Home Analyzes The route of penetration of mustard gas and lewisite into the body. Antidote treatment of lewisite lesions. Complications and consequences

The route of penetration of mustard gas and lewisite into the body. Antidote treatment of lewisite lesions. Complications and consequences

Blistering agents include poisons, characteristic feature the action of which is their ability to cause local inflammatory-necrotic changes in the skin and mucous membranes, while exerting a pronounced resorptive effect. These include representatives of various chemical compounds: distilled mustard gas, nitrogen mustard gas (trichlorotriethylamine), oxygen mustard gas, lewisite, dioxin etc.. The standard chemical agents of the US Army are distilled mustard gas, which is chemically dichlorodiethyl sulfide.

Sulfur mustard has been known since the beginning of the 19th century, but was obtained as a chemically pure substance and was studied in detail in 1886 in Germany in the laboratory of W. Meyer together with Academician N.D. Zelinsky. By the way, during the study, dichlorodiethyl sulfide got on N.D.’s hands and feet. Zelinsky and caused their defeat, as a result of which the experimenter was unable to complete the development of his method for the synthesis of this compound and the work was completed by W. Meyer.

Mustard gas was first used as a chemical agent by the German army against British troops on July 12-13, 1917 near the Belgian city of Ypres. Despite the presence of good gas masks, the British lost 6,000 people in the first battle, and there were repeated uses against French troops. At the same time, due to the versatility of mustard gas, protection against it was very difficult.

Then in 1936 Italy used mustard gas against Abyssinia, and in 1943 Japan used mustard gas in China.

In 1935, an American publication appeared in print about the synthesis of trichlorotriethylamine, which carries all the toxic properties of mustard gas. On this basis, a group of nitrogen mustards was created. They were not used as agents, but gave impetus to the development of antitumor drugs.

Lewisite (an arsenic derivative) was synthesized in 1917 by the American chemist Lewis and the German chemist Wieland. Arsenic compounds are widely used to control agricultural pests (arsenic anhydride, Parisian green, etc.) for the treatment of spirochetosis (novarsenol, miarsenol, osarsol), and some have been used as chemical agents (diphenylchlorarsine, adamsite, etc.)

Tens and hundreds of tons of Zaikov’s mixture are stored at special substance storage bases as a backup BW. This agent consists of 50% dichlorodiethyl sulfide and a similar amount of chlorovinyldichloroarsine. Zaikov's mixture was not used during combat operations. The recipe was tested on laboratory animals and has toxic properties inherent in both mustard gases and lewisite.

In 1961-1969. The United States used military herbicides in South Vietnam. More than 40% of the jungle and arable land (15.5 thousand km²) was processed to the level of saturation with the so-called orange, blue and white formulations. Agent orange contained dioxin in concentrations ranging from 0.1 to 2.4%. Being the most toxic of all known TCAs, dioxin has blister and mutagenic properties. The 44,388 tonnes of orange formulation used in Vietnam contained 110kg of dioxin, creating a contamination density of 70mg per hectare. This was enough to affect approximately 2 million Vietnamese, the consequences of which are mainly associated with dioxin.

After Vietnam, Laos, and Kampuchea, the American company Dow Chemical continued its barbaric experiments with dioxin in South Africa and Brazil. As a result of this, only in the Brazilian state of Pará in 1981-1984. 7,000 people died.

1. General characteristics of areas affected by mustard gases, hazardous chemicals with alkylating properties, and sanitary losses in them.

S‑(CH2‑CH2‑Cl)2 - sulfur or distilled mustard gas (dichlorodiethyl sulfide), boiling point = 217.0°C, melting point = 14.0°C. Solubility in oil 38.0; in water - 0.08; volatility =0.6 mg/l. Inhalation toxicity LCt=4.5 mg/min/l; with resorption Ld=50‑70 mg/kg.

Distilled mustard gas is a chemically pure dichlorodiethyl sulfide, a colorless oily liquid. The volatility is insignificant, but already 3 minutes after inhaling mustard vapors under conditions of maximum saturation, a fatal toxodose penetrates the body. It has the smell of mustard or garlic (contains 17-18% sulfur). Liquid mustard gas dissolves poorly in water and sinks to the bottom of the reservoir (specific gravity = 1.3), but a film remains on the surface of the water. Good solubility in fats ensures high permeability through the skin. Mustard gas vapor is 5.5 times heavier than air. Mixtures of mustard gas with dichloroethane, sarin, and soman freeze at temperatures below -20°C, so they can be used in winter.

The chemical properties of mustard gas are due to the presence in its molecule of divalent unsaturated sulfur, which can be oxidized to four and hexavalent and two halide alkyls. The use of microsomal oxidation inducers such as benzonal in the toxicogenic phase of mustard poisoning activates sulfur to hexavalent, which increases its toxicity by 50-60%.

To degas mustard gas, dichloramine, DTS-HA, and hexachlormelamine are used - chlorination deprives mustard gas of its toxic properties. For PSO, polydegassing liquid IPP-8, 10, 11 and 10% aqueous-alcohol solutions of chloramine are used.

US Army ammunition containing distilled mustard gas includes artillery shells, mines, aircraft bombs and trench-type landmines.

The advancing SME can be hit by two enemy mustard gas mines, which will create a hotbed with an area of 60 hectares, the depth of spread of contaminated air reaching 5-7 km. Mustard gas vapor persists for up to 18 hours at 20°C, in winter - for many days. Losses due to sudden use in companies reach 60% of personnel.

Rear targets can be subject to artillery raids with mustard gas shells, causing outbreaks of up to 20 hectares, and sanitary losses equal to 45-50% of personnel.

Taking into account the physico-chemical and toxic properties of mustard gas and the long-developing clinical picture of lesions, we can conclude that during the combat use of mustard gas, a focus of a persistent, slow-acting agent is formed. The presence of a latent period has a beneficial effect on the time it takes to provide medical care.

However, the high resistance of mustard gas (18 hours in summer, several days in winter) forces personnel to wear protective equipment for a long time, which leads to exhaustion and loss of combat effectiveness and ability to work. Medical service monitoring of the thermal regime is required, as thermal overload is possible. Sanitary losses will be formed depending on the duration of the latent period.

During the First World War, the structure of those affected by mustard gas was distributed as follows: those affected with loss of combat capability for up to 4 weeks - 75%, up to 6 weeks - 15%, up to 4 months or more - 10%. In modern conditions, the proportion of moderate and severe lesions is expected to increase: severe form - 30%, moderate - 40%, mild - 30%. Cutaneous form lesions will prevail over inhalation.

Nitrogen mustard(trichlorotriethylamine) causes the same clinical lesions, but has a number of features. Irritating to the eyes, respiratory system and, to a lesser extent, skin. It is characterized by a pronounced general toxic effect, characterized by a violent convulsive syndrome with respiratory and circulatory disorders, cachexia, and sudden hematological changes (leukopenia with lymphopenia). Skin lesions are less pronounced, dermatitis occurs with folliculitis and papular erythema and small blisters. Vapors have no effect on the skin. The course of ulcers is smoother (2-3 weeks). Damage to the respiratory system and eyes is characterized by a milder course and rapid healing. The use of microsomal oxidation inducers such as benzonal during the toxicogenic period of poisoning accelerates the hydrolysis of trichlorotriethylamine to low-toxic triethylamine. In this case, the toxicity of the agent will decrease to 70%.

To the group dioxins These include polychlorodibenzodioxins (PCDDs) and polychlorodibenzofurans (PCDFs), which have 75 isomers, the toxicity of which varies depending on the number of chlorine atoms and their position in the carbon framework of the molecule. The most toxic are 2,3,7,8 PCDD. These compounds are highly stable: they are not susceptible to hydrolysis, oxidation, are resistant to high temperatures, acids, alkalis, are non-flammable, practically insoluble in water, long time are fixed in the soil, do not evaporate from the soil surface, its half-life is more than 10 years. The toxicity of the substance is known to persist for at least five half-lives. The source of infection is persistent and has a very slow action.

2. The mechanism of occurrence and development of mustard gas lesions.

Poisoning clinic.

The mechanism of action and pathogenesis of mustard gas lesions is very complex and despite the efforts of scientists, especially in the period from 1918 to 1940, when mustard gas was considered the “king of gases”, and even in recent years, it has not been fully disclosed, the pathogenesis has not been fully studied.

The main pathogenetic features of the action of mustard gas on the body are the following: :

1. Absence pain at the moment of tissue contact with the agent. Only at very high concentrations of the poison at the time of inhalation contact may the victim feel the urge to sneeze. The presence of a latent period after the cessation of the action of the poison or its absorption.

