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[脑梗死与血管再通的动态病理生理学。I. 缺血性脑水肿]

[Dynamic pathophysiology of cerebral infarction and revascularization. I. Ischemic cerebral edema].

作者信息

Kawase T, Mizukami M, Tazawa T, Araki G, Nagata K

出版信息

No To Shinkei. 1982 Nov;34(11):1077-83.

PMID:7159539
Abstract

A natural history of ischemic cerebral edema was analyzed in 100 patients with occlusive cerebrovascular diseases admitted within one week of onset, with serial computed tomography (CT) and angiograms. Cerebral edema was defined as a low-density area with mass sign on CT. A total of 446 studies of CT were performed. In 40 patients with major completed stroke admitted 24 hours of onset, a total of 73 studies of CT were taken within 48 hours of onset, and a timing of appearance of cerebral edema was analyzed. Patients were allocated to two groups according to the findings on angiograms; 68 patients who showed occlusive lesions on sequential angiograms (the group of no-recanalization), and 32 patients who showed reopening of occluded vessels on the first or sequential angiograms (the group of no-recanalization). In the group of no-recanalization a low-density area gradually appeared between 6 and 24 hours of onset A. mass sign reached its peak on the 3rd day with a peak incidence of 56%, and midline shift was present in 30% of the cases. It was resolved within 2 weeks in most cases. In the group of recanalization, a low density area appeared after 4 hours and rapidly increase after 6 hours. All patients had a low-density area at 12 hours of onset. A mass sign progressed until the 6th day with a peak incidence of 82%, and midline shift was present in 50% of the cases. The duration of mass sign was longer than that in the group of no-recanalization. These results suggest that the permissible duration of ischemia is considered to be within 6 hours of onset in profound ischemia. After 6 hours, ischemic tissue damage may not be reversible by the revascularization, even if CT shows no change during ischemia. An abrupt revascularization may not contribute to the recovery of brain damage, but accelerate the ischemic cerebral edema.

摘要

对发病一周内入院的100例闭塞性脑血管疾病患者,通过系列计算机断层扫描(CT)和血管造影分析了缺血性脑水肿的自然病程。脑水肿在CT上被定义为有占位征象的低密度区。共进行了446次CT检查。在40例发病24小时内入院的严重完全性卒中患者中,发病后48小时内共进行了73次CT检查,并分析了脑水肿出现的时间。根据血管造影结果将患者分为两组;68例在连续血管造影上显示闭塞病变的患者(未再通组),以及32例在首次或连续血管造影上显示闭塞血管再通的患者(再通组)。在未再通组中,低密度区在发病后6至24小时逐渐出现,占位征象在第3天达到高峰,高峰发生率为56%,30%的病例出现中线移位。大多数病例在2周内消退。在再通组中,低密度区在4小时后出现,6小时后迅速增大。所有患者在发病12小时时均有低密度区。占位征象持续进展至第6天,高峰发生率为82%,50%的病例出现中线移位。占位征象的持续时间比未再通组更长。这些结果表明,在严重缺血时,允许的缺血持续时间被认为是发病后6小时内。6小时后,即使CT在缺血期间无变化,缺血组织损伤可能无法通过血管再通逆转。突然的血管再通可能无助于脑损伤的恢复,反而会加速缺血性脑水肿。

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