DIC
Pathologic activation of coagulation → widespread microvascular thrombosis → consumption of factors and platelets → paradoxical bleeding. Never primary -always find and treat the trigger.
🔍 Overview
Lab Pattern
| Lab | Finding | Why |
|---|---|---|
| Platelets | ↓↓ | Consumed in microthrombi ISTH DIC Score, Taylor 2001 |
| Fibrinogen | ↓ (< 100 = severe) | Consumed. Most specific for DIC severity. |
| PT/INR, aPTT | ↑ | Clotting factors consumed |
| D-dimer | ↑↑↑ | Massive fibrinolysis |
| Smear | Schistocytes | RBCs sheared through fibrin strands |
Common Triggers
- Sepsis (~35% -most common)
- Trauma / major surgery
- Malignancy -APL, mucin-secreting adenocarcinomas (pancreas, prostate)
- Obstetric -placental abruption, amniotic fluid embolism, HELLP
- Massive transfusion, large aortic aneurysm, envenomation
🚨 Management
#1: Treat the underlying cause. DIC will not resolve until the trigger is removed. JAAM DIC Criteria, Gando 2006
| Component | Replacement | Target |
|---|---|---|
| Fibrinogen | Cryoprecipitate 10 units | > 100–150 mg/dL. Most critical to replace. ISTH DIC Guidelines, Levi 2009 |
| Platelets | Platelet transfusion | > 50K if bleeding; > 10K if not |
| Factors | FFP 15 mL/kg | INR < 1.5 if bleeding |
| RBCs | pRBCs | Hgb > 7 (or > 8 if active bleed) |
💊 Medications
Key Medications -Disseminated Intravascular Coagulation
Treat the underlying cause. DIC is ALWAYS secondary -sepsis, malignancy, obstetric emergency, trauma. Transfusion supports hemostasis but does not fix the driver.
| Product | Indication | Dose | Target |
|---|---|---|---|
| Platelets | Plt <10K (any) or <50K with active bleeding | 1 apheresis unit or 6-pack | Plt >50K if bleeding, >10K if stable |
| Cryoprecipitate | Fibrinogen <100-150 mg/dL | 10 units (pools) | Fibrinogen >150 mg/dL. Each pool raises fibrinogen ~50 mg/dL. |
| FFP | PT/aPTT >1.5× normal WITH active bleeding | 15 mL/kg (typically 4 units) | INR <1.5. Replaces all clotting factors. |
| pRBCs | Hgb <7 (or <8 if active hemorrhage) | Per transfusion protocol | Hemodynamic stability, adequate oxygen delivery. |
| Heparin SELECT CASES | Chronic/compensated DIC with thrombosis predominance | Low-dose UFH or prophylactic LMWH | Only when thrombosis outweighs bleeding risk (e.g., Trousseau syndrome, purpura fulminans). Contraindicated in acute DIC with active hemorrhage. |
| Tranexamic acid | Hyperfibrinolysis-predominant DIC | 1g IV load then 1g over 8h | Consider in APL-associated DIC or trauma. Use with caution -can worsen microvascular thrombosis. |
Do NOT transfuse to normalize labs. Transfuse ONLY if actively bleeding or at high risk of bleeding (pre-procedure). Prophylactic transfusion in stable DIC is not indicated and wastes blood products.
📋 On Rounds
How does DIC differ from TTP on labs?
Both: thrombocytopenia + schistocytes. DIC = ↑ PT/INR, ↑ aPTT, ↓ fibrinogen, ↑↑ D-dimer (consumptive coagulopathy). TTP = PT/INR and aPTT are NORMAL, fibrinogen is NORMAL. TTP is platelet consumption only -the coagulation cascade is not activated. If coags are deranged → DIC. If coags are normal → TTP/HUS.
How do you differentiate DIC from TTP? Both have MAHA + thrombocytopenia.
DIC = prolonged PT/INR + low fibrinogen + very high D-dimer. The coagulation cascade is consumed → bleeding predominates. TTP = normal PT/INR + normal fibrinogen + ADAMTS13 < 10%. The problem is platelet microthrombi, not coagulation factor consumption. The key lab: fibrinogen. Low fibrinogen = DIC. Normal fibrinogen = think TTP (or HUS). This distinction is critical because platelet transfusion is treatment in DIC (if bleeding)
What lab value is the most specific for DIC, and why?
Fibrinogen is the most specific and clinically actionable lab. In DIC, the coagulation cascade is massively activated → clotting factors AND fibrinogen are consumed. Low fibrinogen (< 100-150 mg/dL) is highly specific for DIC -it differentiates DIC from other causes of thrombocytopenia + coagulopathy (TTP has normal fibrinogen, liver disease has low fibrinogen but less severely, heparin-induced doesn't affect fibrinogen).
How do you differentiate DIC from severe liver disease?
