2023 Advanced Paediatric Life Support A Practical Approach to Emergencies

Advanced Paediatric

LifeSupport

SEVENTH EDITION

Advanced

Paediatric Life

Support

A Practical Approach

toEmergencies

SEVENTH EDITION

Advanced Life Support Group

EDITED BY

Stephanie Smith

This seventh edition first published 2023

Edition History

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Contributors to seventh edition vii

Foreword xi

Preface to first edition xii

Preface to seventh edition xiii

Acknowledgements xv

Contact details and further information xix

PART 1: Introduction 1

1 Introduction and structured approach to paediatric emergencies 3

2 Getting it right: non- technical factors andcommunication 19

PART 2: The seriously ill child 29

3 Structured approach to the seriously ill child 31

4 Airway and Breathing 45

5 Circulation 65

6 Decreased conscious level (with or without seizures) 93

7 Exposure 115

PART 3: The seriously injured child 125

8 Structured approach to the seriously injured child 127

9 The child withchest injury 147

10 The child with abdominalinjury 157

11 The child withtraumatic brain injury 161

12 The child withinjuries tothe extremities or thespine 173

13 The burned or scalded child 183

14 The child with an electrical injury 191

15 Special considerations 195

Contents

vi Contents

PART 4: Life support 207

16 Basic life support 209

17 Support ofthe airway andventilation 227

18 Management ofcardiac arrest 245

PART 5: Practical application ofAPLS 259

19 Practical procedures: airway andbreathing 261

20 Practical procedures: circulation 277

21 Practical procedures: trauma 295

22 Imaging intrauma 309

23 Structured approach to stabilisation andtransfer 323

PART 6: Appendices 337

Appendix A Acid–base balance andblood gas interpretation 339

Appendix B Fluid andelectrolyte management 357

Appendix C Paediatric major trauma 371

Appendix D Safeguarding 375

Appendix E Advance decisions andend oflife 383

Appendix F General approach topoisoning andenvenomation 397

Appendix G Resuscitation ofthe baby at birth 419

Appendix H Drowning 439

Appendix I Point ofcare ultrasound 445

Appendix J Formulary 455

List ofalgorithms 477

Working group for seventh edition 479

References and further reading 481

Index 487

How to use your textbook 508

vii

Working group chair

Stephanie Smith BM BS FRCPCH, Honorary Emergency Paediatric Consultant, Nottingham

Children’s Hospital, Nottingham, UK

Associate editors

The seriously ill child

Andrew Baldock FRCA FFICM, Consultant Paediatric Anaesthetist and Intensivist, Southampton

Children’s Hospital, Southampton, UK

Els Duval MD PhD, Clinical Head Pediatric Intensive Care Unit, University Hospital Antwerp,

Edegem, Belgium

Jacquie Schutz MBBS FRACP DipObs, Paediatric Emergency Physician, Paediatric Emergency,

Department Women’s and Children’s Hospital, Adelaide, South Australia

The seriously injured child

Alan Charters RGN RSCN RNT DHealthSci MAEd BSc(Hons) PgDip(Ed), Consultant Practitioner,

Paediatric Emergency Care, Portsmouth, UK

Bimal Mehta MBChB BSc FRCPCH FRCEM, Consultant in Paediatric Emergency Medicine, Alder

Hey Children’s Hospital NHS Foundation Trust, Liverpool, UK

Life support

Jason Acworth MBBS FRACP (PEM), Paediatric Emergency Physician, Queensland Children’s

Hospital; Clinical Professor, Faculty of Medicine, University of Queensland, Australia

Marijke van Eerd MSc BSc RN RN(Child) PGCE, Paediatric Advanced Clinical Practitioner, Children

and Young People’s Emergency Department, Nottingham University Hospitals NHS Trust,

Nottingham, UK

Appendices

Peter Davis MRCP(UK) FRCPCH FFICM, Consultant in Paediatric Critical Care Medicine, Bristol

Royal Hospital for Children, University Hospitals Bristol and Weston NHS Foundation Trust,

Bristol, UK

Esyld Watson MBBCH FCEM FAcadMEd PgDip(Med Ed), Consultant in Paediatric and Adult

Emergency Medicine Prince Charles Hospital, Merthyr Tydfil, Wales

Contributors to seventh

edition

viii Contributors to seventh edition

a task, this does not need to be communicated, but

there are times when it is important that followers signal if they have a problem or request the

leader’s attention.

Hierarchy

Within the team there needs to be a hierarchy. This is the power gradient; the leader is at the top of

this as the person coordinating, directing and making the decisions. However, this should not be

absolute. If the power gradient is too steep the leader’s decisions cannot be questioned and

24 PART 1 Introduction

thefollowers blindly follow the orders. This is not safe because leaders are humans too and also

make errors– their team is their safety net. Safe practice is achieved where the followers feel they

can raise concerns or question instructions. This must always be understood by the leaders as much

as by the followers. One way to reduce the hierarchy is for the leader to invite the team’s thoughts

and concerns, particularly around patient safety issues. It is also important for the follower to learn

how to raise concerns appropriately.

One method that is sometimes used to raise concerns appropriately is PACE (probing, alerting,

challenging or declaring an emergency).

These stages are described with examples below:

z Probe– this is used where a person notices something they think might be a problem. They

verbalise the issue, often as a question. ‘Have you noticed that this child is cyanosed?’

z Alert– the observer strengthens and directs their statement and suggests a course of action.

‘Dr Brown, I am concerned, the child is deeply cyanosed, should we start bag–valve–mask

ventilation?’

z Challenge– the situation requires urgent attention. One of the key protagonists needs to be

directly engaged. If possible, the speaker places themself into the eye line of the person with

whom they wish to communicate. ‘Dr Brown, you must listen to me now, this child needs help

with their ventilation’

z Emergency– this is used where all else has failed and/or the observer perceives a critical event

is about to occur. Where possible, a physical signal or physical barrier should be employed

together with clear verbalisation. ‘Dr Brown, you are overlooking this child’s respiratory state,

please move out of the way as I am going to ventilate them’

The PACE structure can be commenced at any appropriate level and escalated until a satisfactory

response is gained. If an adverse event is imminent then it may be relevant to start at the

declaring ‘emergency’ stage, whereas a much lower level of concern may well start at a ‘probing’

question.

An alternative approach that many healthcare settings are using is CUSS. It helps if standard phrases

are used because these can act as collective triggers.

At each of these levels, which increase in assertiveness, the reasoning needs to be re- stated in a

clear, unambiguous way.

Stage Level of concern

P Probe I think you need to know what is happening

A Alert I think something bad might happen

C Challenge I know something bad will happen

E Emergency I will not let it happen

C Concerned I am concerned

U Uncomfortable I am uncomfortable

S Safety issue This is unsafe

S Stop You need to stop

CHAPTER 2 Getting it right: non-technical factors and communication 25

2.7 Situation awareness

A key element of good team working and leadership is to be conscious of what is happening; this is

termed situation awareness. It not only involves seeing what is happening, but also captures how

this is interpreted and understood, how decisions are made and, ultimately, planning ahead. We

can distinguish between individual situation awareness, shared situation awareness and team

situation awareness.

Consider Figure2.2 which illustrates just how easy it is to misinterpret data:

We see what we expect to see, and misperceiving is particularly likely to happen when we are over-

loaded, distracted or the mental demands on us are too high.

Distractions

Within healthcare, distractions become the norm to such an extent individuals are often not even

aware of them. The risk is that mistakes are made and information is missed. It is important to try to

challenge interruptions when doing critical tasks, and when they do occur restart the task from the

beginning, rather than from where it is considered the interruption occurred. Some organisations

have specific quiet areas for critical tasks such as prescribing. Whatever the local set up, the key is

to develop and maintain everyone’s awareness of how distraction greatly increases the chance of

error.

Decision making

To make a good decision a person needs to assess all aspects of a problem and ensure they have the

key information. Good situation awareness is a basic prerequisite for this process. The whole team

should be on the alert for ambiguities or conflicting information. Any inconsistent facts should be

treated as a potential marker for faulty situation awareness. They should never be brushed off as

unimportant anomalies in the absence of evidence to support such a decision.

Where there are no time pressures, the decision- making process should not be concluded until the

team is satisfied they have all the information and have considered all the options. Where time is a

pressure, a certain amount of pragmatism must be employed. There is plenty of evidence to confirm

Figure2.2 Similar package design of two different medications

26 PART 1 Introduction

that practise and experience can mitigate some of the negative effects of abbreviating a decision-

making process. Those making decisions under such circ*mstances need to remain aware of the

shortcuts they have taken. They should be ready to receive feedback from their team, particularly if

any member of the team has significant concerns about the proposed course of action.

Mental models

Our mental models are affected by our previous experiences but also by the information/briefing

that we received before the experience. A good pre- brief, where possible, will positively influence

how the team frame the situation and which mental models they draw on. Where a briefing is

accurate it is extremely helpful, where it is inaccurate, because it influences how we interpret

information, it can lead to error. We are more likely to fit what we see to what we expect to see and

therefore make inaccurate conclusions. Practising good briefings and handovers is time well spent.

There can be a number of reasons why we might fail to have accurate situation awareness.

z Lack of or poor mental model

z A tendency to seek confirming evidence and ignore disconfirming evidence

z Overload on our working memory leading to forgetting vital information

Team situation awareness

We gather information from the world around us using our five senses. Because there is too much

information constantly assaulting us, we selectively attend to only some of it based on our previous

experiences and on what jumps out at us at the time. Different people attend to different aspects

of a complex event, so individuals in a team will have a differing awareness of the situation.

2.8 Improving team andindividual performance

In addition to effective communication, team working, situation awareness, leadership and

followership skills, there are a number of other ways that team and individual performance can be

further developed and improved.

Awareness ofsituations when errors are more likely

If we are aware that errors are more likely we can be more proactive in detecting them. Two common

situations that make errors more likely are stress and fatigue. Stress is not only a source of error

when we are overworked and overstimulated, but also, at the other end of the spectrum, when we

are understimulated we become inattentive.

The acronym HALT has been used to describe situations when error is more likely:

We see what we expect to see

The team’s situation awareness will often be greater than any one individual’s, therefore the

leader should actively encourage this

sharing of perspectives

H Hungry

A Angry

L Late

T Tired

CHAPTER 2 Getting it right: non-technical factors and communication 27

IMSAFE has been used as a checklist in the aviation industry, asking whether the individual may be

affected by:

Ideally, individuals who are potentially compromised need to be supported appropriately, allowed

time to recover and the team made aware. How this can be achieved in the middle of a night shift

can be problematic.

Awareness oferror traps

A common trap that people fall into is only seeing or registering the information that fits in with

their current mental model. This is known as a confirmation bias. When this occurs people favour

information that confirms their preconceptions or hypotheses regardless of whether the information

is true. This may be observed within the healthcare setting during the process of a referral or

handover. An example of this might be a clinician receiving a phone call requesting them to attend

the ward to review an acutely deteriorating child. The clinician is advised that the patient is a known

asthmatic. On their way to the ward the clinician builds up a series of preconceived expectations

around what they will find upon their arrival. They may even formulate a management plan whilst

travelling to the scene, based upon their expectations. Once this mindset is established it can be

difficult to shift.

On arrival, the clinician examines the systems affected by the presumed diagnosis. They seek to

confirm their expectation by focusing on an auscultation of the chest at the expense of a thorough

assessment. Upon hearing bilateral wheeze their preconceived ideas are confirmed and the remain-

der of the assessment is completed without due attention and more as a rehearsed exercise than

an open- minded exploration. They fail to notice that the patient also has a soft stridor and is hypo-

tensive. In this case the eventual diagnosis of anaphylaxis becomes at best a very late consideration,

or at worst a situation that requires an objective newcomer to the team to point out the obvious.

Cognitive aids: checklists, guidelines andprotocols

Well- constructed cognitive aids such as guidelines and algorithms are important because the

human memory is not infallible. They also confer team understanding through the use of a

standardised response. This reduces stress. This is especially true where an uncommon emergency

event occurs. The team may be unfamiliar with one another and each member will be trying to

remember what to do, what treatments are required and in what order. A good team leader will use

the available cognitive aids as a prompt and the team members can use them as a resource so that

they can plan ahead. Safe practice is promoted through the use of these tools in an emergency

rather than relying on memory.

Calling forhelp early

Trainee staff are often reluctant to call for senior help, partly due to not recognising the severity of

the situation and partly due to concerns about wasting the time of seniors. With all emergency

I Illness

M Medication

S Stress

A Alcohol

F Fatigue

E Emotion

28 PART 1 Introduction

events, and in particular with paediatric emergencies, escalation and appropriate help should be

summoned as soon as possible. Remember, help will not arrive instantly, but it is helpful to state

when help is needed and to be clear about what that help should be.

Debriefing

Wherever possible a debriefing should be facilitated following clinical events, even if brief, as this

encourages us to normalise talking about difficult situations. A debrief immediately after an event

is described as a ‘hot’ debrief and it has the aim of ensuring psychological safety. There is a place for

this at the end of a shift or difficult emergency to ensure that staff are ok as they go home. The ‘hot’

debrief is not about learning points or establishing what happened. That can wait for the ‘cold’

debrief, days or even weeks after the event. This is usually facilitated by a trained individual with the

intention of learning from the event and providing pointers moving forwards.

2.9 Summary

In this chapter we have given a brief introduction to the clinical human factors that can lead to poor

team working, patient harm and adverse events. It is important for you to use every opportunity to

reflect and develop your own performance and influence the development of others and the team.

PART 2

The seriously ill child

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

3.1 Introduction

Paediatric cardiac arrests are uncommon and generally have a very poor outcome in comparison

to adults with their primary cardiac causes. Therefore, earlier recognition and management of

potential respiratory, circulatory or central neurological failure will reduce mortality and secondary

morbidity. Rapid, effective assessment and initiation of correct treatment are key and this needs

to be done in a calm, structured way with clear communication to both other team members (if

present) but also to the family and/or child if appropriate.

The structured approach is outlined on the next page (Figures3.1 and3.2).

This can either be done by an individual or ideally with a team working together.

The primary survey and resuscitation involve assessment and management of the vital ABCDE

functions. This primary assessment and any necessary resuscitation must be initiated before the

more detailed secondary assessment is performed. Once the child’s vital functions are supported,

the secondary survey and emergency treatment begins. Illness- specific pathophysiology is sought

and emergency treatments are instituted.

Structured approach to

the seriously ill child

CHAPTER 3

Learning outcomes

After reading this chapter, you will be able to:

z Describe how to recognise the seriously ill child

z Describe a structured approach to the assessment of the seriously ill child

z Describe a structured approach to resuscitation and treatment of the seriously ill child focusing

on the early management

32 PART2 The seriously ill child

During the secondary survey, vital signs should be checked frequently to detect any change in

the child’s condition. If there is deterioration, then return to the primary survey.

3.2 Primary survey andresuscitation ofthe airway

Assess patency of the airway by:

z Looking for chest and/or abdominal movements

z Listening for breath sounds

z Feeling for expired air

Appearance

Circulation to skin

Work of

breathing

Appearance Work of breathing Circulation to skin

Abnormal tone Abnormal sounds Pallor

Decreased interaction Abnormal position Mottling

Decreased consolability Retractions Cyanosis

Abnormal look/gaze Flaring

Abnormal speech/cry Apnoea/gasping

Figure3.1 Paediatric assessment triangle

Primary survey

Resuscitation

Secondary survey

Stabilisation and transfer to

definitive care

Emergency treatment

Figure3.2 Structured approach to paediatric emergencies

CHAPTER 3 Structured approach to the seriously ill child 33

Vocalisations, such as crying or talking, indicate ventilation and some degree of airway patency.

z If there is obvious spontaneous ventilation, note other signs that may suggest upper airway

obstruction such as the presence of stridor or evidence of recession

z If there is no evidence of air movement, then head tilt/chin lift or jaw thrust manoeuvres must

be carried out. Reassess the airway after any airway- opening manoeuvres

z If there continues to be no evidence of air movement then airway patency can be assessed by

performing an airway- opening manoeuvre while giving rescue breaths (see Chapter16)

Resuscitation

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

z Head tilt/chin lift or jaw thrust

z Use of an airway adjunct

z Tracheal intubation

3.3 Primary survey andresuscitation

ofbreathing

A patent airway does not ensure adequate ventilation. The latter requires an intact respiratory

centre and adequate pulmonary function augmented by coordinated movement of the diaphragm

and chest wall.

The effort, efficacy and effect of breathing need to be assessed bearing in mind the effects of

respiratory inadequacy on other organs in the child’s body.

Effort ofbreathing

The degree of effort of breathing is an indication of the severity of respiratory disease. It is important

to assess the following:

1. Respiratory rate. Normal resting respiratory rates at differing ages are shown in the normal

ranges table (inside front cover). Normal rates are higher in infancy and fall with increasing age.

Care should be taken in interpreting single measurements: infants can show wide variation in

respiratory rates depending on their state of activity. The World Health Organization (WHO) uses

a cut- off of 60 breaths per minute for pneumonia in infants and young children. Most useful are

trends in the measurement as an indicator of improvement or deterioration. At rest, tachypnoea

indicates that increased ventilation is needed because of either lung or airway disease, or metabolic

acidosis. A slow respiratory rate indicates fatigue, cerebral depression or a pre- terminal state.

2. Recession. Intercostal, subcostal, sternal or suprasternal (tracheal tug) recession shows increased

effort of breathing. This sign is more apparent in younger infants as they have a compliant chest

wall. If present in older children (i.e. over 6 years) this sign suggests severe respiratory compromise.

The degree of recession gives an indication of the severity of respiratory difficulty, however in the

child who has become exhausted through increased effort of breathing, recession decreases as

respiratory failure develops.

3. Inspiratory or expiratory noises. An inspiratory noise while breathing (stridor) is a sign of laryngeal

or tracheal obstruction. In severe obstruction stridor may also occur in expiration, but the

inspiratory component is usually more pronounced. Wheezing indicates lower airway narrowing

and is more pronounced in expiration. A prolonged expiratory phase also indicates lower airway

narrowing. The volume of the noise is not an indicator of severity, as it may disappear in the pre-

terminal state.

4. Grunting. This 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 of expiration

in children with ‘stiff’ lungs. This is a sign of severe respiratory distress and is characteristically

seen in infants with pneumonia or pulmonary oedema. It may also be seen with raised intracranial

pressure, abdominal distension or peritonism.

34 PART2 The seriously ill child

5. Accessory muscle use. As in adult life, the sternomastoid muscle may be used as an accessory

respiratory muscle when the effort of breathing is increased. In infants, this is ineffectual and just

causes the head to bob up and down with each breath.

6. Flaring of the nostrils. This is seen especially in infants with respiratory distress.

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

Efficacy ofbreathing

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, important information is given

by auscultation of the chest. Listen for reduced, asymmetrical or bronchial breath sounds. A silent

chest is an extremely worrying sign.

Pulse oximetry can be used to measure the arterial oxygen saturation (SpO2). A good plethysmo-

graphic (pulse) waveform is important to help confirm the accuracy of measurements. In severe

shock and hypothermia, there may be poor or absent pulse detection. Measurements are also not

as accurate when the SpO2 is less than 80%, with motion artefact or high levels of ambient light

and in the presence of carboxy- or methaemoglobin. Oximetry in air gives a good indication of the

efficacy of breathing, although to assess the adequacy of ventilation, some measure of carbon

dioxide should be obtained. Any supplemental oxygen will mask problems with oxygenation due to

ineffective breathing unless the hypoxia is severe. Normal SpO2 in an infant or child in air at sea level

is 97–100%, however the aim for oxygen treatment would be 94–98%.

Effects ofrespiratory inadequacy onother organs

1. Heart rate. Hypoxia produces tachycardia in the older infant and child. Anxiety and fever will also

contribute to tachycardia, making this a non- specific sign. Severe or prolonged hypoxia leads

to bradycardia. This is a pre- terminal sign.

2. Skin colour. Hypoxia produces vasoconstriction and skin pallor (via catecholamine release).

Cyanosis is a late and pre- terminal sign of hypoxia as it usually becomes apparent when SpO2

falls to less than 80%, and only in the absence of anaemia. By the time central cyanosis is visible

in acute respiratory disease, the child is close to respiratory arrest. In the anaemic child, cyanosis

may never be visible despite profound hypoxia. A few children will be cyanosed because of

cyanotic heart disease, but may have adequate oxygen uptake within the lungs, and their cyanosis

will be largely unchanged by oxygen therapy.

3. Mental status. The hypoxic or hypercapnic child will be agitated and/or drowsy. Gradually

drowsiness increases and eventually consciousness is lost. These extremely useful and important

signs are often more difficult to detect in small infants. The parents may say that the infant is just

‘not himself’. The healthcare practitioner must assess the child’s state of alertness by gaining eye

contact and noting the response to voice and, if necessary, to painful stimuli. A generalised

muscular hypotonia also accompanies hypoxic cerebral depression.

Exceptions

There may be minimal or no increased effort of breathing if the child with respiratory failure

has:

1. Fatigue due to prolonged respiratory effort; exhaustion is a pre- terminal sign

2. Cerebral depression from raised intracranial pressure, poisoning or encephalopathy. These

children will have respiratory inadequacy without increased effort of breathing. The

respiratory inadequacy in this case is caused by decreased respiratory drive

3. Neuromuscular disease (e.g. spinal muscular atrophy or muscular dystrophy) who may

present in respiratory failure without increased effort of breathing

The diagnosis of respiratory failure in these children is made by observing the efficacy of

breathing and looking for other signs of respiratory inadequacy, as described

CHAPTER 3 Structured approach to the seriously ill child 35

Resuscitation

All children with breathing difficulties should receive oxygen as soon as the airway is opened to

attain SpO2 94–98%. This can be achieved by using a flow up to 10- 15l/min via a non- rebreathing

mask with reservoir bag, or by using high- flow nasal cannula (HFNC) oxygen therapy. With

decreasing oxygen need, low- flow nasal cannula or prongs can be used.

In the child with inadequate respiratory effort, breathing should be supported either with bag–

mask ventilation (two- person technique ideally) or intubation and ventilation with capnography.

Cuffed tubes are now recommended in most instances.

3.4 Primary survey andresuscitation ofthe circulation

The cardiovascular status needs to be assessed bearing in mind the effects of circulatory inadequacy

on other organs.

Factors toassess

1. Heart rate. Normal rates are shown in the normal ranges table (inside front cover). The heart rate

initially increases in shock due to catecholamine release and as compensation for decreased

stroke volume. Fit adolescents can have a heart rate below 60 beats/min without circulatory

problems.

2. Pulse volume. Although blood pressure (BP) in children is maintained until shock is severe, an

indication

of perfusion can be gained by comparative palpation of both peripheral and central

pulses. Absent peripheral pulses and weak central pulses are serious signs of advanced shock

and indicate that hypotension is already present. Bounding pulses may be caused by an increased

cardiac output (e.g. septicaemia), arteriovenous systemic shunt (e.g. patent arterial duct) or

hypercapnia.

3. Capillary refill time. Following cutaneous pressure on the centre of the sternum for 5 seconds,

capillary refill should occur within 2 seconds. A slower refill time than this can indicate poor skin

perfusion, a sign which may be helpful in early septic shock, when the child may otherwise appear

well, with warm peripheries. The presence of fever does not affect the sensitivity of delayed

capillary refill in children with hypovolaemia but a low ambient temperature reduces its specificity.

Poor capillary refill and differential pulse volumes are neither sensitive nor specific indicators of

shock in infants and children but are useful clinical signs when used in conjunction with the

other signs described. They should not be used as the only indicators of shock nor as quantitative

measures of the response to treatment. In children with pigmented skin, the sign is more difficult

to assess. In these cases, the nail beds are used and additionally the soles of the feet in young

babies.

4. Blood pressure. Normal systolic pressures are shown in the normal ranges table (inside front

cover). In septic shock, aim for these normal values and respond to trends along with the other

indicators of shock. Use of the correct cuff size is crucial if an accurate blood pressure measurement

is to be obtained. This caveat applies to both auscultatory and oscillometric devices. The width of

the cuff should be more than 40% of the length of the upper arm and the bladder more than 80%

of the arm’s circumference (Figure3.3). It is important to recognise that BP can be raised due to

pain, movement and being upset, and that it is vital to address these and reassess to obtain a

true BP. A manual device, which is generally tolerated much better, may need to be used. A fall

in BP is a late and pre- terminal sign of shock.

An abnormally slow pulse rate, or bradycardia, is defined as less than 60beats/min or a

rapidly falling heart rate associated with poor systemic perfusion. This is a pre- terminal

sign

36 PART2 The seriously ill child

Effects ofcirculatory inadequacy onother organs

1. Respiratory system. A rapid respiration rate with an increased tidal volume but without recession,

may be compensatory for the metabolic acidosis resulting from circulatory failure.

Olecranon

Acromion

Circumference

(a)

(b)

At least

80%

CuffBladderAt least

40%

Figure3.3 (a, b) Size and position of cuff

(b) Children’s Health Queensland/CC BY 4.0

Cardiac failure

The following features suggest a cardiac cause of respiratory inadequacy:

z Cyanosis, not correcting with oxygen therapy

z Tachycardia out of proportion to respiratory difficulty

z Raised jugular venous pressure (older child/teenager)

z Gallop rhythm/murmur

z Enlarged liver

z Absent femoral pulses

CHAPTER 3 Structured approach to the seriously ill child 37

2. Skin. Mottled, cold, pale skin peripherally indicates poor perfusion. A line of coldness may be felt

to move centrally as circulatory failure progresses.

3. Mental status. Agitation and then drowsiness leading to unconsciousness are characteristic of

circulatory failure. These signs are caused by poor cerebral perfusion. In an infant, parents may

say that their child is ‘not himself’.

4. Urinary output. A urine output of less than 1ml/kg/h in children and less than 2ml/kg/h in infants

may indicate inadequate renal perfusion during shock. A history of reduced wet nappies or urine

production should be sought.

Resuscitation

In every child with an inadequate circulation (shock):

z Give high- flow oxygen via a non- rebreathing mask with reservoir bag, or by using HFNC oxygen

therapy, or via an endotracheal tube if intubation has been necessary for airway control or

inadequate breathing

z Venous or intraosseous (IO) access should be gained without delay and an immediate infusion

of balanced crystalloid (10 ml/kg) given. Urgent blood samples, especially blood glucose and

preferably also a blood gas, may be taken at this point.

3.5 Primary assessment andresuscitation ofdisability (neurological evaluation)

Neurological assessment should only be performed after airway (A), breathing (B) and circulation

ABC. Both 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 a primary neurological

problem.

Both respiratory and circulatory failure will have central neurological effects. Conversely, some

conditions with direct central neurological effects (e.g. meningitis, raised intracranial pressure from

trauma, and status epilepticus) may also have respiratory and circulatory consequences. These

must be addressed to improve the neurological status. In addition, any patient with a decreased

conscious level or convulsions must have an initial glucose stick test performed.

Primary assessment ofneurological function

1. Conscious level. A rapid assessment of conscious level can be made by assigning the patient to

one of the categories shown in the box below.

If the child does not respond to voice, it is important that response to pain is then assessed. A

painful central stimulus can be delivered by sternal pressure, by massaging the mastoid process

or by supraorbital ridge pressure. Commonly, a child who is unresponsive or who only responds

to pain has a significant degree of coma, equivalent to 8 or less on the Glasgow Coma Scale (GCS)

and their airway must be supported. Carry out formal GCS assessment to monitor their response

to treatment.

2. Posture. Many 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 (Figure3.4). These

A Alert

V Responds to Voice

P Responds only to Pain

U Unresponsive to all stimuli

38 PART2 The seriously ill child

postures can be mistaken for the tonic phase of a convulsion. Alternatively, a painful stimulus

may be necessary to elicit these postures. Severe extension of the neck due to upper airway

obstruction can mimic the opisthotonos that occurs with meningeal irritation. A stiff neck and

full fontanelle in infants are signs that suggest meningitis.

3. Pupils. Many drugs and cerebral lesions have effects on pupil size and reactions. However, the

most important pupillary signs to seek are dilatation, unequal sizes and lack of reactivity, which

indicate possible serious brain disorders if new. See Chapter6 for a more detailed explanation.

Effects ofneurological inadequacy onother organs

1. Respiratory effects of central neurological failure. There are several recognisable breathing

pattern abnormalities with raised intracranial pressure. However, they are often changeable and

may vary from hyperventilation to Cheyne–Stokes breathing to apnoea. The presence of any

abnormal respiratory pattern in a child with coma suggests mid- or hindbrain dysfunction. This

is different from Kussmaul breathing, due to the profound acidosis of diabetic ketoacidosis.

2. Circulatory effects of central neurological failure. Systemic hypertension with sinus bradycardia

(Cushing response) indicates compression of the medulla oblongata caused by herniation of the

cerebellar tonsils through the foramen magnum. This is a late and pre- terminal sign.

Resuscitation

z 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)

z If hypoglycaemia has been found, treat hypoglycaemia (less than 2.8mmol/l or 50mg/dl) with a

bolus of glucose (3ml/kg of 10% glucose) followed by an IV infusion of glucose, after taking blood

for glucose measurement in the laboratory and a sample for further studies

z For prolonged or recurrent seizures, treat reversible causes such as hypoglycaemia or

hyponatraemia, then follow the status epilepticus algorithm found in Chapter6

z Manage raised intracranial pressure if present (see Chapter6 for further details)

(a)

(b)

Internal

rotation

Internal

rotation

Arms held

in flexion

Arms held in

extension

Legs held in

extension

Legs held in

extension

Figure3.4 (a) Decorticate posturing, and (b) decerebrate posturing

CHAPTER 3 Structured approach to the seriously ill child 39

3.6 Primary survey andresuscitation ofissues found during exposure

The examination of the seriously ill child involves examination for markers of illness that will help

provide specific emergency treatment. There are a few key indicators:

z Temperature. A fever suggests an infection as the cause of the illness but may also be the result

of prolonged convulsions or shivering. In young infants, infection may present with a low body

temperature

z Rash and bruising. Examination is carried out for rashes, such as urticaria in allergic reactions,

purpura, petechiae and bruising in septicaemia or trauma (accidental or inflicted), or maculopapular

and erythematous rashes in allergic reactions and some forms of sepsis

z Resuscitation. Depends on what factor is identified. Urticarial rash with airway/circulatory

compromise requires IM adrenaline (0.01ml/kg of 1:1000) immediately. Purpuric rash synonymous

with meningococcal sepsis requires early IV/IO access with administration of IV antibiotics and

resuscitation fluids if indicated. Unexplained bruising requires measurement of coagulation

factors and a thorough examination with a very detailed history with the appreciation that there

may be significant trauma such as head injuries or subtle abdominal trauma, which will require

appropriate treatment.

Reassessment

Single observations on respiratory and heart rates, degree of recession, blood pressure, conscious

level, pupils, etc. are useful but much more information can be gained by frequent, repeated

observations to detect a trend in the child’s condition. These are commonly now combined into a

scoring system to provide an early warning of deterioration, such as the paediatric early warning

system (PEWS). There is no single validated tool yet, with different systems being used in different

institutions.

Summary: rapid clinical assessment ofan infant or child

Airway and Breathing

z Effort of breathing

z Respiratory rate/rhythm

z Stridor/wheeze

z Auscultation

z Skin colour

z Oximetry

Circulation

z Heart rate

z Pulse volume

z Capillary refill

z Skin temperature

Disability

z Mental status/conscious level

z Posture

z Pupils

Exposure

z Fever

z Rashes and bruising

The whole assessment should take less than a minute

Remember to obtain information from pre- hospital staff about the initial condition of the

child and any treatment given

Once airway (A), breathing (B) and circulation (C) are clearly recognised as being stable or have

been stabilised, then definitive management of the underlying condition should be started

40 PART2 The seriously ill child

3.7 Secondary survey andemergency treatment

The secondary survey takes place once vital functions have been assessed and the treatment of life-

threatening conditions has been instituted. It includes:

z A focused medical history from parents/carers or child

z A review of notes if available and attention to information obtained from pre- hospital staff

z A clinical examination and specific investigations

It differs from a standard medical history and examination in that it is designed to establish which

further immediate measures are required to stabilise the child. Time is limited and a focused

approach is essential. At the end of the secondary survey, the practitioner should have a better

understanding of the illness affecting the child and may have formulated a differential diagnosis.

Emergency treatments will be appropriate at this stage– either to treat specific conditions (e.g.

asthma) or processes (e.g. raised intracranial pressure). The establishment of a definite diagnosis is

part of definitive care.

Some children will present with an acute exacerbation of a known condition such as asthma or

epilepsy. Such information is helpful in focusing attention on the appropriate system, but the prac-

titioner should be wary of dismissing new pathologies in such children. The structured approach

prevents this problem. Unlike trauma (which is dealt with later), illness affects systems rather than

anatomical areas.

After the presenting system has been dealt with, all other systems should be assessed, and any

additional treatments commenced as appropriate.

The secondary survey is not intended to complete the diagnostic process, but rather is intended to

identify any problems that require further emergency treatment.

The following gives an outline of a structured approach of emergency care. It is not exhaustive

but addresses the majority of emergency conditions that are amenable to specific emergency

treatments in this time period. The symptoms, signs and treatments relevant to each emergency

condition are elaborated in the relevant chapters that follow.

CHAPTER 3 Structured approach to the seriously ill child 41

Respiratory

Secondary survey

Box 3.1 gives common symptoms and signs that should be sought in the respiratory system.

Emergency investigations are suggested.

Emergency treatment

z If ‘bubbly’ noises are heard, the airway is full of secretions, which may require clearance by suction

z 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 the child given nebulised

budesonide or adrenaline

z If there is a quiet stridor, drooling and a short history in a sick- looking child, consider epiglottitis

or tracheitis. Intubation is likely to be urgently required, preferably by a senior anaesthetist. Do

not jeopardise the airway by any unpleasant or frightening interventions. Give IV cefotaxime or

ceftriaxone once the airway is secure

z With a sudden onset and significant history of inhalation, consider a foreign body within the airway.

If the ‘choking child’ procedure has been unsuccessful, the child may require laryngoscopy.

Donot jeopardise the airway by unpleasant or frightening interventions but contact a senior

anaesthetist/ENT surgeon urgently. However, in extreme cases of life threat, immediate direct

laryngoscopy to remove a visible foreign body with a Magill forceps may be necessary

z Stridor following ingestion/injection of a known allergen suggests anaphylaxis. Children in

whom this is likely should receive IM adrenaline

z Children with a history of asthma or with wheeze and significant respiratory distress, decreased

peak flow and/or hypoxia should receive oxygen therapy and inhaled β2- agonists. Infants with

wheeze and respiratory distress are likely to have bronchiolitis and require only oxygen if hypoxic

z In acidotic breathing, take a blood sample for acid–base balance and blood sugar. Treat diabetic

ketoacidosis with IV fluid and insulin

Box 3.1 Common symptoms andsigns that should besought inthe respiratory

system

Symptoms

z Breathlessness

z Coryza

z Cough

z Noisy breathing– grunting, stridor,

wheeze

z Drooling and inability to drink

z Abdominal pain

z Chest pain

z Apnoea

z Feeding difficulties

z Hoarseness

Signs

z Cyanosis

z Tachypnoea

z Recession

z Grunting

z Stridor

z Wheeze

z Chest wall crepitus

z Tracheal shift

z Abnormal percussion note

z Crepitations

on auscultation

z Acidotic breathing

Investigations

z Oxygen saturation

z Peak flow if asthma is suspected

z End- tidal/transcutaneous carbon dioxide if hypoventilation is suspected

z Blood culture if infection is suspected

z Chest X- ray/ultrasound (selective)

z Blood gases (selective)

z Viral polymerase chain reaction (PCR)/swab

42 PART2 The seriously ill child

Cardiovascular (circulation)

Secondary survey

Box3.2 gives common symptoms and signs that should be sought in the cardiovascular system.

Emergency investigations are suggested.

Emergency treatment

z Further boluses of fluid should be given to shocked children who have not had a sustained

improvement to the first bolus given at resuscitation

z Consider inotropes, intubation and invasive arterial blood pressure monitoring particularly if

more than 40ml/kg of fluid is needed with signs of ongoing shock

z Consider IV third generation cephalosporin in shocked children with no obvious fluid loss as

sepsis is likely

z If a child has a cardiac arrhythmia the appropriate protocol should be followed

z If anaphylaxis is suspected, give IM adrenaline in addition to fluid boluses

z Give an IV infusion of dinoprostone (prostaglandin or PGE2) or alprostadil (PGE1) urgently if duct-

dependent congenital heart disease is suspected, for instance in neonates with unresponsive

hypoxia or shock

z Surgical advice and intervention may be needed for gastrointestinal emergencies. The following

symptoms and signs may suggest this:

z Symptoms– bilious vomiting, blood per rectum, abdominal pain

z Signs– abdominal tenderness, abdominal mass, abdominal distension

Box 3.2 Common symptoms andsigns that should besought inthe

cardiovascular system

Symptoms

z Breathlessness

z Fever

z Palpitations

z Feeding difficulties

z Sweating with feeds in infants

z Drowsiness

z Pallor

z Shock

z Poor urine output

Signs

z Tachy- or bradycardia

z Hypo- or hypertension

z Abnormal pulse volume or rhythm

z Abnormal skin perfusion or colour

z Cyanosis/pallor

z Hepatomegaly

z Crepitations on auscultation

z Cardiac murmur

z Peripheral oedema

z Absent femoral pulses

z Raised jugular venous pressure

z Hypotonia

z Purpuric rash

Investigations

z Urea and electrolytes

z Liver function tests

z Full blood count

z Blood gas, lactate

z Coagulation studies

z Blood culture

z Electrocardiogram

z Chest X- ray (selective)

CHAPTER 3 Structured approach to the seriously ill child 43

Neurological (disability)

Secondary survey

Box 3.3 gives common symptoms and signs that should be sought in the nervous system.

Emergency investigations are suggested.

Emergency treatment

z For convulsions follow the status epilepticus protocol (see Chapter6)

z If there is evidence of raised intracranial pressure (decreasing conscious level, asymmetrical

pupils, abnormal posturing and/or abnormal ocular motor reflexes) then the child should

undergo:

z Ventilation to maintain end- tidal CO2 (ETCO2) 3.5–4.0kPa (26–30 mmHg) (this is equivalent

to arterial PaCO2 4.0–4.5kPa (30–34mmHg)

z Nursing with head in- line and 20° head- up position (to help cerebral venous drainage)

z Infusion of IV 3% sodium chloride (3ml/kg) or mannitol 0.25–0.5g/kg (i.e. 1.25–2.5ml/kg of

20% solution IV over 15minutes)

z Consider dexamethasone (only for oedema surrounding a space- occupying lesion) 0.5mg/kg

6- hourly

z In a child with a depressed conscious level or convulsions, consider meningitis/encephalitis. Give

third generation cephalosporins and aciclovir with or without ampicillin and with or without

corticosteroids

z In drowsiness with sighing respirations, check blood sugar, acid–base balance and salicylate

level. Treat diabetic ketoacidosis with IV fluids and insulin

z In unconscious children with pinpoint pupils, consider opiate poisoning. A trial of naloxone could

be considered

Box 3.3 Common symptoms andsigns that should besought inthe nervous

system

Symptoms

z Headache

z Convulsions

z Change in behavior

z Change in conscious level

z Weakness

z Visual disturbance

z Fever

Signs

z Altered conscious level

z Altered pupil size and reactivity

z Abnormal posture

z Abnormal oculocephalic reflexes

z Meningism

z Papilloedema or retinal haemorrhage

z Altered deep tendon reflexes

z Hypertension

z Slow pulse

z Full and tense anterior fontanelle

Investigations

z Urea and electrolytes

z Blood sugar

z Liver function tests

z Ammonia

z Blood culture

z Blood gas

z Coagulation studies

z Blood and urine toxicology including

carboxyhaemoglobin level

z Computed tomography brain scan

z Metabolic screen

44 PART2 The seriously ill child

External

Secondary survey

Box3.4 gives common symptoms and signs that should be sought externally.

Emergency treatment

z In a child with circulatory or neurological symptoms and signs, a purpuric rash suggests

septicaemia/meningitis. The child should receive cefotaxime or ceftriaxone as soon as possible

z In a child with respiratory or circulatory difficulty, the presence of an urticarial rash or angioedema

suggests anaphylaxis. Give IM adrenaline immediately

Further history

Developmental andsocial history

Knowledge of the child’s developmental progress and immunisation status may be useful,

particularly in a small child or infant.

Drugs andallergies

Any medication that the child is currently on or has been on should be recorded. If poisoning is a

possibility, it is important to document any medication in the home that the child might have had

access to, as even relatively benign over- the- counter medications for adults may cause serious

toxicity in small children. A history of allergies should be sought.

3.8 Summary

This chapter has described the structured approach to the seriously ill child which enables the

practitioner to focus on diagnosis and emergency treatment.

The primary survey and resuscitation are concerned with the maintenance of vital functions,

while the secondary survey and emergency treatment allow more specific urgent therapies to be

started.

Box 3.4 Common symptoms andsigns that should besought externally

Symptoms

z Rash

z Swelling of lips/tongue

z Fever

Signs

z Purpura

z Urticaria

z Angioedema

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

4.1 Introduction

Respiratory diseases have the highest prevalence in childhood, accounting for up to 30–40% of

acute hospital admissions of children. Acute respiratory illnesses, such as pneumonia, account for

1.8million deaths per year in children under 5 years of age, more than any other illness, in every

region of the world. Disorders outside the respiratory system may also cause breathing difficulties,

including cardiac disease, metabolic and neurological disorders and poisoning (Table4.1).

