ICD 10 ethanol poisoning. Toxic effect of alcohol. Clinical recommendations. Treatment of hemodynamic disorders

What are alcohol surrogates? What are the signs of poisoning with such counterfeit alcohol? How to help the victim? What could be the consequences of such intoxication? We will look at the answers to these questions in this article.

What applies to alcohol surrogates?

Poisoning with alcohol substitutes in the international classification of diseases ICD-10 corresponds to codes T51.1 - T52.9.

They are divided into two groups: those alcohol substitutes that may contain ethyl alcohol and those that may not contain it. The first group includes:

  1. Butyl alcohol. Death occurs after taking just 30 milliliters.
  2. Hydrolysis and sulfite alcohols, which are obtained from wood. They are more toxic than ethanol due to the presence of a small amount of methyl alcohol.
  3. Denatured alcohol or industrial alcohol. Contains some wood alcohol and aldehyde.
  4. The polish contains several types of toxic alcohols.
  5. The stain, together with ethanol, has dyes that cause the patient’s skin and mucous membranes to turn blue.

The second group, or they are also called “false surrogates,” is represented by:

  • methyl alcohol;
  • ethylene glycol.

Clinical symptoms of alcohol surrogate poisoning

Symptoms of poisoning by alcohol surrogates differ depending on which group they belong to. They will be more favorable if they are alcoholic surrogates of the first group, containing ethyl alcohol, and more severe and dangerous in case of poisoning with methanol or ethylene glycol, so it is worth dwelling on them in more detail.

Symptoms of poisoning with surrogates containing ethyl alcohol

  • emotional and motor arousal;
  • facial redness;
  • state of euphoria;
  • sweating;
  • increased salivation;
  • a feeling of mental and physical relaxation.

Then intoxication gives way to symptoms of alcohol intoxication. The skin becomes pale. There is a frequent urge to urinate. The pupils dilate and the mouth feels dry. Increased mental and physical activity is accompanied by a lack of coordination, movements become sweeping. Concentration becomes reduced, speech is slurred. Criticism of one's words and actions is sharply reduced or completely absent.

Symptoms of methanol (wood alcohol) poisoning

Methyl alcohol is quickly absorbed in the digestive system. About 75% of the absorbed poison is excreted in the breath, the rest in the urine. The lethal dose ranges from 50 to 150 milliliters. The main impact of poisoning falls on the nervous system and kidneys. A psychotropic effect occurs (pathological changes in the psyche) and a neurotoxic effect, accompanied, among other things, by damage to the optic nerves and retina.

  • nausea, vomiting;
  • intoxication and euphoria are weakly expressed;
  • visual impairment: flickering black dots before the eyes, blurred vision, diplopia (double vision) and even blindness;
  • outwardly, in such patients the pupils are dilated and react sluggishly to light;
  • 1-2 days after poisoning, pain in the abdomen, lower back, aches in the muscles and joints appear;
  • the temperature rises to 38⁰;
  • dry skin and mucous membranes;
  • low blood pressure;
  • interruptions in heart function;
  • confusion;
  • attacks of excitement accompanied by convulsions;
  • As the symptoms increase, the victim falls into a coma and paralysis of the limbs develops.

Ethylene glycol is also quickly absorbed into

digestive tract. About 60% of the poison is broken down in the liver, about 20–30% is excreted by the kidneys. Therefore, it is these organs that will suffer the most, up to the development of their acute failure. In severe poisoning, signs of damage to the nervous system appear.

  1. Early period. It lasts about 12 hours and is characterized by signs of alcohol intoxication while feeling well.
  2. Toxic damage to the nervous system. There are: nausea, vomiting, headache, thirst, diarrhea, skin and mucous membranes become cyanotic. The pupils are dilated, body temperature rises, difficulty breathing, tachycardia, and psychomotor agitation appear. Loss of consciousness with the development of convulsions is possible.
  3. The nephro and hepatotoxic period develops 2–5 days from the onset of the disease. A clinical picture of liver and kidney failure is noted. Yellowness of the skin appears, which appears first on the sclera and last of all, the palms turn yellow. Skin itching is characteristic, and darkening of the urine may occur. Renal failure is manifested by a decrease in diuresis up to its absence.

Emergency care for poisoning with alcohol substitutes

If poisoning with alcohol substitutes is suspected, emergency care will depend on the initial condition of the patient. If the patient is unconscious, then he must be laid on a flat, hard surface, turn his head to the side to avoid aspiration of vomit and call an ambulance. If respiratory and cardiac activity is impaired, first call an ambulance, and then perform indirect cardiac massage and artificial respiration.

  • take sorbent;
  • saline laxative;
  • drink an enveloping decoction, for example, jelly;
  • emergency hospitalization in a hospital.

Treatment of poisoning with alcohol surrogates in a hospital:

  1. Gastric lavage through a tube. In case of methanol intoxication, it is repeated for 3 days. They give sorbents.
  2. Antidote treatment in both cases is the same: five percent ethanol is administered intravenously. For mild poisoning, 30% ethyl alcohol can be taken orally.
  3. In case of ethylene glycol poisoning, calcium gluconate is administered to neutralize the breakdown products of the toxic substance.
  4. Forced diuresis is carried out, which is based on the drip administration of large amounts of solutions and diuretics in the absence of renal dysfunction.
  5. Removal of toxins from the blood is also carried out by hemodialysis.
  6. Glucose with novocaine, prednisolone, and vitamins B and C are administered.
  7. In case of methanol poisoning, spinal punctures are performed.
  8. In severe cases of ethylene glycol toxicity, a kidney transplant may be necessary.

Consequences of poisoning with alcohol surrogates

When intoxicated with methanol, complete loss of vision is possible, which is not restored after the poison is removed from the body. Ethylene glycol-based surrogates lead to kidney failure. Such patients mostly die.

The problem of poisoning with alcohol surrogates, unfortunately, remains relevant today. Many people are faced with this disease, so knowing the signs of such intoxication will help not only provide timely emergency assistance to the victim, but also save his life!

Poisoning with alcohol and its substitutes? Symptoms and signs. First aid for alcohol poisoning, what to do?

Poisoning with alcohol substitutes, ICD 10 code

Poisoning with alcohol substitutes

Acute poisoning with alcohol surrogates: signs and symptoms, diagnosis, treatment

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Poisoning with ethanol and alcohol substitutes

Ethanol (ethyl alcohol), a well-known component of alcoholic beverages, is a transparent, volatile, water-soluble liquid with an odor characteristic of alcohols.

It is used extremely widely both in purified form and as part of many technical fluids, cosmetics, etc. Poisoning occurs when it is massively ingested into the body.

ICD-10 T51 Toxic effect of alcohol T51.0 Toxic effect of ethanol T51.1 Toxic effect of methanol T51.2 Toxic effect of 2-propanol T51.3 Toxic effect of fusel oils T51.8 Toxic effect of other alcohols T51.9 Toxic effect of unspecified alcohol T52 Toxic effect of organic solvents T52.3 Toxic effect of glycols T52.4 Toxic effect of ketones T52.8 Toxic effect of other organic solvents T52.9 Toxic effect of organic solvents, unspecified.

EPIDEMIOLOGY

EPIDEMIOLOGY A quarter of all acute poisonings are alcohol poisoning. More than 60% of all fatal poisonings also belong to this group.

CAUSES Risk factors: ■ Chronic alcoholism (about 90% of those hospitalized with acute alcohol poisoning suffer from chronic alcoholism). ■ Drinking alcohol on an empty stomach (food in the stomach slows down the absorption of alcohol). ■ Unique lifestyle: frequent events accompanied by feasts; availability of alcohol, especially cheap alcohol. ■ Alcoholism in the family. The lethal concentration of ethanol (ethyl alcohol) in the blood is 5–8 g/l, a lethal single dose is 4–12 g/kg (300–500 ml of 96% ethanol), however, these indicators vary from person to person and largely depend on the acquired alcohol tolerance. Ethanol easily penetrates tissue membranes and is quickly absorbed in the stomach (20%) and small intestine (80%). On average, after 1.5 hours its concentration in the blood reaches its maximum level. The substance acts as a selective depressant of the central nervous system in low doses and as a general depressant in high doses, has a psychotropic (narcotic) effect, which is accompanied by suppression of excitation processes in the central nervous system due to changes in the metabolism of neurons, disruption of the function of neurotransmitter systems, and slowing down the processes of oxygen utilization. Metabolic toxicosis and acidosis (accumulation of ethanol biotransformation products) play a significant role in the pathogenesis. The main endogenous product is toxic acetaldehyde, which is formed during all types of oxidative degradation of ethyl alcohol. If aldehyde dehydrogenase (an enzyme involved in the metabolism of alcohol) does not have time to transform it into acetate, a picture of severe intoxication develops. Acetaldehyde disrupts the circulation of adrenaline and other catecholamines in the brain and in the periphery, affecting the cardiovascular system, liver, and kidneys. People of Asian descent are especially susceptible to the toxic effects of alcohol, since most of them have aldehyde dehydrogenase in an inactive form in their bodies. In such a situation, even small doses of alcohol can cause serious poisoning.

DIAGNOSTICS

DIAGNOSIS: HISTORY AND PHYSICAL EXAMINATION Alcohol poisoning develops in stages. The clinic depends on the dose (Table 9-7). Acute ethanol poisoning is said to occur when the condition of a person who has taken a large dose of alcoholic beverages sharply worsens, disturbances of consciousness appear, the ability to walk and perceive the environment is lost, stupor and coma occur.

Table 9-7. Stages of acute effects of alcohol (alcohol intoxication) in intolerant individuals (modified according to K.M. Dubovsky)

Blood alcohol concentration, % weight/volume

Alcohol exposure stage

Clinical manifestations

Sobriety

There is no obvious impact. For the average observer, the behavior is normal.

Subtle changes are detected by special tests

Mild euphoria, sociability, talkativeness Increased self-confidence; weakening of inhibitory reactions
Weakening of attention, prudence, self-control In tests - loss of ability to perform subtle operations

Excitation

Emotional instability; weakening of inhibitory reactions Loss of judgment

Weakening of memory and comprehension

Decreased sensory response; increased reaction time

Mild incoordination

Confusion

Disorientation, confusion; dizziness Increased emotionality (fear, anger, sadness, etc.)

Disorder of sensory functions (diplopia, etc.), perception of colors, shapes, movements, sizes

Increased pain threshold

Balance imbalance; quite pronounced disorder of motor coordination; unsteady gait; slurred speech

Apathy; general inertia, approaching paralysis. Noticeable weakening of the reaction to any stimuli.

Loss of coordination of movements; inability to walk and stand

Vomit; urinary and fecal incontinence

Clouding of consciousness; deep sleep or stupor

Complete loss of consciousness; anesthesiaSuppression or absence of reflexes

Decreased body temperature

Urinary and fecal incontinence

Circulatory and respiratory disorders

0.45 and above

Possibly fatal Death from paralysis of the respiratory muscles

The symptoms of alcoholic coma are nonspecific and are a variant of drug coma (see article “Coma”). Characterized by obstructive-aspiration disorders (retraction of the tongue, hypersalivation and bronchorrhea, aspiration of vomit), stridor, tachypnea, acrocyanosis, swelling of the jugular veins, possible coarse rales in the lungs, dilated pupils. Hypothermia is noted. In the absence of medical care, the main cause of death in the prehospital stage is respiratory disorders. Various severe complications may occur due to myocardial damage, including necrosis and acute cardiac death. In case of ethanol poisoning in children, in addition to loss of consciousness, acidosis, hypoglycemia (especially in children under 5 years of age) and hypokalemia come to the fore. Percutaneous intoxication has been described in young children when using alcohol compresses.

ADDITIONAL EXAMINATION

ADDITIONAL EXAMINATION ■ ECG: decreased ST segment, negative T wave, extrasystole; With alcoholic cardiomyopathy, persistent rhythm and conduction disturbances and signs of myocardial damage are possible. ■ During the first examination of the patient, it is advisable to take venous blood for subsequent chemical analysis for alcohol content, which may be required in the future (in the bottle or test tube there should be no free space between the blood and the stopper; otherwise, the result of the study will be underestimated due to with evaporation of alcohol).

DIFFERENTIAL DIAGNOSTICS

DIFFERENTIAL DIAGNOSTICS ■ TBI. The difficulty is that the likelihood of a TBI in a person in a state of deep alcohol intoxication is extremely high. Even if they fall out of the blue, due to lack of coordination, such persons receive severe head injuries. The diagnosis is helped by information received from others (it is important to compare the possible amount of alcohol consumed with the severity of the coma: a discrepancy may indicate a head injury), detection of damage to the soft tissues of the head, and anisocoria. ■ Stroke (acute cerebrovascular accident) can develop independently or be provoked by alcohol consumption (especially hemorrhagic stroke). The diagnosis is based on identifying focal neurological symptoms (see article “Stroke”). ■ Poisoning with alcohol substitutes, drugs, sleeping pills, tranquilizers or other substances, like ethanol, can cause coma (see below and the articles “Coma”, “Drug Poisoning”). ■ Variants of comatose states in diabetes mellitus, diabetic (ketonemic), hyperosmolar and hypoglycemic coma (see articles “Diabetic coma (diabetic ketoacidosis)”, “Hyperosmolar coma”). ■ Alcoholic ketoacidosis, which in turn must be differentiated from diabetic coma. It develops 24–72 hours after stopping alcohol at the end of a heavy binge. The patient complains of nausea, vomiting, abdominal pain, and refuses food. Hypovolemia increases rapidly. Confusion appears and coma develops. Tachypnea and even Kussmaul breathing have been reported as a response to ketoacidosis. Characteristic laboratory signs: normal or reduced blood glucose levels, ketonemia and ketonuria (due to the peculiar set of ketones before treatment - the predominance of β-hydroxybutyrate - the reaction to ketones when using indicator strips can be weakly positive, despite the abundance of ketones in the urine). Such patients are treated with complete restoration of bcc through dextrose infusion without insulin and saline solutions. Monitoring of electrolytes is mandatory, as hypokalemia is possible. Additionally, thiamine is prescribed. It must be borne in mind that as the patient’s condition improves, the reaction to ketones in the urine will become more and more pronounced (as a result of the oxidation of β-hydroxybutyrate to acetoacetate) - this should not be regarded as a sign of worsening pathology.

