What are the morphological signs of barbiturate poisoning. Poisoning and overdose with barbiturates

Poisoning with barbiturates - drugs that are derivatives of barbituric acid - can occur either by accidental overdose or intentionally, for the purpose of committing suicide.

Characteristics of barbiturates

Barbiturates are medications based on barbituric acid. Their main property is the suppression of the central nervous system. Barbiturates are characterized by powerful hypnotic, analgesic and sedative effects.

The effect of such drugs on the body is compared to the effect of alcohol. Soon after taking them, a state of excitement and euphoria is noted, then a heavy sleep-forgetfulness sets in, after which the person feels weak and depressed.

After taking drugs from the barbiturate group, consequences such as unpredictable behavior and inability to control emotions can be observed. Large doses of the drug help reduce levels blood pressure, disrupt activities cardiovascular system, cause disruption of the functioning of the digestive tract. An overdose of barbiturates poses a particular threat not only to health, but also to human life, since in this case there is a high risk of death.

The use of drugs from this drug group causes:

• disturbance of breathing and heart rate;
• speech disorders (slowness, slurring);
• depression;
• clouding of consciousness;
• hallucinations;
• inability to navigate in space;
• loss of balance;
• drowsiness.

Long-term use of barbiturates makes a person dependent on these medications. This condition can be compared to drug addiction. Due to the powerful effect on the central nervous system and the likelihood of developing dependence, barbituric acid preparations are almost never used in therapeutic purposes. They are rarely used to treat epilepsy or have a hypnotic effect. The most well-known barbiturate drugs are “Barbital”, “Barbamil”, “Nembutal”, “Talbutal”. Such well-known products as Valocordin and Corvalol are made on the basis of barbiturates.

What happens during an overdose

Increased doses of barbiturates cause a number of changes in the functioning of organs and body systems. Under these conditions, the following happens:

• blood circulation is disrupted;
• the functions of the brain stem and cortex are inhibited;
• the contractility of the heart muscle decreases;
• the activity of the urinary system decreases;
• the tone of blood vessels is disturbed;
• oxygen starvation of tissues develops;
• the level of toxic compounds and breakdown products in the blood increases;
• body temperature decreases;
• blood pressure drops sharply.

Death in case of barbiturate poisoning occurs as a result of severe cardiac and respiratory failure, since large doses of drugs provoke paralysis of the respiratory and vasomotor centers.

Characteristic symptoms of intoxication with barbituric acid drugs

The severity of symptoms due to excessive use of barbiturates depends on the dosage of the drug and the duration of presence of toxic substances in the bloodstream. If the victim took fast-acting drugs, the manifestations of intoxication are eliminated quite quickly, since the medications disintegrate in the body in a short time. When the dosage of medium- and long-acting barbiturates is exceeded, the clinical picture of intoxication is more pronounced.

Signs of barbiturate poisoning:

• drowsiness and apathy;
• feeling of pleasant relaxation;
• pronounced salivation;
• feeling of weakness in the muscles;
• slurred speech;
• slight constriction of the pupils.

The listed manifestations indicate mild stage intoxication. In this case, reflexes do not become impaired. If the next dose of barbiturates does not enter the body and timely treatment is provided medical care, there will be no serious consequences for the body.

A more severe stage (the so-called “superficial coma”) is expressed in the following manifestations:

• increased heart rate;
• pale skin;
• weak motor reactions;
• difficulty breathing;
• constriction of the pupils;
• decrease in respiratory rate;
• loss of consciousness - the poisoned person is in a state of deep sleep, attempts to wake him up are unsuccessful.

A characteristic feature of this stage of poisoning is the victim’s ability to respond to painful stimuli. A victim who is in a state of superficial coma may begin an attack of vomiting, which can lead to vomit being thrown into the esophagus and entering the respiratory tract. This may cause breathing to stop.

Barbiturate poisoning is most dangerous in the stage of deep coma. In this case, changes occur associated with the complete absorption of toxic substances by tissues. If medical care is not provided in a timely manner, the stage of deep coma ends in death.

This condition is characterized by:

• pale and dry skin;
• lack of reflexes;
• slowness of breathing;
• decreased body temperature;
• a sharp decrease in blood pressure;
• pronounced constriction of the pupils;
• lack of response to painful stimuli;
• arrhythmia.

The victim may remain in a coma for a long time - from an hour to a day. The severe toxic effect of toxins provokes respiratory and cardiac arrest. In this case, death occurs. Each drug that is a derivative of barbituric acid has its own dose indicators that are lethal when taken orally. For example, when using “Barbital” - 6-8 g, “Phenobarbital” - 4-6 g, “Cyclobarbital” - 5-20 g.

When the patient emerges from a coma, during the first 24 hours, manifestations of disturbances in the activity of the central nervous system are observed - hysteria, tearfulness. The victim is in an excited state and suffers from insomnia. Even if the victim was taken to a medical facility and went through all necessary procedures to eliminate excess toxins from the stomach and blood, the possibility of complications cannot be ruled out. These include mental disorders, pulmonary and cerebral edema, metabolic disorders, and acute renal failure.

