Chronic nonspecific lung diseases.

Chronic nonspecific lung diseases is a term adopted in 1958 at a symposium organized by the pharmaceutical company Ciba. COPD includes lung diseases: chronic bronchitis, bronchial asthma, emphysema, chronic pneumonia, bronchiectasis, pneumosclerosis.

Chronic bronchitis.

Chronic bronchitis diffuse progressive damage to the bronchi associated with prolonged irritation of the respiratory tract by harmful agents, characterized by inflammatory and sclerotic changes in the bronchial wall and peribronchial tissue, accompanied by restructuring of the secretory apparatus and hypersecretion of mucus, manifested by a constant or peripheral cough with sputum for at least 3 months per year for 2 or more years, and with damage to the small bronchi - shortness of breath, leading to obstructive ventilation disorders and the formation of chronic pulmonary heart disease.

Classification of chronic bronchitis.

I. Clinical forms:

chronic simple (non-obstructive) bronchitis, occurring with constant or periodic release of mucous sputum and without ventilation disorders; chronic purulent (non-obstructive) bronchitis, occurring with constant or periodic release of purulent sputum and without ventilation disorders; chronic obstructive bronchitis, occurring with the release of mucous sputum and persistent obstructive ventilation disorders; chronic purulent-obstructive bronchitis, accompanied by the release of purulent sputum with persistent obstructive ventilation disorders; special forms: hemorrhagic; fibrinous.

II. Damage level:

bronchitis with predominant damage to large bronchi (proximal);
bronchitis with predominant damage to small bronchi (distal).

III. Flow:

patent;
with rare exacerbations;
with frequent exacerbations;
continuously relapsing.

IV. The presence of bronchopastic (asthmatic) syndrome.

V. Process phase:

exacerbation;
remission.

VI. Complications:

emphysema;
hemoptysis;
respiratory failure (indicating the degree);
chronic pulmonary heart disease (compensated, decompensated).

Obliterating bronchitis, bronchiolitis. On the bronchogram, the left lower lobe bronchus and the bronchi of the basal segments are dilated, there is no peripheral filling. The bronchi of the upper lobe and lingular are not changed and completed to small generations

Etiology of chronic bronchitis.

Inhalation of pollutants - impurities of various natures and chemical structures contained in the air that have a harmful irritating effect on the bronchial mucosa (tobacco smoke, dust, toxic fumes, gases, etc.). Infection (bacteria, viruses, mycoplasmas, fungi). Endogenous factors: congestion in the lungs with circulatory failure, secretion of nitrogen metabolism products by the bronchial mucosa in chronic renal failure. Untreated acute bronchitis.

Predisposing factors:

violation of nasal breathing;
diseases of the nasopharynx chronic tonsillitis, sinusitis, rhinitis;
cooling;
alcohol abuse;
living in an area where the atmosphere is polluted with pollutants (gases, dust, vapors of acids, alkalis, etc.).

Pathogenesis of chronic bronchitis.

Dysfunction of the local bronchopulmonary defense system. Development of the classic pathogenetic triad: hypercrinia (hyperfunctioning of the bronchial mucous glands, hyperproduction of mucus), discrinia (increased sputum viscosity due to changes in its physicochemical properties and a decrease in its rheology), mucostasis (stagnation of thick viscous sputum in the bronchi). Favorable conditions for the introduction of infectious agents into the bronchi. Development of sensitization to microbial flora and autosensitization. The main mechanisms of bronchial obstruction:

bronchospasm;
inflammatory edema and infiltration of the bronchial wall;
hyper and discrimination;
hypotonic dyskinesia of large bronchi and trachea;
collapse of small bronchi on exhalation;
hyperplastic changes in the mucous and submucosal layers of the bronchi.

Clinical symptoms of chronic bronchitis.

Cough with mucopurulent sputum up to 100-150 ml per day, mainly in the morning. In the acute phase - weakness, sweating, with purulent bronchitis - increased body temperature. With purulent perennial chronic bronchitis, thickening of the terminal phalanges (“drumsticks”) and thickening of the nails (“watch glasses”) may develop. When percussing the lungs in the case of emphysema, the percussion sound is “boxy” and the respiratory mobility of the lungs is limited. Auscultation reveals hard breathing with prolonged exhalation, dry whistling and buzzing wheezing, and moist wheezing of various sizes depending on the caliber of the bronchi.

Clinical manifestations of chronic.

Shortness of breath, predominantly of the expiratory type. The changing nature of shortness of breath depending on the weather, time of day, exacerbation of pulmonary infection. Difficult and prolonged exhalation compared to the inhalation phase. Swelling of the neck veins during exhalation and collapse during inhalation. Prolonged, unproductive cough. When percussing the lungs: “box” sound, drooping of the lower border of the lungs (emphysema). On auscultation: harsh breathing with prolonged exhalation, buzzing, whistling wheezing, which can be heard at a distance. Sometimes they can only be heard in a lying position.

Palpation of exhalation according to Votchan: prolongation of exhalation and decrease in its force. Positive match test according to Votchan: the patient cannot extinguish a lit match at a distance of 8 cm from the mouth. With severe obstructive syndrome, symptoms of hypercapnia occur: sleep disturbances, headache, increased sweating, anorexia, muscle twitching, large tremors, and in more severe cases, confusion, convulsions and coma. The syndrome of dyskinesia of the trachea and large bronchi is manifested by attacks of painful bitonic cough with difficult to separate sputum, accompanied by suffocation, sometimes loss of consciousness, and vomiting.

Laboratory data for chronic bronchitis.

CBC: with exacerbation of purulent bronchitis, a moderate increase in ESR, leukocytosis with a shift to the left. BAK: increase in blood sialic acids, fibrin, seromucoid, alpha-2- and gamma-globulin, appearance of PSA. General analysis of sputum: mucous sputum is light in color, purulent sputum is yellowish-greenish in color, mucopurulent plugs may be detected, with obstructive bronchitis, casts of the bronchi; microscopic examination of purulent sputum reveals many neutrophils. In chronic obstructive bronchitis, there is an alkaline reaction in morning sputum and a neutral or acidic reaction in daily sputum. Rheological properties viscosity, increased elasticity. In obstructive bronchitis, Kurshman spirals can be detected.

Instrumental studies for chronic bronchitis.

Bronchoscopy plays a role in the verification of chronic bronchitis. At the same time, signs of chronic inflammation are found: cicatricial changes in the trachea and bronchi, metaplasia of the mucosa. X-ray of the lungs: the X-ray picture in the lungs changes only when the inflammatory process covers the peribronchial or respiratory part of the lungs. In this case, the following symptoms of chronic bronchitis may be detected: reticular pneumosclerosis, deformation of the pulmonary pattern, diffuse increase in the transparency of the pulmonary fields, low standing of the diaphragm and flattening of its dome, a decrease in the amplitude of movements of the diaphragm. Central location of the heart, bulging of the conus pulmonary artery.

Of the spirographic indicators, the most significant are the Tiffno index, the ratio of FEV to VC and the air velocity indicator (the ratio of MVL to VC). The study of ventilation parameters allows us to determine the degree of the reversible component of bronchial obstruction. An ECG is used to detect pulmonary hypertension. Analysis of blood gas composition and acid-base status provides valuable information about the degree of hypoxemia and hypercapnia in chronic bronchitis.

Indications for hospitalization for chronic bronchitis.

Exacerbation of the disease, expressed by an increase in shortness of breath, cough, amount of sputum in the presence of one or more conditions: ineffectiveness of outpatient treatment; high risk of concomitant diseases; long-term progression of symptoms; increase in hypoxia; the occurrence or increase of hypercapnia. The emergence or decompensation of cor pulmonale, which is not amenable to outpatient treatment.

Treatment of chronic bronchitis.

Treatment of chronic bronchitis consists of non-drug and medicinal measures. Non-drug methods of influence on a patient with chronic bronchitis include the following mandatory elements: leveling occupational hazards, improving the environmental situation at work and at home, smoking cessation, psychotherapy and auto-training, dosed physical activity, fortified food with a limitation of table salt and total caloric intake (up to 800 kcal per day) with reduced carbohydrate content.

Drug therapy for chronic bronchitis depends on the nosological diagnosis. For chronic (simple non-obstructive) bronchitis, occurring with constant or periodic production of mucous sputum and without ventilation disturbances, basic therapy includes expectorants. The choice of expectorant drugs depends on the type of cough. For a severe, dry, debilitating cough, drugs that inhibit the cough reflex are prescribed (codeine, tecodine, dionine, glaucine).

For a productive cough with good sputum discharge, substances that enhance its secretion are indicated: expectorants (thermopsis, terpinhydrate, etc.) and bronchodilators (aminophylline, theophylline). When the rheological properties of sputum are unchanged, but mucociliary transport is reduced, derivatives of theophylline and sympathomimetics (theolong, teopec, sinecode) are used.

With high viscoelastic properties of sputum, thiol derivatives (acetylcysteine ​​or mucosolvin), proteolytic enzymes (trypsin, chymotrypsin) are used, and with significant adhesive properties, substances that stimulate the formation of surfactant (bromhexine-bisolvan, lasolvan-ambroxol) and secretion rehydrate (mineral salts) are prescribed , essential oil).

For chronic purulent (non-obstructive) bronchitis, occurring with constant or periodic release of purulent sputum and without ventilation disorders, in addition to drugs that regulate mucociliary clearance, antibacterial agents are indicated. Preference is given to substances active against pneumococci and Haemophilus influenzae.

Since antibacterial drugs worsen the rheological properties of sputum, they must be combined with mucolytics. Antibiotics can be administered orally, parenterally, or in the form of aerosols. Chronic obstructive bronchitis, which occurs with the release of mucous sputum and persistent obstructive ventilation disorders, requires the use of bronchodilators (anticholinergics, beta-2-agonists and methylxanthines) and expectorants, and in the case of hypoxemia, hypercapnia and cor pulmonale, treatment of these complications. When a pronounced purulent component is added to obstructive bronchitis, antibacterial agents are added. Relief of bronchospasm is achieved by prescribing drugs with a bronchodilator effect:

sympathomimetics of selective or predominantly selective action (isadrin, salbutamol, berotec, ventolin); phosphodiesterase inhibitors (theophylline derivatives); anticholinergics (platiphylline, atropine); glucocorticosteroids, mainly of inhalation action (becotide, beclomet, pulmicort), which do not suppress the function of the adrenal cortex.

In case of circulatory failure, cardiac glycosides, diuretics, oxygen therapy (low-flow 24-28% oxygen-air mixture through a mask) are necessary. If, despite active treatment, respiratory acidosis progresses, intubation and mechanical ventilation are indicated. When treating patients with chronic bronchitis, physiotherapeutic procedures (ultraviolet irradiation of the chest, ultrasound, inductothermy, UHF), chest massage, breathing exercises, and spa treatment are widely used.

For frequently relapsing chronic bronchitis, seasonal prophylaxis and anti-relapse therapy are carried out twice a year. Immunomodulatory drugs, phytoncides, methods and means aimed at improving bronchial drainage are prescribed. In purulent forms of bronchitis, a “toilet” of the bronchial tree is performed every morning; the patient performs positional drainage after first taking expectorants, hot tea, and bronchospasmolytics. With secondary pulmonary hypertension and severe respiratory failure, patients are employed or limited in physical activity. Along with bronchospasmolytics, they are prescribed peripheral vasodilators (nitrates or calcium antagonists of the nifedipine group), according to indications - bloodletting, oxygen therapy.

The main tasks of medical examination.

Early diagnosis of the disease. The earliest possible exclusion of external causative factors cessation of smoking, exclusion of harmful production factors, sanitation of chronic foci of infection, restoration of nasal breathing. Selection of individual supportive therapy against the background of non-drug treatment methods.

Organization of special treatment methods on an outpatient basis (aerosol therapy, endobronchial sanitation). Diagnosis of functional breathing disorders, including early diagnosis of bronchial obstruction. Measures to prevent the recurrence of chronic bronchitis involve hardening the body (regulated sports activities), preventing the occurrence of a viral infection (taking ascorbic acid, rimantadine, interferon).

Bronchial asthma.

Bronchial asthma chronic relapsing disease with predominant damage to the bronchi, which is characterized by their hyperreactivity caused by specific (immunological) and (or) non-specific (non-immunological), congenital or acquired mechanisms, and the main (mandatory) symptom of which is an attack of suffocation and (or) asthmatic status due to spasm of bronchial smooth muscles, hypersecretion, discrinia and edema of the bronchial mucosa.

Classification of bronchial asthma.

Traditionally, there are: atopic (exogenous, allergic, immunological); non-atopic (endogenous, non-immunological) bronchial asthma.

By severity:

mild course;
course of moderate severity;
severe course.

A mild degree is characterized by the absence of classic asthma attacks. Symptoms of difficulty breathing occur less than 1-2 times a week and are short-term; Drug therapy is usually not required. The patient's night sleep at this stage of the disease is characterized by awakening from respiratory discomfort less than 1-2 times a year. Outside of attacks, the patient's condition is stable. In bronchial asthma of moderate severity, attacks are controlled by sympathomimetics. Attacks at night are recorded more than twice a month. Severe asthma attacks are characterized by frequent long-term exacerbations with the presence of life-threatening complications, frequent nighttime symptoms, decreased physical activity, and the presence of persistent symptoms in the inter-attack period.

Phases of bronchial asthma: exacerbation, remission. Complications: pulmonary pulmonary emphysema, pulmonary failure, atelectasis, pneumothorax; extrapulmonary myocardial dystrophy, cor pulmonale, heart failure. Bronchial asthma. Direct projection: general swelling of the lungs, the vascular pattern is thinned, can be traced mainly in the hilar zones, the right root is deformed and displaced downward

Stages of development of bronchial asthma Stages of development of bronchial asthma.

I. The presence of congenital and (or) acquired biological defects and disorders in practically healthy people: a) local and general immunity; b) “rapid response” systems (mast cells, macrophages, eosinophils, platelets); c) mucociliary clearance; d) endocrine system, etc. Clinical implementation of biological defects leads to the development of bronchial asthma.

II. State of preasthma. This is a sign of the threat of clinically significant bronchial asthma.

III. Clinically established bronchial asthma after the first attack of asthma or status asthmaticus. Bronchial asthma. Lateral projection: atelectasis of the middle lobe with its reduction to 1/4 of its volume

Etiology and pathogenesis of bronchial asthma.

The general pathogenetic mechanism inherent in different forms of bronchial asthma is a change in the sensitivity and reactivity of the bronchi, determined by the reaction of bronchial patency in response to the influence of physical and pharmacological factors. It is believed that in 1/3 of patients asthma is of autoimmune origin. Nonbacterial and bacterial allergens play a role in the occurrence of allergic forms of asthma. The most studied allergic mechanisms of asthma are based on IgE and IgG-mediated reactions. Leukotrienes play a central role in the pathogenesis of aspirin-induced asthma. In physical exertion asthma, the process of heat transfer from the surface of the respiratory tract is disrupted.

Clinical symptoms of bronchial asthma.

Preasthma. The first group of symptoms of pre-asthma includes acute, recurrent or chronic bronchitis and pneumonia with symptoms of bronchial obstruction. The second group is the presence of extrapulmonary manifestations of allergy: vasomotor rhinitis, urticaria, Quincke's edema. The third group is a hereditary predisposition to various allergic diseases, which is revealed by collecting a family history. The fourth group is eosinophilia of blood and sputum. Bronchial asthma. In the development of an attack of bronchial asthma, three periods are distinguished: precursors, peak (suffocation) and reverse development.

The period of precursors begins several minutes, hours, sometimes days before the attack and is manifested by the following symptoms: vasomotor reactions from the nasal mucosa, sneezing, itching of the eyes, skin, paroxysmal cough, headache, and often mood changes.

The period of height (suffocation) has the following symptoms. There is a feeling of lack of air, compression in the chest, and severe expiratory shortness of breath. Inhalation becomes short, exhalation becomes slow, accompanied by loud, prolonged, wheezing wheezing, audible from a distance. The patient takes a forced position, sits leaning forward, resting his elbows on his knees, gasping for air. The face is pale, with a bluish tint. The wings of the nose swell when inhaling. The chest is in the position of maximum inspiration; the muscles of the shoulder girdle, back, and abdominal wall participate in breathing.

The intercostal spaces and supraclavicular fossae retract when inhaling. The neck veins are swollen. During an attack, there is a cough with very difficult to separate sputum, a percussion sound with a tympanic tint is detected above the lungs, the lower borders of the lungs are lowered, the mobility of the pulmonary edges is limited, against the background of weakened breathing, especially on exhalation, a lot of dry wheezing is heard. The pulse is rapid, weak filling, heart sounds are muffled. An attack of suffocation can develop into asthmatic status. The period of reverse development has different durations. After an attack, patients want to rest, some of them experience hunger and thirst. After an attack of bronchial asthma, a uniform round shadow with clear contours is visible in the upper lobe of the right lung; eosinophilic infiltrate

Laboratory data for bronchial asthma. CBC: eosinophilia, increased ESR. General analysis of sputum: many eosinophils, Charcot-Leyden crystals, Kurshman spirals, neutrophilic leukocytes in patients with infectious-dependent bronchial asthma. BAK: increased levels of alpha-2- and gamma-globulin, sialic acids, seromucoid, fibrin. Resolved infiltrate after an attack of bronchial asthma

Instrumental studies for bronchial asthma.

X-ray examination: in patients with atopic bronchial asthma there are no changes outside of an attack; in infectious-dependent bronchial asthma there are signs of chronic bronchitis with peribronchial sclerosis and pulmonary emphysema. During an attack of bronchial asthma, signs of acute emphysema are revealed. Examination of the nasopharynx. In patients with pre-asthma and bronchial asthma, vasomotor disorders of the nasal mucosa, polyps, deviated nasal septum, inflammation of the paranasal sinuses and tonsils may be detected.

