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