TBI covers a spectrum of injury from trivial to lethal. It is the leading cause of morbidity and mortality in paediatric trauma.¹ The number of children admitted to hospital in a recent study indicated an annual rate in Australia of 232 per 100 000 for those aged 0–4 years, 158 per 100 000 for those aged 5–9 years and 203 per 100 000 for those aged 10–14 years.² These figures are higher than the overall, age standardised, annual rate of between 140 and 150 per 100 000 population.²^,³ It is important to remember that these figures only reflect hospital admissions and the true incidence of TBI in the community is much higher.⁴

In Australia the most common cause of TBI is falls, followed by motor vehicle related accidents.² A much smaller percentage result from being struck by objects, crushed, assaulted (non-accidental injury) and other miscellaneous causes. Males consistently outnumber females, with most studies reporting approximately a 2:1 ratio for all age groups. The overall incidence of spinal cord injury in Australia for children aged 0 to 14 years is unknown.⁴^,⁵ The age standardised incidence in the 15+-year-old population is 14 per million of population per year, with a male to female ratio averaging 4:1, but peaking at 9:1 in the 15–24-year age group.⁵

Preventive strategies have made the most impact on the improved outcomes of paediatric trauma over the past two decades.

Pathophysiology

TBI, like spinal injury, can be divided into primary and secondary trauma. Primary trauma occurs during the initial impact to the head and only preventive measures such as using protective equipment (e.g. helmets and seatbelts), better engineering (e.g. safer roads), education and legislation can alter the extent of this primary injury. Secondary trauma or insult occurs when post-traumatic acute phase response and mediators, or subsequent physiological insults, such as hypoxia, hypotension and increased intracranial pressure, occur and cause further damage to the already traumatised tissues or structures. The prevention of secondary injury, particularly due to cerebral hypoxia and reduced cerebral perfusion, is the primary focus of acute medical intervention, which begins in the field via ambulance and continues in the ED setting.

Children have unique anatomical, physiological and developmental differences when compared to adults. They have a large head to body ratio, leading to a high centre of gravity (falls) and to the head being the primary ‘target’ for trauma. The skull is thinner and more plastic and thus transmits rather than attenuates impact.⁶^,⁷ Skull fractures are therefore more common in children and importantly, serious brain injury can occur without an associated skull fracture.⁸^–¹²

In children, the dura is more closely adherent to the skull compared to adults, making extradural haematomas less common in children, particularly in infants.⁷^,¹³ Unfused sutures and an open fontanelle can expand to accommodate intracranial haemorrhage or cerebral oedema.⁷ Some authors have thought children to be more prone to ‘malignant cerebral swelling’ that can cause rapid and sometimes fatal deterioration even after minor TBI.⁹^,¹⁴^,¹⁵ However, this view has recently been questioned and swelling may be no more common in children than in adults.¹⁶

Physiologically, children have a lower systolic and mean arterial blood pressure, which implies a lower cerebral perfusion pressure (CPP). This, in turn, may cause problems with maintaining adequate cerebral perfusion if they have raised intracranial pressure. Infants and small children may become hypovolaemic with large intracranial bleeds. This is not seen in larger children or adults.⁶

Cerebral blood flow is often very low and may approach ischaemic levels following more severe TBI.¹⁷ This may be related to a low brain metabolic rate in comatose patients, increased intracerebral pressure and vasospasm. Autoregulation of cerebral blood flow (CBF) may be lost following TBI, and in this setting CPP largely determines CBF. This underscores the importance of maintaining an adequate CPP in the head-injured patient, especially those with more severe injuries.

