Morphine-opiates belong to the class of anesthetic drugs and are widely used by physicians to eliminate chronic, acute and other types of pain. Currently, technologies have been developed for taking opiates in any convenient way (orally, injections, droppers, etc.)

Opiates are extracted from a special variety of plants - the opium poppy. The substance itself belongs to the group of natural alkaloids. All opium painkillers are based on morphine and codeine.

At the same time, the term opiates is also used to refer to a variety of drugs that can interact with opium receptors in the body and have similar effects.

Opiates act on the central nervous system. The increased dose capable of causing intoxication varies widely and depends on the individual characteristics of a particular individual. The measure of toxic effects is also determined by the method of taking the drug and the body's tolerance to such substances. Since there is no data on exactly how much of an opiate is an overdose, cases of intoxication with these substances are not uncommon.

Today, medicine widely uses not only natural alkaloids. Morphine and codeine derivatives semi-synthesized at the molecular level are also widespread.

The effect of opiate drugs on the human body

Among opium addicts, the first phase of the action of opium is called the "arrival" and begins after 20-30 seconds. after taking.

At the physiological level, the following happens:

• An increase in heat in the abdominal cavity and lumbar region, which systematically rises up the whole body,
• redness of the skin of the face,
• constricted, immobile pupils,
• Thirst, feeling of dryness in the mouth,
• Itching in the lower part of the face.

On a psycho-emotional level:

• A person feels as if he "has seen the light", "saw the essence of all things",
• The surrounding world is refracted and seems ideal, "sparkling",
• Absence of thoughts, a state of meditation, bliss in the head,
• Consciousness perceives only the “high” of physical sensations.

The first phase lasts about 5 minutes. With prolonged use of opiates, the body's tolerance to them increases, and therefore the time of the first phase is reduced.

The second phase in the relevant areas is called "nirvana". The addict experiences a state of bliss and languor, true bliss and joyful peace. Physiologically, he seems to freeze, his limbs become heavy. A person ceases to pay attention to surrounding objects and events or reacts inadequately. In the imagination, “unearthly fantasies”, dreams and dreams are replaced one after another.

Codeine in action is somewhat different from morphine in the second phase: when it is taken, psychological and motor hyperactivity occurs, speech is fast, but incoherent, thoughts are confused.

The second phase lasts on average about 3-4 hours.

The third phase is a phase of very sensitive sleep, which can be disturbed even by the slightest rustles and sounds. It also lasts about 3-4 hours.

Phase 4 is not found in everyone and depends on the individual characteristics of the organism. It is characterized by headaches and a state of increased anxiety, melancholy, bouts of vomiting, tremors can be observed.

In general, including all phases, the effect of opium exposure lasts 6-10 hours.

Causes of opium poisoning

Opiate intoxication occurs with an overdose of the drug. An overdose can be intentional or accidental, and also happens in chronic opium addiction (addiction), when larger and larger doses are required each time to achieve a “high”. Often drug addicts deliberately increase the doses in an attempt to commit suicide or kill a friend. Childhood cases of intoxication may occur due to the lack of quality control of the substance. There are also cases of childhood poisoning with common cough medicines.

When taking opium for medical purposes, an overdose can occur during preparation for general anesthesia (premedication); in patients suffering from chronic pain and taking opiates on an ongoing basis (usually can occur with hepatic, renal insufficiency). Also, intoxication is possible in individual cases with the rapid introduction of the drug into a vein (bolus).

Symptoms of acute opium poisoning.

Acute intoxication can develop regardless of how the opiate is taken. It is characterized by the following features:

• confused mind,
• There is a coma
• Strongly constricted pupils, regardless of the amount taken,
• Paleness and blueness of the skin (cyanosis),
• Encephalopathy (toxic and hypoxic types),
• Respiratory failure.

If timely assistance is not provided, this is fraught with more serious consequences, such as:

• swelling of the brain,
• Acute respiratory failure when opium is taken orally or inhaled,
• stop breathing,
• dilated pupils,
• immobility of the eyeball
• Pneumonia,
• Arrhythmias, heart failure
• muscle dysfunction (rhabdomyolysis),
• Mendelssohn's syndrome (impaired swallowing function and, as a result, burns of the lungs with hydrochloric acid from the stomach),
• changes in body temperature,
• Vomit.

Opiate intoxication is fraught with serious complications. Some of them may become irreversible. Among them:

• Paresis,
• Paralysis of various nature,
• polyneuropathy,
• Withdrawal syndrome, psychosis, personality disorder,
• Chronic impairment of respiratory function up to respiratory arrest,
• The development of a psycho-organic syndrome - memory and intelligence decrease, a person becomes uncontrollable in a state of passion,
• Renal failure.

For poisoning with opium drugs, withdrawal symptoms (mental disorders) are also characteristic, as well as a withdrawal syndrome.

Stages of acute opium poisoning

In general, doctors divide the development of poisoning into 4 stages.

Stage 1 - the patient is still conscious and can be contacted, despite the fact that he is inhibited, half asleep and stunned. At the level of neurology, the following are characteristic: constricted pupils that do not respond to light stimuli, nystagmus - involuntary, rhythmic movements of the eye muscle, the tone of the muscles of the body decreases, there is no reflex contraction of muscles and tendons. The heart rate drops to only 30-50 beats per minute, breathing is disturbed, and cyanosis of the skin (cyanosis) appears.

Stage 2 - a person falls into a superficial coma, a coma state, there is no consciousness. The above symptoms are also present, the pressure is greatly reduced. There is no response to pain. Convulsions are typical.

Stage 3 - deep coma. The patient does not respond to pain and any external influences. Due to muscle atony, the patient loses the ability to swallow, cough, does not close the eyelid when the cornea is irritated. Impaired respiratory function can lead to cerebral edema. If at the third stage you do not take measures to provide medical care, then a fatal outcome is possible due to a violation of the respiratory function.

Stage 4 - the patient comes out of a coma, regains consciousness. The fourth stage is possible if the dose of the drug is not too high or the body was able to cope with the poisoning on its own. First, the respiratory function returns, then the blood circulation normalizes, after which the patient regains consciousness. At the same time, the motor ability of the eye muscle is limited, emotional instability, hyperactivity and insomnia are noted. A withdrawal syndrome (or withdrawal) is possible if the patient has been injected with an opiate antidote. After leaving the coma, complications are also possible - pulmonary edema, heart attack, aspiration, muscle necrosis.

Diagnosis of intoxication

Diagnosis is carried out by the method of complex laboratory research of the biomaterial. It makes it possible to determine the presence of opiate substances in the blood many days after they have been taken.

Only by combining laboratory tests and analysis of the patient's clinical symptoms, it is possible to diagnose opiate poisoning. Naloxone, an opiate antagonist, is also widely used in diagnostics. The doctor analyzes the body's reaction to it and makes a diagnosis.

