2.1 The seriously ill child: physiology [link]
2.2 The seriously ill child: clinical assessment [link]
2.3 Cardiopulmonary arrest [link]
2.4 Accidental injuries: trauma and burns [link]
2.5 Head injury and drowning [link]
2.6 Poisoning [link]
2.7 Respiratory emergencies [link]
2.8 Septicaemia and septic shock [link]
2.9 Anaphylaxis [link]
2.10 Diabetic ketoacidosis [link]
2.11 Convulsions and coma [link]
2.12 Case-based discussions [link]
Sudden, unexpected cardiopulmonary arrest is very rare in children. Arrest is nearly always preceded by a period of progressive failure of the respiratory, cardiovascular, or nervous system. Care of the critically ill child therefore requires understanding of how these systems function and how the anatomy and physiology of small infants and children differs from that in adults.
Body size and proportions
Infants and children do not have optimal body proportions overall and the head in particular is disproportionately large. This has several unfortunate consequences:
• High ratio of body surface area to weight:
• rapid heat loss predisposes to hypothermia
• high fluid turnover increases susceptibility to dehydration.
• Small body size:
• multisystem involvement is more likely in blunt trauma, e.g. a severe pattern of injury in pedestrian road traffic accidents
• Large head:
• tend to fall head first, increasing the likelihood that the head is the point of impact
• the large head and weak neck of small infants generates large shearing forces if the infant is shaken.
• Up to age 6 months infants are obligate nose breathers and do not tolerate nasal obstruction caused by secretions or soft tissue such as adenoids or cannulae.
• The relatively bulky oropharyngeal soft tissues, combined with passive flexion due to larger occiput and shorter neck, renders the oropharyngeal airway easily occluded. The optimal head position is neutral in an infant and ësniffing’ in a child.
• The diameter of the upper airway is the perfect size for complete occlusion by some inhaled objects.
• The internal diameter of all airways are smaller giving rise to a greater rise in airway resistance for any given reduction in diameter by oedema, secretions, or bronchospasm.
The ribs and chest wall are elastic and compliant in young infants causing
• Intercostal and subcostal recession
• Pulmonary contusions without rib fracture in chest trauma.
Compliance decreases with skeletal maturation. Recession in an older child indicates a greater degree of respiratory distress. The ribs are positioned more horizontally than in adults and afford less protection to the abdominal contents.
The diaphragm is the principle muscle of respiration in infancy. It fatigues easily and air in the stomach, as occurs with bag and mask ventilation, can cause splinting. The sitting position may reduce diaphragmatic work and swallowed air should be decompressed using a nasogastric tube.
Central control of respiration is immature in preterm infants and apnoeic episodes may be spontaneous or provoked by a number of stimuli (see ‘Apparent life threatening events’, Section 2.7).
Cardiac output and oxygen delivery
The volume of blood expelled from each ventricle during systole is called the ‘stroke volume’ and depends on:
• Preload: the degree of ventricular filling during diastole and contractility of the myocardium.
• Afterload: the resistance against which the ventricle pumps.
Cardiac output = heart rate × stroke volume.
The oxygen delivery is the product of cardiac output and arterial oxygen concentration.
Cardiac output is modified by:
• Intracardiac mechanisms: stretching of myocardium causes a more forceful contraction (Frank–Starling curve).
• Extracardiac mechanisms: sympathetic nervous activity increases cardiac performance by increasing venous return (preload), cardiac contractility and heart rate. It also increases afterload and reduces cardiac output by peripheral vasoconstriction.
Whole body oxygen delivery exceeds consumption by a factor of 4, providing a wide safety margin. However, individual organs have different relationships between oxygen delivery and consumption and blood flow to individual organs is influenced by several factors including:
• Metabolism: products of local cellular metabolism cause vasodilatation and match oxygen delivery to consumption.
• Oxygen tension: reduced oxygen delivery causes relaxation of precapillary arterioles with recruitment of capillaries and reduced diffusion distance for oxygen.
• Autoregulation: resistance vessels adapt to pressure changes to maintain flow constant.
In addition to local factors, the sympathetic system has a powerful role in acute regulation of the circulation by noradrenaline mediated vasoconstriction of both arterioles and veins.
In the brain and heart local factors can override sympathetically driven vasoconstriction. In contrast, in organs with a blood flow well in excess of their metabolic needs, such as the kidneys or skin, the action of sympathetic vasoconstriction is more pronounced.
The venous system has a high capacitance and normally contains 75% of the total blood volume. Sympathetic activity tends to reduce venous system compliance and augment venous return. Stretch receptors in the central veins, right atrium, and pulmonary artery mediate enhanced sympathetic activity in response to reduced cardiac filling.
Blood flow in the circulation is determined by the relationship between pressure gradient and resistance. The blood pressure changes from aortic root to arterioles and the driving force available to the arterial tree is best expressed as the mean pressure:
The normal heart rate is higher in small bodies. Increased heart rate increases cardiac output but beyond a certain limit cardiac filling becomes inadequate and cardiac failure ensues.
Following episodes of prolonged and severe hypoxia, a period of bradycardia occurs preceding asystolic cardiac arrest.
Derangements of the nervous system compromise cardiorespiratory function by a variety of distinct mechanisms.
A child with diminished level of consciousness is vulnerable to respiratory compromise because of inability to protect and maintain the airway and depression of central respiratory drive.
A child with convulsive status epilepticus is vulnerable to occlusion of the airway and impaired respiration as a consequence of uncoordinated muscular contractions. In parallel, oxygen consumption of the brain increases. Medications given to control the seizures such as benzodiazepines may cause respiratory depression and apnoea.
Raised intracranial pressure (ICP)
The cranium represents a rigid box with a fixed volume filled by brain, cerebrospinal fluid, and vascular compartments. The normal ICP is 〈10–15 mmHg. Should the space occupied by brain parenchyma increase, e.g. as a result of oedema or blood from an expanding haematoma, compensatory mechanisms such as decreasing the volume of CSF or venous blood are limited in their effects.
When this capacity to compensate is exceeded, further small increases in volume produce large rapid rises in pressure. A raised ICP affects the cardiovascular system in general and the cerebral circulation in particular:
Cerebral perfusion pressure (CPP) = mean arterial pressure – intracranial pressure (ICP)
Increased ICP reduces CPP and therefore brain blood flow.
• Cushing's triad: bradycardia, increased systolic blood pressure, increased pulse pressure. Raised blood pressure and dilatation of cerebral blood vessels causes a further increase in ICP and reduced cerebral perfusion.
The pH scale was introduced because in the environment [H+] varies over an enormous scale. In fact, its use is unnecessary in medicine because [H+] varies over a very small range. pH is the negative logarithm to the base 10 of [H+] in mol/L. As [H+] increases, pH reduces and a change in pH of one point corresponds to a 10fold change in [H+]. Corresponding values over the physiological range are shown in Table 2.1.
Table 2.1. Values of pH and [H+] in the physiological range
Acids, bases, and buffers
An acid is a ‘proton donor’ and forms hydrogen ions in solution whereas a base is a ‘proton acceptor’ and combines with hydrogen ions in solution. A buffer is a compound that limits the change in pH when hydrogen ions are added or removed from a solution.
Production of acid (hydrogen ions)
CO2 from oxidative (aerobic) metabolism: respiratory acid
An enormous quantity of CO2 is produced (15 000 mmol/24 h) which rapidly reacts with water to form carbonic acid which dissociates into hydrogen and bicarbonate (HCO3–) ions. This is described by the equation:
Carbonic acid represents an important buffering system in the body.
Control of hydrogen ion concentrations (pH)
As pH is so critical for many bodily functions it is not surprising that powerful mechanisms exist to maintain pH in the normal range. The main challenge is elimination of acid. Three main mechanisms are:
• Buffers: these include bicarbonate, proteins (e.g. albumin) and haemoglobin. Haemoglobin is a powerful buffer which binds both CO2 and H+ and has the strongest affinity for these in the deoxygenated state.
• Respiration: the respiratory system is the single most important system involved in control of hydrogen ions. The arterial partial pressure of CO2 (PaCO2) is inversely proportional to alveolar ventilation, so small changes in ventilation have a profound and rapid effect on pH: a rise in PaCO2 of 1.0 k Pa results in a fall in pH from 7.40 to 7.34.
• Renal handling of bicarbonate and hydrogen ions: the kidneys secrete hydrogen ions and regenerate bicarbonate ions. Renal handling of electrolytes also influences acid base balance. Bicarbonate ions are freely filtered by the glomerulus and most are reabsorbed in the proximal convoluted tubule. Hydrogen ions are actively secreted in the proximal and distal tubules against a steep concentration gradient and are buffered in the urine by phosphate and ammonia. Channels in the distal tubule controlled by aldosterone exchange sodium for hydrogen or potassium ions. The small capacity of the kidneys for hydrogen ion excretion renders metabolic compensation a slow process.
Early recognition of respiratory failure, circulatory failure, severe neurological dysfunction or acid–base disturbance allows cardiopulmonary arrest to be anticipated and, if possible, prevented.
Rapid clinical assessment
A structured approach is used:
• Primary assessment
• Secondary assessment
• Emergency treatment and stabilization/transfer to ICU.
Primary assessment: ABCDE
• Airway: chest movement, breaths, stridor, wheeze, foreign body, airway opening manoeuvre
• effort: rate, accessory muscles
• efficacy: oxygen saturation
• effects: skin colour, conscious level
• Circulation: heart rate, pulse volume, blood pressure, capillary refill time (CRT)
• Disability: conscious level (AVPU/GCS), posture, pupils: size, symmetry, reaction to light
• Exposure: identify rashes
Secondary assessment involves a focused history and full physical examination in order to establish a diagnosis.
Respiratory failure may be caused by airway obstruction, intrinsic lung disease, or inadequate respiratory effort.
Clinical evaluation should allow recognition of potential respiratory failure. Arterial blood gas analysis is useful to confirm respiratory failure or monitor response to therapy.
Assessment requires evaluation of:
The normal rate decreases from 40–60/min in the newborn to 25–35/min in the 1–2 year old and 15–20/min in an adolescent. Abnormalities include tachypnoea, bradypnoea, and apnoea.
• Tachypnoea: is usually the first manifestation of respiratory distress in an infant and is accompanied by additional signs of changes in the mechanics of respiration such as recession, grunting. Tachypnoea without these signs (‘quiet tachypnoea’) suggests metabolic acidosis with respiratory compensation.
• Bradypnoea: a slow or irregular respiratory rate in an acutely ill child or infant is more ominous and usually indicates fatigue or CNS depression. A decreasing respiratory rate may indicate deterioration rather than improvement.
