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Bronchial asthma

Bronchial asthma - (asthma bronchiale; Greek asthma, panting, asphyxiation) is a disease whose main symptom is seizures or recurrent expiratory asphyxiation due to pathological bronchial hyperreactivity. This hyperreactivity manifests itself when exposed to various endogenous and exogenous stimuli, both causing an allergic reaction and acting without the participation of allergic mechanisms. The given definition corresponds to the idea of ​​B. a. as a nonspecific syndrome and requires coordination with the tendency to preserve the established in the USSR in the 60-70s in the medical and diagnostic practice. allocations from this syndromic concept allergic B. and. as an independent nosological form.

Classification

There is no generally accepted classification of asthma. In most countries of Europe and America from 1918 to the present, B. a. divided into caused by external factors (asthma extrinsic) and related to internal causes (asthma intrinsic). According to modern concepts, the first corresponds to the concept of non-infectious-allergic, or atopic, bronchial asthma, the second includes cases associated with acute and chronic infectious diseases of the respiratory apparatus, endocrine and psychogenic factors. As separate variants, so-called aspirin asthma and asthma of physical effort are distinguished. In the classification of A.D. Ado and P.K. Bulatov, adopted in the USSR since 1968, identified two main forms of B. a.: Atopic and infectious-allergic. Each of the forms is divided into stages on the predastm, the stage of attacks and the stage of asthmatic conditions, and the sequence of stages is not mandatory. According to the severity of the course, they emit light, moderate and severe B. a. In recent years, in light of the approach to B. a. as a syndrome, such a classification, as well as the terminology used, are objectionable. In particular, the proposed allocation of non-immunological form B. a .; introduction of the term "infectious-dependent form", which will combine all cases of B. a. associated with infection, including with non-immunological mechanisms of bronchospasm; allocation of dyshormonal and psychological options of B. and.

Etiology

Atopic B. a. caused by allergens of animal and vegetable origin, as well as those related to simple chemicals that sensitize the airways, usually by inhalation. Food and parasitic allergens can cause hematogenous sensitization. Most often at atopic B. and. in adults, allergy to house dust is detected (about 90% of cases), in which the sensitizing agent is mainly tick Dermatophagoides pteronissimus. Less often atopic B. and. it is a manifestation of Pollinosis - an allergy to pollen of wind-pollinated plants. In some cases, atopic B. a. A significant role belongs to sensitization to mold spores. Sensitization is found to pet dander and dandruff, birds' feathers, dry food for aquarium fish (daphnia), insect emanations (bees, cockroaches, locusts, butterflies), flour, various food products, platinum salts, and some other chemicals, t. h drugs (usually by professional contact).

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Etiology of aspirin B. and. not clear. Patients have an intolerance to acetyl-salicylic acid, all pyrazolone derivatives (amidopirin, analgin, baralgin, butadion), and also indomethacin, mefenamic and flufenamic acids, ibuprofen, voltaren, i.e. most nonsteroidal anti-inflammatory drugs. In addition, some patients (according to various sources, from 10 to 30%) also do not tolerate the yellow food dye tartrazine, used in the food and pharmaceutical industry, in particular for the manufacture of yellow pills and tablets shells.

Infectious-dependent B. a. it is formed and aggravated due to bacterial and especially often viral infections of the respiratory apparatus. According to the works of the school A.D. Ado, the main role belongs to the bacteria Neisseria perflava and Staphylococcus aureus. A number of researchers attach greater importance to influenza viruses, parainfluenza, respiratory syncytial viruses and rhinoviruses, mycoplasma.

The predisposing factors for the development of B. a., In the first place, include heredity, the value of which is more pronounced in atopic B. a., Inherited in a recessive manner with 50% penetrance. It is believed that the ability to produce allergic IgE antibodies (immunoglobulins E) in atopic asthma, as in other manifestations of atopy, is associated with a decrease in the number or decrease in the function of T-lymphocyte suppressors. There is an opinion that the development of B. and. some endocrine disorders and dysfunction of the pituitary - the adrenal cortex; known, for example, exacerbations of the disease in menopause in women. Probably, the predisposing factors include cold, damp climate, as well as air pollution.

Pathogenesis

Pathogenesis of any form B. a. consists in the formation of bronchial hyperreactivity, manifested by spasm of bronchial muscles, edema of the bronchial mucosa (due to increased vascular permeability) and hypersecretion of mucus, which leads to bronchial obstruction and the development of asphyxiation. Bronchial obstruction can occur both as a result of an allergic reaction, and in response to exposure to non-specific irritants — physical (inhalation of cold air, inert dust, etc.), chemical (for example, ozone, sulfur dioxide), strong odors, weather changes (especially barometric pressure, rain, wind, snow), physical or mental stress, etc. Specific mechanisms for the formation of bronchial hyperreactivity have been studied insufficiently and, probably, are not the same for different etiological variants of B. a. with a different ratio of the role of congenital and acquired disorders of the regulation of bronchial tone. The defect of β-adrenergic regulation of the bronchial wall tone is important, the role of the hyperresponsiveness of the α-adrenoreceptors and cholinergic receptors of the bronchi and the so-called non-adrenergic-non-cholinergic system are not excluded. Acute bronchial obstruction in the case of atonic B. a. develops when exposed to the bronchial walls of mediators of an allergic reaction of type I (see Allergy). A possible pathogenetic role in the reaction of immunoglobulins G (subclass lgG4) is discussed. Using inhalation provocative tests with atopic allergens, it was established that they can induce both a typical immediate reaction (15-20 minutes after contact with an allergen) and a late one, which starts in 3-4 h and reaches a maximum in 6-8 h ( about 50% of patients). The genesis of the late reaction is explained by inflammation of the bronchial wall with the involvement of neutrophils and eosinophils by the chemotactic factors of the type I allergic reaction. There is reason to believe that it is a late reaction to an allergen that significantly enhances bronchial hyperreactivity to nonspecific stimuli. In some cases, it is the basis for the development of asthmatic status, but the latter may be due to other causes, arising, for example, after taking nonsteroidal anti-inflammatory drugs in patients with aspirin B. a., With an overdose of adrenergic mimetics. after abnormal cancellation of glucocorticoids, etc. In the pathogenesis of asthmatic status, the blockade of β-adrenoreceptors and mechanical obstruction of the bronchi (viscous mucus, as well as due to edema and cell infiltration of their walls) are considered the most significant.

Pathogenesis of aspirin B. a. not quite clear. In most cases, there is a pseudo-allergy to a number of non-steroidal anti-inflammatory drugs. A violation of the metabolism of arachidonic acid is believed to be of primary importance.

Pathogenesis of infectious-dependent B. a. has no generally accepted explanation. Proof of lgE-mediated allergy to bacteria and viruses is not received. Theories of the β-adrenergic blocking action of a number of viruses and bacteria, as well as the vagal bronchoconstrictive reflex with defeat of the afferent zones by the virus, are discussed. It is established that lymphocytes of sick B. and. A special substance is released in increased amounts that can cause the release of histamine and possibly other mediators from basophils and mast cells. The microbes in the airways of patients, as well as the bacterial allergens manufactured for practical use, stimulate the secretion of this substance by lymphocytes of patients with infectious B. From this it follows that the final pathogenetic links of the formation of an attack of suffocation may be similar in both main forms of bronchial asthma.