Most respiratory illnesses are self- limiting minor infections, but some present as potentially life-

threatening emergencies, especially in children with underlying co- morbidity. Accurate diagnosis

and prompt initiation of appropriate treatment are essential if unnecessary morbidity and mortality

are to be avoided in such cases.

Airway and Breathing

CHAPTER 4

Learning outcomes

After reading this chapter, you will be able to:

z Describe why infants and young children are susceptible to respiratory failure

z Assess and treat children with breathing difficulties

z Resuscitate a child with life- threatening breathing difficulties

Table4.1 Causes ofbreathing difficulty inchildren, according tomechanism

Mechanism Cause

Upper airway obstruction Croup/epiglottitis, foreign body inhalation

Lower airway obstruction Tracheitis, bronchiolitis, asthma, foreign body inhalation

Disorders affecting the lungs Pneumonia, lung oedema (e.g. in cardiac disease)

Disorders around the lungs Pneumothorax, pleural effusion or empyema,

rib fractures

Disorders of the respiratory muscles Neuromuscular disorders

Disorders below the diaphragm Peritonitis, abdominal distension

Increased respiratory drive Diabetic ketoacidosis, shock, anxiety attack and hyperventilation

Decreased respiratory drive Coma, convulsions, raised intracranial pressure, poisoning

46 PART 2 The seriously ill child

4.2 Susceptibility torespiratory failure

Severe respiratory illness may result in the development of respiratory failure, defined as an inability

of physiological compensatory mechanisms to ensure adequate oxygenation and ventilation (carbon

dioxide (CO2) elimination), resulting in hypoxia with or without hypercapnia. Young children and

infants develop respiratory failure more readily than older children and adults, reflecting important

differences in their immune status and the structure and function of the respiratory system.

z Children, and particularly infants, are susceptible to infection with many viruses and bacteria to

which adults have acquired immunity

z The airways in children are smaller and more easily obstructed by mucosal swelling, secretions

or a foreign body. Airway resistance is inversely proportional to the fourth power of the radius of

the airway: a reduction in the radius by a half causes a 16- fold increase in airway resistance. Thus,

1mm of mucosal oedema in an infant’s trachea of 5mm diameter results in a much greater

increase in resistance than the same degree of oedema in a trachea of 10mm diameter

z The thoracic cage of young children is much more compliant than that of adults. When there is

airway obstruction and increased effort, this leads to marked recession and a reduction in the

efficiency of breathing. The compliant thorax also provides less support in maintaining lung volume

z In infants, lung volume at end expiration is similar to closing volume, increasing the tendency to

small airway closure and hypoxia

z Children have fewer alveoli, which makes them more susceptible to ventilation–perfusion

mismatch

z The respiratory muscles of young children are relatively inefficient. In infancy, the diaphragm is

the principal respiratory muscle while intercostal and accessory muscles make relatively little

contribution. Fatigue can develop rapidly, resulting in respiratory failure or apnoea

z The pulmonary vascular bed is relatively muscular in infancy, increasing the tendency with

which pulmonary vasoconstriction can occur in, for example, hypoxia. In turn, this can lead to

right- to- left shunting, ductal opening (in the early neonatal period), ventilation–perfusion

mismatch and further hypoxia

z In the first 1–2months of life there may be a paradoxical inhibition of respiratory drive. This may

result in infections presenting with apnoea or hypoventilation rather than the usual increased effort

4.3 Clinical presentations ofthe child withbreathing difficulties

Respiratory conditions can present with respiratory symptoms but also with symptoms within other

systems:

Noisy breathing may be normal for the child or suggest pathology. Parents and carers commonly under-

stand different meanings from those understood by doctors and nurses for the terms used to describe

breathing noises or may have their own terms. Useful historical features include relieving or aggravating

factors (e.g. sleep, crying, feeding, position, exercise) and whether the voice or vocalisations are normal.

Respiratory Breathlessness, tachypnoea, sub- /intercostal recessions, head bobbing (only

in infants), nasal flaring

Cough

Noisy breathing (stridor, wheeze, grunting)

Chest pain

Non- respiratory Poor feeding (infant)

Abdominal pain

Hypotonia, change in conscious level

Tachycardia, change in colour

CHAPTER 4 Airway and Breathing 47

Stridor is a high- pitched sound usually on inspiration from obstruction of the upper airway and

should be distinguished from stertor or snoring, which are lower pitched inspiratory noises sug-

gestive of poor airway positioning or pharyngeal obstruction. Bubbly noises suggest pharyngeal

secretions, often seen in the child with neurodisability who may have long- standing poor airway

control and inability to spontaneously clear secretions. Wheeze is predominantly expiratory from

lower airway obstruction. Grunting is a physiological response (partial closure of

the glottis during expiration) to prevent end- expiratory alveolar collapse in pneumonia or

pulmonary oedema.

Chest pain is an unusual symptom in children. It does not usually reflect cardiac disease as it so

often does in adults but can suggest pneumonia or pleuritis. Similarly, pneumonia may present as

abdominal pain.

While parents are usually alerted to breathing difficulties in toddlers and older children, abnormal

respiration may be more difficult for them to detect in infants. Infants with breathing difficulties

may present with acute feeding problems. Feeding for an infant is one of the most strenuous

activities, and its ease is often taken by parents as a gauge of their infant’s well- being.

Some features suggest a cardiac cause of respiratory inadequacy. These are:

z Cyanosis, not correcting with oxygen therapy

z Tachycardia out of proportion to respiratory difficulty

z Raised jugular venous pressure (difficult to see in young children)

z Gallop rhythm/murmur

z Enlarged liver

z Absent femoral pulses

4.4 Primary survey andresuscitation

This is dealt with in Chapter2. In general, the following ABCDE principles apply to all children with

breathing difficulties.

Airway

z A patent airway is the first requisite. If the airway is not patent, an airway- opening manoeuvre

should be used and, if needed, secured with a pharyngeal airway device or by intubation with

experienced senior help

Breathing

z All children with breathing difficulties should receive oxygen as soon as the airway is opened to

attain SpO2 94–98%. This can be achieved by using a flow of 10–15l/min via a non- rebreathing

mask with reservoir bag, or by using high- flow nasal cannula (HFNC) oxygen therapy. With

decreasing oxygen need, a low- flow nasal cannula or prongs can be used

z Warning: a child requiring more than 50% oxygen through a mask of HFNC to achieve SpO2

94–98% is significantly hypoxaemic and may be at risk of sudden deterioration and cardiac

arrest. Get senior help and urgent review from the critical care team

z If the child is hypoventilating with a slow rate or weak effort, respiration should be supported

with oxygen via a bag–valve–mask device and experienced senior help summoned

Circulation

Fluid intake may have been reduced, particularly in infants with feeding difficulties. Consider a fluid

bolus (10ml/kg of balanced fluids) if there are signs of circulatory failure.

48 PART 2 The seriously ill child

Table4.2 Causes ofupper airway obstruction

Incidence (UK) Diagnosis Clinical features

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

Uncommon Foreign body aspiration Sudden onset, history of choking

Rare Epiglottitis Drooling, muffled voice, septic appearance, absent

cough

Bacterial tracheitis Harsh cough, chest pain, septic appearance

Trauma Neck swelling, crepitus, bruising

Retropharyngeal or peritonsillar

abscess

Drooling, septic appearance

Inhalation of hot gases Facial burns, perioral soot

Infectious mononucleosis Sore throat, tonsillar enlargement

Angioneurotic oedema Itching, facial swelling, urticarial rash

Diphtheria Travel to endemic area, unimmunised

4.5 Secondary survey andlooking forkey features

While the primary survey and resuscitation are being carried out, a focused history of the child’s

health and activity over the previous days and any significant previous illness should be gained. All

children with breathing difficulties will have varying degrees of respiratory distress and cough, so

these are not useful diagnostic discriminators. Certain key features can point the clinician

to the

likeliest working diagnosis for emergency treatment.

z Inspiratory stridor points to upper airway obstruction

z Expiratory wheeze points to lower airway obstruction

z Fever without upper airway symptoms suggests pneumonia

z Signs of heart failure point to congenital/acquired heart disease

z Acute history, allergen exposure and urticarial rash point to anaphylaxis

z Suspicion of ingestion and no clear cardiorespiratory pathology point to poisoning

4.6 General approach tothe child withupper airway obstruction

Obstruction of the upper airway is potentially life threatening. Its small cross- sectional area renders

the young child particularly vulnerable to obstruction by oedema, secretions or an inhaled foreign

body. Table4.2 shows the different aetiologies of upper airway obstruction in children.

In the child with a compromised but functioning airway, an important principle in all cases is to

avoid worsening the situation by upsetting the child. Crying and struggling may quickly convert a

partially obstructed airway into a completely obstructed one. Parents should be encouraged to help

soothe and settle the child.

Airway

Is the airway partially obstructed or narrowed and what is the likely cause? Note the presence of

inspiratory noises.

z ‘Bubbly’ noises suggest pharyngeal secretions requiring clearance. This might suggest that the child

is fatigued or has a depressed conscious level and is unable to clear secretions with their own cough

CHAPTER 4 Airway and Breathing 49

z Stertorous (snoring) noises suggest partial airway obstruction due to a depressed conscious

level

z A harsh stridor and barking cough are suggestive of croup; a quiet stridor in a sick- looking child

without cough point at epiglottitis or tracheitis

z A stridor of sudden onset with no prodromal symptoms or a history suggestive of inhalation,

could mean foreign body aspiration

Breathing

z What degree of effort is needed for breathing and what is its efficacy and effect? The answer to

this question will inform the clinician as to the severity of the upper airway obstruction. A pulse

oximeter should be put in place and the oxygen saturation noted both on breathing air and

high- flow oxygen

4.7 Specific approach tothe child withupper airway obstruction

Most cases of upper airway obstruction in children are the result of infection, but inhalation of a

foreign body or hot gases (house fires), anaphylaxis and trauma can all result in obstruction. The

airway may also become obstructed in the unconscious, supine child.

Partial obstruction fromsecretions or adepressed conscious level

z Use suction to clear secretions as long as there is no stridor

z Support the airway with the chin lift or jaw thrust manoeuvre in a child with stertorous breathing

due to a depressed conscious level or extreme fatigue and seek senior airway support

z Further maintenance of the airway can be accomplished with an oro- or nasopharyngeal airway,

but the child may require intubation

z Whilst help is summoned, continuous positive airway pressure (CPAP) can be given to children

with a reduced conscious level using a face mask, oxygen flow and breathing circuit (e.g. an

anaesthetic breathing circuit (Ayre’s T- piece)), if familiar with using such circuits

Croup

Background

Croup (acute laryngotracheobronchitis) is defined as an acute clinical syndrome with inspiratory

stridor, a barking cough, hoarseness and variable degrees of respiratory distress. Parainfluenza

viruses are the commonest pathogens, but others include respiratory syncytial virus, influenzavirus

and adenovirus. The peak incidence of croup is in the second year of life and most hospital admissions

are in children aged between 6months and 5 years. Between 1% and 5% of children with croup are

admitted.

The typical features (Figure 4.1) of a barking cough, harsh stridor and hoarseness are often

preceded by fever and coryza for 1–3days. The symptoms usually start, and are worse, at night.

Many children have stridor and a mild fever (less than 38.5°C) with little or no respiratory diff iculty.

If tracheal narrowing is minor, stridor will be present only when the child hyperventilates or is

upset. As the narrowing progresses, the stridor becomes both inspiratory and expiratory, and is

present even when the child is at rest. Some children, and particularly those below the age of 3

years, develop the features of increasing obstruction with marked sternal and subcostal reces-

sion, tachycardia, tachypnoea and hypoxia leading to agitation. If the infection extends distally

to the bronchi, wheeze may also be audible. Some children have repeated episodes

of croup.

50 PART 2 The seriously ill child

Treatment

Steroids modify the natural history of croup – they give rise to clinical improvement within

30minutes, and decrease the need for hospitalisation, the duration of hospitalisation and the need

for intubation. Oral steroids (dexamethasone 0.15–0.6mg/kg or prednisolone 1–2mg/kg) are the

treatment of choice, but if the child will not take oral medication or is vomiting, then nebulised

budesonide 2mg can be used. Dexamethasone can be repeated after 24 hours if clinically indicated;

budesonide aerosol can be given more regularly (every 30–60minutes) based on clinical response.

A small proportion of children will need admission to hospital. Based on clinical severity aerosol with

budesonide or adrenaline will be needed. In both cases they should also receive steroids, such as

dexamethasone.

z Give nebulised adrenaline 5ml of 1:1000 with oxygen through a face mask to children with severe

respiratory distress, provided it does not unduly upset the child. This will produce a transient

improvement beginning within 10–30minutes and lasting for up to 2 hours, giving time for the

corticosteroids to take effect. It may need to be repeated, and if so, additional measures should

be taken to ensure the airway is managed by senior staff. Children should be observed closely

with continuous monitoring (three- lead electrocardiogram (ECG) and SpO2), as they may still

deteriorate and require intubation. Adrenaline may contribute to a tachycardia, but other side

effects are uncommon. This treatment is best used to ‘buy time’ in which to assemble an

experienced team to treat a child with severe croup. Failure to respond to nebulised adrenaline

should question the diagnosis of croup– consider bacterial tracheitis, epiglottitis or foreign body

z Give humidified oxygen and monitor SpO2. Hypoxia is a late sign of croup reflecting alveolar

hypoventilation secondary to airway obstruction and ventilation–perfusion mismatch. The

respiratory rate and the degree of recession are more valuable clinical indicators of severity and

response to treatment

z A very small proportion of these children require intubation. The decision to intubate is a clinical

one based on increasing tachycardia, tachypnoea and chest retraction, or the appearance of

cyanosis, exhaustion or confusion. Ideally, the procedure should be performed under gas

induction anaesthesia by an experienced (paediatric) anaesthetist, unless there is respiratory

arrest. A tube of smaller gauge than usual is often required. If there is doubt about the diagnosis

or difficulty in intubation is anticipated, an ENT surgeon capable of performing a tracheotomy

should be present (see Figure19.8)

Figure4.1 Croup

CHAPTER 4 Airway and Breathing 51

Epiglottitis

Background

Acute epiglottitis shares some clinical features with croup, but it is a quite distinct entity. Although

much less common than croup, its importance is that unless the diagnosis is made rapidly and

appropriate treatment commenced, total obstruction and death may ensue. Epiglottitis is due to

infection with Haemophilus influenza b (Hib), which causes intense swelling of the epiglottis and

the surrounding tissues and obstruction of the larynx (Figure4.2). It is thus less commonly

seen in

countries where Hib immunisation is routine but may still occur in cases of vaccine failure or

unimmunised children.

Epiglottitis is most common in children aged 2–6 years, but it can occur in any age group. The onset

of the illness is usually acute with high fever, lethargy, a soft inspiratory stridor and rapidly increas-

ing respiratory difficulty over 3–6 hours. In contrast to croup, cough is minimal or absent. Typically,

the child sits immobile, with the chin slightly raised and the mouth open, drooling saliva. The child

appears very toxic and pale and has poor peripheral circulation (most are septicaemic). There is

usually a high fever (over 39°C). Because the throat is so painful, the child is reluctant to speak and

unable to swallow drinks or saliva.

Treatment

z Intubation is likely to be required. Contact a senior anaesthetist and an ENT surgeon capable of

performing a tracheotomy urgently. When deeply anaesthetised, the child can be laid on their

back to allow laryngoscopy and intubation. Tracheal intubation may be difficult because of the

intense swelling of the epiglottis (‘cherry red epiglottis’) (Figure4.2a). A smaller tube than the

one usually required for the child’s size will be necessary

(a) (b)

Figure4.2 (a) Larynx in epiglottitis, and (b) normal larynx

Disturbance of the child, and particularly attempts to lie the child down, to examine the throat

with a tongue depressor or insertion of an intravenous cannula should only be considered in

the presence of appropriate senior support

52 PART 2 The seriously ill child

z After securing the airway, blood should be sent for culture and treatment with 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 or accompanying H. influenza meningitis are

rare. In countries where the Hib vaccine is in use, there should be an investigation into vaccine

failure

Bacterial tracheitis

Background

Bacterial tracheitis or pseudomembranous croup is an uncommon but life- threatening form of

upper airway infection. Infection of the tracheal mucosa with Staphylococcus aureus, streptococci

or Hib results in copious, purulent secretions and mucosal necrosis. The child appears toxic, with a

high fever and signs of progressive upper airway obstruction. The croupy cough, absence of

drooling and a longer history help distinguish this condition from epiglottitis.

Treatment

Over 80% of children with this illness need intubation and ventilatory support to maintain an

adequate airway, as well as intravenous antibiotics (cefotaxime or ceftriaxone plus flucloxacillin).

Foreign body aspiration

Background

Foreign body aspiration (FBA) must be suspected for any witnessed choking episode. It is commonest

in children less than 3 years of age– a history of a witnessed choking event is very suggestive as the

child is often too young to give a history. Children have a smaller airway than adults and their larynx

is in a relatively high position with the epiglottis close to the root of the tongue, increasing the risk

of aspiration. Incisors bite through food while molars are necessary to masticate food in preparation

for swallowing. Molars erupt approximately 6months after incisors thus infants are unable to pulp

their food and the bite- sized food they generate is the ideal shape to obstruct an airway if aspirated.

Children often run around and talk while chewing, may put non- organic foreign bodies in their

mouth while playing and may be inattentive and easily distractible. Foodstuffs (nuts, grapes, sweets

and meat) are the commonest foreign bodies. In contrast to croup there is usually no history of

prodromal viral upper respiratory tract infection or pyrexia.

Most suspected FBA should have a chest radiograph. Flat objects such as coins tend to align in the

sagittal plane in the trachea whereas objects in the oesophagus tend to align in the coronal plane. The

majority of foreign bodies are radiolucent and therefore not visible on radiographs, but there may be

secondary evidence of localised gas trapping, atelectasis or mediastinal shift. In approximately 20% of

FBA cases, the chest radiograph is normal. Although a history of inhalation may be elicited from the

parent, FBA cannot be excluded on either normal physical examination or chest radiograph.

Treatment

Removal through a bronchoscope under general anaesthetic should be performed as soon as

possible because there is a risk that coughing will move the object into the trachea and cause life-

threatening obstruction.

z Do not jeopardise the airway by unpleasant or frightening interventions but contact a senior

anaesthetist/ENT surgeon capable of performing a tracheotomy urgently. In the case of a

stridulous child with a relatively stable airway and a strong suspicion of foreign body inhalation,

careful gaseous induction of anaesthesia should be used so the foreign body can then be

removed under controlled conditions

CHAPTER 4 Airway and Breathing 53

z In extreme cases of life threat, immediate direct laryngoscopy with Magill’s forceps to remove a

visible foreign body (Figure4.3) may be necessary

Anaphylaxis

Background

Anaphylaxis is a potentially life- threatening, immunologically mediated reaction with respiratory or

circulatory effects that develop over minutes, often associated with skin or mucosal changes.

Laryngeal oedema causing upper airway obstruction is one manifestation. Food, especially nuts,

drugs (including contrast media and anaesthetic drugs) and venom are the commonest causes of

this. Prodromal symptoms of flushing, itching, facial swelling and urticaria usually precede stridor.

Abdominal pain, diarrhoea, wheeze and shock may be additional or alternative manifestations of

anaphylaxis. A severe episode of anaphylaxis can be predicted in children with a previous severe

episode or a history of increasingly severe reaction, a history of asthma or treatment with

β- blockers.

See Chapter5 for further details and emergency treatment of anaphylaxis.

Other causes ofupper airways obstruction

Although croup accounts for the large majority of cases of acute upper airway obstruction, several

other uncommon conditions need to be considered.

Diphtheria is seen only in children who have not been immunised against the disease. Always ask

about immunisations in any child with fever and signs of upper airway obstruction, particularly if

they have been to endemic areas recently. Specific treatment of diphtheric croup includes penicil-

lin, steroids and antitoxin.

Attempts at endotracheal intubation may push a laryngeal membrane into the trachea causing

total airway obstruction; a tracheostomy may be required for children with laryngeal diphtheria.

Marked tonsillar swelling in infectious mononucleosis or severe acute tonsillitis can occasionally

compromise the upper airway. The passage of a nasopharyngeal tube may give instant relief. If

there is impending airway obstruction, corticosteroids often work fast.

Retropharyngeal or peritonsillar abscesses are uncommon, but both can present with fever and

upper airway obstruction together with feeding difficulties. Treatment is by surgical drainage and

intravenous antibiotics.

Figure4.3 Larynx with foreign body obstruction

54 PART 2 The seriously ill child

4.8 Approach tothe child withwheeze

The two common causes of lower respiratory obstruction are:

z Acute severe asthma

z Bronchiolitis

Bronchiolitis is mostly confined to the under 1- year- olds and asthma is much more commonly

diagnosed in the over 1- year- olds.

Acute severe asthma

Background

Acute exacerbation of asthma is the commonest reason for a child to be admitted to hospital in

the UK. One in 11 children is currently receiving treatment for asthma. In 2018, asthma caused 20

deaths in under 14- year- olds in England

and Wales; reviews of such cases often identify preventable

factors in both the recognition and management of the condition. The classic features of acute

asthma are cough, wheeze and breathlessness.

In young children there may be no triggers other than viral infections and no interval symptoms.

Such cases are often termed viral- induced wheeze or episodic viral wheeze but should be treated

as acute asthma. An increase in symptoms and decreasing response to bronchodilators, along with

difficulty in walking, talking or sleeping, all indicate worsening asthma.

Common exacerbation triggers include:

z Poor adherence to therapy, specifically inhaled corticosteroids

z Viral upper respiratory tract infections (URTIs) (most common in the pre- school child)

z Aero- allergen exposure (e.g. house dust mite, pollens, moulds): it is difficult to attribute a cause

and effect relationship because of their ubiquitous nature and the delay in the allergic response

z Air quality: cold air, exposure to a smoky or polluted atmosphere, or chemical irritants such as

paints and domestic aerosols

z Exercise- induced symptoms

z Emotional upset or excitement

Disease severity

Before progressing to specific treatment for acute asthma in any setting, it is essential to assess

accurately the severity of the child’s condition.

Historical features associated with severe or life- threatening asthma flares include:

z A long duration of symptoms and/or regular nocturnal awakening

z Poor response to treatment already given in this episode

z A severe course of previous attacks, including the use of intravenous therapy and admission to a

paediatric critical care unit (PCCU)

Assessing severity can be difficult since clinical signs correlate poorly with the severity of airway

obstruction. Some children with acute severe asthma do not appear distressed, and young children

with severe asthma are especially difficult to assess. The following clinical signs should be recorded

regularly, for example every 30–60minutes, or before and after each dose of bronchodilator:

z Pulse rate

z Respiratory rate, degree of recession, use of accessory muscles of respiration

z Degree of agitation and conscious level

CHAPTER 4 Airway and Breathing 55

z SpO2 (for assessing severity, monitoring progress and predicting outcome in acute asthma. More

intensive inpatient treatment is likely to be needed if the SpO2 is less than 90% in air after initial

bronchodilator treatment)

z Peak flow (can be valuable, but under- 6- year- olds and those who are very dyspnoeic 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 is severe dyspnoea, uncertainty about the diagnosis,

asymmetry of chest signs or signs of severe infection.

Two degrees of severity are described to indicate the appearance of asthmatic children at the most

severe end of the spectrum: severe and life- threatening asthma (Table4.3 and Figure4.4).

Table4.3 Levels of severity of acute asthma attacks in children

Moderate acute asthma Able to talk in sentences

SpO2 ≥92%

PEF ≥50% best or predicted

Heart rate: ≤140/min in children aged 1–5 years

≤125/min in children >5 years

Respiratory rate: ≤40/min in children aged 1–5 years

≤30/min in children >5 years

Acute severe asthma Can not complete sentences in one breath or too breathless to talk or feed

SpO2 <92%

PEF 33– 50% best or predicted

Heart rate: >140/min in children aged 1– 5 years

>125/min in children >5 years

Respiratory rate: >40/min in children aged 1–5 years

>30/min in children >5 years

Life- threatening asthma Any one of the following in a child with severe asthma:

Clinical signs Measurements

Exhaustion PEF <33% best or predicted

Hypotension SpO2 <92%

Cyanosis

Silent chest

Poor respiratory effort

Confusion

Reproduced from SIGN158: https://www.sign.ac.uk/media/1773/sign158- updated.pdf (last accessed March 2023)

PEF, peak expiratory flow.

https://www.sign.ac.uk/media/1773/sign158-updated.pdf

56 PART 2 The seriously ill child

Mild

6 puffs under 6 /

10 puffs over 6

of salbutamol

Consider

3 x in 1 hour

Assess response

after 10 minutes

Consider oral

corticosteroids

Improving

SpO2 over 92%

Improved work of

breathing

Wheeze may still be

present

Talking

Tolerating oral �uids

No red �ags in

history

Wean MDI (spacer)

dosing

Observe

Improving and

stable

Consider and

discuss admission

to ward

Establish MDI

(spacer)/nebuliser

dose interval

based on

response

No improvement

SpO2 under 92%

Increased work

of breathing

Improving

Decreasing O2

requirement

Improved air entry

Not improving

Increased O2

requirement

Poor or no air

entry

6 puffs under 6 /

10 puffs over 6

of salbutamol

Consider

3 x in 1 hour

Assess response

after 10 minutes

Consider oral

corticosteroids

Apply oxygen

Nebulised salbutamol 2.5–5 mg

and ipratropium bromide

250 mcg together 3 x in 1 hour

Consider nebulised

Magnesium sulphate 150 mg

Continually assess for

deterioration

Oral steroid (if no previous steroids)

Continuous nebulised salbutamol

Venous or capillary gas

Secure IV access

Senior review

IV magnesium sulphate

Consider IV steroids

(if not tolerating oral steroid)

Consider chest X-ray

Discuss with paediatric critical care

IV aminophylline or IV salbutamol

according to local guidelines

(consider ondansetron)

Be aware of salbutamol toxicity

Moderate Severe/life threatening

Assess

severity

Treatment of asthma

Does

not require O2

SpO2 over

90–92%

If suspected severe/life threatening

asthma call for senior help while

starting treatment

Requires

oxygen SpO2 under

90–92%

BTS SIGN British Guideline on the Management of Asthma

For de�nitions of asthma, see

90% is acceptable if

patient is improving,

92% is the cut

off to start severe

treatment if patient is

deteriorating

Figure4.4 Treatment of asthma algorithm

MDI, metered dose inhaler

CHAPTER 4 Airway and Breathing 57

Treatment

Drugs

The cornerstone in the treatment of a severe asthma attack is the repetitive administration of

β2- bronchodilator (to relieve bronchoconstriction), the early introduction of systemic corticosteroids

(to relieve inflammation and bronchial thickening) and controlled or titrated flow oxygen

supplementation.

Short acting β2- agonist (SABA), such as salbutamol:

z In those with moderate asthma maintaining SpO2 greater than 92% in air, give 600micrograms

(6 puffs) to children aged under 6 years, and 1000micrograms (10 puffs) for those over 6years

old (practice may differ, follow local guidelines). Use a valved holding chamber (spacer) with/

without a face mask. Children aged 4 years or under are likely to require a face mask connected

to the mouthpiece of a spacer for successful drug delivery. Inhalers should be sprayed into the

spacer in individual puffs and inhaled immediately by tidal breathing. Spacers help the

medication get straight to where it is needed in the lungs, with less medication ending up in the

child’s mouth or throat

z In those with severe or life- threatening asthma with oxygen need, use nebulised salbutamol

2.5mg (under 6 years) or 5mg (over 6 years) with oxygen at a flow of 6–8l/min in order to

provide small enough particle sizes. Higher flows may be used, but more of the nebulised

drug may be lost from the face mask. This can be repeated every 10–20minutes. If the child is

on high- flow oxygen therapy ultrasonic devices can be used to enhance and fasten drug

delivery

Although inhaled drugs should be given first as they are accessible and more acceptable to the

child, intravenous salbutamol has a place in life- threatening episodes that do not respond promptly

to inhaled therapy. A loading dose (15micrograms/kg in children over 2 years, 5micrograms/kg

under 2 years) can be given, but if frequent doses of nebulised salbutamol were used this can be

omitted

Contributors tochapters

James Armstrong BSc BMBS FRCA, Consultant in Paediatric Anaesthesia, Nottingham University

Hospitals NHS Trust, Nottingham

Dave Bramley FRCSEd(A&E) FRCEM FIMCRCSEd, Consultant in Emergency Medicine and Pre-

Hosptial Emergency Medicine, South Tyneside and Sunderland NHS Foundation Trust; Chief

Medical Officer for the Great North Air Ambulance Service

Andrea Burgess FRCS- ORLHNS, Consultant Paediatric ENT Surgeon, Southampton Children’s

Hospital, Southampton

Jonathan Davies MB BChir MA DCH FRCA, Consultant Paediatric Anaesthetist, Nottingham

University Hospitals NHS Trust, Nottingham

Joe Fawke MBCHB FRPCH, Consultant in Neonatal Medicine, University Hospitals Leicester NHS Trust;

National Course Director, RCUK Newborn Life Support (NLS) and Advanced Resuscitation of the

Newborn Infant Courses; ILCOR NLS Task Force Member; Head of East Midlands School of Paediatrics

Chris FitzSimmons FRCEM, Consultant in Paediatric Emergency Medicine, Sheffield Children’s

Hospital NHS Foundation Trust, Sheffield

Julie Grice MRCPCH, Consultant in Paediatric Emergency Medicine, Alder Hey Children’s Hospital

NHS Foundation Trust, Liverpool

Michael J. Griksaitis MBBS(Hons) MSc MRCPCH FFICM, Consultant Paediatric Intensivist,

Southampton Children’s Hospital; Honorary Senior Clinical Lecturer, Faculty of Medicine,

University of Southampton, Southampton

Rachel Harwood MRCS PhD, Registrar in Paediatric Surgery, Alder Hey Children’s Hospital NHS

Foundation Trust; Honorary Clinical Fellow, University of Liverpool, LIverpool

Dan B. Hawcutt BSc(Hons) MBChB(Hons) MD MRCPCH, Reader in Paediatric Clinical

Pharmacology, University of Liverpool; Honorary Consultant, Alder Hey Children’s Hospital;

Director of NIHR, Alder Hey Clinical Research Facility

Giles Haythornthwaite MRCPCH, Paediatric Emergency Medicine Consultant; Clinical Director for

Medical Specialties, Bristol Royal Children’s Hospital; Clinical Lead for Paediatric Trauma,

Southwest Operational Delivery Network, Bristol

Richard Hollander MD, Consultant in Pediatric Critical Care, Beatrix Children’s Hospital, University

Medical Centre Groningen, the Netherlands

Hasnaa Ismail- Koch DM FRCS- ORLHNS, Consultant Paediatric ENT Surgeon, Southampton

Children’s Hospital

Musa Kaleem MBBS MRCPCH FRCR, Consultant Paediatric Radiologist, Alder Hey Children’s NHS

Foundation Trust, Liverpool

Angela Lee MBE PgDip Bsc(Hons) RGN RSCN, Nurse Consultant Paediatric Trauma and

Orthopaedics, Royal Berkshire NHS Foundation Trust, Reading

Chris Moran MD FRCS, National Clinical Director for Trauma, NHS- England and NHS-

Improvement; Professor of Orthopaedic Trauma Surgery, Nottingham University Hospital;

Honorary Colonel, 144 Parachute Squadron, 16Medical Regiment

Clare O’Connell MB BCh BAO FRCEM, Consultant in Emergency Medicine and Paediatric

Emergency Medicine, North Cumbria Intergrated Care Trust

Ahmed Osman MSc MRCPCH FHEA, Consultant Paediatric Intensivist, Southampton Children’s

Hospital, Southampton

Paul Reavley MBChB FRCEM FRCS (A&E)Ed MRCGP DipMedTox, Paediatric Emergency Medicine

Consultant, Bristol Royal Hospital for Children, Bristol

Martin Samuels MD FRCPCH, Consultant Respiratory Paediatrician, Staffordshire Children’s

Hospital and Great Ormond Street Hospital, London

Nandini Sen DTM&H FRCEM, Consultant in Emergency Medicine, Manchester University NHS

Foundation Trust, Manchester

Contributors to seventh edition ix

Andrew Simpson FRCS(Ed) FRCEM MClinEd DCH, Consultant in Emergency and Paediatric

Emergency Medicine, North Tees and Hartlepool NHS Foundation Trust

Edward Snelson MRCPCH, Consultant Paediatric Emergency Medicine, Clinical Lead, Children’s

Emergency Department, Norfolk and Norwich University Hospital, Norwich

Eleanor Sproson FRCS, Consultant Paediatric ENT Surgeon, Queen Alexandra Hospital,

Portsmouth

Sarah Stibbards FRCEM BSc(Hons), Clinical Director, Major Trauma and Consultant Paediatric

Emergency Medicine, Alder Hey Children’s Hospital NHS Foundation Trust, Liverpool

Neil Thompson BSc BMedSci BM BS RCPCH, Consultant in Paediatric Emergency Medicine,

Imperial College Healthcare NHS Trust, London, UK

Robert Tinnion RCPCH MD, Consultant Neonatologist, Royal Victoria Infirmary, Newcastle

Hospitals NHS Foundation Trust, Newcastle

Paul Turner BM BCh FRCPCH PhD, Clinical Reader and Honorary Consultant in Paediatric Allergy

and Clinical Immunology, Imperial College London; Chairperson, Anaphylaxis Committee, World

Allergy Organization

Jamie Vassallo PgCert DipIMC PhD, Emergency Medicine and Pre Hospital Emergency Medicine

Registrar, Post Doctoral Research Fellow, Academic Department of Military Emergency

Medicine

Julian White AM MB BS MD FACTM, Consultant Clinical Toxinologist and Unit Head, Toxinology

Department, Women’s and Children’s Hospital, North Adelaide; Clinical Academic, Discipline of

Paediatrics, Medical School, University of Adelaide, Australia

Andrea Whitney MRCP, Consultant Paediatric Neurologist, Southampton Children’s Hospital,

Southampton

Sarah Wood Paediatric and Neonatal Surgical Consultant, TPD and Governance Lead, Alder Hey

Childrens Hospital NHS Foundation Trust, Liverpool

Bogdana S. Zoica MD, Paediatric Critical Care Consultant, King’s College Hospital, London

Contributors tothe status epilepticus algorithm

Richard Appleton Alder Hey Children’s Hospital NHS Foundation Trust, Liverpool

Melody Bacon Royal London Hospital, Barts Health NHS Trust, London

Harish Bangalore Great Ormond Street Hospital, London

Celia Brand Royal Hospital for Children and Young People, NHS Lothian, Edinburgh

Juliet Browning University Hospitals Dorset, Poole, Dorset

Richard Chin University of Edinburgh; Royal Hospital for Children and Young People, NHS

Lothian, Edinburgh

Susana Saranga Estevan Addenbrooke’s Hospital, Cambridge

Satvinder Mahal Great Ormond Street Hospital, London

Kirsten McHale Royal Alexandra Children’s Hospital, University Hospitals Sussex NHS Foundation

Trust, Brighton

Ailsa McLellan Royal Hospital for Children and Young People, NHS Lothian, Edinburgh

Nicola Milne Epilepsy Scotland, Glasgow

Suresh Pujar Great Ormond Street Hospital, London

Tekki Rao Luton and Dunstable University Hospital, Luton

Steven Short Scottish Ambulance Service, Edinburgh

Stephen Warriner Portsmouth Hospitals University Trust, Portsmouth

Michael Yoong Royal London Hospital, Barts Health NHS Trust, London

It hardly seems possible that it is 30 years ago that I sat down as an overconfident senior registrar

and wrote the preface for the Advanced Paediatric Life Support manual. Now, three decades later:

older, even balder, definitely less overconfident and most probably a little bit wiser, I have been

given the opportunity to reflect on the evolution of the APLS manual and the APLS course by writing

the Foreword to this- the seventh edition.

Believe it or not, at the time it was first published, APLS was a disruptive intervention. By that I mean

that it challenged the status quo and sought to change the very fundamentals of emergency

paediatric practice. At the most basic level it implied quite bluntly that the old Oslerian paradigm of

history, examination, differential diagnosis, investigation and treatment was not fit for purpose in

an emergency situation. Rather the new concept of primary assessment and resuscitation followed

by secondary assessment and emergency treatment was advocated. To make matters worse it

went on to derive, publish and teach a set, algorithmic approach to many clinical problems that had

traditionally been managed by physician choice. As an example, I can well remember the conversa-

tions we, the editors, had about the algorithm for the management of status epilepticus. We finally

constructed an APLS status epilepticus treatment algorithm from the wisps of published evidence

and filled in the gaps with our best guesses. Our logic was that forearmed with an algorithm any

trained practitioner could manage the situation to the point

and continuous infusion (1–5micrograms/kg/min) can be started immediately. Important

side effects include sinus tachycardia and hypokalaemia: serum potassium levels should be

checked regularly, and supplementation may be needed. If high doses are used, salbutamol-

induced lactic acidosis can occur in the absence of poor circulation. β2- adrenergic agents increase

glycolysis and pyruvate production, which is then converted to lactate. The diagnosis of salbutamol-

induced lactic acidosis must be made by elimination, and could lead to increased tachypnea

despite regression of bronchospasm. It is, however, transient and normalises after stopping or

decreasing salbutamol.

Corticosteroids expedite recovery from acute asthma. Give an initial dose equivalent to predniso-

lone 1–2mg/kg (max. 40mg) on the first day, followed by a further 1 mg/kg/day for 2 days. Unless the

child is vomiting, there is no advantage in giving steroids parenterally.

Nebulised ipratropium bromide should be added only in severe or life- threatening asthma

(250micrograms in nebulised solution in children over 2 years, 125micrograms in nebulised solu-

tion under 2 years) three times during the first hour. If used as an adjunctive therapy, lung function

is improved and hospitalisation rates are decreased.

Intravenous magnesium sulphate is a safe treatment for acute asthma if the child fails to respond

to inhaled or nebulised SABA. A dose of 40mg/kg (max. dose 2g) by slow infusion (over 20minutes)

may be used. Studies of efficacy for severe childhood asthma unresponsive to more conventional

therapies have shown evidence of benefit. Nebulised magnesium sulphate (150 mg added to

nebulised solution) may be useful in severe asthma.

Intravenous aminophylline can have a role as a third line bronchodilator in the child who fails to

respond adequately, after considering other add- on treatment options. In view of its poor efficacy and

safety profile and the greater effectiveness and relative safety of SABA, its use is no longer routinely

recommended. However, if needed in severe or life- threatening asthma unresponsive to other treat-

ment, a 5mg/kg loading dose for 20minutes followed by a continuous infusion at 1mg/kg/h can be

58 PART 2 The seriously ill child

considered. Monitoring of serum levels is necessary and if the child is vomiting then stopping the

infusion should be considered.

There is no evidence to support the routine use of inhaled steroids given in addition to systemic

corticosteroids for the treatment of acute asthma in childhood. There is limited support for inhaled

heliox therapy, which may be considered in children who do not respond to standard therapy. If the

child is still unresponsive, cannot inhale bronchodilators, or is considered to be peri- arrest, consider

IV adrenaline 10micrograms/kg.

Emergency treatment

z Assess ABCDE and give controlled or titrated low oxygen via a face mask with a reservoir bag or

via a HFNC. Aim to keep SpO2 at 94–98%

z Give salbutamol 600–1000micrograms via a spacer in moderate or severe asthma, or nebulised

salbutamol 2.5–5mg with ipratropium bromide in life- threatening asthma. This can be repeated

every 10–20 minutes or even continuously as breaks between doses can lead to a rebound of

symptoms

z Give oral corticosteroids or, if too dyspnoeic to swallow or vomiting, give intravenously

z If an infant or child is clearly in respiratory failure with poor respiratory effort, a depressed

conscious level and poor saturation despite maximum oxygen therapy, attempt to support

ventilation with a bag–valve–mask and arrange for urgent intubation. Give an IV bronchodilator

such as salbutamol

z Reassess ABCDE and monitor the response to treatment carefully. Assessment is based on

physical signs and continuous monitoring of oxygen saturation measurements

If not responding or condition deteriorating

z For severe or life- threatening asthma, intravenous bronchodilators are effective: consider IV

magnesium sulphate or salbutamol

z Contact the PCCU or the retrieval service and senior anaesthetic support

z The evidence regarding non- invasive ventilation in children during acute asthma exacerbations

is limited. Invasive mechanical ventilation is rarely required. There are no absolute criteria, as the

decision to intubate is usually based on the clinical condition of the child. If respiratory effort is

poor or deteriorating, or conscious level is depressed, or SpO2 is low and falling despite maximum

oxygen therapy, attempt to support ventilation with a bag–valve–mask device, or with bag–mask

ventilation or T-piece and bag with high- flow oxygen, whilst arranging for urgent intubation.

Intubation is usually preceded by either rapid sequence induction with IV ketamine or

inhalational anaesthesia; both may help bronchodilatation

In cases of acute severe asthma that responds to treatment, there is usually little value to be gained

from routine blood gas measurement. However, in those responding poorly, a blood gas with raised

CO2 should expedite the decision to intubate. Children with acute asthma who require mechanical

ventilation need to be transferred to the PCCU. The prognosis is good, but complications such as air

leak and lobar collapse are common. All intubated children must have continuous end- tidal CO2

monitoring.

