Monthly Archive December 2019

Acute bronchiolitis

This is an acute respiratory disease, mainly in children of the first year of life, accompanied by obstructive damage to the bronchi and bronchioles.

Etiology of acute bronchiolitis

The causative agent is a virus, especially respiratory syncytial, less often – parainfluenza virus, adenovirus, influenza virus and pneumonia mycoplasma. The etiological role of bacteria is also taken into account. There is an opinion that bronchiolitis is the result of an allergic reaction similar to that in bronchial asthma (a meeting of the respiratory syncytial virus with circulating immunoglobulins). It is impossible to exclude the importance of allergy, since more than 50% of children who have undergone bronchiolitis, subsequently experience bronchospasm and many develop bronchial asthma. A high frequency of allergic manifestations in the immediate family is also detected.

The pathogenesis of acute bronchiolitis

The disease is characterized by the development of respiratory failure due to obstruction in the small bronchi and bronchioles. There is a narrowing of their lumen as a result of thickening of the wall, swelling and infiltration of the mucous membrane. In addition, a large amount of pathological secretion is contained in the lumen of the small bronchi and bronchioles. In the development of obstruction, bronchospasm is also important, although it is not dominant.

Clinic of acute bronchiolitis

The disease begins suddenly, but there is a gradual development. Rhinitis, sneezing and coughing, sometimes paroxysmal, appear.
The general condition of the child can be severe from the first days, sleep worsens, appetite decreases, the child becomes irritable, and sometimes vomiting occurs. Body temperature can be febrile, subfebrile, even normal, but often from the first days of the disease reaches 39 ° C and above. The main symptoms are respiratory failure with an extended expiration (breathing quickens to 60 – 80 in 1 min) and tachycardia (pulse 160 – 180 in 1 min). When examining a patient, cyanosis of the nasolabial triangle, bloating of the wings of the nose, participation in the act of breathing of the supple parts of the chest are determined. In connection with bloating, a boxed shade of pulmonary sound is determined, a decrease in the area of ​​blunting of percussion sound over the liver, heart and mediastinum. Sometimes when examining the chest, it is possible to detect an increase in its anteroposterior diameter. The liver and spleen protrude 2-4 cm below the costal arches, which, apparently, is associated with their displacement as a result of bloating of the lungs.

Auscultation against the background of weakened breathing of both lungs, both on inspiration and on exhalation, multiple finely bubbly are determined, less often – in other parts of the lungs – medium or large bubbly rales. Sometimes wet rales disappear and dry, sometimes whistling, appear instead.

With bronchiolitis, there are violations of water-electrolyte metabolism due to intoxication and vomiting, increased water loss, and often develop exsicosis.

In the blood, usually pronounced changes, with the exception of the sometimes detected lymphopenia, are not determined. The presence of leukocytosis with a shift in the leukocyte count to the left is suspicious of pneumonia.

An X-ray examination reveals bloating, which is manifested by an increase in the transparency of the pulmonary fields. In contrast to pneumonia, there are no areas of continuous infiltration with bronchiolitis.

Differential diagnosis of acute bronchiolitis

Differential diagnoses of bronchiolitis are carried out with pneumonia, which is characterized by the identification of bronchial breathing, bronchophony, crepitating wheezing and localization of the pathological process in any part of the lung.
To distinguish bronchiolitis from attacks of bronchial asthma, anamnestic data are taken into account (history of asthma attacks, their occurrence unrelated to infection, etc.). Use bronchodilators (0.1% solution of adrenaline, etc.), which relieve or alleviate an attack of bronchial asthma and almost do not affect obstruction in bronchiolitis.

Treatment of acute bronchiolitis

Antibiotics are prescribed (methicillin, oxacillin, carbonicillin, kefzol, gentamicin, etc. – p. 232), since from the first hours of the disease it is possible to attach a secondary bacterial infection. The use of interferon is also shown. To reduce the swelling of the mucous membrane of small bronchi and bronchioles, inhalations of 0.1% adrenaline solution (0.3 – 0.5 ml in 4 – 5 ml of isotonic sodium chloride solution) are used 1-2 times a day.
Oxygen therapy is shown, best with the use of an oxygen tent DKP-1. In its absence, oxygen is introduced using the Bobrov apparatus (for the purpose of moisturizing) every 30 to 40 minutes for 5 to 10 minutes with moderate pressure on the oxygen cushion. In order to liquefy the secretion in the bronchi, 2% sodium bicarbonate solution, isotonic sodium chloride solution, etc. are simultaneously administered as aerosols.
When signs of exicosis appear, intravenous drip of liquids is indicated.
Sometimes it is effective to use antispasmodics – aminophylline, ephedrine and antihistamines – glycocorticoids.
Tachycardia, dull heart sounds, enlarged liver are the basis for intravenous use of strophanthin, corglycon.
Of great importance are rational nutrition and sanatorium-hygienic regimen.

The prognosis of acute bronchiolitis

The outcome is almost always favorable. Of the complications, bacterial pneumonia is most common.
Prevention SARS warning. 

Bronchiectatic disease

Bronchiectasis is an irreversible expansion of the bronchi caused by destructive changes in the bronchial wall. The main manifestations of bronchiectasis are cough with purulent sputum, hemoptysis, relapse of bronchopulmonary infection.  

