Nerve Agent Incidents and Public Health Preparedness

Summary by Alex Chen, MD

Spoon Feed
Management of nerve agent (NA) poisoning requires recognition of the syndrome and availability of the antidote. It is important to remember that besides the classic “SLUDGE” and “Killer B’s,” there is also the nicotinic syndrome which can cloud the clinical presentation. Add the “weekdays” mnemonic for nicotinic effects to your list of symptoms in NA toxicity.

Why does this matter?
We are the front lines for patients who may present with these poisonings. We need to be the resident experts. This summary has tips on recognizing NA toxidromes, but you also need to know how to get more help. Chemical Hazards Emergency Medical Management (CHEMM), “provides information that may aid recognition of an NA exposure and how to alert appropriate authorities, protect oneself and others, and decide what onsite actions are and are not safe.” Also, your local Hazmat team and the Poison Center can help.

“Welcome to the Rock.”
NA are organophosphorus compounds (similar to pesticides) and cause their toxicity by inhibition of acetylcholinesterase which normally gets rid of ACh at the neuronal junction. ACh has both muscarinic and nicotinic receptors. The muscarinic receptors tend to get all the mnemonic love (SLUDGE, Killer B’s) and rightfully so, because they are the ones that will likely kill you. However, it is important to remember that the nicotinic symptoms can cloud the picture and potentially lead to a missed diagnosis.

My mentor in residency used to teach the “weekdays” mnemonic to remember nicotinic symptoms (Thanks Saralyn). Nicotinic symptoms eventually fatigue, similar to how a depolarizing paralytic works; however, the muscarinic symptoms will reemerge and continue to manifest.

Possible nicotinic symptoms:

  • (M)onday: Mydriasis, vs the classic miosis

  • (T)uesday: Tachycardia, vs the classic bradycardia

  • (W)ednesday: Weakness –> leads to diaphragmatic weakness

  • t(H)ursday: Hypertension

  • (F)riday: Fasciculations, similar to the action of succinylcholine, which is just two ACh molecules

While it significantly more dramatic to have VX nerve agent potentially melt the faces of the entire population of San Francisco, it is simply not true. The most well-known NAs include the G series (sarin, soman, tabun) and VX. Important characteristics include volatility and persistence, with volatility defined by how easy it is to aerosolize and persistence defined by how long it sticks around in the environment.  Sarin, soman, and tabun are higher volatility nerve agents which make them more desirable for large-scale attacks. VX on the other hand, while it is significantly more potent, is a lower volatility agent, making it harder to spread. Recall the poisoning of Kim Jong-Nam with VX. The NA had to be directly applied to his face. Why does this matter? The more volatile NAs tend to disperse from an area much quicker due to their lower persistence whereas VX can cause secondary contamination to health care workers and other bystanders.

Since it is not financially feasible to stock loads of atropine, 2-PAM, and diazepam in every hospital on the off chance that a NA attack will happen, the government has created the Strategic National Stockpile (SNS) with CHEMPACKs (atropine, 2-PAM, and diazepam) stocked in various strategic areas. Access to these supplies varies by local jurisdiction and it is important to familiarize yourself with them.

Source
Nerve Agent Incidents and Public Health Preparedness. Ann Intern Med. 2018 Dec 18. doi: 10.7326/M18-2428. [Epub ahead of print]

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Reviewed by Clay Smith

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