Bronchial asthma. Clinical picture of bronchial asthma Bronchial asthma classification clinical picture
Clinical presentation and complications
Most often, attacks disturb patients at night, especially in severe forms of the disease. Sometimes they last all night. In cases moderate attacks are observed in the morning or in the morning, when the patient gets out of bed. At the center of the clinical picture of bronchial asthma is an asthma attack. The patient tries, if possible, to maintain a state of rest, avoids unnecessary movements. He usually assumes a high sitting position in bed or sits in a chair with his elbows or palms extended forward; thus fixes the shoulder girdle and is able to bring all the auxiliary muscles into action. Consciousness is preserved. Difficulty breathing in some patients is accompanied by a feeling of excruciating pressure and tightness in the chest, sharp pains in the epigastric region or in the right hypochondrium. Sometimes patients complain of itchy skin, a burning sensation throughout the body, appearing shortly before the attack and continuing to bother them during the attack. Exhalation is most often difficult. Already at the beginning of the attack, breathing becomes noisy, buzzing and sibilant, audible from a distance, sometimes even in the next room. Pure breaths in most cases are reduced (up to 10 or less per minute). At the height of the attack, due to increased tension during breathing, perspiration increases, the patient's entire body becomes covered with perspiration. In these cases, he often complains of chills. The temperature during seizures in adult patients remains normal or subnormal, only in rare cases there is an increase in temperature. The pause between exhalation and inhalation disappears. The rib cage is in a deep inspiratory position, the diaphragm is low, breathing occurs mainly due to the participation of the intercostal muscles. The abdominal muscles are tense. The auxiliary muscles are also tense - scalene, sternocleidomastoid and pectoral muscles. It is characteristic that the inspiratory muscles are in a state of increased tone and even during exhalation they do not completely relax. At the beginning of the attack, the cough is short and painful. Cough is more pronounced in the presence of emphysema and chronic bronchitis. At the first attacks, if they did not appear against the background of previous bronchitis, the cough at the beginning of the attack is mild and may even be absent. At the height of the attack, coughing does not lead to expectoration due to thickening of sputum and bronchospasm. After the attack has passed through the culmination point, the cough intensifies, and a small amount of viscous mucous sputum begins to separate. As the end of the attack approaches, the amount of sputum increases, the latter becomes more liquid, leaves more easily, and the symptoms of suffocation decrease. The attack can last from a few minutes to several days. After an attack, coughing up phlegm may last for several hours. Usually the patient falls asleep soon and wakes up in a satisfactory state.
In some cases, the attack is preceded by prodromal phenomena. Some patients feel the approach of an attack due to the onset of not pronounced shortness of breath, "stuffing" of the nose and profuse mucus from it, tickling in the nose, discomfort in the throat, etc. Among the precursors that remain but the time of the attack, a number of authors point to itching of the skin. In some patients, bronchial asthma attacks are accompanied by stool retention. In cases where bronchial asthma is caused by the influence of a nutritive allergen, dyspeptic symptoms (nausea, vomiting) are pronounced, and the attack is accompanied by itching, urticaria, swelling of the lips, tongue. Before and during an attack, a number of phenomena from the nervous system are observed. Sometimes they portend an attack of sleepiness, yawning, lethargy.
When percussion, a boxed percussion sound is found throughout the pulmonary field, especially pronounced in the lower parts of the chest; the lower boundaries of the lungs are omitted. The dullness of the heart disappears. At the height of the attack, auscultation almost does not catch respiratory sounds, which are weakened in themselves and, moreover, are still drowned out by sonorous wheezing. At the beginning of the attack, wheezing is heard both during inhalation and exhalation. Later, wheezing predominates mainly during exhalation. Dry rales are usually heard at the height of the attack; only at the end of the attack moist rales appear, which become sonorous and are sometimes heard for a day or longer than the attack.
In some patients, single attacks are repeated many years later. Sometimes the first attack is the last at the same time, never repeating itself in the patient's entire subsequent life. However, for the most part, attacks are repeated more and more often, and their intensity also increases. The frequency of seizures depends on a number of factors. In cases where bronchial asthma is caused by a specific sensitivity to a particular allergen, attacks can be very frequent or even continuous, if contact with the allergen is constant or occurs very often. If at the beginning of the disease the patient gets rid of contact with the allergen, a complete cure can occur. Such cases can be observed in the so-called professional bronchial asthma, if the patient stops working in this profession.
In cases where asthma attacks are superimposed on acute respiratory tract infections, a correlation is established between the clinical picture and the main factor. Following a runny nose or bronchitis lasting several days, an asthma attack occurs. Most often, the op begins at night, repeats for several days. Shortness of breath may be continuous or appear only at night. The number of attacks during the year is determined by the frequency of exacerbations and the nature of the respiratory tract disease. More often attacks disturb patients in the cold season and less in summer. In cases where bronchial asthma develops against the background of a chronic respiratory tract infection (eg, bronchitis), attacks can be intense from the very beginning and often recur. Many of these patients endure the pre-paroxysmal stages of bronchial asthma for a number of years without resorting to special treatment, attributing all these phenomena to "bronchitis" or "colds". The course of bronchial asthma in these cases is so severe and continuous that from the very beginning the disease becomes chronic.
The variety and multiplicity of factors that play a role in the course of bronchial asthma determine the individual clinical picture in each individual case. With the loss of sensitivity to some substances and its appearance to other allergens, the nature and frequency of attacks may change. Frequent repeated seizures lead to the development of so groove. habitual asthma. Attacks of bronchial asthma, initially based on a specific increased sensitivity to some allergens, in the future, they may appear under the influence of cold wind, smoking, smells, physical exertion, coughing, strong laughter, a heavy lunch or mental influences. At this stage, each patient has individual characteristics of the course, even if there is a primary factor of the disease common to all such patients.
The most common complications of bronchial asthma include emphysema and chronic bronchitis. Against the background of pneumosclerosis, emphysema is found in patients with bronchial asthma in 30 - 60% of cases: with a more or less prolonged course of the disease, emphysema, as a rule, joins with asthma, which is further complicated by cor pulmonale.
Repeated acute transient expansion of the lungs during an attack of bronchial asthma over time entails a loss of elasticity of the lung tissue and the formation of obstructive emphysema, which is facilitated by the often developing chronic bronchitis with blockage of mucus of small and medium bronchi. Individual characteristics play an important role in each case.
In some cases, asthma and bronchitis have a single basis in the form of an allergic condition of the mucous membrane of the bronchi and upper respiratory tract. In a patient with asthma, with a layer of secondary infection, usually normal temperature may rise. Infectious bronchitis most often joins asthma in the autumn and winter.
The sputum released at the end of an attack of bronchial asthma in an amount of up to 100 ml is a viscous viscous glassy mucus, odorless, slightly alkaline or neutral. When smearing sputum with a thin layer on a black background, you can see mucous plugs in the drink with the naked eye, and through a magnifying glass, Kurshman's spirals, which are casts of mucus formed in the small and medium bronchi spasmodically contracted during a severe attack. They can be seen more clearly with microscopy, along with eosinophils and Charcot-Leiden crystals. Charcot-Leiden crystals are formed as a result of the breakdown of eosinophils and therefore are found in greater quantities not in fresh, but in sputum that has stood for 12 hours.
The greatest diagnostic value is the presence of eosinophils in the sputum, which can be observed only in scanty amounts in other patients. The presence of simultaneous eosinophilia in the blood and punctate of the sternum indicates their bone marrow origin.
The nature and amount of sputum can vary, and the latter can be excreted in large quantities; becomes purulent or mucopurulent when a secondary infection (bronchitis, pneumonia) is attached, pneumosclerosis with bronchiectasis, etc.
The most characteristic change in bronchial asthma in the blood during the period of attacks is eosinophilia, due to the allergic nature of the disease.
The absence of eosinophilia during attacks in patients with bronchial asthma with the simultaneous appearance of neutrophilic leukocytosis is most often due to the complication of secondary infection with the most frequent localization of the process in the lungs or in the upper respiratory tract, or focal infection of another localization.
The occurrence and course of bronchial asthma is influenced by climate and meteorological factors.
Stay at an altitude of 1000-1200 m above sea level has a beneficial effect on most patients. Of great importance is the indirect influence of climate as a factor determining the nature of flora and fauna, the development of certain branches of industry and agriculture associated with the presence of allergens in the working environment, as well as dietary habits associated with climatic conditions, etc. Atmospheric phenomena also affect the course of bronchial asthma. Studies by Cruz-Aunon have shown that low cloudiness, cyclones, and the movement of fronts of large air masses cause an increase in the frequency of attacks of bronchial asthma in Spain, in general, more than twice as compared to their number in calm weather. Weather can also have an indirect effect by increasing or decreasing the circulation of allergens in the air. So, plant, animal, indoor allergens in dry weather are found in greater quantities than in rainy ones.
Along with these patterns, one can often observe such paradoxical reactions to meteorological factors that one has to talk about the individual characteristics of the reaction of each patient with bronchial asthma.
The diagnosis of bronchial asthma is usually not difficult, because clinical picture very typical. However, in some cases, the differential diagnosis between bronchial asthma as a nosological unit and symptomatic asthma, in the pathogenesis of which bronchospasm can also play a role, is difficult. Another S.P. Botkin drew attention to the component of respiratory dyspnea caused by bronchospasm in patients with cardiac asthma. Bronchospasm can be caused by irritation of bronchial interoreceptors by an aspirated foreign body, bronchogenic cancer, as well as due to compression of the bronchi by a mediastinal tumor, aortic aneurysm, etc. Symptomatic asthma can be observed with pneumosclerosis, obstructive emphysema, etc.
During the Great Patriotic War, post-concussion attacks of suffocation of a centrogenic nature were observed (B.P.Kushelevsky). The effectiveness of antispasmodics (adrenaline, etc.) should also be considered ex juvantibus, but with some caution. It should be borne in mind that bronchospasm with these diseases it is also often removed by bronchodilators. Of great differential diagnostic value in these cases, all other things being equal, the patient at the time of the study or in the history of other allergic diseases, indications of bronchial asthma and other allergic diseases in heredity, the presence of eosinophils, crystals and spirals in sputum, eosinophilia in the blood , as well as the patient's age at the onset of the disease (bronchial asthma most often falls ill in childhood or adolescence), profession, etc.
The prognosis for bronchial asthma is generally favorable. Patients with bronchial asthma can maintain their ability to work for many years. The prognosis is determined not so much by the duration of the disease (bronchial asthma is characterized by a cyclic course), as by the frequency, duration and intensity of attacks, the presence or absence of an asthmatic condition and complications (pneumosclerosis, persistent emphysema and pulmonary heart failure, often recurrent perifocal pneumonia, etc.) ... In cases with the presence of these complications, the prognosis is often determined not by bronchial asthma, but by the peculiarities of the course of these diseases. The prognosis for bronchial asthma can be decisive early diagnosis, timely preventive measures (elimination of contact with an allergen in an industrial or household environment, the fight against intercurrent infections, with focal infections, etc.), physiotherapy exercises, as well as the rational use of bronchodilators, to relieve attacks and asthmatic conditions.
Treatment of asthma attacks and asthmatic conditions. Effective remedyadrenaline is quick to stop suffocation. The introduction of adrenaline under the skin already in small doses (0.3-0.5 mg) relieves the attack in 2-3 minutes. The rapid action of adrenaline is associated with the stimulation of the sympathetic nervous system, which has an antispasmodic effect on the smooth muscles of the bronchi. The vasoconstrictor effect of adrenaline results in a decrease in the edema of the bronchial mucosa. However, one cannot but take into account the antagonistic action of adrenaline in relation to the parasympathetic nervous system, the tone of which is invariably increased during seizures and causes spasm of the smooth muscles of the small bronchi. With mild and moderate seizures, especially in the initial stages of the disease, there is no need to resort to high doses of adrenaline, which often cause a number of unpleasant side effects - palpitations, tremors, headache and other symptoms of irritation of the sympathetic nervous system. The action of adrenaline is short-lived, unstable and does not prevent the occurrence of repeated attacks within the next hour or two after the injection. In such cases, it is necessary to resort to repeated and multiple (up to 10-12 times a day) administration of adrenaline.
In order to prevent side effects with prolonged use of adrenaline, it is better to use more frequent injections of small doses than to resort to large doses that cause these phenomena. Over time, in some patients, resistance to adrenaline increases and 1-2 mg is required to stop the attack. Nevertheless, in these cases, in order to avoid side effects, it is necessary to use the minimum effective dose, only gradually increasing it. The rapid destruction of adrenaline in the body allows you to use it repeatedly during the day without fear of causing any persistent pathomorphological changes or functional disorders. An in-depth clinical study of patients with bronchial asthma who have been receiving repeated daily injections of epinephrine continuously for several years does not usually reveal any symptoms that could be attributed to its action. There are no absolute contraindications to the administration of adrenaline (if we exclude the extremely rare hypersensitivity to it).
When bronchial asthma is combined with angina pectoris, heart failure, severe hyperthyroidism, adrenaline should be used with caution. The presence of hypertension in the absence of angina pectoris, coronary or muscular insufficiency of the heart is not a contraindication to the administration of adrenaline. The reflex increase in arterial and venous pressure, often observed during an attack of bronchial asthma in both hypertensive and normotensive patients, decreases to its initial value after the relief of an asthma attack with adrenaline. The disadvantages of using adrenaline include the parenteral route of administration (oral ingestion has no effect), as well as increasing tolerance even to high doses, up to the complete disappearance of the antispasmodic effect. In these cases, it is necessary to interrupt the adrenaline injections for several days, after which the introduction of it usually becomes effective again. Very rarely, patients are refractory to the first adrenaline injections.
