Reply.

Abstract

Potential conflict of interest: Nothing to report. TO THE EDITOR: We thank Kashani et al. for their contribution in reporting successful portosystemic shunt (PSS) embolization in a post–liver transplantation (LT) patient with hepatic encephalopathy (HE). As mentioned in our series, 2 patients underwent PSS embolization for HE in the post‐LT period.1 One was found to have a residual shunt within the first year after LT and enjoyed a sustained benefit at 1 year. The second patient's shunt was discovered nearly 20 years after LT. Clinical improvement was achieved in the short term following embolization, but thereafter required re‐institution of medical therapy. Within 1 year following embolization, the patient was noted to also have allograft cirrhosis and portal hypertension necessitating retransplantation. Available data regarding PSS embolization for refractory HE is sparse,2 but such data in the post‐LT population are extremely limited. An extensive review of the literature demonstrated only a few case reports of PSS embolization in post‐LT patients. Arab et al.7 described the development of HE in a 58‐year‐old patient with cryptogenic cirrhosis 2 months following LT for early stage hepatocellular carcinoma. Further evaluation demonstrated a normal allograft, but severe stenosis of the portal anastomosis and a patent splenorenal shunt that, retrospectively, was present on pretransplant magnetic resonance imaging. Following endovascular dilation of the stenosis and occlusion of the splenorenal shunt with an Amplatzer occluder (AGA Medical Corporation, Golden Valley, MN) and coils, the patient was free of HE for 15 months. At this time, he was again discovered to have recurrent stenosis of the portal vein anastomosis with concurrent development of collateral veins. After stenting of the stenotic anastomosis and providing coil embolization to the collateral veins, he again achieved resolution of HE at follow‐up 13 months later. Herrero et al.8 also reported on a 58‐year‐old male with alcoholic cirrhosis who developed recurrent HE 10 months after transplant. A large portosystemic shunt was discovered, which was also retrospectively noted on pretransplant imaging. Coil embolization and Amplatzer occluder were placed to embolize the large shunt and the patient remained HE‐free 10 months later. We appreciate the report of successful PSS embolization in the post‐LT setting by Kashani et al. As they suggest, the presence of portosystemic shunts should be a consideration in posttransplant patients with normal functioning grafts who are presenting with features suggestive of HE. However, the data on PSS embolization after LT are sparse, and caution should be exercised. If PSS embolization is considered, we postulate that outcomes would be more durable in the early posttransplant period, rather than late after LT when patients would be more likely to have advanced allograft fibrosis and portal hypertension.