Etiology and pathogenesis of bronchiectasis

The leading role in the development of bronchiectasis belongs to bronchopulmonary infections – bacterial (Staphylococcus aureus, Klebsiella, Pfeiffer’s bacillus, Mycobacterium tuberculosis), Viral (adenovirus, influenza, measles), fungal, mycoplasma. Of great importance is also a violation of the clearance (cleansing) of the bronchial tree as a result of bronchial obstruction or impaired mucociliary transport. Bronchial obstruction is observed with aspiration of foreign bodies, neoplasms of the respiratory tract (laryngeal papillomatosis, bronchogenic lung cancer), an increase in bronchopulmonary lymph nodes (with sarcoidosis, tuberculosis, histoplasmosis), as well as chronic obstructive pulmonary diseases (bronchial asthma, chronic bronchitis). Violation of mucociliary transport can be caused by damage to the cilia (fixed cilia syndrome, of which Kartagener syndrome is a variation – the reverse location of organs, sinusitis, bronchiectasis) or a change in the properties of bronchial secretion (with cystic fibrosis, ai-antitrypsin deficiency). Bronchiectasis occurs in patients with immunodeficiency (congenital agammaglobulinemia, acquired deficiency of class A and G immunoglobulins), congenital anatomical defects of the tracheobronchial tree (tracheobronchomegaly, tracheoesophageal fistula), blood (pulmonary aneurysm) and lymphatic vessels. Recurrent aspiration pneumonia in chronic alcoholism, neurological disorders, inhalation of irritating substances (nitrogen oxides, hydrocarbons, silicates), as well as amyloidosis of the trachea and bronchi can cause the disease.    

Mostly medium-sized bronchi expand, less often – distal bronchi and bronchioles. Necrosis with subsequent partial replacement of fibrous tissue undergoes all layers of the bronchi. Depending on the degree of expansion of the bronchi, cylindrical, varicose and saccular bronchiectases are distinguished . Cylindrical bronchiectasis is characterized by moderate (sometimes reversible) expansion of the bronchi, which does not lead to significant deformation or impaired division of the bronchial tree. With varicose bronchiectasis (resembling varicose veins on bronchograms), moderate dilatation and deformation of the bronchi and a decrease in the number of divisions of the bronchial tree are observed. The most severe form is saccular bronchiectasis, which initially affects mainly the proximal (central) bronchi, and subsequently leads to the destruction and fibrosis of the distal bronchi and the formation of pus-filled “bags” on the periphery of the lung. Typically, bronchiectasis develops in the posterior basal segments of the lower lobes of both lungs and the middle lobe of the right lung. The occurrence of bronchiectasis in the upper parts of the lungs is possible with tuberculosis or an abscess. 

Clinic of bronchiectatic disease

The main manifestations are persistent cough with the separation of a large amount of purulent sputum, hemoptysis, repeated pneumonia, which are usually localized in the same segment or lobe of the lung. Coughing may intensify when the patient is lying down or when the body position changes, which is associated with leakage of secretion into large bronchi. Sometimes (especially after a course of antibiotic therapy) a cough becomes unproductive, sputum becomes a mucous membrane. In the period of exacerbation of sputum, as a rule, two to three layers. An admixture of blood is often found in sputum, which is caused by destructive processes in the bronchi and destruction of the walls of blood vessels. Sometimes pulmonary hemorrhages become the leading manifestation of the disease. With frequent exacerbations of the disease, anorexia, weight loss, fatigue, weakness, anemia are observed. A characteristic symptom of bronchiectasis is persistent voiced, small-bubbly moist rales over the affected area of ​​the lung. The auscultatory picture above the remaining parts of the lungs may reflect the presence of concomitant chronic bronchitis: breathing with prolonged expiration, dry rales. During an exacerbation of the disease, percussion is determined by a mildly expressed dullness of sound in the area of ​​inflammation, more often – a boxed shade of percussion sound in connection with the development of emphysema. Often there are drum fingers. Chronic obstructive bronchitis and pulmonary emphysema, which determine the progression of respiratory failure, should be considered complications; pulmonary heart; metastatic abscesses of the brain; amyloidosis; pulmonary hemorrhage. 