The pathogenetic mechanisms of asthma physical effort have not been established. There is a point of view that the leading pathogenesis is the stimulation of the effector endings of the vagus nerve. The reflex can be caused, in particular, by heat loss by the lungs due to forced breathing. The effect of cooling through the mediator mechanism is more likely. It is noticed that asthma of physical effort is more easily triggered by the inhalation of dry air than that of humid air.

At many sick B. and. psychogenic asthma attacks occur, for example, with emotions of fear or anger, with false patient information about inhalation of ostensibly increasing doses of an allergen (when the patient actually ingested saline), etc. Acute, severe stressful situations are more likely to cause a temporary remission of B. a., Whereas chronic psychotrauma usually worsens its course. Mechanisms of influence of psychogenic influences on B.'s current and. remain unclear. Different types of neurosis occurring in patients with B. a. Are more often the result, not the cause of the disease. At present, there are no sufficient grounds for isolating psychogenic asthma in a separate form, but in the complex treatment of patients with B. a. value psychogenic should be considered.

Clinical picture

In the predastmic stage, many patients show allergic or polypous rhinosinusitis. Paroxysmal cough (dry or with a small amount of viscous sputum mucous membrane), which is not relieved by conventional antitussive drugs and is eliminated by the means of treating B. Coughing attacks usually occur at night or in the early morning hours. Most often, the cough remains after the transferred respiratory viral infection or exacerbation of chronic bronchitis, pneumonia. Difficulty breathing the patient is not experiencing. When auscultation of the lungs is sometimes determined by hard breathing, very rarely - dry rales with forced expiration. Eosinophilia is found in the blood and sputum. In the study of respiratory function (respiratory function) before and after inhalation of β-adrenomimetic (izadrina, beroteka, etc.), a significant increase in expiratory power may be established, indicating so-called latent bronchospasm.

In the subsequent stages of development of B. and. its main manifestations are asthma attacks, and in severe cases, it is also a state of progressive suffocation, referred to as asthmatic status (status asthmaticus).

An attack of bronchial asthma develops relatively suddenly, in some patients, following certain individual precursors (sore throat, itchy skin, nasal congestion, rhinorrhea, etc.). There is a feeling of congestion in the chest, shortness of breath, a desire to cough, although the cough during this period is mostly dry and aggravates shortness of breath. The difficulty of breathing, which the patient experiences at the beginning only on expiration, increases, which forces the patient to take a sitting position for inclusion in the work of auxiliary respiratory muscles (see Respiratory system). There are wheezing in the chest, which at first only the patient himself feels (or the doctor’s lungs listening to him), then they are heard at a distance (distance wheezing) as a combination of different pitch of the playing harmonium (music wheezing). At the height of the attack, the patient experiences pronounced suffocation, difficulty not only in exhalation, but also in inhalation (due to the installation in the respiratory pause of the chest and diaphragm in the position of deep inhalation).

The patient sits, leaning his hands on the edge of the seat. Thorax expanded; exhalation is significantly elongated and is achieved by visible tension of the muscles of the chest and trunk (expiratory dyspnea); intercostal space while inhaling; the neck veins on the exhale swell, on the inhale they collapse, reflecting significant differences in the intrathoracic pressure in the phases of inhalation and exhalation. When percussion of the chest is determined by the boxed sound, the lowering of the lower border of the lungs and the restriction of the respiratory mobility of the diaphragm, which is confirmed by x-ray examination also reveals a significant increase in the transparency of the pulmonary fields (acute distention of the lungs). Auscultation of the lungs reveals harsh breathing and dry rales plentiful in various tones, with a predominance of buzzing (at the beginning and at the end of an attack) or whistling (at the height of an attack). Palpitations are speeded up. Heart sounds are often poorly defined due to the distention of the lungs and the muffling volume of audible dry rales.

The attack can last from several minutes to 2-4 hours (depending on the applied treatment). The resolution of the attack is usually preceded by a cough with a small amount of sputum. Difficulty breathing decreases and then disappears.

Asthmatic status is defined as a life-threatening accruing bronchial obstruction with progressive impairment of ventilation and gas exchange in the lungs, which is usually not effective in a patient with bronchodilators.

There are three options for the onset of asthma status: the rapid development of coma (sometimes observed in patients after discontinuation of glucocorticoids), the transition to asthma status of an asthma attack (often against an adrenergic overdose) and the slow development of progressive asphyxiation, most often in patients with infectious B.. According to the severity of the patient's condition and the degree of disturbances in gas exchange, three stages of asthmatic status are distinguished.

Stage I is characterized by the emergence of a stable expiratory dyspnea, against the background of which frequent asthma attacks occur, forcing patients to resort to repeated inhalations of adrenomimetics, but the latter only briefly relieves asphyxiation (without eliminating completely expiratory dyspnea), and after a few hours their action is lost. Patients are a little excited. Percussion and auscultation of the lungs reveal changes similar to those in an attack of B. a., But dry wheezing is usually less abundant and high-pitched wheezing prevails. As a rule, tachycardia is defined, especially pronounced when intoxicated with adrenomimetics, when also finger tremor, pallor, increased systolic blood pressure, sometimes extrasystole, pupillary dilation are detected. The voltage of oxygen (pO2) and carbon dioxide (pCO2) in arterial blood is close to normal, there may be a tendency to hypocapnia.

Stage II asthmatic status is characterized by a severe degree of expiratory asphyxiation, exhaustion of the respiratory muscles with a gradual decrease in the minute volume of respiration, and increasing hypoxemia. The patient either sits leaning on the edge of the bed, or reclines. Arousal is replaced by increasingly lengthening periods of apathy. The tongue, skin of the face and trunk are cyanotic. Breath remains speeded up, but it is less deep than in stage I. Percussion is determined by the picture of acute pulmonary distention, auscultatory - weakened hard breathing, which may not be audible at all over certain parts of the lungs (zones of the “silent” lung). The number of heard dry rales is significantly reduced (determined by the lack of and quiet loud wheezing). Tachycardia, sometimes extrasystole is noted; on ECG - signs of pulmonary hypertension (see Hypertension of the pulmonary circulation), reduced T wave in most leads. Arterial blood pO2 drops to 60-50 mm Hg. Art., Moderate hypercapnia is possible.

Ill stage of asthmatic status is characterized by pronounced arterial hypoxemia (pO2 within 40-50 mm Hg) and increasing hypercapnia (pCO2 above 80 mm Hg) with the development of respiratory acidotic coma (Coma). Marked diffuse cyanosis. Often, dryness of mucous membranes, a decrease in tissue turgor (signs of dehydration) are determined. Breathing gradually decreases and becomes less and less deep, which during auscultation is reflected by the disappearance of wheezing and a significant weakening of respiratory noises with the expansion of the “silent” lung areas. Tachycardia is often combined with various cardiac arrhythmias. Death can occur from respiratory arrest or acute heart rhythm disorders due to myocardial hypoxia.

Separate forms of bronchial asthma have features of history, clinical manifestations and course.