Effort of breathing
• Nasal flaring, head bobbing and intercostal, subcostal or suprasternal recession may occur with airway obstruction or alveolar disease and increased work of breathing.
• Stridor is a sign of extrathoracic airway narrowing and may be accompanied by a tracheal tug.
• Wheeze and prolonged expiration is a sign of intrathoracic airway obstruction usually at bronchial or bronchiolar level.
• Grunting is produced by early glottic closure with late expiratory contraction of the diaphragm and maintains functional residual capacity. It occurs in pneumonia or atelectasis.
Efficacy of breathing: air entry and oxygenation
Chest expansion should be bilateral and breath sounds should be equal and easily heard. Hypoxaemia is manifested as central cyanosis. Oxygenation measured by pulse oximetry is a good guide to hypoxaemia.
Effects of respiratory inadequacy
Pallor, mottling, and peripheral cyanosis occur with hypoxaemia, but these signs can also occur if the child is exposed to a cold environment. Hypoxaemia causes tachycardia and delayed peripheral capillary refill initially and if severe leads on to bradycardia and asystole. Cerebral hypoxaemia is associated with agitation or drowsiness.
Shock is a state in which there is inadequate tissue perfusion; a failure of the circulation to provide adequate oxygen and nutritive substrates to the tissues. It is classified according to the cause and according to the stage reached. It progresses from compensated to decompensated, and then to irreversible shock.
Causes of shock
Shock may be caused by primary cardiac dysfunction or reduced venous return to the heart. Pathological events which cause these circulatory disturbances include:
• Cardiogenic shock: pump failure occurs in congenital heart disease, cardiomyopathies, cardiac arrhythmias, myocardial contusion and sepsis.
• Reduced venous return: This may be due to:
Note that ‘septic shock’ involves several mechanisms: hypovolaemia due to vascular leak, vasodilatation with vasoplegia, and depressed myocardial function.
Stages of shock
In lowflow states such as hypovolaemic or cardiogenic shock, sympathetic outflow from the medulla causes venoconstriction, arterial vasoconstriction, and tachycardia. Arterial vasoconstriction maintains blood pressure and also diverts blood from nonessential areas such as the skin, kidneys, and splanchnic circulation.
In early septic, or anaphylactic shock, there may be a high flow and high cardiac output state with increased skin blood flow and bounding pulses. However, the cardiac output is unevenly distributed and some tissue beds are inadequately perfused as manifested by oliguria and metabolic acidosis.
Decompensated and irreversible shock
Decompensated shock is heralded by a fall in BP. This may occur if volume loss continues and exceeds 40% of circulating volume or if the circulation cannot meet the demands of the heart itself and myocardial function deteriorates.
Decompensation with hypotension exacerbates tissue hypoperfusion leading to increasing acidosis and inadequate oxygenation of respiratory muscles resulting in respiratory failure. Irreversible alterations occur in the microcirculation and tissues associated with multiple organ failure.
Evaluation of cardiovascular function
Tachycardia is a common response to many types of stress, and hypotension is a late and often sudden sign of cardiovascular decompensation. Skin perfusion varies with environmental temperature. CVS assessment can be difficult and requires evaluation of:
Sinus tachycardia is a common response to anxiety, pain, fever, hypoxia, hypercapnia, hypovolaemia and cardiac impairment. Cardiac output of infants and children is primarily increased by increased heart rate. In neonates, bradycardia may be the initial response to hypoxia, but in older infants and children bradycardia is a late and ominous sign.
The lower limit or 5th centile of systolic blood pressure in children 〉1 year is given by the formula:
Hypotension is a sign of decompensated shock.
This is the best guide to recognition of early, compensated shock and requires assessment of:
• Pulse volume: this is related to pulse pressure and is reduced in low cardiac output shock. In early septic shock there may be high output with bounding pulses.
• Skin perfusion: decreased skin perfusion may be an early sign of shock and is manifested as pallor, mottling, peripheral cyanosis, and delayed capillary refill time (〉2 s). However, skin perfusion may also be reduced by fever or by a cold ambient temperature.
• Renal perfusion: urine output of less than 1 mL/kg per hour in a child or 2 mL/kg per hour in an infant indicates poor renal perfusion in the absence of known kidney disease.
• Brain perfusion: cortical hypoperfusion may be manifested initially as altered consciousness with confusion, irritability and agitation alternating with lethargy. More profound hypoperfusion produces greater changes, with failure to respond to a pain an ominous sign.
Evaluation of the CNS should include:
• Conscious level: the AVPU scale is usually sufficient:
• Alert, response to Voice or Pain, Unresponsive
• Pupils: size, symmetry and reaction to light
• Posture: hypotonia, opisthotonus, decorticate (flexed arms, extended legs), or decerebrate (extended arms and legs) may be apparent.
Respiratory acid–base disturbances
Primary respiratory acidosis occurs when the PaCO2 is above normal, i.e. 〉6 kPa, and is due to alveolar hypoventilation. Primary respiratory alkalosis occurs when the PaCO2 is 〈4.5 kPa and is due to alveolar hyperventilation.
Renal compensation in either state is slow. In persistent respiratory acidosis, the most common scenario, renal conservation of bicarbonate occurs, with base excess positive 〉+2.2.
Metabolic acid–base disturbances
This may result from excess acid production or reduced buffering capacity due to a low concentration of bicarbonate. The pH is too acid for the level of PaCO2 observed.
The anion gap allows these two mechanisms to be distinguished. The anion gap is calculated as the difference between the sum of major cations and anions:
It estimates unmeasured anions in plasma and is normally 10–20 mmol/L. The anion gap is increased when acidosis is caused by production of unmeasured acids e.g. lactate, ketoacids, phosphate and sulphate. It is normal when acidosis is caused by excess bicarbonate losses from the GI tract or kidneys or when renal secretion of H+ ions fails.
Causes of metabolic acidosis include:
• Excess H+ production: tissue hypoxia causing anaerobic metabolism and lactate/pyruvate production as in shock, inborn errors of metabolism, diabetic ketoacidosis
• Inadequate renal function: renal failure, renal tubular acidosis, hypoaldosteronism
• Excessive bicarbonate loss: diarrhoea, fistulae, ureteric implantation into colon
This may result from excessive loss of H+, excessive reabsorption of bicarbonate or even ingestion of alkalis. It is uncommon in childhood but may be seen in:
• Pyloric stenosis: metabolic alkalosis is caused by vomiting stomach (not duodenal) contents and loss of H+ ions and CI− ions
• Hypokalaemia: potassium depletion augments renal excretion of hydrogen ions, and causes shift of hydrogen ions into cells. Metabolic alkalosis in turn exacerbates hypokalaemia as urine alkalinization requires potassium excretion.
• Diuretics: thiazide and loop diuretics.
Respiratory compensation may occur with hypoventilation.
Cardiopulmonary resuscitation (CPR)
Paediatric cardiopulmonary arrests are uncommon and usually secondary to respiratory compromise and hypoxia, as may occur in severe airways obstruction with inhaled foreign object, epiglottitis, asthma, suffocation, drowning, or major trauma. The precise mechanisms in sudden unexpected death in infancy (SUDI) are unknown.
The hypoxic myocardium becomes increasingly bradycardic before progressing to asystole, the most common rhythm found in outofhospital arrests.
Primary cardiac arrest is seen in children with underlying cardiac disease. In this case ventricular fibrillation is the most common arrhythmia and early defibrillation is the main determinant of survival.
Resuscitation Council guidelines are provided for:
• Paediatric Basic Life Support: actions of a single rescuer with no equipment.
• Paediatric Advanced Life Support: management in a hospital setting.
Paediatric basic life support (BLS)
BLS is outlined in the algorithm in Fig 2.2. Start by checking responsiveness. Do not shake if suspected cervical spine injury.
A. Open airway
Hand on forehead to tilt head gently backwards (neutral position in infant, ‘sniffing position’ in child) and lift chin with fingertips placed under chin. If this does not open airway, or there is suspected neck injury, perform jaw thrust manoeuvre: lift jaw upwards with two fingers under the angle of the mandible bilaterally.
B. Check breathing
• Look for chest movements
• Listen at nose and mouth for breath sounds
• Feel for air movement on your cheek.
If breathing normally, place in recovery position.
If not breathing, or making agonal gasps (infrequent, irregular breaths) give five initial rescue breaths.
• Rescue breaths for an infant: ensure a neutral head position, take a breath and cover the mouth and nasal apertures with your mouth, blow steadily over 1–1.5 s.
• Rescue breaths for a child 〉1 year: ensure head tilt and chin lift, pinch the nose closed, place lips around mouth and blow steadily over 1–1.5 s.
The chest should be seen to rise. If it does not, the airway is not clear. Readjust the head tilt/chin lift position. If this fails try jaw thrust, and if this fails check for visible obstruction in the mouth.
C. Check for circulation
Check a central pulse for 10 s:
• In an infant: feel for brachial or femoral pulse
• In a child: feel for carotid pulse.
Start chest compressions if there are no signs of circulation (movement, coughing, normal breathing)
or no pulse
or bradycardia (pulse 60/min with poor perfusion)
or you are not sure (it does no harm).
The child should be flat on their back on a hard surface. Chest compressions should compress the lower third of the sternum, one finger's breadth above the xiphisternum, and should depress the sternum by one third of the depth of the chest.
Compression rate is 100/min and ratio of compressions to breaths is 15:2. Lay rescuers who are assumed to be acting alone are taught a ratio of 30:2.
Technique varies with size and number of rescuers:
• Infant: lone rescuer uses two finger tips placed one finger breadth above the xiphisternum. Two or more use hand-encircling approach with both thumbs on lower third of sternum.
• Child: place heel of one hand over lower third of sternum, lift fingers, position vertically over chest with arm straight. For larger children (or smaller rescuers) both hands may be used with fingers interlocked.
This is the management of cardiopulmonary arrest in a hospital setting (see Fig 2.3 for algorithm) and focuses on the procedures necessary after basic life support has been instituted. This may have included intubation and ventilation and gaining intraosseous circulatory access.
The next step is to assess the rhythm and categorize it as non-shockable or shockable:
• pulseless electrical activity (PEA)
• ventricular fibrillation
• pulseless ventricular tachycardia.
These predominate and include asystole and PEA. Asystole appears as a ‘flatline’ on ECG: check the connections and the gain on the ECG monitor. PEA, as the name implies, is the absence of a palpable pulse despite recognizable complexes on ECG. It often precedes asystole and is treated in the same way.
Management of asystole/PEA
Adrenaline 10 micrograms (0.1 mL of 1:10 000 solution) per kg is given intravenously or intraosseously, followed by a normal saline flush 2–5 mL. This stimulates the myocardium and increases aortic diastolic pressure. Continue CPR, pausing every 2 min to assess rhythm and circulation. If no response, repeat adrenaline at 10 micrograms/kg every 4 min. If sinus rhythm and circulation returns, continue post-resuscitation care.