Both have elevated PT/INR, low platelets, and low fibrinogen -making differentiation challenging. Key differentiators: (1) D-dimer: massively elevated in DIC (> 10× ULN), only mildly elevated in liver disease. (2) Factor VIII: LOW in DIC (consumed like all factors), ELEVATED in liver disease (factor VIII is made by endothelium, not hepatocytes -actually increases in liver disease as an acute phase reactant).
Clinical Examples
📋 Case 1, Sepsis-Induced DIC with Active Bleeding
Patient: 65M with septic shock from E. coli urosepsis. Developing diffuse oozing from IV sites, petechiae, and hematuria.
Key findings: Plt 28K, INR 3.2, fibrinogen 62, D-dimer > 20,000. Peripheral smear: schistocytes. ISTH DIC score 7 (overt DIC). Factor VIII LOW (confirming DIC, not liver disease).
Management:
- Treat the underlying cause, antibiotics + source control (this is the ONLY curative treatment)
- Cryoprecipitate 10 units for fibrinogen < 100 (each unit raises fibrinogen ~5-10 mg/dL)
- Platelet transfusion for plt < 50K + active bleeding
- FFP 4 units for prolonged INR + active bleeding
- Trend fibrinogen, plt, INR q4-6h, fibrinogen is the key lab to follow
- Do NOT give heparin (bleeding-predominant DIC)
Teaching point: Fibrinogen is the most specific and actionable lab in DIC. Factor VIII is LOW in DIC but ELEVATED in liver disease, this is the single best lab to differentiate them when the clinical picture is unclear.
📋 Case 2, DIC in APL (Thrombotic Predominant)
Patient: 32F presenting with pancytopenia and gum bleeding. Peripheral smear: blasts with Auer rods. Diagnosed with acute promyelocytic leukemia (APL). Labs: plt 18K, INR 1.8, fibrinogen 85, D-dimer 12,000.
Key findings: APL-associated DIC, unique because it has both bleeding AND thrombotic features. APL blasts release tissue factor and annexin II causing consumptive coagulopathy.
Management:
- Start ATRA (all-trans retinoic acid) immediately, do not wait for confirmatory testing
- Aggressive blood product support: keep fibrinogen > 150, plt > 50K in APL
- Cryoprecipitate and platelet transfusions as needed
- Hematology/oncology emergent consult
- DIC typically resolves within 48-72h of ATRA initiation
Teaching point: APL is a hematologic emergency because of severe DIC. ATRA corrects the DIC by inducing differentiation of the leukemic promyelocytes. In APL, maintain higher fibrinogen (> 150) and platelet (> 50K) thresholds than typical DIC.
📋 Case 3, DIC vs TTP Differentiation
Patient: 44F with thrombocytopenia (plt 22K), schistocytes on smear, and elevated LDH. Presenting with confusion and fever. Is this DIC or TTP?
Key findings: PT/INR NORMAL. Fibrinogen 310 (NORMAL). D-dimer mildly elevated. Cr 2.1. This is NOT DIC, normal coags with thrombocytopenia + MAHA = TTP until proven otherwise.
Management:
- Send ADAMTS13 activity level URGENTLY (do not wait for result to treat)
- Start plasma exchange (PLEX) immediately, untreated TTP mortality > 90%
- Do NOT transfuse platelets in TTP (fuels thrombosis, "adding fuel to fire")
- Start steroids (methylprednisolone 1 g/day x 3 days)
- Consult hematology emergently
Teaching point: The key differentiator: DIC = prolonged PT/INR + low fibrinogen + very high D-dimer. TTP = NORMAL PT/INR + NORMAL fibrinogen. Both have MAHA + thrombocytopenia. If coags are normal, think TTP. Platelet transfusion is treatment in DIC but contraindicated in TTP.
📣 Sample Presentation
One-Liner
"Mr. Ahmed is a 62-year-old with septic shock from cholangitis who developed diffuse oozing from line sites, petechiae, and hematuria. Platelets 32K, INR 2.8, fibrinogen 68, D-dimer >20,000. Consistent with acute DIC."
Key Points to Cover on Rounds
DIC secondary to sepsis (cholangitis -source controlled with ERCP yesterday). Labs: plt 32K, INR 2.8, fibrinogen 68 (<100 → cryoprecipitate 10 units given), D-dimer >20K. Actively bleeding from lines. Treatment: (1) treat underlying cause (antibiotics day 3, source controlled), (2) cryoprecipitate for fibrinogen <100, (3) platelets transfused (plt <50 + active bleeding), (4) FFP 4 units for INR 2.8 + active bleeding. NOT giving heparin (bleeding-predominant DIC). Plan: trend fibrinogen, plt, INR q6h, continue treating sepsis.