Treatment for poisoning

In case of opium poisoning, medical assistance should be provided immediately.

Those who discovered the patient are forbidden to take any action and must wait for the arrival of doctors.

The main treatment for opiate poisoning is the introduction of an opiate antagonist, naloxone, into the body. This substance completely neutralizes their action. If the respiratory arrest is not caused by opium, but by other causes, there will be no reaction in the body to naloxone. Here its introduction is widely used as a way to diagnose an overdose of opium.

With the introduction of naloxone, the doctor observes the patient for an hour to avoid remorphinization - the withdrawal syndrome. Naloxone is usually administered intramuscularly.

Symptomatic treatment methods are also used, such as artificial respiration or tracheal intubation and connecting the patient to an artificial lung ventilation system.

Drug therapy includes a drip with saline and glucose, pyridoxine, neurometabolic stimulants, B vitamins, ethylmethylhydroxypyridine succinate, and some other drugs.

Physiotherapeutic methods include washing the stomach and intestines, introducing adsorbent substances into the gastrointestinal tract.

The term "opiates" refers to a group of physiologically active substances (alkaloids) isolated from opium, which is a hardened milky juice flowing from incisions made on the mature heads of the opium poppy (Papaver somniferum). Opium (opium resin, or raw opium) is a complex mixture of proteins, lipids, resins, waxes, sugars and other substances, including more than 50 alkaloids that make up 10-20% of the total mass of this material.

Opiates include the following drugs:

• opium,
• heroin,
• ethylmorphine (dionine*),
• codeine,
• morphine,
• thebaine.

The most important opium alkaloids are morphine, codeine, papaverine and thebaine. Morphine and codeine are used as medicines, but they are often used for non-medical purposes (as drugs). Papaverine does not have narcotic properties, but is widely used as a medicine. Thebaine is used mainly as a raw material for the production of other drugs.

Heroin (3,6-diacetylmorphine) is the most famous and widespread semi-synthetic opiate.

Pharmacological action: analgesic, narcotic.

Toxic effect: psychotropic, neurotoxic, due to the effect on the central nervous system, a depressing effect on the thalamic regions, a decrease in the excitability of the respiratory and cough centers, and excitation of the center of the vagus nerves.

Morphine

With intravenous administration of morphine, the maximum pharmacological effect develops after a few minutes, with subcutaneous and intramuscular administration - after 15 minutes. In the future, the content of morphine in the blood drops sharply. Morphine is excreted from the body mainly in the urine within 36-48 hours. Up to 80% of the administered morphine can be excreted during the first 8-10 hours after administration, with only less than 3% unchanged. After 72-80 hours, only traces of morphine can be determined in the urine, even when examined by the most sensitive methods. However, a certain part of the injected morphine is fixed in the hair and nails.

When morphine is taken orally, its conjugates with glucuronic and sulfuric acids are found in the urine, and glucuronides (morphine-3- and morphine-6-glucuronide) are much more than sulfate conjugates. Of the two isomeric monoglucuronides, morphine-3-glucuronide has no narcotic properties, while morphine-6-glucuronide exhibits significant activity. Small amounts of normorphine are also found in the urine.

Codeine

Codeine is much less potent than morphine. It is rapidly absorbed after parenteral administration and is metabolized in the liver via O- and N-demethylation to morphine or norcodeine, respectively. About 80% of codeine taken orally is excreted in the urine as free codeine (5-17%), codeine conjugates with glucuronic and sulfuric acids (32-64%), norcodeine conjugates (10-21%), morphine conjugates (5- thirteen%). In the initial period of excretion of codeine in the urine, mainly codeine conjugates are found, after 20-40 hours they are replaced by morphine conjugates.

Heroin

Heroin, when administered intravenously, is rapidly, within 3-7 minutes, metabolized to 6-monoacetylmorphine (6-MAM), which is then slowly deacetylated to morphine over several hours. Due to its high lipid solubility, heroin, unlike morphine, easily crosses the blood-brain barrier, which determines its powerful narcotic effect. Further, the formed morphine is relatively slowly converted into glucuronides. To prove heroin use, it is necessary to identify its metabolite 6-monoacetylmorphine, since other opiates do not form it.

Symptoms of opiate poisoning

The following signs are characteristic:

• significant constriction of the pupils with a weakening of the reaction to light,
• skin hyperemia,
• muscle hypertonicity,
• sometimes clonic-tonic convulsions.

In severe cases, there is often a violation of the respiratory system and asphyxia, characterized by a sharp cyanosis of the mucous membranes, dilated pupils, bradycardia, collapse, hypothermia.

In severe poisoning with codeine, respiratory disorders are possible with the patient's consciousness preserved, as well as a significant drop in blood pressure.

Urgent care

Repeated gastric lavage (in case of taking the drug inside), the appointment of activated charcoal, saline laxative. Alkalinization of the blood is shown, the introduction of 400 ml of a 0.06% solution of sodium hypochlorite intravenously through a catheter.

Subcutaneously and intravenously, 1-2 ml of 0.1% atropine solution, 2 ml of 10% caffeine solution, 2 ml of cordiamine, 3 ml of 5% thiamine solution are injected intravenously repeatedly. It is necessary to warm the patient, oxygen inhalation is indicated.

Specific (antidote) therapy

The antidote naloxone is included in the list of vital drugs (Order of the Ministry of Health of the Russian Federation No. 157 of July 28, 1994) and in the "List of antidotes and other drugs used in acute poisoning as a means of specific pharmacotherapy."

Naloxone- a product of chemical modification of the morphine molecule, a specific pure antagonist of opiates (morphine, etc.) and opioids (fentanyl, dextropropoxyphene, methadone, buprenorphine, nalbuphine), used to completely or partially eliminate their effects, and also used to diagnose acute overdose these compounds. It has no effect on respiratory depression due to other causes.

When administered intravenously, naloxone is rapidly metabolized, metabolism is carried out in the enterohepatic cycle: dealkylation with the reduction of the 6-keto group, glucuronidation with the formation of 2-naloxone-glucuronide. Eliminated in the urine in pure form and in the form of metabolites (70% within 72 hours). The action of naloxone with intravenous administration begins after 30 seconds (3 minutes), with intramuscular or subcutaneous administration - after 3 minutes,

The half-life is from 45 to 90 minutes. The duration of action of naloxone when administered intravenously is from 20 to 30 minutes, when administered intramuscularly or subcutaneously - from 2.5 to 3 hours. It penetrates well through the blood-brain barrier (maximum concentration in brain structures is reached after 15 minutes) and placental barriers.

