How sarin gas affects humans, symptoms of damage to the body. Nerve gases: sarin, soman, tabun and VX

Sarin is one of the most powerful toxic substances. If ingested in high concentrations, it is fatal.. Sarin gas was invented for military purposes as a chemical weapon of mass destruction. It has been banned for use since 1993.

Sarin was found in Germany as a result of numerous experiments by scientists to obtain pesticides. But on the eve of World War II, the substance ended up in a chemical laboratory, where they began to develop chemical weapons based on it.

What is sarin, its physical and chemical properties

Sarin is a liquid (ether), odorless, transparent. Easily mixes with various organic solvents and water. At room temperature 18-22 °C the liquid acquires a faint odor blossoming apple trees. Sarin immediately goes from liquid state into gaseous. When evaporated, it is also odorless and colorless. The substance is not stable in the environment. IN winter time in the air its concentration remains for 2-3 days, in summer period- few hours.

Sarin is a toxic substance that has a nerve-paralytic effect on the body.. Any contact with a person leads to severe poisoning. The most dangerous route is inhalation. When inhaling medium concentrations of the substance, a negative effect occurs within 2 minutes, which is manifested by acute respiratory distress and dilation of the pupil. When entering Airways large doses of sarin, death can occur within 1 minute. Sarin is equally dangerous if it comes into contact with the skin, mucous membranes or the stomach.

The mechanism of action of sarin, clinical symptoms of poisoning

The main target of sarin is the human central nervous system. The gas has a stimulating effect on the transmission of nerve impulses to internal organs and muscles. A continuous process occurs, until the nerves are completely exhausted due to their hyperactive state.

The effects of sarin on humans can be general or local. The mucous membranes are the first to be affected by the substance; a person experiences serous discharge from the nose; due to the increased formation of mucus in the bronchi, difficulty breathing and a feeling of congestion in the chest appear. In the oral cavity, due to damage to the receptors, salivation increases.

Signs of sarin damage to the central nervous system:

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• general damage to the meninges - dizziness, headaches, overexcitation, nervous anxiety, drowsiness, drowsiness or insomnia, general weakness;
• damage to the centers of the brain - tremor (rhythmic contractions of the limbs or the entire body), impaired concentration, slurred speech, violation of the coordination of movements of various muscle groups, convulsions (pseudoconvulsions), shortness of breath due to damage to the respiratory center, drop in blood pressure;
• mental disorders - emotional instability, neurotic outbursts, depression or apathy, nightmares.

Symptoms of damage to the organ of vision - sharp narrowing or dilatation of the pupils, which does not always manifest itself equally in both eyes, sharp pain in the forehead, impaired focusing of the eyes, decreased visual acuity, blurred vision. The conjunctiva (mucous membrane of the eye) becomes bright red.

Signs of damage to the respiratory system:

• pressing chest pain;
• shortness of breath, very rapid, shallow breathing;
• increased production of mucus in the bronchi;
• spastic movements of the respiratory tract;
• continuous cough;
• pulmonary edema;
• cyanosis of the skin.

Symptoms of damage to the gastrointestinal tract are belching, heartburn, nausea, vomiting, discomfort and heaviness in the abdomen, in severe cases, acute, cramping attacks in the abdominal cavity. Then diarrhea occurs, and a false urge to empty the bowel is observed. In severe cases of poisoning, involuntary bowel movements are observed.

Disruption of other organs and systems:

• the heart rhythm is disturbed, the heartbeat slows down;
• the frequency of the urge to urinate increases, emptying in a semi-conscious state Bladder occurs involuntarily;
• fasciculation – contraction of one or a group of muscles.

In severe cases, death occurs from spasm of the respiratory tract and suffocation.

First aid for sarin poisoning

The substance sarin is a potent toxic compound that causes in the human body irreversible consequences . Therefore, it is important to know first aid techniques to prevent the serious consequences of intoxication. The main thing is to prevent the development of a severe form of poisoning, when death is inevitable.

The first thing to do is to remove the victim from the affected area. Then remove all clothing from the person to reduce contact of the toxic substance with the skin. Rinse the victim's body and face with clean pressurized water If possible, wash your face and mucous membranes with a weak solution of baking soda.

There is an antidote to sarin. These are anticholinergic pharmacological drugs - atropine, hyoscyamine, scopolamine, aprofen, cyclodol. If they are absent, you can use antihistamines– diphenhydramine, cyclizine, doxylamine, meclozine. The drugs are administered intramuscularly, for mild and moderate severity - up to 2 ml once, in severe cases the dosage is increased to 4 ml.

The antidote is administered at intervals of 10-15 minutes until signs of improvement appear - restoration of the pupil's reaction to light, relief of convulsions, reduction of pain.

Treatment of patients with poisoning

Sarin poisoning is treated in a hospital, in intensive care and resuscitation.

The patient is placed in a special room in which he is protected from external irritants - sound insulation, adjustment of light intensity. Upon admission, the victim undergoes gastric lavage with alkaline solutions to reduce the degree of influence of sarin on the body.

Rules for administering antidotes:

• Atropine – blocks receptors, prevents physiological destruction of the body.
• Organophosphorus substances – toxogonin, pralidoxime. If you use them in the first hours, you can quickly restore physiological processes in the body.
• Diazepam is an anticonvulsant, relaxes muscles, relieves anxiety, has a hypnotic and sedative effect. It can be used before starting treatment. The drug quickly relieves seizures and epileptic seizures.
• Athene or Budaxim is a drug for use in field conditions. It is produced in a special syringe tube and is part of the military’s individual first aid kit.

