Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by hemorrhage and microvascular thrombosis. Endothelial tissue damage from a variety of underlying disorders (eg, sepsis, trauma, and malignancy) activates the coagulation cascade, which promotes fibrin production and deposition, and consumption of clotting factors. The subsequent consumption of coagulation factors and platelets, enhanced fibrinolysis, and fibrin deposition result in the clinical picture of DIC of a bleeding diathesis accompanied by thrombosis that may lead to end organ damage (algorithm 1 and figure 1).
The etiology, clinical manifestations, diagnosis, and treatment of DIC in infants and children will be reviewed here. DIC in adults is discussed separately. (See "Clinical features, diagnosis, and treatment of disseminated intravascular coagulation in adults".)
The following is a summary of the pathogenesis of disseminated intravascular coagulation (DIC). A more complete discussion is found elsewhere. (See "Pathogenesis and etiology of disseminated intravascular coagulation", section on 'Pathogenesis of DIC'.)
DIC is a secondary process caused by the systemic activation of the coagulation system by tissue damage from a variety of underlying diseases (eg, sepsis, trauma, and malignancies) . The activation of the intravascular coagulation system initiates the following processes (algorithm 1):
●Exposure of blood to procoagulants — Tissue damage from the initiating primary disease releases procoagulants into the bloodstream.