As an initial dose, 0.4-2 mg of the drug is administered intravenously. Mandatory reaction to the introduction of naloxone in case of poisoning with opiates is at least a short-term increase in breathing, dilated pupils, and a decrease in the degree of depression of consciousness. If the desired degree of antagonization and improvement of respiratory functions is not achieved immediately after intravenous administration, it can be repeated at intervals of 2-3 minutes. The lack of effect after 2-3 injections calls into question the diagnosis of opiate poisoning. After intravenous jet administration of the initial dose of naloxone, its intravenous drip is recommended at a dose of up to 2.4 mg in 500 ml of 5% glucose solution or isotonic sodium chloride solution. The rate of infusion is determined by the patient's response (the recommended rate of administration is 0.4 mg over 30 minutes).

The effect of the administration of naloxone is short-lived (30-45 minutes), therefore, due to the risk of remorphinization (repeated depression of consciousness and respiration), even after the restoration of consciousness, it is necessary to monitor the patient (monitoring of respiration and consciousness) for 6-12 hours. For prolonged administration, it is recommended "titration" of naloxone - 1 ml (0.4 mg) is diluted in 4 ml of isotonic sodium chloride solution and administered intravenously at a rate of 1 ml / min.

The lack of a sufficient effect of the administration of naloxone may be due to severe hypoxic brain damage.

Despite the lack of a proven causal relationship, it has been noted that too rapid administration of naloxone to patients with heart disease can lead to arterial hypotension, pulmonary edema, ventricular tachycardia and fibrillation, and cardiac arrest.

For children, the usual starting dose of naloxone is 0.01 mg/kg IV, continued as needed. There is a special dosage form for newborns (Narcan neonatal), containing 0.02 mg of the active ingredient in 1 ml of the drug.

Naltrexone (antaxone) is a specific opioid receptor antagonist. Competitively binds to all types of opioid receptors. Similar to naloxone but longer lasting. The half-life of naltrexone is 4 hours, its metabolite 6-naltrexone is 13 hours. At a dose of 50 mg, naltrexone blocks the pharmacological effects caused by intravenous administration of 25 mg of heroin for 24 hours, at a dose of 100 mg this action is extended to 48 hours, at a dose of 150 mg - up to 72 hours. Naltrexone is used primarily for the treatment of opium dependence in order to maintain the patient's condition in which opioids cannot have a characteristic effect.

Nalorfin chemically similar to morphine. Modification of the structure led to the production of a compound that is an agonist (analgesic effect) and an antagonist in relation to opiate receptors (weakens respiratory depression caused by opiates and lowers blood pressure, cardiac arrhythmias). It is rarely used as an antidote: it has been replaced by naloxone. In the absence of opiates in the body, it can cause depression of consciousness and breathing. Intravenously administered 1-2 ml of 0.5% solution. If the effect is insufficient, the injections are repeated after 10-15 minutes; the total dose should not exceed 8 ml.

Oxygen therapy

Artificial respiration with a mask or Ambu bag, tracheal intubation, artificial lung ventilation, hyperbaric oxygenation.

Pathogenetic therapy

The use of respiratory analeptics (etimizol *, lobelin) is not indicated. With blockade of the respiratory tract, tracheal intubation, artificial lung ventilation (ALV) are necessary, in a coma, intravenous drip of glucose *, cytoflavin *, mexidol *, thiamine, pyridoxine, ascorbic acid, sodium hydroxybutyrate is advisable.

Detoxification therapy

Forced diuresis is shown. After ingestion, a second gastric lavage is recommended (after breathing is restored, very carefully due to the risk of damage to the esophagus, which is in hypertonicity), activated charcoal, enterosorbent, and saline laxative are prescribed. In case of poisoning with a mixture of psychotropic substances, codeine, methadone *, detoxification hemosorption is used.

Syndromic therapy

Assign vasoactive agents, antishock therapy, glucocorticoids. Treat non-cardiogenic pulmonary edema. Antibiotic therapy with broad-spectrum drugs is indicated, starting from the early toxicogenic stage: treatment of positional tissue compression. Hemosorption, plasmapheresis, hemodiafiltration, HD are effective.

Laboratory diagnostics for opiates

When screening biofluids for the presence of opiates, immune methods are used (ICA, IFA, PFIA, RIA). They do not require sample preparation; they are used to determine both free substances (morphine, codeine) and their conjugates with glucuronic acid. Due to cross-reactivity, naloxone, nalorphine, and other substances in plasma at a concentration many times higher than the working concentrations of the method can give a positive result.

Given that opiates are excreted in the urine mainly in the form of conjugates, hydrolysis (acidic or enzymatic), extraction of hydrolysis products and analysis according to accepted standard methods are carried out before chromatographic examination. To establish the fact of heroin use, which is confirmed by the presence of the first active metabolite of heroin - 6-monoacetylmorphine hydrolysis of urine samples is not carried out. In qualitative analysis, TLC, GLC, HPLC, GC-MS are used. Quantification is carried out by GLC or HPLC.

To increase the sensitivity of the method in the determination of opiates, to improve their chromatographic properties, the structure of opiates is transformed before GLC using special reagents to form so-called derivatives.

Morphine and codeine are found in the urine during the day, their glucuronides - within 3 days.

One of the private forms of drug addiction is opium (opioid) addiction - a disease that develops as a result of the use of opiates (opioids) and the formation of drug dependence.

In recent years, there has been a noticeable tendency to distinguish between the concepts of "opium addiction" and "opioid addiction" used by pharmacologists and narcologists. The term "opiates" usually includes narcotic substances of natural origin, derived from plant materials (hypnotic poppy - Papaver somnifeum), including both individual alkaloids of this plant, and primary processed plant products containing a mixture of alkaloids (specially artisanally processed and ready for use raw opium - the so-called acetylated opium). Substances obtained artificially (semi-synthetically or synthetically) that are similar in their pharmacological action to opiates are designated by the term "opioids".

Opium substances are classified according to their origin: natural, semi-synthetic, synthetic ( ), as well as by the type of their pharmacological action: full and partial agonists of opioid receptors, antagonists and drugs of mixed (agonist-antagonistic) action.

The development of dependence on natural, semi-synthetic or synthetic opium substances is based on common pathogenetic mechanisms, which, despite a number of differences (in the picture of drug intoxication, abstinence, etc.), allows us to consider this dependence as a single disease - opium addiction, with its the most common clinical variants (heroinism/heroin addiction; codeineism/codeine addiction, etc.).

Heroin has been the most commonly used drug from the group of opium derivatives in Russia lately.