Depending on the person’s well-being, symptomatic treatment is carried out. If the victim is in extremely serious condition, carry out artificial ventilation lungs. For this, the patient is connected to an oxygen supply apparatus. In case of cardiac arrest, indirect cardiac massage and other resuscitation measures are carried out to restore the vital functions of the body.

Sarin vapor poisoning varies in severity. With small concentrations and timely medical care, human health can be completely restored. With moderate severity, side effects may remain. People after sarin poisoning need not only medicinal support for the body, but also systematic psychological assistance. In severe cases, patients die within minutes, hours or days after exposure to sarin. In this case, the pathological changes caused by the substance are irreversible.

IN ordinary life It is unlikely that you will be poisoned by sarin. But given the current situation in the world, this incident cannot be completely ruled out.

Sarin is a poisonous liquid or gas of the group of organophosphorus substances. In the gaseous state it has neither color nor odor.

During wars, sarin was used as a chemical weapon of mass destruction. Today this substance is prohibited for production in a number of countries, including Russia. However, the likelihood that it is still used for terrorist purposes is still high.

In addition, in laboratories in some countries, sarin is still used to carry out chemical reactions.

The effects of sarin on the body

The principle of action of the gas is nerve-paralytic. That is, the nervous system comes under attack to a greater extent:

• Sarin provokes continuous work nerve cells - neurons. Without external influence on the body, it produces substances that inhibit the process of constant transmission of impulses, and the gas stops the production of these substances. As a result, impulses arrive continuously, the nervous system works in an enhanced mode and is quickly depleted.
• The nerve fibers of organs undergo changes, after which malfunctions occur in the functioning of the whole organism.
• In a chain reaction, the respiratory, digestive and urinary systems begin to suffer.
• As a result of the continuous operation of the nervous system, the acid-base balance is disrupted and cardiac arrest occurs.
• Sarin is converted to decay products in the liver. As a result of the breakdown of the toxin, the organ begins to produce toxic substances, and the body is gradually re-poisoned with some changes in symptoms.

If sarin enters the body, severe poisoning occurs, almost always leading to death.

Ways and causes of poisoning

Sarin can enter the body in three standard ways:

• through inhalation of gas;
• after contact of liquid or gaseous sarin with skin;
• if it enters the digestive system (if contaminated food and water were consumed).

This can happen both in the production and work with sarin in laboratories, and during a terrorist attack using a toxic substance.

To cause severe intoxication by inhaling gas, 0.0005 mg / 1 dm³ is enough, for death - 0.075 mg (and death from sarin in this amount will occur within a minute). The lethal dose of sarin in liquid form upon contact with the skin is 24 mg / 1 kg of body weight. For death from poison entering the digestive tract, only 0.14 mg / 1 kg is enough.

Features of application

It is mainly sarin gas that has the lethal effect. And if we remember that gas has no color, no taste, no smell, then a person will not be able to sense the danger in time. Because of this, the deterioration of the condition occurs quickly and unnoticed.

Detecting the presence of sarin in the air is possible only with the help of special gas traps and similar devices. Moreover, sarin gas is perfectly absorbed into the rubber protective form, so ammunition made from this material cannot fully protect against poisoning.

Sarin also absorbs well into painted surfaces, evaporating from which the gas continues to poison the air and people breathing it for some time.

Read also: Ozone poisoning in humans

How does poisoning manifest itself?

With sarin intoxication, symptoms appear literally within seconds. The clinical picture depends on the degree of poisoning. There are 3 degrees in total: mild, moderate and severe.

Lightweight

The symptoms of this stage resemble poisoning with other gases. In this case, the person feels pain in the sternum, weakness, fog and shortness of breath.

Average

With a higher concentration of sarin, the symptoms of poisoning will be different:

• headache;
• profuse lacrimation;
• pain in the eyes, bright redness of the sclera;
• constriction of the pupils, and this is often more pronounced in one eye;
• nausea and vomiting;
• cold sweat;
• temperature fluctuations up and down;
• shortness of breath even at rest, cough;
• attacks similar to asthmatic ones;
• spasms in the throat;
• slurred, confused speech, confusion in thoughts;
• increased heart rate, pressure surges;
• small muscle twitches turning into tremors;
• mental disorders (increasing fears, anxiety, apathy, depression, trembling, etc.).

Despite the fact that this stage is classified as medium, with such sarin intoxication, in half of the cases deaths are recorded due to the slightest delay in providing assistance.

Heavy

This is the most severe poisoning, in which the concentration of sarin is critical.

The signs of sarin damage here are the same as in the middle stage, but they develop much more severely and faster. In addition to these, additional symptoms are added:

• the person vomits violently (if liquid sarin enters the body, a smell similar to apple tree is felt);
• pain in the head and eyes becomes unbearable;
• uncontrolled urination or defecation occurs;
• after a couple of minutes he loses consciousness;
• convulsions begin, turning into paralysis.

After 10 minutes of torment, a person’s death occurs.

