Chronic bronchitis in the acute phase differential diagnosis. Acute diseases of the lower respiratory tract. Acute bronchitis and pneumonia
Chronic (simple) bronchitis is a diffuse lesion of the mucous membrane of the bronchial tree, caused by prolonged irritation of the airways by volatile household and industrial pollutants and / or damage by a viral-bacterial infection, characterized by a restructuring of the epithelial structures of the mucous membrane, the development of an inflammatory process, accompanied by hypersecretion of mucus and a violation of the cleansing bronchial functions. This is manifested by persistent or recurrent cough with sputum (for more than 3 months a year for more than 2 years), not associated with other bronchopulmonary processes or damage to other organs and systems. In simple (non-obstructive) bronchitis, mainly large (proximal) bronchi are affected.
Epidemiology
The share of chronic bronchitis (CB) in the structure of respiratory diseases of non-tuberculous nature among the urban population is 32.6% among adults. Chronic simple (non-obstructive) bronchitis predominates (in ¾ of patients). Studies carried out in various countries indicate a significant increase in CB over the past 15–20 years. The disease affects the most able-bodied part of the population, forming at the age of 20-39 years. Men, smokers, manual workers at industrial and agricultural enterprises are more likely to suffer from chronic bronchitis.
Etiology
In the occurrence and development of chronic bronchitis, volatile pollutants and non-indifferent dusts play an important role, which have a harmful irritating (mechanical and chemical) effect on the bronchial mucosa. In the first place among them, in terms of importance, should be put the inhalation of tobacco smoke when smoking or the inhalation of the smoke of other smokers (“passive smoking”). Cigarette smoking is the most harmful, and the number of cigarettes smoked per day and the depth of inhalation of tobacco smoke into the lungs matter. The latter reduces the natural resistance of the mucous membrane to volatile pollutants. The second place in terms of etiological significance is occupied by volatile industrial pollutants (products of incomplete combustion of coal, oil, natural gas, sulfur oxides, etc.). All of them, to varying degrees, have an irritating or damaging effect on the bronchial mucosa. Pneumotropic viruses and bacteria (influenza virus, adenoviruses, rhinosincitial viruses, pneumococcus, Haemophilus influenzae, moraxella catarrhalis, mycoplasma pneumonia) most often cause an exacerbation of the disease. As factors predisposing to chronic bronchitis, the pathology of the nasopharynx with impaired breathing through the nose should be attributed, when the functions of cleansing, moisturizing and warming the inhaled air are impaired. Unfavorable climatic and weather factors predispose to exacerbations of the disease.
Pathogenesis
In the pathogenesis of chronic bronchitis, the main role is played by the state of mucociliary clearance of the bronchi with a violation of the secretory, cleansing, protective functions of the mucous membrane and the state of the epithelial lining. In a practically healthy person, bronchial clearance, being an important part of the mechanisms of sanogenesis, occurs continuously, as a result, the mucous membrane is cleared of foreign particles, cellular detritus, microorganisms by transferring them with cilia of the ciliated epithelium along with a more viscous surface layer of bronchial mucus from the deep sections of the bronchial tree along towards the trachea and larynx. Other, in particular, cellular, elements of bronchial contents (first of all, alveolar macrophages) take an active part in this cleansing of the mucosa. The effectiveness of the mucociliary clearance of the bronchi depends on two main factors: the mucociliary escalator, determined by the function of the ciliated mucosal epithelium, and the rheological properties of the bronchial secretion (its viscosity and elasticity), which is ensured by the optimal ratio of its two layers - the “outer” (gel) and the “inner” ( sol). Pathogenic risk factors - volatile pollutants with their constant and intense impact on the bronchial mucosa become etiological. This is facilitated by their combined effect, as well as a decrease in local non-specific resistance of the mucous membrane. The mechanical and chemical (toxic) action of pathogenic irritants on the bronchial mucosa leads to hyperfunction of secretory cells. The resulting hypercrinia initially has a protective character, it causes a decrease in the concentration of antigenic material irritating the mucous membrane due to dilution with an increased volume of bronchial contents, and excites a protective cough reflex. However, along with hypercrinia, a change in the optimal ratio of sol and gel (discrinia) inevitably takes place, the viscosity of the secret increases, making it difficult to remove it. As a result of the toxic effect of pollutants, the movement of the ciliated epithelium, i.e., the mucociliary escalator, changes (slows down, becomes ineffective). Under these conditions, the influence of pathogenic irritants on highly differentiated ciliated epithelium is enhanced, which leads to degeneration and death of ciliated cells. A similar situation occurs when pathogenic respiratory viruses act on the ciliated epithelium. As a result, so-called « bald spots", i.e., areas free of ciliated epithelium. In these places, the function of the mucociliary escalator is interrupted, and it becomes possible for opportunistic bacteria to adhere (adhesion) to the damaged areas of the mucous membrane, primarily high-type pneumococci and Haemophilus influenzae. Possessing a relatively low virulence, these microbes are characterized by a pronounced sensitizing ability, thereby creating conditions for the chronicity of the emerging inflammatory process in the bronchial mucosa (endobronchitis). When the latter occurs, the cellular composition of bronchial contents changes: alveolar macrophages give way to neutrophilic leukocytes, and in allergic reactions, the number of eosinophils increases. The specified change of "leaders" can be traced by the cytogram of sputum or bronchial washings, which is of diagnostic value for characterizing the clinical features of endobronchitis. The development of foci of inflammation against the background of "bald spots" of the mucous membrane of the bronchi is usually a turning point in the deterioration of the habitual state of health of a smoker; cough becomes less productive, symptoms of general intoxication appear, etc., which in most cases is the reason for going to the doctor. In the current inflammatory process, the decay products of neutrophilic leukocytes and alveolar macrophages, in particular, proteinase enzymes, change the ratio of proteinase and antiproteinase (inhibitory) activity, which can give impetus to the destruction of the elastic backbone of the alveoli (the formation of centriacinar emphysema). This is facilitated, apparently, by genetically mediated and insufficiently studied mechanisms of pathogenesis, which are characteristic of patients with COPD.
Pathomorphology
One of the main manifestations of the disease are changes in the mucus-forming cells of the bronchial glands and bronchial epithelium. Changes in the bronchial glands are reduced to their hypertrophy, and bronchial epithelium - to an increase in the number of goblet cells and, conversely, a decrease in the number of ciliated cells, the number of their villi, the appearance of separate areas of squamous metaplasia of the epithelium. These changes occur mainly in the large (proximal) bronchi. Inflammatory changes are superficial. Cellular infiltration of the deeper layers of the bronchi is weakly expressed and is represented mainly by lymphoid cells. Weak or moderate signs of sclerosis are noted only in 1/3 of patients.
HB clinic
Simple (non-obstructive) chronic bronchitis should be considered when the patient complains of cough, sputum, shortness of breath and/or shortness of breath (“bronchitis without shortness of breath”), symptoms without exacerbation do not impair quality of life.
Exacerbations diseases are characterized by an increase in cough and an increase in sputum secretion; in most patients, they occur no more than two to three times a year. Their seasonality is typical - they are noted during the off-season, that is, in early spring or late autumn, when the differences in climatic and weather factors are most pronounced. An exacerbation of the disease in the vast majority of these patients occurs against the background of the so-called cold, which usually hides an episodic or epidemic (during the period of a registered influenza epidemic) viral infection, which is soon joined by a bacterial infection (usually pneumococci and Haemophilus influenzae). An external reason for an exacerbation of the disease is hypothermia, close contact with a coughing "flu" patient, etc. In the exacerbation phase, the patient's well-being is determined by the ratio of two main syndromes: cough and intoxication. Severity intoxication The syndrome determines the severity of the exacerbation and is characterized by general symptoms: an increase in body temperature, usually to subfebrile values, rarely above 38 ° C, sweating, weakness, headache, decreased performance. Complaints and changes in the upper respiratory tract (rhinitis, sore throat when swallowing, etc.) are determined by the characteristics of the viral infection and the presence of chronic diseases of the nasopharynx (inflammation of the paranasal sinuses, compensated tonsillitis, etc.), which usually worsen during this period. Main components cough syndromes of diagnostic value are cough and sputum. At the beginning of an exacerbation, the cough may be unproductive ("dry catarrh"), but is more often accompanied by sputum from several spitting up to 100 g (rarely more) per day. On examination, the sputum is watery or mucous with streaks of pus (with catarrhal endobronchitis) or purulent (with purulent endobronchitis). The ease of coughing up sputum is determined mainly by its elasticity and viscosity. With increased viscosity of sputum, as a rule, there is a long hacking cough, which is extremely painful for the patient. In the early stages of the disease and with its mild exacerbation, expectoration of sputum usually occurs in the morning (when washing), with a more pronounced exacerbation, sputum can be coughed up periodically throughout the day, often against the background of physical exertion and increased breathing. Hemoptysis in such patients is rare, as a rule, thinning of the bronchial mucosa, usually associated with occupational hazards, predisposes to it.
