Symptoms characteristic of the clinic of acute phos. poisoning. Organophosphorus poisoning. SOS: emergency assistance

FOS or organophosphorus compounds are toxic substances used as pesticides, herbicides, and for deratization measures. Typical representatives of the group: Dichlorvos, Karbofos, Metaphos. The lethal dose is 2 g when taken orally.

What are the symptoms of damage from phosphorus compounds? Is there an antidote for phosphate poisoning? How to provide first aid to a victim?

Poisoning with phosphorus and chlorine occurs due to violation of safety rules when working with poisons, or during suicide attempts. Phosphorus drugs block the production of cholinesterase enzymes, which destroy acetylcholine. The mediator is contained in muscle structures, nerve ganglia, sweat glands and accumulates in tissues. An excess of the mediator has an exciting, then depleting effect on cholinergic structures. Leads to persistent forms of paralysis.

Feature of intoxication with phosphorus compounds: they are converted into toxic compounds in the body. They are released cyclically, and 10% of victims experience relapses, although there is no contact with toxins. A diagnosis of chronic intoxication is made.

Symptoms of phos poisoning have a characteristic course. Manifestations of acute intoxication go through 3 stages:

1. Excitation.
2. Cramps and excessive activity of a limited muscle group.
3. Paralysis respiratory center.

Symptoms of initial stage intoxication:

• headache;
• weakness;
• hypersalivation;
• hyperhidrosis;
• lacrimation.

Moderate poisoning from FOS causes shortness of breath, constriction of the pupil, decreased blood pressure, epigastric pain, a convulsive state develops, and relaxation of the sphincters of the bladder and anus is observed. Seizures begin within 30 minutes of exposure to the toxin. In severe cases, the patient falls into a coma.

The sequence of development of symptoms in case of poisoning with organophosphorus compounds depends on the route of penetration of toxic substances into the body. When inhaling phosphorus vapors, signs of damage appear respiratory system– bronchospasm, rhinorrhea.

If the poison is absorbed into the skin, hyperhidrosis develops, muscle fibrillation at the site of contact. When phosphorus compounds come into contact with the scalp, symptoms of central nervous system damage are observed.

If a toxic substance is accidentally ingested, the gastrointestinal tract reacts. Diarrhea, vomiting, pain in the liver, and epigastric pain appear.

During diagnostic measures, the doctor takes into account the clinical manifestations and analyzes the situation in which the poisoning occurred. FOS have a specific garlic smell. Easily detected in wash water and on skin.

Additionally, the presence of phosphorus compounds in the blood, urine, and other biological fluids is determined. Conduct a study on cholinesterase activity. A decrease in activity by 20–30% indicates a mild severity of poisoning, and by 80–90% is a sign of severe intoxication with unpredictable consequences.

Necessary antidotes

The algorithm for providing medical care does not depend on the way phosphates enter the body. At the first stage of therapy, measures are taken to normalize breathing. Intubation, removal of toxic substance residues by washing the bronchoalveolar system, oral cavity.

If it is impossible to breathe independently, the patient is transferred to artificial ventilation. Gastric and intestinal lavage, administration of sorbents, and injection medications are indicated to prevent shock.

An antidote for poisoning with organophosphorus compounds is a drug that restores cholinesterase activity under conditions of inhibition by phosphorus compounds. Injection drugs. Tablets are not used as antidotes.

The following drugs are used in medical practice:

1. Atropine sulfate – intramuscular and intravenous administration is indicated. At the initial stage of therapy, the dose is 1–2 mg. Administration of the drug is indicated before the onset of symptoms of atropine overdose. It manifests itself as dry skin and in the oral cavity, dilated pupils. The maximum dosage is 50 mg per day for severe intoxication.
2. Alloxim - the effective antidote dosage depends on the severity of poisoning with phosphorus-containing drugs. With mild and medium degree In case of intoxication, injections are indicated every 3 hours, in case of severe intoxication - every 2 hours. Daily dosages are 0.3 g - 1.5 g per day.
3. Diethixime - intramuscular administration of 0.5 g of the drug is indicated. For mild intoxication, injections are carried out 6 times a day, for moderate intoxication - 8 times a day. For severe patients, 12–24 injections per day are indicated.
4. The backup antidote for FOS poisoning is dipyroxime. Administered intramuscularly. For mild intoxication, injections are carried out 3 times a day, moderate intoxication - every 2 hours. For severe patients, the antidote is indicated once every 90 minutes.

To prevent malfunctions nervous system the prescription of vitamin preparations is indicated. An obligatory part of therapeutic measures is forcing diuresis. Dialysis and blood transfusions are performed according to indications.

Regardless of the pathogenesis and severity of the victim, in case of intoxication with phosphorus compounds, call an ambulance.