How you can help

Whether the victim survives or not depends on how quickly first aid is provided for sarin poisoning. After calling an ambulance, you need to do the following as quickly as possible:

• immediately remove the poisoned person from the affected area to the air;
• remove clothing from the victim that has become saturated with sarin;
• if sarin gets on your skin, cut off your nails and hair (this can also avoid additional contact with the poison);
• treat the affected area of ​​skin with a weak alkali solution (this will help neutralize the sarin somewhat);
• if you swallow sarin-poisoned water, food, or the poison itself in liquid form, rinse your mouth with a weak alkaline solution and give the poisoned person activated charcoal;
• to restore enzymes that stop the continuous transmission of nerve impulses, the victim needs to take the drugs Dipiroxime, Isonitrozine or Dietixime (these drugs are in in this case may somewhat replace the antidote);
• treat the mucous membranes of the person poisoned with sarin (rinse the eyes with a 1% sodium bicarbonate solution or water), then drip a Novocaine solution.

A special antidote for sarin (Athens) and Taren tablets are unlikely to be found at home. These antidotes are only available in military first aid kits during trials or exercises. But all other measures to provide assistance in case of sarin poisoning must be carried out immediately, without wasting a second, otherwise the victim will die.

Treatment

All therapy will take place only in a hospital. It is impossible to fully help the victim either at home or in the field. What will doctors do:

• immediately - correction of circulatory and respiratory disorders (if they are observed);
• intramuscular antidote Atropine, Scopolamine, Cyclodol, Aprofen or Hyoscyamine at intervals of 10-15 minutes until the condition improves;
• additionally, the antidote Unithiol can be administered for detoxification;
• connection to antioxidant therapy;
• anticonvulsants (Diazepam or magnesium sulfate);
• vitamin E, hydrocortisone;
• plasma expanders and saline solutions for the treatment and prevention of the consequences of sarin poisoning;
• V severe case- Mechanical ventilation or hemodialysis.

Read also: Smoke poisoning in humans

During the treatment period, doctors do not stop monitoring a person who has been poisoned by sarin, since any sudden change in the victim’s condition can result in his death.

What are the risks of poisoning?

Consequences and complications can appear both shortly after sarin poisoning and after a while. Moreover, it does not matter how mild or severe the intoxication was: changes in the functioning of organs will still affect the health of the surviving person:

• relapse of poisoning (can occur after a week and be accompanied by more vivid symptoms) as a result of involuntary production of sarin metabolites by the liver;
• pneumonia;
• disorders of the nervous system (neuritis, headaches, causeless darkening of the eyes, astheno-vegetative syndromes, etc.);
• late sarin intoxication as a long-term consequence;
• sometimes - kidney damage (nephropathy, etc.);
• heart problems, accompanied by chest pain, shortness of breath with slight exertion and changes in rhythm;
• toxic hepatitis with subsequent yellowing of the skin and impaired digestive function (occurs due to the powerful effect of sarin on the liver).

The damage caused to the body by the toxic effect of sarin is destructive. And since the chances of saving the victim are too small due to lack of time, the main consequence may be the death of a person.

Have you ever been poisoned by sarin?

- an organic compound, isopropyl ester of methylfluorophosphonic acid CH 3 P (O) (F) OCH (CH 3) 2. Under normal conditions, it is a colorless liquid, tasteless and odorless, extremely toxic. For military purposes it is used as a chemical warfare agent with a nerve agent.

Has military designations: GB (USA), Trilon 46, T46, Trilon 144, T144 (Germany). On ammunition it is coded with three green rings.

Story

The substance GB was first synthesized in 1939 in the laboratory of the German chemist Gerhard Schrader under the code “sarin”. This name is associated with the combination of the first letters in the surnames of employees of IG Farbenindustrie G. Schrader, A. Ambros and the Armament Directorate of the Ground Forces F. Ritter (German. S chrader, A mbros, Ritter).

In 1993, as a result of the signing of the Chemical Weapons Convention, the use of sarin as chemical weapons was prohibited. It was included in List 1, which regulates the production and circulation of hazardous substances.

Physical properties

Sarin is a colorless, transparent liquid, odorless and tasteless. It is miscible with water and organic solvents in all proportions. When heated to boiling point, it partially decomposes, so it is distilled in vacuum. It is more resistant to short-term temperature increases than the herd.

Gaseous and liquid sarin is easily sorbed by porous materials (wood, concrete, brick, fabric), and does not exceed painted surfaces and rubber.

The volatility of sarin is 4100 mg/m³ (0°C), 16091 mg/m³ (20°C), 22000 mg/m³ (25°C), 29800 mg/m³ (30°C).

Receipt

Methods for synthesizing sarin differ depending on the phosphorus-containing raw materials used. Thus, dichloroanhydride, difluoroanhydride of methylphosphonic acid and their mixture, as well as diisopropyl ester of methylphosphonic acid are used. All of the above compounds can be obtained from phosphorus (III) chloride.

For the synthesis of methylphosphonic acid dichloroanhydride, phosphites (phosphonates) are obtained as intermediates. So, to obtain dimethylphosphite, it is enough to mix phosphorus (III) chloride with anhydrous methanol at a temperature of 0-20 ° C:

The resulting dimethylphosphite under the influence of chlorination agents (SOCl 2, COCl 2, PCl 5) is converted into methylphosphonic acid dichloroanhydride, and then, after treatment with anhydrous hydrogen fluoride, into difluoroanhydride (an equimolar mixture of chloroform and fluorophosphate is formed):

The synthesis of dichloric anhydride without the stage of formation of phosphonates is also known - the interaction of phosphorus trichloride with chloromethane and aluminum chloride in an organic solvent. The resulting complex compound is decomposed by exposure to chilled water, or preferably concentrated hydrochloric acid at -30 ° C, and dichloric acid is isolated from the solution:

This method formed the basis of the Kinnear-Perrin reaction and became the basis for the synthesis of many organophosphorus compounds.

