Delayed cerebral ischaemia (DCI) is a frequent complication of aneurysmal subarachnoid haemorrhage. It contributes substantially to the morbidity and mortality following subarachnoid haemorrhage. It has traditionally been thought to be due to symptomatic vasospasm related to subarachnoid haemorrhage 1, although other aetiologies have been proposed 8.
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Epidemiology
Delayed cerebral ischaemia is demonstrated radiologically in ~30% of patients 9. It usually manifests 4-14 days after subarachnoid haemorrhage.
Clinical presentation
Delayed cerebral ischaemia presents clinically as new focal neurological deficits or altered consciousness (decrease of ≥2 points in the Glasgow Coma Scale) 1,8,9.
Pathology
Although vasospasm has long thought to be the main cause of delayed cerebral ischaemia, other aetiologies have been proposed given the observation that areas of acute cerebral infarction may be identified following subarachnoid haemorrhage despite mild or absent vasospasm 6,8. Thus, it is felt that the pathogenesis of delayed cerebral ischaemia may be complex and multifactorial 9, incorporating vasospasm, but also encompassing factors such as microcirculatory dysfunction, thromboinflammation, and cortical spreading depolarisation 8. The extent to which this understanding overlaps with historical concepts which centralise arterial spasm remains nuanced and uncertain 11.
Radiographic features
Typical features of acute cerebral infarction are seen on CT and/or MRI. The two most common patterns of infarction are single cortical infarct (40%) and multifocal infarcts (often bilateral) distal to the ruptured aneurysm (50%) 5.
CT perfusion may be a useful adjunct 9 with relatively high sensitivity (82.1%) and specificity (79.6%), with changes in MTT most sensitive for the detection of delayed cerebral ischaemia 10.
Vasospasm is also often seen on CT angiography, MR angiography, DSA, or transcranial Doppler ultrasound 9.
Treatment and prognosis
Delayed cerebral ischaemia may be prevented with oral nimodipine, which should be initiated early 9. In patients with severe vasospasm who therefore may have a high risk of delayed cerebral ischaemia-related infarction, use of intra-arterial vasodilators (spasmolysis) or angioplasty may be necessary 9.
Presence of delayed cerebral ischaemia-related infarction is a poor prognostic sign, associated with a 5-fold increase in the odds of an unfavourable outcome at one year 7. Involvement of ischaemia to the left middle cerebral artery territory or either anterior cerebral artery territory are particularly associated with a poor prognosis 7.