Disseminated Intravascular coagulation

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(DIC) – a.k.a. acquired hypofibrinogenemia, defibrination syndrome, consumptive coagulopathy

  1. Etiology is unknown but majority of cases involve sepsis, head trauma, major surgery and liver disease as well as incompatible blood transfusions, malignancy, burns, and fat embolism
  2. DIC results from inappropriate activation of the coagulation cascade resulting in consumption of fibrinogen that in turn results in the deposition of fibrin and thrombin in the microcirculation predisposing to organ dysfunction; degradation products of fibrinogen are subsequently acted upon by plasmin further impeding coagulation
    1. decreased fibrinogen most closely correlates with bleeding in DIC patients
  3. Clinical features: ARDS-picture, oliguric renal failure, progressive lver dysfunction, diffuse bleeding (including GI), limb necrosis, purpura fulminans
  4. Labs: thrombocytopenia, increased PT, PTT, and bleeding time, increased fibrin degradation products; D dimer immunoassay which specifically measure cross-linked fibrin derivates is a more specific assay that fibrin degradation products
  5. Treatment: supportive – give PRBC’s to maintain oxygen carrying capacity, cryoprecipitate for active bleeding, platelet transfusion – and treat underlying cause such as sepsis
    1. Bleeding- replacement of platelets and cryoprecipitate rarely helps
    2. Heparin -ineffective in retarding the microvascular thrombosis
  6. Mortality rate for DIC = 80%
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