhere (Chapter 22).

Gastric tubes

Children are prone to air swallowing and vomiting. Air may also be inadvertentlyforced into the stomach during bag-and-mask ventilation. This may cause vomiting, vagalstimulation and diaphragmatic splinting. A gastric tube will decompress the stomach andsignificantly improve both breathing and general well-being. Withholding the procedure“to be kind to the child” may cause more distress than performing it.

5.4 PRACTICAL SKILLS

The following practical skills are described in detail in Chapter 20:

• Oropharyngeal airway insertionsmall childolder child

• Nasopharyngeal airway insertion• Ventilation without intubation

mouth-to-mask ventilationbag-and-mask ventilation

• Orotracheal intubation (including Rapid Sequence Induction)infant/small childolder child

• LMA insertion• Surgical airway

needle cricothyroidotomysurgical cricothyroidotomy

Tracheal tube placement check

Following the placement of the tracheal tube in the trachea its position must be verifiedby:

• Observing bilateral and symmetrical movement of the chest

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• Auscultation of chest and abdomen• Monitoring expired carbon dioxide in the exhaled air by either colour change cap-

nometry or carbon dioxide capnography

The continued monitoring of expired carbon dioxide is a good indicator of effectiveventilation, but it must be remembered that carbon dioxide will not be detected in theabsence of a circulation (cardiac arrest) or where the lungs have not yet been inflated (atbirth).

Laryngeal mask airway

The laryngeal mask airway (LMA) is an airway device which is widely used in adult andpaediatric anaesthesia. It is also commonly used in adult resuscitation. It is an excellentdevice for ventilation but does not offer the protection against regurgitation and aspirationwhich an endotracheal tube does.

The smaller sizes used in children whilst easy to position are also easy to dislodge, andmay provide a false sense of security to the resuscitator.

The place of the laryngeal mask airway in resuscitation of infants and children is stilluncertain, although for those proficient in its use, it may be life saving in the situation of“can’t intubate, can’t ventilate”. For this reason if for no other, it should be available inany area where intubation might be carried out.

A variety of other, new airway devices have become available in recent years but noneof these are currently recommended for use in paediatrics.

5.5 PUTTING IT TOGETHER: AIRWAY ANDBREATHING MANAGEMENT

In order to respond urgently and yet retain thoroughness, effective emergency man-agement demands a systematic, prioritised approach. Care can be structured into thefollowing phases:

Primary assessment

This consists of a rapid “physiological” examination to identify immediately life-threatening emergencies. It should be completed in less than a minute. It is prioritisedas shown in the box.

AirwayBreathingCirculationDisability (nervous system)Exposure

From the respiratory viewpoint, do the following:

• Look, listen and feel for airway obstruction, respiratory arrest, depression or distress.• Assess the effort of breathing.• Count the respiratory rate.

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• Listen for stridor and/or wheeze.• Auscultate for breath sounds.• Assess skin colour.

If a significant problem is identified, management should be started immediately. Afterappropriate interventions have been performed, primary assessment can be resumed orrepeated.

Resuscitation

During this phase, life-saving interventions are performed. These include such proce-dures as intubation, ventilation, cannulation and fluid resuscitation. At the same time,oxygen is provided, vital signs are recorded and essential monitoring is established.


Airway• perform basic airway-opening manoeuvres• give oxygen• provide suction• place airway adjuncts• proceed to intubation if required

Breathing• establish adequate ventilation via bag – valve mask• intubate if necessary• perform chest decompression if necessary• consider needle cricothyroidotomy if unable to oxygenate by alternative means• initiate pulse oximetry and other monitoring at this time

Secondary assessment

This consists of a thorough physical examination, together with appropriate investiga-tions. Before embarking on this phase, it is important that the resuscitative measures arefully under way.


• Perform a detailed examination of the airway, neck and chest.• Identify any swelling, bruising or wounds.• Re-examine for symmetry of breath sounds and movement.• Do not forget to inspect and listen to the back of the chest.

Emergency treatment

All other urgent interventions are included in this phase.If at any time the patient deteriorates, return to the primary assessment and recycle

through the system.In the very sick or critically injured child, the primary assessment and resuscitation

phases become integrally bound together. As a problem is identified, care shifts to therelevant intervention, before returning to the next part of the primary assessment. Thesimplified airway and breathing management protocol illustrates how this integration canbe achieved.

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Airway and breathing management protocol

Begin airway assessmentAssess the airway and give oxygenIf evidence of blunt trauma

protect cervical spine from the outsetIf evidence of obstruction or altered consciousness

perform airway-opening manoeuvre commonconsider suction, foreign body removal common

If obstruction persistsconsider oro- or nasopharyngeal airway or LMA common

If obstruction still persistsconsider intubation, and if carried out check position of tracheal tube rare

If intubation is impossible or unsuccessfulconsider cricothyroidotomy very, very rare

If stridor but relatively alertallow self-ventilation whenever possibleencourage oxygen but do not force to wear maskdo not force to lie downdo not inspect the airway (except as a definitive procedure under controlled conditions)assemble expert team and equipment

Assess the breathingIf respiratory arrest or depression

administer oxygen by bag – valve – maskconsider intubation and check the position of tube if inserted

If sedative or paralysing drugs possibleadminister reversal agent

If respiratory distress or tachypnoeaadminister oxygen

If lateralised ventilatory deficitconsider haemopneumothorax, inhaled foreign bodylung consolidation, collapse or effusion

If chest injuryconsider tension pneumothorax and massive haemothoraxflail segment, open pneumothorax

If evidence of tension pneumothoraxperform immediate needle decompressionfollow up with chest drain

If evidence of massive haemothoraxinsert chest draincommence blood volume replacement (simultaneously if possible)

If wheeze or cracklesconsider asthma, bronchiolitis, pneumonia, heart failureremember inhaled foreign body

If evidence of acute severe asthmagive inhaled or intravenous β-agonistsgive steroids, consider aminophylline

Continue primary assessmentproceed to assess the circulation and nervous systemIf deterioration from any cause

reassess airway and breathingbe prepared to intubate and ventilate if not already done

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CHAPTER

6The management of cardiac arrest

LEARNING OBJECTIVES

In this chapter you will learn:

• how to assess the collapsed patient and perform advanced life support

6.1 INTRODUCTION

Cardiac arrest has occurred when there are no palpable central pulses. Before anyspecific therapy is started effective basic life support must be established as described inChapter 4.

Three cardiac arrest rhythms will be discussed in this chapter:

1. Asystole2. Ventricular fibrillation and pulseless ventricular tachycardia3. Pulseless electrical activity (including electro-mechanical dissociation)

The initial approach to cardiac arrest is shown in Figure 6.1, but for the purpose ofteaching, the arrest rhythms will be discussed separately.

6.2 ASYSTOLE

This is the most common arrest rhythm in children, because the response of the youngheart to prolonged severe hypoxia and acidosis is progressive bradycardia leading toasystole.

The ECG will distinguish asystole from ventricular fibrillation, ventricular tachycardiaand pulseless electrical activity. The ECG appearance of ventricular asystole is an almoststraight line; occasionally P-waves are seen. Check that the appearance is not caused byan artifact, e.g. a loose wire or a disconnected electrode. Turn up the gain on the ECGmonitor.

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THE MANAGEMENT OF CARDIAC ARREST

Figure 6.1. Initial approach to cardiac arrest

Figure 6.2. Asystole

Drugs in asystole

Before the administration of any drugs the patient must be receivingcontinuous and effective basic life support and ventilation with oxygen.

The protocol for drug use in asystole is shown in Figure 6.3.

Adrenaline (epinephrine)Adrenaline (epinephrine) is the first line drug for asystole. Through adrenergic-

mediated splanchnic and muco-cutaneous vasoconstriction, its action is to increase aorticdiastolic pressure during chest compressions and thus coronary perfusion pressure andthe delivery of oxygenated blood to the heart, which is a critical determinant of successfulresuscitation. It also enhances the contractile state of the heart, stimulates spontaneouscontractions and increases heart rate. The initial intravenous or intraosseous dose is10 micrograms/kg (0.1 ml of 1:10000 solution). This is best given through a central linebut if one is not in place it may be given through a peripheral line.

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Figure 6.3. Protocol for drugs in asystole. CPR = cardiopulmonary resuscitation; IO = intraosseous;IV = intravenous

In the child with no existing intravenous access the intraosseous route is recommendedas the route of choice as it is rapid and effective. In each case the adrenaline (epinephrine)is followed by a normal saline flush (2–5 ml). If circulatory access cannot be gained, thetracheal tube can be used. Ten times the intravenous dose (100 micrograms/kg) shouldbe given via this route. The drug should be injected quickly down a narrow-bore suctioncatheter beyond the tracheal end of the tube and then flushed in with 1 or 2 ml of normalsaline. In patients with pulmonary disease or prolonged asystole, pulmonary oedema andintrapulmonary shunting may make the tracheal route poorly effective. If there has beenno clinical effect, further doses should be given intravenously as soon as circulatory accesshas been secured.

Alkalising agentsChildren with asystole will be acidotic as cardiac arrest has usually been preceded by

respiratory arrest or shock. However, the routine use of alkalising agents has not beenshown to be of benefit. Sodium bicarbonate therapy increases intracellular carbon dioxidelevels so administration, if used at all, should follow assisted ventilation with oxygen, andeffective BLS.

Once ventilation is ensured and adrenaline (epinephrine) plus chest compressions areprovided to maximize circulation, use of sodium bicarbonate may be considered for thepatient with prolonged cardiac arrest or cardiac arrest associated with documented severemetabolic acidosis. These agents should be administered only in cases where profoundacidosis is likely to adversely affect the action of adrenaline (epinephrine). An alkalis-ing agent is usually considered if spontaneous circulation has not returned after the firstor second dose of adrenaline (epinephrine). In addition, sodium bicarbonate is recom-mended in the treatment of patients with hyperkalaemia (see Appendix B) and tricyclicantidepressant overdose (see Appendix H).

In the arrested patient arterial pH does not correlate well with tissue pH. Mixed venousor central venous pH should be used to guide any further alkalising therapy, and it shouldalways be remembered that good basic life support is more effective than alkalising agentsat raising myocardial pH.

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Bicarbonate is the most common alkalising agent currently available, the dose being1 mmol/kg (1 ml/kg of an 8.4% solution). Certain caveats must be kept in mind (seebox).

• Bicarbonate must not be given in the same intravenous line as calcium becauseprecipitation will occur.

• Sodium bicarbonate inactivates adrenaline (epinephrine) and dopamine and thereforethe line must be flushed with saline if these drugs are subsequently given.

• Bicarbonate may not be given by the intra-tracheal route.

Intravenous fluidsIn some situations, where the cardiac arrest has resulted from circulatory failure (for

example septicaemia), a standard (20 ml/kg) bolus of crystalloid fluid should be given ifthere is no response to the initial dose of adrenaline (epinephrine), but the use of fluidshould not delay a second dose of adrenaline (epinephrine).

Second adrenaline (epinephrine) doseThere is no convincing evidence that a tenfold increase in adrenaline (epinephrine)

dose is beneficial in children, and in some adult studies a deleterious effect was ob-served. However, there are some anecdotal cases of return of spontaneous circulationwith large doses of adrenaline (epinephrine) and therefore it can still be used for secondand subsequent doses in patients where cardiac arrest is thought to have been secondaryto circulatory collapse. It is clear that patient response to adrenaline (epinephrine) is veryvariable; therefore if the patient has continuous intra-arterial monitoring (as in arrestsoccurring in the intensive care setting) the adrenaline (epinephrine) dose can be variedand titrated to best effect, with higher doses being given if the aortic diastolic pressure islower than 20 mmHg.

VasopressinVasopressin is now being considered in adult cardiac arrest as an alternative to

adrenaline (epinephrine) in shock-resistant ventricular fibrillation and in asystole. Therehave been no studies and consequently currently no evidence for its efficacy in children,so it is not recommended.

CalciumIn the past, calcium was recommended in the treatment of electro-mechanical dissocia-

tion and asystole, but there is no evidence for its efficacy and there is evidence for harmfuleffects as calcium is implicated in cytoplasmic calcium accumulation in the final com-mon pathway of cell death. This results from calcium entering cells following ischaemiaand during reperfusion of ischaemic organs. Administration of calcium in resuscitationof asystolic patients is not routinely recommended. Calcium is indicated for treatmentof biochemically proven hypocalcaemia and hyperkalaemia, and for the treatment of hy-permagnesaemia and of calcium channel blocker overdose.

GlucoseAlthough sick infants and children may become hypoglycaemic because of their low

glycogen reserves, the routine use of glucose in resuscitation should be avoided. Animaland human studies have shown a correlation between high blood glucose and poorer

50




neurological outcome following resuscitation. Glucose should only be used to treat bio-chemically proven hypoglycaemia (see Chapter 12).

6.3 VENTRICULAR FIBRILLATION AND PULSELESSVENTRICULAR TACHYCARDIA

ECGs showing ventricular fibrillation and ventricular tachycardia are shown in Fig-ures 6.4 and 6.5 respectively.

Figure 6.4. Ventricular fibrillation

Figure 6.5. Ventricular tachycardia

These arrhythmias are uncommon in children but may be expected in those suffer-ing from hypothermia, poisoning by tricyclic antidepressants and with cardiac disease.The protocol for ventricular fibrillation and pulseless ventricular tachycardia is shown inFigure 6.6.

Asynchronous electrical defibrillation should be carried out immediately. A pre cordialthump may be given in monitored children in whom the onset of arrhythmia is witnessedand if the defibrillator is not immediately at hand. Paediatric paddles (4·5 cm) should beused for children under 10 kg. One electrode is placed over the apex in the mid-axillaryline, whilst the other is put immediately below the clavicle just to the right of the sternum.If only adult paddles are available, for an infant under 10 kg one may be placed on theinfant’s back and one over the left lower part of the chest at the front.

The first two shocks are given at 2 J/kg. If these two attempts are unsuccessful the thirdshock should be at 4 J/kg. If three shocks fail to produce defibrillation, attention mustturn to supporting coronary and cerebral perfusion as in asystole. The airway shouldbe secured and the patient ventilated with high-flow oxygen. Adrenaline (epinephrine) is

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Figure 6.6. Protocol for ventricular fibrillation and pulseless ventricular tachycardia

given either as 10 micrograms/kg intravenously or intraosseously or as 100 micrograms/kgvia the tracheal route, then, three further shocks of 4 J/kg are administered. In additionto its role in increasing coronary perfusion, adrenaline (epinephrine) also increases theamplitude of ventricular fibrillations, which increases the likelihood of a successful con-version of the rhythm by defibrillation. In between the shocks basic life support shouldnot be interrupted for any cause.

After each shock the clinician should observe the ECG monitor. If the rhythm hasaltered, a pulse check should be carried out. If the rhythm has not altered, a pulse checkshould be carried out at the end of each set of three shocks.

Antiarrhythmic drugsAmiodarone is the treatment of choice in shock-resistant ventricular fibrillation (VF) and

pulseless ventricular tachycardia. This is based on evidence from adult cardiac arrest andexperience with the use of amiodarone in children in the catheterisation laboratory setting.The dose of amiodarone for VF/pulseless VT is 5 mg/kg via rapid IV/IO bolus followedby continued basic life support and a further defibrillation attempt within 60 seconds.

Further doses of adrenaline (epinephrine) (usually at low dose unless specifically indi-cated by the clinical situation) should be given every 3–5 minutes.

Lidocaine (Lignocaine) (dose 1 mg/kg IV/IO) may still be considered for shock-resistantVF. Its action is to suppress ectopic foci and increase the threshold for the myocardium tofibrillate, so it helps to maintain a pulse-producing rhythm if cardioversion is successful.Bretylium is no longer thought to be an appropriate agent in children.

After each drug CPR should continue for a minute to allow the drug to reach the heartbefore a second defibrillation attempt. It is DC shock that converts the heart rhythm backto a perfusing one, not the drug. The purpose of the antiarrhythmic drug is to stabilise theconverted rhythm, and the purpose of adrenaline (epinephrine) is to improve myocardial

52




oxygenation by increasing coronary perfusion pressure. Adrenaline (epinephrine) alsoincreases the vigour and intensity of ventricular fibrillation, which increases the successof defibrillation.

During resuscitation the underlying cause of the arrhythmia should be considered. Ifthe VF/VT is due to hypothermia then defibrillation may be resistant until core tempera-ture is increased. Active rewarming should be commenced (see Chapter 19). If the VF/VThas been caused by an overdose of tricyclic antidepressants then the patient should bealkalised (see Appendix H) and antiarrhythmic drugs avoided except under expert guid-ance (seek poisons centre advice). The possibility of hyperkalaemia should be consideredand treated if identified with bicarbonate, insulin and glucose (see Appendix B).

If there is still resistance to defibrillation, different paddle positions or another defib-rillator may be tried. In the infant in whom paediatric paddles have been used, largerpaddles applied to the front and back of the chest may be an alternative.

If the rhythm initially converts and then deteriorates back to ventricular fibrillationor pulseless ventricular tachycardia then the lower defibrillation dose should be startedfollowing stabilising medication such as amiodarone.

Automatic external defibrillators (AEDs)

The introduction of automatic external defibrillators in the pre-hospital setting and es-pecially for public access has improved the outcome for VF cardiac arrest for some adults.Standard models have a fixed initial dose of electricity of 150–200 J, which significantlyexceeds the recommended dose of 2–4 J/kg in young children and infants.

In the pre-hospital setting, automatic external defibrillators (AEDs) are commonlyused in adults to assess cardiac rhythm and to deliver defibrillation. In children AEDscan accurately detect ventricular fibrillation at all ages, but there remains concern overtheir ability to identify correctly tachycardic rhythms in infants. At present, therefore,AEDs can be used to identify rhythms in children but not in infants.

The energy dose delivered by both standard monophasic and standard biphasic AEDsexceeds the recommended dose of 2–4 J/kg in most children <8 years of age. The averageweight of children >8 years old is usually more than 25 kg. Therefore the initial dosefrom an AED (150–200 J) will be less than 10 J/kg. Children appear tolerant of highdoses, so this is a safe dose for the over-8-year-old in VF/pulseless VT. Defibrillation ofVF/pulseless VT detected by an AED may be considered in these older children.

Manufacturers are now making available attenuation devices which can be fittedto AEDs to produce a shock of 50 J. This is deemed safe for use with children aged1–8 years. The use of AEDs in infants cannot yet be recommended.

Defibrillation of children younger than approximately 8 years of age with energy dosestypical of standard AEDs cannot be recommended. However, if an AED were the onlydefibrillator available to a clinician confronted with a child in VF/pulseless VT the ma-jority opinion would be to use the device.

Institutions must be advised that AEDs are less suitable for the treatment of childrenthan of adults and that variable defibrillators must continue to be provided until suitableequipment is widely available and experience gained in their use.

Biphasic waveforms

Biphasic waveforms for transthoracic defibrillation appears to be as effective at lowerenergy doses as conventional waveforms in adults. There are currently inadequate data torecommend its use for treatment of VF/VT in children. However, if a biphasic waveform

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defibrillator was the only machine available to a clinician confronted with a child inVF/pulseless VT the majority opinion would be to use the device. Increasingly, defibril-lators with only biphasic waveforms are being produced, so evidence for their successfuluse in children is accruing.

6.4 PULSELESS ELECTRICAL ACTIVITY (PEA)

This is the absence of a palpable pulse despite the presence of recognisable complexeson the ECG monitor. This is often a pre-asystolic state and is treated in the same way asasystole.

Sometimes, pulseless electrical activity is due to an identifiable and reversible cause.In children, this is most often associated with trauma. In the trauma setting, PEA maybe caused by severe hypovolaemia, tension pneumothorax and pericardial tamponade.PEA is also seen in hypothermic patients and in patients with electrolyte abnormalities,including hypocalcaemia from calcium channel blocker overdose. Rarely in children itmay be seen after massive pulmonary thromboembolus.

It is appropriate to give an early bolus of 20 ml/kg of crystalloid because this willbe supportive in cases related to trauma. In addition, however, a tension pneumothoraxand/or pericardial tamponade requires definitive treatment (see Chapter 14). Continuingfluid replacement and the stemming of exsanguination may be required.

Rapid identification and treatment of reversible causes such as hypovolaemia (Chap-ter 13), hypothermia (Chapter 19), electrolyte and acid–base disturbance is vital (Ap-pendices A and B).

6.5 POST-RESUSCITATION MANAGEMENT

Once spontaneous cardiac output has returned, frequent clinical reassessment mustbe carried out to detect deterioration or improvement with therapy. In the emergencydepartment or ward situation, invasive monitoring may not be available. However, allpatients should be monitored for:

• Pulse rate and rhythm – ECG monitor• Oxygen saturation – pulse oximeter• Core temperature – low reading thermometer• Skin temperature• Blood pressure – noninvasive monitor• Urine output – urinary catheter• Arterial pH and gases – arterial blood sample• CO2 monitoring – capnography

Additionally some patients will require:

• Invasive BP monitoring – arterial cannula with pressure transducer• Central venous pressure monitoring – femoral, brachial or jugular catheter• Intracranial pressure monitoring – subarachnoid, subdural, or

intraventricular devices

Some facilities may not be available until transfer to an intensive care setting.The investigations shown in the box should be performed immediately following suc-

cessful resuscitation:

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Post-resuscitation investigations

• Chest radiograph• Arterial and central venous blood gases• Haemoglobin, haematocrit, and platelets• Group and save serum for cross-match• Na+, K+, urea, and creatinine• Clotting screen• Blood glucose• Liver function tests• 12-lead ECG

Chapter 24 gives details on stabilisation after resuscitation from cardiac arrest or seriousillness/injury with guidance on safe transport of the child to a paediatric intensive carefacility.

Hypothermia following resuscitation from cardiac arrest

Recent data suggest that there is some evidence that post-arrest hypothermia (coretemperatures of 32 to 34◦C) have beneficial effects on neurological recovery in adults,but there is insufficient evidence to date to recommend the routine use of hypothermia inchildren. The results of therapeutic hypothermia are generally favourable in laboratorymodels of hypoxic ischaemic injury to immature brains of various species. Until additionalpaediatric data become available, clinicians should tailor therapy for individual patientsbased on their assessment of the risks and benefits of hypothermia.

Current recommendations are that post-arrest patients with core temperatures less than37.5◦C should not be actively rewarmed, unless the core temperature is <33◦C when theyshould be rewarmed to 34◦C. Conversely, increased core temperature increases metabolicdemand by 10–13% for each degree centigrade increase in temperature above normal.Therefore in the post-arrest patient with compromised cardiac output, hyperthermiashould be treated with active cooling to achieve a normal core temperature. Shiveringshould be prevented, since it will increase metabolic demand. Sedation may be adequateto control shivering, but neuromuscular blockade may be needed.

Hypoglycaemia

All children, especially infants, can become hypoglycaemic when seriously ill. Bloodglucose should be checked frequently and hypoglycaemia corrected carefully. It is im-portant not to cause hyperglycaemia as this will promote an osmotic diuresis and, also,hyperglycaemia is associated with worse neurological outcome in animal models of car-diac arrest.

6.6 WHEN TO STOP RESUSCITATION

Resuscitation efforts are unlikely to be successful and can be discontinued if there isno return of spontaneous circulation at any time with up to 30 minutes of cumulative lifesupport and in the absence of recurring or refractory VF/VT. Exceptions are patients witha history of poisoning or a primary hypothermic insult in whom prolonged attempts mayoccasionally be successful. Seek expert help from a toxicologist or paediatric intensivist.

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Figure 6.7. Initial approach to cardiac arrest

6.7 SUMMARY

The teaching in this chapter is consistent with the ILCOR guidelines, Re-suscitation 2000, and there are an enormous number of references which haveinformed this process. These are available on the ALSG website for those whoare interested. See details on “Contact Details and Further Information” page.

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PART

IIITHE SERIOUSLY ILL CHILD

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CHAPTER

7The structured approach to the

seriously ill child

LEARNING OBJECTIVES

In this chapter you will learn:

• how to recognise the seriously ill child• a structured approach to the assessment of the seriously ill child• a structured approach to resuscitation and treatment of the seriously ill child

7.1 INTRODUCTION

As described in Chapter 1, the outcome for children following cardiac arrest is, ingeneral, poor. Earlier recognition and management of potential respiratory, circulatory, orcentral neurological failure will reduce mortality and secondary morbidity. The followingsection outlines the physical signs that should be used for the rapid assessment of children.It is divided systematically into looking for signs of potential respiratory, circulatory andcentral neurological failure and constitutes the primary assessment.

7.2 PRIMARY ASSESSMENT OF AIRWAY AND BREATHING

Recognition of potential respiratory failure

Effort of breathing

The degree of increase in the effort of breathing allows clinical assessment of the severityof respiratory disease. It is important to assess the following.

Respiratory rateNormal resting respiratory rates at differing ages are shown in Table 7.1. Rates are

higher in infancy, and fall with increasing age. Care should be taken in interpreting

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THE STRUCTURED APPROACH TO THE SERIOUSLY ILL CHILD

Table 7.1. Respiratory rate by age at rest

Age (years) Respiratory rate (breaths/min)

<1 30–401–2 25–352–5 25–305–12 20–25>12 15–20

single measurements: infants can show rates of between 30 and 90 breaths per minutedependent on their state of activity. WHO uses a cut-off of 60 breaths per minute forpneumonia in infants and young children. Most useful are trends in the measurement asan indicator of improvement or deterioration.

At rest, tachypnoea indicates that increased ventilation is needed because of either lungor airway disease, or metabolic acidosis. A slow respiratory rate indicates fatigue, cerebraldepression, or a pre-terminal state.

RecessionIntercostal, subcostal or sternal recession shows increased effort of breathing. This

sign is more easily seen in younger infants as they have a more compliant chest wall. Itspresence in older children (i.e. over 6 or 7 years) suggests severe respiratory problems.The degree of recession gives an indication of the severity of respiratory difficulty. Inthe child who has become exhausted through increased effort of breathing, recessiondecreases.

Inspiratory or expiratory noisesAn inspiratory noise while breathing (stridor) is a sign of laryngeal or tracheal obstruc-

tion. In severe obstruction the stridor may also occur in expiration, but the inspiratorycomponent is usually more pronounced. Wheezing indicates lower airway narrowing andis more pronounced in expiration. A prolonged expiratory phase also indicates lowerairway narrowing. The volume of the noise is not an indicator of severity.

GruntingGrunting is produced by exhalation against a partially closed glottis. It is an attempt

to generate a positive end-expiratory pressure and prevent airway collapse at the end ofexpiration in children with “stiff” lungs. This is a sign of severe respiratory distress andis characteristically seen in infants with pneumonia or pulmonary oedema. It may alsobe seen with raised intracranial pressure, abdominal distension or peritonism.

Accessory muscle useAs in adult life, the sternomastoid muscle may be used as an accessory respiratory

muscle when the effort of breathing is increased. In infants, this may cause the head tobob up and down with each breath, making it ineffectual.

Flaring of the alae nasiFlaring of the alae nasi is seen especially in infants with respiratory distress.

GaspingThis is a sign of severe hypoxia and may be pre-terminal.

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Exceptions

There may be absent or decreased evidence of increased effort of breathing in threecircumstances:

1. In the infant or child who has had severe respiratory problems for some time, fatiguemay occur and the signs of increased effort of breathing will decrease. Exhaustion is apre-terminal sign.

2. Children with cerebral depression from raised intracranial pressure, poisoning or en-cephalopathy will have respiratory inadequacy without increased effort of breathing. Therespiratory inadequacy in this case is caused by decreased respiratory drive.

3. Children who have neuromuscular disease (such as spinal muscular atrophy or musculardystrophy) may present in respiratory failure without increased effort of breathing.

The diagnosis of respiratory failure in such children is made by observing the efficacyof breathing, and looking for other signs of respiratory inadequacy. These arediscussed in the text.

Efficacy of breathing

Observations of the degree of chest expansion (or, in infants, abdominal excursion)provide an indication of the amount of air being inspired and expired. Similarly, importantinformation is given by auscultation of the chest. Listen for reduced, asymmetrical orbronchial breath sounds. A silent chest is an extremely worrying sign.

Pulse oximetry can be used to measure the arterial oxygen saturation (Sa2). Theinstruments are less accurate when Sa2 is less than 70%, when shock is present, andin the presence of carboxyhaemoglobin. Oximetry in air gives a good indication of theefficacy of breathing. Supplemented oxygen will mask this information unless the hypoxiais severe. Normal Sa2 in an infant or child at sea level is 97 to 100%.

Effects of respiratory inadequacy on other organs

Heart rateHypoxia produces tachycardia in the older infant and child. Anxiety and a fever will also

contribute to tachycardia, making this a non-specific sign. Severe or prolonged hypoxialeads to bradycardia. This is a pre-terminal sign.

Skin colourHypoxia (via catecholamine release) produces vasoconstriction and skin pallor.

Cyanosis is a late and pre-terminal sign of hypoxia. By the time central cyanosis is visi-ble in acute respiratory disease, the patient is close to respiratory arrest. In the anaemicchild cyanosis may never be visible despite profound hypoxia. A few children will becyanosed because of cyanotic heart disease. Their cyanosis will be largely unchanged byoxygen therapy.

Mental statusThe hypoxic or hypercapnic child will be agitated and/or drowsy. Gradually drowsiness

increases and eventually consciousness is lost. These extremely useful and important signsare often more difficult to detect in small infants. The parents may say that the infantis just “not himself”. The doctor must assess the child’s state of alertness by gaining

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eye contact, and noting the response to voice and, if necessary, to painful stimuli. Ageneralised muscular hypotonia also accompanies hypoxic cerebral depression.

Reassessment

Single observations on respiratory rate, degree of recession, etc. are useful but muchmore information can be gained by frequent repeated observations to detect a trend inthe patient’s condition.

7.3 PRIMARY ASSESSMENT OF THE CIRCULATION

Recognition of potential circulatory failure

Cardiovascular status

Heart rateNormal rates are shown in Table 7.2. The heart rate initially increases in shock due

to catecholamine release and as compensation for decreased stroke volume. The rate,particularly in small infants, may be extremely high (up to 220 per minute).

Table 7.2. Heart rate by age

Age (years) Heart rate (beats/min)

<1 110–1601–2 100–1502–5 95–1405–12 80–120>12 60–100

An abnormally slow pulse rate, or bradycardia, is defined as less than 60 beats perminute or a rapidly falling heart rate associated with poor systemic perfusion. This is apre-terminal sign.

Pulse volumeAlthough blood pressure is maintained until shock is severe, an indication of perfusion

can be gained by comparative palpation of both peripheral and central pulses. Absentperipheral pulses and weak central pulses are serious signs of advanced shock, and indicatethat hypotension is already present. Bounding pulses may be caused by either an increasedcardiac output (e.g. septicaemia), arterio-venous systemic shunt (e.g. patent arterial duct)or hypercapnia.

Capillary refillFollowing cutaneous pressure on the centre of the sternum or on a digit for 5 seconds,

capillary refill should occur within 2–3 seconds. A slower refill time than this indicatespoor skin perfusion. This is a particularly useful sign in early septic shock, when thechild may otherwise be apparently well, with warm peripheries. The presence of feverdoes not affect the sensitivity of delayed capillary refill in children with hypovolaemiabut a low ambient temperature reduces its specificity, so the sign should be used withcaution in trauma patients who have been in a cold environment. Poor capillary refill anddifferential pulse volumes are neither sensitive nor specific indicators of shock in infantsand children, but are useful clinical signs when used in conjunction with the other signs

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described. They should not be used as the only indicators of shock nor as quantitativemeasures of the response to treatment.

In children with pigmented skin the sign is more difficult to assess. In these cases thenail beds are used and additionally the sole of the feet in young babies.

Blood pressureNormal systolic pressures are shown in Table 7.3. Expected systolic blood pressure

can be estimated by the following formula: blood pressure = 80 + (age in years × 2).Use of the correct cuff size is crucial if an accurate blood pressure measurement is to beobtained. This caveat applies to both auscultatory and oscillometric devices. The widthof the cuff should be more than 80% of the length of the upper arm and the bladder morethan 40% of the arm’s circumference.

Table 7.3. Systolic blood pressure by age

Age (years) Systolic blood pressure (mmHg)

<1 70–901–2 80–952–5 80–1005–12 90–110>12 100–120

Hypotension is a late and pre-terminal sign of circulatory failure. Once a child’s bloodpressure has fallen cardiac arrest is imminent. Hypertension can be the cause or result ofcoma and raised intracranial pressure.

Effects of circulatory inadequacy on other organs

Respiratory systemA rapid respiration rate with an increased tidal volume, but without recession, is caused

by the metabolic acidosis resulting from circulatory failure.

SkinMottled, cold, pale skin peripherally indicates poor perfusion. A line of coldness may

be felt to move centrally as circulatory failure progresses.

Mental statusAgitation and then drowsiness leading to unconsciousness are characteristic of circu-

latory failure. These signs are caused by poor cerebral perfusion. In an infant, parentsmay say that he is “not himself”.

Urinary outputA urine output of less than 1 ml/kg/hour in children and less than 2 ml/kg/hour in

infants indicates inadequate renal perfusion during shock. A history of oliguria or anuriashould be sought.

Cardiac failure

The following features suggest a cardiac cause of respiratory inadequacy:

• Cyanosis, not correcting with oxygen therapy• Tachycardia out of proportion to respiratory difficulty

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• Raised jugular venous pressure• Gallop rhythm/murmur• Enlarged liver• Absent femoral pulses

7.4 PRIMARY ASSESSMENT OF DISABILITY

Recognition of potential central neurological failure

Neurological assessment should only be performed after airway (A), breathing (B) andcirculation (C) have been assessed and treated. There are no neurological problems thattake priority over ABC.

Both respiratory and circulatory failure will have central neurological effects. Con-versely, some conditions with direct central neurological effects (such as meningitis,raised intracranial pressure from trauma, and status epilepticus) may also have respira-tory and circulatory consequences.

Neurological function

Conscious levelA rapid assessment of conscious level can be made by assigning the patient to one of

the categories shown in the box.

A ALERTV responds to VOICEP responds only to PAINU UNRESPONSIVE to all stimuli

If the child does not respond to voice, it is important that assessment follows of theresponse to pain. The painful central stimulus can be delivered by sternal pressure, bysupra-orbital ridge pressure or by pulling frontal hair. A child who is unresponsive orwho only responds to pain has a significant degree of coma, equivalent to 8 or less on theGlasgow Coma Scale.

PostureMany children who are suffering from a serious illness in any system are hypotonic. Stiff

posturing such as that shown by decorticate (flexed arms, extended legs) or decerebrate(extended arms, extended legs) children is a sign of serious brain dysfunction. Thesepostures can be mistaken for the tonic phase of a convulsion. Alternatively, a painful stimulusmay be necessary to elicit these postures.

Severe extension of the neck due to upper airway obstruction can mimic the opistho-tonus that occurs with meningeal irritation. A stiff neck and full fontanelle in infants aresigns which suggest meningitis.

PupilsMany drugs and cerebral lesions have effects on pupil size and reactions. However, the

most important pupillary signs to seek are dilatation, unreactivity, and inequality, whichindicate possible serious brain disorders.

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Respiratory effects of central neurological failure

There are several recognisable breathing pattern abnormalities with raised intracranialpressure. However, they are often changeable and may vary from hyperventilation toCheyne–Stokes breathing to apnoea. The presence of any abnormal respiratory patternin a patient with coma suggests mid- or hind-brain dysfunction.

Circulatory effects of central neurological failure

Systemic hypertension with sinus bradycardia (Cushing’s response) indicates compres-sion of the medulla oblongata caused by herniation of the cerebellar tonsils through theforamen magnum. This is a late and pre-terminal sign.

7.5 EXPOSURE

Although not part of the primary assessment, the examination of the seriously ill childwill involve examination for markers of illness that will help provide specific emergencytreatment.

TemperatureA fever suggests an infection as the cause of the illness, but may also be the

result of prolonged convulsions or shivering.340

RashExamination is made for rashes, such as urticaria in allergic reactions, purpura, pe-

techiae and bruising in septicaemia and child abuse, or maculo-papular and erythematousrashes in allergic reactions and some forms of sepsis.

Summary: the rapid clinical assessment of an infant or child

Airway and BreathingEffort of breathingRespiratory rate/rhythmStridor/wheezeAuscultationSkin colourCirculationHeart ratePulse volumeCapillary refillSkin temperatureDisabilityMental status/conscious levelPosturePupilsThe whole assessment should take less than a minute

Once airway (A), breathing (B), and circulation (C) are clearly recognised as being stable orhave been stabilised, then definitive management of the underlying condition can proceed.During definitive management reassessment of ABCD at frequent intervals will be necessaryto assess progress and detect deterioration.

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7.6 THE STRUCTURED APPROACH TO THESERIOUSLY ILL CHILD

Treatment of a child in an emergency requires rapid assessment and urgent interven-tion. The structured approach includes:

• Primary assessment• Resuscitation• Secondary assessment and looking for key features• Emergency treatment• Stabilisation and transfer to definitive care

Primary assessment and resuscitation involve management of the vital ABC functions andassessment of disability (CNS function). This assessment and stabilisation occurs beforeany illness-specific diagnostic assessment or treatment takes place. Once the patient’s vitalfunctions are supported, secondary assessment and emergency treatment begins. Illness-specific pathophysiology is sought and emergency treatments are instituted. During thesecondary assessment vital signs should be checked frequently to detect any change inthe child’s condition. If there is deterioration then primary assessment and resuscitationshould be repeated.

Stabilisation and transfer to definitive care are covered in Chapter 24.

7.7 PRIMARY ASSESSMENT AND RESUSCITATION

In a severely ill child, a rapid examination of vital functions is required. The phys-ical signs described in sections 7.2–7.4 are used in an ABC approach. This primaryassessment and any necessary resuscitation must be completed before the more detailedsecondary assessment is performed.

Airway

Primary assessment• Assess patency by

❝ looking for chest and/or abdominal movement,❝ listening for breath sounds and❝ feeling for expired air.

• Vocalisations, such as crying or talking, indicate ventilation and some degree of airwaypatency.

• If there is obvious spontaneous ventilation, note other signs which may suggest upperairway obstruction:❝ the presence of stridor and❝ evidence of recession.

• If there is no evidence of air movement then chin lift or jaw thrust manoeuvres shouldbe carried out. Reassess the airway after any airway-opening manoeuvres.

• If there continues to be no evidence of air movement then airway patency can beassessed by performing an airway-opening manoeuvre while giving rescue breaths(see “Basic Life Support”, Chapter 4).

Resuscitation• If the airway is not patent, then this can be secured by

❝ a chin lift or jaw thrust,❝ the use of an airway adjunct or❝ tracheal intubation.

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Breathing

Primary assessmentA patent airway does not ensure adequate ventilation. The latter requires an intact res-

piratory centre and adequate pulmonary function augmented by coordinated movementof the diaphragm and chest wall. The adequacy of breathing can be assessed as describedin Section 7.3.

Resuscitation• Give high-flow oxygen (flow rate 15 l/min) through a non-rebreathing mask with a

reservoir bag to any child with respiratory difficulty or hypoxia.• In the child with inadequate breathing, this should be supported either with bag–

valve–mask ventilation or intubation and intermittent positive pressure ventilation.

Circulation

Primary assessmentThe assessment of circulation has been described in Section 7.4. It is more difficult to

assess than breathing and individual measurements must not be over-interpreted.

Resuscitation• Give high-flow oxygen to every child with an inadequate circulation (shock). This will

be through either a non-rebreathing mask with a reservoir bag or an endotracheal tubeif intubation has been necessary for airway control or inadequate breathing.

• Venous or intraosseous access should be gained and an immediate infusion of crys-talloid or colloid (20 ml/kg) given. Urgent blood samples may be taken at this point.

Disability (neurological evaluation)

Primary assessmentBoth hypoxia and shock can cause a decrease in conscious level. Any problem with

ABC must be addressed before assuming that a decrease in conscious level is due to aprimary neurological problem. The rapid assessment of central neurological failure hasbeen described in Section 7.5. In addition, any patient with a decreased conscious levelor convulsions must have an initial glucose stick test performed.

Resuscitation• Consider intubation to stabilise the airway in any child with a conscious level recorded

as P or U (only responding to painful stimuli or unresponsive).• Treat hypoglycaemia with 0·5 g/kg of dextrose (i.e. 5 ml/kg of 10% dextrose) after

having taken blood for glucose measurement in the laboratory and a clotted samplefor further studies.

• Intravenous lorazepam, buccal midazolam or rectal diazepam should be given forprolonged or recurrent fits.

7.8 SECONDARY ASSESSMENT AND EMERGENCYTREATMENT

The secondary assessment takes place once vital functions have been assessed and theinitial treatment of life threat to those vital functions has been started. It includes a med-ical history, a clinical examination and specific investigations. It differs from a standardmedical history and examination in that it is designed to establish which emergency treat-ments might benefit the child. Time is limited and a focused approach is essential. At theend of secondary assessment, the practitioner should have a better understanding of the

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illness affecting the child and may have formulated a differential diagnosis. Emergencytreatments will be appropriate at this stage – either to treat specific conditions (suchas asthma) or processes (such as raised intracranial pressure). The establishment of adefinite diagnosis is part of definitive care.

The history often provides the vital clues that help the practitioner identify the diseaseprocess and provide the appropriate emergency care. In the case of children, the history isoften obtained from an accompanying parent, although a history should be sought fromthe child if possible. Do not forget to ask the paramedic about the child’s initial conditionand about treatments and response to treatments that have already been given.

Some children will present with an acute exacerbation of a known condition such asasthma or epilepsy. Such information is helpful in focusing attention on the appropriatesystem but the practitioner should be wary of dismissing new pathologies in such patients.The structured approach prevents this problem. Unlike trauma (which is dealt with later),illness affects systems rather than anatomical areas. The secondary assessment mustreflect this and the history of the complaint should be sought with special attention to thepresenting system or systems involved. After the presenting system has been dealt with, allother systems should be assessed and any additional emergency treatments commencedas appropriate.

The secondary assessment is not intended to complete the diagnostic process, butrather is intended to identify any problems that require emergency treatment.

The following gives an outline of a structured approach in the first hour of emergencymanagement. It is not exhaustive but addresses the majority of emergency conditionsthat are amenable to specific emergency treatments in this time period.

The symptoms, signs and treatments relevant to each emergency condition are elabo-rated in the relevant chapters that follow.

Respiratory

Secondary assessmentThe box below gives common symptoms and signs that should be sought in the respi-

ratory system. Emergency investigations are suggested.

Symptoms SignsBreathlessness CyanosisCoryza TachypnoeaCough RecessionNoisy breathing – grunting, stridor, wheeze GruntingDrooling and inability to drink StridorAbdominal pain WheezeChest pain Chest wall crepitusApnoea Tracheal shiftFeeding difficulties Abnormal percussion noteHoarseness Crepitations on auscultation

Acidotic breathingInvestigationsOxygen saturationPeak flow if asthma suspectedEnd-tidal/transcutaneous carbon dioxide if hypoventilation suspectedBlood culture if infection suspectedChest X-ray (selective)Arterial blood gases (selective)

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Emergency treatment• If “bubbly” noises are heard, the airway is full of secretions, which may require

clearance by suction.• If there is a harsh stridor associated with a barking cough and severe respiratory

distress, upper airway obstruction due to severe croup should be suspected and thechild given nebulised adrenaline (epinephrine) (5 ml of 1:1000 nebulised in oxygen).

• If there is a quiet stridor, drooling and a short history in a sick-looking child, con-sider epiglottitis or tracheitis. Intubation is likely to be urgently required, preferablyby a senior anaesthetist. Do not jeopardise the airway by unpleasant or frighteninginterventions. Give intravenous cefotaxime or ceftriaxone.

• With a sudden onset and significant history of inhalation, consider a laryngeal foreignbody. If the “choking child” procedure has been unsuccessful, the patient may requirelaryngoscopy. Do not jeopardise the airway by unpleasant or frightening interventionsbut contact a senior anaesthetist/ENT surgeon urgently. However, in extreme casesof life threat immediate direct laryngoscopy to remove a visible foreign body withMagill’s forceps may be necessary.

• Stridor following ingestion/injection of a known allergen suggests anaphylaxis. Chil-dren in whom this is likely should receive IM adrenaline (epinephrine) (10 µg/kg).

• Children with a history of asthma or with wheeze and significant respiratory distress,depressed peak flow and/or hypoxia should receive inhaled β2 agonists and oxygentherapy. Infants with wheeze and respiratory distress are likely to have bronchiolitisand require only oxygen.

• In acidotic breathing, take arterial blood sample for acid–base balance and bloodsugar. Treat diabetic ketoacidosis with IV normal (physiological) saline and insulin.

Cardiovascular (circulation)

Secondary assessmentThe box below gives common symptoms and signs that should be sought in the car-

diovascular system. Emergency investigations are suggested.

Symptoms SignsBreathlessness Tachy- or bradycardiaFever Hypo- or hypertensionPalpitations Abnormal pulse volume or rhythmFeeding difficulties Abnormal skin perfusion or colourDrowsiness Cyanosis / pallorPallor HepatomegalyFluid loss Auscultatory crepitationsPoor urine output Cardiac murmur

Peripheral oedemaRaised jugular venous pressureHypotonia

Investigations Purpuric rashUrea and electrolytesFull blood countArterial blood gasCoagulation studiesECGBlood cultureChest X-ray (selective)

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Emergency treatment• Further boluses of fluid should be given to shocked children who have not had a

sustained improvement to the first bolus given at resuscitation.• Consider inotropes, intubation and central venous pressure monitoring with the third

bolus.• Consider IV cefotaxime/ceftriaxone in shocked children with no obvious fluid loss,

as sepsis is likely.• If a patient has a cardiac arrhythmia the appropriate protocol should be followed.• If anaphylaxis is suspected, give IM adrenaline (epinephrine) 10 micrograms/kg, in

addition to fluid boluses.• Give alprostadil if duct-dependent congenital heart disease is suspected, eg in

neonates with unresponsive shock.• Surgical advice and intervention may be needed for gastro-intestinal emergencies.

The following symptoms and signs may suggest this.

Symptoms SignsVomiting Abdominal tendernessBlood PR Abdominal massAbdominal pain

Neurological (disability)

Secondary assessmentThe box below gives common symptoms and signs that should be sought in the nervous

system.

Symptoms SignsHeadache Altered conscious levelConvulsions ConvulsionsChange in behaviour Altered pupil size and reactivityChange in conscious level Abnormal postureWeakness Abnormal oculo-cephalic reflexesVisual disturbance MeningismFever Papilloedema or retinal haemorrhage

Altered deep tendon reflexesHypertensionSlow pulse

InvestigationsUrea and electrolyteBlood sugarBlood cultureArterial blood gasCoagulation studiesBlood and urine toxicology

Emergency treatment• If convulsions persist, continue the status epilepticus protocol.• If there is evidence of raised intracranial pressure (decreasing conscious level, abnor-

mal posturing and/or abnormal ocular motor reflexes) then the child should undergo:

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❝ intubation and ventilation (to maintain a P2 of 4·0–4·5 kPa)❝ nursing with head in-line and 20–30◦ head-up position (to help cerebral venous

drainage)❝ IV infusion with mannitol 0·25–0·5 g/kg (1·25–2·5 ml of mannitol 20%) over

15 minutes, and repeated as needed, provided serum osmolality remains below325 mOsm/l

❝ consideration of dexamethasone 0·5 mg/kg twice daily (for oedema surrounding aspace occupying lesion)

• In a child with a depressed conscious level or convulsions, consider meningi-tis/encephalitis. Give cefotaxime/acyclovir.

• In drowsiness with sighing respirations check blood sugar, acid–base balance or sali-cylate level. Treat diabetic ketoacidosis with IV normal saline and insulin.

• In unconscious children with pin-point pupils, consider opiate poisoning. A trial ofnaloxone should be given.

External (exposure)

Secondary assessmentThe box below gives common symptoms and signs that should be sought externally.

Symptoms SignsRash PurpuraSwelling of lips/tongue UrticariaFever Angio-oedema

Emergency treatment• In a child with circulatory or neurological symptoms and signs, a pur-

puric rash suggests septicaemia/meningitis. The patient should receive ce-fotaxime preceded by a blood culture. 32

269513616

• In a child with respiratory or circulatory difficulty, the presence of anurticarial rash or angio-oedema suggests anaphylaxis. Give adrenaline(epinephrine) (10 µg/kg) IM.

Further histor1

Developmental and social historyParticularly in a small child or infant, knowledge of the child’s developmental progress

and immunisation status may be useful. The family circumstances may also be helpful,sometimes prompting parents to remember other details of the family’s medical history.

Drugs and allergiesAny medication that the child is currently on or has been on should be recorded and in

addition any medication in the home that the child might have had access to if poisoningis a possibility. A history of allergies should be sought.

7.9 SUMMARY

The structured approach to the seriously ill child outlined here allows the practitionerto focus on the appropriate level of diagnosis and treatment during the first hour ofcare. Primary assessment and resuscitation are concerned with the maintenance of vital

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functions, while secondary assessment and emergency treatment allow more specificurgent therapies to be started. This latter phase of care requires a system-by-systemapproach and this minimises the chances of significant conditions being missed.

In the following chapters and appendices the recognition, resuscitation and emergencymanagement of children with

• breathing difficulties,• shock,• abnormalities of pulse rate or rhythm,• decreased conscious level,• convulsions and• poisoning

are discussed in more detail.

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CHAPTER

8The child with breathing difficulties

LEARNING OBJECTIVES


• why infants and young children are susceptible to respiratory failure• how to assess children with breathing difficulties• how to resuscitate the child with life-threatening breathing difficulties

8.1 INTRODUCTION

There is a wide range of problems that may cause apparent difficulties in breathing inchildren (Table 8.1). Most children with breathing difficulties will have an upper or lowerrespiratory tract illness. These are the commonest causes of acute benign conditions inchildren but are also the most likely causes of life-threatening illness, especially in thevery young. However, there are disorders outside the respiratory system that may causeapparent breathing difficulties, such as cardiac disease, poisoning and metabolic andneurological disorders. This chapter will provide the student with an approach to theassessment, resuscitation and emergency management of such children.

Disorders of the respiratory tract are the commonest illnesses of childhood. Theyare the most frequent reason for children to be seen by their general practitioner, andthey account for 30–40% of acute medical admissions to hospital in children. De-spite advances in the management of respiratory illnesses, they still resulted in almost300 deaths in children between the ages of 4 weeks and 14 years in England and Walesin 1998. In 2002 this figure had fallen to 167 deaths, of which 65 were between the agesof 1 month and 1 year. (ONS 2004)

Most respiratory illnesses are self-limiting minor infections, but a few present as po-tentially life-threatening emergencies. In these, accurate diagnosis and prompt initiationof appropriate treatment are essential if unnecessary morbidity and mortality are to beavoided.

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THE CHILD WITH BREATHING DIFFICULTIES

Table 8.1. Causes of breathing difficulty in children, according to mechanism

Upper airway obstruction Croup/EpiglottitisForeign body

Lower airway obstruction TracheitisAsthmaBronchiolitis

Disorders affecting lungs PneumoniaPulmonary oedema (e.g. in cardiac disease)

Disorders around the lungs PneumothoraxEmpyemaRib fractures

Disorders of the respiratory muscles Neuromuscular disordersDisorders below the diaphragm Peritonitis

Abdominal distensionIncreased respiratory drive Diabetic keto-acidosis

ShockPoisoning (e.g. salicylates)Anxiety attack and hyperventilation

Decreased respiratory drive ComaConvulsionsRaised intracranial pressurePoisoning

8.2 SUSCEPTIBILITY TO RESPIRATORY FAILURE

Severe respiratory illness may result in the development of respiratory failure, definedas an inability of physiological compensatory mechanisms to ensure adequate oxygena-tion and carbon dioxide clearance, resulting in either arterial hypoxia, or hypercapnia,or both. Young children and infants may develop respiratory failure more readily thanolder children and adults, reflecting important differences in the immune status, and thestructure and function of the lungs and the chest wall of children and adults.

• Children, and particularly infants, are susceptible to infection with many organismsto which adults have acquired immunity.

• The upper and the lower airways in children are smaller, and are more easily ob-structed by mucosal swelling, secretions or a foreign body. Airway resistance is in-versely proportional to the fourth power of the radius of the airway: a reduction in theradius by a half causes a 16-fold increase in airway resistance. Thus, 1 mm of mucosaloedema in an infant’s trachea of 5 mm diameter results in a much greater increase inresistance than the same degree of oedema in the trachea of 10 mm diameter. From2 months of age, airway resistance begins to decrease.

• The thoracic cage of young children is much more compliant than that of adults.When there is airways obstruction and increased inspiratory effort, this increasedcompliance results in marked chest wall recession and a reduction in the efficiencyof breathing. The more compliant chest wall also provides less support for the main-tenance of lung volume.

• The lung volume at end expiration is similar to closing volume in infants, increasingthe tendency to small airway closure and hypoxia. This may be exacerbated by anincreased tendency to bronchoconstriction from alveolar or airway hypoxia.

• The number of alveoli is fewer in early childhood and this may increase the suscep-tibility to ventilation–perfusion mismatch.

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• The respiratory muscles of young children are relatively inefficient. In infancy, thediaphragm is the principal respiratory muscle, and the intercostal and accessory mus-cles make relatively little contribution. Respiratory muscle fatigue can develop rapidlyand result in respiratory failure and apnoea.

• The pulmonary vascular bed is relatively muscular in infancy, increasing the tendencywith which pulmonary vasoconstriction occurs. In turn, this can lead to right toleft shunting, ductal opening (in the early neonatal period), ventilation–perfusionmismatch and further hypoxia.

• In the first 1–2 months of life, there may be a paradoxical inhibition of respiratorydrive, with the result that infections can present with apnoea or hypoventilation, ratherthan the usual respiratory distress.

• Foetal haemoglobin is present up until 4–6 months of age, so oxygen is given up lessreadily to the tissues; this results in the oxygen dissociation curve being shifted to theleft. Thus at any given P2, the Sa2 is higher in early infancy.

8.3 CLINICAL PRESENTATIONS OF THE CHILD WITHBREATHING DIFFICULTY

Respiratory conditions do not always present with respiratory symptoms, and mayinclude:

Respiratory BreathlessnessCoughNoisy breathing (stridor or wheeze)Chest pain

Non-respiratory Poor feedingAbdominal painMeningismChanges in tone: hypotoniaChange in colour or conscious level

Noisy breathing may be normal or pathological; parents and carers commonly under-stand different meanings from those understood by doctors and nurses for the terms usedto describe breathing noises, or they may have their own terms. Useful historical featuresinclude relieving or aggravating factors (e.g. sleep, crying, feeding, position) and whetherthe voice or usual vocalisations are normal. Stridor is usually a high pitched sound oninspiration from obstruction of the larynx or trachea and should be distinguished fromstertor or snoring, which are lower pitched inspiratory noises suggestive of poor airwaypositioning or pharyngeal obstruction. Bubbly or gurgly noises suggest pharyngeal secre-tions often seen in the child with cerebral palsy, who may have noises permanently frompoor airway control and inability to spontaneously clear secretions. Wheeze is a predom-inantly expiratory noise from lower airway obstruction, but may be termed a variety ofother names by parents. An expiratory grunt suggests pneumonia.

Chest pain is an unusual symptom in children, and does not usually reflect cardiacdisease, as it so often does in adults.

While parents are usually alert to breathing difficulties in toddlers and older children,abnormal respiration may be more difficult for them to detect in infants. Infants withbreathing difficulties may present with acute feeding problems. Feeding an infant is oneof the most strenuous activities, and parents are accustomed to seeing feeding as a gaugeof their infant’s well-being.

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8.4 PRIMARY ASSESSMENT AND RESUSCITATIONOF THE CHILD WITH BREATHING DIFFICULTY

This is dealt with in Chapter 7, “Structured Approach to the Seriously Ill Child”.Below is a summary:

Assess response

If no response, proceed to life support. If response, assess A–B–C:

Airway

Assess vocalizations – crying or talking indicates ventilation and some degree of airwaypatency.

Assess airway patency by

• looking for chest and/or abdominal movement, symmetry and recession,• listening for breath sounds and stridor and• feeling for expired air.

Reassess after any airway-opening manoeuvres.

Breathing

Effort of breathingrespiratory rate recessionstridor wheeze gruntingaccessory muscle use flaring of alae nasi gasping

Exceptions

Increased effort of breathing DOES NOT occur in three circumstances:

– exhaustion (with imminent respiratory arrest)– central respiratory depression– neuromuscular disease

Efficacy of breathingchest expansion/abdominal excursionbreath sounds – reduced or absent, and symmetry on auscultationSa2 in air

Effects of respiratory failure on other physiologyheart rateskin colourmental status

Circulation

Heart ratePulse volumeCapillary refillSkin temperature

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Disability

Mental status/conscious levelPosturePupils

Exposure – rash or fever

Features suggesting cardiac cause of respiratory inadequacy

• cyanosis, not correcting with oxygen therapy• tachycardia out of proportion to respiratory difficulty• raised jugular venous pressure• gallop rhythm/murmur• enlarged liver• absent femoral pulses

Airway

• A patent airway is the first requisite. If the airway is not patent, an airway-openingmanoeuvre should be used.

• The airway should then be secured with a pharyngeal airway device or by intubationwith experienced senior help.

Breathing

• All children with breathing difficulties should receive high-flow oxygen through a facemask with oxygen as soon as the airway has been demonstrated to be adequate.

• Use a flow of 10–15 l/min via a face mask and reservoir bag to provide the patientwith 100% oxygen. If lower flows maintain adequate Sa2 (ie >95%), then nasalcannulae or nasal catheters may be used (at rates of <2 l/min).

• If the child is hypoventilating, with a slow respiratory rate or weak effort, respirationshould be supported with oxygen via a bag–valve–mask device and experienced seniorhelp summoned.

Circulation

• Fluid intake may have been reduced, particularly in infants presenting with breathingdifficulties. Consider fluid bolus (10–20 ml/kg of 0·9% saline) if there are signs ofcirculatory failure and particularly when intubation and positive pressure ventilation isinitiated. But be aware that respiratory illnesses can cause inappropriate anti-diuretichormone secretion, leading to fluid retention.

8.5 SECONDARY ASSESSMENT AND LOOKINGFOR KEY FEATURES OF THE CHILD WITHBREATHING DIFFICULTIES

While the primary assessment and resuscitation are being carried out, a focused historyof the child’s health and activity over the previous 24 hours and any significant previousillness should be gained.

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All children with breathing difficulties will have varying degrees of respiratory distressand cough, so these are not useful diagnostic discriminators.

Certain key features, which will be identified clinically in the above assessment andfrom the focused history, can point the clinician to the likeliest working diagnosis foremergency treatment.

• Inspiratory noises, i.e. stridor, point to upper airway obstruction Section 8.6• Expiratory noises, i.e. wheeze, point to lower airway obstruction Section 8.7• Fever without stridor suggests pneumonia Section 8.8• Signs of heart failure point to congenital or acquired heart disease Section 8.9• Short history, exposure to allergen and urticarial rash point to anaphylaxis

Section 8.10• Suspicion of ingestion and absence of cardio-respiratory pathology point to poisoning

Section 8.11

8.6 APPROACH TO THE CHILD WITH STRIDOR

Obstruction of the upper airway (larynx and trachea) is potentially life threatening.The small cross-sectional area of the upper airway renders the young child particularlyvulnerable to obstruction by oedema, secretions or an inhaled foreign body.

Table 8.2. Causes of stridor

Incidence (UK) Diagnosis Clinical features

Very common Croup – viral laryngotracheitis Coryzal, barking cough, mild fever,hoarse voice

Common Croup – recurrent or spasmodiccroup

Sudden onset, recurrent, history ofatopy

Uncommon Laryngeal foreign body Sudden onset, history of chokingRare Epiglottitis Drooling, muffled voice, septic

appearanceCroup – bacterial tracheitis Harsh cough, chest pain, septic

appearanceTrauma Neck swelling, crepitus or bruisingRetropharyngeal abscess Drooling, septic appearanceInhalation of hot gases Facial burns, peri-oral sootInfectious mononucleosis Sore throat, tonsillar enlargementAngioneurotic oedema Itching, facial swelling, urticarial rashDiphtheria Travel to endemic area, unimmunised

Reassess airway

Is the airway partially obstructed or narrowed and what is the likely cause? Note thepresence of inspiratory noises.

• If “bubbly” noises are heard, the airway is full of secretions requiring clearance. Thisalso suggests that the child is either very fatigued, or has a depressed conscious level andcannot clear the secretions himself or herself by coughing.

• If stertorous (snoring) respiratory noises are heard, consider partial obstruction ofthe airway due to a depressed conscious level.

• If there is a harsh stridor associated with a barking cough, upper airway obstructiondue to croup should be suspected.

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• If a quiet stridor in a sick-looking child is present, consider epiglottitis.• With a very sudden onset, no prodromal symptoms and a history suggestive of in-

halation, consider a laryngeal foreign body.

Reassess the breathing: what degree of effort is needed for breathing and what is itsefficacy and effect? The answer to this question will inform the clinician as to the severityof the upper airway obstruction. A pulse oximeter should be put in place and the oxygensaturation both on breathing air and high-flow oxygen noted.

8.7 AIRWAY EMERGENCY TREATMENT

In the child with a compromised but functioning airway an important principlein all cases is to avoid worsening the situation by upsetting the child. Crying andstruggling may quickly convert a partially obstructed airway into a completelyobstructed one. Administration of oxygen, nebulised adrenaline (epinephrine)or the performance of a radiograph may all require skill. Parents’ help shouldbe enlisted.

Partial obstruction from secretions/a depressed conscious level• Use suction to clear an airway partially obstructed by secretions as long as there is

no stridor.• Support the airway with the chin lift or jaw thrust manoeuvre in a child with the

stertorous breathing due to a depressed conscious level or extreme fatigue and askan anaesthetist to attend urgently.

• Further maintenance of the airway can be accomplished with an oro-pharyngeal ornaso-pharyngeal airway, but the child may require intubation.

• Continuous positive airway pressure can be given to patients with a reduced consciouslevel, whilst help is summoned, using a face mask, oxygen flow and a breathing circuit,eg an anaesthetic breathing circuit (Ayre’s T-piece).

Croup syndromes• Give nebulised adrenaline (epinephrine) (5 ml of 1:1000) with oxygen through a face

mask to patients with severe respiratory distress in association with harsh stridor andbarking cough. This will produce a transient improvement for 30–60 minutes, but itrarely alters the long-term course of the illness. This treatment should be given onlyto children with signs of severe obstruction.

• Children who require adrenaline (epinephrine) for the emergency treatment of croupshould subsequently promptly receive nebulised or oral steroids (see below).

Adrenaline (epinephrine) reduces the clinical severity of obstruction, but does notimprove arterial blood gases, reduce the duration of hospitalisation or eliminate the needfor intubation. Children who have received adrenaline (epinephrine) will appear improvedfor a short while only and need to be observed very closely with continuous ECG andoxygen saturation monitoring. They may later require tracheal intubation. A markedtachycardia is usually produced by the adrenaline (epinephrine), but other side effectsare uncommon. This treatment is best used to “buy time” in which to assemble anexperienced team to treat a child with severe croup.

• Give humidified oxygen through a face mask, and monitor the oxygen saturation.

Many children admitted to hospital with croup have hypoxia as a result of alveolarhypoventilation secondary to airways obstruction and ventilation perfusion imbalance.Whilst the respiratory rate and the degree of sternal recession are valuable clinical indi-cators of severity and response to treatment, the degree of hypoxia is the best assessment.

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However, hypoventilation may be masked when the child is receiving high ambient oxy-gen. The oxygen saturation with the child breathing air should be checked intermittently.

• Inhalation of warm moist air is widely used but is of unproven benefit.

Foreign body• Laryngoscopy will be needed for children with severe respiratory distress and a sig-

nificant history of foreign body inhalation if the “choking child” procedure has beenunsuccessful.

• Do not jeopardise the airway by unpleasant or frightening interventions, but contacta senior anaesthetist/ENT surgeon urgently.

• In extreme cases of life threat, immediate direct laryngoscopy with Magills forcepsto remove a visible foreign body may be necessary.

EpiglottitisThe diagnosis of acute epiglottitis is made from the characteristic history and clinical

findings, eg drooling and a soft inspiratory stridor.

• Intubation is likely to be required. Contact a senior anaesthetist urgently, who willperform careful gaseous induction of anaesthesia. When deeply anaesthetised thechild can be laid on his back to allow laryngoscopy and intubation. Tracheal intuba-tion may be difficult because of the intense swelling and inflammation of the epiglottis(“cherry red epiglottis”). A smaller tube than the one usually required for the child’ssize will be necessary.

• Do not jeopardise the airway by unpleasant or frightening interventions. Do not liethe child down if he or she prefers sitting up.

• Interventions, such as lateral radiographs of the neck and venepuncture, should beavoided as they disturb the child and have precipitated fatal total airway obstruction.

• There is no evidence that nebulised adrenaline (epinephrine) or steroids arebeneficial.

Anaphylaxis• In addition to oxygen, the specific treatment for anaphylaxis is intramuscular

adrenaline (epinephrine) (10 micrograms/kg).• Nebulised adrenaline (epinephrine) as described above in the treatment of croup may

also be given (see Section 8.11).

Specific upper airway conditions

Most cases of upper airway obstruction in children are the result of infection, but in-halation of a foreign body or hot gases (house fires), angioneurotic oedema and traumacan all result in obstruction and the normal airway will become obstructed in the uncon-scious, supine patient.

Croup

Background – Croup is defined as an acute clinical syndrome with inspiratory stridor,a barking cough, hoarseness and variable degrees of respiratory distress. This definitionembraces several distinct disorders. Acute viral laryngotracheobronchitis (viral croup) isthe commonest form of croup and accounts for over 95% of laryngotracheal infections.Parainfluenza viruses are the commonest pathogens but other respiratory viruses, suchas respiratory syncytial virus and adenoviruses, produce a similar clinical picture. Thepeak incidence of viral croup is in the second year of life and most hospital admissionsare in children aged between 6 months and 5 years.

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The typical features of a barking cough, harsh stridor and hoarseness are usually pre-ceded by fever and coryza for 1–3 days. The symptoms often start, and are worse, atnight. Many children have stridor and a mild fever (<38·5◦C), with little or no respira-tory difficulty. If tracheal narrowing is minor, stridor will be present only when the childhyperventilates or is upset. As the narrowing progresses, the stridor becomes both inspi-ratory and expiratory, and is present even when the child is at rest. Some children, andparticularly those below the age of three, develop the features of increasing obstructionand hypoxia with marked sternal and subcostal recession, tachycardia, tachypnoea andagitation. If the infection extends distally to the bronchi, wheeze may also be audible.

Some children have repeated episodes of croup without preceding fever and coryza. Thesymptoms are often of sudden onset at night, and usually persist for only a few hours. Thisrecurrent or spasmodic croup may be associated with atopic disease (asthma, eczema,hay fever). The episodes can be severe, but are more commonly self-limiting. They aredifficult to distinguish clinically from infectious croup and appear to respond identicallyto treatment, so there is a case for considering both conditions as part of one spectrumof disease.

Treatment – Steroids modify the natural history of croup: they give rise to some clinicalimprovement within 30 minutes and may lead to a reduction in hospital stay. Currenttreatments are either systemic dexamethasone 0·15 mg/kg or inhaled nebulised budeno-side 2 mg. Dexamethasone can be continued once daily for 2 to 3 days if symptoms persistand budenoside may be repeated 30–60 minutes later if clinically indicated. Budenosideand dexamethasone are equally effective. The choice will depend on which route is mostappropriate for the individual child, but oral dexamethasone is the treatment of choicein general.

Fewer than 5% of children admitted to hospital with croup require tra-cheal intubation. The decision to intubate is a clinical one based on increasingtachycardia, tachypnoea and chest retraction, or the appearance of cyanosis,exhaustion or confusion. Ideally, the procedure should be performed undergeneral anaesthetic by an experienced paediatric anaesthetist, unless there hasbeen a respiratory arrest. A much smaller gauge tracheal tube than usual isoften required. If there is doubt about the diagnosis, or difficulty in intubation

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is anticipated, an ENT surgeon capable of performing a tracheotomy should be present.The median duration of intubation in croup is 3 days: the younger the child, the longerthe intubation is usually required. Prednisolone (1 mg/kg every 12 hours) reduces theduration of intubation and the need for re-intubation in children with severe croup. Allintubated children must have continuous CO2 and Sa2 monitoring.

Bacterial tracheitis

Bacterial tracheitis, or pseudomembranous croup, is an uncommon but life-threateningform of croup. Infection of the tracheal mucosa with Staphyloccocus aureus, streptococcior Haemophilus influenzae B (HiB) results in copious, purulent secretions and mucosalnecrosis. The child appears toxic, with a high fever and the signs of progressive upperairway obstruction. The croupy cough and the absence of drooling help distinguish thiscondition from epiglottitis. Over 80% of children with this illness need intubation andventilatory support to maintain an adequate airway, as well as intravenous antibiotics(combination of flucloxacillin and cefotaxime).

Epiglottitis

Background – Acute epiglottitis shares some clinical features with croup but it is a quitedistinct entity. Although much less common than croup, its importance is that unless

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the diagnosis is made rapidly and appropriate treatment commenced, total obstructionand death are likely to ensue. This is far less commonly seen in countries where HiBimmunisation has been introduced. However, it does still occur, in cases of vaccine failureand in unimmunised children.

Infection with Haemophilus influenzae B causes intense swelling of the epiglottis andthe surrounding tissues and obstruction of the larynx. Epiglottitis is most common inchildren aged 1–6 years, but it can occur in infants and in adults.

The onset of the illness is usually acute with high fever, lethargy, a soft inspiratorystridor and rapidly increasing respiratory difficulty over 3–6 hours. In contrast to croup,cough is minimal or absent. Typically the child sits immobile, with the chin slightly raisedand the mouth open, drooling saliva. He looks very toxic and pale, and has poor peripheralcirculation (most are septicaemic). There is usually a high fever (>39◦C). Because thethroat is so painful, the child is reluctant to speak and unable to swallow drinks or saliva.Disturbance of the child, and particularly attempts to lie the child down, to examine thethroat with a spatula, or to insert an intravenous cannula, can precipitate total obstructionand death, and must be avoided.

Treatment – After securing the airway, blood should be sent for culture and treatmentwith intravenous cefotaxime or ceftriaxone commenced. With appropriate treatment,most children can be extubated after 24–36 hours and they recover fully within 3–5 days.Complications such as hypoxic cerebral damage, pulmonary oedema and other seriousHaemophilus infections are rare. In countries where the HiB vaccine is in use there shouldbe an investigation into vaccine failure.

Foreign body

Background – The inquisitive and fearless toddler and the infant with toddler siblings isat risk of inhaling a foreign body. If an inhaled foreign body lodges in the larynx or trachea,the outcome is often fatal at home, unless measures such as those discussed in Chapter4 are performed. Should a child present to hospital with very sudden onset of stridorand other signs of acute upper airway obstruction, especially during waking hours, andparticularly if there is no fever or preceding illness, then a laryngeal foreign body is thelikely diagnosis. A history of eating or of playing with small objects immediately prior tothe onset of symptoms is strong supportive evidence. Foodstuffs (nuts, sweets, meat) arethe commonest offending items. In 2000, nineteen children in England and Wales diedfrom choking. In all but one, food was the cause of obstruction. In some instances, objectsmay compress the trachea from their position of lodgement in the upper oesophagus,producing a similar but less severe picture of airway obstruction.

The object may pass through the larynx into the bronchial tree, where it produces apersistent cough of very acute onset, and unilateral wheezing. Examination of the chestmay reveal decreased air entry on one side or evidence of a collapsed lung. Inspiratoryand expiratory chest radiographs may show mediastinal shift on expiration due to gastrapping distal to the bronchial foreign body.

Treatment – Removal through a bronchoscope under general anaesthetic should be per-formed as soon as possible because there is a risk of coughing moving the object into thetrachea and causing life-threatening obstruction. In the case of the stridulous child with arelatively stable airway and a strong suspicion of foreign body inhalation, careful gaseousinduction of anaesthesia should be induced by an experienced anaesthetist, with the pres-ence of an ENT surgeon to perform a tracheotomy in case of disaster. The foreign bodycan then be removed under controlled conditions. In some cases, prior to anaesthesia, itmay be appropriate to perform a careful lateral neck radiograph in the emergency room(taking extreme care not to distress the child, which might provoke complete obstruction)to ascertain the position and nature of the object.

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Anaphylaxis

Background – Anaphylaxis is a potentially life-threatening, immunologically mediatedsyndrome in which laryngeal oedema can develop over minutes, often with swelling (an-gioneurotic oedema) of the face, mouth and tongue. Food allergies, especially nuts anddrug reactions (contrast media and anaesthetic drugs in particular), are usual causesof this. Prodromal symptoms of flushing, itching, facial swelling and urticaria usuallyprecede stridor. Abdominal pain, diarrhoea, wheeze and shock may be additional oralternative manifestations of anaphylaxis (Section 8.11).

A severe episode of anaphylaxis can be predicted in patients with a previous severeepisode or a history of increasingly severe reaction, a history of asthma or treatment withbeta blockers.

Treatment – If there has not been significant improvement with the initial dose ofadrenaline (epinephrine), a further intramuscular dose can be given after 5 minutes.Chlorphenamine (chlorpheniramine) and steroids are also given to patients with ana-phylaxis but their onset of action (if any) is delayed (see Section 8.11).

Other causes of upper airways obstruction

Although croup accounts for the large majority of cases of acute upper airway ob-struction, several other uncommon conditions need to be considered in the differentialdiagnosis. Diphtheria is seen only in children who have not been immunised against thedisease. Always ask about immunisations in any child with fever and the signs of upperairways obstruction, particularly if they have been to endemic areas recently. Specifictreatment of croup includes penicillin, steroids and anti-toxin.

Marked tonsillar swelling in infectious mononucleosis or acute tonsillitis can rarely com-promise the upper airway. The passage of a nasopharyngeal tube may give instant re-lief. Retropharyngeal abscess is uncommon nowadays, but can present with fever and thefeatures of upper airway obstruction together with feeding difficulties. Treatment is bysurgical drainage and intravenous antibiotics.

8.8 APPROACH TO THE CHILD WITH WHEEZE

The two common causes of lower respiratory obstruction are:

• acute severe asthma see below• bronchiolitis see later

Almost without exception, bronchiolitis is confined to the under-1-year-olds andasthma is much more commonly diagnosed in the over-1-year-olds.

Acute severe asthma

It can be difficult to assess the severity of an acute exacerbation of asthma. Clinical signscorrelate poorly with the severity of airway obstruction. Some children with acute severeasthma do not appear distressed, and young children with severe asthma are especiallydifficult to assess.

Historical features associated with more severe or life-threatening airway obstructioninclude:

• a long duration of symptoms, symptoms of regular nocturnal awakening,• poor response to treatment already given in this episode and• a severe course of previous attacks, including the use of intravenous ther-

apy, and those who have required admission to an intensive care unit.

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Before children can receive appropriate treatment for acute asthma in any setting, it isessential to assess accurately the severity of their symptoms. The following clinical signsshould be recorded every 1–4 hours, or before and after each dose of bronchodilator:

• Pulse rate• Respiratory rate and degree of recession• Use of accessory muscles of respiration• Degree of agitation and conscious level• Sa2

• Peak flow

Two characteristic levels are described to indicate the appearance of asthmatic childrenat the most severe end of the spectrum. These are severe and life-threatening asthma.

Moderate asthma Acute severe asthma Life-threatening asthma

Sa2 ≥ 92%No clinical features of severe

or life-threatening attackPeak flow > 50%

best/predicted

Too breathless to feed or talkRecession/use of accessory

musclesRespiratory rate > 30/min

(>5 years)> 50/min (2–5 years)Pulse rate > 120 beats/min

(>5 years)> 130 beats/min (2–5 years)Peak flow < 50%

best/predicted

Conscious leveldepressed/agitated

ExhaustionPoor respiratory effortSa2 < 92% in air/cyanosisSilent chestPeak flow < 33%

best/predictedHypotension

Arterial oxygen saturation as measured non-invasively by a pulse oximeter (Sa2) isuseful in assessing severity, monitoring progress and predicting outcome in acute asthma.More intensive in-patient treatment is likely to be needed for children with Sp2 < 92%on air after initial bronchodilator treatment.

The peak expiratory flow rate (PEFR) is a valuable measure of severity and should bea routine part of the assessment. Children below the age of 5 and those who are verydyspnoeic are usually unable to produce reliable readings.

Examination features that are poor signs of severity include the degree of wheeze,respiratory rate, and pulsus paradoxus. A chest radiograph is indicated only if there issevere dyspnoea, uncertainty about the diagnosis, asymmetry of chest signs or signs ofsevere infection.

Asthma emergency treatment

• Assess ABC.• Give high-flow oxygen via a face mask with reservoir bag.• Attach pulse oximeter; always aim to keep Sa2 >92%.• Give a beta-2 agonist, such as salbutamol.

❝ In those with mild to moderate asthma and maintaining Sa2 > 92% in air, use pres-surised aerosol 1000 microgram (10 sprays) via valved holding chamber (spacer)with/without face mask. Children with mild to moderate asthma are less likely tohave tachycardia and hypoxia if given beta-2 agonists via a pressurised aerosol andspacer. Children aged <3 years are likely to require a face mask connected to themouthpiece of a spacer for successful drug delivery. Inhalers should be sprayed intothe spacer in individual puffs and inhaled immediately by tidal breathing.

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❝ In those with severe or life-threatening asthma, or when oxygen is needed, usenebulised salbutamol 2·5 mg (<5 years) or 5 mg (>5 years) with oxygen at a flowof 4–6 l/min in order to provide small enough particle sizes. Higher flows may beused, but more of the nebulised drug may be lost from the face mask.

❝ When there is uncertainty about reliable inhalation or where the inhaled drug pro-duces no effective response, give a bolus of intravenous salbutamol (see below),and consider a continuous infusion (on HDU/PICU).

• Give oral prednisolone 1·0 mg/kg or, if vomiting, IV hydrocortisone 4mg/kg.• If receiving nebulised salbutamol, mix with ipratropium bromide 250 micrograms

driven with oxygen. This may be given every 20–30 minutes initially, reducing thedose as improvement occurs.

• If an infant or child is clearly in respiratory failure with poor respiratory effort, adepressed conscious level and poor saturation despite maximum-oxygen therapy,attempt to support ventilation with a bag–valve–mask: give an intravenous salbutamolinfusion (give a loading dose of 15 micrograms/kg) to any in whom a diagnosis ofasthma is suspected, and summon experienced support.

Reassess ABC and monitor the response to treatment carefully. Assessment is based onphysical signs and oxygen saturation measurements performed immediately before and15–30 minutes after inhaled treatment. This should be accompanied by improved peakflow measurement.

If not responding, or deteriorating condition:

• Nebulised salbutamol may be given continuously, or salbutamol IV 15 micrograms/kgover 10 minutes over 2 years. The latter should be followed by IV infusion of1–5 micrograms/kg/min, whilst monitoring ECG and serum K regularly to allowfor detection and treatment of hypokalaemia.

• If respiratory effort is poor or deteriorating, or conscious level is depressed, or Sa2is low and falling despite maximum-oxygen therapy, attempt to support ventilationwith bag–valve–mask, or with a mask, T-piece and bag with high-flow oxygen.

• Summon experienced support.• If the child is not on oral theophylline or other methylxanthines, give a loading dose

of IV aminophylline 5 mg/kg over 20 minutes, monitoring ECG for arrhythmias,followed by an infusion of 1 mg/kg/h.

• Contact the PICU.• Consider magnesium sulphate 25–40 mg/kg over 20 minutes• Consider intubation for mechanical ventilation with IV ketamine or halothane induc-

tion.

Indications for intubation:

• Increasing exhaustion• Progressive deterioration in

❝ clinical condition❝ SaO2 – decreasing and/or oxygen requirement increasing❝ PCO2 – increasing

Mechanical ventilation is rarely required. There are no absolute criteria, as the decisionto intubate is usually based on the clinical condition of the child, and response to previoustreatment. In cases of acute severe asthma that respond to treatment, there is usually littlevalue to be gained from routine blood gas measurement. However, in those responding

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poorly, repeat blood gases help in the decision to intubate. For example, ventilationshould be considered if there is a P2 of >8 kPa, persistent hypoxia (P2 < 8 kPa in aninspired oxygen of 60%), particularly if there is increasing exhaustion, despite intensivedrug therapy. In skilled hands, the prognosis is good but complications such as air leakand lobar collapse are common. Children with acute asthma who require mechanicalventilation should be transferred to a paediatric intensive care unit. All intubated childrenmust have continuous CO2 monitoring.

