#3739 SHUNT PORTOSYSTEMIC COMPLICATED BY HYPERAMMONEMIA AND HEPATIC ENCEPHALOPATHY SUPPORTED BY DAILY DIALYSIS IN A CHRONIC HEMODIALYSIS PATIENT

Abstract

Abstract Background and Aims Hepatic encephalopathy is a neuropsychiatric syndrome that may develop as a consequence of liver insufficiency. In acute liver failure, hepatic encephalopathy suggests the severity of the disease. In end-stage chronic liver diseases, episodes of hepatic encephalopathy are frequently fully and spontaneously reversible. Clinical manifestations vary from mild neuropsychiatric disorders to coma. The pathogenesis of hepatic encephalopathy is complex and not clearly understood. Ammonia plays a key role. In the healthy individual, ammonia is, during its first hepatic passage, directly degraded into urea, itself excreted by the kidney and the stools, and to a lesser degree in glutamine. Ammonia is also metabolized by the muscle striped. In case of liver failure and/or shunts portosystemic, there is a defect in hepatic clearance ammonia which is then found in excess in systemic circulation. Decreased muscle mass, linked to malnutrition, frequent in the patient cirrhotic and chronic hemodialysis, also helps to decrease metabolism ammonia. Due to the increase in permeability of the blood-brain barrier, the brain is exposed to excessive concentrations ammonia causing functional brain abnormalities and structural, which can partly explain the signs neurology of hepatic encephalopathy. In end stage chronic renal failure, clearance of ammonia via extracorporeal treatment has not been systematically evaluated. Several studies with small samples have demonstrated the effectiveness of hemodialysis, compared to peritoneal dialysis, in terms of ammonium purification in chronic renal failure, on dialysis or not on dialysis. The aim of this study was to evaluate the effectiveness of daily dialysis for the purification of ammoniumin a chronic hemodialysis patient with hepatic encephalopathy. Case Report A 40-year-old man undergoing chronic hemodialysis was referred to gastroenterology department of Mohammed VI University center of Marrakesh for inoperable shunt portosystemic complicated by hyperammonemia causing hepatic encephalopathy consisting of headaches and seizures. His medical history was significant for liver cirrhosis caused by infection with hepatitis B, end stage kidney disease due to membranoproliferative glomerulonephritis, for which the patient is on hemodialysis at the rate of 3 sessions per week. The patient went on to develop portal hypertension and ascites requiring frequent hospital admissions and treatment with diuretics. He was on a low-protein and low-sodium diet. While on oral furosemide 250 mg daily and spironolactone 100 mg daily, his diuresis was adequate. Before referral, this patient had already suffered 4 episodes of tonic clonic seizures. His 1st hemodialysis session in our training was on January 10, 2023, he was given daily hemodialysis sessions with daily blood tests, including immediate pre and post dialysis ammonia. Pre-dialytic ammonia levels varied between 103 and 161 µmol/l, as well as post-dialytic ammonia levels varied between 24 and 37 µmol/l, knowing that the normal value of laboratory ammonia varied between 10 and 51 µmol/l. The evolution was marked by a clear clinical improvement, with a disappearance of the seizures without a significant drop in ammonia after 14 daily hemodialysis sessions. Serum creatinine and urea declined, and sodium increased. Accumulation of ascites slowed and the patient could eat and sleep normally and was again independent with self care. The patient returned home on January 24. Conclusion This study shows the interest of daily hemodialysis sessions as a potential treatment for hyperammonemia in a patient on chronic intermittent hemodialysis, with a portosystemic shunt. The interest lies in the fact that the improvement is mainly clinical than biological (persistent hyperammonemia).