In recent years, along with adrenaline, norepinephrine preparations have been increasingly used. more precisely iso-propylnoradrenaline (Aludrin, Isoprctialiii, Euspiran, Izadrin, etc.). Isoproiylnor-adrenaline is prescribed in the form of tablets (under the tongue), as well as in an aerosol. Tablets of 20 mg, slowly disintegrating, stop a moderate attack within 4-5 minutes. If the attack does not stop, then you can take the pill again after 5 minutes, etc. before stopping the attack. In the event of side effects (palpitations), the remains of the pill are immediately removed from the oral cavity, and after 10 to 15 minutes, the heartbeat passes. An even more pronounced and rapid stopping effect will be given within 1 minute by isopropylnoradrenaline in a 1% solution in an aerosol; in this case, side effects are observed less frequently than with the use of tablets (Hegh-fieimer). When refractory to adrenaline appears, isopropylnoradrenaline may be effective and vice versa.
A very effective pathogenetic agent for severe attacks and asthmatic conditions is aminophylline (aminophylline). With intravenous administration, the bronchodilator effect occurs even faster than after subcutaneous injection of adrenaline, and, most importantly, aminophylline acts for 9-10 hours. There are no specific contraindications to the administration of aminophylline. Intravenous injection of 0.24-0.48 g of aminophylline in 10 - 20 ml of 10-20% glucose solution (injected slowly!) In the evening or just before bedtime eliminates the asthmatic state, prevents the occurrence of asthma attacks during the night and provides most patients with a restful sleep and relaxation.
The advantage of aminophylline over adrenaline is that it is not contraindicated in the combination of bronchial asthma with angina pectoris, coronary cardiosclerosis, cardiac asthma and other types of heart failure. Eufillin, along with bronchodilatory vasodilating action against the coronary and renal arteries, and, apparently, increasing the contractility of the heart muscle, is very effective in a combination of pulmonary and heart failure. Euphyllin can be recommended orally (0.1-0.15 g), as well as in the form of suppositories (0.25-0.3 g) or in an enema (0.24 g of aminophylline per 30 ml of 5% glucose solution ") for moderate bronchial asthma.
Intravenous administration of aminophylline during a severe attack and an asthmatic condition, as well as its ingestion and in the form of suppositories for mild asthma, deserve wider use in medical practice.
Bronchial asthma is a chronic inflammatory disease of the airways, accompanied by their hyperreactivity, which is manifested by repeated episodes of shortness of breath, difficulty breathing, a feeling of tightness in the chest and cough, which occurs mainly at night or in the early morning. These episodes are usually associated with widespread but not permanent bronchial obstruction that is reversible either spontaneously or with treatment.
EPIDEMIOLOGY
The prevalence of bronchial asthma in the general population is 4-10%, and among children - 10-15%. Prevailing gender: children under 10 years old - male, adults - female.
CLASSIFICATION
Of the greatest practical importance are the classifications of bronchial asthma by etiology, severity of the course and features of manifestation of bronchial obstruction.
The most important is the division of bronchial asthma into allergic (atopic) and non-allergic (endogenous) forms, since specific methods are effective in the treatment of allergic bronchial asthma, which are not used in the non-allergic form.
International classification of diseases of the tenth revision (ICD-10): J45 - Bronchial asthma (J45.0 - Asthma with a predominance of an allergic component; J45.1 - Non-allergic asthma; J45.8 - Mixed asthma), J46. - Status asthmaticus.
The severity of bronchial asthma is classified by the presence of clinical signs before starting treatment and / or by the amount of daily therapy required for optimal symptom control.
◊ Severity criteria:
♦ clinical: the number of nocturnal attacks per week and daytime attacks per day and per week, the severity of physical activity and sleep disorders;
♦ objective indicators of bronchial patency: forced expiratory volume in 1 s (FEV 1) or peak expiratory flow rate (PSV), daily fluctuations in PSV;
♦ therapy received by patients.
◊ Depending on the severity, there are four stages of the disease (which is especially convenient for treatment).
♦ Step 1 : easy intermittent (episodic) bronchial asthma... Symptoms (cough, shortness of breath, wheezing) are noted less than 1 time per week. Night attacks no more than 2 times a month. In the interictal period, there are no symptoms, lung function is normal (FEV 1 and PSV more than 80% of the proper values), daily fluctuations in PSV are less than 20%.
♦ Step 2 : easy persistent bronchial asthma... Symptoms occur once a week or more often, but not daily. Night attacks more often than 2 times a month. Flare-ups can disrupt normal activity and sleep. PSV and FEV 1 outside the attack are more than 80% of the proper values, daily fluctuations in PSV are 20-30%, which indicates an increasing reactivity of the bronchi.
♦ Step 3 : persistent bronchial asthma average degree gravity... Symptoms occur on a daily basis, exacerbations disrupt activity and sleep, and reduce the quality of life. Night attacks occur more often than once a week. Patients cannot do without daily intake of short-acting β 2 -adrenomimetics. PSV and FEV 1 are 60-80% of the required values, PSV fluctuations exceed 30%.
♦ Step 4 : heavy persistent bronchial asthma... Symptoms persistent throughout the day. Exacerbations and sleep disturbances are frequent. The manifestations of the disease limit physical activity. PSV and FEV 1 are below 60% of the proper values \u200b\u200beven outside an attack, and daily fluctuations in PSV exceed 30%.
It should be noted that it is possible to determine the severity of bronchial asthma by these indicators only before starting treatment. If the patient is already receiving the necessary therapy, the volume should be considered. If a patient's clinical picture corresponds to stage 2, but at the same time he receives treatment corresponding to stage 4, he is diagnosed with severe bronchial asthma.
Phases of the course of bronchial asthma: exacerbation, subsiding exacerbation and remission.
♦ Asthmatic status (status asthmaticus) - a serious and life-threatening condition - a prolonged attack of expiratory suffocation, which is not relieved by conventional anti-asthma drugs for several hours. Distinguish between anaphylactic (rapid development) and metabolic (gradual development) forms of status asthmaticus. Clinically manifests itself as significant obstructive disorders up to the complete absence of bronchial conduction, unproductive cough, severe hypoxia, increasing resistance to bronchodilators. In some cases, signs of an overdose of β 2 -agonists and methylxanthines are possible.
According to the mechanism of bronchial obstruction, the following forms of bronchial obstruction are distinguished.
◊ Acute bronchoconstriction due to smooth muscle spasm.
◊ Subacute bronchial obstruction due to edema of the mucous membrane of the respiratory tract.
◊ Sclerotic bronchial obstruction due to sclerosis of the bronchial wall with prolonged and severe course of the disease.
◊ Obstructive bronchial obstruction caused by impaired discharge and changes in the properties of sputum, the formation of mucous plugs.
ETIOLOGY
Risk factors (causal factors) that determine the possibility of developing bronchial asthma and provocateurs (triggers) that realize this predisposition are distinguished.
The most significant risk factors are heredity and exposure to allergens.
◊ The likelihood of bronchial asthma is associated with the person's genotype. Examples of hereditary diseases accompanied by manifestations of bronchial asthma are increased IgE production, a combination of bronchial asthma, nasal polyposis and acetylsalicylic acid intolerance (aspirin triad), airway hypersensitivity, hyperbradykininemia. Genetic polymorphism in these conditions determines the readiness of the airways for inappropriate inflammatory reactions in response to triggers that do not cause pathological conditions in people without a hereditary predisposition.
◊ Of the allergens, the waste products of house dust mites ( Dermatophagoides pteronyssinus and Dermatophagoides farinae), mold spores, plant pollen, dandruff, saliva and urine components of some animals, bird fluff, cockroach allergens, food and drug allergens.
Provoking factors (triggers) can be respiratory tract infections (primarily acute respiratory viral infections), intake of β-blockers, air pollutants (oxides of sulfur and nitrogen, etc.), cold air, physical activity, acetylsalicylic acid and other NSAIDs in patients with aspirin bronchial asthma, psychological, environmental and professional factors, strong odors, smoking (active and passive), concomitant diseases (gastroesophageal reflux, sinusitis, thyrotoxicosis, etc.).
PATHOGENESIS
The pathogenesis of bronchial asthma is based on chronic inflammation.
For bronchial asthma, a special form of inflammation of the bronchi is characteristic, leading to the formation of their hyperreactivity (increased sensitivity to various nonspecific stimuli compared to the norm); the leading role in inflammation belongs to eosinophils, mast cells and lymphocytes.
Inflamed hyperreactive bronchi respond to triggers by spasm of airway smooth muscles, hypersecretion of mucus, edema and inflammatory cellular infiltration of the airway mucosa, leading to the development of obstructive syndrome, clinically manifested as an attack of shortness of breath or suffocation.
... ◊ An early asthmatic reaction is mediated by histamine, prostaglandins, leukotrienes and is manifested by a contraction of the smooth muscles of the airways, hypersecretion of mucus, edema of the mucous membrane.
... ◊ Late asthmatic reaction develops in every second adult patient with bronchial asthma. Lymphokines and other humoral factors cause the migration of lymphocytes, neutrophils and eosinophils and lead to the development of a late asthmatic reaction. Mediators produced by these cells are capable of damaging the epithelium of the respiratory tract, maintaining or activating the process of inflammation, and stimulating afferent nerve endings. For example, eosinophils can secrete most of the major proteins, leukotriene C 4, macrophages are sources of thromboxane B 2, leukotriene B 4 and platelet activating factor. T-lymphocytes play a central role in the regulation of local eosinophilia and the appearance of excess IgE. In the bronchial lavage fluid in patients with atopic asthma, the number of T-helpers (CD4 + lymphocytes) is increased.
... ♦ The prophylactic administration of β 2 -adrenomimetics blocks only the early reaction, and inhaled HA preparations only blocks the late reaction. Cromones (eg, nedocromil) act on both phases of the asthmatic response.
... ◊ The mechanism of development of atopic bronchial asthma is the interaction of antigen (Ar) with IgE, which activates phospholipase A 2, under the action of which arachidonic acid is cleaved from the phospholipids of the mast cell membrane, from which prostaglandins (E 2, D 2, F 2 α) are formed under the action of cyclooxygenase , thromboxane A 2, prostacyclin, and under the action of lipoxygenase - leukotrienes C 4, D 4, E 4, through specific receptors increasing the tone of smooth muscle cells and leading to inflammation of the airways. This fact provides a rationale for the use of a relatively new class of anti-asthma drugs - leukotriene antagonists.
PATHOMORPHOLOGY
In the bronchi, inflammation, mucous plugs, edema of the mucous membrane, hyperplasia of smooth muscles, thickening of the basement membrane, signs of its disorganization are detected. During an attack, the severity of these pathomorphological changes increases significantly. Signs of pulmonary emphysema are possible (see chapter 20 "Pulmonary emphysema"). Endobronchial biopsy of patients with stable chronic (persistent) bronchial asthma reveals desquamation of bronchial epithelium, eosinophilic infiltration of the mucous membrane, thickening of the basement membrane of the epithelium. With bronchoalveolar lavage, a large number of epithelial and mast cells are found in the lavage fluid. In patients with nocturnal attacks of bronchial asthma, the highest content of neutrophils, eosinophils and lymphocytes in bronchial lavage fluid was noted in the early morning hours. For bronchial asthma, in contrast to other diseases of the lower respiratory tract, the absence of bronchiolitis, fibrosis, and granulomatous reactions is characteristic.
CLINICAL PICTURE AND DIAGNOSTICS
Bronchial asthma is characterized by extremely unstable clinical manifestations, therefore, a thorough history taking and study of the parameters of external respiration are necessary. In 3 out of 5 patients, bronchial asthma is diagnosed only in the later stages of the disease, since clinical manifestations of the disease may be absent during the interictal period.
COMPLAINTS AND ANAMNESIS
The most typical symptoms are episodic attacks of expiratory dyspnea and / or cough, the appearance of distant wheezing, a feeling of heaviness in the chest. An important diagnostic indicator of the disease is the relief of symptoms spontaneously or after taking drugs (bronchodilators, GC). When taking anamnesis, attention should be paid to the presence of recurrent exacerbations, usually after exposure to triggers, as well as seasonal variability of symptoms and the presence of allergic diseases in the patient and his relatives. A careful collection of an allergic history is also necessary to establish the connection between the occurrence of difficulty in exhaling or coughing with potential allergens (for example, contact with animals, eating citrus fruits, fish, chicken meat, etc.).
PHYSICAL EXAMINATION
Due to the fact that the severity of the symptoms of the disease changes during the day, at the first examination of the patient, the characteristic signs of the disease may be absent. Exacerbation of bronchial asthma is characterized by an attack of suffocation or expiratory dyspnea, swelling of the wings of the nose when inhaling, interrupted speech, agitation, participation in the act of breathing of the auxiliary respiratory muscles, persistent or occasional cough, there may be dry wheezing (buzzing) wheezing, intensified on exhalation and hearing distance (distant wheezing). In a severe attack, the patient sits bent forward, resting his hands on his knees (or the headboard, the edge of the table). With a mild course of the disease, the patient remains normally active and sleeps in a normal position.
With the development of emphysema of the lungs, a boxed percussion sound is noted (hyper-airiness of the lung tissue). Dry rales are most often heard on auscultation, but they may be absent even during an exacerbation and even in the presence of a confirmed significant bronchial obstruction, which is presumably associated with the predominant involvement of small bronchi in the process. The expiration phase is lengthened.
ASSESSMENT OF ALLERGOLOGICAL STATUS
During the initial examination, scarification, intradermal and prick test ("prick test") provocative tests with probable allergens are used. It should be borne in mind that sometimes skin tests give false negative or false positive results... Detection of specific IgE in blood serum is more reliable. Based on the assessment of the allergic status, it is highly likely to distinguish between atopic and non-atopic bronchial asthma (Table 19-1).
Table 19-1. Some criteria for the diagnosis of atopic and non-atopic bronchial asthma
LABORATORY RESEARCH
In the general analysis of blood, eosinophilia is characteristic. During the period of exacerbation, leukocytosis and an increase in ESR are detected, while the severity of the changes depends on the severity of the disease. Leukocytosis can also be a consequence of taking prednisone. The study of the gas composition of arterial blood in the late stages of the disease reveals hypoxemia with hypocapnia, which is replaced by hypercapnia.
Microscopic analysis of sputum reveals a large number of eosinophils, epithelium, Kurshmann spirals (mucus that forms casts of small airways), Charcot-Leiden crystals (crystallized eosinophil enzymes). At the initial examination and with non-allergic asthma, it is advisable to bacteriological examination of sputum for pathogenic microflora and its sensitivity to antibiotics.
