创伤性脑损伤后凝血功能异常发生机制的研究进展

Research progress of the mechanism of coagulation dysfunction after traumatic brain injury

创伤性脑损伤（Tmumatic brain injury,TBI）因高致死率和致残率受到极大重视。TBI包括原发性损伤和继发性损伤两部分,其中,继发性损伤主要指TBI后出现脑水肿、脑缺血、进展性出血损伤（progressive hemorrhagic ingury,PHI）等。TBI原发性损伤在暴力损害发生时已经不可改变,具有PHI的颅脑损伤患者预后更差,文献报道PHI患者病死率约为20%（[1]）,所以对TBI的治疗更多在于处理TBI后的继发进展性损伤。

Traumatic brain injury（TBI）often accompanied by coagulation dysfunction which is called TBIrelated coagulopathy,it has many factors caused by a comprehensive coagulation system disorder and can not maintain the basic hemostatic effect after the traumatic bleeding,Its main manifestation is progressive hemorrhagic ingury（PHI）.In recent years,TBI-induced mechanisms of coagulation abnormalities have received more attention,the pathogenesis of TBI-related coagulopathy mainly includes hypoxia,tissue release,tissue activation,protein C activation,inflammatory response,endothelial cell function,hyperplasia,In this article,we reviewed The mechanism of coagulation dysfunction after traumatic brain injury which introduced as follows.