Status epilepticus following inhalational exposure to Bifenthrin, a Type II pyrethroid

To the Editor:

Pyrethroids are commonly used commercial and domestic insecticides that infrequently result in human intoxication. Type I pyrethroids delay closure of voltage-gated sodium channels leading to protracted sodium influx (tail current) and membrane depolarization.^1,2 At high doses, the sodium tail current may be sufficient to prevent further action potential generation. Additional chloride channel inhibition by Type II pyrethroids such as Bifenthrin and Fenvalerate lowers the threshold for action potential generation and increases neuronal hyperexcitability.^2,3 causing profuse salivation, ataxia, hyperactivity, choreoathetosis and seizures in animals.⁴ In humans, dermal exposure leads to paresthesias and ingestion gives rise to nausea, vomiting, abdominal pain, increased secretions and dysphagia. Systemic effects such as dizziness, headache, fatigue, palpitations, chest tightness, blurred vision and convulsions occur by 4–48 h following ingestion. Mortality is low (1–2%) and most patients recover within 6 days following exposure.^1,4 Definitive diagnostic testing is not freely available and management is supportive as no specific antidote exists. Type II pyrethroid poisoning resulting in seizures in humans has been reported only in cases of suicidal or accidental ingestion but not after inhalational exposure. Low systemic toxicity by Type II pyrethroids may be due to poor dermal absorption and 2000-fold higher selectivity for insects over mammals.¹

We report a 45-year-old woman with history of a right fronto-temporal infarct one year prior to presentation who developed acute severe headache, vomiting and confusion and new-onset generalized tonic–clonic seizures in quick succession followed by obtundation and fixed left gaze deviation. Further history revealed that she had sprayed about 4 liters of an unknown dilution of Bifenthrin (original concentration 25.1%) without protection in a closed apartment bedroom prior to the onset of symptoms. There was no suicidal or accidental ingestion of the agent. Skin decontamination was performed and she was stabilized hemodynamically. Metabolic profile, complete blood counts, serum acetylcholine esterase levels, urine drug screen, were unrevealing. Convulsive status epilepticus was treated with intravenous Fosphenytoin and Lorazepam but she persisted to have fixed left-gaze deviation, obtundation and developed hypercarbic respiratory failure requiring intubation and neurointensive care. Continuous EEG monitoring revealed multiple subclinical seizures arising from the right fronto-temporal region suggesting that the previous stroke was the likely focus. MRI of brain excluded a new infarct or new structural lesion. Seizure control was achieved by 72 h with three antiepileptics and she showed clinical improvement by day 4. She made a full recovery and remained seizure-free on 3 anti-epileptics until discharge with no neurological deficits at follow-up.

Overzealous spraying of Bifenthrin in a confined environment in addition to lowered seizure threshold from a previous stroke probably contributed to refractory seizures in our patient, although there was no analytical drug confirmation. A careful drug-exposure history and direct confirmation of the toxic agent are necessary prior to making a diagnosis of pyrethroid intoxication. A high index of suspicion for pyrethroid-toxicity should be maintained even after inhalational exposure to Type II pyrethroids especially in patients who are at higher risk for seizures.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.