Head and Maxillofacial Injuries

Concussion

Concussion is a brain injury associated with brief loss of consciousness, typically for only a few minutes. It causes minor cognitive disturbances, such as temporary confusion or amnesia. By definition, there are no persisting abnormal neurological signs although some patients may report long-term symptoms, such as headache, impaired concentration, poor short-term memory and altered affect (postconcussion syndrome, see later under rehabilitation).

Diffuse Axonal Injury

Diffuse axonal injury (DAI) typically follows large rotational acceleration and deceleration forces, causing widespread damage to axonal tracts. DAI involves microscopic tissue damage and so imaging may appear normal. Abnormalities are seen best on magnetic resonance imaging (MRI), which demonstrates haemosiderin deposition at the junctions of deep grey and white matter, within white matter tracts, or in the basal ganglia. This type of injury does not usually lead to raised ICP. Treatment is supportive. These injuries have a high mortality, and may later produce substantial cognitive impairment and personality change, with or without physical neurodisability.

Focal Brain Injuries

Focal injuries result from trauma to localised brain areas and are readily visible on CT scans. The site and extent of the primary injury depend on the nature of the damaging force ( Fig. 16.2 ). The main lesions are cerebral contusion, laceration or haematoma, all of which can act as space-occupying lesions with a potential for secondary brain injury. Contusions may be small or large and occur beneath the area of impact ( coup ) or contralateral to it ( contre-coup), caused by rebound of the brain within the skull at the time of impact (see Fig. 16.3 ). Serious trauma is needed to cause focal brain injury and hence usually results in a period of loss of consciousness followed by confusion.

Cerebral Hypoxia

Ischaemia and hypoxia are central to most secondary mechanisms of brain injury, and lead to cellular energy failure . Hypoxia causes cerebral oedema, which in turn causes a secondary rise in ICP risking further ischaemia. Common causes of hypoxia are airway obstruction in reduced GCS, alcohol or drug overdose, chest injury, inhalational pneumonitis, acute respiratory distress syndrome or central respiratory depression. Hypotension caused by hypovolaemia contributes to cerebral hypoxia by reducing cerebral perfusion. Resuscitation aims to prevent or treat hypoxia and hypovolaemia.

Intracranial Haemorrhage

Posttraumatic intracranial bleeding is classified into extradural (epidural), subdural , intracerebral or subarachnoid ( Fig. 16.4 ). Intracranial bleeding acts as a mass lesion causing a general rise in ICP, whilst local brain compression can cause focal neurological deficits.

Extradural Haemorrhage

Extradural haemorrhage occurs when blood accumulates in the space between dura and calvarium of the skull. It is most common in children and younger adults because their dura is less adherent to the skull. Most have a fracture, usually in the temporal or parietal region ( Fig. 16.5 ). Almost 90% are caused by rupture of an artery, usually the middle meningeal or a branch running inferior to the temporal region. This normally results in a loss of consciousness immediately following injury. In up to half the patients, this is followed by a lucid interval , with no symptoms other than worsening headache. This is followed by deteriorating conscious level . Temporal lobe herniation then leads to compression of the third nerve and pupillary dilatation . Death quickly follows unless the haematoma is evacuated rapidly. Emergency CT scanning is indicated to confirm the diagnosis and show its position (typically a lentiform-shaped clot— Fig. 16.5B ). Urgent transfer to a neurosurgeon for evacuation of the clot is the ideal course of action.

Subdural Haematoma

Subdural haematoma usually results from tearing of veins passing between cerebral cortex and dura, or from injury to vessels on the brain surface. Blood accumulates in the large potential space between dura mater and arachnoid mater and the haematoma tends to spread laterally over a wide area ( Fig. 16.6 ). In contrast to extradural haemorrhage, there is usually underlying primary brain injury. Acute subdural haemorrhage is more common in older adults because the brain is more mobile within the cranial cavity.

Case History

In acute subdural haemorrhage, there is usually clinical evidence of brain injury at the outset. A lucid interval is rare, except where the pathology is tearing of a bridging vein. Evacuation of an acute subdural haematoma cannot be achieved via burr holes because the blood is clotted. Surgical evacuation via craniotomy may halt deterioration but recovery is often incomplete because of the underlying brain injury. With increasing use of anticoagulation and antiplatelet therapy, acute subdural haematoma is now seen more after relatively inconsequential injury, particularly in the elderly.

Chronic Subdural Haematoma

In the elderly, subdural haematomas may develop gradually following trivial, often unrecalled, head trauma. This is caused by the relative ease with which atrophic brains can accommodate blood under venous pressure. The condition

Case History

only manifests some weeks or months later as the clot lyses and fluid is drawn into the subdural space by osmosis. Symptoms are nonspecific neurological deterioration, chronic headache or coma. At this point the liquid haematoma can be evacuated via burr holes, and the subdural space irrigated with warm saline.

Intracerebral Haemorrhage

Haemorrhage into the brain parenchyma is caused by primary brain injury. Multiple small deep lesions are often associated with DAI. Small haematomas should be managed conservatively and monitored for expansion using serial CT scans. A larger haematoma causing ‘mass effect’ should be evacuated early to prevent secondary brain damage.

Infection

Early debridement of compound depressed fractures is important so as to minimise the risk of infection. Prophylactic antibiotics are not indicated except in contaminated wounds. There is no evidence in favour of prophylactic antibiotics in cases of cerebrospinal fluid (CSF) leakage.