Embolization of portosystemic shunts for treatment of medically refractory hepatic encephalopathy.

Abstract

Potential conflict of interest: Nothing to report. Vinay Sundaram, Amir Kashani, and H.G. Lipshutz were responsible for drafting the manuscript. Vinay Sundaram, Juvelyn Palomique, Andrew S. Klein, Irene Kim, H.G. Lipshutz, and Marc L. Friedman were responsible for critical revision of manuscript. Vinay Sundaram is the guarantor of the article. All authors approved the final version of the article, including the authorship list. TO THE EDITOR: We read with great interest the study by Lynn et al. in Liver Transplantation.1 The authors reported a 92% hepatic encephalopathy (HE)–free rate in patients at 6‐12 months after portosystemic shunt (PSS) embolization. Their study included 2 patients who had undergone transplantation, one of whom received sustained benefit, whereas the other developed allograft dysfunction and recurrent HE. Below, we report a case of a patient who underwent PSS embolization for HE after orthotopic liver transplantation (OLT), without complications and who no longer requires medical therapy for HE. A 60‐year‐old patient with hepatitis C cirrhosis and hepatocellular carcinoma underwent OLT on May 11, 2015. Four months afterward, he was hospitalized with altered mental status. After a negative workup including head computed tomography scan, electroencephalography, and infection testing, combined with an elevated ammonia level of 128 mcmol/L, a diagnosis of hepatic encephalopathy was considered. He was treated with lactulose, which improved his mental status, and he was discharged home. Given the uncertainty surrounding the diagnosis of HE, he was not instructed to take lactulose at home. The patient was readmitted 5 days afterward with another episode of HE. Ammonia level on presentation was 131 mcmol/L, and he again received lactulose with resolution of encephalopathy. Blood tests demonstrated a normally functioning allograft, and liver biopsy demonstrated stage 0 fibrosis. However, a review of his pre‐OLT imaging revealed a large splenorenal shunt. Transhepatic splenoportography revealed hepatofugal flow into the splenorenal shunt and no appreciable filling of intrahepatic portal vein branches. The hepatic venous pressure gradient, measured during his transjugular liver biopsy, was 1 mm Hg. The patient was counseled regarding the findings and treatment options. Given the severity of side effects he experienced with lactulose, he stated that he could not take this medication on a daily basis. Additionally, he could not receive rifaximin due to the expense of this medication. Therefore, it was decided to proceed with embolization of the splenorenal shunt, which successfully reestablished hepatopetal flow (Fig. 1). Subsequently, lactulose was discontinued, and the patient no longer had symptoms of HE. After 7 months of follow‐up, he remains symptom‐free without need for lactulose and with normal allograft function.Figure 1: Images before and after PSS embolization. (A) Before embolization: filling of the proximal main portal vein, with hepatofugal flow into the splenorenal shunt and through the left renal vein into the inferior vena cava. (B) After embolization: restoration of flow through the main portal vein and runoff into the right and left and intrahepatic portal branches.Our case illustrates that when managing HE after OLT, a PSS should be considered as an etiology, either due to shunting which existed prior to OLT or to the development of a PSS de novo after OLT, due to, for instance, increased intrahepatic vascular resistance secondary to acute cellular rejection.2 Furthermore, we report that embolization of PSS was safe and effective after OLT in our patient and can be considered as a therapeutic option for HE occurring after liver transplantation.