If responding andimproving

z If there has been improvement (SpO2 92% or more in air, minimal recession, peak expiratory

flow 50% or more of normal value), it may be possible to consider discontinuing intravenous

treatment

z When oxygen is no longer needed, change from a nebulised bronchodilator to the use of sprays

of a β2- agonist inhaler

z Reduce the frequency of inhaled therapy gradually from every 30minutes to 4- hourly, further

reducing frequency as improvement occurs

CHAPTER 4 Airway and Breathing 59

Inhaler technique should be checked, and an asthma action plan provided. The child’s mainte-

nance treatment should be reviewed and altered if inadequate. Ensure that the child has appropri-

ate medical follow- up.

Other measures

z Reassure the child and avoid upset

z Monitor the heart rhythm and SpO2

z Ensure that there is avoidance of any identifiable trigger

z Intravenous fluids: restrict to two- thirds of the normal requirements

z Antibiotics are usually not indicated as most asthma attacks are triggered by viral infections

Bronchiolitis

Background

Bronchiolitis is the most common serious respiratory infection of childhood: 10% of infants are

affected and 2–3% are admitted to hospital with the disease in their first year of life. Ninety per cent

of patients are aged 1–9months; it is unusual after 1 year of age. There is usually an annual winter

epidemic. Respiratory syncytial virus (RSV) is the pathogen in 60–70% of cases, the remainder being

caused by other respiratory viruses such as influenza or parainfluenza, human metapneumovirus

(hMPV) and adenoviruses. Secondary bacterial involvement is uncommon.

Fever and a clear nasal discharge precede a dry, sharp cough and increasing breathlessness.

Wheezing or fine end- expiratory crackles may be audible on auscultation. There is tachypnoea

and subcostal and intercostal recession, often with head bobbing in the infant. Feeding difficulties

associated with increasing dyspnoea are often the reason for admission to hospital. Apnoea is a

serious and potentially fatal complication and is seen particularly in infants born prematurely.

Infants with co- morbidities including premature birth, immunodeficiency, congenital heart

disease or chronic lung diseases are more prone to develop severe disease, as are very young

infants (less than 6weeks old). The natural history of bronchiolitis is of a self- limiting disease that

usually lasts 7–10days.

Infants with bronchiolitis rarely need a chest radiograph. If performed it usually shows hyperinfla-

tion and often evidence of collapse or consolidation, particularly in

the upper right lobe (Figure4.5).

Figure4.5 Chest radiograph demonstrating lung hyperinflation with a flattened diaphragm and bilateral atelectasis in

the right apical and left basal regions in a 16- day- old infant

Matteo Di Nardo / Wikimedia Commons / CC BY 2.0

60 PART 2 The seriously ill child

RSV and other viruses can be identified on nasopharyngeal secretions. Blood gas analysis, which is

required in only the most severe cases, shows lowered oxygen and raised CO2 levels.

Bronchiolitis may trigger heart failure in an infant with a previously undiagnosed cardiac lesion. On

the other hand, bronchiolitis and cardiac decompensation can have a similar clinical picture in an

infant. Table4.4 lists features to help in distinguishing between these conditions.

Treatment

Management is primarily supportive – fluid replacement, gentle suctioning of nasal secretions,

prone position (if in hospital), oxygen therapy and respiratory support if necessary.

z Assess ABCDE

z Ensure that the airway is patent: use of a suction catheter can clear the nose and nasopharynx,

which can have a significant impact on an infant’s respiratory distress. Installation of sodium

chloride nasal drops may help to ‘thin’ and clear nasal secretions

z Give a high concentration of oxygen via a nasal cannula (max. 2 l/min). Aim at SpO2 94–98%.

Consider using humidity, prone positioning and HFNC humidified systems (flows of 2l/kg/min

for the first 10kg, then 0.5l/kg/min)

z Maintain hydration and nutrition. In infants with significant respiratory distress, maintain

hydration by feeding via a nasogastric tube; intravenous fluid (at two- thirds the usual

maintenance) is seldomly needed. Breastfeeding may be too stressful, in which case breast milk

should be expressed and given via a nasogastric tube

z Monitor for apnoea/hypoventilation (especially in those less than 2months old), SpO2, respiratory

frequency and PCO2 (transcutaneous, capillary or end- tidal)

z HFNC therapy and non- invasive continuous positive airway pressure (nCPAP) are both believed

to improve the work of breathing by preventing dynamic airway collapse during expiration,

thereby reducing air trapping and improving gas exchange. Their place is as rescue therapies

when low- flow oxygen has failed

z Mechanical ventilation is required in 2% of infants admitted to hospital. Indications to intubate

include recurrent apnoea, impending exhaustion or severe respiratory distress. After intubation

SpO2 and end- tidal or transcutaneous PCO2 should be continuously monitored

z Both nebulised 3% sodium chloride and nebulised adrenaline with oral corticosteroids have

been subjected to trials, but without showing substantial benefit. Bronchodilators, steroids and

physiotherapy are not useful. Antibiotics should only be considered if concomitant bacterial

infection is strongly suspected

Table4.4 Features that help distinguish heart failure frombronchiolitis

Heart failure Bronchiolitis

Feeding difficulty with growth failure Feeding difficulty

Coryzal and harsh cough

Tachycardia and tachypnoea Tachycardia, tachypnoea, dyspnoea

Pallor, sweating and cool peripheries Restlessness, sweating

Large heart with displaced apex beat Normal or apparently small heart

Large liver Liver lower than normal due to hyperinflation

Gallop rhythm

Murmur No murmur

Pulmonary congestion and large heart on chest X- ray Hyperinflation on chest X- ray

CHAPTER 4 Airway and Breathing 61

4.9 Approach tothe child withfever andbreathing difficulties

Although many causes of breathing difficulties are associated with infection, a high fever is usually

associated only with pneumonia, epiglottitis and bacterial tracheitis. Many cases of asthma are

precipitated by an URTI, but the asthmatic child is rarely febrile, and a low- grade fever is characteristic

of bronchiolitis. Therefore, in the absence of stridor and wheeze, breathing difficulties in association

with a significant fever are likely to be due to pneumonia.

Pneumonia

Background

Pneumonia in childhood was responsible globally for 14% of deaths of children aged under 5 years in

2019 (WHO data). Infants, and children with congenital abnormalities or chronic illnesses, are at particular

risk. A wide spectrum of pathogens causes pneumonia in childhood, and different organisms are

important in different age groups. The incidence of viral infections decreases with increasing age, while

the incidence of bacterial infections remains stable across all ages. Viral infections typically peak during

the autumn and winter season, whereas bacterial pneumonia exhibits less marked seasonal fluctuation.

Fever, cough, breathlessness and chest recession in the younger child and lethargy are the usual pre-

senting symptoms of pneumonia. 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 is usually swallowed. Pleuritic

chest pain, neck stiffness and abdominal pain may be present if there is pleural inflammation. Classic

signs of consolidation such as decreased percussion, decreased breath sounds and bronchial breathing

are often absent, particularly in infants, and a chest radiograph or ultrasound is needed. This may show

lobar consolidation, widespread bronchopneumonia or, rarely, cavitation of the lung. Pleural effusions

may occur, particularly in bacterial pneumonia and this may organise to empyema. An ultrasound of the

chest will delineate the size and nature of pleural collection and if needed will guide placing of a chest

drain. Blood cultures, swabs for viral isolation and a full blood count can be performed.

Treatment

z Assess ABCDE

z Provide a high concentration of oxygen via a face mask with reservoir bag or HFNC or low- flow

oxygen via a nasal cannula. Attach a pulse oximeter and aim at SpO2 greater than or equal to

92%. Airway and breathing support may be especially needed in children with neurodisability or

Pathogens at different ages

Newborn Escherichia coli, other Gram- negative bacilli

Group B β- haemolytic Streptococcus

Chlamydia trachomatis

Infancy Vi ruses: respiratory syncytial virus (RSV), influenza, parainfluenza, bocavirus,

human metapneumovirus

Adeno- and rhinoviruses

Streptococcus pneumoniae

Haemophilus influenza

Staphylococcus aureus

Bordetella pertussis

School age Streptococcus pneumoniae

Mycoplasma pneumoniae

Chlamydia pneumoniae

Respiratory viruses (see above)

62 PART 2 The seriously ill child

(a) (b)

Figure4.6 (a, b) Chest X- rays of pneumonia with a chest drain in place (b)

(a) Tewan Banditrakkanka/Shutterstock.com

neuromuscular weakness, who may have poor airway control and weak respiratory muscles even

when well. These children could also benefit from secretion management techniques which are

usually not needed in previously healthy children with community- acquired pneumonia

z Maintain hydration: extra fluid may be needed to compensate for loss from fever and tachypnoea,

or restriction (70%) may be needed because of an increase in antidiuretic hormone secretion

leading to SIADH (syndrome of inappropriate antidiuretic hormone). Fluid overload can

contribute to worsening breathlessness

z It is not possible to differentiate reliably between bacterial and viral infection on clinical,

haematological or radiological grounds, so children diagnosed as having significant pneumonia

should receive antibiotics. Oral antibiotics are sufficient in most cases, unless there is vomiting

or severe respiratory distress: that is, infants and children who look toxic, have definite dyspnoea,

an SpO2 below 92%, grunting or signs of dehydration. The initial choice of antibiotics depends on

the age of the child and local policy. Newborns and young infants should receive broad- spectrum

intravenous antibiotics. For older infants and preschool children, oral amoxicillin is suitable.

Check for any antibiotic allergy. Antibiotics should be given

for 3–10days (or as per local policy)

although complicated pneumonias (e.g. with empyema) may require several weeks’ duration.

Other options include the use of:

z Flucloxacillin– if Staphylococcus aureus is suspected

z Macrolides– if atypical pneumonia (school- aged children) or pertussis is suspected

z Clinical examination and the chest radiograph may reveal a pleural effusion (Figure4.6). This

should be confirmed with ultrasound and, if large, it should be drained to relieve breathlessness,

aid diagnosis and allow the instillation of intrapleural fibrinolytic agents. Ultrasound may guide

the positioning of a chest drain. Details of the procedure can be found in Chapter21

Techniques forsecretion management

Airway positioning and suctioning

Nebulised sodium chloride or ipratroprium

Increased humidification: high- flow nasal cannula

Antisialagogues*: hyoscine, glycopyrronium, atropine

Mucolytics: nebulised acetylcysteine, erdosteine, DNAse

Physiotherapeutic adjuvants: use of positive pressure, airway vibration or oscillation

* Use with caution in children with a poor cough (often seen in children with neurodisability) as they may

be prone to mucous plugging and lower airway obstruction

CHAPTER 4 Airway and Breathing 63

Mechanical ventilation is rarely required unless there is a serious underlying condition. Transfer to

the PCCU should be considered with the following: an FiO2 of more than 0.6 to keep SpO2 more than

94%, shock, impending exhaustion, rising PCO2, apnoea or irregular breathing. If a child has recur-

rent or persistent pneumonia, they should be referred to a respiratory specialist so further investiga-

tion may be undertaken.

4.10 Other conditions that may present asbreathing difficulties

Heart failure

Infants and children with serious cardiac pathology may present with breathlessness, cyanosis or

cardiogenic shock. The immediate management of shock is described in Chapter5.

Background

In infancy, heart failure is usually secondary to structural heart disease, and medical management

is directed at improving the clinical condition prior to definitive surgery. There are some complex

congenital heart defects in which the presence of a patent ductus arteriosus (PDA) is essential to

maintain pulmonary or systemic flow. The normal ductus arteriosus closes functionally in the first

24 hours of life. Infants with duct- dependent right or left heart lesions present in the first few days

of life as the ductus arteriosus starts closing in response to transition from fetal to postnatal life.

With modern obstetric management, many infants with congenital heart disease are now diagnosed

antenatally so that they may be delivered within cardiac units. Newborns also more commonly

undergo newborn oximetry screening, which also allows earlier detection of cases. This has resulted

in fewer infants with serious congenital heart disease, including those with duct- dependent disease,

presenting to paediatric or emergency departments.

In the older child, myocarditis and cardiomyopathy are the usual causes of the acute onset of heart

failure. Although there are many causes for myocarditis, in most children it is triggered by an infec-

tion, usually viral. Presenting features include fatigue, effort intolerance, anorexia, abdominal pain

and cough. The presence of chest pain and arrhythmia should also be included as clues towards a

diagnosis of myocarditis. On examination, a marked sinus tachycardia, hepatomegaly and raised

jugular venous pressure are found with inspiratory crackles on auscultation. ECG and cardiac

enzymes may be helpful in diagnosis.

Emergency treatment ofheart failure

z Assess ABCDE

z If needed, give high- flow oxygen by face mask with a reservoir or HFNC

z 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 Chapter5)

Causes of heart failure that may present as breathing difficulties

Left ventricular volume overload or excessive pulmonary blood flow

Ventricular septal defect (VSD) Atrioventricular septal defect (AVSD)

Common arterial trunk Patent ductus arteriosus (PDA)

Left heart obstruction

Hypertrophic cardiomyopathy Critical aortic stenosis

Aortic coarctation Hypoplastic left heart syndrome

Primary ‘pump’ failure

Myocarditis Cardiomyopathy

Dysrhythmia

Supraventricular tachycardia Complete heart block

64 PART 2 The seriously ill child

z If circulation is adequate and SpO2 is normal or improves significantly with oxygen but there are

signs of heart failure, then breathing difficulties are due to pulmonary congestion secondary to

a large left- to- right shunt. The shunt may be through an atrioventricular septal defect (AVSD),

ventricular septal defect (VSD), PDA or, more rarely, an aortopulmonary window or truncus

arteriosus. In many cases a heart murmur will be heard. A chest X- ray usually provides supportive

evidence in the form of cardiomegaly and increased pulmonary vascular markings. Diuretics

should be commenced, for example a combination of loop diuretics (furosemide) with a

potassium- sparing diuretic (amiloride or spironolactone) in twice or thrice daily doses. Electrolytes

should be checked prior to commencing diuretics

z Babies in the first few days of life who present with breathlessness and increasing cyanosis

largely unresponsive to oxygen supplementation are likely to have duct- dependent congenital

heart disease such as tricuspid or pulmonary atresia. Start prostaglandin to maintain the

patency of the ductus arteriosus (see Chapter3 for further details)

z Children of all ages who present with breathlessness from heart failure may have myocarditis.

This is characterised by a marked sinus tachycardia and the absence of signs of structural

abnormality. The patients should be treated with oxygen and diuretics, but often are transferred

to the PCCU in need of inotropes or vasopressors

A full blood count and measurements of serum urea and electrolytes, calcium, glucose, heart

enzymes, inflammatory parameters and (arterial) blood gases with lactate should be performed on

all children in heart failure. A routine infection screen including blood cultures is recommended,

especially in infants. A full 12- lead ECG and a chest radiograph are essential. All patients suspected

of having heart disease should be discussed with a paediatric cardiologist, as transfer to a tertiary

centre will usually be required. Echocardiography will establish the diagnosis in most cases.

Diabetic ketoacidosis

As hyperventilation is a feature of the severe acidosis produced by diabetes, occasionally a child

may present with a primary breathing difficulty. The correct diagnosis is usually easy to establish,

and management is described in Appendix B.

Intoxication

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

respiratory rate may be increased by poisoning with:

z Salicylates

z Ethylene glycol (antifreeze)

z Methanol

z Cyanide

However, usually only poisoning with salicylates causes any diagnostic dilemma. Poisoning with

drugs that cause a depression of ventilation will present as a diminished conscious level. The

management of the poisoned child is dealt with in Appendix F.

4.11 Summary

This chapter has discussed the range of mechanisms and possible causes that make children and

infants particularly susceptible to respiratory failure. The clinician should take a structured approach

to assessing, managing and treating the child with breathing difficulties.

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

5.1 Introduction

The role of the cardiovascular system is to ensure that adequate oxygen is delivered to the end

organs and tissues, and to facilitate the removal of waste products away from

tissues. Failure of the

cardiovascular system to carry out this role can lead to critical illness and shock. Before considering

the pathophysiology of shock, it is important to understand some basic normal physiology.

5.2 Normal physiology ofoxygen delivery

Oxygen delivery (DO2) to tissues is dependent on two factors: (i) the cardiac output; and (ii) the

content of oxygen in arterial blood. Both are needed to ensure tissues are well perfused with

adequate amounts of oxygen.

Cardiac output is the volume of blood ejected from the heart per minute and is calculated as a

product of heart rate multiplied by stroke volume (volume of blood ejected from the heart per

beat). Children have a limited capacity to acutely increase stroke volume, meaning that to increase

the cardiac output in times of illness the main physiological mechanism is to increase the heart

rate.

Circulation

CHAPTER 5

Learning outcomes

After reading this chapter, you will be able to:

z Describe the pathophysiology of shock

z Identify the causes of circulatory failure in infants and children

z Describe how to assess children with cardiovascular failure

z Describe how to resuscitate the child with life- threatening shock

z Describe the emergency treatment of the different causes of circulatory failure including

arrhythmias

z Identify the properties of different resuscitation fluids

This is important as an isolated tachycardia in a child can be the first warning sign that the

cardiac output is compromised

66 PART 2 The seriously ill child

The stroke volume is reliant on three components, all of which can be compromised in critical illness:

1. Preload:

z The circulating volume that returns to the heart (filling of the heart or end diastolic volume)

z This can be reduced in situations such as major haemorrhage, fluid loss (e.g. gastroenteritis) or

fluid redistribution (e.g. capillary leak in sepsis)

2. Contractility:

z The strength of the cardiac muscle contraction to generate the pressure to allow blood to eject

z This can be reduced in situations such as cardiomyopathy or myocarditis

3. Afterload:

z The resistance the heart must eject against

z This is increased when the circulation is vasoconstricted or when there is a fixed obstruction

such as aortic stenosis, and decreased when the circulation is vasodilated (e.g. some presentations

of sepsis). Positive pressure ventilation also reduces left ventricular afterload

Content ofoxygen inarterial blood

The arterial oxygen content of blood is mostly dependent on the amount of haemoglobin and the

percentage of haemoglobin carrying oxygen (oxygen saturation usually measured by peripheral

pulse oximetry). There is also a very small amount of oxygen dissolved in plasma.

Oxygen delivery (DO2) can therefore be calculated by applying an equation to the these concepts

(Figure 5.1). This means when dealing with inadequate oxygen delivery in critical illness (shock),

patient management needs to be orientated to optimising the various aspects of this equation.

5.3 Pathophysiology ofshock

Shock describes a clinical situation of circulatory failure, with inadequate oxygen delivery to

tissues to meet their metabolic demands. This leads to cellular hypoxia and if not recognised and

treated quickly leads to worsening cellular hypoxia, acidosis and loss of normal organ function

and subsequently death.

DO2

Preload

Afterload

Contractility

CaO2

1.34 × [Hb] × SaO2

0.003 × PaO2

DO2 = {Heart rate × stroke volume} × {(Hb × 1.34 × SaO2) + (PaO2 × 0.003)}

Putting it all together...

Factors determining the stroke volume:

Preload

Contractility

Afterload

Factors determining the CaO2:

Hb = Concentration of the haemoglobin (g/l)

1.34 = Oxygen binding capacity of Hb (ml/g)

SaO2 = Arterial oxygen saturation (% expressed as

a function)

PaO2 = Partial pressure of oxygen (mmHg)

0.003 = Solubility constant for oxygen (ml/mmHg)

Factors determining the heart rate:

Intrinsic catecholamine release

Intrinsic electrical cardiac conduction

Figure5.1 Oxygen delivery equation

Hb, haemolglobin; HR, heart rate; SV, stroke volume

CHAPTER 5 Circulation 67

Whilst the causes of the shock can vary, the fundamental physiology remains the same: oxygen delivery

to tissues is inadequate (e.g. cardiomyopathy), oxygen consumption (VO2) is higher than normal (e.g. in

sepsis), oxygen carriage is abnormal (e.g. haemoglobinopathies) or a combination of these reasons.

Without intervention shock will progress, and whilst becoming more clinically obvious will also

carry higher morbidity and mortality with delaying intervention. It is important to have early recog-

nition of shock to try and fully reverse it before end- organ injury occurs.

Homeostasis describes the physiological responses that maintain normal body function, and in this

case, normal oxygen delivery. In young people homeostasis is often very effective, making it difficult

to spot changes in oxygen delivery in the early stages of illness so the clinician must have a low

threshold for considering early shock.

In early shock (sometimes referred to as compensated shock), the body activates a variety of phys-

iological processes to redirect oxygenated blood to the key organs (i.e. heart and brain). Sympathetic

nervous activity leads to a tachycardia (to increase oxygen delivery by increasing the cardiac out-

put) and causes vasoconstriction of peripheral vasculature to increase preload and redivert blood

away from non- essential tissues. There may be a mild tachypnoea to increase oxygen intake and

carbon dioxide (CO2) removal to compensate for the developing metabolic acidosis due to activa-

tion of anaerobic metabolism as a source of energy production. Children can compensate for

early shock very well. Often an isolated tachycardia or tachypnoea are the onlyclues.

As shock progresses, the body’s homeostasis starts to fail (often referred to as uncompensated

shock). At this point cellular hypoxia has worsened and multiorgan failure starts to develop.

If shock is still not managed appropriately then the cellular damage cannot be reversed despite full

management, and cardiac arrest and death will occur. This is often known as irreversible shock.

It is vital that the features of shock are identified before it becomes irreversible, remembering that

not all features will be present as shock is a spectrum. A low threshold for considering shock should

be present when there are only one or two of these features:

General clinical features

z Tachycardia

z Tachypnoea

z Failure to detect pulse oximeter probe tracing

z Cool or very warm, flushed peripheries

z Weak or bounding pulses

z Prolonged capillary refill time OR very rapid (flash) refill time

z Grey/mottled/pale skin appearances or very flushed

z Blood pressure may be normal or low. Sometimes only the diastolic is low with a wide pulse pressure

z Blood pressure can also be high due to peripheral vasoconstriction, sometimes with a narrow

pulse pressure

z Changes in activity level: agitation, not responding to usual social cues, drowsiness or unconsciousness

z Reduced urine output

Blood gas results

z Raised lactate

z Metabolic acidosis

z Low PaCO2 (due to hyperventilation to compensate for metabolic acidosis)

Laboratory results

z Disseminated intravascular coagulation (raised international normalised ratio (INR) and activated

partial thromboplastin time ratio (aPTTr) and low fibrinogen and low platelets)

z Acute kidney injury (raised urea and creatinine)

z Acute liver injury (raised alanine transaminase/aspartate aminotransferase, bilirubin)

z Bone marrow suppression (low platelets, low haemoglobin)

68 PART 2 The seriously ill child

5.4 Classification ofcauses ofshock

Shock is classically divided into five categories based on aetiology: hypovolaemic, distributive,

cardiogenic, obstructive or dissociative. Several mechanisms often coexist.

Some of the potential classifications and

causes of shock are listed in Table5.1. The most common

cause in paediatric patients is hypovolaemia from several different conditions. It must be stated

again that the cause of shock can be multifactorial. For example, in septic shock, hypovolaemia,

cardiogenic and distributive shock frequently occur simultaneously.

5.5 Approach tothe child incirculatory failure

Early recognition and treatment of cardiovascular failure leading to shock is crucial and requires a

high index of suspicion. The initial ABCDE approach is generic and used whatever the underlying

cause, However, it is helpful to have a working knowledge of the conditions that predispose children

of different ages and co- morbidities to shock. For example, it is important to know if there is a

history of congenital heart disease, immunodeficiency, trauma, surgery, toxin ingestion or allergies.

Other than certain obvious causes of shock like external haemorrhage, signs and symptoms of early

compensated shock can be easily missed.

The child may present with fever, rash, pallor, poor feeding or drowsiness. A high level of vigilance

should be maintained during the entire assessment of any patient. It may be difficult to recognise

Table5.1 Categories andexample causes ofshock

Categories Aetiology Cause

Hypovolaemic Loss of fluid Haemorrhage

Gastroenteritis

Surgical abdomen (e.g. intussusception,

volvulus, perforation)

Burns

Diabetic ketoacidosis

Third space fluid loss (e.g. sepsis, pancreatitis)

Distributive Alterations in

vascular tone

Sepsis

Anaphylaxis

Vasodilating drugs (e.g. anaesthesia)

Spinal cord injury

Cardiogenic Pump failure Arrhythmias

Cardiomyopathy/myocarditis

Congenital heart diseases (e.g. coarctation of

the aorta)

Valvular disease

Myocardial contusion

Obstructive Flow restriction Congenital heart disease (e.g. coarctation of

the aorta, hypoplastic left heart, aortic

stenosis)

Pneumothorax

Pleural effusions/haemothorax

Cardiac tamponade

Pulmonary embolism

Dissociative Oxygen- carrying

ability problem

Profound anaemia

Carbon monoxide poisoning

Methaemoglobinaemia

Cyanide poisoning

CHAPTER 5 Circulation 69

shock in children with neurodisability as their baseline physiology may include cool peripheries,

and they may be unresponsive to voice and painful stimuli. A high index of suspicion is needed to

diagnose circulatory shock in these children.

Parents or carers can be valuable in knowing what is normal for these children. Evaluation of car-

diac output is a challenge for any clinician, so multiple parameters should be actively assessed. One

‘good’ value can be often misleading, for example capillary refill time can be normal in toxic shock

syndrome despite shock being present.

5.6 Primary survey andresuscitation

Children with circulatory failure have a high likelihood of collapse and even cardiac arrest. There

should be a low threshold for using a medical emergency call to gather a team with advanced skills

in paediatric resuscitation.

Although our approach is based on the sequential ABCDE method, a well- trained team can do mul-

tiple assessments and tasks simultaneously. When using this team- based approach an understand-

ing of human factors is essential and situational awareness is required of the team leader as well as

different team members (see Chapter2).

[A] Airway

z Ensure the airway is open: consider airway- opening manoeuvres, airway adjuncts or urgent

induction of anaesthesia and intubation to secure the airway

[B] Breathing

z There is often tachypnoea to compensate for metabolic acidosis

z Children can have a combined respiratory and circulatory problem

z Point of care ultrasound (POCUS) may be used for rapid assessment (see Appendix I)

Emergency treatment

z If the child is obviously shocked give high- flow oxygen through a face mask with a reservoir or

start HFNC

z Use pulse oximetry and aim for SpO2 greater than or equal to 94–98%

z If hypoventilating support with oxygen via a bag–valve–mask device or breathing circuit such as

the Ayres T- piece and seek experienced help for early intubation and mechanical ventilation

[C] Circulation

z Monitor the heart rate/rhythm with a continuous three- or five- lead electrocardiogram (ECG).

Measure non- invasive blood pressure and use a short cycle time (1–5minutes) if possible. Note

capillary refill time and central and peripheral pulsations

z If the heart rate is above 200 beats/min in an infant, above 150 beats/min in a child or very slow,

consider arrhythmia and do a 12- lead ECG

z POCUS may be used for rapid assessment of cardiac function (see Appendix I)

Emergency treatment

z Gain intravenous (IV) or intraosseous (IO) access:

z Insert one, or ideally two, IV cannulae if possible; immediately proceed to IO access if peripheral

venous access is difficult

z Central access (femoral, jugular or subclavian) can be used when peripheral or IO access is

impossible and experienced help is available (see Chapter20)

z Take blood for blood gas (normally includes lactate, glucose, haemoglobin, sodium, potassium

and ionised calcium). A raised lactate is a key discriminator of critical illness in the presence of

70 PART 2 The seriously ill child

clinical signs of shock and resuscitation should begin immediately. If the lactate is above 4mmol/l,

referral to paediatric critical care should be made without delay. Other laboratory tests are not a

priority and depend on the potential underlying cause (e.g. full blood count (FBC), electrolytes,

renal and liver function tests, C- reactive protein (CRP) or procalcitonin, blood culture, bacterial

polymerase chain reaction (PCR), crossmatch and coagulation studies)

z Primary treatment of potential hypovolaemic shock is fluid resuscitation. Give 10ml/kg of isotonic

crystalloid over 5–10minutes and reassess after each bolus. Titrate fluid resuscitation at the bedside

to reverse shock (tachycardia, hypotension, capillary refill time, peripheral pulses, lactate and level

of consciousness). If there is no improvement after 20–40ml/kg of fluid, prepare vasoactive drugs

(e.g. adrenaline infusion). Rarely, the total volume of fluid resuscitation can be as high as 60–80ml/kg

in special circ*mstances. In settings without easy access to intensive care facilities which have

inotropes and mechanical ventilation, more caution is warranted. If fluid boluses worsen signs of

shock, pulmonary oedema or hepatomegaly then stop giving fluid

z Expert advice regarding intubation and ventilation should be sought in children with shock who

have not responded to fluid resuscitation. Mechanical ventilation decreases the energy

requirements of the heart and respiratory muscles and helps reduce the risk of development of

pulmonary oedema

z Be cautious in those with primary cardiogenic shock or in those with signs of raised intracranial

pressure (ICP): the first group may still benefit from a judicious fluid bolus (5ml/kg) to optimise

preload but seek the urgent advice of a paediatric cardiologist or paediatric intensivist for further

treatment. In children with signs suggestive of raised ICP (i.e. relative bradycardia and hypertension,

posturing or seizures), hypotension is detrimental for cerebral perfusion, but excessive fluids

carry the theoretical risk of worsening cerebral oedema; hence fluids should be given cautiously

z Also be cautious with fluids in children with diabetic ketoacidosis; follow local guidelines, which

usually start with a 10ml/kg fluid bolus

z Catheterise the child and measure hourly urine output

z In non- hypotensive children with severe haemolytic anaemia (severe malaria or sickle cell

crises), blood transfusion is superior to crystalloid boluses

z In children with suspected severe dengue as the cause of the shock, refer to dengue- specific

resuscitation guidelines (WHO, 2022)

z Give a broad- spectrum antibiotic such as ceftriaxone or cefotaxime for those with an obvious or

suspected diagnosis of septicaemia,

or in those where the aetiology is unknown. Blood cultures

should be obtained before administering antibiotics when possible, but this should not delay

their administration

z In children with trauma, haemorrhage must be looked for and controlled for effective

management of shock (see Chapter8)

z If a tachy- /bradyarrhythmia is identified as the cause of shock, special algorithms should be

used (see Section5.14)

z If anaphylaxis is likely (e.g. in urticarial rash or possible recent allergen exposure) then give IM

adrenaline (see Figure5.3)

[D] Disability

z Conscious level (AVPU): agitation at first, evolving to obtundation and coma

z Posture: children in shock are usually hypotonic

z If there is coexistent evidence of raised ICP, manage as in Chapter6

[E] Exposure

z Rash can help identify the cause of shock, but can also be absent. Haemorrhagic purpura,

although characteristic of meningococcal sepsis, may be seen in sepsis of other aetiologies

particularly pneumococcal sepsis. Generalised erythema, conjunctivitis and mucositis may

indicate toxic shock syndrome

z Bruising may suggest occult trauma due to inflicted injury

z Fever suggests an infective cause

CHAPTER 5 Circulation 71

‘Don’t ever forget glucose’ (DEFG)

Hypoglycaemia may give a similar clinical picture to that of compensated shock. This must always

be excluded by an urgent glucose bedside test and blood glucose estimation. Shock and

hypoglycaemia may coexist due to limited glycogen reserves and the fact that ill children may not

have had adequate nutritional intake.

Treat hypoglycaemia (blood glucose less than 2.8mmol/l or 50mg/dl) with a bolus of 3ml/kg 10%

glucose.

5.7 Key features ofthe child inshock

While the primary survey and resuscitation are being carried out, a focused history of the child’s

health and activity over the previous 24 hours and any significant previous illness should be gained.

Certain key features that will be identified from this– and the initial blood test results– can point

the clinician to the likeliest working diagnosis for emergency treatment.

z A history of vomiting and/or diarrhoea points to fluid loss either externally (e.g. gastroenteritis)

or into the abdomen (e.g. volvulus, intussusception or ruptured appendix)

z The presence of fever and/or rash points to septicaemia

z The presence of urticaria, angioneurotic oedema or a history of allergen exposure points to

anaphylaxis

z The presence of cyanosis unresponsive to oxygen or a grey colour/pallor withsigns of heart

failure in a baby within the first 4weeks of life points to duct- dependent congenital heart

disease

z The presence of heart failure in an older infant or child points to cardiomyopathy or myocarditis

z A history of sickle cell disease, a history of glucose- 6- phosphate dehydrogenase (G6PD)

deficiency or a recent diarrhoeal disease are suggestive of haemolytic uraemic syndrome,

and a very low haemoglobin points to acute haemolysis. Ahistory of sickle cell disease,

abdominal pain and enlarged spleen points to acute splenic sequestration

z An immediate history of trauma points to blood loss or, more rarely, tension pneumothorax,

haemothorax, cardiac tamponade or spinal cord transection. Inflicted injury may present with

no history or an inconsistent history of trauma but with clinical signs of injury such as bruising

z The presence of severe tachy- /bradycardia or an abnormal rhythm on the ECG points to a

cardiac cause for shock

z A history of polyuria, the presence of acidotic breathing and a very high blood glucose

points to diabetic ketoacidosis

z A history of drug ingestion points to poisoning

5.8 Approach tothe child withgastrointestinal fluid loss

Infants are more likely than older children to present with shock due to sudden and rapid fluid losses

due to gastroenteritis or with concealed fluid loss secondary to a ‘surgical abdomen’ such as a volvulus.

In infants, gastroenteritis may occasionally present as circulatory collapse with little or no signifi-

cant history of vomiting or diarrhoea. This is due to sudden massive loss of fluid from the bowel wall

into the gut lumen, causing a depletion of intravascular volume. The infecting organism can be any

of the usual diarrhoeal pathogens, of which viruses are the most common.

Emergency treatment

Having completed the primary survey and resuscitation and identified by means of the key features

that fluid loss is the most likely diagnosis, the child is reassessed to identify the response to the

start of fluid resuscitation.

72 PART 2 The seriously ill child

Reassess ABCDE

z Repeat 10ml/kg boluses of isotonic crystalloid if the shock is responding to fluid but is not fully

resolved. In gastroenteritis, 10–40ml/kg boluses usually restore circulating volume. Once signs

of shock are reversed, rehydration should continue but transitioning to the enteral route (oral or

nasogastric) (see Appendix B) should be started with normal feeding within 4–6 hours

z Do not persist with fluid resuscitation if shock is not improving. Consider vasoactive support,

intubation and ventilation, in discussion with the paediatric critical care team, when shock is

refractory to fluid resuscitation

z Recheck acid–base status and electrolytes:

z Acidosis will usually be corrected by treatment of shock; bicarbonate losses need to be

corrected only in children who have proven large bicarbonate losses (e.g. in stool). There is very

little role for bicarbonate replacement in paediatric resuscitation

z Severe hyponatraemia may occur, and this may cause convulsions. If convulsions are present,

give a dose of 3% sodium chloride 3ml/kg (range 3–5ml/kg) over 15minutes, aiming for a

serum sodium of 125 mmol/l or seizure termination. This dose of sodium chloride may be

repeated once if there is no response to the first dose. Once the seizure has stopped, or if there

is asymptomatic hyponatraemia, slowly correct serum sodium (maximum 8–12mmol/l/day)

z Consider the diagnostic possibilities:

z Abdominal X- ray or ultrasound to detect distended bowel or intra- abdominal air or fluid

z Consider urgent surgical referral especially if bile- stained vomiting or abdominal guarding is

present

z Consider sepsis, which maybe secondary to a surgical abdominal problem, and give appropriate

intravenous antibiotics. It is worth noting that sepsis can present with generalised abdominal

pain without specific abdominal pathology

z The bladder should be catheterised to accurately assess urinary output

z Treatment with an appropriate antiemetic may be helpful

5.9 Approach tothe child withseptic shock

The Third International Consensus in 2016 (Sepsis- 3) defined sepsis in adults as ‘life- threatening

organ dysfunction caused by a dysregulated host response to infection’ and septic shock as ‘a

subset of sepsis in which particularly profound circulatory, cellular and metabolic abnormalities are

associated with a greater risk of mortality than with sepsis alone’. Although formal revisions to

paediatric- specific definitions are outstanding, the clinical manifestations of septic shock are

essentially comparable throughout a person’s life:

z Hypotension (late sign in children who compensate well)

z Reliance on vasoactive agents to maintain a normal blood pressure

z Signs of inadequate tissue perfusion (in particular lactate greater than 2mmol/l, but also other

signs such as increased capillary refill time and oliguria) in the absence of hypovolaemia (after

initial fluid resuscitation)

Shock associated with sepsis can be hypovolaemic (negative fluid balance because of fever,

diarrhoea, vomiting and anorexia and/or capillary leak syndrome causing loss of fluid from the

intravascular compartment), cardiogenic (both the host inflammatory response and infecting

organisms can cause myocardial suppression) or distributive (caused by widespread vasodilatation

resulting in a low systemic vascular

resistance). Children with sepsis can also develop impaired

cellular oxygen utilisation at the mitochondrial level (distributive).

The burden of sepsis in children is considerable and is the cause of 8% of admissions to paediatric

critical care units in high- income countries. The mortality is 4–50% depending on illness severity,

risk factors and geographical location. In 2020, the First International Consensus guidelines for the

care of children with septic shock and other sepsis- associated organ dysfunction were published by

the Surviving Sepsis Campaign (SSC). These guidelines form the basis for the most recent tools for

the recognition and management of sepsis in children, published by the Academy of Medical Royal

Colleges in May 2022, which are shown in Figure5.2. The guidelines use the UK national paediatric

early warning system (PEWS) score.

CHAPTER 5 Circulation 73

Figure5.2 Sepsis Screening Tool

Courtesy of Nutbeam T and Daniels R on behalf of the UK Sepsis Trust, https://sepsistrust.org/professional-resources/clinical/

(last accessed March 2023)

(Continued)

74 PART 2 The seriously ill child

Figure5.2 (Continued)

CHAPTER 5 Circulation 75

Emergency treatment using theSepsis Six

Steps 01, 02 and03

Sepsis is a life- threatening emergency and children should be attended to by senior clinicians without

delay. Oxygen is indicated if the SpO2 is less than 92% or in the presence of shock. Intravenous access can

be difficult and can be an obstacle to time- critical escalation of investigation and resuscitation of critically

unwell children. Attempts should be limited in number and time, and intraosseous access used as an

alternative when indicated. A sample should be taken straight away for blood gas analysis, including

lactate, which is a key discriminator of critical illness. Glucose should be checked and hypoglycaemia

corrected. Blood should also be taken for culture, FBC, urea and electrolytes, liver function tests, CRP,

pro-calcitonin (if available), calcium, phosphate, magnesium and a coagulation screen but this is of

secondary importance and should not delay administration of antimicrobials or escalation of ABCDE

support. Lumbar puncture should be deferred in children with signs of critical illness.

Step04

GIVE IV ANTIBIOTICS, THINK SOURCE CONTROL.

Ensure intravenous antibiotics are given as soon as possible at the maximum dose and according

to local guidance. A third- generation cephalosporin, such as cefotaxime or ceftriaxone, is usual but

there are some specific considerations:

z Aciclovir should be given when sepsis is suspected in the neonatal period to cover herpes

simplex virus

z Clindamycin is usually added in suspected toxic shock syndrome aimed at halting bacterial

exotoxin production

z Amoxicillin is often added in under 3- month old infants to cover Listeria

z Cefotaxime is sometimes preferred to ceftriaxone in premature or jaundiced infants, if there is

hypoalbuminaemia or if a calcium- containing infusion is being used

z Piperacillin/tazobactam ± an aminoglycoside is often used if there is a high risk of Gram- negative

sepsis (e.g. in immunocompromise, urosepsis or known colonisation with a resistant Gram-

negative organism)

z If there are previous cultures of a resistant organism, give the appropriate antibiotic (e.g.

methicillin- resistant Staphylococcus aureus (MRSA): add vancomycin; extended- spectrum β-

lactamases (ESBL): add meropenem)

z If central venous catheters have been in place for more than 48 hours consider adding vancomycin

Source control should be considered part of resuscitation for sepsis. Urgently look for sources of

infection and address. For example, surgical problems such as appendicitis or necrotising fasciitis,

or an infected line which must be removed.

Steps 05 and06

GIVE IV FLUIDS AND CONSIDER INOTROPIC SUPPORT.

Healthcare systems withaccess tointensive care

If the lactate is more than 2 mmol/l and there are no signs of fluid overload, give 10ml/kg of isotonic

crystalloid (based on ideal body weight). Assess the haemodynamic response at the bedside and

repeat if there is evidence of improvement but still signs of shock. If there are signs of fluid overload

do not give further boluses of fluid. POCUS or echocardiography can be used to assess myocardial

function. If myocardial function is impaired, consider starting an adrenaline infusion (0.1–1micrograms/

kg/min).

If normal physiology has not been restored after ≥20ml/kg of fluid boluses (≥10ml/kg in neonates)

or earlier if there are signs of fluid overload, then vasoactive drugs should be considered. These are

usually adrenaline and/or noradrenaline infusions (0.1–1micrograms/kg/min) and should be done in

discussion with the paediatric critical care service. If the lactate is greater than 4 mmol/l, referral to

paediatric critical care should be made without delay.

76 PART 2 The seriously ill child

Healthcare settings without access tointensive care

The FEAST (Fluid Expansion As Supportive Therapy) study was published in 2011 and showed that in a

resource- limited setting in Africa, without access to intensive care, children with severe febrile illnesses

and evidence of impaired perfusion who were treated with fluid boluses had a significantly increased

mortality compared with controls. In systems without access to intensive care, the SSC guidelines only

recommend fluid boluses if there is evidence of both impaired perfusion and hypotension. In the

absence of hypotension, maintenance fluid with vasoactive support (if available) is recommended. In

this context, hypotension is defined as a systolic blood pressure less than 50mmHg in children aged

less than 1 year, less than 60mmHg for age 1–5 years and less than 70mmHg for over 5 years.

