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Coagulopathy in Cirrhosis

John Laurenzano


  • The liver is responsible for production of both pro- (factor II, V, VII, IV, X, and XI) and anti-coagulants (protein C, S) in hemostasis. Factor VIII is the only one not made by the liver.
  • Thrombocytopenia is caused by splenic sequestration from portal HTN, failure to produce thrombopoietin (TPO), and bone marrow failure
  • Hemostatic changes in cirrhotics are incredibly complex, as they involve both procoagulant and anticoagulants. The current thought is that cirrhosis is NO LONGER considered a condition associated with an overall increased bleeding tendency, as the pro-hemostatic and anti-hemostatic pathways are deranged in a way that counterbalance each other.


  • INR/PT, and PTT are poorly reflective of bleeding risk


  • Pre-procedural FFP is not recommended, as it has potential harm w/o proven benefit

  • Low risk procedures (i.e., paracentesis) do not require pre-procedural blood products and per guidelines there is no established INR or platelet cut off

  • In bleeding pts, the following are recommended per AASLD and AGA guidelines

    • IV Vitamin K 10mg x 3 days
    • FFP: Not recommended, unless as part of a balanced transfusion effort to avoid transfusion related coagulopathy, or if a TEG screen suggests potential benefit
    • Cryoprecipitate: if fibrinogen < 120
    • Platelets: No specific targets regardless of bleeding. Pre-procedurally, recommend >50
  • Appropriate DVT ppx should be given with few exceptions (plts <50k, active hemorrhage)
  • For TEG transfusion recommendations are as follows:
    • 10 mg/kg FFP if R-time >10 minutes
    • 1u Plts if maximum amplitude <55 mm
    • 5u cryo if alpha angle <45