Paediatric injuries	Preventative strategies
MVA – occupant	Child car seat
	Seatbelt restraints
	Car design
	Airbags
MVA – pedestrian	Safety programmes in schools
Bicycle	Helmet
Bicycle	Separate sidewalks
Playground	Equipment structural design
Playground	Soft surfaces
Drowning	Surround pool fencing
Burns	Smoke detectors
	Water tap regulators
	Flammable fabric legislation
Poisoning	Preventative packaging
Violence	Hand gun legislation
Violence	Crisis resolution counselling

HEAD INJURY

Significant head injury occurs in 75% of children admitted with blunt trauma,⁵ and 70% of these result in death. Causes of injury are determined by behaviour patterns, which change with age and are commonly due to falls and assaults in infants, and motor vehicle accidents (including bicycle-related injuries) in older children.

ASSESSMENT

The Glasgow Coma Scale (GCS) requires different interpretation in children, because scores tend to be more subjective and prone to misinterpretation. When using the original GCS described for adults, children under 5 years are unable to score normally for verbal and motor responses. Normal aggregate scores for age are:

• 9 at 6 months

• 11 at 12 months

• 13–14 at 5 years.

This has led to attempts to modify the scale by either changing the scoring assessment signs, or by reducing the total score (i.e. eliminating some response categories).⁶ The latter does not allow for comparison of outcome data.

An example of a commonly used scale modified for infants is shown in Table 103.2. However, difficulties remain as regards the accuracy and reproducibility of GCS for infants. Clinical assessment must prioritise the signs and symptoms of cerebral oedema or raised intracranial pressure (ICP) (Table 103.3).

Table 103.2 Glasgow Coma Scale modified for infants

Table 103.3 Signs of raised intracranial pressure

MANAGEMENT

The aims of therapy are to minimise secondary effects on the primary brain injury by maintaining adequate cerebral blood flow and oxygen supply, and preventing secondary ischaemic injury and herniation from raised ICP.

• Deterioration in level of consciousness and the appearance of signs of herniation must be rapidly recognised.

• Airway, oxygenation and respiration should be optimised and intubation performed when the airway is compromised.

• Controlled ventilation with muscle relaxation and sedation should be instituted in the presence of hypoventilation, seizures and signs of raised ICP (see Table 103.3).

• Hypotension significantly increases mortality in children and the systemic circulation must be maintained.

• Management of blood pressure is difficult because the exact ranges of cerebral autoregulation are unknown in children.⁷ Hypotension is most likely from blood loss (especially from scalp lacerations) and not brain injury. Fluid management needs to balance the need for volume resuscitation with the attempt to avoid hypovolaemia.

• Hypotonic and glucose-containing solutions should be avoided because of the association with poor outcomes.⁸

• Studies on the effectiveness of induced hypothermia in paediatric trauma are ongoing.

• Hyperthermia should be avoided with a servo-controlled cooling blanket and adjustment of humidifier temperature because each 1°C temperature rise increases cerebral metabolic rate by 5%.⁹

• Cerebral venous return should be optimised by neutral head positioning. Cerebral perfusion pressure may be best with the bed flat.¹⁰

• Treatment of seizures with phenytoin (20 mg/kg i.v.) provides less central nervous system depression than barbiturates or benzodiazepines. Monitoring for seizures to guard against resulting increases in cerebral blood flow and oxygen consumption is difficult in the paralysed patient. Systems for continuous electroencephalogram monitoring are complex to interpret at the bedside and provide limited information. Post-traumatic seizures are more common under 2 years of age,¹¹ but their long-term incidence is not reduced by acute prophylaxis.¹²

• Continuous measurement of jugular venous oxygen saturation (SjO₂) via fibreoptic reflection oximetry can identify global cerebral hypoperfusion and ischaemia.¹³ However, its use in children is subject to technical difficulties, mainly related to catheter position. Its use is not clinically routine in paediatrics.

DIAGNOSTIC INVESTIGATIONS

Supportive investigations can be performed while emergency assessment and therapy proceed. These include pH and acid–base, serum glucose, osmolality, electrolytes, calcium, magnesium and phosphate, complete blood profile and blood crossmatch.

X-rays of skull and cervical spine (anteroposterior, lateral and C1–C2 views), chest and pelvis are needed. Ultrasound of the skull, where the fontanelle is open, measures ventricular size, and can detect intracranial haemorrhage. It is useful for repeated assessment in the unstable patient.

