"Difficult" asthma: life goes on. Bronchial asthma Treatment of severe bronchial asthma

Bronchial asthma, asthma, choking attacks, suffocation, asphyxia due to illness, shortness of breath

Version: Directory of Diseases MedElement

Asthma (J45)

Pulmonology

general information

Short description

Bronchial asthma* is a chronic inflammatory disease of the respiratory tract, in which many cells and cellular elements are involved. Chronic inflammation causes bronchial hyperreactivity leading to recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing (especially at night or in the early morning). These episodes are usually associated with widespread but variable airway obstruction in the lungs, which is often reversible spontaneously or with treatment.

Bronchial hyperreactivity - increased sensitivity of the lower respiratory tract to various irritating stimuli, which, as a rule, are contained in the inhaled air. These stimuli are indifferent to healthy people. Clinically, bronchial hyperreactivity is most often manifested by episodes of wheezing shortness of breath in response to the action of an irritating stimulus in individuals with a hereditary predisposition.
Latent bronchial hyperreactivity is also distinguished, which is detected only by provocative functional tests with histamine and methacholine.
Bronchial hyperreactivity can be specific and nonspecific.

Specific hyperreactivity occurs in response to exposure to certain allergens, mainly contained in the air (plant pollen, house dust, wool and epidermis of domestic animals, fluff and feathers of poultry, spores and other elements of fungi).

Nonspecific hyperreactivity is formed under the influence of various stimuli of non-allergenic origin (aeropollutants, industrial gases and dust, endocrine disorders, physical activity, neuropsychic factors, respiratory infections, etc.).

Note. Excluded from this subsection are:

Asthmatic status - J46;
- Other chronic obstructive pulmonary disease - J44;
- Lung diseases caused by external agents - J60-J70;
- Pulmonary eosinophilia, not elsewhere classified - J82.

* Definition according to GINA (Global Initiative for Asthma) - Revision 2011.

Classification

Classification of asthma is based on a joint assessment of the symptoms of the clinical picture and indicators of lung function. There is no generally accepted classification of bronchial asthma. Below are examples of the most commonly used classifications.

Classification of bronchial asthma (BA) according to Fedoseev G. B. (1982)

1. Stages of BA development:

1.1The state of betrayal- conditions that threaten the onset of asthma (acute and chronic bronchitis, pneumonia with elements of bronchospasm, combined with vasomotor rhinitis, urticaria, vasomotor edema, migraine and neurodermatitis in the presence of eosinophilia in the blood and an increased content of eosinophils in sputum, due to immunological or non-immunological mechanisms of pathogenesis) .

1.2 Clinically diagnosed BA- after the first attack or asthma status (this term is used mainly in screening studies).

2. BA forms(not included in the formulation of the clinical diagnosis):

immunological form.
- non-immunological form

3. Pathogenetic mechanisms of AD:
3.1 Atonic - indicating the allergenic allergen or allergens.
3.2 Infection-dependent - indicating infectious agents and the nature of infectious dependence, which can be manifested by stimulation of an atopic reaction, infectious allergy and the formation of a primary altered bronchial reactivity (if the infection is an allergen, BA is defined as infectious-allergic).
3.3 Autoimmune.
3.4 Dishormonal - indicating the endocrine organ, the function of which is changed, and the nature of dishormonal changes.
3.5 Neuro-psychic - indicating options for neuro-psychic changes.
3.6 Adrenergic imbalance.
3.7 Primarily altered bronchial reactivity, which is formed without the participation of altered reactions of the immune, endocrine and nervous systems. May be congenital or acquired. Manifested under the influence of chemical, physical and mechanical irritants and infectious agents. Attacks of suffocation are characteristic during physical exertion, exposure to cold air, medicines and other things.

Note to point 3. A patient may have one pathogenetic mechanism of BA or various combinations of mechanisms are possible (by the time of the examination, one of the mechanisms is the main one). During the development of AD, a change in the main and secondary mechanisms is possible.

The separation of BA according to pathogenetic mechanisms and the isolation of the main one are significantly difficult. Nevertheless, this is justified due to the fact that each of the pathogenetic mechanisms involves a certain, unique nature of drug therapy.

4. Severity of BA(in some cases, such a division is conditional; for example, with a mild course, the patient may die from a suddenly developed asthmatic status, and with a rather severe course, a "spontaneous" remission is possible):

4.1 Easy flow: exacerbations are not long, occur 2-3 times a year. Attacks of suffocation are stopped, as a rule, by taking various bronchodilator drugs inside. In the interictal period, signs of bronchospasm, as a rule, are not detected.

4.2 Moderate course: more frequent exacerbations (3-4 times a year). Attacks of suffocation are more severe and are stopped by injections of drugs.

4.3 Severe flow: exacerbations occur frequently (5 or more times a year), differ in duration. The attacks are severe, often turning into an asthmatic state.

5. Phases of the course of bronchial asthma:

1. Aggravation- this phase is characterized by the presence of pronounced signs of the disease, primarily recurring attacks of asthma or an asthmatic condition.

2. fading exacerbation - in this phase, seizures are more rare and not severe. Physical and functional signs of the disease are less pronounced than in the acute phase.

3. Remission - typical manifestations of BA disappear (no asthma attacks occur, bronchial patency is fully or partially restored).

6. Complications:

1. Pulmonary: emphysema, pulmonary insufficiency, atelectasis, pneumothorax and others.

2. Extrapulmonary: myocardial dystrophy, cor pulmonale, heart failure and others.

Classification of asthma according to the severity of the disease and clinical signs before treatment

Step 1 Mild intermittent asthma:
- symptoms less than once a week;
- short exacerbations;
- nocturnal symptoms no more than 2 times a month;
- FEV1 or PSV>= 80% of the expected values;
- variability in FEV1 or PSV< 20%.

Step 2 Mild persistent asthma:

Symptoms more than 1 time per week, but less than 1 time per day;

- nocturnal symptoms more than 2 times a month FEV1 or PEF>= 80% of the expected values;
- variability of FEV1 or PSV = 20-30%.

Step 3 Persistent moderate asthma:

daily symptoms;
- exacerbations can affect physical activity and sleep;
- nocturnal symptoms more than once a week;
- FEV1 or PSV from 60 to 80% of the proper values;
- variability in FEV1 or PSV > 30%.

Step 4 Severe persistent asthma:
- daily symptoms;
- frequent exacerbations;
- frequent nocturnal symptoms;
- restriction of physical activity;
- FEV 1 or PSV<= 60 от должных значений;
- variability in FEV1 or PSV > 30%.

Additionally, the following are BA course phases:
- exacerbation;
- unstable remission;
- remission;
- stable remission (more than 2 years).

Classification according to the Global Asthma Initiative(GINA 2011)
The classification of asthma severity is based on the amount of therapy required to achieve disease control.

1. Mild asthma - disease control can be achieved with a small amount of therapy (low doses of inhaled corticosteroids, antileukotriene drugs or cromones).

2. Severe asthma - A large amount of therapy is needed to control the disease (eg, GINA grade 4) or control cannot be achieved despite a large amount of therapy.

Patients with different AD phenotypes have different responses to conventional treatment. With the advent of specific treatments for each phenotype, AD that was previously considered severe can become mild.
The ambiguity of the terminology associated with the severity of asthma is due to the fact that the term "severity" is also used to describe the severity of bronchial obstruction or symptoms. Severe or frequent symptoms do not necessarily indicate severe asthma, as they may be the result of inadequate treatment.

Classification according to ICD-10

J45.0 Asthma with a predominance of an allergic component (if the disease is associated with an established external allergen) includes the following clinical variants:

allergic bronchitis;

Allergic rhinitis with asthma;

atopic asthma;

Exogenous allergic asthma;

Hay fever with asthma.

J45.1 Non-allergic asthma (when the disease is associated with external factors of a non-allergenic nature or unspecified internal factors) includes the following clinical variants:

Idiosyncratic asthma;

Endogenous non-allergic asthma.

J45.8 Mixed asthma (with signs of the first two forms).

J45.9 Asthma, unspecified, which includes:

asthmatic bronchitis;

Late onset asthma.

J46 Status asthmaticus.

The formulation of the main diagnosis should reflect:
1. The form of the disease (for example, atopic or non-allergic asthma).
2. The severity of the disease (eg, severe persistent asthma).
3. The phase of the course (for example, exacerbation). In remission with steroids, it is reasonable to indicate a maintenance dose of the anti-inflammatory drug (eg, remission at a dose of 800 µg of beclomethasone per day).
4. Complications of asthma: respiratory failure and its form (hypoxemic, hypercapnic), especially asthmatic status.

Etiology and pathogenesis

According to GINA-2011, bronchial asthma (BA) is a chronic inflammatory disease of the respiratory tract, which involves a number of inflammatory cells and mediators, which leads to characteristic pathophysiological changes.

1. Inflammatory cells in the airways in asthma.

1.1 Mast cells. Under the action of allergens with the participation of high-affinity IgE receptors and under the influence of osmotic stimuli, mucosal mast cells are activated. Activated mast cells release mediators that cause bronchospasm (histamine, cysteinyl leukotrienes, prostaglandin D2). An increased number of mast cells in airway smooth muscle may be associated with bronchial hyperreactivity.

1.2 Eosinophils. In the airways, the number of eosinophils is increased. These cells secrete the main proteins that can damage the epithelium of the bronchi. Also, eosinophils may be involved in the release of growth factors and airway remodeling.

1.3 T-lymphocytes. In the respiratory tract, there is an increased number of T-lymphocytes that release specific cytokines that regulate the process of eosinophilic inflammation and the production of IgE by B-lymphocytes. The increase in Th2 cell activity may be partly due to a decrease in the number of regulatory T cells that normally inhibit Th2 lymphocytes. It is also possible to increase the number of inKT cells that secrete Th1 and Th2 cytokines in large quantities.

1.4 Dendritic cells capture allergens from the surface of the bronchial mucosa and migrate to regional lymph nodes, where they interact with regulatory T cells and ultimately stimulate the conversion of undifferentiated T lymphocytes into Th2 cells.

1.5 macrophages. The number of macrophages in the respiratory tract is increased. Their activation may be associated with the action of allergens with the participation of IgE receptors with low affinity. Due to the activation of macrophages, inflammatory mediators and cytokines are released, which enhance the inflammatory response.

1.6 Neutrophils. In the respiratory tract and sputum of patients with severe asthma and smokers, the number of neutrophils increases. Their pathophysiological role has not been elucidated. It is assumed that an increase in their number may be a consequence of GCS therapy. GCS (glucocorticoids, glucocorticosteroids) - drugs one of the leading properties of which is to inhibit the early stages of the synthesis of the main participants in the formation of inflammatory processes (prostaglandins) in various tissues and organs.
.

2.mediators of inflammation. Currently, more than 100 different mediators are known that are involved in the pathogenesis of asthma and the development of a complex inflammatory response in the airways.

3.Structural changes in the airways - are detected in the airways of patients with asthma and are often considered as a process of bronchial remodeling. Structural changes may be the result of repair processes in response to chronic inflammation. Due to the deposition of collagen fibers and proteoglycans under the basement membrane, subepithelial fibrosis develops, which is observed in all patients with asthma (including children) even before the onset of clinical manifestations of the disease. The severity of fibrosis may decrease with treatment. The development of fibrosis is also observed in other layers of the bronchial wall, in which collagen and proteoglycans are also deposited.

3.1 Smooth muscle of the bronchial wall. due to hypertrophy Hypertrophy - the growth of an organ, part of it or tissue as a result of cell multiplication and an increase in their volume
and hyperplasia Hyperplasia - an increase in the number of cells, intracellular structures, intercellular fibrous formations due to enhanced organ function or as a result of a pathological tissue neoplasm.
there is an increase in the thickness of the smooth muscle layer, which contributes to the overall thickening of the bronchus wall. This process may depend on the severity of the disease.

3.2Blood vessels. Under the influence of growth factors, such as vascular endothelial growth factor (VEGF), there is a proliferation Proliferation - an increase in the number of cells of a tissue due to their reproduction
vessels of the bronchial wall, contributing to the thickening of the bronchial wall.

3.3 Mucus hypersecretion observed as a result of an increase in the number of goblet cells in the epithelium of the respiratory tract and an increase in the size of the submucosal glands.

4. Narrowing of the airways- the universal final stage of the pathogenesis of AD, which leads to the onset of symptoms of the disease and typical physiological changes.

Factors causing narrowing of the airways:

4.1 Contraction of the smooth muscles of the bronchial wall in response to the bronchoconstrictor action of various mediators and neurotransmitters is the main mechanism of airway constriction; almost completely reversible under the action of bronchodilators.

4.2 Airway edema due to increased permeability of the microvascular bed, which is caused by the action of inflammatory mediators. Edema can play a particularly important role in exacerbations.

4.3 Thickening of the bronchus wall as a result of structural changes. This factor may be of great importance in severe asthma. Bronchial wall thickening is not fully reversible with existing drugs.

4.4 Mucus hypersecretion can lead to occlusion Occlusion is a violation of the patency of some hollow formations in the body (blood and lymphatic vessels, subarachnoid spaces and cisterns), due to the persistent closure of their lumen in any area.
bronchial lumen ("mucus plugs") and is the result of increased secretion of mucus and the formation of an inflammatory exudate.

