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.

Extrahepatic portosystemic shunts as an unusual but treatable cause of hyperammonemic encephalopathy in a noncirrhotic patient – a case report

“… 9 Hyperammonemic encephalopathy has also been described as a complication of bariatric surgery. 10 , 11 Furthermore, exposure to various substances has been associated with hyperammonemia, including carbamazepine, ribavirin, methamphetamine and chemotherapeutic agents, such as 5-FU. 12 – 16 While the underlying mechanisms are not well understood in most of these agents, a clearer concept exists for the etiopathogenesis of VPA-induced hyperammonemia.…”

Hyperammonemia in the setting of Roux-en-Y gastric bypass presenting with osmotic demyelination syndrome

“…With the increasing rate of obesity in the USA, bariatric surgery continues to be offered as a weight loss treatment. However, over time, there have been multiple case reports on the correlation between RYGB and hyperammonemia in the absence of cirrhosis or liver disease [1][2][3][4]. The onset of hyperammonemic encephalopathy after RYGB has been shown to present at various intervals, ranging from months to years [1].…”

“…Ammonia is a nitrogen-containing compound, mainly produced in the small bowel by glutaminase, which converts glutamine into ammonia and glutamate. Ammonia is then metabolized by the liver, converted to urea -a nontoxic substance -and excreted through the kidneys [4,7]. Any disruption in this process can lead to excess ammonia, which is a potent neurotoxin as it can penetrate the bloodbrain barrier by diffusion [3].…”

“…Any disruption in this process can lead to excess ammonia, which is a potent neurotoxin as it can penetrate the bloodbrain barrier by diffusion [3]. This can manifest as changes in behavior, slurred speech, lethargy, coma and ultimately death [4].…”

“…It can cause a multitude of neurotoxic effects such as cerebral edema, brain herniation and ultimately death. Multiple case reports have now shown that Roux-en-Y gastric bypass (RYGB) can be a causative factor of hyperammonemia in the absence of liver disease [1][2][3][4]. The exact underlying mechanism is not entirely clear, but due to alteration of the gut microbiome in association with nutritional deficiencies, these are thought to be the two main reasons for increased ammonia level [1].…”