Head injury, as opposed to TBI, may be described as extra-axial or intra-axial. Extra-axial injury refers to pathology outside the brain parenchyma.⁷^,¹⁸ Extra-axial structures include the skull, structures between the skull and brain and the ventricular spaces within the brain. Common extra-axial lesions include skull fractures and extradural, subdural, subarachnoid and intraventricular haemorrhages. Extra-dural haemorrhage occurs, as its name implies, outside the dura. Medical literature often refers to this as ‘epidural haemorrhage’ but in Australasia the term ‘epidural’ is generally used only to describe lesions outside the dura of the spinal cord. Intra-axial injuries are true TBIs and include contusion, laceration, haemorrhage and diffuse axonal injury (DAI). DAI may result in considerable disability with little to see on radiological investigation.⁷

Classification

The generally accepted method of classifying severity of TBI is by using the Glasgow Coma Scale (GCS), although other measures such as duration of unconsciousness or amnesia are sometimes used. The GCS was first described for adults in 1974 and scores three variables: eye opening, verbal response and motor response (see ‘examination’ and Table 3.2.1).¹⁹ It has proved to be a very useful tool in rating severity of TBI and prognosis.⁷

Score Adult Child Eye opening 4 Spontaneous 3 To speech only Same 2 To pain only 1 No response Verbal 5 Orientated in person, place and time Happy/smiles/interacts normally 4 Confused Crying but consolable 3 Inappropriate but intelligible speech Inconsistently consolable 2 Incomprehensible sounds Inconsolable and/or irritable 1 No response No response Motor 6 Obeys commands 5 Localises painful stimulus 4 Withdraws to painful stimulus Same 3 Flexor posturing to painful stimulus 2 Extensor posturing to painful stimulus 1 No response

The problem with using the GCS on young children, particularly those aged less than 2 years, is that the best verbal response is limited by their language development. In an attempt to overcome this difficulty, modified GCSs have been proposed, including the so-called Child Coma Scale (CCS).⁹^,²⁰ It is important to note that, unlike the GCS, the CCS has never been properly validated and many studies of head injury in children deliberately exclude those aged less than 2 years.

TBI is usually divided into three categories: mild, moderate and severe.

Mild TBI (GCS 14 to 15)

Mild TBI, sometimes termed ‘minor’ TBI, was originally defined as head trauma patients with a GCS from 13 to 15 (and/or varying periods of loss of consciousness (LOC) and amnesia).²¹ The problem with this definition is that patients with GCS 13 have a significantly higher risk of intracranial injury, with subsequent risks for deterioration and neurosurgery, than patients with a GCS of 14 or 15. They more properly belong in the moderate head injury group.¹⁵^,²²

The original definition of GCS 13 to 15 continues to be used in international and Australasian literature but the recognised definition of mild TBI in Australasia is GCS of 14 or 15.¹⁴ Some authors believe that even this is too liberal and the definition of mild TBI should be restricted to patients with a GCS of 15.²²^,²³

Approximately 80% of children with TBI will fall into this category.²⁴ The reported incidence of intracranial haemorrhage (ICH) varies between 4 and 7% in children with GCS 15, and increases to approximately 10% in children with GCS 14. ¹⁰^,¹⁵^,²⁵^,²⁶ The overall mortality in this group is reported to be as high as 2%.¹⁵ These figures may be subject to significant selection bias.

The terms ‘minimal’ or ‘trivial’ TBI are sometimes used to describe a subgroup of mild TBI who meet the following criteria: GCS 15, normal neurological examination and no signs of a skull fracture.²³^,²⁵^,²⁷ Transient LOC or amnesia does not exclude patients from this subgroup.

Moderate TBI (GCS 9 to 13)

Approximately 18% of children with TBI fall into this category.²⁴ The incidence of ICH and overall mortality in this group of children is uncertain (almost all research focuses on either mild or severe TBI).

Severe TBI (GCS 8 or less)

Approximately 2% of children with TBI fall into this category.²⁴ Patients in this category are, by definition, comatose. Overall mortality in this group is between 30 and 40%.²⁸

Assessment

History

Careful history and examination is important when assessing the significance of the injury and determining the need for further investigation or admission.

Initial assessment and treatment may need to occur simultaneously. Ensuring an adequate airway, breathing and circulation with resuscitation as required is the first priority. The best approach is to undertake a ‘primary survey’ with correction of life threats, followed by a ‘detailed history plus secondary survey’ as for any other trauma patient. Spinal precautions using immobilisation must be maintained until clinical and/or radiological clearance of the spine has been completed.