Atopic B. a. often begins in childhood or adolescence. In the family history of more than 50% of cases, asthma or other atopic diseases are detected, the patient has a history of allergic rhinitis, atopic dermatitis. Asthma attacks in atopic B. a. often prodromal symptoms precede: itching in the nose and nasopharynx, nasal congestion, sometimes itching in the chin, neck, interscapular region. The attack often begins with a dry cough, then a typical pattern of expiratory choking with distant dry rales quickly unfolds. Usually, a seizure can quickly be stopped by using β-adrenomimetics or aminophylline; ends with the release of a small amount of light viscous sputum. After an attack, the auscultatory symptoms of asthma are eliminated completely or remain minimal.

For atopic B. a. characterized by relatively mild, late development of complications. Severe course, development of asthmatic status are rare. In the early years of the disease, remissions are typical when contact with allergens is stopped. Frequent spontaneous remissions. Full recovery at atopic B. and. in adults is rare.

Infectious-dependent B. a. observed in individuals of different ages, but adults are more likely to get sick. In the family history of asthma is relatively common, rarely - atopic diseases. The combination is characteristic B. and. with polypous rhinosinusitis. The onset of the disease is usually associated with acute, often viral infections or exacerbations of chronic diseases of the respiratory apparatus (sinusitis, bronchitis, pneumonia). Asthma attacks differ less than with atopic B. a., Acute development, longer duration, less clear and fast resolution in response to the use of adrenomimetics. After stopping the attack, auscultation of the lungs preserves harsh breathing with a prolonged exhalation, dry buzzing rales, and in the presence of inflammatory exudate in the bronchi, moist rales. At this form B. and. severe course with repeated asthmatic status is more common, complications develop more quickly.

Aspirin asthma in typical cases is characterized by a combination of B. a. with recurrent nasal polyposis and its sinuses and intolerance to acetylsalicylic acid (the so-called aspirin triad, sometimes referred to as the asthmatic triad). However, nasal polyposis is sometimes absent. Adult women are more likely to get sick, but the disease is also found in children. It usually begins with polypous rhinosinusitis; polyps after their removal quickly recur. At some stage of the disease after another polypectomy or aspirin, analgin is joined by B. a., The manifestations of which persist subsequently and without taking nonsteroidal anti-inflammatory drugs. Taking these drugs invariably causes exacerbations of the disease of varying severity - from the manifestations of rhinitis to the most severe asthmatic status with a fatal outcome. Polypectomies are also often accompanied by severe exacerbations of B. a. Most clinicians believe that for aspirin B. a. characterized by severe course. Atopy among these patients is rare.

Asthma of physical effort, or afterload bronchospasm, is not, apparently, an independent form B. a. It is established that at 50 - 90% of patients with any form B. and. physical effort can cause an attack of asphyxiation 2-10 minutes after the end of the load. Attacks are rarely severe, lasting 5-10 minutes, sometimes up to 1 hour; pass without the use of drugs or after inhalation of β-adrenomimetica. Asthma of physical effort is more common in children than in adults. It has been noticed that certain types of physical efforts (running, playing football, basketball) especially often cause postload bronchospasm. Lifting weights is less dangerous; relatively well tolerated swimming and rowing. The duration of physical activity also matters. Under provocative test conditions, loads are usually given for 6–8 minutes; with a longer load (12-16 min), the severity of postload bronchospasm may be less - the patient, as it were, jumps over the bronchospasm.

Complications

Long proceeding B. and. is complicated by emphysema of the lungs, often chronic nonspecific bronchitis, pneumosclerosis, development of pulmonary heart, with the subsequent formation of chronic pulmonary heart disease. Much faster these complications occur with infectious-dependent than with the atopic form of the disease. At the height of a choking attack or a prolonged coughing attack, a short-term loss of consciousness (Bettolepsy) is possible. In severe attacks, lung ruptures are sometimes noted in areas of bullous emphysema with the development of Pneumothorax and pneumomediastinum (see Mediastinum). Complications in connection with long-term therapy are often observed B. and. glucocorticoids: obesity, arterial hypertension, severe osteoporosis, which may be the cause of the onset of seizures B. a. spontaneous rib fractures. With the continuous use of glucocorticoids in a relatively short period (sometimes 3-5 weeks), the hormone-dependent course of B. a is formed; cancellation of glucocorticoids can cause severe asthmatic status, threatening to death.

Diagnosis

Analysis of the clinical picture and targeted examination of the patient allow to solve three main diagnostic tasks: confirm (or reject) the presence of B. a., Determine its shape, establish the spectrum of allergens (with allergic B. a.) Or pseudoallergens (see Pseudo-allergy), with etiological value for B. and. in this patient. The last problem is solved with the participation of allergists.

The diagnosis of bronchial asthma is based on the following criteria: characteristic expiratory asthma attacks with distant wheezing; significant differences in expiratory power during a seizure (sharp decline) and out of seizure: the effectiveness of β-adrenergic mimetics in arresting asthma kits; eosinophilia of the blood and especially sputum; the presence of concomitant allergic or polypous rhinosinusopathy. Confirm the presence of B. and. characteristic changes in respiratory function; less specific data of radiological studies outside of an asthma attack. Of the latter in favor of the possible presence of B. a. signs of chronic emphysema of the lungs (Emphysema of the lungs) and Pneumosclerosis (more often found in infectious-dependent asthma) and changes in the paranasal sinuses may indicate signs of edema of the mucous membrane, a polypous, sometimes purulent process. At atopic B. and. radiological changes in the lungs outside the attack of breathlessness may be absent even years after the onset of the disease.

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From studies of respiratory function of major importance for the diagnosis of B. and. has a detection of bronchial obstruction (as the leading type of ventilation disorders in B. a.) and, most importantly, characteristic of B. a. bronchial hyperreactivity, determined by the dynamics of respiratory function in provocative samples with inhalation of physiological active substances (acetylcholine, histamine, etc.), hyperventilation, physical activity. Bronchial obstruction is determined by the decrease in forced vital capacity in the first second of expiration (FZhEL1) and expiratory power according to pneumotachometry. The latter method is very simple and can be used by a doctor on an ordinary outpatient appointment, incl. for identification of the so-called latent bronchospasm often found in patients B. and. If the expiratory power, measured before and after 5, 10 and 20 minutes after inhalation of a single dose of alupenta (or another β-adrenomimetic in a metered manual inhaler), increases by 20% or more, then the test is considered positive, indicating bronchospasm. At the same time, a negative test in the remission phase with a normal initial expiratory power does not give grounds to reject B.'s diagnosis. A.

The degree of nonspecific bronchial hyperreactivity is estimated in the remission phase of B. a. using provocative inhalation tests with acetylcholine (carbacholine), sometimes histamine, PgF2α, β-adrenoceptor blocking drugs. These researches, sometimes necessary at the doubtful diagnosis of B. and., Are carried out only in the conditions of a hospital. The provocative test is considered positive if after inhalation of the FVC acetylcholine solution, and (or) the expiratory power is reduced by more than 20%; in some cases it is provoked clinically developed attack B. and. A positive acetylcholine test confirms the diagnosis of B. a., Negative allows you to reject it with a high degree of probability.

Diagnosis of separate forms B. and. to a significant extent based on clinical data, the analysis of which, if necessary, is supplemented by special tests and allergological examination.

