Trauma-induced coagulopathy: from biology to therapy

Trauma is a leading cause of death and disability. Hemorrhage is the major mechanism responsible for death during the first 24 hours following trauma. One quarter of severely injured patients present in the emergency room with acute coagulopathy of trauma and shock (ACOT). The drivers of ACOT are tissue hypoperfusion, inflammation, and activation of the neurohumoral system. ACOT is a result of protein C activation with cleavage of activated factor VIII and V and inhibition of plasminogen activator inhibitor-1 (PAI-1). The resuscitation-associated coagulopathy (RAC) is secondary to a combination of acidosis, hypothermia and dilution from intravenous blood and fluid therapy. RAC may further aggravate acidosis and hypoxia resulting in a vicious cycle. This review focuses on the biology of the trauma-associated coagulopathy, and reviews current therapeutic strategies.