Chronical bronchitis- is a progressive lesion of the bronchial tree, caused by prolonged irritation of the airways by various harmful agents, characterized by the restructuring of the secretory apparatus of the mucous membrane and the development of the inflammatory process.

ETIOLOGY:

1. Tobacco smoking(active and passive): among other risk factors, it ranks first. Tobacco smoke contains not only toxic substances such as formaldehyde, benzopyrene, vinyl chloride, but is also a "supplier" of a huge amount of free radicals that trigger lipid peroxidation processes and lead to damage to the bronchial epithelium.

2. Industrial pollutants and industrial dust: ozone, oxides of sulfur, nitrogen, carbon, organic compounds formed during the combustion of oil and gas, cadmium, silicon.

3. Chronic infections of ENT organs, as well as frequent acute respiratory viral infections and acute bronchitis(adenovirus, RS-viruses, influenza virus, mycoplasmas).

Classification of chronic bronchitis:

By functional characteristic: 1. non-obstructive (simple) 2. obstructive

The nature of the inflammation : 1. catarrhal 2. purulent

According to the phase of the disease: 1. Aggravation 2. Remission

Symptoms of chronic bronchitis:

Main symptoms chronic bronchitis - cough, sputum, shortness of breath. Cough is the most typical manifestation of the disease. It can be unproductive (“dry catarrh”), but is more often accompanied by sputum from several spittles up to 100-150 g per day. The sputum may be watery, mucous, streaked with pus and blood, or purulent. The ease of coughing up sputum is mainly determined by its elasticity and viscosity. The viscosity of sputum can vary from watery to very viscous, causing a prolonged cough that is extremely tiring for the patient. In the early stages of the disease, expectoration of sputum occurs only in the morning (usually when washing), in the subsequent sputum may be separated periodically throughout the day, often due to physical stress and increased breathing. Severe sweating is often noted, especially at night (the “wet pillow” symptom) or even with little physical exertion. Wet skin causes a feeling of chilliness, cooling of the body. Hemoptysis is relatively rare. In the phase of exacerbation of the disease, general well-being is usually disturbed, the amount of sputum increases, weakness, sweating, shortness of breath increase, and working capacity decreases.

Treatment of chronic bronchitis:

Treatment of patients with chronic bronchitis should be comprehensive, provide for the impact on the main pathogenetic mechanisms, take into account the individual characteristics and severity of the disease, the presence of complications.

AT exacerbation phase disease, an important element of treatment is the fight against infection, for which antibiotics, sulfonamides and other antibacterial agents are prescribed. The duration of antibiotic treatment is individual.

Foci of infection in the paranasal sinuses, pharyngeal tonsils, teeth, etc. in the acute phase of chronic bronchitis are subject to active treatment.

Antibacterial therapy should be combined with the appointment of agents that affect secretion and help clear the bronchi from a viscous secret. They are more often used orally or in the form of aerosols. Traditional expectorants are prescribed: a 3% solution of potassium iodide, infusions and decoctions of thermopsis, marshmallow, “breast collection” herbs and mixtures based on them, which are prescribed up to 10 times a day, as well as plentiful hot drinks. Patients with chronic obstructive bronchitis, especially those with clinical signs of bronchospasm, usually require more intensive treatment. It usually includes anti-inflammatory and desensitizing agents (acetylsalicylic acid, calcium preparations), according to indications, antihistamines (suprastin, diazolin, etc.). Drugs aimed at restoring bronchial patency are needed.

Effectively - physiotherapy, exercise therapy, massage, breathing exercises. Shown sanatorium treatment during remission.

20) Acute pneumonia. Causes. clinical picture. Principles of treatment.

Acute pneumonia – infectious and inflammatory lesions of the respiratory sections of the lungs, occurring with intoxication and bronchopulmonary syndrome, characteristic radiographic changes.

Acute pneumonia is one of the most common diseases of the respiratory system, often accompanied by complications, causing up to 9% of deaths.

Causes of acute pneumonia:

The dominant role in the etiology of acute pneumonia belongs to infection, primarily bacterial. Usually, the causative agents of the disease are pneumococci, mycoplasma, Staphylococcus aureus, Friedlander's bacillus, less often - hemolytic and non-hemolytic streptococcus, Pseudomonas aeruginosa and Haemophilus influenzae, fungi, influenza virus, adenoviruses.

Acute pneumonia can occur after exposure of the respiratory sections of the lungs to chemical and physical agents (concentrated acids and alkalis, temperature, ionizing radiation), as a rule, in combination with secondary bacterial infection with autogenous microflora from the pharynx and upper respiratory tract.

Various factors that reduce the resistance of the macroorganism predispose to the occurrence of acute pneumonia: prolonged intoxication (including alcohol and nicotine), hypothermia and high humidity, concomitant chronic infections, respiratory allergies, nervous shocks, infancy and old age, prolonged bed rest.

Symptoms of acute pneumonia:

Most forms of acute pneumonia are characterized by the constant presence of general disorders: chills, a sharp rise in temperature and persistent fever, general weakness, sweating, headache, tachycardia, agitation or weakness, sleep disorders.

Cough in acute pneumonia is of a different nature, accompanied by the release of mucopurulent sputum, rapid breathing (up to 25-30 per minute), pain in the chest or under the shoulder blade.

Focal pneumonia (bronchopneumonia) in most cases begins against the background of bronchitis or acute catarrh of the upper respiratory tract. A febrile fever of the wrong type is typical; in elderly and debilitated individuals, a normal or subfebrile temperature may be maintained.

Influenza pneumonia usually develops acutely on the first or third day of the flu. Flowing, as a rule, is easier than bacterial, sometimes it can acquire a severe course with significant intoxication and high fever, persistent cough, and rapid development of pulmonary edema. Late pneumonia that occurs during the recovery period from influenza is due to bacterial microflora.

Treatment of acute pneumonia:

Patients with acute pneumonia require early treatment, usually in a hospital setting.

During the febrile period, bed rest, heavy drinking and easily digestible high-calorie nutrition, vitamin therapy are indicated.

In acute pneumonia, etiotropic therapy with antibacterial drugs prescribed on the basis of clinical and radiological features is effective. Semi-synthetic penicillins (ampicillin, amoxicillin), aminoglycosides (gentamicin), cephalosporins (ceftriaxone), macrolides (erythromycin, azithromycin), tetracyclines are used, rifampicin, lincomycin are used as backup .. The intensity of the course of antibiotic therapy depends on the severity and prevalence of lung damage.

Patients with acute pneumonia are shown bronchodilators and expectorants, mucolytics.

To eliminate intoxication, hemodez, reopoliglyukin infusions are carried out.

In case of shortness of breath and cyanosis, oxygen therapy is required.

With cardiovascular insufficiency, cardiac glycosides are prescribed.

In addition to antibiotic therapy, anti-inflammatory and antihistamines, immunocorrectors are used. In the stage of resolving acute pneumonia, physiotherapy is effective

Version: Directory of Diseases MedElement

Acute bronchitis (J20)

Pulmonology

general information

Short description

acute bronchitis- diffuse acute inflammation of the tracheobronchial tree (bronchial mucosa).

1. Bronchitis, not specified as acute or chronic, in persons under 15 years of age.
2. Acute or subacute bronchitis, including:
- acute bronchitis with bronchospasm;
- fibrinous;
- membranous;
- purulent;
- septic.
3. Acute tracheobronchitis.

Excluded from this section are:
1. Bronchitis (tracheobronchitis), not specified as acute or chronic, in persons 15 years of age and older (see J40).
2. Asthma, unspecified (us. allergic bronchitis) - J45.9.
3. Asthma with a predominance of an allergic component (us. allergic bronchitis) - J45.0.
4. Chronic obstructive pulmonary disease with acute respiratory infection of the lower respiratory tract (J44.0).
5. Acute bronchitis with bronchiectasis (J47.0).
7. Bronchitis and pneumonitis due to chemicals, gases, fumes and vapors (J68.0).
8. Chronic bronchitis and tracheobronchitis:
- unspecified (J42);
- mucopurulent (J41.1);
- simple (J41.0).

Flow period

Minimum flow period (days): 14

Maximum flow period (days): 21

Symptoms (cough, fever, bronchial obstruction) lasting more than 3 weeks should be a reason for expanding the examination and consulting specialists.

Classification

By etiology

:
- viral;
- bacterial (including mycoplasma);
- due to the influence of chemical factors;
- due to the influence of physical factors.

The etiological variants of acute bronchitis associated with chemical and physical effects (for example, toxic and burns) are rarely observed in isolation, but, as a rule, occur as a component of a systemic lesion.

According to the mechanism of development:

Primary;
- secondary (arising against the background of an already existing pathology of the upper and lower respiratory tract).

According to flow options:
- acute;
- acute protracted bronchitis (lasting more than 3 weeks);
- recurrent bronchitis (recurring during the year 3 or more times);

- acute obstructive bronchitis.

