Acute traumatic coagulopathy: mechanisms and diagnosis

Trauma induced coagulopathy (TIC) is defined as an abnormal coagulation process caused by trauma. The condition initially presents as insufficient coagulation, leading to bleeding; a state that is later characterized by hypercoagulability, with associated venous thromboembolism (VTE) and multiple organ failure (MOF). TIC ' s complex pathophysiology involves endothelial dysfunction, immune system activation, which are platelet dysfunction, and coagulation activation, exacerbated by the "lethal triad" (coagulopathy, hypothermia, acidosis). The primary focus of laboratory diagnosis is on conventional coagulation tests and viscoelastic hemostatic assays. However, recent emphasis on cell-mediated hemostasis models has underscored the pivotal roles of platelets and endothelial cells. Moreover, it is noteworthy that metabolicit is noteworthy that metabolic abnormalities induced by tissue damage and hemorrhagic shock are closely associated with TIC. Imbalanced fibrinolytic systems have been demonstrated to engender heightened risks of both bleeding and thrombosis. The management of TIC is predicated on two fundamental objectives: the primary one being the cessation of bleeding, and the secondary one being the restoration of blood volume. Goal-directed transfusion strategies of blood products, in conjunction with antifibrinolytic drugs such as tranexamic acid, have been shown to yield encouraging results. Emerging research areas include microRNA regulation, the relationship between endothelial glycocalyx damage and TIC, and the development of individualized precision treatment strategies. This review summarizes the mechanisms of tissue injury (TIC), the diagnosis and treatment advances, and provides insights for understanding and managing acute traumatic coagulopathy.