Urgent measures:

• stop contact with FOS;
• remove the victim from the affected area into fresh air;
• in case of contact with the skin, rinse the affected area with water; in case of a burn with orthophosphoric acid, use a baking soda solution to neutralize;
• gastric lavage with water;
• If poison gets on your hair, you need to cut it off.

Further treatment is carried out at the base medical institution. Antidotes, vitamin preparations are used, aspiration of the respiratory organs, and anti-shock therapy are performed.

Consequences and prognosis of recovery

The prognosis depends on the dose of the toxic substance, the route of entry into the body, the age of the patient and the response to treatment measures.

Complications of poisoning with phosphorus compounds:

• hepatitis;
• kidney damage;
• polyneuropathy with dysfunction of the central nervous system;
• persistent movement disorders;
• demyelination of the nervous tissue of the limbs;
• periodic relapses associated with the release of phosphorus accumulated in adipose tissue;
• pneumonia;
• death.

OPC poisoning is a difficult diagnosis. Like intoxication with ammonia, heavy metals, zinc can have unpredictable and long-term consequences.

If you use phosphorus compounds at work or at home, follow safety regulations. Do not use Dichlorvos or analogues without a good reason.

At the present stage of scientific development, medicine cannot completely stop the consequences of OPC intoxication. Antidotes have a specific dosage regimen and administration method; have them in home medicine cabinet pointless. Can only be used by a medical professional.

Organophosphorus compounds (OP) are highly toxic substances that are extremely dangerous for the human body. Some OPCs were developed as nerve agents (Sarin was even used by terrorists). Organophosphates and carbamates are commonly used as insecticides. OPC poisoning is accompanied by severe intoxication and requires immediate medical attention at a clinic, as it poses a mortal threat to humans.

Mechanism of poisoning

Poisoning with organophosphorus compounds most often occurs when using chemicals intended for treating premises against rodents and insects and protecting crops from pests. Intoxication is less commonly observed due to the use of FOS as chemical warfare agents (during military operations) and with the improper use of insectoacaricidal agents for animals and medicines, which contain organophosphorus compounds.

The following ways of penetration of the toxin into the body are distinguished:

• eating unpeeled vegetables and fruits treated with phosphorus-based insecticides;
• reception drinking water, which contains toxic compounds;
• inhalation of FOS vapors when treating plants and animals, premises;
• consumption of milk from animals fed on grass and feed poisoned with a toxic substance.

FOS can enter the human body orally, through Airways and skin. Receiving any dose of poison quickly leads to disruption of the production of cholinesterase, the most important enzyme responsible for nervous activity. If cholinesterase activity decreases, this provokes the release of acetylcholine and excessive long-term excitation of M- and H-cholinergic receptors. Such changes entail disturbances in the functioning of vital systems (cardiovascular, nervous, respiratory, visual, digestive).

Signs and symptoms of OP poisoning

Symptoms of OP poisoning depend on the stage of intoxication. There are 3 degrees of poisoning with toxic phosphorus-containing compounds:

1. Excitation.
2. Stage of convulsions and hyperkinesis.
3. Paralysis.

The first phase, which develops approximately 20 minutes after the toxin enters the body, is characterized by the following symptoms:

• headache;
• dizziness;
• excessive sweating;
• lacrimation;
• muscle weakness;
• nausea, vomiting;
• decreased visual acuity;
• abdominal pain, diarrhea;
• bradycardia (decreased heart rate).

At stage 2, the victim experiences hyperkinesis (frequent involuntary twitching of the muscles of the body and face), convulsions, a sharp increase and decrease in blood pressure, confusion and lethargy, cyanosis skin. Patients have no reaction of the pupils to bright light, the sphincters of the bladder and anus relax, and toxic damage to the liver, kidneys, lungs, stomach and intestines develops. At this stage, the victim may fall into a coma.

Organophosphate poisoning of the 3rd degree is accompanied by a complete disruption of nervous activity, which leads to a weakening of all reflexes. The victim experiences paralysis of the body muscles, a strong decrease or increase in heart rate (less than 30 or more than 120 beats per minute), and depression of the functions of the respiratory center. If breathing stops, death occurs. This can happen 3–9 hours after toxic compounds enter the human body.

Possible consequences

Organophosphorus compounds tend to be transformed in the human body into more toxic substances, which lead to disruption of vital systems and provoke the development of dangerous pathologies.

In case of poisoning of 2nd and 3rd degree of severity, paralysis of the entire muscles of the body occurs, including muscle tissue internal organs, which causes deviations in their work.

The victim may experience gastrointestinal diseases, pneumonia, bronchitis, nephropathy, hepatitis, and myocardial dystrophy. In the absence of timely medical care, the person falls into a coma and dies. Survivors often experience long-term effects of toxic poisoning. Problems may arise 2–3 years after intoxication. Such complications include polyneuritis, asthenovegetative syndrome, and inflammatory diseases of the spinal cord.

