Pesticides include insecticides, herbicides, and rodenticides. In addition to active ingredients, many 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.
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.
Table 113-1 SLUDGE, DUMBELS, and “Killer Bees” Mnemonics for the Muscarinic Effects of Cholinesterase Inhibition |Favorite Table|Download (.pdf)
Table 113-1 SLUDGE, DUMBELS, and “Killer Bees” Mnemonics for the Muscarinic Effects of Cholinesterase Inhibition
|M||Muscle weakness, miosis|
|B||Bradycardia, bronchorrhea, bronchospasm|
|Killer Bees||Bradycardia, bronchorrhea, bronchospasm|
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.
Diagnosis and Differential
Organophosphate poisoning is typically a clinical diagnosis based on the toxidrome (Table 113-1), with confirmation available through laboratory cholinesterase assay. 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.
Table 113-2 Treatment for Organophosphate Poisoning |Favorite Table|Download (.pdf)
Table 113-2 Treatment for Organophosphate Poisoning
|Decontamination||Protective clothing must be worn to prevent secondary poisoning of health care workers.|
|Handle and dispose of all clothes as hazardous waste.|
|Wash patient with soap and water.|
|Handle and dispose of water runoff as hazardous waste.|
|Monitoring||Cardiac monitor, pulse oximeter, 100% oxygen.|
|Gastric lavage||No proven benefit.|
|Activated charcoal||No proven benefit.|
|Urinary alkalinization||No proven benefit.|
|Atropine||1 milligram or more IV in an adult or 0.01 ...|