Active substance : suxamethonium iodide - 20 mg;

Excipients: sodium chloride -7 mg;disodium edetate (disodium salt of ethylenediaminetetraaceticacids; trilon B) - 0.05 mg; ascorbic acid - 0.05 mg;hydrochloric acid 0.1 M solution - up to pH 3.3-3.6;water for injection - up to 1 ml.

Short acting depolarizing muscle relaxant. Causes a blockade neuromuscular transmission. Interacting with n-cholinergic receptors, it causes depolarization of the end plate of the motor nerves. The process extends to the adjacent membranes, a generalized disorganized contraction of myofibrils occurs (i.e., the development of the blockade is preceded by muscle twitches - the result of a short-term relief of neuromuscular transmission). The membranes, remaining depolarized, do not respond to additional impulses, since repeated impulses associated with repolarization of the end plate are required to maintain muscle tone, spastic paralysis occurs.

After intravenous administration, muscle relaxation occurs in the following sequence: eyelid muscles, chewing muscles, muscles of the fingers, eyes,limbs, neck, back and abdomen, vocal cords, then intercostal muscles and diaphragm.

It causes an increase in cerebral blood flow and an increase in intracranial pressure. The duration of action is 5-10 minutes.

The severity of the action depends on the size of the administered dose:

0.1 mg/kg - relaxation of skeletal muscles without significant effect on the respiratory system;

0.2-1 mg / kg - complete relaxation of the muscles of the abdominal wall and respiratory muscles (there is a significant limitation or complete cessation of spontaneous breathing).

For prolonged muscle relaxation, repeated administration is necessary. The rapid onset of the effect and the subsequent rapid recovery of muscle tone allow you to create controlled and controlled muscle relaxation.

Suction:After intravenous administration, the action begins after 54-60 seconds, after 2-3 minutes, muscle relaxation reaches a maximum and remains in full for 3 minutes. After intravenous administration, it is distributed in plasma and extracellular fluid. The short duration of action of suxamethonium iodide is due to the rapid inactivation of plasma cholinesterase with the formation of choline and succinylmonocholine. The half-life (T1 / 2) is 90 seconds at a normal level of plasma cholinesterase. Succinylmonocholine is a non-depolarizing muscle relaxant whose activity is 20-50 times lower compared to the original substance. In the future, the metabolic rate slows down and succinylmonocholine breaks down into succinic acid and choline. Excreted by the kidneys. Does not penetrate the intact blood-brain barrier. Does not accumulate.

The drug is used only under general anesthesia to relax the skeletal muscles in order to intubate the trachea, with surgical interventions with a high risk of regurgitation: for example, with intestinal obstruction, "acute abdomen", emergency caesarean section, emergency operations in patients with an unemptied stomach, to reduce the severity of seizures during electrical impulse therapy. Strychnine poisoning, tetanus (symptomatic therapy).

Suxamethonium iodide (ditylin) does not affect the level of consciousness and should not be administered to patients without anesthesia.

- hypersensitivity to suxamethonium iodide or to any of the auxiliary components of the drug;

- predisposition to malignant hyperthermia;

- hyperkalemia and conditions that increase its risk (severe renal failure, taking potassium supplements), due to possible hyperkalemic cardiac arrest;

- severe burns, multiple trauma;

- severe abdominal infections, sepsis;

- prolonged immobilization;

- penetrating eye injury with increased intraocular pressure;

- increased intracranial pressure;

- disorders of neuromuscular conduction in myotonia, poliomyelitis, amyotrophic lateral sclerosis, multiple sclerosis, all forms of muscular dystrophy, myasthenia gravis;

- violation of innervation, leading to secondary muscle atrophy (transverse syndrome);

- congenital cholinesterase deficiency;

- children's age up to 1 year;

- pregnancy;

- breastfeeding period.

The introduction of the drug is allowed only in a specialized department of the hospital in the presence of all conditions for artificial lung ventilation (ALV) or after the patient is transferred to controlled breathing.

The dose is set individually, taking into account the required degree of relaxation, body weight and patient response.

adults: intravenously slowly, by stream or drip (for long-term drip infusion, a 0.1% solution is used). Depending on the clinical situation, with intravenous administration, a single dose varies from 0.1 mg / kg to 1.5-2 mg / kg of body weight.

With tracheal intubation, the dose is 0.2-0.8 mg / kg.

For muscle relaxation and switching off spontaneous breathing 0.2-1 mg / kg.

