Unmasking Hyperammonemia: Psychomotor Slowing as a Diagnostic Trigger During PEG and Enteral Nutrition

A 63-year-old female patient received percutaneous endoscopic gastrostomy (PEG) and continuous enteral nutrition (EEN) for anxiety-related feeding difficulties and weight loss. Notably, she had a background of anxiety and insomnia, managed with escitalopram, zolpidem, and estazolam for several years. One month after PEG and EEN, though weight increased, she exhibited episodes of intermittent psychomotor slowing, and the Montreal Cognitive Assessment (MoCA) revealed significant neuropsychological findings. Cranial computed tomography (CT), cranial and cervical magnetic resonance and angiography imaging (MRI+MRA), and hepatic ultrasonography revealed no significant abnormalities. Notably, the patient’s plasma ammonia levels were persistently elevated, reaching 117.6 μmol/L (normal range 15-45 μmol/L). After PEG tube removed and semi-liquid oral diet received, her plasma ammonia levels normalized, psychomotor symptoms resolved, and MoCA score significantly improved. The patient remains under regular follow-up, with stable ammonia levels and restored cognitive function.

For surgeons and gastroenterologists managing long-term PEG and EEN, hyperammonemia is an easily overlooked but potentially severe complication, particularly when patients present with subtle, non-specific neurocognitive changes. While hyperammonemia typically presents with varying degrees of neurological and hepatic impairment, our patient predominantly exhibited insidious psychomotor slowing and cognitive deficits. ¹ To the best of our knowledge, this is the first reported case of hyperammonemia explicitly associated with PEG and EEN.

Percutaneous endoscopic gastrostomy is a feasible approach for long-term enteral nutrition, significantly improving nutritional status in patients with feeding difficulties. The overall incidence of complications associated with PEG is approximately 20-30%. ² Percutaneous endoscopic gastrostomy and EEN may result in alterations of intestinal microbiota, inappropriate nitrogen input, or deficiencies in substrates and cofactors of the urea cycle. Continuous intragastric feeding with PEG slows gastric emptying and intestinal peristalsis, promoting bacterial overgrowth. ³ Continuous enteral nutrition is also recognized as a potential cause of hyperammonemia. ⁴ High-protein formulas or rapid bolus feedings can saturate hepatic urea cycle capacity. ⁵ Conversely, chronic inadequate protein intake may induce post-receptor glucagon resistance in the liver, significantly reducing urea synthesis. Furthermore, commercial enteral nutrition formulas often have limited micronutrient content, potentially resulting in insufficient supply of substrates or cofactors necessary for the urea cycle. Previous case reported that carnitine deficiency inhibits β-oxidation, ⁶ subsequently leading to saturation of extramitochondrial ammonia transport pathways and ammonia accumulation. In this case, the patient received Peptisorb, which do not include additional carnitine supplementation.

A major target population for PEG tube placement includes patients with severe neuropsychiatric disorders who experience feeding difficulties. Changes in mental status in these patients can be subtle and easily misattributed to their underlying psychiatric conditions or medications. ⁷ Unexplained psychomotor slowing—especially when neuroimaging is unremarkable—should serve as an immediate diagnostic trigger for blood ammonia testing. As demonstrated in this case, immediate management through dietary modification and PEG removal can rapidly reverse the condition. ⁵ Surgeons should remain vigilant regarding specialized enteral formula selection (such as monitoring for carnitine deficiency) and establish routine neurocognitive monitoring for vulnerable patients on long-term EEN.