Fatal Interplay of Over-the-Counter Medications Leading to Acute Liver Failure

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Chest

Abstract

INTRODUCTION: Acetaminophen overdose is a leading cause of drug-induced acute liver failure (ALF), and its hepatotoxic effects are well-documented. However, the concurrent use of propylene glycol, a common excipient in over-the-counter medications such as NyQuil, can significantly exacerbate the clinical presentation and outcomes of acetaminophen toxicity. This case illustrates the critical interaction between acetaminophen and propylene glycol, leading to acute fulminant liver failure and multi-organ dysfunction. CASE PRESENTATION: A 45-year-old man with a history of myotonic dystrophy, type 2 diabetes mellitus, and hypertension presented to an outside hospital after being found unresponsive. He had recently developed an upper respiratory tract infection and had been using acetaminophen and NyQuil. On arrival, he was minimally responsive, hypoxic, and required 6 L/min of supplemental oxygen. He was intubated for airway protection, and respiratory PCR testing confirmed influenza A infection. Initial laboratory findings revealed a severe metabolic acidosis (pH 7.14, bicarbonate 9 mmol/L), high anion gap (29 mmol/L), and lactic acidosis (lactate 15 mmol/L). Serum chemistry showed hyperkalemia (5.3 mmol/L), elevated liver enzymes (AST 15,133 U/L, ALT 2,592 U/L), hyperbilirubinemia (total bilirubin 6.3 mg/dL), and hyperammonemia (277 μmol/L). Blood and respiratory cultures were obtained, and initial toxicology screening identified an elevated acetaminophen level (45.3 μg/mL). Propylene glycol was also elevated (12.6 mg/dL), likely from NyQuil use. Imaging studies revealed multifocal bronchopneumonia without pulmonary embolism, and a right upper quadrant ultrasound confirmed acalculous cholecystitis. The patient was transferred to our tertiary care center for liver transplantation evaluation. N-acetylcysteine was initiated promptly for acetaminophen toxicity, and continuous renal replacement therapy (CRRT) was started for worsening metabolic acidosis and lactic acidosis. Despite intensive resuscitation with vasopressors, the patient's condition deteriorated. His family declined CPR, and he passed away before liver transplantation could be performed. DISCUSSION: Acetaminophen overdose is well-known for its hepatotoxicity, but the addition of propylene glycol exacerbates the clinical presentation. Propylene glycol can cause significant metabolic derangements, including lactic acidosis, hyperosmolality, and renal failure, which compound the effects of acetaminophen-induced hepatotoxicity. The pathophysiology of acetaminophen toxicity involves the formation of a reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI), which depletes glutathione stores and results in oxidative stress and hepatocyte death. Propylene glycol, while generally recognized as safe, can lead to serious metabolic derangements, particularly in patients with pre-existing liver dysfunction or renal impairment. In this case, the elevated propylene glycol level of 12.6 mg/dL, likely from NyQuil use, compounded the effects of acetaminophen toxicity, contributing to severe metabolic acidosis, lactic acidosis and multi-organ failure. Management of acetaminophen and propylene glycol toxicity requires prompt intervention. N-acetylcysteine (NAC) is the antidote for acetaminophen overdose and was initiated in this case. Additionally, continuous renal replacement therapy (CRRT) was employed to address the worsening metabolic acidosis and lactic acidosis. Despite these interventions, the patient's condition deteriorated, highlighting the poor prognosis associated with fulminant hepatic failure, particularly when compounded by additional toxicities. CONCLUSIONS: In conclusion, the interaction between acetaminophen and propylene glycol can lead to severe and life-threatening complications, necessitating careful consideration in clinical practice.

Volume

168

Issue

4S

First Page

3422A

Last Page

3423A

Comments

American College of Chest Physicians CHEST Annual Meeting, October 19-22, 2025, Chicago, IL

DOI

10.1016/j.chest.2025.07.1924

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