Bronchial asthma in concomitant diseases of various organs – features of the clinical course of bronchial asthma in various concurrent diseases. The most common in patients with asthma are allergic rhinitis, allergic rhinosinusopathy, vasomotor rhinitis, nasal and sinus polyposis, arterial hypertension, various endocrine disorders, pathology of the nervous and digestive systems. The presence of arterial hypertension in patients with bronchial asthma is a generally recognized fact. The frequency of the combination of these diseases is increasing. The main factor in increasing systemic blood pressure is central and regional hemodynamic disorders: an increase in peripheral vascular resistance, a decrease in pulse blood supply to the brain, and hemodynamic disturbances in the pulmonary circulation. The increase in blood pressure is promoted by hypoxia and hypercapnia accompanying chronic bronchial obstruction, as well as the influence of vasoactive substances (serotonin, catecholamines and their predecessors). There are two forms of arterial hypertension in bronchial asthma: hypertension (25% of patients), which proceeds benignly and slowly progresses, and symptomatic “pulmonary” (the prevailing form, 75% of patients). In the “pulmonogenic” form, blood pressure rises mainly during severe bronchial obstruction (attack, exacerbation), and in some patients it does not reach the norm and increases with exacerbation (stable phase). Bronchial asthma is often combined with endocrine disorders. A known correlation of asthma symptoms with female genital function. In the puberty period in girls and premenopausal women, the severity of the disease increases. In women suffering from bronchial asthma, premenstrual asthmatic syndrome is often encountered: exacerbation 2-7 days before the onset of menstruation, less often – simultaneously with it; with the onset of menstruation, significant relief comes. Marked fluctuations in bronchial reactivity are not observed. Most patients have ovarian dysfunction. Severe asthma occurs when combined with hyperthyroidism, which significantly disrupts the metabolism of glucocorticosteroids. A particularly severe course of bronchial asthma is observed against the backdrop of Addison’s disease (a rare combination). Sometimes bronchial asthma is combined with myxedema and diabetes mellitus (about 0.1% of cases). Bronchial asthma is accompanied by disorders of the central nervous system of a different nature. In the acute stage, psychotic states with psychomotor agitation, psychoses, and coma are observed. In a chronic course, autonomic dystonia is formed with changes at all levels of the autonomic nervous system. Asthenoneurotic syndrome is manifested by irritability, fatigue, sleep disturbance. Vegetative-vascular dystonia is characterized by a number of signs: palm and foot hyperhidrosis , red and white “dermographism”, tremors, vegetative crises such as sympathoadrenal (sudden shortness of breath with a respiratory rate of 34-38 in 1 mn, fever, tachycardia up to 100-120 in 1 min , rise in blood pressure to 150 / 80-190 / 100 mm Hg. Art., frequent profuse urination, urge to defecate). Crises develop in isolation, mimic an asthmatic attack with a subjective sensation of suffocation, but there is no difficulty in exhaling and wheezing in the lungs. Symptoms of autonomic dystonia occur with the onset of bronchial asthma and become more frequent in parallel with its exacerbations. Autonomic dysfunction is manifested by weakness, dizziness, sweating, fainting and prolongs the period of coughing, asthma attacks, residual symptoms, more rapid progression of the disease and relative resistance to therapy. Concomitant diseases of the digestive system (pancreatic dysfunction, liver, intestinal dysfunction), which are found in a third of patients, especially with prolonged glucocorticosteroid therapy, can have a significant effect on the course of bronchial asthma. Concomitant diseases complicate the course of bronchial asthma, complicate its treatment and need appropriate correction. The treatment of arterial hypertension in bronchial asthma has certain features. “Pulmogenic” arterial hypertension, observed only during asthma attacks (labile phase), can normalize after bronchial obstruction has been eliminated without the use of antihypertensive drugs. In cases of stable arterial hypertension, the combined treatment uses hydralazine, ganglion blockers (arpenal, fubromegan, merpanite, temechin, peitamine), hypothiazide, veroshpiron (has the properties of an aldosterone blocker, corrects electrolyte metabolism disorders) 100-150 mg per day for three weeks . A-blocking adrenergic drugs, in particular pyrroxan, can be effective, calcium antagonists (corinfar, isoptin) are used. Ganglioblockers and anticholinergics can affect the neurogenic components of an attack of bronchial asthma (can be used in combination with bronchodilators: arpenal or fubromegan – 0.05 g three times a day; halidor – 0.1 g three times a day; temehin – 0.001 g three times a day day), which are recommended for mild attacks of a reflex or conditioned reflex nature, with a combination of bronchial asthma with arterial hypertension and pulmonary hypertension. These drugs must be used under the control of blood pressure; they are contraindicated in case of hypotension. For the treatment of patients with a predominance of the neurogenic component in pathogenesis, various variants of novocaine blockades are used (provided novocaine is tolerable), psychotherapy, hypnotic suggestive therapy, electrosleep, reflexology, and physiotherapy. These methods can eliminate the state of fear, conditioned reflex mechanisms of attacks, anxious mood. Treatment of concomitant diabetes is carried out according to the general rules: diet, antidiabetic drugs. Moreover, for the correction of carbohydrate metabolism, it is not recommended to use biguanides, which, due to the increase in anaerobic glycolysis (sugar-lowering mechanism), can aggravate the clinic of the underlying disease. The presence of esophagitis, gastritis, gastric and duodenal ulcers creates difficulties for glucocorticosteroid therapy. In cases of acute gastrointestinal bleeding, it is more advisable to use parenteral glucocorticosteroid drugs, an alternative treatment regimen is preferred. The optimal way to treat bronchial asthma, complicated by diabetes mellitus and peptic ulcer, is the appointment of glucocorticosteroid maintenance inhalation therapy. With hyperthyroidism, there may be a need for increased doses of glucocorticosteroid drugs, since an excess of thyroid hormones significantly increases the speed and changes the metabolic pathways of the latter. Treatment of hyperthyroidism improves the course of bronchial asthma. In cases of concomitant arterial hypertension, angina pectoris, and other cardiovascular diseases, as well as hyperthyroidism, it is necessary to use B-stimulating adrenergic drugs with great care. It is advisable to prescribe enzyme preparations (festal, digestin, panzinorm) for people with impaired digestive function, which reduce the absorption of food allergens and can help reduce shortness of breath, especially in the presence of food allergies. Patients with a positive result of tuberculin tests and a history of tuberculosis during prolonged glucocorticosteroid therapy are prescribed prophylactically tuberculostatic drugs (isoniazid). The use of adrenergic preparations of B-stimulating and methylxanthines in elderly patients is undesirable due to their side effects on the cardiovascular system, especially in coronary atherosclerosis. In addition, the bronchodilating effect of adrenergic drugs decreases with age. When a significant amount of liquid sputum is excreted in patients with bronchial asthma of this age group, anticholinergics are useful, which in some cases are more effective than other bronchodilators. There are recommendations on the use of synthetic androgens for older men suffering from bronchial asthma with a sharp decrease in the androgenic activity of the sex glands (Sustanon-250 – 2 ml intramuscularly with an interval of 14-20 days, course – three to five injections); while remission is achieved faster and the maintenance dose of glucocorticosteroid drugs is reduced. There are indications of the advisability of using antiplatelet agents, in particular dipyridamole (curantyl) – 250,300 mg per day – and acetylsalicylic acid (in the absence of contraindications) – 1.53.0 g per day, especially in elderly patients who have bronchial asthma associated with cardiac pathology -vascular system. In case of microcirculatory disorders and changes in the rheological properties of blood, heparin is used in a dose of 10-20 thousand units per day for 510 days. Concomitant pathology of the upper respiratory tract is being treated.
Diagnosis is based on data from an allergological history, clinic, specific diagnostics, radiological, immunological, and bnochem. and special bronchological and functional studies.