First measures to help the victim

A person with signs of intoxication with barbituric acid preparations requires urgent Care, even if the poisoning is characterized by the mildest degree. The first thing to do is call an ambulance.

First emergency aid before specialists arrive, if the victim has not lost consciousness:

1. Reduce the content of toxic substances in the stomach and blood. For this purpose, it is necessary to give the patient to drink at least a liter of warm water (it is recommended to give from 10 to 13 liters in order to more effectively remove toxic compounds), after which, pressing on the root of the tongue with a finger or a spoon, induce vomiting.
2. After the victim’s bouts of vomiting are over, give an intestinal sorbent - “Smecta”, activated carbon. Then it is necessary to induce vomiting again;
3. Put the patient to bed and give him tea with plenty of sugar.

If a person is unconscious, the washing procedure is strictly contraindicated. The only thing that can be done before the doctor arrives in this case is to lay the person on his side and cover him with a blanket. In no case should the victim be placed on his back and left unattended: in the event of an attack of vomiting and the remnants of undigested food being thrown into the respiratory tract, respiratory arrest and death may occur.

Pulmonologist, Therapist, Cardiologist, Functional Diagnostics Doctor. Doctor of the highest category. Work experience: 9 years. Graduated from Khabarovsk State Medical Institute, clinical residency in therapy. I am engaged in the diagnosis, treatment and prevention of diseases of internal organs, and also conduct medical examinations. I treat respiratory diseases, gastrointestinal tract, cardiovascular system.

Barbiturates are a group of drugs based on barbituric acid, with pronounced sedative and hypnotic effects. Barbiturate poisoning often occurs as a result of taking a high dose of the drug or intentional use large quantity tablets together with alcohol during a suicide attempt.

Depending on the duration of the therapeutic effect, barbitures are divided into several groups:

• ultra-short-acting - most often, barbiturates of this group are used before surgery for premedication, their duration of action is up to 2-3 minutes, usually this is enough for a person not to feel pain and fall asleep;
• short-acting - drugs of this group are used as a sleeping pill, the effect occurs within an hour and lasts up to 6 hours;
• prolonged action - the effect occurs after 40-60 minutes and lasts up to 12 hours; drugs of this group are used to treat epilepsy, stress, and as a hypnotic.

The most well-known drugs from the barbiturate group are presented in more detail in the table.

Barbiturates - indications for use:

Drug name	Which group does it belong to (duration of effect)	Indications for use
Phenobarbital	Long-acting	Epilepsy, chronic alcoholism, diabetes mellitus, severe kidney diseases as part of complex therapy
Barbital	Long-acting	Increased psychomotor agitation, stress, insomnia
Amobarbital	Short acting	Insomnia, feelings of fear and anxiety, chronic stress, aggression
Cyclobarbital	Short acting	Psychomotor overexcitation, insomnia, anxiety

Attention! Self-medication with barbiturates can be life-threatening for the patient, so the dose of the drug should only be selected by a doctor. The instructions attached to the drug cannot determine the dose of the drug, since what is acceptable for one patient is fatal for another.

How do barbiturates act on the body?

Depending on the type, barbiturates can have a wide variety of effects on the human body - from a mild sedative effect to a state of deep coma. For a long period of time, drugs in this group were used as effective sleeping pills, but it soon became clear that barbiturates were addictive, and with prolonged use, chronic poisoning of the body gradually developed.

Drugs from the barbiturate group are almost immediately absorbed into the general bloodstream and have an effect on the brain and central nervous system. When using barbiturates in a moderate dose in the first hours after taking the pill, the patient experiences a state of tranquility, mild euphoria, sometimes speech becomes slurred, and coordination of movements is impaired.

The body quickly gets used to the drug and to obtain the primary effect, an increase in dose is required, as a result of which the nervous system and internal organs– heart, kidneys, lungs.

Barbiturates have the following effects:

• soothing;
• hypnotic;
• narcotic (mild intoxicating);
• relaxing;
• anticonvulsant;
• reduces feelings of anxiety and fear.

Currently, doctors are increasingly trying to prescribe drugs from this group to patients for fear of barbiturate poisoning. Mostly data medicines are used to prepare a patient for surgery or as part of complex therapy for the treatment of epilepsy and other serious diseases.

First signs

Poisoning with drugs based on barbituric acid occurs very often in medical practice.

The severity of clinical symptoms depends on a number of factors:

• medication doses;
• age and body weight;
• the state of the body as a whole and especially the functioning of the heart and kidneys;
• quality of the medicinal product.

The very first sign of poisoning with drugs of this group is sleep, while at first all the patient’s reflexes are preserved. As the drug is absorbed into the bloodstream and influences the central nervous system, sleep turns into deep anesthesia, against which the sensation of pain disappears, touch is not felt, and the patient does not hear loud sounds. The severity of poisoning can be judged by the presence of reflexes - corneal and pupillary.

The corneal reflex is the reaction of quickly closing the eyelids in response to irritation of the cornea. In medicine, to test this reflex, a piece of cotton is used to touch the victim’s cornea. A normal reaction is when, in response to a touch with cotton wool, both eyes quickly close.