INDICATIONS FOR HOSPITALIZATION

TREATMENT INDICATIONS FOR HOSPITALIZATION Persons with severe alcohol intoxication accompanied by coma, respiratory and circulatory disorders are hospitalized. Victims are taken to the emergency room or poison control center.

TREATMENT MEASURES

TREATMENT MEASURES ■ Since the use of analeptic drugs for ethanol poisoning is contraindicated (due to the risk of developing a convulsive syndrome; there is only insufficiently confirmed clinical data on the possible use of flumazenil - 3 mg intravenously), in all cases accompanied by pronounced respiratory and circulatory disorders, it is necessary to resort to resuscitation benefits. It is very likely that breathing will stop while cardiac activity continues. The onset of clinical death requires the implementation of the entire complex of cardiopulmonary resuscitation. ■ Basic resuscitation will be greatly facilitated by the presence of electromechanical or mechanical suction, since the victim usually has profuse salivation and bronchorrhea if dehydration has not yet developed.

■ Gastric lavage through a tube is necessary, but is possible only after ensuring complete protection of the respiratory tract by intubation, which is carried out by a resuscitator on site or already in the hospital. In this regard, all activities in the first stage of assistance must be carried out very quickly.

DRUG THERAPY

DRUG THERAPY ■ At the stage of providing first qualified medical aid, you can begin to implement forced diuresis. To do this, infusion therapy is started through venous access and furosemide is administered (see the article “Poisonings, general aspects”). ■ Maintenance therapy for ethanol poisoning includes the use of dextrose solutions without soluble insulin (if the victim does not suffer from diabetes) to prevent hypoglycemia and ketoacidosis. ■ Parenteral preparations of potassium, magnesium, thiamine, pyridoxine, ascorbic acid, etc. are also indicated. ■ As an auxiliary measure, it may be necessary to use atropine (1 ml of 0.1% solution subcutaneously) to reduce hypersalivation and bronchorrhea. ■ Severe hemodynamic disorders accompanied by arterial hypotension require, in addition to the administration of additional fluid, the use of catecholamines (see articles on shock) and possibly prednisolone at a dose of 90-120 mg intravenously.

POSSIBLE COMPLICATIONS

POSSIBLE COMPLICATIONS ■ Periods of psychomotor agitation with short episodes of auditory and visual hallucinations (during recovery from an alcoholic coma). ■ Aspiration of stomach contents with the development of atelectasis and a full-blown picture of Mendelssohn’s syndrome (asthma-like condition and pulmonary edema that occurs 2–5 hours after aspiration).

PROGNOSIS The prognosis depends not so much on the dose of alcohol, but on the timeliness of assistance provided (98–99% of deaths occur in the prehospital stage). In chronic alcoholics whose poisoning occurs against the background of encephalopathy, hormonal changes, cardiomyopathy, kidney, liver, lung damage, hypomagnesemia, hypovitaminosis, it is logical to expect a more severe clinical picture and a worse prognosis.

Poisoning with alcohol surrogates is a type of intoxication caused by the consumption of low-quality alcoholic beverages containing technical compounds or toxic impurities. Often occurs in people suffering from addiction or teenagers who want to get drunk and at the same time purchase a product at a low price. Accompanied by disorders of the digestive, nervous, and cardiovascular systems. There is a high probability of death and therefore requires emergency care and urgent hospitalization in the toxicology department. It has its own ICD 10 code - T51.

What applies to alcohol surrogates?

According to the classification, they are divided into two groups: true and false. The first include alcoholic drinks that contain ethanol, but also toxic impurities: ethers, heavy metals, harmful dyes. The second type includes those products based on any other alcohol: methyl, isopropyl and others. Poisoning in this case is much more severe, since not only the metabolites are considered poisonous, but also the main compound.

Surrogate substitutes are usually drunk by people suffering from alcoholism and teenagers who do not have the means to purchase high-quality but expensive products. The following compounds are considered to be the causes of intoxication:

TOXINS lead to cancer, blood and vascular diseases, heart disease and many others, including common chronic diseases and colds.

  • denatured alcohols;
  • polishes;
  • wood stain;
  • medicinal medicines (tinctures);
  • cosmetical tools;
  • household supplies in the form of solutions, aerosols;
  • moonshine.

Poisoning due to drinking brake fluid, de-icers and other similar substances also occurs.

Clinical picture of intoxication

Signs of the disease are different, varying depending on what the patient took. The manifestations of pathology when drinking a certain chemical component are described in detail below.

Surrogates containing ethyl alcohol

The first thing the victim feels is euphoria and emotional excitement, which is achieved during the gatherings. Further, the clinic is supplemented by the following symptoms:

  • excessive sweating;
  • increased production of saliva in the oral cavity;
  • pale skin;
  • increase in pupil diameter;
  • dizziness;
  • impaired coordination of movements;
  • nausea;
  • vomit;
  • diarrhea;
  • pain in the abdomen.
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A change in consciousness, the appearance of delusional disorders, and hallucinations are possible.

Methanol (wood alcohol)

They are more toxic; death is possible when consuming fifty milliliters of the surrogate, however, it all depends on the sensitivity of the victim’s body. Signs of poisoning are:

  • depressive syndrome;
  • nausea;
  • vomit;
  • decreased visual acuity up to its complete loss;
  • increase in body temperature;
  • convulsions;
  • weakness;
  • disturbance of consciousness, its absence.

Disorders of the cardiovascular system are often a concern, namely tachycardia, arterial hypotension, and chest pain.

Symptoms of ethylene glycol poisoning

The clinic is divided into three periods. At first, the patient does not present any complaints, feeling only mild euphoria. Further, after 10–12 hours, signs such as:

  • unbearable thirst;
  • nausea;
  • dry mucous membranes;
  • headache;
  • cyanosis;
  • vomiting that does not bring relief;
  • convulsive syndrome.

If proper measures are not taken, renal, liver or heart failure develops on the second or third day. The skin becomes yellow and the volume of urine produced decreases. The man dies in agony.

Diagnosis of intoxication

Must be organized immediately.

The doctor initially collects an anamnesis of the disease, life, conducts a general examination, pays special attention to the smell of the mouth, the consciousness of the victim, and the skin. Afterwards, laboratory and instrumental examination methods are prescribed. The most informative are:

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  • general urine analysis;
  • general and biochemical blood test;
  • electrocardiogram;
  • Ultrasound of the abdominal cavity, heart;
  • CT and MRI;
  • electroencephalogram.

An ECG is usually performed by emergency medical services doctors, which makes it possible to identify disorders that threaten the patient’s life and stop them in a timely manner.

First aid

Carrying out manipulations in the early stages of poisoning with alcohol surrogates will avoid the formation of complications and death. The algorithm of actions includes the following points:

  • gastric lavage with soda solution and pressing on the root of the tongue;
  • sorbent intake;
  • use of saline laxatives;
  • calling a doctor for emergency hospitalization.

During the procedures, it is prohibited to give additional medications; the course of poisoning may worsen.

Antidote

It all depends on what kind of surrogate the person accepted. If intoxication is caused by the true type, then the condition is relieved with the help of pyrazole derivatives. In cases where the disease has developed due to methyl alcohol, ethanol is administered intravenously.

Treatment methods

Therapy is prescribed by a narcologist after a complete examination. The main purpose of taking medications is to detoxify the body, reduce clinical manifestations and reduce the risk of complications.

In most cases, the following groups of drugs are prescribed:

  • saline solutions;
  • diuretics;
  • nootropics;
  • neuroleptics;
  • vitamins;
  • sorbents;
  • antacids;
  • analgesics;
  • antispasmodics.

Treatment is sometimes supplemented with glucocorticoids, beta-blockers, and atropine. Mechanical blood purification is possible using hemodialysis and plasmaphresis. The patient's rehabilitation takes place at home within one month.

Possible consequences

According to statistics, with timely diagnosis and adequate therapy, the prognosis is favorable. Otherwise, complications develop such as:

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  • blindness;
  • cerebral edema;
  • renal, liver failure;
  • mental disorders;
  • acute alcoholic hepatitis;
  • pancreatitis;
  • hypovolemic shock;
  • acidosis.

The most terrible consequence of poisoning with a surrogate is death.

Prevention

  • purchase products in specialized trusted stores;
  • comply with storage and transportation conditions;
  • reduce the amount of alcoholic beverages consumed.

If you buy alcohol, don't skimp. Champagne for 150 rubles or cognac for 300 is most likely not made from the best raw materials and not under the best conditions.

Summary

Such pathologies, unfortunately, occur constantly in medical practice, and their frequency increases every year. If previously everything was attributed to illiteracy of the population and low financial income, now poisoning from even “elite” alcoholic beverages cannot be ruled out. This is why doctors recommend not to drink at all, and if you do drink alcohol, then only high-quality alcohol purchased from trusted outlets.

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Intoxication with alcohol substitutes

Poisoning with alcohol surrogates ranks first among all intoxications with which victims go to medical institutions. This is a very dangerous phenomenon that can not only provoke serious complications, but also lead to death. Poisoning with alcohol substitutes - ICD 10 code:

  • T51.0 - ethyl alcohol;
  • T51.1 - methyl alcohol;
  • T51.2 - isopropyl alcohol;
  • T51.3 - fusel oils;
  • T51.8 - other alcohols;
  • T51.9 - alcohol, unspecified.

Classification of surrogates

The toxicology of poisoning by alcohol and its surrogates distinguishes two types of substances: those produced on the basis of ethanol and those produced using impurities. The first group includes the following:

  1. ethanol produced by hydrolysis from wood;
  2. denatured alcohol;
  3. cosmetic lotions, cologne;
  4. BF glue - the composition includes polyvinyl acetal, phenol-formaldehyde resin, dissolved in acetone, alcohol;
  5. polish - a mixture of ethanol with butyl, amyl, acetone;
  6. nigrosin is a stain containing ethanol and dyes. It is used for processing wood and dyeing leather products blue.

The second type includes chemicals that do not contain ethanol. They are made using ethylene glycol, methyl alcohol with the addition of various impurities.

Symptoms

Symptoms of poisoning with various alcohol substitutes differ from each other. If any signs of intoxication with a dangerous substitute for alcoholic beverages occur, you must immediately contact a medical institution for professional help. Otherwise, everything could end badly.

Surrogate with ethanol

Ethyl alcohol is a substance found in any alcoholic drink. Ethanol poisoning is accompanied by the following symptoms:

  • Gastrointestinal tract: pain in the abdomen, feeling of nausea, vomiting, abnormal stool;
  • Central nervous system: severe excitability, feeling of euphoria, dilated pupils, auditory and visual hallucinations, incoherent speech (resembling the speech of a mute), loss of coordination of movements, increased sweating;
  • cardiovascular system: weakness, redness or pallor of the skin on the face, rapid pulsation, reduced intravenous pressure;
  • respiratory organs: acute respiratory failure, shortness of breath;
  • kidneys: frequent urination or stopping;
  • liver: pain on the right side in the ribs, yellowness of the skin.

Severe poisoning by surrogates can cause coma.

Ethyl alcohol, after entering the body, is absorbed into the walls of the gastrointestinal tract. With the flow of blood fluid, it quickly spreads throughout the body. With small doses of ethanol, the liver is able to cope with its processing. If ethyl alcohol is consumed in large quantities, the organ ceases to perform its functions and poisoning occurs with dangerous alcohol substitutes.

Methanol

The kidneys and central nervous system are most affected by methyl alcohol. It has a psychotropic, neurotoxic effect. The following signs of intoxication with surrogate alcohol occur:

  • feeling of nausea, vomiting;
  • “dots” before the eyes;
  • double vision;
  • in acute situations - complete blindness;
  • dilated pupils;
  • lack of reaction to light.

After a couple of days, the clinical picture worsens. Pain syndrome occurs throughout the body. There is dryness of the mucous membranes and skin. The functionality of the cardiac organ is impaired, intravenous pressure is reduced. The temperature is very high. Convulsions and coma may occur.

Ethylene glycol

This substance is included in the components of brake fluids and antifreezes. Intoxication causes acute liver failure and cerebral edema. The following toxicological symptoms are observed:

  • in the first 12 hours only mild intoxication is observed;
  • after this, nausea, vomiting, migraine, and bowel movements begin;
  • cyanosis of the skin, mucous membranes;
  • high body temperature;
  • heart rhythm disturbance;
  • severe excitability;
  • difficulty breathing;
  • loss of feelings;
  • convulsions;
  • dark color of urine.

If urgent necessary assistance is not provided in case of poisoning with alcohol substitutes, death will occur.

Moonshine

When intoxicated with moonshine, the following symptoms occur:

  • feeling of nausea, vomiting, stool disorders;
  • dizziness, up to loss of consciousness;
  • increased body temperature;
  • severe thirst, dry mouth;
  • labored breathing;
  • surges in intravenous pressure;
  • chills, increased sweating.

