Obstructive lung disease in children: resolved and unresolved issues. How to stop the progression of the disease? Diagnosis of lung obstruction

Yu. E. Veltishcheva, Moscow

Keywords: children, smoking, electronic cigarettes, vaping, chronic obstructive pulmonary disease (COPD)

Key words: children, smoking, e-cigarettes, vaping, chronic obstructive pulmonary disease (COPD)

Today, COPD is understood as an independent disease, which is characterized by partially irreversible airflow limitation in respiratory tract, which, as a rule, is steadily progressive in nature and provoked by an abnormal inflammatory response of lung tissue to irritation by various pathogenic particles and gases. In response to the impact of external pathogenic factors, the function of the secretory apparatus changes (mucus hypersecretion, changes in the viscosity of the bronchial secretion) and a cascade of reactions develops, leading to damage to the bronchi, bronchioles and adjacent alveoli. Violation of the ratio of proteolytic enzymes and antiproteases, defects in the antioxidant defense of the lungs exacerbate damage.

The prevalence of COPD in the general population is about 1% and increases with age, reaching 10% in people over 40 years of age. According to WHO experts, by 2020 COPD will become the third leading cause of morbidity and mortality in the world. COPD is topical issue, since the consequences of the disease are the limitation of physical performance and disability of patients, including modern children and adolescents.

The diagnostic criteria for establishing the diagnosis of COPD in practice include characteristic clinical symptoms (prolonged cough and progressive dyspnea), anamnestic information (presence of risk factors) and functional indicators (progressive decrease in FEV1, and FEV1/FVC ratio).

As an illustration, we give the following clinical example:

Patient Yu., 16 years old, from a family with an uncomplicated allergic history; parents and relatives smoke for a long time, maternal grandfather died of lung cancer. Household history is aggravated by living in a damp apartment where cats are kept. From the age of 3, the girl suffered from recurrent bronchitis with a lingering cough, mainly in the cold season, and repeatedly received courses of antibiotics and mucolytics on an outpatient basis. At the age of 7 she was on a long-term inpatient treatment about a urinary tract infection, in the hospital for the first time began to smoke cigarettes with other children. Subsequently, due to increased episodes of bronchitis and a long-lasting cough, she was registered with a pulmonologist at the place of residence. The disease was regarded as the onset of bronchial asthma, basic treatment was carried out with inhaled glucocorticosteroids in gradually increasing doses, due to the insufficient effect during the last year before contacting the clinic, she received a combined drug Seretide. She was repeatedly hospitalized in a hospital at the place of residence for the relief of exacerbations, inhalations with bronchodilators, mucolytics and antibacterial drugs were added to the therapy. Between exacerbations, she suffered from a paroxysmal obsessive cough (in the mornings with scanty sputum), exercise tolerance did not suffer, but the girl often complained of weakness, fatigue and headaches. She was first sent for examination to clarify the diagnosis at the age of 16. Upon admission, the state of moderate severity; complaints of unproductive cough in the morning with mucopurulent sputum; exacerbation episodes with febrile temperature and increased cough. On examination, there is no dyspnea at rest, physical development is average, harmonious, signs of peripheral osteoarthropathy are not expressed; the chest is not deformed, the percussion sound is boxy, in the lungs, against the background of hard breathing, wet rales of various sizes are heard. When examining deviations from the indicators of general blood tests, urine, biochemical blood tests were not revealed. Immunological study of humoral and cellular immunity, phagocytic activity of neutrophils made it possible to exclude an immunodeficiency state. Allergological examination did not reveal specific sensitization to causative allergens. Morphological analysis of sputum confirmed its mucopurulent character; sputum culture revealed colonies of Staphylococcus aureus and epidermal streptococcus. The radiograph of the lungs showed signs of bronchitis and obstructive syndrome. When conducting spirometry, the volume-velocity parameters were within the proper values, the test with dosed physical activity did not reliably reveal post-exercise bronchospasm. drew attention to himself low level nitric oxide in the exhaled air (FeNO=3.2 ppb at the rate of ppb), as well as sharp increase carbon monoxide content in the exhaled air (COex=20 ppm at a rate of less than 2 ppm), which is pathognomonic for regular active smoking. During body plethysmography, the presence of obstructive disorders detected radiographically was confirmed: a sharp increase in the residual volume of the lungs and its contribution to the total lung capacity. Diaskintest was negative, which ruled out the presence of tuberculosis. The level of sweat chlorides was within the normal range, which disproved the presence of cystic fibrosis.

Markers of persistent viral and bacterial infections were not identified. A carefully collected anamnesis made it possible to clarify that from the age of seven to the present, the girl regularly smoked actively (from ½ to 1 pack of cigarettes per day), i.e. smoking experience by the time of contacting the clinic was 8 years. In her family, parents and close relatives smoked, cigarettes were in the public domain.

At the same time, the girl's parents, knowing about her smoking, did not connect the child's complaints of prolonged cough and repeated bronchitis with smoking and were determined to treat cough with medication. The girl independently made several unsuccessful attempts to quit smoking, but she did not turn to anyone for specialized help. Thus, based on the medical history and the results of the examination, the alleged diagnosis of bronchial asthma was not confirmed, and the patient was diagnosed with Chronic obstructive bronchitis (J 44.8). An explanatory conversation was held with the parents of the teenager and the girl herself, recommendations were given on improving the life, giving up smoking for all family members (including with the help of anti-tuxedo cabinet specialists at the place of residence) and tactics for treating the underlying disease.

In routine clinical practice, portable gas analyzers for determining the level of carbon monoxide in exhaled air (COex) have proven themselves well for detecting active smokers. Thus, 100 patients with bronchial asthma (BA) were examined in our clinic. varying degrees severity of 6-18 years (68 boys, 32 girls) for the content of CO with the help of a Smokerlyzer CO analyzer (Bedfont, England).

The simplicity of the breathing maneuver (15-second breath-hold at the height of inhalation followed by exhalation through the mouthpiece of the gas analyzer) makes the non-invasive measurement of COEX available for most children over 6 years of age. Among the surveyed, 14 active smokers aged 13 to 18 years were identified: their average COvy was 7.9 ppm (4-16 ppm) (1 ppm - 1 particle of gas per 106 particles of air); all of them were in the clinic due to the severe course of BA and denied the fact of smoking. Nineteen patients who belonged to the category of passive smokers (in their families, parents or close relatives smoked at home) had an average level of CO-exp = 1.3 ppm (0-2 ppm), which did not significantly distinguish them from the group of children not exposed to tobacco smoke (67 patients, mean COexp = 1.4ppm (0-2ppm)). However, among patients exposed to passive smoking, children with more severe BA prevailed. The results obtained indicate the potential practical significance of using CO analyzers in a children's pulmonology clinic to identify active smokers in order to conduct targeted anti-smoking programs and monitor their effectiveness.

In addition, the most widely used biomarker for human exposure to cigarette smoke is cotinine, the major nicotine metabolite detected by gas chromatography or radioimmunoassay in blood or, preferably, urine, reflecting the level of absorption of nicotine through the lungs. After smoking cessation, cotinine persists in the urine longer than nicotine and is detected within 36 hours after the last cigarette is smoked. In addition, it was found that the level of cotinine in the urine significantly increases in passive smokers. To date, there are special test strips for the determination of cotinine in urine using the immunochromatographic method.

A particular problem is patients who use vaping as an alternative to smoking (from the English vapor - steam, evaporation). This invention is only 14 years old: in 2003, Hong Kong smoker Hong Lik, whose father died of COPD, patented the first electronic vaporizer cigarette designed to quit smoking. However, the further fate of this invention went along the path of improving various devices and creating flavor mixtures, the benefits of which raise more and more questions.

The following clinical example is proof of this.

Patient G., 15 years old, from a family with a burdened allergic history: his mother and maternal grandmother had allergic rhinitis, his sister had atopic dermatitis.

From the beginning of the visit kindergarten began to get sick often with respiratory infections with a lingering cough, often worried about persistent nasal congestion, when examined at the place of residence allergic genesis complaints are not confirmed. With the beginning of school attendance, acute respiratory infections became less common, but nasal congestion persisted, and he received topical steroids with courses. positive effect. From the age of 12, he began to periodically smoke electronic cigarettes, repeated acute respiratory infections with a prolonged cough resumed. At the age of 15, he began to use a steam inhaler with various flavoring additives. After a month of active “soaring”, against the background of subfebrile temperature, a debilitating paroxysmal cough appeared, periodically to vomiting, aggravated by laughter, deep breathing, going outside and any physical exertion, nasal congestion increased. The boy stopped attending school. At the place of residence, pertussis-parapertussis and chlamydial-mycoplasma infections were excluded, X-ray examination was performed twice to rule out pneumonia. In therapy for two months, inhalations of berodual, pulmicort in high doses, ascoril, antihistamines, 3 courses of antibiotics, lazolvan, singular, intranasal anti-inflammatory drugs with insufficient effect were used: a painful paroxysmal spasmodic cough and persistent nasal congestion persisted. Upon admission to the clinic, there was a rough paroxysmal cough; there was no dyspnea at rest; physical development above average, disharmonious due to overweight(height 181 cm, weight 88 kg); signs of peripheral osteoarthropathy are not expressed; the chest is not deformed; percussion sound with a box shade; in the lungs against the background of hard breathing during forced exhalation, single wet and dry wheezing rales were heard. When examined in general blood tests, urine, biochemical blood tests - without pathological changes. Allergological examination revealed a significant sensitization to the mold of the genus Alternariana against the background of a normal level of total IgE. Plain chest x-ray showed signs of obstructive syndrome, bronchitis. When conducting spirometry, a moderate decrease in VC and FVC was noted, forced expiratory rate indicators were within the proper values, a test with dosed physical activity did not reveal significantly post-exercise bronchospasm. Attention was drawn to the normal level of nitric oxide in the exhaled air (FeNO = 12.5 ppb at a rate of 10-25ppb), as well as a moderate increase in carbon monoxide in the exhaled air (COex = 4ppm at a rate of up to 2ppm), which is pathognomonic for active smoking (although the patient claimed to use nicotine-free vaping mixtures (!)). During body plethysmography, the presence of obstructive disorders detected radiographically was confirmed: a pronounced increase in the residual volume of the lungs and its contribution to the total lung capacity. Diaskintest was negative, which ruled out tuberculosis. When examined for markers of persistent infections, immunoglobulins of the IgG class to respiratory chlamydia were detected in low titers. An ENT doctor diagnosed allergic rhinitis. When clarifying the anamnesis, it turned out that from 12 to 14 years old, the teenager regularly smoked electronic cigarettes with a low nicotine content; has been vaping since the age of 15, using vapor inhalations of various aromatic mixtures without nicotine. The patient strongly believes that vaping is a safe alternative to active smoking. From the words, he uses only expensive devices and liquids for vaping, spends a lot of time in vaping companies, where he tries different mixtures for vaping. Parents are not informed about possible consequences vaping and finance it, while set on active drug treatment of cough, as "it interferes with schoolwork."