First aid for poisoning with organophosphorus compounds

In case of poisoning with organophosphate compounds, the victim must be removed from the poisoned area into fresh air. Contaminated clothing must be removed, skin and eyes should be treated using 2% soda solution(1 teaspoon sodium bicarbonate per 2 cups water). The stomach should be rinsed generously with warm water, after which it is recommended to give the poisoned person a saline laxative. At the same time as providing first aid to the victim, it is necessary to call an ambulance team.

The patient should receive the antidote as quickly as possible. In case of poisoning with organophosphorus compounds, intravenous or intramuscular administration of atropine sulfate, an M-cholinergic receptor blocker, is indicated. Additionally, it is necessary to use cholinesterase reactivators - drugs that restore enzyme activity and reduce the severity of the toxic effect. To such medicines include trimedoxime bromide (Dipiroxime) and isonitrosine.

Treatment

In case of poisoning by toxic compounds, a person undergoes complex intensive therapy in a hospital setting. Treatment includes the following measures:

1. The use of atropine sulfate in combination with cholinesterase reactivators during the first 3–4 days after the development of intoxication.
2. Introduction of M- and N-anticholinergic drugs.
3. The use of drugs for symptomatic treatment aimed at normalizing the functions of internal organs, eliminating seizures, improving general condition (glucocorticosteroids, detoxification, anticonvulsants, vasodilators).
4. The use of antibiotics (for the prevention and treatment of the consequences of toxic damage to internal organs).

Extracorporeal detoxification methods - hemosorption, hemodialysis, hemofiltration - are effective in early dates poisoning

If the victim experiences coma or respiratory arrest, resuscitation measures and the use of artificial ventilation are indicated.

Preventive actions

To avoid intoxication when using organophosphorus substances, it is necessary to follow a number of important rules:

1. When preparing solutions and processing premises or garden areas, it is necessary to use personal protective equipment: gloves, mask, shoes, suit.
2. Chemicals should be stored out of the reach of children and pets.
3. For 3–4 days after applying insecticides to the surface of a room or plant, it is necessary to exclude people and animals from the treated area.
4. After working with toxic substances, you should wash your hands with soap and water. It is necessary to especially carefully clean berries, vegetables and fruits collected from shrubs and trees treated with chemicals under running water.
5. Do not eat or smoke while using solutions.
6. It is best to treat agricultural land in cool weather, since the toxicity of ready-made phosphorus-containing solutions at a temperature of +35 ° C increases several times.

At enterprises using organophosphorus substances in production, worker health and safety standards must be strictly observed. At the first signs of intoxication, you should immediately seek help from specialists.

According to the toxicity of FOS there are:

• potent (LD50<50 мг / кг),
• highly toxic (LD50 from 51 to 200 mg/kg),
• moderately toxic (LD50 from 201 to 1000 mg/kg),
• and low toxicity (LD50 > 1000 mg/kg).

Organophosphorus compounds are crystalline substances or liquids. Most of them are highly soluble in fats and other solvents (xylene, toluene, acetone, chloroform), and have a specific kerosene-garlic odor. Only some of them are soluble in water, in particular chlorophos, methylacetophos, phosphakol. They are quite stable, but in an alkaline environment high temperature hydrolyze within 24 hours. However, in an acidic environment, they can persist in soil for months.

The toxicity of aqueous solutions at a temperature of 35 ° C can increase tens of times per day. Organophosphorus substances enter the body mainly through the mouth, as well as through the respiratory tract and skin. Human intoxication occurs due to the use of contaminated water; consumption of vegetables and fruits after treating gardens and vegetable gardens with appropriate FOS, when spraying them on trees and premises, consumption of milk from cows that have consumed contaminated water and feed, etc.. These same properties and their high volatility determine the intensive intake of poison through the skin and respiratory tract ways.

Effect on the body

Absorption of FOS begins in the oral cavity, then continues in the stomach and intestines. Due to their high lipoidotropy, they soon appear in the blood through any of the indicated penetration routes, in all organs, including the brain. In the body, their toxicity increases sharply, since about 50% of them are biotransformed in the liver according to the type of lethal synthesis, that is, with the formation of very toxic metabolites.

They are excreted from the body by the kidneys, about 30% unchanged, and 20-25% by the respiratory tract.

The toxic effect is due to their anticholinesterase properties. By interacting with acetylcholinesterase, organophosphorus compounds form an inactive phosphorylated complex that is capable of catalyzing acetylcholine. As a result, the content of this mediator in the synaptic cleft of cholinergic synapses sharply increases, which leads to prolonged excitation of m and n-cholinergic receptors.

