What is the appropriate management of pyrethrin/pyrethroid poisoning?

Management of Pyrethrin/Pyrethroid Poisoning

Pyrethrin and pyrethroid poisoning is managed primarily with supportive care, immediate decontamination, and benzodiazepines for seizures or severe agitation—there is no specific antidote. 1, 2

Immediate Priorities and Stabilization

• Contact your regional poison control center immediately upon suspicion of pyrethroid exposure, as expert toxicology guidance improves outcomes and provides case-specific protocols. 1, 3
• Secure airway, breathing, and circulation before attempting toxin identification or awaiting confirmatory laboratory tests—do not delay supportive care. 1, 3
• Assess for the characteristic pyrethroid toxidrome: paresthesias (especially facial), tremor, hyperexcitability, choreoathetosis, seizures, and sympathetic activation (tachycardia, hypertension). Type I pyrethroids cause tremor and hyperreflexia; Type II pyrethroids (containing cyano groups) cause salivation, seizures, and more severe neurological effects. 2, 4, 5

Decontamination

Dermal Exposure

• Remove all contaminated clothing and jewelry immediately to prevent ongoing absorption. 3
• Wash exposed skin thoroughly with soap and water—pyrethroids bind to the epidermis and create a dermal reservoir, so repeated washing may be necessary. 3, 2
• Use personal protective equipment during decontamination to avoid secondary contamination of healthcare workers. 3

Ocular Exposure

• Irrigate eyes with copious tepid water for at least 15 minutes if ocular exposure has occurred. 6

Gastrointestinal Decontamination

• Do NOT induce vomiting—this may worsen gastrointestinal irritation and delay definitive care. 1, 3
• Consider activated charcoal only if presentation occurs within 1-2 hours of ingestion, the airway is protected, and poison control specifically recommends it—evidence for benefit in pyrethroid poisoning is limited. 1, 3
• Gastric lavage is generally not recommended, especially for late presentations. 6

Neurological Management

• Administer benzodiazepines (diazepam or midazolam) for seizures or severe agitation—these are first-line agents for pyrethroid-induced neurological hyperexcitability. 1, 3
• Pentobarbitone may be considered for refractory Type II pyrethroid seizures if benzodiazepines fail, as it acts as both a chloride channel agonist and membrane stabilizer. 5
• Monitor for non-convulsive seizures with electroencephalography in patients with altered mental status. 6
• Avoid neuromuscular blockers without adequate sedation if intubation is required—they mask seizure activity without treating it. 3

Respiratory and Hemodynamic Support

• Provide 100% oxygen and mechanical ventilation when respiratory compromise is present—severe poisoning can cause respiratory failure. 6, 7
• Administer aggressive intravenous fluid resuscitation and vasopressors as needed for hypotension from sympathetic dysregulation. 1, 3
• Monitor cardiovascular status closely—pyrethroids produce potent sympathetic activation with tachycardia and hypertension. 5

Specific Symptom Management

Paresthesias (Most Common Dermal Effect)

• Paresthesias typically resolve within 12-24 hours without specific treatment. 2
• Topical vitamin E (dl-alpha tocopherol acetate) may reduce severity if paresthesias are bothersome, though they are usually self-limited. 2
• Avoid heat, sunlight, scratching, and water application to affected areas, as these exacerbate paresthesias. 2

Gastrointestinal Symptoms

• Expect sore throat, nausea, vomiting, abdominal pain, and mouth ulceration within minutes of ingestion—these are direct irritant effects. 2
• Provide symptomatic treatment with antiemetics and supportive care. 2

Critical Pitfalls to Avoid

• Do not delay treatment while awaiting toxicology confirmation—treat based on clinical presentation and exposure history. 1, 3
• Do not confuse with organophosphate poisoning—severe pyrethroid poisoning can mimic organophosphate toxicity with cholinergic-like symptoms, but high-dose atropine is NOT indicated and may cause complications. Use only low-dose atropine if muscarinic symptoms are present. 7
• Do not underestimate the duration of poisoning—systemic effects can occur 4-48 hours after exposure, and recovery may take up to 6 days. 2
• Be aware of synergistic toxicity—co-formulation with piperonyl butoxide (a metabolic inhibitor) or organophosphates can enhance pyrethroid toxicity significantly. 2, 5

Monitoring and Disposition

• Observe patients for at least 48-72 hours, even if initially stable, due to risk of delayed systemic effects. 3, 2
• Most patients recover within 6 days, though fatalities have been reported (7 deaths among 573 cases in one series). 2
• Early toxicology consultation is recommended for complex or severe cases. 6

Key Mechanistic Considerations

Pyrethroids are approximately 2,250 times more toxic to insects than mammals due to increased sodium channel sensitivity in insects, smaller body size, lower body temperature, and rapid mammalian metabolism. 2 They modify voltage-sensitive sodium channels to delay closure, causing prolonged sodium influx and repetitive neuronal firing. Type II pyrethroids also decrease chloride currents and can affect GABA-gated chloride channels at high concentrations, contributing to seizures. 2, 4, 5