Clinical recommendations for broncho-obstructive syndrome. Broncho-obstructive syndrome in children. Symptoms of biofeedback in children

S.L. Babak, L.A. Golubev, M.V. Gorbunova

Broncho-obstructive syndrome (BOS) is a clinical symptom complex caused by impaired air flow through the bronchi due to narrowing or occlusion of the airways with a subsequent increase in the resistance of the airways to the inhaled air flow.

Biofeedback is one of the pathophysiological disorders that can affect the outcomes and progressive course of many acute and chronic bronchopulmonary diseases. BOS, not being an independent nosological entity, can occur in various diseases of the lungs and heart, leading to obstruction of the airways. The main clinical manifestations of BOS are paroxysmal cough, expiratory shortness of breath and sudden attacks of suffocation. Based on clinical manifestations, biofeedback is usually divided into latent and pronounced clinical manifestations. According to the course, biofeedback is divided into acute (suddenly occurring) and chronic (permanent).
Functional changes in biofeedback are associated with a decrease in the main spirometric indicators, reflecting the degree of bronchial obstruction (BO) and the nature of the “air trap”, namely:

Forced expiratory volume in 1 second (FEV1);
FEV1/FVC ratio

These indicators are a diagnostic criterion for bronchial obstruction and serve to determine the severity of biofeedback.
Based on the severity of clinical and functional manifestations, BOS is divided into mild, moderate and severe.
The main clinical manifestations of BOS are shortness of breath, suffocation (refers to life-threatening conditions), paroxysmal cough, wheezing, noisy breathing. Symptoms are more noticeable with physical activity. Other manifestations of BOS - increased sweating, sleep disturbance, headache, confusion, convulsions - are detected in severe cases of the syndrome complex.

Variant forms of biofeedback
Spastic is the most common variant of BOS (>70% of all cases), the development of which is due to bronchospasm due to dysfunction in the systems of control of bronchial tone.
Inflammatory – the mechanism is caused by edema, infiltration of the airways, hyperemia of the bronchial membrane.
Discrinic - observed with excessive stimulation of enzymes of goblet cells and glands of the bronchial layer, leading to a deterioration in the properties of sputum, dysfunction of mucus formation and mucociliary transport.
Dyskinetic - bronchial patency is impaired due to congenital underdevelopment of the membranous part of the trachea and bronchi, which contribute to the closure of their lumen during inhalation.
Emphysematous - accompanied by collapse (collapse) of small bronchi due to reduction and loss of elasticity by the lungs.
Hemodynamic – occurs secondary to the background of hemodynamic disorders of the pulmonary circulation: with hypertension of the pre- and postcapillaries, congestion in the bronchial veins and with a hypertensive crisis in the pulmonary circulation.
Hyperosmolar - observed when there is a decrease in hydration of the mucous membranes of the bronchi (inhalation of cold air), when a high osmotic concentration on the surface of the cells causes irritation of the receptors and bronchospasm.
Bronchial obstruction is based on reversible (functional) and irreversible (organic) changes. The functional mechanisms of bronchial obstruction include spasm of smooth muscles, hypersecretion of mucus and swelling of the bronchial mucosa. Spasm of smooth muscles and hypersecretion of mucus occur as a result of exposure to irritating factors (pollutants, infectious agents) on the mucous membrane of the respiratory tract. In response to this, inflammatory mediators are released, which irritate the endings of the vagus nerve and promote the release of acetylcholine, which realizes its effect through muscarinic cholinergic receptors. Activation of these receptors causes cholinergic bronchoconstriction and hypersecretion. In the wall of the bronchi there is a sharp congestion of the microvasculature and an increase in their permeability. Thus, swelling of the mucous membrane and submucosal layer develops, their infiltration with mast cells, basophils, eosinophils, lymphoid and plasma cells.
The cough can be dry and productive. The initial period of the inflammatory or edematous process is characterized by a dry cough. The appearance of a productive cough indicates a violation of mucociliary clearance and bronchial drainage.
Among the infectious agents that most often cause obstructive syndrome are respiratory syncytial virus (about 50%), parainfluenza virus, mycoplasma pneumoniae, and less commonly, influenza viruses and adenovirus.

Biofeedback treatment
The manifestation of biofeedback, regardless of etiology, requires the doctor to take urgent measures to eliminate bronchial obstruction by influencing its reversible component.
It should be noted that the reversibility of bronchial obstruction is determined by the degree of bronchial hyperreactivity (BHR). GRB is defined as the response of the bronchi to various chemical, physical or pharmacological stimuli, when bronchospasm develops in response to an influence that does not cause such a reaction in healthy individuals. The higher the GRB and the duration of exposure to the provocative agent, the more severe and life-threatening the biofeedback is.
In modern pulmonology, there are highly effective methods of delivering drugs directly to the bronchi. This technology is called inhalation nebulizer therapy (from the Latin nebulae - fog) therapy. Its characteristic feature is a high fraction (>80%) of particles ranging in size from 0.5 to 5 microns, which can easily reach the receptor zone in the small bronchi and quickly relieve bronchial obstruction.
The undeniable advantages of inhalation therapy in general are:

Effective creation of high concentrations of medications in the respiratory tract;
insignificant concentration of the drug in the blood;
rapid onset of action of drugs;
possibility of dose adjustment;
minimum systemic side effects.

The treatment tactics for biofeedback are quite clear and logical. To relieve bronchial obstruction, bronchodilators (bronchodilators) are used. Despite the differences in the mechanism of action of various bronchodilators, their most important property is the ability to eliminate spasm of the bronchial muscles and facilitate the passage of air into the lungs. All modern bronchodilators used for biofeedback therapy can be divided into several main groups:

Short- and long-acting B2 agonists;
short- and long-acting anticholinergics;
combination drugs;
methylxanthines.

Inhaled b2-agonists
Inhaled short-acting b2-agonists. This group includes two fairly selective b2-agonists - fenoterol and salbutamol. The main properties of this group of drugs are:

Relaxation of bronchial smooth muscles;
reduction of airway hyperresponsiveness;
improvement of mucociliary clearance of the bronchi;
decreased vascular permeability and plasma exudation;
reducing swelling of the bronchial mucosa;
stabilization of mast cell membranes, reducing the release of inflammatory mediators.

The advantages of these drugs are their rapid (within 3-5 minutes) and pronounced bronchodilator effect. The duration of action of the drugs is short, ranging from 3 to 6 hours, which is why they are classified as short-acting b2-agonists (SABA). Obviously, if it is necessary to effectively control the lumen of the bronchi within 24 hours, it is necessary to perform from 4 to 8 inhalations of SABA per day.
However, like any b2-agonists, drugs in this group have a large number of side effects, especially when used frequently (more than 4 times a day).
One of the serious side effects of b2-agonists is tremor due to the direct effect of the drug on b2-adrenergic receptors of skeletal muscles. Tremor is more often observed in elderly and senile patients. Tachycardia is often observed, either as a result of a direct effect on atrial beta-adrenergic receptors, or under the influence of a reflex response due to peripheral vasodilation through beta-receptors. Particular attention should be paid to prolongation of the QT interval, which can cause sudden death in patients with cardiovascular pathology. Less common and less severe complications include hypokalemia, hypoxemia, and irritability. In addition, short-acting b2-agonists are characterized by the phenomenon of tachyphylaxis - a rapid decrease in the therapeutic effect with repeated use of drugs.
Long-acting inhaled b2-agonists. Drugs in this group have a duration of action from 12 to 24 hours and are used as part of the basic therapy of diseases most often accompanied by biofeedback, such as bronchial asthma (BA). They are most effective when administered in combination with anti-inflammatory drugs – inhaled glucocorticosteroids (ICS). Today, the combination of LABA + ICS is recognized as an effective basic therapy for BA.
The most prominent representative of this group is formoterol fumarate (formoterol), which has the ability to relax bronchial smooth muscles, enhance mucociliary clearance, reduce vascular permeability and the release of mediators from mast cells and basophils, and provide long-term protection from factors leading to bronchospasm. However, there is insufficient evidence of the effect of formoterol on persistent inflammation in asthma; In addition, a number of studies have shown that with long-term use, the severity of the bronchodilator effect can vary greatly.
The undesirable effects of LABAs are not very different from those of CDBAs; they develop when the average daily recommended doses are exceeded and manifest themselves in the form of anxiety, skeletal muscle tremor, and stimulation of the cardiovascular system.

Inhaled M-anticholinergics
Inhaled short-acting M-anticholinergics. The main representative of this group, short-acting anticholinergic drugs (SDA), is ipratropium bromide (ipratropium), which has a pronounced bronchodilator effect.
The mechanism of bronchodilator action is due to the blockade of muscarinic cholinergic receptors, as a result of which the reflex narrowing of the bronchi caused by irritation of irritative cholinergic receptors is suppressed and the tone of the vagus nerve is reduced.
In almost all published guidelines on BA, anticholinergics are recognized as the “drugs of choice” for the treatment of this disease, as well as as additional bronchodilators for moderate and severe BOS in the elderly, senile and children.
The undeniable advantages of M-anticholinergics are:

Lack of cardiotoxic effect, which makes them “drugs of choice” for patients with cardiac and circulatory disorders, as well as in elderly patients;
absence of tachyphylaxis upon repeated use;
stable receptor activity (the number of M-cholinergic receptors does not decrease with age, unlike the number and activity of b2-adrenergic receptors);
rare side effects (dryness, bitter taste in the mouth).

The positive effects of anticholinergics are multifaceted and are not limited only to the bronchodilation effect. They are expressed in a decrease in the sensitivity of cough receptors, a change in the secretion of viscous sputum, and a decrease in oxygen consumption by the respiratory muscles. The positive features of ipratropium bromide include a long duration of action – up to 8 hours.
A conditional disadvantage of short-acting M-anticholinergics or short-acting anticholinergics (SAC) is the slow onset of action (30-60 minutes) after inhalation, which makes it difficult to quickly relieve symptoms of BOS.
Long-acting inhaled M-anticholinergics. The main representative of this group - long-acting anticholinergic drugs (LAADs) - is tiotropium bromide (tiotropium), which has a long-lasting and strong bronchodilator effect.
Tiotropium is advisable to use to eliminate BOS in “severe refractory asthma”, when high therapeutic doses of b2-agonists do not provide the desired bronchodilation and do not relieve BOS.

Combined bronchodilators
Short-acting inhaled combination bronchodilators. The main representative of this group - short-acting combined bronchodilators (SACDs) - is the combination of SABA (ipratropium 20 mcg) + SABA (fenoterol 50 mcg), which has become widespread in modern therapeutic practice under the commercial name "Berodual N" in the form of a metered-dose aerosol inhaler and "Berodual" in the form of a solution for inhalation (Boehringer Ingelheim, Germany).
The idea of ​​combining CDAC+CDBA is not new and has a long history. Suffice it to say about the high expectations from salbutamol + ipratropium, which have not yet found their widespread use. That is why we consider it necessary to note a number of features of combining fenoterol and ipratropium.
First, the M-anticholinergic ipratropium acts predominantly in the proximal bronchi, whereas the selective β2-agonist fenoterol acts predominantly in the distal bronchial tree. This leads to a “double effect” of bronchodilation, the possibility of reducing the dose of each drug to the minimum therapeutic level, and eliminates the possibility of third-party adverse events. Secondly, both substances have the same state of aggregation (aqueous solutions), which makes it possible to create a high respirable fraction during nebulizer therapy, and therefore effectively stop BOS.
It is justified to prescribe the drug Berodual for the relief of biofeedback in asthma in the following cases:

The presence of an altered b2 receptor in patients (genetic abnormality of the b2 receptor, consisting in the replacement of Gly at position 16 by Arg with the formation of the b2-APB16 Arg/Arg receptor genotype, which is not sensitive to any b2 agonists);
with a decrease in receptor b2 activity;
in the presence of pronounced manifestations of cardiovascular diseases;
with the phenomena of “night asthma” (a variant of asthma in which attacks of suffocation occur in the second half of the night against the background of bronchial obstruction caused by vagal activity);
with viral infections that can reduce the expression of the M2 gene and increase bronchial obstruction.

Of interest are randomized clinical trials examining the effectiveness of combination therapy compared with monotherapy with one of the components. Thus, in a randomized controlled crossover study, N. Gross et al. , which included 863 patients, combination therapy led to an increase in FEV1 by 24% compared with salbutamol monotherapy (p). Another study (a meta-analysis of two large 3-month studies in 1067 patients (E.J. Weber et al., 1999) demonstrated the advantage of combination therapy Biofeedback in patients with chronic obstructive pulmonary disease (COPD).It was found that with salbutamol monotherapy, the frequency of exacerbations of COPD (18%) and the number of days of exacerbations (770 person-days) were significantly higher than with combination therapy (12% and 554 person-days). ) (pThus, Berodual N was considered as a drug with a high cost/effectiveness ratio. Today, a fixed combination of a short-acting b2-agonist and ipratropium bromide (Berodual N) is included in international clinical guidelines for the treatment of patients with bronchial asthma COPD.
The undeniable proven advantages of Berodual N and Berodual solution for inhalation are:

Quick (5-10 minutes) and fairly long-lasting (6-8 hours) effect;
safe clinical profile (no cardiotoxic effects);
absence of tachyphylaxis;
no effect on mortality in elderly patients (unlike b2-agonists);
moderate anti-inflammatory effect (reducing the release of inflammatory mediators);
a more pronounced bronchodilatory response in combination than with each drug individually;
effective relief of acute BOS (with BA) and chronic BOS (with chronic obstructive pulmonary disease - COPD).

Methylxanthines
The main representative of this group is a bronchodilator, a purine derivative, called Theophylline (from Latin: theo-tea, phyllin-leaf). Theophylline has a weak bronchodilator effect, but has a positive effect on the respiratory muscles, improves sputum separation, and stimulates the respiratory center. This combination of positive properties, along with the availability of theophylline, once led to its widespread use.
The use of methylxanthines is accompanied by numerous side effects: nausea, vomiting, headache, agitation, gastroesophageal reflux, frequent urination, arrhythmia, tachycardia, etc. The drugs are used orally or parenterally.
Long-acting theophylline preparations have faded into the background. They are recommended in special cases to be used as an additional bronchodilator for biofeedback in patients with asthma and COPD with insufficient bronchodilation response from modern inhaled bronchodilator therapy.

