Decrease in platelet count as an independent risk factor for symptomatic vasospasm following aneurysmal subarachnoid hemorrhage
Decrease in platelet count as an independent risk factor for symptomatic vasospasm following aneurysmal subarachnoid hemorrhage
复制标题
DOI：
10.3171/jns.2005.102.5.0882
复制
发表时间：
2005-05-01
影响因子：
4.1
通讯作者：
Endo, S
中科院分区：
文献类型：
--
作者：
Hirashima, Y;Hamada, H;Endo, S
目的。根据临床和实验研究的数据，脑血管痉挛患者的血小板消耗预计会增加。作者研究了蛛网膜下腔出血 (SAH) 患者血小板计数的连续变化，以及有和无症状血管痉挛 (SV) 患者之间血小板消耗的差异。与血小板计数相关的变量以及其他临床和放射学变量作为 SV 的独立预测因子进行分析。方法。 100 名在 SAH 发病后 48 小时内接受手术的连续患者被纳入该研究。回顾性检查 SAH 后的临床和放射学变量以及血细胞计数，包括红细胞、白细胞和血小板。其中 20 个变量被输入单变量和多变量分析以确定 SV 的预测因子。SAH 后，血小板计数降至最低，然后迅速增加至高于入院时记录的水平。这种变化是 SAH 所特有的，患有 SV 的患者的血小板消耗比没有 SV 的患者更严重。 SV 有三个独立的预测因素：最低血小板计数与入院计数的比率大于 0.7（比值比 [OR] 0.322，95% 置信区间 [CI] 0.124-0.834 p = 0.0196）和高血压病史（OR 0.338，95% CI 0.126-0.906，p = 0.0311）负显着（即减少 SV 的发生），Fisher Grade 3（OR 4.42，95% CI 1.48-13.2，p = 0.0077）为正显着（即增加 SV 的发生）。结论。血小板计数减少与 SV 发生之间的关联表明血小板在 SAH 后血管痉挛的病理生理学中发挥重要作用。
Object. Increased platelet consumption is expected in patients with cerebral vasospasm, according to data from clinical and experimental studies. The authors investigated sequential changes in platelet counts in patients with subarachnoid hemorrhage (SAH) and the difference in platelet consumption between patients with and those without symptomatic vasospasm (SV). Variables related to platelet count as well as other clinical and radiological variables were analyzed as independent predictors of SV.Methods. One hundred consecutive patients who had undergone surgery within 48 hours after SAH onset were entered in the study. Clinical and radiological variables and blood cell counts, including red blood cells, white blood cells, and platelets, after SAH were retrospectively examined. Twenty of these variables were entered into univariate and multivariate analyses to determine predictors for SV.After SAH, the platelet count decreased to a minimum and then increased rapidly to levels greater than those recorded on admission. This change was specific to SAH, and platelet consumption was more severe in patients with SV than in those without. There were three independent predictors of SV: a ratio of the lowest platelet count and the admission count greater than 0.7 (odds ratio [OR] 0.322, 95% confidence interval [CI] 0.124-0.834 p = 0.0196) and a history of hypertension (OR 0.338, 95% CI 0.126-0.906, p = 0.0311) were negatively significant (that is, decreases the occurrence of SV), and a Fisher Grade 3 (OR 4.42, 95% CI 1.48-13.2, p = 0.0077) was positively significant (that is, increases the occurrence of SV).Conclusions. The association between a decrease in platelet count and the occurrence of SV indicates the important role of platelets in the pathophysiology of vasospasm following SAH.