Organophosphorus insecticides include diazinon, acephate, maalthion, parathion, and chlorpyrofos. Absorption occurs through ingestion, inhalation (eg, nerve gas agents), and dermal routes. Toxicity is produced through binding to acetylcholinesterase, which becomes irreversible within hours, causing excess stimulation of acetylcholine receptors; this results in a cholinergic crisis known as “sludging” (Table 113-1). Most patients become symptomatic within 8 hours of dermal exposure, though some fat-soluble agents (eg, fenthion) can cause delayed symptoms. Nicotinic stimulation leads to fasciculations and muscle weakness, which is most pronounced in the respiratory muscles, worsening the pulmonary muscarinic effects. Nicotinic effects can also cause paradoxical tachycardia and mydriasis. Central nervous system (CNS) effects, which often predominate in children, include tremor, restlessness, confusion, seizures, and coma.
A variety of subacute and chronic effects are associated with organophosphorus insecticide poisoning. An intermediate syndrome, 1 to 4 days after acute poisoning, may present with paralysis or weakness of neck, facial, and respiratory muscles, which can result in respiratory arrest if not treated. Organophosphate-induced delayed neuropathy can occur 1 to 3 weeks after acute poisoning, resulting in a distal motor-sensory polyneuropathy with leg weakness and paralysis.