It is necessary to single out a number of emergency conditions associated with the use of narcotic (substance addicts) substances, among which, according to statistics, opiates occupy one of the leading positions:

• severe intoxication (poisoning);
• withdrawal syndrome;
• psychosis (due directly to exogenous intoxication or complicating the corresponding withdrawal syndrome);
• pseudo-withdrawal syndrome (the so-called "false abstinence" - a condition that occurs in patients with drug addiction and substance abuse during remission, months and even years after the last use of the usual psychoactive drug, resembling withdrawal symptoms in all manifestations);
• convulsive conditions;
• various mixed conditions (combination of severe somatic pathology and narcological symptoms);
• acute conditions that occur in patients during inpatient treatment as side effects and complications of ongoing therapy (for example, neuroleptic syndrome).

Such emergency conditions can be conditionally divided into two groups: Group I - conditions directly related to the use of a psychoactive substance (the first five points); Group II - conditions arising in the course of ongoing therapeutic measures (the last two points). At the prehospital stage (DGE) in the practice of an emergency physician (EMP), the first two conditions are most common - opium overdose (acute poisoning) and abstinence (withdrawal syndrome). This fact determines the need to focus the doctor's attention on these two urgent conditions. The remaining listed pathological conditions are much less common and usually require symptomatic treatment.

An overdose of opiates is deadly. According to various sources, up to 50-60% of opium addicts who inject themselves with opium preparations by parenteral route have suffered an overdose of the drug at least once. Among the causes of death in patients with opium addiction, lethal drug overdose is the leader - up to 30-40%. Overdose may be due to a significant excess of the usual dose of the drug in chronic users (most cases). Less often, the state of overdose is associated with physiological causes and occurs when the usual dose of the drug enters the body.

As a rule, full opioid agonists - morphine, heroin, methadone, as well as a short-acting full opioid agonist - fentanyl and its derivatives, pose the greatest danger in terms of overdose.

Compiling a social “portrait” of patients treated by EMS teams for opium poisoning, it can be noted that these are young men, approximately 24 years old, who use intravenous opiates, usually in the company of their own kind outside the home (4/5 of all cases). The low reliability of the obtained anamnestic data makes it difficult to separate these patients into systematic and episodic consumers.

The clinical picture of opiate poisoning (overdose) is characterized primarily by depression of the central nervous system (CNS), manifested by the switching off of consciousness of varying severity, from the stage of falling asleep (drowsiness, stupor) to a disorder of consciousness in the form of a coma - superficial or deep. In the neurological picture, the most specific is a sharp narrowing of the pupil (miosis) up to a point (with a "pin" or "match head", and sometimes even in the form of "needle punctures"). In addition, the state of the pupil is characterized by a significant decrease or complete absence of reaction to light. In severe hypoxia of the brain, miosis can be replaced by mydriasis with no pupillary response to light.

The danger to the life of patients with an overdose of drugs is the violation of two vital functions - respiration and blood circulation.

The most typical for the toxic effect of opiates is the depression of external respiration with a decrease in its frequency and depth to bradypnea with a respiratory rate of up to 4-6 per minute, up to the complete cessation of respiratory movements (apnea), including in patients who are in a state of stupor or superficial coma. This condition is accompanied by blanching or cyanosis of the skin. It is respiratory failure that determines the severity of the course, the outcome of the disease and the need to choose therapeutic measures. The most severe are combined poisonings with opiates with alcohol or other psychotropic drugs.

Inhibition of hemodynamics in patients with an overdose of opiates is manifested by acute left ventricular failure, severe peripheral vasodilation and vascular collapse (blood pressure (BP) is critically reduced, the pulse becomes thready).

On DHE, with an overdose of opiates / opioids, irreversible respiratory arrest, aspiration of vomit and adult respiratory distress syndrome, pulmonary edema, and cardiac depression can be deadly. Of these complications, non-cardiogenic pulmonary edema is characteristic and most life-threatening for the patient.

The basic principles of treatment of opium poisoning on DHE do not differ from those developed for the treatment of other poisonings, including other psychoactive substances (SAS). This is to ensure the normalization of respiration and hemodynamics, stopping the entry of poison into the body, neutralizing the poison, conducting symptomatic and initiating infusion therapy, and transporting the patient to a hospital.

In turn, therapeutic measures that reduce the harm caused by exposure to the poison on the body in acute opiate poisoning include:

• decrease in adsorption, including: a) probe gastric lavage (with stupor or coma - aspiration of vomit with preliminary tracheal intubation); b) the introduction of activated charcoal (before and after gastric lavage);
• increased elimination, carried out by: a) the introduction of liquid inside in the form of a plentiful drink, when possible, and parenterally; b) stimulation of diuresis (administration of diuretics); c) the introduction of a saline laxative; d) re-introduction of activated charcoal (to prevent re-absorption of opiates in the intestines and stomach);
• antidote therapy - the introduction of the blocker of opiate receptors naloxone.

The introduction of naloxone can currently be considered the only pathogenetically substantiated and effective medical intervention.

Naloxone (synonyms: narcan, intrenone, narcanti) is a complete opiate receptor antagonist, available as a 0.04% solution in ampoules (0.4 mg / ml) or 0.1% (1 mg / ml), displaces opiates from specific receptors, as a result of which oppressed breathing and consciousness are quickly restored. The drug is especially indicated for DHE, even if it is not possible to intubate the trachea and start mechanical ventilation (ALV).

Naloxone is used for opium intoxication of any severity. For the treatment of opium poisoning, the drug is administered intravenously by stream, slowly, at an initial dose of 0.4 mg (1 ml of a 0.04% solution) diluted in isotonic sodium chloride solution, or endotracheally. The action of naloxone with intravenous administration begins almost immediately - after 2 minutes - and lasts for 20-45 minutes. If necessary, after 3-5 minutes, the administration of the drug (1.6-2 mg, 4-5 ml of a 0.04% solution) is repeated until the level of consciousness rises, spontaneous breathing is restored and mydriasis appears. To eliminate hypersalivation, bronchorrhea and bradycardia, 1-2 ml of a 0.1% solution of atropine is prescribed subcutaneously.

The indication for repeated administration of naloxone is the deterioration of the patient's condition. However, it must be taken into account that the half-life of most opioids (for example, heroin) exceeds the half-life of naloxone. In such cases, the administration of the drug is repeated after 20-30 minutes. With repeated appointment, a combined intravenous and subcutaneous administration of the drug is possible. When a stable therapeutic effect is achieved, the administration is stopped, fixing the result with a single intramuscular or intravenous drip injection of an additional dose of naloxone at a dose of 0.4 mg (1 ml - 0.04% solution).

The scheme for the use of naloxone for suspected acute poisoning with surfactants is shown in .

It should be noted that some authors, such as J. C. M. Brust, believe that stopping the administration of naloxone and searching for other and / or concomitant causes of coma should be carried out after reaching a total dose of 20 mg (Yu. P. Sivolap, V. A. Savchenkov, 2005 ).

