Acute bronchitis. Definition. Causes. Clinic, diagnostics. Treatment. Bronchitis: clinical manifestations, causes, mechanism of development Clinic and principles of treatment of acute bronchitis

Cough is the main symptom of any bronchitis. Complaints of a cough - dry or wet, paroxysmal or isolated coughs - always suggest bronchitis. But in order to figure out whether it is bronchitis and what type of bronchitis, you need to know the clinical features of this disease.

Clinic and symptoms of acute bronchitis

Most often, the onset of the disease is preceded by signs of ARVI: weakness and malaise, pain in muscles and joints, runny nose, sore throat, rise in body temperature.

Bronchitis itself begins with a rise in body temperature and the appearance of a cough. Clinical signs can suggest what causes acute bronchitis. Thus, bronchitis of influenza and parainfluenza etiology is characterized by a sharp onset and persistence of fever for 2-3 days. If the temperature does not drop for about 7 days, this may indicate that the cause of bronchitis is adenoviruses or mycoplasmas.

A cough may appear before the development of bronchitis, as a manifestation of damage to the larynx and trachea. This is either a rough, barking cough (laryngitis) or a dry, painful cough, accompanied by painful sensations and a burning sensation in the chest (tracheitis). Quite often, the pathological process covers all the respiratory tract, laryngotracheobronchitis occurs, in which there is no point in isolating the symptoms of bronchitis. Complex treatment is required.

At the beginning of the disease, the cough is paroxysmal in nature. This is an unproductive, dry, persistent cough. Sometimes coughing attacks are so intense that they lead to headaches and chest pain. When auscultating the lungs during this period, hard breathing and scattered dry rales are heard.

Gradually, the cough becomes moist, mucopurulent sputum begins to leave, and moist fine bubbling rales are heard in the lungs. Laboratory tests may not reveal any abnormalities. But the x-ray will show an increase in the pulmonary pattern, expansion of the roots of the lungs.

In cases of severe disease, the cough is accompanied by shortness of breath, difficulty breathing, and abundant fine wheezing is heard in the lungs against the background of weakened breathing. With this clinical picture, laboratory tests show signs of an acute inflammatory reaction: leukocytosis, increased ESR.

Particular attention should be paid to acute obstructive bronchitis, which usually occurs in children and is fraught with serious complications. In such cases, the appearance of noisy wheezing with prolonged exhalation attracts attention. During the breathing process, auxiliary muscles are involved, retraction of the pliable areas of the chest is noted: supra- and subclavian fossae, intercostal spaces. On auscultation, abundant dry wheezing is heard, indicating bronchospasm.

Obstructive bronchitis is dangerous due to a possible attack of suffocation and the development of bronchial asthma.

Clinic and diagnosis of chronic bronchitis

Unlike acute bronchitis, chronic bronchitis begins imperceptibly and can remain unnoticed for a long time, manifesting itself only as a slight cough in the morning, without affecting well-being or performance. Gradually, the cough becomes more frequent and becomes a constant complaint of the patient, slightly “letting go” in the warm season. The amount of sputum increases and its properties change: from mucous, it gradually becomes mucopurulent or purulent. On auscultation, hard breathing is noted. Dry or moist fine bubbling rales are possible.

In the later stages of chronic bronchitis, a characteristic symptom is shortness of breath, which occurs first during physical exertion and during exacerbation, gradually becoming more permanent. The appearance of shortness of breath indicates the spread of the process to the small bronchi and the development of ventilation (obstructive) disorders.

Chronic bronchitis is characterized by severe sweating, especially during physical activity and at night; warm acrocyanosis – the limbs are slightly bluish, but at the same time warm.

Diagnosis of chronic bronchitis at the initial stage is based primarily on clinical symptoms, since laboratory and x-ray examination methods do not reveal any abnormalities.

At later stages and in the phase of exacerbation of chronic bronchitis, a general blood test (leukocytosis, ESR) can be informative; biochemical blood test (appearance of CRP, changes in blood protein fractions (alpha-2-globulin), seromucoid, sialic acids); sputum examination (increased number of leukocytes, epithelial cells, macrophages).

Bronchoscopy helps to confirm the presence of a diffuse inflammatory process and clarify the nature of morphological changes in the bronchi, which allows not only to conduct a visual examination of the bronchi from the inside, but also to take a biopsy specimen for histological examination.

Functional diagnostic methods make it possible to assess the degree of respiratory impairment using pneumotachometry, spirography, peak flowmetry. In a patient with chronic bronchitis, the vital capacity of the lungs (VC), forced expiratory volume (FEV) and peak expiratory volume flow (PEF) decrease, and the residual lung volume (RLV) increases.

The progression of chronic bronchitis inevitably leads to the appearance of clinical signs of respiratory and heart failure.

Bronchitis: clinical manifestations, causes, mechanism of development

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:

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 in 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.

JMedic.ru

Acute obstructive bronchitis is an inflammatory lesion of the bronchial tree (mainly medium and small caliber bronchi), which is accompanied by obstruction (spasm) of smooth muscle cells located in the wall of the bronchi, which is accompanied by respiratory failure and oxygen starvation of internal organs and systems.
The main symptoms of the disease in adults are cough, expiratory shortness of breath (difficulty in exhaling), the appearance of copious amounts of sputum, wheezing and impaired ventilation.

Acute obstructive bronchitis is common throughout the globe and mainly occurs in regions with cold and humid climates, or in the autumn and winter months. This is due to the fact that during these periods people are most often susceptible to viral and bacterial infections.

The prognosis for the life and ability to work of sick individuals is favorable. Full recovery is observed in 90% within 10–14 days.

Main causes of the disease

A viral infection in which viruses such as:

Bacterial infection of the respiratory tract. The most common infectious agents in adults are:

  • staphylococci;
  • streptococci;
  • pneumococci;
  • Pseudomonas aeruginosa;
  • legionella;
  • Proteus.

