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Abstract: SA-PO501

Fireball Whiskey-Induced Severe Lactic Acidosis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Maheshwari, Priya Kumari, HCA Florida West Hospital, Pensacola, Florida, United States
  • Sabra, Michel J., HCA Florida West Hospital, Pensacola, Florida, United States
  • Goldsmith, William W., HCA Florida West Hospital, Pensacola, Florida, United States
  • Issac, Maro, German University in Cairo, New Cairo, Cairo, Egypt
  • Harrison, Anil, HCA Florida West Hospital, Pensacola, Florida, United States
  • Fahim, Peter, HCA Florida West Hospital, Pensacola, Florida, United States
Introduction

Propylene glycol (PG) is metabolized by alcohol dehydrogenase in the liver into lactate, which further converts to pyruvate. Excessive consumption of Fireball whiskey, containing PG, can lead to lactic acidosis.

Case Description

A 36-year-old patient with a history of alcoholism presented to the ED due to increased work of breathing and SOB. Upon arrival, the patient was afebrile with a heart rate of 128 bpm, BP of 112/52 mmHg, RR of 28 breaths per minute, and SpO2 of 98% on room air. He was encephalopathic, and the rest of his physical examination was unremarkable.

Initial laboratory investigations were significant for severe anion gap metabolic acidosis with a bicarbonate level of 13 mmol/L and an anion gap of 31, elevated lactic acid of 19.3 mmol/L, hyponatremia, hypomagnesemia, hypophosphatemia, elevated transaminases, elevated total bilirubin, and neutrophilic leukocytosis. A chest CT scan with IV contrast was unremarkable. Additionally, an EKG revealed sinus tachycardia. ABG revealed a pH of 7.4, pCO2 of 16, and bicarbonate of 8.8. The ethanol level was negative.

The patient received fluid resuscitation with 30 ml/kg and empiric antibiotics and was admitted to the medical floor. Subsequently, the patient was transferred to ICU due to respiratory distress and concerns regarding potential intubation needs. In the ICU, serum osmolality was measured at 281 mosm/kg with no osmolar gap, and a urine drug screen returned negative. Further inquiry revealed heavy Fireball whiskey consumption over recent days with concern for PG intoxication. Treatment included fluid resuscitation and aggressive electrolyte replacement, resulting in the clearance of lactic acid. However, the patient's hospital course was complicated by acute respiratory failure secondary to aspiration pneumonia, necessitating intubation, critical illness myopathy leading to extubation failure and requiring tracheostomy, and acute kidney injury which resolved. Fortunately, the patient was successfully decannulated before discharge.

Discussion

This case illustrates a low threshold to consider PG intoxication in alcoholic patients presenting with severe lactic acidosis. Our patient didn't have a high osmolar gap as the PG had already been metabolized to lactic acid. Hence, fomepizole was not administered, and given that he cleared lactic acid with fluid resuscitation, hemodialysis was not performed.