Chronic bronchitis (CB) is a diffuse inflammation of the mucous membranes of the bronchial tree and deeper layers of the bronchial wall, characterized by a long course with periodic exacerbations. Patients with CB include those who have a cough with sputum for at least three months a year for two years, excluding other diseases of the upper respiratory tract, bronchi and lungs that could cause these symptoms

Etiology

In the occurrence and development of CB, the following closely interact:

· exogenous factors: a significant role is played by irritating and damaging pollutants (domestic and professional), as well as non-indifferent dusts, which have a harmful (chemical and mechanical) effect on the bronchial mucosa. Pollutants are various chemical substances that, when accumulated in high concentrations, can cause deterioration in human health;

· endogenous factors: pathology of the nasopharynx, changes in breathing through the nose with impaired purification, humidification and warming of inhaled air; repeated acute respiratory diseases, acute bronchitis and focal infection of the upper respiratory tract, impaired immunity and metabolism;

· viruses (influenza viruses, adenoviruses) and mycoplasma;

· bacterial infection (pneumococcus, Haemophilus influenzae, moraxella).

nursing process chronic bronchitis

Classification

HB classification:

· simple uncomplicated bronchitis - occurs with the release of mucous sputum and without ventilation disturbances;

· purulent chronic bronchitis - occurs with the release of purulent sputum constantly or in the phase of exacerbation of the disease, without ventilation disorders;

· chronic obstructive bronchitis (COB) - occurs with the release of mucous sputum and persistent obstructive ventilation disorders;

· purulent-obstructive bronchitis - occurs with the release of purulent sputum and persistent obstructive ventilation disorders;

· special forms of chronic bronchitis: hemorrhagic and fibrous.

Clinic

The clinical picture of CB may vary depending on the nature of the inflammation and the variant of the disease. Typical clinical manifestations are cough, sputum production and shortness of breath.

Symptoms:

· cough - at the beginning of the disease it occurs only in the morning and is accompanied by the release of a small amount of sputum, after which, as a rule, it stops. This type of cough is due to the accumulation of sputum overnight, which, when changing body position, irritates the receptors, causing a cough reflex. It is typical for the cough to intensify during the cold and damp seasons; in the summer it may stop completely. Initially, the cough occurs only during exacerbations, later it grows and becomes disturbing during the period of remission. With an exacerbation of chronic disease, the sensitivity of the receptors increases, which is accompanied by an increase in coughing, which becomes hacking, barking, painful and paroxysmal. When bronchial obstruction occurs, the nature of the cough also changes; to expel sputum, the patient requires not 2-3 cough impulses, but much more. At the same time, he tenses painfully, the neck veins swell, the skin of the face and chest turns red, and the strength of the cough impulse is significantly reduced. This annoying, unproductive cough often occurs in the morning and is the most important clinical symptom of COB;

· sputum production is an essential clinical sign of CB. In the early stages of the disease, scanty sputum is produced; it can be mucous, light or gray. Subsequently, mucopurulent and purulent sputum appears, which has a characteristic yellow color. Its appearance is usually associated with another exacerbation. Purulent sputum is characterized by increased viscosity, especially at the beginning of the disease and in the morning. Sputum production is worse in cold weather and after drinking alcohol;

Shortness of breath is also a characteristic symptom. At first it occurs only with significant physical exertion or with an exacerbation of the process. Most often it bothers you in the morning and disappears after sputum is discharged. In this case, shortness of breath increases with changes in temperature, inhalation of odorous substances, emotional stress, etc. It intensifies when moving from a horizontal to a vertical position. As the disease progresses, shortness of breath begins to bother you with minimal physical activity and at rest;

· hemoptysis - in some cases possible, especially characteristic of hemorrhagic bronchitis;

· distortion of sleep rhythm (drowsiness during the day and insomnia at night);

· headache, worse at night;

· increased sweating;

· muscle tremors;

· impaired concentration;

· convulsions are possible.

During an external examination of the patient, the following is noted:

cyanosis of the skin;

· When examining the chest in the early stages of the disease, no changes can be noted. As complications develop, the chest becomes barrel-shaped;

· the location of the ribs is approaching horizontal;

The supraclavicular fossae bulge.

Auscultation of the lungs reveals:

· prolongation of exhalation;

· hard breathing, exhalation is heard as clearly as inhalation;

· Presence of dry wheezing;

· Moist rales are heard only in the presence of a large amount of liquid sputum.

When examining the cardiovascular system, it is noted:

· tachycardia;

· Blood pressure is increased.

Of the special forms, it is necessary to focus on hemorrhagic bronchitis. As a rule, this is non-obstructive bronchitis, the clinical picture of which is dominated by long-term hemoptysis. The diagnosis is established by excluding other causes of hemoptysis and according to characteristic bronchoscopy findings (thinned, easily bleeding mucosa). Less common is fibrinous bronchitis, which is characterized by the deposition in the bronchial tree of fibrin, Charcot-Leyden crystals and Courshman spirals, obliterating the airways. The clinical picture is dominated by a cough with periodic expectoration of “bronchial tree dummies.”

Acute bronchitis– acute diffuse inflammation of the mucous membrane (endobronchitis) or the entire wall of the bronchi (panbronchitis).

The etiology of acute bronchitis is a number of pathogenic factors affecting the bronchi:

1) physical: hypothermia, dust inhalation

2) chemical: inhalation of vapors of acids and alkalis

3) infectious: viruses - 90% of all acute bronchitis (rhinoviruses, adenoviruses, respiratory syncytial viruses, influenza), bacteria - 10% of all acute bronchitis (Mycoplasma pneumoniae, Chlamydia pneumoniae, Bordetella pertusis, Streptococcus pneumoniae) and their associations.

The main etiological factor is infectious, the others play the role of a trigger mechanism. There are also predisposing factors: smoking, alcohol abuse, heart disease with stagnation in the pulmonary circulation, the presence of foci of chronic inflammation in the nasopharynx, oral cavity, tonsils, genetic inferiority of the bronchial mucociliary apparatus.

Pathogenesis of acute bronchitis:

Adhesion of pathogens to epithelial cells lining the trachea and bronchi + reduction in the effectiveness of local protective factors (the ability of the upper respiratory tract to filter inhaled air and free it from coarse mechanical particles, change the temperature and humidity of the air, cough and sneeze reflexes, mucociliary transport) Þ pathogen invasion Þ hyperemia and edema of the bronchial mucosa, desquamation of the cylindrical epithelium, the appearance of mucous or mucopurulent exudate Þ further disturbance of mucociliary clearance Þ edema of the bronchial mucosa, hypersecretion of the bronchial glands Þ development of an obstructive component.

Classification of acute bronchitis:

1) primary and secondary acute bronchitis

2) according to the level of damage:

a) tracheobronchitis (usually against the background of acute respiratory diseases)

b) bronchitis with predominant damage to the medium-caliber bronchi

c) bronchiolitis

3) according to clinical symptoms: mild, moderate and severe severity

4) according to the state of bronchial patency: obstructive and non-obstructive

Clinic and diagnosis of acute bronchitis.

If bronchitis develops against the background of an acute respiratory viral infection, hoarseness, sore throat when swallowing, a feeling of rawness behind the sternum, and an irritating dry cough (manifestations of tracheitis) first appear. The cough intensifies and may be accompanied by pain in the lower chest and behind the sternum. As inflammation in the bronchi subsides, the cough becomes less painful, and copious mucopurulent sputum begins to be released.

Symptoms of intoxication (fever, headaches, general weakness) vary greatly and are determined more often by the causative agent of the disease(with adenoviral infection - conjunctivitis, with parainfluenza virus - hoarseness, with influenza virus - high fever, headache and mild catarrhal symptoms, etc.).

Objectively-percussion: clear pulmonary sound, auscultation: hard breathing, dry wheezing of varying heights and timbres, and when a sufficient amount of liquid sputum is released - small amounts of wet wheezing; wheezing intensifies with forced breathing of the patient.

Laboratory findings are not specific. Inflammatory changes in the blood may be absent. During a cytological examination of sputum, all fields of view are covered with leukocytes and macrophages.

Treatment of acute bronchitis.

1. Stay at home, drink plenty of fluids

2. Mucolytic and expectorants: acetylcysteine ​​(fluimucil) orally 400-600 mg/day in 1-2 doses or 10% solution in inhalation 3 ml 1-2 times/day for 7 days, bromhexine orally 8-16 mg 3 times/day for 7 days, ambroxol 30 mg, 1 tablet. 3 times/day 7 days.

3. In the presence of broncho-obstructive syndrome: short-acting beta-agonists (salbutamol in a dosage aerosol, 2 puffs each).

4. For uncomplicated acute bronchitis, antimicrobial therapy is not indicated; The effectiveness of prescribing antibiotics to prevent bacterial infection has not yet been proven. In case of acute bronchitis against the background of influenza, the earliest possible use of rimantadine according to the regimen is indicated. ABs are used most often in elderly people with serious concomitant pathologies and in children in the first years of life. AB of choice – amoxicillin 500 mg 3 times/day for 5 days, alternative AB – cefaclor 500 mg 3 times/day for 5 days, cefuroxime axetil 500 mg 2 times/day for 5 days, if intracellular pathogens are suspected – clarithromycin 500 mg 2 times/day or josamycin 500 mg 3 times a day for 5 days.

5. Symptomatic treatment (NSAIDs, etc.).

Chronic bronchitis (CB) is a chronic inflammatory disease of the bronchi, accompanied by a constant cough with sputum production for at least 3 months a year for 2 or more years, and these symptoms are not associated with any other diseases of the bronchopulmonary system, upper respiratory tract or other organs and systems.

HB is distinguished:

A) primary– an independent disease not associated with damage to other organs and systems, most often of a diffuse nature

b) secondary– etiologically associated with chronic inflammatory diseases of the nose and paranasal sinuses, lung diseases, etc., most often it is local.

Etiology of chronic bronchitis:

1) smoking:

Nicotine, polycyclic aromatic hydrocarbons of tobacco (benzopyrene, cresol) are strong carcinogens

Dysfunction of the ciliated epithelium of the bronchi, mucociliary transport

Components of tobacco smoke reduce the phagocytic activity of macrophages and neutrophils of the respiratory tract

Tobacco smoke leads to metaplasia of the ciliated epithelium and Clara cells, forming the precursors of cancer cells

Stimulation of proteolytic activity of neutrophils, hyperproduction of elastase --> destruction of elastic fibers of the lungs and damage to the ciliated epithelium --> emphysema

- ACE activity of alveolar macrophages --> AT II synthesis --> pulmonary hypertension

Nicotine increases the synthesis of IgE and histamine, predisposing to allergic reactions

2) inhalation of polluted air– inhaled aggressive substances (nitrogen and sulfur dioxide, hydrocarbons, nitrogen oxides, aldehydes, nitrates) cause irritation and damage to the bronchopulmonary system.

3) influence of occupational hazards- various types of dust (cotton, floury wood), toxic vapors and gases (ammonia, chlorine, acids, phosgene), high or low air temperature, drafts, etc. can lead to CB.

4) damp and cold climate– contributes to the development and exacerbation of chronic disease.

5) infection– more often it is secondary, joining when the conditions for infection of the bronchial tree have already been formed. The leading role in exacerbations of chronic disease is played by pneumococcus and Haemophilus influenzae, as well as viral infection.

6) previous acute bronchitis(most often untreated, protracted or recurrent)

7)genetic factors and hereditary predisposition

Pathogenesis of chronic bronchitis.

1. Dysfunction of the local bronchopulmonary defense system and immune systems:

A. dysfunction of mucociliary transport (ciliated epithelium)

b. dysfunction of the surfactant system of the lungs --> increased viscosity of sputum; violation of nonciliary transport; collapse of the alveoli, obstruction of small bronchi and bronchioles; colonization of microbes in the bronchial tree

V. violation of the content of humoral protective factors in the bronchial contents (deficiency of IgA, complement components, lysozyme, lactoferrin, fibronectin, interferons

d. violation of the ratio of proteases and their inhibitors (a 1 -antitrypsin and a 2 -macroglobulin)

d. decreased function of alveolar macrophages

e. dysfunction of local broncho-associated lymphoid tissue and the body’s immune system as a whole

2. Structural restructuring of the bronchial mucosa- a significant increase in the number and activity of goblet cells, hypertrophy of the bronchial glands --> excess mucus production, deterioration of the rheological properties of sputum --> mucostasis

3. Development of the classical pathogenetic triad(hypercrinia - increased mucus production, discrinia - mucus becomes viscous, thick, mucostasis - stagnation of mucus) and the release of inflammatory mediators and cytokines (histamine, arachidonic acid derivatives, TNF, etc.) --> a sharp violation of the drainage function of the bronchi, good conditions for microorganisms --> penetration of infection to deep layers and further damage to the bronchi.

Clinical picture of chronic bronchitis.

Subjectively:

1) cough– at the beginning of the disease it is periodic, bothers patients in the morning soon after waking up, the amount of sputum discharge is small; The cough increases in the cold and damp seasons, and in the summer it may stop completely. As CB progresses, the cough becomes constant, disturbing not only in the morning, but throughout the day and even at night. When the process worsens, the cough sharply intensifies, becomes annoying and painful. In the late stage of the disease, the cough reflex may fade, and the cough ceases to bother the patient, but bronchial drainage is sharply disrupted.

2) sputum separation– it can be mucous, purulent, mucopurulent, sometimes streaked with blood; in the early stages of the disease, the sputum is light, mucous, easily separated, as the process progresses it acquires a mucopurulent or purulent character, is separated with great difficulty, and as the process worsens, its quantity increases sharply. Hemoptysis may be caused by damage to the blood vessels of the bronchial mucosa during a hacking cough (requires differential diagnosis with tuberculosis, lung cancer, bronchiectasis).

3) shortness of breath– begins to bother the patient with the development of bronchial obstruction and emphysema.

Objectively:

1) upon inspection, no significant changes are revealed; During an exacerbation of the disease, sweating and an increase in body temperature to subfebrile levels may be observed.

2) percussion clear pulmonary sound, with the development of emphysema - box sound.

3) auscultation: lengthening of exhalation, hard breathing (“roughness”, “unevenness” of vesicular breathing), dry wheezing (due to the presence of viscous sputum in the lumen of the bronchi, in large bronchi - low-pitched bass, in the middle bronchi - buzzing, in small bronchi - whistling) . If there is liquid sputum in the bronchi - moist rales (in large bronchi - large-bubble, in the middle bronchi - medium-bubble, in small bronchi - fine-bubble). Dry and wet wheezing is unstable and may disappear after vigorous coughing and expectoration of sputum.

Variants of the clinical course of chronic disease: with and without symptoms of bronchial obstruction; latent course, with rare exacerbations, with frequent exacerbations and continuously relapsing course of the disease.

Clinical and diagnostic signs of exacerbation of chronic disease:

Increased general weakness, the appearance of malaise, decreased overall performance

The appearance of severe sweating, especially at night (a symptom of a damp pillow or sheet)

Low-grade body temperature

Tachycardia at normal temperature

Increased cough, increased amount and “purulence” of sputum

The appearance of biochemical signs of inflammation

A shift in the leukocyte formula to the left and an increase in ESR to moderate numbers

Diagnosis of chronic bronchitis.