Routine use of sodium bicarbonate is not recommended but should be considered in a patient with prolonged cardiac arrest or cardiac arrest associated with severe metabolic acidosis, hyperkalaemia or tricyclic antidepressant overdose. The dose is 1 mL/kg of 8.4% sodium bicarbonate (1 mmol/kg.)
Calcium is only indicated for hypocalcaemia, hyperkalaemia, hypermagnesaemia, or calcium channel blocker overdose.
Ventricular fibrillation and pulseless ventricular tachycardia are uncommon but may occur in cardiac disease, hypothermia or tricyclic antidepressant poisoning. Sudden collapse occurs and rescue depends on defibrillation.
The protocol (see Fig 2.3) is the same for either rhythm:
1 Asynchronous DC shock of 4 J/kg
An automatic external defibrillator (AED) can be used in children over 1 year. Paediatric paddles are required for children 〈10 kg when using a manual defibrillator. Resume CPR.
2 Second DC shock of 4 J/kg
After 2 min of continued CPR, if monitor still shows VF/VT when compressions paused. Immediately resume CPR for further 2 min. Consider and correct reversible causes (4Hs and 4Ts).
3 Adrenaline 10 micrograms/kg IV or IO
And third DC shock of 4 J/kg
After 2 min of continued CPR if rhythm still VF/VT
As CPR proceeds, reversible causes should be considered and treated. These are the 4 ‘H's and 4 ‘T's (see box)
Reversible causes of cardiopulmonary arrest
Hypoxia: the usual cause
Toxic substances: iatrogenic, accidental, deliberate
Hyper/hypokalaemia: in renal failure, DKA
Hypovolaemia: sepsis, anaphylaxis
When to stop resuscitation
Successful outcome from resuscitation is not common. Resuscitation attempts may be discontinued if there is no return of spontaneous circulation after 30 min of cumulative life support. Exceptions are recurring or refractory VF/VT, a primary hypothermic insult,or patients with a history of poisoning. The team leader, not the parents (if present) decides when to stop.
The important principles are:
• Place child in lateral position with mouth dependent to allow free drainage of fluid such as saliva or vomitus
• Position should be stable: support back with pillow
• No pressure on chest that impairs breathing
• Airway accessible and easily observed.
An accident is an ‘unforeseen event’, but although individually unforeseen, many childhood accidents can be both predicted and prevented. The main varieties of accidental injuries include:
• Trauma: falls, transport accidents
• Burns and scalds: exposure to smoke, fire, hot liquids
• Drowning, choking, suffocation
Inflicted (non-accidental) injury is often an important differential diagnosis and is discussed in Chapter 18.
Epidemiology and aetiology
The type and location of childhood accidents relate closely to age and development stage. Babies and toddlers have most accidents at home as this is where they spend their time. Pre-mobile infants may be dropped or fall from elevated surfaces if left unattended. This is a risk from birth as uncoordinated limb movements may be sufficient to cause a fall. Rolling is not a prerequisite. By school age more accidents are occurring on the roads, at play, and at school.
Boys are twice as likely as girls to have accidents. Boys may be more exposed to risks as they may be more active and adventurous and more subject to peer pressure.
Children in lower socio-economic classes are estimated to be up to four times more likely to die in accidents than other children.
Accidental injury is the leading cause of death in children over the age of one year in the developed world. In the UK in 2005, 251 children aged 〈5 died as the result of injury or poisoning.
The number of children attending hospital emergency departments after accidental injury is almost 1 million/year. The breakdown by type of accident is:
• Falls at home: 390 000
• Sporting injuries: 180 000
• Poisoning: 52 000
• Burns and scalds: 37 000
• Playground injuries: 33 000
• Road and traffic accidents: 29 000.
Most minor trauma care lies outside the direct responsibility of the paediatrician. This section deals with the management of pain and the basic management of major multiple trauma.
The recognition and assessment of acute pain in infants and children must be adapted to the age and development stage of the child. Infants, including preterm infants, demonstrate measurable behavioural and physiological responses to pain.
Changes in a child's behaviour such as silent withdrawal, fighting behaviour, appearance, activity level, and vital signs (heart rate, respiratory rate) may indicate the presence of pain. Behavioural tools allow pain assessment in young children, including assessment of facial expression, leg posture, activity, and cry. Self-reporting tools in common use include the Wong and Baker ‘faces’ pain scale used for children 〉3, and the visual analogue ‘pain-ladder’ scale for children〉7:
Analgesia should be given orally if possible, given regularly, and titrated to pain severity.
• Mild: paracetamol, with or without NSAID
• Moderate: add dihydrocodeine
• Severe: add opiate or Entonox.
Hurts little bit
Hurts little more
Hurts even more
Hurts whole lot
The seriously injured child
A structured approach to clinical evaluation and management is based on primary, secondary and tertiary surveys.
This is directed towards identification of life-threatening injuries and implementation of resuscitation according to the ABCDE paradigm (see Section 2.2).
Life-threatening injuries which should be identified and treated in the primary survey include:
• Respiratory system: airway obstruction, tension pneumothorax, open pneumothorax, haemothorax, flail chest
• Cardiovascular system: cardiac tamponade
• CNS: extradural haematoma.
Resuscitation measures include:
• Airway opening manoeuvres and high flow oxygen
• Control of external haemorrhage
• Intravenous access and volume resuscitation
• Nasogastric tube and urinary catheter placement
• Monitoring ECG, blood volume, oxygen saturations
• Investigations: baseline bloods and crossmatch specimens. Imaging: chest XR, lateral C-spine, pelvis.
A detailed physical examination to identify all injuries. ‘Log-rolling’ manoeuvre required to enable survey of the neck, spine, back, and rectum. Any additional investigations (blood tests, imaging, special investigations) are then requested.
Burns and scalds
About 40 000 children 〈15 years are injured in burn or scald accidents in the UK each year, the majority (75%) being 〈5 years. Of these about 1/7 are admitted and 500 have severe burns. 95% of thermal injuries happen at home and half of all severe injuries in the kitchen.
Accidental thermal injuries are most commonly scalds caused by hot drinks, hot tap water, hot oil or fat, and steam or water from kettles. Burns occur after contact with open fires, cookers, irons, fireworks, candles, etc. Young children are vulnerable to sunburn. Most burns are preventable.
Non-accidental burn injuries also occur, although the true incidence is uncertain. Features suggesting a non-accidental injury are discussed in Chapter 18.
Most thermal injuries affect the skin and are defined by the total burn surface areas (TBSA) involved, their anatomical location and their thickness. The thickness is a major determinant of healing and is classified into:
• Superficial: affects epidermis only. Erythematous, painful, heals rapidly.
• Superficial dermal: affects epidermis and upper dermis. Blistering and intense pain.
• Deep dermal: affects epidermis and deep dermis. Mottled, cherry red colour, dry, non-blanching. Painless.
Involves all of epidermis and dermis, and may involve muscle and bone. Pearly white, dry skin with no hair, no sensation and no capillary return. Regenerative elements are destroyed but spontaneous healing can occur in healthy skin at the burn margin with considerable scarring. Excision and grafting is required for all but smallest injuries.
Assess TBSA and depth. For TBSA, remember the ‘rule of nines’ does not apply to children 〈14 years because they have a relatively larger head surface area and smaller surface area of the extremities. Lund and Browder charts are used (Fig 2.4).
Attention should also be directed towards:
• Anatomic location: involvement of face and upper airway may compromise the upper airway due to laryngeal oedema with stridor, hoarseness and dyspnoea.
• Circumferential full thickness chest or limb burns may impair ventilation and perfusion respectively. Escharotomy (an eschar is a deep, cutaneous slough or scab caused by a thermal burn) should be considered to lessen the pull on surrounding tissues.
• Coexistent smoke or carbon monoxide inhalation
• Life-threatening or spinal injuries
• Occult blood loss causing circulatory compromise.
Initial management of all burns includes:
• Remove heat source and apply active cooling for 20 min
• Analgesia: opiates may be necessary
• Dressing: clingfilm is sterile and non-adherent
• Elevate limbs to reduce oedema
• Check tetanus status
Major burns require application of the ABCDE paradigm with the addition of F for fluid.
IV fluid replacement is required for burns involving TBSA 〉 ≥10%, or 5% in infants 〈6 months. The Parkland formula is used to calculate the volume of Hartmann's fluid to be given over 24 h:
Give 50% in the first 8 h and 50% in next 16 h from time of injury.
Maintenance fluid is given in addition as 0.45% NaCl/5% dextrose. The rate should be titrated to maintain urine output at 1.0–1.5 mL/kg per hour although some centres accept 0.5 mL/kg per hour if electrolytes are normal.
Assessment of adequacy of fluid resuscitation can be difficult. Poor capillary refill time, a core–peripheral temperature gap, and metabolic acidosis are indicators of circulatory compromise. Excessive fluids may cause pulmonary oedema and hyponatraemia with cerebral oedema and seizures.
Transfer to a specialist burns facility should be considered in children 〈5 years, full thickness burns 〉5% or if there are complications such as circumferential burns or inhalation injury.
The most important cause of morbidity. Diagnosis can be difficult as fever is not a specific predictor of infection in burned children. Although children with sepsis usually have a fever 〉38° C, 73% of those without infection also have a fever due to the inflammatory response to the burn. The most useful indicators of sepsis are intolerance of enteral feeding and a rise in CRP.
Toxic shock syndrome (TSS)
This can complicate even small, ‘clean’ burns. It is caused by toxic shock toxin-1 (TSST-1) from strains of Staphylococcus. A sudden deterioration occurs with fever (〉39° C), diarrhoea, vomiting, and rash accompanied by circulatory failure. Treatment includes antibiotics and anti-TSST1 antibodies (human immunoglobulin or fresh frozen plasma). Mortality is up to 50%.
Up to 500 000 children attend emergency departments with head injury each year in the UK. A fatal outcome is fortunately rare, about 1/500, but head injuries account for 40% of injury-related deaths in childhood.
Aetiology and pathogenesis
The causes of head injuries vary markedly with age:
• 〈2 years: inflicted, non-accidental injury is the most common cause, accounting for up to 25%. In addition, babies may be accidentally dropped or fall from elevated surfaces such as changing tables.
• 1–4 years: falls
• 5–15 years: road traffic accidents. Pedestrians most commonly, followed by cyclists and car passengers
• 〉15 years: sports injuries, assaults.
There is a peak incidence in summer, in children 〈10 years, and in late afternoon and early evening.