Aspirin asthma is considered with a high probability in the case of a clear connection with seizures with aspirin or other nonsteroidal anti-inflammatory drugs, as well as if asthma is the first manifestation of intolerance to these drugs, especially in women over 30 years old who have no atopy in their personal and family history and suffer from pansinusitis or nasal polyposis, complementing the aspirin triad. The diagnosis is more reliable if during the attacks of B. and. a normal level of lgE in the blood is detected in the presence of blood eosinophilia. In doubtful cases, a provocative oral test with acetylsalicylic acid (in minimal doses) is sometimes carried out in specialized institutions, but the widespread use of this test cannot be recommended due to the possibility of severe reactions.

Physical effort asthma is established according to anamnesis and the results of a provocative test with a dosed (using a bicycle ergometer) exercise, which is usually performed in the hospital in the remission phase of the disease and in the absence of contraindications (heart disease, thrombophlebitis of the lower extremities, a high degree of myopia, etc.) . The test is considered positive if within 20 minutes after performing physical effort FVC) and (or) expiratory power is reduced by 20% or more or a clinically pronounced attack of suffocation occurs (usually not severe). A positive test is an objective indicator of bronchial hyperreactivity and can be used to confirm the diagnosis of B. a. A negative result does not exclude this diagnosis.

Atopic B. a. they are recognized by the characteristics of the clinical course, the presence of concomitant manifestations of atopy (pollinosis, atopic dermatitis, food allergies, etc.) according to the family and allergic history. Confirm the diagnosis by identifying in the patient sensitization of the reagin type (see Allergy) and positive results of elimination tests (cessation of contact with suspected allergens), as well as provocative tests with certain allergens. For atonic B. a. characterized by elevated levels of total lgE in serum, as well as the presence of allergen-specific lgE. Relatively often there is a decrease in the number of T-lymphocytes, especially T-suppressors.

Infectious-dependent B. a. it is supposed primarily in cases of manifestations of asthma attacks on the background of already formed chronic bronchitis, chronic pneumonia or in the presence of chronic foci of infection in the upper respiratory tract. However in all cases it is necessary to differentiate infectious-dependent and atopic forms of B. a. In favor of infectious B. evidence of a delayed onset and a long duration of asthma attacks, the frequent association of their increased frequency with acute or exacerbated chronic respiratory infection, a tendency to develop asthmatic status, the absence of reagin-type sensitization in patients, positive skin and provocative inhalation tests with bacterial allergens.

The differential diagnosis is carried out most often between infectious B., and., Chronic obstructive bronchitis, the manifestations of which, including the auscultative picture, may be similar. In favor of B. and. eosinophilia of blood and sputum, the presence of allergic or polypous rhinosinusitis, a positive test for latent bronchospasm, therapeutic efficacy of anti-asthma drugs. The same criteria, as well as the results of allergic examination, are used for the differential diagnosis of B. a. with asthma-like bronchospasm with carcinoid syndrome, systemic mastocytosis, with irritation of the trachea or bronchi with a foreign body, compression of their tumor, enlarged lymph nodes, aortic aneurysm. Tracheobronchial dyskinesia (expiratory stenosis of the trachea and bronchi) in combination with chronic bronchitis is accompanied by expiratory difficulties in breathing, without other characteristic symptoms of B. a., The diagnosis is established using a bronchoscopic examination. At radiological detection in lungs of infiltrates at patients with a hypereosinophilia of blood and asthma attacks the differential diagnosis of B. is necessary. And. with volatile eosinophilic infiltrates (see Lefflera syndrome), allergic bronchopulmonary aspergillosis (Aspergillosis), as well as with pulmonary form of periarteritis nodosa (see Periarteritis nodosa). It is based on the results of targeted diagnostic studies confirming or excluding these diseases. Sometimes it is necessary to differentiate B. and. with hyperventilation syndrome (with hysteria, organic brain lesions), which manifests itself tachypnea and hypocapnia, but there are no typical signs of bronchospasm. In doubtful cases for B.'s exception and. apply inhalation acetylcholine test.

Treatment

In the treatment of sick B. and. highlight the urgent measures for stopping the attack of suffocation and the removal of patients from asthmatic status and comprehensive therapy aimed at the disease itself and the secondary prevention of attacks B. a. Indications for hospitalization at the onset of the disease are determined by the need to clarify the diagnosis, the severity of the condition of patients with marked exacerbations (in prostate status and asthmatic status); Hospitalization in allergological departments is desirable in the remission phase of the disease, when specific diagnostics and immunotherapy can be performed.

Emergency treatment of an asthma attack with mild and at an early stage of its development is usually carried out by the patient himself according to the previously received recommendations of the doctor. Often it is limited to the inhalation of 1-2 doses of β-adrenomimetic (alupente, salbutamol, berotok, etc.) or atropine-like bronchodilator (atrovent), or a combined drug, berodual (berotek and atrovent) from a metered-dose manual inhaler. The choice of the drug, its single and maximum daily dose is made by the doctor, based on the results of a comparative assessment of the effect of different doses of these bronchodilators (Bronchodilators) in a given patient both on bronchial permeability (according to FZhEL1 dynamics, expiratory power) and on heart rate and HELL. When prescribing β-adrenomimetics, the patient is warned about the danger of overdosing (due to the possibility of exacerbation of bronchospasm by the so-called ricochet mechanism and cardiotoxic action) and allow no more than 8 doses per day without direct supervision of a doctor; If there is a need for more inhalations, the patient should consult a doctor.

With moderate and severe B., a., Especially with insufficient effect of dosed inhalations of bronchodilators from a manual inhaler, the doctor provides emergency care, using not only medication, but also non-drug effects on the patient, including psychotherapy. Begin with the introduction of 5-10 ml of a 2.4% solution of aminophylline into the vein, and in the absence of such an opportunity (and in a relatively early stage of the attack), the adult patient should be taken inside of aminophylline, poured from the ampule into a glass and mixed with 1 dessert spoon of vodka, or 1-2 tablespoons of an alcohol solution in a mixture containing 3 g of aminophylline, 40 ml of simple syrup and 360 ml of a 12% solution of wine alcohol. At the same time, to quickly get an expectorant and enhance the bronchodilator effect, the patient is given to drink (2-3 glasses) hot milk with the addition of Borjomi (1: 1) or sodium bicarbonate (1/2 teaspoon per glass), tea from nursing infants (excluding at atopic B A. herbs, to which the patient is allergic) or ordinary hot tea or coffee (given the patient's desire and experience in stopping such attacks earlier).

Much attention should be paid to the mental state of the patient, the elimination of the frequently occurring "respiratory panic" - irrational increase and respiratory dysrhythmia, aggravating impaired ventilation of the lungs. The patient needs to be reassured, to instill confidence in the imminent resolution of the attack, to help the patient choose the rhythm of breathing optimal for the conditions of attack (the ratio of expiration and inhalation, depth and frequency of breathing), posture and location of the patient in the room (distance from heating devices, open vent) sources of odors, etc.). Often relief to the patient brings breathing with resistance to exhalation at the level of the lip crevice (exhalation with almost closed lips); at the same time, expiratory decay of the trachea and bronchi walls decreases. In some cases, simple means of reflex therapy help to resolve the attack: placing hands or feet in hot water, rubbing the skin of the limbs and chest, applying mustard plaster, etc.