ECG: signs of increased load on the right atrium, sometimes partial or complete blockade of the right bundle branch, formation of cor pulmonale. ECG changes develop earlier in patients with atopic bronchial asthma than in patients with infection-dependent asthma. Spirographic and pneumotachometric studies: impaired bronchial obstruction (reduced forced expiratory volume in the first second, maximum ventilation of the lungs, decreased expiratory velocity), with frequent exacerbations and the development of pulmonary emphysema decreased vital capacity of the lungs.

Diagnosis of clinical and pathogenetic variants of bronchial asthma

Diagnostic criteria for atopic bronchial asthma:

Allergological history. Hereditary predisposition. Allergic constitution. Pollen allergy. Food allergies. Drug allergy. Occupational allergies. Predominantly young age (80% of patients under the age of 30 years). Positive skin tests with certain allergens. Positive provocative tests for certain allergens (carried out according to strict indications). Identifying a specific food allergen.

Laboratory criteria: elevated blood levels of IgE; increased levels of eosinophils in the blood and sputum, Shelley's basophil test; positive reaction of alteration of neutrophils of a patient with an allergen; increased viscosity of sputum under the influence of an allergen. The atopic form of bronchial asthma is characterized by periods of long-term remission in the event of cessation of contact with specific allergens, a relatively mild course with the late development of complications, and the absence of signs of infectious damage to the upper respiratory tract and bronchi.

Diagnostic criteria for infection-dependent bronchial asthma:

Clinical examination: complaints, anamnesis, objective data indicating a connection between bronchial asthma and a previous respiratory infection, acute bronchitis, influenza, pneumonia. CBC: leukocytosis, increased ESR. BAK: appearance of PSA, increase in sialic acids, alpha-2- and gamma-globulin, seromucoid. General analysis of sputum: mucopurulent, neutrophilic leukocytes predominate in the smear, detection of pathogenic bacteria in the diagnostic titer.

X-ray examination: identification of infiltrative fields in pneumonia, signs of pneumosclerosis, darkening of the paranasal sinuses. Bronchoscopy: signs of inflammation of the mucous membrane, thick mucopurulent secretion, predominance of neutrophilic leukocytes in the bronchial secretion, detection of pathogenic bacteria. Determination of bacterial sensitization: positive tests with relevant bacterial allergens. Mycological examination of sputum: sowing of yeast of the genus Candida.

Virological research: detection of viral antigens in the epithelium of the nasal mucosa using immunofluorescence, serodiagnosis. Identification of foci of chronic infection in the upper respiratory tract, nasopharynx and oral cavity. An attack of suffocation in this variant of the course of bronchial asthma is characterized by a gradual development, long duration, and relative resistance to beta-agonists. Patients quickly develop complications: emphysema, diffuse pneumosclerosis, chronic pulmonary heart disease.

Diagnostic criteria for dishormonal variant of bronchial asthma. For the dishormonal variant, the deterioration of the condition of patients before or during the menstrual cycle, during pregnancy or menopause, against the background of hypothalamic syndrome, after a skull injury, when the dose of corticosteroids is reduced or withdrawn is typical. Laboratory data based on determination of the level of 11-OCS in the blood, hormonal function of the ovaries, a radioimmunological method for studying estrogen and progesterone in the blood plasma, and a cytological examination of a smear confirm the diagnosis.

Diagnostic criteria for the autoimmune form of bronchial asthma. Severe, continuously relapsing course. Positive intradermal test with autolymphocytes. High levels of acid phosphatase in the blood. Positive reaction of blast transformation of lymphocytes with phytohemagglutinin. Reduction of complement levels in the blood and detection of circulating immune complexes.

Diagnostic criteria for the neuropsychic variant of bronchial asthma. Mental factors can cause asthma attacks, but much more often they provoke the development of bronchospasm in patients already suffering from bronchial asthma. Psychogenic stimuli can cause bronchospasm through blockade of beta-adrenergic receptors, stimulation of alpha-adrenergic receptors and the vagus nerve. The patient has a history of neuropsychiatric disorders, mental and traumatic brain injuries, conflict situations in the family, at work, and disorders in the sexual sphere.

Aspirin asthmaAspirin asthma (asthmatic triad). Bronchial asthma in the presence of recurrent nasal polyposis, chronic inflammation of the paranasal sinuses and intolerance to one or more non-steroidal anti-inflammatory drugs (usually aspirin) is called “aspirin asthma”. The disease most often affects people in older age groups. Before the development of asthma attacks, patients suffer from polypous rhinosinusitis for many years, for which they undergo repeated surgical treatment. Suddenly, after taking aspirin, 15-20 minutes later, a severe attack of suffocation develops, sometimes ending in death. Laboratory indicators are most characterized by high eosinophilia in blood and sputum.

Exercise asthma, or post-exertional bronchospasm, is characterized by the occurrence of asthma attacks in the next 2-10 minutes after physical activity. Among various sports, running is the most powerful, and swimming is the weakest stimulator of bronchospasm. The anaphylactic variant is characterized by a sudden onset with rapid (within several hours) development of a coma. Its appearance is usually associated with increased sensitivity to drugs.

The metabolic variant of the asthmatic state is formed over a long period of time (over several days and weeks) under the influence of rapid withdrawal of corticosteroids, respiratory tract infections, adverse meteorological factors against the background of functional blockade of beta-adrenergic receptors and intensive use of sympathomimetics. With the increase and severity of asthma attacks, the patient more often resorts to non-selective beta stimulants (apupent, asthmament, etc.). The use of such high doses of sympathomimetics leads to the fact that each subsequent attack of suffocation becomes more severe than the previous one. This is the “rebound syndrome”. There is another undesirable effect of sympathomimetics. When taken for a long time, they can contribute to swelling of the bronchial mucosa and hypersecretion of mucus, as a result of which the attack of suffocation may increase.

The first stage of status asthmaticus (relative compensation). The patient is able to mainly hyperventilate the alveoli, which is accompanied by normo- or hypercapnia (35-40 pCO2 mm Hg). Some patients may develop hypoxemia (pO2 60-70 mm Hg). Clinically, this stage is characterized by a prolonged attack of suffocation, moderate shortness of breath and tachycardia (up to 100-120 beats per minute), non-productive cough and sometimes mild cyanosis. Percussion reveals a “box” sound above the surface of the lungs, and dry whistling rales are detected on auscultation.

The second stage is accompanied by a decrease in the ability to hyperventilate the alveoli (“silent lung”). This leads to increased hypoxemia (PaO2 50-60 mm Hg) and the appearance of hypercapnia (PaCO2 50-60 mm Hg). The general condition of the patients is serious, a change in the psyche occurs (psychomotor agitation is replaced by depression, hallucinations are possible). An important sign of this stage is the discrepancy between noisy, wheezing breathing and the almost complete absence of wheezing in the lungs. The auscultatory picture of the lungs is characterized by a mosaic pattern: areas with weakened breathing are replaced by “silent” areas. Tachycardia reaches 140 beats per minute, arrhythmia and hypotension are often recorded.

The third stage corresponds to the clinical picture of hypoxemic and hypercapnic coma. Development of acidosis and severe hypoxia (pO2 40-50 mm Hg) and hypercapnia (pCO2 80-90 mm Hg). The condition of the patients is extremely severe; a pronounced disturbance of nervous and mental activity precedes a disturbance of consciousness. An objective examination reveals diffuse cyanosis, collapse, arrhythmic breathing, and threadlike pulse.

Treatment of bronchial asthma.

Treatment of patients with bronchial asthma should be individualized and based on the idea of ​​the allergic nature of the disease. A comprehensive program for the treatment of bronchial asthma includes: an educational program for patients; dynamic monitoring of the severity of the disease and the adequacy of therapy using clinical and functional studies; measures that exclude the impact of the “culprit allergen” on the patient’s body, or control of causative factors;

For quotation: Latysheva T.V., Shubina O.V. Broncho-Vaxom. Treatment of diseases of the bronchopulmonary system // RMZh. 2005. No. 21. S. 1438

Introduction The most common diseases of the bronchopulmonary system, in the pathogenesis of which the infectious component plays an important role, are chronic obstructive pulmonary disease (COPD) and infection-dependent bronchial asthma. The prevalence of COPD and infection-related bronchial asthma throughout the world is very high. COPD affects 4–6% of men and 1–3% of women. According to official medical statistics, the number of patients suffering from COPD is about 1 million. This is primarily due to the delayed diagnosis of COPD and the rapid progression of the disease. Chronic obstructive pulmonary disease is one of the leading diseases in terms of the number of days of disability, which also causes economic losses. COPD significantly affects the quality of life of patients, is the cause of hospitalization and subsequent disability, and ranks fourth among the causes of death. In the near future, mortality from COPD is predicted to increase in developed countries.

The most common diseases of the bronchopulmonary system, in the pathogenesis of which the infectious component plays an important role, are chronic obstructive pulmonary disease (COPD) and infection-dependent bronchial asthma. The prevalence of COPD and infection-related bronchial asthma throughout the world is very high. COPD affects 4–6% of men and 1–3% of women. According to official medical statistics, the number of patients suffering from COPD is about 1 million. This is primarily due to the delayed diagnosis of COPD and the rapid progression of the disease. Chronic obstructive pulmonary disease is one of the leading diseases in terms of the number of days of disability, which also causes economic losses. COPD significantly affects the quality of life of patients, is the cause of hospitalization and subsequent disability, and ranks fourth among the causes of death. In the near future, mortality from COPD is predicted to increase in developed countries.
There is currently no precise definition of COPD. From the point of view of clinical and pathogenetic characteristics, chronic obstructive pulmonary disease is a group of diseases characterized by progressive, partially reversible or irreversible bronchial obstruction, which is associated with inflammatory changes in the respiratory tract. The group of diseases united under the concept of COPD includes such chronic diseases of the respiratory system as chronic obstructive bronchitis (COB), pulmonary emphysema (PE), and severe bronchial asthma (BA). All of these diseases are characterized by a progressive course and increasing respiratory failure.
One of the most important factors leading to the development of COPD and provoking its exacerbations is a persistent infectious process in the bronchi. Treatment of COPD is quite complex and in some cases it is not possible to reduce the frequency of exacerbations and the rate of progression of the disease. The majority of drugs used to treat COPD are symptomatic drugs and do not in any way affect the pathogenesis of the disease. Of great interest is the possibility of using immunotropic drugs in this category of patients, which can positively affect the course of infectious inflammation in the respiratory tract.
Etiology and pathogenesis of COPD
The main risk factor for COPD in 80–90% of cases is smoking. Smokers experience rapid development of irreversible obstructive changes in the bronchi, an increase in shortness of breath and other manifestations of the disease. This category of patients has the highest mortality rates from COPD, but COPD can also develop in non-smokers.
Another risk factor for developing COPD is exposure to occupational irritants, of which the most harmful are dusts containing cadmium and silicon. At the same time, smoking, as a rule, enhances the adverse effects of occupational factors.
Genetic predisposition plays a significant role in the occurrence of COPD. A genetic pathology, the influence of which on the formation of COPD has already been proven, is a1-antitrypsin (AAT) deficiency, which leads to the development of emphysema, chronic obstructive bronchitis and bronchiectasis.
The formation of COPD is also influenced by other negative environmental factors: increased levels of nitrogen dioxide, high humidity in living quarters, etc.
The presence of bronchial asthma (of any etiology) in a patient, the progressive course of the disease and the lack of adequate therapy also leads to the subsequent formation of COPD. Exacerbation of infectious diseases of the upper respiratory tract (rhinitis, sinusitis) is another possible cause of exacerbation of chronic obstructive pulmonary disease.
The etiopathogenesis, nature of the course and severity of broncho-obstructive changes in COPD are largely determined by the development of the infectious process in the lungs. Respiratory infection is the cause of approximately 80% of COPD exacerbations of established etiology. In 40–60% of cases they are caused by bacteria. Persistence of bacterial infection leads to deterioration of mucociliary clearance, disruption of neurogenic regulation of bronchial smooth muscle tone, damage to the epithelium of the respiratory tract and increased vascular permeability, the formation of hyperreactivity, which can, in turn, aggravate the course of bronchial asthma, if present. The severity largely depends on the microorganism that caused it. The most common infectious inflammatory process is caused by Streptococcus pneumonia, Haemophilus influenzae, Moraxella catarralis, Staph. aureus, P. aeruginosa, enterobacteria. Long-term persistence of a bacterial infection in the bronchial tree in the presence of chronic bronchitis leads to sensitization with the subsequent development of severe infectious bronchial asthma.
The causes of exacerbation of COPD can be a viral infection (influenza viruses, rhinoviruses, RSV, adenorviruses), as well as intracellular infection, pollutants, drugs, heart failure and cardiac arrhythmias, respiratory failure caused by other reasons.
All of the above factors are directly involved in the formation of the disease, provoke frequent exacerbations and subsequent progression of broncho-obstructive changes. The irreversible component of bronchial obstruction is associated with developing emphysema and peribronchial fibrosis, a consequence of chronic inflammation. The development of emphysema leads to a reduction in the vascular network in areas of the lung tissue, disruption of gas exchange, and aggravates the development of respiratory failure. Impaired drainage of bronchial secretions and its high viscosity further aggravate the inflammatory process and promote more active colonization by microorganisms.
Immunological disorders in COPD
The results of repeated studies of the functioning of the immune system in patients suffering from chronic bronchitis indicate the presence of a number of immunological abnormalities (the number and functional activity of T and B lymphocytes): a decrease in the number of T suppressors (CD8+), a decrease in the absolute number of T helper cells (CD4+) , as well as CD19+ cells; a pronounced decrease in the phagocytic activity of cells, a decrease in interferon production, a decrease in the level of IgA and IgG.
Significant changes in the state of local immunity and nonspecific resistance to infection are also detected. In COPD, both in the acute and remission stages, there is a decrease in the number of macrophages and an increase in the number of neutrophils in the bronchial contents. The activity of phagocytic cells is also reduced (especially in the presence of a purulent process).
The identified disturbances in the immune status of patients with COPD are a consequence of a long-term inflammatory infectious process, as well as repeated courses of antibacterial therapy. Moreover, the degree of their severity, as a rule, increases with the severity of the patient’s condition. The presence of immunological disorders, in turn, leads to a decrease in the effectiveness of the therapy and progression of the disease.
Clinical
COPD picture
Clinical manifestations of COPD are the result of pathophysiological changes in the lungs: damage to the mucous membrane by an infectious agent, increased bronchial hyperreactivity, development of edema of the bronchial mucosa, hypersecretion of mucus, increased mucus viscosity and decreased mucociliary clearance, impaired perfusion, cellular infiltration of the bronchial wall. These changes lead to a severe cough with sputum (usually viscous), shortness of breath, weakness, and decreased performance. These symptoms are leading, despite the heterogeneity of the diseases that make up COPD.
The function of external respiration is characterized by an obstructive type of ventilation disorders, a progressive decrease in maximum expiratory flow due to increasing resistance in the airways and a gradual deterioration in gas exchange function of the lungs, which indicates the irreversible nature of airway obstruction.
The severity of symptoms depends on the stage of the disease, the rate of disease progression, the predominant level of damage to the bronchial tree, the intensity of the impact of etiological factors and their total impact.
Principles of COPD therapy
The main components of COPD therapy are patient education, symptomatic therapy and immunotropic therapy.
Patient education
Patient education involves outreach to patients about the need to comply with preventive measures aimed at stopping exposure to adverse environmental factors and reducing the frequency of exacerbations of the disease (quitting smoking, stopping exposure to occupational irritants, improving living conditions); about methods of treating the disease and the importance of adequate therapy, as well as self-control techniques.
Symptomatic therapy
Symptomatic therapy includes: bronchodilators (b2-adrenergic agonists, anticholinergics, methylxanthines); mucolytic therapy, anti-inflammatory therapy (inhaled, oral, parenteral forms of GCS), anti-infective therapy (antibacterial drugs are prescribed only during an exacerbation in the presence of clinical signs of intoxication, an increase in the amount of sputum and signs of purulent inflammation). In case of severe exacerbation of COPD, accompanied by a significant degree of respiratory failure, oxygen therapy is indicated. In addition to therapy aimed at relieving the symptoms of COPD, treatment of concomitant diseases (rhinitis, sinusitis and bronchial asthma) is indicated. This is a necessary condition for successful treatment of COPD, because exacerbation of the above diseases often leads to its exacerbation.
Immunotropic therapy
Violations of the function of local and systemic immune defense, as well as nonspecific resistance to infection, lead to a decrease in the effectiveness of traditional therapy, therefore immunotropic therapy is an important component of the complex treatment of COPD. Considering the importance of the infectious factor in the occurrence and chronicity of the inflammatory process in the bronchi, the use of immunotropic drugs becomes especially relevant.
Exacerbations associated with infection of patients with COPD most often occur in the cold season, during epidemics of viral diseases. In some cases, acute viral diseases are complicated by the addition of a bacterial infection. Therefore, vaccination against severe infections such as influenza, which can not only lead to exacerbation of COPD and the development of severe respiratory failure, but in severe cases to death, is a very important preventive measure.
The use of bacterial vaccines makes COPD therapy more successful and improves the prognosis of the disease, which is associated with a decrease in the frequency of exacerbations of the disease. Considering the diversity of the microflora of the bronchial contents of patients with COPD, the most effective are bacterial preparations containing lysates of several bacteria that most often cause exacerbation of diseases. The use of multicomponent bacterial vaccines has a positive effect not only on the course of COPD, but also other concomitant chronic infectious diseases of the respiratory tract - rhinitis, sinusitis, laryngitis, tracheitis. In Russian practice, there is already experience in the use of bacterial vaccines in patients with COPD. The results of the studies indicate their effectiveness and safety. When these drugs were included in the treatment regimen for patients with COPD, an increase in the effectiveness of therapy was noted, along with positive dynamics in indicators of the immune status of patients (both in peripheral blood and in lavage fluid).
Immunomodulators of bacterial origin provide more stable and long-term remission, preventing the activation of bacterial flora in the bronchial tree. By limiting or preventing the persistence of bacterial infection, they also have a positive effect on the course of infectious bronchial asthma, reducing the severity of the allergic reaction.
One of the drugs that helps increase immune resistance to bacterial infections is Broncho-Vaxom (manufactured by OM PHARMA). Broncho-Vaxom is a multicomponent bacterial vaccine that contains dried extracts of Haemophilus influenzae, Klebsiella, Staphylococcus aureus, Streptococcus and Neisseria. The course of treatment includes three cycles of 10 days, 1 capsule per day. The interval between cycles is 20 days. Broncho-Vaxom is also effective in the treatment of bacterial infections of other parts of the respiratory tract (rhinitis, sinusitis, laryngotracheitis). The drug is highly effective in patients with viral infections of the upper and lower respiratory tract.
Conclusion
Therapeutic approaches to the treatment of many infectious diseases of the upper and lower respiratory tract have recently undergone changes. The participation of the infectious process in the etiopathogenesis of these diseases, identified immunological disorders that tend to worsen with increasing severity of the disease, the insufficient effectiveness of traditional therapy and associated complications dictate the need to create methods of pathogenetic treatment of chronic infectious diseases of the respiratory tract (including such severe ones as COPD).
The use of multicomponent bacterial vaccines (Broncho-Vaxoma) improves the quality of treatment and the patient’s quality of life, reduces the frequency of exacerbations of diseases, reduces the risk of rapid progression of the inflammatory process and respiratory failure in COPD, reduces the frequency of exacerbations of concomitant diseases of the respiratory tract (rhinitis, sinusitis, laryngitis, tracheitis ), which can also provoke the development of exacerbations of COPD. The use of bacterial vaccines helps to reduce the number of courses of antibacterial therapy, which avoids the immunosuppressive effects of antibiotics, the emergence of resistant strains, mucosal dysbiosis and the development of other complications.