When examining a patient, there may be no visible deviations from the norm on the part of the respiratory system. In the physical examination of the chest organs, the results of auscultation are of the greatest diagnostic value. Chronic simple (non-obstructive) bronchitis is characterized by hard breathing, usually heard over the entire surface of the lungs and dry scattered wheezing. Their occurrence is associated with a violation of the drainage function of the bronchi. The timbre of wheezing is determined by the caliber of the affected bronchi. Buzzing rales of a low timbre, aggravated by coughing and forced breathing, are heard in endobronchitis with lesions of large and medium bronchi; with a decrease in the lumen of the affected bronchi, wheezing becomes high-pitched. When a liquid secret appears in the bronchi, moist rales can also be heard, usually finely bubbling, their caliber also depends on the level of damage to the bronchial tree. The ventilation capacity of the lungs in non-obstructive bronchitis in the phase of clinical remission can remain normal for decades. In the acute phase, the ventilation capacity of the lungs may also remain within normal limits. In such cases, one can speak of functionally stable bronchitis. However, in some patients, usually in the exacerbation phase, the phenomena of moderately pronounced bronchospasm join, the clinical signs of which are the emerging difficulty in breathing during physical exertion, the transition to a cold room, at the time of a strong cough, sometimes at night, and dry high-pitched wheezing. The study of respiratory function during this period of time reveals moderate obstructive disorders of lung ventilation, i.e., there is a bronchospastic syndrome. In such patients, one can speak of functionally unstable bronchitis, unlike COPD, obstruction is completely reversible after treatment. It is assumed that transient bronchial obstruction is associated with persistent viral infection (influenza B virus, adenovirus and rhinosincitial virus). For the progression or, conversely, stabilization of CNB, the state of local immunological reactivity is important. In the acute phase, the level of secretory immunoglobulin A, the functional ability of alveolar macrophages (AM) and the phagocytic activity of neutrophils in the blood serum are usually reduced; the level of interleukin - 2 increases, the higher, the more pronounced the activity of inflammation; about half of the patients showed an increase in the level of circulating immune complexes (CIC) in the blood. These indicators remain in about half of the patients and in the remission phase, with a disease duration of up to 5 years. This, apparently, is due to the presence of pneumococcal and Haemophilus influenzae antigens in the bronchial contents, which remain there even in the phase of clinical remission. Changes in other organs and systems are either absent or reflect the severity of the disease exacerbation (intoxication, hypoxemia) and concomitant pathology.
Diagnostics simple bronchitis is based on an assessment of the patient's history, the presence of symptoms indicating a possible lesion of the bronchi (cough, sputum), the results of a physical examination of the respiratory organs and the exclusion of other diseases that may be characterized by largely similar clinical symptoms (pulmonary tuberculosis, bronchiectasis, bronchial cancer).
Laboratory research.
Laboratory data are used to diagnose exacerbation of chronic bronchitis, clarify the degree of activity of the inflammatory process, the clinical form of bronchitis and differential diagnosis. Indicators of a clinical blood test and ESR with catarrhal endobronchitis, they rarely change, more often with purulent, when moderate leukocytosis and a shift of the leukocyte formula to the left appear. ABOUT With trophasic biochemical tests( determination of total protein and proteinogram, C-reactive protein, haptoglobin, sialic acids and seromucoid in blood serum) . have diagnostic value in sluggish inflammation.
Cytological examination of sputum, and in its absence - the contents of the bronchi, obtained during bronchoscopy characterizes the degree of inflammation. Yes, at severe exacerbation of inflammation (3 degrees) in the cytograms, neutrophilic leukocytes predominate (97.4–85.6%), in a small number there are dystrophically altered cells of the bronchial epithelium and AM; at moderate inflammation (2 degrees) along with neutrophilic leukocytes (75.7%) in the contents of the bronchi there is a significant amount of mucus, AM and cells of the bronchial epithelium; with mild inflammation (grade 1) the secret is predominantly mucous, desquamated cells of the bronchial epithelium predominate, there are few neutrophils and macrophages (52.3–37.5% and 26.7–31.1%, respectively). A certain relationship is revealed between the activity of inflammation and the physical properties of sputum (viscosity, elasticity). With purulent bronchitis in the acute phase, the content of acid mucopolysaccharides and fibers of deoxyribonucleic acid increases in sputum and the content of lysozyme, lactoferrin and secretory IgA decreases. This reduces the resistance of the bronchial mucosa to the effects of infection.
Instrumental research.
Bronchoscopy in chronic bronchitis, it is indicated for diagnostic and / or therapeutic purposes. endoscopy is required. With persistent cough syndrome, expiratory collapse (dyskinesia) of the trachea and large bronchi is often detected, manifested by an increase in respiratory mobility and expiratory narrowing of the airways. Dyskinesia of the trachea and main bronchi of II-III degree has an adverse effect on the course of the inflammatory process in the bronchi, impairs the effectiveness of expectoration of sputum, predisposes to the development of purulent inflammation, causes the appearance of obstructive disorders of lung ventilation. With purulent endobronchitis, the bronchial tree is sanitized.
Radiography
On chest x-ray in patients with simple bronchitis, there are no changes in the lungs. In case of purulent bronchitis after therapeutic and diagnostic bronchoscopy and a course of sanitation of the bronchial tree, computed tomography is indicated, which allows diagnosing bronchiectasis and determine further treatment tactics.
Differential Diagnosis
Acute bronchitis
Simple (non-obstructive) bronchitis should be distinguished from acute protracted And recurrent bronchitis. The first is characterized by: the presence of a protracted (more than 2 weeks) course of an acute cold, for the second - repeated short episodes of it three or more times a year. bronchiectasis are characterized by cough since childhood after suffering "epitheliotropic" infections (measles, whooping cough, etc.), discharge of purulent sputum "full mouthful", there is a relationship between sputum discharge and body position, bronchoscopy reveals local purulent (mucopurulent) endobronchitis, CT lungs and bronchography revealed bronchiectasis.
cystic fibrosis
cystic fibrosis is a genetically determined disease, which is characterized by the appearance of symptoms in childhood, damage to the exocrine glands with the presence of purulent bronchitis, violation of the secretory function of the pancreas, a diagnostic marker is an increased content of Na in the sweat fluid (40 mmol / l.).
Tuberculosis of the respiratory organs
For tuberculosis signs of intoxication, night sweats, mycobacterium tuberculosis in sputum and bronchial washings are characteristic, bronchoscopy reveals local endobronchitis with scars, fistulas with positive serological reactions to tuberculosis, positive results from the use of tuberculostatic drugs (therapia ex juvantibus).
Lung cancer
Central cancer more common in men over 40, heavy smokers; characteristic hacking cough, streaks of blood and "atypical" cells in the sputum, characteristic results of bronchoscopy and biopsy.
Tracheobronchial dyskinesia
Tracheobronchial dyskinesia (expiratory collapse of the trachea and large bronchi) is characterized by a pertussis-like whooping cough; bronchoscopy reveals prolapse of the membranous part of the trachea into the lumen of varying severity.
Bronchial asthma
With functionally unstable bronchitis with bronchospastic syndrome, it is necessary to carry out a differential diagnosis with b ronchial asthma, which is characterized by young age, a history of allergies or a respiratory infection at the onset of the disease, an increase in the number of eosinophils in sputum and blood (> 5%), paroxysmal difficulty in breathing or coughing both during the day and especially during sleep, mainly high-pitched scattered dry wheezing, therapeutic effect of bronchodilator drugs (mainly 2-agonists).
Classification
By pathogenesis:
primary bronchitis- as an independent nosological form;
secondary bronchitis- as a consequence of other diseases and pathological conditions (tuberculosis, bronchiectasis, uremia, etc.).
By functional characteristic(shortness of breath, spirometry FEV 1, FVC, FEV 1 / FVC):
non-obstructive (simple) chronic bronchitis (CNB)): no shortness of breath, spirometric parameters - FEV 1 , FVC, FEV 1 /FVC are not changed;
obstructive: expiratory dyspnea and changes in spirometric parameters (decrease in FEV 1 , FEV 1 / FVC) during an exacerbation.
According to clinical and laboratory characteristics(nature of sputum, cytological picture of bronchial washings, degree of neutrophilia in peripheral blood and acute phase biochemical reactions):
catarrhal;
mucopurulent.
According to the phase of the disease:
exacerbation;
clinical remission.
Obligate complications of bronchial obstruction:
chronic cor pulmonale;
respiratory (lung) failure, heart failure.
Treatment
In the phase of exacerbation of the disease with an increase in body temperature, patients are subject to release from work. With severe intoxication, obstructive syndrome, in the presence of severe concomitant diseases, especially in elderly patients, hospitalization is advisable. Tobacco smoking is strictly prohibited.
Given the large role of a respiratory viral infection in exacerbating the disease, all kinds of measures are being taken to accelerate the removal of antigenic material (toxins) from the body. It is recommended to drink plenty of warm liquids: hot tea with lemon, honey, raspberry jam, lime blossom tea, dry raspberry tea, heated alkaline mineral waters - table and medicinal (Borzhom, Smirnovskaya, etc.); official "sweating" and "breast" collections of medicinal herbs. Steam ("not deep") indifferent inhalations are useful. Of the antiviral drugs, amexin, ingavirin, relenza, arbidol, interferon or interlock are prescribed in the form of nasal drops, 2–3 drops in each nasal passage with an interval of 3 hours, or in the form of inhalations of 0.5 ml 2 times a day for 2–5 days; anti-influenza -globulin (for influenza and other respiratory viral infections), anti-measles -globulin (for adeno- and PC-infections). All gamma globulins are administered intramuscularly in 2-3 doses, daily or every other day, usually 6 injections, depending on the patient's condition. Perhaps one-day local application of immunoglobulins (instillation into the nose) with an interval of 3 hours. Among other antiviral drugs, it is advisable to prescribe chigain (the active principle is secretory IgA) 3 drops in each nasal passage 3 times a day. In the presence of allergy manifestations and an increase in the level of eosinophils in sputum and blood (> 5%), the appointment of antihistamines, ascorbic acid is indicated. These measures, as a rule, reduce the symptoms of intoxication, improve overall well-being. With an increase in the degree of purulence of sputum (a change in the color of sputum from light to yellow, green), the presence of neutrophilic leukocytosis in the peripheral blood, and the persistence of symptoms of intoxication, antibiotics are indicated (natural and semi-synthetic penicillins, macrolides or tetracyclines), dioxidine in inhalations (1% -10 ml ) . These chemotherapy drugs are used under the control of clinical symptoms, usually not longer than 2 weeks. To cleanse the bronchi of excess viscous secretions, expectorants should be prescribed orally or inhaled: 3% solution of potassium iodide (in milk, after meals), infusions and decoctions of thermopsis, marshmallow, herbs "breast collection" and mixtures based on them, in a warm form up to 10 times a day, ambroxol, bromhexine, acetylcysteine. Bronchial clearance largely depends on the degree of hydration of the bronchial contents, this is facilitated by inhalation of warm sodium bicarbonate solution or hypertonic saline. With functionally unstable bronchitis and bronchospastic syndrome, short-acting 2 -agonists (Berotek and its analogues), anticholinergics (Atrovent) or their combination (Berodual) should be included in the complex of drug therapy.