Damage to the bronchopulmonary system by protozoan microorganisms:

Predisposing factors that contribute to the development of a disease such as acute obstructive bronchitis:

  • Immune system diseases:
  1. HIV infection (human immunodeficiency virus);
  2. AIDS (acquired immunodeficiency syndrome);
  3. Mononucleosis;
  4. Cytomegalovirus infection.
  • Decreased immunity due to diseases of other organs and systems:
  1. Frequent upper respiratory tract infections;
  2. Oncological pathologies;
  3. Diabetes;
  4. Hypothyroidism;
  5. Rheumatism;
  6. Reactive arthritis;
  7. Scleroderma;
  8. Dermatomyositis;
  9. Systemic lupus erythematosus, etc.
  1. Alcoholism;
  2. Tobacco smoking;
  3. Addiction.
  • Lack of vitamins in the body.

Classification of the disease

  • According to severity, acute obstructive bronchitis is divided into:
  1. Easy;
  2. Moderate;
  3. Heavy;
  4. Extremely heavy.
  • According to the nature of inflammation in adults, there are:
  1. Purulent obstructive bronchitis;
  2. Catarrhal obstructive bronchitis;
  3. Catarrhal-purulent obstructive bronchitis;
  4. Fibrinous obstructive bronchitis;
  5. Hemorrhagic obstructive bronchitis.

Signs of the disease

  • Symptoms of damage to the bronchopulmonary system:
  1. A dry cough, which over time becomes unproductive and productive with the release of copious amounts of sputum. The appearance of a symptom such as sputum is the first stage in the recovery of the body;
  2. Expiratory dyspnea is difficulty in exhaling air from the lungs after inhalation. This type of shortness of breath occurs exclusively in diseases of the bronchi and is an important diagnostic criterion;
  3. Feeling short of air.

  1. Increased body temperature;
  2. Chills;
  3. Cold sweat;
  4. Fever;
  5. Increased fatigue;
  6. A sharp decrease in performance;
  7. Body aches;
  8. Arthralgia (joint pain);
  9. Myalgia (muscle pain).
  • Associated syndromes that indicate damage to other organs and systems:
  1. Symptoms of damage to the cardiovascular system: pain in the heart area, increased heart rate, increased blood pressure;
  2. Symptoms of damage to the central nervous system: headaches, dizziness, decreased visual acuity, convulsions, hallucinations (only in very severe cases);
  3. Symptoms of damage to the digestive system: nausea, vomiting of intestinal contents, pain in the right hypochondrium, bloating, constipation;
  4. Symptoms of damage to the urinary system: pain in the kidneys, swelling of the lower extremities.

Diagnosis of the disease

  • Medical examination;

Patients with acute obstructive bronchitis usually go to the clinic at their place of residence or work after developing shortness of breath, i.e. somewhere on the 3rd–4th day from the onset of the disease. Considering the specific complaints and the identification during examination of an expanded chest, a box sound over the lung fields and dry wheezing against the background of weakened or hard breathing, determining a preliminary diagnosis - acute obstructive bronchitis is not difficult.

To confirm the diagnosis, general clinical tests are prescribed, which will monitor the inflammatory reaction, sputum analysis, where there will be characteristic changes, and chest x-ray.


  1. A general blood test, which will be characterized by an increase in leukocytes, lymphocytes, monocytes, ESR (erythrocyte sedimentation rate) and a shift in the leukocyte formula to the left. In hemorrhagic obstructive bronchitis, an increased level of reticulocytes may be observed. Also in this analysis, a slight decrease in the number of red blood cells and hemoglobin may be observed;
  2. A general urine test, which will be characterized by an increase in squamous epithelial cells and leukocytes in the field of view. Often, along with these changes, there is an increase in the number of red blood cells in the field of view, the appearance of mucus, bacteria and traces of protein;
  3. General analysis of sputum, which will note the appearance of a large number of ciliated columnar epithelial cells, alveolar macrophages, leukocytes and Kurshman spirals (casts of small-caliber bronchioles) in the field of view.
  • Instrumental examination.

X-ray of the chest, which will show a uniform increase in the transparency of the lung fields on both sides.

Treatment of the disease

  • Drug treatment
  1. Protected penicillins (Amoxiclav, Flemoxin-solutab, Augmentin) have a bacteriostatic effect (inhibit microbial cell division). Prescribed to adults: 1000 mg 2 times a day or 625 mg 3 times a day for 7–14 days;
  2. 2nd generation cephalosporins (Cefamandol, Ciprofloxacin, Norfloxacin) have a pronounced bactericidal effect (targetedly destroy the bacterial cell). Adults are prescribed 200 mg 2 times a day. Duration of treatment is up to 10–14 days.

Inosine pranobex (Groprinosin) has a pronounced immunomodulatory (increases the formation, division and reproduction of cells of the human immune system - lymphocytes, interleukins, cytokines, immunoglobulins that fight viral infection) and immunostimulating (increases the release of the above cells from the depot (lymph nodes) into the bloodstream ) action.

Prescribed to adults for the first 3 days at the maximum dosage - 2 tablets 4 times a day, then the dose is reduced to 6 tablets per day. Prophylactic dose: 1 tablet 1 time per day 2 weeks after starting the drug.

  1. Ambroxol (Lazolvan, Flavamed), which has a pronounced mucolytic and expectorant effect. Prescribed 30 mg 3 times a day or 75 mg 1 time a day. The course of treatment for adults should be at least 10 days;
  2. For intense dry coughs, the drug Erespal or Inspiron is often used, which locally eliminates the inflammatory focus in the bronchial wall and promotes better coughing. Adults are prescribed 1 tablet 2 times a day. The course of treatment is 10 days. When taking the drug, heart rate may increase up to 100 beats per minute.

Treatment of shortness of breath:

  1. Short-acting beta2-agonists (Salbutamol, Ventolin, Berodual) help eliminate bronchial spasm and thereby have a bronchodilator effect. Adults are prescribed 2 breaths 4–6 times a day;
  2. Long-acting beta2-agonists (Salmeterol, Formoterol) have, like beta2-agonists, a bronchodilator effect, but the effect, unlike the former, lasts several times longer and lasts almost 12 hours. The drugs are prescribed 2 puffs 2 times a day (morning and evening).

