What are the treatment guidelines for organophosphorus (OP) poisoning?

Treatment Guidelines for Organophosphorus Poisoning

The treatment of organophosphorus poisoning requires immediate administration of atropine, pralidoxime, and benzodiazepines, along with supportive care including decontamination, airway management, and close monitoring for at least 48-72 hours. 1

Initial Management

• Healthcare providers must use proper personal protective equipment (PPE) when caring for patients with organophosphate exposure to prevent self-contamination 1
• Immediate dermal decontamination is essential for external exposure by removing contaminated clothing and copious irrigation with soap and water 1
• Secure airway, breathing, and circulation as the first priority in management 1
• Early endotracheal intubation is recommended for life-threatening organophosphate poisoning, with observational data suggesting better outcomes with early intubation 1
• Avoid neuromuscular blockers metabolized by cholinesterase (succinylcholine and mivacurium) as they may cause prolonged paralysis in patients with anticholinesterase activity 1, 2

Atropine Administration

• Administer atropine immediately at 1-2 mg IV for adults (0.02-0.1 mg/kg for children) for severe poisoning manifestations such as bronchospasm, bronchorrhea, seizures, or significant bradycardia 1
• Double the atropine dose every 5 minutes until full atropinization is achieved (secretions are inhibited) 1, 2
• Maintain some degree of atropinization for at least 48 hours, and until any depressed blood cholinesterase activity is reversed 2
• Atropine should not be given in the presence of significant hypoxia due to the risk of atropine-induced ventricular fibrillation 2

Pralidoxime (Oxime) Therapy

• Administer pralidoxime early to reactivate the acetylcholinesterase enzyme: initial adult dose of 1-2 g IV administered slowly, preferably by infusion 1, 2
• Maintenance therapy of pralidoxime: 400-600 mg/hour for adults or 10-20 mg/kg/hour for children 1
• Pralidoxime is most effective when administered early, before "aging" of the phosphorylated enzyme occurs 1
• Generally, little is accomplished if pralidoxime is given more than 36 hours after termination of exposure to the poison 2
• Always administer atropine concurrently with pralidoxime, as pralidoxime alone is insufficient to manage respiratory depression 1, 2

Seizure Management

• Administer benzodiazepines (such as diazepam or midazolam) to treat seizures and agitation in patients with organophosphate poisoning 1
• Use of morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning 2

Ongoing Management

• Monitor patients for at least 48 to 72 hours after exposure, as fatal relapses have been reported after initial improvement 1, 2
• In cases where poison has been ingested, consider the likelihood of continuing absorption from the lower bowel which constitutes new exposure 2
• Additional doses of pralidoxime may be needed every three to eight hours if signs of poisoning recur 2
• Watch for complications such as delayed muscle weakness (which can follow the initial cholinergic crisis even as late as 4 days after acute exposure), myonecrosis, rhabdomyolysis, and renal damage 1

Emerging Therapies

• Magnesium sulfate has shown promise in recent studies, potentially decreasing hospitalization duration and improving outcomes 3, 4
• Other potential adjunctive therapies under investigation include calcium channel blockers (nimodipine), plasma alkalinizing agents, β-2 agonists, nicotinic receptor antagonists, and lipid emulsions, though large clinical trials are still needed 3
• Sodium bicarbonate administration for mild to moderate alkalinization has shown effectiveness in recent investigations 4
• Bio-scavengers including fresh frozen plasma or albumin may be useful through clearing of free organophosphates 4

Special Considerations

• Organophosphates form a covalent bond with acetylcholinesterase causing permanent inactivation ("aging"), while carbamates spontaneously dissociate 1
• The role of pralidoxime in carbamate poisoning is less clear, but should not be withheld when the class of poison is unknown 1
• The bone injection gun (BIG) for intraosseous administration might provide necessary fast response for rapid termination of convulsions when intravenous access is difficult, especially in field conditions 5