Raabe Andreas, Zimmermann Michael, Setzer Matthias, Vatter Hartmuth, Berkefeld Jürgen, Seifert Volker
Department of Neurosurgery and Neurosurgery Center, Johann Wolfgang Goethe University, Frankfurt am Main, Germany.
Neurosurgery. 2002 May;50(5):1006-13; discussion 1013-4. doi: 10.1097/00006123-200205000-00013.
Sodium nitroprusside (SNP) was recently suggested as a treatment for cerebral ischemia in patients with severe, medically refractory vasospasm after subarachnoid hemorrhage. In this study, we sought to objectify the effect on cerebral hemodynamics and oxygenation (PbrO2) when using intraventricular SNP as a last resort therapy in poor-grade patients with subarachnoid hemorrhage; severe, medically refractory vasospasm; and compromised cerebral blood flow.
Thirteen of 185 consecutive patients with subarachnoid hemorrhage developed severe, medically refractory vasospasm and were treated with intraventricular SNP. All of these patients' neurological conditions were classified as Hunt and Hess Grade IV. SNP doses ranged from 10 to 40 mg with single-dose treatment and from 2 to 8 mg/h with continuous infusion. Angiography or PbrO2 measurement was used to assess the treatment effects.
In 6 of the 13 patients, SNP improved cerebral hemodynamics, as demonstrated by increased PbrO2 or decreased cerebral circulation time. Only 1 patient showed increased diameter of the spastic vessel, however. Maximum increase in PbrO2 ranged from 5 to 52 mmHg. Adverse effects were hypertension in five patients, vomiting in three patients, and cardiac arrhythmia in one patient. Cerebral infarctions caused by vasospasm occurred in 6 (46%) of the 13 patients. No differences between SNP responders and SNP nonresponders were noted.
In patients with severe, medically refractory vasospasm, intraventricular SNP may improve PbrO2 and cerebral blood flow, but the effect is highly variable. On the basis of the improvements we observed in 6 of 13 patients, intraventricular SNP administration is justified as a last resort therapy in patients with cerebral ischemia and impending infarction. Our findings suggest that SNP may be more effective when initiated early and administered continuously.
最近有人提出硝普钠（SNP）可用于治疗蛛网膜下腔出血后出现严重、药物难治性血管痉挛的患者的脑缺血。在本研究中，我们试图明确在病情较差的蛛网膜下腔出血患者中，当作为最后手段使用脑室内SNP治疗严重、药物难治性血管痉挛且脑血流受损时，其对脑血流动力学和氧合（脑组织氧分压，PbrO2）的影响。
185例连续的蛛网膜下腔出血患者中有13例发生严重、药物难治性血管痉挛，并接受了脑室内SNP治疗。所有这些患者的神经状况均被分类为Hunt和Hess IV级。SNP单剂量治疗时剂量范围为10至40mg，持续输注时为2至8mg/h。采用血管造影或PbrO2测量来评估治疗效果。
13例患者中有6例，SNP改善了脑血流动力学，表现为PbrO2升高或脑循环时间缩短。然而，只有1例患者痉挛血管直径增大。PbrO2的最大升高范围为5至52mmHg。不良反应包括5例患者出现高血压，3例患者出现呕吐，1例患者出现心律失常。13例患者中有6例（46%）发生了由血管痉挛引起的脑梗死。SNP反应者和非反应者之间未观察到差异。
在严重、药物难治性血管痉挛患者中，脑室内SNP可能改善PbrO2和脑血流量，但效果差异很大。基于我们在13例患者中的6例观察到的改善情况，脑室内给予SNP作为脑缺血和即将发生梗死患者的最后手段治疗是合理的。我们的研究结果表明，SNP早期开始并持续给药可能更有效。
