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Published on: February 4, 2014
Clinical course and toxicokinetic data following isolated citalopram overdose in an infant
Lawrence N Masullo1, Michael A Miller, S David Baker
1Darnall Army Community Hospital, Ft Hood, TX 76544, USA.
Insights
Citalopram overdose in a 10-month-old infant caused refractory seizures but no cardiovascular issues. The infant recovered fully, with citalopram elimination half-life estimated at 17.38 hours.
Area of Science:
- Pediatric Toxicology
- Clinical Pharmacology
- Emergency Medicine
Background:
- Citalopram is a commonly prescribed selective serotonin reuptake inhibitor (SSRI).
- Limited data exists on citalopram overdose effects and pharmacokinetics in pediatric patients.
- Understanding overdose management is crucial for this age group.
Observation:
- A 10-month-old female ingested an unknown quantity of citalopram.
- The infant experienced refractory generalized tonic-clonic seizures, treated with midazolam and fosphenytoin.
- No cardiovascular abnormalities (hypotension, dysrhythmia, QTc prolongation) were observed.
Findings:
- Plasma citalopram levels were monitored over 23 hours post-ingestion.
- The calculated elimination half-life (t1/2) of citalopram was approximately 17.38 hours.
- Despite seizures, the infant experienced an uneventful recovery and was discharged without sequelae.
Implications:
- This case highlights the potential for severe neurological effects in pediatric citalopram overdose.
- The observed elimination half-life provides valuable pharmacokinetic data for infant overdose scenarios.
- Prompt and aggressive seizure management is critical for favorable outcomes in pediatric SSRI poisoning.
Objective:
Despite the frequency of use of citalopram, its clinical effects and pharmacokinetics in overdose in the pediatric patient are not well described. We describe the clinical course and drug levels following the ingestion of citalopram by a 10-month-old female.
Case Report:
A 10 month-old female ingested an unknown amount of citalopram. Approximately 40 min after ingestion, the child developed horizontal nystagmus, followed by a generalized, tonic-clonic seizure that lasted 2 to 3 min very shortly thereafter. The child received 1 mg of midazolam intramuscularly (IM), followed by 1 mg of midazolam intravenously (IV) for termination of this seizure, and was given a loading dose of 20 mg/kg of fosphenytoin IV. Elective orotracheal intubation was done to protect the airway. Despite the use of midazolam and fosphenytoin, the child had another seizure approximately 85 min following the ingestion. A third seizure was noted at approximately 100 min post-ingestion. In the course of treatment, activated charcoal was administered via nasogastric tube, and IV midazolam and phenobarbital were given. The child was transferred to a nearby facility with pediatric intensive care capabilities in stable condition. The child did not experience any hypotension or dysrhythmia, and the electrocardiographic QTc and QRS complex were normal throughout the clinical course. During the subsequent 48 h, the child awoke and regained normal function. This child's recovery was uneventful, and the child was discharged home without sequelae. Plasma levels of citalopram were 1400 ng/ml, 583 ng/ml, 416 ng/ml, and 296 ng/ml, at one, six, 13, and 23 h post-ingestion, respectively. The first level likely represents a predistributional level with subsequent levels giving an elimination t1/2 of 17.38 h.
Conclusion:
We report a case of citalopram poisoning in a 10-month-old infant with refractory seizures, and an absence of cardiovascular events with subsequent excellent outcome. The elimination of the parent drug corresponds to an approximate t1/2 of 15-20 h in this single case.
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