Intubation andventilation

There are no clear recommendations for the timing of intubation and ventilation in septic shock. Some

children present in extremis and intubation is required as part of the initial ABCDE resuscitation. In

other children, respiratory failure may be a presenting feature or may develop as a result of fluid boluses.

Intubation and ventilation should also be strongly considered in children with fluid refractory shock,

even without evidence of respiratory failure. Mechanical ventilation reduces oxygen consumption and

positive intrathoracic pressure reduces left ventricular afterload, therefore improving oxygen supply

and reducing demand. Septic shock can be associated with an impaired level of consciousness and

agitation is a common barrier to delivering the care that is required, which is another indication for

intubation. Meningitis causes raised ICP and there should be a low threshold for induction of

anaesthesia and intubation as part of the medical management of raised ICP (see Chapter6). When

vasoactive infusions are required to support the circulation, a central line, arterial line, urinary catheter

and continuous saturation and ECG monitoring are required. The reality in many children is that this

can only realistically be delivered after intubation and there should be a low threshold for doing this.

Induction of anaesthesia should be with ketamine (1 or 2mg/kg) and a rapid acting muscle relaxant

(e.g. rocuronium 1–2mg/kg). Adrenaline should be prepared to support the circulation (see Chapter19).

Refractory shock

Hydrocortisone (2–4mg/kg 6 hourly, maximum 100mg) can be given if shock remains refractory to

fluid and vasoactive drugs. Veno- arterial or veno- venous extracorporeal life support (ECLS) for

refractory shock or oxygenation/ventilation failure (after addressing other causes of shock and

respiratory failure) could be considered in discussion with the regional paediatric critical care service.

Causative organisms

The most common causes of community- acquired sepsis in children include Streptococcus

pneumoniae, Neisseria meningitidis, Streptococcus pyogenes (group A Streptococcus) and

Staphylococcus

aureus, with epidemiology varying depending on geographical region and

vaccination access/coverage. Streptococcus agalactiae (group B Streptococcus) and Gram- negative

sepsis are more prevalent in the neonatal age range. Herpes simplex virus should also not be

forgotten as a possible cause of neonatal sepsis and early empirical IV aciclovir should be considered.

The cardinal sign of meningococcal septicaemia is a purpuric rash in an ill child. At the onset,

however, the rash may be absent or mistaken for viral exanthems and a careful search should be

made for purpura in any unwell child. In about 15% of children with meningococcal septicaemia, a

blanching erythematous rash replaces or precedes a purpuric one, and in 7% of cases no rash occurs.

In toxic shock syndrome the initial clinical picture includes a high fever, diffuse erythema, head-

ache, confusion, conjunctival and mucosal hyperaemia (strawberry tongue), scarlatiniform rash

(can look like sunburn), subcutaneous oedema, vomiting and watery diarrhoea. Findings may

include a trivial injury such as an infected wound, cut, scratch, minor burn or scald, surgical wound

infection or coexistent deep- seated infection such as pneumonia or bone/joint infection. Early

administration of intravenous antibiotics (e.g. ceftriaxone and clindamycin), concurrent with initial

resuscitation, is vital. Intravenous immunoglobulin should be considered in discussion with infec-

tious disease specialists, along with urgent drainage of any localised abscess.

CHAPTER 5 Circulation 77

Many hospitals use adrenaline auto- injectors (e.g. Epipen®) for a first dose of adrenaline, in

which case a dose of 300 or 500micrograms is appropriate. Importantly, if further doses are

needed, these should be given by ampoule/needle/syringe

Source control andfurther investigations

It is important to seek expert advice from the microbiology/infectious diseases team after initial

empirical management, especially if there has been a slow response to treatment. Further investi-

gations might include specific PCRs (N. meningitidis, Streptococcus pneumoniae, S. pyogenes,

S.agalactiae Staphylococcus aureus, Enterobacterales) or broad- range PCR (16S) depending on the

most likely pathogens.

5.10 Approach tothe child withanaphylaxis

Anaphylaxis is a serious systemic hypersensitivity reaction that is usually rapid in onset and may

cause death. Severe anaphylaxis is life threatening and may present with either shock and/or severe

respiratory distress. Life- threatening features include breathing difficulties (due to upper airway

swelling and/or bronchospasm) and/or shock (due to acute vasodilatation, fluid loss from the

intravascular space caused by increased capillary permeability and cardiac involvement). Any of

these may lead to respiratory or cardiac arrest.

Symptoms of anaphylactic shock include dizziness, collapse, pallor and floppiness; peripheral

perfusion may be compromised (cold extremities) or warm due to systemic vasodilatation.

Respiratory symptoms of anaphylaxis include swelling of the throat, stridor or wheeze and may or

may not be associated with shock. Other allergic symptoms/signs include skin flushing, itchy rash

(urticaria), facial swelling, abdominal pain and vomiting; these may or may not precede shock. Skin

symptoms/signs are absent in 10–20% of cases.

Individuals allergic to food allergens will often have a history of previous allergic reactions; some

may have a ‘medic- alert’ bracelet or carry their own adrenaline autoinjector device. Possible risk

factors for more severe reactions include:

z Previous poor response to IM adrenaline

z Poorly controlled asthma

z Treatment with β- blockers

Symptoms and signs vary according to the body’s response to the allergen. These are shown in

Table5.2.

Table5.2 Symptoms andsigns inallergic reaction

Symptoms Signs

Allergic

reactions

Itchy mouth/lips/throat, throat clearing, feeling

of warmth, nausea, vomiting, abdominal pain,

loose bowel motions, sweating

Urticarial rash, angioedema, conjunctivitis,

erythema/flushing

Anaphylaxis Difficulty breathing, noisy breathing,

persistent cough, cyanosis, agitation,

collapse

Wheeze, stridor, tachycardia, hypotension,

poor pulse volume and pallor, respiratory

or cardiac arrest

IM adrenaline 1:1000 dosages

z Under 6months: 100micrograms or 0.1ml

z 6months to 6 years: 150micrograms or 0.15ml

z 6 to 12 years: 300micrograms or 0.3ml

z Over 12 years: 500micrograms or 0.5ml

78 PART 2 The seriously ill child

The management of anaphylactic shock or severe airways involvement (Figure5.3) requires airway

management, administration of adrenaline and aggressive fluid resuscitation. Intubation will be

required for severe cases. Note that the intramuscular route is the preferred route for initial doses of

adrenaline. IV/IO adrenaline should be reserved for children with life- threatening shock or airway

obstruction who have not responded to repeated doses of IM adrenaline, or those in cardiac arrest.

The child must be carefully monitored.

Having completed the primary survey and resuscitation and identified by means of the key features

that anaphylaxis is the most likely diagnosis, the child is reassessed.

Corticosteroids and/or antihistamines are no longer recommended for the initial acute manage-

ment of anaphylaxis, although antihistamines can be used to treat (emerging) skin conditions once

the patient is stabilised.

Nebulised

adrenaline

Nebulised

salbutamol

IV access,

fluid 10 ml/kg

Definitive care

If resolution: consider

steroids and

antihistamines

10 mcg/kg (0.01 ml/kg

1 : 1000 adrenaline)

IM adrenaline - auto injector

6 months–6 yrs - 150 mcg

6 yrs–12 yrs - 300 mcg

12 yrs–adult - 500 mcg

High flow oxygen

Stridor

Wheeze

Shock

Improvement?

No effect

After 5–10 min:

Repeat adrenaline

YES

Remove allergen

Call for help

Adrenaline IM

Evaluate ABCDE

Refractory anaphylaxis

management

see text for guidance

Emergency treatment of anaphylaxis

Figure5.3 Emergency treatment of anaphylaxis algorithm

CHAPTER 5 Circulation 79

Further emergency management

For anaphylaxis features that do not respond to initial IM adrenaline, continue with a bolus of

balanced crystalloid and/or ventilatory support, and give a second dose of IM adrenaline 5minutes

after the first. If the reaction does not respond to two doses of IM adrenaline, commence refractory

anaphylaxis management. Give a rapid fluid bolus and commence an IV/IO adrenaline infusion

according to local guidelines and titrate to clinical response. While waiting for the infusion to be

prepared, continue IM adrenaline every 5minutes.

The child should be closely monitored with continuous pulse oximetry, blood pressure and ECG. If the

shock is refractory to the adrenaline infusion a second vasopressor, such as noradrenaline, vasopressin

or metaraminol, could be considered. Guidance from a paediatric intensive care specialist is vital.

Take a blood sample for mast cell tryptase for future analysis as soon as possible, and a second

sample 2–4 hours later.

In addition to this treatment, corticosteroids (e.g. hydrocortisone) are still recommended for refrac-

tory reactions. The role these drugs have in acute management is limited, as their onset of action is

too delayed to be of much benefit in the first hour.

In cardiac arrest, resuscitation should be aggressive– do not give up too soon. Prolonged cardio-

pulmonary resuscitation, including extracorporeal membrane oxygenation (ECMO), should be

considered as the cause of arrest is potentially reversible and the tissue oxygenation prior to arrest

is likely to have been normal.

5.11 Approach tothe child withprofound anaemia

Severe anaemia exists if the haemoglobin level is less than 50g/l. The child will be lethargic with severe

pallor of the conjunctiva, palms and soles, and there may be signs of heart failure. If acute haemolysis is

the cause of anaemia,

urine will usually be dark brown. The most usual situation in which a child develops

sudden severe haemolysis in high- income western countries is septicaemia associated with sickle cell

disease or haemolytic uraemic syndrome (HUS). In children returning from or living in endemic areas,

severe malaria may present with severe anaemia, with or without haemolysis. G6PD deficiency may

also present with severe haemolytic anaemia following exposure to triggers.

Emergency treatment

z Red blood cell transfusion should be considered when the haemoglobin level is less than 50g/l

z The presence of heart failure affects the decision to transfuse; diuretics will be required. Fluid

overload may exacerbate or lead to cardiogenic shock and pulmonary oedema

z Treatment may also be required as for sepsis with volume support, inotropes and intubation

Management of these children includes early discussion with paediatric critical care services.

5.12 Approach tothe child withsickle cell crisis

Sickle cell disease is characterised by episodic clinical events called ‘crises’. A vaso- occlusive crisis is the

most common and occurs when abnormal red cells occlude small vessels, causing tissue ischaemia.

The other crises are acute chest syndrome, sequestration crisis (severe anaemia and hypotension,

resulting from pooling of blood in the spleen and liver), aplastic crisis and hyper- haemolytic crisis.

Factors that precipitate or modulate the occurrence of sickle cell crises 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 treatment in sickle

cell crises. Parenteral opioids are essential for relieving pain in severe vaso- occlusive crises and acute

chest syndrome.

Oxygen saturation monitoring may be falsely reassuring in children who are in profound anaemia

80 PART 2 The seriously ill child

5.13 Approach tothe child withcardiogenic shock

Overview

Cardiogenic shock describes inadequate oxygen delivery to tissues due to failure of the ‘pump’ (i.e.

the heart) to deliver an adequate cardiac output. Whilst the pump failure can be due to primary

cardiac disease (e.g. congenital heart disease, cardiomyopathy, myocarditis, arrhythmias or

ischaemic heart disease), it is important to recognise that ventricular failure can also be seen

secondary to pathologies such as sepsis, and this is more often seen in younger children.

Specific recognition of cardiogenic shock is important as these children often need early positive

pressure ventilation, inotropic support and limited use of fluid resuscitation.

Clinical features that may suggest cardiogenic shock include tachycardia, heart murmurs, gallop

rhythms, hepatomegaly, weak pulses, narrow pulse pressure, pallor, distended neck vessels and

deterioration on administration of fluid boluses. Failure to pick up a SpO2 trace can suggest poor

peripheral perfusion due to low cardiac output. POCUS can be helpful to assess left ventricular

function and look for cardiac tamponade (see Appendix I).

Duct- dependent congenital heart diseases

Overview

The ductus arteriosus connects the systemic and pulmonary circulations in fetal life, allowing blood

to bypass the pulmonary circulation in utero as gas exchange occurs at the placenta. In the first few

days of life the ductus arteriosus (duct) starts closing as part of the transition from fetal to postnatal

life. Some neonatal congenital heart lesions are dependent upon a duct to supply either pulmonary

or systemic blood flow (Figure5.4) or to support adequate mixing between parallel circulations (e.g.

in transposition of the great arteries). These lesions are known as duct- dependent congenital heart

diseases. Anatomical examples are shown in Figure5.5.

• Usually right-sided

lesions

• Presents with cyanosis,

unresponsive to O2

(Worsens as duct

closes)

• Usually left-sided

lesions

• Presents with severe

cardiogenic shock

when duct closes

• Usually normal PaO2

• Critical aortic stenosis

• Coarctation of the aorta

• Hypoplastic left heart

• Interrupted aortic arch

• Tetralogy of Fallot (severe)

• Pulmonary atresia

• Tricuspid atresia

Duct-dependent circulation

Systemic-dependent

circulation

Pulmonary-dependent

circulation

Figure5.4 Summary of two main groups of duct- dependent lesions

CHAPTER 5 Circulation 81

Recognition

The most common time to present with compromise to the systemic or pulmonary circulations

due to a closing duct is at 7–10days of age. However, there should be a high index of suspicion for

duct- dependent congenital heart when dealing with any critically unwell neonatal patient. Whilst

many are diagnosed antenatally, normal antenatal scans do not exclude congenital heart disease.

Clinical features that can suggest duct- dependent lesions include:

z Features of cardiogenic shock (discussed earlier in this chapter)

z Cyanosis (especially if not fully responding to oxygen therapy)

z Weak or absent femoral pulses

z Discrepancy between upper and lower limb blood pressure and oxygen saturations

z Hepatomegaly

z Cardiomegaly

z Abnormal ECGs

Emergency treatment

When neonates present critically unwell, the differential diagnosis is broad. The mnemonic SCAM

stands for sepsis, cardiac, abuse and metabolic disorders and is a helpful way of remembering

possible causes. However, distinguishing between these can be very difficult during resuscitation

and the priority should be the standardised ABCDE approach to resuscitation, with the additional

consideration of resuscitating the ductus arteriosus. Some people find it useful to think ABCDDE

when resuscitating critically unwell neonates. The additional ‘D’ standing for duct.

(a)

(b)

There is no opening in the right ventricular outflow

tract so blood cannot exit the small right ventricle to

get to the pulmonary circulation for oxygenation. All

blood must mix via an intracardiac shunt (atrial or

ventricular septal defect) by shunting right to left. In

this case, the blood gets to the pulmonary circulation

by going via the duct from the aorta to the pulmonary

artery (left-to-right shunt). In these cases, the

systemic cardiac output is usually good, with the main

problem being increasing hypoxia as the duct closes

and pulmonary blood flow is reduced. The systemic

cardiac output is deoxygenated and as the hypoxia

worsens shock can develop

There is obstruction to blood flow within the aorta at

the level of the coarctation. Blood flow distal to the

obstruction is supplied by the duct by going from the

pulmonary artery to the aorta (right-to-left shunt). This

means the blood supplying the lower body is at a

lower blood pressure and is deoxygenated. As the duct

closes, blood flow is maintained to the coronary

arteries and brain from the left ventricle, but blood flow

to the lower body is reduced or absent, leading to

cardiogenic shock

Figure5.5 Examples of duct- dependent pulmonary circulation. (a) Pulmonary atresia with intact interventricular septum.

(b) Coarctation of the aorta

82 PART 2 The seriously ill child

Specific management points for the neonate with suspected duct- dependent circulation include:

z Obtain early support from the local paediatric or neonatal critical care service. In some lesions

urgent intervention is needed (e.g. balloon atrial septostomy in transposition of the great arteries)

z Ensure blood pressure and pulse oximetry monitoring is placed on the right arm (preductal

circulation) and use this monitoring as your target blood pressure and SpO2. This is because

preductal blood perfuses the coronary arteries and brain. The postductal observations (obtained

on the lower limbs) are helpful for diagnosis but not as a target for physiological parameters

z Oxygen therapy should be given to maintain the preductal right arm SpO2 greater than 75%. Use

as much as required to achieve

this target. There is no condition in which withholding oxygen

improves hypoxia and there are no concerns about oxygen accelerating duct closure when

prostaglandin is being used

z Give IV infusion of dinoprostone (prostaglandin E2 or PGE2) or alprostadil (PGE1) urgently:

z This acts by reopening the duct and restores either systemic or pulmonary blood flow

z It should be started early if duct- dependent circulation is suspected and can always be

stopped later after a detailed echocardiogram

z The side effects are dose dependent and include apnoea, pyrexia and vasodilatation (leading

to hypotension)

z The impact on the duct is dose dependent. This means low doses of dinoprostone (5–10ng/

kg/min) will keep open a duct that is already open. Higher doses (20–100 ng/kg/min) will

reopen a closing or closed duct and therefore the starting dose depends on the clinical

situation of the neonate

z If signs of shock/absent pulses: 20–50ng/kg/min increasing to 100ng/kg/min in discussion

with paediatric critical care services

z Lower doses (5–10ng/kg/min) are only useful in the immediate postnatal period or the very

stable neonate

z Doses can be titrated to saturations and the presence or return of femoral pulses

z Manage preductal right arm hypotension. Whilst a cautious 5ml/kg of fluid can be tried, it is

likely that these children will need inotropic support with an infusion of adrenaline

z The following are indications for intubation and ventilation:

z Apnoea due to dinoprostone

z Extreme hypoxia

z Any degree of hypoxia with respiratory distress

z Signs of shock

z Need for interventional procedure

z All neonates presenting shocked should be covered for sepsis with IV antibiotics and aciclovir

Throughout management of this complex patient group ensure early and regular discussions with

your local paediatric or neonatal critical care service.

Cardiomyopathy or myocarditis

Overview

Cardiomyopathy is a disease of the heart muscle itself, resulting in pump failure. It is a cause of

cardiogenic shock in children. It is usually caused by a genetic pathology, toxins (especially

chemotherapy), unrecognised arrhythmias or metabolic disorders. It can also be caused by

myocarditis. Myocarditis is an infection of the heart muscle, usually from a viral pathology, and leads

to pump failure, and so is a cause of cardiomyopathy. Cardiomyopathy can also be secondary to

non- cardiac diseases such as sepsis.

These children can present with varying degrees of heart failure and cardiogenic shock. It can be

difficult to distinguish this from other causes of shock. A chest X-ray and 12 lead ECG may help with

the diagnosis of cardiomyopathy, while assessment with POCUS can help to differentiate these

similar clinical pictures. Fluid resuscitation can often worsen the condition of these children, and

this is a clue ventricular function is impaired. If such a patient is in the first few weeks of life, a trial

of prostaglandin (PGE1 or PGE2) may be appropriate and would be beneficial for duct- dependent

circulations as discussed earlier.

CHAPTER 5 Circulation 83

Emergency management

Management depends on whether the child presents with cardiac failure without signs of shock or

cardiac failure with signs of shock. Ensure other pathologies (such as sepsis) have been considered

and managed as indicated.

Children with cardiomyopathy/myocarditis can be very difficult to manage and can rapidly deterio-

rate if they develop an arrhythmia. Ensure they are on continuous monitoring. A blood gas is

mandatory and a raised lactate should prompt referral to the paediatric critical care service.

Those presenting in heart failure without signs of shock need to be referred to the paediatric cardi-

ologist quickly for treatment of their heart failure, so they do not develop shock. If the child is not

shocked consider diuretics to offload the heart, such as furosemide 0.5–1mg/kg, and consider non-

invasive ventilation or high- flow nasal oxygen therapy.

For those already in shock who are suspected to have myocarditis or cardiomyopathy, aggressive

fluid resuscitation needs to be avoided and early use of inotropes (e.g. adrenaline infusion) with

positive pressure ventilation are likely to be indicated. This should be in close discussion with the

paediatric critical care team. Afterload reduction (e.g. with milrinone or dobutamine) may be con-

sidered. The availability of ECLS with ECMO and ventricular assist devices (VADs) for the most seri-

ous cases needs to be considered, with the focus on the child being stabilised and transferred

urgently to the right centre.

Early discussion about transfer to a cardiac centre should take place with your local paediatric critical

care service.

5.14 Approach tothe child withabnormal rhythm or pulse rate

Overview

Sinus tachycardia and bradycardia can occur in normal physiological states, such as during exercise

and sleep. However, they can both also be signs of critical illness from a variety of non- cardiac

pathologies. In some situations these rhythms are not sinus, in which case the child may have a

primary arrhythmia (Table5.3). This may be haemodynamically significant and lead to cardiogenic

shock. An ECG should be performed in situations of tachycardia or bradycardia when it is not clear

that the rhythm is sinus from a rhythm strip.

Treatment of children with an abnormal rhythm or pulse is highly protocolised and depends on the

underlying rhythm. Basic recognition of the arrhythmia is essential. To use the right management

protocol, answer three basic questions (Figure5.6).

Table5.3 Example causes oftachyarrhythmias andbradyarrhythmia

Causes of tachyarrhythmia Causes of bradyarrhythmia

Supraventricular tachycardias

Ventricular tachycardias

Poisoning

Metabolic disturbance

After cardiac surgery

Cardiomyopathy

Primary arrhythmia syndromes (e.g. long QT syndrome, Brugada

syndrome)

Pre- terminal event in hypoxia or shock

Raised intracranial pressure

Heart blocks (iatrogenic or congenital)

Poisoning

84 PART 2 The seriously ill child

Abnormal rhythm or pulse: bradyarrhythmia

Overview

An abnormally slow pulse rate is defined as one less than 60 beats/min or a rapidly falling heart rate

associated with poor systemic perfusion.

Most sinus bradycardia in children is a pre- terminal rhythm due to hypoxia and/or myocardial

ischaemia from untreated shock but it can sometimes be precipitated by vagal stimulation (e.g.

during intubation or airway suctioning). Sinus bradycardia can also be a sign of raised ICP, which

could be with or without an altered conscious level (see Chapter6). Any sinus or non- sinus brady-

cardia can also point to poisoning (e.g. with digoxin or β- blockers).

Incidental sinus bradycardia in a clinically well child may be seen in athletic and sporty children and

does not require any treatment.

Non- sinus bradycardias usually indicate a type of heart block. Complete heart block is known as

third degree heart block. This can be seen as a congenital phenomenon, after cardiac surgery, due

to drug overdose or idiopathic. It is recognised as a slow heart rate, with widely spaced QRS com-

plexes (which can be broad) with dissociation of P wave activity from the QRS complexes.

Rhythm

Regular

QRS broad QRS narrow

RegularIrregular Irregular

FAST

More than 200 bpm (infant)

More than 150 bpm (child)

SLOW

Less than 60 bpm

Commonly

atrial fibrillation

(AF)

Supraventricular

(SVT) or sinus

tachycardia

Ventricular

tachycardia

(VT)

Usually due

to conduction

abnormalities

or fitness

training or

preterminal

Usually

vagally

induced or

preterminal

Basic recognition of arrhythmia

QRS

complex

Broad/

Narrow

Rhythm

Regular/

Irregular

Rate

Fast/

Slow

Questions

to ask:

Figure5.6 Basic recognition of arrhythmia algorithm

CHAPTER 5 Circulation 85

Emergency treatment

As described, in paediatric practice bradycardia is predominantly a pre- terminal finding in children

with

of arrival of an expert. This approach

upset a number of established clinicians who felt that, as practitioners of the art of medicine, they

could craft personalised treatment only by having free choice, and that anything that interfered

with that free choice was bad for patients. Over the next 6 editions of APLS these arguments have

abated and, indeed, the algorithms themselves are often now owned and regularly updated by

expert sub- speciality groups. The smell of paraldehyde and the need for glass syringes has become

history, and debates continue as evidence based medicine evolves.

Most practitioners who deal with paediatric emergencies nowadays will never have known

anything other than the ‘APLS approach’ to emergency care, and that is the true success of the

disruption the manual and course started all those years ago. There are, of course, dangers in

becoming the new normal, in particular it is easy to rest on the laurels of success. Avoiding

complacency is important and is why this latest (seventh) edition is as important as the first edition

was all those years ago. The current APLS working group and the book editors are at the peak of

their careers and are wholly committed to keeping the content and teaching of APLS at the very

cutting edge of current practice. Knowing the energy they bring as the current custodians of APLS

is why I have no hesitation in recommending this new edition to you. It will serve you, and sick and

injured children, well.

Kevin Mackway- Jones

Manchester, 2023

Foreword

xii

Advanced Paediatric Life Support: The Practical Approach was written to improve the emergency

care of children, and has been developed by a number of paediatricians, paediatric surgeons,

emergency physicians and anaesthetists from several UK centres. It is the core text for the APLS

(UK) course, and will also be of value to medical and allied personnel unable to attend the course. It

is designed to include all the common emergencies, and also covers a number of less common

diagnoses that are amenable to good initial treatment. The remit is the first hour of care, because it

is during this time that the subsequent course of the child is set.

The book is divided into six parts. Part I introduces the subject by discussing the causes of child-

hood emergencies, the reasons why children need to be treated differently and the ways in which a

seriously ill child can be recognised quickly. Part II deals with the techniques of life support. Both

basic and advanced techniques are covered, and there is a separate section on resuscitation of the

newborn. Part III deals with children who present with serious illness. Shock is dealt with in detail,

because recognition and treatment can be particularly difficult. Cardiac and respiratory emergen-

cies, and coma and convulsions, are also discussed. Part IV concentrates on the child who has been

seriously injured. Injury is the most common cause of death in the 1–14- year age group and the

importance of this topic cannot be overemphasised. Part V gives practical guidance on performing

the procedures mentioned elsewhere in the text. Finally, Part VI (the appendices) deals with other

areas of importance.

Emergencies in children generate a great deal of anxiety – in the child, the parents and in the

medical and nursing staff who deal with them. We hope that this book will shed some light on the

subject of paediatric emergency care, and that it will raise the standard of paediatric life support. An

understanding of the contents will allow doctors, nurses and paramedics dealing with seriously ill

and injured children to approach their care with confidence.

Kevin Mackway- Jones

Elizabeth Molyneux

Barbara Phillips

Susan Wieteska

Editorial Board

1993

Preface to first edition

xiii

The Advanced Paediatric Life Support (APLS) course is now delivered in 76 centres across the United

Kingdom and 17 centres on every continent across the world. This amazing achievement is due to

the small, dedicated team based at the Advanced Life Support Group (ALSG) in Manchester and

tothe thousands of trained instructors from many disciplines, who give their time and expertise so

generously. Thank you all.

This manual (the seventh in the last 30 years) supports the APLS and Paediatric Life Support (PLS)

courses, as well as being used as a gold standard for acute paediatric clinical practice. It builds on

the contributions from previous authors whose names can be found on the ALSG website. Thank

you to them and to all those who have worked so hard to produce this edition.

This manual has been updated throughout. There is an increased emphasis on preparation for

effective team working to improve patient safety. The seriously ill child section has been restruc-

tured to consolidate information into chapters reflecting the ABCDE approach.

Evolving techniques such as point of care ultrasound (POCUS) are included in several chapters, and

POCUS is described in more detail in an excellent appendix at the end of the manual. APLS does not

specifically teach this skill, rather we acknowledge its place in many aspects of emergency

management and care.

The entire manual has been updated in line with the 2021 International Liaison Committee on

Resuscitation (ILCOR) guidelines as well as with consensus best practice. The international nature

of APLS means the manual is written to reflect different cultures and clinical practices wherever

possible.

Additional and detailed information for those who wish to take their learning further is included in

the 10 appendices. This information is not essential knowledge for all but we hope will be

interesting reading for many.

Since the sixth edition of APLS there has been the worldwide COVID- 19 pandemic which had an

impact on the way courses were delivered as well as the timescale for this edition of the manual.

It is essential that we incorporate the lessons learned from this experience into delivery of both

healthcare and the way it is taught.

Stephanie Smith

May 2023

Preface to seventh edition

Acknowledgements

A great many people have put a lot of hard work into the production of this book, and the

accompanying Advanced Paediatric Life Support course. The editors would like to thank all the

contributors for their efforts and all the APLS instructors who took the time to send us their

comments on the earlier editions.

We are greatly indebted to Kirsten Baxter and Kate Denning for their exceptional hard work and

dedication towards this publication; their encouragement and guidance throughout the process

has been gratefully received.

We would like to express our special thanks to Ayşe Mehta for producing the excellent line drawings,

Jason Acworth and Children’s Health Queensland for the new photographs that illustrate the text

and Catherine Giaquinto for designing the new algorithms for this edition.

For the cover image, thank you to Russell Ashworth and his son Noah Ashworth, Chloe Donaldson,

Manivannan Manoharan, Julia Maxted, Angela Armitage and Nila Prince.

We would also like to thank Laura May for kindly allowing adaptation of the UHCW NHS Trust

Paediatric TRAUMATIC list. Rowan Pritchard Jones and Michael Watts for allowing images from the

Mersey Burns App. Michael J. Griksaitis and Bogdana Zoica for the POCUS chapter and figures.

Jamie Vassallo for the PTCA algorithm. Marijke van Eerd for the Paediatric Major Trauma and

analgesia calculation chart. Ross Smith on behalf of the Child and Young Person’s Advance Care

Plan. Tim Nutbeam and Ron Daniels on behalf of the UK Sepsis Trust. The Status Epilepticus

Guidelines development group.

For the shared use of their images, illustrations, tables and algorithms, we would like to thank:

Alder Hey Radiology Department Teaching Library

ASIA– American Spinal Injury Association

Bristol Royal Hospital for Children and RTIC Severn

British Society for Paediatric Endocrinology and Diabetes

British Thoracic

respiratory and/or circulatory insufficiency. Airway, breathing and circulation should be

assessed and treated during the primary survey, with particular focus on reversing hypoxia and/or

shock. Hypoxia leading to bradycardia results in cardiac arrest if not addressed quickly. Stabilisation

of the airway and breathing should be started immediately, and bradycardia will often resolve once

oxygenation is restored.

After this basic ABCDE management then pharmacological management of bradycardia can be

considered, primarily for the non- sinus bradyarrhythmias and heart block (Figure5.7).

Seek expert adviceTreat hypoxia2 and shock/

decompensation

Atropine

20 mcg/kg

(max dose

1.2 mg)

Give adrenaline

0.5 mcg/kg per dose

and titrate to effect

Seek expert advice

and consider

adrenaline infusion/

pacing

Shock present?YES NO

If unresponsive and heart rate

less than 60 beats per minute

despite oxygen, start chest

compressions

Management of bradycardia

General signs of shock:

bradycardia, tachycardia,

BP < 5th centile1,

CRT > 2 secs , weak or

impalpable peripheral pulses

Signs of circulatory

compromise:

signs of vital organ

perfusion compromise, altered

consciousness, tachypnoea

1 See table on inside front cover

2 Treat hypoxia, optimise oxygenation, including

positive pressure ventilation if required

Figure5.7 Management of bradycardia algorithm

BP, blood pressure; CRT, capillary refill time

86 PART 2 The seriously ill child

If the bradycardia persists following treatment of hypoxia and shock then slowly titrate adrenaline

up to 10micrograms/kg IV/IO. If this is ineffective, consider an adrenaline infusion of 0.05–2micro-

grams/kg/min IV/IO.

z In non- sinus bradycardias (e.g. complete heart block), consider giving atropine 20micrograms/

kg IV (maximum dose 1.2 mg). The dose may be repeated after 5minutes (maximum total dose

of 1mg in a child and 2mg in an adolescent)

z Consider transcutaneous pacing if the bradycardia is caused by atrioventricular block or

abnormal atrioventricular node and arrange more definitive pacing system

z Consider use of isoprenaline infusion (0.02–0.2micrograms/kg/min in neonates and 1microgram/

kg/min in non- neonatal age groups)

z If there has been vagal stimulation, remove the vagal stimulus if possible and stabilise airway

and breathing. Atropine can be used at the doses discussed above

z If there has been poisoning, seek expert toxicology help

z If bradycardia is due to raised ICP, urgent action is needed (see Section6.3)

Abnormal rhythm or pulse: tachyarrhythmia

Overview

Most tachycardia in children is sinus tachycardia. In infants this may be as high as up to 220 beats/

min and in children up to 180 beats/min. Rates over these figures are highly likely to be

tachyarrhythmias, but in case of any significant tachycardia (i.e. more than 200 beats/min in an

infant and more than 150 beats/min in a child) an ECG rhythm strip should be examined and, if in

doubt, a full 12- lead ECG performed.

Recognition of sinus tachycardia is of vital importance as this can be the first sign of critical illness.

Causes of sinus tachycardia can include inadequate cardiac output states (e.g. cardiomyopathy,

congenital heart diseases), high metabolic demand (e.g. sepsis), hypovolaemia (e.g. gastroenteritis,

haemorrhage, third space fluid loss) or situations such as pain, anxiety or exercise.

There are two main types of tachyarrhythmias to recognise: supraventricular tachycardia (SVT) and

ventricular tachycardia (VT).

Approach tothe child withsupraventricular tachycardia

A SVT is the most common non- arrest arrhythmia during childhood and the most common

arrhythmia that produces cardiovascular instability during infancy. SVT in infants generally produces

a heart rate more than 220 beats/min, and sometimes much higher. Lower heart rates occur in

older children during SVT. SVT is an umbrella term for many types of atrial arrhythmias.

Cardiopulmonary stability during episodes of SVT is affected by the child’s age, duration of SVT,

prior ventricular function and ventricular conduction rate. Older children can complain of light

headedness, dizziness or chest discomfort or they note a racing heart rate. Very rapid rates may be

Clues to suggest a non- sinus tachycardia on a rhythm strip include:

z Extreme tachycardia (more than 200 beats/min)

z Absent P waves, or P waves not before each QRS complex

z Very narrow or wide QRS complex

z Irregular rhythms

z Sudden and abrupt changes in heart rate

z No variability in heart rate when variability would be expected (e.g. child crying versus settled)

z Heart rate fixed despite interventions (e.g. trial of fluid bolus)

CHAPTER 5 Circulation 87

undetected for long periods in young infants until they develop a low cardiac output state and

cardiogenic shock. This deterioration occurs because of increased myocardial oxygen demand and

limitation in myocardial oxygen delivery during the short diastolic phase associated with very rapid

heart rates. The systemic cardiac output is reduced because the ventricular function deteriorates

due to ischaemia, the short diastolic filling time reduces the ventricular volumes and the loss of

atrioventricular synchrony removes the atrial component of the cardiac output. If baseline myocar-

dial function is impaired (e.g. in a child with a cardiomyopathy), SVT can produce signs of shock in a

relatively short time.

It is easy to mistake SVT for a significant sinus tachycardia and vice versa. Careful interpretation

of the clinical situation must be undertaken to try and correctly identify which you are dealing

with. The following characteristics may help distinguish sinus tachycardia from SVT (Figures5.8

and5.9):

z Look at the child’s presenting complaint: a history consistent with high fever or other causes of

shock (e.g. gastroenteritis or sepsis) may suggest sinus tachycardia

z Look at the pattern in heart rate: SVT starts and ends abruptly, whereas sinus tachycardia

changes more gradually

z Look for heart rate variability: in sinus tachycardia the heart rate varies from beat to beat and is

often responsive to stimulation or interventions such as fluid bolus, but there is no beat- to- beat

variability in SVT and the heart rate remains fixed

z Look carefully for P waves (they may be difficult to identify at faster heart rates even in sinus

tachycardia). P waves in sinus rhythm should be seen before every QRS complex and should be

upright in leads I, II, III and aVF and inverted in aVR. If the P waves are inverted in leads I, II, III and

aVF then the options are: (i) the ECG leads are not correctly placed; (ii) the child has dextrocardia;

or (iii) the child has a form of SVT. The paper speed of the ECG machine may need to be increased

to make the identification of P waves easier.

Figure5.8 Rhythm strip of sinus tachycardia showing upright P waves before each QRS complex

Figure5.9 Rhythm strip of supraventricular tachycardia showing absent P waves, narrow complex QRS and extreme

tachycardia

88 PART 2 The seriously ill child

Emergency treatment forSVT

Treatment for SVT should follow the appropriate algorithm (Figure5.10).

It is important to ensure the child has continuous monitoring applied. IV or IO access should be

obtained. Ensure the electrolytes have been checked, including magnesium.

Vagal manoeuvreVagal manoeuvre

(if no delays)

Synchronous shock 1 J/kg

Synchronous shock 2 J/kg

Seek expert advice and

consider synchronous

shock 4 J/kg

Seek expert advice and

consider amiodorone

Give appropriate sedation and

analgesia

Adenosine 100 mcg/kg

(max 6 mg)2

Adenosine 200 mcg/kg

(max 12 mg)2

Adenosine 300 mcg/kg

(max 12 mg)2

Assess rhythm

SVT identified

Shock present?

Adequate

vascular access quicker

than obtaining

defibrillator

YES

2 mins

Management of supraventricular tachycardia

1 See table on inside front cover

2 These are maximum adult doses

Ensure ABCs

have been

addressed, IV/IO access

achieved and patient is

attached to a monitor

General signs of shock:

bradycardia, tachycardia,

BP < 5th centile1,

CRT > 2 secs, weak or

impalpable peripheral pulses

Signs of circulatory

compromise:

signs of vital organ

perfusion compromise, altered

consciousness, tachypnoea

Figure5.10 Management of supraventricular tachycardia algorithm

BP, blood pressure; CRT, capillary refill time

CHAPTER 5 Circulation 89

If the child is not shocked, then it is reasonable to consider a vagal manoeuvre whilst adenosine is

being prepared. This can be achieved by:

z Eliciting the diving reflex to increase vagal tone by placing a glove with ice cold water over the face

z Performing a Valsalva manoeuvre in older children. This can be done by asking the child to blow

into an empty syringe with the plunger pulled back or blowing hard through a straw. If able, ask

the child to do a handstand and hold the position for 30 seconds

z Do not use ocular pressure in children because ocular damage may result

If these manoeuvres are unsuccessful or IV/IO access is available then use IV adenosine, which acts

by blocking the atrioventricular node and breaking any abnormal electrical conduction pathways,

or unmasking an arrhythmia that will require additional treatment. Adenosine has a very short half- life

(less than 10 seconds) and is safe for use, even if the rhythm is not SVT. In fact, an adenosine trial can

be helpful to distinguish sinus tachycardia from SVT. The only contraindication to adenosine is an

irregularly irregular rhythm (incredibly rare in paediatric practice). During adenosine administration

the side effects include flushing, nausea, dyspnoea and chest tightness and older children should

be warned of this. Due to the short half- life, the side effects wear off quickly.

When giving adenosine, ensure the drug is injected rapidly into the largest possible vein available.

Ensure continuous ECG monitoring is recording and printing the rhythm strip. Doses may need to

be escalated:

z Start with a rapid bolus of 100 micrograms/kg (max. dose 6mg)

z If success is not achieved then after 2 minutes use 200 micrograms/kg (max. dose 12mg)

z If still unsuccesful then after another 2 minutes use 300micrograms/kg (max. dose 12mg)

z In older children 500micrograms/kg may be required

If sinus rhythm is not obtained after adenosine, ensure it is SVT you are managing and not sinus

tachycardia and consult your local paediatric critical care service. Some rhythms (e.g. atrial flutter)

will require direct current (DC) cardioversion or additional antiarrhythmic medications.

If the child is shocked with SVT, do not delay adenosine if IV access is available. If this is not available

then a synchronous DC shock of 1J/kg should be delivered, followed by 2J/kg up to a maximum of

4J/kg. Ensure anaesthesia/intensive care are involved for appropriate sedation and support for the

DC shock. Ventricular function may remain impaired even after successful DC cardioversion, so

vasoactive support and intubation may be required. All these cases should be discussed with local

paediatric critical care services.

Approach tothe child withventricular tachycardia witha pulse

Ventricular tachycardia is a less common tachyarrhythmia seen in children. It is recognised by a

broad complex, rapid QRS with P waves absent or very difficult to see. It can be associated with

cardiac arrest or severe haemodynamic instability. All cases should be discussed with your local

paediatric critical care services.

VT can be caused by congenital heart disease and cardiac surgery, myocarditis or cardiomyopathy,

poisoning with tricyclic antidepressants, procainamide or quinidine, renal disease or other causes of

hyperkalaemia or channelopathies (e.g. long QT syndromes).

Torsade de pointes describes a specific type of polymorphic VT, with QRS complexes that change

in amplitude and polarity so that they appear to rotate around an isoelectric line. This is seen in

conditions characterised by a long QT interval or drug poisoning, such as with quinine, quinidine,

disopyramide, amiodarone, tricyclic antidepressants or digoxin.

Sometimes, wide- complex tachycardia can be SVT with bundle branch block and aberrant conduc-

tion. This can be very difficult to differentiate from VT by a non- specialist. A dose of adenosine may

help identify the underlying aetiology of the arrhythmia but should be used with extreme caution

in haemodynamically stable children with wide- complex tachycardia because acceleration of the

tachycardia and significant hypotension are known risks. This should not delay definitive treatment

in children with shock. A safer approach is to treat it as VT. Seek early advice.

90 PART 2 The seriously ill child

Give appropriate sedation/

analgesia

Synchronous shock

1 J/kg

Amiodarone 5 mg/kg

over 20 minutes

Seek expert advice and

consider synchronous shock

Synchronous shock

2 J/kg

Seek expert advice

Consider amiodarone and

synchronous shock 4 J/kg

VF/pVT algorithm Check pulse

Assess rhythm

VT rhythm identified

Shock present?

