Cerebral protection requires generalised sedation and abolition of seizures to reduce cerebral metabolic rate, cerebral oedema and neuronal damage during ischaemia and reperfusion.

Mannitol reduces cerebral interstitial water by the osmotic load. The effect is transient and at its best where the blood-brain barrier is intact. Interstitial water is mainly reduced in normal areas of brain and this may accentuate cerebral shift. Repeated doses accumulate in the interstitium and may eventually increase oedema formation; mannitol should only be given 4-5 times in 48h. In addition to its osmotic effect, there is some evidence of cerebral vasoconstriction due to a reduction in blood viscosity and free radical scavenging.

The loop diuretic effect of furosemide encourages salt and water loss. There may also be a reduction of CSF chloride transport reducing the formation of CSF.

Dexamethasone reduces oedema around space occupying lesions such as tumours. Steroids are not currently considered useful in head injury or after a cerebrovascular accident but benefit has been shown if given early after spinal injury. Steroids encourage salt and water retention and must be withdrawn slowly to avoid rebound oedema.

Nimodipine is used to prevent cerebral vasospasm during recovery from cerebrovascular insults. As a calcium channel blocker it also prevents calcium ingress during neuronal injury. This calcium ingress is associated with cell death. It is commonly used in the management of subarachnoid haemorrhage for 5-14 days.

Thiopental reduces cerebral metabolism thus prolonging the time that the brain may sustain an ischaemic insult. However, it also reduces cerebral blood flow, although blood flow is redistributed preferentially to ischaemic areas. Thiopental acutely reduces intracranial pressure and this is probably the main cerebroprotective effect. Seizure control is a further benefit. Despite these effects, barbiturate coma has not been shown to improve outcome in cerebral insults of various causes.


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