To obtain sarin, combine difluoranhydride with isopropanol. The dichloroanhydride present in the reaction mixture also reacts to form sarin. The yield of the final product is about 85%:

Chemical properties

Sarin hydrolyzes to form isopropyl ester of methylphosphonic acid and hydrogen fluoride:

The rate of hydrolysis depends on the pH of the medium. Thus, at pH 1.8, the period of beer hydrolysis is 7.5 hours, 5:00 at pH 9. With a solution concentration of less than 14 mg/l, the period of beer hydrolysis is 54 hours. At temperatures exceeding 25 °C, hydrolysis is capable of self-producing through the catalytic action of its products. This is explained by the dissociation of the isopropyl ether produced by hydrolysis to form H+ ions, which can form hydrogen bonds with the fluorine atoms, weakening their interaction with the phosphorus atom and promoting the cleavage of the FP bond followed by hydrolysis. Adding any acid to a sarin solution increases the rate of hydrolysis.

Alkali solutions affect the course of hydrolysis even more than acids, since the hydroxide ion has greater nucleophilicity compared to undissociated water molecules:

Thus, solutions of acids and alkalis can be used to neutralize sarin.

Aqueous solutions of ammonia and amines act on sarin almost similarly to alkalis. Phenolates and alcoholates degas sarin very easily (even in a dry state).

When sarin is heated above 100 °C, it begins to decompose and near its boiling point it decomposes almost completely. The main products formed as a result of pyrolysis are propene and methylphosphonic acid fluoroanhydride. Depending on the pyrolysis conditions, 2-fluoropropane, an oligomer of methylphosphonic anhydride CH 3 PO (O) and some further decomposition products may also be formed.

Toxicity

Sarin is 4-5 times more poisonous than herd. Poisoning can be caused by inhalation of vapors or penetration through the skin (especially due to injury). Sarin easily penetrates the body through the mucous membrane of the eyes and respiratory tract. It is also easily absorbed by objects environment, brick, fabric and may cause poisoning in the future. This increases the risk of poisoning for people who left the affected area but did not get rid of clothing, personal belongings, and the like contaminated with sarin. When favorable weather conditions Sarin can remain in the area in the form of a liquid for up to 5 days, its vapor is effective for 20 hours. In winter, the stability of sarin decreases to two days.

At concentrations of 0.0002-0.002 mg/l and with its action within 2 minutes, mild poisoning, which, however, leads to loss of ability to work for 4-5 days and is accompanied by constriction of the pupils, sweating, difficulty breathing, and increased salivation. The effects of sarin of the same concentration within 15 minutes can become lethal. Severe poisoning occurs at concentrations of 0.005-0.01 mg/l and effects within 5 minutes, they cause miosis, convulsions, dizziness, increased salivation, and can also lead to death. When exposed for 2-5 minutes to sarin with a concentration of 0.02-0.05 mg/l, a person dies from cardiac arrest within 15-20 minutes.

Protection

An effective protection against sarin is a filter gas mask. To avoid the absorption of sarin on clothing, it is necessary to use protective suits. If sarin gets on your skin or clothing, it should be neutralized as soon as possible using individual anti-chemical bags.

If symptoms of sarin poisoning appear, solutions of atropine, Athena or Budaxim should be immediately administered subcutaneously or intramuscularly. When administered no later than 10 minutes after injury, the drug is capable of neutralizing a lethal dose. If necessary, artificial respiration can be performed.

Aqueous solutions of alkalis, ammonia, hydrogen peroxide, as well as a solution of hydroxylamine in a slightly alkaline environment are suitable for disinfecting objects, premises and clothing.

Video on the topic

According to their chemical structure, nerve agents belong to the organophosphorus substances (OPS). These include sarin, soman, and V-gases.

In addition to toxic substances, a large number of organophosphorus substances for peaceful purposes have been synthesized and continue to be synthesized. These are primarily organophosphorus insecticides (chlorophos, thiophos, metaphos, karbofos, fosamide, etc.), organophosphorus drugs (pyrophos, phosphakol, armin, fosarbine, fadaman, etc.), organophosphorus additives for lubricating oils, synthetic fibers, and organophosphorus polymers.

Organophosphate poisonous substances are esters phosphoric acids (ortho- and pyrophosphoric). So, sarin is isopryl ether.

Sarin and soman are colorless (or slightly yellowish) liquids with a characteristic odor for each substance; specific gravity of these substances is slightly higher than unity (1.02-1.1). They dissolve well in organic solvents, including fats and fat-like substances, are less soluble in water, and quickly create lethal concentrations of vapors in the air. In a droplet-liquid state they can contaminate the area in summer: sarin for up to 8 hours, soman for up to a day.

Sarin and soman are not stable in an alkaline environment: 8-10% solutions of caustic alkalis (caustic potassium and caustic sodium), as well as a 10% solution of ammonia in water, quickly destroy the toxic substance.

The chemical name of V-gases is phosphorylthiocholines. O-ethyl-3-dimetcan be cited as a representative of this subgroup of organophosphorus substances. This substance is a colorless liquid, poorly soluble in water, well soluble in organic solvents, flammable substances, and lubricants. Penetrates well into rubber products and is absorbed paint and varnish coatings. Due to its low volatility (10-8 mg/l at a temperature of 20 ° C), it remains in place for a long time.