1. Bronchitis

Classification of bronchitis (1981)

Acute (simple) bronchitis

Acute obstructive bronchitis

Acute bronchiolitis

Recurrent bronchitis, obstructive and non-obstructive

Downstream:

exacerbation,

remission

1.1. Acute (simple) bronchitis- This is usually a manifestation of a respiratory viral infection. The general condition of the patients was slightly impaired. Characterized by a cough and fever for 2-3 days, maybe more than 3 days (the duration of the temperature reaction is determined by the underlying viral disease). There are no percussion changes in the lungs.

Auscultation-widespread (scattered) dry, large- and medium-bubbling wet rales. The duration of the disease is 2-3 weeks.

Examination methods: patients with acute bronchitis do not need x-ray and laboratory examination in most cases. A chest x-ray and blood test are necessary if pneumonia is suspected.

Treatment of patients with bronchitis is carried out at home. Hospitalization is required for young children and patients with persistent temperature reactions. Children stay in bed for 1-2 days; at low temperatures, a general regime can be allowed. Treatment table 15 or 16 (depending on age). Drinking regimen with sufficient fluid intake; compotes, fruit drinks, water, sweet tea, oralit, for older children - warm milk with Borjom.

Drug therapy is aimed at reducing and alleviating cough. To reduce cough, the following are prescribed:

libexin 26-60 mg per day, i.e. Swallow 1/4-1/2 tablets 3-4 times a day without chewing);

tusuprex 6-10 mg per day, i.e. 1/4-1/2 tablets 3-4 times a day or Tusuprex syrup 1/2-1 tsp. (in 1 tsp - 6 ml);

Glauvent 10-25 mg, i.e. 1/1--1/2 tablets 2-3 times a day after meals.

Bromhexine and mucolytic drugs relieve cough, help thin sputum, improve the function of the ciliated epithelium. Bromhexine is recommended for children aged 3 to 6 years - at a dose of 2 mg, i.e. 1/4 tablet 3 times a day, from 6 to 14 years - 4 mg, i.e. 1/2 tablet 3 times a day. Bromhexine is not prescribed to children under 3 years of age! Ammonia-anise drops and breast elixir (as many drops as the child’s age), percussion (from 1/2 tsp to 1 tsp 3 times a day) and breast tea (No. 1) have a mucolytic effect : marshmallow root, coltsfoot leaf, oregano herb - 2:2:1; No. 2: coltsfoot leaf, plantain, licorice root - 4:3:3; No. 3: sage herb, anise fruits, pine buds, marshmallow root, licorice root - 2:2:2:4:4). Prepared decoctions give 1/4-1/3 cup 3 times a day.

In the hospital, from the first days of illness, steam inhalations are prescribed (for children over 2 years old!) with a decoction of breast tea or infusions of chamomile, calendula, mint, sage, St. John's wort, wild rosemary, pine buds (decoctions are prepared immediately before use in the form of 5-10% solutions , inhalations are carried out 3-4 times a day). You can use ready-made tinctures of mint, eucalyptus, cadendula, plantain juice, colanchoe from 15 drops to 1-3 ml for inhalation, depending on age. Thermal procedures: mustard plasters on the chest, warm baths.

Dispensary observation for 6 months. In order to prevent relapses of bronchitis, the nasopharynx is sanitized in those surrounding the sick child. In 2-3 months. Prescribe (for children over 1.6-2 years old) inhalations with decoctions of sage, chamomile or St. John's wort daily for 3-4 weeks and a complex of vitamins. Preventive vaccinations are carried out after 1 month. subject to complete recovery.

1.2. Acute obstructive bronchitis is the most common form of acute bronchitis in young children. Obstructive bronchitis has all the clinical signs of acute bronchitis in combination with bronchial obstruction. Observed; prolonged exhalation, expiratory noise (“whistling” exhalation), wheezing on exhalation, participation of auxiliary muscles in the act of breathing. At the same time, there are no signs of severe respiratory failure. The cough is dry and infrequent. The temperature is normal or low-grade. The severity of the condition is due to respiratory disorders with mild symptoms of intoxication. The current is favorable. Respiratory distress decreases within 2-3 days, wheezing can be heard for a longer period of time.

Young children with bronchial obstruction syndromes must be hospitalized.

Examination methods:

General blood test

Consultation with an ENT specialist

Allergy examination of children after 3 years of age for the purpose of early diagnosis of bronchospasm of allergic origin

Consultation with a neurologist if there is a history of perinatal CNS injury.

1. Eufillin 4-6 mg/kg IM (single dose), if the symptoms of bronchial obstruction decrease, continue to give aminophylline 10-20 mg/kg per day evenly every 2 hours orally.

2. If aminophylline is ineffective, administer a 0.05% solution of alupent (orciprenaline) 0.3-1 ml intramuscularly.

3. If there is no effect and the condition worsens, administer prednisolone 2-3 mg/kg IV or IM.

In the following days, antispasmodic therapy with aminophylline is indicated for those children in whom the first administration of the drug was effective. You can use a 1-1.5% solution of etimizol IM 1.5 mg/kg (single dose).

Clinical observation is to prevent repeated episodes of bronchial obstruction and relapses of bronchitis. For this purpose, inhalations of decoctions of sage, St. John's wort, and chamomile are prescribed daily for 3-4 weeks in the autumn, winter and spring seasons of the year.

Preventive vaccinations are carried out every 1 month. after obstructive bronchitis, subject to complete recovery.

1.3. Acute bronchiolitis is a common lesion of the smallest bronchi and bronchioles, leading to the development of severe airway obstruction with the development of symptoms of respiratory failure. Mostly children in the first months of life are affected (parainfluenza and respiratory syncytial bronchiolitis), but children in the second or third year of life can also be affected (adenoviral bronchiolitis).

Obstructive syndrome often develops suddenly and is accompanied by a loud, dry cough. The increase in respiratory distress is accompanied by severe anxiety in the child, low-grade fever (with parainfluenza and respiratory syncytial infections) or febrile (with adenovirus infection) temperature. The patient's severe and extremely serious condition is caused by respiratory failure. Chest swelling, a box-shaped percussion sound are detected, and upon auscultation of the lungs, a mass of fine-bubbly and crepitating rales are heard. Diffuse changes in the lungs against the background of severe obstruction with a very high probability (up to 90-95%) exclude pneumonia. X-ray reveals swelling of the lungs, increased bronchovascular pattern, and possible microatelectasis. Complications of bronchiolitis may include reflex cessation of breathing, the development of pneumonia, and repeated episodes of bronchial obstruction (in almost 50% of patients).

Examination methods:

X-ray of the lungs in two projections

General blood test

Determination of the acid-base state of blood (ABC)

Mandatory hospitalization in hospital for emergency care

Oxygen inhalation. Supply of humidified oxygen through nasal catheters for children over 1-1.6 years old in an oxygen tent DPK-1 - 40% oxygen with air

Removing mucus from the respiratory tract

Infusion therapy in the form of intravenous drip infusions is indicated only taking into account hyperthermia and fluid loss due to shortness of breath

Antibiotic therapy is indicated because in the first day of increasing severity of the patient’s condition it is difficult to exclude pneumonia. Semi-synthetic penicillins are prescribed, in particular, ampicillin 100 mg/kg per day in 2-3 injections (it should be noted that antibiotic therapy does not reduce the degree of obstruction!)

Eufillin 4-5 mg/kg IV or IM (single dose), but not more than 10 mg/kg per day (a decrease in the severity of obstruction is observed in only 50% of patients!!)

If aminophylline is ineffective, administer a 0.05% solution of adupent (orciprenaline) 0.3-0.5 ml intramuscularly. You can use Alupent inhalations 1 or 1 per inhalation, inhalation duration 10 minutes.

Obstructive syndrome, which is not relieved for a long time by the administration of aminophylline, alupent, requires the administration of corticosteroids: prednisolone 2-3 mg/kg parenterally (iv or i.m.)

Cardiotonic drugs for tachycardia!) - intravenous drip administration of a 0.05% solution of corglycone 0.1-0.6 ml every 6-8 hours.

Antihistamines are not indicated! Their drying, atropine-like effect can increase bronchial obstruction.

In severe cases of respiratory failure, mechanical ventilation is prescribed.

Clinical observation of children who have had bronchiolitis is aimed at preventing further sensitization and repeated episodes of bronchial obstruction. For children with repeated obstructive episodes, after the age of 3 years, it is recommended to perform skin tests with the most common allergens (dust, pollen, etc.).

Positive skin tests, as well as attacks of obstruction due to viral infection, indicate the development of bronchial asthma.

Preventive vaccinations for patients who have had bronchiolitis. carried out no earlier than after 1 month. subject to complete recovery.

1.4. Recurrent bronchitis is bronchitis that recurs 3 times or more during the year with an exacerbation lasting at least 2 weeks, occurring without clinical signs of bronchospasm, and tending to be protracted. It is characterized by the absence of irreversible, sclerotic changes in the bronchopulmonary system. The onset of the disease can be in the first or second year of life. This age is of particular importance in the occurrence of relapses of bronchitis due to poor differentiation of the epithelium of the respiratory tract and immaturity of the immune system. However, a diagnosis can be made with certainty only in the third year of life. Recurrent bronchitis mainly affects children of early and preschool age.

The clinical picture of relapse of bronchitis is characterized by an acute onset, an increase in temperature to high or low-grade levels. Recurrence of bronchitis is possible even at normal temperatures. At the same time, a cough appears or intensifies. Cough has a wide variety of characters. More often it is wet, with mucous or mucopurulent sputum, less often dry, rough, paroxysmal. It is a cough that increases in intensity that often serves as a reason to consult a doctor. Cough can be triggered by physical activity.

The percussion sound over the lungs is unchanged or with a slight boxy tint. The auscultatory picture of relapse of bronchitis is varied: against the background of harsh breathing, moist large and medium bubbles are heard. as well as dry wheezing, variable in character and location. Wheezing is usually heard for a shorter period of time than complaints of cough. It should be noted that patients with recurrent bronchitis often exhibit increased cough readiness, i.e. children begin to cough after slight cooling, physical exertion, or during the next acute respiratory viral infection.

Forecast. In the absence of adequate therapy, children remain ill for years, especially those who become ill at early and preschool age. There may be a transformation of recurrent bronchitis into asthmatic and bronchial asthma. A favorable course of recurrent bronchitis is observed in children in whom it is not accompanied by bronchospasm.

Examination methods:

Blood test

Bacteriological examination of sputum

X-ray of the lungs (in the absence of X-ray examination during periods of previous relapses of bronchitis and if pneumonia is suspected)

Bronchoscopy for the purpose of diagnosing the morphological form of endobronchitis (catarrhal, catarrhal-purulent, purulent)

Cytological examination of bronchial contents (imprint smears from the bronchi)

Study of external respiration function; pneumotachometry to determine the state of airway patency, spirography to assess the ventilation function of the lungs

Immunogram

It is advisable to hospitalize patients with exacerbation of recurrent bronchitis, but treatment is also possible on an outpatient basis

It is necessary to create an optimal air condition with an air temperature of 18-20C and a humidity of at least 60%

Antibacterial therapy, including antibiotics, is prescribed if there are signs of bacterial inflammation, in particular purulent sputum. Courses of antibiotic therapy (ampicillin 100 mg/kg, gentamicin 3-5 mg/kg, etc.) are prescribed for 7-10 days

Inhalation therapy is one of the most important types of therapy in the treatment complex, prescribed to eliminate bronchial obstruction.

It is carried out in three stages. At the first stage, he prescribes inhalations of solutions of salts, alkalis and mineral waters. A mixture prepared from equal volumes of 2% sodium bicarbonate solution and 5% ascorbic acid solution, the volume of the inhalation mixture according to age, is effective for liquefying and removing sputum. In the presence of mucopurulent sputum, enzyme preparations are administered by inhalation (Appendix No. 1). The duration of the first stage is 7-10 days.

At the second stage, antiseptics and phytoncides are administered by inhalation. For this purpose, onion and garlic juice, decoctions of St. John's wort (Novoimanin), wild rosemary, pine buds, ready-made tinctures of mint, eucalyptus, calendula, plantain juice, colanchoe, inhalations with lysozyme, propolis are prescribed (Appendix No. 2). The duration of the second stage is 7-10 days.

At the third stage, oil inhalations are prescribed. Uses vegetable oils that have a protective effect. The duration of the third stage is also 7-10 days.

Mucolytic (secretolytic) agents (see section acute simple bronchitis) are prescribed only at the first stage of inhalation therapy

Expectorants (secretomotor) drugs; decoctions and infusions of herbs (thermopsis, plantain, coltsfoot, thyme, wild rosemary, oregano), marshmallow root, licorice and elecampane, anise fruits, pine buds. These medicines make up medicinal mixtures used to relieve cough

Physiotherapeutic procedures: microwaves on the chest (electromagnetic oscillations of ultra-high frequency in the centimeter range, SMV, device "Luch-2" and decimeter range, UHF, device "Romashka".

Treatment for patients with exacerbation of recurrent bronchitis is carried out (at home or in a hospital) for 3-4 weeks. Patients with recurrent bronchitis should be registered at a dispensary. Children are monitored by local pediatricians. The frequency of examinations depends on the duration of the disease and the frequency of relapses, but at least 2-3 times a year. If there is no recurrence of bronchitis within 2-3 years, the patient can be removed from the register. Consultations with specialists are carried out according to indications: a pulmonologist if the development of a chronic bronchopulmonary process is suspected; an allergist if bronchospasm appears; otolaryngologist to monitor the condition of the ENT organs.

Rehabilitation of patients with recurrent bronchitis is carried out according to the principle of improving the health of frequently ill children:

1. Sanitation of foci of chronic infection in the ENT organs: chronic tonsillitis, sinusitis, adenoiditis

2. Elimination of concomitant diseases of the digestive system: dyskinesia of the biliary system, intestinal dysbiosis, etc.

3. Correction of metabolic disorders is prescribed throughout the year. Approximate diagram:

August - riboxin and potassium orotate;

September - vitamins B1, B2, calcium panthetonate and lipoic acid;

October - tincture of Eleutherococcus;

November multivitamin preparations (decamevit, aerovit, undevit, hexavit, kvadevit, etc.), lipoic acid;

December - Aralia tincture, inhalation with plantain decoction;

January - vitamins B1, B2. calcium pantetonate and lipoic acid;

February - riboxin and potassium orotate;

March - multivitamin preparations;

April - vitamins B1, B2, calcium pantetonate, lipoic acid;

May - tincture of Eleutherococcus (pantocrine).

The complexes are prescribed in age-specific dosages in 10-day courses

4. Adaptogen drugs: methyluracil 0.1-0.6 orally 3-4 times a day after or during meals, 3-4 weeks. Dibazol 0.003-0.03 once a day. 3-4 weeks

b. Inhalations with sage decoction, 25-30 inhalations daily in winter and spring

6. Reaferon (genetically engineered - interferon) intranasally in doses of 300 and 600 units for 6 days (winter, spring)

7. Speleotherapy for children over 5 years of age in order to normalize mucociliary clearance and improve sputum evacuation, daily, 20 sessions

8. Physical therapy

9. Massage: acupressure, classic, vibration

10. Hardening procedures.

During the rehabilitation period, immunological examination of patients is carried out. In cases of immunodeficiency syndrome, immunocorrective therapy is indicated after consultation with a clinical immunologist.

1.6. Recurrent obstructive bronchitis has all the clinical symptoms of recurrent bronchitis, accompanied by episodes of bronchial obstruction. Like recurrent bronchitis, it refers to preasthma.

