Bronchial asthma, mixed, severe, uncontrolled, hormone dependent. Severe bronchial asthma Moderate persistent bronchial asthma is characterized by

Bronchial asthma, asthma, asthma attacks, suffocation, asphyxia due to illness, difficulty breathing

Version: MedElement Disease Directory

Asthma (J45)

Pulmonology

general information

Short description

Bronchial asthma* is a chronic inflammatory disease of the airways in which many cells and cellular elements are involved. Chronic inflammation causes bronchial hyperresponsiveness, 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 either spontaneously or with treatment.

Bronchial hyperreactivity - increased sensitivity of the lower respiratory tract to various irritating stimuli, which are usually contained in the inhaled air. These stimuli are indifferent to healthy people. Clinically, bronchial hyperreactivity most often manifests itself as episodes of wheezing, difficult breathing in response to an irritating stimulus in individuals with a hereditary predisposition.
There is also a hidden hyperreactivity of the bronchi, 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, fur and epidermis of domestic animals, down and feathers of poultry, spores and other elements of fungi).

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

Note. Excluded from this subcategory:

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) - 2011 revision.

Classification

Asthma classification is based on a combined assessment of clinical symptoms and pulmonary function tests. 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 G. B. Fedoseev. (1982)

1. Stages of AD development:

1.1State of pre-asthma- conditions that pose a threat 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 the sputum, caused by immunological or non-immunological mechanisms of pathogenesis) .

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

2. Forms of BA(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 Infectious-dependent - indicating the infectious agents and the nature of the infectious dependence, which can manifest itself as 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 Dyshormonal - indicating the endocrine organ whose function is altered and the nature of the dishormonal changes.
3.5 Neuropsychic - indicating options for neuropsychic changes.
3.6 Adrenergic imbalance.
3.7 Primary altered bronchial reactivity, which is formed without the participation of altered reactions of the immune, endocrine and nervous systems. May be congenital or acquired. Manifests itself under the influence of chemical, physical and mechanical irritants and infectious agents. Attacks of suffocation during physical exertion, exposure to cold air, medications, and other things are typical.

Note to point 3. A patient may have one pathogenetic mechanism of asthma, or various combinations of mechanisms are possible (at the time of 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 division of AD into pathogenetic mechanisms and the identification of the main one is significantly difficult. Nevertheless, this is justified due to the fact that each of the pathogenetic mechanisms presupposes a certain, unique nature of drug therapy.

4. Severity of asthma(in some cases, such a division is arbitrary; for example, with a mild course, the patient may die from suddenly developing status asthmaticus, and with a rather severe course, “spontaneous” remission is possible):

4.1 Mild course: exacerbations are not long-lasting, occurring 2-3 times a year. As a rule, attacks of suffocation are stopped by taking various bronchodilators orally. During 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 can be stopped with injections of medications.

4.3 Severe: exacerbations occur frequently (5 or more times a year) and vary in duration. The attacks are severe and often progress to an asthmatic state.

5. Phases of bronchial asthma:

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

2. Fading exacerbation - in this phase, attacks are more rare and mild. Physical and functional signs of the disease are less pronounced than in the acute phase.

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

6. Complications:

1. Pulmonary: emphysema, pulmonary failure, 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

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

Stage 2. Mild persistent asthma:

Symptoms more often than once a week, but less than once a day;

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

Stage 3. Persistent asthma of moderate severity:

Daily symptoms;
- exacerbations can affect physical activity and sleep;
- nighttime symptoms more than once a week;
- FEV1 or PSV from 60 to 80% of the required values;
- variability of FEV1 or PEF >30%.

Stage 4. Severe persistent asthma:
- daily symptoms;
- frequent exacerbations;
- frequent nighttime symptoms;
- limitation of physical activity;
- FEV 1 or PSV<= 60 от должных значений;
- variability of FEV1 or PEF >30%.

Additionally, the following are highlighted phases of asthma progression:
- exacerbation;
- unstable remission;
- remission;
- stable remission (more than 2 years).