Features of the pathogenesis are described for the following forms of AD:
- exacerbation of BA;
- night BA;
- irreversible bronchial obstruction;
- BA, difficult to treat;
- BA in smokers;
- aspirin triad.

Epidemiology

In the world, bronchial asthma affects about 5% of the adult population (1-18% in different countries). In children, the incidence varies from 0 to 30% in different countries.

The onset of the disease is possible at any age. Approximately half of the patients develop bronchial asthma before the age of 10 years, in a third - up to 40 years.
Among children with bronchial asthma, there are twice as many boys as girls, although the sex ratio levels off by the age of 30.

Factors and risk groups

Factors affecting the risk of developing AD are divided into:
- factors causing the development of the disease - internal factors (primarily genetic);
- factors that provoke the onset of symptoms - external factors.
Some factors belong to both groups.
The mechanisms of influence of factors on the development and manifestations of AD are complex and interdependent.

Internal factors:

1. Genetic (for example, genes predisposing to atopy and genes predisposing to bronchial hyperreactivity).

2. Obesity.

External factors:

1. Allergens:

Room allergens (house dust mites, pet hair, cockroach allergens, fungi, including mold and yeast);

External allergens (pollen, fungi, including molds and yeasts).

2. Infections (mainly viral).

3. Professional sensitizers.

4. Tobacco smoking (passive and active).

5. Air pollution indoors and outdoors.

6. Nutrition.

Examples of substances that cause the development of asthma in certain occupations

Profession	Substance
	Proteins of animal and vegetable origin
Bakers	Flour, amylase
Cattle farmers	Warehouse tongs
Detergent production	Bacillus subtilis enzymes
Electrical soldering	Rosin
Crop farmers	soy dust
Production of fish products
Food production	Coffee dust, meat tenderizers, tea, amylase, shellfish, egg whites, pancreatic enzymes, papain
Granary workers	Warehouse mites, Aspergillus. Weed particles, ragweed pollen
Medical workers	Psyllium, latex
poultry farmers	Poultry mites, bird droppings and feathers
Researchers-experimenters, veterinarians	Insects, dander and animal urine proteins
Sawmill workers, carpenters	wood dust
Movers/transport workers	grain dust
Silk workers	Butterflies and silkworm larvae
	inorganic compounds
Beauticians	Persulfate
Platters	Nickel salts
Oil refinery workers	Salts of platinum, vanadium organic compounds
Car painting	Ethanolamine, diisocyanates
Hospital workers	Disinfectants (sulfathiazole, chloramine, formaldehyde), latex
Pharmaceutical production	Antibiotics, piperazine, methyldopa, salbutamol, cimetidine
Rubber processing	Formaldehyde, ethylenediamide
Plastics production	Acrylates, hexamethyl diisocyanate, toluine diisocyanate, phthalic anhydride

Elimination of risk factors can significantly improve the course of asthma.

In patients with allergic asthma, elimination of the allergen is of paramount importance. There is evidence that in urban areas in children with atopic asthma, individual complex measures for the removal of allergens in the homes led to a decrease in soreness.

Clinical picture

Clinical Criteria for Diagnosis

Unproductive hacking cough, prolonged expiration, dry, wheezing, usually treble, wheezing in the chest, more at night and in the morning, attacks of expiratory choking, chest congestion, dependence of respiratory symptoms on contact with provoking agents.

Symptoms, course

Clinical diagnosis of bronchial asthma(BA) is based on the following data:

1. Identification of bronchial hyperreactivity, as well as reversibility of obstruction spontaneously or under the influence of treatment (decrease in response to appropriate therapy).
2. Unproductive hacking cough; prolonged exhalation; dry, whistling, usually treble, rales in the chest, more marked at night and in the morning; expiratory dyspnea, attacks of expiratory suffocation, congestion (stiffness) of the chest.
3. Dependence of respiratory symptoms on contact with provoking agents.

Also of great importance are the following factors:
- the appearance of symptoms after episodes of contact with the allergen;
- seasonal variability of symptoms;
- a family history of asthma or atopy.

When diagnosing, you need to find out the following questions:
- Does the patient have episodes of wheezing, including recurring ones?

Does the patient have a cough at night?

Does the patient have wheezing or cough after exercise?

Does the patient have episodes of wheezing, chest congestion, or coughing after exposure to aeroallergens or pollutants?

Does the patient report that the cold "goes down to the chest" or continues for more than 10 days?

Does the severity of symptoms decrease after the use of appropriate anti-asthma drugs?

On physical examination, there may be no symptoms of asthma, due to the variability in the manifestations of the disease. The presence of bronchial obstruction is confirmed by wheezing that is detected during auscultation.
In some patients, wheezing may be absent or detected only during forced exhalation, even in the presence of severe bronchial obstruction. In some cases, patients with severe exacerbations of asthma do not wheeze due to severe limitation of airflow and ventilation. In such patients, as a rule, there are other clinical signs indicating the presence and severity of an exacerbation: cyanosis, drowsiness, difficulty in speaking, swollen chest, participation of auxiliary muscles in the act of breathing and retraction of the intercostal spaces, tachycardia. These clinical symptoms can only be observed when examining the patient during the period of pronounced clinical manifestations.

Variants of clinical manifestations of AD

1.Cough variant of BA. The main (sometimes the only) manifestation of the disease is a cough. Cough asthma is most common in children. The severity of symptoms increases at night, and during the day the manifestations of the disease may be absent.
For such patients, it is important to study the variability of lung function or bronchial hyperreactivity, as well as the determination of eosinophils in sputum.
The cough variant of asthma is differentiated from the so-called eosinophilic bronchitis. In the latter, patients present with cough and sputum eosinophilia, but have normal lung function on spirometry and normal bronchial reactivity.
In addition, cough can occur due to the use of ACE inhibitors, gastroesophageal reflux, postnasal drip syndrome, chronic sinusitis, dysfunction of the vocal cords.

2. Bronchospasm induced by physical activity. Refers to the manifestation of non-allergic forms of asthma, when the phenomena of airway hyperreactivity dominate. In the majority of cases, physical activity is an important or only cause of the onset of symptoms of the disease. Bronchospasm as a result of physical activity, as a rule, develops 5-10 minutes after the cessation of exercise (rarely - during exercise). Patients have typical symptoms of asthma or sometimes a prolonged cough that resolves on its own within 30-45 minutes.
Forms of exercise such as running cause asthma symptoms more frequently.
Exercise-induced bronchospasm often develops when inhaling dry, cold air, more rarely in hot and humid climates.
In favor of asthma is evidenced by the rapid improvement in the symptoms of post-exercise bronchospasm after inhaled β2-agonist, as well as the prevention of the development of symptoms due to inhaled β2-agonist before exercise.
In children, asthma can sometimes manifest itself only during exercise. In this regard, in such patients or in the presence of doubts about the diagnosis, it is advisable to conduct a test with physical activity. Diagnosis is facilitated by a protocol with an 8-minute run.

Clinical picture of an asthma attack quite typical.
In case of allergic etiology of BA, before the development of suffocation, itching (in the nasopharynx, auricles, in the chin area), nasal congestion or rhinorrhea, feelings of lack of "free breathing", dry cough can be observed. elongated; the duration of the respiratory cycle increases and the respiratory rate decreases (up to 12-14 per minute).
During listening to the lungs in the bulk of cases, against the background of an extended expiration, a large number of scattered dry rales, mostly whistling, are determined. As the asthma attack progresses, wheezing wheezes on expiration are heard at a certain distance from the patient in the form of "wheezing" or "bronchial music".

With a prolonged attack of suffocation, which lasts more than 12-24 hours, there is a blockage of the small bronchi and bronchioles with an inflammatory secret. The general condition of the patient is significantly aggravated, the auscultatory picture changes. Patients experience excruciating shortness of breath, aggravated by the slightest movement. The patient takes a forced position - sitting or half-sitting with fixation of the shoulder girdle. All auxiliary muscles participate in the act of breathing, the chest expands, and the intercostal spaces are drawn in during inspiration, cyanosis of the mucous membranes, acrocyanosis, arises and intensifies. It is difficult for the patient to speak, the sentences are short and jerky.
During auscultation, there is a decrease in the number of dry rales, in some places they are not heard at all, as well as vesicular breathing; so-called silent lung zones appear. Above the surface of the lungs, percussion is determined by a pulmonary sound with a tympanic shade - a box sound. The lower edges of the lungs are lowered, their mobility is limited.
The completion of an asthma attack is accompanied by a cough with a discharge of a small amount of viscous sputum, easier breathing, a decrease in shortness of breath and the number of auscultated wheezing. Even for a long time, a few dry rales can be heard while maintaining an elongated exhalation. After the cessation of the attack, the patient often falls asleep. Signs of asthenia persist for a day or more.

Exacerbation of asthma(attacks of asthma, or acute asthma) according to GINA-2011 is divided into mild, moderate, severe, and such an item as "breathing is inevitable." The severity of the course of BA and the severity of exacerbation of BA are not the same thing. For example, with mild asthma, exacerbations of mild and moderate severity can occur; with asthma of moderate severity and severe, exacerbations of mild, moderate, and severe are possible.

The severity of BA exacerbation according to GINA-2011

	Lung	Middle gravity	heavy	Stopping breathing is inevitable
Dyspnea	When walking. May lie	When talking; children crying getting quieter and shorter having difficulty feeding. Prefers to sit	At rest, children stop eating. Sitting leaning forward
Speech	Offers	Phrases	words
Level wakefulness	May be aroused	Usually aroused	Usually aroused	Inhibited or confused mind
Breathing rate	Increased	Increased	More than 30 min.
Participation of auxiliary muscles in the act of breathing and retraction of the supraclavicular fossae	Usually no	Usually there	Usually there	Paradoxical movements chest and abdominal walls
wheezing	Moderate, often only exhale	Loud	Usually loud	Missing
Pulse (in min.)	<100	>100	>120	Bradycardia
Paradoxical pulse	Absent <10 мм рт. ст.	May have 10-25 mmHg st	Often available >25 mmHg Art. (adults) 20-40 mmHg Art. (children)	Absence allows assume fatigue respiratory muscles
PSV after the first injection bronchodilator in % of due or the best individual value	>80%	About 60-80%	<60% от должных или наилучших individual values (<100 л/мин. у взрослых) or the effect lasts<2 ч.	Impossible to rate
PaO 2 in kPa (when breathing air)	Normal. Analysis is usually not needed.	>60 mmHg Art.	<60 мм рт. ст. Possible cyanosis
PaCO 2 in kPa (when breathing air)	<45 мм рт. ст.	<45 мм рт. ст.	>45 mmHg Art. Possible respiratory failure
SatO 2,% (when breathing air) - oxygen saturation or the degree of saturation of arterial blood hemoglobin with oxygen	>95%	91-95%	< 90%

Notes:
1. Hypercapnia (hypoventilation) develops more often in young children than in adults and adolescents.
2. Normal heart rate in children:

Infant (2-12 months)<160 в минуту;

Younger age (1-2 years old)<120 в минуту;

Preschool and school age (2-8 years)<110 в минуту.
3. Normal respiratory rate in awake children:

Under 2 months< 60 в минуту;

2-12 months< 50 в минуту;

1-5 years< 40 в минуту;

6-8 years old< 30 в минуту.

Diagnostics

Fundamentals of diagnosing bronchial asthma(BA):
1. Analysis of clinical symptoms, which are dominated by periodic attacks of expiratory suffocation (for more details, see the "Clinical picture" section).
2. Determination of indicators of pulmonary ventilation, most often with the help of spirography with registration of the "flow-volume" curve of forced expiration, identification of signs of reversibility of bronchial obstruction.
3. Allergological research.
4. Identification of nonspecific bronchial hyperreactivity.

The study of indicators of the function of external respiration

1. Spirometry Spirometry - measurement of vital capacity of the lungs and other lung volumes using a spirometer
. In patients with asthma, signs of bronchial obstruction are often diagnosed: a decrease in indicators - PEF (peak expiratory volumetric velocity), MOS 25 (maximum volumetric velocity at the point of 25% FVC, (FEF75) and FEV1.

To assess the reversibility of bronchial obstruction is used pharmacological bronchodilation test with short-acting β2-agonists (most often salbutamol). Before the test, you should refrain from taking short-acting bronchodilators for at least 6 hours.
Initially, the initial curve "flow-volume" forced breathing of the patient is recorded. Then the patient makes 1-2 inhalations of one of the short and fast acting β2-agonists. After 15-30 minutes, the flow-volume curve is recorded. With an increase in FEV1 or FOS ex by 15% or more, airway obstruction is considered reversible or bronchodilator-reactive, and the test is considered positive.

For asthma, it is diagnostically important to identify a significant daily variability in bronchial obstruction. For this, spirography (when the patient is in the hospital) or peak flowmetry (at home) is used. Scatter (variability) of FEV1 or POS vyd more than 20% during the day is considered to confirm the diagnosis of BA.

2. Peakflowmetry. It is used to evaluate the effectiveness of treatment and to objectify the presence and severity of bronchial obstruction.
Peak expiratory flow rate (PEF) is estimated - the maximum speed at which air can exit the respiratory tract during a forced exhalation after a full breath.
The patient's PSV values ​​are compared with normal values ​​and with the best PSV values ​​observed in this patient. The level of decrease in PSV allows us to draw conclusions about the severity of bronchial obstruction.
The difference between PSV values ​​measured during the day and in the evening is also analyzed. A difference of more than 20% indicates an increase in bronchial reactivity.