V-gases, soman, sarin are persistent toxic substances.

When using these gases, injuries will most often occur when a droplet-liquid substance gets on the skin or by inhalation of vapors of these agents.

Lethal concentrations and doses: sarin inhalation dose is 0.06; soman - 0.002; V-gases - 0.001.

All representatives of FOV have a pronounced cumulative effect.

Compounds found in nature and in production have been used as chemical weapons.

Entry and distribution in the body. The entrance gates for FOV are the skin, respiratory organs, conjunctiva, and digestive organs. Once in the body and in the blood, OPAs find themselves in unfavorable conditions, since they are unstable in an alkaline environment, and the blood has a slightly alkaline reaction.

That part of the agent that does not bind to biochemical structures is neutralized in the blood after some time. It is assumed that the process of destruction of OPA can be catalyzed by enzymes. The products of the transformation of OPA in the form of simple compounds (in particular, phosphorus) are removed by the kidneys.

Clinical picture

Clinic of acute lesions. The first symptoms of FOV damage appear, as a rule, after a certain period of latent phenomena; Then the clinic develops rapidly.

The prodromal period is more extended (10-15 minutes) when the agent enters the body through the skin. In case of inhalation damage and damage through gastrointestinal tract the period of latent phenomena may be practically absent. The first symptoms of the disease are a feeling of tightness in the chest and suffocation. The visible mucous membranes and skin become cyanotic, the neck veins are tense. The breathing is noisy, the patient breathes with an open mouth, and is fixed in the asthmatic pose (sitting with his hands resting to include auxiliary muscles in the act of breathing).

Noteworthy is the increase in intercostal spaces, barrel-shaped widened rib cage. The lower border of the lungs is lowered. Percussion sound is boxed.

On auscultation, dry and coarse moist rales are heard diffusely. Pulse is frequent, good filling at first, then it becomes sparse and easily compressible. Blood pressure, after a small short-term increase, decreases, sometimes falls catastrophically. At the same time, vision is impaired: the patient complains of pain in the eye sockets, he has difficulty distinguishing objects far away, he sees poorly in the twilight (like a patient with hemerolopia - “night blindness”), his eyelashes seem sharply thickened. Abdominal pain appears intermittently. Nausea, profuse salivation, vomiting, and diarrhea are noted. Twitching of muscle fibers and muscle groups occurs. Further, the twitching becomes generalized. The patient loses consciousness and falls. At the same time, clonic-tonic convulsions of the muscles of the face, neck, upper belt and finally total clonic-tonic convulsions appear. Sometimes convulsions occur continuously and end in paralysis, sometimes they occur in paroxysms: a cascade of convulsions is replaced by a period of relaxation, followed by a new attack of clonic-tonic convulsions. During the period of convulsions, cyanosis increases. Death occurs when breathing stops. Cardiac activity continues for several minutes.

Depending on the route of entry, some features may occur in the development of the disease. Thus, when an agent penetrates through the skin and wound surface, the first signs of damage will be muscle twitching in the area where the poison is absorbed. In case of poisoning through the gastrointestinal tract, drooling, vomiting, diarrhea, and cramping abdominal pain develop more quickly. Vision and breathing are quickly impaired in case of inhalation damage to FOV and somewhat more slowly in case of poisoning through the skin or gastrointestinal tract.

Damage from organophosphorus substances, depending on the dose of poison, can be mild, moderate or severe.

Easy defeat. Due to its predominant syndrome, some toxicologists call this form “mystical.” The patient complains of a state of “tension,” weakness, restless sleep, headache, which is localized in the eye sockets, poor vision of distant objects, absence or sharp deterioration of twilight vision, and excessive salivation. Some complain of a feeling of tightness behind the sternum and repeated loose stools.

On examination, one notices the narrowing of the pupil, sometimes to the size of a pinhead, and the injection of conjunctival vessels. A well-filled pulse is usually increased. Blood pressure is slightly elevated or normal. In the lungs, the percussion sound is pulmonary; wheezing is not audible. The tongue is clean and moist. The abdomen is soft and painless. In the descending colon, liquid contents are noted on palpation.

The diagnosis is made based on a combination of visual disturbances (such as deterioration of twilight vision, development of acute myopia, miosis), pain in the orbital area with sleep disorders and increased salivation.

Moderate damage. Moderate lesions are sometimes called the bronchospastic form of the disease. The patient complains of suffocation, paroxysmal abdominal pain, frequent loose stools, poor vision of distant objects, deterioration or absence of night vision. The patient is in the asthmatic position. The skin and visible mucous membranes are cyanotic, the neck veins are swollen, and breathing is noisy. Twitching of individual muscle groups is noted. The patient sweats profusely. The pupils are constricted, the conjunctival vessels are injected. The pulse is well filled and rare. Blood pressure is normal or slightly elevated. The chest is barrel-shaped expanded. Percussion sound is boxed. The lower border of the lung is lowered.

Auscultation reveals a large number of dry and moist coarse bubbling rales, a moist tongue, profuse salivation, vomiting, the abdomen is soft, the spleen is not palpable, the large intestine is palpated in the form of cords, the stool is liquid with an admixture of mucus.

The diagnosis is made on the basis of bronchial asthma syndrome, miosis, fibrillary twitching of individual muscle groups, cramping abdominal pain and diarrhea, and a decrease in blood cholinesterase activity (by 60-70%).

