Prednisolone hemisuccinate

GLUCOCORTICOID DRUGS

Toolkit

PREDNISOONE BUFUS

Interaction

There may be pharmaceutical incompatibility of prednisolone with other intravenously administered drugs; it is recommended to administer it separately from other drugs (intravenous bolus, or through another dropper, as a second solution).
When mixing a solution of prednisolone with heparin, a precipitate forms. Simultaneous administration of prednisolone with:

- inducers of microsomal liver enzymes (phenobarbital, rifampicin, phenytoin, theophylline, ephedrine) leads to a decrease in its concentration;

- diuretics (especially thiazide and carbonic anhydrase inhibitors) and amphotericin B - can lead to increased excretion of potassium ions (K+) from the body and an increased risk of developing heart failure;

- with sodium-containing drugs - to the development of edema and increased blood pressure;

- cardiac glycosides worsen their tolerability and increase the likelihood of developing ventricular extrasytolia (due to hypokalemia);

- indirect anticoagulants - weakens (less often enhances) their effect (dosage adjustment required);

- anticoagulants and thrombolytics - increases the risk of bleeding from ulcers in the gastrointestinal tract;

- ethanol and nonsteroidal anti-inflammatory drugs (NSAIDs) - increases the risk of erosive and ulcerative lesions in the gastrointestinal tract and the development of bleeding (in combination with NSAIDs in the treatment of arthritis, it is possible to reduce the dose of glucocorticosteroids due to the summation of the therapeutic effect);

- paracetamol - the risk of developing hepatotoxicity increases (induction of liver enzymes and the formation of a toxic metabolite of paracetamol);

- acetylsalicylic acid - accelerates its elimination and reduces its concentration in the blood (when prednisolone is discontinued, the level of salicylates in the blood increases and the risk of side effects increases);

- insulin and oral hypoglycemic drugs, antihypertensive drugs - their effectiveness decreases;

- vitamin D - its effect on the absorption of calcium ions (Ca2+) in the intestine is reduced;

- growth hormone - reduces the effectiveness of the latter, and with praziquantel - its concentration;

- M-anticholinergics (including antihistamines and tricyclic antidepressants) and nitrates - helps increase intraocular pressure;

- isoniazid and mexiletine - increases their metabolism (especially in “fast acetylators”), which leads to a decrease in their plasma concentrations.

Carbonic anhydrase inhibitors and loop diuretics may increase the risk of osteoporosis.

Indomethacin, displacing prednisolone from its connection with albumin, increases the risk of developing its side effects.

Adrenocorticotropic hormone enhances the effect of prednisolone.

Ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by prednisolone.

Cyclosporine and ketoconazole, by slowing down the metabolism of prednisolone, can in some cases increase its toxicity.

The simultaneous use of androgens and steroidal anabolic drugs with prednisone contributes to the development of peripheral edema and hirsutism, and the appearance of acne. Estrogens and oral estrogen-containing contraceptives reduce the clearance of prednisolone, which may be accompanied by an increase in the severity of its action.

Mitotane and other inhibitors of adrenal function may necessitate an increase in the dose of prednisolone.

When used simultaneously with live antiviral vaccines and against the background of other types of immunizations, it increases the risk of viral activation and the development of infections.

Antipsychotics (neuroleptics) and azathioprine increase the risk of developing cataracts when prednisolone is prescribed.

When used simultaneously with antithyroid drugs, the clearance of prednisolone decreases and with thyroid hormones increases.

Prednisolone-induced hypokalemia may increase the severity and duration of muscle blockade caused by muscle relaxants.

Immunosuppressants increase the risk of developing injections and lymphoma or other lymphoproliferative disorders caused by the Epstein-Barr virus.

Tricyclic antidepressants may increase the severity of depression caused by taking prednisolone (not indicated for the treatment of these side effects).

CHARACTERISTICS OF INDIVIDUAL DRUGS

Depending on their structure, glucocorticoids differ in duration of action, severity of anti-inflammatory, mineralocorticoid, metabolic and immunosuppressive activity (Table 5). Moreover, there is no direct correlation between their immunosuppressive and anti-inflammatory effects. For example, dexamethasone has a powerful anti-inflammatory effect and relatively low immunosuppressive activity.

CORTISONE

The drug is a natural glucocorticoid, biologically inactive. Activated in the liver, turning into hydrocortisone. Has a short-term effect. Compared to other glucocorticoids, it has more pronounced mineralocorticoid activity, that is, it has a significant effect on water-electrolyte metabolism.

Features of application

Mainly used for replacement therapy

adrenal insufficiency in patients with normal liver function.

Release forms:

• tablets of 25 and 50 mg (cortisone acetate)
  .

HYDROCORTISONE

A natural glucocorticoid, its glucocorticoid activity is 4 times weaker than prednisolone, but its mineralocorticoid activity is slightly superior. As with cortisone, there is a high risk of edema, sodium retention, and potassium loss.

Features of application

Hydrocortisone, like cortisone, is not recommended for pharmacodynamic therapy

, especially in patients with edema, hypertension, and heart failure.
It is used
mainly
for replacement therapy
for primary and secondary adrenal insufficiency. In acute adrenal insufficiency and other emergency conditions, the drug of choice is hydrocortisone hemisuccinate.

Release forms:

• hydrocortisone hemisuccinate, dry substance or solution in ampoules and bottles of 100 and 500 mg (hydrocortisone-meva, panukort, solu-cortef)
  ;
• hydrocortisone acetate, suspension in ampoules and vials of 25 mg/ml.

PREDNISOONE

Synthetic glucocorticoid, most often used in clinical practice for pharmacodynamic therapy

and is considered as a standard drug. In glucocorticoid activity it is 4 times stronger than hydrocortisone, and in mineralocorticoid activity it is inferior to it. Refers to glucocorticoids with an average duration of action.

Release forms:

• tablets of 5, 10, 20 and 50 mg (ano-prednisone, decortin N, tednisol);
• prednisolone phosphate, 1 ml ampoules, 30 mg/ml;
• prednisolone hemisuccinate, powder in ampoules of 10, 25, 50 and 250 mg (decortin salt);
• prednisolone acetate, suspension in ampoules of 10, 20, 25 and 50 mg ( prednihexol).

PREDNISONE

In terms of activity and other parameters it is close to prednisolone. Initially, prednisone is a metabolically inactive drug (prodrug). Activated in the liver by hydroxylation and conversion to prednisolone. Therefore, it is not recommended to use it for severe liver diseases. The main advantage of prednisone is its lower cost.

Release forms:

• 5 mg tablets (prednisone).

METHYLPREDNISOLONE

Compared to prednisolone, it has slightly greater (20%) glucocorticoid activity, minimal mineralocorticoid effect, and is less likely to cause undesirable reactions (especially changes in the psyche, appetite, ulcerogenic effect). It has a higher cost than prednisolone.

