SummaryPostshunt hepatic encephalopathy after liver transplantation (LT) is an infrequent condition and is commonly associated with portal occlusion or stenosis and the presence of a patent portosystemic shunt. Portal vein stenosis (PVS) or thrombosis (PVT) are uncommon complications after LT. The overall frequency of both complications is reported to be less than 3%. 1,2 When PVS or PVT develop early after LT, the occlusion of the portal vein can have catastrophic consequences to the graft including acute liver failure and graft loss. Late PVT/PVS are asymptomatic in 50% of the cases 2 and mainly diagnosed by a routine ultrasound. Symptomatic postshunt hepatic encephalopathy (HE) is a very infrequent condition after LT that has been scarcely reported in the literature. 3,4 We present here the case of a liver recipient with normal graft function who presented with hepatic encephalopathy 3 months after LT with stable liver function but a severe portal stenosis and the presence of a spontaneous portosystemic shunt whose successful endovascular treatment was followed by the complete resolution of the HE.
Case ReportA 58-year-old man with cryptogenic cirrhosis (Child-Pugh score A, MELD 9) was listed for LT in June 2010 due to an early stage 2.5 cm hepatocellular carcinoma. He also had experienced a few episodes of grade 2 episodic HE which were properly treated with lactulose. He underwent an LT with a deceased-donor liver graft on January 2011. The patient had an uneventful postsurgical evolution and was discharged on a cyclosporine-based immunosuppression protocol. Four weeks after LT a severe stenosis of the biliary anastomosis was diagnosed and successfully treated employing an endoscopic approach.Two months later, the patient was admitted because of evident bradypsychia, confusion, and flapping tremor. Serum ammonia levels were raised (80 lmol/ L, normal range 16-60). Liver function tests were in the normal range with preserved synthetic and excretory function and renal function was normal. Also, common precipitating factors of HE (infection, constipation, gastrointestinal bleeding, not-prescribed medications, etc.) were excluded. At admission his 2-hour postdose cyclosporine blood level (C2) was 601 ng/mL, which ruled out calcineurin inhibitor-related neurotoxicty. A brain magnetic resonance imaging (MRI) only showed high signal intensity in the globus pallidum on T1-weighted images with no other abnormalities. An abdominal MRI showed a normal liver graft but a severe stenosis of the portal anastomosis and a patent splenorenal shunt (Fig. 1), which was confirmed by angiography ( Fig. 2A). Persistent isolated small type 1 gastric varices (diagnosed before LT) were visualized with an upper digestive endoscopy. Employing a balloon, an endovascular dilation of the stenosis was successfully performed. Simultaneously, the splenorenal shunt was successfully occluded with a plug Amplatzer II and metallic coils (Fig. 2B). Twenty-four hours after the procedure, neurological examination was completely normal with no flap...