Diagnosis and differential diagnosis of bronchiectasis

Bronchiectasis is suspected in patients complaining of a constant productive cough, often accompanied by hemoptysis, as well as with recurrent pneumonia affecting the same segments or lobes of the lung. Differential diagnosis is carried out with chronic bronchitis, tuberculosis and lung abscess. X-ray with bronchiectatic disease, depending on the volume and nature of the lesion, it is possible to identify unchanged lung tissue, increased and (or) deformation of the pulmonary interstitial pattern, cystic formations with a diameter of 1-2 cm, often with levels liquids. In recent years, computed tomography has been widely used in the diagnosis of bronchiectasis. The presence of bronchiectasis is confirmed by bronchography, which allows to determine their prevalence, size and shape. Bronchography should be performed in patients with unchanged radiographs (without exacerbation of the disease), as well as with local bronchiectasis to solve the issue of surgical intervention. Bronchoscopy may be useful to determine the cause of bronchial obstruction, the presence of anatomical defects, localization of bleeding sources or foreign bodies. external respiration reveals signs of bronchial obstruction, and with a common process – a decrease in VC. In the period of exacerbations of the disease in the blood can observe leukocytosis with a shift of the leukocyte formula to the left, an increase in ESR, hypochromic anemia are given. Of great importance for establishing a diagnosis and determining treatment tactics is the study of sputum, especially its sowing and staining of smears to identify the pathogen. hired for pneumonia). Therapy with antibacterial drugs is recommended to be carried out already at the beginning of any viral infection of the upper respiratory tract (without waiting for an exacerbation of bronchopulmonary infection), as well as annually in winter. An important link in the treatment is to improve the drainage of the bronchi – breathing exercises, chest thumping, taking mucolytic drugs, positional drainage. Bronchoscopy is indicated only for removal of a foreign body or elimination of bleeding and should not be used for therapeutic purposes to remove secretions or endobronchial administration of antibiotics. Surgical interventions are possible in the presence of local bronchiectasis, as well as to stop bleeding. A complete diet rich in proteins and vitamins, sufficient drinking is required . Prevention of bronchiectasis – timely adequate treatment of bronchopulmonary infection, elimination of factors predisposing to the development of bronchiectasis. 

Acute bronchitis

Etiology of acute bronchitis

The causative agents of the disease are influenza virus, parainfluenza, respiratory syncytial virus, adenovirus, pneumonia mycoplasma, streptococcus, pathogenic staphylococcus, pneumococcus, Afanasyev-Pfeiffer coli or a combination of virus and microbes. It is important to consider the role of endogenous microbial invasion, especially staphylococcal, which occurs most often against the background of influenza or adenovirus infection.
Bronchitis or tracheobronchitis may be the initial manifestation of measles, less commonly whooping cough and other childhood infections.
The predisposing factors for the occurrence of bronchitis are the following: hypothermia, defects in care (inadequate stay of the child in fresh air, clothing not suitable for the weather, etc.), air pollution with industrial dust and rooms in which children are located, with tobacco smoke.

Pathomorphology of acute bronchitis

Depending on the etiological factors, more or less pronounced pathomorphological changes occur. So, tracheobronchitis in influenza is characterized by hemorrhages in the mucous membrane of the bronchi and the presence of fibrinous effusion. With parainfluenza, pillow-like growths of the epithelium are found, mainly in the small bronchi, narrowing their lumen. With adenovirus infection, mucus on the mucous membrane is noted. In the wall of the bronchus, round-cell infiltrates are formed. With respiratory syncytial infection, changes in the small, medium bronchi and bronchioles are most pronounced. Characterized by an abundance of foamy semi sputum. Microscopically determined a certain increase in epithelial cells, their reproduction with the formation of multinuclear papillary growths, occupying a significant part of the lumen of the bronchus. In bacterial bronchitis, infiltration of the mucous membrane by polynuclear cells and lymphocytes is microscopically detected; in severe cases, the formation of a fibrinous film.

Clinic of acute bronchitis

The onset is acute. The temperature rises to subfebrile, but often its short (1 – 2 days) increase to 38 – 39 ° С is observed. The main symptom is a cough, worse at night. At the beginning of the disease, a cough is dry, sometimes paroxysmal in nature, may be accompanied by vomiting. On the 3rd – 4th day of the disease, sputum mucus begins to discharge, later replacing purulent. Older children complain of chest pain and tightness, headache, sleep disturbance.

In acute (non-spastic) bronchitis in the first days of the disease, scattered dry rales are heard, on the 3rd – 5th day the rales become wet. Sometimes wet rales are heard at a distance both on inhalation and on exhalation, you can also hear small bubbling rales, which differ from the rales in diffuse pneumonia. Localization of changes in bronchitis is mainly bilateral. With unilateral auscultatory changes, pneumonia should be excluded, although unilateral bronchitis is observed even in young children (S.V. Rachinsky et al., 1978). Percussion changes are usually not.

On the 6th – 8th day of the disease, cough decreases, body temperature normalizes, wheezing disappears in the lungs; recovery comes.
Bronchitis can occur not only from the first days of an acute respiratory viral infection, but at a later date in connection with the addition of a secondary bacterial infection. The clinical picture of the disease in such cases changes: the general condition worsens, body temperature rises, cough intensifies, moist large and medium bubbling rales appear in the lungs. In infants and young children, the disease can be complicated by pneumonia. In uncomplicated bronchitis, there is no marked respiratory failure. In infants, breathing can increase up to 60 in 1 min, accompanied by a slight participation in the act of breathing of the supple parts of the chest in the absence of cyanosis.

Radiologically in acute bronchitis, a symmetrical increase in the pattern of the lungs is detected mainly in the basal and lower medial zones. The enhancement of the pattern is also determined along the bronchovascular structures, which is a consequence of vascular hyperemia and increased lymph production mainly in the peribronchial spaces. These reactive changes in the lungs last longer than the clinical manifestations of bronchitis.
A separate clinical variety of acute bronchitis is spastic bronchitis (bronchitis spastica).