2.1 Intermittent asthma (stage I). Daytime attacks of shortness of breath, cough, wheezing occur less than 1 time per week. Duration of exacerbations - from several hours to several days. Night attacks - 2 or less times a month. In the period between exacerbations, lung function is normal; PSV - 80% of normal or less.

2.2 Mild persistent asthma (stage II). Daytime attacks are observed 1 or more times a week (not more than 1 time per day). Night attacks are repeated more often than 2 times a month. During an exacerbation, the activity and sleep of the patient may be disturbed; PSV - 80% of normal or less.

2.3 Persistent asthma of moderate severity (stage III). Daily attacks of suffocation, once a week there are nocturnal attacks. As a result of exacerbations, the patient's activity and sleep are disturbed. The patient is forced to use short-acting inhaled beta-adrenergic agonists daily; PSV - 60 - 80% of the norm.

2.4 Severe course of persistent asthma (stage IV). Daytime and nighttime symptoms are permanent, which limits the patient's physical activity. The PSV index is less than 60% of the norm.

3. Allergological study. Allergological history is analyzed (eczema, hay fever, family history of asthma or other allergic diseases). Positive skin tests with allergens and elevated blood levels of total and specific IgE testify in favor of AD.

4. Provocative Tests with histamine, methacholine, physical activity. They are used to detect nonspecific bronchial hyperreactivity, manifested by latent bronchospasm. Performed in patients with suspected asthma and normal spirography.

In the histamine test, the patient inhales nebulized histamine in progressively increasing concentrations, each of which is capable of causing bronchial obstruction.
The test is assessed as positive if the air flow rate deteriorates by 20% or more as a result of histamine inhalation at a concentration one or more orders of magnitude lower than that which causes similar changes in healthy people.
Similarly, a test with methacholine is carried out and evaluated.

5. Additional research:
- radiography of the chest in two projections - most often show signs of emphysema (increased transparency of the lung fields, depletion of the lung pattern, low standing of the domes of the diaphragm), while the absence of infiltrative and focal changes in the lungs is important;
- fibrobronchoscopy;

Electrocardiography.
Additional studies are being carried out in atypical asthma and resistance to anti-asthma therapy.

Main diagnostic criteria for AD:

1. The presence in the clinical picture of the disease of periodic attacks of expiratory suffocation, which have their beginning and end, passing spontaneously or under the influence of bronchodilators.
2. Development of asthmatic status.
3. Determination of signs of bronchial obstruction (FEV1 or POS vyd< 80% от должной величины), которая является обратимой (прирост тех же показателей более 15% в фармакологической пробе с β2-агонистами короткого действия) и вариабельной (колебания показателей более 20% на протяжении суток).
4. Identification of signs of bronchial hyperreactivity (hidden bronchospasm) in patients with initial normal indicators of pulmonary ventilation using one of three provocative tests.
5. The presence of a biological marker - a high level of nitric oxide in the exhaled air.

Additional diagnostic criteria:
1. The presence in the clinical picture of symptoms that may be "small equivalents" of an attack of expiratory suffocation:
- unmotivated cough, often at night and after exercise;
- recurring sensations of chest tightness and / or episodes of wheezing;
- the fact of awakening at night from the indicated symptoms strengthens the criterion.
2. Aggravated allergic history (presence of eczema, hay fever, pollinosis in a patient) or aggravated family history (BA, atopic diseases in the patient's family members).

3. Positive skin tests with allergens.
4. An increase in the patient's blood level of general and specific IgE (reagins).

Professional BA

Bronchial asthma due to professional activity is often not diagnosed. Due to the gradual development of occupational asthma, it is often regarded as chronic bronchitis or COPD. This leads to incorrect treatment or its absence.

Occupational asthma should be suspected when symptoms of rhinitis, cough and/or wheezing appear, especially in nonsmokers. Establishing a diagnosis requires a systematic collection of information about work history and environmental factors in the workplace.

Criteria for the diagnosis of occupational asthma:
- well-established occupational exposure to known or suspected sensitizing agents;
- the absence of symptoms of asthma before employment or a clear worsening of the course of asthma after employment.

Laboratory diagnostics

Non-invasive determination of markers of airway inflammation

1. The study of spontaneously produced or induced by inhalation of hypertonic sputum solution on inflammatory cells - eosinophils or neutrophils. It is used to assess the activity of inflammation in the airways in asthma.

2. Determination of levels of nitric oxide (FeNO) and carbon monoxide (FeCO) in exhaled air. In patients with BA, there is an increase in the level of FeNO (in the absence of inhaled corticosteroids) compared with individuals without BA, however, these results are not specific for this disease. The role of FeNO in the diagnosis of AD has not been evaluated in prospective studies.

3. Skin tests with allergens - are the main method for assessing allergic status. Such samples are highly sensitive, easy to use and do not require much time. It should be borne in mind that incorrect sample performance can lead to false positive or false negative results.

4. The determination of specific IgE in blood serum is a more expensive method than skin tests, which does not surpass them in reliability.
In some patients, specific IgE may be detected in the absence of any symptoms and play no role in the development of AD. Thus, positive test results do not necessarily indicate the allergic nature of the disease and the association of the allergen with the development of asthma.
The presence of allergen exposure and its association with asthma manifestations should be supported by history data. The measurement of total IgE in serum is not a method of diagnosing atopy.

Clinical Tests

1. Complete blood count: during the period of exacerbation, an increase in ESR and eosinophilia are noted. Eosinophilia is not determined in all patients and cannot serve as a diagnostic criterion.

2. General sputum analysis:
- a large number of eosinophils;
- Charcot-Leiden crystals;
- Kurshman's spirals (formed due to small spastic contractions of the bronchi);
- neutral leukocytes - in patients with infectious-dependent BA in the stage of an active inflammatory process;
- release of Creole bodies during an attack.

3. Biochemical analysis of blood: changes are of a general nature. BAC is not the main diagnostic method and is prescribed to monitor the patient's condition during an exacerbation.

Differential Diagnosis

1. Differential diagnosis of BA variants.

The main differential diagnostic features of atopic and infection-dependent variants of BA(according to Fedoseev G. B., 2001)

signs	Atopic variant	infection dependent variant
Allergic diseases in the family	Often	Rare (except asthma)
Atopic disease in a patient	Often	Rarely
Connection of an attack with an external allergen	Often	Rarely
Features of an attack	Acute onset, rapid onset, usually of short duration and mild course	Gradual onset, long duration, often severe
Pathology of the nose and paranasal sinuses	Allergic rhinosinusitis or polyposis without signs of infection	Allergic rhinosinusitis, often polyposis, signs of infection
Bronchopulmonary infectious process	Usually absent	Often chronic bronchitis, pneumonia
Eosinophilia of blood and sputum	Usually moderate	Often high
Specific IgE antibodies to non-infectious allergens	Present	Missing
Skin tests with extracts of non-infectious allergens	Positive	Negative
Exercise test	More often negative	More often positive
Allergen Elimination	Possible, often effective	Impossible
Beta-agonists	Very effective	Moderately effective
Cholinolytics	Ineffective	Effective
Eufillin	Very effective	Moderately effective
Intal, Thailed	Very effective	Less effective
Corticosteroids	Effective	Effective

2. Differential diagnosis of BA is carried out with chronic obstructive pulmonary disease(COPD), which is characterized by more permanent bronchial obstruction. In patients with COPD, there is no spontaneous lability of symptoms typical of BA, there is no or significantly less daily variability in FEV1 and POS exud, complete irreversibility or less reversibility of bronchial obstruction is determined in the test with β2-agonists (increase in FEV1 is less than 15%).
Sputum in COPD is dominated by neutrophils and macrophages rather than eosinophils. In patients with COPD, the effectiveness of bronchodilator therapy is lower, more effective bronchodilators are anticholinergics, and not short-acting β2-agonists; pulmonary hypertension and signs of chronic cor pulmonale are more common.

Some features of diagnosis and differential diagnosis (according to GINA 2011)

1.In children aged 5 years and younger wheezing episodes are common.

Types of wheezing in the chest:

1.1 Transient early wheezing, which children often "outgrow" in the first 3 years of life. Such wheezing is often associated with prematurity of children and smoking parents.

1.2 Persistent wheezing with early onset (under 3 years of age). Children usually have recurrent episodes of wheezing associated with acute respiratory viral infections. At the same time, children do not have signs of atopy and there is no family history of atopy (in contrast to children of the next age group with late onset wheezing/bronchial asthma).
Wheezing episodes typically continue into school age and are still detected in a significant proportion of children as young as 12 years of age.
The cause of wheezing episodes in children under 2 years of age is usually a respiratory syncytial virus infection, in children 2-5 years of age - other viruses.

1.3 Late-onset wheezing/asthma. Asthma in these children often lasts throughout childhood and continues into adulthood. Such patients are characterized by a history of atopy (often manifested as eczema) and airway pathology typical of asthma.

With repeated episodes of wheezing, it is necessary to exclude other causes of wheezing:

Chronic rhinosinusitis;

Gastroesophageal reflux;

Recurrent viral infections of the lower respiratory tract;

cystic fibrosis;

bronchopulmonary dysplasia;

Tuberculosis;

Aspiration of a foreign body;
- immunodeficiency;

Syndrome of primary ciliary dyskinesia;

Malformations causing narrowing of the lower respiratory tract;
- Congenital heart defect.

The possibility of another disease is indicated by the appearance of symptoms in the neonatal period (in combination with insufficient weight gain); wheezing associated with vomiting, signs of focal lung damage or cardiovascular pathology.

2. Patients over 5 years of age and adults. Differential diagnosis should be carried out with the following diseases:

Hyperventilation syndrome and panic attacks;

Obstruction of the upper respiratory tract and aspiration of foreign bodies;

Other obstructive pulmonary diseases, especially COPD;

Non-obstructive lung disease (eg, diffuse lesions of the lung parenchyma);

Non-respiratory diseases (for example, left ventricular failure).

3. Elderly patients. BA should be differentiated from left ventricular failure. In addition, BA is underdiagnosed in the elderly.

Risk Factors for Underdiagnosis of AD in Elderly Patients

3.1 From the side of the patient:
- depression;
- social isolation;
- impaired memory and intelligence;


- Decreased perception of dyspnea and bronchoconstriction.

3.2 From the doctor's point of view:
- misconception that asthma does not start in old age;
- difficulties in examining lung function;
- perception of asthma symptoms as signs of aging;
- accompanying illnesses;
- underestimation of dyspnea due to a decrease in the patient's physical activity.

Complications

Complications of bronchial asthma are divided into pulmonary and extrapulmonary.

Pulmonary complications: chronic bronchitis, hypoventilation pneumonia, pulmonary emphysema, pneumosclerosis, respiratory failure, bronchiectasis, atelectasis, pneumothorax.

Extrapulmonary complications:"pulmonary" heart, heart failure, myocardial dystrophy, arrhythmia; in patients with a hormone-dependent variant of BA, complications associated with prolonged use of systemic corticosteroids may occur.

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Treatment

Objectives of the treatment of bronchial asthma(BA):

Achieve and maintain control of symptoms;

Maintaining a normal level of activity, including physical activity;

Maintaining lung function at a normal or as close to normal level as possible;

Prevention of asthma exacerbations;

Prevention of unwanted effects of anti-asthma drugs;

Prevention of deaths from AD.

BA control levels(GINA 2006-2011)

Characteristics	controlled BA(all of the above)	Partially controlled asthma(presence of any manifestation within a week)	uncontrolled asthma
daytime symptoms	None (≤ 2 episodes per week)	> 2 times a week	3 or more signs of partially controlled asthma in any week
Activity restriction	No	Yes - any expression
Night symptoms/ awakenings	No	Yes - any expression
Need for emergency medicines	None (≤ 2 episodes per week)	> 2 times a week
Pulmonary function tests (PSV or FEV1) 1	Norm	< 80% от должного (или от наилучшего показателя для данного пациента)
Exacerbations	No	1 or more times a year 2	Any week with aggravation 3

1 Pulmonary function testing not reliable in children 5 years of age and younger. Periodic assessment of the level of control over BA in accordance with the criteria indicated in the table will allow individual selection of a pharmacotherapy regimen for the patient.
2 Each exacerbation requires an immediate review of maintenance therapy and an assessment of its adequacy
3 By definition, the development of any exacerbation indicates that asthma is not controlled

Medical therapy

Medications for the treatment of AD:

1. Drugs that control the course of the disease (maintenance therapy):
- inhalation and systemic corticosteroids;
- anti-leukotriene agents;
- long-acting inhaled β2-agonists in combination with inhaled corticosteroids;
- sustained release theophylline;
- cromones and antibodies to IgE.
These drugs provide control over the clinical manifestations of asthma; they are taken daily and for a long time. The most effective for maintenance therapy are inhaled corticosteroids.

2. Rescue drugs (to relieve symptoms):
- inhaled β2-rapid agonists;
- anticholinergics;
- short-acting theophylline;
- short-acting oral β2-agonists.
These drugs are taken to relieve symptoms as needed. They have a fast action, eliminate bronchospasm and stop its symptoms.

