Management of DIC is always directed at correcting the underlying tissue destruction, whether due to leukemia, infection, a burn or crush injury, or an obstetric complication. In the meantime, the consumption of coagulation proteins through fibrin formation and its associated secondary fibrinolysis can be brought under control by administration of exogenous cryoprecipitate, platelets, and fresh frozen plasma, as well as by the use of heparin. A continuous intravenous infusion of heparin at 5 units/kg per hour is well tolerated even in thrombocytopenic patients and allows fresh frozen plasma or cryoprecipitate to be transfused safely without concern about adding substrate for renewed intravascular coagulation. Nonetheless, there are no randomized clinical trials demonstrating benefit from the use of heparin products in DIC. Subcutaneous and/or low-dose intravenous heparin should be used with great care in patients with DIC and particularly in actively bleeding patients. Cryoprecipitate infusions should be used to maintain the fibrinogen concentration at greater than 100 mg/dL. Several doses of vitamin K (10 mg/d) should be given. If the liver is functioning normally, the vitamin K–dependent factors II, VII, IX, and X, as well as antithrombin, will be repleted rapidly, thereby avoiding the need for transfusion of large volumes of fresh frozen plasma. If after 24 hours of heparin therapy the fibrinogen level has not stabilized and the FDP levels have not decreased, the heparin infusion should be increased to 10 U/kg per hour; a higher dose of heparin is rarely necessary. Lack of response to heparin may indicate a deficiency of the heparin cofactor antithrombin, which can be repleted by transfusion of fresh frozen plasma. The optimal approach to DIC in leukemia remains to be determined. It is usually possible to manage the coagulopathy associated with APL with all-trans-retinoic acid, intensive chemotherapy, and blood product support without the routine use of heparin.19,20