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因血管痉挛导致延迟性缺血性神经功能缺损患者进行高血容量治疗的颅内并发症。

Intracranial complications of hypervolemic therapy in patients with a delayed ischemic deficit attributed to vasospasm.

作者信息

Shimoda M, Oda S, Tsugane R, Sato O

机构信息

Department of Neurosurgery, Tokai University School of Medicine, Kanagawa, Japan.

出版信息

J Neurosurg. 1993 Mar;78(3):423-9. doi: 10.3171/jns.1993.78.3.0423.

Abstract

This investigation has revealed the frequency of various intracranial complications that may result from hypervolemic therapy for a delayed ischemic deficit following subarachnoid hemorrhage (SAH). Among 323 patients with SAH, 112 patients developed a delayed ischemic deficit, 94 of whom underwent hypervolemic therapy. Infarction due to vasospasm was found ultimately in 43 of these 94 patients. Twenty-six patients (28%) developed an intracranial complication during hypervolemic therapy: cerebral edema was aggravated in 18, and a hemorrhagic infarction developed in eight. In 13 of 18 patients with aggravation of edema, delayed ischemic deficit developed within 6 days after the SAH; at that time, a massive new infarction was found in four and edema in 10 patients. After hypervolemic therapy, the 18 patients with aggravation of edema deteriorated rapidly, and 14 of them died. In every case in which hemorrhagic infarction followed hypervolemic therapy, a new infarct was found on computerized tomography (CT) when the delayed ischemic deficit became apparent. Hemorrhagic infarction developed as the delayed ischemic deficit resolved, with one exception. In patients who sustained no complication from hypervolemia, the incidence of both massive new infarction and edema at the time when the delayed ischemic deficit was manifested was only 1%. In 44 of 68 patients who sustained no complication from hypervolemia, the delayed ischemic deficit was manifested on or after the 7th day following the SAH. This study suggests that hypervolemic therapy is contraindicated in a patient who is found to have a massive abnormality on CT at the time when a delayed ischemic deficit is manifested, especially when it occurs within 6 days after the SAH. To avoid hemorrhagic infarction, it is important to discontinue hypervolemic therapy as soon as the delayed ischemic deficit resolves.

摘要

本研究揭示了蛛网膜下腔出血(SAH)后为治疗迟发性缺血性神经功能缺损而进行的高血容量疗法可能导致的各种颅内并发症的发生率。在323例SAH患者中,112例出现迟发性缺血性神经功能缺损,其中94例接受了高血容量疗法。这94例患者中最终有43例因血管痉挛发生梗死。26例患者(28%)在高血容量治疗期间出现颅内并发症:18例脑水肿加重,8例发生出血性梗死。在18例脑水肿加重的患者中,13例在SAH后6天内出现迟发性缺血性神经功能缺损;此时,4例发现有大量新梗死灶,10例有脑水肿。高血容量治疗后,18例脑水肿加重的患者病情迅速恶化,其中14例死亡。在高血容量治疗后发生出血性梗死的每一例中,当迟发性缺血性神经功能缺损明显时,计算机断层扫描(CT)均发现有新梗死灶。除1例例外,出血性梗死在迟发性缺血性神经功能缺损缓解时发生。在未发生高血容量并发症的患者中,迟发性缺血性神经功能缺损出现时大量新梗死灶和脑水肿的发生率仅为1%。在68例未发生高血容量并发症的患者中,44例在SAH后第7天或之后出现迟发性缺血性神经功能缺损。本研究提示,当迟发性缺血性神经功能缺损出现时,尤其是在SAH后6天内出现,且CT发现有大量异常的患者,高血容量疗法是禁忌的。为避免出血性梗死,迟发性缺血性神经功能缺损一旦缓解,应立即停止高血容量治疗。

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