Drugs for the treatment of asthma can be administered in various ways - inhalation, oral or injection. Advantages of the inhalation route of administration:
- delivers drugs directly to the respiratory tract;
- a locally higher concentration of the medicinal substance is achieved;
- Significantly reduces the risk of systemic side effects.

For maintenance therapy, inhaled corticosteroids are most effective.

The drugs of choice for the relief of bronchospasm and for the prevention of exercise-induced bronchospasm in adults and children of any age are fast-acting inhaled β2-agonists.

Increasing use (especially daily) of rescue drugs indicates worsening asthma control and the need to reconsider therapy.

Inhaled corticosteroids are most effective for the treatment of persistent asthma:
- reduce the severity of asthma symptoms;
- improve quality of life and lung function;
- reduce bronchial hyperreactivity;
- inhibit inflammation in the respiratory tract;
- reduce the frequency and severity of exacerbations, the frequency of deaths in asthma.

Inhaled corticosteroids do not cure BA, and when they are canceled in some patients, a worsening of the condition is observed within weeks or months.
Local undesirable effects of inhaled corticosteroids: oropharyngeal candidiasis, dysphonia, sometimes cough due to irritation of the upper respiratory tract.
Systemic side effects of long-term therapy with high doses of inhaled corticosteroids: a tendency to bruising, inhibition of the adrenal cortex, a decrease in bone mineral density.

Calculated equipotent daily doses of inhaled corticosteroids in adults(GINA 2011)

A drug	Low daily allowance doses(µg)	Medium daily allowance doses(µg)	High daily allowance doses(µg)
Beclomethasone dipropionate CFC*	200-500	>500-1000	>1000-2000
Beclomethasone dipropionate HFA**	100-250	>250-500	>500-1000
Budesonide	200-400	>400-800	>800-1600
Cyclesonide	80-160	>160-320	>320-1280
Flunisolide	500-1000	>1000-2000	>2000
fluticasone propionate	100-250	>250-500	>500-1000
mometasone furoate	200	≥ 400	≥ 800
Triamcinolone acetonide	400-1000	>1000-2000	>2000

*CFC - chlorofluorocarbon (freon) inhalers
** HFA - hydrofluoroalkane (CFC-free) inhalers

Calculated equipotent daily doses of inhaled corticosteroids for children over 5 years of age(GINA 2011)

A drug	Low daily allowance doses(µg)	Medium daily allowance doses(µg)	High daily allowance doses(µg)
beclomethasone dipropionate	100-200	>200-400	>400
Budesonide	100-200	>200-400	>400
Budesonide Neb	250-500	>500-1000	>1000
Cyclesonide	80-160	>160-320	>320
Flunisolide	500-750	>750-1250	>1250
fluticasone propionate	100-200	>200-500	>500
mometasone furoate	100	≥ 200	≥ 400
Triamcinolone acetonide	400-800	>800-1200	>1200

Antileukotriene drugs: subtype 1 cysteinyl leukotriene receptor antagonists (montelukast, pranlukast and zafirlukast), as well as a 5-lipoxygenase inhibitor (zileuton).
Action:
- weak and variable bronchodilatory effect;
- reduce the severity of symptoms, including cough;
- improve lung function;
- reduce the activity of inflammation in the respiratory tract;
- reduce the frequency of asthma exacerbations.
Anti-leukotriene drugs can be used as second-line drugs for the treatment of adult patients with mild persistent asthma. Some patients with aspirin asthma also respond well to therapy with these drugs.
Antileukotriene drugs are well tolerated; side effects are few or absent.

Long-acting inhaled β2-agonists: formoterol, salmeterol.
Should not be used as monotherapy for asthma because there is no evidence that these drugs reduce inflammation in asthma.
These drugs are most effective in combination with inhaled corticosteroids. Combination therapy is preferred in the treatment of patients in whom the use of medium doses of inhaled corticosteroids does not achieve control of asthma.
With regular use of β2-agonists, the development of relative refractoriness to them is possible (this applies to both short-acting and long-acting drugs).
Therapy with inhaled long-acting β2-agonists is characterized by a lower incidence of systemic adverse effects (such as stimulation of the cardiovascular system, skeletal muscle tremor and hypokalemia) compared with oral long-acting β2-agonists.

Oral long-acting β2-agonists: sustained-release formulations of salbutamol, terbutaline, and bambuterol (a prodrug that is converted to terbutaline in the body).
Used in rare cases when additional bronchodilator action is required.
Undesirable effects: stimulation of the cardiovascular system (tachycardia), anxiety and skeletal muscle tremor. Undesirable cardiovascular reactions can also occur when oral β2-agonists are used in combination with theophylline.

Rapidly acting inhaled β2-agonists: salbutamol, terbutaline, fenoterol, levalbuterol HFA, reproterol and pirbuterol. Due to its rapid onset of action, formoterol (a long-acting β2-agonist) can also be used to relieve asthma symptoms, but only in patients receiving regular maintenance therapy with inhaled corticosteroids.
Fast-acting inhaled β2-agonists are emergency medicines and are the drugs of choice for the relief of bronchospasm during exacerbation of asthma, as well as for the prevention of exercise-induced bronchospasm. Should be used only as needed, with the lowest possible doses and frequency of inhalations.
The growing, especially daily, use of these drugs indicates a loss of control over asthma and the need to reconsider therapy. In the absence of a rapid and stable improvement after inhalation of a β2-agonist during an exacerbation of asthma, the patient should also continue to be monitored and, possibly, a short course of therapy with oral corticosteroids should be prescribed.
The use of oral β2-agonists in standard doses is accompanied by more pronounced than when using inhaled forms, undesirable systemic effects (tremor, tachycardia).

Short-acting oral β2-agonists(refer to emergency medicines) can be prescribed to only a few patients who are not able to take inhaled drugs. Side effects are observed more often.

Theophylline It is a bronchodilator and, when administered in low doses, has a slight anti-inflammatory effect and increases resistance.
Theophylline is available in sustained-release dosage forms that can be taken once or twice a day.
According to available data, sustained release theophylline has little efficacy as a first-line agent for the maintenance treatment of bronchial asthma.
The addition of theophylline may improve outcomes in patients in whom inhaled corticosteroid monotherapy does not achieve asthma control.
Theophylline has been shown to be effective as monotherapy and as a supplement to inhaled or oral corticosteroids in children over 5 years of age.
When using theophylline (especially at high doses - 10 mg / kg of body weight per day or more), significant side effects are possible (usually decrease or disappear with prolonged use).
Undesirable effects of theophylline:
- nausea and vomiting - the most common side effects at the beginning of the application;
- disorders of the gastrointestinal tract;
- liquid stool;
- heart rhythm disturbances;
- convulsions;
- death.

Sodium cromoglycate and nedocromil sodium(cromones) are of limited value in the long-term treatment of asthma in adults. There are known examples of the beneficial effects of these drugs in mild persistent asthma and exercise-induced bronchospasm.
Cromones have a weak anti-inflammatory effect and are less effective than low doses of inhaled corticosteroids. Side effects (cough after inhalation and sore throat) are rare.

Anti-IgE(omalizumab) are used in patients with elevated serum IgE levels. Indicated for severe allergic asthma, control over which is not achieved with the help of inhaled corticosteroids.
In a small number of patients, the appearance of an underlying disease (Churg-Strauss syndrome) was observed when glucocorticosteroids were discontinued due to anti-IgE treatment.

Systemic GCS in severe uncontrolled asthma, they are indicated as long-term therapy with oral drugs (recommended use for a longer period than with the usual two-week course of intensive therapy with systemic corticosteroids - standardly from 40 to 50 mg of prednisolone per day).
The duration of the use of systemic corticosteroids is limited by the risk of developing serious adverse effects (osteoporosis, arterial hypertension, depression of the hypothalamic-pituitary-adrenal system, obesity, diabetes mellitus, cataracts, glaucoma, muscle weakness, striae and a tendency to bruise due to thinning of the skin). Patients taking any form of systemic corticosteroids for a long time require the appointment of drugs for the prevention of osteoporosis.

Oral antiallergic drugs(tranilast, repyrinast, tazanolast, pemirolast, ozagrel, celatrodust, amlexanox and ibudilast) are offered for the treatment of mild to moderate allergic asthma in some countries.

Anticholinergic drugs - ipratropium bromide and oxitropium bromide.
Inhaled ipratropium bromide is less effective than inhaled rapid-acting β2-agonists.
Inhaled anticholinergics are not recommended for the long-term treatment of asthma in children.

Comprehensive treatment program BA (according to GINA) includes:

Patient education;
- clinical and functional monitoring;
- elimination of causative factors;
- development of a long-term therapy plan;
- prevention of exacerbations and drawing up a plan for their treatment;
- dynamic observation.

Drug Therapy Options

Treatment for AD is usually lifelong. It should be borne in mind that drug therapy does not replace measures to prevent the patient from coming into contact with allergens and irritants. The approach to the treatment of the patient is determined by his condition and the goal currently facing the doctor.

In practice, it is necessary to distinguish between the following therapy options:

1. Relief of an attack - is carried out with the help of bronchodilators, which can be used by the patient himself situationally (for example, for mild respiratory disorders - salbutamol in the form of a metered aerosol device) or by medical personnel through a nebulizer (for severe disorders of respiratory function).

Basic anti-relapse therapy: a maintenance dose of anti-inflammatory drugs (the most effective are inhaled glucocorticoids).

3. Basic anti-relapse therapy.

4. Treatment of status asthmaticus - is carried out using high doses of systemic intravenous glucocorticoids (SGK) and bronchodilators in the correction of acid-base metabolism and blood gas composition with the help of medications and non-drugs.

Long-term maintenance therapy for asthma:

1. Assessment of the level of control over BA.
2. Treatment aimed at achieving control.
3. Monitoring to maintain control.

Treatment aimed at achieving control is carried out according to step therapy, where each step includes therapy options that can serve as alternatives when choosing maintenance therapy for asthma. The effectiveness of therapy increases from stage 1 to stage 5.

Stage 1
Includes the use of rescue drugs as needed.
It is intended only for patients who have not received maintenance therapy and occasionally experience short-term (up to several hours) symptoms of asthma during the daytime. Patients with more frequent onset of symptoms or episodic worsening of the condition are indicated for regular maintenance therapy (see step 2 or higher) in addition to rescue drugs as needed.

Rescue drugs recommended in step 1: Rapid-acting inhaled β2-agonists.
Alternative drugs: inhaled anticholinergics, short-acting oral β2-agonists, or short-acting theophylline.

Stage 2
Relief drug + one disease control drug.
Drugs recommended as initial maintenance therapy for asthma in patients of any age at stage 2: low-dose inhaled corticosteroids.
Alternative agents for asthma control: antileukotriene drugs.

Step 3

3.1. Emergency drug + one or two drugs to control the course of the disease.
At step 3, children, adolescents and adults are recommended: a combination of a low dose of inhaled corticosteroids with a long-acting inhaled β2-agonist. Reception is carried out using one inhaler with a fixed combination or using different inhalers.
If control over BA has not been achieved after 3-4 months of therapy, an increase in the dose of inhaled corticosteroids is indicated.

3.2. Another treatment option for adults and children (the only one recommended in the management of children) is to increase the doses of inhaled corticosteroids to medium doses.

3.3. Step 3 treatment option: Combination of low dose inhaled corticosteroids with an antileukotriene drug. A low-dose extended-release theophylline may be used instead of an antileukotriene (these options have not been fully investigated in children 5 years of age and younger).

Step 4
Emergency drug + two or more drugs to control the course of the disease.
The choice of drugs in Step 4 depends on prior prescriptions in Steps 2 and 3.
Preferred option: combination of inhaled corticosteroids in a medium or high dose with a long-acting inhaled β2-agonist.

If asthma control is not achieved with a combination of a medium-dose inhaled glucocorticosteroid and a β2-agonist and/or a third maintenance drug (eg, antileukotriene or sustained-release theophylline), high-dose inhaled glucocorticosteroids are recommended, but only as trial therapy. duration 3-6 months.
With prolonged use of high doses of inhaled corticosteroids, the risk of side effects increases.

When using medium or high doses of inhaled corticosteroids, drugs should be prescribed 2 times a day (for most drugs). Budesonide is more effective when the frequency of administration is increased up to 4 times a day.

The effect of treatment increases by adding a long-acting β2-agonist to medium and low doses of inhaled corticosteroids, as well as the addition of antileukotriene drugs (less compared to a long-acting β2-agonist).
The addition of low doses of sustained release theophylline to inhaled corticosteroids in medium and low doses and a long-acting β2-agonist may increase the effectiveness of therapy.

Step 5
Emergency drug + additional options for the use of drugs to control the course of the disease.
The addition of oral corticosteroids to other maintenance drugs may increase the effect of treatment, but is accompanied by severe adverse events. Therefore, this option is only considered in patients with severe uncontrolled asthma on treatment at the appropriate stage 4, if the patient has daily symptoms that limit activity, and frequent exacerbations.

The use of anti-IgE in addition to other maintenance drugs improves the control of allergic asthma if it is not achieved during treatment with combinations of other maintenance drugs that include high doses of inhaled or oral corticosteroids.