In severe cases, seizures may occur. The victim loses his vision. First, visual and auditory hallucinations occur. After this, the person may fall into a coma.

Diagnostic tests

Before prescribing adequate treatment, the specialist performs a full examination of the victim. First of all, he conducts a visual inspection. After this, he collects an anamnesis of the pathology: the stage of alcoholism, substances used, the presence of concomitant diseases, etc.

Additional diagnostic methods are also prescribed. This is necessary to study the heart rhythm and the amount of toxic element in the blood. Research is complicated by the fact that those who have been poisoned most often end up in the clinic already in a coma. But modern medicine does not stand still; with properly provided first aid and modern hospitalization, the patient can be saved.

Emergency measures

Timely first aid can save a person’s life. Therefore, it is necessary not to get confused in an emergency situation and do everything right. First of all, call a team of medical workers, and then proceed to action:

  1. Provide air supply to the victim. To do this, open all windows and vents. If possible, take the patient out into the fresh air. Unbutton your collar, remove your tie, belt, and corset.
  2. Lay the victim on a horizontal surface on his side. Extend your lower arm forward. Make sure that the poisoned person does not choke on the escaping liquid or choke on his own tongue.
  3. If the patient is conscious, he needs to perform gastrointestinal lavage. To do this, give the poisoned person to drink plenty of liquid. After this, provoke a gag reflex by pressing on the beginning of the tongue with your fingers or a spoon. Repeat this action until the escaping liquid becomes clear. The stomach is washed well with water-salt, slightly pink potassium permanganate solutions.
  4. If the victim is unconscious, bring a cotton pad soaked in ammonia to his nose. Rubbing your earlobes and tickling the tip of your nose will also help you come to your senses.
  5. After the release of vomit, the water-salt balance is disrupted. To bring it back to normal, it is necessary to give the patient sorbents. For example, activated carbon.
  6. If the patient is poisoned as a result of taking ethylene glycol or methyl alcohol, give the victim a little vodka or other high-quality alcoholic drink.
  7. If the victim is cold, wrap him in a blanket.

If the heartbeat and breathing stop, it is necessary to perform an indirect massage of the cardiac organ and perform artificial ventilation.

What not to do

In case of a pathological condition, it is prohibited to do the following:

  • turn a person upside down;
  • place the victim under a cold shower or in a bathtub;
  • force the patient to be physically active;
  • provoke vomiting if the poisoned person is in an unconscious state;
  • give any medications, with the exception of sorbents;
  • leaving a person alone, unattended;
  • refuse hospitalization in a hospital, even if the victim feels better.

If this is not taken into account, the patient may be harmed.

Therapy

Treatment measures are carried out in a hospital setting, in the intensive care ward in the toxicology department. Treatment of acute poisoning with alcohol surrogates should be carried out under the round-the-clock supervision of medical workers.

  1. In the hospital, the body is detoxified using a special probe. Alcohol 5% is introduced. Diuretics are prescribed and the blood fluid is cleared.
  2. For ethylene glycol intoxication, calcium gluconate is prescribed. They use a solution of glucose with novocaine, vitamin complexes B and C. In case of poisoning with methyl alcohol, spinal punctures are performed.
  3. After cleansing the body, a special diet must be followed. Meals should be light and balanced. There is a complete abstinence from alcoholic products, even good quality ones.

Consequences

Alcohol addiction is a serious disease that must be treated. Otherwise, regular intoxication with alcohol and its surrogates can lead to serious consequences, including death:

  • acute hepatitis;
  • pancreatitis;
  • cirrhosis of the liver;
  • liver failure;
  • the occurrence of thoughts of suicide;
  • vascular-vegetative disorders;
  • loss of vision;
  • hand tremors and other severe pathologies.

If you cannot get rid of alcoholism on your own, contact a drug treatment clinic for help. They will not only cleanse the body, but also help cope with addiction on a psychological level.

Treatment

Therapy is prescribed by a narcologist after a complete examination. The main purpose of taking medications is to detoxify the body, reduce clinical manifestations and reduce the risk of complications.

In most cases, the following groups of drugs are prescribed:

  • saline solutions;
  • diuretics;
  • nootropics;
  • neuroleptics;
  • vitamins;
  • sorbents;
  • antacids;
  • analgesics;
  • antispasmodics.

Treatment is sometimes supplemented with glucocorticoids, beta-blockers, and atropine. Mechanical blood purification is possible using hemodialysis and plasmaphresis. The patient's rehabilitation takes place at home within one month.

The effectiveness of treatment and the overall prognosis for the victim will depend entirely on the dose of surrogate taken and on the timeliness of medical care. In addition, an important factor is the initial physical condition of the patient.

Thus, chronic alcoholics are more difficult to tolerate the toxic effects of surrogates. However, the consequences for both can be the same - from loss of vision and paralysis to death due to kidney or liver failure.

In general, in a hospital a number of specific measures are applied to the victim. Emergency care for poisoning looks like this:

  • Tube gastric lavage. Indicated if the victim is conscious.
  • Taking sorbents to bind and remove toxins.
  • Administration of intravenous antidotes. In most cases, ethanol is used. In the case of ethylene glycol poisoning, calcium gluconate is used as an antidote.
  • Increasing diuresis for rapid elimination of toxins through the kidneys (indicated only if the kidneys are functioning normally).
  • Introduction of vitamins B and C into the body. Having been poisoned, a person loses all electrolytes, minerals and vitamins, which requires restoring their balance.

    At the primary health care stage, it is recommended to normalize impaired breathing and restore or maintain adequate hemodynamics (see 3.1 “Treatment of hemodynamic disorders.”

Conviction level: D (level of evidence: 4)

  1. in cases of aspiration-obstructive breathing disorders, oral toileting is recommended; atropine** (1–2 ml of 0.1% solution) is administered subcutaneously to reduce hypersalivation and bronchorrhea;
  2. in case of superficial coma - aspiration of the contents of the upper respiratory tract is carried out using an air duct;
  3. in case of deep coma, tracheal intubation is performed.
  4. in case of central respiratory failure, artificial ventilation of the lungs is necessary after preliminary tracheal intubation.
  5. in case of a mixed form of disorders, aspiration-obstructive breathing disorders are first eliminated, and then artificial ventilation is connected.
  6. oxygen inhalation is indicated.
  7. to resolve atelectasis - performing sanitation FBS.

    In case of severe hemodynamic disorders, anti-shock therapy is recommended: plasma-substituting solutions intravenously, saline solutions and glucose solutions.

    After relief of respiratory failure and associated hypoxia, the use of succinic acid preparations (meglumine sodium succinate solution** - 1.5% - 400.0) and cardiovascular drugs in therapeutic doses (cordiamin, caffeine) is recommended.

    It is recommended to correct the water-electrolyte balance with crystalloid, colloid solutions and glucose under the control of pulse, blood pressure (BP) and central venous pressure (CVP), cardiac index, total peripheral resistance, hematocrit, hemoglobin and electrolyte concentrations, as well as diuresis.

    General hypothermia of the body is below a critical level in persons with alcoholic coma who were outside closed heated rooms during the cold season;

    Chronic alcohol intoxication in the terminal stage with signs of multiple organ failure (liver, cardiovascular, metabolic disorders) alcoholic cardiomyopathy;

    Acute alcoholic delirium against the background of chronic alcohol intoxication, which develops almost immediately after the patient emerges from an alcoholic coma, is dangerous due to complications (pnemonia, cerebral edema, acute cardiovascular failure.

    Order No. 520n of the Ministry of Health of the Russian Federation dated June 15, 2016 “On approval of criteria for assessing the quality of medical care, clause 3.13.6;

    Toxic effects of substances, mainly for non-medical purposes (T51-T65) / World Health Organization // International statistical classification of diseases and health problems. Tenth revision. Volume 1 (part 2).- M.: Medicine, 1995.- P. 337-344.;

    Order of the Ministry of Health of the Russian Federation No. 925n dated November 30, 2012 “On approval of the procedure for providing medical care for acute chemical poisoning”;

    Order of the Ministry of Health of the Russian Federation dated October 5, 1998 No. 298 “On the analytical diagnosis of narcotic drugs, psychotropic and other toxic substances in the human body”;

    Order of the Ministry of Health of the Russian Federation dated January 27, 2006 No. 40 “On the organization of chemical and toxicological studies for analytical diagnostics of the presence of alcohol, narcotic drugs, psychotropic and other toxic substances in the human body.”

Chronic alcohol intoxication is poisoning of human organs by the breakdown products of alcohol when consumed in excessive doses. There may not be any alcohol dependence. In contrast to the long-term negative effects of alcohol on the body during alcoholism, chronic intoxication is caused even by irregular drinking, if the doses of alcohol are large enough.

TREATMENT Management tactics (see Nonspecific drug therapy (see also Poisoning, general provisions) For acidosis - 4% sodium bicarbonate solution IV up to 1,000–1,500 ml/day For agitation and convulsions - 10 ml 25% solution magnesium sulfate intramuscularly Prednisolone, thiamine, trifosadenine, ascorbic acid, glucose-procaine mixture (200 ml of 40% glucose solution and 20 ml of 2% procaine solution) intravenously.

Mild intoxication does not require medical attention. The patient should be allowed to sleep, after which his condition will return to normal.

In case of moderate and severe poisoning, assistance is provided according to the following algorithm:

  • stabilization of condition;
  • gastric lavage;
  • detoxification of the body;
  • combating complications and symptomatic treatment.

Treatment of alcohol intoxication at home is possible only if the victim is conscious, does not turn blue, breathes well and does not show signs of severe toxic effects of ethanol (shortness of breath, decreased blood pressure, severe abdominal pain, low body temperature, etc.).

Stabilization of condition

Measures to stabilize the patient's condition are aimed primarily at restoring adequate spontaneous breathing. To do this, using an electric suction, residual vomit, saliva and sputum are removed from the upper respiratory tract.

In the absence of the necessary equipment, the procedure is carried out by wrapping a bandage or napkin around two fingers and thus cleaning the oral cavity. In case of severe breathing disorders of the central type, the patient is intubated and transferred to mechanical ventilation. As a rule, this only happens during a deep alcoholic coma.

The level of hypersalivation can be reduced by subcutaneous administration of atropine sulfate (0.5-1 ml). It should be remembered that the drug can significantly increase the heart rate and provoke mental agitation. The latter is treated with the use of chlorpromazine, haloperidol, and relanium.

Low blood pressure is corrected by prescribing vasopressors to the victim. With a slight decrease in blood pressure, caffeine and mesaton are injected under the skin in a dose of 0.5 ml. Coma in combination with significant hypotension is an indication for drip intravenous administration of dopamine, norepinephrine, and mesatone.

Gastric lavage

Gastric lavage can be done at home or in a hospital setting. At home, the victim is given 0.5-1 liter of water to drink, after which they induce vomiting. The procedure is repeated several times.

For rinsing, you can use clean water, water with the addition of activated carbon powder or sodium bicarbonate (baking soda). Gastric lavage in this way is possible only if the patient’s consciousness and ability to swallow are preserved.

In the hospital and at the EMS stage, lavage is carried out through a thick gastric tube. The latter is inserted into the stomach through the mouth, and after the procedure is removed.

Alcohol surrogates are alcohol-based liquids not intended for oral consumption. When consuming alcohol substitutes, poisoning develops, which often leads to death.

Alcohol surrogates are considered to be liquids containing alcohol that are not drinks. Once in the human body, they cause intoxication with serious health consequences.

Ethyl alcohol may or may not be present in surrogates. The group containing ethanol includes:

  • Butyl alcohol.
  • Wood alcohols.
  • Denatured alcohol.
  • Colognes.
  • Varnish.
  • Stain.

Surrogates are much more toxic than alcohol. Thus, wood alcohols contain methanol, denatured alcohol contains aldehyde, and the polish contains a whole combination of different toxic alcohols. The stain contains chemical dyes, which, when entering the body, cause the skin and mucous membranes to turn blue.

The second group includes “false surrogates”:

  • Methanol.
  • Ethylene glycol.
  • Isopropanol
  • BF glue.
  • Dichloroethane.

Toxic doses

Alcohol surrogates are dangerous because even a small amount of these liquids, when entering the body, provokes death.

Their toxic doses for the development of acute poisoning vary depending on the composition:

  • methanol - 7-8 ml.;
  • ethylene glycol - 50 ml.;
  • polish - 50 ml;
  • acetone - 30 ml;
  • isopropanol - 0.5 - 2 ml/kg;
  • BF glue - 20-50 ml.;
  • dichloroethane - 5 ml.

Methanol in the human body breaks down into formic acid and formaldehyde. These substances are very toxic and cause serious damage to the central nervous system. 7 ml. enough for acute poisoning with fainting and loss of vision. 50 g cause lightning death.

Poisoning with alcohol surrogates is very dangerous, as it is often accompanied by severe pathological damage to the liver, kidneys, and central nervous system. Such lesions often result in the death of the poisoned person.

Some poisonings are associated with the consumption of low-quality alcohol, but in most cases, poisoning with alcohol substitutes occurs in chronic alcoholics who use household chemicals, medicinal liquids and industrial alcohols.

Classification of alcohol surrogates

What are alcohol surrogates? These are liquids that contain alcohol and are used in everyday life and for technical needs. They are consumed for the purpose of intoxication when regular alcoholic drinks are not available. The group of alcohol surrogates also includes low-quality/counterfeit wine, cognac, vodka and other types of alcoholic beverages.