The most characteristic radiological changes in bronchial asthma are emphysema, stiffness of the roots, increased pulmonary pattern, mooring, fusion in the sinuses, and other changes in the pleura. Normal pulmonary pattern is rare. In the presence of an active inflammatory process in the lungs, peribronchial type infiltration predominates; focal and mixed types of infiltration are observed in 89% of patients.
Syndrome of bronchial obstruction during an attack is accompanied by characteristic changes in pulmonary volumes: an increase in OOL and its share in the OEL, as well as a sharp increase in bronchial resistance on exhalation, a decrease in FVC of the MVL and Tiffno index. These disorders are caused by bronchial obstruction (the main cause) and a deterioration in the elastic properties of the lung. Due to the unevenness of alveolar ventilation and violations of the ratio of ventilation and blood flow, ventilation and alveolar respiratory failure develop. The severity of respiratory failure in the interictal period depends on the severity of the disease; in accordance with this, obstructive changes of varying degrees are observed. The chronic course of bronchial asthma is characterized by a complex set of ventilation defects associated with obstruction of the bronchi. An objective measurement of the partial pressures of oxygen and carbon dioxide allows you to judge blood gases and ventilation status. In the acute stage of uncomplicated bronchial asthma, the severity of obstruction is associated with hypoxemia, respiratory alkalosis, a decrease in partial pressure and oxygen transport, and in some patients, respiratory acidosis. These disorders are especially pronounced with asthmatic status. Changes in peripheral blood are not characteristic. During seizures, the number of red blood cells and hemoglobin increases; white blood cell count depends on the activity of inflammation; eosinophilia is noted (bone marrow eosinophilia is more pronounced and constant), lymphocytosis. Leukocytosis and eosinophilia are evaluated with caution after administration of adrenaline and glucocorticosteroid drugs. Very high eosinophilia requires differential diagnosis with allergic bronchopulmonary aspergillosis, parasitic infections, Leffler’s syndrome. ESR and biochem. indicators of inflammation activity depend on the phase of the inflammatory process. Diagnostic value are proteinogram, C-reactive protein, serum glycoproteins, a2-globulinemia, hypergammaglobulinemia.
Eosinophilia is detected in sputum, there may be Kurshman spirals, Charcot-Leiden crystals (may be absent in freshly isolated sputum and appear when it is defended); increased activity of acid phosphatase (ten times higher than in serum), which indicates deep damage to the lysosomal membranes of neutrophils and macrophages. Histological examination reveals non-mucoid and degenerated cell elements, as well as eosinophilic detritus. In bronchial contents (bronchoalveolar lavage) with atopic asthma there is a decrease in the number of macrophages in two – two and a half times, an increase in the number of eosinophils in 5-10, neutrophils – in two to three times. In infectious bronchial asthma, macrophages prevail, there are few eosinophils, there are neutrophils. Bronchoscopy reveals diffuse catarrhal inflammation (in 50% of patients), diffuse catarrhal endobronchitis of the II degree (about 20% of patients), atrophic bronchitis (about a third of patients). Biochem. violations are different. They to a certain extent depend on the form, stage and severity of bronchial asthma and are characterized by changes in the blood levels of adaptive hormones, allergy mediators, proteolytic enzymes and other factors. Changes in cellular and humoral immunity are heterogeneous. In some patients, secondary immunological deficiency is noted; some have a relationship between the degree of immunity disorders and the severity of the disease and there is an improvement as a result of immunocorrective therapy.
Differential diagnosis. Bronchial asthma is differentiated with other allergic lung diseases (allergic bronchopulmonary aspergillosis, allergic exogenous bronchioalveolitis, chronic bronchitis, many bronchospastic syndromes that develop in various pathological conditions). Within the framework of bronchial asthma itself, various forms and variants are diagnosed.
Differential diagnosis of allergic and bacterial inflammation in the bronchopulmonary system in bronchial asthma is difficult. Activation of the bacterial inflammatory process in bronchial asthma is accompanied by an increase in the number of microbes in sputum (the main pathogens are pneumococcus and hemophilic bacillus, there is a significantly higher frequency of detection of opportunistic microorganisms, especially staphylococcus, than with other chronic non-specific lung diseases).
The treatment of bronchial asthma is still difficult. There are four basic rules for the treatment of bronchial asthma, an
individual approach with the determination of the leading factor in the etiology, pathogenesis and clinic of the disease;
elimination of the cause (complete or partial elimination of antigen), non-specific irritants, provoking factors;
the implementation of specific hyposensitization when it is impossible to eliminate the antigen;
conducting complex nonspecific therapy with an unknown etiology and the presence of contraindications for hypersensitivity.
Nonspecific complex therapy consists in the rehabilitation of infectious and inflammatory processes in the bronchopulmonary system (antibacterial agents, bronchial tree sanitation) and foci of infection outside the respiratory tract, the elimination of airway obstruction, the improvement of alveolar ventilation, the effective dilution and evacuation of sputum using hydrating and mucolytic drugs immunocorrecting and desensitizing non-specific therapy, sanatorium and other treatment.
One of the main places is the treatment of bronchial obstruction, which in bronchial asthma has a complex nature. Medicines of various classes contribute to its elimination: bronchodilators (relieve bronchospasm), expectorants (dilute and remove sputum), glucocorticosteroid drugs (eliminate allergic inflammation), antibacterial agents (eliminate bacterial inflammation).
Due to the pronounced allergenic properties of many drugs, especially antibiotics and sulfonamides, as well as the tendency of patients to drug allergies, a careful choice of therapy is necessary in each case. Drug allergy in bronchial asthma is most often manifested by an increase and aggravation of asthma attacks, the formation of asthmatic status. The treatment failure, especially in the absence of activation of the infectious and inflammatory process in the lungs and steroid dependence, indicates the need to review the therapy in terms of the possibility of drug allergy.
Treatment of individual forms and options A. b has featurs.
Mild attacks are stopped by oral administration of theophedrine or ephedrine, as well as by inhalation of adrenergic drugs, especially B2 stimulants. At the same time, distracting means (banks, mustard plasters, hot foot baths) are used. In the absence of effect, ephedrine or adrenaline is administered subcutaneously, and in the case of contraindications to their use, aminophylline is administered intravenously, atropine is subcutaneous. Highly effective B2-stimulants with parenteral administration. Adequate hydration is required, moistened oxygen is used. In severe bronchial asthma, resistance to adrenergic drugs is often observed. In this case, euphyllium is introduced (4 mg per 1 kg of body weight) – slowly intravenously, moistened oxygen is given. With resistance to adrenergic drugs and methylxanthines, parenteral administration of glucocorticosteroid drugs is indicated, especially for patients receiving maintenance doses of these drugs. It is preferable to use hydrocortisone (hemisuccinate, phosphate), since a high plasma concentration is achieved within a short time. In patients not receiving hormones, an infusion of 100-200 mg of hydrocortisone every 6 hours can give a satisfactory result . For steroid-dependent patients, large doses are required, in some cases the effect does not occur until the concentration of glucocorticosteroid drugs in the plasma reaches 1 μg / ml (corresponds to dose of 4 mg per 1 kg of body weight every 2 hours). The response to glucocorticosteroid drugs correlates with a decrease in the number of eosinophils (absolute amount) by 50% or more. Treatment of severe, non-stopping attacks of asthma, passing into asthmatic status, is in the nature of intensive care.
Specific hyposensitization in the treatment of bronchial asthma refers to pathogenetic methods of therapy, is carried out according to general rules in the absence of exacerbation of bronchial asthma and inflammatory processes in the foci of infection after thorough rehabilitation. Most allergist clinicians assess hyposensitization as the primary treatment for atopic bronchial asthma. It is most developed and effective in atopic dust bronchial asthma and pollen etiology. The effectiveness of treatment with food extracts in cases of suspected food allergies has not been confirmed. the number and frequency of allergen injections depend on the severity of sensitization and patient tolerance. The duration of specific desensitization is at least two years, with a significant decrease in symptoms, a break is made, when symptoms return, treatment is resumed. There are a number of reports on the greater effectiveness of inhalation immunotherapy for asthma with dust etiology (carried out according to the same scheme as injection, aerosols are sprayed with AI-1 inhalers), note a long duration of remission, and it is recommended to conduct three courses of local immunotherapy in a row. There are no reliable criteria for determining the duration of treatment: in each case this is determined by the clinical situation. The specific hyposensitization of infectious bronchial asthma is less developed and less effective. The points of view on the effectiveness of bacterial vaccines are different. There is evidence in favor of both auto and hetero vaccines. Significantly more often than with atopic bronchial asthma, exacerbations during hypersensitivity by microbial allergens are described.