Well antibiotic therapy indicated in the presence of purulent sputum, high leukocytosis, accelerated ESR. Taking into account antibiograms appoint:
- spiramycin 3,000,000 IU x 2 times, 5-7 days;
- amoxicillin + clavulanic acid 625 mg x 2 times, 7 days;
- clarithromycin 250 mg x 2 times, 5-7 days;
- ceftriaxone 1.0 x 1 time, 5 days;
- Metronidazole 100 ml IV drip.

Forecast

The prognosis is favorable with regular dispensary observation (at least 2 times a year) and rationally selected treatment.
The lethal outcome may be associated with severe infectious complications, progressive pulmonary heart failure in patients with cor pulmonale, untimely and irrational therapy.

The following points should be kept in mind:
- in the presence of bronchial asthma (BA) of any severity, the progression of dysfunctions of the bronchopulmonary system occurs faster than in healthy people;

With a mild course of the disease and adequate therapy, the prognosis is quite favorable;
- in the absence of timely therapy, the disease can go into a more severe form;

In severe and moderate BA, the prognosis depends on the adequacy of treatment and the presence of complications;
- comorbidities can worsen the prognosis of the disease.

X The nature of the disease and long-term prognosis depend on the age of the patient at the time of the onset of the disease.

In asthma that began in childhood, about long-term prognosis is favorable. As a rule, by puberty, children "outgrow" asthma, but they still have impaired lung function, bronchial hyperreactivity, and deviations in the immune status.
With asthma that began in adolescence, an unfavorable course of the disease is possible.
In asthma that began in adulthood and old age, the nature of the development and prognosis of the disease is more predictable.
The severity of the course depends on the form of the disease:
- allergic asthma is easier and prognostically more favorable;
- "pollen" asthma, as a rule, has a milder course compared to "dust";
- in elderly patients, a primary severe course is noted, especially in patients with aspirin BA.

AD is a chronic, slowly progressive disease. With adequate therapy, the symptoms of asthma can be eliminated, but treatment does not affect the cause of their occurrence. Remission periods can last for several years.

Hospitalization

Indications for hospitalization:
- severe attack of bronchial asthma;

There is no rapid response to bronchodilator drugs and the effect lasts less than 3 hours;
- no improvement within 2-6 hours after the start of oral corticosteroid therapy;
- there is a further deterioration - an increase in respiratory and pulmonary heart failure, "silent lung".

Patients at high risk of death:
- having a history of conditions close to lethal;
- requiring intubation, artificial ventilation, which leads to an increase in the risk of intubation during subsequent exacerbations;
- who have already been hospitalized or sought emergency care in the past year due to bronchial asthma;
- taking or recently discontinued oralglucocorticosteroids;
- using inhaled fast-acting β2-agonists in excess, especially more than one pack of salbutamol (or equivalent) per month;
- with mental illness, a history of psychological problems, including the abuse of sedatives;
Poor adherence to the asthma treatment plan.

Prevention

Preventive measures for bronchial asthma (BA) depend on the patient's condition. If necessary, it is possible to increase or decrease the activity of treatment.

Asthma control should begin with a thorough study of the causes of the disease, since the simplest measures can often have a significant impact on the course of the disease (it is possible to save the patient from the clinical manifestations of the atopic variant of asthma by identifying the causative factor and eliminating contact with it later).

Patients should be educated on proper drug administration and proper use of drug delivery devices and peak flow meters to monitor peak expiratory flow (PEF).

The patient must be able to:
- control PSV;
- to understand the difference between drugs of basic and symptomatic therapy;
- avoid asthma triggers;
- identify signs of deterioration of the disease and stop attacks on your own, as well as seek medical help in a timely manner to stop severe attacks.
The control of asthma over a long period requires a written treatment plan (algorithm of patient actions).

List of preventive measures:

Termination of contact with cause-dependent allergens;
- termination of contact with non-specific irritating environmental factors (tobacco smoke, exhaust gases, etc.);
- exclusion of occupational hazard;
- with aspirin form of BA - refusal to use aspirin and other NSAIDs, as well as compliance with a specific diet and other restrictions;
- refusal to take beta-blockers, regardless of the form of asthma;
- adequate use of any medicines;
- timely treatment of foci of infection, neuroendocrine disorders and other concomitant diseases;
- timely and adequate therapy of asthma and other allergic diseases;
- timely vaccination against influenza, prevention of respiratory viral infections;
- Carrying out therapeutic and diagnostic measures using allergens only in specialized hospitals and offices under the supervision of an allergist;
- carrying out premedication before invasive examination methods and surgical interventions - parenteral administration of drugs: GCS (dexamethasone, prednisolone), methylxanthines (aminophylline) 20-30 minutes before the procedure. The dose should be determined taking into account age, body weight, severity of asthma and the extent of intervention. Before carrying out such an intervention, a consultation with an allergist is indicated.

Information

Sources and literature

1. Global strategy for the treatment and prevention of bronchial asthma (revised 2011) / ed. Belevsky A.S., M.: Russian Respiratory Society, 2012
2. Russian therapeutic reference book / edited by acad.RAMN Chuchalin A.G., 2007
   1. pp 337-341
3. http://lekmed.ru
4. http://pulmonolog.com

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Bronchial asthma is a recurrent chronic inflammation of the respiratory system associated with bronchial hyperreactivity. In this case, an inflammatory edema of the bronchial mucosa occurs, which causes asthma attacks, shortness of breath, whistling and congestion in the chest, cough.

What causes asthma

The causes of asthma can be divided into two classifications: non-infectious allergens and infectious. They define several types of this disease - atopic bronchial asthma (allergic), caused by the first classification, infectious-allergic and mixed type. Non-infectious allergens include household dust, pets, tobacco smoke, pollen of various plants, food products (fish, milk, eggs), household chemicals, drugs (antibiotics, hormones, pancreatin).

The most common infectious allergens include Staphylococcus aureus and white, as well as all kinds of bacteria, fungi and viruses. Infectious allergens contribute to the development of infectious-allergic bronchial asthma and its mixed type.

Heredity and predisposition of the disease can also be attributed to the factor in the occurrence of asthma. The causes of this disease can also be the frequent occurrence of SARS and colds.

Symptoms of bronchial asthma

In order to start treatment on time and prevent a severe course of the disease, it is important to see the symptoms of pre-asthma in time, such as the presence of bronchitis (obstructive, chronic asthmatic), allergic syndromes, hereditary predisposition. As a consequence, coughing fits at night, shortness of breath or suffocation begin to occur. At the same time, the cough is dry, although it constantly seems to the person that he cannot cough up something. Dry whistling rales appear, which can sometimes be heard even at a distance from a sick person. Breathing in is difficult, and exhaling requires great effort.

At this point, you need to contact a specialist for diagnosis in time. It includes such studies as the collection of anamnesis; immunoglobulin studies; blood and sputum analysis for the presence of characteristic signs of eosinophilia; allergological tests on the skin, sometimes inhalation provocation. To determine the strengthening of the pulmonary pattern, radiography is performed. The study also includes: a test with physical activity (usually for children) and a functional study of the lungs.

Severity

Such a diagnosis has several degrees of severity:

Intermittent degree (mild course)

It is characterized by the occurrence of symptoms less than once a week. Exacerbations are short-lived. Night attacks - no more than two per month. Between exacerbations, the absence of symptoms and the normalization of respiratory functions.

Mild persistence (moderate condition)

Symptoms recur more than once a week, but no more than once a day. Night attacks more than twice a month. Sleep disturbance and physical activity during an exacerbation.

Severe persistence (severe course)

daily symptoms. Violation of physical condition, sleep and normal vitality. Night attacks more than once a week.

Persistent asthma (extremely severe)

Constant onset of symptoms throughout the day. Protracted and frequent exacerbations. Frequent nocturnal attacks. Severe physical condition, limited mobility.

In some cases, complications arise. Such as acute respiratory failure, enphysematous lung disorders, pneumothorax - air entering the pleural cavity.

With a severe and complex degree of bronchial asthma, the patient is supposed to receive a disability group. To do this, you will need to make an extract from the medical history, undergo an additional examination and obtain opinions from a number of doctors, and then contact the ITU bureau with the results. In a mild and moderate degree of the disease, most often, disability is not required, since life restrictions at such stages are insignificant.

Treatment

Treatment of bronchial asthma is prescribed after establishing an accurate diagnosis and the degree of development of the disease. For each, an individual treatment plan is determined. Medical care is divided into emergency therapy, treatment during an exacerbation (anti-inflammatory therapy) and treatment in remission.

Anti-inflammatory

In anti-inflammatory therapy, the use of hormonal drugs by inhalation is characteristic. This method is more effective than oral administration of tablets, since it does not irritate the gastrointestinal tract, and most importantly, the drug enters directly into the bronchi. Bronchospasmolytic drugs in the form of an aerosol inhaler are used in emergency therapy to relieve an attack and eliminate suffocating symptoms. These inhalers are compact, it is recommended to always keep them at hand.

The course of therapy also includes non-drug treatment. It includes massage, physiotherapy exercises, spa treatment.

A good effect is achieved by the use of nebulizers - small devices that spray medicines using ultrasound. With its help, you can stop seizures.

Nutrition

Patients with this disease are advised to follow a diet. Such a diet excludes foods that provoke allergic reactions. Such foods are citrus fruits, strawberries, fish, raw cabbage, seafood, beans, tomatoes, eggs, chocolate, alcohol, melons and peaches. Fats, strong tea, coffee, and spicy spices should also be limited. It is recommended to eat onions and garlic, mustard, as these products help to relieve breathing. But it is worth considering individual intolerance when using them. Calcium-containing products are added to the menu, they have anti-allergic and anti-inflammatory effects. Liquid is limited to 1-1.5 liters per day. It is recommended to eat fractionally 4-5 times a day and avoid overeating.

According to statistics, in the uncontrolled course of the disease of bronchial asthma, a high number of deaths was recorded, compared with patients who are under observation and strictly comply with all recommendations. Therefore, the key to successful treatment is timely access to specialists.

Video: Dr. Komarovsky about bronchial asthma

Bronchial asthma is one of the most common chronic diseases in modern society. It is registered in more than 5% of the adult population and in almost 10% of children.

T.A. Pertseva, Corresponding Member of the Academy of Medical Sciences of Ukraine, MD, Professor, E.Yu. Gashinova, PhD, Department of Faculty Therapy and Endocrinology, Dnipropetrovsk State Medical Academy

Dum spiro spero.
(While I breathe I hope)
Ovid

Epidemiology
General practitioners and pulmonologists who provide daily care to patients with bronchial asthma know firsthand the severity of the disease, its increasing prevalence, and the ever-increasing economic costs associated with it.
Data on the prevalence of severe asthma are conflicting, partly due to the lack of a universal definition for this form of the disease. However, along with the worldwide increase in the overall number of asthma patients, there has been a steady trend towards an increase in the number of patients requiring emergency care, often hospitalized due to a severe course of the disease, the exacerbation of which is often life-threatening.

Definition
In the Global Strategy for the Treatment and Prevention of Asthma (GINA, 2005), a severe disease is defined as a disease that is characterized by daily symptoms that limit physical activity, frequent exacerbations and nocturnal manifestations, as well as a decrease in FEV1 less than 60% of predicted values, and diurnal fluctuations in peak expiratory flow (PEF). ) over 30%.
The British Thoracic Society classifies severe asthma, with sufficient medical therapy, as a disease in which control is achieved only with the use of high doses of inhaled corticosteroids and / or those that have a systemic effect.
In 2000, the American Thoracic Society defined "refractory asthma" as a condition with one or more major and two or more minor criteria, taking into account the need for medication, asthma symptoms, frequency of exacerbations, and degree of airway obstruction.
In the ENFUMOSA European Community study, severe asthma was diagnosed in patients with persistent symptoms and recurrent exacerbations despite high doses of inhaled corticosteroids and long-acting bronchodilators; patients with asthma who need constant intake of corticosteroids that have a systemic effect in order to achieve disease control; patients with a history of life-threatening asthma attacks.
The most precise definition should be considered in which severe asthma is considered as severely controlled, treatment-resistant, refractory asthma, poor control of which is confirmed by persistent symptoms, frequent exacerbations and persistent variable bronchial obstruction, despite the use of high doses of inhaled corticosteroids or providing systemic action.

Clinical variants (terminology)
In the world medical literature, a number of terms are used to denote difficult-to-treat bronchial asthma: acute and chronic severe, resistant to therapy, difficult to control, refractory, steroid-dependent, steroid-resistant, fatal (fatal), "difficult", "fragile" (unstable). This abundance of names reflects the heterogeneity of the clinical manifestations of severe asthma. They characterize the sequence of occurrence of symptoms and exacerbations, the chronization and speed of the development of attacks, the response to ongoing therapy. Systematizing all the variety of available terms, three main clinical variants of severe asthma can be distinguished.