Conclusion
Biofeedback accompanies many diseases, especially diseases of the respiratory system, such as bronchial asthma, COPD, ARVI, pneumonia, etc. All of them require appropriate medication correction.
The standard of treatment for BOS can be confidently considered to be inhaled drugs and the nebulizer method of their delivery, which allows creating the maximum concentration of the drug in the receptor zone and causing the maximum bronchodilator response in the absence of systemic action of the drug.
Various parts of the nervous system take part in the occurrence of BOS: sympathetic (b-receptors) and parasympathetic (M1-2 and M3 receptors). Quite often, it is clinically difficult to determine what predominates in the mechanism of bronchial obstruction: insufficient adrenergic stimulation or excessive vagal innervation. In this case, it is optimal to prescribe a combination of a short-acting b2-agonist and the M-anticholinergic ipratropium bromide (Berodual N).
We can confidently say that Berodual N in the form of a metered dose aerosol inhaler and Berodual solution for inhalation via a nebulizer are indicated for the prevention and symptomatic treatment of obstructive respiratory diseases with reversible bronchospasm, such as acute and chronic obstructive bronchitis, bronchial asthma, chronic obstructive pulmonary disease.

Literature
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4. Geppe N. A. Modern ideas about the tactics of treating bronchial asthma in children. RMJ. 2002; 10:7:12-40.
5. Gavalov S.M. Bronchial hyperreactivity syndrome and its clinical varieties. Consilium. 1999; 1:3-11.
6. Bradley B.L., Azzawi M., Jacobson M., et al. Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness. J. Allergy Clin. Immunol. 1991; 88.
7. Savelyev B.P., Reutova V.S., Shiryaeva I.S. Bronchial hyperreactivity according to the histamine inhalation test in children and adolescents. Medical scientific and educational journal. 2001; 5: 121-146.
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… from 30 to 50% of children in the first three years of life have certain manifestations of broncho-obstructive syndrome.

Broncho-obstructive syndrome is a pathophysiological concept that characterizes a violation of bronchial obstruction in a very wide range of acute and chronic diseases. Broncho-obstructive syndrome is not synonymous with bronchospasm, although in many cases bronchospasm plays an important and sometimes leading role in the genesis of the disease.

Typically, broncho-obstructive syndrome is detected in children in the first four years of life, but can also be diagnosed at an older age.

The genesis of bronchial obstruction involves various pathogenetic mechanisms, which can be divided into:
reversible (functional): bronchospasm, inflammatory infiltration, edema, mucociliary insufficiency, hypersecretion of viscous mucus;
irreversible: congenital bronchial stenoses, their obliteration, etc.

In the development of bronchial obstruction, age-related characteristics characteristic of children in the first three years of life play a certain role:
narrowness of the bronchi and the entire respiratory apparatus, which significantly increases aerodynamic resistance (according to Poiselle’s rule, the resistance of the airways is inversely proportional to their radius to the 4th power);
pliability of bronchial tract cartilage;
insufficient rigidity of the bone structure of the chest, which freely reacts by retracting compliant places to increase resistance in the airways;
features of the position and structure of the diaphragm;
features of the bronchial wall: a large number of goblet cells that secrete mucus;
the mucous membrane of the trachea and bronchi quickly reacts with swelling and hypersecretion of mucus in response to the development of a viral infection;
increased viscosity of bronchial secretions associated with high levels of sialic acid;
imperfection of immunological mechanisms: the formation of interferon in the upper respiratory tract, serum immunoglobulin A, secretory immunoglobulin A is significantly reduced, the functional activity of the T-system of immunity is also reduced;
Functional disorders of the respiratory system in a small child are also influenced by factors such as longer sleep, frequent crying, and a predominant position lying on the back in the first months of life.

Broncho-obstructive syndrome most often has an infectious-allergic nature. The viruses that most often cause broncho-obstructive syndrome include respiratory syncytial virus, parainfluenza, and less commonly, influenza viruses and adenovirus; a large role is given to intracellular pathogens (chlamydial and mycoplasma infections). A connection between broncho-obstructive syndrome and certain types of pathogenic microflora isolated from sputum or bronchial secretions, for example with Moraxella catarrhalis and Candida fungi, has been reported.

Of particular importance among environmental factors that can lead to the development of obstructive syndrome (especially in children in the first three years of life) is given to:
passive smoking in the family (tobacco smoke provokes hypertrophy of the bronchial mucous glands, impaired mucociliary clearance, slower movement of mucus, destruction of the bronchial epithelium);
pollution of the surrounding atmosphere with industrial gases, organic and inorganic dust.

The following groups of diseases accompanied by broncho-obstructive syndrome are distinguished::
respiratory diseases: bronchitis, bronchiolitis, pneumonia, obstructive bronchitis, bronchial asthma, bronchopulmonary dysplasia, malformations of the bronchopulmonary system, tumors of the trachea and bronchi;
foreign bodies of the trachea, bronchi, esophagus;
diseases of aspiration origin (or aspiration obstructive bronchitis): gastroesophageal reflux, tracheoesophageal fistula, malformations of the gastrointestinal tract, diaphragmatic hernia;
diseases of the cardiovascular system of a congenital and acquired nature: congenital heart disease with hypertension of the pulmonary circulation, vascular anomalies, congenital non-rheumatic carditis, etc.);
diseases of the central and peripheral nervous system: birth trauma, myopathies, etc.;
hereditary metabolic abnormalities: cystic fibrosis, 1-antitrypsin deficiency, mucopolysaccharidosis;
congenital and acquired immunodeficiency conditions;
rare hereditary diseases;
other conditions: injuries and burns, poisoning, exposure to various physical and chemical environmental factors; compression of the trachea and bronchi of extrapulmonary origin (tumors, lymphogranulomatosis).

Clinical picture broncho-obstructive syndrome (BOS) in children is determined primarily by the factors that caused bronchoconstriction. Since in most cases, as noted above, BOS is associated with manifestations of an acute respiratory viral infection, therefore, let us consider the clinical picture of BOS associated with an acute respiratory viral infection (acute obstructive bronchitis).

At the onset of the disease, there is a rise in body temperature, catarrhal changes in the upper respiratory tract, and a disturbance in the general condition of the child; their severity and character vary largely depending on what pathogen led to the disease.

Signs of expiratory difficulty breathing can appear both on the first day of the disease and during the course of the viral infection (on the 3-5th day of the disease). The respiratory rate and duration of exhalation gradually increase. Breathing becomes noisy and whistling, which is due to the fact that as hypersecretion develops, secretion accumulates in the lumen of the bronchi due to shortness of breath and fever, the viscosity properties of the secretion change - it “dries out”, which leads to the appearance of buzzing (low) and whistling sounds. (high-pitched) dry wheezing.

Damage to the bronchi is widespread, and therefore hard breathing with dry whistling and buzzing wheezing is heard equally over the entire surface of the chest. Wheezing may be heard from a distance. The younger the child, the more often, in addition to dry, moist medium-bubbly rales can be heard. If the spastic component plays a leading role in the genesis of bronchial obstruction, then auscultatory data over the lungs are usually more varied and labile during the day.

As the severity of shortness of breath increases, the participation of auxiliary muscles becomes greater - retraction of the intercostal spaces, epigastrium and supraclavicular fossa, swelling (tension) of the wings of the nose. Perioral cyanosis and pallor of the skin are often detected, the child becomes restless and tries to take a sitting position with support on his hands.

Respiratory failure is more pronounced the younger the child, but usually with biofeedback it does not exceed degree II. On physical examination, in addition to scattered dry wheezing and hard breathing, signs of lung swelling are detected: narrowing of the boundaries of relative cardiac dullness, a boxy tint to percussion tone.

Bloating of the lungs is a consequence of the collapse of small bronchial branches during exhalation, which leads to the so-called ventilation emphysema. Lung volume increases. The chest is, as it were, constantly in a state of inhalation, that is, it is enlarged in anteroposterior size.

Changes in peripheral blood correspond to the nature of the viral infection. Bacterial flora is rarely layered - no more than 5%. X-ray examination, in addition to bilateral enhancement of the pulmonary pattern and expansion of the roots of the lungs, reveals: low standing of the flattened domes of the diaphragm, increased transparency of the pulmonary fields, elongation of the pulmonary fields, horizontal arrangement of the ribs on the radiograph, that is, signs of swelling of the lungs.

Treatment broncho-obstructive syndrome is based on the etiological principle (etiotropic therapy) and is complex in nature. For example, for chronic lung diseases, treatment includes the use of antibacterial drugs (according to indications), mucolytics, bronchodilators and various methods that improve sputum evacuation (therapeutic bronchoscopy, positional drainage, vibration chest massage), etc.

1. Respiratory diseases:

Infectious and inflammatory diseases (bronchitis, bronchiolitis, pneumonia).

Allergic diseases (asthmatic bronchitis, bronchial asthma).

Bronchopulmonary dysplasia.

Malformations of the bronchopulmonary system.

Tumors of the trachea and bronchi.

2. Foreign bodies of the trachea, bronchi, esophagus.

3. Diseases of aspiration origin (or aspiration obstructive bronchitis) - gastroesophageal reflux, tracheoesophageal fistula, malformations of the gastrointestinal tract, diaphragmatic hernia.

4. Diseases of the cardiovascular system of congenital and acquired nature (CHD with hypertension of the pulmonary circulation, vascular anomalies, etc.)

5. Diseases of the central and peripheral nervous system.

6. Hereditary metabolic abnormalities.

7. Congenital and acquired immunodeficiency conditions.

8. Rare diseases: Lawrence-Moon-Bardet-Biedl syndrome, Kartagener syndrome, etc.

9. Other conditions: injuries and burns. Poisoning.

Impact of various physical and chemical environmental factors.

Compression of the trachea and bronchi of extrapulmonary origin.

3. From a practical point of view, depending on the etiological pathogenetic mechanisms, there are 4 variants of broncho-obstructive syndrome:

Infectious, developing as a result of viral and (or) bacterial inflammation in the bronchi and bronchioles;

Allergic, developing as a result of spasm and allergic inflammation of bronchial structures with a predominance of spastic phenomena over inflammatory ones;

Obstructive, observed during aspiration of a foreign body, with compression of the bronchi;

Hemodynamic, occurring in heart failure of the left ventricular type.

4. Manifestations of broncho-obstructive syndrome are of the same type, despite the variety of etiological factors and pathogenetic mechanisms of obstruction. Cardinal symptoms:

More often - expiratory shortness of breath due to increased resistance to air flow due to pathology of small and medium bronchi or the reflux of a small amount of stomach contents into the lumen of the bronchi (against the background of gastroesophageal reflux disease). Inspiratory dyspnea occurs less frequently with pathology of the large bronchi, trachea or heart;

Choking as an extreme degree of acute respiratory failure (refers to life-threatening conditions);

Paroxysmal cough with sputum (or without it);

Noisy breathing (whisking);

Distant wheezing.

More rare manifestations of broncho-obstructive syndrome are symptoms of hypercapnia (increase in pCO2): headache, sleep disturbance, increased sweating, tremor: in severe cases - confusion, convulsions and even hypercapnic coma.

5. Obstructive syndrome is observed with such forms of respiratory allergosis as bronchial asthma atopic in nature. Obstruction in this disease is manifested mainly by spasm of small bronchi and bronchioles (tonic type) and to a lesser extent by hypersecretion and edema. Heredity burdened with allergic diseases, a burdened personal allergic history (skin manifestations of allergies, “minor” forms of respiratory allergosis - allergic rhinitis, laryngitis, tracheitis, bronchitis, intestinal allergosis), the presence of a connection between the occurrence of the disease and a causally significant allergen and the absence of such a connection with infection, positive effect of elimination, recurrence of attacks, their uniformity.

The clinical picture is characterized by the following signs: absence of intoxication, distant wheezing, expiratory shortness of breath with the participation of auxiliary muscles; mainly wheezing and a few wet wheezes are heard in the lungs, the number of which increases after relief of bronchospasm. An attack occurs, as a rule, on the first day of exacerbation of the disease and is eliminated in a short time with adequate therapy (salbutamol, Berotek, etc.). The cardinal signs of bronchial asthma are an attack of suffocation, eosinophilia of blood and sputum, the presence of allergic or polypous rhinosinusitis, a positive test for detection of hidden bronchospasm. The same criteria, as well as the results of an allergological examination, are used for the differential diagnosis of bronchial asthma with asthma-like bronchospasm in carcinoid syndrome, irritation of the trachea or bronchi by a foreign body, compression by a tumor, enlarged lymph nodes, or aortic aneurysm.

6. COPD- diffuse progressive inflammation of the bronchi, not associated with local or generalized damage to the lungs and manifested by cough. It is customary to speak of the chronic nature of the process if a productive cough, not associated with any other disease, continues for at least 3 months a year for 2 years in a row.

The main cause of COPD is prolonged smoking, repeated inhalation of dust (in working conditions, for example in textile, wool, tobacco factories), irritating gases, disintegration aerosols, disaggregation. The etiological significance of unfavorable climatic conditions and microclimate (large fluctuations in temperature and humidity, air pollution) is undeniable.

What distinguishes COPD from bronchial asthma is, first of all, the absence of asthma attacks - COPD is characterized by constant coughing and shortness of breath. In the bronchial variant of COPD, the difference between morning and evening peak flow measurements is reduced (variability less than 15%), the irreversible component of bronchial obstruction predominates, in bronchial asthma it is increased (variability more than 20% indicates increased bronchial reactivity), in addition, COPD is not characterized by concomitant allergic diseases, eosinophilia of blood and sputum.

State educational institution

higher professional education

Altai State Medical University

Ministry of Health and Social Development of the Russian Federation

Department of Pediatrics FPC and teaching staff

BRONCHO-OBSTRUCTIVE SYNDROME IN CHILDREN

A textbook for intern doctors,

clinical residents, pediatricians

Barnaul - 2010

Published by decision of the Central

Altai Coordination and Methodological Council

State Medical University

Seroklinov Valery Nikolaevich - Ph.D. honey. Sciences, Associate Professor,

Fedorov Anatoly Vasilievich - Dr. med. sciences, professor,

Ponomareva Irina Aleksandrovna - chief pediatric pulmonologist in Barnaul

Reviewer: Klimenov Leonid Nikanorovich, Dr. med. Sciences, Professor, Department of Pediatrics No. 2, State Educational Institution of Higher Professional Education, ASMU, Ministry of Health and Social Development of the Russian Federation

Definition, epidemiology

Definition. Broncho-obstructive syndrome (BOS) or bronchial obstruction syndrome is a complex of clinical manifestations resulting from a generalized narrowing of the lumen of the bronchi of various etiologies. The narrowing of the lumen of the small bronchi requires greater positive intrathoracic pressure to produce exhalation, which contributes to greater compression of the large bronchi; this causes them to vibrate and produce whistling sounds (1). Clinical manifestations of biofeedback consist of prolongation of exhalation, the appearance of expiratory noise (wheezing), attacks of suffocation, participation of auxiliary muscles in the act of breathing, and unproductive cough. With severe obstruction, an increase in respiratory rate, fatigue of the respiratory muscles, and a decrease in the partial tension of blood oxygen may occur (2).