Heavy defeat. This form of damage is called convulsive-paralytic. After the appearance of symptoms of FOB damage, characteristic of a moderately severe disease, as a rule, the patient quickly falls into an unconscious state. The eyes are open, the pupils are sharply constricted. The skin and mucous membranes are cyanotic. Clonic-tonic convulsions are noted, which occur continuously, or periods of convulsions are replaced by periods of relaxation. The longer and longer the periods of relaxation, the more favorable the outcome of the lesion. Against the background of convulsions and during periods of relaxation, twitching of various muscle groups is observed. The pulse is weak, rare. Blood pressure is reduced, sometimes falling catastrophically. Breathing is noisy, the chest is barrel-shaped, the percussion sound is boxy, the lower border of the lungs is lowered. On auscultation, a mass of dry and coarse rales are heard. During the period of convulsions, pulmonary ventilation completely stops, and the cyanosis of the skin and mucous membranes sharply increases. There is profuse salivation and vomiting is possible. The abdomen is soft during the interconvulsive period, the liver and spleen are not palpable. The large intestine is palpated in the form of a cord. The rectal sphincter is gaping. There is involuntary separation of the contents of the intestines and bladder. Death usually occurs from primary respiratory arrest. The diagnosis is made on the basis of a combination of clonic-tonic convulsions with bronchial asthma syndrome, generalized fibrillations, miosis, diarrhea, bluish discoloration of the skin and mucous membranes, and a decrease in blood cholinesterase activity (by 80-90%).

Complications and consequences of acute injury. When a person affected by FOB combines convulsions with vomiting, due to the fact that the natural outlet for vomit is closed due to a spasm of the masticatory muscles, aspiration of vomit can occur and suffocation may develop due to blockage of the bronchial lumen. If the vomiting was not profuse and the vomit entered the lungs, then aspiration bronchopneumonia is possible, which is often suppurative in nature (abscess pneumonia).

Bronchopneumonia, which is a consequence of blockage of spasmodic bronchioles and bronchi with abundant secretion of the bronchial glands - mucus plugs, is quite common. Bruises, dislocations and even fractures are very likely, which can occur during convulsions. As a result of severe damage to FOB, paresis, paralysis, and mental disorders are noted. The nature of the patients' behavior changes sharply: they become uncooperative and their professional skills decline. Long-term polyneuritis with severe muscle atrophy was noted. Long-term consequences of FOB damage are vegetative neuroses from the cardiovascular system (vascular dystonia, angina pectoris), digestive organs (disorders of the secretory and motor functions of the gastrointestinal tract, which can simulate gastritis, gastroenteritis, enterocolitis, spastic colitis), respiratory organs (bronchial asthma).

Chronic Poisoning Clinic

In case of repeated damage to OPA in small doses, as well as in case of violations of safety regulations during production, storage, transportation, irrational use of organophosphorus compounds as insecticides and medicines Chronic poisoning may develop, since these poisons have a pronounced cumulative ability.

The clinical picture of chronic FOV poisoning is very diverse and depends on a number of reasons: entrance gate, duration of contact, total dose, initial state of the autonomic nervous system. When organophosphate poisons enter the conjunctival sac, temporary myopia and deterioration of night vision may develop. When OPA enters the body through inhalation, attacks of suffocation are early manifestations of poisoning. Visual disturbances are also common in patients.

If poisoning occurs as a result of the intake of OPV through the gastrointestinal tract, the first signs of the disease are nausea, vomiting, diarrhea, and cramping abdominal pain. Lesion selectivity various systems and organs largely depends on the ratio of the tone of the sympathetic and parasympathetic nerves in various organs: the prevalence of the tone of the parasympathetic nerves creates conditions for increased sensitivity of a given organ to FOB. Thus, in people with physiologically increased secretion and peristaltic activity of the gastrointestinal tract, the first manifestations of chronic FOB poisoning are nausea, cramping abdominal pain, and diarrhea. In people prone to hypotonic reactions and spasms of heart vessels, cardiovascular disorders primarily occur. With any route of admission, mental disorders are noted. Initially, patients complain of disturbing sleep with frightening dreams, a state of causeless anxiety, tension, decreased memory, and attention. They become difficult to communicate in a team, often lose professional skills - they degrade as specialists.

Thus, chronic poisoning with organophosphorus compounds can cause serious disorders in both the mental sphere and internal organs. The picture of chronic poisoning is very diverse, which can lead the patient to doctors of various profiles: a psychiatrist, a neurologist, a therapist, an ophthalmologist.

Pathogenesis

Organophosphorus substances, absorbed through the mucous membranes and skin, enter the blood and penetrate with it into all tissues of the body.

It is known that FOBs have the property of inhibiting the function of vital enzymes, such as cholinesterase, dehydrogenase, phosphatase, thrombin, trypsin, etc. The greatest consequences for the poisoned organism result from inhibition of the activity of cholinesterases.

Cholinesterases are enzymes that regulate the amount of active substance involved in the conduction of nerve impulses through synaptic formations - acetylcholine. Substances with such properties are called mediators. Acetylcholine is released at the ends of excited centrifugal nerves and causes excitation of the innervated cell. Nerves that excite the cell using acetylcholine are called cholinergic. As soon as the excitation of the cholinergic nerve stops, the excited cell must go into a resting state, for which acetylcholine must be destroyed. Acetylcholine, with the participation of cholinesterases, is broken down into choline and acetic acid.