In addition, these compounds can reduce the activity of proteases, acid and alkaline phosphatases, phosphorylate some proteins, disrupt blood composition, block membrane ATPases and disrupt the permeability of myocardial cell membranes.

Stages of poisoning

There are two stages of acute poisoning with organophosphorus compounds:

• first (cholinergic),
• the second (non-cholinergic).

First stage manifested by the effects of significant stimulation of m and n-cholinergic receptors, i.e.:

• miosis,
• spasm of accommodation,
• visual impairment,
• salivation,
• bronchorrhea,
• increased peristalsis and intestinal spasm,
• diarrhea,
• bradycardia,
• acute respiratory failure due to peripheral respiratory impairment (cholinomimetic effect).

In this case, psychomotor agitation, ataxia, shortness of breath, tremors, clonic-tonic convulsions, confusion, coma, paralysis of the respiratory center develop as a consequence of the central n-cholinomimetic effect.

In addition, as a result of excitation and subsequent paralysis of vital centers, nerve nodes and executive organs, there is first an increase and then a decrease in blood pressure, disorder heart rate, an increase followed by a decrease in body temperature, signs of adrenal exhaustion, hyperglycemia, hypokalemia, the appearance of pulmonary edema.

At the second stage of acute FOS poisoning the signs of the first stage begin to weaken somewhat, but signs of exotoxic shock appear:

• cyanosis,
• areflexia,
• heart rhythm disturbance,
• hypotension,
• manifestations of acidosis,
• cerebral edema,
• convulsions.

Sometimes, on the 2-8th day, a relapse of poison intoxication occurs.

Death in the first stage of acute OP poisoning can occur at the height of convulsions due to overexcitation and paralysis of the respiratory center, and in the second - through fibrillation of the ventricles of the heart, sudden cardiac arrest or paralysis of the respiratory center. Acute heart failure can be the result of aspiration-obstruction, peripheral respiratory disorders or toxic pulmonary edema.

Clinical symptoms of FOS poisoning

During acute FOS poisoning, it is customary to distinguish 3 periods:

1. acute - 1-3 days;
2. complications - 4-14 days;
3. long-term consequences - up to 3 years.

Manifestations of acute poisoning are determined by the stage and severity of intoxication and complications (of course, at the second stage - in the form of pneumonia, toxic hepatitis, nephropathy, myocardial dystrophy, etc.), and long-term consequences - in the form of asthenovegetative syndrome, myeloradiculoneuritis, polyneuritis.

Based on the rate of increase in the manifestations of acute poisoning with organophosphorus compounds, lightning-fast and slow-flowing forms are distinguished (mild poisoning, moderate poisoning, severe, extremely severe).

In victims with a fulminant form of intoxication, convulsive syndrome develops within the first 30 minutes after the poison enters the body.

Victims with mild poisoning complain about:

• dizziness,
• headache,
• Pain in the eyes,
• photophobia,
• "fog in the eyes"
• sometimes psychomotor agitation or depression,
• nausea,
• vomit,
• spasmodic pain in the abdomen,
• diarrhea,
• sometimes difficulty breathing,
• feeling of tightness in the chest.

They have sweating, pale skin, salivation, in some - moderate bronchorrhea, moderate miosis, with impaired pupillary reactions to light, trembling of the eyelids and outstretched fingers. Tachycardia, slight hypertension. Frequent urination. Cholinesterase activity is reduced by 20-50%.

More severe manifestations are typical for moderate poisoning. Victims show signs of bronchospasm and central nervous system disorders:

• psychomotor agitation,
• hallucinations,
• disorientation,
• ataxia,
• movement coordination disorders,
• myofibrillation (tongue, face, legs, chest),
• miosis,
• spasm of accommodation and visual impairment.

From the cardiovascular system, bradycardia or tachycardia, respiratory hypertension - shortness of breath with difficulty in exhalation, noisy or Cheyne-Stokes breathing are noted; glands - salivation, bronchorrhea, sweating; in the lungs - dry and moist wheezing; in case of oral poisoning - nausea, vomiting, abdominal pain, diarrhea. Urination is involuntary. There are no convulsions. Cholinesterase activity is reduced by 51-70%.

For severe forms Slow acute poisonings, in addition to the indicated cholinomimetic manifestations, are characterized by convulsions and loss of consciousness, and later bronchospasm. Breathing becomes bubbling, and a significant amount of foamy secretion is noted. Fibrillation covers all muscles. During convulsions, consciousness is lost. Body temperature rises. The development of acute respiratory failure is very dangerous. Involuntary not only urination, but also defecation are possible. Cholinesterase activity drops by 71-80%.