Examination methods:

Functional ventilation test with bronchodilators. The following indicators are used: vital capacity of the lungs (VC). maximum ventilation (MVV), expiratory pneumotachometry (EPT), forced vital capacity (FVC).

The listed ventilation parameters are recorded before and after the administration of a bronchodilator (ephedrine, aminophylline). The presence of bronchospasm in the examined patients is indicated by an increase in 2-3 of 4 indicators, most often VC and MVL. A positive functional ventilation test with bronchodilators, indicating bronchospasm, requires differential diagnosis of recurrent obstructive bronchitis with asthmatic bronchitis.

Other methods of examining patients with obstructive recurrent bronchitis are similar to examining children with recurrent bronchitis.

Treatment of patients with recurrent obstructive bronchitis is carried out according to the same principle as for patients with recurrent bronchitis. Additionally, bronchospasmolytics are prescribed - aminophylline, alupent (see Treatment of acute obstructive bronchitis). Clinical observation of patients is aimed at preventing relapses of bronchial obstruction and bronchitis. Rehabilitation of patients is based on the same principle as for patients with recurrent bronchitis. Rehabilitation measures are planned taking into account the results of an allergological examination with the most common allergens. In the process of clinical observation and according to allergological examination, the diagnosis of “recurrent obstructive bronchitis” can be verified. Probable diagnoses may be asthmatic bronchitis, and in the presence of typical asthma attacks - bronchial asthma.

1.6. Bronchial asthma is a chronic allergic disease in which the immunopathological process is localized in the bronchopulmonary system and is clinically characterized by recurrent, reversible attacks of suffocation caused by acute impairment of bronchial obstruction.

Classification of clinical forms of bronchial asthma (S.S. Kaganov, 1963)

Form of the disease

1. Atopic

2. Infectious-allergic

3. Mixed

Typical:

1. Severe attacks of bronchial asthma

2. Asthmatic bronchitis

Atypical:

Attacks of acute emphysematous bloating

Severity

2. Moderate

3. Heavy

Severity indicators:

1. Frequency, nature and duration of attacks

2. The presence and severity of changes in the interictal period from:

a) respiratory system;

b) cardiovascular system;

c) nervous system;

d) metabolic processes:

e) physical development;

1. With isolated attacks, with an asthmatic condition, with asphyxial syndrome

2. With bronchopulmonary infection, with inflammatory changes in the nasopharynx

3. With concomitant allergic diseases:

a) with allergic dermatoses (eczema, urticaria, Quincke's edema);

b) with other clinical forms of respiratory allergies (allergic rhinitis, sinuitis, tracheitis, bronchitis, pneumonia, eosinophilic pulmonary infiltrate)

4. With complications:

a) chronic (persistent) pulmonary emphysema;

b) cor pulmonale;

c) pulmonary atelectasis;

d) pneumothorax;

e) mediastinal and subcutaneous emphysema;

f) neurological disorders;

With a mild degree of the disease, exacerbations are rare and short-lived; with moderate-severe bronchial asthma, exacerbations occur monthly. Severe bronchial asthma is characterized by frequent exacerbations. Attacks of suffocation occur weekly, and often daily, with the transition to an asthmatic state. An attack of bronchial asthma, lasting from several minutes to several hours and days, is determined by acute bronchospasm. There is expiratory shortness of breath with noisy wheezing exhalation. Patients are bothered by a cough with difficult to separate viscous sputum. Percussion of the lungs reveals a boxy tint of the percussion sound, and upon auscultation multiple dry rales. In young children, moist rales of various sizes are heard in the lungs, since at this age, during an attack of bronchial asthma, it is not bronchospasm that predominates, as in older children, but inflammatory swelling of the bronchial mucosa and excess mucus production.

The atopic form of bronchial asthma is characterized by the acute development of an attack and in mild cases, bronchial patency can be restored quite quickly.

Exacerbation of infectious-allergic bronchial asthma begins slowly and gradually. Obstructive syndrome, when prescribed bronchospasmolytics, is relieved slowly.

In the lungs, not only dry rales, but also moist rales of various sizes can be heard for a long time.

With a mild attack of bronchial asthma, the patient’s well-being suffers little. A moderate-to-severe attack has a clinical picture of asthmatic suffocation. Accessory muscles are involved in the act of breathing, tachycardia and increased blood pressure are observed. A severe attack is characterized by clinical symptoms of respiratory failure against the background of severe asthmatic suffocation.

An intractable attack of bronchial asthma lasting 6 hours or more is classified as an asthmatic condition, which can develop into asthmatic status. For status asthmaticus II and III degrees. total obstruction of the bronchi occurs as a result of their filling with thick viscous secretions, severe inflammatory infiltration of the mucous membrane and spasm of smooth muscles. Breathing sounds disappear in the lungs (silence syndrome), a decrease in blood pressure, muscle hypotension, and a drop in cardiac activity are observed.

Prognosis: the course of bronchial asthma is difficult to predict. Parents of sick children should not expect a quick recovery. Their energy should be directed toward long-term treatment that would prevent new attacks and alleviate their severity. The atopic form of bronchial asthma has a more favorable prognosis with timely identification of causally significant allergens and specific hyposensitization. Infectious-allergic and mixed forms of bronchial asthma more often than atopic asthma remain throughout childhood, adolescence and become a disease of adults.

Examination methods:.

1. General blood test

2. Immunogram (determination of T-I B-lymphocytes. Tn-helpers, Ts-suppressors, Tn/Ts indicator, content of serum immunoglobulins, circulating immune complexes (CICs)

3. Study of the acid-base state of the blood (ABS)

5. Consultation with an ENT specialist followed by sanitation of foci of chronic infection in the ENT organs

6. In the interictal period, performing skin prick tests with non-infectious allergens.

7. Radioallergosorbent test (RAST), which allows to detect specific immunoglobulins (class E-IgE) in blood serum.

A mild attack of bronchial asthma can be relieved at home. For these purposes, bronchospasmolytics are prescribed orally or by inhalation: ephedrine (children from 2 to 6 years old, 0.003-0.01 g, from 6 to 12 years, 0.01-0.02 g), aminophylline 3-4 mg/kg (single dose) up to 12-16 mg/kg per day. You can use combination drugs: theophedrine, antasman (children from 2 to 6 years old 1/4-1/3 tablets per dose, children from 6 to 12 years old 1/2-3/4 tablets), solutan in a dosage of 1 drop for 1 year life. Orciprenaline (0.76 mg per inhalation or 1/4-1/2 tablets orally), alupent (1-2 inhalations or 1/4 tablet for children under 6 years old, 1/2 tablet for children aged 6 years and older) is also recommended. .5% solution of Asthmopent and Berotec 1-2 inhalations, salbutamol (inhalation package - 0.1 mg of the drug, children from 4 to 7 years old 1 inhalation, school-age children 1-2 inhalations), ventolin (in inhalation packages prescribed in the same dosage, like salbutamol, orally for children 3-4 years old 1/6 tablet, 6-7 years old 1/3 tablet, 7-14 years old 1/2 tablet).

Patients with moderate to severe attacks of bronchial asthma should be immediately hospitalized. The following activities should be carried out in the hospital.

A moderate-to-severe attack can be stopped with fast-acting sympathomimetics, for example, parenteral administration of a 0.1% solution of adrenaline subcutaneously at a rate of 0.01 mg/kg in combination with a 5% solution of ephedrine 0.6-0.75 mg/kg. The effect of adrenaline occurs after 15 minutes, ephedrine after 45 minutes, the duration of action of these drugs is 4-6 hours. Alupent IM or SC (0.3-0.5 ml), aminophylline IM (4- 6 mg/kg single dose). After removing the acute manifestations of a moderate-severe attack, in order to stabilize the patients’ condition, it is advisable to carry out a 5-7-day course of treatment with aminophylline or ephedrine, prescribing a single dose of the drugs orally 3-4 times a day.

Antihistamines are used if there is no difficulty in sputum discharge. Oxygen therapy is required!

A severe attack of bronchial asthma requires immediate intravenous administration of aminophylline at the rate of 6-8 mg/kg (single dose) or 1 ml per year of life, but not more than 10 ml. Outside the hospital, the drug can be administered in a stream, but slowly, over 5-10 minutes. in 10-15 ml of 15-20% glucose solution. In the hospital, it is necessary to administer aminophylline intravenously, dropwise in 150-250 ml of isotonic sodium chloride solution. Severe respiratory failure and resistance to previously used sympathomimetics requires intravenous administration of prednisolone (1-2 mg/kg) or hydrocortisone (5-7 mg/kg).

Oxygen therapy in a somatic hospital: humidified oxygen for 20-30 minutes. every 2 hours, in a specialized department, an oxygen-air mixture containing 35-40% oxygen.

After the attack of bronchial asthma is relieved, treatment with aminophylline should be continued until the obstructive syndrome is completely eliminated, but the method of administration of the drug can be changed by prescribing it intramuscularly or orally, or in suppositories. Treatment is supplemented by the prescription of mucolytic drugs (mucaltin, bromhexine, herbal decoctions: thyme, elecampane, plantain, infusions of birch buds, pine needles, etc.).

Treatment of patients with stage I status asthmaticus, which is a prolonged severe attack of bronchial asthma, is carried out according to the same program with the addition of antibiotic therapy due to the activation of bronchopulmonary infection. Semi-synthetic penicillins or aminoglycoaids are recommended; cephalosporins may be prescribed.

If metabolic acidosis is detected, in order to correct it, a 4% sodium bicarbonate solution is prescribed at a rate of 2-2.5 ml/kg under the control of blood pH (required level 7.25); heparin 180-200 units/kg (under the control of a coagulogram); 1% Lasix solution 0.5 mg/kg per day (for insufficient diuresis); cardiotonic drugs - 0.06% solution of corglycone for children aged 2 to 5 years 0.2-0.5 ml, from 6 to 12 years 0.5-0.75 ml. Repeated drip administration of aminophylline! Continue the administration of prednisolone, but orally for 5-7 days with gradual withdrawal over a period of two weeks. Treatment of status asthmaticus is carried out by prescribing a hypoallergenic diet or a fasting day with kefir.

Asthmatic status II degree. requires expanding the scope of therapeutic intervention aimed at restoring bronchial patency. In this condition, the dosage of prednisolone is increased to 3-5 mg/kg, which is administered intravenously along with zufillin. Correction of metabolic acidosis is necessary. Clinical signs of heart failure require the administration of cardiotonic drugs with simultaneous intravenous administration of 50-100 mg of cocarboxylase and potassium preparations. Therapeutic bronchoscopy with removal of mucus and injection of sodium bicarbonate solutions into the bronchial lumen is indicated. As the patient's condition improves, the dose of prednisolone is reduced to 1-1.5 mg/kg, administered orally for 2-2.5 weeks, followed by discontinuation.

Asthmatic status III degree. requires transfer of the child to the intensive care unit and the appointment of mechanical ventilation. It is possible to carry out plasmapheresis or hemosorption. The dose of prednisolone is increased to 6-10 mg/kg, of which 4-8 mg/kg is administered intravenously, 2 mg/kg orally. At the same time, aminophylline and cardiotonic drugs are prescribed according to the previous program. Treatment with corticosteroids is carried out with their gradual withdrawal over 3-4 weeks. During the period of corticosteroid withdrawal, it is advisable to prescribe calcium pantetonate (vitamin B5). vitamin B6, etimizol, glyceram, inductothermy on the adrenal gland area. Withdrawal syndrome can be prevented by prescribing aerosols of hormones: becotide, beclamate.

Rehabilitation

1. Home regimen with the exclusion of causally significant allergens. Complete prohibition of smoking, keeping animals, fish, birds in the apartment and house, refusal of medications to which an allergic reaction has been noted

2. Medical nutrition with the exclusion of obligate food allergens

3. Sanitation of foci of chronic infection of the ENT organs in the patient and in those surrounding the sick child

4. Identification and treatment of chronic diseases of the digestive system (biliary dyskinesia and cholecystitis, duodenogastric reflexes and gastroduodenitis), deworming, treatment of giardiasis, intestinal dysbiosis. Prescription of biologically active drugs (lacto-, coli-, bifidumbacterin, fermented milk bifidumbacterin) for 1-1.5 months, enzyme preparations for 2 weeks, enterosorbents (activated carbon from 10 to 30 g per day, cholestyramine according to 4-8 g per day for 5-7 days and vazazan-r at the same dosage for 5-7 days at night; enterodesis 10% solution up to 150-200 ml orally, in 3-4 doses during the day.

5. Vitamin B6 courses of 50-100 mg for 1-2 months.

6. Inhalation of intal or ifiral 2-4 times a day for 2-4 months. Longer use of Intal is also possible (from 1 to 3 years), if it maintains stable remission

7. Zaditen (ketotifen), single dose 0.025 mg/kg, 2 times a day or 0.125 ml/kg in the form of syrup 2 times a day, morning and evening, 6-9 months; astafen 1 mg 2 times a day with food for several weeks

8. Teopek - first 1/2 tablet 1-2 times a day, and then 1 tablet 2 times a day, orally after meals with water, for 1-2 months. Do not chew or dissolve in water!!

9. Histaglobulin: course of treatment is 5 injections with an interval of 3-4 days, start with 0.5 ml, then 1 ml. Repeated courses after 2-3 months.

human placental blood 6 ml 2 times a month for 2 months.

11. Acupuncture 15-20 sessions daily/or every other day, 2-3 courses per year

12. Speleotherapy

13. Patients with hormone-dependent bronchial asthma are prescribed prednisolone in a maintenance dosage of 5-15 mg per day. During treatment with zaditen (ketotifen, astafen), it is sometimes possible to discontinue corticosteroids or reduce their dosage

14. For atopic bronchial asthma, 15% solution of dimephosphone 75-100 mg/kg (10-15 ml 3 times a day, orally, for one month)

15. Inhalation of a 5% solution of unithiol (0.1 ml/kg) in combination with oil inhalations of vitamin E 2-3 mg/kg, 10-15 inhalations per course of treatment. Repeated preventive courses 2-3 times a year, 10 inhalations of each drug every other day (the best effect with moderate-severe mixed and atopic forms of bronchial asthma)

16. Long-term (from several months to a year), continuous use of theophylline is possible

17. Vilosen electrophoresis on the chest, 8-10 procedures daily. Repeated courses in autumn-winter-spring

18. Specific hyposensitization (SH therapy) is carried out mainly with household and pollen allergens

19. Regular physical therapy, 2-3 times a day, for a long time

20. Various forms of massage (general, vibration, acupressure)

21. Sanatorium treatment in mountain climatic conditions. People with bronchial asthma are not removed from dispensary registration. They are subject to supervision by a local doctor and a doctor at an allergy clinic. During the rehabilitation period, an immunological examination of patients is carried out and, according to indications, immunocorrective therapy is prescribed.

Asthmatic bronchitis is a type of bronchial asthma. The development of asthmatic bronchitis is based on allergic swelling of the bronchial mucosa and blockage of the airways with mucous secretions. In asthmatic bronchitis, the allergic reaction develops mainly in the bronchi of medium and large caliber, as opposed to bronchial asthma, in which small bronchi and bronchioles are involved in the pathological process. This is associated with the peculiarities of clinical symptoms: during exacerbation of asthmatic bronchitis there are no typical attacks of suffocation (!), shortness of breath of a mixed type with a predominance of the expiratory component, with the participation of auxiliary muscles, wet frequent cough, distant wheezing.

The classification of asthmatic bronchitis is identical to the classification of bronchial asthma. Treatment and rehabilitation of patients is carried out according to the same program as for bronchial asthma.

1.7. Acute pneumonia is an acute inflammatory process in the lung tissue, occurring as an independent disease or as a manifestation or complication of any disease.

Classification of acute pneumonia

Focal (including focal-confluent)

Segmental

Krupoznaya

Interstitial

2. Current

Lingering

3. Manifestations (complications)

Respiratory failure

Cardiovascular failure

Pulmonary edema

Destruction of lung tissue

Pneumothorax

Meningitis, etc.

Characterized by an acute onset of the disease with an increase in temperature to febrile levels. The high temperature lasts for at least 3 days, accompanied by chills. Pneumonia can occur not only suddenly, but also against the background of an ongoing respiratory viral infection. The cough is less often dry, more often wet. There are disturbances in the general condition in the form of decreased appetite, changes in behavioral reactions (excitement or, on the contrary, apathy), sleep, decreased emotional tone, indicating pneumonic toxicosis. From the first days of the disease, patients experience shortness of breath; in severe cases, moaning or groaning breathing is observed. When examining patients, changes in breathing over the affected area of ​​the lung are revealed: harsh or bronchial, very often weakened breathing. During percussion in the area of ​​the inflammatory process, a shortening of the percussion sound is observed. Listening to moist fine rales over a limited area of ​​the lung makes the diagnosis of pneumonia very likely, but in patients with acute pneumonia, rales may not be heard throughout the entire illness.

Infants and young children with pneumonia require immediate hospitalization. The duration of hospital stay is 20-21 days, in complicated cases 1-1.5 months. Patients of preschool age and schoolchildren, at the request of parents, can be treated at home, subject to all the recommendations of the local doctor.

Examination methods:

1. X-ray of the lungs in two projections, taking into account the localization of the inflammatory bronchopulmonary process (right or left-sided pneumonia)

2. General blood test.

1. Organization of medical and protective regime.

2. Treatment table 16 or 15 (depending on age). Additional administration of liquid in a volume of 300-500 ml in the form of tea, berry and fruit decoctions, fruit drinks, juices, mineral water, Oralite (oralite formulation: per 1 liter of water 3.5 g of sodium chloride, 2.5 g of sodium bicarbonate, 1. 6 g potassium chloride, 20-40 g glucose). With properly organized oral rehydration, in almost all cases, IV infusion therapy can be abandoned. In case of uncomplicated pneumonia, you should limit yourself to parenteral administration (IM) of one antibiotic, preferably the penicillin series (benzyl-penicillin 150 mg/kg, semi-synthetic penicillins - ampicillin, ampiox 150-200 mg/kg, carbenicillin 200 mg/kg).