Treatment of symptoms of intoxication:

  1. Drinking plenty of fluids or intravenously administering Ringer's solution 200.0 ml, Rheosorbilact 200.0 ml or physiological solution 5% glucose 200.0 ml - eliminates headaches, dizziness, nausea, vomiting;
  2. Nonsteroidal anti-inflammatory drugs (Nimesulide, Ibuprofen) have antipyretic, analgesic and anti-inflammatory effects. Prescribed to adults: 200 mg 1–2 times a day. Duration of treatment is up to 5–7 days.
  • Physiotherapeutic treatment:

Indicated after the 7th–10th day of drug treatment and only when the patient’s temperature is normalized and there are no symptoms of intoxication.

LECTURE No. 19 Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention

Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention

1. Acute bronchitis

Acute bronchitis is an acute diffuse inflammation of the tracheobronchial tree. Classification:

1) acute bronchitis (simple);

2) acute obstructive bronchitis;

3) acute bronchiolitis;

4) acute obliterating bronchiolitis;

5) recurrent bronchitis;

6) recurrent obstructive bronchitis;

7) chronic bronchitis;

8) chronic bronchitis with obliteration. Etiology. The disease is caused by viral infections (influenza viruses, parainfluenza viruses, adenoviruses, respiratory syncytial viruses, measles, whooping cough, etc.) and bacterial infections (staphylococci, streptococci, pneumococci, etc.); physical and chemical factors (cold, dry, hot air, nitrogen oxides, sulfur dioxide, etc.). Cooling, chronic focal infection of the nasopharyngeal area and impaired nasal breathing, and chest deformation predispose to the disease.

Pathogenesis. The damaging agent enters the trachea and bronchi with inhaled air through the hematogenous and lymphogenous route. Acute inflammation of the bronchial tree is accompanied by a violation of bronchial patency due to an edematous-inflammatory or bronchospastic mechanism. Characterized by hyperemia, swelling of the mucous membrane; on the wall of the bronchus and in its lumen there is a mucous, mucopurulent or purulent secretion; degenerative disorders of the ciliated epithelium develop. In severe forms of acute bronchitis, inflammation is localized not only on the mucous membrane, but also in the deep tissues of the bronchial wall.

Clinical signs. Clinical manifestations of bronchitis of infectious etiology begin with rhinitis, nasopharyngitis, moderate intoxication, increased body temperature, weakness, a feeling of weakness, rawness behind the sternum, a dry cough that turns into a wet cough. Auscultatory signs are absent or hard breathing is detected over the lungs, dry rales are heard. There are no changes in peripheral blood. This course is observed more often with damage to the trachea and bronchi. In moderate cases of bronchitis, general malaise, weakness, severe dry cough with difficulty breathing, shortness of breath, and pain in the chest and abdominal wall appear, which is associated with muscle strain when coughing. The cough gradually turns into a wet cough, and the sputum becomes mucopurulent or purulent in nature. In the lungs, upon auscultation, hard breathing, dry and moist fine bubbling rales are heard. Body temperature is subfebrile. There are no pronounced changes in the peripheral blood. A severe course of the disease is observed with predominant damage to the bronchioles. Acute clinical manifestations of the disease begin to subside by the 4th day and, with a favorable outcome, almost completely disappear by the 7th day of the disease. Acute bronchitis with impaired bronchial obstruction has a tendency to protracted course and transition to chronic bronchitis. Acute bronchitis of toxic-chemical etiology is severe. The disease begins with a painful cough, which is accompanied by the release of mucous or bloody sputum, bronchospasm quickly develops (dry wheezing can be heard during auscultation against the background of prolonged exhalation), shortness of breath progresses (up to suffocation), symptoms of respiratory failure and hypoxemia increase. An X-ray examination of the chest organs can determine the symptoms of acute emphysema.

Diagnostics: based on clinical and laboratory data.

Treatment. Bed rest, plenty of warm drinks with raspberries, honey, linden blossom. Prescribe antiviral and antibacterial therapy, vitamin therapy: ascorbic acid up to 1 g per day, vitamin A 3 mg 3 times a day. You can use cups on the chest, mustard plasters. For a severe dry cough - antitussive drugs: codeine, libexin, etc. For a wet cough - mucolytic drugs: bromine-hexine, ambrobene, etc. Inhalation of expectorants, mucolytics, heated mineral alkaline water, eucalyptus, anise oil using a steam inhaler is indicated Duration inhalations – 5 minutes 3–4 times a day for 3–5 days. Bronchospasm can be stopped by prescribing aminophylline (0.25 g 3 times a day). Antihistamines are indicated, Prevention. Elimination of the etiological factor of acute bronchitis (hypothermia, chronic and focal infection in the respiratory tract, etc.).

2. Chronic bronchitis

Chronic bronchitis is a progressive diffuse inflammation of the bronchi, not associated with local or generalized damage to the lungs, manifested by a cough. We can talk about chronic bronchitis if the cough continues for 3 months in the 1st year - 2 years in a row.

Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other compounds of a chemical nature) and recurrent respiratory infection (a major role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), less commonly occurs in cystic fibrosis. Predisposing factors are chronic inflammatory, suppurative processes in the lungs, chronic foci of infection and chronic diseases localized in the upper respiratory tract, decreased reactivity of the body, hereditary factors.

Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion and a change in the composition of the secretion, as well as an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not improve the emptying of the bronchial tree; normally, the entire layer of secretion is renewed (partial cleansing of the bronchi is possible only with a cough). Long-term hyperfunction is characterized by depletion of the mucociliary apparatus of the bronchi, the development of dystrophy and atrophy of the epithelium. When the drainage function of the bronchi is disrupted, a bronchogenic infection occurs, the activity and recurrence of which depend on the local immunity of the bronchi and the occurrence of secondary immunological deficiency. With the development of bronchial obstruction due to hyperplasia of the epithelium of the mucous glands, swelling and inflammatory thickening of the bronchial wall, obstruction of the bronchi, excess viscous bronchial secretion, and bronchospasm are observed. With obstruction of the small bronchi, overstretching of the alveoli during exhalation and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or unventilated zones develop, and therefore the blood passing through them is not oxygenated and arterial hypoxemia develops. In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance develop; pericapillary pulmonary hypertension develops. Chronic hypoxemia leads to an increase in blood viscosity, which is accompanied by metabolic acidosis, which further increases vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi and bronchioles it is deep with the development of erosions and the formation of meso- and panbronchitis. The remission phase is manifested by a decrease in inflammation and a large decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane.