Classification according to the Global Initiative for Asthma(GINA 2011)
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 volume of therapy is required to control the disease (for example, GINA stage 4) or control cannot be achieved despite a large volume of therapy.

Patients with different asthma phenotypes have different responses to traditional treatment. With the advent of specific treatments for each phenotype, asthma that was previously considered severe may become mild.
The ambiguity of terminology associated with asthma severity 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 a consequence of inadequate treatment.

Classification according to ICD-10

J45.0 Asthma with a predominance of an allergic component (if there is a connection between the disease and an identified 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 (if the disease is associated with external factors of a non-allergenic nature or unknown 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. Severity of the disease (for example, severe persistent asthma).
3. Current phase (for example, exacerbation). In case of remission with the help of steroid drugs, it is advisable to indicate a maintenance dose of an anti-inflammatory drug (for example, remission at a dose of 800 mcg of beclomethasone per day).
4. Complications of asthma: respiratory failure and its form (hypoxemic, hypercapnic), especially status asthmaticus.

Etiology and pathogenesis

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

1. Inflammatory cells in the airways of asthma.

1.1 Mast cells. Under the influence 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). Increased numbers of mast cells in airway smooth muscle may be associated with bronchial hyperresponsiveness.

1.2 Eosinophils. In the respiratory tract, the number of eosinophils is increased. These cells secrete basic proteins that can damage the bronchial epithelium. Eosinophils may also be involved in the release of growth factors and airway remodeling.

1.3 T lymphocytes. In the airways there is an increased number of T lymphocytes, which release specific cytokines that regulate the process of eosinophilic inflammation and the production of IgE by B lymphocytes. Increased Th2 cell activity may be due in part to a decrease in the number of regulatory T cells, which normally suppress Th2 lymphocytes. It is also possible to increase the number of inKT cells, which 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 transformation 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 low-affinity IgE receptors. 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 smoking patients, the number of neutrophils increases. Their pathophysiological role is not clear. It is assumed that an increase in their number may be a consequence of GCS therapy GCS (glucocorticoids, glucocorticosteroids) are drugs whose main properties are to inhibit the early stages of 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 respiratory tract - are detected in the airways of patients with asthma and are often considered as a process of bronchial remodeling. Structural changes may result from 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 is the growth of an organ, its part or tissue as a result of cell proliferation and an increase in their volume
and hyperplasia Hyperplasia is an increase in the number of cells, intracellular structures, intercellular fibrous formations due to enhanced organ function or as a result of pathological tissue neoplasm.
there is an increase in the thickness of the smooth muscle layer, which contributes to a general thickening of the bronchial wall. This process may depend on the severity of the disease.

3.2Blood vessels. Proliferation occurs under the influence of growth factors, such as vascular endothelial growth factor (VEGF). Proliferation - an increase in the number of cells of any tissue due to their reproduction
vessels of the bronchial wall, promoting thickening of the bronchial wall.

3.3 Hypersecretion of mucus 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 asthma, which leads to the appearance of symptoms of the disease and typical physiological changes.

Factors that cause 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 narrowing of the airways; almost completely reversible under the influence of bronchodilators.

4.2 Swelling of the airways, resulting from increased permeability of the microvascular bed, which is caused by the action of inflammatory mediators. Edema can play a particularly important role during exacerbations.

4.3 Thickening of the bronchial wall as a result of structural changes. This factor can be of great importance in severe asthma. Thickening of the bronchial wall is not completely reversible under the influence of 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), caused by persistent closure of their lumen in any area.
lumen of the bronchi (“mucus plugs”) and is the result of increased secretion of mucus and the formation of inflammatory exudate.

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

Epidemiology

Around 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. In approximately half of patients, bronchial asthma develops before 10 years of age, and in a third - before 40 years of age.
Among children with bronchial asthma, there are twice as many boys as girls, although the sex ratio levels off at age 30.