Monitoring Parameters -Disseminated Intravascular Coagulation
| Parameter | Frequency | Target / Action |
|---|---|---|
| CBC (platelets, Hgb) | q6-8h in acute DIC | Platelet trend (rising = improving). Hgb drop = ongoing hemorrhage or hemolysis. Check smear for schistocytes. |
| Fibrinogen | q6-8h in acute DIC | Target >150 mg/dL. Most specific lab for DIC severity. Replete with cryoprecipitate if <100-150. |
| PT/INR, aPTT | q6-8h in acute DIC | Trend toward normalization. Prolonged + bleeding → FFP. Improving PT/fibrinogen = resolving DIC. |
| D-dimer | q6-12h | Massively elevated in DIC. Trending down = resolving. Not specific -use in context of ISTH score. |
| ISTH DIC score | Daily recalculation | ≥5 = overt DIC. Track serial scores -declining score confirms resolution. Components: platelets, D-dimer, PT, fibrinogen. |
| Clinical bleeding assessment | q2-4h | IV sites, surgical sites, mucosal bleeding, petechiae, hematuria, GI bleeding. Simultaneous bleeding AND thrombosis is pathognomonic. |
| Thrombotic complications | Each assessment | Skin necrosis (purpura fulminans), acral ischemia, organ dysfunction (renal, hepatic). DVT/PE screening if clinical concern. |
⚡ Summary
Summary
The Paradox That Defines It
Pathologic activation of coagulation causes widespread microvascular thrombosis, which consumes clotting factors and platelets, so the patient bleeds. Thrombosis and hemorrhage are happening at the same time, which is why the labs look like a bleeding disorder while the pathology is clotting.
Read the Lab Pattern
Platelets low (consumed in microthrombi), fibrinogen low with below 100 mg/dL indicating severe disease, PT and aPTT prolonged, D-dimer markedly raised, and schistocytes on the smear from red cells sheared through fibrin strands. Fibrinogen is the most specific marker of severity, and because it is an acute phase reactant a 'normal' value in a septic patient may already represent a large fall.
Trend the Labs, Do Not Read Them Once
A single set can look unremarkable early. A falling platelet count and a falling fibrinogen over hours are more informative than any absolute value, and the ISTH DIC score is designed to be applied serially rather than as a one-off.
DIC Is Never Primary
Always find and treat the trigger, because DIC will not resolve until it is removed. Sepsis is the commonest, about 35%, then trauma and major surgery, malignancy (acute promyelocytic leukemia and mucin-secreting adenocarcinomas of pancreas and prostate), obstetric emergencies (abruption, amniotic fluid embolism, HELLP), massive transfusion, large aortic aneurysm and envenomation.
Do Not Transfuse to Normalize Numbers
Transfuse only for active bleeding or before a procedure with high bleeding risk. Prophylactic transfusion in a stable DIC patient is not indicated, wastes product and adds transfusion risk without changing outcomes. The abnormal numbers are a marker of the underlying illness, not a target.
Know What to Give When They Do Bleed
Platelets for a count below about 50,000 with bleeding. Cryoprecipitate for fibrinogen below 100 to 150, which is the most efficient way to replace it. Fresh frozen plasma for a prolonged PT or aPTT with bleeding. Follow the response with repeat labs rather than giving fixed volumes.
Heparin Is Only for the Thrombotic Phenotype
Consider low-dose heparin when thrombosis dominates: purpura fulminans, digital ischemia, large vessel thrombosis, or chronic compensated DIC in malignancy. Avoid it when bleeding dominates, and be aware that antithrombin depletion in DIC blunts its effect. Antifibrinolytics such as tranexamic acid are generally contraindicated, since blocking fibrinolysis in a microthrombotic state worsens organ ischemia.
APL Is the Exception Worth Knowing
Acute promyelocytic leukemia causes a catastrophic DIC with early fatal hemorrhage, and ATRA started on clinical suspicion reverses it. Support aggressively while it takes effect: keep fibrinogen above 150 and platelets above 50,000, which are higher thresholds than in ordinary DIC precisely because intracranial hemorrhage is what kills these otherwise curable patients.
📄 One Pager
Text version
Disseminated Intravascular Coagulation (DIC) -Quick Reference Card
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DISSEMINATED INTRAVASCULAR COAGULATION (DIC) -AT A GLANCE
📋 Diagnose: See Overview tab for criteria
🧪 Workup: Focused labs + imaging → see Workup tab
⚡ Treat: Evidence-based algorithm → see Management tab
💊 Drugs: Key medications with dosing → see Medications tab
📣 Present: One-liner + key points → see Rounds tab
🧪 Workup: Focused labs + imaging → see Workup tab
⚡ Treat: Evidence-based algorithm → see Management tab
💊 Drugs: Key medications with dosing → see Medications tab
📣 Present: One-liner + key points → see Rounds tab
🧪 Workup
Workup
- CBC + smear -thrombocytopenia + schistocytes
- PT/INR, aPTT -prolonged
- Fibrinogen -most specific. Cryo if <100.
- D-dimer -markedly elevated
- Factor VIII -LOW in DIC, HIGH in liver disease
- ISTH DIC score ≥5
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