1. Bronchial asthma with frequent severe exacerbations
Today, a large number of factors are known to cause the development of severe exacerbations. These are respiratory viral infections, atypical bacterial pathogens (Mycoplasma pneumoniae, Chlamydia pneumoniae), exposure to allergens, industrial and household pollutants, discontinuation of basic drugs, hormonal imbalance (for example, premenstrual tension syndrome). An important role is played by the psychosocial status of the patient, which directly affects the desire and ability to fulfill the doctor's prescriptions, and hence the achievement of control over asthma.
A variant of asthma with frequent exacerbations is “brittle” (unstable) asthma, a disease characterized by high chaotic variability in PSV despite high doses of inhaled corticosteroids. The pathogenetic basis of unstable asthma is airway hyperreactivity. There are two clinical phenotypes of brittle asthma. The first is characterized by persistently high variability in PSV, despite treatment selected according to existing standards. In patients with the first type of unstable asthma, psychological disorders are often noted. One of the likely causes of exacerbation may be gastroesophageal reflux as a consequence of the use of anti-asthma drugs in high doses. Perhaps the instability of asthma is associated with the content of freon in inhalers, and by prescribing the same drugs in the form of dry powder, the condition of patients can be significantly improved. Patients with unstable type 1 asthma respond well to nebulized beta2-agonists or their long-acting forms.
The second phenotype is characterized by a sudden sporadic decrease in PEF in patients with well-controlled disease at baseline. An example of this clinical variant is intolerance to aspirin and other NSAIDs, in which patients with a good initial condition after taking the provoking drug can develop a severe exacerbation. Patients with type 2 unstable asthma often have food allergies. Since the occurrence of an exacerbation in them is almost always unpredictable, it is extremely difficult to prevent it. The prognosis for such patients is always serious.
The terms “status asthma”, “suddenly onset severe asthma attack”, “slowly developing asthma attack”, which reflect the processes of exacerbation of the disease, should be specially characterized.
Asthmatic status is characterized by a clinical picture of increasing exacerbation and a sharp decrease in the effectiveness of bronchodilator drugs. In the clinical picture of an exacerbation of bronchial asthma, such a syndrome as "silent lung" appears, in especially severe cases, hypoxic coma develops. The main reason for the development of status asthmaticus is the uncontrolled intake of β 2 -agonists.
A sudden or slow-onset asthma attack reflects the rate at which an asthma attack develops. So, an example is the delayed exacerbation of the disease in a respiratory viral infection.
The term "fatal asthma" is used to describe a severe exacerbation or sudden death in a patient with bronchial asthma. Patients with an episode of acute respiratory failure requiring intubation, respiratory acidosis, two or more hospitalizations for asthma despite treatment with systemic corticosteroids, two or more pneumothorax or pneumomediastinum associated with with asthma. Patients receiving three or more classes of drugs for asthma are also at high risk of sudden death. Among the causes of fatal asthma, low socioeconomic status, unavailability of medical care, depression, conscious refusal of treatment, and drug addiction should be singled out.

2. Chronic severe bronchial asthma
Distinctive features of this form of the disease are the constant presence of symptoms that limit physical activity and sleep, low (less than 60% of the norm) indicators of forced expiratory volume, the presence of slightly reversible bronchial obstruction, despite full-fledged drug therapy using maximum doses of drugs. Factors contributing to the development of "refractory" asthma are persistent eosinophilic airway inflammation, exposure to tobacco smoke and industrial pollutants, onset of asthma in childhood with an early decrease in lung function, non-atopic asthma, and the presence of chronic respiratory tract infection.

3. Severe asthma with steroid resistance or steroid dependence
Another form of severe asthma is "steroid-dependent" and "steroid-resistant" or "therapy-resistant" bronchial asthma. Patients with steroid dependence do not always have frequent exacerbations or have little reversible severe airway obstruction. However, to maintain control of asthma, they constantly need to take high doses of inhaled or systemic corticosteroids. Reducing the dose of basic drugs leads to a progressive deterioration in the condition of such patients, and an increase can reduce the severity of symptoms and stabilize the course of the disease. It has been proven that this form of severe asthma develops more often in patients who become ill at an older age and do not have signs of atopy.
A possible mechanism for the development of steroid resistance in severe asthma may be a secondary dysregulation of glucocorticosteroid receptors due to uncontrolled long-term administration of hormones that have a systemic effect, or a decrease in the number of steroid receptors. The decrease in the effectiveness of glucocorticosteroids in severe forms of asthma is associated with changes in the spectrum of inflammatory cells that accumulate in the mucous membrane of the respiratory tract. Eosinophilic infiltration gives way to predominant neutrophilic infiltration, which may have an impact on the biological effects of steroids.
Another explanation for the development of resistance may be that glucocorticosteroids not only do not affect bronchial smooth muscle hypertrophy, but also aggravate myopathy of the respiratory muscles (diaphragm, intercostal muscles and muscles of the upper shoulder girdle). The cause of secondary steroid resistance can also be long-term use of β 2 -agonists, viral infection and endogenous disturbance of the level of female sex hormones. Complete steroid resistance in asthma (lack of effect from taking 40 mg of prednisolone per day for 14 days) is rare and is most likely due to a congenital anomaly of glucocorticosteroid receptors.

Severe Asthma: Reasons for Lack of Control
Not all patients with symptoms of severe asthma actually suffer from this form of the disease. In this section, we would like to consider the main reasons why it is not possible to establish adequate control over the symptoms of the disease.

1. Wrong diagnosis
Since the symptoms of asthma (suffocation, shortness of breath, wheezing in the lungs) are not strictly specific, the possibility that the patient has another disease should not be denied. The list of pathological conditions that most often masquerade as difficult-to-control asthma is given in table 1.
A large number of diseases with which it is necessary to conduct a differential diagnosis in the presence of symptoms of severe asthma determines the thoroughness and large volume of examination of such patients (Table 2). The diagnosis of severe asthma must be supported by objective evidence of reversible bronchial obstruction or airway hyperresponsiveness.

2. The presence of concomitant pathology
Some concomitant diseases may cause an increase in the frequency and severity of asthma exacerbations (Table 3). Proper diagnosis and treatment of these pathological conditions contributes to better control of the symptoms of severe asthma.

3. Constant exposure to irritants
Constant exposure to allergens, even at low concentrations, contributes to maintaining inflammation in the airways, exacerbating the severity of asthma symptoms. The most common causes of atopy are house dust, mold fungus, pet hair, cockroaches, plant pollen, food allergens.
Inorganic irritants such as tobacco smoke, sulfur and nitrogen dioxide, and ozone may also cause inhaled corticosteroid therapy to be ineffective.
Taking certain medications (non-steroidal anti-inflammatory drugs, β-blockers) can cause severe exacerbation of asthma in some patients.
Avoidance of contact with allergens, industrial and household pollutants, smoking cessation and controlled therapy significantly improve the condition of patients with bronchial asthma.

4. Inadequate treatment
The reason for the persistence of symptoms of severe asthma may be an underestimation of the severity of the patient's condition and, as a result, an insufficient amount of anti-asthma therapy. In 15-20% of cases, the cause of severe asthma is inadequate treatment tactics. An indispensable condition for proper treatment should be a sufficient (up to high) dose of inhaled corticosteroids.
The willingness and ability of the patient to cooperate plays a large role in achieving asthma control. The factors predisposing to poor adherence to treatment are psychological problems in patients, irregularity in seeking medical help, lack of faith in traditional methods of treatment with excessive enthusiasm for traditional medicine, a large number of prescribed medications, and underestimation by patients of the severity of their condition.
Another reason for poor asthma control may be improper inhalation technique. In this regard, preference should be given to easier-to-use delivery devices with a spacer or powder inhalers.
To exclude the influence of inadequate treatment on the course and prognosis of asthma, a reasonable and clear diagnostic and treatment program should be followed.

Treatment of patients with severe asthma
Patients with symptoms of difficult-to-control asthma should be treated in specialized pulmonology centers by highly qualified specialists. Only in such medical institutions is it possible to conduct differential diagnosis using laboratory and instrumental examination methods that are not used in routine practice (determination of the level of nitric oxide in the exhaled air, the study of the cellular composition of bronchoalveolar lavage, biopsy specimens of the bronchial mucosa, computed tomography, immunological examination and genetic testing). In addition, during hospitalization, exposure to allergens and inorganic irritants that provoke an exacerbation of the disease can be avoided. The algorithm for managing patients with symptoms of severe asthma is shown in the figure.
It is required to draw up an individual treatment plan for each patient. After differential diagnosis, it is important to identify the causative factor in the development of exacerbations and, if possible, eliminate it: stop smoking, identify causal allergens, prevent infections, sanitize infections in the paranasal sinuses, normalize sleep, affect gastroesophageal reflux, etc.
Be sure to evaluate and maximize the cooperation between doctor and patient. Patient education is important. The patient should be taught the elements of self-control (in particular, peak flowmetry) and the tactics of behavior in the developing exacerbation of the disease.
Among other measures to establish asthma control, the correct use of delivery devices and inhalation techniques should be assessed.
Patients with severe asthma need to be rehabilitated. Many patients are weakened by the disease, suffer from side effects of anti-inflammatory therapy, and are forced to change their lifestyle. The appointment of a program of physical exercises and psychological correction helps to improve the tolerance of physical activity and the quality of life of patients.
Asthma drug therapy, according to current recommendations, uses a stepwise approach, in which the intensity of therapy increases as the severity of the disease increases.
In severe asthma, high-dose inhaled corticosteroids (eg, fluticasone, beclamethasone, mometasone) are the mainstay of therapy. Typically, these drugs are taken twice a day, although there is evidence that four times a day is more effective. In some cases, the introduction of drugs in high doses through a nebulizer can significantly improve asthma control. However, it should be remembered that monotherapy with inhaled corticosteroids is not effective enough in severe asthma, and if their dose is increased >800 mcg / day, the likelihood of systemic effects increases with a not always pronounced increase in clinical efficacy.
Long-acting β 2 -Agonists (salmeterol, formoterol) in severe asthma must be prescribed in addition to inhaled corticosteroids. They improve respiratory function, reduce the frequency of exacerbations, reduce the use of short-acting β 2 -agonists and reduce the dose of inhaled corticosteroids. Combined preparations containing inhaled corticosteroids and long-acting β2-agonists (eg, Seretide, Seroflo, Symbicort*) are considered more effective and convenient to use.
As with any severity of asthma, in severe cases, short-acting β 2 -agonists (salbutamol, fenoterol) are taken only “on demand”. Their frequent use leads to a decrease in effectiveness, and therefore, to a loss of control over asthma. In the second phenotype of brittle asthma, parenteral administration of epinephrine is possible in extreme situations.
Corticosteroids that have a systemic effect (prednisolone, dexamethasone, triamcinolone) are prescribed for severe persistent symptoms of severe asthma and severe exacerbation of the disease with further gradual withdrawal. Patients who develop frequent exacerbations despite high doses of inhaled corticosteroids may also be advised to use intermittent high doses of systemic agents followed by a transition to a maintenance low dose.
In the case of persisting, despite the constant use of systemic corticosteroids, symptoms of severe asthma, an increase in their daily dose should be considered.
In patients (especially women) receiving systemic corticosteroids, due to severe side effects, correction of mineral metabolism and hormonal status is necessary.
Methylxanthines (theophylline) in some cases may be prescribed in addition to basic drugs. In some patients, taking them allows you to reduce the dose of inhaled and / or systemic corticosteroids. However, due to the toxicity of methylxanthines, their use requires regular monitoring of theophylline plasma levels.
Antileukotrienes (zafirlukast*, montelukast*) are used together with steroidal anti-inflammatory drugs. They are especially effective in aspirin asthma.
The widespread use of immunosuppressants and antimetabolites for the treatment of bronchial asthma is limited by their severe toxicity. In addition, in clinical trials on the use of inhaled forms, conclusive data on their clinical effectiveness have not yet been obtained.
A promising group of drugs prescribed for severe asthma are monoclonal antibodies (omalizumab*). They have proven to be an effective addition to traditional basic therapy, improving the function of external respiration and the quality of life of patients. When using these drugs, the consumption of short-acting β 2 -agonists is also reduced. Monoclonal antibodies are included in the guidelines for the treatment of severe bronchial asthma of the latest revision.
Today, there is evidence of a pronounced anti-inflammatory effect of type 4 phosphodiesterase inhibitors (rolipram *, roflumilast *, cilomilast *) in severe asthma.

Conclusion
Severe bronchial asthma is a multicomponent process that combines pathological conditions with different sequences of symptoms and exacerbations, rates of chronicity and speed of attacks. Accurate identification of the clinical variant of the disease allows you to better understand the mechanism of its occurrence, and therefore, to choose the right treatment for a particular patient.
Not every patient with symptoms of severe asthma is confirmed by a detailed examination of the initial diagnosis. Many of them have either another pathology of the respiratory organs, or moderate asthma and inadequately chosen treatment tactics.
Treatment of severe asthma includes a range of non-drug interventions and multicomponent drug therapy. Clinical studies in recent years have led to the recommendation of several fundamentally new groups of drugs to achieve control of severe asthma. However, there are still a number of patients with persistent asthma symptoms despite intensive therapy, which means that there is a need to develop new drugs.

Persistent symptoms throughout the day. - Frequent exacerbations. - Frequent nocturnal symptoms.

Physical activity is limited by the manifestations of asthma.

PSV less than 60% of due; fluctuations of more than 30%.

Survey: complete blood count, general urinalysis, determination of general and specific IgE, chest x-ray, sputum analysis, respiratory function with a beta-2-agonist test, daily peak flowmetry, if necessary, skin allergy tests.