For relaxation of skeletal muscles during orthopedic and traumatic interventions (fractures, reposition of bone fragments, reduction of dislocations, and others) dose of 0.1-0.2 mg / kg.

For endoscopy - 0.2 mg / kg.

In order to prevent complications of electropulse therapy (convulsions, avulsion of muscles and tendons) 0.1-1 mg / kg intravenously and up to 2.5 mg / kg intramuscularly, but not more than 150 mg. For long-term relaxation of the muscles during the entire operation, fractional administration is administered, after 5-7 minutes, at a dose of 0.5-1 mg/kg. Repeated doses last longer.

Children over 1 year old:

Intravenously 1-2 mg / kg or intramuscularly in doses up to 2.5 mg / kg, but not more than 150 mg.

Elderly patients:

Dose adjustment in elderly patients is not required. However, older patients are more susceptible to heart rate, especially in the case of the use of cardiac glycosides.

From the side immune system: allergic reactions (sharp redness of the skin, urticaria); anaphylactic shock with or without bronchospasm and hypotension; anaphylactoid reactions; bronchospasm as a result of anaphylactoid reactions; circulatory failure as a result of anaphylactoid reactions.

From the side of metabolism and nutrition: hyperglycemia, transient increase in potassium levels, life-threatening hyperkalemia. porphyria, malignant hyperthermia with orwithout muscle rigidity (spasm chewing muscles), severe acidosis, hypercalcemia, especially in children with unidentified skeletal muscle disease (Duchenne myopathy).

From the side nervous system: increased intracranial pressure.

From the side of the organ of vision: increase in intraocular pressure.

From the side of the cardiovascular system: increase or decrease in blood pressure, hot flashes, short-term bradycardia (more often in children, with repeated administration - in children and adults), asystole, tachycardia, arrhythmia (including ventricular arrhythmias), cardiovascular complications (tachyarrhythmias, unstable blood pressure); ventricular fibrillation, cardiac conduction disorder, cardiogenic shock, collapse.

From the side of the respiratory system chest and mediastinum: apnea, bronchospasm, prolonged paralysis of the respiratory muscles (associated with a genetically determined violation of the production of pseudocholinesterase), laryngospasm, late respiratory failure with neuromuscular transmission disorders, laryngeal edema, pulmonary edema, increased carbon dioxide concentration at the end of exhalation (with capnometry).

From the side gastrointestinal tract: hypersalivation, increasedintragastric pressure (risk of regurgitation in pregnant patients, patients with hiatal hernia, atony of the stomach and intestines, ascites, and tumors of the abdominal cavity).

From the side of the liver and biliary tract: liver dysfunction.

From the side of the musculoskeletal and connective tissue: the appearance of muscle pain 10-12 hours after the administration of the drug, muscle fasciculations, rhabdomyolysis followed by the development of myoglobinemia and myoglobinuria, myalgia as a result of muscle fasciculations, most often develops in the neck. shoulder girdle, chest and back, especially in middle-aged patients, mild trismus (up to 60 seconds), which can be reduced with propofol or a small dose of a non-depolarizing muscle relaxant, muscle contractions instead of relaxation (often against the background of dystrophic myotonia or congenital myotonia), prolonged paralysis as a result of the development of a "double block" and impaired neuromuscular transmission, which can also be the result of idiosyncrasy (hereditary cholinesterase variant), overdose or a decrease in plasma cholinesterase activity, myoglobinemia (this effect is not dose dependent and may develop with or without muscle fasciculations), myoglobinuria, and increased creatine phosphokinase activity, mainlyway in children receiving suxamethonium in combination with halothane.

From the skin and subcutaneous tissue: redness of the skin.

From the side of the kidneys and urinary tract: myoglobinuria leading to renal failure, mainly in patients with diagnosed or latent muscular dystrophy, hemoglobinuria.

General disorders : hyperthermia.

Pharmaceutically incompatible with donor blood and blood products (hydrolysis occurs), blood and serum preservatives, barbiturate solutions and alkaline solutions (precipitation forms). Compatible with 0.9% (isotonic) sodium chloride solution, Ringer's solution, 5% fructose solution and 6% dextran solution.

The effect of suxamethonium is enhanced and lengthened: anticholinesterase drugs, beta-blockers, aminoglycoside antibiotics, amphotericin B, cyclopropane, organophosphorus insecticides (infusion of magnesium salts should be stopped 20-30 minutes before drug administration) and lithium salts, quinine, pancuronium, class I antiarrhythmic drugs, blockers of "slow "calcium channels," loop "diuretics, antiepileptic drugs, alcohol and CNS depressants - enhance and lengthen the muscle relaxant effect of suxamethonium iodide.

