Disseminated Intravascular Coagulation: Pathogenesis and Management

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Abstract
Disseminated intravascular coagulation (DIC) is a clini-copathological syndrome secondary to an underlying disease. Characteristic laboratory abnormalities of DIC should suggest, much like the recognition of fever, anemia, or congestive heart failure, that an inciting disease process must be searched for. The clinical and laboratory consequences of DIC can be ascribed to the unregulated and unbalanced formation of thrombin, the main clot-forming enzyme, and plasmin, the main clot-lysing enzyme. If too much plasmin is formed in relation to thrombin, a hemorrhagic state, which appears in 60 to 75% of patients with deep vein thrombosis, will occur. Alternatively, if too much thrombin is formed in relation to the degree of secondary fibrinolysis, a thrombotic condition, which appears in 25 to 40% of patients with DIC, will become manifest. The diagnosis of DIC is dependent on the presence of an appropriate clinical situation with concurrent laboratory evidence of thrombin and plasmin formation. Thrombin formation, plasmin formation, or both, can be assessed by detection of fibrin monomer, fibrin/fibrinogen degradation products, and D-dimer or E fragment, respectively. Treatment of DIC should initially be addressed to treatment of the primary, underlying condition inciting the disorder. If treatment for DIC is specifically needed, blood product replacement is the first order of therapy. This replacement should be tailored to each patient's specific needs (i.e., platelets, fibrinogen, or plasma proteins). Heparin has a definite but limited use in conditions associated with acral cyanosis and dermal ischemia. Other specific therapies for DIC may be of use in individualized situations.