Authors: Fathima Murthuza , Wasim Ahmad , Mohamed Abdou Saad , Maitha Almatrooshi

Abstract

Introduction: Pyrethroids are synthetic analogs of natural pyrethrins and are used as insecticides because of their perceived low mammalian toxicity and high insecticidal efficacy. Despite this reputation, large volume ingestion can result in systemic toxicity which may closely mimic cholinergic toxidromes, leading to diagnostic uncertainty.

Case Presentation: A 21 year old male presented with vomiting, drowsiness, hypersalivation, miosis, bronchorrhea, and respiratory distress after ingesting  500 mL of a beverage mixed with Katmal, a cockroach killing powder. On examination, he was lethargic with pinpoint pupils, cold extremities, excessive oral secretions, and bilateral lung crackles. Blood gas analysis revealed primary metabolic acidosis with an elevated lactate. Organophosphate poisoning was assumed and atropine was administered, which led to improvement in secretions and respiratory distress. The ingested compound was later identified as lambda cyhalothrin, a type II pyrethroid.

Discussion: This case highlights the diagnostic challenge posed by atypical toxidromes following insecticide ingestion. The initial clinical picture closely resembled a cholinergic crisis, yet the underlying etiology was pyrethroid toxicity. Pyrethroids exert toxicity through neuronal ion channel dysfunction rather than acetylcholinesterase inhibition. Delayed closure of voltage gated sodium channels leads to prolonged neuronal depolarization, while type II pyrethroids additionally inhibit GABA gated chloride channels, impairing inhibitory neurotransmission. This results in neuronal hyperexcitability manifesting as tremors, hypersalivation, seizures, altered mental status, and respiratory compromise.

Type I agents cause the T syndrome characterized by tremors and hyperreflexia, whereas type II agents cause the CS syndrome marked by choreoathetosis, salivation, and seizures. Despite overlapping features, true cholinergic toxicity does not occur. Respiratory compromise in pyrethroid poisoning is more often due to central nervous system depression rather than bronchospasm. Ingestions greater than 250 mL and elevated lactate levels have been associated with severe outcomes, consistent with this presentation. Management remains primarily supportive, as no specific antidote exists, though atropine may provide symptomatic benefit in cases with excessive secretions.

Conclusion: Pyrethroid poisoning should be considered in patients presenting with cholinergic like features after insecticide ingestion. Despite clinical overlap with cholinergic syndromes, management relies on supportive care rather than antidotal therapy, and outcomes are favorable with timely intervention.

Keywords: Pyrethroid poisoning; Lambda cyhalothrin; Cholinergic like toxidrome; Insecticide ingestion