A 53-yr-old man with uncompensated cirrhosis due to hepatitis B and hepatocellular carcinoma received a living-donor liver transplantation (LDLT) from his healthy son. His BMI was 25.9 kg m⁻² (height, 172 cm; weight, 66.2 kg). He had previously experienced episodes of massive oesophageal variceal bleeding which were treated by endoscopic injection sclerotherapy (EIS). Preoperative oesophageal endoscopy showed no signs or symptoms of rupture. Laboratory evaluations included: haemoglobin, 9.9 g dl⁻¹; white blood cell count, 4400 μl⁻¹; platelet count, 37 000 μl⁻¹; aspartate aminotransferase (AST), 78 IU litre⁻¹; alanine aminotransferase (ALT), 52 IU litre⁻¹; albumin (Alb), 2.5 g dl⁻¹; prothrombin time–international normalized ratio (PT–INR), 1.99; total bilirubin (T-Bil), 6.3 mg dl⁻¹; creatinine, 0.61 mg dl⁻¹; and NH₃, 45 μg dl⁻¹. His Child–Turcotte–Pugh score was 13 and the model of end-stage liver disease (MELD) score was 21. A large number of collateral veins were observed on contrast abdominal computed tomography (CT) and prophylactic splenic artery modulation was used to decompress the portal hypertension. Anaesthesia was induced with midazolam, remifentanil, and isoflurane with rocuronium for tracheal intubation. Anaesthesia was maintained with isoflurane and remifentanil. The pre-anhepatic phase proceeded uneventfully, with stable systemic arterial pressure and central venous pressure (CVP) remaining at 5–10 mm Hg. However, after the ligation of the ligamentum teres hepatis, arterial pressure gradually reduced. A definite bleeding source was not identified in the surgical field, but sudden gastric distension was observed. The CVP also gradually decreased and rapid transfusion was initiated. The circulation was supported pharmacologically with phenylephrine and a norepinephrine infusion at 0.05–0.1 μg kg⁻¹ min⁻¹ to maintain a mean arterial pressure >55 mm Hg. The nasogastric tube was blocked by clots, but sudden haemorrhage from the mouth and nose helped to identify the bleeding as coming from an upper gastrointestinal varix. The stomach was opened in an attempt to control the bleeding under direct vision. The varix was overseen in stages by intermittently releasing the applied pressure and allowing time for blood volume to be restored. All respective collateral veins were ligated after liver implantation, and the haemodynamic status was gradually stabilized. In total, 90 units of packed red cells, 150 units of fresh-frozen plasma (FFP), and 60 units of platelets were required. After transplantation, further transfusions were required, but the haemodynamic status and laboratory data remained stable (haemoglobin: 9.1, 8.9, and 9.1 mg dl⁻¹ and INR: 1.61, 1.44, and 1.54 on postoperative days 1, 2, and 3). Endoscopic examination confirmed the absence of bleeding and the trachea was extubated in the intensive care unit on postoperative day 1. No bleeding from the varix occurred after operation.