Antibacterial therapy is carried out in cases of exacerbation of bronchial asthma caused by an acute infectious and inflammatory process in the respiratory system or activation of a chronic one. Sulfanilamides of prolonged action (sulfapyridazine, sulfamonomethoxin, sulfadimethoxine, sulfalene, septrin, kelfisin – course of 7-10 days) and combined preparations (bactrim, biseptol, merafin, potesepil) are used as antibacterial agents in the treatment of bronchial asthma. Of the sulfa drugs most often cause allergic reactions in patients with bronchial asthma, kelfizin and septrin. In necessary cases, semi-synthetic penicillins and tetracyclines are prescribed (until the results of bacteriological examination of sputum are obtained, in the future, taking into account the sensitivity of microflora to antibiotics). A good effect of the use of erythromycin is noted (for 5-7 days, 1 million -1 million 200 thousand units per day). In bronchial asthma, the etiology of which is associated with a hemophilic bacillus and pathogenic staphylococcus, chloramphenicol (up to 2 million units per day) and tetracycline antibiotics (metacyclin up to 900 thousand units per day) can be used. Nitrofuran drugs are effective for the treatment of staphylococcal inflammatory processes: furazolidone (50 mg is recommended six to eight times a day), furazolin, furagin, soluble furagin (solafur). High activity, especially in cases of combination with candidal infection, is possessed by 5-NOC (nitroxoline), which can be combined with the sodium salt of levorin.
ACT However, antibiotics and other antibacterial agents should be prescribed with convincing evidence of an infectious (bacterial) etiology of the inflammatory process in the lungs, which is especially true for atopic bronchial asthma, since antibiotics are not indicated for most viral infections.
After a course of antibacterial therapy for a sluggish, protracted process, as well as intolerance to antibiotics and sulfonamides, treatment with phytoncides is recommended: garlic juice, onion, lingonberry condensate in the form of inhalation, tincture of ordinary myrtle (20-25 drops three times a day two weeks for 15 -20 minutes before meals). Antibacterial therapy is combined with desensitizing, and if necessary with immunocorrective therapy.
Therapeutic bronchoscopy in the complex treatment of bronchial asthma is positively evaluated by many experts. However, there are opponents of this method. Remediation is urgent and planned. The former are a component of intensive care and are carried out at the II-III stage of asthmatic status. They are based on the segmental lavage of the bronchi using the phenomenon of injection (developed by G.I. Lukomsky and collaborators). The second is carried out with infectious- allergic bronchial asthma with clinical, laboratory and endoscopic signs of exacerbation of purulent or catarrhal-purulent endobronchitis with the failure of other measures. The method is considered effective. There is an opinion about the preferred use of bronchial lavage in bronchial asthma with non-purulent forms of endobronchitis (lavage is performed after reduction of bronchial obstruction, alternates with debridement bronchofibroscopy).
Remediation of bronchi with bronchial asthma can increase bronchospasm, therefore it cannot be recommended as widely as with chronic bronchitis.
Bronchodilators in the treatment of asthma are divided into the following main groups: adrenergic drugs, anticholinergics, methylxanthines. One of the main principles of long-term bronchodilator therapy is the restrained use of p-stimulating adrenergic drugs, which can cause serious complications. A comparative study of the effectiveness of B-stimulants and methylxanthines (aminophylline) showed that the combined use of their low doses and the isolation of each drug in high doses provide similar bronchodilatory effects, but in the first case, side effects are much less pronounced. The use of bronchodilators can be differentiated depending on the partial pressure of oxygen in the blood, which they affect in case of bronchial asthma differently change it, increase it, reduce it. Decrease most often causes aminophylline, less often – stimulants and atrovent, increase – berotek. The reaction of the bronchi to bronchodilators and a shift in the partial pressure of oxygen depend on the severity of exacerbation of bronchial asthma. In bronchial asthma with the participation of the parasympathetic nervous system, increased sensitivity of the bronchi to various inhalation irritants, as well as the presence of concomitant obstructive bronchitis, preparations of the atropine group are recommended. There is evidence of greater effectiveness of the combined use of berotek with atrovent. There are a number of complex ready-made bronchodilators, which are various combinations of the three main groups of bronchodilators with vasodilators (aminophylln complex “Polfa”, one or two tablets three times a day), analgesic (Antastman “Spofa”), expectorant and soothing drugs (asthmatol “ Spofa ”, theophedrine, etc.). Certain principles of the rational use of bronchodilators in bronchial asthma have been developed.
Hydrating and mucolytic drugs in the treatment of bronchial asthma occupy a significant place. Adequate hydration is important – frequent and sufficient intake of fluid (at least 1.5 liters per day), which helps to thin and expectorate sputum. Many clinicians prescribe (subject to tolerance) a 1 – 3% solution of potassium iodide five to six times a day (drink warm water). However, it is contraindicated in persons with intense irritation of the salivary glands, severe acne and generalized maculopapular rash. Side effects when using potassium iodide – increased salivation, urticaria, acne, rhinitis, conjunctivitis, hypothyroidism, may be serum sickness. It is not recommended for acute inflammation in the respiratory system, bronchoremia, tuberculosis in the evolutionary phase. In the absence of effect from the use of potassium iodide and contraindications for its use, bromhexine (512 days), bisolvonum inside or in the form of inhalation is advisable. In cases of concomitant purulent bronchitis with sputum difficult to separate, Nacetylcysteine (used carefully, in combination with bronchodilators, can cause bronchospasm), in the absence of effect for two weeks, further use is useless. Particular care in the treatment of asthma requires the use of aerosols of proteolytic enzymes (chymotrypsin, chymopsin, deoxyribonuclease), which can cause a severe attack and even asthmatic status. As a hydrating and mucolytic drugs, herbal decoctions and infusions are used: elecampane high, angelica officinalis, coltsfoot, tricolor violets, oregano, thyme, marshmallow, which are effective only with frequent use (every 1-2 hours); ready-made medicinal plant forms: mucaltin – dry marshmallow mucus, allantoin (drug from elecampane). Sputum separation is facilitated by exercise therapy, positional drainage, vibration massage.
Abundant discharge of green-brown sputum with “casts” of the bronchi indicates the release of the distal parts of the bronchial tree. During this period, it is advisable to strengthen bronchodilator therapy, since a strong cough is possible, contributing to an increase in bronchospastic reactions.
Nonspecific antiallergic agents in the treatment of bronchial asthma include calcium preparations, heparin, antikinin agents, glyciram, angiulin preparations and native plasma, etimizol, intal, ketotifen, antihistamines, glucocorticosteroid drugs.
Glucocorticosteroid drugs in the treatment of bronchial asthma are most effective. They are absolutely indicated for the treatment of asthmatic status, in which high doses are prescribed at frequent intervals. After the elimination of acute symptoms, the dose is gradually reduced to the previous level or the drug is canceled (if possible in cases of primary use). Sudden cancellation of hormones can cause severe exacerbation of bronchial asthma. Long-term supportive glucocorticosteroid therapy is indicated for severe to moderate bronchial asthma with no effect of complex treatment with non-steroid drugs with a tendency to frequent seizures and asthmatic conditions.