Treatment: stage 4. patients with severe asthma cannot be fully controlled. The goal of treatment is to achieve the best possible outcomes: the minimum number of symptoms, the minimum need for short-acting beta-2-agonists, the best possible PEF values, the minimum variation in PEF, and the minimum side effects of drugs. Treatment is usually with a large number of asthma-controlling drugs.

Primary treatment includes high-dose inhaled corticosteroids (800 to 2000 micrograms per day of beclomethasone dipropionate or equivalent).

Oral corticosteroids continuously or in long courses.

Long-acting bronchodilators.

An anticholinergic drug (ipratropium bromide) can be tried, especially in patients who report side effects when taking beta-2 agonists.

Short-acting inhaled beta-2 agonists can be used as needed to relieve symptoms, but should not be taken more than 3-4 times per day.

It should be noted that the determination of the severity of asthma by these indicators is possible only before the start of treatment. If the patient is already receiving the necessary therapy, then its volume should also be taken into account. Thus, if a patient has mild persistent asthma according to the clinical picture, but at the same time he receives medical treatment corresponding to severe persistent asthma, then this patient is diagnosed with severe bronchial asthma.

The method for optimizing asthma therapy can be described in the form of blocks in the following way:

Block 1. The first visit of the patient to the doctor, assessment of the degree of severity, determination of the tactics of managing the patient. If the patient's condition requires emergency care, then it is better to hospitalize him. At the first visit, it is difficult to accurately determine the severity, because. this requires fluctuations in PSV during the week the severity of clinical symptoms. Be sure to take into account the volume of therapy before the first visit to the doctor. Continue therapy for the period of monitoring. If necessary, additional intake of short-acting beta-2 agonists can be recommended.

An introductory weekly monitoring period is prescribed if the patient is presumed to have mild or moderate asthma that does not require emergency full therapy. Otherwise, it is necessary to carry out adequate treatment and monitor the patient for 2 weeks. The patient fills out a diary of clinical symptoms and records PSV values ​​in the evening and morning hours.

Block 2. Determining the severity of asthma and choosing the appropriate treatment. It is carried out on the basis of the classification of the severity of bronchial asthma. Provides a visit to the doctor a week after the first visit, if therapy is not prescribed in full.

Block 3. A two-week monitoring period against the background of ongoing therapy. The patient, as well as during the introductory period, fills out a diary of clinical symptoms and records PEF values.

Block 4. Evaluation of the effectiveness of therapy. Visit after 2 weeks against the background of ongoing therapy.

step up A: An increase in the volume of therapy should be given if asthma control cannot be achieved. However, it should be taken into account whether the patient is taking medications of the appropriate level correctly and whether there is any contact with allergens or other provoking factors. Control is considered unsatisfactory if the patient:

Episodes of coughing, wheezing, or difficulty breathing occur

more than 3 times a week.

Symptoms appear at night or in the early morning hours.

Increased need for bronchodilators

short action.

The spread of PSV indicators is increasing.

step down: Reduced maintenance therapy is possible if asthma remains under control for at least 3 months. This helps to reduce the risk of side effects and increases the patient's susceptibility to the planned treatment. Reduce therapy should be "stepped", lowering or canceling the last dose, or additional drugs. It is necessary to monitor the symptoms, clinical manifestations and indicators of respiratory function.

Thus, although bronchial asthma is an incurable disease, it is reasonable to expect that the majority of patients can and should achieve control over the course of the disease.

It is also important to note that the approach to the diagnosis, classification and treatment of asthma, taking into account the severity of its course, allows you to create flexible plans and special treatment programs depending on the availability of anti-asthma drugs, the regional healthcare system and the characteristics of a particular patient.

It should be noted once again that one of the central places in the treatment of asthma is currently occupied by the educational program of patients and dispensary observation.

Bronchial asthma

Bronchial asthma(asthma bronchiale; Greek asthma, heavy breathing, suffocation) is a disease whose main symptom is attacks or periodic conditions of expiratory suffocation due to pathological hyperreactivity of the bronchi. This hyperreactivity manifests itself under the influence of various endo- and exogenous stimuli, both causing an allergic reaction and acting without the participation of allergic mechanisms. The given definition corresponds to idea about B. and. as a non-specific syndrome and requires coordination with the trend towards preservation in medical and diagnostic practice that developed in the USSR in the 60-70s. allocation from this syndromic concept of allergic B. and. as an independent nosological form.

Classification

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

Etiology

Etiology of aspirin B. a. is not clear. Patients have intolerance to acetylsalicylic acid, all pyrazolone derivatives (amidopyrine, analgin, baralgin, butadione), as well as indomethacin, mefenamic and flufenamic acids, ibuprofen, voltaren, i.e. most non-steroidal anti-inflammatory drugs. In addition, some patients (according to various sources, from 10 to 30%) also do not tolerate the yellow food coloring tartrazine, which is used in the food and pharmaceutical industries, in particular for the manufacture of yellow shells of dragees and tablets.

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

The predisposing factors in the development of B. a., first of all, include heredity, the value of which is more pronounced in atopic B. a., inherited according to a recessive type with 50% penetrance. It is believed that the ability to produce allergic IgE antibodies (immunoglobulins E) in atopic asthma, as in other manifestations of atopy, is associated with a decrease in the number or function of suppressor T-lymphocytes. There is an opinion that B.'s development and. contribute to some endocrine disorders and dysfunction of the pituitary - adrenal cortex; known, for example, exacerbations of the disease in menopause in women. Probably, the cold, damp climate, as well as air pollution, should be attributed to the predisposing factors.

Pathogenesis

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

The pathogenesis of aspirin B. a. not quite clear. In most cases there is pseudo-allergy To a number of non-steroidal anti-inflammatory drugs. It is believed that the disruption of the metabolism of arachidonic acid by these drugs is of paramount importance.

Pathogenesis of infection-dependent B. a. has no generally accepted explanation. Evidence of IgE-mediated allergy to bacteria and viruses has not been obtained. Theories b - adrenoblocking action of a number of viruses and bacteria, as well as a vagal bronchoconstrictor reflex when the afferent zones are affected by the virus. It has been established that the lymphocytes of patients with B. a. secrete in increased quantities a special substance that can cause the release of histamine and, possibly, other mediators from basophils and mast cells. Microbes that are in the respiratory tract of patients, as well as bacterial allergens manufactured for practical use, stimulate the release of this substance by lymphocytes of patients with infection-dependent B. a. From this it follows that the final pathogenetic links in the formation of an asthma attack may be similar in both main forms of bronchial asthma.

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

At many patients B. and. psychogenic attacks of suffocation are noted, which occur, for example, with emotions of fear or anger, with false information from the patient about the inhalation of supposedly increasing doses of the allergen (when the patient actually inhaled saline), etc. Acute, severe stressful situations tend to cause a temporary remission of B. a., whereas chronic psychotraumas usually worsen its course. Mechanisms of influence of psychogenic influences on B.'s course and. remain unclear. Different types of neurosis occurring in patients with B. a. are more often a consequence, and not a cause of the disease. Currently, there are no sufficient grounds to single out psychogenic asthma in a separate form, but in the complex treatment of patients with B. a. the importance of psychogeny should be taken into account.

Clinical picture

In the pre-asthma stage, many patients develop allergic or polypous rhinosinusitis. The manifestations of pre-asthma itself 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 means of treating B. a. Coughing fits usually occur at night or in the early morning hours. Most often, the cough remains after a respiratory viral infection or exacerbation of chronic bronchitis, pneumonia. The patient does not experience any difficulty in breathing. During auscultation of the lungs, hard breathing is sometimes determined, very rarely - dry wheezing during forced exhalation. Eosinophilia is found in blood and sputum. When examining the functions of external respiration (RF) before and after inhalation of a b-agonist (izadrin, berotek, etc.), a significant increase in expiratory power can be established, indicating the so-called latent bronchospasm.

In the subsequent stages of B.'s development and. its main manifestations are attacks of suffocation, and in severe cases, also states of progressive suffocation, referred to as asthmatic status (status asthmaticus).

Asthma attack develops relatively suddenly, in some patients following certain individual precursors (sore throat, pruritus, nasal congestion, rhinorrhea, etc.). There is a feeling of congestion in the chest, shortness of breath, a desire to cough up, although the cough during this period is mostly dry and exacerbates shortness of breath. Difficulty in breathing, which the patient experiences at first only on exhalation, increases, which forces the patient to take a sitting position to engage the auxiliary respiratory muscles ( cm. Respiratory system ). There are wheezing in the chest, which at first is felt only by the patient himself (or the doctor listening to his lungs), then they become audible at a distance (remote wheezing) as a combination of different pitches of voices 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 installation of the chest and diaphragm in the respiratory pause in the position of a deep breath).

The patient sits, leaning his hands on the edge of the seat. The chest is expanded; expiration is significantly lengthened and is achieved by a visible tension of the muscles of the chest and trunk (expiratory dyspnea); the intercostal spaces are retracted on inspiration; the cervical veins swell on exhalation, collapse on inspiration, reflecting significant differences in intrathoracic pressure in the phases of inhalation and exhalation. With percussion of the chest, a box sound, lowering of the lower border of the lungs and limitation of the respiratory mobility of the diaphragm are determined, which is also confirmed by an X-ray examination, which also reveals a significant increase in the transparency of the lung fields (acute swelling of the lungs). Auscultatory examination of the lungs reveals hard breathing and abundant dry rales of different tones with a predominance of buzzing (at the beginning and end of the attack) or whistling (at the height of the attack). Heartbeats are quickened. Heart sounds are often poorly defined due to the swelling of the lungs and the drowning volume of audible dry rales.

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

asthmatic status is defined as a life-threatening progressive bronchial obstruction with progressive impairment of ventilation and gas exchange in the lungs, which is not stopped by bronchodilators that 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 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 infection-dependent B. a . According to the severity of the condition of patients and the degree of gas exchange disorders, three stages of asthmatic status 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 briefly relieve suffocation (without completely eliminating expiratory dyspnea), and after a few hours this effect is lost. The patient is somewhat agitated. Percussion and auscultation of the lungs reveal changes similar to those during an attack of B. a., but dry rales are usually less abundant and high-pitched rales predominate. As a rule, tachycardia is determined, especially pronounced in case of intoxication with adrenomimetics, when tremor of the fingers, pallor, increased systolic blood pressure, sometimes extrasystole, 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 asthmatic status is characterized by a severe degree of expiratory suffocation, fatigue of the respiratory muscles with a gradual decrease in the minute volume of breathing, and increasing hypoxemia. The patient either sits, leaning on the edge of the bed, or reclining. Excitation is replaced by ever longer periods of apathy. The tongue, skin of the face and trunk are cyanotic. Breathing remains rapid, but it is less deep than in stage I. Percussion determines the picture of acute swelling of the lungs, auscultatory - weakened hard breathing, which over certain areas of the lungs may not be heard at all (zones of the "silent" lung). The number of audible dry rales is significantly reduced (non-abundant and quiet wheezing rales are determined). There is tachycardia, sometimes extrasystole; on the ECG - signs of pulmonary hypertension (see. Hypertension of the pulmonary circulation ), Decreased T wave in most leads. Arterial blood pO 2 drops to 60-50 mmHg Art., moderate hypercapnia is possible.

Ill stage of asthmatic status is characterized by pronounced arterial hypoxemia (pO 2 within 40-50 mmHg Art.) and increasing hypercapnia (pCO 2 above 80 mmHg Art.) with the development of respiratory acidotic coma. There is marked diffuse cyanosis. Dryness of the mucous membranes, a decrease in tissue turgor (signs of dehydration) are often determined. Breathing gradually slows down and becomes less and less deep, which is reflected by the disappearance of wheezing and a significant weakening of respiratory noises with the expansion of the “silent” lung zones during auscultation. Tachycardia is often combined with various cardiac arrhythmias. Death can occur from respiratory arrest or acute cardiac arrhythmias due to myocardial hypoxia.

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

atopic B. a. often begins in childhood or adolescence. In a family history, asthma or other atonic diseases are detected in more than 50% of cases, in the patient's anamnesis - allergic rhinitis, atopic dermatitis. Attacks of suffocation in atopic B. a. 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 a typical picture of expiratory suffocation with remote dry rales quickly unfolds. Usually, an attack can be quickly stopped with the use of b-adrenergic agonists or aminophylline; the attack ends with the release of a small amount of light viscous sputum. After an attack, auscultatory symptoms of asthma are eliminated completely or remain minimal.

For atopic B. a. characterized by a relatively mild course, late development of complications. Severe course, the development of status asthmaticus are rare. In the first years of the disease, remissions are typical when contact with allergens is stopped. Spontaneous remissions are not uncommon. Complete recovery from atopic B. a. rarely occurs in adults.

Infectious-dependent B. a. observed in people of different ages, but adults are more likely to get sick. Asthma is relatively common in a family history, and atopic diseases are rare. B.'s combination is characteristic and. with polyposis rhinosinusitis. The onset of the disease is usually associated with acute, often viral infections or with exacerbations of chronic diseases of the respiratory apparatus (sinusitis, bronchitis, pneumonia). Attacks of suffocation differ less than in atopic B. a., acuteness of development, longer duration, less clear and rapid resolution in response to the use of adrenomimetics. After stopping the attack during auscultation of the lungs, hard breathing with an extended exhalation, dry buzzing rales, and moist rales in the presence of inflammatory exudate in the bronchi persist. With this form B. a. a severe course with repeated asthmatic statuses is more common, complications develop faster.

