Head and maxillofacial injuries
Head injuries
Introduction
Head injury is a potentially devastating problem with an enormous social and economic cost. Up to a million people attend emergency departments in the UK each year following head injury. Using the Glasgow Coma Scale (GCS, Table 16.1) as a clinical indicator, 90% are classified as mild/minor, with scores of 13–15 respectively, 5% as moderate (score 9–12) and 5% as severe (score 3–8). Head injuries cause approximately 3500 deaths each year in the UK, amounting to about 0.6% of all deaths. Figure 16.1 shows how serious injuries represent the tip of an iceberg of the impact of head injury on health care. The greatest burdens are the acute management of all these cases and dealing with the chronic disability these injuries can cause.
Table 16.1
| Clinical observation | Score* |
| Eye opening: | |
| Spontaneous | 4 |
| To verbal command | 3 |
| To pain | 2 |
| None | 1 |
| Motor response: | |
| Obeys commands | 6 |
| Localises pain | 5 |
| Flexion withdrawal to pain | 4 |
| Abnormal flexion (decorticate) | 3 |
| Extension to pain (decerebrate) | 2 |
| None | 1 |
| Verbal response: | |
| Orientated | 5 |
| Confused conversation | 4 |
| Inappropriate words | 3 |
| Incomprehensible words | 2 |
| None | 1 |
*On this scale, a patient’s Glasgow Coma score is the sum of the scores from all three sections. The worst total score is 3, the best is 15. After the initial score, the observations and scoring are repeated at intervals to look for deterioration
Less than half the head injury patients attending emergency departments require CT scanning or hospital admission and only a small proportion require specialist neurosurgical investigation and care. The difficulty is to recognise those at risk without over-investigating or admitting patients unnecessarily. In order to streamline this process, various triage algorithms have been produced, notably NICE guidelines (http://guidance.nice.org.uk/CG56/Guidance—summarized in Box 16.4, see below). The main focus is detecting clinically important brain injuries (and cervical spine injuries—Box 16.1) whilst avoiding admission of those with low risk of sequelae.
Primary brain injury
Focal brain injuries
Focal injuries are the result of trauma to localised brain areas and are readily visible on CT scanning. The main lesions are cerebral contusion, laceration or haematoma, all of which may act as space-occupying lesions and are liable to result in secondary brain injury. The site and extent of the primary injury depend on the nature of the damaging force (see Fig. 16.2). Contusions may be small or large and occur either 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 (Fig. 16.3). The severity of trauma required to cause focal brain injury will usually result in a period of loss of consciousness, followed by confusion.
Fig. 16.2 Mechanisms of brain injury
(a) The mechanism of ‘coup’ or direct injury is similar to a deceleration injury (shown in horizontal section). (b) A ‘contre-coup’ injury affects the side opposite to the blow because of rebound (horizontal section). (c) In rotational injury the inertia of the brain suspended within the cranium leads to the tearing of surface vessels and subdural haemorrhage (horizontal and sagittal sections)
Case History
Fig. 16.3 Focal brain injury
A cyclist was knocked off his bike by a car and suffered a head injury with loss of consciousness of 45 minutes. CT scan of head shows signs of soft tissue injury I, I in both left temporal (‘coup’) and right fronto-parietal regions (‘contre-coup’). There is a depressed segment of skull bone in the left temporal region D and signs of intracerebral contusion C beneath both areas of injury. He gradually recovered without need for operation, but full cerebral functional recovery took several months
Secondary brain injury
Intracranial bleeding
Post-traumatic intracranial bleeding is classified into extradural (epidural), subdural, intracerebral or subarachnoid (see Fig. 16.4). Intracranial bleeding acts as a mass lesion causing a general rise in ICP, whilst local brain compression can cause focal neurological deficit. Untreated, raised ICP may cause ‘coning’. One or both temporal lobes herniate through the tentorium cerebelli, compressing the third nerve and midbrain, whilst herniation of the cerebellar tonsils through the foramen magnum compresses the medulla, causing neurological deterioration and often death. Rising intracranial pressure manifests initially with deteriorating conscious level. Late clinical signs are:
• An enlarging, unresponsive pupil
• Central respiratory depression
Extradural (epidural) haemorrhage: Extradural haemorrhage occurs when blood accumulates in the space between dura and calvarium. It is most common in children and younger adults, because their dura is less adherent to the skull. Most have a skull fracture, usually in the temporal region (Fig. 16.5). Almost 90% are due to rupture of an artery, usually the middle meningeal or a branch. Immediately after injury causing loss of consciousness, in up to half the patients, there will be a lucid interval, perhaps with no symptoms other than worsening headache. In either group, 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 (typically a lentiform-shaped clot—see Fig. 16.5b) and to show its position. With increased awareness of the condition and widespread availability of CT scanning, emergency ‘blind’ burr hole drainage is almost never appropriate. Urgent transfer to a neurosurgeon for craniotomy is the best course of action, almost without exception.
Case History
Fig. 16.5 Temporo-parietal fracture with extradural haematoma
(a) This 20-year-old man was admitted fully conscious after being knocked off a bicycle but deteriorated rapidly 2 hours later. Lateral skull X-ray showing a linear fracture (arrowed F) of the right temporo-parietal bones crossing the course of the anterior branch of the middle meningeal artery M on the temporal bone. (b) Classical CT appearance of extradural haematoma
Subdural haematoma: Subdural haematoma usually results from tearing of veins passing between cerebral cortex and dura, or from injury to vessels on the surface of the brain. Blood accumulates in the large potential space between dura mater and arachnoid mater. 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
Fig. 16.6 Subdural haematoma
An elderly man suffered a head injury in a road traffic collision without loss of consciousness 48 hours previously. His conscious level gradually deteriorated and so this CT scan was performed. On the right side, there is a large subdural haematoma of mixed attenuation M M (black arrows define the edge of the brain). Such mixed attenuation suggests old liquefying thrombus and is consistent with its origin around the time of the accident. There is a smaller subdural haematoma on the left side (white arrows) of consistent attenuation suggesting that it arose more recently. Note the midline of the brain is shifted to the left by the mass effect of the larger haematoma and there is compression of the lateral ventricles. The patient required neurosurgical drainage
Chronic subdural haematoma: In the elderly, subdural haematomas may develop gradually following trivial, often unrecalled, head trauma. This is due to the relative ease with which their atrophic brains can accommodate blood under venous pressure. Only as the clot lyses and fluid is drawn into the subdural space by osmosis does the condition manifest, some weeks or months later, as non-specific 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.