When the signs of activity of the inflammatory process subside, the above can be used inhalations of garlic or onion juice, which are prepared ex temporae on the day of inhalation, mixed with a 0.25% solution of novocaine in a ratio of 1:3; using up to 1.5 ml of solution per inhalation twice a day, a total of 9-15 procedures. The above treatment is combined with the use of vitamins C, A, group B, biostimulants (aloe juice, propolis, licorice root, sea buckthorn oil, prodigiosan, etc.), methods of physical therapy and physical methods of rehabilitation treatment. With purulent endobronchitis, such treatment should be supplemented with sanitation of the bronchial tree. The duration of the course of treatment depends on the speed of elimination of purulent secretions in the bronchial tree. This usually requires 2-4 therapeutic bronchoscopies at intervals of 3-7 days. If clinically, with repeated bronchoscopy, a clear positive dynamics of the inflammatory process in the bronchi is revealed, the course of sanitation is completed with the help of endotracheal infusions or aerosol inhalations with iodinol and other symptomatic agents.
Prevention
Primary prevention includes combating the bad habit of smoking tobacco, improving the external environment, prohibiting work in a polluted (dusty or gassed) atmosphere, hardening the body, treating foci of infection in the nasopharynx, and establishing normal breathing through the nose. To prevent exacerbations of simple chronic bronchitis, it is recommended to exclude the fact of active and passive smoking, to carry out hardening (water) procedures and methods of rehabilitation exercise therapy that increase nonspecific resistance and tolerance to physical activity, rational employment. During the off-season, it is recommended to take adaptogens (Eleutherococcus, Schisandra chinensis, etc.), as well as antioxidants (vitamin C, rutin, etc.). During the period of remission of the inflammatory process, it is necessary to radically sanitize the foci in the nasopharynx, oral cavity, correct defects in the nasal septum that make it difficult to breathe through the nose. To prevent the expected exacerbation of the disease during an impending influenza epidemic, vaccination against influenza can be carried out; to prevent exacerbation in the most dangerous period of the year (late autumn), vaccination with a pneumococcal or combined vaccine is possible. Prophylactic use of antibiotics is not advisable.
In functionally unstable chronic bronchitis, annual spirographic control should be carried out. For the purposes of restorative treatment and rehabilitation of these patients, the possibilities of sanatorium treatment at climatic resorts should be more widely used. In patients over 50 years of age and with multiple pathologies from other organs and systems, preference should be given to local sanatoriums.
Forecast
The prognosis for chronic bronchitis is favorable. Usually, CB does not cause a persistent decrease in lung function. However, an association has been found between mucus hypersecretion and a decrease in FEV1, and it has also been found that in young smokers, the presence of chronic bronchitis increases the likelihood of developing COPD.
Version: Directory of Diseases MedElement
Acute bronchitis (J20)
Pulmonology
general information
Short description
acute bronchitis- diffuse acute inflammation of the tracheobronchial tree (bronchial mucosa).
1. Bronchitis, not specified as acute or chronic, in persons under 15 years of age.
2. Acute or subacute bronchitis, including:
- acute bronchitis with bronchospasm;
- fibrinous;
- membranous;
- purulent;
- septic.
3. Acute tracheobronchitis.
Excluded from this section are:
1. Bronchitis (tracheobronchitis), not specified as acute or chronic, in persons 15 years of age and older (see J40).
2. Asthma, unspecified (us. allergic bronchitis) - J45.9.
3. Asthma with a predominance of an allergic component (us. allergic bronchitis) - J45.0.
4. Chronic obstructive pulmonary disease with acute respiratory infection of the lower respiratory tract (J44.0).
5. Acute bronchitis with bronchiectasis (J47.0).
7. Bronchitis and pneumonitis due to chemicals, gases, fumes and vapors (J68.0).
8. Chronic bronchitis and tracheobronchitis:
- unspecified (J42);
- mucopurulent (J41.1);
- simple (J41.0).
Flow period
Minimum flow period (days): 14
Maximum flow period (days): 21
Symptoms (cough, fever, bronchial obstruction) lasting more than 3 weeks should be a reason for expanding the examination and consulting specialists.
Classification
By etiology
:
- viral;
- bacterial (including mycoplasma);
- due to the influence of chemical factors;
- due to the influence of physical factors.
The etiological variants of acute bronchitis associated with chemical and physical effects (for example, toxic and burns) are rarely observed in isolation, but, as a rule, occur as a component of a systemic lesion.
According to the mechanism of development:
Primary;
- secondary (arising against the background of an already existing pathology of the upper and lower respiratory tract).
According to flow options:
- acute;
- acute protracted bronchitis (lasting more than 3 weeks);
- recurrent bronchitis (recurring during the year 3 or more times);
- acute obstructive bronchitis.
Etiology and pathogenesis
Etiology
In adults, 85-95% of acute bronchitis is caused by viruses.
According to Russian researchers, in children over 4 years of age, viral bronchitis is recorded in approximately 20% of cases, in children from 14 days to 4 years - in less than 10% of cases.
As a rule, viral bronchitis is associated with bacteria (more often), with fungi (less often), protozoa. Acute bronchitis can be caused by a variety of bacteria. At the same time, the etiological structure of acute community-acquired and nosocomial bacterial bronchitis differs significantly.
According to the results of Russian studies on the identification of topical pathogens of acute bronchitis in patients without concomitant pulmonary pathology, it was possible to verify the pathogen only in 16-29% of patients.
The long-held hypothesis of acute bacterial bronchitis caused, for example, by Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, and Gram-negative bacteria, was not confirmed by Russian pediatricians (except for patients who underwent surgical procedures).
Evidence of participation in the development of the disease Bordatella pertussis and B. parapertussis, Mycoplasma pneumoniae and Chlamydophila pneumoniae was obtained in 5-10% of cases.
However, according to foreign authors, the role of chlamydia and mycoplasmas as an etiological factor has recently grown significantly; mycoplasma and chlamydial etiology in children can be from 25 to 40%, and it is highest in the first year of life and after 10 years.
Etiology of acute bronchitis depending on age(Geppe N.A., Safronova A.N., 2009):
- 0-3 months: cytomegalovirus, enterovirus, herpes viruses;
- 0-6 months: chlamydia (Chl.trachomatis);
- from 6 months to 3 years: respiratory syncytial virus, parainfluenza virus type 3;
- 6-17 years old: chlamydia (Chl.pneumoniae), mycoplasmas (M.pneumoniae).
Note. In all age groups: adenovirus, rhinovirus, influenza virus (especially in the cold season).
Pathogenesis
Viruses, penetrating into the epithelial cells of the bronchial mucosa, lead to their death. The infection also spreads to smaller airways (this is especially true for influenza viruses and respiratory syncytial viruses), contributing to the development of bronchial hyperreactivity. Viral infection sensitizes the respiratory tract, disrupts mucocellular clearance up to complete cessation, and suppresses defense mechanisms against bacterial infection. After the attachment of a bacterial infection, the amount of mucus increases, which prevents the penetration of antibiotics into the respiratory tract and makes phagocytosis difficult. Under the influence of infectious agents, various inflammatory mediators are released.
pathological anatomy
The mucous membrane of the bronchi in acute bronchitis appears swollen and hyperemic, there is exudate on its surface Exudate is a protein-rich fluid that exits small veins and capillaries into surrounding tissues and body cavities during inflammation.
, which in small bronchi and bronchioles can fill the entire lumen of the respiratory tubes. The exudate of the bronchial mucosa can be serous, mucous, mucopurulent or purulent.
In the discharge almost always (with the exception of serous exudate) erythrocytes are found. In such severe forms as influenza B, hemorrhages in the bronchial mucosa are possible, due to which the exudate becomes bloody. Almost constantly in the exudate, individual cells of the cylindrical epithelium of the mucous membranes are detected. In mild cases of bronchitis, changes are limited only to the mucosa itself, in more severe cases, they capture all layers of the bronchial wall. When conducting a microscopic examination of the wall of the inflamed bronchus, a picture of hyperemia is observed Hyperemia - increased blood supply to any part of the peripheral vascular system.
and inflammatory edema of the mucosa and submucosal tissue.
Even with mild bronchitis, there is infiltration with leukocytes and lymphocytes (later with an admixture of plasma cells). It is present in the mucous membrane and submucosal tissue, in other layers of the bronchial wall, captures the peribronchial tissue in the small bronchi.
In the case of significant cell infiltration, the bronchial wall thickens, the infiltrate and edema in it loosen the elastic tissue and the smooth muscle layer, and the muscle fibers undergo degenerative obesity. All this creates conditions for the expansion of small intrapulmonary bronchi, the formation of bronchiectasis Bronchiectasis - expansion of limited areas of the bronchi due to inflammatory-dystrophic changes in their walls or anomalies in the development of the bronchial tree
(typical for measles and influenza bronchitis in children).
