急性创伤性凝血病:分子机制及诊疗进展  

Acute coagulopathy of trauma: molecular mechanisms,diagnosis and management

作　　者：文科[1] 林哲绚[2] 韩溟[1] KEN Ke;LIN Zhe -xuan;HAN Ming(The Second Affiliated Hospital＆Shantou University Medical College＆Shantou＆Guangdong 515041 ,China;Bio-analytical Laboratory, Shantou University Medical College, Shantou,Guangdong 515041 ,China)

机构地区：[1]汕头大学医学院第二附属医院,广东515041 [2]汕头大学医学院第二附属医院生物分析实验室,广东515041

出　　处：《创伤外科杂志》2018年第1期72-76,共5页Journal of Traumatic Surgery

基　　金：国家自然科学基金资助项目(81172088);广东省科学技术厅-广东省中医药科学院联合科研专项基金资助项目(2012A032500009)

摘　　要：在世界范围内,创伤是引起人类死亡的第二大原因。虽然建立了区域性急救体系并且在创伤治疗方面有所提高,但是病死率仍居高不下。创伤所致的凝血障碍约占创伤后死因的40%。创伤性凝血病的发病机制复杂,涉及多个系统。目前认为,急性创伤性凝血病并非简单的消耗性凝血障碍,而是凝血系统、纤溶系统、组织灌注、炎症反应及血管内皮功能动态平衡的紊乱。因此,凝血障碍应以血小板及内皮细胞为核心的细胞分子模型解释而不是过去的血浆模型。现对创伤性凝血病的发病机制作一总结。Traumatic injury is the second leading cause of death worldwide. High mortality maintains despite establishment of regionalized trauma systems and advances in the management of injured patients. And as much as 40% of injury-related mortality is attributed to traumatic coagulopathy. The pathogenesis of acute coagulopathy of trauma（ ACo T） is complicated,owing to multiple factors,including coagulation system,fibrinolytic system,tissue perfusion,inflammation and endothelium. Therefore,ACo T is not merely a consumptive coagulopathy,but a systemic imbalance involving multiple factors,which is understood by cell-molecules based model rather than plasma based model. It is still critical to make a summary about the mechanisms of ACo T.

关 键 词：创伤 凝血障碍 纤溶亢进 活化蛋白C 

分 类 号：R641[医药卫生—外科学]