Etiology and pathogenesis

Etiology

In adults, 85-95% of acute bronchitis is caused by viruses.
According to Russian researchers, in children over 4 years of age, viral bronchitis is recorded in approximately 20% of cases, in children from 14 days to 4 years - in less than 10% of cases.
As a rule, viral bronchitis is associated with bacteria (more often), with fungi (less often), protozoa. Acute bronchitis can be caused by a variety of bacteria. At the same time, the etiological structure of acute community-acquired and nosocomial bacterial bronchitis differs significantly.
According to the results of Russian studies on the identification of topical pathogens of acute bronchitis in patients without concomitant pulmonary pathology, it was possible to verify the pathogen only in 16-29% of patients.
The long-held hypothesis of acute bacterial bronchitis caused, for example, by Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, and gram-negative bacteria, was not confirmed by Russian pediatricians (except for patients who underwent surgical procedures).
Evidence of participation in the development of the disease Bordatella pertussis and B. parapertussis, Mycoplasma pneumoniae and Chlamydophila pneumoniae was obtained in 5-10% of cases.
However, according to foreign authors, the role of chlamydia and mycoplasmas as an etiological factor has recently grown significantly; mycoplasma and chlamydial etiology in children can be from 25 to 40%, and it is highest in the first year of life and after 10 years.

Etiology of acute bronchitis depending on age(Geppe N.A., Safronova A.N., 2009):
- 0-3 months: cytomegalovirus, enterovirus, herpes viruses;
- 0-6 months: chlamydia (Chl.trachomatis);
- from 6 months to 3 years: respiratory syncytial virus, parainfluenza virus type 3;
- 6-17 years old: chlamydia (Chl.pneumoniae), mycoplasmas (M.pneumoniae).

Note. In all age groups: adenovirus, rhinovirus, influenza virus (especially in the cold season).

Pathogenesis
Viruses, penetrating into the epithelial cells of the bronchial mucosa, lead to their death. The infection also spreads to smaller airways (this is especially true for influenza viruses and respiratory syncytial viruses), contributing to the development of bronchial hyperreactivity. Viral infection sensitizes the respiratory tract, disrupts mucocellular clearance up to complete cessation, and suppresses defense mechanisms against bacterial infection. After the attachment of a bacterial infection, the amount of mucus increases, which prevents the penetration of antibiotics into the respiratory tract and makes phagocytosis difficult. Under the influence of infectious agents, various inflammatory mediators are released.

pathological anatomy
The mucous membrane of the bronchi in acute bronchitis appears swollen and hyperemic, there is exudate on its surface Exudate is a protein-rich fluid that exits small veins and capillaries into surrounding tissues and body cavities during inflammation.
, which in small bronchi and bronchioles can fill the entire lumen of the respiratory tubes. The exudate of the bronchial mucosa can be serous, mucous, mucopurulent or purulent.
In the discharge almost always (with the exception of serous exudate) erythrocytes are found. In such severe forms as influenza B, hemorrhages in the bronchial mucosa are possible, due to which the exudate becomes bloody. Almost constantly in the exudate, individual cells of the cylindrical epithelium of the mucous membranes are detected. In mild cases of bronchitis, changes are limited only to the mucosa itself, in more severe cases, they capture all layers of the bronchial wall. When conducting a microscopic examination of the wall of the inflamed bronchus, a picture of hyperemia is observed Hyperemia - increased blood supply to any part of the peripheral vascular system.
and inflammatory edema of the mucosa and submucosal tissue.
Even with mild bronchitis, there is infiltration with leukocytes and lymphocytes (later with an admixture of plasma cells). It is present in the mucous membrane and submucosal tissue, in other layers of the bronchial wall, captures the peribronchial tissue in the small bronchi.
In the case of significant cell infiltration, the bronchial wall thickens, the infiltrate and edema in it loosen the elastic tissue and the smooth muscle layer, and the muscle fibers undergo degenerative obesity. All this creates conditions for the expansion of small intrapulmonary bronchi, the formation of bronchiectasis Bronchiectasis - expansion of limited areas of the bronchi due to inflammatory-dystrophic changes in their walls or anomalies in the development of the bronchial tree
(typical for measles and influenza bronchitis in children).
During the period of acute bronchitis, the inflammatory process often passes to the connective tissue surrounding the bronchus, captures the descending lymphatic vessels here and spreads along the bronchus through them. Inflammatory changes from the peribronchial connective tissue can move to the lung tissue. Often there is the development of bronchopneumonia, when inflammation inside the bronchi goes down to their terminal branches and to the lung tissue. In case of blockage of the lumen of the small bronchi with a secret, the corresponding sections of the lung tissue collapse and atelectasis is formed.

The main morphological types of acute inflammation of the bronchi:
- acute catarrhal;
- catarrhal-purulent;
- hemorrhagic;
- fibrinous-ulcerative;
- suppurative.

For acute catarrhal bronchitis hyperemia and edema of the bronchus wall, an increase in the number of goblet cells, hypersecretion of glands and liquefaction of mucus, accumulation of a small number of leukocytes and desquamated epithelium in the lumen of the bronchus are characteristic. Inflammatory infiltration is moderate and limited to the mucous membrane, defects in the epithelial lining are superficial and small, quickly recovering.

At catarrhal-purulent bronchitis(purulent catarrh of the bronchi, purulent bronchitis) the mucous membrane of the bronchi is swollen and has a bright pink or red color. Exudate accumulates in the lumen of the bronchi, which contains a large number of leukocytes; the epithelium has more persistent and deep surface defects, erosion may form Erosion - superficial defect of the mucous membrane or epidermis
. There are pronounced degenerative changes in the ciliated epithelium. Inflammatory process - limited or widespread; captures most of the bronchial tree down to the smallest bronchi. In the case of a severe course of the disease, the inflammatory process, along with the mucous membrane, also covers the deep tissues of the bronchial wall.

At hemorrhagic bronchitis in exudate a large number of erythrocytes comes to light.

Acute fibrinous bronchitis(croupous bronchitis, plastic bronchitis, bronchial croup) is observed in diphtheria, lobar pneumonia and is accompanied by the release of a fibrinous film on the surface of the inflamed mucous membrane. In rare cases, isolated croupous inflammation of the bronchi occurs without fibrinous lesions of the larynx, trachea, or lung tissue. The nature of the inflammation is croupous, the epithelial cover in the large bronchi can be preserved (with the exception of superficial rows) and the fibrinous film looks like a tube. In small ones, it looks like a continuous cylindrical mass and fills the entire lumen of the bronchi. Acute fibrinous bronchitis is a rather rare disease with unclear etiology and pathogenesis. In the future, it usually takes on a relapsing character with exacerbation intervals from several months to several years. May cause minor bleeding in the lungs (hemoptysis).

Membrane bronchitis(a variant of fibrinous bronchitis with the formation of a large number of films) develops against the background of pronounced alterative changes. Fibrinous (croupous or diphtheritic) inflammation is characteristic, which is manifested by the presence of a whitish-gray fibrinous film on the surface of the mucous membrane, more or less tightly soldered to the underlying tissues. After the film is melted by neutrophil enzymes and its rejection, defects of various depths are exposed - ulcers that heal, filling with granulation tissue with its subsequent scarring.

Suppurative bronchitis (suppuration of the bronchi, septic bronchitis) is characterized by purulent fusion of the bronchial mucosa and underlying tissues with the formation of deep ulcerative defects, destruction of glands, muscles and cartilage. The granulation tissue that gradually fills the ulcers becomes sclerosed, which leads to the formation of rough scars. This occurs mainly when a large amount of secretion accumulates in the lumen of the bronchi as a result of a violation of its evacuation (for example, with obstruction) and its purulent inflammation.

Options for the course of acute bronchitis

Acute obstructive bronchitis(OHB) of infectious genesis can be caused by various respiratory viruses, mycoplasmas, chlamydia. In young children, the majority of obstructive forms of bronchitis are caused by RS-viral and parainfluenza type 3 infections; other viruses (usually cytomegalovirus and adenoviruses) cause no more than 10-20% of cases.
Some authors consider mycoplasma to be one of the main etiological factors of acute obstructive bronchitis (especially in older children). In recurrent obstructive bronchitis, the role of M.pneumoniae increases (according to Nazarenko N.M. et al. (2001), infection with this pathogen is detected in 85% of children with recurrent obstructive bronchitis).
The complex mechanisms of bronchial obstruction in children include narrowness of the airways, swelling of the mucous membranes and hypersecretion of the bronchial glands and, to a lesser extent, spasm of the smooth muscles of the bronchi. Difficulty in expiration in AOB of infectious origin is not a consequence of allergic inflammation. It is due to the peculiarities of the age-related reactivity of young children and the biological characteristics of the infectious agent.

Acute recurrent bronchitis(ARB) is acute bronchitis that occurs three or more times a year. Patients with this variant of acute bronchitis should be evaluated for asthma, COPD, and immunodeficiency. In about 50% of cases, these patients are later diagnosed with bronchial asthma.

Epidemiology

The epidemiology of acute bronchitis is directly related to the epidemiology of influenza and other respiratory viral diseases. Typically, the typical peaks of the increase in the incidence of these diseases are the end of December and the beginning of March.

Data on incidence in adults are very contradictory. The incidence of bronchitis, according to a number of authors, ranges from 15 to 50%. This percentage is significantly higher (up to 50-90%) among children who often suffer from acute respiratory infections, especially in environmentally unfavorable regions, as well as with passive smoking.