During the period of acute bronchitis, the inflammatory process often passes to the connective tissue surrounding the bronchus, captures the descending lymphatic vessels here and spreads along the bronchus through them. Inflammatory changes from the peribronchial connective tissue can move to the lung tissue. Often there is the development of bronchopneumonia, when inflammation inside the bronchi goes down to their terminal branches and to the lung tissue. In case of blockage of the lumen of the small bronchi with a secret, the corresponding sections of the lung tissue collapse and atelectasis is formed.
The main morphological types of acute inflammation of the bronchi:
- acute catarrhal;
- catarrhal-purulent;
- hemorrhagic;
- fibrinous-ulcerative;
- suppurative.
For acute catarrhal bronchitis hyperemia and edema of the bronchus wall, an increase in the number of goblet cells, hypersecretion of glands and thinning of mucus, accumulation of a small number of leukocytes and desquamated epithelium in the lumen of the bronchus are characteristic. Inflammatory infiltration is moderate and limited to the mucous membrane, defects in the epithelial lining are superficial and small, quickly recovering.
At catarrhal-purulent bronchitis(purulent catarrh of the bronchi, purulent bronchitis) the mucous membrane of the bronchi is swollen and has a bright pink or red color. Exudate accumulates in the lumen of the bronchi, which contains a large number of leukocytes; the epithelium has more persistent and deep surface defects, erosion may form Erosion - superficial defect of the mucous membrane or epidermis
. There are pronounced degenerative changes in the ciliated epithelium. Inflammatory process - limited or widespread; captures most of the bronchial tree down to the smallest bronchi. In the case of a severe course of the disease, the inflammatory process, along with the mucous membrane, also covers the deep tissues of the bronchial wall.
At hemorrhagic bronchitis in exudate a large number of erythrocytes comes to light.
Acute fibrinous bronchitis(croupous bronchitis, plastic bronchitis, bronchial croup) is observed in diphtheria, lobar pneumonia and is accompanied by the release of a fibrinous film on the surface of the inflamed mucous membrane. In rare cases, isolated croupous inflammation of the bronchi occurs without fibrinous lesions of the larynx, trachea, or lung tissue. The nature of the inflammation is croupous, the epithelial cover in the large bronchi can be preserved (with the exception of superficial rows) and the fibrinous film looks like a tube. In small ones, it looks like a continuous cylindrical mass and fills the entire lumen of the bronchi. Acute fibrinous bronchitis is a rather rare disease with unclear etiology and pathogenesis. In the future, it usually takes on a relapsing character with exacerbation intervals from several months to several years. May cause minor bleeding in the lungs (hemoptysis).
Membrane bronchitis(a variant of fibrinous bronchitis with the formation of a large number of films) develops against the background of pronounced alterative changes. Fibrinous (croupous or diphtheritic) inflammation is characteristic, which is manifested by the presence of a whitish-gray fibrinous film on the surface of the mucous membrane, more or less tightly soldered to the underlying tissues. After the film is melted by neutrophil enzymes and its rejection, defects of various depths are exposed - ulcers that heal, filling with granulation tissue with its subsequent scarring.
Suppurative bronchitis (bronchial suppuration, septic bronchitis) is characterized by purulent fusion of the bronchial mucosa and underlying tissues with the formation of deep ulcerative defects, destruction of glands, muscles and cartilage. The granulation tissue that gradually fills the ulcers becomes sclerosed, which leads to the formation of rough scars. This occurs mainly when a large amount of secretion accumulates in the lumen of the bronchi as a result of a violation of its evacuation (for example, with obstruction) and its purulent inflammation.
Options for the course of acute bronchitis
Acute obstructive bronchitis(OHB) of infectious genesis can be caused by various respiratory viruses, mycoplasmas, chlamydia. In young children, the majority of obstructive forms of bronchitis are caused by RS-viral and parainfluenza type 3 infections; other viruses (usually cytomegalovirus and adenoviruses) cause no more than 10-20% of cases.
Some authors consider mycoplasma to be one of the main etiological factors of acute obstructive bronchitis (especially in older children). With recurrent obstructive bronchitis, the role of M.pneumoniae increases (according to Nazarenko N.M. et al. (2001), infection with this pathogen is detected in 85% of children with recurrent obstructive bronchitis).
The complex mechanisms of bronchial obstruction in children include narrowness of the airways, swelling of the mucous membranes and hypersecretion of the bronchial glands and, to a lesser extent, spasm of the smooth muscles of the bronchi. Difficulty in expiration in AOB of infectious origin is not a consequence of allergic inflammation. It is due to the peculiarities of the age-related reactivity of young children and the biological characteristics of the infectious agent.
Acute recurrent bronchitis(ARB) is acute bronchitis that occurs three or more times a year. Patients with this variant of acute bronchitis should be evaluated for asthma, COPD, and immunodeficiency. In about 50% of cases, these patients are later diagnosed with bronchial asthma.
Epidemiology
The epidemiology of acute bronchitis is directly related to the epidemiology of influenza and other respiratory viral diseases. Typically, the typical peaks of the increase in the incidence of these diseases are the end of December and the beginning of March.
Data on incidence in adults are very contradictory. The incidence of bronchitis, according to a number of authors, ranges from 15 to 50%. This percentage is significantly higher (up to 50-90%) among children who often suffer from acute respiratory infections, especially in environmentally unfavorable regions, as well as with passive smoking.
Individual clinical forms
Acute obstructive bronchitis(AOB) is a clinical form of acute bronchitis that occurs with severe signs of obstruction. It occurs mainly in children of the first 4 years of life. According to various authors, approximately 20-25% of bronchitis in children occur in the form of AOB. This figure is significantly higher than in adults. At the same time, obstructive conditions against the background of a respiratory viral infection are recorded in 10-30% of infants. The frequency of AOB, as a manifestation of SARS, is especially high in young children (mainly up to 4 years).
Recurrent acute bronchitis has a prevalence of 16.4 per 1000 children. Children of preschool age are ill. Among frequently ill children (according to referrals), recurrent bronchitis was found in 27% and recurrent obstructive - in 17.2%.
Factors and risk groups
The following factors predispose to the development of acute bronchitis:
- climatic and weather conditions;
- unfavorable working and living conditions (hypothermia, dampness, drafts) or vice versa excessively dry, hot, polluted air;
- smoking;
- alcoholism;
- chronic focal infection in the nasopharyngeal region;
- influenza and other acute respiratory viral infections, acute pneumonia in history;
- chronic obstructive pulmonary disease (COPD);
- allergic diseases (bronchial asthma, allergic rhinitis, allergic conjunctivitis);
- violation of nasal breathing;
- immunodeficiency states;
- deformity of the chest;
- reflux esophagitis;
- elderly or children's age;
- congestive changes in the lungs with right ventricular failure;
- genetic (hereditary) predisposition to respiratory diseases.
Clinical picture
Symptoms, course
Bronchitis of infectious etiology often begins against the background of acute rhinitis or laryngitis.
Symptoms:
- sore behind the sternum;
- dry (rarely wet) cough, with a small amount of sputum (with a bacterial infection, sputum becomes purulent); sometimes the cough is hacking and painful;
- weakness, feeling of weakness;
- hoarseness of voice, pain when swallowing (rarely);
- signs of acute rhinitis, laryngitis, tracheitis (depending on the pathogen).
There are no physical signs, or hard breathing and widespread dry rales are determined over the lungs. Body temperature - subfebrile or normal.
With the defeat of the bronchi of medium and small calibers, the exhalation can become elongated, wheezing - dry and whistling.
When a secret appears in the bronchi, moist small bubbling rales are heard, which, unlike pneumonia, are less sonorous, do not have a clear localization and disappear after coughing.
In the case of the development of bronchospasm, signs of bronchial obstruction are added:
- shortness of breath with little physical exertion;
- box shade of percussion sound;
- prolonged exhalation on auscultation Auscultation is a method of physical diagnostics in medicine, which consists in listening to sounds generated during the functioning of organs.
;
- dry high-pitched rales.
Moderate course the disease is accompanied by a significantly pronounced general malaise, weakness; characterized by a strong dry cough with difficulty breathing and shortness of breath; pain in the lower parts of the chest and abdominal wall, caused by muscle strain when coughing. Gradually, the cough becomes wet with mucopurulent or purulent sputum.
Above the surface of the lungs, harsh breathing, dry and moist small bubbling rales are heard. For several days, the body temperature remains subfebrile. There are no pronounced changes in the composition of peripheral blood.
With a predominant lesion of the bronchioles (see "Acute bronchiolitis" - J20), as a rule, a severe course of the disease is observed.
Acute symptoms of the disease become less pronounced by the fourth day and, with a favorable outcome, completely disappear by the seventh day.
In acute bronchitis with impaired bronchial patency, there is a tendency to a protracted course and transition to chronic bronchitis.
Separate clinical forms of acute bronchitis
Acute obstructive bronchitis
At the onset of the disease, the clinical picture is characterized by symptoms of a respiratory viral infection: rise in body temperature, catarrhal changes in the upper respiratory tract, a violation of the general condition.
The severity and nature of symptoms vary greatly depending on the causative agent of the disease.
Signs of expiratory difficulty in breathing can be observed on the first day of the disease or during the course of a viral infection (on the third to fifth days). The respiratory rate and expiratory duration gradually increase.
Breathing becomes noisy and wheezing. This is due to the fact that as hypersecretion develops, secretion accumulates in the lumen of the bronchi due to shortness of breath and fever, the viscous properties of the secret change - it "dries up". This results in buzzing (low) and whistling (high) dry rales.
The defeat of the bronchi is widespread and therefore hard breathing with dry whistling and buzzing rales is heard equally over the entire surface of the chest. Wheezing can be heard from a distance.
The onset of the disease is the same as with SARS. Later, expiratory dyspnea develops with a respiratory rate of 60-80 per minute and cough. With the first episode, these symptoms are noted on the 2nd-4th day, with repeated episodes - on the 1st-2nd day.