Treatment begins with urgent gastric lavage and administration of sodium sulfate through a tube. In case of methanol poisoning, the patient is given ethanol (antidote) orally or a 2-5% alcohol solution is administered intravenously.

In case of poisoning with substances containing ethylene glycol, a sodium bicarbonate solution administered orally or intravenously is used to eliminate acidosis. The tactics of further treatment for poisoning by true surrogates are determined by the identified violations of various organs and systems.

All patients undergo detoxification therapy, are prescribed vitamins, nootropics, etc.

In case of poisoning with alcohol surrogates containing methanol, prednisolone, atropine, ATP and lumbar punctures are used to correct visual impairment. In case of ethylene glycol poisoning, the first priority is to combat kidney damage.

Patients are prescribed diuretics, plenty of fluids, and magnesium sulfate. The water-salt balance is corrected.

In severe cases, hemodialysis or peritoneal dialysis is performed. The prognosis for poisoning with alcohol surrogates is determined by the type and amount of liquid taken.

After consuming true surrogates, death rarely occurs; long-term consequences are possible as a result of damage to internal organs. As a result of taking substances containing methanol and ethylene glycol, death is often observed, and many surviving patients become disabled.

Titles

Alcohol poisoning.

Titles

Russian name: Piracetam.
English name: Piracetam.

Latin name

Piracetamum (Piracetami).

Chemical name

2-Oxo-1-pyrrolidinacetamide.

Pharm Group

Nootropics.

Nosologies

A89 Viral infection of the central nervous system, unspecified.
D57 Sickle cell disorders.
F00 Dementia due to Alzheimer's disease (G30).
F01 Vascular dementia.
F03 Dementia, unspecified.
F04 Organic amnesic syndrome not caused by alcohol or other psychoactive substances.
F05 Delirium not caused by alcohol or other psychoactive substances.
F06.7 Mild cognitive impairment.
F07.1 Postencephalitic syndrome.
F07.2 Post-concussion syndrome.
F07.9 Organic disorder of personality and behavior due to disease, damage or dysfunction of the brain, unspecified.
F09 Organic or symptomatic mental disorder, unspecified.
F10.2 Alcohol dependence syndrome.
F10.3 Withdrawal state.
F10.4 Withdrawal state with delirium.
F10.5 Alcoholic psychosis.
F11 Mental and behavioral disorders caused by opioid use.
F13 Mental and behavioral disorders caused by the use of sedatives or hypnotics.
F29 Inorganic psychosis, unspecified.
F32 Depressive episode.
F34.1 Dysthymia.
F41.2 Mixed anxiety and depressive disorder.
F48.0 Neurasthenia.
F60.3 Emotionally unstable personality disorder.
F63 Disorders of habits and inclinations.
F79 Mental retardation, unspecified.
F80 Specific developmental disorders of speech and language.
F90.0 Impaired activity and attention.
F91 Behavioral disorders.
G21.8 Other forms of secondary parkinsonism.
G25.3 Myoclonus.
G30 Alzheimer's disease.
G40.9 Epilepsy, unspecified.
G46 Vascular cerebrovascular syndromes in cerebrovascular diseases.
G80 Cerebral palsy.
G93.4 Encephalopathy, unspecified.
H55 Nystagmus and other involuntary eye movements.
I61 Intracerebral hemorrhage.
I63 Cerebral infarction.
I67.2 Cerebral atherosclerosis.
I69 Consequences of cerebrovascular diseases.
P15 Other birth injuries.
P91 Other disorders of cerebral status in a newborn.
R26.8 Other and unspecified disorders of gait and mobility.
R40.2 Coma, unspecified.
R41.0 Disorientation, unspecified.
R41.3. 0* Memory loss.
R41.8. 0* Intellectual-mnestic disorders.
R42 Dizziness and loss of stability.
R45.1 Restlessness and agitation.
R46.4 Lethargy and slow reaction.
R47.0 Dysphasia and aphasia.
R51 Headache.
R53 Malaise and fatigue.
R54 Old age.
S06 Intracranial injury.
T40 Poisoning with drugs and psychodysleptics [hallucinogens].
T42.3 Barbiturate poisoning.
T51 Toxic effects of alcohol.
Z55 Problems related to learning and literacy.

CAS code

Characteristics of the substance

Cyclic derivative of GABA.

Pharmacodynamics

Pharmacological action - nootropic.
Pharmacodynamics.

Improves connections between the cerebral hemispheres and synaptic conduction in neocortical structures, improves cerebral blood flow.
It has an effect on the central nervous system in various ways: it modifies neurotransmission in the brain, improves metabolic conditions that promote neuronal plasticity, improves microcirculation, affecting the rheological characteristics of the blood and without causing vasodilation.
In case of cerebral dysfunction, it increases concentration and improves cognitive functions, including learning ability, memory, attention and consciousness, mental performance, without having a sedative or psychostimulating effect. The use of piracetam is accompanied by significant changes in the EEG (increased α- and β-activity, decreased δ-activity).
Helps restore cognitive abilities after various cerebral injuries due to hypoxia, intoxication or electroconvulsive therapy.
Indicated for the treatment of cortical myoclonus both as monotherapy and as part of complex therapy.
Reduces the duration of vestibular neuronitis and nystagmus.
The hemorheological effects of piracetam are associated with its effect on red blood cells, platelets and the vascular wall.
In patients with sickle cell anemia with pathological rigidity of red blood cells, piracetam restores the elasticity of the red blood cell membrane, increases their ability to deform and filter, reduces blood viscosity and prevents the formation of coin columns. In addition, it inhibits increased aggregation of activated platelets without significantly affecting their number. At a dose of 9.6 g, it reduces the level of fibrinogen and von Willebrand factor by 30–40% and prolongs bleeding time.
Animal studies have shown that piracetam inhibits vasospasm and counteracts various vasospastic substances.
In studies on healthy volunteers, piracetam reduced the adhesion of red blood cells to the vascular endothelium and stimulated the production of prostacyclins in the endothelium.

Definition and general information [edit]

Acute alcohol intoxication (without consequences and development of the disease).

Etiology and pathogenesis[edit]

Types of alcohol intoxication

1. Simple alcoholic intoxication.

Alcohol intoxication with hebephrenic features;

Alcohol intoxication with hysterical features.

2. Pathological intoxication.

Clinical manifestations[edit]

Acute alcohol intoxication: Diagnosis[edit]

- impaired concentration;

Narrowing of mental capabilities;

Decrease in mental and production productivity.

Negative Romberg test;

A thorough somatoneurological examination of the patient is necessary, taking into account the possibility of injuries and infections. The patient should always be assessed for possible multi-substance toxicity.

Differential diagnosis[edit]

Acute alcohol intoxication: Treatment[edit]

Indications for hospitalization

1. Presence of convulsive phenomena.

2. Associated acute consequences of TBI.

4. High temperature.

5. Physical exhaustion or dehydration.

7. Severe depression or obvious risk of suicidal behavior.

Therapeutic measures include monitoring the patient, symptomatic therapy, and, if necessary, parenteral nutrition.

Bibliography

BP - blood pressure

ADH – alcohol dehydrogenase

ALAT – alanine transferase

ACAT – aspartate transferase

GGTP – gamma-glutamyl transpeptidase

GGTP – gamma-glutamyltransferase

HD - hemodialysis

HDF - hemodiafiltration

GLC – gas-liquid chromatography

Gastrointestinal tract - gastrointestinal tract

IVL - artificial lung ventilation

AOS – acid-base state

CT – computed tomography

CPK - creatine phosphokinase

LDH – lactate dehydrogenase

ICD10 – international statistical classification classification of diseases and health-related problems, tenth revision

MRI – magnetic resonance imaging

ARDS – acute respiratory distress syndrome

ICU - intensive care unit

PZh – gastric lavage

Ultrasound – ultrasound examination

FBS – fibrobronchoscopy

FD – forced diuresis

CVP - central venous pressure

ALP – alkaline phosphatase

ES – ethyl alcohol

EGDS – esophagogastroduodenoscopy

ECG – electrocardiography (cardiogram)

EEG – electroencephalography

EAPCCT – European Association of Poison Centers and Clinical Toxicologists

LD – lethal (lethal) dose

Rg – radiograph

Terms and Definitions

In response to the question “what is surrogate alcohol,” it is worth conveying to the reader the information that surrogate alcoholic beverages are considered to be those that were produced in an artisanal way in violation of the recipe or those that have expired their shelf life/sales.

Such alcohol is so toxic to the human body that in ICD 10 (the international classification of diseases) such conditions have their own code. In particular, it is poisoning of this type that is indicated by coding in the T51 range.

Moreover, according to ICD-10, each component, which is the main active ingredient in a surrogate drink, is classified with certain codes.

All low-quality (surrogate) alcoholic drinks can be divided into two main groups:

  • Alcohol containing ethyl alcohol and its derivatives. These include drinks based on butyl alcohol (lethality within an hour when taking 30 ml), sulfite and hydrolytic alcohol, technical alcohol or denatured alcohol. Also included in this category are all lotions/colognes/varnishes and stains. In the latter case (when using stain), the patient’s skin and mucous membranes become blue.
  • False surrogate. This is the most dangerous category of low-quality alcoholic beverages for human life. To reduce the cost of alcohol production, methyl alcohol or ethylene glycol is used here instead of ethanol. Both lead to paralysis or death of a person.

0 Thus, the term alcohol is essentially used as a synonym for alcoholic beverages.

Alcohol intoxication is a phrase that characterizes a health disorder caused by excessive consumption of alcoholic beverages. Historically, the term “alcohol intoxication” is used by medical specialists of various profiles, including toxicologists, psychiatrists and narcologists (mainly), and forensic doctors.

Currently, the concept of “alcohol intoxication” is present in ICD10 under code F10 - Mental and behavioral disorders caused by alcohol consumption, including: F.10. 0 “Acute intoxication” – like acute intoxication in alcoholism and alcohol intoxication.

At the same time, it is customary to distinguish the following clinical forms: acute alcohol intoxication: simple alcohol intoxication; altered forms of alcohol intoxication; pathological intoxication; chronic alcoholism stages 1, 2, 3; alcoholic psychoses (alcoholic delirium, acute alcoholic hallucinosis, acute alcoholic paranoid, etc.).

“Chronic alcohol intoxication” characterizes a disease that has developed as a result of prolonged alcohol abuse and is not accompanied by coma (with the exception of the terminal stage of multiple organ failure).

This disease is more characterized by various behavioral and mental disorders. Substitution of the concepts “alcohol intoxication”, “acute alcohol intoxication” and “alcohol poisoning” often leads to incorrect diagnosis, hospitalization and treatment of the victim.

Alcoholic coma is a coma that develops as a result of consuming ES predominantly in the form of alcoholic beverages in a toxic/lethal dose with the appearance of a toxic/lethal concentration of ethanol in the blood.

Alcohols are a large and highly diverse class of organic compounds: they are widespread in nature, have critical industrial importance, and have exceptional chemical properties.

Aliphatic saturated alcohols with a long chain of up to 5 carbon atoms (methyl, ethyl, propyl, butyl and amyl) are of greatest toxicological importance.

The toxic effect of alcohol (according to the formulation of ICD10) implies a health disorder caused by the ingestion of one or more representatives of this group and is interpreted as acute poisoning.

At the same time, from the point of view of clinical characteristics, the predominant value, both in terms of the frequency of occurrence of this pathology and in terms of medical consequences, is the leading one - poisoning with ES (ethanol) or the commonly used concept - alcohol poisoning, which, from the point of view of toxicologists, is a disorder of consciousness (coma) caused by excessive immediate intake of ethanol.

Poisoning with other alcohols of this group can manifest itself with various symptoms while consciousness is preserved.

Considering the higher toxicity and specificity of clinical manifestations and complications, these recommendations do not consider the toxic effect (poisoning) of methanol (methyl alcohol), which is highlighted in separate clinical recommendations.

Surrogate alcoholic products are considered to be those drinks that are not originally intended for drinking. Conventionally, they can be divided into 2 groups.

First group

Short description

Acute alcohol (ethanol) poisoning is usually associated with ingestion of ethyl alcohol or drinks containing more than 12% ethyl alcohol. The lethal concentration of ethanol in the blood is 5–8 g.l, the lethal single dose is 4–12 g.kg (300–500 ml of 96% ethanol); however, this rate varies between patients and often depends on acquired tolerance to alcohol.

Acute alcohol poisoning is most widespread in countries of northern and middle latitudes.

Frequency. 25% of all acute poisonings. More than 60% of all fatal poisonings are caused by alcohol. The predominant gender is male. Risk factors Alcoholism (about 90% of those hospitalized with acute alcohol poisoning are alcoholic) Drinking alcohol on an empty stomach (food masses in the stomach slow down the absorption of alcohol) Alcoholic drinks with a strength of up to 30% are absorbed faster.

Acute poisoning with alcohol surrogates is associated with the intake of ethyl alcohol containing impurities of various substances prepared on the basis of ethanol or other monohydric or polyhydric alcohols.

Alcohol surrogates prepared on the basis of ethyl alcohol containing various impurities. The clinical picture, course and treatment are similar to those for alcohol intoxication (see.

When taken orally - alcohol intoxication; intense staining of the skin and mucous membranes in a blue color, which persists for 3–4 months. Differential diagnosis - methemoglobinemia.

Alcohol surrogates that do not contain ethyl alcohol and are other monohydric or polyhydric alcohols (false surrogates) Methyl alcohol (methanol, wood alcohol). The lethal dose when taken orally is about 100 ml (without prior intake of ethanol).