Aspirin asthma in typical cases it 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. Adult women get sick more often, but the disease also occurs in children. It usually begins with polypous rhinosinusitis; polyps after their removal quickly recur. At some stage of the disease, after another polypectomy or taking aspirin, analgin joins B. a., the manifestations of which persist in the future even without taking non-steroidal anti-inflammatory drugs. Taking these drugs invariably causes exacerbations of the disease of varying severity - from manifestations of rhinitis to the most severe asthmatic status with a fatal outcome. Polypectomy is also often accompanied by severe exacerbations of B. a. Most clinicians believe that for aspirin B. a. characterized by a severe course. Atopy among these patients is rare.

Asthma of physical effort, or post-load bronchospasm, does not, apparently, represent an independent form of B. a. It has been established that in 50-90% of patients with any form of B. a. physical effort can cause an asthma attack in 2-10 min after the end of the load. Seizures are rarely severe, lasting 5-10 min, sometimes up to 1 h; pass without the use of drugs or after inhalation of a b-agonist. Exercise asthma is more common in children than in adults. It has been noted that some types of physical effort (running, playing football, basketball) especially often cause post-exercise bronchospasm. Lifting weights is less dangerous; relatively well tolerated swimming and rowing. The duration of physical activity also matters. Under the conditions of a provocative test, they usually give loads for 6-8 min; with a longer load (12-16 min) the severity of post-exercise bronchospasm may be less - the patient, as it were, jumps over bronchospasm.

Complications

Long flowing B. a. complicated by pulmonary emphysema, often chronic nonspecific bronchitis, pneumosclerosis, development of cor pulmonale, with subsequent formation of chronic pulmonary heart failure. These complications occur much faster in the infection-dependent than in the atopic form of the disease. At the height of an attack of suffocation or a prolonged attack of coughing, a short-term loss of consciousness is possible ( bettolepsy ). In severe attacks, lung ruptures are sometimes noted in areas of bullous emphysema with the development pneumothorax and pneumomediastinum (see Mediastinum ). Quite often complications in connection with long therapy B. are observed and. glucocorticoids: obesity, arterial hypertension, severe osteoporosis, which may be the cause of B. a. spontaneous rib fractures. With the continuous use of glucocorticoids in a relatively short period of time (sometimes in 3-5 weeks), a hormone-dependent course of B. a. is formed; the abolition of glucocorticoids can cause severe status asthmaticus, which is fatal.

An analysis of the clinical picture and a targeted examination of the patient allow us to solve three main diagnostic tasks: confirm (or reject) the presence of B. a., determine its form, establish the spectrum of allergens (with allergic B. a.) or pseudo-allergens (see. Pseudoallergy ), having etiological significance for B. a. in this patient. The last task is solved with the participation of allergists.

The diagnosis of bronchial asthma is based on the following criteria: characteristic attacks of expiratory suffocation with remote wheezing; significant differences in expiratory power during an attack (sharp decrease) and outside an attack: the effectiveness of b-adrenomimetics in stopping asthma attacks; eosinophilia of blood and especially sputum; the presence of concomitant allergic or polyposis rhinosinusopathy. Confirm the presence of B. a. characteristic changes in respiratory function; less specific are x-ray findings outside of an asthma attack. Of the latter in favor of the possible presence of B. a. may indicate signs of chronic emphysema And pneumosclerosis (more often found in infectious-dependent asthma) and changes in the paranasal sinuses - signs of mucosal edema, polypous, sometimes purulent process. With atopic B. a. X-ray changes in the lungs outside of an asthma attack may be absent even years after the onset of the disease.

From researches of FVD the main value for the diagnosis of B. and. has the identification of bronchial obstruction (as the leading type of ventilation disorders in B. a.) and, most importantly, characteristic of B. a. bronchial hyperreactivity, determined by the dynamics of respiratory function in provocative tests with inhalation of physiological active substances (acetylcholine, histamine, etc.), hyperventilation, physical activity. Bronchial obstruction is determined by the decrease in forced vital capacity in the first second of expiration (FVC 1) and expiratory power according to pneumotachometry. The latter method is very simple and can be used by a doctor at a regular outpatient appointment, incl. to identify the so-called latent bronchospasm, often found in patients with B. a. If the expiratory power measured before and after 5, 10 and 20 min after inhalation of a single dose of alupent (or another b-agonist in a metered-dose manual inhaler) by a patient, increases by 20% or more, then the test is considered positive, indicating the presence of bronchospasm. At the same time, a negative test in the remission phase with normal initial expiratory power does not give grounds to reject the diagnosis of B. a.

The degree of nonspecific bronchial hyperreactivity is assessed in the remission phase of B. a. using provocative inhalation tests with acetylcholine (carbocholine), sometimes histamine, PgF 2a, b-blockers. These studies, sometimes necessary for a dubious diagnosis of B. a., are carried out only in a hospital setting. A provocative test is considered positive if, after inhalation of an acetylcholine solution, FVC and (or) expiratory power decrease by more than 20%; in some cases, a clinically developed attack of B. is provoked and. A positive acetylcholine test confirms the diagnosis of B. a., a negative one allows you to reject it with a high degree of probability.

The diagnosis of separate forms B. and. is largely based on clinical data, the analysis of which, if necessary, is supplemented by special tests and allergological examination.

Aspirin asthma is highly suspected when attacks are clearly associated with aspirin or other non-steroidal anti-inflammatory drugs, and when asthma is the first manifestation of intolerance to these drugs, especially in women over 30 years of age who do not have a personal and family history of atopy and suffer from pansinusitis or nasal polyposis, complementing the aspirin triad. The diagnosis is more reliable if during B.'s attacks and. a normal level of lgE in the blood is detected in the presence of blood eosinophilia. In doubtful cases, a provocative oral test with acetylsalicylic acid (in minimal doses) is sometimes performed in specialized institutions, but the widespread use of this test cannot be recommended due to the possibility of severe reactions.

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

Atopic B. a. are recognized by the features of the clinical course, the presence of concomitant manifestations of atopy (hay fever, atopic dermatitis, food allergies, etc.), family and allergic history data. The diagnosis is confirmed by identifying reaginic type sensitization in the patient (see. Allergy ) and positive results of elimination tests (cessation of contact with suspected allergens), as well as provocative tests with certain allergens. For atonic B. a. characterized by an increased content of total lgE in serum, as well as the presence of allergen-specific lgE. Relatively often there is a decrease in the number of T-lymphocytes, especially T-suppressors.

Infection-dependent B. a. it is assumed primarily in cases of manifestation of asthma attacks against the background of already formed chronic bronchitis, chronic pneumonia, or in the presence of chronic foci of infection in the upper respiratory tract. However, in all cases it is necessary to differentiate infectious-dependent and atopic forms of B. a. In favor of infection-dependent B. a. evidence of a delayed onset and a long duration of asthma attacks, a frequent association of their increase with an acute or exacerbated chronic respiratory infection, a tendency to develop asthmatic status, the absence of reagin-type sensitization in patients, positive skin and provocative inhalation tests with bacterial allergens. The main differences between atopic and infection-dependent forms of B. a. given in the table .

Bronchial asthma is one of the most serious diseases of the respiratory system and has several varieties. A persistent form of bronchial asthma is a type of disease that is accompanied by constant manifestations, including regular spasms of the bronchi.

Depending on the severity, bronchial asthma is divided into intermittent, that is, episodic, and persistent, a chronic type of pathology. Such a disease can last for years, it is characterized by a severe course with many complications and requires constant treatment.

When diagnosing bronchial asthma, the words "persistent course" indicate that the pathology is chronic, accompanied by regular spasms of the bronchi. It is one of the most common and dangerous forms of this disease of the respiratory system.

The constant exacerbations that accompany the persistent course of asthma occur against the background of inflammation of the airways caused by exposure to certain irritants. As a result of this, the bronchial mucosa swells and begins to actively produce an increased amount of mucous secretion necessary for protection.

The clinical picture of persistent bronchial asthma includes a feeling of heaviness in the chest area, asthma attacks, heavy breathing, and a persistent cough. The patient is not able to breathe deeply or exhale completely.

The disease develops over many years, periods of remission are regularly replaced by periods of exacerbation, giving a person discomfort, interfering with normal life.

Classification of persistent asthma

Depending on the severity of the disease of the respiratory system, several varieties of persistent asthma are distinguished, each of which has characteristic manifestations and course features:

• light;
• average;
• heavy.

With mild persistent bronchial asthma, asthma attacks disturb the patient 1-2 times during the week and 2-4 times a month at night. There are no daily attacks if there is no aggressive influence of external factors. Seizures can interfere with the life of the patient, disrupt sleep.

In case of severity, the following symptoms are observed: night attacks more often 1-2 times a week, daytime attacks can occur several times over 7 days. A person cannot lead an active, full life, as he has increasing manifestations of respiratory failure.

Severe asthma is accompanied by regular suffocating attacks, which can disturb the patient every day and night. Physical activity is severely limited. Relief of suffocation is carried out with the help of special medications.

Also stands out the concept of status asthmaticus - a pathological condition that is dangerous to human life. Most often, it develops abruptly and unexpectedly, accompanied by severe attacks of suffocation, resistant to medical treatment.

For their relief, drugs from the group of corticosteroids are used. Treatment of status asthmaticus is carried out only in a hospital, as this condition poses a serious threat to the life of the patient.

Causes of Persistent Asthma

The development of persistent asthma is associated with the aggressive effects of certain environmental factors and the characteristics of the human body. The most common causes of this disease include:

1. hereditary factor.
2. Allergy.
3. infectious diseases.
4. Obesity of varying degrees.
5. Work in hazardous industries.
6. Bad environmental situation.

Genetic predisposition plays an extremely important role in the formation of persistent bronchial asthma. If one of the parents is diagnosed with this pathology, the likelihood of its development in the child increases significantly.

Allergic reactions are one of. Allergens can enter the respiratory tract both at home and on the street, in the office or at work. The most common allergens include food, drugs, pet hair, cosmetics or household chemicals, dust particles, tobacco smoke, perfumes.

Infectious diseases such as bronchitis, pneumonia, SARS or influenza have a negative effect on the weakened body of an allergic person, which can cause the development of another suffocating attack, for which medications are used.

Clinical picture

With a persistent course of bronchial asthma, a pronounced clinical picture is observed, so the diagnosis of the disease does not cause great difficulties.

The main symptoms of the disease:

• choking, heavy breathing;
• feeling of heaviness in the bronchi and chest;
• wheezing and whistling sounds that appear during exhalation;
• barking type unproductive cough;
• sleep disturbances due to exacerbation of seizures at this particular time;
• excessive pallor of the skin;
• swelling of the blood vessels in the neck.

Asphyxiation attacks differ in frequency - they can disturb the patient both several times a month and every day. The disease is characterized by an increasing exacerbation of symptoms, but regardless of the severity of bronchial asthma, the signs of pathology themselves are always the same. Incorrectly selected or untimely treatment can aggravate the clinical picture.

Diagnostic methods

The main diagnostic methods used in persistent asthma are the examination of the patient and the collection of an anamnesis of the disease. In most cases, the symptoms of the pathology clearly indicate the presence of bronchial asthma in the patient.

Additional diagnostic measures:

1. Laboratory blood test.
2. The study of sputum separated by coughing.
3. Conducting electrocardiography.
4. Spirometry, that is, the study of the function of external respiration.
5. X-ray of the chest organs.

If an allergic origin of persistent bronchial asthma is suspected, the patient is examined by an allergist, who determines which allergen provoked the development of the disease.

Treatment

Persistent asthma is treated with various medications, which are selected individually depending on the characteristics of the development and severity of the disease.

Bronchial asthma of a mild course is stopped by corticosteroids intended for inhalation use, as well as bronchodilators, which eliminate the symptoms of the disease. Asthmatics diagnosed with moderate pathology are prescribed short-acting beta-agonists for urgent relief of choking and long-acting agonists to prevent daytime and nighttime attacks.

In a severe form of the disease of the respiratory system, the use of inhaled corticosteroids is combined with the simultaneous administration of drugs in the form of tablets. But since such medicines can become addictive over time, their dosage is gradually increased. Relief of allergic manifestations is carried out by taking antihistamines.

Prevention

In order to prevent asthma, several important recommendations must be followed.

Allergy sufferers are not recommended to keep pets, as their hair is one of the main allergens that provoke the development and exacerbation of persistent bronchial asthma. It is also necessary to stop smoking - both active and passive.

It is very useful to regularly take walks in the fresh air, away from noisy roads and harmful industries. Performing breathing exercises helps to improve the functioning of the bronchi and lungs, as well as prevent the onset of a suffocating attack.

Persistent bronchial asthma is one of the most severe diseases of the respiratory system, which is accompanied by attacks of suffocation, severe coughing, and sleep disturbances. Treatment of the disease of mild and moderate severity is allowed to be carried out at home.

Pathology that occurs in severe form is treated only in a hospital, as it poses a serious danger to the patient's life.