In this episode of Hospital Medicine Unplugged, we cut through DIC—systemic coagulation activation that causes microvascular thrombosis + consumptive bleeding—and show how to diagnose fast, treat the trigger, and tailor hemostatic support without fueling harm.

We open with the core phenotypes: SIC (sepsis) → early microthrombosis/organ dysfunction with modest bleeding; TIC (trauma) → early bleeding that later flips prothrombotic. Always anchor to context (sepsis, trauma, malignancy, obstetrics).

Recognition & labs you can’t skip:
• Think DIC with new bleeding, ischemia, or organ failure in a compatible illness.
• ISTH DIC score (platelets, PT, fibrinogen, D-dimer) for overt DIC; SIC criteria for earlier sepsis-phase disease.
• Typical pattern: thrombocytopenia, ↑PT/aPTT, low fibrinogen, ↑D-dimer—but phenotypes vary.
• Don’t miss mimics: TTP/HUS, HIT, severe liver disease, primary hyperfibrinolysis—because management diverges.

Treatment—fix the cause, then the clotting:
• Treat the trigger now: source control/antibiotics, hemorrhage control, cancer/APL therapy, obstetric management. This is the cornerstone.
• Supportive hemostasis (only if bleeding or high risk):
– Platelets: keep >50×10⁹/L if bleeding; 20–30×10⁹/L acceptable if not bleeding.
– FFP to target PT/aPTT <1.5× control.
– Fibrinogen: maintain >1.5 g/L (cryoprecipitate or FFP).
– Transfuse to clinical need, not to normalize every number.
• Anticoagulation (select cases):
– Predominantly thrombotic DIC, purpura fulminans, or proven VTE: consider heparin (e.g., UFH 300–500 U/h infusion) if no active bleeding/critical thrombocytopenia.
– Thromboprophylaxis (LMWH) for most hospitalized patients until bleeding ensues or platelets <30×10⁹/L.
• What not to expect: Antithrombin, recombinant thrombomodulin, activated protein C have no consistent mortality benefit in broad RCTs; bleeding risk is real. rTM may help selected SIC subgroups, but evidence remains emerging.

ICU moves & monitoring that matter:
• Reassess daily (or q24–48 h): platelets, PT/INR, fibrinogen, D-dimer, ISTH score trend. Rising scores → re-hunt the trigger and escalate support.
• Watch for both bleeding and new thrombosis; manage organ failure (vasopressors, ventilation, RRT).
• Use viscoelastic testing (where available) to guide targeted transfusion—not blanket product use.

Pitfalls you’ll avoid:
• Treating labs instead of the disease (over-transfusing the nonbleeder).
• Withholding prophylactic anticoagulation in a stable, thrombosis-dominant phenotype.
• Missing TTP/HIT—order ADAMTS13/PF4 when the story fits.
• Forgetting that COVID-19 coagulopathy is thrombotic-heavy (high D-dimer, often normal/↑fibrinogen) and only occasionally evolves to overt DIC.

We close with the system bundle: auto-trigger DIC/SIC scoring in sepsis/trauma, embed cause-first pathways (source control, hemostasis, oncology/OB), protocolized transfusion thresholds, VTE prophylaxis by platelet cutoffs, daily score-tracked rounds, and a hematology consult for thrombotic-dominant or refractory cases.

Treat the cause, individualize support, anticoagulate thoughtfully, and track the score—DIC management without the whiplash.