Toxic concentration in the blood is 300 mg/l, lethal - more than 800 mg/l Ethylene glycol is classified as dihydroxyl higher alcohols; Part of antifreeze and brake fluid. The lethal dose when taken orally is 100 ml.

Symptoms

Poisoning with alcohol substitutes can manifest itself in different ways; it directly depends on what was drunk and in what quantity. If it was a substance from group I, then most likely the threat to life will not be very great and in 9 out of 10 cases the poisoned person will be able to be safely “pumped out”.

But if we are talking about the internal use of group II surrogates, then the poisoning will be extremely difficult, and the consequences can be the most unpredictable.

Intoxication with alcohol surrogates includes initial symptoms such as:

  • emotional arousal;
  • increased motor activity;
  • strong euphoria;
  • dizziness, loss of space;
  • redness of the facial skin;
  • excessive salivation;
  • physical and emotional relaxation.

After some time, intoxication begins to manifest itself in the following symptoms:

  • pale skin;
  • severe dry mouth;
  • frequent urination;
  • dilated pupils that do not respond to light;
  • impaired motor coordination;
  • affected nervous system;
  • labored breathing;
  • loss of ability to speak and reason.

The first sign of alcohol poisoning is loss of consciousness, deep sleep, coma. There are three stages of coma with alcohol poisoning according to severity.

Superficial coma. The pupils are constricted, but react to light.

From the mouth there is a pungent odor of the alcoholic drink that the patient had previously consumed. When trying to bring him to his senses with ammonia vapor, the patient reacts with an appropriate grimace and defensive movements of his hands, but does not come to his senses.

The prognosis is usually favorable. If at this stage the patient is given gastric lavage using a gastric tube, he quickly regains consciousness.

Moderate coma. It differs from the previous one in the pronounced relaxation of muscle tone.

It reacts weakly to inhalation of ammonia vapors. Gastric lavage does not restore consciousness.

Such patients require hospitalization in the toxicology department. Deep coma.

Complete absence of tendon reflexes. The pupils are constricted or (if breathing is impaired) wide and do not respond to light.

There is no pain sensitivity or reaction to ammonia. Emergency hospitalization to the toxicology department is required.

You should know that all types of alcohol intoxication can be accompanied by retraction of the tongue, which blocks the access of air to the larynx and lungs, and the entry of mucus and vomit into the respiratory tract.

Blood pressure in a state of mild coma is usually elevated, but in a state of deep coma it drops to critical levels. An increase in heart rate is typical.

Alcoholic coma should be distinguished from traumatic brain injury (often a combination of both in drunk people), from a stroke, and also from drug poisoning.

If the poisoned person drank surrogates containing ethanol, this is not so bad, although sometimes in these cases the poisoning is too severe. Alcohols from the group that does not contain ethanol are especially dangerous. When poisoned by them, a person first looks like he is under normal alcoholic intoxication:

  • the drinker's face turns red;
  • the person becomes agitated emotionally and physically;
  • a state of euphoria appears;
  • sweating increases;
  • saliva is produced more abundantly;
  • excitement gives way to relaxation.
  • the skin turns pale;
  • pupils become wider;
  • the mouth becomes dry;
  • diuresis increases;
  • movements become uncoordinated, their amplitude expands;
  • physical and mental activity increases again;
  • attention weakens;
  • speech becomes confused and unintelligible.

These symptoms of poisoning are still more similar to a severe degree of intoxication. However, when using different surrogates, the signs will differ.

Methanol

Quickly absorbed into the blood, methanol deals a crushing blow to the kidneys and nervous system. As a result of toxic exposure, a person will display a number of characteristic symptoms:

  • the optic nerve is affected;
  • the person feels sick and vomits;
  • vision deteriorates (black spots appear, double vision, vision of objects becomes blurry, blindness may gradually develop);
  • the pupils are dilated, the response to the light stimulus is insufficient.

After 1–2 days, other signs of poisoning with burnt vodka or other counterfeit alcoholic drinks are added:

  • the whole body hurts (ache in the muscles, lower back and joints, cramps and pain in the abdomen);
  • temperature rises to 38 °C;
  • pressure drops;
  • drying of the mucous membranes and skin is observed;
  • the heart works intermittently;
  • consciousness becomes clouded;
  • agitation and convulsions occur.

As symptoms increase without assistance, a person develops a coma, followed by paralysis and death.

Ethylene glycol

This surrogate is also absorbed quickly, and the liver and kidneys suffer from its toxic effects. In severe intoxication, damage to the nervous system is observed. The clinical picture develops progressively, according to the three stages of poisoning:

  1. Early. During the first 12 hours after consuming surrogate alcohol, symptoms of intoxication do not appear. The person simply looks drunk, but does not yet complain about his health.
  2. Toxic damage to the nervous system. At this stage, a person vomits, complains of headache and thirst. Diarrhea appears, the skin and mucous membranes acquire a bluish tint, the temperature rises and the pupils dilate. The poisoned person finds it difficult to breathe, the heart beats faster, and a phase of excitation begins. If you do not help, the victim will lose consciousness and begin to have convulsions.
  3. Hepato- and nephrotoxic stages. This stage begins on days 2-3. A person's kidneys and liver fail. The skin turns yellow and itching begins. Urine darkens, its production decreases and disappears altogether. Liver and kidney failure develops, resulting in organ failure.

Symptoms of poisoning by alcohol surrogates differ depending on which group they belong to. They will be more favorable if they are alcoholic surrogates of the first group, containing ethyl alcohol, and more severe and dangerous in case of poisoning with methanol or ethylene glycol, so it is worth dwelling on them in more detail.

Symptoms of poisoning with surrogates containing ethyl alcohol

Clinically, signs of alcohol intoxication are first observed:

  • emotional and motor arousal;
  • facial redness;
  • state of euphoria;
  • sweating;
  • increased salivation;
  • a feeling of mental and physical relaxation.

Poisoning with alcohol substitutes ICD 10 (international classification of diseases) is represented by codes T51.1 - T52.9.

Symptoms will depend primarily on the type of surrogate accepted. So, in people who are poisoned by alcohol with ethanol, the symptoms are not so dangerous. Surrogates that do not contain ethyl alcohol pose a great danger.

In both cases, common symptoms will be nausea, vomiting, abdominal pain, and dizziness. They are similar to those that occur with ordinary poisoning. The type of surrogate accepted can be determined by the symptoms characteristic of each of them.

This poisoning is not so terrible compared to poisoning by surrogates of the second group, since ethanol is used to make alcoholic beverages. First, the person gets drunk, feels relaxed, peaceful, and is in a euphoric state.

With further use of the surrogate, symptoms of ordinary poisoning appear, as well as:

  • The face and skin become pale;
  • A person increasingly wants to go to the toilet;
  • Pupils dilate;
  • The mouth becomes dry and the person feels thirsty;
  • A person cannot control his movements;
  • It is difficult for a poisoned person to speak, speech is confused;
  • Confusion or loss of consciousness may occur.

Methanol or wood alcohol acts on the body as psychotropic drugs. You can die by taking just 50 milliliters of the substance. Symptoms of methanol poisoning include:

  • Symptoms of common poisoning: nausea, dizziness, etc.;
  • Virtually absent feeling of intoxication;
  • Dilated pupils that do not respond to light;
  • Vision problems: inability to focus, black spots before the eyes, etc.;
  • A few days after poisoning, the patient begins to experience pain in the joints and muscles;
  • The temperature rises;
  • The skin becomes dry, as do the mucous membranes;
  • The pressure drops;
  • The patient is worried about palpitations;
  • Consciousness becomes confused;
  • The person becomes agitated, which may be accompanied by convulsions.

Ethylene glycol quickly spreads throughout the body, and the liver and kidneys take the brunt of it, since it is through them that the substance is excreted. Symptoms of ethylene glycol poisoning include:

  • Feeling of intoxication in the first 12 hours, no signs of poisoning;
  • Then nausea, vomiting, and diarrhea begin;
  • A feeling of thirst appears;
  • The skin takes on a blue tint, as do the mucous membranes;
  • The pupils dilate;
  • The temperature rises;
  • It becomes difficult to breathe;
  • Heart rate increases.

If the patient does not seek help or treatment does not help, his skin begins to turn yellow, his kidneys and liver fail, his skin itches and his urine darkens. In this case, death is possible.

Russia is among the top ten countries in the world in terms of the number of people who abuse alcohol.

A huge number of deaths occur from poisoning with alcohol substitutes, the use of which leads to serious intoxication of the body, in most cases ending in the death of a person.

It is rarely possible to save people, because not everyone pays attention to the terrible symptoms of poisoning with scorched vodka, the development of which quickly leads to death. Knowledge of how to provide assistance to the victim will save him from death.

What is surrogate alcohol

Alcohol is drunk to change the emotional state to a more comfortable one. However, there are products approved by the state for internal consumption that have passed certification, and there are products that are not intended for drinking at all.

Why do we need surrogate vodka and analogues? Such a “scorched” product is cheaper than a certified one, it is easier to get, and the intoxication effect is almost the same. Poisoning by surrogates, according to the classification codes according to ICD 10, belongs to disease groups T5.1.1 - T5.2.

9. Surrogate alcohol includes:

  • Chemical liquids containing ethyl alcohol as the main component - lotions, cosmetic and medicinal tinctures, denatured alcohols, industrial alcohols, insect stains.
  • Deceptive or false substitutes for alcohol-containing drinks that do not contain ethanol, but do contain methanol, dichloroethane, ethylene glycol.

Poisoning with surrogate alcohol containing ethyl alcohol is very common, since alcoholics consider such liquids to be the safest to drink.

However, all these substances are by no means intended for the human body; they contain a high concentration of potent chemicals, the impact of which destroys internal organs.

These include: BF-based glue, glass cleaners, colognes, deodorants, mouth fresheners, and other household chemicals that contain ethyl alcohol.

False surrogates

Poisoning with alcohol substitutes that do not contain ethyl alcohol is considered the most severe and leads to almost instant death, since methyl alcohol and ethylene glycol are quickly absorbed by the body and decompose into separate, extremely toxic substances.

At best, when drinking methyl alcohol, the alcoholic will end up with blindness. Ethylene glycol is part of brake and defrosting fluid for cars, dichloroethane is a solvent for adhesive bases.

The WHO organization presented impressive and scary figures - approximately 60% of men in Russia aged 15 to 60 years die from intoxication with surrogates, which sharply reduces the age of survival of men before retirement in the country to 59 years instead of 75, as, for example, in the UK.

Ethanol is a toxic substance, and poisoning with alcohol and its surrogates depends on the individual reaction of the body. A lethal dose for any person is considered to be three bottles of cognac consumed less than 5 hours apart.

At the same time, doctors stipulate that for counterfeit drugs, the lethal dose may not exceed one sip, depending on the concentration of toxins in the substance that the person drinks.

Paradoxically, excessive snacking can lead to death, since the body does not have time to cope with the incoming food that accumulates in the gastrointestinal tract, and alcohol is simply not absorbed at first, but then enters the blood in huge quantities, which can lead to death.

The mechanism of action of the poison on the body

Each toxic substance has its own effect on internal organs, however, since the poison passes through the digestive tract, all organs of the gastrointestinal tract, from the stomach to the kidneys, are at risk.

Unable to cope with incoming poisons, the gastric mucosa reacts with ulcerative formations.

Approximately one third of methanol and ethylene glycol are excreted by the kidneys, which leads to acute failure of organ functions, including the absence of urination, the rest enters the blood, causing a serious blow to the cells of the central nervous system, even leading to cardiac arrest.

Signs of alcohol poisoning

It is not uncommon for people to buy a bottle of alcohol in a store, labeled and certified, but it turns out to be “scorched.”

It is difficult to notice poisoning by surrogates if alcohol is drunk in a cheerful company, especially when you consider that the first signs of the effects of alcohol are euphoria, liberation, and high spirits.

And only a few hours after drinking alcohol with toxic impurities, frightening symptoms of a hangover may appear, indicating that poisoning with alcohol substitutes has occurred.

Ethyl alcohol

Poisoning with alcohol surrogates is fatal in most cases if the victim is not provided with emergency medical care in a timely manner. The poison quickly not only affects the organs of the gastrointestinal tract, but is also spread by the blood throughout the body. The person experiences severe intoxication, the symptoms of which can be very painful.

Alcohol surrogates are conventionally divided into several types. The first is those that contain ethyl alcohol. These can be cosmetics, liquids for cleaning household items, etc.

The second type is surrogates that do not contain ethyl alcohol. These include products for treating materials against the negative effects of insects, mold, as well as dyes, adhesives, etc. There is also a third type. They are called false surrogates.

Poisoning with alcohol surrogates occupies a leading position in the statistics of all intoxications. Moreover, 98% of patients die before hospitalization. A brief description of the alcohol surrogate will help to understand the reason for such a high mortality rate.

What are alcohol surrogates? What are the signs of poisoning with such counterfeit alcohol? How to help the victim? What could be the consequences of such intoxication? We will look at the answers to these questions in this article.

Alcohol carries considerable danger to the body. By consuming a low-quality product, you can not only get poisoned, but also die.

According to statistics, poisoning with alcohol surrogates occurs quite often and often leads to irreparable consequences. For example, in Russia in 2011, according to statistics, about 11,700 people died from poisoning, but the true result exceeds this figure.

And every year the number of victims of surrogacy is growing.

