In case of confirmed or suspected Lewisite presence in the gas attack, procedure are exactly the same. Lewisite is an arsine, 2-chlorovinyl-dichloroarsine, and is colourless and odorless but when used or mixed with impurities has an odor of geranium oil. As said the main symptomatic difference is that Lewisite causing immediate pain in the affected areas. In addition there might be arsenic poisoning, with severe increase in capillary permeability, loss of fluids in the interstitial compartment, hemoconcentration, shock and death There is an antidote to Lewisite, but is not presently available. This antidote is the dimercaprol (2,3-dimercapto-propanol) better known as BAL (British Anti Lewisite), which is also used for treatment of heavy metals poisoning such as lead poisoning.
The BAL would be used in form of cream or ointment for the skin. It should be applied after removing any other ointment. It is incompatible with silver sulphadiazine.
For systemic treatment, indicated for severe exposure and subsequent symptoms, the dosage would be 3 mg/Kg body weight given IM by deep injection, repeated every four hours the first two days, then every six hours for the third day, then every 12 hours up to the tenth day.
There are new drugs being investigated, so called chelating agents, with same indications as for BAL, which can be given orally, are less toxic, and are more effective. These are DMSA (meso-dimercaptosuccinic acid) DMPS (2,3-dimercapto-1-propanelsulfonic acid) and DMPA (N-(2,3-dimercaptopropyl)-phthalamidic acid)

Basic Neurophysiology
As it is known nerve transmission at the end receiving organ or structure such as a muscle fiber or a smooth muscle cell or a glandular cell is mediated by chemicals molecules called neurotransmitters. One of such neurotransmitter is acetylcholine. It is the neurotransmitter of the junction (called also synapsis) between nerve fibers of the Central Nervous System and muscles, involved in all body motion and in respiratory muscles. Acetylcholine is also one of the neurotransmitters between nerve fibers of the nervous system and smooth muscle cells of the eye pupil, gastrointestinal tract, heart, and ureter and bladder, and gland cells such as salivary glands and sweats glands. It is also one of the neurotransmitter between nerve fibers of the nervous system. Acetylcholine is one of the many neurotransmitters within the Central Nervous System. Acetylcholine is the neurotransmitter between the Central Nervous System nervous fibers and peripheral groups of nervous cells called ganglions (which are part of the autonomic nervous system).
How does it work? Neurotransmitter molecule is formed in the nerve ending expansion, and stored there. On receiving the nerve impulse it is carried through the end wall of the expansion (called pre-junction membrane or pre-synaptic membrane), cross the junction (synapsis) and goes to install itself on the membrane of the receiving cell (post-synaptic membrane). The installation on the post-synaptic membrane is in particular places, called receptors, which are good only for that particular molecule or any molecule of very similar structure. Just like a key in the locker. By sitting on those receptors they elicit the response (muscle contraction or secretion etc.). Just like a key in a locker, sometime a key very similar to the right one can enter the locker but does not turn the mechanism. Various chemical substances have structures very similar to a variety of neurotransmitters, and have a variety of similar functions. Like a similar key sometimes opens the locker, sometimes fits in to the locker without opening it, sometime fits the locker without coming out, so molecules of various type similar to neurotransmitters can in various way adversely affect nerve impulse transmission at the junction (synapsis). For instance, some snake venom behaves exactly so, they are a key similar to acetylcholine, which fit in the post synaptic acetylcholine receptors. However as an imperfect key does not work properly, and in just sitting there do not let (inhibit) the normal neural transmission to work. In the case of muscle neuromuscular junction, this causes paralysis of the muscle.
In the post junction membrane of smooth cells and gland cells, the acetylcholine fit in receptors which are slightly different from acetylcholine receptors present in the post junction membrane of muscle cells. They are called with different names, muscarinic receptors the first and nicotinic receptors the second. Conversely different but similar molecules can, like a key in a locker, fit or not fit in those receptors. This is one of the basic mechanism involved in many pharmacologic use of chemical molecules (drugs) and or damaging activity of other chemical molecules (poisons or toxins).
In the case of organophosphate pesticides, or, which is the same, nerve agents, the poisonous molecules do work in a different manner but within the same mechanism.
Now it becomes slight more difficult: once our acetylcholine has installed itself on the acetylcholine receptors in the post synaptic membrane, a stimulus is elicited in that membrane and the muscle fiber contracts, or the gland cell secretes, and so on. In order to prevent acetylcholine from continuously firing those receptors there is an enzyme called acetyl cholinesterase whose job it to degrade acetylcholine. This happens immediately after the stimulus is carried through, in hundreds of one second. So the story goes like this: acetylcholine is one of the chemical message used by the body to activate neuronal responses, and acetylcholinesterase brings the message to an end by destroying acetylcholine. The effect having being obtained, the receptor is ready for a new stimulus. A nicely controlled biological loop.

