Posttraumatic hemorrhage is one of the leading causes of preventable human deaths. Acute traumatic coagulopathy (ATC) is a hypocoagulable state that has been observed during the first hours following trauma. ATC is an endogenous hypocoagulable state with hyperfibrinolysis mediated by activation of the Protein C pathway. These abnormalities are suspected to be a manifestation of severe tissue injury, shock induced hypoperfusion, worsening base deficit and head injury.1 In humans, it is hypothesized that coagulation alterations are associated with the degree of injury sustained.2 With mild injuries, normal coagulation status has been documented. Next, people with moderate injury have a hypercoagulable state, then a hypocagulable state and hyperfibrinolysis are present with severe injury.3 Activation of the coagulation system occurs in people with severe trauma because of exposure of subendothelial tissue factor and cytokine release. ATC along with acidosis and hypothermia contributes to the phenomenon referred to as "trauma induced coagulopathy".
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