The preservation of this reflex indicates a shallow degree of poisoning of the body and timely measures taken help to quickly remove the patient from of this state. The absence of a corneal reflex indicates a severe lesion; in this case, if medical care is not provided in a timely manner, the prognosis can be disappointing.

Pupillary reflex

The pupillary reflex is the reaction of the pupil to light. Normally, when light enters the eyes, the pupil sharply constricts, and when the eyelid closes or when being in a dark room, the pupil dilates.

If the pupil does not constrict when exposed to artificial light in the victim’s eyes, then the patient has a severe form of poisoning and immediate resuscitation is necessary.

Reaction from the respiratory system

Depending on the severity of the condition, the victim’s breathing changes:

• becomes less frequent;
• becomes intermittent and superficial;
• There is a violation of the respiratory rhythm - breathing every once in a while;
• complete cessation of breathing.

When barbiturates are taken in large doses, paralysis of the respiratory center and complete cessation of breathing occurs. Against the background of such a complication, the amount of carbon dioxide in the blood sharply increases and the level of oxygen in the internal organs decreases.

As a result, acidosis quickly develops - a violation of the acid-base balance in the body. Along with acidosis, the patient’s blood pressure drops, acute vascular and heart failure develops - against the background of this, the blood vessels stop responding to adrenaline.

Against the background of disruption of the full functioning of the respiratory system and deterioration of gas exchange, the patient often experiences congestion in the lungs, resulting in the development of broncho-obstruction and pneumonia. In severe cases, patients died from pulmonary edema.

Changes in pulse and heart rate

Against the background of a decrease in blood pressure, the victim’s pulse rate changes. At first, the pulse becomes rapid, which is associated with changes in pressure and the response of baroreceptors (receptors in the heart and blood vessels).

As barbiturates are absorbed into the bloodstream and the drug affects the central nervous system, disturbances in the transmission of nerve impulses occur, which affects the pulse rate - this occurs in several stages:

• pulse becomes weak;
• the pulse becomes thread-like and is faintly palpable;
• The pulse cannot be felt at all, it disappears.

At the same time, the heart rate decreases.

Changes in the gastrointestinal tract and urinary system

As a result of poisoning the body with barbiturates, changes occur in the functioning of the urinary system and gastrointestinal tract. The pituitary gland increases the production of the hormone vasopressin, which reduces daily diuresis. In addition, urine production decreases due to a decrease in blood pressure and blood pressure in the kidney vessels, as a result of which the organ cannot function fully.

On the part of the gastrointestinal tract, there is a decrease in the production of gastric juice, a decrease in intestinal tone and a decrease in its peristalsis. Changes in metabolic processes are also observed, namely, body temperature decreases as a result of vasodilation, and the process of heat production decreases.

Attention! A sudden increase in body temperature against the background of barbiturate poisoning after hypothermia indicates a deterioration in the victim’s condition. Against the background of hyperthermia, acidosis in the blood can intensify even more, which can be fatal, so it is extremely important to provide resuscitation measures to the patient and closely monitor any changes in the body.

Severity of barbiturate poisoning

Doctors have identified forms of poisoning with drugs based on barbituric acid, depending on the severity of clinical symptoms:

1. Mild form - as a rule, everything goes away on its own without medical intervention within 24 hours after taking the drug. Clinically, it is accompanied by constant drowsiness of the patient, but he can be awakened and his reflexes are still preserved. The patient's breathing is normal, the skin is of normal color, the pulse is clearly palpable, the pressure is within normal limits or slightly reduced, but not critical.
2. The average form is when the victim sleeps all the time, and it is almost impossible to wake him up. Respiration and blood pressure are within normal limits, reflexes are preserved. If the patient’s liver and kidneys are working normally, then moderate poisoning may go away on its own within 2-3 days, after which the victim will feel weak and lethargic for some time. When diagnosing this form, the patient needs constant monitoring and observation, as his condition can sharply worsen.
3. Severe form - the corneal reflex is absent, but the pupillary reflex is preserved. With this pathology, the victim’s body is relaxed, breathing is intermittent, pulse and blood pressure are reduced. If severe barbiturate poisoning is detected, the patient needs resuscitation measures and constant medical supervision, otherwise cardiac arrest may occur.
4. Critical form - all reflexes are absent, breathing is rare, Cheyne-Stokes type (every other time), the skin is bluish, which indicates severe acidosis. The pulse is thready or not palpable at all, blood pressure is low, and the heartbeat is weak or absent.

Attention! In severe cases of poisoning, the patient needs artificial support of vital functions - breathing, heartbeat, as well as the necessary resuscitation and detoxification actions.

First aid to the victim

It is extremely dangerous when the victim is alone in the apartment and there is no one to help him - in such a situation, death most often occurs. However, if relatives or close people are nearby, then negative consequences completely avoidable.

An overdose of barbiturates and poisoning of the body can be suspected by sudden drowsiness and lethargy of the victim. The first step is to urgently call an ambulance.

Important! There is no need to decide on your own whether the poisoning is serious or not, since the patient’s condition can worsen at any time, so first call a doctor, and then provide pre-hospital emergency care.