Symptoms of poisoning with surrogates are different, since it all depends on the type of substance and its quantity. A more favorable prognosis with the use of low-risk surrogates. And in case of poisoning with methanol and ethylene glycol, the consequences are severe and most often fatal.

Since there are 2 groups of surrogates, it is important to understand that the symptoms will vary greatly depending on the cause of the poisoning. Even if it is known which group the surrogate that provoked the poisoning belonged to (for example, it was a true surrogate), it is necessary to know what kind of impurity was contained in the drink in order to competently provide assistance to the victim.

Symptoms of poisoning by true surrogates

The signs of poisoning with surrogates are similar to the symptoms that indicate that the patient has consumed ethyl alcohol, but in the first case the ailment is more pronounced and is observed after a shorter period of time. The consequences of poisoning from low-quality alcoholic beverages depend on the amount of alcohol ingested.

In case of poisoning with true surrogates, intoxication occurs due to toxic impurities. For example, after drinking hydrolytic alcohol, all the same symptoms appear as after drinking high-quality alcohol:

  • nausea;
  • vomit;
  • weakness;
  • drowsiness;
  • sudden changes in blood pressure.

However, the speed at which the first signs appear is much higher. Intoxication is often reported when taking alcohol-based heart medications. In this case, the following will be added to the symptoms of poisoning:

  • bradycardia;
  • decompensated dysfunction of the myocardium.

Poisoning with surrogate alcohol is often caused by the use of alcohol-containing products for external use. In this case, the patient will experience a sharp blue discoloration of the lips and mucous membranes, and the blood will become more brown. This is due to the presence of anesthesin in the composition, which tends to prevent oxygen from entering tissues and internal organs.

Drinking alcohol in the form of cosmetics leads to disruption of the functioning of the digestive tract along with signs of simple alcohol poisoning. This is due to the presence of butyl and methyl alcohols in most cosmetics, which can lead to acute gastritis and even provoke the development of hepatitis.

When using stain, a change in the color of the mucous membranes is observed, but this is due to the presence of dyes in the composition.

The main harm of moonshine lies in the danger of fusel oils, which have an extremely destructive effect on the liver and lead to acute liver failure, and in the most advanced cases, even cirrhosis. To provoke severe poisoning by surrogates of this group, you need to drink a relatively small portion of alcoholic liquid.

Symptoms of poisoning by false surrogates

The most common “substitute” for ethyl alcohol is methyl alcohol, which in itself does not pose any particular harm to the human body. The main danger comes from its breakdown products - formic acid and formaldehyde.

It is possible to avoid acute poisoning with surrogate alcohol if ethyl alcohol is present in the drink along with methyl alcohol. The thing is that ethanol is an “antidote” that prevents the transformation of methanol into substances harmful to the body.

Therefore, people suffering from chronic alcoholism mix two types of alcohol, but such experiments are extremely dangerous for health.

A small dose of the surrogate causes a mild stage of intoxication, during which the person feels satisfactory and only the main signs of alcohol intoxication appear. Poisoning with low-quality alcohol occurs at the end of this “hidden” period.

If the amount of alcohol consumed is slightly larger, signs of intoxication appear instantly: death can occur in just a few hours if the person is not given proper assistance.

In cases of mild to moderate poisoning, the following are observed:

  • sharp deterioration of vision followed by its restoration;
  • dizziness;
  • nausea.

In the severe stage, very pronounced symptoms of acute alcohol poisoning are present. A person can fall into an alcoholic coma within 2 hours after the first symptoms appear:

  • drowsiness;
  • violation of self-control;
  • sudden changes in blood pressure;
  • strong thirst;
  • joint pain.

Another common substitute for ethyl alcohol is ethylene glycol, which is present in brake fluid. The danger comes from the breakdown products of this substance, the most toxic of which is oxalic acid, which causes kidney destruction. Main symptoms:

  • redness of the skin;
  • change in color of mucous membranes;
  • increase in heart rate;
  • hyperthermia;
  • disturbance of perception of the surrounding world;
  • psychomotor disorders;
  • convulsions.

Oxalic acid leads to acute heart failure, disrupts liver function and provokes acute renal failure, which is the most common cause of death in human poisoning with ethylene glycol.

At the first signs of poisoning by surrogates, you must seek qualified help, as the ailment progresses at a very high speed. First aid should always be gastric lavage with warm water.

Further treatment measures directly depend on the cause of poisoning:

  1. Methanol. For treatment, ethanol is used in small doses, which prevents the breakdown of methanol. Atropine and prednisolone are used to restore vision.
  2. Ethylene glycol. A sodium bicarbonate solution is used. It is necessary to adjust the water-electrolyte balance and take diuretics to restore kidney function.
  3. True surrogates. Here, treatment is prescribed depending on which organs and systems of the body are affected. It all depends on the amount of alcohol taken and its type.

Poisoning with alcohol and any of its substitutes can be extremely dangerous. Surrogate alcohol very often leads to death, and many people who have undergone treatment after poisoning with surrogates become disabled. It is important to protect people from drinking such alcohol.

Surrogate alcohol has become a real national problem due to the increasing cases of poisoning with toxic compounds instead of alcoholic beverages.

The later stages of alcoholism are characterized by degradation of personality and thinking, which leads to ill-considered actions, including drinking cheap products that are unsuitable for food consumption and life-threatening.

The effect of surrogate alcohol on mortality

Toxic doses

Surrogate alcohol has become a real national problem due to the increasing cases of poisoning with toxic compounds instead of alcoholic beverages. The later stages of alcoholism are characterized by degradation of personality and thinking, which leads to ill-considered actions, including drinking cheap products that are unsuitable for food consumption and life-threatening.

However, not only chronic alcoholism can cause poisoning - illegally manufactured low-quality products can be found on store shelves under a harmless label.

Poisoning with alcohol and its surrogates is accompanied by a rapid loss of consciousness and the development of a soporous and comatose state. First of all, the brain and circulatory system are affected by toxic drinks, therefore, in addition to disturbances of consciousness, the symptoms are accompanied by problems with breathing and blood vessels.

The clinical picture of poisoning may differ slightly - it all depends on the type of product that caused it. Thus, moonshine poisoning is accompanied by persistent irreversible changes, since this highly toxic alcohol surrogate contains a number of heavy and dangerous compounds.

The main danger of low-quality alcohol is due to fusel oils, from which it is either not purified at all, as is the case with moonshine, or is partially purified. Moreover, it is very difficult to clean burnt vodka or moonshine at home from fusel oils.

The taste and smell of methyl alcohol are the same as ethyl alcohol. Death can occur after consuming just 100 ml.

Individual sensitivity varies, so after consuming the same dose, one patient may experience more severe alcohol poisoning than another. The severity of poisoning also depends on whether the patient simultaneously took ethanol, which is an antidote to methanol - some alcoholics dilute methyl alcohol with ethyl alcohol to avoid poisoning.

However, such attempts to save money are associated with an immediate risk to life. Methanol itself is not toxic, but when it breaks down in the body, strong poisons formaldehyde and formic acid are formed.

When consuming a large dose, signs of poisoning with alcohol surrogates appear almost instantly, and death occurs within a few hours. When taking a small dose, there is a latent period during which the patient feels satisfactory.

A mild form of poisoning with alcohol surrogates is manifested by nausea, repeated vomiting, headache, dizziness, epigastric pain, mild visual disturbances - flickering of spots, impaired clarity of perception (“seen as if through fog”).

Symptoms persist for several days and then gradually disappear. In case of poisoning with moderate alcohol surrogates, the manifestations are similar, but all the symptoms are more pronounced.

After 1-2 days the patient loses vision. Subsequently, vision is partially restored, but then deteriorates again.

Such poisonings usually do not pose a threat to life, but can lead to visual impairment leading to disability.

Causes

The cause of severe poisoning and death of a person can be a single use of surrogates in large dosages or their regular use over many years. Predisposing factors are:

  • antisocial lifestyle;
  • bad Company;
  • alcohol addiction;
  • burdened heredity;
  • addiction;
  • lack of permanent residence;
  • difficult family incidents.

Ethanol

1.2 Etiology and pathogenesis

Alcohols included in the T51 group are characterized by limited volatility and, with relatively low toxicity, acute inhalation poisoning with alcohols practically does not occur in clinical practice, with the exception of cases of inhalation use of certain alcohols (isopropyl) and some technical formulations containing alcohols for the purpose of drug intoxication.

The most common occurrence in clinical practice is acute oral poisoning with alcohol consumed for the purpose of alcohol intoxication.

Acute alcohol poisoning usually occurs when taking ethyl alcohol or various alcoholic beverages with an ethyl alcohol content of more than 12%. The lethal dose of 96% ethanol ranges from 4 to 12 g per 1 kg of body weight (approximately 700-1000 ml of vodka in the absence of tolerance).

Alcoholic coma occurs when the concentration of ethanol in the blood is 3 g.l and above, death - at a concentration of 5-6 g.l and above. Poisonings, as a rule, are of a domestic nature - accidental, with the purpose of intoxication.

Poisoning with pure higher alcohols - propyl, butyl, amyl - occurs in toxicological practice much less frequently than with ethyl alcohol; poisoning with their mixture with ethyl alcohol is more common.

Lethal doses and concentrations: cases of fatal poisoning have been described when ingested - 0.1–0.4 liters of propyl alcohol or more. Death occurred in the period from 4–6 hours to 15 days, coma - when the content of propanol in the blood was about 150 mg%.

However, fatal poisoning has also been described when 40 ml of alcohol is ingested. The lethal dose (LD100) of isopropyl alcohol taken orally for adults is considered to be 240 ml, with lethal concentration levels ranging from 0.04 mg/L in children and 4.4 mg/L in adults.

Routes of entry into the body are inhalation, oral, percutaneous; however, in clinical practice, poisoning as a result of oral ingestion of these alcohols predominates.

1.3 Epidemiology

Acute ES poisoning is one of the leading causes of emergency hospitalization for poisoning. According to reports from toxicological centers in Russia (Form No. 64), there were 37 patients with this pathology.

9%, 30.7%. of all hospitalized in these units in 2008 – 2011, respectively.

In 2015, this figure averaged 32.7%. In federal districts, the proportion of patients hospitalized with ethanol poisoning in 2015 ranged from 7.1% in the Northwestern Federal District to 69% in the Ural and Siberian Federal Districts.

The average hospital mortality rate for ethanol poisoning was 3.0% in 2005-2012, and 4.7% in 2015. Mortality due to ethanol poisoning in relation to other causes of death due to poisoning in the Russian Federation is the leading factor for the same period, ranging from 55.8% in 2005 to 42.1% in 2012, 2015 - 43. 7%, other alcohols – 3.3% – 4.0%.

Criteria for assessing the quality of medical care

Quality criteria

Level of evidence

An examination was performed by a toxicologist and/or an anesthesiologist-resuscitator no later than 15 minutes from the moment of admission to the hospital

Gastric lavage by tube was performed no later than 30 minutes from the moment of admission to the hospital (if this was not performed at the stage of primary health care)

Forced diuresis with urine alkalization was performed no later than 30 minutes from the moment of admission to the hospital (in the absence of medical contraindications)

A study of the acid-base state of the blood (pH, PaCO2, PaO2, BE, SB, BB, SO2, HbO) was performed no later than 1 hour from the moment of admission to the hospital

A blood glucose level test was performed no later than 1 hour from the moment of admission to the hospital

A study of the level of ethanol and methanol in the blood was performed (gas-liquid chromatography) no later than 2 hours from the moment of admission to the hospital

A study of the level of ethanol and methanol in urine was performed (gas-liquid chromatography) no later than 2 hours from the moment of admission to the hospital

A study of the level of 2-propanol and fusel oils in the blood was performed (gas-liquid chromatography) - in case of suspected poisoning with higher alcohols

An electrocardiographic study was performed no later than 2 hours from the moment of admission to the hospital

An X-ray of the chest organs was performed no later than 2 hours from the moment of admission to the hospital (in a coma state)

An X-ray of the entire skull was performed in one or more projections no later than 2 hours from the moment of admission to the hospital

Hematocrit assessment performed

A detailed general (clinical) blood test was performed

A general urine test was performed

A general therapeutic biochemical blood test was performed (total bilirubin, creatine phosphokinase, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, urea, creatinine, potassium, sodium, calcium) at least 2 times during the hospitalization period

Ultrasound examination of the abdominal organs (comprehensive) was performed

Intravenous drip administration of detoxification medications was performed (in the absence of medical contraindications)

Therapy with hepatoprotectors was carried out (with an increase in aspartate aminotransferase and alanine aminotransferase and alkaline phosphatase by more than 2 times and in the absence of medical contraindications)

Therapy was carried out with medications to correct water and electrolyte disorders (in the absence of medical contraindications)

A study of the level of myoglobin in urine was performed (with an increase in the level of creatine phosphokinase and creatinine and urea by more than 2 times)

Normalization of homeostasis indicators was achieved at the time of discharge from the hospital

Restoration of consciousness was achieved at the time of discharge from the hospital

Normalization of spontaneous breathing and hemodynamics was achieved at the time of discharge from the hospital

Classification

Classification of coma due to the toxic effect (acute poisoning) of ethanol, which is divided by depth, respectively

    superficial coma, uncomplicated,

    superficial complicated coma,

    deep uncomplicated coma

    deep complicated coma.

Toxic effect of alcohols:

    2-propanol (propyl alcohol),

    fusel oils (alcohol: amyl;

butyl; propyl

classified according to severity:

    mild - not accompanied by loss of consciousness,

    moderate severity - with a disorder of consciousness such as stupor, toxic encephalopathy, but without complications,

    severe - characterized by complete loss of consciousness (coma), which may be accompanied by various complications.

