Cardenas Jessica C, Wade Charles E, Holcomb John B
Department of Surgery, The Center for Translational Injury Research, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Curr Opin Hematol. 2014 Sep;21(5):404-9. doi: 10.1097/MOH.0000000000000063.
Hemorrhage is the leading cause of potentially preventable death following injury. Excessive and uncontrolled bleeding, commonly referred to as trauma-induced coagulopathy (TIC), affects a quarter of all trauma patients and is associated with substantial injuries, increased transfusion requirements, and poor outcomes. Recent data have contributed to our current understanding of the molecular mechanisms driving TIC.
The current literature offers evidence supporting proposed mechanisms that induce TIC, such as platelet dysfunction, endogenous anticoagulation, endothelial activation, fibrinogen modifications, and hyperfibrinolysis. However, the majority of these data are mere associations; causative data are slowly unfolding through the utilization of animal models of hemorrhagic shock coupled with prospective observational clinical studies.
As both clinical and basic science research expands our understanding of TIC, trauma patient care is improving substantially. Future studies should focus on the interplay between the coagulation pathways whose simultaneous or codependent dysregulation could offer the most advantageous points for intervention.
出血是受伤后潜在可预防死亡的主要原因。过度且不受控制的出血，通常称为创伤性凝血病（TIC），影响四分之一的创伤患者，与严重损伤、输血需求增加及不良预后相关。近期数据有助于我们当前对驱动TIC的分子机制的理解。
当前文献提供了支持引发TIC的机制的证据，如血小板功能障碍、内源性抗凝、内皮激活、纤维蛋白原修饰及高纤溶状态。然而，这些数据大多只是关联；通过出血性休克动物模型结合前瞻性观察性临床研究，因果关系数据正逐渐显现。
随着临床和基础科学研究扩展我们对TIC的理解，创伤患者的护理正在大幅改善。未来研究应聚焦于凝血途径之间的相互作用，其同时或相互依赖的失调可能为干预提供最有利的切入点。