For obstructive bronchitis, the prevalence of symptoms of damage to large bronchi is typical: wheezing, dry, often musical wheezing. For bronchiolitis, a more "wet" picture is characteristic: a mass of diffuse finely bubbling rales.
Elongation of expiration and whistling sounds with a significant increase in breathing can weaken up to complete disappearance. In this regard, when assessing obstruction, one should focus on the severity of lung swelling (percussion of the borders), respiratory rate and the degree of retraction of the "compliant" places of the chest, as well as the levels of Po and Pco 2.
Severe obstruction lasts 1-4 days (longer with bronchiolitis), complete normalization of the condition occurs after 1-2 weeks.
Recurrent obstructive bronchitis(3 or more episodes of acute obstructive bronchitis within a year)
The exacerbation proceeds with symptoms characteristic of SARS. After 1-3 days, these symptoms are accompanied by a cough (usually dry, more frequent at night). Cough and wheezing (dry or coarse and medium bubbling) persist longer than in acute bronchitis, sometimes up to 3-4 weeks. Symptoms, their duration and order of appearance tend to recur in ARVI of different etiologies. The expressed obstruction does not develop, but the latent bronchospasm often comes to light.
Diagnostics
1. The diagnosis of "acute bronchitis" is made clinically:
- in the presence of a carefully collected anamnesis, including the detection of smoking, adverse environmental factors and / or other predisposing factors;
- in the presence of an acute cough that lasts no more than 3 weeks, regardless of the presence of sputum;
- in the absence of signs of pneumonia and chronic lung diseases (COPD Chronic obstructive pulmonary disease (COPD) is an independent disease characterized by partially irreversible airflow limitation in the airways.
, bronchial asthma), which can also cause coughing;
- in the absence of reflux esophagitis Reflux esophagitis - inflammation of the esophageal mucosa due to gastroesophageal reflux; manifested by retrosternal pain, heartburn.
.
2. Physical examination and auscultation are performed.
3. When X-ray of the chest, as a rule, there is an increase in the pulmonary pattern and indistinctness of the roots of the lungs. In the case of attachment of a bronchospastic component, signs of "acute swelling of the lungs" appear: increased transparency of the lung fields, descent of the dome of the diaphragm.
X-ray examination is not indicated if:
- acute cough and sputum production indicate acute bronchitis;
- heart rate HR - heart rate
<100 уд./мин.;
- breathing rate<24 вдохов/мин.;
- temperature (oral)<38 о С (100,4 F).
4. Spirometry Spirometry - measurement of vital capacity of the lungs and other lung volumes using a spirometer
is not decisive in the diagnosis of acute bronchitis, but may help in the differential diagnosis.
Laboratory diagnostics
1. General blood analysis. Changes are nonspecific and depend on the type of pathogen. In the first days, leukopenia may be observed, bacterial inflammation is characterized by neutrophilia with a moderate shift to the left, a slight increase in ESR ESR - erythrocyte sedimentation rate (non-specific laboratory blood indicator, reflecting the ratio of plasma protein fractions)
.
2. Sputum analysis: a large number of desquamated epithelial cells, macrophages, single erythrocytes.
When a bacterial infection is attached, the sputum becomes mucopurulent, contains a large number of neutrophils.
Routine, mandatory, planned typing of the pathogen in uncomplicated and mild acute bronchitis is not recommended. Typing of the pathogen is indicated for a protracted course of acute bronchitis. PCR applied PCR - polymerase chain reaction
, serological (especially in paired blood sera taken at intervals of 3 weeks) research methods.
Differential Diagnosis
The most important in the differential diagnosis of acute bronchitis are:
- pneumonia;
- whooping cough;
- bronchial asthma;
- acute and chronic sinusitis;
- miliary pulmonary tuberculosis;
- foreign body;
- emphysema;
- ciliary dyskinesia syndrome (for example, Kartagener's syndrome);
- cystic fibrosis.
Differential diagnosis of acute bronchitis (WILLIAM J. HUESTON & ARCH G. MAINOUS III, 1998)
| Pathological process | Signs and symptoms |
| reactive respiratory disease | |
| Asthma | Evidence of reversible airway obstruction, even with infection |
| Allergic aspergillosis |
- Transient infiltrates in the lungs - Eosinophilia in sputum and peripheral blood |
| Occupational hazards | Symptoms are pronounced during the working week, but tend to improve on weekends, holidays and vacations |
| Chronical bronchitis |
- Chronic daily cough with sputum production for at least three months - Commonly seen in smokers |
| Respiratory tract infection | |
| Sinusitis |
- Congestion and pain in the sinuses - Nasal discharge |
| Cold | Inflammation of the upper airways without bronchial wheezing |
| Pneumonia | Characteristic changes on a chest x-ray |
| Other reasons | |
| Congestive heart failure |
- Basilar rales - Orthopnea - Cardiomegaly - Evidence of increased interstitial or alveolar fluid on chest x-ray - S 3 (gallop rhythm) - Tachycardia |
| Reflux esophagitis | Symptoms worsen when lying down Heartburn |
| Bronchogenic tumors |
- Constitutional signs (weight loss) - Chronic cough, sometimes with hemoptysis |
| Aspiration syndromes |
- Usually associated with a specific event, such as smoke inhalation - Vomit - Decreased level of consciousness |
Differential diagnosis between acute bronchitis and acute pneumonia
| Clinical signs | Acute (simple) bronchitis | Acute pneumonia |
| Degree of fever | Below 38 o C | Above 38 o C |
| Fever duration | Less than 3 days | More than 3 days |
| The nature of the cough | Superficial, dry, painless | Deep, wet, painful |
| Dyspnea | No | Eat |
| Cyanosis | No | Eat |
| Participation of auxiliary muscles in the act of breathing | No | Eat |
| Voice jitter | Not changed | Enhanced |
| Shortening of percussion sound | No | Eat |
| Local fine bubbling sonorous rales | No | Eat |
| Crepitus | No | Eat |
| Bronchophony | Not changed | reinforced |
Differential diagnosis of broncho-obstructive syndrome (BOS) of allergic and infectious genesis
(Lasitsa O.I., Lasitsa T.S.)
|
signs
|
Infection
|
Allergy
|
| Epidemiology | Contact with a patient with SARS | Contact with household, pollen and other allergens |
| Heredity | Not weighed down | hereditary predisposition to atopy |
| Clinic | Fever, intoxication and other signs of an infectious process | The temperature is normal, there is no intoxication |
| Persistence of clinical signs of BOS (cough, tympanitis, dry whistling and various wet rales) | Characterized by the cyclical nature of the pathological process | Typical lability of clinical signs during the day and in the dynamics of observation |
| Adaptation to bronchial obstruction | Pronounced respiratory failure | Sufficient adaptation to biofeedback |
| BOS duration | More often - 1-2 weeks | Very uncertain, dependent on exposure and allergen elimination |
| Relapses | Rare, except in cases of persistence of the virus | Very characteristic |
| Immunofluorescence study of nasopharyngeal swabs | Find allergens of RS viruses, parainfluenza, adenovirus, etc. | More often negative |
| The growth of the titer of antibodies to viruses in the reactions of RSK, RNGA | characteristic | not characteristic |
| Immunological study | There may be a decrease in cellular immunity, an increase in the CEC | Increase in Ig E, there may be a decrease in Ig A, CIC is often normal |
| Eosinophilia | Not typical | Very characteristic |
| Skin tests with household and other atopic allergens | negative | positive |
| Sensitization to atopic allergens in in vitro samples | Absent | Present |
| bronchial hypersensitivity | Not typical | typical |
| Infestation with worms | As in the population | Happens more often |
Complications
Atelectasis Atelectasis is a condition of the lung or part of it in which the alveoli contain little or no air and appear to be collapsed.
, respiratory failure.
Treatment abroad
Chronic bronchitis is a diffuse progressive inflammation of the bronchi, not associated with local or generalized lung damage and manifested by cough. Chronic bronchitis is called such, in which a productive cough that is not associated with any other disease (for example, tuberculosis, bronchial tumor, etc.) lasts at least 3 months a year for 3 consecutive years.
Chronic bronchitis is a disease characterized by chronic diffuse inflammation of the bronchial mucosa, restructuring of its epithelial structures, hypersecretion and increased viscosity of bronchial secretions, impaired protective bronchial cleansing function and persistent or recurrent cough with sputum, not associated with other diseases of the bronchopulmonary system. Chronic inflammation of the bronchial mucosa is caused by prolonged irritation of the airways by volatile household or industrial pollutants (most often tobacco smoke) and/or a viral-bacterial infection.
The above definition of chronic bronchitis is fundamentally important, because, firstly, it allows you to clearly identify and diagnose chronic bronchitis as an independent nosological form and, secondly, it forces the therapist to make a differential diagnosis with lung diseases accompanied by cough with sputum (pneumonia, tuberculosis and etc.).
ICD-10 code
J41.0 Chronic simple bronchitis
J41 Simple and mucopurulent chronic bronchitis
J41.1 Mucopurulent chronic bronchitis
J41.8 Mixed, simple and mucopurulent chronic bronchitis
J42 Chronic bronchitis, unspecified
Epidemiology of chronic bronchitis
Chronic bronchitis is a widespread disease and occurs in 3-8% of the adult population. According to A. N. Kokosov (1999), the prevalence of chronic bronchitis in Russia is 16%.
Most pulmonologists suggest distinguishing between primary and secondary chronic bronchitis.
Primary chronic bronchitis is understood as chronic bronchitis as an independent disease not associated with any other bronchopulmonary pathology or damage to other organs and systems. In primary chronic bronchitis, there is a diffuse lesion of the bronchial tree.
