Comparison of histidine-tryptophan-ketoglutarate and University of Wisconsin in living-donor liver transplantation.

For cadaveric transplantations, histidine-tryptophan-ketoglutarate (HTK) and University of Wisconsin (UW) solutions have been shown to engender similar outcomes. In September 2004, our institution changed from UW to HTK as the primary preservation solution for liver and kidney transplantations. We reviewed records of living-donor liver transplant recipients from September 2001 to December 2005. This study compared early postoperative outcomes of liver transplantation using the 2 solutions. Perfusion was performed first via the portal vein and then via the hepatic artery until the outflow became clear. Patients were compared based on the organ preservation solution. The analysis included patient demographics, early postoperative complication rates, mortality rates, number of acute rejection episodes, costs for preservation solutions, and results of 1-, 7-, 14-, and 30- day liver function tests. Patients in both groups were managed with similar operative techniques, immunosuppressive regimens, and donor liver criteria. Statistical analyses were performed with chi- square and Mann-Whitney U tests. Donor and patient demographics were similar. No statistically significant differences were observed between the groups with regard to posttransplantation liver biochemistry, complication rates, number of acute rejection episodes, and mortality rates. The mean infused volume of preservation solution was 1000 +/- 400 mL (range, 500-2000 mL) for all patients. These volumes corresponded to a cost savings of US 148 dollars/L when using HTK solution. In conclusion, UW and HTK were equally effective and safe for perfusion of living-donor liver grafts; however, the use of HTK solution provided significant cost savings.

Arterial steal syndrome after orthotopic liver transplantation.

Arterial steal syndrome after orthotopic liver transplantation (OLT) is characterized by arterial hypoperfusion of the graft, which is caused by a shift in blood flow into the splenic or gastroduodenal arteries. In this report, we present mechanisms by which this syndrome caused ischemia in our patients. Steal was suspected by elevated levels of liver enzymes and the results of Doppler ultrasonography and computed tomographic angiography; it was confirmed by celiac angiography. Patients with established hepatic arterial thrombosis before angiography were excluded from this study. Steal was treated by embolization with a coil or by placement of an endoluminal narrowing stent. Ten patients at our institution (seven men and three women; mean age, 24.7 +/- 11 years; range, 6 to 40 years) exhibited biochemical evidence of liver ischemia and graft failure at 1 to 170 days after having undergone orthotopic liver transplantation. Nine of those patients had splenic steal, and one had both splenic and left gastric artery steal syndrome. None of the patients had gastroduodenal artery steal syndrome. The eight patients with splenic steal syndrome and the patient with both splenic and left gastric steal syndrome were treated by transcatheter occlusion with a coil. The remaining patient with splenic steal syndrome was treated with an endoluminal narrowing stent placement. All patients improved clinically within 24 hours after treatment, exhibiting significant changes in their biochemical and radiological parameters. Follow-up ranged from 1 to 22 months (mean, 6.7 +/- 6.6 months). One patient died from sepsis 1 month after having undergone coil embolization. He had no vascular anomalies at the time of death. We conclude that steal is a significant problem after OLT. Embolization and stenting are minimally invasive and successful treatments for steal, usually resulting early clinical improvement.