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Disseminated intravascular coagulation (DIC, also called consumptive coagulopathy) is a catastrophic activation of the coagulation system that classically presents as the abrupt onset of uncontrolled spontaneous diffuse bleeding from multiple sites (venipuncture sites, catheter sites, endotracheal tubes, recent surgical sites) in patients with severe illness such as shock states, major trauma, sepsis, obstetric emergencies, and advanced cancer.


  1. The common denominator of conditions that cause DIC is tissue injury and activation of the clotting cascade via entry of procoagulants into the circulation.

  2. A variety of conditions activate the clotting cascade.

    1. Trauma

    2. Advanced adenocarcinomas of any site, such as colon, pancreas, or lung.

    3. Obstetric crises such as amniotic fluid embolism or placental abruption.

    4. Acute promyelocytic leukemia, wherein the granules of the malignant promyelocytes activate the clotting system.

  3. Although the classic presentation is major bleeding due to activation of the clotting cascade leading to secondary consumption of clotting factors, in some cases clotting manifestations may predominate.

    1. Patients with advanced cancer may have recurrent deep venous thrombosis or pulmonary embolism or arterial emboli in the extremities without signs of bleeding.

    2. This is considered chronic DIC.

  4. Renal, hepatic, and pulmonary dysfunction may accompany acute DIC.


  1. In acute DIC, consumption of clotting factors is demonstrated by thrombocytopenia, prolongation of the PT/INR and aPTT, reduction of plasma fibrinogen level, and increases in D-dimer and fibrin degradation products (FDP).

  2. The D-dimer and FDP reflect fibrinolytic activity acting upon fibrin formed during the clotting process.

    1. D-dimer is the product of lysis of cross-linked fibrin.

    2. FDP is the product of lysis of both fibrin and fibrinogen.

    3. Fibrinogen levels below 100 mg/dL may correlate with bleeding risk.

  3. image If DIC is suspected, testing should include platelet count, PT/INR, aPTT, fibrinogen, and D-dimer.


  1. Treat the underlying condition if possible.

  2. Replete clotting factors that have been depleted, with platelet transfusions, fresh frozen plasma, and cryoprecipitate if fibrinogen is particularly low.

  3. In rare instances, the use of low-dose heparin is considered. While it is logical to consider undertaking anticoagulation if the initiation of the process was coagulation, the additional bleeding risk is of great concern, and efforts are generally focused more on providing clotting factors while addressing the underlying cause.

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