Assessment of the child may be extremely difficult, if not impossible, if the child is distressed with pain or is cerebrally irritated. The early use of a very small dose of parenteral narcotic such as morphine 0.05 mg kg^–1 intravenously may make assessment and management much easier. Concern about masking changes in neurological function should not prevent the use of adequate analgesia for children who are distressed by pain.

The following historical information is relevant and should be ascertained if possible:

• time and mechanism of the injury;

• any loss of consciousness or period of altered level of consciousness and its duration;

• any post-trauma seizure-type activity;

• any post-injury vomiting;

• any headache or other neurological symptoms such as diplopia, weakness or altered sensation;

• any retro- or anterograde amnesia;

• progression of any symptoms and signs from the time of injury;

• details of pre-hospital care assessment and therapies.

The possibility of non-accidental injury (NAI) must always be considered in children with skull fractures or intracranial injuries. Be particularly vigilant with children aged <2 years, when a parent or carer has delayed seeking medical care or the stated mechanism is not in keeping with degree of injury observed.¹²

Past history that is particularly relevant in the context of neurotrauma is:

• previous head or spinal injury;

• congenital central nervous system (CNS) problems;

• CNS surgery (such as the insertion of a VP shunt);

• bleeding diatheses such as haemophilia or thrombocytopenia;

• psychomotor or developmental problems, such as autism, that make assessment particularly difficult.

It is important to remember:

• medications, and other ingestants that may influence assessment of a head injury including possible illicit drugs or medications and chemicals to which a young child may have gained access at home;

• allergies;

• immunisation status;

• last food or fluid intake.

Examination

Check vital signs, including bedside blood sugar level, to immediately exclude:

• hypoxia (SaO₂ ≤90% or PaO₂ ≤60 mmHg)

• hypotension (SBP ≤5th percentile for age or SBP <90 mmHg)

• hypoglycaemia (blood sugar level <3.0 mmol L^–1).

These reversible factors may be contributing to the child’s altered level of consciousness and also cause secondary brain injury. Ascertain the child’s weight, early, either by measurement or inference from the child’s age, as it is necessary for calculating drug and fluid requirements.

Glasgow Coma Scale (GCS)

This should be used to define the child’s level of consciousness and to monitor any change over time. Serial neurological observations should be performed regularly to monitor for deterioration or improvement in the child’s conscious state. Once a child’s GCS is normal and stable, the frequency of neurological observations can be decreased. It is important to note that the GCS is intended to score global function not focal deficit. When using the GCS to classify the severity of TBI, the best post-resuscitation score should be used.

If a painful stimulus is needed to test motor function, apply pressure to the supra-orbital margin to test for localisation of pain. This is superior to a ‘sternal rub’. To test for withdrawal or abnormal flexion/extension, use a pen or pencil to apply pressure to finger-nail or toe-nail beds. Abnormal flexion is usually termed ‘decorticate posturing’ and abnormal extension termed ‘decerebrate posturing’ although this was discouraged in the original description of the GCS as it implied a specific physio-anatomic correlation.¹⁹ The best score should be recorded after testing all four limbs and any discrepancy between limbs should be recorded separately.⁵

It should also be noted that it may not be possible to score verbal or motor function in some patients, for example those who are intubated (verbal score) or have a high-level spinal cord injury or limb injuries (motor score).

Table 3.2.1 allows comparison of the GCS and the CCS used by Hahn et al and others.⁹^,²⁹ The CCS has never been properly validated and assessment of verbal response is somewhat subjective, particularly in children aged less than 6 months.²⁰

A rapid assessment of a child’s neurological disturbance can also be made using the AVPU scale, which denotes the child’s response to stimuli (Table 3.2.2). The child who demonstrates a non-purposeful response to pain (withdrawal, flexor or extensor responses) has a level of consciousness consistent with a GCS of <9 and the unresponsive child, a GCS of 3.