Introduction

Patients with end stage liver disease (ESLD), who are presented for orthotopic liver transplantation (OLT), often have multiple disturbances in haemostasis. These disturbances can result from imbalances in the clotting and the fibrinolytic systems. Excessive bleeding may occur, requiring increased blood product transfusion to replace blood loss due to medical coagulopathy. Occasional thrombotic complications may also occur, leading to potentially catastrophic intravascular or intracardiac thrombosis, cardiac arrest, or death. In addition, use of immunosuppressant drugs at the time of transplantation can have an impact on coagulation.

Intra-operative management of blood loss requires not only exceptional surgical skill, but also an understanding of the derangements in haemostasis. Thrombocytopenia can result from sequestration secondary to portal hypertension and hypersplenism.1 In addition, platelet production can be impaired due to chronic disease with diminished thrombopoietin synthesis (natural growth factor for megakaryocytes), and there may be immune-mediated platelet destruction. Malabsorption of vitamin K in patients with cholestatic disease will lead to a decrease in vitamin K dependent clotting factors (Factors II, VII, IX and X). An inability to clear tissue plasminogen activator (tPA) may lead to primary fibrinolysis.1 This often occurs during the anhepatic phase of the OLT procedure. Primary fibrinolysis, usually manifest by elevated circulating fibrin split products, can be present in critically ill patients when they are first brought to the operating room.

The presence of deficiencies in anti-thrombin III, protein C or S; Factor V Leiden or Factor 11 mutations; anti-phospholipid syndrome; and MTHFR gene mutation must all be considered as risk factors for intravascular thrombosis. This is especially true in patients with known portal vein thrombosis.2 The imbalance in the haemostatic mechanisms usually leads to excessive bleeding. It is, however, known that patients with primary liver tumours, primary scleros-ing cholangitis (PSC), or primary biliary cirrhosis (PBC) tend to be hypercoagulable.3

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