Dynamics of falls
Factors that determine injury severity include:
• Distance fallen and impact surface: most domestic falls are short (〈1.5 m), and very rarely cause death or serious injury. However, a fall of 1 m may be sufficient to cause skull fracture and falls 〉1.5 m can cause serious injury. The impact surface is critical. A soft surface provides slower deceleration and absorbs more kinetic energy, reducing the peak forces acting on the head.
• Whether the fall was ‘broken’: protective reflexes may break the fall, but do not operate in babies or in backwards falls.
• Impact area: focal or diffuse: the fall may be on to a point or edge, or more commonly on to a flat, blunt surface.
• Impact part: the disproportionate large head size in infants and young children makes them fall ‘head first’.
Intracranial pathology or traumatic brain injury (TBI) is classified as primary or secondary and focal or diffuse.
Primary pathology: direct result of trauma
• cerebral contusions and lacerations which may occur under or opposite (contre-coup) the site of impact.
• intracranial bleeding which may be extradural (very uncommon), subdural, or intracerebral.
• Diffuse: shearing forces cause immediate axonal damage.
Secondary pathology: indirect consequence of primary insult
• Focal: ischemia due to intracerebral haematoma
• Diffuse: brain ischaemia due to hypoxia or impaired cerebral perfusion due to raised ICP secondary to brain oedema, hypercapnia, and impaired ‘autoregulation’ or hypotension.
Infection may occur with a compound depressed fracture or basal skull fracture causing meningitis or brain abscess.
History and examination aims to identify the minority of patients at high risk of significant intracranial pathology. Risk features indicating a need for cranial CT include:
• Mechanism consistent with severe injury: high-speed RTA as pedestrian, cyclist, or car occupant; fall from 〉3 m; injury from high-speed projectile or object.
• Witnessed loss of consciousness lasting 〉5 min
• Amnesia, antegrade or retrograde, lasting 〉5 min
• Abnormal drowsiness
• Three or more discrete episodes of vomiting
• Post-traumatic seizure but no history of epilepsy
• Clinical suspicion of inflicted, non-accidental injury.
• Age 〉1 year: GCS 〈14 in emergency department
• Age 〈1 year: GCS 〈 15 in emergency department or tense fontanelle; bruise, swelling or laceration 〉5 cm on head
• Suspicion of open or depressed skull injury
• Signs of basal skull fracture: these include blood or CSF from ear or nose, bilateral periorbital haematomas (panda eyes), Battle's sign (bruising over mastoid, may take 24 h to develop), haemotympanum
• Focal neurological deficit: additional features may include history of drug or alcohol intoxication, history of neurosurgery, presence of a bleeding diathesis such as haemophilia or anticoagulant medication.
A child who has had a minor head injury and has none of the risk factors listed above, is fully conscious and has no adverse medical or social factors, does not require hospital admission. A clear written advice sheet should be provided with criteria for seeking medical advice again.
The child with a severe head injury and GCS ≤8 requires intubation and ventilation with full cervical spine immobilization (cervical spine injury is present in 10% of patients with severe head injury). Cranial CT with scanning of the cervical spine down to C2 should be done within 1 h.
Children with the risk factors listed above should undergo cranial CT combined with a period of observation. Skull radiographs are not generally indicated. Although the presence of a skull fracture increases the likelihood of intracranial pathology fourfold, significant intracranial pathology can exist in the absence of a fracture, especially in injuries inflicted by shaking. If non-accidental injury is diagnosed, early cranial MRI is indicated to assist in clarifying the timing and mechanism of any injury (see Chapter 18).
Consultation with a neurosurgical unit is indicated for:
• Intracranial pathology on cranial CT
• A compound depressed or basal skull fracture
• Coma persisting for 〉4 h or deteriorating level of consciousness
• Progressive focal neurological signs.
Prevention by individual, local, and national policy is of course most important. Children with significant head injury should be followed up by a specialist multidisciplinary team and both the school medical service and primary health care team should be notified.
Drowning describes the process of primary respiratory impairment from immersion in a liquid medium. The final outcome, whether alive or dead, is not part of the definition so the distinction between near-drowning with survival and drowning with a fatal outcome is no longer made.
Accidental drowning is the third most common cause of accidental death in childhood in the UK, after road traffic accidents and burns. In 2005, 26 children 〈15 years were drowned in the UK.
Drowning is more common in children aged 4 years or less (60%) and in boys (male:female ratio 4:1). One third of drownings occur in the summer. The location is age dependent:
• 〈1 year: bathtubs and buckets
• 1–4 years: home settings: garden ponds, pools
• 5–14 years: open water sites: lakes, rivers and seas.
Many drownings are preventable by active adult supervision, safe water environments such as isolation fencing and use of personal flotation devices (PFDs). There is no conclusive evidence that drowning rates are higher for less experienced swimmers. 80% of childhood drowning accidents occur in unsupervised children.
Drowning can happen in as little as 2.5 cm (1 inch) of water and is usually quick and silent. Most children who survive are discovered within 2 min of submersion and most who die are found after 10 min. Submersion of 〉3 min confers a poor outcome.
The sequence of events following submersion is:
• Voluntary breath holding and reflex bradycardia: the diving reflex
• Hypoxia, hypercarbia, and acidosis stimulates compensatory mechanisms with tachycardia and hypertension
• After at most 2–5 min involuntary breathing occurs and inhaled fluid causes laryngeal spasm on touching the glottis which initially protects the lower airway.
• Secondary apnoea gives way to further respiratory efforts with inhalation of water and debris into lower airways.
• Bradycardia, arrhythmia, and cardiac arrest occur.
If this sequence of events can be interrupted and the child survives, additional complications include:
• Respiratory: surfactant depletion, pulmonary oedema, pneumonia
• CVS: arrhythmias, pulmonary hypertension
• Metabolic: hyponatraemia, hypernatraemia
• Hypothermia: is common and classified according to deep body temperature (rectal or oesophageal) into mild (〉34° C), moderate (30–34° C) and severe (〈30° C)
• Spinal injury (diving injury)
• Multiorgan failure from hypoxia/ischaemia.
Primary survey and resuscitation
Cardiac arrest may be due to asystole, PEA, ventricular tachycardia, or ventricular fibrillation (VF). Arrhythmias such as VF are not only more common in hypothermia, but also refractory at temperatures 〈30° C.
Drowning in icy water can provide some protection against the effects of hypoxia on the heart and brain.
External re-warming is sufficient for temperatures 〉32° C, but below this active core re-warming should also be used. Anticipate the need for volume replacement to counter the ‘rewarming shock’ which occurs to peripheral vasodilatation.
• Remove cold, wet clothing
• Apply warm blankets
• Infrared radiant lamp
• Forced air re-warming blanket, e.g. Bair Hugger.
• Warm intravenous fluids to 39° C
• Warm ventilator gases to 42° C
• Gastric or bladder lavage with 0.9% saline at 42° C
• Lavage of peritoneum, pleura or pericardium and extracorporeal blood warming are extreme measures.
Resuscitation should be continued until core temperature is ≥32° C or cannot be raised despite active measures. Careful monitoring of cardiovascular function is vital.
This should include a careful survey for injuries that may have occurred preceding submersion, especially spinal injuries. Investigations to consider include:
• Blood glucose, gases, electrolytes
• Coagulation screen
• CXR, cervical spine imaging
• Blood and sputum cultures.
Fever 〉24 h post drowning suggests systemic infection, e.g. with gram-negative organisms such as Pseudomonas spp., and broad-spectrum antibiotics should be given.
A poor prognosis is conferred by submersion for more than 3–8 min, no gasp after 40 min of full CPR, rectal temperature 〉33°C on arrival, persisting coma, acidosis (pH 〈7.0) or hypoxia (PaO2 〈8.0 kPa).
70% of children survive when early basic life support is provided at the waterside. Of those who survive 25% have mild neurological sequelae and 5% are severely disabled. 75% make a full recovery.
Types of poisoning
Poisoning may be:
• Accidental: common in toddlers, mean age 2.5 years
• deliberate self-harm is most common in adolescents
• fabricated or induced illness (FII) may involve administration of poisons
• drug misuse involving alcohol, solvents or opiates occurs in adolescents
• Iatrogenic: poisoning usually involves dosage errors rather than wrong drug or route.
The poisonous substances include drugs, household chemicals, alcohol, cosmetics, plants, berries, and mushrooms.
Most poisons are ingested and exert their ill effects following enteral absorption, but some caustic agents cause local damage and inhalation of volatile agents can cause direct damage to the respiratory system.
Specific effects reflect the toxic actions of specific poisons and are considered below. However, many poisons act via important final common pathways such as CNS depression and recognizable poison syndromes do exist.
Important systemic effects in poisoning include:
• Central nervous system (CNS): a reduced level of consciousness is the most common problem and impairs respiration by causing airway obstruction and central depression of respiratory drive. Convulsions may also occur.
• Cardiovascular system (CVS): hypotension is common in poisoning with CNS depressants. Hypertension, usually transient, is less frequent but occurs with sympathomimetic drugs. Cardiac conduction defects and arrhythmias may occur especially in poisoning with tricyclic antidepressants.
• Body temperature: hypothermia may develop in prolonged coma, especially after overdose with barbiturates or phenothiazines. Hyperthermia can develop in children taking CNS stimulants or antimuscarinic drugs.
Recognizable poison syndromes include those resulting from altered autonomic nervous system activity (sympathomimetics, parasympathomimetics, anticholinergics), metabolic acidosis, chemical pneumonia, acute cerebellar dysfunction, methaemoglobinaemia, renal failure, and violent emesis.
The constituents of the substance ingested, the timing and the dosage per kg body weight should be identified as accurately as possible. Some idea of the maximum possible amount can be estimated from comparing the number of tablets or volume of liquid remaining with the total described on packaging. Ingestion may have been unobserved and in older children may not be disclosed.
In the UK, the National Poisons Information Service maintains an online database, TOXBASE and telephone advice which is freely available to NHS hospitals (www.toxbase.org)
Management encompasses primary assessment and resuscitation, initial investigations, measures to prevent absorption or enhance excretion, and specific measures if available.
Attention to obstructed airway with airway opening measures and insertion of oropharyngeal or nasopharyngeal airway, administer high-flow oxygen and use bag–valve–mask device for assisted ventilation. Intubation and ventilation should be considered if GCS ≤8, airway protection inadequate, or respiration depressed. Treat hypotension by tilting head down and volume replacement with normal saline.
Baseline investigations and monitoring
• Blood glucose: hypoglycaemia in alcohol poisoning
• U&E: hypokalaemia with β-agonists
• Hyperkalaemia: digoxin
• Blood gases: metabolic acidosis in carbon monoxide poisoning, salicylates
• LFTs, coagulation: hepatotoxicity with paracetamol
• Drug levels: paracetamol, salicylates, iron, digoxin
• Urine: toxicology screen.