INSTRUMENTAL STUDIES
Peak flowmetry (PSV measurement) is the most important and available technique in the diagnosis and control of bronchial obstruction in patients with bronchial asthma (Fig. 19-1). This study, carried out daily 2 times a day, makes it possible to diagnose bronchial obstruction on early dates development of bronchial asthma, determine the reversibility of bronchial obstruction, assess the severity of the disease and the degree of bronchial hyperreactivity, predict exacerbations, determine occupational bronchial asthma, evaluate the effectiveness of treatment and carry out its correction. Every patient with bronchial asthma should have a peak flow meter.
Investigation of FVD: an important diagnostic criterion is a significant increase in FEV 1 by more than 12% and PSV by more than 15% of the appropriate values \u200b\u200bafter inhalation of short-acting β 2 -adrenomimetics (salbutamol, fenoterol). An assessment of bronchial hyperreactivity is also recommended - provocative tests with inhalation of histamine, methacholine (with a mild course of the disease). Measurement standard bronchial reactivity - the dose or concentration of the provoking agent that causes a 20% decrease in FEV 1. Based on the measurement of FEV 1 and PSV, as well as daily fluctuations in PSV, the stages of bronchial asthma are determined.
Chest x-rays are performed primarily to rule out other respiratory diseases. Most often, they find increased airiness of the lungs, sometimes - quickly disappearing infiltrates.
◊ When pleuritic pain appears in a patient with an attack of bronchial asthma, an X-ray is necessary to exclude spontaneous pneumothorax and pneumomediastinum, especially when subcutaneous emphysema occurs.
◊ In case of a combination of asthma attacks with elevated body temperature, an X-ray examination is performed to exclude pneumonia.
◊ In the presence of sinusitis, it is advisable to x-ray the sinuses to detect polyps.
Bronchoscopy is performed to rule out any other causes of bronchodilator obstruction. During the initial examination, it is advisable to assess the cellular composition of the fluid obtained during bronchoalveolar lavage. The need for medical bronchoscopy and medical bronchial lavage with this disease is assessed ambiguously.
The ECG is informative in severe bronchial asthma and reveals overload or hypertrophy of the right heart, conduction disturbances along the right bundle of His bundle. Sinus tachycardia is also characteristic, decreasing in the interictal period. Supraventricular tachycardia can be a side effect of theophylline.
NECESSARY STUDIES AT DIFFERENT STAGES OF BRONCHIAL ASTHMA
. Step 1 ... General blood analysis, general analysis urine analysis, study of high pressure concentration with a sample with β 2 -adrenomimetics, skin provocative tests to detect allergies, determination of general and specific IgE, chest x-ray, sputum analysis. Additionally, provocative tests with bronchoconstrictors, exercise and / or allergens can be carried out in a specialized institution to clarify the diagnosis.
. Step 2 ... General blood test, general urine analysis, study of high-pressure function with a sample with β 2 -adrenomimetics, skin provocative tests, determination of general and specific IgE, chest x-ray, sputum analysis. Daily peak flow is desirable. Additionally, provocative tests with bronchoconstrictors, exercise and / or allergens can be carried out in a specialized institution to clarify the diagnosis.
. Steps 3 and 4 ... General blood test, general urine analysis, study of high-pressure function with a sample with β 2 -adrenomimetics, daily peak flowmetry, skin provocative tests, if necessary - determination of general and specific IgE, chest x-ray, sputum analysis; in specialized institutions - blood gas analysis.
OPTIONS AND SPECIAL FORMS OF BRONCHIAL ASTHMA
There are several variants (infectious-dependent, dyshormonal, disovarial, vagotonic, neuropsychic, a variant with a pronounced adrenergic imbalance, a cough variant, as well as autoimmune and aspirin bronchial asthma) and special forms (occupational, seasonal, bronchial asthma in the elderly) of bronchial asthma ...
INFECTIOUS-DEPENDENT OPTION
The infectious-dependent variant of bronchial asthma is inherent primarily in persons over 35-40 years old. In patients with this variant of the course, the disease is more severe than in patients with atopic asthma. The reason for the exacerbation of bronchial asthma in this clinical and pathogenetic variant is inflammatory diseases respiratory organs (acute bronchitis and exacerbation of chronic bronchitis, pneumonia, tonsillitis, sinusitis, acute respiratory viral infections, etc.).
Clinical picture
Asthma attacks in such patients are characterized by a lesser severity of development, last longer, and are less well controlled by β 2 -adrenomimetics. Even after the relief of an attack in the lungs, hard breathing with a prolonged exhalation and dry wheezing remain. Often the symptoms of bronchial asthma are combined with symptoms of chronic bronchitis. Such patients have a constant cough, sometimes with mucopurulent sputum, the body temperature rises to subfebrile values. Quite often in the evening there is a chill, a feeling of chilliness between the shoulder blades, and at night - sweating, mainly in the upper back, neck and occiput. These patients are often diagnosed with polypoid-allergic rhinosinusitis. Attention is drawn to the severity and persistence of obstructive changes in ventilation, which are not fully restored after inhalation of β-adrenergic agonists and relief of an attack of suffocation. In patients with infectious-dependent bronchial asthma much faster than in patients with atopic asthma, pulmonary emphysema, cor pulmonale with CHF develop.
Laboratory and instrumental research
Radiographically, as the disease progresses in patients, signs of increased airiness of the lungs appear and grow: increased transparency of the pulmonary fields, expansion of the retrosternal and retrocardial spaces, flattening of the diaphragm, signs of pneumonia can be detected.
In the presence of an active infectious-inflammatory process in the respiratory organs, leukocytosis is possible against the background of severe blood eosinophilia, an increase in ESR, the appearance of CRP, an increase in the content of α- and γ-globulins in the blood, an increase in the activity of acid phosphatase by more than 50 units / ml.
Cytological examination of sputum confirms its purulent character by the predominance of neutrophils and alveolar macrophages in the smear, although eosinophilia is also observed.
When bronchoscopy reveals signs of inflammation of the mucous membrane, hyperemia, mucopurulent nature of the secret; in the washings from the bronchi in cytological examination, neutrophils and alveolar macrophages predominate.
Necessary laboratory research
Laboratory studies are required to establish the presence and identify the role of infection in the pathological process.
Determination of antibodies to chlamydia, moraxella, mycoplasma in blood serum.
Sowing from sputum, urine and feces of fungal microorganisms in diagnostic titers.
Positive skin tests for fungal allergens.
Detection of viral Ag in the epithelium of the nasal mucosa by immunofluorescence.
A fourfold increase in serum AT titers to viruses, bacteria and fungi when observed in dynamics.
DISHORMONAL (HORMONE-DEPENDENT) OPTION
With this option, for the treatment of patients, the systemic use of GCs is mandatory, and their cancellation or reduction in dosage leads to a worsening of the condition.
As a rule, patients with a hormone-dependent course of the disease take GC, and the formation of hormonal dependence is not significantly related to the duration of administration and the dose of these drugs. In patients receiving GC, it is necessary to check for the presence of complications of therapy (suppression of the function of the adrenal cortex, Itsenko-Cushing's syndrome, osteoporosis and bone fractures, hypertension, increased blood glucose concentration, gastric and duodenal ulcers, myopathy, mental changes).
Hormonal dependence can be a consequence of HA deficiency and / or HA resistance.
Glucocorticoid insufficiency, in turn, can be adrenal and extra-adrenal.
... ◊ Adrenal glucocorticoid insufficiency occurs when the synthesis of cortisol by the adrenal cortex decreases, with the predominance of synthesis by the adrenal cortex is much less biologically active corticosterone.
... ◊ Extra-adrenal glucocorticoid insufficiency occurs with increased binding of cortisol to tracortin, albumin, disorders in the "hypothalamus-pituitary-adrenal cortex" regulation system, with increased cortisol clearance, etc.
HA-resistance can develop in patients with the most severe bronchial asthma; at the same time, the ability of lymphocytes to adequately respond to cortisol decreases.
Necessary laboratory research
Laboratory studies are needed to identify the mechanisms that form the hormone-dependent variant of bronchial asthma.
Determination of the level of total 11-hydroxycorticosteroids and / or cortisol in blood plasma.
Determination of the concentration of 17-hydroxycorticosteroids and ketosteroids in urine.
Daily clearance of corticosteroids.
The absorption of cortisol by lymphocytes and / or the number of glucocorticoid receptors in lymphocytes.
Small dexamethasone test.
DESIGN VERSION
The disovarial variant of bronchial asthma, as a rule, is combined with other clinical and pathogenetic variants (most often with atopic) and is diagnosed in cases when exacerbations of bronchial asthma are associated with the phases of the menstrual cycle (usually exacerbations occur in the premenstrual period).
Clinical picture
Exacerbation of bronchial asthma (resumption or increased frequency of asthma attacks, increased shortness of breath, cough with viscous sputum difficult to separate, etc.) before menstruation in such patients is often accompanied by symptoms of premenstrual tension: migraine, mood changes, pasty face and extremities, algomenorrhea. This variant of bronchial asthma is characterized by a more severe and prognostically unfavorable course.
Necessary laboratory research
Laboratory studies are needed to diagnose violations of the hormonal function of the ovaries in women with bronchial asthma.
Basal thermometry test in combination with cytological examination of vaginal smears (colpocytological method).
Determination of the content of estradiol and progesterone in the blood by the radioimmunoassay method on certain days of the menstrual cycle.
EXPRESSED ADRENERGIC IMBALANCE
Adrenergic imbalance is a violation of the relationship between β - and α -adrenergic reactions. In addition to an overdose of β-adrenergic agonists, the factors contributing to the formation of adrenergic imbalance are hypoxemia and changes in the acid-base state.
Clinical picture
Adrenergic imbalance is most often formed in patients with atopic variant of bronchial asthma and in the presence of viral and bacterial infections in the acute period. Clinical data suggesting the presence of adrenergic imbalance or a tendency to develop it:
Aggravation or development of bronchial obstruction with the introduction or inhalation of β-adrenomimetic;
Absence or progressive decrease in the effect with the introduction or inhalation of β-adrenergic agonist;
Long-term use (parenteral, oral, inhalation, intranasal) β-adrenergic agonists.
Necessary laboratory research
The simplest and most accessible diagnostic criteria for adrenergic imbalance include a decrease in the bronchodilation reaction [according to the indications of FEV 1, instantaneous volumetric velocity (MFV) of inspiration, MFV, and maximum ventilation of the lungs] in response to inhalation of β-adrenomimetics or a paradoxical reaction (an increase 20% after inhalation of β-adrenergic agonist).
CHOLINERGIC (VAGOTONIC) OPTION
This variant of the course of bronchial asthma is associated with a violation of the metabolism of acetylcholine and increased activity of the parasympathetic division of the autonomic nervous system.
Clinical picture
The cholinergic variant is characterized by the following features of the clinical picture.
It occurs mainly in the elderly.
Formed several years after bronchial asthma disease.
The leading clinical symptom is shortness of breath, not only during exercise, but also at rest.
The most striking clinical manifestation of the cholinergic variant of the course of bronchial asthma is a productive cough with the separation of a large amount of mucous, frothy sputum (300-500 ml or more per day), which gave reason to call this variant of bronchial asthma "wet asthma".
Rapidly onset bronchospasm under the influence physical activity, cold air, strong odors.
Violation of bronchial patency at the level of medium and large bronchi, which is manifested by an abundance of dry rales over the entire surface of the lungs.
The manifestations of hypervagotonia are nocturnal attacks of suffocation and coughing, excessive sweating, hyperhidrosis of the palms, sinus bradycardia, arrhythmias, arterial hypotension, frequent combination of bronchial asthma with peptic ulcer disease.
NERVO-MENTAL OPTION
This clinical and pathogenetic variant of bronchial asthma is diagnosed when neuropsychic factors contribute to the provocation and fixation of asthmatic symptoms, and changes in the functioning of the nervous system become the mechanisms of the pathogenesis of bronchial asthma. In some patients, bronchial asthma is a kind of pathological adaptation of the patient to the environment and the solution of social problems.
The following clinical variants of neuropsychic bronchial asthma are known.
The neurasthenic variant develops against the background of low self-esteem, high demands on oneself and a painful consciousness of one's own inadequacy, from which it "protects" an attack of bronchial asthma.
An hysterical variant may develop against the background of an increased level of the patient's claims to significant persons of the microsocial environment (family, production team, etc.). In this case, with the help of an attack of bronchial asthma, the patient tries to achieve the satisfaction of his desires.
The psychasthenic variant of the course of bronchial asthma is distinguished by increased anxiety, dependence on significant persons microsocial environment and low ability to make independent decisions. The "conditional pleasantness" of an attack is that it "relieves" the patient from the need to make a responsible decision.
The seizure shunt mechanism relieves the neurotic confrontation of family members and receives attention and care during an attack from a significant environment.
Diagnostics of the neuropsychic variant is based on anamnestic and test data obtained by filling out special questionnaires and questionnaires.
AUTOIMMUNE ASTHMA
Autoimmune asthma occurs as a result of sensitization of patients to Ar of the lung tissue and occurs in 0.5-1% of patients with bronchial asthma. Probably, the development of this clinical and pathogenetic variant is due to allergic reactions of types III and IV according to the classification of Coombs and Gell (1975).
The main diagnostic criteria for autoimmune asthma are:
Severe, continuously recurrent course;
Formation of GK-dependence and GK-resistance in patients;
Detection of anti-pulmonary antibodies, increase in the concentration of CEC and the activity of acid phosphatase in blood serum.
Autoimmune bronchial asthma is a rare, but the most severe variant of the course of bronchial asthma.
"ASPIRAL" BRONCHIAL ASTHMA
The origin of the aspirin variant of bronchial asthma is associated with a violation of the metabolism of arachidonic acid and an increase in the production of leukotrienes. In this case, the so-called aspirin triad is formed, including bronchial asthma, polyposis of the nose (paranasal sinuses), intolerance to acetylsalicylic acid and other NSAIDs. The presence of the aspirin triad is observed in 4.2% of patients with bronchial asthma. In some cases, one of the components of the triad - nasal polyposis - is not detected. Sensitization to infectious or non-infectious allergens is possible. Anamnesis data on the development of an attack of suffocation after taking acetylsalicylic acid and other NSAIDs are important. In specialized institutions, these patients are tested with acetylsalicylic acid with an assessment of the dynamics of FEV 1.
