Head injury

Published on 10/04/2015 by admin

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Last modified 22/04/2025

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Head injury

Head injury is an important cause of disability and death. In western countries, trauma is the most common cause of death in patients aged under 45 years. Half of these patients die as a result of head injury. Overall there is a mortality rate of 20–30 per 100 000 per year. The survivors are often disabled with a prevalence of disabled survivors of up to 400 per 100 000.

The causes of head injury are falls, assaults and road traffic accidents (RTAs). The relative frequency varies from country to country and according to age. About a quarter of head injuries are due to RTAs in all age groups. In those aged under 15 years and over 65 years, falls are the most common cause; in those between the ages of 15 and 65 years, assaults are the most common cause.

Patients with acute head injuries are looked after by neurosurgeons or orthopaedic surgeons. Neurologists can be involved in their care, particularly in the recognition and management of the sequelae of head injury.

Pathology and pathogenesis

Cerebral injury

Head injury may lead to a brief loss of consciousness without associated pathological changes in the brain. The mechanism for the loss of consciousness is not clear.

With more severe head injury, brain damage can occur because of the direct trauma to the brain. This arises from direct disruption of the brain, shearing of axons and intracerebral haemorrhage. These injuries occur at the site of trauma and opposite the site of injury, so-called contre-coup injury. Contre-coup injury results from acceleration/deceleration forces moving the brain within the skull.

There may be secondary brain injury (Fig. 1) due to brain oedema, which causes raised intracranial pressure and can lead to cerebral herniation (p. 48). The raised intracranial pressure, usually associated with hypotension, leads to hypoperfusion of the brain and therefore cerebral ischaemia. Infratentorial lesions can obstruct CSF flow and lead to hydrocephalus.

image

Fig. 1 Mechanisms of secondary head injury.

Intracranial haematomas

Extradural haematomas occur when the middle meningeal artery bleeds into the extradural space (Fig. 2). This can occur some time after the head injury and should be considered in any patient with deterioration following an apparently good recovery from a head injury.

image

Fig. 2 CT scan showing an extradural haematoma (arrow) and intracranial haemorrhage (double arrow).

Subdural haematomas occur either acutely, usually with some intracerebral bleeding, or chronically (Fig. 3). The latter occurs when damaged cortical veins ooze into the subdural space.

image

Fig. 3 CT scan showing a subdural haematoma (arrow) producing some mass effect with displacement of the midline structures.

Intracerebral haematomas (Fig. 2) are the most common, occurring both at the site of direct trauma and at the contre-coup site.

The mass effect of any of these bleeds may lead to cerebral herniation.

Skull fractures

These can be divided into simple and depressed fractures and basal skull fractures. The latter are difficult to see on skull X-rays but are associated with particular physical signs such as periorbital bruising or Battle’s sign (Fig. 4). These may also be associated with cranial nerve damage, especially facial and auditory nerves. Basal fractures also produce bleeding into the middle ear, seen as either blood behind the ear drum or coming from the external ear, or CSF rhinorrhoea. CSF rhinorrhoea is seen as clear fluid coming from the nose – fluid which, unlike mucus, contains glucose, which is easily tested for. (A more specific test is isotransferrin.) The presence of a skull fracture substantially increases the risk of significant intracranial haemorrhage.

image

Fig. 4 Signs of basal skull fracture: Battle’s sign.

Basal and compound fractures can produce a dural leak, which provides a potential route of entry of infection into the CNS.

Clinical features

The clinical features of head injury are varied and depend on the severity of the injury and the part of the brain affected. This can be complicated by delayed events such as intracranial haemorrhage. The clinical setting alters the evaluation. For example, in patients with multiple injuries, there can be trauma elsewhere, with multiple fractures and abdominal and chest trauma. In these and other patients, there may be associated cervical spine trauma.

The severity of a head injury can be assessed in several ways:

image The level of consciousness, reliably and easily measured using the Glasgow Coma Scale (p. 129), which is an important clinical measure.
image Signs indicative of a basal skull fracture (see above).
image The pupil reactions, an important indicator of herniation.
image The finding of focal neurological signs.

These measures can be monitored and any change is particularly important in the management of these patients. The vital signs need to be monitored.