Adequate vascular

access quicker than

obtaining

defibrillator

YES NO

YES

Ensure ABCs have been

addressed, IV/IO access

achieved and patient is

attached to a monitor

Management of ventricular tachycardia

1 See table on inside front cover

General signs of shock:

bradycardia, tachycardia,

BP < 5th centile1,

CRT > 2 secs, weak or

impalpable peripheral pulses

Signs of circulatory

compromise:

signs of vital organ perfusion

compromise, altered

consciousness, tachypnoea

Figure5.11 Management of ventricular tachycardia (VT) algorithm

BP, blood pressure; CRT, capillary refill time; pVT, pulseless ventricular tachycardia; VF, ventricular fibrillation

CHAPTER 5 Circulation 91

Emergency treatment forVT witha pulse

In the absence of a cardiac output, this is a shockable cardiac arrest and the algorithm for cardiac

arrest for ventricular fibrillation/pulseless VT should be followed (see Chapter18).

If there are any signs of cardiac output, then follow the algorithm for ventricular tachycardia

(Figure 5.11). It is important not to delay treatment in VT as the rhythm often deteriorates quite

quickly into pulseless VT or ventricular fibrillation.

Ensure IV/IO access is obtained, and electrolytes are checked, including magnesium.

z In the shocked child, the treatment is synchronised DC cardioversion starting at 1J/kg, followed

by 2J/kg up to a maximum of 4J/kg if needed. Ensure anaesthesia/intensive care are involved

for appropriate sedation and support for the DC shock, as in these children the ventricular

function may still be reduced after DC cardioversion. All these cases should be discussed with

your local paediatric critical care service

z If the child with VT is not shocked, then early consultation with paediatric critical care services

and paediatric cardiology are mandatory. They may suggest amiodarone (5 mg/kg over

20minutes) that may then need to be followed by a continuous infusion of 5–20micrograms/kg/

min. Other antiarrhythmic drugs may be used.

z Many antiarrhythmic drugs can cause hypotension, which should be treated appropriately

z The use of magnesium sulphate as an IV infusion of 25–50mg/kg (up to 2g) is helpful in VT,

especially when it is due to torsade de pointes

z In catecholamine- driven VT, IV β- blockers may help calm the adrenergic storm, but this should

only be used after discussion with local paediatric critical care services

5.15 After resuscitation andemergency treatment ofshock

Following successful restoration of adequate circulation, varying degrees of organ dysfunction may

remain, and should be actively sought and managed. The problems are similar but of a lesser degree

than those expected following resuscitation from arrest. Thus, after the initial resuscitation and

emergency treatment, the child should have a review of ABCDE, as

well as a full systems review to

ensure stabilisation for safe and effective transfer (see Chapter23).

5.16 Use offluids inresuscitation

Which fluid?

For paediatric fluid resuscitation three types of fluid are available:

1. Isotonic crystalloids:

z 0.9% sodium chloride solution (this can result in hyperchloraemic acidosis)

z Balanced solutions like Ringer’s lactate or Plasma- Lyte (electrolyte composition similar to

extracellular fluid)

2. Colloids:

z Human albumin 4% solution is usually available for fluid resuscitation while 20% is used as a

replacement

z Synthetic colloids become less available but are still used in some countries

3. Blood products:

z Packed red cells

z Fresh frozen plasma

z Cryoprecipitate

z Platelets

z Whole blood

92 PART 2 The seriously ill child

Outside trauma there is no conclusive evidence about any benefit of one fluid over the other.

However, there seems to be a consensus on common practice. Fluid resuscitation is started preferably

with a balanced crystalloid or, if not readily available, 0.9% sodium chloride. When large volumes of

crystalloid are used there is the potential detrimental effect of haemodilution and tissue oedema.

In this case, the use of colloids like albumin can be considered. Colloids are suspensions of larger

molecules and may provide swifter and more sustained volume expansion of the intravascular

space. This is controversial and potential risks of colloids include allergic reactions and renal failure.

Packed red cells or clotting products might be used if the haemoglobin is low or there is evidence

of coagulopathy. Intravenous fluid resuscitation is difficult to fully protocolise and patient- tailored

therapy is appropriate. Consultation with the regional paediatric critical care service can help.

Remember that IV fluids (both bolus and maintenance) are drugs: they should be prescribed for the

right indication, at the right dose, via the right route and at the right speed/interval.

If blood is needed, a full crossmatch should be undertaken, which takes about 1 hour to perform. For

urgent need, type- specific non- crossmatched blood (which is ABO rhesus compatible but has a

higher incidence of transfusion reactions) takes about 15minutes to prepare. In dire emergencies

O- negative blood must be given.

How much fluid?

The volume of fluid needed will depend on clinical assessment, and the clinical situation also

dictates the rapidity with which boluses are given. Although life- saving capacities of fluid

resuscitation are well known, the evidence that fluid overload can be detrimental has become

evident in recent literature. So if large volumes are needed, resuscitation is best guided by advanced

haemodynamic monitoring such as measurement of the central venous pressure, invasive blood

pressure, urine output and/or POCUS. Children requiring large- volume resuscitation need early

involvement from and transfer to a paediatric critical care unit. When large volumes are used, fluids

should be warmed.

In conclusion, there is no definitive evidence demonstrating which fluid is best for resuscitation.

Other important questions about how much and when fluids should be used also remain to be

answered. Clinical trials are underway to answer these questions, although they are unlikely to

provide simple answers. At present, optimal management should be guided by knowledge of the

pathophysiology underlying the disease, and of the different roles of the different fluids.

5.17 Summary

This chapter has discussed how the structured approach should be used in the assessment and

management of the child with circulatory failure. Specific conditions and their management have

been looked at in greater depth.

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

6.1 Introduction

The conscious level may be altered by disease, injury or intoxication, as well as by cerebral hypoxia

or hypoperfusion due to respiratory or circulatory failure. The level of awareness decreases as a child

passes through stages from drowsiness (mild reduction in alertness and increase in hours of sleep)

to unconsciousness (unrousable, unresponsive).

Because of variability in the definition of words describing the degree of conscious level, the Glasgow

Coma Scale (GCS) and the Children’s Glasgow Coma Scale (Table6.1) have been developed as semi-

quantitative measures and, more importantly, as an aid to communication between carers. The

GCS was developed and validated for use in the head- injured patient but has come to be used as an

unvalidated tool for the description of conscious states from all pathologies. Coma occurs when a

child is unconscious and unresponsive to painful stimuli and equates to a GCS of 3–8. It represents

an acute, life- threatening emergency that requires prompt action to prevent both life- long neuro-

logical morbidity and mortality.

In children, causes of coma are either traumatic or non- traumatic. The most common aetiologies

are summarised in Box6.1, with infection being the overall leading cause in all ages.

Children with a decreased conscious level are usually presented by parents who are very aware of

the seriousness of the symptom. They may also have noted other features such as fever, headache

or exposure to poisoning, which may aid the clinician in making a presumptive diagnosis. In children

with neurodevelopmental delay, parents can provide vital information about the child’s usual level

of responsiveness; deviation from this baseline should be taken as a sign of reduced conscious level.

Decreased conscious

level (with or without

seizures)

CHAPTER 6

Learning outcomes

After reading this chapter, you will be able to:

z List the causes of decreased conscious level in infants and children

z Describe the pathophysiology and management of raised intracranial pressure

z Describe how to assess a child with a decreased conscious level

z Describe how to resuscitate a child with a decreased conscious level

z Describe how to assess and treat a child presenting with seizures

94 PART 2 The seriously ill child

Box 6.1 Disorders causing reduced conscious level inchildren

z Hypoxic ischaemic brain injury following

respiratory or circulatory failure

z Epileptic seizures

z Trauma:

z intracranial haemorrhage

z brain swelling

z Infections:

z sepsis

z meningitis

z encephalitis

z cerebral and extracerebral abscesses

z malaria

z Intoxication:

z alcohol

z drugs, including accidental ingestion

z Metabolic:

z renal or hepatic failure

z hypo- or hypernatraemia

z hypoglycaemia

z hypothermia

z hypo- or hypercapnia

z inborn errors of metabolism

z hyperammonaemia

z Cerebral tumour

z Stroke or cerebrovascular event (haemor-

rhagic or ischaemic)

z Cerebral venous sinus thrombosis

z Hydrocephalus, including blocked intra-

ventricular shunts

Table6.1 Glasgow Coma Scale andChildren’s Glasgow Coma Scale

Glasgow Coma Scale (4–15 years) Children’s Glasgow Coma Scale (less than 4 years)

Response Score Response Score

Eye opening Eye opening

Spontaneously 4 Spontaneously 4

To verbal stimuli 3 To verbal stimuli 3

To pain 2 To pain 2

No response to pain 1 No response to pain 1

Best verbal response Best verbal response

Orientated and converses 5 Alert, babbles, coos words to usual ability 5

Disorientated and converses 4 Less than usual words, spontaneous

irritable cry

Inappropriate words 3 Cries only to pain 3

Incomprehensible sounds 2 Moans to pain 2

No response to pain 1 No response to pain 1

Best motor response Best motor response

Obeys verbal command 6 Spontaneous or obeys verbal command 6

Localises to pain 5 Localises to pain or withdraws to touch 5

Withdraws from pain 4 Withdraws from pain 4

Abnormal 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 1

CHAPTER 6 Decreased conscious level (with or without seizures) 95

6.2 Primary survey andresuscitation

ABCDE

The first steps in the management of the child with a decreased conscious level are to assess and,

if necessary, support airway, breathing and circulation. This will ensure that the diminished conscious

level is not secondary to hypoxia and/or ischaemia and that whatever the cerebral pathology, it will

not be worsened by a lack of oxygenated blood supply to the brain.

Follow the algorithm for coma (Figure6.1).

Assess and stabilise ABC

Give high-flow oxygen

Establish IV /IO access

Identification and

immediate treatment

of the treatable

Commence diagnostic workup

Inform specialist teams

DEFINITIVE CARE

Give glucose

10% 3 ml/kg

Check glucose

Reassess

Rapid assessment

of conscious level

URGENT

Intubation and

ventilation

Raised ICP

management

CONSIDER

intubation and

ventilation

CONSIDER

naloxone trial

Insecure

airway

Inadequate

breathing

Possible

raised

ICP

Alert or responds

to voice or pain

Less than 2.8 mmol/l

Less than 50 mg/dl

Unresponsive

Initial management of coma

Figure6.1 Initial management of coma algorithm

ICP, intracranial pressure

96 PART 2 The seriously ill child

Features specific forchild withdecreased conscious level

Airway

z Ensure the airway is open. Assess the need for airway- opening manoeuvres, airway adjuncts or

intubation to secure the airway

z If the child has an AVPU score of ‘P’ or ‘U’ or the gag or cough reflex is absent, then the airway is

at risk. It should be maintained by an airway manoeuvre or adjunct, and preparations for

intubation made as soon as possible

Breathing

z Assess if breathing is adequate and provide appropriate respiratory support

z Some causes of coma may also affect breathing patterns. For example, acidotic sighing

respirations may suggest metabolic acidosis from diabetes, an inborn error of metabolism or

salicylate/ethylene glycol poisoning

Resuscitation

z All children with a decreased conscious level should receive high- flow oxygen through a face

mask with a reservoir or high- flow nasal cannula

z If the child is hypoventilating, respiration should be supported with oxygen via a bag–valve–mask

device while preparations are made for intubation and ventilation. Inadequate breathing in coma

can lead to a rise in arterial PCO2, which can cause a dangerous rise in intracranial pressure (ICP)

Circulation

z Hypertension and/or bradycardia indicate critically raised ICP, until proven otherwise. Conversely

hypotension and/or tachycardia indicate shock

Resuscitation

z Establish IV/IO access quickly

z Take a blood gas, look at the glucose and send blood urgently for an ammonia level. Correct

hypoglycaemia (less than 2.8mmol/l or 50mg/dl) with a 3ml/kg bolus of 10% glucose. Note that

if a metabolic condition is suspected, subsequent maintenance rates of 8mg/kg/min of glucose

may be required

z If hypoglycaemia is a new condition for the child, send blood to the laboratory for plasma to be

frozen for specific hypoglycaemia investigations as per local protocol. This will allow later

investigation of the cause of the hypoglycaemic state. The blood should be taken on initial

cannulation before administering glucose but do not delay correcting hypoglycaemia with

further attempts

z Blood should also be sent for urea and electrolytes (U&E), liver function test (LFT), full blood

count (FBC) and blood culture

z Give a broad- spectrum intravenous antibiotic such as cefotaxime or ceftriaxone. Consider

adding amoxicillin to cover Listeria. Aciclovir should be given to cover herpes simplex encep-

halitis if central nervous system infection is suspected. If meningitis is suspected, also consider

giving dexamethasone

z Reverse shock with 10 ml/kg boluses of isotonic crystalloid. Reassess and repeat only if fluid

responsive

z Vasopressors (noradrenaline, metaraminol, phenylephrine) may be required to maintain blood

pressure at a level to ensure cerebral perfusion pressure of 40–60mmHg, especially if there are

concerns about raised ICP. To start, all can temporarily be given through a peripheral vein when

a diluted solution is used

CHAPTER 6 Decreased conscious level (with or without seizures) 97

Disability

z Abnormal tonic posturing might suggest raised ICP presenting as decerebrate posturing and

may be mistaken for seizure activity

z Look for evidence of seizure activity (subtle findings may include fixed eye deviation and

nystagmus)

z Look for neck stiffness in a child and a full or tense fontanelle in an infant, which suggest

meningitis

z A purpuric rash suggests meningococcal/streptococcal sepsis

z Petechiae or bruising might point to trauma, non- accidental injury or coagulopathy

z Fever is suggestive evidence of an infectious cause (but its absence does not exclude it) or

poisoning with ecstasy, cocaine or salicylates. Hypothermia suggests poisoning with barbiturates

or ethanol

z Look for evidence of poisoning: history or characteristic smell (see Appendix F)

z Acute focal neurological deficit (e.g. motor weakness, facial palsy) or speech disturbance suggest

potential stroke

z Consider a metabolic cause particularly if a prolonged period of poor caloric intake preceded the

illness

Resuscitation

z Manage the causes identified above, aiming to reduce secondary insult due to hypoxia or

hypoglycaemia

There should be a specific assessment for raised ICP. A history taken from parents might contain

evidence of preceding symptoms. The symptoms and signs in Box6.2 are suggestive of raised

ICP.In infants there may be a bulging fontanelle, an increase in head circumference and a high-

pitched cry.

Box 6.2 Symptoms andsigns ofraised intracranial pressure

z Headache (often worse in the morning or on waking the child from sleep)

z Persistent vomiting or history of early morning vomiting

z Seizures

z Abnormal posturing (see Figure3.4)

z Reduced visual acuity

z Pupillary reaction to light impaired or lost

z Pupillary dilatation, unilateral or bilateral

z Sixth nerve palsy, as a false localising sign

z Hypertension and bradycardia, which together with rapid, irregular breathing form

‘Cushing’s triad’. This is a late, pre- terminal sign

z Papilloedema, not always present in the acute phase

98 PART 2 The seriously ill child

6.3 Pathophysiology ofraised intracranial pressure

Children with a closed fontanelle have a fixed volume cranium, meaning an expansion of intracranial

contents due to brain swelling, haematoma or cerebrospinal fluid (CSF) blockage will cause raised

ICP. In very young children, before the cranial sutures are closed, considerable intracranial volume

expansion may occur if the disease process is slow (e.g. hydrocephalus), but raised ICP can still

develop quickly if the process is rapid.

Initially, CSF and venous blood within the cranium decrease in volume. Soon, this compensating

mechanism fails and as the ICP continues to rise the cerebral perfusion pressure (CPP) falls and the

cerebral arterial blood flow is reduced. CPP is defined as mean arterial pressure (MAP) minus ICP:

CPP MAP ICP

Reduced CPP reduces cerebral blood flow, leading to secondary injury caused by cerebral ischae-

mia. The aim is to keep CPP above 40–60mmHg, with infants at the lower end and adolescents at

the upper end of this range. In the absence of direct ICP monitoring, an ICP of at least 20mmHg

can be used to calculate the MAP target to maintain CPP.

Increasing ICP will push brain tissue against more rigid intracranial structures. A brain herniation

can be classified by where the brain tissue has shifted (Figure6.2).

Subfalcine

Uncal

Cerebellar

tonsillar

Descending transtentorial

Ascending transtentorial

Figure6.2 Herniations of the brain

1. Subfalcine. The brain tissue moves underneath the falx cerebri in the middle

of the brain. Brain

tissue ends up being pushed across to the other side.

2. Transtentorial:

z Descending or uncal. The 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

tentorial opening and compressed against the fixed free edge of the tentorium. If the pressure

is unilateral (e.g. from a subdural or extradural haematoma), this leads to third nerve compression

and an ipsilateral dilated pupil. Next, an external oculomotor palsy appears, and the eye appears

deviated ‘down and out’ and there may be a ptosis. Hemiplegia may then develop on either or

both sides of the body, depending on the progression of the herniation

z Ascending. The cerebellum and the brain stem move upward through a notch in a membrane

called the tentorium cerebelli

CHAPTER 6 Decreased conscious level (with or without seizures) 99

3. Cerebellar tonsillar. The 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, raised

blood pressure and irregular respiration leading to apnoea are seen terminally, usually preceded by

significant tachycardia. The presence of hypertension and bradycardia are late signs of raised

ICP; their absence should not be taken to mean that the ICP is normal.

It is important to note that there is a widely held misconception that critically rising ICP is always

accompanied by a progressive deterioration in conscious level. In fact, a GCS of 15 can be main-

tained right up until the point of brain- stem herniation and should not be considered reassuring in

children with signs and symptoms of critically raised ICP. Immediate medical control of ICP, diag-

nostic imaging and definitive treatment are required in these circ*mstances.

6.4 Management ofraised intracranial pressure

Management of raised ICP is a time- critical emergency. A full paediatric emergency team should be

assembled, and the following actions taken immediately. These actions are collectively referred to

as ‘neuroprotection’.

z Intubate and ventilate. Initially target normal oxygen saturations and maintain end-tidal carbon

dioxide (CO2) at 3.5–4 kPa (26–30 mmHg), equivalent to PaCO2 4–4.5 kPa (30–34 mmHg)

z Deeply sedate and fully muscle relax to reduce ICP and cerebral oxygen demand

z Treat seizures to reduce cerebral oxygen demand

z Manage 20° head up

z Give 3% sodium chloride in 3–5ml/kg boluses IV/IO over 10minutes

z Mannitol may be used as an alternative if sodium chloride is not available (0.25–0.5 g/kg; i.e.

1.25–2.5ml/kg of 20% solution IV over 15minutes)

z Maintain blood pressure at a level to ensure CPP of 40–60mmHg

z Arrange an urgent computed tomography (CT) scan of the head and contact the neurosurgical

centre and the paediatric critical care unit (PCCU)

6.5 Lumbar puncture

Lumbar puncture should not be performed acutely in a child presenting with altered conscious

level or signs or symptoms of raised ICP.

There is no benefit in performing an acute lumbar puncture, which carries the risk of coning and

death if it is performed in a child with significantly raised ICP. Normal fundi or a normal CT scan do not

exclude raised ICP. Treatment for meningoencephalitis should be commenced without delay when

infection is part of the differential diagnosis. A blood culture should be taken. If it is considered important,

a lumbar puncture can be performed later in the clinical course, when it is safe to do so and polymer-

ase chain reaction (PCR) tests used to look for evidence of specific bacterial or viral infection.

When todefer lumbar puncture

Defer preforming a lumbar puncture if the child has:

z Signs of raised intracranial pressure (see Box6.2)

z A reduced or deteriorating GCS score

z Focal neurological signs

z Had a prolonged seizure

z Shock

z Clinical evidence of meningococcal/streptococcal sepsis

z A CT or MRI scan suggesting blockage or impairment of the cerebrospinal fluid pathways,

e.g. by blood, pus, tumour or coning

z Coagulopathy

From RCPCH (2019)

100 PART 2 The seriously ill child

6.6 Secondary survey andlooking forkey features

While the primary survey and resuscitation are being carried out, a focused history should be taken

of the child’s health and activity over the previous 24 hours and of any significant previous illnesses.

In a child in a coma, it is often impossible to be certain of the diagnosis in the first hour and so the

focus should be on resuscitation and stabilisation while looking for and treating reversible causes.

Specific points for history taking include:

z Recent trauma

z Pre- existing neurological disability

z History of epilepsy

z Poison ingestion: specifically enquire about medicine/agents that the child might have been

exposed to

z Known chronic condition (e.g. renal disease, cardiac abnormality, diabetes)

z Known metabolic disorder or family history of one

z Previous episodes of encephalopathy with illness

z Recent foreign travel

z Ear or paranasal sinus infection

Specific additional neurological examination includes:

z Eye examination:

z Pupil size (may be subjective) and reactivity (Table6.2)

z Fundal changes: haemorrhage and papilloedema (trauma, hypertension)

z Ophthalmoplegia: lateral or vertical deviation

z Reassess posture, tone and power: look for lateralisation

z Assess deep tendon reflexes and plantar responses and look for lateralisation

z Assess for facial palsy or speech disturbance

Lateralisation suggests a localised rather than a generalised lesion, but this is often a false indicator

in childhood. The child will need urgent CT or magnetic resonance imaging (MRI) scan for further

evaluation.

A general physical examination may add clues to point to a working diagnosis. Specific findings

include the following:

z Skin: rash, haemorrhage, trauma and evidence of neurocutaneous syndromes

z Scalp: evidence of trauma

z Ears and nose:

z Bloody or clear discharge from a base of skull fracture (see Chapter11)

z Evidence of otitis media or mastoiditis: can point to meningitis

z Neck tenderness or rigidity: meningitis or cerebrovascular accident

z Odour: alcohol intoxication, ketones in diabetic ketoacidosis or metabolic disorders

z Abdomen: enlarged liver may indicate inherited metabolic disease

Table6.2 Summary ofpupillary changes

Pupil size and reactivity Potential causes

Small reactive pupils Metabolic disorders, medullary lesion

Pinpoint pupils Narcotic/organophosphate ingestions, metabolic disorders

Fixed mid- size pupils Midbrain lesion

Fixed dilated pupils Hypothermia, severe hypoxia, brain- stem herniation, barbiturates (late sign), during

and post seizure, anticholinergic drugs, recent administration of high- dose adrenaline

Unilateral dilated pupil Rapidly expanding ipsilateral lesion, tentorial herniation, third nerve lesion,

epileptic seizures

CHAPTER 6 Decreased conscious level (with or without seizures) 101

The key features, which will be identified clinically, from the history, examination and the initial blood

test results, can point the clinician to the likeliest working diagnosis for emergency treatment.

z Coma that develops over several hours, associated with irritability and/or fever and a rash points

to meningitis/encephalitis

z A history of drug or poison ingestion and pinpoint pupils point to poisoning with opiates

z Coma occurring in the setting of, or just after, a minor illness presenting with vomiting,

hepatomegaly and hypoglycaemia points to metabolic encephalopathy

z A history of travel to a malaria endemic country and splenomegaly might point to malaria

z Coma associated with significant hypertension points to hypertensive encephalopathy

z A vague and inconsistent history and/or suspicious bruising in an infant are suggestive of non-

accidental head injury; the presence of retinal haemorrhage is supportive

evidence of this

z Hyperglycaemia points to diabetes

z A history of very sudden onset of coma, sometimes with a preceding headache, points

to an intracerebral bleed. Speech disturbance or focal deficit might suggest ischaemic stroke

Note that unless meningitis can be excluded by the clear identification of another cause for coma,

antibiotics should be given. The consequence of a missed diagnosis is catastrophic and the risk of

unnecessary treatment with antibiotics small. This also applies to meningoencephalitis from

Mycoplasma and herpes, and the use of a macrolide (e.g. azithromycin or erythromycin) and aciclo-

vir, respectively. Early initiation of treatment is important because these have a worse prognosis

when treatment is seriously delayed. Senior advice should be sought.

6.7 Approach tothe child withmeningitis/encephalitis

After the neonatal period, the two most common causes of bacterial meningitis are Streptococcus

pneumoniae and Neisseria meningitidis (meningococcus). There is still a mortality rate of around

5% and a similar rate of permanent serious sequelae. Infection with S. pneumoniae may follow an

upper respiratory tract infection with or without otitis media. Long- term morbidity and mortality

occur in up to 30% of cases. Widespread Hib vaccination has reduced the incidence of Haemophilus

influenzae infection. Pneumococcal and meningococcus B vaccines are now part of the childhood

immunisation schedule in most countries. A history of weight loss, contact, fever and slow onset of

meningeal signs suggests tuberculous meningitis.

For infants presenting at under 1month of age, the most common causes of bacterial meningitis

are group B Streptococcus and Escherichia coli. This may present some time after delivery, and lead

to readmission.

A wide range of infections may also cause encephalitis. The most common viral infection, in infants

particularly, is herpes simplex.

Diagnosis ofbacterial meningitis

In children of3 years andunder

Bacterial 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. A bulging fontanelle is a sign

of advanced meningitis in an infant, but even this serious and late sign will be masked if the baby is

dehydrated from fever and vomiting. Almost all children with meningitis have some degree of

raised ICP, so that, in fact, the signs and symptoms of meningitis are primarily those of raised ICP.

The following are signs of possible meningitis in infants and young children:

z Coma

z Drowsiness (often shown by lack of eye contact with parents or doctor)

z High- pitched cry or irritability that cannot be easily soothed by parent

z Poor feeding

z Unexplained pyrexia

z Convulsions with or without fever

z Apnoeic or cyanotic attacks

z Purpuric rash

102 PART 2 The seriously ill child

In children of4 years andover

These 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 unwell children, and

children with fever without an apparent source, a careful search should be made for neck stiffness

and for a purpuric rash. The finding of such a rash in an ill child is indicative of meningococcal or

other bacterial sepsis, for which immediate treatment is required (see Chapter5).

Emergency treatment ofmeningitis

Reassess ABCDE

z Specific assessment should be made of the severity of raised ICP, as many of the clinical signs of

meningitis arise from this

z Give IV ceftriaxone or cefotaxime (child under 3 months) or another suitable antibiotic if

meningitis cannot be excluded and this has not yet been given. Empirically treat a child with

raised ICP and meningitis, and defer or do not perform a lumbar puncture. Ensure blood cultures

and PCR have been taken, as these may help in the diagnosis

z Treat a febrile child with reduced conscious level or focal neurology with aciclovir and a macrolide

to cover herpes simplex virus and Mycoplasma encephalitis

It is generally recommended that dexamethasone be administered before or with the first dose of

antibiotics and no more than 6 hours later, when bacterial meningitis is confirmed or strongly

suspected to reduce the rate of severe hearing loss and other long- term neurological sequelae

(150micrograms/kg up to a max. of 10mg four times a day).

6.8 Approach tothe child poisoned withopiates

These children have usually accidentally ingested oral opioids such as methadone, oxycodone or

oramorph. The sedative effect of the drug may reduce the conscious level sufficiently to put the

airway at risk and cause hypoventilation.

Emergency treatment ofopiate poisoning

Reassess ABCDE

Following stabilisation of the airway, breathing and circulation, the specific antidote is naloxone,

with rapid titration to reverse potential life- threatening effects, starting with an initial bolus dose of

100micrograms/kg IV in children under 12 years. If there is no response, repeat the dose at intervals

of 1minute to the maximum dose of 2mg, then review the diagnosis. In children over 12 years, the

initial dose is 400micrograms, then 800micrograms for up to two doses at 1minute intervals, then

one dose of 2mg if there is still no response. Naloxone has a short half- life, relapse often occurring

after 20minutes. Further boluses, or an infusion of 5–20micrograms/kg/min, may be required. For

older children, intranasal is an alternative route for delivery (1 spray = 1.8mg).

Adverse events such as ventricular arrhythmias, acute pulmonary oedema, asystole or seizures have

incidentally been described, due to the sudden rise in catecholamine (pro- arrhythmogenic) or cen-

tral neurogenetic responses to narcotic reversal. Assess ABCDE and prepare for resuscitative meas-

ures prior to naloxone administration.

CHAPTER 6 Decreased conscious level (with or without seizures) 103

6.9 Approach tothe child withmetabolic coma

The most common metabolic disorders that can result in encephalopathy are hypoglycaemia

and diabetic ketoacidosis (see Appendix B). Diabetic ketoacidosis can be associated with cerebral

oedema and cerebral venous sinus thrombosis. Nevertheless, metabolic coma can arise from a

variety of conditions, including a number of rare, inborn errors of metabolism. These illnesses often

present with a rapidly progressive encephalopathy, vomiting, drowsiness and convulsions or

coma. There may be associated hepatomegaly, hypoglycaemia, abnormal liver enzymes and/or

hyperammonaemia. In a case of otherwise unexplained decreased consciousness, a key urgent

investigation is a plasma ammonia, particularly in infants. Ideally, the plasma ammonia sample

should be sent rapidly on ice for the most accurate measurement. Interpretation of the concentration

can be difficult, as can specific treatment of the hyperammonaemia. Seek advice from a specialist

in inherited metabolic disease and the PCCU, as children with hyperammonaemia may need urgent

transfer for renal replacement therapy to reduce the ammonia level. Sodium benzoate and sodium

phenylbutyrate infusions should be used as the ammonia scavenging agent in the first instance.

Carglumic acid can also be used. Encephalopathy secondary to hyperammonaemia commonly

presents in the neonatal period but can occur even as late as adulthood.

6.10 Approach tothe child withmalaria

Plasmodium falciparum causes 95% of deaths and the most severe complications in children with

malaria. It is transmitted by the bite of an infected Anopheles mosquito, and less commonly by

infected blood transfusion, needle stick injuries or by the transplacental route.

The clinical features of severe disease include reduced conscious level, convulsions, metabolic

acidosis, hypoglycaemia and severe normocytic anaemia. Cerebral malaria may produce encepha-

lopathy, rapid- onset coma and raised ICP. Diagnosis requires microscopy

of a thick film (quick

diagnosis) and thin film (species identification). Rapid diagnostic tests also have a high sensitivity

and specificity, but always need to be followed by a thick smear. Obtain a complete history, includ-

ing the likely country or region of origination and get expert advice.

Specific emergency treatment ofcerebral malaria

Reassess ABCDE

z Artesunate IV/IO (3mg/kg if the child weighs less than 20kg, 2.4mg/kg if more than 20kg) is

the recommended treatment for severe P. falciparum malaria. It is given on admission, then

exactly at 12 and 24 hours, then once a day, to get the parasitaemia down as soon as possible

in the first 24 hours. Monitor cytology since there is a risk of haemolysis. Consider adding

clindamycin when the mortality risk is high (parasitaemia more than 10% or severely ill) after

discussion with a specialist. Complete the treatment with artemisinin combined treatment

orally, after at least three doses of artesunate IV if the child is clinically better. IV quinine is only

an acceptable alternative if artesunate is not available (loading dose 20mg/kg over 4 hours in

glucose 5%, then 10mg/kg every 8 hours). Use electrocardiogram (ECG) monitoring during

administration. Do not give quinine in bolus because of the risk of severe arrhythmia/

hypotension. In renal/hepatic failure, reduce the quinine dose by a third after 48 hours. After

at least 24 hours or when clinically well enough to switch to oral medication, complete by

enteral treatment

z Consider IV antibiotics (e.g. cefotaxime) since the risk of concomitant bacterial (especially Gram-

negative) infections is high in children

z Monitor and treat hypoglycaemia as needed

z If there is evidence of life- threatening anaemia (haemoglobin less than 5 g/dl) consider

transfusion, especially if there are signs of heart failure. Be cautious with fluid administration,

reduce maintenance to 70% of normal and beware fluid overload and cerebral oedema

104 PART 2 The seriously ill child

6.11 Approach tothe child presenting withstroke

Stroke is an important childhood disorder, leading to significant mortality and morbidity. However,

the condition is often missed due to a low index of suspicion, leading to delayed diagnosis. Better

recognition of childhood stroke can facilitate early imaging, assessment and intervention, leading

to better outcomes.

Identification ofpotential stroke

Signs of stroke in children include:

z Acute focal neurological deficit

z Speech disturbance

z Unexplained change in conscious level (GCS of less than 12)

Stroke should also be considered in children with:

z New- onset focal seizures

z New- onset severe headache

z Ataxia

z Vertigo

z Resolved acute focal neurological deficit of unknown cause

Initial management andinvestigation ofsuspected stroke

z As with any child with neurological concerns, the priority is to perform a rapid ABCDE assessment

and quickly reverse any compromise to airway, breathing and circulation that poses an

immediate risk to life. This includes urgent intubation and ventilation if the GCS is less than 8, if

the child’s airway is not being maintained or if there is suspicion of raised ICP

z Obtain intravenous access and send blood tests for FBC, U&E, LFT, C- reactive protein (CRP),

coagulation screen, glucose, blood gas analysis, blood cultures and group and save

z Record time of symptom onset and assess neurological deficit using the PedNIHSS (Paediatric

National Institute of Health Stroke Scale) score (https://www.mdcalc.com/calc/10270/

pediatric- nih- stroke- scale- nihss, last accessed January 2023) to determine suitability for

potential thrombolysis

z Arrange urgent brain imaging. A CT scan with angiography (CTA) should be performed within 1

hour of admission to facilitate potential thrombolysis. MRI with stroke- specific sequences may

be performed in children in whom there is diagnostic uncertainty after the CT scan; this should

be discussed with specialist paediatric neurology services

Management ofconfirmed stroke

All children with confirmed stroke should be urgently discussed with local paediatric neurology

and/or critical care specialists to guide further management. Treatment may need to be initiated

locally, but children should subsequently be transferred to a centre with paediatric neurology and

critical care expertise on site.

Haemorrhagic stroke

Children with haemorrhagic stroke should be urgently discussed with local paediatric critical care

and/or neurosurgical teams and will usually require time- critical transfer for neurosurgical intervention.

Arterial ischaemic stroke

Children with confirmed arterial ischaemic stroke should be considered for emergency intervention,

including thrombolysis, thrombectomy or decompressive craniectomy.

https://www.mdcalc.com/calc/10270/pediatric-nih-stroke-scale-nihss

CHAPTER 6 Decreased conscious level (with or without seizures) 105

Thrombolysis can be considered in children over 2 years old in whom all of the following are true,

and if there are no contraindications:

z PedNIHSS score between 4 and 24

z Thrombolysis can be administered within 4.5 hours of symptom onset

z CT has excluded intracranial haemorrhage

z CT demonstrates normal brain parenchyma or minimal early ischaemic change

z CTA demonstrates partial/complete occlusion of the intracranial artery corresponding to the

clinical/radiological deficit or MRI and magnetic resonance angiography (MRA) show evidence

of acute ischaemia on diffusion weighted imaging and partial/complete occlusion of the

intracranial artery corresponding to the clinical/radiological deficit

Local protocols and specialist advice should be sought before initiating thrombolysis.

If thrombolysis is not indicated, and there is no evidence of parenchymal haemorrhage, the admin-

istration of aspirin (5mg/kg PO/NG) or anticoagulation should be considered.

Thrombectomy may be considered up to 12 hours after symptom onset (including prior thrombolysis)

in children with a PedNIHSS score of more than 6 and favourable brain imaging; this should be

discussed by paediatric neurology and interventional radiology specialists.

Decompressive craniectomy may be required in children with vascular infarction caused by stroke

and signs of raised ICP or deteriorating conscious level. These children should have immediate

raised ICP management as discussed earlier and urgent discussion with neurosurgery.

6.12 Approach tothe child withsystemic hypertensive crisis

Hypertension is uncommon in children. Renal disorders such as dysplastic kidneys, reflux nephropathy

or glomerulonephritis account for most children presenting with severe hypertension. Coarctation of

the aorta is another important cause. Blood pressure is rarely measured routinely in otherwise healthy

children and therefore hypertension usually presents with symptoms that may be diverse in nature.

Neurological symptoms are more common in children than in adults. There may be a history of severe

headaches, with or without vomiting. Children may also present acutely with convulsions or in a

coma. Some children will present with a facial palsy or hemiplegia, and small babies may even present

with apnoea or cardiac failure. Any child presenting with hypertension and neurological signs or

symptoms should be assumed to have critically raised ICP and treated accordingly until proven

otherwise.

Blood pressure measurement

This may be difficult in small children and misleading if not done correctly. The following guidelines

should be observed:

z Always use the biggest cuff that will fit comfortably on the upper arm. A small cuff will give

erroneously high readings

z The systolic blood pressure may give a more reliable reading than the diastolic because the

fourth Korotkoff sound is frequently either not heard or is audible down to zero

z When using an electronic device,

if the result is unexpected recheck it manually before acting

on it

z A raised blood pressure in a child who is seizing, in pain or screaming must be rechecked when

the child is calm

Blood pressure increases with age– the reading should be checked against normal ranges for the

child’s age (see the normal ranges table (inside front cover)). Any blood pressure over the 95th

centile should be repeated and if persistently raised will need treatment. Blood pressures leading

to symptoms will be grossly elevated for the child’s age and the diagnosis should not be

difficult.

106 PART 2 The seriously ill child

Emergency treatment ofhypertension

Reassess ABCDE

Airway, breathing and circulation should be assessed and managed in the usual way and the

neurological status assessed and monitored. Convulsions should be managed as per the status

epilepticus algorithm (see Figure 6.4) and children with clinical signs of raised ICP should be

managed accordingly.

Once the child has been resuscitated, management of the hypertension is urgent, but should only

be commenced after discussion with a paediatric nephrologist, cardiologist or intensivist. The aim

of treatment is to achieve a safe reduction in blood pressure to alleviate the urgent presenting

symptoms whilst avoiding the optic nerve or neurological damage that may occur with too rapid a

reduction. Typically, the aim is to bring the blood pressure down to the 95th centile for age (or

height) over 24–48 hours, with perhaps one- third of the reduction in the first 8 hours. This must be

undertaken in conjunction with close blood pressure monitoring and a titratable infusion of the

antihypertensive drug. PCCU admission is mandatory during the initial treatment and children

should be cared for in a unit experienced in managing paediatric hypertension. This will usually be

the regional paediatric nephrology (or paediatric cardiology) centre. It is essential that adequate

consultation takes place before transfer.

Monitoring of visual acuity and pupils is crucial during this time as rapidly lowering the blood pressure

may lead to infarction of the optic nerve heads. Any deterioration must be treated by urgently raising

the blood pressure by lowering the antihypertensive treatment and/or using IV crystalloids or colloids.

Some children may be anuric– renal function (serum creatinine, U&E) should be analysed promptly.

Some drugs commonly used to achieve blood pressure reduction in children are shown in Table6.3

and the usual starting point would be oral/sublingual nifedipine.

6.13 Further stabilisation andtransfer todefinitive care

Children presenting with altered conscious level of unknown cause need an urgent CT scan, especially

if there are signs of raised ICP or focal neurological signs, as soon as possible after resuscitation and

stabilisation. If the imaging shows evidence of an intracranial bleed or other pathology requiring

urgent neurosurgical intervention (e.g. blocked ventriculo- peritoneal shunt), time- critical transfer to

a neurosurgical centre may be required. Children shown to have an ischaemic stroke on imaging will

need urgent discussion regarding the need for thrombolysis and may also need time- critical transfer

to facilitate this. Time- critical transfers are sometimes done by referring teams rather than specialist

paediatric critical care transport teams. Early communication is essential.

Table6.3 Drug therapy forsevere hypertension

Drug Dose Comments

Nifedipine 0.25–0.5mg/kg oral/

sublingual, emergency dose

for hypertensive crisis; may be

repeated once

Fluid can be drawn up from capsules and squirted into

mouth sublingually

Better to bite the capsule and swallow

May cause unpredictable and severe reduction of blood

pressure– monitor closely

Labetalol 0.25–3mg/kg/h IV infusion α- and β- blocker

Titratable infusion

Do not use in patients with fluid overload or acute heart failure

Sodium

nitroprusside

0.5–8 micrograms/kg/min IV

infusion (max. 4 micrograms/

kg/min if used for longer than

24 hours)

Vasodilator

Very easy to adjust dose

Titratable infusion

Protect from light

Monitor cyanide levels if used at max. dose beyond 48 hours

CHAPTER 6 Decreased conscious level (with or without seizures) 107

6.14 Approach tothe child withseizures

Some children presenting with reduced conscious level are having seizures. The overall approach

should be considered similar to other presentations, but there are some specific considerations.

The Neurocritical Care Society guidelines from 2012 define status epilepticus as a seizure with 5min-

utes or more of continuous clinical and/or electrographic seizure activity or recurrent seizure activity

without recovery between seizures. In general, seizures that persist beyond 5minutes are unlikely to

stop spontaneously and so it is usual practice to commence anticonvulsive treatment at this point.

Important causes of convulsions in children include fever (usually in a child less than 6 years old),

meningitis/encephalitis, epilepsy, hypoxia and metabolic abnormalities. Status epilepticus occurs in

approximately 1–5% of patients with epilepsy and up to 5% of children with febrile seizures will pre-

sent with convulsive status epilepticus (CSE).

Status epilepticus can have a significant morbidity. Adverse neurological outcomes are a recognised

complication, which are much more common in patients under 1 year of age. Status epilepticus can

also be fatal, with an all- cause mortality rate in children of about 4–6% (i.e. one in 20 children). A

proportion of these deaths are caused by the primary pathology and it is therefore important to

remember that CSE is not a diagnosis and the treatment algorithm is not necessarily the cure.