The main pathogenetic essence of spastic bronchitis is a narrowing of the lumen of the bronchi, a violation of their patency, due to vaso-secretory changes that occur under the influence of acute respiratory viral infections. Due to inflammatory changes, the mucous membrane of the bronchi thickens, becomes swollen and swollen, in the lumen of the bronchi there is an abundant accumulation of mucus, sometimes viscous. These changes are the cause of the development of obstructive syndrome. It is possible that viral bacterial allergy is important in the mechanism of the occurrence of spastic bronchitis, as 5-30% of such patients subsequently develop bronchial asthma.

In connection with obstructive disorders, tracheobronchial resistance to air flow increases, especially on exhalation, with its subsequent delay in the lungs and the development of functional emphysema, determined radiologically as bloating of the lungs.
Spastic bronchitis is most common in children of the second half of life and differs from bronchiolitis in a lower degree of respiratory failure due to damage to the bronchi of a larger caliber. Breathing becomes moderately rapid. The clinical picture of the disease is dominated by signs of expiratory difficulty breathing, although in infants there is an involvement in the act of breathing of the supple parts of the chest, which may also indicate difficulty in breathing.
In addition to expiratory difficulty breathing, coughing and wheezing noisy breathing are observed. Auscultation of dry wheezing is determined. Percussion in connection with the phenomena of emphysema is a boxed shade of sound.

Spastic bronchitis in most cases ends in recovery within 5 to 10 days, simultaneously with acute respiratory viral infections, sometimes delayed up to 2 to 3 weeks. More severe forms of spastic bronchitis can be complicated by bronchiolitis.

Significant differential diagnostic difficulties, especially in infants and young children, arise between spastic bronchitis due to airway obstruction as a result of a response to infection and an asthmatic component that complicates pneumonia. For this purpose, it is important to take into account anamnestic data indicating the manifestation of allergy during acute respiratory viral infections in the past, the presence of drug allergy, exudative diathesis, hereditary allergy, etc.

The diagnosis of acute bronchitis is established on the basis of diffuse lesion (physical changes on both sides). Pneumonia is characterized by the presence of physical changes over a limited area of ​​the lung. If pneumonia occurs against the background of diffuse bronchitis or simultaneously with it, the deterioration of the general condition of the child, the identification of limited areas of shortening of percussion sound and changes in auscultation data are taken into account. X-ray with pneumonia revealed infiltrative changes in the lung tissue.

Treatment of acute bronchitis

In acute bronchitis, it is necessary to systematically ventilate the ward or room in which the patient is located. Given that the disease can be caused by a viral bacterial or bacterial infection, antibiotics are indicated for children, especially for infants and infants (ampicillin, oxacillin, methicillin, ampiox, carbenicillin, kefzol – p. 232). With viral etiology bronchitis, the use of antibiotics is less justified, although in such cases they can be effective in order to prevent bacterial complications.

Children older than three years and with a mild course of acute bronchitis can be prescribed bactrim, erythromycin, oleandomycin phosphate, sulfonamide drugs (0.15 – 0.1 g / kg / day for 4 or 6 doses).
When applying symptomatic therapy, it is important to take into account that in patients with profuse sputum, antitussive agents can make it difficult to evacuate and worsen bronchial obstruction.
If there is a thick viscous secretion in the tracheobronchial ducts, measures are shown that contribute to its dilution and evacuation. To dilute sputum, reduce inflammatory edema of the bronchial mucosa, inhalations of 1–2% sodium bicarbonate solution are prescribed 2–3 times a day. Humidification and warming of the inhaled air is shown, best of all with the help of ultrasonic humidifiers, aeroionizers, aerosol devices. If they are absent, central heating radiators are used to humidify the air in the room where the patient is located, covering them with a wet, thick cloth.

Apply therapeutic baths for 5 to 10 minutes, daily increase the water temperature from 37 ° C to 40 ° C, warm wraps, distracting agents (mustard, jars, mustard foot baths), warm drink, expectorant medicines, etc.
With an abundance of sputum, postural drainage, contributing to the outflow of it from the affected bronchi. The patient is in Quincke position (with the head down) for 15 to 20 minutes (intermittently). In this position, coughing movements are desirable. The procedure is repeated 2 to 3 times a day. The effectiveness of the drainage increases when it is combined with a vibration massage, which in older children is performed by patting the chest over the affected area with a palm folded in a “boat”. In young children, this procedure is performed by applying rhythmic hits with the ends of the fingers of one hand on the chest or on the finger of the other hand, located along the intercostal space.

To relieve bronchospasm, aminophylline and ephedrine are used. Eufillin is administered orally in a single dose of 2–4 mg / kg 2–3 times a day, intravenously in the form of a 2.4% solution at the rate of 0.1–0.15 ml / kg, but not more than 5–7.5 ml in 150 – 200 ml of 5% glucose solution. Ephedrine is prescribed orally for children up to 1 year old – at 0.002 – 0.003 g; 2 – 5 years – 0.003 – 0.01 g; 6 – 12 years old – 0.15 – 0.02 g; older – 0.025 g 2 to 3 times a day. Prescribe combined powders of ephedrine, diphenhydramine and aminophylline in age doses.

The prognosis of acute bronchitis is favorable, but complications are possible – bronchiolitis, pneumonia. Prevention of acute bronchitis boils down to the prevention of acute respiratory viral infections and increase nonspecific resistance of the body by hardening, proper care of the child, compliance with the indoor air regime, rational nutrition, etc. 

