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目的:探讨高血压脑出血后血肿局部凝血酶与脑水肿、神经功能缺损的相关性。方法:本实验按临床病例对照研究的方法,在决定微创治疗组的同时选择同期住院的与之匹配的病例作常规治疗组对照。常规治疗组30例,微创治疗组32例。微创治疗组在常规治疗的基础上,行颅内血肿微创治疗。常规治疗组分别在起病1d、3d、5d和7d测定外周血清凝血酶浓度、神经功能缺损程度评分以及影像学的脑水肿比值。微创治疗组分别在起病1 d、3 d、5 d和7 d测定外周血清凝血酶浓度和血肿液中凝血酶浓度、神经功能缺损程度评分以及影像学的脑水肿比值。结果:常规治疗组和脑水肿比值第3、5天比值达高峰(P<0.05),微创治疗组脑水肿比值第3天达高峰(P<0.05)。两组脑水肿比值第1、3天比较无差异(P>0.05),第5、7天比较有差异(P<0.05),常规治疗组高于微创治疗组。血肿局部凝血酶浓度和脑水肿比值呈正相关(r=0.663,P<0.05);常规治疗组临床神经功能缺失程度评分第3、5天高于1、7天(P<0.05),微创治疗组临床神经功能缺失程度评分第3天达高峰(P<0.05)。两组第1、3天临床神经功能缺失程度评分比较无差异(P>0.05),第5、7天比较有差异(P<0.05),常规治疗组高于微创治疗组。血肿局部凝血酶和神经功能缺损评分呈正相关(r=0.553,P<0.05)。结论:血肿内凝血酶可能导致脑水肿形成以及影响神经功能缺损评分。
Objective: To investigate the correlation between local thrombin in hematoma and cerebral edema and neurological impairment after hypertensive intracerebral hemorrhage. Methods: According to the method of clinical case control study, we selected the matched matched cases in the same period as the routine treatment group to decide the minimally invasive treatment group. The conventional treatment group 30 cases, minimally invasive treatment group 32 cases. Minimally invasive treatment group on the basis of conventional treatment, minimally invasive intracranial hematoma treatment. Routine treatment group were measured at the onset of 1d, 3d, 5d and 7d determination of serum thrombin concentration, neurological deficit score and imaging brain edema ratio. In the minimally invasive treatment group, the peripheral blood thrombin concentration, the thrombin concentration in the hematoma fluid, the neurological deficit score, and the imaging cerebral edema ratio were measured on the 1st, 3rd, 5th, and 7th days after onset. Results: The ratio of routine edema and brain edema peaked on day 3 and day 5 (P <0.05), and the ratio of cerebral edema in minimally invasive treatment group reached the peak on the third day (P <0.05). There was no significant difference between the two groups on the 1st and 3rd day (P> 0.05). There was significant difference on the 5th and 7th day (P <0.05). The conventional treatment group was higher than the minimally invasive treatment group. The hematoma local thrombin concentration was positively correlated with the ratio of cerebral edema (r = 0.663, P <0.05). The score of clinical neurological deficit in the conventional treatment group was higher than that of the first and third days (P <0.05) The scores of clinical neurological deficit reached the peak on the third day (P <0.05). There was no significant difference in the score of clinical neurological deficit between the two groups on the 1st and 3rd day (P> 0.05). There was significant difference on the 5th and 7th day (P <0.05). The routine treatment group was higher than the minimally invasive treatment group. Local thrombin and neurological deficit scores were positively correlated (r = 0.553, P <0.05). Conclusion: Thrombin in the hematoma may lead to the formation of cerebral edema and affect the neurological deficit score.