First group

Low hazard

Low hazard

The toxicology of poisoning by alcohol and its surrogates distinguishes two types of substances: those produced on the basis of ethanol and those produced using impurities. The first group includes the following:

  1. ethanol produced by hydrolysis from wood;
  2. denatured alcohol;
  3. cosmetic lotions, cologne;
  4. BF glue - the composition includes polyvinyl acetal, phenol-formaldehyde resin, dissolved in acetone, alcohol;
  5. polish - a mixture of ethanol with butyl, amyl, acetone;
  6. nigrosin is a stain containing ethanol and dyes. It is used for processing wood and dyeing leather products blue.

The second type includes chemicals that do not contain ethanol. They are made using ethylene glycol, methyl alcohol with the addition of various impurities.

Diagnostics

Must be organized immediately. The doctor initially collects an anamnesis of the disease, life, conducts a general examination, pays special attention to the smell of the mouth, the consciousness of the victim, and the skin. Afterwards, laboratory and instrumental examination methods are prescribed. The most informative are:

  • general urine analysis;
  • general and biochemical blood test;
  • electrocardiogram;
  • Ultrasound of the abdominal cavity, heart;
  • CT and MRI;
  • electroencephalogram.

An ECG is usually performed by emergency medical services doctors, which makes it possible to identify disorders that threaten the patient’s life and stop them in a timely manner.

2.3.1 Chemical-toxicological laboratory diagnostics

The basis is chemical-toxicological laboratory diagnostics. It is not recommended to use for diagnostic purposes the determination of the presence and level of ES in the blood using an analysis of exhaled air (alcometer), since this method does not allow determining the presence of other alcohols, is inferior in accuracy to GLC, and also does not allow obtaining the required amount of exhaled air (maximum complete active exhalation) in a patient in a coma).

    Determination of ethyl alcohol in blood and urine is recommended to be carried out 2 times with an interval of 1 hour in order to confirm the result of the first study and determine the phase of poisoning by the ratio of ethanol concentration in these biological media (resorption or elimination).

Instrumental diagnostics have no specificity and are carried out for the purpose of differential diagnosis and monitoring of the patient’s condition.

    electrocardiography (ECG) - the likelihood of cardiomyopathy, chronic cardiac pathology (especially since the life history of such patients upon admission to the hospital is practically unknown),

    X-rays of the chest organs,

    X-rays of the skull in two projections - for patients brought from the street, public places, in the presence of signs of injury.

    esophagogastroduodenoscopy (EGDS) - higher alcohols have a local irritating effect on the mucous membrane of the digestive tract (frequency of up to 2 times).

    Additional instrumental diagnostic methods are recommended to be carried out once in order to identify injury, concomitant pathology or possible complications (ultrasound examination (ultrasound) (ECHO-scopy) of the brain, computed tomography (CT) and magnetic resonance imaging (MRI) of the brain, ultrasound of the abdominal organs, kidneys, pancreas, fibrobronchoscopy FBS.

    At the stage of primary health care, it is recommended to exclude diseases or conditions that caused coma due to alcohol intoxication, in particular:

      traumatic brain injury, acute cerebrovascular accident;

      hypoglycemic coma;

      infectious disease (meningitis, encephalitis, etc.)

      hepatic and uremic coma, comas with endocrinological diseases, severe encephalopathy with water-electrolyte and metabolic disorders.

    In the hospital, upon admission of the patient, it is also recommended to exclude the diseases or conditions listed above, and in the absence of positive dynamics, 2.0-4.0 hours after the start of infusion therapy, a more in-depth study is recommended, including a chemical-toxicological one, in order to exclude the presence of a combination of any -or psychotropic drugs or other somatic or infectious disease.

Arriving doctors will first interview witnesses to the poisoning and examine the victim himself. If necessary, medical assistance will be provided on the spot, after which the patient will be transported to the hospital for further examination:

  • a blood test from a vein to identify the alcohol that the burnt vodka you drank contained;
  • blood for methanol detection;
  • ECG to study the activity of the heart (is the rhythm disturbed, is there any myocardial damage, etc.).

After diagnosis, when a specific surrogate is known and the true picture of the patient’s condition is revealed, doctors will prescribe targeted treatment.

Methods for studying EEG ECG (decreased S-T segment, negative T wave, extrasystole; with alcoholic cardiomyopathy, persistent rhythm and conduction disturbances are possible) Microdiffusion test and gas-liquid chromatography - tests for the presence of ethanol in the blood.

Differential diagnosis of TBI Acute cerebrovascular accident Poisoning with false substitutes for alcohol (chlorinated hydrocarbons, methanol, ethylene glycol) Poisoning with sleeping pills, drugs and tranquilizers Hypoglycemic coma.

EEG research methods Gas-liquid chromatography. Differential diagnosis is carried out with acute alcohol poisoning.

TREATMENTManagement tactics (see The absence of positive dynamics in the patient’s condition within 3 hours during therapy indicates unrecognized complications (TBI, pulmonary atelectasis, etc.) or an erroneous diagnosis.

Toxic doses

2.1 Complaints and anamnesis

In case of ethanol poisoning, there are practically no complaints, since the patient is unconscious. In case of poisoning with higher alcohols while consciousness is preserved, complaints are characteristic of the effects of narcotic and irritant substances: weakness, dizziness, headache, pain in the epigastric region, nausea, vomiting.

In case of poisoning with butanol and amyl alcohols, there may be complaints of diarrhea.

The anamnesis should be aimed at clarifying the following data: type of toxic substance (vodka, wine, beer, technical alcohol, solvent - its name, brand, etc.), dose, time of taking the toxicant.

In addition, it is advisable to find out some life history data: past illnesses, injuries, bad habits.

2.2 Physical examination

    In case of poisoning with ethanol and higher alcohols, it is recommended to evaluate the following:

    The appearance of the skin - there is no specific coloring; in case of respiratory failure, shock, cyanosis of the lips, face, acrocyanosis, coldness is noted; in deep coma there may be dampness. It is necessary to identify the presence/absence of a rash, local changes, the so-called. “bedsores” due to positional trauma due to pressure from the weight of one’s own body, the so-called positional pressure on individual areas of soft tissue, leading to the appearance of areas of skin hyperemia, which are often regarded as bruises, hematomas, burns, phlebitis, allergic edema, etc. and are usually detected in the early stages (1-3 days).

    Assess the psychoneurological status: state of consciousness (clear, lethargy, stupor, coma, psychomotor agitation, hallucinations). If there is a coma, assess its depth, the presence or absence of reflexes, the width of the pupils, their reaction to light, the presence (absence) of anisocoria, the state of muscle tone. When identifying anisocoria and pathological reflexes, pay attention to their constancy (“play of the pupils”), since with a superficial alcoholic coma, anisocoria and pathological reflexes can appear and quickly disappear.

    Assess the state of breathing: adequacy, frequency, depth, uniformity of participation in the act of breathing of all parts of the chest, auscultatory picture.

    Examine visible mucous membranes - some higher alcohols have irritating properties and can cause a burning sensation and pain when swallowing.

    Pay attention to the presence/absence of damage, especially in the face, head, abdomen, and lower back.

    Pay attention to the presence/absence of the exhaled air odor characteristic of ES, higher alcohols, but this is not an absolute fact confirming ES poisoning, since the state of alcohol intoxication can accompany various somatic, infectious diseases, injuries.

Pharmacodynamics

Nootropics.

Pharmacological action - nootropic. Pharmacodynamics.

Piracetam binds to the polar heads of phospholipids and forms mobile piracetam-phospholipid complexes. As a result, the two-layer structure of the cell membrane and its stability are restored, which in turn leads to the restoration of the three-dimensional structure of membrane and transmembrane proteins and the restoration of their function.

At the neuronal level, piracetam facilitates various types of synaptic transmission, having a predominant effect on the density and activity of postsynaptic receptors (data obtained from animal studies).

Improves connections between the cerebral hemispheres and synaptic conduction in neocortical structures, improves cerebral blood flow. It has an effect on the central nervous system in various ways: it modifies neurotransmission in the brain, improves metabolic conditions that promote neuronal plasticity, improves microcirculation, affecting the rheological characteristics of the blood and without causing vasodilation.

In case of cerebral dysfunction, it increases concentration and improves cognitive functions, including learning ability, memory, attention and consciousness, mental performance, without having a sedative or psychostimulating effect.

The use of piracetam is accompanied by significant changes in the EEG (increased α- and β-activity, decreased δ-activity). Helps restore cognitive abilities after various cerebral injuries due to hypoxia, intoxication or electroconvulsive therapy.

Indicated for the treatment of cortical myoclonus both as monotherapy and as part of complex therapy. Reduces the duration of vestibular neuronitis and nystagmus.

The hemorheological effects of piracetam are associated with its effect on red blood cells, platelets and the vascular wall. In patients with sickle cell anemia with pathological rigidity of red blood cells, piracetam restores the elasticity of the red blood cell membrane, increases their ability to deform and filter, reduces blood viscosity and prevents the formation of coin columns.

In addition, it inhibits increased aggregation of activated platelets without significantly affecting their number. At a dose of 9.6 g, it reduces the level of fibrinogen and von Willebrand factor by 30–40% and prolongs bleeding time.

Animal studies have shown that piracetam inhibits vasospasm and counteracts various vasospastic substances. In studies on healthy volunteers, piracetam reduced the adhesion of red blood cells to the vascular endothelium and stimulated the production of prostacyclins in the endothelium.

Nosologies

A89 Viral infection of the central nervous system, unspecified. D57 Sickle cell disorders.

F00 Dementia due to Alzheimer's disease (G30). F01 Vascular dementia.

F03 Dementia, unspecified. F04 Organic amnesic syndrome not caused by alcohol or other psychoactive substances.

F05 Delirium not caused by alcohol or other psychoactive substances. F06.7 Mild cognitive impairment.

F07.1 Postencephalitic syndrome. F07.2 Post-concussion syndrome.

F07.9 Organic disorder of personality and behavior due to disease, damage or dysfunction of the brain, unspecified. F09 Organic or symptomatic mental disorder, unspecified.

F10.2 Alcohol dependence syndrome. F10.3 Withdrawal state.

F10.4 Withdrawal state with delirium. F10.5 Alcoholic psychosis.

F11 Mental and behavioral disorders caused by opioid use. F13 Mental and behavioral disorders caused by the use of sedatives or hypnotics.

F29 Inorganic psychosis, unspecified. F32 Depressive episode.

F34.1 Dysthymia. F41.2 Mixed anxiety and depressive disorder.

F48.0 Neurasthenia. F60.3 Emotionally unstable personality disorder.

F63 Disorders of habits and inclinations. F79 Mental retardation, unspecified.

F80 Specific developmental disorders of speech and language. F90.0 Impaired activity and attention.

F91 Behavioral disorders. G21.8 Other forms of secondary parkinsonism.

G25.3 Myoclonus. G30 Alzheimer's disease.

G40.9 Epilepsy, unspecified. G46 Vascular cerebrovascular syndromes in cerebrovascular diseases.

G80 Cerebral palsy. G93.4 Encephalopathy, unspecified.

H55 Nystagmus and other involuntary eye movements. I61 Intracerebral hemorrhage.

I63 Cerebral infarction. I67.2 Cerebral atherosclerosis.

I69 Consequences of cerebrovascular diseases. P15 Other birth injuries.

P91 Other disorders of cerebral status in a newborn. R26.8 Other and unspecified disorders of gait and mobility.

R40.2 Coma, unspecified. R41.0 Disorientation, unspecified.

R41.3. 0* Memory loss.

R41.8. 0* Intellectual-mnestic disorders.

R42 Dizziness and loss of stability. R45.1 Restlessness and agitation.

R46.4 Lethargy and slow reaction. R47.0 Dysphasia and aphasia.

R51 Headache. R53 Malaise and fatigue.

R54 Old age. S06 Intracranial injury.

T40 Poisoning with drugs and psychodysleptics [hallucinogens]. T42.3 Barbiturate poisoning.

T51 Toxic effects of alcohol. Z55 Problems related to learning and literacy.

In addition, all drinks, including those made at home, may contain other alcohols: methanol, isobutanol, isobutylcarbinol, etc. All of them are the main components of fusel oil. Excessive concentrations of this byproduct of alcoholic fermentation can cause severe poisoning.

Ethanol

At a blood alcohol concentration of 0.4%, coma occurs. Concentrations greater than 0.6% may cause cardiac arrest.

Ethanol poisoning is characterized by respiratory failure due to aspiration of mucus and retraction of the tongue. The development of acute renal failure is also possible.

If, after taking ethyl alcohol, there is no loss of consciousness, then doctors regard this as alcohol intoxication, which does not require emergency assistance. A person comes out of this state on his own. Commonly available headache medications are used to relieve mild hangover symptoms.

Methanol

Methyl or wood alcohol is inferior to ethanol in its narcotic effect. In terms of toxicity, it is significantly superior to ethyl alcohol, since it decomposes into formaldehyde and formic acid. The central nervous system is severely affected by these toxic substances. Blood pressure increases when taking methanol, and then drops sharply.

Intoxication is fully manifested when taking no more than 300 ml of methyl alcohol. A person's reflexes decrease, breathing becomes impaired, vomiting occurs, and involuntary urination occurs. Vision problems begin, which can lead to blindness.

Death from methanol poisoning occurs from respiratory failure.

