Hostname: page-component-cd9895bd7-lnqnp Total loading time: 0 Render date: 2024-12-26T08:57:33.723Z Has data issue: false hasContentIssue false

Lamotrigine as a possible cause of QRS prolongation in a patient with known seizure disorder

Published online by Cambridge University Press:  21 May 2015

Thomas J.S. Herold*
Affiliation:
Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas
*
Department of Emergency Medicine, Darnall Army Community Hospital, 36000 Darnall Loop, Fort Hood TX 76544-4752; 254 288-8302, fax 254 288-8093, HeroldTJ64@aol.com

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Lamotrigine and felbamate are 2 newer anticonvulsant medications used to control refractory partial and generalized seizures. Although several cases of lamotrigine toxicity secondary to acute intentional or unintentional overdose have been described, there is little published information related to potential side-effects associated with the therapeutic use of these agents. Described is a case of a 22-year-old woman who presented to the emergency department after experiencing 2 seizure-like episodes. Findings on evaluation included nystagmus, ataxia, widening of the QRS complex and right-axis deviation on ECG. The patient reported only therapeutic use of her medications. The lamotrigine level was 14.8 mg/L. The mechanism of action for lamotrigine is blockade of the sodium channels; therefore, the patient was treated with intravenous sodium bicarbonate with resultant QRS narrowing following administration.

Type
Case Report • Observations de cas
Copyright
Copyright © Canadian Association of Emergency Physicians 2006

References

1.Verrotti, A, Trotta, G, Morgese, G, et al. New antiepileptic drugs in childhood. Panminerva Med 2002;44:221–5.Google Scholar
2.Ticku, MK, Kamatchi, GL, Sofia, RD. Effect of anticonvulsant felbamate on GABA receptor system. Epilepsia 1991;32:389–91.Google Scholar
3.Cohen, AF, Land, GS, Breimer, DD, et al. Lamotrigine, a new anticonvulsant: pharmacokinetics in normal humans. Clin Pharm Ther 1987;42:535–41.Google Scholar
4.Dollery, C, editor. Therapeutic drugs. CD Release 1.0, 1999.Google Scholar
5.Buckley, NA, White, IM, Dawson, AH. Self-poisoning with lamotrigine. Lancet 1993;342:1552–3.Google Scholar
6.Peano, C, Leikin, JB, Hanashiro, PK. Seizures, ventricular tachycardia, and rhabdomyolysis as a result of ingestion of venlafaxine and lamotrigine. Ann Emerg Med 1997;30:704–8.Google Scholar
7.Pricone, MG, King, CV, Drummer, OH, et al. Postmortem investigation of lamotrigine concentrations. J Forensic Sci 2000;45:11–5.Google Scholar
8.Triage drugs of abuse plus TCA [pamplet]. San Diego (CA):Biosite Inc; 1996.Google Scholar
9.Poklis, A, Edinboro, LE, Lee, JS, et al. Evaluation of a colloidal metal immunoassay device for detection of tri-cyclic antidepressants in urine. J Toxicol Clin Toxicol 1997;35:7782.Google Scholar
10. Hill, AB. The environment and disease: association or causation? Proc R Soc Med 1965;58:295300.Google Scholar
11.O’ Donnell, J, Bateman, DN. Lamotrigine overdose in an adult. J Toxicol Clin Toxicol 2000;38:659–60.Google Scholar
12.Briassoulis, G, Kalabalikis, P, Tamiolaki, M, et al. Lamotrigine childhood overdose. Ped Neuro 1998;19:239–42.Google Scholar