2. The occurrence of inflammation, necrosis in any tissue affected by mustard gas.

3. Extreme sluggishness of tissue regeneration and recovery processes, development of cachexia, depression.

4. A sharp weakening of the body’s protective immunological reactions, the addition of a secondary infection.

5. Activation of peroxide processes in tissues, damage to proteins - the so-called “radiomimetic” effect, i.e. resembling damage from ionizing radiation.

6. Mutagenic and teratogenic effects in the long term.

7. Sensitization of the body to repeated contact with poison.

Most pronounced defeat tissues are noted at the place of their primary contact with mustard gas; when exposed to poison in large quantities, tissue necrosis can develop quite quickly. Along with this, with all forms of poison application, its pronounced resorptive effect is observed, manifested in damage to the nervous system (dystrophy), the hematopoietic system, immune system. A feature of dystrophies is the delayed restoration of the normal state of tissue elements.

Mechanism of action Mustard gas, based on modern data and studied features of pathogenesis, is as follows:

1. Due to its high solubility in lipids, mustard gas penetrates into cells within 20-30 minutes. Possessing high activity, intracellularly it quickly undergoes hydrolytic dissociation, i.e. is neutralized, but this does not prevent the development of body damage and tissue necrosis at the site of contact with the poison after a latent period (10 minutes after penetration into the blood, 90% of the mustard gas disappears from the bloodstream). During the process of hydrolytic dissociation, hydrochloric acid is formed at the point of contact, shifting the pH to the acidic side, and primary damage to cellular structures develops.

2. As a result of the rapid breakdown of mustard gas, intermediate toxic compounds are formed. In the metabolism of sulfur mustard a sulfonium cation is formed, nitrogenous - ammonium cation. Onium compounds cause ionization of water and lipids, which, when reacting with the thiol groups of proteins, disrupt their structure. The so-called “radiomimetic” effect develops:

a) lymphocytes and leukocytes responsible for the body’s immune defense are among the first to be damaged;

b) a polyenzymatic effect develops; about 40 different enzymes are damaged, including deamine oxidase, which inactivates histamine. In this case, histamine accumulates in high concentrations and activates inflammation processes. In general, those tissues and organs in which increased cell proliferation occurs are most affected - red bone marrow, intestinal mucosa, cells of the endocrine glands.

3. Acting as a whole molecule and through onium compounds, mustard interacts with the sulfhydryl groups of amino acids that make up DNA and RNA. The amino acid guanine is most sensitive to mustard gas. As a result of the interaction of the poison with guanine, alkylation of the latter occurs. In this case, damage develops nucleic acids by the type of rupture and cross-linking of their molecules.

4. By blocking hexokinase, mustard gas selectively acts on anaerobic glycolysis, which leads to disruption of primary glucose phosphorylation, and trophic processes in tissues are inhibited.

5. When mustard gases are destroyed in the liver, haptens are formed, leading to sensitization of the body.

As we said earlier, the induction of microsomal oxidation of mustard gases leads to a significant increase in the toxicity of sulfur mustard and a decrease in the toxic properties of nitrogen mustard.

3. Mustard poisoning clinic.

Depending on the route of penetration, mustard gas affects the skin, respiratory organs, organs of vision, digestion and causes general intoxication.

During combat use, damage to the eyes is most common, somewhat less common to the respiratory system, and only in third place in frequency are skin lesions. The nature of the poison determines a number of general clinical patterns: “silent” contact, the presence of a latent period, a tendency to infection, sluggishness of reparative processes, sensitization to repeated exposure.

Skin lesions most typically occur when affected by droplet-liquid mustard gas; vapors cause milder lesions. There are three successive stages: erythematous, bullous, ulcerative-necrotic. Depending on the dose, the process may be limited to any of the stages. Therefore, mild skin lesions are characterized by the development of erythematous dermatitis, moderate severity - erythematous-bullous dermatitis, severe severity - ulcerative necrotic dermatitis.

Mild forms of damage caused by vapor mustard (C=0.002 mg/l and exposure 3 hours) and liquid (density 0.01 mg/cm²). After a latent period (about 12 hours), erythema appears, on days 4-5 it gives way to pigmentation followed by peeling of the skin, on days 7-10 all phenomena disappear and pronounced pigmentation remains in place of the erythema for a long time.

Moderate forms of damage mustard gas at a concentration of vapor mustard gas of 0.15 mg/l and liquid mustard gas at a contamination density of 0.1 mg/cm². The latent period lasts 2-4 hours. Then, against the background of mustard erythema, after 8-12 hours, small blisters appear - “pearl necklaces”, increasing in size and subsiding after the 4th day, exposing the erosive surface, which epithelializes after 2-3 weeks.

With deep damage of the skin, after damage to the bladder membrane, an ulcerative surface with undermined edges is exposed. A secondary infection occurs, resulting in the development of necrotizing ulcerative dermatitis, which heals slowly (3-4 months) resulting in a white scar surrounded by a pigmentation zone.

Features of facial skin lesions are: faster healing without pronounced scars; scrotum - continuous erosive surface and reflex anuria, slow healing; feet and lower third of legs - long-term recurrent course, “trophic ulcers”.

The eyes are most sensitive to mustard gas; their damage occurs when exposed to vapors at a concentration of 0.005 mg/l. After a latent period of 0.5-3 hours, a burning sensation and a feeling of sand in the eyes, photophobia, lacrimation and swelling of the mucous membrane of the eyes appear - i.e. a picture of uncomplicated conjunctivitis (mild degree of damage), which disappears without a trace after 1-2 weeks. However, in the acute stage, combat effectiveness is lost.

With more high concentration vapors, moderate damage occurs (complicated conjunctivitis). The symptoms of conjunctivitis are more pronounced, they spread to the skin of the eyelids, conjunctival hyperemia, and a swollen ridge around the cornea (chemosis). The duration of the course is 20‑30 days. The outcome is favorable.

Severe eye damage occurs when exposed to droplet-liquid mustard gas.

After a short latent period, conjunctivitis develops; on the 2nd day, excoriation of the cornea is noted against the background of its opacification, resulting in necrosis and rejection of the cornea, then ulcers and opacification. A picture of keratoconjunctivitis develops. A secondary infection occurs, corneal perforation is possible, pus penetrates into the anterior chamber of the eye (hypopyon), and iridocyclitis occurs. When the infection spreads into the deep tissues of the eye, panophthalmitis and death of the eye occurs. There is always deformation of the eyelids.

Long-term consequences: photophobia, corneal clouding. Severe lesions occur in 10%.

When inhaling mustard vapors, damage occurs respiratory tract varying degrees severity (mild, moderate and severe).

For mild lesions after a latent period of more than 12 hours, signs of respiratory tract damage appear in the form of rhinitis, pharyngitis, laryngitis - i.e. the process is limited to the picture of acute nasopharyngolaryngitis, which completely disappears after 1.5 weeks.

Moderate damage severity is characterized by an earlier appearance (after 6 hours) of symptoms of pharyngolaryngitis; on the 2nd day the clinical picture of mustard gas tracheobronchitis develops, which is characterized by a protracted course and is necrotic (pseudomembranous in nature). Dead mucous membrane of the trachea and bronchi can be rejected and cause atelectasis, pneumonia, and suppurative processes. Long-term consequences: chronic bronchitis.

In severe cases lesions appear within 2 hours and reach significant severity on the 2nd day; symptoms of inflammation of the respiratory tract. On the 3rd day, mustard gas pneumonia develops, characterized by severe symptoms of resorption (fever, respiratory failure, neutrophilic leukocytosis with lymphopenia and aneosinophilia). Pneumonia occurs due to the toxic effect of poison on the respiratory tract, the addition of an infection against the background of a decrease in immunobiological reactivity and a decrease in the phagocytic activity of leukocytes. Possible bronchogenic spread of infection. The lesion is of a descending nature: on the 1st day - nasopharyngolaryngitis, on the 2nd day - tracheobronchitis, on the 3rd day - pneumonia. The course of pneumonia is protracted. Complications: lung abscess, cachexia, lung atelectasis. Long-term consequences: pulmonary emphysema, chronic asthmatic bronchitis, bronchiectasis, diffuse pulmonary cirrhosis.

With inhalation of very high concentrations or aspiration of droplet-liquid mustard gas, necrotizing pneumonia develops, the signs of which appear on the first day: hemoptysis, respiratory failure, leukopenia. The condition is extremely serious, the prognosis is poor. Complications: gangrene of the lung. Death occurs from resorption.