Potentially reversible primary critical illness must be sought and treated. Death can also occur as a

consequence of the known complications of prolonged convulsive seizures. These include airway

obstruction, aspiration, respiratory failure, heart failure, cardiac arrhythmias, hypertension, pulmo-

nary oedema and disseminated intravascular coagulation.

Pathophysiology ofprolonged seizures

A generalised convulsion increases the cerebral metabolic rate at least threefold. Initially, there is an

increased sympathetic activity with the release of catecholamines, which lead to peripheral

vasoconstriction and increased systemic blood pressure. There is also a loss of cerebral arterial

regulation and, following the increase in systemic blood pressure, there is a resulting increase in

cerebral blood flow to provide the necessary oxygen and energy. If convulsions continue, the

systemic blood pressure falls and this is followed by a fall in cerebral blood flow. Lactic acid rapidly

accumulates and there is subsequently cell death, oedema and raised intracranial pressure resulting

in further worsening of cerebral perfusion. Prolonged seizure activity causes downregulation of

inhibitory γ- aminobutyric acid receptors in the brain. These changes perpetuate seizure activity and

mean that first line anticonvulsants that act on these receptors (benzodiazepines, e.g. lorazepam,

midazolam) become less effective as the seizure continues.

Primary survey andresuscitation ofchildren withseizures

ABCDE

Look specifically for any evidence of red flags in a child presenting with prolonged seizures (Figure

6.3). The priority is to assess and quickly reverse any compromise to airway, breathing and circulation

that pose an immediate risk to life. Look specifically for any of the following:

If any of these red flags are present, then it is likely that the child needs to be intubated and ventilated

urgently, while reversible causes are identified and treated. Ketamine is the induction agent of choice due

to relative haemodynamic stability. It is anticonvulsant and does not increase ICP as previously thought.

A Airway obstruction not responding to a jaw thrust or airway adjunct

B Respiratory failure

C Shock

D Signs

or symptoms of raised ICP, encephalopathy or focal neurology

E Purpuric rash, puncture marks or signs of head trauma

108 PART 2 The seriously ill child

URGENT INTERVENTIONS

Correct hypoglycaemia with

3 ml/kg 10% glucose

Treat hyponatraemia less than

125 mmol/l with 3–5 ml/kg of 3%

sodium chloride

Aim for normothermia

Treat meningoencephalitis with

IV ceftriaxone and aciclovir

Check ammonia

Consider specific antidotes

DO NOT DO A LUMBAR

PUNCTURE

INDICATIONS FOR CT SCAN

New prolonged seizure

New focal seizure

Refractory seizures

New neurological deficit

Suspected raised ICP

Suspected space occupying

lesion

VP shunt in situ

Trauma

Possible NAI

Remember to request a

contrast enhanced scan if

suspicion of venous sinus

thrombosis or abscess

Rapid ABCDE assessment

Check glucose

status

epilepticus

algorithm

Anaesthetise to

terminate seizure

Intubate to secure airway

Ventilate to restore

gas exchange

Reverse shock

Neuroprotect

Airway

compromise or respiratory

failure not responding to basic manoeuvres?

Shock unresponsive to fluid resuscitation?

Raised ICP or trauma?

YES NO

Continuous

reassessment

Red flags in the child with seizures

Figure6.3 Red flags in the child with seizures algorithm

CT, computed tomography; ICP, intracranial pressure; NAI, non- accidental injury; VP, ventriculo- peritoneal

If none of these red flags are present then the algorithm follows the familiar pathway (Figure6.4),

through two doses of benzodiazepines to levetiracetam and finally induction of anaesthesia, intu-

bation and ventilation. Continually reassess for red flags when treating any child with seizures and

be ready to intubate and ventilate when it is indicated.

CHAPTER 6 Decreased conscious level (with or without seizures) 109

Secure airway

High flow oxygen

Consider reversible causes

(Don’t ever forget glucose)

Monitor

Lorazepam (IV / IO)

or IV midazolam

Lorazepam (IV / IO)

or IV midazolam

Midazolam

(buccal or intranasal)

Midazolam

(buccal or intranasal)

Diazepam (rectal)

Vascular access

Vascular access?

Convulsion

ongoing?

(check ABCDE)

Convulsion

ongoing?

(check ABCDE)

YES

ANTICIPATE

Get 2nd dose

benzodiazepine

ready

Maximum 2 doses

(including pre-

hospital doses)

• Individual emergency plan

takes precedence

• Early anaesthetic support if

ABC concern

• Pre-hospital benzodiazepine

doses count

Pre-hospital

(trained parent(s) /

carer(s) / paramedics)

In hospital

Pre-hospital (with

paramedics)

In hospital

5 MINS From onset

of convulsion

5 MINS After 1st

benzodiazepine

ANTICIPATE

Get levetiracetam

ready

Levetiracetam

Refer to local monograph for dilution

and infusion

ANTICIPATE

Get phenytoin /

phenobarbitone

ready

Prepare for RSI

5 MINS After 2nd

benzodiazepine

Status epilepticus

Figure6.4 Status epilepticus algorithm

(Continued)

110 PART 2 The seriously ill child

Team ready for immediate RSI?

Rapid sequence induction (RSI)

Ketamine

OR Thiopental

OR Propofol

Status epilepticus (continued)

Refer to local monograph for dilution and

infusion. Cardiac monitoring.

Monitor

Convulsion

ongoing?

(check ABCDE)

YES

Monitor

Convulsion

ongoing?

(check ABCDE)

YES

In hospital with

paediatric registrar

and/or consultant

Anaesthetic team

MUST be present

Inform PCCU and/or

paediatric retrieval

team

10 MINS After

infusion finished

After infusion finished

Already on

phenytoin?

Phenytoin Phenobarbitone

YES

Lorazepam (IV/IO) 0.1 mg/kg (max 4 mg)

Midazolam (IV/IO) 0.15 mg/kg (max 10 mg)

Midazolam (buccal

or intranasal)

3–11 months 2.5 mg

1–4 years 5 mg

5–9 years 7.5 mg

10–17 years 10 mg

~ 0.3 mg/kg (max 10 mg)

Diazepam (rectal)

1 month–1 year 5 mg

2–11 years 5–10 mg

12–17 years 10–20 mg

~ 0.5 mg/kg (max 20 mg)

Levetiracetam

40 mg/kg IV/IO (max 3 g)

Give over 5 minutes

Phenytoin

20 mg/kg IV/IO (max 2 g)

0.8 ml/kg (max 20 ml) PR of

premixed 50:50 solution in olive oil

give over 20 minutes

Phenobarbitone

Paraldehyde

20 mg/kg IV/IO (max 1 g)

give over 20 minutes

Ketamine 1–2 mg/kg

Thiopental

(thiopentone)

3–5 mg/kg IV/IO

Propofol (refer to local monograph)

Figure6.4 (Continued)

CHAPTER 6 Decreased conscious level (with or without seizures) 111

This consensus guideline is not intended to cover all circ*mstances. There are patients with recur-

rent convulsive status whose physicians recognise that they respond to certain drugs and not to

others and for these children an individual protocol is more appropriate. In addition, seizures in

neonates are managed differently to those of infants and children.

It is important to recognise that the timings for interventions are listed from the onset of the seizure

not from arrival into hospital. Pre- hospital treatment should be noted and not repeated unless there

is concern about efficacy of administration. More than two doses of benzodiazepine are associated

with an increased risk of respiratory depression.

In all cases

z Continuous ABCDE assessment with immediate treatment if compromised

z Intubate and ventilate immediately if evidence of red flags is identified

z Take blood for glucose, blood gas analysis, U&E and calcium and correct metabolic abnormalities

z Treat hypoglycaemia with 3ml/kg 10% glucose

z Treat pyrexia with paracetamol or ibuprofen

z Give sodium chloride (3–5ml/kg of 3% solution) if signs of increased ICP are present, followed by

immediate treatment of ICP as described earlier

Five minutes fromseizure onset

z If in a pre- hospital setting or when IV/IO access is not established and if the seizure has lasted

longer than 5minutes, give buccal/intranasal midazolam. This can be given by prefilled syringe

by age (see later in this section) or 0.3mg/kg (max. 10mg). Alternatively, rectal diazepam 0.5mg/

kg (max. 20mg) can be used

z If IV/IO access is already established or can be established quickly, give IV/IO lorazepam 0.1mg/kg

(max. 4mg) or IV midazolam 0.15mg/kg (max. 10 g)

Five minutes after first dose ofbenzodiazepine

z In the hospital setting, give a second dose of benzodiazepine, and call for senior help

z If the child has received buccal midazolam or rectal diazepam before or in hospital, and is still

convulsing, obtain intravenous access to give one dose of IV lorazepam 0.1mg/kg (max. 4mg) or

IV midazolam 0.15mg/kg (max. 10 g). Do not give more than two adequate doses of benzodiazepine,

including any pre- hospital medication

z If intravenous access still has not been achieved, obtain intraosseous access

z Start to prepare levetiracetam or phenytoin for next step

z Reconfirm it is an epileptic seizure

Five minutes after second dose ofbenzodiazepine

z At this stage senior help is needed to reassess the child and advise on management. Anaesthetic

or intensive care support should be obtained urgently, as the child could need anaesthetising

and intubating if this step is unsuccessful

z Give IV levetiracetam 40mg/kg (max. 3g) over 5minutes even if the child usually takes oral

levetiracetam

z If the child is still seizing after loading with IV levetiracetam then termination with induction of

anaesthesia and intubation is expected. However, if the advanced airway team is not yet prepared

and the ABCDE assessment is stable, then either phenytoin (20 mg/kg by IV infusion over

20minutes, max. 2g)– or phenobarbitone (20mg/kg by IV infusion over 20minutes, max. 1g) if

the child already takes phenytoin– can be given. Continuous ECG, blood pressure and pulse

oximetry should be checked throughout

z Rectal paraldehyde (0.8 ml/kg) mixed with an equal volume of olive oil may still appear on

individual seizure management plans and should be given accordingly. The maximum single

dose of paraldehyde is 20ml

112 PART 2 The seriously ill child

Ten minutes after

finish ofinfusion

z By this stage, a full paediatric emergency team, including an anaesthetist, paediatric intensivist

or other practitioner with advanced paediatric anaesthesia and airway skills must be present

z Emergency induction of anaesthesia should be performed. Ketamine is the safest choice of

induction agent. Propofol and thiopentone are sometimes used by experienced practitioners

but these drugs can cause profound hypotension and even cardiac arrest. All induction agents

should be used with a rapid- onset muscle relaxant (e.g. rocuronium)

z Following induction, commence ongoing analgesia and sedation infusions as per local paediatric

critical care guidelines

z Most seizures will stop by this stage. These children can sometimes be safely woken and

extubated without transfer to a PCCU, provided seizures are controlled, physiology has normalised

and serious reversible causes have been excluded; this should be discussed with local paediatric

critical care services

z If seizures continue, commence a midazolam infusion at 100 micrograms/kg/h and arrange

transfer to a PCCU

z Further advice on management should be sought from a paediatric intensivist and/or

neurologist

z In children under 3 years with a history of chronic, active epilepsy, a trial of pyridoxine should be

considered

Post- seizure management

Many children presenting with seizures respond to treatment without the need for intubation and

ventilation. There is commonly a post- ictal period which, in combination with antiepileptic drugs,

results in a reduced conscious level. This period requires close and continuous monitoring. There is

a high risk of airway obstruction and respiratory depression. Potential reversible causes and red

flags need to be continually reassessed. Children not protecting their airway after an oro- /

nasopharyngeal airway has been put in place, should be intubated and ventilated to keep them

safe during this period, even if there is no ongoing seizure activity. There should be a low threshold

for a CT scan and other investigations for reduced conscious level for children not showing signs of

improving GCS score within 30–60minutes of seizure termination.

Other post- seizure management includes:

z Maintain normoglycaemia using 5% or 10% glucose, preferably with isotonic crystalloid (e.g.

Plasma- Lyte 148with 5% glucose or 0.9% sodium chloride with 5% glucose)

z Keep serum sodium in the normal range of 135–145mmol/l

z Consider a nasogastric tube to aspirate the stomach contents

z Regulate temperature, ensuring temperatures above 37.5°C are avoided

Drugs used instatus epilepticus

Lorazepam

Lorazepam is equally or more effective than diazepam and possibly produces less respiratory

depression. It has a longer duration of action (12–24 hours) than diazepam (less than 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 substituted at a dose of 0.25mg/kg IV/IO or midazolam at a dose

of 0.15mg/kg IV/IO.

Midazolam

This is an effective, quick- acting anticonvulsant that takes effect within minutes but has a

shorter lasting effect than lorazepam. It can be given by IV/IO/IM routes or via the buccal or

nasal mucosa. Buccal/nasal midazolam may be twice as effective as rectal diazepam, but both

CHAPTER 6 Decreased conscious level (with or without seizures) 113

drugs produce the same level and degree of respiratory depression. Most children do not

convulse again once the seizure has been terminated. All benzodiazepines have the potential

to cause signif icant respiratory depression requiring active management of both airway

and breathing.

Buccal midazolam is available in prefilled syringes. The dosing schedule is as follows:

The tip of the syringe is inserted into the buccal area between the lower bottom lip and the gum

margin at the side of the mouth. If the licensed preparation is not available, draw up the higher dose

(0.5mg) of the intravenous preparation. For nasal application, commercially available nasal spray

can be used or the dose (0.3mg/kg) can be given using a mucosal atomisation device (MAD) on a

standard syringe.

Continuous midazolam IV/IO infusion is often used as a treatment in a ventilated patient because of

its relative ease of use, its high response rate and low complication rate. The starting dose is

100micrograms/kg/h, increased in steps of 100micrograms/kg/h up to a maximum of 1mg/kg/h.

Diazepam

This 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 midazolam where the latter is

available. The rectal dose is well absorbed.

Paraldehyde

The dose is 0.8ml/kg (max. 20ml) PR of the premixed 50:50 solution in olive oil or 0.9% sodium chloride.

Arachis oil should be avoided because children with peanut allergy may react to it. Paraldehyde can

cause rectal irritation, but IM 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. Do not leave

paraldehyde standing in a plastic syringe for longer than a few minutes. If paraldehyde is given, this

should be at the same time as the levetiracetam is being drawn up or infused. It is also important

that the infusion of phenytoin must not be delayed because paraldehyde has been given.

Levetiracetam

Levetiracetam is a newer antiepileptic drug that is now being used as an alternative to phenytoin

for second line treatment of CSE. The dose is 40mg/kg IV/IO (max. 3g), given over 5minutes. It has

fewer drug interactions and side effects than phenytoin, and the full 40mg/kg dose can be given

even if the child is on regular maintenance levetiracetam.

Phenytoin

The dose is 20mg/kg IV/IO (max. 2g), which must be given over at least 20minutes. The infusion

should be made up in 0.9% sodium chloride to a maximum concentration of 10mg in 1ml. Phenytoin

z 1–2months: 300micrograms/kg (max. dose 2.5mg)

z 3–11months: 2.5mg

z 1–4 years: 5mg

z 5–9 years: 7.5mg

z 10–17 years: 10mg

114 PART 2 The seriously ill child

can cause dysrhythmias and hypotension, therefore monitor the ECG and blood pressure. It has

little depressant effect on respiration.

Ketamine

Ketamine is a short- acting dissociative anaesthetic agent that does not cause cardiovascular

depression. Recent studies have shown that ketamine administration is safe and effective in cases

of refractory status epilepticus, and that it does not raise ICP; therefore, it should be the first line

induction agent for most cases of status epilepticus in order to avoid hypotension associated with

other agents. The induction dose is 1–2mg/kg IV/IO.

Propofol

The induction dose is 2.5–4mg/kg IV and is usually available in dilutions of 1% (10mg/ml) or 2%

(20 mg/ml). It is a white oil- in- water emulsion that commonly causes irritation on intravenous

administration. It is very effective for the induction of general anaesthesia, although its use for

ongoing sedation for children in critical care has been controversial due to the associated risk of

propofol infusion syndrome (potentially fatal effects, including metabolic acidosis, arrhythmias,

cardiac failure, rhabdomyolysis, hyperlipidaemia, hyperkalaemia, hepatomegaly and renal failure).

Propofol should only be administered by, or under the direct supervision of, experienced staff.

Thiopental (thiopentone) sodium

The induction dose is 3–5mg/kg IV/IO. It is an alkaline solution, which will cause irritation if the

solution leaks into subcutaneous tissues. It is a general anaesthetic agent, with no analgesic effect.

Repeated doses have a cumulative effect. It is a potent drug with marked cardiorespiratory effects

and must be used only by experienced

Society/Scottish Intercollegiate Guidelines Network

Children’s Health Queensland

National Tracheostomy Safety Project: Paediatric Working Party

Northern Neonatal Network

Resuscitation Council UK

Royal College Paediatrics and Child Health and Harlow Printing

Safeguard Medical Technologies

Teleflex Medical Australia and New Zealand

Victorian Department of Health

ALSG gratefully acknowledge the support of the Royal College of Paediatrics and Child Health (UK).

The Specialist Groups of the RCPCH agreed to advise on the clinical content of chapters relevant to

their specialism. ALSG wish to thank the following:

xvi Acknowledgements

Association ofPaediatric Emergency Medicine

Anastasia Alco*ck FRCPCH DTM&H DRCOG PgDIP, Paediatric Emergency Medicine Consultant,

Evelina London

Jane Bayreuther FRCPCH, Consultant in Paediatric Emergency Medicine, Southampton. On behalf

of APEM

Charlotte Clements BSc(Hons) MBChB MRCPCH MSc PGCert (Darzi), Consultant Paediatrician,

Clinical Lead for the Paediatric Emergency Department, North Middlesex University Hospital NHS

Trust; Secretary, Association of Paediatric Emergency Medicine

Miki Lazner MBChB MMSc (Child Health) FRCPCH, Paediatric Emergency Medicine Consultant,

Clinical Lead Paediatric Trauma, University Hospitals Sussex NHS Foundation Trust; Paediatric Lead,

Sussex Trauma Network; Guidelines Representative and Executive Committee Member, Association

of Paediatric Emergency Medicine (APEM)

Michael Malley MA MBBS MRCPCH DTMH, Consultant in Paediatric Emergency Medicine, Bristol

Royal Hospital for Children

Rachael Mitchell MRCPCH MA (Cantab), Consultant in Paediatric Emergency Medicine, Kings

College Hospital NHS Foundation Trust

British Association General Paediatrics

Christine Brittain RCPCH, Sub- speciality PEM, Acute Paediatric Consultant, PAU Lead, Musgrove

Park Hospital Somerset Foundation Trust

British Association ofPerinatal Medicine

Hannah Shore MBChB MRCPCH MD, Consultant Neonatologist, Lead Clinician for Leeds Centre for

Newborn Care

Tim J. van Hasselt MBChB BMedSc MRCPCH, Neonatal sub- specialty trainee, West Midlands, NIHR

Doctoral Research Fellow, University of Leicester

British Paediatric Allergy, Immunity andInfection Group

Alasdair Bamford MBBS FRCPCH DTM+H PhD, Consultant and Specialty Lead in Paediatric Infectious

Diseases, Great Ormond Street Hospital for Children NHS Foundation Trust; Honorary Associate

Professor, UCL GOSH Institute of Child Health; British Paediatric Allergy Infection and Immunity

Group (BPAIIG) secretary

Enitan Carrol MBChB MD DTMH FRCPCH, Professor and Honorary Consultant in Paediatric

Immunology and Infectious Diseases, University of Liverpool and Alder Hey Children’s NHS

Foundation Trust

Saul Faust MBBS PhD FRCPCH OBE, Professor and Honorary Consultant in Paediatric Immunology

and Infectious Diseases, University of Southampton and University Hospital Southampton NHS

Foundation Trust

Paul Turner BM BCh FRCPCH PhD, Clinical Reader and Honorary Consultant in Paediatric Allergy

and Clinical Immunology, Imperial College London; Chairperson of Anaphylaxis Committee, World

Allergy Organization

Elizabeth Whittaker MB BAO BCh MRCPCH DTM&H PhD, Consultant in Paediatric Infectious

Diseases; Clinical Lead in Paediatric Infectious Diseases, Imperial College Healthcare NHS Trust,

London; Senior Clinical Lecturer in Paediatric Infectious Diseases, Imperial College London; Convenor

for British Paediatric Allergy Immunity and Infectious Diseases Group (BPAIIG)

Acknowledgements xvii

British Paediatric Respiratory Society

Elise Weir MBChB MRCPCH PGCert Child Health, Consultant in Paediatric Respiratory Medicine,

Royal Hospital for Children, Glasgow

British Society ofPaediatric Radiology– trauma imaging

Judith Foster MB ChB(Hons) FRCR, Consultant Paediatric Radiologist, University Hospitals Plymouth;

Paediatric Trauma Lead for British Society of Paediatric Radiology

Child Protection Special Interest Group

David Lewis MBBS MSc(Paeds) MRCP FRCPCH, Consultant Community Paediatrician and

Designated Doctor for Child Protection (Herefordshire and Worcestershire ICB); Chair of the Child

Protection Specialist Interest Group (affiliated to the Royal College of Paediatrics and Child Health)

Paediatric Critical Care Society

David Finn MBBS MRPCH MSc, Paediatric Intensive Care Consultant, Leeds Children’s Hospital

Rum Thomas MB BS DNB (Paediatrics) FRCPCH, Consultant in Paediatric Critical Care, Sheffield

Children’s NHS Foundation Trust; Clinical Lead, Paediatric Critical Care Operational Delivery Network

Yorkshire and Humber South

Hanna Tilly BSc BMedSci BMBS, Specialist Registrar in Paediatrics, North Central and East London

Mark Worrall MB ChB FRCA MRCPCH FFICM, Consultant in Paediatric Intensive Care and Paediatric

Anaesthesia, Royal Hospital for Children, Glasgow; Consultant in Paediatric Critical Care Transport,

ScotSTAR, Scottish Ambulance Service

RCEM Intercollegiate group

Anne Frampton MPhil BSc MB ChB MRCP DipIMC DCH FRCEM, Consultant in Emergency Medicine

(Paediatrics), Bristol Royal Hospital for Children, UHBW NHS FT

Michelle Jacobs BSc MB BCh FRCEM ARSM, Consultant in Paediatric Emergency Medicine, ED

Clinical Lead for Paediatric Emergency Department, London North West University Healthcare NHS

Trust (Northwick Park Hospital)

Damian Roland B(Med)Sci BMBS FRCPCH PhD, Honorary Professor and Consultant in Emergency

Medicine, Head of Service, Children’s Emergency Department, Leicester Hospitals and University

Rob Stafford MBBS MRCA PGCertMedEd FHEA FRCEM, Consultant in Adult and Paediatric

Emergency Medicine; Chair, RCEM Paediatric Emergency Medicine Professional Advisory Group

We would like to thank, in advance, those of you who will attend the Advanced Paediatric Life

Support course and others using this text for your continued constructive comments regarding the

future development of both the course and the manual.

xix

ALSG: www.alsg.org

For details on ALSG courses visit the website or contact:

Advanced Life Support Group

ALSG Centre for Training and Development

29–31 Ellesmere Street

Swinton, Manchester

M27 0LA

Tel: +44 (0) 161 794 1999

Email: enquiries@alsg.org

Updates

The material contained within this book is updated on approximately a 4- yearly cycle. However,

practice may change in the interim period. We will post any changes on the ALSG website, so we

advise you to visit the website regularly to check for updates (www.alsg.org).

References

To access references, visit the ALSG website www.alsg.org– references are on the course pages as

well as at the end of this book.

On- line feedback

It is important to ALSG that the contact with our providers continues after a course is completed.

We now contact everyone 6months after their course has taken place asking for on- line feedback

on the course. This information is then used whenever the course is updated to ensure that the

course provides optimum training to its participants.

Contact details and

further information

http://www.alsg.org

PART 1

Introduction

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

1.1 Introduction

The Advanced Paediatric Life Support (APLS) course equips those caring for children with the

necessary skills and structured approach to identify and safely manage ill or injured children

whenever or wherever they encounter them.

Children continue to die from preventable causes throughout the world. The reasons for their

deaths differ between countries, however the structure and principles for managing the underlying

causes are universal.

Child mortality is the lowest it has ever been and has halved in the last three decades, which is a huge

achievement (12.5million deaths of under 5‐ year‐ olds worldwide in 1990 compared with 5million in 2020).

Worldwide data from

staff who can intubate a child.

6.15 Summary

This chapter has described how the structured approach should be used in the assessment and

management of the child with reduced conscious level with or without seizures. Children presenting

acutely with a reduced conscious level should worry treating teams. There are potentially reversible,

life- threatening causes and there should be a low threshold for an aggressive approach, especially

when the cause is not known. Specifically, this means intubation, neuroprotection, cover for

meningoencephalitis and urgent investigations for treatable causes, including glucose, ammonia

and CT head. The Royal College or Paediatrics and Child Health (RCPCH) guideline The Management

of Children and Young People with an Acute Decrease in Conscious Level (DECON) provides an

excellent summary of this topic.

115

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

7.1 Introduction

As discussed in Chapter3, the structured approach is:

z Primary survey

z Resuscitation

z Secondary survey and looking for key features to aid diagnosis

z Emergency treatment

z Stabilisation and transfer to definitive care

Once ABCD have been managed to an optimum stage then progress to E. The E for exposure

should encompass a survey of the whole child looking for rashes, bruises, bleeding, etc. At this

stage of the assessment it would also be appropriate to do the following if they have not already

been done:

z Take a temperature

z Actively seek indicators of chronic conditions

z Look for signs of intoxication

z Consider pain management

Exposure

CHAPTER 7

Learning outcomes

After reading this chapter, you will be able to:

z Complete a full assessment relating to exposure

z Resuscitate dependent on findings

z Describe how to undertake a pain assessment

z Understand the variety and methods of administering analgesia to children

It is vital when completing E (exposure) to ensure that the child or young person has their

dignity protected throughout and that they feel as comfortable as possible whilst the full

examination is undertaken

116 PART 2 The seriously ill child

7.2 Temperature

This is the time to ensure that the temperature is checked if it has not been done previously.

High body temperature

An elevated body temperature can be due to fever, as the result of cytokine release causing an

increase in the hypothalamic setpoint, in response to various triggers, or to hyperthermia due to

loss of thermoregulation.

Fever

A fever is one of the most common reasons for parents to seek medical help; in addition, it is one of

the commonest causes for admission. Fever is defined as a temperature over 38°C and can be

caused by a variety of conditions including infections, inflammatory conditions and a reaction to

immunisation.

Symptom relief is with antipyretics, such as paracetamol and ibuprofen, although they should be

spaced out correctly and not given persistently without the child being reviewed by a clinical

practitioner.

Infections

Infections caused by bacteria, viruses, fungi and atypical organisms often result in a temperature

rise as the body mounts an immune response. It is important that the temperature is measured

accurately either using a tympanic thermometer or, in extremely unwell children, a rectal

thermometer. A fever in an infant under 3 months is significant and the baby needs a full

assessment.The clinician needs to maintain a low threshold for instigating a full septic screen and

starting sepsis treatment. It is important to assess whether the child/baby is unwell and whether

there is a significant infection (e.g. meningitis) or mild viral infection which will resolve in a few days.

This may require watching for a period of time and repeat observations.

Sepsis can be said to occur when the body’s response to infection causes injury to its own tissues

and organs. This is a very significant condition and a leading cause of paediatric mortality world-

wide. It needs to be identified and treated correctly with intravenous antibiotics and fluids initially

and escalating care as required. There are a number of systems to aid in the diagnosis such as the

National Institute for Health and Care Excellence (NICE) guidance traffic light system.

Inflammatory conditions

Inflammatory conditions may cause fever. Examples include juvenile chronic arthritis and Kawasaki

disease. These conditions will have indicators in the history or other signs visible on examination.

Post immunisation

After immunisation some children can develop a fever, but these are not usually high or prolonged.

Reassurance and antipyretic treatments are recommended.

Hyperthermia

Drug ingestion, thyrotoxicosis, central nervous system (CNS) damage and heat stroke are all

examples of hyperthermia. Their treatment differs to the management of fever, as antipyretics

may not be helpful and specific therapies are often required as well as physical cooling.

CHAPTER 7 Exposure 117

Low body temperature

Hypothermia occurs when the temperature is below 35oC. This can be due to a number of

factors:

z Infection, as described above, especially in young children

z Exposure to a cold environment: warm using external warmers, warmed fluids and removal of

wet clothes unless there are indications not to warm, for example neuroprotection in significant

head injuries or post cardiac arrest

z Secondary to toxins

z As a result of metabolic derangements

z Dysfunction of central nervous and endocrine systems

7.3 Rashes

Rashes take a number of forms and appearances dependent on cause, severity and skin colour.

z Petechiae (less than 2mm)/purpura (greater than or equal to 3mm):

z Meningococcal or any disease that causes coagulation disorders

z Immune thrombocytopenia (ITP) or any cause of low platelet count

z Traumatic– accidental or non- accidental

z Henoch–Schönlein purpura (HSP)

z Specific infectious exanthema:

z Cold sores– herpes infection has the potential to lead to encephalitis

z COVID- 19 rash

z Measles, scarlet fever, mumps, chickenpox, rubella and impetigo

z Urticaria relating to allergic reaction

7.4 Indicators ofchronic conditions

Look for indicators of chronic conditions especially if the child is unaccompanied and unable to give

a history. Examples include:

z Insulin pumps

z Pacemakers

z Ventriculo- peritoneal shunts

z Cochlear implants

z Surgical scars

z Medic alerts bands

7.5 Signs ofingestion

The most obvious indicator of ingestion comes in the history and would be evident in missing

medicines, tablets, button batteries or empty packaging (see Appendix F for management). It is

also important to look for:

z Discoloration or burns in or around the mouth

z Drooling due to difficulty in swallowing or increased saliva

z Breath smelling of chemicals or alcohol

z Vomiting

z Clinical signs such as drowsiness, confusion or pupillary changes

118 PART 2 The seriously ill child

7.6 Managing pain

The adequate management of pain is integral to all emergency care. Optimising patient comfort

not only allows the practitioner to make a more accurate assessment of illness severity, but also

minimises the adverse physiological responses to pain that worsen outcome.

It is important that the language used when assessing and improving a child’s comfort is carefully

selected. The power of the ‘nocebo effect’, where the use of words describing negative sensations

and experiences increases the likelihood of the child actually experiencing these sensations, must

be recognised. Enquire about negative experiences such as pain and nausea by using open- ended

questions such as ‘Do you need something to make you more comfortable?’ rather than ‘How much

pain are you in?’ Reassuring the child that they are safe, that they will be made comfortable and

that we will help their body to heal

can be powerful.

These principles are also important when obtaining consent for procedures. Further information

can be found on the Society for Paediatric Anaesthesia in New Zealand and Australia (SPANZA)

EPIC website https://www.spanza.org.au/epic (last accessed January 2023).

Recognition andassessment ofpain

There are three main ways to recognise that a child is in pain:

z Listening to the child for statements that they are in pain or listening to their parent or carer

z Observing the child’s behaviour and physiology for things such as crying, guarding of the injured

part, facial grimacing, pallor, stillness and withdrawal, tachycardia and tachypnoea

z Anticipating pain because of the nature of the underlying problem

The purpose of pain assessment is to establish, as far as possible, the degree of pain experienced by

the child to allow selection of the right level of pain relief. Reassessment using the same pain tool

will indicate whether the pain management has been successful or whether further analgesia is

required– the assess, treat and reassess cycle. The use of suitable pain tools and protocols in the

emergency setting has been shown to shorten the time to delivery of analgesia.

An observational pain scale overcomes the problems caused by anxiety at presentation and is more

appropriate. The Alder Hey Triage Pain Score (AHTPS) is one such tool that has been developed spe-

cifically for this situation and is shown to have some validity as well as good levels of inter- rater

reliability (Table7.1). It is an observation- based pain score, which is quick and easy to use.

Other commonly used pain scales are self- assessment tools, for example a faces scale or pain ladder

(Figure7.1). Self- assessment tools, however, were primarily developed for use with children where

there was the opportunity for explanation of the scale prior to the painful event (e.g. before surgery).

This is rarely the case in the emergency department.

Table7.1 The Alder Hey Triage Pain Score: reference scoring chart

Response Score 0 Score 1 Score 2

Cry/voice No complaint/cry Consolable Inconsolable

Normal conversation Not talking/negative interaction Complaining of pain

Facial

expression

Normal Short grimace or similar less

than 50% of time

Long grimace more

than 50% of time

Posture Normal Touching/rubbing/sparing Defensive/tense

Movement Normal Reduced or restless Immobile or thrashing

Colour Normal Pale Very pale/’green’

https://www.spanza.org.au/epic

CHAPTER 7 Exposure 119

Both or either of these tools can be used to assess the pain experienced by the child and help to

guide the level and route of analgesia required. The tools can then be used again to assess the

efficacy of the intervention and to guide further analgesia.

Pain management

There are various strategies for managing pain in the emergency situation that do not require

pharmacological interventions.

Environment

The emergency department and the treatment room of the paediatric ward can be frightening

places for children. Negative aspects of the environment should be removed or minimised. This

includes an overly ‘clinical’ appearance and evidence of invasive instruments. An attractive

environment with toys, themes and colour schemes should be substituted.

Preparation

Approaching the child in a calm, quiet manner, assuring them that they will be looked after well,

they will be comfortable and giving them the suggestion that healing can begin immediately, can

rapidly settle an anxious child. Simple, age- appropriate explanations about what is happening to

them are also important. Except in a life- threatening emergency or when dealing with an

unconscious child, an explanation of the procedure to be undertaken and the ways to make it as

comfortable as possible should be given to the child and their parents. Words which foretell negative

sensations, such as ‘pain’, ‘sharp scratch’, ‘be brave’, ‘feel sick’ or ‘vomit’ should be avoided. Studies

No pain

at all

Mild

Stinging

Quite bad

Moderate

Very bad

Severe

Excruciating

Worst ever

No control

Disabling

Stops normal activities

Severe difficulties

Stops some things

A few problems

Can do most things

Normal activities

Figure7.1 Faces scale and pain ladder

Assess, treat, reassess

120 PART 2 The seriously ill child

suggest that, contrary to previous assumptions, these words are more likely to result in a negative

experience for the child. Open- ended statements invoking curiosity and suggesting success and

the desired outcome are more likely to lead to a comfortable experience. Permission can be given

for the child not to be bothered by the procedure. Positive messages such as ‘I am going to help

you’, ‘you are doing great’ or ‘this will make you more comfortable’ are helpful. If a play therapist is

available they may be able to assist with the preparation and the procedure.

Physical treatments: supportive anddistractive techniques

During an invasive procedure, the presence of suitably prepared parents or carers is important. In

one study, almost all children between the ages of 9 and 12 years reported that ‘the thing that

helped most’ was to have a parent present during a painful procedure. Parents need some guidance

on how to help their child during the procedure beyond just being present. Studies suggest that

talking to and touching the child during the procedure is both soothing and anxiety relieving. Other

distractive strategies include:

z Looking at pop- up books or interactive toys

z Listening through headphones to stories or music

z Blowing bubbles

z Video or interactive computer games

z Moving images projected onto a nearby wall, such as fish swimming or birds flying

z The presence of transitional objects (comforters), for example a favourite blanket or soft toy

z Lived imagination– have the child imagine a place or an activity that they enjoy. Parents can be

helpful with this. Ask them to describe what they are experiencing, using all the senses and

taking time for the child to immerse themselves in their imagination. Suggest that they might

like to stay and enjoy the place and leave us behind to get the procedure finished

Some emergency departments use hypnosis to manage pain effectively. Hypnosis is a state involving

focused attention, reduced peripheral awareness and an enhanced capacity to respond to suggestion.

Outpatient- based hypnotherapy to prepare children for unpleasant procedures or to treat other

conditions such as enuresis can be very successful. Similar techniques ‘on the fly’ in emergency

settings can also be very effective in reducing the discomfort experienced during procedures.

Children are open to new experiences, crave mastery and have powerful imaginations, all of which

increase the likelihood of success with hypnosis. With some basic training and practice a child can

be helped to tolerate uncomfortable procedures such as venepuncture or reduction of joint

dislocations.

Further information can be found on the Society for Paediatric Anaesthesia in New Zealand and

Australia (SPANZA) EPIC website https://www.spanza.org.au/epic (last accessed January 2023).

Pharmacological treatment

Local anaesthetics: topical onintact skin

Ametop® gel. This contains tetracaine (amethocaine) base 4%.

z It is used under an occlusive dressing

z Analgesia is achieved after 30–45minutes

z Anaesthesia remains for 4–6 hours after removal of the gel

z Slight erythema, itching and oedema may occur at the site

z Not to be applied on broken skin, mucous membranes, eyes or ears

z Can cause sensitisation on repeated exposure

z Not recommended for a patient under 1month of age

Emla®. A mixture of lidocaine 2.5% and prilocaine 2.5% can be used in a similar fashion where

sensitivity to Ametop® gel occurs. Emla®, however, takes around 60minutes to work effectively and

tends to cause vasoconstriction rather than vasodilatation.

Alternatively, ethyl chloride spray works immediately.

https://www.spanza.org.au/epic

CHAPTER 7 Exposure 121

Local anaesthetics: infiltrated

Local anaesthetics are manufactured to a pH of 5 (to improve shelf- life) and are painful for this

reason. A buffered solution (i.e. 9ml of lidocaine with 1ml of 8.4% sodium bicarbonate) and the use

of smaller needles will lessen the pain associated with infiltration, but local adrenaline cannot then

be used because the bicarbonate buffer inactivates it.

Overdose or inadvertent injection of local anaesthetics into an artery or vein may result in cardiac

arrhythmias and convulsions. Resuscitative facilities and skills must therefore be available wherever

and whenever these drugs are injected.

Lidocaine. 1% lidocaine (lignocaine, contains 10 mg of lidocaine per 1 ml) is used for rapid and

intense sensory nerve block.

z The onset of action is significant within 2minutes and is effective for up to 2 hours

z It is often used with adrenaline to prolong the duration of sensory blockade and to limit toxicity

by reducing absorption (adrenaline concentration 5 micrograms/ml). Adrenaline- containing

local anaesthetic should not be used in areas served by an end artery, such as a digit

z The maximum body dose is 3mg/kg for plain solutions and 7mg/kg for solutions that contain

adrenaline

Bupivacaine and ropivacaine. Long- acting local anaesthetics such as bupivacaine or ropivacaine

are used – at a concentration of 0.25% or 0.5% (2.5 or 5 mg per ml) – when longer lasting local

anaesthesia is required, such as in femoral nerve blocks.

z Onset takes up to 15minutes, but its effects last up to 8 hours

z Maximum body dosage is 2mg/kg

Non- opioid analgesics

These drugs exhibit varying degrees of analgesic, antipyretic and anti- inflammatory activity.

Paracetamol. This is probably the most widely used analgesic in paediatric practice. It may be

administered by the oral, rectal and intravenous routes. It is thought to work through inhibiting

cyclo- oxygenase in the CNS but not in other tissues, so that it produces analgesia without any anti-

inflammatory effect. It does not cause respiratory depression. It is very safe when administered at

the recommended dose although overdosage in a large single dose, or too frequent smaller doses,

may cause hepatotoxicity. Higher loading doses have been shown to improve pain control (see

Appendix J).

Non- steroidal anti- inflammatory drugs (NSAIDs). These are anti- inflammatory and antipyretic

drugs with moderate analgesic properties. They are less well tolerated than paracetamol, causing

gastric irritation, platelet disorders, bronchospasm and renal impairment. They should, therefore,

be avoided in children with a history of gastric ulceration, platelet abnormalities and dehydration or

renal problems. Their advantage is that they are especially useful for post- traumatic pain because

of the additional anti- inflammatory effect. Ibuprofen is given by mouth, and if rectal administration

is necessary then diclofenac can be used. Ketorolac can be given intravenously.

Opiate analgesics

Morphine. This produces a rapid onset of excellent analgesia and remains the treatment of

choice in many situations. It may be titrated to effect and (temporarily) reversed with naloxone

if necessary. The intranasal route for the administration of opiates such as diamorphine and

fentanyl has been shown to be a safe and effective route and is increasingly popular for

children. It also has the advantage of being quick and easy, avoiding the trauma of an

intravenous cannula.

Side effects include respiratory depression, nausea and vomiting. Cardiovascular effects include

peripheral vasodilatation and venous pooling, but in single doses it has minimal haemodynamic

effect in a supine child with normal circulating volume. In hypovolaemic patients it will contribute

to hypotension but this is not a contraindication to its use and merely an indication for cardiovascular

122 PART 2 The seriously ill child

monitoring and action as appropriate. Opioids produce a dose- dependent depression of ventila-

tion primarily by reducing the sensitivity of brain- stem respiratory centres to hypercarbia and

hypoxia. This means that a child who has received a dose of an opioid requires observation and/or

monitoring and should not be discharged home until it is clear that the effects of the opiate are

significantly reduced. The nausea and vomiting produced in adults by morphine seems to be less

common in children.

Opiate antagonists

Naloxone. Naloxone is a potent opioid antagonist. It antagonises the sedative, respiratory- depressive

and analgesic effects of opioids. It is rapidly metabolised and is given parenterally because of its

rapid first pass extraction through the liver following oral administration. Following intravenous

administration, naloxone reverses the effects of opiates almost immediately. Its duration of action,

however, is much shorter than the opiate agonist. Therefore, repeated doses or an infusion may be

required if continued opiate antagonism is wanted.

