Lamotrigine overdose
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Lamotrigine overdose Metabolic encephalopathy secondary to drug toxicity: case report
A 38-year-old man developed metabolic encephalopathy secondary to toxicity following an overdose of lamotrigine for suicidal purposes. The man, who had a history of hypertension and migraine, presented with abnormal movements and sudden episodes of loss of consciousness. Cerebral MRI and video EEG showed no pathological findings. However, he had been receiving oral lamotrigine 150 mg/12h with limited therapeutic adherence. Later, he attempted suicide by ingesting lamotrigine of approximately 1000mg. On presentation, 8 hours after ingestion, he had tachycardia, blood pressure 148/70 [unit not stated], baseline oxygen saturation 95%, blood glucose 182 mg/dL and axillary temperature 36.2°C. Marks on the lateral edges of the tongue were observed with nausea and vomiting indicating epileptic seizure. Neurological findings showed the following: partially oriented, somnolent, bradypsychic, dysarthria, mildly myotic, pupils reactive, obeys commands, no campimetric disturbances, no speech alteration, downward vertical nystagmus, no limitations of external eye movements, no cranial pairs impairment, muscle balance in the limbs, generalised hyperreflexia, ataxia in the upper limbs and perpetual bilateral Achilles’ clonus. Bilateral Hoffman’s sign showed bilateral flexorplantar cutaneous reflex with no nuchal rigidity or other evidence of meningeal compromise and associated with mild oppressive headache. The emergency study revealed he had metabolic acidosis and isolated leukocytosis. Renal function, hepatic panel, calcium and magnesium ion level were normal. The urine toxins panel was negative, and no alteration in urinary sediment. Brain CT and baseline EEG showed no pathological findings, and lumbar puncture with an opening pressure of 22.5cm H2O. No alteration was found in cerebrospinal fluid. Blood lamotrigine levels were found to be 17.2 mg/L, giving the diagnosis of metabolic encephalopathy secondary to drug toxicity and overdose. Also, the impaired level of consciousness with perpetual spontaneous clonus indicated a serotonin syndrome. The man received serum therapy to promote renal excretion. Clinical and haemodynamic surveillance was maintained until the washout of the drug. His condition improved gradually, and he was asymptomatic after 48 hours. Lambea Gil A, et al. Encephalopathy secondary to lamotrigine toxicity. Neurologia 35: 439-440, No. 6, Jul-Aug 2020. Available from: URL: http://doi.org/10.1016/ j.nrl.2018.03.017 [Spanish; summarised from a translation]
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Reactions 10 Oct 2020 No. 1825
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