Head and maxillofacial injuries

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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

Glasgow Coma Scale (GCS)

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.

Pathophysiology of traumatic brain injury

Traumatic brain injuries can be divided into primary injury, from the initial trauma, and secondary brain injury, which evolves later. Treatment cannot reverse the primary brain injury but aims to minimise sequelae that add to it. Secondary brain injury is mostly caused by raised intracranial pressure (e.g. from intracranial haematoma or brain swelling), ischaemia or hypoxia, and is amenable to treatment by prophylactic measures and timely intervention. Prospects for improving care of head-injured patients depend on prompt triage, adequate resuscitation, ready access to CT scanning, safe and rapid transfer to neurosurgery units, and the availability of specialist critical care.

At the cellular level, brain injury disrupts the neuronal cytoskeleton, which over a few hours can lead to irreversible axonal injury. High levels of glutamate accumulate extracellularly, damaging neighbouring cells and causing a ripple effect of neuronal death and release of further toxic molecules. Potential neuroprotective agents such as glutamate and calcium antagonists have so far proved ineffective.

The brain has minimal capacity to regenerate after injury but in general, the younger the patient the better the prognosis. Young children may make a remarkable functional recovery despite suffering severe injuries because of the plasticity of the developing nervous system, although some will suffer high level cognitive impairment (‘executive dysfunction’) in their late teens from failure of frontal maturation. In adults, the primary injury consequences are likely to be more severe with advancing age. One important factor here is that the brain atrophies, allowing greater mobility under impact within the cranial vault.

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.

Secondary brain injury

Secondary brain injury can be caused by cerebral hypoxia, intracranial bleeding or infection. These are discussed in detail below.

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:

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.

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.

In an acute subdural haemorrhage, there is usually clinical evidence of brain injury at the outset. A lucid interval between initial loss of consciousness and later deterioration 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 seen more commonly after relatively inconsequential injury, particularly in the elderly.

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