Left renal vein ligation for spontaneous splenorenal shunts during deceased-donor orthotopic liver transplant is safe and can mitigate complications from portal steal: A case series

Objectives: Large spontaneous splenorenal shunts can result in portal vein steal syndrome and is a risk factor for portal vein thrombosis after orthotopic liver transplant. Disconnection of these shunts by left renal vein ligation has been suggested as a potential technique for improving portal venous flow and mitigating risk of portal vein thrombus, thus improving graft perfusion. We present a series of 6 patients who underwent left renal vein ligation for spontaneous splenorenal shunts and their outcomes. Materials and Methods: This retrospective analysis included all orthotopic liver transplant recipients who underwent left renal vein ligation for spontaneous splenorenal shunts between 2016 and 2017. Portal venous flow, patency, and renal function were assessed postoperatively. Liver Doppler ultrasonography scans were obtained 1, 3, and 5 days postligation, and serum creatinine was evaluated at 1 and 2 weeks and 1, 3, 6, and 12 months postligation. Results: Over the 1-year study period, 92 orthotopic liver transplants were performed. In 6 patients who underwent left renal vein ligation, spontaneous splenorenal shunts were identified preoperatively. One patient received a retransplant complicated by portal vein thrombus and underwent thrombectomy with left renal vein ligation. Concurrent left renal vein ligation and liver transplant were performed in 5 patients, 2 with known portal vein thrombus at the time of transplant requiring thrombectomy. All patients had subjective intraoperative improvements in portal venous flow after ligation. Zero patients developed postoperative portal vein thrombus. No patients developed clinically significant renal dysfunction at 1-year follow-up. Conclusions: Left renal vein ligation is technically feasible, has minimal and transient effects on renal function, and can improve portal venous flow, thus mitigating the risk for portal vein thrombus, graft hypoperfusion, and possible dysfunction.