Clinical manifestations. The onset of the disease is gradual. The first and main symptom is a cough in the morning with the discharge of mucous sputum; gradually the cough begins to occur at any time of the day, intensifies in cold weather and becomes constant over the years. The amount of sputum increases, the sputum becomes mucopurulent or purulent. Shortness of breath appears. With purulent bronchitis, purulent sputum may periodically be released, but bronchial obstruction is less pronounced. Obstructive chronic bronchitis is manifested by persistent obstructive disorders. Purulent-obstructive bronchitis is characterized by the release of purulent sputum and obstructive ventilation disorders. Frequent exacerbations during periods of cold, damp weather: cough intensifies, shortness of breath, the amount of sputum increases, malaise and fatigue appear. Body temperature is normal or subfebrile, hard breathing and dry wheezing over the entire pulmonary surface can be detected.

Diagnostics. A slight leukocytosis with a rod-nuclear shift in the leukocyte formula is possible. With exacerbation of purulent bronchitis, a slight change in the biochemical parameters of inflammation occurs (C-reactive protein, sialic acids, fibronogen, seromucoid, etc. increase). Sputum examination: macroscopic, cytological, biochemical. With severe exacerbation, the sputum becomes purulent in nature: a large number of neutrophilic leukocytes, an increased content of acidic mucopolysaccharides and DNA fibers, the nature of the sputum, predominantly neutrophilic leukocytes, an increase in the level of acidic mucopolysaccharides and DNA fibers, which increase the viscosity of the sputum, a decrease in the amount of lysozyme, etc. Bronchoscopy, with the help of which endobronchial manifestations of the inflammatory process are assessed, the stages of development of the inflammatory process: catarrhal, purulent, atrophic, hypertrophic, hemorrhagic and its severity, but mainly to the level of the subsegmental bronchi.

Differential diagnosis is carried out with chronic pneumonia, bronchial asthma, tuberculosis. Unlike chronic pneumonia, chronic bronchitis always develops from a gradual onset, with widespread bronchial obstruction and often emphysema, respiratory failure and pulmonary hypertension with the development of chronic cor pulmonale. On X-ray examination, the changes are also diffuse in nature: peribronchial sclerosis, increased transparency of the pulmonary fields due to emphysema, expansion of the branches of the pulmonary artery. Chronic bronchitis differs from bronchial asthma in the absence of asthma attacks; it is associated with pulmonary tuberculosis by the presence or absence of symptoms of tuberculosis intoxication, Mycobacterium tuberculosis in sputum, the results of X-ray and bronchoscopic examination, and tuberculin tests.

Treatment. In the phase of exacerbation of chronic bronchitis, therapy is aimed at eliminating the inflammatory process, improving bronchial patency, as well as restoring impaired general and local immunological reactivity. Antibiotic therapy is prescribed, which is selected taking into account the sensitivity of the sputum microflora, administered orally or parenterally, and sometimes combined with intratracheal administration. Inhalations are indicated. Use expectorants, mucolytic and bronchospasmolytic drugs, and drink plenty of fluids to restore and improve bronchial patency. Herbal medicine using marshmallow root, coltsfoot leaves, and plantain. Proteolytic enzymes (trypsin, chymotrypsin) are prescribed, which reduce the viscosity of sputum, but are currently rarely used. Acetylcysteine ​​has the ability to break disulfide bonds of mucus proteins and promotes strong and rapid liquefaction of sputum. Bronchial drainage is improved with the use of mucoregulators that affect secretions and the production of glycoproteins in the bronchial epithelium (bromhexine). In case of insufficient bronchial drainage and existing symptoms of bronchial obstruction, bronchospasmolytics are added to treatment: aminophylline, anticholinergic blockers (atropine in aerosols), adrenergic stimulants (ephedrine, salbutamol, Berotec). In a hospital setting, intratracheal lavages for purulent bronchitis must be combined with sanitation bronchoscopy (3–4 sanitation bronchoscopy with a break of 3–7 days). When restoring the drainage function of the bronchi, physical therapy, chest massage, and physiotherapy are also used. When allergic syndromes develop, calcium chloride and antihistamines are used; if there is no effect, a short course of glucocorticoids can be prescribed to relieve allergic syndrome, but the daily dose should not be more than 30 mg. The danger of activation of infectious agents does not allow long-term use of glucocorticoids. In patients with chronic bronchitis, complicated respiratory failure and chronic cor pulmonale, the use of veroshpiron (up to 150–200 mg/day) is indicated.

The food of patients should be high-calorie and fortified. Use ascorbic acid 1 g per day, nicotinic acid, B vitamins; if necessary, aloe, methyluracil. With the development of complications of a disease such as pulmonary and pulmonary-heart failure, oxygen therapy and auxiliary artificial ventilation are used.

Anti-relapse and maintenance therapy is prescribed in the subsiding phase of exacerbation, carried out in local and climatic sanatoriums, this therapy is prescribed during clinical examination. It is recommended to distinguish 3 groups of clinical patients.

1st group. It includes patients with cor pulmonale, severe respiratory failure and other complications, and loss of ability to work. Patients are prescribed maintenance therapy, which is carried out in a hospital or by a local doctor. These patients are examined at least once a month.

2nd group. It includes patients with frequent exacerbations of chronic bronchitis, as well as moderate dysfunction of the respiratory system. Such patients are examined by a pulmonologist 3–4 times a year, and anti-relapse therapy is prescribed in the fall and spring, as well as for acute respiratory diseases. An effective method of administering drugs is the inhalation route; according to indications, it is necessary to carry out sanitation of the bronchial tree using intratracheal lavages, sanitation bronchoscopy. In case of active infection, antibacterial drugs are prescribed.

3rd group. It includes patients in whom anti-relapse therapy led to a subsidence of the process and the absence of relapses for 2 years. Such patients are indicated for preventive therapy, which includes means aimed at improving bronchial drainage and increasing its reactivity.

