The two tales of coagulation in liver transplantation

Hemostatic alterations in cirrhosis involve molecular pathways that both promote and stabilize blood clotting and pathways that mediate clot dissolution. Orthotopic liver transplantation for end-stage liver disease historically was a long and risky procedure, accompanied by substantial blood loss. The aim of this review paper is to provide an overview of recent studies and developments that have gradually changed our understanding about the hemostatic system and changes that may occur in patients undergoing liver transplantation.

Patients with severe liver disease not only have a deficiency of procoagulant and antifibrinolytic factors, but also have a deficiency of naturally occurring anticoagulants and profibrinolytics. Studies using modern laboratory technology have shown that thrombin generation in these patients is less abnormal than traditionally believed based on standard coagulation tests. In addition, clinical observations indicated that patients with cirrhosis are not protected against thromboembolic complications.

Hemostatic alterations in cirrhosis concern both pro- and antihemostatic pathways and the net result is a rebalancing of the hemostatic system, albeit with narrower margins. This delicate balance will become precarious when the system is heavily challenged such as during liver transplantation. The balance may than be turned to either hypocoagulation or hypercoagulation, making patients with cirrhosis both prone to bleeding as well as thromboembolic complications.