The etiology of disseminated intravascular coagulation (DIC) can be classified into three processes: (1) endothelial cell injury which activates Hageman factor and the intrinsic clotting system, (2) tissue injury which activates the extrinsic clotting system, or (3) red cell or platelet injury with the release of coagulant phospholipids. These initiating mechanisms result in a final common product, thrombin, which cleaves fibrinogen, activates factor XIII, aggregates platelets, releases platelet constituents and triggers secondary fibrinolysis. Plasmin produces fibrinogen degradation products which participate in the hemorrhagic diathesis. Detection of these fragments provides a sensitive method of diagnosing DIC. DIC usually presents with bleeding at multiple sites, and occasionally with thrombotic episodes or acrocyanosis. The diagnostic manifestations of DIC include a hemorrhagic-thrombotic diathesis, a specific coagulation test profile, the presence of fibrin thrombi and the response to heparin therapy. Analysis of our large series of patients finds the presence of three abnormal screening tests to be diagnostic (prothrombin time, fibrinogen and platelets). If only two of the three are abnormal, a test for fibrinolysis (thrombin time, euglobulin clot lysis time or fibrinogen degradation products) should be abnormal in order to establish the diagnosis. Treatment with heparin usually results in decreased bleeding. The prothrombin time, fibrinogen level and euglobulin lysis become normal within one to three days in those who stop bleeding. The titer of fibrinogen degradation products may respond rapidly but if greatly elevated remains abnormal for more than a week. Platelet levels do not respond uniformly to heparin therapy; when they do respond, it frequently requires several weeks. Even severe fibrinolysis responds to heparin therapy and is probably always secondary to DIC. Epsilon aminocaproic acid (EACA) therapy alone aggravates DIC and often results in thrombosis.
ASJC Scopus subject areas