The pathogenesis and management of disseminated intravascular coagulation.

The pathologic and progressive generation of thrombin in human blood can result in the development of disseminated intravascular coagulation (DIC), a syndrome associated with many underlying conditions and manifested as microvascular thrombosis, tissue hypoxia, and organ damage. DIC can be either acute or chronic, with acute DIC resulting from generation of a large amount of thrombin in a brief time period and chronic (compensated) DIC developing as a result of exposure of the coagulation system to small amounts of tissue factor leading to increased but nonacute levels of thrombin generation. DIC can also be considered a thrombohemorrhagic syndrome. Acute DIC at first manifests in a hypercoagulable state and leads to thrombosis, but can be followed by the development of a so-called hypocoagulable phase caused by depletion of clotting factors. This depletion can sometimes lead to bleeding. Bleeding is less common in chronic DIC, as coagulation factors and platelets are more likely to be able to be replenished in the majority of patients. Diagnosis of DIC can sometimes be difficult, depending upon the stage and presentation of the syndrome. During the thrombotic phase of DIC, many common laboratory parameters remain normal, with the important exception of an early drop in circulating platelets. DIC is easier to diagnose when the patient is bleeding, as abnormalities can normally be detected in global coagulation tests and factor assays. Therapy involves identification and treatment of the underlying condition, if possible. In the interim, measures to control bleeding can be administered, if necessary, and may include supportive care with blood products, antithrombin, heparin, and other agents.