Penetration of mustard gas inside along with food and water leads to the development of mustard gas stomatitis, phlegmonous-necrotic esophagitis, and hemorrhagic gastritis. Morphological changes in the intestines are not characteristic, since mustard gas is fixed in the wall of the stomach, from there it is absorbed into the blood.

The general toxic effect is manifested in an increase in body temperature, the appearance of adynamia, nausea, vomiting, diarrhea, bradycardia - tachycardia, acute cardiovascular failure, cachexia, phase shifts in the blood picture, toxic nephropathy.

Depending on the severity of the lesion, there are three main forms of general resorptive action of mustard gas.

The most severe form is shock, it is caused by the pronounced effect on the body of significant doses of poison and its metabolic products, peroxide, hydroperoxide and other toxins of protein and non-protein nature. Death at this form develops in the first 18 hours - 3 days.

The second form - leukopenic or gastrointestinal, develops on days 6-9. In the blood, neutrophilic leukocytosis with a shift to the left (neutrophilic phase) is noted at the beginning, then leukopenia with lympho- and neutropenia with relative monocytosis.

In more severe cases, a secondary infection occurs and general weakness, fever, gastrointestinal disorders. Death may occur within 1-2 weeks.

With a favorable course of the disease, recovery begins with an increase in the number of lymphocytes - the lymphocytic stage.

After 24–40 days, with a relatively satisfactory course of the disease, a cachectic form develops. Mortality from cachexia, anemia, secondary infection

Overall in clinical picture general resorptive action of mustard gas is isolated following periods: latent, toxemia, period of leukopenia with damage to the gastrointestinal tract, period of cachexia and anemia.

4. Prevention and provision of medical care for mustard gas lesions.

In contrast to FOV, when damage to all systems appears in the first minutes, damage to mustard gas can only appear hours later. The process of admission of those affected to EME will be extended over time depending on the severity. Symptoms of poisoning, in the first hours, will allow the affected to leave the source themselves. Approximately, only 30% will not be able to leave the infected area on their own.

Prevention of mustard gas lesions.

Since mustard gases enter the body through the respiratory system, mucous membranes and skin, the use of gas masks and protective suits is a mandatory preventive measure.

In order to remove mustard gases from the skin, it is necessary to immediately carry out a partial sanitization(ChSO) using liquid IPP‑8,10,11. PPI liquid neutralizes drops of mustard gas located on the surface of the skin, as well as in the superficial layers of the epidermis. The liquid has antiseptic effect, preventing infection of the affected area. To treat skin affected by mustard gas, a 10-15% aqueous-alcohol solution of chloramine is also used, and nitrogen mustard is degassed with a 5% solution of potassium permanganate in 5% acetic acid. If the agent is ingested with contaminated water or food, it is necessary to rinse the stomach copiously with water or a solution of 0.02% potassium permanganate.

General principles for treating lesions with mustard gas:

Avoid the haphazard use of various drugs, especially those acting on the same principle, since the effect of drugs in case of mustard gas damage does not appear immediately.

It is necessary to take into account that the process of damage by mustard gas proceeds through a number of sequential periods of general resorptive action (latent, toxemia, leukopenia, cachexia) and stages of skin damage (exudation, dehydration and rejection of necrotic masses, regeneration), therefore various therapeutic agents should be used in strict accordance with the state of the affected person at that moment. Compliance with this principle is also necessary when treating various forms general resorptive action and skin lesions.

Treatment for the resorptive effect of mustard gas as in the same forms and periods of the course of the disease, one etiopathogenetic factor is taken into account, and in general it is of the same type. The difference is that, for example, in the shock, the most severe form, intoxication during the period of toxemia will be much more pronounced than in the cachectic form, and therefore general detoxification therapy in the first case should be more intense.

During the period of toxemia, intensive detoxification therapy is carried out, aimed at neutralizing and removing from the body both exotoxins and toxins of endogenous origin: hemodez (400 ml), 4% sodium bicarbonate solution (400 ml), 40% glucose solution (40 ml) with 5% ascorbic acid (10 mg) and insulin (8 U); furosemide (80 mg). In case of damage, especially by nitrogen mustard, intravenous administration of 30% sodium thiosulfate solution (20-30 ml) is indicated. Treatment with antihistamines is carried out.

On the eve of development period of leukopenia In order to prevent infectious complications, bactericidal antibiotics with a wide spectrum of action are used (oxacillin, ampicillin 2 g per day). If a secondary infection occurs, the doses of antibiotics are increased (oxacillin up to 8-12 g per day, ampicillin up to 3-6 g per day).

When severe gastrointestinal disorders develop in patients during this period, due to damage to the intestinal epithelium, poorly absorbable antibiotics such as kanamycin (3-4 g per day) are prescribed to sterilize the intestines.

In order to stimulate hematopoiesis and leukopoiesis, improve the coordinated functioning of the immune system and increase the body's immune response, transfusions of the nuclear fraction are carried out bone marrow, vitamin B 12, ATP, ascorbic and folic acids, sodium nucleic acid are introduced.

Of the new generation drugs to stimulate leuko-thrombopoiesis and accelerate bone marrow proliferation, 15 ml of 0.5% deoxynate solution is administered intramuscularly or subcutaneously.

To stimulate cellular immunity and accelerate phagocytosis, Thymalin is prescribed deep intramuscularly at 0.01-0.03 g per day for 20 days; levamisole (Decaris) - orally 0.15 g per day every other day for a week.

During the period of cachexia and anemia washed and thawed erythrocytes, erythrocyte mass 250-300 ml are administered 2-3 times a week.

To stimulate metabolism - diucifon 5% solution, 4-5 ml once a day or orally, 0.2 g 3 times a day, in two or three five-day cycles.

In order to stimulate reparative processes, etadene 1% solution is administered intramuscularly, 10 ml 2 times a day.

To correct malnutrition, parenteral administration of protein hydrolysates (aminopeptide, aminokrovin, hydrolysine, etc.) and balanced solutions of amino acids (polyamine, amexin) are prescribed. The drugs are administered 400-800 ml daily.

Throughout the disease, for the purpose of symptomatic therapy, various drugs are used according to indications - cardiac glycosides, anticonvulsants, pressor amines, hormones, therapy for pulmonary and cerebral edema, and antibiotic therapy.

The most common and effective treatment methods for mustard gas skin lesions include:

In the exudation stage - application of wet-dry dressings with a 2% chloramine solution (in the first 2-3 days);

At the stage of erosive-ulcerative course and dehydration, antibiotics are prescribed. At the bladder stage, the bladder is emptied with a sterile needle, and the surface of the bladder is treated with a disinfectant solution. Then the method of creating a coagulation film on the affected surface is applied locally using a 5% aqueous solution of potassium permanganate or a 0.5% solution of silver nitrate, a 1-2% solution of collargol, a 5% solution of tannin. The film protects the affected surface from the penetration of secondary infections and limits the absorption of toxic products.

To prevent suppuration of lesions, especially when they are infected and wet necrosis, putrefactive melting of tissues, application of bandages with a 1% solution of iodopyrone is indicated.

IN regeneration stages To stimulate reparative processes, an aerosol of lyoxazole is applied to the affected surfaces once a day. At the same time, blood supply to the tissues improves. Physiotherapy procedures are carried out: irradiation with a quartz lamp, Sollux, dry air baths.

Treatment of extensive lesions must be carried out under a protective sterile frame.

5. Providing medical care in areas of chemical contamination with mustard gas and at EME.

When conducting medical triage of those affected by mustard gases, it is necessary to take into account the following factors, which determine a number of features of its organization. Firstly, those affected will be admitted to EME at different times, which is due to the duration of the latent period. Secondly, those affected in a state of shock, collapse, convulsions, with severe irritation of the eyes and respiratory tract will require urgent measures according to vital indications. Thirdly, some of those affected will require partial or complete special treatment. Fourthly, those who are mildly affected, whose symptoms are completely eliminated after receiving qualified medical care and are in good health, can be returned to duty. Fifthly, treatment of those affected will be carried out in multidisciplinary hospitals of the Great Britain, based on the leading lesion of a particular system.

First medical care includes putting on a gas mask after preliminary treatment of the eyes with water from a flask and the face with the contents of the PPI, partial sanitary treatment, and inducing vomiting if the agent enters the stomach (outside the affected area). First of all, those affected with severe symptoms of damage to the eyes and respiratory tract are evacuated, having previously prescribed ficillin inhalation.

