Treatment of Organophosphorus Poisoning
The treatment of organophosphorus poisoning requires immediate administration of atropine, early endotracheal intubation, benzodiazepines for seizures, proper personal protective equipment, dermal decontamination, and consideration of pralidoxime for organophosphate poisoning. 1
Initial Management
- Ensure proper personal protective equipment (PPE) when caring for patients with organophosphate exposure to prevent contamination of caregivers 1
- Perform immediate dermal decontamination for external exposure by removing contaminated clothing and copious irrigation with soap and water 1
- Administer atropine immediately for severe poisoning manifestations such as bronchospasm, bronchorrhea, seizures, or significant bradycardia 1
- Initial doses are often higher than for typical bradycardia
- Double the dose every 5 minutes until full atropinization is achieved (clear chest on auscultation, heart rate >80/min, systolic blood pressure >80 mm Hg)
- Maintenance of atropinization can be achieved by an atropine infusion 1
Airway Management
- Perform early endotracheal intubation for life-threatening organophosphate poisoning 1
- Observational data suggest better outcomes with early intubation in significant organophosphate poisoning 1
- Avoid neuromuscular blockers metabolized by cholinesterase (succinylcholine and mivacurium) as they are not recommended for patients with organophosphate poisoning 1
Seizure Management
- Administer benzodiazepines to treat seizures and agitation 1
- Diazepam (first line) or midazolam have demonstrated efficacy in patients with organophosphate poisoning 1
Oxime Therapy
- Pralidoxime is reasonable for organophosphate poisoning (Class 2a recommendation, Level A evidence) 1
- When administered early (before aging), oximes reactivate the acetylcholinesterase enzyme, reversing nicotinic effects and improving respiratory and skeletal muscle strength 1, 2
- For adult dosing, inject an initial dose of 1000 to 2000 mg of pralidoxime, preferably as an infusion in 100 mL of normal saline, over a 15-30 minute period 3
- If infusion is not practical or if pulmonary edema is present, give the dose slowly (over not less than five minutes) by intravenous injection as a 50 mg/mL solution in water 3
- A second dose of 1000 to 2000 mg may be given after about one hour if muscle weakness persists 3
- Additional doses may be given every 10-12 hours if muscle weakness continues 3
- Continuous intravenous infusion may maintain therapeutic levels longer than short intermittent infusion therapy 3
Special Considerations
- Organophosphates eventually form a covalent bond with the acetylcholinesterase enzyme, causing permanent inactivation ("aging"), while carbamates spontaneously dissociate from acetylcholinesterase 1
- Although data are insufficient to support a recommendation for or against oxime use in carbamate poisoning, oximes should not be withheld when the class of poison is unknown 1
- Monitor for delayed muscle weakness which can follow the initial cholinergic crisis even as late as 4 days after acute exposure 1
- Watch for complications such as myonecrosis, rhabdomyolysis, and renal damage due to calcium overload in skeletal muscle 1, 4
Common Pitfalls and Caveats
- Atropine should not be given in the presence of significant hypoxia due to the risk of atropine-induced ventricular fibrillation 3
- Intravenous administration of pralidoxime should be carried out slowly as temporary worsening of cholinergic manifestations may occur with rapid administration 3
- Avoid use of morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers in patients with organophosphate poisoning 3
- Patients should be observed for at least 48 to 72 hours after poisoning as fatal relapses have been reported after initial improvement, particularly when the poison has been ingested 3, 5
- Treatment is most effective if initiated immediately after poisoning; little is accomplished if pralidoxime is given more than 36 hours after termination of exposure 3, 5