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Key Features

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  • Characterized by tissue factor–mediated coagulation activation in the patient

  • Involves dysregulated, excessive thrombin generation, with consequent intravascular fibrin deposition and consumption of platelets and procoagulant factors

  • Microthrombi, composed of fibrin and platelets, may produce tissue ischemia and end-organ damage

  • Fibrinolytic system is frequently activated, leading to plasmin-mediated destruction of fibrin and fibrinogen; this results in fibrin-fibrinogen degradation products (FDPs) that exhibit anticoagulant and platelet-inhibitory functions

  • DIC commonly accompanies severe infection and other critical illnesses

  • Conditions known to trigger DIC include

    • Endothelial damage (eg, endotoxin, virus)

    • Tissue necrosis (eg, burns)

    • Diffuse ischemic injury (eg, shock, hypoxia acidosis)

    • Systemic release of tissue procoagulants (eg, certain cancers, placental disorders)

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Clinical Findings

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  • Signs of shock, often including end-organ dysfunction

  • Diffuse bleeding tendency (eg, hematuria, melena, purpura, petechiae, persistent oozing from needle punctures or other invasive procedures)

  • Evidence of thrombotic lesions (eg, major vessel thrombosis, purpura fulminans)

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Diagnosis

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  • Tests that are most sensitive, easiest to perform, most useful for monitoring, and best reflect the hemostatic capacity of the patient are

    • Prothrombin time (PT)

    • Activated partial thromboplastin time (aPTT)

    • Platelet count

    • Fibrinogen

    • Fibrin split products (FSPs).

  • The PT and aPTT are typically prolonged and the platelet count and fibrinogen concentration may be decreased

  • However, fibrinogen level may be normal until late in the course

  • Levels of FSPs are increased

  • D-dimer

    • Elevated levels may be helpful in monitoring the degree of activation of both coagulation and fibrinolysis

    • However, may be elevated in the context of a triggering event (eg, severe infection) without concomitant DIC

  • Often, physiologic inhibitors of coagulation, especially antithrombin III and protein C, are consumed, predisposing to thrombosis

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Treatment

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  • When underlying condition is treated, often no other therapy needed

  • Replacement of consumed procoagulant factors with fresh frozen plasma (FFP) and of platelets via platelet transfusion is warranted in the setting of DIC with hemorrhagic complications, or as periprocedural bleeding prophylaxis

    • Infusion of 10–15 mL/kg FFP typically raises procoagulant factor activities by approximately 10–15%

    • Cryoprecipitate can also be given as a rich source of fibrinogen; one bag of cryoprecipitate per 3 kg in infants or one bag of cryoprecipitate per 6 kg in older children typically raises plasma fibrinogen concentration by 75–100 mg/dL

  • Continuous intravenous infusion of unfractionated heparin is sometimes given to attenuate coagulation activation and consequent consumptive coagulopathy

  • Prophylactic doses of unfractionated heparin or low-molecular-weight heparin (LMWH) in critically ill and nonbleeding patients with DIC may be considered for prevention of venous thromboembolism

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