A worker exposed to a military nerve agent receives pralidoxime 6 hours after the exposure, yet muscle weakness does not improve. The most likely explanation is:

• A Pralidoxime was degraded before reaching the neuromuscular junction
• B Pralidoxime acts only at central nervous system synapses
• C Atropine co-administration antagonizes pralidoxime at nicotinic sites
• D The phosphorylated enzyme complex has undergone aging, making reactivation impossible ✓

Explanation

Organophosphates inhibit acetylcholinesterase by phosphorylating the serine hydroxyl group at the active site. Over time one alkyl group is lost spontaneously, a process called aging, after which the bond is irreversible and pralidoxime can no longer reactivate the enzyme. Aging occurs within minutes for soman and within hours for many insecticides, hence pralidoxime must be given early. Pralidoxime is a quaternary compound that does not enter the brain.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

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Written and medically reviewed by the StethoPrep medical team.