颅脑创伤相关性凝血障碍发病机制

Pathogenesis of traumatic brain injury-associated coagulopathy:a review

在颅脑创伤患者中,凝血功能障碍较为常见。该病发病机制复杂,主要包括了凝血系统异常、低灌注、血液稀释、代谢性酸中毒、低体温、炎症反应等多种因素。其中,凝血系统异常又包括了组织因子释放、纤溶亢进和血小板异常。近年来,组织因子释放激活外源性凝血途径的主导地位受到挑战,低灌注及其相关蛋白C通路的地位日益受到重视。在凝血障碍后期,炎症反应的作用也逐渐受到关注。本文将就上述颅脑创伤相关性凝血障碍发病机制作一综述。

Coagulation disorder, also known as coagulopathy, is commonly associated with traumatic brain injury. The exact mechanisms underlying their association are poorly understood although multiple factors, including abnormalities of coagulation system, hypoperfusion, dilution, metabolic acidosis, hypothermia and inflammation, have been proposed. The abnormalities of coagulation system mainly include tissue factor release, hyperfibrinolysis, and platelet abnormalities. Recently, the dominant role of tissue factor has been challenged by hypoperfusion and the related protein C signaling pathway. The role of inflammation is gradually acknowledged in the late stage of traumatic brain injury-associated coagulopathy. This review was aimed to discuss the above pathogenesis.