1. Laboratory data:

A) UAC– little change, inflammatory changes are typical during exacerbation of the process

b) sputum analysis– macroscopic (white or transparent – ​​mucous or yellow, yellow-green – purulent; streaks of blood, mucous and purulent plugs, bronchial casts can be detected) and microscopic (a large number of neutrophils, bronchial epithelial cells, macrophages, bacteria), bacteriological examination of sputum and determination of pathogen sensitivity to antibiotics.

V) TANK– biochemical indicators of inflammation activity allow us to judge its severity (decrease in albumin-globulin ratio, increase in haptoglobin, sialic acids and seromucoid).

2. Instrumental research:

A) bronchoscopy– bronchoscopically, diffuse (inflammation covers all endoscopically visible bronchi) and limited (inflammation covers the main and lobar bronchi, segmental bronchi are not changed) bronchitis is isolated, the intensity of bronchial inflammation is determined (I degree - the bronchial mucosa is pale pink, covered with mucus, does not bleed; II degree - the bronchial mucosa is bright red, thickened, often bleeds, covered with pus; III degree - the bronchial and tracheal mucosa is thickened, purple-bluish in color, bleeds easily, covered with purulent secretion).

b) bronchography– carried out only after sanitation of the bronchial tree; Chronic bronchitis is characterized by:

The bronchi of the IV-VII orders are cylindrically expanded, their diameter does not decrease towards the periphery, as is normal; the lateral branches are obliterated, the distal ends of the bronchi are blindly broken off (“amputated”);

In a number of patients, the dilated bronchi are narrowed in some areas, their contours are changed (the shape of a “rosary”), the internal contour of the bronchi is jagged, and the architectonics of the bronchial tree is disrupted.

V) chest x-ray– signs of chronic disease are detected only in long-term patients (intensification and deformation of the pulmonary pattern according to the loop-cellular type, increased transparency of the pulmonary fields, expansion of the shadows of the roots of the lungs, thickening of the walls of the bronchi due to peribronchial pneumosclerosis).

G) pulmonary function test(spirography, peak flowmetry) – to identify obstructive disorders

Complications of chronic disease.

1) directly caused by infection: a) pneumonia b) bronchiectasis c) broncho-obstructive syndrome d) bronchial asthma

2) due to the evolution of bronchitis: a) hemoptysis b) emphysema c) diffuse pneumosclerosis d) respiratory failure e) cor pulmonale.

Treatment of CB is different during the period of remission and during the period of exacerbation.

1. During remission: for chronic disease of mild severity - elimination of foci of infection (caries, tonsillitis, etc.), hardening of the body, therapeutic physical training, breathing exercises; for moderate and severe CB – additional courses of pathogenetic treatment are carried out aimed at improving bronchial patency, reducing pulmonary hypertension and combating right ventricular heart failure.

2. During an exacerbation:

A) etiotropic treatment: oral AB taking into account the sensitivity of flora cultured from sputum (semi-synthetic penicillins: amoxicillin 1 g 3 times/day, protected penicillins: amoxiclav 0.625 g 3 times/day, macrolides: clarithromycin 0.5 g 2 times/day, respiratory fluoroquinolones: levofloxacin 0.5 g 1 time/day, moxifloxacin 0.4 g 1 time/day) for 7-10 days. If treatment is ineffective, parenteral administration of III-IV generation cephalosporins (cefepime IM or IV 2 g 2 times a day, cefotaxime IM or IV 2 g 3 times a day).

b) pathogenetic treatment, aimed at improving pulmonary ventilation, restoring bronchial patency:

Mucolytic and expectorant drugs: ambroxol 30 mg orally 3 times a day, acetylcysteine ​​200 mg orally 3-4 times a day for 2 weeks, herbal preparations (Thermopsis, ipecac, mucaltin)

Therapeutic bronchoscopy with bronchial rehabilitation

Bronchodilators (M-anticholinergics: ipratropium bromide 2 puffs 3-4 times/day, beta-agonists: fenoterol, their combination - Atrovent inhalation, prolonged aminophylline: theotard, teopek, theobilong orally 1 tablet 2 times/day)

Medicines that increase the body's resistance: vitamins A, C, B, immunocorrectors (T-activin or thymalin 100 mg subcutaneously for 3 days, ribomunil, bronchomunal orally)

Physiotherapeutic treatment: diathermy, calcium chloride electrophoresis, quartz on the chest area, chest massage, breathing exercises

V) symptomatic treatment: drugs that suppress the cough reflex (for an unproductive cough - libexin, tusuprex, for a hacking cough - codeine, stoptussin)

Outcome of chronic bronchitis: in the obstructive form or CB with damage to the distal parts of the lungs, the disease quickly leads to the development of pulmonary failure and the formation of cor pulmonale.

Vermeirc (1996) proposed the following diagnostic criteria for chronic obstructive bronchitis:

• bronchial obstruction itself (clinical manifestations and a decrease in FEV1 less than 84% and/or a decrease in the Tiffno index below 88% of the expected values);
• irreversibility or partial reversibility of bronchial obstruction, variability (spontaneous variability) of FEV values ​​by less than 12% during the day;
• stably confirmed bronchial obstruction - at least 3 times during one-year observation;
• age is usually over 50 years;
• detection of the disease usually in smokers or persons exposed to industrial air pollutants;
• physical and radiological signs of emphysema;
• steady progression of the disease in the absence of adequate treatment, which is manifested by increasing shortness of breath and an annual decrease in FEV1 by more than 50 ml.

Assessing the severity of chronic obstructive bronchitis

According to the methodological recommendations “Chronic obstructive bronchitis” of the Russian Society of Pulmonologists (Moscow, 1997), the severity of chronic obstructive bronchitis is assessed by the FEV1 value. The approach to assessing the severity of patients with chronic obstructive bronchitis is complemented by determining the stage of the disease, based on the overall picture of the severity of the disease, bronchial obstruction according to the recommendations of the American Thoracic Society.

• Stage I. FEV1 is more than 50% of the normal value. The disease has little impact on quality of life. Patients do not need frequent examinations by a general practitioner. The presence of severe shortness of breath in such patients requires additional examinations and consultation with a pulmonologist.
• Stage II FEV1 is 35-49% of the normal value. The disease significantly reduces the quality of life. Frequent visits to a medical facility and observation by a pulmonologist are required.
• Stage III. FEV1 is less than 34% of the expected value. The disease sharply reduces the quality of life. Frequent visits to medical institutions and observation by a pulmonologist are required.

Examination program for chronic obstructive bronchitis

1. General blood and urine analysis.
2. BAC: content of total protein and protein fractions, fibrin, haptoglobin, seromucoid, sialic acids, bilirubin, aminotransferases, glucose, creatinine.
3. IAC: blood content and determination of the functional ability of T- and B-lymphocytes, determination of subpopulations of T-lymphocytes, immunoglobulins, circulating immune complexes.
4. X-ray examination of the lungs.
5. Spirography; peak flowmetry or pneumotachometry.
6. Echocardiography.
7. General and bacteriological analysis of sputum.

Laboratory and instrumental diagnostics

At the initial stages of the development of the disease, a thorough questioning of the patient, assessment of anamnestic data and possible risk factors are of great importance. During this period, the results of an objective clinical study, as well as data from laboratory and instrumental methods, are not very informative. Over time, when the first signs of broncho-obstructive syndrome and respiratory failure appear, objective clinical, laboratory and instrumental data become increasingly important diagnostically. Moreover, an objective assessment of the stage of development of the disease, the severity of COPD, and the effectiveness of the therapy is possible only using modern research methods.

X-ray examination

X-ray examination of the chest in two projections is a mandatory method of examining all patients with COPD. The study allows us to identify the presence of signs of broncho-obstructive syndrome, including pulmonary emphysema, some complications of COPD (bronchiectasis, pneumonia, pneumothorax, pulmonary arterial hypertension, chronic pulmonary heart disease, etc.), and indirectly assess the phase of the disease.

An important objective of the study is the radiological differential diagnosis of COPD with diseases also accompanied by prolonged cough and shortness of breath (lung cancer, pulmonary tuberculosis, bronchiectasis, cystic fibrosis, etc.).

In the initial stage of COPD, radiographic changes may be absent. As the disease progresses, distinct radiological signs of pulmonary emphysema begin to appear, reflecting, first of all, an increase in the airiness of the lungs and a reduction in the vascular bed. These radiological signs include:

• increase in the total area of ​​the pulmonary fields;
• persistent decrease in lung transparency;
• depletion of the pulmonary pattern at the periphery of the pulmonary fields;
• the appearance of limited areas of ultra-high transparency, corresponding to large emphysematous bullae;
• flattening of the dome of the diaphragm and significant limitation of its mobility during breathing (less than 3-5 cm);
• reduction in the transverse dimensions of the heart (“drip” or “hanging” heart);
• increase in retrospinal space and others.

The listed radiological signs of pulmonary emphysema are the most important confirmation of the presence of broncho-obstructive syndrome in the patient.

It is more difficult to identify radiological signs of inflammatory damage to the bronchi. In patients with moderate and severe COPD, inflammation of the bronchi may be accompanied by edema, and then the development of sclerosis of peribronchial and interstitial tissue and a peculiar heaviness of the pulmonary pattern. In relatively rare cases, usually with a long-term history of the disease, a reticular deformation of the pulmonary pattern is observed in the form of reticular pneumosclerosis, localized mainly in the lower parts of the lungs. Deformation of the pulmonary pattern is a change in the normal course and shape of the elements of the pulmonary pattern, which forms a randomly branching network. These changes are caused by sclerosis of peribronchial tissues, as well as interlobular and intersegmental septa.

One of the reasons for the depletion of the pulmonary pattern is severe disturbances of bronchial obstruction in patients with COPD, often accompanied by the development of microatelectasis. In these cases, the depletion of the pulmonary pattern is due to the simultaneous compensatory overextension of the lung tissue in a limited zone located directly adjacent to the microatelect area.

Finally, in severe cases, radiographic evidence of pulmonary arterial hypertension and chronic cor pulmonale with hypertrophy and dilatation of the right ventricle can be detected. The development of pulmonary arterial hypertension is evidenced by the expansion of all large branches of the pulmonary artery in the roots (more than 1.5-1.6 cm) and a decrease in the caliber of small peripheral arteries of the muscular type (the “jump in caliber” symptom). There is also a bulging of the cone of the pulmonary artery trunk in the form of an increase in the 2nd arch of the left contour of the heart.

Well-known radiographic signs of right ventricular hypertrophy in patients with COPD are not always detected, primarily due to a decrease in the overall transverse size of the heart (“hanging” heart) and the presence of severe emphysema, which increases the retrosternal space and, as it were, moves the wall of the right ventricle away from the anterior chest wall.

X-ray computed tomography (CT) has significant advantages over traditional x-ray examination and allows you to identify signs of inflammatory damage to the bronchi and emphysema even in the earliest stages of the disease.

To diagnose pulmonary emphysema, for example, a CT technique is used with a quantitative measurement of the transparency of the lung during inhalation and exhalation. However, despite its high information content, CT technology is rarely used in patients with COPD to confirm damage to the bronchi and pulmonary parenchyma. More often, CT is used to exclude lung tumors, tuberculosis, or other diseases that resemble the clinical picture of COPD.

Blood test

Exacerbation of COPD may be accompanied by neutrophilic leukocytosis with a shift in the blood count to the left and an increase in ESR, although these changes are not obligatory.

With a long course of the disease, accompanied by the occurrence of chronic respiratory failure and hypoxemia, signs of secondary erythrocytosis can be detected in the peripheral blood (increased number of red blood cells, increased hemoglobin content, increased blood viscosity and hematocrit value (in women more than 47% and in men more than 52%). Against this background, a decrease in ESR to 1-3 mm/h is often noted.

There is also an increase in the content of acute phase proteins in the blood serum (a1-antitrypsin, a2-glycoprotein, a2-macroglobulin, haptoglobulin, ceruloplasmin, seromucoid, C-reactive protein), as well as a2- and beta-globulips, which indicates the activity of the inflammatory process in bronchi.

Sputum examination

Sputum examination in patients with COPD differs little from the corresponding procedure in patients with pneumonia. When microscopy of mucopurulent sputum, which usually corresponds to moderate activity of the inflammatory process in the bronchi, neutrophils (up to 75%) and alveolar macrophages predominate in the smears. Purulent endobronchitis is characterized by an even higher content of neutrophils (up to 85-95%) and dystrophically altered bronchial epithelial cells.

In patients with severe exacerbation of obstructive bronchitis, purulent sputum or frequent relapses of bronchial inflammation, it becomes necessary to determine the causative agent of endobronchitis. For this purpose, a bacteriological examination of sputum or BAL fluid is carried out.

Most often, exacerbations of chronic bronchitis are caused by Haemophilus influenzae or the association of Haemophilus influenzae with Moraxella. This association is especially often found in smokers, including people who do not suffer from chronic obstructive bronchitis. In other cases, the causative agent of endobronchitis is pneumococci and other streptococci.

In elderly, weakened patients with severe COPD, staphylococci, Pseudomonas aeruginosa and Klebsiella may predominate in the sputum.

Finally, in recent years, in relatively young and middle-aged patients, intracellular (“atypical”) microorganisms: chlamydia, legionella or mycoplasma are increasingly (in some countries up to 20-30%) the causative agent of the inflammatory process in the bronchi.

Bronchoscopy

Bronchoscopy is currently one of the most common and informative methods for studying the respiratory tract. The method allows:

1. visually assess the anatomical features of the respiratory tract, the condition of the trachea, main, segmental and subsegmental bronchi;
2. conduct a biopsy of the areas of interest in the tracheobronchial tree and obtain material for histological and cytological examination;
3. using aspiration of bronchial lavage water, obtain material for cytological, immunological and bacterioscopic examination
4. For therapeutic purposes, perform bronchial lavage.

Bronchoscopy in patients with COPD is advisable in the following cases:

• in the presence of clinical and radiological signs suspicious for the presence of a lung tumor;
• with purulent sputum;
• if you suspect the presence of tracheobronchial dyskinesia;
• when clarifying the source of pulmonary hemorrhage;
• if it is necessary to obtain aspiration material to clarify the etiology of the disease (for example, identifying the causative agent of the infectious process in the bronchi and lungs);
• if necessary, for therapeutic purposes, local administration of medications (for example, antibiotics) directly to the affected area;
• when performing therapeutic bronchial lavage.

The main contraindications to bronchoscopy are:

• acute myocardial infarction or unstable angina;
• severe circulatory failure stage II6-III and/or hemodynamic instability;
• paroxysmal heart rhythm disturbances;
• arterial hypertension with an increase in blood pressure above 200 and 110 mm Hg. Art. or hypertensive crisis;
• acute cerebrovascular accident;
• rapidly progressing hypercapnia;
• unconscious state of the patient, complete lack of contact with the patient;
• acute inflammatory diseases or tumors of the upper respiratory tract (acute laryngitis, laryngeal cancer, etc.);
• insufficient instrumentation and training of medical personnel.

It should be emphasized that in patients with arterial hypoxemia and even in patients with blood coagulation disorders and thrombocytopenia, bronchoscopy is completely safe. However, in the latter cases, a biopsy of the bronchial mucosa and pulmonary parenchyma and other invasive procedures are not indicated.