Epidemiology. BOS is quite common in children, especially in children in the first 3 years of life. But biofeedback is not always recorded in the final diagnosis and in this case is not subject to statistical recording.

The frequency of biofeedback developed against the background of infectious diseases of the lower respiratory tract in young children, according to various authors, ranges from 5% to 40% (1, 2, 3, 4). At the same time, in children with a family history of allergic diseases, BOS develops more often (in 30-40% of cases). This is also typical for children who often (more than 6 times a year) suffer from respiratory infections. Among young children (from 3 months to 3 years) with acute infectious disease of the lower respiratory tract, BOS occurred in 34% of patients, and with bronchitis it was 3 times more common than with pneumonia. Slightly less than half of the hospitalized children had repeated episodes of biofeedback, most of them over the age of 1 year (2).

Risk factors

Risk factors. The development of biofeedback in young children is predisposed by age-related characteristics of the respiratory system: hyperplasia of glandular tissue, secretion of predominantly viscous sputum, relative narrowness of the respiratory tract, insufficiency of local immunity, structural features of the diaphragm.

The development of BOS is influenced by premorbid background factors: a burdened allergic history, hereditary predisposition to atopy, perinatal pathology of the central nervous system, rickets, malnutrition, thymic hyperplasia, early artificial feeding.

Among the environmental factors that can lead to the development of biofeedback, great importance is attached to unfavorable environmental conditions and passive smoking.

The development of bronchial asthma (BOS, caused by chronic allergic inflammation of the airways) is associated with the complex influence of internal and external factors. Internal (congenital) factors are a genetic predisposition to the development of bronchial asthma, atopy and airway hyperresponsiveness. Today, these factors are considered uncontrollable. External factors are numerous and, in many respects, controllable, directly trigger the manifestation of bronchial asthma or cause its exacerbation. The main ones include exposure to allergens, viral and bacterial infections, early transfer to artificial feeding, and passive smoking (5).

Etiology.

The reasons for the development of biofeedback in children are numerous. In children of the first year of life, the cause of biofeedback may be aspiration caused by impaired swallowing, congenital anomalies of the nasopharynx, tracheobronchial fistula, or gastroesophageal reflux. Malformations of the trachea and bronchi, respiratory distress syndrome, cystic fibrosis, bronchopulmonary dysplasia, immunodeficiency states, intrauterine infections, and passive smoking are also causes of biofeedback in children of the first year of life.

In the second and third years of life, clinical manifestations of BOS may first appear in children with bronchial asthma, with aspiration of a foreign body, migration of round helminths, bronchiolitis obliterans, in patients with congenital and hereditary diseases of the respiratory system, in children with heart defects occurring with pulmonary hypertension (2).

In children over 3 years of age, the main causes of BOS are bronchial asthma, congenital and hereditary respiratory diseases (cystic fibrosis, ciliary dyskinesia syndrome, bronchial malformations).

Pathogenesis.

BOS is based on various pathogenetic mechanisms, which can be divided into reversible (inflammation, edema, bronchospasm, mucociliary insufficiency, hypersecretion of viscous mucus) and irreversible (congenital bronchial stenosis, bronchial obliteration).

Inflammation can be caused by infectious, allergic, toxic, physical, neurogenic factors. The mediator that initiates the acute phase of inflammation is interleukin 1. It is synthesized by phagocytes and tissue macrophages when exposed to infectious or non-infectious factors and activates a cascade of immune reactions that promote the release of type 1 mediators (histamine, serotonin, etc.) into the peripheral bloodstream. Histamine is released from granules of mast cells and basophils, usually during an allergic reaction when an allergen interacts with allergen-specific IgE antibodies. However, degranulation of mast cells and basophils can also be caused by non-immune mechanisms. In addition to histamine, type 2 mediators (eicosanoids), generated during the early inflammatory reaction, play an important role in the pathogenesis of inflammation. The source of eicosanoids is arachidonic acid, which is formed from phospholipids of cell membranes. Under the action of cyclooxygenase, prostaglandins, thromboxane and prostocycline are synthesized from arachidonic acid, and leukotrienes are synthesized under the action of lipoxygenase. It is with histamine, leukotrienes and pro-inflammatory prostaglandins that increased vascular permeability, the appearance of edema of the bronchial mucosa, hypersecretion of viscous mucus, the development of bronchospasm and the formation of a biofeedback syndrome are associated. In addition, these events initiate the development of a late inflammatory reaction, which contributes to the development of hyperreactivity and alteration (damage) of the epithelium of the mucous membrane of the respiratory tract. Damaged tissues have increased sensitivity of bronchial receptors to external influences, including viral infection and pollutants, which significantly increases the likelihood of developing bronchospasm (5).

Disturbance of bronchial secretion accompanied by an increase in the amount of secretion and an increase in its viscosity. The mediator of the parasympathetic nervous system, acetylcholine, stimulates the functioning of the mucous and serous glands. Stagnation of bronchial contents and inevitable infection leads to the development of endobronchial inflammation. In addition, the thick and viscous secretion produced, in addition to inhibiting ciliary activity, can cause bronchial obstruction due to the accumulation of mucus in the respiratory tract. In severe cases, ventilation disorders are accompanied by the development of atelectasis.

Edema and hyperplasia of the mucous membrane lead to disruption of bronchial obstruction due to thickening of all layers of the bronchial wall. With recurrent bronchopulmonary diseases, the structure of the epithelium is disrupted, its hyperplasia and squamous metaplasia are noted.

Bronchospasm.Cholinergic nerves end on bronchial smooth muscle cells, which have not only cholinergic receptors, but also H1-histamine receptors, b 2 -adrenergic receptors and neuropeptide receptors.

Activation of cholinergic nerve fibers leads to an increase in the production of acetylcholine and an increase in the concentration of guanylate cyclase, which promotes the entry of calcium ions into the smooth muscle cell, thereby stimulating bronchoconstriction. M-cholinergic receptors in infants are quite well developed, which implies the production of very viscous bronchial secretions and explains the pronounced bronchodilator effect of M-cholinergic drugs in children of the first years of life.

Stimulation of b 2 -adrenergic receptors by catecholamines reduces the manifestations of bronchospasm. Hereditary blockade of adenylate cyclase reduces the sensitivity of b 2 -adrenergic receptors to adrenergic agonists, which is quite common in patients with bronchial asthma. Some researchers point to the functional immaturity of b 2 -adrenergic receptors in children in the first months of life.

Neuropeptide system carries out the integration of the nervous, endocrine and immune systems. The relationship between inflammation and the neuropeptide system suggests the development of bronchial obstruction, especially in children in the first years of life. In addition to the classical cholinergic and adrenergic innervation, there is non-cholinergic and non-adrenergic innervation. The main mediators of this system are neuropeptides. Neurosecretory cells have the properties of exocrine secretion and can cause a distant humoral-endocrine effect. The hypothalamus is the leading link in the neuropeptide system. The most studied neuropeptides are substance P, neurokines A and B, calcitonin gene-related peptide, and vasoactive intestinal peptide. Neuropeptides can interact with immunocompetent cells, activate degranulation, increase bronchial hyperreactivity, and directly affect smooth muscles and blood vessels. Infectious pathogens and allergens stimulate the release of substance P, which increases bronchospasm. At the same time, vasoactive intestinal peptide has a pronounced bronchodilator effect (2).

Genetically determined connective tissue deficiency may be accompanied by tracheobronchial dyskinesia - narrowing of the lumen of the trachea and large bronchi during exhalation due to prolapse of their walls. The mechanism of its development is due to the fact that in the bronchi of large and medium caliber there is a powerful connective tissue frame, the elasticity of which is reduced due to the primary “weakness” of the connective tissue. The tendency to form obstructive disorders and the presence of bronchial hyperreactivity in connective tissue dysplasia has been noted by many authors (6,7,8,9). In this case, flattening of the diaphragm and swelling of the lungs are detected. These manifestations of respiratory muscle fatigue are caused by a narrowing of the lumen of the bronchi during exhalation, deformation of the chest and spine due to connective tissue dysplasia (6). Another aggravating factor is the presence of immunological deficiency in connective tissue dysplasia, which at the clinical level is expressed by chronic inflammation of dysplastic bronchi. The combination of chronic inflammation and dysplasia of the tracheobronchial tree results in obstructive changes in the bronchi, partial obliteration of small bronchial branches, the formation of areas of pneumosclerosis with deformation of the bronchi, and the occurrence of expiratory prolapse of the tracheobronchial wall (6,10,11).

The syndrome of undifferentiated connective tissue dysplasia in bronchial asthma is observed in 59-67% of cases (11, 12), which significantly exceeds the frequency of this syndrome (9.8-34.3%) in different populations, and also confirms the certain role of genetically determined connective tissue deficiency tissue in the development of bronchial obstruction (12,13).

Previously, many researchers identified three pathogenetic mechanisms of BOS. First - active mechanism - realized through hyperreactivity of the bronchial tree and spasm of bronchial smooth muscles. Second - passive mechanism. This mechanism consists of the following processes: allergic inflammation or increased permeability of bronchial capillaries, swelling of the mucous and submucosal layers, thickening of the basement membrane, hypersecretion and hypertrophy of the bronchial glands with the release of mucus of increased viscosity, obliteration of the airways. The third mechanism is related to decreased static elasticity of the lungs. This mechanism increases resistance to upward air flow.

The degree of severity of biofeedback is directly dependent on all three mechanisms, and the more components are included in the process, the more severe the child’s condition. The severity of each of the three mechanisms of bronchial obstruction is determined by the leading etiological factor of biofeedback and the age of the child.

Thus, there are several main mechanisms for the development of bronchial obstruction. The proportion of each of them depends on the cause of the pathological process and the age of the child. The anatomical, physiological and immunological characteristics of young children determine the high incidence of BOS in this group of patients. An important feature of the formation of reversible bronchial obstruction in children of the first 3 years of life is the predominance of inflammatory edema and hypersecretion of viscous mucus over the bronchospastic component of obstruction, which must be taken into account in treatment.

Classification.

About 100 diseases are known that are accompanied by biofeedback (1, 5, 14, 15, 16, 17, 18, 19, 20, 21, radiating bronchial obstruction in a frequently painful syndrome such as “). The following groups of diseases accompanied by biofeedback are distinguished.

Groups of diseases accompanied by bronchial obstruction syndrome:

1. Respiratory diseases:

1.1. Infectious and inflammatory diseases (acute respiratory infections, bronchitis, bronchiolitis, pneumonia).

1.2. Allergic diseases (bronchial asthma).

1.3. Bronchopulmonary dysplasia.

1.4. Malformations of the bronchopulmonary system.

1.5. Obliterating bronchiolitis.

1.6. Tuberculosis.

1.7. Tumors of the trachea and bronchi.

2. Foreign bodies of the trachea, bronchi, esophagus.

3. Diseases of the gastrointestinal tract (aspiration obstructive bronchitis) - gastroesophageal reflux, tracheoesophageal fistula, malformations of the gastrointestinal tract, diaphragmatic hernia.

4. Diseases of the cardiovascular system of a congenital and acquired nature - congenital heart defects with hypertension of the pulmonary circulation, anomalies of large vessels, congenital non-rheumatic carditis.

5. Diseases of the central and peripheral nervous system:

5.1. Traumatic spinal injury.

5.2. Cerebral palsy.

5.3. Myopathies.

5.4. Neuroinfections (poliomyelitis, etc.).

5.5. Hysteria, epilepsy.

6. Hereditary diseases:

6.1. Cystic fibrosis.

6.2. Malabsorption syndrome.

6.3. Rickets-like diseases.

6.4. Mucopolysaccharidoses.

6.5. Alpha-1 antitrypsin deficiency.

6.6. Kartagener's syndrome.

7. Congenital and acquired immunodeficiency conditions.

8. Other conditions:

8.1. Injuries and burns.

8.2. Poisoning.

8.3. Impact of various physical and chemical environmental factors.

8.4. Compression of the trachea and bronchi of extrapulmonary origin (thymomegaly, etc.).

From a practical point of view, depending on the etiopathogenesis of bronchial obstruction, 4 variants of biofeedback can be distinguished: 1) infectious, 2) allergic, 3) obstructive, 4) hemodynamic.

The course of BOS can be acute (clinical manifestations of BOS persist for no more than 10 days), protracted, recurrent and continuously relapsing (in the case of bronchopulmonary dysplasia, bronchiolitis obliterans, etc.).

According to the severity of obstruction, one can distinguish: mild, moderate, severe and hidden bronchial obstruction. Criteria for the severity of biofeedback are: the presence of wheezing, shortness of breath, cyanosis, participation of auxiliary muscles in the act of breathing, indicators of external respiratory function (ERF) and blood gases. Cough is observed with any degree of severity of biofeedback.

A mild course of biofeedback is characterized by the presence of wheezing on auscultation, the absence of shortness of breath and cyanosis at rest. Blood gas indicators are within normal limits, respiratory function indicators (forced expiratory volume in 1 second and maximum expiratory flow rate) are more than 80% of normal. The child’s well-being, as a rule, does not suffer.

The course of biofeedback of moderate severity is accompanied by the presence at rest of expiratory or mixed shortness of breath, cyanosis of the nasolabial triangle, and retraction of the compliant areas of the chest. Wheezing can be heard from a distance. Indicators of respiratory function are 60-80% of the norm, PaO 2 is more than 60 mm Hg. Art., PaCO 2 less than 45 mm Hg. Art.

In severe cases of an attack of bronchial obstruction, the child’s well-being suffers; noisy, difficult breathing with the participation of auxiliary muscles, and the presence of cyanosis are characteristic. Indicators of respiratory function are below 60% of the norm, PaO 2 is less than 60 mm Hg. Art., PaCO 2 more than 45 mm Hg. Art.

In case of latent bronchial obstruction, clinical and physical signs of BOS are not determined, but a study of FEV reveals a positive test with a bronchodilator (an increase in FEV 1 by more than 12% after inhalation with a bronchodilator and/or an increase in the amount of increase in maximum volumetric expiratory flow rates (MOF 25-75) by 37% or more).

Clinic.

Clinical manifestations of biofeedback consist of prolongation of exhalation, the appearance of a whistling timbre, and the participation of auxiliary muscles in the act of breathing. Usually accompanied by an unproductive cough. With severe obstruction, noisy inspiration may appear, an increase in the frequency of respiratory movements, and the development of fatigue of the respiratory muscles. Air retention in the lungs is accompanied by hypoxemia. During physical examination, prolonged exhalation and dry wheezing are detected by auscultation. In young children, moist rales of various sizes are often heard, and with bronchiolitis, a lot of fine bubbling and crepitating rales are heard throughout all fields of the lungs during inhalation and exhalation. During percussion, a boxy sound appears above the lungs.