Individual clinical forms

Acute obstructive bronchitis(AOB) is a clinical form of acute bronchitis that occurs with severe signs of obstruction. It occurs mainly in children of the first 4 years of life. According to different authors, about 20-25% of bronchitis in children occur in the form of AOB. This figure is significantly higher than in adults. At the same time, obstructive conditions against the background of a respiratory viral infection are recorded in 10-30% of infants. The frequency of AOB, as a manifestation of ARVI, is especially high in young children (mainly up to 4 years).

Recurrent acute bronchitis has a prevalence of 16.4 per 1000 children. Children of preschool age are ill. Among frequently ill children (according to referrals), recurrent bronchitis was found in 27% and recurrent obstructive - in 17.2%.

Factors and risk groups

The following factors predispose to the development of acute bronchitis:
- climatic and weather conditions;
- unfavorable working and living conditions (hypothermia, dampness, drafts) or vice versa excessively dry, hot, polluted air;
- smoking;
- alcoholism;
- chronic focal infection in the nasopharyngeal region;
- influenza and other acute respiratory viral infections, acute pneumonia in history;
- chronic obstructive pulmonary disease (COPD);
- allergic diseases (bronchial asthma, allergic rhinitis, allergic conjunctivitis);
- violation of nasal breathing;
- immunodeficiency states;
- deformity of the chest;
- reflux esophagitis;
- elderly or children's age;
- congestive changes in the lungs with right ventricular failure;
- genetic (hereditary) predisposition to respiratory diseases.

Clinical picture

Symptoms, course

Bronchitis of infectious etiology often begins against the background of acute rhinitis or laryngitis.

Symptoms:
- sore behind the sternum;
- dry (rarely wet) cough, with a small amount of sputum (with a bacterial infection, sputum becomes purulent); sometimes the cough is hacking and painful;
- weakness, feeling of weakness;
- hoarseness of voice, pain when swallowing (rarely);
- signs of acute rhinitis, laryngitis, tracheitis (depending on the pathogen).

There are no physical signs, or hard breathing and widespread dry rales are determined over the lungs. Body temperature - subfebrile or normal.
With the defeat of the bronchi of medium and small calibers, the exhalation can become elongated, wheezing - dry and whistling.
When a secret appears in the bronchi, moist small bubbling rales are heard, which, unlike pneumonia, are less sonorous, do not have a clear localization and disappear after coughing.

In the case of the development of bronchospasm, signs of bronchial obstruction are added:
- shortness of breath with little physical exertion;
- box shade of percussion sound;
- prolonged exhalation on auscultation Auscultation is a method of physical diagnostics in medicine, which consists in listening to sounds generated during the functioning of organs.
;
- dry high-pitched rales.

Moderate course the disease is accompanied by a significantly pronounced general malaise, weakness; characterized by a strong dry cough with difficulty breathing and shortness of breath; pain in the lower parts of the chest and abdominal wall, caused by muscle strain when coughing. Gradually, the cough becomes wet with mucopurulent or purulent sputum.
Above the surface of the lungs, harsh breathing, dry and moist small bubbling rales are heard. For several days, the body temperature remains subfebrile. There are no pronounced changes in the composition of peripheral blood.
With a predominant lesion of the bronchioles (see "Acute bronchiolitis" - J20), as a rule, a severe course of the disease is observed.

Acute symptoms of the disease become less pronounced by the fourth day and, with a favorable outcome, completely disappear by the seventh day.
In acute bronchitis with impaired bronchial patency, there is a tendency to a protracted course and transition to chronic bronchitis.

Separate clinical forms of acute bronchitis

Acute obstructive bronchitis
At the onset of the disease, the clinical picture is characterized by symptoms of a respiratory viral infection: rise in body temperature, catarrhal changes in the upper respiratory tract, a violation of the general condition.
The severity and nature of symptoms vary greatly depending on the causative agent of the disease.
Signs of expiratory difficulty in breathing can be observed on the first day of the disease or during the course of a viral infection (on the third to fifth days). The respiratory rate and expiratory duration gradually increase.
Breathing becomes noisy and wheezing. This is due to the fact that as hypersecretion develops, secretion accumulates in the lumen of the bronchi due to shortness of breath and fever, the viscous properties of the secret change - it "dries up". This results in buzzing (low) and whistling (high) dry rales.
The defeat of the bronchi is widespread and therefore hard breathing with dry whistling and buzzing rales is heard equally over the entire surface of the chest. Wheezing can be heard from a distance.
The onset of the disease is the same as with SARS. Later, expiratory dyspnea develops with a respiratory rate of 60-80 per minute and cough. With the first episode, these symptoms are noted on the 2nd-4th day, with repeated episodes - on the 1st-2nd day.
For obstructive bronchitis, the prevalence of symptoms of damage to large bronchi is typical: wheezing, dry, often musical wheezing. For bronchiolitis, a more "wet" picture is characteristic: a mass of diffuse finely bubbling rales.
Elongation of expiration and whistling sounds with a significant increase in breathing can weaken up to complete disappearance. In this regard, when assessing obstruction, one should focus on the severity of pulmonary distension (percussion of the borders), respiratory rate and the degree of retraction of the "compliant" places of the chest, as well as the levels of Po and Pco 2.
Severe obstruction lasts 1-4 days (longer with bronchiolitis), complete normalization of the condition occurs after 1-2 weeks.

Recurrent obstructive bronchitis(3 or more episodes of acute obstructive bronchitis within a year)
The exacerbation proceeds with symptoms characteristic of SARS. After 1-3 days, these symptoms are accompanied by a cough (usually dry, more frequent at night). Cough and wheezing (dry or coarse and medium bubbling) persist longer than in acute bronchitis, sometimes up to 3-4 weeks. Symptoms, their duration and order of appearance tend to recur in ARVI of different etiologies. The expressed obstruction does not develop, but the latent bronchospasm often comes to light.

Diagnostics

1. The diagnosis of "acute bronchitis" is made clinically:
- in the presence of a carefully collected anamnesis, including the detection of smoking, adverse environmental factors and / or other predisposing factors;
- in the presence of an acute cough that lasts no more than 3 weeks, regardless of the presence of sputum;
- in the absence of signs of pneumonia and chronic lung diseases (COPD Chronic obstructive pulmonary disease (COPD) is an independent disease characterized by partially irreversible airflow limitation in the airways.
, bronchial asthma), which can also cause coughing;
- in the absence of reflux esophagitis Reflux esophagitis - inflammation of the esophageal mucosa due to gastroesophageal reflux; manifested by retrosternal pain, heartburn.
.

2. Physical examination and auscultation are performed.

3. When X-ray of the chest, as a rule, there is an increase in the pulmonary pattern and indistinctness of the roots of the lungs. In the case of attachment of a bronchospastic component, signs of "acute swelling of the lungs" appear: increased transparency of the lung fields, descent of the dome of the diaphragm.

X-ray examination is not indicated if:
- acute cough and sputum production indicate acute bronchitis;
- heart rate HR - heart rate
<100 уд./мин.;
- breathing rate<24 вдохов/мин.;
- temperature (oral)<38 о С (100,4 F).

4. Spirometry Spirometry - measurement of vital capacity of the lungs and other lung volumes using a spirometer
is not decisive in the diagnosis of acute bronchitis, but may help in the differential diagnosis.

Laboratory diagnostics

1. General blood analysis. Changes are nonspecific and depend on the type of pathogen. In the first days, leukopenia may be observed, bacterial inflammation is characterized by neutrophilia with a moderate shift to the left, a slight increase in ESR ESR - erythrocyte sedimentation rate (non-specific laboratory blood indicator, reflecting the ratio of plasma protein fractions)
.

2. Sputum analysis: a large number of desquamated epithelial cells, macrophages, single erythrocytes.
When a bacterial infection is attached, the sputum becomes mucopurulent, contains a large number of neutrophils.

Routine, mandatory, planned typing of the pathogen in uncomplicated and mild acute bronchitis is not recommended. Typing of the pathogen is indicated for a protracted course of acute bronchitis. PCR applied PCR - polymerase chain reaction
, serological (especially in paired blood sera taken at intervals of 3 weeks) research methods.

Differential Diagnosis

The most important in the differential diagnosis of acute bronchitis are:
- pneumonia;
- whooping cough;
- bronchial asthma;
- acute and chronic sinusitis;
- miliary pulmonary tuberculosis;
- foreign body;
- emphysema;
- ciliary dyskinesia syndrome (for example, Kartagener's syndrome);
- cystic fibrosis.