Research technique

Bronchoscopy, which is a rather complex technically instrumental research method associated with a certain risk for the patient, should be performed only in specialized pulmonology departments of hospitals with intensive care services. The study is carried out in special X-ray and bronchology rooms that meet the requirements of a small operating room or surgical dressing room, or in an endoscopic room equipped with a mobile X-ray unit, preferably with an electron-optical converter and a TV.

In patients with COPD, the study is carried out using a flexible bronchofiberscope under local anesthesia with a 2.4% trimecaine solution, 2-4% lidocaine solution or 1% dicaine solution. First, by irrigation or lubrication with a local anesthetic, anesthesia is achieved in the upper respiratory tract - the oropharynx and vocal cords. After 5 minutes, a bronchofiberscope is inserted through the lower nasal passage or oral cavity and, while inhaling, it is passed through the glottis. By installing aseptics through a bronchoscope, the trachea and large bronchi are anesthetized.

Research using a bronchofiberscope includes several stages:

Aspiration of bronchial contents using a special bronchofiberscope. The contents of the bronchus are aspirated for subsequent bacteriological, cytological and other types of research. If there is a small amount of bronchial secretion, about 20 ml of an isotonic solution is first instilled into the bronchus, and then this solution is aspirated along with the contents of the bronchus, obtaining the so-called bronchial lavage modes, which are subsequently subjected to bacteriological and cytological examination.

Diagnostic subsegmental bronchoalveolar lavage (BAL) for cytological and bacteriological examination of bronchoalveolar contents. To carry out this procedure, a bronchofibroscope is brought under visual control to the mouth of the subsegmental bronchus and about 50-60 ml of an isotonic sodium chloride solution is injected into the bronchus through the aspiration channel of the bronchofibroscope, then the liquid coming from the lumen of the bronchus (BAL) is aspirated into a special polyethylene glass. The introduction of the solution and aspiration of BALF is repeated 2~3 times. The composition of BALF includes cellular, protein; and other components of alveolar and, to a lesser extent, bronchial contents. To reduce the admixture of bronchial secretions, not the first, but the second or third portion of the resulting BALF is used for bacteriological and cytological examination. Bronchial biopsy, which is carried out using special flexible forceps (direct bronchial biopsy) or a brush with a diameter of about 2 mm (brush or brush biopsy), brought to the site of interest through the aspiration channel of a bronchofibroscope under visual endoscopic control. After receiving the biopsy material, smears are immediately prepared from it.

If necessary, transbronchial (intrapulmonary) biopsy and puncture biopsy of trachsobronchial lymph nodes can be performed.

Some of the listed methods are very complex and unsafe for the patient, so the choice of each of them depends on the specific indications and contraindications for bronchoscopy, the equipment of the bronchoscopic room, in particular X-ray television equipment, and the qualifications of the endoscopist. Visual assessment of the condition of the trachea and bronchi is carried out in all cases of bronchofibroscopy

Visual assessment of the condition of the trachea and bronchi

The effectiveness of diagnosing respiratory diseases using bronchoscopy depends not only on the equipment of the endoscopic room and the qualifications of the endoscopist, but also on the correct choice of a particular research technique, as well as on the attending physician’s knowledge of the diagnostic capabilities of the method

A thorough examination of the vocal folds, subglottic space, trachea and bronchi allows one to assess the anatomical features of the upper and lower respiratory tract, identify inflammatory, neoplastic and other changes in the mucosa, as well as evaluate some dysfunctions of the trachea and bronchi.

Hypotonic tracheobronchial dyskinesia. For patients with COPD, a violation of the elastic-elastic properties of the walls of the bronchi is very characteristic, with the appearance in some cases of a clinical picture of hypotonic tracheobronchial dyskinesia, the diagnosis of which can only be confirmed endoscopically.

Tracheobronchial dyskinesia is a prolapse of the posterior membranous part of the mucous membrane of these organs into the lumen of the trachea or large bronchi, causing attacks of painful hacking cough, accompanied by an attack of suffocation, stridor breathing and even loss of consciousness. It should be remembered that the only reliable and at the same time accessible method for identifying tracheobronchial dyskinesia is bronchoscopy.

The main endoscopic sign of tracheobronchial dyskinesia is a significant increase in the amplitude of respiratory movements of the membranous wall of the trachea and main bronchi and, accordingly, the degree of their expiratory narrowing compared to the norm. Let us recall that normally, during a quiet exhalation, there is a faintly noticeable bulging of the membranous part of the mucosa into the lumen of the trachea and bronchi; upon inhalation, it returns to its original position. With forced breathing or coughing, the expiratory bulging of the wall of the trachea and main bronchi increases; however, normally such expiratory narrowing of the lumen does not exceed 30%.

With dyskinesia of the first degree, expiratory narrowing of the trachea and main bronchi to 2/3 of their lumen is observed while maintaining their normal (rounded) configuration or some flattening of the lumen. Dyskinesia of the second degree is characterized by complete closure of the posterior and anterior membranous walls during exhalation and significant flattening of the lumen of the trachea and bronchi.

Tracheobronchial dyskinesia in patients with COPD can significantly increase the resistance of the trachea and main bronchi during forced expiration and aggravate expiratory airway obstruction.

Inflammatory changes in the mucous membrane. Endoscopic signs of inflammatory changes in the mucous membrane of the trachea and bronchi include:

• hyperemia of the mucous membrane of the trachea and bronchi;
• swelling of the mucous membrane;
• bleeding of the mucous membrane during instrumental palpation;
• changes in the vascular pattern of the mucous membrane;
• individual accumulations of mucous or mucopurulent secretion (with catarrhal endobronchitis) or abundant purulent contents in the lumen of the bronchi (for example, with purulent endobronchitis), etc.

The last sign has an independent and very important diagnostic value and indicates a suppurative process in the lung, although it may not always be caused by purulent bronchitis (pus can enter the lumen of the bronchi from alveolar tissue, abscess, etc.). Such an endoscopic picture always requires further in-depth examination of patients.

According to the most common classification by J. Lemoine (1965), there are three main forms of inflammatory damage to the bronchi, detected by visual examination:

1. Diffuse endobronchitis, characterized by the spread of inflammation to all visible bronchi and the absence of a distal border of mucosal inflammation.
2. Partially diffuse endobronchitis, in which signs of inflammation persist in all visible bronchi, with the exception of the upper lobe bronchi.
3. Limited (local) endobronchitis with clearly defined boundaries of inflammatory changes, which are localized in the main and lobar bronchi and are absent in the segmental and subsegmental bronchi.

When studying the visual endoscopic picture, as well as histological and cytological changes within the described forms of endobronchitis, different morphological types of bronchitis can be distinguished:

• simple (catarrhal) endobronchitis;
• purulent endobronchitis;
• atrophic endobronchitis.

Catarrhal (simple) endobronchitis is most common in patients with COPD. In this case, endoscopically reveals hyperemia, swelling and increased bleeding of the bronchial mucosa. Purulent endobronchitis is distinguished, first of all, by the presence of purulent sputum in the lumen of the bronchi. Finally, atrophic endobronchitis is characterized by thinning and dryness of the mucous membrane, increased vascular pattern, the appearance of characteristic fine folding of the mucous membrane, desolation and expansion of the mouths of the bronchial glands and a tendency to bleeding.

When assessing the results of an endoscopic examination, it should be remembered that a visual examination of the mucous membrane can only be carried out to the level of gradation 5-7 of the segmental bronchi. To obtain information about damage to smaller bronchi, which is typical for patients with COPD, you can use the results of a study of materials from bronchial washings or BALF.

Examination of BALF obtained by bronchoscopy includes:

1. study of the cellular composition of bronchoalveolar contents;
2. identification of pathogenic microorganisms, and, if possible, identification of the causative agent of the infectious inflammatory process and, if necessary,
3. biochemical analysis of BALF (determining the content of protein, lipids, enzymes, immunoglobulins, etc.).

The scope of the BALF examination is determined each time by the specific diagnostic tasks facing the doctor.

Cytological analysis of BALF. To study the cellular composition of the bronchoalveolar contents, BALF is centrifuged at a temperature of + 4 ° C and smears are prepared from the sediment, which are stained with Romanovsky-Giemsa or other dyes and subjected to microscopy. The total number of cells in 1 ml of BALF is counted using a hemocytometer or an automatic hemoanalyzer.

Normally, the number of cells in 1 ml of BALF is 0.5-10.5 x 10 5. Of these, alveolar macrophages account for more than 90% of all cellular elements, lymphocytes - about 7% and neutrophils - less than 1%. Other cellular elements are extremely rare.

Diagnosis of lung diseases based on the results of a cytological study of BALF is based on changes in the ratio of the main cellular elements (alveolar macrophages, lymphocytes and neutrophils), identification of additional inclusions in these cells and disruption of their morphology and histochemical properties, as well as the detection of new pathological cells. In patients with COPD, an increase in the content of neutrophils and lymphocytes is found in the BALF.

Microbiological examination of BALF

Of great practical importance is the identification of pathogens of the inflammatory process in the lungs in the bronchial and bronchoalveolar contents. The diagnostic significance of microbiological examination of tracheobronchial washings (bronchial washings) and BALF is somewhat higher than the corresponding examination of sputum, since the material for research can be obtained directly from the lesion. Microbiological examination of BALF has a particularly high diagnostic value for respiratory tract infections caused by Pneumocystis carini, Mycobacterium tuberculosis, cytomegalovirus, fungi and other pathogens.

At the same time, the complexity of the bronchoscopy procedure with aspiration of bronchial or bronchoalveolar contents does not yet allow the widespread use of this method to identify the causative agent of the inflammatory process and determine the sensitivity of microflora to antibiotics. Therefore, in most cases, microbiological examination of sputum is still preferable.

The bronchoscopic method of obtaining BALF to determine the causative agent of the infectious process, apparently, is justified only in cases where, for various reasons, sputum is absent or the results of its microbiological examination are questionable, and the rapid progression of the inflammatory process and the lack of effect from the prescribed therapy are clinically revealed. In clinical practice, the method of microbiological examination of BALF obtained during bronchoscopy is usually used if there are other indications for bronchoscopy.

Biochemical study of BALF with determination of the content of protein, sialic acids, haptoglobin, lipid peroxidation products, antioxidants and other substances is a very promising direction for assessing the activity and degree of the inflammatory process in the lungs and bronchi and differential diagnosis of some forms of bronchial damage. However, they have not yet found widespread use in clinical practice.

Study of material obtained from biopsy

Cytological examination. The material for cytological examination is smears obtained during bronchoscopy, scrapings with a brush on the affected area, aspirates of bronchial contents, BALF, punctates, as well as prints of a biopsied piece of tissue. Cytological examination of material obtained from a biopsy makes it possible with a high degree of probability to diagnose morphological changes in cells characteristic of large groups of lung lesions (for example, acute or chronic inflammatory diseases) or even signs that are pathognomonic of individual diseases.

Thus, acute inflammatory changes in the lungs and bronchi (bronchitis, pneumonia, abscess) are characterized by the presence of amorphous necrotic masses, a large number of polymorphonuclear leukocytes, reactive structural changes in epithelial cells up to the development of their atypia.

In chronic inflammatory diseases, the biopsy material reveals cells of the inflammatory infiltrate (polymorphonuclear leukocytes, lymphocytes, monocytes, plasma cells, macrophages, etc.), reactive changes in bronchial epithelial cells, and goblet cell hyperplasia.

Histological examination of biopsy specimens. For histological examination, microslides prepared from a piece of tissue obtained from a direct biopsy of the mucous membrane of the trachea and bronchi, transbronchial, transbronchial and other types of biopsy of the tracheobronchial tree, lung tissue, lymph nodes and pleura are used.

In patients with COPD, using this method, characteristic morphological signs of chronic inflammation of the bronchial mucosa can be identified - changes in the bronchial epithelium, swelling and infiltration of bronchial walls with leukocytes, hyperplasia of the bronchial glands, etc. In patients with atrophic endobronchitis, a decrease in the number of secreting goblet cells and basal layer cells is found , a significant increase in the content of degenerated cells of the bronchial epithelium, histological signs of atrophy and metaplasia of the bronchial epithelium.

Assessment of respiratory function

The most important method for quantitatively assessing the degree of ventilation disturbances in patients with COPD, the severity of the disease and the nature of bronchial obstruction is the determination of external respiratory function (ERF).

The most complete picture of these disorders can be obtained by analyzing the structure of the total lung capacity, determined using the method of general body plethysmography. However, the use of this complex, expensive research method is limited in general clinical practice. Therefore, assessment of respiratory function in patients with COPD is usually carried out using the method of computed spirography and quantitative analysis of the flow-volume loop. In patients with COPD, this method gives quite acceptable results for assessing the severity of broncho-obstructive syndrome.

According to modern concepts, the main spirographic sign of obstructive syndrome is a slowdown in forced expiration due to an increase in airway resistance. The main indicators of the spirogram reflecting these violations are:

• FEV1 - forced expiratory volume in 1 second;
• FEV1/FVC (Tiffno index);
• The average forced expiratory volumetric flow rate is 25-75% of FVC (FVC 25%-75%).
• Maximum forced expiratory volumetric flow rate at 25%, 50% and 75% of FVC (MOF25%, MEF50%, MEF75%).

In widespread clinical practice, the FEV1 indicator is used, which is considered a marker of broncho-obstructive syndrome. It is believed that a decrease in this indicator below 80% of the required values ​​is a sign of broncho-obstructive syndrome.

At the same time, it should be remembered that the absolute values ​​of FEV1 can decrease not only with bronchial obstruction, but also with severe restrictive disorders due to a proportional decrease in all pulmonary volumes and capacities, including FVC and FEV1. Therefore, a more reliable indicator of broncho-obstructive syndrome is the Tiffio index - the ratio of FEV1 to FVC (FEV1/FVC). A decrease in this indicator less than 70% in most cases indicates the presence of bronchial obstruction syndrome.

An even more informative indicator of small airway obstruction is probably the SOS rate of 25-75%, i.e. the average volumetric air flow rate during forced expiration, measured at the level of relatively small lung volumes. It has been shown, for example, that the SOS25-75% indicator is an earlier and more sensitive spirographic marker of increased resistance of the small airways. In this case, the shape of the flow-volume loop changes: the final region of the expiratory part of the loop becomes concave. This indicates that part of the FVC at the level of small lung volumes is exhaled at relatively low volumetric velocities, which is characteristic of small airway obstruction.

At the same time, it should be remembered that the above interpretation of changes in the COC25-75% indicators and the shape of the final part of the flow-volume loop is not yet generally accepted.

Assessment of the degree of bronchial obstruction

According to the recommendations of the European Respiratory Society (ERS) in 1995, FEV1 values ​​are currently used in clinical practice to assess the degree of bronchial obstruction in patients with COPD and, accordingly, the severity of COPD, since, despite all the limitations, this indicator is extremely ease of measurement and sufficient reproducibility. There are three degrees of decrease in relative values ​​of FEV1%

• mild degree - FEV1 > 70% of the required values;
• moderate degree - FEV1 ranging from 50 to 69%;
• severe - FEV1

The degree of decrease in absolute FEV1 values ​​correlates well with the prognosis of the disease. Thus, in patients with moderate signs of airway obstruction and FEV1 greater than 1 l, the 10-year mortality rate is slightly higher than that in persons who do not suffer from COPD. If in patients with COPD the absolute values ​​of FEV1 are less than 0.75 l, mortality only during the first year from the start of observation is about 30%, and over 10 years of observation it reaches 90-95%.