Inhalational analgesia

Nitrous oxide. This is a colourless, odourless gas that provides analgesia in subanaesthetic

concentrations. It is supplied in premixed cylinders at a 50% concentration with oxygen (Entonox®,

Kalinox®) or at a concentration of up to 70% with oxygen via a blender. Delivery devices either act

on a demand principle (i.e. the gas is only delivered when the child inhales and applies a negative

pressure) or via a free- flowing circuit. The latter delivery system requires a scavenger circuit.

Generally during nitrous oxide therapy, the child has to be awake and cooperative to be able to

inhale the gas; this is an obvious safeguard with the technique.

z Because nitrous oxide is inhaled and has a low solubility in blood, its onset of effect is very

rapid. It takes 2–3minutes to achieve its peak effect. For the same reason, the drug wears off over

several minutes, enabling children to recover considerably quicker than if they received narcotics

or sedatives. Laryngeal protective reflexes do not always remain intact

z Nitrous oxide is therefore most suitable for procedures where short- lived intense analgesia is

required, for example dressing changes; suturing and needle procedures such as venous

cannulation; lumbar punctures; and for pain relief during splinting or transport. It is also of

benefit for immediate pain relief on presentation until definitive analgesia is effective

z Using a free- flow circuit, nitrous oxide can be used by children as young as 2 years of age,

although children will need to be 4 or 5 years of age before they can trigger the demand valve

of a premixed cylinder

z Nitrous oxide may cause nausea, vomiting, euphoria and disinhibition. Prolonged exposure to

high concentrations can cause bone marrow depression and neuronal degeneration

z Nitrous oxide is contraindicated in children with possible intracranial or intrathoracic air because

gas diffusion into the confined space may increase pressure

z As there are no adequate data and the potential risk is unknown, passive exposure to nitric

oxide during pregnancy and lactation should be avoided

Sedative anddissociative drugs

In addition to analgesics, psychotropic drugs may also be useful when undertaking lengthy or

repeated procedures. Sedatives relieve anxiety but not pain and may reduce the child’s ability to

communicate discomfort and therefore should not be given in isolation. The problems associated

with the use of sedatives are side effects (usually hyperexcitability) and the time required for the

child to be awake enough to be allowed home if admission is not necessary. This does not apply to

dissociative agents such as ketamine which have a different mode of action, and are widely used for

procedures.

CHAPTER 7 Exposure 123

Midazolam. Midazolam is an amnesic and sedative drug. It can be given intravenously, intramuscu-

larly, orally or intranasally (although this is unpleasant). It has an

onset time of action of 15minutes

after an oral administration and recovery occurs after about an hour. It may cause respiratory

depression, necessitating monitoring of respiratory function and pulse oximetry. A few children

become hyperexcitable with this drug (paradoxal reaction). Whilst its action can be reversed by

flumazenil, intravenously this is rarely necessary and can precipitate seizures.

Ketamine. This is a potent anaesthetic agent that has an established place in paediatric procedural

pain relief in many emergency settings. It causes a dissociative anaesthesia, which is amnesic and

analgesic, but has little effect on breathing and protective airway reflexes are maintained. Side

effects include hypersalivation, tachycardia and hypertension, but previous concerns with regard to

increasing intracranial pressure are no longer valid. Laryngospasm is a rare complication that may

be precipitated by instrumentation of the upper airway or rapid administration.

Ketamine should be considered as an anaesthetic agent and used with all the precautions gener-

ally associated with anaesthesia. Emergence phenomenon (delirium following use of ketamine)

can be treated with a low dose of midazolam if necessary but is much less common in paediatric

than in adult practice.

Specific clinical situations

Severe pain

Children in severe pain (e.g. major trauma, femoral fracture, significant burns, displaced or

comminuted fractures) should receive IV morphine at an initial dose of 0.1–0.2mg/kg infused

over 2–3minutes (see Appendix J). A further dose can be given after 5–10minutes if sufficient

analgesia is not achieved. The child should be monitored using pulse oximetry and

electrocardiography.

Low- dose IV ketamine (0.1mg/kg) can be additionally given if the pain has not responded to maxi-

mal doses of opiates.

Higher doses of ketamine are a safe and alternative initial option for treating severe and acute pain

in the emergency room.

Head injuries

There is often concern about giving morphine to a child who has had a head injury and who

could therefore potentially lose consciousness secondary to the head injury. If the child is

conscious and in pain, then the presence of a potential deteriorating head injury is not a

contraindication to giving morphine. First, an analgesic dose is not necessarily a significant

sedative; second, if the child’s conscious level does deteriorate, then the clinician’s f irst action

should be to assess airway, breathing and circulation, intervening where appropriate. If these are

stable, then a dose of naloxone will quickly ascertain whether the diminished conscious level is

secondary to morphine or (as is much more likely) represents increasing intracranial pressure.

There are significant benefits for the head- injured child in receiving adequate pain relief as the

physiological response to pain may increase intracranial pressure.

In the common situation of the patient who has an isolated femoral shaft fracture and a possible

head injury, a femoral nerve block may be an effective alternative (see Chapter21).

Emergency venepuncture andvenous cannulation

At present, the management of this problem is difficult as topical anaesthetics take up to an hour

to be effective. Inhaled nitrous oxide, given by one of the methods described earlier, gives excellent

results. Alternatives in an emergency include ethyl chloride spray, an ice cube inside the finger of a

124 PART 2 The seriously ill child

plastic glove placed over the vein to be cannulated or local anaesthetic infiltration (1% buffered

lidocaine) using a very fine gauge (e.g. 29gauge) needle. Verbal or other distraction techniques can

also be very effective.

7.7 Summary

This chapter gives an outline of the elements that should be considered in the E assessment if they

have not yet been assessed and managed in the ABCD primary assessment. Pain management,

both pharmacological and non- pharmacological, should be considered.

125

PART 3

The seriously injured

child

127

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

8.1 Introduction

Internationally, unintentional injuries are a leading cause of death in children. The World Health

Organization (WHO) estimates 18000injury- related deaths in children under 15 years of age each

year. The predominant mechanisms are from preventable causes such as road traffic collisions,

drownings and fire- related incidents.

In the UK, data from the Trauma Audit and Research Network (TARN) show that pedestrian children

suffer the most severe injuries secondary to traumatic brain injury. Mortality is between 8% and 10% of

those with major trauma (injury severity score greater than 15), particularly if there is a reduced Glasgow

Coma Scale (GCS) score, injury to multiple organ systems or the need for admission to a critical care

facility. Infants are more susceptible to severe injuries resulting from suspected physical abuse.

Many more children are injured in accidents that, although not causing death, cause pain, distress

and permanent disability. There has been an increase in penetrating injury, particularly knife crime,

in the UK over the past decade.

The majority of these events are predictable and preventable. This introduction to the seriously

injured child will consider the important role of injury prevention, trauma systems and some specif-

ics about trauma teams.

8.2 Injury prevention

Over the last few decades, injury prevention programmes, together with increased education in

schools and public health campaigns, in some countries have succeeded in significantly reducing

childhood death rates from injury by introducing key legislation such as child restraints, speed

restrictions and laws on the use of motorcycle helmets. This is a remarkable achievement. Injury

prevention is a multifaceted, multidisciplinary process that provides many opportunities for clinicians,

who are primarily involved in the management of acutely injured children, to play a major role.

Structured approach to

the seriously injured child

CHAPTER 8

Learning outcomes

After reading this chapter, you will be able to:

z Identify the importance of injury prevention

z Describe the role of trauma systems

z Describe the team- based, structured approach to the seriously injured child

128 PART 3 The seriously injured child

8.3 Epidemiology

Circ*mstances andtype ofincident

A multitude of injury scenarios are possible, each of which involve the child interacting with their

environment. The commonest injuries that cause death are those resulting from motor vehicle

accidents, drownings, burns, falls from a height and poisonings. Children in urban environments

are at particular risk of motor vehicle collisions and playground falls whilst children in a rural

environment are at risk of farm equipment injuries or unintentional chemical exposure. Exposure

to different circ*mstances also varies with age. Children under 5 years of age experience injuries at

home, with infants and toddlers at greater risk of inflicted injury. School- age children experience

injuries at school, sport and play, and are especially at risk of death as pedestrians and cyclists.

Adolescents may unintentionally place themselves at risk of injury, especially where alcohol and

drugs may impair their judgement. Self- harm is an increasing cause of death and disability in

young people.

Children with major injuries are affected differently– physically, physiologically and psychologically.

Initial presentation can be deceptive because the relative elasticity of their tissues allows more

energy to be transmitted to other body parts, with less being dissipated at the impact site. This will

influence assessment and management.

Understanding the mechanism of injury will help assess how likely it is that a child has major inju-

ries. For example, a fall from above the child’s head height is much more significant than a fall from

ground level.

Sex

Males are more frequently injured than females. The difference emerges at 1–2 years of age. How

much of this difference is innate and how much cultural is a subject for speculation. Females 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. Take falls as an

example. A newborn baby can only fall if dropped, or if a parent falls holding the baby. An older

baby can wriggle and roll off a changing table or a bed. A crawling baby 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. It is important to the healthcare professionals to know the stages of development

of children. This will allow professionals to understand the mechanism of injury and judge whether

a given history is plausible when considering non- accidental injury. A child’s developmental stage

will also influence the clinical assessment and decisions on investigation and treatment.

Social class

It is well- recognised that inequalities in children’s environments are linked to health problems.

Children in lower socioeconomic groups are twice as likely to die from an injury as children in

higher social class groups. For some injury types, the chances of sustaining an injury are

increased. Burns, for example, are six times more likely to be sustained by children in lower

socioeconomic groups. Pressures such as overcrowding, poor housing or poverty are likely

contributory factors.

Psychological factors

Injuries are more common in families where there is stress from mental illness, substance abuse,

marital discord, moving home or a variety of similar factors.

CHAPTER 8 Structured approach to the seriously injured child 129

8.4 Trauma systems

A trauma system is described as an organised, coordinated effort in a defined geographical area

that delivers the full range of care to all injured patients and is integrated with the local healthcare

system. After pre- hospital assessment, ambulance crews may bypass hospitals to reach those

trauma centres with specialised care, investigations and interventions 24/7.

If a trauma system is in place, then the response to a seriously injured child will be adapted to

take into account the pathway for major trauma patients in a certain area. This includes the

recognition that secondary transfer of children may become more prevalent. This may also

increase the number of time- critical transfers as children are transferred to the place where

definitive care for the life- threatening condition can be delivered. Pre- hospital practitioners may

consider going directly to a hub trauma centre or moving on at the earliest possibility. The

‘ moving on’ should potentially be seen as an extension of the pre- hospital phase. Clinicians

should start planning for transfer as soon as the child arrives and make contact early with

theplace where definitive care for the life- threatening condition can be delivered. The phrase

‘stop/sort/go’ emphasises this point.

Trauma systems have an important role in the planning and management of mass casualty events,

which are major incidents that present serious threat to the health of the community or cause such

numbers or types of casualties as to require special arrangements to be implemented. It is likely

that such an event will include children, and indeed some incidents may almost exclusively involve

children. It is essential that all healthcare workers are familiar with their own organisations’

major incident plans and procedures.

Some knowledge of the initial management of blast and ballistic injuries is necessary, and clinical

guidelines such as those produced by NHS England (https://www.england.nhs.uk/publication/

clinical- guidelines- for- major- incidents- and- mass- casualty- events/; last accessed January 2023)

should be immediately available for reference in emergency departments.

Following the terrorist attack at the Manchester Arena in 2017, a number of learning points and rec-

ommendations were identified around the initial hospital response, including:

z Casualties may arrive at hospital before a major incident has been recognised or declared

z Re- triage of all casualties on arrival at hospital is essential

z Expect difficulties in identifying children– they will often not carry identification

z Plans should allow for children and their parents/carers to remain together where practical

z Use of improvised tourniquets may be life saving on scene, but need to be specifically looked for

on arrival at hospital in order to keep the tourniquet time as short as possible

z Whole- body computed tomography (CT) is essential in blast injuries

z Consider the potential for blood- borne virus transmission if a penetrating wound may have

been caused by projectile body matter from another victim, or from a bladed weapon that may

have been used on multiple casualties. Hepatitis B vaccination may be indicated

z Antibiotics should be given for penetrating injuries according to local guidelines

z Check carefully for penetrating eye injuries, especially in casualties with a reduced level of

consciousness

z A terrorist incident will require a forensic investigation– any removed foreign bodies, etc. need

carefully labelling and keeping for the police

z Do not underestimate the psychological impact that critically injured or dying children will have

on all levels of staff

z Regular simulation and table- top exercises are essential

When reading the chapters in this section, it is important that they are placed in the context of

your local trauma system

https://www.england.nhs.uk/publication/clinical-guidelines-for-major-incidents-and-mass-casualty-events/

130 PART 3 The seriously injured child

Irrespective of the presence of a trauma system, it is essential that hospitals that receive paediatric

traumas should have:

z Specific paediatric guidelines and protocols (Box8.1)

z Standard operating procedures and pathways (Box8.1)

z Paediatric equipment and monitoring

z Immediate access to staff with paediatric expertise

8.5 Trauma teams

Paediatric major trauma happens infrequently, therefore it is important that trauma teams are

familiar with all of the elements listed above and that they receive regular training and practice. The

roles required in a trauma team are detailed in Box8.2. Considerations of non- technical skills are to

be found in Chapter2.

Box 8.1 Paediatric guidelines, protocols, procedures andpathways

z Trauma team activation

z Rapid sequence intubation/difficult airway procedures

z Head injury management

z Penetrating cardiac injury management

z Chest drain insertion

z Open fracture management

z Pelvic fracture management

z Drowning pathway

z Burns referral pathway

z Major haemorrhage protocol:

z tranexamic acid

z blood products

z haemostatic agents

z recombined factor VIIa

z analgesia

z Imaging:

z CT guidance

z X- ray guidance

z abdominal injury

z Urethrogram and cystogram

z Tetanus prevention

z Safeguarding

z Youth support organisations

z Brain injury pathway

CHAPTER 8 Structured approach to the seriously injured child 131

Trauma alert, team briefing andpreparation

Preparation is the key to effective and efficient trauma management. Capturing the information

given when the trauma alert is received using a structured approach, for example ATMISTER,

enables appropriate briefing and planning prior to the arrival of the child.

It also allows the team leader to decide on the appropriate response, either a full paediatric trauma

team or a targeted specialty response. However, it is important to have an awareness that 30% of

children

with significant trauma may arrive by car with friends/family without a pre- alert. With less

information available another structured approach can be STEP UP.

Box 8.2 Trauma team andexample roles

Actual roles will depend on local processes

z Team Leader– coordinates team actions and communication, directs treatment

z Operating Department Practitioner– assists Airway Specialist in managing airway

z Airway Specialist/Anaesthetist- manages airway

z Assistant 1– monitors vital signs and administers medication

z Assistant 2– assists with emergency procedures and checks medications with Nurse 1

z Clinician 1– conducts primary survey and necessary procedures

z Clinician 2– gains vascular access and other emergency procedures

z Scribe– liaises closely with Team Leader to maintain an accurate record of assessment,

treatments and decisions

z Emergency Department Assistant

z Radiographer– undertakes appropriate trauma imaging

z Radiologist– provides expert review of trauma imaging; may undertake focused point of

care imaging and/or interventional procedures

z Lead Nurse

z Specialists– provide expert assessment and relevant interventions and treatments:

z trauma and orthopaedics

z surgery

z paediatric critical care

A Age/sex

T Time of incident

M Mechanism of injury

I Injury suspected

S Signs including vital signs, Glasgow Coma Scale

T Treatment so far

E Estimated time of arrival to emergency department

R Requirements, i.e. bloods, specialist services, tiered response, ambulance call sign

S Self Prepare communication, recognise stresses

T Team Plan roles and positions of the team

E Environment Prepare equipment

P Patient/Primary survey Clear roles/ABCDE

U Update Treatment so far

P Plan Requirements

132 PART 3 The seriously injured child

After the call has been received from ambulance control, the team leader should complete the

following actions (Box8.3).

In role allocation consideration must be given to specific roles, including primary survey, airway,

breathing and circulation, plus scribe, family support and drug management, taking into account

the competencies of the team available.

On arrival, unless the child has a catastrophic haemorrhage, traumatic cardiac arrest or obstructed air-

way, a controlled ‘eyes- on, hands- off’ handover occurs. At this point, the team leader completes a

5- second review and adapts the plan accordingly. The form of the structured approach is shown in

Box8.4.

8.6 Primary survey andresuscitation

Box 8.4 Structured approach

Immediate

z Primary survey (identify immediate life threats and act on them)

z Resuscitation

Focused

z Secondary survey (elicit key features)

z Emergency treatment

Detailed review

z Reassessment (system control)

z Further stabilisation and definitive care

During the primary survey, life- threatening problems should be treated as they are identified

(Box8.5)

Box 8.5 ABCDE

A Airway (with cervical spine control)

B Breathing with ventilatory support

C Circulation with haemorrhage control

D Disability with prevention of secondary insult

E Exposure with temperature control

Consider F for family and discuss presence of family at the briefing

Box 8.3 Team leader actions: plan andreview

z Remember early management of catastrophic haemorrhage requires urgent blood

products so activate the massive haemorrhage protocol early

z Make a plan and back- up plan according to age, mechanism and expected injuries

z Child arrives: 5- second review and adapt plan accordingly

CHAPTER 8 Structured approach to the seriously injured child 133

In major trauma ABCDE has become the established approach. Obvious external exsanguinating

haemorrhage becomes the immediate priority.

‘Blood on the floor and five more Bs’: a life- threatening amount of blood may be lost as a result of

traumatic haemorrhage. The haemorrhage may be obvious bleeding outside the body (it can be

seen on the ‘floor’– remember to check the back and skin folds, including between the buttocks).

Or the blood loss may be hidden with the haemorrhage occurring in internal compartments. The

most likely areas are:

z Thorax (Breast)

z Abdomen (Belly)

z Pelvis (Buttock)

z Femur (Bone)

z Do not forget that babies can lose significant blood volume into their head (Brain)

These areas are where blood loss should be looked for in the context of ongoing shock without obvi-

ous cause, and where initial attempts to control catastrophic haemorrhage should be directed.

z Simple direct pressure, specialised haemostatic dressings or a tourniquet (or indirect pressure

on a major artery above the injury) must be applied instantly to stem active external haemorrhage

z Apply a pelvic binder if there is concern for pelvic injury with haemodynamic instability

z Tranexamic acid should be given intravenously 15mg/kg (max. 1000mg) as soon as possible

The assessment can then continue with the ABCDE sequence.

Airway andcervical spine

Look for anything compromising the airway.

z Material in the lumen (blood, vomit, teeth or a foreign body)

z Damage to or loss of control of the structures in the wall (the mouth, tongue, pharynx, larynx or

trachea)

z External compression or distortion from outside the wall (e.g. compression from a pre- vertebral

haematoma in the neck or distortion from a displaced maxillary fracture)

Whatever the cause, airway management should follow the structured sequence (see Chapter17),

bearing in mind the need to protect the cervical spine. This is summarised in Box8.6.

Problems can develop after the primary survey, e.g. bleeding or progressive swelling in facial

trauma or burns

A child with a GCS score of 8 or less is unlikely to be adequately protecting their airway

The commonest cause is from occlusion by the tongue in an unconscious, head- injured child

Box 8.6 Airway management sequence

z Jaw thrust

z Suction/removal of foreign body under direct vision

z Oro- /nasopharyngeal airways

z Tracheal intubation

z Surgical airway

134 PART 3 The seriously injured child

Head tilt/chin lift is not recommended following trauma because this manoeuvre can move the

cervical spine and may exacerbate an injury. For 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

(spinal cord injury without radiological abnormality (SCIWORA)). If ignored, ligamentous instability

in the absence of radiological evidence of a fracture can have devastating consequences.

If protection is considered necessary, start with manual in- line stabilisation (MILS) by a competent

assistant or, if this is not possible, consider using a head block and appropriate strapping. Rigid

immobilisation of the head risks increasing leverage on the neck as the child struggles. Minimise

anxiety by avoiding unnecessary interventions and encouraging the parents to remain at the

bedside.

Vomiting poses an obvious threat to the unprotected airway, especially if there is also a risk of spinal

injury. Before providing airway suction, tilt the patient trolley head down, ensuring they are secure.

The child should be taken off the extrication stretcher as soon as possible, using the 20° tilt method

(see Chapter21), and placed directly onto a trauma mattress (Figure8.1) or an emergency depart-

ment trolley. If the spine has not been cleared, manual in- line immobilisation will be needed for

intubation if indicated. If the child is paralysed, sedated and ventilated the cervical spine cannot be

cleared, and spinal immobilisation needs to be maintained until definitive imaging (see Chapter22)

and neurological examinations can take place. A child should not be on a spinal board/scoop for any

longer than for the initial survey and transfer to scan.

Breathing

Adequacy of breathing is checked in three domains (see Chapter3):

z Effort

z Efficacy

z Effects on other organ systems

When examining the chest, look, listen and feel:

Look– remembering asymmetry and asymmetrical movement (flail chest)

Listen– for reduced air entry or crackles

Feel– remember to check for crepitus (surgical emphysema) and tracheal deviation, and percuss to

distinguish a tension pneumothorax from a massive haemothorax

Figure8.1 Vacuum mattress in use

CHAPTER 8 Structured approach to the seriously injured child 135

Conditions identified

By the end of the primary survey, the following conditions may have been recognised, all of which

can have a detrimental effect on respiration, with treatment initiated as soon as they are found:

z Airway obstruction

z Tension pneumothorax

z Open pneumothorax

z Massive haemothorax

z Flail chest

z Cardiac tamponade

z Decompensating head injury

z Shock

If breathing is inadequate, commence ventilation with a bag–valve–mask and prepare for intuba-

tion, which is likely to be required. The indications for intubation and mechanical ventilation are

summarised in Box8.7.

If breath sounds are unequal consider and institute correct management (see Chapter9):

z Pneumothorax

z Haemopneumothorax

z Misplaced tracheal tube

z Blocked main bronchus or pulmonary collapse

z Diaphragmatic rupture

z Pulmonary contusion

z Aspiration of vomit or blood

Circulation

Circulatory assessment in the primary survey involves the rapid assessment of heart rate and

rhythm, pulse volume and peripheral perfusion including colour, temperature and capillary return

and blood pressure (Table8.1). Circulatory assessment must take into account the fact that resting

Box 8.7 Indications forintubation andventilation

z Persistent airway obstruction

z Predicted airway obstruction, e.g. inhalational burn

z Loss of airway reflexes (reduced Glasgow Coma Scale (GCS) score and responding to pain

or unresponsive)

z Inadequate ventilatory effort or increasing fatigue

z Disrupted ventilatory mechanism, e.g. severe flail chest

z Persistent hypoxia despite supplemental oxygen

z Controlled ventilation required to prevent secondary brain injury (see Chapter11)

Table8.1 Recognition ofclinical signs indicating blood loss requiring urgent treatment

Sign Indicator

Heart rate Marked or increasing tachycardia or relative bradycardia

Systolic blood pressure Falling

Capillary refill time (normal less than 2 seconds) Increasing

Respiratory rate Tachypnoea unrelated to thoracic problem

Mental state Altered conscious level unrelated to isolated head injury

136 PART 3 The seriously injured child

heart rate, blood pressure and respiratory rate vary with age (see the normal ranges table (inside

front cover)).

Additionally in trauma:

z Check peripheral pulses in limb injury

z Look for internal haemorrhage (chest, abdomen, pelvis and femurs), including consideration of

bleeding from multiple sites and progressive deterioration

z Apply pressure to significant external haemorrhage (if appropriate)

z Remember that exposure to cold prolongs the capillary refill time in healthy people

z Check lactate and haemoglobin as early indicators of circulatory compromise

z Consider the possibility of blood loss from a head injury in infants

All seriously injured children require vascular access to be established urgently using two relatively

large intravenous cannulae. Peripheral veins are preferred; other options are:

z Intraosseous cannulation of the tibia, femur or humerus

z If there is no suspicion of a cervical spine injury– direct cannulation of the external jugularvein

z Indirect or direct cannulation of the femoral vein using the Seldinger technique (‘wire through

needle’ followed by ‘catheter over wire’)

z Cut- down onto the cephalic vein at the elbow or the long saphenous vein at the ankle

Vascular access techniques are discussed in detail in Chapter20. When vascular access is achieved,

bloods should be taken, prioritising an urgent cross- match as well as a blood gas for haemoglobin

and lactate and a venous sample for clotting. If there are signs of circulatory compromise, uncon-

trolled bleeding must be considered and appropriate teams summoned, if they are not already part

of the trauma team. The initial haemoglobin is unlikely to change in the first instance; be careful not

to be reassured by a normal haemoglobin in the first hour. If the child is stable with no signs of

shock, an immediate fluid bolus is not required. The principles behind this are ‘the first clot is the

best clot’.

There are four key treatments of circulation (Figure8.2):

1. Stop obvious external bleeding.

2. Replace ongoing blood loss with blood products.

3. Ensure the blood is warm.

4. Give the replacement fast.

Massive haemorrhage following injury is not common in children. Its management requires an

understanding of concepts that have become standard in adult trauma care (Figures 8.3

and8.4):

z Use of tranexamic acid (bolus dose 15 mg/kg; max. 1000 mg followed by an infusion of

2mg/kg/h)

z Effective use of adjuncts (e.g. tourniquets, pelvic splints)

z Implementation of massive haemorrhage protocols (MHPs)

z Avoidance of hypothermia using heating devices

z Maintenance of an adequate haematocrit used to aid clotting by promoting platelet aggregation

in small blood vessels, by use of optimal ratios of red cells to other blood products

z Prompt restoration of perfusion after controlling haemorrhage (monitored by the lactate level

returning to normal within a few hours)

z Damage control interventions, involving surgery and interventional radiology

z Massive transfusion can cause an increase in potassium and citrate so careful monitoring of

calcium and potassium is necessary as homeostasis will alter significantly

If abdominal haemorrhage is suspected, CT with contrast should be performed. In children, FAST

(focused assessment with sonography for trauma) has very limited application and there is limited

evidence of its worth in detecting abdominal haemorrhage.

CHAPTER 8 Structured approach to the seriously injured child 137

Give 10 ml/kg fluid bolus

Either blood product or balanced

crystalloid (WARMED)

Give further 10 ml/kg fluid bolus

Blood if available otherwise

balanced crystalloid

(WARMED)

Massive Haemorrhage in

Trauma Algorithm

Continue to

monitor for

further

features of

shock

and treat

accordingly

Identify

and treat

sources of

haemorrhage

Simultaneously

identify and

manage sources

of haemorrhage:

"Blood on the

floor and FIVE

more"

(see text)

Give tranexamic acid 15 mg/kg

bolus IV/IO if not already given if

within 3 hours of injury

Start tranexamic acid infusion

(2 mg/kg/hr) if bolus already given

Signs of shock?

Reassess

Shock remains?

Reassess

Shock remains?

YES

Activate Massive Haemorrhage

Protocol (MHP)

Fluid resuscitation in trauma

Figure8.2 Blood and fluid therapy in severe uncontrolled haemorrhage after trauma

FFP, fresh frozen plasma

138 PART 3 The seriously injured child

Once in haemorrhagic shock and no response to

20ml/kg fluid, declare massive haemorrhage protocol

Reduce bleeding:

Physical haemorrhage control - direct pressure,

tourniquet, stabilise fractures

Give tranexamic acid 15 mg/kg bolus IV/IO if not

already given if within 3 hours of injury

Start tranexamic acid infusion (2 mg/kg/hr) if bolus

already given

Send blood for:

Crossmatch, clotting studies, FBC, gas, lactate,

calcium, U&E

Use point of care clotting studies (ROTEM/TEG)

if expertise to interpret available

Give warmed red blood cells (RBC) and plasma

10 ml/kg aiming for a balanced 1:1 ratio

Regularly reassess ongoing shock and response

to blood

Continue to give blood products and

cryoprecipitates to achieve therapeutic aims

Continuing haemorrhage and/or shock

Continue to give RBC and

plasma 10 ml/kg

Give platelets 10 ml/kg

Give cryoprecipitate 10

ml/kg

Correct calcium

Repeat FBC, clotting and gas

Continue to monitor for

further features of shock

and treat accordingly

Reassess

Shock remains?

YES

Do not wait for

blood results

before starting

resuscitation

Stand down Massive Haemorrhage when bleeding controlled

AND therapeutic aims achieved

Continue to monitor FBC, clotting, U&Es

Massive haemorrhage in trauma

Therapeutic aims:

Bleeding controlled

Hb > 80 g/l

Platelets > 75 x 109/l

APTT ratio < 1.5

PT ratio < 1.5

Fibrinogen > 1.5 g/l

Ionised Ca > 1.0 mmol/l

Lactate < 2.0 mmol/l

pH > 7.35

Temp > 36°C

Avoid hyperkalaemiaDiscuss with

consultant

haematologist if on

anticoagulants

CONSIDER

Damage control

surgery and/or

interventional

radiology

Order RBC,

plasma, platelets

and cryoprecipitate

ANTICIPATE need

for further blood

products after

20 ml/kg of RBC/

plasma

Figure8.3 Massive haemorrhage in trauma algorithm

APTT, activated partial thromboplastin time; FBC, full blood count; Hb, haemoglobin; PT, prothrombin time; U&E, urea and

electrolytes.

CHAPTER 8 Structured approach to the seriously injured child 139

Figure8.4 Paediatric major trauma checklist

Adapted from UHCW NHS Trust Paediatric TRAUMATIC (Copyright (c): L May, A Kelly, M Wyse, K Thies, T Newton)

ContactLaura.May@uhcw.nhs.uk

aPTTR, activated partial thromboplastin time ratio; INR, international normalised ratio; MHP, major haemorrhage protocol;

PCCU, paediatric critical care unit; PRBC, packed red blood cells

Paediatric major trauma

T Tranexamic acid • If not administered already 15 mg/kg bolus (max 1 g), followed by

• 2 mg/kg/hr over 8 hours (max 125 mg/h)

R Resuscitation

• Activate MHP and consider:

• Rapid infuser

• Cell salvage

• Normotensive resuscitation (unless post pubertal)

• Pelvic binder/splint fractures/tourniquet

• Limit crystalloid and colloid use

Avoid

hypothermia

• Target temperature over 36 degrees Celsius

• Remove wet clothing and sheets

Warm fluids•

• Warming blanket/mattress/external warmer

Unstable?

Damage control

surgery

• If unstable, coagulopathic, hypothermic or acidotic, consider damage control surgery

• Aim surgery time less than 90 minutes

• Haemorrhage control, decompression, decontamination and splintage

M Metabolic

• Avoid acidosis

• Base excess guides resuscitation

• If lactate more than 5 mmol/litre or rising, consider stopping surgery, splint and

transfer to PCCU

• Monitor blood glucose

Avoid

vasoconstrictors

• Inappropriate use of vasoconstrictors doubles mortality

• However, use may be required in cases of spinal cord or traumatic brain injury

T Test clotting

• Consider TEG® (thromboelastographic)/ROTEM®

• Check clotting every 15 ml PRBC/kg body weight

• Aim platelets over 75 x 10/litre

• Aim INR & aPTTR less than or equal to 1.5

Aim fibrinogen more than 1.5 g/litre•

I Imaging

• Consider:

• Local guidelines for paediatric trauma

• Does this child need imaging at all?

• If imaging is required which anatomical area(s) need to be covered?

Calcium

gluconate

• Maintain ionised calcium more than 1.0 mmol/litre

• Administer 0.2 ml/kg 10% calcium gluconate over 10 minutes as required

• Give calcium routinely after MHP pack one

140 PART 3 The seriously injured child

Disability

The assessment of disability (neurological function) during the primary survey consists of a focused

neurological examination to determine the conscious level and to assess pupil size and reactivity.

The conscious level is described by the child’s response to voice and (where necessary) to pain. The

AVPU method describes the child as alert, responding to voice, responding to pain or unresponsive

and is a rapid, and simple, assessment.

A children’s Glasgow Coma Scale (GCS) score should be performed as soon as possible (see Table6.1),

particularly in the context of traumatic brain injury and prior to drugs that alter conscious level such

as sedatives and anaesthetics.

If the primary survey reveals that the child has a decompensating head injury, neurological

resuscitation is required. If the GCS score is less than 8 and/or AVPU equivalent of P or U, imme-

diate intervention is necessary. Remember that the GCS is modified in the smaller child (see

Table6.1).

Interventions to be considered whilst organising urgent transfer (if required) include:

z Oxygenation with 15l/min

z Head up 20°

z Control of carbon dioxide (CO2) levels (by intubation and controlled ventilation)

z Maintenance of normal blood pressure to support cerebral perfusion including use of inotropes

z Sodium chloride or mannitol osmotic diuretics to help reduce (if indicated) the intracranial

pressure

z Anaesthesia/paralysis/sedation/analgesia to reduce cerebral metabolism

z Prompt treatment of any seizures and raised temperature

Tranexamic acid (15mg/kg, max. 1g) should be considered if within 3 hours of injury and there is

suspicion of head injury and evidence of reduced conscious level (GCS less than 15 or V, P, U) or

confirmed intracranial bleed on imaging.

See further details in Chapter11.

If the child is deteriorating neurologically, the child might need urgent transfer to a neurological

centre prior to CT.

The child’s condition should be constantly reassessed and immediate damage control surgical

intervention to stop the haemorrhage considered

A Alert

V Responds to Voice

P Responds only to Pain

U Unresponsive to all stimuli

Agitation in a child may suggest cerebral hypoxia

As soon as a serious head injury is suspected, a CT scan of the brain should be ordered and the

neurosurgical team (which may be off site) alerted

CHAPTER 8 Structured approach to the seriously injured child 141

Exposure

In order to assess a seriously injured child fully, it is necessary to take their clothes off. Children

become cold very quickly, and may be acutely embarrassed when undressed in front of strangers.

Although exposure is necessary the duration should be minimised, and a blanket provided at all

other times.

This is achieved by having a warm resuscitation area and tasking one or more of the nursing team

members to keep the child covered with a blanket or hot air warming device at all times and to

warm all fluids given.

It is important to examine the child fully. In the context of penetrating injury it is particularly impor-

tant to ensure that all creases including the perineum and anus are examined as there can be hid-

den wounds.

Other procedures carried out during theresuscitation phase

Imaging

See Chapter22.

Investigations

When venous access is achieved and blood is taken for cross- matching, samples for other

investigations should be taken at the same time, including full blood count, blood gas, lactate,

clotting studies (where available thrombelastograph (TEG®) and thromboelastometry (ROTEM®)

analysis may be used), amylase, liver transaminases, urea and electrolytes. Remember to measure

the glucose, especially in adolescents (who are prone to both injury and hypoglycaemia after

drinking alcohol) and in very small children. Serum β- human chorionic gonadotrophin should also

be taken in adolescent females to identify pregnancy.

Oro/nasogastric tube placement

Gastric stasis is a frequent consequence of major trauma and acute gastric dilatation is common in

children. If suspected, particularly in the obtunded child, the stomach should be decompressed. If

there is evidence or suspicion of base of skull fracture, the tube should not be passed by the nasal

route. In the intubated child, the oral route is a simple alternative.

Analgesia

Analgesia can usually be administered just after completing the primary survey and resuscitation.

See Chapter3.

8.7 Secondary survey andlooking 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 this phase is the

secondary survey, a systematic clinical examination to identify injuries. It is supplemented by

observations, imaging and other investigations. Further information is gathered at this time,

especially the history of the events leading up to the injury and the presence of any co- morbid

factors. It is important for the team leader to instigate a summary of what the findings are and

ensure the team are aware of them.

Ensure that the child’s temperature is maintained and hypothermia is prevented

142 PART 3 The seriously injured child

History

History should be sought from the child, ambulance personnel, relatives and witnesses of the

accident. An AMPLE history can be used to obtain relevant information.

In addition, consider the mechanism of injury. The following should alert the team to an increased

likelihood of significant injury:

z Fall more than twice the height of the child

z Death or serious injury of another occupant of the vehicle

z Ejection from or trapped under vehicle/prolonged extrication

z Greater than 40mph head- on collision/bullseye or significant damage to the vehicle

z Stabbing

Secondary survey

The secondary survey is a thorough head- to- toe, front- to- back examination searching for key

anatomical features of injury. It is helpful to think in terms of:

z Surface (head to toe, front and back)

z Orifice (mouth, nose, ears, orbits, rectum, genitals)

z Cavity (chest, abdomen, pelvic cavity, retroperitoneum)

z Extremity (upper limbs including shoulders; lower limbs including pelvic girdle)

Occasionally, a full secondary survey may be delayed if immediate life- saving interventions are

required. Ensure that this decision is clearly documented and a secondary survey carried out at a

later stage.

Special considerations ininjury

z Consider otoscopy (for haemotympanum) and ophthalmoscopy (for retinal haemorrhage)

z Inspect the mouth inside and out– intraoral bruising may represent fractures

z Palpate the teeth for looseness

z Assess for nasal septal haematoma

z Assess for midface stability

z Look for signs of base of skull injury (panda eyes, mastoid bruising)

z Perform a full neurological examination

z Inspect neck veins and pulses if there is a neck injury

z Observe for movement

z Inspect for any external evidence of injury – tyre marks, bruising, lacerations and swelling,

including inspection of all creases

z Note unusual injury and bruising patterns suggesting non- accidental injury

z Inspect the perineum

z Inspect the external urethral meatus for blood

A Allergies

M Medication

P Previous medical history (pre- existing medical conditions and immunisations)

L Last meal

E Environment and events

Throughout this stage of management, the vital signs and neurological status should be

continually reassessed, and any deterioration should lead to an immediate return to the

primary survey

CHAPTER 8 Structured approach to the seriously injured child 143

Investigations

See Chapter22 for details on requesting and interpreting trauma imaging. An electrocardiogram

(ECG) should be performed in children with chest trauma or unexplained collapse/seizure.

8.8 Emergency treatment

Emergency treatment represents the early response to key findings in the secondary survey and its

adjunct investigations. While the interventions are less urgent than those in the resuscitation phase,

they will still need to be carried out promptly to minimise the risk of deterioration or unnecessary

morbidity. The emergency treatment plan will include treatments for any potentially life- threatening

or limb- threatening injuries discovered during the secondary survey. If it does not put the child at

undue risk, this plan may be extended to include definitive care of other (more minor) injuries

discovered at the same time.

Emergency treatments are discussed in more detail in subsequent chapters.

8.9 Further stabilisation

Further stabilisation and definitive care constitute the final part of the structured approach to

trauma care. Good note taking and appropriate, timely referral are essential. If definitive care is to

be undertaken in a specialist centre then transfer may be necessary at this stage.

The initial emphasis was on crude physiological assessment (ABCDE) in the primary survey,

followed by focusing on the anatomical evaluation of injuries in the secondary survey. From the time

of the initial resuscitation, pulse rate, blood pressure, respiratory rate, oxygen saturation and tempera-

ture (avoid hypo- and hyperthermia) should be measured and charted frequently (every 5minutes

initially). Beyond these continuing observations, there is now a need to return to overall physiological

control by considering the following systems in more detail, especially in a critically injured child:

z Respiration

z Circulation

z Nervous system

z Metabolism

z Host defence

Respiration (A andB)

The airway should be rechecked. If intubated, is the endotracheal tube of an expected length at the

teeth (for the size of the child)? Are the breath sounds symmetrical? Could the tube have migrated

into a main- stem bronchus?

Arterial blood gas analysis provides essential information in the child with serious head, chest or multi-

ple injuries (arterial oxygen and CO2 tensions) or in any child who has been intubated. Inserting an arte-

rial line facilitates repeated measurements; in an unintubated child, a venous blood gas should suffice.

Pulse oximetry readings should be displayed continuously. End- tidal CO2 monitoring is mandatory

in the ventilated child. It shows that the breathing circuit is still connected and that the endotracheal

tube has not become dislodged. The end- tidal CO2 should not be 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 be regarded 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 electrocardiographically.

Non- invasive blood pressure readings are generally reliable, although in serious head injuries and

In the face of a serious deterioration, return to the primary survey

144 PART 3 The seriously injured child

multiple injuries, it is better to monitor on a beat- to- beat basis using direct arterial measurements

via an arterial line usually at the radius. This also allows estimation of the haemoglobin (or

haematocrit) at hourly intervals to help detect ongoing bleeding and to determine the requirement

for further transfusion. Base deficit (or lactate) measurements indicate the adequacy of tissue

perfusion, although it is still important to reassess the child clinically. Other invasive techniques,

such as central venous pressure monitoring, may be considered at this stage, but should only be

undertaken by appropriately trained personnel.

After major blood loss, plasma, platelets and cryoprecipitate may be needed to correct coagulopathy

following the measurement of clotting times and platelet count. Remember that hypothermia affects

clotting. Also consider using viscoelastic assays such as TEG® or ROTEM® which may give a more rapid

assessment of clotting at the bedside. If not available, recheck coagulation profile frequently.

Urinary catheterisation

In 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 stabilisation after a serious

physiological insult. The route (urethral or suprapubic) will depend 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 Chapter10). 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

subsequent urethral stricture formation.

If any doubt exists then the decision to catheterise the child

can be left to the responsible surgeon. Urine should have dipstick urinalysis and sent for microscopy.

In seriously injured children, the urinary output serves as an indicator of systemic perfusion and

should be recorded hourly. It should be maintained at 1–2ml/kg/h, or higher if 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, although other causes should be considered. If it is high, it may reflect excessive fluid therapy,

but remember that diabetes insipidus can occur within a few hours of a serious head injury.

