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Disseminated
intravascular coagulation (DIC) involves abnormal, excessive generation
of thrombin and fibrin in the circulating blood. During the process,
increased platelet aggregation and coagulation factor consumption
occur. DIC that evolves slowly (over weeks or months) causes primarily venous
thrombotic and embolic manifestations; DIC that evolves rapidly
(over hours or days) causes primarily bleeding. Severe, rapidly
evolving DIC is diagnosed by demonstrating thrombocytopenia, an elevated
PTT and PT, increased levels of serum fibrin degradation products,
and a decreasing plasma fibrinogen level. Treatment includes correction
of the underlying cause and replacement of platelets, coagulation
factors (in fresh frozen plasma), and fibrinogen (in cryoprecipitate)
to control severe bleeding. Heparin is used as therapy (or prophylaxis)
in patients with slowly evolving DIC who have (or are at risk for)
venous thromboembolism.
Etiology
and Pathophysiology
DIC usually results from exposure of tissue factor to blood, initiating the coagulation cascade (see Fig. 2: Hemostasis: Fibrinolytic pathway. ). DIC occurs in the following clinical circumstances:
Less common causes of DIC include severe tissue damage from head trauma, burns, frostbite, or gunshot wounds; complications of prostate surgery that allow prostatic material with tissue factor activity (along with plasminogen activators) to enter the circulation; venomous snake bites in which enzymes enter the circulation that activate one or several coagulation factors and generate thrombin or directly convert fibrinogen to fibrin; profound intravascular hemolysis; and aortic aneurysms or cavernous hemangiomas (Kasabach-Merritt syndrome) associated with vessel wall damage and areas of blood stasis.
Slowly evolving DIC primarily causes venous thromboembolic manifestations (eg, deep venous thrombosis, pulmonary embolism), although occasionally cardiac valve vegetations occur; abnormal bleeding is uncommon. In contrast, in severe, rapidly evolving DIC, thrombocytopenia and depletion of plasma clotting factors and fibrinogen cause bleeding. Bleeding into organs, along with microvascular thromboses, may cause hemorrhagic tissue necrosis in multiple organs.
Symptoms and Signs
In slowly evolving DIC, symptoms of venous thrombosis and pulmonary embolism may be present.
In severe, rapidly evolving DIC, skin puncture sites (eg, IV or arterial punctures) bleed persistently, ecchymoses form at sites of parenteral injections, and serious GI bleeding may occur. Delayed dissolution of fibrin polymers by fibrinolysis may result in the mechanical disruption of RBCs and mild intravascular hemolysis (see Thrombocytopenia and Platelet Dysfunction: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)). Occasionally, microvascular thrombosis and hemorrhagic necrosis produce dysfunction and failure in multiple organs.
Diagnosis
DIC is suspected in patients with unexplained bleeding or venous thromboembolism, especially if a predisposing condition exists. If DIC is suspected, platelet count, PT, PTT, plasma fibrinogen level, and plasma d-dimer (an indication of in vivo fibrin deposition and degradation) are obtained.
Slowly evolving DIC produces mild thrombocytopenia, a normal to minimally prolonged PT (results are typically reported as INR) and PTT, a normal or moderately reduced fibrinogen level, and an increased plasma d-dimer level. Because a variety of illnesses stimulate increased synthesis of fibrinogen as an acute-phase reactant, a declining fibrinogen level on 2 consecutive measurements can help make the diagnosis of DIC.
Severe, rapidly evolving DIC results in more severe thrombocytopenia, more prolonged PT and PTT, rapidly declining plasma fibrinogen concentrations, and a high plasma d-dimer level.
A factor VIII level can sometimes be helpful if severe, acute DIC must be differentiated from massive hepatic necrosis, which can produce similar abnormalities in coagulation studies. The factor VIII level is elevated in hepatic necrosis, because factor VIII is made in hepatocytes and released as they are destroyed; factor VIII is reduced in DIC because of the thrombin-induced generation of activated protein C, which proteolyses factor VIII.
Treatment
Immediate correction of the underlying cause is the priority (eg, broad-spectrum antibiotic treatment of suspected gram-negative sepsis, evacuation of the uterus in abruptio placentae). If treatment is effective, DIC should subside quickly. If bleeding is severe, adjunctive replacement therapy is indicated, consisting of platelet concentrates to correct thrombocytopenia; cryoprecipitate to replace fibrinogen and factor VIII; and fresh frozen plasma to increase levels of other clotting factors and natural anticoagulants (antithrombin, proteins C and S). The effects of infusion of concentrates of antithrombin or activated protein C in severe, rapidly evolving DIC are under study.
Heparin usually is not indicated in DIC. An exception is in women with a retained dead fetus and evolving DIC with a progressive decrease in platelets, fibrinogen, and coagulation factors. In this circumstance, heparin is administered for several days to control DIC, increase fibrinogen and platelets, and decrease excessive coagulation factor consumption before uterine evacuation.
Last full review/revision November 2005
Content last modified November 2005
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