If responding and improving

• If there has been considerable improvement (Sa2 > 92% in air, minimal recession,PEFR > 50% of normal value) intravenous treatment can be discontinued.

• Change from nebulised bronchodilator to the use of 8–10 aerosol sprays of a beta2-agonist inhaler, such as salbutamol or terbutaline, given one spray at a time duringtidal breathing through a spacer with mouthpiece or face mask – this can usually bedone when additional oxygen is no longer needed.

• Reduce the frequency of inhaled therapy from 12-hourly to 4-hourly, reducing fre-

quency as improvement occurs.• The child’s maintenance treatment should be reviewed and altered if inadequate.

Inhaler technique should be checked.

Other measures

• Reassure child and avoid upset.• Monitor ECG and Sa2.• Ensure that there is avoidance of any identifiable trigger.• Intravenous fluids – restrict to two-thirds of the normal requirements.• Antibiotics – do not give routinely, as most asthma attacks are triggered by viral

infections.

Drug notes

• Corticosteroids expedite recovery from acute asthma. Although an oral single doseof prednisolone is effective, many paediatricians use a 3–5-day course. There is noneed to taper off the dose for courses up to 10–14 days, or unless the child is onmaintenance treatment with oral or high-dose inhaled steroids. Unless the child isvomiting, there is no advantage in giving steroids parenterally.

• Intravenous salbutamol has been shown to offer an advantage over inhaled delivery.Although inhaled drugs should be given first as they are accessible and more ac-ceptable to the child, intravenous salbutamol has a place in severe or life-threateningepisodes that do not respond promptly to inhaled therapy. Important side effects in-clude sinus tachycardia and hypokalaemia: serum potassium levels should be checked12-hourly, and supplementation may be needed.

• Intravenous aminophylline still has a role in the child who fails to respond adequatelyto nebulised therapy. A loading dose is given over 20 minutes, followed by a continu-ous infusion. The pulse should be regularly checked for irregularities with continuousECG monitoring during infusion of the loading dose. If the child has received a slow-release theophylline in the previous 12 hours, the loading dose should be omitted.Seizures, severe vomiting, and fatal cardiac arrhythmias may follow rapid infusion.There is no place for rectal administration of these drugs, as absorption is unpre-dictable.

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• Intravenous magnesium sulphate is a safe treatment for acute asthma although its placein management is not yet established. Doses of up to 40 mg/kg/day (maximum 2 g)by slow infusion have been used. Studies of efficacy for severe childhood asthmaunresponsive to more conventional therapies have been inconsistent in providingevidence of benefit.

• There is no evidence to support the routine use of heliox or leukotriene receptorantagonists for the treatment of acute asthma in childhood.

Table 8.3. Drug treatment of severe acute asthma

Oxygen High flow

Nebulised beta-2-bronchodilator Salbutamol 2·5–5 mg 30-min–4-hourlyTerbutaline 2–10 mg 30-min–4-hourly

Prednisolone 2 mg/kg/day for 3 days (max dose/day 60 mg) ORIntravenous hydrocortisone succinate loading dose4 mg/kg by continuous infusion 1 mg/kg/hour

Aminophylline Loading dose 5 mg/kg IV over 20 minutes∗ bycontinuous infusion 1 mg/kg/h

Intravenous salbutamol Loading dose 15 µg/kg over 2 yrs. Continuousinfusion 1–5 µg/kg/min

Nebulised ipratropium 125–250 µg every 20–30 minutes

∗Omit if child has received oral theophylline in previous 12 hours.

Background information on asthma

Acute exacerbation of asthma is the commonest reason for a child to be admitted tohospital in the UK. Admissions for acute asthma in children aged 0–4 years increasedsevenfold between 1970 and 1986 and admissions for children in the 5–14 age grouptripled. In the early 1990s asthma represented 10–20% of all acute medical admissions inchildren, but by 2000 hospital admission rates had declined by about 50%. Consultationswith general practitioners for an acute asthma episode peaked in the early 1990s and by2000 had declined quite substantially. Despite the continuing high prevalence of asthmain children in England and Wales, there appears to be a decrease in acute episodesrequiring medical care. However, there were still 26 deaths from asthma in England andWales in 2002 (ONS).

Except in the young infant, there is rarely any problem in making a diagnosis of acuteasthma. An inhaled foreign body, bronchiolitis, croup and acute epiglottitis should be con-sidered as alternative diagnoses. The classic features of acute asthma are cough, wheezeand breathlessness. An increase in these symptoms and difficulty in walking, talking orsleeping all indicate worsening asthma. Decreasing relief from increasing doses of a bron-chodilator always indicates worsening asthma.

Upper respiratory tract infections are the commonest precipitant of symp-toms of asthma in the preschool child. Viruses cause 90% of these infections.Exercise-induced symptoms are more frequent in the older child. Heat andwater loss from the respiratory mucosa appears to be the mechanism by whichexercise induces bronchoconstriction. Emotional upset, laughing or excite-ment may also precipitate acute exacerbations. It is hard to assess the impor-tance of allergen exposure to the onset of acute symptoms in an individualasthmatic, partly because of the ubiquitous nature of the common allergens(house dust mite, grass pollens, moulds) and partly because delay in the allergicresponse makes a cause-and-effect relationship difficult to recognise. A rapidfall in air temperature, exposure to a smoky atmosphere and other chemicalirritants such as paints and domestic aerosols may trigger an acute attack.

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Bronchiolitis emergency treatment

Management is usually supportive, as although there is specific anti-viral treatmentfor respiratory syncitial virus (RSV, the commonest cause of bronchiolitis), this is notfrequently used.

• Assess ABC.• Ensure that the airway is patent and clear: use of a Yankauer suction catheter applied

to the nares can help to ensure that the nose and nasopharynx are cleared, which canhave a significant impact on an infant’s respiratory distress.

• Give a high concentration of oxygen via mask with reservoir bag. Monitor Sa2 andkeep above 94%. Milder and improving cases may use oxygen via nasal cannulae at<2 l/min. Consider using humidity.

• Maintain hydration and nutrition. In infants with significant respiratory distress,maintain hydration by feeding via a nasogastric tube, or intravenously. Remember,nasogastric tubes may partially occlude the airway. Breastfeeding may be too stressful,in which case breast milk should be expressed and given via a gastric tube.

• Monitor for apnoea/hypoventilation in those <2 months old:– Sa2– Respiratory frequency/apnoea monitor– Arterial/capillary hypercapnia

• Mechanical ventilation is required in 2% of infants admitted to hospital. Whilst non-invasive methods of respiratory support (e.g. CPAP) have been used, there are norandomised controlled data to show that this avoids intubation. In severe cases, infantswith the following may need intubation and mechanical ventilation:– Recurrent apnoea– Exhaustion– Severe hypercapnia and hypoxia

• All intubated infants must have continuous Sa2 and CO2 monitoring.• Bronchodilators, steroids and antibiotics are of no proven value. The precise role

of the nebulised antiviral agent ribavirin is unclear – it is sometimes used for chil-dren with pre-existing lung disease, those with impaired immunity and infants withcongenital heart disease, although these groups are by now likely to have receivedpalivizumab, which is expected to lessen the severity of the RSV disease.

Most children recover from the acute infection within 2 weeks. However, as many ashalf will have recurrent episodes of cough and wheeze over the next 3–5 years. Rarelythere is severe permanent damage to the airways (bronchiolitis obliterans).

Background information on bronchiolitis

Bronchiolitis is the most common serious respiratory infection of childhood:it occurs in 10% of all infants and 2–3% are admitted to hospital with the dis-ease each year. Ninety per cent of patients are aged 1–9 months – it is rareafter 1 year of age. There is an annual winter epidemic. Respiratory syncytialvirus is the pathogen in 75% of cases, the remainder of cases being caused byother respiratory viruses, such as parainfluenza, influenza and adenoviruses.Acute bronchiolitis is never a primary bacterial infection, and it is likely thatsecondary bacterial involvement is uncommon.

Fever and a clear nasal discharge precede a dry cough and increasing breath-lessness. Wheezing is often, but not always, present. Feeding difficulties asso-ciated with increasing dyspnoea are often the reason for admission to hospital.Recurrent apnoea is a serious and potentially fatal complication, and is seen

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particularly in infants born prematurely. Children with pre-existing chronic lung disease(e.g. cystic fibrosis, bronchopulmonary dysplasia in premature infants), and children withcongenital heart disease or immune deficiency syndromes are at particularly high risk ofdeveloping severe respiratory failure with bronchiolitis.

The findings on examination are characteristic.

Table 8.4. Bronchiolitis – characteristic findings on examination

Tachypnoea 50–100 breaths/minRecession Subcostal and intercostalCough Sharp, dryHyperinflation of the chest Sternum prominent, liver depressedTachycardia 140–200 beats/minCrackles Fine end-inspiratoryWheezes High-pitched expiratory > inspiratoryColour Cyanosis or pallorBreathing pattern Irregular breathing/recurrent apnoea

The chest radiograph shows hyperinflation with downward displacement and flatten-ing of the diaphragm due to small airways obstruction and gas trapping. In one-thirdof infants there is also evidence of collapse or consolidation, particularly in the upperlobes. Respiratory syncytial virus and other viruses can be cultured or identified with afluorescent antibody technique on nasopharyngeal secretions. Blood gas analysis, whichis required in only the most severe cases, shows lowered oxygen and raised carbon dioxidelevels.

Risk factors for severity in bronchiolitis

• Age under 6 weeks• Premature birth• Chronic lung disease• Congenital heart disease• Immunodeficiency

Bronchiolitis can be difficult to differentiate from heart failure, or may trigger it in aninfant with a previously undiagnosed cardiac lesion. Distinguishing features include:

Heart failure Bronchiolitis

Feeding difficulty with growth failureRestlessness, sweatingTachycardia and tachypnoea Coryzal and harsh coughPallor, sweating and cool peripheriesLarge heart with displaced apex beat Normal or apparently small heartLarge liver Liver lower than normalGallop rhythmMurmur No murmurChest X-ray shows pulmonary congestion

and large heartHyperinflation on chest X-ray

Although many causes of breathing difficulties are associated with infection, a high feveris usually associated only with pneumonia, epiglottitis and bacterial tracheitis. Although

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many cases of asthma are precipitated by an URTI, the asthmatic child is rarely febrileand a low grade fever is characteristic of bronchiolitis. Therefore in the absence of stridorand wheeze, breathing difficulties in association with a significant fever are likely to bedue to pneumonia.

8.9 APPROACH TO THE CHILD WITH FEVER

Pneumonia emergency treatment

• Assess ABC.• Provide a high concentration of oxygen via a face mask with reservoir bag. Attach a

pulse oximeter; if a low flow maintains Sa2 at >94%, then nasal cannulae may beused with a flow <2 l/min.

• As it is not possible to differentiate reliably between bacterial and viral infectionon clinical, haematological or radiological grounds, all children diagnosed as havingsignificant pneumonia should receive antibiotics. The preferred antibiotics in theseriously ill child are:❝ cefuroxime – effective against most bacteria❝ cefotaxime – if there is a septic component❝ flucloxacillin – if Staphylococcus aureus is suspected❝ erythromycin – if chlamydia/mycoplasma pneumonia or pertussis (unimmunised

infant) is suspected• Maintain hydration – extra fluid may be needed to compensate for loss

from fever, but restriction may be needed because of inappropriate ADHsecretion. Fluid overload can contribute to worsening breathlessness.

514• Clinical examination and the chest radiograph may reveal a pleural effu-sion. Large pleural effusions should be diagnosed where possible by ultrasound andif this is large, it should be tapped to relieve breathlessness, as well as to help in thediagnosis. Pleural drainage with a chest drain should be performed under ultrasoundcover to avoid placing the chest drain into the heart, liver or an undiagnosed tumour.Details of the procedure can be found in Chapter 22.

• Airway and breathing support may be especially needed in children with neurologicalhandicap who may have poor airway control and weak respiratory muscles even whenwell.

Background to pneumonia

Pneumonia in childhood was responsible for 63 deaths of children aged between 1month and 14 years in England and Wales in 2002 (ONS). Infants, and children withcongenital abnormalities or chronic illnesses, are at particular risk. In adults, two-thirdsof cases of pneumonia are caused by either Streptococcus pneumoniae or Haemophilus in-fluenzae. A much wider spectrum of pathogens causes pneumonia in childhood, anddifferent organisms are important in different age groups.

In the newborn, organisms from the mother’s genital tract, such as Escherichia coliand other Gram-negative bacilli, group B beta-haemolytic Streptococcus and, increasingly,Chlamydia trachomatis are the most common pathogens. In infancy, respiratory viruses,particularly respiratory syncytial virus, are the most frequent cause, but Streptococcuspneumoniae, Haemophilus and, less commonly, Staphylococcus aureus are also important.In older children, viruses become less frequent pathogens and bacterial infection is moreimportant. S. pneumoniae remains the commonest cause in this age group but Mycoplasmapneumonia is also a cause of pneumonia in the school-age child. Bordatella pertussis can

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present with pneumonia as well as with classical whooping cough, even in children whohave been fully immunised. It can cause a severe pneumonitis, leading to respiratoryfailure in unimmunised infants.

Fever, cough, breathlessness and chest recession in the younger child and lethargy arethe usual presenting symptoms. The cough is often dry initially but then becomes loose.Older children may produce purulent sputum but in those below the age of 5 years it isusually swallowed. Pleuritic chest pain, neck stiffness and abdominal pain may be presentif there is pleural inflammation. Classical signs of consolidation such as impaired percus-sion, decreased breath sounds and bronchial breathing are often absent, particularly ininfants, and a chest radiograph is needed. This may show lobar consolidation, widespreadbronchopneumonia or, less commonly, cavitation of the lung. Pleural effusions are quitecommon, particularly in bacterial pneumonia. An ultrasound of the chest will delineatea pleural effusion and be helpful in the placing of a chest drain. Blood cultures, swabs forviral isolation, and a full blood count should also be performed. It can be useful to savean acute serum for further microbiological diagnosis.

As it is not possible to differentiate reliably between bacterial or viral infection onclinical or radiological grounds, all children diagnosed as having significant pneumoniashould receive antibiotics. The initial choice of antibiotics depends on the age of thechild. Antibiotics should be given for 7–10 days, except in staphylococcal pneumonia,where a flucloxacillin course of 4–6 weeks’ duration is needed. Many older children haveno respiratory difficulty and can be treated at home with penicillin, a cephalosporin orerythromycin. Infants, and children who look toxic, have definite dyspnoea, Sa2 below93%, grunting or signs of dehydration should be admitted and usually require intravenoustreatment initially (see above).

Oxygen (if Sa2 < 93%) and an adequate fluid intake (80% maintenance, as inappro-priate anti-diuretic hormone secretion occurs in pneumonia) are also required. Mechan-ical ventilation is rarely required unless there is a serious underlying condition. Transferto the PICU should be considered with the following: an Fi2 > 0·6 to keep Sa2 > 92%,shock, exhaustion, rising CO2, apnoea or irregular breathing. Chest physiotherapy is notbeneficial in previously healthy children with community-acquired pneumonia, but mayhelp children who are known to have problems with secretion clearance. If a child hasrecurrent or persistent pneumonia, investigations to exclude underlying conditions suchas cystic fibrosis or immunodeficiency should be performed.

8.10 APPROACH TO THE CHILD WITH HEART FAILURE

Infants and children with serious cardiac pathology may present with breathlessness,cyanosis or cardiogenic shock. The immediate management of the latter is described inChapter 9.

Table 8.5. Causes of heart failure which may present as breathing difficulties

Left ventricular volume overload or excessive pulmonary blood flowVentricular septal defect Atrioventricular septal defectCommon arterial trunk Persistent arterial duct

Left heart obstructionHypertrophic cardiomyopathy Critical aortic stenosisAortic coarctation Hypoplastic left heart syndrome

Primary “pump” failureMyocarditis Cardiomyopathy

DysrhythmiaSupraventricular tachycardia Complete heart block

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Heart failure emergency treatment

• Reassess ABC• If there are signs of shock – poor pulse volume or low blood pressure with extreme

pallor and depressed conscious level – treat the child for cardiogenic shock (see Sec-tion 10.10).

• If circulation is adequate and oxygen saturation is normal or improves significantlywith oxygen by face mask but there are signs of heart failure, then the breathingdifficulty is due to pulmonary congestion secondary to a large left to right shunt.The shunt may be through a VSD, AVSD, PDA or, more rarely, a truncus arterio-sus. In many cases a heart murmur will be heard. A chest radiograph will also giveconfirmatory evidence, with a large, usually globular heart and radiological signs ofpulmonary congestion. Give❝ high-flow oxygen by face mask with a reservoir and❝ diuretics such as furosemide (frusemide) (1 mg/kg IV followed by initial mainte-

nance dose of 1–2 mg/kg/day in 1–3 divided doses); if there is no diuresis within2 hours, the intravenous bolus can be repeated.

• Babies in the first few days of life who present with breathlessness and increasingcyanosis largely unresponsive to oxygen supplementation are likely to have a duct-dependent congenital heart disease such as tricuspid or pulmonary atresia. An in-fusion of alprostadil at an initial dose of 0·05 micrograms/kg/min will maintain orincrease the patent ductus arteriosus size temporarily until the patient can be trans-ferred to a neonatal cardiology unit. Patients should be intubated and ventilated fortransfer, both because of the seriousness of their condition and because the alprostadilmay cause apnoea. As oxygen tends to promote ductal closure, oxygen concentrationfor ventilation should be individually adjusted using pulse oximetry to monitor themost effective concentration for each infant.

• Children of all ages who present with breathlessness from heart failure may havemyocarditis. This is characterised by a marked sinus tachycardia and the absenceof signs of structural abnormality. The patients should be treated with oxygen anddiuretics.

Full blood count, and measurements of serum urea and electrolytes, calcium, glucoseand arterial blood gases should be performed on all patients in heart failure. A routineinfection screen including blood cultures is recommended, especially in infants. A full12-lead electrocardiogram and a chest radiograph are essential. All patients suspected ofhaving heart disease should be discussed with a paediatric cardiologist; echocardiographywill establish the diagnosis in almost all cases. Transfer to a tertiary centre will usuallybe required.

Background to heart failure in infancy and childhood

In infancy, heart failure is usually secondary to structural heart disease, and medicaltreatment is directed at improving the clinical condition prior to definitive surgery. Withmodern obstetric management many babies are now discharged from the maternity unitonly hours after birth. Therefore babies with serious congenital neonatal heart diseasemay present to paediatric or accident and emergency departments.

Infants with common congenital heart diseases are usually diagnosed in utero or at thepost-natal examination, but a few will present acutely after discharge from medical careas the lowering pulmonary vascular resistance over the first hours to weeks of life allowsincreasing pulmonary flow in infants with left to right shunts such as VSD, persistentPDA, truncus arteriosus. The increasing left to right shunt causes increasing pulmonary

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congestion and heart failure, and the infant presents with poor feeding, sweating andbreathlessness. In addition, some may present at a few months of age when heart failureis precipitated by a respiratory infection, usually bronchiolitis.

Duct-dependent congenital heart disease

There are also several rarer and more complex congenital heart defects in which thepresence of a patent ductus arteriosus is essential to maintain pulmonary or systemicflow. The normal patent ductus arteriosus closes functionally in the first 24 hours of life.This may be delayed in the presence of congenital cardiac anomalies.

The pulmonary obstructive lesions include pulmonary atresia, critical pulmonary valvestenosis, tricuspid atresia, severe Fallot’s tetralogy and some cases of transposition of thegreat vessels. In all of these lesions there is no effective route for blood to take from theright ventricle into the pulmonary circulation, and therefore pulmonary blood flow andoxygenation of blood are dependent on flow from the aorta via a patent ductus.

Babies with critical pulmonary obstructive lesions present in the first few days of lifewith increasing cyanosis, breathlessness or cardiogenic shock. On examination there maybe a characteristic murmur but more frequently there is no murmur audible. An enlargedliver is a common finding. The clinical situation has arisen from the gradual closure of theductus arteriosus. Complete closure will result in the death of the infant from hypoxia.

In addition, there are some congenital heart malformations where systemic blood flowis dependent on the ductus arteriosus delivering blood to the aorta from the pulmonarycirculation. This is characteristic of severe coarctation, critical aortic stenosis and hy-poplastic left heart syndrome.

In these congenital heart lesions the baby ceases to be able to feed and becomes breath-less and grey and collapses with a poor peripheral circulation. On examination the babiesare in heart failure and in more severe cases in cardiogenic shock. In this situation, evenin coarctation of the aorta all pulses are difficult to feel.

In the older child myocarditis and cardiomyopathy are the usual causes of the acuteonset of heart failure and remain rare (see Table 8.1). Presenting features include fa-tigue, effort intolerance, anorexia, abdominal pain and cough. On examination a markedsinus tachycardia, hepatomegaly and raised JVP are found with inspiratory crackles onauscultation.

How to differentiate the infant with heart failure from the infantwith bronchiolitis

Bronchiolitis can be difficult to differentiate from heart failure, or may trigger it in aninfant with a previously undiagnosed cardiac lesion. Distinguishing features include:

Heart failure Bronchiolitis

Feeding difficulty with growth failureRestlessness, sweatingTachycardia and tachypnoea Coryzal and harsh coughPallor, sweating and cool peripheriesLarge heart with displaced apex beat Normal or apparently small heartLarge liver Liver lower than normalGallop rhythmMurmur No murmurChest X-ray shows pulmonary congestion

and large heartHyperinflation on chest X-ray

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In babies and children peripheral oedema is less commonly seen than in adults. Itcan therefore be difficult to differentiate the infant with heart failure from the infant withbronchiolitis, but the cardinal additional features in the infant in heart failure is the greaterdegree of hepatomegaly, the enlarged heart with displaced apex beat and the presence ofa gallop rhythm and/or a murmur. A chest radiograph will often be helpful in showingcardiomegaly and pulmonary congestion rather than the over-inflation of bronchiolitis.

8.11 APPROACH TO THE CHILD WITH ANAPHYLAXIS

Anaphylaxis is an immunologically mediated reaction to ingested, inhaled or topicalsubstances, which may present as either shock or respiratory distress. Common causes in-clude allergy to penicillin, to radiographic contrast media, and to certain foods, especiallynuts. This situation is potentially life-threatening and may result in breathing difficultieswith stridor or wheeze, shock, change in conscious level, collapse and respiratory orcardiac arrest. Some patients may carry their own adrenaline (epinephrine).

Emergency treatment of anaphylaxis

Figure 8.1. Emergency treatment of anaphylaxis

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Specific treatment includes:

• oxygen,• intramuscular adrenaline (epinephrine) 10 micrograms/kg,• nebulised adrenaline (epinephrine) 5 ml of 1:1000, as for croup and• nebulised bronchodilator.

Adrenaline (epinephrine) 10 microgram/kg is given intramuscularly, unless intractableshock or cardiac arrest is present – in these cases give via the intravenous or intraosseousroute. Intubation and ventilation will be required for severe cases.

Background to anaphylaxis

Consider with any of the following symptoms:

Symptoms Signs

Mild Burning sensation in mouth,itching of lips, mouth andthroat, feeling of warmth,nausea, abdominal pain

Urticarial rash, angio-oedema,conjunctivitis

Moderate (Mild +) Coughing/wheezing, loosebowel motions, sweating,irritability

Bronchospasm, tachycardia, pallor

Severe (Moderate +) Difficulty breathing,collapse, vomiting,uncontrolled defecation

Severe bronchospasm, laryngealoedema, shock, respiratoryarrest, cardiac arrest

When there is:

• a history of previous severe reaction,

• rapidly progressive or increasingly severe symptoms,

• a history of asthma, eczema or rhinitis (atopy) and

• in the presence of treatment with β-blockers.

8.12 APPROACH TO THE CHILD WITH METABOLICAND POISONING PROBLEMS

Diabetes

As hyperventilation is a feature of the severe acidosis produced by diabetes, occasionallya child may be presented with a primary breathing difficulty. The correct diagnosis isusually easy to establish and management is described in Appendix B.

Poisoning

There may be apparent breathing difficulties following the ingestion of a number ofpoisons.

The respiratory rate may be increased by poisoning with:

• Salicylates• Ethylene glycol (antifreeze)• Methanol• Cyanide

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But usually only poisoning with salicylates causes any diagnostic dilemma. Poisoningwith drugs that cause a depression of ventilation will present as a diminished consciouslevel. The management of the poisoned child is dealt with in Appendix H.

8.13 SUMMARY

You should use the structured approach in the assessment and management of thechild with breathing difficulties:


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CHAPTER

9The child in shock

LEARNING OBJECTIVES


• the causes of shock in infants and children• about the pathophysiology of shock• how to assess children with shock• how to resuscitate the child with life-threatening shock• the emergency treatment of the different causes of shock• the properties of different resuscitation fluids

9.1 INTRODUCTION

Shock results from an acute failure of circulatory function. This involves inadequateamounts of nutrients, especially oxygen, delivered to body tissues and inadequate removalof tissue waste products. Maintenance of adequate tissue perfusion depends on a pump(the heart) delivering the correct type and volume of fluid (blood) through controlledvessels (arteries, veins and capillaries) without abnormal obstruction to flow. Inadequatetissue perfusion resulting in impaired cellular respiration (ie shock) may result from de-fects of the pump (cardiogenic), loss of fluid (hypovolaemic), abnormalities of vessels(distributive), flow restriction (obstructive), or inadequate oxygen-releasing capacity ofblood (dissociative). As these functions involve several body systems, there are severalcauses of shock, and therefore the clinician must consider which of several alternativeemergency treatments will be effective for an individual patient.

9.2 CLASSIFICATION OF THE CAUSES OF SHOCK

The causes of shock are listed in the box, with the more common in bold. It can beseen that the most common causes in the paediatric patient are hypovolaemia from anycause, septicaemia and the effects of trauma.

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THE CHILD IN SHOCK

Cardiogenic • Arrhythmias (see Chapter 10)

• Cardiomyopathy

• Heart failure (see Chapter 8)

• Valvular disease

• Myocardial contusion (see Chapter 14)Hypovolaemic • Haemorrhage (see Chapter 13)

• Gastroenteritis (see Chapter 9)

• Intussusception (see Chapter 9)

• Volvulus (see Chapter 9)

• Burns (see Chapter 18)

• PeritonitisDistributive • Septicaemia (see Chapter 9)

• Anaphylaxis (see Chapter 9)

• Vasodilating drugs

• Spinal cord injury (see Chapter 17)Obstructive • Tension pneumothorax (see Chapter 14)

• Haemopneumothorax (see Chapter 14)

• Flail chest (see Chapter 14)

• Cardiac tamponade (see Chapter 14)

• Pulmonary embolismDissociative • Profound anaemia (see Chapter 9)

• Carbon monoxide poisoning (seeChapter 18)

• Methaemoglobinaemia

9.3 THE PATHOPHYSIOLOGY OF SHOCK

Shock results from an acute failure of circulatory function. Inadequate amounts ofnutrients, especially oxygen, are delivered to body tissues and there is inadequate removalof tissue waste products. Shock is a complex clinical syndrome that is the body’s responseto cellular metabolic deficiency.

In hypovolaemic or distributory shock the initial haemodynamic abnormality of fluidloss or fluid shift is followed by compensatory mechanisms under neuroendocrine control.Later, shock is worsened by the production of vasoactive mediators and the products ofcellular breakdown. The identity and relative importance of these chemicals are as yetpoorly understood.

Shock is a progressive syndrome but it can be divided into three phases: compensated,uncompensated and irreversible. Although artificial, this division is useful because eachphase has characteristic clinicopathological manifestations and outcome.

Phase 1 (compensated) shock

In this phase vital organ function (brain and heart) is conserved by sympathetic reflexeswhich increase systemic arterial resistance, divert blood away from non-essential tissues,constrict the venous reservoir and increase the heart rate to maintain cardiac output. Thesystolic blood pressure remains normal whereas the diastolic pressure may be elevateddue to increased systemic arterial resistance. Increased secretion of angiotensin and va-sopressin allows the kidneys to conserve water and salt, and intestinal fluid is reabsorbedfrom the digestive tract. The clinical signs that we see at this stage include mild agitation

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THE CHILD IN SHOCK

or confusion, skin pallor, increased heart rate and cold peripheral skin with decreasedcapillary return.

Phase 2 (uncompensated) shock

In uncompensated shock, the compensatory mechanisms start to fail and the circula-tory system is no longer efficient. Areas that have poor perfusion can no longer metaboliseaerobically, and anaerobic metabolism becomes their major source of energy production.Anaerobic metabolism is comparatively inefficient. Only 2 moles of adenosine triphos-phate (ATP) are produced for each mole of glucose metabolised compared with 38 molesof ATP per mole of glucose metabolised aerobically.

Anaerobic pathways produce excess lactate, leading to systemic acidosis. The acidosisis compounded by intracellular carbonic acid formed because of the inability of thecirculation to remove CO2. Acidosis reduces myocardial contractility and impairs theresponse to catecholamines.

A further result of anaerobic metabolism is the failure of the energy-dependent sodium–potassium pump, which maintains the normal homoeostatic environment in which thecell functions.

Lysosomal, mitochondrial and membrane functions deteriorate without this ho-moeostasis. Sluggish flow of blood and chemical changes in small vessels lead to plateletadhesion and may produce damaging chain reactions in the kinin and coagulation sys-tems, leading to a bleeding tendency.

Numerous chemical mediators have been identified in shocked patients, but the rolesof each have not been clearly identified. They include histamine, serotonin, cytokines(especially tumour necrosis factor and interleukin 1), xanthine oxidase (which generatesoxygen radicals), platelet-aggregating factor and bacterial toxins. They are largely pro-duced by cells of the immune system, especially monocytic macrophages. It has beensuggested that these mediators, which developed as initial adaptive responses to severeinjury and illness, may have deleterious consequences in the “unnatural” setting of theresuscitated patient. When the role of these chemical mediators is more fully understood,blocking agents may be produced, which will improve the treatment in phase 2 shock.

The result of these cascading metabolic changes is to reduce tissue perfusion andoxidation further. Blood pools in some areas because arterioles can no longer controlflow in the capillary system. Furthermore, abnormal capillary permeability allows furtherfluid loss from the circulation into the interstitium.

Clinically, the patient in phase 2 shock has a falling blood pressure, very slow capillaryreturn, tachycardia, cold peripheries, acidotic breathing, depressed cerebral state andabsent urine output.

Phase 3 (irreversible) shock

The diagnosis of irreversible shock is a retrospective one. The damage to key organssuch as the heart and brain is of such magnitude that death occurs despite adequaterestoration of the circulation. Pathophysiologically, the high-energy phosphate reservesin cells (especially those of the liver and heart) are greatly diminished. The ATP has beendegraded via adenosine to uric acid. New ATP is synthesised at only 2% an hour andthe body can be said to have run out of energy. This underlies the clinical observationthat during the progression of shock a point is reached at which death of the patient isinevitable, despite therapeutic intervention. Hence early recognition and effective treatmentof shock are vital.

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A closer study of septic shock illustrates the clinical patterns of these phases forshock.

Septic shock

In sepsis the cardiac output may be normal or raised but may still deliver insufficient oxygento the tissues. This is because abnormal distribution of blood in the microcirculation leadsto decreased tissue perfusion.

The release of bacterial toxins triggers complex interacting haemodynamic andmetabolic changes. Mediators and activators are released and react to produce the “septicsyndrome”. These activators may be vasodilators or vasoconstrictors; some promote andactivate the coagulation cascade; others are cardiac depressants.

In septic shock cardiac function may be depressed. Oxygen delivery to the heart from thecoronary arteries occurs mainly in diastole, and the tachycardia and increased oxygen de-mand of the myocardium in septic shock may jeopardise cardiac oxygenation. Metabolicacidosis also damages myocardial cells at the mitochondrial level. The function of the leftventricle is affected more than that of the right ventricle. This may be due to myocardialoedema, adrenogenic receptor dysfunction, or impaired sarcolemmal calcium influx. Theright ventricle is less important in maintaining cardiac output than the left, but increasedpulmonary vascular resistance can limit the hyperdynamic state and oxygen delivery.

In septic shock, cells do not use oxygen properly. There appears to be a block at the mito-chondrial level in the mechanism of oxygen uptake, and in progressive shock the differencebetween arterial and venous saturation levels of oxygen is inappropriately narrow. Thisprogressive deterioration in cell oxygen consumption heralds multiple organ failure.

Early (compensated) septic shockThis is characterised by a raised cardiac output, decreased systemic resistance, warm

extremities and a wide pulse pressure. This pattern is seen more typically in adults andmay never be seen in infants in whom cold peripheries are much more common. The hy-perdynamic state is recognised by hyperpyrexia, hyperventilation, tachycardia and mentalconfusion. All of these signs may be minimal: mental confusion in particular needs tobe looked for carefully, if septic shock is not to be overlooked at this stage. Decreasedcapillary return is a useful sign in these circumstances.

Late (uncompensated) septic shockIf no effective therapy is given, the cardiovascular performance deteriorates and cardiac

output diminishes. Even with a normal or raised cardiac output, shock develops. Thenormal relationship between cardiac output and systemic vascular resistance breaks downand hypotension may persist as a result of decreased vascular resistance.

The cardiac output may fall gradually over several hours, or precipitously in minutes.As tissue hypoxia develops, plasma lactic acid levels increase. Infants, who have littlecardiac reserve, often present with hypotension and a hypodynamic picture. These sickbabies are a diagnostic challenge but sepsis must be assumed and treated as quickly aspossible.

Survival in septic shock depends on the maintenance of a hyperdynamic state. Severalfactors mitigate against this by encouraging hypovolaemia:

1. Increased microvascular permeability2. Arteriolar and venous dilatation with peripheral pooling of blood3. Inadequate fluid intake4. Fluid loss secondary to fever, diarrhoea and vomiting5. Inappropriate polyuria

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9.4 APPROACH TO THE CHILD IN SHOCK

Children in shock are usually presented by parents who are aware that their child isworryingly ill even though they may not be able to express their concerns clearly. The childmay be presented primarily with a fever, a rash, with pallor, poor feeding, or drowsiness orwith a history of trauma or poisoning. The initial assessment will identify which patientsare in shock.

9.5 PRIMARY ASSESSMENT

This is dealt with in Chapter 7 “Structured Approach to the Seriously Ill Child”. Belowis a summary.

Airway

Assess vocalisations – crying or talking indicate ventilation and some degree of airwaypatency.



Reassess after any airway-opening manoeuvres. If there is still no evidence of air movementthen airway patency can be assessed by performing an opening manoeuvre and givingrescue breaths (see “Basic Life Support”, Chapter 4).

Breathing

Effort of breathingrespiratory raterecession stridorwheeze gruntingaccessory muscle use flaring of the alae nasigasping

ExceptionsIncreased effort of breathing DOES NOT occur in three circumstances:

– exhaustion– central respiratory depression– neuromuscular disease



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Features suggesting a cardiac causeof circulatory inadequacy

• Cyanosis, not correcting withoxygen therapy

• Tachycardia out of proportionto respiratory difficulty

• Raised jugular venous pressure• Gallop rhythm• Murmur• Enlarged liver• Absent femoral pulses

Circulation

Heart ratePulse volumeBlood pressureCapillary refill timeSkin temperature and colourEffects on breathing and mental status

Monitor heart rate/rhythm, blood pressureand core–toe temperature difference. If heartrate is above 200 in an infant or above 150 ina child, or if the rhythm is abnormal perform astandard ECG.

Disability

Mental status/conscious level (AVPU)Pupillary size and reactionPosture, children in shock are usually hypotonicNote: In meningococcal disease there may be signs of abnormal neurological function

from both the underlying shock and a meningitic element of the illness.

Exposure

Rash: This is often a key clinical indicator for the cause of shock (see Sections 9.9 and9.10).

Fever: suggests an infective cause.Consider evidence for poisoning.

9.6 RESUSCITATION

Airway

• Use an opening manoeuvre, if not patent, or partially obstructed. If there is improve-ment, use airway adjuncts to support the airway.

• Suction• The airway may need to be secured by intubation.

Breathing

• All children in shock should receive high-flow oxygen through a face mask with areservoir as soon as the airway has been demonstrated to be adequate.

• If the child is hypoventilating, respiration should be supported with oxygen via abag–valve–mask device and experienced, senior help summoned.

Circulation

• Gain intravenous or intra-osseous access:

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❝ Use a short, wide-bore IV cannula if possible.❝ Try to obtain two vascular access sites to give large volumes quickly and in case one

line is lost.❝ Femoral vein access is a good option if peripheral or intraosseous access is impos-

sible. Long saphenous vein cut down may also be considered.❝ Ideally do not use upper central venous lines initially – there is a risk of pneumoth-

orax, or exacerbation of an unsuspected neck injury.❝ Techniques for vascular access are described in Chapter 21.

• Take blood for FBC, U&Es, renal and liver function, blood culture, cross-match,coagulation studies, glucose stick test and laboratory test.

• Give 20-ml/kg rapid bolus of crystalloid to all patients except to those with signs ofheart failure as their primary pathology. Apart from septic shock, it is uncommonto need more than one or two 20-ml/kg fluid boluses for resuscitation – too muchfluid too quickly may cause cerebral oedema. In septic shock the first bolus of fluidmay be given as 4·5% human albumin if shock is severe. But extreme caution, withfrequent re-assessment, is required in giving IV fluid boluses in patients who mayhave cerebral oedema or cardiogenic shock.

• Give an antibiotic such as cefotaxime 80 mg/kg for those with an obvious or suspecteddiagnosis of septicaemia, eg in the presence of a purpuric rash.❝ In paediatric practice, septicaemia is the commonest cause of a child presenting in

shock. So unless an alternative diagnosis is very clear (such as trauma, anaphylaxisor poisoning), an antibiotic is given as soon as a blood culture has been taken.

❝ A third-generation cephalosporin, such as cefotaxime or ceftriaxone, is usually used,but an anti-staphylococcal antibiotic (flucloxacillin or vancomycin) should be con-sidered in possible toxic shock syndrome i.e. post burns/cellulitis.

• If a tachyarrhythmia is identified as the cause of shock, up to three synchronouselectrical shocks at 0·5, 1·0 and 2·0 J/kg should be given. (see Chapter 10)❝ If the arrhythmia is broad-complex and the synchronous shocks are not activated

by the defibrillator then attempt an asynchronous shock.❝ A conscious child should be anaesthetised first if this can be done in a timely

manner.❝ If the shocked child’s tachyarrhythmia is SVT then this can be treated with intra-

venous/intraosseous adenosine, as this can often be administered more quickly thana synchronous electrical shock.

If anaphylaxis is obvious give adrenaline (epinephrine) 10 micrograms/kg IM.

Disability

If there is coexistent evidence of raised intracranial pressure, manage as in Chapter 11.

“Don’t ever forget glucose” (DEFG)

Hypoglycaemia may give a similar clinical picture to that of compensated shock. Thismust always be excluded by urgent glucose stick test and blood glucose estimation.Shock and hypoglycaemia may coexist as the sick infant or small child has poor glucose-producing reserves.

9.7 KEY FEATURES OF THE CHILD IN SHOCK

While the primary assessment and resuscitation are being carried out, a focused historyof the child’s health and activity over the previous 24 hours and any significant previous

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illness should be gained. Certain key features which will be identified from this – andthe initial blood test results – can point the clinician to the likeliest working diagnosis foremergency treatment.

A history of vomiting and/or diarrhoea points to fluid loss ei-ther externally (e.g. gastroenteritis) or into the abdomen (e.g.volvulus, intussusception).

see Section 9.8

The presence of fever and/or a rash points to septicaemia. see Section 9.9The presence of urticaria, angio-neurotic oedema or history of

allergen exposure points to anaphylaxis.see Section 9.10

The presence of cyanosis unresponsive to oxygen or a greycolour with signs of heart failure in a baby under 4 weekspoints to duct-dependent congenital heart disease.

see Section 9.11

The presence of heart failure in an older infant or child pointsto cardiomyopathy.

see Section 9.12

A history of sickle cell disease or a recent diarrhoeal illness anda very low haemoglobin points to acute haemolysis.

see Section 9.13and 9.14

An immediate history of major trauma points to blood lossand, more rarely, tension pneumothorax, haemothorax, cardiactamponade or spinal cord transection. A history of sickle celldisease, abdominal pain and enlarged spleen points to acutesplenic sequestration.

see Part IVsee Section 9.14

The presence of severe tachycardia and an abnormal rhythmon the ECG points to an arrhythmia.

See Chapter 10

A history of polyuria and the presence of acidotic breathing anda very high blood glucose points to diabetes.

See Appendix B

A history of drug ingestion points to poisoning. See Appendix H

9.8 APPROACH TO THE CHILD WITH FLUID LOSS

Infants are more likely than older children to present with shock due to sudden fluid lossin gastroenteritis or with concealed fluid loss secondary to a “surgical abdomen” suchas a volvulus. This is due both to the infant’s low physiological reserve and increasedsusceptibility to these conditions.

In infants, gastroenteritis may occasionally present as a circulatory collapse with littleor no significant preceding history of vomiting or diarrhoea. The infecting organismcan be any of the usual diarrhoeal pathogens, of which viruses are the most common indeveloped countries. The mechanism leading to this presentation is that there is a suddenmassive loss of fluid from the bowel wall into the gut lumen, causing depletion of theintravascular volume and the appearance of shock in the infant. This occurs before thestool is passed so that the diagnosis may be unsuspected. Usually during resuscitation ofthese infants, copious watery diarrhoea is evacuated.

Having completed the primary assessment and resuscitation and identified by meansof the key features that fluid loss is the most likely diagnosis, the child is reassessed toidentify the response to the first fluid bolus.

Emergency treatment of fluid loss

Reassess ABC

• The child has had one fluid bolus of 20 ml/kg IV.• If signs of shock persist after the first bolus, give a second fluid bolus of crystalloid

or colloid:

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❝ In gastroenteritis, one to two boluses usually restore circulating volume.❝ In gastroenteritis initiate enteral or gastric tube oral rehydration solution (see Ap-

pendix B).• Check acid–base status and electrolytes

585

❝ Acidosis will usually be corrected by treatment of shock.❝ Sodium imbalance may occur, and this may cause convulsions (see

Appendix B).• Consider diagnostic possibilities:

❝ Abdominal X-ray or ultrasound scan to detect distended bowel, intra-abdominalair or fluid.

❝ Consider urgent surgical referral especially if bile-stained vomiting or abdominalguarding is present.

❝ Consider sepsis (secondarily to the surgical abdomen) and give appropriate IVantibiotics.

• Consider intubation and ventilation, particularly if more than two boluses of fluid arerequired.

• Consider third fluid bolus if still shocked; at this stage, colloid (human albumin) iscommonly used.

• Consider the need for inotropes and monitoring of central venous pressure – thesewill usually be essential if a third fluid bolus is given.

• The child should be catheterised in order to assess accurately the urinary output.

9.9 APPROACH TO THE CHILD WITH SEPTICAEMIA

The commonest cause of septicaemia in infants and children is meningococcal, butother causes include Group B streptococcal in young infants, Gram-negative sepsis inrelation to underlying urinary tract or gut problems and group A streptococcal sepsis.

The cardinal sign of meningococcal septicaemia is a purpuric rash in an ill child. Atthe onset, however, the rash is not florid and a careful search should be made for pur-pura in any unwell child. In about 15% of patients with meningococcal septicaemia, ablanching erythematous rash replaces or precedes a purpuric one, and in 7% of casesno rash occurs. In the rarer toxic shock syndrome, the initial clinical picture includesa high fever, headache, confusion, conjunctival and mucosal hyperaemia, scarlatini-form rash with secondary desquamation, subcutaneous oedema, vomiting and waterydiarrhoea. Early administration of antibiotics, concurrent with initial resuscitation, isvital.

In countries where the vaccine against Meningococcus C has been introduced, there hasbeen a fall in the number of cases of infection.

Having completed the primary assessment and resuscitation and identified by meansof the key features that septicaemia is the most likely diagnosis, the child is reassessed.

Emergency treatment of septicaemia

Reassess ABC

• Give fluid bolus(es)❝ The initial bolus can be 20 ml/kg of 0·9% saline or 4·5% human albumin. Subse-

quent boluses are 4·5% human albumin.❝ Children often require several boluses of fluid to achieve relative stability (up to

200 ml/kg in the first 24 hours has been used to treat severe shock, i.e. 2·5 timesthe blood volume).

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❝ After 40 ml/kg it is necessary to consider inotropes and ideal to monitor CVP.❝ Central venous access will be valuable, particularly in shock needing ≥40 ml/kg. It

should ideally be achieved using a multi-lumen catheter coated with heparin andplaced in the intra-thoracic IVC or SVC. The femoral approach can be used. Anormal CVP is +4 to +10 cmH2O, and optimising CVP can improve cardiacoutput with less risk of inducing heart failure. Take great care if CVP > 12 cmH2Osince cardiac failure may be induced by excessive IV fluids, especially if severeanaemia, malnutrition or a primary cardiac disorder is present. Inotropic supportwill be required.

• Ensure that an antibiotic such as cefotaxime or ceftriaxone has been given.• Consider intubation by rapid sequence induction of anaesthesia and provide assisted

ventilation:❝ Consider after two to three 20-ml/kg boluses of fluid have been given.❝ Positive pressure ventilation can improve oxygenation, and prevents/treats pul-

monary oedema. It can improve cardiac output.❝ All intubated children must have continuous Sa2 and capnography and blood gas

monitoring.• Consider an intravenous infusion of dobutamine and/or dopamine:

❝ These are considered if a third bolus of fluid is required. Start at a dose of 10 mi-crograms/kg/min and increase to 20 micrograms/kg/min if there is a poor response.

❝ These infusions can initially be given through a peripheral vein until central venousaccess is obtained. Do not hesitate to increase the infusion rapidly in the face of apoor response.

❝ Sometimes adrenaline (epinephrine) by IV infusion at 0·05–2 micrograms/kg/minmay be required if there is no response to other inotropes. Ideally, this should begiven centrally but do not hesitate to infuse adrenaline peripherally if no otheraccess is immediately available.

❝ In severe, refractory shock, whilst infusions are being prepared, an arrest dose ofadrenaline (epinephrine) can be drawn up in 50 ml of 0·9% saline and infusedslowly to reverse hypotension.

• Patients who require ventilation and inotropic support should be cared for in a pae-diatric intensive care unit with invasive monitoring. Seek early advice.

Further investigations

In addition to the blood tests taken during resuscitation, the following blood testsare needed in the septic child: calcium, magnesium, phosphate, coagulation screen andarterial blood gas. Electrolyte and acid–base derangements can have a deleterious effecton myocardial function. They should be sought and corrected.

Table 9.1. Corrective measures for electrolyte and acid–base derangements

Result Treat if less than Correct with

Glucose 3 mmol/l 5 ml/kg 10% dextroseAcid–base 7·2 1 mmol/kg NaHCO3 over 20 min of ventilationPotassium 3·5 mmol/l 0·25 mmol/kg KCl over 30 min: ECG monitoringCalcium 2 mmol/l 0·3 ml/kg 10% Ca gluconate over 30 min (max 20 ml)Magnesium 0·75 mmol/l 0·2 ml/kg 50% MgSO4 over 30 min (max 10 ml)

It is difficult to manage a patient so seriously ill as to require ventilation and inotropicsupport without intensive care facilities and invasive monitoring. If these treatments are

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required, a paediatric intensive care unit must be involved early to give advice and toretrieve the patient.

Reassess disability

Meningitis may accompany meningococcal septicaemia. Assess neurological status(conscious level, using the Glasgow Coma Score, pupillary size and reaction, and pos-ture, using a painful stimulus to demonstrate its presence), particularly looking for raisedintracranial pressure. If, despite effective treatment of shock, there is decreasing con-scious level or abnormal posturing or focal neurological signs, treat for raised intracranialpressure.

Emergency treatment of disability in shock

• Intubate using rapid sequence induction.• Monitor CO2 levels by capnography and keep in a normal range (4–5 kPa).• If there are signs of raised intracranial pressure, relatively slow pulse, raised BP

and localising signs such as abnormal pupillary reactions, give intravenous mannitol250 mg/kg IV over 20 minutes followed by 1mg/kg furosemide (frusemide) IV andrepeat as required.

• Insert a urinary catheter once the child is sedated, and monitor output.• Nurse the child with 30◦ head elevation and midline position.• Maintenance of a normal blood pressure to ensure an adequate cerebral perfusion

pressure is mandatory. Treatment of the shocked state takes priority. An adequateblood pressure is necessary to perfuse a swollen brain.

• Lumbar puncture must be avoided as its performance may cause death throughconing of the brain through the foramen magnum.

Paediatric intensive care skills and monitoring is paramount in these patients. Seek adviceearly.

9.10 APPROACH TO THE CHILD WITH ANAPHYLAXIS

Anaphylaxis is a potentially life-threatening syndrome, which may progress to shock,upper or lower airway obstruction, or all three. It is immunologically mediated, with themost common causes including allergy to penicillin, to radiographic contrast media, andto certain foods, especially nuts.

Prodromal symptoms of flushing, itching, facial swelling, urticaria, abdominal pain,diarrhoea, wheeze and stridor may precede shock or may be the only manifestationsof anaphylaxis. The presence of these additional symptoms confirms anaphylaxis as thecause of shock in a child. Most patients will have a history of previous attacks, and somemay have a “medic-alert” bracelet.

Anaphylaxis can be life-threatening because of the rapid onset of airwaycompromise due to laryngeal oedema, breathing difficulties due to suddensevere broncho-constriction and/or the development of shock due to acutevasodilatation and fluid loss from the intravascular space caused by increasedcapillary permeability.

Key points in the history may point to a severe reaction. These are shownin the box.

549334

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Previous severe reactionHistory of increasingly severe reactionHistory of asthmaTreatment with β-blockers

Symptoms and signs vary according to the body’s response to the allergen. These areshown in Table 9.2.

Table 9.2. Symptoms and signs in allergic reaction

Symptoms Signs

Mild Burning sensation in mouth Urticarial rashItching of lips, mouth, throat Angio-oedemaFeeling of warmth ConjunctivitisNauseaAbdominal pain

Moderate (Mild +) Coughing/wheezing BronchospasmLoose bowel motions TachycardiaSweating PallorIrritability

Severe (Moderate +) Difficulty breathing Severe bronchospasmCollapse Laryngeal oedemaVomiting ShockUncontrolled defecation Respiratory arrest

Cardiac arrest

Emergency treatment of anaphylaxis

The management of anaphylactic shock requires good airway management, adminis-tration of adrenaline (epinephrine) and aggressive fluid resuscitation.

Note that the intramuscular route is the preferred route for the delivery of adrenaline(epinephrine). Intravenous adrenaline (epinephrine) should be reserved for children withlife-threatening shock for whom intramuscular injection has been ineffective. The patientmust be carefully monitored.

Having completed the primary assessment and resuscitation and identified by meansof the key features that anaphylaxis is the most likely diagnosis, the child is reassessed.

Further emergency management of anaphylaxis

For severe shock, and shock resistant to treatment, continue with boluses of colloidand ventilatory support and give further doses of adrenaline (epinephrine) intramuscu-larly every 5 minutes if the symptoms are not reversed. Additional inotropes will not beneeded because the adrenaline (epinephrine) used for the treatment of anaphylaxis is apowerful inotrope. However, in the face of shock resistant to intramuscular adrenaline(epinephrine) and one or two boluses of fluid, an infusion of intravenous adrenaline(epinephrine) may be life-saving. The dose is 0·1–5·0 micrograms/kg/min and the pa-tient should be closely monitored for pulse and blood pressure.

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Figure 9.1. Emergency treatment of anaphylaxis

In addition to the above treatment it is also customary to give patients with anaphy-laxis an antihistamine and steroids. There is no evidence of the part these drugs play inmanagement, and their onset of action is too delayed to be of much benefit in the firsthour.

Drug doses in anaphylaxis

Adrenaline (epinephrine) 10 µg/kg 1MChlorphenamine (chlorpheniramine)>12 years 10–20 mg6–12 years 5–10 mg1–5 years 2·5–5 mg1 month–1 year 250 µg/kgDo not use in neonatesHydrocortisone 4 mg/kg

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9.11 APPROACH TO THE INFANT WITH ADUCT-DEPENDENT CONGENITAL HEART DISEASE

Infants with critical pulmonary obstructive lesions present in the first few days of lifewith increasing cyanosis, breathlessness or cardiogenic shock. On examination there maybe a characteristic murmur but more frequently there is no murmur audible. An enlargedliver is a common finding.

Babies with critical systemic obstructive lesions also present in the first few days of lifewith inability to feed, breathlessness, a grey appearance and collapse with poor peripheralcirculation. On examination the babies are in heart failure and in more severe cases incardiogenic shock. In this situation, even in coarctation of the aorta, all pulses are difficultto feel.

The clinical situation has arisen from the gradual closure of the arterial duct, on whicha functioning circulation depends in these congenital heart anomalies. Complete closurewill result in the death of the infant.

Having completed the primary assessment and resuscitation and identified by means ofthe key features that duct-dependent congenital heart disease is the most likely diagnosis,the child is reassessed.

9.12 EMERGENCY TREATMENT OF DUCT-DEPENDENTCONGENITAL HEART DISEASE

Reassess ABC

• Oxygen therapy will usually have little beneficial effect, and may accelerate ductclosure. Do not use high-flow oxygen, but a flow that causes an increase in Sa2, andno higher.

• Give an intravenous infusion of prostaglandin E2:❝ Initial dose of 3–5 nanograms/kg/min (may be increased to 10–20 nanograms/

kg/min in 5-nanograms/kg/min increments until side effects).❝ This will keep the arterial duct patent.❝ This commonly causes apnoea, so intubate and ventilate.

• Investigations:❝ Chest X-ray❝ ECG❝ Full blood count❝ Arterial blood gases❝ Urea and electrolytes, and calcium❝ Glucose❝ Blood cultures

• Discuss with and transfer to a neonatal cardiology unit.

9.13 APPROACH TO THE CHILD WITH CARDIOMYOPATHY

Cardiomyopathy/myocarditis is most uncommon, but may rarely be found in an infantor child presenting in shock and with signs of heart failure but with no history of congenitalheart disease.

If such a patient were in the first few weeks of life, a trial of alprostadil would beappropriate and harmless.

Having completed the primary assessment and resuscitation and having identified bymeans of the key features that cardiomyopathy/myocarditis is the most likely diagnosis,the child is reassessed.

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Emergency treatment of cardiomyopathy

Reassess ABC

• Give high concentration oxygen.• Give a diuretic, such as furosemide (frusemide) 1 mg/kg IV, and repeat if required.• Start an intravenous infusion of dobutamine 10 micrograms/kg/min.• Investigations

❝ Chest X-ray❝ ECG❝ Full blood count❝ Arterial blood gases❝ Urea and electrolytes, and calcium❝ Glucose❝ Blood cultures

• Urgent cardiology advice should be sought. Echocardiography should establish thediagnosis in almost all cases.

9.14 APPROACH TO THE CHILD WITHPROFOUND ANAEMIA

Severe anaemia exists if the haemoglobin level is less than 50 g/l. If acute haemolysisis the cause of the anaemia, the urine will usually be dark brown in colour, the child willbe weak, with palms and soles near white, and there may be signs of heart failure. Themost usual situation in which a child develops sudden severe haemolysis is in the case ofsepticaemia associated with sickle cell disease. In children returning from endemic areas,severe malaria may present with severe anaemia, with or without haemolysis.

Emergency treatment of profound anaemia

• Transfusion should in general be considered when the Hb is less than 50 g/l.• The presence of heart failure affects the decision to transfuse, diuretics will be re-

quired or an exchange transfusion may be safer.• Over-hydration may exacerbate or lead to cardiogenic shock and pulmonary oedema.• Treatment may also be required as for sepsis with volume support, intubation and

inotropes.• Fresh blood should be used, where possible.• These children will all need early paediatric intensive care advice and transfer.

9.15 APPROACH TO THE CHILD WITH SICKLECELL CRISIS

Sickle cell disease is characterised by episodic clinical events called “crises”. Vaso-occlusive crisis is the most common and occurs when abnormal red cells clog smallvessels causing tissue ischaemia. The other crises are acute chest syndrome, sequestra-tion crisis (severe anaemia and hypotension, resulting from pooling of blood in the spleenand liver), aplastic crisis and hyper-haemolytic crisis. Factors that precipitate or modu-late the occurrence of sickle cell crisis are not fully understood, but infections, hypoxia,dehydration, acidosis, stress and cold are believed to play some role.

Oxygen therapy, rehydration, antibiotics and analgesia are considered standard treat-ment in sickle cell crises. Parenteral morphine is also considered essential for relievingpain in severe vaso-occlusive crises and acute chest syndrome.

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9.16 AFTER RESUSCITATION AND EMERGENCYTREATMENT OF SHOCK

Following successful restoration of adequate circulation, varying degrees of organ dam-age may remain, and should be actively sought and managed. The problems are similarbut of a lesser degree than those expected following resuscitation from cardiac arrest.Thus after the initial resuscitation and emergency treatment, the patient should have areview of ABC, as well as a full systems review to ensure stabilisation for safe and effectivetransfer (see Chapter 24).

9.17 USE OF FLUIDS IN RESUSCITATION

Which fluid? Crystalloid or colloid fluids are available for volume replacement. Dextroseinfusions do not constitute appropriate fluid resuscitation and can be dangerous by,for example, lowering serum sodium and producing seizures. For further details of thecomposition of different fluids, see Appendix B.

Compared with colloids, crystalloid fluids:

• diffuse more readily into the interstitial space;• may be associated with more peripheral oedema;• where capillary leak exists, allow more water to enter the interstitial space, because

of a lower osmotic pressure;• need 2–3 times the volume of colloids to expand the vascular space and• have been reported to be associated with lower mortality (however this is unproven

for shock in many childhood conditions).

There has been a long-standing debate about whether crystalloid or colloid should beused in resuscitation. No definitive answer can be given. Where small volumes of fluid areused it may not matter. When larger volumes of fluid are used it must be more important.

In acute collapse, a smaller volume of colloid is needed than crystalloid to produce agiven increase in intravascular volume, and so a more rapid correction of haemodynamicderangement may be possible with colloid if it is readily available.

When larger volumes of fluid are used, the choice of fluid becomes more important.As the circulating volume of a child is approximately 80 ml/kg, if more than 40 ml/kg offluid is used over a short time, one half of the child’s circulating volume will have beengiven. If much more fluid transfusion is needed, significant haemodilution may result, andconsideration should be given to using blood for fluid resuscitation with measurements ofthe central venous pressure (effectively cardiac preload) to guide fluid resuscitation andthe haematocrit to guide the need for blood transfusion. Where large volumes are used,human albumin solution is generally preferred in paediatric practice, although most adultpatients are resuscitated with synthetic colloids, crystalloid or hypertonic solutions.

If blood is needed, a full cross-match is to be undertaken, which takes about 1 hour toperform. For urgent need, type-specific non–cross-matched blood (which is ABO rhesuscompatible but has a higher incidence of transfusion reactions) takes about 15 minutesto prepare. In dire emergencies O-negative blood must be given.

How much? The volume of fluid needed will depend on clinical assessment. However,the clinical situation may dictate the rapidity with which repeat boluses are given. Forexample, in a retrospective review of children with septic shock, early administration oflarge volumes of fluid (>40 ml/kg in the first hour) was associated with better outcomethan smaller-volume resuscitation, encouraging a vigorous approach in septicaemia. Incontrast, where shock is caused by penetrating trauma requiring definitive surgical man-agement, maximal fluid resuscitation may be best delayed until operation, as improvingperfusion without improving oxygen-carrying capacity as well results in a worse outcome.

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THE CHILD IN SHOCK

If large volumes are needed, resuscitation is best guided by measurement of cardiacfilling pressures, and therefore patients requiring large-volume resuscitation need promptpaediatric intensive care advice and timely transfer. When large volumes are used, fluidsshould be warmed. In the absence of specific fluid warmers, bags of fluid/blood can bewarmed by placing them in warm water, or under the clothes of the mother next to herskin.

In conclusion, there is no definitive evidence demonstrating which fluid is best for re-suscitation. Other important questions – how much and when should fluids be used alsoremain to be answered. Clinical trials will be needed to answer these questions, thoughthey are likely to be difficult to perform. Whilst awaiting more clinical trials, fluid resus-citation guided by knowledge of the pathophysiology underlying the disease, and of thedifferent roles of the different fluids, will remain optimal management.

9.18 SUMMARY

You should use the structured approach in the assessment and management of thechild with shock:


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114



CHAPTER

10The child with an abnormal pulse

rate or rhythm

LEARNING OBJECTIVES


• how to assess children with an abnormal pulse rate or rhythm• how to resuscitate the child with life-threatening brady- or tachyarrhythmia

10.1 INTRODUCTION

In tachyarrhythmias in children, the rate is fast but the rhythm largely regular. Causesinclude:

• Re-entrant congenital conduction pathway abnormality (common)• Poisoning• Metabolic disturbance• After cardiac surgery• Cardiomyopathy• Long QT syndrome (rare)

In bradyarrhythmias in children the rate is slow and the rhythm usually irregular.Causes include:

• Pre-terminal event in hypoxia or shock• Raised intracranial pressure• After conduction pathway damage during cardiac surgery• Congenital heart block (rare)• Long QT syndrome (rare)

Presentations include:

• History of palpitations (verbal child)• Poor feeding (preverbal child)• Heart failure or shock

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THE CHILD WITH AN ABNORMAL PULSE RATE OR RHYTHM


This is dealt with in Chapter 7 “Structured Approach to the Seriously Ill Child”. Belowis a summary.

Airway




Reassess after any airway-opening manoeuvres. If there continues to be no evidence of airmovement then airway patency can be assessed by performing an opening manoeuvreand giving rescue breaths (see “Basic Life Support”, Chapter 4).

Breathing

Effort of breathingrespiratory raterecession stridorwheeze gruntingaccessory muscle use flaring of alae nasigasping




chest expansion/abdominal excursionbreath sounds – reduced or absent, and symmetry on auscultationSa2 in air

Effects of respiratory failure on other physiology

heart rateskin colourmental status

Circulation

Heart rate – This is the defining observation for this presentation. An abnormal pulserate is defined as one falling outside the normal range given in Chapter 2. In prac-tice, most serious disease or injury states are associated with a sinus tachycardia. In

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infants this may be as high as up to 220 beats per minute (bpm) and in children up to180 bpm. Rates over these figures are highly likely to be tachyarrhythmias, but in anycase of significant tachycardia, i.e. 200 in an infant and 150 in a child, an ECG rhythmstrip should be examined and, if in doubt, a full 12-lead ECG performed. Very high ratesmay be impossible to count manually and the pulse oximeter is often unreliable in thisregard. Again a rhythm strip is advised.

An abnormally slow pulse rate is defined as less than 60 bpm or a rapidly falling heartrate associated with poor systemic perfusion. This will almost always be in a child whorequires major resuscitation.

Features suggesting cardiac cause ofrespiratory inadequacy

• Cyanosis, not correcting withoxygen therapy

• Tachycardia out of proportionto respiratory difficulty

• Raised jugular venous pressure• Gallop rhythm/murmur• Enlarged liver• Absent femoral pulses

Pulse volumeCapillary refillSkin temperature

Disability

Mental status/conscious levelPosturePupils

Exposure – rash or fever

10.3 RESUSCITATION

Airway

If the airway is not open, use:

• an airway-opening manoeuvre,• an airway adjunct or• urgent induction of anaesthesia followed by intubation to secure the airway.

Breathing

• Give high-flow oxygen through a face mask with a reservoir as soon as the airway hasbeen shown to be adequate.

• If the child is hypoventilating or has bradycardia, respiration should be supportedwith oxygen via a bag–valve–mask device and consideration given to intubation andventilation.

Circulation

If there is shock and

• the heart rate <60/min, start chest compressions.• the ECG shows ventricular tachycardia, give up to three synchronous electrical shocks

at 0.5, 1 and 2 J/kg.– The child who is responsive to pain should be anaesthetised or sedated first– If the synchronous shocks for VT are ineffectual (because the defibrillator cannot

recognise the abnormally shaped QRS complex), then the shocks may have to begiven asynchronously – recognising that this is a more risky procedure – becausewithout conversion the rhythm may deteriorate to VF and asystole.

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– Synchronisation relies on the ability of the defibrillator to recognise the QRSTcomplex, and is designed to avoid shock delivery at a point in the cardiac cyclelikely to precipitate ventricular fibrillation.

• Gain intravenous or intraosseous access.• If the tachyarrhythmia is SVT then give intravenous/intraosseous adenosine (see for-

mulary for more on adenosine) 50 micrograms/kg to a maximum of 3 mg if this canbe administered more quickly than a synchronous electrical shock.

• Take blood for FBC, renal function, glucose stick test and glucose laboratory test.• Give a bolus of 20 ml/kg IV of crystalloid to a patient with bradycardia who is in shock.

While the primary assessment and resuscitation are being carried out, a focused historyof the child’s health and activity over the previous 24 hours should be gained. Certain keyfeatures which will be identified clinically in the primary assessment, from the focusedhistory, from the initial blood tests and from the rhythm strip and 12-lead ECG can pointthe clinician to the likeliest working diagnosis for emergency treatment.

From the ECG the arrhythmia can be categorised by the following simple questions:1. Is the rate

too fast?too slow?

2. Is the rhythmregular?irregular?

3. Are the QRS complexesnarrow?broad?

❝ Bradycardia

– is usually a pre-terminal rhythm. It is seen as the final response to profoundhypoxia and ischaemia and its presence is ominous.

– is precipitated by vagal stimulation as occurs in tracheal intubation and suctioningand may be found in post-operative cardiac patients. The rhythm is usually irreg-ular.

– may be seen in patients with raised intracranial pressure. These patients will havepresented with coma and their management can be found in Chapters 11 and 16.

– can be a side effect of poisoning with digoxin or beta-blockers and the managementcan be found in Appendix H.

❝ Tachyarrhythmia

– with a narrow QRS complex on the ECG is supra-ventricular tachycardia. Therhythm is usually regular.

– with a wide QRS complex on the ECG is ventricular tachycardia; this can beprovoked by– hyperkalaemia.– poisoning with tricyclic antidepressants, or a combination of cisapride and

macrolide antibiotics. Additional details on the management of the poisonedchild with ventricular tachycardia can be found in Appendix H.

10.4 APPROACH TO THE CHILD WITH BRADYCARDIA

In paediatric practice bradycardia is almost always a pre-terminal finding in pa-tients with respiratory or circulatory insufficiency. Airway, breathing and circulationshould always be assessed and treated if needed before pharmacological management ofbradycardia.

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Emergency Treatment of Bradycardia

Reassess ABC

• If there is hypoxia and shock, treat with– high concentration of oxygen, bag–mask ventilation, intubation and IPPV;– volume expansion (20 ml/kg of 0.9% saline repeated as recommended in the treat-

ment of shock);– if the above is ineffective give a bolus of adrenaline (epinephrine) 10 micrograms/kg

IV and– if the above is ineffective try an infusion of adrenaline (epinephrine) 0.05 to

2 micrograms/kg/min IV.• If there has been vagal stimulation, treat with

– adequate ventilation;– atropine 20 micrograms/kg IV/IO (minimum dose 100 micrograms; maximum dose

600µg)– the dose may be repeated in 5 minutes (maximum total dose of 1·0 mg in a child

and 2·0 mg in an adolescent) and– if IV/IO access is unavailable, atropine (0·04 mg/kg) may be administered tracheally,

although absorption into the circulation may be unreliable.• If there has been poisoning, seek expert toxicology help.

10.5 APPROACH TO THE CHILD WITHSUPRAVENTRICULAR TACHYCARDIA

Supraventricular tachycardia (SVT) is the most common non-arrest arrhythmia duringchildhood and is the most common arrhythmia that produces cardiovascular instabilityduring infancy. SVT in infants generally produces a heart rate >220 bpm, and often250–300 bpm. Lower heart rates occur in children during SVT. The QRS complex isnarrow, making differentiation between marked sinus tachycardia due to shock and SVTdifficult, particularly because SVT may also be associated with poor systemic perfusion.

The following characteristics may help to distinguish between sinus tachycardia andSVT:

1. Sinus tachycardia is typically characterised by a heart rate less than 200 bpm ininfants and children whereas infants with SVT typically have a heart rate greater than220 bpm.

2. P-waves may be difficult to identify in both sinus tachycardia and SVT once theventricular rate exceeds 200 bpm. If P-waves are identifiable, they are usually uprightin leads I and AVF in sinus tachycardia while they are negative in leads II, III andAVF in SVT.

3. In sinus tachycardia, the heart rate varies from beat to beat and is often responsiveto stimulation, but there is no beat-to-beat variability in SVT.

4. Termination of SVT is abrupt whereas the heart rate slows gradually in sinus tachy-cardia in response to treatment.

5. A history consistent with shock (e.g. gastroenteritis or septicaemia) is usually presentwith sinus tachycardia.

Cardiopulmonary stability during episodes of SVT is affected by the child’s age, du-ration of SVT and prior ventricular function and ventricular rate. Older children usuallycomplain of lightheadedness, dizziness or chest discomfort or they note the fast heartrate, but very rapid rates may be undetected for long periods in young infants until theydevelop a low cardiac output state and shock. This deterioration in cardiac function

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occurs because of increased myocardial oxygen demand and limitation in myocardialoxygen delivery during the short diastolic phase associated with very rapid heart rates.If baseline myocardial function is impaired (e.g. in a child with a cardiomyopathy), SVTcan produce signs of shock in a relatively short time.

Figure 10.1. Sinus tachycardia

Figure 10.2. Supraventricular tachycardia

Emergency Treatment of Supraventricular Tachycardia

Reassess ABC

• Try vagal stimulation while continuing ECG monitoring. The following techniquescan be used:– Elicit the “diving reflex”, which produces an increase in vagal tone, slows atri-

oventricular conduction and interrupts the tachycardia. This can be done by theapplication of a rubber glove filled with iced water over the face, or if this is inef-fectual, wrapping the infant in a towel, and immersing the face in iced water for5 seconds.

– One-sided carotid body massage.– Older children can try a Valsalva manoeuvre. Some children know that a certain

position or action will usually effect a return to sinus rhythm. Blowing hard througha straw may be effective for some children.

• Do not use ocular pressure in an infant or child, because ocular damage may result.• If these manoeuvres are unsuccessful, give:

Intravenous adenosine: Start with a bolus dose of 50 micrograms/kg intravenously andincrease the dose to 100 micrograms/kg after 2 minutes if success is not achieved. Thenext dose should be 250 micrograms/kg. The maximum total dose that should be given

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is 500 micrograms/kg (300 micrograms/kg under 1 month) up to a maximum of 12 mg.Adenosine is a very rapidly acting drug with a half-life of less than 10 seconds. Thismeans that side effects (flushing, nausea, dyspnoea, chest tightness) are short-lived. It alsomeans, however, that the effect may be short-lasting and the supraventricular tachycardiamay recur.

Owing to the same reason, if the drug is given through a small peripheral vein, aninsufficiently high concentration may reach the heart and therefore a larger dose mayneed to be given. Preferably, the drug should be injected into a large peripheral vein andrapidly followed by a saline flush. Adenosine is the drug of choice for supraventriculartachycardia because of its efficacy and safety record.

If the stable supraventricular tachycardia of a child has not been converted to a nor-mal rhythm with intravenous adenosine, it is essential to seek the advice of a paediatriccardiologist before further treatment. The use of one of the following may be suggested.

Flecainide (2 mg/kg over 20 minutes): This drug is particularly useful in refractoryWolff–Parkinson–White-type tachycardia. It is a membrane stabiliser but can be proar-rhythmic and has a negative inotropic effect.

Figure 10.3. Algorithm for the management of supraventricular tachycardia

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Digoxin: Dosage schedules vary with age and underlying condition. Seek advice.Verapamil: This drug has been associated with irreversible hypotension and asystole

when given to infants. It therefore should not be used in children under 1 year of age. Thedose is 100–300 µg/kg, maximum 5 mg. The drug should be terminated when sinusrhythm is seen, even if the calculated dose has not been given. Do not use if a patient hasreceived β-blockers, flecainide or amiodarone.

Amiodarone: This drug can be used in refractory atrial tachycardia. The dose is 5 mg/kgover 30 min diluted in approximately 4 ml/kg of 5% dextrose.

Propranolol (50 micrograms/kg slowly intravenously): Only if pacing is available, be-cause asystole may occur. Do not give propranolol if the patient has been given verapamil.

It is unsafe to give verapamil and propranolol to the same patient because they bothhave negative inotropic actions. It is, however, safe to give propranolol and digoxin.

10.6 APPROACH TO THE CHILD WITHVENTRICULAR TACHYCARDIA

In the haemodynamically stable child with ventricular tachycardia a history should becarefully obtained to identify an underlying cause for the tachycardia because this willoften determine ancillary therapy.

Consider underlying causes:

• Congenital heart disease and surgery• Poisoning with tricyclic antidepressants, procainamide, quinidine, cisapride and

macrolide antibiotics, or terfenadine with grapefruit juice• Renal disease or other cause of hyperkalaemia• Long QT syndrome

Look for:

• Characteristics of the ECG indicative of torsade de pointes: polymorphic VT withQRS complexes which change in amplitude and polarity so that they appear to rotatearound an isoelectric line. Seen in conditions characterised by a long QT intervalquinine, quinidine, disopyramide, amiodarone, tricyclic antidepressant and digoxinpoisoning and cisapride with erythromycin.

Check serum K, Mg and Ca levels.

Analysis of the ECG should be done in consultation with a paediatric cardiologist, whoshould be sent a copy urgently.

Emergency Treatment of Ventricular Tachycardia

Reassess ABC

• The treatment of the haemodynamically stable child with ventricular tachycardiashould always include early consultation with a paediatric cardiologist. They maysuggest– amiodarone (5 mg/kg over 60 minutes) or– intravenous procainamide (15 mg/kg over 30–60 minutes).Both can cause hypotension, which should be treated with volume expansion.

• In cases where the ventricular arrhythmia has been caused by drug toxicity, seda-tion/anaesthesia and DC shock may be the safest approach. Use synchronous shocks

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Figure 10.4. Algorithm for the management of ventricular tachycardia

initially, as these are less likely to produce ventricular fibrillation than an asynchronousshock. If synchronous shocks are ineffectual, subsequent attempts will have to beasynchronous.

• The treatment of torsade de pointes ventricular tachycardia is magnesium sulphatein a rapid IV infusion (several minutes) of 25–50 mg/kg (up to 2 g).

It is important not to delay a safe therapeutic intervention for longer than necessary inVT as the rhythm often deteriorates quite quickly into pulseless VT or VF.

Wide-QRS SVT (i.e. SVT with aberrant conduction) is uncommon in infants andchildren. Correct diagnosis and differentiation from ventricular tachycardia depends oncareful analysis of at least a 12-lead ECG that may be supplemented by information froman oesophageal lead. The patient and family history should be evaluated to help identifythe presence of an underlying condition predisposing to stable ventricular tachycardia.Because either SVT or VT can cause haemodynamic instability, assumptions about themechanism (i.e. ventricular versus supraventricular) should not be based solely on thehaemodynamic status of the patient.

A dose of adenosine may help identify the underlying aetiology of the arrhythmia, butshould be used with extreme caution in haemodynamically stable children with wide-complex tachycardia because acceleration of the tachycardia and significant hypotensionare known risks.

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10.7 SUMMARY

You should use the structured approach in the assessment and management of thechild with an abnormal pulse rate or rhythm:


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CHAPTER

11The child with a decreased

conscious level

LEARNING OBJECTIVES


• the causes of a decreased conscious level in infants and children• about the pathophysiology of raised intracranial pressure• how to assess children with a decreased conscious level• how to resuscitate the child with a decreased conscious level

11.1 INTRODUCTION

The conscious level may be altered by disease, injury or intoxication. The level ofawareness decreases as a child passes through stages from drowsiness (mild reductionin alertness and increase in hours of sleep) to unconsciousness (unrousable, unrespon-sive). Because of variability in the definition of words describing the degree of coma,the Glasgow and the Children’s Coma Scales have been developed as semi-quantitativemeasures and, more importantly, as an aid to communication between carers. TheGlasgow Coma Scale was developed and validated for use in the head-injured patient buthas come to be used as an unvalidated tool for the description of conscious states from allpathologies.

In children, coma is caused by a diffuse metabolic insult (including cerebral hypoxiaand ischaemia) in 95% of cases, and by structural lesions in the remaining 5%. Metabolicdisturbances can produce diffuse, incomplete and asymmetrical neurological signs falselysuggestive of a localised lesion. Early signs of metabolic encephalopathy may be sub-tle, with reduced attention and blunted affect. The conscious level in metabolic en-cephalopathies is often quite variable from minute to minute. The most common causesof coma are summarised in the box.

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THE CHILD WITH A DECREASED CONSCIOUS LEVEL

Disorders causing coma in children

Hypoxic ischaemic brain injuryFollowing respiratory or circulatory failure

Epileptic seizuresTrauma

Intracranial haemorrhage, brain swellingInfections

MeningitisEncephalitisMalaria

PoisoningMetabolic

Renal, hepatic failure, Reye’s syndrome, hypoglycaemia, diabetes, hypothermia,hypercapnia

Vascular lesions

Table 11.1. Glasgow Coma Scale and Children’s Coma Scale

Glasgow Coma Scale (4–15 years) Child’s Glasgow Coma Scale (<4 years)

Response Score Response ScoreEye opening Eye opening

Spontaneously 4 Spontaneously 4To verbal stimuli 3 To verbal stimuli 3To pain 2 To pain 2No response to pain 1 No response to pain 1

Best motor response Best motor responseObeys verbal command 6 Spontaneous or obeys verbal

command6

Localises to pain 5 Localises to pain or withdrawsto touch

5

Withdraws from pain 4 Withdraws from pain 4Abnormal flexion to pain

(decorticate)3 Abnormal flexion to pain

(decorticate)3

Abnormal extension topain (decerebrate)

2 Abnormal extension to pain(decerebrate)

2

No response to pain 1 No response to pain 1Best verbal response Best verbal response

Orientated and converses 5 Alert; babbles, coos words tousual ability

5

Disorientated andconverses

4 Less than usual words,spontaneous irritable cry

4

Inappropriate words 3 Cries only to pain 3Incomprehensible sounds 2 Moans to pain 2No response to pain 1 No response to pain 1

Children with a decreased conscious level are usually presented by parents who arevery aware of the seriousness of the symptom. They may also have noted other featuressuch as fever, headache or exposure to poisoning which may aid the clinician in makinga presumptive diagnosis.

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11.2 THE PATHOPHYSIOLOGY OF RAISEDINTRACRANIAL PRESSURE

In very young children, before the cranial sutures are closed, considerable intracra-nial volume expansion may occur if the process is slow (i.e. hydrocephalus). However,if the process is rapid and in children with a fixed-volume cranium, increase in vol-ume due to brain swelling, haematoma or cerebrospinal fluid (CSF) blockage will causeraised intracranial pressure (ICP). Initially cerebrospinal fluid and venous blood withinthe cranium decrease in volume. Soon, this compensating mechanism fails and as theintracranial pressure continues to rise the cerebral perfusion pressure (CPP) falls andcerebral arterial blood flow is reduced.

CPP = MAP − ICP

where MAP is mean arterial pressure. Reduced CPP reduces cerebral blood flow (CBF).Normal CBF is over 50 ml/100 g brain tissue/min. If the CBF falls below 20 ml/100 gbrain tissue/min, the brain suffers ischaemia. The aim is to keep CPP above 50–60 mmHg.

Increasing intracranial pressure will push brain tissue against more rigid intracra-nial structures. Two clinical syndromes are recognisable by the site of localised braincompression.

Central syndromeThe whole brain is pressed down towards the foramen magnum and the cerebellar

tonsils herniate through it (“coning”). Neck stiffness may be noted. A slow pulse, raisedblood pressure and irregular respiration leading to apnoea are seen terminally.

Uncal syndromeThe intracranial volume increase is mainly in the supratentorial part of the intracranial

space. The uncus, which is part of the hippocampal gyrus, is forced through the tentorialopening and compressed against the fixed free edge of the tentorium. If the pressureis unilateral (e.g. from a subdural or extradural haematoma), this leads to third nervecompression and an ipsilateral dilated pupil. Next, an external oculomotor palsy appears,so the eye cannot move laterally. Hemiplegia may then develop on either or both sides ofthe body, depending on the progression of the herniation.

