摘要： 目的 探讨阿替普酶静脉溶栓过程中微循环障碍症状加重原因及临床转归。方法 回顾13例阿替普酶静脉溶栓治疗过程中症状与体征加重患者的临床资料，分析其发病特点及临床转归，总结急救经验。结果 13例患者均为颅内大动脉狭窄造成载体动脉封闭穿支所致梗死（颈内动脉系统梗死8 例、椎-基底动脉系统梗死5 例），溶栓治疗过程中症状加重主要表现为皮质缺血症状、四肢瘫痪、意识障碍加重；影像学检查显示皮质及分水岭区多发点状新鲜梗死灶，或小脑及脑干梗死灶数目增加。经对症治疗均获得良好预后，溶栓治疗后24h（美国国立卫生研究院卒中量表 评分：8.69 ± 3.42 ）和 3 个月随访时（改良Rankin量表评分：0.94 ± 0.37 ）神经功能缺损程度和预后明显改善。结论 阿替普酶静脉溶栓治疗过程中临床症状与体征加重与多种因素有关，栓子“崩解”所致微循环障碍可能为其主要原因。对于溶栓过程中出现的并发症，经积极救治、对症治疗患者仍能获得良好预后。

关键词: 脑缺血, 卒中, 组织型纤溶酶原激活物, 血栓溶解疗法, 脑静脉

Abstract: Objective  To explore the causes of aggravation of microcirculation disorders in the process of intravenous thrombolysis with alteplase and the clinical outcomes. Methods  The clinical data of the aggravated signs and symptoms of 13 cases treated by alteplase were reported, and the onset characteristics and clinical outcomes were analysed to summarize emergency experiences. Results  There were 13 patients with stenosis of intracranial large arteries occurred perforating branch infarctions caused by the blocking of carried arteries (8 cases in internal carotid system, 5 cases in vertebral-basilar system). In the process of thrombolytic therapy, main aggravated presentations including cortical ischemic symptom, quadriplegia, exacerbated disturbance of consciousness were seen. Imaging examinations showed multiple new petechial ischemic foci in cortex and watershed region or increasing of infarct foci in cerebellum and brain stem. The prognosis was favorable after expectant treatment. NIHSS score was 8.69 ± 3.42 at 24 h after treatment, and mRS score was 0.94 ±0.37 at 3 month-follow-up. Neurologic deficit and quality of life were evidently improved. Conclusion  In the course of intravenous thrombolytic therapy with alteplase. Aggravated clinical signs and symptoms may be related to various factors. Emboli disintegration inducing microcirculation disorder is inferred to be the main cause. For patients presenting aggravated signs and symptoms in thrombolysis process, favorable outcomes may occur as long as intensive care and timely treatment are performed. 

Key words: Brain ischemia, Stroke, Tissue plasminogen activator, Thrombolytic therapy, Cerebral veins