Long Live the Liver! Accidental Prophylaxis With N-acetylcysteine in Intentional Acetaminophen Overdose 2401

Acetaminophen overdose is one of the most common causes of poisoning worldwide, and can lead to fulminant hepatic failure necessitating transplant if untreated. While the risk of dose-dependent injury is high without intervention, outcomes are generally positive if the antidote, N-acetylcysteine (NA...

Full description

Saved in:
Bibliographic Details
Published in:The American journal of gastroenterology Vol. 113; no. Supplement; p. S1340
Main Authors: Soliman, Megan, Soliman, Youssef, Gurell, Michael
Format: Journal Article
Language:English
Published: New York Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins 01-10-2018
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Acetaminophen overdose is one of the most common causes of poisoning worldwide, and can lead to fulminant hepatic failure necessitating transplant if untreated. While the risk of dose-dependent injury is high without intervention, outcomes are generally positive if the antidote, N-acetylcysteine (NAC), is administered within 8-10 hours from acetaminophen ingestion. We present a case of intentional acetaminophen overdose of unknown duration wherein the liver enzymes remained relatively stable, possibly due to NAC consumption as part of a mental health supplement prior to admission. A 66-year-old female with history of depression presented after her husband found her unresponsive. Three empty bottles of acetaminophen-codeine and acetaminophen-oxycodone were found. The timeline of ingestion was not known. Her depression was previously controlled on lithium, but this had recently been discontinued due to development of diabetes insipidus. She was instead taking an over-the-counter mental health supplement called MethylCare™. Cardiopulmonary resuscitation was initiated by a family member until the ambulance arrived. Her initial heart rhythm was pulseless electrical activity and she received multiple rounds of CPR along with epinephrine and naloxone. She was intubated and transferred to the critical care unit. Her initial acetaminophen level was 320 ug/ml. She was given both intravenous and oral NAC as well as activated charcoal through a nasogastric tube. Her initial liver function tests were as follows: AST 142 U/L, ALT 101 U/L, alkaline phosphatase 89 IU/L, total bilirubin of 0.3 mg/dL, and INR of 1.3. Her INR peaked at 1.9 and then trended back to normal range within 48 hours. She was extubated and transferred to the psychiatry unit for titration of depression medications. It was discovered later that an ingredient in her MethylCare™ supplement was 600mg of NAC. NAC acts as a glutathione substitute in acetaminophen overdose which helps convert toxic metabolites to a nontoxic conjugate that can be excreted. When this is given within 8-10 hours of acetaminophen overdose, it can prevent liver damage. While our patient's timeline of overdose is not clear, she fully recovered, possibly because she was already taking NAC. This raises the possibility of a prophylactic role for NAC in patients at risk for overdose that has not been previously described.
ISSN:0002-9270
1572-0241
DOI:10.14309/00000434-201810001-02400