Head Injury

SECONDARY BRAIN DAMAGE (contd)

2. Cerebral swelling

This may occur with or without intracranial haematoma. It results from either vascular engorgement or an increase in extra- or intracellular fluid, the exact causative mechanisms in different injuries remaining unknown.

3. Tentorial/tonsillar herniation (syn. 'cone')

It is unlikely that high intracranial pressure alone directly damages neuronal tissue, but brain damage occurs as a result of tonsillar or tentorial herniation (see page 77). A progressive increase in intracranial pressure due to a supratentorial haematoma initially produces midline shift. Herniation of the medial temporal lobe through the tentorial hiatus follows (lateral tentorial herniation), causing midbrain compression and damage. Uncontrolled lateral tentorial herniation or diffuse bilateral hemispheric swelling will result in central tentorial herniation. Herniation of the cerebellar tonsils through the foramen magnum (tonsillar herniation) and consequent lower brainstem compression may follow central tentorial herniation or may result from the infrequently occurring traumatic posterior fossa haematoma.

Vasodilatation Oedema

Cerebral swelling

Subfalcine ^ herniation

Subfalcine ^ herniation

Lateral tentorial herniation

Tonsillar herniation

Tonsillar herniation

4. Cerebral ischaemia

Cerebral ischaemia commonly occurs after severe head injury and is caused by either hypoxia or impaired cerebral perfusion. In the normal subject, a fall in blood pressure does not produce a drop in cerebral perfusion since 'auto-regulation' results in cerebral vasodilatation. After head injury, however, autoregulation is often defective and hypotension may have more drastic effects. Glutamate excess and free radical accumulation may also contribute to neuronal damage (see page 241).

Hypotension

I Cerebral perfusion

Lateral tentorial herniation

Central tentorial herniation

Î Intracranial pressure

Hypoxia

Cerebral ischaemia

5. Infection

Compound depressed fracture Basal fracture

Dural tear

Meningitis

Cerebral abscess

The presence of a dural tear provides a potential route for infection. This seldom occurs within 48 hours of injury. Meningitis may develop after several months or years.

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