Figure 11.1. Herniations of the brain

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Lumbar puncture should not be performed in a child in coma. The purpose of a lumbarpuncture is to confirm the diagnosis of meningitis and to identify the organism and itsantibiotic sensitivity. There is a risk of coning and death if a lumbar puncture is performedin a child with significantly raised intracranial pressure. Normal fundi do not excludeacutely, severely raised intracranial pressure. The lumbar puncture can be performedsome days later when the child’s condition allows, to confirm or refute the diagnosisof meningitis or encephalitis if antibiotic treatment or acyclovir, respectively, has beenstarted. In addition, the results of blood cultures and PCR are therefore important.

The relative contraindications to a lumbar puncture are shown in the box.

318Relative contraindications to lumbar puncture

• Prolonged or focal seizures• Focal neurological signs, e.g. asymmetry of limb movement and

reflexes, ocular palsies• A widespread purpuric rash in an ill child. In this case intravenous

cefotaxime should be given immediately after a blood culture• Glasgow Coma Scale – score of less than 13• Pupillary dilatation• Impaired oculocephalic reflexes (doll’s eye reflexes)• Abnormal posture or movement, decerebrate or decorticate

posturing, or cycling movements of the limbs• Inappropriately low pulse, elevated blood pressure, and irregular

respirations (i.e. signs of impending brain herniation)• Thrombocytopenia or coagulation disorder• Papilloedema• Hypertension

11.3 PRIMARY ASSESSMENT OF THE CHILD WITH ADECREASED CONSCIOUS LEVEL

The first steps in the management of the patient with a decreased conscious level areto assess and if necessary support airway, breathing and circulation. This will ensurethat the diminished conscious level is not secondary to hypoxia and/or ischaemia andthat whatever the cerebral pathology it will not be worsened by lack of oxygenated bloodsupply to the brain.

This is dealt with in Chapter 7, “Structured Approach to the Seriously Ill Child”.Below is a summary.

Airway



• looking for chest and/or abdominal movement, symmetry and recession• listening for breath sounds and stridor• feeling for expired air

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Breathing

Effort of breathingrespiratory raterecession stridorwheeze gruntingaccessory muscle use flaring of alae nasigasping





Circulation

Heart rate: The presence of an inappropriate bradycardia will suggest raised intracranialpressure

Pulse volumeBlood pressure: Significant hypertension indicates a possible cause for the coma or

may be a result of itCapillary refill timeSkin temperature and colourEffects on breathing and mental status: Acidotic sighing respirations may suggest

metabolic acidosis from diabetes, or salicylate or ethylene glycol poisoning as a causefor the coma.

Heart rate/rhythm, blood pressure and core–toe temperature difference.

Disability

Mental status/conscious level (AVPU)Pupillary size and reaction (see table below)Posture: Decorticate or decerebrate posturing in a previously normal child should

suggest raised intracranial pressure.Look for neck stiffness in a child and a full fontanelle in an infant, which suggest

meningitis.

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The presence of convulsive movements should be sought: these may be subtle.

Summary of pupillary changes

Pupil size and reactivity CauseSmall reactive pupils Metabolic disorders

Medullary lesionPin-point pupils Metabolic disorders

Narcotic/organophosphate ingestionsFixed midsize pupils Midbrain lesionFixed dilated pupils Hypothermia

Severe hypoxiaBarbiturates (late sign)During and post seizureAnticholinergic drugs

Unilateral dilated pupil Rapidly expanding ipsilateral lesionTentorial herniationThird nerve lesionEpileptic seizures

There should be a specific assessment for raised intracranial pressure. There are veryfew absolute signs of raised ICP, these being papilloedema, a bulging fontanelle, andabsence of venous pulsation in retinal vessels. All three signs are often absent in acutelyraised ICP.

In a previously well, unconscious child (Glasgow Coma Scale score < 9) who is not ina post-ictal state, the signs in the box are suggestive of raised intracranial pressure:

Signs of raised intracranial pressure

1. Abnormal oculocephalic reflexes; avoid in patients with neck injuries:when the head is turned to the left or right a normal response is for the eyes to move

away from the head movement; an abnormal response is no (or random) movement;when the head is flexed, a normal response is deviation of the eyes upward, a loss of

his conjugate upward gaze is a sign suggestive of raised ICP.2. Abnormal posture:

(a) decorticate (flexed arms, extended legs)(b) decerebrate (extended arms, extended legs).

Posturing may need to be elicited by a painful stimulus.3. Abnormal pupillary responses, unilateral or bilateral dilation suggests raised ICP.4. Abnormal breathing patterns. There are several recognisable breathing pattern abnormal-

ities in raised ICP. However, they are often changeable and may vary from hyperventilationto Cheyne–Stokes breathing to apnoea.

5. Cushing’s triad: slow pulse, raised blood pressure and breathing pattern abnormalities area late sign of raised ICP.

Exposure

Rash: If one is present, ascertain if it is purpuric as an indicator of meningococcaldisease or non-accidental injury.

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Fever: A fever is suggestive evidence of an infectious cause (but its absence does not sug-gest the opposite) or poisoning with ecstasy, cocaine or salicylates. Hypothermia suggestspoisoning with barbiturates or ethanol.

Look for evidence of poisoning.

11.4 RESUSCITATION

Figure 11.2. Algorithm for the initial management of coma

Airway

• A patent airway is the first requisite. If the airway is not patent it should be opened andmaintained with an airway manoeuvre and the child ventilated by bag–valve–maskoxygenation. An airway adjunct can be used. The airway should then be secured withintubation by experienced senior help.

• If the child has an AVPU score of “P” or “U”, or the gag or cough reflex is absent,the airway is at risk. It should be maintained by an airway manoeuvre or adjunct andsenior help requested to secure it.

Breathing

• All children with a decreased conscious level should receive high-flow oxygen througha face mask with a reservoir as soon as the airway has been demonstrated to beadequate.

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• If the child is hypoventilating, respiration should be supported with oxygen via a bag–valve–mask device and consideration given to intubation and ventilation. Inadequatebreathing in coma can lead to a rise in arterial P2, which can cause a dangerousrise in intracranial pressure.

Circulation

Circulation needs to be optimised and if intracranial pressure is high, then cerebralperfusion will be compromised. However, overenthusiastic fluid administration shouldbe avoided.

• Establish IV access quickly or use the intraosseous route.• Check blood glucose – don’t ever forget glucose.

❝ If in doubt or test unavailable, it is safer to treat as if hypoglycaemia is present(<3 mmol/l) with 5 ml/kg (2 ml/kg for neonates) 10% glucose bolus IV.

• Take blood samples for blood culture, FBC, renal and liver function tests, plasmaammonia (send rapidly to the laboratory on ice), group & save/X-match, and bloodgas analysis.

• Give a broad-spectrum antibiotic, e.g. cefotaxime 80 mg/kg or ceftriaxone, to anychild in whom sepsis is suspected – e.g. meningococcal disease or other meningitis.

• Give 20-ml/kg rapid bolus of crystalloid to any patient with signs of shock (and seetreatment of coexistent shock and meningitis in meningococcal disease, Section 9.8).

Disability

Undertake appropriate medical management of raised intracranial pressure, if noted:

• Intubate and support ventilation (maintain a Pco2 of 4·0–4·5 kPa 30–34 mmHg).• Nurse with the head in-line in a 20–30◦ head-up position (to help cerebral venous

drainage).• Give mannitol (250–500 mg/kg; i.e. 1·25–2·5 ml of 20% IV over 15 minutes, and give

2-hourly as required, provided serum osmolality is not greater than 325 mOsm/l).• Consider dexamethasone (for oedema surrounding a space occupying lesion)

0·5 mg/kg 6-hourly.

If the situation remains unstable or is deteriorating, further urgent primary assessmentand resuscitation must be initiated. If the patient is stable, a further and more detailedneurological examination will reassess the earlier findings, help localise the site of neuro-logical dysfunction, and provide a reference for further examinations.

11.5 SECONDARY ASSESSMENT AND LOOKINGFOR KEY FEATURES

While the primary assessment and resuscitation are being carried out, a focused his-tory of the child’s health and activity over the previous 24 hours and any significantprevious illness should be gained. In a patient in coma, it is often impossible to be certainof the diagnosis in the first hour. The main immediate aims are therefore to maintainhomoeostasis and “treat the treatable”.

Specific points for history taking include:

• Recent trauma• Pre-existing neurological disability• History of epilepsy

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• Poison ingestion• Known chronic condition (e.g. renal disease, cardiac abnormality, diabetes)• Last meal• Family history or patient’s history of metabolic disorder• Recent trips abroad

Specific additional neurological examination includes:

• Eye examination:– Pupil size and reactivity (see table)– Fundal changes – haemorrhage and papilloedema (trauma, hypertension)– Ophthalmoplegia – lateral or vertical deviation

• Reassess posture and tone – look for lateralisation• Assess deep tendon reflexes and plantar responses – look for lateralisation

Lateralisation suggests a localised rather than a generalised lesion, but this is often afalse indicator in childhood. The child will almost certainly need a CT scan.

General physical examination may add clues to point to a working diagnosis. Specificfindings include the following:

1. Skin: rash, haemorrhage, trauma, evidence of neurocutaneous syndromes2. Scalp: evidence of trauma3. Ears and nose:

Bloody or clear discharge. Base of skull fracture (Chapter 16)Evidence of otitis media. May accompany meningitis

4. Neck: tenderness or rigidity. Meningitis, cerebrovascular accident5. Odour. Metabolic disorders and poisoning6. Abdomen: enlarged liver. (In conjunction with hypoglycaemia: Reye’s-like metabolic

syndrome)

The key features, which will be identified clinically, from the history, examination andthe initial blood test results, can point the clinician to the likeliest working diagnosis foremergency treatment.

• Coma that develops over several hours, associated with irritabil-ity and/or fever and a rash points to meningitis/encephalitis (butthis should also be a default working diagnosis in the absence ofa clear alternative one).

See Section 11.7

• A history of opiate ingestion and/or pin-point pupils points topoisoning with opiates.

See Section 11.8

• Coma occurring in the setting of, or just after, a minor illness pre-senting with vomiting, hepatomegaly and hypoglycaemia pointsto metabolic encephalopathy.

See Section 11.9

• A history of travel abroad might point to malaria. See Section 11.10• Coma associated with significant hypertension points to hyper-

tensive encephalopathy.See Section 12.7

• A history of onset of coma over an hour or so in an otherwisewell child is suggestive of poisoning.

See Appendix H

• A vague and inconsistent history and/or suspicious bruising in aninfant are suggestive of intracerebral bleeding from child abuse: thepresence of retinal haemorrhage is strong presumptive evidenceof the same.

See Chapter 16

• Hyperglycaemia points to diabetes. See Appendix B.• A history of very sudden onset of coma often with a preceding

headache points to a cerebrovascular accident (rare in childhood)

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In addition, unless meningitis can be excluded by the clear identification of anothercause for coma, it should be assumed present as the consequence of missed diagnosis iscatastrophic and the risk of unnecessary treatment with antibiotics small. Acyclovir shouldalso be considered because herpes encephalitis has a worse prognosis when treatment isseriously delayed. Senior advice should be sought.

11.6 FURTHER GENERAL TREATMENT OF COMA

• Maintain normo-glycaemic state.❝ Be wary of administering insulin to hyperglycaemic patients, since hyperglycaemia

may be stress induced.• Restrict fluids to 60% of maintenance if evidence of water retention is seen.• Assess and maintain electrolyte balance.

❝ If possible keep serum sodium in the normal range, 135–145 mmol/l.❝ Avoid hyponatraemia by using normal saline or 0·45% saline.

• Treat seizures if present and give prophylactic anticonvulsants if the child has repeatedseizures.

• Insert gastric tube to aspirate stomach contents. Perform gastric lavage in appropriatecircumstances see Appendix H.

• Regulate temperature, ensuring hyperthermia above 37·5◦C is avoided.• Undertake appropriate medical management of acute RICP if noted:

❝ Support ventilation (maintain a Pco2 of 4·0–4·5 kPa).❝ Maintain a 20–30◦ head-up position with the head in-line.❝ Give mannitol (250–500 mg/kg, i.e. 1·25–2·5 ml of 20% IV over 15 minutes, and

give 2-hourly as required, provided serum osmolality stays <325 mOsm/l.❝ Dexamethasone (for oedema surrounding a space occupying lesion) 0·5 mg/kg

twice daily.• Catheterise the bladder (bladder distension may aggravate raised intracranial pres-

sure) and monitor urine output.• Maintain skin care to prevent bedsores, and eye padding to avoid xerophthalmia.

11.7 APPROACH TO THE CHILD WITHMENINGITIS/ENCEPHALITIS

After the neonatal period, the commonest cause of bacterial meningitis is Neisseriameningitidis (Meningococcus). There is still a mortality rate of around 5% and a similar rateof permanent serious sequelae. Widespread Hib vaccination has reduced the incidence ofHaemophilus influenzae infection. Infection with Streptococcus pneumoniae is less commonand may follow an upper respiratory infection with or without otitis media. Long-termmorbidity and mortality occur in up to 30% of cases. A wide range of infections may alsocause encephalitis.

Diagnosis of bacterial meningitis

In the 3-year-old child and underBacterial meningitis is difficult to diagnose in its early stages in this age group. The

classic signs of neck rigidity, photophobia, headache, and vomiting are often absent. Abulging fontanelle is a sign of advanced meningitis in an infant, but even this serious andlate sign will be masked if the baby is dehydrated from fever and vomiting. Almost allchildren with meningitis have some degree of raised intracranial pressure, so that, in fact,

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the signs and symptoms of meningitis are primarily those of raised intracranial pressure.The following are signs of possible meningitis in infants and young children:

• Coma• Drowsiness (often shown by lack of eye contact with parents or doctor)• High-pitched cry or irritability that cannot be easily soothed by parent• Poor feeding• Unexplained pyrexia• Convulsions with or without fever• Apnoeic or cyanotic attacks• Purpuric rash

Older children of 4 years and overThese children are more likely to have the classic signs of headache, vomiting, pyrexia,

neck stiffness, and photophobia. Some present with coma or convulsions. In all unwellchildren, and children with an unexplained pyrexia, a careful search should be made forneck stiffness and for a purpuric rash. The finding of such a rash in an ill child is almostpathognomic of meningococcal infection, for which immediate treatment is required (seeChapter 9).

Emergency treatment of meningitis

Reassess ABCD

• Specific assessment should be made of the severity of raised intracranial pressure, asmany of the clinical signs of meningitis arise from this.

• After the above assessment, give intravenous cefotaxime or other suitable antibioticif meningitis is suspected and this has not yet been given. Treat a child with possibleraised intracranial pressure and meningitis without performing a lumbar puncture.Ensure blood cultures and PCR have been taken, as these may help in diagnosis.

• Consider acyclovir in a febrile comatose child to treat the rare possibility of herpessimplex virus encephalitis.

• Give dexamethasone (0·15 mg/kg) intravenously before or at the same timeas the initial antibiotic; in bacterial meningitis, this can reduce the rate ofsevere hearing loss.

11.8 APPROACH TO THE CHILD POISONEDWITH OPIATES

These children are usually toddlers who have drunk the green liquid form ofmethadone. The sedative effect of the drug may reduce the conscious level sufficiently toput the airway at risk and cause hypoventilation.

Emergency treatment of opiate poisoning

Reassess ABC

Following stabilisation of airway, breathing and circulation, the specific antidote isnaloxone. An initial bolus dose of 10 micrograms/kg is used but some children needdoses as high as 100 micrograms/kg up to a maximum of 2 mg. Naloxone has a shorthalf-life, relapse often occurring after 20 minutes. Further boluses, or an infusion of10–20 micrograms/kg/min, may be required.

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It is important to normalise CO2 before the naloxone is given because adverse eventssuch as ventricular arrhythmias, acute pulmonary oedema, asystole or seizures may oth-erwise occur. This is because the opioid system and the adrenergic system are interre-lated. Opioid antagonists and hypercapnia stimulate sympathetic nervous system activity.Therefore if ventilation is not provided to normalise carbon dioxide prior to naloxoneadministration, the sudden rise in adrenaline (epinephrine) concentration can cause ar-rhythmias.

11.9 APPROACH TO THE CHILD WITH METABOLIC COMA

Metabolic coma can arise from a variety of conditions, including a number of rareinborn errors of metabolism. An idiopathic form, Reye’s syndrome, was found to beassociated with aspirin ingestion, which is now banned from routine use in childrenunder 12 years of age.

These illnesses, now called “Reye-like” conditions, often present with a rapidly pro-gressive encephalopathy, vomiting, drowsiness and convulsions or coma. There may beassociated hepatomegaly (from fatty change), hypoglycaemia, abnormal liver enzymes orhyperammonaemia. In a case of otherwise unexplained coma with a GCS of <12 a keyurgent investigation is a plasma ammonia. Interpretation of the level can be difficult as canspecific treatment of the hyperammonaemia. In this event seek advice from a specialistin inherited metabolic disease and the paediatric intensive care unit.

11.10 APPROACH TO THE CHILD WITH MALARIA

Plasmodium falciparum causes 95% of deaths and most severe complications. It is trans-mitted by the bite of an infected Anopheles mosquito, and less commonly by infectedblood transfusion, needle stick injuries or by the transplacental route.

The clinical features of severe disease include reduced conscious level, convulsions,acidosis and severe anaemia. Cerebral malaria may produce encephalopathy, rapid-onsetcoma and raised intracranial pressure. Diagnosis requires microscopy of thick film (quickdiagnosis) and thin film (species identification).

Emergency Treatment of Cerebral Malaria

Reassess ABCD

• Intravenous quinine loading dose 20 mg/kg over 4 hours in dextrose 5%.– Give with ECG monitoring.

• Also give antibiotic, e.g. intravenous cefotaxime.• If Hb < 5 g/dL consider transfusion, especially if there are signs of heart failure.

11.11 APPROACH TO THE CHILD WITH SYSTEMICHYPERTENSIVE CRISIS

See Section 12.7.

11.12 STABILISATION AND TRANSFER TODEFINITIVE CARE

After the child has been stabilised and conditions such as hypoglycaemia, meningi-tis and opiate poisoning treated as indicated, some children will remain undiagnosed.

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These children and those in whom there is any suggestion of lateralisation or intracranialbleeding should have an urgent CT scan. Children who remain very ill and those in whomthe cause of coma is as yet unidentified will require transfer to a paediatric intensive careunit and the involvement of other specialists such as from neurology, inherited metabolicdiseases, endocrinology etc. as indicated.

Patients will almost certainly need intubation and ventilation for safe transfer by theretrieval team (see Chapter 24). In such patients neurological assessment cannot becontinued, and there should therefore be clear documentation of neurological signs,including their progression before transfer is commenced.

11.13 SUMMARY

You should use the structured approach in the assessment and management of thechild with a decreased conscious level:


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138



CHAPTER

12The convulsing child

LEARNING OBJECTIVES


• the causes of convulsions in infants and children• how to assess the convulsing child• how to resuscitate the child with convulsions• how to terminate a tonic–clonic convulsion• the emergency treatment of the different causes of convulsions

12.1 INTRODUCTION

Generalised convulsive (tonic–clonic) status epilepticus (CSE) is currently defined as ageneralised convulsion lasting 30 minutes or longer or when successive convulsions occurso frequently over a 30-minute period that the patient does not recover consciousnessbetween them. Although the outcome of CSE is mainly determined by its cause, theduration of the convulsion is also relevant. In addition, the longer the duration of theepisode, the more difficult it is to terminate it. In general, convulsions that persist beyond5 minutes may not stop spontaneously, so it is usual practice to institute anti-convulsivetreatment when the episode has lasted 5 or more minutes.

Tonic–clonic status occurs in approximately 1–5% of patients with epilepsy. Up to 5%of children with febrile seizures will present with status epilepticus.

Status epilepticus can be fatal, but mortality is lower in children than in adults – atabout 4%. Death may be due to complications of the convulsion, such as obstruction ofthe airway, hypoxia, and aspiration of vomit, to overmedication, cardiac arrhythmias or tothe underlying disease process. Complications of prolonged convulsions include cardiacarrhythmias, hypertension, pulmonary oedema, hyperthermia, disseminated intravascu-lar coagulation and myoglobinuria.

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THE CONVULSING CHILD

Neurological sequelae (persistent epilepsy, motor deficits, learning and behaviouraldifficulties) are age dependent, occurring in 6% of those over 3 years but 29% of thoseunder 1 year.

12.2 PATHOPHYSIOLOGY OF PROLONGED CONVULSIONS

A generalised convulsion increases the cerebral metabolic rate at least threefold. Ini-tially, there is an increased sympathetic activity with release of catecholamines, whichlead to peripheral vasoconstriction and increased systemic blood pressure. There is alsoa loss of cerebral arterial regulation and, following the increase in systemic blood pres-sure, there is a resulting increase in cerebral blood flow to provide the necessary oxygenand energy. If convulsions continue, the systemic blood pressure falls and this is followedby a fall in cerebral blood flow. Lactic acid accumulates and there is subsequently celldeath, oedema, and raised intracerebral pressure resulting in further worsening of cere-bral perfusion. Cellular metabolism of calcium and sodium is also impaired, with furthercell death.


The first steps in the management of the convulsing patient are to assess and, if nec-essary, support airway, breathing and circulation. This will ensure that the convulsion isnot secondary to hypoxia and/or ischaemia and that whatever the cerebral pathology, itwill not be worsened by lack of oxygenated blood supply to the brain. An important earlystep is to identify and treat any hypoglycaemia.

This is dealt with in Chapter 7, “Structured Approach to the Seriously Ill Child”.Below is a summary, with additional notes relevant to this presentation:

Airway




Breathing

Effort of breathingrespiratory rate stridorrecession wheezeaccessory muscle use flaring of alae nasigasping grunting

Grunting may be caused by the convulsion and not be a sign of respiratory distress inthis instance.

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Circulation

Heart rate: The presence of an inappropriate bradycardia will suggest raised intracranialpressure.

Pulse volumeBlood pressure: Significant hypertension indicates a possible cause for the convulsion

or more likely is a result of it.Capillary refill timeSkin temperature and colourEffects on breathing and mental statusMonitor heart rate/rhythm, blood pressure and core–toe temperature difference.

Disability

Mental status/conscious level (AVPU)

Pupillary size and reaction (see table in section 11.3)Posture – Decorticate or decerebrate posturing in a previously normal child should

suggest raised intracranial pressure. These postures can be mistaken for the tonic phaseof a convulsion. Consider also the possibility of a drug-induced dystonic reaction or apsychogenic, pseudo-epileptic attack. All these movement disorders are distinguish-able from tonic–clonic status epilepticus as long as they are considered.

Look for neck stiffness in a child and a full fontanelle in an infant, which suggestmeningitis.

Exposure

Rash: If one is present, ascertain if it is purpuric as an indicator of meningococcaldisease or non-accidental injury.

Fever: A fever is suggestive evidence of an infectious cause (but its absence does notsuggest the opposite) or poisoning with ecstasy, cocaine or salicylates. Hypothermia sug-gests poisoning with barbiturates or ethanol.

Consider the evidence for poisoning: History or characteristic smell (see Appendix H).

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12.4 RESUSCITATION

Airway

• A patent airway is the first requisite. If the airway is not patent it should be openedand maintained with an airway manoeuvre or an airway adjunct.

• Even if the airway is open the oropharynx may need secretion clearance by gentlesuction.

• If the child is breathing satisfactorily, the recovery position should be adopted tominimise the risk of aspiration of vomit.

Breathing

• All convulsing children should receive high-flow oxygen through a face mask with areservoir as soon as the airway has been demonstrated to be adequate.

• If the child is hypoventilating, respiration should be supported with oxygen via abag–valve–mask device and consideration given to intubation and ventilation.

Circulation

Gain intravenous or intraosseous access.

• Take blood for glucose stick test and laboratory test. Give 5 ml/kg of 10% dextrose toany hypoglycaemic patient. If hypoglycaemia is a new condition for the patient take10 ml of clotted blood before giving the dextrose for later investigation of the causeof the hypoglycaemic state.

• Give 20-ml/kg rapid bolus of crystalloid to any patient with signs of shock. Colloidand an antibiotic such as cefotaxime should be used for those in whom a diagnosis ofsepticaemia is made obvious by the presence of a purpuric rash after blood has beentaken for culture.

• Give an antibiotic such as cefotaxime or ceftriaxone to any child in whom a diagnosisof meningitis is made obvious by a stiff neck or bulging fontanelle after blood hasbeen taken for culture.

12.5 SECONDARY ASSESSMENT AND LOOKING FORKEY FEATURES

While the primary assessment and resuscitation are being carried out a focused historyof the child’s health and activity over the previous 24 hours and any significant previousillness should be gained.

Specific points for history taking include:

647• Current febrile illness• Recent trauma• History of epilepsy• Poison ingestion• Last meal• Known illnesses

The immediate emergency treatment requirement, after ABC stabilisation and exclu-sion or treatment of hypoglycaemia is to stop the convulsion.

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12.6 EMERGENCY TREATMENT OF THE CONVULSION

Figure 12.1. Status epilepticus algorithm

Reassess ABC

This evidence-based consensus guideline is not intended to cover all circumstances.There are patients with chronic epilepsy whose physicians recognise that they respondto certain drugs and not to others and for these children an individual protocol is moreappropriate. In addition, seizures in neonates are managed differently to those of infantsand children.

The protocol is for the majority of children in CSE who present acutely onwards or in an accident and emergency department.

100128Step 1

• If intravenous access is already established or can be established quickly, give lo-razepam 0·1 mg/kg in the first instance.

• In children in whom intravenous access is unsuccessful, give buccal midazolam 0·5mg/kg or rectal diazepam 0·5 mg/kg.

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Step 2

• After 10 minutes, give a second dose of lorazepam 0·1 mg/kg, if the convulsioncontinues.

• If the child has received buccal midazolam or rectal diazepam, now has intravenousaccess and is still convulsing, he should be given a dose of intravenous lorazepam(0·1 mg/kg).

• If intravenous access still has not been achieved, then a dose of rectal paraldehyde(0·4 ml/kg) can be given mixed with an equal volume of olive oil.

In the majority of children, treatment in steps 1 to 2 will be effective.

Step 3

At this stage senior help is needed to reassess the child and advise on management. It isalso wise to seek anaesthetic or intensive care advice as the child will need anaesthetisingand intubating if this step is unsuccessful.

• While the phenytoin (18 mg/kg over 30 minutes) is being prepared, paraldehydeshould be given to any child who has not yet received it.

• If the convulsion stops before phenytoin is started, the infusion should not be com-menced without specialist advice.

• If the convulsion stops after phenytoin has been started, the complete dose shouldstill be given, as this will have an anticonvulsant effect for up to 24 hours.

• In the case of children already receiving phenytoin as maintenance treatment for theirepilepsy, phenobarbital (phenobarbitone) (20 mg/kg over 20 minutes) should be usedin place of phenytoin.

Step 4

If 20 minutes after Step 3 has started, the child remains in CSE, an anaesthetist mustbe present. Check airway, breathing, and circulation. Take blood for glucose, arterialblood gas, urea, electrolytes and calcium. Treat any vital function problem and correctmetabolic abnormalities slowly. Treat pyrexia with paracetamol or diclofenac rectally.Consider mannitol (0·25 g/kg intravenously over 30–60 minutes).

• Rapid sequence induction of anaesthesia is performed with thiopental (thiopentone)and a short-acting paralysing agent.

• Further advice on management should be sought from a paediatric neurologist.

In children under 3 years with a history of chronic, active epilepsy, a trial of pyridoxineshould be instituted.

Drugs

LorazepamLorazepam is equally or more effective than diazepam and possibly produces less res-

piratory depression. It has a longer duration of action (12–24 hours) than diazepam (lessthan 1 hour). It appears to be poorly absorbed from the rectal route.

Lorazepam is not available in every country. If this is the case, diazepam can be sub-stituted at a dose of 0·25 mg/kg IV/IO.

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MidazolamThis is an effective quick-acting anticonvulsant, which takes effect within minutes but

has a shorter lasting effect than lorazepam. However, most children do not convulse againonce the seizure has been terminated. It has a depressant effect on respiration (which isenhanced by the addition of phenobarbital (phenobarbitone) but occurs only in about5% of patients, is short-lived and usually easily managed with bag–valve–mask ventilatorysupport. It is given by the buccal route by the following methods:

• by drawing up the correct dose of the IV preparation using a needle (to avoid anyfragments of glass from the ampoule) and

• removing the needle and injecting the drug into the buccal area between the lowerbottom lip and the gum margin at the side of the mouth.

A recent large, multi-centre randomised controlled trial of the safety and efficacy of buccalmidazolam versus rectal diazepam for the emergency treatment of seizuresin children showed that buccal midazolam was twice as effective as rectal di-azepam. Both drugs produced the same level and degree of respiratory depres-sion.

DiazepamThis is also an effective, quick-acting anticonvulsant with similar characteristics to

midazolam. It is widely used but may now be superseded by the more effective midazolamwhere the latter is available. The rectal dose is well absorbed.

ParaldehydeDose: 0·4 ml/kg per rectum (0·3 ml/kg under 6 months of age), made up as a 50:50

solution in olive oil or physiological saline. Arachis oil should be avoided because chil-dren with peanut allergy may react to it. Paraldehyde can cause rectal irritation, butintramuscular paraldehyde causes severe pain and may lead to sterile abscess formation.Paraldehyde causes little respiratory depression. It should not be used in liver disease.

Paraldehyde takes 10–15 minutes to act and its action is sustained for 2–4 hours. Donot leave paraldehyde standing in a plastic syringe for longer than a few minutes.

PhenytoinDose: 18 mg/kg intravenously. Rate of infusion no greater than 1 mg/kg/min. Infusion

to be made up in 0·9% sodium chloride solution to a maximum concentration of 10 mgin 1 ml.

Measure plasma phenytoin levels 60–90 minutes after the completion of the infusion.Phenytoin can cause dysrhythmias and hypotension, and therefore an ECG monitor

should be used and the BP monitored. It has little depressant effect on respiration.Do not use this if the child is known to be on oral phenytoin until the blood level of

phenytoin is known. Then only give it if the phenytoin level is less than 5 micrograms/ml.Phenytoin has a peak action within 1 hour but a long half-life that is dose-dependent. Itsaction therefore is more sustained than diazepam.

FosphenytoinThis is a recently produced pro-drug of phenytoin. It is not itself anticonvulsant but is

rapidly converted into phenytoin once administered. Because it does not need propyleneglycol as a solvent, it can be administered more rapidly than phenytoin over 7–10 minutesand is said to cause fewer cardiac side effects. It can be given intramuscularly. At presentthere are no paediatric efficacy data on use in CSE in children. If used it is prescribed in“phenytoin equivalents”, which could cause confusion: 75 mg fosphenytoin is equivalentto 50 mg phenytoin.

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Thiopental (thiopentone) sodiumInduction dose 4–8 mg/kg intravenously.This is an alkaline solution, which will cause irritation if the solution leaks into subcu-

taneous tissues.It has no analgesic effect and is a general anaesthetic agent. Repeated doses have a

cumulative effect. It is a potent drug with marked cardiorespiratory effects and shouldbe used only by experienced staff who can intubate a child.

It is not an effective long-term anticonvulsant and its principal use in status epilepticusis to facilitate ventilation and the subsequent management of cerebral oedema due to theprolonged seizure activity. Other antiepileptic medication must be continued.

The child should not remain paralysed as continued seizure activity cannot universallybe adequately monitored by cerebral function analysis monitoring. When the child isstable he or she will need transfer to a paediatric intensive care unit. A paediatric neu-rologist should continue to give clinical advice and support. There are several regimesfor continued drug control of the convulsions but they are outside the scope of thistext.

General measures

• Maintain normo-glycaemic state.❝ Be wary of administering insulin to hyperglycaemic patients, since hyperglycaemia

will usually be stress induced.• Restrict fluids to 60% of maintenance and monitor urine output.• Assess and maintain electrolyte balance.

252❝ If possible keep serum sodium in the normal range, 135–145mmol/l.❝ Avoid hyponatraemia by using normal saline or 0·45% saline.

• Insert a gastric tube to aspirate stomach contents. Perform gastric lavage in circum-stances such as drug or chemical ingestion if appropriate for the drug concerned (seeAppendix H).

• Regulate temperature, ensuring temperatures above 37·5◦C are avoided.• Undertake appropriate medical management of RICP if noted:

❝ Support ventilation (maintain a P2 of 4·0–4·5 kPa).❝ Maintain a 20–30◦ head-up position with the head in-line.❝ Give mannitol (250–500 mg/kg; that is 1·25–2·5 ml of 20% IV over 15 minutes,

and give 2-hourly as required, provided serum osmolality stays <325 mOsm/l.❝ Dexamethasone (for oedema surrounding a space occupying lesion) 0·5 mg/kg

twice daily.❝ Catheterise the bladder (bladder distension may aggravate raised intracranial

pressure).

Frequent reassessment of ABC is mandatory as therapy may cause depression of venti-lation or hypotension. This particularly applies after treatment with benzodiazepines usedto control the fit. Although it is appropriate to continue face mask oxygen treatment, itsuse may mask hypoventilation if breathing efficacy is being monitored by Sa2. Ensurethat Sa2 when breathing room air is assessed several times and support ventilation if thisunmasks hypoventilation. Alternatively monitor carbon dioxide levels.

The role of cerebral function analysis monitoring is still unclear. Currently, clinicalfeatures and standard EEG are the preferred methods of assessing seizure activity.

After the fit has been controlled the clinician must consider the underlying cause of theconvulsion. In many cases there will be an infectious cause: either a benign, self-limitinginfection causing “febrile status” or possibly meningitis (see Chapter 11). Additionaltreatments will depend on the clinical situation.

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12.7 APPROACH TO THE CHILD WITH SYSTEMICHYPERTENSIVE CRISIS

Hypertension is uncommon in children. Renal disorders such as dysplastic kidneys,reflux nephropathy or glomerulonephritis account for the majority of children presentingwith severe hypertension. Coarctation of the aorta is another important cause. Bloodpressure is rarely measured routinely in otherwise healthy children and therefore hyper-tension usually presents with symptoms which may be diverse in nature. Neurologicalsymptoms are more common in children than in adults. There may be a history of severeheadaches, with or without vomiting, suggestive of raised intracranial pressure. Childrenmay also present acutely with convulsions or in coma. Some children will present witha facial palsy or hemiplegia, and small babies may even present with apnoea or cardiacfailure.

Blood pressure measurement

This may be difficult in small children and misleading if not done correctly. The fol-lowing guidelines should be observed:

• Always use the biggest cuff that will fit comfortably on the upper arm. A small cuffwill give erroneously high readings.

• The systolic blood pressure may give a more reliable reading than the diastolic becausethe fourth Korotkoff sound is frequently either not heard or is audible down to zero.

• When using an electronic device, if the result is unexpected recheck it manually beforeacting on it.

• Raised blood pressure in a child who is fitting, in pain or screaming must be recheckedwhen the child is calm.

• If the child is very small or uncooperative, using a Doppler device may be helpful.Approximate systolic blood pressures may be obtained by the palpation method.

Blood pressure increases with age – the reading should be checked against normalranges for the child’s age. Any blood pressure over the 95th centile should be repeatedand if persistently raised will need treatment. Blood pressures leading to symptomatologywill be grossly elevated for the child’s age and the diagnosis should not be difficult.

12.8 HYPERTENSION EMERGENCY TREATMENT

Reassess ABC

Initial treatment will be that of the presentation. Airway, breathing and circulationshould be assessed and managed in the usual way and neurological status assessed andmonitored. Convulsions usually respond to lorazepam, midazolam or diazepam and pa-tients with clinical signs of raised intracranial pressure should be managed with intuba-tion, maintenance of normal P2, 20–30◦ nurse head-up and mannitol (see Chapter 11).

Once the patient has been resuscitated, management of the hypertension is urgent, butshould only be commenced after discussion with a paediatric nephrologist, cardiologistor intensivist. The aim of treatment is to achieve a safe reduction in BP to alleviate theurgent presenting symptoms whilst avoiding the optic nerve or neurological damage thatmay occur with too rapid reduction. Typically the aim is to bring the BP down to the95th centile for age (or height) over 24–48 hours, with perhaps one-third of the reductionin the first 8 hours. This can be difficult to do without very close BP monitoring and atitratable infusion of the antihypertensive drug.

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Monitoring of visual acuity and pupils is crucial during this time as lowering the bloodpressure may lead to infarction of the optic nerve heads. Any deterioration must be treatedby urgently raising the blood pressure using intravenous saline or colloid. Some childrenmay be anuretic – renal function (serum creatinine, urea and electrolytes) should beanalysed promptly.

Some drugs commonly used to achieve blood pressure reduction in children are shownin Table 12.1.

Table 12.1. Drug therapy of severe hypertension

Drug Dose Comments

Labetalol Bolus Loading dose250–500 mcg/kg α– and β-blockers.1–3 mg/k/h Titratable infusion. DO NOT USE in

patients with fluid overload or acuteheart failure.

Sodium nitroprusside 0·2–1 µg/kg/min Vasodilator. Very easy to adjust dose.Titratable infusion. Protect from light.Monitor cyanide levels.

Nifedipine 0·25 mg/kg Fluid can be drawn up from capsulesand squirted into mouth sublingually.Better to bite the capsule andswallow. May be difficult to control BPdrop because it is given as a bolus.

Some specialists may recommend the use of nifedipine as a temporary measure beforetransfer; if any drug is used, the child should have the blood pressure monitored as aboveand an intravenous infusion in place.

These children should be cared for in a unit experienced in paediatric hypertension.This will usually be the regional paediatric nephrology (or paediatric cardiology) centre.It is essential that adequate consultation takes place before transfer.

12.9 SUMMARY

You should use the structured approach in the assessment and management of theconvulsing child:


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PART

IVTHE SERIOUSLY INJURED CHILD

149



150



CHAPTER

13The structured approach to the

seriously injured child

LEARNING OBJECTIVES


• the structured approach to the seriously injured child

13.1 INTRODUCTION

Children and adults are affected differently by major injuries – physically, physiolog-ically and psychologically. A young child cannot describe pain, or even localise symp-toms. The more frightened children become, the “younger” they behave, and the lessthey can cooperate with management. Symptoms may be denied vehemently. Their in-experience, lack of awareness of danger and denial of threats posed puts them at par-ticular risk of trauma. The relative elasticity of their tissues allows more energy to betransmitted to other body parts, with less being dissipated at the impact site. Theirrelatively small size affects the pattern of injuries sustained. For example, the point ofimpact of a car bumper is more cephalad on the body of a child pedestrian, leadingto different anatomical injuries than those sustained in the same incident involving anadult.

Although traumatised children have a number of unique problems, this in no wayaffects the validity of a structured approach. By following the principles outlined, prob-lems should be identified and treated in the same order of priority as for adults.It should be emphasised from the start that, although assessment and managementare discussed separately, this is purely to allow the steps to be shown clearly. Intrauma resuscitation, it is essential to intervene immediately, as soon as a problem isfound.

The form of the structured approach is shown in the box.

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THE STRUCTURED APPROACH TO THE SERIOUSLY INJURED CHILD

Structured Approach

Immediate

• Primary survey (immediate life threats)• Resuscitation

Focussed

• Secondary survey (key features)• Emergency treatment

Detailed Review

• Reassessment (system control)• Continuing stabilisation and definitive

care

13.2 PRIMARY SURVEY

During the primary survey life-threatening conditions are identified. Assessment fol-lows the familiar ABC pattern with significant additions:

Airway with cervical spine controlBreathing with ventilatory supportCirculation with haemorrhage controlDisability with prevention of secondary insultExposure with temperature control

Airway and cervical spine

Airway assessment following trauma has the highest priority and should follow thestandard

LOOKLISTENFEEL

technique discussed in Chapters 4 and 5.Unless the mechanism of injury clearly excludes the possibility of a cervi-

cal spine injury, spinal precautions must be implemented from the outset, untilsuch injury can be excluded by adequate clinical evaluation and (when indi-cated) radiological examination. This requires that either the child should beimmobilised on a firm surface with the neck placed in a hard collar of theappropriate size, with side supports provided by blocks and straps, or that thehead should be held in manual in-line stabilisation by a competent assistant.

553559

Breathing

After dealing with any immediate airway problems, breathing should be assessed asthe next priority. As discussed in earlier chapters, the adequacy of breathing is checkedin three domains – the effort of breathing, the efficacy of breathing and the effects of

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inadequate respiration on other organ systems. These are summarised in the box. Whenexamining the chest, the look, listen and feel approach is again appropriate, but it is impor-tant to remember to percuss also to distinguish a tension pneumothorax from a massivehaemothorax.

Assessment of the adequacy of breathing

Effort of breathing

RecessionRespiratory rateInspiratory or expiratory noisesGruntingAccessory muscle useFlare Flaring of the alae nasi


Breath soundsChest expansionAbdominal excursion

Effects of inadequate respiration

Heart rateSkin colourMental statusDon’t forget to percuss each side of the chest

The normal resting respiratory rate changes with age. These changes are summarisedin Table 13.2.

Circulation

Circulatory assessment in the primary survey involves the rapid assessment of heart rateand rhythm, pulse volume and peripheral perfusion (colour, temperature and capillaryreturn, remembering that exposure to cold prolongs the capillary refill time in healthypeople – test on the sternum). In addition, a rapid check should be made for significantexternal haemorrhage (and pressure applied if appropriate). Blood pressure takes toolong to perform as part of the primary survey itself, but it should be measured as anadjunct (afterwards or by other personnel). An abnormal respiratory rate and alteredmental status in the presence of circulatory compromise indicate the effect of shock onother organ systems. Using these measures an estimate of the need for fluid replacementcan be made as shown in Table 13.1. Again, remember the caveats about heart rate,differential pulse volume and capillary refill time outlined in Chapter 7. It canbe difficult to assess the circulatory state of an injured child: in blunt traumalarge blood losses are the exception rather than the rule. A single abnormalsign is not predictive of shock, but more than two of the signs tending to thesame conclusion is predictive of the requirement for fluid replacement. SeeTable 13.1.

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Circulatory assessment must take into account the fact that resting heart rate, bloodpressure and respiratory rate vary with age. The normal values are shown in Table 13.2.Note that the systolic blood pressure in children who have been injured is raised above

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Table 13.1. Recognition of clinical signs indicating blood loss requiring urgent treatment

Sign

Heart rate Marked or increasing tachycardia or relative bradycardiaSystolic BP FallingCapillary refill time (Normal <2 sec) Increased to >4–5 secRespiratory rate Tachypnoea unrelated to thoracic problemMental state Altered conscious level unrelated to head injury

Table 13.2. Vital signs: approximate range of normal

Age (years) Respiratory rate (breaths/min) Systolic BP (mmHg) Pulse (beats/min)

<1 30–40 70–90 110–1601–2 25–35 80–95 100–1502–5 25–30 80–100 95–1405–12 20–25 90–110 80–120>12 15–20 100–120 60–100

normal and that the degree of hypertension is unrelated to age or trauma severity. Theclinician should therefore view with suspicion a systolic pressure in the lower part of thenormal range in an injured child.

Disability

The assessment of disability during the primary survey consists of a brief neurologicalexamination to determine the conscious level and to assess pupil size and reactivity. Theconscious level is described by the child’s response to voice and (where necessary) topain. The AVPU method describes the child as alert, responding to voice, responding to painor unresponsive and is a rapid, if crude, assessment.

A AlertV Responds to VoiceP Responds only to PainU Unresponsive to all stimuli

The score will identify whether or not there is an abnormality of the child’s consciouslevel and alert the clinician to the possible need for airway protection if the level is P or U.

Exposure

In order to assess a seriously injured child fully, it is necessary to take his or her clothesoff. Children become cold very quickly, and may be acutely embarrassed when undressedin front of strangers. Although exposure is necessary the duration should be minimised,and a blanket provided at all other times.

Conditions identified

By the end of the primary survey, the following conditions may have been recognisedand should be treated as soon as they are found:

• Airway obstruction• Tension pneumothorax

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• Open pneumothorax• Massive haemothorax• Flail chest• Cardiac tamponade• Shock (haemorrhagic or otherwise)• Decompensating head injury

13.3 RESUSCITATION

Life-threatening problems should be treated as they are identified during theprimary survey.


AirwayThe airway may be compromised by material in the lumen (blood, vomit, teeth or a

foreign body), by damage to or loss of control of the structures in the wall (the mouth,tongue, pharynx, larynx or trachea) or by external compression or distortion from outsidethe wall (e.g. compression from a pre-vertebral haematoma in the neck or distortion froma displaced maxillary fracture). The commonest cause is from occlusion by the tonguein an unconscious, head-injured child. Whatever the cause, airway management shouldfollow the sequence described in Chapters 4 and 5 bearing in mind the need to protectthe cervical spine. This is summarised in the box.

Airway management sequence

• Jaw thrust• Suction/removal of foreign body under direct vision• Oro/nasopharyngeal airways• Tracheal intubation• Surgical airway

Head tilt/chin lift is not recommended following trauma, because cervical spine injuriesmay be made worse.

Cervical spineFor any mechanism of injury capable of causing spinal injury (or in cases with an

uncertain history), the cervical spine is presumed to be at risk, until it can be cleared.Children (and adults) can suffer spinal cord injury despite normal plain radiographs.If ignored, ligamentous instability without radiographic evidence of a fracture can havedevastating consequences.

If the child is unconscious or cooperative, the head and neck should be immobilisedinitially by manual in-line stabilisation and then by using a hard collar, blocks and straps.Uncooperative or combative children should simply have a hard collar applied, if they willtolerate it. Too rigid immobilisation of the head in such cases may increase leverage onthe neck as the child struggles. It is imperative that the child is treated from the outset ina gentle, supportive atmosphere in a way that is appropriate for their age and that parentsremain at the bedside, so that anxiety is minimised and unnecessary interventions areavoided.

Vomiting poses an obvious threat to the unprotected airway, especially if there is also arisk of spinal injury. Positioning the child safely and providing airway suction are the key

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interventions if the child vomits. If the child has only just arrived and the head, chest,pelvis and legs are still strapped securely to a spine board, then it is feasible to tilt theboard temporarily while clearing the airway. Once the body straps have been removed,turning the child into the lateral position puts the spine at risk, unless it can be carriedout immediately by three or four carers as a properly coordinated log-roll. It is generallymuch simpler and more effective to tip the trolley head-down (so that the trachea runs“uphill”) and provide suction to the mouth and pharynx.

If the spine has not been cleared, manual in-line immobilisation will be needed forintubation if indicated. Intubation is significantly harder with the collar left on, as jawopening is hindered. Having weighed up the risk of failed intubation against any benefitof the collar being left in place, it is generally accepted that manual in-line immobilisationwith the collar off is by far the best option. Full immobilisation with the collar, blocksand straps reapplied is necessary after securing the endotracheal tube. The cervical collarmay only be removed when radiographs are normal, the child has no neck pain andthe neurological examination is normal. Clearly, if the child is paralysed, sedated andventilated the neurological examination cannot be done and spinal immobilisation mayneed to be maintained for prolonged periods in such cases. Computed tomog-raphy or magnetic resonance imaging may be necessary to assess the risk tothe spinal cord in this event. It is important to ensure that the cervical collardoes not restrict venous outflow in the neck as this may increase intracranialpressure.

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Breathing

If breathing is inadequate, ventilation must be commenced. Initially bag–mask ventila-tion should be performed. Generally speaking, a child who requires bag–mask ventilationinitially following trauma will subsequently require intubation to control the airway. Fol-lowing intubation, mechanical ventilation can be commenced.

The indications for intubation and mechanical ventilation are summarised in the box.

Indications for intubation and ventilation

• Persistent airway obstruction• Predicted airway obstruction eg inhalational burn• Loss of airway reflexes• Inadequate ventilatory effort or increasing fatigue• Disrupted ventilatory mechanism eg severe flail chest• Persistent hypoxia despite supplemental oxygen• Controlled hyperventilation required to prevent

secondary brain injury.

If breath sounds are unequal then pneumothorax, haemo-pneumothorax, misplacedtracheal tube, blocked main bronchus or pulmonary collapse, diaphragmatic rupture,pulmonary contusion and aspiration of vomit or blood should be considered, and appro-priate measures should be taken. (see relevant chapters)

Circulation

All seriously injured children require vascular access to be established urgently. Tworelatively large intravenous cannulae are mandatory. Peripheral veins are preferred, butin the event of failure, other options should be considered:

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• Direct cannulation of the external jugular vein• Indirect cannulation of the femoral vein using the Seldinger technique (“wire through

needle” followed by “catheter over wire”)• Intraosseous cannulation of the tibia• Cut-down onto the cephalic vein at the elbow or the long saphenous vein at the ankle

Intraosseous infusion is warranted from the outset in very urgent situations or laterif other options have failed. It usually proves to be quicker and easier than the morespecialised techniques mentioned above. Vascular access techniques are discussed indetail in Chapter 21.

Central venous cannulation (other than by the femoral route) is hazardous in childrenand should not be attempted by the inexperienced clinician. Femoral cannulation is notwithout risk, given the proximity of the site to the femoral joint. The main use of aninternal jugular or subclavian line is for monitoring central venous pressure.

Guidelines for fluid therapy following trauma are under frequent review.There is some evidence in adults that vigorous fluid administration is harm-ful in the presence of uncontrolled bleeding, especially following penetratingtrauma. This has led to a much more cautious fluid regime, until the risk ofuncontrolled bleeding has been ruled out. The concern is that increasing the blood pres-sure back to normal rapidly may disrupt early clot formation with subsequent exsanguina-tion. This is a typical concern in the pre-hospital situation, where surgical interventionto stop concealed bleeding is unavailable. In the pre-hospital setting paramedics are nowlikely to be using boluses of fluid of 5 ml/kg.

It is appropriate to use similar guidelines for children with potentially uncontrolledbleeding (modified for the size of the child), although there is insufficient evidence in thecurrent literature as trauma in children, while a major cause of death and disability, is lesswell studied than that in adults. In the absence of further evidence, it is recommendedthat aliquots of fluid of 10 ml/kg be given with frequent re-assessment, rather than thefull 20 ml/kg recommended in other life-threatening situations such as sepsis. Similarvolumes may be repeated if there is continuing evidence of haemorrhagic shock, afterre-evaluating the state of the circulation. Early surgical involvement is essential.

While cautious fluid administration is desirable in ongoing haemorrhage, other consid-erations may lead us in the opposite direction. In particular, head injury may be worsenedby hypotension. It is important to consider all possibilities in early trauma care. If un-controlled bleeding is shown to be unlikely during the early evaluation, in the presenceof a significant head injury blood pressure should be kept at normal levels to maintainthe perfusion pressure to the brain.

When a fluid bolus is indicated, it should be given in aliquots of 10 ml/kg of crystalloid(e.g. 0.9% saline) with careful review after each aliquot. The need for emergency surgicalcontrol of bleeding should be considered immediately.

If 40 ml/kg of crystalloid has been administered to a child who remains unstable,blood should be used for further fluid replacement. The surgical team must be involvedin the child’s management as soon as it is clear that 20 ml/kg has not stabilised the child.Cross-matching of blood takes time, and clinical urgency may dictate that type-specificor O-negative blood must be given. The times necessary to obtain blood are shown inTable 13.3.

Disability

If the primary survey reveals that the child has a de-compensating head injury, neurolog-ical resuscitation is required. If the Glasgow Coma Score is less than 8 and there are pupilinequalities, immediate intervention is necessary. Lesser degrees of unconsciousness orthe presence of focal signs also indicate the need for urgent action.

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Figure 13.1. Fluids in hypovolaemic shock after trauma

Table 13.3. Cross-match times

Blood type Cross-match Time (min)

O-negative Nil 0Type-specific ABO 10–15Full cross-match Full 45–60

Remember that the scale is modified in the smaller child.Interventions to be considered include:

• Oxygenation (which will already have been addressed)• Control of carbon dioxide tension (by controlling ventilation)• Maintenance of blood pressure to support cerebral perfusion• Mannitol (if indicated) to lower the intracranial pressure• Anaesthesia/sedation/analgesia to reduce cerebral metabolism• Prompt treatment of any fits

As soon as a serious head injury is suspected, a CT scan should be ordered and theneurosurgical team (which will usually be off-site) alerted. This will help to reduce delayin reaching a decision on the need for neurosurgical intervention. A full Glasgow ComaScore is needed at this point.

Other procedures carried out during the resuscitation phase

Chest and pelvic radiographs are not required to identify the conditions (refer to listabove) that should be found during the primary survey – these life-threatening conditionsare clinical diagnoses – but they contribute to resuscitation and subsequent decisionmaking. In unstable or high-risk children, it is appropriate to perform these radiographsduring the resuscitation phase in the resuscitation room bay.

When venous access is achieved and blood is taken for cross-matching, samples forother investigations should be taken at the same time, including full blood count, clottingscreen, amylase/trypsinogen, urea and electrolytes. Remember to measure the glucose,especially in adolescents (who are prone to both injury and hypoglycaemia after drinkingalcohol) and in very small children.

A brief history will usually have been given by the ambulance staff together with detailsof the child’s condition at the scene. This information is useful in allowing the clinician to

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consider what injuries the mechanism might have produced and to assess whether clinicaldeterioration is occurring. Monitoring of the respiratory rate, pulse rate, blood pressure,and oxygen saturation are important adjuncts to the primary survey and resuscitation. Aurinary catheter and a gastric tube may be inserted during this phase in severely injuredchildren.

Urinary catheterisationIn a child, a urinary catheter should only be inserted if the child cannot pass urine

spontaneously or if continuous accurate output measurement is required to achieve sta-bilisation after a serious physiological insult. The route (urethral or supra-pubic) willdepend on factors related to signs of urethral, bladder, intra-abdominal or pelvic injury(such as blood at the external meatus, or bruising in the scrotum or perineum; see Chap-ter 15). If a boy requires urethral catheterisation, urethral damage must be excluded first.The smallest possible silastic catheter should be used in order to reduce the risk of sub-sequent urethral stricture formation. If any doubt exists then the decision to catheterisethe child can be left to the responsible surgeon. Urine should be stick-tested and sent formicroscopy.

Nasogastric tube placementAcute gastric dilatation is common in children and the stomach should be decom-

pressed. If there is evidence or suspicion of basal skull fracture, the tube should not bepassed by the nasal route. In the intubated patient, the oral route is a simple alternative.

AnalgesiaAnalgesia can usually be administered just after completing the primary survey and

resuscitation. A brief examination of the conscious level and of the body part in pain helpsto set the baseline for titrating the dose. Morphine is the standard drug in acute traumacare. A dose of 0.1–0.2 mg/kg should be drawn up in a convenient concentration (e.g.1 mg/ml in 0.9% saline) according to the size of the child and administered in increments.Remember that morphine may take more than 10 minutes to provide maximal effect.Fentanyl given in increments of 0.5 µg/kg is a useful alternative (in the first instance) asit has a much quicker onset, though it is of shorter duration. Both of these opioids shouldbe at least halved in dose if there is any alteration in the conscious level or any evidence ofhypovolaemia. There is no place for the administration of intramuscular analgesia in trauma.Entonox (a 50:50 mix of O2/N2O) may be considered, but is contraindicated if there isa possibility of pneumothorax or basal skull fracture.

13.4 SECONDARY SURVEY AND LOOKING FORKEY FEATURES

Having finished the primary survey and set in place appropriate resuscitative measures,focused care is the next phase of management. The central diagnostic process during thisphase is the secondary survey, a systematic clinical examination to identify injuries. It issupplemented by observations, imaging and other investigations. Further information isgathered at this time, especially the history of the events leading up to the injury and thepresence of any co-morbid factors.

History

History should be sought from the child, ambulance personnel, relatives and witnessesof the accident. Some history may have already been relayed from the ambulance controlprior to admission, though it will need to be confirmed as the initial information is often

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sketchy and incomplete. On arrival, ambulance staff should be able to provide a greatdeal of information, including details of the accident site and of the pre-hospital caregiven. Relatives should be able to give the child’s past medical history, allergies and anyregular medications. Pre-existing medical conditions such as haemophilia or osteogenesisimperfecta will affect how the child is treated. It is conventional to seek details of the timeof the last meal, but it is never wise to assume that the stomach is empty, as gastric stasis isa frequent consequence of major trauma. The child may withhold relevant information,such as glue sniffing or drug abuse, especially in the presence of parents. Alcohol ingestionis usually obvious despite earnest denial.

The mechanism of injury is useful in predicting potential injuries and setting the levelof concern. The information in Table 13.4 should be sought.

Table 13.4. Relevant history of injury mechanism

Road accident Other

Car occupant/cyclist/pedestrian Nature of accidentPosition in vehicle Objects involvedRestraints worn Height of fallHead protection Landing surfaceThrown from vehicle EnvironmentSpeed of impact TemperatureDamage to vehicle ContaminationOther victim’s injuries

Secondary survey

The secondary survey is a simple but thorough search for key anatomical features ofinjury. It is helpful to think in terms of:

• Surface (head to toe, front and back)• Orifice (mouth, nose, ears, orbits; rectum, genitals)• Cavity (chest, abdomen, pelvic cavity, retroperitoneum)• Extremity (upper limbs including shoulders; lower limbs including pelvic girdle)

In blunt trauma, the child is often brought to hospital on a spine board. It is generallyconvenient to perform the “anterior” part of the secondary survey first. The head re-straints and collar are then taken off, while an assistant holds the neck in line, to examinethe head, neck, face, ears, nose and mouth. The collar can then be reapplied and, withthe assistant still holding the neck in alignment, a log roll is performed to examine thespine, scapula, renal angles, sacro-iliac joints and other posterior structures. The spineboard is removed at this time, if it has not been earlier.

Occasionally, a full secondary survey is delayed. If immediate life-saving interventionsin the operating theatre are required, the secondary survey will have to be completedpost-operatively.

Throughout this stage of management, the vital signs and neurological status shouldbe continually reassessed, and any deterioration should lead to an immediate return tothe primary survey.

Head

Clinical examination• Inspect for bruising, haemorrhage, deformity and CSF leak from nose or ears• Palpate for lacerations, bruising and skull depressions

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• Perform otoscopy (for haemotympanum) and ophthalmoscopy (for retinalhaemorrhage)

• Perform a mini-neurological examination:pupillary reflexesconscious level – according to the Glasgow Coma Scale (see Chapter 16)motor function – reflexes, tone, power (noting symmetry)sensation

Investigations (as indicated)• CT scan of the head (see Chapter 16 for indications)• Skull radiographs (now rarely indicated)

Face

Clinical examination• Inspect for bruising, lacerations and deformity• Inspect the mouth inside and out• Palpate the bones for deformity and stability• Palpate the teeth for looseness

Investigations (as indicated)• Facial radiographs• CT scan

Neck

Clinical examinationCare should be taken not to move the cervical spine during the initial assess-

ment, when the spine has not been cleared. While the hard collar, blocks andstraps are removed, an assistant should maintain in-line cervical stabilisationthroughout.

• Inspect the front and back of the neck for bruising, lacerations and swelling• Palpate the cervical spine for tenderness, bruising, swelling and deformity• Palpate for surgical emphysema

Investigations (as indicated)Cervical spine imaging, according to a locally agreed protocol. In the UK,

this will be according to the NICE guidelines.

• Lateral view (with the arms pulled down)• Antero-posterior view• Odontoid (open mouth) view – omit if a CT scan of the head is separately

required; a CT of the upper cervical spine should then be done instead 559638• Oblique views (if the lower cervical spine is inadequately visualised on the

lateral view – rarely needed in children)• CT scan• MRI scan (especially if there are features of neurological deficit)

Flexion and extension views are controversial and should only be obtained in veryspecific circumstances.

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Chest

Clinical examination• Inspect for bruising, lacerations, deformity, and movement.• Inspect neck veins.• Feel for tracheal deviation.• Feel for tenderness, crepitus and paradoxical movement.• Percuss.• Listen for breath sounds and added sounds.• Listen for heart sounds.

Investigations (as indicated)• ECG• Further chest radiographs• Special radiographs as indicated (e.g. arch aortogram)• CT scan

Abdomen

Clinical examination• Observe for movement.• Inspect for bruising, lacerations and swelling.• Palpate for tenderness, rigidity and masses.• Auscultate for bowel sounds.

Rectal examination should only be performed if the result is going to alter managementof the child. In major blunt trauma, it is necessary (in males) to exclude evidence ofurethral disruption. It may be necessary to assess anal tone in spinal injuries or to excluderectal penetration by bony fragments in major pelvic fractures. Vaginal examinationsshould not be performed on children.

Investigations (as indicated)• Ultrasound• CT scan (double contrast)• Intravenous urogram

Diagnostic peritoneal lavage has been replaced by ultrasound and CTscanning.

258Pelvis

Clinical examination• Inspect for bruising, lacerations and deformity• Inspect the perineum• Inspect the external urethral meatus for blood• Press over the anterior iliac crests for tenderness and check for abnormal mobility –

do this once, to minimise the risk of dislodging clots and re-starting bleeding

Investigations (as indicated)• Ultrasound• Retrograde urethrography

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Spine

Clinical examinationExamination of the spine requires the child to be log-rolled (see Chapter 22).

• Observe for swelling and bruising• Palpate for tenderness, bruising, swelling and deformity• Assess motor and sensory function

Investigations (as indicated)• Radiographs• CT scans• MRI scans

Extremities

Clinical examination• Observe for bruising, swelling and deformity• Palpate for tenderness. Crepitus and abnormal movement may be found, but do not

elicit deliberately as these are painful. The pattern and degree of tenderness alonewill identify the need for X-ray

• Assess peripheral circulation – pulses and capillary return• Assess peripheral sensation – to touch. It is rarely useful to test pin prick in a frightened

child

Investigations (as indicated)• Radiographs• Angiograms

13.5 EMERGENCY TREATMENT

Emergency treatment represents the early response to key findings in the secondarysurvey and its adjunct investigations. While the interventions are less urgent than those inthe resuscitation phase, they will still need to be carried out promptly to minimise the riskof deterioration or unnecessary morbidity. The emergency treatment plan will includetreatments for any potentially life-threatening or limb-threatening injuries discoveredduring the secondary survey. If it does not put the child at undue risk, this plan may beextended to include definitive care of other (more minor) injuries discovered at the sametime.

Emergency treatments are discussed in more detail in subsequent chapters.

13.6 REASSESSMENT

The initial emphasis was on crude physiological assessment (ABCD) in the primarysurvey, followed by focusing on the anatomical evaluation of injuries in the secondarysurvey. From the time of the initial resuscitation, pulse rate, blood pressure, respiratoryrate and oxygen saturation should be measured and charted frequently (every 5 minutesinitially). Beyond these continuing observations, there is now a need to return to overall

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physiological control by considering the following systems in more detail, especially in acritically injured child:

• Respiration• Circulation• Nervous system• Metabolism• Host defence

Respiration (A and B)The airway should be re-checked. If intubated, is the endotracheal tube of an expected

length at the teeth (for the size of the child)? Are the breath sounds symmetrical? Couldthe tube have migrated into a main-stem bronchus?

Arterial blood gas analysis provides essential information in the child with serious head,chest or multiple injuries (arterial oxygen and CO2 tensions) or any child who has beenintubated. Inserting an arterial line facilitates repeated measurements.

Pulse oximetry readings should be displayed continuously. End-tidal CO2 monitoringis mandatory in the ventilated child. It shows that the breathing circuit is still connectedand that the endotracheal tube has not become dislodged. The end-tidal CO2 should notbe regarded as a reliable indicator of arterial CO2 tension, especially in a shocked child.Ventilation–perfusion mismatch causes it to under-represent the arterial level. It can beregarded as a crude indicator of pulmonary perfusion.

Circulation (C)This system comprises the three “haems”: haemodynamics, haemoglobin and haemostasis.In a child with serious injuries, the pulse rate and rhythm should be monitored elec-

trocardiographically. Non-invasive blood pressure readings are generally reliable, thoughin serious head injuries and multiple injuries, it is better to monitor on a beat-to-beatbasis using direct arterial measurements via an arterial line usually at the radius. This alsoallows estimation of the haemoglobin (or haematocrit) at hourly intervals to help detecton-going bleeding and determine the requirement for further transfusion. Base-deficit(or lactate) measurements indicate the adequacy of tissue perfusion, though it is still im-portant to reassess the child clinically. Other invasive techniques, such as central venouspressure monitoring, may be considered at this stage, but should only be undertaken byappropriately trained personnel.

In seriously injured children, the urinary output serves as an indicator of systemic perfu-sion and should be recorded hourly. It should be maintained at 1–2 ml/kg/hour, or higherif there has been a major crush injury or electrical burn with a high risk of myoglobinuria.If it is low, hypovolaemia is the likely cause, though other causes should be considered.If it is high, it may reflect excessive fluid therapy, but remember that diabetes insipiduscan occur within a few hours of a serious head injury. After major blood loss, fresh frozenplasma and platelets may be needed to correct coagulopathy following measurement ofclotting times and platelet count. Remember that hypothermia affects clotting.

Nervous system (D)Pupil size and reactivity and the Glasgow Coma Score should be checked and recorded

every 15 minutes initially. Any deterioration should prompt the need to discuss the casewith a neurosurgeon or consider a CT scan (or repeat one). Intracranial pressure (ICP)monitoring is an important means of identifying life-threatening rises in pressure. Inconjunction with invasive blood pressure measurements, it provides a means of trackingcerebral perfusion pressure. ICP monitoring can be established in the operating theatre orthe intensive care unit. Its use should be confined to hospitals with appropriately skilledpersonnel, but the importance of cerebral perfusion pressure should be understood byall those who deal with critical head injuries in children.

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Metabolism (Electrolytes, Fluid balance, Gut and Hormones)This system refers to biochemical processes and includes renal, hepatic, gastro-

intestinal and endocrine problems. Glucose control (Don’t Ever Forget Glucose, es-pecially in very young children and in adolescents who have taken alcohol) and urineoutput are key issues (see Circulation above).

Host defence (Injury, Infection, Immunity, Intoxication) Host defence represents the in-teraction between the body as a whole and external influences. As such, it encompassesinjury (including injury from poor positioning and thermal injury), infection (includ-ing wound care), immunity (including need for tetanus prophylaxis) and intoxication(including alcohol and drugs that may be present in the circulation)

Thermal injury is an important concern: hypothermia hinders blood clotting and pre-disposes to infection, while fever must be avoided in the severely head injured child.Wound care, antibiotic prophylaxis for open fractures, and checking that tetanus immu-nisations are up to date (has the child been immunised at all?) are all considered at thisstage, as is careful positioning to avoid problems such as pressure injury from a badlyfitting collar.

The “tertiary survey”In addition to physiological system control, it is essential for transport escorts, in-

tensive care staff or receiving-unit medical staff, who may take over care at this stage,to re-examine the child and review the investigations (especially the imaging) from ananatomical viewpoint to seek out any missed injuries.

Returning to the primary surveyAny sudden deterioration in the child’s condition should trigger an immediate reassess-

ment of the airway, breathing, circulation and disability so resuscitation can once morebe undertaken.

In the face of a serious deterioration, return to the primary survey

13.7 CONTINUING STABILISATION

Continuing stabilisation and definitive care constitute the final part of the structuredapproach to trauma care. It goes hand in hand with the detailed physiological systemcontrol outlined above and is often carried out by teams other than those which initiallyreceived the patient. Good note taking and appropriate, timely referral are essential iftime is not to be lost. If definitive care is to be undertaken in a specialist centre thentransfer may be necessary at this stage.

Note takingThe structured approach discussed in this chapter can provide a framework for the

writing of notes. It is recommended that these should be set out as shown in Table 13.5.

ReferralMany teams may be involved in the definitive care of a seriously injured child. It is

essential that referrals are made appropriately, clearly and early. Guidance about whichchildren to refer to which teams is given in subsequent chapters.

TransferInjured children may require transfer either within the hospital or to another centre. In

either case thorough preparation of equipment, patient, and documentation is essential.Secondary transfer should not be undertaken until all life-threatening problems havebeen addressed, and the child is stable. Occasionally, transfer is the means of delivering

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life-saving care (e.g. an acute extradural haematoma) and a careful balance must beachieved between delaying such care and setting off with an inadequately stabilised child.Transport of children is discussed in more detail in Chapter 24.

Table 13.5. Template for note taking

History• Mechanism of injury

• Past history

Primary survey and resuscitative interventions

• A

• B

• C

• D

Secondary survey and emergency treatment of injuries

• Head

• Face

• Neck

• Chest

• Abdomen

• Pelvis

• Spine

• Extremities

Continuing stabilization

• Respiration

• Circulation

• Nervous system

• Metabolism

• Host defence

13.8 SUMMARY

The structured approach to initial assessment and management allows the clinician to carefor the seriously injured child in a logical, effective way.

Assessment of vital functions (airway, breathing, circulation and disability) is carried outfirst and resuscitation for any problems found is instituted immediately:

• Primary survey• Resuscitation

A complete head-to-toe examination is then carried out, adjunct investigations areperformed and emergency treatment is instituted:

• Secondary survey and the search for key features• Emergency treatment

Finally, a detailed review is undertaken and definitive care is provided:

• Reassessment and physiological system control• Continuing stabilisation and definitive care

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CHAPTER

14The child with chest injury

LEARNING OBJECTIVES


• which chest injuries post an immediate threat to life and those that are discovered later• how to manage these injuries

14.1 INTRODUCTION

Establishing a secure airway is the first priority in the resuscitation of a child. Thenext most important consideration is the assessment of breathing. Respiratory problemsmay result from direct chest injury or may reflect the effect of other anatomical injurieson breathing (especially tachypnoea from shock and respiratory irregularity from headinjury). General consequences of severe trauma, such as gastric dilatation or pulmonaryaspiration after vomiting or regurgitation, may further compromise respiratory function.

Children have relatively elastic tissues. Substantial amounts of kinetic energy may betransferred through a child’s chest wall to deep structures with little or no external signof injury and without rib fractures. A lack of evident rib fractures on the chest radio-graph does not exclude major thoracic visceral disruption; conversely, the presence ofrib fractures indicates high-energy transfer. Children have relatively little respiratory re-serve. Their high metabolic rate and small functional residual capacity allow them tode-saturate more rapidly – when their oxygen supply is curtailed. Their horizontal ribsand underdeveloped musculature make them tolerate chest wall disruption badly. Flailchest, for example, is poorly tolerated.

The risk of iatrogenic chest problems must be appreciated. The child’s relativelyshort trachea allows the endotracheal tube to become easily displaced into a main-stembronchus or into the oesophagus. Mask ventilation can cause inadvertent gastric dis-tension and overinflation of the lungs can result in a pneumothorax (especially afterintubation, if the endotracheal tube has migrated beyond the carina). If a traumatic

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THE CHILD WITH CHEST INJURY

pneumothorax already exists, ventilation will cause it to increase in size and turn it intoa tension pneumothorax.

Thoracic injuries must be considered in all children who suffer major trauma. Somemay be life-threatening and require immediate resuscitative therapy during the primarysurvey and resuscitation. Others may be discovered during the secondary survey (and itsassociated investigations) and be dealt with by emergency treatment. Some situations willneed prompt, specialist surgical intervention, but most chest injuries can be managed inthe first hour using general advanced life support skills. Practical procedures are describedin detail in Chapter 22. During subsequent detailed review, attention will be re-directedto the chest to maintain respiratory control and to search for missed injuries.

14.2 INJURIES POSING AN IMMEDIATE THREAT TO LIFE

The following conditions are life-threatening. They should be identified during theprimary survey and treated immediately. They do not need to be confirmed by adjunctinvestigations.

Tension pneumothorax

This is a relatively common life-threatening emergency that can be rapidly fatal if nottreated promptly. Yet treatment is simple and effective.

Air accumulates under pressure in the pleural space. This pushes the mediastinumacross the chest and kinks the great vessels, compromising venous return to the heartand reducing cardiac output. The diagnosis is a clinical one. A radiograph that shows atension pneumothorax should never have been taken.

Signs• The child will be hypoxic and may be shocked.• Unless the child is deeply unconscious, there will be signs of respiratory distress.• There will be decreased air entry and hyper-resonance to percussion on the side of

the pneumothorax.• Distended neck veins may be apparent in thin children.• The trachea deviates away from the side of the pneumothorax, though this is not

always easy to identify clinically.

Resuscitation• High-flow oxygen should be given through a reservoir mask.• Immediate needle thoracocentesis should be performed to relieve the tension.• A chest drain should be inserted urgently to prevent recurrence.

Air may be forced into the pneumothorax by positive pressure ventilation. If the childis ventilated, a simple pneumothorax is very likely to progress rapidly into a tensionpneumothorax.

Massive haemothorax

A massive haemothorax will be identified during the B (breathing) stage of the primarysurvey, though it is even more of a circulatory problem than a respiratory one.

Blood accumulates in the pleural space. This may result from damage to blood ves-sels (arteries or veins from the pulmonary or systemic vessels) within the lung, the me-diastinum or the chest wall (or from a combination). The hemi-thorax can contain a

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substantial proportion of a child’s blood volume, causing haemorrhagic shock as well aslocal pressure effects.

Signs• The child will show signs of shock and may be hypoxic despite added oxygen.• There will be decreased chest movement, decreased air entry and dullness to percus-

sion on the side of the haemothorax.

Resuscitation• High-flow oxygen should be given through a reservoir mask.• Intravenous access should be established and volume replacement commenced.• A relatively large chest drain should be inserted urgently.

Open pneumothorax

There is a penetrating wound in the chest wall with associated pneumothorax. Thewound may be obvious, but if it is on the child’s back, it will not be seen unless activelylooked for. If the diameter of the defect is greater than about one third of the diameterof the trachea, air will preferentially enter the pleural space via the defect rather than bedrawn into the lungs via the trachea when the child takes a breath. It is then referred toas a sucking chest wound.

Signs• Air may be heard sucking and blowing through the wound.• The other signs of pneumothorax will be present.• There may be an associated haemothorax (i.e. a haemo-pneumothorax).

Resuscitation• High-flow oxygen should be given through a reservoir mask.• The conventional immediate treatment for a sucking wound is to cover it with an

occlusive dressing that is taped down on three sides. This is intended to act as aflap valve, allowing air to escape from the un-taped side during expiration. A morereliable solution is to use an Asherman chest seal, provided that the defect is notlarger than the base of this device. The Asherman seal consists of an adhesive base,similar to that on a colostomy or ileostomy stoma bag, and a short, flexible pipethat protrudes outwards, acting as a one-way valve. Alternatively, the wound may beoccluded completely and a separate chest drain inserted.

• Whichever immediate treatment option is undertaken, a chest drain will be requiredas part of emergency treatment. It should not be inserted through the defect itself asthis may spread contamination and re-start bleeding.

Flail chest

If a number of adjacent ribs are fractured in two or more places, a segment of the chestwall may be free-floating, moving inwards with inspiration and outwards with expiration(paradoxical movement). Such a flail segment is rare in children because of the elasticity ofthe child’s chest wall. When it does occur, we expect major force to have been involved andserious underlying lung (and mediastinal) injury should be anticipated. If the reportedmechanism does not involve significant force, suspect an erroneous history (remembernon-accidental injury) or, more rarely, osteogenesis imperfecta.

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Flail segments may not be noticed on initial examination for three separate reasons:severe pain on breathing will cause the child to splint the chest wall (this may be unmaskedby analgesia); a child who has already been intubated will be receiving positive pressureventilation, which moves the floating segment in unison with the rest of the chest wall;the flail segment may be posterior and unnoticed if the back of the chest is not examinedcarefully. Rib fractures do not always show up well on the chest radiograph, so thatimaging should not be relied upon in making the diagnosis.

Signs• The child may be hypoxic despite added oxygen and in considerable pain.• Paradoxical chest movement is characteristic, but may not be obvious as indicated

above. A high index of suspicion should be retained.• Other evidence of rib fractures (e.g. crepitus on palpation) may be seen.

Resuscitation• High-flow oxygen should be given through a reservoir mask.• Tracheal intubation and ventilation should be considered immediately, if the child

is compromised. If ventilation is necessary, it may need to be continued for up to2 weeks before the flail segment becomes “sticky” and stabilises. On the other hand,minor cases may do well simply with good pain relief and with oxygen by face mask.Nasal or facial CPAP (continuous positive airway pressure), combined with painrelief, may be effective in intermediate cases.

• Pain relief should be given using titrated intravenous opioids in the first instance.Local or regional neural blockade avoids the respiratory depressant effects of opioidsand should be considered. However, intercostal blocks and epidural catheters arehazardous in the uncooperative patient and may need sedation to achieve safety – therisks and benefits of the decision must be carefully considered. Epidural analgesiain children should be carried out by an expert and only after injury to the spine hasbeen ruled out formally.

Cardiac tamponade

Cardiac tamponade can occur after both penetrating and blunt injury, though it ismuch more common after penetrating trauma. The blood that accumulates in the fibrouspericardial sac reduces the volume available for cardiac filling during diastole. As moreblood accumulates, the cardiac output is progressively reduced.

Signs• The child will be in shock.• The heart sounds may be muffled.• The neck veins may be distended; though this will not be apparent if the child is also

hypovolaemic.

Resuscitation• High-flow oxygen should be given through a reservoir mask.• Intravenous access should be established and volume replacement commenced. This

may temporarily increase cardiac filling.• Emergency needle pericardiocentesis should be performed. Removing even a small

volume of fluid from within the pericardial sac can dramatically increase cardiacoutput.

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• Emergency thoracotomy will generally be required. A cardiothoracic surgeon (or asurrogate general or paediatric surgeon, in centres without cardiothoracic surgery)should be involved as soon as the diagnosis is suspected.

14.3 SERIOUS INJURIES DISCOVERED LATER

These conditions will generally be discovered during the secondary survey and itsassociated investigations, but delayed presentation and masking by other injuries canoccur, demanding continual vigilance into the detailed review phase and beyond.

Pulmonary contusion

Children have a high incidence of pulmonary contusion. Energy is readily transmittedto the lungs, as the ribs are elastic and do not easily dissipate energy by fracturing. Ifthe ribs do fracture, the degree of force is such that pulmonary contusion is likely too.Pulmonary contusion usually results from blunt trauma, though the shock wave froma high-speed bullet can cause it too. At the microscopic level, pulmonary contusionmanifests itself as oedema and interstitial and intra-alveolar haemorrhage.

Clinical features include hypoxia, dyspnoea and haemoptysis, but are not specific. Ini-tially, there may be little to show on the chest radiograph, though an area of non-segmentalopacification may be clearly visible from the outset. It is important to realise that theclinical features and radiological findings may progress over the next few hours. The ap-pearance on the plain chest film is not specific and may be confused with aspiration, othercauses of consolidation/collapse, and even with haemothorax (on a supine film). A CTscan, when indicated for other reasons, helps to distinguish pulmonary contusion fromother diagnoses, but it is not warranted for this purpose alone. There are simpler means ofdemonstrating a haemothorax, for example, clinical examination and bedside ultrasound.

Treatment consists of the administration of high-flow oxygen and artificial ventilation ifnecessary. Uncomplicated contusion will largely resolve within the next 36 hours. Physio-therapy plays an important role in reducing the risk of pulmonary collapse and secondaryinfection.

Tracheal and bronchial rupture

Tracheo-bronchial disruption has a high mortality and requires prompt referral to a spe-cialist cardiothoracic surgeon. It presents as a pneumothorax or haemo-pneumothorax,typically with a persistent (and often vigorous) air leak after the insertion of a chest drain.Subcutaneous emphysema is frequently present.

Emergency care may involve the insertion of more than one chest drain (with suctionapplied). When intubation is required, the passage of the endotracheal tube may furtherdisrupt a tracheal tear. An expert in airway care must be involved. When mechanical ven-tilation is needed, it is important to limit the pressure applied to the airway. This requiresspecialist ventilation techniques. Unless the leak is small enough to seal spontaneously,definitive surgical repair will be needed.

Disruption of great vessels

This is usually due to a high-speed motor vehicle crash and is generally fatal at thescene. A child with aortic rupture who survives to get to hospital has a tear that hastamponaded itself within an intact adventitial (outermost) layer. The commonest site ofrupture is at the insertion of the ligamentum arteriosum (the residual ligament from theductus arteriosus that connected the pulmonary and systemic circulations in utero), close

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to the origin of the left subclavian artery – this structure tethers the otherwise mobileaorta during severe deceleration.

The patient may be shocked and peripheral pulses may be poorly palpable. On theother hand, if the leak has (temporarily) sealed itself with little blood loss, interferencewith the baroreceptors in the aortic arch can lead to relative hypertension. Symptoms aregenerally non-specific. The diagnosis should be suspected if the mediastinum is widenedor has an abnormal profile on chest radiograph. Remember that a supine antero-posteriorfilm will increase the apparent width of the mediastinum and that the thymus is shownas a prominent mediastinal mass in small children. Sternal and spinal fractures can alsocause apparent mediastinal widening.