SPECIAL FORMS OF BRONCHIAL ASTHMA
. Bronchial asthma at elderly... In elderly patients, both the diagnosis of bronchial asthma and the assessment of the severity of its course are difficult due to a large number of concomitant diseases, for example, chronic obstructive bronchitis, pulmonary emphysema, coronary artery disease with signs of left ventricular failure. In addition, the number of β 2 -adrenergic receptors in the bronchi decreases with age, so the use of β-adrenergic agonists in the elderly is less effective.
. Professional bronchial asthma accounts for an average of 2% of all cases of this disease. More than 200 substances are known that are used in production (from highly active low molecular weight compounds, for example isocyanates, to known immunogens such as platinum salts, plant complexes and animal products) that contribute to the occurrence of bronchial asthma. Occupational asthma can be both allergic and non-allergic. An important diagnostic criterion is considered the absence of symptoms of the disease before the start of this professional activity, the confirmed connection between their appearance at the workplace and their disappearance after leaving it. The diagnosis is confirmed by the results of measuring PSV at work and outside the workplace, specific provocative tests. It is necessary to diagnose occupational asthma as early as possible and to stop contact with the damaging agent.
. Seasonal bronchial asthma usually associated with seasonal allergic rhinitis. In the period between the seasons, when an exacerbation occurs, the manifestations of bronchial asthma may be completely absent.
. Tussive option bronchial asthma: dry paroxysmal cough is the main and sometimes the only symptom of the disease. It often occurs at night and is usually not accompanied by wheezing.
ASTMATIC STATUS
Status asthmaticus (life-threatening exacerbation) is an asthmatic attack, unusual in severity for this patient, resistant to the usual bronchodilator therapy for this patient. Status asthmaticus is also understood as a severe exacerbation of bronchial asthma, requiring medical care in a hospital setting. One of the reasons for the development of status asthmaticus may be the blockade of β 2 -adrenergic receptors due to an overdose of β 2 -adrenomimetics.
The development of status asthmaticus can be facilitated by the inaccessibility of constant medical care, the lack of objective monitoring of the condition, including peak flowmetry, the inability of the patient to self-control, inadequate previous treatment (usually the absence of basic therapy), a severe attack of bronchial asthma, aggravated by concomitant diseases.
Clinically, status asthmaticus is characterized by pronounced expiratory dyspnea, anxiety up to the fear of death. The patient assumes a forced position with a forward tilt of the body and an emphasis on the arms (shoulders are raised). The muscles of the shoulder girdle, chest and abdominal muscles take part in the act of breathing. The duration of exhalation is sharply lengthened, dry wheezing and humming rales are heard, with progression, breathing becomes weakened up to "mute lungs" (no breathing sounds on auscultation), which reflects the extreme degree of bronchial obstruction.
COMPLICATIONS
Pneumothorax, pneumomediastinum, pulmonary emphysema, respiratory failure, cor pulmonale.
DIFFERENTIAL DIAGNOSTICS
The diagnosis of bronchial asthma should be excluded if, when monitoring the parameters of external respiration, no violations of bronchial patency are detected, there are no daily fluctuations in PSV, bronchial hyperreactivity and coughing attacks.
In the presence of broncho-obstructive syndrome, differential diagnosis is carried out between the main nosological forms, which are characterized by this syndrome (Table 19-2).
Table 19-2. Differential diagnostic criteria for bronchial asthma, chronic bronchitis and pulmonary emphysema
. Signs | . Bronchial asthma | . COPD | . Emphysema lungs |
Age at onset of the disease | Often less than 40 years old | Often over 40 years old | Often over 40 years old |
History of smoking | Not necessary | Characteristically | Characteristically |
The nature of the symptoms | Episodic or persistent | Exacerbation episodes, progressive | Progressing |
Sputum discharge | Little or moderate | Constant in varying amounts | Little or moderate |
Having atopy | |||
External triggers | |||
FEV 1, FEV 1 / FVC (forced vital capacity of the lungs) | Norm or reduced | ||
Airway hyperreactivity (tests with methacholine, histamine) | Sometimes possible |
||
Total lung capacity | Norm or slightly increased | Norm or slightly increased | Sharply reduced |
Diffusion capacity of the lungs | The norm or slightly increased | The norm or slightly increased | Sharply reduced |
Variable | |||
Hereditary predisposition to allergic diseases | Not typical | Not typical |
|
Combination with extrapulmonary manifestations of allergy | Not typical | Not typical |
|
Blood eosinophilia | Not typical | Not typical |
|
Sputum eosinophilia | Not typical | Not typical |
When carrying out the differential diagnosis of broncho-obstructive conditions, it must be remembered that bronchospasm and cough can be caused by certain chemicals, including drugs: NSAIDs (most often acetylsalicylic acid), sulfites (found, for example, in chips, shrimps, dried fruits, beer, wines, and also in metoclopramide, injectable forms of epinephrine, lidocaine), β-blockers (including eye drops), tartrazine (yellow food coloring), ACE inhibitors. Cough caused by ACE inhibitors, usually dry, poorly controlled by antitussives, β-adrenomimetics and inhaled HA, completely disappears after the withdrawal of ACE inhibitors.
Bronchospasm can also be triggered by gastroesophageal reflux. Rational treatment of the latter is accompanied by the elimination of attacks of expiratory dyspnea.
Symptoms similar to bronchial asthma occur with dysfunction of the vocal cords ("pseudo-asthma"). In these cases, it is necessary to consult an otolaryngologist and phoniatrist.
If infiltrates are detected during chest X-ray in patients with bronchial asthma, differential diagnosis should be made with typical and atypical infections, allergic bronchopulmonary aspergillosis, pulmonary eosinophilic infiltrates of various etiologies, allergic granulomatosis in combination with angiitis (Churg-Strauss syndrome).
TREATMENT
Bronchial asthma is an incurable disease. The main goal of therapy is to maintain a normal quality of life, including physical activity.
TREATMENT TACTICS
Treatment goals:
Achieving and maintaining control over the symptoms of the disease;
Prevention of exacerbation of the disease;
Maintaining lung function as close to normal values \u200b\u200bas possible;
Maintaining a normal level of activity, including physical activity;
Elimination of side effects of anti-asthma drugs;
Prevention of the development of irreversible bronchial obstruction;
Prevention of asthma-related mortality.
Control of bronchial asthma can be achieved in most patients, it can be determined as follows:
Minimal severity (ideally no) of chronic symptoms, including nocturnal;
Minimal (infrequent) exacerbations;
No need for ambulance and emergency care;
The minimum need (ideally no) for the use of β-adrenergic agonists (as needed);
No restrictions on activity, including physical;
Daily fluctuations in PSV less than 20%;
Normal (close to normal) PSV values;
Minimal severity (or absence) of undesirable effects of drugs.
The management of patients with bronchial asthma includes six main components.
1. Education of patients for the formation of partnerships in the process of their management.
2. Assessment and monitoring of the severity of the disease, both by recording symptoms and, if possible, by measuring lung function; for patients with moderate and severe course, daily peak flowmetry is optimal.
3. Elimination of exposure to risk factors.
4. Development of individual plans of drug therapy for long-term management of the patient (taking into account the severity of the disease and the availability of anti-asthma drugs).
5. Development of individual plans for relief of exacerbations.
6. Providing regular follow-up monitoring.
EDUCATIONAL PROGRAMS
The basis of the educational system for patients in pulmonology is asthma schools. According to specially developed programs, patients are explained in an accessible form the essence of the disease, methods of preventing seizures (elimination of the effect of triggers, preventive use of drugs). In the course of the implementation of educational programs, it is considered mandatory to teach the patient to independently manage the course of bronchial asthma in various situations, to develop a written plan for getting out of a severe attack, to ensure the availability of access to a medical professional, to teach how to use a peak flow meter at home and maintain a daily PSV curve, as well as correctly use metered dose inhalers. Asthma schools are most effective among women, non-smokers and patients with high socioeconomic status.
MEDICAL THERAPY
Based on the pathogenesis of bronchial asthma, bronchodilators (β 2 -adrenomimetics, m-anticholinergics, xanthines) and anti-inflammatory anti-asthma drugs (GCs, mast cell membrane stabilizers and leukotriene inhibitors) are used for treatment.
ANTI-INFLAMMATORY ANTIASTHMIC PREPARATIONS (BASIC THERAPY)
. GK: the therapeutic effect of the drugs is associated, in particular, with their ability to increase the number of β 2 -adrenoreceptors in the bronchi, inhibit the development of an immediate allergic reaction, reduce the severity of local inflammation, edema of the bronchial mucosa and secretory activity of the bronchial glands, improve mucociliary transport, reduce bronchial reactivity ...
. ◊ Inhalation GK * (beclomethasone, budesonide, fluticasone), unlike systemic ones, have a predominantly local anti-inflammatory effect and practically do not cause systemic side effects. The dose of the drug depends on the severity of the disease.
* When taking medications in the form of dosing cans, it is recommended to use a spacer (especially with a valve that excludes exhalation into the spacer), which contributes to more effective control of bronchial asthma and reduces the severity of some side effects (for example, associated with the sedimentation of drugs in the oral cavity, ingestion) ... A special form of aerosol delivery is represented by the "light breathing" system, which does not require pressing the can, the aerosol dose is issued in response to negative pressure on the patient's inhalation. When using preparations in powder form with the help of cyclohaler, turbuhaler, etc., the spacer is not used.
. ◊ Systemic GK (prednisolone, methylprednisolone, triamcinolone, dexamethasone, betamethasone) is prescribed for severe bronchial asthma in minimal doses or, if possible, every other day (alternating regimen). They are administered intravenously or orally; the latter route of administration is preferable. Intravenous administration is justified if oral administration is impossible. Appointment of depot drugs is permissible only for severe patients who do not follow medical recommendations, and / or when the effectiveness of other drugs has been exhausted. In all other cases, their appointment is recommended to be avoided.
. Stabilizers membranes mast cells (cromoglycic acid and nedocromil, as well as drugs combined with short-acting β 2 -adrenomimetics) act locally, preventing the degranulation of mast cells and the release of histamine from them; suppress both immediate and delayed bronchospastic reaction to inhaled Ag, prevent the development of bronchospasm when inhaling cold air or during physical exertion. With prolonged use, they reduce bronchial hyperreactivity, reduce the frequency and duration of bronchospasm attacks. They are more effective in childhood and youth. Drugs in this group are not used to treat an attack of bronchial asthma.
. Antagonists leukotriene receptors (zafirlukast, montelukast) - a new group of anti-inflammatory anti-asthma drugs. The drugs reduce the need for short-acting β 2 -adrenomimetics and are effective for the prevention of bronchospasm attacks. Used internally. Reduces the need for blood glucose ("sparing effect").
BRONCHOOLING PREPARATIONS
It should be remembered that all bronchodilators in the treatment of bronchial asthma have a symptomatic effect; the frequency of their use serves as an indicator of the effectiveness of basic anti-inflammatory therapy.
... β 2 - Adrenomimetics short actions (salbutamol, fenoterol) are administered by inhalation, they are considered the means of choice for the relief of attacks (more precisely, exacerbation) of bronchial asthma. When administered by inhalation, the action usually begins in the first 4 minutes. The drugs are produced in the form of metered aerosols, dry powder and solutions for inhalers (if necessary, long-term inhalation, the solutions are inhaled through a nebulizer).
◊ Metered dose inhalers, powder inhalers, and nebulization are used to administer drugs. For the correct use of metered-dose inhalers, the patient needs certain skills, since otherwise only 10-15% of the aerosol gets into the bronchial tree. The correct application technique is as follows.
♦ Remove the cap from the mouthpiece and shake the can well.
♦ Exhale fully.
♦ Turn the can upside down.
♦ Position the mouthpiece in front of your mouth wide open.
♦ Start a slow inhalation, at the same time press the inhaler and continue deep inhalation to the end (inhalation should not be sharp!).
♦ Hold your breath for at least 10 seconds.
♦ After 1-2 minutes, repeat inhalation (for 1 breath, the inhaler must be pressed only 1 time).
◊ When using the "light breathing" system (used in some dosage forms of salbutamol and beclomethasone), the patient must open the mouthpiece cap and take a deep breath. It is not required to press the can and coordinate the inhalation.
◊ If the patient is unable to comply with the above recommendations, a spacer (a special plastic flask into which an aerosol is sprayed before inhalation) or a spacer with a valve - an aerosol chamber from which the patient inhales the drug should be used (Fig. 19-2). The correct technique for using the spacer is as follows.
♦ Remove the cap from the inhaler and shake it, then insert the inhaler into the special opening of the device.
♦ Put the mouthpiece in your mouth.
♦ Press the can to receive the dose of the drug.
♦ Take a slow and deep breath.
♦ Hold your breath for 10 seconds and then exhale into the mouthpiece.
♦ Inhale again, but do not press on the can.
♦ Move the device away from the mouth.
♦ Wait 30 seconds before taking the next inhalation dose.
Figure: 19-2. Spacer. 1 - mouthpiece; 2 - inhaler; 3 - hole for the inhaler; 4 - spacer body.
... β 2 - Adrenomimetics long actions used by inhalation (salmeterol, formoterol) or orally ( dosage forms sustained release salbutamol). The duration of their action is about 12 hours. The drugs cause expansion of the bronchi, increased mucociliary clearance, and also inhibit the release of substances that cause bronchospasm (for example, histamine). β 2 -Adrenomimetics are effective for preventing asthma attacks, especially at night. They are often used in combination with anti-inflammatory anti-asthma drugs.
M- Holinoblockers (ipratropium bromide) after inhalation act in 20-40 minutes. The method of administration is inhalation from a balloon or through a spacer. Specially produced solutions are inhaled through a nebulizer.
. Combined bronchodilators drugscontaining β 2 -adrenomimetic and m-anticholinergic (balloon and nebulizer solution).
