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Pesticides include insecticides, herbicides, and rodenticides. In addition to active toxic ingredients, many pesticides also contain “inert” products such as petroleum distillates, which may be toxic as well. Although the mainstay of treatment is supportive care, some antidotes are essential.


Clinical Features

Organophosphate insecticides include agents such as diazinon, acephate, malathion, parathion, and chlorpyrifos. Absorption occurs through ingestion, inhalation (e.g., nerve gas agents), and dermal routes. Toxicity is produced through binding and inhibition of acetylcholinesterase, causing excess accumulation of acetylcholine and stimulation of cholinergic receptors, of both the muscarinic and nicotinic receptor types. The muscarinic receptor agonism results in a cholinergic crisis known as “SLUDGE” and “DUMBELS” effects (Table 113-1).

Table 113-1

SLUDGE, DUMBELS, and “Killer Bees” Mnemonics for the Cholinergic

Onset of symptoms, ranging from minutes to hours, varies based on amount and route of exposure. Most patients become symptomatic within 8 hours of acute exposure, though some fat-soluble agents (e.g., fenthion) can cause delayed symptoms with dermal exposure. Nicotinic receptor stimulation leads to fasciculations and muscle weakness, which is most pronounced in the respiratory muscles, which leads to worsening of pulmonary dysfunction caused by bronchorrhea from muscarinic effects. Nicotinic effects can also cause tachycardia and mydriasis, paradoxical to the expected muscarinic cholinergic effects. 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 organophosphate insecticide poisoning. An intermediate syndrome, 1 to 5 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.

Diagnosis and Differential

Organophosphate poisoning is typically a clinical diagnosis based on the toxidrome and history of exposure (Table 113-1); laboratory cholinesterase assay can aid in confirmation. An ECG may be useful to monitor for prolonged QT, which is associated with increased morbidity and mortality in organophosphate poisoning.

Emergency Department Care and Disposition

Treatment of organophosphate poisoning is listed in Table 113-2, and should not be delayed pending confirmatory tests.

  1. In symptomatic patients, administer 100% oxygen and focus on airway management, with gentle suctioning of secretions. Nondepolarizing agents should be used for rapid sequence ...

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