TABLE 2118 Laboratory Abnormalities Characteristic of Disseminated Intravascular Coagulation

The management of acute DIC is based on the symptoms demonstrated by the patient and the underlying disease state. Many patients with DIC require no specific therapy if there is no evidence of bleeding or thrombosis and laboratory studies are not deteriorating. The first principle of management is to stabilize the patient hemodynamically, providing oxygen, fluids, and life support as needed. If possible, the primary cause of the DIC needs to be treated. The high mortality rate in severe DIC is primarily due to the underlying disorder. Antibiotics can be given and the fetus or retained uterine products removed; however, in many circumstances, little can be done rapidly. Further management depends on the predominant symptoms of the patient—bleeding or thrombosis.

Bleeding requires replacement therapy based on the amount of bleeding, risk of bleeding (i.e., postoperative), and the extent of depletion of coagulation factors and platelets. The PT is the best indicator of clotting factor depletion. If the PT is prolonged by more than 2 to 3 s and there is bleeding, replacement is indicated. Factor levels also can be used to guide therapy if they are readily available. The fibrinogen level should be maintained above 100 to 150 mg/dL and the other factor levels at or above 50 percent of normal. FFP is used to replace clotting factors; each unit contains 200 to 250 units of each factor. Usually given 2 units at a time, there are 200 to 250 mL of fluid per unit, making volume overload a potential problem. Cryoprecipitate is used to replace fibrinogen. There are 100 to 250 mg fibrinogen per bag of cryoprecipitate; 10 bags are typically given at one time. Platelet replacement is indicated if the count is less than 50,000/pL and there is bleeding or if it is less than 20,000/pL regardless of bleeding. Each unit of platelets transfused should raise the platelet count 10,000/pL; typically, 6 units of random donor platelets (or one apheresis unit) are given at a time. As with the use of any blood products, there is a small risk of viral transmission. Patients with DIC also should be given vitamin K and folate.

The treatment of microthromboses in DIC with systemic heparinization is controversial. Its use has not been conclusively shown to improve survival and may make the overall clinical situation worse. Heparin should be considered and may be beneficial for some patients with DIC if the underlying condition is carcinoma, acute promyelocytic leukemia, or retained uterine products. Patients with purpura fulminans may also benefit from anticoagulation. In this setting, the continuous infusion of low-dose heparin (5-10 units/kg/h) is recommended. Patients with large thromboses, such as seen with Trousseau's syndrome, should receive full-dose heparinization. Antifibrinolytic agents such as a e-aminocaproic acid (EACA) and tranexamic acid are used in DIC with great caution. Although these drugs may reduce bleeding and fibrinogen consumption, they may convert a bleeding disorder into a thrombotic disorder. When used, these antifibrinolytic agents usually are given in conjunction with low-dose heparin infusion to minimize the potential for thrombosis. They are occasionally used in DIC patients with acute promyelocytic leukemia or prostate cancer.

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