Nonfatal Hyperammonemic Encephalopathy as a Late Complication of Roux-en-Y Gastric Bypass

Abstract

Roux-en-Y gastric bypass (RYGB) is the most common weight loss procedure performed in the US. Gastric bypass-related hyperammonemia (GaBHA) is a potentially fatal entity, characterized by encephalopathy associated with hyperammonemia and various nutritional deficiencies, which can present at variable time intervals after RYGB. Twenty-five cases of hyperammonemic encephalopathy after bariatric surgery have been previously reported in the literature. We describe the case of a 48-year-old Hispanic woman with no prior history of liver disease, presenting with nonfatal hyperammonemic encephalopathy as a late postoperative complication 20 years after undergoing a RYGB. Hyperammonemic encephalopathy in the absence of known hepatic dysfunction presents a diagnostic dilemma. An early diagnosis and intervention are crucial to decrease morbidity and mortality.

Figure 1

Urea cycle. Ammonia is the source of the first amino group in the urea cycle, required in the synthesis of carbamoyl phosphate (CPS), which happens in the hepatocyte mitochondria. The second amino group comes from glutamate in the formation of aspartate, which happens in the hepatocyte cytoplasm. This reaction produces α-ketoglutarate, which then becomes available for the Krebs cycle. The synthesis of argininosuccinate links the Krebs cycle and urea cycle. In the peripheral tissues, glutamate accepts free ammonia from amino acid catabolism. Glutamine transports ammonia from the peripheral tissues to the liver, where glutamine is broken back to glutamate and ammonia via glutaminase. AST, aspartate transaminase.