The absence of a positive effect after 24-49 hours, namely: a decrease in temperature to normal or low-grade levels, a reduction or elimination of symptoms of intoxication, an improvement in general condition and appetite, as well as an increase in pulmonary changes require therapeutic correction in the form of prescribing a second antibiotic (i.e. in administration) or changing antibiotics with the prescription of cephalosporil 100 mg/kg, aminoglycosides (gentamicin 3-5 mg/kg), lincomycin 30-50 mg/kg, chloramphenicol 50 mg/kg, erythromycin 20 mg/kg. Enteral use of antibiotics is not recommended due to the risk of developing dysbacteriosis!

4. Infusion therapy (iv) includes the administration of glucose-saline solutions: 1056 glycose solution in a 1:1 ratio with saline, hemodez, rheopolyglucin (glucose 50 ml/kg, rheopolyglucin 10 ml/kg, hemodez 10-20 ml/kg ), plasma or albumin 5-10 ml/kg. The calculation of the infusion fluid is based on pathological losses, which in pneumonia are limited to high fever and shortness of breath, while the volume of fluid, as a rule, does not exceed 30 ml/kg.

5. Cardiotonic drugs; 0.065% solution of corglycone 0.1-0.15 ml per year of life or 0.05% solution of strophanthin 0.1 ml per year of life, i.v. You can use digoxin 0.007-0.01 mg/kg per day on the first day of pneumonia complicated by pneumonic toxicosis

6. Corticooteroids (prednisolone) are used as a means of combating toxic-infectious shock, cerebral edema, secondary cardiopathy, pulmonary edema and microcirculation disorders. Prescribed for severe condition of patients at a dose of 4-6 mg/kg IV for 1-3 days

7. If a destructive form of pneumonia is suspected and there is a threat of disseminated intravascular coagulation syndrome, the following are prescribed: antiproteases (contrical 1000 units/kg, but not more than 15 thousand), heparin 200-250 units/kg (under the control of a coagulogram)

8. Immunotherapy is indicated for severe, complicated staphylococcal and pseudomonas pneumonia. Proteus etiology. It is recommended to use immunoglobulin at a rate of 1-2 ml/kg IM, hyperimmune antistaphylococcal immunoglobulin 100 IU daily for 3-5 days, hyperimmune plasma with high titers of the corresponding antitoxin at a dose of 5-15 ml/kg

9. Attention! Blood transfusions(!) are indicated for long-term purulent-destructive process in a child with a hemoglobin content of 65 g/l

10. Oxygen therapy: administration of humidified oxygen through a nasal catheter or in an oxygen tent DPK-1

11. Physiotherapy: SMT-phoresis on the chest No. 7-10, intraorgan electrophoresis of antibiotics No. 5-6 daily for acute inflammatory process, calcium electrophoresis No. 10, daily during the period of resolution of pneumonia

12. Symptomatic therapy, including a complex of vitamins, enzyme preparations, biologically active drugs, is prescribed after improvement of general well-being, elimination of clinical symptoms of intoxication and respiratory failure. The duration of stay of patients in the hospital is 21-24 days, with a complicated form up to 1-1.5 months.

Rehabilitation. Rehabilitation activities are carried out for 3 months.

Children are deregistered after a year. In the first month after discharge from the hospital they are examined weekly, in the second or third month of observation once every 2 weeks, then monthly.

Repeated X-ray examination is recommended in cases where patients are discharged with residual effects of pneumonia. In the autumn-winter-spring period, inhalation therapy is carried out with the appointment of inhalations of a decoction of St. John's wort (novoimanin), chamomile, calendula, plantain, and phytoncides (see Rehabilitation of recurrent bronchitis). Seasonal courses of vitamins and biologically active drugs. Chest massage No. 15-20.

Classes in the physical therapy room for 1-1.5 months. Schoolchildren can continue classes in sports sections after 1-1.5 months. after the control ECG.

Preventive vaccinations are carried out no earlier than after 2 months. after recovery (in cases of uncomplicated form), after 6 months. after suffering destructive pneumonia. If the course of pneumonia was accompanied by neurotoxicosis, preventive vaccinations are carried out after consultation with a neurologist.

1.8. Chronic pneumonia is a chronic nonspecific bronchopulmonary process, which is based on irreversible morphological changes in the form of bronchial deformation and pneumosclerosis in one or more segments and is accompanied by relapses of inflammation in the lung tissue and (or) in the bronchi. Chronic pneumonia with deformation of the bronchi (without their expansion) and bronchiectasis is distinguished. The severity of chronic pneumonia is determined by the volume and nature of bronchial lesions, the frequency and duration of exacerbation, and the presence of complications.

In children with chronic pneumonia, a history of acute pneumonia is detected, often its complicated course or destructive form. Repeated pneumonia and increased incidence of acute respiratory viral infections and bronchitis are noted.

The clinical symptoms of chronic pneumonia are determined by the localization and extent of the pathological process. Most often, the bronchopulmonary process is localized in the lower lobe of the left lung, then in the lingular segments, then in the lower and middle lobes of the right lung, and only in some cases in the segments of the upper lobe. Exacerbation of chronic pneumonia occurs, as a rule, of the bronchitis type. The onset of exacerbation is gradual. The temperature rises, the wet cough intensifies, the amount of sputum increases, which becomes mucopurulent or purulent in nature. The amount of sputum is small (20-50 silt), and only in the bronchiectasis version of chronic pneumonia is there a large amount of sputum “mouthful” (up to 100-150 ml per day). Physical changes in the lungs are increasing in the form of the appearance of a large number of wet rales of different sizes or dry rales both in the area of ​​previously diagnosed chronic pneumonia and in places where they have not previously been heard. It is important to emphasize the increase in auscultation pattern in the lungs, since the constant presence of wet or dry rales in the area of ​​the affected segment or segments is one of the most characteristic signs of chronic pneumonia. Mixed shortness of breath (inspiratory-exspiratory) is intensifying, which before the exacerbation was observed only during physical activity. The exacerbation lasts from 2-3 to 4-6 weeks.

Exacerbation of chronic pneumonia can occur with symptoms of acute pneumonia. The onset of exacerbation is acute, with an increase in temperature to febrile levels. The severity of the general condition, signs of intoxication, shortness of breath, cyanosis increase, and the cough intensifies. Moist, fine-bubbling and crepitating rales are heard, first in the area of ​​the primary lesion, and then in neighboring areas and in the unaffected lung. The exacerbation period lasts from 3 weeks to 2-3 mod.

Currently, it is proposed to distinguish 2 variants of the course of chronic pneumonia. The first is “small” forms, in which the general condition of children and their physical development do not suffer. Exacerbations are rare, 1-2 times a year, with a short-term increase in temperature, a scant amount of sputum, and an increase in the physical picture. Outside of exacerbation, children feel quite satisfactory; in the affected area, wheezing is heard only with deep inspiration and forced exhalation. The second option is bronchiectasis. In recent years it has been rare. With this option, exacerbation is observed 2-3 times a year. The cough is wet, with the release of purulent sputum, almost constant. These children always show signs of intoxication. They are lagging behind in physical development. Physical symptoms in the form of weakened breathing, wet and dry wheezing in the affected area are observed almost constantly.

Examination methods:

1. X-ray of the lungs

2. Bronchoscopy

3. General blood test over time

4. Bacteriological examination of lavage fluid, i.e. bronchial lavage water during bronchoscopy with determination of sensitivity to antibiotics

5. Immunogram

6. Consultation with an ENT specialist

1. Hospitalization of patients during an exacerbation period

2. Regimen depending on the general condition of the patient

3. Table 15 with additional protein: meat, cottage cheese, eggs, cheese. Unlimited fruits and vegetables

4. Antibiotic therapy is carried out according to the same principle as for acute pneumonia and recurrent bronchitis. Duration of antibiotic therapy is 7-12 days

5. Inhalation therapy (see Recurrent bronchitis) is carried out in 3 stages

6. Mucolytic (secretolytic) and expectorant (secretomotor) drugs are prescribed in the same way. as with recurrent bronchitis

7. Physiotherapy: for exacerbation, ozokerite, paraffin applications, calcium, magnesium, copper, iodine electrophoresis, 10-12 procedures (2-55% solutions, galvanic current density 0.03-0.06 ml/cm3).

When the exacerbation subsides, high-frequency electrotherapy; microwaves - "Romashka" device, 10 procedures, 7-12 W, procedure duration 8-10 minutes. "Luch-3" device, 9-10 procedures, 48 ​​W, procedure duration 6-10 minutes. Inductothermy - IKV-4 device, 8-10 procedures, 160-200 mA, procedure duration 8-12 minutes.

8. Therapeutic bronchoscopy, course of 2-6 bronchoscopy

9. Therapeutic exercise: postural drainage 2-3 times a day (Quincke position: in the morning after waking up, hanging the torso from the bed with your hands resting on the floor, 5-10 minutes, making coughing movements). Performing a handstand against a wall, 5-10 minutes, 1-2 times a day. Vibration massage.

Attention! These types of physical therapy are prescribed only after the exacerbation has been eliminated (!) and during the rehabilitation period.

Rehabilitation

1. Examination by a pediatrician 2-3 times a year

2. Sanitation of foci of chronic infection in ENT organs

3. Immunological examination with immunotherapy (if indicated)

4. Treatment of concomitant diseases of the digestive system, prescription of biologically active drugs in courses of 2-4 weeks, 2-3 times a year

5. Inhalation therapy during unfavorable seasons of the year - spring-autumn-winter and during epidemic outbreaks of ARVI

6. Sanatorium-resort treatment in local sanatoriums in Crimea, Anapa, Kislovodsk. Balneotherapy: mineral baths of chloride, sodium, carbon dioxide, radon, sulfide. oxygen Therapeutic mud in the form of applications to the chest (in the absence of respiratory and cardiovascular disorders)

7. Physical therapy no earlier than a month after an exacerbation! Postural drainage and vibration massage 3-4 times a year. A set of measures is prescribed by the methodologist of the exercise therapy room

8. Tempering procedures, swimming, skiing, taking into account individual tolerance

9. A complex of vitamins and adaptogen drugs according to the program used in patients with recurrent bronchitis (see Rehabilitation of patients with recurrent bronchitis)

10. Consultation with a thoracic surgeon to determine the indication for surgical treatment. The decision on surgical intervention can be made after a repeat x-ray and bronchological examination, a full course of conservative therapy and observation of the patient for at least a year.

The prognosis for the majority of patients with chronic pneumonia is favorable, provided conservative therapy is carried out methodically. Children are not removed from the dispensary register and are transferred to doctors in adolescent clinics.

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Acute respiratory diseases of the upper respiratory tract

Acute respiratory diseases, or acute respiratory infections, as they are commonly called for short, are the most common diseases of childhood. There are practically no children who do not suffer from acute respiratory infections. Sometimes children are extremely susceptible to these diseases; they can occur several times a year or even several times a month, separating the child from the team and parents from work.

Acute respiratory diseases (ARIs) are infectious and inflammatory diseases that occur with primary damage to the mucous membranes of the upper respiratory tract, that is, the nose, nasopharynx, larynx, paranasal sinuses, etc.

A viral infection is transmitted from a sick person to a healthy person through airborne droplets during talking, coughing, sneezing, or very close contact. The infection penetrates various parts of the upper respiratory tract. With the normal functioning of the barrier protective mechanisms of the nose, pharynx, larynx and bronchi, pathogens quickly die and the disease does not develop, however, if the protective mechanisms are insufficient or disrupted, the infection penetrates into the mucous membrane of the respiratory tract, which causes its damage and the development of an infectious-inflammatory process.

Causes of the disease. The cause of acute respiratory infections is often a variety of viruses - the smallest microorganisms. They are extremely widespread in the environment and can cause both isolated cases of disease in the most weakened children and epidemics when the majority of the child population begins to get sick. The most dangerous viruses for children are influenza viruses, parainfluenza, adenoviruses, respiratory syncytial viruses, etc. Acute respiratory infections can also be caused by bacteria, especially streptococci, pneumococci, etc.
Acute respiratory infections mainly affect young children - from 1 year to 3 years. From 4-5 years, the incidence of acute respiratory infections decreases. Children with impaired immunity are especially often affected.

Factors predisposing to the development of acute respiratory infections:

Unfavorable environmental factors - atmospheric pollution, environmental pollution, air pollution inside the home, parental smoking, unfavorable sanitary conditions for the child, etc.;
overcrowding of the child population is a factor contributing to the rapid transmission of the pathogen from one child to another. This situation is typical for child care institutions, city vehicles, dormitories, that is, places where children are in close contact with each other;
impaired nasal breathing - enlarged adenoids, deviated nasal septum, etc.;
chronic or recurrent nasopharyngeal infections - adenoiditis, chronic tonsillitis, chronic rhinitis, otitis media, etc.;
allergic predisposition of the child.

Preventive measures for acute respiratory infections should include mandatory improvement of the environment, compliance with sanitary standards for keeping the child, treatment of nasopharyngeal infections and isolation of sick children in cases of acute respiratory infections in the team.

Symptoms of acute respiratory infections. Acute respiratory diseases begin in both large and small children, most often suddenly, against the background of complete health. For any viral disease, the main characteristic symptoms are:

Increased temperature (fever);
intoxication;
signs of damage to the upper respiratory tract - nose, larynx, pharynx, trachea, bronchi.

Attentive parents can determine even before the development of the disease that the child is ill, by such manifestations as poor health, malaise, lethargy, lack of appetite, chilling.

An increase in body temperature is an alarming signal for parents, indicating that the child is sick. This is the most common symptom that causes you to worry and see a doctor. We can talk about an increase in body temperature if there is a temperature above 37 degrees. Typically, body temperature rises from the first day of illness and remains elevated for 3-5 days, without posing a danger to the sick child. However, an increase in temperature to high numbers, above 39 degrees, is dangerous and requires the child to be prescribed antipyretic medications.

Along with fever, acute respiratory infections are characterized by manifestations of intoxication. Older children may complain of headaches, dizziness, pain or burning in the eyeballs, and inability to look at bright lights. Sometimes vague, intermittent, low-intensity pain in muscles or joints appears. The child may be bothered by nausea, vomiting, and loose stools.

In young children, intoxication can be suspected when anxiety appears or, conversely, lethargy, refusal to eat or a sharp decrease in appetite, regurgitation, or loose stools.

In severe forms of acute respiratory infections, coldness of the extremities, severe pallor and marbling of the skin, tilting of the head back, and convulsive twitching of the extremities may appear against the background of a high temperature. In older children, hallucinations and delusions are possible. The occurrence of convulsions and loss of consciousness is especially dangerous. This requires emergency, immediate medical care for the child.

However, as a rule, the duration of intoxication in mild acute respiratory infections is several days (2-3 days).

Signs of respiratory tract damage during acute respiratory infections can be very diverse. They can appear from the first days of the disease, but more often appear from the second day of the disease. For acute respiratory infections, damage to the upper respiratory tract is more typical: the nose and its paranasal sinuses, pharynx, larynx. Often, simultaneously with damage to the respiratory tract, an inflammatory disease of the ears - otitis media - and the eyes - conjunctivitis occurs. Somewhat less frequently, the disease manifests itself as damage to the lower respiratory tract and is characterized by clinical signs of inflammation of the bronchial mucosa - bronchitis and even lung tissue - pneumonia.

Symptoms of upper respiratory tract damage

Rhinitis (runny nose) is characterized by itching in the nose, sneezing, sometimes watery eyes, and very quickly difficulty in nasal breathing - “nasal congestion” and mucous discharge from the nasal passages. The nose is red and slightly swollen. And with significant nasal discharge, redness can be observed under the nose and even above the child’s upper lip. The child breathes through his mouth, sleep is disturbed. The duration of a runny nose is usually about 7 days, but in children with a predisposition to allergies it can persist for a longer period of time.

If the paranasal sinuses are affected (sinusitis, sinusitis, frontal sinusitis), which can be suspected in older children (over 5 years old), the child complains of headache, nasal congestion, and prolonged runny nose. Very often, inflammation of the paranasal sinuses accompanies rhinitis.

Pharyngitis (infection of the pharynx) is characterized by dryness, soreness, and sometimes tingling in the throat. Moreover, these symptoms may be accompanied by a dry cough or pain when swallowing. If you look into a child's throat, you can see its redness.

Laryngitis, an inflammatory lesion of the larynx, which often occurs against the background of acute respiratory infections in children aged 1-3 years, is characterized by the appearance of hoarseness. The inflammatory process spreads to the trachea, and sometimes from the first days of the illness a rough, painful, barking cough occurs. In such cases, the disease is usually called laryngotracheitis. In more severe cases, inflammatory swelling of the larynx may occur, resulting in difficulty breathing.

Inhalation is usually difficult, it becomes noisy, audible at a distance, especially when the child is restless, during a conversation or physical stress.

In severe cases, difficulty in breathing is determined both at rest and even during sleep. The appearance of difficulty breathing is often accompanied by fear, increased sweating,
retraction of compliant places of the chest - supraclavicular areas, intercostal spaces, etc. Sometimes blue discoloration appears around the mouth, rapid breathing and heartbeat. This is an alarming sign, and you should urgently call an ambulance.

The duration of uncomplicated laryngitis is usually 7-9 days.

Treatment of acute respiratory infections in a child

If signs of illness appear, the child should be isolated, since there is a danger of infecting other children, as well as the addition of another additional pathogen, which can make the course of the disease more severe.

