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Hypertension associated with clonidine ingestion
Insights
Accidental Clonidine hydrochloride (CH) ingestion in children can cause serious toxicity, including apnea, even with small doses. Prompt supportive care led to full recovery in all patients within hours.
Area of Science:
- Pediatric Toxicology
- Emergency Medicine
- Pharmacology
Background:
- Clonidine hydrochloride (CH) is an antihypertensive medication with complex alpha-adrenergic and CNS effects.
- Accidental ingestion of CH can lead to significant toxicity in pediatric patients.
Purpose of the Study:
- To review the clinical presentation and outcomes of pediatric patients admitted to the ICU after accidental Clonidine hydrochloride ingestion.
- To highlight the potential for severe toxicity from relatively small ingestions of CH.
Main Methods:
- Retrospective review of medical records for 5 children admitted to a Pediatric Intensive Care Unit (PICU) following accidental CH ingestion.
- Analysis of clinical signs, symptoms, ingested dose, treatment, and patient outcomes.
Main Results:
- All 5 patients presented with lethargy/stupor within 20-60 minutes post-ingestion.
- Four patients experienced respiratory depression or apnea, with 2 requiring intubation and 1 mechanical ventilation.
- Transient hypertension was observed in all patients; 3 developed asymptomatic bradycardia. Significant toxicity occurred despite estimated small ingestions (0.2-0.4 mg in 4/5 patients).
Conclusions:
- Apnea was the most critical adverse event observed following CH overdose in children.
- Even small ingestions of Clonidine hydrochloride can cause significant pediatric toxicity.
- Supportive care and GI decontamination were effective, with rapid resolution of toxicity and good patient outcomes.
Abstract:
Clonidine hydrochloride (CH) is an antihypertensive drug with complex pharmacologic activity including central and peripheral alpha-adrenergic stimulation and CNS depression. We reviewed the records of 5 children admitted to our Pediatric Intensive Care Unit following accidental ingestion of CH. All patients presented with lethargy or stupor, beginning 20-60 minutes after ingestion. Respiratory depression or apnea occurred in 4, requiring endotracheal intubation in 2 and mechanical ventilation in 1. All 5 developed mild to moderate hypertension, and 3 developed asymptomatic bradycardia. The dose of CH ingested was estimated to be 0.2-0.4 mg in 4 out of 5 patients. Treatment consisted of efforts to prevent absorption of CH from the GI tract and supportive care. All signs of CH toxicity resolved within 6-14 hours. Four patients were transferred from ICU within 24 hours and discharged home the following day. One patient developed post-extubation stridor and atelectasis. Significant toxicity occurred even though the amount of CH ingested was relatively small in at least 4 or 5 patients. Transient hypertension occurred early in the hospital course of all patients and resolved without treatment. Hypotension and symptomatic bradycardia were not observed. Apnea was the most serious abnormality observed. All patients recovered without significant morbidity.