C EREBRAL edema and infarction are common causes of morbidi ty and dea th af ter rup ture or surgical t reatment of an intracranial aneurysm. Crompton 2 found infarct ion in 75% of his autopsied cases of rup tured aneurysms and felt it should be considered significant from the s tandpoint of morbid i ty , if not mortal i ty . Schneck and Kricheff 7 suggested tha t vasospasm migh t be responsible for infarction of unknown etiology in their autopsied series. In an effort to improve or prevent circulatory impa i rment caused by spasm or other factors, we have resorted to Rheomacrodex , t a low-molecular-weight dextran tha t supposedly improves the microcirculation by decreasing cellular aggregation, which can lead to stasis, thrombosis, and finally to cerebral edema or infarction. The beneficial use of Rheolnacrodex in other fields 4,s,9 and its an t i thrombot ic effect in small vessel surgery ~,t~ p rompted our clinical investigation. In addition, Cyrus, et al., s have demonstrated its protect ive action after experimental occlusion of the middle cerebral ar tery, while H a m m a r g r e n , et al.,S have shown tha t it protec ts the brain from damaging doses of Hypaque . Our repor t is based on a series of 101 cases of proven intracranial aneurysm. Nine tyfive pat ients were operated on by the attending and resident staffs of the Neurological Ins t i tu te of New York since April, 1964. Six pat ients , too sick for surgery, were not operated upon. F o r most of the 95 intracranial operat ions, modera te hypo the rmia (r to 30~ t e m p o r a r y clips, and intravenous urea or ]Y[annitol were used. Th i r ty eight control pa t ients were not t reated with
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McMurtry et al. (1967) studied this question.
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