Thus, based on the history and the results of the examination, the following diagnosis was established: Chronic obstructive bronchitis (J 44.8). allergic rhinitis(J 31.0).

An explanatory conversation was held with parents and a teenager, recommendations were given on the categorical refusal to use steam inhalers and smoking. In order to achieve stabilization of the condition and relief of obsessive cough, it was necessary for another 2 months. use inhaled steroids in high doses in combination with combined bronchodilators through a nebulizer, followed by switching to taking a combined inhaled corticosteroid in high doses (symbicort) while taking an antileukotriene drug (montelukast) for 6 months.

To date, more than 500 brands of devices designed for “soaring” and almost 8,000 types of liquids with and without nicotine are being sold in the world, the vapors of which are inhaled. It has been found that between high school students' fascination with electronic cigarettes and vaporizers has tripled. It is believed that the number of teen vapers already exceeds the number of teens who smoke conventional cigarettes.

Vaping liquids are known to contain glycerin, propylene glycol, distilled water, and various flavors. Propylene glycol and glycerin - two-and trihydric alcohols, viscous, colorless liquids; widely used in household chemicals, cosmetics, are permitted as food additives (E1520 and E422). When heated, propylene glycol (bp.=187°C) and glycerin (b.p.=290°C) evaporate with the formation of a number of carcinogens: formaldehyde, propylene oxide, glycidol, etc. It has been shown that lung tissue cells respond to exposure to water vapor from vaping, as well as to exposure to cigarette smoke, which increases the likelihood of developing lung cancer (compared to non-smokers). To date, some US states equate vapers to smokers, they are prohibited from vaping on board aircraft, in in public places and in stores.

According to the FDA (Food and Drug Administration, USA - US Food and Drug Administration), liquids for electronic devices may contain 31 toxic chemicals, including acrolein, diacetyl and formaldehyde, the levels of which increase depending on temperature and type of devices. Thus, liquids in these devices can be heated up to 300°C (for example, Tbp. acrolein = 52.7°C), which entails the release of substances hazardous to health. In addition, in experiments on animals after vaping, the development of acute lung failure up to half an hour. In addition, only in 8 months of 2016, 15 people were treated with burns to the face, hands, thighs and groin, which were obtained as a result of the explosion of electronic cigarettes and steam devices; most patients required skin grafting.

In Russia, there are no strict legal restrictions on electronic cigarettes and vaporizers, and statistics of related diseases are not kept; we came across a single report of the death of a 15-year-old teenager from the Leningrad region after using a steam inhaler due to acute respiratory failure. Electronic cigarettes and vaporizers are currently certified as electronic devices - neither their effectiveness in trying to quit smoking, such as nicotine replacement drugs (chewing gum, patches), nor the composition of the contents of cartridges and liquids are tested. Electronic cigarettes and vaping devices are freely available (including in large shopping centers and on the Internet).

Therefore, an important task of modern pediatricians and pulmonologists is to create effective barriers to the "rejuvenation" of COPD. To this end, it is advisable to recommend anonymous surveys of children and adolescents to identify the prevalence of smoking, the use of electronic cigarettes and vaporizers, regular monitoring using portable spirometers, CO analyzers and determining the level of cotinine. An active educational position of the medical community can be facilitated by amendments to existing legislative acts on the mandatory certification of electronic cigarettes and vapor inhalers, as well as liquids for them as medical devices; their free sale to persons under 18 years of age should also be restricted. In addition, it is necessary to involve the media in the discussion of this topic, including through the use of Internet resources and television.

Before it's too late, we must make every effort so that COPD does not have a chance to become a reality in childhood!

The bibliography is under revision.

Therapy-Chronic obstructive pulmonary disease in children

E.V. Klimanskaya

Doctor of Medical Sciences, Professor, Head. Laboratory of Endoscopy in Pediatrics at the Department of Children's Diseases of the Moscow Medical Academy. THEM. Sechenov, Moscow

Chronic obstructive pulmonary disease (COPD) is a heterogeneous group of diseases caused by impaired airway patency. Under the violation of the patency of the respiratory tract is understood such a condition of the bronchi and lungs, which prevents pulmonary ventilation and outflow of bronchial contents. In children of the first years of life, violations of the free patency of the respiratory tract to a greater or lesser extent accompany many bronchopulmonary diseases, manifested broncho-obstructive syndrome(BOS), which is understood as a symptom complex, including cough, cyanosis, shortness of breath.

In the last two decades, the spectrum of chronic inflammatory lung pathology has undergone significant changes, which decisively affected the modern characteristics of its structure. The incidence of allergic diseases has increased significantly, while bronchial asthma is gaining more and more weight. Epidemiological studies testify to the negative trend in the increase in the incidence of bronchial asthma, especially in children, according to which currently 4 to 8% of the population suffer from bronchial asthma, and in childhood this figure increases to 10%.

Beginning in childhood, respiratory diseases leading to obstructive syndrome are the most common cause of disability and premature disability. Therefore, the problem of COPD is becoming more and more important every year.

Etiology and pathogenesis

The causes of stenosing lesions of the respiratory tract in children are different. These lesions may be due to malformations, acquired and traumatic injuries, etc. But most often they are the result of inflammatory bronchopulmonary diseases. Bronchial obstruction occurs as a result of exposure to intra- and extra-bronchial factors. The former plays a dominant role in the development of obstructive lesions of the respiratory tract - these are inflammatory changes in the mucous membrane with hypersecretion, dyskrinia and congestion, various mechanical obstacles. Extrabronchial factors - enlarged mediastinal lymph nodes, parabronchial cysts and tumors, abnormal vessels - put pressure on the bronchi from the outside.

The symptomatology of biofeedback is determined by the leading link in pathogenesis, which has its own characteristics in various nosological forms. The basis for biofeedback in case of insufficiency of the muscular-elastic frame of the bronchi are dyskinesia and abrupt changes in the lumen of the lower respiratory tract during breathing and coughing. Profound disturbances in the mucociliary transport system, causing obstruction and shortness of breath, are observed with congenital defects in the structure of the ciliated cells of the respiratory apparatus, with pathological viscosity of an altered physical and chemical composition bronchial secretions. Developing on the basis of chronic allergic inflammation bronchospasm, hypersecretion, dyskrinia, and mucosal edema are essential pathophysiological components of asthma attacks.

Development of violations bronchial patency age-related anatomical and physiological features of the respiratory organs contribute, among which the most important are the narrowness of the airways, the softness and compliance of their cartilaginous framework, the tendency of the mucous membrane to generalized edema and swelling.

The free patency of the bronchi is directly dependent on the mechanisms of self-purification of the lungs: bronchial peristalsis, the activity of the ciliated epithelium of the mucous membranes of the respiratory tract, cough, which accelerates the movement of mucus through the bronchi and trachea. In young children, due to the weakness of the respiratory muscles and the small amplitude of movement of the ribs and diaphragm, the cough impulse is weak and ineffective, the excitability of the respiratory center is reduced, and the lumen of narrow airways with pliable walls decreases even with their slight swelling. Therefore, in children it is much easier than in adults, there may be a violation of the patency of the bronchi.

Pathomorphology

Pathological changes in the lungs are largely determined by the size of the narrowing and the duration of its existence. According to the generally accepted classification of bronchial obstruction disorders (C.Jackson), there are three degrees of bronchial constriction.

At first degree the lumen of the bronchus is narrowed slightly. As a result, during inspiration, less air enters the corresponding segments of the lung than other areas. Coming obstructive hypoventilation.

With the second degree of bronchial obstruction, only a small free space remains for the passage of air, a so-called valve mechanism is created. During inhalation, when the bronchi expand, air partially enters below the obstruction. On exhalation, the bronchi collapse, preventing the reverse flow of air. Repeated respiratory movements under such conditions lead to swelling of the corresponding section of the lung parenchyma. Obstructive emphysema develops. The degree of lung swelling depends on the duration of the valve mechanism and the conditions for air circulation through the narrowed lumen of the bronchus.