Differential diagnosis of acute bronchitis (WILLIAM J. HUESTON & ARCH G. MAINOUS III, 1998)

Pathological process	Signs and symptoms
reactive respiratory disease
Asthma	Evidence of reversible airway obstruction, even with infection
Allergic aspergillosis	- Transient infiltrates in the lungs - Eosinophilia in sputum and peripheral blood
Occupational hazards	Symptoms are pronounced during the working week, but tend to improve on weekends, holidays and vacations
Chronical bronchitis	- Chronic daily cough with sputum production for at least three months - Commonly seen in smokers
Respiratory tract infection
Sinusitis	- Congestion and pain in the sinuses - Nasal discharge
Cold	Inflammation of the upper airways without bronchial wheezing
Pneumonia	Characteristic changes on a chest x-ray
Other reasons
Congestive heart failure	- Basilar rales - Orthopnea - Cardiomegaly - Evidence of increased interstitial or alveolar fluid on chest x-ray - S 3 (gallop rhythm) - Tachycardia
Reflux esophagitis	Symptoms worsen when lying down Heartburn
Bronchogenic tumors	- Constitutional signs (weight loss) - Chronic cough, sometimes with hemoptysis
Aspiration syndromes	- Usually associated with a specific event, such as smoke inhalation - Vomit - Decreased level of consciousness

Differential diagnosis between acute bronchitis and acute pneumonia

Clinical signs	Acute (simple) bronchitis	Acute pneumonia
Degree of fever	Below 38 o C	Above 38 o C
Fever duration	Less than 3 days	More than 3 days
The nature of the cough	Superficial, dry, painless	Deep, wet, painful
Dyspnea	Not	There is
Cyanosis	Not	There is
Participation of auxiliary muscles in the act of breathing	Not	There is
Voice jitter	Not changed	Enhanced
Shortening of percussion sound	Not	There is
Local fine bubbling sonorous rales	Not	There is
Crepitus	Not	There is
Bronchophony	Not changed	reinforced

Differential diagnosis of broncho-obstructive syndrome (BOS) of allergic and infectious genesis

(Lasitsa O.I., Lasitsa T.S.)

signs	Infection	Allergy
Epidemiology	Contact with a patient with SARS	Contact with household, pollen and other allergens
Heredity	Not weighed down	hereditary predisposition to atopy
Clinic	Fever, intoxication and other signs of an infectious process	The temperature is normal, there is no intoxication
Persistence of clinical signs of BOS (cough, tympanitis, dry whistling and various wet rales)	Characterized by the cyclical nature of the pathological process	Typical lability of clinical signs during the day and in the dynamics of observation
Adaptation to bronchial obstruction	Pronounced respiratory failure	Sufficient adaptation to biofeedback
BOS duration	More often - 1-2 weeks	Very uncertain, dependent on exposure and allergen elimination
Relapses	Rare, except in cases of persistence of the virus	Very characteristic
Immunofluorescence study of nasopharyngeal swabs	Find allergens of RS viruses, parainfluenza, adenovirus, etc.	More often negative
The growth of the titer of antibodies to viruses in the reactions of RSK, RNGA	characteristic	not characteristic
Immunological study	There may be a decrease in cellular immunity, an increase in the CEC	Increase in Ig E, there may be a decrease in Ig A, CIC is often normal
Eosinophilia	Not typical	Very characteristic
Skin tests with household and other atopic allergens	negative	positive
Sensitization to atopic allergens in in vitro samples	Is absent	Present
bronchial hypersensitivity	Not typical	typical
Infestation with worms	As in the population	Happens more often

Complications

Atelectasis Atelectasis is a condition of the lung or part of it in which the alveoli contain little or no air and appear to be collapsed.
, respiratory failure.

Treatment abroad

Bronchitis: clinical manifestations, causes, mechanism of development

Bronchitis refers to diseases of the respiratory system, is a diffuse inflammation of the mucous membrane of the trachea and bronchi. The clinic 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, dry cough, worse at night. After a few days, the cough becomes wet, sputum begins to move away. Acute bronchitis usually lasts 2-4 weeks.

In accordance with the guidelines of the World Health Organization, the 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 a chronic process, the lesion spreads to the bronchial tree, the protective functions of the bronchi are disturbed, there is difficulty breathing, abundant 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 terms of 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);
• stay in adverse 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 rhino-, adenoviruses, influenza, parainfluenza, respiratory-interstitial.

Of the bacteria, the disease is more often caused by pneumococci, streptococci, Haemophilus influenzae and Pseudomonas aeruginosa, Moraxella catarrhalis, Klebsiella. Pseudomonas aeruginosa and Klebsiella are more often detected in immunocompromised patients 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, reduces the protective functions of the immune system. This creates favorable conditions for the attachment of a secondary infection.

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

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

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

Features of the pathogenesis of inflammation of the bronchi

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 noted in the walls of the bronchi. Infectious disease begins with the adhesion of the infecting pathogen to the epithelial cells of the mucous membrane of the airways of the lungs. At the same time, local protective mechanisms are violated, such as air filtration, moisturizing, cleansing, the activity of the phagocytic function of alveolar macrophages and neutrophils decreases.

The penetration of pathogens into the lung tissue is also facilitated by a disruption in the functioning of the immune system, an increase in the body's sensitivity to allergens or toxic substances formed during the vital activity of pathogens of the inflammatory process. With constant smoking or contact with harmful conditions, the purification of the lungs from small irritants slows down.

With further progression of the disease, obstruction of the tracheobronchial tree develops, redness, swelling of the mucosa is 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 a complete blockage of the lumen of the bronchioles, bronchi.

In severe cases, yellowish or greenish purulent sputum is formed. With hemorrhages from the blood vessels of the mucous membrane, the exudate acquires 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. With a favorable outcome, the consequences of the inflammatory process disappear in 2-3 weeks. In the case of panbronchitis, the restoration of deep layers of the mucosa lasts about 3-4 weeks. If pathological changes become irreversible, the acute phase of the disease acquires a chronic course.

The conditions for the transition of pathology into a chronic form are:

• decrease in the body's defenses to diseases, exposure to allergens, 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 failures in motor skills and disorders of the ciliated epithelium;
• the presence of a tracheostomy;
• socially unfavorable living conditions;
• violations of the functioning of the neurohumoral system of regulation;
• smoking, alcoholism.

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

Set of manifestations of bronchitis

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

The clinical picture of the acute form of bronchitis

The clinic of acute bronchitis in the initial stage is manifested by signs of acute respiratory infections, runny nose, general weakness, headache, slight fever, redness, sore throat). Simultaneously with these symptoms, a dry, painful cough occurs.

Patients complain of a sore feeling in the chest. After a few days, the cough acquires a wet character, becomes softer, mucous exudate begins to move away (catarrhal form of the disease). If infection with a bacterial agent joins the viral pathology, sputum acquires a mucopurulent character. Purulent sputum in acute bronchitis is extremely rare. With severe coughing fits, the exudate may be streaked with blood.

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

When tapping the chest, percussion sound and trembling of the voice usually do not change. Harsh breathing is heard. In the initial stage of the course of the disease, dry rales are noted, when sputum begins to depart, they become wet.

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, an increased level of sialic acids, alpha 2-globulins.

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

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

In acute bronchitis, recovery occurs in 10-14 days. In immunocompromised patients, the disease is protracted and can last more than a month. In children, there are more pronounced signs of bronchitis, 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 in different ways, 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 form.

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

• increased secretion and secretion of purulent sputum;
• whistling during inspiration;
• difficult breathing process, hard breathing when listening;
• strong painful cough;
• more often dry rales, wet with a large amount of viscous sputum;
• heat;
• sweating;
• muscle tremor;
• change in the frequency and duration of sleep;
• severe headaches at night;
• attention disorders;
• heart palpitations, increased blood pressure;
• convulsions.

The main sign of chronic bronchitis is a strong paroxysmal barking cough, especially in the morning, with copious secretion of thick sputum. After a few days with such a cough comes soreness of the chest.

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

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

With the progression of bronchitis, the patient begins to be disturbed by shortness of breath even without physical exertion. Outwardly, this is manifested by cyanosis of the skin. The chest takes the form of a barrel, the ribs rise to a horizontal position, the pits above the collarbones begin to bulge.

In a separate form, hemorrhagic bronchitis is isolated. The disease is non-obstructive in nature, the course is long-term, a distinctive feature is hemoptysis, due to an increase in the 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 the mucous secretion of the lungs with an admixture of blood. To do this, during bronchoscopy, the thickness of the walls of the blood vessels of the mucosa is determined.

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

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

Acute Bronchitis - Symptoms, Diagnosis and Treatment of Acute Bronchitis

Bronchitis Acute

Bronchitis Acute- diffuse acute inflammation of the tracheobronchial tree is one of the most common diseases of the respiratory system.

Most often, it occurs during periods of temperature fluctuations in nature - autumn and spring periods during an influenza epidemic, after hypothermia of the body;

Chilling, tobacco smoking, alcohol consumption, chronic focal infection in the nasopharyngeal region, impaired nasal breathing, chest deformity, malnutrition and stress predispose to the disease, reducing the defenses of the immune system.

Etiology and pathogenesis

Mechanism of acute bronchitis - The damaging agent enters the trachea and bronchi with inhaled air, hematogenous or lymphogenous route (uremic bronchitis).

The disease is caused by:

• Viruses(influenza viruses, parainfluenza, adenoviruses, respiratory syncytial, measles, whooping cough, etc.),
• bacteria(staphylococci, streptococci, pneumococci, etc.);
• Physical and chemical factors(dry, cold, hot air, nitrogen oxides, etc.). Acute toxic-chemical bronchitis occurs when inhaling air containing chromium, nickel, vanadium, tungsten, cobalt, fluorine, diphosgene, formaldehyde, arsenic anhydride, sulfur dioxide, benzene, acetone, gasoline vapors, acids, dimethyl sulfate, Thomas slag,. Inhalation of air with a high content of dust, especially organic, causes the development of acute dusty bronchitis.