In the absence of positive dynamics in the patient's condition, 15-25 minutes after the administration of aminophylline, drug therapy should be continued. If there are no signs of an adrenergic overdose (tremor of the fingers, severe tachycardia, an increase in systolic blood pressure), it is advisable to repeat their inhalation (2 doses) with the control of the correctness of its performance (sometimes the drug is not inhaled by the patient, is delayed in the oral cavity) or enter the adrenaline subcutaneously (0, 3 ml of 0.1% solution) or ephedrine (0.5-1 ml of 5% solution). If the attack failed to stop within 1 hour, 60 mg of prednisolone or 8 mg of dexamethasone are injected intravenously. and the patient is hospitalized with suspected asthmatic status.

Intensive therapy of asthmatic status, and, if necessary, also resuscitation measures can be fully implemented only in a hospital. Therefore, all patients with asthmatic status (as well as in case of suspicion of its development) are subject to urgent hospitalization, if possible in the ward or intensive care and resuscitation ward. The main directions of therapeutic effects include restoration of sensitivity (unblocking) of bronchial β-adrenoreceptors, elimination of mechanical obstruction of the bronchi, correction of hypoxemia, hypercapnia and acid-base balance disorders, as well as the introduction of fluids, which is mandatory not only for general bronchial hydration, necessary to reduce the viscosity of secretion of bronchial glands and sputum.

At the prehospital stage, prednisone (60–90 mg) is administered intravenously to the patient. If there are signs of an overdose of adrenergic mimetics, the additional introduction of the latter is contraindicated: the use of manual inhalers is immediately stopped. In the absence of overdose, a patient can subcutaneously inject 0.3 ml of a 0.1% solution of epinephrine or 0.5 ml of a 0.05% solution of alupenta (orciprenaline sulfate), but preferably slow intravenous administration of 10 ml of a 2.4% solution of aminophylline. Because of the danger of ventricular fibrillation of the heart, the simultaneous administration of korglikon, strophanthin or other cardiac glycosides with euphyllin is categorically contraindicated. Indications for the use of the latter in patients without pulmonary heart decompensation are completely absent (in asthmatic status, the pathogenesis of tachycardia excludes the possibility of arresting it with cardiac glycosides, and the occurrence of extrasystole creates direct contraindications to their use). Further treatment is carried out in the hospital.

In stage I of the asthmatic status, prednisolone in a dose of 60 mg (or methylprednisolone, dexamethasone in equivalent doses) is administered intravenously every 4-6 hours before the patient is removed from the asthmatic status. At the same time, glucocorticoids are administered orally (30–60 mg per day of prednisone or equivalent doses of other drugs). If necessary, especially in patients with a hormone-dependent B. course, the doses of prednisolone can be significantly increased - up to 1000 mg in the first 12 hours. Upon reaching the effect, the daily dose of glucocorticoids is reduced quickly and after 7-8 days they switch to maintenance doses ( patients with a hormone-dependent B.'s course. and.) or cancel these drugs. From the moment of receipt of the patient begin infusion therapy. Euphylline is injected intravenously in an isotonic solution of sodium chloride - 1.5-2 g per day: with poor tolerance (nausea, vomiting, cardiac arrhythmia), the drug dose is halved, and in the absence of a bronchodilatory effect, its administration is stopped. The volume of injected fluid should be at least 2 liters per day. In addition to an isotonic solution of sodium chloride, a 5% glucose solution, polyglucin, reopolyglucin is injected. Apply continuous inhalation of moistened oxygen through a nasal catheter. In order to improve bronchial drainage in this stage of asthmatic status, a 3% potassium iodide solution is prescribed (in the absence of contraindications to iodine) 20 ml every 3-4 hours until the sputum viscosity decreases or signs of iodism appear (rhinorrhea, tearing), after which the drug is canceled or reduce the frequency of its admission to the same dose up to 2-3 times per day; at the same time, bisolvone is prescribed (its expectorant effect is manifested later), and a vibrating massage of the chest is performed.

In stage II of the asthmatic status, in addition to the above-described therapy, additional measures are taken to eliminate hypoxemia, and the therapy is intensified, aimed at improving bronchial patency and drainage of the bronchi. Apply inhalation of helium-oxygen mixture. The volume of injected fluids is increased to 3 liters per day, and with severe dehydration - up to 4 liters. In order to obtain an expectorant effect, a 5% solution of sodium bicarbonate — 100 ml is administered intravenously (if necessary, correction of respiratory acidosis — 200 ml or more). If bronchial obstruction is still increasing, sometimes bronchoscopic lavage is used, i.e. washing the bronchial tree (under anesthesia with a predione or sodium hydroxybutyrate in combination with seduxen or droperidol) with warm saline sodium chloride through an injection fibrobronchoscope.

The transformation of asthmatic status in stage III, as evidenced by severe hypercapnia, decompensation of respiratory acidosis, is an indication for mechanical ventilation (ALV), which is carried out with the following features: it is necessary to create high pressure in the respiratory system (80-100 cm of water column), respiratory the volumes should not be less than 0.8–1.2 l, the minute volume of ventilation at the beginning of the ventilator should be significantly increased (up to 30–35 l). Active exhalation is not recommended. Against the background of artificial ventilation of the lungs, the bronchial tree is washed and cleaned through an endotrache tube in combination with an active shock massage of the chest.

Comprehensive treatment of patients with bronchial asthma is aimed at achieving remission of the disease and secondary prevention of its exacerbations and asthma attacks. All methods of treatment B. and. conditionally can be divided into specific, used in allergic B. a. (restriction or cessation of contact with identified allergens, and desensitization by specific immunotherapy), and non-specific, used in all forms of B. a. and including drug therapy, physiotherapy, spa treatment, physical therapy, psychotherapy, acupuncture.

Specific treatment methods used by allergists, based on the results of allergological examination of the patient. The local therapist may suspect a “guilty” allergen (for example, pet dander or feed for aquarium fish) and must give advice about stopping contact with the suspected allergen even before consulting with the allergist. Specific immunotherapy is carried out by subcutaneous administration of allergen extracts in gradually increasing doses. It is generally accepted for the treatment of atopic asthma. This type of treatment is especially effective at an early stage of the disease, when it is possible to achieve long-term remissions in 60-70% of patients. Infectious allergens for medical purposes are used less frequently. In some cases, immunosorption, plasmapheresis, lymphocytepheresis, which have a temporary effect, are used.

Treatment with immunoglobulins of antiallergic action is of secondary importance in atopic B. a. Immunomodulators (levamisole, T-activin, sodium nucleinate, etc.) are indicated for the treatment of associated inflammatory processes of the respiratory apparatus, rather than asthma itself.

Medical nonspecific therapy of patients B. and. limited to the minimum number of drugs, because polypharmacy at B. and. fraught with serious complications. Patients B. and. cholinomimetics are absolutely contraindicated, for example pilocarpine (even eye drops), or cholinesterase inhibitors (physostigmine), as well as β-adrenergic blockers (obzidan, etc.). Rauwolfia preparations can provoke a choking attack, as well as vasomotor rhinitis. It is undesirable to use opiates with histamine-absorbing activity. With indications for antibiotic therapy, the use of penicillins should be avoided, to which patients with B. a. Allergies are often detected. When B. aspirin and. categorically prohibit the use of acetylsalicylic acid, derivatives of pyrazolone and all other analgesics and nonsteroidal anti-inflammatory drugs with antiprostaglandin effect (paracetamol can be used as an analgesic). These patients should not be prescribed tablets in the yellow shell.

