摘要
Trauma-induced coagulopathy （TIC） is a clinical syndrome caused by imbalance between clotting, anti- coagulation and fibrinolysis resulting from multiple pathological factors such as hemorrhage and tissue injury in the early stage of trauma, and is closely related to the outcome of trauma patients. It is proved in growing evidence that the endogenous coagulation disturbance in trauma itself is the activating factor of TIC, rather than dilution or other acquired coagulopathy. Therefore, a thorough understanding of the molecular mechanisms in the pathogenesis and progression is crucial for effective prevention and treatment in patients with TIC. This review focuses on transitions in the concept of TIC and mechanical progress.