Features of application

Just like prednisolone, it is used mainly for pharmacodynamic therapy. It is preferable in patients with mental disorders, obesity, peptic ulcer disease, as well as during pulse therapy.

Release forms:

• tablets of 4 and 16 mg (Medrol, Metypred, Urbazon, Prednol);
• methylprednisolone succinate, dry substance in ampoules and vials of 8, 20, 40, 125, 250, 500 mg, 1.0 and 2.0 g (metipred, prednol-L, solu-medrol);
• methylprednisolone acetate, suspension in 40 mg bottles (depo-medrol, metypred);
• methylprednisolone suleptanate, ampoules of 50 and 100 mg/ml (promedrol).

TRIAMCINOLONE

It is a fluorinated glucocorticoid. It has a stronger (20%) and longer-lasting glucocorticoid effect than prednisolone. Has no mineralocorticoid activity. More often causes undesirable reactions, especially from muscle tissue (“triamcinolone” myopathy) and skin (striae, hemorrhages, hirsutism).

Release forms:

• tablets of 2, 4 and 8 mg ( berlicort, delficort, kenacort, polcortolone
  );
  triamcinolone acetonide, suspension in ampoules of 40 mg/ml ( kenalog, tricort
  );
• triamcinolone hexacetonide, suspension in ampoules of 20 mg/ml ( Lederspan
  ).

DEXAMETHASONE

Just like triamcinolone, it is a fluorinated drug. One of the most powerful glucocorticoids: 7 times stronger than prednisolone in glucocorticoid activity. Does not have mineralocorticoid effect. It causes severe depression of the hypothalamic-pituitary-adrenal system, severe disturbances of carbohydrate, fat, calcium metabolism, and a psychostimulating effect, therefore it is not recommended to prescribe it for a long period.

Features of application

The drug has some special indications for use: bacterial meningitis; cerebral edema; in ophthalmology (keratitis, uveitis and others); prevention and treatment of nausea and vomiting during chemotherapy; treatment of severe withdrawal syndrome in alcoholism; prevention of respiratory distress syndrome in premature infants (dexamethasone stimulates the synthesis of surfactant in the alveoli of the lungs); leukemia (replacing prednisolone with dexamethasone in acute lymphoblastic leukemia significantly reduces the incidence of damage to the central nervous system).

Release forms:

• tablets of 0.5 and 1.5 mg (daxin, dexazone, cortidex);
• dexamethasone phosphate, ampoules of 1 and 2 ml, 4 mg/ml (daxin, dexabene, dexazone, sondex).

BETAMETHASONE

A fluorinated glucocorticoid, similar in strength and duration of action to dexamethasone. Glucocorticoid activity is 8-10 times higher than that of prednisolone. Does not have mineralocorticoid properties. It has a somewhat weaker effect on carbohydrate metabolism than dexamethasone. The best known drug is betamethasone phosphate/dipropionate, intended for intramuscular, intra-articular and periarticular administration. It consists of two esters, one of which - phosphate - is quickly absorbed from the injection site and gives a quick (within 30 minutes) effect, and the other - dipropionate - is absorbed slowly, but provides a prolonged effect - up to 4 weeks or more. It is a fine-crystalline suspension that cannot be administered intravenously. Water-soluble betamethasone phosphate is administered intravenously and subconjunctivally.

Prednisolone hemisuccinate

GCS is a dehydrated analogue of hydrocortisone, inhibits the release of interleukin1, interleukin2, interferon gamma from lymphocytes and macrophages. It has anti-inflammatory, antiallergic, desensitizing, antishock, antitoxic and immunosuppressive effects.

Suppresses the release of ACTH and beta-lipotropin by the pituitary gland, but does not reduce the concentration of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.

Increases the excitability of the central nervous system, reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (stimulates the production of erythropoietins).

Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus and stimulates the synthesis of mRNA; the latter induces the formation of proteins, incl. lipocortin, mediating cellular effects. Lipocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, Pg, leukotrienes, which contribute to inflammation, allergies, etc.

Protein metabolism: reduces the amount of protein in plasma (due to globulins) with an increase in the albumin/globulin ratio, increases the synthesis of albumins in the liver and kidneys; enhances protein catabolism in muscle tissue.

Lipid metabolism: increases the synthesis of higher fatty acids and TG, redistributes fat (fat accumulation mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.

Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase, leading to an increase in the flow of glucose from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases, leading to the activation of gluconeogenesis.

Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (MCS activity), reduces the absorption of Ca2+ from the gastrointestinal tract, “washes out” Ca2+ from the bones, increases the excretion of Ca2+ by the kidneys.

The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; inducing the formation of lipocortin and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes and organelle membranes (especially lysosomal ones).

The antiallergic effect develops as a result of suppression of the synthesis and secretion of allergic mediators, inhibition of the release of histamine and other biologically active substances from sensitized mast cells and basophils, a decrease in the number of circulating basophils, suppression of the development of lymphoid and connective tissue, a decrease in the number of T- and B-lymphocytes, mast cells, reducing the sensitivity of effector cells to allergy mediators, inhibiting antibody formation, changing the body's immune response.

In COPD, the action is based mainly on inhibition of inflammatory processes, inhibition of development or prevention of swelling of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of the bronchial epithelium, deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of beta-adrenergic receptors of small and medium-caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by inhibiting or reducing its production.

Antishock and antitoxic effects are associated with an increase in blood pressure (due to an increase in the concentration of circulating catecholamines and restoration of the sensitivity of adrenergic receptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane protective properties, and activation of liver enzymes involved in the metabolism of endo- and xenobiotics.

The immunosuppressive effect is due to inhibition of the release of cytokines (interleukin1, interleukin2; interferon gamma) from lymphocytes and macrophages.

Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.

Prednisolone-Ferein solution for IV and IM administration 30 mg/ml in 1 ml ampoules No. 5x2

Name

Prednisolone-Ferein

Main active ingredient

Prednisolone

Release form

solution for intravenous and intramuscular administration 1 ml of the drug in glass ampoules or glass ampoules with a break ring. 3, 5 or 10 ampoules of the drug, together with instructions for medical use and a ceramic cutting disc for opening the ampoules, are placed in a pack of cardboard boxes with partitions or a corrugated insert, or with a polymer insert made of polyvinyl chloride film for placing and fixing the ampoules. 1 ml of the drug in glass ampoules with a break ring of 1 ml. 5 ampoules of the drug are placed in a blister made of polyvinyl chloride film, which is covered with a pack of boxed cardboard (chrome-ersatz).