There is a limited number of medications that are really effective in asthma. These include bronchodilators, in particular β-adrenomimetics and xanthine derivatives (aminophylline, caffeine), as well as intal and glucocorticoids. Base course of sick B. and. usually includes the use of drugs one or two of these groups. Of the bronchodilators, β-adrenergic drugs (alupente, berotok, etc.), as well as atrovent, berodual, contained in manual metered-dose inhalers, are most convenient for stopping mild attacks of asthma (severe attacks usually require intravenous administration of aminophylline) and their prevention. So, in case of occurrence of seizures, mainly at night, they can be warned only by inhalation of bronchodilator just in a day just before bedtime. With relatively light, but frequent attacks, it is possible to recommend inhalations of these drugs by 1-2 doses up to 3-4 times per day (without the physician's control no more than 8 doses per day) for a long time (several weeks), but you should strive to reduce the daily dose or temporary cancellation of β-adrenomimetics with each relief of the patient's condition and even more so during the remission of B. a. In a number of patients, the use of non-inhalation forms of adrenomimetics and other bronchodilators, administered orally or rectally (in enemas or in candles), is effective, which makes it possible to lengthen the time of the preventive attack of the drug by 2-3 hours (compared to the inhalation route). Ephedrine, theofedrine, anastastman, aminophylline (in tablets, mixtures, solutions for microcysticism), prolonged theophylline preparations, including, are successfully used. domestic teolong and canofillin. To prevent physical asthma, fenigidine (adalat, corinfar) is also recommended. The use of these drugs allows you to temporarily cancel or significantly harm the inhalation of bronchodilators and thereby reduce the immediate, for some time, incl. irritating, their effect on the bronchial wall.

One of the goals of the use of bronchodilators is to increase the effectiveness of bronchial drainage, which plays an important role during periods of exacerbations of the disease, especially in patients with infectious B. Bronchodilator inhalation is performed 10 minutes before the start of the drainage procedure (positional and with the help of special breathing exercises), carried out in the same way as in patients with chronic Bronchitis. Expectorants are used for the same purpose - bromhexine, lasolvan, mucosolvin; iodine preparations (potassium iodide or sodium) are most effective, but sometimes vasomotor rhinitis (possibly exacerbation) and the presence of idiosyncrasy are prevented from using them. The use of inhaled proteic and mucolytics (N-acetylcysteine, trypsin, etc.) should be avoided due to the possibility of provoking a severe attack of suffocation.

Intal, mast cell stabilizing, is prescribed to achieve remission during B. a. (ability to stop the arising attack intal does not possess). It is more often effective at an atonic form B. and., But attempt of its use is justified at any form. For the same purpose, ketotifen (zaditen) possessing a wider spectrum of action is prescribed. It is difficult to predict in advance the effectiveness or inefficiency of these drugs as well as the comparative effectiveness of bronchodilators in this patient in most cases because of pronounced individual differences in drug reactions in patients with B. a. Therefore, greater importance in the treatment of patients with B. a. they have empirical criteria and flexibility of medical tactics in the choice of therapies, based on a timely assessment of their effectiveness in a given patient. For the objectification of the effect, it is necessary to use more extensively the research of FZhEL1, expiratory power (especially when selecting a bronchodilator) and other indicators of the functions of external respiration; however, in some cases, their dynamics under the influence of the medicinal product is less expressive than the dynamics of the clinical manifestations of an asthma attack and the relief of breathing observed in patients.

Glucocorticoids as a means of basic therapy are used only for severe B. and a. and the apparent lack of effectiveness of all other possible treatments. When for the first time there is a need to use glucocorticoids, for example, due to asthmatic status, you should strive to cancel them in the next 3-5 days, regardless of the size of the initial daily dose, because the formation of a hormone-dependent B. flow. and. and the likelihood of known side effects is determined not so much by daily and course doses as by the duration of use of glucocorticoids (even in small doses). Matters and dosage form used drugs. The safest of them is beclomethasone dipropionate (bekotid, beclomet) in manual metered-dose inhalers. The average daily dose corresponds to 8 breaths (2 breaths 4 times a day), but you can prescribe up to 16 breaths per day. In case of severe bronchospasm, a preliminary inhalation of β-adrenomimetic is advisable for better penetration of the drug into the respiratory tract. In the absence of effect, methylprednisolone or other glucocorticoids are shown by short courses of parenteral or oral, followed by transfer to becotide or intal, and if cancellation is not possible, transfer to the intermittent administration of the drug: every other day in an individual dose for each patient.

Surgical treatment (glomectomy) is not very effective and is considered to be insufficiently substantiated.

Diet of sick B. and. must be sufficiently high in calories, but not conducive to overweight; liquid is not limited. Food that should, according to the anamnesis, cause allergic reactions in a patient, and products containing exogenous histamine-liberators (fish, raw cabbage, radishes, citrus fruits) should be excluded from the diet. in case of aspirin asthma, culinary and confectionery products such as dragee, creams, etc., are colored with yellow paint (tartrazine may be present) are contraindicated.

Physiotherapy is used to treat chronic inflammatory processes in the lungs and sinuses, as well as to stimulate the function of the adrenal glands (inductothermia). A special place is occupied by acupuncture. which in some cases leads to a long-lasting stable remission B. and., and with exacerbations of the disease helps in many patients to achieve improvement with a smaller amount of pharmacotherapy.

The climatotherapy quite often promotes remission of B. and., Especially at young patients. Cases of the full termination of moderately heavy manifestations of B. are known. And. on the day of the patient’s arrival in a favorable climate zone. Sometimes this effect of climate change persists for many months and even years, which induces the patient to change his permanent place of residence. However, in most patients, the effect of climatotherapy is temporary, and in different patients the response to the particular climate is different. More often for sick B. and. favorable climatic zones of the middle mountains with a warm dry climate (Kislovodsk), as well as the southern coast of Crimea. Trips to these zones are recommended in the remission phase or mild clinical manifestations of the disease.

Physical therapy is important as a means of secondary prevention, and as an auxiliary element of the treatment of seizures B. a. Systematic physical exercises and special breathing exercises “discipline” breathing, help the patient to reduce fatigue of the respiratory muscles during bronchial obstruction due to better distribution of the load on them, more efficient use of the diaphragm movements with a rational ratio of respiration rate and depth, and the duration of inhalation and exhalation. During the periods of remissions and at not heavy course B. and. without signs of afterloading bronchospasm, intense muscular work causes an expansion of the lumen of the bronchi, leads in the process of training to reorganization of the regulation of respiration, makes it economical and contributes to the reduction and relief of asthma attacks.

With frequent attacks and prolonged difficulty in breathing, special breathing exercises that promote complete expiration are appropriate. These include the so-called sound gymnastics (long exhalation with pronouncing whistling or hissing sounds) and exhalation with resistance (through a straw under water, into various devices and devices).

