In a cluster of patients with bradycardia and miosis after exposure to a crop-duster or pesticide, in addition to high-flow oxygen, the MOST appropriate treatment includes:

In a cluster of patients with bradycardia and miosis after exposure to a crop-duster or pesticide, in addition to high-flow oxygen, the MOST appropriate treatment includes:

• A. Atropine and pralidoxime chloride (neurotoxin)
• B. Epinephrine and albuterol
• C. Activated charcoal and laxatives
• D. Naloxone and diazepam

Answer: (A)

Exposure to a crop-duster or similar pesticide can cause organophosphate poisoning, which blocks acetylcholinesterase and leads to an excess of acetylcholine at muscarinic and nicotinic receptors. This produces bradycardia, miosis, increased secretions, bronchospasm, and other cholinergic symptoms. The most effective additional treatment beyond high-flow oxygen is atropine to counteract the muscarinic effects (reducing bronchorrhea, bronchospasm, salivation, sweating, and bradycardia) and pralidoxime chloride to reactivate acetylcholinesterase, reversing both muscarinic and nicotinic symptoms by restoring the breakdown of acetylcholine. Early administration is important because aging of the enzyme-inhibitor complex can limit pralidoxime’s effectiveness. Other options don’t address the underlying mechanism. Epinephrine and albuterol may help with bronchospasm, but they don’t counteract acetylcholine buildup. Activated charcoal is only helpful if the substance was ingested recently and isn’t the primary antidote in organophosphate exposure. Naloxone and diazepam target opioid overdose and seizures, not cholinergic toxicity from organophosphates.

Exposure to a crop-duster or similar pesticide can cause organophosphate poisoning, which blocks acetylcholinesterase and leads to an excess of acetylcholine at muscarinic and nicotinic receptors. This produces bradycardia, miosis, increased secretions, bronchospasm, and other cholinergic symptoms. The most effective additional treatment beyond high-flow oxygen is atropine to counteract the muscarinic effects (reducing bronchorrhea, bronchospasm, salivation, sweating, and bradycardia) and pralidoxime chloride to reactivate acetylcholinesterase, reversing both muscarinic and nicotinic symptoms by restoring the breakdown of acetylcholine. Early administration is important because aging of the enzyme-inhibitor complex can limit pralidoxime’s effectiveness.

Other options don’t address the underlying mechanism. Epinephrine and albuterol may help with bronchospasm, but they don’t counteract acetylcholine buildup. Activated charcoal is only helpful if the substance was ingested recently and isn’t the primary antidote in organophosphate exposure. Naloxone and diazepam target opioid overdose and seizures, not cholinergic toxicity from organophosphates.