Bronchial asthma due to physical stress

Bronchial asthma due to physical stress is a variant of bronchial asthma, characterized by the obligatory development of asthma attacks 1-10 minutes after exercise. Asthma due to physical stress is especially often observed in children.

Etiology of bronchial asthma due to physical exertion

The type of physical activity matters. Most often, asthma attacks occur when running, playing soccer, basketball, mountain climbing, less often – with intermittent loads (weight lifting); swimming is well tolerated. The formation of an attack is more affected by the duration of the load than its intensity.

Pathogenesis of bronchial asthma due to physical stress

In connection with the rapid and complete reverse development of asthma attacks due to physical stress, it is believed that bronchial obstruction is caused by bronchospasm without the presence of inflammation, swelling, and mucus secretion. Bronchospasm is not associated with immunological mechanisms. In the pathogenesis of asthma attacks due to physical stress, various regulatory disorders are expected to be involved: a relative decrease in the functions of adrenergic B receptors due to the hyperreactivity of adrenergic a receptors in combination with the peculiarities of the release of catecholamines during exercise. The participation of adrenergic mechanisms is confirmed by the effectiveness of adrenergic drugs (3-stimulating in the prevention and relief of bronchospasm induced by physical stress, as well as by provoking bronchospasm with a-adrenoreceptor stimulants and the preventive effect of a-blocking adrenergic drugs in people who are sensitive to stress; isolation of mediators of immediate allergy, which is proved by the following facts: the presence of a refractory period after an attack (depletion of copper reserves is assumed tori under load); Protective effect Intalum and calcium antagonists preventing mast cell degranulation, and antihistamines; sensitization cells of patients to degranulation and release of mediators; hyperstimulation irritant vagal receptors due to rapid cooling of the upper respiratory tract and hyperventilation during the loading process Participation. of these mechanisms is confirmed by: a pronounced correlation between the sensitivity of the bronchi to vagotonic agents and to physical. stress; the preventive effect of atropine and lidocaine (pharyngeal ring anesthesia); increased sensitivity of the bronchi to anticholinergics in some patients; heat loss during breathing. It is assumed non-immunological stimulation of the release of mediators due to mechanical irritation (body shake during exercise), direct action of physical. factors, in particular cooling, on the peripheral respiratory tract, the effect of catecholamines and acetylcholine. In the genesis of bronchospasm on physical. metabolic acidosis and impaired fatty acid utilization also matter . The central and peripheral airways are involved in the pathological reaction to the load, however, obstruction of the large bronchi most often dominates.

Clinic of bronchial asthma due to physical stress

Attacks of suffocation induced by physical. load, mainly observed in atopic asthma and are not observed in chronic bronchitis. They occur 1-2 minutes after the load is stopped and in mild cases they stop spontaneously after
5-10 minutes (increase in individuals within 30-60 minutes), in severe cases, the attack begins during the load and lasts more than 1 hour (without treatment ); bronchospasm progresses with alternating different loads with an interval of less than 1 hour. The initial condition of the patient is not critical: in sensitive individuals, an attack may appear during complete remission, while in resistant individuals it does not develop even with initial bronchial obstruction. The initial level of obstruction affects the severity of bronchospasm, which can be short-term and asymptomatic (subclinical form of bronchial asthma due to physical stress) in 25% of cases, especially in children, moderate bronchospasm is observed in 25-30% of patients, and severe bronchospasm in 15-25%.

Diagnosis of bronchial asthma due to physical stress

Reaction to physical. the load is established using clinical observation and pulmonary function tests, studied before and after the standard load –
6-8 minutes of running on the treadmill (p-stimulating adrenergic drugs are canceled in 3-4 hours, intal is removed in 8-12). A decrease in FVC1 by more than 15% of the initial level indicates the development of bronchospasm. In the first 24 minutes, FVC increases, then decreases, reaching 40-50% of the initial value in individuals. In mild cases, two-, three-fold testing is necessary before a reaction is detected. Diagnostic value is the constant nature of the reaction – the mandatory occurrence of bronchospasm on the physical. voltage. Load tests are not performed for concomitant heart diseases.

Treatment of bronchial asthma due to physical exertion

Attacks of suffocation due to physical. loads can prevent aerosols of adrenergic drugs that stimulate p2-adrenergic receptors, intala, methylxanthines (the latter are prescribed 30 minutes before the load, intal – immediately before or at the same time as the load).
Glucocorticosteroid drugs are relatively ineffective. In certain cases, certain sports are allowed (swimming). Before sports, it is recommended
to prophylactically take theophylline and intal, the appointment of p-stimulating adrenergic drugs is prohibited. Recently, reports appeared about the effectiveness of calcium antagonists (nifedipine, 20 mg sublingually) and a-adrenergic receptors (prazosin, 2 mg, inhalation).