Obstructive bronchitis

Obstructive bronchitis– diffuse inflammation of the bronchi of small and medium caliber, occurring with a sharp bronchial spasm and progressive impairment of pulmonary ventilation. Obstructive bronchitis is manifested by cough with sputum, expiratory shortness of breath, wheezing, and respiratory failure. Diagnosis of obstructive bronchitis is based on auscultatory, radiological data, and the results of a study of external respiration function. Therapy for obstructive bronchitis includes the prescription of antispasmodics, bronchodilators, mucolytics, antibiotics, inhaled corticosteroid drugs, breathing exercises, and massage.

Obstructive bronchitis

Bronchitis (simple acute, recurrent, chronic, obstructive) constitutes a large group of inflammatory diseases of the bronchi, varying in etiology, mechanisms of occurrence and clinical course. In pulmonology, obstructive bronchitis includes cases of acute and chronic inflammation of the bronchi, occurring with the syndrome of bronchial obstruction, which occurs against the background of swelling of the mucous membrane, hypersecretion of mucus and bronchospasm. Acute obstructive bronchitis often develops in young children, chronic obstructive bronchitis in adults.

Chronic obstructive bronchitis, along with other diseases that occur with progressive obstruction of the respiratory tract (emphysema, bronchial asthma), is usually referred to as chronic obstructive pulmonary disease (COPD). In the UK and US, COPD also includes cystic fibrosis, bronchiolitis obliterans and bronchiectasis.

Causes of obstructive bronchitis

Acute obstructive bronchitis is etiologically associated with respiratory syncytial viruses, influenza viruses, parainfluenza virus type 3, adenoviruses and rhinoviruses, and viral-bacterial associations. When studying bronchial washings in patients with recurrent obstructive bronchitis, DNA of persistent infectious pathogens - herpesvirus, mycoplasma, chlamydia - is often isolated. Acute obstructive bronchitis mainly occurs in young children. The most susceptible to the development of acute obstructive bronchitis are children who often suffer from acute respiratory viral infections, have a weakened immune system and an increased allergic background, and a genetic predisposition.

The main factors contributing to the development of chronic obstructive bronchitis are smoking (passive and active), occupational risks (contact with silicon, cadmium), air pollution (mainly sulfur dioxide), deficiency of antiproteases (alpha1-antitrypsin), etc. To the group Those at risk for the development of chronic obstructive bronchitis include miners, construction workers, metallurgical and agricultural workers, railway workers, office employees associated with printing on laser printers, etc. Chronic obstructive bronchitis most often affects men.

Pathogenesis of obstructive bronchitis

The summation of genetic predisposition and environmental factors leads to the development of an inflammatory process, which involves small and medium-sized bronchi and peribronchial tissue. This causes disruption of the movement of the cilia of the ciliated epithelium, and then its metaplasia, loss of ciliated cells and an increase in the number of goblet cells. Following the morphological transformation of the mucosa, a change in the composition of the bronchial secretion occurs with the development of mucostasis and blockade of small bronchi, which leads to disruption of the ventilation-perfusion balance.

In the bronchial secretions, the content of nonspecific factors of local immunity that provide antiviral and antimicrobial protection decreases: lactoferin, interferon and lysozyme. Thick and viscous bronchial secretions with reduced bactericidal properties are a good breeding ground for various pathogens (viruses, bacteria, fungi). In the pathogenesis of bronchial obstruction, a significant role is played by the activation of cholinergic factors of the autonomic nervous system, causing the development of bronchospastic reactions.

The complex of these mechanisms leads to swelling of the bronchial mucosa, hypersecretion of mucus and spasm of smooth muscles, i.e. the development of obstructive bronchitis. In case of irreversibility of the bronchial obstruction component, one should think about COPD - the addition of emphysema and peribronchial fibrosis.

Symptoms of acute obstructive bronchitis

As a rule, acute obstructive bronchitis develops in children during the first 3 years of life. The disease has an acute onset and occurs with symptoms of infectious toxicosis and bronchial obstruction.

Infectious-toxic manifestations are characterized by low-grade body temperature, headache, dyspeptic disorders, and weakness. The leading clinical manifestations of obstructive bronchitis are respiratory disorders. Children are bothered by a dry or wet obsessive cough that does not bring relief and worsens at night, and shortness of breath. Note the flaring of the wings of the nose during inhalation, the participation of auxiliary muscles in the act of breathing (neck muscles, shoulder girdle, abdominal muscles), the retraction of compliant areas of the chest during breathing (intercostal spaces, jugular fossa, supra- and subclavian region). For obstructive bronchitis, a prolonged wheezing exhalation and dry (“musical”) wheezing, heard at a distance, are typical.

The duration of acute obstructive bronchitis is from 7-10 days to 2-3 weeks. In case of repetition of episodes of acute obstructive bronchitis three or more times a year, they speak of recurrent obstructive bronchitis; If symptoms persist for two years, a diagnosis of chronic obstructive bronchitis is made.

Symptoms of chronic obstructive bronchitis

The basis of the clinical picture of chronic obstructive bronchitis is cough and shortness of breath. When coughing, a small amount of mucous sputum is usually released; during periods of exacerbation, the amount of sputum increases, and its character becomes mucopurulent or purulent. The cough is constant and is accompanied by wheezing. Against the background of arterial hypertension, episodes of hemoptysis may occur.

Expiratory shortness of breath in chronic obstructive bronchitis usually occurs later, but in some cases the disease can debut immediately with shortness of breath. The severity of shortness of breath varies widely: from sensations of lack of air during exertion to severe respiratory failure. The degree of shortness of breath depends on the severity of obstructive bronchitis, the presence of exacerbation, and concomitant pathology.

Exacerbation of chronic obstructive bronchitis can be provoked by respiratory infection, exogenous damaging factors, physical activity, spontaneous pneumothorax, arrhythmia, the use of certain medications, decompensation of diabetes mellitus and other factors. At the same time, signs of respiratory failure increase, low-grade fever, sweating, fatigue, and myalgia appear.

The objective status of chronic obstructive bronchitis is characterized by prolonged exhalation, the participation of additional muscles in breathing, distant wheezing, swelling of the neck veins, and changes in the shape of the nails (“hour glass”). As hypoxia increases, cyanosis appears.

The severity of chronic obstructive bronchitis, according to the methodological recommendations of the Russian Society of Pulmonologists, is assessed by FEV1 (forced expiratory volume in 1 second).