Most often, before the development of acute bronchitis, a person suffers from other inflammatory diseases of the upper respiratory tract: acute respiratory infections, tracheitis, wounds, tonsillitis, sinusitis - untreated or severe.

pathological anatomy

In mild cases changes are limited to the mucous membrane, in severe cases they capture all layers of the bronchial wall. The mucous membrane appears edematous, hyperemic with the presence of mucous, mucopurulent or purulent exudate on the surface.

In severe forms of the disease often there are hemorrhages in the mucous membrane, the exudate can become hemorrhagic. In some cases, there is a complete obturation with a secret of the lumen of the small bronchi and bronchioles. The inflammation may be widespread or limited.

Clinical picture (Symptoms of acute bronchitis)

Bronchitis of infectious etiology often begins against the background of acute rhinitis, laryngitis.

For mild disease there are soreness behind the sternum, dry, less often wet cough, feeling of weakness, weakness. There are no physical signs or severe breathing, dry rales are determined above the lungs. Body temperature is subfebrile or normal. The composition of peripheral blood does not change. This course is observed more often with damage to the trachea and large bronchi.

For moderate flow general malaise, weakness are significantly expressed, a strong dry cough with shortness of breath and shortness of breath, pain in the lower parts of the chest and abdominal wall, associated with muscle strain when coughing, are characteristic. The cough gradually becomes wet, the sputum acquires a mucopurulent or purulent character. Harsh breathing, dry and moist small bubbling rales are heard above the surface of the lungs. The body temperature remains subfebrile for several days. There are no pronounced changes in the composition of peripheral blood.

Severe illness observed, as a rule, with a predominant lesion of the bronchioles (the spread of the inflammatory process to the smallest branching of the ventilation tracts bordering the respiratory sections of the lungs) (see Bronchiolitis). Acute symptoms of the disease subside by the 4th day and, with a favorable outcome, completely disappear by the 7th day. Acute bronchitis with impaired bronchial patency tends to protracted course and transition to chronic bronchitis.

Acute bronchitis of toxic-chemical etiology is difficult. The disease begins with a painful cough with the release of mucous or bloody sputum, bronchospasm quickly joins (against the background of an extended exhalation, dry whistling rales are heard) and shortness of breath progresses (up to suffocation), respiratory failure and hypoxemia increase.

Radiological symptoms of acute pulmonary emphysema can be determined. Symptomatic erythrocytosis breaks down, hematocrit indicators increase. Acute dust bronchitis can also take a severe course. In addition to coughing (at first dry and then wet), marked shortness of breath, cyanosis of the mucous membranes are noted. A boxed shade of percussion sound, hard breathing, dry wheezing are determined. Slight erythrocytosis is possible. X-ray revealed increased transparency of the lung fields and a moderate expansion of the roots of the lungs.

With percussion above the lungs, a clear pulmonary sound is determined, often with a box shade.
During auscultation in the first days of the disease, vesicular breathing with an extended expiration is determined, dry - whistling or buzzing - wheezing. Sometimes, after coughing, the number of wheezing decreases, and with calm breathing, wheezing is absent, but is heard only with forced breathing. After 3-4 days, wet rales of various sizes (large, medium and fine bubbling) may join.

Changes from other organs often insignificant. There may be tachycardia, vegetative symptoms (excessive sweating), loss of appetite, sleep disturbance.
On x-ray examination, changes are often absent. In some cases, there is an expansion of the shadow of the roots of the lungs.
The study of the function of external respiration often reveals a decrease in the vital capacity of the lungs (by 15–20% of the due). Blood oxygen saturation initially remains normal - due to an increase in breathing volume (due to an increase in the depth and frequency of breathing). When small bronchi are involved in the pathological process, violations of bronchial conduction are revealed: a decrease in pneumotachymetry (up to 80% of the due) and forced vital capacity of the lungs.
Blood tests most often detect neutrophilic leukocytosis (up to 10–12 G/l), accelerated ESR.

Bronchitis

There is hardly a person on earth who has never encountered bronchitis. Excruciating cough - the main symptom of bronchitis - the result of an acute or chronic inflammatory process in the bronchial mucosa.

Causes of bronchitis

When a person is healthy, the air, passing through the upper respiratory tract, is cleared of dust and suspended particles, warmed, moistened. Therefore, a stream of already purified disinfected air enters the bronchi. However, in some cases, for example, when the upper respiratory tract is affected by a viral infection, the air in contact with the bronchial mucosa contains microbes or irritants. In such cases, the mucous membrane reacts to the introduction of an infectious agent or irritant by secreting a large amount of mucus. Excess mucus makes it difficult for air to move through the respiratory tract and causes coughing. This is how acute bronchitis develops.

When a pathogenic factor regularly affects the mucous membrane of the bronchial tree, inflammation develops and proceeds slowly: the bronchial wall thickens and becomes less elastic, the patency of the bronchial tree decreases, deformation and narrowing of the bronchi develops. This happens with systematic irritation of the bronchi with irritating or toxic substances, with chronic infectious processes, as well as with reduced immunity. In this case, we speak of chronic bronchitis.

Clinical picture of the disease

The symptomatology of bronchitis depends on the severity and form of the pathological process. The onset of the disease is usually preceded by a runny nose, hoarseness, muscle pain, headache, weakness.

Acute bronchitis begins with a rise in temperature, general weakness and malaise. The main symptom of bronchitis is coughing. At the beginning of the disease, it is dry, paroxysmal, at the height of the disease it becomes wet, with the release of copious sputum. In some cases, a broncho-obstructive syndrome is added, associated with a reflex spasm of the small bronchi, manifested by shortness of breath, difficulty breathing.

The disease proceeds for 7-10 days.

In chronic bronchitis, cough may be present constantly or appear sporadically. As a rule, it is a wet cough with the release of a large amount of purulent sputum, which is worse in the morning.

Diagnosis, prevention and treatment of bronchitis

Diagnosis of bronchitis is based on the analysis of complaints and symptoms, as well as on the auscultatory picture: hard breathing is heard with an extended breath, dry rales, which, in the stage of resolution of the disease, are replaced by moist rales, indicating the removal of sputum. Additionally, more often to exclude complications, they resort to x-ray diagnostics. With bronchitis, the radiograph shows some expansion of the roots of the lungs and an increase in the pulmonary pattern.

In the treatment of bronchitis, several groups of drugs are used. Mucolytics and mucokinetics (expectorants) help thin the mucus and remove it from the bronchi. Bronchodilators in combination with expectorants are used when symptoms of bronchial obstruction appear. Antibiotics are designed to cope with the infectious process in the bronchial tree. Folk remedies are widely used: decoctions of medicinal plants and herbal preparations that have an expectorant effect. With bronchitis, it is advisable to prescribe immunostimulants and vitamins, since the disease most often occurs against the background of a decrease in general immunity.

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Chronic bronchitis (CB)- a chronic progressive disease, which is based on a degenerative-inflammatory lesion of the mucous membrane of the tracheobronchial tree, usually developing as a result of prolonged irritation of the airways by harmful agents with a restructuring of the secretory apparatus and sclerotic changes in the bronchial wall, clinically manifested by cough, sputum and (or) shortness of breath.

According to the WHO criteria, one can speak of CB only when the main symptom of the disease- cough can be traced in the patient for at least two years (during each year, episodes of coughing must be recorded by the patient or doctor for at least three months). In other cases, it is necessary to raise the question of whether the patient has either recurrent acute or prolonged bronchitis.

In addition, the diagnosis of chronic bronchitis can be made in a patient only after the exclusion of the so-called "secondary bronchitis" (B.E. Votchal) associated with other organs and systems of the body or another type of inflammation of the tracheobronchial tree (bronchial asthma, tuberculosis, tumor, uremia, circulatory failure, cystic fibrosis, etc.).

Etiology and pathogenesis

The basis of chronic bronchitis in all cases is a degenerative-inflammatory lesion of the mucosa of the tracheobronchial tree, manifested in chronic inflammation of the mucosa with its subsequent irreversible restructuring with the replacement of the ciliated epithelium with a multilayer one, hypertrophy, and subsequently atrophy of the bronchial glands, destruction of the elastic collagen base of the lungs and the formation fibrosis and secondary obstructive emphysema.

At the same time, the main factors leading to the formation of chronic bronchitis are long-term exposure to the airways of various pollutants (tobacco smoke from active and passive smoking, carbon monoxide, various industrial dusts, etc.), leading to damage to the mucous membrane of the tracheobronchial tree. Quite rarely, the development of chronic bronchitis is associated with recurrent viral and bacterial infections (whooping cough, parainfluenza, etc.), accompanied by deep necrotic, and subsequently cicatricial-atrophic lesions of the mucous membrane of the tracheobronchial tree.