Bronchial asthma

Bronchial asthma is a disease characterized by the development of reversible bronchial obstruction under the influence of various stimuli and caused by hyperreactivity of the bronchi. With bronchial astmenus, a triad of clinical symptoms is observed – asphyxiation, cough and shortness of breath, in a small part of patients the only manifestation of the disease may be a paroxysmal cough. More often, young people are sick: in half of patients, asthma develops in childhood, in 1/3 – under the age of 40. There is no single classification of bronchial asthma. Two main types of bronchial asthma are distinguished – exogenous (atopic, allergic) and endogenous, which is believed to be caused by non-immune mechanisms. Endogenous bronchial asthma includes asthma of physical effort, aspirin psychogenic, infectious, hypereosinophilic asthma, asthma associated with environmental pollution, as well as many cases of occupational bronchial asthma. The main differences between the two types of bronchial asthma are given below.

Etiology and pathogenesis of bronchial asthma

To date, the most fully studied mechanisms of development of atopic bronchial asthma. An allergen (pollen, house dust, fungal spores, food, medicines), when ingested, causes the production of antibodies of the IgE class, which are fixed on the membrane of mast cells. With repeated exposure to the allergen, antibodies combine with it, causing mast cells to release a number of biologically active substances – histamine, eosinophilic anaphylaxis factor, neutrophilic chemotactic factor. Following degranulation, mast cells synthesize a slow-reacting anaphylaxis substance (which includes leukotrienes), a platelet activating factor and, possibly, prostaglandins, some mast cell mediators (histamine, most leukotrienes, prostaglandins E1 and E2, platelet activating factor) cause bronchospasm increase vascular wall permeability and mucus secretion. Others (eosinophilic, lymphocytic, neutrophilic chemotactic factors, leukotriene B4) attract neutrophils, lymphocytes, eosinophils and thrombodites.

In recent years, new data have been obtained that better understand the role of mediators in the occurrence of bronchial asthma. The metabolism of arachidonic acid 5 and the synthesis of slow-reacting anaphylaxis substances were studied. Arachidonic acid is a product of the phospholipid membrane of a mast cell activated by a phospholipase under the influence of the antigen-antibody reaction. There are two ways of converting arachidonic acid – cyclooxygenase, which results in the formation of prostaglandins E2 and E2a and thromboxanes, and lipoxygenase, leading to the synthesis of leukotrienes, some of which form slowly reactive anaphylaxis substances. Leukotrienes and thromboxanes have a stronger effect on the smooth muscles of the bronchi than histamine and prostaglandins, while their point of application is mainly small bronchi.

It is assumed that the process of bronchial obstruction passes through two phases, the first, which occurs several minutes after inhalation of the allergen and lasts from 30 to 60 minutes, due to mediators that directly act on the vessels and bronchial wall; the second (repeated wave of bronchial obstruction several hours after the end of the first phase) is caused by the action of chemotactic factors and the effector cells attracted by them. The leading role in this period is played by eosinophils, the proteins of which damage the ciliary epithelium of the respiratory tract and increase the permeability of the mucous membrane, bronchi for allergens. At the same time, eosinophils secrete substances that inhibit histamine, platelet activating leukotrienes. Factor release of bronchospasm mediators depends on the ratio of cAMP and cGMP content in mast cells. cAMP inhibits the release of histamine, slow-reacting anaphylaxis, other mediators, while cGMP has the opposite effect. B-adrenoreceptors are known to activate adenylate cyclase, which is involved in the synthesis of cAMP. Drugs that stimulate a-adrenergic receptors increase the content of intracellular cAMP, which is destroyed by phosphodiesterase. Methylxanthines, potent phosphodiesterase inhibitors, also increase cAMP levels in cells. The synthesis of cAMP is enhanced by the excitation of H2 receptors and prostaglandin receptors, which respond to increased levels of histamine and other mediators. Cholinergic receptors are responsible for the activation of guanyl cyclase, which is involved in the synthesis of cGMP, so cholinolytic agents can also prevent the release of mediators. The role of calcium ions in the occurrence of bronchospasm is not fully understood. Moving them from the outer membrane of the cell and dealing with the cytoplasm is a sign of mast cell activation. It is also known that a decrease in the content of calcium ions in the smooth muscle cells of the bronchi contributes to the expansion of the latter.

The pathogenesis of endogenous bronchial asthma is not well understood. In development, it attaches importance to violations of the parasympathetic innervation of the bronchial tree, leading to the development of bronchospasm and a change in the secretion of bronchial glands, as well as a decrease in the threshold of sensitivity of the vagus nerve receptors to irritants. However, it is not possible to explain the development of various forms of endogenous bronchial asthma using a single hypothesis.

In the pathogenesis of asthma, physical effort suggests the importance of cooling the bronchial tree as a result of hyperventilation and inhalation of cold air. In this case, the excitation of specific temperature receptors in the airways that respond to a decrease in temperature occurs. Other mechanisms for the development of this form of asthma are discussed, in particular, IgE-independent mast cell degranulation with the release of mediators, activation of cholinergic receptors.

