Citation

Forbes RA, Kalra H, Hackett LP, Daly FF. Emerg. Med. Australas. 2007; 19(6): 556-558.

Affiliation

Intensive Care Unit, Royal Perth Hospital, Perth, WA, Australia.

Copyright

(Copyright © 2007, Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine, Publisher John Wiley and Sons)

DOI

10.1111/j.1742-6723.2007.00973.x

PMID

18021110

Abstract

Tiagabine is an anticonvulsant acting by selective inhibition of neuronal and glial gamma-aminobutyric acid uptake, resulting in increased gamma-aminobutyric acid-mediated inhibition in the brain. Few reports in the literature describe the clinical course of severe tiagabine intoxication. A 44-year-old woman presented after deliberate self-poisoning with 100 tiagabine 15 mg tablets (1500 mg; 25 mg/kg). Serum tiagabine level was 4600 microg/L (1725 mmol/L) at presentation, 20 times levels associated with therapeutic dosing. Intoxication was manifested by profuse vomiting, coma, myoclonus, generalized rigidity, bradycardia, hypertension, hypersalivation and generalized piloerection within 2 h of ingestion. The patient was intubated and management was supportive. Coma lasted until 10 h post-ingestion, but recovery was complicated by severe agitated delirium lasting 12 h. The patient recovered fully within 26 h of ingestion. Tiagabine deliberate self-poisoning was associated with the rapid onset of coma and an unusual toxidrome. Recovery, although complicated by agitated delirium, was complete within 26 h.

Language: en