PREVENTION STRATEGIES

Paediatric trauma requires resources and separate systems to successfully reduce mortality and morbidity.³ New emphasis has seen the development of prevention strategies (Table 103.1), including:

• injury surveillance, prevention research, legislation and public safety campaigns

• education programmes directed at care-givers

• nationally coordinated approaches to trauma care

Table 103.1 Prevention strategies ⁴

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)

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