. Drugs theophyllineand short actions (theophylline, aminophylline) as bronchodilators are less effective than inhaled β 2 -adrenomimetics. They often cause severe side effects that can be avoided by prescribing the optimal dose and controlling the concentration of theophylline in the blood. If the patient is already taking long-acting theophylline preparations, intravenous administration of aminophylline is possible only after determining the concentration of theophylline in the blood plasma!
. Drugs theophyllineand prolonged actions used internally. Methylxanthines cause bronchial expansion, inhibit the release of inflammatory mediators from mast cells, monocytes, eosinophils and neutrophils. Due to their long-term effect, the drugs reduce the frequency of nocturnal attacks, slow down the early and late phases of the asthmatic response to allergen exposure. Theophylline drugs can cause serious side effects, especially in older patients; treatment is recommended to be carried out under the control of theophylline content in the blood.
OPTIMIZATION OF ANTIASTHMIC THERAPY
For the rational organization of anti-asthma therapy, methods of its optimization have been developed, which can be described in the form of blocks.
. Block 1 ... The first visit by the patient to the doctor, assessment of the severity of bronchial asthma [although it is difficult to establish it exactly at this stage, since accurate information is needed about PSV fluctuations (according to home peak flow measurements during the week) and the severity of clinical symptoms], determination of patient management tactics. If the patient needs urgent help, it is better to hospitalize him. It is imperative to take into account the amount of previous therapy and continue it in accordance with the degree of severity. If the condition worsens during treatment or inadequate previous therapy, an additional intake of short-acting β 2 -adrenomimetics can be recommended. Assign an introductory weekly observation period for the patient's condition. If the patient is suspected to have mild or moderate bronchial asthma and there is no need to immediately prescribe full treatment, the patient should be observed for 2 weeks. Monitoring the patient's condition involves filling out a diary of clinical symptoms by the patient and registering PSV indicators in the evening and morning hours.
. Block 2 ... Doctor visit 1 week after the first visit. Determining the severity of asthma and choosing appropriate treatment.
. Block 3 ... A two-week monitoring period during therapy. The patient, as well as during the introductory period, fills in the diary of clinical symptoms and records the PSV values \u200b\u200bwith a peak flow meter.
. Block 4 ... Evaluation of the effectiveness of therapy. A visit to the doctor after 2 weeks on the background of the treatment.
DRUG THERAPY IN ACCORDANCE WITH THE STAGES OF BRONCHIAL ASTHMA
The principles of treatment of bronchial asthma are based on a stepwise approach, recognized in the world since 1995. The purpose of this approach is to achieve the most complete control of the manifestations of bronchial asthma using the least amount of drugs. The number and frequency of drug intake increase (step up) with the aggravation of the course of the disease and decrease (step down) with the effectiveness of therapy. At the same time, it is necessary to avoid or prevent the influence of trigger factors.
. Step 1 ... Treatment of intermittent bronchial asthma includes prophylactic intake (if necessary) of drugs before exercise (inhaled short-acting β 2 -adrenomimetics, nedocromil, their combined drugs). Instead of inhaled β 2 -adrenomimetics, m-anticholinergics or short-acting theophylline preparations can be prescribed, but their action begins later, and they often cause side effects. With an intermittent course, it is possible to carry out specific immunotherapy with allergens, but only by specialists, allergists.
. Step 2 ... With a persistent course of bronchial asthma, a daily long-term prophylactic drug intake is required. Prescribe inhaled GC at a dose of 200-500 mcg / day (based on beclomethasone), nedocromil, or prolonged-release theophylline preparations. Inhaled short-acting β 2 -adrenomimetics continue to be used as needed (with proper basic therapy, the need should decrease until they are canceled).
... ◊ If, against the background of treatment with inhaled GC (at the same time, the doctor is sure that the patient inhales correctly), the frequency of symptoms does not decrease, the dose of the drug should be increased to 750-800 μg / day, or in addition to GC (at a dose of at least 500 μg), prescribe prolonged-acting bronchodilators at night (especially to prevent nocturnal attacks).
... ◊ If, with the help of prescribed drugs, control of bronchial asthma manifestations cannot be achieved (symptoms of the disease occur more often, the need for short-acting bronchodilators increases, or PSV values \u200b\u200bdecrease), treatment should be started according to stage 3.
. Step 3 ... Daily use of anti-asthma anti-inflammatory drugs. Prescribe inhaled HA at 800-2000 mcg / day (based on beclomethasone); the use of an inhaler with a spacer is recommended. Additional bronchodilators may be prescribed long acting, especially for the prevention of nocturnal attacks, for example, oral and inhaled long-acting β 2 -adrenomimetics, long-acting theophylline preparations (under the control of the concentration of theophylline in the blood; therapeutic concentration is 5-15 μg / ml). Symptoms can be relieved by short-acting β 2 -adrenomimetics. For more severe exacerbations, a course of treatment with oral GC is carried out. If it is not possible to control the manifestations of bronchial asthma (symptoms of the disease occur more often, the need for short-acting bronchodilators increases or the PSV indices decrease), treatment should be started according to step 4.
. Step 4 ... In severe cases of bronchial asthma, it cannot be completely controlled. The goal of treatment is to achieve the maximum possible results: the least number of symptoms, the minimum need for short-acting β 2 -adrenomimetics, the best possible PSV values \u200b\u200band their minimum spread, the least number of side effects of drugs. Usually, several drugs are used: inhaled HA in high doses (800-2000 mcg / day in terms of beclomethasone), HA inside permanently or in long courses, long-acting bronchodilators. You can prescribe m-anticholinergics (ipratropium bromide) or their combination with β 2 -adrenomimetic. Inhaled short-acting β 2 -adrenomimetics can be used as needed to relieve symptoms, but not more often 3-4 times a day.
. Step up (worsening). They move to the next stage if treatment is ineffective at this stage. However, it should be taken into account whether the patient is taking the prescribed drugs correctly, and whether he has contact with allergens and other provoking factors.
. Step down (improvement). A decrease in the intensity of maintenance therapy is possible if the patient's condition is stabilized for at least 3 months. The volume of therapy should be reduced gradually. The transition to a step down is carried out under the control of clinical manifestations and FVD.
The above basic therapy should be accompanied by carefully performed elimination measures and supplemented with other drugs and non-drug methods of treatment, taking into account the clinical and pathogenetic variant of the course of asthma.
Patients with infectious-dependent asthma need sanitation of foci of infection, mucolytic therapy, barotherapy, acupuncture.
Patients with autoimmune changes, in addition to HA, can be prescribed cytostatic drugs.
Patients with hormone-dependent asthma need individual regimens for the use of GC and control over the possibility of complications of therapy.
Patients with disovarial changes can be prescribed (after consultation with a gynecologist) synthetic progestins.
Patients with a pronounced neuropsychic variant of the course of bronchial asthma are shown psychotherapeutic methods of treatment.
In the presence of adrenergic imbalance, GCs are effective.
Patients with a pronounced cholinergic variant are shown the anticholinergic drug ipratropium bromide.
Patients with bronchial asthma of physical effort need exercise therapy methods, antileukotriene drugs.
All patients with bronchial asthma need various methods of psychotherapeutic treatment, psychological support. In addition, all patients (in the absence of individual intolerance) are prescribed multivitamin preparations. When the exacerbation subsides and during remission of bronchial asthma, exercise therapy and massage are recommended.
Particular attention should be paid to teaching patients the rules of elimination therapy, inhalation techniques, individual peak flowmetry and monitoring their condition.
PRINCIPLES OF TREATMENT OF EXCERATIONS OF BRONCHIAL ASTHMA
Exacerbation of bronchial asthma - episodes of a progressive increase in the frequency of attacks of expiratory suffocation, shortness of breath, cough, wheezing, feelings of shortness of breath and chest compression or a combination of these symptoms, lasting from several hours to several weeks or more. Severe exacerbations, sometimes fatal, are usually associated with the doctor's underestimation of the severity of the patient's condition, incorrect tactics at the onset of an exacerbation. The principles of treating exacerbations are as follows.
A patient with bronchial asthma should know the early signs of an exacerbation of the disease and begin to stop them on their own.
The optimal route of drug administration is inhalation using nebulizers.
The drugs of choice for the rapid relief of bronchial obstruction are inhaled short-acting β 2 -adrenomimetics.
In case of ineffectiveness of inhaled β 2 -adrenomimetics, as well as in severe exacerbations, systemic GCs are used orally or intravenously.
To reduce hypoxemia, oxygen therapy is performed.
The effectiveness of therapy is determined using spirometry and / or peak flowmetry based on changes in FEV 1 or PSV.
TREATMENT FOR ASTMATIC STATUS
It is necessary to examine the FVD every 15-30 minutes (at least), PSV and oxygen pulse. The hospitalization criteria are given in Table. 19-3. Complete stabilization of the patient's condition can be achieved within 4 hours of intensive care in the emergency department, if during this period it is not achieved, follow-up is continued for 12-24 hours or hospitalized in the general department or intensive care unit (with hypoxemia and hypercapnia, signs fatigue of the respiratory muscles).
Table 19-3. Spirometry criteria for hospitalization of a patient with bronchial asthma
condition | Indications to hospitalizations |
Primary examination | Inability to conduct spirometry OFV 1 ‹0.60 l |
Peak flowmetry and response to treatment started | Lack of effect of bronchodilators and PSV \u003c60 l / min PSV gain after treatment ‹16% FEV 1 \u003c150 ml increase after subcutaneous administration of bronchodilators FEV 1 ‹30% of the required values \u200b\u200band not\u003e 40% of the required values \u200b\u200bafter treatment for more than 4 hours |
Peak flowmetry and response to treatment | PSV \u003c100 l / min initially and \u003c300 l / min after treatment FEV 1 \u003c0.61 L at baseline and \u003c1.6 L after the full course of treatment Increase in FEV 1 \u003c400 ml after using bronchodilators Reduction of PSV by 15% after an initial positive reaction to bronchodilators |
In case of status asthmaticus, as a rule, inhalation of β 2 -adrenomimetics is usually carried out first (in the absence of a history of overdose data), it is possible in combination with an m-holinobokator and better through a nebulizer. For most patients with severe seizures, GC supplementation is indicated. Inhalation of β 2 -adrenomimetics through nebulizers in combination with systemic GCs usually relieves the attack within 1 hour. In a severe attack, oxygen therapy is required. The patient remains in the hospital until the nocturnal attacks disappear and the subjective need for short-acting bronchodilators decreases to 3-4 inhalations per day.
GCs are prescribed orally or intravenously, for example, methylprednisolone 60-125 mg intravenously every 6-8 hours or prednisolone 30-60 mg orally every 6 hours. The effect of drugs with both modes of administration develops after 4-8 hours; the duration of admission is determined individually.
... β 2 -Short-acting adrenergic agonists (in the absence of anamnestic data on overdose) are used in the form of repeated inhalations in a severe condition of the patient in the form of metering balloons with spacers or prolonged (within 72-96 hours) inhalation through a nebulizer (7 times more effective than inhalation from a balloon safe for adults and children).
You can use a combination of β 2 -adrenergic agonist (salbutamol, fenoterol) with an m-anticholinergic antagonist (ipratropium bromide).
The role of methylxanthines in emergency care is limited, since they are less effective than β 2 -adrenomimetics, are contraindicated in older patients, and, in addition, their concentration in the blood must be monitored.
If the condition has not improved, but there is no need for mechanical ventilation, inhalation of an oxygen-helium mixture is indicated (it causes a decrease in resistance to gas flows in the airways, turbulent flows in small bronchi become laminar), the introduction of magnesium sulfate intravenously, auxiliary non-invasive ventilation. Transfer of a patient with status asthmaticus to mechanical ventilation is carried out for health reasons in any conditions (outside the hospital, in the emergency department, in the general department or intensive care unit). The procedure is performed by an anesthesiologist or resuscitator. The purpose of mechanical ventilation in bronchial asthma is to maintain oxygenation, normalize blood pH, and prevent iatrogenic complications. In some cases, mechanical ventilation of the lungs requires an intravenous infusion of sodium bicarbonate solution.
BRONCHIAL ASTHMA AND PREGNANCY
On average, 1 out of 100 pregnant women suffers from bronchial asthma, and in 1 out of 500 pregnant women it has a severe course with a threat to the life of the woman and the fetus. The course of bronchial asthma during pregnancy is highly variable. Pregnancy in patients with a mild course of the disease can improve the condition, while in severe cases it usually worsens. An increase in seizures is more often noted at the end of the second trimester of pregnancy, during childbirth severe attacks are rare. Within 3 months after childbirth, the nature of the course of bronchial asthma returns to the initial prenatal level. Changes in the course of the disease in repeated pregnancies are the same as in the first. Previously, it was believed that bronchial asthma is 2 times more likely to cause pregnancy complications (gestosis, postpartum hemorrhage), but recently it has been proven that with adequate medical control, the likelihood of their development does not increase. However, these women are more likely to have children with low body weight, and the need for surgical delivery is also more common. When prescribing anti-asthma drugs for pregnant women, one should always take into account the possibility of their effect on the fetus, however, most modern inhaled anti-asthma drugs are safe in this regard (Table 19-4). In the US FDA * developed a guideline according to which all drugs are divided into 5 groups (A-D, X) according to the degree of danger of use during pregnancy * .
* According to the classification of the FDA (Food and Drug Administration, Committee on the Control of Medicines and Food Additives, USA), medicines according to the degree of danger (teratogenicity) for fetal development are divided into categories A, B, C, D, X. Category A (for example, potassium chloride) and B (for example, insulin): adverse effects on the fetus have not been established either in animal experiments or in clinical practice; category C (eg isoniazid): adverse effects on the fetus established in animal experiments, but not in clinical practice; category D (for example, diazepam): there is a potential teratogenic risk, but the effect of drugs on a pregnant woman usually outweighs this risk; category X (for example, isotretinoin): the drug is definitely contraindicated in pregnancy and if you wish to become pregnant.
Among patients who are indicated for operations with inhalation anesthesia, an average of 3.5% suffer from bronchial asthma. In these patients, complications are more likely during and after surgery, therefore, it is extremely important to assess the severity and control over the course of bronchial asthma, assess the risk of anesthesia and this type of surgery, as well as preoperative preparation. The following factors should be considered.