When poisoning with OPA, as a result of their ability to inhibit the activity of cholinesterases, a large amount of acetylcholine accumulates in the body, which maintains cells sensitive to this mediator in a state of prolonged excitation. The mediator acetylcholine causes excitation of cells in various organs and tissues: in the central nervous system, autonomic ganglia, in all internal organs, as well as in motor muscles. With the accumulation and retention of acetylcholine in these organs, pathological excitation remains, and if exposed to a very large amount of the mediator, paralysis of their function may occur. Thus, an excess of acetylcholine in skeletal muscles initially leads to its tension and causes twitching of individual fibers (fibrillation). If the mediator continues to accumulate, muscle tone decreases - they relax and become unable to contract.

If these phenomena develop in the respiratory muscles, death occurs from cessation of external respiration. This phenomenon is called neuromuscular block, or relaxation of the respiratory muscles. The accumulation of acetylcholine in the bronchi and intestines leads to a reduction in the muscles of these organs - bronchial spasm, intestinal spasm or increased peristalsis develop. The muscles of the arterioles relax under the influence of acetylcholine, so blood pressure decreases and the heart rate slows down. There is an indication that FOBs affect the cholinoreactive structures of the body not only indirectly (through acetylcholine), but also directly (by interacting with them).

Inhibition of FOB enzymes phosphoglucomutases and dehydrogenases, which are involved in the activation of oxidative processes occurring in cells and providing them with the necessary energy, leads to energy starvation of tissues. This exacerbates the harmful effects of excess acetylcholine.

Thus, inhibition of cholinesterase activity and the associated accumulation of acetylcholine in the body during FOB poisoning distorts the normal functioning of the central and peripheral nervous systems and, naturally, all organs.

The effectiveness of treatment of affected FOVs largely depends on the timely cessation of further entry of FOVs into the body. If chemical agents come into contact with the skin in a droplet-liquid state or in the form of drizzle, the exposed skin areas should be treated with the liquid of an individual anti-chemical package (IPP). If it is unavailable, you can use a 10% ammonia solution - ammonia. If the skin comes into contact with FOV, wipe it vigorously with a degasser, and then wash it with soap and water. If FOV gets into the eyes, the conjunctival sac is washed with a 2% solution of baking soda.

In case of poisoning through the gastrointestinal tract, give copious amounts of soda (2% solution of baking soda) and induce vomiting. If possible, wash the stomach with a 2% solution of baking soda, followed by the administration of a suspension of activated carbon (10-15 g of activated carbon is stirred in 3/4 cup of a 2% solution of baking soda). To treat affected FOBs, antidotes (antidotes), syndromic drugs and symptomatic drugs are used.

Cholinesterase reactivators have been proposed as antidotes, but acetylcholine antagonists - anticholinergics (atropine) and adrenergic agonists (adrenaline, ephedrine) are more common. Atropine is administered intramuscularly in a 0.1% solution of 1-3 ml repeatedly. The daily dose of atropine in the treatment of severe forms of FOV damage can reach 24-30 ml and more than 0.1% solution. The atropine prescription regimen is designed in such a way that the patient does not complain of difficulty breathing and notices mild dry mouth. The appearance of severe dryness of the mucous membranes, thirst, sharp dilation of the pupil, redness of the face indicate an overdose of atropine. In case of severe damage to FOV, anticholinergics are used in combination with cholinesterase reactivators: diperoxime, 1 ml of a 15% aqueous solution, is administered intramuscularly at intervals of 4-6 hours. Adrenaline in a 0.1% solution, 1 ml each, and ephedrine in a 5% solution 1 ml solution is administered intramuscularly.

If the administration of antidotes does not relieve seizures, then to relieve them, one of the medicinal substances of the barbituric acid group is used - barbiturates (sodium thiopental, hexenal, barbamyl). Sodium thiopental is administered intramuscularly in a 2.5% solution, 5 ml each, hexenal - 5 ml of a 10% solution, also intramuscularly. A reliable anticonvulsant effect is achieved by intramuscular injection of 2 ml of a 2.5% solution of aminazine, 2 ml of a 2% solution of diphenhydramine and 2 ml of a 2% solution of promedol. In case of severe respiratory distress, the affected FOV is given artificial respiration and oxygen is prescribed.

Due to the fact that one of the causes of respiratory distress is the narrowing of the lumen of the bronchi, conventional two-handed methods of artificial respiration are ineffective. Such affected people need active artificial respiration - instrumental (DP-3, GS-6, RPA-3, etc.) or using the mouth-to-mouth method. Symptomatic drugs are also used that increase blood pressure (10% solution of caffeine-sodium benzoate, 1 ml intramuscularly or subcutaneously, etc.), stimulating breathing while simultaneously administering oxygen (cytiton, 1 ml intramuscularly). Severely affected FOVs, as a rule (for the purpose of prevention and treatment of pneumonia), require antibiotics and sulfonamides. All manipulations should be as gentle as possible.

Such patients require constant monitoring medical personnel. In addition, when vomiting occurs, severely affected patients should be promptly introduced with mouth dilators, and if vomit is aspirated, they should be sucked out.

Prevention

If there is a threat of contact with FOV, it is necessary to wear gas masks and use skin protection. If infected with droplet-liquid FOV, the skin and visible areas of clothing should be treated with IPP degassers, and personal weapons should be degassed with the liquid of an individual degassing package (IDP). If there is no PPI, the skin should be wiped with a 10% ammonia solution (V-gases are not destroyed). Mucous membranes should be protected from the IPP degasser and ammonia. The mucous membranes accessible to treatment are washed with a 2% soda solution. If you don’t have a PPI or ammonia on hand, then exposed skin should be washed with water and soap (preferably household soap). When infected with FOV, a prophylactic antidote is administered before symptoms of poisoning appear.