Extremely severe acute poisoning with FOS characterized by the cessation of seizures, the appearance of paralysis and coma. Consciousness, like reflexes, is lost, cyanosis increases, and body temperature decreases. Breathing is arrhythmic, shallow, frequent. The heart rate increases, and paroxysmal ventricular tachycardia is possible. There is acute vascular insufficiency (collapse). Cholinesterase activity does not exceed 10% of normal.

Mortality at the toxic stage of FOS poisoning is quite high. Affected individuals die from sudden cardiac arrest or ventricular fibrillation, central paralysis, or from acute respiratory failure due to paralysis of the respiratory muscles.

Clinical manifestations of acute OP poisoning are largely determined by the routes by which the poison enters the body. When a lethal dose of poison is administered orally, signs of acute intoxication appear within 10-15 minutes, coma after 20-30 minutes, and death after 3-9 hours. In case of prolonged acute poisoning, death occurs on the 2-6th day.

With percutaneous penetration, the first signs appear later, sometimes even after 2-3 days. They can occur suddenly after mild symptoms, in the form of weakness, headache, muscle twitching, sweating at the site of contact of the poison with the skin.

Treatment of acute OP poisoning

When creating individual programs for providing emergency care to victims of acute OP poisoning, the efforts of medical personnel are directed, first of all, to eliminating the most dangerous manifestations of intoxication, in particular: the primary specific cardiotoxic effect (disorders of heart rhythm and conduction, acute heart failure, sudden cardiac arrest) , central respiratory paralysis, acute respiratory failure due to paralysis of the respiratory muscles.

The treatment program should include: a complex of intensive resuscitation measures and an active complex of specific and pathogenetic therapy. Of the resuscitation measures carried out at the scene of the incident, particularly important is gastric lavage (if the poison has entered the body orally), washing the eyes and washing it off the skin with plenty of water and soap or a 2% solution of sodium chloride, chloramine or ammonia. In case of acute inhalation poisoning, the victim should be removed from the contaminated room or area and the same measures should be taken. In the hospital they resort to forced diuresis or peritoneal dialysis.

Antidote atropine

From medications Atropine sulfate is of leading importance as a remedy that eliminates all manifestations of the cholinomimetic effect of the poison and thus provides specific protection for the victim. It is administered intravenously, intramuscularly or subcutaneously in the form of a 0.1% solution in doses determined by the severity of acute poisoning, and repeatedly and for a long time, preferably in combination with cholinesterase reactivators.

Intensive atropinization is carried out within an hour. To do this, the patient is administered 2-4 ml of 0.1% atropine sulfate solution every 10-15 minutes, until characteristic features the effect of this remedy is to reduce bronchorrhea, dry skin and oral mucosa, noticeable tachycardia, etc.

It is advisable to carry out this stage of treatment in accordance with the severity of the condition.

In particular, it is recommended that in case of mild FOS intoxication, 2-3 ml of this solution should be administered intravenously to victims; patients with moderate acute poisoning should be given 5 ml intravenously; 3 ml intramuscularly and 4 ml subcutaneously; and 10-14 ml intravenously for severe and extremely severe poisoning; intramuscularly and subcutaneously 3-5 ml.

Over the next 3-4 days, maintenance atropinization is carried out by repeated administration of a 0.1% solution of atropine sulfate in 30-50 ml or more per day.

In addition to this drug, it is advisable for patients, especially with severe acute poisoning, to administer such central and peripheral m and n-cholinergic drugs as aprofen and Arpenal (1 ml each). It is advisable to combine atropine treatment with the administration of cholinesterase reactivators: dipyroxime, dietixime. Thus, dipyroxime is administered intravenously or intramuscularly, 1 ml of a 15% solution 6-7 times during the first day, dietixime - 3-5 ml of a 10% solution intramuscularly.

At the same time, to prevent cardiac disorders, they resort to the administration of 5-10 ml of a 5% solution of unithiol, 300 mg of tocopherol acetate and 60 mg of prednisolone. For arrhythmia, antiarrhythmic drugs are indicated.

If breathing stops or suddenly weakens, you should resort to artificial ventilation. If convulsions are not relieved by specific therapy, use magnesium sulfate intramuscularly 10 ml of a 25% solution, sodium hydroxybutyrate intravenously 5-120 mg/kg in 20 ml of a 5% glucose solution. An effective combination of aminazine (2.5% solution), diphenhydramine (2% solution) and promedol (2% solution) - 2 ml of each.

Also used vascular agents, and to prevent pneumonia - antibiotics.

After emergency care, all injured persons must be hospitalized in intensive care units of hospitals that have artificial kidney devices, or in poison control centers.

Of the chemical characteristics of these substances, attention should be paid to their high distribution coefficient between oil and water, which determines their free penetration through intact skin, biological membranes, and the blood-brain barrier.

