Cerebral Aneurysms Complications


Following subarachnoid haemorrhage, patients are at risk of developing cerebral ischaemia or infarction and this is an important contributory factor to mortality and morbidity. Cerebral ischaemia/infarction may occur as an immediate and direct result of the haemorrhage, but more often develops 4-12 days after the onset, either before or after operation - hence the term 'delayed cerebral ischaemia'. Approximately 25% of patients develop clinical evidence of delayed ischaemia/ infarction; of these 25% die as a result. About 10% of the survivors remain permanently disabled.

Incidence of cerebral ischaemia/infarction in 217 patients with SAH

Estimated infarction risk per day

Adapted from Vcrmculen, Lindsay, Murray et al 1984 New England Journal of Medicine 311 432-437

Estimated infarction risk per day

5-6 7-8 9-io 11-12 13-14 15-16 17-18 19-20 Days from SAH to onset Aetiology of cerebral ischaemia/infarction

Several factors probably contribute to the development of cerebral ischaemia or infarction: ' Vasospasm': arterial narrowing on angiography occurs in up to 60% of patients after SAH and is either focal or diffuse. The development of 'vasospasm' shows a similar pattern of delay to that of cerebral ischaemia.

The angiogram appearance was initially thought to result from arterial constriction; this may be so, but the pathogenesis of 'vasospasm' now seems more complex. Many vasoconstrictive substances either released from the vessel wall or from the blood clot appear in the CSF after SAH, e.g. serotonin, prostaglandin, oxyhaemoglobin, but numerous studies with vasoconstrictor antagonists have failed to reverse the angiographic narrowing or to reduce the incidence of ischaemia. This failure may be a result of the arteriopathic changes which have been observed in the vessel wall. Only calcium antagonists appear to have a beneficial effect (see page 241).

Blood clot

3-4 days

Subintimal oedema,. lymphocyte, leucocyte and macrophage infiltration and myonecrosis

The greater the amount of blood in the basal cisterns (as shown on CT scan), the higher the incidence of arterial narrowing and associated ischaemic deficits.

Inflammatory reaction around tunica adventitia

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