In the third degree of violation of bronchial patency, the bronchus is completely obstructed and air does not penetrate into the lung. The air contained in the parenchyma is rapidly absorbed, and obstructive atelectasis develops. In the zone of atelectasis, favorable conditions are created for the reproduction of microbes and the development inflammatory process, the course and outcome of which depend on the duration of the existence of occlusion.

Classification

To date, no unified classification of COPD has been formulated. it not an easy task, since it is necessary to combine diseases that are different in etiology and pathogenesis into a single group. Approaches to diagnosis and subsequent therapy are largely determined by pathogenesis. They are not the same with common types of bronchial obstruction and with limited bronchial lesions, with congenital pathology or acquired diseases. Therefore, when systematizing COPD, it seems important to group them taking into account the localization of pathological changes that cause obstruction, etiology and nosological forms.

Table 1. Classification of COPD in children

Tracheobronchomalacia, tracheobronchomegaly (Mounier-Kuhn syndrome), Williams-Campbell syndrome.

Primary ciliary dyskinesia, immovable cilia syndrome, Kartagener's syndrome.

Anomaly of the aorta (double arch) and pulmonary artery

Recurrent and chronic obstructive bronchitis.

Diagnostics

The negative trend towards irreversible pathoanatomical changes in COPD requires their earliest possible recognition and individual therapy, the purpose of which is to eliminate bronchial obstruction. The BOS symptom complex leading in COPD should not become self-sufficient when making a diagnosis. Diagnosis should be carried out based on the results of a comprehensive examination, highlighting the decisive diagnostic signs(see table 2).

Table 2. Differential diagnosis of COPD in children

At history taking important information about the presence of pulmonary pathology in the family, the frequency of spontaneous abortions and stillbirths, the presence of closely related marriages. Information about the course of pregnancy and childbirth is also extremely important (medication, alcohol, occupational hazards). These data contribute to improving the efficiency of diagnosing congenital diseases. Allergological vigilance in the collection of anamnesis will help to avoid errors in recognition allergic diseases.

The variety of symptoms and early onset of infectious complications make it difficult to clinically recognize COPD. Along with this, it is possible to identify some diagnostic features due to etiological and pathogenetic factors.

An important role is given to the results of the study of the function of external respiration (RF). For COPD, the most typical obstructive type of violations of respiratory function. The fact of reversibility of functional disorders or their progression can be used in the differential diagnosis of bronchial asthma and other COPD.

Clinical signs of congenital diseases appear early, in the first year of life, most often against the background of an associated infection. Subsequently, diseases common type violations of bronchial patency are manifested by symptoms of chronic non-specific inflammation, characterized by an undulating course with periods of exacerbation, the presence of a wet productive cough with purulent or purulent-mucous sputum, moist widespread rales in the lungs. Many patients with congenital broncho-obstructive diseases lag behind in physical development, are emaciated, have deformity nail phalanges in the form of drum sticks. An x-ray examination reveals changes characteristic of chronic bronchopulmonary inflammation: deformation of the lung pattern, isolated shadows of compacted lung tissue, mediastinal displacement with a decrease in lung volumes. Plain radiography confirms the reverse arrangement of organs and the diagnosis of Kartagener's syndrome.

Contrasting bronchi - bronchography - with exhaustive completeness provides data on the morphological deformation of the bronchi and allows you to diagnose such nosological forms as Mounier-Kuhn and Williams-Campbell syndromes. During bronchoscopy, along with nonspecific inflammatory changes symptoms typical of some defects are found: excessive mobility and sagging of the posterior membranous wall of the trachea and bronchi in tracheobronchomalacia, pronounced folding of the tracheal walls with prolapse of intercartilaginous spaces, a symptom of "loss of light" in tracheobronchomegaly (Mounier-Kuhn's syndrome).

History, characteristic appearance, elevated sweat electrolytes, and genetic testing are diagnostic of cystic fibrosis.

AT clinical picture local types obstruction, respiratory disorders come to the fore. The most important diagnostic symptom is shortness of breath on exhalation, accompanied by noise - expiratory stridor. However, pure expiratory stridor is rare. With high localization of stenosis, both inhalation and exhalation are difficult (mixed stridor). Depending on the degree of narrowing, participation of auxiliary muscles, retraction of compliant chest areas, and cyanosis are noted. With local types of obstruction, X-ray examination, including layer-by-layer, in some cases can help to make not only a symptomatic, but also an etiological diagnosis. With stenosis of the trachea and large bronchi, radiographs show a break or narrowing of the air column, and with neoplasms, the shadow of the tumor and the narrowing of the lumen caused by it.

Bronchoscopy is an objective research method that allows identifying endobronchial causes of stenosis and making a final etiological diagnosis. The endoscopic picture in congenital stenosis is quite typical. The lumen of the trachea looks like a narrow ring bordered by a whitish cartilage without a membranous part. Cystic formations are located eccentrically and cause narrowing of varying degrees. Compression stenoses of the trachea caused by an anomaly large vessels, are characterized by narrowing the lumen of the anterior and lateral walls of the suprabifurcation part of the trachea. In this case, a clear pulsation is determined. Comprehensive data allows you to get aortography.

At acquired local obstructive lesions, the importance of anamnestic information about possible aspiration of a foreign body, traumatic injuries of the respiratory tract (burn), instrumental interventions (intubation), etc. is undoubted. X-ray examination helps to clarify this information. However, the final diagnosis, as with congenital stenosis, is possible only with bronchoscopy.

A special problem is the differential diagnosis of bronchial asthma. As mentioned earlier, bronchial asthma dominates among obstructive diseases, the frequency of which has increased in last years not only in the population as a whole, but also in children under 5 years of age, in whom its diagnosis mainly presents certain difficulties, due primarily to the fact that one of the leading criteria for bronchial asthma - recurrent BOS - is clinically indistinguishable at an early age, regardless on whether it develops on the background of atopy (bronchial asthma) or as a result of inflammatory edema mucous membrane caused by a viral infection (obstructive bronchitis). Obstructive conditions against the background of a respiratory viral infection are recorded in 10-30% of infants, and only a third of them are a manifestation of bronchial asthma. At the same time, hiding under the guise of a viral disease, bronchial asthma at this age is often not recognized for a long time. At the same time, BOS polymorphism significantly complicates clinical recognition of etiology and topical diagnosis of the level of bronchial obstruction. It leads to misdiagnosis bronchial asthma, for which patients with various congenital and acquired bronchopulmonary diseases are treated for a long time and unsuccessfully.

Indications of a hereditary burden for allergic diseases, allergic reactions to food and medicine, a clear effect of bronchodilator therapy with the exclusion of congenital and acquired obstructive diseases can help clarify the likelihood and make a final diagnosis of bronchial asthma. In children older than 6 years, the results of the study of respiratory function can provide some assistance in the differential diagnosis of bronchial asthma. An important difference between asthma and other COPD is the reversibility of obstruction and functional parameters. However, in some cases, even the entire complex of modern clinical, radiological and laboratory (determination of the level of general and specific IgE, skin allergic tests) studies is insufficient for a reliable diagnosis of bronchial asthma, and the true nature of the disease can only be clarified by bronchoscopy with a biopsy of the mucous membrane.

In conclusion, it should be repeated that in recent years the incidence of COPD among children has increased significantly and their etiological structure has changed significantly. Due to the uniformity of clinical symptoms, COPD is often diagnosed with a delay, already with a progressive course of the disease, and is the most common cause of disability in children. Introduction into clinical practice of modern instrumental, laboratory and radiological methods The study allowed a new approach to explaining the mechanisms of development of broncho-obstructive diseases and their diagnosis. Timely etiological diagnosis is necessary for targeted therapy and prevention of irreversible changes in the respiratory system.

Literature:

Kaganov S.Yu. Modern problems of pediatric pulmonology. Pulmonology 1992; 2:6-12.
Sears M R. Descriptive epidemiology of asthma. Lancet 1997; 350 (suppl 11): 1-4.
Johansen H, Dutta M, Mao Ychagani K, Sladecek I. An investigation of the increase in preschool-age asthma in Manitoba. Canada Health Rep 1992; four:.
Kaganov S.Yu., Rozinova N.N., Sokolova L.V. Difficulties and errors in the diagnosis of bronchial asthma in children. Russian Bulletin of Perinatology and Pediatrics 1993; 4:13-8.
Dodge R R, Burrows B: The prevalence and incidence of asthma and asthma-like symptoms in a general population sample. Am Rev Respir Dis 1980; 122(4):.
Brandt PL, Hoekstra MO. Diagnosis and treatment of recurrent coughing and wheezing in children younger than 4 years old. Ned Tijdschr Geneeskd 1997; 141:467-7.
Foucard T. The wheezy child. Acta Paediatr Scand 1985; 74(2): 172-8.
Rabbit E.B., Lukina O.F., Reutova V.S., Dorokhova N.F. Broncho-obstructive syndrome in ARVI in young children. Pediatrics 1990; 3:8-13.
Klimanskaya E.V., Sosyura V.Kh. Bronchoscopy under anesthesia in children with bronchial asthma. Pediatrics 1968; 9:39-42.