All these factors trigger a single pathomorphological process: first, irritation of the mucous membrane occurs with hyperproduction of mucus, followed by the death of the ciliated epithelium, replacing it with a multilayer one, and hypertrophy of the mucous glands develops. All this leads to disturbances in the mucociliary clearance of the tracheobronchial tree and there is a delay in the lumen of the airways of mucus and foreign substances, which, along with advancing disturbances in the system of local protection of the lungs, contributes to the addition of purulent inflammation, which further exacerbates deep irreversible damage to the mucous and submucosal layers of the bronchi and bronchioles up to the development of bronchiectasis.

At the same time, the developing inflammatory edema of the mucosa of the distal bronchi and bronchioles, transient bronchospasm due to activation of the parasympathetic nervous system of the bronchial tree, as well as blockage of the lumen of small bronchi with mucus lead to the development of bronchial obstruction, which determines gas exchange disorders and disorders of alveolar ventilation in the form of alveolar hypoxemia and hypercapnia . There is a gradual development of emphysema due to overstretching of the alveoli, which is also facilitated by the destruction of the elastic collagen base of their walls due to a secondary deficiency of the alpha-1 antitrypsin enzyme as a result of exposure to tobacco smoke.

The resulting emphysema, in turn, triggers a vicious circle - there is a progressive mechanical compression of the terminal bronchioles by the swollen alveoli and an increase in alveolar hypoventilation with alveolar and, subsequently, arterial hypoxemia.

In order to overcome the adverse effect on the body of uneven ventilation of the alveoli, a reflex spasm of the arterioles of the pulmonary circulation occurs, which, as the disease progresses and develops hypoxemia, takes on a generalized character, determining the development of persistent arterial hypertension in the pulmonary circulation and the development of regular hypertrophy of the right ventricle, the so-called cor pulmonale . The terminal phase of the development of the disease is the onset of cor pulmonale decompensation.

Clinical picture

The clinical picture of chronic bronchitis is diverse and depends on the form of the disease, the stage and the presence of certain complications. Traditionally consider several clinical forms of chronic bronchitis.

Chronic simple (catarrhal, smoker's cough) bronchitis

With this form of the disease, the main, and often the only symptom of the disease is a cough, usually productive with the separation in the morning and during the day of small amounts of mucous sputum. Most often, a cough does not bother a significant patient, often people consider it characteristic of their body and consider it as a natural reaction to smoking. To establish this stage (form) of CB, as practice shows, the patient succeeds only with targeted, often screening, examination and questioning. At the same time, it is not possible to identify any physical symptoms during the physical and instrumental examination of the patient (only some hardness of breathing is detected only sometimes).

Endoscopic examination of the tracheobronchial tree can reveal signs of local, and less commonly diffuse catarrhal endobronchitis with hyperemia and edematous mucosa.

Chronic purulent bronchitis (CGB)

A characteristic feature of this form of chronic bronchitis is the addition (permanently or during periods of exacerbation) of purulent inflammation, most often associated with such etiological agents as Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae. A distinctive symptom is the release of purulent sputum when coughing. Often, the development of chronic hepatitis B is promoted by secondary defects of the immune system that are formed in the body in the form of hypogammaglobulinemia, a deficiency in the production of immunoglobulins of certain classes, primarily secretory immunoglobulin A.

With this form of the disease, the phases of exacerbation and remission are quite clearly traced, an exacerbation often occurs with hypothermia and with the addition of a respiratory viral infection and manifests itself in the form of subfebrile condition, increasing weakness and weakness, and a noticeable increase in the amount of sputum discharge. Characteristic are the endoscopic signs of the disease - the detection during bronchoscopy of the pattern of local or diffuse catarrhal-purulent (purulent) endobronchitis. With prolonged presence of purulent inflammation in the tracheobronchial tree, the course of CHB is complicated by the development of bronchiectasis.

Chronic obstructive bronchitis

Chronic obstructive bronchitis (COB)- a special clinical form of chronic bronchitis, characterized by progressive airway obstruction, consisting of reversible (swelling of the mucous membrane, hypersecretion of mucus with obstruction of the lumen of the bronchioles and, to a lesser extent, spasm of the smooth muscles of the bronchi) and irreversible (obstructive emphysema with compression of small airways, inflammatory obliteration bronchioles) components.

A characteristic syndrome of this form of chronic bronchitis is expiratory dyspnea that grows over time, varying over a very wide range - from feeling short of breath during significant physical exertion to severe respiratory failure, determined even with minor physical exercises and at rest. At the same time, the patient is concerned about coughing with sputum, which in some cases can become purulent (chronic purulent-obstructive bronchitis). As the disease progresses, the course is complicated by the addition of secondary obstructive emphysema of the lungs and cor pulmonale, which further aggravates respiratory failure and the severity of the patient's condition.

The clinical picture of the advanced complicated stage of COB, with which doctors most often meet, is quite well known - the doctor sees a patient in front of him who complains of shortness of breath, aggravated by physical exertion and cough with sputum. At the same time, the patient notes that at rest he feels quite well, and shortness of breath begins to bother him only with a certain physical exertion.

In contrast to patients with bronchial asthma, asthma attacks at rest or during sleep, as a rule, are not observed; patients with COB tolerate inhalation of strong odors and cold air quite calmly. During examination and physical examination, attention is drawn to an increase in the volume of the chest and limitation of its excursion during breathing, enlarged intercostal spaces, bulging of the supraclavicular fossae, and the presence of epigastric pulsation.

With percussion, a box sound is determined, often with difficulty, due to the severity of emphysema, it is possible to determine the boundaries of cardiac dullness. Breathing is usually significantly weakened (sometimes doctors mistakenly diagnose "silent lung" or even pneumothorax in these patients), against the background of it, only single low-tone whistling rales can be heard. Often in advanced cases, an enlarged liver and the presence of pastosity and swelling of the legs can be detected.

X-ray examination of the chest organs reveals the classic signs of emphysema and pneumosclerosis, and the study functions of the external respiration apparatus (EPD)- the presence of airway obstruction in the form of a decrease forced expiratory volume in 1 second (FEV1), the ratio of FEV1 to vital capacity (VC) or to forced vital capacity (FVC), a decrease in the maximum expiratory flow rate at the level of 25%, 50% or 75% FVC. At the same time, there may be a decrease in VC and an increase in residual lung capacity.

Also characteristic for such a course of COB is the presence of hypercapnia and hypoxemia of arterial blood. Early verification of the development of cor pulmonale and emerging hypertension in the pulmonary artery system is important for determining the prognosis. In this regard, it is mandatory to determine the pressure in the pulmonary artery by recording jugular phlebography or plethysmography, as well as an ultrasound examination of the right heart (wall thickness of the right ventricle).

Patients with the initial stages of chronic obstructive bronchitis, when the obstructive component is transient, reversible and subjectively does not bother the patient, turn to the doctor much less often. In these cases, in a long-term coughing patient during a physical examination, only during periods of exacerbation of the disease, it is possible to determine the presence of single wheezing over the lungs, and in the study of respiratory function, it is possible to identify obstructive respiratory disorders and, on the basis of this, establish the presence of the initial stage of COB in the patient. In these cases, it is of paramount importance to conduct a test with bronchodilators to establish the reversibility of the existing broncho-obstructive component and the feasibility of long-term bronchodilator therapy.

In this regard, all patients after the initial determination of the state of bronchial patency are inhaled with a bronchodilator. During the period of screening studies in an outpatient setting, preference should be given to berodual (2 breaths from a metered-dose aerosol canister), and in a hospital, inhalation with atrovent or traventol is performed (2 breaths). After 10-15 minutes, the state of bronchial patency is again recorded. With an improvement in bronchial patency by 15 percent or more from the initial level, a conclusion is made about a positive test. After 12 hours or the next day, the test is repeated using a sympathomimetic (berotek, ventolin, etc.).

Classification

According to the WHO International Classification of Diseases, Injuries and Causes of Death 10 (1995) revision of HB to:

• J.41 simple and mucopurulent chronic bronchitis;
• J.41. 0 simple chronic bronchitis;
• J.41. 1 mucopurulent chronic bronchitis;
• J.44 other chronic obstructive pulmonary diseases, including: chronic asthmatic (obstructive) bronchitis, emphysematous chronic bronchitis, obstructive CP, CP with difficulty breathing.

It should be noted that in ICD 10 chronic asthmatic bronchitis is classified under J.46.9 - bronchial asthma. That is why it is not advisable to use the term "asthmatic bronchitis", as this prevents a clear distinction between two different nosological forms - bronchial asthma and COB.

Survey program

The plan of laboratory and instrumental examination of patients with chronic bronchitis includes:

A) In outpatient clinics and clinics:

• general blood analysis;
• general sputum analysis, including the determination of the content of eosinophils;
• study of the function of external respiration - pneumotachometry and spirometry, recording the FVC curve, as well as conducting a pharmacological test with berodual;
• radiography of the chest and paranasal sinuses; - ECG;
• examination by an ENT specialist.

b) In the conditions of the therapeutic (pulmonological) department of the hospital (additionally in the above):

• conducting a pharmacological profile in the study of respiratory function with atrovent and berotek (ventolin);
• determination of blood protein fractions, and in COB - alpha-antitrypsin (if possible);
• study of the immunological status (with chronic purulent bronchitis);
• conducting bronchoscopy, and in chronic purulent bronchitis - bronchography;
• determination of the partial pressure of oxygen and carbon dioxide in capillary blood (with chronic obstructive bronchitis);
• study of pressure in the pulmonary artery (jugular phlebography, plethysmography, ECHO-cardiography) in COB.

