Case Report
Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2014; 20(25): 8288-8291
Published online Jul 7, 2014. doi: 10.3748/wjg.v20.i25.8288
Novel therapy for non-cirrhotic hyperammonemia due to a spontaneous splenorenal shunt
Shari S Rogal, Angela Hu, Rupal Bandi, Obaid Shaikh
Shari S Rogal, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, United States
Angela Hu, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, United States
Rupal Bandi, Department of Radiology, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, United States
Obaid Shaikh, Division of Gastroenterology, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, United States
Author contributions: All authors contributed to writing and editing the manuscript.
Supported by Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development
Correspondence to: Shari S Rogal, MD, MPH, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, 200 Lothrop Street, M Level, C Wing, PUH, Pittsburgh, PA 15213, United States. rogalss@upmc.edu
Telephone: +1-412-6489115 Fax: +1-412-6489378
Received: October 2, 2013
Revised: December 10, 2013
Accepted: January 14, 2014
Published online: July 7, 2014
Processing time: 274 Days and 13.2 Hours
Abstract

Spontaneous splenorenal shunts in the absence of cirrhosis have rarely been reported as a cause hyperammonemia with encephalopathy. Several closure techniques of such lesions have been described. Here we report a case of a patient with no history of liver disease who developed significant confusion. After an extensive workup, he was found to have hyperammonemia and encephalopathy due to formation of a spontaneous splenorenal shunt. There was no evidence of cirrhosis on biopsy or imaging and no portal hypertension when directly measured. The shunt was 18 mm and too large for embolization so the segment of the splenic vein between the portal vein and the shunt was occluded using an Amplatzer plug. Thus, the superior mesenteric flow was directed entirely to the liver. After interventional radiology closure of the shunt using this technique there was complete resolution of symptoms. The case represents the first report of a successful closure of splenorenal shunt via percutaneous embolization of the splenic vein with an amplatzer plug using a common femoral vein approach.

Keywords: Splenorenal shunt; Gastric bypass; Hyperammonemia; Encephalopathy

Core tip: This is the first reported case of non-portal hypertension associated hepatic encephalopathy related to a large splenorenal shunt that was successfully closed percutaneously with an Amplatzer plug applied to the splenic vein.