Chlorpyrifos Poisoning: Symptoms and Treatment
What is Chlorpyrifos?
Chlorpyrifos is an organophosphate (OP) insecticide that causes irreversible acetylcholinesterase inhibition, leading to acetylcholine accumulation and cholinergic syndrome, with toxicity extending beyond simple cholinesterase inhibition to include neuroinflammation and disruption of multiple neurotransmitter systems 1, 2.
Clinical Presentation
Acute Cholinergic Symptoms
The symptoms of chlorpyrifos poisoning follow a predictable pattern based on severity, ranging from mild muscarinic effects to life-threatening cholinergic crisis 3.
Mild symptoms include:
- Blurred vision and eye pain 3
- Excessive tearing and runny nose 3
- Sudden drooling and increased salivation 3
- Chest tightness or difficulty breathing 3
- Tremors and muscular twitching 3
- Nausea and vomiting 3
- Involuntary respiratory secretions 3
Severe symptoms include:
- Confusion or altered behavior 3
- Severe respiratory distress with excessive secretions 3
- Severe muscular twitching and generalized weakness 3
- Involuntary urination and defecation 3
- Seizures 3
- Loss of consciousness 3
Special considerations for infants and young children: Symptoms like tearing, runny nose, and drooling may occur normally in healthy infants, so these must be considered collectively when exposure is known or suspected 3. Infants may present with drowsiness, unconsciousness, and muscle floppiness rather than twitching 3.
Delayed Neurological Effects
A critical pitfall is failing to anticipate delayed neuropathy: Chlorpyrifos can cause delayed myelopathy and pure motor neuropathy appearing 6-8 weeks after initial recovery from cholinergic crisis, resulting in permanent paralysis at sites of dermal exposure, particularly affecting hands and feet with atrophy and loss of function 1.
Some patients develop mild reversible sensory neuropathy after subchronic exposure, with five of eight reported cases also experiencing memory loss and cognitive slowing 4.
Treatment Algorithm
Immediate Management (First 36 Hours)
Treatment is most effective if initiated immediately after poisoning and should include decontamination, atropinization, supportive care, and pralidoxime (PROTOPAM Chloride) 3.
Step 1: Decontamination
- Remove all clothing if dermal exposure occurred 3
- Wash hair and skin thoroughly with sodium bicarbonate or alcohol as soon as possible 3
- Consider continuing absorption from the lower bowel if ingested, as fatal relapses have been reported after initial improvement 3
Step 2: Supportive Care
- Ensure airway management 3
- Provide respiratory and cardiovascular support 3
- Correct metabolic abnormalities 3
- Control seizures if present 3
Step 3: Atropinization
- Do not give atropine in the presence of significant hypoxia due to risk of atropine-induced ventricular fibrillation 3
- Once hypoxemia is improved, give atropine 2-4 mg IV in adults 3
- Repeat at 5-10 minute intervals until full atropinization (secretions are inhibited) or signs of atropine toxicity appear (delirium, hyperthermia, muscle twitching) 3
- Maintain some degree of atropinization for at least 48 hours until depressed blood cholinesterase activity reverses 3
Step 4: Pralidoxime Administration
- Administer pralidoxime after atropine effects become apparent 3
- Give slowly, preferably by infusion; if IV not feasible, use IM or subcutaneous injection 3
- Generally little is accomplished if given more than 36 hours after termination of exposure 3
- "Titrate" the patient with additional doses every 3-8 hours as long as signs of poisoning recur 3
Medications to Avoid
Critical drug interactions: Avoid morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers in organophosphate poisoning 3. Use succinylcholine with caution as prolonged paralysis has been reported when given with anticholinesterase drugs 3.
Observation Period
Keep the patient under observation for at least 48-72 hours 3. This is essential because continuing absorption from the GI tract constitutes new exposure, and fatal relapses have been documented 3.
Long-Term Monitoring
Monitor for delayed neuropathy at 6-8 weeks post-exposure, particularly in patients with significant dermal exposure, as permanent motor deficits can develop at exposure sites 1. Cognitive and sensory function should also be assessed, as some patients develop memory impairment and sensory neuropathy 4.
Important Clinical Caveats
The mechanism involves acetylcholinesterase inhibition, but acetylcholinesterase levels are uninformative regarding neurodevelopmental effects from chronic low-level exposure, as toxic effects occur at concentrations too low to inhibit cholinesterase 1. Cognitive and motor deficits can return to normal well before recovery of AChE activity 5.