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平均动脉压极度升高后脑血管造影显示的脑血管痉挛几乎完全缓解:病例报告

Near-complete resolution of angiographic cerebral vasospasm after extreme elevation of mean arterial pressure: case report.

作者信息

Ray Wilson Z, Moran Christopher J, Derdeyn Colin P, Diringer Michael N, Dacey Ralph G, Zipfel Gregory J

机构信息

Department of Neurological Surgery, Washington University School of Medicine, St Louis, MO 63110, USA.

出版信息

Surg Neurol. 2009 Oct;72(4):347-53; discussion 353-4. doi: 10.1016/j.surneu.2008.10.006. Epub 2009 Jan 14.

Abstract

BACKGROUND

Cerebral vasospasm is a widespread and potentially treatable complication after aneurysmal SAH. Aggressive treatment often includes hemodynamic augmentation, although the exact mechanism by which such therapy leads to improved cerebral blood flow and reduced neurologic deficits is incompletely established. This case report is only the second to provide compelling evidence that hypertension can lead to direct dilation of vasospastic arteries, thereby providing valuable insight into its potential mechanism.

CASE DESCRIPTION

We present a patient with SAH from a ruptured anterior communicating artery aneurysm who developed marked decline in mental status on posthemorrhage day 11, consistent with symptomatic cerebral vasospasm. A diagnostic cerebral angiogram was performed demonstrating extensive and diffuse cerebral vasospasm. After receiving a nonselective slow infusion of verapamil, the patient developed an episode of extreme hypertension. Repeat angiography immediately after hypertensive crisis revealed near-complete resolution of the previously noted cerebral vasospasm. Rapid improvement in the patient's neurologic status ensued.

CONCLUSION

The present case illustrates that extreme hypertension can lead to direct dilation of vasospastic arteries and suggests that hypertensive-type hemodynamic therapy may act not only through increasing the pressure gradient across vasospastic arteries but also via direct induction of arterial vasodilation.

摘要

背景

脑血管痉挛是动脉瘤性蛛网膜下腔出血(SAH)后一种广泛存在且可能可治疗的并发症。积极治疗通常包括血流动力学强化,尽管这种治疗导致脑血流量改善和神经功能缺损减少的确切机制尚未完全明确。本病例报告是第二篇提供有力证据表明高血压可导致血管痉挛动脉直接扩张的报告,从而为其潜在机制提供了有价值的见解。

病例描述

我们报告一名因前交通动脉瘤破裂导致SAH的患者,在出血后第11天出现精神状态明显下降,符合症状性脑血管痉挛。进行了诊断性脑血管造影,显示广泛弥漫性脑血管痉挛。在接受非选择性缓慢输注维拉帕米后,患者出现了一次极度高血压发作。高血压危象后立即进行的重复血管造影显示,先前记录的脑血管痉挛几乎完全缓解。随后患者的神经功能状态迅速改善。

结论

本病例表明极度高血压可导致血管痉挛动脉直接扩张,并提示高血压型血流动力学治疗可能不仅通过增加血管痉挛动脉两端的压力梯度起作用,还可通过直接诱导动脉血管舒张起作用。

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