Hemorrhagic infarction following vasospasm due to ruptured intracranial aneurysms

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Among 293 cases admitted from May 1976 to December 1980, due to ruptured intracranial aneurysms, 219 cases (91 anterior communicating, 67 internal carotid, and 61 middle cerebral aneurysms) admitted within 14 days after the onset without intracerebral hematoma, sudden death, or troubled operation were chosed for analysis. Among which 153 cases (70%) developed angiographically detectable vasospasm, 56 cases (26%) presented symptomatic vasospasm and 44 cases (20%) showed cerebral infarction due to vasospasm. 14 (32%) of these 44 cases revealed hemorrhagic infarction confirmed by CT. Detection of hemorrhagic infarction by CT occurred between 13 and 42 days after the onset (average: 24±7 days). This period almost coincided with that of the maximum contrast enhancement of the infarcted region (23±4 days) and that of angiographical relaxation of vasospasm (21±4 days). Among these 14 cases, 71% showed capillary blush and 64% revealed early venous filling just before the appearance of hemorrhagic infarction. The incidence of these phenomena were clearly higher than in the cases with ischemic infarction only. On CT examination, 11 cases revealed a high density area mainly in the cortical area, 2 cases in the subcortical area, and one case accompanied ventricular hematoma. Twelve cases developed hemorrhagic infarction without a worsening of the neurological signs with a slight increase of brain swelling. However, one case died due to severe brain swelling and another case needed ventricular drainage because of intraventricular hematoma. The case who died was of the “swelling stage type”. Severe brain swelling due to ischemia and increased perfusion pressure due to a slight release of vasospasm with concomitant arterial hypertension must have caused the hemorrhagic infarction. The other 13 cases fell into the “neovascularization stage type”. Here, increased perfusion pressure following relaxation of vasospasm and development of neovascularization lacking blood brain barrier after ischemic cerebral infarction might explain the cause of hemorrhagic infarction. These phenomena coincided with the decreasing stage of brain swelling and the stage of marked contrast enhancement on CT. In both types, increase of cerebral blood flow despite low metabolism in the damaged brain—the concept of “luxury perfusion syndrome”—may explain the development of hemorrhagic infarction. Concerning the management of vasospasm, care should be paid not to worsen hemorrhagic infarction by monotonus methods for the increase cerebral blood flow such as the induced hypertensive-hypervolemic therapy. Appropriate evaluation of the ischemic stage is important for suitable treatment.