Dosage

30 mg / 1 ml 1 ml

Pharmacodynamics

It has anti-inflammatory, antiallergic, immunosuppressive, antishock and antitoxic effects. In relatively large doses, it inhibits the activity of fibroblasts, the synthesis of collagen, reticuloendothelium and connective tissue (inhibition of the proliferative phase of inflammation), delays synthesis and accelerates protein catabolism in muscle tissue, but increases its synthesis in the liver. The antiallergic and immunosuppressive properties of the drug are due to inhibition of the development of lymphoid tissue with its involution with long-term use, a decrease in the number of circulating T- and B-lymphocytes, inhibition of mast cell degranulation, and suppression of antibody production. The antishock effect of the drug is due to an increase in the vascular response to endo- and exogenous vasoconstrictor substances, with restoration of the sensitivity of vascular receptors to catecholamines and an increase in their hypertensive effect, as well as a delay in the excretion of sodium and water from the body. The antitoxic effect of the drug is associated with the stimulation of protein synthesis processes in the liver and the acceleration of inactivation of endogenous toxic metabolites and xenobiotics in it, as well as with an increase in the stability of cell membranes, incl. hepatocytes. Enhances the deposition of glycogen in the liver and the synthesis of glucose from the products of protein metabolism. An increase in blood glucose levels activates the release of insulin. Inhibits the uptake of glucose by fat cells, which leads to activation of lipolysis. However, due to increased insulin secretion, lipogenesis is stimulated, which promotes fat accumulation. Reduces calcium absorption in the intestine, increases its leaching from bones and excretion by the kidneys. Suppresses the release of adrenocorticotropic hormone and β-lipotropin by the pituitary gland, and therefore, with long-term use, the drug can contribute to the development of functional insufficiency of the adrenal cortex. The main factors limiting long-term prednisone therapy are osteoporosis and Cushing's syndrome. Prednisolone inhibits the secretion of thyroid-stimulating and follicle-stimulating hormones. In high doses, it can increase the excitability of brain tissue and help lower the threshold for convulsive readiness. Stimulates excessive secretion of hydrochloric acid and pepsin in the stomach, and therefore may contribute to the development of peptic ulcers.

Pharmacokinetics

When administered intramuscularly, it is absorbed into the blood quickly, however, compared to reaching the maximum level in the blood, the pharmacological effect of the drug is significantly delayed and develops within 2-8 hours. In the blood plasma, most of prednisolone binds to transcortin (cortisol-binding globulin), and when the process is saturated, to albumin. With a decrease in protein synthesis, a decrease in the binding capacity of albumin is observed, which can cause an increase in the free fraction of prednisolone and, as a consequence, the manifestation of its toxic effect when using normal therapeutic doses. The half-life in adults is 2-4 hours, in children it is shorter. It is biotransformed by oxidation mainly in the liver, as well as in the kidneys, small intestine, and bronchi. Oxidized forms are glucuronidated or sulfated and excreted by the kidneys in the form of conjugates. About 20% of prednisolone is excreted from the body unchanged by the kidneys; a small part is excreted in bile. In liver diseases, the metabolism of prednisolone slows down and the degree of its binding to plasma proteins decreases, which leads to an increase in the half-life of the drug.

Indications for use

Intramuscular, intravenous administration: systemic connective tissue diseases: systemic lupus erythematosus, dermatomyositis, scleroderma, periarteritis nodosa, ankylosing spondylitis; hematological diseases: acute hemolytic anemia, lymphogranulomatosis, granulocytopenia, thrombocytopenic purpura, agranulocytosis, various forms of leukemia; skin diseases: eczema vulgaris, exudative erythema multiforme, pemphigus vulgaris, erythroderma, exfoliative dermatitis, seborrheic dermatitis, psoriasis, alopecia, adrenogenital syndrome; replacement therapy: Addison's crisis; emergency conditions: severe forms of nonspecific ulcerative colitis and Crohn's disease, shock (burn, traumatic, surgical, anaphylactic, toxic, transfusion), status asthmaticus, acute adrenal insufficiency, hepatic coma, severe allergic and anaphylactic reactions, hypoglycemic reactions; Intra-articular administration: chronic polyarthritis, osteoarthritis of large joints, rheumatoid arthritis, post-traumatic arthritis, arthrosis; For infectious diseases and latent forms of tuberculosis, the drug should be prescribed only in combination with antibiotics and anti-tuberculosis drugs. If it is necessary to use prednisolone while taking oral hypoglycemic drugs or anticoagulants, it is necessary to adjust the dosage regimen of the latter. In patients with thrombocytopenic purpura, the drug should be used only intravenously. After cessation of treatment, withdrawal syndrome, adrenal insufficiency, and exacerbation of the disease for which prednisolone was prescribed may occur. If, after finishing treatment with prednisolone, functional adrenal insufficiency is observed, use of the drug should be resumed immediately, and the dose reduction should be carried out very slowly and with caution (for example, the daily dose should be reduced by 2-3 mg over 7-10 days). Because of the risk of developing hypercortisolism, a new course of treatment with cortisone, after a previous long-term treatment with prednisone over several months, should always be started with low initial doses (except in acute life-threatening conditions). Electrolyte balance should be especially carefully monitored when prednisolone is used in combination with diuretics. With long-term treatment with prednisolone to prevent hypokalemia, it is necessary to prescribe potassium supplements and an appropriate diet due to a possible increase in intraocular pressure and the risk of developing subcapsular cataracts. During treatment, especially long-term treatment, observation by an ophthalmologist is necessary. If there is a history of psoriasis, use prednisolone in high doses with extreme caution. If there is a history of psychosis or seizures, prednisolone should be used only in minimal effective doses. Particular caution should be taken when prescribing the drug for migraines or a history of certain parasitic diseases (especially amoebiasis). Prednisolone should be prescribed to children with special caution. Prescribe with particular caution in immunodeficiency states (including AIDS or HIV infection). Also prescribe with caution after a recent myocardial infarction (in patients with acute, subacute myocardial infarction, expansion of the focus of necrosis, slowdown in the formation of scar tissue, and rupture of the heart muscle are possible). It is prescribed with particular caution for liver failure, conditions that cause the occurrence of hypoalbuminemia, and obesity of III-IV degree. Women during menopause need to undergo research regarding the possible occurrence of osteoporosis. In case of liver use of glucocorticoids for a long time, it is recommended to regularly monitor blood pressure, determine the level of glucose in urine and blood, perform a fecal occult blood test, blood clotting tests, and x-ray monitoring of the spine. Before starting treatment with glucocorticoids, a thorough examination of the gastrointestinal tract should be performed to exclude gastric and duodenal ulcers.

