Abstract | March 15, 2024
Portosystemic Shunt Occlusion as Treatment for Recurrent Hepatic Encephalopathy Secondary to Congestive Hepatopathy
Learning Objectives
- Recognize chronic congestive hepatopathy as a potential cause of hepatic disorders (cirrhosis, hepatic encephalopathy, ascites, etc)
- Demonstrate understanding the pathophysiology of cardiac cirrhosis versus other etiologies of cirrhosis (alcohol, NAFLD, viral, etc)
Introduction: Congestive hepatopathy promotes susceptibility to ammonia (NH4) accumulation through multiple mechanisms but markedly from decreased hepatic flow/clearance secondary to increased portal pressures. Hyperammonemia can manifest as hepatic encephalopathy (HE) and can be challenging to manage medically with the progression of heart failure and potential cirrhosis.
Case Presentation: A 65-year-old male with a history of heart failure with reduced ejection fraction complicated by congestive hepatopathy, moderate mitral stenosis, and end-stage renal disease on hemodialysis presented to the ED for the eleventh time in eighteen months for acutely worsening confusion. HE with hyperammonemia was determined as the root cause of altered mentation at every prior admission. NH4 levels during active encephalopathy ranged from 65mcMol/L to 222mcMol/L. Prior episodes of encephalopathy were associated with events resulting in a femur fracture and a subdural hematoma. Prior liver biopsy and right heart catheterization with hepatic circulatory measures were consistent with congestive hepatopathy. Genetic studies for inherent urea cycle defects were also unremarkable. Despite strict home management with oral lactulose, rifaximin, zinc, and lactulose enemas; the patient once again presented with altered mentation. During this admission, NH4 was elevated to 152mcMol/L which clinically presented with a GCS score of 8.
Management/Outcome: Initially, the patient responded to multiple lactulose enemas, improving alertness and orientation. However, this was followed by multiple encephalopathic relapses despite aggressive medical management and consecutive dialysis sessions. Repeat abdominal CT imaging did reveal a portosystemic splenorenal shunt, routinely seen in patients with portal hypertension. In theory, closure of this shunt would reduce systemic NH4 levels and promote NH4 processing by the liver. After deliberation with a multidisciplinary team and shared decision-making with the patient’s family, the decision was made to pursue the occlusion of the splenorenal shunt. Interventional radiology performed a successful balloon-occluded retrograde transvenous obliteration (BRTO) of the splenorenal shunt. Over the next four days, improvements in alertness, orientation, and cognition were reported with the patient returning to baseline per family. At the two-week follow up patient had remained at baseline without further deterioration. Repeat NH4, four weeks after the procedure was <9 mcMol/L.
References and Resources
- Rodriguez Ziccardi M, Pendela VS, Singhal M. Cardiac Cirrhosis. [Updated 2023 Apr 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431053/.
- Suk KT. Hepatic venous pressure gradient: clinical use in chronic liver disease. Clin Mol Hepatol. 2014 Mar;20(1):6-14. doi: 10.3350/cmh.2014.20.1.6. Epub 2014 Mar 26. PMID: 24757653; PMCID: PMC3992331.