The minimum dose is established in the process of gradually reducing the initial therapeutic dose (usually 25-30 mg in the equivalent of prednisolone). In the future, the dose is temporarily increased with exacerbation of bronchial asthma, the need for surgical interventions, climate change, stressful situations, which make increased demands on adaptive mechanisms. If possible, an alternating hormone regimen is preferred. Long-term hormonal therapy of steroid-dependent patients can be carried out using steroid aerosols, which have advantages due to a mild systemic effect. Dexamethasone and beclamethasone dipropionate (becotide, beclamet), triamcinoloneacetonide are used. The minimum maintenance dose is 400 mcg (two breaths four times a day with prior use of bronchodilators in the form of an aerosol and orally). In moderate cases, the initial dose is 400-1600 mcg.
Injection depot preparations (Kenalog, Valon A-40, fluorocort-40) are preferred if tablets cannot be used, in particular with concomitant gastric ulcer. Long-term glucocorticosteroid therapy is combined with the introduction of anabolic hormones, vitamin C, potassium preparations, and veroshpiron. When the inflammatory process in the lungs is activated, antibiotic therapy is prescribed. In order to reduce the dose of glucocorticosteroid drugs, ethnmizole, glycyram, intal are used.
Immunosuppressants in the treatment of bronchial asthma began to be used in connection with the notion of autoimmune pathology in bronchial asthma. Currently, they are used in a limited way: they are prescribed in certain cases with a very severe, progressive course of bronchial asthma with a pronounced immunopathological component in the absence of the effect of all other treatment methods, including glucocorticosteroid drugs, and pronounced steroid-induced complications. Treatment is carried out only in a hospital. Immunosuppressants should be used very carefully. In recent years, a selective effect of these agents on subpopulations of immunoregulatory cells has been identified, which can lead to irreversible changes in the regulatory link of immunity. Long-term use of immunosuppressants increases the risk of viral and bacterial diseases. A number of experts consider the use of immunosuppressants in bronchial asthma pathogenetically unjustified and note that the long-term results of treatment are significantly worse than the nearest ones. Aminoquinoline drugs (delagil, plaquenil) are sometimes used to treat bronchial asthma: in the first month, take a tablet at night, several months – half a tablet.
Immunocorrective agents for treatment. The feasibility of using immunocorrective agents is justified by the presence of secondary immunological deficiency in bronchial asthma, therefore, when prescribing immunomodulators, the severity of the clinical symptoms of the disease and the state of immunity must be assessed. For the purpose of immunomodulation in bronchial asthma, decaris, diutsifon, sodium nucleinate, transfer factor, thymosin are used. However, these drugs pass the stage of clinical trials, so the indications and treatment regimens need to be studied. There are several treatment regimens for decaris: 100 mg once after eating four days in a row, two days off; 150 mg every other day, course dose of 900 mg or more; 150 mg for three consecutive days, four days off; 150 mg twice a week, course dose of 1200 mg. It is believed that decaris is indicated for patients with asthma with T-cell deficiency and functional deficiency of T lymphocytes. A positive effect was noted with exacerbations of bronchial asthma caused by respiratory diseases, influenza; in patients with moderate course of bronchial asthma, severe T lymphocyte deficiency and insufficient cvpressor activity. There is an opinion that decaris with bronchial asthma favorably affects the course of concomitant infections and does not affect allergy mechanisms. The effect of decaris is observed less frequently and is not sufficient in steroid-dependent patients (perhaps, in this case, other treatment regimens are necessary). In the process of therapy, hemogram and immunity are monitored. In case of infectious bronchial asthma with leukemia lymphopenia, a decrease in the number of B and T lymphocytes and inhibition of their function, it is advisable to use sodium nucleinate: inside 0.8 g per day (three days taken, three days off), course dose 1018 g. Long-term remissions were noted in some sick. There is evidence of a positive effect of the transfer factor with a decrease in the frequency and severity of respiratory infections.
In the treatment of bronchial asthma, uglobulin preparations and native plasma transfusions (100-120 ml once a week, five to six transfusions per course) are used with a favorable effect. Splenin also possesses certain immunocorrective sva, which is thought to act on target cells of an allergic reaction like the anti-allergic drug ketotifen. Along with this, splenin has a desensitizing, detoxifying effect, has a positive effect on liver function, adrenal cortex, and vascular permeability. Assigned to 2.0 ml twice a day intramuscularly for three weeks. Included in complex therapy, including steroid-dependent patients.
Normalization of the functional state of the central nervous system is of great importance in the treatment of bronchial asthma, especially in cases of severe neuropsychiatric disorders. As sedatives, bromides, valerian, motherwort, antihistamines are used. If necessary (stressful situations), Elenium, Seduxen are briefly prescribed. The appointment of “large” tranquilizers to patients with asthma is undesirable.
There are general rules for using sedatives: they cannot be overdosed and prescribed for respiratory failure; courses during a period of situational stress should be short. Treatment of patients with bronchial asthma with a predominance of the neurogenic component in the pathogenesis has features.
Detoxification hemosorption during treatment. There is evidence of the use of this method in infectious-allergic bronchial asthma of moderate and severe course. The best results were obtained in individuals with an initial increase in the level of circulating immune complexes – remission was observed from two months to a year. With a normal content of immune complexes, treatment results are worse.
A general hypoallergenic diet is recommended, as certain types of food can be an additional provoking factor in some patients.
In patients with bronchial asthma with metabolic disorders (obesity), concomitant pathology of the cardiovascular system (stage I-II hypertension, atherosclerosis), gastrointestinal tract, metabolic-dystrophic joint lesions, the choice of choice may be unloading and dietary therapy. A good effect of this method is described for infectious-allergic bronchial asthma (carried out according to the method of Yu. S. Nikolaev). Contraindications: deep degree of exhaustion, active pulmonary tuberculosis, malignant neoplasms, cirrhosis, organic diseases of the central nervous system, pregnancy and lactation, helminth infections.
Physiotherapeutic methods in the treatment of bronchial asthma are used very widely. They are used differentially depending on the characteristics of the course of bronchial asthma and the biological effects of physiotherapy. At the stage of exacerbation, electrophoresis of various drugs (adrenaline, magnesium, bromine, calcium iodine) is carried out, as well as aeroinotherapy. During the period of exacerbation, the use of ultraviolet radiation of certain reflexogenic zones (contraindicated in case of hypersensitivity to ultraviolet rays); ultrasound therapy; high-frequency inductothermy and electromagnetic field of microwave frequency on the projection area of the adrenal glands (stimulates their function). In the presence of a concomitant inflammatory process in the lungs, high-frequency electrotherapy is performed. The positive effect of barotherapy is described under conditions of reduced or increased barometric pressure.
Sanatorium treatment is one of the stages of treatment and prevention of bronchial asthma. Climatotherapy (air and sun baths, sea bathing), which uses various climatic and geographical zones: the North Caucasus (Kislovodsk), the highlands (Bakuriani, Shovi, Elbrus region), and the South-East and South Coast of Crimea, is most widely used. Sanatorium-resort treatment is recommended for pre-asthma in the phase of remission, prolonged exacerbation of the underlying disease (chronic bronchitis or pneumonia), infectious-allergic and atopic bronchial asthma with mild and moderate severity in the phase of remission or mild exacerbation with pulmonary insufficiency no higher than II degree.
Recently, speleotherapy based on salt mines (Solotvino settlement, Transcarpathian region) has been used for the treatment of patients with bronchial asthma, the microclimate of which is characterized by the following parameters: air temperature 23-24 ° C, relative humidity 20-60%, highly dispersed aerosol of sodium chloride 0.5 -5 mg / m3, oxygen content of 20.7% by volume, carbon dioxide – 0.03, atmospheric pressure 750-775 mm Hg. Art., the absence of pathogenic microorganisms and allergens, the noise level is not more than 25 dB. Speleotherapy consists in the systematic stay of the patient in the underground department (session time 2-12 hours depending on the condition of the patients, the average course is 30 days). Indications for speleotherapy: predastma, atopic and infectious bronchial asthma of mild and moderate course, pulmonary insufficiency of I-II degree and pulmonary-cardiac I, stage I bronchial asthma with concomitant chronic bronchitis and pneumonia in the remission phase.