O.V. Zaitseva identifies several clinical variants of biofeedback in children of the first three years of life (22).

The first clinical variant of the clinical course of biofeedback is characterized by the development of signs of broncho-obstruction against the background of an acute respiratory infection with an acute onset of the disease, an increase in body temperature to febrile levels, mucous rhinitis, and the presence of intoxication phenomena: the child becomes lethargic, capricious, sleeps poorly, refuses breastfeeding, and declines. appetite. The cough is unproductive, “dry”, usually short-lived with a quick transition to wet. On days 2-4, already against the background of pronounced catarrhal phenomena and an increase in body temperature, broncho-obstructive syndrome develops: shortness of breath of an expiratory nature without pronounced tachypnea (40-60 breaths per minute), sometimes distant wheezing in the form of noisy, wheezing breathing, a percussion-box-like tone of sound, on auscultation - prolonged exhalation, dry, buzzing wheezing, moist wheezing of various sizes on both sides. Broncho-obstructive syndrome lasts for 3-7-9 or more days, depending on the nature of the infection and disappears gradually, parallel to the subsidence of inflammatory changes in the bronchi. The course of biofeedback according to this clinical variant has been established in children with acute obstructive bronchitis that developed against the background of acute respiratory viral infection, and in children with bronchial asthma in the presence of acute respiratory viral infection.

The main clinical symptoms in the second variant of the clinical course of BOS were moderate catarrhal manifestations and signs of severe respiratory failure: perioral cyanosis, acrocyanosis, tachypnea up to 60-90 breaths per minute, with a predominance of the expiratory component, retraction of the compliant areas of the chest. Percussion above the lungs determines a boxy tint of the percussion sound; During auscultation, many moist, fine-bubbly and crepitating rales are heard throughout all fields of the lungs during inhalation and exhalation, exhalation is prolonged and difficult. This clinical picture develops gradually, over several days, less often - acutely, against the background of a respiratory infection and is accompanied by a sharp deterioration in condition. In this case, a paroxysmal cough occurs, appetite decreases, and anxiety appears. The temperature is often subfebrile. Bronchoobstruction persists for a long time, at least two to three weeks. The second option is typical for children of the first year of life with acute bronchiolitis.

The third variant of the clinical course of BOS is characterized by the following signs: absence of intoxication, distant wheezing, expiratory shortness of breath in some children with the participation of auxiliary muscles. Dry whistling sounds and a few wet sounds are heard in the lungs, the number of which increases after relief of bronchospasm. Some children experience pronounced anxiety, bloating of the chest, tachypnea with a slight predominance of the expiratory component, impaired breathing in the basal parts of the lungs, and severe perioral cyanosis. An attack occurs, as a rule, “for no reason” or against the background of minimal catarrhal manifestations; in some children, the development of BOS coincides with spring pollination and is accompanied by symptoms of allergic conjunctivitis and, less often, allergic rhinitis. The vast majority of children in this group are diagnosed with bronchial asthma.

In children with the fourth variant of BOS, moderate signs of bronchial obstruction appear against the background of non-infectious factors: during an allergic reaction of post-vaccination origin, after a bee sting, to the smell of paint. Clinical signs of bronchial obstruction in these children are limited to the appearance of multiple scattered dry wheezing. The child’s condition depends on the severity of the underlying disease (generalized allergic reaction, Quincke’s edema, etc.). Signs of biofeedback disappear within 4-7 days.

It must be remembered that BOS is not an independent diagnosis, but a symptom complex of a disease, the nosological form of which should be established in all cases of the development of bronchial obstruction (23).

Diagnostics

The diagnosis of bronchial obstruction is made on the basis of clinical and anamnestic data and the results of a physical and functional examination. The study of respiratory function using the methods of spirography (flow-volume curve) and pneumotachometry (peak flowmetry) is carried out in children over 5-6 years of age, since children under 5 years of age are unable to perform the forced expiration technique.

In order to diagnose a disease occurring with biofeedback, it is necessary to study in detail the clinical and anamnestic data, paying special attention to the presence of atopy in the family, previous diseases, and the presence of relapses of bronchial obstruction.

Newly diagnosed mild BOS, which developed against the background of a respiratory infection, does not require additional research methods. In case of recurrent BOS, the complex of examination methods should include:

1. Study of peripheral blood.

2. Serological tests (specific IgM and IgG are required, IgA testing is desirable) for the presence of chlamydial, mycoplasma, cytomegalovirus and herpetic infections; in the absence of IgM and the presence of diagnostic IgG titers, the study must be repeated after 2-3 weeks (paired sera).

3. Serological tests for the presence of helminthiasis (toxocariasis, ascariasis).

4. Allergy examination (level of total IgE, specific IgE, skin prick tests); other immunological examinations are carried out after consultation with an immunologist.

Bacteriological examination methods and PCR diagnostics are highly informative when collecting material during bronchoscopy and deep coughing up of sputum from the lower respiratory tract; smear examination characterizes mainly the flora of the upper respiratory tract.

Chest X-ray is not a mandatory method of examination in children with biofeedback. This study is carried out in the following situations:

Suspicion of a complicated course of biofeedback (atelectasis, etc.);

Rule out pneumonia;

Suspicion of a foreign body;

Recurrent course of biofeedback (if x-rays were not previously performed).

According to indications, bronchoscopy, scintigraphy, computed tomography of the lungs, sweat test, etc. are performed. The scope of the examination is determined individually for each patient.

Severe cases of bronchial obstruction and recurrent BOS require mandatory hospitalization to clarify the genesis and differential diagnosis of BOS.

Differential diagnosis.

BOS of infectious origin often occurs in young children with viral and viral-bacterial respiratory tract infections. BOS occurs in 5-40% of ARVI cases with an average frequency of 45-50 per 1000 young children (24).

In the genesis of bronchial obstruction in acute respiratory infections, swelling of the mucous membrane, inflammatory infiltration, and hypersecretion are of primary importance. A clear effect of a number of viruses on increasing the level of IgE and IgG and suppressing the T-suppressor function of lymphocytes was noted.

The occurrence of bronchial obstruction in children is facilitated by perinatal damage to the central nervous system, constitutional anomalies (allergic, lymphatic diathesis), as well as age-related morphofunctional features: narrowness of the airways, pliability of cartilage and rigidity of the chest, less elasticity of the lung tissue, its abundant vascularization, tendency to edema and exudation.

Research by domestic authors has established that 75% of young children with obstructive bronchitis had perinatal damage to the central nervous system of hypoxic-ischemic and/or traumatic origin. In 55.6% of these infants, autonomic-visceral disorders were detected (respiratory dysfunction in the form of apnea, dyspnea, false stridor, spasm and dystonia of peripheral vessels, prolonged low-grade fever, dyskinesia of the gastrointestinal tract). In children with obstructive bronchitis, the syndrome of vegetative-visceral dysfunctions rarely occurred in isolation, and was more often combined with other neurological syndromes: in 36% of children - with hypertensive-hydrocephalic syndrome, in 64% - with the syndrome of motor disorders. In these infants, the duration of the obstructive period (15-16 days) was 2 times longer compared to children with obstructive bronchitis and encephalopathy without severe autonomic disorders and 3 times longer than children with obstructive bronchitis without perinatal CNS damage. They also had a more severe course of obstructive bronchitis, 74.6% of patients had moderate BOS, and 13.4% were diagnosed with severe BOS with a predominance of hypersecretion (25,26).

In the etiology of acute obstructive bronchitis and bronchiolitis in children of the first 3 years of life, the leading role is played by RS viruses and parainfluenza viruses type 3, other viruses (adenoviruses, rhinoviruses, cytomegaloviruses, etc.) cause no more than 20% of cases of these diseases (27,28) . The most common causative agent of ARVI in children is the RS virus, and in 25-40% of sick young children complications occur in the form of bronchiolitis and pneumonia, often leading to death (29). The highest incidence of RS infection is observed in children from 6 weeks to 6 months, and by 1-2 years of age, most children are already infected with the RS virus. However, reinfection with this virus has been observed in schoolchildren and adolescents, despite the presence of antibodies to RS viruses after the primary infection (30).

The second pathogen after the RS virus in terms of severity of respiratory disease are parainfluenza viruses type 3. This virus infects children already in the first months of life, causing bronchiolitis and bronchopneumonia in 30% of patients (31). Recently, a new paramyxovirus was discovered that causes ARVI - metapneumovirus. This virus causes a disease, mainly in young children, that is clinically similar to that caused by the RS virus, with complications such as bronchiolitis and pneumonia. This virus mainly causes illness in winter, and among those who became ill and hospitalized with complications, metapneumovirus was isolated from 35% of children (32).

The share of the RS virus as the cause of acute infectious BOS in young children accounts for from 50% to 85% (33,34,35), parainfluenza viruses - 10-21% (28,34, 36), Mycoplasma pneumoniae - up to 8% (28.37), Chlamydia trachomatis - 5-20% (27,37).

In children over 3 years of age and adolescents with acute and recurrent BOS, rhinovirus is detected in 60% of patients (33), Mycoplasma pneumoniae- in 10-40% of patients (25,33,37), Chlamydophila pneumoniae - in 27-58% of patients (27,34,35,37,38). In this age group, even the first episode of biofeedback may be based on an allergic nature.

Clinical biofeedback was detected in 41.4% of older children with whooping cough. Whooping cough in older children, regardless of the period of the disease, is characterized by the development of impaired bronchial obstruction and bronchial hyperreactivity caused by hypergammaglobulinemia E. There is evidence of the possibility of the formation of chronic allergic inflammation and bronchial asthma in children who have had whooping cough (39).

In most patients, acute obstructive bronchitis begins with an increase in body temperature to febrile levels, mucous rhinitis, a short dry cough with a rapid transition to a wet cough, intoxication phenomena (breast refusal, loss of appetite, poor sleep, lethargy, moodiness). On days 2-4, already against the background of pronounced catarrhal phenomena and an increase in body temperature, broncho-obstructive syndrome develops: shortness of breath of an expiratory nature without pronounced tachypnea, oral crepitus, sometimes distant wheezing in the form of noisy, wheezing breathing, a boxy tint of percussion sound, during auscultation - an extended exhalation, dry, whistling rales, moist rales of various sizes on both sides. Biofeedback lasts for 3-7-9 or more days, depending on the nature of the infection and disappears gradually in parallel with the subsidence of inflammatory changes in the bronchi.

Mycoplasma etiology of BOS is most likely in children over 10 years of age. Mycoplasma bronchitis occurs against the background of normal or subfebrile, and often high temperature, but without toxicosis, with the involvement of small bronchi (fine bubbling rales, on a chest x-ray there is an increase in small elements of the pulmonary pattern in the area of ​​bronchitis). Asymmetry of wheezing is characteristic, which should alert you to pneumonia. In most children, these changes are combined with dry catarrh and conjunctivitis without effusion, which allows one to suspect a mycoplasma etiology of BOS. In some cases, severe bronchial obstruction develops. With mycoplasma infection, the ESR may increase against the background of a normal or reduced number of leukocytes.

Chlamydial BOS caused by Chl. trachomatis, in children of the first half of the year it often occurs without severe shortness of breath, toxicosis and hematological changes. In half of the cases, conjunctivitis occurs, and the cough is of a whooping cough-like nature. Respiratory chlamydia caused by Chl. pneumoniae, in children over 3 years of age and adolescents, it is manifested by the following clinical symptoms: prolonged and recurrent broncho-obstructive syndrome with long periods of coughing, low-grade fever, absence of severe intoxication, asthenic state (weakness, lethargy).

To identify chlamydial and mycoplasma etiology of BOS, immunological and molecular genetic (PCR - polymerase chain reaction) methods are used.

Determination of immunoglobulin classes allows not only to determine the presence of infection, but also to clarify the phase of the disease. In the acute phase of the disease, on the 5-7th day of the onset of acute infection, IgM class antibodies are detected, a week later IgA appears, and only by the end of 2-3 weeks of the disease can IgG class antibodies be detected.

The transition from the acute to the chronic stage is always characterized by a fairly high IgA titer, which persists for a long time, while the IgM titer quickly decreases. The chronic course of the disease is characterized by the presence of antibodies of the IgG and IgA classes that persist for a long time, and low titers of these antibodies may indicate persistent pathogens. During reinfection or reactivation, an abrupt rise in IgG titers occurs, which in untreated patients remains at a constant level for a long time. Low titers of IgG may indicate the initial stage of infection or indicate a long-standing infection (“serological scars”).

For timely diagnosis and treatment of chlamydial infection, it is important to take into account that the production of antibodies to chlamydial antigens and phagocytosis of chlamydial macrophages occur only at the elementary body stage, when chlamydial cells are in the intercellular space and are available for contact with antibodies, lymphocytes and macrophages. At the stage of reticular bodies, immune reactions of the host organism (cellular and humoral) are impossible, which creates difficulties for the diagnosis of the disease, and chlamydia itself is protected, not only from various influences from the host organism, but also from most antibacterial drugs that are not able to penetrate inside the cell.

Currently the following are distinguished: laboratory diagnostic criteria for respiratory chlamydia:

The presence of chlamydial antigen/DNA (ELISA, PCR methods) in material from the oropharynx;

Detection of chlamydial IgM (or IgA) antibodies in diagnostically significant titers (ELISA);

Seroconversion with the appearance of chlamydial IgM antibodies, then IgG (ELISA);

Increase in IgG titers ≥ 2-4 times during repeated testing (ELISA).

To the main laboratory methods for diagnosing respiratory mycoplasmosis relate:

Determination of IgM and IgG by ELISA (or passive hemagglutination reaction) to determine antibody titers to Mycoplasma pneumonia;

PCR for diagnosing pathogen DNA ( M. pneumoniae) in an oropharyngeal smear.

Acute bronchiolitis is observed mainly in children in the first six months of life, but can also occur up to 2 years of age. Premature babies are 4 times more likely to develop bronchiolitis (40). In most cases it is caused by respiratory syncytial infection. Bronchiolitis affects the small bronchi and bronchioles. Narrowing of the lumen of the bronchi and bronchioles, due to edema and cellular infiltration of the mucous membrane, leads to the development of severe respiratory failure.