Conducted by the National Scientific and Practical Society of the NSR in 2000-2003. An open-label, multicenter, controlled study aimed at improving the quality of emergency care for patients with acute PAS poisoning on DHE included a study of the efficacy of naloxone in opium coma.

In the group of persons with acute PAS poisoning who received naloxone, 18% more cases were noted when the recovery of consciousness on DHE was achieved in a shorter time. At the same time, the need for mechanical ventilation arose much less frequently, three times fewer patients were sent for hospitalization. In addition, there was a significant reduction (by an average of 7.6 minutes) of the time spent at the exit of the ambulance crews, which indicates a clear economic effect of the use of naloxone.

As the results of the study showed, on DHE, regardless of the administered dose, naloxone did not cause complications and was well tolerated by patients.

When prescribing naloxone, it is important to remember the following.

• With prolonged severe hypoxia, especially with possible aspiration (vomiting), the introduction of naloxone should be preceded by tracheal intubation (after premedication, intravenous atropine is indicated) and mechanical ventilation.
• In patients with aspiration syndrome with prolonged hypoxia, in the case of the administration of naloxone, an undesirable effect can be obtained in the form of pronounced psychomotor agitation and pulmonary edema, which occur after 30-60 minutes.

In addition, there are some features that must be considered in the treatment of opium coma. In severe cases, in the absence of the effect of the introduction of antagonists or the impossibility of prescribing other drugs, it is necessary to carry out mechanical ventilation in the hyperventilation mode. It is necessary to constantly give the patient to inhale oxygen until the breathing problems are eliminated.

At present, on DGE, especially in the absence of modern immunochromatographic strip tests for the presence of various surfactants in saliva and urine in the equipment of the ambulance teams, a test with naloxone has an important differential diagnostic value. When conducting such a diagnostic and treatment test, naloxone is used in the above doses (1-2 ml of a 0.04% solution intravenously) as a means of making pharmacological diagnosis of unclear cases of poisoning.

If the reaction to naloxone is negative, the absence of an "awakening effect" of the drug suggests the presence of concomitant pathology:

• traumatic brain injury;
• overdoses of "street" narcotic analgesics;
• drug poisoning;
• hypoxic encephalopathy;
• hypoglycemic state;
• conditions after convulsions (if there are indications of a convulsive syndrome in history);
• any other pathology.

It should be remembered that the use of unreasonably high doses of naloxone in case of opiate poisoning (up to 1.2-1.6 mg - 3-4 ampoules initially) leads to the rapid development of opium withdrawal syndrome (see below).

In the absence of naloxone, the current practice of using the “traditional” drug allowance for patients in coma with suspected acute opiate poisoning - cordiamine (2-4 ml), both in the form of monotherapy and with caffeine (up to 8-10 ml), by doctors of the ambulance service, is more like a forced measure. Such a benefit, especially if the most effective in this situation, tracheal intubation and mechanical ventilation, makes it difficult to restore breathing, and patients are admitted to the hospital in an extremely serious condition with severe hypoxia and convulsive readiness.

In addition to the introduction of naloxone, intravenous drip infusion with electrolyte solutions is carried out to increase blood pressure. This is done, as a rule, with caution - because of the possibility of developing pulmonary edema. Usually, vascular tone and blood pressure recover spontaneously as hypoxemia resolves and blood volume increases. However, pronounced collapse and a significant decrease in pressure in the pulmonary circulation are an indication for the administration of dobutamine in high doses.

Attention should be paid to the fact that in methadone coma (with an overdose of methadone often leads to pulmonary edema), the introduction of large doses of naloxone without tracheal intubation and transfer to mechanical ventilation is categorically contraindicated, especially in patients with aspiration syndrome, due to the likely development of intractable respiratory disorders.

Opium withdrawal syndrome (OSA), a withdrawal syndrome, is represented by intense mental, somatovegetative and neurological disorders that occur when opium poppy preparations are discontinued.

The severity of any withdrawal syndrome is determined by a specific substance, the degree of its narcogenicity and toxicity, the duration of the disease, the dosage of the drug used, the range of possible complications, and the general reactivity of the body also matter.

The rate of development of OSA, as well as its duration, is also determined by a number of factors, primarily the pharmacokinetic characteristics of opiates. Thus, with dependence on intravenous methadone, abstinence begins at a later date than with dependence on acetylated opium poppy preparations. Various psychoactive additives (for example, antihistamines, benzodiazepine derivatives, etc.) can significantly prolong the effect of opiates.

OSA usually develops 6-18 hours after the last dose of the drug. In typical cases of heroin addiction, the maximum development of withdrawal symptoms is recorded 48-72 hours after the last use of the drug. In the treatment of OSA, its duration, depending on the nature of therapy, ranges from 3 to 10 days (rarely 12-15 days), while in the absence of treatment, the duration of OSA can increase significantly.

There are several phases in the development of OSA (IN Pyatnitskaya, 1969). The first phase develops 8-12 hours after the last opiate intake. Signs of mental addiction to drug addiction are states of dissatisfaction, tension, they are accompanied by somatovegetative reactions - mydriasis (dilated pupils), yawning, lacrimation, runny nose with sneezing, piloerection ("goose bumps"). Appetite disappears, there is a violation of falling asleep.

Signs of the second phase of OSA are most pronounced 30-36 hours after the last opiate intake. Characterized by chills, followed by a feeling of heat, bouts of sweating and weakness, constant piloerection. A feeling of discomfort appears in the muscles of the back, then the legs, neck and arms. The muscles of the body are tense. There is pain in the temporomandibular joints and chewing muscles. The symptoms of the first phase persist and intensify: pupils are wide, frequent sneezing (up to 50-100 times), intense yawning and lacrimation.

The third phase of OSA develops 40-48 hours after the last dose. The attraction to the drug acquires a compulsive (irresistible) character. Signs of the first two phases are intensifying. There are muscle pains. The muscles of the back, limbs, less often - the neck reduces, pulls, twists.

Some patients experience convulsions of peripheral muscles (calf, foot muscles, etc.), the need to constantly move, because at the beginning of the movement the pain weakens, but then intensifies. Patients cannot find a place for themselves, lie down, get up, lie down again, spin in bed. There are no pains in the joints. Patients are tense, dissatisfied, angry, depressed, experiencing a sense of hopelessness and hopelessness.

The fourth phase of OSA appears on the third day after drug withdrawal and lasts up to 5-10 days. The difference between this phase and the previous one is in the development of a new symptom of dyspeptic phenomena: abdominal pains appear, and then, after a few hours, vomiting and diarrhea (loose stools up to 10-15 times a day, accompanied by tenesmus).