First aid(OPM, VG) includes repeated PSO using PPI. If the eyes are affected, wash them with a 2% soda solution or 0.02% potassium permanganate, and apply synthomycin ointment to the eyes. If the respiratory system is affected, wash the oral cavity and nasopharynx with 2% soda solution. If the chemical agent gets into the stomach, the stomach is washed with a sorbent inside. According to indications, oxygen inhalation and administration of cardiovascular drugs are carried out. First of all, in providing first aid Patients with keratoconjunctivitis, tracheobronchitis, erythematous-bullous dermatitis, and vomiting will need it.

First medical aid (FMA) includes PSO, applying a wet bandage with a 1-2% solution of monochloramine or anti-burn emulsion to the affected areas of the skin, washing the eyes with a solution of monochloramine (0.25-0.5%) or soda (2%), placing under eyelids 5% syntomycin ointment, tube gastric lavage with the administration of sorbents, according to indications, administration of oxygen and cardiovascular drugs, administration of antibiotics,

alkaline inhalations, application safety glasses and a visor. The triage is based on the principle of the need for an emergency response with the replacement of uniforms for those seriously injured, and the need for first medical aid.

Subsequently, the affected people are evacuated to the VG, where they undergo complete sanitary treatment and receive qualified medical care. Patients with local lesions remain in the recovery group or return to duty. Those slightly affected by vapor mustard gas with symptoms of nasopharyngolaryngitis and conjunctivitis are referred to VPGLR. Patients with erythematous-bullous and ulcerative-necrotic forms are treated in the VPHG and the dermatovenerological hospital, severe eye lesions in the VPHG for those wounded in the head and neck, inhalation and oral lesions - in the VPTG.

6. Toxicological characteristics of lewisite.

Lewisite(chlorovinyldichlorarsine) - oily liquid with a specific gravity of 1.9, chemically pure - colorless, technical - dark brown with a purple tint, has the smell of geranium. Boiling point - 190°C, vapor density 7.2, volatility 4.4 mg/l. Solubility in water is low - 0.5 g/l, in organic solvents - high.

The chemical properties of lewisite are determined by the easy mobility of two chlorine atoms with arsenic, which can be replaced by other atoms and radicals, as well as the possibility of oxidizing trivalent arsenic to pentavalent arsenic.

Hydrolysis of lewisite occurs with the replacement of chlorine atoms. The resulting lewisite oxide is not inferior to lewisite in toxicity.

Oxidation of lewisite is caused by many substances (hydrogen peroxide, iodine, monochloramine), so its degassing on human skin can be done with tincture of iodine.

Alkalis also react well with lewisite, which is used in its degassing.

The interaction of lewisite with sulfhydryl compounds with the formation of non-toxic products made it possible to create highly effective antidotes - BAL, unithiol.

In terms of toxicity, lewisite is superior to mustard gas: the average incapacitating concentration (Ict50) is 0.03 mg/l/min, the average lethal dose (LD50) is 2.5 mg/kg.

Lewisite penetrates the body quickly in various ways, even through intact skin within 5 minutes. There is no hidden period.

The lesions created when using lewisite are persistent and quick-acting.

Mechanism of action of lewisite is realized due to chlorine atoms and trivalent arsenic. The resorptive toxicity of lewisite is generally ensured by the action of arsenic.

When absorbed, lewisite hydrolyzes quite quickly in the tissues, and a very stable metabolite is formed - vinyl chloride and hydrochloric acid. The latter leads to a shift in pH to the acidic side, resulting in tissue necrosis at the site of application of the poison.

Lewisite itself and its oxide interact with the sulfhydryl groups of enzymes and bind them due to arsenic. Arsines interact with more than a hundred different enzymes containing thio groups, and their activity is impaired. As a result, vascular permeability increases, capillary paresis and tissue edema, including pulmonary edema, develop.

When arsines interact with monothiol enzymes (cholinesterase, lipase, MAO, glutathione, etc.), the body can independently restore the activity of enzyme systems. In the case of interaction of arsines with the dithiol enzyme - lipoic acid, which is a component of the pyruvate oxidase system, a powerful binding of the enzyme occurs, as a result of which oxidation in mitochondria is disrupted, trophic and energy processes in tissues are disrupted, inflammatory and necrotic processes are activated not only at the site of contact with the poison, but also in other organs and tissues.

Inhibition of pyruvate in the kidney, the main organ that secretes trivalent arsenic, explains the nephrotoxic effect of the poison.

Lewisite damage in the vapor state appears almost immediately. There is a sharp irritation of the mucous membranes of the eyes and respiratory tract - lacrimation, runny nose, sneezing, sore throat, profuse drooling, the clinic resembles the effect of irritating agents. With a large toxic dose of poison, chest pain, anxiety, nausea, vomiting, depression, and adynamia occur. If the victim does not die as a result of developing collapse, then after a few hours toxic pulmonary edema and fluid accumulation in the cavities develop (ascites, hydrothorax, swelling of the skin and mucous membranes). Intoxication in general is similar to the defeat of suffocating agents. Blood thickening, respiratory failure and hypotension lead to oxygen starvation in the body.

If death does not occur and the body tolerates acute stage poisoning, necrotizing bronchopneumonia develops with extensive tissue destruction. Death can occur from an abscess or gangrene of the lungs during symptoms of acute cardiovascular failure.

When poison enters the stomach with contaminated water or food, vomiting immediately occurs, but part of the agent has time to act locally and be absorbed. Extensive lesions of the esophagus and stomach develop, along with a pronounced resorptive effect of the poison. If significant doses of lewisite enter the stomach, death may occur within a few hours as a result of collapse or pulmonary edema.

When lewisite acts on the skin, pain and burning immediately develop at the site of contact with the poison; after 30 minutes, bright red erythema appears, quickly spreading over a large surface, and tissue swelling is pronounced. After 8-12 hours, large single bubbles form. Maximum inflammation develops by the end of the second day. The blisters break open and a bright red ulcer forms with multiple hemorrhages at the bottom.

Healing, unlike mustard gas lesions, occurs relatively quickly within 2-3 weeks. There is no pigmentation, and secondary infection is rare.

When affected by lewisite for a year or more, most patients experience clinical changes in their health status in the form of: vegetative-vascular dystonia, chronic gastroduodenitis, chronic erythema of the affected skin areas, etc.

Treatment of those affected by lewisite, in contrast to those affected by mustard gas, is more effective due to the possibility of using antidotes. Sulfur-containing BAL antidotes (“British anti-lewisite” - dimercaptopropanol) and domestic unithiol (sodium dimercaptopropane sulfate) interact with both free lewisite and its oxide, and with the poison associated with the enzyme, which restores the activity of the latter. Unithiol is more effective than BAL, because it is highly soluble in water and can, therefore, be administered intravenously in severe cases. BAL is oil-based and is not administered intravenously. The therapeutic breadth of unithiol is significantly higher than that of BAL, 1:20 and 1:4, respectively.

The arsine-unithiol complex is low-toxic, highly soluble in water and easily excreted from the body in urine.

Unithiol is available as a 5% solution in 5 ml ampoules. The drug is administered subcutaneously or intramuscularly according to the following scheme: on day 1 - 3-4 times with an interval of 6-8 hours, on days 2 - 2-3 times, on days 3-5 1-2 times, if necessary on 6 On day 10, the drug is administered once a day.

To treat eye and skin lesions, dithiones are used in the form of ointments - 30% unithiol ointment with lanolin.

Otherwise, when affected by lewisite, methods typical for treating lesions with mustard gas are used.

7. Toxicological characteristics of dioxin.

Clinic of dioxin damage.

In the process of studying the effect of dioxins on the body, their special insidiousness was revealed, which manifests itself even in acute poisoning; symptoms of intoxication develop weeks and months after exposure to the poison.

Clinical manifestations of poisoning are marked by the development of pronounced immunodeficiency, and therefore very diverse and nonspecific syndromes are identified, which significantly complicates diagnosis in the event of mass destruction.

The toxic syndrome that develops with TCDD poisoning includes hyperkeratosis, dermatitis, hair loss, hepatotoxic effect (enlargement, necrosis of hepatocytes, pain), hypoplasia of lymphocytic tissue, edema (hydropericarditis, ascites), sudden changes in metabolism with activation of enzyme systems.

Characteristic in long term the development of teratogenic, carcinogenic effects, cytogenetic and cytotoxic effects, which were studied in people exposed to dioxin by chromosomal analysis of peripheral blood lymphocytes.

