Abstract: SA-PO0607
Mind the Gap: Pyroglutamic Acidosis Secondary to Acetaminophen Use for Postoperative Pain Control
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Pickford, Ashley, University of Utah Health, Salt Lake City, Utah, United States
- Conlon, Luke, University of Utah Health, Salt Lake City, Utah, United States
- Abraham, Josephine, University of Utah Health, Salt Lake City, Utah, United States
Introduction
Pyroglutamic acidosis is a rare cause of high anion gap metabolic acidosis.Pyroglutamic acidosis is commonly iatrogenic due to acetaminophen use which depletes glutathione and leads to a buildup of the metabolic intermediates. Acquired pyroglutamic acidosis is common in females and with malnutrition,alcohol use disorder, kidney disease, pregnancy, and infection.We present a case of pyroglutamic acidosis in a patient with acetaminophen use in the setting of a post-surgical infection.
Case Description
A 66-year-old woman with past medical history of alcohol use disorder, peripheral arterial disease and a complex history of vascular surgery with recent thrombectomy presented to the emergency department for wound dehiscence. Wound infection was managed with a course of daptomycin and cefepime. During the hospitalization she had persistently low oral intake in the setting of poor appetite and refusal of enteral nutrition. The patient received a multi-modal pain control regimen which included scheduled acetaminophen. On hospital day 31,an elevation of her creatinine from her baseline of 0.5 mg/dl to 2.6 mg/dl was observed along with oliguria and altered mentation. She developed a gap and non-gap metabolic acidosis with a serum bicarbonate of 8 mmol/L. Nephrology was consulted in the setting of the acute kidney injury and severe acidosis.Urine organic acid screen was positive for elevated levels of pyroglutamic acid (5-oxo-proline). Serum glutathione was checked and was found to be low. Acetaminophen was discontinued and N-acetylcysteine started at a dose of 600mg orally twice daily to replenish glutathione stores. Her acidosis improved and resolved at the time of discharge.
Discussion
Pyroglutamic acidosis is a rare complication of acetaminophen use. Factors such as malnutrition, alcohol use, infection contribute to depletion of glutathione and the buildup of pyroglutamic acid though depletion of cysteine and inhibition of 5-oxoprolinase enzyme.While this patient developed pyroglutamic acidosis due to acetaminophen administration during her extended hospitalization, her acidosis was ultimately correctible with the discontinuation of acetaminophen and administration of N-acetylcysteine.This case emphasizes that acetaminophen while an important component of a multi-modal pain control is not benign and should be carefully considered in patients with multiple risk factors for pyroglutamic acidosis.