Arch angiography remains the cornerstone of definitive diagnosis, though multi-sliceCT promises to serve as an alternative. It is important to avoid surges in blood pressurethat could precipitate re-bleeding. Definitive repair requires cardiothoracic surgery.

Ruptured diaphragm

Diaphragmatic rupture is a rare blunt injury in children. It is generally thought tobe more common on the left side, though some recent studies have questioned this.Penetrating trauma may also involve the diaphragm, usually in the form of knife stabwounds entering the chest or abdomen. Unless other structures are damaged at thesame time, such knife wounds may be asymptomatic, only to present many years later asdiaphragmatic hernias.

The child with a ruptured diaphragm may be hypoxic owing to diaphragmatic dys-function and to pulmonary compression from a herniated viscus. Shock may result frommediastinal distortion that affects venous return or to haemorrhage from adjacent struc-tures. The plain chest radiograph may show an apparently raised hemi-diaphragm orevidence of abdominal contents within the chest, e.g. bowel shadowing or a nasogastrictube. Surgical referral should be made. Most ruptures can be repaired from the abdomen,without the need for thoracotomy.

14.4 OTHER INJURIES

Simple pneumothorax

Air is present in the pleural space with some degree of lung collapse, but it is not yetunder pressure (tension). Signs of hypoxia with decreased chest wall movement, dimin-ished breath sounds and normal or increased resonance to percussion on the side of thepneumothorax may be found, but the signs may be subtle or barely perceptible comparedwith tension pneumothorax. The diagnosis is usually made on the plain chest radiographas a lung edge with no lung markings beyond it. However, an anterior pneumothorax isoften difficult to recognise. The increasing use of thoracic CT scanning in severe blunttrauma is picking up injuries that may have been missed on plain films.

As traumatic pneumothoraces do not usually resolve spontaneously, a chest drainshould be inserted as a planned procedure, even if the child is relatively asymptomatic. Ifthe patient needs to be ventilated, a chest drain must be inserted as a matter of urgencyto avoid a simple pneumothorax developing into a tension pneumothorax.

14.5 PRACTICAL PROCEDURES

Needle thoracocentesis, chest drain insertion and pericardiocentesis are described inChapter 22.

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14.6 REFERRAL

A competent clinician, trained in advanced life support skills, can provide immediatemanagement for most of the life-threatening injuries discovered during the primary sur-vey. Emergency cardiothoracic surgical involvement will be needed if cardiac tamponadeis diagnosed. Other serious injuries discovered during the secondary survey will needcardiothoracic referral. The major reasons for referral are shown in the box.

Indications for cardiothoracic surgical referral

Continuing massive air leak after chest drain insertionContinuing haemorrhage after chest drain insertionCardiac tamponadeDisruption of the great vessels

Patients who require ventilation as part of the treatment of their chest injury (such asthose with significant pulmonary contusion) will need transfer to a paediatric intensivecare unit. Critical care management will be needed for transfer and as part of continuingstabilisation in general. Appropriate medical and nursing referrals should be made.

14.7 CONTINUING STABILISATION

In serious chest injuries, the oxygen saturation and pulse rate must be continuouslymonitored through to the detailed review stage and beyond. The respiratory rate andblood pressure need to be checked frequently. Chest drains must be well secured. Arterialblood gas monitoring is invaluable in severe cases for confirming adequate oxygenationand adjusting carbon dioxide tensions (particularly if there is a concomitant head injury).Remember that many conditions worsen with time, especially pulmonary contusion. Anarterial line will also allow haemoglobin, base deficit and lactate to be tracked.

Continual clinical review is required. Changes in the respiratory pattern and in theapparent degree of illness, in conjunction with trends in the monitoring data, will alertthe vigilant clinician to new problems and missed injuries.

14.8 SUMMARY

A clear airway must be established before attending to chest injuries.All children should receive high-concentration oxygen through a reservoir mask (if breathing

spontaneously), through a mask and self-inflating bag with an oxygen reservoir (if receivingassisted ventilation) or via a ventilator (if intubated).

Chest injuries are life-threatening, but most can be managed successfully by any cliniciancapable of performing the following techniques:

• Needle thoracocentesis• Chest drain insertion• Intubation and ventilation• Fluid replacement• Pericardiocentesis

Cardiothoracic surgical referral may be necessary once immediate management oflife-threatening conditions has been carried out.

Intensive care involvement will be needed for the continuing stabilisation of severe cases.

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CHAPTER

15The child with abdominal injury

LEARNING OBJECTIVES


• how to assess the injured abdomen• the options for definitive care

15.1 INTRODUCTION

Blunt trauma causes the majority of abdominal injuries in children. Most occur becauseof accidents on the roads, although a significant number happen during recreationalactivities. A high index of suspicion is necessary if some injuries are not to be missed.

The abdominal contents are very susceptible to injury in children for a number ofreasons. The abdominal wall is thin and offers relatively little protection. The diaphragmis more horizontal than in adults, causing the liver and spleen to lie lower and moreanteriorly. Furthermore, the ribs, being very elastic, offer less protection to these or-gans. Finally, the bladder is intra-abdominal, rather than pelvic, and is therefore moreexposed when full. Respiratory compromise can complicate abdominal injury because di-aphragmatic irritation or splinting may occur – reducing the use of the diaphragm duringbreathing.

15.2 HISTORY

A precise history of the mechanism of injury may help in diagnosis. Rapid deceler-ation, such as experienced during road accidents, causes abdominal compression. Thesolid organs (liver, spleen and kidneys) are at risk from such forces, and the duodenummay develop a large haematoma or may rupture at the duodenojejunal flexure. Directblows, such as those caused by punching or impact with bicycle handlebars, readily

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THE CHILD WITH ABDOMINAL INJURY

injure underlying solid organs. Injury to the pancreas or duodenum is a particular fea-ture of handlebar injury. Finally, straddling injuries associated with a significant perinealhaematoma or urethral bleeding suggest urethral injury.

15.3 ASSESSMENT OF THE INJURED ABDOMEN

Initial assessment and management must be directed to the care of the airway, breathingand circulation as discussed in Chapter 13.

Examination

If shock is not amenable to fluid replacement during the primary survey and resuscita-tion, and no obvious site of haemorrhage exists, then intra-abdominal injury may be thecause of blood loss. The abdomen should be assessed urgently to establish whether earlyoperative intervention is necessary. In other circumstances, the abdominal examinationis carried out during the secondary survey.

The abdomen should be inspected for bruising, lacerations, and penetrating wounds.Although major intra-abdominal injury can occur without obvious external signs, visiblebruising increases the likelihood of significant injury. A high index of suspicion andfrequent, repeated clinical assessment is appropriate in such cases. The external urethralmeatus should be examined for blood.

Gentle palpation should be carried out. This will reveal areas of tenderness and rigidity.Care should be taken not to hurt the child because his or her continued cooperation isimportant during the repeated examinations that form an important part of management.

Rectal and vaginal examination are rarely required in the injured child. Internal digitalexamination therefore should be limited to the surgeon who has overall responsibility forthe child.

Aids to assessment

Both gastric and urinary bladder drainage may help the assessment by decompressingthe abdomen.

Gastric drainageAir swallowing during crying with consequent acute gastric dilatation is common in

children. Early passage of a gastric tube of an appropriate size is essential. The tube shouldbe aspirated regularly and left on free drainage at other times. A massively distendedstomach can mimic intra-abdominal pathology needing laparotomy, and cause seriousdiaphragm splintage with consequent respiratory compromise.

Urinary catheterisationCatheterisation of a child should only be performed if the child cannot pass urine

spontaneously, or if continuous accurate output measurement is required. The route(urethral or suprapubic) will depend on factors related to signs of urethral, bladder, orintra-abdominal or pelvic injury (such as blood at the external meatus, or bruising in thescrotum or perineum). If a boy requires urethral catheterisation, urethral damage mustbe excluded first. The catheter should be silastic and as small as possible in order toreduce the risk of subsequent urethral stricture formation.

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Investigations

Blood tests Intravenous access will have already been secured during the primary surveyand resuscitation, and at that time blood will have been drawn for baseline blood counts,urea and electrolytes, and cross-matching. An amylase estimation should be requestedand can usually be performed on the sample sent for urea and electrolytes. Arterialblood gases should be sent if indicated. Repeated monitoring of blood parameters maybe appropriate in some patients.

RadiographsViews of the chest and pelvis will have been obtained earlier. Neither a normal chest

radiograph nor a normal pelvic radiograph excludes abdominal injury. Subsequent plainabdominal radiography may be helpful to look for gastric tube position, abdominal gasdistribution and free gas, in cases of suspected small bowel injury, where diagnosis isoften delayed and notoriously difficult. Blood at the external urethral meatus may requireinvestigation using retrograde urethrography.

Computed tomographyA single-contrast CT scan of the abdomen is the radiological investigation of choice

in children. CT will confirm renal perfusion and identify solid organ injury. While freeintraperitoneal air is pathognomonic of a perforated viscus, the presence of significantfree fluid in the absence of solid organ injury heightens suspicion of a bowel or, rarely,bladder injury.

UltrasoundThis may be readily available and give early information on free fluid and

lacerations in the liver, spleen, or kidneys. A normal ultrasound early on doesnot exclude injury. 234

258Diagnostic peritoneal lavage

The use of this investigation in children has been rendered virtually obsolete in thetrauma setting by modern imaging modalities. The presence of intraperitoneal bloodper se is not an indication for laparotomy. Once lavage fluid has been introduced, theperitoneum shows signs of irritation for up to 48 hours, and hence reduces the possibilityof accurate repeated assessment. The technique is nevertheless described in Chapter 22,as peritoneal lavage may be used to re-warm the hypothermic “near-drowned” patient,and access to the peritoneum may provide a temporary dialysis route in children withacute renal failure.

15.4 DEFINITIVE CARE

Non-operative management

Until the early 1980s, both adult and paediatric patients with haemoperitoneum wouldundergo laparotomy. Damage to the spleen or liver would result in splenectomy or partialhepatectomy, respectively. It has since been shown that the haemorrhage is often self-limiting, and many of these operations can therefore be avoided. As well as avoiding themorbidity associated with laparotomy, this approach also reduces the number of childrenat risk of overwhelming, potentially fatal sepsis following splenectomy.

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For non-operative management to be undertaken the following are essential:

• Adequate observation and frequent monitoring• Precise fluid management• The immediate availability of a surgeon trained to operate on the paediatric abdomen

(should this become necessary)

The need for clotting factors such as platelets, fresh frozen plasma or cryoprecipitatemust be monitored. Vigorous and early management of coagulopathy is indicated in orderto improve clotting and hence achieve haemostasis.

Indications for operative intervention

Children whose circulation is not stable after replacement of 40 ml/kg of fluid areprobably bleeding into the thoracic or abdominal cavities. In the absence of clear thoracicbleeding, urgent laparotomy may be necessary. All children with penetrating abdominalinjuries and those with definite signs of bowel perforation will require urgent laparotomy.

A non-functioning kidney, as demonstrated on contrast studies, may have sufferedrenal pedicle injury. Exploration will not salvage the kidney since the warm ischaemiatime is only 45–60 minutes.

Indications for operative intervention following abdominal injury

LaparotomyRefractory shock with evidence of solid organ injury on CT scanPenetrating injuriesSigns of bowel perforation

It is essential that the surgeon performing these procedures is competent to deal withpaediatric trauma and can perform any reconstructive surgery that may be required.

15.5 SUMMARY

• The assessment and management of airway, breathing, and circulation must be carriedout first. Abdominal assessment is only carried out at this stage if shock is refractory.

• Abdominal assessment consists of careful observation and gentle, repeated palpation.Gastric and urinary drainage aid this assessment.

• Abdominal CT scan is the investigation of choice.• The majority of children with solid organ injury may be managed non-operatively. Urgent

operative intervention is required when children with solid organ injury have persistinghaemodynamic instability despite adequate blood replacement, or for penetratingabdominal injury, or signs of a perforated viscus.

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CHAPTER

16The child with trauma to the head

LEARNING OBJECTIVES


• the structured approach in the context of the child with a head injury

16.1 INTRODUCTION

Epidemiology

Head injury is the most common single cause of trauma death in children aged1–15 years. It accounts for 40% of deaths from injury and many (but largely unstud-ied) cases of permanent brain injury, probably up to two or even three thousand childrenper year in the UK alone. Head injury deaths in children most commonly result fromroad traffic accidents – pedestrians are the most vulnerable, followed by cyclists, and thenpassengers in vehicles. Falls are the second most common cause of fatal head injuries. Ininfancy, the most common cause is child abuse.

Pathophysiology

Primary brain injury is the damage incurred as a direct consequence of the impact.Neurones, axonal sheaths and blood vessels may be physically disrupted at the momentof impact, often with irreversible cell damage. Secondary brain injury represents furtherdamage to central nervous system tissue by secondary insults, and adverse physiologicalevents that can occur minutes, hours or days after the initial injury. Such insults includehypotension, hypoxia, intracranial hypertension and seizures. A key aim of head injurymanagement is to prevent or minimise secondary brain injury.

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THE CHILD WITH TRAUMA TO THE HEAD

Primary damage

• Injury to neural tissue:❝ Focal cerebral contusions and lacerations (direct impact and contrecoup)❝ Diffuse axonal injury (shearing injury)

• Injury to intracranial blood vessels:❝ Extradural haematoma (especially middle meningeal artery)

53❝ Subdural haematoma (especially dural bridging veins)❝ Intracerebral haematoma❝ Subarachnoid haemorrhage

Injury to the cranium and to the dural sac may be associated with the above neural andvascular injuries. Open skull fractures, where there is a breach in the skull (vault or base)and in the dural membrane, allow brain tissue to come into contact with the externalenvironment (directly or via the sinuses), with consequent risk of infection.

Secondary damage

This may result from either the direct secondary effects of cerebral injury or from thecerebral consequences of associated injuries and stress.

• Ischaemia from poor cerebral perfusion secondary to raised intracranial pressure❝ Expanding intracranial haematoma (exacerbated by coagulopathy)❝ Cerebral swelling/oedema

• Ischaemia secondary to hypotension and anaemia❝ Haemorrhage with hypovolaemia or dilutional anaemia❝ Other causes of hypotension (spinal cord injury, drug-induced vasodilatation or

later sepsis)• Hypoxia

❝ Airway obstruction❝ Inadequate ventilation (loss of respiratory drive or mechanical disruption of chest

wall or diaphragm)❝ Shunt from pulmonary contusion or later respiratory failure

• Hypoglycaemia and hyperglycaemia• Fever• Convulsions• Later infection

Hypothermia may have a protective effect on neural tissue, but at temperatures below35◦C it affects platelet function and may exacerbate bleeding.

Raised intracranial pressure

Once sutures have closed at 12–18 months of age, the child’s cranial cavity behaves likean adult’s with a fixed volume. If cerebral oedema worsens or if intracranial haematomasincrease in size, the pressure within the cranium increases. Initial compensatory mecha-nisms include diminution in the volume of cerebrospinal fluid and venous blood withinthe cranial cavity. When these mechanisms fail, intracranial pressure rises, compromisingcerebral perfusion:

Cerebral perfusion pressure = Mean arterial pressure − Mean intracranial pressure

Normal cerebral blood flow is 50 ml of blood per 100 g brain tissue per minute. A fallin cerebral perfusion pressure decreases cerebral blood flow. A flow of below 20 ml per100 g of brain tissue per minute will produce ischaemia. This in turn increases cerebral

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oedema, causing a further rise in intracranial pressure. A cerebral blood flow of below10 ml/100 g/min leads to electrical dysfunction of the neurones and loss of intracellularhomoeostasis.

A generalised increase of intracranial pressure in the supra-tentorial compartment ini-tially causes trans-tentorial (uncal) herniation, leading to trans-foraminal (central) her-niation and death. In uncal herniation, the third nerve is nipped against the free borderof the tentorium, causing ipsilateral pupillary dilatation secondary to loss of parasympa-thetic constrictor tone to the ciliary muscles. In central herniation, also known as coning,the cerebellar tonsils are forced into the foramen magnum.

In childhood, the most common cause of raised intracranial pressure following headinjury is cerebral oedema. Children are especially prone to this problem. They may,of course, also have expanding extradural, subdural, or intracerebral haematomas thatrequire prompt surgical treatment.

Depending on the aetiology of the raised intracranial pressure, treatment is eitheraimed at preventing it rising further, or removing its cause (by surgical evacuation ofhaematomas).

There are special considerations in infants with head injuries. Unfused sutures allowthe cranial volume to increase initially. Large extradural or subdural bleeds may occurbefore neurological signs or symptoms develop. Such infants may show a significant fall inhaemoglobin concentration. In addition, the infant’s vascular scalp may bleed profusely,causing shock. In children over 1 year with shock associated with head injury, seriousextracranial injury should be sought as the cause of the shock.

16.2 TRIAGE

Head injuries vary from the trivial to the fatal. Triage is necessary in order to give moreseriously injured patients a higher priority. Factors indicating a potentially serious injuryare shown in the box.

Factors indicating a potentially serious injury

• History of substantial trauma such as involvement in a road traffic accident or a fall froma height

• A history of loss of consciousness• Children who are not fully conscious and responsive• Any child with obvious neurological signs/symptoms such as headache, convulsions, or

limb weakness• Evidence of penetrating injury

16.3 PRIMARY SURVEY

The first priority is to assess and stabilise the airway, breathing and circulation asdiscussed in Chapter 13. Head injury may be associated with cervical spine injury, andneck immobilisation must be achieved as previously described.

Pupil size and reactivity should be examined and a rapid assessment of conscious levelshould be made. In the first place the AVPU classification may be used.

A AlertV Responds to VoiceP Responds only to PainU Unresponsive to all stimuli

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In a time-limited situation, it is not essential to work out the numerical Glasgow Comascore immediately, though the EMV (eye, motor, verbal) responses will have been noted.But it is important to note the response to voice or pain (if not responding to voice) inmore detail before proceeding with neurological resuscitation, using the Glasgow ComaScale. The assessment serves as a baseline for continuing care and as a key indicator ofthe need to intervene immediately.

16.4 RESUSCITATION

Immediate control of the airway, breathing and circulation should be carried out inresponse to the primary survey findings, according to the general approach in Chapter13. This support will help to prevent secondary cerebral damage caused by hypoxia andshock arising from both the head injury and other coexistent injuries.

During the primary survey assessment of disability, evidence of decompen-sating head injury will have been recognised. In the severely injured child, extrainformation from blood gas sampling will be obtained during the resuscita-tion phase or ongoing monitoring. On the basis of simple clinical evaluation,supported when necessary by blood gas data, a set of indications for immediate intubationand ventilation in severe head injury have been recommended (in the UK, the NationalInstitute for Clinical Excellence (NICE) has produced evidence-based guidelines fortreatment, imaging and referral):

• Coma – not obeying commands, not speaking, not eye opening (equivalent to a GCS <8)• Loss of protective laryngeal reflexes• Ventilatory insufficiency as judged by blood gases: hypoxaemia (PaO2 < 9 kPa on air or

<13 kPa with added oxygen) or hypercarbia (PaCO2 > 6 kPa)• Spontaneous hyperventilation (causing PaCO2 < 3·5 kPa)• Respiratory irregularity

16.5 SECONDARY SURVEY AND LOOKINGFOR KEY FEATURES

History

The history of the injury and the child’s course since the injury occurredshould be established from bystanders and pre-hospital personnel. Other his-tory should be obtained from parents or carers.

230Examination

The head should be carefully observed and palpated for bruises and lacerations to thescalp and for evidence of depressed skull fracture. Look for evidence of basal skull fracture,such as blood or cerebrospinal fluid (CSF) from the nose or ear, haemotympanum, pandaeyes or Battle’s sign (bruising behind the ear over the mastoid process).

The conscious level should be reassessed using the modified Glasgow Coma Scale ifthe child is less than 4 years old, or the standard scale in older children. These scales areshown in Table 16.1. It should be noted that the coma scales reflect the degree of braindysfunction at the time of the examination. Assessment should be repeated frequently –every few minutes if the level is changing. Communication with the child’s caregivers isrequired to establish the child’s best usual verbal response. A “grimace” alternative toverbal responses should be used in pre-verbal or intubated patients (Table 16.2).

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Table 16.1. Glasgow Coma Scale and Children’s Coma Scale

Glasgow Coma Scale (4–15 years) Child’s Glasgow Coma Scale (<4 years)

Response Score Response Score

Eye opening Eye openingSpontaneously 4 Spontaneously 4To verbal stimuli 3 To verbal stimuli 3To pain 2 To pain 2No response to pain 1 No response to pain 1Best motor response Best motor responseObeys verbal command 6 Obeys verbal command or performs

normal spontaneous movements6

Localises to pain 5 Localises to pain or withdraws to touch 5Withdraws from pain 4 Withdraws from pain 4Abnormal flexion to pain

(decorticate)3 Abnormal flexion to pain (decorticate) 3

Abnormal extension to pain(decerebrate)

2 Abnormal extension to pain (decerebrate) 2

No response to pain 1 No response to pain 1Best verbal response Best verbal responseOrientated and converses 5 Alert; babbles, coos, words or sentences

to usual ability5

Disorientated andconverses

4 Less than usual ability and/orspontaneous irritable cry

4

Inappropriate words 3 Cries inappropriately 3Incomprehensible sounds 2 Occasionally whimpers and/or moans 2No response to pain 1 No response to pain 1

Table 16.2. The Best Grimace Response

Best Grimace Response

Spontaneous normal facial/oro-motor activity 5Less than usual spontaneous ability or only

response to touch stimuli4

Vigorous grimace to pain 3Mild grimace to pain 2No response to pain 1

The pupils should be re-examined for size and reactivity. A dilated non-reactive pupilindicates third nerve dysfunction due to an ipsilateral intracranial haematoma until provenotherwise.

The fundi should be examined using an ophthalmoscope. Papilloedema will not beseen in acute raised intracranial pressure, but the presence of retinal haemorrhage mayindicate non-accidental injury in a young infant.

Motor function should be assessed. This includes examination of extra-ocular musclefunction and facial and limb movements. Limb tone, movement and reflexes should beassessed and any focal or lateralising signs noted.

Investigations

Blood testsBlood for full blood count, clotting, glucose, urea and electrolytes should already have

been taken during the immediate care phase. Blood for cross-matching should have been

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sent off at the same time. Arterial blood gases should be taken in head-injured patientsto allow careful control of Pa2 and Pa2, as well as to check pH and base deficit orlactate.

ImagingPlain radiographs of the chest and pelvis may have been taken during the

immediate-care phase, depending on the mechanism of injury and the currentstate of the child. If not, reconsider the need for them at this stage. Remem-ber that the chest film will need to be repeated if the child is subsequentlyintubated.

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In severe head injury, a skull radiograph will usually be superfluous, asequivalent information (and more) will be contained within the CT scan. Innon-accidental injury and in some cases of penetrating head trauma, plainskull films still have a useful role. For other head injuries, this once-commoninvestigation has been supplanted by CT scanning, on the basis of evidence in the lit-erature. Indications for performing an emergency head CT scan are summarised below(NICE guidelines):

• GCS less than 13 at any point since the injury• GCS 13 or 14 at 2 hours after the injury• Suspected open or depressed skull fracture• Any sign of basal skull fracture 23• Focal neurological deficit• More than one episode of vomiting (clinical judgement should be used regarding the

cause of vomiting in children aged 12 years and under, and whether imaging isnecessary) (see note)

• Amnesia for more than 30 minutes of the events before the injury• Dangerous mechanism, e.g. ejection from a motor vehicle or fall if there was any loss of

consciousness or amnesia (see note)• Post-traumatic seizure• Coagulopathy, provided some loss of consciousness or amnesia has been experienced

Note: (1) small children are perceived to vomit more readily than older children oradults following a head injury. In general a CT would be requested in children who havethree or more episodes of vomiting.

(2) The height of a fall likely to be associated with significant injury is unclear asseveral factors are present. Falls from more than twice the patient’s height, falls onto anunyielding surface, would prompt concern.

(3) Note that a skull radiograph still has a role in detecting non-accidental injury inchildren, especially babies.

An area of concern especially in small children is the need, on occasion, to anaesthetisethem for a CT scan, if they are non-cooperative or the scanner is slow. This must only bedone where skills and facilities are available for the anaesthetic care of young children.

Remember that the cervical spine is at risk and that in the presence of altered conscious-ness, neck pain or tenderness, or distracting pain from other injuries, spinal imaging willbe required.


The initial aim of management of a child with a serious head injury is pre-vention of secondary brain damage. The key aims are to maintain oxygenation,ventilation and circulation, and to avoid rises in intracranial pressure.

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These can best be achieved by paying attention to the ABCs discussed earlier. If theairway is at risk, it should be secured. Children with a Coma Score of 8 or less shouldbe intubated and ventilated without delay using rapid-sequence induction of anaesthe-sia. Capnogaphy must be used immediately after intubation to confirm endotrachealtube placement, to serve as a disconnection monitor, and to help maintain normocapniaor mild hypocapnia if there is evidence of raised intracranial pressure. Remember thatthe end-tidal CO2 level may differ significantly from the arterial level, especially in theshocked child – it is essential to check the arterial P2 level with a blood gas sample. Whileroutine hyperventilation has not been shown to improve outcome, arterial P2 levels of4–4.5 kPa are considered to be appropriate in the presence of raised intracranial pressure.Lower levels may adversely affect cerebral perfusion in the areas of brain still responsiveto changes in P2. Except in life-threatening uncontrolled bleeding (see Chapter 13),hypotension should be treated vigorously to avoid hypoperfusion of the brain.

Analgesia

There have been concerns that opioid analgesic agents will lower the conscious level,cause respiratory depression and conceal pain in the abdomen and elsewhere. However,withholding analgesia may contribute to deterioration of the child’s condition by leadingto a rise in intracranial pressure. Failing to control pain will leave the child agitated anduncooperative, making any assessment of the pain more difficult, rather than easier.

Following initial assessment, sufficient analgesia should be administered by carefultitration. It is important to appreciate that head-injured children are often more sensitiveto opioids. If the child’s conscious level is normal, despite other evidence of head injury,intravenous morphine in an initial standard dose of 0·1–0·2 mg/kg (administered in in-crements) is appropriate. In obtunded children, particularly if the Glasgow Coma Scoreis 8 or less, intubation and ventilation will have a higher priority than analgesia alone. Inintermediate cases, a useful rule of thumb is to expect that half the standard dose maybe sufficient in the first instance.

Remember that opioids can be rapidly reversed with naloxone if necessary, althoughit is clearly better to avoid overadministration by cautious titration. Alternative opioidssuch as fentanyl that act more quickly when given intravenously or that can be givenby an alternative route (e.g. mucosal) may be considered, as described in Chapter 13.Local anaesthetic techniques such as femoral nerve block may also be used to good effect,avoiding opioid side effects altogether.

Management of specific problems

Deteriorating conscious levelIf airway, breathing and circulation are satisfactory and hypoglycaemia has been ex-

cluded, then a deteriorating conscious level is assumed to be due to increased intracranialpressure, resulting from an intracranial haematoma or cerebral oedema. CT scan and ur-gent neurosurgical referral are indicated and the temporising manoeuvres shown in thebox may be instituted.

Measures to increase cerebral perfusion temporarily

• Nurse in the 20◦ head-up position to help venous drainage• Ventilation to PaCO2 of 4·0–4·5 kPa• Infusion of intravenous mannitol 0·25–0·5 g/kg• Combat hypotension if present with colloid infusion

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Signs of uncal or central herniationThese signs (discussed in Chapter 11) should lead to immediate institution of the

measures in the box and emergency neurosurgical referral.

ConvulsionsA focal seizure should be regarded as a focal neurological sign of considerable concern.

A general convulsion, while also worrying, has less prognostic significance in children.Seizure activity raises intracranial pressure in both non-paralysed and paral-ysed patients, as well as causing an acidosis and increased cerebral metabolicdemand. The lack of limb or facial movement makes it more difficult to recog-nise a seizure if the child has been paralysed, but fitting should still be suspectedif there is a sharp increase in heart rate and blood pressure, with dilatation ofthe pupils.

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Seizures due to head injury should be controlled promptly. Hypoglycaemia should beexcluded, especially in small children and in adolescents who have been drinking alco-hol. The initial drugs of choice are diazepam, midazolam or lorazepam (see Chapter 12).However, phenytoin should be used for prolonged or persistent convulsions as it is lesssedative. The dose is 18 mg/kg intravenously over 30 minutes, with appropriate moni-toring for rhythm irregularities and hypotension.

Neurosurgical referral

Agreed indications for neurosurgical referral are shown in the box (NICEguidelines):

Indications for referral to a neurosurgeon

• Persisting coma (GCS < 8) after initial resuscitation• Unexplained confusion lasting for more than 4 hours• Deteriorating conscious level (especially motor response changes)• Focal neurological signs• Seizure without full recovery• Definite or suspected penetrating injury• A cerebrospinal fluid leak

Other cases may be discussed to consider referral and to ensure optimal management,such as when there is evidence of a depressed or basal skull fracture or if the initial GCSis between 8 and 12. In general, the care of all children with new, surgically significantabnormalities on imaging should be discussed with a neurosurgeon.

16.7 DETAILED REVIEW AND CONTINUINGSTABILISATION

Review of anatomical injuries and physiological system control

It is easy to miss injuries in the face of an altered conscious level. A high index of suspi-cion is essential. Reconsider the mechanism of injury, review the physical and radiologicalfindings, and make sure that the appropriate specialists have been involved.

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In the severely head-injured child, physiological system control is of critical importancein preventing secondary insults. The airway and ventilation have been dealt with as part ofemergency treatment. The position of the endotracheal tube should now be checked ona chest radiograph and the tube fixation adjusted and re-secured, if necessary. Attentionto detail in adjusting the ventilator settings, according to repeated arterial blood gas sam-pling, is vital. An adequate blood pressure and circulating haemoglobin level are requiredfor cerebral perfusion. Preventing rises in intracranial pressure will help achieve the samegoal. Sedation and paralysis play an important role in tolerating the endotracheal tubeand in suppressing rises in ICP, but must not be allowed to cause hypotension. Bleedingfrom other injuries should already have been stopped and the blood volume restored.Normoglycaemia and a normal or slightly reduced temperature help to guarantee anoptimal outcome.

Vigilance is needed to recognise any significant deterioration in the child’scondition. Any of the following examples of neurological deterioration shouldprompt urgent reappraisal by the supervising medical team (NICE guidelines):

• Development of agitated or abnormal behaviour• A sustained (>30-minute) drop of 1 point in the GCS (especially in the motor score)• Any drop of 2 points in the GCS• Severe/increasing headache/vomiting• New neurological signs

16.8 TRANSFER TO DEFINITIVE CARE

Transport of critically ill children is increasingly the responsibility of the receiving hos-pital. In general, the quality of transfer is more important than absolute speed. Withinthe time constraints imposed by the particular diagnosis, adequate time should be spentpreparing the child before setting off (see checklist and Chapter 24). Despite this empha-sis, remember that some conditions (especially an expanding intracranial haematoma)depend on timely surgical intervention for a successful outcome, and a proactive ap-proach is necessary to optimise outcome. In such circumstances, the delay in waiting fora retrieval team to arrive may be unacceptable, so that the responsibility for transfer mayrevert to the primary hospital.

Checklist for transfer of the ventilated head-injured child (also see Chapter 24)

• Secure endotracheal tube with position confirmed• Adequate sedation and full neuromuscular paralysis• Intermittent positive pressure ventilation (IPPV) using a portable paediatric ventilator• Continuous pulse oximetry and end-tidal capnography to monitor ventilation (with arterial

blood gas checks before setting off)• Adequate, secure vascular access• Naso- or oro-gastric tube• Equipment box• Adequate oxygen supply• Drugs and fluids for planned needs and emergency back-up• Heat conservation• Full medical and nursing notes, charts, and radiographs• Full parental information

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16.9 SUMMARY

• The impact causes primary brain damage. Secondary damage occurs principally as aresult of hypoxia and poor cerebral perfusion and cerebral bleeding, but can also resultfrom hypoglycaemia, seizures and fever.

• The first priority is assessment and management of the airway, breathing and circulation.• The response to voice or pain (if not responding to voice) and the pupillary responses

are checked to identify decompensanting head injury. Immediate measures are taken toimprove cerebral perfusion, when indicated.

• A thorough secondary survey involves an assessment of external signs of head injuryand a more detailed neurological examination. This includes a repeated assessment ofconscious level and pupillary responses, together with examination of the fundi andmotor function.

• A head CT scan should be performed, if indicated.• The aim of initial management is to prevent secondary damage. This is achieved by

attention to airway, breathing and circulation, and by prompt neurosurgical referral andtransfer for operative decompression or neurocritical care, when indicated.

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CHAPTER

17The child with injuries to the

extremities or the spine

LEARNING OBJECTIVES


• how to use the structured approach in the assessment and management of the child withinjuries to the extremities or the spine

17.1 EXTREMITY TRAUMA

17.2 INTRODUCTION

Skeletal injury accounts for 10–15% of all childhood injuries – of these 15% involvephyseal disruptions. It is uncommon for extremity trauma to be life-threatening in themultiply injured child. It is crucial to recognise and treat associated life-threatening in-juries before assessing and managing the skeletal trauma. This can often be difficult inchildren as the pain associated with the extremity trauma can mask serious life-threateninginjuries. Although rarely life-threatening, fractures and associated extremity trauma mustbe managed well or else they can have devastating implications for subsequent rehabil-itation. This chapter deals with problems from the perspective of multiple injury; theprinciples apply equally to individual injuries.

The differences between the mature and immature skeleton have a bearing on initialtreatment and eventual outcome. Use of the principles usually applied to injuries of themature skeleton will result in errors of both diagnosis and treatment. Children’s bones areprone to a greater range of injury than those of adults. This is a reflection of the differentmechanical properties of the immature skeleton, in particular the greater plasticity ofbones and the presence of growth plates. These differences explain the occurrence offractures unique to childhood. Greenstick and torus fractures occur because one or bothcortices deform without fracturing. The growth plate is 2–5 times weaker than any otherstructure in the paediatric skeleton (including ligament and tendon), so it is not surprising

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THE CHILD WITH INJURIES TO THE EXTREMITIES OR THE SPINE

that it is commonly involved in fractures. The chance of fracture propagation is reducedand comminuted fractures are relatively rare. It should be remembered that children’sbones can absorb more force than adults and this may result in an underestimation ofthe degree of trauma to associated soft tissues.

17.3 ASSESSMENT

Unless extremity injury is life-threatening, evaluation is carried out during the sec-ondary survey and treatment commenced during the definitive care phase. Single, closedextremity injuries may produce enough blood loss to cause hypovolaemic shock, but thisis not usually life-threatening. Multiple fractures can, however, cause severe shock. Pelvicfractures are relatively uncommon in children – the energy that would have fractured apelvis in an adult may have been transmitted to vessels within the pelvis of a child, leadingto disruption and haemorrhage. Closed fractures of the femur may cause loss of approxi-mately 20% of the intravascular volume into the thigh, and blood loss from open fracturescan be even more significant. This blood loss begins at the time of the injury, and it canbe difficult to estimate the degree of pre-hospital loss.

17.4 PRIMARY SURVEY AND RESUSCITATION

All multiply injured children should be approached in the structured way discussedin Chapter 13. Relevant history should be sought from relatives and pre-hospital staff.Extremity deformity and perfusion prior to arrival at hospital are especially important,and information concerning the method of injury is helpful.

Life-threatening injuriesThese include the following:

• Crush injuries of the abdomen and pelvis• Traumatic amputation of an extremity• Massive, open long-bone fractures

They should be dealt with immediately and take precedence over any other extremityinjury.

Crush injuries to the abdomen and pelvisThe pelvic bones of a child are much more cartilaginous and thus more flexible than

those of an adult; therefore if fractures occur it will only be after significant impact. Achild’s pelvis tends to be narrower than that of an adult and thus does not offer the sameprotection to the internal structure and organs. The significance of a fracture in itself isnot important but the subsequent damage caused to the associated organs and structurescan be life-threatening and must be treated accordingly. Pelvic disruption can lead to life-threatening blood loss. The child will present with hypovolaemic shock; this may remainresistant to treatment until either the pelvic disruption is stabilised or the injured vesselsare occluded.

Initial treatment during the primary survey and resuscitation phase consists of splintingof the pelvis with a temporary sling, rapid fluid and blood infusions. The diagnosis may beobvious if disruption is severe or if fractures are open. More often this cause of resistanthypovolaemia is discovered when the pelvic radiograph is taken.

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Emergency orthopaedic opinion should be sought, and urgent external fixation of thepelvis should be considered. In some hospitals, radiographic identification and therapeu-tic embolisation of bleeding vessels may be attempted.

Traumatic amputationTraumatic amputation of an extremity may be partial or complete. Paradoxically, it is

usually the former that presents the greatest initial threat to life. This is because com-pletely transected vessels go into spasm, whereas partially transected vessels may not.Blood loss can be large and the pre-hospital care of these injuries is critical; an exacthistory of this should be sought.

Once in hospital the airway should be cleared and breathing assessed as previouslydiscussed. Exsanguinating haemorrhage must be controlled. Two wide-bore cannulaeshould be inserted. If the child is in shock, but the bleeding points are well controlled,vigorous fluid therapy may be instituted. If the bleeding is still uncontrolled, fluid bolusesshould be commenced in 5–10-ml/kg aliquots until control is achieved (Chapter 13). Iflocal pressure and elevation are not sufficient, pressure may also be applied temporarilyover the femoral and brachial artery. The use of a tourniquet is now contraindicated.Bleeding continues through bones that are not compressed by the tourniquet and tis-sue viability is generally compromised. On the basis of experience from land-mine in-juries, an elasticated compression bandage and dressing, if applied carefully, may helpstem the haemorrhage and better preserve tissue viability. Emergency orthopaedic andplastic surgical opinions sought. If no active bleeding is taking place, the stump shouldbe dressed with a sterile dressing soaked in normal saline and the limb splinted andelevated.

Reimplantation techniques are available in specialist centres. The success rate is im-proving, particularly in children. Urgent referral and transfer are necessary – the ampu-tated part will only remain viable for 8 hours at room temperature, or for 18 hours ifcooled. The amputated part should be cleaned, wrapped in a moist sterile towel, placedin a sterile, sealed plastic bag and transported in an insulated box filled with crushed iceand water in the same vehicle as the child. Care should be taken to avoid direct contactbetween the ice and tissue.

If, after discussion with the specialist centre, it is decided that reimplantation is notappropriate, the amputated part should still be saved because it may be used for graftingof other injuries.

The child must be stabilised before transfer.

Massive, open long-bone fracturesThe blood loss from any long-bone fractures may be significant; open fractures bleed

more than closed ones because there is no tamponade effect from surrounding tissues.As a general rule an open fracture causes twice the blood loss of the corresponding closedfracture. Thus a single, open, femoral shaft fracture may result in 40% loss of circulatingblood volume. This in itself is life-threatening.

After airway and breathing have been assessed and treated, two relatively large-borecannulae should be inserted and fluid boluses should be commenced according to thechild’s overall circulatory state (Chapter 13). Exsanguinating haemorrhage should becontrolled both by the application of pressure at the fracture site, and by correct splintingof the limb.

Emergency orthopaedic opinion should be sought. Angiography may be necessaryto examine whether any major vessel rupture has occurred, and if such an injury isconsidered likely then a vascular surgical opinion should be obtained immediately.

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In a conscious child, inspection is usually the most productive part of the examina-tion. Causing pain or eliciting crepitus in an injured extremity will only increase anxiety,ultimately making the child more difficult to manage.

The extremities should be inspected for discolouration, bruising, swelling, deformity,lacerations and evidence of open fractures.

Next, gentle palpation should be undertaken to establish any areas of tenderness. Limbtemperature and capillary refill should be assessed, and pulses sought – a Doppler flowprobe should be used if necessary.

Finally, the active range of motion should be assessed if the child is cooperative. If thereis an obvious fracture or dislocation, or the child refuses to move a limb actively, passivemovement should be avoided.

Limb-threatening injuryThe viability of a limb may be threatened by vascular injury, compartment syndrome,

or by open fractures. These situations are discussed below.

Vascular injury Assessment of the vascular status of the extremity is a vital step in evalu-ating an injury. Vascular damage may be caused by traction (resulting in intimal damageor complete disruption), or by penetrating injuries caused by either a missile or the endof a fractured bone. Brisk bleeding from an open wound or a rapidly expanding massis indicative of active bleeding. Complete tears are less likely to bleed for a prolongedperiod due to contraction of the vessel. It should be remembered that nerves usually passin close proximity to vessels and are likely to have been damaged along with the vessel.

The presence of a pulse, either clinically or on Doppler examination, does not rule outa vascular injury. A diminished pulse should not be attributed to spasm.

The signs of vascular injury are shown in the box.

Signs of vascular injury

• Abnormal pulses• Impaired capillary return• Decreased sensation• Rapidly expanding haematoma• Bruit

If these signs are present, urgent investigation and emergency treatment should becommenced. The fracture should be aligned and splints checked to ensure that theyare not restrictive; if no improvement occurs a vascular surgeon should be consultedand angiography considered. Vascular damage may not always be immediately apparent;constant reassessment is therefore essential.

Compartment syndrome If the interstitial pressure within a fascial compartment risesabove capillary pressure, then local muscle ischaemia occurs. If this is unrecognised, iteventually results in Volkmann’s ischaemic contracture.

Compartment syndrome usually develops over a period of hours and is most oftenassociated with crush injuries. It may, however, occur following simple fractures. Theclassic signs are shown in the box.

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Classic signs of compartment syndrome

• Pain, accentuated by passively stretching the involved muscles• Decreased sensation• Swelling• Pallor of limb• Paralysis• Pulselessness

Distal pulses only disappear when the intra-compartmental pressure rises above arterialpressure; by this time irreversible changes have usually occurred in the muscle bed. Initialtreatment consists of releasing constricting bandages and splints. If this is ineffective thenurgent surgical fasciotomy should be performed.

Open fractures

Any wound within the vicinity of a fracture should be assumedto communicate with the fracture.

Open wounds are classified according to the degree of soft tissue damage, amount ofcontamination and the presence or absence of associated neurovascular damage. Initialtreatment includes removal of gross contamination, and covering of the wound with asterile dressing. No attempt should be made to ligate bleeding points because associatednerves may be damaged as this is done. Bleeding should be controlled by direct pressure.Broad-spectrum antibiotics should be given, and tetanus immunisation status checked.Further management is surgical – debridement should be carried out within 6 hours bythe orthopaedic surgeons under operating theatre conditions. It may be useful to take apicture of the wound with either a digital or Polaroid camera to reduce the number oftimes the dressing is removed.

Other injuries

Non-accidental injuryThis must always be considered if the history is not consistent with the injury pattern.

It is discussed in detail in Appendix C.

Fracture–dislocationIt is difficult to distinguish fractures and fracture–dislocations on clinical grounds.

Radiology is often helpful, but in very young children, where ossification centres havenot yet formed, an ultrasound examination or MR scan may be necessary. In an olderchild (when some of the ossification centres are present), a comparative radiograph ofthe normal side may be helpful before more invasive investigations are considered. Theseinvestigations should be performed in the definitive-care phase, unless there are vascularor neurological complications. If suspected, early orthopaedic assistance must be sought.

DislocationsDislocations, other than of the elbow and hip, are rare in children but, as for adults, may

produce neurovascular injury that can result in permanent impairment. All dislocationsshould therefore be reduced as soon as possible.

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Epiphyseal injuriesFractures involving the epiphysis may be displaced or non-displaced. An orthopaedic

surgeon should manage them.


Life-threatening problems identified during the primary survey in the multiply injuredpatient are managed first. Only then should attention be turned to the extremity in-jury. The specific management of complications such as vascular injury, compartmentsyndrome, traumatic amputation, and open wounds have been discussed earlier in thischapter.

Alignment

Severely angulated fractures should be aligned. Gentle traction should be applied to thelimb to facilitate alignment, particularly when immobilising long-bone fractures. Splintsshould extend one joint above and below the fracture site. Perfusion of the extremity,including pulses, skin colour, temperature, and neurological status, must be assessedbefore and after the fracture is aligned. Radiographs, including arteriograms, should notbe obtained until the extremity is splinted.

When aligning a fracture, analgesia is usually necessary. Entonox or intra-venous opiates should be used. Analgesia and further pain management isdiscussed in Appendix F. In femoral fractures, femoral nerve block is veryeffective – the technique is discussed in Chapter 22. 130

Immobilisation

Fractures (or suspected fractures) should be immobilised to control pain and preventfurther injury. Splintage is a most effective way of controlling pain, and subsequent dosesof analgesia may be reduced. If pain increases after immobilisation, then an ischaemicinjury and/or compartment syndrome must be excluded. Emergency splinting techniquesfor various injured extremities are described below.

Upper limbHand Splinted in the position of function with the wrist slightly dorsiflexed and thefingers slightly flexed at all joints. This is best achieved by gently immobilising the handover a large roll of gauze.

Forearm and wrist Splinted flat on padded pillows or a dorsal above elbow plaster backslab should be applied.

Elbow Immobilised in a flexed position to a maximum of 80˚ of flexion from full exten-sion with a sling and an above elbow plaster back slab.

Arm Immobilised by a sling, which can be augmented with splints for unstable fractures.Circumferential bandages should be avoided, as they may be the cause of constriction,particularly when swelling occurs.

Shoulder Immobilised by a sling.

Lower limbFemur Femoral fractures should be treated in traction splints or skin traction withThomas splint. Ipsilateral femoral and tibial fractures can be immobilised in the same

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splint. Excess traction may cause perineal injury and neurovascular problems, and shouldbe avoided.

Tibia and ankle Tibial and ankle fractures should be aligned and immobilised in paddedbox splints or above/below knee back slab depending on position of fracture. Foot per-fusion should be assessed before and after application of the splint.

17.7 SUMMARY

• Extremity trauma is rarely life threatening per se, unless exsanguinating haemorrhageensues. Multiple fractures can cause significant blood loss

• The first priority is assessment of the airway, breathing, and circulation• Full assessment of the extremities takes place during the secondary survey.

Limb-threatening injuries should be identified at this stage and further investigation andmanagement begun. Other injuries should be treated by splintage

17.8 SPINAL TRAUMA

17.9 INTRODUCTION

Spinal injuries are rare in children, which does not mean that they are unimportant.For any mechanism of injury capable of causing cervical spine damage (or in cases withuncertain history), the cervical spine is presumed to be at risk. A high index of suspicion,correct management, and prompt referral are necessary in order to prevent exacerbationof underlying cord injury. Every severely injured child should be treated as though he orshe has spinal injury until adequate examination and investigation exclude it.

Who to immobilise

If the child is unconscious, uncooperative or has had a significant mechanism of injurythe head and neck should be immobilised initially by manual in-line stabilisation andthen triple point immobilised using a hard collar, block and tape/straps. Once a childhas been immobilised, a member of staff must remain with the child at all times as thechild’s airway is at risk. The immobilisation of the cervical spine can be very frighteningand disorientating to a child and thus must be carried out supportively and sensitivelywith careful explanation appropriate to the child’s age and cognitive level throughoutthe procedure. Uncooperative or combative children should simply have a hard collarapplied, and in-line manual stabilisation continued, if they tolerate it. Too rigid im-mobilisation of the head in such cases may increase leverage on the neck as the childstruggles.

Guidelines for clearing a cervical spine

1. No midline cervical tenderness on direct palpation2. No focal neurological deficit3. Normal alertness4. No intoxication5. No painful distracting injuries

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17.10 INJURIES OF THE CERVICAL SPINE

Injuries to the cervical spine are rare in children; however they are associated withsubstantial levels of impact. The upper three vertebrae are usually involved – injury is morecommon in the lower segments of an adult. The low incidence (0–2% of all children’sfractures and dislocations) of bony injury is explained by the mobility of the cervical spinein children, which dissipates applied forces over a greater number of segments.

Radiographs

A lateral cervical spine radiograph may have been obtained during the secondary survey.Injury must be presumed until excluded radiologically and clinically. Spinal injury maybe present even with a normal radiograph. The development of the cervical vertebraeis complex. There are numerous physeal lines (which can be confused with fractures),and a range of normal sites for ossification centres. Pseudosubluxation of C2 on C3and of C3 on C4 occurs in approximately 9% of children, particularly those aged 1–7 years. Interpretation of cervical radiographs can therefore be difficult even for the mostexperienced.

Indirect evidence of trauma can be detected by assessing retropharyngeal swelling. Atthe inferior part of the body of C3, the pre-vertebral distance should be one-third thewidth of the body of C2. This distance varies during breathing and is increased in a cryingchild. Cervical spine X-rays are discussed in more detail in Chapter 23.

Injury types

Atlantoaxial rotary subluxation is the most common injury to the cervi-cal spine. The child presents with torticollis following trauma. Radiologicaldemonstration of the injury is difficult, and computed tomography or mag-netic resonance imaging may be necessary. Other injuries of C1 and C2 includeodontoid epiphyseal separations and traumatic ligament disruption.

638

It should be noted that significant cervical cord injuries have been reported withoutany radiological evidence of trauma.

Immediate treatment

Despite the rarity of fractures a severely injured child’s spine should besecurely immobilised until spinal injury has been excluded. If in any doubt the

child should continue to be immobilised and senior help sought.

Cervical spine immobilisation techniques are described in Chapter 22.

17.11 INJURIES OF THE THORACIC AND LUMBAR SPINE

Injuries to the thoracic and lumbar spine are rare in children. They are most commonin the multiply injured child. In the second decade, 44% of reported injuries resultfrom sporting and other recreational activity. Some spinal injuries may result from non-accidental injury.

When an injury does occur, it is not uncommon to find multiple levels of involvementbecause the force is dissipated over many segments in the child’s mobile spine. Thisincreased mobility may also lead to neurological involvement without significant skeletalinjury.

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The most common mechanism of injury is hyperflexion, and the most common radio-graphic finding is a wedge- or beak-shaped vertebra resulting from compression.

The most important clinical sign is a sensory level. Neurological assessment is difficultin children, and such a level may only become apparent after repeated examinations.Because of the difficulties of assessment, a child with multiple injuries should be assumedto have spinal injury, and should therefore remain immobilised. However they should belog-rolled off the long spinal board onto a firm emergency department trolley. If injuryis confirmed, further treatment is similar to that in adults. Unstable injuries may requireopen reduction and stabilisation with fusion.

If cord damage does occur methyl prednisolone should be started within8 hours at an initial infusion of 30 mg/kg over 1 hour and followed by aninfusion of 5.2 mg/kg per hour for 24 hours.

17.12 SPINAL CORD INJURY WITHOUTRADIOLOGICAL ABNORMALITY

Spinal cord injury without radiological abnormality (SCIWORA) is said to have oc-curred when the spinal cord has been injured without an obvious accompanying injuryto the vertebral column. The cervical spine is affected more frequently than the thoracicspine. Because the upper segments of the cervical spine have the greatest mobility, theupper cervical cord is most susceptible to this injury.

Children who are seriously injured should have immobilisation of the spine maintaineduntil such time as a full neurological assessment can be carried out, since normal X-raysdo not exclude a cord injury. If there is any doubt, MRI scans should be obtained.

17.13 SUMMARY

• Spinal injuries are rare in children but must be considered when associated withsignificant mechanism of injury.

• Assessment can be difficult and significant cord damage can occur without fractures.• Spinal immobilisation must be applied until the assessment is complete and then can

only be removed if the spine has been cleared.

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CHAPTER

18The burned or scalded child

LEARNING OBJECTIVES


• how to use the structured approach to assess and manage the burned or scalded child

18.1 INTRODUCTION

Epidemiology

Each year some 50 000 burned or scalded children attend emergency departments.Of these, 5000–6000 require hospital admission. In England and Wales in 2001,23 children died from burns. Seventy per cent of those burnt are pre-school children, themost common age being between 1 and 2 years. Scalds occur mostly in the under-4s.Boys are more likely to suffer burns and serious scalds.

Most fatal burns occur in house fires and smoke inhalation is the usual cause of death.The number of deaths from burns has decreased because of a combination of factors.The move away from open fires, safer fireguards, smoke alarms and more stringent low-flammability requirements for night clothes have all played a part. Non-fatal burns ofteninvolve clothing and are often associated with flammable liquids.

Scalds are usually caused by hot drinks, but bath water and cooking oil scalds are notuncommon. The improvement in survival following scalding (which followed improve-ments in treatment) has reached a plateau.

There is a strong link between burns to children and low socioeconomic status. Familystress, poor housing conditions, and over-crowding are implicated in this.

PathophysiologyTwo main factors determine the severity of burns and scalds – these are the temperature

and the duration of contact. The time taken for cellular destruction to occur decreases ex-ponentially with temperature. At 44◦C, contact would have to be maintained for 6 hours,

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THE BURNED OR SCALDED CHILD

at 54◦C for 30 seconds, and at 70◦C epidermal injury happens within a second. Thisrelationship underlies the different patterns of injury seen with different types of burn.Scalds generally involve water at below boiling point and contact for less than 4 seconds.Scalds that occur with liquids at a higher temperature (such as hot fat or steam), or inchildren incapable of minimising the contact time (such as young infants and the handi-capped), tend to result in more serious injuries. Flame burns involve high temperaturesand consequently produce the most serious injuries of all.

It must be re-emphasised that the most common cause of death within the first hourfollowing burn injuries is due to smoke inhalation. Smoke-filled rooms not only containsoot particles, hot gases and noxious substances but are also depleted of oxygen. Inhala-tion of all or any of which can lead to cardiac arrest. Thus, as with other types of injury,attention to the airway and breathing is of prime importance.


When faced with a seriously burned child it is easy to focus on the immediate problemsof the burn, and forget the possibility of other injuries. The approach to the burned childshould be the structured one advocated in Chapter 13.


The airway may be compromised either because of inhalational injury and oral scaldsor because of severe burns to the face. The latter are usually obvious, whereas the formertwo may only be indicated more subtly. The indicators of inhalational injury are shownin the box.

Indications of inhalational injury

• History of exposure to smoke in a confined space• Deposits around the mouth and nose• Carbonaceous sputum

Because oedema occurs following thermal injury, the airway can deteriorate rapidly.Thus even suspicion of airway compromise, or the discovery of injuries that might beexpected to cause problems with the airway at a later stage, should lead to immediateconsideration of tracheal intubation. This procedure increases in difficulty as oedemaprogresses; it is therefore important to perform it as soon as possible. All but the mostexperienced should seek expert help urgently, unless apnoea requires immediate inter-vention.

If there is any suspicion of cervical spine injury, or if the history is unobtainable,appropriate precautions should be taken until such injury is excluded.

Breathing

Once the airway has been secured, the adequacy of breathing should be assessed.Signs that should arouse suspicion of inadequacy include abnormal rate, abnormal chestmovements and cyanosis (a late sign). Circumferential burns to the chest or abdomen(the latter in infants) may cause breathing difficulty by mechanically restricting chestmovement.

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All children who have suffered burns should be given high-flow oxygen. If there aresigns of breathing problems then intubation and ventilation should be commenced.

Circulation

In the first few hours following injury, signs of hypovolaemic shock are rarely at-tributable to burns. Therefore any such signs should raise the suspicion of bleedingfrom elsewhere, and the source should be actively sought. Intravenous access should beestablished with two cannulae during resuscitation and fluids started. If possible, dripsshould be put up in unburnt areas, but burned skin, eschar, can be perforated if nec-essary. Remember that the intraosseous route can be used. Blood should be taken forhaemoglobin, haematocrit, electrolytes and urea, blood glucose and cross-matching atthis stage.

Disability

Reduced conscious level following burns may be due to hypoxia (remember smoke-filled rooms may contain little oxygen), head injury or hypovolaemia. It is essential that aquick assessment is made during the primary survey as described in Chapter 13, becausethis provides a baseline for later observations.

Exposure

Exposure should be complete. Burned children lose heat especially rapidly, and shouldbe kept in a warm environment and be covered with blankets when not being examined.


As well as being burned, children may suffer the effects of blast, may be injured byfalling objects, or may fall while trying to escape from the fire. Thus other injuries are notuncommon and a thorough head-to-toe secondary survey must be carried out. This isdescribed in Chapter 13. Any injuries discovered, including the burn, should be treatedin order of priority.

Assessing the burn

The severity of a burn depends on its relative surface area and depth. Burns to particularareas require special attention.

Surface areaThe surface area is usually estimated using burns charts. It is particularly important to

use a paediatric chart when assessing burn size in children, because the relative surfaceareas of the head and limbs change with age. This variation is illustrated in Figure 18.1and the table accompanying it.

Another useful method of estimating relative surface area relies on the fact that thepatient’s palm and adducted fingers cover an area of approximately 1% of the bodysurface. This method can be used when charts are not immediately available, and isobviously already related to the child’s size.

Note that the “rule of 9s” cannot be applied to a child who is less than 14 years old.

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Figure 18.1. Body surface area (percent). (Reproduced courtesy of Smith & NephewPharmaceuticals Ltd)

Surface area at

Area indicated 0 year 1 year 5 years 10 years 15 years

A 9·5 8·5 6·5 5·5 4·5B 2·75 3·25 4·0 4·5 4·5C 2·5 2·5 2·75 3·0 3·25

DepthBurns are classified as being superficial, partial-thickness, or full-thickness. The first

causes injury only to the epidermis, and clinically the skin appears red, with no blisterformation. Partial-thickness burns cause some damage to the dermis; blistering is usuallyseen and the skin is pink or mottled. Deeper (full-thickness) burns damage both theepidermis and dermis, and may cause injury to deeper structures as well. The skin lookswhite or charred, and is painless and leathery to touch.

Special areasBurns to the face and mouth have already been dealt with above. Burns involving the

hands or feet can cause severe functional loss if scarring occurs. Perineal burns are proneto infection and present particularly difficult management problems. Circumferential,full- or partial-thickness burns of the limbs or neck may require urgent incision to relievedistal ischaemia. Similarly circumferential burns to the torso may restrict ventilation andalso require urgent incision. This procedure is called escharotomy and usually needs tobe done before transfer to a burns centre.


Analgesia

Most burned children will be in severe pain, and this should be dealt with urgently.Some older children may manage to use Entonox, but most will not. Any child with burns

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that are anything other than minor should be given intravenous morphine at a dose of0·1 mg/kg as soon as possible. Further doses are often required but must be titratedagainst pain and sedation. There is no place for administration of intramuscular analgesiain burns because absorption is unreliable.

Fluid therapy

Two cannulae should already have been sited during the primary survey and resusci-tation and therapy for shock (20 ml/kg) commenced if indicated. Children with burns of10% or more will require intravenous fluids as part of their burns care. This fluid is inaddition to their normal fluid requirement. The additional fluid (in ml) required per dayto treat the burn can be estimated using the following formula:

Percentage burn × Weight (kg) × 4

Half of this should be given in the first 8 hours following the time of their burn. Thefluid given is usually crystalloid. Remember that this is only an initial guide; subsequenttherapy will be guided by urine output, which should be kept at 2 ml/kg/hour or more.Urethral catheterisation should therefore be performed as soon as is practicable.

Wound care

Infection is a significant cause of mortality and morbidity in burns victims, and woundcare should start as early as possible to reduce this risk. Furthermore, appropriate woundcare will reduce the pain associated with air passing over burnt areas.

Burns should be covered with sterile towels, and unnecessary re-examination shouldbe avoided. Blisters should be left intact. Although cold compresses and irrigation withcold water may reduce pain, it should be remembered that burned children lose heatrapidly. These treatments should only be used for 10 minutes or less, and only in patientswith superficial or partial-thickness burns totalling less than 10%. Children should neverbe transferred with cold soaks in place. Cling film is often used as a sterile dressing andcan be applied loosely onto the burned area. No additional ointments or creams shouldbe applied.

Management of carbon monoxide poisoning

During a fire, burning of organic compounds in a low-oxygen environment producescarbon monoxide. Inhalation by the victim induces production of carboxyhaemoglobin,which has a 200-fold greater affinity for the oxygen molecule than haemoglobin. A highlevel will therefore cause cellular hypoxia as the oxygen will not be given up to cells. Chil-dren who have been in house fires should have their blood carboxyhaemoglobin measured.(Note: Most pulse oximeters show the oxygen saturation, regardless of haemoglobin con-centration i.e. normal Sp2 does not exclude carbon monoxide poisoning)

Levels of 5–20% are treated with oxygen (which speeds up the removal of CO). Levelsover 20% should prompt consideration of hyperbaric oxygen chamber treatment – discusswith the paediatric burns unit.

In some environments the burning of plastics, wool and silk can produce cyanide.Assessment and treatment are complex. Be aware of the possibility of cyanide poisoningand consider it in a child from a house fire who is in a coma without apparent cause. Ingeneral, antidotes are used when blood levels of cyanide are greater than 3 mg/l. Discusstreatment with a poisons centre as other factors such as the concomitant presence ofcarboxyhaemoglobin are contraindications for some antidotes.

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18.5 CONTINUING STABILISATION AND TRANSFERTO DEFINITIVE CARE

Definitive care requires transfer to a paediatric burns facility. Criteria for transfer areshown in the box.

Criteria for transfer to a burns unit

• 10% partial- and/or full-thickness burns• 5% full-thickness burns• Burns to special areas: face, hands, feet or perineum.• Any circumferential burn• Significant inhalational burn (excluding pure carbon monoxide poisoning)• Chemical, radiation or high voltage electrical burns

If in doubt discuss the child with the paediatric burns unit.As with any injury in childhood, consider the possibility of child abuse. Note the

timeliness of presentation, and assess whether the history given to account for the burnor scald fits in with the clinical appearance of the injury in size, shape, age and location.Consider whether the injury is consistent with the child’s developmental attainments. Ifconcerned or in doubt, consult with a child protection specialist.

18.6 SUMMARY

• Initial assessment and management of the burned child should be directed towards careof the airway, breathing, and circulation. Intubation and ventilation should be performedearly if indicated.

• Assessment of the area and depth of the burn should be undertaken during thesecondary survey.

• Fluid replacement should be used initially to treat shock. Additional fluids will be neededto treat the burn, and a guide to the amount required can be calculated. Urine outputshould be used as an indicator of the efficacy of treatment.

• Specialist burns centres should be contacted, and transfer arranged if indicated.

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CHAPTER

19The child with an electrical

injury or drowning

LEARNING OBJECTIVES


• how to use the structured approach to assess and manage the child with an electricalinjury or drowning

19.1 ELECTRICAL INJURIES

19.2 INTRODUCTION

Epidemiology

Many minor electrical injuries do not require medical treatment and the instance ofthis sort of injury is unknown. Only a small percentage of electrical injuries requiringhospital attention occur in children. Electrical injuries usually occur in the home andinvolve relatively low currents and voltage. The mortality from electrical injuries fromhigh power external sources such as electrified railways is high.

Other injuries may occur during the event: for example, the child may fall or be thrownoff. As with all injuries, a systematic approach is required.

Pathophysiology

Alternating current (AC) produces cardiac arrest at lower voltages than does directcurrent (DC). Regardless of whether the electrocution is caused by AC or DC, the riskof cardiac arrest is related to the size of the current and the duration of exposure. Thecurrent is highest when the resistance is low and the voltage is high.

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THE CHILD WITH AN ELECTRICAL INJURY OR DROWNING

CurrentA lightning strike is a massive direct current of very short duration which can depolarise

the myocardium and cause an immediate asystole.The typical effects of increase in current are given in the following list:

Above 10 mA: Tetanic contractions of muscles may make it impossible for the child tolet go of the electrical source.

50 mA: Tetanic contraction of the diaphragm and intercostal muscles leads to respira-tory arrest, which continues until the current is disconnected. If hypoxia is prolonged,secondary cardiac arrest will occur.

Over 100 mA to 50 A: Primary cardiac arrest may be induced. (defibrillators used inresuscitation deliver around 10 A)

50 A to several 100 A: Massive shocks cause prolonged respiratory and cardiac arrestand more severe burns.

ResistanceThe resistance of the tissues determines the path which the current will follow. Gener-

ally the current will follow the path of least resistance from the point of contact to earth.The relative resistance of the body tissues is in increasing order: tissue fluid, blood, mus-cle, nerve, fat, skin, bone. Electrocution generates heat, which causes a variable degree oftissue damage. Nerves, blood vessels, the skin and muscles are damaged most. Bone cancontinue to increase in temperature after the current has stopped because of the Jouleeffect and this can lead to necrosis of adjacent structures. Swelling of damaged tissues,particularly muscle, can lead to a crush or compartment syndrome requiring fasciotomy.Water decreases the resistance of the skin and will increase the amount of current whichflows through the body.

VoltageHigh-voltage sources such as lightning or high-tension cables cause extremely high cur-

rents and severe tissue damage. However, very high voltages can cause severe superficialburns without damage to deeper structures (flash burns and arcing).

19.3 INITIAL TREATMENT

The first priority is to disconnect the current. Be aware that high voltage sources candischarge through several centimetres of air.


The upper airway should be opened and secured especially if this is compromisedby facial or other injuries. The cervical spine should be immobilised especially in anunconscious child. Other injuries should be treated in an appropriate and structuredmanner.

The entry and exit point of the current should be sought in order to determine the sortof possible internal injuries that could have occurred.


Associated injuries are common in electrocution. Almost all possible injuries can occuras a result of falls or being thrown from the source. Burns are particularly common and

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are caused either by the current itself or by burning clothing. Tetanic contraction ofmuscles can cause fractures, luxations or muscle tearing.

Associated problems

Burns cause oedema and fluid loss. Myoglobinuria occurs after significant muscledamage. In this case it is important to maintain a urine production of more than2 ml/kg/hour with the judicious use of diuretics such as mannitol and appropriate fluidloading. Alkalisation of the urine with sodium bicarbonate increases the excretion ofmyoglobin.

Dysrhythmias can occur up to a considerable time after the electrocution, and con-tinuous ECG monitoring is essential. Children with significant internal injuries havea greater fluid requirement than one would suspect on the basis of the area of theburn.

19.6 STABILISATION AND TRANSFER TODEFINITIVE CARE

A significant electrical burn is an indication for transfer to a burns centre.

19.7 SUMMARY

• The first priority in electrical injuries is to switch off the current.• The management of electrocution should be structured according to the A-B-C-D-E

principal, including the appropriate treatment of a possible cervical spine injury.• Almost all injuries can be associated with electrocution.• The entry and exit wounds should be sought in order to form a picture of the possible

internal injuries.• Dysrhythmias can occur some considerable time following the electrocution.

Myoglobinuria should be treated aggressively.

19.8 DROWNING

19.9 INTRODUCTION

The new uniform definition of drowning – “the process of experiencing respiratory im-pairment from submersion/immersion in liquid” – was agreed upon during the first WorldCongress on Drowning in 2002. The term “near drowning” is no longer an official termmainly because it has been used differently worldwide, which has caused confusion. Ifused, “near drowning” is said to have occurred if there is any recovery (however transient)following a submersion incident.

Epidemiology

According to the annual World Health Organization report some 450,000 die annuallyas a result of drowning worldwide. For children under the age of 15 years drowning isthe leading cause for accidental death in the world. The age group from 0 to 4 years hasa mortality rate of 18.9 per 100 000, the older age group up to 15 years has an incidence

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of 9.5 deaths per 100 000. Male victims are more likely to die from drowning thanfemale victims. Infants die most commonly in bathtubs, older children die in privateswimming pools, garden ponds and other inland waterways. It is estimated that up to80% of drownings are preventable. Prevention strategies like fencing of private pools andreinforcing the importance of adult supervision may reduce this number. Death fromdrownings is the reinforcing third most common cause of accidental death in children inthe UK (after road accidents and burns).

Pathophysiology

Bradycardia and apnoea occur shortly after submersion as a result of the diving reflex.As apnoea continues, hypoxia and acidosis causes tachycardia and a rise in blood pressure.Between 20 seconds and 5 minutes later a breakpoint is reached, and breathing occurs.Fluid is inhaled and on touching the glottis causes immediate laryngeal spasm. After avariable but short period of time the laryngospasm subsides and fluid is aspirated into thelungs, resulting in alveolitis and pulmonary oedema. Hypoxia is by this time severe andthe patient will have lost consciousness. Bradycardia and other dysrhythmias can alsooccur and may be fatal (ventricular fibrillation is rare). Ultimate death usually occursfrom hypoxia.

Children who survive because of interruption of this chain of events not only requiretherapy for drowning, but also assessment and treatment of concomitant hypothermia,hypovolaemia and injury (particularly spinal). Major electrolyte abnormalities due to theamount of water swallowed seldom occur.

The type of water does not predict the clinical course of drowning. The differencesbetween freshwater and seawater drowning do not usually have an impact on the degreeof pulmonary oedema. However, immersion in severely contaminated water is associ-ated with infections with unusual organisms, and aspiration of water contaminated withpetroleum products can lead to a severe ARDS.

Submersion injuries are generally associated with hypothermia. The large body surfacearea to weight ratio in infants and children put them at particular risk. Hypothermiamay have a protective effect against the neurological sequelae following hypoxia andischaemia but is also associated with life-threatening dysrhythmias, coagulation disordersand susceptibility to infections.

The initial approach to drowning patients focuses on the correction of hypoxia, hy-pothermia and the treatment of associated injuries, which are common in older childrenand often overlooked. Cervical spine injury should always be suspected in drowningvictims for whom the mechanism of injury is unclear.


The initiation of early and effective basic life support is one of the most importantfactors for survival. If needed it must be commenced as early as possible.

The neck must be presumed to be injured, and the cervical spine should be immo-bilised until such injury is excluded. A history of diving is especially significant in thisregard.

Following a drowning episode, the stomach is usually full of swallowed water. The riskof aspiration is therefore increased and the airway must be secured as soon as possibleusually by endotracheal intubation. Gastric decompression by an oro- or nasogastric tubeshould also be performed.

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After an initial good recovery there can still be a rapid clinical deterioration after4–6 hours with respiratory compromise and the need for endotracheal intubation andmechanical ventilation. Chest X-ray changes may occur later.

Whatever the method of rescue, patients should be lifted out of the water in a ho-risontal position and if possible with their spine immobilised. Vertical rescue may leadto cardiovascular collapse due to loss of pressure from surrounding water and venouspooling.

HypothermiaA core temperature reading (rectal or oesophageal) should be obtained as soon as

possible and further cooling should be prevented immediately. Hypothermia is commonfollowing drowning, and adversely affects resuscitation attempts unless treated. Not onlyare arrhythmias more common but some, such as ventricular fibrillation, may be refrac-tory at temperatures below 30◦C. According to CPR guidelines, defibrillation with threeshocks may be attemped at temperatures below 30◦C; if unsuccessful, further shocksmust be delayed until there has been a rise in temperature to above 30◦C. Administra-tion of inotropic or antiarrhythmic drugs should not be given when the core temperatureis below 30◦C. Resuscitation should be continued until the core temperature is at least32◦C or cannot be raised despite active measures.

Rewarming strategies depend on the core temperature and signs of circulation. Externalrewarming is usually sufficient if the core temperature is above 30◦C. Active core rewarm-ing should be added in patients with a core temperature of less than 30◦C, but bewareof “rewarming shock”. Most hypothermic patients are hypovolaemic. During rewarmingthe peripheral vascular resistance falls more rapidly as core rewarming is accomplished.As a result of vasodilation and impaired myocardial dysfunction, hypotension ensues.

External rewarming

• Remove cold, wet clothing• Supply warm blankets• Infrared radiant lamp• Heating blanket• Warm air system

Core rewarming

• Warm intravenous fluids to 39◦C to prevent further heat loss• Warm ventilator gases to 42◦C to prevent further heat loss• Gastric or bladder lavage with normal (physiological) saline at 42◦C• Peritoneal lavage with potassium-free dialysate at 42◦C. Use 20 ml/kg cycled every

15 minutes• Pleural or pericardial lavage• Endovascular warming• Extracorporeal blood rewarming

The temperature is generally allowed to rise by 1◦C per hour to reduce haemodynamicinstability. However, recent evidence suggests that in post-cardiac-arrest patients withrestoration of adequate spontaneous circulation there has been a beneficial effect onneurological outcome of mild hypothermia (32–34◦C) for 12–24 hours when the initialrhythm was ventricular fibrillation. The data on the use of therapeutic hypothermia inchildren are so far insufficient.

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External and internal rewarming methods are shown in the box. Rhythm, pulse rateand blood pressure monitoring should be undertaken. In severe hypothermia, admissionto a high-dependency area is necessary.


During the secondary survey, the child should be carefully examined from head totoe. Any injury may have occurred during the incident that preceded immersion; spinalinjuries are particularly common. Ingestion of alcohol and/or drugs may have precededthe drowning incident in the older child.

Investigations

• Blood glucose• Blood gas analysis (preferably arterial) and blood lactate• Urea and electrolytes• Coagulation status• Blood and sputum cultures• Chest X-ray• Lateral cervical spine X-ray or CT scan.

19.12 EMERGENCY TREATMENT AND STABILISATION

The brain is the most vulnerable organ for asphyxia, and cerebral impairment occursbefore cardiac problems in submersion. Except for bystander cardiopulmonary resus-citation and mild hypothermia in specific patients, there are few effective measures forreducing brain damage in drowning.

It is essential to monitor the vital functions closely, especially during the first couple ofhours. An early suggestion of respiratory insufficiency or haemodynamic instability is anindication for admission to the intensive care unit.

Fever is common during the first 24 hours following immersion and this is not necessar-ily a sign of infection. In fact infections usually become manifest after the first day whengram-negative organisms, especially Pseudomonas aeruginosa, are common. Aspergillusspecies has also been reported in drowning victims. Broad-spectrum intravenous antibi-otic therapy (such as cefotaxime) should be started after blood and sputum cultures havebeen repeated.

Signs of raised intracranial pressure (ICP) may develop, probably as a result of a post-hypoxic injury. Aggressive treatment of a raised ICP has not however been shown toimprove the prognosis. Other therapeutic measures, such as barbiturates, calcium chan-nel blockers and free-radical scavengers have not shown any beneficial effects in clinicalpractice. But keeping the patient normoglycaemic is of importance for the optimal re-covery of the injured brain.

19.13 PROGNOSTIC INDICATORS

The clinical course of drownings is determined by the duration of hypoxic–ischaemicinjury and the adequacy of initial resuscitation. It is assumed that hypoxic brain damageis reduced when the brain cools before the heart stops. There is no single factor that canreliably predict good or poor outcome in drowning. Still, the following factors may givean indication on outcome.

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Immersion time

Most children who have been submerged for more than 8 minutes have a very smallchance of intact neurological recovery or survival. Details of the incident are thereforevital.

Time to first respiratory effort

If this occurs within 3 minutes after the start of basic cardiopulmonary support, theprognosis is good. If there has been no respiratory effort after 40 minutes of full cardiopul-monary resuscitation, there is little or no chance of survival unless the child’s respirationhas been depressed (e.g. by hypothermia, medication or alcohol).

Core temperature

If the victims are hypothermic before they drown (and suffer from asphyxia) they havea better prognosis. If the core temperature is less than 33◦C on arrival, the chances ofsurvival are increased because rapid cooling seems to protect vital organs. This is morelikely to occur in small children because of their large surface area to weight ratio. Agealone however does not seem to be a prognostic factor.

Persisting coma

This indicates a bad prognosis.

Arterial blood pH

If this remains less than 7·0 despite treatment, the prognosis is poor.

Arterial blood PO2

If this remains less than 8·0 kPa (60 mmHg), despite treatment, the prognosis is poor.

Type of water

Whether the water was salt or fresh has no bearing on the prognosis.The decision to discontinue resuscitation attempts is particularly difficult in cases of

drowning, and should be taken only after all the prognostic factors discussed above havebeen considered carefully.

19.14 OUTCOME

Seventy percent of children survive drowning when basic life support is provided at thesite of drowning. Only 40% survive without early basic life support, even if full advancedcardiopulmonary resuscitation is given in hospital.

Of those who do survive, having required full cardiopulmonary resuscitation in hospital,around 70% will make a complete recovery and 25% will have a mild neurological deficit.The remainder will be severely disabled or remain in a persisting vegetative state.

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19.15 SUMMARY

• There is a high incidence of associated cervical spine injury, especially during divingaccidents.

• Other associated injuries may arise during the incident leading to submersion.• Hypothermia should be actively sought and treated.• The decision to stop resuscitation should be taken after all prognostic indicators have

been considered.

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PART

VPRACTICAL PROCEDURES

213



214



CHAPTER

20Practical procedures – airway

and breathing

Procedures explained in this chapter

• Oropharyngeal airway insertionsmall childolder child

• Nasopharyngeal airway insertion• Orotracheal intubation including Rapid Sequence Induction

infant/small childolder child

• Laryngeal Mask Airway insertion• Surgical airway

needle cricothyroidotomysurgical cricothyroidotomy

• Ventilation without intubationmouth-to-mask ventilationbag-and-mask ventilation

• Management of a blocked tracheostomy (for guidance for parents)

20.1 OROPHARYNGEAL AIRWAY INSERTION

If gag reflex is present, it may be best to avoid the use of an oropharyngeal tube orother artificial airway, because it may cause choking, laryngospasm or vomiting.

Small child

1. Select an appropriately sized Guedel airway (see Chapter 5).2. Open the airway using the chin lift, taking care not to move the neck if trauma has

occurred.

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PRACTICAL PROCEDURES – AIRWAY AND BREATHING

3. Use a tongue depressor or a laryngoscope blade to aid insertion of the airway “theright way up”.

4. Recheck airway patency and look for improvement.5. If necessary, consider a different size from the original estimate.6. Provide oxygen; consider ventilation by pocket mask or bag-and-mask.

Older child

1. Select an appropriately sized Guedel airway (see Chapter 5).2. This can be inserted either

(a) using the technique as described for the younger child or(b) inserting the airway upside down until the tip has passed the soft palate and then

rotating it 180◦ so that the natural curve of the Guedel airway follows the curveof the tongue and pharynx (see Figure 20.1–20.3).

3. Recheck airway patency, looking for improvement following insertion.4. Be prepared to change to a different size.5. Provide oxygen and consider augmenting ventilation using either a pocket mask or a

bag–valve–mask device.

Figure 20.1. Airway insertion in an older child



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20.2 NASOPHARYNGEAL AIRWAY INSERTION

Assess for any contraindications such as a base of skull fracture.

1. Select an appropriate size (length and diameter) (see Chapter 5).2. Lubricate the airway with a water-soluble lubricant and insert a large safety pin

through the flange.3. Insert the tip into the nostril and direct it posteriorly along the floor of the nose (rather

than upwards).4. Gently pass the airway past the turbinates with a slight rotating motion. As the tip

advances into the pharynx, there should be a palpable “give”.5. Continue until the flange and safety pin rest on the nostril.6. If there is difficulty inserting the airway, consider using the other nostril or a smaller

size from the original estimate.7. Recheck airway patency.8. Finally provide oxygen, consider ventilation by pocket mask or bag-and-mask.

20.3 OROTRACHEAL INTUBATION (INCLUDING RAPIDSEQUENCE INDUCTION)

Introduction

As resuscitation and stabilisation improve due to application of the APLS principlesfewer children will require intubation when they are in extremis.

Conversely, more will require intubation as a planned urgent rather than emergentprocedure. This will often be outside the first hour during stabilisation or prior to transferto definitive care.

Intubation may need to be carried out in the referring hospital prior to the arrival of aretrieval team and will require anaesthesia/sedation and muscle relaxation if the child isconscious. The technique used to secure the airway rapidly and safely in this situation isknown as rapid sequence induction (RSI).

Figure 20.4. Technique 1: using the straight-bladed laryngoscope

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Rapid sequence induction

This has largely been the province of anaesthetists, for whom it is a core skill. However,it may also fall within the remit of paediatricians and emergency medicine specialists.Crucially, the person carrying out the procedure should be a confident, competent andexperienced intubator. They should have at least one and ideally two skilled assistantsand all equipment available as previously listed for intubation. In particular they shouldhave the patient on a tilting trolley or bed and have available a powerful, high-volumesucker. They must have a plan of action for a failed intubation. It is also appropriate forthose clinicians who will not have the skills to perform RSI to learn about the techniqueso that they can provide support for those who undertake it.