Exacerbation of bronchial asthma can be triggered by an infection of the upper respiratory tract, and the main role in the occurrence of bronchospasm is played not by bacteria, but by viruses (influenza, parainfluenza). Possible causes of bronchospasm are virus replication in the epithelium of the respiratory tract, causing cell damage and the release of arachidonic acid metabolites, as well as a decrease in the sensitivity threshold of bronchial tree receptors to various external stimuli under the influence of a viral infection, “Aspirin” or prostaglandin, asthma is observed in patients with polyposis nasal cavity and intolerance to acetylsalicylic acid, indomethacin, phenacetin or yellow food coloring (yellow tartrazine). Its development is associated with a violation of the synthesis of prostaglandins and an increase in the synthesis of leukotrienes due to a violation of the metabolism of arachidonic acid under the action of acetylsalicylic acid and its derivatives.

Occupational bronchial asthma occurs when in contact with various substances: 1) metal salts (chromium, nickel, manganese); 2) wood (dust of pine, oak) and vegetable (cotton, linen) dust; 3) industrial chemicals (phthalic anhydride, ethylenediamine, formaldehyde); 4) drugs (antibiotics, cimetidine, piperazine); 5) enzymes; 6) animal proteins (bird droppings, fish isolations, beekeeping products). Occupational factors can induce an immune response (metal salts, animal proteins, certain types of plant dust), act on specific cellular receptors (cotton, a substance that promotes the release of histamine, organophosphorus insecticides with anticholinesterase effects) and irritate, causing inflammation mucous membrane of the bronchi (silicon dioxide, ammonia, hydrochloric acid). Psychogenic bronchial asthma was described as early as the 17th century. In its pathogenesis, an increase in vagus nerve activity plays a role.

Bronchial asthma resulting from environmental pollution has become widespread in recent years. In its pathogenesis, along with the effect on the bronchial mucosa of irritating substances that pollute the atmosphere (sulfur oxides, ozone, carbon oxides, nitrogen dioxide), bronchial hyperreactivity plays a role. Hypereosinophilic bronchial asthma is also distinguished, which may be one of the manifestations of periarteritis nodosa (asthmatic variant). Its peculiarity is the presence of a large number of eosinophils in the blood (40-60% or more) and sputum.

Clinic of bronchial asthma

In most patients, asthma attacks begin with an unproductive cough. Usually they occur upon contact with allergen 1} at night, after exercise, in the cold, when inhaling substances with irritating properties or a pungent odor. Attacks can last up to several hours and stop on their own or under the influence of treatment. The end of the attack is preceded by the discharge of sputum in the form of mucous plugs. During an attack of suffocation, exhalation is difficult, wheezing can be heard at a distance during both phases of the respiratory cycle; with a more severe attack, an increase in shortness of breath is sometimes accompanied by a decrease or disappearance of wheezing. The patient occupies a forced position – he usually hoarsens, resting his hands on his knees or the edge of the bed and thus fixing the shoulder girdle. The auxiliary muscles actively participate in the act of breathing; the chest is enlarged (“swollen”), its anteroposterior dimensions are enlarged, percussion sound with a box-like tint or box-like sound, the lower borders of the lungs are omitted; sharply elongated exhalation and a large number of dry rales are heard in the lungs, after the discharge of sputum, the exhalation is shortened, the number of dry snores decreases, but the last two symptoms can persist for some time after the attack of suffocation.

Frequent asthma attacks or in time an uncured, prolonged asthma attack can go into asthmatic status (status asthmaticus). In many patients, the development of it is preceded by uncontrolled (up to tens of times) use of inhalers of B-adrenergic agonists (drug blockade of B-adrenergic receptors). Asthmatic status is characterized by an increase in bronchial obstruction with tachypnea and shallow breathing and the lack of effect in the treatment of adrenomimetic drugs. As a result of the formation of mucous plugs, clogging the lumen of the boronchus and disrupting the conduct of sound to the surface of the chest, the sonority and the number of dry rales are reduced (until they disappear, the “dumb” lung). The progression of respiratory failure leads to the development of decompensated respiratory acidosis and hypercapnia. Death occurs with hypoxemic coma due to paralysis of the respiratory center. Bronchial asthma can be complicated by obstructive pulmonary emphysema, pulmonary heart, pneumothorax, pneumomediastinum.

Diagnosis and differential diagnosis of bronchial asthma

Eosinophilia is detected in the blood during attacks of suffocation or with their increased frequency. With atopic bronchial asthma, the level of IgE is increased in the blood. Kurshman spirals (elements of mucus), Charcot-Leiden crystals (decay products of eosinophils), a large number of eosinophils are found in sputum. An X-ray examination of the chest organs increased the transparency of the pulmonary fields. In severe cases, atelectasis may develop due to obstruction of the bronchi with mucous plugs.
Examination of the function of external respiration is an important method for determining the severity of an attack, as well as the effectiveness of the treatment used. In the acute period, there is a significant decrease in FEV1, other speed indicators, in addition, a decrease in VC and an increase in residual lung volume can be recorded. In the interictal period, especially at the beginning of the disease, only a decrease in FEV1 is detected . In patients with a severe or protracted attack of suffocation, hypoxemia is observed, usually accompanied by hypocapnia, and an increase in the pH of arterial blood. Hypocapnia and respiratory alkalosis are caused by hyperventilation. Normalizing or increasing PaCO2, indicating severe bronchial obstruction or progressive respiratory failure, is considered a poor prognostic symptom.

