Pathophysiology of delayed ischaemic dysfunction after subarachnoid haemorrhage: experimental and clinical data.

Cerebral arterial spasm from subarachnoid haemorrhage (SAH) may be associated with the clinical syndrome of delayed cerebral ischaemic dysfunction, but the two conditions are by no means synonymous. Patients in good clinical condition may be seen with severe vasospasm and vice versa. A variety of mechanisms may be responsible for the neurological dysfunction: current evidence indicates that most of these mechanisms produce a reduction in cerebral blood flow (CBF). In the early stages after SAH, there is a loss of autoregulation so that reduction in cerebral perfusion pressure (CPP) may produce ischaemia. This fall in CPP may be due to elevated intracranial pressure (ICP) or reduced mean arterial blood pressure (MABP). Delayed cerebral ischaemic dysfunction following SAH is a clinical syndrome which may also be caused by re-bleeding, hydrocephalus, dehydration, reduced cardiac output and/or blood pressure, hyperglycemia or epilepsy. Experimental evidence has indicated that at the time of an intracranial haemorrhage there is a profound and extensive focal ischaemic insult. The severity of the ischaemia depends upon the nature, size and rapidity of onset of haemorrhage. The focal ischaemic lesion around an intracerebral haemorrhage becomes smaller with the passage of time and is the result of two interacting phenomena: a) The physical properties of the haemorrhage result in increased local tissue pressure around the lesion. This produces squeezing of the microcirculation and focal ischaemia. b) Vasoconstrictor elements in blood produce spasm which may further reduce CBF, sometimes even remotely from the lesion. Treatment of delayed ischaemia therefore depends upon its cause.