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S. E. Dyakova, Candidate of Medical Sciences, Leading Researcher, Yu. Yu. E. Veltishcheva, Moscow

Considering the prevalence of electronic cigarettes and steam inhalers among children and adolescents and based on real clinical practice, it should be stated that chronic obstructive bronchitis, which is one of the forms of chronic obstructive pulmonary disease (COPD), can debut in childhood, which previously seemed impossible.
Keywords Key words: children, smoking, electronic cigarettes, vaping, chronic obstructive pulmonary disease (COPD)
key words: children, smoking, e-cigarettes, vaping, chronic obstructive pulmonary disease (COPD)

To date, COPD is understood as an independent disease, which is characterized by a partially irreversible restriction of airflow in the respiratory tract, which, as a rule, is steadily progressive and provoked by an abnormal inflammatory response of lung tissue to irritation by various pathogenic particles and gases. In response to the impact of external pathogenic factors, the function of the secretory apparatus changes (mucus hypersecretion, changes in the viscosity of the bronchial secretion) and a cascade of reactions develops, leading to damage to the bronchi, bronchioles and adjacent alveoli. Violation of the ratio of proteolytic enzymes and antiproteases, defects in the antioxidant defense of the lungs exacerbate damage.

The prevalence of COPD in the general population is about 1% and increases with age, reaching 10% in people over 40 years of age. According to WHO experts, by 2020 COPD will become the third leading cause of morbidity and mortality in the world. COPD is an urgent problem, since the consequences of the disease are the limitation of physical performance and disability of patients, including modern children and adolescents.

As an illustration, we give the following clinical example:
Patient Yu., 16 years old, from a family with an uncomplicated allergic history ; parents and relatives smoke for a long time, maternal grandfather died of lung cancer. Household history is aggravated by living in a damp apartment where cats are kept. From the age of 3, the girl suffered from recurrent bronchitis with a lingering cough, mainly in the cold season, and repeatedly received courses of antibiotics and mucolytics on an outpatient basis. At the age of 7 she was on long-term inpatient treatment for a urinary tract infection, in the hospital for the first time she began to smoke cigarettes with other children. Subsequently, due to increased episodes of bronchitis and a long-lasting cough, she was registered with a pulmonologist at the place of residence. The disease was regarded as the onset of bronchial asthma, basic treatment was carried out with inhaled glucocorticosteroids in gradually increasing doses, due to the insufficient effect during the last year before contacting the clinic, she received a combined drug Seretide. She was repeatedly hospitalized in a hospital at the place of residence for the relief of exacerbations, inhalations with bronchodilators, mucolytics and antibacterial drugs were added to the therapy. Between exacerbations, she suffered from a paroxysmal obsessive cough (in the mornings with scanty sputum), exercise tolerance did not suffer, but the girl often complained of weakness, fatigue and headaches. She was first sent for examination to clarify the diagnosis at the age of 16. Upon admission, the state of moderate severity; complaints of unproductive cough in the morning with mucopurulent sputum; episodes of exacerbations with febrile temperature and increased cough. On examination, there is no dyspnea at rest, physical development is average, harmonious, signs of peripheral osteoarthropathy are not expressed; the chest is not deformed, the percussion sound is boxy, in the lungs, against the background of hard breathing, wet rales of various sizes are heard. When examining deviations from the indicators of general blood tests, urine, biochemical blood tests were not revealed. Immunological study of humoral and cellular immunity, phagocytic activity of neutrophils made it possible to exclude an immunodeficiency state. Allergological examination did not reveal specific sensitization to causative allergens. Morphological analysis of sputum confirmed its mucopurulent character; sputum culture revealed colonies of Staphylococcus aureus and epidermal streptococcus. The radiograph of the lungs showed signs of bronchitis and obstructive syndrome. When conducting spirometry, the volume-velocity parameters were within the proper values, the test with dosed physical activity did not reliably reveal post-exercise bronchospasm. Attention was drawn to the low level of nitric oxide in the exhaled air (FeNO=3.2 ppb at a rate of 10-25 ppb), as well as a sharp increase in carbon monoxide in the exhaled air (COex=20 ppm at a rate of less than 2 ppm), which is pathognomonic for regular active smoking. During body plethysmography, the presence of obstructive disorders detected radiographically was confirmed: a sharp increase in the residual volume of the lungs and its contribution to the total lung capacity. Diaskintest was negative, which ruled out the presence of tuberculosis. The level of sweat chlorides was within the normal range, which disproved the presence of cystic fibrosis.
Markers of persistent viral and bacterial infections were not identified. A carefully collected anamnesis made it possible to clarify that from the age of seven to the present, the girl regularly smoked actively (from ½ to 1 pack of cigarettes per day), i.e. smoking experience by the time of contacting the clinic was 8 years. In her family, parents and close relatives smoked, cigarettes were in the public domain.
At the same time, the girl's parents, knowing about her smoking, did not connect the child's complaints of prolonged cough and repeated bronchitis with smoking and were determined to treat cough with medication. The girl independently made several unsuccessful attempts to quit smoking, but she did not turn to anyone for specialized help. Thus, based on the medical history and the results of the examination, the alleged diagnosis of bronchial asthma was not confirmed, and the patient was diagnosed with Chronic obstructive bronchitis (J 44.8). An explanatory conversation was held with the parents of the teenager and the girl herself, recommendations were given on improving the life, giving up smoking for all family members (including with the help of anti-tuxedo cabinet specialists at the place of residence) and tactics for treating the underlying disease.

In routine clinical practice, portable gas analyzers for determining the level of carbon monoxide in exhaled air (COex) have proven themselves well for detecting active smokers. Thus, in our clinic, 100 patients with bronchial asthma (BA) of varying severity aged 6–18 years (68 boys, 32 girls) were examined for CO2 content using a Smokerlyzer CO analyzer (Bedfont, England).
The simplicity of the breathing maneuver (15-second breath-hold at the height of inhalation followed by exhalation through the mouthpiece of the gas analyzer) makes the non-invasive measurement of COEX available for most children over 6 years of age. Among the surveyed, 14 active smokers aged 13 to 18 years were identified: their average COvy was 7.9 ppm (4-16 ppm) (1 ppm - 1 particle of gas per 106 particles of air); all of them were in the clinic due to the severe course of BA and denied the fact of smoking. Nineteen patients who belonged to the category of passive smokers (in their families, parents or close relatives smoked at home) had an average level of CO-exp = 1.3 ppm (0-2 ppm), which did not significantly distinguish them from the group of children not exposed to tobacco smoke (67 patients, mean COexp = 1.4ppm (0-2ppm)). However, among patients exposed to passive smoking, children with more severe BA prevailed. The results obtained indicate the potential practical significance of using CO analyzers in a children's pulmonology clinic to identify active smokers in order to conduct targeted anti-smoking programs and monitor their effectiveness.

The following clinical example is proof of this.

Patient G., 15 years old, from a family with a burdened allergic history : her mother and maternal grandmother had allergic rhinitis, her sister had atopic dermatitis.
Since the beginning of the visit to the kindergarten, he often began to suffer from respiratory infections with a prolonged cough, persistent nasal congestion was often disturbing, and during examination at the place of residence, the allergic genesis of complaints was not confirmed. With the start of school attendance, acute respiratory infections became less common, but nasal congestion persisted, and he received topical steroids with a positive effect in courses. From the age of 12, he began to periodically smoke electronic cigarettes, repeated acute respiratory infections with a prolonged cough resumed. At the age of 15, he began to use a steam inhaler with various flavoring additives. After a month of active “soaring”, against the background of subfebrile temperature, a debilitating paroxysmal cough appeared, periodically to vomiting, aggravated by laughter, deep breathing, going outside and any physical exertion, nasal congestion increased. The boy stopped attending school. At the place of residence, pertussis-parapertussis and chlamydial-mycoplasma infections were excluded, X-ray examination was performed twice to rule out pneumonia. In therapy for two months, inhalations of berodual, pulmicort in high doses, ascoril, antihistamines, 3 courses of antibiotics, lazolvan, singular, intranasal anti-inflammatory drugs with insufficient effect were used: a painful paroxysmal spasmodic cough and persistent nasal congestion persisted. Upon admission to the clinic, there was a rough paroxysmal cough; there was no dyspnea at rest; physical development above average, disharmonious due to overweight (height 181 cm, weight 88 kg); signs of peripheral osteoarthropathy are not expressed; the chest is not deformed; percussion sound with a box shade; in the lungs against the background of hard breathing during forced exhalation, single wet and dry wheezing rales were heard. When examined in general blood tests, urine, biochemical blood tests - without pathological changes. Allergological examination revealed a significant sensitization to the mold of the genus Alternariana against the background of a normal level of total IgE. Plain chest x-ray showed signs of obstructive syndrome, bronchitis. When conducting spirometry, a moderate decrease in VC and FVC was noted, forced expiratory rate indicators were within the proper values, a test with dosed physical activity did not reveal significantly post-exercise bronchospasm. Attention was drawn to the normal level of nitric oxide in the exhaled air (FeNO = 12.5 ppb at a rate of 10-25ppb), as well as a moderate increase in carbon monoxide in the exhaled air (COex = 4ppm at a rate of up to 2ppm), which is pathognomonic for active smoking (although the patient claimed to use nicotine-free vaping mixtures (! )). During body plethysmography, the presence of obstructive disorders detected radiographically was confirmed: a pronounced increase in the residual volume of the lungs and its contribution to the total lung capacity. Diaskintest was negative, which ruled out tuberculosis. When examined for markers of persistent infections, immunoglobulins of the IgG class to respiratory chlamydia were detected in low titers. An ENT doctor diagnosed allergic rhinitis. When clarifying the anamnesis, it turned out that from 12 to 14 years old, the teenager regularly smoked electronic cigarettes with a low nicotine content; has been vaping since the age of 15, using vapor inhalations of various aromatic mixtures without nicotine. The patient strongly believes that vaping is a safe alternative to active smoking. From the words, he uses only expensive devices and liquids for vaping, spends a lot of time in vaping companies, where he tries different mixtures for vaping. Parents are not informed about the possible consequences of vaping and finance it, while they are set on active drug treatment of cough, as "it interferes with schoolwork."