Directions for use and doses

The dose of the drug and the duration of treatment are determined by the doctor individually depending on the indications and severity of the disease. Prednisolone is administered intravenously (drip or stream) or intramuscularly. Intravenously, the drug is usually administered first as a stream, then as a drip. In case of acute adrenal insufficiency, a single dose of the drug is 100-200 mg, a daily dose is 300-400 mg. For severe allergic reactions, Prednisolone is administered in a daily dose of 100-200 mg for 3-16 days. For bronchial asthma, the drug is administered depending on the severity of the disease and the effectiveness of complex treatment from 75 mg to 675 mg per course of treatment from 3 to 16 days; in severe cases, the dose can be increased to 1400 mg per course of treatment or more with a gradual dose reduction. For status asthmaticus, Prednisolone is administered at a dose of 500-1200 mg per day, followed by a reduction to 300 mg per day and switching to maintenance doses. In case of thyrotoxic crisis, 100 mg of the drug is administered in a daily dose of 200-300 mg; if necessary, the daily dose can be increased to 1000 mg. The duration of administration depends on the therapeutic effect, usually up to 6 days. In case of shock that is resistant to standard therapy, Prednisolone is usually administered as a bolus at the beginning of therapy, after which it is switched to drip administration. If blood pressure does not increase within 10-20 minutes, repeat the infusion of the drug. After recovery from the shock state, drip administration is continued until blood pressure stabilizes. A single dose is 50-150 mg (in severe cases - up to 400 mg). The drug is re-administered after 3-4 hours. The daily dose can be 300-1200 mg (with subsequent dose reduction). In case of acute hepatic-renal failure (in acute poisoning, in the postoperative and postpartum periods, etc.), Prednisolone is administered at 25-75 mg/day; if indicated, the daily dose can be increased to 300-1500 mg/day and higher. For rheumatoid arthritis and systemic lupus erythematosus, Prednisolone is administered in addition to systemic drug intake at a dose of 75-125 mg per day for no more than 7-10 days. In acute hepatitis, Prednisolone is administered at a dose of 75-100 mg/day for 7-10 days. For poisoning with cauterizing liquids with burns of the digestive tract and upper respiratory tract, Prednisolone is prescribed at a dose of 75-400 mg/day for 3-18 days. If intravenous administration is not possible, Prednisolone is administered intramuscularly in the same doses. After relief of the acute condition, Prednisolone tablets are prescribed orally, followed by a gradual reduction in the dose. When taking the drug for a long time, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly! Children: Use in children over 6 years of age only as directed and under the supervision of a physician. The doctor determines the dose and duration of therapy individually, depending on the age and severity of the disease. Long-term use in children may cause growth retardation, so it is necessary to limit the use of minimal doses for certain indications for the shortest possible time. The benefit of treatment must outweigh the possible risk of adverse reactions.

Use during pregnancy and lactation

Do not use the drug during pregnancy. If it is necessary to use the drug during lactation, it is recommended to stop breastfeeding.

Precautionary measures

The ability to influence the speed of reaction when driving vehicles or other mechanisms. Patients treated with prednisone should refrain from potentially hazardous activities that require increased attention to the speed of mental and motor reactions. Special groups of patients Elderly During long-term therapy, muscle atrophy, muscle pain or weakness, delayed wound healing, atrophy of the protein matrix of the bone leading to osteoporosis, vertebral compression fractures, avascular necrosis of the femoral head or humeral head, and pathological fractures of long tubular bones may be observed. Particularly serious complications may occur in elderly and debilitated patients. Before initiating glucocorticoid therapy in postmenopausal women, it is necessary to take into account that such patients are especially prone to osteoporosis. Use with caution in patients with osteoporosis. Liver dysfunction In patients with cirrhosis, an increased effect of glucocorticoids is observed. Renal dysfunction. Use with caution.

Interaction with other drugs

Anticoagulants: when used simultaneously with glucocorticoids, the effect of anticoagulants may be increased or decreased. Parenteral administration of prednisolone causes the thrombolytic effect of vitamin K antagonists (fluindione, acenocoumarol). Salicylates and other non-steroidal anti-inflammatory drugs: Concomitant use of salicylates, indomethacin and other non-steroidal anti-inflammatory drugs may increase the likelihood of gastric ulceration. Prednisolone reduces the level of salicylates in the blood serum, increasing their renal clearance. Caution is necessary when reducing the dose of prednisolone during long-term concomitant use. Hypoglycemic drugs: Prednisolone partially inhibits the hypoglycemic effect of oral hypoglycemic agents and insulin. Hepatic enzyme inducers, for example, barbiturates, phenytoin, pyramidone, carbamazepine and rifampicin increase the systemic clearance of prednisolone, thereby reducing the effect of prednisolone by almost 2 times. CYP3A4 inhibitors, such as erythromycin, clarithromycin, ketoconazole, diltiazem, aprepitant, itraconazole and oleandomycin, increase the elimination and plasma levels of prednisolone, which increases the therapeutic and side effects of prednisolone. Estrogen may potentiate the effect of prednisolone by slowing its metabolism. It is not recommended to adjust the dose of prednisolone for women using oral contraceptives, which contribute not only to an increase in the half-life, but also to the development of the atypical immunosuppressive effect of prednisolone. Fluoroquinolones: Concomitant use may cause tendon damage. Amphotericin, diuretics and laxatives: Prednisolone may increase potassium excretion in patients receiving these drugs concomitantly. Immunosuppressants: Prednisolone has active immunosuppressive properties, which may cause an increase in therapeutic effects or the risk of developing various adverse reactions when used simultaneously with other immunosuppressants. Only some of them can be explained by pharmacokinetic interactions. Glucocorticoids increase the antiemetic effectiveness of antiemetic drugs that are used in parallel during therapy with anticancer drugs that cause vomiting. Corticosteroids can increase the concentration of tacrolimus in the blood plasma when used simultaneously; when they are withdrawn, the concentration of tacrolimus in the blood plasma decreases. Immunization: Glucocorticoids may reduce the effectiveness of immunization and increase the risk of neurological complications. The use of therapeutic (immunosuppressive) doses of glucocorticoids with live viral vaccines may increase the risk of developing viral diseases. Emergency vaccines may be used during drug therapy. Anticholinesterase agents: In patients with myasthenia gravis, the use of glucocorticoids and anticholinesterase agents may cause muscle weakness, especially in patients with myasthenia gravis. Cardiac glycosides: the risk of developing glycoside intoxication increases. Others: Two serious cases of acute myopathy have been reported in elderly patients who took doxocarium chloride and high-dose prednisolone. With long-term therapy, glucocorticoids may reduce the effect of somatotropin. Cases of acute myopathy have been described with the use of corticosteroids in patients who are simultaneously receiving treatment with neuromuscular transmission blockers (for example, pancuronium). Cases of seizures have been reported with the simultaneous use of prednisolone and cyclosporine. Because coadministration of these drugs causes mutual inhibition of metabolism, it is likely that seizures and other side effects associated with the use of each of these drugs as monotherapy may occur more frequently when administered concomitantly. Concomitant use may cause an increase in the concentration of other drugs in the blood plasma. Antihistamines reduce the effect of prednisolone. When prednisolone is used simultaneously with antihypertensive drugs, the effectiveness of the latter may be reduced. Prednisolone should not be mixed or used simultaneously with other drugs in the same infusion system or syringe. When mixing a solution of prednisolone with heparin, a precipitate forms. Incompatible with aerosols of sympathomimetic drugs for the treatment of bronchial asthma in children (risk of respiratory paralysis).

