What is DIC?
- Systemic activation of coagulation → widespread intravascular fibrin deposition → consumption of clotting factors and platelets → both thrombosis and bleeding.
- It is always secondary to an underlying condition.
Common Causes
- Oncology:
- Acute promyelocytic leukemia (APL, t(15;17)) → strongest association.
- Advanced solid tumors.
- Other:
- Sepsis (esp. Gram-negative).
- Trauma, burns.
- Obstetric complications (amniotic fluid embolism, abruptio placentae).
- Severe liver failure.
Clinical Features
- Bleeding: mucosal oozing, petechiae, ecchymoses, GI/GU bleeding.
- Thrombosis: digital ischemia, organ dysfunction (renal, hepatic, CNS).
- APL-related DIC: often dominates with catastrophic bleeding (intracranial, pulmonary).
Laboratory Findings
Typical consumptive coagulopathy pattern:
- ↓ Platelets (thrombocytopenia).
- Prolonged PT, aPTT.
- ↓ Fibrinogen (<100 mg/dL often).
- ↑ D-dimer (or FDP).
- Blood smear: schistocytes (microangiopathy).
Management
1. Treat underlying cause
- APL → ATRA (tretinoin) immediately + arsenic trioxide or chemotherapy.
- Sepsis → antibiotics & source control.
2. Supportive care (balance bleeding vs thrombosis):
- Platelet transfusion if <10–20K (higher threshold if bleeding or procedure).
- Cryoprecipitate if fibrinogen <100 mg/dL.
- Fresh frozen plasma (FFP) for prolonged PT/aPTT + bleeding.
- RBC transfusion as needed.
3. Anticoagulation (selective):
- Low-dose heparin sometimes used if thrombosis predominates and bleeding risk is low.
- In APL, ATRA reverses coagulopathy → supportive transfusions until remission induction kicks in.
Key Oncology Pearls
- DIC in APL is an emergency — start ATRA at diagnosis, before cytogenetics confirm.
- Monitor: CBC, PT, aPTT, fibrinogen, D-dimer at least daily during acute phase.
- Drug-induced coagulopathy (e.g., asparaginase) is different from DIC (low antithrombin III, not consumptive fibrinolysis).