Intoxicacion Por Acetaminofen

Clinical Toxicology (2013), 51, 50–53
Copyright © 2013 Informa Healthcare USA, Inc.
ISSN: 1556-3650 print / 1556-9519 online
DOI: 10.3109/15563650.2012.748195

BRIEF COMMUNICATION

Acetaminophen/diphenhydramine overdose in profound
hypothermia
A. D. ROLLSTIN1 and S. A. SEIFERT2
1UNM

Clinical Toxicology Downloaded from informahealthcare.com by HINARI on 01/21/13
For personal useonly.

2New

School of Medicine, Emergency Medicine & Anesthesia, Albuquerque, NM, USA
Mexico Poison Center, MSC09 5080, 1 University of New Mexico, Albuquerque, NM, USA

Background. There are few reports of acetaminophen overdose in hypothermic patients and even fewer reports describing profound
hypothermia. The kinetics, risk of hepatotoxicity, and the possible dose adjustments toN-acetylcysteine (NAC) therapy are not known in
this setting. Case report. A 37-year-old female was found unconscious outside in December and was brought by ambulance to a tertiary care
Emergency Department (ED) following a presumed overdose of acetaminophen and diphenhydramine. She later confirmed the ingestion
and reported the ingestion had occurred approximately 18 hours prior to being found. Onarrival, she was profoundly hypothermic, with
a core rectal temperature of 17°C. Her initial serum acetaminophen concentration was 232 mcg/mL 19 hours post ingestion of a reported
dose of approximately 50 grams of acetaminophen and 2.5 grams of diphenhydramine. Active rewarming was started immediately and
IV NAC was initiated using the standard treatment protocol. The patient did not develop serioussigns of hepatic injury or NAC toxicity.
The patient’s AST and ALT peaked 12 hours after admission at 84 IU/L (ref 10–37 U/L) and 104 IU/L (ref 12–78 U/L), respectively.
Her INR peaked 2 hours after admission at 1.46 (ref 1.2). Discussion. Despite the significant ingestion of acetaminophen, delayed
presentation, prolonged period of decreased responsiveness, and profound hypothermia, thepatient did not develop any signs/symptoms of
liver injury. NAC was administered in a standard dose during her rewarming period without apparent toxicity. The patient’s absorption and/
or metabolism of acetaminophen were likely slowed by her hypothermia and possibly by the anticholinergic coingestant. Initiation of IV
NAC at a standard dose was apparently safe and effective in preventinghepatotoxicity as the patient was rewarmed. Conclusions. Profound
hypothermia may be protective of hepatic injury in acetaminophen overdose. Delayed absorption from the coingestant, diphenhydramine,
may also have played a role. IV NAC was given in a standard dose without apparent toxicity in the setting of profound hypothermia.
Lastly, IV NAC, in standard dosing, appeared to be effective in preventinghepatotoxicity during rewarming in a patient with a potentially
hepatotoxic concentration of acetaminophen with a coingestion of the anticholinergic agent, diphenhydramine.
Keywords Analgesics; Complications of poisoning, Other; Pharmaceuticals, Metabolic; Organ/tissue specific; Paracetamol; Complications
of poisoning, Liver

Introduction

Her heart rate was between 28 and 40 bpm, with anundetermined rhythm, oxygen saturation was 96%, and a blood
pressure could not be obtained. The patient moaned occasionally but was otherwise not responsive. Blue pills found in her
pocket upon arrival at a tertiary care emergency department
(ED) were identified as “Tylenol PM®” (acetaminophen
and diphenhydramine; McNeil-PPC, Inc.). On arrival at
the hospital, her core body temperature was 17°C.She was
moaning, with incomprehensible words, and her initial GCS
was 10 (Eyes 4; Verbal 1; Motor 5). Patient was in the ED for
approximately 40 minutes. While in the ED, two 18-gauge
peripheral IVs were placed. Her rewarming/resuscitation was
begun using warmed fluids, a forced air warming blanket,
warming lights, and her Foley catheter, which was lavaged
with warm fluid.

There are few...