Risk factors and groups

Factors influencing the risk of developing asthma are divided into:
- factors determining the development of the disease - internal factors (primarily genetic);
- factors that provoke the occurrence of symptoms - external factors.
Some factors apply 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 hyperresponsiveness).

2. Obesity.

External factors:

1. Allergens:

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

External allergens (pollen, fungi, including mold and yeast).

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 people of certain professions

Profession	Substance
	Proteins of animal and plant origin
Bakers	Flour, amylase
Farmers-pastoralists	Warehouse tongs
Production of detergents	Bacillus subtilis enzymes
Electric 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 house mites, bird droppings and feathers
Experimental researchers, veterinarians	Insects, dander and animal urine proteins
Sawmill workers, carpenters	Wood dust
Loaders/transport workers	grain dust
Silk workers	Butterflies and silkworm larvae
	Inorganic compounds
Cosmetologists	Persulfate
Cladding	Nickel salts
Oil refinery workers	Platinum salts, vanadium Organic compounds
Car painting	Ethanolamine, diisocyanates
Hospital workers	Disinfectants (sulfathiazole, chloramine, formaldehyde), latex
Pharmaceutical production	Antibiotics, piperazine, methyldopa, salbutamol, cimetidine
Rubber processing	Formaldehyde, ethylene diamide
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 primary importance. There is evidence that in urban areas, in children with atopic asthma, individual comprehensive measures to remove allergens in the home led to a decrease in pain.

Clinical picture

Clinical diagnostic criteria

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

Symptoms, course

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

1. Detection of bronchial hyperreactivity, as well as reversibility of obstruction spontaneously or under the influence of treatment (decrease in response to appropriate therapy).
2. Non-productive hacking cough; extended exhalation; dry, whistling, usually treble-like, wheezing in the chest, occurring more at night and in the morning; expiratory shortness of breath, attacks of expiratory suffocation, congestion (stiffness) of the chest.
3. Dependence of respiratory symptoms on contact with provoking agents.

Also essential 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, it is necessary to clarify the following questions:
- Does the patient have episodes of wheezing, including repeated episodes?

Does the patient have a cough at night?

Does the patient wheeze or cough after exercise?

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

Does the patient notice that his cold “goes down into the chest” or lasts more than 10 days?

Do symptoms improve with appropriate asthma medications?

During physical examination, symptoms of asthma may be absent due to the variability of manifestations of the disease. The presence of bronchial obstruction is confirmed by wheezing sounds detected during auscultation.
In some patients, wheezing may be absent or detected only during forced expiration, 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 speaking, distended chest, participation of auxiliary muscles in the act of breathing and retraction of 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 asthma

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

2. Bronchospasm induced by physical activity. Refers to the manifestation of non-allergic forms of asthma, when the phenomena of airway hyperreactivity dominate. In most cases, physical activity is an important or sole cause of the onset of symptoms of the disease. Bronchospasm as a result of physical activity usually develops 5-10 minutes after cessation of exercise (rarely during exercise). Patients experience typical symptoms of asthma or sometimes a prolonged cough that goes away on its own within 30-45 minutes.
Forms of exercise such as running cause asthma symptoms more often.
Bronchospasm caused by physical activity often develops when inhaling dry, cold air, and more rarely in hot and humid climates.
Evidence in favor of asthma is the rapid reduction of symptoms of post-exertional bronchospasm after inhalation of a β2-agonist, as well as the prevention of the development of symptoms due to inhalation of a β2-agonist before exercise.
In children, asthma can sometimes manifest itself only during physical activity. In this regard, in such patients or if there is doubt about the diagnosis, it is advisable to conduct an exercise test. The diagnosis is facilitated by an 8-minute running protocol.