Bronchospasm in bronchiolitis is not of great importance, which is confirmed by the lack of effect from the use of bronchospasmolytics. The clinical picture is determined by severe respiratory failure: perioral cyanosis, acrocyanosis, tachypnea up to 60-80-100 breaths per minute, with a predominance of the expiratory component, “oral” crepitus, retraction of the compliant areas of the chest. Percussion reveals a percussion-type box shade over the lungs; on auscultation - many small moist and crepitating rales throughout all fields of the lungs during inhalation and exhalation, exhalation is prolonged and difficult. This clinical picture of the disease develops gradually over several days. In this case, a paroxysmal cough occurs, appetite decreases, and anxiety appears. The temperature is often febrile, sometimes subfebrile or normal. An X-ray examination of the lungs reveals swelling of the lungs, a sharp increase in the bronchial pattern with a high prevalence of these changes, a high position of the dome of the diaphragm, and a horizontal arrangement of the ribs.

The course of bronchiolitis is usually favorable, obstruction reaches a maximum within 1-2 days, then the retraction of the intercostal spaces decreases, and obstruction completely disappears on days 7-10. Complications (pneumothorax, mediastinal emphysema, pneumonia) are rare. Pneumonia is supported by asymmetry in the distribution of wheezing, persistent febrile temperature, severe toxicosis, leukocytosis and infiltrative changes on the radiograph.

Biofeedback as a manifestation of chronic obstructive pulmonary disease in children

Chronic obstructive pulmonary disease (COPD) in children is characterized by non-allergic inflammation of the lower respiratory tract with predominant damage to the small bronchi and bronchioles (changes in their shape and obliteration), destruction of the collagen basis of the lungs with the formation of emphysema, leading to impaired pulmonary ventilation and gas exchange in an obstructive type and clinically manifested by cough, shortness of breath of varying severity and persistent physical changes in the lungs.

In childhood, including early childhood, diseases such as bronchopulmonary dysplasia (BPD) and bronchiolitis obliterans can be considered forms of COPD in children (48). But at the same time, BPD and bronchiolitis obliterans are included in the modern classification of respiratory diseases in children as independent nosological forms.

Bronchopulmonary dysplasia. In the domestic classification of clinical forms of bronchopulmonary diseases (2008) in children, the following definition of BPD is given (44). BPD (P27.1) is a polyetiological chronic disease of morphologically immature lungs, developing in newborns, mainly in very premature infants receiving oxygen therapy and artificial ventilation. Occurs with primary damage to the bronchioles and lung parenchyma, the development of emphysema, fibrosis and/or impaired replication of the alveoli; manifests itself as oxygen dependence at the age of 28 days of life and older, broncho-obstructive syndrome and other symptoms of respiratory failure; is characterized by specific radiographic changes (interstitial edema alternating with areas of increased transparency of the lung tissue, fibrosis, band-like compactions) in the first months of life and regression of clinical manifestations as the child grows.

Clinical criteria for diagnosing BPD: mechanical ventilation in the first week of life and/or respiratory therapy with continuous positive airway pressure through nasal catheters (nCPAP); oxygen therapy more than 21% at 28 days of age and older; respiratory failure, bronchial obstruction at the age of 28 days and older, oxygen dependence developing during oxygen therapy (ventilator, nCPAP).

X-ray criteria for diagnosing BPD: interstitial edema alternating with areas of increased transparency of the lung tissue, fibrosis, band-like compactions.

They are classified according to their form: BPD full-term, BPD premature(classical and new forms). Classic shape develops in premature infants in whom surfactant preparations were not used to prevent SDR, and “strict” mechanical ventilation regimens took place. Radiologically characteristic: pulmonary distension, fibrosis, bullae.

New form develops in children of gestational age< 32 недель, у которых применялись препараты сурфактанта для профилактики СДР, а респираторная поддержка была щадящей. Рентгенологически характерно гомогенное затемнение легочной ткани без ее вздутия.

BPD in term develops in children born at term and is clinically and radiologically similar to the classic form of BPD of prematurity.

Based on severity, BPD is divided into light, medium and heavy. There are periods of BPD disease: exacerbation, remission. Complications of BPD are: chronic respiratory failure, acute respiratory failure against the background of chronic, atelectasis, pulmonary hypertension, cor pulmonale, systemic arterial hypertension, circulatory failure, malnutrition.

The diagnosis of “bronchopulmonary dysplasia” is valid as an independent diagnosis only in children under 3 years of age. At older ages, BPD is only listed as a history of the disease (44).

According to many researchers, BPD is defined as a chronic obstructive pulmonary disease in young children who had respiratory disorders in the early postnatal period that required artificial ventilation and subsequent oxygen therapy for 21-28 days, with the presence of radiological changes in the form of pulmonary distension and atelectasis ( 54.55). A special place among the etiopathogenetic factors of BPD is occupied by the infectious process as a result of colonization of the respiratory tract by such microorganisms as Chlamydia trachomatis, Chlamydophila pneumoniae, Mycoplasma pneumoniae, Mycoplasma hominis, Ureaplasma urealyticum, cytomegalovirus (45,46).

BPD is characterized by: flat metaplasia of the ciliated epithelium and hypertrophy of bronchial smooth muscles, the formation of bronchiolitis obliterans with collapse of the alveoli and the formation of air cysts (emphysema). The cardiovascular system may be affected secondarily (hypertension of the pulmonary circulation, cor pulmonale), and this condition is often accompanied by impaired physical development of the child.

Clinically, the disease manifests itself as symptoms of bronchial obstruction (rapid wheezing and persistent cough, persistent physical changes in the lungs in the form of dry, moist fine bubbling and crepitant rales) in young children of varying severity, which intensifies with the accumulation of a viral infection. Characteristic data from the anamnesis: premature birth, the presence of respiratory distress syndrome in the early postnatal period, mechanical ventilation with strict parameters and oxygen dependence for at least 1 month (48).

Bronchiolitis obliterans(J43) is a polyetiological chronic disease of the small respiratory tract, resulting from acute bronchiolitis. The morphological basis is concentric narrowing or complete obliteration of the lumen of bronchioles and arterioles in the absence of changes in the alveolar ducts and alveoli, leading to the development of emphysema and disruption of pulmonary blood flow.

Clinical diagnostic criteria: history of acute bronchiolitis, shortness of breath, unproductive cough, physical changes in the form of crepitus and fine wheezing, persistent irreversible airway obstruction.

X-ray diagnostic criteria: mosaic pulmonary pattern due to multiple areas of increased transparency and reduced vascularization, signs of an “air trap”. Scintigraphy shows a violation of pulmonary blood flow.

Unilateral hyperlucent lung syndrome (McLeod syndrome) is a special case of this disease (44).

Bronchiolitis obliterans In patients in the first two years of life, it has a respiratory syncytial and adenoviral (types 3, 7 and 21) etiology, and at an older age it is caused by ligionella and mycoplasma infections (27, 41, 42, 43). The disease is characterized by extreme severity and high frequency of chronicity. The clinical picture of bronchiolitis obliterans occurs cyclically.

In the first (acute) period, clinical signs characteristic of the course of acute bronchiolitis are observed, but with more pronounced disorders. A mass of fine bubbling rales and crepitus, often asymmetrical, are heard against the background of prolonged and difficult exhalation. As a rule, hypoxemia and cyanosis develop. In addition, respiratory failure in these cases persists for a long time and even increases over the course of 2 weeks, which often requires artificial pulmonary ventilation (ALV). The temperature remains persistently at febrile levels. A clinical blood test revealed an increase in ESR, a neutrophil shift, and moderate leukocytosis. Radiographs reveal extensive, often one-sided, soft-shadowed, confluent lesions without clear contours (“cotton lung”). Severe obstructive phenomena also occur after temperature normalization.

In the second period, the child’s well-being improves, but obstruction remains pronounced; moist rales of various sizes and wheezing on exhalation are heard in the lungs. The obstruction may periodically worsen, sometimes resembling an asthma attack. After 6-8 weeks, some children develop the “super-transparent lung” phenomenon. At the same time, respiratory failure persists, indicating persistent changes in the lungs. The outcome of the process is sclerosis of a lobe or the entire lung, but more often obliteration of bronchioles and arterioles occurs with preservation of the airiness of the unventilated lung tissue, described radiographically as a “supertransparent lung” (28). With a favorable outcome, the temperature drops in 2-3 weeks and physical and radiological symptoms completely disappear. In this case, hypoperfusion of the lung lobe (grade 1-2) may persist without typical McLeod syndrome; for many years, during ARVI, wheezing can be heard in such patients.

The key to diagnosis is the identification of irreversible widespread or localized increased transparency of the lungs on a plain chest x-ray, the “air trap” symptom detected by fluoroscopy or radiography during inhalation and exhalation (during the exhalation phase, the transparency of the lung tissue in the affected lung does not decrease). Computed tomography using high-resolution scanning techniques during inhalation and exhalation makes it possible to confirm bronchiolitis obliterans in all cases. Symptoms of increased transparency and depletion of the pulmonary pattern or inhomogeneity of ventilation, signs of emphysema, air trapping on exhalation in combination with fibrous-sclerotic changes in large and small bronchi and lung tissue are specific to children with bronchiolitis obliterans (41,49,50).

Biofeedback of allergic origin. Obstruction in these diseases is caused by two underlying mechanisms: hyperreactivity of the bronchial tree and inflammation of the mucous membrane. Bronchospasm, which gives clinical symptoms to the disease, is a consequence of these two processes, as well as edema, discrinia, hypercrinia, which are less pronounced.

Etiological factors can be various allergens: house dust, plant and tree pollen, dander and animal hair, medications, food products, dry food for aquarium fish, etc. Nonspecific factors can also provoke attacks, such as physical activity, cooling, sudden changes in weather conditions, odors, chemical agents, and mental stress.

Respiratory viral infection is a powerful etiological factor in the formation and course of bronchial asthma (BA). The main pathogenetic links in the development of virus-induced BA are the development of acute viral catarrhal inflammation in the bronchial epithelium, causing its gross morphofunctional changes, swelling of the mucous membrane and hypersecretion of mucus, increased vascular permeability, bronchial hyperreactivity syndrome and the formation of allergic reactions with the participation of immunoglobulin E (51,52,53) .

Respiratory viruses are the trigger of asthma in children in 90% of cases. The leading viral agent, detected in 60-90% of cases, is the RS virus. According to Vartanyan (54), an RS viral disease that occurred with broncho-obstructive syndrome led to the formation of asthma in children in 10% of cases, and in case of relapse of the disease - in 29.1% (while in a similar group of patients with other acute respiratory viral infections BA formed in only 2.5% of cases). Back in the early 70s of the last century, it was shown that 40-50% of children who suffered from RS-viral bronchiolitis developed chronic obstructive bronchitis or asthma over the next 5 years (55). Currently, most authors associate the formation of persistent bronchial hyperreactivity with chronic forms of respiratory viral infection - RS viruses, adenoviruses, parainfluenza viruses (55).

In children suffering from bronchial asthma, it is very often found Mycoplasma pneumoniae. If mycoplasma infection was detected in 4.1-16.4% of children with a favorable premorbid background (56.57), then among patients with bronchial asthma - in 64.2-77% of children (56.58). The positive effect of macrolide therapy with a favorable premorbid background confirms the mycoplasma etiology of BOS.

Significant difficulties are presented by the differential diagnosis between bronchial asthma and obstructive bronchitis of infectious origin. In favor of bronchial asthma is evidenced by a family history, a burdened allergic history (skin manifestations of allergies, “minor” forms of respiratory allergosis - allergic rhinitis, laryngitis, tracheitis, bronchitis, intestinal allergosis, the presence of a connection between the occurrence of the disease and a causally significant allergen and the absence of such a connection with infection , positive effect of elimination, recurrence of attacks, their uniformity). The clinical picture of asthma is characterized by the following signs: absence of intoxication phenomena, distant wheezing or “sawing” nature of breathing, expiratory shortness of breath with the participation of auxiliary muscles, dry wheezing and a few wet ones are heard in the lungs, the number of which increases after relief of bronchospasm. The attack usually occurs on the first day of the disease and is eliminated in a short time, within 1-3 days. Bronchial asthma is also supported by the positive effect of the administration of bronchospasmolytics (xanthines, adrenergic agonists, etc.), eosinophilia in a general blood test, a high level of total IgE in the blood, and the presence of specific IgE in the blood to various allergens.

The initial manifestations of bronchial asthma, as a rule, are of the nature of biofeedback that accompanies respiratory viral infections. Therefore, quite often the diagnosis of asthma is made 5-10 years after the appearance of the first clinical symptoms of the disease. In almost half of young children hospitalized for BOS, the disease is the onset of asthma. At the same time, among preschool children who often (more than 6 times a year) suffer from respiratory diseases, asthma occurred in 20% (23).

For the differential diagnosis of bronchial asthma and obstructive bronchitis with biofeedback against the background of acute respiratory viral infections in early childhood, the following clinical symptom complex has been used for many years (Table 1).

Differential diagnosis of bronchial asthma

(Mizernitsky Yu.L., 2002)

Table 1

Values ​​that are highly diagnostically significant for:	Bronchial	Obstructive bronchitis
1. Age	Over 1.5 years old
2. Beginning of biofeedback	On the 1st day of ARVI	On the 3rd day and later
3. Duration of biofeedback	Less than 2 days	4 days or more
4. Repeatability of biofeedback earlier	2 or more times	1 time or for the first time
5. Hereditary burden of allergic diseases
6. Presence of maternal bronchial asthma
7. History of allergic reactions to foods, medications, preventive vaccinations
8. Infectious diseases of the mother during pregnancy
9. History of pregnancy nephropathy
10. Excessive household antigen load, presence of dampness, mold in a residential area

The presence of any 4 of the 10 above listed diagnostically significant signs for bronchial asthma with a probability of more than 95% indicates this diagnosis (24).

Toxocariasis is a disease caused by the migration of Toxocara canis larvae into the skin or internal organs of humans. The development of toxocariasis occurs as a result of infection with a large number of larvae and is associated in children with the habit of geophagy. The main symptoms of toxocariasis are recurrent fever, pulmonary syndrome, enlarged liver, lymphadenopathy, eosinophilia, hypergammaglobulinemia.

Lung damage syndrome occurs in 65% of patients with visceral toxocariasis and varies from catarrhal phenomena to severe asthmatic conditions. A study conducted in the Netherlands showed that among children with bronchial asthma or recurrent bronchitis, toxocariasis is detected with a frequency of 19.2% (in the control group - 9.9%). The diagnosis is confirmed by the detection of anti-toxocariasis antibodies in the blood serum in the diagnostic titer using enzyme-linked immunosorbent assay (59).