Monitoring in addition to standard nursing observations and neuro observations should include ECG and pulse oximetry.
Induction of emesis is not recommended. Gastric lavage is rarely required but may be considered for life-threatening amounts of certain drugs including iron and lithium ingested within the previous hour. It is contraindicated if a corrosive substance or petroleum product has been ingested.
Activated charcoal may be useful in prevention of absorption of poisons toxic in small amounts, e.g. antidepressants. It may be effective up to 1 h after ingestion. Repeated doses may be used as an active elimination technique.
Enhancing excretion: active elimination
This is rarely performed, but may be useful in cases of prolonged, high concentration exposure to dangerous toxins. Methods include:
• Repeated doses of activated charcoal for quinine, theophylline, carbamazepine, phenobarbital
• Whole bowel irrigation for enteric-coated drugs, iron
• Urine alkalinization for salicylates.
Antidotes are available for certain poisons: see Table 2.2. Management of specific poisons is considered in turn.
Table 2.2. Specific poisons and their antidotes
Alcohol intoxication occurs in toddlers and adolescents. The main risks are respiratory depression, vomiting with aspiration, and hypoglycaemia. It is potentially fatal.
Most cases of paracetamol poisoning occur as episodes of self-harm in adolescents. As little as 150 mg/kg of paracetamol taken within a 24 h period may cause severe hepatocellular necrosis. If it is certain that the dose ingested is 〈150 mg/kg, no further action is required. Children seem less sensitive to the hepatotoxic effects.
Initial symptoms of nausea and vomiting settle within 24 h. Persistence beyond 24 h associated with right subcostal pain and tenderness indicates development of hepatic necrosis which is maximal 3–4 days after ingestion.
Administration of activated charcoal should be considered if a toxic dose has been ingested within the previous hour.
Children at risk and requiring treatment are identified by a single measurement of the plasma paracetamol concentration taken not less than 4 h after ingestion. Patients whose concentration is above the ‘normal treatment line’ are treated with acetylcysteine by intravenous infusion (Parvolex), or if acetylcysteine cannot be used, with oral methionine provided it is within 12 h of ingestion.
A lower treatment threshold, 50% of the standard concentration threshold (‘high-risk treatment line’) is used for high risk groups which include malnourished children and those on enzyme-inducing drugs (e.g. carbamazepine, phenobarbital). Patients who have taken a staggered overdose should be treated regardless of initial paracetamol concentration.
All patients require baseline measurements of electrolytes, creatinine (renal necrosis can occur), liver enzymes, and INR.
Normal results at 48 h exclude hepatic damage. ALT levels 〉1000 IU/L indicate significant injury and serial measurements of INR provide an important guide to residual liver function.
Opioids and compound analgesics, antimotility drugs
Opioids cause coma, respiratory depression, and pinpoint pupils. The specific antidote naloxone is indicated if there is coma or depressed respiration. Its effects are immediate but short-lived (2 h) and an IV infusion may be optimal. Opioids such as methadone have a very long duration of action. Opioids are also encountered in antimotility drugs: Co-phenotrope (as Lomotil) is the most common and dangerous. The delayed gastric emptying may delay symptoms of severe opioid poisoning for up to 36 h.
Co-proxamol, a combination of dextropropoxyphene and paracetamol, is dangerous as the former has direct cardiotoxic effects and arrhythmias may occur for up to 12 h.
Salicylate poisoning is now uncommon. Symptoms include tinnitus, deafness, dizziness, pyrexia, nausea, vomiting, and metabolic acidosis. Asymptomatic children who have consumed 〈120 mg/kg of aspirin do not require treatment. Treatment options depending on severity include activated charcoal, urinary alkalinization, and haemodialysis.
This group includes ibuprofen, mefenamic acid, and diclofenac. Toxicity is generally low. Ibuprofen may cause vomiting, epigastric pain, and tinnitus. Activated charcoal is indicated for ≥400 mg/kg taken within the preceding hour.
Antidepressants: tricyclic compounds, monoamine oxidase inhibitors, and selective serotonin re-uptake inhibitors (SSRIs)
Tricyclic compounds cause anticholinergic effects, ataxia, coma and convulsions, hypotension, cardiac conduction defects, and arrhythmias. Activated charcoal should be given and an ECG performed. A prolonged QRS (〉0.1 s) is the best indicator of risk for cardiac toxicity. Intravenous infusion of sodium bicarbonate can treat compromising arrhythmias or prevent them in those with a long QRS duration. The use of antiarrhythmic drugs is best avoided.
SSRI poisoning can cause vomiting, agitation, tremor, and rarely convulsions. Severe poisoning results in the ‘serotonin syndrome’: hyperpyrexia, convulsions, rhabdomyolysis.
Early features of iron poisoning are gastrointestinal and include nausea, vomiting, abdominal pain, and gastrointestinal haemorrhage. Signs of multiorgan failure, with fulminant hepatic failure, develop 12–48 h after ingestion.
Asymptomatic children with a definite history of consuming 〈30 mg/kg of elemental iron require no further treatment. If 〉30 mg/kg may have been ingested an abdominal radiograph is done. If tablets are confined to the stomach repeated gastric lavage or endoscopic removal are options. If large quantities are visible, whole bowel irrigation should be undertaken. Serum iron concentrations are measured 4 h post ingestion (8 h for sustained release preparations). Further treatment depends on levels: if ≥90 micromole/L, intravenous desferrioxamine is given.
Treatment is continued until symptoms have abated and urine discoloration clears. In multiorgan failure higher dose may be required and haemodialysis may be indicated.
Ecstasy (methylenedioxymethamphetamine, MDMA) can cause severe idiosyncratic reactions including coma, convulsions, arrhythmias, hyperthermia, and rhabdomyolysis. Asymptomatic children should receive activated charcoal. Blood levels can confirm exposure.
Respiratory emergencies include upper airway obstruction and respiratory failure caused by airway obstruction, intrinsic lung disease, or inadequate respiratory effort. So-called ‘apparent life threatening events’ (ALTEs) are considered here as disturbed respiration appears to be a common final pathway, although there are many causes.
‘Apparent life threatening events’
An ALTE is defined as an episode that is frightening to an observer and characterized by some combination of:
• Apnoea, central or occasionally obstructive
• Change in muscle tone, usually limpness.
• Choking or gagging, observed or heard.
Despite the alarming term, few episodes fulfilling this definition actually require cardiopulmonary resuscitation. The incidence is 0.6/1000 live births and ALTEs account for almost 1% of emergency visits for infants. The peak age incidence is between 1 week and 2 months and two thirds are 〈10 weeks.
This cluster of symptoms and signs has many causes, but no cause is identified in about half of cases. The three most common identified causes are:
• Gastro-oesophageal reflux disease, GORD: 30%
• Seizures from hypoglycaemia, hypocalcaemia: 11%
• Lower respiratory tract infection: 8% (This includes pertussis, bronchiolitis and pneumonia.)
A number of less common causes exist which should be considered especially if ALTEs are recurrent, severe or in an older infant. These include:
• ENT or airway problems
• Urinary tract infection
• Inborn errors of metabolism
• Cardiac arrhythmia
• Breath-holding attacks
• Fabricated or induced illness (FII).
FII should be considered especially in recurrent ALTEs and may be a feature of fabrication, repeated smothering, or deliberate poisoning.
The history should establish the exact description of the episode and its relationship to feeding. Physical examination is often normal but careful examination for respiratory infection is appropriate. SaO2 should be measured and fundoscopy considered to identify non-accidental head injury.
A single, short, self-correcting episode associated with feeding in a well infant with no abnormal physical findings requires no action other than addressing parental anxiety and arranging follow-up and health visitor input.
A more significant episode or recurrent episodes warrants admission and cardiorespiratory monitoring for 24 h. Investigations are dependent on whether a likely cause is identified clinically but may include:
• Full blood count, C-reactive protein
• Biochemistry: urea and electrolytes, calcium, magnesium, glucose, lactate
• Microbiology: urine microscopy and culture; per-nasal swab for pertussis
• ECG rhythm strip including QTc interval
• EEG, USS brain
• Blood and urine for toxicology and metabolic studies
• Investigation for GORD.
It is important to empathize with the high level of parental anxiety and provide adequate support. Resuscitation training may be considered but home apnoea monitoring is not of proven value. Any association of ALTEs with SUDI is very weak if indeed it exists at all.
Upper airway obstruction
Obstruction to the upper airway is always potentially life threatening. Each year in the UK about 70 children die from suffocation, strangling, or choking (foreign body airway obstruction). A proportion of these episodes are inflicted (non-accidental) and most deaths are out of hospital. See Chapter 3.4 for a discussion of acute stridor.
Important causes of upper airways obstruction (apart from suffocation and strangulation) include:
• Foreign body airway obstruction (FBAO): ‘choking’
• acute epiglottitis
• bacterial tracheitis
• retropharyngeal abscess
• diphtheria (rare in the UK)
• peritonsillar abscess (quinsy)
• Smoke inhalation.
In addition, patients with chronic upper airway obstruction may decompensate acutely, particularly with superadded infection. This may occur with subglottic stenosis, vascular rings, tracheomalacia, Pierre–Robin syndrome, and laryngeal webs.
The length of history provides a guide to aetiology.
Inhaled foreign bodies cause acute symptoms with choking. Angio-oedema develops over minutes and acute epiglottitis over a few hours.
Croup and retropharyngeal abscess have a prodromal history lasting several days although progression may occur over several hours.
Specific signs occur in some disorders. A ‘barking cough’ and hoarse voice reflects the laryngeal inflammation present in croup. Drooling and dysphagia are caused by the painful swelling of epiglottitis or retropharyngeal abscess. Systemic toxicity occurs in bacterial infection: epiglottitis, bacterial tracheitis, retropharyngeal abscess.
Severity of obstruction is evident clinically. Marked stridor, tracheal tug, and prolonged inspiratory phase all indicate severe obstruction. Hypoxia is a late sign.
This depends on cause but is always a matter of urgency. Active treatment is indicated. Investigations are not indicated initially.
Foreign body airway obstruction (FBAO)
Most choking episodes occur in preschool children during play or while eating. If the diagnosis is clear cut the strategy depends on whether an effective cough is present, conscious state, and age of the child (see Fig 2.5).
If the child is coughing effectively, this should be encouraged: a spontaneous cough is more likely to be effective than any external manoeuvre.
If coughing is ineffective, and the child unable to vocalize, or has a silent cough or cyanosis and the child is conscious five back blows should be given, followed if necessary by five chest thrusts in an infant or abdominal thrusts in a child. In an unconscious child, proceed with basic life support after opening the mouth to look for any obvious removable object.