You should create a friendly, calm environment at home for the sick child.
If the baby’s well-being is not affected, the temperature is low (up to 38 degrees), it is not necessary to put the child to bed, but it is necessary, however, to protect him from noisy games that require a lot of physical stress. If the disease occurs with high fever and severe intoxication, bed rest is necessary until the temperature normalizes.
The room where the patient is located must be frequently ventilated, since the causative agent of the disease is released into the atmosphere of the room with breathing and the child breathes it.

The air should be warm. It is very important that it is well moisturized, since with breathing the child loses moisture, and secretions of the respiratory tract often become viscous, sticky, and difficult to remove from the respiratory tract. How to achieve this? You can use special humidifiers, or you can make do with improvised means: hang wet diapers on heating devices, place basins of water in the corners of the room, and periodically spray water from a spray bottle. We should not forget about wet cleaning of the room. This is an effective fight against the pathogen and at the same time humidifies the air.

The diet during illness should not differ from age. You should not force-feed a child if he or she has no appetite, as force-feeding may cause vomiting. Feeding should be done more often, in small portions. As a rule, as the condition improves, appetite is restored.

It is necessary to pay special attention to the child's drinking. If the body temperature is not high and health does not suffer, the child should drink the usual amount of liquid. But if the symptoms of intoxication are severe, the child has a high temperature, and his health is disturbed, then in order to reduce intoxication it is necessary to give the child more to drink than usual, often, in small portions, evenly throughout the day. You should not drink very large volumes of liquid, as this can also lead to vomiting. It is necessary to drink between feedings. In cases where it is not possible to give the child something to drink (he does not drink or vomits after repeated attempts to give him something to drink), it is necessary to urgently seek medical help.

A sick child should drink from 800 ml to 1.5 liters of liquid per day, depending on age. It is better to give your child slightly alkaline mineral water (Essentuki, Borjomi, etc.), but you can also use slightly acidified liquids: tea with lemon, cranberry or lingonberry juice. Acidified liquids are good for relieving nausea. Decoctions of raisins, dried apricots, and rose hips are a very good drink. You should not give your child sugary drinks, as they can lead to bloating and sometimes even pain in the abdomen.

The food a child receives should not be rough, hot or spicy. It should be easily digestible, rich in vitamins and, if possible, meet the wishes of the patient.
The child's medical treatment must be determined by the doctor. The doctor takes into account the cause of the disease, the age of the child, and the characteristics of the course of the disease. However, parents can take some therapeutic measures on their own.

Medicines

All medications used for acute respiratory infections can be divided into two groups: drugs aimed at eliminating the causative agent of the disease, and drugs that relieve individual symptoms of the disease.
Since acute respiratory infections are most often caused by viruses, early use of antiviral drugs is first of all necessary. Treatment should be started immediately when the first symptoms of the disease appear. What medications can be given to a sick child?

Remantadine. The drug is used in children over 3 years of age. When symptoms of acute respiratory infections appear, children aged 3 to 6 years can be given 1/2 tablet 3 times a day; children from 7 to 14 years old - 1-2 tablets 3 times a day. The medicine is given only on the first or second day of illness.
Aflubin. In the first days of the disease, it is recommended to take the drug every half hour to an hour: children under 1 year old - 1 drop, children under 12 years old - 3-5 drops; for adolescents - 8-10 drops until the condition improves, but no more than 8 times. After the condition improves, take the drug 3 times a day.

Careful toileting of the nose is necessary - removing the contents by blowing your nose. This must be done correctly - alternately from the right and left half of the nose, since when they are simultaneously blown out, purulent mucus from the nose can enter through the Eustachian tube (auditory tube) into the middle ear cavity and cause inflammation - otitis media, as well as onto the conjunctiva of the eyes and cause conjunctivitis .

If the child does not have an allergic reaction, swelling of the mucous membrane of the nose and nasopharynx can be reduced by instilling herbal infusions into the nose - chamomile, sage, linden.
How to put medicine into your nose correctly. It is necessary to lay the child on his back, place a pillow under his shoulders, and his head should be thrown back. Place 2-3 pipettes of infusion into each nostril. After 2-3 minutes, you need to blow your nose well. The procedure must be done 2-3 times a day for 7-10 days.

How to prepare a decoction of medicinal herbs. To prepare a decoction, pour 1-2 tablespoons of medicinal herbs into a thermos with boiling water and leave for several hours.

If nasal breathing is completely absent and the child breathes through the mouth, it is necessary to instill vasoconstrictor drops into the nose or inject medicine through a special nasal spray to relieve swelling and restore nasal breathing.

Vasoconstrictor medications for young children

Xymelin: children from 3 to 6 years old - 1-2 drops in the nose or 1 portion of nasal spray 3 times a day; children aged 6 years and older - 2-3 drops or 1 portion of nasal spray no more than 3 times a day.
Tizin: children aged 2 to 6 years - 0.05% solution in the nose, 2-4 drops no more than 3 times a day; children aged 6 years and older - 0.1% solution of the drug, 2-4 drops of the drug 3 times a day.

Rhinopront: medicine in syrup or capsules, which is very convenient to give to small children, and the medicine lasts 10-12 hours (all day): children from 1 to 6 years old - 1 measuring spoon of syrup 2 times a day; children from 6 to 12 years old - 2 measuring spoons of syrup 2 times a day; children aged 12 years and older - 3 scoops of syrup or 1 capsule 2 times a day.

Medicines for older children (6 years and older)

In addition to the above, you can use drugs such as afrin, pinosol, xylometazoline, naphthyzin, galazolin, sanorin: 2-3 drops in each nostril 3-4 times a day. It should be remembered that these medications should not be used for more than 5 days in a row, as prolonged use can damage the nasal mucosa.
In addition, after using these drugs, as well as for viral runny noses, lubricating the nasal mucosa with 0.25% oxolinic ointment is effective.

For inflammation of the pharynx - laryngitis - gargling with infusions of chamomile, sage, eucalyptus, raspberry leaves, aqueous solutions of garlic and onion has a good effect. The rinse solution should not be hot; rinse frequently.
In cases of laryngitis symptoms, warm inhalations with ordinary boiled water (steam inhalations) have a good effect.

What antipyretic drugs should be kept in your home medicine cabinet?

If the patient has a high temperature (over 39 degrees), antipyretic drugs are indicated and should always be on hand. These are paracetamol, Panadol, Coldrex, children's Tylenol.

It is better not to give aspirin to children. Physical cooling methods can be used at very high temperatures, but not earlier than 20 minutes after giving the medicine. To lower the temperature faster and more effectively, you can undress the child, place him near a fan for a while, wipe him with cool water, and place a vessel with ice near the child’s head. You can add a little table vinegar to the rubbing water. Rub with a soft terry towel or a special mitten until the skin appears slightly red.
Under no circumstances should you give a child with acute respiratory infections antibiotics on your own, without a doctor’s prescription. These medications do not reduce fever, do not act on viral infections, and may cause unwanted effects. Antibacterial drugs can only be prescribed by a doctor for special indications.

How to perform steam inhalations for children

Inhalation should always be carried out under adult supervision. It can be done over a pan of boiling water or over boiled potatoes in their skins.

Inhalation in adult children can be done by covering the head with a towel or sheet, but it is better to breathe through a funnel made of thick paper. In this case, you need to cover the pan with the wide end, and inhale the steam through the narrow gap.

To avoid burns to the respiratory tract in children, it is more convenient to inhale using a coffee pot or heating pad. The vessel should be filled with boiling water to 1/3 of its volume and placed on a hard, flat surface (for example, a table). Place a pacifier with the tip cut off or a rubber tube on the spout of the coffee pot through which to inhale.

In cases of signs of respiratory distress due to laryngitis (difficulty in inhaling), before the doctor arrives, a 0.05% solution of naphthyzine should be dripped into the nose, which can also be added (5-7 drops) to the water for inhalation.

How to properly perform warming procedures

The favorite procedures of all parents - warming ones, such as compresses, hot foot baths, mustard plasters on the chest or calf muscles, warming up the nose using special bags of salt or cereal, etc. - can be used, but it should be remembered that they are contraindicated in cases when a child has a high fever, or the child is allergic to mustard, or the procedure is unpleasant for him, it causes severe anxiety.

For pharyngitis, laryngitis and other diseases of the upper respiratory tract, compresses have a good therapeutic effect.

A compress is a specially prepared medicinal bandage. The compress dilates blood vessels, increases blood flow to the body area, and has an anti-inflammatory effect. For acute respiratory infections, compresses can be placed on the child’s neck or chest. There are dry and wet (warming, medicinal) compresses. It is better to use a damp warming compress at night, and a dry compress during the day.

How to prepare a compress? Moisten a piece of cloth or gauze folded in several layers with vodka or wine alcohol diluted in half with water, wring it out well, and place it on the neck or chest area. Place wax paper or plastic film on top of the fabric so that it extends 1-2 cm beyond the edges of the fabric, cover the top with a large layer of cotton wool and tightly bandage the compress with a bandage or scarf so that it does not move, but does not embarrass the child. Keep the warm compress for 10-12 hours.

It is rational to use a dry compress after a wet one in the daytime. Cover several layers of dry gauze with cotton wool and bandage it to the neck or chest. Such a compress can remain on the patient’s body throughout the entire waking period.

An extremely popular warming procedure is mustard plasters. Mustard plaster is a piece of paper coated with a thin layer of mustard powder. Mustard plasters have an irritating, distracting, analgesic, and anti-inflammatory effect. They can be used for inflammatory diseases of both the upper and lower respiratory tract.

Mustard plasters can be bought at the pharmacy, or you can prepare them yourself at home. To prepare homemade mustard plaster, dry mustard must be diluted in warm water until a paste-like mass is obtained. Spread the resulting mass onto a thick cloth in a layer of about 0.5 cm, and cover with the same piece of cloth on top.

For diseases of the upper respiratory tract, mustard plasters are applied to the chest (in the center of the chest) or to the calf muscles. In this case, before use, mustard plaster must be moistened in warm water, and then through a layer of gauze or directly placed on the skin, pressed, and covered with a blanket for the patient. After a few minutes, the child will feel a slight burning sensation. Usually mustard plasters are kept for 5-10 minutes until the skin turns red. After removing the mustard plasters, the remaining mustard must be washed off with warm water, gently wipe the skin; if the skin is significantly reddened, it must be lubricated with Vaseline.

How to properly prepare and take a medicinal bath

For diseases of the upper respiratory tract of a cold nature, medicinal baths can be used - general or foot baths using only water or with the addition of medicinal substances.

When taking a shared bath, the child’s entire body is immersed in water. In this case, you need to ensure that the head, neck, upper chest, including the heart area, are free of water. The child’s face should be well lit, since the reaction of the facial skin vessels can be used to judge the tolerability of the procedures. So, if the face of a child taking a bath becomes very pale or, conversely, turns sharply red, the procedure must be stopped immediately.

The bath water temperature should be 36-38 degrees for small children, 39-40 degrees for older children. The duration of the bath is 10-15 minutes. A child should take a bath in the presence of a family member to avoid an accident. After the bath, the child should be wrapped in a towel and wrapped in a blanket for 30-60 minutes.
Warm medicinal baths are best taken at night. To increase the therapeutic effect of the bath, you can add some medicinal substances to the water: pine extract (from 50 to 70 g or 1-2 tablets per 200 liters of water), bronchicum - a liquid additive to the therapeutic bath (20-30 ml per 1/3 of the bath with warm water). Essential vapors penetrate the respiratory tract, facilitate breathing and remove mucus. Such baths have a double therapeutic effect.
Mustard foot baths have a good healing effect. However, you need to remember that they should not be used in children with skin diseases and intolerance to the smell of mustard.
To prepare a mustard foot bath, you need to dilute 5-10 g of dry mustard in a small volume of water, strain through cheesecloth and pour into a bucket of water at a temperature of 38-39 degrees, mix the water and mustard solution well. The bath is carried out in a sitting position, the child’s legs are gradually lowered into the bucket and covered with a sheet on top to protect the eyes and respiratory tract from the irritating effects of mustard.

The duration of the local bath is 10-15 minutes.

After the bath, the child’s feet should be washed with warm water, wiped dry, put on socks and put the child to bed.

After taking therapeutic baths, rest for 1-1.5 hours is necessary.

Lower respiratory tract diseases

Diseases of the lower respiratory tract are somewhat less common in children than diseases of the upper respiratory tract. Often their symptoms do not appear from the first days of the disease, but somewhat later and indicate the spread of infection from the nasopharynx to the deeper parts of the bronchopulmonary system. The most common diseases of the lower respiratory tract for children are tracheitis, bronchitis and bronchiolitis.

Tracheitis

This is an infectious and inflammatory disease of the trachea. Tracheitis can be recognized by the appearance of a particularly frequent, rough, low-pitched cough. They say about such a cough that the patient coughs “like a barrel.” The cough may be accompanied by rawness, chest pain, and sometimes discomfort when breathing. There is usually no sputum, or a small amount of very thick mucus (lumps) may be coughed up.

Tracheitis is often combined with laryngitis (laryngotracheitis). The duration of the disease is on average 7-10 days.

Bronchitis

Bronchitis is the most common disease of the lower respiratory tract.
Bronchitis is commonly called acute inflammatory damage to the bronchial mucosa.
As a result of the vital activity of the infectious agent, swelling of the bronchial mucosa occurs, which narrows the diameter of their lumen and leads to impaired bronchial obstruction.

The inflammatory process leads to dysfunction of the bronchial glands and often contributes to the production of an excess amount of thick, viscous secretion, which can be very difficult for a child to cough up.

Damage to the cilia of the bronchial epithelium under the influence of viruses, microbes, toxins, and allergic substances leads to disruption of the self-cleaning processes of the bronchi and the accumulation of sputum in the respiratory tract.

The accumulation of secretions in the respiratory tract, as well as irritation of special cough receptors by inflammatory products, causes a cough. Coughing helps cleanse the bronchi, but if the secretion is very thick and viscous, even a cough is sometimes unable to push through the mucus accumulated in the respiratory tract.

Thus, the main symptoms of bronchitis are cough and sputum.
If we look inside the bronchi during bronchitis, we can see the following picture: the mucous membrane of the bronchus is inflamed, thickened, swollen, bright red, easily vulnerable, and on the walls of the bronchi lies a cloudy, sometimes purulent-looking secretion, while the lumen of the diseased bronchus is narrowed.

Causes of bronchitis

First of all, it is a viral infection. Viruses from the nasopharynx enter the bronchi during breathing, settle on the mucous membrane of the bronchi, multiply in the cells of the mucosa and damage it. At the same time, the protective systems of the mucous membrane of the respiratory tract are affected and favorable conditions are created for the infection to penetrate deep into the body. Viral bronchitis is the most common bronchitis in children.

Bronchitis can be caused by a variety of bacteria. Bacterial bronchitis develops, as a rule, in weakened children and children with impaired immunity. Bacteria can seriously damage not only the bronchial mucosa, but also deeper structures, as well as tissues around the respiratory tract.

In very weakened, small, premature children, children who have received many antibiotics, bronchitis of a fungal nature may occur. This, like bacterial bronchitis, is a very serious disease with deep damage to the bronchial mucosa. Fungal bronchitis is less common than viral and bacterial ones.

In recent years, allergic bronchitis has become increasingly common, the cause of which is allergic inflammation of the bronchial mucosa in response to exposure to various antigens - dust, pollen, etc.

Toxic bronchitis, a disease associated with the action of chemicals in contaminated inhaled air, is also possible. Toxic substances can very severely and sometimes irreversibly damage the mucous membrane of the respiratory tract and lead to a chronic course of the disease.

Factors predisposing to the development of bronchitis

These factors are:
cold;
dampness;
nasopharyngeal infection;
overcrowding (dormitories, children's groups, etc.);
violation of nasal breathing;
passive or active smoking.

It should be noted that prolonged inhalation of tobacco smoke by a child is especially seriously damaging to the mucous membrane of the respiratory tract.

Tobacco smoke contains about 4,500 potent substances that have:

Respiratory allergies are common allergic diseases with predominant damage to the respiratory system.

Etiology

Allergoses develop as a result of sensitization by endogenous and exogenous allergens.

Exogenous allergens of non-infectious nature include: household - washing powders, household chemicals; epidermal - wool, skin scales of domestic animals; pollen - pollen of various plants; food – food products; herbal, medicinal. Allergens of an infectious nature include bacterial, fungal, viral, etc.

Classification

The classification is as follows.

1. Allergic rhinitis or rhinosinusitis.

2. Allergic laryngitis, pharyngitis.

3. Allergic tracheitis.

4. Allergic bronchitis.

5. Eosinophilic pulmonary infiltrate.

6. Bronchial asthma.

Symptoms and diagnosis

Allergic rhinitis and rhinosinusitis. History – the presence of allergic diseases in the parents and close relatives of the child, the connection of diseases with allergens.

Symptomatically manifested by an acute onset: the sudden onset of severe itching, burning in the nose, bouts of sneezing, copious liquid, often foamy discharge from the nose.

Upon examination, swelling of the mucous membrane of the nasal septum, inferior and middle turbinates is revealed. The mucous membrane has a pale gray color with a bluish tint, the surface is shiny with a marble pattern.

X-ray examination shows thickening of the mucous membrane of the maxillary and frontal sinuses and the ethmoidal labyrinth on photographs of the skull.

Positive skin tests with infectious and non-infectious allergens are characteristic.

Laboratory diagnostics revealed an increase in the level of immunoglobulin E in nasal secretions.

Allergic laryngitis and pharyngitis can occur in the form of laryngotracheitis.

Characterized by an acute onset, dryness of the mucous membrane, a feeling of soreness, soreness in the throat, attacks of dry cough, which later becomes “barking”, rough, hoarseness appears, up to aphonia.

