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DIC

DIC. DIC. acute, subacute or chronic widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms. DIC.

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DIC

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  1. DIC

  2. DIC • acute, subacute or chronic widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms

  3. DIC • consumption of platelets, fibrin and coagulation factors and secondarily, activation of fibrinolytic mechanisms • tissue hypoxia • infarction • hemorraghic disorder

  4. DIC • Two major mechanisms trigger DIC • Release of tissue factor or thromboplastic substances into the circulation - thromboplastic substances - mucus - bacterial endotoxin 2. Widespread injury to the endothelial cells - TNF - antigen-antibody complexes - temperature extremes

  5. DIC

  6. Differential Diagnosis

  7. Differential Diagnosis • The differential diagnosis between DIC and severe liver disease is challenging and requires serial measurements of the laboratory parameters of DIC

  8. Differential Diagnosis • Patients with severe liver disease are at risk for bleeding and manifest laboratory features including • Thrombocytopenia (due to platelet sequestration, portal hypertension, or hypersplenism) • Decreased synthesis of coagulation factors and natural anticoagulants • Elevated levels of fibrin degradation products (FDP)

  9. Differential Diagnosis • In contrast to DIC, these laboratory parameters in liver disease do not change rapidly • Other important differential findings include the presence of portal hypertension, or other clinical or laboratory evidence of underlying liver disease

  10. Differential Diagnosis • Microangiopathicdisorders such as thrombotic thombocytopenicpurpurapresent an acute clinical onset of illness accompanied by: • Thrombocytopenia • Red cell fragmentation • Multiorgan failure • There is, however no consumption of clotting factors or hyperfibrinolysis

  11. Management of Disseminated Intravascular Coagulation

  12. Management of DIC

  13. Management of DIC

  14. Management of Hemorrhagic Sx • Fresh Frozen Plasma • Indicated for an elevated PT. • PT (>1.5xnormal) provides a good indicator for severity of clotting factor consumption • 1 unit of FFP increases most coagulation factors by 3% in an adult without DIC

  15. Management of Hemorrhagic Sx • Cryoprecipitate • Plasma fraction enriched for fibrinogen, FVIII, and vWF • Indicated in low levels of fibrinogen (<100 mg/dL) or brisk hyperfibrinolysis • The replacement of 10 U of cryoprecipitate for every 2–3 U of FFP is sufficient to correct the hemostasis

  16. Management of Hemorrhagic Sx • Platelet Concentrates • Indicated for patients with severe thrombocytopenia (20 K) or active bleeding. • The dose is 1–2 U/10 kg body weight

  17. Replacement of Coagulation or Fibrinolysis inhibitors • Heparin • Low doses of continuous infusion heparin (5–10 U/kg per h) may be effective in patients with: • Low-grade DIC associated with solid tumor or APL • Malignancy with thrombotic complications • Also indicated: • Purpura fulminans (gangrene of digits/extremities) • During surgical resection of giant hemangiomas • During removal of dead fetus / amniotic fluid embolism

  18. Replacement of Coagulation or Fibrinolysis inhibitors • Heparin • In acute DIC, the use of heparin is likely to aggravate bleeding • To date, the use of heparin in severe DIC patients is of no proven survival benefit

  19. Replacement of Coagulation or Fibrinolysis inhibitors • Fibrinolytic inhibitors • e-aminocaproic acid; tranexamic acid • prevent fibrin degradation by plasmin may reduce bleeding episodes in patients with DIC and confirmed hyperfibrinolysis • However, these drug increase the risk of thrombosis, and concomitant use of heparin is indicated • Indicated: APL, chronic DIC associated with giant hemangiomas

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