See Chapter 3 for details. Principles include:
• Keep child upright and comfortable; minimize upsetting procedures
• Oxygen to keep SaO2 〉93%
• Steroids in all but mildest cases. Options include:
• oral dexamethasone 0.15 mg/kg to maximum 12 mg
• oral prednisolone 1 mg/kg
• nebulized budesonide 2 mg
• Nebulized adrenaline for significant respiratory distress. Use 1 in 1 000 (1 mg/mL) solution in a dose of 400 micrograms/kg (to maximum 5 mg) repeated after 30 min if necessary.
Symptomatic relief may begin within 10 min and lasts up to 1 h. Intubation and ITU admission is required in 〈2% of hospital admissions.
Respiratory failure is not the same as respiratory distress.
• Respiratory distress describes an increase in the work of breathing as manifested by tachypnoea, nasal flaring, recession, use of accessory muscles, grunting, and if airway obstruction is present stridor (upper airway) or wheeze (lower airway). In respiratory compensation for metabolic acidosis there is tachypnoea but no other signs of respiratory distress and this is an important differential.
• Respiratory failure describes inadequate oxygenation and or ventilation. Although often accompanied by respiratory distress this may be absent if there is respiratory depression due to coma or exhaustion.
Clinical signs of hypoxia include cyanosis, tachycardia, circulatory failure and ultimately bradycardia followed by asystole. A raised arterial PCO2 generates no easily detectable clinical signs but lack of adequate chest movements or obvious exhaustion provides a clue to inadequate ventilation. In children, a mixture of hypoxaemia and hypercapnia usually coexists and is confirmed on blood gas analysis.
The most common context in which respiratory failure occurs in infants and children is primary respiratory disease:
• Acute asthma (severe)
• Croup (severe).
Respiratory depression is less common but may be seen e.g. in poisoning by opiates or Guillain–BarrÈ syndrome.
In addition to specific measures supportive treatment involves:
• Oxygen: supplemental oxygen is prescribed to provide a FiO2 in the range of up to 100%. Oxygen toxicity is not a risk in infants and children. Delivery systems vary with age and include:
• nasal cannulae
• face mask
• head box.
• Continuous positive airways pressure (CPAP)
• Assisted ventilation.
Endotracheal intubation and intermittent positive pressure ventilation should be instituted if progressive respiratory failure is diagnosed.
Invasive bacteraemia triggers a series of inflammatory and immune mediated metabolic and circulatory changes, the clinical manifestations of which are called sepsis or septicaemia. Septic shock is the end point in which tissue perfusion is compromised.
The incidence has been reduced by the introduction of vaccination against causative pathogens: Haemophilus influenza (Hib), Neisseria meningitidis (Men C), and Streptococcus pneumoniae.
Aetiology and pathogenesis
The main pathogens causing septic shock are:
• Gram-negative bacteria: E. coli, Pseudomonas, Meningococcus
• Gram-positive bacteria: Pneumococcus, Haemophilus influenzae, Staphylococcus aureus.
Meningococcal septicaemia remains the most common infectious cause of death in childhood in developed countries (see Chapter 15.14).
Invasion of the blood stream
The mechanisms by which organisms which reside in the nasopharynx in a harmless fashion invade the circulation remain uncertain but are assumed to reflect both factors in the pathogen and host susceptibility.
Transient bacteraemia which is rapidly cleared is not uncommon in febrile children. Continued replication and septicaemia occurs in a minority and may reflect factors in the host immune response.
Bacterial toxins activate a series of inflammatory cascades, the systemic inflammatory response syndrome. Endotoxin, a cell wall constituent of gram-negative bacteria, causes release of mediators such as tumour necrosis factor alpha and interleukin-1. These responses cause shock by a variety of mechanisms which are initially ‘distributive’ (‘warm’ shock) and progress to a combination of hypovolaemic and cardiogenic shock. These include:
• Vasodilatation: high cardiac output state
• Capillary leak: increased microvascular permeability is associated with massive fluid loss from the circulation and hypovolaemia due to ‘redistribution’
• Tissue hypoxia: metabolic acidosis due to raised plasma lactate levels
• Myocardial depression: a combination of hypoxia, acidosis and other mechanisms depresses myocardial function and impairs cardiac output
• Cellular metabolism: progressive deterioration in cellular oxygen consumption heralds multiple organ failure and irreversible shock
• Disseminated intravascular coagulation (DIC).
Early recognition of the ‘septic’ infant or child remains a major challenge especially because of the potentially fulminant course.
A high fever causes tachycardia and peripheral vasoconstriction which is difficult to distinguish from early compensated shock. In meningococcal septicaemia signs of an associated meningitis (if present) may assist diagnosis and a non-blanching petechial or purpuric rash is a well known and subtle early sign. However, in 30% of cases the rash is blanching and maculopapular.
Signs of early ‘compensated’ shock are listed in the algorithm.
The differential diagnosis in the infant with unequivocal signs of ‘shock’ includes
• Cardiac disease: supraventricular tachycardia, congenital heart disease, cardiomyopathy, myocarditis
• Inborn errors of metabolism
• Gastrointestinal obstruction: intussusception, volvulus
• Inflicted injury, non-accidental head injury
• Toxic shock syndrome and HUS.
Investigations: the septic screen
• Full blood count and differential, C-reactive protein
• Urea and electrolytes, glucose, Ca, phosphate, LFTs
• Coagulation screen, blood gases
• Microbiology: blood cultures, urine cultures, etc.
• Lumbar puncture: this is unnecessary and even contraindicated in septic shock or if there are signs of raised intracranial pressure.
A CRP of 〈0.5 mg/dL renders sepsis less likely and either leucopaenia or leucocytosis render invasive bacterial disease more likely.
The management of meningococcal septicaemia is set out in the algorithm in Fig 2.6.
An intravenous broad-spectrum antibiotic, e.g. cefotaxime, is indicated for suspected invasive bacterial disease. A ‘wait and see’ policy is often inadvisable, but it is reasonable to await investigation results in a well child with concern generated by a localized petechial rash.
Initial management of septicaemic shock includes:
• Oxygen by face mask
• Insertion of two large cannulae (IV or intraosseous)
• Antibiotics: IV cefotaxime
• Fluids: bolus of colloid (4.5% human serum albumin) at 20 mL/kg. Repeat if necessary.
Further management depends on clinical response as judged by cardiovascular and respiratory parameters and the presence or absence of raised intracranial pressure.
A total of 60 mL/kg (or more) of colloid should be administered if signs of shock persist. It is increasingly recognized that a massive capillary leak may exist with a corresponding high requirement for fluid volume replacement.
Inotropic support is indicated if poor perfusion persists despite fluid replacement. Dopamine (up to 10 micrograms/kg per minute) is first line. Dobutamine may be added but should not be used alone.
If severe metabolic acidosis (pH 〈7.15) persists despite adequate fluid replacement, sodium bicarbonate may be necessary. Hypoglycaemia, hypocalcaemia, hypokalaemia, hypomagnesaemia should be sought and corrected.
Elective intubation and ventilation is indicated if shock persists following adequate fluid replacement or requires 〉60 mL/kg of fluid.
Clinical features of meningitis may or may not coexist with signs of raised intracranial pressure (ICP). This is managed as shown in Fig 2.6).
The terms anaphylaxis or anaphylactic reaction are best reserved for a severe multisystem allergic reaction caused by interaction of a soluble antigen with IgE bound to mast cells and basophils leading to degranulation and release of histamine and other substances, a type I allergic reaction.
Anaphylactoid reactions are clinically indistinguishable from anaphylaxis but are mediated by a drug or substance acting on mast cells directly and not via sensitized IgE antibodies.
No reliable epidemiological data on incidence are available because of difficulty in the exact definition of anaphylactic reactions. However, fatal allergic reactions to food account for about 1 death in children 〈16 years each year in the UK.
Aetiology and pathogenesis
The antigen interacts with specific IgE molecules fixed to mast cells and basophils leading to influx of calcium and degranulation with release of preformed (histamines and tryptase) and newly generated (thromboxane, leukotrienes and platelet activating factor) mediators. These induce reactions in several systems:
• Respiratory: bronchospasm, mucosal oedema, upper airway obstruction from oedema of glottis and tongue (angio-edema)
• Cardiovascular: vasodilatation and increased capillary permeability
• Gastrointestinal: abdominal pain, vomiting
• Skin: flushing, erythema, urticaria.
The leading causes of anaphylaxis in childhood differ from those in adults:
• Foods: account for 〉95% of cases and 41% of hospital admissions. Peanuts, tree nuts and seeds, milk, eggs, fish, shellfish, soya, and wheat account for 90% of food-induced cases.
• Drugs: B-lactamase antibiotics (e.g. penicillin), vaccines (e.g. MMR)
• Insect venom: Hymenoptera (bee and wasp) stings are a rare cause. Children with venom allergy have a high rate of spontaneous improvement.
• Latex: a rare cause in childhood and usually in children requiring frequent surgical procedures or indwelling catheters. Cross-reaction to banana, melon, and avocado occurs.
Rare causes of anaphylaxis include exercise (sometimes food dependent) and physical pressure on the skin or cold such as after swimming in cold water.
Activation of mast cells and basophils by IgE-independent mechanisms cause ‘anaphylactoid’ reactions with an identical clinical picture. Mechanisms include inhibition of prostaglandin synthetase by NSAIDs, complement activation producing C3a and C5a by pooled immunoglobulin in IgA deficient patients, and direct activation by opiates or hyperosmolar compounds such as radiocontrast media and mannitol.
There may be a history of atopy, food allergy, or previous severe reactions. Episodes range from minor to life threatening. Onset may be within seconds of exposure or delayed by 15–30 min or even 1 h. A biphasic response may occur 4–12 h later.
Symptoms and signs usually evolve, affecting the skin, respiratory and cardiovascular system in succession.
• Skin: itching with flushing of skin and an urticarial rash (hives)
• Angio-oedema: swelling of mouth, lips, face and upper respiratory tract (laryngeal oedema) causing stridor, hoarseness and drooling.
• Bronchospasm and oedema: cough, wheeze, dyspnoea and cyanosis
• Cardiovascular collapse: faintness and dizziness followed by syncope with pallor, tachycardia and hypotension i.e. shock.
Diagnosis is clinical and is usually not in doubt. It is rare for children to present with syncope, in which case an arrhythmia should be excluded. It may be mistaken for severe acute asthma and panic attacks can cause confusion, especially in victims of previous anaphylaxis.