The principles of first aid are as follows:

• stop the absorption of the drug into the blood - to do this, induce vomiting, wash the stomach, give sorbents (see);
• supporting normal breathing - the main thing here is to ensure that the victim does not fall into a state of deep sleep - hit him on the cheeks, talk loudly to him, wash with cold water, whatever you want, just don’t let him sleep;
• prevention of falling into a coma - if the victim is conscious, then the concentration of the drug in the blood should be reduced as much as possible, for this they give enemas, introduce enterosorbents inside, induce vomiting, give a lot of water.

Attention! If the patient’s consciousness is impaired, then there can be no talk of injecting drugs or inducing vomiting - such actions can lead to the victim choking on vomit or choking.

If the victim is unconscious, then before the ambulance arrives, it is important to ensure that his head is elevated and his tongue does not fall back. In addition, ensure that the patient maintains optimal body temperature - cover him, apply a warm heating pad to his limbs. The video in this article explains how to help a person who has been poisoned by barbiturates before the ambulance arrives.

Remember that self-medication can be life-threatening, so any medicines should be taken only as prescribed by a doctor. You cannot increase the dose of barbiturates without permission, even if this drug was recommended to you by your doctor; the cost of such self-medication may be too high.

Barbiturates are a group of drugs derived from barbituric acid that have a depressant effect on the central nervous system. The therapeutic effect is determined by the dose taken - from light sedation to surgical stages of anesthesia.

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Previously, barbiturates were widely used as hypnotics, sedatives and anticonvulsants, but due to the narrow therapeutic action, as well as the ability to quickly cause drug dependence, their use is currently limited.

Barbiturate poisoning occurs intentionally (during attempted murder or suicide) or accidentally when the therapeutic dose of the drug is exceeded.

After entering the body in toxic doses, barbiturates inhibit the functions of the cerebral cortex and brain stem. This leads to loss of consciousness up to the development of coma and severe breathing problems. Tendon, tactile and pain reflexes disappear.

The toxic effect of barbiturates on the vasomotor center causes a decrease in the tone of blood vessels and a deterioration in myocardial contractility. As a result, the victim experiences severe hemodynamic disturbances:

• a sharp decrease in venous and blood pressure;
• decreased cardiac output;
• decrease in circulating blood volume;
• significant tissue hypoxia.

Severe barbiturate poisoning leads to paralysis of the vasomotor and respiratory centers, resulting in death due to severe respiratory and heart failure.

Hemodynamic disturbances cause metabolic disorders, increased heat transfer and, as a result, a decrease in body temperature. However, in children with barbiturate poisoning, body temperature, on the contrary, can increase, which is associated with severe hypoxia of the subcortical centers of the brain, including the thermoregulation center, as well as dehydration of the body.

High doses of barbiturates have a toxic effect on the hypothalamic-pituitary system. The result is a significant decrease in diuresis, up to the development of anuria (cessation of urination) and an increase in the concentration of residual nitrogen in the blood.

Symptoms of poisoning

Clinical picture barbiturate poisoning includes several stages. With the exception of the first stage, the rest may have a complicated or uncomplicated course.

Falling asleep stage

The first stage is characterized by:

• drowsiness;
• apathy;
• muscle weakness;
• ataxia;
• slurred speech;
• slight constriction of the pupils while maintaining their reaction to light;
• increased salivation.

Respiratory and cardiovascular disorders are not detected, reflex activity is preserved.

Superficial coma stage

The victim loses consciousness and falls into deep sleep. The pupils are constricted. Tendon, pupillary and corneal reflexes are weakened. At this stage of poisoning, slight stiffness of the neck muscles may be observed, as well as the appearance of pathological Rossolimo and Babinski reflexes.

The frequency of respiratory movements decreases, which is accompanied by periodic cyanosis. Blood pressure is within normal limits, the pulse is somewhat rapid, but its rhythm and filling are normal.

Deep coma stage

If the victim is not provided with medical assistance in the previous stages of barbiturate poisoning, a deep coma develops, which is manifested by the following symptoms:

• areflexia;
• lack of muscle tone;
• sharp constriction of the pupils, which, with severe hypoxia, is replaced by dilation;
• cyanosis of the mucous membranes and skin;
• coldness of the skin of the extremities;
• slow shallow breathing (in terminal stage poisoning, the development of noisy breathing of the Cheyne-Stokes type is possible);
• bradycardia;
• hypotension;
• decrease in body temperature.

Postcomatose period

After emerging from a comatose state, the patient retains the following symptoms for some time (the duration depends on the severity of intoxication):

• impaired coordination of movements;
• diplopia;
• nystagmus;
• eyelid ptosis;
• eye convergence;
• transient neurological disorders;
• emotional lability;
• mental deafness;
• motor restlessness.

Acute poisoning barbiturates occurs during an overdose, and chronic develops with prolonged abuse. Based on the symptoms and signs, you can determine the stage of poisoning with sleeping pills and provide assistance correctly. Here you will find an algorithm for action in case of poisoning and find out what to do if a person is poisoned with drugs containing barbituric acid.

Barbiturates are drugs that contain salts of barbituric acid. Teenagers use them as a drug, which in its effects resembles alcohol intoxication.