2, 3, 7, 8-tetrachlorodibenzo-paradioxin is a colorless, crystalline powder, odorless, insoluble in water (0.001%), limitedly soluble in organic solvents, chemically inert. Has high thermal stability and very resistant to hydrolysis. Melting point 320 - 323 C. The substance has a toxic effect in the form of dust or aerosol, when introduced into the stomach and when applied to the skin. Doses that produce the same effect in in different ways revenues are approximately equal. Sources of pollution environment are by-products pulp and paper industry, waste from the metallurgical industry, exhaust gases from internal combustion engines, herbicides and by-products of their production. Dioxin in the body accumulates in the liver, adipose tissue, thyroid gland and lung tissue . The most low levels dioxin found in the brain and testes. They are excreted from the body very slowly. In soil, the half-life of decomposition is 6 - 12 months.

The mechanism of the toxic effect of dioxin is not fully understood. Histochemically, a complete suppression of the ATPase activity of hepatocytes is revealed, indicating that the “target” of the poison is mainly the plasma membrane of liver cells. Dioxin is a powerful inducer of microsomal enzymes, which sharply increases tissue oxygen demand . Dioxin can become intertwined with DNA in places corresponding to the location of only certain genes. Already Six such “dioxin genes” have been identified. One of them has been studied most closely: the gene corresponding to the enzyme from cytochromes P-450. The duty of this enzyme is to protect cells from toxic effects. However, biochemists did not find any damage in the DNA structure affected by dioxin. It only bends a little, becomes more pliable, more accessible to the influence of other proteins. Hence the assumption that dioxin itself does not cause diseases, but only contributes to them. In particular, dioxin, without a doubt, stimulates the development of cancer, but only in the presence of a carcinogen in the cell and unfavorable environmental conditions: it is not an initiator, but rather a provocateur of tumor growth.

The fact of the teratogenic effect of dioxin has been established. It is known to cause wasting syndrome, manifested by severe hypophagia, a decrease in fat content in the body and changes in intermediate metabolism, and causes a disruption in the production of carbohydrates. However, the mechanisms of these changes are not yet clear.

Once in the human body, dioxin can clinically cause both acute and chronic poisoning. A feature of its toxic effect is the presence of a long latent period and the slow development of signs of intoxication.

For acute poisoning dioxin- a latent period is characteristic, lasting 5-7 days after the poison enters the body. At this time, symptoms of intoxication may appear due to the action of dioxin-related substances: organic solvents, herbicides, etc.

Dioxin - polytropnog poison o action, affects almost all organs and systems. The most frequently expressed symptoms are damage to the skin, liver and nervous system.

Skin manifestations of intoxication are characterized by the development of chloracne, meibomitis, and later cutaneous porphyria.

Chloracne is the only one specific sign dioxin poisoning, but there are individuals who are genetically resistant to the development of chloracne.

Chloracne- acne-like rash localized on the upper eyelids and under the eyes, on the skin of the zygomatic part of the cheeks, behind the ears, on the skin of the nose. May spread to the skin of the armpits and groin area, chest, back, buttocks, thighs, external genitalia. The appearance of chloracne is preceded by swelling and erythema of the skin. The rash is accompanied by itching and is activated by exposure to solar radiation. Infection may occur, leading to the development of pyoderma, superficial follicles, and even abscess formation. Subsequently, rough scars and hyperkeratosis may form.

Meibomyites- an inflammatory process localized in the meibomian glands of the upper eyelids.

Porphyria cutanea tarda characterized by a triad: pigmentation, blisters, hypertrichosis. Pigmentation usually occurs on exposed areas of the skin - on the face, neck, upper chest, back of the hands and is diffuse in nature. Skin color ranges from earthy gray to reddish-bluish, with a bronze tint. The blisters are most often located on the back of the hands and face, ranging in size from a millet grain to a bean. The skin is hypersensitive to mechanical trauma and solar radiation. Hypertrichosis occurs mainly on the face, in the temporomygomatic region, on the back, and around the navel.

The urine of patients with porphyria cutanea tarda is dark, orange-brown in color due to increased excretion of porphyrins, especially uroporphyrin; coproporphyrin is contained, but in much smaller quantities.

Porphyria cutanea tarda is usually accompanied by an enlarged liver and impaired functional state. Liver damage can be expressed to varying degrees: from a short-term increase without pronounced functional disorders, to severe dysfunction and structure, up to necrosis. Due to the inducing effect of dioxin on the biosynthesis of liver enzymes, their content in the blood serum may increase.

During intoxication, changes in fat and carbohydrate metabolism may occur, which are accompanied by triglyceridemia, hypercholesterolemia, and an increase in the content of total lipids in the blood serum.

Pathology of the nervous system often develops - from subclinical neuritis to polyneuropathy and polyneuritis. There may be a decrease in hearing, olfactory and taste sensitivity. Deviations in the mental sphere with the development of asthenic or depressive syndrome may be observed.

Clinical manifestations of the respiratory system can be expressed in the development of bronchitis.

Damage to the gastrointestinal tract is manifested by gastritis and chronic colitis.

In some cases, muscle pain, swelling of the limbs, and the development of bursitis in the area of large joints may be observed.

Hematological changes are not typical for intoxication, but in severe cases anemia and even pancytopenia can develop.

Exposure to lethal doses of dioxin can lead to progressive weight loss and suppression of cellular immunity. IN pathological process the cardiovascular, urinary and endocrine systems are involved.

Mild dioxin damage - characterized by complaints of headache, weakness, lacrimation for several days after exposure to the poison, or no complaints. Objectively - the appearance of chloracne 10-14 days after exposure or later. The prognosis for mild lesions is favorable, complete recovery occurs.

Moderate lesions are characterized by complaints of headache, nausea, vomiting, eye irritation, lacrimation, anorexia, pain in the right hypochondrium, paresthesia. Objectively - the appearance of chloracne of a more severe and widespread nature, liver enlargement, functional signs of toxic hepatitis, subclinical neuritis, polyneuritis. The prognosis with active treatment is relatively favorable, but symptoms of intoxication can persist for a long time, for several years.

Severe lesions - characterized by complaints (except those listed above) about muscle weakness, pain in muscles, joints, depression. Objectively (besides what has already been said) - progressive loss of body weight, hair and eyelash loss, asthenia, signs of toxic hepatitis, pancreatitis, anemia and pancytopenia, respiratory, renal and cardiovascular failure. The prognosis is unfavorable. Death can occur as early as 14–30 days of intoxication.

The course of chronic intoxication is protracted, uneven, and scanty symptoms in the initial period are not yet the basis for a favorable prognosis, since pathological changes can appear after several months or even years.

The severity of clinical symptoms and the predominance of certain pathological syndromes are very diverse and depend on the dose and duration of exposure to the poison, on the individual sensitivity of the body. Provoking factors in the development of certain manifestations of intoxication may be stressful situations or heavy physical activity.

First aid if drugs containing dioxin come into contact with the skin is to remove them with a swab (without rubbing), then rinse the skin with running water and rinse the eyes repeatedly. After washing, drip a few drops of a 2 - 3% solution of novocaine with adrenaline.

If it gets into the stomach, induce vomiting, if possible, immediately rinse the stomach with plenty of water (10 - 15 l), give an adsorbent (activated carbon, kaolin, bentonite, 20.0 - 30.0 per glass of water), then a saline laxative.

If exposed in aerosol form, remove the victim from the infection zone, carry out complete sanitization with a change of clothes and shoes.

Antidote treatments for dioxin poisoning have not been developed. Treatment is carried out using symptomatic and some pathogenetic drugs, syndromic, taking into account the leading symptom complexes.

Prescribe carbolene 1.0 3 - 5 times a day for 15 - 20 days; choleretic agents. If the victim’s condition remains good within 3 to 7 days, he can be discharged from the hospital. Such patients are monitored at the dispensary. It is recommended to avoid physical overload and insolation. Diet with limited fat, fried and spicy foods. Products containing pectin are shown (marmalades, jellies, etc.)

Chloracne requires long-term treatment. Anti-inflammatory drugs, antibiotics and vitamin therapy are prescribed. Ointments based on simpone or T-2 emulsifier are used locally. Ichthyol, tar, naphthalan, boric and salicylic acids or their combinations are introduced into the ointment filler in increasing concentrations. Papulous-pustular elements can be treated 1 - 2% alcohol solutions aniline dyes. For torpid abscess and phlegmonous forms of chloracne, 0.05% chlortrypsin or 1% mefenam creams are indicated. It is better to administer them using iontophoresis 30 - 40 minutes after treating the lesions with a 40 - 50% dimexide solution. Prescribing steroid hormones and antibiotics in ointments should be avoided to avoid possible skin sensitization.