A cranial computed tomography (CT) scan in stable patients excludes surgically treatable lesions, assesses the size of cerebrospinal fluid (CSF) spaces, including the basal cisterns, detects herniation and shift, and shows the presence of hyperaemia, oedema, intracerebral haematomas, contusions and fractures. A normal CT scan does not exclude raised ICP. Intracranial blood collections are less common than in adults.⁵ The following are poor prognostic signs:

• subdural haemorrhage (as an indication of severe trauma and damage to underlying brain tissue)

• ablated basal cisterns and midline shift

• lack of or reversal of grey/white differentiation

CEREBRAL PERFUSION PRESSURE

Maintenance of cerebral perfusion pressure (CPP) in children is important and has significant implications, but the minimal required CPP in children has not been determined. CPP depends on the difference between mean systemic blood pressure and ICP and these values vary with age. In particular, blood pressure assumes great importance in the younger age group, where physiological systolic pressures are lower:

• 85 mmHg (11.3 kPa) at 6 months

• 95 mmHg (12.6 kPa) at 2 years

• 100 mmHg (13.3 kPa) at 7 years ¹⁴

Normal ICP is also lower,¹⁵ being normally less than 5 mmHg (0.67 kPa) at 2 years and less than 10 mmHg (1.3 kPa) at 5 years. Thus, in younger age groups, relative hypotension has a more profound effect on CPP and outcome,¹⁶ and hypotension may be the main cause of cerebral ischaemia. For adolescents, therapy should aim to sustain CPP at 60–70 mmHg (8.0–9.3 kPa), while maintaining normal blood volume and adequate blood pressure (with pressor agents if required). A CPP less than 40 mmHg (5.3 kPa) reduces the likelihood of intact survival. Younger patients should have therapeutic targets adjusted to age-related realistic end-points.

INTRACRANIAL PRESSURE

Mechanisms of raised ICP in childhood trauma are listed in Table 103.4. If ICP remains persistently raised and uncompensated, cerebral ischaemia and herniation result. This herniation can be cingulate, uncal (temporal lobe), cerebellar tonsillar, upward cerebellar (posterior fossa hypertension) or transcalvarian (through vault defects). Signs of herniation are as for raised ICP (Table 103.3).

Table 103.4 Mechanisms of raised intracranial pressure

Increased intracranial blood volume

Intracranial bleeding (epidural, subdural, subarachnoid, intracerebral)

Cerebral hyperaemia (in the first 1–2 days post injury ¹⁷)

Increased cerebral blood flow (increased PaCO₂, decreased PaO₂, and convulsions)

Cerebral oedema (after day 2 ¹⁸)

Hydrocephalus from intraventricular blood

MEASUREMENT OF INTRACRANIAL PRESSURE

Measurement of ICP is indicated when intracranial hypertension is likely or potential (e.g. GCS 8 or less), or where signs are hidden by muscle relaxation. Technically, measurement in children can be more difficult. Subdural catheters and intracranial transducers require careful placement in children. Ventricular catheters allow removal of CSF, but are difficult to insert when ventricles are small, and readings are difficult to interpret when ventricles collapse. Strain-gauge technology will allows easier and more meaningful measurement of ICP (including intracerebral pressure).

REDUCTION OF RAISED INTRACRANIAL PRESSURE

Several mechanisms allow physiological compensation for raised ICP in children (Table 103.5). In the child under 18 months of age, a gradual increase in intracranial volume is achieved by an increase in head circumference. Measurement of the circumference is important, because compensation can delay recognition of clinical signs and diagnosis in emerging intracranial pathology. The important factor in the rate of change in compliance and ICP is the elasticity of the dura, which is dependent on the rate of change in intracranial volume.

Table 103.5 Physiological compensatory mechanisms for raised intracranial pressure in children

Displacement of CSF to distensible spinal subarachnoid space

Compression of intracranial venous system

Increased CSF reabsorption

Reduced CSF production

Stretching of dura, unfused skull bones and skin (less than 18 months of age)

Hyperventilation is effective in lowering raised ICP. However, excessive hyperventilation may cause cerebral ischaemia, and PaCO₂ should be maintained between 35 and 40 mmHg (4.7–5.3 kPa). Weaning from hyperventilation should be slow, to minimise rebound rises in ICP.¹⁹ Fluid restriction is helpful, provided circulating blood volume is maintained.

Mannitol (0.25–0.50 g/kg i.v. slowly) reduces raised ICP by increasing the osmotic gradient across the intact blood–brain barrier and reducing cerebral oedema. Its effects may also be due to reduced blood viscosity and induced cerebral vasoconstriction. Serum osmolality should be monitored to avoid hyperosmolar states.