Acute airway obstruction causes ventilation and perfusion disturbances, increasing hypoxemia and hypercapnia.
Endotracheal intubation can cause bronchospasm.
Drugs used during surgery (for example, morphine, trimeperidine) can provoke bronchospasm.
Severe bronchial obstruction in combination with postoperative pain syndrome can disrupt the coughing process and lead to the development of atelectasis and nosocomial pneumonia.
To prevent exacerbation of bronchial asthma in patients with a stable condition with regular inhalation of HA, it is recommended to prescribe prednisolone at a dose of 40 mg / day by mouth 2 days before the operation, and give this dose in the morning on the day of the operation. In severe bronchial asthma, the patient should be hospitalized a few days before the operation to stabilize the FVD (intravenous HA administration). In addition, it should be borne in mind that in patients who received systemic GC for 6 months or more, there is a high risk of adrenal-pituitary insufficiency in response to surgical stress, therefore, they are shown prophylactic administration of 100 mg of hydrocortisone intravenously before, during and after surgery. ...
FORECAST
The prognosis of the course of bronchial asthma depends on the timeliness of its detection, the level of education of the patient and his ability to self-control. The elimination of provoking factors and the timely appeal for qualified medical care are of decisive importance.
DISPENSERIZATION
Patients need constant supervision by a physician at the place of residence (with complete control of symptoms at least once every 3 months). With frequent exacerbations, constant monitoring by a pulmonologist is indicated. According to the indications, an allergic examination is carried out. The patient should know that in Russian Federation free (according to special prescriptions) provision of anti-asthma drugs is provided in accordance with the lists approved at the federal and local levels.
Factors that determine the need for careful and continuous monitoring, which is carried out in a hospital or in outpatient, depending on the available options, include:
Insufficient or decreasing response to therapy in the first 1-2 hours of treatment;
Persistent severe bronchial obstruction (PSV less than 30% of the proper or individual best value);
Recent history of severe bronchial asthma, especially if hospitalization and stay in the intensive care unit was required;
The presence of factors of high risk of death from bronchial asthma;
Prolonged presence of symptoms before seeking emergency care;
Insufficient availability of medical care and drugs at home;
Poor living conditions;
Difficulty transporting to hospital in case of further deterioration.
2. The clinical picture and schemes for assessing the status of a patient with bronchial asthma
During the course of the disease, the following periods are distinguished:
1) harbingers;
2) seizure;
3) post-attack;
4) interictal.
The period of precursors of bronchial asthma occurs a few minutes, sometimes days before the attack and is characterized by the appearance of anxiety, irritability, sleep disturbance. Sneezing, itching of eyes and skin, nasal congestion and serous discharge, obsessive dry cough, and headache are often noted.
Asthma asthma is characterized by a feeling of lack of air, chest compression, severe expiratory shortness of breath. Breathing wheezing, wheezing is heard in the distance. Small children are frightened, rush about in bed, older children take a forced position - they sit, leaning forward, resting their elbows on their knees, gasping for air. Speech is almost impossible. The face is pale, with a bluish tinge, covered with cold sweat. The wings of the nose are inflated upon inhalation. The chest is in a state of maximum inspiration, the auxiliary muscles are involved in breathing. The phlegm when coughing is difficult, viscous, thick. Percussion determines the box sound. Auscultation against a background of hard or weakened breathing is heard a large number of dry wheezing, often - crepitus.
External changes of cardio-vascular system: with bronchial asthma
tachycardia, muffling of heart sounds, increased blood pressure; the skin is pale gray, perioral cyanosis, cyanosis of the lips, auricles, and hands are expressed.
An attack of bronchial asthma ends, as a rule, with the discharge of thick foamy sputum and a gradual relief of breathing.
The duration of an attack of bronchial asthma ranges from several minutes to several hours or days.
If an attack of bronchial asthma did not stop within 6 hours, then they talk about the development of status asthmaticus.
In the post-attack period of bronchial asthma, the following are noted:
general weakness, drowsiness, lethargy;
changes in the respiratory system: auscultated bronchial breathing, scattered dry rales on exhalation;
changes in the cardiovascular system:
bradycardia, lowering blood pressure.
But the complete restoration of breathing can be judged only by the results of peak flowmetry.
In the interictal period of bronchial asthma - the condition depends on the severity of the disease and the function of external respiration.
Measurement of lung function in bronchial asthma is as necessary as measuring blood pressure in hypertension.
Respiratory function is measured using a peak flow meter (PEP meter).
Peak flowmetry (English - peak flow) is a method of determining the peak forced expiratory flow rate. It allows you to determine the maximum speed at which air passes through the airway during forced expiration.
Continuous recording of peak flowmetry values \u200b\u200bhelps to timely identify the period of precursors of an attack of bronchial asthma.
Daily measurement of peak expiratory flow rate for 2-3 weeks allows to assess the severity of bronchial asthma and develop an appropriate treatment plan.
If, within 2-3 weeks, the patient fails to achieve a peak expiratory flow rate of 80% of the proper value (tables of proper values \u200b\u200bare attached to all peak flow meters), then a course of treatment with corticosteroid drugs may be required to determine the patient's maximum functionality.
Long-term measurement of peak expiratory flow rate makes it possible to evaluate the effectiveness of the treatment.
Characteristics of the severity of bronchial asthma in children.
When deciding on the severity of bronchial asthma, the pediatrician must take into account:
medical history (frequency, severity, duration of asthma attacks and their equivalents, the effectiveness of medications and procedures); physical examination data; instrumental examination data; laboratory examination results.
1. Mild degree: characterized by rare attacks (less than 1 time per month), relatively quickly disappearing as a result of treatment. In the period of remission, the general condition does not suffer, the indicators of external respiration fluctuate within the age norm.
2. Moderate degree: asthma attacks are repeated 3-4 times a month. They proceed with pronounced violations of the respiratory and circulatory function: tachypnoe, tachycardia, muffling of heart sounds, fluctuations in the maximum arterial pressure during the respiratory cycle are clearly recorded - its increase during exhalation and decrease during inhalation. Respiratory function indicators range from 60 to 80%.
3. Severe degree: characterized by frequent (several times a week) attacks of suffocation, occurring against the background of severe distension, shortness of breath and tachycardia. Patients assume a forced position. Skin pale gray, perioral cyanosis, cyanosis of the lips, auricles, and hands are expressed. The cough is unproductive, exhalation is noisy, prolonged, chest retraction appears during inhalation, auxiliary muscles participate in the act of breathing. Respiratory function indicators are less than 60%.
When assessing the severity of the disease, take into account
number of nocturnal symptoms per month, week, day
number of daytime symptoms per week, day
severity of physical activity and sleep disorders
the best FEV1 and PSV indicators per day
daily fluctuations of FEV1 and PSV
In the stratification of asthma by severity, there is the concept of a stage corresponding to certain gradations of symptoms of asthma symptom complex. There are four stages, if the patient does not take basic drugs, then each of these stages corresponds to one of four degrees of severity:
Stage 1. Intermittent asthma
Illness attacks are rare (less than once a week)
Short exacerbations
Nocturnal attacks of the disease are rare (no more than twice a month)
PSV spread less than 20%
Stage 2. Mild persistent asthma
Symptoms of the disease occur more often than 1 time per week, but less often than 1 time per day
Exacerbations can disrupt the patient's sleep, inhibit physical activity
Nocturnal attacks of the disease occur at least 2 times a month
FEV1 or PSV more than 80% of the norm
PSV spread 20-30%
Stage 3. Moderate persistent asthma
Asthma attacks occur almost daily
Exacerbations disrupt the patient's sleep, reduce physical activity
Nocturnal attacks of the disease occur very often (more often than 1 time per week)
FEV1 or PSV decreases to 60% to 80% of normal
PSV spread over 30%
Stage 4. Severe persistent asthma
Disease attacks occur daily
Asthma attacks are very common at night
Limiting physical activity
FEV1 or PSV is about 60% of normal
PSV spread over 30%
If the patient is on basic therapy, the severity of the disease is determined by the step and dosage of the basic drug:
Scheme 1. Assessment of complaints, clinical symptoms and medical history
Scheme 2. Evaluation of the physical examination of the patient
Scheme 3. Study of the function of external respiration
Scheme 4. Assessment of allergic status
Bronchial asthma in children
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The clinical picture of bronchial asthma of physical effort
An attack of suffocation in this variant of the disease is caused by hyperventilation against the background of physical activity.Hyperventilation leads to cooling and drying of the airways, which causes the activation of mast cells and the release of bronchospastic mediators by them.
In addition, bronchospasm is probably due to the activation of afferent nerves.
Factors contributing to the development of an asthma attack of physical effort are: continuous heavy exertion with inhalation of cold and / or dry air for 6-8 minutes; physical activity in patients with atopic bronchial asthma (BA) during an exacerbation; impossibility for any reason to take the necessary medicine in a timely manner. Difficulty breathing is also triggered by brisk walking, running, laughing, fright, and other manifestations of physical exertion or emotion. BA symptoms do not appear during the action of the provoking factor, but 5-40 minutes after it.
In fact, bronchial asthma of physical exertion is one of the manifestations of bronchial hypersensitivity, and not a special form of asthma, therefore it often serves as an indicator of poor control of bronchial asthma. In this regard, adequate anti-inflammatory therapy leads to a decrease in symptoms associated with exercise, however, in some cases, additional inhalation of a short-acting 2-agonist before exercise is recommended.
The clinical picture of bronchial asthma and pregnancy
Pregnancy has a different effect on the course of asthma. It is believed that in 1/3 of women the course of asthma improves during pregnancy, in 1/3 it does not change and in 1/3 it worsens, and women with a severe course of the disease are more prone to exacerbation during pregnancy than women with a mild course of bronchial asthma. Exacerbations of asthma occur early in the third trimester, and asthma symptoms rarely appear during childbirth.Uncontrolled (untreated or poorly treated) asthma can lead to the development of complications in the mother (preeclampsia, placental abruption, hypertension of pregnant women, toxemia, caesarean section) and the fetus (increased risk of perinatal death, intrauterine growth retardation, low birth weight, preterm labor, and neonatal hypoxia).
It has been established that anti-asthma drugs - in 2 -agonists, sodium cromoglycate and inhaled steroids do not have a negative effect on the fetus or mother. It is preferable to use inhaled glucocorticosteroids in the minimum effective dose, and the drug of choice is budesonide (Pulmicort), since it was with it that multicenter studies were conducted on the efficacy and safety of inhaled glucocorticoids in pregnant women.
If necessary, oral systemic corticosteroids can be safely used, and in such cases prednisolone is recommended over dexamethasone. Thus, the treatment of pregnant women suffering from bronchial asthma should be carried out in accordance with the accepted recommendations for BA treatment.
The clinical picture of aspirin bronchial asthma
Aspirin asthma is a special type of asthma, when one of the bronchoconstrictor factors in a patient is non-steroidal anti-inflammatory drugs (NSAIDs)... From 5 to 30% of patients with bronchial asthma have an increased sensitivity to aspirin. Asthma attacks in aspirin-sensitive patients can be caused not only by aspirin, but also by other NSAIDs that block the cyclooxygenase pathway of arachidonic acid metabolism. Once developed intolerance to aspirin or NSAIDs continues throughout life."Aspirin" asthma, as mentioned above, consists of a triad of symptoms: asthma attacks, NSAID intolerance and polypous rhinosinusitis ("asthmatic triad").
In its course, aspirin BA refers to severe forms, is characterized by a high incidence of disability and the possibility of sudden death, and is characterized by more frequent hospitalization of patients in intensive care units.
To confirm the diagnosis of aspirin AD, the skin test is not used as having no diagnostic value, but a provocative dosed test with aspirin is performed. This study is a complex diagnostic procedure and is performed only by specially trained doctors in allergological or pulmonological centers (departments).
Treatment of aspirin bronchial asthma is carried out in accordance with the recommendations of clinical guidelines for the treatment of other forms of bronchial asthma. In addition to this, in a number of patients (with low sensitivity to aspirin), aspirin desensitization is carried out, that is, the administration of the drug in small, gradually increasing doses. Desensitization with aspirin is especially indicated for patients for whom NSAIDs are vital for the treatment of other diseases (coronary heart disease, rheumatic diseases, etc.).
It is carried out only in a hospital under the guidance of a specialist - pulmonologist (allergist). A key component to achieving symptom control of aspirin asthma is eliminating the use of NSAIDs in aspirin-sensitive patients.
Determination of the key role of leukotrienes in the pathogenesis of aspirin asthma has expanded the possibilities for its effective therapy. The most important pathogenetic group of drugs for patients with aspirin asthma are antileukotriene drugs, such as zafirlukast (acolate) and montelukast (singular).
When leukotriene receptor antagonists are used in combination with topical steroids, a pronounced sparring effect is noted (saving effect of both drugs), which allows them to be used in lower doses. Antileukotriene drugs are basic, preventive therapy and are not used to relieve acute attacks of bronchial obstruction.
Rhinosinusitis and nasal polyps in patients with aspirin asthma require active treatment with nasal steroids, which must be prescribed in the correct dosage in order to stop the growth of polyps and regress the process. Removing polyps, as a rule, not only does not bring relief, but, on the contrary, makes the condition worse. In addition, recurrence of polyps is natural. Therefore, polypectomy is not recommended.
The clinical picture of occupational bronchial asthma
In developed countries, AD is the most common occupational disease. Occupational asthma is defined as asthma caused by contact with an agent present in the environment in which the patient is at work. According to existing estimates, occupational factors are the cause of about 1 out of every 10 cases of bronchial asthma in adults, including newly diagnosed cases, as well as exacerbations of existing bronchial asthma. Occupations with a high risk of occupational asthma include agriculture, paint handling (including painting), cleaning and janitorial jobs, and plastics manufacturing.There are two types of occupational asthma: immunologically mediated and non-immunologically mediated. Immunologically mediated is more common and has a latency period from several months to several years after the onset of contact with provoking factors.
