PREVENTION OF CEREBRAL ISCHAEMIA/INFARCTION
Despite considerable clinical and experimental research, cerebral ischaemia is still a major cause of morbidity and mortality after subarachnoid haemorrhage. In recent years some advances have proved beneficial.
Calcium antagonists: several large studies have confirmed that Nimodipine and Nicardipine both reduce the incidence of cerebral infarction by about one third and improve outcome. Whether these act by improving collateral circulation, by reducing the harmful effect of calcium flooding into brain cells or by reducing cerebral 'vasospasm' remains uncertain.
Avoidance of antihypertensive therapy: antihypertensive therapy was once widely used after SAH to reduce 'reactive' hypertension and theoretically to minimise the risk of rebleeding. In the normal subject a drop in BP results in cerebral vasodilatation to maintain cerebral flow (autoregulation, page 75). After SAH, autoregulation is often impaired; a drop in BP causes a reduction in cerebral blood flow with a subsequent risk of cerebral ischaemia. Accumulated evidence shows that patients with SAH on antihypertensive therapy have a significantly higher risk of cerebral infarction.
High fluid intake: maintenance of a high fluid input (3 litres per day) may help prevent a fall in plasma volume from sodium and fluid loss. If hyponatraemia develops do not restrict fluids (this significantly increases the risk of cerebral infarction). If sodium levels fall below 130 mmol/1, give fludrocortisone or hypertonic saline.
Plasma volume expansion: expanding the plasma volume with colloid, e.g. plasma proteins, dextran 70, Haemacel, increases blood pressure and improves cerebral blood flow. This should be given either prophylactically in high risk patients (heavy cisternal blood load on CT scan or with high Dopplcr velocities) or at the first clinical sign of ischaemia. If clinical evidence of ischaemia develops despite this treatment, then combine with:
Hypertensive therapy: treatment with inotropic agents, e.g. dobutamine, increases cardiac output and blood pressure. Since cerebral autoregulation commonly^fails after subarachnoid haemorrhage, increasing blood pressure increases cerebral blood flow. Up to 70% of ischaemic neurological deficits developing after aneurysm operations can be reversed by inducing hypertension; often a critical level of blood pressure is evident.
Early recognition and treatment of a developing neurological deficit may prevent progression from ischaemia to infarction. Delayed treatment may merely aggravate vasogenic oedema in an ischaemic area. This technique of induced hypertension is now widely applied, with good results, but requires careful, intensive monitoring. In view of the risk of precipitating aneurysm rupture, it is reserved until after aneurysm clipping.
Brain protective agents: several newly developed neuroprotective drugs (other than the calcium antagonists (see page 241) are currently under study in patients with subarachnoid haemorrhage but as yet their value remains unknown.
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