Steps in rapid sequence induction:

1. Prepare as above.2. Pre-oxgenate with 100% O2 for at least 3 minutes.3. Induce anaesthesia using a sedative or anaesthetic induction agent [see “Drugs” later].4. Apply cricoid pressure via your skilled assistant. Cricoid pressure causes compres-

sion of the oesophagus against the vertebral body behind, thereby preventing passiveregurgitation of gastric contents. It significantly enhances the safety of the intubation,but needs to be applied carefully and skilfully by an assistant specifically trained inthe technique. It should be noted that in the trauma patient at risk of C spine injurycricoid pressure should be applied with a two-handed technique, with the secondhand behind the neck to provide additional stabilisation [in addition to the assistantwho is stabilising the C spine by manual in-line immobilisation].

5. Administer a rapid-acting, short-lasting muscle relaxant. This should be suxametho-nium [1–2 mg/kg] in virtually all circumstances. There are contraindications such ashyperkalaemia, but it otherwise offers unique advantages in terms of rapidity of onset,and very short duration of action. The rapidity of onset is due to its very close re-semblance to acetyl choline. It causes depolarisation at the neuromuscular junction,and therefore prior to full relaxation the muscles are seen to twitch [fasciculate].

6. Wait for muscle fasciculation to stop, then intubate in the normal way.7. Check that intubation is successful in the usual way.

The assistant should NOT remove cricoid pressure until you are happy with tube place-ment, and that it has been secured in place.

Drugs

It must be stressed that all sedative and anaesthetic drugs may cause cardiovascularcollapse in the ill, particularly hypovolaemic, child.

Drugs to support the failing circulation should be immediately to hand and the seda-tive/anaesthetic drugs should be given with extreme caution, often in very low doses.

Anaesthetic induction agents which may be used are listed in the table below:

Drug Dose Important notes

Ketamine Dose 1–2 mg/kg Potent analgesia, dissociativeanaesthesia, less hypotensive.Causes intracranial pressure to riseand should not be used in case ofhead injury or potentially high ICP

Etomidate Dose 0.1–0.3 mg/kg Less hypotensive

Continued

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Drug Dose Important notes

Propofol Dose in a healthy childaround 5 mg/kg, but1–2 mg may suffice ina sick child

Most commonly usedinduction agent,therefore familiar. Verygood intubatingconditions, but muchless CVS stability

(Thiopental) Thiopentone Dose in healthy child atleast 5 mg/kg but 1–2mg may be enough ina sick child

Historically the agentof choice. Very smoothonset, but may inducemarked cardiovascularimpairment

Sedative drugs Again, much lowerdoses may be neededin the sick child

Benzodiazepines:midazolam is the mostcommonly used drugin this groupOpioid drugs:fentanyl and morphineare commonly used

Technique of tracheal intubation: for immediate intubation in theapnoeic child or following RSI in the planned intubation

Infant or small child1. Ensure that adequate ventilation and oxygenation by face mask are in progress. It is

much less worrying for you and much safer for the child if adequate pre-oxygenationhas been carried out. However, it should be realised that as one of the indicationsfor intubation is failure to ensure adequate patency by any other means, this may notalways be possible.

2. Prepare and check equipment. (before inducing RSI if used under these circum-stances)

3. Ensure manual immobilisation of the neck by an assistant if cervical spine injury ispossible. Because of the relatively large occiput, it may be helpful to place a foldedsheet or towel under the baby’s back and neck to allow extension of the head.

4. The laryngoscope should be held in the left hand and inserted initially into the right-hand side of the mouth, thereby displacing the tongue to the left. Lift the epiglottisforward. The vocal cords should be sought in the midline directly underneath. It iseasy to obscure the view by either looking too far to the left or too far to the right intoeither the piriform fossa or by inserting the blade too far past the larynx and downinto the oesophagus. In the circumstance where the laryngoscope blade has beeninserted too far into the oesophagus, if the blade is cautiously and slowly withdrawnthe vocal cords may suddenly pop into view.

In the unconscious baby being intubated by the relatively inexperienced doctor,it is often easiest to place the laryngoscope blade well beyond the epiglottis. Thelaryngoscope blade is placed down the right side of the tongue into the proximaloesophagus. With a careful lifting movement, the tissues are gently tented up to “seekthe midline”. The blade is then slowly withdrawn until the vocal cords come into view.In some situations, it may be better to stay proximal to the epiglottis to minimise therisk of laryngospasm. This decision must be based on clinical judgement.

5. The tube should then be inserted through the cords, with due attention to the factthat in small children the trachea is very short. Whilst it is important not to insert

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the tube too far, thereby avoiding inadvertent bronchial intubation, it is much, muchmore dangerous to have a tube which is too short as this may be displaced any timeby movement of the child’s head.

6. Following intubation, placement of the tube should be confirmed by both inspect-ing the chest for equal bilateral movement and by auscultating the chest. It is alsoworth listening over the epigastrium for the absence of classic borborygmi followingoesophageal intubation.

7. If intubation is not achieved within 30 seconds discontinue the attempt, re-establishpre-oxygenation and try again.

8. The definitive test for successful placement is the presence of expired CO2 in theexhaled air. This can be tested by either chemical colour-change devices or evenbetter, by definitive end-tidal CO2measurement. This is not yet accepted in neonates.A large randomised trial is underway.

9. Once the tube is inserted and fixed into place, arrangements should be made to obtaina chest X-ray to confirm correct tube length. The end of the tube on X-ray shouldbe below the level of the vocal cords, but above the carina.

Older child1. Ensure that adequate ventilation and oxygenation by face mask are in progress.2. Prepare and check equipment. (before inducing RSI if used under these circum-

stances)3. Select an appropriate tube size, but prepare a range of sizes, including the size above

and below the best estimate (see Chapter 5).4. Ensure manual immobilisation of the neck of cervical spine injury by an assistant is

possible.5. Hold the laryngoscope in the left hand and insert it into the right-hand side of the

mouth, displacing the tongue to the left.6. Visualise the epiglottis and place the tip of the laryngoscope anterior to it in the

vallecula. The epiglottis is then pulled forwards by anterior pressure in the valleculaas demonstrated in the illustration.

7. Gently but firmly lift the handle towards the ceiling on the far side of the room, whilebeing careful not to lever on the teeth (Figure 20.5).

8. Insert the endotracheal tube into the trachea, concentrating on how far the tip isbeing placed below the vocal cords. The tip should lie at least 2 cm below the vocalcords, depending on age. If the tube has a “vocal cord level” marker, place this atthe vocal cords. Be aware that flexion or extension of the neck may cause migrationdownwards or upwards, respectively.

9. Inflate the cuff if present, to provide an adequate seal.10. Check the placement of the tube by inspecting the chest for movement and auscul-

tating the chest (including the axillae) and epigastrium.11. If endotracheal intubation is not achieved in 30 seconds, discontinue the attempt,

ventilate and oxygenate by mask and try again.12. Monitor expired carbon dioxide in the exhaled air by either colour-change capnom-

etry or end-tidal capnography.13. Once the tube is in place obtain a chest X-ray to confirm correct placement.

Complications of endotracheal intubationThese include:

• Oesophageal intubation – This is the most dangerous complication of attemptedintubation. Will cause severe hypoxia if not immediately recognised and is particularlydangerous when it occurs secondary to tube misplacement.

• Endobronchial intubation, resulting in lung collapse and/or risk of pheumothorax.

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Figure 20.5. Technique 2: using the curved-bladed laryngoscope

• Severe hypoxia from a prolonged attempt to intubate should not occur. It is not failedintubation which kills people, it is hypoxia.

• Chipping or loosening of the teeth. This is more likely in the trauma patient and inthe age group of children who are shedding their deciduous teeth.

• Overextension of the neck does not aid intubation; on the contrary, it makes the vocalcords more difficult to visualise, and should never be done.

Exacerbation of an existing cervical spine injury leading to neurological deteriorationshould be preventable with a high index of suspicion and the use of trained assistant(s)to provide immobilisation during airway manipulation.

20.4 LARYNGEAL MASK AIRWAY (LMA) INSERTION

Equipment

• Laryngeal mask airway, sizes 1, 1·5, 2 and 2·5 according to body weights roughly lessthan 5 kg, 5–10 kg, 10–20 kg and over 20 kg, respectively

• Lubricant• Syringe to inflate cuff• Adhesive tape to secure laryngeal mask airway• Suction• Ventilating device

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Procedure

1. Whenever possible, ventilate the patient with 100% oxygen using a bag–valve–maskdevice before inserting the laryngeal mask airway. During this time, check that all theequipment is present and working, particularly the integrity of the cuff.

2. Deflate the cuff and lightly lubricate the back and sides of the mask.3. Tilt the patient’s head (if safe to do so), open the mouth fully, and insert the tip of the

mask along the hard palate with the open side facing, but not touching the tongue(Figure 20.6a).

4. Insert the mask further, along the posterior pharyngeal wall, with your index fin-ger initially providing support for the tube (Figure 20.6b). Eventually, resistance isfelt as the tip of the laryngeal mask airway lies at the upper end of the oesophagus(Figure 20.6c).

5. Fully inflate the cuff .The LMA will rise slightly at this point.

Figure 20.6a–d. Insertion of the laryngeal mask airway

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6. Secure the laryngeal mask airway with adhesive tape and check its position duringventilation as for a tracheal tube. You will not usually obtain a completely gas tightfit.

7. If insertion is not accomplished in less than 30 seconds, re-establish ventilation usinga bag–valve–mask.

Complications

• Incorrect placement is usually due to the tip of the cuff folding over during insertion.The laryngeal mask airway should be withdrawn and reinserted.

• Inability to ventilate the patient, because the epiglottis has been displaced over thelarynx. Withdraw the laryngeal mask airway and reinsert, ensuring that it closelyfollows the hard palate. This may be facilitated by the operator or an assistant liftingthe jaw upwards. Occasionally rotation of the laryngeal mask airway may prevent itsinsertion. Check that the line along the tube is aligned with the patient’s nasal septum;if not, reinsert.

• Coughing or laryngeal spasm is usually due to attempts to insert the laryngeal maskairway into a patient whose laryngeal reflexes are still present.

• Inadvertant displacement. This is very common with smaller LMAs, usually due torotation, once a circuit or a self-inflating bag is attached.

20.5 SURGICAL AIRWAY

Cricothyroidotomy is a “technique of failure”. It is indicated if a patent airway cannot beachieved by other means. It must be performed promptly and decisively when necessary.

In children under the age of 12 years, needle cricothyroidotomy is preferred to sur-gical cricothyroidotomy. In the adolescent either technique can be used, but the surgi-cal technique allows better protection of the airway. The relevant anatomy is shown inFigure 20.7.

Figure 20.7. Surgical airway anatomy

In a very small baby, or if a foreign body is below the cricoid ring, direct trachealpuncture using the same technique can be used.

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Needle cricothyroidotomy

This technique is simple in concept, but far from easy in practice. In an emergencysituation the child may be struggling and attempts to breathe or swallow may result inthe larynx moving up and down:

1. Attach a cricothyroidotomy cannula-over-needle (or if not available, an intravenouscannula and needle) of an appropriate size to a 5-ml syringe.

2. Place the patient in a supine position.3. If there is no risk of cervical spine injury, extend the neck, perhaps with a sandbag

under the shoulders.4. Identify the cricothyroid membrane by palpation between the thyroid and the cricoid

cartilages.5. Prepare the neck with antiseptic swabs.6. Place your left hand on the neck to identify and stabilise the cricothyroid membrane

and to protect the lateral vascular structures from needle injury.7. Insert the needle and cannula through the cricothyroid membrane at a 45◦ angle

caudally, aspirating as the needle is advanced (Figure 20.8).

Figure 20.8. Needle cricothyroidotomy

8. When air is aspirated, advance the cannula over the needle, being careful not todamage the posterior tracheal wall. Withdraw the needle.

9. Recheck that air can be aspirated from the cannula.10. Attach the hub of the cannula to an oxygen flowmeter via a Y-connector. Initially the

oxygen flow rate (in litres) should be set at the child’s age (in years).11. Ventilate by occluding the open end of the Y-connector with a thumb for 1 second to

direct gas into the lungs. If this does not cause the chest to rise, the oxygen flow rateshould be increased by increments of 1 litre and the effect of 1 second of occlusionof the Y-connector reassessed.

12. Allow passive exhalation (via the upper airway) by taking the thumb off for 4 seconds.13. Observe chest movement and auscultate breath sounds to confirm adequate ventila-

tion.14. Check the neck to exclude swelling from the injection of gas into the tissues rather

than the trachea.15. Secure the equipment to the patient’s neck.

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16. Having completed emergency airway management, arrange to proceed to a moredefinitive airway procedure, such as tracheostomy or intubation if more skilled helphas arrived.

Important notes

There are two common misconceptions about transtracheal insufflation. The first is that it ispossible to ventilate a patient via a needle cricothyroidotomy using a self-inflating bag. Themaximum pressure from a bag is approximately 4·5 kPa (45 cm H2O – the blow-off valvepressure) and this is insufficient to drive gas through a narrow cannula. In comparison, walloxygen is provided at a pressure of 4 atmospheres (approximately 400 kPa or 4000 cm H2O.The second misconception is that expiration can occur through the cannula, or through aseparate cannula inserted through the cricothyroid membrane. This is not possible. Theintratracheal pressure during expiration is usually less than 3 kPa (30 cm H2O)–less thanone – hundredth of the driving pressure in inspiration). Expiration must occur via the upperairway, even in situations of partial upper airway obstruction. Should upper airway obstructionbe complete, it is necessary to reduce the gas flow to 1–2 l/min. This provides someoxygenation but little ventilation.

Nevertheless, insufflation buys a few minutes in which to attempt surgical airway.

Surgical cricothyroidotomy

This should only be considered in the older child (12 years or over):

1. Place the patient in a supine position.2. If there is no risk of neck injury, consider extending the neck to improve access.

Otherwise, maintain a neutral alignment.3. Identify the cricothyroid membrane.4. Prepare the skin and if the patient is conscious, infiltrate with local anaesthetic.5. Place your left hand on the neck to stabilise the cricothyroid membrane and to protect

the lateral vascular structures from injury.6. Make a small vertical incision in the skin and press the lateral edges of the incision

outwards, to minimise bleeding.7. Make a transverse incision through the cricothyroid membrane, being careful not to

damage the cricoid cartilage.8. Insert a tracheal spreader, or use the handle of the scalpel by inserting it through the

incision and twisting it through 90◦ to open the airway.9. Insert an appropriately sized endotracheal or tracheostomy tube. It is advisable to

use a slightly smaller size than would have been used for an oral or nasal tube.10. Ventilate the patient and check that this is effective.11. Secure the tube to prevent dislodgement.

Complications of cricothyroidotomyThese include:

• Asphyxia• Aspiration of blood or secretions• Haemorrhage or haematoma• Creation of a false passage into the tissues• Surgical emphysema (subcutaneous or mediastinal)• Pulmonary barotrauma

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• Subglottic oedema or stenosis• Oesophageal perforation• Infection

20.6 VENTILATION WITHOUT INTUBATION

Mouth-to-mask ventilation

1. Apply the mask to the face, using a jaw thrust grip, with the thumbs holding themask. If using a shaped mask, it should be the right way up in children (Figure 20.9),or upside down in infants (Figure 20.10).

Figure 20.9. Mouth-to-mask in a child

Figure 20.10. Mouth-to-mask in an infant

2. Ensure an adequate seal.3. Blow into the mouth port, observing the resulting chest movement.4. Ventilate at 15–30 breaths/min, depending on the age of the child.5. Attach oxygen to the face mask if possible.

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Bag-and-mask ventilation

1. Apply the mask to the face, using a jaw thrust grip. The fourth and fifth fingersshould perform a jaw thrust and the other fingers hold the mask tightly in place(Figure 20.11).

Figure 20.11. Bag-and-mask ventilation

2. Ensure an adequate seal.3. Squeeze the bag observing the resulting chest movement.4. Ventilate at 15–30 breaths/min, depending on the age of the child.

If a two-person technique is used, one rescuer maintains the mask seal withboth hands, while the second person squeezes the self-inflating bag.

This is to be recommended

20.7 MANAGEMENT OF BLOCKED TRACHEOSTOMYFOR FIRST RESPONDERS (INCORPORATING GUIDANCEFOR PARENTS)

When you suspect a child with the tracheostomy tube is not breathing, the procedure to follow is:

1. Stimulate2. Shout for help3. Suction4. Check for breathing – IF NO BREATHING5. Tube change6. Check for breathing7. Give up to five breaths if necessary8. Check for pulse9. Give five chest compressions if necessary

10. Give 20 cycles of five chest compressions to one breath11. Reassess the child’s ABC12. Summon more help

Do not leave the child alone if his or her breathing returns to normal.

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Basic Life Support1. Stimulate the child2. Shout for help

Don’t leave the child alone and commence basic life support immediately.3. Open and check the airway

If the child is unresponsive, it is essential to safeguard the air passage, to enableoxygen to pass to the lungs. To do this, you must tilt the head. Lay the child on hisor her back on a flat, firm surface and place one of your hands around the top of thehead to support it. With the fingers of your other hand, gently lift the tip of the child’schin upwards, taking care not to press under the jaw. This exposes the tracheostomy tube(Figure 20.12).

Figure 20.12. “Lift the tip of the child’s chin upwards”

4. If tube blocked attempt to clear with suction catheter if you are unable to pass thesuction catheter down the tracheostomy tube – then the tube must be changed immediately.If you are unable to insert the new tube:– try a smaller tube; if unable to insert this– thread a suction catheter through the tracheostomy tube. Insert the tip of the suction

catheter into the stoma, then attempt to guide the tracheostomy tube along thecatheter and into the stoma.

– If this is unsuccessful then:attempt breathing via the suction catheter through the stoma (only if a large suctioncatheter)orattempt mouth-to-stoma/mouth-to-mouth resuscitation.

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Figure 20.13. Check for breathing

5. Check for breathingSupporting the new tube, place the side of your face over the tracheostomy tube tolisten and feel for any breaths, and at the same time look at the child’s chest to observeany breathing movement (Figure 20.13).If the child is not breathing, or there are only infrequent gasps, you will have to breathefor the child by performing rescue breathing.

6. Give up to five rescue breathsYou must inflate the child’s lungs by blowing into their tracheostomy tube. To dothis, cover the child’s tracheostomy tube with your mouth and blow into the childuntil you see their chest rising (this tells you that their lungs are inflating).

Remove your mouth from the child’s tube to let the breath escape from their lungs(you will see their chest fall again). Repeat this five times at a rate of about one breathinto the child, every 2 seconds.

You will know your breathing has been effective if you can see the child’s chest riseand fall with each breath. After up to five breaths of mouth-to-tracheostomy rescuebreathing (at least two with good chest movement), you must check to see whetheror not the child is still circulating oxygen around their body. To do this you must seeif the child has a pulse, or any other signs of circulation.

7. If there is no pulse present or you are not sure and the child has not responded tothe rescue breathing, you will need to perform chest compressions (heart massage)as well as provide the child with rescue breathing.

8. Chest compressionsIdentify the position to deliver heart compressions. To do this, use two fingers to traceup along the lower margin of the child’s rib cage to the notch where the ribs join thebreastbone.

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Have a look at where the upper finger is on the chest, so that you can place the heelof that hand above it.

Supporting the tracheostomy tube with the other hand, press down on the chestfive times, depressing the breastbone by up to 4–5 cm.

9. Give 20 cycles of five chest compressions to one breathAs both chest compressions and rescue breathing are now required, you must giveone breath after every five compressions.

10. Reassess the child’s own breathing and pulse after about 1 minute of breathing andchest compressions (or 20 cycles). If they are still not breathing you must continueto breathe for them. If there is no pulse you must continue both breathing and chestcompressions until professional help is obtained.

11. Calling for helpThis is the time (i.e. after one full minute of Basic Life Support) to phone for helpby dialling 999, if no one else has done it in response to your earlier shout for help.

If the child recovers before help arrives, lay them in a safe position (recovery posi-tion).This will help to keep the airway clear and allows any vomit or mucus to drain fromtheir mouth. Keep them warm and do not leave them alone until help arrives.

Emergency equipment for tracheostomy change

This should be checked daily

1. Usual-size tracheostomy tube with tapes attached2. Smaller-size tracheostomy tube with tapes attached3. Scissors4. Sterile sodium chloride 0.9% ampoules5. Five 2-ml syringes6. Tracheal dilators7. Spare tape8. Gauze swab9. KY Jelly

10. Gloves

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CHAPTER

21Practical procedures – circulation


Vascular accessPeripheral venous access

upper and lower extremity veinsscalp veinsexternal jugular veinvenous cut-downumbilical vein

Central venous accessfemoral veininternal jugular veinexternal jugular veinsubclavian vein

Arterial cannulationIntraosseous access

Defibrillation

21.1 VASCULAR ACCESS

Access to the circulation is a crucial step in delivering advanced paediatric life support.Many access routes are possible; the one chosen will reflect both clinical need and theskills of the operator.

If fluids are to be given, infusion pumps or paediatric infusion sets must be used. Thisavoids inadvertent over-transfusion in small children.

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PRACTICAL PROCEDURES – CIRCULATION

Peripheral venous access

Upper and lower extremity veinsVeins on the dorsum of the hand, the elbow, the dorsum of the feet and the saphenous

vein at the ankle can be used for cannulation. Standard percutaneous techniques shouldbe employed if possible. Topical or injected local anaesthetic should be used whenevertime allows.

Scalp veinsThe frontal superficial, temporal posterior, auricular, supraorbital and posterior facial

veins can be used.

Equipment• Skin-cleansing swabs• Butterfly needle• Syringe and 0·9% saline• Short piece of tubing or bandage

Procedure1. Restrain the child.2. Shave the appropriate area of the scalp.3. Clean the skin.4. Have an assistant distend the vein by holding a taut piece of tubing or bandaging

perpendicular to it, proximal to the site of puncture.5. Fill the syringe with 0·9% saline and flush the butterfly set.6. Disconnect the syringe and leave the end of the tubing open.7. Puncture the skin and enter the vein. Blood will flow back through the tubing.8. Infuse a small quantity of fluid to see that the cannula is properly placed and then

tape into position.

External jugular vein

Figure 21.1. The course of the external jugular vein

Equipment• Skin-cleansing swabs• Appropriate cannula• Tape

Procedure1. Place child in a 15–30◦ head-down position (or with padding under the shoulders so

that the head hangs lower than the shoulders).

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2. Turn the head away from the site of puncture. Restrain the child as necessary in thisposition.

3. Clean the skin at the appropriate side of the neck.4. Identify the external jugular vein, which can be seen passing over the sternocleido-

mastoid muscle at the junction of its middle and lower thirds (Figure 21.1).5. Have an assistant place his or her finger at the lower end of the visible part of the

vein just above the clavicle. This stabilises it and compresses it so that it remainsdistended.

6. Puncture the skin and enter the vein.7. When free flow of blood is obtained, ensure no air bubbles are present in the tubing

and then attach a giving set.8. Tape the cannula securely in position.

Venous cut-downIf speed is essential, it may be more appropriate to use the intraosseous route for

immediate access, and to cut down later for continued fluid and drug therapy.

Equipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1% for local anaesthetic with a 2-ml syringe and a 25-gauge

needle• Scalpel• Curved haemostats• Suture and ligature material• Cannula

Figure 21.2. Site of long saphenous cut-down and its technique

Procedure1. Immobilise the appropriate limb.2. Clean the skin.3. Identify the surface landmarks for the relevant vein. These are shown in Table 21.1.

Table 21.1. Surface anatomy of the brachial and long saphenous veins

Child Brachial Saphenous (Figure 21.2)

Infant One finger-breadth lateral to themedial epicondyle of the humerus

Half a finger-breadth superior andanterior to the medial malleolus

Small children Two finger-breadths lateral to themedial epicondyle of the humerus

One finger-breadth superior andanterior to the medial malleolus

Older children Three finger-breadths lateral to themedial epicondyle of the humerus

Two finger-breadths superior andanterior to the medial malleolus

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4. If the child is responsive to pain, infiltrate the skin with 1% lidocaine (lignocaine).5. Make an incision perpendicular to the course of the vein through the skin.6. Using the curved haemostat tips, bluntly dissect the subcutaneous tissue.7. Identify the vein and free 1–2 cm in length.8. Pass a proximal and a distal ligature (Figure 21.2).9. Tie off the distal end of the vein, keeping the ends of the tie long.

10. Make a small hole in the upper part of the exposed vein with a scalpel blade orfine-pointed scissors.

11. While holding the distal tie to stabilise the vein, insert the cannula.12. Secure this in place with the upper ligature. Do not tie this too tightly; doing so would

cause occlusion.13. Attach a syringe filled with 0·9% saline to the cannula and ensure that fluid flows freely

up the vein. If free flow does not occur, then either the tip of the cannula is againsta venous valve or the cannula may be wrongly placed in the adventitia surroundingthe vein. Withdrawing the catheter will improve flow in the former case.

14. Once fluid flows freely, tie the proximal ligature around the catheter to help immo-bilise it.

15. Close the incision site with interrupted sutures.16. Fix the catheter or cannula to the skin and cover with a sterile dressing.

Umbilical veinVenous access via the umbilical vein is a rapid and simple technique. It is used during

resuscitation at birth.

Equipment• Skin-cleansing swabs• Umbilical tape• Scalpel• Syringe and 0·9% saline• Catheter

Figure 21.3. Umbilical cord cross section

Procedure1. Loosely tie the umbilical tape around the cord.2. Cut the cord with a scalpel, leaving a 1-cm strip distal to the tape.3. If there is bleeding from the vein gently tighten the tape, to stop it.4. Identify the umbilical vein. Three vessels will be seen in the stump: two will be small

and contracted (the arteries sited inferiorly), and one at the head end will be dilated(the vein) (Figure 21.3).

5. Fill a French 5-gauge catheter with 0·9% saline.6. Insert the catheter into the vein, and advance it approximately 5 cm.7. Tighten the umbilical tape to secure the catheter. A purse-string suture may be used

later to stitch the catheter in place.

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Central venous access

Central access can be obtained through the femoral, internal jugular, external jugularand (in older children) subclavian veins. The Seldinger technique is safe and effective.The femoral vein is often used as it is relatively easy to cannulate away from the chestduring cardiopulmonary resuscitation. Central venous access via the neck veins is notwithout dangers, and may be difficult in emergency situations. The course of the centralveins of the neck is shown in Figure 21.4.

Figure 21.4. The course of the central veins of the neck

Femoral veinEquipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1% for local anaesthetic with a 2-ml syringe and a 23-gauge

needle• Syringe and 0·9% saline• Seldinger cannulation set

syringeneedleSeldinger guide wirecannula

• Suture material• Prepared paediatric infusion set• Tape

Procedure1. Place the child supine with the groin exposed and leg slightly abducted at the hip.

Restrain the child’s leg and body as necessary.2. Clean the skin at the appropriate side.3. Identify the puncture site. The femoral vein is found by palpating the femoral artery.

The vein lies directly medial to the artery.4. If the child is responsive to pain, infiltrate the area with 1% lidocaine (lignocaine).5. Attach the needle to the syringe.

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6. Keeping one finger on the artery to mark its position, introduce the needle at a 45◦angle pointing towards the patient’s head directly over the femoral vein. Keep thesyringe in line with the child’s leg. Advance the needle, pulling back on the plungerof the syringe all the time.

7. As soon as blood flows back into the syringe, take the syringe off the needle. Imme-diately occlude the end of the needle to prevent blood loss.

8. If the vein is not found withdraw the needle to the skin, locate the artery again andadvance as in (6) above.

9. Insert the Seldinger wire into the needle, and into the vein.10. Withdraw the needle along the wire, ensuring that the wire is not dislodged from the

vein.11. Place the catheter over the wire and advance it through the skin, into the vein.12. Suture the catheter in place.13. Withdraw the wire, immediately occluding the end of the cannula to prevent blood

loss.14. Attach the infusion set.15. Tape the infusion set tubing in place.

Internal jugular veinEquipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1% for local anaesthetic with a 2-ml syringe and a 23-gauge




Procedure1. Place the child in a 15–30◦ head-down position.2. Turn the head away from the side that is to be cannulated and restrain the child as

necessary.3. Clean the skin at the appropriate side of the neck.4. Identify the puncture site. This is found at the apex of the triangle formed by the two

lower heads of the sternomastoid and the clavicle.5. If the child is responsive to pain, infiltrate the area with 1% lidocaine (lignocaine).6. Attach the needle to the syringe and puncture the skin at the appropriate place (see

(4) above).7. Direct the needle downwards at 30◦ to the skin; advance the needle towards the

nipple, pulling back on the plunger of the syringe all the time.8. As soon as the blood flows back into the syringe, take the syringe off the needle.

Immediately occlude the end of the needle to prevent air embolism.9. If the vein is not found withdraw the needle to the skin and advance it again some

5–10◦ laterally.10. Insert the Seldinger wire into the needle, and into the vein.11. Withdraw the needle along the wire, ensuring that the wire is not dislodged from the

vein.12. Place the catheter over the wire and advance it through the skin, into the vein.

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13. Suture the catheter in place.14. Withdraw the wire, immediately occluding the end of the cannula to prevent air

embolism.15. Attach the infusion set.16. Tape the infusion set tubing in place.17. Obtain a chest radiograph in order to see the position of the catheter and to exclude

a pneumothorax.

External jugular veinBy using the Seldinger technique it is possible to obtain central venous access via the

external jugular vein as described below. The anatomy is such that passage into the centralveins can sometimes be more difficult compared with other approaches.

Equipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1% for local anaesthetic with a 2-ml syringe and a 25-gauge


syringeneedleSeldinger guide wire (J wire)cannula


Procedure1. Place child in a 15–30◦ head-down position (or with padding under the shoulders so

that the head hangs lower than the shoulders).2. Turn the head away from the site of puncture. Restrain the child as necessary in this

position.3. Clean the skin at the appropriate side of the neck.4. Identify the external jugular vein, which can be seen passing over the sternocleido-

mastoid muscle at the junction of its middle and lower thirds.5. Have an assistant place his or her finger at the lower end of the visible part of the

vein just above the clavicle. This stabilises it and compresses it so that it remainsdistended.

6. Attach the needle to the syringe and puncture the vein.7. As soon as blood starts to flow freely, take off the syringe and occlude the end of the

needle.8. Insert a J wire into the needle and into the vein.9. Advance the J wire. There may be some resistance as the wire reaches the valve at the

proximal end of the vein. Gently advance and withdraw the wire until it passes thisobstacle.

10. Gently advance the wire.11. Withdraw the needle along the wire, ensuring that the wire is not dislodged from the

vein.12. Place the catheter over the wire and advance it through the skin, into the vein.13. Suture the catheter in place.14. Withdraw the wire, immediately occluding the end of the cannula to prevent air

embolism.

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15. Attach the infusion set.16. Tape the infusion set tubing in place.17. Obtain a chest radiograph in order to see the position of the catheter and to exclude

a pneumothorax.

Subclavian veinEquipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1% for local anaesthetic with a 2-ml syringe and a 23-gauge




Procedure1. Place the child in a 15–30◦ head-down position.2. Turn the head away from the site that is to be cannulated and restrain the child as

necessary.3. Clean the skin over the upper side of the chest to the clavicle.4. Identify the puncture site. This is 1 cm below the mid-point of the clavicle.5. If the child is responsive to pain, infiltrate the area with 1% lidocaine (lignocaine).6. Attach the needle to the syringe and puncture the skin at the appropriate place (see

(4) above).7. Direct the needle under the clavicle, “stepping down” off the bone.8. Once under the clavicle, direct the needle towards the suprasternal notch. Advance

the needle, pulling back on the plunger of the syringe all the time and staying assuperficial as possible.

9. As soon as the blood flows back into the syringe, take the syringe off the needle.Immediately occlude the end of the needle to prevent air embolism.

10. If the vein is not found, slowly withdraw the needle, continuing to pull back on theplunger. If the vein has been crossed inadvertently, free flow will often be establishedduring this manoeuvre.

11. If the vein is still not found repeat (7) to (10) aiming at a point a little higher in thesternal notch.

12. Insert the Seldinger wire into the needle, and into the vein.13. Withdraw the needle along the wire, ensuring that the wire is not dislodged from the

vein.14. Place the catheter over the wire and advance it through the skin, into the vein.15. Suture the catheter in place.16. Withdraw the wire, immediately occluding the end of the cannula to prevent air

embolism.17. Attach the infusion set.18. Tape the infusion set tubing in place.19. Obtain a chest radiograph in order to see the position of the catheter and to exclude

a pneumothorax.

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Arterial cannulation

Arterial cannulation is used to monitor arterial blood pressure, guide dosage adjust-ments in shock and hypertensive crisis, obtain blood samples for respiratory and acid–basestatus and calculate cerebral perfusion pressure.

It should not be performed in sites where there is skin infection or interruption, orabsent collateral circulation, and care should be taken in severe haemorrhagic sites. Inchildren, the preferred sites include radial, posterior tibial, dorsalis pedis, ulnar andfemoral arteries. The site should remain visible and not prone to contamination.

Radial artery cannulationEquipment• Skin-cleansing swabs• Lidocaine (lignocaine) 1%• Heparinised syringe• Cannula

❝ Pre-term, 24-gauge❝ Infant–pre-school, 22-gauge❝ School-aged, 20–22-gauge❝ Adolescent–adult, 18–20-gauge

• T-connector or three-way tap with extension• Gauze, pad and tapes• Transparent sterile dressing• Flushed infusion set (saline 0.9% with heparin 0.5–1.0 U/ml) with pressure infusion

bag or pump• Pressure transducer and monitor

Procedure1. Before using the radial artery check that the ulnar artery is present and patent. Oc-

clude both arteries at the wrist and then release the pressure on the ulnar artery;circulation should return to the hand. (It will flush pink.) If this does not happen, donot proceed with a radial puncture on that side.

2. Keep the wrist hyperextended and restrained, and palpate the radial artery (usuallylocated in the middle of the lateral third of the wrist).

3. Clean the skin, and infiltrate with local anaesthetic.4. Insert the cannula over the artery at 45◦ to the skin and advance it slowly. When the

artery is punctured blood will be seen to pulsate into the syringe.5. Advance the cannula over the needle and into the artery, and remove the needle whilst

compressing the artery proximal to the position of the cannula tip.6. Connect the T-connector or three-way tap with extension, ready-flushed with 0.9%

saline to test cannula patency.7. Tape the cannula securely in place and cover with transparent dressing.8. Connect the infusion set and calibrate the monitoring equipment.

Complications

• Arteriospasm• Haematoma• Thrombosis• Bacterial colonisation and sepsis

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Intraosseous infusion

The technique of intraosseous infusion is not new. It was used in the 1930s as a quickmethod of gaining vascular access (the only alternative was to use a reusable, resharpenedmetal needle or to perform a venous cut-down). Because it is important to achievevascular access quickly in many life-threatening situations, intraosseous infusion is againbeing recommended. Specially designed needles make this quick and easy. It is indicatedif other attempts at venous access fail, or if they will take longer than 1·5 minutes tocarry out. It is the recommended technique for circulatory access in cardiac arrest.

Equipment• Alcohol swabs• An 18-gauge needle with trochar (at least 1·5 cm in length)• A 5-ml syringe• A 20-ml syringe• Infusion fluid

Procedure1. Identify the infusion site. Fractured bones should be avoided, as should limbs with

fractures proximal to possible sites. The landmarks for the upper tibial and lowerfemoral sites are shown below, and the former approach is illustrated in Figure 21.5.

2. Clean the skin at the chosen site.3. Insert the needle at 90◦ to the skin.4. Continue to advance the needle until a “give” is felt as the cortex is penetrated.5. Attach the 5-ml syringe and aspirate or flush to confirm correct positioning.6. Attach the filled 20-ml syringe and push in the infusion fluid in boluses.

Figure 21.5. Tibial technique for intraosseous infusion

Surface anatomy for intraosseous infusions

Tibial FemoralAnterior surface, 2–3 cm below the Anterolateral surface, 3 cm above

tibial tuberosity the lateral condyle

21.2 DEFIBRILLATION

In order to achieve the optimum outcome, defibrillation must be performed quicklyand efficiently. This requires the following:

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• Correct paddle position• Correct paddle placement• Good paddle contact• Correct energy selection

Many defibrillators are available. Providers of advanced paediatric life support shouldmake sure that they are familiar with those they may have to use.

Correct paddle selection

Most defibrillators are supplied with adult paddles attached (13-cm diameter, or equiv-alent area). Paddles of 4·5-cm diameter are suitable for use in infants, and ones of 8-cmdiameter should be used for small children.

Correct paddle placement

The usual placement is anterolateral. One paddle is put over the apex in the midaxillaryline and the other is placed just to the right of the sternum, immediately below the clavicle(Figure 21.6).

Figure 21.6. Standard anterolateral paddle placement

If the anteroposterior placement is used, one paddle is placed just to the left side of thelower part of the sternum and the other just below the tip of the left scapula (Figure 21.7).

Figure 21.7. Anteroposterior paddle placement

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Good paddle contact

Gel pads or electrode gel should always be used (if the latter, care should be taken notto join the two areas of application). Firm pressure should be applied to the paddles.

Correct energy selection

The recommended levels are shown in Chapters 6 and 10.If the only device available is a standard AED, then energy levels are pre-set at 150 or

200 J. This is suitable for a child over 8 years (25 kg) and may be used if no other optionsare available in younger children. Some manufacturers are now producing attenuationdevices that reduce the energy level to 50 J. These devices are suitable for children aged1–8 years.

Safety

A defibrillator delivers enough current to cause cardiac arrest. The user must ensurethat other rescuers are not in physical contact with the patient (or the trolley) at themoment the shock is delivered. The defibrillator should only be charged when the paddlesare either in contact with the child or replaced properly in their storage positions.

Disconnect the oxygen supply to the patient.

Procedure

Basic life support should be interrupted for the shortest possible time (5–9 below)

1. Apply gel pads or electrode gel2. Select the correct paddles3. Select the energy required4. Place the paddles onto the gel pads, and apply firm pressure5. Press the charge button6. Wait until the defibrillator is charged7. Shout “Stand back!”8. Check that all other rescuers are clear9. Deliver the shock

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CHAPTER

22Practical procedures – trauma


• Chest decompressionneedle thoracocentesischest drain placement

• Pericardiocentesis• Femoral nerve block• Diagnostic peritoneal lavage• Spinal care

cervical spine immobilisationapplication of a cervical collarapplication of head blocks and strapslog-rolling

• Helmet removal

22.1 NEEDLE THORACOCENTESIS

This procedure can be life-saving and can be performed quickly with minimum equip-ment. It should be followed by chest drain placement.

Minimum equipment

• Alcohol swabs• Large over-the-needle intravenous cannula (16-gauge or larger)• 20-ml syringe

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PRACTICAL PROCEDURES – TRAUMA

Procedure

1. Identify the second intercostal space in the mid-clavicular line on the side of thepneumothorax (the opposite side to the direction of tracheal deviation).

2. Swab the chest wall with surgical preparation solution or an alcohol swab.3. Attach the syringe to the cannula. Fluid in the cannula will assist in the identification

of air bubbles.4. Insert the cannula vertically into the chest wall, just above the rib below, aspirating

all the time (Figure 22.1).5. If air is aspirated remove the needle, leaving the plastic cannula in place.6. Tape the cannula in place and proceed to chest drain insertion as soon as possible.

Figure 22.1. Needle thoracocentesis

If needle thoracocentesis is attempted, and the patient does not have a tensionpneumothorax, the chance of causing a pneumothorax is 10–20%. Patients whohave had this procedure must have a chest radiograph, and will require chest

drainage if ventilated.

22.2 CHEST DRAIN PLACEMENT

Chest drain placement should be performed using the open technique described here.This minimises lung damage. In general, the largest size drain that will pass between theribs should be used.

Minimum equipment

• Skin prep and surgical drapes• Scalpel• Large clamps × 2• Suture• (Local anaesthetic)• Scissors• Chest drain tube

Procedure

1. Decide on the insertion site (usually the fifth intercostal space in the mid-axillaryline) on the side with the pneumothorax (Figure 22.2).

2. Swab the chest wall with surgical prep or an alcohol swab.

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Figure 22.2. Chest drain insertion – landmarks

3. Use local anaesthetic if necessary.4. Make a 2–3-cm skin incision along the line of the intercostal space, just above the rib

below.5. Bluntly dissect through the subcutaneous tissues just over the top of the rib below,

and puncture the parietal pleura with the tip of the clamp.6. Put a gloved finger into the incision and clear the path into the pleura (Figure 22.3).

This will not be possible in small children.7. Advance the chest drain tube into the pleural space during expiration.8. Ensure the tube is in the pleural space by listening for air movement, and by looking

for fogging of the tube during expiration.9. Connect the chest drain tube to an underwater seal.

10. Suture the drain in place, and secure with tape.11. Obtain a chest radiograph.

Figure 22.3. Chest drain insertion – clearing the path

22.3 PERICARDIOCENTESIS

The removal of a small amount of fluid from the pericardial sac can be life-saving. Theprocedure is not without risks and the ECG should be closely monitored throughout.An acute injury pattern (ST segment changes or a widened QRS) indicates ventriculardamage by the needle.

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Minimum equipment

• ECG monitor• (Local anaesthetic)• 20-ml syringe• Skin prep and surgical drapes• 6-inch over-the-needle cannula (16- or 18-gauge).

Procedure

1. Swab the xiphoid and subxiphoid areas with surgical prep or an alcohol swab.2. Use local anaesthetic if necessary.3. Assess the patient for any significant mediastinal shift if possible.4. Attach the syringe to the needle.5. Puncture the skin 1–2 cm inferior to the left side of the xiphoid junction at a

45◦ angle (Figure 22.4).6. Advance the needle towards the tip of the left scapula, aspirating all the time (Fig-

ure 22.5).7. Watch the ECG monitor for signs of myocardial injury.8. Once fluid is withdrawn, aspirate as much as possible (unless it is possible to withdraw

limitless amounts of blood, in which case a ventricle has probably been entered).9. If the procedure is successful, remove the needle, leaving the cannula in the pericardial

sac. Secure in place and seal with a three-way tap. This allows later repeat aspirationsshould tamponade recur.

Figure 22.4. Needle pericardiocentesis – angle

Figure 22.5. Needle pericardiocentesis – direction

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22.4 FEMORAL NERVE BLOCK

The femoral nerve supplies the femur with sensation, and a block is useful in casesof femoral fracture. The technique may also be of benefit when analgesic agents wouldinterfere with the management or assessment of other injuries. A long-acting local anaes-thetic agent should be used so that radiographs and splinting can be undertaken withminimal distress to the child.

Equipment

• Antiseptic swabs to clean• Lidocaine (lignocaine) 1%• A 2-ml syringe and a 25-gauge needle• A syringe (5- or 10-ml) and a 21-gauge needle• Bupivacaine 0·25%

0·8 ml/kg of 0·25% (maximum 2 mg/kg)

Procedure

1. Move the fractured limb gently so that the femur lies in abduction and the ipsilateralgroin is exposed.

2. Swab the groin clean with antiseptic solution.3. Identify the femoral artery and keep one finger on it. The femoral nerve lies imme-

diately lateral to the artery.4. Using the 2-ml syringe filled with lidocaine (lignocaine) and 25-gauge needle, infil-

trate the skin just lateral to the artery. Aspirate the syringe frequently to ensure thatthe needle is not in a vessel.

5. Inject the bupivacaine around the nerve using the 21-gauge needle, taking care notto puncture the artery or vein.

6. Wait until anaesthesia occurs (bupivacaine may take up to 20 minutes to have its fulleffect).

22.5 DIAGNOSTIC PERITONEAL LAVAGE

The technique described here is designed to maximise the sensitivity and specificity ofdiagnostic peritoneal lavage. Special care should be taken when performing diagnosticperitoneal lavage in children, otherwise the unwary operator may be caught out by therelative thinness of the abdominal wall, the intra-abdominal position of the bladder andthe high incidence of acute gastric dilatation.

Equipment

• Antiseptic solution• Lidocaine (lignocaine) 1% with adrenaline (epinephrine)• Scalpel• Self-retaining retractors• Suture material• 500 ml sterile normal (physiological) saline (warmed)• Sterile drapes• Syringe and needle

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• Artery forceps• Scissors• Peritoneal lavage catheter• Giving set

Procedure

1. Ensure that the urinary bladder is catheterised and drained, and that a gastric tubehas been passed to decompress the stomach.

2. Surgically prepare the abdomen with antiseptic solution and drapes.3. Identify the site for incision – one-third of the way down from the umbilicus towards

the pubis in the mid-line.4. Anaesthetise the area to the peritoneum with 1% lidocaine (lignocaine) and

adrenaline (epinephrine).5. Make a vertical incision through skin and subcutaneous tissue in the mid-line.6. Incise the fascia.7. Ensure haemostasis.8. Apply two clips to the peritoneum and gently lift it away from underlying structures.9. Using the scissors cut between the two clips – making a small hole in the peritoneum.

10. Insert the dialysis catheter through the hole, and gently advance it caudally into thepelvis.

11. Connect the dialysis catheter to a syringe and aspirate.12. If blood is not aspirated, connect the catheter to the giving set and infuse 10 ml/kg

of the warmed saline.13. Use as indicated for dialysis or treating hypothermia (see Chapter 15).

22.6 CERVICAL SPINE IMMOBILISATION

All children with serious trauma must be treated as though they have a cervical spineinjury. It is only when adequate investigations have been performed and a neurosurgicalor orthopaedic consultation obtained, if necessary, that the decision to remove cervicalspine protection should be taken. In-line cervical stabilisation should be continued untila hard collar has been applied, and sandbags and tape or head blocks and straps are inposition as described below.

Two techniques are described. It is necessary to apply both of these to achieve adequatecervical spine control.

Once the collar is in place, the neck is largely obscured. Before placing the collar lookfor the following signs quickly and without moving the neck.

1. Distended veins2. Tracheal deviation3. Wounds4. Laryngeal crepitus5. Subcutaneous emphysema

Application of a cervical collar

The key to successful, effective collar application lies in selecting the correct size.

Minimum equipment• Measuring device• Range of paediatric hard collars

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Figure 22.6. In-line cervical stabilisation

Method1. Ensure in-line cervical stabilisation is maintained throughout by a second person.2. Using the manufacturer’s method, select a correctly sized collar.3. Fully unfold and assemble the collar.4. Taking care not to cause movement, pass the flat part of the collar behind the neck.5. Fold the shaped part of the collar round and place it under the child’s chin.6. Fold the flat part of the collar with its integral joining device (usually Velcro tape)

around until it meets the shaped part.7. Reassess the correct fit of the collar.8. If the fit is wrong, slip the flat part of the collar out from behind the neck, taking care

not to cause movement. Select the correct size and recommence the procedure.9. If the fit is correct secure the joining device.

10. Ensure that in-line cervical stabilisation is maintained until head blocks and strapsor sandbags and tape are in position.

Application of head blocks and tape

Equipment• Two head blocks• Attachment system

Method

1. Ensure in-line cervical stabilisation is maintained by a second person throughout.2. Place a head block either side of the head.3. Apply the forehead strap and attach it securely.4. Apply lower strap across the chin piece of the hard collar and attach it securely.5. Apply tape across the chin piece of the hard collar and securely attach it to the long

spinal board.

Exceptions

Two groups of children cause particular difficulty. The first (and most common) is thefrightened, uncooperative child; the second is the child who is hypoxic and combative. In bothcases, overzealous immobilisation of the head and neck may paradoxically increase cervicalspine movement. This is because these children will fight to escape from any restraint. Insuch cases a hard collar should be applied, and no attempt made to immobilise the head withhead blocks and straps or sandbags and tape.

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22.7 LOG-ROLLING

In order to minimise the chances of exacerbating unrecognised spinal cord injury,non-essential movements of the spine must be avoided until adequate examination andinvestigations have excluded it. If manoeuvres that might cause spinal movement areessential (e.g. during examination of the back in the course of the secondary survey),then log-rolling should be performed. The aim of log-rolling is to maintain the alignmentof the spine during turning of the child. The basic requirements are an adequate numberof carers and good control.

Method

1. Gather together enough staff to roll the child. In larger children four people will berequired; three will be required in smaller children and infants.

2. Place the staff as shown in Table 22.1.3. Ensure each member of staff knows what they are going to do as shown in Table 22.2.4. Carry out essential manoeuvres as quickly as possible.

Figure 22.7. Log-rolling a child (four-person technique)

Table 22.1. Position of staff in log-rolling

Position of staff for

Staff member no. Smaller child and infant Larger child

1 Head Head2 Chest Chest3 Legs and pelvis Pelvis4 Legs

22.8 HELMET REMOVAL

Cycle or motorcycle helmets must be removed without causing cervical spine move-ments. This requires a minimum of two staff.

1. Obtain history of mechanism of injury.2. Explain procedure to patient and parent(s).

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Figure 22.8. Log-rolling a small child or infant (three-person technique)

Table 22.2. Tasks of individual members of staff

Staff member – position Task

Head Hold either side of the head (as for in-line cervicalstabilisation), and maintain the orientation of the head withthe body in all planes during turning.

Control the log-roll by telling other staff when to roll andwhen to lay the child back onto the trolley.

Chest Reach over the child and carefully place both hands underthe chest. When told to roll the child, support the weight ofthe chest and maintain stability. Watch the movement ofthe head at all times and roll the chest at the same rate.

Pelvis and legs This only applies to smaller children and infants. If it is notpossible to control the pelvis and legs at the same time,get additional help immediately.

Place one hand either side of the pelvis over the iliac crests.Cradle the child’s legs between the forearms. When told toroll the child, grip the pelvis and legs and move themtogether. Watch the movement of the head and chest at alltimes, and roll the pelvis and legs at the same rate.

Pelvis Place one hand over the pelvis on the iliac crest and theother under the top of the far leg. When told to roll thechild, watch the movement of the head and chest at alltimes and roll the pelvis at the same rate.

Legs Support the weight of the far leg by placing both handsunder it. When told to roll the child, watch the movementof the chest and pelvis and roll the leg at the same rate.

3. Carry out brief neurological examination.4. Demonstrate position of hands on each side of the helmet with thumbs on the

mandible and fingers on the occipital ridge. Keep this position whilst an assistantremoves the chin straps.

5. Direct the assistant to take control of the in-line stabilisation by holding the occipitalridge with one hand and placing the thumb and forefinger of the other hand alongthe mandible.

6. Gently remove the helmet, spreading it laterally if necessary. Then resume in-linestabilisation with both thumbs on the mandible, and fingers of both hands on theoccipital ridge.

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7. Ensure removal of any jewellery from the neck.8. Place the patient in a cervical collar, head blocks and straps and secure to the spinal

board.∗9. Carry out a brief neurological exam again.

∗A restless, agitated child should not be head-blocked or sandbagged and taped becauseof the risk that his or her struggling may cause further cervical spine damage.

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BYO33-23 BMJ Books BY033-Jones-v8.cls September 1, 2004 16:18

CHAPTER

23Interpreting trauma X-rays

23.1 INTRODUCTION

This chapter provides an overview of emergency imaging of the spine, chest and pelvisin children. It provides an introduction to interpretation for the clinician involved inmanaging paediatric trauma in the resuscitation room.

Radiological advice should be sought if there is any doubt that a film is normal. Dis-cussing the film with an experienced emergency physician or trauma, orthopaedic orneurosurgeon may also help. An experienced emergency radiographer (technician) is avaluable asset to any department and, if they consider a film is abnormal, their commentsshould be carefully noted.

Radiography of a seriously injured child is technically challenging as access is oftenlimited and films are often taken with a mobile machine. Equipment such as neck collarsmay obscure bony landmarks, and the position in which the child is lying may causedifficulty in radiographic interpretation due to rotation.

The radiology department is not a place to leave a sick or unstable patient withoutadequate clinical supervision. Plain films are taken by a radiographer, who will not beable to supervise an ill patient. Complex investigations including ultrasound scanning,computed tomography (CT) or contrast studies take time, during which the child maydeteriorate significantly without appropriate treatment.

Three standard trauma films are available to the emergency clinician:

1. Lateral cervical spine radiograph2. Chest radiograph3. Pelvic radiograph

These three provide a basic screen for major injuries. They should only be taken afterimmediately-life-threatening injuries have been identified and treated.

Viewing the film

Before reviewing any film, check the information shown over.

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INTERPRETING TRAUMA X-RAYS

• The name of the patient• The date and time that the film was taken• The orientation (side marker position)

View the film on a light box – not against the ceiling lights or a nearby window. Lightboxes give uniform illumination and should be available in all resuscitation rooms.

The ABCD approach to radiographic interpretation is shown in the box below.

Adequacy, Alignment and ApparatusBonesCartilage and soft tissuesDisc spaces (in the spine), Diaphragm (in the chest)

23.2 CERVICAL SPINE

Cervical spine immobilisation should take place before any radiographs are performed.The standard film is a lateral radiograph, which may be supplemented by AP (lower cervi-cal spine and odontoid peg views) when appropriate. If the child has an adequately fittedcervical collar for immobilisation, it is very difficult to get good quality AP views, includ-ing the odontoid peg. If sandbags rather than head blocks are used for immobilisationthey may obscure bony landmarks.

Bony injury in itself is not the prime concern in spinal injury. The main risk is actualor potential injury to the cord. Any unstable fracture, if inadequately immobilised, maylead to progressive cord damage.

A lateral cervical spine film is often requested to “clear” the cervical spine, but a normalfilm may be falsely reassuring. The plain film only shows the position of the bones at thetime the film was taken, and gives no idea of the magnitude of flexion and extensionforces applied to the spine at the time of injury. The cord may be injured even in a childwithout any apparent radiographic abnormality.

Unlike adult spines most paediatric cervical spine injuries occur either through thediscs and ligaments, at the cranio-vertebral junction (C1, C2 and C3) or at C7/T1.The relatively large mass of the head, moving on a flexible neck with poorly supportivemuscles, leads to injury in the higher cervical vertebrae.

Children develop three patterns of spinal injury:

1. Subluxation or dislocation without fracture2. Fracture with or without subluxation or dislocation3. SCIWORA (spinal cord injury without radiographic abnormality)

The last of these, SCIWORA, is said to have occurred when radiographic films aretotally normal in the presence of significant cord injury. If the film is normal in a consciouschild with clinical symptoms (such as pain, loss of function or paraesthesia in a limb) thenneck protection measures should be continued. In an unconscious child at high risk, acord injury cannot be excluded until the patient is awake and has been assessed clinically,even in the presence of a normal cervical spine film. Adequate spinal precautions shouldbe continued until the child is well enough to be assessed clinically, or magnetic resonanceimaging has been carried out.

The most common site of a “missed” spinal injury is where a flexible part of thespine meets the fixed part. In the neck these are the cervicocranial junction and thecervicothoracic junction.

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AdequacyThe whole spine should be viewed from the lower clivus down to the upper body of T1

vertebra. If the C7/T1 junction is not seen initially then gentle traction should be appliedby pulling the arms down, holding them above the elbow joint. If the child is consciousthey should be asked to relax their shoulders as traction is applied. If the child is on aspinal board then this must be stabilised by an assistant.

AlignmentSee Figure 23.1.

Figure 23.1. Lateral cervical spine showing anatomy and four review lines

The four lines shown in Figure 23.1 are reviewed. These are:

1. Anterior vertebral line2. Posterior vertebral line (anterior wall of the spinal canal)3. Facet line4. Spino-laminar line (posterior wall of the spinal canal)

The continuity of these lines should be maintained, no matter what the degree of flexionor extension seen on the neck film is. There should be no “steps” or angulation.

The spinal cord lies in the canal between the posterior vertebral (2) and the spinolam-inar (4) line. The former should line up with the clivus and the latter with the back ofthe foramen magnum.

BonesThe outline of each vertebra should be reviewed in turn. Fracture lines going through

the cortex, vertebral bodies, laminae or spinous processes should be sought.The spaces between the facet joints and the gaps between adjacent spinous processes

should be similar (Figure 23.2).The joint between the odontoid peg and the anterior arch of the atlas should be less

than 3 mm in a child. This is illustrated in Figure 23.3.The gap between the posterior arch of C1 and the spinous process of C2 may be slightly

larger than the gaps at the other levels in flexion. The base of the odontoid peg may not

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Figure 23.2. Lateral cervical spine showing disc spaces, facet joints and spinous process spaces

Figure 23.3. C1/C2 anatomy in the older child

be completely fused onto the body of the axis (C2) in a small child, but the orientationof the odontoid peg should always be perpendicular to the body of C2.

In adolescence, ring apophyses are seen related to the vertebral bodies as shown inFigure 23.4. These are sometimes a site for fracture separation from the vertebral body.The appearances of the apophyses at each level should be compared with the vertebraabove and below.

Cartilage and soft tissuesAbnormal widening of the pre-vertebral soft tissues may indicate a haematoma due

to cervical spine injury. There may however be a significant spinal injury with normalsoft tissues – thus the absence of soft tissue swelling does not exclude major bony orligamentous injury. When a child is intubated, it is difficult to assess pre-vertebral soft

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Figure 23.4. Ring apophyses in the adolescent spine

tissue swelling. Small children have large adenoids, which are seen as well-demarcatedsoft tissue swelling at the base of the clivus. This is shown in Figure 23.5.

Figure 23.5. Lateral cervical spine – soft tissues

Acceptable soft tissue thicknesses are:

• Above the larynx – less than one-third of the vertebral body width• Below the larynx – not more than one vertebral body width

Below the level of the larynx the pre-vertebral soft tissues become progressively narrowertowards the cervicothoracic junction. If the pre-vertebral soft tissues are wider at C7 thanat the C5 level, then this suggests trauma at the C7/T1 level.

Any soft tissue swelling outside these limits should be regarded as abnormal and neckprotection measures maintained until a further clinical and radiological opinion can beobtained. In small children the soft tissues may appear abnormally wide if the film is

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taken with the infant lying in flexion – if in doubt maintain the neck protection and askfor advice.

DiscsThe height of the vertebral disc should be compared from C2/C3 to C7/T1. The discs

should all be of similar height, as shown earlier in Figure 23.2.Flexion and extension cervical spine films should never be performed in the

acute trauma situation. Further imaging is obtained when the patient is stable,including CT to assess the bones or magnetic resonance imaging (MRI) forthe spinal cord. 638

AP films of the cervical spine may be taken. The films should be reviewedusing the same system as was used for the lateral cervical spine film:

Figure 23.6 shows five lines of alignment to assess. The spinal cord lies between lines2 and 4.

Figure 23.6. AP cervical spine showing anatomy and five review lines, discs and spinous processes

Chest radiograph

Adequacy and alignmentAdequacy can be assessed by considering both penetration and the depth of inspiration.The film should be sufficiently penetrated to just visualise the disc spaces of the lower

thoracic vertebrae through the heart shadow. At least five anterior rib ends should beseen above the diaphragm on the right side. An expiratory film may mimic consolidation.

Alignment can be assessed by ensuring that the medial ends of both clavicles are equallyspaced about the spinous processes of the upper thoracic vertebrae as shown in Fig-ure 23.7. Abnormal rotation may create apparent mediastinal shift. The trachea shouldbe equally spaced between the clavicles.

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Figure 23.7. Assessing rotation – straight-chest film

ApparatusCheck the position of any apparatus, including:

• Tracheal tube• Central venous lines• Chest drains

Misplacement of the tracheal tube (ETT) should be evident clinically, but may be seenon a chest film if you look for it. Do this first when reviewing any CXR on an intubatedpatient. Malposition of an ETT can result in reduced ventilation and hypoxia.

The ideal position for an ETT is below the clavicles and at least 1 cm above the carina.To find the carina, identify the slope of the right and left main bronchi – the carina iswhere the two lines meet in the midline.

BonesThe posterior, lateral and anterior aspects of each rib must be examined in detail. This

can be done by tracing out the upper and lower borders of the ribs from the posteriorcostochondral joint to where they join the anterior costal cartilage at the mid-clavicularline. The internal trabecular pattern can then be assessed.

The ribs in children are soft and pliable and only break when subjected to considerableforce. Even greater force is required to fracture the first rib or to break multiple ribs.Consequently, presence of these fractures should stimulate you to look for other sites ofinjury both inside and outside the chest.

Finish assessing the bones by inspecting the visible vertebrae, the clavicles, scapulaeand proximal humeri.

Thoracic spine injuries may be overlooked on a chest radiograph. Abnormal flatteningof the vertebral bodies, widening of the disc spaces, or gaps between the spinous processesor pedicles may be seen. On the AP views increased vertical or horizontal distances

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between the pedicles or spinous processes on the AP views indicates an unstable fractureas shown in Figure 23.8

Figure 23.8. Vertical fracture of the thoracic spine

If there are rib fractures in the first three ribs, these may be associated with major spinaltrauma and great vessel injury.

Cartilage and soft tissuesLungs

In a well-centred film, the lungs should appear equally black on both sides.Compare the left and right lungs in the upper third, middle third and lower third of

the chest.Check that the lungs go all the way out to the rib cage – i.e. there is no pleural effusion or

pneumothorax. A lung black on one side may be due to a pneumothorax or air trapping.A lung white on one side may be due to collapse, pulmonary haemorrhage, contusion oreffusion (including haemothorax).

On the supine film, blood or fluid lies posteriorly, giving a generalised greyness to thelung, rather than the typical meniscus sign seen on the erect film. At the apex of eachlung, an effusion displacing the lung down (apical cap) may indicate spinal injury ormajor vessel damage.

A suspected tension pneumothorax should be treated clinically in the emergency situ-ation, without confirmatory X-ray. On a supine film, the air in a simple pneumothoraxrises anteriorly and may only be evident from an abnormal blackness or “sharpness” ofthe diaphragm or cardiac border. The standard appearances of a pneumothorax, wherethere is a sharp lung edge and the vessels fail to extend to the rib cage and the lung edges,may not occur in the supine film.

The heartThe cardiac outline should lie one-third to the right of midline and two-thirds to the

left of midline. If the film is not rotated, then mediastinal shift is due to the heart beingeither pushed from one side or pulled from the other. For example, mediastinal shift to

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the left may be due either to a pneumothorax, air trapping or effusion on the right side,or to collapse of the left lung.

All trauma radiographs are taken in the supine position, often using portable X-ray ma-chines. The tube is near to the patient and the heart is anterior with the film posterior. Theheart in this situation appears abnormally magnified (widened) and the cardiothoracicratio is difficult to assess on supine AP films.

The mediastinal cardiac outline should be clear on both sides. Any loss of definitionsuggests consolidation (de-aeration) of adjacent lungs. A “globular” shape to the heartmay suggest a pericardial effusion. Tamponade is managed clinically, not radiologically.A cardiac echo is useful in equivocal cases.

The upper mediastinumIn the teenager the mediastinum should appear as narrow as in an adult. In children un-

der the age of 18 months, the normal thymus may simulate superior mediastinal widening(above the level of the carina). A normal thymus may touch the right chest wall, left chestwall, left diaphragm or right diaphragm, making it very difficult to exclude mediastinalpathology. Fortunately, mediastinal widening due to aortic dissection or spinal trauma isvery rare in small children.

In cases of doubt, where there is a normal clinical examination, an opinion from a radi-ologist should be sought. In the older child involved in trauma, mediastinal widening maymean aortic dissection, or major vessel or spinal injury. Ultrasound, CT or angiographymay be required to resolve this, when the child is stable.

DiaphragmsThe cardiophrenic and costophrenic angles should be clear on both sides. The di-

aphragms should be clearly defined on both sides and the left diaphragm should beclearly visible behind the heart. Loss of definition of the left diaphragm behind the heartsuggests left lower lobe collapse, an abnormal hump suggests diaphragmatic rupture andan elevated diaphragm suggests effusion, lung collapse or nerve palsy.

At the end of the systematic ABCD review of the X-ray, check again in the key areasshown in the box below.

• Behind the heart (left lower lobe consolidation or collapse)• Apices for effusions, pneumothorax, rib fractures and collapse/consolidation• Costophrenic and cardiophrenic angles – fluid or pneumothorax• Horizontal fissure – fluid or elevation (upper lobe collapse)• Trachea for foreign body (and ETT)

Pelvis

A single, anteroposterior pelvic view is usually taken. As with other films this can bereviewed using the ABC approach.

Adequacy and alignmentRotation of the pelvic film causes great difficulty in interpretation. In a non-rotated

pelvic film the tip of the sacrum and spine will be aligned with the symphysis pubis.The whole of the pelvis from the top of the iliac crests to the ischial tuberosities

should be included, as should both hips, with the femoral necks shown to the level of thetrochanters.

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BonesThe pelvis is made up from the sacrum, innominate bones (iliac wings), ischium and

pubic bones. These come together to form a Y-shaped cartilage in the floor of the ac-etabulum. In young children the joint between the ischium and the pubis (ischiopubicsynchondrosis) is commonly seen and may simulate a fracture.

The pelvis is reviewed as a series of rings, including the pelvic brim, the two obturatorrings and both acetabular fossae. These should appear smooth and symmetrical in a well-centred film. They are illustrated in Figure 23.9. The femoral necks must be checked forfracture and symmetry of the “tear drop” gap.

Figure 23.9. Normal, straight pelvis in a young child

Cartilage and soft tissuesMinor degrees of rotation, hip flexion or hip rotation will distort the fat plane and make

assessment of soft tissue displacement difficult. Abnormal widening of the obturator fatpad may indicate a pelvic side wall haematoma.

Figure 23.10. Multiple pelvic fractures

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The paediatric pelvis is held together by cartilage. Separation through the cartilage ofthe sacroiliac joint, the symphysis pubis or the “Y” cartilage of the acetabular floor mayoccur without apparent bony injury. Comparison of both hips and sacroiliac joints on awell-centred film may show this. On a well-centred film the distance between the femoralhead and the floor of the acetabular “teardrop” should be symmetrical – it is abnormalin effusion or dislocation.

If further assessment is needed, a CT scan is performed after the patient is stabilised.Angiography may be needed for vessel injury, or cystourethrography to assess associatedurethral or bladder damage.

The place of further imagingOnce the patient has been stabilised or resuscitated, further imaging of the

brain and spine may be needed, to exclude intracranial haemorrhage or spinalfracture. CT scanning is the first modality, but has a relatively high radiationdose.

NICE (National Institute for Clinical Excellence) NHS guidance on head injuriesThe NICE evidence is extrapolated from adult practice, as there are few studies to

form a scientific basis for this guidance in the paediatric age group.

Plain X-rays of the cervical spineUnder 10 years: AP views of the odontoid peg are difficult to obtain and are often

obscured by overlying un-erupted teeth – request lateral cervical spine. AP lowercervical spine.

Over 10 years – request lateral cervical spine. AP lower cervical spine, AP odontoidpeg view.

CT of the cervical spineIF the plain films are unclear, or there is a high-risk mechanism of injury:

Under 10 years of age the recommendation is for CT of the upper cervical spine (fromoccipital condyles and foramen magnum down to C3) – this covers the craniocervicaljunction. This is the most common site of fracture in this age group and it excludesthe radiosensitive thyroid gland from the scan.

Over the age of 10 years the recommendation is to image as adults – i.e. from theoccipital condyles down to the C7/T1 junction.

BRAIN imagingCT brain scanning is the prime modality for excluding acute intracranial haemorrhage.

A child with clinical features of intracranial bleeding (focal neurology, reduced GCS,etc.) requires a CT scan, not a skull film, as intracranial bleeding in children often occurswithout a skull fracture. Before the child is sent into the radiology department for ascan, he or she must be resuscitated, stabilised and supervised at all times by a doctor orappropriately trained senior nurse.

If a child has an indication for a head CT and when the mechanism of injury mightalso have caused a neck injury, then the cervical spine is included at the same time (seecervical spine CT above).

MR brain imaging is not suitable for an acutely ill patient. Specific MR-compatibleanaesthetic equipment is needed and scanning takes much longer than CT. MR is usefulin assessing spinal cord injury, disc injury and soft tissue injury in the spine. It is asecondary imaging modality rather than a modality used in the acute phase.

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Body imagingThere is often a temptation to scan the chest, abdomen and pelvis at the

same time as the head. This extends the time a sick child spends in radiologyand away from a high-dependency area. CT scanning is a high-radiation-doseprocedure, and the benefit from more areas imaged has to be carefully balanced againstthe time this takes and the radiation dose incurred. The decision to extend the scan toinclude the body must be based on clinical features and not requested simply “whilst thechild is being scanned”.

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CHAPTER

24Structured approach to stabilisation

and transfer

24.1 STABILISATION OF THE CHILD

After cardiac arrest, or after successful resuscitation of the seriously ill or injured child,frequent clinical reassessment must be carried out to detect deterioration or improvementwith therapy. In the emergency department or ward situation, invasive monitoring maynot be available. However, all patients should have the following monitored:

• Pulse rate and rhythm – ECG monitor• Oxygen saturation – pulse oximeter• Core temperature – low reading thermometer• Skin temperature• Blood pressure – non-invasive monitor• Urine output – urinary catheter• Arterial pH and gases – arterial blood sample• CO2 monitoring – capnography or transcutaneous CO2

Additionally some patients will require:

• Invasive BP monitoring – arterial cannula with pressure transducer• Central venous pressure monitoring – femoral, brachial or jugular catheter• Intracranial pressure monitoring – subarachnoid, subdural or

intraventricular devices

Some facilities may not be available until transfer to an intensive care setting.However, the investigations shown in the box should be performed following successful

resuscitation or during subsequent stabilisation:

Post-resuscitation investigations

• Chest radiograph• Arterial and central venous blood gasses• Haemoglobin, haematocrit and platelets

(Continued)

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STRUCTURED APPROACH TO STABILISATION AND TRANSFER

• Group and save serum for cross-match• Na+, K+, urea and creatinine• Clotting screen• Blood glucose• Liver function tests• Urinalysis and microscopy• 12-lead ECG

Children who have been resuscitated from cardiac arrest often die hours or days laterfrom multiple organ failure. In addition, to the cellular and homeostatic abnormalities thatoccur during the preceding illness, and during the arrest itself, cellular damage continuesafter spontaneous circulation has been restored. This is called reperfusion injury and iscaused by the following:

• Depletion of ATP• Entry of calcium into cells• Free fatty acid metabolism activation• Free-radical oxygen production

Similarly, children resuscitated with serious illness or injury may suffer multi-systemdysfunction as a result of hypoxia or ischaemia. Ongoing activation of inflammatorymediators, as occurs in serious sepsis, also contributes to multi-system organ failure.Post-resuscitation management aims to achieve and maintain homeostasis in orderto optimise the chances of recovery. Management should be directed in a systematicway.

Airway and breathing

After cardiac arrest, there is usually an impaired conscious level or depressed gag reflex.This may also apply after resuscitation of the critically ill or injured child. Intubation willusually have occurred.

• Intubation should be maintained and monitored by capnography.• Ventilation settings should be maintained to keep blood gases normal (P2 <

5·0 kPa), to minimise cerebral oedema and avoid raised intracranial pressure. If thisis difficult because of airway or lung disease, urgent advice should be obtained froma paediatric intensivist.

• Whether intubated or not, sufficient inspired oxygen should be given to maintainSa2 above 95%.

Circulation

Following resuscitation from any cause, there will usually be poor cardiac output. Thismay be due to any combination of the following factors:

• Underlying cardiac abnormality• Effects on myocardium of hypoxia, acidosis, and toxins, preceding and during arrest• Continuing acid–base or electrolyte disturbance• Hypovolaemia

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The following steps should be taken if there are signs of poor perfusion:

• Assess cardiac output clinically.• Infuse crystalloid or colloid 20 ml/kg and reassess cardiac output clinically.• Ensure normal arterial pH and oxygenation: this may require inotropic drug support

with/without further fluid boluses.• Support and monitor ventilation.• Identify and start to correct electrolyte abnormality or hypoglycaemia.• Following cardiac arrest, normalise body temperature to about 34◦C if initially be-

low 33◦C, reduce hyperthermic temperatures to normal, and avoid temperatures>37·5◦C.

A central venous pressure line will give useful information about systemic venous pres-sure, which will assist in the decisions about fluid infusion or inotropic support. Thecentral venous pressure measures right ventricular function and the effect of venous re-turn on preload.

The central venous pressure is best used in assessing the response to a fluid challenge.In hypovolaemic patients, central venous pressure alters little with a fluid bolus, but ineuvolaemia or hypervolaemia it shows a sustained rise.

Drugs used to maintain perfusion following cardiacarrest or treatment of shock

There are no research data comparing one drug to another that shows an advantageof any specific drug on outcome. In addition, the pharmacokinetics of these drugs varyfrom patient to patient and even from hour to hour in the same patient. Factors thatinfluence, in an unmeasurable manner, the effects of these drugs include the child’sage and maturity, underlying disease process, metabolic state, acid–base balance, thepatient’s autonomic and endocrine response, and liver and renal function. Therefore, therecommended infusion doses are starting points: the infusions must be adjusted accordingto patient response.

DobutamineDobutamine increases myocardial contractility and has some vasodilating effect by

decreasing peripheral vascular tone. Dobutamine is therefore particularly useful in thetreatment of low cardiac output secondary to poor myocardial function, for examplein septic shock and following cardiac arrest. It is infused in a dose range of 2–20 mi-crograms/kg/min. Higher infusion rates may produce tachycardia or ventricular ectopy.Pharmacokinetics and clinical response vary widely, so the drug must be titrated accord-ing to individual patient response.

Infusion concentration: 15 mg/kg in 50 ml of 5% dextrose or normal saline will give5 micrograms/kg/min if run at 1 ml/h.

For a dose of 2–20 micrograms/kg/min give 0·4–4 ml/h of the above dilution.

DopamineDopamine is an endogenous catecholamine with complex cardiovascular effects. At low

infusion rates (1–5 micrograms/kg/min), dopamine increases renal perfusion with littleeffect on systemic haemodynamics. At infusion rates greater than 5 micrograms/kg/min,dopamine directly stimulates cardiac β-adrenergic receptors and releases noradrenaline(norepinephrine) from cardiac sympathetic nerves. Myocardial noradrenaline (nore-pinephrine) stores are low in chronic congestive heart failure and in infants, so the drugis less effective in these groups. Dopamine can be used instead of dobutamine in the

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treatment of circulatory shock following resuscitation or when shock is unresponsive tofluid administration. It can also be used with dobutamine, but at the lower renal perfu-sion dose. Infusions are usually begun at 1–5 micrograms/kg/min and may be increasedto 10–20 micrograms/kg/min.

Dopamine infusions may produce tachycardia, vasoconstriction and ventricular ectopy.Infiltration of dopamine into tissues can produce local tissue necrosis. Dopamine andother catecholamines are partially inactivated in alkaline solutions and therefore shouldnot be mixed with sodium bicarbonate.

Infusion concentration: 15 mg/kg in 50 ml of 5% dextrose or normal saline will give5 micrograms/kg/min if run at 1 ml/h.

For a dose of 2–20 micrograms/kg/min, give 0·4–4 ml/h of the above dilution.

Adrenaline (epinephrine)An adrenaline (epinephrine) infusion is used in the treatment of shock with poor

systemic perfusion from any cause that is unresponsive to fluid resuscitation. Adrenaline(epinephrine) may be preferable to dobutamine or dopamine in patients with se-vere, hypotensive shock and in very young infants in whom other inotropes may beineffectual. The infusion is started at 0·1–0·3 microgram/kg/min and increased to1 microgram/kg/min depending on clinical response. Adrenaline (epinephrine) shouldbe infused only into a secure intravenous line because tissue infiltration may cause localischaemia and ulceration.

Infusion concentration: 0·3 mg/kg in 50 ml of 5% dextrose or normal saline will give0·1 microgram/kg/min if run at a rate of 1 ml/h.

For a dose of 0·1–2·0 micrograms/kg/min, give 1–20 ml/h of the above dilution.3 mg/kg in 50 ml of 5% dextrose or normal saline will give 1 microgram/kg/min if run

at a rate of 1 ml/h.For a dose of 0·5–2·0 micrograms/kg/min, give 0·5–2 ml/h of the above dilution.

Kidney

It is important both to maximise renal blood flow and to maintain renal tubular patencyby maintaining urine flow. To achieve this, the following are necessary:

• Maintenance of good oxygenation• Maintenance of good circulation using inotropes and fluids as required• Use diuretics (e.g. furosemide (frusemide) 1 mg/kg) to maintain urine output at or

above 1 ml/kg/h• Monitoring and normalisation of electrolytes (Na+, K+, urea, creatinine) and acid–

base balance in blood and urine

Liver

Hepatic cellular damage can become manifest up to 24 hours following an arrest.Among other things coagulation factors can become depleted, and bleeding may beworsened by concomitant, ischaemia-induced intravascular coagulopathy. The patient’sclotting profile and platelets should be monitored and corrected, as indicated, with freshfrozen plasma, cryoprecipitate or platelets.

Brain

The aim of therapy is to protect the brain from further (secondary) damage. To achievethis, the cerebral blood flow must be maintained, normal cellular homeostasis must beachieved and cerebral metabolic needs must be reduced.

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Adequate cerebral blood flow can only be achieved if the cerebral perfusion pressure(mean arterial pressure – intracranial pressure) is kept above 50 mmHg. Cellular home-ostasis is helped by normalisation of the acid–base and electrolyte balances. Cerebralmetabolic needs can be reduced by sedating the child and by controlling convulsions.Although barbiturate coma does reduce cerebral metabolism, it has not been shown toimprove neurological outcome.

Practical steps to minimise secondary brain injury are:

• Maintenance of good oxygenation• Maintenance of good circulation using inotropes and fluids as required• Monitoring and normalisation of electrolytes (Na+, K+, urea, creatinine) and acid–

base balance• Normalisation of blood glucose• Maintenance of adequate analgesia and sedation• Control of seizures• Reduction of intracranial pressure

❝ intubation and maintenance of normal blood gases❝ nurse 20–30◦ head-up❝ consider mannitol 0·25g/kg IV over 15 minutes

• Following cardiac arrest, normalise body temperature to about 34◦C if initially below33◦C and keep temperature <37·5◦C.

Post-cardiac-arrest hypothermia

Recent data suggest that there is some evidence that post-arrest hypothermia (coretemperatures of 32–34◦C) have beneficial effects on neurological recovery in adults,but there is insufficient evidence to date to recommend the routine use of hypother-mia in children. The results of therapeutic hypothermia are generally favourable inlaboratory models of hypoxic ischaemic injury to immature brains of various species.Until additional paediatric data becomes available, however, clinicians should tailor ther-apy for individual patients on the basis of their assessment of the risks and benefits ofhypothermia.

Current recommendations are that post-arrest patients with core temperatures less than37·5◦C should not be actively rewarmed, unless the core temperature is <33◦C, when theyshould be rewarmed to 34◦C. Conversely, increased core temperature increases metabolicdemand by 10–13% for each degree Centigrade increase in temperature above normal.Therefore, in the post-arrest patient with compromised cardiac output, hyperthermiashould be treated with active cooling to achieve a normal core temperature. Shiveringshould be prevented, since it will increase metabolic demand. Sedation may be adequateto control shivering, but neuromuscular blockade may be needed.

24.2 ASSESSMENT AFTER STABILISATION

After resuscitation and emergency treatment have been provided, the patient will usu-ally be transferred to where definitive care can continue. Before this happens, it is impor-tant to regularly reassess the child’s condition, firstly to ensure that no life-threateningdeterioration has occurred, and secondly to ensure that stability is maintained. The for-mer can be achieved by the ABCD rapid clinical assessment. Patient stability will beassessed effectively by use of one of a variety of checklists commonly used to reviewpatients receiving intensive care. An example is given in the box.

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Respiratory endotracheal tube, humidification, ventilation parameters, chestX-ray, blood gases

Cardiovascular circulatory status, hepatic size, use of inotropes, ECG, chest X-rayNeurological GCS, pupils, use of sedation, analgesia and paralysis, imaging

neuro-protection for RICPGastro-enterological nutrition, gastro-protection, ileusRenal and fluids urine output, fluid balance, urea and creatinine, need for renal

supportHepatic liver function testsBiochemistry electrolytes, blood sugar, calcium, magnesiumHaematology Hb, clotting studiesInfection temperature, WCC, review cultures/swabs, CRP, specific PCR,

antibioticsSkin / Joints skin, mouth and eye care, rashes, passive movementsDrugs complete list of enteral and IV drugs, drug levelsLines and tubes access for monitoring, blood sampling and IV drugs security of

catheters and drainsParents and family communications, concerns, support

24.3 PREPARING FOR TRANSPORT

Sick or injured children may initially be taken to a unit that can offer adequate resusci-tation or stabilisation, but is unable to offer further acute or long-term medical manage-ment. Such children must be transported to another hospital or department. Critically illchildren transferred by untrained personnel have been shown to suffer largely preventabletransfer-related morbidity. In the United Kingdom, the Paediatric Intensive Care Societyhas set a standard of practice for the transport of critically ill children. This may involvespecialised paediatric transfer teams, which are usually based at a paediatric intensivecare unit. These teams can be contacted in the event of requests for transfer of a childto a paediatric intensive care facility or a specialised facility such as a neurosurgical orburns unit. Often a patient needs to be transported from the emergency department toanother department within the same hospital. Not surprisingly, such transfers are alsoassociated with a high incidence of serious transport-related adverse events.

