Olga N. Tucker

Successful outcome following transplantation of an injured liver from a nonheart beating donor

Nonheart beating donation (NHBD) of the liver is a relatively new potential source of grafts. Guidelines to indications and contraindications to donation from controlled nonheart beating donors are still being formulated. We report a successful case of transplantation of a liver from a controlled nonheart beating donor who sustained significant injuries following a road traffic accident. Emergency laparotomy with peri‐hepatic packing was performed to control haemorrhage from lacerations in segments VI and VII. Forceful packing resulted in an area of focal ischaemia in segment VI. Trauma to the liver should not be considered an absolute contraindication to controlled NHBD.

Graft positioning at liver transplantation in situs inversus

Situs inversus (SI) totalis is a rare congenital anomaly. In the past it was considered an absolute contraindication to liver transplantation (LT) because of associated malformations, and difficulty achieving accurate graft positioning. We describe successful outcome following LT in a 41-year-old with alcoholrelated chronic liver disease and complete SI using a novel technique (Fig. 1). Recipient hepatectomy was uncomplicated. A donor whole liver was implanted using a piggyback technique. Reduced space in the right upper quadrant from the stomach and spleen resulted in 40% clockwise graft rotation. To attenuate this effect, the left diaphragm was plicated and a Sengstaken-Blakemore tube was inserted percutaneously into the left upper quadrant (LUQ). The gastric balloon was inflated with 400 ml of normal saline to support the left lobe (Fig. 2). The donor remnant falciform ligament was fixed to the recipient diaphragmatic surface to effect long-term optimal positioning. Abdominal CT scan on day 7 demonstrated the gastric balloon elevating and supporting the graft (Figure 3). On day 12, 200 ml of normal saline was aspirated with gradual balloon deflation over the next 3 days, and removal of the Sengstaken-Blakemore tube on day 15. Serial Doppler ultrasonography demonstrated normal hepatic venous flow. An abdominal CT scan at 3 months demonstrated no change in graft position (Figure 4A). The hepatic veins, portal vein and hepatic artery appeared patent (Figure 4B). The patient remains well 17 months following LT with normal graft function. Abdominal SI is described in association with the polysplenia syndrome with inferior vena caval absence, preduodenal portal vein, midgut malrotation, aberrant hepatic arterial anatomy, and portal vein hypoplasia. Anatomic anomalies result in a more complex recipient hepatectomy. Consideration has to be given to correct donor graft positioning, and additional vascular reconstruction. However, LT has been performed successfully using modified surgical techniques. Most cases are in the paediatric population in whom graft displacement and hepatic venous pedicle torsion are less due to a smaller abdominal cavity when even split and reduced grafts are typically large-for-size, and greater use of caval replacement techniques. Cadaveric segmental and living related left lateral segment grafts have been successfully placed with suitable orientation for hilar vessel anastomoses. However, in adults following recipient hepatectomy, a large empty space exists in the LUQ predisposing to lateral displacement with supero-lateral graft rotation and torsion of the hepatic venous pedicle particularly with a piggyback technique. Split, reduced, and right lobe living related LT have been performed successfully. Technical modifications with an intact recipient cava include piggyback implantation over the right suprahepatic vein with orthotopic graft position, and graft rotation by 90°. In our patient, only partial volume reduction of the left hepatic fossa was achieved by diaphragmatic plication. Due to its large size, filling the defect with omentum and mobilized hepatic flexure would have been inadequate. The use of a Sengstaken-Blakemore tube represents an innovative and simple technique to provide effective graft support, and reduce the risk of outflow obstruction. Subsequent peri-hepatic adhesion formation and migration of bowel loops into the LUQ would be expected to provide longterm graft fixation.

Peribiliary Cysts Can Mimic Caroli’s Disease: A Case Report

Peribiliary cysts, otherwise known as cystic dilatation of the peribiliary glands, are uncommon, and are usually discovered incidentally at autopsy, or in explants following liver transplantation. Preoperative diagnosis is often difficult owing to their asymptomatic nature and small size. Exclusion of a premalignant or malignant cystic condition is mandatory. We report a case of peribiliary cysts, initially thought to represent Caroli’s disease, and briefly discuss the management of this condition.

Liver transplantation with caval thrombectomy and cavoatrial shunt in acute Budd‐Chiari syndrome

A 38-year-old woman was admitted to her local hospital with acute-onset upper abdominal pain and vomiting. Examination revealed mild jaundice, ascites, smooth, tender hepatomegaly, and bilateral lower limb edema. Liver function tests were abnormal, with increased serum bilirubin of 37 mol/L and aspartate transaminase of 515 IU/L. Abdominal ultrasound revealed a diffusely enlarged hypoechoic liver with thrombus in the inferior vena cava (IVC) extending to the hepatic veins, moderate ascites, and a patent portal vein. A procoagulant screen was normal, with the exception of lupus anticoagulant, which was increased at 1.46 (normal range 0.8-1.2). No anticoagulation therapy had been used. Abdominal computed tomographic scan confirmed the presence of luminal caval thrombus extending from the level of the bifurcation superiorly to the right atrium (RA) (Fig. 1). The patient was transferred to our liver intensive care unit for further management of acute Budd-Chiari syndrome. Her clinical condition deteriorated over several days, and she was listed for urgent liver transplantation. Intraoperative findings included moderate ascites, severe portal hypertension, and an enlarged, hard, congested liver. The IVC was thrombosed along its length from the iliac veins to the RA. Access for left axillary vein to portal vein venovenous bypass was prepared early. The femoral veins were not cannulated because of the presence of iliac thrombus. The supradiaphragmatic IVC was severely stenosed, with extensive hard caval thrombus. A midline sternotomy was performed, the RA cross-clamped just below the coronary sinus, and the stenotic IVC excised. The infrahepatic vena cava was thrombectomized with a Foley and a large Fogarty catheter, followed by retrograde infusion of 3 mg of recombinant tissue plasminogen activator. The liver was removed after clamping the infrahepatic vena cava. Because the donor heart had been retrieved leaving a very short suprahepatic cava, donor infrarenal IVC was used as an interpositional graft, with anastomosis to the RA (Fig. 2). The graft was implanted by first suturing the suprahepatic vena cava to the caval interpositional graft. The infrahepatic vena cava was re-bled, and a further thrombectomy performed. Portal, arterial, and