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    Recipient Splenic Artery Utilization for Arterial Re-Anastomosis in Living Donor Liver Transplantation: Single-Center Experience
    (H G E Update Medical Publishing S A, 2012) Piskin, Turgut; Demirbas, Tolga; Yalcin, Levent; Yaprak, Onur; Dayangac, Murat; Guler, Necdet; Bulutcu, Fusun
    Thrombosis of recipient hepatic artery is a life threatening complication for liver transplantation. The etiology of hepatic arterial thrombosis is multi-factorial and can be caused by intimal dissection, poor surgical technique and coagulopathies. The patency of hepatic arterial flow is very important for both graft survival and patient survival. Intraoperative diagnosis of inadequate hepatic arterial flow found with Doppler ultrasonography is essential in order to achieve good results after liver transplantation. Urgent re-anastomosis is necessary when the arterial blood flow is insufficient. We performed 317 living donor liver transplantations from July 2004 to July 2011. We used recipient splenic artery for hepatic artery reconstruction in six patients. These six patients were included in this study. Using the recipient splenic artery is a simple, safe and practical alternative for hepatic artery re-anastomosis in living donor liver transplantations.
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    Right-lobe Liver Transplant From Donors With Gilbert Syndrome
    (Baskent Univ, 2012) Demirbas, Tolga; Piskin, Turgut; Dayangac, Murat; Yaprak, Onur; Akyildiz, Murat; Tokat, Yaman; Yuzer, Yildiray
    Objectives: Donor safety is one of the most important aspects of living-donor liver transplant. The preoperative evaluation of candidates for such transplants essentially starts with serologic and biochemical analyses. However, some potential liver donors with normal liver function test results may have isolated mild hyperbilirubinemia (serum indirect bilirubin level > 20.5 mu mol/L [1.2 mg/dL]). Gilbert syndrome is an autosomal recessive condition that is a common cause of nonhemolytic unconjugated hyperbilirubinemia, and its prevalence is 3% to 10% in the healthy US population. Mild hyperbilirubinemia episodes are expected in people with Gilbert syndrome when they are exposed to physical stress, such as operative intervention or low energy intake. The liver morphologic findings of these individuals are normal; however, there is a debate on the use of people with Gilbert syndrome as living-liver donors. The purpose of this study was to assess the results of right-lobe living-donor hepatectomy of liver donors with Gilbert syndrome. Materials and Methods: Between 2004 and 2010, two hundred twenty-five living-donor liver transplants using right-lobe grafts were performed in our hospital. Donors with Gilbert syndrome were defined as those whose serum bilirubin level was greater than 20.5 mu mol/L (1.2 mg/dL). Six of 225 right-lobe living-donor liver transplants were performed using donors with Gilbert syndrome. Results: The median follow-up after transplant was 34 months (range, 18 to 51 mo). One week after the operation, the median bilirubin level for rightlobe liver donors was 34.5 mu mol/L (2.02 mg/dL) (range, 17.1 to 51.3 mu mol/L [1 to 3 mg/dL]), and the median prothrombin time (international normalized ratio) was 1.36 (range, 1.1 to 1.7). The median bilirubin level of the donors after 6 months was 29 mu mol/L (1.7 mg/dL) (range, 20.5 to 41 mu mol/L [1.2 to 2.4 mg/dL]). Conclusions: Living-donor liver transplant from Gilbert syndrome donors can be safely performed.