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Abstract: SA-PO495

Unexplained Metabolic Acidosis: Look for Acetaminophen!

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

  • Sriperumbuduri, Sriram, The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Harris, Liliia, The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Avula, Uma Mahesh R., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Osman, Safa, The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Schwartz, Carter V., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Tio, Maria Clarissa, The University of Mississippi Medical Center, Jackson, Mississippi, United States
Introduction

High anion gap metabolic acidosis (HAGMA) is a common clinical scenario and often presents as a diagnostic challenge. We present an often-overlooked etiology of HAGMA in a hospitalised patient.

Case Description

A 65-year-old-female with atrophic right kidney and hypertension was referred to our hospital for management of a recently diagnosed urothelial bladder malignancy. She had multiple hospitalisations for urosepsis in the past 3 months. Labs showed low serum albumin of 2.3 mg/dl and serum creatinine of 0.65 mg/dl at the time of current admission. She underwent radical cystectomy and open right nephroureterectomy (for recurrent urosepsis). Post operatively she developed ileus and was started on total parenteral nutrition (TPN).

One week later, she developed progressively worsening HAGMA. Initial evaluation at the onset of acidosis showed high blood glucose with normal serum beta hydroxybutyrate (BHB) level. Insulin infusion was started and TPN was held. Despite giving sodium bicarbonate, HAGMA continued to worsen with decline in serum bicarbonate up to 10 mEq/l and increase in anion gap (AG) to 36 mEq/l by post operative day 17.

Serum lactate was normal and there was no exposure to salicylates or alcohol. Serum creatinine was 0.9 mg/dl indicating mild acute kidney injury. Chart review showed a cumulative exposure of 49.7 grams to Acetaminophen over 19 days after the surgery. Urine 5-oxoproline was ordered and it was elevated at 1401 mmol/mol of creatinine. Liver function tests remained normal. Acetaminophen was held and intravenous N-Acetyl cysteine (NAC) was given for a total dose of 300 mg/kg over one day. Serum AG normalized after 3 days of NAC to 12 mEq/L and bicarbonate improved to 23 mEq/L after one week.

Discussion

This case highlights 5-oxoprolinemia as a differential for HAGMA in a hospitalized patient with chronic acetaminophen exposure. Exposure to high cumulative doses of acetaminophen in patients with predisposing factors (elderly, females, malnutrition, sepsis, chronic acetaminophen exposure) should raise concern for this condition.