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Disseminated Intravascular Coagulation (DIC)

Hannah Angle, Eric Singhi


Background

  • Abnormal activation of coagulation and fibrinolysis, leading to simultaneous clotting and bleeding
  • Widespread thrombi formation results in consumption of coagulation factors and platelets (consumption coagulopathy)

Etiologies

  • Sepsis (especially gram-negative rods), liver disease, pancreatitis, trauma (especially CNS), severe burns, insect/snake venom
  • Malignancies: acute leukemia (especially APL), mucin-secreting pancreatic/gastric adenocarcinoma, brain tumors, prostate cancer
  • Obstetric complications: preeclampsia/eclampsia, placental abruption, acute fatty liver of pregnancy
  • Acute hemolytic transfusion reaction (ABO incompatible transfusion)

Evaluation

  • Exam findings: petechiae, ecchymoses, bleeding (mucosal, IV sites, surgical wound sites, hematuria), thrombosis (cold, pulseless extremities)
  • Laboratory evaluation
    • Initial workup: CBC, PT/INR, aPTT, fibrinogen, d-dimer, peripheral blood smear
    • Serial DIC labs: q6-8h fibrinogen, PT/INR, aPTT (space out when lower risk)
    • Lab abnormalities suggestive of DIC: prolonged aPTT and PT/INR, thrombocytopenia, low fibrinogen, elevated D-dimer, schistocytes
    • Since Factor VIII is not produced in the liver, it can help distinguish between DIC and liver dysfunction: Factor VIII should be elevated/normal in liver disease and decreased in DIC

Management

  • TREAT THE UNDERLYING CAUSE
  • Supportive measures:
    • Vitamin K for INR > 1.7 or bleeding
    • Cryoprecipitate (10 units) if fibrinogen < 100
    • Platelet transfusion as normally indicated
    • DVT ppx if not bleeding and platelet > 50
    • VTE: therapeutic anticoagulation if platelet > 50 and no massive bleeding