Furosemide (1 mg/kg) reduces cerebral water and CSF production, but excessive diuresis from mannitol or furosemide may compromise the circulation. The use of hypertonic saline in children (3%) reduces ICP and appears to be more beneficial in resuscitation. CSF drainage is possible if a ventricular drain is in situ. Controlled hypothermia reduces raised ICP in patients with refractory intracranial hypertension, but improvement in outcomes is uncertain. Surgical decompression or removal of cerebral contusion in the face of intractably raised ICP in head trauma is advocated,⁵ with improved results in unremitting focal oedema.

SPINAL CORD INJURY

Spinal cord injury is rare in children. Anatomical differences in children under 8 years render their spines more mobile and subject to stress with flexible ligaments and joint capsules, less muscular support, and horizontal facet joints. In addition, the relatively large head mass increases momentum, with the fulcrum of mobility at C2–C3 as opposed to C4–C5 in the adult. Thus paediatric cervical spine injuries tend to be above C4. The use of seat belts has led to an increase in lumbar spinal cord injury in children.²⁰

ASSESSMENT

Clinical assessment can be difficult, as can the interpretation of radiological investigations because of normal variation and age-dependent ossification changes. Spinal cord injury without obvious radiological abnormality (SCIWORA) occurs in 10–20% of all paediatric spinal cord injuries.²¹ Sensory-evoked potentials can be a valuable adjunct to diagnosis. Spinal cord injury can only be dismissed after imaging assessments (which may include magnetic resonance imaging in the non-acute setting) and careful and repeated examination of the lucid patient.

MANAGEMENT

From the time of injury, the spine should be assumed to be unstable until proved otherwise. Immobilisation, which at times is difficult, is necessary from the time of injury in the presence of:

• signs or symptoms suggesting neurological spinal deficit

• a history of loss of consciousness

• altered mental status

• history of a high-speed accident or significant fall (including diving)

• significant head or chest trauma

Immobilisation should continue until appropriate assessment can be made, looking for abnormal peripheral neurological signs and spinal distraction pain in the presence of normal imaging.

It is often difficult to decide whether the spinal-injured child is initially best cared for in a paediatric ICU or a specialised spinal unit. This decision will be ultimately determined on the age of the child and the stability of the spine. Certainly, infants should not be managed in adult spinal units, whereas for older children, expertise in spinal care may be more important. However, once spinal column stability and surgical fixation have been achieved, children are best managed in paediatric facilities for ongoing management and rehabilitation.²² Ongoing care is complex, and requires a multidisciplinary approach. Attention to pressure areas, bladder and bowel care and training, nutrition and prevention of contractures is essential. Symptoms of hypercalcaemia (e.g. vomiting, anorexia, nausea and malaise) can be distressing and difficult to control. Depression is common in adolescents. With high spinal cord injury, chin-operated battery-powered wheelchairs, portable ventilators and computer-activated environment control devices allow for relative independence and a functional lifestyle.

THORACIC TRAUMA

Despite a low incidence in children, thoracic trauma is usually associated with multiorgan injury and high mortality.²³ The mechanism of injury is almost entirely related to motor vehicle accidents, with penetrating trauma being uncommon. The child’s small size and more elastic chest wall allow transmission of more kinetic energy to intrathoracic structures, with a high incidence of pulmonary contusions without rib fractures or flail chest.

As for adults, life-threatening injuries which require immediate intervention are upper-airway obstruction, tension pneumothorax, open pneumothorax, flail chest, pericardial tamponade and massive haemothorax (see Chapter 69). Potentially life-threatening injuries are airway rupture, pulmonary contusion, ruptured aorta, diaphragmatic rupture, oesophageal perforation and myocardial contusion. Contrast CT scan and angiography are the methods of choice in diagnosing aortic rupture in children.

ABDOMINAL TRAUMA

Abdominal trauma is usually associated with blunt injury ²⁴ and recognition maybe difficult in the presence of multisystem injury. Mortality is relatively high and missed abdominal trauma is the leading cause of preventable morbidity and mortality.²⁵ The abdominal wall and thoracic cage of children provide less protection to intra-abdominal organs. Also, the liver and spleen are relatively large and more exposed below the rib cage. Forces need not be excessive to cause rupture of internal organs. Absence of bruising does not exclude injury while bruising means severe injury is likely. Lap seat belt injuries are an important cause of abdominal injury in restrained children.

Improvements in radiological imaging techniques have allowed blunt abdominal trauma to be managed conservatively in children.²⁶ This approach requires appropriate monitoring and supervision in a paediatric intensive care setting, with an awareness of the need for urgent intervention, i.e. laparotomy (Table 103.6).