BOS can occur with tuberculosis of the trachea and bronchi. Bronchial tuberculosis occurs as a complication of other local forms of tuberculosis. The transition of a specific process to the bronchial wall is usually associated with caseous-changed intrathoracic lymph nodes adjacent to the bronchi (contact path), and can also occur by hematogenous and lymphogenous routes from the caseous focus. But more often, tuberculosis of the trachea and bronchi in children and adolescents develops as a complication of tuberculosis of the lung tissue as a result of infection of the trachea and bronchi by expectorated sputum with Mycobacterium tuberculosis during progressive destructive processes.

Involvement of the bronchi in a specific process in children is often asymptomatic. There are complaints of increased coughing, often acquiring an annoying character and turning into wheezing or whooping cough, sometimes with a metallic tint, often with pain behind the sternum, as well as complaints of hemoptysis. There may be difficulty in exhaling, or the appearance or intensification of shortness of breath. On auscultation, dry local rales are heard. When the bronchial wall is perforated, lumps of lime can be seen in the sputum.

Tuberculosis with tracheobronchial complications is characterized by more pronounced and long-lasting symptoms of intoxication. In the event of a breakthrough of caseous masses from tumor-modified lymph nodes into the lumen of the bronchi, a picture of a bronchial foreign body may develop. Children with bronchial tuberculosis often develop bronchial obstruction: when narrowing by 1/3 of the diameter of the bronchus - hypoventilation, when reduced by 2/3 - emphysema, with complete closure of the bronchial lumen - atelectasis(usually segmental or lobar).

In the diagnosis of tuberculous lesions of the trachea and bronchi, bronchoscopy with biopsy for bacteriological and morphological verification is required (60).

Biofeedback for developmental defects of the bronchopulmonary system. The frequency of malformations in patients with chronic lung diseases ranges from 1.4% to 20-50% according to various authors. BOS with developmental defects is often detected already in the first year of life against the background of a newly emerging infectious process in the respiratory tract. Defects of the bronchopulmonary system are characterized by great diversity.

Anomalies of bronchial branching can contribute to changes in the aerodynamic characteristics of the air flow.

Tracheal stenosis may be associated both with congenital defects of its wall and with external compression. Compression of the trachea can be caused by developmental anomalies of the aorta and its branches, pulmonary artery anomalies, enlarged thymus gland, congenital cysts and mediastinal tumors.

In the case of significant narrowing of the trachea by a vascular ring, children early begin to suffer from pneumonia, which in them takes a protracted course and is accompanied by broncho-obstructive syndrome. The child's posture is characteristic - the head thrown back, which reduces pressure on the trachea. These patients are characterized by a combination of bronchial obstruction and dysphagia.

In the clinic of tracheal stenosis, expiratory stridor, sometimes mixed, the participation of auxiliary muscles in the act of breathing, attacks of cyanosis and asphyxia come to the fore. Stridor can increase with physical activity, anxiety, eating, and especially with acute respiratory infections. The observed noisy breathing can have a different character: “wheezing”, “crackling”, “sawing”. The bronchopulmonary process is recurrent or continuously recurrent in nature. Diagnosis of tracheal stenosis is based on clinical, radiological and endoscopic data. Among the X-ray methods used are computed tomography, contrast examination of the esophagus, tracheobronchoscopy, and in the case of aortic anomaly - aortography.

Williams-Campbell syndrome(CRS) manifests itself as generalized bronchiectasis caused by a defect of bronchial cartilage at the level of 2 to 6-8 generations. With CRS, bronchiolitis obliterans is detected, which is a consequence of infection. The clinical picture of CRS is characterized by the presence of bronchial obstruction and bronchopulmonary infection, most often manifesting itself in the first year of life. The onset of the disease is most often acute and accompanied by severe respiratory failure. Characterized by constant shortness of breath, aggravated by physical activity, distant wheezing, paroxysmal cough with sputum discharge, centrally located keeled deformity of the chest, “drumsticks”, “watch glasses”, lag in physical development; percussion - box sound; Auscultation - weakened breathing everywhere, dry whistling, buzzing and moist rales of various sizes; X-ray - chest swelling. During bronchoscopy, closure of the cartilaginous and membrane walls of large bronchi is noted. When performing a high-resolution CT scan of the lungs, widespread dilatations of the bronchi are found, starting with the subsegmental ones.

Biofeedback during aspiration of foreign bodies. The greatest number of aspirations is observed between the ages of 1 and 3 years (54%). The distribution of foreign bodies in the tracheobronchial tree depends on the size, shape of the foreign body, the nature of its surface and the possibility of movement along the tracheobronchial tree. According to the literature, foreign bodies are most often localized in the right lung (from 54 to 70%). Despite the variety of clinical symptoms, the most characteristic of them can be identified for a specific localization of a foreign body in the respiratory tract. The main symptoms of a foreign body in the larynx are inspiratory shortness of breath, hoarseness or aphonia, and the development of suffocation. In addition to laryngoscopy and tracheoscopy, an indication in the anamnesis of the sudden development of the clinical picture of the disease against the background of complete health helps in diagnosis.

Foreign bodies of the trachea are somewhat more common - from 43 to 66% (versus 2.9-18% in cases of localization in the larynx). At the moment of aspiration, an attack of suffocation is possible, and a paroxysmal cough is noted.

When a foreign body is localized in the bronchi, a reflex spasm of the bronchioles occurs, which is clinically expressed by the sudden appearance of bronchial obstruction. Percussion and auscultation data, in contrast to bronchial obstruction of other origins, are clearly asymmetrical in nature - weakening of breathing corresponds to the zone in which the foreign body caused hypoventilation. X-ray can determine the shadow of an aspirated object, atelectasis, and mediastinal displacement. If the foreign body is small, penetrated through the glottis and was fixed in one of the bronchi, then breathing becomes free, the child calms down after a coughing attack. The development of BOS in this case can be gradual - local bronchitis transforms into diffuse, which complicates diagnosis. With complete obstruction of the bronchus, atelectasis develops. A carefully collected anamnesis helps make a diagnosis. In this regard, it is especially necessary to note the clinical signs characteristic of foreign bodies in young children:

1. Underdevelopment of the reflexogenic zones of the larynx, the funnel-shaped shape contributes to the asymptomatic penetration of a foreign body into the respiratory tract.

2. One of the striking symptoms is vomiting, often multiple times, which can simulate the ingestion of a foreign body rather than its aspiration.

3. Independent release of foreign bodies is extremely rare.

4. Characterized by the rapid development of bacterial complications (from several hours to 1-2 days, especially in the case of aspiration of foreign bodies of an organic nature), which occur with severe purulent endobronchitis on the affected side and the subsequent development of pneumonia, which takes a protracted course.

5. Frequent development of broncho-obstructive syndrome.

Biofeedback of aspiration origin. At the core broncho-obstructive syndrome of aspiration genesis Various diseases and conditions may lie: gastroesophageal reflux (GER), tracheoesophageal fistula, gastrointestinal malformations, diaphragmatic hernia.

GER develops as a result of persistent and frequent entry of stomach contents into the esophagus or as a result of aspiration of small quantities of gastric contents into the respiratory tract (chronic microaspiration), mainly during sleep. The main cause of GER is considered to be a decrease in tone and periodic relaxation of the lower esophageal sphincter. Autonomic disorders of the sphincter, including those resulting from traumatic brain injury, play an important role in the development of GER. GER can be a manifestation of functional and organic lesions of the central nervous system.

Tracheo- and bronchoesophageal fistulas often manifest themselves during the first feeding of the child with attacks of suffocation, coughing, and cyanosis. This is observed in cases of wide communication between the esophagus and the respiratory tract. Subsequently, either aspiration bronchitis or pneumonia quickly develops. Narrow fistulas can remain undetected for a long time, even until preschool age. Aspiration bronchitis is characterized by persistent physical changes, diffuse nature of the process, frequent development of biofeedback, as well as the discharge of large amounts of mucus.

Biofeedback for diseases of the cardiovascular system of congenital and acquired nature. More often BOS observed for heart defects with enrichment of the pulmonary circulation and is caused by hemodynamic disturbances. Changes in the cardiovascular system come to the fore in the clinical picture of the disease, which facilitates the interpretation of the biofeedback mechanism.

Congenital early and late carditis. The most constant sign of this pathology should be considered cardiomegaly and cardiovascular failure with a predominance of left ventricular failure, which appears in the first half of life. Along with shortness of breath, in 25% of patients, various types of wet and dry wheezing are heard in the lungs, often interpreted as “obstructive syndrome.”

Acquired carditis (acute carditis). As a rule, the first signs of the disease appear against the background of acute respiratory viral infection or 1-2 weeks after it. At the very beginning, acute carditis is manifested by signs of left ventricular failure: shortness of breath, sometimes noisy wheezing breathing, which is why a diagnosis of pneumonia with obstructive syndrome, asthmatic bronchitis or congenital stridor is often made. Simultaneously with shortness of breath, cardiomegaly and cardiac arrhythmias are detected: tachycardia, brady- or tachyarrhythmia.

Malformations of the pulmonary vessels. Characterized by frequent acute respiratory infections, mainly with broncho-obstructive syndrome. On examination, there is flattening of the chest on the affected side, and there is weakened breathing with intermittent wheezing. Radiographically, on the affected side, a narrowing of the pulmonary field and a depletion of the vascular pattern are noted, resulting in the impression of hypertransparency. Scintigraphy reveals either a complete absence of pulmonary blood flow or a gross disruption of it. Angiopulmonography and high-resolution CT of the lungs are important for diagnosing this defect.

Biofeedback for diseases of the central and peripheral nervous systems. In children with natal craniospinal injury, damage to the central nervous system, hypertensive-hydrocephalic syndrome, and severe malformations of the brain, the coordination of the act of swallowing and sucking may be impaired, as a result of which aspiration of food, mainly liquid, with the development of biofeedback is possible. With myopathies (Werdnig-Hoffmann amyotrophy, Oppenheim disease), dysphagia develops associated with paresis of the swallowing muscles with the subsequent development of aspiration bronchitis. The development of biofeedback in congenital myopathies, neuroinfections (poliomyelitis), flaccid forms of cerebral palsy, very premature infants, and alcoholic fetopathy may also be associated with dyskinesia of the bronchial tree.

Biofeedback for metabolic abnormalities. Broncho-obstructive syndrome quite often occurs with hereditary metabolic abnormalities that occur with damage to the bronchopulmonary system. Most often, BOS occurs with cystic fibrosis, malabsorption syndrome, rickets-like diseases, and less often with alpha-1-antitrypsin deficiency, mucopolysaccharidosis.

Cystic fibrosis is the most common monogenic disease with early manifestation, severe course and serious prognosis. Cystic fibrosis is transmitted in an autosomal recessive manner; the risk of birth in the patient's family is 25% with each new pregnancy. It is known that cystic fibrosis is caused by mutations in the gene (localized in the middle of the long arm of chromosome 7), responsible for the molecular structure of the protein, which is located in the membrane of glandular cells lining the excretory ducts of the pancreas, intestines, bronchopulmonary system, urogenital tract and regulates electrolyte (mainly chloride ) transport between these cells and the intercellular fluid. The defective protein is destroyed in the cell, which leads to dehydration of secretions, that is, the release of secretions of increased viscosity and the development of clinical symptoms and syndromes from the above organs and systems.

A mixed pulmonary-intestinal form is identified - in 76.5%, predominantly pulmonary - in 21% and predominantly intestinal - in 2.5% of patients. Bronchopulmonary changes dominate the clinical picture and determine its course and prognosis in 90-95% of patients with cystic fibrosis.

Respiratory syndrome most often begins to manifest itself between the ages of 2 months and 1 year, either with pneumonia, or with broncho-obstructive syndrome, or with a combination of both.

The disease begins with a cough that is unproductive, whooping cough, painful. Sputum, saliva, and mucus in the nose of sick children are viscous, sticky, and thick. The genesis of bronchial obstruction in cystic fibrosis is caused by a violation of mucociliary clearance due to the phenomena of discrinia, dyskinesia, edema and hyperplastic processes. Biofeedback in cystic fibrosis is an example of the second pathogenetic mechanism of bronchial obstruction ( passive) due to the production of viscous sputum and mucostasis.

Broncho-obstructive syndrome immediately becomes protracted or recurrent. Obstruction is enhanced by purulent endobronchitis, which develops as a result of infection. The process involves small bronchi and bronchioles. As a result of persistent airway obstruction, sick children develop bloating, which is an early and persistent sign of the disease. The long course of the bronchopulmonary process leads to the formation of bronchiectasis and pneumosclerosis. Atelectasis often occurs in cystic fibrosis. Most children with cystic fibrosis are delayed in physical development. The lag in physical development is caused not so much by intestinal syndrome, which is well compensated by enzyme preparations, but by the presence of chronic hypoxia and purulent intoxication due to bronchopulmonary changes. On examination, attention is drawn to the deformation of the chest, often in the form of a barrel-shaped form (due to swelling), less often due to a keeled deformity. Deformation of fingers and toes appears in the form of “drumsticks”, nails in the form of “watch glasses”. When percussing the lungs, the “variegation” of the pulmonary sound is determined, namely the alternation of areas of shortened pulmonary sound with areas of boxed sound. Typical for cystic fibrosis is the presence of constantly audible moist wheezing of various sizes, however, in some children, especially during the period of exacerbation of the process, wheezing may not be heard, but a significant weakening of breathing is detected mainly in the basal parts of the lungs due to the accumulation of a large amount of viscous sputum.

With an exacerbation of the bronchopulmonary process, obstructive syndrome occurs or intensifies, shortness of breath appears at rest, cyanosis (perioral, acrocyanosis), tachycardia, wheezing either disappears or their number increases. The presence of massive upper lobe pneumonia in infants is more characteristic of cystic fibrosis. Radiologically, one of the most constant signs of cystic fibrosis is swelling of the lungs, diffuseness of pulmonary changes - pronounced thickening of the walls of the bronchi, blurring of small elements of the bronchovascular pattern, general turbidity of the background, expansion of the shadow of the roots of the lungs to the peripheral parts, their deformation.

As the disease progresses, there is a consistent change in pathogens of the infectious process. A particularly severe group of patients consists of patients with chronic seeding of Pseudomonas aeruginosa from the respiratory tract. The syndrome of bronchial obstruction is pronounced in them and is difficult to treat, which is associated with the peculiarity of Pseudomonas aeruginosa, which increases the viscosity of sputum and enhances the gene defect (2).

Treatment of biofeedback should first of all be aimed at eliminating the cause of the disease that led to the development of biofeedback.

Main directions biofeedback therapy for respiratory infections include activities for improving the drainage function of the bronchi, anti-inflammatory and bronchodilator therapy. A severe course of an attack of bronchial obstruction requires oxygen therapy, and sometimes mechanical ventilation.