Prevention of further attacks by allergen avoidance is the cornerstone of treatment. Referral should be made to a specialist allergy clinic where the allergen can be identified by skin prick tests, serum testing, or oral challenge if necessary. Advice is given on allergen avoidance and injectable adrenaline (Epipen, Anapen) provided with training.
Treatment of acute severe anaphylaxis
See algorithm in Fig 2.7.
Timely administration of IM adrenaline is life saving but complete management includes:
• Stop administration of causal agent
• Maintain airway and administer 100% oxygen
• Lie flat with leg elevation if hypotensive (unless respiratory distress increased)
• IM adrenaline 1:1000 solution:
• child 〈6 years 150 micrograms IM (0.15 mL)
• child 6–12 years 300 micrograms IM (0.3 mL)
• 〉12 years 500 micrograms IM (0.5 mL)
• Repeat in 5 min if no improvement.
Additional measures may include:
• IV hydrocortisone: for all severe or recurrent reactions and patients with severe asthma
• Nebulized salbutamol: for severe bronchospasm or anaphylaxis in an asthmatic
• IV or IM antihistamine (chlorpheniramine): may be helpful and unlikely to be harmful, but IV injection must be slow
Adrenaline causes α-receptor effects (vasoconstriction) and β-receptor effects (bronchodilation, enhanced myocardial contraction, suppression of histamine release). It should be given IM to all patients with clinical signs of shock, airway swelling, or breathing difficulty. Intravenous adrenaline is hazardous and used only in profound, life-threatening shock by experienced personnel. Hydrocortisone appears to be of particular importance for asthmatics and must be given if they have been treated previously with corticosteroids.
Recurrence may occur for up to 24 h and observation for this period is indicated in asthmatics, episodes in which continued allergen exposure is possible, or patients with a previous history of biphasic reactions.
A blood sample (clotted) should be taken up to 1 h after onset for mast cells tryptase measurement and serum specific IgE levels to suspected allergens.
Diabetic ketoacidosis (DKA) is a clinical state caused by absolute or relative deficiency of insulin and characterized by dehydration and metabolic acidosis.
Biochemical criteria for diagnosis of DKA include hyperglycaemia, blood glucose 〉11 mmol/L and metabolic acidosis, pH 〈7.3, HCO3− 〈15 mmol/L with associated glycosuria and ketonuria.
The exact incidence of DKA is uncertain. Hospitalization rates for DKA in established and new cases with type 1 diabetes mellitus (T1DM) are stable at about 10 per 100 000 children. DKA at onset of T1DM is more common in younger children 〈4 years. The risk of DKA in established T1DM is up to 10% per patient per year. The mortality rate is about 1/300 with cerebral oedema accounting for the majority of deaths.
Aetiology and pathogenesis
DKA is the end stage of a period of absolute or relative insulin deficiency and is more common in T1DM, occurring both at onset and in established T1DM.
DKA at onset is more common in younger children, those without a first degree relative with T1DM and those from families of lower socio-economic status.
DKA in established T1DM is usually due to inadequate insulin therapy during intercurrent illness, treatment error, or insulin omission. Risk is increased in children with poor control or previous episodes of DKA, adolescent girls, children with psychiatric disorders including eating disorders, and those with difficult family circumstances.
Insulin deficiency leads to hyperglycaemia which causes an osmotic diuresis with excessive loss of free water and electrolytes. This is compensated by increased oral intake until vomiting occurs, at which point severe dehydration rapidly develops with hypovolaemia and poor tissue perfusion.
Glucagon stimulates lipolysis with formation of keto-acids and poor tissue perfusion leads to lactic acidosis. At presentation a patient with severe DKA has:
• Dehydration: 5–10% body weight loss
• Depletion of whole body sodium and potassium.
Measured plasma Na+ and K+ concentrations are determined by a variety of factors:
• Na+: hyponatraemia is common because of a dilutional effect as free water shifts extracellularly. In addition hyperlipidaemia, if present, causes an artefactual reduction.
• K+: serum potassium may be high, normal, or low, depending on renal function and the degree of metabolic acidosis. Acidosis and reduced renal function tends to cause hyperkalaemia.
• Metabolic acidosis: due to a combination of keto-acid formation from lipolysis and lactic acidosis due to poor tissue perfusion.
In DKA complicating onset of T1DM the classical history is several weeks of polyuria, polydipsia, malaise, and weight loss. Vomiting often heralds the onset of DKA and abdominal pain is a common symptom. Classical symptoms are often absent in toddlers in whom the diagnosis is easy to miss, especially if tachypnoea is misinterpreted as respiratory pathology. In a known diabetic, intercurrent infection or poor adherence are common precipitants.
The physical findings depend on whether DKA is mild, moderate or severe. In mild DKA there is hyperglycaemia and ketosis (pH 〉7.30) without vomiting or significant dehydration. Most cases, however, are moderate or severe and clinical examination reveals:
• Dehydration: 5–10% dehydration is manifested by dry mucous membranes, sunken eyes and signs of hypovolaemia: tachycardia, increased capillary refill time, poor perfusion. Hypotension indicates decompensated shock.
• Metabolic acidosis: tachypnoea (Kussmaul breathing) occurs as respiratory compensation develops for the metabolic acidosis. Odour of ketones may be detectable on the breath (like pear-drop sweets).
• Altered mental status: level of consciousness may be reduced but coma is extremely unusual.
Always consult with a more senior doctor on call if you suspect DKA even if you feel confident of your management. Children can die from DKA. The clinical diagnosis is confirmed by demonstrating biochemical criteria for DKA:
• Hyperglycaemia: blood glucose 〉11 mmol/L
• Acidaemia: pH 〈7.3, bicarbonate 〈15 mmol/L
Children who are clinically well, 〈5% dehydrated, and tolerating oral fluids can be managed with oral rehydration and subcutaneous soluble insulin. Those with severe DKA or at increased risk of cerebral oedema should be considered immediately for treatment in a paediatric ICU.
Management of moderate (pH 〈7.2, HCO–3 〈10 mmol/L) to severe (pH 〈7.1, HCO–3 〈5 mmol/L) DKA is as follows.
• If decreased conscious state, or recurrent vomiting an oral airway and nasogastric tube should be inserted. Aspirate nasogastric tube and leave on free drainage.
• Give 100% O2 by face mask
• Insert IV cannula.
Take blood samples for glucose, U&E, PCV, FBC, and arterial, capillary, or venous sample for blood gases. If shocked with poor capillary return and tachycardia and/or hypotension give 10 mL/kg 0.9% normal saline as a bolus and repeat as necessary to a maximum of 30 mL/kg.
Once circulating blood volume has been restored using up to 30 mL/kg of 0.9% saline calculate fluid requirement as deficit plus maintenance and give the total volume evenly over 48 h.
20 kg 6 year old 10% dehydrated given 20 mL/kg 0.9% saline
20 kg boy aged 6 years
This boy requires a total of 4000 mL over 48 h (see Table 2.3).
Excessive urinary losses are not included in calculations.
Table 2.3 Fluid maintenance requirements
mL/kg per 24 h
Type of fluid
Initially use 0.9% saline. Add KCl at 40 mmol/L to rehydration fluid after initial volume repletion unless anuria is suspected (failure to micturate is not the same as anuria). Plasma levels of K+ will fall once insulin therapy is commenced. Add dextrose to fluid when blood glucose has fallen to 14–17 mmol/L. In first 6 h this may be 0.9% saline/5% dextrose. After first 6 h, if plasma sodium stable, use 0.45% saline/5% dextrose. Administration of bicarbonate or phosphate is rarely indicated.
Soluble insulin is given at a rate of 0.1 u/kg per hour.
Make up a solution of 1 u/mL by adding 50 u insulin to 50 mL 0.9% saline in a syringe pump.
Try to maintain insulin at this rate and keep glucose levels in range of 4–12 mmol/L by increasing the dextrose concentration in fluids up to 10%, until the pH is 〉7.3.
Once pH is 〉7.3 and dextrose-containing fluid has been started, consider reducing insulin infusion rate to 0.05–0.1 u/kg per hour.
Monitoring and investigations
This should include
• Hourly BP, HR, and respiratory rate
• Neuro observations
• ECG: monitor T waves for hyper or hypokalaemia
• Initial weight and twice daily thereafter
• Fluid balance: hourly input/output
• Hourly blood glucose (capillary) measurement
• Electrolytes and blood gases: 2 h after onset of IV therapy then 4 hourly, or more frequent if unstable.
Principles of DKA management
Fluid and electrolytes
All patients with moderate to severe DKA have a significant whole-body deficit of Na+ and K+ and dehydration with some hypovolaemia. Rapid volume expansion to restore circulation is the most important initial step, usually requiring 10–20 mL/kg of 0.9% saline. Subsequent fluid management aims to restore the deficit slowly over 48 h.
Even severe acidosis will respond to insulin and fluid replacement, as keto-acids are metabolized and tissue perfusion is improved.
Insulin and dextrose
An infusion rate of 0.1 u/kg per hour equates to 2.4 u/kg per day, which is about twice the usual requirement in established T1DM (1.0 u/kg per day). It is essential to include dextrose in the IV fluids when blood glucose is in the range 14–17 mmol/L or if blood glucose levels fall faster than 5 mmol/L per hour. While acidosis persists it is better to increase dextrose administration than reduce insulin infusion rates.
It is vital to carefully monitor all therapy. Do not write fluid and insulin prescriptions and walk away, as delays or mistakes in administration can occur and be life threatening.
Complications of DKA
The most important is cerebral oedema, but hypokalaemia, aspiration pneumonia, and hypoglycaemia may also occur.
Cerebral oedema in DKA
Cerebral oedema is rare, occurring in 〈1% of cases of DKA, but the mortality rate is ∼25% and it accounts for ∼75% of all deaths. Risk factors include young age, newly diagnosed T1DM, and longer duration of symptoms, all of which correlate with greater likelihood of severe DKA.
The causes are complex and multifactorial but probably relate to osmotic disequilibrium between plasma and brain extracellular fluid. The brain has equilibrated with hyperosmolar plasma and as plasma osmolarity falls water shifts into the brain. Epidemiological associations exist with severity of acidosis, greater hypocapnia, and high urea levels but not with the degree of hyperglycaemia.
Onset is typically 4–12 h after initiation of treatment but cerebral oedema may occur at any time. Symptoms and signs variable but may include:
• Headache, restlessness, irritability, reduced level of consciousness
• Bradycardia and rising BP
• Focal neurological signs: altered pupillary responses, cranial palsies
• Abnormal posturing.