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Symptoms of acute barbiturate poisoning

Most often, people are poisoned by barbiturates of medium and long duration of action. There is also a third option - a short-acting one, but it is more difficult to get poisoned by them and basically, this happens in the clinic, under the supervision of medical staff who know how to quickly correct the situation.

Acute poisoning with barbituric sedatives has 4 stages. Signs that a person has been poisoned by barbituric acid manifest themselves in different ways.

Stage 1 – falling asleep. A person wants to sleep, he is apathetic to everything that happens, and his reaction to stimuli is reduced. At this stage it is still possible to establish contact with the victim.

Stage 2 – superficial coma. At this stage, the victim loses consciousness and responds to painful stimulation with a weak motor reflex or short-term dilation of the pupils. This stage is also characterized by difficulty swallowing and a weakened cough reflex. Breathing may be impaired due to a sunken tongue, and body temperature at this time may rise to 40 degrees.

Stage 3 – deep coma. At the stage of poisoning progression, a person falls into a deep coma, while reflexes are inhibited, muscle tone decreases, and the pupils dilate. In this condition, the patient does not react to pain in any way, breathing becomes rare and shallow, and may even stop. In a deep coma with an overdose of barbituric sleeping pills, a person can stay from 1-3 hours to a day.

Stage 4 – post-comatose state. When a barbiturate addict comes out of a coma, this is accompanied by motor agitation. Consciousness is gradually restored. On the first day after waking up, most patients suffer from sleep disturbances, depression and tearfulness.

Clinical signs of barbiturate poisoning

• Comatose state together with other neurological disorders;
• Breathing disorders;
• Disruption of the cardiovascular system
• Renal dysfunction, trophic disorders

In case of barbiturate poisoning, death occurs from paralysis of the respiratory center and circulatory disorders. Lethal dose The most common drugs containing barbituric acid are approximately 10 times higher than usual.

Amobarbital 2-4g.
Barbital 6-8g.
Heptabarbital 20g.
Diallylbarbituric acid 6-8g.
Phenobarbital 4-6g.
Cyclobarbital 5-20g.

First emergency aid for barbiturate poisoning

A person who has been poisoned by barbiturates needs to urgently call an ambulance. Before the doctors arrive, the patient can be helped by washing the stomach. The algorithm of actions in case of barbiturate poisoning must be followed clearly.

1. Take activated carbon.
2. 10 minutes after taking charcoal, double gastric lavage (induce vomiting + enema). Repeat rinsing, using at least 10-12 liters of water.
3. To speed up the elimination of absorbed barbituric acid, the patient is prescribed plenty of fluids and a saline laxative.

IN outpatient setting Treatment of barbiturate poisoning is selected individually, depending on the stage. Doctors administer infusion therapy and forced diuresis to the patient. If a barbiturate addict falls into a coma, he will undergo hemosorption, hemodialysis and ultraviolet irradiation of the blood. If the coma is superficial, then analeptics (physiological antagonists) are used for barbiturate poisoning.

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Relevance. Acute barbiturate poisoning is quite common in the structure of modern toxicological pathology. Thus, among the contingent of patients admitted to specialized centers for the treatment of acute poisoning, specific gravity persons with poisoning by psychopharmacological compounds, including barbituric acid derivatives, is at least 20 - 25%; they account for 3% of all deaths. In severe barbiturate poisoning with the development of a coma, the mortality rate increases to 15% even under conditions of use modern methods intensive care.

Barbiturates- an extensive group of barbituric acid derivatives (phenobarbital [luminal], sodium amytal [barbamyl], sodium etaminal [nembutal], benzonal, hexenal, sodium thiopental, barbital [veronal], butobarbital, secobarbital [seconal], etc. [phenobardital is included in the composition ]), which are used as sedatives and hypnotics with a narcotic type of action; phenobarbital, in addition, is an effective antiepileptic drug (barbituric acid was first synthesized in 1863 by the famous chemist Adolf von Bayer; since the discovery occurred on December 4 - St. Barbara's Day - this is where the first part of the name of the acid came from; the second part - from English word"urea", that is, "urine"). Their use as hypnotics has decreased due to the widespread use of benzodiazepine anxiolytics.

The action of barbiturates is opposite to that of amphetamines: they suppress the central nervous system. In small doses they act as tranquilizers, and in large doses they are hypnotics (while sleeping with barbiturates is abnormal sleep, since they suppress all types of normal activity during sleep). In general, barbiturates have an inhibitory effect on the central nervous system, which is clinically manifested by hypnotic, euphoric, as well as sedative, anxiolytic and anticonvulsant effects.

The main mechanism of action of barbiturates is due to the fact that they penetrate the internal lipid layers and liquefy the membranes nerve cells, disrupting their function and neurotransmission. Barbiturates block the excitatory neurotransmitter acetylcholine, while stimulating the synthesis and increasing the inhibitory effects of GABA. Barbiturates can cause an increase in the stability of nerve cell membranes over time. With an overdose of barbiturates, previously intact individuals consistently develop disturbances of consciousness: stupor, stupor and coma. Severe poisoning is accompanied by a decrease in cardiovascular activity and hyporeflexia. Causes of death: respiratory failure, acute liver failure, shock reaction with cardiac arrest.