The microclimate of karst caves (Tskhaltubo, Novy Afon) is also used to treat bronchial asthma, the main therapeutic factors of which are a relatively high degree of ionization, highly dispersed aerosol, relatively low temperature and humidity, a high degree of air purity, and the absence of pathogenic microorganisms.
Contraindications to spa treatment: predastma and bronchial asthma in the phase of severe exacerbation; severe bronchial asthma, frequent exacerbations and asthmatic conditions; stage II bronchial asthma; active inflammatory process in the bronchopulmonary system, regardless of the severity of the disease; severe concomitant; diseases. Elderly patients, as well as people with concomitant diseases of the cardiovascular system, are recommended treatment in local sanatoriums. When referring patients to resorts during the transition period (spring, autumn), the contrast of the climate of the place of residence and resort area, as well as the possibility of mechanisms for compensating the cardiovascular system, should be taken into account.
Treatment and prophylactic measures for bronchial asthma include a set of measures: elimination of the harmful effects of nonspecific irritants; timely and adequate treatment of the infectious-inflammatory process in the bronchopulmonary system; improvement of bronchial drainage (timely intake of expectorants, mucolytic drugs, rational use of bronchodilators, postural drainage, vibration massage) and pulmonary ventilation; elimination of hypoxemia; rehabilitation of extrapulmonary foci of chronic infection; restoration of nasal breathing; physiotherapy courses (two to three times a year); Exercise therapy (“respiratory”, “drainage”), hardening procedures; dynamic adequate glucocorticosteroid therapy, corresponding to changes in the patient’s condition and his environment; rational use of antihistamines, sedatives, antihypertensives, adrenergic drugs Rstimulating. Prevention of severe asthma attacks is consistent with asthmatic status.
The possibilities of using adrenergic preparations of a-blocking and antihistamines of H-2-blocking are currently being studied. The use of potential bronchodilators, synthetic prostoglandins of the E1 prostaglandins series and E2 prostaglandins in the form of aerosols, is under study. However, they have a pronounced local irritant effect and can cause a paradoxical increase in airway resistance. It is believed that the systemic administration of prostaglandins in bronchial asthma is not very effective due to their rapid inactivation by PG dehydrogenase in the lungs and other tissues. Studies are being conducted in the direction of the synthesis and testing of drugs that block MPC-A (such substances may be lipoxygenase inhibitors that catalyze the synthesis of leukotrienes from arachidonic acid). It is assumed that these agents will significantly expand the therapeutic possibilities in bronchial asthma. In particular, the Hertrazan adrenaline synergist in vitro blocks the antigen-induced release of MPC-A highly efficiently. With an asthmatic triad, the possibility of desensitization to acetylsalicylic acid is studied, followed by treatment with non-steroidal anti-inflammatory drugs. The indications and possibilities of non-specific immunocorrective therapy are studied, and the effectiveness of various combination drugs (a combination of glucocorticosteroid drugs among themselves, as well as with bronchodilators) is evaluated.
New inhaled glucocorticosteroid preparations, derivatives of flunisolide (pulmicort, bronelide), have been created and are being tested. They have a pronounced anti-inflammatory activity, without causing systemic effects and fungal infections of the mucous membranes. Calcium antagonists attract attention. Good results were obtained with the use of nifedipine derivatives (Corinfar, Adalat), which may become the preferred means for combining bronchial asthma with coronary heart disease, arterial hypertension, but further studies are needed for final conclusions. Combined preparations of bronchodilators are studied, including theophylline, sympathomimetics and atropine-like substances.
Certain prospects are associated with the development of methods of extracorporeal detoxification (hemo-, plasmosorption, plasmapheresis) and specific immunosorption. The prospects of specific immunotherapy are associated with the effect on immunoregulatory cells and other ways.
Bronchospastic syndromes are secondary syndromes that develop in diseases of various organs and systems, in the clinical picture of which bronchospasm is the dominant or one of the main symptoms. Depending on the leading pathogenetic symptom, the following types of bronchospastic syndrome are distinguished: allergic bronchospastic syndromes ; hemodynamic bronchospastic syndromes; syndromes bronchospastic infectious and inflammatory; bronchospastic irritative syndromes; bronchospastic drug syndromes; bronchospastic neurogenic syndromes; obstructive bronchospastic syndromes; bronchospastic syndromes in autoimmune diseases; bronchospastic syndromes with rare diseases; bronchospastic syndromes with tracheobronchial dyskinesias; syndromes bronchospastic endocrine-humoral.
Allergic bronchospastic syndromes – bronchospastic syndromes that develop with respiratory tract diseases, which are based on immunological damage of various types. Allergic bronchospastic syndromes are observed with allergic bronchopulmonary aspergillosis, allergic exogenous bronchioalveolitis, allergic pulmonary vasculitis, pulmonary eosinophilia.
Pulmonary vasculitis is associated with allergic bronchospastic syndrome and Leffler syndrome. In particular, with periarteritis, nodular allergic bronchospastic syndrome can appear in the form of a prolonged stage of a generalized form of the disease: a variant of classical nodular periarteritis can be the Charch-Strauss syndrome, which develops in people with atopy and is characterized by persistent asthma, bronchial, skin vasculitis, and multiple neuritis. Involvement in the process of other organs (kidneys, gastrointestinal tract, central nervous system) is not typical for the disease. Allergic bronchospastic syndromes can accompany various pulmonary eosinophilic diseases, including those caused by parasitic infections: nematodes, trematodes, cystodes, which cause Leffler’s syndrome and asthmatic attacks, the number of eosinophils in the peripheral blood increases significantly with unusually high levels of immunoglobulin E (pulmonary symptoms usually during the passage of parasites through the lungs during the specific phase of their life cycle). Hemodynamic bronchospastic syndromes can develop with drug allergies.
Hemodynamic bronchospastic syndromes – bronchospastic syndromes that form with hemodynamic disorders in the pulmonary circulation.
Hemodynamic bronchospastic syndromes develop with primary pulmonary hypertension, thrombosis and embolism in the pulmonary artery system, venous congestion in the pulmonary circulation (heart defects, cardiosclerosis, anomalies of development and aneurysm of large vessels).
To conduct rational therapy, it is important to distinguish between asthma attacks of bronchial and cardiac, especially in old age, when chronic infectious and inflammatory diseases of the respiratory system are often combined with hypertensive and coronary heart disease, cardiosclerosis, especially since asthma is bronchial infectious-allergic and cardiovascular diseases first occur in the same age group. In a number of cases, mixed cardiac and bronchial asthma have been reported.
Bronchoconstriction stimulating bronchial asthma is sometimes observed in patients with an embolism in the pulmonary artery system. The frequency of embolic asthma has not been established, but may be high in patients with cardiac asthma. In the pathogenesis of acute bronchoconstriction during embolism, stimulation of pulmonary irritant receptors by serotonin released from aggregated platelets is important; the role of other mediators is less defined. With extensive embolism in the blood serum, lactate dehydrogenase is detected, levels of bilirubin and fibrinogen increase; ECG shows signs of a pulmonary heart, and an X-ray examination reveals lung infiltration. In difficult cases, selective angiography is used.
Bronchospastic infectious and inflammatory syndromes that develop during infectious and inflammatory processes in the respiratory tract: chronic bronchitis, chronic pneumonia, bronchiectasis, pulmonary tuberculosis, adenovirus, fungal, parasitic and protozoal infectious diseases.
Most often, there is a need for differential diagnosis of bronchospastic infectious and inflammatory syndromes and bronchial infectious-allergic asthma. The differential diagnosis of bronchospastic infectious and inflammatory syndromes developing in chronic obstructive bronchitis and bronchial asthma is also difficult. Typical signs of this kind of bronchospastic infectious and inflammatory syndromes are the duration of the disease, cough with mucous mucous sputum. A history of prolonged exposure to occupational hazards and smoking. In bronchial asthma, a reversible obstruction of the airways is more often observed, which is determined using a functional test with bronchodilators ( 15–20% improvement in FEV1 is noted ). A set of diagnostic criteria includes physical data, lung radiography, bronchoscopy, bronchoalveolar lavage, microbiological examination of sputum, detection of eosinophilia in peripheral blood and secrets.