Secondary chronic bronchitis is etiologically associated with chronic inflammatory diseases of the nose, paranasal sinuses; with chronic limited inflammatory diseases of the lungs (chronic pneumonia, chronic abscess); with past pulmonary tuberculosis; with severe heart disease occurring with congestion in the small circle; with chronic renal failure and other diseases. Usually secondary chronic bronchitis is local, less often - diffuse.
Chronic bronchitis is the most common disease of the bronchopulmonary system. In the USA, for example, only chronic obstructive bronchitis (COB), ie. The most prognostically unfavorable form of chronic bronchitis affects about 6% of men and 3% of women, in the UK - 4% of men and 2% of women. In people older than 55 years, the prevalence of this disease is about 10%. The proportion of chronic bronchitis in the overall structure of respiratory diseases of a non-tuberculous nature currently reaches more than 30%.
Depending on the nature of the course, the severity of the pathological process in the bronchi and the characteristics of the clinical picture of the disease, there are two main forms of chronic bronchitis:
- Chronic simple (non-obstructive) bronchitis (CNB) is a disease characterized by lesions predominantly of the proximal (large and medium) bronchi and a relatively favorable clinical course and prognosis. The main clinical manifestation of chronic non-obstructive bronchitis is persistent or intermittent and cough with sputum. Signs of unexpressed bronchial obstruction occur only during periods of exacerbation or in the most advanced stages of the disease.
- Chronic obstructive bronchitis (COB) is a disease characterized by deeper degenerative-inflammatory and sclerotic changes not only in the proximal but also in the distal airways. The clinical course of this form of chronic bronchitis, as a rule, is unfavorable and is characterized by a prolonged cough, gradually and steadily increasing shortness of breath, and a decrease in exercise tolerance. Sometimes, with chronic obstructive bronchitis, signs of local damage to the bronchi (bronchiectasis, cicatricial changes in the bronchial wall, pneumosclerosis) are revealed.
The main distinguishing feature of chronic obstructive bronchitis is an early lesion of the respiratory sections of the lungs, manifested by signs of respiratory failure, slowly progressing in parallel with the increase in the degree of bronchial obstruction. It is believed that in chronic obstructive bronchitis, the annual decrease in VC is more than 50 ml per year, while in chronic non-obstructive bronchitis it is less than 30 ml per year.
Thus, the clinical assessment of patients with chronic bronchitis implies the mandatory allocation of two main forms of the disease. In addition, the diagnosis of the phase of the course of the disease (exacerbation, remission), the nature of inflammation of the bronchial mucosa (catarrhal, mucopurulent, purulent), the severity of the disease, the presence of complications (respiratory failure, compensated or decompensated chronic pulmonary heart, etc.) .
Below is the simplest and most accessible classification of chronic bronchitis.
Cause of chronic bronchitis
The disease is associated with prolonged irritation of the bronchi by various harmful factors (smoking, inhalation of air polluted with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other chemical compounds) and recurrent respiratory infection (respiratory viruses, Pfeiffer bacillus, pneumococci), less often occurs when cystic fibrosis, alpha1-antitrypsin deficiency. Predisposing factors - chronic inflammatory and suppurative processes in the lungs, upper respiratory tract, reduced body resistance, hereditary predisposition to respiratory diseases.
Pathological anatomy and pathogenesis
Hypertrophy and hyperfunction of the bronchial glands, increased secretion of mucus, a relative decrease in serous secretion, a change in the composition of the secret - a significant increase in acid mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not provide cleansing of the bronchial tree and the normal renewal of the entire secret layer; emptying of the bronchi in this state of mucociliary clearance occurs only when coughing. Such conditions for the mucociliary apparatus turn out to be disastrous: dystrophy and atrophy of the ciliated epithelium occur. At the same time, the glandular apparatus, which produces lysozyme and other antibacterial protectors, undergoes the same degeneration. Under these conditions, a bronchogenic infection develops, the activity and relapses of which largely depend on the local immunity of the bronchi and the development of secondary immune deficiency.
In the pathogenesis of the disease, spasm, edema, fibrous changes in the bronchus wall with stenosis of its lumen or its obliteration are important. Obstruction of the small bronchi leads to hyperextension of the alveoli on expiration and disruption of the elastic structures of the alveolar walls, as well as to the appearance of hyperventilated and completely non-ventilated zones that function as an arteriovenous shunt. Due to the fact that the blood passing through these alveoli is not enriched with oxygen, arterial hypoxemia develops. In response to alveolar hypoxia, a spasm of the arterioles of the lungs occurs with an increase in the total pulmonary arterial resistance; precapillary pulmonary hypertension occurs. Chronic hypoxemia leads to polycythemia and increased blood viscosity, accompanied by metabolic acidosis, further enhancing vasoconstriction in the pulmonary circulation.
Superficial infiltration develops in large bronchi, in medium and small bronchi, as well as in bronchioles, this infiltration can be deep with the development of erosions, ulcerations and the formation of meso- and panbronchitis. The remission phase is characterized by a decrease in inflammation in general, a significant decrease in the amount of exudate, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane. The final phase of the chronic inflammatory process in the bronchi is the sclerosis of their walls, atrophy of the glands, muscles, elastic fibers, cartilage. Perhaps irreversible stenosis of the lumen of the bronchus or its expansion with the formation of bronchiectasis.
Symptoms and clinical course of chronic bronchitis
The onset of the disease is gradual. The first symptom is a morning cough with mucous sputum. Gradually, the cough begins to occur at night and during the day, aggravated, as in chronic bronchitis, by inhalation of cold damp or hot dry air. The amount of sputum increases, it becomes mucopurulent and purulent. Shortness of breath appears and progresses, first during physical exertion, and then at rest.
In the clinical course of chronic bronchitis, four stages are distinguished: catarrhal, purulent, obstructive and purulent-obstructive. The third stage is characterized by emphysema and bronchial asthma, the fourth - purulent complications (bronchiectasis).
The diagnosis is established using fnbrobronchoscopy, in which the endobronchial manifestations of the inflammatory process (catarrhal, purulent, atrophic, hypertrophic, hemorrhagic, fibrous-ulcerative endobronchitis) and its severity (but only to the level of subsegmental bronchi) are visually assessed. Bronchoscopy allows biopsy of the mucous membrane and histological methods to clarify the nature of its morphological changes, as well as to identify tracheobronchial hypotonic dyskinesia (increased mobility of the walls of the trachea and bronchi during breathing, up to expiratory collapse of the walls of the trachea and main bronchi - as with laryngomalacia, only with the opposite sign ) and static retraction (change in configuration and decrease in the lumen of the trachea and bronchi), which can complicate chronic bronchitis and be one of the causes of bronchial obstruction. However, in chronic bronchitis, the main pathological changes occur in smaller bronchi, so broncho- and radiography are used in the diagnosis of this disease.
Classification of chronic bronchitis
Form of chronic bronchitis:
- simple (non-obstructive);
- obstructive.
Clinical, laboratory and morphological characteristics:
- catarrhal;
- mucopurulent or purulent.
Disease phase:
- exacerbation;
- clinical remission.
Severity:
- mild - FEV1 more than 70%;
- medium - FEV1 ranging from 50 to 69%;
- severe - FEV1 less than 50% of the proper value.
Complications of chronic bronchitis:
- emphysema;
- respiratory failure (chronic, acute, acute on the background of chronic);
- bronchiectasis;
- secondary pulmonary arterial hypertension;
- cor pulmonale (compensated and decompensated).
The above classification takes into account the recommendations of the European Respiratory Society, in which the severity of chronic bronchitis is assessed by the magnitude of the decrease in FEV1 compared to the proper values. It is also necessary to distinguish between primary chronic bronchitis - an independent nosological form, and secondary bronchitis, as one of the manifestations (syndrome) of other diseases (for example, tuberculosis). In addition, when formulating a diagnosis of chronic bronchitis in the acute phase, it is advisable to indicate a possible causative agent of bronchopulmonary infection, although this approach has not yet become widespread in wide clinical practice.
Chronic bronchitis (CB)- diffuse inflammatory lesion of the bronchial tree, caused by prolonged irritation of the bronchi by various harmful agents, which has a progressive course and is characterized by impaired mucus formation and drainage function of the bronchial tree, which is manifested by cough, sputum and shortness of breath.
According to WHO recommendations, bronchitis can be considered chronic if the patient coughs up sputum on most days for at least 3 consecutive months for more than 2 consecutive years. Chronic bronchitis is divided into primary and secondary.
Primary HB is an independent disease, not associated with any other bronchopulmonary processes or damage to other organs and systems. In primary chronic bronchitis, a diffuse lesion of the bronchial tree is observed.
Secondary HB develops against the background of other diseases, both pulmonary (tuberculosis, bronchiectasis, CP, etc.) and extra-pulmonary (uremia, congestive heart failure, etc.). Most often, secondary CB is segmental, i.e. is local.
This section considers only various forms of primary chronic bronchitis, which accounts for about 30% in the structure of nonspecific lung diseases among the urban population.
Classification. There is currently no generally accepted classification of HB. Of fundamental importance is the division of HB into obstructive and non-obstructive variants. With each of these options, a catarrhal (mucous), catarrhal-purulent or purulent inflammatory process can develop in the bronchi. Thus, catarrhal, catarrhal-purulent and purulent non-obstructive chronic bronchitis and the same forms of chronic obstructive bronchitis are distinguished.
The classification includes rare forms - hemorrhagic and fibrinous CB. CB is also subdivided according to the level of bronchial damage: with a predominant lesion of large (proximal bronchitis) or small bronchi (distal bronchitis) [Paleev N.R. et al., 1985].
Etiology. The development of CB is largely determined by external influences - exogenous factors: tobacco smoke (with active and passive smoking); air pollution; unfavorable conditions of professional activity; climatic factors; infectious factors (viral infection).