Please note! The clinical picture of barbiturate poisoning is characterized by a “calm” coma and has no pathognomonic signs; it boils down to depression of consciousness, respiratory failure of mixed origin, decreased blood pressure, and muscle hypotonia with hyporeflexia.

Barbiturates primarily depress the central nervous system, so one of the main symptoms is impaired consciousness. Depending on the severity of poisoning (intoxication) with barbiturates, the degree of depression of consciousness can vary from mild drowsiness and stupor to the development of coma. In the case of a rapid decrease in the concentration of barbiturates in the blood, for example, against the background of extracorporeal treatment methods, the development of a convulsive syndrome may occur.

Rough neurological symptoms distinguish barbiturate intoxication from alcohol intoxication. Therefore, the doctor’s attention should be drawn to dysarthria, ataxia, lack of coordination of movements, large lateral nystagmus, sharp dilation of the pupils with a sluggish reaction to light, hypersalivation, hyperhidrosis, a tendency to anger and aggression. Intoxication with sleeping pills differs from opiate anesthesia by impaired consciousness, the above-mentioned neurological symptoms, pupil size, skin color, hypersalivation, hyperhidrosis, inability to dissimulate, and lack of ease of emotions. In contrast to hashish intoxication, in these cases there are pronounced neurological symptoms and more severe affective reactions with anger and aggressiveness.

Respiratory disorders due to barbiturate poisoning have a mixed origin. The central type of acute respiratory failure is associated with depression of the respiratory center. This type of respiratory failure is manifested by an increase in respiratory rate and a decrease in tidal volume. Another important pathogenetic link in respiratory failure is the development of obstructive breathing disorders, which can be caused by both a decrease in muscle tone and retraction of the tongue, and the development of broncho-obstruction due to increased tone of the vagus nerve. It is significant that the mechanism of formation of the obstructive type of respiratory failure is often obstruction of the upper respiratory tract by gastric contents. Aspiration of gastric contents leads to aspiration pneumonitis and the development of aspiration pneumonia, acute lung injury and acute respiratory distress syndrome. Ultimately, breathing disorders will lead to the development of hypoxemia, hypercarbia and mixed hypoxia.

Barbiturates, acting on the central nervous system, inhibit the cardiovascular center, which causes vasodilation, also caused by the nonspecific release of histamine. Also, in case of poisoning with barbiturates, a direct negative inotropic effect is possible, due to disruption of the transmembrane current of calcium and NO uptake. Thus, vasodilation, relative hypovolemia and decreased myocardial contractility lead to a decrease in blood pressure. It is obvious that the listed pathological processes are characterized high risk development of perfusion disorders.

In case of barbiturate poisoning, hypothermia is often detected, associated with decreased metabolism and vasodilation (peripheral). Often poisoning with barbiturates is accidental in nature for the purpose of intoxication, and therefore such patients are long time in a stationary state. This leads to disruption of local blood supply and ischemia and necrosis of soft tissues, characteristic of positional compression syndrome, as well as ischemic neuropathies and bullous dermatitis, which aggravates the somatogenic stage of barbiturate poisoning.

read also the article “Toxic effects of barbiturates” by G.V. Esin, P.A. Livanov, V.Yu. Soldatova, V.Yu. Pikovsky (Moscow State Medical and Dental University named after A.I. Evdokimov, Ministry of Health of Russia, Moscow), A.S. Livanov (GBUZ "City Clinical Hospital No. 5" of the Moscow Department of Health); magazine "Medical Alphabet" No. 3/2015, volume No. 1 (Emergency medicine) [read]

stage 1 – “falling asleep”: characterized by drowsiness, apathy, decreased reactions to external stimuli, but contact with the patient can be established;

stage 2 – “superficial coma”: loss of consciousness is noted; Patients may respond to painful stimulation with a weak motor reaction and short-term dilation of the pupils; swallowing becomes difficult and the cough reflex weakens, breathing problems occur due to the retraction of the tongue; characterized by an increase in body temperature to 39 - 40 C° (toxic hyperthermia);

stage 3 – “deep coma”: characterized by the absence of all reflexes, hypothermia (toxic hypothermia); there are signs of a threatening violation of the vital functions of the body; breathing disorders from superficial, arrhythmic to complete paralysis, associated with inhibition of the central nervous system, come to the fore;

stage 4 – “post-comatose state”: consciousness is gradually restored; on the first day after waking up, most patients experience tearfulness, sometimes moderate psychomotor agitation, and sleep disturbances (withdrawal syndrome - with regular use of barbiturates for 6 months).

Withdrawal syndrome Abuse of barbiturates is dangerous due to the occurrence of convulsive seizures and psychosis. They are observed when taking large doses of drugs and can replace each other. So, a patient may have 1 or 2 convulsive seizures during the first day after stopping the drug, and psychosis develops on the 2nd - 3rd day (usually at night). But more often, convulsive phenomena occur on the 3rd - 5th day of deprivation or a significant reduction in barbiturate doses. They are characterized by full-blown convulsive seizures, indistinguishable from seizures in genuine epilepsy. Psychosis occurs on the 3rd to 8th day of deprivation or a sharp reduction in large daily doses of barbiturates. Psychoses are usually represented by delirium, less often - verbal hallucinosis. Delirium is similar in clinical manifestations to alcoholic delirium. However, it is distinguished by the greater severity of anxiety, tension, and anger of patients, the rarity of tactile hallucinations, the greater proportion of auditory hallucinations, and the presence of muscle twitching. Rarely occurring hallucinatory delusional psychoses resemble schizophrenic psychoses. Their structure includes hallucinations and delusions; patients may be in a substupor or, on the contrary, exhibit panic reactions. Withdrawal syndrome from barbiturate abuse lasts an average of 3 weeks.