Contraindications

Hypersensitivity to the components of the drug; peptic ulcer of the stomach and duodenum, osteoporosis, Itsenko-Cushing's disease, tendency to thromboembolism, renal failure, arterial hypertension, viral infections (including viral lesions of the eyes and skin), decompensated diabetes mellitus, vaccination period (at least 14 days before and after preventive immunization), lymphadenitis after BCG vaccination, active form of tuberculosis, glaucoma, cataracts, productive symptoms in mental illness, psychosis, depression; systemic mycosis, herpetic diseases, syphilis, severe myopathy (except for myasthenia gravis), poliomyelitis (except for the bulbar-encephalitic form), pregnancy and lactation. For intra-articular injections - infections at the injection site.

Compound

active ingredient: 1 ml of solution contains prednisotokg for prednisolone - 30 mg; excipients: sodium hydrogen phosphate anhydrous, sodium dihydrogen phosphate dihydrate, propylene glycol, water for injection. Basic physical and chemical properties: transparent, colorless or almost colorless solution.

Overdose

In case of overdose, nausea, vomiting, bradycardia, arrhythmia, increased symptoms of heart failure, cardiac arrest are possible; hypokalemia, increased blood pressure, muscle cramps, hyperglycemia, thromboembolism, acute psychosis, dizziness, headache, possible development of symptoms of hypercortisolism: weight gain, development of edema, arterial hypertension, glucosuria, hypokalemia. In children with an overdose, suppression of the hypothalamic-pituitary-adrenal system, Itsenko-Cushing syndrome, decreased excretion of growth hormone, and increased intracranial pressure is possible. There is no specific antidote. Treatment: discontinuation of the drug, symptomatic therapy, and, if necessary, correction of electrolyte balance.

Side effect

The development of severe adverse reactions depends on the dose and duration of treatment. Adverse reactions usually develop with long-term treatment with the drug. Over a short period, the risk of their occurrence is unlikely. Infections and invasions: increased sensitivity to bacterial, viral, fungal infections, their severity with masking of symptoms, opportunistic infections. From the blood and lymphatic system: an increase in the total number of leukocytes with a decrease in the number of eosinophils, monocytes and lymphocytes. The mass of lymphoid tissue decreases. Blood clotting may increase, which leads to thrombosis and thromboembolism. From the endocrine system and metabolism: suppression of the hypothalamic-pituitary-adrenal system, growth retardation in children and adolescents, menstrual irregularities, impaired secretion of sex hormones (amenorrhea), postmenopausal bleeding, Cushingoid face, hirsutism, weight gain, decreased tolerance to carbohydrates , increased need for insulin and oral hypoglycemic drugs, hyperlipidemia, negative balance of nitrogen and calcium, increased appetite, disturbance of mineral metabolism and electrolyte balance, hypokalemic alkalosis, hypokalemia, possible fluid and sodium retention in the body. Mental disorders: irritability, euphobia, depression, suicidal tendencies, insomnia, labile mood, increased concentration, psychological dependence, mania, hallucinations, exacerbation of schizophrenia, dementia, psychosis, anxiety, sleep disturbances, epileptic seizures, cognitive dysfunction (including amnesia and impaired consciousness), increased intracranial pressure, which is accompanied by nausea and swelling of the optic disc in children. From the nervous system: increased intracranial pressure, epileptic seizures, peripheral neuropathies, paresthesia, dizziness, headache, autonomic disorders. From the organs of vision: increased intraocular pressure, glaucoma, swelling of the optic nerve, cataracts, thinning of the cornea and sclera, exacerbation of ocular viral and fungal infections, exophthalmos. From the cardiovascular system: myocardial rupture due to myocardial infarction, arterial hypo- or hypertension, bradycardia, combined ventricular arrhythmia, asystole (due to rapid administration of the drug), atherosclerosis, thrombosis, vasculitis, heart failure, peripheral edema. In patients with acute myocardial infarction, the necrosis focus spreads, scar formation slows down. From the immune system: allergic reactions that cause anaphylactic shock with a fatal outcome, angioedema, allergic dermatitis, changes in the reaction to skin tests, relapse of tuberculosis, immunosuppression, hypersensitivity reactions, including rash, itching of the skin. From the gastrointestinal tract: nausea, bloating, unpleasant taste in the mouth, dyspepsia, peptic ulcers with perforation and bleeding, esophageal ulcer, esophageal candidiasis, pancreatitis, gallbladder perforation, gastric bleeding, local ileitis and ulcerative colitis. During the use of the drug, an increase in ALT, AST and alkaline phosphatase may be observed, which is usually not significant and is reversible after discontinuation of the drug. From the skin: slower regeneration, skin atrophy, formation of hematomas and atrophic stripes of the skin (striae), telangiectasia, acne, acne, hirsutism, microhemorrhages, ecchymosis, purpura, hypo- or hyperpigmentation, post-steroid panniculitis, which is characterized by the appearance of erythematosis, hot subcutaneous thickenings for 2 weeks after discontinuation of the drug, Kaposi's sarcoma. From the musculoskeletal system: proximal myopathy, osteoporosis, tendon rupture, muscle weakness, atrophy, myopathy, fractures of the spine and long bones, aseptic osteonecrosis. From the urinary system: increased risk of urolith formation and the content of leukocytes and red blood cells in the urine without obvious kidney damage. General: malaise, persistent hiccups when using the drug in high doses, adrenal insufficiency leading to hypotension, hypoglycemia and death in stressful situations such as surgery, trauma or infection if the dose of prednisolone is not increased. With abrupt withdrawal of the drug, withdrawal syndrome is possible, the severity of symptoms depends on the degree of adrenal atrophy, headache, nausea, abdominal pain, dizziness, anorexia, weakness, mood changes, lethargy, fever, myalgia, arthralgia, rhinitis, conjunctivitis, skin pain, weight loss. In more severe cases - severe mental disorders and increased intracranial pressure, steroid pseudorheumatism in patients with rheumatism, death. Reactions at the injection site: pain, burning, changes in pigmentation (depigmentation, leucoderma), skin atrophy, sterile abscesses, rarely - lipoatrophy.