The symptomatology of severe OSA is usually represented by a strong craving for the drug in order to alleviate one's painful condition. Disorders of the somatovegetative sphere (intense muscle and joint pain, muscle hypertension and muscle cramps, hyperhidrosis, chills or a feeling of heat, nausea, vomiting, lability of blood pressure, heart rate), psychopathological manifestations (lowered mood background with a dysphoric shade, anxiety , feeling of fear, restlessness, insomnia). There is a general weakness, weakness, capriciousness, malice with dysphoric outbursts, which, however, quickly subside.

Despite the versatility of OSA manifestations, the main targets of therapy for the relief of acute manifestations of opiate withdrawal syndrome include the vegetative-algic symptom complex and sleep disorders.

It should be remembered about the aggravational tendencies that are characteristic of the behavior of many patients with opium addiction, who tend to exaggerate the severity of their own condition. This is usually due to a number of reasons. Let's note some main points.

• Opium addicts experience persistent and almost uncorrectable fears associated with the deterioration of their condition due to drug withdrawal, this determines their desire to receive inflated (clinically unjustified) doses of drugs in order to “guaranteedly” avoid withdrawal discomfort.
• What matters is the mutual mental induction of drug addicts, exchanging impressions about the experience of their own experiences of such states and about the effectiveness of ongoing therapeutic measures. This determines the perseverance of such patients, who are confident in the need to prescribe certain (even completely unjustified) methods of therapy.
• Patients often deliberately exaggerate the severity of their own condition and insistently require the appointment of additional drugs, based on their euphoric effect, which is directly due to the pathological craving for the drug.

Despite the fact that OSA is a subjectively extremely painful condition, and for a number of drug addicts, according to them, “almost unbearable”, nevertheless, it almost never threatens the life of an opium addict. OSA is much less dangerous to health than alcohol withdrawal syndrome. Exaggeration of the severity of the abstinent state experienced by patients with opium addiction gives rise to fear of the developing symptoms of OSA, which not only forces the patient to resort to aggravation of his condition, but even “demonstrate” his own feelings in the form of violent psychopathic reactions. Quite often, especially within a few days immediately after the onset of withdrawal, the behavior of drug addicts becomes demonstrative: they scream loudly, cry, moan, roll on the floor, demand a drug, and in its absence, medical help. Typically, such a scenario is designed mainly for the surrounding people and aims to achieve the next dose of the drug in various ways. Such a phenomenon should be regarded as blackmail within the framework of hysterical behavior. In these cases, therapeutic measures are reduced to the relief of excitation.

At the DGE, an emergency physician who has encountered manifestations of severe OSA should notify the patient of the need for treatment in a specialized psychiatric (narcological) hospital. The decision on hospitalization of a patient with opium addiction is made independently. The exception is cases when the developed complications threaten the life of the patient.

V. G. Moskvichev, Candidate of Medical Sciences
MGMSU, NNPOSMP, Moscow

Unfortunately, opiate poisoning is common and in most cases caused by drug addiction. In order to avoid a tragedy, relatives of those subject to the “habit” should be persistent in treating the patient, stop attempts to purchase drugs.

ICD code 10 T36-T50.

Effects of opiates on the body

Currently, analgesics based on morphine or codeine are widely used in medical practice. This type includes natural and semi-synthetic alkaloids that effectively eliminate pain. Assigned orally, drip, injection. The raw material for production is the opium poppy.

The action is directed to the central nervous system. At the same time, it is impossible to predict when intoxication will develop, the properties appear depending on the individual qualities of the patient.

There are 4 phases of the effect of an opiate on the body:

Coming

Begins 10-20 seconds after ingestion. Heat appears in the lower back and abdomen, which slowly rises through the body. You can identify by the following symptoms:

• red face;
• constricted pupils;
• dry mouth;
• sometimes itching in the nose and chin.

Sometimes there is a feeling of insight, but soon thoughts are completely focused on sensations. The duration rarely exceeds 5 minutes. When an opiate is used by an experienced addict, the severity decreases.

If morphine is introduced, the exposure algorithm is as follows:

• languor;
• pleasure;
• peace;
• dreams;
• inadequate response to stimuli.

The limbs become heavy, the person practically does not move.

When codeine is used, the clinical picture changes:

• mental arousal;
• high physical activity;
• speech is fast and incoherent.

In this state, the patient is 3-4 hours.

Duration 3-4 hours. There is no deep immersion, light irritants are capable of waking up.

Effects

It does not appear to everyone. Characteristic signs:

• anxiety;
• headache;
• depression;
• bouts of nausea;
• tremor.

In general, the duration of the 4 phases is 6-10 hours.

Causes of intoxication

An overdose of opiates can be intentional or unintentional. There are several contributing factors:

1. Addiction. The addicted person becomes disoriented and may inject an excessive amount of, for example, heroin, which leads to poisoning.
2. Suicide attempt.
3. Bad control. In medicine, there are cases when drugs were stored improperly due to the negligent attitude of the management. As a result, both patients and doctors could use them.
4. If opiates are used at home, try the taste and the child is able.
5. In preparation for general anesthesia, an incorrect calculation was made.
6. Significantly increases the risks of joint use with ethyl alcohol. Ethanol enhances respiratory suppression.
7. For analgesic effect, codeine is introduced into the composition of some antitussive drugs. Therefore, you can face intoxication with an overdose of a seemingly safe medication.

Most often, people with addiction or undergoing therapeutic treatment for pathologies accompanied by intense pain are at risk of poisoning with opium and its derivatives.

The main symptoms of acute intoxication

This course is observed with any method of administration.

Characteristic signs:

• confused mind;
• coma;
• constriction of the pupils;
• cyanosis of breath;
• hypoxic and toxic encephalopathy;
• cyanosis of the skin;
• apnea.

The following symptoms may be attached:

• swelling of the brain;
• acute heart failure;
• convulsions;
• pneumonia;
• temperature change;
• vomiting even in the absence of consciousness;
• delayed emptying of the bladder and intestines:
• dilated pupils, fixed gaze;
• problems with swallowing, leading to burns of the mucous membranes as a result of exposure to gastric juice;
• muscle tissue dysfunction.

With severe opiate poisoning, deviations in the mental state and withdrawal syndrome are likely.

stages

There are 4 stages:

1. At first, lethargy, drowsiness are observed. The main signs of mild intoxication:

• constriction of the pupils;
• muscle hypotension;
• lack of response to light;
• decreased tendon reflexes;
• respiratory failure;
• acrocyanosis;
• bradycardia.

But you can still contact the patient.

1. The person is unconscious, a superficial coma is likely. The blood pressure drops, there is practically no sensitivity to pain. Seizures often develop.
2. Drug use causes a coma. There is no reaction to external stimuli, there is muscle atony, apnea. In the absence of first aid, breathing stops within 6-12 hours, death is declared.
3. At this stage of acute intoxication with opiates, recovery from coma is noted. Gradually, normal breathing is restored, blood flow stabilizes, consciousness returns, and the hypnotic effect disappears.

