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Toxicology Rounds: Five Things to Know about the Nerve Agent VX

Gussow, Leon MD

Emergency Medicine News: May 2017 - Volume 39 - Issue 5 - p 22
doi: 10.1097/01.EEM.0000516462.62273.f5
Toxicology Rounds

Dr. Gussowis a voluntary attending physician at the John H. Stroger Hospital of Cook County in Chicago, an assistant professor of emergency medicine at Rush Medical College, a consultant to the Illinois Poison Center, and a lecturer in emergency medicine at the University of Illinois Medical Center in Chicago. Read his blog atwww.thepoisonreview.com, follow him on Twitter @poisonreview, and read his past columns athttp://bit.ly/EMN-ToxRounds.

Figure

Figure

Security camera footage from Kuala Lumpur International Airport in Malaysia documenting the assassination of Kim Jong-nam, the half-brother of North Korea's leader Kim Jong-un, is horrifying and riveting. (http://bit.ly/2ohtLR9.)

Mr. Kim is seen walking through the airport in the Feb. 13 video when two women approach him from behind and rub their hands over his face. Mr. Kim is then seen talking with security guards, who direct him to the airport medical clinic. He walks, somewhat slowly and unsteadily, to the clinic where he collapses. Mr. Kim died in the ambulance taking him to the hospital. The elapsed time from attack to collapse seems to have been 10 to 15 minutes at most.

Malaysian officials revealed days later that tests had identified traces of the chemical weapon VX on Mr. Kim's face. The use of such a lethal weapon in a crowded international airport is alarming and serves as a reminder that all emergency practitioners should be familiar with the basic toxicology of VX.

VX is a nerve agent that produces toxicity like that of organophosphate insecticides. The poison is acetylcholinesterase, the enzyme that breaks down and terminates the action of acetylcholine, a crucial neurotransmitter in the peripheral and central nervous systems. Without this “off” switch, acetylcholine-activated processes run amok.

There are three types of acetylcholine receptors. Muscarinic receptors are found where the parasympathetic system innervates secretory glands and smooth (involuntary) muscles such as those in the respiratory and gastrointestinal tracts. Nicotinic receptors occur at the neuromuscular junction, and central cholinergic receptors are abundant in the brain. (Table.)

When VX inactivates acetylcholinesterase, glands secrete profusely, smooth muscle contracts uncontrollably, skeletal muscle fasciculates, and brain activity ignites to the point of seizure.

Just as there are three categories of acetylcholine receptors and three types of effects, there are three antidotes to counter the various manifestations of toxicity. The first and most important antidote, the antimuscarinic drug atropine sulfate, dries up secretions and relaxes smooth muscle, but will not alleviate nicotinic or central manifestations.

The nicotinic effects — skeletal muscle hyperactivity and weakness — are treated with pralidoxime (2-PAM), which removes the nerve agent from the active site on cholinesterase, regenerating functioning enzyme. Benzodiazepines, most frequently diazepam and midazolam, are also used to prevent and treat central effects of VX, including seizures.

Table C

Table C

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The Triple-Whammy

Victims of nerve agent exposure generally die from suffocation. They get hit by a respiratory triple-whammy: airway obstruction from muscarinic effects, dysfunction of voluntary muscles of respiration from nicotinic stimulation, and central apnea. Bronchorrhea and bronchospasm, the so-called Killer Bs, are the most important clinical effects on presentation, and can make ventilating and oxygenating the victim impossible unless he has received adequate doses of antidote. Atropine should be given in whatever dose is needed to dry up respiratory secretions, relax bronchial muscle constriction, and allow ventilation and oxygenation.

VX has low volatility and is a persistent agent, meaning its consistency is similar to motor oil and it does not vaporize quickly or easily. Any victim who becomes symptomatic shortly after exposure to VX has likely had direct contact with the liquid and will need thorough wet decontamination (showering). Onset of symptoms after dermal exposure to VX can be delayed, possibly for hours, so these patients will also need prolonged observation.

On the other hand, sarin, the nerve agent released in the Tokyo subway system in 1995, has a consistency and volatility like water and vaporizes easily. Sarin, unlike VX, is predominantly an inhalation threat.

It is still somewhat of a mystery why bystanders weren't affected by the VX that killed Kim Jong-nam. One of the alleged attackers reportedly developed some cholinergic symptoms, but both attackers purportedly washed their hands immediately after contact with Mr. Kim. Some reports also speculated that Mr. Kim may have been exposed to a binary agent composed of two harmless chemicals that combine to form VX. This may explain why neither attacker became severely ill.

Mr. Kim's assassination was the second time VX has been used as a targeted murder weapon. The Aum Shinrikyo cult, the group behind the 1995 sarin attack in Tokyo, used VX in the mid-1990s against three people, spraying the liquid on their necks as they walked or jogged outside. One person died.

Hiroyuki Nagaoka, now 78, survived the attack after weeks in the intensive care unit. He was interviewed by Japan Times, which described his experience: “[T]he toxin was causing his pupils to shrink. He then started feeling hot inside and, sweating profusely, took off his clothes. His wife later told him that he got down on all fours like an animal, twisting and scratching his neck and chest, before rolling onto his back in pain and losing consciousness.” (Feb. 25, 2017; http://bit.ly/2nHAHWH.)

Mr. Kim reportedly died a very painful death. It seems that unusual pain after being exposed to an unknown liquid might be a clue to VX toxicity.

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