What is the management for chlorpyrifos poisoning?

Management of Chlorpyrifos Poisoning

Immediate management of chlorpyrifos poisoning requires aggressive supportive care with atropinization and pralidoxime (PROTOPAM), initiated as rapidly as possible after exposure, with treatment most effective when started immediately. 1

Initial Stabilization and Decontamination

Airway, breathing, and circulation management takes absolute priority, as acute respiratory failure occurs in approximately 49% of chlorpyrifos poisoning cases and is the primary cause of mortality. 2 Intubation should be performed early if respiratory distress, excessive secretions, or altered mental status are present. 1, 3

Decontamination Steps:

• Remove all contaminated clothing immediately and wash hair and skin thoroughly with sodium bicarbonate or alcohol 1
• Gastric lavage and activated charcoal are routinely used for ingestions, though their definitive benefit remains unproven 3
• Critical caveat: Continuing absorption from the lower bowel after ingestion can cause fatal relapses after initial improvement, requiring extended monitoring 1

Atropine Administration

Atropine is the mainstay of therapy and can reverse life-threatening features of organophosphate poisoning. 3

Atropine Protocol:

• Do NOT give atropine until hypoxemia is corrected - atropine administration in the presence of significant hypoxia risks ventricular fibrillation 1
• Initial adult dose: 2-4 mg IV, repeated at 5-10 minute intervals until full atropinization (secretions inhibited) or atropine toxicity appears (delirium, hyperthermia, muscle twitching) 1
• Maintain some degree of atropinization for at least 48 hours until depressed blood cholinesterase activity reverses 1
• No clear guidelines exist on exact dosing and duration, highlighting ongoing controversies in management 3

Pralidoxime (PROTOPAM) Administration

After atropine effects become apparent, administer pralidoxime to reactivate acetylcholinesterase. 1 This can reverse both nicotinic and muscarinic effects, though clinical trial benefits have been inconsistent. 3

Pralidoxime Guidelines:

• Administer slowly, preferably by infusion 1
• Most effective if initiated immediately after poisoning - little benefit if given more than 36 hours after exposure termination 1
• "Titrate" the patient with additional doses every 3-8 hours as long as signs of poisoning recur 1
• Continue monitoring for relapses, particularly with ingestions where ongoing bowel absorption constitutes new exposure 1

Clinical Monitoring Parameters

Key Symptoms to Monitor:

Mild symptoms include blurred vision, excessive tearing, rhinorrhea, salivation, chest tightness, tremors, nausea/vomiting, and respiratory secretions 1

Severe symptoms include confusion, severe respiratory distress, severe muscle twitching and weakness, involuntary urination/defecation, seizures, and unconsciousness 1

Common complications requiring specific attention:

• Aspiration pneumonia (45% of cases) 2
• Salivation (43%) 2
• Acute respiratory failure (41%) 2
• Acute kidney injury (14%) 2
• Seizures (8%) 2

Laboratory Monitoring:

• Leukocytosis and elevated C-reactive protein are common (mean WBC 12,700/uL, CRP 36.8 mg/L) 2
• Serum cholinesterase levels correlate with severity 2
• Monitor for metabolic abnormalities requiring correction 1

Medications to AVOID

Absolutely avoid morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers in organophosphate poisoning. 1

Use succinylcholine with extreme caution - prolonged paralysis reported when given with anticholinesterase activity drugs. 1

Duration of Observation

Keep patients under observation for at least 48-72 hours minimum, as fatal relapses can occur after initial improvement, particularly with ingestions. 1, 3 The mortality rate for chlorpyrifos poisoning is approximately 17%, underscoring the need for intensive monitoring. 2

Special Considerations

Chlorpyrifos causes irreversible acetylcholinesterase inhibition, leading to cholinergic syndrome through acetylcholine accumulation. 4, 3 The toxicity extends beyond simple cholinesterase inhibition to include neuroinflammation and disruption of multiple neurotransmitter systems. 4

Intermediate syndrome and delayed polyneuropathy are potential sequelae requiring extended follow-up beyond the acute phase. 3