Clinical picture of an asthma attack quite typical.
With an allergic etiology of asthma, before the development of suffocation, itching (in the nasopharynx, ears, in the chin area), nasal congestion or rhinorrhea, a feeling of lack of “free breathing”, and a dry cough may be observed. With the development of an attack of suffocation, expiratory shortness of breath occurs: inhalation is shortened, exhalation lengthened; the duration of the respiratory cycle increases and the respiratory rate decreases (up to 12-14 per minute).
When listening to the lungs, in most cases, against the background of prolonged exhalation, a large number of scattered dry rales, mainly whistling, are detected. As the attack of suffocation progresses, wheezing sounds on exhalation are heard at a certain distance from the patient in the form of “wheezing” or “music of the bronchi.”

With a prolonged attack of suffocation, which lasts more than 12-24 hours, the small bronchi and bronchioles become blocked with inflammatory secretions. The patient's general condition worsens significantly, and the auscultatory picture changes. Patients experience painful shortness of breath, which worsens with the slightest movements. The patient takes a forced position - sitting or half-sitting with the shoulder girdle fixed. All auxiliary muscles are involved in the act of breathing, the chest expands, and the intercostal spaces are drawn in during inhalation, cyanosis of the mucous membranes and acrocyanosis occurs and intensifies. It is difficult for the patient to speak; sentences are short and abrupt.
On auscultation, a decrease in the number of dry rales is noted; in some places they are not heard at all, as is vesicular breathing; so-called silent lung zones appear. Above the surface of the lungs, a pulmonary sound with a tympanic tint is determined by percussion - a box sound. The lower edges of the lungs are lowered, their mobility is limited.
The end of an attack of suffocation is accompanied by a cough with the release of a small amount of viscous sputum, easier breathing, a decrease in shortness of breath and the number of wheezing heard. For a long time, a few dry rales may be heard while maintaining an extended exhalation. After the attack stops, 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 a point as “respiratory arrest is inevitable.” The severity of asthma and the severity of exacerbation of asthma are not the same thing. For example, with mild asthma, mild and moderate exacerbations may occur; with moderate and severe asthma, mild, moderate, and severe exacerbations may occur.

Severity of asthma exacerbation according to GINA-2011

	Lung	Average gravity	Heavy	Stopping breathing is inevitable
Dyspnea	When walking. Can lie	When talking; children cry becomes quieter and shorter, there are difficulties with feeding. Prefers to sit	At rest, children stop eating. Sit leaning forward
Speech	Offers	In phrases	In words
Level wakefulness	May be excited	Usually excited	Usually excited	Inhibited or confused
Breathing rate	Increased	Increased	More than 30 per minute
Participation of auxiliary muscles in the act of breathing and retraction of the supraclavicular fossa	Usually no	Usually there is	Usually there is	Paradoxical movements chest and abdominal walls
Wheezing	Moderate, often only when exhale	Loud	Usually loud	None
Pulse (per minute)	<100	>100	>120	Bradycardia
Paradoxical pulse	Absent <10 мм рт. ст.	There may be 10-25 mm Hg. st	Often available >25 mmHg Art. (adults), 20-40 mm Hg. Art. (children)	Absence allows assume fatigue respiratory muscles
PEF after the first injection bronchodilator in % of due or the best individual meaning	>80%	About 60-80%	<60% от должных или наилучших individual values (<100 л/мин. у взрослых) or the effect lasts<2 ч.	Impossible to evaluate
RaO 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 breathing failure
SatO 2,% (during breathing air) - oxygen saturation or the degree of saturation of hemoglobin in arterial blood 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:

Infancy (2-12 months)<160 в минуту;

Younger (1-2 years)<120 в минуту;

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

Under 2 months< 60 в минуту;

2-12 months< 50 в минуту;

1-5 years< 40 в минуту;

6-8 years< 30 в минуту.

Diagnostics

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

Study of external respiratory function indicators

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 - POSV (peak expiratory volume flow), MEF 25 (maximum volume flow at the point of 25% FVC, (FEF75) and FEV1.