Improved drainage functionincludes active oral rehydration, usage expectorants and mucolytic drugs, vibration massage and postural drainage of the chest, breathing exercises (2).

Oral rehydration. It is better to use alkaline mineral waters as a drink; the additional daily volume of liquid is about 50 ml/kg of the child’s weight.

Purpose mucolytic and expectorant therapy is to thin sputum and increase the effectiveness of cough (61). In children with bronchial obstruction and an unproductive cough with viscous sputum, it is advisable to combine inhalation (via a nebulizer) and oral route of administration mucolytics, the best of which for ARVI are the active metabolites of bromhexine - drugs ambroxol(lasolvan, ambrohexal, ambrobene, ambrosan, chalixol, ambrolan, bronchovern, deflegmin). These drugs are indirect-acting mucolytics, have a moderate anti-inflammatory effect, increase the synthesis of surfactant, do not increase bronchial obstruction, and practically do not cause allergic reactions. Ambroxol preparations for ARVI are prescribed orally after meals for children (tablets, syrup, oral solution): up to 2 years - 7.5 mg 2 times a day, from 2 to 5 years - 7.5 mg 2-3 times a day, from 5 to 12 years - 15 mg 2-3 times a day, over 12 years - 30 mg 2-3 times a day. Ambroxol solution (7.5 mg/1 ml) is used in inhalation through a nebulizer: up to 2 years - 1 ml 1-2 times a day, from 2 to 5 years - 1-2 ml 1-2 times a day, over 5 years - 2-3 ml 1-2 times a day.

A weaker mucolytic of indirect action is bromhexine(flexoxin, bromoxin, bronchosan, solvin, phlegamine). Prescribed orally for children: up to 2 years - 2 mg 3 times a day, from 2 to 6 years - 4 mg 3 times a day, from 6 to 10 years - 6-8 mg 3 times a day, over 10 years - 8 mg 3 once a day. The maximum effect from taking bromhexine and ambroxol occurs on days 4-6.

The most pronounced mucolytic effect has N-acetylcysteine, which is used mainly for chronic broncho-obstructive processes. N-acetylcysteine ​​is a direct-acting mucolytic. Breaks the disulfide bonds of sputum glycoproteins, which leads to its liquefaction. With long-term use, it reduces the production of lysozyme and IgA, increases bronchial hyperreactivity (in children over 3 years old in 1/3 of cases). Strong liquefaction of sputum can lead to “swamping” of the lungs, so good drainage for sputum must be ensured (postural drainage, vibration massage of the chest). N-acetylcysteine ​​is prescribed for BOS of infectious origin of mild to moderate severity orally after meals: up to 2 years, 100 mg 2 times a day, 2-6 years - 100 mg 3 times or 200 mg 2 times a day, over 6 years - 200 2-3 times a day. Inhaled forms of acetylcysteine ​​are not used in pediatrics, since the drug has an unpleasant odor of hydrogen sulfide. The duration of use for acute respiratory infections is 5-7 days.

For acute obstructive bronchitis with pronounced bronchial secretion, it is more acceptable carbocisteine, diluting sputum without disturbing its layered structure. Refers to mucoregulators, the effect of which is associated with the normalization of the rheological parameters of sputum, regardless of their initial state. Improves mucociliary transport, promotes restoration of damaged ciliated epithelium. Carbocysteine ​​(broncatar, drill, mucodin, mucopront, fluvik, mucosol) is prescribed orally for 1 month. up to 2.5 years - 50 mg 2 times a day, 2.5-5 years - 100 mg 2 times a day, over 5 years - 200-250 mg 3 times a day. The drug has a negative effect on the gastric mucosa due to its high acidity. In this regard, the lysine salt of carbocysteine ​​( fluifort), which does not irritate the gastric mucosa . Fluifort (syrup 450 mg/5 ml) is prescribed orally at the age of 1-5 years - 2.5 ml (225 mg) 2-3 times a day, at the age of 5-12 years - 5 ml (450 mg) 2- 3 times a day, over the age of 12 years - 15 ml 2-3 times a day.

In the treatment of patients with cystic fibrosis and other chronic obstructive pulmonary diseases occurring with purulent endobronchitis, a direct-acting mucolytic - recombinant human deoxyribonuclease ( dornase alfa, pulmozyme). The mechanism of action is associated with the destruction of DNA of leukocytes contained in sputum during pulmonary infections. It is prescribed in inhalation via a nebulizer, 2.5 ml (2.5 mg) 1 time per day for a course of 14 days to 6 months for chronic purulent-inflammatory diseases of the bronchopulmonary system, and in patients with cystic fibrosis - continuously.

For children with an obsessive, unproductive cough and lack of sputum, it is advisable to prescribe expectorants- alkaline drinking, herbal remedies. Herbal medicines should be prescribed to children with allergies with caution. A combination of expectorants and mucolytic drugs is possible. However, in severe cases of BOS (especially in young children), mucolytics and expectorants are prescribed only after relief of severe bronchial obstruction (61).

Expectorant drugs include substances of plant origin that enhance the peristalsis of bronchioles by stimulating the gastropulmonary reflex, which is an analogue of the gag reflex. This promotes the movement of mucus from the lower respiratory tract to the upper and its evacuation. These drugs help to increase the secretion of the bronchial glands, which increases the liquid lower layer of mucus and, thereby, the activity of the ciliated epithelium. It is recommended to take expectorants frequently in small doses (every 2-4 hours) in combination with plenty of fluids. They should be used with caution in young children and infants as they may cause vomiting (61).

Drugs in this group, mostly combined, are available in ready-made forms. Bronchicum elixir(tincture of herbs grindelia, wildflower, quebracho, thyme, primrose) has an expectorant, antimicrobial and antispasmodic effect, relieves paroxysmal cough. Prescribed to children 3-6 years old, ½ tsp. 2-3 times/day, 6-14 years - 1 tsp. 2-3 times/day, over 14 years old, every 2-3 hours, 1 tsp. (up to 6 times/day).

Bronchosan(menthol, fennel oil, anise, oregano, mint, eucalyptus, bromhexine) has mucolytic, expectorant, antimicrobial and antispasmodic effects. It is used for acute and chronic diseases of the respiratory tract, accompanied by the formation of difficult-to-discharge bronchial secretions. Available in drops for oral administration and inhalation. For oral administration, a single dose for adults and children over 6 years old is 20 drops, for children 2-6 years old - 10 drops, for children under 2 years old - 5 drops. Frequency of administration - 4 times/day. For inhalations, a single dose for adults is 4 ml, for children over 10 years old - 2 ml, 6-10 years old - 1 ml, 2-6 years old - 10 drops, under 2 years old - 5 drops. Inhalations are carried out 2 times a day.

Glycyram(ammonium salt of glycyrrhizic acid isolated from licorice roots) has an anti-inflammatory effect associated with stimulation of the adrenal cortex and a moderate expectorant effect. Prescribed 1-2 tablets. (0.05-0.1) 3-6 times/day. in 30 min. before meals.

Breast Elixir(licorice root extract, anise oil, aqueous ammonia) children are prescribed as many drops as the child is old, adults - 20-40 drops per dose. Frequency of administration - 4-6 times/day.

Doctor Mom(extracts of licorice, basil, elecampane, aloe, ginger, curcuma longa, Indian nightshade, menthol) has a bronchodilator, mucolytic, expectorant and anti-inflammatory effect. Prescribed orally for children 3-5 years old, ½ tsp. 3 times/day, 6-14 years - ½-1 tsp. 3 times/day, over 14 years old - 1-2 tsp. 3 times/day.

Mukaltin(marshmallow herb extract, sodium bicarbonate) has an expectorant, enveloping, anti-inflammatory effect. Prescribe ½-1-2 tablets before meals. depending on age 3-4 times/day.

Pertussin(thyme extract or thyme extract, potassium bromide, sugar syrup, ethyl alcohol) softens cough. Prescribed orally in syrup, ½ tsp - 1 tbsp. l. 3 times/day.

Guaifenesin(tussin) is a glycerin ester of guacol, thins mucus and improves the vibrations of the cilia of the ciliated epithelium. Prescribed orally for children 2-6 years old - 50-100 mg, 6-12 years old - 100-200 mg, over 12 years old - 200 mg every 4-6 hours.

Guaifenesinis part of the combination product a reproached(in 10 ml of syrup: bromhexine - 4 mg, guaifenesin - 100 mg, salbutamol - 2 mg), which has an expectorant, mucolytic and bronchodilator effect. Dosage: 3-6 years 1 tsp. (5 ml) 3 times a day, 6-12 years - 1-2 tsp. (5-10 ml) 3 times a day, adults - 1 dec. l. (10 ml) 3 times a day.

Sinupret(extracts of gentian root, primrose flowers, sorrel herb, elderberry flowers, verbena herb) has a secretolytic, secretomotor, anti-inflammatory effect, has antiviral and immunostimulating activity. Prescribed to children 2-6 years old, 15 drops 3 times/day, to school-age children - 25 drops 3 times/day.

Bronchipret(syrup - extracts of thyme herbs, ivy leaves) has an expectorant, secretolytic, anti-inflammatory, bronchodilator effect, helps reduce the viscosity of sputum and accelerate its evacuation. It is recommended to use after meals, washing down the syrup with water. Using the included measuring cup: children 3-12 months - 1.1 ml 3 times a day; children 1-2 years old - 2.2 ml 3 times a day; children 2-6 years old - 3.2 ml 3 times a day; children 6-12 years old - 4.3 ml 3 times a day; adolescents from 12 years old - 5.4 ml 3 times a day.

Codelac Broncho with thyme(elixir - ambroxol, sodium glycyrrhizinate, liquid thyme extract) has an expectorant, secretolytic, secretokinetic, anti-inflammatory, bronchodilator effect. Dosage regimen: children 2-6 years old, 2.5 ml 3 times a day, children 6-12 years old, 5 ml 3 times a day for 7 days.

All patients with BOS of infectious origin are excluded from antitussive drugs (2).

Bronchodilator therapy(2,5,62). Short-acting β2-agonists, anticholinergic drugs, short-acting theophyllines, and their combination are used as bronchodilator therapy for BOS of infectious origin. Preference should be given to inhalation forms of drug administration.

The drugs of choice for reducing acute bronchial obstruction are Short-acting β2-agonists(salbutamol, fenoterol). When used inhalation, they provide a rapid (within 5-10 minutes) bronchodilator effect. They should be prescribed 3-4 times a day. Drugs in this group are highly selective and therefore have minimal side effects. However, with long-term uncontrolled use of short-acting β2-agonists, it is possible to increase bronchial hyperreactivity and reduce the sensitivity of β2-adrenergic receptors to the drug. A single dose of salbutamol inhaled through a spacer is 100-200 mcg (1-2 doses); when using a nebulizer, the single dose can be significantly higher and amount to 2.5 mg (nebulas of 2.5 ml of 0.1% solution). In case of severe torpid course of biofeedback, three inhalations of a short-acting β 2 -agonist are allowed as “emergency therapy” within 1 hour with an interval of 20 minutes.

Anticholinergic drugsblock muscarinic M3 receptors for acetylcholine. The bronchodilator effect of the inhaled form of ipratropium bromide (Atrovent) develops 15-20 minutes after inhalation. Through a spacer, 2 doses (40 mcg) of the drug are inhaled once, through a nebulizer - 8-20 drops (100-250 mcg) 3-4 times a day. M-anticholinergics in cases of BOS arising from a respiratory infection are somewhat more effective than short-acting β 2 agonists. However, the tolerability of Atrovent in young children is somewhat worse than that of salbutamol.

A physiological feature of young children is the presence of a relatively small number of β 2 -adrenergic receptors; with age, there is an increase in their number and an increase in sensitivity to the action of mediators. The sensitivity of M-cholinergic receptors, as a rule, is quite high from the first months of life. These observations served as a prerequisite for the creation of combination drugs.

Most often in complex therapy of biofeedback in young children is currently used combination drug berodual, combining two mechanisms of action: stimulation of β 2 -adrenergic receptors and blockade of M-cholinergic receptors. Berodual contains ipratropium bromide and fenoterol, the action of which in this combination is synergistic. The best way to deliver the drug is a nebulizer; a single dose in children under 5 years of age is on average 1 drop/kg of body weight 3-4 times a day. In the nebulizer chamber, the drug is diluted with 2-3 ml of physiological solution.

Short-acting theophylline (aminophylline),Having bronchodilator and anti-inflammatory activity, it has a large number of undesirable effects on the digestive system (nausea, vomiting, diarrhea), the cardiovascular system (risk of arrhythmia), and the central nervous system (insomnia, hand tremors, agitation, convulsions). Currently, aminophylline is classified as a second-line drug and is prescribed when short-acting β 2 agonists and M-anticholinergics are insufficiently effective. Eufillin in mixture is prescribed to children at the rate of 5-10 mg/kg per day in 4 divided doses. In case of severe bronchial obstruction, aminophylline is prescribed intravenously (in saline solution) at a dose of 4-5 mg/kg every 6 hours (daily dose up to 16-18 mg/kg) (2).

Anti-inflammatory drugs.

Glucocorticoid therapy. In children with bronchial obstruction, inhalation of glucocorticosteroids through a nebulizer is effectively used: budesonide suspension (pulmicort suspension for nebulizer in plastic containers of 2 ml; 0.5 mg or 0.25 mg per 1 ml). Pulmicort suspension can be diluted with saline and also mixed with solutions of bronchodilators (salbutamol, ipratropium bromide, berodual). The dose used in children is 0.25-0.5 mg (up to 1 mg) twice daily. Thus, in modern biofeedback therapy, the principle of combining bronchodilators and glucocorticosteroid drugs is used.

When treating children with severe biofeedback, other glucocorticosteroid drugs (hydrocortisone and methylprednisolone intravenously, prednisolone orally) can also be used. The dose of hydrocortisone is 125-200 mg intravenously (4 mg/kg) every 6 hours, methylprednisolone is 60 to 125 mg every 6-8 hours intravenously, prednisolone is 30 to 60 mg orally every 6 hours. Prednisolone is prescribed orally 1-2 times a day at a rate of 1-2 mg/kg/day (children under 1 year); 20 mg/day (children 1-5 years old); 20-40 mg/day (children over 5 years old) for 3-5 days (5).

For bronchiolitis, corticosteroids are prescribed immediately along with sympathomimetics. The onset of the effect is judged by a decrease in the respiratory rate by 15-20 per minute, a decrease in intercostal space retractions, and the intensity of expiratory noises. With this tactic, the condition of most patients improves on the 2nd day of treatment.