The criteria for classifying patients with COPD according to the stages of the disease, recommended by the American Thoracic Society and widely presented in modern domestic medical literature, are also based mainly on assessing the degree of decrease in FEV1. However, they differ somewhat from the EPO recommendations given above. According to the proposal of the American Thoracic Society, three stages of COPD should be distinguished:

• Stage 1 - FEV1 is more than 50% of the normal value. The disease slightly reduces the quality of life and requires periodic visits to a general practitioner (general practitioner). A more in-depth examination of patients, including studying the gas composition of arterial blood and pulmonary volumes, is not required.
• Stage 2 - FEV1 from 35% to 49% of the normal value. There is a significant decrease in quality of life. Frequent visits to medical institutions, observation by a pulmonologist and determination of the gas composition of the blood, the structure of the total lung capacity, the diffusion capacity of the lungs and other parameters are necessary.
• Stage 3 - FEV1 is less than 35% of the normal value. The disease sharply reduces the quality of life. Frequent visits to medical institutions, observation by a pulmonologist, and in-depth examination of patients are required, including determination of the blood gas composition, the structure of the total lung capacity, the diffusion capacity of the lungs, bronchial resistance, etc. If arterial hypoxemia is detected (PaO2 less than 55 mm Hg), patients are candidates for oxygen therapy.

Thus, according to this classification, a decrease in FEV1 of less than 50% can be regarded as a sign of the second stage of the disease (and moderate severity of COPD), while according to the criteria for the degree of bronchial obstruction recommended by ERS, the same decrease in this indicator corresponds to severe impairment of bronchial obstruction.

The criteria for the degree of bronchial obstruction recommended by the European Respiratory Society are more consistent with the tasks of domestic medical practice, since they guide the doctor towards the earlier involvement of specialists (pulmonologists) in the management of patients with COPD. In addition, it would be more correct to indicate in the diagnosis not the stage of COPD, which, by the way, depends not only on FB1 values, but the objective functional and morphological characteristics of the disease: the degree of bronchial obstruction and respiratory failure, the presence of pulmonary emphysema, the degree and nature of gas exchange disorders , the presence of signs of pulmonary arterial hypertension, as well as compensated and decompensated chronic pulmonary heart disease, etc.

Determination of reversibility of bronchial obstruction

To determine the reversibility of bronchial obstruction in patients with COPD, it is advisable to use bronchodilation tests. Most often, the test is performed using inhaled administration of short-acting beta 2 adrenergic receptor agonists:

• salbutamol (2.5-5 mg);
• fenoterol (0.5-1.5 mg); .
• tebutamine (5-10 mg).

In this case, the bronchodilator effect is assessed after 15 minutes.

It is also possible to use anticholinergic drugs, for example, ipratropium bromide at a dose of 0.5 mg (inhalation) with measurement of the bronchodilator effect 30 minutes after inhalation.

An increase in FEV1 values ​​by 15% or more indicates the presence of a reversible component of bronchial obstruction, in particular bronchosnasm, which, of course, makes it advisable to prescribe appropriate bronchodilators to treat the patient’s data. At the same time, it should be borne in mind that the lack of response to inhaled bronchodilator during a single test is not at all the reason for failure to prescribe bronchodilator therapy.

FEV1 monitoring

Repeated determination of FEV1 (monitoring) allows you to definitively confirm the diagnosis of COPD, since this disease is considered to be characterized by an annual decrease in FEV1 of more than 50 ml. Normally, in adulthood and old age, starting from 35-40 years, the physiological decrease in this indicator usually does not exceed 25-30 ml per year. The magnitude of the annual decrease in FEV1 in patients with COPD serves as the strongest prognostic indicator indicating the rate of progression of broncho-obstructive syndrome. Moreover, the rate of decline in FEV1 in patients with COPD depends on the age of the patients, duration of smoking, the number of cigarettes currently smoked daily, and on the frequency and severity of annual exacerbations of the inflammatory process in the bronchi. It has been shown that clinically significant exacerbations of chronic obstructive bronchitis lead to a sharp decrease in FEV1, which persists for up to 3 months after relief of inflammation.

Determination of the structure of total lung capacity (TLC)

In most cases, to characterize the degree of bronchial obstruction in patients with COPD, determining FEV1, FEV1/FVC, and SOS25-75% is sufficient. However, with a significant decrease in FEV1 (less than 50% of the expected value), as a rule, there is a need for a more detailed study of the mechanisms of decreased pulmonary ventilation. Let us recall that inflammatory and structural changes in large and small bronchi, expiratory tracheobronchial dyskinesia, expiratory collapse of small bronchi, pulmonary emphysema, etc. can contribute to the occurrence of these disorders. A more detailed characterization of the participation of these mechanisms in the decrease in pulmonary ventilation is possible only by studying the structure of the total lung capacity (TLC).

In general, COPD patients experience increases in total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV), and TLC/TLC ratio. However, not all patients experience a proportional increase in TLC and TLC, since the latter indicator may remain normal. This is explained primarily by differences in the level of bronchial obstruction. Thus, if obstruction of the large airways predominates, an increase in TLC is observed, while TLC usually does not increase. On the contrary, with obstruction of smaller peripheral bronchi, both indicators increase in parallel.

In patients with the emphysematous type of COPD, there is a significant increase in TLC and TLC, which reflects a pronounced overextension of the lung parenchyma. In these patients, a significant decrease in FEV1 is detected, while the total bronchial inspiratory resistance remains normal.

In patients with bronchitis COPD, there is a significant increase in residual lung volume (RLV), although total lung capacity (TLC) may remain normal or only slightly increase. FEV1 decreases in parallel with the increase in bronchial resistance during inspiration.

With the predominance of restrictive disorders, the TLC and TLC remain normal or decrease along with the FRC. With obstructive syndrome, I increase TLC/TLC (more than 35%) and FRC/TLC (more than 50%). With mixed ventilation disorders, a decrease in the value of TLC and at the same time an increase in the ratios TLC/TLC and FRC/TLC are observed.

It should still be remembered that determining the structure of the total lung capacity still remains the prerogative of large specialized medical centers.

Lung diffusion capacity study

Impaired lung diffusion capacity is also one of the most important rhythms in the occurrence of arterial hypoxemia in COPD patients with pulmonary emphysema. A decrease in the diffusion capacity of the lungs is associated with a decrease in the effective area of ​​the alveolar-capillary membrane, which is very typical for patients with primary pulmonary emphysema. In the bronchitis type of COPD, the diffusion capacity of the lungs is less affected.

Blood gas composition

Determination of gas composition (PaO2, PaCO2) and blood pH is one of the most important characteristics of respiratory failure developing in patients with severe COPD. Let us recall that the cause of arterial hypoxemia (decrease in PaO2) in patients with COPD is a violation of ventilation-perfusion relationships in the lungs, caused by pronounced unevenness of alveolar ventilation, as well as a violation of the diffusion capacity of the lungs during the development of emphysema. Hypercapnia (increase in PaCO2 > 45 mm Hg), which occurs in later stages of the disease, is associated with ventilation respiratory failure caused by an increase in functional dead space and a decrease in the function of the respiratory muscles of the diaphragm).

Respiratory acidosis (a decrease in blood pH less than 7.35), characteristic of patients with chronic respiratory failure, is compensated for a long time by increasing the production of sodium bicarbonate by the kidneys, which is the reason for maintaining a normal pH level.

The need to determine the blood gas composition and acid-base status usually arises in patients with COPD who are in critical condition, for example in patients with acute respiratory failure. These measurements are carried out in intensive care units (resuscitation). Since to determine the gas composition it is necessary to obtain an arterial blood sample using a puncture of the femoral or brachial artery, the technique cannot be considered routine and completely safe. Therefore, in practice, to assess the ability of the lungs to saturate the blood with oxygen (oxygenation), a fairly simple method is often used - pulse oximetry.

Pulse oximetry is a method for determining the oxygen saturation (saturation) of hemoglobin (SaO2) in pulsating arterial vessels.

The method does not allow assessing the PaCO2 level, which significantly limits its diagnostic capabilities. In addition, it should be remembered that the O2 indicator is influenced by many factors, such as body temperature, hemoglobin concentration in the blood, blood pH and some technical characteristics of the device.

It is believed that when SaO2 decreases below 94%, it is advisable to carry out an invasive determination of the gas composition of arterial blood, if the condition requires a more accurate assessment of oxygenation and ventilation of the lungs.

Examination of patients

The examination data depend on the severity and duration of chronic obstructive bronchitis. In the early stages of the disease there are no characteristic features. As chronic obstructive bronchitis progresses due to the development of pulmonary emphysema, the shape of the chest changes, it becomes barrel-shaped, the neck becomes short, the location of the ribs becomes horizontal, the anteroposterior size of the chest increases, kyphosis of the thoracic spine becomes pronounced, and the supraclavicular spaces bulge. Excursion of the chest during breathing is limited, retraction of the intercostal spaces is more pronounced.

In severe cases of chronic obstructive bronchitis, the neck veins swell, this is especially pronounced during exhalation; During inhalation, the swelling of the neck veins decreases.

With the development of respiratory failure and arterial hapoxemia, diffuse warm cyanosis of the skin and visible mucous membranes appears. With the development of pulmonary heart failure, acrocyanosis develops, edema of the lower extremities and epigastric pulsation appear, and orthopnea becomes characteristic.

A typical sign of chronic obstructive bronchitis is slowing of forced expiration. To identify this symptom, the patient is asked to take a deep breath and then exhale as quickly and fully as possible. Normally, full forced exhalation lasts less than 4 s, but with chronic obstructive bronchitis it lasts much longer.

Lung examination

Percussion sound with the development of pulmonary emphysema has a box-like tint, the lower borders of the lungs are lowered, and the mobility of the lower pulmonary edge is significantly reduced.

Auscultation of the lungs reveals prolongation of expiration and harsh vesicular breathing. The classic auscultatory sign of chronic obstructive bronchitis is whistling dry rales during normal breathing or during forced exhalation. It should be noted that with mild bronchial obstruction, whistling or buzzing wheezing can only be detected in a horizontal position, especially with forced exhalation (“hidden bronchial obstruction”). With severe bronchial obstruction, whistling dry rales can be heard even at a distance.

To diagnose bronchial obstruction, you can use the exhalation palpation and match test proposed by B. E. Votchal.

Exhalation palpation is performed as follows. In a standing position, the patient inhales deeply, then exhales with maximum force into the doctor’s palm, located at a distance of 12 cm from the patient’s mouth. The doctor determines the strength of the exhaled air stream (strong, weak, moderate) by comparing it with the force of his exhalation. At the same time, the duration of exhalation is determined (long - more than 6 s, short - from 3 to 6 s, very short - up to 2 s). If bronchial obstruction is impaired, the force of exhalation is reduced and its duration lengthens.

The match test is performed as follows. A burning match is placed at a distance of 8 cm from the patient’s mouth and the patient is asked to blow it out. If the patient cannot extinguish it, this indicates a severe impairment of bronchial obstruction.

Cardiovascular research

When examining the cardiovascular system, tachycardia is often detected, and blood pressure may be increased. These changes are explained by hypercapnia with peripheral vasodilation and increased cardiac output.

In many patients, epigastric pulsation is detected due to the right ventricle. This pulsation may be due to hypertrophy of the right ventricle (with chronic cor pulmonale) or positional shifts of the heart due to pulmonary emphysema.

Heart sounds are muffled due to emphysema; the accent of the second tone is often determined on the pulmonary artery due to pulmonary hypertension.

With severe chronic obstructive bronchitis, chronic gastritis with reduced secretory function is often detected, and the development of a stomach or duodenal ulcer is possible. With severe pulmonary emphysema, the liver is drooped, its diameter is normal; Unlike congestive liver, it is painless and its size does not change after the use of diuretics.

Clinical manifestations of hypercapnia

With steady progression of bronchial obstruction, chronic hypercapnia may develop. Early clinical signs of hypercapnia are:

• sleep disturbance - insomnia, which may be accompanied by slight confusion;
• headache, worsening mainly at night (at this time of day, hypercapnia intensifies due to worsening ventilation);
• increased sweating;
• sharp decrease in appetite;], [

  Typically, FEV1 is calculated as a percentage of vital capacity - the Tiffno index. It is normally 75-83%. In chronic obstructive bronchitis, the Tiffno index is significantly reduced. The prognosis for chronic obstructive bronchitis correlates with FEV1 values. With an FEV1 of more than 1.25 L, the ten-year survival rate is about 50%; with FEV1 equal to 1 l, the average life expectancy is 5 years; with an FEV1 of 0.5 l, patients rarely live more than 2 years. According to the recommendations of the European Respiratory Society (1995), the severity of chronic obstructive bronchitis is assessed taking into account the FEV1 value. Repeated FEV1 determinations are used to determine disease progression. A decrease in FEV1 by more than 50 ml per year indicates progression of the disease.

  Bronchial obstruction is characterized by a decrease in the maximum volumetric expiratory flow rate in the range of 25-75% FVC (MOV25%), which is determined by analyzing the volume-flow curve.

  MOC25-75 is less dependent on effort than FEV1 and therefore serves as a more sensitive indicator of bronchial obstruction in the early stages of the disease.

  In chronic obstructive bronchitis, maximum pulmonary ventilation (MVV) is significantly reduced - the maximum amount of air ventilated by the lungs within 1 minute with deep and frequent breathing.

  Normal MVL values:

  • men under 50 years old - 80-100 l/min;
  • men over 50 years old - 50-80 l/min;
  • women under 50 years old - 50-80 l/min;
  • women over 50 years old - 45-70 l/min;

  Proper maximum ventilation (DMV) is calculated using the formula:

  DMVL = vital capacity x 35

  Normally, the MVL is 80-120% of the MVL. In COB, MVL is significantly reduced.

  Pneumotachometry

  Using pneumotachometry, the volumetric velocity of the air stream during inhalation and exhalation is determined.

  In men, the maximum expiratory flow is about 5-8 l/s, in women - 4-6 l/s. These indicators also depend on the age of the patient. It is proposed to determine the proper maximum expiratory flow (MEF).

  DMSV = actual vital capacity χ 1.2

  If bronchial obstruction is impaired, the speed of the air stream during exhalation is significantly reduced.

  Peak flowmetry

  In recent years, determining the state of bronchial patency using peak flowmetry - measuring the maximum volumetric expiratory flow rate (l/min) has become widespread.

  In fact, peak flowmetry allows you to determine peak expiratory flow (PEF), i.e. the maximum speed at which air can leave the respiratory tract during forced exhalation after a maximally complete inspiration.

  The patient’s PEF indicators are compared with normal values, which are calculated depending on the patient’s height, gender and age.

  If bronchial obstruction is impaired, PSV is significantly lower than normal. The value of PEF closely correlates with the values ​​of forced expiratory volume in the first second.

