Massive bleeding in patients with major trauma is the most common cause of in-hospital mortality during the first 48 h and in the early postoperative period. It interferes with the coagulation process, resulting in a coagulopathy, even in patients with previously normal hemostasis. The presence of trauma-induced coagulopathy (TIC) reflects the severity of injury and is an independent predictor of mortality in trauma. The pathogenesis of TIC is complex and multifactorial, involving physiological, biochemical, immunological, and cellular mechanisms. In particular, TIC has a number of causal factors, including dilutional coagulopathy after fluid resuscitation and consumption of clotting factors and platelets due to major blood loss. Increased fibrinolysis, activation of anticoagulant pathways, hypocalcemia, and disseminated-intravascular-coagulation-like syndrome may also play a role. Moreover hypothermia and acidosis contribute to the occurrence of TIC. In this setting the interpretation of blood coagulation tests can be unreliable since they are performed at a normal pH and temperature, whereas these patients are often hypothermic and acidotic. Besides the surgical repair of the bleeding source, if feasible, the prompt recognition and correction of these latter conditions and the administration of both procoagulant and antifibrinolytic substances are the cornerstones of the treatment.
