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Clinical Effects of Pediatric Clonidine Exposure: A Retrospective Cohort Study at a Single Tertiary Care Center
Michael S Toce1, Eli Freiman2, Katherine A O'Donnell3
1Harvard Medical Toxicology Program, Boston Children's Hospital, Boston, Massachusetts; Division of Emergency Medicine, Department of Pediatrics, Boston Children's Hospital, Boston, Massachusetts.
Insights
Pediatric clonidine ingestions commonly cause vital sign abnormalities, including bradycardia and hypotension. Naloxone showed some effectiveness, and safe medication storage is crucial, especially for adolescents.
Area of Science:
- Pediatric Emergency Medicine
- Clinical Toxicology
- Pharmacology
Background:
- Pediatric clonidine ingestions lead to frequent emergency department visits and hospital admissions.
- Limited data exists on the clinical course and timing of vital sign abnormalities in these pediatric cases.
Purpose of the Study:
- To analyze the rates and onset of vital sign abnormalities in pediatric clonidine poisoning.
- To describe treatment, disposition, and outcomes in a cohort of children with clonidine exposure.
Main Methods:
- Retrospective cohort study of patients under 21 with clonidine exposure (2004-2017).
- Patients were divided into younger (≤9 years) and older (10-21 years) age groups.
- Analysis focused on vital sign changes, mental status, and naloxone administration.
Main Results:
- 45% of patients experienced bradycardia, 32% bradypnea, and 44% hypotension.
- 80% of pediatric patients presented with depressed mental status.
- 38% received naloxone, with 50% showing a clinical response.
Conclusions:
- Clonidine exposure in children frequently causes altered mental status and vital sign abnormalities.
- Naloxone demonstrated partial effectiveness; high-dose use is suggested for severe non-opioid-dependent cases.
- Adolescents are more prone to self-ingestion, highlighting the need for secure medication storage education.
Background:
Pediatric clonidine ingestions frequently result in emergency department visits and admission for cardiac monitoring. Detailed information on the clinical course and specifically time of vital sign abnormalities of these patients is lacking.
Objective:
The objective of this study was to provide descriptive analysis of the rates and times to vital sign abnormalities, treatment, disposition, and outcomes in a single-center cohort of pediatric patients with report of clonidine poisoning.
Methods:
We performed a retrospective cohort study of patients younger than 21 years who presented to a large, urban, tertiary care center with a report of single substance clonidine exposure between January 2004 and November 2017. Patients were dichotomized into younger (≤9 years or younger) and older (10-21 years) groups based on the expected physiologic and psychologic differences between older and younger children.
Results:
Eighty-eight patients met our inclusion criteria. Younger patients (≤9 years or younger; n = 47) were more likely to be exposed to someone else's medication (53%) and older patients (10-21 years; n = 41) overwhelmingly (85%) were exposed to their own medication. Thirty-nine (45%) became bradycardic, 27 (32%) became bradypneic, and 38 (44%) became hypotensive. Eighty percent of patients had depressed mental status. Thirty-three (38%) patients received at least one dose of naloxone (median 0.07 mg/kg; interquartile range 0.03-0.11 mg/kg). Of those who received naloxone, 50% had a documented clinical response.
Conclusions:
In this study of patients at a pediatric tertiary referral center, pediatric patients with report of clonidine exposures were likely to exhibit altered mental status and frequently develop vital sign abnormalities. Naloxone exhibited some effectiveness; given its wide safety margin, high-dose naloxone should be used in critically poisoned non-opioid-dependent patients. Because adolescents are much more likely to ingest their own clonidine medication, counseling with parents and other caregivers regarding safe medication storage is paramount.
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