Diagnosis and differential diagnosis

The diagnosis of chronic bronchitis is based on the establishment of a patient with a prolonged (for at least 2 years) cough with or without sputum, the presence of exposure to the tracheobronchial tree of risk factors for the development of chronic bronchitis (long-term smoking, exposure to harmful working conditions, severe viral infections, etc. .).

If it is assumed that a patient has chronic bronchitis, it is necessary to exclude other diseases and pathological conditions (cancer or adenoma of the bronchus, tuberculosis, chronic sinusitis, bronchial asthma, foreign body of the bronchi, etc.) using the entire volume of clinical, radiological, endoscopic and other methods, which may be manifested by prolonged cough and shortness of breath. In other words, the diagnosis of chronic bronchitis can only be made by exclusion, after excluding the possibility that a patient with a long-term cough has "secondary bronchitis".

Of particular importance is the diagnosis of COB, since this form of chronic bronchitis is the most severe and, with progression, leads to the development of severe complications (emphysema, cor pulmonale), quickly disabling patients and leading to death. In this regard, two areas of diagnostics are of paramount importance. First, the diagnosis of chronic bronchitis. Secondly, a targeted study of the function of the external respiration apparatus in all patients with CB for the purpose of early (preclinical) detection of the presence of bronchial obstruction (FVC1 study, determination of the maximum expiratory flow rate at the level of 75-25% of the forced vital capacity of the lungs).

When obstructive respiratory disorders are detected in order to establish the reversibility of broncho-obstructive syndrome, and subsequently the choice of bronchodilator therapy, pharmacological tests with bronchodilators (sympathomimetic-ventolin or berotek and anticholinergic blocker-atropine or atrovent) are indicated. The test is considered positive (reversible bronchial obstruction) in cases where, after inhalation of a bronchodilator, there is an increase in the indicator of bronchial patency by 15% or more compared to the baseline.

Doctors face the greatest difficulties in the differential diagnosis of COB and bronchial asthma (BA), especially since it is not uncommon for cases of asthma to develop in elderly patients who have been smoking for a long time. In addition, it is necessary to take into account the fact that in a number of patients with BA proceeds without outlined attacks - they have a clinic of prolonged bronchial obstruction, periodically increasing and decreasing spontaneously or under the influence of treatment. In these diagnostically difficult cases, the detection of eosinophils in the sputum is important for establishing the diagnosis of AD (sputum must be re-examined and must be stained according to Ziehl-Nielson or Romanovsky-Giemsa before microscopy!).

The study of biopsy specimens of the mucous membrane of the tracheobronchial tree (BA is characterized by thickening of the basement membrane and infiltration of the submucosal layer by eosinophils), as well as ex juvantibus diagnosis - a significant improvement in the patient's condition against the background of a short course of active anti-inflammatory therapy with inhaled glucocorticoid drugs (ingacort, ventolin, etc.), as well as the detection of an increased content of total immunoglobulin E in the blood. For BA, in contrast to chronic obstructive bronchitis, a pronounced variability in peak fluometry is also characteristic.

Treatment of chronic bronchitis

The main direction of treatment and prevention of progression of CB is the elimination of the impact on the airways of harmful impurities in the inhaled air (smoking ban, rational employment, etc.). The very same treatment of chronic bronchitis should be differentiated depending on the form of the disease and the presence of certain complications.

With simple (catarrhal) chronic bronchitis, the main, and in most cases the only method of treatment is the use of expectorant drugs aimed at normalizing mucociliary clearance and preventing the addition of purulent inflammation.

Traditionally, expectorant drugs are divided depending on the mechanism of their action:

• reflex action - thermopsis and epicuan, marshmallow, wild rosemary, which directly irritate the nerve endings located in the gastric mucosa, and thereby reflexively cause an increased secretion of mucus by the bronchial glands;
• resorptive action - potassium iodide, bromhexine (bisolvon), thyme oil, etc., which, being absorbed into the blood, reach the bronchial glands and, through direct action on them, cause an increased secretion of mucus;
• mucolytics and mucoregulators - ambroxol (lazolvan) acetylcestein (fluimucil, mucomist), carbocysteine ​​(bronkatar, mucodin, mistabron), which destroy mucopolysaccharides and disrupt the synthesis of sputum sialumucins.

As a rule, in chronic catarrhal bronchitis, long-term (many months) therapy is carried out with expectorant preparations of predominantly plant origin - decoctions of wild rosemary herbs, breast preparations, bronchicum, etc., in combination with methods of breathing exercises.

In chronic catarrhal-purulent bronchitis, along with the use of expectorant drugs in case of exacerbations of the disease, and this is said in cases of a change in the nature of sputum to purulent, the appearance of low-grade fever and malaise, 1-2 week courses of antibiotic therapy are carried out.

At the same time, preference (until the results of sputum culture and antibiogram of the isolated pathogen) is given to antibacterial drugs, to which influenza bacillus, pneumococci and moraxella are highly sensitive - macrolides of new generations (sumamed, rovamycin), amoxicillin, amoxicillin + clavulanic acid (augmentin, clavocillin) , clindamycin in combination with mucolytic drugs. Upon receipt of the results of bacteriological examination, depending on the clinical effect and the isolated microflora, adjustments are made to the treatment (cephalosporins, fluoroquinolones, etc.).

In cases of severe purulent endobronchitis during the period of exacerbation of chronic purulent bronchitis, it is advisable to conduct repeated sanitation bronchofibroscopy.

Treatment of chronic obstructive bronchitis is a difficult complex task. It has several strategic directions.

Leveling (reduction) of manifestations of bronchial obstruction, contributing to the development of irreversible changes due to the formation of obstructive em[physema and reflex hypertension in the pulmonary artery and pulmonary heart in response to alveolar hypoxemia. This direction of treatment is of particular importance in the initial stages of COB, when the existing secondary changes are still functional in nature and can be corrected with medication.

In this regard, it is necessary to take into account that various pathogenetic factors are involved in the formation of broncho-obstructive syndrome in patients with COB, many of which can be actively influenced. So, spasm of the smooth muscles of the bronchi and swelling of the mucous membrane, as well as blockage of the lumen of the bronchi and bronchioles with mucus, have a certain value in the genesis of broncho-obstructive syndrome. That is why, along with the use of mucolytics, an important place in the treatment of COB belongs to various bronchodilators. The purpose of these drugs should be differentiated depending on the results of the study of respiratory function and testing with bronchodilators.

Traditionally, in the treatment of chronic obstructive bronchitis, inhaled selective sympathomimetics (salbutamol, berotek) and anticholinergics (Atrovent) are used. Usually they are prescribed in medium therapeutic doses of 1 inhalation 3-4 times a day. However, practice shows that, unlike patients with bronchial asthma in COB, sympathomimetics are much less effective, often inferior to drugs with anticholinergic action. That is why anticholinergics are of primary importance in the treatment of COB patients, especially during long-term therapy, including in patients with developed pulmonary emphysema, and they are rightly considered as the drugs of first choice in the treatment of COB.

Atrovent (ipratropium bromide), which is a competitive antagonist of acetylcholine, is commonly used. It blocks the muscarinic receptors of the smooth muscles of the trachebronchial tree, reduces the secretion of the bronchial glands and swelling of the mucous membrane, and also prevents acetylcholine-mediated stimulation of the sensory fibers of the vagus nerve when irritated by various factors. Usually the drug is used for a long time (months) 2 inhalations 3-4 times a day.

At the same time, it is traditional and justified to use bronchodilator drugs in the treatment of patients with chronic obstructive bronchitis, which are a combination of anticholinergic and sympathomimetic - solutan, theofedrine. A good alternative to this is the use of the drug berodual - a combination of ipratropium bromide and fenoterol hydrobromide, both in the form of inhalations (2 inhalations 3-4 times a day) using a metered dose inhaler and using a portable nebulizer. Methylxanthines, especially their prolonged retard forms, also have a certain value in the treatment of patients with COB.

Due to the fact that the resulting sputum can also aggravate the phenomena of bronchial obstruction, the use of mucolytic drugs is mandatory in the treatment of COB.

The most important direction in the treatment of COB, especially when its course was complicated by the development of emphysema and cor pulmonale, is long-term low-flow oxygen therapy. The main objective of this treatment is to slow down the development and leveling of the existing alveolar hypoxemia, which leads to an improvement in the gas composition of the blood (the goal is to maintain the partial pressure of oxygen at the level of 55-60 mm Hg), a decrease in pressure in the pulmonary artery and, ultimately, to improve the clinical condition and prognosis of the patient. Low-flow oxygen therapy is prescribed in cases of a constant decrease in the partial pressure of oxygen below 55 mm Hg. Art. (saturation of hemoglobin with oxygen 55%).

When oxygen therapy is given, it is usually sufficient to use a low flow (2-5 L/min) of 100% humidified oxygen through nasal cannulas for at least 18 hours a day, including during sleep (when oxygen therapy is given during sleep, it reduces the risk of arrhythmias).

