The acute treatment of nerve agent exposure

Nerve agents (NA) are simple and cheap to produce but can produce casualties on a massive scale. They have already been employed by terrorist organizations and rogue states on civilians and armed forces alike. By inhibiting the enzyme acetylcholine esterase, NAs prevent the breakdown of the neurotransmitter acetylcholine. This results in over-stimulation of muscarinic and nicotinic receptors in the autonomic and central nervous systems and at the neuromuscular junction. Increased parasympathetic stimulation produces miosis, sialorrhea, bronchospasm and bronchorrhea. Effects at the neuromuscular junction cause weakness, fasciculations, and eventually paralysis. Central effects include altered behavior and mental status, loss of consciousness, seizures, or apnea. Most deaths are due to respiratory failure. Treatment with atropine competitively blocks the parasympathetic effects. Oximes like pralidoxime salvage acetylcholine esterase by “prying off” NA, provided the attachment has not “aged” to an irreversible bond. This reverses weakness. Benzodiazepines like diazepam are effective against NA induced seizures. Mortality has been surprisingly low. If victims can survive the first 15 to 20 min of a vapor attack, they will likely live. The low mortality rate to date underscores that attacks are survivable and research reveals even simple barriers such as clothing offer substantial protection. This article reviews the properties of NAs and how to recognize the clinical features of NA intoxication, employ the needed drugs properly, and screen out anxious patients who mistakenly believe they have been exposed.