Chapter 113. Pesticides

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.

Clinical Features

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.

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.

1. In symptomatic patients, administer 100% oxygen and focus on airway management, with gentle suctioning of secretions. The use of succinylcholine for intubation, which is metabolized by plasma cholinesterase, may result in prolonged paralysis.

2. The key in treatment is large amounts of atropine titrated to attenuation of tracheobronchial secretions. Tachycardia and dilated pupils are not a contraindication to atropine. High dose diphenhydramine can be substituted for atropine.

3. Minimal exposures require only 6 to 8 hours observation. Recrudescence can occur due to reexposure to contaminated clothing, particularly leather. Significant poisonings require intensive care monitoring.

4. Other commonly encountered pesticides and their treatment are listed in Table 113-3.

Herbicides are agents used to kill weeds. In addition to intrinsic toxicity, they may also be packaged with surfactants or solvents with their own toxic effects. The most dangerous are bipyridyl herbicides, namely paraquat and diquat. Nonbipyridyl herbicides and their treatment are depicted in Table 113-4.

Paraquat is especially toxic with lethal oral doses of 20% solution being only 10 to 20 mL in an adult and 4 to 5 mL in children. Both agents are toxic via inhalation, dermal exposure, or ingestion. Due to their caustic properties, ulceration of skin and mucous membranes and gastrointestinal corrosion can occur. Paraquat ingestions result in renal, cardiac, and hepatic failure along with progressive pulmonary fibrosis. Due to the latter, treatment often includes restriction of supplemental oxygen. Decontamination of skin is important to prevent continued absorption. Early after ingestion, GI decontamination with activated charcoal, fuller's earth, or bentonite may be helpful. Charcoal hemoperfusion may remove paraquat. Because of poor prognosis, especially with paraquat ingestions, admit patients with ingestion for further observation and treatment.

The most commonly used rodenticides are superwarfarins, including bordifacoum, diphenacoum, and bormadoline. Coagulopathy typically develops within 48 hours and lasts for weeks to months due to the long half-lives of these agents. Single ingestions in children usually do not result in toxic effects. Acute intentional or repeated ingestions may present with delayed hemorrhage, including hematuria, gastrointestinal hemorrhage, or epistaxis. Screening for toxic effect can be performed with an INR obtained 24 to 48 hours after ingestion. If the INR is elevated (>2), then start oral vitamin K1, typically at doses of 20 milligrams a day in adults (1 to 5 milligrams for children) and continue for up to 10 months. Acute hemorrhage requires more aggressive therapy with fresh frozen plasma, IV vitamin K1, and addition of prothrombin complex or recombinant activated factor VII for refractory hemorrhage. Nonanticoagulant rodenticides are described in Table 113-5.