With the development of stenosis, inspiratory shortness of breath appears, the participation of auxiliary muscles in the act of breathing, retraction of the pliable parts of the chest, flaring of the wings of the nose, and abdominal breathing acquires greater intensity and amplitude.

Obstruction of the bronchi develops due to edema, spasm and exudate and, as a consequence, obstructive ventilation failure.

The use of antibacterial agents does not have a positive effect, and the condition may even worsen.

Laboratory data - positive skin tests, increased levels of immunoglobulin E in the blood serum.

Allergic bronchitis occurs in the form of asthmatic bronchitis.

The anamnesis contains evidence of allergization of the body. Unlike true bronchial asthma, asthmatic bronchitis develops spasm of large and medium-caliber bronchi, so asthma attacks do not occur.

Eosinophilic pulmonary infiltrate develops with sensitization of the body.

The most common cause is ascariasis. In a general blood test, high eosinophilia (more than 10%) appears against the background of leukocytosis. Foci of infiltration appear in the lungs, homogeneous, without clear boundaries, which disappear without a trace after 1–3 weeks. Sometimes an infiltrate, having disappeared in one place, may appear in another.

2. Bronchial asthma

Bronchial asthma– an infectious-allergic or allergic disease of a chronic course with periodically recurring attacks of suffocation caused by impaired bronchial obstruction as a result of bronchospasm, swelling of the bronchial mucosa and accumulation of viscous sputum.

Bronchial asthma is a serious health problem worldwide. It affects 5 to 7% of the Russian population. There is an increase in morbidity and mortality.

Classification (A.D. Ado and P.K. Bulatova, 1969)

1) atopic;

2) infectious-allergic;

3) mixed. Type:

1) asthmatic bronchitis;

2) bronchial asthma. Gravity:

1) mild degree:

a) intermittent: attacks of bronchial asthma less than twice a week, exacerbations are short, from several hours to several days. Attacks occur rarely at night - twice or less per month;

b) persistent: attacks do not occur every day, no more than two per week.

At night, symptoms of bronchial asthma are observed more than twice a month;

2) moderate degree - manifests itself every day, requires daily use of bronchodilators. Night attacks occur more than once a week;

3) severe degree - bronchial obstruction, expressed to varying degrees constantly, physical activity is limited.

The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen with the occurrence of allergic inflammation in the mucous membrane of the bronchial tree.

When collecting anamnesis from a patient, it is necessary to establish the nature of the first attack, place and time of year, duration and frequency of attacks, the effectiveness of the therapy, and the patient’s condition during the non-attack period.

Pathogenesis

The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen and the occurrence of allergic inflammation.

Clinic

The main symptom is the presence of attacks of expiratory suffocation with distant wheezing and paroxysmal cough. The forced position of the patient during an attack: the legs are lowered down, the patient is sitting on the bed, the body is tilted forward, and his hands are resting on the bed on either side of the body.

Symptoms of respiratory failure appear (participation of auxiliary muscles in the act of breathing, retraction of intercostal spaces, cyanosis of the nasolabial triangle, shortness of breath). The chest is emphysematously distended, barrel-shaped.

Percussion-box sound, the boundaries of the lungs shift downward. Auscultation - weakened breathing (short inhalation, long exhalation), an abundance of dry wheezing, moist rales of various sizes. From the cardiovascular system - narrowing of the boundaries of absolute cardiac dullness, tachycardia, increased blood pressure.

On the part of the nervous system, increased nervous excitability or lethargy, changes in autonomic reactions (sweating, paresthesia) appear.

Laboratory diagnostics

The general blood history includes lymphocytosis and eosinophilia. In the general analysis of sputum - eosinophilia, epithelial cells, macrophages, or Charcot-Leiden crystals, and Kurshman spirals.

Instrumental research methods. X-ray shows pulmonary emphysema (increased transparency, the borders of the lungs are shifted downwards). Spirography: decreased expiratory flow (pneumotachometry), decreased vital capacity, hyperventilation at rest.

Allergy examination. Skin testing with bacterial and non-bacterial allergens gives a positive result. Provocative tests with allergens are also positive.

Immunological indicators. In atopic bronchial asthma, the level of immunoglobulins A decreases and the content of immunoglobulins E increases; in mixed and infectious asthma, the level of immunoglobulins G and A increases.

In the atopic form, the number of T-lymphocytes decreases, in the infectious-allergic form it increases.

In the atopic form, the number of suppressors is reduced and the content of T-helper cells is increased. When sensitized by fungal agents, the level of CEC increases.

Patient examination

Interview (collection of medical history, complaints). Inspection (palpation, percussion, auscultation). General blood test. Microscopy and sputum culture.

X-ray of the chest organs. Study of external respiration parameters. Allergological, immunological examination.

Differential diagnosis

Differential diagnosis of bronchial asthma is carried out with diseases manifested by bronchospastic syndrome of non-allergic nature, which are called “syndromic asthma”; chronic obstructive bronchitis, diseases of the cardiovascular system with left ventricular failure (cardiac asthma), hysteroid breathing disorders (hysteroid asthma), mechanical blockage of the upper respiratory tract (obstructive asthma).

Differentiate with diseases of an allergic nature: polyposis, allergic bronchopulmonary aspergillosis with obstructive respiratory disorders.

It is necessary to take into account the presence of a combination of two or more diseases in the patient.

Unlike bronchial asthma, in chronic obstructive bronchitis, the obstructive syndrome persists and does not develop reversely even when treated with hormonal drugs, and there is no eosinophilia in the sputum analysis.

With left ventricular failure, cardiac asthma may develop, which is manifested by an attack of shortness of breath at night; the feeling of lack of air and tightness in the chest develops into suffocation.

Combined with arrhythmia and tachycardia (with bronchial asthma, bradycardia is more common). Unlike bronchial asthma, both phases of breathing are difficult. An attack of cardiac asthma can be prolonged (before the use of diuretics or neuroglycerin).

Hysteroid asthma has three forms. The first form is similar to a respiratory spasm. Breathing of a “driven dog” - inhalation and exhalation are intensified. There are no pathological signs on physical examination.

The second form of suffocation is observed in hysterical people and is caused by impaired contraction of the diaphragm. During an attack, breathing is difficult or impossible, and there is a feeling of pain in the solar plexus area.

To stop the attack, the patient is offered to inhale hot water vapor or given anesthesia.

Obstructive asthma is a symptom complex of suffocation, which is based on a violation of the patency of the upper respiratory tract.

The cause of obstruction may be tumors, foreign bodies, stenosis, or aortic aneurysm. The greatest importance in making a diagnosis belongs to tomographic examination of the chest and bronchoscopy.

The combination of symptoms of shortness of breath and suffocation also occurs in other conditions (anemic, uremic, cerebral asthma, periarthritis nodosa, carcinoid syndrome).

Hay fever, or hay fever, is an independent allergic disease in which the body becomes sensitized to plant pollen.

These diseases are characterized by: bronchospasm, rhinorrhea and conjunctivitis. Seasonality of diseases is characteristic. It begins with the flowering period of plants and decreases when it ends.

The exacerbation stage is characterized by a persistent runny nose, pain in the eyes and lacrimation, coughing until an attack of suffocation develops.

Possible fever and arthralgia. A general blood test shows eosinophilia (up to 20%). During the period of remission there is no clinical manifestation.

Allergic bronchopulmonary aspergillosis– a disease caused by sensitization of the body to Asperginel fungi. With this disease, damage to the alveoli, blood vessels of the lungs, bronchi, and other organs is possible.

The clinical sign is the symptom complex of bronchial asthma (obstructive syndrome, eosinophilia, increased immunoglobulin E).

Confirmation of the diagnosis is carried out by identifying skin sensitization to aspergillus allergens.

An example of a diagnosis. Bronchial asthma, atopic form, with frequent relapses, period of remission, uncomplicated.

Treatment

The goal of treatment is to prevent the occurrence of attacks of suffocation, shortness of breath during physical activity, cough, and nocturnal breathing difficulties. Elimination of bronchial obstruction. Maintaining normal lung function.

Objectives of the therapy:

1) stop exposing the body to the allergen – the cause of the disease. In case of pollen allergy, the patient is asked to move to another area during the flowering period of the plants. In case of occupational allergies, change the place and working conditions. For food – strict adherence to an elementary diet;

2) carry out specific desensitization followed by the production of blocking antibodies (immunoglobulins G);

3) stabilize the walls of mast cells and prevent the secretion of biologically active substances;

4) limit the impact of irritants on the respiratory tract - cold air, strong odors, tobacco smoke;

5) rehabilitation of chronic foci of infection (teeth with inflammation, sinusitis, rhinitis);

6) limit developing allergic inflammation by prescribing glucocorticoids in inhaled form;

7) prevent taking non-steroidal anti-inflammatory drugs.

Principles of treatment.

1. Elimination of the allergen (exclusion, elimination).

2. Bronchospasm therapy:

1) selective β-adrenergic agonists (Berotec, salbutalone, Ventosin, terbutamol, phenotyrol, guoetarin);

2) non-selective adrenergic agonists (adrenaline, ephedrine, asthmapent, fulprenaline, isadrin, euspiran, novodrin);

3) phosphodiesterase antagonists, xanthines (theobramines, theophylline, euphylkin);

4) anticholinergics (atropine, ipratropine).

3. Histamine H2 receptor blockers (tavegil, fenkarol, suprastin, atosinil, pipolfen, displeron).

4. Drugs that reduce bronchial reactivity (glucocorticoids, intal, betotifen).

5. Expectorants:

1) increasing the liquid phase of sputum (thermopsis, licorice root, marshmallow, potassium iodide, alkyonium chloride);

2) mucolytic drugs (acetylcysteine ​​(ACC)), ribonuclease, deoxyribonuclease);

3) drugs that combine a mucoliptic effect with an increase in the level of surfactant (bromgesin, ambrocagn, lazolvan).

6. Antibiotics.

7. Vibration massage with postural drainage.

8. Physiotherapeutic procedures, reflexology (acupuncture, oxygen therapy).

9. Bronchoscopy, intranasal tracheobronchial sanitation.

10. Rehabilitation in the gnotobiological department.

11. Sauna therapy.

3. Acute bronchitis

Bronchitis is a disease of the bronchi, accompanied by gradually developing inflammation of the mucous membrane with subsequent involvement of the deep layers of the walls of the bronchi.

Etiology

More often it develops with the activation and reproduction of the opportunistic flora of the body itself with a violation of mucocilar clearance due to ARVI.

Predisposing factors are cooling or sudden heating, polluted air, smoking.

Pathogens: viruses, bacteria, mixtures, allergens.

Classification:

1) acute bronchitis (simple);

2) acute obstructive bronchitis (with symptoms of bronchospasm);

3) acute bronchiolitis (with respiratory failure);

4) recurrent bronchitis.

Pathogenesis

Viruses, bacteria, mixtures or allergens multiply, damaging the bronchial epithelium, reducing barrier properties and causing inflammation, disruption of nerve conduction and trophism.

Narrowing of the bronchial passages occurs as a result of swelling of the mucous membrane, excess mucus in the bronchi and spasm of the smooth muscles of the bronchi.

Clinic

The current is wavy. By the end of the first week of illness, the cough becomes wet, the temperature returns to normal.

The main clinical symptom is cough with mucous or purulent sputum; low-grade fever, no symptoms of intoxication. Auscultation - dry and moist, medium-caliber wheezing sounds on exhalation, hard breathing are heard.

Wheezing is scattered and practically disappears after coughing. The general blood test revealed moderate hematological changes: increased ESR, monocytosis.

X-ray shows increased bronchovascular pattern, expansion of roots, symmetrical changes.

Acute obstructive bronchitis is characterized by shortness of breath on exertion; painful cough with scanty sputum.

Auscultation - lengthening of exhalation. With forced breathing - wheezing when exhaling. In the general blood test, hematological changes are most often leukopenia.

The X-ray shows pulmonary emphysema, increased transparency of the lung tissue, and expansion of the roots of the lungs.

Acute bronchiolitis (capillary bronchitis) is characterized by generalized obstructive damage to the bronchioles and small bronchi.

Pathogenesis is associated with the development of edema of the mucous wall of the bronchioles and papillary proliferation of their epithelium.

Clinically manifested by severe shortness of breath (up to 70–90 breaths per minute) against a background of persistent febrile temperature; increased nervous excitability associated with respiratory failure within a month after temperature normalization; perioral cyanosis; On auscultation, fine-bubbly, crepitating asymmetrical rales are heard. The cough is dry and high-pitched. The chest is distended.

In the general blood test - hematological changes: increased ESR, neutrophil shift, moderate leukocytosis.

The radiograph shows alternation of areas with increased density with areas of normal pneumatization; low standing of the diaphragm, sometimes total darkening of the pulmonary field, atelectasis.

Recurrent bronchitis is diagnosed if there are three or more illnesses during the course of a year with a prolonged cough and auscultatory changes in bronchitis without an asthmatic component, but with a tendency to have a protracted course. This disease does not cause irreversible changes and sclerosis. The pathogenesis is due to a decrease in the barrier function of the bronchial mucosa to resist infections.

Predisposing factors: immunity defects, heredity, predisposition, polluted air, damage to the bronchial mucosa by exogenous factors, bronchial hyperreactivity. Recurrent bronchitis develops against the background of clinical signs of ARVI.

Moderate fever. The cough is initially dry, then wet, with mucous or mucopurulent sputum. Percussion-pulmonary sound with a boxy tint. Auscultation - hard breathing, dry, moist rales of medium and small caliber, scattered on both sides.

In the general blood test, hematological changes - leukocytosis or leukopenia, monocytosis.

The radiograph shows increased pulmonary pattern, expansion of the roots, atelectasis, hypoventilation. Bronchological examination - signs of bronchospasm, delayed filling of the bronchi with contrast, narrowing of the bronchi.

Survey plan

The patient's examination plan is as follows.

1. Collection of anamnesis (previous acute respiratory viral infections, premorbid background, concomitant diseases, frequency of acute respiratory viral infections, hereditary predisposition, allergies to anything, assessment of the effect of treatment).

2. Examination of the patient (assessment of cough, breathing, chest shape).

3. Palpation (presence of emphysema, atelectasis).

4. Percussion – mobility of the lungs during breathing, air filling.

5. Auscultation (vesicular, hard breathing, diffuse wheezing).

6. Blood test - increased ESR, shift in leukocyte formula.

7. General urine analysis.

8. Analysis of sputum from the nasopharyngeal mucosa with determination of sensitivity to antibiotics.

10. Study of the ventilation function of the lungs.

11. X-ray – study of the vascular and pulmonary patterns, the structure of the roots of the lungs.

12. Bronchoscopy and examination of the mucous membrane.

13. Tomography of the lungs.

14. Immunological study.

Differential diagnosis

Differential diagnosis is carried out with:

1) bronchopneumonia, which is characterized by local lung damage, intoxication, and a persistent increase in body temperature; X-ray changes characteristic of focal lesions;

2) bronchial asthma, which is accompanied by attacks of suffocation, hereditary predisposition, contact with an infectious allergen;

3) with congenital or acquired heart disease, which are characterized by congestion in the lungs. An example of a diagnosis. Acute infectious-allergic obstructive bronchitis DN 2.

Treatment

Treatment principles:

1) antibacterial therapy: antibiotics: ampicillin, tetracycline and others, sulfonamide drugs: sulfapyridazine, sulfomonolitaxin;

2) mucolytic drugs: acetylcysteine, bromhexine, trypsin, chymotrypsin;

3) expectorants: breast milk (coltsfoot, wild rosemary, marshmallow, elecampane), broncholithin;

4) bronchilitics: amupect, berotene;

5) endobroncholitin: aminophylline in aerosol;

6) vitamins B, A, C (cocarboxylase, biplex);

7) immunostimulants (immunal, timolin);

8) physiotherapy, massage, breathing exercises.

4. Respiratory failure

Respiratory failure is a pathological condition of the body, characterized by insufficient provision of blood gas composition, or it can be achieved using compensatory mechanisms of external respiration.

Etiology

There are five types of factors leading to impaired external respiration:

1) damage to the bronchi and respiratory structures of the lungs:

a) disturbance of the structure and function of the bronchial tree: increased tone of the smooth muscles of the bronchi (bronchospasm), edematous-inflammatory changes in the bronchial tree, damage to the supporting structures of the small bronchi, decreased tone of the large bronchi (hypotonic hypokinesia);

b) damage to the respiratory elements of the lung tissue (infiltration of the lung tissue, destruction of the lung tissue, dystrophy of the lung tissue, pneumosclerosis);

c) decrease in functioning lung tissue (underdeveloped lung, compression and atelectasis of the lung, absence of part of the lung tissue after surgery);

2) violation of the musculoskeletal framework of the chest and pleura (impaired mobility of the ribs and diaphragm, pleural adhesions);

3) violation of the respiratory muscles (central and peripheral paralysis of the respiratory muscles, degenerative-dystrophic changes in the respiratory muscles);

4) circulatory disorders in the pulmonary circulation (damage to the vascular bed of the lungs, spasm of the pulmonary arterioles, stagnation of blood in the pulmonary circulation);

5) violation of the control of the act of breathing (suppression of the respiratory center, respiratory neuroses, changes in local regulatory mechanisms).

Classification

1) ventilation;

2) alveolorespiratory.

Type of ventilation failure:

1) obstructive;

2) restrictive;

3) combined.

Degree of severity: DN I degree, DN II degree, DN III degree.

Obstructive ventilation failure is caused by a violation of the gas flow through the airways of the lungs as a result of a decrease in the lumen of the bronchial tree.

Restrictive ventilation failure is the result of processes that limit the compliance of lung tissue and a decrease in lung volumes. For example: pneumosclerosis, adhesions after pneumonia, lung resection, etc.

