Kidney Week

Abstract: PUB100

Beyond the Threshold: Early Hemodialysis in a Patient with Severe Acetaminophen Toxicity with Mitochondrial Dysfunction

Session Information

• Publication Only

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

• Imam, Nimrah H., Olive View UCLA Medical Center, Sylmar, California, United States

Nimrah H. Imam, DO

• Kamarzarian, Anita, Olive View UCLA Medical Center, Sylmar, California, United States

Anita Kamarzarian, MD, FASN

• Gunasekaran, Vidhya, Olive View UCLA Medical Center, Sylmar, California, United States

Vidhya Gunasekaran, MD

• Jafari, Golriz, Olive View UCLA Medical Center, Sylmar, California, United States

Golriz Jafari, MD

• Pham, Phuong-Chi T., Olive View UCLA Medical Center, Sylmar, California, United States

Phuong-Chi T. Pham, MD, FASN

Introduction

Acetaminophen overdose is a leading cause of acute liver failure. N-acetylcysteine (NAC) is the primary therapy, while kidney replacement therapy (KRT) is recommended in massive ingestions, typically when serum levels exceed 900 µg/mL with metabolic acidosis or altered mental status. However, early mitochondrial toxicity may warrant dialysis even below this threshold.

Case Description

A 34-year-old man with depression presented after suspected intentional acetaminophen overdose with unknown timing. He required intubation for altered mental status. Initial evaluation showed acetaminophen level 776 µg/mL and lactate 7.9 mmol/L, creatinine of 0.27mg/dL, and normal transaminases (with peak INR 1.5). Despite a level below the conventional dialysis threshold, the presence of severe lactic acidosis and encephalopathy raised concern for early mitochondrial toxicity. Following toxicology consultation, intravenous NAC was initiated, and the patient underwent urgent intermittent hemodialysis. After NAC initiation and first dialysis, acetaminophen levels decreased to 615 µg/mL and then 439 µg/mL. A second dialysis session further reduced levels to 261 µg/mL, ultimately reaching <5 µg/mL, with normalization of lactate to 1 mmol/L. Liver enzymes remained within normal limits throughout hospitalization. The patient was extubated and discharged without evidence of hepatotoxicity.

Discussion

Massive acetaminophen toxicity can cause early mitochondrial dysfunction manifesting as lactic acidosis and altered mental status prior to hepatocellular injury. While guidelines emphasize level based thresholds for dialysis, this case demonstrates that clinical severity may justify earlier KRT. Hemodialysis facilitates rapid drug clearance and correction of acidosis, while NAC mitigates hepatotoxicity. Of note, NAC is dialyzable and requires dose adjustment during dialysis.

Conclusion:
In severe acetaminophen toxicity, early dialysis should be considered in the presence of metabolic acidosis and encephalopathy, even when serum levels are below traditional thresholds. A physiology driven approach may prevent progression to acute liver failure and improve outcomes.