Storage conditions

Store in original packaging to protect from light at a temperature not exceeding 25°C. Keep out of the reach of children.

Buy Prednisolone-Ferein solution for IV and IM administration 30 mg/ml in 1 ml ampoules No. 5x2 in the pharmacy

Price for Prednisolone-Ferein solution for IV and IM administration 30 mg/ml in 1 ml ampoules No. 5x2

Instructions for use for Prednisolone-Ferein solution for IV and IM administration 30 mg/ml in 1 ml ampoules No. 5x2

Providing emergency medical care for acute allergic diseases

Ph.D.
A.V. Topolyansky, professor A.L. Vertkin Scientific Center for Children's Health of the Russian Academy of Medical Sciences, Moscow MMA named after I.M. Sechenov MGMSU named after. ON THE. Semashko Station of ambulance and emergency medical care, Moscow National Scientific and Practical Society of Emergency Medical Care, Moscow
P

According to the National Scientific and Practical Society of Emergency Medical Services, over the past 3 years the number of calls for acute allergic diseases in the Russian Federation as a whole has increased by 18%. Moreover, their frequency in different regions ranges from 1 to 5% of all cases of emergency medical team visits.

Main causes and pathogenesis

The pathogenesis of allergic reactions has been studied quite fully today and is described in detail in many domestic and foreign monographs on allergology and clinical immunology. In any case, in the tissue of the shock organ or the “target” organ, which can be the skin, bronchi, gastrointestinal tract, etc., signs of allergic inflammation appear. The central role in the implementation of these immunopathological reactions belongs to class E immunoglobulins

(IgE), the binding of which to the antigen leads to the release of allergy mediators (histamine, serotonin, cytokines, etc.) from mast cells.

Most often, allergic reactions develop when exposed to inhaled allergens in homes, epidermal, pollen, food allergens, medications, parasite antigens, as well as stings and insect bites. Drug allergies most often develop when using analgesics, sulfonamides and antibiotics from the penicillin group, and less often cephalosporins. In addition, the incidence of latex allergy is high.

Clinical picture, classification and diagnostic criteria

From the point of view of providing assistance and assessing the prognosis, acute allergic diseases can be classified as follows (Table 1):

Lungs
– allergic rhinitis (year-round or seasonal), allergic conjunctivitis (year-round or seasonal), urticaria.

Moderate to heavy

– generalized urticaria, angioedema, acute laryngeal stenosis, moderate exacerbation of bronchial asthma, anaphylactic shock.

The greatest concern when providing medical care at the prehospital stage should be caused by prognostically unfavorable cases of development of life-threatening conditions in patients: severe asthma attack (status asthmaticus), anaphylactic shock, Quincke's edema in the larynx, acute laryngeal stenosis.

When analyzing the clinical picture of an allergic reaction, the emergency physician should receive answers to the questions presented in Table 2.

The initial examination should assess for the presence of: stridor, dyspnea, wheezing, dyspnea, or apnea; hypotension or syncope; changes on the skin (urticaria-type rashes, Quincke's edema, hyperemia, itching); gastrointestinal manifestations (nausea, abdominal pain, diarrhea); changes in consciousness. If the patient has stridor, severe shortness of breath, hypotension, arrhythmia, convulsions, loss of consciousness or shock, then this condition is considered life-threatening.

Treatment of acute allergic diseases

In case of acute allergic diseases at the prehospital stage, emergency therapy is based on the following areas:

Stopping further entry of the suspected allergen into the body

. For example, in case of a reaction to a drug administered parenterally or to an insect bite/sting, apply a tourniquet above the injection or sting site for 25 minutes (every 10 minutes, loosen the tourniquet for 1–2 minutes); to the injection or bite site - ice or a heating pad with cold water for 15 minutes; pricking at 5–6 points and infiltrating the injection or bite site with 0.3–0.5 ml of 0.1% epinephrine solution with 4.5 ml of isotonic sodium chloride solution.

Antiallergic therapy (antihistamines or glucocorticosteroids)

.
The administration of antihistamines is indicated for allergic rhinitis, allergic conjunctivitis, and urticaria. Glucocorticoid therapy (GCS) is carried out for anaphylactic shock and angioedema (in the latter case, the drug of choice): prednisolone
(adults - 60-150 mg, children - at the rate of 2 mg per 1 kg of body weight).
For generalized urticaria or when urticaria is combined with Quincke's edema, betamethasone
1-2 ml intramuscularly is highly effective. In case of angioedema, to prevent the effect of histamine on tissues, it is necessary to combine new generation antihistamines (loratadine) with glucocorticoids.

Symptomatic therapy

. With the development of bronchospasm, inhaled administration of b2-agonists and other bronchodilators and anti-inflammatory drugs through a nebulizer is indicated. Correction of arterial hypotension and replenishment of circulating blood volume is carried out by administering saline and colloid solutions (isotonic sodium chloride solution 500–1000 ml, hydroxyethyl starch 500 ml, polyglucin 400 ml). The use of vasopressor amines (dopamine 400 mg per 500 ml of 5% glucose, norepinephrine 0.2 - 2 ml per 500 ml of 5% glucose solution; the dose is titrated until a systolic pressure level of 90 mm Hg is achieved) is possible only after replenishment of the circulating blood volume . For bradycardia, it is possible to administer atropine in a dose of 0.3–0.5 mg subcutaneously (if necessary, the administration is repeated every 10 minutes). In the presence of cyanosis, dyspnea, and dry wheezing, oxygen therapy is also indicated.

Anti-shock measures

(Fig. 1). In case of anaphylactic shock, the patient should be laid down (head lower than legs), head turned to the side (to avoid aspiration of vomit), protract the lower jaw, and remove removable dentures. Epinephrine is administered subcutaneously in a dose of 0.1 - 0.5 ml of a 0.1% solution (drug of choice); if necessary, injections are repeated every 20 minutes for an hour under blood pressure monitoring. In case of unstable hemodynamics with the development of an immediate threat to life, intravenous administration of epinephrine is possible. In this case, 1 ml of 0.1% epinephrine solution is diluted in 100 ml of isotonic sodium chloride solution and administered at an initial rate of 1 mcg/min (1 ml per min). If necessary, the rate can be increased to 2–10 mcg/min. Intravenous administration of epinephrine is carried out under the control of heart rate, respiration, and blood pressure (systolic blood pressure must be maintained at a level of more than 100 mm Hg in adults and > 50 mm Hg in children). Medicines used for allergic diseases of varying severity and their effectiveness are presented in Table 3.