If awakening is due to the introduction of an antidote, a withdrawal syndrome occurs.

Diagnosis of intoxication

Upon admission to the hospital, a thorough examination is necessary, since an overdose of a narcotic drug can be confused with hypothermia, benzodiazepine poisoning, hypoglycemia, and hypoxia.

The program includes pathogenesis, observation of the clinical picture and laboratory tests:

1. Study biological material. In samples, the presence of opiates can be detected several days after intoxication.
2. Perform a reaction with nalaxone - an antagonist of a narcotic substance.

However, the main diagnostic methods require time, which is not available in acute poisoning. Therefore, treatment begins immediately after the patient arrives.

Urgent care

If during an overdose there were relatives next to the person, it is necessary to call an ambulance and urgently perform the following procedures:

1. Stop access to opiates.
2. In case of cardiac arrest, perform indirect massage, perform artificial respiration.
3. If the lesion occurred due to ingestion, rinse the stomach, induce vomiting.
4. As an antidote, camphor oil can be injected subcutaneously.

The emergency team will arrive to administer nalaxone to the patient, which will restore lung function. Further treatment takes place in a hospital.

Therapy of poisoning

The program includes:

1. If this has not been done before, inject the antidote.
2. Apply the Ambu bag for artificial respiration.
3. Tracheal intubation and connection to ventilation is possible.
4. Drip solutions of glucose, mexidol, thiamine, nootropics are administered.

Often, drug addicts suffer from HIV, hepatitis. Therefore, when providing first aid, it is advisable to use protective equipment.

Possible Complications

The consequences of opiate poisoning are quite severe:

• paralysis and paresis;
• polyneuropathy;
• psychoses;
• withdrawal syndrome;
• personality disorder;
• decreased intelligence and memory;
• degradation;
• chronic renal failure.

It is not uncommon for a patient who has undergone poisoning to require further psychiatric help.

Prevention

It is not so easy for a person who is not subject to addiction to get poisoned - the drugs are under strict control in the clinic, it is impossible to purchase at a pharmacy without a prescription. But if someone from the family is undergoing therapy with opiates, it is necessary to store funds as far as possible from children and adolescents.

Knowing that someone close to you uses drugs, you should be persistent and persuaded to take a course that helps get rid of the habit.

Acute poisoning with opiates and opioids has long occupied one of the first places in the general structure of accidental and targeted acute poisonings. According to the World Health Organization, the number of deaths associated with overdose of opiates and opioids in the world annually reaches 69,000.

In 2013, between 0.3 and 0.4% (13-20 million people) of the world's population aged 15 to 65 received opiates. WHO estimates that 15 million people are addicted to opioids each year.

Most of them use illicitly produced heroin, but there is a clear trend towards an increase in the number of drug addicts as a result of the prescription of opiates and opioids by physicians. At the same time, no more than 10% of those who need it receive effective treatment.

Terminology and classification of opioids

Traditionally, opiates are narcotic alkaloids derived from the sleeping pills poppy (papaver somniferum). The mixture of these alkaloids is called opium. Natural alkaloids include morphine, codeine, thebaine, oripavine.

Other opiates are semi-synthetic: heroin (diacetylmorphine), dihydrocodeine, desomorphine, etc. Heroin, for example, is obtained by acetylation of morphine with acetic anhydride when heated.

Opioids are substances of other origin, often synthetic, that in the body have effects similar to those of opiates through interaction with opioid (opiate) receptors.

The term "opioids" was first used in 1963 by George Acheson, who emphasized that he meant substances with biological activity similar to morphine. Currently, the term "opiates" is rarely used in foreign literature and the term "opioids" is predominantly used, regardless of the nature of narcotic substances. Obviously, the term "opiates" will not be used soon.

According to the international anatomical-therapeutic-chemical classification (Anatomical Therapeutic Chemical) of drugs, the following groups of opioids are distinguished.

ATX: N02A Opioids

• N02AE Oripavine derivatives (buprenorphine (bupranal))
• N02AF Morphine derivatives (butorphanol (stadol, moradol), nalbuphine)
• N02AX Other opioids (tramadol (tramal, protradon, sintradon, zaldiar), tilidine (valorone, galidin, centrak, kitadol, perdolate, tilidate, tilifort, volaren), dezocin (dalgan), etc.)
• N02AA Natural opium alkaloids (morphine, opium, hydromorphone, nycomorphone, oxycodone, dehydrocodeine, diamorphine, papaveretum, morphine in combination with other drugs, codeine in combination with other drugs, etc.)
• N02AB Phenylpiperidine derivatives (fentanyl, pethidine (demerol, meperidine, mepergan), ketobemidone, trimeperidine (promedol), etc.)
• N02AC Diphenylpropylamine derivatives (dextromoramide, methadone, pyrithramide (dipidolor), dextropropoxyphene, bezitramid, levacetylmethadol, etc.)
• N02AD Benzomorphan derivatives (pentazocine (Lexir, Fortran), phenazocine, etc.)
• N02AG Opioids and antispasmodics

Epidemiology of opioid distribution

In some countries (USA) opioids are prescribed very frequently, as are, for example, non-steroidal anti-inflammatory drugs or antispasmodics. According to the Automation of Reports and Consolidated Orders System (ARCOS) reports, opioid prescription increased by 100% between 2004 and 2011. At the same time, the prescription of codeine decreased by 20%, but the prescription of other drugs increased as follows: buprenorphine - by 2318%, hydromorphone - by 140%, oxycodone - by 117%, hydrocodone - by 73%, morphine - by 64%, methadone - by 37%, fentanyl by 35%.

According to another US drug prescription monitoring system, the Drug Abuse Warning Network (DAWN), for the period 2006-2011. buprenorphine prescriptions increased by 384%, and from 2004 to 2011 other opioid prescriptions increased as follows: hydromorphone by 438%, oxycodone by 263%, morphine by 146%, hydrocodone by 107%, fentanyl by 104%, methadone - by 82%.

In the last decade, there has been a significant increase in the number of opioid prescriptions that are not associated with the presence of chronic pain syndrome characteristic of oncological pathology. In 2010, there were 16,651 deaths in the US from overdose of prescribed opioids alone. 3,036 deaths were due to heroin overdose.

In 2012, the US Centers for Disease Control and Prevention stated that in cases where the death of the victims was due to an overdose of medications, in 72% of cases (16,007 out of 22,114) opioids were taken. Almost 40% of deaths (39.8%) in the period 1999-2010 from opioid overdose were due to methadone.