To treat moderate and severe forms of chloracne, antibiotic therapy (tetracycline group) is used. The course of treatment can be continued from 5 to 14 days to 6 months. Rondomycin and rifampicin are also effective. It is recommended to use vitamin A derivatives for 30 days. Other vitamins are prescribed: B1, B6, B12, C, P, E. For phlegmonous and abscessive forms of rash, the use of indomethacin 25 mg 3 times a day after meals has a certain effect.

To activate the body's defenses, plasma, blood serum, and gamma globulin are used. For the treatment of fresh keloid scars - vitreous, aloe extract.

For symptoms of hyperkeratosis and the presence of pigmented areas of the skin, salicylic, benzoic, lactic acids, and resorcinol are used.

Porphyria cutanea tarda is difficult to treat. Currently, the most effective use of quinoline drugs is in small doses: delagil (hingamin) according to the regimen of 0.125 (1/2 tablet) 2 times a day for 2 weeks, then 0.125 every other day for 2 weeks. If well tolerated, further doses of 0.125 are prescribed once a day for a month, then 0.125 2 times a day for a month, followed by 0.25 2 times a day for three months. Delagil is contraindicated in case of severe heart damage, diffuse kidney damage and severe impairment of liver function. A good effect is achieved by combining delagil with riboxin; the latter is prescribed 0.2 3 - 4 times a day for 2 - 3 months.

Complexons can be used to remove porphyrins from the body, but they are less effective than delagil. You can resort to bloodletting: every 10 days, 500 ml of blood is removed from the patient. At severe forms Treatment of porphyria with hemosorption and hemodialysis is indicated.

Basic therapy for liver damage should be aimed at improving metabolic processes in the liver, stimulating hepatocyte regeneration. For this purpose, cocarboxylase, amino acids and protein hydrolysate are used. In addition to the above vitamins, they also use folic acid 5 mg 3 times a day for a month.

IN acute period in case of severe intoxication, detoxification measures are indicated: intravenous administration of alvesin, hemodez, serum albumin, glucose; with the development of acute liver failure syndrome, glucocorticosteroids are prescribed high doses, protease inhibitors (contrical, epsilon-aminocaproic acid), colloidal and crystalloid solutions. Partial shown exchange transfusion blood.

In order to stimulate the general resistance of the body, methyluracil is prescribed 3.0 per day for 5 days and sodium nucleinate 1 tablet 5 times a day for 10 - 12 days. In case of pronounced inhibition of the cellular component of immunity (decrease in T-lymphocytes by 30% or more), immunomodulators are used: levamisole 150 mg for 3 days daily, then a 3-day break and repeat the 3-day cycle, then a 1-day break and taken for 4 days at a daily dose of 37.5 mg prodigiozam, pirogue-nal.

Symptomatic treatment is carried out with the help of replacement drugs (allochol, cholenzym, festal), desensitizing agents (diazolin, suprastin, tavegil).

Much attention should be paid to the diet of patients. Alcohol is completely excluded. The diet should be energetically complete (3000 - 3500 kcal), but with a limited amount of extractive and cholesterol-rich substances (fatty meats and fish, spicy snacks and fried foods, salted and smoked foods, margarine, lamb, pork, goose fats); The use of canned food with the addition of various chemical preservatives is excluded. Preference should be given to dairy and vegetable products, lean meats and fish, butter, vegetable fats.

Persons exposed to dioxin are subject to long-term clinical observation and, if necessary, repeated courses of treatment.

LEWISITE, a chemical warfare agent belonging to the group of blister agents, is present in the following three fractions representing liquid axins: 1) chlorovinyldichloroarsine CHCl:CHAsCl 2; 2) dichlorovinylchloroarsine (CHCl:CH) 2 AsCl; 3) trichlorovinyl-arsine (CHCl:CH) 3 As. L. is named after Lewis, who obtained L. in its pure form and described it in 1918, although L. was first obtained in its impure form in 1904. Of the three fractions, the most active is the first, to swarm and belongs primarily to the name L. It freezes at -13° and at normal pressure boils at 190°. Ud. V. at 0° -1.92 and at 20° -1.885. Vapor pressure is insignificant: 0.087 at 0° and 0.395 at 20°. At this t° 1 l air saturated with L. vapors contains 15.6 mg. At 0° 1 liter of air contains, under saturation conditions, about 1 mg L. In weak concentrations, L. vapors have the smell of geranium. Water slowly hydrolyzes L., and toxic arsine oxides are formed. Alkalis decompose lewisite with the release of acetylene. Oxidizing agents convert L. into slightly toxic compounds of pentavalent As. Lethal concentration, according to Vedder, - 0.048 mg by 1 l(with half an hour exposure). Concentration that gives an abscess effect, according to the same author, is 0.334 mg by 1 l. L. was not used in the war, and therefore its effect on people has been little studied. In dogs, when they are exposed to a poisoned atmosphere, irritation of the open mucous membranes, especially the eyes, is observed, accompanied by lacrimation and profuse nasal discharge, and then symptoms of damage to the digestive tract occur: profuse salivation, nausea and vomiting. The consequences of poisoning are reflected in pronounced symptoms of mucous, and later purulent conjunctivitis and rhinitis. Further, the animals are depressed, have difficulty breathing and coughing. Vomiting of foamy mucus is often observed, probably previously swallowed after it is released from the respiratory tract. At fatal poisonings many animals die in the first 2 days. In survivors, symptoms reflect- 4о phenomena from both the external mucous membranes and the respiratory tract progress until the 5th day; sharp wheezing is observed, indicating intense bronchitis. During this time, some more animals die. Survival for more than 5 days is a favorable sign. False membranes in the nose disappear, and the symptoms of conjunctivitis and bronchitis also regress. In the period from the 7th to the 10th day, complete recovery usually occurs. Other symptoms of poisoning include a temporary drop in temperature by half a degree during the first hour after poisoning, a slowing of the pulse during the first day with some acceleration during the second, increased breathing immediately after poisoning with a return to normal on the second day. In fatal cases, slowing of breathing was observed before death. Autopsy of dead animals reveals the formation of abundant false membranes in the nose, larynx and trachea, purulent bronchitis, often the same bronchopneumonia, along with overflow of the lungs with blood and their edema, emphysema and atelectasis, not always expressed equally sharply. At the same time, congestion in the liver and kidneys and enlargement of the right heart are observed. The cause of acute death in dogs that died in the first 30 hours after poisoning, in the vast majority of cases, according to Vedder, is bronchopneumonia. Thus, the picture of poisoning in general is very similar to mustard gas poisoning. In the same way, when exposed to L. vapors on the skin, phenomena similar to the effect of mustard gas vapors are observed, and hyperemia occurs after 4-6 hours, and the formation of a blister after 16-48 hours. Lubrication with liquid L. also produces a reaction similar to mustard gas. but a more pronounced result. Significant differences in the action of both substances are as follows: 1) the latent period for L. is much shorter; when using liquid L., a burning sensation appears immediately after use; 2) the presence of arsenic causes local painful irritation, which is much less pronounced with mustard gas, and when absorbed through the skin, L. can also cause a resorptive toxic effect. Animal experiments have shown that the use of 0.02 hedgehog 3 to 1 kg weight (provided that it acts on a skin surface equal to as many square centimeters as the number of kilograms the animal weighs) causes the death of the latter. That. for a person over 70 kg weight, the use of 1.4 ohm 3 L. at 70 should be fatal cm 2, skin, i.e., in a space smaller than the palm. - When subltal doses of L. are used on the skin of animals, deeply penetrating, gradually more and more spreading tissue necrosis is observed. Subsequently, the process proceeds slowly, and the necrotic tissues are separated by suppuration, and secondary infections of the affected areas occur very easily. In fatal cases of poisoning through the skin, damage to the lungs, kidneys, sometimes the liver, duodenum, and heart is found during autopsies. With chem. analysis LUMINAL^ arsenic was discovered in all tissues of the body, but most of all in places adjacent to the lesion, as well as in the liver, kidneys and spleen. As a rule, arsenic was also found in urine. -When applied to one’s forearm 2 mg undiluted lewisite Rovida (Rovi-da) observed after 2 hours 20 minutes the appearance of ■erythema, which then became hemorrhagic and edematous, and a slight itching was felt. After 18 hours, a blister appeared and, upon opening it, a scab appeared, which fell off after 26 days. That. and in humans the effect of L. turned out to be stronger than mustard gas. In case of poisoning, the following measures are suggested. When liquid L. acts on the skin, the immediate use of substances that hydrolyze L., which, if it does not protect against local damage to L., will protect it from its resorptive effect by disintegrating it. With this goal in mind, Vedder recommends a 5% aqueous solution NaOH, applied as soon as possible after the lesion. Due to the irritating properties of this solution, it should then be washed off. Oxidizing agents, including bleach, can also be used to destroy lye. Further treatment may consist of excision of the affected area, which can be successfully applied up to 12 and 24 hours after the lesion. The result may be healing by spontaneous tension and, in less favorable cases, a significant reduction in healing time. When affected by lewisite vapors, Vedder recommends the use of a paste consisting of aqueous iron oxide with glycerin. The recipe for preparation is as follows: to an almost saturated solution of chlorine chloride, add a strong solution of ammonia until the faint odor of the latter is preserved. The resulting precipitate is allowed to settle in narrow vessels. The top layer of liquid is removed with a siphon and the vessel is again filled with distilled water, repeating this washing until the washing liquid is free of chlorides. Such washing may require weeks of time. After this, the precipitate of aqueous iron oxide is dried on a filter, and thick mass(6 parts) mixed with pure glycerin (1 part). The resulting ointment is placed in metal tubes, and is well preserved out of air. The paste is thickly applied to the affected area and then covered with parchment paper, etc. The dressing is resumed after 12 hours.* The same ointment can be used for liquid lewisitis immediately after the lesion. Lit.: R o v i d a &., Ricerche sperimentali con la lewisite; azione della lewisite sulla cute dei comuni animali da esperiraento, Sperimentale, Arch, di biologia, v. LXXXIII, 1929. See also pit. to Art. Chemical warfare agents. A. Likhachev. L YN AC Keys (Keith Lucas, 1871-1916), eminent English. physiologist."L.'s work was concentrated in the field of research of excitation phenomena, where L. was one of the founders of the direction seeking to approach the explanation complex processes summation and inhibition in the central nervous system from the elementary properties of excitable tissues. According to his concept, at the junctions of individual links of a conducting heterogeneous tissue system (myoneural connections, synapses), there are areas with imperfect conductivity, in which the impulse propagates with decrement. Their presence leads to the fact that a series of impulses, each of which falls on a relative period of the refractory phase from the previous impulse and reaches such a section in a weakened state, fades within the latter. On the contrary, impulses following one after another during the supernormal period of the refractory phase are transmitted through the site. Being an excellent experimenter who carried out precise quantitative calculations of the time relationships between individual moments in the development of an impulse, Ch. L. substantiated his ideas with great convincingness. This, combined with the breadth of his coverage of the fundamental problems of arousal, places him among the ranks of outstanding modern physiologists, despite the fact that many of his views have undergone radical revision in recent years. L.'s main monograph was published posthumously - “The conduction of the nervous impulse” (London, 1917). Lit.:L a n g 1 e y J., Keith Lucas, Nature, v. XCVIII, p. 109, 1916.