Drugs with the potential ability to reduce the activity of blood cholinesterase (, estrogens, high-dose glucocorticosteroids, oral contraceptives,), as well as cytostatics (, thiophosfamide), monoamine oxidase inhibitors (MAO) and some antipsychotics (for example,), sympathomimetics enhance and lengthen the muscle relaxant effect suxamethonium iodide.

The effect of suxamethonium reduces concomitant whole blood or plasma transfusion.

Effect of suxamethonium on other drugs. compatible with other muscle relaxants, narcotic analgesics. Strengthenscardiac effects of cardiac glycosides (bradycardia).

Suxamethonium iodide reduces the effectiveness of antimyasthenic drugs. Halogen-containing agents for general anesthesia increase, and sodium thiopental and reduce the undesirable effect of suxamethonium on the cardiovascular system.

They are used only in the conditions of a specialized department of a hospital by decision and under the supervision of an experienced anesthetist in the presence of equipment for urgent tracheal intubation and artificial lung ventilation (ALV). oxygen inhalation. (prozerin) or other anticholinesterase agents are not antagonists of suxamethonium iodide, on the contrary, by inhibiting the activity of cholinesterase, they can enhance and prolong the action of suxamethonium. Adverse reactions from the side of the heart are more common in children (first bradycardia, then tachycardia, replacement nodal rhythm, ventricular extrasystole are possible). There have been cases of death in children and adolescents as a result of resistance to resuscitation therapy. Some of these cases had unrecognized neuromuscular transmission disorders.

Slow administration of suxamethonium. as well as a preliminary intravenous injection of atropine at a dose of 1-1.5 mg largely prevent bradycardia and increased bronchial secretion.

Preliminary (for 1 min) administration of 3-4 mg of tubocurarine chloride or 10-15 mg of diplacin chloride almost completely prevents muscle fasciculations and subsequent myalgia. For long operations, non-depolarizing muscle relaxants are usually used. which are administered after preliminary intubation of the trachea against the background of suxamethonium iodide. Prolonged muscle relaxation with possible apnea can be caused by several reasons: "atypical" serum cholinesterase, hereditaryinsufficiency of serum cholinesterase or a temporary decrease in its concentration in blood plasma.

If the drug is administered repeatedly and 25-30 minutes after the end of the injection, the patient does not recover muscle tone, breathing remains superficial, one can think about the transition of the depolarizing block to the anti-depolarizing one (the so-called "double block"). To remove this effect, it is administered intravenously at a dose of 0.5-0.7 mg (0.5-0.7 ml of a 0.1% solution), after an increase in heart rate, after 1-2 minutes, prozerin is administered at a dose of 1.5 mg (3 ml of 0.05% solution).

The introduction of suxamethonium may be accompanied by the intake of a significant amountpotassium inside the cell. Increasing the concentration of potassium inserum can lead tolife-threatening hyperkalemia with the development of ventricular fibrillation and asystole. Patients with renal insufficiency, severe burns or multiple injuries are at particular risk. In patients with renal insufficiency (without signs of hyperkalemia and neuropathy), the drug is administered once at medium doses, but not used for multiple injections or at higher doses due to the risk of developing hyperkalemia.

Cholinesterase or pseudocholinesterase deficiency can markedly prolong the action of suxamethonium. Cholinesterase deficiency can be congenital, develop against the background of severe liver dysfunction, terminal renal failure, hypothyroidism or severe diseases of various etiologies (malignant tumors, cachexia), burns or medicines(see section "Interaction with other drugs"). Physiological inhibition of cholinesterase activity is noted in newborns, at a young age and in women in late pregnancy.

Under certain circumstances, patients with hereditary serum cholinesterase deficiency should continue to be on mechanical ventilation for several hours.

Hypothermia can potentiate and prolong the effects of suxamethonium by slowing down physical and biochemical membrane processes.

The effect of suxamethonium can be enhanced and prolonged by hypermagnesemia and hypocalcemia due to inhibition of presynaptic release of acetylcholine and hypokalemia, by reducing the resting membrane potential.

The drug is used only in a hospital setting. Patients should not administer vehicles or mechanisms for at least 24 hours after administration of suxamethonium iodide.

Solution for intravenous and intramuscular administration 20 mg/ml.

But 5 ml in neutral glass ampoules.