To assess the reversibility of bronchial obstruction, it is used pharmacological bronchodilation test with short-acting β2-agonists (most often salbutamol). Before the test, you should avoid taking short-acting bronchodilators for at least 6 hours.
First, the initial flow-volume curve of the patient's forced breathing is recorded. Then the patient takes 1-2 inhalations of one of the short-acting β2-agonists. After 15-30 minutes, the flow-volume curve is recorded. When FEV1 or POS increases by 15% or more, airway obstruction is considered reversible or bronchodilator-responsive, and the test is considered positive.

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

2. Peak flowmetry. It is used to assess the effectiveness of treatment and objectify the presence and severity of bronchial obstruction.
Peak expiratory flow (PEF) is assessed - the maximum speed at which air can exit the airways during forced exhalation after a full inhalation.
The patient's PEF values ​​are compared with normal values ​​and with the best PEF values ​​observed in this patient. The level of decrease in PEF allows us to draw conclusions about the severity of bronchial obstruction.
The difference in PSV values ​​measured during the day and 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, coughing, and wheezing occur less than once a week. The duration of exacerbations ranges from several hours to several days. Night attacks - 2 or less times a month. In the period between exacerbations, lung function is normal; PEF - 80% of normal or less.

2.2 Mild course of persistent asthma (stage II). Daytime attacks occur 1 or more times a week (no more than 1 time per day). Night attacks recur more often than 2 times a month. During an exacerbation, the patient's activity and sleep may be disrupted; PEF - 80% of normal or less.

2.3 Persistent asthma of moderate severity (stage III). Daily attacks of suffocation, night attacks occur once a week. Due to exacerbations, the patient’s activity and sleep are disrupted. The patient is forced to use short-acting inhaled beta-agonists daily; PSV - 60 - 80% of the norm.

2.4 Severe persistent asthma (stage IV). Daytime and nighttime symptoms are constant, which limits the patient’s physical activity. The PEF indicator is less than 60% of the norm.

3. Allergy research. An allergy history (eczema, hay fever, family history of asthma or other allergic diseases) is analyzed. Positive skin tests with allergens and increased levels of general and specific IgE in the blood 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. It is performed in patients with suspected asthma and normal spirography values.

During a histamine test, the patient inhales nebulized histamine in progressively increasing concentrations, each of which can cause bronchial obstruction.
The test is assessed as positive when the volumetric air flow rate deteriorates by 20% or more as a result of inhalation of histamine in a concentration one or several orders of magnitude less than that which causes similar changes in healthy people.
A test with methacholine is carried out and evaluated in the same way.

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

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

Main diagnostic criteria for asthma:

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 status asthmaticus.
3. Determination of signs of bronchial obstruction (FEV1 or POS ext.< 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. Detection of signs of bronchial hyperreactivity (hidden bronchospasm) in patients with initial normal levels 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 physical activity;
- repeated sensations of chest tightness and/or episodes of wheezing;
- the fact of waking up at night from these symptoms strengthens the criterion.
2. A burdened allergic history (the patient has eczema, hay fever, hay fever) or a burdened family history (BA, atopic diseases in the patient’s family members).

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

Professional BA

Bronchial asthma caused by professional activities 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 lack thereof.

Suspicion of occupational asthma should arise when symptoms of rhinitis, cough and/or wheezing appear, especially in non-smoking patients. Establishing a diagnosis requires systematic collection of information about work history and workplace environmental factors.

Criteria for diagnosing professional asthma:
- clearly established occupational exposure to known or suspected sensitizing agents;
- absence of asthma symptoms before hiring or a clear worsening of asthma after hiring.

Laboratory diagnostics

Non-invasive determination of markers of airway inflammation

1. Study of sputum spontaneously produced or induced by inhalation of a hypertonic solution on inflammatory cells - eosinophils or neutrophils. 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 asthma, there is an increase in FeNO levels (in the absence of therapy with inhaled corticosteroids) compared to individuals without asthma, however, these results are not specific for this disease. The value of FeNO for the diagnosis of AD has not been assessed in prospective studies.

3. Skin tests with allergens are the main method for assessing allergic status. Such tests are highly sensitive, easy to use and do not require much time. Please be aware that performing samples incorrectly may result in false positive or false negative results.

