Current opinion in critical care · 2013
Coagulation pattern in critical liver dysfunction.
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Schaden Eva, Saner Fuat H, Goerlinger Klaus
Аннотация
PURPOSE OF REVIEW: This article reviews the current literature dealing with pathophysiology, diagnostics, bleeding management, and thromboprophylaxis in patients with acute and chronic liver dysfunction.
RECENT FINDINGS: Routine coagulation tests such as prothrombin time and International Normalized Ratio (INR) are not able to define whether a patient with critical liver dysfunction is hypocoagulable or hypercoagulable and are not able to predict the risk of bleeding in patients with liver dysfunction. Therefore, prophylactic transfusion of fresh frozen plasma and platelets in order to correct laboratory values is not appropriate. Notably, patients with liver dysfunction and increased INR are not 'autoanticoagulated'. In contrast, thrombin generation assays in the presence and absence of thrombomodulin or Protac, a snake venom that activates protein C in a manner similar to thrombomodulin, as well as viscoelastic tests (thrombelastography/thromboelastometry) indicate that patients with liver dysfunction are rather hypercoagulable with the inherent risk of thrombosis.
SUMMARY: Coagulopathy in patients with critical liver dysfunction is complex and can quickly decompensate to bleeding as well as to thrombosis. Both are associated with worse outcome. Hemostatic interventions should only be performed in case of clinically relevant bleeding and thromboprophylaxis should strongly be considered.
RECENT FINDINGS: Routine coagulation tests such as prothrombin time and International Normalized Ratio (INR) are not able to define whether a patient with critical liver dysfunction is hypocoagulable or hypercoagulable and are not able to predict the risk of bleeding in patients with liver dysfunction. Therefore, prophylactic transfusion of fresh frozen plasma and platelets in order to correct laboratory values is not appropriate. Notably, patients with liver dysfunction and increased INR are not 'autoanticoagulated'. In contrast, thrombin generation assays in the presence and absence of thrombomodulin or Protac, a snake venom that activates protein C in a manner similar to thrombomodulin, as well as viscoelastic tests (thrombelastography/thromboelastometry) indicate that patients with liver dysfunction are rather hypercoagulable with the inherent risk of thrombosis.
SUMMARY: Coagulopathy in patients with critical liver dysfunction is complex and can quickly decompensate to bleeding as well as to thrombosis. Both are associated with worse outcome. Hemostatic interventions should only be performed in case of clinically relevant bleeding and thromboprophylaxis should strongly be considered.