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CBRN and the Trauma Victim
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Nerve agents cause an overstimulation of the cholinergic parts of the nervous system including the parasympathetic nervous system (pinpoint pupils, bradycardia, excessive secretions, bronchospasm), neuromuscular junctions (muscle paralysis) and central nervous system (confusion, coma, convulsions). This is due to the inhibition of the enzyme acetylcholinesterase and accumulation of acetylcholine.
Chemical and Biological Threats to Public Safety
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The onset of symptoms is within seconds for inhalation of vapors and hours for dermal contact or oral ingestion. In addition, they all decompose in the presence of bleach (or base). As with all the nerve agents, VX produces a severe cholinergic syndrome, terminating in convulsions, respiratory failure, and death with high doses. Recovery from mild or moderate exposure to a nerve agent is possible. Treatment relies on removal from exposure, supportive measures, decontamination, and rapid administration of atropine (antimuscarinic) and pralidoxime (ACh-∑ reactivator). The FDA has recently approved pyridostigmine bromide, an anticholinesterase agent, as a prophylactic drug for U.S. military personnel to increase survival after exposure to soman poisoning during combat.
Military Chemical Casualty Treatment
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Timothy J. Byrne, Raymond Vazquez, Dan Boehm, Laukton Rimpel, Charles. G. Hurst
Nerve agents are the most toxic of the known chemical agents. They are hazards in their liquid, aerosol, and vapor states and can cause death within minutes after exposure. Nerve agents inhibit the enzyme acetylcholinesterase in tissue and blood, and their effects are caused by the resulting excess of acetylcholine, a neurotransmitter, in tissue. This creates what is called a “cholinergic crisis.” Organs with cholinergic receptor sites include the smooth muscles, skeletal muscles, central nervous system (CNS), and most exocrine glands (sweat, tears, saliva, and mucosal secretions). In addition, cranial efferents and ganglionic afferents are cholinergic nerves. Exposure to a small amount of nerve agent vapor causes effects in the eyes, nose, and airways. These effects are from local contact of the vapor with the organ and do not alone indicate systemic absorption of the agent. In this circumstance, the circulating erythrocyte-cholinesterase may be depressed and used as a possible indicator of exposure. A very small amount (usually non-lethal) of liquid agent on the skin causes systemic effects initially in the gastrointestinal (GI) tract. Localized sweating and muscle fasciculations may be seen at the spot. Lethal amounts of vapor (almost immediate) or liquid (once absorption takes place) cause a rapid cascade of events culminating within a minute or two in loss of consciousness and convulsive activity, followed by apnea (breathing cessation) and muscular flaccidity within several more minutes.
Anticonvulsant effectiveness of scopolamine against soman-induced seizures in African green monkeys
Published in Drug and Chemical Toxicology, 2022
John H. McDonough, Joseph D. McMonagle, Benedict R. Capacio
Nerve agents are highly toxic organophosphate compounds. They exert their toxic effects by inhibiting the cholinesterase (ChE) family of enzymes to include acetylcholinesterase (AChE), the enzyme that hydrolyzes the neurotransmitter acetylcholine (ACh). Nerve agents bind to the active site of the AChE enzyme, thus preventing it from hydrolyzing ACh. ACh is the neurotransmitter at the neuromuscular junction of skeletal muscle, the preganglionic nerves of the autonomic nervous system, and the postganglionic parasympathetic nerves, as well as muscarinic and nicotinic cholinergic synapses within the central nervous system (CNS). Following nerve agent exposure and the inhibition of the AChE enzyme, levels of ACh rapidly increase at the various effector sites, resulting in continuous overstimulation. This hyperstimulation of the cholinergic system at central and peripheral sites leads to the toxic signs of poisoning with these compounds. The signs of poisoning include miosis (constriction of the pupils), increased tracheobronchial secretions, bronchial constriction, laryngospasm, increased sweating, urinary and fecal incontinence, muscle fasciculations, tremor, convulsions/seizures of CNS origin, and loss of respiratory drive from the CNS (Departments of the Army, Navy, Air Force, and Commandant Marine Corps 1995, Aas 2003, Chemical Casualty Care Division 2014).
Inhibition of cholinesterases following percutaneous intoxication with V agents in rats
Published in Toxin Reviews, 2021
Jiri Bajgar, Kamil Kuca, Jiri Kassa
Percutaneous exposure to nerve agents is one of the important routes of administration of chemical warfare agents under field conditions. The use of nerve agents is not excluded though there is the international agreement (Chemical Weapons Convention) dealing with prohibition of these agents, as well as their misuse as it was demonstrated previously in Syria (United Nations 2013). From this group, V agents are the most toxic at different routes of administration including percutaneous intoxication. VX weaponized in the US Army is the most important representative though they are also Chinese and Russian VX (Bajgar 2012). These agents are under control of the Organization for the Prohibition of Chemical Weapons (OPCW) and they have to be destroyed; see, for example, Hart and Trapp (2017). They were also misused by terrorists for two assasinations that were done in Japan (Tsuchihashi et al.2005) and Kuala Lumpur airport (Patocka 2017), in both cases, VX was used.
Efficient agent degradation within skin is important for decontamination of percutaneously exposed VX
Published in Cutaneous and Ocular Toxicology, 2021
Lina Thors, Elisabeth Wigenstam, Johanna Qvarnström, Anders Bucht
In medical management guidelines for victims percutaneously exposed to nerve agents, rapid skin decontamination is critical to prevent absorption and uptake in the blood circulation, as well as to avoid secondary contamination to prehospital responders and hospital personnel1. In acute exposures, the skin contact risk is particularly high for low volatile nerve agents such as VX, as in the case of the alleged assassination of Kim Jong-Nam in 20172,3. Studies of the skin penetration ability of VX in animal exposure models have shown that the maximum blood level of the agent is reached several hours after percutaneous exposure and is followed by a slow elimination due to the agent’s high persistency4–7. In addition, following percutaneous exposure to VX, a significant proportion of the applied dose is reported to remain in the deeper layers of the skin8,9. This depot effect may cause prolonged agent release and delayed symptoms as demonstrated by analysis of toxicokinetics and cholinesterase inhibition in guinea pigs, even when decontamination was performed10. Consequently, extended preparedness for intensive medical care may be necessary post-exposure to the nerve agent10–12.