If cerebral oedema is suspected inform senior staff and arrange intensive care transfer. Immediate measures while awaiting transfer:
• Exclude hypoglycaemia as cause of CNS signs
• Reduce IV fluids to two-thirds maintenance and replace deficit over 72 h rather than 48 h
• Give IV 2.5–5 mL/kg of mannitol 20% over 15 min. Repeat after 2 h if no response
• Nurse in head-up position
• When stable arrange cranial CT to exclude other causes of raised ICP (thrombosis, haemorrhage)
• Neurointensive care may be necessary including intubation and ventilation to control arterial PCO2.
Convulsive status epilepticus (CSE)
Generalized convulsive (tonic-clonic) status epilepticus (CSE) is defined as a generalized convulsion lasting 30 min or more, or repeated convulsions occurring over a 30 min period without recovery of consciousness. However, the management approach is the same for any child with a tonic-clonic seizure lasting 〉5 min.
The outcome is mainly determined by the cause. Neurological sequelae are age dependent: 29% in those under a year but only 6% in those 〉3 years. Overall mortality is 4%.
Aetiology and pathogenesis
The most common cause of a generalized tonic-clonic seizure lasting 〉5 min is a febrile seizure. Other less common causes include:
• Intracranial infection: encephalitis or meningitis
• Metabolic disorders: e.g. hypoglycaemia
• Traumatic brain injury: accidental or non-accidental.
A generalized seizure causes an increase in brain metabolic rate and oxygen and glucose requirement which is met by compensatory mechanisms which are effective for at least 30 min unless there is hypoglycaemia or the seizure compromises ventilation.
Beyond 30 min decompensation occurs and additional comp-lications may arise such as hypoxia and aspiration, cardiac arrhythmias, hypotension, and reduced cardiac output.
Primary assessment and resuscitation (see below) obviously precedes history taking and examination which are an important component of the secondary assessment.
Important points in history are:
• Duration and nature of any current seizure activity
• Treatment given pre-hospital
• Prior history of seizures including medication
• Recent intercurrent illness
• Recent head injury or toxic exposure
• Conditions associated with hypoglycaemia: T1DM, congenital adrenal hyperplasia, ethanol ingestion.
Physical examination should be directed towards identifying:
• Fever: fever suggests a febrile seizure, intercurrent illness, or intracranial infection
• Intracranial infection: signs of meningitis or encephalitis
• Intracranial pressure: bulging fontanelle in an infant, bradycardia and hypertension.
• Traumatic brain injury: soft tissue swelling of scalp, retinal haemorrhages
• Neurocutaneous syndromes: depigmented macules of tuberous sclerosis complex (TSC)
• Focal or asymmetrical neurological signs.
Protocols for management of CSE differ only in detail.
Primary assessment and resuscitation follows the standard ABC routine:
• Airway: ensure airway is patent. Put child in recovery position.
• assess respiratory rate, O2 saturation
• give high flow oxygen via a non-rebreathe face mask; support hypoventilation with oxygen via a bag–valve–mask device and consider intubation.
• assess heart rate, blood pressure, capillary refill time
• establish intravenous or intraosseous access
• blood tests: capillary glucose testing, FBC, urea and electrolytes, calcium, magnesium, blood gases, blood cultures.
• Treat hypoglycaemia with 5 mL/kg of 10% dextrose IV.
Seizures are treated in a series of steps as shown in Fig 2.8.
Step 1: benzodiazepines: lorazepam 0.1 mg/kg IV or IO or, if no vascular access, diazepam 0.5 mg/kg PR or, midazolam by buccal or intranasal route.
Step 2: if the convulsion has not stopped after 10 min a second dose of lorazepam 0.1 mg/kg IV/IO is given or, if there is still no vascular access, paraldehyde 0.4 mL/kg PR
Step 3: if convulsions still persist after a further 10 min a longer acting antiepilepsy drug is indicated. Phenytoin 18mg/kg IV or IO is given over 20 min. If child already on phenytoin, use phenobarbital 20 mg/kg IV or IO over 10 min.
Step 4: if 20 min after step 3 has commenced the child remains in CSE, then rapid sequence of anaesthesia is performed with thiopentone 4 mg/kg IV or IO.
Decreased conscious level is defined as a modified Glasgow Coma Score (GCS) 〈15, or being responsive only to voice or pain or being unresponsive on the AVPU scale. Coma is a state of profoundly reduced conscious level.
Specific causes other than sepsis or shock include:
• Traumatic brain injury: accidental and non-accidental
• Intracranial infection: meningitis, tuberculous meningitis, brain abscess, herpes simplex encephalitis
• Seizures: ictal or post-ictal states
• Metabolic disorders: hypoglycaemia, hyperammonaemia
• Poisoning: opiates, barbiturates, tricyclic antidepressants
• Raised intracranial pressure: hypertension.
Important points in history include:
• Prodromal illness: headache, vomiting, fever, or seizures
• Speed of onset, head trauma: remember that inflicted trauma such as shaking will not usually be disclosed.
• Ingestion of medications: accidental or deliberate,
• Family history of metabolic disorders, previous history of epilepsy, diabetes mellitus.
Primary assessment is focused on Airway, Breathing, and Circulation but secondary assessment should focus on clues to aetiology.
• General examination: fever (absence makes intracranial infection unlikely), trauma: bruising or scalp swellings
• Neurological examination: level of consciousness: GCS or AVPU score’, signs of meningism or raised intracranial pressure, fundi (papilloedema or retinal haemorrhages), focal neurological signs, or abnormal posturing.
Glasgow Coma Scale
Best Eye Response (4)
Best Verbal Response (5)
Best Motor Response (6)
Initial management follows the ABC paradigm for the sick child. A capillary blood glucose should be checked immediately as hypoglycaemia is an important remedial cause of altered consciousness.
• glucose, gases, urea and electrolytes
• LFTs, plasma ammonia, plasma lactate
• full blood count, coagulation screen
• blood culture
• Plasma/serum/urine: save for later analysis
• Plasma/urine for toxicology, organic, and amino acids.
Consideration is given to:
A cranial CT should be considered when the patient is stable if the working diagnosis is raised intracranial pressure, intracranial abscess, traumatic brain injury, or the cause of altered consciousness remains uncertain.
Lumbar puncture (LP)
An LP should be performed, if no contraindications exist, if the working diagnosis is intracranial infection (meningitis, encephalitis) or the cause remains uncertain. CSF should be analysed by gram staining and microscopy, culture, protein, glucose, PCR for HHV1 and other viruses.
Contraindications to performing an LP include:
• Clinical evidence of systemic meningocococcal disease, e.g. shock
• GCS ≤8 or deteriorating
• Pupillary abnormalities
• Focal neurological signs, abnormal posturing
• Signs of raised intracranial pressure
• Bleeding diathesis.
A normal cranial CT does not exclude acute raised intracranial pressure. The decision to perform an LP in a child with reduced conscious level should be made by an experienced paediatrician who has examined the child.
If the cause remains obscure, after reviewing initial core investigations, further helpful investigations might include:
• EEG: detects non-convulsive status epilepticus
• Acyl-carnitine profile (on Guthrie card)
• ESR and autoimmune screen (cerebral vasculitis).
Further management depends of course on whether a cause for which specific treatment exists has been identified. If no obvious cause can be identified, consideration is given to starting antibiotics and intravenous aciclovir.
A child in convulsive status
A 3 year old child is brought into the hospital emergency department by ambulance. The child has been convulsing for almost 15 min.
What is your initial management?
Management should follow the Airway, Breathing, Circulation sequence. The child is placed in the recovery position and oxygen should be given by face mask. Blood glucose should be checked as hypoglycaemia is an easily treatable cause of seizures and will cause brain damage if unrecognized and untreated.
Diazepam may be given rectally 0.5 mg/kg, or buccal midazolam at the same dose if vascular access is not obtained. If vascular access is obtained, lorazepam should be given intravenously at 0.1 mg/kg.
The blood glucose was normal. A dose of lorazepam was given, but the seizures continued. After 10 min, a further dose was given, to no avail.
What is your subsequent management?
The child should be loaded with phenytoin, followed by a phenytoin infusion, with blood pressure and ECG monitoring. If seizures are not controlled, the next step is rapid sequence induction with thiopentone, followed by mechanical ventilation.
What secondary assessment and investigations might be appropriate?
Secondary assessment is focused on identifying a cause. Enquiry should be made about any history of previous seizures, recent intercurrent illness, or head trauma.
General examination should assess whether the child is febrile or has any evidence of head trauma. The child should be inspected for features suggesting known epilepsy (Medicalert bracelet, helmet). Features of a neurocutaneous syndrome should also be sought.
Neurological examination for evidence of meningism, raised intracranial pressure, focal neurological signs. Blood tests should be sent to investigate for sepsis, electrolyte abnormalities and toxicology.
The child was apyrexial with no circulatory or respiratory compromise. There were no signs of meningism or focal neurological signs. Several small hypopigmented lesions were seen on his limbs (Fig 2.9).
Sudden unexpected death in an infant
A 3 month old baby boy is brought by ambulance to the hospital emergency department having been found in his cot blue and not breathing. Parents tried mouth-to-mouth resuscitation when they found him, while waiting for the ambulance to arrive. After 30 min there has been no response and resuscitation is discontinued.
When and what samples do you collect?
This is a sudden unexplained death in infancy (SUDI) and the Department of Health guidelines in Working Together 2006 need to be followed:
• A full physical examination must be carried out, with documentation of all lesions and abnormalities, including any iatrogenic lines and tubes.
• If possible take specimens before child declared dead; if not, obtain the permission of the coroner.
• Blood samples can be taken from a venous or arterial site. A larger gauge needle may be necessary. The femoral vein can be used for sampling blood. Cardiac puncture should be avoided if possible as this may damage intrathoracic structures.
• Record the site from which all samples were taken and document all samples.
• Retain infant's clothes and nappy in labelled bags.
Toxicology, culture, chromosomes, metabolic screen
Viral/bacterial cultures, immunofluorescence
Swab lesions; throat swab
Culture and sensitivity
Urine (if available from SPA)
Toxicology, organic/amino acids
Whom do you inform?
Coroner (post-mortem), police child abuse investigation team, social work team, GP, health visitor, designated doctor for SUDI, and consultant in charge must all be informed.
What happens to the parents?
Good practice is that within 24 h, they will have a joint police/paediatric home visit, preferably and if possible with the consultant paediatrician. Support, advice and information for parents may include details of the Foundation for the Study of Infant Deaths (FSID, www.sids.org.uk/fsid), Child Death Helpline and Cruse: Bereavement Support and Advice.
The consultant should arrange to meet with the parents a few days after the post-mortem has been performed to provide preliminary results and meet the parents again 2 months later to provide his/her views on the cause of death.
Subsequent infants of these parents may be placed on the Care of the Next Infant Scheme (CONI) for parental support (see also Chapter 18.13).