  For a more detailed characterization of the state of bronchial patency and to establish the reversible component of bronchial obstruction, tests with bronchodilators (anticholinergics and beta2-agonists) are used.

  A test with Berodual (a combined aerosol preparation containing the anticholinergic ipratropium bromide and the beta2-adrenergic stimulant fenoterol) allows for an objective assessment of both the adrenergic and cholinergic components of the reversibility of bronchial obstruction. In most patients, after inhalation of anticholinergics or beta2-agonists, an increase in FVC occurs. Bronchial obstruction is considered reversible when FVC increases by 15% or more after inhalation of these drugs. Before prescribing treatment with bronchodilators, it is recommended to carry out the indicated pharmacological tests. The result of the inhalation test is assessed after 15 minutes.

  Formulating a diagnosis

  When formulating a diagnosis of chronic bronchitis, it is necessary to reflect, as far as possible and as fully as possible, the following characteristics of the disease:

  • form of chronic bronchitis (obstructive, non-obstructive);
  • clinical, laboratory and morphological characteristics of the inflammatory process in the bronchi (catarrhal, mucopurulent, purulent);
  • phase of the disease (exacerbation, clinical remission);
  • degree of severity (according to ERS classification);
  • the presence of complications (pulmonary emphysema, respiratory failure, bronchiectasis, pulmonary arterial hypertension, chronic cor pulmonale, heart failure).

  In addition, if possible, decipher the infectious nature of the disease, indicating the possible causative agent of the inflammatory process in the bronchi. In those cases where the nosological affiliation of the disease (bronchitis) can be clearly determined, the term “COPD” need not be used. For example:

  • Chronic catarrhal simple (non-obstructive) bronchitis, exacerbation phase caused by pneumococcus.
  • Chronic obstructive purulent bronchitis, exacerbation phase.
  • Chronic obstructive catarrhal bronchitis, pulmonary emphysema. Mild severity. Exacerbation phase. Respiratory failure stage I.

  The term “COPD” is usually used when formulating a diagnosis in more severe cases (moderate and severe severity), when identifying the nosological affiliation of the disease causes certain difficulties, but there are clinical manifestations of broncho-obstructive syndrome and damage to the respiratory structures of the lungs. In this case, the term “COPD” is, if possible, deciphered with an indication of the diseases that led to its development. For example:

  • COPD: chronic obstructive catarrhal bronchitis, pulmonary emphysema. Moderate severity. Exacerbation phase. Respiratory failure stage II. Chronic cor pulmonale, compensated.
  • COPD: chronic obstructive purulent bronchitis, obstructive pulmonary emphyema. Heavy current. Clinical remission phase. Respiratory failure degree II. Polycythemia. Chronic pulmonary heart, decompensated. Chronic heart failure II FC.
  • COPD: bronchial asthma, chronic obstructive purulent bronchitis, pulmonary amphysema. Heavy current. Exacerbation phase caused by the association of Haemophilus influenzae and Moraxella. Respiratory failure stage II. Chronic pulmonary heart, decompensated. Chronic heart failure II FC.

MINISTRY OF HEALTH OF THE REPUBLIC OF BELARUS

BELARUSIAN STATE MEDICAL UNIVERSITY

DEPARTMENT OF PROPAEDEUTIICS OF INTERNAL DISEASES

E. A. DOTSENKO, I. M. ZMACHINSKAYA, S. I. NEROBEEVA

Approved by the University Scientific and Methodological Council as methodological recommendations on March 29, 2006, protocol No. 5

Authors: Dr. med. sciences, prof. E. A. Dotsenko; Ph.D. honey. Sciences, Associate Professor I. M. Zmachinskaya; Ph.D. honey. Sciences, Associate Professor S. I. Nerobeeva

REVIEWERS: Dr. med. prof. I. P. Danilov; Ph.D. honey. Sciences, Associate Professor V. K. Koshelev

Dotsenko, E. A.

D 71 Chronic obstructive bronchitis: method. recommendations / E. A. Dotsenko, I. M. Zmachinskaya, S. I. Nerobeeva. – Minsk: BSMU, 2006. – 16 p.

The issues of etiology and pathogenesis of chronic obstructive bronchitis are reflected, the clinical picture and diagnosis of the disease are described in detail. Particular attention is paid to issues of primary and secondary prevention.

Intended for 4th year students of the Faculty of Preventive Medicine.

UDC 616.233–002–036.12 (075.8) BBK 54.12 i 73

Educational edition

Dotsenko Eduard Anatolyevich Zmachinskaya Irina Mikhailovna Nerobeeva Svetlana Ivanovna

CHRONIC OBSTRUCTIVE BRONCHITIS

Responsible for the issue I. M. Zmachinskaya Editor N. V. Onoshko

Computer layout N. M. Fedortsova Proofreader Yu. V. Kiseleva

Signed for seal ___________. Format 60×84/16. Writing paper "KumLux". Offset printing. Times typeface.

Conditional oven l. _____. Academic ed. l. _____. Circulation ____ copies. Order ________.

Publisher and printing - Belarusian State Medical University.

LI No. 02330/0133420 dated 10/14/2004; LP No. 02330/0131503 dated 08/27/2004. 220030, Minsk, Leningradskaya, 6.

© Design. Belarusian State Medical University, 2006

MOTIVATIONAL CHARACTERISTICS OF THE TOPIC

Topic of the lesson: “Chronic obstructive bronchitis. Etiology. Pathogenesis. Clinic. Diagnostics. Prevention".

Total lesson time: 5 hours.

In recent years, the problem of chronic bronchitis and especially its most severe obstructive form has increasingly attracted the attention of the medical community. According to WHO, in terms of economic damage caused, chronic obstructive pulmonary diseases will move from 12th place in 1990 to 5th by 2020, ahead of all other diseases of the respiratory system, including pulmonary tuberculosis.

Purpose of the lesson: to train students in the methods of physical examination of a patient with chronic obstructive bronchitis (COB), its complications, differential diagnosis using diagnostic search algorithms, to familiarize them with the basic methods of instrumental and laboratory research, patient management tactics, principles of pharmacotherapy, and prevention.

Lesson objectives:

1. To familiarize students with the definition, etiology, pathogenesis, classification, clinical picture and methods of examining patients with chronic bronchitis.

2. To consolidate practical skills in examining patients with respiratory pathology (history taking, examination, palpation, percussion and auscultation of the lungs).

3. Teach students to correctly interpret the findings of a physical examination.

4. To teach how to analyze the results of laboratory and instrumental examinations of patients, draw up a plan for a targeted examination of the patient, formulate a clinical diagnosis, identify the principles of treatment, and outline a plan of preventive measures.

Requirements for the initial level of knowledge. To prepare for the lesson, the student should repeat the sections: “General examination and examination of the chest for pathologies of the respiratory system”, “Palpation of the chest”, “Percussion of the lungs”, “Auscultation of the lungs”, “X-ray diagnostics for pathologies of the lungs”, “Study of the function of external breathing."

Test questions from related disciplines

1. Anatomy of the bronchial tree.

2. Gas exchange in the lungs.

3. Study of external respiration function.

Test questions on the topic of the lesson

1. Define the concept of “chronic obstructive bronchitis”.

2. Epidemiology, etiology and pathogenesis of COB.

3. Classification of COB.

4. COB Clinic.

5. The role of instrumental and laboratory research methods in the diagnosis of COB.

6. Differential diagnosis of COB.

7. Principles of treatment of COB.

8. Primary and secondary prevention of COB.

CHRONIC OBSTRUCTIVE BRONCHITIS

Definition

Chronic obstructive bronchitis is a disease characterized by chronic diffuse non-allergic inflammation of the bronchi, leading to a progressive impairment of pulmonary ventilation and gas exchange of the obstructive type and manifested by cough, sputum production, shortness of breath, not associated with damage to other organs and systems.

Epidemiology

Currently, the term “chronic obstructive bronchitis” is increasingly being replaced by the concept of “chronic obstructive pulmonary disease” (COPD), which largely reflects modern ideas about the essence of pathology and emphasizes the involvement in the pathological process of not only the airways, but also the respiratory parts of the lungs. In the structure of all patients with COPD, chronic obstructive bronchitis accounts for approximately four

In fact, the remaining ¾ are accounted for by non-obstructive bronchitis (CNB), or “simple and mucopurulent chronic bronchitis” according to the ICD-10 nomenclature. Mortality from COPD accounts for more than 80% of all mortality from chronic lung diseases, ranks 4th in the structure of causes of death in the world and tends to increase. Calculations based on assessing the prevalence of COB using epidemiological markers suggest that in the CIS countries this figure is currently twice as high as the prevalence of bronchial asthma.

Classification of chronic bronchitis

According to the functional characteristics, chronic bronchitis is:

1. Non-obstructive (simple).

2. Obstructive.

Based on the nature of inflammation, there are two types of chronic bronchitis:

1. Catarrhal.

2. Purulent.

The following phases of the disease are distinguished:

1. Exacerbation.

2. Remission.

Also, when formulating a diagnosis, it is necessary to note possible complications characteristic of this pathology, namely: respiratory failure (I, II, III degrees) and chronic pulmonary heart disease.

Examples of the formulation of a detailed chronic diagnosis:

1. Chronic non-obstructive bronchitis in the acute phase. DN 0.

2. Chronic purulent-obstructive bronchitis, exacerbation phase. Pulmonary emphysema, diffuse pneumosclerosis. DN III. Pulmonary heart failure, chronic pulmonary heart disease in the stage of decompensation.

Etiology

There are 3 known risk factors for developing COB:

1) smoking;

2) severe congenital deficiencyα 1 -antitrypsin;

3) increased levels of dust and gas in the air associated with occupational hazards and poor environmental conditions.

In addition, there are many probable factors: passive smoking, respiratory viral infections, socio-economic factors, living conditions, alcohol consumption, age, gender, etc. Most researchers consider infection a secondary factor in the development of the disease. Its role is manifested against the background of adverse effects on the bronchial mucosa in combination with endogenous factors (pathology of the nasopharynx, impaired nasal breathing, disorder of local immunity, etc.), which creates conditions conducive to infection. At the same time, infection (pneumococcus, viruses, mycoplasmas) is the main cause of exacerbation of the disease.

The role of allergies in the occurrence of chronic bronchitis has not been sufficiently studied. However, the presence of vasomotor disorders of the upper respiratory tract, drug allergies, and eosinophilia in the peripheral blood is noted in more than 80% of patients with this disease.

Pathogenesis

With prolonged exposure to etiological factors, a number of pathological processes occur in the bronchial tree. First of all, the structural and functional properties of the mucous membrane change:

– goblet cell hyperplasia;

– hypersecretion of mucus;

– metaplasia and atrophy of the epithelium;

– decreased production of immunoglobulin A;

– swelling of the mucous membrane.

Inflammation of the mucous membrane causes:

– reflex spasm of the bronchi;

– disruption of surfactant production.

The outcome of the inflammatory process is the collapse of small bronchi and obliteration of bronchioles (pneumosclerosis). This leads to irreversible bronchial obstruction, which is characterized as widespread narrowing

bronchi, refractory to treatment with bronchodilators, including corticosteroids, which leads to disruption of the drainage function of the bronchial tree.

Obstruction of the small bronchi causes overstretching of the alveoli during exhalation and disruption of the elastic structures of their walls, which contributes to the development of pulmonary emphysema. As a result of the development of emphysema and pneumosclerosis, uneven ventilation of the lungs occurs with the formation of hypo- and hyperventilated areas, which, in combination with local inflammatory changes, leads to:

– to disruption of gas exchange;

– development of respiratory failure;

– arterial hypoxemia;

– to pulmonary hypertension.

The right ventricle of the heart works under load, hypertrophies and enlarges. Subsequently, right ventricular failure develops and cor pulmonale is formed.

Clinic

IN the onset of the disease occurs in the morning cough, which is accompanied by the release of a small amount of sputum. This is due to the daily rhythm of mucociliary transport, the insufficiency of which manifests itself only at night. Active physical movements are important, accompanied by increased ventilation, increased tone of sympathetic innervation and adequate bronchodilation.

If at first the cough occurs only during an exacerbation (usually in the cold and damp season), then with a long course of the disease it becomes permanent.

IN In the case of distal chronic bronchitis, there may be no cough for a long time due to the absence of a cough reflex in the small bronchi. In chronic bronchitis, it intensifies during an exacerbation of the process, becomes annoying, painful (especially with obstructive bronchitis), contributing to the development of pulmonary emphysema and bronchiectasis.

Sputum production: in the early stages of chronic bronchitis, scanty mucous sputum is released, later mucopurulent and purulent sputum appears, which, as a rule, is associated with the next exacerbation of the disease.

With long-term chronic bronchitis, patients constantly secrete purulent sputum. Its amount per day is usually no more than 50 ml, but with the formation of bronchiectasis it can increase.

Purulent sputum has increased viscosity and is difficult to cough up. During exacerbation, its quantity increases, sometimes it becomes more liquid due to the mucolytic action of bacterial and leukocyte enzymes.

IN In some cases, hemoptysis (streaks of blood in the sputum) is possible. Shortness of breath initially occurs only with significant physical exertion.

ke, during an exacerbation of the process.

The appearance and increase in shortness of breath as the disease progresses is associated with obstruction of the bronchial tree, as well as with the development of pulmonary emphysema. Over time, it becomes a constant symptom.

Manifestations of intoxication: during an exacerbation, patients note weakness, increased fatigue, low-grade fever, which are manifestations of intoxication.

Objective research:

1. General inspection. At the onset of the disease, pathological changes are not detected. The development of respiratory failure (and then pulmonary-cardiac failure) manifests itself:

– diffuse cyanosis and acrocyanosis;

– swelling of the lower extremities;

– changes in hands;

– fingers in the form of “drumsticks”;

– nails in the form of “hour glasses”.

2. Cardiovascular system:

– in the early stages - normal;

– later stages:

1) swelling of the neck veins;

2) epigastric pulsation (signs of damage to the right ventricle during the development pulmonary heart failure);

3) reduction of the zone of absolute cardiac dullness (development of emphy-

4) outward displacement of the right border of relative cardiac dullness (dilatation of the right ventricle);

5) uniform weakening of both heart sounds(due to emphysema);

6) emphasis of the second tone on the pulmonary artery (due to pulmonary hypertension

7) weakening of the first tone at the base of the xiphoid process (as a sign of damage to the myocardium of the right ventricle).

3. Respiratory system:

– emphysema:

1) barrel chest;

2) boxed percussion sound;

3) decrease in excursion of the lower pulmonary edge;

– weakened breathing;

– in the presence of obstruction - dry wheezing;

– in the acute phase, moist, silent wheezing appears, the caliber of which depends on the level of damage to the bronchial tree.

4. Digestive system:

– the edge of the liver protruding from under the costal arch, which is explained by its prolapse due to severe emphysema, the liver is painless, its size according to Kurlov is not changed;

– with the development of right ventricular failure and stagnation in the systemic circulation, the liver increases in size.

5. Additional research methods:

General blood analysis:

– moderate neutrophilic leukocytosis with a shift in the leukocyte formula to the left;

– acceleration of ESR;

– with severe emphysema and respiratory failure, there may be erythrocytosis and a slight increase in hemoglobin levels.

