Head injury

It has been estimated that in the UK, between 200 and 300 per 100 000 of the population are admitted to hospital each year with a head injury, making it one of the most common causes for attending accident and emergency departments. Trauma, in which severe head injury often plays a major role, is also the leading cause of death in the population below 45 years of age. Craniocerebral trauma is consequently a source of major disability and a huge financial and psychological burden upon society.

Despite being encased in a rigid protective skull and cushioned by CSF, the brain is still very vulnerable to trauma, having only the consistency of a well-set jelly. This trauma can take the form of translational acceleration/deceleration forces, rotational forces or direct local sharp penetrating or blunt trauma to the cranium and can involve the scalp, skull or brain, in any combination.

  Scalp

Scalp lacerations are common and can give rise to exanguinating haemorrhage if not controlled. This is due to the vessels in the dense fibrous layer being held open. Scalp hair plays an important protective role and by matting into wounds can effectively assist haemostasis but likewise mask significant scalp lacerations. The scalp’s rich vascular supply plays an important role in healing, making it a very resilient structure.

Skull

Different types of skull injury may follow blunt trauma.

Simple linear fractures

These require no specific neurosurgical management but are usually markers of the force to which the head was subjected. Patients are usually CT scanned but should also be admitted for at least 48 hours’ observation.

Depressed skull fracture

These fractures are a result of blunt trauma, usually to the left -frontal region. If the pericranium has been breached the fractures are technically compound. The integrity of the dora is however more important. The dura and brain may be lacerated by the depressed fragment.

The damage done at the time of impact with subsequent risk of epilepsy is irreversible. Surgery is usually undertaken to prevent the risk of infection, to alleviate mass effect and for cosmetic purposes. Contaminated wounds require extensive debridement, a duraplasty and irrigation before closure. A full course of intravenous antibiotics should be administered.

Base of skull fracture

These are relatively frequent fractures, usually diagnosed on clinical grounds. They often result in CSF fistula which may persist but usually seal off after a few days. Anterior fossa fractures present with subconjunctival haematomas, anosmia, epistaxis and CSF rhinorrhoea and may occasionally be associated with caroticocavernous fistulae (Fig. 35.11). Periorbital haematomas or ‘racoon eyes’ indicate subgaleal haemorrhage and not necessarily base of skull fracturing as do subconjuntival haemorrhages extending beyond the conjunctival reflections (Fig. 35.12). Middle fossa fractures present with CSF otorrhoea or rhinorrhoea via the eustachian tube, heamotympanum, ossicular disruption, ‘battle sign’ (Fig. 35.13) or VII and VIII cranial nerve palsies.

There is no evidence that prophylactic~ antibiotics diminish the incidence of meningitis. Administering them may just select out more virulent organisms in those that become infected, increasing morbidity and mortality. If one suspects a CSF fistula, the fluid should be screened for beta-transferrin to confirm that it is in fact CSF. Before repair of CSF fistula, it is mandatory to exclude the presence of hydrocephalus. The dura should then be sealed with autologous, vascularised grafts and fibrin glue after cranialisation of the frontal sinuses.

Ping-pong fracture

This is a smooth depression of the cranial vault usually seen in children. Also known as a ‘pond’ fracture.

Blow-out fracture

These are caused by fracturing of the orbital walls with herniation of orbital contents and subsequent tethering of the globe, resulting in pain and diplopia.