Activité fibrinolytique chez les patients opérés pour transplantation hépatique

Abstract

Bleeding complications during liver transplantation have been attributed to accelerated fibrinolysis. In order to determine its cause, 11 adults (mean age : 38.9 ± 13.2 yr) undergoing liver transplantation were studied. There were three groups of patients : cirrhosis (n = 4), fulminating hepatitis (n = 4) and one group including a primary biliary cirrhosis, a hepatic metastasis and a hepatoma. The following factors were studied in the immediate preoperative period, at different surgical times throughout the procedure and 2–3 h after the end of the abdominal sutures : platelet count, prothrombin concentration, fibrinogen, activated kephalin time, factors II, V, VII + X and VIIIc, antithrombin III, protein C, D-dimers, fibrinogen and fibrin degradation products (PDF), plasma plasminogen, tissue plasminogen activator (tPA) and the fast tPA inhibitor (PAi). Preoperatively, only the two patients with hepatic cancer had a normal haemostatic profile. Throughout the procedure, all patients had only moderate changes in platelets, coagulation factors and their inhibitors, and plasminogen, because platelet concentrates and fresh frozen plasma were transfused. Levels of tPA rose, becoming very high during the anhepatic period and just after graft reperfusion. An abrupt fall occurred at the end of surgery. There were important individual differences in tPA activity. PAi activity was low during the preanhepatic and anhepatic stages, rising rapidly after revascularization. The cause of the increased fibrinolytic activity during liver transplantation would therefore seem to be an increase in tPA activity with a fall in PAi. None of the patients had haemorrhagic complication. The possible sources of tPA release from endothelial cells during liver transplantation were very important, including graft injury and veno-venous bypass. Slow or absent hepatic tPA clearance explained the high levels. The fall in platelet count was due to haemodilution, trapping by the spleen and the donor liver, destruction by the veno-venous bypass, as well as by disseminated intravascular coagulation. The rather low PDF and D-dimer levels were not in favour of secondary fibrinolysis. The balance between activators and inhibitors being impaired, the occurrence of primary fibrinolysis during liver transplantation is not surprising.