Acta Anaesthesiol Scand 2001; 45: 914–918 Copyright C Acta Anaesthesiol Scand 2001 Printed in Denmark. All rights reserved ACTA ANAESTHESIOLOGICA SCANDINAVICA ISSN 0001-5172 Case Report Anticoagulation with hirudin for continuous veno-venous hemodialysis in liver transplantation F. SANER, M. HERTL and C. E. BROELSCH Department of General and Transplantation Surgery, University Hospital Essen, Germany Postoperative encephalopathy after orthotopic liver transplan- tation can be difficult to diagnose. We report a case of heparin- induced thrombocytopenia in a liver transplant patient who had seizures. Due to poor liver function the patient developed hepa- torenal syndrome requiring continuous veno-venous hemo- dialysis (CVVHD). Initially we used heparin as the anticoagu- lant. After the diagnosis of heparin-induced thrombocytopenia (HIT) was made, we switched to r-hirudin. No serious side ef- fects, e.g. bleeding or immune sensitization, were seen. E XTRACORPORAL thrombogenesis is a major prob- lem associated with hemodialysis. The use of an anticoagulant is therefore necessary to prevent throm- botic events. Heparin is currently the standard antico- agulation, whose effect is achieved through antithrombin III (AT III (1)). It potentiates the inacti- vation of thrombin by forming a complex with its co- factor AT III. Heparin-induced thrombocytopenia (HIT) and thrombosis are characterized by progress- ive thrombocytopenia, most often occurring 5–10 days after heparin exposure. It has long been recognized that heparin administration can cause a drop in plasma platelet concentration. In 1941, Copley and Robb (2) observed thrombocytopenia in heparin- treated dogs, and Fidlar and Jaques observed a similar finding in humans (3) seven years later. In 1958 Weiss- mann and Tobin (4) described heparin-induced thrombocytopenia in 10 patients. Six of them died from recurrent diffuse arterial thromboses. The em- bolic fragments were composed of platelets and fibrin, forming a ‘‘white clot’’. Although the syndrome of heparin-induced throm- bocytopenia during heparin therapy is now well-rec- ognized and the pathophysiological mechanisms characterized, substantial questions regarding diag- nosis and treatment remain; there is some evidence for HIT being thought to be immune-mediated, be- cause platelet-associated immunoglobin G antibodies that bind to complexes of heparin and platelet factor 4 have been identified in most of these patients (5). 914 Received 31 October 2000, accepted for publication 29 March 2001 Key words: Hirudin; continuous veno-venous hemodialysis; liver transplantation; heparin-induced thrombocytopenia. c Acta Anaesthesiologica Scandinavica 45 (2001) Therefore, in the face of HIT, an alternative anticoagu- lant is needed. We used the recombinant hirudin, lepi- rudin, for anticoagulation during hemodialysis in a patient with heparin-induced thrombocytopenia. The anticoagulant treatment with hirudin was successful, although the patient’s outcome was fatal; there were no adverse side effects in terms of bleeding or im- mune sensitization. Case report A 60-year-old male patient suffering from autoim- mune-induced liver cirrhosis was admitted for ortho- topic liver transplantation. Preoperative evaluation in- cluded a thorough examination by a neurologist, who found no signs of neurological deficits. During the transplantation 16 U packed red cells, 32 U fresh frozen plasma, and re-transfusion of 3100 ml from the ‘‘cell saver’’ had been given, intraoperatively. After transplantation, the patient was transferred sedated, intubated and ventilated to the Intensive Care Unit (ICU). To improve arterial perfusion of the liver, an epop- rostenol perfusion at 4 ng kg ª1 min ª1 was initiated. Heparin was given for thrombosis prophylaxis. The initial platelet count directly after transplantation was 60/nl (preoperative platelet count was 137/nl). Due to continuous bleeding via the drains, a sec- ond-look operation was performed 22 h after the