  • Stage I chronic obstructive bronchitis is characterized by an FEV1 value exceeding 50% of the normative value. At this stage, the disease has little impact on the quality of life. Patients do not need constant medical monitoring by a pulmonologist.
  • Stage II chronic obstructive bronchitis is diagnosed when FEV1 decreases to 35-49% of the normative value. In this case, the disease significantly affects the quality of life; patients require systematic monitoring by a pulmonologist.
  • Stage III chronic obstructive bronchitis corresponds to an FEV1 indicator of less than 34% of the expected value. In this case, there is a sharp decrease in stress tolerance; inpatient and outpatient treatment is required in pulmonology departments and offices.

Complications of chronic obstructive bronchitis are emphysema, cor pulmonale, amyloidosis, and respiratory failure. To make a diagnosis of chronic obstructive bronchitis, other causes of shortness of breath and cough must be excluded, primarily tuberculosis and lung cancer.

Diagnosis of obstructive bronchitis

The examination program for persons with obstructive bronchitis includes physical, laboratory, radiological, functional, and endoscopic examinations. The nature of physical findings depends on the form and stage of obstructive bronchitis. As the disease progresses, vocal tremors weaken, a boxy percussion sound appears over the lungs, and the mobility of the pulmonary edges decreases; Auscultation reveals hard breathing, wheezing during forced exhalation, and during exacerbation - moist rales. The tone or amount of wheezing changes after coughing.

X-ray of the lungs allows you to exclude local and disseminated lung lesions and detect concomitant diseases. Usually, after 2-3 years of obstructive bronchitis, an increase in the bronchial pattern, deformation of the roots of the lungs, and pulmonary emphysema are detected. Therapeutic and diagnostic bronchoscopy for obstructive bronchitis allows you to examine the bronchial mucosa, collect sputum and perform bronchoalveolar lavage. To exclude bronchiectasis, bronchography may be necessary.

A necessary criterion for diagnosing obstructive bronchitis is a study of external respiration function. The most important data are spirometry (including inhalation tests), peak flowmetry, and pneumotachometry. Based on the data obtained, the presence, degree and reversibility of bronchial obstruction, impaired pulmonary ventilation, and the stage of chronic obstructive bronchitis are determined.

The complex of laboratory diagnostics examines general blood and urine tests, biochemical blood parameters (total protein and protein fractions, fibrinogen, sialic acids, bilirubin, aminotransferases, glucose, creatinine, etc.). Immunological tests determine the subpopulation functional ability of T-lymphocytes, immunoglobulins, and CEC. Determination of CBS and blood gas composition makes it possible to objectively assess the degree of respiratory failure in obstructive bronchitis.

Microscopic and bacteriological examination of sputum and lavage fluid is carried out, and in order to exclude pulmonary tuberculosis, sputum analysis is carried out using PCR and AFB. Exacerbation of chronic obstructive bronchitis should be differentiated from bronchiectasis, bronchial asthma, pneumonia, tuberculosis and lung cancer, pulmonary embolism.

Treatment of obstructive bronchitis

For acute obstructive bronchitis, rest, drinking plenty of fluids, air humidification, alkaline and medicinal inhalations are prescribed. Etiotropic antiviral therapy (interferon, ribavirin, etc.) is prescribed. For severe bronchial obstruction, antispasmodic (papaverine, drotaverine) and mucolytic (acetylcysteine, ambroxol) agents, bronchodilator inhalers (salbutamol, orciprenaline, fenoterol hydrobromide) are used. To facilitate the discharge of sputum, percussion massage of the chest, vibration massage, massage of the back muscles, and breathing exercises are performed. Antibacterial therapy is prescribed only when a secondary microbial infection occurs.

The goal of treatment of chronic obstructive bronchitis is to slow the progression of the disease, reduce the frequency and duration of exacerbations, and improve the quality of life. The basis of pharmacotherapy for chronic obstructive bronchitis is basic and symptomatic therapy. Quitting smoking is a mandatory requirement.

Basic therapy includes the use of bronchodilators: anticholinergics (ipratropium bromide), b2-agonists (fenoterol, salbutamol), xanthines (theophylline). If there is no effect from the treatment of chronic obstructive bronchitis, corticosteroid drugs are used. To improve bronchial patency, mucolytic drugs (ambroxol, acetylcysteine, bromhexine) are used. Drugs can be administered orally, in the form of aerosol inhalation, nebulizer therapy, or parenterally.

When the bacterial component accumulates during periods of exacerbation of chronic obstructive bronchitis, macrolides, fluoroquinolones, tetracyclines, b-lactams, cephalosporins are prescribed for a course of 7-14 days. In case of hypercapnia and hypoxemia, oxygen therapy is a mandatory component of the treatment of obstructive bronchitis.

Forecast and prevention of obstructive bronchitis

Acute obstructive bronchitis responds well to treatment. In children with an allergic predisposition, obstructive bronchitis can recur, leading to the development of asthmatic bronchitis or bronchial asthma. The transition of obstructive bronchitis to a chronic form is prognostically less favorable.

Adequate therapy helps delay the progression of obstructive syndrome and respiratory failure. Unfavorable factors that aggravate the prognosis are the elderly age of patients, concomitant pathology, frequent exacerbations, continued smoking, poor response to therapy, and the formation of cor pulmonale.

Primary prevention measures for obstructive bronchitis include maintaining a healthy lifestyle, increasing overall resistance to infections, and improving working conditions and the environment. The principles of secondary prevention of obstructive bronchitis involve the prevention and adequate treatment of exacerbations to slow the progression of the disease.

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 - 7.4x10 9, 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.


Hospital pediatrics: lecture notes by N. V. Pavlov

LECTURE No. 19 Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention

LECTURE No. 19

Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention

1. Acute bronchitis

Acute bronchitis is an acute diffuse inflammation of the tracheobronchial tree. Classification:

1) acute bronchitis (simple);

2) acute obstructive bronchitis;

3) acute bronchiolitis;

4) acute obliterating bronchiolitis;

5) recurrent bronchitis;

6) recurrent obstructive bronchitis;

7) chronic bronchitis;

8) chronic bronchitis with obliteration. Etiology. The disease is caused by viral infections (influenza viruses, parainfluenza viruses, adenoviruses, respiratory syncytial viruses, measles, whooping cough, etc.) and bacterial infections (staphylococci, streptococci, pneumococci, etc.); physical and chemical factors (cold, dry, hot air, nitrogen oxides, sulfur dioxide, etc.). Cooling, chronic focal infection of the nasopharyngeal area and impaired nasal breathing, and chest deformation predispose to the disease.