The basic principles of good transport should be applied to all sick children movedwithin or between hospitals, whether or not a specialised team is involved. Effectivepreparation and planning are the keys to the safe, successful, smooth transport of illchildren. This will ensure that the right patient is taken at the right time by the right peopleto the right place by the right form of transport and receives the right care throughout.

Thus important considerations are:

• How urgent is the transfer?• Is the child in the optimal condition for transfer?• Does the benefit of transfer outweigh the risks involved?• Who are the most appropriate people to transfer this child?• What type and mode of transfer is required for this child?

Whilst some transfers are time-critical (e.g. an expanding extradural haematoma), inmost cases, time spent ensuring the patient is stable, and appropriate staff and equipmentare available, is more likely to ensure an effective and safe transfer.

It is essential to evaluate, resuscitate and stabilise a child’s condition before movinghim or her – no child must be stabilised “on the way”. Whatever the injury or illness,

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the airway must be secured and ventilation must be adequate. Intravenous access mustbe established and fluids and/or life-saving drugs given. Proper evaluation requires athorough examination to show whether any orthopaedic, surgical or medical proceduresshould be carried out prior to transportation. Baseline haematological and biochemicalsamples should be taken when the intravenous lines are placed and essential imagingshould be carried out at this time.

Communication

The team organising the transfer should ensure good communication. Issues listed inthe box should be discussed as part of the organisation.

• Talk to the receiving hospital/unit/department early on.❝ Obtain advice from them and advise them concerning the child.❝ Find out what facilities are available there (especially transfers within the hospital).❝ Find out whether the parents will be required for consent for any procedures.

• Talk to the ambulance or portering service.❝ Make sure that they are aware of the condition of the child.❝ Make sure that they know what is required of them.

• Talk to your own team.❝ Make sure that everyone knows what is his or her job and responsibility.❝ Make sure that they know what is planned for the child.

• Talk to the parents.❝ Keep them up-to-date with their child’s condition.❝ Make sure that they know why and where their child is being transferred.

The staff at the receiving hospital or department must be contacted before arrangingtransport. Referring and receiving units should record their conversation, as well as thenames and contact details of the clinicians responsible for current and ongoing care.The receiving hospital must be clearly told what has happened, the state of the child, thetreatment received and what transport facilities and staff are needed. Both teams can thendecide if the child is stable enough for transport and whether the referring or receivinghospital will provide the staff to supervise transfer.

Joint management by the referring hospital and transport team should commenceimmediately, since successful initial resuscitation and stabilisation is crucial to ultimateoutcome. It must be stressed that this initial role is, and must remain, the responsibilityof the referring unit and should be provided at a senior level in conjunction with advicegiven by the receiving hospital staff. It is the responsibility of the team transporting thechild, however, to make sure that all necessary equipment and drugs are at hand, workingand that they know how to use them. It should never be assumed that ambulances willhave equipment.

Equipment

Dedicated transport equipment for monitoring and therapy should be available inthe emergency department. Familiarity with such equipment is a prerequisite for allemergency staff that are involved in the transport of a critically ill child. A list of essentialequipment is shown in the box.

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Paediatric resuscitation equipment

Airway

1. Oropharyngeal airway sizes 000, 00, 0, 1, 2, 32. Tracheal tubes sizes 2·5–7·5 mm uncuffed (in 0·5-mm steps) and 7·5 mm cuffed3. Laryngoscopes

• straight paediatric blades• adult curved blades

4. Magill forceps5. Yankauer sucker6. Soft suction catheters7. Humidity moisture exchange unit8. Needle cricothyroidotomy set

Breathing

1. Oxygen masks with reservoir2. Self-inflating bags (with reservoir)

• 240 ml, infant size (for pre-term infants)• 500 ml, child size• 1600 ml, adult size

3. Portable ventilator4. Face masks

• infant – circular 01, 1, 2• child – anatomical 2, 3• adult – anatomical 4, 5

5. Catheter mount and connectors6. Ayre’s T-piece

Circulation

1. ECG monitor – defibrillator (with paediatric paddles)2. Non-invasive blood pressure monitor (with infant- and child-sized cuffs)3. Pulse oximeter (with infant- and child-sized probes)4. Capnogram5. Intravenous access requirements

• Intravenous cannulae (as available) 18–25 g• Intraosseous infusion needles 16–18 g• Graduated burette• Intravenous giving sets• Syringes 1–50 ml

6. Intravenous drip monitoring device/syringe pumps7. Cut-down set

Fluids

• 0·9% saline• Hartmann’s solution or Ringer’s lactate• 4% dextrose and 0·18% saline• 5% dextrose• Colloid• 4·5% albumin

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Drugs

• Adrenaline (epinephrine) 1:10 000• Adrenaline (epinephrine) 1:1000• Atropine 0·6 or 1 mg/ml• Sodium bicarbonate 8.4%• Dopamine 40 mg/ml• Dobutamine• Lidocaine (lignocaine) 1%• Amiodarone• Dextrose 5 and 10%• Calcium chloride 10%• Furosemide (frusemide) 20 mg/ml• Mannitol 10 or 20%• Antibiotics – penicillin, gentamicin, ampicillin, cefotaxime, cefuroxime

Miscellaneous

• Stick test for glucose• Chest drain set

The ability to monitor and record the vital functions shown in the box is essentialduring transport.

• ECG and heart rate• Oxygen saturation• Non-invasive blood pressure• Temperature (core and peripheral)• End-tidal CO2

• Respiratory rate

All the equipment must be kept in a constant state of readiness and be checked at frequentintervals. Batteries must be capable of supporting full function for a period of at least twicethe maximum anticipated length of the transfer.

24.4 THE TRANSFER

The basic principles of transporting the seriously ill or injured patient are ongoingABCDE. Always assume that the worst might happen.

Airway and breathing

• The airways must be patent and secure, before moving and throughout the entiretransfer.❝ Nasal endotracheal tubes are better secured than oral.❝ The length and position of endotracheal tubes must be known before moving the

child.

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• Suction must be available and working throughout the entire transfer.❝ Portable suction is necessary when transporting a ventilated patient.❝ A condenser humidifier should be used to reduce tube blockage.

• Appropriate analgesic, sedative and muscle-relaxant drugs are usually required for thesafe and comfortable transfer of intubated patients. They will also minimize accidentalextubation.

• Full intubation equipment and drugs should be taken in case of an emergencyintubation/re-intubation.

• Ventilation should be provided by a mechanical ventilator, rather than manually.• A fully pressurised, size E oxygen cylinder contains approximately 600 l of gas and is

the most practical portable means of carrying oxygen. Check that oxygen cylindersare both full and working.

Calculate the amount of oxygen required for the journey using the following formula:

Number of cylinders = 2 × duration of journey × flow [l/min]cylinder capacity [litres]

For example, if oxygen is provided at 10 l/min for a journey intended to take 120 minutes, thiswould need 4 size E cylinders, each containing 600 l. This allows for at least twice as muchoxygen as the estimated journey time requires

Circulation

• Stabilise and optimise perfusion before moving the child.• Two good secure intravenous lines are the minimum.• These IV lines should be easily accessible during the transfer.• Central venous access is usually required in haemodynamically unstable or potentially

haemodynamically unstable children.• Blood pressure monitoring is needed regularly throughout the transfer – either non-

invasive cuff monitoring or direct intra-arterial.• Heart rate and rhythm must be monitored, preferably continuously.• Inotrope infusions should be delivered by a reliable means – e.g. battery-powered

syringe pump.• Pumps and monitors should be securely fastened for the transfer – preferably to the

stretcher and not to the patient.• Monitors must be easily viewable during the transfer.

The aim of the treatment of shock is to optimise the perfusion of critical vascular bedsand to prevent and correct metabolic abnormalities arising from cellular hypoperfusion.To this end, besides attention to ABC, other important therapeutic measures – such asinotropic support, the correction of metabolic derangements (hypoglycaemia, acidosis,severe electrolyte derangements) – may be required.

Disability

The transfer of the comatose child requires consideration, especially in the contextof head injuries. Coma is the sign of significant “brain failure” and requires emergencytreatment to prevent secondary central nervous system damage. Full assessment andinitial management of ABC and seizures along APLS guidelines take precedence overthe need to get the patient to the CT or MRI scanner.

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• The development of rising intracranial pressure should be anticipated and activelymanaged.

• A spinal board should be used if there is any suspicion of a spinal injury.• Fractured limbs must be properly splinted and immobilised.

Exposure

• Children, especially infants and those who are very ill, can become cold very quickly.• Blanket or duvets/quilts should cover exposed areas.• Do not forget to cover the child’s head (a relatively large surface area with a lot of

heat loss, particularly in infants).• Ensure that the transport vehicle is heated effectively.• Cold IV infusion fluids will further cool the child down, so consider warming them

up

Documentation

• All clinical findings, treatments and procedures should be documented, and the spe-cific time of the findings and all treatments/drugs given.

• All investigations [even if still awaiting the results] and their results should be docu-mented.

• The child’s notes, X-rays and any cross-matched blood should be taken with thechild.

• The child’s full name, age, date of birth and body weight (actual or the estimate usedin resuscitation) should be available and logged.

• The names of the medical and nursing staff involved [both at the referring and re-ceiving hospital/unit/department] should be documented.

• Parents’/care givers’ names and contact addresses and telephone numbers should bedocumented and they should be given details of the receiving hospital.

• If parents/guardians are unable to travel to the receiving hospital, it should be ensuredthat consent issues have been managed.

Dialogue

• Talk to your patient – sick children need explanations and verbal encouragement.Find out if they are in pain.

• Ensure the receiving unit knows when the child is leaving the referring hospital.• Update the receiving hospital on the child’s present status and problems.• Keep the parents/care givers up-to-date – clear explanations lessen anxiety and in-

crease cooperation.• Motivate and encourage your team – this is usually a stressful time.• A mobile telephone with an adequately charged battery is useful but be aware of its

possible interference with equipment (especially syringe drivers supplying inotropes).

Drugs

• Have the emergency drugs at hand and when appropriate already drawn up – e.g.intubation drugs, adrenaline (epinephrine), intravascular expanders.

• Make sure that you have the constituents to make any necessary infusions – bothinfusions that may run out and those that might be needed.

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• Do not forget appropriate analgesia and sedation; this should last for the entiretransfer.

• Check the blood glucose – you will need to carry IV fluids with glucose in them.

24.5 SUMMARY

Meticulous attention to initial assessment and resuscitation together with appropriateemergency treatment will reduce the chance of transport-related morbidity and mortality.A specialised paediatric transport team can transfer critically ill and injured children withminimal related complications. A checklist is shown in the box.

Checklist prior to transporting a child

1. Is the airway protected and is ventilation satisfactory? (substantiated by blood gases, pHand pulse oximetry if possible)

2. Is the neck properly immobilised?3. Is there sufficient oxygen available for the journey?4. Is vascular access secure and will the pumps in use during transport work by battery?5. Have adequate fluids been given prior to transport?6. Are fractured limbs appropriately splinted and immobilised?7. Are appropriate monitors in use?8. Will the child/baby be sufficiently warm during the journey?9. Is documentation available? Include:

child’s nameagedate of birthweightradiographs takenclinical notesobservation chartsneurological observation chartthe time and route of all drugs givenfluid chartsventilator recordsresults of investigations

10. Has the case been discussed with the receiving team directly?11. Have plans been discussed with the parents?

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PART

VIAPPENDICES

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APPENDIX

AAcid–base balance

Under normal circumstances the blood pH is tightly controlled between 7·35 and 7·45.Although this sounds like very little variation, it has to be remembered that there is alogarithmic relationship between pH and hydrogen ion concentration ([H+]). Thus a pHrise from 7·35 to 7·45 represents a fall in [H+] from 45 to 35 nmol/1. By the time the pHhas fallen to 7·1, [H+] has doubled to 80 nmol/l.

A normal intracellular pH is required for the functioning of the many enzyme systems inthe body. The body thus has mechanisms to maintain normal pH, and many buffers existto protect against the pH changes that occur as H+ production increases in sepsis, injury,poor perfusion and catabolism, or if there is failure to excrete normal acids produced.

Abnormalities of acid–base balance are important to understand for 2 major reasons.Firstly it is essential to identify and treat the cause of the acid–base disturbance, andsecondly the acid–base abnormality may require correction.

It is the intracellular pH that will affect the function of cells, and correction of theblood pH does not necessarily correct the intracellular pH. In the setting of poor tissueperfusion, administration of bicarbonate (which will increase the blood pH) may actuallyaggravate intracellular acidosis. There is evidence that administration of bicarbonate insituations such as diabetic ketoacidosis may actually increase the risk of cerebral oedemaand death.

The pH of blood affects the distribution of ions (such as calcium) throughout the body,and changes in pH may be associated with changes in ion concentration, which may haveeffects on body systems and thus require monitoring.

The acid–alkali balance equation

In the blood, bicarbonate reacts with hydrogen ions to produce CO2 and water:

H+ + HCO3 ↔ H2O + CO2

The balance of this equation is reflected by the Henderson Hasselbach equation:

pH = pKa + log[HCO3−]/0·03P2

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which is used by blood gas analysers to calculate [HCO3–] once P2 and pH have been

measured.The base deficit is calculated as the amount of base that would have to be added to

the system to correct the pH to normal, while the base excess is the amount of base thatwould have to be removed (or balanced with H+) in order to correct the pH. Unfortunatelythe base deficit is frequently expressed as a negative base excess, which may give rise toconfusion unless great care is exercised. In practice, blood gas analysers calculate the basedeficit from the difference between the calculated [HCO3

–] and a predicted “normal” of24 mmol/l. As normal values of [HCO3

–]are lower in young infants (18–20 mmol/l) thismay be a source of confusion.

The acid–base balance is also affected by “strong ions” in the body such as chloride.The term “strong” simply refers to the fact that these ions have a strong tendency toexist in the ionic form. The presence of ions affects the amount of H+ and HCO3

–produced, as electrochemical neutrality must be maintained in the body. An increase inthe concentration of chloride ions will tend to produce acidosis, while low chloride ionconcentrations will tend to induce metabolic alkalosis.

Short-term control of the blood pH is exerted via the respiratory system. Increasedventilation will drop the P2 and thus increase the pH within minutes, while decreasedventilation will have the opposite effect. The respiratory centre is driven by the pH of thecerebrospinal fluid (CSF). Any drop in CSF pH will result in an increase in respiratorydrive, with increased ventilation and loss of CO2. Conversely an increase in CSF pH willtend to decrease the respiratory drive.

Longer-term control of the acid–base status of the body is exerted by the productionof bicarbonate in the kidney, and the excretion of acid (over hours).

Figure A.1 shows the relationship between pH and bicarbonate concentration at dif-ferent levels of CO2. It can be seen that at a given bicarbonate concentration the pHfalls as the CO2 level rises. Also, it can be seen that at lower pH levels small falls inbicarbonate concentration produce dramatic reductions in pH. Similarly at low pH, ad-ministration of small amounts of bicarbonate may cause large shifts in pH. The nearerthe pH gets to normal the larger the amount of bicarbonate required to produce anychange.

Figure A.1. The relationship between pH, bicarbonate and carbon dioxide

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Abnormalities of acid–base

A drop in pH is referred to as acidosis, while an increase in pH above normal isalkalosis. Acidosis or alkalosis may be the result of respiratory or metabolic problems.Abnormalities of acid–base that are the result of respiratory dysfunction are generallyreferred to as respiratory acidosis or alkalosis, while acid–base abnormalities from allother systems are referred to as metabolic acidosis or alkalosis.

The body always attempts to correct abnormalities of pH and this may give rise to a“corrected acidosis or alkalosis”.

It is possible to have concomitant metabolic acidosis and respiratory alkalosis (or viceversa). In this situation the pH will be normal, but the P2, [HCO3

–] and base ex-cess/deficit will be abnormal.

Acidosis (low pH)

Respiratory acidosis is characterised by a low pH with a high P2, and results fromthe retention of CO2. In acute respiratory acidosis the [HCO3

–] will be normal, but inprolonged respiratory acidosis there is a tendency for the [HCO3

–] to gradually increasefrom renal compensation. It is important to note that the body will never overcompensate,so if the pH is normal or elevated in the face of an elevated P2, it means that there isconcomitant metabolic alkalosis.

In any patient with respiratory acidosis the questions to be asked are, is this a prob-lem of respiratory drive, a problem of respiratory function or a combination of both?The presence of nasal flaring is strong evidence of adequate respiratory drive. Respi-ratory function may fail as a result of problems in the airways, the lung, the thorax,the musculoskeletal system, the brain or finally the neuromuscular system. Manage-ment must be directed at identifying the problem(s) and providing adequate respiratorysupport.

Metabolic acidosis (characterised by a low pH, low or normal P2, and base deficit >2)is caused by:

Abnormal production of acidLactic acid in patients with shock and poor tissue perfusion, and mitochondrialdysfunctionKetoacidosis in patients with diabetic ketoacidosisAbnormal acids in children with inborn errors of metabolism, including lactic aci-doses, organic acidurias and amino-acidopathies

Abnormal excretion of acidRenal failureRenal tubular acidosis

Excessive levels of chlorideA feature of salt poisoning, or following resuscitation with large volumes of 0.9%sodium chloride

Toxin ingestionSalicylates

The body will attempt to correct for the metabolic acidosis. A “corrected metabolicacidosis” is characterised by a low pH with a low P2.

In the acute life-threatening illness or injury scenario, metabolic acidosis is most com-monly due to a combination of lactic acidosis and acute renal failure. The primary man-agement is thus to ensure that there is adequate resuscitation (ABC in particular) withcorrection of renal and other tissue perfusion.

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If the pH remains <7.15 in the face of adequate resuscitation, and it is felt that theacidosis is contributing to the clinical problems, a single dose of 1–2 mmol/kg (1–2 ml/kgof 8·4% NaHCO3) may be given. This is based on the knowledge that this raises the[HCO3

–] by about 1.5–3 mmol/l, which should improve the pH by 0.1–0.2 units (FigureA.1), whilst being unlikely to cause troublesome hypocalcaemia or hypokalaemia. If onrecheck of the pH, after this dose has been given, significant correction has not occurredthen it is due to the presence of a high acid load or high acid production rate. Expertassistance is required.

When correcting an acidosis the serum calcium and potassium should be monitoredcarefully. Correction of acidosis reduces the ionised calcium and may produce symp-tomatic hypocalcaemia. Hypocalcaemia will have a negative inotropic effect on the heart.Although the serum potassium is often high in the face of acidosis, correction will causeit to fall because of intracellular movement, and supplementation may be required. Con-tinued use of sodium bicarbonate will lead to hypernatraemia.

Where metabolic acidosis is inadequately explained, or more severe than expected, it isessential to collect specimens of blood and urine for later investigation of the causes of themetabolic acidosis. If this is not done, inborn errors of metabolism and toxin ingestionwill be missed.

A “compensated metabolic acidosis” is characterised by a low or normal pH with a lowP2, while a “compensated respiratory acidosis” is characterised by a low or normalpH with a high P2.

Alkalosis (high pH)

Respiratory alkalosis is characterised by a high pH with low P2 and results fromexcessive blowing off of CO2. In this situation it is important to identify what is causingthe patient to overventilate. Pain and anxiety are the most common causes, but cerebralirritation (e.g. meningitis) may also cause overventilation. The CO2 level can fall quitemarkedly, causing a significant rise in pH, which is often enough to produce hypocal-caemic tetany.

If a patient is overventilating from anxiety, the well-known remedy of breathing into apaper bag makes the patient rebreathe his or her own CO2 and is very effective. Organiccauses of overventilation must always be excluded before instituting rebreathing therapy.

Certain toxins such as salicylates may also be associated with respiratory alkalosis(although in children this is usually offset by a concomitant metabolic acidosis).

Metabolic alkalosis is characterised by a high pH in the face of a normal or high P2.The base excess is >2.

Metabolic alkalosis is commonly associated with severe vomiting of gastric contents.Severe vomiting causes alkalosis in two ways. First there is direct loss of acid from thestomach. Second, vomiting may induce severe hypovolaemia. This causes hyperaldostero-nism in an attempt to promote salt and water retention, which, in turn, leads to increasedrenal potassium and hydrogen ion loss, with bicarbonate retention. This exacerbates thealkalosis. Volume expansion with normal saline promotes correction. Congenital hyper-trophic pyloric stenosis is a good example of this pathophysiological process in action.It is important to exclude gastric outlet obstructions in small children with significantmetabolic alkalosis. Renal causes of alkalosis, such as Bartter’s syndrome, are rare, but di-uretic agents such as a furosemide (frusemide) are relatively common causes of metabolicalkalosis.

In most of the cases of metabolic alkalosis noted above, hypochloraemia is a commonfeature. Administration of additional chloride may often be the most effective way ofcorrecting the alkalosis. Very occasionally, agents such as acetazolamide may be used,but then only under specialist supervision.

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A.1 ANALYSIS OF ARTERIAL BLOOD GAS (ABG)

The proper interpretation of an ABG sample requires clinical history, examination,knowledge of treatments given, and other laboratory investigations. In emergencies, whenmuch of the data is lacking, interpret the findings with caution.

What is the pH? (normal: 7·36–7·44)

Is there an acidosis or alkalosis? If the pH is near normal it may be due to respiratoryor metabolic compensation. This compensation is never complete, so if the pH is nearnormal it will still always tell you if the child has a compensated acidosis (pH slightlylower than normal) or a compensated alkalosis (pH slightly higher than normal).

What is the Paco2? (normal: 4·7–6·0 kPa, 35–45 mmHg)

This is a good indicator of ventilatory adequacy because it is inversely proportional toalveolar minute volume (Respiratory rate × alveolar tidal volume). When the pH is knownit can be used to determine if there are primary or compensatory ventilatory changes.

A higher than normal Pa2 indicates underventilation. In association with a low pH,this indicates respiratory acidosis.

A lower than normal Pa2 indicates overventilation. In association with a high pHthis indicates respiratory alkalosis.

What is the base excess or deficit? (normal: ±2)

A base excess indicates a metabolic alkalosis, while base deficit indicates a metabolicacidosis. A base deficit is only treated if it is >6 and the pH is low (and then only inspecific circumstances).

Bicarbonate and base excess/deficit are calculated by blood gas analysers using theHenderson Hasselbach equation. These results must always be interpreted cautiously inclinical situations.

What is the PaO2? (normal: 10·6 kPa, >80 mmHg in air)

The partial pressure of oxygen in an arterial blood sample must be interpreted in thelight of the inspired oxygen concentration and the pressure of its delivery.

An easy method for blood gas interpretation

Step 1Assess the pH. Is it raised, >7·44 (alkalosis), or lowered, <7·36 (acidosis)? This is the

overall status of the patient, regardless of compensatory mechanisms.

Step 2Acidosis Alkalosis

Respiratory CO2 ↑ CO2 ↓Metabolic Base excess ↓ or Bicarbonate ↓ Base excess ↑ or Bicarbonate ↑

Look at the CO2 on the chart above.

• If the CO2 provides a cause for the abnormal pH, i.e. low pH with high CO2 (acidosis)and high pH with low CO2 (alkalosis), then the overall picture is a respiratory acidosisor alkalosis.

• If the CO2 does not provide a cause for the pH, it is compensating for a metabolicabnormality.

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Step 3Confirm your findings by looking at the base excess of bicarbonate.

• If the base excess provides a cause for the abnormal pH, i.e. low pH with negativebase excess (acidosis) and high pH with positive base excess (alkalosis), the overallpicture is a metabolic acidosis or alkalosis.

• If the base excess does not provide a cause for the pH, it is compensating for arespiratory abnormality.

Example

In a patient with shock, showing sighing respirations:

pH 7·24P2 31 mmHg[HCO3

−] 14 mmol/lBase deficit 8

• The pH is low, showing acidosis.• The P2 does not provide a cause for the abnormal pH (a low CO2 indicates a

respiratory alkalosis, not an acidosis); therefore it is compensating for a metabolicacidosis.

• The base deficit accounts for the abnormal pH (a base deficit indicates a metabolicacidosis).

• Therefore the patient has a metabolic acidosis, which is being partially compensatedby a blowing off of CO2.

Precautions when taking an arterial blood sampleThe taking of arterial blood samples is described in Chapter 21. Certain errors must beavoided:

• Note the inspired oxygen concentration.• Ensure an adequate sample and avoid bubbles. Air in the syringe will allow CO2 and

O2 to diffuse in or out of the sample. Seal the syringe with a plastic cap for the samereasons.

• Avoid excess heparin (which may produce an artefactual acidosis). Fill the dead spaceof a 2-ml syringe and attached needle with 1:1000 heparin. A pre-heparinised syringeis preferable.

• Minimise metabolism in the sample. Delay in analysis allows O2 consumption andCO2 generation to continue in the syringe sample. If a delay of more than a fewminutes is anticipated store the sample on ice.

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APPENDIX

BFluid and electrolyte management

B.1 INTRODUCTION

Between 70 and 80% of a child’s body is made up of water. That water is distributedbetween the intracellular, interstitial and intravascular spaces. Fluid moves from onecompartment to another depending on various pressure and osmotic gradients. In illnessand injury these fluid shifts may be rapid, with significant clinical consequences.

B.2 FLUID BALANCE

In health, fluid balance is tightly controlled by thirst, hormonal responses and renalfunction. In this context the formulae in Table B.1 provide a guideline to appropriatefluid intake. These formulae are based on an assumption of 100 kcal/kg/day of caloricintake, 3 ml/kg/day of urine output and normal stool output.

Table B.1. Normal fluid requirements

Body weight Fluid requirement per day (ml/kg) Fluid requirement per hour (ml/kg)

First 10 kg 100 4Second 10 kg 50 2Subsequent kilograms 20 1

For example, a 6-kg infant would require 600 ml/day,

a 14-kg child would require 1000 + 200 = 1200 ml/day anda 25-kg child would require 1000 + 500 + 100 = 1600 ml/day.

In critical illness or injury some or all of these mechanisms may be profoundly dis-rupted, and fluid therapy has to be tailored to the needs of the specific child. In thepresence of acute respiratory or CNS pathology, fluid requirements may be as low as30 ml/kg/day, while in diarrhoea requirements may be as high as 300–400 ml/kg/day.

Fluid intake is required to replace fluid losses, and to enable the excretion of variouswaste products through the urine. Insensible losses (via respiration, sweat) generally

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amount to between 10 and 30 ml/kg/day. The actual volume of insensible fluid loss isrelated to the caloric content of the feeds, the ambient temperature, humidity of inspiredair, presence of pyrexia and the quality of the skin. Insensible losses from a child on aventilator in a cool environment and with minimal caloric intake may be minimal. Usuallybetween 0 and 10 ml/kg/day are lost in stool (obviously this will increase markedly indiarrhoea, where losses in excess of 300 ml/kg/day are not uncommon). Urinary lossesare between 1 and 2 ml/kg/hour (i.e. approximately 30 ml/kg/day).

Dehydration and shock

Concepts

1) Dehydration does not cause death, shock does. Shock may occur with the loss of20 ml/kg, while clinical dehydration is only evident after losses of >25 ml/kg.

2) The treatment of shock requires rapid administration of intravascular volume of fluid thatapproximates in electrolyte content to plasma.

3) The treatment of dehydration requires gradual replacement of fluids, with electrolytecontent that relates to the electrolyte losses, or to the total body electrolyte content.

4) Damage from electrolyte changes is related to either extreme levels, or rapid rates ofchange.

5) Administration of sodium bicarbonate is rarely indicated.6) Overhydration is potentially much more dangerous than dehydration.

The intravascular volume is approximately 80 ml/kg. Rapid loss of 25% of this volume(i.e. 20 ml/kg) will cause shock unless that volume is replaced from the interstitial fluidat a similar rate. Clinical signs of dehydration (see table) only occur when the patient is2.5–5% dehydrated. Five percent dehydration implies that the body has lost 5 g/100 gbody weight, i.e. 50 ml/kg. Clearly, shock may occur in the absence of dehydration,dehydration may occur in the absence of shock or both may occur together – all dependenton the rate of fluid loss and the rate of fluid shifts.

Fluid and electrolyte losses occur in a number of situations:

Abnormal renal losses

• abnormal renal function (both high and low urine output may occur)• endocrine problems: both high (e.g. diabetes mellitus, diabetes insipidus) and

low urine output (syndrome of inappropriate ADH secretion) may occur

Abnormal GIT losses

• Mostly high output, with vomiting, diarrhoea or both.• Abnormal intake: excessive intake may be iatrogenic, with excessive fluid admin-

istration; accidental excessive intake of electrolytes such as sodium may occur,and occasionally this may be given deliberately (a form of child abuse).

The priorities of management are to identify shock and treat it effectively and rapidly(see chapter 9), identify dehydration and devise a treatment programme that will enableeffective rehydration over 24–48 hours, identify the presence and aetiology of acid–baseproblems and correct these where necessary, identify the presence and aetiology of elec-trolyte abnormalities and correct these gradually without precipitating complications.

One factor remains unknown at the initiation of therapy, namely the ongoing fluid lossesthat will occur during therapy. Thus any plan of fluid management represents a startingpoint, and this will have to be modified in the light of data from constant monitoring.

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The critical clinical questions are therefore:

Is the patient shocked?Is the patient dehydrated?Does the patient have a significant acid–base abnormality?Are there significant electrolyte problems?

Shock

The clinical signs of shock from fluid loss are:

Cardiovascular signs Tachycardia usually associated with poor volumeperipheral pulses

Poor peripheral perfusion with prolonged capillaryrefill time and cool peripheries

Low blood pressure as a pre-terminal signConsequences of poor perfusion Alteration of mental status

Development of metabolic acidosis withcompensatory tachypnoea

Poor urine output

The treatment of hypovolaemic shock secondary to fluid loss (after securing the airwayand providing high-flow oxygen) is the rapid administration of crystalloid. The startingvolume is 20 ml/kg, and this can be repeated if there is inadequate clinical response (withno evidence of intravascular overload). The fluids used should approximate in electrolyteconcentrations to those of serum (options include 0.9% saline, Hartmann’s solution).The presence of hyper- or hyponatraemia does not affect the choice of fluids during thisphase of resuscitation.

Occasionally, shock may be precipitated by cardiac dysrhythmia secondary to elec-trolyte abnormalities (most commonly of potassium). In this situation rapid correctionof the electrolyte anomaly may be essential. Usually electrolyte abnormalities should becorrected gradually.

Once shock has been adequately treated, attention can turn to management of hy-dration. Frequent reassessment is however necessary, as the patient may well becomeshocked again if the basic cause of the fluid shifts (e.g. gastro-enteritis) is ongoing.

Dehydration

The clinical signs of dehydration are:

Sign Comment

Drop in weight Only objective measure of acute changes in hydration.Unfortunately the child’s pre-sickness weight is usually notavailable, and so this is not usually useful in the initialevaluation of the child.

Depressed fontanelle Only useful if fontanelle well-patent, and in absence of disorderssuch as meningitis.

Sunken eyes Mothers may well recognize this sign, but it is poorly reproducibleamong clinical staff, especially if first contact with the patient.

(Continued)

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Sign Comment

Dry mouth Mouth breathers tend to have dry mouths, and mouth will be wet iffluids have just been administered orally.

Decreased skin turgor Difficult to interpret in malnourished children. Particularlyunreliable in fat children and in children with hypernatraemicdehydration.

Decreased urine output In renal disorders, patient may be dehydrated in association withinappropriately high urine output (same happens in diabetes).In the presence of gastroenteritis it is very difficult to establishurine output accurately, particularly in girls.

The clinical signs of dehydration are individually unreliable (see table) and have poorinter-observer reproducibility, but taken together they provide a reasonable estimate oftotal body fluid losses. Weight is the only objective measure of total body fluid shifts,and enables an accurate assessment of fluid balance over time (unfortunately initial fluidtherapy must usually be based on a clinical assessment of hydration because the pre-sickness weight is usually not available).

The weight loss or percentage dehydration (5% dehydration = loss of 5 ml of fluid per100 g body weight, or 50 ml per kg) provides an estimate of the volume of fluid requiredto replace the dehydration.

Management of dehydration consists of administration of calculated daily maintenancefluids in addition to calculated replacement fluids over a 24-hour period. The patientshould thus achieve normal body weight over a 24-hour period (this may increase to48 hours if there are electrolyte problems). Therapy must be monitored at 3–4-hourlyintervals using weight as an objective measure, to ensure that the patient is gaining weightat an appropriate rate. If the calculated fluid administration rate is too slow or too fast,then the rate should be modified appropriately.

Table B.2. Commonly available crystalloid fluids

Fluid Na+ (mmol/l) K+ (mmol/l) Cl− (mmol/l) Energy (kcal/l) Other

Isotonic crystalloid fluidsSaline 0·9% 150 0 150 0 0Saline 0·45%, dextrose 2·5% 75 0 75 100 0Saline 0·18%, dextrose 4% 30 0 30 160 0Dextrose 5% 0 0 0 200 0Hartmann’s solution 131 5 111 0 Lactate

Hypertonic crystalloid solutionsSaline 0·45%, dextrose 5% 75 0 75 200 0Dextrose 10% 0 0 0 400 0Saline 0·18%, dextrose 10% 30 0 30 400 0Dextrose 20% 0 0 0 800 0

When there is excessive vomiting or there are signs of damaged bowel, fluid therapyshould be given intravenously.

Example

A 6-kg child is clinically shocked and 5% dehydrated as a result of gastroenteritis.

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Initial therapy

20 ml/kg for shock = 6 × 20 = 120 ml of 0.9% saline given as a rapid intravenousbolus

Estimated fluid therapy

50 ml/kg for 5% dehydration = 50 × 6 = 300 ml100 ml/kg for daily maintenance fluid = 100 × 6 = 600 mlRehydration + maintenance = 900 ml∴ Start with infusion of 900/24 = 37 ml/h

Application of fluid therapy

Reassess clinical status and weight at 4–6 hours, and if satisfactory continue. If the childis losing weight increase the fluid rate, and if the weight gain is excessive decreasethe fluid rate. Start giving more of the maintenance fluid as oral feeds if the child istolerating the fluids.

When the gut is functioning, oral rehydration using standard solutions is ideal (WHOformulation provides 75 mmol Na, 20 mmol K, 65 mmol Cl, 10 mmol citrate and75 mmol glucose per litre. The formulations generally used in the UK have lower Naconcentrations of 50–60 mmol/l). This fluid should be administered frequently in smallvolumes (cup and spoon works very well for this process). Generally normal feeds shouldbe administered in addition to the rehydration fluid, particularly if the infant is breast-fed.

Fluid overload and overhydration

In the same way that fluid losses may cause shock, dehydration or both, excessive fluidadministration can cause intravascular fluid overload, overhydration or both.

In the patient with nephrotic syndrome, fluid has leaked out of the intravascular spaceand into the tissues because of a low serum albumin. Such children may be grossly over-hydrated, with diffuse severe oedema (see table). However, many patients with nephroticsyndrome have a contracted intravascular space, and attempts to diurese these patientswithout first expanding the intravascular space with albumin may result in shock.

By contrast the patient with myocardial dysfunction may have an intravascular com-partment that is grossly overfilled. The clinical signs of intravascular overload (see table)may be present, and yet the patient (particularly if they have been on diuretics) mayactually be total body fluid depleted and may appear dehydrated.

Children with other renal conditions may often have a combination of intravascular andtotal body fluid overload. They are then oedematous, but this is combined with featuresof intravascular fluid overload, and administering albumin would be dangerous.

Signs of intravascular fluid overload

Raised jugular venous pressure May be difficult to elicit in young childEnlarged (and often tender) liver Difficult to assess in the patient who already has a large

liver. May also be difficult to assess if the patient hasascites

Cardiac gallop, usually togetherwith cardiomegaly

May be difficult to assess in the patient with severetachycardia, and particularly if pulmonary oedema orother signs are present.

(Continued)

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Hypertension An important clinical feature of excessive intravascularfluid, particularly in patients with renal problems.

Pulmonary signs Diffuse fine crepitations in the bases of the lungs,together with other clinical signs of fluid in the lungs.

Signs of overhydration

Oedema Usually in dependent areas. In the infant or child who is either lying or sitting,this may not affect areas such as the buttocks or lower legs. Marked facialpuffiness may be a feature.

Weight gain Sudden increases in weight are often markers of excessive fluid intake.

Therapy is critically dependent on an understanding of the fluid balance.The patient with nephrotic syndrome who is overhydrated should not be treated by

diuresis alone. The management consists of fluid restriction, and in some cases diuresisfollowing the prior administration of albumin, so that fluid is brought into the intravas-cular compartment, prior to initiation of diuresis and thus preventing shock.

The patient with intravascular overload as well as overhydration requires fluid restric-tion and administration of diuretics. It is inappropriate (and potentially dangerous) totry and treat the resultant hypertension with agents such as β-blockers because this mayprecipitate heart failure.

In patients with cardiac failure, which has led to intravascular overload because ofpump failure, a situation may be reached where treatment with diuretics of intravascularoverload is causing dehydration. Attention must then be focused on a way of increasingcardiac output (using measures such as afterload reduction, or in the acute phase inotropicsupport) – in other words, treating the underlying cause.

The treatment of fluid overload is complex and the non-specialist shouldseek help.

Electrolyte abnormalities

Table B.3. Normal water, electrolyte, energy

Water Sodium Potassium Energy ProteinBody weight (ml/kg/day) (mmol/kg/day) (mmol/kg/day) (kcal/day) (g/day)

First 10 kg 100 2–4 1·5–2·5 110 3·00Second 10 kg 50 1–2 0·5–1·5 75 1·5Subsequent

kilograms20 0·5–1 0·2–0·7 30 0·75

Sodium

In situations of critical illness or major fluid and electrolyte abnormality, very variablefluid and electrolyte intake may be required.

Both low and high sodium levels are potentially dangerous to the patient. Severe hy-pernatraemia may be associated with severe brain damage, because brain tissue shrinksas a result of intracellular dehydration and blood vessels may tear or clot up. Toorapid correction of hypernatraemia may lead to cerebral oedema and injury. Similarly,

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rapid correction of hyponatraemia may also be associated with brain damage. Thussodium levels must be brought back to normal, but at a rate that does not exceed0.5–1 meq/l/h.

The electrolyte losses during dehydration depend on the reason for dehydration. In gas-troenteritis, sodium losses in diarrhoea range from approximately 50 meq/l (rotavirus)to approximately 80 meq/l (cholera and enteropathogenic Escherichia coli). In renal dys-function sodium losses may be minimal (diabetes insipidus) or significant (renal tubulardysfunction).

Hypernatraemia

Hypernatraemia in the dehydrated patient may be the end result of excessive loss ofwater (e.g. diabetes insipidus, diarrhoea), excessive intake of sodium (e.g. iatrogenic poi-soning, or non-accidental injury) or a combination of both (children with gastroenteritisgiven excessive sodium in rehydration fluid).

The electrolyte content of the replacement solutions depends on the cause of the de-hydration. In general 0.45% NaCl is a safe starting solution for rehydration. This isbased largely on the electrolyte content of stool in diarrhoea. If a patient is dehydratedfrom diabetes insipidus then virtually no sodium losses have occurred and fluid replace-ment could be done with fluid containing 0–0.18% NaCl. By contrast patients with renaltubular dysfunction and natriuresis may require 0.9% saline to replace the renal lossesof sodium. Measurement of Na content of urine and stool may facilitate replacementtherapy considerably.

As part of the monitoring of therapy electrolyte specimens should be collected. Fre-quent reassessment of fluid and electrolyte needs by repeated weighing and biochemi-cal measurement of serum electrolytes is the key to safe rehydration under all circum-stances.

Ongoing therapy for severe hypernatraemic dehydration

Start with (calculated) maintenance fluidvolume + (estimated) rehydration volumegiven as constant infusion over 24 hoursusing 0.45% saline with 5% dextrose.

Weigh and check serum sodium levels every4 hours.

IF:Sodium levels are correcting at a rate of

0.5–1 meq/l/h, and the weight is increasingat the estimated rate for rehydration over24–48 hours.

Therapy is appropriate.

Sodium levels are coming down at a rate of<0.5 meq/l/h, and the weight is correctingappropriately.

Decrease sodium content of IV fluid (e.g.change to 0.18% saline with dextrose).Could also consider careful administrationof diuretic in the context of sodiumoverload.

Sodium levels are dropping >1–1.5 meq/l/h,and the weight is increasing too rapidly.

Decrease rate of fluid administration.

Sodium levels are dropping >1–1.5 meq/l/hand the weight is not increasing toorapidly.

Increase sodium content of replacementsolution.

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Hyponatraemia

Hyponatraemia may be due to excessive water intake or retention, excessive sodiumlosses or a combination of both.

If hyponatraemia is due to excessive water intake or retention, and the patient is notsymptomatic, the restriction of fluid intake to 50% of normal estimated requirementsmay be adequate therapy. If however the patient is fitting from hyponatraemia, it may beappropriate to use hypertonic saline administration carefully to bring the sodium levelsup towards normal at a rate not exceeding 1 meq/L/h.

In hyponatraemia in the context of excessive losses sodium intake will have to exceedthe normal daily requirements. A reasonable starting fluid is 0.9% NaCl, with appropriateadjustment of fluid and electrolyte therapy on the basis of ongoing tests.

Potassium

Unlike sodium, potassium is mainly an intracellular ion and the small quantities mea-surable in the serum and extracellular fluid represent only a fraction of the total bodypotassium. However, the exact value of the serum potassium is important as cardiac ar-rhythmias can occur at values outside of the normal range. The intracellular potassiumacts as a large buffer to maintain the serum value within its normal narrow range. Thushypokalaemia is usually only manifest after significant total body depletion has occurred.Similarly, hyperkalaemia represents significant total body overload, beyond the abilityof the kidney to compensate. The exception to both these statements is the situation inwhich the cell wall pumping mechanism is breached. A breakdown of the causes of hyper-and hypokalaemia is given in Table B.4.

Table B.4. Causes of hypo- and hyperkalaemia

Hypokalaemia Hyperkalaemia

Diarrhoea Renal failureAlkalosis AcidosisVolume depletion Adrenal insufficiencyPrimary hyperaldosteronism Cell lysisDiuretic abuse Excessive potassium intake

In the critically ill neonate, inadequate cardiac output mustalways be excluded as a cause.

Hypokalaemia

Hypokalaemia is rarely a great emergency. It is usually the result of excessive potassiumlosses from acute diarrhoeal illnesses. As total body depletion will have occurred, largeamounts are required to return the serum potassium to normal. The fastest way of givingthis is with oral supplementation. In cases where this is unlikely to be tolerated, IVsupplements are required. However, strong potassium solutions are highly irritant andcan precipitate arrhythmias, thus the concentration of potassium in IV solutions oughtnot to exceed 80 mmol/l when given centrally, except on intensive care units. Fortunatelythis is not usually a problem as renal conservation of potassium aids restoration of normalserum levels.

Patients who are alkalotic, hyperglycaemic (but not diabetic) or are receiving insulinfrom exogenous sources will have high intracellular potassium stores. Thus hypokalaemiain these cases is the result of a redistribution of potassium rather than potassium defi-ciency, and treatment of the underlying causes is indicated.

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Hyperaldosteronism is a cause of hypokalaemic alkalosis. Patients with this conditionwill have salt and water retention and will be hypertensive on presentation. Secondaryhyperaldosteronism is the body’s natural response to hypovolaemia and salt deficiencyand is thus a common cause of hypokalaemic alkalosis. As there is primary salt andwater deficiency the patient is not usually hypertensive. The most common causes arediarrhoeal illness and salt-losing conditions such as cystic fibrosis. Other causes includeexternal loss of fluid from intestinal stomas or drains. Although potassium replacementis required in this condition the main thrust of therapy has to be with salt and waterreplacement to re-expand the circulation and cut down on aldosterone production.

Hyperkalaemia

Hyperkalaemia is a dangerous condition. Although the normal range extends up to5·5 mmol/l it is rare to get arrhythmias below 7·5 mmol/l. The most common causeof hyperkalaemia is renal failure – either acute or chronic. Hyperkalaemia can also re-sult from potassium overload, loss of potassium from cells due to acidosis or cell lysis,hypoaldosteronism and hypoadrenalism.

The immediate treatment of hyperkalaemia is shown schematically in Figure B.1. Ifthere is no immediate threat to the patient’s life because of an arrhythmia then a logi-cal sequence of investigation and treatment can be followed. Beta-2 stimulants, such assalbutamol, are the immediate treatment of choice. They act by stimulating the cell wallpumping mechanism and promoting cellular potassium uptake. They are best adminis-tered by a nebuliser. The dose to be given is shown in Table B.5. The serum potassiumwill fall by about 1 mmol/l with these dosages.

Figure B.1. Algorithm for the management of hyperkalaemia

Table B.5. Salbutamol dose by age

Age (years) Salbutamol dose (mg)

≤2·5 2·52·5–7·5 5>7·5 10

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Sodium bicarbonate is also effective at rapidly promoting intracellular potassium up-take. The effect is much greater in the acidotic patient (in whom the hyperkalaemia islikely to be secondary to movement of potassium out of the cells). The dosage is the sameas that used for treating acidosis, and 1–2 ml/kg of 8.4% NaHCO3 is usually effective. It ismandatory to also check the serum calcium, because hyperkalaemia can be accompaniedby marked hypocalcaemia, particularly in patients with profound sepsis or renal failure.The use of bicarbonate in these situations can provoke a crisis by lowering the ionisedcalcium fraction, precipitating tetany, convulsions or hypotension and arrhythmias.

Insulin and dextrose are the classic treatment for hyperkalaemia. They are not, however,without risk, and the use of salbutamol has fortunately reduced the requirement for suchtherapy. It is very easy to precipitate hypoglycaemia if monitoring is not adequate. Largevolumes of fluid are often used as a medium for the dextrose and, particularly in thepatient with renal failure, hypervolaemia and dilutional hyponatraemia can then be aproblem. Many patients are quite capable of significantly increasing endogenous insulinproduction in response to a glucose load, and this endogenous insulin is just as capable ofpromoting intracellular potassium uptake. It thus makes sense to start treatment with justan intravenous glucose load and then to add insulin as the blood sugar rises. The initialdosage of glucose ought to be 0·5 g/kg/h, i.e. 2·5 ml/kg/h of 20% dextrose. Once the bloodsugar is above 10 mmol/l, insulin can be added if the potassium level is not falling. Thedosage of insulin is initially half that used in diabetic ketoacidosis, i.e. 0·05 units/kg/h.This can then be titrated according to the blood sugar.

The above treatments are the fastest means of securing a fall in the serum potassium,but all work through a redistribution of the potassium into cells. Thus the problem ismerely delayed rather than treated in the patient with potassium overload. The only waysof removing potassium from the body are with dialysis or ion-exchange resins such ascalcium resonium. If it is anticipated that the problem of hyperkalaemia is going to persistthen the use of these treatments ought not to be delayed. Dialysis can only be startedwhen the patient is in an appropriate environment, but will be the most effective andrapid means of lowering the potassium. Ion-exchange resins can be used at the outset.The dosage of calcium resonium is 1 g/kg as an initial dose either orally or rectally,followed by 1 g/kg/day in divided doses.

In an emergency situation where there is an arrhythmia (heart block or ventriculararrhythmia) the treatment of choice is intravenous calcium. This will stabilise the my-ocardium but will have no effect on the serum potassium. Thus the treatments dis-cussed above will still be necessary. The dosage is 0·5 ml/kg of 10% Ca gluconate (i.e.0·1 mmol/kg Ca). This dose can be repeated twice. With a very high potassium, morethan one treatment can be used simultaneously.

Calcium

Some mention of disorders of calcium metabolism is relevant because both hyper- andhypocalcaemia can produce profound clinical pictures.

Hypocalcaemia

Hypocalcaemia can be a part of any severe illness, particularly septicaemia. Otherspecific conditions that may give rise to hypocalcaemia are severe rickets, hypoparathy-roidism, pancreatitis, or rhabdomyolysis, and citrate infusion (in massive blood trans-fusions). Acute and chronic renal failure can also present with severe hypocalcaemia.In all cases hypocalcaemia can produce weakness, tetany, convulsions, hypotension andarrhythmias. Treatment is that of the underlying condition. In the emergency situation,however, intravenous calcium can be administered. As most of the above conditions are

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associated with a total body depletion of calcium and because the total body pool is solarge, acute doses will often only have a transient effect on the serum calcium. Contin-uous infusions will also often be required, and must be given through a central venousline as calcium is so irritant to peripheral veins. In renal failure, high serum phosphatelevels may prevent the serum calcium from rising. The use of oral phosphate binders ordialysis or haemofiltration may be necessary in these circumstances.

Hypercalcaemia

Hypercalcaemia usually presents as long-standing anorexia, malaise, weight loss, failureto thrive and vomiting. Causes include hyperparathyroidism, hypervitaminosis D or A,idiopathic hypercalcaemia of infancy, malignancy, thiazide diuretic abuse and skeletaldisorders. Initial treatment is with volume expansion with normal saline. Following this,investigation and specific treatment are indicated.

B.3 DIABETIC KETOACIDOSIS (DKA)

DKA is a special case in which a relative or absolute lack of insulin leads to an inabilityto metabolise glucose. This leads to hyperglycaemia and an osmotic diuresis.

Once urine output exceeds the ability of the patient to drink, dehydration sets in. Inaddition, without insulin, fat is used as a source of energy, leading to the production oflarge quantities of ketones and metabolic acidosis. There is initial compensation for theacidosis by hyperventilation and a respiratory alkalosis but, as the condition progresses,the combination of acidosis, hyperosmolality and dehydration leads to coma. DKA isoften the first presentation of diabetes; it can also be a problem in known diabeticswho have decompensated through illness, infection or non-adherence to their treatmentregimes.

History

The history is usually of weight loss, abdominal pain, vomiting, polyuria and polydipsia,though symptoms may be much less specific in under-5-year-olds who also have anincreased tendency to ketoacidosis.

Examination

Children are usually severely dehydrated with deep and rapid (Kussmaul) respiration.They have the smell of ketones on their breath. Salicylate poisoning and uraemia are dif-ferential diagnoses that should be excluded. Infection often precipitates decompensationin both new and known diabetics, and must be sought.

Management

Assess

• Airway• Breathing• Circulation

Give 100% oxygen and place on a cardiac monitor.

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Take blood for:

• Bicarbonate/blood gases• Urea and electrolytes, creatinine, calcium, albumin• Glucose• Culture (if clinically indicated)

449• Haemoglobin and differential white cell count

Take urine for:

• Culture• Sugar• Ketones

The principles of management are to reverse shock, provide rehydration over24–48 hours, avoid hypokalaemia, avoid rapid changes in serum osmolarity (focus es-pecially on sodium and glucose levels), return glucose to normal levels and treat theunderlying precipitating cause of the DKA.

In order to provide appropriate therapy and avoid complications, it is essential to mon-itor these patients meticulously. Hourly monitoring should include heart rate, respiratoryrate and blood pressure (more frequently if these are unstable), oxygen saturation, neu-rological observations, urine output (if depressed level of consciousness or young child,insert urinary catheter) and fluid balance. Glucose must be monitored hourly (can usecapillary specimens if reasonable perfusion, and where possible check with laboratoryspecimens). Serum electrolytes and acid–base must be monitored at least 2-hourly un-less markedly abnormal, in which case hourly levels must be checked until more stable.

Shock is treated by the administration of oxygen and then 10–20 ml/kg of Ringer’slactate or 0.9% saline given over approximately 1 hour. Despite the fluid losses, shock isrelatively uncommon in DKA.

Rehydration is administered by calculating the expected 24-hour maintenance require-ment and the estimated fluid deficit. Administer maintenance fluids together with rehy-dration fluids, with rehydration calculated to happen over 24 hours. Initial rehydrationcan be given using normal saline, switching to 0·45% saline after the initial 1–2 hours.Once glucose levels fall below 14–17 mmol/l, 5% dextrose should be added to the fluidinfusions. Actual fluid volumes given should rarely exceed 1.5–2 times the usual mainte-nance requirements. Fluid administration needs to be adjusted to the actual fluid balanceon an hourly basis.

Insulin should be given by continuous infusion. The initial dose is 0·1 units/kg/h. Donot stop using insulin. This is the child’s prime requirement. Administer the insulinby a separate line. Add 25 units of soluble insulin to 50 ml saline. This solution is0·5 unit/ml:0·1 unit/kg/h is equal to 0·2 × weight in kg, as ml/h. Thus a 20-kg childwould have 4 ml/hour, a 35-kg child 7 ml/hour. The insulin infusion should continueuntil the acidosis is cleared. If the blood sugar falls below 15 mmol/l, then additionaldextrose must be added to the infusion, in order to maintain the glucose levels. Theinsulin dose can then be reduced to 0.05 units/kg/h but should not be reduced below thisif acidosis remains.

Potassium supplementation should be started as soon as insulin therapyis initiated, unless the patient is (unusually) hyperkalaemic. Hypokalaemia ismore of a risk than hyperkalaemia. Start with a concentration of 40 mmol/l ofKCl in the infusion. While there is little evidence that phosphate supplemen- 498tation is beneficial, severe hypophosphataemia should be treated. Potassium phosphatecan be given instead of KCl in the presence of hypophosphataemia. If phosphate is given,then the serum calcium must be monitored closely as it may precipitate hypocalcaemia.

The acidosis of DKA is initially compensated for by hyperventilation. Acidosis willresolve with treatment of shock, insulin supplementation and rehydration. Treatment with

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bicarbonate has been associated with the development of cerebral oedema and shouldtherefore be avoided unless essential. If the pH remains less than 7.1 despite replacementof intravascular volume, and appropriate insulin and glucose therapy for several hours,it may be reasonable to give bicarbonate. This should be discussed with the endocrineteam.

Regular, frequent (i.e. initially half-hourly) assessment of conscious level by the Glas-gow Coma Score is required to recognise early cerebral oedema. This complication ofdiabetic ketoacidosis is uncommon but may be devastating. It usually occurs in the moreseverely ill, but not always. A headache may be the first indication of the condition andshould be taken seriously. Early recognition of reduced conscious level should lead tomeasures for reducing raised intracranial pressure, and transfer to intensive care for in-tracranial pressure monitoring.

Complications

Major complications of diabetic ketoacidosisCerebral oedema Most important cause of death and poor neurological outcome.

Attempt to avoid by slow normalisation of osmolarity withattention to glucose and sodium levels, and hydration over36–48 hours.

Monitor for headache, recurrence of vomiting, Glasgow ComaScale, inappropriate slowing of heart rate and rising bloodpressure.

Treat with mannitol infusion (0.25–0.5 g/kg over 20 minutes), oralternatively hypertonic saline may be used.Hyperventilation has been associated with worse outcomes.

Cardiac dysrhythmias Usually secondary to electrolyte disturbances, particularlypotassium.

Pulmonary oedema Careful fluid replacement may limit the occurrence ofpulmonary oedema.

Acute renal failure Uncommon because of high osmotic urine flow.

All of these complications require intensive monitoring on an intensive care unit.

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BY033-APXC BMJ Books BY033-Jones-v8.cls September 1, 2004 16:20

APPENDIX

CChild abuse

C.1 INTRODUCTION

Child abuse is a universal occurrence. The medical aspects of this chapter are relevantin all settings, but the guidance for health professionals and legal details are specific tothe countries indicated in the relevant parts of the text.

Health care workers will come into contact with:

1. children who have been abused by adults or by other children,2. children who have abused other children and3. adults who were abused as children

Historical

The standard of care of children has varied over the centuries. Up to the nineteenthcentury, children were used in industry in a manner that today we would classify asabuse. In previous eras beating children as a means of discipline was accepted by mostsocial groups. The extremes of physical abuse were described in 1962 by Kempe, anAmerican paediatrician, as the “battered baby syndrome” – multiple bruises, intracranialhaemorrhages, fractures, and internal injuries in children under the age of 1 year.

Since 1962 we have gradually recognised many more forms of abuse. Present classifi-cations are as follows.

Classification of child abuse

NeglectNeglect means the persistent or severe neglect of a child, or the failure to protect

a child from exposure to any kind of danger, including cold or starvation, abandon-ment or extreme failure to carry out important aspects of care, resulting in the signifi-cant impairment of the child’s health or development, including non-organic failure tothrive.

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CHILD ABUSE

Physical injuryThis is actual or probable physical injury to a child, or failure to prevent physical

injury (or suffering) to a child, including deliberate poisoning, suffocation, and illnessesor injuries, which are fabricated or induced.

Sexual abuseThis is the involvement of dependent, developmentally immature children and adoles-

cents in sexual activities which they do not truly comprehend, to which they are unable togive informed consent or which violate the social taboos of family roles. There are manytypes of sexual abuse:

• Touching, fondling, or licking of genitals or breasts• Masturbation of child by adult or adult by child; or of an adult in the presence of the

child• Body contact with the adult genitals including rubbing or simulated intercourse by

the adult against or between thighs, buttocks, or elsewhere• Heterosexual or homosexual intercourse with actual or attempted vaginal, anal or

oral penetration• Exhibitionism (the display of genitals)• Involvement in pornography, including photography and erotic talk• Involvement in prostitution, male or female• Other varieties of sexual exploitation. Including internet child pornography and

“grooming” of a child

Most of these abusive acts will leave no physical signs on the victim.

Emotional abuseThis is described as actual or probable severe adverse effect on the emotional and

behavioural development of a child caused by persistent or severe emotional ill treatmentor rejection. All abuse involves some emotional ill treatment. This category should beused where it is the main or sole form of abuse.

Grave concernThis is described in children whose situations do not currently fit the above categories,

but where social and medical assessments indicate that they are at significant risk of abuse.These could include situations where another child in the household has been harmed orthe household contains a known abuser including situations where an adult is the subjectof domestic violence.

Organised abuseThis characteristically involves multiple perpetrators, involves multiple victims and is

a form of organised crime. There are three sub-sections. The first is paedophile and/orpornographic rings. The second is cult-based ritualistic abuse in which the abuse hasspiritual or social objectives. The third is pseudoritualistic abuse in which the degradationof children is the end rather than the means.

Presentations of physical abuse

• Head injuries – fractures, intracranial injury• Fractures of long bones 134

135335499145

– single fracture with multiple bruises– multiple fractures in different stages of healing, possibly with no bruises

or soft tissue injury– metaphyseal or epiphyseal injuries, often multiple

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CHILD ABUSE

• Fractured ribs, spinal injuries• Internal damage, e.g. rupture of bowel• Burns and scalds – “glove and stocking” appearance for scalds, implement imprints

for contact burns• Cold injury – hypothermia, frostbite• Poisoning – drugs or household substances, suffocation• Cuts and bruises – imprints of hands, sticks, whips, belts, bites, etc. may be present.

Presentations of sexual abuse

• Disclosure by child• Disclosure by witness• Suspicion by third party because of behaviour of child, especially changes in be-

haviour. These include insecurity; fear of men; sleep disorders; mood changes,tantrums, aggression at home; anxiety, despair, withdrawal, secretiveness; poor peerrelationships; lying, stealing, arson; school failure; eating disorders: anorexia, com-pulsive overeating; running away, truancy; suicide attempts, self-poisoning, self-mutilation, abuse of drugs, solvents, alcohol; unexplained acquisition of money; sexu-alised behaviour: drawings with a sexual content; knowledge of adult sexual behaviourshown in speech, play, or drawing; apparently sexual approaches; promiscuity

• Symptoms such as sore bottom, vaginal discharge, bleeding perirectum, inflamedpenis which caregiver believes is due to sexual abuse

• Symptoms as above and/or signs, e.g. unexplained perineal tear and/or bruising, tornhymen, perineal warts; but doctor is the first person to suspect abuse

• Sexually transmitted disease• Faecal soiling or relapse of enuresis• Child (usually adolescent girl) presents frequently with a variety of problems including

recurrent abdominal pain, overdose of drugs and reluctance to go home• Pregnancy but girl refuses to name the putative father or even indicate the category,

e.g. boyfriend, casual acquaintance

C.2 ASSESSMENT

The child who has disclosed abuse, or who is the subject of suspected abuse, will beoverwhelmed by the number of professional people who are involved in the assessmentof the situation. If the disclosure or suspicion arises in a nursery or school, then teachersand health visitors/school nurses will make preliminary enquiries and referrals. In allintra-familial abuse, social workers will speak to the child and the family. They willbe responsible for the safety of the child, for ongoing care of the family, and for anysubsequent civil proceedings. All child abuse is criminal activity, so police officers willinterview the alleged victim, the alleged offender, and any other witnesses to the incidents.There should be good liaison between social workers and police officers so joint interviewscan be done to minimise the number of times the child will have to relate the details of theincident(s). Whenever possible, these interviews are recorded on videotape to be used asevidence. Under the Criminal Justice Act 1991 (England and Wales), videotapes couldbe used as evidence in chief for children under the age of 14 years, provided that the childis available for cross-examination, and then a video link may be allowed by the judge.Under the Youth Justice and Criminal Evidence Act 1999, the age for child witnesses isnow 17 years but any vulnerable or intimidated adult is now also eligible for the samespecial measures.

Medical assessment will be carried out by a paediatrician with forensic training or jointlyby a police surgeon and a paediatrician. If the child has severe psychological disturbance

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CHILD ABUSE

or psychiatric symptoms, then a psychologist and/or psychiatrist will also see the childand the family. The basic medical assessment should follow the pattern used for all otherdiagnostic problems. Consent is not mandatory for child protection concerns but it isgood practice to involve the family wherever feasible.

Details of medical assessment

HistoryFull details of the history of the incident(s) should be obtained from the child and the

caregivers. If social workers and police officers have previously talked to the child, thentaking this history from them may be appropriate, especially for alleged sexual offences.Frequent repetition of the details can be very disturbing to the child and can jeopar-dise evidence. Remember to remain objective and show professional sensitivity. Systemicenquiry is then done for the cardiovascular system, respiratory system, gastrointestinaltract (remember to ask about soiling, constipation, rectal pain, rectal bleeding), uro-genital system (remember to ask about wetting, vaginal bleeding, vaginal discharge and,when appropriate, menarche, cycle, sanitary protection and previous sexual intercourse),central nervous system, musculoskeletal system, skin and behaviour.

Personal history must start with pregnancy, birth, the neonatal period, and subsequentdevelopmental milestones. Then details of immunisations, drug history (including alco-hol and street drugs), and allergies are obtained. Information on the child’s performanceat nursery or school should include social factors.

Enquiries are made about previous illnesses and injuries, with dates of attendanceat hospital or at the surgery of the family doctor. Past records should be obtained andrelevant information should be extracted.

The traditional family history should include details of the natural parents, all cohab-itees and any other people who regularly care for the child, e.g. relatives, childminders.Parental illness should be discussed, particularly psychiatric illness. The presence of do-mestic violence should be explored. Then the names, ages and medical histories of allsiblings and half-siblings are obtained. Any miscarriages, stillbirths or deaths of siblingsare discussed sensitively. Familial illnesses which are particularly important are inheritedskin or blood disorders.

ExaminationThe general examination starts while the history is being taken. During that time the

doctor observes the affect of the child, the relationships between child, mother, fatherand others present and any behavioural problems. If the child is reluctant to be examined,then playing with toys or the doctor’s stethoscope often breaks the ice. No child shouldbe examined against his or her will as this constitutes an assault. Sometimes a child whorefuses to be examined one day will come back quite cheerfully another day. Examinationunder anaesthesia is rarely required.

Each child is examined from head to toe rather than in systems. Height and weightare checked, as is head circumference in babies. Careful notes are made of all normaland abnormal findings, including any marks on clothing, e.g. tears, blood stains. Suchclothing may be required by the police. All marks, contusions, abrasions and lacerationsmust be measured and related to anatomical landmarks and described as fully as possible.Drawings must be made. If an abnormality is found that has not been discussed previouslyin the history, then further questions are asked – most undisclosed events are recentminor childhood accidents or previous ones that have left scars. When the upper part ofthe body has been examined, the child is asked to put the clothes back on to that areabefore taking the clothes off the abdomen and legs. Finally, the genitalia and anal regionare examined; this part of the examination should be recorded using a videocolposcope

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CHILD ABUSE

whenever possible, enabling future review of the videotape evidence and discussion withmedical colleagues, avoiding unnecessary repeat examinations. This method minimisesthe embarrassment of the child.

InvestigationsDuring the examination, specimens needed for forensic investigation will be taken by a

police surgeon or a paediatrician with forensic experience. These are relevant when therehas been contact within 7 days of the examination. Swabs for microbiological investigationwill be taken if there is a vaginal discharge or if threadworms may be present. Investigationsfor sexually transmitted diseases are done ideally 7 days after the last alleged offence iforal, vaginal or anal intercourse has taken place.

If bruises are found, then organic disease may be present with or without abuse, sohaematological investigations are needed. Venous blood is taken for full blood count,bleeding and clotting studies.

Radiograph interpretationOccasionally old rib fractures may be seen on a chest radiograph. Posterior rib fractures

in adjacent ribs are very suggestive of non-accidental injury due to abnormal squeezingor compression of the chest. Recent rib fractures, unless displaced, may be difficult todetect radiographically and may only be seen in the healing phase. Small children’s ribsare relatively pliable compared to adults and will tend to bend rather than fracture withcompressive forces. It is exceptionally unusual to fracture a child’s ribs during cardiopul-monary resuscitation in a child with a normal skeleton. The presence of a rib fracture,recent or healed, is a significant finding. Metaphyseal fractures seen in the shoulders ona chest radiograph are significant.

Skull fractures may occur in small infants who fall from a significant height onto a hardfloor, but are rarely seen when a child rolls off a sofa onto a carpeted floor. Femoral andhumeral fractures occur infrequently in domestic accidents in infants. The history alwaysneeds to be correlated with the clinical and radiographical findings.

In suspected non-accidental injury the child should be protected from further assaultand further assessment made. In physical abuse of children under the age of 2 years thisinvolves a full skeletal survey. A skeletal survey can only be performed after adequateexplanation to the child’s carers, and does not normally need to be performed in theemergency situation. The components of a skeletal survey are shown in the box.

• Front and lateral skull films• Lateral whole spine• Chest radiograph• AP views of all the long bones• AP views of lumbar spine, pelvis and hips• Supplemented with lateral views of the metaphyses where there is any suspected

abnormality or clinical symptoms• Neurocranial imaging (e.g. CT and/or MRI) as appropriate to the child’s symptoms

DiagnosisClassic pointers to the diagnosis of inflicted injury are:

• There is delay in seeking medical help or medical help is not sought at all.• The story of the “accident” is vague, is lacking in detail and may vary with each telling

and from person to person. Innocent accidents tend to have vivid accounts that ringtrue.

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• The account of the accident is not compatible with the injury observed.• The injury is not compatible with the child’s level of development or of the level of

development of another child alleged to have caused the injury.• The parents’ affect is abnormal. Normal parents are full of anxiety for the child

who has been injured. Abusing parents tend to be more preoccupied with their ownproblems – for example, how they can return home as soon as possible.

• The parents’ behaviour gives cause for concern. They may become hostile, rebutaccusations that have not been made, or leave before the consultant arrives.

• The child’s appearance and his interaction with his parents are abnormal. He maylook sad, withdrawn or frightened. There may be visible evidence of a failure to thrive.Full-blown frozen watchfulness is a late stage and results from repetitive physical andemotional abuse over a period of time.

• The child may disclose abuse. Always make a point of talking to the child in a safe placein private if the child is old enough to be separated from the parents. Interviewingthe child as an outpatient may fail to let the child open up as he is expecting to bereturned home in the near future. He may disclose more in the safety of a fosterhome.

At the end of the medical assessment the diagnosis may be clear. More often thedoctor has a differential diagnosis which includes abuse. Discussion then takes placeamong the social workers, health care workers and police officers, who have informationabout the family, to balance the probabilities of abuse having occurred. A child protectionconference will be held as soon as possible. In the meantime it may be necessary to arrangefor the child to be taken to a place of safety (see “Emergency Protection Orders”).

C.3 MANAGEMENT

All child protection work is based on cooperation between families, social workers,police officers, health care workers, and educationalists. This multi-agency approach isto ensure that all aspects of the care of the family are considered when decisions arebeing made. Certain decisions in management must be made by a professional, e.g. onlya doctor can decide on the treatment required for fracture and only a police officer candecide the charge that is appropriate for the alleged offence. However, whenever possible,unilateral decisions are avoided in the best interests of the child and the family.

Because of the complexity of interaction between these agencies, the most commonreason for child protection disasters has been failure of communication. Over the years,in the United Kingdom, there have been a number of high-profile cases that have beeninvestigated and led to various reports. The most recent has been the Laming report(2004), which has made recommendations for health care professionals in the acutesetting. The recommendations are designed to improve communication and to identifyaccountabilities. They include:

• taking a history from the child where possible, with an interpreter when necessary;• having access to previous records and the Child Protection Register;• making comprehensive and contemporaneous records of all findings and communi-

cations;• seeking further opinion where needed and allowing discharge of the child only by a

senior doctor and with a plan for future care;• having clear lines of responsibility and a single set of hospital records and• training and update in child protection for those managing children.

Doctors may be concerned about sharing information with other professionals be-cause of the ethical consideration of confidentiality. In the United Kingdom the GeneralMedical Council (2004) gives the following advice:

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Disclosures where a patient may be a victim of neglect or abuse

If you believe a patient to be a victim of neglect or physical, sexual or emotional abuse andthat the patient cannot give or withhold consent to disclosure, you must give informationpromptly to an appropriate responsible person or statutory agency, where you believethat the disclosure is in the patient’s best interests. If, for any reason, you believe thatdisclosure of information is not in the best interests of an abused or neglectedpatient, you should discuss the issues with an experienced colleague. If youdecide not to disclose information, you must be prepared to justify your deci-sion.

When the diagnosis is one of child abuse then the decisions to be made on managementare the following:

• Does the child need admission for treatment of the injuries?• Will the child be safe if returned home?• If the child needs protection from an abuser who is in his or her own home, how can

this be done?• What support/protection is needed for the rest of the family, including siblings?

If the alleged abuser is not in the same household as the child and the caregivers canprotect the child, then he or she can return home. If the alleged abuser is in the samehousehold as the child but is in custody, then the child will still be safe at home withanother caregiver. When a person is charged and is allowed bail, one condition mustbe that he or she lives away from the household of the child. If this is not done thenalternative care will be needed for the child.

Whenever there is a disclosure or suspicion of abuse, the whole family needs support.Siblings may have been at risk of injury and so will need to be assessed. Spouses maybe ambiguous in their loyalties to the child and to the alleged abuser. The child willneed much support to withstand the stress of the investigation, especially if there aresubsequent legal proceedings.

The details of management of these many facets are decided in the child protectionconference. In this all the professional people meet with the family to share informationand to produce a plan of care.

C.4 MEDICOLEGAL ASPECTS

Health care professionals must be familiar with the medicolegal aspects of their work.In England and Wales the most important are the following:

• Emergency Protection Orders, Child Assessment Orders, Residence Orders, PoliceProtection Orders

• Consent to examination• Writing of statements and reports for criminal and civil proceedings• Presentation of evidence

Emergency Protection Order (EPO)

The Emergency Protection Order (Children Act 1989, sections 44 and 45) replacedthe Place of Safety Order. It may be made for a maximum of 8 days, with a possible furtherextension of up to 7 days. An application for discharge of that order may be made. Thecourt may only make the order if it is satisfied that there is reasonable cause to believethat the child is likely to suffer significant harm if either he is not removed to anotherplace or his removal from a safe place (such as a hospital) is not prevented. Anotherclause is that, in the case of an application made by a Social Services Department or

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the NSPCC, the applicant “has reasonable cause to suspect that a child is suffering or islikely to suffer significant harm” and enquiries which are being made with respect to thechild “are frustrated by access to the child being unreasonably refused” and the applicantbelieves that access is required as a matter of urgency.

Child Assessment Order (CAO)

This Order (Children Act 1989, section 43) addresses those situations where thereis good cause to suspect that a child is suffering or is likely to suffer significant harmbut is not at immediate risk, and the applicant believes that an assessment (medical,psychiatric or other) is required. If the parents are unwilling to cooperate, the SocialServices Department or the NSPCC can apply for a Child Assessment Order. The Orderhas a maximum duration of 7 days from the date on which it comes into effect. The courtwill direct the type and nature of the assessment that is to be carried out, and whetherthe child should be kept away from home for the purposes of the assessment. A childof reasonable understanding may refuse to have this assessment. Lawyers suggest that achild of reasonable understanding is a normal child of 10 years of age or more.

Residence Order

A Residence Order states with whom the child is to live. It has the effect of ending anycare order and gives parental responsibility to the person with the order.

Police Protection Order

A constable has powers (Children Act 1989, section 46) to take a child “into policeprotection” for up to 72 hours. This power can be used to prevent the removal of a childfrom hospital.

Consent to examination

Consent for all examinations that are for evidential purposes must be obtained froma person with parental responsibility. In the Children Act 1989 (section 3), parentalresponsibility is defined as “all the rights, duties, powers, responsibilities and authoritywhich by law a parent has in relation to the child and his property”. Those with parentalresponsibility are specified in the Children Act 1989 (section 2). This can be summarisedas in the box.

Parental responsibility

• Parents married at time of birth both have parental responsibility, which continues afterseparation or divorce

• An unmarried mother always has parental responsibility unless the child has beenadopted

• An unmarried father has parental responsibility if he is named on the child’s birthcertificate and the birth is registered on or after 1st December 2003

• An unmarried father of a child born before this date or un-named on the birth certificatecan acquire parental responsibility, by marrying the mother, by a parental responsibilityagreement with the mother (stamped by the court) or by an order from the court

(Continued)

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• Person in whose favour a Residence Order has been made – this is for the duration ofthe Order

• Appointed guardian• Local Authority while a Care Order is in force• Person who applied for an Emergency Protection Order• Person in whose favour an Adoption Order has been made

When more than one person has parental responsibility, each of them can act alone andwithout the other in meeting that responsibility. Parents do not lose parental responsibilityif a Care Order or an Emergency Protection Order is in force, but their responsibility maybe limited by the Local Authority. Parents lose parental responsibility with an AdoptionOrder. Parental responsibility can be delegated to a person acting on their behalf, e.g.while they are on holiday.

To cover emergency situations, those caring for a child, who do not have parentalresponsibility may do what is reasonable in all the circumstances for the purpose ofsafeguarding or promoting the child’s welfare.

Consent from the child or young person is needed if that person is of sufficient un-derstanding to make an informed decision. Lawyers suggest that in a normal child thiswould be at age 10 years. The Fraser (previously known as Gillick) ruling (1986) allowsan individual under the age of 16 years to submit to examination and treatment withoutthe parents being informed, provided that is the wish of the child or young person.

Court reports

When preparing a written report on a child for the court all health care profession-als should keep in mind that the written report may be used in subsequent court ap-pearances. Therefore, the report should be confined to the facts. Whenever possible,objective and measurable evidence of the child’s health and development should be pre-sented. Where subjective views must be given they should reflect balanced professionaljudgement. If the report is comprehensive and comprehensible, then the health care pro-fessional may not be called to give verbal evidence in person. Always keep a copy of yourreport.

Statements

The purpose of a statement is to provide the court with an informative and relevantaccount of the medical assessment of the child. The statement will give details of thepersons involved, the observations, and the findings. Information given by another per-son should not be included unless this has been requested. In many areas, the CrownProsecution Service wish statements to record all information, although hearsay may beexcluded before presentation to the court.

A statement is a professional document. It should be well written in good, basicEnglish. Technical terms should be avoided or, if used, should be followed immedi-ately by appropriate lay terms. Most statements will be for the prosecution and a printedstatement form will be provided. The standard sequence of writing a statement is asshown in the box.

Each page must be signed at the bottom, and the final page must be signed on the linebelow the completion of the writing. Any alterations must be initialled.

Always keep a copy of the statement.

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Sequence for writing a statement

1. Full name with surname in capitals2. Qualifications3. Occupation4. Name of person requesting the assessment5. Date, time, and place of the assessment6. Name of person who was examined7. Name of persons present8. Details of the relevant history – if general history taken produced nothing significant then

make a general comment including the sight of the detailed notes9. Details of examination – if joint examination then specify who did each part

10. Investigations11. Opinion on findings12. The time at which examination ended

Presentation of evidence

Dress in a professional manner. Arrive early in court. Take along all notes relevant tothe case. Revise these on the day before the court proceedings. With permission from themagistrate or judge, you may refer to contemporaneous notes. However, revision helpsto put the whole picture of the incident into the forefront of your mind so that you canfind the appropriate notes more quickly.

When giving evidence stay calm even when challenged. Do not be persuaded to answerquestions which are outside your knowledge or experience.

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APPENDIX

DPrevention of injury in children

D.1 INTRODUCTION

In developed countries, injury is the leading cause of death in children aged between1 and 14 years. Millions more children worldwide are injured in accidents that, althoughnot causing death, cause pain, distress and permanent disability. The majority of theseincidents are predictable and preventable.

Over the last few decades, injury prevention programs in some countries have suc-ceeded in halving childhood death rates from injury. This is a remarkable achievementand a good start to reducing childhood injury as far as possible. Injury prevention isa multifaceted, multidisciplinary process that provides many opportunities for clinicianswho are primarily involved in the management of acutely injured children, to play a majorrole.

D.2 EPIDEMIOLOGY

Circumstances and type of incident

A multitude of injury scenarios are possible each of which involve the child interactingwith their environment. The commonest injuries that cause death are those resultingfrom motor vehicle accidents, drownings, burns, falls from a height and poisonings.The commonest incidents overall, however, are falls leading to injuries such as bruises,abrasions and fractured limbs.

Children in urban environments are at particular risk of motor vehicle accidents andplayground falls whilst children in a rural environment are at risk of farm equipmentinjuries, unintentional chemical exposure and, in some countries, snakebite. Exposure todifferent circumstances also varies with age. Children under 5 years experience injuries athome. School-age children experience injuries at school, sport and play, and are especiallyat risk of death as pedestrians and cyclists. Adolescents may deliberately place themselvesat risk of injury especially where alcohol and drugs may impair their judgement.

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Sex

Boys are more frequently injured than girls. The difference emerges at age 1–2 yearsof age. How much of this difference is innate and how much cultural is a subject forspeculation. Girls may mature more rapidly in terms of perception and coordination.

Age

The type of injury sustained is closely related to the child’s stage of development. Takefalls as an example. A newborn baby can only fall if dropped, or if a parent falls holdingthe baby. An older baby can wriggle and roll off a changing table or a bed. A crawlingbaby can climb upstairs and fall back. A small child can climb and fall out of a window.An older child can climb a tree, or fall in a playground.

Social class

As with so many other health problems, injuries are linked to inequalities in envi-ronments. Children in social class V, derived from the occupation of the head of thehousehold, are twice as likely to die from an injury as children in social class I and, forsome injury types, such as burns, the chances are 6 times higher.

This does not mean that working-class parents care less about their children thanmiddle-class parents, or that they do not know about risk. It may mean that there areother pressures such as overcrowding, lack of money or poor housing, and there is lessability for financial reasons to make safety-related changes.

Psychological factors

Injuries are more common in families where there is stress from mental illness, maritaldiscord, moving home and a variety of similar factors.

D.3 INJURY PREVENTION

There are three levels of injury prevention. Primary injury prevention is any measuredesigned to reduce the incidence of injury. Examples of this are the use of speed limits,pool fences, fireguards and child-resistant medication closures. Secondary injury preven-tion is any measure designed to minimise injury even though an incident has occurred.Examples of this are the proper use of seat belts, bicycle helmets and other personal pro-tective clothing. Tertiary injury prevention is any measure designed to limit the extent orconsequences of an injury that has already occurred. Examples include the applicationof cold water to burns and scalds, or direct pressure on a laceration.

Whilst injury prevention can be addressed on an individual level it is most effective forthe community as a whole when viewed as a public health issue. The most successful in-jury prevention campaigns have a number of common attributes. Firstly they are carefullyplanned, with attention given to data collection and the identification of specific issuesin the target population. Secondly they attempt to permanently change behaviour by theuse of education and enforcement. Finally they include methods to monitor effectiveness,provide feedback and modify the campaign as necessary.

Clinicians involved in the acute management of injured children are in a unique positionto be able to assist in injury prevention. Their daily work gives them first-hand knowledgeof injured children and credibility with parents and government. Some of the ways thatclinicians may be involved include the following.

