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Disseminated Intravascular Coagulation (DIC) (Ref. Hari. 18th ed., Pg- 978)

Essentials of Diagnosis
  1. Underlying serious illness.
  2. Microangiopathic hemolytic anemia may be present,
  3. Hypofibrinogenemia. Thrombocytopenia, fibrin degradation products, and prolonged prothrombin time.
  1. Sepsis (especially with gram-negative bacteria), P. falciparum
  2. Severe tissue injury (especially burns and head injury), Snake bite
  3. Obstetric complications (amniotic fluid embolus, septic abortion, retained fetus)
  4. Cancer (acute promyelocytic leukemia, mucinous adenocarcinomas)
  5. Major hemolytic transfusion reactions.
The pathophysiology of DIC. (Ref. Hari. 18th ed., Pg- 979, Fig 116.3)

Clinical Findings

Symptoms and Signs:
  1. DIC leads to both bleeding and thrombosis.
  2. Bleeding is far more common than thrombosis. Bleeding may occur at any site.
  3. Thrombosis is most commonly manifested by digital ischemia and gangrene, but catastrophic events such as renal cortical necrosis and hemorrhagic adrenal infarction may occur.
  4. DIC may also secondarily produce microangiopathic hemolytic anemia > heart > lung > kidney > adrenal gland.
Laboratory Findings:
  1. Hypofibrinogenemia
  2. Elevated fibrin degradation products (most sensitive test)
  3. Thrombocytopenia
  4. Prolonged prothrombin time.
Important Points
  1. Of the fibrin degradation products, the D-dimer is the most sensitive, since its cross-linking implies origin from fibrin in a clot. P/S schistocyte helmet cell
  2. All fibrin degradation products are cleared by the liver and thus may be elevated in hepatic dysfunction.
  3. All blood test (BT, CT, PT, PTT) are abnormal except clot retardation time which is normal. (LQ 2012)
  4. Coombs test is negative, (LQ 2012)
Coagulation Disorders and Hemostasis in Liver Disease
  1. Bleeding
    1. Portal hypertension - Esophageal varices
    2. Thrombocytopenia due to
      1. Splenomegaly
      2. Chronic or acute DIC
    3. Decreased synthesis of clotting factors due to
      1. Hepatocyte failure
      2. Vitamin K deficiency
    4. Systemic fibrinolysis due to
      1. DIC
      2. Dysfibrinogenemia
  2. BThrombosis
    1. Decreased synthesis of coagulation inhibitors: protein C, protein S, antithrombin
    2. Hepatocyte failure
    3. Failure to clear activated coagulation proteins
  3. Iatrogenic: Transfusion of prothrombin complex concentrates
  4. Antifibrinolytic agents: ε-aminocaproic acid (EACA), tranexamic acid

Pathophysiology of disseminated intravascular coagulation.

Treatment of DIC
  1. Treatment of the underlying disorder
  2. Replacement therapy
    1. Platelet transfusion
    2. Fibrinogen is replaced with cryoprecipitate.
    3. Coagulation factor deficiency may require replacement with fresh-frozen plasma.
  3. The role of heparin in the treatment of DIC is controversial.

Extra Edge: But Heparin therapy is routinely used in the treatment of acute promyelocytic leukemia.

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