In the daily work of toxicology departments, the most common household oral poisonings (accidental or intentional) with karbofos, dichlorvos, chlorophos, and industrial poisonings are more often inhalation. Percutaneous poisonings in peacetime are occasional cases.

Pathogenesis. FOS disrupt or block the function of cholinesterase (ChE), forming a phosphorylated enzyme resistant to hydrolysis, unable to react with acetylcholine (ACh) molecules, as a result of which ACh, which is a mediator in the transmission of excitation in synapses, ceases to be destroyed in a timely manner and accumulates on the postsynaptic membrane, causing its persistent depolarization, which is clinically manifested by the formation of four specific effects: muscarinic-like, nicotine-like, curare-like and central action.

1. Muscarinic-like effect associated with stimulation of M-cholinergic receptors. Clinically, this is manifested by profuse sweating, salivation, bronchorrhea, spasm of the smooth muscles of the bronchi and intestines, and miosis.

2. Nicotine-like effect is associated with stimulation of H-cholinergic receptors and is clinically manifested by hyperkinesis and convulsions.

3. Curare-like effect manifested by the development of peripheral paralysis.

4. Central action FOS is manifested by the development of clonic and tonic seizures and mental disorders.

Clinic. In case of oral poisoning with OPs, three stages of poisoning are distinguished.

Stage I (excitation stage) observed in patients after 15-20 minutes. after taking FOS. Psychomotor agitation, dizziness, headache, nausea, and sometimes vomiting appear. Objectively, moderate miosis, sweating, salivation are noted, and sometimes moderate bronchorrhea occurs. Vomiting and cramping pain in the abdomen appear. Blood pressure is elevated, moderate tachycardia.

Stage II (stage of hyperkinesis and convulsions) develops approximately 1-2 hours after taking FOS (the time of its onset largely depends on the amount of the substance ingested). Specific signs of poisoning reach their maximum and create a clear clinical picture. The patient complains of general poor health, spontaneous muscle twitching, blurred vision, difficulty breathing, drooling, profuse sweating, frequent urination, painful tenesmus. The excitement characteristic of the onset of the disease is replaced by stupor, then stupor, up to the development of a coma.
On examination it is noted significant miosis, There is no reaction of the pupils to light. The chest is rigid, its excursion is limited. Hyperhidrosis reaches its maximum development- the patient is literally flooded with saliva, auscultation reveals a large number of wirey moist rales as a result of hypersecretion of the tracheobronchial tree. The most characteristic sign of this stage of the disease is the appearance of myofibrillations first in the area of ​​the face, neck, chest muscles, forearms and legs, and subsequently in other muscle groups (similar myofibrillation can be observed in patients in the operating room, with the intravenous administration of short-acting muscle relaxants during induction of anesthesia). Periodically, general hypertonicity develops with the transition to tonic convulsions. Against the background of the existing initial tachycardia a trend is starting to develop To distinct bradycardia. The increase in blood pressure reaches a maximum level (250/160 mm Hg), then a drop in cardiovascular activity and the development of a collaptoid state are possible. Frequent urination, painful tenesmus, and involuntary loose stools are noted.

Stage III (stage of paralysis). Paralysis of striated muscles takes first place in the clinic. Consciousness is usually absent. The pupils are pinpoint, there is no reaction to light. Tendon reflexes are sharply weakened, or complete areflexia. Signs of acute respiratory failure and respiratory depression of central origin appear. Bradycardia (heart rate up to 40-20 per minute), hypotension.

Laboratory diagnostics. Specific research methods are quantitative and qualitative reactions to the toxic substance of the FOS group, determination of ChE activity.

Urgent Care. The principle of treatment of patients with acute OP poisoning is complex antidote therapy in combination with nonspecific methods.

Antidote therapy consists of the combined use of anticholinergic drugs (most often atropine) and ChE reactivators.

When using atropine, a distinction is made between “intensive” and “maintaining” atropinization. “Intensive” atropinization is carried out within the first hour from the start of treatment of the patient until all symptoms of the muscarinic-like action of FOS are relieved, which manifests itself in the form of characteristic signs of atropinization: moderate tachycardia develops, miosis disappears, pupils dilate, dry skin and mucous membranes appear. The approximate doses of administered atropine for intensive atropinization are as follows: stage I - 2-3 mg, stage II 20-25 mg, stage 111 - 30-50 mg IV. “Maintenance” doses are administered when signs of the end of the “intensive” dose of atropine appear and amount to approximately 80-90% of its amount. The daily dose of atropine for severe poisoning can reach 150-200 mg or more. Decrease daily dose atropine should be produced gradually, parallel to the increase in the level of ChE activity. If the maintenance dose of atropine is abruptly discontinued when the level of ChE is not restored, sudden death is possible.