Due to the fact that the disease does not occur in all those exposed to the same adverse effects, there are also internal causes that determine the development of CB - endogenous factors: pathology of the nasopharynx, impaired breathing through the nose and purification of the inhaled air, repeated acute respiratory diseases (ARI), acute bronchitis and focal infection of the upper respiratory tract, hereditary predisposition (violation of enzyme systems - oi-antitrypsin, etc., local immunity), violation metabolism (obesity).
Among exogenous factors, the main role in the occurrence of chronic bronchitis belongs to pollutants - impurities of various nature contained in the inhaled air. Infection in the development of chronic bronchitis plays a secondary role, but it is the main cause of exacerbation of the disease.
Pathogenesis. Under the influence of exogenous and endogenous factors, a number of pathological processes occur in the tracheobronchial tree (Scheme 5).
The structural and functional properties of the mucous membrane and submucosal layer change.
3935 0
Chronic bronchitis (CB) is an independent diffuse lesion of the mucous membrane of the bronchial tree, mainly medium and large (proximal) bronchi, caused by prolonged irritation of the airways by volatile pollutants of a domestic and industrial nature and / or damage by a viral-bacterial infection with the development of an inflammatory process (endobronchitis), manifested by constant or intermittent cough, usually with sputum production (according to WHO epidemiological criteria, lasting 3 months or more per year for at least 2 years in a row), which is not associated with other bronchopulmonary processes or damage to other organs and systems.
It is necessary to distinguish between primary bronchitis as an independent nosological form and secondary bronchitis, which is a consequence of other diseases and pathological conditions (tuberculosis, bronchiectasis, uremia, etc.).
In recent years, there have been significant changes in the concept of this disease.
The term "chronic bronchitis" that existed earlier included two types of bronchitis, differing in functional characteristics: non-obstructive (simple) and obstructive. Currently, "chronic bronchitis" refers only to non-obstructive, and obstructive bronchitis refers to chronic obstructive pulmonary disease (COPD).
Epidemiology
Due to the long-term oligosymptomatic course of chronic bronchitis and the late treatment of patients with a doctor, it is not possible to judge the true prevalence of this disease. Chronic bronchitis occurs in 7.3% of the total number of the surveyed population and in 62.4% of identified patients with chronic nonspecific lung diseases. It is registered 3 times more often than COPD. Men are ill mainly (70.1%), the highest prevalence of the disease occurs at the age of 50-59 years, and among women - 40-49 years.Etiology
Causing and predisposing factors closely interact in the occurrence and development of chronic bronchitis, irritating and damaging volatile pollutants (domestic and professional), as well as non-indifferent dusts that have a harmful (chemical and mechanical) effect on the bronchial mucosa play a significant role.In the first place in terms of importance among these factors, inhalation of tobacco smoke should be placed, in which about 4,000 potentially toxic components were found. At the same time, the depth of inhalation of tobacco smoke is important, which reduces the natural resistance of the bronchial mucosa to its damaging oxidants, and the number of cigarettes smoked per day.
To assess the severity of the pathogenic effects of tobacco smoke, the index of a smoker is calculated, for which the average number of cigarettes smoked per day is multiplied by 12. If the index of a smoker is > 200, then after 15-20 years of smoking or earlier, symptoms of bronchial and lung disease will inevitably appear. The so-called “passive smoking”, that is, being in smoky rooms, also has a negative effect on the respiratory system.
The second place among the damaging factors that create a threat of disease should be occupied by volatile industrial pollutants (products of incomplete combustion of coal, oil, natural gas, sulfur oxides, etc.). All of them have an irritating and / or damaging effect on the bronchial mucosa.
The cause of the disease may be air pollution by various impurities. These include products of incomplete combustion of various types of fuel, vehicle exhaust gases. Smog has a particularly adverse effect on the respiratory organs, which is understood as rapidly developing massive air pollution, mainly by fuel combustion products, and is associated with special meteorological conditions (complete absence of wind and cooling with the development of thick fog). As a result, polluted air accumulates under a layer of warm air lying in low places under a layer of cold air.
Much less often, in 10-15% of cases, mainly in children and in non-smoking women and men, the cause of chronic bronchitis is an infection. With this variant of development, the disease is formed from an acute one, especially with viral-viral, viral-mycoplasmal and viral-bacterial associations. The transition of acute bronchitis to chronic is facilitated by the presence of chronic inflammatory diseases of the nasopharynx.
If infection has a modest place as the immediate and main cause of the disease, then it is of primary importance as the cause of exacerbation of chronic bronchitis.
Etiologically the most significant pathogens are:
1. Bacteria: H.influenzae; S.pneumoniae; M. catarrhalis;
2. "Atypical" (intracellular) microorganisms: Mycoplasmapneumoniae; Chlamidiapneumoniae;
2. Viruses: influenza/parainfluenza, PC virus, rhinoviruses, coronaviruses.
Not all persons exposed to the same adverse environmental influences develop chronic bronchitis. Even in many and long-term smokers, the latter may be absent. This indicates that the violation of the protective function of the bronchi, in particular, local immunity, plays an important role in the occurrence of chronic bronchitis.
Pathogenesis
In the pathogenesis of chronic bronchitis, the main role is played by a violation of the secretory, cleansing and protective functions of the bronchial mucosa. In a practically healthy person, bronchial clearance, being an important part of the mechanisms of sanogenesis, occurs continuously; as a result, the mucous membrane is cleared of foreign particles, cellular detritus, microorganisms by transferring them with the cilia of the ciliated epithelium along with a more viscous surface layer of bronchial mucus from the deeper sections of the bronchial tree towards the trachea and larynx.At the same time, other, in particular cellular, elements of bronchial contents (first of all, alveolar macrophages) take an active part in the cleansing of the mucosa. The effectiveness of the mucociliary clearance of the bronchi depends on two main factors: the mucociliary escalator, determined by the function of the ciliated epithelium of the mucosa, and the rheological properties of the bronchial secretion (its viscosity and elasticity), which depends on the optimal ratio of its two layers - "outer" (gel) and "internal" (sol).
The mechanical (toxic) effect of volatile pollutants causes structural changes in the bronchial mucosa (hyperplasia and metaplasia of goblet cells, squamous cell metaplasia of the epithelium, hypertrophy of the tracheobronchial glands). The resulting hypercrinia initially has a protective character: with an increase in the volume of bronchial contents, the concentration of antigenic material irritating the mucous membrane decreases, a protective cough reflex is excited, and pathogenic material is removed from the bronchi.
However, along with hypercrinia, the optimal ratio of sol and gel is inevitably violated (discrinia develops); the viscosity of the secret increases, making it difficult to remove it. In addition, as a result of the toxic effect of etiological factors, the movement of the cilia of the ciliated epithelium slows down, becomes ineffective, and further dystrophy and death of the ciliated cells occur. On the mucous membrane, "bald spots" are formed, i.e., areas free of ciliated epithelium.
In these places, the function of the mucociliary escalator is interrupted and there is a possibility of sticking (adhesion) to the damaged areas of the mucous membrane of opportunistic bacteria, primarily pneumococci and Haemophilus influenzae. These microbes, like other representatives of conditionally pathogenic microflora, with normal function of the mucociliary system, cannot adhere to an intact mucous membrane and locally accumulate in a diagnostically significant concentration (10 6 microbial cells in 1 ml of sputum).
In parallel with the development of mucociliary insufficiency, the phagocytic activity of alveolar macrophages and neutrophils decreases, the activity of T-lymphocytes is disturbed, the synthesis of antibodies, in particular, secretory immunoglobulin A (SIgA) and the content of lysozyme and lactoferrin in the mucus, decrease. Secondary immunological deficiency also contributes to the maintenance of the inflammatory process.
Recurrence of inflammation, associated primarily with the presence of a permanent depot of infection in the bronchi, leads to the development of panbronchitis, followed by the formation of deforming bronchitis and secondary bronchiectasis, which aggravate the course of the disease.
Pathomorphology
The morphological picture in chronic bronchitis depends on the severity, prevalence of the lesion and the presence of complications. The most characteristic are changes in the mucus-forming cells of the bronchial glands and the epithelium of predominantly medium and large bronchi in the form of hypertrophy of the tracheobronchial glands, hyperplasia and metaplasia of goblet cells, squamous metaplasia of the epithelium, which is manifested by an increase in the Reid index more than 0.5 (Reid index is the ratio of the thickness of the glandular layer to large bronchi to the thickness of the bronchial wall).At the same time, there is a decrease in the number of ciliated cells, and areas free of ciliated epithelium (“bald spots”) are formed. With an exacerbation of the inflammatory process, hyperemia of the mucosa is noted with the presence of purulent or mucopurulent contents in the lumen of the bronchi.
In the later stages of the disease, atrophy of the mucous membrane develops. Very often, the deeper layers of the bronchial wall also undergo changes: areas of thickening may alternate with areas of thinning due to uneven development of the connective tissue, which is accompanied by deformation and curvature of the bronchi. In areas of thinning, bronchiectasis is often found.
Clinical picture
It is not easy to establish the onset of the disease, since smokers often get used to a prolonged cough, mainly in the morning, and do not perceive it as a disease, but consider it as a morning “bronchial toilet”. Cough is estimated by them as a natural consequence of smoking and exposure to adverse production factors. It is accompanied by the release of a small amount of serous sputum (smoker's cough) and does not significantly affect performance and does not impair the quality of life.During their physical examination, the state of the respiratory organs usually does not differ from that of practically healthy people. Over the years, the cough becomes constant, regardless of the season, it worries the patient not only in the morning, when it is more pronounced, but also throughout the day. The amount of sputum increases and even without exacerbation can reach 50-75 ml per day.