Lewisite is a toxic substance with a generally toxic, irritating, skin-vesicant effect.

R-chlorovinidedichlorarsine. Chemically pure lewisite is a colorless liquid. Technical lewisite - heavy oily liquid dark brown color with a strong unpleasant odor. At low concentrations, lewisite vapors have an odor reminiscent of geranium leaves. The vapor density relative to air is 7.2. Boiling point 119 °C. The melting point is 18 °C, so in winter, without solvents, it is used only at temperatures above 18 °C. Insoluble in water, highly soluble in organic solvents. It is used in droplet-liquid form (steam or fog).

Intolerable concentration irritating the upper respiratory tract - 0.02 mg/l, lethal concentration when exposed through the respiratory system -
0.25 mg/l (15 min), in case of contact with the skin - 25 mg/kg.

Lewisite is a contact poison with virtually no latent period of action. Upon contact with the skin, the victim immediately feels a burning sensation, the skin turns red and swells. After 10-12 hours, blisters appear at the site of the lesion. The action of the vapor also begins immediately. A pain appears in the eyes and nose, which is accompanied by watery eyes and irritation in the throat. After 2-3 hours, pulmonary edema develops if lewisite enters the respiratory organs. Inhalation of air containing vapors in an amount of 0.4 mg/l for 5 minutes entails death. Fog damage is more severe than lewisite vapor damage.

Water and food products, contaminated with lewisite, are not suitable for consumption even after degassing. Lewisite also contributes to the appearance of rust, and drip-liquid causes the destruction of aluminum alloys.

On the ground and in the air, lewisite is detected by external signs and using indicator tubes included in chemical reconnaissance devices. In water, products and materials it is determined by laboratory methods.

To protect against lewisite, use a gas mask and personal skin protection. For degassing (neutralization) chloroactive compounds are used.
Lewisite was proposed as a toxic substance at the end of the First World War (1917) by the American chemist W. L. Lewis, but did not find any combat use.

Lewisite- a mixture of isomers of β-chlorovinyldichloroarsine (α-lewisite), bis-(β-chlorovinyl)chloroarsine (β-lewisite) and arsenic chloride. A dark brown liquid with a sharp irritating odor reminiscent of geranium, a poisonous substance with blister action, named after the American chemist Winford Lee Lewis (1879–1943).

Synthesis and properties

Lewisite is synthesized by the addition of acetylene to arsenic trichloride catalyzed by mercuric dichloride or Lewis acids, resulting in the formation of both β-chlorovinyldichloroarsine (α-lewisite) and the product of the addition of a second acetylene molecule to α-lewisite - bis-(β-chlorovinyl)chloroarsine (β- lewisite):

HC≡CH + AsCl 3 ClCH=CHAsCl 2

HC≡CH + ClCH=CHAsCl 2 (ClCH=CH) 2 AsCl 2

β-Chlorovinyldichloroarsine, a colorless, odorless liquid, is the main component of lewisite and can exist in the form of two isomers - trance- And cis-; in technical lewisite prevails trance-isomer.

Lewisite properties:

Technical lewisite is a complex mixture of three organoarsenic substances and arsenic trichloride. It is a heavy, almost twice as heavy as water, oily, dark brown liquid with a characteristic pungent odor (some resemblance to the smell of geranium). Lewisite is poorly soluble in water, highly soluble in fats, oils, petroleum products, and easily penetrates various natural and synthetic materials (wood, rubber, polyvinyl chloride). Lewisite boils at temperatures above 190C, freezes at temperatures -10 - - 18C. Lewisite vapor is 7.2 times heavier than air: the maximum vapor concentration at room temperature is 4.5 g/m3.
Depending on the time of year, weather conditions, relief, and the nature of the terrain, lewisite retains its tactical resistance as a chemical warfare agent from several hours to 2-3 days. Lewisite is chemically active. It easily interacts with oxygen, atmospheric and soil moisture, and burns and decomposes at high temperatures. The arsenic-containing substances formed in this process retain their “hereditary” characteristic - high toxicity.

Toxic effect

Lewisite is classified as a persistent toxic substance. It has a general toxic and vesicant effect. Toxic to humans under any form of exposure, capable of penetrating through the materials of protective suits and gas masks. Lewisite also has an irritating effect on mucous membranes and respiratory organs.

General toxic effect

The general toxic effect of lewisite on the body is multifaceted: it affects the cardiovascular, peripheral and central nervous systems, respiratory organs, and gastrointestinal tract. The general toxic effect of lewisite is due to its ability to interfere with the processes of intracellular carbohydrate metabolism. Acting as an enzymatic poison, lewisite blocks the processes of both intracellular and tissue respiration, thereby preventing the ability to convert glucose into products of its oxidation, which comes with the release of energy necessary for normal functioning all systems of the body.

Blistering action

The mechanism of the blister effect of lewisite is associated with the destruction of cellular structures. Acting in a drop-liquid state, lewisite quickly penetrates into the thickness of the skin (3-5 minutes). The latent period is practically absent. Signs of damage immediately develop: pain and burning at the site of exposure. Then inflammatory changes in the skin appear, the severity of which determines the severity of the lesion. Mild lesions are characterized by the presence of painful erythema. Moderate damage leads to the formation of a superficial bubble. The latter quickly opens. The erosive surface epithelializes within several weeks. A severe lesion is a deep, long-lasting ulcer. When the skin is damaged by lewisite vapors, a latent period lasting 4-6 hours is observed, followed by a period of diffuse erythema, primarily on open areas of the skin. Acting in high concentrations, the substance can cause the development of surface blisters. Healing takes on average 8-15 days.