Now, organophosphate pesticides and nerve agents inhibit the activity of acetylcholinesterase by chemically binding to it in a key central position This means the loop is not working. Now, with all these pesticides or nerve agents around there is continuous presence of acetylcholine activating the receptors; there is no-more the enzyme (acetyl cholinesterase) to bring it to an end. So the good doctor decides to reduce the levels of acetylcholine artificially. This is achieved in two way, one by "freeing" the enzyme and restoring its activity, which is done with drugs called collectively oximes. One other way is by adding inhibitors of acetylcholine receptors. Atropine is one such inhibitor. Unfortunately Atropine does fit only in the muscarinic type of receptors.

As said muscarinic receptor is the name of the acetylcholine receptors in the smooth muscle cells (eye pupil, gastrointestinal tract, ureter and bladder) and some glands (salivary glands and sweat glands), while the name of the acetylcholine receptor in the skeletal muscles is nicotinic receptor. To a different name does correspond a slightly different molecular structure. Again just as in the cases of similar keys some molecules, being similar to acetylcholine, can fit in only one of the two types of receptors, some fit in the muscarinic ones, some fit in the nicotinic ones, some in both.
Atropine is a muscarinic antagonist, that is to say it attaches to the muscarinic receptor and prevents acetylcholine from doing so. It "looks like" acetylcholine in some way, that is why it binds to muscarinic receptors, only once attached it does not activate the receptor. Overall it is a competitive inhibitor; the more atropine you have the less acetylcholine can bind to the muscarinic receptor. In other words Atropine inhibit acetylcholine at the muscarinic receptor site. It is consequently a corrector, an antidote, to the damaging effect of the nerve agents. In facts nerve agents cause increase activity of acetylcholine, the increased activity of acetylcholine keeps on stimulating disorderly the receptors, which keep on discharging signal. By occupying the receptors but not stimulating them, Atropine counteract the activity of nerve agent at the muscarinic receptor site.
Unfortunately Atropine is not enough similar to acetylcholine to install on the nicotinic receptors, is therefore ineffective in the skeletal muscles.
What about the neuromuscular junction then? The nerve agents cause an excessive amount of acetylcholine to be present and permanently in the nicotinic receptors, which therefore keeps on firing. The muscle fibers keep on receiving order to contract, contractions of overall fibers does not result in generalized contraction of all muscles but rather in a generalized uncoordinated contraction of single muscle fibers. There will be involuntary muscular twitching in all part of the body, scattered muscular fasciculations and occasional muscle cramps. All this picture is followed by generalized muscle weakness and this situation on the respiratory muscle causes arrest of the ventilation and death by lack of breathing and consequently lack of oxygen. In fact opposite to smooth muscle cell, the skeletal muscle cannot contract continuously and fatigue will supervene, causing the generalized weakness. To counteract the effect of nerve agent the oximes (such as Pralidoxime -Pralidoxime chloride, Protopam chloride, 2-PAMCl. Mark I Kit) are used. Oximes are given IM or IV. The oximes break the bond between nerve agents and acetylcholinesterase, freeing the enzyme and therefore restoring its activity. Therefore the oximes are active everywhere, in the skeletal muscle (nicotinic receptors) and in the glands and smooth muscles (muscarinic receptors). All these informations are coming from oximes uses in organophosphate insecticide poisoning.Oximes are not presently available in North Iraqi Kurdistan.
In addition to the action of nerve agents on skeletal muscles and glands and smooth muscle cells, there is also an action on the Central Nervous System -CNS- and particularly a depressive effect on the respiratory center in the CNS. Atropine, which is not effective on the muscle, is however effective in the Central Nervous System where it does counteract the depressing activity on the respiratory center. Unfortunately Atropine does not penetrate easily through the blood brain barrier, and to have a central effect the dose must be somewhat higher then in the periphery.
Oximes do not penetrate blood brain barrier, or even much less so than Atropine. Even though they are on theory acting everywhere because they free the acetylcholinesterase, they do not reach the enzyme within the CNS. Atropine still needs to be given.

Botulinum toxins act also at the neuromuscular junction but with a different mechanism. The toxins localize themselves at the nerve ending expansion and interfere with normal extrusion through the presynaptic membrane of the small vesicles containing the stored acetylcholine. In this way acetylcholine cannot be released and go through the junction to install on the post synaptic receptor. The neurotransmission is completely arrested.

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