Currently, a number of prescriptions for a prophylactic antidote are used, one of which may consist of an aqueous solution of proserin and an aqueous solution of atropine sulfate.

In case of infection with FOV, a full dose is administered; in case of suspicion or threat of infection, a half dose of the prophylactic antidote is administered. As soon as possible, you need to take a shower, change your underwear and uniform.

First aid. Put on a gas mask, inject an antidote intramuscularly from a syringe tube, treat exposed skin and visible areas of contaminated clothing with PPI degassers, and degas personal weapons. In case of suffocation, perform artificial respiration without removing the gas mask. In case of convulsions, re-administer the antidote.

First aid. The exposed skin areas are re-treated with a PPI degasser and an antidote is administered. In case of suffocation, oxygen is given by connecting a gas mask helmet to an oxygen device. Carry out artificial respiration. Adrenaline (1 ml of 0.1% aqueous solution), ephedrine (1 ml of 5% aqueous solution), caffeine-sodium benzoate (1 ml of 10% aqueous solution), 1 ml of cititon are administered intramuscularly. In cold weather, the affected person should be wrapped warmly and covered with heating pads.

Sarin

Sarin is a nerve agent. It is a colorless liquid that produces vapor when heated. In its pure form, sarin has virtually no odor, so at high concentrations, which are easily created in the field, a lethal dose can quickly and unnoticeably accumulate inside the body.

This is very important property sarin, which increases the possibility of its sudden use, especially in cases where delivery systems are used that can quickly and relatively imperceptibly create very high concentrations in the target area. Under such conditions, personnel subjected to a chemical attack will not detect the danger in time and will not be able to put on gas masks and use skin protection in a timely manner.

Presence of nerve agents 0V in the air, on the ground, in weapons and military equipment detected using chemical reconnaissance instruments ( indicator tube with a red ring and dot) and gas detectors. AP-1 indicator film is used to detect VX aerosols.

When sarin vapor is inhaled, its damaging effect manifests itself very quickly, so it is possible to create such high concentrations in the field that they will be enough to receive a lethal dose into the body in a few breaths. In this case, death can occur within a few minutes.

At low concentrations of sarin in the air, if gas masks are not used, those affected primarily experience a severe runny nose, heaviness in the chest, as well as constriction of the pupils, as a result of which vision deteriorates. These symptoms are sometimes mild. When a large dose of sarin is inhaled, symptoms of damage occur very quickly, they manifest themselves in the form of severe shortness of breath, nausea and vomiting, spontaneous discharge, severe headache, loss of consciousness and convulsions leading to death.

Sarin, being in a liquid or vapor state, can penetrate into the body and through the skin. In this case, the nature of its damaging effect will be the same as when entering through the respiratory system. However, damage to the body when sarin enters through the skin will occur somewhat more slowly. It takes a few drops of sarin or very high concentrations of its vapor to infect the body through the skin.

It should be noted that when exposed both through the skin and through the respiratory tract, sarin has a cumulative effect, that is, it tends to accumulate in the body.

Sarin (GS) is a colorless or yellowish volatile liquid, practically odorless, and does not freeze in winter. Miscible with water and organic solvents in any ratio, soluble in fats. Resistant to water, which causes contamination of stagnant bodies of water long time up to 2 months When it comes into contact with human skin, uniforms, shoes and other porous materials, it is quickly absorbed into them.

Sarin is used to destroy manpower by contaminating the ground layer of air through short fire raids by artillery, missile strikes and tactical aircraft. The main combat state is steam. Sarin vapor can spread downwind under average weather conditions. up to 20 km from the place of application. Durability of sarin (in funnels): in summer - several hours, in winter - up to 2 days.

When units operate military equipment in an atmosphere contaminated with sarin, gas masks and a combined arms comprehensive protective kit are used for protection. When operating in contaminated areas on foot, additionally wear protective stockings.

When staying for a long time in areas with high levels of sarin vapor, it is necessary to use a gas mask and a general protective kit in the form of overalls. Protection against sarin is also ensured by the use of sealed equipment and shelters equipped with filter-ventilation units. Sarin vapor can be absorbed by uniforms and, after leaving the contaminated atmosphere, evaporate, contaminating the air. Therefore, gas masks are removed only after special processing uniforms, equipment and air pollution control.

The first signs of sarin damage are observed at concentrations of about 0.0005 mg/l after a minute (constriction of the pupils of the eyes, difficulty breathing). The lethal concentration in the air is 0.07 mg/l. with exposure 1 min. The lethal concentration for resorption through the skin is 0.12 mg/l.

Exist antidotes, for example atropine.

Protection against sarin - gas mask and protective clothing.

Clinical picture

The first signs of exposure to sarin (and other nerve agents) on a person are nasal discharge, chest congestion and constriction of the pupils. Soon after this, the victim has difficulty breathing, nausea and increased salivation. Then the victim completely loses control over body functions, vomits, and involuntary urination and defecation occur. This phase is accompanied by convulsions. Ultimately, the victim falls into a comatose state and suffocates in a fit of convulsive spasms followed by cardiac arrest.

Short- and long-term symptoms experienced by the victim include:

Prevention