Pathogenesis. The damaging agent enters the trachea and bronchi with inhaled air through the hematogenous and lymphogenous route. Acute inflammation of the bronchial tree is accompanied by a violation of bronchial patency due to an edematous-inflammatory or bronchospastic mechanism. Characterized by hyperemia, swelling of the mucous membrane; on the wall of the bronchus and in its lumen there is a mucous, mucopurulent or purulent secretion; degenerative disorders of the ciliated epithelium develop. In severe forms of acute bronchitis, inflammation is localized not only on the mucous membrane, but also in the deep tissues of the bronchial wall.

Clinical signs. Clinical manifestations of bronchitis of infectious etiology begin with rhinitis, nasopharyngitis, moderate intoxication, increased body temperature, weakness, a feeling of weakness, rawness behind the sternum, a dry cough that turns into a wet cough. Auscultatory signs are absent or hard breathing is detected over the lungs, dry rales are heard. There are no changes in peripheral blood. This course is observed more often with damage to the trachea and bronchi. In moderate cases of bronchitis, general malaise, weakness, severe dry cough with difficulty breathing, shortness of breath, and pain in the chest and abdominal wall appear, which is associated with muscle strain when coughing. The cough gradually turns into a wet cough, and the sputum becomes mucopurulent or purulent in nature. In the lungs, upon auscultation, hard breathing, dry and moist fine bubbling rales are heard. Body temperature is subfebrile. There are no pronounced changes in the peripheral blood. A severe course of the disease is observed with predominant damage to the bronchioles. Acute clinical manifestations of the disease begin to subside by the 4th day and, with a favorable outcome, almost completely disappear by the 7th day of the disease. Acute bronchitis with impaired bronchial obstruction has a tendency to protracted course and transition to chronic bronchitis. Acute bronchitis of toxic-chemical etiology is severe. The disease begins with a painful cough, which is accompanied by the release of mucous or bloody sputum, bronchospasm quickly develops (dry wheezing can be heard during auscultation against the background of prolonged exhalation), shortness of breath progresses (up to suffocation), symptoms of respiratory failure and hypoxemia increase. An X-ray examination of the chest organs can determine the symptoms of acute emphysema.

Diagnostics: based on clinical and laboratory data.

Treatment. Bed rest, plenty of warm drinks with raspberries, honey, linden blossom. Prescribe antiviral and antibacterial therapy, vitamin therapy: ascorbic acid up to 1 g per day, vitamin A 3 mg 3 times a day. You can use cups on the chest, mustard plasters. For a severe dry cough - antitussive drugs: codeine, libexin, etc. For a wet cough - mucolytic drugs: bromine-hexine, ambrobene, etc. Inhalation of expectorants, mucolytics, heated mineral alkaline water, eucalyptus, anise oil using a steam inhaler is indicated Duration inhalations – 5 minutes 3–4 times a day for 3–5 days. Bronchospasm can be stopped by prescribing aminophylline (0.25 g 3 times a day). Antihistamines are indicated, Prevention. Elimination of the etiological factor of acute bronchitis (hypothermia, chronic and focal infection in the respiratory tract, etc.).

2. Chronic bronchitis

Chronic bronchitis is a progressive diffuse inflammation of the bronchi, not associated with local or generalized damage to the lungs, manifested by a cough. We can talk about chronic bronchitis if the cough continues for 3 months in the 1st year - 2 years in a row.

Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other compounds of a chemical nature) and recurrent respiratory infection (a major role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), less commonly occurs in cystic fibrosis. Predisposing factors are chronic inflammatory, suppurative processes in the lungs, chronic foci of infection and chronic diseases localized in the upper respiratory tract, decreased reactivity of the body, hereditary factors.

Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion and a change in the composition of the secretion, as well as an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not improve the emptying of the bronchial tree; normally, the entire layer of secretion is renewed (partial cleansing of the bronchi is possible only with a cough). Long-term hyperfunction is characterized by depletion of the mucociliary apparatus of the bronchi, the development of dystrophy and atrophy of the epithelium. When the drainage function of the bronchi is disrupted, a bronchogenic infection occurs, the activity and recurrence of which depend on the local immunity of the bronchi and the occurrence of secondary immunological deficiency. With the development of bronchial obstruction due to hyperplasia of the epithelium of the mucous glands, swelling and inflammatory thickening of the bronchial wall, obstruction of the bronchi, excess viscous bronchial secretion, and bronchospasm are observed. With obstruction of the small bronchi, overstretching of the alveoli during exhalation and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or unventilated zones develop, and therefore the blood passing through them is not oxygenated and arterial hypoxemia develops. In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance develop; pericapillary pulmonary hypertension develops. Chronic hypoxemia leads to an increase in blood viscosity, which is accompanied by metabolic acidosis, which further increases vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi and bronchioles it is deep with the development of erosions and the formation of meso- and panbronchitis. The remission phase is manifested by a decrease in inflammation and a large decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane.

Clinical manifestations. The onset of the disease is gradual. The first and main symptom is a cough in the morning with the discharge of mucous sputum; gradually the cough begins to occur at any time of the day, intensifies in cold weather and becomes constant over the years. The amount of sputum increases, the sputum becomes mucopurulent or purulent. Shortness of breath appears. With purulent bronchitis, purulent sputum may periodically be released, but bronchial obstruction is less pronounced. Obstructive chronic bronchitis is manifested by persistent obstructive disorders. Purulent-obstructive bronchitis is characterized by the release of purulent sputum and obstructive ventilation disorders. Frequent exacerbations during periods of cold, damp weather: cough intensifies, shortness of breath, the amount of sputum increases, malaise and fatigue appear. Body temperature is normal or subfebrile, hard breathing and dry wheezing over the entire pulmonary surface can be detected.