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Data collection and analysis

The provision of accurate and reliable data regarding incidence and circumstances ofchild injury occurring in a particular city or country underpins any injury-preventionstrategy. It identifies areas of high priority and enables the monitoring of effectiveness.In addition, it assists in the recognition of local and national factors that contribute toinjury that may need to be specifically addressed. The power of the information and theability to identify trends will be increased if the data is pooled into a national databasethat is accessible by many sources.

Education

Parents, community groups and politicians need information regarding childhood in-juries and the methods likely to prevent them. Information can be delivered directly faceto face in talks and interviews or by posters, books, pamphlets and the Internet. Theinformation must be relevant, accurate and presented at a level appropriate to the targetgroup. Information based on local data presented by a credible person is most likely tobe well received.

Publicising cases in the media can be an effective strategy to convey messages to parents,especially if the topic is newsworthy. Such publicity tends to be immediate and short-livedbut may be particularly useful in certain circumstances such as at the start of summer(i.e. snakebite, drowning).

The Injury Minimisation Programme for Schools (IMPS) provides an ed-ucation pack with accident lessons drawn on the National Curriculum in theUK and includes a hospital visit. Health professionals are actively encouragedto contact this group as its reach through schools in the UK has expanded and requiresfurther support from interested health professionals.

Advocacy for legislation and design

Child injury prevention is all about changing behaviour. Whist education is the pre-ferred way of encouraging people to do this, the introduction of legislation, regulationsand enforceable standards have been an extremely effective adjunct. For example legis-lation regarding pool fencing and regulations concerning the packaging of medicationsare two important legal measures specifically directed at child safety.

Whilst clinicians do not generally draft and enact legislation and regulations they canplay an important role in convincing politicians that such measures are necessary and inensuring that they are enforced.

People must not only have the knowledge of what is safe, they must have the abilityto select safe products and be protected against things that are inherently unsafe. Safedesign of products designed for use by and around children is essential. Clinicians havea responsibility to notify authorities when they become aware of a dangerous toy that hasinjured a child.

Involvement with child safety organisations

Many countries have organisations dedicated to preventing childhood injury. Theseorganisations are often involved in all facets of injury prevention and provide ideal ve-hicles for individuals to work within. Be prepared to participate in working groups andcampaigns. You have special expertise and influence to offer. Local initiatives involvinghealth professionals have had an impact, e.g. work in bicycle helmet use and playground

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safety has led to a better understanding of the effects of altering the environment and onimplementing advances in design.

The collection of data about accidents can lead to a decrease in childhood injury;e.g. by identifying accident black spots and collaborating with police and local councilauthorities, effective safety changes can be implemented. Similarly, types of frequentlyoccurring domestic injuries can lead to targeted campaigns.

Children’s accidents and injuries are the major public health problem tochildren in developed and developing countries today. All health care workerscan learn more about them, and can be active in reducing their toll. Healthcareprofessionals can form powerful alliances with heads of schools, playgroup leaders, localmedia, police and the local council to launch injury-prevention schemes. Support forsuch initiatives can be given by charitable agencies such as Child Accident PreventionTrust, the Gloucestershire Home Safety Check and the Royal Society for the Preventionof Accidents in the UK and Kidsafe in Australia.

Primary Prevention Measures

• Parental knowledge regarding behaviour and supervision of young children• Fencing around domestic swimming pools• Child-resistant closures on medication containers• Fireguards surrounding open fireplaces• Motor vehicle speed limits around schools• Automatic water temperature regulation in bathroom• Use of stair-guards, window-guards and toughened glass• Installation of electrical safety switches• Removal of unsafe toys from retail outlets

Secondary Prevention Measures

• Properly fitted child restraints in motor vehicles• Wearing of bicycle helmets at all times• Personal protective equipment such as mouth guards and wrist guards• Installation of domestic smoke alarms, fire extinguishers and fire blankets

Tertiary Prevention Measures

• Cardiopulmonary resuscitation training• Compressive bandage in snake bite• Rapidly responding, well-trained ambulance service

218• Excellent trauma care from retrieval to rehabilitation

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APPENDIX

EWhen a child dies

E.1 INTRODUCTION

Even with the best preventative measures in place and the use of the most effectiveresuscitation methods, children will continue to die from serious illness and severe injury.When a death occurs, medical and nursing staff must be able to deal effectively with thechild’s family and the legal requirements of death as well as cope with their own emotionalreactions. Sympathetic and sensitive support of the family at this time can do much tohelp the grief process and adjustment to the bereavement.

The principles in dealing with a family that has experienced a sudden childdeath are:

• Display caring, kindness and compassion• Spend as much time as necessary with the family in an unhurried fashion• Offer information regarding the death as the family requires• Talk to colleagues later regarding your experience and feelings

Unless there is a clear “do not resuscitate” (DNR) order negotiated in advance withthe parents and recorded in the medical records, full resuscitation should be undertaken.Parental presence during resuscitation is increasingly common, and whether this occursshould be a decision made jointly by the child’s parents and staff. Although being presentat their child’s resuscitation is always extremely traumatic for the parents, when it is overthey are almost always left with the impression that everything possible was done to savetheir child. If parents are present during resuscitation, then a member of staff must beavailable exclusively for their support.

Breaking the news

Telling the parents that their child has died is a difficult task and is usually undertakenby a senior and experienced staff member. Before speaking to the parents ensure they arein a private, comfortable environment and that you know the name of the child.

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A direct and sympathetic approach is best, avoiding euphemisms and cliches. If it isappropriate and you feel comfortable doing it you may show sympathy by holding theparent’s hand or putting an arm around them. Usually the parents will turn away to-wards each other for a while but may wish to ask questions about the cause of deathand what they should do now. The parents will often want to know what happenedand what treatments were instituted. If you are asked about the cause of death an-swer as simply and honestly as you can, making it clear that some answers are not yetavailable.

Caring for the parents

Provide the family with a private room in which they can be alone with their child foras long as they wish. Encourage the family to touch and hold the child. Offer to stay withthe family; however if they wish to be left alone, assure them you will be nearby if theywish to speak with you. In cases where there have been child protection concerns it willbe necessary for the parents to be accompanied by a professional when they are with thechild.

Accept the families’ distress as natural and support them in this by acknowledging theirfeelings. Be prepared for a variety of responses: there is no “correct” way to grieve andeach person will have a different reaction. Be sensitive to and respectful toward varyingcultural norms and rituals surrounding death.

Facilitate contact with other family members and friends as required. Even very youngchildren may be included in the grief process right from the start: assist the family infeeling comfortable with this.

Each institution will have its own bereavement support programme: ensure that you arefamiliar with local resources and that the family is offered ongoing support and medicaladvice.

Post-death procedures

Every jurisdiction will have specific legal requirements that need to be adhered to. It isusually necessary for the coroner, the police or another statutory authority to be informedof the death. The requirements for a police or coronial investigation, an autopsy and aninquest will vary from case to case.

A customised checklist is invaluable for ensuring that procedures or information arenot forgotten.

The table gives an outline of such a list; however local hospital guidelines should befollowed. Especially in the case of Sudden Unexpected Death in Infancy and any in whomchild protection issues are suspected, local forensic procedures agreed with the coronermust be followed.

Take care of the staff

The sudden and unexpected death of a child is extremely distressing for all involved.Some staff members may be profoundly affected. Encourage staff members to talk aboutthe event and their feelings in private soon afterwards with a colleague. Formal staffcounselling should be available if needed.

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The child

• Full and thorough examination• Core temperature• Wrap child in clean warm clothes for parents to see and hold (if consistent with forensic

requirements)• Samples or swabs if agreed as mandatory in local protocol

The parents

• Explain that the child (use name) has died• Gently get as full a history as possible• Ask if they would like a priest/religious leader present• Ask if they want any close relative to be contacted• Encourage the parents to see and hold the child• Let them know if a post-mortem examination needs to be carried out and ensure that

they understand all that they wish to know about the procedure and have given theirwritten consent where appropriate

• Let them know that police are always informed of sudden unexpected deaths and willneed to ask a few simple questions of the carers

• Ask what address the family will be going to on leaving hospital• Arrange transport from hospital to home and if alone make sure they are accompanied

on the journey and not left alone at home• Be gentle, unhurried, calm and careful• Do not guess at the diagnosis

Obtain details of

• Child’s and parents’ names• Child’s date of birth• Address at which death occurred• Time of arrival in department• Time last seen alive• Usual address if different from above

Inform

• GP – advise of child’s death and give the address to which parents will be going fromhospital

• Health visitor• Social worker• Any relative as requested by the family• Coroner – who will need to know the full name and address and date of birth of child,

time of arrival, place of death, brief recent history, any suspicious circumstances

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APPENDIX

FManagement of pain in children

F.1 INTRODUCTION

In general, children, especially very young ones, are undertreated for pain. They receivefewer, smaller doses of opiate drugs and instead are prescribed less powerful analgesicsthan adults. The reasons for this include:

• fear of the harmful side effects;• failure to accept that children, especially infants, feel pain like adults;• fear of inducing addiction and• the child’s fear of receiving injections.

Inadequate analgesia can be detrimental in the critically ill child. Bronchoconstrictionand increases in pulmonary vascular resistance caused by pain can lead to hypoxia whereasgood pain control facilitates the assessment of the severity of illness.

F.2 RECOGNITION AND ASSESSMENT OF PAIN

There are four main ways in which we recognise that a child is in pain:

• A description from the child or parent• Behavioural changes such as crying, guarding of the injured part, facial grimacing• Physiological changes, such as pallor, tachycardia and tachypnoea, which are ob-

served by the clinician• An expectation of pain because of the pathophysiology involved, e.g. fracture, burn

or other significant trauma, especially where the assessor is experienced

The purpose of pain assessment is to establish, as far as possible, the degree of painexperienced by the child so as to select the right level of pain relief. Additionally, re-assessment using the same pain tool will indicate whether the pain management has beensuccessful or whether further analgesia is required. The use of pain tools and protocolsin the emergency setting has been shown to shorten the time to delivery of analgesia.

Pain assessment at triage in the emergency situation is unique and therefore a pain as-sessment tool, specifically designed for this situation, is desirable. The anxiety associated

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with a sudden and unexpected presentation in pain confound the ability of an individ-ual, especially a child, to make a satisfactory self-assessment of pain that can be used toguide analgesic requirements. Therefore an observational pain scale appears to be moreappropriate in this setting. The Alder Hey Triage Pain Score is one such toolthat has been developed specifically for this situation and shown to have somevalidity as well as good levels of inter-rater reliability. It is an observation-basedpain score, which is quick and easy to use. (Table F:1) 45

Table F.1. The Alder Hey Triage Pain Score: reference scoring chart

Response Score 0 Score 1 Score 2

1. Cry No complaint/cry Consolable InconsolableVoice Normal conversation Not talking negative Complaining of pain

2. Facial expression Normal Short grimace Long grimace<50% time >50% time

3. Posture Normal Touching/rubbing/sparing Defensive/tense4. Movement Normal Reduced or restless Immobile or thrashing5. Colour Normal Pale Very pale/“green”

Note. Guidance notes for the use of the score can be found at the end of the chapter.

Other commonly used pain scales are self-assessment tools (Figure F.1) based on aFaces scale or pain ladder. However self-assessment tools were primarily developed foruse with children where there was the opportunity for explanation of the scale priorto the painful event, e.g. before surgery. This is clearly not the case in the emergencydepartment.

Figure F.1. Faces Scale and Pain Ladder

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All or any of these tools can be used to assess the pain experienced by the child and help,in the setting of the specific clinical situation, to guide the need for the level and route ofanalgesia. The tools can then be used again to assess the efficacy of the intervention andto guide further analgesia.

F.3 PAIN MANAGEMENT

Environment

The emergency department and the treatment room of the paediatric ward are fright-ening places for children. Negative aspects of the environment should be removed orminimised. This includes an overly “clinical” appearance and evidence of invasive in-struments. An attractive, decorated environment with toys, mobiles and pictures shouldbe substituted.

Preparation

Except in a life-threatening emergency or when dealing with an unconscious child,an explanation of the procedure to be undertaken and the pain relief plannedshould be given to the child and his parents. If time permits, they shouldcontribute to the pain management plan by relating previous pain experiencesand successful relief measures. 450

Physical treatments: supportive and distractive techniques

The presence of parents during an invasive procedure on their child is important. Inone study almost all children between the ages of 9 and 12 reported that “the thingthat helped most” was to have a parent present during a painful procedure. As well ashaving to be present, parents need some guidance on how to help their child during theprocedure. Studies suggest that talking to and touching the child during the procedureis both soothing and anxiety-relieving. Other distractive strategies include:

• looking at pop-up books or interactive toys;• listening through headphones to stories or music;• blowing bubbles;

358• video or interactive computer game;• moving images projected on a nearby wall, e.g. fish swimming, birds flying and• presence of transitional objects (comforters), e.g. favourite blanket, soft toy.

Pharmacological treatment

Local anaesthetics: topical on intact skinAmetop gel This contains Tetracaine (amethocaine) base 4%.

• Used under an occlusive dressing• Analgesia achieved after 30–45 minutes 210

381• Anaesthesia remains for 4–6 hours after removal of gel• Slight erythema, itching and oedema may occur at site but capillary vessels may be

dilated, making venesection easier• Not to be applied on broken skin, mucous membranes, eyes or ears• Can cause sensitisation on repeated exposure• Not recommended under 1 month of age

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EMLA A mixture of lidocaine 2.5% and prilocaine 2.5% can be used similarily wheresensitivity to Ametop occurs.

Local anaesthetics: infiltratedLidocaine(lignocaine) 1 % lidocaine (lignocaine) is used for rapid and intense sensorynerve block.

• The onset of action is significant within 2 minutes and is effective for up to 2 hours.• Often used with adrenaline (epinephrine) to prolong the duration of sensory block-

ade and limit toxicity by reducing absorption – adrenaline concentration 5 µg/ml.Adrenaline (epinephrine) containing local anaesthetic should not be used in areasserved by an end artery, such as a digit.

• Maximum dose given locally is 3 mg/kg.

Bupivacaine This local anaesthetic is used – at a concentration of 0·25% or 0·5% –when longer-lasting local anaesthesia is required. -Bupivacaine used in the same dose isassociated with less toxicity. Bupivacaine is used in femoral nerve blocks.

• The onset of anaesthesia is for up to 15 minutes but its effects last up to 8 hours.• Maximum dosage is 2 mg/kg.

Local anaesthetics are manufactured to a pH of 5 (to improve shelf-life) and are painfulfor this reason. A buffered solution and the use of smaller needles will lessen the pain as-sociated with infiltration, but local adrenaline (epinephrine) cannot then be used becausethe bicarbonate buffer inactivates it.

The suggested upper limits given are for local anaesthetics without the addition ofadrenaline (epinephrine). Direct intra-arterial or intravenous injection of even a fractionof these doses may result in systemic toxicity or death.

Overdose or inadvertent circulatory injection of local anaesthetics results in cardiacarrhythmias and convulsions. Resuscitative facilities and skills must therefore be availablewhere these drugs are injected.

Non-opiate analgesicsThese drugs are analgesic, antipyretic and anti-inflammatory to varying degrees.

Paracetamol Paracetamol is probably the most widely used analgesic in paediatric prac-tice. It is thought to work through inhibiting cyclo-oxygenase in the central nervous systembut not in other tissues, so that it produces analgesia without any anti-inflammatory ef-fect. It does not cause respiratory depression. It has a bad taste, which has to be disguised.It is very dangerous in overdose but very safe in the recommended dose. Higher loadingfirst doses have been shown to optimise pain control (see table).

Non-steroidal anti-inflammatory drugs (NSAID) These are anti-inflammatory and an-tipyretic drugs with moderate analgesic properties. They are less well tolerated thanparacetamol, causing gastric irritation, platelet disorders and bronchospasm. They shouldtherefore be avoided in children with a history of gastric ulceration, platelet abnormal-ities and significant asthma. Their advantage is that they are especially useful for post-traumatic pain because of the additional anti-inflammatory effect. Ibuprofen is given bymouth, and if rectal administration is necessary then diclofenac can be used.

Opiate analgesicsMorphine Morphine is the standard for analgesia against which all other opiates aremeasured. When small doses are administered, analgesia occurs without loss of con-sciousness. It produces peripheral vasodilatation and venous pooling, but in single doses

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has minimal haemodynamic effect in a supine patient with normal circulating volume. Inhypovolaemic patients it will contribute to hypotension but this is not a contraindicationto its use and merely an indication for cardiovascular monitoring and action as appropri-ate. Opiates produce a dose-dependent depression of ventilation primarily by reducingthe sensitivity of brain stem respiratory centres to hypercarbia and hypoxia. This meansthat the patient who has received a dose of an opiate requires observation and/or moni-toring and should not be discharged home until it is clear that the effects of the opiate aresignificantly reduced. The nausea and vomiting produced in adults by morphine seemsto be less common in children.

Parenteral morphine given intravenously is the route of choice for emergency painrelief. The therapeutic effects and side effects are much more easily controlled with theIV or intraosseous route than with intramuscular injection.

Diamorphine given intra-nasally has been shown to be a safe and effectiveroute of opiate administration and is becoming increasingly popular for chil-dren. Further studies are being undertaken to establish the exact role for thisdrug in the emergency setting. 16

Codeine Oral codeine is almost always prescribed in combination with paracetamol forthe treatment of moderate pain. It is a less potent opiate than morphine but similarly hasless effect on the central nervous system. Codeine must not be given intravenously as itcan cause profound hypotension.

Opiate antagonistsNaloxone Naloxone is a potent opiate antagonist. It antagonises the sedative, respi-ratory depressive and analgesic effects of opiates. It is rapidly metabolised and is bestgiven parenterally because of its rapid first-pass extraction through the liver followingoral administration. Following IV administration naloxone reverses the effects of opiatesvirtually immediately. Its duration of action, however, is much shorter than the opiateagonist. Therefore, repeated doses or an infusion may be required if continued opiateantagonism is wanted.

Inhalational analgesiaEntonox Nitrous oxide is a colourless, odourless gas that provides analgesia in sub-anaesthetic concentrations. It is supplied as a 50% mixture with oxygen to prevent hy-poxia. Most devices act on a demand principle, i.e. the gas is only delivered when thepatient inhales and applies a negative pressure. The patient has to be awake and cooper-ative to be able to inhale the gas; this is an obvious safeguard with the technique.

Because nitrous oxide is inhaled and has a low solubility in blood, its onset of effect isvery rapid. It takes 2–3 minutes to achieve its peak effect. For the same reason, the drugwears off over several minutes, enabling patients to recover considerably quicker than ifthey received narcotics or sedatives. Laryngeal protective reflexes do not always remainintact.

Nitrous oxide is therefore most suitable for procedures where short-lived intense anal-gesia is required, e.g. dressing changes, suturing, needle procedures such as venous can-nulation, lumbar punctures and for pain relief during splinting or transport. It is also ofbenefit for immediate pain relief on presentation until definitive analgesia is effective.

Entonox can be used by children as young as 5 years of age if they are well supported.The black rubber masks that are used are unacceptable to some children but a mouthpiececan overcome some of these problems.

Toxicity in the emergency situation is not a problem, but prolonged exposure to highconcentrations can cause bone marrow depression and neuronal degeneration.

Entonox must not be used in children with possible intracranial or intrathoracic airbecause replacement of the air by Entonox may increase pressure.

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Sedative drugsIn addition to analgesics, psychotropic drugs may also be useful when undertaking

lengthy or repeated procedures. Sedatives relieve anxiety and not pain. They may reducethe child’s ability to communicate discomfort and therefore should not be given in isola-tion. The problems associated with the use of sedatives are those of side effects (usuallyhyperexcitability) and the time required for the child to be awake enough to be allowedhome if admission is not necessary.

Midazolam This is an amnesic and sedative drug. It can be given orally orintranasally (although this is unpleasant). It has an onset time of action of15 minutes and recovery occurs after about an hour. In some cases there isrespiratory depression, necessitating monitoring of respiratory rate and depthand pulse oximetry. A few children become hyperexcitable with this drug. Itsaction can be reversed by flumazenil intravenously.

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Ketamine This drug is now increasingly used for sedation in the emergency situationespecially for minor procedures in children. It causes dissociative sedation as well as anal-gesia; however brain stem reflexes are maintained. Laryngospasm is a rare complicationTherefore the drug should be used in the fasted child who is fully monitored and cared forby staff with paediatric advanced airway skills. Emergence phenomenon can be treatedwith midazolam if necessary but are much less common in paediatric than adult practice.Two isomeric forms of the drug are available: S(+) ketamine and R(–) Ketamine. TheS(+) isomer is more potent and associated with fewer side effects although R(–) is morewidely available.

The use of ketamine in any individual situation or organisation requires a local as-sessment of relative benefits and risks as it is a drug that lies between a sedative and ananaesthetic and has not yet fully found its place outside the anaesthetic room.

F.4 SPECIFIC CLINICAL SITUATIONS

Severe pain

Children in severe pain (e.g. major trauma, femoral fracture, significant burns, dis-placed or comminuted fractures, etc.) should receive IV morphine at an initial dose of0·1–0·2 mg/kg infused over 2–3 minutes. A further dose can be given after 5–10 min-utes if sufficient analgesia is not achieved. The patient should be monitored using pulseoximetry and electrocardiography.

Duration of Common sideAnalgesic Pain severity Single dose effect effects Comments

Morphine IV Moderate tosevere

Over 1 yr: 0·1–0·2mg/kg; 3 months to1 yr: 0·05–0·1mg/kg; 0–3 months:0·025 mg/kg

4 h RespiratorydepressionHypotension

Monitorrespiration andpulse oximetryECG

Diamorphineintranasal spray

Moderate tosevere

Single dose 0·1mg/kg diluted to avolume to 0·2 ml

As above As aboveDilute withsaline

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Duration of Common sideAnalgesic Pain severity Single dose effect effects Comments

Morphine oral Moderate Over 1 yr: 0·2–0·5mg/kg; under 1 yr:0·08 mg/kg

4 h Observerespiration

Codeine Mild tomoderate

Oral 1–1·5 mg/kg 4–6 h Avoid inpatients <1 yr.Do not give IV

Paracetamol Mild Over 3 months:

Single loadingdoses – 20 mg/kgorally or 40 mg/kgrectally;

Maintenance dose– 15 mg/kg orally

or rectally

Under 3 months:

20 mg/kg orally or30 mg/kg rectally

4–6 h

Furtherdoses after6 h

8-hourly if>36weeks’gestation

Avoid in liverimpairmentTotal daily doseshould notexceed 90mg/kg

Total daily doseshould notexceed 60mg/kg

Ibuprofen Mild tomoderate

5 mg/kg 4–6 h Avoid inasthmatics; notrecommendedfor patients<10 kg

Diclofenac Moderate 1 mg/kg orally orrectally

8 h Avoid inasthmatics; notfor patientsunder 1 yr ofage

Midazolam Not analgesic 0·5 mg/kg orally RespiratorydepressionHyperexcitability

Monitor SaO2

Head injuries

There is often concern about giving morphine to a patient who has had a head injuryand who could therefore potentially lose consciousness secondary to the head injury.If the patient is conscious and in pain then the presence of a potential deterioratinghead injury is not a contraindication to giving morphine. First, an analgesic dose is notnecessarily a significant sedative; second, if the child’s conscious level does deteriorate,then the clinician’s first action should be to assess airway, breathing and circulation,intervening where appropriate. If these are stable then a dose of naloxone will quicklyascertain whether the diminished conscious level is secondary to morphine or (as is much

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more likely) represents increasing intracranial pressure. There are significant benefits forthe head-injured patient in receiving adequate pain relief as the physiological response topain may increase intracranial pressure.

In the common situation of the patient who has an isolated femoral shaft fractureand a possible head injury, a femoral nerve block may be an effective alternative (seeChapter 22).

Emergency venepuncture and venous cannulation

At present the management of this problem is difficult as anaesthetics take up to anhour to be effective. Alternatives in an emergency include an ice cube inside the fingerof a plastic glove placed over the vein to be cannulated or local anaesthetic infiltration(1% buffered lidocaine (lignocaine)) using a very fine gauge, e.g. 29-gauge, needle. Ofcourse, in some instances the urgency of the situation is such that no local anaestheticcan be used.

F.5 EXPLANATORY NOTES OF ALDER HEYTRIAGE PAIN SCORE

F.6 CRY/VOICE

Score 0 Child is not crying and, although may be quiet, is vocalising appropriatelywith carer or taking notice of surroundings

Score 1 Child is crying but consolable/distractible or is excessively quiet andresponding negatively to carer. On direct questioning says it is painful

Score 2 Child is inconsolable, crying and/or persistently complaining about pain

F.7 FACIAL EXPRESSION

Score 0 Normal expression and affectScore 1 Some transient expressions that suggest pain/distress are witnessed but less

than 50% of timeScore 2 Persistent facial expressions suggesting pain/distress more than 50% of time

Grimace – Open mouth, lips pulled back at corners, furrowed forehead and/or betweeneyebrows, eyes closed, wrinkled at corners.

F.8 POSTURE

This relates to the child’s behaviour to the affected body area.

Score 0 NormalScore 1 Exhibiting increased awareness of affected area, e.g. by touching, rubbing,

pointing, sparing or limpingScore 2 Affected area is held tense and defended so that touching it is deterred;

non-weight-bearing

F.9 MOVEMENT

This relates to how the child moves the whole body.

Score 0 NormalScore 1 Movement is reduced or child is noted to be restless/uncomfortableScore 2 Movement is abnormal, either very still/rigid or writhing in agony/shaking

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F.10 COLOUR

Score 0 NormalScore 1 PaleScore 2 Very pale “green”, the colour that can sometimes be seen with nausea or

fainting – extreme pallor.

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APPENDIX

GTriage

G.1 INTRODUCTION

Nurse triage is the process whereby each child presenting with potentially serious illnessor injury is assigned a clinical priority. It is an essential clinical risk management step andis part of the process of recognition of the seriously ill or injured child that has beendiscussed earlier.

In the United Kingdom, Canada and Australia, five-part national triage scales havebeen agreed. The UK scale is shown in the table below. While the names of the triagecategories and the target times assigned to each name vary from country to country, theunderlying concept does not.

Table G.1. The UK triage scale

Number Name Colour Max time (min)

1 Immediate Red 02 Very Urgent Orange 103 Urgent Yellow 604 Standard Green 1205 Non-urgent Blue 240

G.2 TRIAGE DECISION MAKING

There are many models of decision making, each requiring three basic steps. Theseare, identification of a problem, determination of the alternatives and selection of themost appropriate alternative. The commonest triage method in the UK is that developedby the Manchester Triage Group. This method uses the following five steps:

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• Identifying the problem• Gathering and analysing information related to the solution• Evaluating all the alternatives and selecting one for implementation• Implementation of the selected alternative• Monitoring the implementation and evaluation of outcomes

Identify the problem

This is done by taking a brief and focused history from the child, his or her parentsand/or any pre-hospital care personnel. This phase is always necessary whatever themethod used.

Gather and analyse information related to the solution

Once the presentation has been identified, discriminators can be sought at each level.Discriminators, as their name implies, are factors that discriminate between patientssuch that they allow them to be allocated to one of the five clinical priorities. They canbe general or specific. The former apply to all patients irrespective of their presentation,whilst the latter tend to relate to key features of particular conditions. Thus severe painis a general discriminator, but cardiac pain and pleuritic pain are specific discriminators.General discriminators would include life threat, pain, haemorrhage, conscious level andtemperature.

Life threatTo an APLS provider life threat is perhaps the most obvious general discriminator of

all. Any cessation or threat to the vital (ABC) functions means that the patient is inthe immediate group. Thus the presence of an insecure airway, inspiratory or expiratorystridor, absent or inadequate breathing, or shock are all significant.

PainFrom the child’s and parent’s perspectives pain is a major factor in determining priority.

Pain assessment and management is dealt with elsewhere in this book and not reiteratedhere. Children with severe pain should be allocated to the very urgent category whilethose with moderate pain should be allocated to the urgent category. Any child with anylesser degree of pain should be allocated to the standard category.

HaemorrhageHaemorrhage is a feature of many presentations particularly those following trauma.

If haemorrhage is exsanguinating, death will ensue rapidly unless bleeding is stopped.These children must be treated immediately. A haemorrhage that is not rapidly controlledby the application of sustained direct pressure, and which continues to bleed heavily orsoak through large dressings quickly, should be treated very urgently.

Conscious levelAll unresponsive children must be an immediate priority, and those who respond to

voice or pain only are categorised as very urgent. Children with a history of unconscious-ness should be allocated to the urgent category.

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TemperatureTemperature is used as a general discriminator. It may be difficult to obtain an ac-

curate measurement during the triage process; however modern rapid-reading tympanicmembrane thermometers should make this aim attainable. A hot child (over 38·5◦C) isalways seen very urgently, as are children who are cold (less than 32◦C).

Evaluate all alternatives and select one for implementation

Clinicians collect a huge amount of information about the children they deal with.The data is compared to internal frameworks that act as guides for assessment. Thepresentational flow diagrams developed by the Manchester Triage Group provide theorganisational framework to order the thought process during triage.

Implement the selected alternative

As previously noted there are only five possible triage categories to select from and thesehave specific names and definitions. The urgency of the patient’s condition determinestheir clinical priority. Once the priority is allocated the appropriate pathway of care begins.

Monitor the implementation and evaluate outcomes

Triage categories may change as the child deteriorates or gets better. It is important,therefore, that the process of triage (clinical prioritisation) is dynamic rather than static.To achieve this end all clinicians involved in the pathway of care should rapidly assesspriority whenever they encounter the child. Furthermore any changes in priority mustbe noted and the appropriate actions taken.

G.3 SECONDARY TRIAGE

It may not be possible to carry out all the assessments necessary at the initial triageencounter – this is particularly so if the workload of the department is high. In suchcircumstances the necessary assessments should still be carried out, but as secondaryprocedures by a receiving nurse. The actual initial clinical priority cannot be set until theprocess is finished. More time-consuming assessments (such as blood glucose estimationand peak flow measurement) are often left to the secondary stage.

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APPENDIX

HGeneral approach to poisoning

and envenomation

H.1 POISONING

H.2 INTRODUCTION

Suspected poisoning in children results in about 40,000 attendances at emergency de-partments each year in England and Wales. Around half of these children are admittedto hospital for treatment or observation. Precise data on hospital admissions for poison-ings are altered by the fact that many emergency departments and paediatric wards havespecial areas where children who have taken a substance of low toxicity can be observedfor a few hours without being formally admitted.

Deaths from ingested poisons are uncommon, and are due to drugs (especially tricyclicantidepressants), household products and, rarely, plants. As can be seen from Table H.1,more children die each year from inhalation of carbon monoxide and other gases inhousehold fires, than from accidental poisoning by drugs.

Table H.1. Deaths in children (ages 1–14) from poisons in England and Wales

Cause of death 1988 1998 2001

From poisoning by drugs, medicaments and biologicalsubstances

16 18 2

From toxic effects of carbon monoxide 36 15 21From toxic effect of other gases, fumes or vapours, includingunspecified factors

56 24 7

Office of National Statistics 2001

There has been a steady decline in the number of childhood deaths from poisonings.The selective introduction of child-resistant containers (CRCs) in 1976, together withother measures, has reduced the number of poisonings and hospital attendances. Inthe case of salicylate poisoning the introduction of CRCs saw an 85% fall in hospital

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GENERAL APPROACH TO POISONING AND ENVENOMATION

admissions from 1975 to 1978. It should be remembered, however, that 20% of childrenunder the age of 5 years are capable of opening CRCs!

The decrease in deaths from the inhalation of toxic fumes may be related to the gradualeffect of the legislation in the UK on the banning of toxic substances in furnishing items.The continued substantial death rate from carbon monoxide poisoning is disappointingbut may be related to the fact that although smoke alarms are more readily found indwellings, they are often non-functional. The decline in mortality from drug poisoningmay be due both to more effective treatment and possibly to the more widespread use ofless toxic antidepressant drugs.

Accidental poisoning

This is usually a problem of the young child or toddler, with a mean age of presentationof 21

2 years. Accidental poisoning usually occurs when the child is unsupervised, and thereis an increased incidence in poisoning following recent disruption in households, such asa new baby, moving house or where there is maternal depression.

Intentional overdose

Suicide or parasuicide attempts are usually made by young people in their teens; how-ever, sometimes they may be as young as 8 or 9 years. These children or adolescentsshould undergo psychiatric and social assessment.

Drug abuse

Alcohol and solvent abuse are the commonest forms of drug abuse in children in theUK.

Iatrogenic

The commonest offender is diphenoxylate with atropine (Lomotil). This combina-tion is toxic to some children at therapeutic doses. The most frequently fatal drug isdigoxin.

Deliberate poisoning

Rarely, symptoms are induced in children by adults via the administration of drugs. Ahistory of poisoning will often not be given at presentation.

Most poisoning episodes in childhood and adolescence are of low lethality and little orno treatment is required. This chapter will not address the milder cases but will enablethe student to develop an approach to the seriously ill poisoned child, with additionaladvice on the management of specific poisons.

H.3 PRIMARY ASSESSMENT

Airway

Assess airway patency by the “look, listen, and feel” method.If the child can speak or cry in response to a stimulus, this indicates that the airway

is patent, that breathing is occurring and that there is adequate circulation. If the child

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responds only with withdrawal to a painful stimulus (AVPU score “P”) his airway is atrisk.

If there is no evidence of air movement then chin lift or jaw thrust manoeuvres shouldbe carried out and the airway reassessed. If there continues to be no evidence of airmovement then airway patency can be assessed by performing an opening manoeuvreand giving rescue breaths (see “Basic Life Support”, Chapter 4).

Breathing

Assess the adequacy of breathing.

• Effort of breathingRecessionRespiratory rate: the rate may be increased in poisoning from amphetamines,

ecstasy, salicylates, ethylene glycol and methanol• Efficacy of breathing

Breath soundsChest expansion/abdominal excursion

Monitor oxygen saturation with a pulse oximeter.

Circulation

Assess the adequacy of circulation.

• Cardiovascular statusHeart rate: tachycardia is caused by amphetamines, ecstasy, β-agonists, phenoth-

iazines, theophylline and tricyclic antidepressants; bradycardia is caused by beta-blockers, digoxin and organophosphates

Pulse volumeCapillary refillBlood pressure: hypotension is commonly seen in serious poisoning; hypertension

is caused by ecstasy and monoamine oxidase inhibitors• Effects of circulatory inadequacy on other organs

Acidotic sighing respirations: this may suggest metabolic acidosis from salicylateor ethylene glycol poisoning as a cause for the coma

Pale, cyanosed or cold skin

Monitor heart rate/rhythm, blood pressure and core–toe temperature difference.If heart rate is above 200 in an infant or above 150 in a child, or if the rhythm is

abnormal, perform a standard ECG. QRS prolongation and ventricular tachycardia isseen in tricyclic antidepressant poisoning.

Disability

Assess neurological function.

• A rapid measure of level of consciousness should be recorded using the AVPU scale.Depression of conscious level suggests poisoning with opiates, sedatives (such as benzodi-azepines) antihistamines and hypoglycaemic agents.

• Pupillary size and reaction should be noted. Very small pupils suggest opiate ororganophosphate poisoning, large pupils amphetamines, atropine and tricyclic antidepres-sants.

• Note the child’s posture. Hypertonia is seen in amphetamine, ecstasy, theophylline andtricyclic antidepressant poisoning.

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• The presence of convulsive movements should be sought. Convulsions are associ-ated with any drug that causes hypoglycaemia (ethanol) and with tricyclic antidepressantpoisoning.

Exposure

Take the child’s core and toe temperatures. A fever suggests poisoning with ecstasy, cocaineor salicylates. Hypothermia suggests poisoning with barbiturates or ethanol.

H.4 RESUSCITATION

Airway

• A patent airway is the first requisite. If the airway is not patent it should be opened andmaintained with an airway manoeuvre and the child ventilated by bag–valve–maskoxygenation. An airway adjunct can be used. The airway should then be secured byintubation by experienced senior help.

• If the child has an AVPU score of “P”, his airway is at risk. It should be maintainedby an airway manoeuvre or adjunct and senior help requested to secure it.

Breathing

• All children with respiratory abnormalities, shock or a decreased conscious levelshould receive high-flow oxygen through a face mask with a reservoir as soon as theairway has been demonstrated to be adequate.

• A number of agents taken in overdose (particularly narcotics) can produce respira-tory depression. Oxygen should be given, but it is important to remember that thesepatients may have an increasing carbon dioxide level despite a normal oxygen sat-uration whilst breathing oxygen. Inadequate breathing should be supported using abag–valve–mask device with oxygen or by intermittent positive pressure ventilationin the intubated patient.

Circulation

• A number of poisons can produce shock, by a number of different mechanisms.Hypovolaemia may be caused by gastrointestinal bleeding from iron poisoning orthere may be vasodilatation from barbiturates. Shock should be treated with a fluidbolus, as usual. If possible, inotropes should be avoided in poisoning cases as thecombination of toxic substance producing shock and an inotrope may be proarrhyth-mogenic.

• Cardiac dysrhythmias can be expected in tricyclic antidepressant (TCA), digoxin,quinine and antiarrhythmic drug poisoning. Some antiarrhythmic treatments are con-traindicated with certain poisons. See below for advice on TCA poisoning and contacta poisons centre urgently for other advice.

Gain intravenous or intraosseous access

• Take blood for FBC, U&Es, toxicology, paracetamol and salicylate levels (in patientswho have taken an unknown drug), glucose stick test and laboratory test. Give 5 ml/kgof 10% dextrose to any hypoglycaemic patient.

• Give 20-ml/kg rapid bolus of crystalloid to any patient with signs of shock.

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• If a child has a tachyarrhythmia and is shocked, up to three synchronous electricalshocks at 0·5, 1 and 2 J should be given. If the arrhythmia is broad complex andthe synchronous shocks are not activated by the defibrillator then attempt an asyn-chronous shock. A conscious child should be anaesthetised first if this can be donein a timely manner. DC shock may be dangerous in digoxin poisoning. Use lidocaine(lignocaine), amiodarone or phenytoin.

Disability

• Treat convulsions with either diazepam, midazolam or lorazepam.• Give a trial of naloxone in cases where depressed conscious level and small pupils

suggest opiate poisoning.

In all cases of serious poisoning early consultation with a poisons centre is mandatory.Such centres have a wealth of expertise in the management of poisoning and will adviseon the individual patient’s needs.

Monitoring

• ECG• Blood pressure (use appropriate size of cuff)• Pulse oximetry• Core temperature• Blood glucose• Urea and electrolytes• Blood gases (where indicated)

Lethality assessment

At the end of the primary assessment, it is important to assess the potential lethalityof the overdose. This requires knowledge of the substance that has been taken, the timeit was taken and the dosage. This information may be unattainable in the unwitnessedpoisoning episode of a toddler or that of an unconscious or uncooperative adolescent.Some clues about the drug ingested may be available from physical signs noted duringthe primary assessment (Table H.2).

Table H.2. Diagnostic clues from the primary assessment

Signs Drug

Tachypnoea Aspirin, theophylline, carbon monoxide, cyanideBradypnoea Ethanol, opiates, barbiturates, sedativesMetabolic acidosis (sighing respirations) Ethanol, carbon monoxide, ethylene glycolTachycardia Antidepressants, sympathomimetics,

amphetamines, cocaineBradycardia β-blockers, digoxin, clonidineHypotension Barbiturates, benzodiazepines, β-blockers, calcium

channel blockers, opiates, iron, phenothiazines,phenytoin, tricyclic antidepressants

Hypertension Amphetamines, cocaine, sympathomimetic agentsSmall pupils Opiates, organophosphate insecticides,

phenothiazines

(Continued)

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Table H.2. Continues

Signs Drug

Large pupils Amphetamines, atropine, cannabis,carbamazepine, cocaine, quinine, tricyclicantidepressants

Convulsions Carbamazepine, lindane, organophosphateinsecticides, phenothiazines, tricyclicantidepressants

Hypothermia Barbiturates, ethanol, phenothiazinesHyperthermia Amphetamines, cocaine, ecstasy, phenothiazines,

salicylates

Some investigation results can add clues to the diagnosis of an unknown poison.

1. Metabolic acidosis can be found in poisoning from:

• Carbon monoxide• Ecstasy• Ethylene glycol• Iron• Methanol• Salicylates• Tricyclic antidepressants

2. Enlarged anion gap (Na + K)-(HCO3 – Cl) > 18 can be found in poisoning from:

• Ethanol• Ethylene glycol• Iron• Methanol• Salicylates

3. Hypokalaemia can be found in poisoning from:

• β-agonists• Theophylline

4. Hyperkalaemia can be found in poisoning from:

• Digoxin

The risks of a particular overdose can be assessed once all the information has beengathered. Complex or life-threatening cases should be discussed with a poisons centre.The poisons centre will require the following information:

• Age and weight of the patient• The time since exposure• The substance• The amount taken together with any description or labelling• The patient’s condition

If the nature of the overdose is unknown then a high potential lethality should beassumed. Many childhood poisoning incidents have zero lethality and no treatment isrequired.

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H.5 POISONING EMERGENCY TREATMENT

Drug elimination

Many children have taken a trivial overdose or an overdose of a non-poisonous sub-stance. If the overdose episode is assessed as having a low lethality, then no treatment isrequired.

If the drug overdose is assessed as having a potentially high lethality or its exact natureis unknown, then measures to minimise blood concentrations of the drug should beundertaken. In general this means stopping further absorption. Occasionally measuresto increase excretion can be employed and in some circumstances specific antidotes maybe available. Seek advice from a poisons centre.

Activated charcoalActivated charcoal has a surface area of 1000 m2/g and is capable of binding a number

of poisonous substances without being systemically absorbed. It is now widely used incases of poisoning. However, there are some substances which it will not absorb. Theseinclude alcohol and iron. Repeated doses of activated charcoal are useful in some typesof poisoning because they promote drug reabsorption from the circulation back into thebowel and interrupt enterohepatic cycling. These types include aspirin, barbiturates andtheophylline.

It is often difficult to give charcoal to children as it is unpalatable. Flavouring maybe necessary but can diminish the charcoal’s activity. The charcoal can be given viaa nasogastric or lavage tube after a gastric washout. The dose is at least 10 times theestimated dose of poison ingested. Children should usually be given 25–50 g.

Aspirated charcoal causes severe lung damage, so airway protection is especiallyimportant in the child who is not fully conscious.

EmesisEmesis caused by ipecacuanha is now rarely used although for many years was routinely

given for the management of poisoning incidents in children. The dose schedule is 15 mlwith water (10 ml in children of 6 months to 2 years), repeated once after 20 minutesif necessary. It must not be used in the child with a depressed conscious level. Evidencenow suggests that unless emesis occurs within 1 hour of ingestion of the poison, little ofthe poison will be eliminated. Only about 30% is retrieved even up to 1 hour.

Emesis should only be used for those poisons requiring removal which are not boundby charcoal or in children who are at risk from developing symptoms from the poison theyhave taken, who present within 1 hour of ingestion and who will not take the charcoal.

Gastric lavageThis is indicated in children who have ingested significant amounts of drugs at a high

lethality but is likely to be effective only if performed within an hour of ingestion. Intuba-tion (under anaesthetic) will be necessary for children who cannot protect their airway.After evacuation, the lavage tube can be used as a route for a specific antidote or activatedcharcoal. The lavage fluid can be water or isotonic saline and aliquots of 10–20 ml/kgused. In children the usual indication is iron poisoning.

There are a number of active elimination techniques such as haemoperfusion andplasmapheresis: their use is infrequent and should be guided by the advice of the poisonscentre.

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H.6 EMERGENCY TREATMENT OF SPECIFIC POISONS

Iron

The child with iron poisoning presents with shock, which may be due to gut haemor-rhage. If over 20 mg/kg of elemental iron has been taken, toxicity is likely. Over 150 mg/kgmay be fatal. Intubation, ventilation and circulatory support are necessary in the severelyaffected child.

Initial symptoms of toxicity are vomiting, diarrhoea and abdominal pain. These maylead on to drowsiness, fits and circulatory collapse.

Gastric lavage should be performed once the airway is secured and circulatory accesshas been gained. Charcoal is not helpful. Desferrioxamine can be left in the stomach, butthe main treatment is to infuse desferrioxamine at a dose of 15 mg/kg/h. This treatmentshould be given immediately to children with serious symptoms such as shock, coma orfits and to all with a serum iron level (4 hours or more after ingestion) of 3 mg/l andgastrointestinal symptoms, leucocytosis or hyperglycaemia.

Radiography of the abdomen can help to show how much iron remains within. Whole-bowel irrigation with polyethylene glycol–electrolyte solutions may have a place in severecases.

Tricyclic antidepressant (TCA) poisoning

The toxic effects of these agents result from their inhibition of fast sodium channels inthe brain and the myocardium, which action is known as “quinidine-like”. With seriousintoxication, the cardiac problems are due to intraventricular conduction delay. Thisresults in QRS prolongation (a QRS of more than 4 little squares on the ECG paper ispredictive of serious effects).

TCA poisoning causes anticholinergic effects (tachycardia, dilated pupils, convulsions)and cardiac effects (conduction delay, any arrhythmia). Convulsions should be treatedas described in Chapter 12.

In addition, alkalinisation up to an arterial pH of at least 7·45, and preferably 7·5, hasbeen shown to reduce the toxic effects on the heart. This can be achieved by hyperven-tilation (P2 no lower than 3·33 kPa (25 mmHg)) and by infusing sodium bicarbonate(1–2 mmol/kg). Hypotension should be treated with volume expansion, and if an inotropeis necessary, noradrenaline (norepinephrine) is preferable to dopamine, dobutamine andadrenaline (epinephrine). Glucagon has an inotropic effect and can be used in thiscircumstance.

The use of antiarrhythmics should be guided from a poisons centre. Lidocaine (lig-nocaine) and phenytoin may be helpful. Quinidine, procainamide and disopyramide arecontraindicated.

Opiates (including methadone)

Following stabilisation of airway, breathing and circulation, the specific antidote isnaloxone. An initial bolus dose of 10 micrograms/kg up to a maximum of 0·8 mg shouldbe given. Naloxone has a short half-life, relapse often occurring after 20 minutes. Largerboluses, or an infusion of 5–20 micrograms/kg/hr, may be required.

It is important to normalise CO2 before the naloxone is given because adverse eventssuch as ventricular arrhythmias, acute pulmonary oedema, asystole or seizures mayotherwise occur. This is because the opioid system and the adrenergic system are in-terrelated. Opioid antagonists and hypercapnia stimulate sympathetic nervous system

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activity. Therefore if ventilation is not provided to normalise carbon dioxide prior to nalox-one administration, the sudden rise in adrenaline (epinephrine) concentration can causearrhythmias.

Paracetamol

Significant paracetamol poisoning in childhood is almost always intentional: the acci-dental ingestion of paediatric paracetamol elixir preparations by the toddler very rarelyachieves toxicity. Doses of less than 150 mg/kg will not cause toxicity except in a childwith hepatic or renal disease. Current treatment of paracetamol poisoning includes oralcharcoal and a paracetamol blood level to be taken at 4 hours or later. Figure H.1 showsa nomogram indicating the level of blood paracetamol at which acetylcysteine shouldbe given intravenously. A total dose of 300 mg/kg is given over approximately 24 hours.Contact a poisons centre for individual details.

Figure H.1. Nomogram showing level of blood paracetamol

Salicylates

Aspirin slows stomach emptying, so gastric lavage can be undertaken up to 4 hoursafter ingestion. Repeated charcoal doses should be given for patients who have ingestedsustained-release preparations. The salicylate level can be measured initially at 2 hours.However, repeated measurements are necessary and no reliance should be placed ona single salicylate level. The levels will usually rise significantly over the first 6 hours(longer if an enteric coated preparation is used). Salicylate poisoning causes a respiratoryalkalosis and metabolic acidosis. Arterial blood gas estimation is necessary for managingthe patient. Alkalinisation of the patient improves the excretion of salicylate: 1 mmol/kgof sodium bicarbonate should be infused over 4 hours. Forced diuresis is no longer used.

Ethylene glycol

This sweet-tasting substance is available as an antifreeze and de-icer fluid for vehicles.It produces a clinical appearance of inebriation accompanied by metabolic acidosis and

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causes widespread cellular damage, especially to the kidneys. In unwitnessed ingestionsthe clue is in the metabolic acidosis with an inexplicable anion gap. Activated charcoalis ineffective. Ethanol is a competitive inhibitor of alcohol dehydrogenase and can blockmetabolism of the ethylene glycol to its poisonous metabolic byproducts. An oral loadingdose of 2·5 ml/kg of 40% ethanol (the strength of most spirits) should be started. The aimis to have a blood ethanol concentration of 100 mg/dl. Haemodialysis may be necessary.Cofactors, thiamine and pyridoxine are also recommended.

Cocaine

Cocaine poisoning leads to local accumulation of the neurotransmitters noradrenaline(norepinephrine), dopamine, adrenaline (epinephrine) and serotonin. Accumulation ofnoradrenaline (norepinephrine) and adrenaline (epinephrine) leads to tachycardia, whichincreases myocardial oxygen demand while reducing the time for diastolic coronary per-fusion. Vasoconstriction causing hypertension results from the accumulation of neu-rotransmitters at the peripheral β-adrenergic receptors, and peripheral 5-HT receptorstimulation causes coronary artery vasospasm. In addition, cocaine stimulates plateletaggregation. Together, these changes can produce what is effectively a coronary event ina child or an adolescent.

Acute coronary syndrome producing chest pain and varying types of cardiac rhythmdisturbances is the most frequent complication of cocaine use, which leads to hospitalisa-tion. Cocaine is also a sodium channel inhibitor, similar to a type I antiarrhythmic agent,and so can prolong the QRS duration and impair myocardial contractility. Through thecombination of adrenergic and sodium channel effects, cocaine use may cause varioustachyarrhythmias including ventricular tachycardia and ventricular fibrillation. Treat-ment should be guided by a poisons centre.

Initial treatment of acute coronary syndrome consists of oxygen administration, contin-uous ECG monitoring, administration of a benzodiazepine (e.g. diazepam or lorazepam),aspirin and heparin. Hyperthermia should be treated with cooling. β-adrenergic blockersare contraindicated in the setting of cocaine intoxication.

Ventricular tachycardia should be treated with DC shock as antiarrhythmic drugs maycause further proarrhythmic effects.

Since cocaine is a sodium channel blocker, administration of sodium bicarbonate in adose of 1–2 meq/kg should be considered in the treatment of ventricular arrhythmias.

Ecstasy

Most ecstasy tablets contain 30–150 mg of 3,4-methylenedioxymethamphetamine(MDMA). This drug, which has a half-life of around 8 hours, most probably stimu-lates both the peripheral and the central alpha- and beta-adrenergic receptors. Earlydeaths are usually due to cardiac dysrhythmias, while deaths after 24 hours occur from aneuroleptic malignant-like syndrome.

Mild adverse effects occur at low doses and include increased muscle tone, agitation,anxiety and tachycardia. Mild elevation of temperature may also occur. At higher doses,hypertonia with hyperreflexia, tachycardia, tachypnoea and visual disturbance can beseen. In the worst affected children, coma, convulsions and cardiac dysrhyth-mias can occur. Hyperpyrexia with increased muscle tone can lead to rhab-domyolysis, metabolic acidosis with acute renal failure and disseminatedintravascular coagulation.

Activated charcoal should be given to conscious patients. Blood pressure and temper-ature must be monitored. Diazepam can be used to control anxiety – major tranquilisersshould not be used because they exacerbate symptoms. If core temperature exceeds 39◦C

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then active cooling should be commenced and the use of dantrolene sodium (1 mg/kgover 10–15 min) should be considered. Some children may require ventilation.

H.7 ENVENOMATION

H.8 INTRODUCTION

Envenomation may occur as a result of bites or stings from a wide variety of animals in-cluding snakes, bees, scorpions, spiders, jellyfish and fish. In many cases envenomation isunavoidable, but appropriate behaviour and clothing will limit exposure to envenomation.

Symptoms of envenomation may be the direct result of the venom, or allergic reactions(e.g. bee sting) to those toxins. In all cases the principles of management consist of:

• standard resuscitation practice of managing airway, breathing and circulation;• limiting the uptake of venom into the circulation where possible;• administration of antitoxin where available and appropriate;• supportive care to the systems involved by the toxin;• management of pain and• treatment of sites of local injury.

Diagnosis of envenomation is often difficult, but essential to appropriate management.The symptoms of stings are usually rapid in onset, and the diagnosis of envenomation isusually straightforward. Envenomation does not occur with all bites, even from venomousspecies, and it may be difficult to decide whether or not envenomation has occurred im-mediately after a bite. In this context it is appropriate to apply measures to reduce systemicuptake of venom from the site of the bite, and to delay the administration of antitoxin untila more definitive diagnosis of envenomation has been made. Occasionally, envenomationis part of the differential diagnosis of symptoms experienced by a patient who either wasnot aware of a sting or bite, or is too young to provide an appropriate history. Diagnosisof envenomation may be made by the development of specific symptoms, or by the use ofdiagnostic kits which identify the presence of specific venoms. Unfortunately, diagnosticsystems are not generally available in many areas where stings or bites are common.

Although accurate identification of the cause of the envenomation may assist withspecific therapy, attempts to capture the source of the bite or sting are more likely toresult in extra victims than useful information.

H.9 RESUSCITATION AND SUPPORT

Airway

The airway may be threatened for a number of reasons including depressed level ofconsciousness, bulbar palsy, paralysis and swelling of tissues around the airway.

The airway must be assessed frequently. Clearance of secretions from the pharynxis the most common problem. Patients who require intubation for reasons other thana depressed level of consciousness require anaesthesia for intubation. It is extremelyimportant to note that a totally paralyzed patient may be fully conscious.

Breathing

Many venoms cause paralysis, and patients affected by these venoms require ventilatorysupport. The support must be provided prior to respiratory arrest. As patients may beparalysed but fully awake, anaesthesia for intubation is recommended.

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Severe muscle spasm or seizures may occur following some envenomation, and thesepatients will require ventilatory support. Also, secretions may contribute to respiratoryembarrassment and ventilatory support may prevent the accumulation of secretions.

Circulation

Shock may occur for a variety of reasons including massive leakage of fluid intotissues damaged by cytotoxic venoms, cardiac arrhythmia and bleeding secondary tocoagulopathy.

Adequate vascular access must be secured with fluid resuscitation appropriate to theclinical situation.

Some venoms are associated with the development of renal and/or electrolyte problems,and fluid and electrolyte therapy must be adapted to the specific venom.

Disability

Assess the patient’s conscious level, remembering that failure to respond may be aconsequence of paralysis and not of the level of consciousness. Look specifically to localneurological problems such as ophthalmoplegia and/or bulbar palsy.

Exposure

Full exposure may be required to identify the site of a bite, and in the case of stings itis also important to examine areas of the body covered by hair.

H.10 SPECIFIC ENVENOMATION ISSUES

Limiting the uptake of venom

Where possible, the rate of uptake of venom or toxin into the circulation should belimited. If the bite or sting has affected a limb, it may be possible to slow the rate ofabsorption of toxin from the bite or sting by the application of a crepe bandage to the limb,together with immobilization of the limb. Neither the application of a pressure bandagenor immobilization alone will significantly slow uptake of toxin into the circulation. Bothmeasures should be applied. The bandage should be firmly applied (similar pressure tothat required to strap a strained ankle), but should not interfere with the circulation to thelimb. Splints should be applied to immobilize the limb. The pressure bandage should notbe removed before the child is in a facility that can provide supportive care, and antiveninshould be administered prior to the release of the bandage if envenomation has occurred.

There is little data about the efficacy of limb bandaging in the case of cytotoxic venoms.Theoretically, localisation of the venom may increase the local damage (controversial inthe various articles). However, in children, uptake of predominantly cytotoxic venominto the circulation will cause systemic effects, and it is probably safer to immobilize thelimb and apply a pressure bandage.

In the case of jellyfish stings there is a concern that application of pressure to the site ofthe sting may increase the release of toxin from stings on the skin. In this situation liberalwashing of the site with vinegar and then gentle application of a vinegar-soaked bandageis appropriate.

Some marine toxins are heat-sensitive, and application of warmth to the site of theinjury may reduce symptoms considerably. Great care must be taken to avoid burningthe patient.

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If there is a specific antivenin or antiserum available, this should be administeredas soon as possible. If there is doubt as to whether envenomation actually occurred,then there may be a place for observation and some delay in administration. Symptomsare usually evident within 1 hour of snakebite envenomation. In reality, antivenins arenot usually available at the site of the incident, and by the time the victim has actuallyreached a medical facility it is usually clear whether envenomation has occurred. Thedose of antiserum should not be based on the patient size, but on the amount requiredto neutralize the toxin; thus in general children will receive the full adult dose.

Although allergic reactions to antivenin are relatively common, they may be preventedor ameliorated by premedication with subcutaneous adrenaline (epinephrine) 5–10 micro-grams/kg. Additional protective agents such as a steroid (hydrocortisone) and an antihis-tamine may be indicated if the patient has a known allergic history.

Treatment of sites of local injury

If venom is sprayed into the eyes, it is important to wash out any venom as soon aspossible, using clean fluids.

There is no evidence that suction, electrotherapy or local incision provides any benefitto the patient. There is likewise no evidence that administration of prophylactic antibioticsis useful. Patients who suffer a snakebite and have not been immunised against tetanuswithin the last 5 years should receive antitetanus toxoid.

Envenomation by cytotoxic venoms may cause severe local swelling and pain. Limbsmust be carefully observed for the development of compartment syndromes and if theydevelop early, fasciotomies must be performed. In these patients careful assessment ofcoagulation status with appropriate support is essential as severe bleeding may occurfollowing fasciotomy.

Figure H.2. Management of potentially venomous bite

Local and systemic infections may occur following bites. Although there is no placefor prophylactic antibiotics, any necrotic tissue should be debrided, and infection treatedvigorously with antibiotics based on bacterial cultures. Initial therapy prior to cultureresults should cover both gram-negative and gram-positive organisms.

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Drugs

In addition to antivenin (where available) there are a number of problems that mayrequire symptomatic therapy.

Analgesia

Pain may be an extremely important feature of envenomation, and adequate analgesiais critical. Severe pain is best treated with intravenous opiates titrated to effect. Localtherapy with agents that neutralize toxins may be possible, e.g. application of vinegar inthe case of jellyfish stings or application of warm water in some stonefish stings. In casesof severe limb-related pain regional anaesthesia may be helpful, but must be used withcare in view of potential bleeding problems.

Sedation

Bites or stings may be associated with extreme anxiety. Reassurance and supportivecare is the basis of therapy, but sedation and anxiolysis may be helpful, particularly ifpatients require transportation.

Coagulation support

Antivenins do not correct coagulation defects, and coagulation problems must betreated using supportive administration of clotting factors.

Figure H.3. Management of potentially venomous sting

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Monitoring

If envenomation has occurred a wide range of side effects are possible depending onthe particular source of envenomation, the dose of venom administered, the time toadequate therapy, the dose of antivenom administered, etc. It is essential to monitorpatients carefully for all the potential side effects of the supposed envenomation.

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BY033-APPXI BMJ Books BY033-Jones-v8.cls September 1, 2004 16:25

APPENDIX

IResuscitation of the baby at birth

I.1 OBJECTIVES

This will teach you:

• the physiological differences in the newly born baby• the equipment used for resuscitation at birth• how to assess the baby at birth• how to resuscitate the baby at birth• additional measures for special situations

I.2 INTRODUCTION

The resuscitation of babies at birth is different from the resuscitation of all other agegroups, and knowledge of the relevant physiology and pathophysiology is essential. How-ever, the majority of newly born babies will establish normal respiration and circulationwithout help. Ideally, someone trained in newborn resuscitation should be present atall deliveries. It is advisable that all those who attend deliveries attend courses such asthe Newborn Life Support Course, organised by the Resuscitation Council (UK) or theNeonatal Resuscitation Programme, organised by the American Academy of Pediatrics.However, some babies are born in unexpected places such as A&E departments. Forthese situations it is important that clinicians have an understanding of the differences inresuscitating a baby at birth.

I.3 NORMAL PHYSIOLOGY

At birth the baby must change, within a matter of moments, from an organism withfluid-filled lungs whose respiratory function is carried out by the placenta to a separatebeing whose air-filled lungs can successfully take over this function. Preparation for thisbegins during labour, when the fluid-producing cells within the lung cease secretion and

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begin re-absorption of that fluid. Delivery by caesarean section before the onset of labourmay slow the clearance of pulmonary fluid from the lungs.

During vaginal delivery some lung fluid, perhaps 35 ml in a term baby, is expelledby passage through the birth canal. In a healthy baby the first spontaneous breaths maygenerate a negative pressure of between –40 cmH2O and –100 cmH2O (–3·9 and –9·8 kPa), which aerates the lungs for the first time. This pressure is 10–15 times greaterthan that needed for later breathing but is necessary to overcome the viscosity of the fluidfilling the airways, the surface tension of the fluid-filled lungs and the elastic recoil andresistance of the chest wall, lungs and airways. These powerful chest movements causefluid to be displaced from the airways into the lymphatics.

After delivery, a healthy term baby usually takes its first breath within 60–90 secondsof clamping or obstructing the umbilical cord. Separation of the placenta and clampingof the cord leads to the onset of asphyxia, which is initially a major stimulant to startrespiration. Physical stimuli such as cold air or physical discomfort may also provokerespiratory efforts.

In a 3-kg baby up to 100 ml of fluid is cleared from the airways following the initialbreaths, a process aided by full inflation and prolonged high pressure on expiration, i.e.crying. The effect of the first few breaths is to produce the baby’s functional residual ca-pacity. Neonatal circulatory adaptation commences with the detachment of the placenta,but lung inflation and alveolar distension releases mediators, which affect the pulmonaryvasculature as well as increase oxygenation.

Pathophysiology

Our knowledge of the pathophysiology of foetal asphyxia is based on pioneering animalwork in the early 1960s. The results of these experiments, which followed the physiologyof newborn animals during acute, total, prolonged asphyxia and subsequent resuscitationare summarised in Figure I.1.

When the placental oxygen supply is interrupted, the foetus attempts to breathe. Shouldthese attempts fail to provide an alternative oxygen supply – as they will inevitably fail todo so in utero – the baby will lose consciousness. If hypoxia continues, the respiratorycentre becomes unable, through lack of sufficient oxygen, to continue initiating breathingand the breathing stops, usually within 2–3 minutes (primary apnoea, Figure I.1). Foetalbradycardia ensues but blood pressure is maintained, primarily by peripheral vasocon-striction and diversion of blood away from non-vital organs, and also by an increasedstroke volume. After a latent period of apnoea (primary), primitive spinal centres, nolonger suppressed by neural signals from the respiratory centre, exert an effect by initi-ating primitive gasping breaths. These deep spontaneous gasps are easily distinguishablefrom normal breaths as they occur 6–12 times per minute and involve all accessory mus-cles in a maximal inspiratory effort. After a while, if hypoxia continues, even this activityceases (terminal apnoea). The time taken for such activity to cease is longer in the newlyborn baby than in later life, taking up to 20 minutes.

The circulation is almost always maintained until all respiratory activity ceases. Thisresilience is a feature of all newborn mammals at term, largely due to the reserves ofglycogen in the heart. Resuscitation is therefore relatively easy if undertaken before allrespiratory activity has stopped. Once the lungs are inflated, oxygen will be carried tothe heart and then to the brain provided the circulation is still functional (Figure I.2).Recovery will then be rapid. Most infants who have not progressed to terminal apnoeawill resuscitate themselves if their airway is patent. Once gasping ceases, however, thecirculation starts to fail and these infants are likely to need more extensive resuscitation(Figure I.3).

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10 20 30 40

Heart rate

Minutes

Excess acid

BP

Northern Neonatal Network

160

120

80

40

00

RespsPrimaryapnoea

Terminalapnoea

1 2 3

PaO2

PaCO2

Figure I.1. Effects of asphyxia. Babies requiring resuscitation may be born at 1, 2 or 3 (reproducedwith permission from the Northern Neonatal Network)

10 20 30 40

Primaryapnoea

Terminalapnoea

Resps

LungInflation

Heart rate

Minutes


Excess acid

BP

160

120

80

40

00

PaO2

PaCO2

Figure I.2. Effects of lung inflation prior to failure of the cardiovascular system (reproduced withpermission from the Northern Neonatal Network)

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10 20 30 40

Primaryapnoea

Terminalapnoea

Resps

LungInflation IPPV

PaO2

PaCO2

Heart rate

Minutes


Excess acid

BP

160

120

80

40

00

CC

Figure I.3. Response of babies born in terminal apneoa requiring lung inflation, chest compressions(CC) and ventilation (IPPV) (reproduced with permission from the Northern Neonatal Network)

I.4 EQUIPMENT

For many newborn babies, especially those born outside the delivery room, the needfor resuscitation cannot be predicted. It is therefore useful to plan for such an eventuality.Equipment which may be required to resuscitate a newborn baby is listed in Table I.1.This will vary between departments; however, most babies can be resuscitated with a flatsurface, warmth, knowledge and a way to deliver air or oxygen at a controlled pressure.

Table I.1. Equipment for newborn resuscitation

• A flat surface

• Source of warmth and dry towels

• A suction system with catheters at least 12 Fr

• Face masks

• Bag–valve–mask or pressure-limiting device

• Source of air and/or oxygen

• Oropharyngeal airways

• Laryngoscopes with straight, 0 and 1, blades

• Nasogastric tubes

• Device to clamp cord

• Scissors

• Endotracheal tubes sizes 2.5 to 4.0 mm

• Endotracheal stylet

• Umbilical cannulae

• Adhesive tape

• Disposable gloves

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Practical aspects of neonatal resuscitation

Most babies, even those born apnoeic, will resuscitate themselves given a clear airway.However, the basic approach to resuscitation is Airway, Breathing and Circulation, withthe following initial actions:

• Get help• Start the clock• Dry, wrap and keep baby warm• Assess baby

Call for help

Ask for help if you expect or encounter any difficulty.

Start clock

If available, or note the time.

Keep the baby warm

Dry the baby off immediately and then wrap in a dry towel. A cold baby has increasedoxygen consumption and cold babies are more likely to become hypoglycaemic and aci-dotic. They also have an increased mortality. If this is not addressed at the beginningof resuscitation it is often forgotten. Most of the heat loss is caused by the baby beingwet and in a draught – hence the need to dry the baby and then to wrap the baby ina dry towel. Babies also have a large surface area to weight ratio; thus heat can be lostvery quickly. Ideally, delivery should take place in a warm room, and an overhead heatershould be switched on. However, drying effectively and wrapping the baby in a warm drytowel is the most important factor in avoiding hypothermia. A naked wet baby can stillbecome hypothermic despite a warm room and a radiant heater, especially if there is adraught. (see “Pre-Term Babies”)

Assessment of the newborn baby

The APGAR score was proposed as a tool for evaluating a baby’s condition at birth.Although the score, calculated at 1 and 5 minutes, may be of some use retrospectively,it is almost always recorded subjectively and it is not used to guide resuscitation. Acuteassessment is made by assessing:

• Respiration• Heart rate• Colour• Tone

(rate and quality) Airway and Breathing(fast, slow, absent)(pink, blue, pale)(unconscious, apnoeic Circulation

babies are floppy)

Respiration

Most babies will establish spontaneous regular breathing sufficient to maintain theheart rate above 100 beats/min and to improve the skin colour within 3 minutes of birth.If apnoea or gasping persists after drying, intervention is required.

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Heart rate

Auscultating at the cardiac apex is the best method to assess the heart rate. Palpatingperipheral pulses is not practical and cannot be recommended. Palpation of the umbilicalpulse can only be relied upon if it is >100 beats/min. A rate less than this should bechecked by auscultation if possible. An initial assessment of heart rate is vital because anincrease in the heart rate will be the first sign of success during resuscitation.

This assessment will categorise the baby into one of the three following groups:

1. Pink, regular respirations, heart rate fast (more than 100 beats/min). These are healthybabies and they should be kept warm and given to their mothers.

2. Blue, irregular or inadequate respirations, heart rate slow (60 beats/min or less). If gentlestimulation (such as drying) does not induce effective breathing, the airway shouldbe opened and cleared. If the baby responds then no further resuscitation is needed.If there is no response, progress to lung inflation.

3. Blue or pale, apnoeic, heart rate slow (less than 60 beats/min) or absent. Whether anapnoeic baby is in primary or secondary apnoea (Figure I.1) the initial managementis the same. Open the airway and then inflate the lungs. A reassessment of any heartrate response then directs further resuscitation. Reassess the heart rate and respirationat regular intervals throughout.

Pallor, apnoea and low or absent heart rate suggest terminal apnoea. However, initialmanagement of such babies is unchanged but resuscitation may be prolonged.

After assessment, resuscitation follows:

• Airway• Breathing• Circulation• With the use of drugs in a few selected cases

Airway

The baby should be positioned with the head in the neutral position (see Figure I.4 andChapter 4). The newborn baby’s head has a large, often moulded, occiput, which tendsto cause the neck to flex when the baby is supine on a flat surface. However, overextensionmay also collapse the newborn baby’s pharyngeal airway, leading to obstruction. A foldedtowel placed under the neck and shoulders may help to maintain the airway in a neutralposition and a jaw thrust may be needed to bring the tongue forward and open the airway,especially if the baby is floppy (Figure I.5). Visible secretions may be removed by gentlesuction with a paediatric Yankauer or 12–14-Fr suction catheter, although these rarelycause airway obstruction. Blind deep pharyngeal suction should be avoided as it maycause vagally induced bradycardia and laryngospasm. Suction, if it is used, should notexceed –100 mmHg (9·8 kPa).

Meconium aspirationMeconium-stained liquor is relatively common and occurs in up to 10% of births.

Happily, meconium aspiration is a rare event. Meconium aspiration usually happens interm infants in utero before delivery. There is no advantage to suctioning the airwaywhilst the head is on the perineum. If the baby is vigorous, a randomised trial has shownthat suctioning at any time offers no advantage and no specific action (other than dryingand wrapping the baby) is needed. If the baby has absent or inadequate respirations,a heart rate <100 beats/min or hypotonia, inspect the oropharynx with a laryngoscopeand aspirate any particulate meconium seen using a wide-bore catheter. If intubation is

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Figure I.4. Chin lift in infants

Figure I.5. Jaw thrust

possible and the baby is still unresponsive, aspirate the trachea using the tracheal tubeas a suction catheter. However, if intubation cannot be achieved immediately, clear theoropharynx and start mask inflation. If, while attempting to clear the airway, the heartrate falls to less than 60 beats/min then stop airway clearance, give aeration breaths andstart ventilating the baby.

Breathing (aeration breaths and ventilation)

The first five breaths in term babies should be aeration breaths in order to replacelung fluid in the alveoli with air/oxygen. These should be 2–3-second sustained breathsusing a continuous gas supply, a pressure-limiting device and a mask. Use a transparent,circular soft mask big enough to cover the nose and mouth of the baby (Figure I.7). Ifno such system is available then a 500-ml self-inflating bag and a blow-off valve set at30–40 cmH2O can be used. This is especially useful if compressed air or oxygen is notavailable.

The chest may not move during the first 1–3 breaths as fluid is displaced. Once thechest is aerated, reassess the heart rate. It is safe to assume the chest has been inflatedsuccessfully if the heart rate responds. If you need to assess air entry, do so by checking forchest movement, not by auscultation. In fluid-filled lungs, breath sounds may be heardwithout lung inflation.

Once the chest is aerated and the heart rate has increased or the chest has been seento move, ventilation is continued at a rate of 30–40 per minute.

Circulation

If the heart rate remains slow (less than 60 beats/min) even after the lungs have beenaerated, chest compressions must be started. However, the commonest reason for the

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Newborn Life SupportDry the baby

Remove any wet towels and coverStart the clock or note the time

Assess colour, tonebreathing and heart rate

Open the airway

Give 5 inflation breaths

Recheck head positionApply jaw thrust

Repeat inflation breaths

Try alternative airwayopening manoeuvres

Repeat inflation breaths

Give ventilation breathsCheck the heart rate

Start chest compressions

Reassess heart rateevery 30 seconds

if not breathing

If still not breathing

if no response

If still no response

When the chest is moving

if the heart rate is not detectableor slow (<60) and not increasing

if no increase in heart ratelook for chest movement



Look for a response

Look for a response

Look for a response

3 compressions to each breath

Consider venous access and drugs

If heart rate is increasing:

If the chest is still not moving:

If the chest is not moving:

If heart rate is satisfactory butincreasing:

If heart rate is satisfactory butincreasing:

If breathing:

–baby floppy and not breathing well:

If meconium present and–baby breathing well: Do not suction the airway

Consider inspection and suction before inflation breaths

Reassess heart rate and monitor

baby

Continue ventilation breaths at

about 30 per minute until baby isbreathing adequately

Continue ventilation breaths at

about 30 per minute until baby isbreathing adequately

Recheck head position andrepeat inflation breathsIf competent, consider intubation

The airway is the problem

Stop compressionsContinue ventilation breaths atabout 30 per minute until baby isbreathing adequately

Head in neutral position

Get help from a second person

Chest compressions

to support the airwayand/or inspect the oropharynx underdirect vision and consider suctionand/or insert an oropharyngeal airway

Comp/vent ratio 3:1Rate: 120 events per minute

Inflation breathsUse a well-fitting face maskconnected to pressure-limitedgas supplyEach breath of 2–3 seconds' durationat 30 cm H2O for a term baby

Figure I.6. Algorithm for resuscitation at birth (Reproduced with permission from the NLSSub-Committee Resuscitation Council (UK))

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Figure I.7. Bag-and-mask ventilation

Figure I.8. Infant chest compression: hand-encircling technique

heart rate to remain low is that lung inflation has not been successful – chest compressionsare rarely needed. Cardiac compromise is always the result of respiratory failure and canonly be effectively treated if effective ventilation is occurring.

The most efficient way of delivering chest compressions in the neonate is to encirclethe chest with both hands, so that the fingers lie behind the baby and the thumbs areapposed on the sternum just below the inter-nipple line (Figure I.8). Compress the chestbriskly, by one third of its depth. Current advice is to perform three compressions for eachventilation breath (3:1 ratio).

The purpose of chest compression is to move oxygenated blood or drugs to the coro-nary arteries in order to initiate cardiac recovery. Thus there is no point in starting chestcompression before effective lung inflation has been established. Similarly, compressionsare ineffective unless interposed by ventilation breaths of good quality. Therefore, theemphasis must be upon good-quality breaths, followed by effective compressions. Simulta-neous delivery of compressions and breaths should be avoided, as the former will reducethe effectiveness of the breaths.

Once the heart rate is above 60 beats/min and rising, chest compression can bediscontinued.

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Drugs

If after adequate lung inflation and cardiac compression the heart rate has not re-sponded, drug therapy should be considered. However, the most common reason forfailure of the heart rate to respond is failure to achieve lung inflation, and there is nopoint in giving drugs unless the airway is open and the lungs have been inflated. Airwayand breathing must be reassessed as adequate before proceeding to drug therapy. Venousaccess will be required via an umbilical venous line, because ideally drugs should be givencentrally. The outcome is poor if drugs are required for resuscitation.

Adrenaline (epinephrine)The alpha-adrenergic effect of adrenaline (epinephrine) increases coronary artery

perfusion during resuscitation, enhancing oxygen delivery to the heart. In the pres-ence of profound unresponsive bradycardia or circulatory standstill, 10 micrograms/kg(0·1 ml/kg 1:10000) adrenaline (epinephrine) may be given intravenously or tracheally.Further doses of 10–30 micrograms/kg (0·1–0·3 ml 1:10000) may be tried at 3–5-minuteintervals if there is no response. For this drug the tracheal route is accepted but effective-ness is unproven in resuscitation at birth.

BicarbonateAny baby who is in terminal apnoea will have a significant metabolic acidosis. Acidosis

depresses cardiac function. Bicarbonate 1 mmol/kg (2 ml/kg of 4·2% solution) may beused to raise the pH and enhance the effects of oxygen and epinephrine.

Bicarbonate use remains controversial and it should only be used in the absence ofdiscernible cardiac output despite all resuscitative efforts or in profound and unresponsivebradycardia.

DextroseHypoglycaemia is a potential problem for all stressed or asphyxiated babies. It is treated

using a slow bolus of 5 ml/kg of 10% dextrose intravenously, and then providing a secureintravenous dextrose infusion at a rate of 100 ml/kg/day of 10% dextrose. BM stix arenot reliable in neonates when reading less than 5 mmol/l.

FluidVery occasionally hypovolaemia may be present because of known or suspected blood

loss (antepartum haemorrhage, placenta or vasa praevia, unclamped cord) or it may besecondary to loss of vascular tone following asphyxia. Volume expansion, initially with10 ml/kg, may be appropriate. Normal saline can be used; alternatively Gelofusine hasbeen used safely and if blood loss is acute and severe, non-cross-matched O-negativeblood should be given immediately. Albumin cannot be recommended. However, mostnewborn or neonatal resuscitations do not require fluid unless there has been knownblood loss or septicaemic shock.

NaloxoneThis is not a drug of resuscitation. Occasionally, a baby who has been effectively re-

suscitated – is pink, with a heart rate of over 100 beats/min – may not breathe sponta-neuosly because of the effects of maternal opiates. If respiratory depressant effects aresuspected the baby should be given naloxone intramuscularly (200 micrograms in a full-term baby). Smaller doses of 10 micrograms/kg will also reverse the sedation but the effectwill only last a short time (20 minutes IV or a few hours IM). Intravenous naloxone hasa half-life shorter than opiates, and there is little evidence to recommend intra-trachealadministration.

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Atropine and calcium gluconateAtropine and calcium gluconate have no place in newborn resuscitation. Atropine

may, rarely, be useful in the neonatal unit, when vagal stimulation has produced resistantbradycardia or asystole (see bradycardia protocol).

I.5 RESPONSE TO RESUSCITATION

The first indication of success will be an increase in heart rate. Recovery of respiratorydrive may be delayed. Babies in terminal apnoea will tend to gasp first as they recoverbefore starting normal respirations. Those who were in primary apnoea are likely to startwith normal breaths, which may commence at any stage of resuscitation.

Tracheal intubation

Most babies can be resuscitated using a mask system. Swedish data suggests that ifthis is applied adequately, only 1:500 babies may actually need intubation. However,tracheal intubation remains the gold standard in airway management. It is especiallyuseful in prolonged resuscitations, pre-term babies and meconium aspiration. It shouldbe considered if mask ventilation has failed, although the most common reason for failurewith mask inflation is poor positioning of the head with consequent failure to open theairway.

The technique of intubation is the same as for infants and is described in Chapter 20.A normal full-term newborn usually needs a 3·5-mm tracheal tube, but 4·0-, 3·0- and2·5-mm tubes should also be available.

I.6 SPECIAL CASES

Pre-term babies

Pre-term babies are more likely to get cold (higher surface area to mass ratio), andmore likely to become hypoglycaemic (fewer glycogen stores). There are now severaltrials which support the use of plastic bags placed over babies of <29 weeks’ gestation or<1000 g before drying in order to keep them warm. This technique is especi-ally suited to the unexpected pre-term birth outside a delivery unit but is atemporary insulating measure. Large, food-grade microwaveable roasting bagsare suitable. (see box below)

GUIDELINES FOR USE OF PLASTIC BAGS FOR PRE-TERM BABIES

(<29 WEEKS) AT BIRTH

1. Pre-term babies born below 29 completed weeks’ gestation may be placed in plastic bagsfor temperature stability during resuscitation. They should remain in the bag until theyare on the NICU and the humidity within their incubator is at the desired level. This isa recognised modality to use. It is a way of preventing heat loss and cannot replaceincubators etc. Neither should it replace all efforts to maintain a high ambient temperaturearound babies born outside delivery suites.

2. At birth the baby should not be dried, but should be slipped straight into the preparedplastic bag. There is no need to wrap in a towel so long as this is done immediately afterbirth. This gives immediate humidity.

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3. Suitable plastic bags are food-grade bags designed for microwaving and roasting. Theyshould be large. The bag is prepared with a V cut in the closed end.

4. The bag should be slipped from the head up to the legs, covering in full, and let the headbe completely accessible from the V-cut. This is easiest if the hand is placed through theV, the head placed in the hand, and the bag drawn back down over the baby.

5. The head will stick out of the V-cut and will be dried as usual and resuscitation commencedas per standard guidelines. A hat should be placed over the head if practical to furtherreduce heat loss.

6. The standard resuscitation would be carried out without any limitations of access, but ifthe umbilicus is required for any access then a quick hole can be made above the areaand the desired intervention done.

7. For any cardiac massage as part of resuscitation, the bag should not be removed unlessdeemed necessary by the registrar or consultant.