Confirmation of acute barbiturate intoxication is carried out using qualitative chemical-toxicological analysis using immunochemical methods for determining barbiturates in biological media: enzyme immunoassay, immunochemical analysis, polarization fluoroimmunoassay, etc. They are based on a specific antigen-antibody reaction, where the antigen is various barbiturates from the patient’s biological media, and the antibody is a pre-prepared IgG fraction of the blood of an immunized animal, fixed by a certain method. Similar methods used as express diagnostics. They make it possible to qualitatively determine the presence of barbiturates in a given biological environment (for a one-stage, rapid qualitative determination of barbiturates and their metabolites in urine at the prehospital stage and in the emergency department, it is possible to use “ImmunoChrome-BARBITURATES-Express” test strips, the operating principle of which is based on the immunoassay method -chromatographic analysis). In case of a negative result, no further chemical-toxicological analysis is carried out. In the case of a positive rapid reaction, further chemical and toxicological analysis is carried out using one of the confirmatory methods to quantify the concentration of barbiturates in a sample of biological media. Gas-liquid chromatography, high-performance liquid chromatography, and gas chromatography-mass spectrometry are used as confirmatory methods.

There is no specific antidote to treat barbiturate poisoning. Treatment of barbiturate poisoning is aimed at increasing drug excretion and symptomatic therapy. In all cases of acute barbiturate poisoning, it is necessary to rinse the stomach and intestines with warm water and activated carbon or 2% soda solution (if more than 8 - 10 hours have passed after taking barbiturates, rinsing is useless), give a saline laxative, prescribe oxygen inhalation with 5% carbon dioxide, suck out mucus from the bronchi, prescribe cardiovascular drugs and, for the purpose of preventing and treating pneumonia, antibiotics. If breathing is impaired, lobeline (1 ml of 1% solution) is injected under the skin and artificial respiration is used. In case of collapse and pulmonary edema, the necessary set of measures is carried out. Great value given to patient care (warming, body and oral hygiene, catheterization bladder, treatment of bedsores, etc.). To recover from a comatose state, large doses of analeptics (strychnine, caffeine, cordiamine, bemegride) are used, which stimulate the central nervous system and are physiological antagonists of barbiturates. [ ! ] Their use requires absolute certainty in barbiturate poisoning.

REFERENCE INFORMATION: syndrome of psychoneurological disorders in acute poisoning

Psychoneurological disorders in acute poisoning consist of a combination of mental, neurological and somatovegetative symptoms due to a combination of direct toxic effects on various structures of the central and peripheral nervous system and lesions of other organs and systems that develop as a result of intoxication.

Disturbances of consciousness are manifested by depression (stupefaction, somnolence, coma) or excitement (psychomotor agitation, delirium, hallucinations) of mental activity, often replacing each other. The most severe cases are acute intoxication psychosis and toxic coma.

Toxic coma is more often observed in case of poisoning with substances that have a narcotic effect, although severe poisoning with any toxic substances with a sharp disruption of the vital functions of the body (blood circulation, respiration, metabolism, etc.) can be accompanied by profound inhibition of brain functions.

Clinical manifestations comas in acute poisoning are caused in the toxicogenic stage by the direct specific effect of poisons on the central nervous system, and in the somatogenic stage of poisoning they are determined by the development of endotoxicosis.

The general neurological picture of toxic coma in the early toxicogenic stage is characterized by the absence of persistent focal neurological symptoms (symmetrical symptoms predominate neurological signs) and rapid positive dynamics of neurological symptoms under the influence of adequate emergency treatment measures.

Each type of toxic coma, caused by the action of a certain group of toxic substances, is characterized by its own neurological symptoms, most clearly manifested at the stage of superficial coma.

Along with narcotic toxic coma, with neurological symptoms of superficial or deep anesthesia (muscular hypotonia, hyporeflexia), comatose states with severe hyperreflexia, hyperkinesis, and convulsive syndrome are observed.

The most noticeable in the neurological picture of acute poisoning, in particular coma, are the following somato-vegetative disorders: symmetrical changes in the size of the pupils, sweating disorders with dysfunction of the salivary and bronchial glands.

With M-cholinomimetic (muscarinic-like) syndrome, miosis, hyperhidrosis, hypersalivation, bronchorrhea, pallor of the skin, hypothermia, bronchospasm, bradycardia, hyperperistalsis are observed, caused by an increase in the tone of the parasympathetic division of the autonomic nervous system. Develops from poisoning with substances that have M-cholinergic activity (muscarine, organophosphorus compounds, barbiturates, alcohol, etc.).

