Pediatrics
Prospective evaluation of mild to moderate pediatric acetaminophen exposures

Preliminary data presented at the Society for Academic Emergency Medicine annual meeting, Washington, DC, May 1997.
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Abstract

Study objective: To determine whether pediatric patients with acute, mild to moderate acetaminophen exposures, treated with home monitoring alone, develop systemic signs of hepatic injury. Methods: A prospective, observational study of calls to a regional poison center over a 25-month period was performed. Patients were eligible for the study if they were younger than 7 years and had an acute maximum possible acetaminophen exposure of up to 200 mg/kg. Exclusion criteria included previous decontamination measures, possibility of ingestion of an extended-release preparation, health or medication issues that could increase susceptibility to hepatotoxicity, current symptoms of hepatotoxicity, and indeterminable ingestions. Study protocol included reviewing the signs and symptoms of early and late acetaminophen toxicity, a 4- to 6-hour follow-up call, and a 72-hour follow-up call. Outcome measures were defined as a verbal report by the patient’s parent or guardian of the presence or absence of signs or symptoms of hepatotoxicity. Results: A total of 1,039 patients were enrolled in the study, including 519 girls and 520 boys, with exposures ranging from 20 to 200 mg/kg. Eighteen patients were lost to follow-up; data were incomplete for 2 patients. At 72-hour follow-up, the remaining 1,019 patients were all doing well, without signs or symptoms of hepatotoxicity. Conclusion: On the basis of these data, pediatric patients with acute acetaminophen exposures of up to 200 mg/kg, treated with home monitoring alone, do not develop signs or symptoms of hepatic injury. [Mohler CR, Nordt SP, Williams SR, Manoguerra AS, Clark RF. Prospective evaluation of mild to moderate pediatric acetaminophen exposures. Ann Emerg Med . March 2000;35:239-244.]

Section snippets

INTRODUCTION

Acetaminophen is one of the most commonly ingested medications in the United States. Although generally considered to be a safe drug, acetaminophen poisoning can result in significant morbidity and mortality, including fulminant hepatic necrosis, acute renal failure, and liver transplantation.1, 2, 3, 4, 5 Millions of dollars in health care expenditures are spent annually to rule out and treat acetaminophen poisoning.6, 7, 8 During 1997, the American Association of Poison Control Centers

MATERIALS AND METHODS

We performed a prospective, observational study of telephone calls involving acute mild to moderate pediatric acetaminophen or acetaminophen-containing products presenting to a regional PCC, from March 1, 1996, to March 31, 1998. All children who had not yet reached their seventh birthday, with acute maximum possible acetaminophen ingestions of up to 200 mg/kg, were entered into the study protocol. Patients were excluded from the study if any gastrointestinal decontamination procedures had been

RESULTS

During the study period, the PCC received 89,679 calls regarding human exposures. Of these, 1,039 cases (520 boys and 519 girls) were enrolled in the study; average patient age was 2.3 years (Figure).

Figure. Algorithm of cases of mild to moderate acetaminophen exposures reported to San Diego Division of the California Poison Control System during the study period. APAP, Acetaminophen.

Data for 2 cases were incomplete. Estimated exposures ranged from 20 to 200 mg/kg; 236 patients had exposures of

DISCUSSION

In this study, we followed 1,019 children with acute acetaminophen ingestions of up to 200 mg/kg with home monitoring alone. There were no adverse outcomes at 72-hour follow-up in this population.

Acetaminophen remains a common pediatric exposure in the United States.6, 7, 8 A number of studies have recognized that children appear to be somewhat protected from severe hepatotoxicity from acute acetaminophen ingestions.3, 9, 10, 11, 12, 13 Authors have postulated that this is partly due to the

Acknowledgements

We thank the staff of the San Diego Division of the California Poison Control System, without whom this study would not have been possible. We also acknowledge the statistical assistance of Reena Deutsch, PhD, and G. Paul Shragg, MA, of the General Clinical Research Center at the University of California, San Diego, who are supported by NIH grant M01 RR00827.

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    Address for reprints: Christy Rosa Mohler, MD, UCSD Medical Center, Department of Emergency Medicine, 200 West Arbor Drive, MCH 8676, San Diego, CA 92103; fax 619-543-3115; E-mail [email protected] .

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