4. Determination of specific IgE in blood serum is a more expensive method compared to skin tests, which is not superior to them in reliability.
In some patients, specific IgE may be detected in the absence of any symptoms and may not play any role in the development of asthma. Thus, positive test results do not necessarily indicate the allergic nature of the disease or the connection of the allergen with the development of asthma.
The presence of allergen exposure and its relationship with manifestations of asthma should be confirmed by medical history. Measuring the level of total IgE in serum is not a method for diagnosing atopy.

Clinical tests

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

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

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

Differential diagnosis

1. Differential diagnosis of asthma variants.

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

Signs	Atopic variant	Infectious variant
Allergic diseases in the family	Often	Rarely (except asthma)
Atopic diseases in a patient	Often	Rarely
Relationship between an attack and an external allergen	Often	Rarely
Features of the attack	Acute onset, rapid development, usually short duration and mild course	Gradual onset, long duration, often severe course
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	Typically moderate	Often high
Specific IgE antibodies to non-infectious allergens	Present	None
Skin tests with extracts of non-infectious allergens	Positive	Negative
Exercise test	Mostly negative	Mostly positive
Allergen elimination	Possible, often effective	Impossible
Beta-agonists	Very effective	Moderately effective
Anticholinergics	Ineffective	Effective
Eufillin	Very effective	Moderately effective
Intal, tiled	Very effective	Less effective
Corticosteroids	Effective	Effective

2. Conduct differential diagnosis of BA with chronic obstructive pulmonary disease(COPD), which is characterized by more persistent bronchial obstruction. In patients with COPD, the spontaneous lability of symptoms typical of BA is not observed, there is no or significantly less daily variability in FEV1 and POS, and complete irreversibility or less reversibility of bronchial obstruction is determined in a test with β2-agonists (increase in FEV1 is less than 15%).
In COPD sputum, neutrophils and macrophages predominate rather than eosinophils. In patients with COPD, the effectiveness of bronchodilator therapy is lower; anticholinergic drugs are more effective bronchodilators rather than 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 Episodes of wheezing 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 and parental smoking.

1.2 Persistent wheezing with early onset (before age 3 years). Children commonly experience recurrent episodes of wheezing associated with acute respiratory viral infections. In this case, children do not have signs of atopy and there is no family history of atopy (unlike children of the next age group with late onset of wheezing/bronchial asthma).
Episodes of wheezing typically continue into school age and are still present in a significant proportion of children aged 12 years.
The cause of episodes of wheezing in children under 2 years of age is usually a respiratory syncytial viral infection; in children 2-5 years of age - other viruses.

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

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

Chronic rhinosinusitis;

Gastroesophageal reflux;

Repeated viral infections of the lower respiratory tract;

Cystic fibrosis;

Bronchopulmonary dysplasia;

Tuberculosis;

Foreign body aspiration;
- immunodeficiency;

Primary ciliary dyskinesia syndrome;

Developmental defects that cause 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;

Upper airway obstruction and foreign body aspiration;

Other obstructive pulmonary diseases, especially COPD;

Non-obstructive pulmonary diseases (for example, 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, asthma is underdiagnosed in old age.

Risk factors for underdiagnosis of asthma in elderly patients

3.1 From the patient's side:
- depression;
- social isolation;
- memory and intelligence impairment;


- decreased perception of shortness of breath and bronchoconstriction.

3.2 From the doctor's side:
- misconception that asthma does not begin in old age;
- difficulties in studying pulmonary function;
- perception of asthma symptoms as signs of aging;
- accompanying illnesses;
- underestimation of shortness of breath due to decreased physical activity of the patient.

Complications

Complications of bronchial asthma are divided into pulmonary and extrapulmonary.

Pulmonary complications: chronic bronchitis, hypoventilation pneumonia, 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 long-term use of systemic corticosteroids may occur.