Propanol

Isopropyl (propyl) alcohol can enter the body through inhalation, oral administration, and through the skin.

The release of propanol and acetone (a metabolite of propyl alcohol) with exhaled air begins 15 minutes after administration. The process of releasing the body from these substances also occurs in the urine. The release of acetone may continue for several days.

Propyl alcohol provokes headache, dizziness, photophobia, and palpitations. Possible deterioration of vision and hearing. In case of severe poisoning, coma occurs, and subsequently death caused by respiratory arrest.

Fusel oils

Fusel oil is a mixture of higher monohydric aliphatic alcohols, ethers and other compounds. It is present in almost all alcoholic beverages, but only certain monohydric alcohols have toxicological significance: isoamyl, isopropyl and isobutyl.

The danger of surrogates

Alcohol substitutes based on components from the group of monohydric and polyhydric alcohols and organic solvents have a narcotic effect on the central nervous system. They are similar in action to ethanol, but more toxic.

Surrogates are used in everyday life and in production for technical purposes. They are not originally intended for oral administration.

Moonshine, a product of artisanal distillation of mash, is also considered a surrogate.

With a high concentration of monohydric alcohols, it is characterized by rapid impairment of consciousness, deep damage to the central nervous system and severe post-intoxication syndrome.

Frequent use of surrogates provokes the development of psychoorganic syndrome. It is characterized by memory deterioration and a drop in the level of thinking.

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Which drinks are more harmful?

In order to determine which type of alcohol will cause the most harm, you need to know the dose of ethanol you plan to take, the degree of purification of the drink, as well as possible additives that add color or aroma.

To obtain a sufficiently high degree of intoxication, it is recommended to opt for concentrated drinks: vodka or cognac. If you want to drink a little, then it is better to give preference to low-proof alcohol - beer or wine.

If you want to drink a little, then it is better to give preference to low-proof alcohol - beer or wine.

It is undesirable to consume liqueurs, since the cheapest alcohol is often used in their production.

For whom is it more dangerous?

Despite the fact that beer is a low-alcohol drink, doctors do not recommend drinking it every day. It can harm both men and women with a large amount of phytoestrogens - female hormones of plant origin.

Alcoholic cocktails are also dangerous, especially for women and teenagers. In addition to alcohol, these drinks contain fruit juices, dyes, sugar, essential oils and spices. This combination of components causes damage to the liver and pancreas.

It is unacceptable to drink alcohol during pregnancy and breastfeeding. With perinatal alcohol intake, a phenomenon such as dysmorphia - fetal alcohol syndrome - may occur. These are congenital anomalies and chromosomal disorders.

If the pregnancy is at the planning stage, then the man should also give up alcohol 4 months before conception. Otherwise, intrauterine malformations may occur.

When a nursing woman drinks alcohol, the child may experience heart rhythm disturbances, severe intestinal colic, and delayed mental and physical development.

Women who drink often experience gynecological diseases, including menstrual irregularities.

Against the background of alcohol abuse, both women and men develop chronic skin diseases: eczema, neurodermatitis, psoriasis. Weakening of the immune system caused by alcohol leads to rosacea and herpes.

Alcoholic cocktails are also dangerous, especially for women and teenagers. In addition to alcohol, these drinks contain fruit juices, dyes, sugar, essential oils and spices.

The symptoms that occur after consuming true surrogates depend on the impurities contained in the alcohol-containing liquid. After taking hydrolytic alcohol, the symptoms are the same as after drinking too much of regular alcohol: nausea, vomiting, headache, dizziness, dry mouth. Hydrolytic alcohol is more toxic than ethyl alcohol, so signs of poisoning with alcohol surrogates are observed after drinking less alcohol.
In patients with severe alcoholism, poisoning with alcohol substitutes often occurs when taking alcohol-containing cardiac medications. Such drugs contain cardiac glycosides that provoke bradycardia. With systematic use or taking a large dose, acute heart failure may develop. Anesthesin is often added to external alcohol-containing products, which blocks the blood’s ability to deliver oxygen to organs and tissues. Poisoning with alcohol surrogates is manifested by symptoms of oxygen starvation. The mucous membranes become bluish, the blood takes on a brown tint.
The taste and smell of methyl alcohol are the same as ethyl alcohol. Death can occur after consuming just 100 ml. Individual sensitivity varies, so after consuming the same dose, one patient may experience more severe alcohol poisoning than another. The severity of poisoning also depends on whether the patient simultaneously took ethanol, which is an antidote to methanol - some alcoholics dilute methyl alcohol with ethyl alcohol to avoid poisoning.
However, such attempts to save money are associated with an immediate risk to life. Methanol itself is not toxic, but when it breaks down in the body, strong poisons formaldehyde and formic acid are formed. When consuming a large dose, signs of poisoning with alcohol surrogates appear almost instantly, and death occurs within a few hours. When taking a small dose, there is a latent period during which the patient feels satisfactory.
A mild form of poisoning with alcohol surrogates is manifested by nausea, repeated vomiting, headache, dizziness, epigastric pain, mild visual disturbances - flickering of spots, impaired clarity of perception (“seen as if through fog”). Symptoms persist for several days and then gradually disappear. In case of poisoning with moderate alcohol surrogates, the manifestations are similar, but all the symptoms are more pronounced. After 1-2 days the patient loses vision. Subsequently, vision is partially restored, but then deteriorates again. Such poisonings usually do not pose a threat to life, but can lead to visual impairment leading to disability.
In severe cases, pronounced typical symptoms of poisoning with alcohol substitutes, drowsiness and stupor, occur. After a few hours, increasing thirst, pain in the legs, dryness and cyanosis of the mucous membranes, rhythm disturbances, tachycardia and increased blood pressure appear. Subsequently, tachycardia gives way to bradycardia, and blood pressure drops. Confusion is observed, convulsions and psychomotor agitation are possible. In case of particularly severe poisoning with alcohol surrogates, the time interval between the appearance of the first symptoms and the occurrence of pronounced impairments in life is only 2-3 hours. The result is coma and death as a result of respiratory arrest and cardiac dysfunction.
Another common poisoning occurs when consuming brake fluid containing ethylene glycol. The lethal dose, as for methanol poisoning, is only 100 ml. The cause of poisoning is the formation of toxic intermediate products of the breakdown of ethylene glycol, in particular oxalic acid, which provokes acidosis and has a destructive effect on the kidneys as a result of the formation of sodium oxalate crystals.

Acute alcohol poisoning(ethanol) is usually associated with the consumption of ethyl alcohol or drinks containing more than 12% ethyl alcohol. The lethal concentration of ethanol in the blood is 5-8 g/l, the lethal single dose is 4-12 g/kg (300-500 ml of 96% ethanol); however, this rate varies between patients and often depends on acquired tolerance to alcohol. Acute alcohol poisoning is most widespread in countries of northern and middle latitudes.

Code according to the international classification of diseases ICD-10:

  • T51.0

Frequency. 25% of all acute poisonings. More than 60% of all fatal poisonings are caused by alcohol. The predominant gender is male.
Risk factors. Alcoholism (about 90% of those hospitalized with acute alcohol poisoning are alcoholic). Drinking alcohol on an empty stomach (food masses in the stomach slow down the absorption of alcohol). Alcoholic drinks with a strength of up to 30% are absorbed faster.

Causes

Pathogenesis. Ethanol easily penetrates tissue membranes and is quickly absorbed in the stomach (20%) and small intestine (80%); on average, after 1.5 hours its concentration in the blood reaches its maximum level. Ethanol has a psychotropic (narcotic) effect, accompanied by suppression of excitation processes in the central nervous system, which is caused by changes in the metabolism of neurons, dysfunction of neurotransmitter systems, and a decrease in oxygen utilization. Development of metabolic acidosis (accumulation of acidic products of its biotransformation).

Symptoms (signs)

Clinical picture
. General signs.. Emotional lability.. Impaired coordination of movements.. Redness of the face.. Nausea and vomiting.. Respiratory depression.. Impaired consciousness.
. Alcoholic coma develops when the concentration of ethanol in the blood is 0.3-0.7 mg%. The symptoms of alcoholic coma (especially deep) are nonspecific and are a variant of drug coma.. Superficial coma: lack of speech contact, loss of consciousness, decreased corneal and pupillary reflexes, sharp suppression of pain sensitivity. Neurological symptoms - decreased or increased muscle tone and tendon reflexes (trismus of the masticatory muscles, meningeal symptoms, myofibrillations usually occur in the chest and neck); pathological eye symptoms (floating movements of the eyeballs, anisocoria) are inconsistent, the pupils are usually constricted (miosis), and dilate as breathing disorders increase. Usually there are 2 periods of superficial alcoholic coma... 1st period: an injection or pressure in the pain points of the trigeminal nerve, inhalation of ammonia vapors are accompanied by dilation of the pupils, a facial reaction, protective movements of the hands... 2nd period: in response to such irritations only a weak hypertonicity of the arms and legs, myofibrillation; the pupillary reaction is inconsistent.. Deep coma: complete loss of pain sensitivity, absence or sharp decrease in corneal, pupillary, tendon reflexes, muscle atony, decrease in body temperature.
. External respiration disorders are the main cause of death in the prehospital stage in the absence of medical care. Obstructive and aspiration disorders (retraction of the tongue, hypersalivation and bronchorrhea, aspiration of vomit), stridor, tachypnea, acrocyanosis, swelling of the neck veins, possible coarse rales in the lungs, dilation pupils.. Central respiratory failure occurs only in deep alcoholic coma.
. Disturbances in the functions of the cardiovascular system.. Tachycardia is the most constant clinical symptom.. During deep coma, blood pressure decreases sharply.. Hypercoagulation with acidosis and general hypothermia lead to microcirculation disorders.

Diagnostics

Research methods. EEG. ECG (decreased S-T segment, negative T wave, extrasystole; with alcoholic cardiomyopathy, persistent rhythm and conduction disturbances are possible). Microdiffusion test and gas-liquid chromatography are tests for the presence of ethanol in the blood.
Differential diagnosis. TBI. Acute cerebrovascular accident. Poisoning with false alcohol substitutes (chlorinated hydrocarbons, methanol, ethylene glycol). Poisoning with sleeping pills, drugs and tranquilizers. Hypoglycemic coma.

Treatment

TREATMENT
Lead tactics(see also Poisoning, general provisions). Hospitalization for severe alcohol intoxication (coma, respiratory and circulatory disorders) to a poison control center. Ensuring adequate ventilation of the lungs.. Toilet of the oral cavity, fixation of the tongue with a tongue holder.. In case of superficial coma, an air duct is inserted; in case of deep coma, intubation is indicated, followed by suction of mucus and vomit from the upper respiratory tract.. In case of respiratory failure of the central type - mechanical ventilation after tracheal intubation . Gastric lavage through a tube is carried out after ensuring adequate ventilation of the lungs. Intensive supportive care; measures aimed at preventing hypoglycemia and ketoacidosis. Forced diuresis. Hemodialysis (according to indications). In case of severe obstruction-aspiration syndrome - emergency bronchoscopy; to resolve atelectasis - postural drainage. Treatment of complications. The absence of positive dynamics in the patient’s condition within 3 hours during therapy indicates unrecognized complications (TBI, pulmonary atelectasis, etc.) or an erroneous diagnosis.

Drug therapy. Atropine 1-2 ml 0.1% solution s.c. to reduce hypersalivation and bronchorrhea. Antishock therapy (for severe hemodynamic disorders) .. Plasma substitutes (polyglucin, hemodez, reopoliglucin) IV drip.. 5% glucose solution, 0.9% sodium chloride solution IV drip.. Analeptics (introduction of bemegride or large doses of analeptics are contraindicated due to the risk of developing convulsive syndrome and obstructive forms of breathing disorders).. Prednisolone 60-100 mg IV drip for persistent arterial hypotension. To correct metabolic acidosis - 600-1000 ml of 4% sodium bicarbonate solution intravenously. To accelerate the oxidation of alcohol and normalize metabolic processes - glucose (40-60 ml of 40% solution with insulin) IV; thiamine, pyridoxine, nicotinic and ascorbic acids. If complications develop, antibiotics are prescribed.

Complications. Periods of psychomotor agitation with short episodes of auditory and visual hallucinations (when recovering from an alcoholic coma). Convulsive syndrome (more often in persons suffering from alcoholic encephalopathy). Alcohol delirium. Alcoholic amaurosis. Inflammatory diseases of the respiratory system (tracheobronchitis and pneumonia). Aspiration of stomach contents often leads to the development of pulmonary atelectasis or Mendelssohn's syndrome. Myorenal syndrome (rare).
Course and prognosis depend on the timeliness of care provided (98-99% of deaths occur in the prehospital stage).
Prevention - promotion of a healthy lifestyle, treatment of alcoholism.
Synonym. Alcohol intoxication

ICD-10. T51.0 Toxic effects of ethanol

Application. Myorenal syndrome - general microcirculation disorders in alcoholic coma are aggravated by local disorders: compression of the great vessels in the uncomfortable position of the patient’s body in a coma (limbs tucked under themselves), positional pressure from the weight of one’s own body on individual muscle groups. This leads to ischemic coagulative tissue necrosis. Clinically: when consciousness returns, patients complain of pain, limitation of movements, increasing swelling of the affected limbs (the swelling is dense, usually circular, sometimes spreading to the buttock or chest); usually one side of the body is affected; neuritis with a decrease in all types of sensitivity; urine is dirty brown and contains a large amount of myoglobin (1-2 days); toxic nephropathy; with delayed or inadequate treatment - development of acute renal failure.