Cholinesterase reagents (oximes) should be administered in parallel with atropinization. The main drug in this group is dipyroxime

In stage I of poisoning, dipyroxime is prescribed 150 mg IM 1-2 times a day (ampoules of 1 ml of 15% solution).

At II stages dipyroxime is administered 150 mg intramuscularly every 1-3 hours in a total dose of up to 1.2-2 g. In the presence of disturbances of consciousness, it is necessary to administer centrally acting drugs.

For treatment Stage III a combination of dipyroxime is used with another oxime of central and peripheral action - diethixime, the therapeutic dose of which is 250 mg, the total dose is 5-6 g.

Note. Intensive reactivation is effective only until a stable blockage of ChE occurs, which occurs 6-8 hours after poisoning, therefore, the introduction of ChE reactivators on the 2nd day after poisoning and later will be ineffective and even dangerous due to their pronounced toxic effect, which is manifested by a violation of intracardiac conductivity, relapse of acute symptoms of poisoning FOV, and also toxic.

Poisoning with organophosphorus compounds is often recorded, since the substances are widely distributed in everyday life and, in the absence of safety measures, easily lead to intoxication. In case of direct contact, it is necessary to call a medical team and, if possible, provide first aid. In this case, the risks of health complications will be significantly reduced.

Phosphorus compounds in everyday life

They are complex chemicals that are used not only in production, but also at home and in veterinary medicine. Currently, FOS is used:

The toxic properties of organophosphorus substances can be judged by army developments. Based chemical element poisons such as Soman, Zorin, and V-gases have been developed.

FOS can be solid, volatile, liquid. Basically they have a specific garlic-kerosene aroma, dissolve well in fatty media and poorly in H2O. In this case, the toxicity of aqueous liquid when heated to 35° C increases 35 times.

Almost every day a person encounters such connections. The following organophosphorus agents are considered the most dangerous:

• metaphos;
• DCVF;
• thiophos;
• heterophos;
• phthalophos;
• methyl mercaptophos;
• coral;
• chlorophos;
• dichlorvos;
• karbofos.

IN agriculture apply:

1. Dimethoate Plants are sprayed that become poisonous to sucking insects.
2. Fenitrothion. Used in industry to protect citrus and fruit crops. Also in demand for processing vegetable seeds.
3. Diazinon. Recommended for surface application and soil application. Over the course of several days, the roots absorb the substance, which saturates the entire bush.

The compositions of these phosphorus-containing drugs contain malathion, diazinon and pirimiphosmethyl, which are extremely dangerous for humans.

Routes of poisoning by FOS

Intoxication occurs in 3 ways:

1. Orally. It develops as a result of the ingestion of phosphates, phosphides, and phosphines through the gastrointestinal tract with water containing toxins, poorly washed fruits, and unsterilized milk.
2. Inhalation. The cause is inhalation of vapors.
3. Percutaneously. Direct contact with skin.

Penetrating into the body, phosphorus compounds block cholinesterase (AChE). An enzyme is formed that is highly resistant to the hydrolysis process. It destroys acetylcholine and gradually accumulates, leading to the development of a clinical picture. Effect classification:

At the slightest symptoms of poisoning with organophosphorus compounds, it is necessary to urgently call emergency help; it is advisable to show doctors the substance that caused it.

Signs of FOS poisoning

After contact, organic phosphorus compounds are absorbed into the blood. In this case, they can penetrate through the mucous membranes of the mouth, stomach and intestines, lungs, and skin. The processes are characterized by a cyclical feature. The chemical is transformed, creating new toxic substances, and repeated interaction with drugs is not required. Both adults and children are at risk from such chronic intoxication. According to statistics, relapses develop in approximately 10% of patients.

Stages of FOS poisoning

Phosphorus damage has a general clinical picture, which practically does not depend on the type of agent. Symptoms develop in 3 phases:

1. Excitation.

Already 15 minutes after intoxication with organophosphorus compounds, initial signs appear:

• cephalgia;
• attacks of nausea;
• gagging;
• abdominal pain;
• constriction of the pupils;
• increased salivation;
• profuse sweat;
• blood pressure jump;
• increased heart rate.

It is advisable to provide first aid to the victim already at this stage.

2. Hyperkinesis and convulsions.

If no measures are taken, after a few hours, a person experiences the following symptoms of poisoning with organophosphorus compounds:

• general malaise;
• vision problems;
• difficulty breathing;
• profuse sweat;
• pain when urinating and bowel movements;
• muscle twitching.

Stupor is noted as coma progresses. In this case, the pupils do not respond to light, the tone of the skeletal muscles is increased, chest movements are limited, and blood pressure rises to critical levels. The spasms gradually move to the muscle tissues of the neck, synergists of the legs, and forearms. Collapse is likely.