The use of glucocorticoids is justified only in cases of a combination of chronic obstructive bronchitis with bronchial asthma, when it is proved, including laboratory (detection of eosinophils in sputum), the participation of an allergic mechanism in the formation of a bronchial obstructive component.

During the exacerbation of COB, in the presence of clinical signs of intoxication and the appearance of purulent sputum, a course of antibiotic therapy is mandatory.

Quite controversial and often contradictory is the use of various cardiovascular drugs in COPD patients with signs of circulatory decompensation. So, there is no doubt that the careful use of cardiac glycosides is justified in cases of signs of circulatory failure in the pulmonary circulation, in other cases, the use of these drugs is not always justified. The widespread use of drugs that have a direct vasodilating effect (nitrates, calcium antagonists, etc.) is not advisable, since due to vasodilation in the pulmonary artery system, these drugs can reduce blood flow in sufficiently ventilated areas with its increase in areas of limited ventilation, which leads to to a decrease in partial pressure in the blood and exacerbates tissue hypoxia.

This unfavorable effect of nitrates is to a certain extent offset by a distinct bronchodilatory effect of calcium antagonists (nefidipine), and therefore these drugs are quite successfully used in the treatment of severe cases of COB. Promising are the first experience of using angiotensin-converting enzyme inhibitors for the treatment of chronic obstructive bronchitis.

An important place in the treatment of COB belongs to the methods of therapeutic breathing exercises aimed at improving the drainage function of the bronchial tree and training the respiratory muscles. At the same time, physiotherapeutic methods of treatment and therapeutic massage of the respiratory muscles are of particular importance.

V.G. Alekseev, V.N. Yakovlev

Acute bronchitis is an acute inflammatory process that develops in the bronchial mucosa. The disease is characterized by an increase in bronchial secretion, which leads to sputum production and a prolonged cough. The defeat of the small bronchi provokes shortness of breath. The causative agents of pathology are viruses or bacteria, in more rare cases - fungi. It is also possible the manifestation of bronchitis due to exposure to chemical factors.

causative agents of the disease

In most cases, acute bronchitis develops due to the penetration of influenza, parainfluenza, AVRI, rubella, and measles viruses into the bronchi. Much less often, bacteria act as pathogens: staphylococcus aureus, pneumococcus, chlamydia, mycoplasmas, and various representatives of the typhoid-paratyphoid group.

The main ways of their penetration into the body:

• air;
• hematogenous;
• lymphogenous.

Causes of acute bronchitis

The causes of acute bronchitis are factors that, to a greater or lesser extent, contribute to the reduction of the general and local resistance of the organism. The most significant of them:

• hypothermia;
• unfavorable working conditions (in particular, increased dampness);
• exposure to cigarette smoke;
• alcohol abuse;
• the presence of a focus of infection in the nasopharynx;
• violation of nasal breathing;
• heart failure leading to congestive changes in the lungs;
• violation of the small circle of blood circulation;
• national nutrition
• decreased immunity as a result of a serious illness.

Of the etiological causes that provoke acute bronchitis, it should be distinguished:

• exposure to physical factors (very cold, hot or dry air);
• chemical factors (contact with various chemical compounds: alkalis, acids, nitrogen oxides, chlorine, ammonia, sulfur dioxide, etc.);
• infectious (viruses, bacteria, other pathogens);
• allergic (plant pollen, organic dust, etc.).

The cause of acute bronchitis can also be a combination of infection with the action of irritants of a physicochemical nature. The allergic form of bronchitis develops in the presence of a genetic predisposition to an allergic reaction.

Clinical picture

Symptoms of acute bronchitis can vary to a certain extent depending on the cause of the disease, the degree of its spread, the severity of pathological changes and the inflammatory process, the degree of bronchial damage.

The disease begins acutely, with symptoms of damage to the lower and upper respiratory tract, general intoxication. Acute bronchitis of infectious etiology at the stage of occurrence is characterized by signs of SARS:

• runny nose;
• nasal congestion;
• perspiration and pain in the throat;
• hoarseness of voice.

With the development of intoxication,:

• chills;
• fever (up to subfebrile levels) - absent in case of a mild course of the disease;
• fatigue;
• weakness;
• sweating;
• headache;
• muscle pain with localization in the limbs and back.

If acute bronchitis is caused by pathogens of rubella, measles, whooping cough, its manifestations are similar to the symptoms of the underlying disease.

A characteristic symptom of the pathology is a painful dry cough, which manifests itself at the earliest stage and persists throughout the illness. Cough in acute bronchitis occurs paroxysmal, characterized by rudeness, sonority, may have a barking character. Attacks provoke increased burning and soreness in the retrosternal region.

Overexertion of the pectoral muscles and spasmodic contraction of the diaphragm lead to pain in the lower segment of the chest, which can also spread to the abdominal wall.

When coughing, sputum is released: at first it is scanty, viscous, gradually becomes more fluid and easier to move away. Sometimes it is mucopurulent.

In the case of a severe and prolonged course of acute bronchitis, the inflammatory process can spread to the bronchioles, which leads to a significant narrowing or complete blockage of the bronchiolar lumen with the subsequent development of an obstructive syndrome, impaired blood circulation and gas exchange. In this case, a sudden deterioration in the patient's condition occurs with the manifestation of the following symptoms:

• pallor of the skin;
• fever;
• severe shortness of breath;
• a state of anxiety and arousal with a transition to lethargy and drowsiness;
• signs of cardiovascular insufficiency (tachycardia, low blood pressure).

With an allergic component there is an association with the effect of the allergen. The main symptoms of acute allergic bronchitis are:

• paroxysmal cough accompanying obstructive syndrome;
• light glassy sputum.

If the disease develops as a result of inhalation of toxic fumes, there are:

• painful cough;
• feeling of tightness in the chest;
• suffocation;
• laryngospasm.

Diagnosis of acute bronchitis

Diagnosis of acute bronchitis is carried out on the basis of the clinical picture, data from laboratory and instrumental studies.

In the process of examining a patient, it must be taken into account that the disease can become a manifestation of various pathologies of an infectious nature: whooping cough, measles, etc.

Auscultation (listening to the lungs and bronchi) reveals:

• hard breathing of obstructive type;
• scattered dry rales;
• finely bubbling moist rales - are heard with the accumulation of liquid secretion in the bronchi and disappear after coughing.

For the diagnosis of acute bronchitis is carried out:

• blood test (general, biochemical, immunological);
• general urine analysis;
• sputum culture for microflora;
• x-ray examination of the lungs;
• bronchoscopy;
• spirography, peak flowmetry (to study the functions of external respiration).
• ECHOCG;

Examination of external respiration shows an obstructive lung ventilation disorder.

A blood test reveals:

• acceleration of ESR;
• neutrophilic leukocytosis;
• with allergic bronchitis - an increased number of eosinophils.

X-ray with viral acute bronchitis shows a fuzzy pattern and an average expansion of the roots of the lungs.

Differential diagnosis is also carried out with miliary pulmonary tuberculosis and bronchopneumonia.

Treatment of acute bronchitis

In acute bronchitis, treatment in most cases is carried out on an outpatient basis. In case of severe course, hospitalization is required.

If acute bronchitis is accompanied by fever and fever, prescribe:

• Bed rest, diet and drinking plenty of water.
• Smoking must be abandoned.
• The room should be wet cleaned daily, maintaining a high level of humidity.
• To relieve the pain syndrome, compresses, banks, mustard plasters are used on the sternum area, between the shoulder blades.
• Mustard foot baths give a good effect.

Medication use

In acute bronchitis against the background of SARS, drug treatment is based on the use of the following agents:

• antiviral drugs: interferon, rimantadine.
• painkillers;
• antipyretic;
• non-steroidal anti-inflammatory drugs.

In the presence of a secondary bacterial infection, a long course of the disease, the severity of the inflammatory process, antibiotics, sulafanilamides are prescribed.

In the treatment of acute bronchitis with a painful dry cough, apply:

• to suppress the cough reflex - codeine, libexin, dionin;
• to thin sputum with an increase in its amount - expectorants, mucolytics: lazolvan, bromhexine, alkaline inhalations, as well as infusions of medicinal plants: marshmallow, thermopsis.

Bronchospasm with obstruction is removed with the help of:

• adrenollytics (ephedrine);
• antispasmodics (papaverine, aminophylline);
• steroid hormones (prednisolone) - they are treated according to indications;

If necessary, an intensive course of therapy for respiratory and acute heart failure is indicated.

In acute allergic bronchitis, treatment includes the use of antihistamines: suprastin, tavegil, diazolin, ketotifen, sodium cromglycate.

With a severe clinical picture, the treatment of acute bronchitis is associated with the use of glucocorticoids.

Physiotherapy and other methods

Physiotherapy treatments for acute bronchitis include:

• ultraviolet irradiation;
• diathermy of the chest area;
• inductothermy;

The uncomplicated form of the disease generally ends with clinical recovery in 14-20 days. With regard to the restoration of functional indicators (bronchial patency and respiratory functions), this requires one month.

With a long course of acute bronchitis, clinical recovery takes a little longer - from 30 to 50 days.