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白细胞增多作为动脉瘤性蛛网膜下腔出血后脑血管痉挛的独立危险因素。

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

作者信息

McGirt Matthew J, Mavropoulos John C, McGirt Laura Y, Alexander Michael J, Friedman Allan H, Laskowitz Daniel T, Lynch John R

机构信息

Division of Neurology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.

出版信息

J Neurosurg. 2003 Jun;98(6):1222-6. doi: 10.3171/jns.2003.98.6.1222.

Abstract

OBJECT

The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm.

METHODS

A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 +/- 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5-15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02-1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01-0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04-0.45). A serum leukocyte count greater than 15 x 10(9)/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74-6.38).

CONCLUSIONS

During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 x 10(9)/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

摘要

目的

识别蛛网膜下腔出血(SAH)后发生脑血管痉挛风险增加的患者,可能有助于采取更积极的治疗措施并改善患者预后。然而,需注意入院时血凝块大小仍是唯一经一致证实会增加SAH后脑血管痉挛风险的因素。本研究的目的是评估临床、影像学或血清学变量是否可用于识别发生脑血管痉挛风险增加的患者。

方法

对1995年至2001年间入住作者所在机构的所有动脉瘤性或自发性非动脉瘤性SAH患者进行回顾性研究。评估潜在血管疾病(高血压或慢性糖尿病)、Hunt和Hess分级及Fisher分级、患者年龄、动脉瘤位置、开颅手术与血管内动脉瘤栓塞术的比较、入院时用药情况、术后类固醇药物使用情况以及发热、脑积水或白细胞增多症的发生情况,将其作为血管痉挛的预测因素。在回顾期间,224例患者接受了SAH治疗。101例患者(45%)发生了症状性血管痉挛。血管痉挛高峰出现在SAH后5.8±3天。血管痉挛有四个独立预测因素:Fisher 3级SAH(比值比[OR]7.5,95%置信区间[CI]3.5 - 15.8)、血清白细胞计数峰值(OR 1.09,95% CI 1.02 - 1.16)、大脑后动脉(PCA)动脉瘤破裂(OR 0.05,95% CI 0.01 - 0.41)和自发性非动脉瘤性SAH(OR 0.14,95% CI 0.04 - 0.45)。血清白细胞计数大于15×10⁹/L与发生血管痉挛的可能性独立增加3.3倍相关(OR 3.33,95% CI 1.74 - 6.38)。

结论

在这7年期间,自发性非动脉瘤性SAH和破裂的PCA动脉瘤分别使发生血管痉挛的几率降低了7倍和20倍。入院时存在Fisher 3级SAH或白细胞计数峰值大于15×10⁹/L分别使血管痉挛的几率增加了7倍和3倍。监测血清白细胞计数可能有助于早期诊断和治疗血管痉挛。

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