Combined ventilation failure occurs as a result of a combination of restrictive and obstructive changes.

Alveolorespiratory insufficiency develops as a result of impaired pulmonary gas exchange due to a decrease in the diffusion capacity of the lungs, uneven distribution of ventilation and ventilation-perfusion deposits in the lungs.

Main stages of diagnosis

Respiratory failure stage I. Manifested by the development of shortness of breath without the participation of auxiliary muscles, it is absent at rest.

Cyanosis of the nasolabial triangle is unstable, increases with physical activity, anxiety, and disappears when breathing 40–50% oxygen. The face is pale, puffy. Patients are restless and irritable. Blood pressure is normal or slightly elevated.

Indicators of external respiration: minute volume of respiration (MRV) is increased, vital capacity of the lungs (VC) is decreased, respiratory reserve (RR) is decreased, respiratory volume (VR) is slightly decreased, respiratory equivalent (RE) is increased, oxygen utilization factor (O2) is decreased . The gas composition of the blood at rest remains unchanged; blood saturation with oxygen is possible. The carbon dioxide tension in the blood is within normal limits (30–40 mm Hg). Violations of the CBS are not determined.

Respiratory failure stage II. Characterized by shortness of breath at rest, retraction of yielding areas of the chest (intercostal spaces, supraclavicular fossa), possibly with a predominance of inhalation or exhalation; P/D ratio 2 – 1.5:1, tachycardia.

Cyanosis of the nasolabial triangle, face, and hands does not disappear when inhaling 40–50% oxygen. Diffuse skin pallor, hyperhidrosis, pale nail beds. Blood pressure rises.

Periods of anxiety alternate with periods of weakness and lethargy, vital capacity is reduced by more than 25–30%. AP and RP reduced to 50%. DE is increased, which occurs due to a decrease in oxygen utilization in the lungs; blood gas composition, CBS: blood oxygen saturation corresponds to 70–85%, i.e., decreases to 60 mm Hg. Art. Normocapnia or hypercapnia above 45 mm Hg. Art. Respiratory or metabolic acidosis: pH 7.34 – 7.25 (normal 7.35 – 7.45), base deficiency (BE) is increased.

Respiratory failure stage III. Clinically manifested by severe shortness of breath, respiratory rate exceeds 150% of the norm, aperiodic breathing, bradypnea periodically occurs, asynchronous, paradoxical breathing.

There is a decrease or absence of breathing sounds during inspiration.

The P/D ratio changes: cyanosis becomes diffuse, generalized pallor is possible, marbling of the skin and mucous membranes, sticky sweat, and blood pressure is reduced. Consciousness and response to pain are sharply reduced, skeletal muscle tone is reduced. Cramps.

Precoma and coma. External respiration indicators: MOD is reduced, vital capacity and OD are reduced by more than 50%, RD is 0. Blood gas composition CBS: blood oxygen saturation is less than 70% (45 mm Hg).

Decompensated mixed acidosis develops: pH less than 7.2; VE is more than 6–8, hypercapnia is more than 79 mmHg. Art., the level of bicarbonates and buffer bases is reduced.

The examination plan includes:

1) survey and inspection;

2) objective examination (palpation, percussion, auscultation);

3) determination of CBS, partial pressure of O 2 and CO 2 in the blood;

4) study of external respiration parameters.

Differential diagnosis

Differential diagnosis of respiratory failure is carried out based on a comparison of clinical symptoms and indicators of external respiration and tissue respiration. If respiratory failure develops no more than stage II, it is necessary to find the cause of its development.

For example, in case of impaired alveolar patency, signs of depression of the central nervous system, impaired neuromuscular regulation of breathing and destructive processes are differentiated.

With the development of symptoms of obstruction, it is necessary to distinguish between diseases and conditions that cause high obstruction (acute stenosing laryngitis, tracheitis, allergic laryngeal edema, foreign body) and low obstruction (bronchitis, bronchiolitis, bronchial asthma attack and status asthmaticus. Circulatory failure with symptoms of stagnation in the pulmonary circle blood circulation).

An example of a diagnosis. Bronchopneumonia, complicated by cardiorespiratory syndrome, acute respiratory failure of the second degree, ventilation obstructive form.

Treatment principle:

1) creation of a microclimate (room ventilation, humidification, aeronization);

2) maintaining free patency of the airways (suction of mucus, bronchodilators, expectorants, breathing exercises, vibration massage with postural drainage);

3) oxygen therapy (through a mask, nasopharyngeal catheter, oxygen tent, mechanical ventilation, hyperbaric oxygenation);

4) spontaneous breathing under continuous positive pressure (CPBP);

5) normalization of pulmonary blood flow (aminophylline, pentamin, benzohexonium);

6) correction of CBS;

7) to improve the utilization of oxygen by tissues - glucose-vitamin-energy complex (glucose 10–20; ascorbic acid, cocarboxylase, riboflavin, ceichrome C, calcium pantothenate, union);

8) treatment of the underlying disease and accompanying pathological conditions.

5. Acute pneumonia

Pneumonia is an infectious lesion of the alveoli, accompanied by infiltration of inflammatory cells and exudation of the parenchyma in response to the introduction and proliferation of microorganisms into the usually sterile parts of the respiratory tract. One of the most common respiratory diseases; 3–5 cases per 1,000 people.

Etiology

The etiology of pneumonia may be due to:

1) bacterial flora (pneumococcus, streptococcus, staphylococcus, E. coli, Proteus, etc.);

2) mycoplasma;

4) fungi.

1) bacterial flora (pneumococcus, streptococcus, staphylococcus, Haemophilus influenzae, Friednender's bacillus, enterobacteria, Escherichia coli, Proteus);

2) mycoplasma;

3) influenza viruses, parainfluenza, herpes, respiratory sensitial, adenoviruses, etc.;

4) fungi.

Classification

1) focal bronchopneumonia;

2) segmental pneumonia;

3) interstitial pneumonia;

4) lobar pneumonia.

1) spicy;

2) protracted.

Severity is determined by the severity of clinical manifestations or complications:

1) uncomplicated;

2) complicated (cardiorespiratory, circulatory, extrapulmonary complications).

Diagnostic criteria. Anamnestic:

1) presence of respiratory diseases in the family (tuberculosis, bronchial asthma);

2) previous ARVI infections, adenoviral infection;

3) hypothermia.

Clinic

Complaints of cough, fever, weakness, sweating.

Signs of respiratory failure: groaning, rapid breathing, number of breaths up to 60–80 breaths per minute, flaring of the wings of the nose, retraction of the pliable parts of the chest, irregular breathing rhythm, inhalation is longer than exhalation, cyanosis of the skin, nasolabial triangle is very pronounced, especially after physical activity ; gray complexion, pallor of the facial skin as a result of hypoxemia and hypercapnia, caused by the exclusion of a more or less significant part of the alveoli from participating in normal respiratory gas exchange.

It is characterized by intoxication syndrome: fever, weakness, adynamia or agitation, sometimes accompanied by convulsions, sleep disturbances, and decreased appetite.

Disorders of the cardiovascular system: muffled heart sounds, tachycardia, expansion of the borders of the heart, pulse filling is reduced, blood pressure is sometimes increased, emphasis of the second tone on the aorta. Slowing cardiac function in severe pneumonia is an ominous symptom.

Changes in the gastrointestinal tract develop due to a decrease in secretory and enzymatic activity: nausea, vomiting, flatulence due to impaired peristalsis, abdominal pain due to irritation of the lower intercostal nerves innervating the diaphragm, abdominal muscles and abdominal skin.

Objective changes in the lungs: functional data are expressed in segmental (polysegmental) and confluent pneumonia, less pronounced in focal pneumonia and bronchopneumonia.

Minimal changes in interstitial pneumonia. Examination and palpation of the chest reveals swelling, more in the anterior sections, tension, which is a characteristic sign of pulmonary enphysema.

During percussion, the percussion sound is mottled (dullness during percussion alternates with areas of tympanic sound); dullness of percussion sound in the lower posterior parts of the lungs is characteristic of confluent pneumonia.

There may be no changes on percussion due to the small size of the inflammatory focus.

During auscultation, breathing disturbances are heard: hard, puerile, weakened, moist wheezing, small, medium and large caliber, depending on the involvement of the bronchi in the inflammatory process; wheezing can be dry, of various types (wheezing, musical). With a deep location of inflammatory foci in the lungs, there may be no percussion and auscultation changes.

Research methods

X-ray examination: in the images, emphysematous changes are combined with foci of infiltration of the lung tissue. The entire segment of the lung may be affected, including the root on the affected side.

In the general blood test, hematological changes: in the peripheral blood, neutrophilic leukocytosis with a shift to the left, increased ESR. If the body's reactivity decreases, the indicators may be within normal limits.

Examination plan:

1) general blood and urine analysis;

2) biochemical study of blood serum (protein fractions, sialic acids, seromucoid, fibrin, LDH);

3) radiography of the chest organs in two projections;

5) blood test for immunoglobulins, T- and B-lymphocytes;

6) bacteriological examination of mucus from the nasopharynx, sputum with determination of the sensitivity of the isolated flora to antibacterial drugs;

7) assessment of the main indicators of external respiration;

8) study of pH and blood gas composition;

9) radiography of the paranasal sinuses according to indications (complaints of pain when tilting the head, palpation in the projection of the sinuses, nasal discharge).

Differential diagnosis

Differential diagnosis is carried out with bronchitis, bronchiolitis, acute respiratory viral infection, acute dissimilated pulmonary tuberculosis.

An example of a diagnosis. Focal bronchopneumonia is uncomplicated, acute.

Treatment

Treatment principle:

1) the patient is prescribed bed rest, aerotherapy, and a diet corresponding to the severity of the condition;

2) antibacterial drugs, antibiotics (semi-synthetic penicillins, aminoglycosides, cephalosporins), sulfonamide drugs (sulfadimezin, sulfalopanetaxine, biseptol), nitrofuran drugs (furagin, furadonin, furazolidone);

3) treatment of respiratory failure, elimination of obstructive syndrome (removal of mucus from the upper respiratory tract, expectorants and mucolytics, bronchodilators);

4) antihistamines (diphenhydramine, fenkarol, kistin, telfast);

5) increasing the patient’s immunological activity (immunoglobulin, dibazol, pentoxin, methyluracil, immunomodulators - immunal);

6) vitamin therapy.

6. Pleurisy

Pleurisy is an inflammation of the pleura, accompanied by tension in the function and structure of the pleural layers and altering the activity of the external respiratory system.

Etiology

The development of pleurisy may be associated with an infectious agent (staphylococcus, pneumococcus, tuberculosis pathogen, viruses, fungi); non-infectious effects - a complication of the underlying disease (rheumatism, systemic lupus erythematosus, pancreatitis).

Pleurisy may be of unknown etiology (idiopathic pleurisy).

Classification

The classification is as follows:

1) dry pleurisy (fibrous);

2) effusion pleurisy: serous, serous-fibrinous, purulent, hemorrhagic (depending on the nature of the exudate).

Diagnostic criteria

History of previous infectious diseases, pneumonia, inflammation of the paranasal sinuses; frequent hypothermia of the body; presence in the family or close relatives of tuberculosis or other respiratory diseases.

Clinical signs of pleurisy include a painful, wet cough with a small amount of mucous sputum; the patient complains of pain in the chest (one half), which intensifies with breathing.

Respiratory failure syndrome appears: shortness of breath, pale skin, perioral cyanosis, which worsens with physical activity; acrocyanosis. Characterized by intoxication syndrome: fatigue, poor appetite, lethargy, adynamia.

An objective examination reveals asymmetry of signs: forced position of the child on the affected side with fixation of the diseased half of the chest.

The side with the source of inflammation looks smaller, lags behind in the act of breathing, the shoulder is lowered.

When exudate accumulates in the pleural cavity during percussion, there is a shortening of the percussion sound with an upper border that goes from the spine upward outward and to the inner edge of the scapula (Damoiso line).

This line and the spine limit the area of ​​clear pulmonary sound (Garland's triangle). On the healthy side of the chest there is a triangular area of ​​shortening of percussion sound (Grocco-Rauchfuss triangle).

Auscultation: with exudative pleurisy, a sharp weakening of breathing is heard or there is no opportunity to listen to it; with dry pleurisy, a pleural friction noise is heard.

Additional research methods

The x-ray shows an oblique darkening of the diseased lung (fluid level), a shift of the mediastinum to the healthy side, and infiltrates in the lung tissue.

The blood test shows changes in the form of increased ESR, neutrophilic leukocytosis.

When examining the exudate of the pleural cavity, its nature is determined (serous, purulent, hemorrhagic), the specific gravity, the nature and number of formed elements, and the level of protein are determined.

Inflammatory exudate is characterized by: density greater than 1018, amount of protein more than 3%, positive Rivalta test. In a cytological examination of the sediment, neutrophils predominate at the beginning of the development of inflammation.

During development, the number of neutrophils increases and they can be destroyed. If eosinophils predominate in the sediment, then the patient has allergic pleurisy. Transudate is characterized by a sediment with a small amount of desquamated epithelium. In case of serous and hemorrhagic pleurisy, cultures on simple media do not give results.

Tuberculous pleurisy can be diagnosed by inoculation on a special medium or infection of guinea pigs. Research is complemented by biopsy and morphological studies of altered areas of the pleura during thoracoscopy. If there is exudate in the pleural cavity, bronchoscopy is indicated.

Examination plan:

1) biochemical, general blood and urine tests;

2) blood serum examination (protein, seromucoid, sialic acids, fibrinogen);

3) bacteriological studies of mucus from the throat and nose, sputum, fluid from the pleural cavity with determination of the sensitivity of the isolated flora to antibiotics;

4) study of immunological status with determination of T- and B-lymphocytes;

5) radiography of the chest organs in two projections in a vertical position;

6) pleural puncture;

7) tuberculin diagnostics.

Differential diagnosis

Differential diagnosis is carried out between pleurisy of various etiologies (rheumatic pleurisy, with systemic lupus erythematosus, leukemia, lymphogranulomatosis, hemophilia, kidney disease, liver cirrhosis, liver amebiasis, tumors, brucellosis, syphilis, mycosis), between effusion pleurisy and atelectasis of the lower lobe, lobar pneumonia .

Diagnosis example:

1) exudative pleurisy, purulent (pleural empyema, interlobar, pneumococcal);

2) dry pleurisy (fibrinous), effusion (purulent) pleurisy.

Treatment

Treatment principle:

1) elimination of pain syndrome;

2) influence on the cause that caused pleurisy (antibiotics, anti-inflammatory therapy);

3) therapeutic pleural punctures;

4) symptomatic therapy;

5) physiotherapy, exercise therapy.

7. Chronic nonspecific lung diseases

Chronic nonspecific lung diseases are a group of diseases with different etiologies and pathogenesis, characterized by damage to the lung tissue.

The classification is as follows:

1) chronic pneumonia;

2) malformations of the bronchopulmonary system;

3) hereditary lung diseases;

4) lung damage due to hereditary pathology;

5) bronchial asthma.

Chronic pneumonia is a chronic nonspecific bronchopulmonary process, which is based on irreversible structural changes in the form of bronchial deformation, pneumosclerosis in one or more segments and is accompanied by inflammation in the lung or bronchi.

Etiology

Most often, chronic pneumonia develops as a result of recurrent or prolonged pneumonia of staphylococcal nature, with destruction of the lungs.

Chronic secondary pneumonia is based on immunodeficiency states, foreign body aspiration, and malformations of the pulmonary system.

Classification

1) with deformation of the bronchi (without their expansion);

2) with bronchiectasis. Period of illness:

1) exacerbation;

2) remission.

The severity of the disease depends on the volume and nature of the lesion, the frequency and duration of exacerbations, and the presence of complications.

Clinic

Chronic pneumonia: history of repeated pneumonia with a protracted course and destruction of the lungs. Clinically manifested by a constant wet cough, intensifying during an exacerbation.

The sputum is mucopurulent, more often in the morning. Symptoms of intoxication are clearly expressed: pale skin, cyanosis of the nasolabial triangle, decreased appetite. Chronic heart and pulmonary failure syndrome; cyanosis, shortness of breath, tachycardia, nail phalanges in the form of “watch glasses” and “drumsticks”.

The chest is deformed - flattening, asymmetry in the act of breathing; percussion – shortening of sound over the affected area. Auscultation - bronchial amphoric, weakened breathing. The wheezes are varied, wet and dry.

Polycystic lung disease is characterized by a wet cough with purulent sputum, shortness of breath, bulging and retraction of individual parts of the chest. Percussion – shortening of sound over foci of inflammation. Auscultation – amphoric breathing, moist rales.

Lung damage in primary immunodeficiency conditions. Characteristic frequent acute respiratory viral infections, sinusitis, otitis, hepatolienal syndrome. Reduction of immunoglobulins of a certain class. In the general blood test there is lymphopenia; decrease in T- and B-lymphocytes.

Primary pulmonary hypertension. Clinical manifestations: cough may be absent, patients are severely exhausted, ECG shows right ventricular hypertrophy; X-ray shows expansion of the roots of the lungs, expansion of the branches of the pulmonary artery.

Kartagener syndrome is characterized by a triad of symptoms:

1) reverse arrangement of internal organs;

2) bronchiectasis;

3) sinusitis.

Percussion – shortening of sound over the lesion; Auscultation – wet rales. On the radiograph, the lung damage is diffuse in nature with localization to a greater extent in the basal segments.

Idiopathic pulmonary hemosiderosis is characterized by damage to the lungs and deposition of iron in them and anemia.

In the sputum there are macrophages with gynosiderin. There is an increased level of indirect bilirubin in the blood. The radiograph shows small cloud-like (1–2 cm) focal shadows, often symmetrical.