Thus, based on the history and the results of the examination, the following diagnosis was established: Chronic obstructive bronchitis (J 44.8). Allergic rhinitis (J 31.0).

To date, more than 500 brands of devices designed for “soaring” and almost 8,000 types of liquids with and without nicotine are being sold in the world, the vapors of which are inhaled. It was found that between 2013-2014. high school students' fascination with electronic cigarettes and vaporizers has tripled. It is believed that the number of teen vapers already exceeds the number of teens who smoke conventional cigarettes.

Vaping liquids are known to contain glycerin, propylene glycol, distilled water, and various flavors. Propylene glycol and glycerin - two-and trihydric alcohols, viscous, colorless liquids; widely used in household chemicals, cosmetics, allowed as food additives (E1520 and E422). When heated, propylene glycol (bp.=187°C) and glycerin (b.p.=290°C) evaporate with the formation of a number of carcinogens: formaldehyde, propylene oxide, glycidol, etc. It has been proven that lung tissue cells respond to exposure to water vapor from vaping, as they do to exposure to cigarette smoke, which increases the likelihood of developing lung cancer (compared to non-smokers). To date, some US states equate vapers with smokers, they are prohibited from vaping on board aircraft, in public places and in stores.

According to the FDA (Food and Drug Administration, USA - US Food and Drug Administration), liquids for electronic devices may contain 31 toxic chemicals, including acrolein, diacetyl and formaldehyde, the levels of which increase depending on temperature and type of devices. Thus, liquids in these devices can be heated up to 300°C (for example, Tbp. acrolein = 52.7°C), which entails the release of substances hazardous to health. In addition, in experiments on animals after vaping, the development of acute pulmonary insufficiency lasting up to half an hour was recorded. In addition, only in 8 months of 2016, 15 people were treated with burns to the face, hands, thighs and groin, which were obtained as a result of the explosion of electronic cigarettes and steam devices; most patients required skin grafting.

Before it's too late, we must make every effort so that COPD does not have a chance to become a reality in childhood!

The bibliography is under revision.

Chronic obstructive pulmonary disease (COPD) is considered a disease of people over 40 years of age. The main cause of the disease is long-term smoking or inhalation of other particles and gases. The definition of COPD noted its characteristic irreversible airflow limitation, which is progressive in nature and is associated with an abnormal inflammatory response of the lungs to harmful particles and gases. It is emphasized that chronic airflow limitation is a consequence of damage to the small airways (obstructive bronchiolitis) and destruction of the lung parenchyma (emphysema). Exactly chronic inflammation small airways leads to these changes. Recent Scientific research indicate that COPD is treatable and may be preventable.

Among the causes of COPD, the main attention is paid to environmental factors such as smoking, long-term exposure to occupational factors (dust, chemical irritants, fumes) and atmospheric/household air pollution.

It is known that not all risk factors cause COPD. The mechanisms by which this disease occurs are still largely unexplored, and it is possible that chronic inflammatory diseases lungs, arising in childhood, continuing in adolescents and passing to adults. First of all, these are diseases that cover both lungs and occur with a predominant lesion of the small airways and lung parenchyma. There is evidence that antenatal lung injury may be a risk factor for COPD in adults.

The frequency of chronic lung disease (CLD) in children in Russia is not known. There are data on general respiratory morbidity and the prevalence of individual nosological forms (bronchial asthma, cystic fibrosis), as well as data from individual pulmonological centers, which differ significantly due to the ambiguous approach to diagnosing certain diseases. Official statistics do not take into account all nosological forms of CLD. The frequency of chronic lung diseases without bronchial asthma is estimated at 0.6-1.2 per 1000 children.

However, epidemiological studies of the prevalence of only bronchial asthma, conducted in children in accordance with international criteria, indicate a frequency of 4-10%.

In recent years, there has been an increase in respiratory morbidity, as well as an increase in the number of patients with chronic lung diseases and congenital malformations, which are the basis of some chronic lung diseases.

The table presents the main nosological forms of chronic lung diseases in children that meet the criteria mentioned above.

Bronchial asthma

Bronchial asthma and COPD, despite the similarity of symptoms, are various diseases. Although their combination is not excluded. Asthma is characterized by chronic eosinophilic airway inflammation regulated by CD4+ T-lymphocytes, while in COPD inflammation is neutrophilic in nature and is characterized by an increased content of macrophages and CD8+ T-lymphocytes. In addition, airflow limitation in asthma may be completely reversible. Asthma is considered a risk factor for the development of COPD. Smokers with asthma develop lung function decline faster than non-asthma smokers. Despite the more favorable course of bronchial asthma in children, in most patients, the symptoms of the disease persist into adolescence. Currently, the proportion of adolescents among children with asthma is 36-40%. Moreover, 20% of adolescents develop a more severe course of the disease, and 33% have a stable course of the disease. 10% of adolescents have persistent respiratory dysfunction (RF) in the absence of clinical symptoms of asthma.

Since asthma is the most common chronic lung disease in childhood and its frequency is increasing, these patients should be considered as a risk group due to possible development COPD

Malformations of the trachea, bronchi, lungs and pulmonary vessels

This group of diseases includes malformations associated with underdevelopment of bronchopulmonary structures: agenesis, aplasia, lung hypoplasia; malformations of the wall of the trachea and bronchi, both common and limited, pulmonary cysts, sequestration of the lungs, malformations of the pulmonary veins, arteries and lymphatic vessels. Many malformations are the cause of recurrence of bronchopulmonary inflammation and form the basis for the secondary formation of a chronic inflammatory process.

As a possible basis for the formation of COPD, common malformations of the bronchi (bronchomalacia, tracheobronchomalacia, Williams-Campbell syndrome) are of the greatest interest. Depending on the prevalence and degree of bronchial damage, clinical symptoms can vary from recurrent obstructive bronchitis to severe chronic bronchopulmonary process with hypoxemia, respiratory failure, purulent endobronchitis, formation cor pulmonale. Recent symptoms more characteristic of Williams-Campbell syndrome. Clinical symptoms are characterized by: wet cough, shortness of breath, deformity of the chest, the presence of widespread moist mixed and dry rales. Obstructive syndrome is a consequence of underdevelopment of the cartilage framework and increased mobility walls of the bronchi, as well as a bacterial inflammatory process that quickly forms in the bronchial tree. In the study of FVD revealed combined disorders ventilation with a predominance of obstruction. Endobronchitis visually has a catarrhal or purulent character, with pronounced neutrophilic cytosis.

Age dynamics depends on the prevalence of the process and the effectiveness of therapeutic and preventive measures. In most patients, the condition improves and stabilizes; over 18 years of age, they are observed with a diagnosis of bronchiectasis or chronic bronchitis. In some patients, cor pulmonale is formed and early disability occurs.

Obliterating bronchiolitis

Bronchiolitis obliterans is a disease of small bronchi, the morphological basis of which 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.

The disease is a consequence of bronchiolitis, an acute infectious disease that mainly affects children aged 6-24 months. In children of the first two years, the cause of the disease is most often respiratory syncytial and adenovirus (types 3, 7, 21) infection. In older children - legionella and mycoplasma. The development of the disease after lung transplantation is possible. Unilateral opaque lung syndrome (McLeod's syndrome) is a variant of this disease. Clinically, obliterating bronchiolitis is manifested by recurrent, unproductive cough, shortness of breath, broncho-obstructive syndrome, local physical data in the form of weakened breathing and fine bubbling wheezing.

The diagnosis is made on the basis of characteristic clinical findings and the presence of radiological signs of increased transparency of a part of the lung. Scintigraphy reveals a sharp decrease in blood flow in the affected area, and bronchography reveals local bronchial obliteration below generation 5-6 in the absence of signs of pneumosclerosis. Bronchoscopy often reveals catarrhal endobronchitis. Most patients (75%) are characterized by persistent obstructive ventilation disorders and moderate hypoxemia.

The age dynamics of the disease depends on the extent of the lesion. The absence of progression of obliteration of bronchioles and ventilation disorders is characteristic, but with a bilateral process, the development of cor pulmonale and early disability of patients is possible. The disease, with a lesion volume of no more than one lobe of the lung, has a favorable prognosis, but signs of chronic obstructive bronchitis persist.

Chronical bronchitis

The disease is characterized by a diffuse lesion of the bronchial tree, a chronic course with periods of exacerbation and remission [at least two or three exacerbations in two consecutive years], a productive cough, and persistent, moist rales of various sizes in the lungs. In children, a disease similar to chronic bronchitis in adults is rare. Most often, chronic bronchitis is a symptom of other chronic lung diseases and is diagnosed with the exclusion of bronchial asthma, local pneumosclerosis, cystic fibrosis, ciliary dyskinesia syndrome, immunodeficiency states and other chronic lung diseases. In adolescents, chronic bronchitis may occur due to causes that cause chronic bronchitis in adults (smoking, occupational hazards, environmental pollution).

Diagnostic criteria: wet cough, diffuse moist rales in the lungs in the presence of 2-3 exacerbations of diseases per year for two years.

Age dynamics: depends on the underlying disease.

Bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic lung disease in children during the first two years of life that occurs in the perinatal period, mainly in very preterm infants receiving respiratory therapy in the neonatal period, occurring with a predominant lesion of the bronchioles and lung parenchyma, the development of emphysema, fibrosis, and/or impaired replication alveoli, manifested by oxygen dependence at the age of 28 days of life and older, respiratory failure, broncho-obstructive syndrome, radiographic changes and characterized by regression of clinical manifestations as the child grows.

The cause of BPD is more often rigid modes of artificial lung ventilation (ALV) with high concentrations of oxygen and/or high pressure on the inhale. Usually develops in the treatment of severe syndrome respiratory disorders. There is evidence of a hereditary predisposition to BPD.

The disease is based on a violation of the architectonics of the lung tissue and, often, bronchial hyperreactivity. Pathological processes develop in the first days of life in the form interstitial edema with hyaline membranes, atelectasis, alternating with areas of emphysema. In the next 15-20 days, metaplasia and hyperplasia of the epithelium and the muscular layer of the small bronchi develops, which leads to progressive atrophy of the alveolar parenchyma. In the second month, the process ends with massive fibrosis with destruction of the alveoli, the formation of bullous areas in the lung, a reduction in blood flow, and often right ventricular failure. Violation of gas exchange in the lung can lead to the need for prolonged mechanical ventilation.

Clinically manifested by hypoxemia, respiratory failure, symptoms of bronchial obstruction; X-ray usually reveals gross changes in the form of fibrosis, cysts, changes in the transparency of the lung tissue, bronchial deformities.

Age dynamics. Most children, even those with severe forms of bronchopulmonary dysplasia, tend to improve over time. By the age of five, the functional state of the respiratory system becomes comparable to the development of the respiratory system in their peers. . At an early age, signs of obstruction of the small bronchi are noted. In many children, the course of the disease is complicated by airway hyperreactivity, which leads to the need for their hospitalization for acute viral diseases and puts children at risk for developing asthma. Long-term prognosis is difficult because patients who this pathology was first isolated into an independent nosological form, by now they have reached only the period of puberty.

Interstitial lung disease

Of this group of diseases, the chronic variant of the course of hypersensitivity pneumonitis (exogenous allergic alveolitis).

Exogenous allergic alveolitis is an immunopathological disease caused by inhalation of organic dust containing various antigens, and manifested by diffuse damage to the alveolar and interstitial tissue of the lung, followed by the development of pneumofibrosis. The course of the disease is characterized by cough, diffuse crepitating and finely bubbling rales, shortness of breath, restrictive and obstructive ventilation disorders. An indication of contact with the source of the causally significant allergen is required. Radiologically it is characterized by diffuse infiltrative and interstitial changes.

Age dynamics. The disease is more often detected in school-age children and is characterized by a slowly progressive course. The use of modern methods of therapy makes it possible to achieve a long-term remission.

Other variants of alveolitis can either be cured in childhood (acute exogenous allergic alveolitis), or have a rapidly progressive course with poor prognosis(idiopathic fibrosing alveolitis).

Alpha-1 antitrypsin deficiency

Alpha-1-antitrypsin (A-1-AT) is a protein produced by liver cells. Its main function is a blocking action against the elastase enzyme produced by leukocytes to destroy microorganisms and the smallest inhaled particles. A-1-AT inactivates excess elastase, and in its absence, elastase has a damaging effect on the alveolar structures of the lungs, causing the development of emphysema. 24 variants of the A-1-AT molecule have been identified, which are encoded by a series of co-dominant alleles, designated as the Pi system. The majority (90%) of people are homozygous for the M gene (PiM phenotype), 2-3% - PiMZ, 3-5% - PiMS (i.e., heterozygous for the M gene) and provide a normal level of A-1-AT in serum blood (20-53 mmol/L or 150-350 mg/dL). Most often, A-1-AT deficiency is associated with the Z allele or PiZ (ZZ) homozygotes. The content of A-1-AT in these patients is 10-15% of the norm. The concentration of A-1-AT above 11 mmol/L is considered protective. Emphysema develops if the A-1-AT level is below 9 mmol/L. Other genotypes are associated with the PiSZ, PiZ/Null and PiNull alleles. The role of A-1-AT deficiency in the pathogenesis of COPD has been reported. The disease is characterized by the formation of panlobular emphysema. Deficiency of A-1-AT usually begins to manifest itself at the age of 35-40 years with moderate dyspnea, increased transparency of the lung fields (especially the lower areas) and irreversible obstructive changes. Over time, emphysema intensifies, signs of chronic bronchitis develop; smoking and repeated lung infections speed up the process. In adolescents, cases of progressive emphysema have been described, but in young children the disease does not reveal specific features: acute respiratory diseases in them can occur with an obstructive syndrome or recurrent bronchitis. The question of A-1-AT deficiency arises in children with severe diffuse emphysema on x-ray, persistent obstruction, and impaired pulmonary blood flow. Impoverishment of blood flow in areas of the lungs may be the first manifestation of the disease; repeated pneumonias with the rapid formation of bullous emphysema are also described.

ciliary dyskinesia syndrome

The disease is based on a hereditary defect of the ciliary epithelium - the absence of dynein handles and the dislocation of internal structures in the cilia of the ciliary epithelium. The consequence of this is the stagnation of secretions in the respiratory tract, infection and the formation of a chronic inflammatory process. Dysfunction of the ciliary epithelium can be combined with immobility of spermatozoa in men and dysfunction of the epithelium of the fallopian tubes in women. Kartagener's syndrome (reversed position of internal organs, chronic sinusitis and bronchiectasis) is a special case of ciliary dyskinesia syndrome. Clinical manifestations usually occur at an early age. After repeated diseases of the upper respiratory tract, bronchitis and pneumonia, signs of a chronic bronchopulmonary process are revealed. Typically, persistent, difficult-to-treat lesions of the nasopharynx (chronic sinusitis, rhinitis, adenoiditis) are also typical. In some patients, a deformity of the chest and changes in the terminal phalanges of the fingers are formed according to the type of "drumsticks". The main type of pulmonary changes is limited pneumosclerosis with deformation of the bronchi, often bilateral. A common purulent endobronchitis, which has a persistent course, is characteristic. In patients with Kartagener's syndrome, other defects (heart, kidney), as well as hypofunction of the endocrine glands, are also described.

Ciliary dyskinesia in the absence of a reverse arrangement of organs is also manifested by repeated bronchitis and pneumonia, the development of chronic bronchitis, but in many patients a gross pathology of the lungs does not develop, which is obviously associated with a lesser degree of dysfunction of the cilia. The diagnosis is confirmed by electron microscopy of a biopsy of the nasal or bronchial mucosa, as well as by the study of the mobility of cilia in a phase-contrast microscope.

In patients with ciliary epithelial dysfunction syndrome, with age, there is a positive trend in the course of the disease, although signs of chronic bronchitis and chronic sinusitis persist. In patients with Kartagener's syndrome, with insufficiently effective therapy, it is possible to develop widespread pneumosclerotic changes in the lungs and the formation of cor pulmonale.

It should be noted that a number of hereditary diseases, such as cystic fibrosis, immunodeficiency states, occur with chronic lesion lungs. However, these diseases, as a rule, manifest in early childhood, occur with purulent endobronchitis and respiratory failure. The prognosis of these diseases is serious.

Environmental factors are mentioned among the main causes of COPD. The same reasons contribute to the formation of chronic lung diseases in children and adolescents. First, it is tobacco smoking. According to the Ministry of Health and Social Development of the Russian Federation, 8-12 percent of schoolchildren in grades 7-8 systematically smoke. By the 11th grade of the school, about half of the boys and a quarter of the girls already smoke. In Moscow (2000 data) 36.9% of adolescents start smoking before the age of 13. 79.9% of boys and 73.7% of girls have tried smoking, and 52% of 11th grade students smoke systematically. More than 60% of non-smokers are forced to inhale ambient tobacco smoke for at least an hour a week. Second hand smoke 2-3 times increases the respiratory morbidity of young children and, in particular, recurrent bronchitis. At the same time, there is a direct dependence of the incidence on the number of cigarettes smoked by parents.

Air pollution from industrial emissions adversely affects the function of the respiratory system. The main polluting factors are dust particles and gases (SO2, nitrogen oxides, phenols and other organic substances) that irritate mucous membranes.

Short-term emission peaks under adverse weather conditions lead to an increase in the number of bronchitis and laryngitis, obstructive episodes in children with asthma, observed over the next few days.

With prolonged exposure, there is a decrease in the functional parameters of respiration, an increase in the reactivity of the bronchi. In areas of industrial air pollution, the percentage of frequently ill children and the frequency of recurrent bronchitis, including obstructive ones, are high, which is especially pronounced in preschoolers. The prevalence of these types of pathology at school age is reduced, but in a large percentage of schoolchildren, the speed indicators of respiratory function remain reduced by 10-20%. This decrease is all the more pronounced, the longer the period of residence of the child in the gassed area. Children practically do not have specific dust diseases (silicosis, asbestosis, etc.).

In microdistricts adjacent to enterprises whose emissions contain organic dust (mold spores, down and feathers, flour, wood and straw dust), the number of allergic diseases (asthma, alveolitis) is growing. Increased allergization is also noted in areas near gas stations. Open fire strongly pollutes the air, especially kitchen gas stoves, especially with insufficient ventilation; the concentration of nitrogen oxides in a kitchen with a gas stove can reach a high level; respiratory morbidity in children living in apartments with gas stoves is higher than in apartments with electric stoves. Jedrychowski W. et al. attempted to determine how postnatal indoor air quality affects lung function in schoolchildren. After examining 1096 children, the authors found that a decrease in respiratory function may be associated with air pollution in residential premises when using stove heating and prolonged exposure of children to environmentally unfavorable conditions.

