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Coagulation Abnormalities Following Primary Intracerebral Hemorrhage

机译:原发性脑出血后凝血异常

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Systemic hemostatic activation following primary intracerebral hemorrhage (PICH) has been described, particularly with intraventricular or subarachnoid extension, Our objective was to study the occurrence of abnormalities of coagulation as measured by partial thromboplastin time, international normalized ratio, and platelet count in patients with PICH and no obvious cause for a pre-existing coagulopathy. Charts of PICH patients admitted between November 1991 and December 2001 were reviewed We excluded patients with an underlying lesion, cranial trauma, anticoagulation, liver failure or sepsis. All patients had partial thromboplastin time, international normalized ratio, and platelet count measured on admission. An international normalized ratio > 1,4, partial thromboplastin time > 35, and platelet count < 100,000 were considered abnormal based on standardized values for our laboratory. All patients underwent a computed tomography (CT) scan on admission. Repeat CT was obtained for evidence of neurological deterioration. One hundred ninety-two patients with intracerebral hemorrhage were studied. Thirty-seven were excluded because of a possible underlying cause for a pre-existing coagulopathy. Thirteen of one hundred and fifty-five (8.4%) patients were found to have a coagulopathy based on our criteria. Three of thirteen (23%) patients with coagulopathy versus 3/142 (2%) without suffered neurological deterioration with evidence of hematoma enlargement (P = .008). Eleven of sixty-seven (17%) patients with intraventricular /subarachnoid extension versus 2/88 (2%) without had a coagulopathy (P = .002). Eight of thirteen (61%) patients with coagulopathy versus 29/142 (20%) without were dead at 30 days (P = .003). Coagulation abnormalities without an obvious etiology that may be consistent with low grade disseminated intravascular coagulation are seen in 8.4% of patients with PICH and are associated with extension into the subarachnoid and intraventricular compartments, neurological deterioration with hematoma expansion, and mortality at 30 days. This may represent a target for therapeutic intervention.
机译:已经描述了原发性脑出血(PICH)后的全身止血激活,尤其是脑室内或蛛网膜下腔扩张时。我们的目标是研究通过部分凝血活酶时间,国际标准化比率和血小板计数对PICH患者凝血功能异常的发生也没有明显的原因导致先前存在凝血病。回顾了1991年11月至2001年12月间收治的PICH患者图表。我们排除了具有潜在病变,颅外伤,抗凝,肝功能衰竭或败血症的患者。所有患者入院时均具有部分凝血活酶时间,国际标准化比率和血小板计数。根据我们实验室的标准值,国际标准化比率> 1,4,部分凝血活酶时间> 35和血小板计数<100,000被视为异常。所有患者入院时均接受计算机断层扫描(CT)扫描。重复进行CT检查以发现神经功能恶化。研究了192例脑出血患者。由于可能存在先前存在的凝血病的潜在原因,三十七位患者被排除在外。根据我们的标准,发现一百三十五名患者(8.4%)患有凝血病。十三名(23%)患有凝血病的患者与三名/ 142名(2%)没有神经系统恶化且有血肿扩大迹象的患者(P = .008)。 67例(17%)脑室内/蛛网膜下腔扩张患者中有11例患者,而2/88(2%)没有凝血病的患者(P = .002)。 13例有凝血病的患者中有8例(61%)则在30天时死亡,而29/142例(20%)没有死亡(P = .003)。在8.4%的PICH患者中观察到凝血异常异常而没有明显的病因,可能与低度弥散性血管内凝血相一致,并与伸入蛛网膜下腔和脑室内腔,神经系统恶化,血肿扩大以及30天死亡率相关。这可能代表治疗干预的目标。

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