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🔴 DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

Complete Pathology Summary — NEET PG 2026

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1. DEFINITION

DIC is a clinicopathologic syndrome characterized by systemic activation of the coagulation and fibrinolysis systems, resulting in simultaneous formation of thrombin and plasmin, leading to:

• Widespread microvascular fibrin-platelet thrombi (thrombosis)
• Consumption of coagulation factors, inhibitors, and platelets
• Secondary hemorrhage

• Also called: Consumptive coagulopathy / Defibrination syndrome
• DIC is never a primary disease — it always has an underlying cause
• It is primarily a thrombotic process pathophysiologically, but clinically presents as hemorrhage in acute cases

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2. ETIOLOGY / CAUSES ⭐ (HIGH-YIELD)

Key Mnemonic for causes: STOP Making New Thrombi Sepsis, Trauma, Obstetric complications, Promyelocytic leukemia (APL), Malignancy, Neoplasm, Transfusion reactions

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3. PATHOGENESIS / MECHANISM ⭐⭐ (MOST IMPORTANT)

Central Trigger: Tissue Factor (TF)

• Tissue factor (TF) = lipoprotein not normally exposed to blood
• In DIC, TF gains access to blood by:
  1. Tissue injury → exposes TF
  2. Malignant cells elaborate TF (especially APL granules releasing tissue thromboplastin)
  3. Monocytes and endothelial cells express TF in response to inflammatory mediators (TNF, IL-1 in sepsis)

Cascade of Events:

Triggering event (infection/trauma/APL/obstetric)
           ↓
  Tissue Factor enters circulation
           ↓
  TF + VIIa → activates X and IX
           ↓
  Thrombin generation (key enzyme)
           ↓
    ┌──────────────────────────────────┐
    ↓                                  ↓
Fibrinogen → Fibrin              Platelet activation
(microthrombi in vessels)        (thrombocytopenia)
    ↓
Consumption of factors I, II, V, VIII, XIII
Consumption of inhibitors (AT-III, Protein C, S)
    ↓
Secondary fibrinolysis → Plasminogen → PLASMIN
    ↓
FDPs / D-dimers released
(FDPs inhibit thrombin → further impair coagulation)
    ↓
BLEEDING (from consumption + FDP inhibition)

Key Points in Pathogenesis:

• Thrombin induces fibrin formation + platelet activation
• Plasmin degrades fibrin → generates FDPs (fibrin degradation products) and D-dimers
• FDPs inhibit thrombin and platelet aggregation → worsening hemorrhage
• Microthrombi → microangiopathic hemolytic anemia (MAHA) with schistocytes
• Antithrombin III (AT-III) is consumed → cannot inhibit thrombin
• Protein C and S consumed → cannot inhibit factors Va and VIIIa
• Net result: both thrombosis AND hemorrhage occurring simultaneously

In APL specifically:

• Malignant cells release Auer rods and granules containing tissue thromboplastin and proteases
• Prominent fibrinolysis component → severe bleeding tendency
• Treated with ATRA (all-trans retinoic acid) which causes differentiation of APL cells → mitigates DIC

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4. TYPES OF DIC

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5. CLINICAL FEATURES ⭐

Hemorrhagic Manifestations (Acute DIC):

• Bleeding from multiple sites simultaneously
• Oozing from IV puncture sites, surgical wounds
• Petechiae, ecchymoses, purpura
• Mucosal bleeding (gum, nose, GI tract)
• Internal hemorrhage (intracranial, adrenal → Waterhouse-Friderichsen in meningococcemia)

Thrombotic Manifestations:

• Microthrombi → end-organ damage
• Acute renal failure (renal cortical necrosis)
• Pulmonary insufficiency / ARDS
• Hepatic dysfunction
• Neurological changes

Microangiopathic Hemolytic Anemia (MAHA):

• RBCs sheared by fibrin strands → schistocytes, helmet cells on peripheral smear
• Hemolysis → anemia, elevated LDH, low haptoglobin, indirect hyperbilirubinemia

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6. LABORATORY FINDINGS ⭐⭐ (MOST TESTED)

Classic DIC lab picture: ↑PT + ↑aPTT + ↓Fibrinogen + ↑D-dimer + ↓Platelets + Schistocytes

D-dimer is the MOST SPECIFIC test for DIC (indicates cross-linked fibrin degradation)

FDPs = both cross-linked and non-cross-linked degradation products; elevated in DIC and fibrinolysis

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7. ISTH SCORING SYSTEM FOR OVERT DIC ⭐

Score ≥5 = Overt DIC (repeat daily) Score <5 = Suggestive of non-overt DIC (repeat in 1–2 days)

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8. DIFFERENTIATION FROM OTHER CONDITIONS ⭐

Key distinction: In liver disease, Factor VIII is normal or elevated (because Factor VIII is made by endothelium, not just liver). In DIC, Factor VIII is consumed/decreased. ⭐

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9. SPECIFIC HIGH-YIELD ASSOCIATIONS FOR NEET PG

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10. PATHOLOGY / MICROSCOPY ⭐

• Microthrombi in small vessels of multiple organs (kidney, lung, adrenal, brain)
• Renal cortical necrosis (bilateral symmetric — pathognomonic of DIC in obstetric cases)
• Adrenal hemorrhage (Waterhouse-Friderichsen in meningococcemia)
• Diffuse alveolar damage (lung)
• Schistocytes (helmet cells, burr cells) on peripheral blood smear — mechanical fragmentation
• Microangiopathic hemolytic anemia (MAHA) morphology

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11. TREATMENT PRINCIPLES (Pathology-relevant)

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12. QUICK REVISION FLASH CARDS

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13. MEMORY AIDS

• UP: PT ↑, aPTT ↑, D-dimer ↑, FDPs ↑, Bleeding time ↑
• DOWN: Platelets ↓, Fibrinogen ↓, Factors V & VIII ↓, Antithrombin III ↓, Hb ↓

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Sources: Goldman-Cecil Medicine (26th ed.) | Tietz Textbook of Laboratory Medicine (7th ed.) | Wintrobe's Clinical Hematology — Medical Library