In the conditions of out-patient treatment of sick B. and. the method of volitional restriction of pulmonary ventilation and delays in breathing on exhalation may be applied, but it is contraindicated in cases of asthmatic status, in case of circulatory failure, as well as in mental diseases that prevent the necessary contact with the doctor. The method is based on the possibility of restructuring the regulation of respiration (with appropriate training at rest) without additional oxygen demand for muscle work. A patient is given a calming conversation, the purpose of the exercises is explained, and then they are taught how to relax the muscles of the shoulder girdle, back, and abdomen in the most comfortable position - sitting at the table, putting their hands on their knees or leaning on the table. In the first classes, the doctor (or an exercise therapy instructor) inspires the patient to breathe superficially, restraining a cough. Short breathing pauses of 2-3 s help. The patient learns volitional breath hold on a quiet exhalation. In the future, such training of respiratory delays up to 30-40 times a day, but with interruptions of at least 5-7 minutes, the patients perform independently with periodic medical monitoring. At the same time, the duration of arbitrary apnea gradually increases. As the patient's condition improves, the frequency of use of bronchodilators should be reduced to their complete abolition. These recommendations can not be extended to other medicines, especially hormonal drugs. After reaching remission in uncomplicated cases, general developmental exercises are prescribed - walking, jogging, swimming, cycling. Maximum and submaximal loads for sick B. a. not shown.

When infectious B. and. against the background of chronic nonspecific lung diseases (pneumosclerosis, emphysema, chronic bronchitis, chronic pneumonia), targeted breathing exercises are recommended that contribute to bronchial drainage and short breathing after exhalation and coughing; mandatory continuous training long-willed delays in breathing.

Forecast

In sick B. adult recovery is rare. In relation to the ability to work and the life of patients, the prognosis depends on the form and hardness of B. a. At atopic form B. and. long-term remissions are possible - spontaneous (at the termination of contact with the allergen) or after specific immunotherapy. With a mild course of the disease, the ability to work is usually preserved, with moderately severe, it is disturbed in the phases of exacerbation, and in severe cases, there is often a persistent disability (disability of group III or II). The development of repeated asthmatic conditions worsens the vital prognosis; with asthmatic status stage III, even in conditions of use of mechanical ventilation, there is often a lethal outcome.

Primary prevention

General decrease in incidence of B. and. It is considered possible with the combined use of socio-hygienic and medical measures. Improving the working and living conditions of the population, reducing air pollution in cities and at industrial enterprises, combating smoking, developing physical education and sports are directly related to B. prevention. A. Medical aspects of the problem of prevention B. a. include a rational restriction of vaccinations, the fight against self-medication, polyphragmas (especially for individuals with atopic constitution). The correct and timely treatment of the so-called predastmatic diseases - acute and chronic bronchitis, pneumonia, inflammatory diseases of the upper respiratory tract, pollinosis, year-round allergic rhinitis is very important. In persons suffering from such diseases for individual prophylaxis B. a. Of great importance is the hardening of the body, physical education, employment in enterprises with clean and normal air in terms of temperature and humidity. Particularly differentiated should be the choice of profession and the organization of everyday life for persons with signs of atopic constitution and the presence of asthma in the family history, to avoid their massive contact with highly antigenic substances.

Features of bronchial asthma in children

Since the 60s. an increase in the incidence of children with bronchial asthma was noted; the proportion of B. and. in the structure of bronchopulmonary pathology in childhood is, according to various sources, from 27.6 to 60%. The disease begins more often in preschool age; revealed a tendency to more frequent disease of children in the first year of life. The number of sick children with a heavy course of B. increased.

Etiology and pathogenesis of B. a. in children, as in adults, in most cases are associated with sensitization of the body by exogenous and endogenous allergens. Children are characterized by the rapid development of polyallergy (3–12 months from the onset of the disease); monoallergy is rare. The most frequently observed allergy to house dust, pollen and food products. At allergy to pollen of an aggravation B. and. are seasonal depending on the time of flowering plants. From food cause sensitization and development B. a. most often citrus fruits, raspberries, strawberries, cantaloupe, pineapple, chocolate, coffee, cocoa, fish, caviar, eggs, honey, nuts, less often milk (milk protein), chicken meat (broiler chickens), red apples, carrots. In case of infectious allergy, hypersensitivity to hemolytic staphylococcus, streptococcus, Escherichia coli, and mold fungi is more often detected. Often in children, sensitization to non-infectious allergens precedes the appearance of an infectious allergy; over time, the same child may experience allergic reactions of both immediate and delayed type. Delayed type reactions are also possible.

Earlier occurrence of B. and. hereditary predisposition to allergic reactions (polygenic inheritance), perinatal hypoxia of the child, anomalies of the constitution (lymphatic-hypoplastic and exudative diathesis) contribute to children and its more severe course. A certain role in B.'s development and. play frequent respiratory viral infections that violate the protective role of the mucous membrane of the respiratory tract against allergens. Conditionally-reflex connections are important (the onset of an attack in a situation in which it was previously caused by exposure to an allergen), as well as a decrease in the excitability threshold of bronchial receptors as a cause of an attack of B. a. when exposed to non-specific factors (irritating particles in the air, physical or emotional stress, changing meteorological conditions, etc.).

Classification. In pediatric practice, the classification of S.Yu. Kaganova (1980), in which three forms of the disease are identified: atopic, infectious-allergic and mixed - with typical (marked attacks of B. a. Or asthmatic bronchitis) and atypical (in the form of attacks of acute distention of the lungs), with a subdivision according to severity three degrees (mild, moderate and severe). Indicators of severity B. and. are the frequency, nature and duration of asthma attacks, as well as the presence and severity in the interictal period of pathological abnormalities in the respiratory system, blood circulation, nervous system, metabolism, physical development. The classification also implies the characterization of the characteristics of the B. a. Stream: 1. Separate seizures, an asthmatic condition, an asphyxial syndrome; 2. The presence of bronchopulmonary infections, microbial-inflammatory changes in the nasopharynx; 3. Concomitant allergic diseases: allergic dermatosis (eczema, urticaria, angioedema), respiratory allergies (allergic rhinitis, sinusitis, tracheitis, tracheobronchitis, bronchitis, pneumonia, eosinophilic pulmonary infiltration); 4. Complications: chronic pulmonary emphysema; pulmonary heart; atelectasis of the lungs; pneumothorax; mediastinal and subcutaneous emphysema; neurological disorders.

The stated classification is used for the differentiated assessment of manifestations and B.'s course and. in a child and for formulating a diagnosis of the disease, which also indicates the period of the disease (attack, interictal).

Clinical manifestations of B. and. in children in the form of attacks of asthma and asthmatic status are the same. as in adults. There are entrepreneurial, paroxysmal, post-offensive and interictal periods. The entrepreneurial period lasts from several minutes to 2-3 days. There is a deterioration of the child’s condition: lethargy or irritability, tearfulness, emotional instability, fatigue, and loss of appetite. At atopic B. and. before an attack, itchy nose, sneezing, copious watery nasal discharge (or nasal congestion), sore throat, dry cough, conjunctivitis. When food and drug allergies before the development of an attack can be a rash, dyspeptic disorders, sometimes angioedema. At infectious and allergic B. and. seizures often occur on the 3-5th day from the onset of acute respiratory infection. The starting period for children lasts from several minutes to several hours and even days. In young children, cough from the very beginning of the attack is moist and during auscultation of the lungs, in addition to dry a lot of medium and finely wheezing due to a pronounced exudative component (edema and hypersecretion prevail).

