Case scenario for fluid management in liver resection

Abstract

Patients undergoing liver resection, especially those with intrinsic liver disease (e.g., alcoholic liver cirrhosis or hepatitis C), frequently demonstrate a prolongation of PT-INR (prothrombin time/international normalized ratio). Simultaneous thromboelastographic tracings, however, typically show a normal coagulation function in these patients, with transient hypercoagulability occurring immediately after the partial hepatectomy. Liver resection reduces the synthetic function of the liver, resulting in a decrease in the level of both procoagulant and anticoagulant factors synthesized by the liver. Concomitantly, there is an up-regulation on non-hepatically synthesized factors, especially factor VIII and von Willebrand factor, which can maintain coagulation. The release of large amounts of factor VIII, von Willebrand factors, and tissue factor from the cut liver parenchyma can activate the coagulation cascade and subsequent fibrinolysis. This can explain the observed decrease in platelet count, fibrinogen (with the formation of fibrin platelet complexes), the increase in D dimer, and the prolongation in PT-INR that is observed when individual coagulation tests are performed. It is therefore not advisable, and dangerous, to base plasma transfusion decisions solely on prolonged PT/INR values.