In recent years, as a nonspecific anti-inflammatory agent successfully used for respiratory diseases in children fenspiride (erespal). The anti-inflammatory mechanism of action of erespal is caused by blocking H1-histamine and β-adrenergic receptors, reducing the formation of leukotrienes and other inflammatory mediators, and suppressing the migration of effector inflammatory cells. Erespal reduces the effect of the main pathogenetic factors that contribute to the development of inflammation, mucus hypersecretion, bronchial hyperreactivity and bronchial obstruction. For children, the drug is prescribed before meals at the rate of 4 mg/kg per day in the form of syrup (1 ml of syrup contains 2 mg of fenspiride hydrochloride): children weighing up to 10 kg - 2-4 teaspoons (10-20 ml) of syrup per day, more 10 kg - 2-4 tablespoons of syrup (30-60 ml) syrup per day (61).

Antihistamines. The use of antihistamines in children with respiratory infection is justified if it is accompanied by the appearance or intensification of any allergic manifestations, as well as in children with concomitant allergic diseases in remission.

In children under 6 months of age, it is permissible to prescribe only the first generation of these drugs: fenistil 3-10 drops 3 times a day (20 drops = 1 mg); fenkarol 5 mg 2 times a day (Table 0.01 and 0.025); peritol 0.15 mg/kg 3 times a day (1 ml syrup = 0.4 mg); suprastin 6.25 mg (1/4 tablet) 2 times a day (table 0.025). First generation antihistamines should not be prescribed in the presence of thick and viscous bronchial secretions, as they have a pronounced “drying” effect.

From 6 months of age, only cetirizine (Zyrtec) is allowed to be used at 0.25 mg/kg 1-2 times a day (1 ml = 20 drops = 10 mg). From 2 years of age, loratadine (Claritin), deslorotadine (Erius) can be prescribed (62).

Ventilation or breathing under increased pressure during exhalation(about 10 cm of water column) is rarely performed in children with bronchiolitis, the indications for this are:

Weakening of breath sounds during exhalation.

Persistence of cyanosis when breathing 40% oxygen.

Reduced pain response.

The drop in partial pressure of oxygen is less than 60 mmHg. Art.

An increase in the partial pressure of carbon dioxide more than 55 mmHg. Art.

Vibration massage and postural drainage already from the 2nd day it allows to improve the evacuation of sputum and reduce the severity of bronchospasm.

Indications for antibiotics for infectious biofeedback (61):

Signs indicating the bacterial nature of inflammation are mucopurulent and purulent sputum, severe intoxication, hyperthermia for more than 3 days.

Bronchiolitis, the mortality rate of which is 1-3%.

Prolonged course of obstructive bronchitis, especially if the intracellular nature of the disease is suspected.

It is most appropriate to prescribe macrolide antibiotics for the treatment of obstructive bronchitis. Macrolides are active both against pneumotropic gram-positive cocci (pneumococci, Staphylococcus aureus) and against intracellular pathogens (mycoplasma, chlamydia).

1st generation drug - erythromycin - 40-50 mg/kg per day in 4 doses is given orally 1 hour before meals in children. Food significantly reduces bioavailability (30-65%) when taken orally. The half-life is 1.5-2.5 hours. It has an unpleasant bitter taste and is characterized by a high frequency (up to 20-23%) of side effects from the gastrointestinal tract in the form of nausea, vomiting, diarrhea, pain, caused not by a violation of the intestinal biocenosis, but by the prokinetic, motilium-like effect of the drug. Intravenously for adults - 0.5-1.0 g. x 4 times a day, for children - 40-50 mg/kg per day in 3-4 administrations. Before intravenous administration, a single dose should be diluted in at least 250 ml of 0.9% sodium chloride solution and administered over 45-60 minutes. Can be prescribed during pregnancy and breastfeeding.

Macrolides 2nd generation (spiramycin) And 3 generations (roxithromycin, clarithromycin, azithromycin, josamycin) do not have the disadvantages inherent in erythromycin. They have a satisfactory taste. The frequency of side effects does not exceed 4-6% of cases. The weakness of these drugs is that not all drugs are injectable, which limits the use of macrolides in severe cases.

Clarithromycin- inside: children over 6 months. - 15 mg/kg per day in 2 divided doses.

Roxithromycin- orally (1 hour before meals): children - 5-8 mg/kg per day in 2 divided doses.

Azithromycin- orally: children - 10 mg/kg/day for 3 days or on the 1st day - 10 mg/kg, then on days 2-5 - 5 mg/kg in one dose.

Spiramycin- orally: children - body weight less than 10 kg - 2-4 sachets of 0.375 million IU per day in 2 divided doses, 10-20 kg - 2-4 sachets of 0.75 million IU per day in 2 divided doses, more than 20 kg - 1.5 million IU per day in 2 divided doses.

Josamycin- orally: children - 30-50 mg/kg per day in 3 divided doses.

Midecamycin- orally, children over 12 years old - 0.4 x 3 times a day, children under 12 years old - 30-50 mg/kg per day in 2-3 doses (61).

Treatment of bronchiolitis obliterans presents great difficulties due to the lack of etiotropic drugs. In connection with suspected pneumonia, antibiotics are used, which do not prevent persistent obliteration of bronchioles. Early use of steroids (prednisolone 2-3 mg/kg/day) promotes faster elimination of obstruction and gives hope for reducing residual changes. Treatment of toxicosis is carried out with a minimum of intravenous fluid infusion. In the second period, with a gradual reduction in the dose of steroids, sympathomimetics are prescribed according to indications, and vibration massage and postural drainage are mandatory (1).

Treatment of biofeedback of allergic origin is a therapy for exacerbations of bronchial asthma in children. The amount of therapy depends on the severity of the asthma exacerbation and whether the patient is treated at home, outpatient or in hospital (5,62).

At mild exacerbation of asthma Prescribe short-acting β 2 -agonists through a metered-dose aerosol inhaler (1-2 doses (100-200 mcg) of salbutamol) with a spacer or nebulizer (2.5-5 mg of salbutamol) every 20 minutes for 1 hour. If there is no effect, the child should be hospitalized.

At moderate exacerbation of asthma prescribe:

- Short-acting β2-agonists via metered-dose inhaler with spacer or nebulizer every 20 minutes for 1 hour;

-

-

- glucocorticosteroids by mouth are possible - in the absence of an immediate response or if the patient has previously taken systemic glucocorticosteroids.

Severe exacerbation of asthmaassumes the purpose:

- inhaled short-acting β2-agonists + anticholinergics via nebulizer every 20 minutes or continuously for 1 hour;

- oxygen until saturation reaches more than 90%;

- pulmicort suspension via nebulizer;

- glucocorticosteroids by mouth.

If there is no effect from the treatment, the patient is transferred to the intensive care unit in order to intensify treatment measures:

- inhaled short-acting β2-agonists + anticholinergics via nebulizer every hour or continuously;

- oxygen therapy;

- inhalation of pulmicort through a nebulizer;

-

- aminophylline intravenously;

- Intubation and mechanical ventilation are possible.

Extremely severe exacerbation of asthma (silent mild stage) is an indication for immediate hospitalization in the intensive care unit and emergency care to save the patient:

- intubation and mechanical ventilation with 100% oxygen;

- glucocorticosteroids intravenously;

- aminophylline intravenously;

- inhaled short-acting β2-agonists + anticholinergic drugs via nebulizer.

If the patient's condition improves, the patient is transferred to a specialized department, where treatment with bronchodilators and glucocorticosteroids (by mouth and/or nebulizer) is continued. Then basic combination drugs are added (Seretide, Symbicort), the doses of these drugs are selected in accordance with the severity of the patient, and the child is discharged under the supervision of a specialist (5, 62).

Summarizing the above, we can say that almost every pediatrician in his practice encounters such a condition as broncho-obstructive syndrome - a symptom complex of impaired bronchial patency of a functional or organic origin. It should be taken into account that BOS is heterogeneous and can be a manifestation of many diseases. Therefore, before prescribing treatment, it is important to establish the cause of biofeedback in each individual child and prescribe the correct appropriate therapy.

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Broncho-obstructive syndrome causes a lot of harm to the child’s body. He occurs against the background of existing diseases.

If left untreated, complications may occur. Clinical recommendations for the treatment of broncho-obstructive syndrome in children will be presented in the article.

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Concept and characteristics

This pathology is not a disease, but a syndrome, which is characterized by a set of certain symptoms.

Broncho-obstructive syndrome is not a separate diagnosis, but its symptoms describe problems of the respiratory system, namely bronchial obstruction.

Occurs most often at an early age: from 1 to 5 years. There is a high likelihood of the disease occurring in children who have had respiratory infections.

Causes and risk factors

Pathology occurs for the following reasons:

TO risk group include children who have suffered respiratory tract diseases.

There is a high likelihood of the syndrome occurring in those children whose mothers suffered from viral and infectious diseases during pregnancy. The syndrome occurs as a complication.

How does it develop and what forms does it take?

The syndrome develops against the background of an existing disease. The development of the disease occurs quickly. In just one or two weeks, the child’s condition can deteriorate significantly. Recovery will take two weeks, in severe cases a month. This syndrome can take the following forms:

Classification

Depending on the pathogenesis of the syndrome, experts distinguish these types of pathology:

1. Syndrome allergic genesis. Appears against the background of allergies, bronchial asthma.
2. Syndrome caused infections. Causes: viral and infectious diseases, colds, pneumonia, bronchiolitis.
3. Syndrome caused by neonatal pathologies. Formed against the background of stridor, diaphragmatic hernia.
4. Syndrome caused by hereditary, congenital diseases. Causes of appearance: cystic fibrosis, hemosiderosis, emphysema.
5. The syndrome against the background of the development of other nosologies. Appears due to foreign bodies in the bronchial tree, thymomegaly, hyperplasia of regional lymph nodes.

Clinical picture and symptoms

The syndrome is characterized by the following symptoms:

• loud breathing. It can be very difficult for children to breathe, wheezing and whistling are heard;
• cough. In severe cases of the disease, it is accompanied by the release of mucus not only from the bronchi, but also from the nose;
• weakness, moodiness. The child does not play and lies down a lot. Sleep disturbance may occur;
• loss of appetite. The baby refuses to eat food. Becomes pale and dizzy;
• expansion of intercostal spaces. The child's chest becomes disproportionate;
• vomit. It is a consequence of impaired digestion. The syndrome negatively affects the digestive system.

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Diagnostics

Carried out in a hospital by a pediatrician, or neonatologist. To diagnose the syndrome, the following are used:

1. Blood and urine tests. Such tests are necessary to collect general information about the condition of the body.
2. Bronchoscopy. Identifies and helps remove foreign bodies from the bronchi. Evaluates the patency and condition of the mucous membranes of the respiratory system.
3. Spirometry. Necessary for assessing respiratory function.
4. Radiography chest. Makes it possible to examine the expanded roots of the lungs, signs of damage to individual areas, and the presence of neoplasms. This method can identify enlarged lymph nodes.

What is the differential diagnosis? The syndrome should be distinguished from diseases:

1. . The syndrome has a number of symptoms: cough, shortness of breath, weakness. However, with the syndrome there is no severe suffocation or fainting.
2. Pneumonia. When the disease occurs, there is a high temperature, fever, and the child has a severe cough. The syndrome does not have fever or chills.
3. Whooping cough. The disease and syndrome are very similar. Only sputum examination can distinguish them. It differs significantly in the two cases presented.
4. Chronic sinusitis. The presence of mucus in the lungs is typical, and the nose may be stuffy. The disease and syndrome can only be distinguished by a CT scan of the paranasal sinuses.

Urgent Care

The syndrome can worsen the child's condition. If the baby suddenly becomes ill, necessary:

1. Call an ambulance immediately.
2. While the doctors are driving, the collar of the child’s clothes is unbuttoned to make it easier to breathe.
3. You need to calm the child down; you can’t show excitement.
4. It is necessary to provide a flow of fresh air. To do this you need to open a window.
5. The baby needs to take a comfortable position.
6. It is necessary to give the child an antihistamine (Claritin, Zyrtec) in the amount of one tablet.

Reduce bronchospasms hot foot baths. You need to pour hot water into the basin.

Very carefully, the child’s legs are lowered into a bowl of water. The water should not be too hot so as not to burn the child.

The procedure lasts at least ten minutes. During this time the child will feel better Perhaps the doctors will arrive by this time.

These measures will help alleviate the child’s condition and avoid complications. By the time the doctors arrive, the baby will feel better.

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Treatment methods

Doctors recommend using drugs to dilate the bronchi: Salbutamol, Berotec. They prevent the development of the syndrome, act instantly, do not enter the blood, and therefore do not have side effects. They are used twice a day, the dosage is determined by the doctor.

Mucolytic therapy is necessary. The child takes mucolytic drugs, which slightly thin the mucus and remove it from the lungs along with the cough. Such medications include Lazolvan and Ambrobene. Take the medication 2-3 times a day. The exact dosage is prescribed by a specialist.

It is strictly forbidden to give No-shpa to a child. It relieves headaches, but leads to complications of the syndrome. The respiratory system functions worse after taking this drug.

To relieve inflammation and stop the development of the syndrome, it is recommended to take medication Erespal. It is taken twice a day, one tablet.

It is useful massotherapy. To do this, the child's back and chest are lightly rubbed and tapped with the pads of the fingers.

The baby shouldn't be in pain. The duration of the massage is ten minutes. The procedure is carried out twice a day. It helps remove mucus from the lungs and promotes recovery.

It is not recommended to treat a child with folk remedies, since their effect has not been proven in medical research. Such drugs can lead to a significant deterioration in the baby’s condition, rather than recovery.

On the diagnosis and treatment of broncho-obstructive syndrome in children.

To stop the development of the syndrome and cure the child, you need to follow some recommendations:

1. If the child's temperature does not exceed 37 degrees, It is recommended to take him for a walk, get some fresh air. The baby’s body must be saturated with oxygen, ventilation of the lungs will take place, and this will help to recover.
2. Food should be healthy. This will strengthen the body and help fight the syndrome.
3. You should not take warm baths. This will lead to increased sputum and complications.
4. The room must be ventilated regularly, wet cleaning must be performed. If this is not done, dust will accumulate, which will lead to a deterioration in the baby’s condition. Breathing dust in this condition is very dangerous.
5. It is prohibited to choose medications to treat your baby on your own. Medicines are prescribed by a doctor after examining the child and diagnosing the pathology. If you purchase medications yourself, can harm the baby.

This syndrome is dangerous for the child’s body; the pathology is accompanied by unpleasant symptoms.

It can be cured with various drugs, timely treatment will help the child recover faster.

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We kindly ask you not to self-medicate. Make an appointment with a doctor!