Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage.
Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage.
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DOI：
10.1186/cc5958
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Diringer MN
中科院分区：
文献类型：
--
作者：
Keyrouz SG;Diringer MN
血管痉挛是蛛网膜下腔出血（SAH）后发病和死亡的主要原因之一。放射性血管痉挛通常在初次出血后5 - 15天发生，并且在三分之一的患者中与临床上明显的迟发性缺血性神经功能缺损（DID）相关。这种可逆性血管病变的病理生理学尚未完全了解，但似乎涉及血管内皮细胞和平滑肌细胞水平的结构变化和生化改变。蛛网膜下腔的血液被认为是引发这些变化的原因。此外，低血容量和脑自动调节功能受损可能同时损害脑灌注。这些过程的综合作用可导致脑血流量减少，严重到引起缺血，导致梗死。结合临床、脑血管造影和经颅多普勒超声等因素进行诊断。尼莫地平是一种钙离子通道拮抗剂，是迄今为止唯一一种有效的治疗方法，已被证明可减轻DID的影响。结合血流动力学增强、经腔球囊血管成形术和血管扩张药物动脉内输注的积极治疗通常在不同程度上实施。一系列具有不同作用机制的药物已经在SAH相关的血管痉挛中进行了研究。目前，最有前途的是硫酸镁，3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂，一氧化氮供体和内皮素-1拮抗剂。本文综述了血管痉挛的既定和新兴疗法。
Vasospasm is one of the leading causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually develops between 5 and 15 days after the initial hemorrhage, and is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients. The pathophysiology of this reversible vasculopathy is not fully understood but appears to involve structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells. Blood in the subarachnoid space is believed to trigger these changes. In addition, cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function. The combined effects of these processes can lead to reduction in cerebral blood flow so severe as to cause ischemia leading to infarction. Diagnosis is made by some combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors. Nimodipine, a calcium channel antagonist, is so far the only available therapy with proven benefit for reducing the impact of DID. Aggressive therapy combining hemodynamic augmentation, transluminal balloon angioplasty, and intra-arterial infusion of vasodilator drugs is, to varying degrees, usually implemented. A panoply of drugs, with different mechanisms of action, has been studied in SAH related vasospasm. Currently, the most promising are magnesium sulfate, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, nitric oxide donors and endothelin-1 antagonists. This paper reviews established and emerging therapies for vasospasm.
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