Exacerbations of the disease in most patients occur no more than twice a year, they usually develop in early spring or late autumn, when changes in climatic and weather factors are most pronounced. Exacerbations occur against the background of the so-called cold, which usually hides an episodic or epidemic (during the period of a registered influenza epidemic) viral infection, which is soon joined by a bacterial infection (usually pneumococci and Haemophilus influenzae). In some cases, the cause of exacerbations of chronic bronchitis is the activation of saprophytic flora.
In the acute phase, the patient's well-being is determined by the ratio of two main syndromes - cough and intoxication), the latter is characterized by the presence of general symptoms: fever (usually to subfebrile values, rarely above 38 ° C), sweating, weakness, headache, decreased performance.
Complaints and changes in the upper respiratory tract (rhinitis, sore throat when swallowing, etc.) are determined by the characteristics of a viral infection (for example, rhinovirus, adenovirus) and the presence of chronic diseases of the nasopharynx (inflammation of the paranasal sinuses, compensated tonsillitis, etc.), which in this period is usually aggravated. The cough intensifies, the amount of sputum increases to 100-150 ml, and its quality changes (the degree of purulence and viscosity increases).
On examination, the sputum is watery or mucous with streaks of pus (with catarrhal endobronchitis) or purulent (with purulent endobronchitis). With increased viscosity of sputum, as a rule, there is a long hacking cough, which is extremely painful for the patient.
When examining patients, visible deviations from the norm on the part of the respiratory organs may not be detected. In a physical examination of the chest organs, the results of auscultation are of the greatest diagnostic value: during exacerbation, hard breathing is characteristic, usually heard over the entire surface of the lungs, and dry, low-pitched rales of a diffuse nature.
Dry buzzing rales of a low timbre are heard in endobronchitis with lesions of large and medium bronchi; being associated with a violation of the drainage function of the bronchi, they are aggravated by coughing and forced breathing. The timbre of wheezing becomes higher with a decrease in the lumen (caliber) of the affected bronchi, which is of diagnostic value.
When a liquid secret appears in the bronchi, moist rales, usually finely bubbling, can also be heard; their timbre also depends on the level of damage to the bronchial tree. In some patients, wheezing may also be in remission, but their number decreases, which can only be judged during dynamic observation.
The ventilation capacity of the lungs in the phase of clinical remission can remain normal for more than a dozen years. In the acute phase, the ventilation capacity of the lungs may also remain within the normal range (functionally stable bronchitis).
However, in some patients, during an exacerbation, a moderately pronounced bronchospasm joins, the clinical signs of which are expiratory dyspnea that occurs during exercise, transition to a cold room, at the time of a strong cough, sometimes at night, and dry high-pitched (whistling) wheezing; a study of respiratory function during this period of time reveals moderate obstructive disorders of lung ventilation, i.e., there is a bronchospastic syndrome (functionally unstable bronchitis).
Chronic bronchitis is not characterized by the presence of constant shortness of breath and its progression, the development of emphysema, respiratory and heart failure. Such unfavorable dynamics of the disease is inherent in patients with chronic obstructive bronchitis, which is currently included in COPD.
Diagnostics
Diagnosis of chronic bronchitis is based on anamnesis, the presence of symptoms indicating a possible damage to the bronchi (cough, sputum), the results of a physical examination of the respiratory organs and the exclusion of other diseases that may be characterized by largely similar clinical symptoms (pulmonary tuberculosis, bronchiectasis, bronchial cancer, etc.). .).Often in the anamnesis there are indications of past influenza or frequent acute respiratory viral infections, childhood infections (measles, whooping cough), after which a cough periodically recurs.
Laboratory data are used mainly to clarify the activity of the inflammatory process, the clinical form of bronchitis and differential diagnosis.
Indicators of the general blood test in catarrhal endobronchitis rarely change, with purulent - more often: moderate leukocytosis appears, a shift of the leukocyte formula to the left is noted, acceleration erythrocyte sedimentation rate (ESR). With sluggish inflammation, deviations of acute-phase biochemical tests are of relatively great diagnostic value: dysproteinemia with an increase in the content of 1- and 2-globulins, detection of C-reactive protein, haptoglobin, sialic acids and seromucoid in the blood serum.
Of particular importance is the cytological examination of sputum and bronchial washings, which determines the degree of inflammation; thus, with severe inflammation (III degree), in cytograms against the background of a mass of neutrophilic leukocytes, dystrophically altered cells of the bronchial epithelium and single alveolar macrophages are poorly represented; with moderate inflammation (grade II), along with neutrophilic leukocytes, a significant amount of mucus, alveolar macrophages and bronchial epithelial cells are found in the contents of the bronchi; with mild inflammation (I degree), the secret is predominantly mucous, desquamated cells of the bronchial epithelium predominate, there are few neutrophils and alveolar macrophages.
A certain relationship is revealed between the activity of inflammation and the physical properties of sputum (viscosity, elasticity). With purulent bronchitis in the acute phase in sputum, there is an increase in the content of acid mucopolysaccharides, deoxyribonucleic acid fibers and a decrease in the level of lysozyme, lactoferrin and SIgA. This reduces the resistance of the bronchial mucosa to the effects of infection.
Bacteriological examination of sputum should be carried out if there are signs of active inflammation in the bronchi and for the selection of rational antibiotic therapy.
An immunological study is usually indicated for signs of immune deficiency (repeated recurrence, poor curability of infectious foci) and progression of the infectious inflammatory process. In HB, more changes are recorded in the study of local immune reactivity compared to systemic; at the same time, deviations from cellular immunity (unlike obstructive pathological conditions) are weakly expressed.
In the acute phase, SIgA, the functional ability of alveolar macrophages and the phagocytic activity of neutrophils in the blood serum are usually reduced; the level of interleukin-2 is the higher, the more pronounced the activity of inflammation; about half of the patients showed an increase in the level of circulating immune complexes in the blood. Such indicators persist in about half of the patients and in the remission phase with a disease duration of up to 5 years.
In the majority of patients with chronic bronchitis for 3-5 years, both in the phase of remission and during exacerbation of the process, changes in the radiograph are not detected. In the future, there is an expansion and strengthening of the pattern of the roots of the lungs, thickening of the walls of the bronchi due to peribronchial pneumosclerosis.
The ventilation capacity of the lungs with functionally stable bronchitis is not changed. With functionally unstable bronchitis during the period of exacerbation, moderate obstructive disorders of lung ventilation are found ( forced expiratory volume in 1 secondFEV 1 ) > 50-60% of due).
Of great importance, especially in the diagnosis of the early stages of the disease, belongs to endoscopic examination, which allows to clarify the prevalence, activity, depth and nature of the inflammatory process (catarrhal or purulent endobronchitis). Value fibrobronchoscopy (FBS) increases when it is supplemented with a cytological examination of bronchial washings, biopsy of the mucosa, inoculation of the contents of the bronchi for microflora and a study of its sensitivity to antibiotics.
Bronchoscopy also makes it possible to judge the presence of tracheobronchial dyskinesia, it is also necessary for the differential diagnosis with cancer and bronchial tuberculosis.
Differential Diagnosis
Chronic bronchitis should be distinguished from:Acute protracted and recurrent bronchitis: they are characterized by a protracted (more than 2 weeks) course acute respiratory viral infection (SARS)(with acute protracted) or repeated short (up to 3-4 weeks) episodes of it 3 times a year or more (with recurrent bronchitis);
Secondary purulent (mucopurulent) bronchitis with bronchiectasis: it is characterized by a cough since childhood, after suffering "epitheliotropic" infections (measles, whooping cough, etc.), purulent sputum can be separated by a "full mouth", there is a connection between sputum discharge and position body; in the lungs, against the background of scattered dry buzzing rales, local changes are found in the lower sections (shortening of percussion sound, wet rales); with FBS, local purulent (mucopurulent) endobronchitis is detected, with bronchography - bronchiectasis;
Tuberculous lesions of the bronchi: it is characterized by signs of tuberculous intoxication, night sweats, the presence of Mycobacterium tuberculosis in sputum and bronchial washings, local endobronchitis with scars, fistulas with FBS; possible local radiographic changes in the lungs in the form of focal shadows, infiltration or cavities; positive serological tests for tuberculosis and positive results from the use of tuberculostatic drugs (therapia ex juvantibus);
Bronchial cancer: it is more common in men over 40 years of age, heavy smokers; characteristic cough, streaks of blood and atypical cells in the sputum; the results of FBS and biopsy are crucial;
Expiratory collapse (dyskinesia) of the trachea and large bronchi, which is characterized by a pertussis-like whooping cough, with FBS - bronchial dyskinesia of the II–III degree;
Bronchial asthma: it should be distinguished from functionally unstable bronchitis with broncho-obstructive syndrome. Asthma is more characteristic of: young age, a history of allergies, an increase in the number of eosinophils in sputum and blood (more than 5%), paroxysmal difficulty in breathing or coughing both during the day and (especially) during sleep, accompanied by wheezing in the chest; predominantly high-pitched scattered dry rales, a positive pharmacological functional test with β 2 -agonists (increase in FEV 1 more than 15% after inhalation of β 2 -agonists).
Code of chronic bronchitis in ICD-10
J 41.0 Chronic simple bronchitis.
Examples of the formulation of the diagnosis
The diagnosis of chronic bronchitis should include the nature of endobronchitis (catarrhal or purulent, it is desirable to indicate the pathogen), the phase of the disease (exacerbation or remission), functional characteristics in case of functionally unstable bronchitis:
Chronic catarrhal bronchitis, remission phase.
Chronic catarrhal bronchitis, exacerbation phase.
Chronic catarrhal bronchitis, functionally unstable, exacerbation phase. Respiratory failure (RD) I.
Chronic purulent bronchitis, exacerbation phase (caused by pneumococcus).
Saperov V.N., Andreeva I.I., Musalimova G.G.