Nervous system (D)

Pupil size and reactivity and the GCS score should be checked and recorded every 15minutes initially.

Any deterioration should prompt the need to discuss the case with 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. In conjunction with invasive blood pressure measurements, it provides

a means of tracking cerebral perfusion pressure. ICP monitoring can be established in the operating

theatre or the critical care unit. Its use should be confined to hospitals with appropriately skilled

personnel, but the importance of cerebral perfusion pressure should be understood by all those who

deal with critical head injuries in children. See further details in Chapter11.

Metabolism (electrolytes, fluid balance, gut andhormones)

This system refers to biochemical processes and includes renal, hepatic, gastrointestinal and

endocrine problems. Glucose (‘don’t ever forget glucose’) monitoring and control, is important in

both young children and in adolescents who may have have taken alcohol or unknown drugs.

Monitor urine output and check serum biochemistry (see Circulation section above).

Host defence (injury, infection, immunity, intoxication)

Host defence represents the interaction between the body as a whole and external influences. As

such, it encompasses injury (including injury from poor positioning and thermal injury), infection

(including 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 predisposes to infec-

tion, while fever increases metabolic demand and must be avoided in the severely head- injured child.

Wound care, antibiotic prophylaxis for open fractures, and checking that tetanus immunisations are

up to date (has the child been immunised at all?) are all considered at this stage, as is careful positioning

CHAPTER 8 Structured approach to the seriously injured child 145

to avoid problems such as pressure injury from a poorly fitted splint. Consider tetanus toxoid and

tetanus immunisation in a heavily contaminated wound (soil or faeces) as per national guidelines.

‘Tertiary survey’

In addition to physiological system control, it is essential for transport escorts, intensive 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 an anatomical viewpoint to seek out any missed injuries.

Returning tothe primary survey

Any sudden deterioration in the child’s condition should trigger an immediate reassessment of the

airway, breathing, circulation and disability so resuscitation can once more be undertaken.

Note taking

The 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 Table8.2. Many trauma centres have

dedicated trauma booklets.

Table8.2 Template fornote taking

History

Mechanism of injury and pre- hospital/pre- major trauma centre interventions

Past history

Primary survey and resuscitative interventions

D and E

Secondary survey and emergency treatment of injuries

Head

Face

Neck

Chest

Abdomen

Pelvis

Spine/back

Extremities

Further stabilisation

Respiration

Circulation

Nervous system

Metabolism

Host defence

146 PART 3 The seriously injured child

Referral

Many 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 which children to refer to which

team is given in subsequent chapters.

Transfer

Injured children may require transfer either within the hospital or to another centre to deliver life-

saving and definitive care. In either case, thorough preparation of the equipment, patient and

documentation is essential. A careful balance must be achieved between delaying such care and

setting off with an inadequately stabilised child. Transport of children is discussed in more detail in

Chapter23.

8.10 Summary

This chapter has described how the structured approach to initial assessment and management

allows the clinician to care effectively for the seriously injured child. Life-threatening issues should

be treated when found, before progressing to secondary survey, emergency treatment and definitive

care. Knowledge of local major incident guidance is important and needs to be practised regularly.

147

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

9.1 Introduction

Isolated chest injuries are uncommon in children; they are usually associated with multisystem

injury. Problems may result directly from chest injury or may be secondary to other injuries.

Consequences of severe trauma, such as gastric dilatation or pulmonary aspiration after vomiting

or regurgitation, may further compromise respiratory function.

Children have relatively elastic tissues. Substantial amounts of kinetic energy may be transferred

through a child’s chest wall to deep structures with little or no external sign of injury and without rib

fractures. A lack of evident rib fractures on the chest radiograph does not exclude major thoracic

visceral disruption; conversely, the presence of rib fractures indicates high- energy transfer.

Children have relatively little respiratory reserve. Their high metabolic rate and small functional

residual capacity allow them to desaturate more rapidly when their oxygen supply is curtailed. Their

horizontal ribs and underdeveloped musculature make them tolerate chest wall disruption badly.

Flail chest, for example, is poorly tolerated.

The risk of iatrogenic chest problems must be appreciated. The child’s relatively short trachea allows

the endotracheal tube to become easily displaced into a main- stem bronchus or into the oesopha-

gus. Mask ventilation can cause inadvertent gastric distension and overinflation of the lungs can

result in a pneumothorax (especially after intubation if the endotracheal tube has migrated beyond

the carina). If a traumatic pneumothorax already exists, ventilation will cause it to increase in size

and may turn it into a tension pneumothorax.

Thoracic injuries must be considered in all children who suffer major trauma. Some may be life

threatening and require immediate resuscitative therapy during the primary survey and

resuscitation. Others may be discovered during the secondary survey (and its associated investiga-

tions) and be dealt with by emergency treatment. Some situations will need prompt, specialist

surgical intervention, but most chest injuries can be managed in the first hour using general

advanced life support skills. Practical procedures are described in detail in Chapter 21. During

subsequent detailed review, attention will be redirected to the chest to maintain respiratory control

and to search for missed injuries. See Box9.1 for Imaging in chest trauma.

The child withchest

injury

CHAPTER 9

Learning

the World Health Organization (WHO) show the leading cause of death in this

age group is pneumonia, followed by preterm birth and then diarrhoeal illnesses. This compares

with recent data from the USA showing the leading cause in children to be gun‐ related injuries. In

the UK, Office for National Statistics (ONS) data show that cancer is the leading cause of death in all

children followed by accidents and then congenital abnormalities.

The COVID‐ 19 pandemic has not directly had a significant impact on child mortality. However, there

are ongoing concerns about the indirect impact due to strained and under‐ resourced health

systems; a reduction in care‐ seeking behaviours; a reduced uptake of preventative measures such

as vaccination and nutritional supplements; and socioeconomic challenges.

Introduction and

structured approach to

paediatric emergencies

CHAPTER 1

Learning outcomes

After reading this chapter, you will be able to:

z Appreciate the focus and principles of the APLS course

z Describe the structured approach to identifying and managing paediatric emergencies

z Identify the important differences in children and the impact these have on the management

of emergencies

z Appreciate that the absolute size and relative body proportions change with the age of the

child

z Identify the approach to triage of a child

4 PART 1 Introduction

Pathways to cardiac arrest

Respiratory

obstruction

Foreign body

Asthma

Croup

Respiratory

depression

Convulsions

Poisoning

Raised ICP

Fluid

loss

Blood loss

Burns

Vomiting

Fluid

maldistribution

Sepsis

Anaphylaxis

Cardiac failure

Respiratory failure Circulatory failure

Cardiac arrest

Figure1.1 Pathways leading to cardiac arrest in childhood (with examples of underlying causes)

ICP, intracranial pressure

1.2 The APLS approach

In the structured approach it is essential to remember that:

z The child’s family will need support from a qualified member of the team

z Absolute size and body proportions change with age

z Observations and therapy in children must be related to their age and weight

z The psychological needs of children must be considered

z It is key to support each other as the clinical team

Physiological differences

Children, especially young ones, have significantly lower physiological reserves than adults. As a

consequence, they may deteriorate rapidly when severely ill or injured and respond differently

from adults to various interventions. It is essential to manage and support their respiratory and

cardiovascular systems in a timely and structured manner to prevent further deterioration or even

cardiovascular arrest. (See normal ranges table, inside front cover.)

Relationship between disease progression andoutcomes

The further a disease process is allowed to progress, the worse the outcome is likely to be. The

outcomes for children who have a cardiac arrest out of hospital are generally poor. This may be

because cardiac arrest in children is less commonly related to cardiac arrhythmia, but is more

commonly a result of hypoxaemia and/or shock with associated organ damage and dysfunction.

By the time that cardiac arrest occurs, there has already been substantial damage to various

organs. This is in contrast to situations (more common in adults) where the cardiac arrest is the

consequence of cardiac arrhythmia– with preceding normal perfusion and oxygenation. Thus the

focus of the course is on early recognition and effective management of potentially life‐ threatening

problems before there is progression to respiratory and/or cardiac arrest (Figure1.1).

CHAPTER 1 Introduction and structured approach to paediatric emergencies 5

Standardised structure forassessment andstabilisation

A standardised approach for resuscitation enables the provision of a standard working environment

and access to the necessary equipment to manage ill or injured children. The use of the standardised

structure enables the whole team to know what is expected of them and in which sequence.

Once basic stabilisation has been achieved, it is appropriate to investigate the underlying diagnoses

and provide definitive therapy.

Resource management

Provision of effective emergency treatment depends on the development of teams of healthcare

providers working together in a coordinated, well‐ led manner (Figure1.2). It is important that all

training in paediatric life support focuses on how to best use the equipment and human resources

available and emphasises the key nature of effective communication.

Early referral toappropriate teams fordefinitive management

Emergency departments are unlikely to be able to provide definitive management for all paediatric

emergencies, and a component of stabilisation of critically ill or injured children is the capacity to

call for help as soon as possible, and where necessary transfer the child to the appropriate site safely.

Ongoing care until admission toappropriate care

In most parts of the world it is impossible to transfer critically ill children into intensive care units or

other specialised units within a short time of their arrival in the emergency area. Therefore, it is

important to provide training in the ongoing therapy that is required for a range of relatively

common conditions once initial stabilisation has been completed.

Definitive therapy (such as surgical intervention) may be a component of the resuscitation

Figure1.2 Advanced paediatric life support (APLS) in action

6 PART 1 Introduction

1.3 Important differences inchildren

Children are a diverse group, varying 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 immature immune system. They are capable of

limited movement, have immature emotional responses though still perceive pain and are

dependent upon adults for all their needs. At the other end of childhood, the adolescent may be

more than 60kg, 160cm tall and look physically like an adult, often exhibiting a high degree of

independent behaviour but who may still require support in ways that are different from adults.

Competent management of a seriously ill or injured child who may fall anywhere between these

two extremes requires a knowledge of these anatomical, physiological and emotional differences

and a strategy of how to deal with them.

Weight

The most rapid changes in weight occur during the first year of life. An average birth weight of

3.5kg will have increased to 10kg by the age of 1 year. After that time weight increases more slowly

until the pubertal growth spurt. This is illustrated in the weight charts shown in Figure1.3.

As most drugs and fluids are given as the dose per kilogram of body weight, it is important to deter-

mine a child’s weight as soon as possible. The most accurate method for achieving this is to weigh

the child on scales; however, in an emergency this may be impracticable. Very often, especially with

infants, the child’s parents or carer will be aware of a recent weight. If this is not possible, various

formulae or measuring tapes are available. The Broselow or Sandell tapes use the height (or length)

of the child to estimate weight. The tape is laid alongside the child and the estimated weight read

from the calibrations on the tape. This is a quick, easy and relatively accurate method. Various

formulae may also be used although they should be validated to the population in which they are

being used.

If a child’s age is known, the normal ranges table will provide you with an approximate weight

(inside front cover) and allow you to prepare the appropriate equipment and drugs for the

child’s arrival in hospital. Whatever the method, it is essential that the carer is sufficiently

familiar with the tools to use them quickly and accurately under pressure. When the child

arrives, you should quickly review their size

outcomes

After reading this chapter, you will be able to:

z Identify the chest injuries that pose an immediate threat to life and those that are discovered later

z Describe how to manage these injuries

148 PART 3 The seriously injured child

9.2 Thoracic Injuries posing animmediate threat tolife

The following conditions are life threatening. They should be identified during the primary survey

and treated immediately. They do not need to be confirmed by adjunct investigations.

Airway obstruction

The management of airway obstruction is discussed in Chapter17.

Tension pneumothorax

This is a life- threatening emergency that can be rapidly fatal if not treated promptly. Air accumulates

under pressure in the pleural space. This pushes the mediastinum across the chest and kinks the

great vessels, compromising venous return to the heart and reducing cardiac output (Figure9.1).

The diagnosis is a clinical one.

Signs

z The child will be hypoxic and may be shocked

z Unless the child is deeply unconscious, there will be signs of respiratory distress

z There will be decreased air entry and possible asymmetrical air movement on inspection, with

hyper- resonance to percussion on the side of the pneumothorax

z Distended neck veins may be apparent in some children

z The trachea deviates away from the side of the pneumothorax, although this is not always easy

to identify clinically

z Point of care ultrasound (POCUS) (see Appendix I) mid- axillary of the chest may be useful

Box 9.1 Imaging inchest trauma

Chest X- ray (CXR)

The primary investigation for blunt chest trauma is the chest X- ray. This will detect pneumothorax,

haemothorax, gross mediastinal injuries, flail chest and may show rib fractures

Point ofcare ultrasound (POCUS)

Focused ultrasound used in the emergency situation to identify pneumothorax, haemothorax

or cardiac tamponade

Computed tomography (CT)

CT chest should be performed for penetrating chest injuries

CT chest in blunt trauma should be dictated by the nature of the trauma, the clinical condition

of the child and the initial CXR findings

A Airway obstruction

T Tension pneumothorax

O Open pneumothorax

M Massive haemothorax

F Flail chest

C Cardiac tamponade

CHAPTER 9 The child withchest injury 149

Resuscitation

z High- flow oxygen should be given through a reservoir mask

z Immediate finger thoracostomy (an incision to allow continuous drainage (Figure9.2)) or needle

thoracocentesis should be performed to relieve the tension (Figure9.3)

z A chest drain should be inserted urgently to prevent recurrence or progression to a tension

pneumothorax

Trachea

Pleural space

Chest wall

Pressure from

air entering

pleural space

Tracheal shift

Collapsed lung

Air in pleural

spaceExpanded

lung

Figure9.1 Tension pneumothorax

(a) (b)

Figure9.2 (a, b) Finger thoracostomy

Air may be forced into the pneumothorax by positive pressure ventilation. If the child is

ventilated, a simple pneumothorax is very likely to progress rapidly into a tension pneumothorax

150 PART 3 The seriously injured child

Open pneumothorax

In this situation there is a penetrating wound in the chest wall with associated pneumothorax. The

wound may be obvious, but if it is on the child’s back it will not be seen unless actively looked for. If

the diameter of the defect is greater than about one- third of the diameter of the trachea, air will

preferentially enter the pleural space via the defect rather than be drawn into the lungs via the

trachea when the child takes a breath. It is then referred to as a sucking chest wound.

Signs

z Air may be heard sucking and blowing through the wound

z The other signs of pneumothorax will be present

z There may be an associated haemothorax (i.e. a haemopneumothorax)

z POCUS of the chest may be useful

Resuscitation

z High- flow oxygen should be given through a reservoir mask

z The immediate treatment for a sucking wound is to occlude the wound site by using a ported

chest seal, provided that the defect is not larger than the base of this device (Figures9.4 and9.5).

If a ported seal is unavailable, use a three-sided occulsive dressing (Figure 9.4)

z A chest drain will be required as part of emergency treatment. It should not be inserted through

the defect itself as this may spread contamination and restart bleeding

(a)

(b)

Mid-clavicular line

5th intercostal space

between anterior axillary

and mid-axillary lines

Lateral edge of

pectoris major Base of axilla

Lateral edge of

latissimus dorsi

5th intercostal space

Figure9.3 (a, b) Landmarks for chest decompression

CHAPTER 9 The child withchest injury 151

Massive haemothorax

A massive haemothorax will be identified during the B (breathing) stage of the primary survey,

although 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 vessels (arteries or

veins from the pulmonary or systemic vessels) within the lung, the mediastinum or the chest wall

(or from a combination). The hemithorax can contain a substantial proportion of a child’s blood

volume, causing haemorrhagic shock as well as local pressure effects.

Opening in

chest wall

(but not gauze pad)

Free edge

Figure9.4 Occlusive dressing (taped on three sides)

(a)

(b)

Figure9.5 (a) Ported chest seal, and (b) Russell chest seal

Reproduced by permission of Safeguard Medical Technologies

152 PART 3 The seriously injured child

Signs

z The child will show signs of shock and may be hypoxic despite added oxygen

z There will be decreased chest movement, decreased air entry and dullness to percussion on the

side of the haemothorax

z POCUS of the chest may be helpful to confirm if a haemothorax is present

Resuscitation

z High- flow oxygen should be given through a reservoir mask

z Intravenous access ×2 should be established and blood volume replacement commenced

z A relatively large chest drain should be inserted urgently

Flail chest (or chest wall instability or deformity)

If a number of adjacent ribs are fractured in two or more places, a segment of the chest wall 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 of the child’s chest wall. When it does

occur, we expect major force to have been involved and serious underlying lung (and mediastinal)

injury should be anticipated. If the reported mechanism does not involve significant force, suspect

an erroneous history (remember non- accidental injury) or, more rarely, osteogenesis imperfecta.

Flail segments may not be noticed on initial examination for three separate reasons: firstly, severe pain

on breathing will cause the child to splint the chest wall (this may be unmasked by analgesia); secondly,

a child who has already been intubated will be receiving positive pressure ventilation, which moves the

floating segment in unison with the rest of the chest wall; or thirdly, the flail segment may be posterior

and unnoticed if the back of the chest is not examined carefully. Rib fractures do not always show up

well on the chest radiograph, so imaging should not be relied upon in making the diagnosis.

Signs

z The child may be hypoxic despite added oxygen and in considerable pain

z Paradoxical chest movement is characteristic but may not be obvious as indicated above. A high

index of suspicion should be retained

z Other evidence of rib fractures (e.g. crepitus on palpation) may be seen

Resuscitation

z High- flow oxygen should be given through a reservoir mask

z 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 to 2weeks 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

to check if it is much larger or smaller than predicted.

If you have a child who looks particularly large or small for their age, you can go up or down

one age group.

CHAPTER 1 Introduction and structured approach to paediatric emergencies 7

Figure1.3 Example of centile chart for weight in girls (2–18 years)

(Continued)

8 PART 1 Introduction

Figure1.3 (Continued)

CHAPTER 1 Introduction and structured approach to paediatric emergencies 9

Anatomical

As the child’s weight increases with age the size, shape and proportions of various organs 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 occiput is relatively large and the neck short, potentially resulting in neck flexion and

airway narrowing when the child is laid flat in the supine position. The face and mandible are small,

and teeth or orthodontic appliances may be loose. The tongue is relatively large and not only tends

to obstruct the airway in an unconscious child, but may also impede the view at laryngoscopy.

Finally, the floor of the mouth is easily compressible, requiring care in the positioning of fingers

when holding the jaw for airway positioning. These features are summarised in Figure1.4.

The anatomy of the airway itself changes with age, and consequently different problems affect dif-

ferent age groups. Infants less than 6months old are primarily nasal breathers. As the narrow nasal

passages are easily obstructed by mucous secretions, and as upper respiratory tract infections are

common in this age group, these children are at particular risk of airway compromise. Adenotonsillar

hypertrophy may be a problem at all ages, but is more usually found between 3 and 8 years. This not

only tends to cause obstruction, but also may cause difficulty when the nasal route is used to pass

pharyngeal, gastric or tracheal tubes.

The trachea is short and soft. Overextension of the neck as well as flexion may therefore cause

tracheal compression. The short trachea and the symmetry of the carinal angles (the angle between

the right and left main bronchi) mean that not only is tube displacement more likely, but a tube or

a foreign body is also just 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 small total surface

area in the infant (less than 3m2). In addition, there is a 10‐ fold increase in the number of small

airways from birth to adulthood. Both the upper and lower airways are relatively small and are

consequently more easily obstructed. As resistance to flow is inversely proportional to the fourth

power of the airway radius (halving the radius increases the resistance 16‐ fold), seemingly small

obstructions can have significant effects on air entry in children. This may partially explain why so

much respiratory disease in children is characterised by airway obstruction.

Infants rely mainly on diaphragmatic breathing. Their muscles are more likely to fatigue as they

have fewer type I (slow‐ twitch, highly oxidative, fatigue‐ resistant) fibres compared with adults.

Preterm infants’ muscles have even fewer type I fibres. These children are consequently more prone

to respiratory failure.

The ribs lie more horizontally in infants, and therefore contribute less to chest expansion. In the

injured child, the compliant chest wall may allow serious parenchymal injuries to occur without

necessarily incurring rib fractures. For multiple rib fractures to occur the force must be very large;

the parenchymal injury that results is consequently very severe and flail chest is tolerated badly.

Narrow nostrils

Large tongue

Loose teeth

Horseshoe-shaped epiglottis

High anterior larynx

Compressible floor of mouth

Figure1.4 Summary of significant upper airway anatomy

10 PART 1 Introduction

Figure1.5 Differences in children

TAGSTOCK2/Adobe Stock

Circulation

At birth the two cardiac ventricles are of similar weight; by 2months of age the RV:LV weight ratio

is 0.5. These changes are reflected in the infant’s electrocardiogram (ECG). During the first months

of life the right ventricle (RV) dominance is apparent, but by 4–6months of age the left ventricle (LV)

is dominant. As the heart develops during childhood, the sizes of the P wave and QRS complex

increase, and the P‐ R interval and QRS duration become longer.

The child’s circulating blood volume per kilogram of body weight (70–80ml/kg) is higher than that

of an adult, but the actual volume is small. This means that in infants and small 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 (Figure1.5). Small children,

with a high ratio, lose heat more rapidly and consequently are relatively more prone to hypothermia.

At birth, the head accounts for 19% of BSA; this falls to 9% by the age of 15 years.

CHAPTER 1 Introduction and structured approach to paediatric emergencies 11

Physiological

Respiratory

The infant has a relatively greater metabolic rate and oxygen consumption. This is one reason for an

increased respiratory rate. However, the tidal volume remains relatively constant in relation to body

weight (5–7 ml/kg) through to adulthood. The work of breathing is also relatively unchanged at

about 1% of the metabolic rate, although it is increased in the preterm infant.

In the adult, the lung and chest wall contribute equally to the total compliance. In the newborn,

most of the impedance to expansion is due to the lung, and is critically dependent on the presence

of surfactant. The lung compliance increases over the first week of life as fluid is removed from the

lung. The infant’s compliant chest wall leads to prominent sternal recession when the airways are

obstructed or lung compliance decreases. It also allows the intrathoracic pressure to be less ‘nega-

tive’. This reduces small airway patency. As a result, the lung volume at the end of expiration is simi-

lar to the closing volume (the volume at which small‐ airway closure starts to take place).

The combination of high metabolic rate and oxygen consumption with low lung volumes and limited

respiratory reserve means that infants in particular will desaturate much more rapidly than adults.

This is an important consideration during procedures such as endotracheal intubation.

At birth, the oxygen dissociation curve is shifted to the left and P50 (PO2 at 50% oxygen saturation)

is greatly reduced. This is due to the fact that 70% of the haemoglobin (Hb) is in the form of fetal

haemoglobin (HbF); this gradually declines to negligible amounts by the age of 6months.

The immature infant lung is also more vulnerable to insult. Following prolonged respiratory support

of a preterm infant, chronic lung disease of the newborn may cause prolonged oxygen depend-

ence. Many infants who have suffered from bronchiolitis remain ‘chesty’ for a year or more.

Cardiovascular

The infant has a relatively small stroke volume (1.5ml/kg at birth) but has the highest cardiac index

seen at any stage of life (300ml/min/kg). Cardiac index decreases with age and is 100ml/min/kg in

adolescence and 70–80ml/min/kg in the adult. At the same time the stroke volume increases, the

heart gets bigger and muscle mass relative to connective tissue increases. As cardiac output is the

product of stroke volume and heart rate, these changes underlie the heart rate changes seen during

childhood. In addition, the average infant is only able to increase their heart rate by approximately

30% versus the adult who may be able to increase heart rate under stress by up to 300%.

As the stroke volume is small and relatively fixed in infants,

cardiac output is principally related to

heart rate. The practical importance of this is that the response to volume therapy is blunted when

normovolaemic because stroke volume cannot increase greatly to improve cardiac output. By the

age of 2 years, myocardial function and response to fluid are similar to those of an adult.

Systemic vascular resistance rises after birth and continues to do so until adulthood is reached. This

is reflected in the changes seen in blood pressure.

Immune function

At birth the immune system is immature and, consequently, babies are more susceptible than older

children to many infections such as bronchiolitis, septicaemia, meningitis and urinary tract

infections. Maternal antibodies acquired across the placenta provide some early protection but

these progressively decline during the first 6 months. These are replaced slowly by the infant’s

antibodies as they grow older. Infants may be particularly susceptible to infectious diseases in the

period between the waning of maternal antibodies and development of their own antibodies

(sometimes in response to immunisation). Breastfeeding provides increased protection against

respiratory and gastrointestinal infections.

12 PART 1 Introduction

Children with developmental differences due to pre‐ existing conditions such as autism,

chromosome abnormalities or cerebral palsy may require different means of communication

Knowledge allays fear and it is important to explain things as clearly as possible to the child in

language they understand

Psychological

Fear

Children vary enormously in their intellectual ability and their emotional response. A knowledge of

child development assists in understanding a child’s behaviour and formulating an appropriate

management strategy. Particular challenges exist in communicating with children. Many situations

that adults would not classify as fearful, engender fear in children. This causes additional distress to

the child and adds to parental anxiety. Physiological parameters, such as pulse rate and respiratory

rate, are often raised because of it, and this in turn makes clinical assessment of pathological

processes such as shock more difficult.

Fear is a particular problem in the pre‐ school child who often has a ‘magical’ concept of illness and

injury. This means that the child may think that the problem has been caused by some bad wish or

thought that they have had. School‐ age children and adolescents may have fearsome concepts of

what might happen to them in hospital because of ideas they have picked up from adult conversa-

tion, films and television.

Play can be used to help with explanations (e.g. applying a bandage to a teddy first), and also helps

to maintain some semblance of normality in a strange and stressful situation. Parents must be

allowed to stay with the child at all times (including during resuscitation if at all possible); impor-

tantly, they too must be supported and fully informed at all times.

Communication

Infants and young children either have no language ability or are still developing their speech. This

causes difficulty when symptoms such as pain need to be described. Even children who are usually

fluent may remain silent in healthcare settings when unwell or injured. Information has to be

gleaned from the limited verbal communication and from the many non‐ verbal cues (such as

facial expression and posture) that are available. Older children are more likely to understand

aspects of their illness and treatment and so be reassured by adequate age‐ appropriate

communication.

CHAPTER 1 Introduction and structured approach to paediatric emergencies 13

1.4 Structured approach topaediatric emergencies

A structured approach to paediatric emergencies will enable a clinician to manage emergencies in

a logical and effective fashion and assist in ensuring that vital steps are not forgotten even in

unfamiliar or infrequent emergency situations (Figure1.6). This allows:

z Identification of life‐ threatening situations: closed or obstructed airway, absent or ineffective

breathing, or absent pulse or shock requiring immediate interventions which comprise resuscitation

z Following resuscitation, looking for key features which signpost likely working diagnosis

z Initiation of emergency treatment

z Stabilisation and transfer for definitive care

Remember to utilise newer techniques such as point of care ultrasound (POCUS) if practitioners

have the skill set to do so (see Appendix I).

Throughout this book, in the virtual learning environment (VLE) and on APLS courses, the same

structure will be used so that the clinician will become familiar with the approach and be able to

apply it to any clinical emergency situation.

Structured approach to paediatric emergencies

Prepare for child’s arrival

Primary survey

ABCDE looking for

life-threatening issues

Resuscitation

Secondary survey

looking for key features to aid

diagnosis

Reassessment and

physiological system control

Emergency treatment

Continuing stabilisation

Transfer to definitive care

Figure1.6 Structured approach to paediatric emergencies

14 PART 1 Introduction

Table1.1 Triage scale

Number Colour Name Maximum time to clinician

1 Red Immediate 0min

2 Orange Very urgent 10min

3 Yellow Urgent 60min

4 Green Standard 240min

5 Blue Non‐ urgent N/A

1.5 Preparation

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

z Ensure that appropriate help is available: critical illness and injury need a team approach

z Work out the likely drug, fluid and equipment needs

For unexpected emergencies, ensure that all areas where children may be treated are stocked with

the drugs, fluid and equipment needed for any childhood emergencies.

1.6 Teamwork

A well‐ functioning team is vital in all emergency situations. Success depends on each team member

carrying out their own tasks and being aware of the tasks and the skills of other team members. The

whole team must be under the direction of a team leader. Scenario practice by teams who work

together is an excellent way to keep up skills, knowledge and team coordination in preparation for

the ‘real thing’. See Chapter2 on non‐ technical skills.

1.7 Communication

Communication with the ill or injured child and their family has been discussed previously.

Communication is no less important with clinical colleagues. When things have gone wrong,

investigations have identified that an issue in communication has often been involved. Structured

communication tools may be useful in ensuring that all relevant information is conveyed to all the

teams involved in the child’s care. Contemporaneous recording of clinical findings, of the child’s

history and of test results and management plans seems obvious but in the emergency situation

may be overlooked. A template for note taking can be found in Chapter8.

1.8 Triage

Triage is the process whereby each child presenting with potentially serious illness or injury is

assigned a clinical priority. It is an essential clinical risk management step, and also a tool for

optimisation of resource allocation in any emergency.

In the UK, Canada and Australia, five‐ part national triage scales have been agreed. Such a scale is

shown in Table1.1. While the names of the triage categories and the target times assigned to each

name vary from country to country, the underlying concept does not.

CHAPTER 1 Introduction and structured approach to paediatric emergencies 15

Triage is used to identify children who require urgent intervention.

Accuracy of triage and assigning a priority is an important basis for any triage system. However,

there are instances when even for lower acuity patients the management may be deemed urgent,

for example in an epidemic it may be important to get potentially uninfected children away from

possible infection as soon as possible

but the assessed triage priority will not change, just the action

post triage. Never forget the need for repeated triage/reassessment– children can deteriorate rap-

idly and if there is no reassessment process, this may be missed.

Remember also that being triaged green does not mean that a child does not have a serious prob-

lem that requires specialist attention. It simply means the risk has been assessed and it would be

acceptable for that child to wait for definitive management.

It is important to make sure that the family understands the nature of the triage process (and why

they will see other children receiving treatment who arrived after their child).

Triage decision making

There are many models of decision making, each including: identification of a problem, determination

of the alternatives and selection of the most appropriate alternative.

Discriminators are factors normally expressed as a word or short statement that allow patients to be

allocated to one of five clinical priorities as in the algorithm in Figure1.7. They can be general or spe-

cific. The former apply to all patients irrespective of their presentation and include life threat, pain,

haemorrhage, conscious level and temperature and appear across the priorities (e.g. very hot, hot

and warm). Specific discriminators tend to relate to key features of particular conditions, for exam-

ple an asthmatic child ‘unable to talk in sentences’. Thus severe pain is a general discriminator, but

cardiac pain and pleuritic pain are specific discriminators.

16 PART 1 Introduction

Airway compromise

Inadequate breathing

Shock unresponsive

Currently fitting

Hypoglycaemia

Low SpO2

Signs of dehydration

Not feeding

Not passing urine

Inappropriate history

History of recent foreign travel

Significant haematological or metabolic

history

Hot

Moderate pain

Atypical behaviour

Warm

Recent mild pain

Recent problem

Very low SpO2

New abnormal pulse

Responds to voice or pain only

Fails to react to parents

Signs of meningism

Purpura

Known or likely immunosuppression

Special risk of infection

Non-blanching rash

Very hot

Possible sepsis

Cold

Severe pain

RISK

LIMIT

BLUE

Unwell child

RED

ORANGE

YELLOW

GREEN

1 2 3 4 5

Figure1.7 Paediatric triage for an unwell child

CHAPTER 1 Introduction and structured approach to paediatric emergencies 17

Secondary triage

It may not be possible to carry out all the assessments necessary at the initial triage encounter– this

is particularly so if the workload of the department is high. In such circ*mstances, the necessary

assessments should still be carried out, but as secondary procedures by the receiving healthcare

professional. The actual initial clinical priority cannot be set until the process is finished. More time‐

consuming assessments (e.g. blood glucose estimation and peak flow measurement) are often left

to the secondary stage.

1.9 Summary

This chapter has given an overview of management of paediatric emergencies, outlining the

structured approach which is central to APLS. Subsequent chapters will focus in depth on the

elements of the ABCDE approach in both the ill and the injured child.

Advanced Paediatric Life Support: A Practical Approach to Emergencies, Seventh Edition. Edited by Stephanie Smith.

2.1 Introduction

This chapter provides a brief introduction to some of the non- technical skills that can affect the

performance of individuals and teams in the healthcare environment. Non- technical skills, also

referred to as human factors or ergonomics, is an established scientific discipline and clinical

human factors have been described as:

Enhancing clinical performance through an understanding of the effects of teamwork, tasks, equipment,

workspace, culture and organisation on human behaviour and abilities and application of that

knowledge in clinical settings. (Kohn etal., 2010)

2.2 Extent ofhealthcare error

In 2000 an influential report entitled To Err is Human: Building a Safer Health System suggested

that across the USA somewhere between 44000 and 98000 deaths each year could be attributed

to medical error. A pilot study in the UK demonstrated that approximately one in 10 patients

admitted to healthcare experienced an adverse event.

Healthcare has been able to learn from a number of other high- risk industries including the nuclear,

petrochemical, space exploration, military and aviation industries about how team issues have been

managed. These lessons have been gradually adopted and translated to healthcare.

Specialist working groups and national bodies have been instrumental in promoting awareness of

the importance of human factors in healthcare. One such example of this in the UK is the Human

Factors Clinical Working Group.

Getting it right:

non- technical factors

andcommunication

CHAPTER 2

Learning outcomes

After reading this chapter, you will be able to:

z Describe how clinical human factors affect the performance of individuals and teams in the

healthcare environment

20 PART 1 Introduction

2.3 Causes ofhealthcare error

Consider this example of an adverse event:

A child needs to receive an infusion of a particular drug. An error occurs and the child receives an

incorrect drug. There are a number of potential causes of this situation. A few of these are given

below.

However many checks and procedures are put in place, mistakes will still occur and may cause

harm to patients. It is vital therefore that we look to work in a way that, wherever possible, reduces

the occurrence of mistakes and ensures that when they do occur the chance of the error resulting

in harm to children in our care is minimised. Reason’s taxonomy of errors (Figure2.1) provides further

insight by illustrating how errors can be sharp or blunt or a combination of the two.

Because errors are multifactorial, it is typically found that the organisational or blunt issues often

coexist with the clinical or sharp errors; in fact it is rare for an isolated error to occur– often there is

a chain of events that results in the adverse event. Apparently random, unconnected events and

organisational decisions can all make errors more likely. Conversely, a standardised system with

good defences can often capture these errors and prevent adverse events and subsequent impact

on the patient.

Blunt end

Design phase

Decreasing time to think

Errors in:

Policies

Procedures

Infrastructure

Building layout

Sharp end

Clinical practice

Error types:

Mistake

Slip or lapse

Deliberate violation

Figure2.1 Reason’s taxonomy of errors

Prescription error Wrong drug prescribed

Prescription error Incorrect amount prescribed

Preparation error Correct drug prescribed but misread

Preparation error Contents mislabelled during manufacture

Drawing up error Incorrect drug selected

Administration error Patient ID mix- up, drug given to wrong patient

CHAPTER 2 Getting it right: non-technical factors and communication 21

In the example of drug error just given, the first potential error is the doctor writing the prescription,

the second is the organisation’s drug policy, the third is the nurse who draws up the drug and the

fourth is the nurse who second checks the drug.

Now consider the following:

z What if the doctor is very junior and not familiar with that area or drugs used?

z What if the doctor is very senior and makes untested assumptions about drugs available?

z What if the organisation has failed to develop a robust drug policy that is fit for purpose?

z What if the nurse is a bank nurse who does not normally work on this ward and is not familiar

with commonly used drugs?

z What if this area is always short of staff so that other staff do not routinely attempt to get the

drug second checked?

The end result is that multiple defences have been weakened or removed and error is not only more

likely to occur, but, if it does, there is a greater

chance that it will cause harm.

2.4 Improving team andindividual performance

Raising awareness of clinical human factors and being able to practise these skills and behaviours

within multiprofessional teams allows the development of effective teams in all situations. Simulation

activity allows a team to explore these new ideas, practise them and develop them. To do this we

need feedback on our performance within a safe environment where no patient is at risk and egos

and personal interests can be set aside. Consider how you developed a clinical skill. It was something

that needed to be practised again and again until eventually it started to become automatic and

routine. The same applies for our non- technical behaviours. In addition, recognising our inherent

human limitations and the situations when errors are more likely to occur, will encourage us to aim

to be hypervigilant when required. It is important to remember that paying attention alone does

not guarantee improved awareness of a situation as attentional control is subconscious and

therefore beyond volitional control.

2.5 Communication

Poor communication is a leading cause of adverse events. This is not surprising; to have an effective

team there needs to be good communication. The leader needs to communicate with the followers,

and followers need to communicate with leaders and other followers. Communication is not just

saying something– it is ensuring that information is accurately passed on and received. There are

multiple components to effective communication (Table2.1).

Table2.1 Elements ofcommunication

Sender Sender Transmitted Receiver Receiver

Thinks of what to

say

Says

message

Through air, over phone, via

Hears it Thinks about it and

acts

22 PART 1 Introduction

When communicating face- to- face, in an emergency setting, a message is often announced to a

room where nobody acknowledges it. Targeting our communications towards specified individuals

in what is sometimes referred to as ‘directed communication’ is now seen to be an essential element

in improving communication. Many emergency settings, where staff change frequently, have

people’s names prominently displayed to encourage this.

Information is also transmitted non- verbally and processed in different ways by different people

dependent on cultural, linguistic, neurodivergent and contextual variables. Communication can be

more difficult when talking across professional, cultural, specialty or hierarchal barriers as we do not

always talk the same technical language, have the same levels of understanding, or even have a full

awareness of the other person’s role.

There are a variety of tools to aid communication, such as SBAR (situation, background, assessment

and recommendation) which facilitates planning and organising a message, making it succinct

and focused. A good SBAR provides a handover in a logical and expected order. It is also an empow-

erment tool allowing the sender (who may be more junior) to request an action from a more senior

individual.

Effective communication witha feedback loop

Consider a busy clinical situation and the team leader shouts ‘We need an ECG connecting’

while looking at the blood pressure– what happens? The majority of times nothing– nobody

goes to connect the electrocardiogram (ECG) because responsibility for the task has been

diffused. The larger the group, the more likely it is that no- one will take responsibility for this

vaguely phrased request. So how can this be improved? Most obviously an individual can be

identif ied to perform the task, by name: ‘Michael can you please connect the ECG?’ If Michael

says ‘Yes’, effective communication might be assumed, but not always. What has Michael heard

and what will he do? At the moment we do not really know what message has been received.

Michael might dash over with the defibrillator as this is what he thought he heard. This may

seem a slightly strange thing to happen, but how often in a clinical emergency have you asked

for something and been presented with something else? People are less likely to ask questions

in emergencies as everyone is busy. This could be the catalyst for an error or precipitate a missed

task. So how do we f ind out what message Michael received? The easiest way is to include a

feedback loop in which we request that the other person let us know when they’ve completed

the task.

Now the conversation goes:

We now know that the message has been transmitted and received correctly. For this process to

work both parties (the sender and receiver) need to understand and expect it– again demonstrating

the need for us to practise and train together.

Team leader ‘Michael, can you please connect the ECG, and let me know when you’ve

done it?’

Michael ‘Okay’

Michael (later) ‘I have connected the ECG’

CHAPTER 2 Getting it right: non-technical factors and communication 23

2.6 Team working, leadership andfollowership

At a basic level a team is a group of individuals with a common cause. Historically we have tended

to train individually or in professional silos; the risk here is that we are making a ‘team of experts’

rather than an ‘expert team’. Often within healthcare, our teams form at short notice and arrive at

different times. Emphasis tends to be placed on the significance of the role of the leader, but a

leader cannot be a team on their own. As much emphasis should be given to developing the other

team members, the active followers. A good leader will be able to swap from the role of leader to

follower as more senior staff arrive and agree to take over.

The leader

The leader’s role is multifaceted and includes directing the team, assigning tasks and assessing

performance, motivating and encouraging the team to work together, and planning and organising.

Additionally, a leader needs to maintain standards, support others and see where needs arise. All

leadership skills and behaviours need to be developed and practised. Constructive feedback on

efficacy of communication should both be given and sought in order to facilitate continuously

improving performance.

It is important to clearly identify who is leading. The leader may change as more people arrive in an

emergency situation. If there is a scribe recording events, they should record and update who is

leading at any time.

As soon as the leader becomes hands on, and task focused, they are primarily concentrating on the

task at hand. This becomes the focus of their thoughts and they lose situation awareness, their

objective overview of the situation. The leader should be standing in an optimal position where they

can gather all the information and ideally view the patient, the team members and the monitoring

and diagnostic equipment. This enables them to recognise when a member is struggling with a

task or procedure and support them appropriately.

Team roles

Ideally, the team should meet before the event and have the opportunity to introduce themselves

to each other and clarify roles and actions in emergencies. Sometimes this can be facilitated at

the beginning of a shift but at other times it is impossible to predict or arrange. It is important,

therefore, that individuals identify themselves to the leader as they arrive and roles are agreed,

allocated and understood. Much of the time their role may be determined purely in relation to the

specific bleep the individual carries, but it is important that team members are flexible, for

example if three airway providers are first on the scene we would expect other tasks to also be

allocated and undertaken.

Followership

Followers are expected to work within their scope of practice and take the initiative. They should be

attentive to the needs of the rest of the team and know where they fit within the bigger picture. It

is important to think about the level of communication required between the leader and followers.

If it is obvious that a team member is doing

2023 Advanced Paediatric Life Support A Practical Approach to Emergencies - Emergência e Primeiros Socorros (2024)

References