Signs of defeat

Lewisite has almost no period of latent action; signs of damage appear within 3-5 minutes after it comes into contact with the skin or the body. The severity of the damage depends on the dose or time spent in an atmosphere contaminated with lewisite. When inhaling lewisite vapors or aerosols, the upper respiratory tract is primarily affected, which manifests itself after a short period of latent action in the form of coughing, sneezing, and nasal discharge. In case of mild poisoning, these phenomena disappear after a few days. Severe poisoning is accompanied by nausea, headaches, loss of voice, vomiting, and general malaise. Shortness of breath, chest cramps are signs of very severe poisoning. The organs of vision are very sensitive to the action of lewisite. Contact with drops of this agent in the eyes leads to loss of vision within 7-10 days.

Dangerous concentrations

Staying for 15 minutes in an atmosphere containing lewisite at a concentration of 0.01 mg per liter of air leads to redness of the mucous membranes of the eyes and swelling of the eyelids. At higher concentrations, there is a burning sensation in the eyes, lacrimation, and spasms of the eyelids. Lewisite vapors act on the skin. At a concentration of 1.2 mg/l, skin redness and swelling are observed within one minute; at higher concentrations blisters appear on the skin. The effect of liquid lewisite on the skin manifests itself even faster. When the skin infection density is 0.05-0.1 mg/cm², redness occurs; at a concentration of 0.2 mg/cm² bubbles form. Lethal dose for a person is 20 mg per 1 kg of weight, i.e. Lewisite during skin resorption is approximately 2-2.5 times more toxic than mustard gas. However, this advantage is somewhat offset by the absence of a period of latent action, which makes it possible to take the antidote in a timely manner and/or treat the affected areas of the skin using an individual anti-chemical package. When lewisite enters the gastrointestinal tract, profuse salivation and vomiting occur, accompanied by sharp pains, fall blood pressure, damage to internal organs. The lethal dose of lewisite when ingested is 5-10 mg per 1 kg of weight.

Lewisite is a contact poison that belongs to (BOV). It is a dark brown oily compound with a pungent odor. On the battlefield, the substance can be used in liquid, vapor or mist form.

This chemical weapon was first synthesized by the American chemist Lewis at the end of the First World War. But according to official data, it was never used during combat operations. For many years, in some countries, including the USSR, lewisite was considered as a potential weapon of mass destruction, and was accumulated in large quantities. It was also used as an additive to mustard gas to lower the freezing point.

Over time, the idea of using lewisite was rejected: it demonstrated low efficiency compared to other chemical agents - mustard gas, sarin, VX. Later, in 1992, the UN General Assembly adopted the Chemical Weapons Convention. To date, 192 countries have already signed it. Now lewisite and mustard gas are classified as toxic substances that are prohibited from being used during combat operations due to unjustifiably large quantity possible victims.

Lewisite reserves accumulated during the arms race are being destroyed. This process produces pure arsenic, a valuable raw material for semiconductor production. Due to the economic benefits obtained from the destruction of warheads, disarmament is quite active.

Synthesis and properties

According to its chemical structure, lewisite is a compound of acetylene with arsenic trichloride, catalyzed by Lewis acids or mercuric dichloride. In low concentrations it has an odor reminiscent of geranium leaves.

Lewisite is a toxic substance that is practically insoluble in water and easily penetrates into the structure of natural and artificial materials, including wood and rubber. This property makes it difficult to provide the army with means of protection in the event of the likely use of BW. Lewisite is able to penetrate the structure of a protective suit and gas mask in a few minutes.

IN liquid form this toxic substance provokes corrosive processes and even destroys aluminum alloys. Its vapors are 7 times heavier than air, so when spread over an open area they spread along the ground.

Toxic effect

When inhaling lewisite vapors, severe irritation of the mucous membranes occurs. The victim experiences a burning sensation in the throat, watery eyes, and pain in the eyes and nose. Subsequently, the toxic substance penetrates deeper into the respiratory tract, and after 2–3 hours bronchitis develops, and later pulmonary edema.

Fog exposure causes a more acute and rapid reaction in the body than exposure to vapor. The liquid-droplet form of a chemical weapon, when it comes into contact with the skin, spreads over its surface: a small drop the size of a lentil provokes redness in an area the size of a child’s palm. Liquid lewisite is especially dangerous for the membrane of the eyes - it destroys it within 7-10 days, leading to complete blindness.

Food and water contaminated with BWAs are not suitable for consumption even after decontamination. If this rule is neglected, the chemical compound enters the body through digestive tract. It causes death of the tongue, cheeks, palate, larynx, walls of the esophagus and stomach. Then there are disturbances in swallowing and breathing, abdominal pain, vomiting and diarrhea; food poisoning in most cases it ends in death.

Blistering action

The rate and nature of skin damage upon contact with BW depends on the form of the chemical compound. The most toxic with this method of exposure to the body is the droplet-liquid form of the poison. Within 3–5 minutes after contact with the skin, the chemical warfare agent lewisite causes:

pain;
redness;
burning;
swelling.

Further development inflammatory process depends on the severity of the lesion:

with a mild degree, painful erythrema appears on the surface of the skin;
with moderate damage, the damaged area becomes covered with blisters, which heal within 4–5 weeks;
in severe cases, deep ulcers form, sometimes with perforation.

Vapor and mist forms of BWA are less toxic to the skin. Signs of their effects appear only after 4–6 hours.

General toxic effect

Lewisite affects several internal systems of the body at once:

respiratory;
cardiovascular;
nervous (central and peripheral);
digestive tract.

It disrupts protein, carbohydrate and lipid metabolism, mechanisms of tissue and cellular respiration, process of glucose breakdown. For these properties, lewisite is called an enzyme poison.

Signs of defeat

The following general signs of lewisite damage are distinguished:

After poisoning with a large amount of BWA vapors or with prolonged exposure to them, changes occur in the human body similar to those that occur with.

Dangerous concentrations

A concentration of lewisite in the air stream exceeding 0.02 ml/l, when inhaled, causes irritation of the upper respiratory tract and subsequent inflammation of the mucous membrane. Such a quantity of chemically active substances is called intolerable: upon contact with it, it is impossible to avoid harm to human health.

Concentrations above 0.25 mg/l are lethal. If the substance enters the body through the respiratory system, the person dies within 15 minutes. At a higher concentration – 0.4 mg/l – death occurs three times faster.

Contact with chemical pesticides on the surface of the skin also leads to death. In this case, the concentration of the substance should be quite high - 25 mg/kg.

First aid

In case of lewisite poisoning, it is necessary to urgently remove the victim from the area of exposure to chemical agents. Then you can provide first aid:

place a crushed ampoule with an anti-smoke mixture under the mask;
treat exposed areas of the body.

The anti-smoke mixture is a combination of wine alcohol, chloroform, ether and ammonia. It is available in ampoules for single use. The mixture is placed under a gas mask already worn by the patient. In the absence of protective equipment, you can inhale a cotton swab moistened with the composition, but this is less effective.

Before the doctor arrives, you can re-wipe the affected skin with a degasser, and then apply a bandage with a chloramine solution. The nasopharynx and conjunctival sac must be washed with a weak solution of potassium permanganate. When chills appear, the patient should be wrapped or covered with heating pads.

If poisonous substance entered the body through the digestive tract, you need to do a gastric lavage. To do this, the patient is given to drink from 5 to 8 liters of warm water with the addition of baking soda. After the procedure, you need to take any sorbent.

Further therapy is carried out in the clinic and depends on the severity of the victim’s condition. First medical aid includes complete sanitization and the use of antidotes. If pulmonary edema or collapse develops, transportation of the victim is not recommended.

Appropriate symptomatic therapy– cardiovascular, antihistamines. For the purpose of prevention, the patient is prescribed antibiotics, vitamins and alkaline inhalations. If the course is favorable, complete recovery occurs no earlier than 4–6 weeks.

Antidotes

When in contact with thiols, lewisite forms a less toxic compound, therefore Unithiol is used as an antidote for damage by this chemical agent. It's detoxifying medicine It is administered intramuscularly, and in case of severe damage - intravenously. Maximum concentration in the patient’s blood occurs within 15–30 minutes.

Dimercaptopropanol, or “British Anti-Lewisite,” is also used as an antidote. It is used in an oil solution and is less effective than Unithiol.

Skin cleansing

This procedure can only be performed when the victim is already outside the area of action of the toxic substance. Traces of drops of poison remaining on the surface of the skin are removed using:

degasser IPP (individual anti-chemical package);
chloramine B solution (10–15%);
iodine tincture.

After treating the affected areas, the patient’s clothes and shoes are removed, which can become a source of lewisite evaporation. They are hidden in sealed bags, tied and handed over for disposal.