Rice. 1. Treatment algorithm for anaphylactic shock

Clinical pharmacology of drugs used for the treatment of acute allergic diseases.
The method of administration and dosage of antiallergic drugs are presented in Table 4.

Epinephrine
Epinephrine is a direct stimulator of a- and b-adrenergic receptors, which determines all its pharmacodynamic effects. The mechanism of antiallergic action is realized:

The method of administration and dosage of antiallergic drugs are presented in Table 4. Epinephrine is a direct stimulator of - and - adrenergic receptors, which determines all its pharmacodynamic effects. The mechanism of antiallergic action is realized:

• stimulation of a-adrenergic receptors, vasoconstriction of the abdominal organs, skin, mucous membranes, increased blood pressure;

• positive inotropic effect (the strength of heart contractions increases due to stimulation of b1-adrenergic receptors of the heart);

• stimulation of b2-adrenergic receptors of the bronchi (relief of bronchospasm);

• suppression of degranulation of mast cells and basophils (due to stimulation of intracellular cAMP).

When administered parenterally, the drug has a short-term effect (intravenous - 5 minutes, subcutaneously - up to 30 minutes), as it is quickly metabolized in the endings of sympathetic nerves, in the liver and other tissues with the participation of monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) .

Side effects:

dizziness, tremor, weakness; strong heartbeat, tachycardia, various arrhythmias (including ventricular), the appearance of pain in the heart area; difficulty breathing; increased sweating; excessive increase in blood pressure; urinary retention in men suffering from prostate adenoma; increased blood sugar levels in patients with diabetes. Tissue necrosis has also been described with repeated subcutaneous injection into the same place due to local vasoconstriction.

Contraindications:

arterial hypertension; severe cerebral atherosclerosis or organic brain damage; cardiac ischemia; hyperthyroidism; angle-closure glaucoma; diabetes; prostatic hypertrophy; pregnancy. However, even with these diseases, it is possible to prescribe epinephrine for anaphylactic shock for health reasons and under strict medical supervision.

Glucocorticosteroids

The mechanism of the antiallergic action of glucocorticoids is based on the following effects:

• immunosuppressive property (suppression of growth and differentiation of immune cells - lymphocytes, plasma cells, reduction in antibody production);

• prevention of degranulation of mast cells and the release of allergy mediators from them;

• decreased vascular permeability, increased blood pressure, improved bronchial obstruction.

Prednisolone is used for parenteral administration during emergency treatment at the prehospital stage.

.
For the treatment of bronchial asthma, allergic rhinitis, and allergic conjunctivitis, topical forms of glucocorticosteroids ( fluticasone, budesonide
) have been developed. Side effects of systemic corticosteroids: arterial hypertension, agitation, arrhythmia, ulcerative bleeding. Side effects of topical corticosteroids: hoarseness, disturbance of microflora with further development of mucosal candidiasis, when using high doses - skin atrophy, gynecomastia, weight gain, etc. Contraindications: peptic ulcer of the stomach and duodenum, severe arterial hypertension, renal failure , history of hypersensitivity to glucocorticoids.

Betamethasone

– glucocorticosteroid drug, consists of 2 mg of disodium phosphate and 5 mg of betamethasone dipropionate. Betamethasone disodium phosphate provides rapid onset of effect. Prolonged action is ensured by betamethasone dipropionate. The drug has immunosuppressive, antiallergic, desensitizing and antishock effects. Betamethasone is biotransformed in the liver. The dose of the drug depends on the severity of the disease and the clinical picture of the course. It is used for the treatment of acute allergic diseases in the form of intramuscular injections of 1–2 ml. With a single administration, no significant side effects were noted.

Antihistamines (H1-histamine receptor blockers)

There are several classifications of antihistamines. According to one of them, drugs of the first, second and third generation are distinguished (at the same time, the question of whether different drugs belong to the 2nd or 3rd generation is still debated). Another classification, more popular among clinicians, distinguishes between classic antihistamines, for example, chloropyramine, and new generation drugs (acrivastine, fexofenadine, loratadine, etc.)

It should be noted that classical antihistamines, in contrast to new generation drugs, are characterized by a short duration of action with a relatively rapid onset of clinical effect. Many of them are available in parenteral forms. All this determines the widespread use of classical antihistamines at the present time.

Chloropyramine

– one of the widely used classical antihistamines. It has significant antihistamine activity, peripheral anticholinergic and moderate antispasmodic effects. When taken orally, it is quickly and completely absorbed from the gastrointestinal tract. The maximum concentration in the blood is achieved within the first 2 hours, the therapeutic level of concentration remains for 4–6 hours. Effective in most cases for the treatment of seasonal and year-round allergic rhinitis and conjunctivitis, urticaria, atopic dermatitis, eczema; in parenteral form – for the treatment of acute allergic diseases requiring emergency care. Has a wide range of therapeutic doses used. It does not accumulate in the blood serum, therefore it does not cause an overdose with long-term use. The drug is characterized by a rapid onset of effect and a short duration (including side effects). Can be combined with other H1 blockers to increase the duration of the antiallergic effect. Available in tablets and ampoules for intramuscular and intravenous administration.

New generation antihistamines are devoid of cardiotoxic effects, have a competitive effect on histamine, are not metabolized by the liver (for example, the pharmacokinetics of acrivastine does not change even in patients with impaired liver and kidney function) and do not cause tachyphylaxis.

Akrivastine

– a drug with high antihistamine activity with minimally expressed sedative and anticholinergic effects. A feature of its pharmacokinetics is a low level of metabolism and the absence of accumulation and addiction. Acrivastine is preferred in cases where there is no need for continuous antiallergic treatment. The gelatin capsule is quickly absorbed in the stomach, providing a rapid onset of effect. The drug has a short period of action, which allows the use of a flexible dosage regimen. No cardiotoxic effect. Selectively influencing H1 receptors, it does not irritate the gastric mucosa. There is no effect on H2 receptors.

Loratadine

– a new generation antihistamine over-the-counter.

Indications for use: allergic rhinitis (seasonal and year-round), allergic conjunctivitis, urticaria, generalized urticaria, Quincke's edema, allergic reactions to insect bites, itchy dermatoses (contact allergic dermatitis, chronic eczema).

The drug has no side effects such as drowsiness, dry mouth, headache, dizziness.

Bronchospasmolytics: short-acting b2-agonists and anticholinergics

Berodual is a combined bronchospasmolytic drug containing two bronchodilators: fenoterol (b2-agonist) and ipratropium bromide (anticholinergic). One dose of Berodual contains 0.05 mg of fenoterol and 0.02 mg of ipratropium bromide.

Method of use: using a nebulizer to relieve an attack of suffocation, inhale 10–20 drops of Berodual in 1–4 ml of physiological solution for 5–10 minutes. If there is no improvement, repeat inhalation after 20 minutes.