Irridative bronchospastic syndromes – bronchospastic syndromes that develop with mechanical, physical, chemical. and thermal influences (dust, powder, acid, alkali, etc.).
Medicinal bronchospastic syndromes – bronchospastic syndromes that develop due to the main pharmacological effect of the corresponding drugs.
Medicinal bronchospastic syndromes can form with the use of medications that block adrenergic B receptors, especially with lung pathology; monoamine oxidase inhibitors, rauwolfia preparations, etc. Bronchospasm in these cases is not a consequence of allergic reactions, but is due to the pharmacological properties of certain drugs.
Neurogenic bronchospastic syndromes – bronchospastic syndromes that develop with disorders of the central and autonomic nervous systems of a functional nature. Neurogenic bronchospastic syndromes occur with hysteria, irritations (reflex, toxic, compression) of the vagus nerve. Along with neurogenic bronchospastic syndromes, there are states of suffocation that do not have an organic basis: hyperventilation da Costa syndrome, autonomic neurotic dysregulation of respiration, “neurotic asthma”. The state of suffocation is also accompanied by laryngospasm, while wheezing in the lungs is absent. A history of “neurotic asthma” is the impact of psychotraumatic factors, a pronounced tendency to neurotic (especially hysterical) reactions, daily and often seasonal fluctuations in the affective state. The disease begins most often between the ages of 15-25 and 35-45 years. Dyspnea in neurogenic bronchospastic syndromes is associated with paroxysmal hyperventilation, characterized by respiratory arrhythmia with periodic deep breaths and a subsequent short-term breath-holding. Cyanosis and bronchospasm in patients are absent, wheezing in the lungs is not heard; functional systolic murmur at the apex of the heart is possible; sputum does not stand out. Signs of cardiopulmonary failure do not appear even with a long course of neurogenic bronchospastic syndromes. Blood saturation with oxygen is normal, hypocapnia, compensated respiratory alkalosis are noted (in some patients – in combination with compensated metabolic acidosis). With neurogenic bronchospastic syndromes, tranquilizers, antidepressants, antipsychotics, psychotherapy are effective.
Obstructive bronchospastic syndromes – bronchospastic syndromes accompanying bronchial occlusion diseases.
Obstructive bronchospastic syndromes develop in the presence of malignant tumors of the trachea, bronchi and lungs, foreign bodies in the bronchi, broncholithiasis, cystic fibrosis, mediastinal formations: cysts, teratomas, angiomas, thymomas. They are caused either by endobronchial obstruction (bronchogenic carcinoma, foreign bodies, endobronchial tuberculosis, bronchial
adenoma, allergic bronchopulmonary aspergillosis), or extrabronchial compression (enlargement of radical lymph nodes in sarcoidosis, lymphoma, tuberculous lymphadeniosis, various;
In the presence of foreign bodies in the bronchi, the symptoms of obstructive bronchospastic syndromes can be different and depend on the type of object, its location and the duration of the bronchi. Foreign bodies can cause bilateral bronchospasm, however, unilateral, appearing or intensifying in the supine position is more typical: inspiratory and expiratory shortness of breath is characteristic. In the case of an undeleted foreign body, obstruction may progress due to increased local edema and inflammation, and obstructive emphysema, atelectasis, or lung abscess may develop depending on the nature of the foreign material. Plant foreign bodies (particularly nuts) are particularly prone to cause severe tracheobronchitis and pneumonia. The diagnosis of Obstructive Bronchospastic Syndrome is easily diagnosed with radiopaque foreign bodies. However, most foreign bodies are not radiopaque; in these cases, special studies are required. Only 2-4% of foreign bodies clears their throat spontaneously, so the main treatment method is to remove them using direct laryngi or bronchoscopy. For the diagnosis of obstructive bronchospastic syndromes using a range of methods, special radiographic study on inhalation and exhalation, tomography, bronchoscopy, bronchial biopsy.
Bronchospastic syndromes in autoimmune diseases – bronchospastic syndromes associated with lung lesions in collagen diseases (dermatomyositis, rheumatoid arthritis, systemic scleroderma, periarteritis nodosa).
Bronchospastic syndromes with rare diseases Bronchospastic syndromes that develop with rare diseases of various organs with a variety of pathogenesis: systemic mastocytosis, A1 antitrypsin deficiency, Goodpasture syndrome, pulmonary alveolar fibrosis, sarcoidosis, pulmonary fibrosis, idiopathic pulmonary fibrosis, mydrolinosis, pulmonary fibrosis, and pulmonary fibrosis; manifestations in combination with skin lesions and high eosinophilia), certain types of pat ogy gastrointestinal system (foreign bodies, hernia or stenosis of the esophagus, esophageal reflux).
Severe emphysema in the lower parts of the lungs in adolescents suggests a deficiency of a1-antitrypsin. Intensive discharge of mucopurulent sputum in a patient younger than 25 years of age requires examination for the presence of cystic fibrosis.
In some patients with systemic mastocytosis, bronchospastic syndrome can simulate bronchial asthma. In contrast to asthma, with this type of syndrome, a pronounced symptomatic effect of antihistamines is observed. The most reliable method of confirming the diagnosis is a skin biopsy.
Bronchospastic syndromes with tracheobronchial dyskinesias – bronchospastic syndromes that form with abnormalities in the development of the trachea and bronchi.
Bronchospastic syndromes in tracheobronchial dyskinesias can simulate bronchial asthma. These include: tracheobronchomegaly (Mounier-Kuhn syndrome); tracheobronchomalacia; Williams-Campbell syndrome; bronchioloectatic emphysema.
Bronchioloectatic emphysema affects the peripheral parts of the bronchial tree and is associated with a defect in elastic fibers (the lesion is usually diffuse, bilateral). It occurs at any age, is manifested by symptoms of chronic obstructive emphysema, stubborn cough, wheezing, constant dry and mixed wet rales, frequent pneumonia, severe respiratory failure; spontaneous pneumothorax is possible. The disease can occur with asthma attacks, sometimes it becomes asthmatic. Patients develop rapidly pulmonary heart. Diagnostics – radiological (bronchography). Williams-Cambell syndrome is characterized by a deficiency of cartilage rings in the wall of the bronchi from III to VI-VIII. It is usually detected in children of early and primary school age. This syndrome may be erroneously interpreted as bronchial asthma. It begins after respiratory diseases, repeated infections provoke its exacerbation. In patients, obstruction of the small bronchi progresses, pulmonary emphysema develops, often segmented or lobar atelectasis. The course of the syndrome is chronic, with frequent exacerbations; pulmonary heart is formed. Sick children lag behind in growth and development; they have a barrel-shaped chest, a symptom of “drumsticks”, shortness of breath with minimal load; during auscultation, constant or periodic dry rales are heard. The diagnosis is established using x-ray examination. Tracheobronchomalacia is characterized by excessive softness of the cartilage of the trachea and large bronchi, is manifested by symptoms of stenosis of the trachea and main bronchi (stridor, “sawing breathing”, “barking” cough, asthma attacks that cannot be stopped by bronchodilators), obstructive type of ventilation disorders is observed. Diagnosed with x-ray and bronchoscopy. Tracheobronchomegaly is most often found in men (the ratio between sick men and women is 6: 1), is characterized by a pronounced expansion of the trachea and main bronchi, combined with chronic respiratory infections. Tracheobronchomegaly is characterized by a long history of pulmonary disease, frequent exacerbations of the inflammatory process with a loud, vibrating cough of a specific timbre (“goat bleating”), hoarseness, profuse purulent sputum, expiratory dyspnea. Attacks of coughing and suffocation can occur with a change in body position. The course is stubborn, difficult to treat, the condition worsens all the time, patients die from infectious complications and respiratory failure. The diagnosis is made using tomoy bronchography. The function of external respiration is characterized by the obstructive type of ventilation disorders. Tracheobronchial dyskinesia is detected (the forced expiration curve has a stepwise character).