Biochemical blood test: positive “acute phase” indicators are noted (the presence of C-reactive protein, increased levels of fibrinogen, sialic acids, dysproteinemia).

Sputum examination:

– the nature of inflammation is clarified;

– identifies the type of infectious pathogen and its sensitivity to antibacterial agents.

X-ray reveals:

– strengthening and deformation bronchovascular pattern - signs of pneumosclerosis;

– signs of emphysema: increased transparency of the pulmonary fields, low diaphragm;

– subsequently - manifestations of pulmonary hypertension and cor pulmonale (bulging of the pulmonary artery trunk, dilatation of the hilar arteries).

Bronchography:

– the presence of bronchiectasis and deformation of the bronchial tree;

– differential diagnosis with tumors.

Bronchoscopy allows:

– evaluate changes in the mucous membrane: inflammation, atrophy, hemorrhagic component;

– determine the severity of the inflammatory process;

– obtain material for microscopic and cytological examination

– carry out differential diagnosis with tracheobronchial dyskinesia and tumors.

Pulmonary function testing reveals restrictive and obstructive pulmonary ventilation disorders.

If obstruction is present:

– there is a decrease in external respiration speed indicators (MVL and FEV 1, exceeding the degree of decrease in vital capacity);

– bronchial resistance increases during exhalation;

Bronchitis is a disease of the respiratory tract that occurs as a result of the development of an inflammatory process in the bronchi. The main mechanism for the appearance of pathology is the entry of pathogenic microorganisms and bacteria into the human body. From this article you will learn about the etiology, pathogenesis, and clinical picture of bronchitis, the treatment and diagnosis of which should be carried out under the supervision of a specialist. What is a disease?

The clinical manifestations of bronchitis directly depend on the form and stage of development of the disease. The symptoms of acute bronchitis have a number of significant differences from the clinical picture and symptoms of bronchitis in its chronic form. So, the main manifestations of acute bronchitis include the following:

• in the acute initial stage, a dry cough is noted, which is often accompanied by painful sensations behind the sternum, the voice becomes hoarse, and swallowing is painful;
• symptoms of general intoxication are expressed: fever, weakness, headache, increased body temperature;
• Along with this, symptoms of the primary disease are noted (ARVI, influenza, upper respiratory tract infections).

The clinical picture of chronic bronchitis is characterized by the following symptoms:

• coughing attacks are present continuously for three months for two years;
• when coughing, sputum is released (the consistency of sputum depends on the degree of damage to the bronchi: from mucous and light to mucopurulent and opaque);
• in advanced stages, shortness of breath appears and breathing becomes difficult as a consequence of obstructive processes in the bronchi and lungs.

Etiology of bronchitis

The main cause of obstructive bronchitis is infection of the upper respiratory tract. The development of bronchitis is mainly promoted by viral colds (rhinoviruses, acute respiratory viral infections, adenoviruses, influenza), as well as bacterial infections (for example, streptococcus or chlamydia). It should be noted that the development of bronchitis during colds often occurs in an organism weakened by smoking, an unhealthy lifestyle, as well as a history of a number of diseases.

The clinic of acute bronchitis in children and adults indicates that the disease can also be triggered by various external influences: inhalation of harmful chemicals, dusty premises, regular hypothermia. Chronic bronchitis, as a rule, is a consequence of untimely treatment of acute bronchitis. Among the main etiological reasons, the following should also be considered:

• environmental problems (air pollution with emissions harmful to health);
• smoking;
• hazardous working conditions (for example, work in chemical production);
• severe tolerance to cold climates.

Pathogenesis of acute and chronic bronchitis

With the progressive development of bronchitis, the walls of the bronchi are primarily affected by pathological effects, in which atrophic processes begin. This, in turn, leads to a weakening of the protective functions of the bronchi, which causes a decrease in the function of the immune system. When an infection enters the respiratory tract, an acute inflammatory process develops in the body. If appropriate drug therapy is not carried out, then the further development of the pathological process leads to swelling and hyperemia of the mucous membranes, and the appearance of mucopurulent exudate. With full treatment, it is possible to get rid of bronchitis in two to three weeks; it will take about a month to restore bronchial function; if atrophic processes lead to irreversible changes, then bronchitis becomes chronic.

Causes

With bronchitis, the walls of the bronchi are damaged, which can happen due to a number of reasons such as:

1. Infection with viral infections - acute bronchitis is caused in 90% of cases by viruses. In adults, the disease is usually caused by myxoviruses (influenza, parainfluenza).
2. Infection with bacterial infections - in 5-10% of cases, the cause of bronchitis is bacteria (streptococci, hemophilia and chlamydia); bacterial infections often become secondary infections as a result of infection by a virus.
3. Weakened immunity and vitamin deficiency.
4. Hypothermia.
5. Living in places with high humidity, polluted air and poor ecology.
6. Active and passive smoking - when you inhale cigarette smoke, various chemicals deposit on the lungs, which leads to irritation of the walls.
7. Inhalation of toxic and harmful gases and toxins that damage the walls of the lungs and bronchi (ammonia, hydrochloric acid, sulfur dioxide, etc.).
8. A consequence of other chronic or acute diseases - if treatment is incorrect or not completed, bacteria can enter the lungs and begin to spread there.
9. Poor nutrition.
10. Due to an allergic reaction.

Symptoms

The manifestation of acute bronchitis begins with a cold. Severe fatigue, weakness, tickling and cough. At the height of the disease, the cough is dry, soon followed by sputum. The discharge can be either mucous or purulent in nature. Bronchitis may be accompanied by fever. A form of chronic bronchitis is diagnosed after several months of illness. A wet and painful cough with phlegm torments a person every day. When in contact with irritants, the cough reflex may be strengthened. A long process leads to difficulty breathing and the development of emphysema.

What symptoms are accompanied by infectious bronchitis? At the beginning of the disease, a dry cough, a feeling of weakness, an increase in body temperature are disturbing; when a dry cough changes to a wet one, discomfort in the chest area occurs.

How does allergic bronchitis manifest? Contact with the pathogen causes discomfort and coughing. Sputum in allergic bronchitis always has a mucous secretion. There is no increase in body temperature. Symptoms of bronchitis disappear when the irritant is eliminated.

With toxic bronchitis, a severe cough causes difficulty breathing, shortness of breath or suffocation.

Diagnosis of bronchitis

The easiest disease, if we consider the issue of diagnosis, is bronchitis. Currently, many objective and modern methods for diagnosing clinical bronchitis in children and adults are available:

1. Conversation with a doctor. In most cases, the diagnosis of bronchitis is made based on interviewing the patient and identifying complaints related to the respiratory system. During the interview, the doctor also finds out the approximate onset of the disease and possible causes.
2. Inspection. The doctor checks for breath sounds in the chest using a phonendoscope. Auscultation reveals harsh breathing, as well as the presence of dry and moist rales. For differential diagnosis and exclusion of pneumonia and pleurisy, it is possible to use the percussion method. In chronic bronchitis, percussion sound changes due to changes in lung tissue.
3. Clinical tests. Blood and sputum examination is performed to substantiate the diagnosis. With bronchitis, blood counts in the general analysis will vary depending on the pathogen. Bacterial flora will lead to an increase in ESR, as well as the number of leukocytes and neutrophils. With viral bronchitis, there is a decrease in the number of leukocytes and an increase in lymphocytes.
4. Chest X-ray in two projections is a method for diagnosing diseases of the bronchial tree.
5. Spirography. A modern method for identifying decreased respiratory tract function. With bronchitis, due to the inflammatory component, there is an obstacle to inhalation and exhalation, which will undoubtedly affect a decrease in the total volume of the lungs.

Treatment of bronchitis

The clinic and treatment of acute bronchitis consists of following the following doctor’s recommendations:

1. Bed rest and complete physical and mental rest of the patient are prescribed.
2. It is necessary to provide the patient with enough fluids.
3. Application of necessary physiotherapeutic treatment methods.
4. Taking necessary medications.
5. It should also be noted that depending on the reasons contributing to the development of the disease, the methods of treating the disease differ.

Antiviral

Thus, in the treatment of bronchitis of viral etiology, the following types of antiviral drugs are prescribed:

1. "Viferon". This is a drug containing combined human interferon. This substance is a broad-spectrum medicine, available in the form of ointments and suppositories of various dosages. The course of therapy ranges from five to ten days. Possible side effects may include an allergic reaction.
2. "Laferobion". This drug can be used both for the prevention and treatment of diseases caused by pathogens of various viruses. Available in the form of a solution. The course of therapy should not exceed ten days.

Antibacterial

As a rule, the following groups of drugs are selected for the treatment of bronchitis of bacterial origin:

• Aminopenicillins.
• Cephalosporins.
• Macrolides.
• Fluoroquinolones.

Prebiotics

The necessary prebiotics are also prescribed to prevent the development of intestinal dysbiosis in the patient. All of the listed substances must be used in combination to treat the disease. Also, all patients with bronchitis, regardless of etiology, are prescribed physiotherapeutic methods. This treatment method is one of the oldest in medical practice; its use allows you to achieve an effective result in influencing the disease in a safe way for health.

Physiotherapy

The following physiotherapeutic methods of treatment are used in the treatment of the disease:

1. Inhalation. This method of influencing the respiratory system allows it to be used in the treatment of pregnant women and children with bronchitis. A special inhaler device is used to carry out the procedure. This method of exposure can effectively eliminate such clinical manifestations of the disease as the presence of sputum, cough, and pathogens. Also, the undoubted advantage of this method is the possibility of home use.
2. Massage techniques. To treat bronchitis, the massage therapist performs dynamic tapping and stroking with his fingertips. The use of essential oils is mandatory during the procedure. Manipulations are carried out only on the human thoracic spine. The duration of the procedure is from five to ten minutes daily, the course of treatment is five days.
3. Inductothermy. The basis of this method is the effect of heat rays on a person. Under the influence of electromagnetic waves, blood circulation increases in the tissues affected by inflammation. The duration of the manipulation is twenty minutes. Depending on the severity of the condition, the course of the procedure can vary from six to twelve manipulations.
4. Electrophoresis. This technology is used to liquefy secretions released from the bronchi. The procedure is performed using a special apparatus that allows the substance to penetrate into the deep layers of the epidermis, which helps to expand the bronchi and restore damaged mucous membranes of the organ.
5. Halotherapy. This method consists of artificially creating a climate similar to that existing in salt caves. Used to improve lung ventilation.
6. Heat therapy. For this procedure, special paraffin pads are used, which are preheated and then applied to the patient’s chest, which helps reduce spasms during coughing attacks. The duration of this manipulation is ten minutes.

The best herbs

You can also use medicinal herbs and breast infusions to treat the disease. Preparing herbal infusions from licorice root and thyme helps accelerate the removal of secretions from the bronchi. Collecting herbs such as coltsfoot, elecampane root, and anise will help against coughing attacks.

Take a test to control your asthma - More details ⇒

Bronchitis is a disease of the respiratory tract, characterized by an inflammatory process in the bronchial mucosa.

Classification

Classification is made according to various criteria.

The following forms are distinguished along the flow:

1. Acute (the disease usually lasts 2-3 weeks, after which recovery occurs).
2. Prolonged (this form characterizes acute bronchitis, which lasts more than 3 weeks).
3. Chronic (the diagnosis is made if the patient has signs of bronchitis for at least 3 months a year over 2 years of observation).
4. Recurrent (the diagnosis criterion is as follows: at least 2 infectious-inflammatory lesions of the bronchial tree are diagnosed throughout the year).

According to the independence of development, bronchitis is primary and secondary:

• A primary disease is a condition in which some pathological factor initially acts on the mucous membrane of the bronchial tree, causing its inflammation. That is, primary bronchitis is an independent pathological process that begins in the bronchi and is limited to them. This option is extremely rare in clinical practice.
• Secondary damage to the bronchi is a manifestation or complication of another disease occurring in the respiratory tract (for example, influenza, whooping cough) or in other organs and systems of the body. Secondary bronchitis against the background of other diseases of the respiratory tract is the pathology that is most often encountered in doctor’s practice.

The causes of inflammation are:

1. Infection.
2. Allergy.
3. Physico-chemical factors (for example, inhalation of air containing irritating chemical compounds).

Important! Typically, damage to the bronchial tree is caused by exposure to viruses. Among them, the most common are influenza viruses, adenoviruses, respiratory syncytial virus, and rhinoviruses.

A bacterial or fungal agent may join a viral infection as the process progresses. Much less often, bacteria or fungi act as the root cause of bronchitis. Sometimes the causative agents of bronchitis are chlamydia and mycoplasma.

Physical, chemical, and allergic agents act as independent causes or factors predisposing to infection.

Based on the presence of signs of narrowing of the lumen of the bronchi, obstructive and non-obstructive bronchitis are distinguished.

According to the level of damage, bronchitis is:

• proximal (the base of the bronchial tree is affected);
• distal (inflammation occurs in bronchi with a small diameter; this disease is called “bronchiolitis”).

Depending on the degree of spread, inflammation of the bronchi is distinguished:

According to the type of inflammatory manifestations, bronchitis is:

1. Catarrhal.
2. Serous-purulent.
3. Purulent.
4. Hemorrhagic.
5. Ulcerative.
6. Necrotic.

Clinic

The onset of the infectious variant of the disease in question is usually manifested by symptoms of ARVI. A runny nose, sore throat, general weakness, chills, and a slight increase in body temperature appear. The cough is initially dry, without sputum production. It intensifies with deep breathing, which accompanies, for example, emotional conversation or laughter. Pain in the tracheal area is often observed. Gradually the cough becomes softer. It acquires a productive character, that is, sputum begins to cough up.

In the obstructive form of the disease, a characteristic symptom is noisy, wheezing breathing and the participation of auxiliary muscles in breathing.

The degree of increase in body temperature depends on the cause that caused the development of bronchitis, the specific form of the disease and the individual characteristics of the body.

Diagnostics

Main diagnostic signs:

• cough;
• shortness of breath with difficulty exhaling (with obstructive forms of the disease and bronchiolitis);
• signs revealed by listening with a phonendoscope: hard breathing, dry and varied wet rales.

Important! A chest x-ray is required to rule out pneumonia. With bronchitis, there may be a bilateral increase in the pulmonary pattern and the pattern of the roots of the lungs. In the presence of narrowing of the lumen of the bronchi, an increase in the transparency of the pulmonary fields, flattening and low placement of the domes of the diaphragm, and horizontal lines of the ribs are determined.

The function of external respiration is also examined. Obstructive type disorders can be identified here.

In severe chronic cases, diagnostic procedures such as bronchography and bronchoscopy are sometimes performed.

From laboratory tests the following are prescribed:

1. General blood analysis.
2. General urine analysis.
3. Microscopic examination of sputum (including examination for the presence of the causative agent of tuberculosis).
4. Sputum culture for microflora.
5. Biochemical analysis.

Differential diagnosis

Depending on the signs of the disease, differential diagnosis can be made with pathologies such as:

• pneumonia;
• bronchiectasis;
• cystic fibrosis;
• foreign body of the bronchi and others.

Treatment program

Treatments are usually carried out on an outpatient basis. Hospitalization is indicated only for people with an unfavorable course of bronchitis or those who have severe concomitant pathology. Treatment of bronchitis is complex.

