Etiology

Any life-threatening severe systemic disease associated with hypoxia, acidosis, tissue necrosis, shock, and/or endothelial damage may trigger DIC. A large number of conditions have been reported to be associated with DIC (Table 477-1). Although the clinical symptoms are more often hemorrhagic, the initiating event is usually excessive activation of clotting that consumes both the physiologic anticoagulants (protein C, protein S, and antithrombin III) and procoagulants, resulting in a deficiency of factor V, factor VIII, prothrombin, fibrinogen, and platelets. Commonly, the clinical result of this sequence of events is hemorrhage. The hemostatic dysregulation may also result in thromboses in the skin, kidneys, and other organs. Better understanding of the pathophysiology of hemostasis has lead to an appreciation of the critical interaction of the coagulation pathways with the innate immune system and inflammatory response that likely contributes to the widespread dysregulation present in DIC.