Endocrine-humoral bronchospastic syndromes are bronchospastic syndromes that develop with endocrine disorders due to the release of biologically active substances with bronchoconstrictive action or other endocrine-humoral mechanisms.
Endocrine-humoral bronchospastic syndromes occur with carcinoid syndrome, hypothalamic syndrome and hypoparathyroidism. They are detected in approximately 20% of patients with carcinoid syndrome, in 7% of cases there is a primary bronchial carcinoid.
The main etiological factor is cigarette smoking compared to pipe and cigar smoking. It should be noted that smoking cessation to a lesser extent than with lung cancer, affects the reduction in mortality from COPD. Using spirography, the presence of small bronchial obstruction in young smokers can be demonstrated even in the absence of any clinical symptoms. Recently, much attention has been paid to the effects of passive inhalation of tobacco smoke. It was shown that wives and children of smokers are much more likely to experience symptoms of lung damage, in particular cough and dry rales, than in non-smoking families.
Smoking leads to the development of chronic inflammation of the respiratory tract and hypertrophy of the glands of the mucous membrane, characteristic of chronic bronchitis. Smokers have an increased number of neutrophils in the bronchoalveolar washout, possibly due to the allocation of chemotactic factors by alveolar macrophages and epithelial cells. Neutrophils and, to a lesser extent, alveolar macrophages secrete elastase and other proteolytic enzymes, myeloperoxidase and oxidants. Proteinases destroy the elastic tissue of the lungs, while myeloperoxidase and oxidants damage the lung parenchyma cells and inactivate proteinase inhibitors. Proteins formed during the destruction of collagen, elastin and other components of the interstitium of the lungs, in turn, attract new neutrophils and support the course of chronic inflammation. In addition, inhalation of tobacco smoke inhibits elastin biosynthesis. Thus, smoking causes an imbalance between proteolytic enzymes and their inhibitors, which, apparently, is the main reason for the development of emphysema in smokers. An important role in the etiology of COPD is played by environmental pollution and various occupational factors. The degree of air pollution is especially high in industrial densely populated cities, especially with the formation of sedentary air masses. In this case, a significant increase in the number of exacerbations of COPD can be observed. Air mainly pollutes SO2 and ozone, resulting from incomplete combustion of combustible substances and exposure to UV radiation with the release of oxidants. Some harmful substances (nitric oxide, carbon monoxide), irritating to the respiratory tract, are formed in apartments when using gas stoves. Irritation of the bronchial mucosa and hypersecretion of mucus is caused by many organic (cotton, grain, etc.) and inorganic (cement, coal, cadmium, etc.) dusts that a person comes into contact with during production activities. Occupational dust bronchitis can occur alone or in combination with other occupational diseases, in particular pneumoconiosis. Especially severe consequences are observed when toxic substances (toxic bronchitis) are exposed to the bronchi – phthalic anhydrite, ozone, phosgene, etc. In patients with chronic bronchitis, bronchopulmonary infections are much more common than in healthy individuals, in which the phenomena of airway obstruction increase due to accumulation viscous sputum, swelling and infiltration of the bronchial mucosa. In patients with pulmonary emphysema, any bronchopulmonary infection can be the cause of death as a result of acute respiratory failure. During bacteriological examination of sputum in patients with chronic bronchitis, various types of bacteria and viruses can be detected. Hereditary factors have a greater effect on the development of emphysema than chronic bronchitis. However, in recent years, the possibility of a genetic predisposition to chronic bronchitis in twins has been shown, regardless of bad habits and the degree of air pollution. The specific genetic transmission of such a predisposition is still unknown. In contrast to chronic bronchitis, acute bronchitis (tracheobronchitis, bronchiolitis) most often develops due to viral (influenza, parainfluenza, respiratory syncytial viruses), bacterial (pneumococcus, Pfeiffer’s stick), mycoplasma infection, but also under the influence of chemical (chlorine vapor , nitrogen oxides) and physical (hot air) factors. The main symptoms of acute bronchitis is characterized by enough – paroxysmal dry unproductive cough, is replaced by the painful emergence of a small amount of sputum mucous or muco-purulent character. Body temperature rarely reaches febrile numbers. Symptoms of bronchitis disappear on the 4th-7th day, although a slight cough may persist for 2 weeks. A prolonged course of bronchitis is observed with bacterial superinfection, when antibiotics (ampicillin, erythromycin) are required, as well as in smokers. Smoking, impaired immunological reactivity, adverse environmental factors contribute to the transition of the disease into a chronic form.
Chronic bronchitis is characterized by cough with sputum for at least 3 months a year for more than 2 years. Hypersecretion of mucus is considered to be the cause of the cough, the earliest sign of the disease. The secretion of mucus in the bronchial tree occurs in healthy people, however, its quantity is not enough for sputum formation. In addition, the composition of the mucous secretion is different from normal. Hypersecretion of mucus begins in the large bronchi and may not be accompanied by bronchial obstruction. In the presence of bronchopulmonary infection, sputum becomes mucopurulent or purulent. Depending on the nature of sputum, catarrhal and purulent bronchitis is secreted. Sometimes when sowing sputum, bacteria growth may be observed, despite the absence of pus in secret. Morphologically, in large bronchi, hypertrophy of the glands in the submucosa is detected. As chronic bronchitis persists and progresses, the process extends to smaller bronchi, in which goblet cell hyperplasia, formation of mucous plugs, edema and inflammatory infiltration of the mucous and submucous layers, an increase in smooth muscle cells, and peribronchial fibrosis are observed. The listed structural changes are accompanied by a narrowing of the lumen of the bronchioles and the development of bronchial obstruction. Chronic bronchitis, proceeding with a violation of bronchial obstruction, is often called obstructive. In the early stages of chronic bronchitis, obstruction is partially reversible due to a possible reduction in edema and inflammatory infiltration of the bronchial wall and improved sputum discharge. However, over time, its degree of reversibility decreases as a result of increased fibrosis and other irreversible changes. In some patients with chronic bronchitis, bronchospasm plays a role in the development of transient airway obstruction, which is usually observed against irritation of the respiratory tract and bronchopulmonary infections, chronic bronchitis with a bronchospastic component or chronic asthmatic bronchitis, which is difficult to differentiate from bronchial asthma. In contrast to bronchial asthma, the main symptom of chronic asthmatic bronchitis is a long-term productive cough, asthma attacks join much later. In bronchial asthma, reverse kartinia is observed
Emphysema is characterized by stretching of air spaces distal to the terminal bronchiole. There are two main types of emphysema – centroacinar, in which respiratory bronchioles and alveolar passages in the center of the acinus are affected, and panacinar with the defeat of the entire acinus. Centroacinar emphysema, which is not accompanied by impaired respiratory function, is often detected by autopsy of patients older than 40-50 years, who during life had no clinical and radiological signs of lung damage. Sites of centroacinar emphysema are more often found in men in the upper lobes of the lungs. Signs of limited panacinar emphysema are found in half of people over the age of 70 years. Emphysema (predominantly panacinar) is of clinical importance, accompanied by obstruction of the airways as a result of a decrease in the elastic properties of the acinus and the decline of respiratory bronchioles on exhalation. With common emphysema, the respiratory surface is significantly reduced and ventilation-perfusion disorders develop.