Low socioeconomic status is known to lead to increased respiratory morbidity. But in our country, such systematic studies have not yet been carried out.

Conclusion

Thus, none of the chronic lung diseases that occur in childhood is an analogue of COPD in adults in the sense that corresponds to this nosological form at present. But a number of diseases and environmental factors can contribute to the occurrence of this disease. The role of these conditions in the pathogenesis of COPD deserves further study.

What are the options for COPD prevention in childhood?

First of all, it is the prevention of smoking in children and adolescents. A number of measures are needed to help reduce the number of teenagers who smoke, to ensure the prevention of passive smoking in children and smoking in pregnant women.

Prevention respiratory infections, such as respiratory syncytial virus, adenovirus, will lead to a decrease in the frequency of chronic bronchiolitis, which may be one of the causes of COPD. The use of methods of immunization of the child population will help reduce the incidence of these infections.

Improving the system of nursing premature babies, the use of sparing methods of mechanical ventilation will reduce the incidence of bronchopulmonary dysplasia.

The best way to prevent COPD lies in optimizing fetal antenatal health by preventing maternal smoking and its impact on both placental function and fetal airway growth; as well as limiting postpartum exposures that can cause bronchial obstruction, such as viral infections, unfavorable environmental and home ecology.

It is promising to study the genetic predisposition to the formation of broncho-obstructive syndrome.

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I. K. Volkov, doctor of medical sciences, professor

First MGMU them. I. M. Sechenov, Moscow

In recent years, Russia has seen an increase in the number of children with chronic diseases and congenital malformations of the lungs (COPD). And before it was believed that if you do not take action, then any of these problems can lead to COPD. But ... a few decades later, when the child grows up and crosses the 40-year mark. Little COPD is not threatened. Bronchial asthma, chronic bronchitis, bronchopulmonary dysplasia are completely different ailments. Serious, dangerous, but not so irreversible. And suddenly the situation changed...

COPD in children: a false alarm?

Now pediatricians in polyclinics say that a number of diseases of the respiratory system and environmental factors can trigger the development of COPD at a very early age. The main manifestation of COPD is shortness of breath due to interference with airflow into the lungs. To receive a portion of oxygen, the lung tissue stretches and becomes too thin, sluggish and can no longer perform its functions.

Asthma, bronchopulmonary dysplasia and COPD have the same manifestations. And not only them. If mom or dad smokes and the baby continuously inhales tobacco smoke, that is, passive smoker, then he is threatened with emphysema from an early age. The process develops as follows: the bronchial mucosa is inflamed all the time due to toxic smoke. And this leads to chronic bronchitis and narrowing of the lumen of the bronchi. As a result, air hardly enters the lungs and even worse leaves them. After exhalation, processed oxygen remains in the cavities of the organ, which is no longer involved in respiration, but takes up a lot of space, overstretching the tissue. Over time, the lungs lose their ability to contract normally, receive oxygen, and expel carbon dioxide. Shortness of breath appears. If physiological emphysema is planned in preschoolers (doctors call it "vicarious"), then at the age of 10-11 years they already show signs of COPD. Currently, military doctors, assessing the health of conscripts, often identify the first and even the second stage of COPD. Despite the achievements in the fight against the disease, one should try to prevent it at an early age, reducing the impact of risk factors.

Expert opinion

Leila Namazova-Baranova, pediatrician, MD Sciences, Professor, Academician of the Russian Academy of Sciences, Deputy Director of the Research Institute of Pediatrics, Ministry of Health of the Russian Federation, Moscow

When diagnosing babies in district clinics, doctors sometimes confuse COPD with asthma and bronchopulmonary dysplasia. Despite the similarity of symptoms, namely asthma attacks, these are different diseases. Asthma develops as allergic reaction, and bronchopulmonary dysplasia is the lot of "hurry-ups", children who were born ahead of time. And above all, those who received oxygen support incorrectly immediately after their birth in the maternity hospital. At present time runs scientific discussion whether asthmatics and children with bronchopulmonary dysplasia in infancy are potential patients with COPD. It seems that data appeared in favor of such a conclusion, but so far science still cannot give a reliable answer to this question. Extensive and long-term observations are needed.

But what can be done right now? I advise parents of those children who have any respiratory (breathing) problems to be sure to vaccinate against pneumococcus, influenza and Haemophilus influenzae. These bacteria cause diseases that occur with complications. And the main blow falls on the bronchi and lungs. The listed vaccinations are included in the National vaccination calendar and are free of charge. The prevention of infection with pneumococcal infection, which annually claims about a million children's lives, is especially relevant. Vaccination can be started in babies from 2-4 months.

Natalia Lev, pulmonologist, Ph.D. honey. Sci., Leading Researcher, Department of Chronic Inflammatory and Allergic Lung DiseasesResearch Clinical Institute of Pediatrics. acad. Yu. E. Veltishcheva, Moscow

Although COPD is an “adult” disease, there are a number of pediatric pulmonary diseases that can be considered within COPD. These are diseases that are accompanied by a severe, difficult to treat severe obstructive syndrome (suffocation), in which bronchial conduction is impaired. They swell, overflow with mucus. And as a result, there is a spasm that interferes with breathing. The kid breathes noisily with a whistle, all the time trying to exhale the remaining air, coughing. Cough can be either dry or wet. Any physical effort is accompanied by shortness of breath. The general condition is disturbed: the little one has poor sleep and appetite, general weakness, headaches, dizziness. The state of health worsens all the time, the treatment does not help, doctors and parents are sounding the alarm. Clinical blood tests are normal, except that the ESR is elevated. This continues for at least a week, sometimes it is not possible to get rid of the cough even in a month. The temperature may not rise. The picture is absolutely similar to that observed in adult patients with COPD. And doctors involuntarily come to the conclusion that the child has COPD. Although this is not so, and we must continue to search for the correct diagnosis.

Figures and facts

In 2015, 42,000 people died from COPD in Russia, and every year the disease claims more than 3 million lives in the world.
Women are more sensitive to tobacco smoke than men.
According to international estimates, bronchial asthma occurs in 10% of children.
Asthma is the most common respiratory disease in children. And as a rule, with age passes into COPD.
The question remains: at what age can COPD be diagnosed.

If a child has pulmonary diseases that are accompanied by an obstructive syndrome, it is necessary:

exclude passive smoking of children and women during pregnancy;
prevent smoking in children and adolescents;
limit the impact on the baby of factors that can cause bronchial obstruction, namely viral infections and the unfavorable ecology of the external environment and housing, observe sanitary standards;
protect the baby from infectious diseases, since any of them - viral or bacterial - overloads respiratory system and causes complications
during the cold season, one should not neglect the observance of banal precautions: limit the contact of the child, follow the rules of personal hygiene;
carry out the prevention of respiratory infections: vaccinate, including against influenza, pneumococcus, Haemophilus influenzae, respiratory syncytial virus.

Chronic obstructive pulmonary disease or COPD is a chronic lung diseases associated with respiratory failure. Bronchial damage develops with emphysema complications against the background of inflammatory and external stimuli and has a chronic progressive character.

The alternation of latent periods with exacerbations requires a special approach to treatment. The risk of developing serious complications is quite high, which is confirmed by statistical data. Respiratory dysfunction causes disability and even death. Therefore, patients with this diagnosis need to know COPD, what it is and how the disease is treated.

general characteristics

When exposed to the respiratory system of various irritating substances in people with a predisposition to pneumonia, negative processes begin to develop in the bronchi. First of all, the distal sections are affected - located in close proximity to the alveoli and lung parenchyma.

Against the background of inflammatory reactions, the process of natural discharge of mucus is disrupted, and small bronchi become clogged. When an infection is attached, inflammation spreads to the muscle and submucosal layers. As a result, bronchial remodeling occurs with replacement by connective tissues. In addition, lung tissue and bridges are destroyed, which leads to the development of emphysema. With a decrease in the elasticity of the lung tissues, hyperairiness is observed - the air literally inflates the lungs.

Problems arise precisely with the exhalation of air, since the bronchi cannot fully expand. This leads to a violation of gas exchange and a decrease in the volume of inhalation. A change in the natural process of breathing manifests itself in patients as shortness of breath in COPD, which is greatly enhanced by exertion.

Persistent respiratory failure causes hypoxia - oxygen deficiency. All organs suffer from oxygen starvation. With prolonged hypoxia, the pulmonary vessels narrow even more, which leads to hypertension. As a result, irreversible changes in the heart occur - the right section increases, which causes heart failure.

Why is COPD classified as a separate group of diseases?

Unfortunately, not only patients, but also medical workers little is known about the term chronic obstructive pulmonary disease. Doctors habitually diagnose emphysema or chronic bronchitis. Therefore, the patient does not even realize that his condition is associated with irreversible processes.

Indeed, in COPD, the nature of symptoms and treatment in remission are not much different from the signs and methods of therapy for pulmonary pathologies associated with respiratory failure. What then made physicians single out COPD as a separate group.

Medicine has determined the basis of such a disease - chronic obstruction. But the narrowing of the gaps in the airways are also found in the course of other pulmonary diseases.

COPD, unlike other diseases such as asthma and bronchitis, cannot be permanently cured. Negative processes in the lungs are irreversible.

So, in asthma, spirometry shows improvement after bronchodilators are used. Moreover, the indicators of PSV, FEV may increase by more than 15%. While COPD does not provide significant improvements.

