Disseminated Intravascular Coagulation (DIC)
Eric Singhi
Background
- Concurrent activation of the coagulation pathway and fibrinolytic pathway
- Consumption of platelets, fibrin, and coagulation factors → fibrinolysis → end organ damage and hemolysis
- Etiologies:
- Infection/sepsis, liver disease, pancreatitis, trauma
- Malignancies: mucin-secreting pancreatic/gastric adenocarcinoma, brain tumors, prostate cancer, all acute leukemias, acute promyelocytic leukemia
- Obstetric complications: preeclampsia/eclampsia, placental abruption
- Acute hemolytic transfusion reaction (e.g. ABO incompatible transfusion)
Evaluation
- Exam: petechiae, bleeding (mucosal, IV site, surgical wound site, hematuria), ecchymoses, thrombosis (i.e. cold, pulseless extremities)
- Laboratory evaluation
- CBC, PT/INR, aPTT, fibrinogen, d-dimer, peripheral blood smear
- “DIC labs”: q6h fibrinogen, PT/INR, aPTT (space out when lower risk)
- Findings suggestive of DIC: thrombocytopenia, prolonged aPTT and PT/INR, hypofibrinogenemia, elevated D-dimer, fibrin degradation products, schistocytes
- A FVIII level can help distinguish between the DIC and liver dysfunction: elevated or normal in liver dysfunction and decreased in DIC since it is not hepatically derived
Management
- Treat the underlying cause
- Vitamin K for INR > 1.7 or bleeding
- Hypofibrinogenemia treatment: Cryoprecipitate 5-10 units if fibrinogen < 100
- Thrombocytopenia treatment: platelet transfusion as normally indicated
- DVT ppx if not bleeding and platelet > 50
- VTE: anticoagulation if platelet > 50 and no massive bleeding