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Graft Portal Vein Thrombosis Before Liver Transplant.

S injuries during organ procurement and vascular thrombosis may deteriorate liver graft quality and post–liver transplant (LT) outcome, regardless of donor characteristics. Graft hepatic artery thrombosis before LT has been described. Conversely, there are no reports on graft portal vein thrombosis (gPVT) recognized during organ procurement. The aim of this letter is to describe 2 cases of gPVT recognized and treated within donor procedures. In the first case, a 75-year-old woman died of an embolic stroke (brain death donor [DBD]) during arteriovenous extracorporeal membrane oxygenation after cardiocirculatory arrest. Once donor hepatectomy was completed, gPVT became evident and thrombectomy was performed. The histopathologic analyses showed 50% macrovesicular and 40% microvesicular steatosis, focal microthrombosis, and multifocal sinusoidal dilatation. Based on the presence of steatosis, portal vein thrombosis (PVT), and sinusoidal damage, the graft was discarded. In the second case, a 62-year-old man DBD, who died for subarachnoid hemorrhage, was allocated to our Center as rescue allocation due to 40% macrovesicular steatosis. The procurement was performed by a separate transplant center team using in situ aortic cold perfusion and portal vein perfusion after hepatectomy. No abnormalities, except for steatosis and vasoactive drug infusion, were reported. The unexpected allocation (eg, urgent allocation) imposed to use a back-base dual hypothermic oxygenated machine perfusion (DHOPE) to extend cold ischemia time and recondition a steatotic graft (Table 1). Upon the beginning, suboptimal portal flow and resistances indicated poor graft viability (Figure 1). These hemodynamic data imposed an additional evaluation. The graft was then handled for a macroscopic inspection, and a gPVT was identified. A Doppler ultrasound (US) confirmed this diagnosis. We disconnected the graft and performed a thrombectomy (Figure 1). To evaluate the efficacy of thrombectomy and the possible presence of an intrahepatic PVT, we reconnected the graft to DHOPE. Portal and hepatic artery flow/resistances immediately reached normal values. After 345 minutes of DHOPE, the graft was successfully transplanted. Total cold ischemia time was 710 minutes. No liver (eg, early allograft dysfunction) or kidney complications occurred. Post-LT computed tomography and US showed no residual intraparenchymal PVT. Posttransplant vascular complications are the most common causes of graft failure after LT. Among them, post-LT PVT was reported in 5% of the patients. The most documented risk factors for post-LT PVT are related to primary liver disease and pre-LT medical history, while donor influence has not been exhaustively