A 53-year-old man was referred to our department for LRLT. At 39 years of age he had been diagnosed with liver dysfunction secondary to hepatitis B virus (HBV) infection. Liver cirrhosis and hepatocellular carcinoma (HCC) subsequently developed, and he was treated by trans-arterial embolization at 48 years of age. The HCC recurred at 52 years of age, and he developed an umbilical hernia caused by a huge volume of ascitic fluid. Living-related liver transplantation of an ABO-compatible right hepatic lobe donated by his wife was performed. Preoperative three-dimensional dynamic enhanced computed tomography of the donor revealed that drainage veins from the middle hepatic vein had not developed in Couinaud segments V and VIII, that the main drainage route of venous return from right lobe of the liver was the right hepatic vein, and that there was no stenosis (Figure 1). The graft-to-recipient weight ratio was 0.89%. The main hepatic vein of the donor was anastomosed to the right hepatic vein of the recipient without reconstruction of the middle hepatic vein. The length of the orifice and the cuff of the right hepatic vein of the graft were 27 mm and 14 mm, respectively, and the length of the remnant right hepatic vein of the recipient was 8 mm. The detailed surgical procedure for hepatic vein reconstruction was as follows. The vascular clamp holding the stump of the right hepatic vein was positioned vertically on the inferior vena cava (IVC). The IVC was incised at the inferior end of the right hepatic vein orifice to adjust it to the length of the orifice of the hepatic vein of the graft. A portion of the anterior wall of the IVC was removed to make the orifice oval-shaped. End stitches of 5–0 polypropylene monofilament suture were placed on the superior and inferior ends. The superior stitch of 5–0 polypropylene monofilament suture was knotted, and one arm of the knotted stitch was passed through the posterior wall of the graft vein from the outside in, close to the first knot, and continued intraluminally to the inferior end. The anterior wall closure was completed in simple running suture fashion with the same stitch. There were no areas of congestion in the graft. Cold ischemic time was 47 min, and warm ischemic time was 59 min. Intraoperative Doppler ultrasound examinations showed no evidence of either stenosis or obstruction of the hepatic venous, portal venous, or hepatic arterial blood flow after reperfusion. Portal venous pressure was monitored with a catheter inserted into the superior mesenteric vein via a branch of the ileocolic vein. Before hepatectomy, it was 33 mmHg, but it decreased to 20 mmHg after transplantation, and ultimately to 9 mmHg on postoperative day (POD) 7. HBIg and lamivudine were given postoperatively, and immunosuppressive treatment with tacrolimus was started immediately after transplantation. On POD 10 the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (T-bil) values had decreased to 56 international units (IU)/mL, 41 IU/mL, and 2.8 mg/dL, respectively (Figure 2), and by POD 12 they had increased to 103 IU/mL, 81 IU/mL, and 3.6 mg/dL, respectively. The daily volume of ascitic fluid increased from less than 5000 mL to more than 10 000 mL on POD 11 (Figure 2). Ascitic fluid cultures were negative for mycobacteria and fungi, and no cytomegalovirus–antigen was detected on granulocytes in the ascitic fluid. A Doppler ultrasound examination on POD 12 revealed flat waveforms and low-flow velocity of 9.6 cm/s in the right hepatic vein (Figure 2), and a low-flow velocity of 11.7 cm/s in the right main portal vein. A hepatic venogram was performed on POD 13 because of clinical suspicion that hepatic venous obstruction had developed. The venogram showed stenosis of an intrahepatic vein, not of the anastomosis (Figure 3A), and examination of both the anterior-posterior view and lateral view (Figure 3B) hepatic venograms revealed that the stenotic intrahepatic vein was tortuous. Manometric venous pressure data obtained by withdrawing the catheter from the intrahepatic vein into the inferior vena cava showed a gradient of 14 mmHg across the intrahepatic stenosis (Figure 3C). The wedge pressure of the distal hepatic vein branch was 33 mmHg. We immediately inserted an EMS (diameter: 1.4 cm, length: 5 cm; Wallsten™, Boston Scientific, Nagoya, Japan K. K) into the right hepatic vein via the right internal jugular vein (Figure 4A), and the venous pressure gradient was found to have decreased to 4 mmHg (Figure 4B). A Doppler ultrasound examination after EMS placement showed a pulsatile waveform in the right hepatic vein and an increase in flow velocity at the same sites in the intrahepatic vein and the right main portal vein of 30.9 cm/s and 23.9 cm/s, respectively. The AST and ALT values had decreased to 31 IU/L and 30 IU/L, respectively, on POD 14. The daily volume of ascitic fluid decreased to less than 5000 mL from POD 18 onward, and continued decreasing to less than 500 mL from POD 25 onward. The patient developed to severe sepsis caused by coagulase-negative Staphylococcus aureus associated with increasing AST- and T-bil-values and decreasing flow velocity from POD 16 to POD 24, but treatment with Vancomycin was followed by recovery of their values. The patient was discharged on POD 55, and he has been working and enjoying a good quality of life for the past 7 months.