8. After the baby is transferred to a neonatal unit, the temperature should be recorded aftersecuring ventilation. The bag is only removed when the incubator humidity is satisfactory,and further care provided as per nursing protocols.

The more pre-term a baby the less likely it is to establish adequate respirations. Pre-term babies (<32 weeks) are likely to be deficient in surfactant especially after unexpectedor precipitate delivery. The surfactant, secreted by pneumocytes in the alveolar epithe-lium, reduces alveolar surface tension and prevents alveolar collapse on expiration. Smallamounts of surfactant can be demonstrated from about 20 weeks’ gestation, but a surgein production occurs at 30–34 weeks. Surfactant is released at birth due to aeration anddistension of the alveoli. The half-life of the surfactant is approximately 12 hours. Pro-duction is reduced by hypothermia (<35◦C), hypoxia and acidosis (pH <7·25). In babiesborn before 32 weeks, one must anticipate a lack of surfactant. The effort of respirationwill be increased, although the musculature will be less developed. They may require helpto establish prompt aeration and ventilation, and may subsequently require exogenoussurfactant therapy.

The lungs of pre-term babies are more fragile than those of term babies and thus aremuch more susceptible to damage from over-distension. Therefore, it is appropriate tostart with a lower inflation pressure of 2·0–2·5 kPa (20–25 cmH2O) but do not be afraidto increase this to 30 cmH2O if there is no heart rate response.

Actions in the event of poor initial response to resuscitation

1. Check airway and breathing.2. Check for a technical fault.

(a) Is mask ventilation effective? Observe movement.(b) Is the tracheal tube in the trachea? Auscultate both axillae, listen at the mouth for

a large leak, and observe movement.(c) Is the tracheal tube in the right bronchus? Auscultate both axillae and observe

movement.(d) Is the tracheal tube blocked? If there is doubt about the position or patency of the

tracheal tube re-place it.(e) Is a longer inflation time required?(f) Is the oxygen connected? This is least likely to be a cause.

3. Does the baby have a pneumothorax? This occurs spontaneously in up to 1% of new-borns, but those needing action in the delivery unit are exceptionally rare. Auscultate

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the chest for asymmetry of breath sounds. A cold light source can be used to tran-silluminate the chest – a pneumothorax may show as a hyper-illuminating area. If atension pneumothorax is thought to be present clinically, a 21-gauge butterfly needleshould be inserted through the second intercostal space in the mid-clavicular line. Al-ternatively, a 22-gauge cannula connected to a three-way tap may be used. Rememberthat you may well cause a pneumothorax during this procedure. (Chapter 22)

4. Does the baby remain cyanosed despite breathing with a good heart rate? There maybe a congenital heart malformation, which may be duct-dependent (Chapter 9), ora persistent pulmonary hypertension.

5. If, after resuscitation, the baby is pink and has a good heart rate but is not breathingeffectively, it may be suffering the effects of maternal opiates. Naloxone 200 micro-grams IM may be considered. This should outlast the opiate effect.

6. Is there severe anaemia or hypovolaemia? In case of large blood loss, 20 ml/kgO-negative blood or a volume expander should be given.

Birth outside the delivery room

Whenever a baby is born unexpectedly, the greatest difficulty lies often in keeping itwarm. Drying and wrapping, turning up the heating and closing windows and doors areall important in maintaining temperature. Special care must be taken to clamp and cutthe cord to prevent blood loss.

Hospitals with accident and emergency departments should have guidelines for resus-citation at birth, summoning help and post-resuscitation transfer of babies born withinthe department.

Babies born unexpectedly, outside hospital, will be at greater risk of being pre-termand of getting cold. However, the principles of resuscitation are identical to the hospitalsetting. Transport will need to be discussed according to local guidelines.

Discontinuation of resuscitation

The outcome for a baby with no cardiac output after 10–15 minutes of resuscitation islikely to be very poor. Stopping resuscitation early, or not starting resuscitation at all, maybe appropriate in situations of extreme prematurity (<23 weeks), birth weight of <400 g,or in the presence of lethal abnormalities such as anencephaly or confirmed trisomy 13 or18. Such decisions should be taken by a senior member of the team, ideally a consultant.This means that help must have been called for.

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BY033-App-J BMJ Books BY033-Jones-v8.cls September 19, 2004 14:37

APPENDIX

JFormulary

The formulary is intended as a reference to be used in conjunction with this book. Tothis end the drugs mentioned elsewhere are set out alphabetically below, along with theirroutes of administration, dosage and some notes on their use.

J.1 GENERAL GUIDANCE ON THE USE OF THE FORMULARY

When dosage is calculated on a basis of per kilogram and a maximum dose is not stated,then the dose given should not exceed that for a 40-kg child.

The exact dose calculated on a basis of per kilogram may be difficult to administerbecause of the make-up of the formulations available. If this is the case the dose may berounded up or down to a more manageable figure.

Doses in the formulary are sometimes written as “µg” or “ng”. When prescribing suchdoses these terms should be written in full (micrograms or nanograms, respectively) inorder to avoid confusion.

Although every effort has been made to ensure accuracy, the writers, editors, publishersand printers cannot accept liability for errors or omissions.

More detailed information about individual drugs is available from the manufactur-ers, from the British National Formulary, from hospital drug information centres, from“Medicines for Children” (RCPCH 2003) and from the pharmacy departments of chil-dren’s hospitals.

Abbreviations

The following abbreviations are used:

IO intraosseousIM intramuscularIV intravenousSC subcutaneousETT endotracheal tube

The final responsibility for delivery of the correct dose remains with thephysician prescribing and administering the drug.

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Indication Route Age/Weight Frequency Notes

Under 12 years

Acetylcysteine <20 kg >20 kg 12–18 years

Treatment ofparacetamoloverdose

IV infusionover15 min

150 mg/kgin 3ml/kg

150 mg/kgin 100 ml

150 mg/kgin 200 ml

Single dose May be used up to24 h afterparacetamoloverdose. After24 h seekguidance from aNational PoisonsInformationCentre. Infuse inglucose 5%; ifthis is unsuitable,use Nsaline0·9%. Use withcaution if patienttaking liverenzyme inducingdrugs, e.g.phenytoin.Contraindicatedif previoushypersensitivityto any of theingredients. Usewith caution inpatients withasthma or ahistory ofbronchospasm.Monitor serumpotassium

Then IVinfusionover 4 h

Then 50mg/kg in7 ml/kg

Then 50mg/kg in250 ml


Single dose

Then IVinfusionover16 h

Then 100mg/kg in14 ml/kg


Then 100mg/kg in1 l

Single dose

Up to 2 2–12 12–18Acyclovir years years years

Herpessimplexvirustreatment

IV infusion <3 months,10 mg/kg;3 months–2 years,250 mg/m2

250 mg/m2 5 mg/kg 3 times daily Normal immunestatus

<3 months,10 mg/kg;3 months–2 years,500 mg/m2

500 mg/m2 10 mg/kg 3 times daily Immuno-compromised orencephalitisIn both cases:Adjust dose if renalimpairment. Notgiven by IV bolus,infuse over 1 h

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1 month–Activated charcoal 2 years 2–12 years 12–18 years

Absorption ofpoisons

Oral Dose by weight: 1 g/kg

Dose by age

Single dose

Single dose

– 25–50 g 50 g

Single dose treatment.Because of the riskof aspiration,charcoal shouldnever be given to achild with an absentgag reflex orimpairedconsciousness,unless the airway isfirst protected by anendotracheal tube

Adenosine Birth–12 years 12–18 years

Antiarrhythmicto terminateSVT and toelucidatemechanismoftachycardia

IV Bolus 50-µg/kg increaseafter 2 min ifnecessary to100 µg/kg.Increase furtherin 50-µg/kgincrements at2-min intervalsuntil tachycardiaterminated or toa maximumdose of300 µg/kg,<1 month, and500 µg/kg,>1 month

3-mg increaseafter 2 minif necessaryto 6 mg.Increaseafter further2 min ifnecessaryto 12 mg

Single dose Initial dose:Subsequent doses ifrequired as shown.Increments shouldnot be given ifhigh-level AV blockdevelops at anyparticular doseContraindications orwarnings: Second-or third-degree heartblock, AV block, sicksinus syndrome andasthma. Beware oftorsades de pointesin child withprolonged QTinterval

Adrenaline Birth– 1 month– 2–12 12–18(epinephrine) 1 month 2 years years years

Cardiopulmonaryresuscitation(CPR)

IV/endotrachealtube (ETT)

10 µg/kg(0·1ml/kg of1:10000)

– – – Initial dose Endotracheal routeis accepted buthas unproveneffectiveness inresuscitation atbirth

10–30µg/kg(0·1–0·3ml/kg of1:10000)

– – – Subsequentdoses

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Adrenaline Birth– 1 month– 2–12 12–18(epinephrine) 1 month 2 years years years

Cardiopulmonaryresuscitation(CPR)

IV rapidbolus/IO

– 10 µg/kg(0·1 ml/kg of1:10000)

1 mg(10 ml of1:10000)

Initial andusualsubsequentdose

If given by IO routeflush with NaCl0·9%

– 100 µg/kg(0·1 ml/kg of1:1000 or1 ml/kg of1:10000)

5 mg (5 mlof1:1000)

Maximum dose is5 ml of 1:1000.Subsequentdoses inexceptionalcircumstances,e.g. arterialmonitoring,septicaemia,anaphylaxis

ETT – 100 µg/kg(0·1 ml/kg of1:1000 or1 ml/kg of1:10000)

5 mg (5 mlof1:1000)

Acuteanaphylaxis

Deep IM 10 µg/kg (0·01 ml/kg of1:1000)

0·5–1 mg(0·5–1ml of1:1000)

Single dose Repeat at 5-minintervals ifnecessaryaccording toclinical response

Low cardiacoutput

IV infusion 10 ng–1 µg/kg/min Continuous Start at lowerdoses

Croup Nebulised 1–5 ml of 1:1000 Single dose Produces atransientimprovement,rarely alters thelong-term courseof the illness.Observe closelywith ECG andoxygensaturationmonitoring

Alprostadil Neonates

Duct-dependentcongenitalheart defectsin neonates

IV infusion 50–100 ng/kg/min Single dose Intensive supportrequired

Then IVinfusion

Then decrease to lowesteffective dose

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Aminophylline 1 month–12 years 12–18 years

Bronchodilatorin asthma oranaphylaxis

IV infusionover 20–30 min

5 mg/kg (maximum 500 mg) Singleloadingdose over20–30 min

Loading dose if notheophylline oraminophylline hasbeen given in thelast 24 h

IV infusion 1 mg/kg/h 500 µg/kg/h Continuous Maintenance dose.Infusion can usuallybe stopped and nottapered down

Amiodarone Birth–12 years 12–18 years

Stablearrhythmias

IV loadingdose

5 mg/kg Single dose Slow IV injection over30 min. Loading dosesup to 15 mg/kg havebeen reported. Givevia a central line ifpossible. Adjust rateaccording to clinicalresponse. Solutionscontaining more than150 mg of amiodaronein 250 ml of glucose5% (600 µg in 1 mlamiodarone) areunstable and shouldnot be used

IV infusion 5–15 µg/kg/min (maximum Continuous1·2 g in 24 h)

In CPR, shock-resistant VFand pulselessVT

Rapid IVbolus

5 mg/kg (maximum 300 mg) Single dose The injection iscompatible withglucose 5% only. Maybe used inconcentrations of15 mg in 1 ml ofglucose 5%

Birth–1 1 month– 2–12 12–18Atropine sulphate month 2 years years years

Pre-intubationdose or tobe given inbradycardiaif induced byvagalstimulation

IV bolusover1 min

15 µg/kg 20 µg/kg(minimum100 µg,maximum600 µg)

300 µg–600 µg

Single dose May be repeated

Budesonide 1 month–18 years

Croup Nebuliser 2 mg Single dose

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Bupivacaine Birth– 1 month– 2–12 12–18hydrochloride 1 month 2 years years years

Infiltration andregionalanaesthesiaincludingperipheralnerve block

Localinfiltration

Up to 0·8 ml/kg of 0·25%(up to 2 mg/kg)

Up to 60ml of0·25%(up to150 mg)

Single dose Do notadministermorefrequentlythan every8 h

Calcium gluconate Birth–18 years

CPR only whenthere iselectrolytedisturbanceand insepticaemia,where there ishypocalcaemia

IV bolus 0·3 ml/kg of 10% solution Single dose Tissue damageif there isextravasation

Calcium resonium Birth–18 years

Hyperkalaemiaassociatedwith anuria orsevere oliguriaand in dialysispatients

Orally 0·5–1 g/kg Daily individeddoses

Contraindicatedin obstructiveboweldisease

Birth– 1 month– 2–12 12–18Cefotaxime 1 month 2 years years years

Severe neonatalinfections,meningitis

IV <7 days,50 mg/kg

2 timesdaily

7–21 days,50 mg/kg

3 timesdaily

>21 days 3–4timesdaily

Meningitis;respiratory-tract,urinary-tractand soft-tissueinfections;epiglottitis

IV – 50 mg/kg 1–3 g 2 The frequency shouldbe increased tofour times daily inmeningitis andother severeinfections. In thesecases a loadingdose of 80 mg/kgcan be given

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Birth– 1 month– 2–12 12–18Ceftriaxone 1 month 2 years years years

Severe neonatalinfections,meningitis

IV 20–50mg/kg

– – – 1 timedaily

Do not exceed50 mg/kg. Infuseover 10–30 min(doses of 50 mg/kgover at least 60 min).Avoid in premature,acidotic orhyperbilirubinaemicneonates

Meningitis;respiratory-tract,urinary-tract,soft-tissueinfections;epiglottitis

IV orIM

– 20–50 mg/kg 1 timedaily

Maximum singledose 4 g

IV – 80 mg/kg 1 timedaily

Severe infections ormeningitis, infuseover at least 30 min

Chlorphenamine 1 month– 2–12 12–18(chlorpeniramine) 2 years years years

Antihistamine withsedative andantimuscariniceffects

IV, IMorSC

Dose byweight:<1 yr,250 µg/kg

2–5 years,2·5–5 mg

10–20mg

Singledose

Can be repeated up to4 times in 24 h ifnecessary. Note: adultmaximum daily dose is40 mg. In anaphylaxis,administer IV, becauseSC or IM rarely actsquicker than oraldosing

Dose by age:>1 yr,2·5–5 mg

6–12 years,5–10 mg

Codeine phosphate Birth–18 years

Mild to moderate pain Orally 1–1·5 mg/kg Loadingdose

Contraindicated inparalytic ileus.Warning: avoid inacute respiratorydepression.Caution: renalimpairment; hepaticimpairment mayprecipitate coma

1 month– 2–12 12–18Dantrolene 2 years years years

Malignanthyperthermia

IV bolus 1 mg/kg Single dose Repeat as required, at5–10-min intervals to amaximum cumulativedose of 10 mg/kg

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Desferrioxamine 1 month– 2–12 12–18mesilate 2 years years years

Acute ironpoisoning

IV infusion Initially 15 mg/kg/h,reducing after 4–6 h asindicated

Continuous If shocked, hypotensiveor seriously ill,administer IV.Decrease the rate ofadministration after4–6 h to ensure thattotal maximum dosedoes not exceed80 mg/kg/day.Continue until serumiron level is less thantotal iron-bindingcapacity. Use withcaution in patients withrenal impairment

1 month– 2–12 12–18Dexamethasone 2 years years years

Croup Oral 150 µg/kg 2 times daily No definitive standard dosehas been agreed in the UK.Suggested maximum singledose of 12 mg

600 µg/kg Single dose

Short courseto relievesymptomsof braintumour

IV/oral 500 µg/kg 2 times daily Can also be used to reduceoedema around tumourscompressing nerves

Birth– 1 month– 2–12 12–18Diamorphine 1 month 2 years years years

Control ofsevere pain

Intranasal Notrecommended

0·1 mg/kg Singledose

Dilute withsaline to avolume of0·2 ml. Avoidin acuterespiratorydepression.Naloxone isan antidote.Use withcaution inhead injury

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Birth–1 1 month– 2–12 12–18Diazepam month 2 years years years

Treatment ofstatusepilepticus

Rectal 0·5 mg/kg Singledose

If needed, repeat after5 min. Parenteral andrectal use can depressrespiration. Caution withother CNS depressants

In place oflorazepam whennot available

IV/IO 0·25 mg/kg

1 month– 2–12 12–18Diclofenac 2 years years years

Nonsteroidalanti-inflammatorydrug (NSAID)

Oral/rectal <6 months, notrecommended;>6 months,300 µg–1 mg/kg

300 µg–1mg/kg

3 timesdaily

Up to amaximum of150 mg/day

Birth–1 1 month– 2–12 12–18Dobutamine month 2 years years years

Providesinotropicsupport inthe treatmentof low-outputcardiacfailure, e.g. insepticaemia

IV infusion 2–10 µg/kg/min Continuous Dose can beincreased up toa maximum of20 µg/kg/min innewborn infants(but side effectsare more likelyat this higherdose) and40 µg/kg/min inolder children, ifnecessary

Dopaminehydrochloride Birth–1 month 1 month–18 years

Treatment oflow cardiacoutput states

IV infusion 1–5 µg/kg/min Continuous Low dose for renaleffect. Somedebate over itsuse – see“Medicines forChildren”

IV infusion Start at3 µg/kg/min,increasing asclinicallyindicated to amaximum of20 µg/kg/min

5–20µg/kg/min

Continuous Direct inotropiceffect, butvasoconstrictionmay occur athigher doses

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Birth–1 1 month– 2–12 12–18Erythromycin month 2 years years years

Upper and lowerrespiratorytract infections

Oral/IV 12·5 mg/kg – – – 4

Oral – 125 mg 2–8 years,250 mg;9–12years,500 mg

500 mg 4 Doses can bedoubled insevereinfections.Maximumsingle dose1 g

Birth– 1 month– 2–12 12–18Flecainide acetate 1 month 2 years years years

Treatment ofresistant re-entrySVT, ventricularectopics orventriculartachycardia (VT)

IV bolus 2 mg/kg 2 mg/kg Singledose

Give over at least10 min with ECGmonitoring; avoidin patients withpre-existing heartblock. Maximumdose 150 mg

Birth– 1 month– 2–12 12–18Flucloxacillin 1 month 2 years years years

Treatment ofinfections due toGram-positiveorganisms (anti-staphylococcal)

Oral/IV <7 days,25–50mg/kg

– – – 2 Dose may beincreased to100 mg/kg perdose IV in severeinfection(meningitis,cerebral abscess,staphylococcalosteitis). Oral routeonly recommendedfor minor infection

Oral/IV 7–21days,25–50mg/kg

– – – 3

Oral/IV >21days,25–50mg/kg

– – – 4

IV or IMbolus

– 12·5–25 mg/kg 4 Maximum single dose1 g. Dose may bedoubled in severeinfection, maximumsingle dose 2 g

Oral – <1 yr,62·5mg;>1 yr,125 mg

<5 years,125 mg;>5 years,250 mg

250 mg 4 Doses may bedoubled in severeinfection

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Birth– 1 month– 2–12 12–18Flumazenil 1 month 2 years years years

Reversal of acutebenzodiazepineoverdose

IV bolusover15 sec

10 µg/kg 10 µg/kg(maximumdose 200 µg)

200 µg Singledose

Initial dose. If thedesired effectis not achieved– repeat at1-min intervalsto a maximumtotal dose of40 µg/kg (2 mgmaximumdose in 12–18years)

IV infusion 2–10 µg/kg/h (maximumdose of 400 µg/h)

100–400µg/hdose

Continuous This should beindividuallyadjusted toachieve thedesired level ofarousal. Thereis limitedexperience ofthe use offlumazenil inchildren

Furosemide Birth– 1 month– 2–12 12–18(frusemide) 1 month 2 years years years

To inducediuresis incardiac orrenal failure orfluid overload;hypertension

IV bolus 500 µg/kg–1 mg/kg 20–40 mg Singledose

Single doses up to4 mg/kg havebeen used. Dosecan be repeatedevery 8 h

Birth– 1 month– 2–12 12–18Glucagon 1 month 2 years years years

Severeinsulin-inducedhypoglycaemiain the treatmentof diabetes

IM, SC Notrecommended

500 µg 500 µg–1 mg(<25 kg:500 µg;>25 kg:1 mg)

Singledose

Should beeffective within10 min. Onlyuse when IVglucosedifficult orimpossible toadminister. Ifnot, give IVglucose5–10%

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Birth– 1 month– 2–12 12–18Hydrocortisone 1 month 2 years years years

Anaphylaxis;emergencytreatment ofsevere acuteasthma

IV bolus/IM/IO

2·5 mg/kg 4 mg/kg (maximum100 mg)

100 mg–300 mg

Singledose

Maintenancedose may berepeated ifnecessaryevery 6 h. Maybe given by IOroute if IV notpossible

Then 2mg/kg

Then 2–4 mg/kg Then100 mg–300 mg

4

1 month 2–12 12–18Ibuprofen –2 years years years

Pyrexia, mildto moderatepain

Oral Doseby weight:

5 mg/kg – 3–4 Maximum of 20mg/kg/day upto 2·4 g/day

Oral Doseby age:

1–2years,50 mg

3–7 years,100 mg;8–12 years,200 mg

200–600mg

3–4

Birth– 1 month– 2–12 12–18Insulin 1 month 2 years years years

Primary treatmentfor patients withtype 1 and2 diabetesuncontrolled byother means

IV infusion inketoacidosis

0·1 unit/kg/h Continuous Adjust doseaccording toblood glucoselevel

Birth– 1 month– 2–12 12–18Ipratropium 1 month 2 years years years

Treatment ofchronicreversibleairwaysobstruction.May be usedwith a beta-2agonist in thetreatment ofsevere acuteasthma.

Nebulised 25 µg/kg <1 yr,62·5 µg;>1 yr,125–250 µg

<5 years,125–250 µg;>5 years,250–500 µg

500 µg Singledose

Can be repeatedevery 20–30min in the first2 h in acutesevereasthma.Reduce dosefrequency asclinicalimprovementoccurs

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Birth– 1 month– 2–12 12–18Labetalol 1 month 2 years years years

Hypertensionandhypertensivecrises

IV bolus – 250–500 µg/kg 50 mg Single dose Loading dose

IV infusion 500 µg/kg/hup to amaximum of4 mg/kg/h

1–3 mg/kg/h 120 mg/h Continuous Start at lowdose andtitrateaccording toresponse,until the bloodpressure hasbeen reducedto anacceptablelevel. Avoid inasthma, heartfailure andheart block

Birth– 1 month– 2–12 12–18Lidocaine (lignocaine) 1 month 2 years years years

Antiarrhythmic IV bolus 500 µg/kg–1 mg/kg 50–100 mgtheninfusion –see below

Single dose Loading dose: Inthe 12–18-yrage groupgive 50 mg inlighterpatients orthose whosecirculation isseverelyimpaired

IV infusion Then 10–50 µg/kg/min(600 µg–3 mg/kg/h)

4 mg/min for30 minthen2 mg/minfor 2 hthen1 mg/min*

Continuous In the 12–18-yrgroup:*reducingconcentrationfurther ifinfusion iscontinuedbeyond 24 h

Maintenancedosing: ECGmonitoringwith infusion

373

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Lidocaine (lignocaine) 1 month 2 years years years

VF orpulselesstachycardia

IV/IO 1 mg/kg (maximum dose100 mg)

50–100 mg Single dose Repeat every5 min if neededto a totalmaximum of3 mg/kg. In the12–18-yr agegroup give50 mg in lighterpatients orthose whosecirculation isimpaired

Localanaesthetic

Localinfiltration

Up to 3 mg/kg Up to200 mg

Single dose Not more oftenthan every 4 h.Use fineneedles(27–29-gauge).Less painful ifbuffered beforeuse with 8·4%sodiumbicarbonate1 ml to every10 ml lidocaine(lignocaine) 1%

Intra-urethral

3–4 mg/kg Single dose Prior to urinarycatheterisation.Warm thesolution to bodytemperatureand inject it veryslowly to reducelocal stinging

Birth– 1 month– 2–12 12–18Lorazepam 1 month 2 years years years

Statusepilepticus

IV/rectal/sublingual

100 µg/kg (maximumdose 4 mg)

4 mg Single dose Generally given as asingle dose; maybe repeated onceif initial dose isineffective. Limitedexperience inneonates. Maycause apnoea.Flumazenil is anantidote

374

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Magnesium sulphate 1 month 2 years years years

Hypo-magnesaemiain septicaemia

IV 0·2 ml/kg; 50%MgSO4 over 30min (maximum10 ml)

Singledose

Repeat later ifserummagnesiumremains low

Treatment ofasthma

IV Notrecommended

Noexperience

25–40 mg/kgover6 years

Singledoseover20 min

Not establishedpractice butappears safe

Treatment oftorsades depointes

IV Notrecommended

25–50 mg/kg Singledose

Maximum of 2 g

Birth– 1 month– 2–12 12–18Mannitol 1 month 2 years years years

Treatment ofRICP

IV infusionover30 min

250 mg/kg–500 mg/kg (1·25–2.5 ml/kgof 20% solution)

Singledose

Cerebraloedema. Maybe repeatedonce or twice

Birth– 1 month– 2–12 12–18Midazolam 1 month 2 years years years

Buccal/intranasal

– Dose byweight:<6 months,300 µg/kg

1–4 years,5 mg;5–9 years,7·5 mg;>10 years,10 mg

10 mg Singledose

Buccaladministrationis the preferredroute overintranasaladministration.The parenteralpreparationcan be usedfor this route.The dose byweight for thebuccal route is0·5 mg/kg from6 months.Maximumdose 10 mg

Dose by age:>6 months,2·5 mg

375

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Morphine 1 month 2 years years years

Control ofseverepain

IV infusion Pre-term:25–50 µg/kg

– – – Single dose Loading dose

Then5 µg/kg/h

– – – Continuous

Term: 50–100 µg/kg

– – – Single dose Loading dose

Then 10–20 µg/kg/h


IV bolus – 100–200 µg/kg 2·5–10 mg <6 months,up to4 times in24 h;>6 months,up to6 times in24 h

Respiratorymonitoring ismandatory.Give IV overat least5–10 min.For <1 yruse the lowerstated doseand consideroxygensaturationmonitoring

IV infusion – 10–30 µg/kg/h: <6 months initialrate is 10 µg/kg/h; >6 monthsinitial rate is 20 µg/kg/h

Continuous Use IV bolus asstarting dosefirst

Orally – <1 yr,80 µg/kg;>1 yr,200–400µg/kg

200–500µg/kg

10–15 mg Up to 6 timesin 24 h

Starting doses,which shouldbe reviewedregularly andadjustedaccording tothe patient’sresponse

Birth– 1 month– 2–12 12–18Naloxone 1 month 2 years years years

Reversal ofopioid-inducedCNS andrespiratorydepression

IV bolus,IM or SC

10 µg/kg – – – Single dose May be repeatedusing doses up to100 µg/kg asrequired, at2–3-min intervals

IV infusion 5–20µg/kg/h


376

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Naloxone 1 month 2 years years years

Specificallyindicatedfor thereversal ofrespiratorydepressionin anewborninfantwhosemotherhasreceivednarcoticswithin 4 hof delivery.It isgenerallypreferredto give anIMinjectionfor aprolongedeffect

IM 100 µg/kg – – – Single dose Use400 µg/mlnaloxonepreparation.Gradualonset ofaction(3–4 min),but theeffect isprolonged

IV Bolus 10 µg/kg 10 µg/kg(maximumdose800 µg)

Single dose Initial dosefollowed bya higherdose if noresponse.Becausenaloxonehas a shorthalf-life,repeatdoses asnecessaryto maintainopioidreversal.Observe forrecurrenceof CNS andrespiratorydepression

Then 100 µg/kg(maximum dose2 mg)

Then 2 mg Single dose

IV infusion – 5–20 µg/kg/h Infuse asolution of4 µg/ml ata rateadjustedaccordingtoresponse

Continuous

Do not administer to newborns whose mothers are suspected of narcotic abuse, as a withdrawalsyndrome may be precipitated. ALWAYS establish and maintain adequate ventilation beforeadministration of naloxone.

377

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Nifedipine 1 month 2 years years years

Hypertensivecrisis

Oral – 250–500 µg/kg Single dose Bite the capsule,releasing thecontents into themouth, and thenswallow. Aspirateliquid from capsulefor young children

Birth– 1 month– 2–12 12–18Paracetamol 1 month 2 years years years

Analgesic/antipyretic

Oral loadingdose

Pre-term,28–32 wks;pre-term,32–36 wksandfull-term to1 month:All above20 mg/kg

20 mg/kg Single dose

Oralmaintenancedose

Pre-term,28–32 wks,15 mg/kg

12-hourly Maximumdaily dose30 mg/kg

Pre-term,32–36 wks,20 mg/kg;Full-term to1 month,20 mg/kg

1–3 months,dose byweight:20 mg/kg


– >3 months, doseby weight:15 mg/kg

– 4–6-hourly Maximumdaily dose90 mg/kg

– Dose by age:3 months–1 yr,60–120 mg;1–5 years,120–250 mg;6–12 years,250–500 mg


– – 500 mg–1 g

4–6-hourly Maximumdaily dose4 g

378

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Paracetamol 1 month 2 years years years

Rectal loadingdose

Pre-term,28–32 wks,20 mg/kg;pre-term,32–36 wks,30 mg/kg;full-term to1 month,30 mg/kg

1–3 months,30 mg/kg;>3 months,40 mg/kg

Single dose

Rectalmaintenancedose

Pre-term,28–32 wks,15 mg/kg


Pre-term,32–36 wks,20 mg/kg;full-term to1 month,20 mg/kg

1–3 months,dose byweight:20 mg/kg


– Dose by weight:3 months–12 years,20 mg/kg


– Dose by age:3 months–1 year,60–125 mg;1–5 years,125–250 mg;6–12 years,250–500 mg


– – 500 mg–1 g

4–6-hourly Maximumdaily dose4 g

Caution in patients with hepatic or renal disease.

379

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Paraldehyde 1 month 2 years years years

Statusepilepticus

Rectal 0·4 ml/kg 5–10 ml Single dose Doses stated in ml/kg oras ml of paraldehyde.Dilute with an equalvolume of olive orsunflower oil beforeadministration; or ifusing a ready-prepared“special”, rememberthat it is already dilutedand dose accordingly

IM 0·2 ml/kg 0·1–0·15 ml/kg 5–10 ml Single dose IM use should be avoidedwhenever possible.May cause pain andsterile abscess.Maximum 5 ml (1 ml inneonates) at one site.Consider addinghyaluronidase150 units

Phenobarbital Birth– 1 month– 2–12 12–18(phenobarbitone) 1 month 2 years years years

Status epilepticus; IV slowbolus

20 mg/kg 20 mg/kg Single Loading doserespiratorydepression,especially whenused withbenzodiazepines

Then 2·5–5 mg/kg Then300 mgdose

Twice daily(oncedaily inneonatalperiod)

Maintenance

Birth– 1 month– 2–12 12–18Phenytoin 1 month 2 years years years

Antiepileptic IV 20 mg/kg 18 mg/kg Single dose Loading dose (over30–45 min); monitorECG and BP

2·5–5 mg/kg – 2 Usual maintenance doseover 30 min

– 100 mg 3–4

Antiarrhythmic IV – 18 mg/kg Single dose

Reduce dose in liver disease

380

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Potassium chloride 1 month 2 years years years

Acutehypokalaemia

IV infusion – 0·08–0·25 mmol/kg/h Continuous Always check thedose carefully, anoverdose can berapidly fatal, dilutewith at least 50times its volumeand mix well.Restrict to criticalcare areas, store inlocked cupboard,document as forcontrolled drug.Recheck thepotassium levelafter 3 h

Birth– 1 month– 2–12 12–18Prednisolone 1 month 2 years years years

Acute asthma Oral – 1–2 mg/kg (maximumdose 40 mg)

Once daily Treat for 1–5 days andthen stop (no need totaper doses)

Suppression ofinflammatoryand allergicdisorders

Oral – 1–2 mg/kg Once daily The daily dose can begiven in 2–3 divideddoses if necessary.Consider alternate daytreatment in long-term

Croup requiringintubation

Oral – 1 mg/kg – Twice daily Start within 24 h ofintubation, continuinguntil 24 h afterextubation

Birth– 1 month– 2–12 12–18Propanolol 1 month 2 years years years

Dysrhythmias IV bolus 25–50 µg/kg 1 mg Single dose Repeat the injectionas needed up tofour times daily.Give injectionslowly over 5 minunder ECG control

381

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Quinine 1 month 2 years years years

Treatment ofP. falciparummalaria

IV infusionat leastover 4 h

20 mg/kg (maximum 1·4 g) Single loadingdose

For seriously illpatients or thoseunable to taketablets

Then 10 mg/kg (maximum 700 mg) Then after8–12 hmaintenancedose

Maintenance dosecan be repeatedevery 8–12 h butchange to oraltherapy as soonas possible

Then 5–7 mg/kg Maintenancedose after48-hr IVtherapy

If IV therapy isrequired after48 h, use thismaintenancedose every 8 h

Risk of arrhythmias with amiodarone, flecainide, cisapride. Common side effects: tinnitus, headache,visual disturbance, hypoglycaemia.

Monitor ECG and blood sugar

Birth– 1 month– 2–12 12–18Salbutamol 1 month 2 years years years

Aerosolinhaler

– Up to 1 mg Single dose Asthma reliever given asrequired; 1–2-hourlyinitially, then reducefrequency to 4–6-hourly

Nebulisersolution

1·25–2·5 mg

2·5–5 mg Single dose Asthma: reliever given asrequired; 1–2-hourlyinitially, then reducefrequency to 4–6-hourly inhospital with monitoring.In severe acute asthmahalf-hourly or continuousdoses may be given inhospital. NB only licensedfor use up to 4 times daily

IV bolusover5 min

5 µg/kg initial dose 15 µg/kg(maximum250 µg)

Single dose Status asthmaticus.Maximum concentration50 µg in 1 ml

IV infusion 1–5 µg/kg/min Continuous Status asthmaticus: dosesup to 10 µg/kg/min havebeen used. Solutioncompatible withpotassium but not withaminophylline

382

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Salbutamol 1 month 2 years years years

Renalhyperkalaemia

IV bolus 4 µg/kg Single dose Repeat if necessary

Nebuliser 2·5–5 mg Single dose Repeat if necessary

Birth– 1 month– 2–12 12–18Sodium bicarbonate 1 month 2 years years years

Resuscitation Slow IV 1 ml/kg of 8·4% initially if indicated

Followed by: 0·5 ml/kg of 8·4% ifneeded

Metabolicacidosis

Slow IV 1–2 mmol/kg Only after attention toventilation andperfusion. Alwaysinfuse slowly. Ifacidosis persistentconsider inborn errorsor toxins

Renalhyperkalaemia

Slow IV 1 mmol/kg Single dose Dose adjustedaccording to plasmabicarbonate level

Birth– 1 month– 2–12 12–18Sodium nitroprusside 1 month 2 years years years

Hypertensivecrisis

IV infusion 500 ng/kg/min Continuous Initial dose – increase inincrements of 200ng/kg/min asnecessary to amaximum of 8µg/kg/min. Use onlywith expert advice

Birth– 1 month– 2–12 12–18Terbutaline 1 month 2 years years years

Relief ofbronchospasmin bronchialasthma

Nebuliser – 2·5–5 mg <5 years,2·5–5 mg;>5 years,5–10 mg

10 mg Single dose Reliever: dosesare given asrequired; upto 8 timesdaily ifnecessary or12 times dailyunder hospitalsupervision

383

P1: IML


FORMULARY


Birth– 1 month– 2–12 12–18Verapamil 1 month 2 years years years

Treatment forSVT(adenosinefirst-line)

Slow IVbolus

— >1 yr, 100–300 µg/kg(maximum5 mg)

100–300 µg/kg(maximum5 mg)

Single dose:over2–3 min

ECG and BPmonitoringrequired. Dosemay berepeated after30 min ifnecessary.Many cases arecontrolled bydoses at thelower end of therange. Cautionin liver disease.Do not use withbeta-blockers.Use only withexpert advice

384


BY033-IND BMJ Books BY033-Jones-v8.cls October 18, 2004 19:41

INDEX

Note: page numbers in italics refer to figures and boxes, those in bold refer to tables

ABC (airway, breathing, circulation) 21,23–9

abdominal injury 175–8assessment 176crush injuries 190definitive care 177–8examination 176gastric drainage 176history 175–6investigations 177non-operative management 177–8operative intervention 178seriously injured child 162urinary catheterisation 176

abdominal thrusts 34accidents, data collection 312acetabular tear drop 262, 263acetazolamide 282acetylcysteine 362acid–base balance 279–84

equation 279–80acid–base disturbance 106, 279,

281–2pulseless electrical activity 54

acidosis 281–2, 283compensated 282convulsions 186diabetes mellitus 95metabolic 49, 281–2

poisoning 336respiratory 6, 281see also diabetic ketoacidosis

acute respiratory distress syndrome(ARDS) 208

acyclovir 135, 362adenosine 363

supraventricular tachycardia 120–1ventricular tachycardia 123

adenosine triphosphate (ATP) 99adenotonsillar hypertrophy 9adolescents 309Adoption Order 307adrenaline 363–4

administration of nebulised 79anaphylaxis 83, 94, 95, 108, 109asystole 48–9, 50defibrillation 51–2function in cardiac arrest 52–3intramuscular 80nebulised 79, 80neonates 356perfusion maintenance 268second dose 50

AEDs see defibrillators, automaticexternal

age of child 310air swallowing 43airway

abnormal pulse rate/rhythm 116,117

advanced support 37–45, 46

anatomy 9–10at birth 348breathing difficulties 76burns 200cardiac arrest 266chest injury 167convulsions 140, 142decreased conscious level 128–9,

131emergency treatment 79–83envenomation 341initial assessment 22–3management 44–5, 46

equipment 37–41mucosal swelling 74neonates 352–3obstruction 26, 31, 69

partial 79respiratory failure 74

poisoning 332–3, 334practical procedures 215–30practical skills 43–4primary assessment 23–5, 44–5, 46

seriously ill child 59–62, 66resistance 74resuscitation

poor initial response 358seriously ill child 66–7

scalds 200secondary assessment 45, 46secretions 79seriously ill child 66–7seriously injured child 152, 155–6, 164shock 101, 102support 79surgical 223–6transfer of child 273–4

alae nasi, flaring 60alcohol abuse 309, 332Alder Hey Triage Pain Score 318,

324–5aldosterone 293alkalising agents 49–50alkalosis 282, 283allergies/allergic reactions 108

antivenin 343history 71

alprostadil 110, 364alveoli, number 74Ametop gel 319aminophylline 85, 86, 365amiodarone 52, 53, 365

supraventricular/ventricular tachycardia122

amputation, traumatic 190, 191amylase estimation 177anaemia

neonate 359profound 111

anaesthesia, local 319–20anaesthetic induction agents 218–19

analgesiaburns 202–3envenomation 344flail chest 170fracture alignment 194head injury 185inhalational 321non-opiate 320opiates 320–1seriously injured child 159

anaphylaxis 69, 83, 94–5, 107–9emergency treatment 70, 71, 80, 94, 95,

108–9symptoms 108

anatomy 9–10anencephaly 359angiography

arch 172open long-bone fractures 191

angioneurotic oedema 71, 80anion gap 336antiarrhythmic drugs 52–3antibiotics

macrolide combination with cisapride118

meningitis 135prophylactic 30

antibodies 12antidepressants, tricyclic

overdose 49ventricular fibrillation/tachycardia 51,

53poisoning 118, 338

antihistamine 109antihypertensive drugs 148antiserum 343antivenin 343, 344aortic rupture 171–2APGAR score 351apnoea

central neurological failure 65fetal 348recurrent in bronchiolitis 88–9submersion 208terminal 348, 350

apophyses, ring 256, 257arcing, electrical 206arterial blood gases 184

analysis 283–4arterial cannulation 239arterial pH 49, 211arterial pressure, mean 127, 180Asherman chest seal 169Aspergillus 210asphyxia 348, 349aspirated fluid removal 41aspiration risk with drowning 208aspirin

poisoning 339Reye’s syndrome 136

assessment, primary 21–30

385



INDEX

asthma 69, 90acute exacerbation 87acute severe 83–4deteriorating 85–6diagnosis 87emergency treatment 84–5

asystole 47–51lightning strike 206

atlantoaxial rotary subluxation 196atropine 365

neonates 357

back blows 32, 33Bartter’s syndrome 282base excess/deficit 283basic life support 21–35

blocked tracheostomy 228–30cardiac arrest 35infection risk 30–1sequence 22

Battle’s sign 182beta-2 agonists 84, 86beta-blockers, poisoning 118bicarbonate 383

acid–base balance 279–80, 283asystole 49diabetic ketoacidosis 297hyperkalaemia treatment 53, 293,

294neonates 356

biphasic waveforms 53–4birth

airway 348outside delivery room 359pre-term 357–8resuscitation 234, 347, 350–9weight 7, 8see also neonates

bites 341–5infection 343

bloodcross-matching 158, 177

head injury 183–4pH

arterial 49, 211control 280level 281–2, 283

blood gases see arterial blood gasesblood loss 10

nose/ear 182open long-bone fractures 191seriously injured child 157traumatic amputation 191

blood pressuremeasurement 147seriously ill child 63

blood samples 158arterial 284

blood tests, head injury 183–4blood transfusion 112body surface area 8, 10borborygmi absence 220brachial artery palpation 26brachial vein 233bradyarrhythmia 115bradycardia 117, 118

approach to child 118–19emergency treatment 119submersion 208

brainherniation 127, 181, 186hypernatraemia 290–1imaging 263stabilisation 268–9

brain injury 179primary 179secondary 179, 269

breastfeeding 12breathing/breathing difficulties 10, 11,

25–6abnormal pulse rate/rhythm 116,

117acidotic 69airway 76, 77at birth 348burns 200–1cardiac arrest 266causes 74

Cheyne–Stokes 65circulation 76, 77clinical presentations 75convulsions 140–1, 142decreased conscious level 129, 131–2disability 77efficacy 61effort 59–60envenomation 341–2key features 77–8management 44–5, 46neonates 353noisy 75, 78–9poisoning 333, 334practical procedures 215–30primary assessment 76–7

seriously ill child 59–62, 67resuscitation 37, 76–7

poor initial response 358seriously ill child 67

scalds 200–1secondary assessment 77–8seriously ill child 59–62, 67seriously injured child 152–3, 156shock 101, 102transfer of child 273–4see also ventilation

bronchial rupture 171bronchial secretions, removal 41bronchiolitis 11, 12

emergency treatment 88heart failure differential diagnosis

93–4bronchoconstriction 74bronchopulmonary dysplasia 11Broselow tape 9budesonide 365bupivacaine 247, 320, 366burns 199–204

airway 200breathing 200–1cervical spine 200circulation 201continuing stabilisation 204depth 202disability 201emergency treatment 202–3epidemiology 199–200exposure 201flash 206fluid loss 207key features 201–2oedema 207primary survey 200–1resuscitation 200–1secondary survey 201–2seriously injured child 165special areas 202surface area 201, 202transfers 204

calciumasystole 50hypercalcaemia 295hyperkalaemia treatment 294infusions 295metabolic disorders 294–5serum level 282see also hypocalcaemia

calcium channel blockersoverdose 50pulseless electrical activity 54

calcium gluconate 357, 366calcium resonium 294, 366cannula, intravenous

emergency 324emergency airway management 41

cannulation, arterial 239capillary refill 62–3capnography, head injury 185carbon dioxide

acid–base balance 280end-tidal 164, 185normalisation before naloxone use

338–9partial pressure 283

carbon monoxide poisoning 203,332

cardiac apex, auscultation 352cardiac arrest 5–6

airway 266approach 56basic life support 35breathing 266hypoglycaemia 55hypothermia 269

following resuscitation 55intraosseous infusion 240investigations 54, 55management 47–56monitoring 54–5outcome 6perfusion maintenance 267–8post-resuscitation management 54–5resuscitation 266

cardiac arrhythmias 53emergency treatment 70

cardiac compression 27–9infants 27, 28older children 29small children 28

cardiac disease, ventricularfibrillation/tachycardia 51

cardiac dysrhythmiasdiabetic ketoacidosis 297drowning 208electrical injuries 207shock 287

cardiac index 11cardiac output 11, 12cardiac tamponade 170–1cardiomyopathy 93, 110–11

emergency treatment 111cardiophrenic angle 261cardiopulmonary resuscitation 23

active compression–decompression 29audio prompts 30continuing 29, 30drowning 211

cardiorespiratory arrest 5–6cardiovascular physiology 11–12cardiovascular status, severely ill child

62–3Care Order 307carotid artery palpation 26carotid body massage 120cartilage

cervical spine 255–8chest radiograph 260, 261pelvis 262–3

catheters, tracheal suction 41cefotaxime 366ceftriaxone 367central herniation 181, 186central syndrome 127central venous pressure 267cerebral blood flow 127, 269cerebral depression 61cerebral oedema 180–1, 297cerebral perfusion

increase 185pressure 127, 180, 269

cerebrospinal fluid loss from nose/ear 182cervical collar application 248–9cervical spine

alignment 255bones 255–6burns 200cartilage 256–8clearing 195CT 263disc spaces 256immobilisation 248–9, 254injuries 25, 196, 254

drowning 208types 196

mobility 196neck examination 161radiography 196scalds 200seriously injured child 152, 155–6, 161soft tissues 256–8spinal cord injury without radiological

abnormality 197vertebral discs 258X-rays 254–63

386



INDEX

cervicocranial junction 254cervicothoracic junction 254charcoal, activated 337, 339, 340,

363chemical exposure 309chest

aeration 353auscultation 61expansion 61iatrogenic problems 167pain 75seriously injured child 162sucking wound 169

chest compression 27asystole 49audio prompts 30blocked tracheostomy 229–30infants 27, 28mechanical adjuncts 29neonates 353, 355older children 29small children 28

chest drain 43placement 244–5

chest injury 167–73continuing stabilisation 173discovered later 171–2immediate threat to life 168–71referral 173

chest radiograph 258–61adequacy 258alignment 258, 259apparatus 259cartilage 260, 261soft tissues 260–1

chest thrusts 32, 33chest wall

compliance 74disruption 167paradoxical movement 169

Cheyne–Stokes breathing 65child abuse 299–308

assessment 301–4classification 299–300communication 304diagnosis 303–4disclosures 305examination of child 302–3history 302investigations 303management 304–5medical assessment 301–4medicolegal aspects 305–8organised 300radiographs 303see also non-accidental injury

Child Assessment Order (CAO) 306child safety organisations 311–12Children’s Coma Scale 125, 126

head injury 183child-resistant containers 331–2chin lift 23–4, 25

readjustment 26chloride ions 281, 282chlorphenamine 83, 367

anaphylaxis 109choking 31–5

infants 31, 32lay people actions 35

circulation 10, 26–9abnormal pulse rate/rhythm 116–17,

117–18assessment 26–7at birth 348breathing difficulties 76, 77burns 201central neurological failure 65convulsions 141, 142decreased conscious level 129, 132emergency treatment 70envenomation 342neonates 353, 355poisoning 333, 334practical procedures 231–42primary assessment 62–4

seriously ill child 67resuscitation 266–7

seriously ill child 67

scalds 201secondary assessment 69seriously ill child 62–4, 67, 69–70seriously injured child 153–4, 156–7,

164shock 102–3transfer of child 274

circulatory failurecardiac arrest 6potential 62–4

cisapride, macrolide combination 118clotting factors 344coagulation support in envenomation

344coagulopathy, seriously injured child

164coarctation of the aorta 147cocaine poisoning 340codeine 321, 323, 367colloid solutions 104–5, 112

anaphylaxis 108colour assessment of child 325

skin in respiratory inadequacy 61coma 125

causes 126drowning 211metabolic 136transfer of child 274treatment 134

communication 12child abuse 304emergency paediatrics 17transfer of child 271, 275

compartment syndrome 192–3electrical injuries 206

computed tomography (CT) 264abdominal injury 177brain imaging 263cervical spine 263head injury 158, 184

confidentiality 304–5congenital abnormalities 4

heart malformation 359congenital heart disease 92

bronchiolitis 89diagnosis 92duct-dependent 93, 110

emergency treatment 110conscious level, assessment 64

diabetic ketoacidosis 297triage 328

conscious level, decreased 71, 78,125–37

burns 201cardiac arrest 266head injury 185key features 133–4presentation 126primary assessment 128–31resuscitation 131–2scalds 201secondary assessment 132–3stabilisation of child 136–7transfer of child 136–7see also intracranial pressure,

raisedconsent

emergency paediatrics 17examination in child abuse 306–7

continuous positive airway pressure(CPAP) 79

convulsions 139–48cause 146emergency treatment 143–6fever 65general measures 146head injury 186neurological sequelae 140pathophysiology 140primary assessment 140–1respiratory arrest 5–6resuscitation 142secondary assessment 142

coronary syndrome, acute 340coroner investigation 314, 315costophrenic angle 261cough, choking 31court reports 307

cricoid pressure 218cricoid ring 10, 40cricothyroidotomy 223–6

complications 225–6needle 224–5, 226surgical 225

cricothyroidotomy cannulae 41croup 80–1

airway obstruction 31, 69emergency treatment 79–80pseudomembranous 81stridor 78syndromes 79–80

crush injuries 190–1compartment syndrome 192electrical injuries 206

cry assessment 324crystalloid solutions 104–5, 112, 288

poisoning 334seriously injured child 157

Cushing’s response 65cyanide poisoning 203cyanosis 61, 359

heart failure 91, 92cycle helmets 250–2cystic fibrosis 293

dantrolene 367death 313–15

breaking news 313–14care of child 315causes of 4expected 5infant mortality 3–4poisoning 331–2post-death procedures 314

defibrillation 53, 240–2abnormal pulse rate/rhythm 117–18asynchronous electrical 51–2automatic external defibrillators 53biphasic waveforms 53–4electrode gel 242energy selection 242gel pads 242paddles 241–2poisoning 335procedure 242safety 242

defibrillators, automatic external 23, 30,53

dehydration 286–7clinical signs 287–8electrolyte losses 291management 288–9

desferrioxamine 338, 368design, safe 311developmental history 71dexamethasone 368dextrose 294, 356diabetes insipidus

head injury 164sodium loss 291

diabetes mellitus 95diabetic ketoacidosis 69, 295–7

complications 297emergency treatment 71management 295–7

dialysisethylene glycol poisoning 340hyperkalaemia treatment 294peritoneal lavage 248renal failure 295

diamorphine 368diaphragm 75

chest radiograph 261ruptured 172

diarrhoeahypokalaemia 292, 293sodium loss 291

diazepam 143, 144, 145, 369convulsions in head injury 186ecstasy poisoning 340

diclofenac 323, 369digoxin

poisoning 118, 335supraventricular tachycardia 122

diphenoxylate with atropine 332diphtheria, airway obstruction 83

387



INDEX

disabilitybreathing difficulties 77burns 201convulsions 141decreased conscious level 129–30,

132emergency treatment 70–1

shock 107envenomation 342poisoning 333–4, 335primary assessment 64–5, 67resuscitation 67scalds 201septicaemia 107seriously injured child 154, 157–8shock 102, 103transfer of child 274–5

dislocations 193diuresis, osmotic 295diving reflex 120, 208dobutamine 106, 267, 369domestic injuries 312dopamine 106, 267–8, 369drowning 207–12

cardiopulmonary resuscitation 211coma 211emergency treatment 210epidemiology 207–8hypothermia 208, 209–10immersion time 211key features 210outcome 211pathophysiology 208prevention 208primary survey 208–10prognostic indicators 210–11publicity 311resuscitation 208–10, 211secondary survey 210stabilisation 210time to first respiratory effort

211drowsiness 61–2

emergency treatment 71drug abuse 309, 332ductus arteriosus, patent 93

ecstasy poisoning 340–1electrical injuries

epidemiology 205key features 206–7pathophysiology 205–6primary survey 206resuscitation 206secondary survey 206–7stabilisation 207transfer to definitive care 207

electrocardiography (ECG)abnormal pulse rate/rhythm

117–18asystole 47electrical injuries 207infant 10pericardiocentesis 245–6severe pain 322ventricular tachycardia 122

electrolyte disturbance 106, 290–5pulseless electrical activity 54shock 287

Emergency Medical Services (EMS)system 22–3

emergency paediatrics 15–17communication 17consent 17preparation 15, 16teamwork 16

Emergency Protection Order (EPO)305–6, 307

emergency treatment 45airway 79–83anaemia 111anaphylaxis 70, 71, 80, 94, 95,

108–9asthma 84–5bradycardia 119bronchiolitis 88burns 202–3cardiac arrhythmias 70

cardiomyopathy 111circulation 70convulsions 143–6croup 79–80diabetic ketoacidosis 71disability 70–1

shock 107drowning 210drowsiness 71duct-dependent congenital heart disease

110epiglottitis 80fluid loss 104–5foreign body 80fractures 194–5gastro-intestinal emergencies 70head injury 184–6heart failure 92hypertension 147–8malaria 136meningitis 135opiate poisoning 71, 135–6pneumonia 90poisoning 71, 135–6, 337–41respiration 68–9resuscitation 45scalds 202–3septicaemia 105–6seriously ill child 67–71seriously injured child 163shock 70supraventricular tachycardia

120–2unconsciousness 71ventricular tachycardia 122–3

emesis 337EMLA 320emotional abuse 300encephalitis 71

approach to child 134–5herpes 134

encephalopathy, metabolic 125endobronchial intubation 220–1Entonox 321

burns 202–3fracture alignment 194seriously injured child 159

envenomation 341–5analgesia 344coagulation support 344cytotoxic venom 343diagnosis 341local injury 343monitoring 345resuscitation 341–2sedation 344support 341–2venom uptake limitation 342–3

epiglottis 9–10cherry red 80movement 39

epiglottitis 81–2airway obstruction 31emergency treatment 80stridor 79tracheitis differential diagnosis 81

epilepsy 144epinephrine see adrenalineepiphyseal injuries 194erythromycin 370ethanol

ethylene glycol poisoning 340see also alcohol abuse

ethylene glycol poisoning 339–40etomidate 218evidence presentation

professional 308video link 301

exhaustion 61expiratory noise 60explanations of illness 13exposure 65

abnormal pulse rate/rhythm 117burns 201convulsions 141decreased conscious level

130–1envenomation 342

poisoning 334scalds 201seriously injured child 154shock 102transfer of child 275

extradural bleeds 181extremities

dislocations 193fracture–dislocations 193injuries 189–95

key features 192–4secondary survey 192–4

seriously injured child 163vascular injury 192venous access 232see also fractures

faceexpression assessment 324seriously injured child 161

face mask 42, 216falls 309

head injury 179farm equipment injuries 309fatigue 78, 79fear 12–13feeding problems

breathing difficulties 75bronchiolitis 88

femoral artery, palpation 26femoral nerve block 194, 247, 324femoral vein access 235–6femur, fractures 194, 324fetus, hypoxia 348, 349fever 65, 90–1

convulsions 141decreased conscious level 131shock 102

finger sweep technique 25fires, house 80flail chest 10, 167, 169–70flecainide 370

supraventricular tachycardia 121flucloxacillin 370fluid(s)

balance 285–95intake 285–6

pneumonia 91overload 289–90requirements 285

fluid loss 104–5burns 207emergency treatment 104–5insensible 285–6shock 286–7

fluid therapy 285anaphylaxis 108burns 203dehydration 288–9fluid loss 104–5neonates 356oral rehydration solutions 289septicaemia 105–6seriously injured child 153, 154,

157vomiting 288–9

flumazenil 322, 371foreign body 25

airway obstruction 26, 69, 74aspiration 31emergency treatment 80inhaled 82laryngeal 79removal 31, 82

formulary 361–84fosphenytoin 145fracture–dislocations 193fractures 189–90

alignment 194assessment 190emergency treatment 194–5epiphyseal 194femur 194, 324greenstick 189immobilisation 194–5open 193

long-bone 190, 191primary survey 190–1

388



INDEX

resuscitation 190–1ribs 10, 167, 259, 260

child abuse 303skull 182, 263, 303splinting 194–5surgical debridement 193torus 189transfer of child 275

Fraser ruling 307furosemide 282, 371

gag reflex, depressed 266gasping 60gastric decompression 208gastric drainage 176gastric lavage 337, 338gastric tubes 43gastroenteritis

electrolyte losses 291shock 104

gastrointestinal emergencies 70gender

injury incidence 310mortality rates 4

General Medical Council (UK), disclosureadvice 304–5

Gillick ruling 307Glasgow Coma Scale 125, 126

diabetic ketoacidosis 297head injury 158, 182, 183seriously injured child 164

glomerulonephritis 147glucagon 338, 371glucose

asystole 50–1blood levels 55, 132

convulsions 142drowning 210seriously injured child 158

hyperglycaemia 55, 295hyperkalaemia treatment 53shock 103see also hypoglycaemia

grave concern 300great vessel disruption 171–2grimace, best response 182, 183growth, pubertal spurt 7Guedel airway 38, 215, 216

haemodialysisethylene glycol poisoning 340see also dialysis

haemodynamics, seriously injured child164

haemofiltration 295haemoglobin 11

HbF 11, 75seriously injured child 164

haemoperitoneum 177Haemophilus influenzae pneumonia 90Haemophilus influenzae type b 134

epiglottitis 82tracheal infection 81

haemorrhage, triage 328haemostasis, seriously injured child 164haemothorax, massive 168–9haemotympanum 182HbF 11, 75head

manual in-line stabilisation 152, 155,156

seriously injured child 160–1head blocks and tape 249head injury 158, 179–88

continuing stabilisation 186–7deteriorating conscious level 185diabetes insipidus 164emergency treatment 184–6epidemiology 179examination 182–3history 182imaging 184intracranial pressure monitoring

164investigations 183–4key features 182–4NICE guidance 263pain management 323–4

pathophysiology 179physiological system control

186–7primary damage 180primary survey 181–2resuscitation 182review 186–7secondary damage 180secondary survey 182–4transfer of child 187triage 181

head tilt 23–5readjustment 26

heartchest radiograph 260–1murmur 92see also cardiac entries

heart failure 91–4bronchiolitis differential diagnosis 89,

93–4congenital lesions 93emergency treatment 92intravascular overload 290respiratory inadequacy 63–4

heart rate 12abnormal pulse rate/rhythm

116–17changes 11chest compression 355neonates 352, 353

drug administration 356–7respiratory inadequacy 61severely ill child 62

Heimlich manoeuvre 33–4helmet removal 250–2Henderson–Hasselbalch equation 279,

283hepatic cellular damage 268herpes encephalitis 134hind-brain dysfunction 65HIV/AIDS

cause of death 5transmission risk in resuscitation 31

host defence, seriously injured child165

hot gas inhalation 80, 200hydrocortisone 372hyperaldosteronism 293hypercalcaemia 295hyperglycaemia 55, 295hyperkalaemia 292, 293–4

bradycardia 118calcium therapy 50management 293–4poisoning 336sodium bicarbonate 49tachyarrhythmia 118ventricular fibrillation/tachycardia

53hypermagnesaemia 50hypernatraemia 290–1hypertension

emergency treatment 147–8persistent pulmonary 359systemic 65

crisis 147hyperventilation

acidosis 95central neurological failure 65diabetic ketoacidosis 296

hypocalcaemia 294–5acidosis correction 282calcium therapy 50pulseless electrical activity 54

hypochloraemia 282hypoglycaemia

cardiac arrest 55convulsions 142decreased conscious level 132glucose therapy 51head injury 186shock 103

hypokalaemia 292–3poisoning 336

hyponatraemia 292hypotension

circulatory failure 63convulsions 146

hypothermiacardiac arrest 55, 269drowning 208, 209–10peritoneal lavage 248poisoning 334pulseless electrical activity 54resuscitation from cardiac arrest 55ventricular fibrillation/tachycardia 51,

53hypovolaemia

neonate 359pulseless electrical activity 54vomiting 282

hypoxia 6bradycardia 61, 118, 119bronchoconstriction 74croup 79fetal 348, 349gasping 60intubation 221skin pallor 61tachycardia 61

ibuprofen 323, 372immobilisation

cervical spine 248–9, 254fractures 194–5spinal injury 195

immune deficiency 89immune function 12infants

cardiac compression 27, 28choking 31, 32mortality 3–4

infections/infectious diseasesairway obstruction 31bites 343burn wounds 203cause of death 5drowning 210transmission during resuscitation

30–1see also respiratory tract infections

infectious mononucleosis 83informed decisions 307inhalation injury 200injury

advocacy for legislation/design 311data collection/analysis 311, 312education 311epidemiology 309–10incidents 309–10prevention 310–12

Injury Minimisation Programme forSchools (IMPS) 311

inspiratory noise 60insulin 372

diabetic ketoacidosis 295hyperkalaemia treatment 53, 294infusion 296potassium levels 292

intercostal recession 60interviews with children 301intracranial bleeding 263intracranial pressure

mean 180monitoring

diabetic ketoacidosis 297seriously injured child 164

raised 5–6assessment 130bradycardia 118diabetic ketoacidosis 297drowning 210head injury 180–1meningitis 135pathophysiology 127–8signs 130systemic hypertensive crisis 147transfer of child 275

intraosseous access 334–5intraosseous infusion 240intravascular overload 289, 290intravenous fluids, asystole 50intubation see tracheal intubationion-exchange resins 294ipratropium bromide 85, 372iron poisoning 338

389



INDEX

jaw thrust 24–5, 26jellyfish stings 342, 344jugular vein

external, access 232–4, 237–8internal, access 236–7

ketamine 218, 322kidneys

dysplastic 147stabilisation 268see also renal entries

knowledge 13

labetalol 148, 373Laerdal pocket mask 42Laming report 304laparotomy, urgent 178laryngeal mask airway 44

complications 223equipment 221insertion 221–3procedure 222–3

laryngoscopes 39, 219blade 219

laryngoscopy, foreign body 80laryngotracheobronchitis, acute viral

80larynx 9–10legislation, safety 311lidocaine 52, 247, 320, 373–4

vein cannulation 324life threat, triage 328lightning strike 206limbs, viability threat 192liver stabilisation 268log-rolling 250, 251Lomotil 332lorazepam 143, 144, 374

convulsions in head injury 186lumbar puncture 128lumbar spine injuries 196–7lungs

anatomy 10chest radiograph 260compliance 11inflation 348, 349, 350pre-term babies 358stiff 60volume 11see also pulmonary entries

Magill’s forceps 25, 41, 80magnesium sulphate 85, 87, 375magnetic resonance imaging (MRI), brain

imaging 263malaria 136Manchester Triage Group 327, 328manikins, resuscitation practice 31mannitol, decreased conscious level

132marine toxins 342masks, oxygen 42, 216MDMA 340–1mean arterial pressure 127, 180meconium aspiration 352–3mediastinum, chest radiograph 261medication history 71medicolegal aspects 305–8medulla oblongata compression 65meningitis 71

approach to child 134–5bacterial 134–5convulsions 141, 142decreased conscious level 129diagnosis 134–5emergency treatment 135meningococcal septicaemia 107

meningococcal diseaseconvulsions 141rash in decreased conscious level 130

mental statuscirculatory inadequacy 63respiratory inadequacy 61–2

metabolic coma 136metabolic problems 95metabolic rate 11metabolism, seriously injured child 165methadone poisoning 338–9

midazolam 143, 144, 145, 322, 323, 375convulsions in head injury 186

mid-brain dysfunction 65morphine 320–1, 375

head injury 323–4seriously injured child 159severe pain 322, 322–3sickle cell crisis 111

mortality rates 3–4motor function, head injury 183motor vehicle accidents 179, 309motorcycle helmets 250–2movement assessment 324multiple organ failure 266multiply injured child 190–1

spinal injuries 196–7muscle spasm, envenomation 342myocardial dysfunction 289myocardial pH 49myocarditis 92, 93, 110–11myoglobinuria

electrical injuries 207seriously injured child 164

naloxone 135, 136, 376–7head injury 323–4maternal opiates 359neonates 356opiate poisoning 338–9opioid reversal 185, 321

nasal prongs 42nasogastric tube placement 159nasopharyngeal airway 38, 79

contraindications 38insertion 217

natriuresis 291near drowning see drowningneck

immobilisation 23seriously injured child 161

needle thoracocentesis 243–4neglect 299Neisseria meningitidis 134Neonatal Resuscitation Programme

347neonates

airway 348, 352–3assessment 351breathing 348, 353causes of death 4chest compression 353, 355circulation 348, 353, 355heart rate 352, 353

drug administration 356–7normal physiology 347–8pathophysiology 348, 349, 350pneumothorax 358–9pre-term 357–8respiration 351resuscitation 234, 347, 350–9

response to 357tracheal intubation 357ventilation 353see also birth

nephropathy, reflux 147nephrotic syndrome 289, 290nervous system, seriously injured child 164neurological assessment 64

poisoning 333–4secondary 70seriously ill child 67, 70

neurological failure, central 64, 65neurological function 64neuromuscular disease 61neurosurgical referral for head injuries

186Newborn Life Support Course 347nifedipine 148, 378nitrous oxide 321non-accidental injury 193

convulsions 141flail chest 169head injury 179presentations 300–1rash in decreased conscious level

130sodium intake 291see also child abuse

non-steroidal anti-inflammatory drugs(NSAIDs) 320, 323

noradrenaline 338note taking, seriously injured child 165,

166

oesophageal intubation 220opiates 320–1

antagonists 321fracture alignment 194maternal 359poisoning 135–6, 338–9

emergency treatment 71opioids

flail chest 170head injury 185

oral rehydration solutions 289electrolyte content 291

oropharyngeal airway 38, 79insertion 215–16

orotracheal intubation 217–21see also tracheal intubation

osteogenesis imperfecta 169overdose, intentional 332overhydration 289–90oxygen

administration 79abnormal pulse rate/rhythm 117decreased conscious level 131–2pneumonia 91

arterial blood 211arterial saturation 61, 84

convulsions 146concentration 42consumption 11equipment for provision 41–3flowmeter 42high-flow 84humidified 79partial pressure 283requirement for transfer 274wall supply 42

oxygen dissociation curve 11shift in infants 75

oxygenation 37

painassessment 317–19chest 75envenomation 344management 319–25recognition 317–19scales 318–19self-assessment tools 318severe 322, 322–3treatment 319–22triage 328see also analgesia

panda eyes 182papilloedema 183paracetamol 320, 323, 378–9

poisoning 339parainfluenza viruses 80paraldehyde 144, 145, 380paralysis, envenomation 341–2parental responsibility 306–7parents

caring for at death of child 314, 315presence

at invasive procedures 319at resuscitation 313

peak expiratory flow rate 84pelvis

bones 262cartilage 262–3crush injuries 190–1external fixation 191radiographs 261–4seriously injured child 162soft tissues 262–3splinting 190

perfusiondrugs used to maintain 267–8poor 267see also cerebral perfusion

pericardiocentesis 170, 245–6peritoneal lavage, diagnostic 247–8

abdominal injury 177

390



INDEX

persistent pulmonary hypertension 359pharyngeal airways 38phenobarbital 380phenytoin 144, 145, 380

convulsions in head injury 186phosphate binders 295phosphate supplementation 296physical injury 300physiology 11–12placental oxygen supply 348plastic bags for pre-term babies 357–8pneumonia 89–91

grunting 60pneumothorax

needle thoracocentesis 244neonates 358–9open 169simple 172tension 168

poisoning 95–6, 331–6abnormal pulse rate/rhythm 118accidental 332airway 332–3, 334aspirin 339beta-blockers 118bradycardia 118, 119breathing/breathing difficulties 333, 334carbon monoxide 203, 332circulation 333, 334cocaine 340convulsions 141crystalloid solutions 334cyanide 203deaths 331–2defibrillation 335deliberate 332diagnostic clues 335–6digoxin 118, 335disability 333–4, 335drug elimination 337ecstasy 340–1emergency treatment 71, 135–6,

337–41ethylene glycol 339–40exposure 334hyperkalaemia 336hypokalaemia 336hypothermia 334iatrogenic 332intentional overdose 332iron 338lethality assessment 335–6metabolic acidosis 336methadone 338–9monitoring 335neurological assessment 333–4opiates 135–6, 338–9

emergency treatment 71paracetamol 339primary assessment 332–4respiratory arrest 5–6respiratory rate 95resuscitation 334–6salicylates 339shock 334, 335sodium intake 291tachyarrhythmia 335temperature 334tricyclic antidepressants 118, 338vascular access 334–5

poisons centre 336police investigation 314Police Protection Order 306Portex system 41posture assessment 64, 324potassium 292–4

hypokalaemia 292–3, 336serum level 282supplementation 296see also hyperkalaemia

potassium chloride 381prednisolone 381prematurity 357–8

causes of death 4extreme 359

pre-terminal signs 60, 61circulatory failure 63medulla oblongata compression 65

procainamideventricular tachycardia 122

propofol 219propranolol 381

supraventricular tachycardia 122Pseudomonas aeruginosa 210psychological factors 12

injuries 310puberty, growth spurt 7pulmonary atresia 92pulmonary circulation obstruction 93pulmonary congestion 92pulmonary contusion 171pulmonary hypertension, persistent

359pulmonary obstructive lesions 110pulmonary oedema

diabetic ketoacidosis 297grunting 60

pulmonary thromboembolus 54pulmonary vascular bed 75pulmonary vasoconstriction 75pulse 27

abnormal rate/rhythm 115–24primary assessment 116–17resuscitation 117–18

absence 27checks 52volume in severely ill child 62

pulse oximetry 61, 322asthma 84

pulseless electrical activity 54pulsus paradoxus 84pupils

assessment 64decreased conscious level 130head injury 183hypertension treatment 148seriously injured child 164

pyloric stenosis, congenital hypertrophic282

pyridoxine 144

quinine 382

radial artery cannulation 239radiography

abdominal injury 177body imaging 264cervical spine 196, 254–63child abuse 303head injury 184performance 79

rapid sequence induction 217–18rash 71

convulsions 141decreased conscious level 130seriously ill child 65shock 102urticarial 71

recovery position 30referral

chest injury 173neurosurgical for head injuries

186seriously injured child 165

rehydration 296reimplantation techniques 191renal disorders

sodium loss 291systemic hypertensive crisis 147

renal failurediabetic ketoacidosis 297dialysis 295

renal tubular dysfunction 291rescue breaths 25, 229reservoir bags 42Residence Order 306resistance, tissue to electric current

206respiration

central neurological failure 65emergency treatment 68–9neonates 351secondary assessment 68–9seriously injured child 164

respiratory arrest 5–6respiratory distress, severe 60

respiratory drivedecrease 61paradoxical inhibition 75

respiratory failure 10potential 59–62susceptibility 74–5

respiratory function deterioration 37respiratory illness, severe 74respiratory inadequacy

cardiac failure 63–4effects on other organs 61–2

respiratory muscles 75accessory 60

respiratory physiology 11respiratory rate

asthma 84poisoning 95seriously ill child 59–60

respiratory syncytial virus 88, 89respiratory system, circulatory inadequacy

63respiratory tract disorders 73respiratory tract infections 74

asthma 87bronchiolitis 88–90

resuscitation 21–30airway poor initial response 358arrhythmia cause 53at birth 234, 347, 350–9

algorithm 354equipment 350procedure 351–3, 354, 355–7

blood transfusion 112burns 200–1cardiac arrest 266cardiopulmonary 23, 29, 30

audio prompts 30continuing 29

circulation 266–7convulsions 142decreased conscious level 131–2discontinuation 359drowning 208–10, 211electrical injuries 206emergency treatment 45envenomation 341–2equipment 272–3, 350exhaled air 26, 27fluid use 112–13fractures 190–1head injury 182hypothermia following 55investigations following 265–6management 45, 46mouth-to-mouth 30neurological 157–8parental presence 313poisoning 334–6poor initial response 358–9practice manikins 31priority 37scalds 200–1seriously ill child 66–7seriously injured child 155–9shock 102–3

treatment after 112stopping 55

retinal haemorrhage 183retrolental fibroplasia 42retropharyngeal abscess 83rewarming

active 53hypothermia with drowning

209–10Reye’s syndrome 136ribs 10

chest radiograph 259fractures 10, 167, 259, 260

child abuse 303rifampicin 30road traffic accidents 179, 309

sacroiliac joint 263SAFE approach 22–3salbutamol 84–5, 86, 293, 294, 382–3salicylates 282

poisoning 339salt-losing conditions 293

391



INDEX

saphenous vein, long 233scalds 199–204

airway 200breathing 200–1cervical spine 200circulation 201continuing stabilisation 204disability 201emergency treatment 202–3epidemiology 199–200exposure 201key features 201–2primary survey 200–1resuscitation 200–1secondary survey 201–2surface area 201, 202transfers 204

scalpbleeding 181venous access 232

sedatives 218, 219, 322envenomation 344

seizuresenvenomation 342head injury 186

Seldinger technique 235self-inflating bags 42sepsis, splenectomy 177septic shock 62–3, 100septic syndrome 100septicaemia 71, 105–7

emergency treatment 105–6hypocalcaemia 294meningococcal 107

seriously ill childemergency treatment 67–71primary assessment 59–62, 66–7resuscitation 66–7secondary assessment 67–71structured approach 66

seriously injured child 151–66continuing stabilisation 165–6emergency treatment 163history 159–60key features 159–63note taking 165, 166primary survey 152–5, 165reassessment 163–5resuscitation 155–9secondary survey 159–63tertiary survey 165

sexual abuse 300presentations 301

shivering, fever 65shock 97–113

abdominal injury 176advanced 62anaemia 111aortic rupture 172blood gas analysis 284bradycardia 119capillary refill 62–3cardiogenic 91, 93, 98

duct-dependent congenital heartdisease 110

cardiomyopathy 110–11classification 97, 98compensated 98–9, 100convulsions 142decreased conscious level 132diabetic ketoacidosis 296dissociative 98distributive 98electrolyte disturbance 287emergency treatment 70

treatment after 112envenomation 342fluid loss 104–5, 286–7hypovolaemic 98, 158, 190, 287irreversible 99–100key features 103–4obstructive 98pathophysiology 98–100perfusion maintenance 267–8phases 98–100poisoning 334, 335presentation 101primary assessment 101–2

resuscitation 102–3fluid use 112–13treatment after 112

scalp bleeding 181septic 62–3, 100septicaemia 105–7seriously injured child 153sickle cell crisis 111synchronous DC 122–3uncompensated 99, 100

shunts, left to right 92sickle cell crisis 111sinus bradycardia 65sinus tachycardia 119skeletal injury 189–90

child abuse 303skeletal survey 303skin

circulatory inadequacy 63colour in respiratory inadequacy 61perfusion 62

skull fracturebasal 182child abuse 303imaging 263

smoke inhalation 200snakebite 309

envenomation 343publicity 311tetanus immunisation 343

social history 71socioeconomic status

burns 199injuries 310

sodium abnormalities 290–2sodium bicarbonate see bicarbonatesodium nitroprusside 148, 383solvent abuse 332spinal cord

canal 255damage 197

log-rolling 250injury without radiological abnormality

(CSIWORA) 197, 254spinal injury 23, 25, 195–7

chest radiograph 259–60cord damage 197dislocation 254hyperflexion 197immobilisation 195log-rolling 250missed 254seriously injured child 155–6subluxation 254transfer of child 275trauma 195–7

spineimmobilisation 23, 155, 156, 197precautions in seriously injured child

152seriously injured child 163

splenectomy, sepsis 177splinting of fractures 194–5stabilisation of child 136–7, 265–9, 270

assessment after 269, 270continuing with chest injury 173

staff at death of child 314Staphylococcus aureus 81statements, child abuse cases 307, 308status epilepticus 139

algorithm 143sternal recession 60steroids

anaphylaxis 109asthma 85, 86croup 81decreased conscious level 132meningitis 135nebulised 79oral 79

stings 341–5stonefish sting 344streptococci, tracheal infection 81Streptococcus pneumoniae 134

pneumonia 90stridor 75, 78–9

causes 78stroke volume 11, 12

subclavian vein access 238subcostal recession 60subdural bleeds 181submersion injuries 208suction devices 41sudden infant death syndrome (SIDS) 4Sudden Unexpected Death in Infancy 314supraventricular tachycardia 119–22

emergency treatment 120–2wide-QRS 123

surfactant 358surgical airway 223–6suxamethonium 218symphysis pubis 263systemic vascular resistance 12systemic venous pressure 267

tachyarrhythmia 103, 115, 118poisoning 335

tachycardia 117see also supraventricular tachycardia;

ventricular tachycardiateamwork 16tear drop, acetabular 262, 263temperature, body

core 269drowning 209, 211poisoning 334seriously ill child 65triage 329

tension pneumothorax 168needle thoracocentesis 244

terbutaline 86, 383tetanus immunisation 343thermal injury

seriously injured child 165see also burns; scalds

thiopental sodium 146thiopentone (thiopental) 219thoracic cage compliance 74thoracic spine injuries 196–7, 259–60thoracocentesis, needle 243–4thoracotomy, emergency 171thorax see chestthymus 261tibial technique for intraosseous infusion

240tidal volume 11tonic–clonic status 139tonsillitis, acute 83toxic fume inhalation 332T-piece and open-ended bag 43trachea 10

puncture 223tracheal intubation 266

complications 220–1croup 81epiglottitis 80flail chest 170indications 156neonates 357orotracheal 217–21placement checking 220seriously injured child 156technique 219–21

tracheal rupture 171tracheal suction catheters 41tracheal tubes 39–41

connectors 40–1introducers 40misplacement 259placement check 43–4

tracheitis, bacterial 81tracheostomy 25

blocked 227, 228–30emergency equipment for change 230

tracheostomy tube 228, 229transfer of child 136–7, 273–6

airway 273–4breathing 273–4burns 204checklist 276circulation 274communication 271, 275disability 274–5documentation 275drugs 275–6electrical injuries 207

392



INDEX

equipment 271, 272–3exposure 275head injuries 187oxygen requirement 274planning 270–3preparation for 270–3seriously injured 165–6vital function monitoring/recording 273

transport, preparation for 270–3transtracheal insufflation 225trauma 151

airway obstruction 80amputation 190, 191blunt 175cause of death 5cervical spine injury 248chest injury 167extremities 189–95fluid therapy 157, 158head tilt/chin lift 25initial assessment 23penetrating 172pneumothorax 172practical procedures 243–52pulseless electrical activity 54X-ray interpretation 253–64

triagedecision making 327–9head injury 181secondary 329

tricuspid atresia 92trisomy 13, 359trisomy 18, 359tuberculosis 5

ultrasound, abdominal injury 177umbilical vein access 234uncal herniation 181, 186uncal syndrome 127unconsciousness

emergency treatment 71see also coma; conscious level, decreased

understanding of child 307urinary catheterisation 176

seriously injured child 159urinary output

circulatory inadequacy 63seriously injured child 164

urine flow 268

vagal stimulationbradycardia 118, 119supraventricular tachycardia 120

Valsalva manoeuvre 120vascular access 231–40

poisoning 334–5seriously injured child 156–7

vascular injury, extremities 192vasopressin, asystole 50venepuncture, emergency 324venom

cytotoxic 343uptake limitation 342–3

venous access 158central 235–8peripheral 232–4

ventilationadvanced support 37–45, 46asthma 85–6bag-and-mask 227, 228, 353, 355bag–valve–mask 42, 85, 216decreased conscious level 132depression with treatment of

convulsions 146envenomation 341–2equipment for provision 41–3flail chest 170indications 156mechanical 43, 85–6mouth-to-mask 226mouth-to-mouth 42neonates 353

poor initial response 358partial 41

practical skills 43–4without intubation 226–7

ventilation–perfusion mismatch74, 75

ventilators, mechanical 43ventricles, cardiac 10ventricular fibrillation 51–4

shock-resistant 50ventricular tachycardia

abnormal pulse rate/rhythm117–18

approach to child 122–3emergency treatment 122–3pulseless 51–4torsade de pointes 123

verapamil 384supraventricular tachycardia 122

vertebral discs, cervical 258videotape interviews 301visual acuity 148vital signs, seriously injured child 154voice assessment 324Volkmann’s ischaemic contracture 192voltage 206vomiting 43

fluid therapy 288–9metabolic alkalosis 282seriously injured child 155–6

water intake/retention 292weighing 7, 9weight 7, 8, 9

estimation 9wheeze 69, 75, 83–90

bronchiolitis 88wheezing 60Wolff–Parkinson–White tachycardia 121wound care, burns 203

X-rays see radiography

Yankauer sucker 41, 352

393

pediatric life support

Health & Medicine