• Ultrasonography is an important screening tool for detecting free fluid ²⁷ and confirming intra-abdominal bleeding.

• CT scan assessment with intraluminal and i.v. contrast is indicated with clinical suspicion of abdominal injury or when physical examination is unreliable. It allows for examination of solid organs and renal tract, and detection of intraperitoneal blood and free air.

• Diagnostic peritoneal lavage is less important, and is only indicated when the source of continued bleeding is undetermined, when an urgent procedure is required for a non-abdominal injury or when a prolonged observation period is anticipated and ultrasonography or CT scan is not available.

Table 103.6 Indications for laparotomy in paediatric abdominal trauma ²⁸

Profound hypovolaemia

Persistent haemorrhage

Haemodynamic instability after replacement 40 ml/kg

Penetrating injury

Gastrointestinal perforation

Signs of peritonism

Pancreatic injury

NON-ACCIDENTAL INJURY

Non-accidental injuries to children are seen in younger age groups, and include physical assault, sexual and emotional abuse and neglect (especially inadequate supervision and deprivation of nutrition and medical care). Injuries resulting from intentional assault can be difficult to diagnose, unless a high index of awareness is maintained.

With regard to the history, suspicion should be raised when:

• the cause of the injury cannot be explained

• there is discrepancy between the volunteered history and the sustained injury, especially when the child’s stage of development is taken into account

• there is a history of repeated injuries

• it is alleged that the injury is self-sustained; or

• there is a delay in seeking care

Physical examination should be thorough, to establish a pattern of injury.²⁹ Multiple bruises in differing stages of development can be separately estimated for age. Patterns for burns are typical for forced immersion in hot water (with sparing of the groin area) and from cigarettes. Suspicion should be raised where cerebral trauma is associated with retinal haemorrhages, subdural haematomas or fractures. Findings of retinal haemorrhages on ophthalmological examination increases suspicion for inflicted injury but do not confirm the diagnosis.³⁰ The most common intracranial pathology is subdural and subarachnoid haemorrhage, which account for the higher morbidity and mortality. A whole-body X-ray series and bone scan will detect fractures in differing stages of healing from multiple assaults.

Whenever non-accidental injury is suspected or diagnosed, a multidisciplinary approach is required by a specialised child protection unit to deal with medical and legal issues, and with the counselling. Urgent intervention may be necessary where the safety of other siblings is threatened.

TRANSPORT

The outcome of trauma in remote locations is optimal when advice, prehospital stabilisation and transport are provided by teams based in tertiary paediatric ICUs.³¹ Secondary insults occur more frequently when paediatric-trained personnel are not used for transport.³² A referral and retrieval infrastructure which links a tertiary centre to outlying areas within the region is necessary. Local health care providers must have sufficient skills to stabilise any critically ill child adequately. The transport team must offer a level of care during the stabilisation and transport phases that is equivalent to that of the receiving paediatric ICU.

It is important for regional hospitals not used to routinely caring for paediatric trauma patients to recognise and acknowledge their individual abilities and limitations. A relationship with a tertiary PICU is essential to allow appropriate and timely communication regarding advice on clinical care, prehospital stabilisation and safe transport for individual patients.

BRAIN DEATH

Determination of brain death in children has different implications.³³ Isoelectric EEGs have been reported in neonates with partially preserved clinical brain function, and cerebral death can occur without marked increase in ICP, allowing partial cerebral blood flow in the presence of brain death criteria and electrocerebral silence. In addition, partial brain recovery has been demonstrated after prolonged periods of clinical unresponsiveness. So for determination of brain death, consideration needs to be given to longer observation periods, more frequent use of confirmatory tests, and an emphasis on the history and clinical findings.

The American Academy of Pediatrics has set longer observation times which include the requirement for two separate EEGs or one EEG and a cerebral radionucleotide angiogram. These longer observation times depend on the child’s age, namely:

• over 1 year of age – 12 hours’ observation

• ages 1 month to 12 months – 24 hours’ observation

• ages 7 days to 2 months – 48 hours’ observation

• under 7 days of age – no recommendation

The Australian and New Zealand Intensive Care Society recommendations on brain death and organ donation only make reference to the under 2 months age group when ‘determination of brain death may be more difficult and different time periods may be required’.³⁴ Importantly, there is a lack of evidence for any required observation periods, so that cerebral blood flow imaging may be required in the neonate and infant. The most important factors when determining brain death are in knowing the cause of coma, and being certain of its irreversibility. Time must be allowed for relatives to come to terms with the diagnosis, and there is a responsibility to discuss organ donation. Having relatives watch the physical examination for brain death testing is helpful.