Its development involves IgE-mediated and, possibly, cellular allergic reactions due to sensitization of the body to a professional factor. Non-immunologically mediated AD has no latency period and occurs most often within 24 hours after exposure to a high concentration of gas, smoke or chemical in previously healthy individuals and lasts at least 3 months.
To diagnose occupational asthma, it is necessary to carefully collect anamnesis about the patient's working conditions, possible exposure to various substances. In typical cases, asthma gradually worsens during the working week.
On weekends or during holidays, that is, when contact with a professional factor ceases, patients, on the contrary, notice an improvement in their condition. To confirm the diagnosis, it is recommended to monitor the peak expiratory flow rate at least four times a day during two weeks when the patient is working and during the same period when he is not at work. In some cases, a provocative test has to be carried out to make a diagnosis.
Once the diagnosis is established, the best treatment is to completely eliminate contact with the relevant provoking factors, however, in some cases, it becomes necessary for regular anti-asthma treatment. The disease often persists even after a job change.
The clinical picture of bronchial asthma in old and senile age
The group of patients in whom the diagnosis of bronchial asthma is often not established or is established erroneously is the elderly and senile. This is due to the peculiarities of the course of the disease in this age group. Most patients do not have typical attacks of suffocation, and the disease is clinically manifested by episodes of respiratory discomfort, dyspnea of \u200b\u200ba mixed nature, constant difficulty breathing with prolonged exhalation and paroxysmal cough. Another characteristic feature of elderly and senile AD patients is pronounced hyperreactivity of the bronchi to nonspecific stimuli: pungent odors, cold air, changes in weather conditions.One of the most important features of AD in elderly and senile age is multimorbidity - the presence of concomitant diseases (from 2 to 6). Most often there are concomitant cardiovascular pathology, diabetes mellitus, diseases of the gastrointestinal tract, kidneys. Often in these patients, with exacerbation of bronchial asthma, cardiac decompensation rapidly develops, which, in turn, aggravates the dysfunction of external respiration, maintaining a more severe course of the disease. Formed "syndrome of mutual burdening."
The described features of the course of bronchial asthma in elderly and senile people require correction of therapeutic measures. In particular, cromones are ineffective in these patients, so inhaled corticosteroids are the drugs of choice. Given the frequent presence of concomitant cardiovascular pathology, from bronchodilators, anticholinergic (atrovent) or combined drugs (berodual) are preferred.
All inhaled drugs are recommended to be used with a spacer, as patients often cannot synchronize their inhalation with inhalation of the drug. Treatment of concomitant diseases is also shown, but one should not forget about polypharmacy and the interaction of various drugs.
The clinical picture of severe bronchial asthma
Patients with severe asthma occur in 10-14% of cases.The term "severe bronchial asthma" includes a number of clinical syndromes, which are united by an exacerbation of the disease that threatens the life of a sick person. Clinical forms of severe asthma are listed below.
Asthmatic condition (severe exacerbation of asthma), which will be covered in a separate chapter of this manual.
“Unstable bronchial asthma” is a term that defines the condition of BA patients with supposedly well-chosen treatment, but with the development of severe exacerbations in them in the future. There are two forms of unstable bronchial asthma, which are characterized by sudden and delayed asthmatic attacks. An example of the first form is aspirin asthma, when a sudden severe exacerbation is provoked by taking NSAIDs. An example of the second form is the delayed exacerbation of the disease that occurs with a respiratory viral infection.
About "chronic severe bronchial asthma" is said in cases where the disease is poorly controlled by inhaled glucocorticosteroids and it becomes necessary to prescribe systemic steroid hormonal drugs. This category of patients includes patients with "hormone-dependent" asthma.
Thus, severe asthma is not a homogeneous concept, but its various forms combine a decrease in the effectiveness of anti-inflammatory and bronchodilator drugs up to their paradoxical effect and exacerbations that threaten the patient's life.
Factors that can lead to a severe exacerbation of bronchial asthma include:
1) infectious viral diseases of the respiratory tract;
2) medications: NSAIDs, β-blockers, antibiotics;
3) environmental factors (pollutants, allergens, "black smoke");
4) socio-economic problems.
Timely diagnosis of severe exacerbation of asthma (Table 3) will help the doctor to begin adequate treatment of the patient as early as possible.
Table 3. Criteria for severe exacerbation of bronchial asthma
Differential diagnosis
Bronchial asthma must be differentiated from various diseases that are accompanied by paroxysmal dyspnea or shortness of breath. Such conditions are observed in diseases of the lungs and bronchi ( chronic obstructive pulmonary disease (COPD), tracheobronchial dyskinesia, occlusion and compression of the trachea and large bronchi), diseases of the cardiovascular system (cardiac asthma, pulmonary embolism (TELA)), disturbances in the nervous regulation of respiration (neurocirculatory dystonia, hysteria), polyarteritis nodosa and hormone-active tumors.Most often, it is necessary to carry out a differential diagnosis between chronic obstructive pulmonary disease and bronchial asthma.
The main difference from COPD is the presence of typical asthma attacks with asthma with predominant difficulty in exhaling or respiratory discomfort, which occurs sporadically and is accompanied by coughing, chest congestion and wheezing. In COPD, shortness of breath and difficulty in breathing do not have a paroxysmal nature, they are observed constantly and only intensify with physical exertion, sometimes when inhaling cold air and irritating odors, which, as in BA, is associated with increased bronchial reactivity.
Cough in COPD with sputum, often purulent in nature, is constantly observed, although it can acquire a paroxysmal character. However, such paroxysms of cough are not preceded by difficulty in breathing. In asthma, paroxysmal cough is accompanied by wheezing in the chest, and viscous mucous sputum, usually in small amounts, is separated at the end or after an attack of suffocation.
Difficulties in the differential diagnosis with COPD usually do not arise with exogenous and aspirin bronchial asthma, which typically occur with complete reversibility of obstruction according to clinical data (elimination of shortness of breath, hard breathing, wheezing). Differential diagnosis with COPD is much more difficult in endogenous asthma, in which asthma attacks have a less vivid clinic and are prolonged. Moreover, this form of asthma is often combined with COPD.
In contrast to COPD, in endogenous asthma, dyspnea is paroxysmal in nature and, as a rule, is not associated with physical activity. The results of a pharmacological functional test are of great importance for differential diagnosis: an increase in forced expiratory volume in 1 second (FEV 1 ) or POS VYD after inhalation of 2 -agonists or M-anticholinergics by 15% or more indicate in favor of bronchial asthma. In patients with COPD, according to clinical data and the results of functional examination, there is no complete reversibility of obstruction. Differential diagnosis takes into account the presence of polyposis-allergic rhinosinusitis, blood eosinophilia, and especially sputum in AD.
With tracheobronchial dyskinesia (expiratory collapse of the trachea and large bronchi), the prolapse of the thinned and stretched membranous part of the trachea and large bronchi into the lumen of the airways occurs during exhalation or coughing, which leads to narrowing of their lumen until it is completely closed. Clinically, this pathology is manifested by paroxysmal cough and expiratory dyspnea or dyspnea, which can lead to an erroneous diagnosis of asthma.
Unlike asthma, cough with tracheobronchial dyskinesia has a rattling, nasal shade; in the larynx, during a coughing attack, it is often possible to hear a characteristic whistling sound on exhalation. The main difference is the absence of widespread wheezing, characteristic of bronchial asthma. Bronchodilators have no effect, improvement occurs with the transition to more shallow breathing, which decreases intrathoracic pressure and prolapse. Bronchoscopy is crucial for diagnosis.
AD has to be differentiated by acute respiratory viral diseases accompanied by widespread obstructive bronchiole disease, which can lead to dyspnea attacks and mimic asthma attacks, which is especially pronounced in children. It is assumed that bronchial obstruction is caused by transient bronchial hyperreactivity caused by a viral infection.
Choking syndrome can be observed with mechanical obstruction of the large airways. Occlusion of the larynx, trachea and large bronchi is observed with endophytic tumor growth, with foreign bodies and cicatricial stenosis of the trachea and large bronchi. Similar breathing disorders can be observed when the trachea and large bronchi are compressed by mediastinal tumors, enlarged lymph nodes, and aortic aneurysms.
Unlike asthma, during these processes, dyspnea is inspiratory in nature, and a loud whistling noise is heard during inspiration (stridor breathing). Inhalation is performed with the active participation of the auxiliary respiratory muscles, while exhalation is carried out without effort. An important difference is also the absence of dry wheezing, and with the defeat of large bronchi, the predominance of physical symptoms on the one hand.
In some cases, bronchial asthma has to be differentiated from bronchial tuberculosis. The latter is characterized by a cough with a small amount of sputum, sometimes hemoptysis. Complications may develop in the form of a decrease in pneumatization or atelectasis due to a violation of bronchial patency, which are detected during an X-ray examination. Of decisive importance for the diagnosis is bronchoscopic examination, which reveals tuberculous lesions of the bronchi, detection of mycobacterium tuberculosis in the lavage of the bronchi (sputum).
Often there is a need, especially in men, for differential diagnosis of bronchial asthma with bronchial cancer. As you know, with central cancer initial signs diseases are associated with irritation of the mucous membrane receptors and with impaired bronchial patency. A common symptom is cough, dry or with little phlegm, sometimes streaked with blood, which does not bring relief.
Periodically, there is an increase in temperature, signs of intoxication associated with the development of secondary inflammatory changes in the lung tissue. In diagnostics lung cancer anamnesis data (prolonged smoking, occupational hazards), X-ray, including tomographic, research, bronchoscopy with biopsy and histological study of biopsy help.
In recent years, in the literature, especially foreign, there have been many works on sleep apnea syndrome, the development of which in patients poses a serious threat to health and life. By pathogenesis, there are two main types of sleep apnea syndrome: obstructive and central. The central type of sleep apnea is relatively rare and is observed with primary alveolar hypoventilation, which is caused by a violation of the automatic regulation of respiration due to a decrease in the sensitivity of the respiratory center to carbon dioxide.
It is observed sometimes after suffering encephalitis, as well as in case of opiate poisoning. In many cases, it is not possible to determine the cause of central apnea. Clinically, in addition to sleep apnea, it is manifested by a decrease and decrease in the depth of breathing, drowsiness, and headache. In the blood, hypoxemia, hypercapnia, compensatory hyperglobulinemia and an increase in the amount of hemoglobin are detected.
The cause of obstructive apnea, which has to be differentiated from nocturnal attacks of asthma, is a temporary complete violation of the patency of the upper airways as a result of hypotension and retraction of the soft palate, the root of the tongue, collapse of the posterior pharyngeal wall, which is facilitated by adenoids and hyperplasia of the tonsils in children, as well as developmental defects of the lower jaw. However, the causes of sleep apnea are not fully understood. It occurs at any age, but most often occurs in middle-aged and older men who are obese, less often in women during menopause.
The clinical features of patients with sleep apnea syndrome include lethargy and drowsiness during the daytime, and night sleep, especially in the supine position, is usually characterized by loud snoring, which is suddenly interrupted at the time of apnea. Loud snoring, during which a short awakening may occur, marks the end of the apnea period. Sleep apnea syndrome is considered severe if the breaks in breathing occur with a frequency of at least 5 per hour and last for 10 or more seconds. To clarify the diagnosis, monitoring of the external respiration function in patients at night is carried out.
Serious difficulties arise in the differential diagnosis of an attack of heart and bronchial asthma in the elderly, who often have chronic bronchitis and pulmonary emphysema combined with ischemic heart disease (cardiosclerosis, various rhythm disturbances, angina pectoris and other forms ischemic heart disease (Ischemic heart disease)), hypertension, atherosclerotic lesions of the aorta and peripheral arteries. In such cases, it is necessary to take into account the presence of a history of cardiovascular diseases in patients, the absence of manifestations of allergies and a different clinical picture of an attack of heart and bronchial asthma.
Cardiac asthma is a manifestation of acute left ventricular failure in coronary artery disease (especially in acute heart attack myocardium and postinfarction cardiosclerosis), hypertension, heart defects and myocardiopathies.
Cardiac asthma often develops at night, at first patients experience a feeling of tightness in the chest, soon turning into suffocation. Acute left ventricular failure leads to venous congestion in the lungs and proceeds in two stages: 1st stage - interstitial edema, which usually quickly passes into the 2nd stage - the stage of alveolar edema.
Significant difficulties in differential diagnosis with asthma are present in the initial period of left ventricular failure, at the stage of interstitial pulmonary edema, when in connection with venous hyperemia of the mucous membrane of the bronchi and bronchioles, their narrowing develops and the flow of air from the alveoli into the airways is disturbed. At this stage, there is a dry paroxysmal cough and pronounced shortness of breath, dry rales can be heard over the lungs. Sputum during this period is not separated. This condition resembles an attack of asthma.
The main distinguishing features of bronchial asthma are:
1) anamnestic indications of the presence of cardiovascular diseases, and with coronary artery disease, suffocation often develops against the background of an anginal attack, with hypertension may initially be accompanied by an additional rise in blood pressure;
2) forced semi-sitting position of the patient;
3) sharply increased (up to 40-50 per minute) respiratory rate, which is not observed during an asthma attack;
4) suffocation in cardiac asthma is predominantly inspiratory or mixed, while in asthma, expiratory suffocation is observed.
Symptoms of acute left ventricular failure progress rapidly and soon a picture of alveolar pulmonary edema develops: cough with a large amount of foamy sputum, often pink in color; in the lungs, a lot of different-sized wet rales are heard, which first appear in the lower parts, but soon begin to be heard over all parts of the lungs.
The accumulation of liquid phlegm in the upper respiratory tract produces bubbling breathing, which can be heard from a distance. In contrast to this, during an attack of asthma, a small amount of viscous, mucous sputum is released, and dry wheezing rales are heard in the lungs. At the stage of alveolar edema, such differences from bronchial asthma as the forced (sitting) position of the patient, rapid breathing and the inspiratory or mixed nature of suffocation, remain.
Thromboembolism of the branches of the pulmonary artery in some patients is accompanied by bilateral or unilateral dry wheezing and an attack of suffocation resembling an asthma attack. In differential diagnosis, it is necessary to take into account the presence of thrombosis (thrombophlebitis) of the veins of the lower extremities and pelvis, pain in the chest. Patients, as a rule, in contrast to BA patients, do not strive to assume the "orthopnea" position, but prefer the horizontal position.
