Treatment of Organophosphate Poisoning
Immediate Life-Saving Interventions
Administer atropine immediately at 1-2 mg IV for adults (0.02 mg/kg for children, minimum 0.1 mg, maximum single dose 0.5 mg) as soon as severe organophosphate poisoning is recognized, doubling the dose every 5 minutes until full atropinization is achieved. 1, 2, 3
Critical First Steps (Within Minutes)
Personal protective equipment (PPE) must be worn by all healthcare workers to prevent secondary contamination—documented cases exist of providers requiring atropine, pralidoxime, and intubation after exposure to contaminated gastric contents 1
Immediate dermal decontamination by removing all contaminated clothing and copious irrigation with soap and water for external exposure 1, 3
Secure airway early—endotracheal intubation is recommended for life-threatening poisoning, with observational data showing better outcomes with early intubation 1, 3
Atropine Dosing Algorithm
Initial Dosing
- Adults: 1-2 mg IV immediately (substantially higher than the 0.5-1.0 mg used for bradycardia from other causes) 2, 3
- Children: 0.02 mg/kg IV (minimum 0.1 mg, maximum single dose 0.5 mg)—higher doses than standard pediatric resuscitation are required 1, 2
Dose Escalation Protocol
- Double the dose every 5 minutes until all atropinization endpoints are achieved—this doubling strategy is critical and differs from fixed-dose repetition 2, 3
- Continue escalation regardless of heart rate—tachycardia is NOT a contraindication to continued atropine administration 2, 3
- The tachycardia may originate from nicotinic receptor overstimulation by the organophosphate itself, not from atropine 1, 3
Endpoints of Full Atropinization (All Must Be Achieved)
- Clear chest on auscultation (resolution of bronchorrhea) 2, 3
- Heart rate >80 beats/min 2, 3
- Systolic blood pressure >80 mm Hg 2, 3
- Dry skin and mucous membranes 2, 3
- Mydriasis (pupil dilation) 2, 3
Maintenance Therapy
- Administer 10-20% of the total loading dose per hour (up to 2 mg/hour in adults) 2
- Continuous infusion is preferred over intermittent boluses 2
- Cumulative doses may reach 10-20 mg in the first 2-3 hours, with some patients requiring up to 50 mg in 24 hours 2
- Maintain some degree of atropinization for at least 48 hours 4
Pralidoxime (2-PAM) Administration
Pralidoxime should be administered early to reactivate acetylcholinesterase enzyme (Class 2a recommendation, Level A evidence) and is most effective before "aging" of the phosphorylated enzyme occurs. 1, 4
Dosing Protocol
- Initial adult dose: 1-2 g IV administered slowly over 15-30 minutes (preferably by infusion in 100 mL normal saline) 1, 3, 4
- If pulmonary edema is present, give slowly over not less than 5 minutes as a 50 mg/mL solution 4
- Maintenance infusion: 400-600 mg/hour for adults or 10-20 mg/kg/hour for children 1, 3
Timing Considerations
- Do not withhold pralidoxime when the class of poison (organophosphate vs. carbamate) is unknown 1
- Treatment is most effective if initiated immediately—little is accomplished if given more than 36 hours after exposure termination 4
- A second dose of 1000-2000 mg may be indicated after one hour if muscle weakness has not been relieved 4
Critical Principle
- Always administer atropine concurrently with pralidoxime—pralidoxime alone is insufficient to manage respiratory depression 1, 3
- Pralidoxime reverses nicotinic effects (muscle weakness, potentially some tachycardia) that atropine cannot address 3
Seizure and Agitation Management
- Administer benzodiazepines (diazepam or midazolam) for seizures and agitation 1, 3
- Benzodiazepines may also facilitate mechanical ventilation 1
Monitoring and Observation Period
Duration of Monitoring
- Maintain close observation for at least 48-72 hours as delayed complications and relapses can occur 1, 3, 4
- With ingested organophosphates, continuing absorption from the GI tract constitutes new exposure—fatal relapses have been reported after initial improvement 4
Additional Monitoring Parameters
- Continuous cardiac monitoring to detect dysrhythmias (not to limit atropine dosing) 3
- Serial respiratory assessments every 5-10 minutes during escalation phase 3
- Monitor for delayed muscle weakness (intermediate syndrome) which can occur as late as 4 days after acute exposure 1
- Check creatine kinase and potassium levels for rhabdomyolysis detection 1
Complications to Anticipate
Intermediate Syndrome
- Delayed muscle weakness can follow the initial cholinergic crisis even 4 days after exposure 1
- May require prolonged mechanical ventilation 5, 6
Rhabdomyolysis
- Severe myonecrosis from excessive acetylcholine causing calcium flux into skeletal muscle 1
- Treatment includes adequate hydration, forced diuresis, and urine alkalinization when urine turns reddish from myoglobin 1
Atropine-Related Effects
- Fever is an expected adverse effect with high-dose atropine therapy and does not indicate treatment failure 1
- Never withhold or prematurely discontinue atropine due to fever—inadequate atropinization leads to respiratory failure and death 1
- Repeated atropine administration may produce hallucinations and fever 1
Critical Pitfalls to Avoid
- Never delay atropine administration—it is the immediate life-saving intervention with Class 1, Level A evidence 2
- Never stop atropine escalation due to tachycardia—the risk of undertreating organophosphate poisoning far exceeds the risk of atropine-induced tachycardia 3
- Never use succinylcholine or mivacurium for intubation 1, 3, 4
- Never handle gastric contents without PPE—organophosphates in emesis and gastric aspirate can cause severe secondary poisoning 1
- Avoid morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers in organophosphate poisoning 4
Special Considerations
Pediatric Patients
- Children require relatively higher atropine doses compared to standard pediatric resuscitation doses 1, 2
- Tachycardia is even less of a concern in children than adults 1
- Children accounted for 35% of OP-poisoned victims in epidemiologic reviews 7
Mechanism of Toxicity
- Organophosphates form a covalent bond with acetylcholinesterase causing permanent inactivation ("aging"), while carbamates spontaneously dissociate 1
- Restoration of normal enzyme activity may take up to 6 weeks in untreated patients 2