Data from 2015 indicates that oxycodone prescriptions in the US and Canada have already increased 14-fold. It is possible that about 1.7% of the population of these countries is already receiving opioids. A large number of prescriptions lead to the misuse of opioids, namely to improve mood and relaxation.

In European countries, the increase in opioid use is much slower, but an increase in the number of prescriptions of this type of medication should also be expected in the near future.

According to The Office for National Statistics (ONS), in 2012 there were 579 heroin and morphine-related deaths in England and Wales. 414 deaths were attributable to methadone use. In Scotland, the number of deaths associated with the use of heroin and morphine decreased by 25% from 2009 to 2012. But 7% increased mortality associated with the use of methadone.

Numerous studies indicate that opioids have a pronounced anti-inflammatory effect with few side effects when used at therapeutic doses. Moreover, the cost of opioids is often significantly less than the cost of modern non-steroidal anti-inflammatory drugs.

A five-year monitoring of the use of opioids in Europe (Access to Opioid Medication in Europe, ATOME) showed an unreasonable restriction of their availability in the treatment of severe chronic pain, even in cancer patients.

In conclusion, it was pointed out that in the 12 countries of the European Union belonging to Eastern Europe, patients' access to opioids is seriously limited. It was noted that the same problem exists in Ukraine, Belarus, Montenegro and the Russian Federation. The conclusion also states that the availability of opioids should be considered as one of the components of human rights.

Opioid-based drugs are the mainstay of drug therapy for severe pain, respiratory distress, and opioid addiction itself.

Mechanism of action of opioids

Opioids increase the activity of one or more G protein-coupled transmembrane molecules called mu, kappa, and delta opioid receptors. Opioid receptors are activated by both endogenous (enkephalins, endorphins, and dynorphins) and exogenous ligands. The prototype of most of the latter is morphine.

Opioid receptors are widely present in the human body. A significant number of them are located in the brain and spinal cord. Their highest density was found in the anterior and ventrolateral thalamus, amygdala, and spinal ganglia.

Together with dopaminergic neurons, brainstem opioid receptors modulate respiratory activity in response to hypoxemia and hypercapnia, and together with the Edinger-Westphal nucleus receptors of the oculomotor nerve control changes in pupil diameter. Activation of opioid receptors in the central nervous system mediates the inhibition of neurotransmission. Both the release of excitatory neurotransmitters and sensitivity to them are inhibited. Activation of opioid receptors in the gastrointestinal tract leads to inhibition of its motility.

Mu-opioid receptors are the most widely represented in the central nervous system. In this regard, their stimulation provides the most powerful analgesic effect. In addition, euphoria, physical dependence, miosis, respiratory depression and peristalsis are realized through mu receptors.

Through stimulation of opioid delta receptors, analgesic, antidepressant effects and physical dependence are also realized. Stimulation of kappa receptors provides analgosedation, dysphoria and inhibition of the production of arginine vasopressin.

According to the nature of the interaction with opioid receptors, all opioidergic drugs are divided into:

• agonists (activate all types of receptors) - morphine, trimeperidine, tramadol, fentanyl, etc.;
• partial agonists (activate mainly mu receptors) - buprenorphine;
• agonist-antagonists (activate kappa and block mu- and delta-receptors) - pentazocine, nalorphine (blocks mainly mu-opioid receptors and is not used as an analgesic);
• antagonists (block all types of opioid receptors) - naloxone, naltrexone.

Clinical manifestations of opioid intoxication

The classic triad of opioid intoxication includes severe depression of respiratory function, depression of consciousness to the point of stupor or coma, and the development of bilateral miosis. Administration of opioids to opioid-intolerant individuals results in dose-dependent inhibition of all phases of respiratory activity, even when opioids are used at therapeutic doses.

Respiratory rate less than 12 per minute in a patient who is not in a state of physiological sleep is the most important sign of opioid intoxication. The probability of an event is greatly increased if respiratory depression is combined with depression of the function of consciousness.

Miosis is not a mandatory symptom of opioid intoxication. Miosis is not characteristic of an overdose of meperidine, propoxyphene and tramadol.

In cases where opioid respiratory depression provides adequate evacuation of carbon dioxide from the body, but does not provide sufficient oxygenation, that is, arterial hypoxemia is combined with normocapnia for a long time, there is a threat of developing hypoxemic pulmonary edema, similar to that which is characteristic of staying at high altitudes. .

Other manifestations of opioid intoxication may be arterial hypotension, moderate bradycardia. Individuals with a complete lack of tolerance may vomit. Rhabdomyolysis with the development of myoglobinuria and renal failure is caused by muscle ischemia from positional compression, when the victim is in a motionless unconscious state for a long time.

According to observations deposited by WHO, the most susceptible to overdose of opioids are:

• people who are opioid dependent, especially if they have completed detoxification therapy;
• just released from places of restriction of freedom;
• discontinued treatment;
• using the intravenous route of administration into the body;
• patients using high-dose prescribed opioids;
• persons taking opioids in conjunction with sedatives;
• patients with HIV, liver and respiratory failure;
• family members of patients receiving opioids.

Emergency Medical Services

Measures of emergency medical care (EMA) consist in ensuring the patency of the respiratory tract, carrying out artificial ventilation of the lungs by any available method, as well as in the introduction of naloxone.

Respiratory support is considered more important than the use of naloxone. Naloxone is not effective unless the depression of consciousness and breathing is due to an opioid overdose. Naloxone can be administered intravenously, intramuscularly, subcutaneously, and intranasally.

The accumulated experience with the use of naloxone has led to a gradual increase in the dosage of the drug used for both diagnosis and detoxification, with official statements and recommendations for this use. In the USA in 2011-2012. 50,000 doses of naloxone prevented death from opioid overdose in about 10,000 patients.

In November 2015, the Food and Drug Administration (USA) approved the intranasal administration of naloxone for EMT for suspected opioid intoxication. The spray should provide a single dose of 0.4 mg of naloxone.

The doses of naloxone recommended for intravenous administration in Ukraine fully comply with modern international recommendations (0.4-2 mg for adults and 0.1 mg/kg for children). Intravenous drip administration of naloxone in isotonic sodium chloride solution and in 5% glucose solution is allowed.

Long-term infusions are usually used for methadone poisoning. The half-life of naloxone ranges from 20-60 minutes. The duration of action can be up to 2-3 hours, but most often it is much shorter - 40-45 minutes.

An overdose of naloxone leads to the manifestation of an abstinence syndrome, the severity of which can be different. To stop heroin intoxication, naloxone is often used together with buprenorphine, which very effectively displaces other opioid agonists from binding to opioid mu receptors, but by itself has weak analgesic activity, without causing severe dependence.

The routine use of opioid antagonists with a long half-life (nalmefene, naltrexone) for EMT is not recommended.

Kursov S.V., Skoroplet S.M.