A cough with bloody sputum is common. On examination, swelling of the cervical veins, a positive venous pulse, increased cardiac impulse, an accent of the II tone, systolic and diastolic murmurs on the pulmonary artery, and sometimes pericardial friction are also noted. On the ECG, in 70-80% of cases, signs of acute overload of the right chambers of the heart are found. Moist wheezing in the lung, which is a sign of infarction pneumonia, appears 4-5 days after the development of thromboembolism of the branches of the pulmonary artery. In these cases, pleural friction noise may be heard.
Violation of the nervous regulation of breathing is more often observed with hysteria and neuro-circulatory dystonia (NDC).
In hysteria, suffocation may be associated with spasm of the glottis. This leads to a sharp obstruction of inhalation, which is performed with a whistling sound (stridor breathing). Respiratory movements slow down, become deep; at the height of the attack, temporary respiratory arrest may occur. Due to the strong opposition to the flow of air into the lungs, the lower part of the chest is drawn in with each inhalation (it normally expands). With laryngoscopy, prolonged convulsive contractions of the vocal cords can be observed after short-term opening. The inspiratory nature of suffocation, the absence of wheezing in the lungs distinguish this form of hysterical asthma from asthma.
In another variant of hysterical asthma, difficulty breathing is associated with a convulsive contraction of the respiratory muscles. For this reason, the chest during an attack makes frequent (up to 50-60 or more per minute) and usually intensified respiratory movements, which are compared to "breathing of a driven dog." Such rapid breathing is not typical for bronchial asthma. Another important difference is the absence of changes during a hysterical attack of suffocation during physical examination of the lungs (boxed percussion sound, hard breathing, wheezing on exhalation).
An attack of hysterical asthma lasts from 2-3 minutes to several tens of minutes and, due to an unusual emotional coloring (often accompanied by inappropriate behavior, convulsive crying or, conversely, hysterical laughter) creates a painful impression on others. Correct diagnosis of these attacks and the use of inhalation of hot water vapor, sedatives, in severe cases, giving anesthesia relieve the attack.
In our practice, we have often observed erroneous diagnosis of asthma in patients with NCD, when a violation of the nervous regulation of respiration is associated with the functional lability of the respiratory center. With NCD, the syndrome of respiratory disorders is manifested by a feeling of lack of air (shortness of breath), "dissatisfaction" with inhalation, a feeling of a "lump" in the throat and respiratory arrhythmia: the patient makes frequent (up to 30-50 per minute), then more rare respiratory movements, periodically may to stop breathing for 5-10 s, after which the patient takes deep breaths, called "melancholy sighs", or "deep sighs of a neurasthenic".
The described subjective symptomatology is completely different from changes in breathing in AD. An objective examination, in contrast to asthma, with a respiratory disorder in patients with NCD (da Costa's syndrome), no objective changes in the respiratory system is determined.
Bronchial asthma as an independent disease must be differentiated from the so-called hypereosinophilic bronchial asthma, which is a manifestation of the Churg-Strauss syndrome, which was previously considered one of the variants of polyarteritis nodosa, and now it has been isolated into an independent nosological form. Diagnosis of this syndrome is facilitated when a patient is diagnosed with polysystemic symptoms: weight loss, kidney damage with secondary arterial hypertension, asymmetric polyneuritis, coronaritis, abdominal syndrome.
Differential diagnosis is significantly complicated in cases when asthma attacks in patients with Churg-Strauss syndrome appear at the onset of the disease, sometimes several months or years before the appearance of other signs of the disease.
In such cases, in favor of hypereosinophilic asthma, the severity of asthma attacks, insufficient effectiveness of bronchodilators (the effect occurs when glucocorticosteroids (GKS)), higher eosinophilia (usually more than 20%, and in absolute numbers more than 1,500 in 1 μl, while in AD, eosinophilia usually does not exceed 20%) in combination with hyperleukocytosis, frequent detection of pulmonary eosinophilic infiltrates or allergic pneumonia on the radiograph ... Of course, the diagnosis becomes convincing only as other signs of Churg-Strauss syndrome appear. By this time, the severity of asthma attacks and the severity of eosinophilia usually diminish up to complete disappearance.
Of the hormone-active tumors, paroxysmal bronchial obstruction syndrome is most often found in carcinoid tumors originating from the cells of the APUD system and producing biologically active substances and hormones, mainly serotonin, bradykinin, prostaglandins, gastrin, glucagon, adrenocorticotropic hormone (ACTH)... Carcinoid tumor is more often localized in organs abdominal, much less often (in 5-7% of cases) - in the bronchus. It is for this localization of the tumor that the development of an acute broncho-obstructive syndrome, reminiscent of an asthma attack, is characteristic.
Unlike bronchial asthma, when suffocating in patients with carcinoid tumor due to the release of biologically active substances, mainly serotonin, there are hot flushes and hyperemia of the face and upper half of the body, diarrhea (watery stools), rumbling in the abdomen. In the blood, the content of serotonin is increased, in the urine - the product of its metabolism - 5-hydroxyindoleacetic acid. To detect a tumor, x-ray and endoscopic examination, supplemented by a biopsy, are performed.
The bronchial obstruction syndrome due to dysfunction of the digestive system is most often caused by gastroesophageal reflux and is associated with repeated aspiration of stomach contents. Such a mechanism of bronchial obstruction can be suspected in the presence of heartburn and dysphagia that appear at night.
Thus, asthma must be differentiated from a large number of other diseases, but the greatest practical value is differential diagnosis bronchial asthma with
In the pre-asthma stage, many patients have allergic or polypous rhinosinusitis. The manifestations of predastma proper include paroxysmal cough (dry or with the release of a small amount of mucous viscous sputum), which is not relieved by conventional antitussive drugs and is eliminated by B.'s treatment. Coughing fits usually occur at night or in the early morning hours. Most often, a cough remains after a postponed respiratory viral infection or exacerbation of chronic bronchitis, pneumonia. The patient does not yet experience breathing difficulties. With auscultation of the lungs, hard breathing is sometimes determined, very rarely - dry rales with forced expiration. Eosinophilia is found in the blood and sputum. When examining the functions of external respiration (FVD) before and after inhalation of a β-adrenergic agonist (Izadrin, Beroteka, etc.), a significant increase in the expiratory power can be established, indicating the so-called latent bronchospasm.
In the subsequent stages of B.'s development and. its main manifestations are asthma attacks, and in severe cases, also states of progressive suffocation, designated as status asthmaticus.
Bronchial asthma attack develops relatively suddenly, in some patients after certain individual precursors (sore throat, itchy skin, nasal congestion, rhinorrhea, etc.). There is a feeling of chest congestion, shortness of breath, a desire to cough up, although the cough during this period is mostly dry and aggravates shortness of breath. Difficulty breathing, which the patient experiences at first only on exhalation, increases, which forces the patient to take a sitting position to activate the auxiliary respiratory muscles (see Respiratory system). There are wheezing in the chest, which at first is felt only by the patient himself (or the doctor who listens to his lungs), then they become audible at a distance (distant wheezing) as a combination of different heights of the voices of the playing accordion (musical wheezing). At the height of the attack, the patient experiences severe suffocation, difficulty not only exhaling, but also inhaling (due to the setting in the respiratory pause of the chest and diaphragm in the position of deep inhalation).
The patient sits, resting his hands on the edge of the seat. The chest is expanded; exhalation is significantly lengthened and is achieved by visible tension of the muscles of the chest and trunk (expiratory dyspnea); the intercostal spaces are drawn in on inhalation; the cervical veins swell on exhalation, collapse on inhalation, reflecting significant differences in intrathoracic pressure in the phases of inhalation and exhalation. With percussion of the chest, the box sound, the lowering of the lower border of the lungs and the restriction of the respiratory mobility of the diaphragm are determined, which is also confirmed with x-ray examination, revealing also a significant increase in the transparency of the pulmonary fields (acute distention of the lungs). Auscultation over the lungs reveals hard breathing and abundant dry rales of different tones with a predominance of buzzing (at the beginning and at the end of the attack) or sibilant (at the height of the attack). Palpitations are quickened. Heart sounds are often poorly defined due to the distention of the lungs and the muffling volume of audible dry wheezing.
The attack can last from several minutes to 2-4 hours (depending on the treatment used). The resolution of the attack is usually preceded by a cough with a small amount of phlegm. The difficulty in breathing decreases and then disappears.
Asthmatic status is defined as a life-threatening increasing bronchial obstruction with progressive impairment of ventilation and gas exchange in the lungs, which is not relieved by bronchodilators, which are usually effective in this patient.
There are three options for the onset of status asthmaticus: the rapid development of coma (sometimes observed in patients after the withdrawal of glucocorticoids), the transition to the asthmatic status of an asthma attack (often against the background of an overdose of adrenergic agonists) and the slow development of progressive suffocation, most often in patients with infectious B. a ... According to the severity of the patient's condition and the degree of gas exchange disorders, three stages of status asthmaticus are distinguished.
Stage I is characterized by the appearance of persistent expiratory dyspnea, against the background of which frequent attacks of suffocation occur, forcing patients to resort to repeated inhalations of adrenomimetics, but the latter only temporarily relieve suffocation (without completely eliminating expiratory dyspnea), and after a few hours this effect is also lost. The patients are somewhat agitated. Percussion and auscultation of the lungs reveal changes similar to those in B.'s attack and., But dry wheezing is usually less abundant and high-tone wheezing prevails. As a rule, tachycardia is determined, especially pronounced with intoxication with adrenergic agonists, when tremors of the fingers of the hands, pallor, increased systolic blood pressure, sometimes extrasystole, and dilated pupils are also found. The tension of oxygen (pO 2) and carbon dioxide (pCO 2) in arterial blood is close to normal, there may be a tendency to hypocapnia.
Stage II of status asthmaticus is characterized by a severe degree of expiratory suffocation, fatigue 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 reclining. Excitement is replaced by more and more prolonged periods of apathy. The tongue, skin of the face and trunk are cyanotic. Breathing remains quickened, but it is less deep than in stage I. Percussion is determined by the picture of acute swelling of the lungs, auscultatory - weakened hard breathing, which over some parts of the lungs may not be heard at all (zones of the "silent" lung). The amount of audible dry wheezing is significantly reduced (there are not abundant and quiet wheezing wheezes). Tachycardia, sometimes extrasystole is noted; on the ECG - signs of pulmonary hypertension (see. Hypertension of the pulmonary circulation), a decrease in the T wave in most leads. The pO 2 of arterial blood drops to 60-50 mm Hg. Art., moderate hypercapnia is possible.
Stage III of status asthmaticus is characterized by pronounced arterial hypoxemia (pO 2 within 40-50 mm Hg) and increasing hypercapnia (pCO 2 above 80 mm Hg) with the development of respiratory acidotic coma. Severe diffuse cyanosis is noted. Dryness of mucous membranes, decreased tissue turgor (signs of dehydration) are often 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 sounds with the expansion of the zones of the "silent" lung. 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 brochial asthma have features of anamnesis, clinical manifestations and course.
Atopic B. and. often begins in childhood or adolescence. A family history of more than 50% of cases reveals asthma or other atonic diseases, in the patient's history - allergic rhinitis, atopic dermatitis. To attacks of suffocation at atopic B. and. often preceded by prodromal symptoms: 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 the typical pattern of expiratory suffocation with remote dry wheezing quickly develops. Usually, an attack can be quickly stopped by using? -Adrenomimetics or aminophylline; the attack ends with the release of a small amount of light viscous sputum. After an attack, auscultatory symptoms of asthma are completely eliminated or remain minimal.
For atopic B. and. characterized by a relatively mild course, late development of complications. A severe course, the development of status asthmaticus are rare. In the first years of the disease, remissions are typical when contact with allergens is terminated. Spontaneous remissions are not uncommon. Complete recovery at atopic B. and. rarely in adults.
Infection-dependent B. and. observed in individuals different ages, but adults are more likely to get sick. A family history of asthma is relatively common, and atopic diseases are rare. B.'s combination is characteristic 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 system (sinusitis, bronchitis, pneumonia). Asthma attacks differ less than with atopic B. and., The severity of development, longer duration, less clear and rapid resolution in response to the use of adrenergic agonists. After the relief of the attack during auscultation of the lungs, hard breathing with prolonged exhalation, dry buzzing rales persist, in the presence of inflammatory exudate in the bronchi - moist rales. With this form B. and. a severe course with repeated asthmatic states is more common, complications develop faster.
Aspirin asthma in typical cases is characterized by B.'s combination and. with recurrent polyposis of the nose and its paranasal sinuses and intolerance to acetylsalicylic acid (the so-called aspirin triad, sometimes referred to as the asthmatic triad). However, nasal polyposis is sometimes absent. More often adult women are ill, but the disease also occurs in children. It usually begins with polyposis rhinosinusitis; polyps after their removal quickly recur. At some stage of the disease, after the next polypectomy or taking aspirin, analgin is joined by B. and., The manifestations of which persist in the future and without taking non-steroidal anti-inflammatory drugs. Taking these drugs invariably causes exacerbations of the disease of varying severity - from manifestations of rhinitis to severe asthmatic status with a fatal outcome. Polypectomy is also quite often accompanied by severe exacerbations of B. and. The majority of clinicians believe that for aspirin B. and. severe course is characteristic. Atopy is rare among these patients.
Asthma of physical effort, or post-exercise bronchospasm, is not, apparently, an independent form of B. a. It has been established that in 50-90% of patients with any form of B. and. physical effort can cause an attack of suffocation 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? -adrenomimetic. Exercise asthma is more common in children than in adults. It has been noticed that some types of physical efforts (running, playing football, basketball) especially often cause post-exercise bronchospasm. Lifting weights is less dangerous; swimming and rowing are relatively well tolerated. The duration of physical activity also matters. In a provocative test, loads are usually given for 6-8 minutes; with a longer load (12-16 minutes), the severity of post-exercise bronchospasm may be less - the patient, as it were, jumps over bronchospasm.