At this stage, there are no tendon reflexes, bradycardia and a drop in blood pressure appear. Greater risk of death if left untreated.

Long-term consequences of poisoning with organophosphorus compounds can appear even after several years.

Symptoms of possible complications resulting from intoxication

Defeat of FOS negatively affects almost all groups of internal organs:

1. Suffering the cardiovascular system. The pulse rate reaches 120–130 beats. Arterial hypertension is observed, after which collapse usually develops.
2. Excessive production of acetylcholine provokes profuse secretion of sweat and saliva. Miosis appears - a sharp constriction of the pupils, which is accompanied by loss of the light reflex.
3. Initial convulsions when cholinesterase is inhibited lead to paralysis of the striated and respiratory muscles. Muscle tone disappears, nervous activity is disrupted.

The comatose state can last up to 6 days.

Diagnosis of intoxication

The examination includes the study of indirect and direct signs of poisoning with organophosphorus compounds. For pathogenesis, it is advisable to have an idea of ​​the location of the lesion and to warn doctors about the presence of a characteristic odor.

A biochemical study of blood composition helps confirm the presence of FOS. In addition, pay attention to the speed of the reaction - the clinic appears very quickly, which makes it possible to separate it from the manifestations of intoxication with chlorine, zinc, hydrogen sulfide, ammonia and other chemicals.

First aid

As soon as the victim shows signs of organophosphate damage, several steps must be followed in succession.

Algorithm of pre-medical actions:

1. In case of oral poisoning, it is recommended to rinse the stomach using such agents as magnesium sulfate, petroleum jelly, universal antidote for poisoning - Activated carbon, which take 1 tablet for every 10 kg of weight.
2. If vapors penetrate into the pulmonary system, the person is taken out into fresh air and the gastrointestinal tract is also cleaned. An antidote and laxative are indicated.
3. If the skin comes into contact with a substance that can poison, use a soap solution, 20% soda, or chloramine. When direct phosphorus damage is observed, the damaged area should be kept moist while otherwise ignition is possible.
4. If necessary, resort to indirect massage of the heart muscle.

The patient is quickly transported by ambulance to the hospital, where further therapy will take place.

Treatment

People exposed to organophosphate toxic substances are sent to the intensive care unit.

The program includes diagnostics, on the basis of which an optimal scheme is developed:

1. In case of acute intoxication, it is recommended to administer 2–3 ml of Atropine 0.1% intravenously or subcutaneously. Injections are repeated every 15 minutes until symptoms such as sweating and saliva disappear. Dilated pupils and dry mouth are evidence indicating discontinuation of this treatment method. Sometimes the daily dosage reaches 50–70 ml. But usually 5–10 ml is enough to normalize the condition.
2. Antidotes are used to neutralize the poison - Dipiroxime 15%, 1 ml, Isonitrozine 40%, 2 ml. With their help, they eliminate cramps and restore breathing.
3. To reduce the absorption of organophosphorus compounds, the stomach is cleansed again with activated carbon.
4. For persistent high blood pressure, use 3% Dibazol, 25% magnesium sulfate. Drip administration of 2.5% Aminosine helps. But this drug must be used carefully, as there are risks of collapse.

Doctors need to select a specific antidote that will eliminate the severe symptoms of poisoning as soon as possible. Pharmacology offers an extensive list of drugs that can be included in the treatment program:

• cholinesterase reactivators;
• Pentafen;
• Amizil;
• Dipiroxime;
• Isonitrosine;
• Tropacin.

The following activities are carried out:

1. If necessary, connect to an artificial respiration apparatus.
2. Antibiotics are prescribed to exclude infection.
3. To prevent blood thickening, anticoagulants are used.

Antidote therapy is carried out depending on the degree of poisoning. Most effective in the first 6 hours. For damage caused by certain compounds, it is not required. For example, if avenin or methylacetophos is detected in the body, the patient will be treated symptomatically, using drugs that eliminate common toxic manifestations.

Late use of antagonists is dangerous, since the compounds have a negative effect on the liver, heart and provoke re-intoxication.

Prevention

To prevent both acute and chronic poisoning by organophosphorus compounds, it is necessary to adhere to safety recommendations:

1. To prevent pathology from becoming an occupational disease, work using protective equipment.
2. Limit children's access to household products containing the chemical.
3. Promptly dispose of empty containers and expired substances.
4. In case of contact with skin, immediately remove clothing, rinse areas thoroughly, and trim nails and hair.

If prevention was not followed and you managed to poison yourself with phosphorus, phosgene, tetrachloroethane, organochlorine acid or other substances, you should urgently call doctors - symptoms appear quickly, often severe. Timely hospitalization will reduce the existing risks of complications, and possibly save the life of a seriously injured person.