Dextromethorphan Overdose with Refractory Status Epilepticus and Reversible Cranial Nerve Reflex Loss: A Case Report
Akifumi Okamoto, Naoki Yonezawa, Kazuhiro Yoshizawa, Reiki Kumashiro, Shinya Suzuki
The American journal of case reports February 7, 2025 DOI: 10.12659/ajcr.946447 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | A 21-year-old woman with schizophrenia who attempted suicide by ingesting dextromethorphan and other prescribed medications |
| Interventions | Dextromethorphan Propofol Midazolam Endotracheal intubation |
| Dose | 20 280 mg |
| Duration | 9-day hospital stay |
| Key findings | The patient survived a massive dextromethorphan overdose (20,280 mg) that caused refractory status epilepticus and reversible cranial nerve reflex loss, with full recovery by discharge on day 9. Serum dextromethorphan concentrations declined from 5.8 mg/L to 1.1 mg/L over two days while dextrorphan remained within therapeutic limits, which the authors interpret as suggesting dextromethorphan rather than its metabolite was responsible for the symptoms. |
Abstract
Patient: Female, 21-year-old Final Diagnosis: Dextromethorphan overdose with refractory status epilepticus and reversible cranial nerve reflex loss Symptoms: Status epilepticus Clinical Procedure: — Specialty: Toxicology
Objective: Unusual clinical course
Background: Dextromethorphan is a widely used over-the-counter antitussive medication. Generally safe within the recommended dosages, its misuse can lead to severe adverse effects, particularly in large amounts. However, comprehensive descriptions of severe overdose cases – including pharmacokinetic data of dextromethorphan and its active metabolite (dextrorphan) – are scarce. Case Report: A 21-year-old woman with schizophrenia ingested 20 280 mg of dextromethorphan along with other prescribed medications during a suicide attempt. She was discovered semiconscious and experienced a generalized seizure en route to the hospital. Despite intensive treatments – including endotracheal intubation and administration of propofol and midazolam – she continued to experience refractory status epilepticus. Subsequent neurological examination revealed cranial nerve reflex loss. The serum concentration of dextromethorphan was 5.8 mg/L on admission and decreased to 2.2 mg/L by day 1 and 1.1 mg/L by day 2, contrasting with that of dextrorphan, which remained within the therapeutic limits. By day 4, her condition stabilized; she became alert, responsive to commands, and was successfully extubated. She was discharged on day 9 without any sequelae.
Conclusions: This report describes the case of a patient who survived a massive dextromethorphan overdose, who presented with refractory status epilepticus followed by reversible suppression of cranial nerve reflexes. The pharmacokinetic profiles suggested that dextromethorphan, rather than dextrorphan, was responsible for the symptoms. High-dose dextromethorphan ingestion can lead to varied and potentially fatal outcomes, especially when compounded by metabolism-altering factors such as CYP2D6 inhibition, genetic variability, or co-ingested medications. This case underscores the importance of prompt, intensive supportive care in managing severe dextromethorphan toxicity.