Important! Antibiotics or antiviral drugs are prescribed only when indicated.

• organization of regime and nutrition. Bed rest during fever, then gentle rest. The diet at the height of the disease should be predominantly dairy-vegetable. It is recommended to drink plenty of fluids (the volume should be 2 times the age-specific daily norm). It is necessary to drink more warm liquid in the form of tea with raspberries, lemon, mint, cranberry juice, rosehip infusion;

• symptomatic treatment;

• vitamin therapy;
• physiotherapeutic treatment, physical therapy.

The photo is for illustrative purposes only. From open sources

Bronchitis - inflammation of the bronchial mucosa without signs of damage to the lung tissue - is one of the most common acute respiratory diseases.

Elena Lapteva, Head of the Department of Pulmonology and Phthisiology of BelMAPO, Doctor of Medical Sciences. Sciences, Associate Professor; Irina Kovalenko, Associate Professor of the Department of Pulmonology and Phthisiology of BelMAPO, Candidate of Medical Sciences. Sci.

Bronchitis - inflammation of the bronchial mucosa without signs of damage to the lung tissue - is one of the most common acute respiratory diseases. It usually occurs against the background of acute respiratory viral infection, which in 20% of cases is an independent cause of the disease. However, in 80% of patients, the main role in the etiology of the disease belongs to viral-bacterial associations. Among the viral pathogens, the most common are influenza, parainfluenza, adenoviruses, respiratory syncytial, adeno-, corona- and rhinoviruses. Among the bacterial pathogens, the leading ones are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, opportunistic microflora and their associations.
All ARVIs are characterized by signs of intoxication (fever, headache, weakness, myalgia, etc.) with symptoms of respiratory tract damage. Intoxication is usually not as severe as with the flu. The clinical picture is dominated by catarrhal syndrome: with adenoviral diseases - pharyngitis and conjunctivitis (pain or sore throat, pain in the eyes, lacrimation, cough, often productive), laryngitis (hoarseness, dry cough), with respiratory syncytial infection - frequent obsessive cough for a long time, obstructive syndrome.

Acute bronchitis is characterized by diffuse damage to bronchi of different sizes, which causes certain clinical symptoms. The course can be acute (up to 3 weeks) and protracted (more than 3 weeks). In cases of repeated (2–3 or more during the year) episodes, we can talk about recurrent bronchitis or (if there are signs of obstructive ventilation failure) about recurrent acute obstructive bronchitis.

Infectious factors play a decisive role in the formation of a relapsing course of the disease. When viruses act on immature tissue structures, bacterial inflammation may occur, damaging the ciliated epithelium and impairing the self-cleaning function of the bronchi. The proliferation of microorganisms contributes to the progression of inflammation both due to independent damage to the structure of the bronchus and due to the activation of lysosomal enzymes of cells. The consequence of this is mucociliary disorders, leading to the development of panbronchitis, peribronchitis and contributing to the formation of deforming bronchitis when areas of fibrosis occur.

Prolonged and recurrent course of bronchitis can be provoked by intracellular pathogens, such as chlamydia, mycoplasma (they can also cause severe variants of its course).

Mycoplasma infection is manifested by pharyngitis, general malaise, weakness, sweating and is accompanied by a long-term (up to 4-6 weeks) paroxysmal cough. Respiratory chlamydia is characterized by pharyngitis, laryngitis and bronchitis. Patients' most common complaints include hoarseness, sore throat, low-grade body temperature, and a persistent, unproductive cough with the discharge of a small amount of mucous sputum.

Risk factors for developing bronchitis

Hypothermia, influenza and other respiratory viral diseases, smoking (including passive smoking), alcoholism, congestion in the lungs due to heart failure, viral and allergic diseases, immunodeficiency conditions, epidemic situation (contact with the patient), autumn-winter period, the presence of a tracheostomy, old age or childhood, reflux esophagitis, chronic sinusitis, exposure to physical (cold and hot air) and chemical (inhalation of sulfur vapor, hydrogen sulfide, chlorine, bromine, ammonia) factors.

Diagnostic criteria

The diagnosis of “acute bronchitis” is made when a cough appears that lasts no more than 3 weeks, regardless of the presence of sputum in the absence of signs of pneumonia and chronic lung diseases, which can also cause cough. The diagnosis is determined by excluding other diseases characterized by cough and is based on the clinical picture. The main clinical manifestations: symptoms of intoxication (malaise, chills, low-grade fever, pain in the chest, muscles), cough - first dry, then productive with mucous sputum, shortness of breath, which may be due to obstructive syndrome or underlying pathology of the lungs or heart. Auscultation reveals scattered dry or moist rales in the lungs.

The viral etiology of the disease is accompanied by fever with chills, pharyngitis, conjunctivitis, rhinitis, headache, aches in the joints and muscles, and cough. A general blood test may reveal leukocytosis and an increase in ESR. In general urine analysis, slight proteinuria is possible, but more often there are no pathological changes.

Principles of treatment of bronchitis

• Bronchosanation therapy;
• anti-inflammatory therapy;
• detoxification therapy;
• antibacterial therapy (according to indications);
• restorative therapy.

At present, there is no doubt that treatment should be carried out taking into account the etiology of the disease and the presence of bronchial obstruction, the genesis of which is dominated by inflammatory edema and hypersecretion of viscous mucus. Therefore, anti-inflammatory, bronchodilator and mucolytic drugs are pathogenetic and symptomatic methods of therapy. However, treatment should first of all be aimed at eliminating the cause of the disease - the infectious pathogen. The most difficult at the present stage, both from the point of view of diagnosis and therapy, is the treatment of recurrent broncho-obstructive diseases associated with atypical pathogens of respiratory infections (Mycoplasma pneumoniae, Chlamydia pneumonia, etc.), which is associated with the ability of these pathogens to persist and have an unfavorable immunotropic effect.

Due to irrational pharmacotherapy, bronchitis can develop into a protracted form, which leads to a decrease in the ability to work and quality of life of patients, and an increase in economic costs associated with treatment.
Rationally selected etiological therapy will reduce the risk of developing severe forms of the disease and its chronicity.

Drug therapy

Expectorant drugs that irritate the stomach receptors

Products based on medicinal plants: istod, ivy, plantain, thyme, licorice, marshmallow, thermopsis, guaifenesin, etc.

These drugs have a moderate irritating effect on the receptors of the gastric mucosa and reflexively enhance the secretion of the bronchi and bronchial glands. Promote the movement of mucus from the lower to the upper parts of the respiratory tract. The effect of some drugs (thermopsis, istod, etc.) is associated with a stimulating effect on the vomiting and respiratory centers.

Expectorants with resorptive action

• Carriers of sulfhydryl groups: acetylcysteine, carbocysteine.
• Vasicine derivatives: synthetic analogues of the alkaloid Adhatoda vasica: bromhexine, ambroxol.

After oral administration, these drugs are absorbed, enter the blood, are delivered to the bronchi, are secreted by the mucous membrane of the respiratory tract, stimulate the secretion of the bronchial glands, dilute and facilitate the separation of sputum, and enhance bronchial peristalsis.

Non-opioid antitussives with central action

• Butamirate - inhibits respiratory tract receptors, acts on the central nervous system, does not depress the respiratory center (sinecode, codelac, stoptussin).
• Glaucine is a yellow poppy alkaloid from the poppy family. Selectively inhibits the cough center (glaucine, glauvent).
• Oxeladin - suppresses the cough center and does not suppress the respiratory center. Does not cause drowsiness (paxeladine, tusuprex).
• Pentoxyverine - suppresses the cough reflex, reduces stimulation of the cough center (sedotussin).
• Ledin is a derivative of the essential oil of wild rosemary shoots, 8-hydroxyaromadendran. The antitussive effect is achieved by inhibiting the central cough reflex (ledin).
• Dextromethorphan - inhibiting respiratory tract receptors, does not inhibit the respiratory center, partially acts on the central nervous system (tussin plus).

Combined drugs with mucolytic and bronchodilator action in the form of syrups

Recently, combination drugs have appeared, the purpose of which is to have a complex effect on the symptoms of the disease that caused the cough. There are many combinations in which antitussives, expectorants, and mucolytics are found in a variety of combinations, and due to the combined effect, treatment results are significantly superior to those with monotherapy.

The variety of drugs for treating cough is due, on the one hand, to the need to solve various therapeutic problems depending on the nature of the cough, the stage of the infectious process and the combination of certain pathological factors underlying it, and on the other hand, to the insufficient effectiveness of the therapy.

Joset, Cashnol, Ascoril - combined with salbutamol. Baladex combined with theophylline, clenbuterol.

In the pathogenetic therapy of bronchitis, an inhibitor of anti-inflammatory mediators has appeared, which includes fenspiride, which has bronchodilator and anti-inflammatory activity. The drug reduces the manifestations of bronchospasm, reduces the production of a number of biologically active substances involved in the development of inflammation and helps to increase bronchial tone, including cytokines, arachidonic acid derivatives, and free radicals. Fenspiride also suppresses the formation of histamine - this is associated with its antispasmodic and antitussive effect.

In symptomatic and pathogenetic therapy in the acute period with obstructive syndrome, it is advisable to choose inhaled bronchodilators and inhaled glucocorticosteroids.

The use of the “bronchodilator + mucolytic + inhaled glucocorticosteroid” regimen in comparison with the “bronchodilator + mucolytic” regimen and with the use of a single bronchodilator in the symptomatic treatment of recurrent obstructive bronchitis is most optimal from a pharmacoeconomic point of view. The likelihood of positive clinical effects using this regimen is very high.

Nebulizer therapy Currently, nebulizers used for inhalation therapy in pulmonology are widely used. The operation of the devices is based on the principle of spraying liquid medications into an aerosol mist using compressed air or ultrasound. There are two types of nebulizers: jet, using a stream of gas (air or oxygen), and ultrasonic, using the energy of vibration of a piezocrystal. Jet nebulizers are more popular.

For lung diseases, the inhalation route of drug administration is the most logical, since the drug is delivered by the shortest route, acts faster at a lower dose and with a lower risk of systemic side effects compared to drugs that are administered orally or parenterally.
The use of nebulizers allows you to:

• improve drug delivery to the lungs without increasing the dose;
• achieve significant drug savings;
• use treatment regardless of age and severity of the disease.

Nebulizer therapy provides the highest percentage of drug delivery to the distal parts of the respiratory tract (compared to any other delivery devices), regardless of the patient’s inhalation force, and is most suitable for relieving an attack of suffocation (or cough) of any severity, as well as for basic step-by-step therapy with transferring the patient, when the condition is stabilized, to the use of drugs using other delivery devices.

Bronchodilators

• Fenoterol (Berotec). The drug helps to dilate the bronchi and facilitate the passage of air flow through the respiratory tract narrowed by inflammation. For inhalation, 1–2 ml of the drug is used, the effect lasts for 3 hours. It is used symptomatically depending on the severity of bronchospasm. During an exacerbation, on average it is used up to 4 times a day. Inhalation of Berotek through a nebulizer has significant advantages over a metered aerosol can: the drug acts directly in the smallest bronchioles, and does not settle in the oropharynx, is not absorbed into the blood and does not cause a lot of side effects (increased blood pressure, arrhythmias, tremor). When using a spray can, you must hold your breath for a few seconds after administering the drug, which is not always possible during a severe attack, or in children. This is not necessary when using a nebulizer.
• Salbutamol. Used when bronchospasm occurs. Available in special nebulas of 2.5 ml. One nebula is used for inhalation; the therapeutic effect lasts for 4–6 hours. The number of inhalations depends on the severity of the underlying disease.
• Ipratropium bromide (Atrovent). Inhale 2–4 ml, the effect lasts 5–6 hours. The bronchodilating properties of the drug are somewhat weaker than those of Berotek, but it is practically free of side effects and is more often prescribed to patients with cardiovascular diseases.
• Combined bronchodilator Berodual (fenoterol + atrovent). 2–4 ml of solution are inhaled, the number of procedures depends on the patient’s condition.

Agents affecting sputum rheology

• Lazolvan. The solution intended for inhalation is available in 100 ml bottles. Effectively dilutes viscous, difficult to separate sputum, as a result of which it becomes liquid and the patient can easily cough it up. Inhale 3 ml of the drug 4 times a day.
• Fluimucil (acetylcysteine). Used as an expectorant, 3 ml several times a day.
• Slightly alkaline mineral waters: “Borjomi”, “Narzan”, physiological solution in a dose of 3 ml 4 times a day.

Antibacterial and antiseptic agents

Should be used only in the presence of a clinical diagnosis of bacterial damage to the bronchi.

• Fluimucil antibiotic IT. A two-component drug containing the antibiotic thiamphenicol and acetylcysteine, which effectively thins sputum. Prescribed for purulent bronchitis. The dry powder is dissolved in 5 ml of 0.9% sodium chloride and divided into 2 doses.
• Dioxidin, miramistin. Broad-spectrum antiseptics. Used for purulent processes in a dose of 4 ml 2 times a day.
• Furacilin. Antiseptic. Use a ready-made 0.02% solution, 4 ml 2 times a day.

Inhaled corticosteroids

Dexamethasone, budesonide, pulmicort. Nebulas 2 ml in various dosages. Used for broncho-obstructive syndrome. The dose and frequency depend on the severity of the disease and are selected by the doctor.

Lidocaine

In cases of obsessive dry cough, lidocaine inhalation through a nebulizer can be used as a symptomatic remedy. The drug, having local anesthetic properties, reduces the sensitivity of cough receptors and effectively suppresses the cough reflex. The most common indications for lidocaine inhalation are viral tracheitis, laryngitis and even lung cancer. You can inhale a 2% solution, available in ampoules, 2 ml 2 times a day. When prescribing several drugs simultaneously, the order should be observed. The first is a bronchodilator, after 10-15 minutes - an expectorant, after sputum is discharged - an anti-inflammatory or disinfectant.

Antibiotic therapy Treatment of prolonged and recurrent bronchitis of bacterial etiology should be aimed at eliminating the cause of the disease and eradicating the infectious pathogen. The leading role belongs to antibiotic therapy. Adequate antibiotic therapy allows not only to relieve the symptoms of acute inflammation, but also to eradicate the pathogen, reduce the frequency of relapses, and increase the interval between exacerbations, which ultimately improves the quality of life of patients.

Indications for use:

• temperature above 38 °C, not decreasing for more than 3 days, temperature increase during treatment;
• discharge of purulent sputum;
• prolonged course (2–3 weeks without improvement);
• serious condition: high fever, weakness, signs of intoxication;
• increase in ESR up to 20 mm/hour, band shift, changes in blood count.

The choice of antibiotic was made empirically, taking into account the probable etiology and sensitivity of the suspected pathogen to antimicrobial drugs (see table).

General restorative therapy for recurrent bronchitis

In recent years, among immunomodulatory drugs, bacterial lysates of pathogens of respiratory infections have attracted particular interest in pulmonology. These drugs have a dual purpose: specific (vaccinating) and nonspecific (immunomodulatory).