It is common to establish the diagnosis of asthmatic status in children if an attack is a B. a. does not stop for 6 hours or more, occurs with severe hypoxia and hypoxemia, with the development of resistance to bronchodilators from the group of adrenergic mimetics. Massive or prolonged contact with allergens, the development of adrenal insufficiency, the cancellation of hormones during a B.-dependent hormone-dependent course can lead to asthmatic status, and later onset of treatment of an attack, blockade of bronchial β-adrenergic receptors with prolonged use of adrenergic mimetics. There are 3 stages of asthmatic status in children. Stage I (relative compensation) - difficult, noisy breathing, cough, swelling of the lungs, a large number of dry and often moist rales in the lungs, tachycardia, increased blood pressure, pallor of the skin, cyanosis; respiratory and metabolic acidosis, hypoxemia, often - hypercapnia, general dehydration. Stage II - increasing respiratory failure with the identification of “silent” lung areas during auscultation: respiration in all fields is weakened, and in some areas it is not audible at all due to obstruction of the small bronchi and bronchioles with viscous secretion; dyspnea, cyanosis, tachycardia, respiratory and metabolic acidosis, hypercapnia increase, blood pressure falls III stage (hypoxemic coma, or asphyxia syndrome) - respiratory sounds are not heard in all fields of the lungs, pronounced diffuse cyanosis, adynamia, loss of consciousness, hypoxic convulsions, falling blood pressure . More often the asphyctic syndrome is observed in patients B. children in puberty.

The post-criminal period in children is longer than in adults and lasts from 2–5 days to 2–3 weeks. The state and state of health are improved, scattered dry, sometimes wet rales (more with deep breathing), a rare wet cough are determined, emphysema is reduced: functional tests reveal bronchospasm.

Difficult breathing in a child without pronounced attacks of asphyxiation may not promptly attract the attention of adults, even with obvious shortness of breath, aggravated by physical exertion, the presence of cough (especially at night), dry whistling, and sometimes moist rales in the lungs. Children often adapt to respiratory failure and do not complain, attend day care centers and schools. Such option of an aggravation B. and. may last for several weeks; protracted course is often caused by inflammation in the airways or in the lungs, which can be indicated by low-grade fever, leukocytosis, neutrophilia with a left shift, increased ESR, and the appearance of moist rales in the lungs. If the child had no asthma attacks at all, then this type of manifestation B. a. defined as asthmatic bronchitis. It is often observed at an infectious dependent form B. and. however, it may be in atopic asthma, especially in cases of prolonged contact of the child with the allergen.

The interictal period, or remission of B. and., Is characterized by full restoration of function of breath, its duration is various.

B.'s current and. children may have frequent or rare exacerbations, with concomitant other allergic diseases, with or without complications. With an easy course of attacks rare and short, easily stop. With a moderate course of asthma attacks are observed almost monthly, are removed by complex treatment with antispasmodic and antihistamine drugs. A severe course is characterized by frequent exacerbations, against the background of which an asthmatic condition often develops, the presence of complications, a lag in physical development. Heavy current B a. more often observed in children with burdened heredity, with concomitant allergic dermatitis, with impaired tryptophan metabolism. B. aggravations and. depend on contact with allergens. Thus, when sensitizing to plant pollen, seizures occur during the flowering period of the respective plants. If you are allergic to house dust, pet dander, bird feathers, aquarium fish feed, seizures are more frequent and more difficult at night in the autumn and winter, when the child spends more time in the apartment. In children with infectious B. a. there are more prolonged exacerbations, often accompanied by a bronchopulmonary infection.

Complications B. a. in children with severe asthma, lung atelectasis, subcutaneous or mediastinal emphysema, spontaneous pneumothorax, acute pulmonary heart, hypoxic convulsions can occur. Typical complications of long-lasting B. a. are chronic emphysema of the lungs (persisting after an attack for more than 3 months), pneumosclerosis, chronic pulmonary heart, impaired physical development of the child. With severe B. and. in children receiving glucocorticoids, there is often a lack of adrenal function.

B.'s diagnosis and in children it settles in the same way as in adults. B. and. differentiate with Laryngospasm, as well as with bronchitis, bronchiolitis, trachea and bronchi foreign body, compression of the respiratory tract by a tumor or bronchopulmonary lymph nodes, in young children with bronchopneumonia.

Treatment is based on the same principles as adults. For the purpose of the prevention of attacks of asthma at atopic B. and. patient's contact with the allergen should be interrupted (remove the allergen from the apartment, exclude food allergens, hospitalize the child, etc.), prescribe antihistamines.

For stopping and the prevention of attacks of B. and. use bronchodilator drugs inside or in the form of inhalation. Apply ortsiprenalina sulfate (alupente, astmopent) in the form of inhalation (1-2 breaths) or inside 1/4—1 / 2 tablets, fenoterol (berotok), salbutamol (ventolin), as well as eufillin, antastman, theofedrin, solutan, sometimes adrenaline . Salbutamol and ventolin in metered manual inhalers are prescribed to children up to 7 years old in a single dose of not more than 1 breath, older than 7 years - up to 2 breaths. Antastman and teofedrin for children from 2 to 5 years give 1 / 4-1 / 3 tablets per reception, from 6 to 12 years - 1/2 tablet. Single dose solutan - 1 drop for 1 year of life. If necessary, arrest the moderate attack of B. a. with adrenaline, the latter is administered in the form of a 0.1% solution subcutaneously at the rate of 0.01 mg per 1 kg of the child’s mass in combination with a 5% solution of ephedrine (at the rate of 0.5-0.75 mg per 1 kg of weight). In the absence of effect, the introduction of adrenaline should not be repeated, since usually we are talking about the blockade of bronchial β-adrenergic receptors, to which often leads to the frequent use of inhaled β-adrenomimetics.

Eufillin in case of moderate severity is administered intramuscularly (24% solution) or a 2.4% solution is diluted in 50 ml of isotonic sodium chloride solution to be administered intravenously at the rate of 4-5 mg per 1 kg of child weight (no more than 5-7 mg per 1 kg masses per day). In severe attacks of B. a. in addition to aminophylline, prednisone is administered intravenously at the rate of 2 mg per 1 kg of weight. In the case of asthmatic status, euphyllinum is administered intravenously, up to 15–20 mg per 1 kg of weight per day; Intravenous administration of prednisolone is repeated every 3-4 hours (up to 7-10 mg per 1 kg of weight per day). Protease inhibitors and heparin are also used. In the case of asphyxial syndrome, the patient is transferred to a ventilator, the sputum is washed out of the bronchi through a bronchoscope. Sometimes hemosorption is used. Diphenhydramine and pipolfen can increase the viscosity of sputum, so they are prescribed only to young children who have B. and a. exudation and hypersecretion in the bronchi and sputum are rarely viscous.

In the interictal period, sanitation of chronic infection foci, treatment with inhalations of intratalum or ketotifen (infusion) orally for 3-6 months, as well as specific hyposensitization are carried out, and with polyallergy or allergy not established - treatment with histaglobulin. An important role is played by hardening, therapeutic exercises. Acupuncture is often effective. Sanatorium treatment is shown in local specialized sanatoriums.

Children, sick B. and., Are on a dispensary, supervision at the local pediatrician and the allergist.

The main difference of the prognosis in children is that with light and moderate B. recovery is much more common than in adults (usually in the prepubertal period). Prevention in its principles does not differ from that in adults.

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