10 ampoules with instructions for use and an ampoule knife or an ampoule scarifier are placed in a cardboard box.

5 or 10 ampoules are placed in a blister pack of filmpolyvinyl chloride or polyethylene terephthalate tape and aluminum foil, orPE-coated paper, or without foil, or without paper.

1 or 2 blister packs with instructions for use and an ampoule knife or ampoule scarifier are placed in a cardboard pack.

When packing ampoules with a break ring or a break point, an ampoule knife or an ampoule scarifier is not included.

In a place protected from light at a temperature of 2 to 8 ° C.

Do not freeze.

Keep out of the reach of children.

Active ingredient: suxamethonium iodide - 20.0 mg.

Auxiliary components: sodium chloride, disodium edetate, ascorbic acid, 0.1 M hydrochloric acid solution, water for injection - up to 1 ml.

Adults: intravenously slowly, by stream or drip (for long-term drip infusion, a 0.1% solution is used). Depending on the clinical situation with intravenous administration, a single dose varies from 0.1 to 1.5-2 mg / kg.

Intramuscularly - 3-4 mg / kg, but not more than 150 mg. Intramuscularly used in children in W doses up to 2.5 mg / kg, but not more than 150 mg, intravenously 1-2 mg / kg.

For tracheal intubation - 0.2-0.8 mg / kg; for muscle relaxation and switching off spontaneous breathing - 0.2-1 mg / kg; for relaxation of skeletal muscles during reduction of dislocations and reposition of bone fragments in fractures - 0.1-0.2 mg / kg; for endoscopy and electroencephalography - 0.2 mg / kg; for the prevention of complications during electrical impulse therapy (convulsions, avulsion of muscles and tendons) - 0.1-1 mg / kg intravenously and up to 2.5 mg / kg intramuscularly, but not more than 150 mg.

For long-term relaxation of the muscles during the entire operation, the drug can be administered fractionally after 5-7 minutes at a dose of 0.5-1 mg/kg. Repeated doses of suxamethonium iodide last longer.

Symptoms: respiratory arrest.

Treatment: artificial ventilation of the lungs, in case of a decrease in serum cholinesterase - transfusion of fresh blood.

Enhances the effects of cardiac glycosides. Reduces the effectiveness of antimyasthenic drugs. Pharmaceutically incompatible with donor blood (hydrolysis occurs), blood preservatives, serum preservatives, blood products, barbiturate solutions (precipitation) and alkaline solutions. Compatible with 0.9% sodium chloride solution, Ringer's solution, 5% fructose solution and 6% dextran solution. Anticholinesterase drugs, beta-blockers, aminoglycoside antibiotics, amphotericin B, cyclopropane, organophosphorus insecticides, magnesium and lithium salts, quinine, pancuronium bromide enhance and lengthen the muscle relaxant effect. Compatible with other muscle relaxants, narcotic analgesics.

Halogen-containing drugs for general anesthesia increase, and sodium thiopental and reduce the undesirable effect on the cardiovascular system. Drugs with the potential ability to reduce blood cholinesterase activity (estrogen, high-dose glucocorticoids, oral contraceptives) enhance and prolong the muscle relaxant effect of suxamethonium iodide.

Introduction 1 min before suxamethonium iodide 3-4 mg of non-depolarizing muscle relaxants almost completely prevents muscle twitching and subsequent myalgia. With an appropriate dose and repeated administration, it can also be used for longer operations, however, for prolonged muscle relaxation, non-depolarizing muscle relaxants are usually used, which are administered after preliminary tracheal intubation against the background of suxamethonium iodide.

They are used only in the conditions of a specialized department in the presence of equipment for artificial ventilation of the lungs and personnel who own this technique, and against the background of general anesthesia. To prevent severe bradycardia, increase bronchial secretion and other effects associated with the m-anticholinergic effect, it is recommended to administer suxamethonium iodide before administration. Patients with renal insufficiency (without signs of hyperkalemia and neuropathy) are administered once at medium doses, but are not used for multiple injections or at higher doses due to the risk of developing hyperkalemia.

Protracted muscle relaxation with possible apnea can be caused by several reasons: "atypical" serum cholinesterase, hereditary deficiency of serum cholinesterase or a temporary decrease in its concentration in severe liver diseases, severe anemia, after prolonged fasting, with cachexia, dehydration, febrile conditions, after acute poisoning or chronic exposure to insecticides - cholinesterase inhibitors (when ingested) or anticholinesterase drugs (