Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is an acquired hypercoagulable state, induced by the progressive generation of thrombin in circulation. It is a pathophysiologic term describing a continuum of events that occur in the coagulation pathway as a complication of many different serious and lifethreatening disease states. The International Society on Thrombosis and Hemostasis has suggested the following definition for DIC: “An acquired syndrome, characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction. DIC occurs in acute and chronic forms. In its acute (overt) form it is a hemorrhagic disorder, characterized by multiple ecchymoses, mucosal bleeding and consumption of platelets and clotting factors. Chronic (nonovert) DIC, on the other hand, is more subtle and involves venous thromboembolism (VTE) accompanied by evidence of activation of the coagulation system and is associated with conditions like malignancies and intrauterine death of fetus. With chronic DIC, coagulation factors may be normal, increased, or moderately decreased, as may the platelet counts. The syndrome can be considered to involve a 2 phase phenomenon: a hypercoagulable phase that leads into a hypocoagulable phase manifesting in bleeding. Most physicians encounter patients in the hypocoagulable state with bleeding manifestations in critical illnesses. The thrombotic complications are more frequently seen in patients with malignancies who run a chronic course. In acute promyelocytic leukemia the patient usually presents with bleeding tendency secondary to DIC triggered by the granules released from the promyelocytes.