Over a long period of time, the development of pulmonary emphysema was explained by mechanical factors, for example, pulmonary emphysema in musicians playing wind instruments. In 1963, COPD was found to be associated with a deficiency of si-antitrypsin and a model of emphysema was introduced in an animal experiment by introducing proteolytic enzymes from plants into the lungs. These observations have shown that the cause of emphysema can be an imbalance between proteinases and their inhibitors. An increase in the activity of proteolytic enzymes as a result of their enhanced isolation or deficiency of inhibitors is accompanied by the destruction of the structural proteins of the acinus and the violation of the elastic properties of the lung tissue. It is known that in a healthy person, neutrophils and alveolar macrophages in the lungs secrete proteolytic enzymes (primarily elastase) in sufficient quantities for the development of emphysema, but this is prevented by their inhibitors circulating in the blood. The highest level of si-proteinase inhibitor, or ai-antitrypsin (AT), which can be found in bronchoalveolar washout and other tissue fluids is highest in the blood. Glycoprotein AT is synthesized in the liver. It is more correct to call it an ai-proteinase inhibitor, since it has an effect not only on trypsin, but also on other enzymes. There are more than 80 phenotypes of AT, the synthesis of which is encoded by genes located on the 14th chromosome. In 90% of people, the M-phenotype AT (genotype MM) is detected. In individuals with the AT Z-phenotype (ZZ genotype), as a result of the replacement of glutamic acid in the amino acid chain with lysine, AT accumulates in the endoplasmic reticulum of hepatocytes and is not secreted into the blood. Changes in AT metabolism increase the risk of developing not only pulmonary emphysema, but also liver diseases. In particular, cirrhosis of the liver is observed in 10-20% of patients with Z-phenotype AT over the age of 50 years. Various complex and inaccessible methods are used to determine the level of AT in the blood and its phenotype, however, AT deficiency can also be suspected during electrophoresis of blood serum proteins (the absence of a curve peak in the region of si-globulin).
Chronic bronchitis and pulmonary emphysema develop in parallel and almost always to one degree or another accompany each other, especially since COPD patients often consult a doctor during the advanced stage of the disease, when it is extremely difficult to distinguish between chronic bronchitis and pulmonary emphysema. In this regard, it is more correct to talk about the predominance of emphysema or chronic bronchitis. Accordingly, two clinical types of COPD are distinguished: emphysema and bronchitis.
Patients suffering mainly from pulmonary emphysema have complained of shortness of breath for many years. The cough is slight and is accompanied by the release of only a small amount of sputum. Bronchopulmonary infection rarely joins, but can lead to death as a result of the development of ONE. The appearance of patients is characteristic – thin asthenics with a barrel-shaped chest, which are often called “pink puffs”, given the presence of severe shortness of breath with difficulty wheezing, and the absence of cyanosis. Auxiliary muscles are actively involved in breathing. Such patients usually breathe through closed lips, which prevents the bronchioles from falling down at the end of exhalation due to increased intrabronchial pressure. On examination, signs of severe emphysema are seen: a barrel-shaped chest, weakened voice trembling, boxed percussion sound, lowering of the lower borders of the lungs and decrease in excursion of their lower edge, weakening of vesicular respiration. At the end of the exhalation, dry wheezing can be heard. The boundaries of the relative dullness of the heart are determined with difficulty or not at all. Heart sounds are muffled. Patients are characterized by tympanic fingers, nails of Hippocrates. When examining the function of external respiration, an increase in OEL due to the residual volume is observed, while the VC decreases. FEV1 and diffusion capacity of the lungs are also sharply reduced. Due to rapid breathing, the values of PaCO2 and PaCO2 are not significantly changed. Patients with pulmonary emphysema sometimes have no objective symptoms and radiological changes. Thus, changes in radiographs appear only with panacinar emphysema, involving at least 2/3 of the lung. In severe disseminated pulmonary emphysema, radiographs show an increase in the airiness of the lung tissue, bullous changes, diaphragm prolapse, vertical position of the heart.
The main symptom is a long-term cough with sputum separation. In the initial period of the disease, exacerbations are observed in the cold season and are characterized by an increase in cough and an increase in the amount of sputum. In the presence of bronchopulmonary infection, patients develop fever or subfebrile condition, sputum becomes mucopurulent or purulent, impaired bronchial obstruction due to edema and inflammatory infiltration of the bronchial wall, bronchospasm, and accumulation of sputum with the formation of mucous plugs. When a blood test is observed leukocytosis and an increase in ESR. Over time, the cough becomes almost constant, episodes of bronchopulmonary infection become more frequent, shortness of breath joins. Exacerbations of the disease are more severe and longer. Unlike pulmonary emphysema, in which any episode of bronchopulmonary infection can be fatal, with exacerbation of chronic bronchitis, antibiotic therapy allows, as a rule, to achieve a rapid improvement in the patient’s condition. At the same time, the general condition improves, body temperature normalizes, the amount of sputum decreases, which gradually becomes mucous, dry wheezing and other signs of bronchial obstruction disappear. Another feature of chronic bronchitis that distinguishes it from emphysema is the rapid development of pulmonary hypertension, the severity of which increases with physical exertion. The cause of increased pressure in the pulmonary artery is considered to be a spasm of the pulmonary vessels in response to hypoxia, a violation of the rheological properties of blood against the background of secondary erythrocytosis. Long-term pressure overload of the right ventricle leads to the development of a pulmonary heart, decompensation of which is usually observed during exacerbations of chronic bronchitis as a result of an increase in the degree of airway obstruction and hypoxemia. In patients with a predominance of chronic bronchitis, body weight is increased, pronounced edematous syndrome and cyanosis are noted, in connection with which they are called “blue edema”. At rest, the respiratory rate is not significantly increased, auxiliary muscles in the act of breathing are clearly not involved. On examination, signs of severe emphysema are absent. Percussion sound is clear or slightly dull. Vesicular or hard breathing, exhalation is elongated. Scattered dry rales of various caliber are heard, in the lower parts of the lungs – inaudible moist small-bubbling rales that disappear after coughing and sputum discharge. The right border of the relative dullness of the heart is shifted. Accent II tone over the pulmonary artery. With decompensation of the pulmonary heart, in addition to edema, there is an increase in the liver, expansion of the jugular veins, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium).
When radiography, the transparency of the lungs can be reduced, the pulmonary pattern is enhanced. As pulmonary hypertension increases, the shadow of the heart increases, and pulmonary arteries expand. On the ECG , signs of hypertrophy of the right atrium and ventricle are detected (an increase in the amplitude of tooth I in lead III and AVF, wave R in leads V1-2, the appearance of tooth S in leads K5-6, conduction disturbances in the right leg of the atrioventricular bundle). An electrocardiogram is a relatively insensitive method for diagnosing a pulmonary heart and in most cases does not reveal the initial hypertrophy of the right ventricle. To determine the wall thickness of the right ventricle and the size of its cavity during diastole in patients with COPD, echocardiography is increasingly being used. Signs of pulmonary hypertension during echocardiography are considered to be hypertrophy of the wall of the right ventricle (more than 5 mm), an increase in the amplitude of its movement, dilatation of the right ventricle (more than 25 mm with an increase in the ratio of the sizes of the right and left ventricles over 0.5). There are other methods for indirectly assessing pulmonary pressure, in particular rheography under conditions of a Valsalva test.
Unlike pulmonary emphysema, chronic obstructive pulmonary hypertension does not change significantly; VC and diffusion capacity are close to normal or moderately reduced. FEV1 and expiratory flow rate are sharply reduced. Ventilatron-perfusion disturbances in the absence of an increase in MOD lead to a decrease in PaO2, and an increase in PaCO2. Hypoxemia stimulates erythropoiesis and leads to secondary erythrocytosis. The main complication is ARF, due to an increase in the volume and (or) viscosity of sputum against a background of bronchopulmonary infection. In addition, ONE can cause pneumonia, left ventricular failure, pulmonary thromboembolism, the diagnosis of which is very difficult. Symptoms of menacing ONE are increasing shortness of breath, insomnia, agitation. Often, such patients are prescribed sedatives, which can contribute to the development of respiratory failure. Reliable criteria for the diagnosis of ODN in patients with COPD are considered to be a rapid decrease in RaO2 by 10-15 mm RT. Art. and pH below 7.30. A change in the latter indicator reflects the development of metabolic acidosis against the background of hypercapnia.