It should be noted that specific active immunization against the most common pathogens of respiratory diseases compares favorably with nonspecific immunostimulation in its focus and effectiveness. This is also due to the fact that, unfortunately, the most highly effective method of preventing infectious diseases - vaccination - today has rather limited possibilities in pulmonology. There are vaccinations against pneumococcus, Haemophilus influenzae, etc., and new vaccines against influenza virus and staphylococcus appear every year. However, there are no vaccines against most respiratory pathogens, not to mention the absence of multivaccines with antigens of the main pathogens of respiratory infections. In addition, respiratory pathogens are characterized by rapid variability, and specific immunity against them is short-lived.

Therefore, so-called vaccine-like drugs, the action of which is aimed at creating specific immunity against a specific pathogen of respiratory tract infections, are becoming of great importance. In this regard, in recent years, immunocorrectors of bacterial origin have become widely used for the treatment and prevention of respiratory infections, primarily bacterial lysates, which cause the formation of a selective immune response against specific pathogens. The drugs can also be prescribed for prophylactic purposes during the acute period of respiratory infections (more effective in combination with appropriate etiotropic therapy).

The main representatives of bacterial lysates are broncho-munal (capsules), IRS-19 (nasal spray), ribomunil (tablets). The drugs initiate a specific immune response to bacterial antigens present in these drugs. The use of oral lysates causes the contact of antigens of the most significant pathogens of respiratory infections with macrophages located in the mucous membranes of the gastrointestinal tract, with their subsequent presentation to lymphocytes in the lymphoid tissue. As a result, committed clones of B lymphocytes appear, producing specific antibodies to pathogen antigens contained in bacterial lysates, and secretory IgA for the development of effective local immune defense of the mucosa against the main pathogens of respiratory diseases. Since bacterial immunomodulatory drugs are intended to stimulate the body's specific defense against the pathogenic effects of those microorganisms whose antigenic substrates are included in its composition, this vaccine-like effect is accompanied by the induction of a specific response of both local and general immunity. They are able to increase the overall resistance of the body, which has a positive effect on the preventive effect against respiratory infections.

Criteria for transfer to the inpatient stage of treatment. It is advisable to transfer to the inpatient stage of treatment if complications develop: pneumonia, obstructive syndrome, increasing intoxication, fever, and signs of respiratory failure. Thus, the treatment of bronchitis should be comprehensive, taking into account the etiology of the disease, its severity and the nature of its course. Table. Etiotropic prescription of antibiotics

Microflora	Antibiotics
Pneumococcus	macrolides (clarithromycin).
Streptococcus	Amoxicillin, including with clavulanic acid; 1st and 2nd generation cephalosporins; macrolides (clarithromycin).
Staphylococcus	Amoxicillin, including with clavulanic acid; 1st and 2nd generation cephalosporins; macrolides (clarithromycin); fluoroquinolones; vancomycin (for methicillin resistance).
Haemophilus influenzae	Amoxicillin, including with clavulanic acid; 1st and 2nd generation cephalosporins; macrolides (clarithromycin).
Legionella	Macrolides (clarithromycin); fluoroquinolones.
Mycoplasma Chlamydia	Macrolides (clarithromycin).

Note.
The low effectiveness of protected penicillins and cephalosporins in the treatment of bronchitis in the absence of concomitant diseases may indicate the atypical nature of the disease.

Case from practice

In practice, 3 types of erroneous use of antibacterial agents most often occur: belated (4 hours after diagnosis) prescription in patients, for example, with pneumonia; inadequate initial therapy for non-severe diseases, including reserve antibiotics; unjustified prescription to patients with a viral infection (most often). The latter is demonstrated by the clinical case below.

Patient G., born in 1984, came to the clinic with complaints of malaise, body temperature above 38 °C, non-productive cough, pain and sore throat, runny nose. Upon objective examination: the skin and visible mucous membranes are of normal color, sweating is increased, the temperature is 37.8 °C. On auscultation, hard breathing, isolated dry wheezing, and rhythmic, clear, and somewhat muffled heart sounds are heard in the lungs.

Research results. Complete blood count: leukocytes - 7.4×109, lymphocytes - 41%, eosinophils - 4%, ESR - 19 mm/h; urine analysis without pathological changes; radiography - increased pulmonary pattern, focal and infiltrative shadows were not detected.

Diagnosis: acute bronchitis.

The patient was prescribed: amoxicillin 0.5 g 3 times a day, lazolvan 0.03 g 3 times a day.

Sick leave issued. After 3 days, the patient returned to the clinic to extend his sick leave. He reported that the temperature had dropped to 37.3–37.0 °C, but complained of a paroxysmal nonproductive cough and periodic difficulty breathing that occurred in the early morning hours. When auscultating the lungs, dry whistling rales are heard mainly in the lower parts of both lungs. A referral was made for a spirogram; moderate obstruction of the distal bronchi was detected, which was reversible when performing a bronchodilator test with salbutamol.

Diagnosis: acute bronchitis with symptoms of bronchospasm.

The patient was discontinued amoxicillin, Berodual (1 inhalation 3 times a day) was prescribed while taking lazolvan at the same dose, tylol hot (symptomatically), fenkarol (0.025 g 2 times a day), gargling.

Sick leave extended. After 4 days, the patient visited the clinic with complaints of slight malaise and a rare nonproductive cough. During auscultation of the lungs, no wheezing was heard, and harsh breathing persisted. Spirometry revealed mild obstruction at the level of the distal bronchi, reversible. It is recommended to continue taking Berodual 1 inhalation 2 times a day. Control spirogram - after 10 days. Sick leave is closed.

This case demonstrates a typical, unfortunately, mistake when prescribing initial therapy in this category of patients - the use of antibacterial agents in cases of viral infection, which is the most common cause of acute bronchitis. Despite the correct diagnosis in this case, such treatment tactics aggravated the symptoms of bronchial hyperreactivity in a predisposed patient, which were detected already at the first time of seeking medical help in the form of dry wheezing. Probably, the increased reactivity of the bronchi was provoked by a viral infection and “supported” by the antibiotic. However, during the follow-up visit, the doctor correctly assessed the situation and made appropriate adjustments to the treatment regimen.

In the future, this patient needs to be examined to exclude bronchial asthma.

Bronchitis refers to diseases of the respiratory system and is a diffuse inflammation of the mucous membrane of the trachea and bronchi. The clinical picture of bronchitis may differ depending on the form of the pathological process, as well as the severity of its course.

According to the international classification, bronchitis is divided into acute and chronic. The first is characterized by an acute course, increased sputum production, and a dry cough that gets worse at night. After a few days, the cough becomes wet and sputum begins to come out. Acute bronchitis usually lasts 2-4 weeks.

In accordance with the guidelines of the World Health Organization, signs of bronchitis, which allows it to be classified as chronic, is a cough with intense bronchial secretion, lasting more than 3 months for 2 years in a row.

In the chronic process, the damage spreads to the bronchial tree, the protective functions of the bronchi are disrupted, there is difficulty breathing, copious formation of viscous sputum in the lungs, and a prolonged cough. The urge to cough with expectoration is especially intense in the morning.

Reasons for the development of bronchitis

Various forms of bronchitis differ significantly from each other in their causes, pathogenesis and clinical manifestations.

The etiology of acute bronchitis is the basis for the classification, according to which diseases are divided into the following types:

• infectious (bacterial, viral, viral-bacterial, rarely fungal infection);
• staying in unfavorable harmful conditions;
• unspecified;
• mixed etiology.

More than half of all cases of the disease are caused by viral pathogens. The causative agents of the viral form of the disease in most cases are rhinoviruses, adenoviruses, influenza, parainfluenza, and respiratory interstitial.

Of the bacteria, the disease is most often caused by pneumococci, streptococci, Haemophilus influenzae and Pseudomonas aeruginosa, Moraxella catarrhalis, and Klebsiella. Pseudomonas aeruginosa and Klebsiella are more often detected in patients with immunodeficiencies who abuse alcohol. In smokers, the disease is more often caused by Moraxella or Haemophilus influenzae. Exacerbation of the chronic form of the disease is often provoked by Pseudomonas aeruginosa and staphylococci.

Mixed etiology of bronchitis is very common. The primary pathogen enters the body and reduces the protective functions of the immune system. This creates favorable conditions for the addition of a secondary infection.

The main causes of chronic bronchitis, in addition to bacteria and viruses, are exposure to harmful physical and chemical factors on the bronchi (irritation of the bronchial mucosa by coal, cement, quartz dust, vapors of sulfur, hydrogen sulfide, bromine, chlorine, ammonia), prolonged contact with allergens. In rare cases, the development of pathology is caused by genetic disorders. A connection has been established between the incidence rate and climatic factors; an increase is observed during the cold, damp period.

Atypical forms of bronchitis are caused by pathogens that occupy an intermediate niche between viruses and bacteria. These include:

• legionella;
• mycoplasma;
• chlamydia.

Atypical diseases are characterized by uncharacteristic symptoms with the development of polyserositis, damage to joints and internal organs.

Features of the pathogenesis of bronchial inflammation

The pathogenesis of bronchitis consists of neuro-reflex and infectious stages of the development of the disease. Under the influence of provoking factors, trophic disorders are observed in the walls of the bronchi. An infectious disease begins with the adhesion of an infecting pathogen to the epithelial cells of the mucous membrane of the airways of the lungs. In this case, local protective mechanisms, such as air filtration, humidification, purification, are disrupted, and the activity of the phagocytic function of alveolar macrophages and neutrophils is reduced.

The penetration of pathogens into lung tissue is also facilitated by disruption of the immune system, increased sensitivity of the body to allergens or toxic substances formed during the life of pathogens of the inflammatory process. With constant smoking or contact with harmful conditions, the clearance of small irritants from the lungs slows down.

With further progression of the disease, obstruction of the tracheobronchial tree develops, redness and swelling of the mucous membrane are noted, and increased desquamation of the integumentary epithelium begins. As a result, an exudate of a mucous or mucopurulent nature is produced. Sometimes there may be complete blockage of the lumen of the bronchioles and bronchi.

In severe cases, purulent sputum of a yellowish or greenish color is formed. With hemorrhages from the blood vessels of the mucous membrane, the exudate takes on a hemorrhagic form with brown lumps (rusty sputum).

A mild degree of the disease is characterized by damage to only the upper layers of the mucous membrane; in severe cases, all layers of the bronchial wall undergo morphological changes. If the outcome is favorable, the consequences of the inflammatory process disappear within 2-3 weeks. In the case of panbronchitis, restoration of the deep layers of the mucosa lasts about 3-4 weeks. If pathological changes become irreversible, the acute phase of the disease becomes chronic.

The conditions for the pathology to become chronic are:

• a decrease in the body’s defenses to diseases, exposure to allergens, and hypothermia;
• viral respiratory diseases;
• foci of infectious processes in the organs of the respiratory system;
• allergic diseases;
• heart failure with congestion in the lungs;
• deterioration of drainage function due to disruptions in motility and disruption of the ciliated epithelium;
• presence of tracheostomy;
• socially unfavorable living conditions;
• dysfunction of the neurohumoral regulatory system;
• smoking, alcoholism.

The most significant thing in this type of pathology is the functioning of the nervous system.

The totality of manifestations of bronchitis

The symptoms of bronchitis, depending on the form of the disease, have significant differences, therefore, in order to correctly assess the patient’s condition, as well as prescribe appropriate treatment, it is necessary to identify the distinctive features of the pathology in time.

Clinical picture of acute bronchitis

The clinical picture of acute bronchitis in the initial stage is manifested by signs of acute respiratory infections, runny nose, general weakness, headache, slight increase in body temperature, redness, sore throat). Along with these symptoms, a dry, painful cough occurs.

Patients complain of a sore feeling behind the sternum. After a few days, the cough acquires a wet character, becomes softer, and mucous exudate begins to disappear (catarrhal form of the disease). If infection with a bacterial agent is added to a viral pathology, the sputum becomes mucopurulent in nature. Purulent sputum in acute bronchitis is extremely rare. During severe coughing attacks, the exudate may be streaked with blood.

If inflammation of the bronchioles develops against the background of bronchitis, symptoms of respiratory failure may occur, such as shortness of breath and bluish skin. Rapid breathing may indicate the development of bronchial obstruction syndrome.

When tapping the chest, the percussion sound and trembling of the voice usually do not change. Hard breathing can be heard. In the initial stage of the disease, dry wheezing is observed, when sputum begins to leave, it becomes moist.

In the blood there is a moderate increase in the number of leukocytes with a predominance of neutrophils. The erythrocyte sedimentation rate may increase slightly. There is a high probability of the appearance of C-reactive protein, increased levels of sialic acids, alpha 2-globulins.

The type of pathogen is determined by bacterioscopy of lung exudate or sputum culture. For timely detection of blockage of the bronchi or bronchioles, peak flowmetry or spirometry is performed.

In acute bronchitis, pathology of the lung structure is usually not observed on an x-ray.

In acute bronchitis, recovery occurs within 10-14 days. In patients with weakened immune systems, the disease has a protracted course and can last more than a month. In children, more pronounced signs of bronchitis are observed, but the tolerance of the disease in pediatric patients is easier than in adults.

Symptoms of chronic bronchitis

Chronic non-obstructive or obstructive bronchitis manifests itself differently, based on the duration of the disease, the likelihood of heart failure or emphysema. The chronic form of the disease has the same varieties as the acute one.

In chronic bronchitis, the following clinical manifestations of the disease are noted:

• increased secretion and release of purulent sputum;
• whistling during inspiration;
• difficulty breathing, hard breathing when listening;
• severe painful cough;
• more often dry wheezing, moist with a large amount of viscous sputum;
• heat;
• sweating;
• muscle tremors;
• changes in the frequency and duration of sleep;
• severe headaches at night;
• attention disorders;
• rapid heartbeat, increased blood pressure;
• convulsions.

The main symptom of chronic bronchitis is a severe paroxysmal barking cough, especially in the morning, with copious discharge of thick sputum. After a few days of this cough, chest pain occurs.

The nature of the sputum secreted, its consistency, color, differ depending on the following types of chronic bronchitis:

• catarrhal;
• catarrhal-purulent;
• purulent;
• fibrinous;
• hemorrhagic (hemoptysis).

As bronchitis progresses, the patient begins to experience shortness of breath even without physical exertion.. Externally, this is manifested by cyanosis of the skin. The chest takes on the shape of a barrel, the ribs rise to a horizontal position, and the pits above the collarbones begin to protrude.

Hemorrhagic bronchitis is classified as a separate form. The disease is non-obstructive in nature, has a long-term course, and is characterized by hemoptysis caused by increased permeability of the vascular wall. The pathology is quite rare; in order to establish a diagnosis, it is necessary to exclude other factors in the formation of mucous secretion from the lungs mixed with blood. To do this, bronchoscopy determines the thickness of the walls of the mucosal blood vessels.

The fibrinous form of bronchitis is detected very rarely. A distinctive feature of this pathology is the presence of fibrin deposits, Kurshman spirals, and Charcot-Leyden crystals. The clinic is manifested by a cough, with expectoration of casts in the form of a bronchial tree.

Bronchitis is a common disease. With adequate therapy, it has a favorable prognosis. However, with self-medication, there is a high probability of developing serious complications or the disease becoming chronic. Therefore, at the first symptoms characteristic of bronchial inflammation, you should consult a doctor.