White Nathan J
1Division of Emergency Medicine, University of Washington, Seattle, WA.
Hematology Am Soc Hematol Educ Program. 2013;2013:660-3. doi: 10.1182/asheducation-2013.1.660.
The identification and management of coagulopathy is a critical component of caring for the severely injured patient. Notions of the mechanisms of coagulopathy in trauma patients have been supplanted by new insights resulting from close examination of the biochemical and cellular changes associated with acute tissue injury and hemorrhagic shock. Acute intrinsic coagulopathy arising in severely injured trauma patients is now termed trauma-induced coagulopathy (TIC) and is an emergent property of tissue injury combined with hypoperfusion. Mechanisms contributing to TIC include anticoagulation, consumption, platelet dysfunction, and hyperfibrinolysis. This review discusses current understanding of TIC mechanisms and their relative contributions to coagulopathy in the face of increasingly severe injury and highlights how they interact to produce coagulation system dysfunction.
凝血功能障碍的识别与处理是重症创伤患者救治的关键环节。对创伤患者凝血功能障碍机制的传统认知，已被对急性组织损伤和失血性休克相关生化及细胞变化的深入研究所带来的新见解所取代。严重创伤患者出现的急性内源性凝血功能障碍现被称为创伤性凝血病（TIC），它是组织损伤与灌注不足共同作用的结果。导致TIC的机制包括抗凝、消耗、血小板功能障碍和纤维蛋白溶解亢进。本文综述了目前对TIC机制的理解，以及在损伤日益严重的情况下它们对凝血病的相对影响，并强调了它们如何相互作用导致凝血系统功能障碍。
