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Àcute Traumatic Coagulopathy happens instantly after massive trauma when shock, hypoperfusion, and vascular damage are extant. Mechanisms for this acute coagulopathy incorporate activation of protein C, endothelial glycocalyx interruption, consumption of fibrinogen, and platelet dysfunction. Hypothermia and acidaemia enhance the endogenous coagulopathy and regularly accompany trauma. These multifactorial processes lead to diminished clot strength, autoheparinization, and hyperfibrinolysis. Moreover, the impacts of aggressive crystalloid organization, haemodilution from improper blood product transfusion, and extended surgical times may get worse clinical results.