With M-cholinergic (atropine-like) syndrome, mydriasis, hyperemia, dry skin and mucous membranes, hyperthermia, and tachycardia are observed. Develops from poisoning with substances that have anticholinergic effects (atropine, diphenhydramine, amitriptyline, asthmatol, aeron, etc.).

Adrenergic syndrome is caused by cocaine, ephedrine, amphetamines, melipramine, aminophylline, etc. It manifests itself as hyperthermia, impaired consciousness, agitation, hypertension, tachycardia, rhabdomyolysis, disseminated intravascular coagulation (DIC).

Serotonergic syndrome has been described in recent years, sometimes poses a danger to life. Caused by a large group of drugs - selective agonists of serotonergic receptors (buspirone, cisapride, new generation antidepressants, etc.), manifested by hyperthermia, impaired consciousness, vegetative dystonia (profuse sweat, pressure instability are observed), hyperreflexia, myoclonus, trismus, muscle rigidity. Characterized by rapid reverse development.

Miosis is caused by substances that increase the activity of the cholinergic system: M-cholinomimetics (muscarine, pilocarpine), anticholinesterases with an M-choline potentiating effect (aminostigmine, organophosphorus compounds, etc.); opiates, reserpine, cardiac glycosides, barbiturates, etc., as well as substances that reduce the activity of the adrenergic system: clonidine and its homologues, depressants; industrial agents (carbamate insecticides).

Mydriasis is caused by substances that increase the activity of the adrenergic system: indirect adrenergic agonists (amphetamines, ephedra, cocaine), catecholamine precursors (L-DOPA, dopamine), inhibitors of enzymes that inactivate catecholamines (MAO inhibitors); LSD; substances that reduce the activity of the cholinergic system: atropine and its homologues, antihistamines, tricyclic antidepressants.

Toxic encephalopathy is the occurrence of persistent toxic damage to the brain (hypoxic, hemodynamic, liquorodynamic with degenerative changes in brain tissue, edema of the meninges, its plethora, disseminated areas of necrosis in the cortex and subcortical formations). The most well-known psychoneurological symptoms of toxic encephalopathy in case of poisoning with compounds heavy metals and arsenic, carbon monoxide, opiates, as well as substance abuse.

Cerebral edema is a complication of toxic coma, accompanied by a variety of neurological symptoms corresponding to the topic of the lesion: transient paralysis, hemiparesis, pyramidal signs, cerebellar and extrapyramidal symptoms, epileptiform convulsions, hyperthermia, bulbar disorders, etc. Characteristic features Brain edema is congestion in the fundus of the eye, such as swelling of the optic discs, lack of pulsation, dilated veins and an increase in the size of the blind spot. Signs of intracranial hypertension are detected - stiff neck, tension in the eyeballs, bradypnea, bradycardia, etc. During a spinal puncture, an increase in intracranial pressure is determined.

Lifetime brain death is the most severe and irreversible complication of toxic coma with symptoms of hypoxia and edema of brain tissue. Brain vitality is determined by EEG. In acute poisoning with sleeping pills and drugs that cause deep but reversible anesthesia, intravital brain death can be judged only after 30 hours of continuous recording of isoelectric EEG.

Acute intoxication psychosis is a mental disorder with a predominance of symptoms of “floating” consciousness, hallucinosis (usually visual and tactile), and catatonic disorders. Observed when exposed to psychotomimetic substances (cocaine, marijuana, LSD, phenamines), carbon monoxide, tetraethyl lead, bulbocapnin (catatonia). Poisoning with anticholinergic drugs (atropine, atropine-like, antihistamines, amitriptyline) is accompanied by central anticholinergic syndrome.

Convulsive syndrome. In case of poisoning, clonic (corazol, cicutotoxin), clonic-tonic (physostigmine, organic phosphorus poisons) and tonic (strychnine) convulsions can occur. In case of poisoning with anticholinesterase poisons, general convulsions are preceded by intense myofibrillations.

Toxic hyperthermia can develop as a result of central disturbances of thermoregulation during poisoning with amphetamines, anesthetics (initial stage), zincofene, cocaine, dinitrocresol, dinitrophenol, ecstasy and its derivatives, MAO inhibitors, phenothiazines, theophylline, salicylates, serotonergic drugs, succinylcholine, xanthines. Most often, hyperthermia can be caused by infectious complications (such as pneumonia, including aspiration pneumonia, bacteremia and septicemia in drug addicts, etc.). Convulsive syndrome may be accompanied by hyperthermia.

Toxic hypothermia is a decrease in body temperature below 35 °C. Hypothermia can be observed in case of poisoning with alcohol, central analgesics, anesthetics, tricyclic antidepressants, barbiturates, benzodiazepines, carbamates, clonidine, cyanides, chloral hydrate, methyldopa, carbon monoxide, phenothiazines. In case of drug poisoning, it occurs in 7-10% of cases.

Toxic visual, auditory neuritis and polyneuritis develop in acute poisoning methyl alcohol, quinine, salicylates, antibiotics, organic phosphorus substances, thallium, arsenic, magnesium salts. Impaired color vision is observed in cases of poisoning with salicylates, aconite, digitalis, etc.