1. DIC

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

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

4. Two major mechanisms trigger DIC 1.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 DIC

6. Differential Diagnosis

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

8. 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) Differential Diagnosis

9. 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 Differential Diagnosis

10. Microangiopathic disorders such as thrombotic thombocytopenic purpura present an acute clinical onset of illness accompanied by: – Thrombocytopenia – Red cell fragmentation – Multiorgan failure There is, however no consumption of clotting factors or hyperfibrinolysis Differential Diagnosis

11. Management of Disseminated Intravascular Coagulation

12. Management of DIC Identify and aggressively treat the underlying disease Maximize cardiovascular and pulmonary support

13. Management of DIC Manage hemorrhagic symptoms Replace coagulation or fibrinolysis inhibitors

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