DIC

1. Definition

• DIC = systemic activation of the coagulation cascade → widespread microthrombi in the microcirculation (small infarcts).
• Consequence is two-fold: (1) microthrombi → ischemia/microinfarcts (esp. organs with intense blood supply — brain, kidney, lung); (2) consumption of platelets + clotting factors + activated fibrinolysis → bleeding (consumptive coagulopathy).

2. Pathogenesis

• Triggered by release of tissue factor into circulation and/or widespread endothelial damage.

3. Causes

• Obstetric: abruptio placentae, amniotic fluid embolism, retained dead fetus, septic abortion.
• Infections: sepsis (esp. Gram−, meningococcus), malaria, aspergillosis.
• Neoplasms: mucin-secreting carcinomas, acute promyelocytic leukemia (APL).
• Massive tissue injury: crush syndrome, burns, extensive surgery (head/neck).

4. Labs

• ↑PT & ↑aPTT, ↓platelets, ↓fibrinogen, ↑D-dimer/FDP, schistocytes (MAHA).

5. Morphology & Clinical

• Microthrombi in arterioles/capillaries of kidney (fibrin thrombi → cortical necrosis), adrenal (Waterhouse-Friderichsen), brain (focal hemorrhage), lung, GI.
• Bleeding tendency: petechiae, ecchymoses, oozing.
• Acute DIC (obstetric) = bleeding-dominant; chronic DIC (cancer) = thrombosis-dominant.
• Severe → acute renal failure, ARDS, coma.

6. Treatment

• Treat the underlying cause; support with platelets / FFP / cryoprecipitate; heparin if thrombosis-predominant.

💡 High-yield: DIC = simultaneous thrombosis + bleeding from consumption. Labs: ↑PT/aPTT, ↓platelets, ↓fibrinogen, ↑D-dimer, schistocytes. Classic triggers: sepsis (Gram−), obstetric emergencies, APL, massive trauma. Adrenal involvement → Waterhouse-Friderichsen.