Live donor liver transplantation for Budd-Chiari syndrome: Anastomosis of the right hepatic vein to the right atrium
Makaleler > Tam Makale · 2009
Yazarlar: Mircelal Kazimi, Can Karaca, Mustafa Ozsoy, Murat ÖZDEMİR, Anil Ziya Apaydin, Sezgin ULUKAYA, Murat ZEYTÜNLÜ, Murat KILIÇ
Liver Transplantation, SCI Expanded İndekslerine Giren Dergi, Uluslararası, Wos, 2009, cilt 15, ss 1374-1377
DOI: 10.1002/lt.21815
Özet
A 29-year-old male patient with the diagnosis of end-stage liver disease due to Budd-Chiari syndrome was referred to our hospital for liver transplantation. The patient had been diagnosed 4 years earlier and initially was managed with anticoagulant therapy and diuretics. Later, he developed end-stage liver disease, and anticoagulant therapy was withdrawn. He was admitted with massive ascites, jaundice, and fatigue complaints, and his Child and Model for End-Stage Liver Disease scores were 12 and 23, respectively. The workup for the etiology of Budd-Chiari syndrome, including bone marrow biopsy, autoantibodies, and mutations for thrombosis, did not demonstrate a specific cause. Multislice computed tomography of the abdomen and chest and vena cavography were performed, revealing total thrombosis of the inferior vena cava ascending from the renal vein orifices to the diaphragm (Fig. 1). Multislice computed tomography image of the patient showing a thrombosed retrohepatic vena cava right above the renal veins up to the diaphragm. His 22-year-old brother volunteered for right lobe liver donation, and his workup to be a live donor did not show any abnormalities. The donor and the recipient simultaneously underwent surgery for regular live donor liver transplantation. Technically, in these kind of cases, the mobilization of the liver and the piggyback maneuver are not easy because of diffuse fibrotic reactions in the retroperitoneum, which also involves the inferior vena cava.1, 2 The recipient liver was removed, and the vena cava was observed to be fibrotic and totally thrombosed from the renal vein orifices to the right atrium. The pericardium was cut, and the supradiaphragmatic vena cava was encircled (Fig. 2). As the vena cava was totally obstructed and there was no place to perform an anastomosis on the vena cava, the right atrium was used for the outflow reconstruction. The diaphragm surrounding the vena cava was excised with electrocautery, and the pericardial space was widely exposed (Fig. 3). The suprahepatic vena cava was also fibrotic and did not have enough distance to allow an anastomosis; thus, a Satinsky clamp was placed diagonally on the right atrium without causing any arrhythmia, and the bottom of the atrium was cut 2 cm wide so that anastomosis could be performed (Fig. 4). The fibrotic native vena cava was removed, and anastomosis between the right atrium and right hepatic vein was performed with 5/0 polypropylene sutures in a continuous fashion (Figs. 5 and 6). The pericardium was left open at the end of the procedure. The portal vein, hepatic artery, and bile duct anastomoses were performed in the usual fashion. The patient was hemodynamically stable during the operation, and the postoperative period was uneventful. Mild sinus tachycardia occurring after surgery resolved in 5 days, and the patient did not develop any further arrhythmias. He was taken out of the intensive care unit on postoperative day 4, and he was discharged home on postoperative day 20. His liver function tests recovered gradually after the transplant, and his control echocardiogram did not demonstrate any abnormalities in the first postoperative week. Oral anticoagulation with warfarin was started on postoperative day 5, targeting a prothrombin time international normalized ratio of 2. Currently, the patient is doing well with normal liver function tests and without any cardiac problems 4 months after surgery. Multislice computed tomography obtained 3 months after surgery demonstrated a patent anastomosis (Fig. 7). The opening of the pericardial cavity through the diaphragm and the suprahepatic vena cava was encircled with a blue vessel loop. After the pericardial cavity was opened, the diaphragm surrounding the vena cava was excised with electrocautery (white arrow). A Satinsky clamp was placed diagonally on the right atrium, and the bottom of the atrium was opened as the suprahepatic vena cava was also fibrotic. The fine muscles of the right atrium were grabbed with forceps (white arrow). The native vena cava was resected, and the outflow reconstruction was performed between the right atrium and the donor right hepatic vein. First, the posterior wall of the anastomosis was finished, and then, the anterior wall was completed in a continuous fashion. Multislice computed tomography image demonstrating patent anastomosis between the right hepatic vein and the right atrium 3 months after surgery. Note the absence of the inferior vena cava above the renal veins. Both medical treatment and surgical treatment of Budd-Chiari syndrome are challenging.1 Transplantation is the best method of treatment for individuals with end-stage liver disease, but it has many complications, especially for patients with caval thrombosis. A donor organ from a deceased donor has the advantage of the vena cava and right atrium of the donor.3 Live donor liver transplantation is technically more challenging for Budd-Chiari syndrome, but successful cases using various cavaplasty techniques have been reported recently.4 In our case, because of the technical difficulty, the vena cava could not be used for anastomosis, so the right atrium was exposed through the abdominal cavity and used for the anastomosis. On the donor site, the right hepatic vein was deliberately dissected along the vena cava to obtain an additional 5-mm cuff. Opening the pericardium wide and excising the surrounding diaphragm allowed us to clamp the right atrium easily, and anastomosis between the right atrium and right hepatic vein could be performed easily without cardiopulmonary bypass.