Diagnostics. A slight leukocytosis with a rod-nuclear shift in the leukocyte formula is possible. With exacerbation of purulent bronchitis, a slight change in the biochemical parameters of inflammation occurs (C-reactive protein, sialic acids, fibronogen, seromucoid, etc. increase). Sputum examination: macroscopic, cytological, biochemical. With severe exacerbation, the sputum becomes purulent in nature: a large number of neutrophilic leukocytes, an increased content of acidic mucopolysaccharides and DNA fibers, the nature of the sputum, predominantly neutrophilic leukocytes, an increase in the level of acidic mucopolysaccharides and DNA fibers, which increase the viscosity of the sputum, a decrease in the amount of lysozyme, etc. Bronchoscopy, with the help of which endobronchial manifestations of the inflammatory process are assessed, the stages of development of the inflammatory process: catarrhal, purulent, atrophic, hypertrophic, hemorrhagic and its severity, but mainly to the level of the subsegmental bronchi.

Differential diagnosis is carried out with chronic pneumonia, bronchial asthma, tuberculosis. Unlike chronic pneumonia, chronic bronchitis always develops from a gradual onset, with widespread bronchial obstruction and often emphysema, respiratory failure and pulmonary hypertension with the development of chronic cor pulmonale. On X-ray examination, the changes are also diffuse in nature: peribronchial sclerosis, increased transparency of the pulmonary fields due to emphysema, expansion of the branches of the pulmonary artery. Chronic bronchitis differs from bronchial asthma in the absence of asthma attacks; it is associated with pulmonary tuberculosis by the presence or absence of symptoms of tuberculosis intoxication, Mycobacterium tuberculosis in sputum, the results of X-ray and bronchoscopic examination, and tuberculin tests.

Treatment. In the phase of exacerbation of chronic bronchitis, therapy is aimed at eliminating the inflammatory process, improving bronchial patency, as well as restoring impaired general and local immunological reactivity. Antibiotic therapy is prescribed, which is selected taking into account the sensitivity of the sputum microflora, administered orally or parenterally, and sometimes combined with intratracheal administration. Inhalations are indicated. Use expectorants, mucolytic and bronchospasmolytic drugs, and drink plenty of fluids to restore and improve bronchial patency. Herbal medicine using marshmallow root, coltsfoot leaves, and plantain. Proteolytic enzymes (trypsin, chymotrypsin) are prescribed, which reduce the viscosity of sputum, but are currently rarely used. Acetylcysteine ​​has the ability to break disulfide bonds of mucus proteins and promotes strong and rapid liquefaction of sputum. Bronchial drainage is improved with the use of mucoregulators that affect secretions and the production of glycoproteins in the bronchial epithelium (bromhexine). In case of insufficient bronchial drainage and existing symptoms of bronchial obstruction, bronchospasmolytics are added to treatment: aminophylline, anticholinergic blockers (atropine in aerosols), adrenergic stimulants (ephedrine, salbutamol, Berotec). In a hospital setting, intratracheal lavages for purulent bronchitis must be combined with sanitation bronchoscopy (3–4 sanitation bronchoscopy with a break of 3–7 days). When restoring the drainage function of the bronchi, physical therapy, chest massage, and physiotherapy are also used. When allergic syndromes develop, calcium chloride and antihistamines are used; if there is no effect, a short course of glucocorticoids can be prescribed to relieve allergic syndrome, but the daily dose should not be more than 30 mg. The danger of activation of infectious agents does not allow long-term use of glucocorticoids. In patients with chronic bronchitis, complicated respiratory failure and chronic cor pulmonale, the use of veroshpiron (up to 150–200 mg/day) is indicated.

The food of patients should be high-calorie and fortified. Use ascorbic acid 1 g per day, nicotinic acid, B vitamins; if necessary, aloe, methyluracil. With the development of complications of a disease such as pulmonary and pulmonary-heart failure, oxygen therapy and auxiliary artificial ventilation are used.

Anti-relapse and maintenance therapy is prescribed in the subsiding phase of exacerbation, carried out in local and climatic sanatoriums, this therapy is prescribed during clinical examination. It is recommended to distinguish 3 groups of clinical patients.

1st group. It includes patients with cor pulmonale, severe respiratory failure and other complications, and loss of ability to work. Patients are prescribed maintenance therapy, which is carried out in a hospital or by a local doctor. These patients are examined at least once a month.

2nd group. It includes patients with frequent exacerbations of chronic bronchitis, as well as moderate dysfunction of the respiratory system. Such patients are examined by a pulmonologist 3–4 times a year, and anti-relapse therapy is prescribed in the fall and spring, as well as for acute respiratory diseases. An effective method of administering drugs is the inhalation route; according to indications, it is necessary to carry out sanitation of the bronchial tree using intratracheal lavages, sanitation bronchoscopy. In case of active infection, antibacterial drugs are prescribed.

3rd group. It includes patients in whom anti-relapse therapy led to a subsidence of the process and the absence of relapses for 2 years. Such patients are indicated for preventive therapy, which includes means aimed at improving bronchial drainage and increasing its reactivity.

From the book Hospital Pediatrics: Lecture Notes by N.V. Pavlova

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

Classification is made according to various criteria.

The following forms are distinguished along the flow:

  1. (the illness usually lasts 2-3 weeks, after which recovery occurs).
  2. (this form characterizes acute bronchitis, which lasts more than 3 weeks).
  3. (the diagnosis is made if the patient has signs of bronchitis for at least 3 months a year over a 2-year follow-up period).
  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 ““).

Depending on the degree of distribution, the following are distinguished:

  • limited;
  • widespread;
  • diffuse.

According to the type of inflammatory manifestations, bronchitis is:

  1. Catarrhal.
  2. Serous-purulent.
  3. Hemorrhagic.
  4. Ulcerative.
  5. 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. . It acquires a productive character, that is, sputum begins to cough up.

A characteristic sign 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 urine analysis.
  2. Microscopic examination of sputum (including examination for the presence of the causative agent of tuberculosis).
  3. Sputum culture for microflora.
  4. Biochemical analysis.

Differential diagnosis

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

  • pneumonia;
  • 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.