Bronchospastic syndrome also occurs in congestive heart failure (cardiac asthma), pulmonary thromboembolism, chronic bronchitis, and airway volume formations. Attacks of shortness of breath with cardiac asthma occur when lying down and can be stopped with nitroglycerin. Cough usually does not appear at the beginning, but at the end of the attack. During auscultation of the lungs, moist rales are heard, mainly in the lower sections. Distinctive features of recurrent thromboembolism of the pulmonary artery are pleural pain, signs of overload of the right heart chambers (ECG). Crucial for the diagnosis are the data of scanning and angiography of the lungs. Volumetric formations of large bronchi (tumors, polyps, foreign bodies) are detected using bronchoscopy and X-ray examination. For chronic asthmatic bronchitis, a long-term cough is characteristic. Eosinophilia is not observed; there are no elements of bronchial asthma in sputum.

Bronchiectasis in children

Bronchiectasis is an irreversible local expansion of the bronchi, accompanied by infection.

Etiology and pathogenesis of bronchiectasis

The disease is polyetiological. The main factors contributing to the formation of bronchiectasis: congenital lung defects; recurrent non-specific inflammatory diseases of the respiratory system; childhood infectious diseases (measles, whooping cough) foreign bodies of the tracheobronchial tree, tuberculosis, some hereditary diseases and systemic lesions (cystic fibrosis, Cartagener syndrome, agammaglobulinemia); bacterial destruction of the lungs. There are various theories of the pathogenesis of bronchiectatic disease. Some authors consider the main significance of chronic bronchitis, others consider pneumosclerosis to be primary, and others – malformations and inferiority of the bronchopulmonary system. The main importance in the pathogenesis of bronchiectasis is the interaction of two factors: the inflammatory process and the violation of the drainage function of the bronchi. An important role in the occurrence of bronchiectasis is played by atelectases of various genesis (congenital, aspiration, pneumonic, with foreign bodies, bronchial tumors, with cystic fibrosis, with compression by bronchial lymph nodes). It is not excluded that nasopharyngeal diseases (rhinosinusopathies) are associated with bronchiectasis. With joint inflammation of the nasopharynx and lungs, a reactive increase in the lymph nodes of the submandibular region, neck, mediastinum, paratracheal and bronchopulmonary arises. Enlarged lymph nodes are not only a source of infection, but also a factor that disrupts pulmonary blood flow, which contributes to the development of chronic pneumonia. Thus, the pathogenesis of bronchiectasis is a chain of pathological processes that interact and affect each other.

Classification of bronchiectasis

Classification of bronchiectasis. F. Isakov, E. A. Stepanov, V. I. Geraskin (1978).
By origin:
congenital (dysontogenetic), acquired (atelectatic, emphysematous, mixed).
In shape:
cylindrical, bubble-frequent, brush-like.
For distribution:
unilateral, bilateral (large, non-distributed), – with an indication of the segment.
By the severity of bronchitis:
localized, diffuse.
With the course:
with exacerbations (frequent, rare).

Clinic of bronchiectasis

The clinical picture depends on the spread of the lesion, the severity and spread of bronchitis in the unaffected areas of the lung, on the presence of exacerbation or remission. The general condition may be slightly impaired, but with a common process, symptoms of intoxication join early. Children quickly tire, vststayuturouroz-turn. Hemoptysis is rare. With limited bronchiectasis, shortness of breath at rest is usually not observed, with bilateral damage – severe shortness of breath with little physical exertion. Some children complain of headache, bone pain. During periods of exacerbation, the amount of sputum increases, coughing throughout the day is constant, shortness of breath intensifies or appears, fever, more often to subfebrile numbers. One of the most important diagnostic signs of chronic pulmonary disease is chest deformity – chest retraction on the side of the lesion, its lag in the act respiration, a slight omission of the angle of the scapula, rapprochement of the ribs, narrowing of the intercostal spaces. Auscultatory moist rales of various sizes, decreasing after expectoration of sputum.

Diagnosis of bronchiectasis

An X-ray examination of the chest can reveal a spotted eclipse of the affected lobe of the lung, the presence of bronchiectasis is further confirmed by computed tomography. However, the main method to establish a diagnosis of bronchiectasis is bronchography – a contrast study of the bronchial tree. Evaluation of the bronchogram allows you to determine the localization of bronchiectasis, their distribution , form. Changes found during angiopulmonography of children with bronchiectasis depend on the depth and prevalence of pa process in the bronchi and lung parenchyma. The complete absence of blood flow in the affected areas of the lung indicates a functional failure and the need to remove these areas, which are only cells of purulent intoxication.

Treatment of bronchiectasis

Conservative treatment is used as a preoperative preparation in the postoperative period and is aimed at maximizing the rehabilitation of the tracheobronchial tree, as well as all associated foci of inflammation. For the rehabilitation of the trachea and bronchi, bronchoscopy is used, which is repeated 2-3 times. Inhalations, exercise therapy are prescribed. postural drainage, bronchial and mucolytics, vitamins, desensitizing agents. During surgical treatment, the volume of resection is determined according to bronchography and is specified during the operation. Resection of the lobe, several segments of two lobes of the lung is performed (with localization on the right), very rarely it is necessary to remove the entire lung – pulmonectomy. In case of bilateral localization of bronchiectasis, the operation is performed in 2 stages at intervals of 6-12 months.