## Pathophysiology of DIC **Key Point:** DIC is a syndrome of widespread intravascular coagulation triggered by tissue factor release, endotoxins, or malignancy-associated procoagulants. It results in consumption of clotting factors, platelets, and fibrinogen, leading to both thrombosis and bleeding. ## Laboratory Features of DIC | Parameter | Expected Finding in DIC | Mechanism | |-----------|------------------------|----------| | PT / aPTT | **Prolonged** | Consumption of factors II, V, VII, X | | Fibrinogen | **Decreased** | Consumption in clot formation | | Platelet count | **Decreased** | Consumption in microthrombi | | D-dimer / FDP | **Elevated** | Excessive fibrin formation and breakdown | | Antithrombin III | **Decreased** | Consumption during coagulation cascade | | Protein C | **Decreased** | Consumption and inhibition | **High-Yield:** Antithrombin III is a natural anticoagulant that is **consumed** (not elevated) during DIC because it is used up in binding to and neutralizing activated clotting factors (thrombin, Xa, IXa, XIa). Low antithrombin III is a marker of severe DIC and indicates poor prognosis. **Clinical Pearl:** The coagulopathy in DIC is paradoxical—patients have simultaneous thrombosis (microthrombi in organs) and bleeding (due to factor/platelet consumption). This distinguishes DIC from other coagulopathies like liver disease (where factors are not consumed but synthesized less). ## Why Antithrombin III Is Decreased in DIC 1. Antithrombin III inhibits thrombin and other serine proteases (Xa, IXa, XIa) 2. In DIC, massive activation of coagulation causes increased binding and consumption of antithrombin III 3. Decreased antithrombin III levels correlate with severity and poor outcome 4. Serial measurement of antithrombin III can be used to monitor DIC progression **Mnemonic:** **COAGULOPATHY in DIC** = **C**onsumption of factors, **O**ver-activation of coagulation, **A**ntithrombin depleted, **G**eneration of thrombin-antithrombin complexes, **U**nderline cause (APL, sepsis, trauma), **L**ow platelets, **O**ver-production of FDP, **P**rolonged PT/aPTT, **A**cute bleeding/thrombosis, **T**issue factor release, **H**ypofibrinogenemia, **Y**ield poor prognosis if untreated.
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