S4126 A Rare Case of Hyperammonemic Encephalopathy Following Roux-en-Y Gastric Bypass Surgery

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Introduction: As bariatric surgery becomes increasingly common, clinicians must remain vigilant for rare but life-threatening complications like hyperammonemic encephalopathy. In Roux-en-Y gastric bypass (RYGB) patients, catabolic stress, rapid weight loss, and nutritional deficiencies can unmask latent urea cycle disorders (UCDs). Prompt recognition is critical to prevent irreversible neurologic injury. We report a case of hyperammonemic encephalopathy in a post-RYGB patient, unmasked by infection and nutritional stress, highlighting the importance of early metabolic evaluation in patients with unexplained altered mental status. Case Description: A 54-year-old woman with a history of bipolar disorder, chronic obstructive pulmonary disease, recurrent urinary tract infections (UTI), and prior RYGB presented with acute confusion. She was found to have a UTI due to Enterococcus faecalis and started on intravenous antibiotics, but her mental status worsened, prompting intensive care unit transfer. On admission: Blood pressure 93/55 mmHg, heart rate 116 bpm, SpO₂ 91%, and temperature 98.9°F. Labs revealed ammonia of 186 µmol/L with normal liver function tests. Electroencephalogram was consistent with metabolic encephalopathy; brain magnetic resonance imaging showed no acute pathology. She was started on lactulose, rifaximin, vitamin B12, and thiamine. Wernicke’s encephalopathy was ruled out and psychiatric medications were tapered. Despite treatment, her encephalopathy worsened, requiring intubation, with persistently elevated ammonia levels. Given her severe protein-calorie malnutrition, she had been receiving protein-enriched enteral nutrition, which was suspected to be exacerbating hyperammonemia. L-carnitine was initiated and protein intake discontinued. Ammonia declined to <10 µmol/L within 24 hours, and she was successfully extubated with cognitive improvement. She was transitioned to a low-protein diet and discharged to a long-term acute care facility for outpatient metabolic and genetic evaluation for suspected UCD. Discussion: This case underscores the importance of considering UCDs in post-RYGB patients with persistent hyperammonemia and normal liver function. Postoperative catabolic stress and nutritional deficiencies can unmask partial enzyme defects. Diagnosis relies on elevated ammonia with preserved liver function. Management includes ammonia-lowering agents, protein restriction and nutritional support. Early recognition is critical to prevent neurologic deterioration. Clinician awareness and further research are needed to guide screening in high-risk bariatric populations.

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