Salbutamol

– selective agonist of b2- adrenergic receptors. The bronchodilator effect of salbutamol occurs within 4–5 minutes. The effect of the drug gradually increases to its maximum at 40–60 minutes. The half-life is 3–4 hours, duration of action is 4–5 hours.

Directions for use: using a nebulizer; nebulas of 2.5 ml containing 2.5 mg of salbutamol in saline solution. 1–2 nebulas (2.5–5.0 mg) are prescribed for inhalation, undiluted. If there is no improvement, repeat inhalations of 2.5 mg every 20 minutes. In one hour.

Typical errors in the use of drugs in the treatment of acute allergic diseases at the prehospital stage

• Isolated administration of H1-histamine blockers for severe allergic reactions, as well as for broncho-obstructive syndrome, has no independent significance and at the prehospital stage only leads to unjustified loss of time.

• The use of diprazine is also dangerous because it worsens hypotension.

• Late administration of GCS; unreasonable use of small doses of corticosteroids.

• Use of certain drugs not indicated for the treatment of allergic diseases (calcium gluconate, calcium chloride, etc.).

• The presence of unidirectional drugs in the equipment list of ambulance teams is not economically justified.

• Non-use of topical corticosteroids and b2-agonists for allergic laryngeal stenosis and bronchospasm.

Patients with severe allergic diseases must be hospitalized. For mild allergic diseases, the issue of hospitalization is decided on an individual basis in each case.

APPENDIX
Allergic stenosis of the upper respiratory tract in children
Main causes and pathogenesis

Upper respiratory tract obstruction syndrome (croup, acute stenosing laryngotracheitis) in children is one of the common reasons for seeking emergency care. There are acute allergic stenosis of the larynx and stenosis developing against the background of ARVI.

The main reason for the development of allergic stenosis of the upper respiratory tract with a predominant localization of the process in the larynx is the body’s sensitization to food and drug allergens, as well as to allergens of house dust mites (Dermatophagoides pteronyssinus and Dermatophagoides farinae), animals, etc.

Acute allergic stenosis of the upper respiratory tract

more often observed in children with a hereditary predisposition to allergies. The development of croup is often preceded by the appearance of symptoms of skin and respiratory allergies. The occurrence of allergic stenosis of the larynx is also favored by such anatomical features of this organ in children as the softness of the cartilaginous skeleton, a short and narrow vestibule and a high-lying larynx, the presence of a delicate mucous membrane rich in cellular elements and a loose submucosal layer with an abundant vascular network and a large number of mast cells. . These structural features of the mucous and submucous membranes are especially characteristic of the area of ​​the larynx surrounded by dense cricoid cartilage. This area is projected onto the subglottic space, where the most pronounced edema develops in children. Croup most often develops in children aged 6 months to 3 years, and boys suffer from it 3–4 times more often than girls.

The pathogenetic basis of allergic stenosis of the upper respiratory tract is IgE-mediated allergic reactions, causing the development of inflammation in the laryngeal mucosa in the form of edema, hypersecretion of mucus, spasm of the smooth muscles of the upper respiratory tract; In some patients, bronchospasm also occurs. The development of acute stenosing laryngotracheitis may also be associated with exposure to a viral infection, chemical pollutants, and changes in the weather situation.

Clinical picture, classification and diagnostic criteria

Acute laryngeal stenosis causes the development of respiratory failure and disruption of the child’s general condition. There are three degrees of stenosis

depending on the severity of the narrowing of the larynx:

I degree

laryngeal stenosis – compensated stenosis;

II degree

– subcompensated stenosis;

III degree

– decompensated stenosis (Table 5).

Children with allergic laryngeal stenosis are usually found to have heredity burdened by allergic reactions and diseases; they often also have manifestations of atopic dermatitis, food and drug allergies.
This variant of croup is characterized by the sudden development of stenosis “against the background of complete health,” in the absence of catarrhal symptoms, normal body temperature, as well as relatively rapid relief of symptoms of the disease when adequate therapy is prescribed. In a number of children, simultaneously with manifestations of allergic laryngeal stenosis, broncho-obstructive syndrome develops. Acute laryngeal stenosis, developing against the background of an acute respiratory infection, is characterized by a more gradual onset of the disease, the occurrence of stenosis against the background of catarrhal phenomena in the upper respiratory tract, an increase in temperature, the development of symptoms of intoxication, and inflammatory changes in a general blood test.

Laryngeal stenosis must be differentiated from laryngeal diphtheria, foreign body in the respiratory tract, obstructive bronchitis, retropharyngeal abscess, bronchial asthma, whooping cough, pneumonia with manifestations of respiratory failure.

Treatment of acute laryngeal stenosis

Children with acute laryngeal stenosis are subject to mandatory hospitalization. Therapy carried out for acute laryngeal stenosis should be pathogenetic and aimed at restoring air patency of the upper respiratory tract. Treatment is carried out taking into account the severity of laryngeal stenosis, begins with emergency medical services teams on call, and continues along the way to the hospital. The time required to provide prehospital care to a patient should not exceed 60 minutes.

For the treatment of acute laryngeal stenosis in the compensated stage (I degree) at the prehospital stage, inhalations of glucocorticosteroids are used (budesonide through a nebulizer at a dose of 0.25 mg; if nebulizers are ineffective or unavailable, antihistamines are used: intramuscularly (chloropyramine, 2% solution, 0.1 ml in the first year of life) or orally (for children over 12 years old - acrivastine (7 mg, capsule) or loratadine 10 mg (1 tablet or 2 teaspoons of syrup).

Treatment of acute laryngeal stenosis in the stage of incomplete compensation (II degree) begins with inhalation of glucocorticosteroids through a nebulizer at a dose of 0.5 mg. If ineffective, repeat budesonide inhalations in the same dose through a nebulizer with an interval of 20 minutes (maximum 3 times).

In the absence of nebulizers, antihistamines (chloropyramine intramuscularly) and systemic glucocorticosteroids (prednisolone at a rate of 2 mg/kg) are used. If the effect is insufficient, subcutaneous administration of a 0.1% epinephrine solution at the rate of 0.01 mg/kg body weight is additionally prescribed.

III degree laryngeal stenosis occurs with manifestations of respiratory and cardiovascular failure, metabolic disorders, and signs of toxicosis, which necessitates immediate hospitalization. At the prehospital stage, treatment of grade III laryngeal stenosis also begins with inhalation of glucocorticosteroids through a nebulizer at a dose of 1 mg.

If broncho-obstructive syndrome occurs, treatment is carried out with solutions of short-acting b2-agonists (berodual 10-20 drops for children under 6 years old or salbutamol - 1/2-1 nebul for children over 6 years old) through a nebulizer.