Fortunately, most patients will have less severe head injuries. The same measurements need to be made but a history may be obtainable from the patient. From the history of the episode, perhaps from witnesses, some estimate of the potential forces involved can be made. The occurrence and duration of loss of consciousness are important indicators. The duration of memory lost by the patient, before the injury (retrograde amnesia) or after the injury (anterograde amnesia), are important indicators of severity of injury.

One group of patients of particular concern are those who have made an initial recovery from their head injury but then later deteriorate again after a ‘lucid interval’. This is the classical history of patients with extradural haemorrhage, though it can occur with subdural haemorrhage. It can also occur because of neck trauma resulting in carotid dissection. These complications are rare in patients who have not fractured their skull (1 in 1000).

Differential diagnoses

The differential diagnosis of head injury will depend on the clinical presentation. In patients who present unconscious or confused, the differential diagnosis is wide and is discussed on page 50. In patients who have had a head injury with a period of anterograde and retrograde amnesia, there may be uncertainty as to whether the head injury was the primary event or the result of a blackout.

Investigation and management

The investigation and management depend on the severity of the head injury. Patients with mild head injuries without loss of consciousness or with loss of consciousness of less than 5 min, with a normal examination and no skull fracture, can be allowed home in the care of a responsible adult with a warning card outlining the possible types of deterioration. Patients at risk from developing complications are those with longer than 5–10 min unconsciousness, a seizure at onset, altered consciousness or focal signs on examination and evidence of a skull fracture. These patients need to be admitted and monitored. CT or MRI of the brain is needed in most of these patients. These are optimally managed in a neurosurgical centre.

The aim of treatment is to prevent secondary brain damage. This focuses on avoiding hypotension, maintaining oxygenation and avoiding raised intracranial pressure. Intracranial pressure may be reduced by surgical procedures to evacuate intracranial haematomas and shunt for hydrocephalus, and medical interventions with mannitol, mechanical ventilation and forced hyperventilation; this may need monitoring with intracranial pressure monitors. Cytotoxic oedema is maximal about 3–4 days after the injury. This specific treatment needs to be combined with general medical care as for any unconscious patient.

Once the patient is stable and improving, there are many aspects that will require rehabilitation. This will involve physiotherapy and occupational therapy, and may require speech therapy. There are frequently psychological and behavioural difficulties with personality change, frontal disinhibition and memory loss. These latter problems make the rehabilitation of patients following severe head injuries somewhat different from patients with other brain injuries such as stroke and are often most effectively managed at a specialist unit.

Other complications

In addition to the consequences of brain damage there are other complications.

Post-traumatic syndromes

Even after a mild head injury, patients can become anxious, have difficulty concentrating and sleep poorly. This may be associated with particular recollections of the accident and a change in behaviour, for example avoiding driving. This is a post-traumatic stress disorder. There is uncertainty about whether this is affected by compensation claims relating to any accident. Patients may develop a migraine-like headache following head injury, which usually spontaneously improves over 2 years.

Anosmia (loss of sense of smell) can occur as a result of damage to the fibres passing through the cribriform plate. This is permanent. Patients may still appreciate tastes and chemical irritation such as ammonia.

Post-traumatic vertigo can occur and is most commonly benign positional vertigo (p. 46).

The frequency of post-traumatic epilepsy depends on the severity and type of the head injury. Severe head injuries with intracranial haematomas or post-traumatic amnesia (PTA) over 24 h have a 12% risk of epilepsy in 5 years. More moderate injury with skull fracture or PTA over 30 min has a 1.6% risk at 5 years. Milder head injuries have the same rate as the background population of 0.5%.

Prognosis

The outcome of head injury depends on the severity of the injury and age of the patient, with younger patients doing better. Most head injuries are mild or moderate and there is a good recovery: if PTA is less than 1 h, 90% of patients are back at work in 2 months; if PTA is longer than 24 h then 80% of patients return to work in 6 months. Patients with more severe head injuries are often left with some disability. They do, however, continue to improve for longer, over 2 years, than patients with other brain injuries such as stroke.

Head injury

image Head injury is a common cause of death and neurological disability.
image Brain injury results from a combination of direct trauma, haemorrhage, hypoxia and raised intracranial pressure.
image Acute management of head injuries aims to control the secondary mechanisms of brain injury: haemorrhage, hypoxia and raised intracranial pressure.

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