Bronchitis and COPD are two different diseases. But chronic obstructive pulmonary disease can develop against the background of bronchitis or proceed as an independent pathology, just like bronchitis can not always provoke COPD.

Bronchitis is characterized by a prolonged cough with sputum hypersecretion and the lesion extends exclusively to the bronchi, while obstructive disorders are not always observed. Whereas sputum separation in COPD is not increased in all cases, and the lesion extends to structural elements, although bronchial rales are auscultated in both cases.

Why does COPD develop?

Not so few adults and children suffer from bronchitis, pneumonia. Why, then, chronic obstructive pulmonary disease develops only in a few. In addition to provoking factors, predisposing factors also affect the etiology of the disease. That is, the impetus for the development of COPD can be certain conditions in which people who are prone to pulmonary pathologies find themselves.

Predisposing factors include:

hereditary predisposition. It is not uncommon to have a family history of certain enzyme deficiencies. This condition has a genetic origin, which explains why the lungs do not mutate in a heavy smoker, and COPD in children develops for no particular reason.
Age and gender. For a long time it was believed that pathology affects men over 40. And the rationale is more related not to age, but to smoking experience. But today is the number smoking women with experience meets no less than men. Therefore, the prevalence of COPD among the fair sex is no less. In addition, women who are forced to breathe also suffer. cigarette smoke. Passive smoking negatively affects not only the female, but also the children's body.
Problems with the development of the respiratory system. And it's like talking about negative impact on the lungs during intrauterine development, and the birth of premature babies, in which the lungs did not have time to develop for full disclosure. In addition, in early childhood, the lag in physical development negatively affects the state of the respiratory system.
Infectious diseases. For frequent respiratory problems infectious origin, both in childhood and at an older age, increases the risk of developing COL at times.
Hyperreactivity of the lungs. Initially, this condition is the cause of bronchial asthma. But in the future, the addition of COPD is not ruled out.

But this does not mean that all patients at risk will inevitably develop COPD.

Obstruction develops under certain conditions, which can be:

Smoking. Smokers are the main patients diagnosed with COPD. According to statistics, this category of patients is 90%. Therefore, it is smoking that is called the main cause of COPD. And the prevention of COPD is based primarily on smoking cessation.
Harmful working conditions. People forced by their kind labor activity, inhale regularly dust of various origins, air saturated with chemicals, smoke suffer from COPD quite often. Work in mines, construction sites, in the collection and processing of cotton, in metallurgical, pulp, chemical production, in granaries, as well as in enterprises producing cement, other building mixtures leads to the development of respiratory problems to the same extent in smokers and non-smokers .
Inhalation of combustion products. We are talking about biofuels: coal, wood, manure, straw. Residents who heat their homes with such fuel, as well as people who are forced to be present during natural fires, inhale combustion products that are carcinogens and irritate the respiratory tract.

In fact, any external effect on the lungs of an irritating nature can provoke obstructive processes.

Main complaints and symptoms

The primary signs of COPD are associated with coughing. Moreover, cough, to a greater extent, worries patients in the daytime. At the same time, sputum separation is insignificant, wheezing may be absent. The pain practically does not bother, sputum leaves in the form of mucus.

Sputum with the presence of pus or a cough that provokes hemoptysis and pain, wheezing - the appearance of a later stage.

The main symptoms of COPD are associated with the presence of shortness of breath, the intensity of which depends on the stage of the disease:

With mild shortness of breath, breathing is forced against the background brisk walking, as well as when climbing a hill;
Moderate shortness of breath is indicated by the need to slow down the pace of walking on a flat surface due to breathing problems;
Severe shortness of breath occurs after several minutes of walking at a free pace or walking a distance of 100 m;
For shortness of breath of the 4th degree, the appearance of breathing problems during dressing, performing simple actions, immediately after going outside is characteristic.

The occurrence of such syndromes in COPD may accompany not only the stage of exacerbation. Moreover, with the progress of the disease, the symptoms of COPD in the form of shortness of breath, cough become stronger. On auscultation, wheezing is heard.

Breathing problems inevitably provoke systemic changes in the human body:

The muscles involved in the breathing process, including the intercostal ones, atrophy, which causes muscle pain and neuralgia.
In the vessels, changes in the lining, atherosclerotic lesions are observed. Increased tendency to form blood clots.
A person is faced with heart problems in the form of arterial hypertension, coronary disease and even a heart attack. For COPD, the pattern of cardiac changes is associated with left ventricular hypertrophy and dysfunction.
Osteoporosis develops, manifested by spontaneous fractures of the tubular bones, as well as the spine. Constant joint pain, bone pain cause a sedentary lifestyle.

The immune defense is also reduced, so any infections are not rebuffed. Frequent colds, at which it is observed heat, headache, and other signs of infection are not uncommon in COPD.

There are also mental and emotional disorders. Working capacity is significantly reduced, a depressive state, unexplained anxiety develops.

correct emotional disorders arising against the background of COPD is problematic. Patients complain of apnea, stable insomnia.

In the later stages, cognitive disorders also appear, manifested by problems with memory, thinking, and the ability to analyze information.

Clinical forms of COPD

In addition to the stages of development of COPD, which are most often used in medical classification,

There are also forms of the disease according to the clinical manifestation:

bronchial type. Patients are more likely to cough, wheezing with sputum discharge. In this case, shortness of breath is less common, but heart failure develops more rapidly. Therefore, there are symptoms in the form of swelling and cyanosis of the skin, which gave the name to the patients "blue edema".
emphysematous type. The clinical picture is dominated by shortness of breath. The presence of cough and sputum is rare. The development of hypoxemia and pulmonary hypertension seen only in later stages. In patients, the weight decreases sharply, and the skin becomes pink-gray, which gave the name - "pink puffers".

However, it is impossible to speak of a clear division, since in practice COPD of a mixed type is more common.

Exacerbation of COPD

The disease can be aggravated unpredictably under the influence of various factors, including external, irritating, physiological and even emotional. Even after eating in a hurry, choking may occur. At the same time, the condition of a person is deteriorating rapidly. Increasing cough, shortness of breath. The use of the usual basic COPD therapy in such periods does not give results. During the period of exacerbation, it is necessary to adjust not only the methods of COPD treatment, but also the doses of the drugs used.

Usually treatment is carried out in a hospital, where it is possible to provide emergency assistance the patient and conduct the necessary examinations. If exacerbations of COPD occur frequently, the risk of complications increases.

Urgent care

Exacerbations with sudden attacks of suffocation and severe shortness of breath must be stopped immediately. Therefore, emergency assistance comes to the fore.

It is best to use a nebulizer or spacer and provide fresh air. Therefore, a person predisposed to such attacks should always have inhalers with them.

If first aid does not work and suffocation does not stop, it is urgent to call an ambulance.

Video

Chronic obstructive pulmonary disease

Principles of treatment for exacerbations

Treatment of chronic obstructive pulmonary disease during an exacerbation in a hospital is carried out according to the following scheme:

Short bronchodilators are used with an increase in the usual dosages and frequency of administration.
If bronchodilators do not have the desired effect, Eufilin is administered intravenously.
It can also be prescribed for exacerbation of COPD treatment with beta-stimulants in combination with anticholinergic drugs.
If pus is present in the sputum, antibiotics are used. Moreover, it is advisable to use antibiotics with a wide spectrum of action. It makes no sense to use narrowly targeted antibiotics without bakposev.
The attending physician may decide to prescribe glucocorticoids. Moreover, Prednisolone and other drugs can be prescribed in tablets, injections or used as inhaled glucocorticosteroids (IGCS).
If oxygen saturation is significantly reduced, oxygen therapy is prescribed. Oxygen therapy is carried out using a mask or nasal catheters to ensure proper oxygen saturation.

In addition, drugs can be used to treat diseases that frolic against the background of COPD.

Basic treatment

To prevent seizures and improve the general condition of the patient, a set of measures is taken, among which are not last place occupies behavioral and drug treatment, dispensary observation.

The main drugs used at this stage are bronchodilators and corticosteroid hormones. Moreover, it is possible to use long-acting bronchodilator drugs.

Together with taking medications, it is necessary to pay attention to the development of pulmonary endurance, for which breathing exercises are used.

As for nutrition, the emphasis is on getting rid of excess weight and saturation with the necessary vitamins.

Treatment of COPD in the elderly, as well as in severe patients, is associated with a number of difficulties due to the presence of comorbidities, complications and reduced immune protection. Often such patients require constant care. Oxygen therapy in such cases is used at home and, at times, is the main way to prevent hypoxia and related complications.

When the damage to the lung tissue is significant, cardinal measures are necessary with resection of a part of the lung.

To modern methods cardinal treatment refers to radiofrequency ablation (ablation). It makes sense to do RFA when detecting tumors, when for some reason the operation is not possible.

Prevention

Basic Methods primary prevention directly depend on the habits and lifestyle of a person. Smoking cessation, the use of personal protective equipment significantly reduces the risk of developing lung obstruction.

Secondary prevention is aimed at preventing exacerbations. Therefore, the patient must strictly follow the recommendations of doctors for treatment, as well as exclude provoking factors from their lives.

But even cured, operated patients are not fully protected from exacerbations. Therefore, tertiary prevention is also relevant. Regular medical examination allows you to prevent the disease and detect changes in the lungs in the early stages.

Periodic treatment in specialized sanatoriums is recommended for both patients, regardless of the stage of COPD, and cured patients. With such a diagnosis in the anamnesis, vouchers to the sanatorium are provided on a preferential basis.

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