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Treatment

Objectives of treatment of bronchial asthma(BA):

Achieving and maintaining symptom control;

Maintaining a normal level of activity, including physical activity;

Maintaining lung function at normal or as close to normal levels as possible;

Prevention of exacerbations of asthma;

Preventing unwanted effects of anti-asthma drugs;

Preventing deaths from asthma.

Levels of asthma control(GINA 2006-2011)

Characteristics	Controlled asthma(all of the above)	Partially controlled asthma(presence of any manifestation within a week)	Uncontrolled asthma
Daytime symptoms	No (≤ 2 episodes per week)	> 2 times a week	Presence of 3 or more signs of partially controlled asthma in any week
Activity Limit	No	Yes - of any severity
Nocturnal symptoms/awakenings	No	Yes - of any severity
Need for emergency medications	No (≤ 2 episodes per week)	> 2 times a week
Pulmonary function tests (PEF 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 exacerbation 3

1 Pulmonary function testing is not reliable in children 5 years of age and younger. Periodic assessment of the level of asthma control in accordance with the criteria specified 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 assessment of its adequacy
3 By definition, the development of any exacerbation indicates that asthma is not controlled

Drug therapy

Medicines for the treatment of asthma:

1. Drugs that control the course of the disease (maintenance therapy):
- inhaled and systemic corticosteroids;
- antileukotriene drugs;
- inhaled long-acting 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. Emergency medications (to relieve symptoms):
- inhaled rapid-acting β2-agonists;
- anticholinergics;
- short-acting theophylline;
- oral short-acting β2-agonists.
These medications are taken to relieve symptoms as needed. They have a rapid effect, eliminate bronchospasm and relieve its symptoms.

Drugs for the treatment of asthma can be administered in different 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 drug is achieved;
- the risk of systemic side effects is significantly reduced.

For maintenance therapy, inhaled corticosteroids are most effective.

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

Increasing use (especially daily use) of rescue medications indicates worsening asthma control and the need for a review of 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 asthma, and when they are discontinued, some patients experience a worsening of their condition within weeks or months.
Local undesirable effects of inhaled corticosteroids: oropharyngeal candidiasis, dysphonia, and sometimes cough due to irritation of the upper respiratory tract.
Systemic side effects of long-term therapy with high doses of inhaled corticosteroids: tendency to bruise, suppression of the adrenal cortex, decreased bone mineral density.

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

A drug	Low daily allowance doses(mcg)	Average daily allowance doses(mcg)	High daily allowance doses(mcg)
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 (Freon-free) inhalers

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

A drug	Low daily allowance doses(mcg)	Average daily allowance doses(mcg)	High daily allowance doses(mcg)
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: antagonists of cysteinyl leukotriene receptors of the 1st subtype (montelukast, pranlukast and zafirlukast), as well as a 5-lipoxygenase inhibitor (zileuton).
Action:
- weak and variable bronchodilator 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.
Antileukotriene drugs can be used as second-line drugs for the treatment of adult patients with mild persistent asthma. Some patients with aspirin-induced 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.
They should not be used as monotherapy for asthma, since there is no evidence that these drugs suppress inflammation in asthma.
These drugs are most effective in combination with inhaled corticosteroids. Combination therapy is preferable in the treatment of patients in whom the use of medium doses of inhaled corticosteroids does not allow them to achieve control of asthma.
With regular use of β2-agonists, it is possible to develop relative refractoriness to them (this applies to both short- and long-acting drugs).
Therapy with long-acting inhaled β2-agonists is characterized by a lower incidence of systemic adverse effects (such as cardiovascular stimulation, skeletal muscle tremor, and hypokalemia) compared with long-acting oral β2-agonists.

Long-acting oral β2-agonists: sustained-release dosage forms of salbutamol, terbutaline and bambuterol (a prodrug that is converted into 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. Adverse cardiovascular reactions may also occur when oral β2-agonists are used in combination with theophylline.

Rapid-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.
Inhaled rapid-acting β2-agonists are emergency medications and are the drugs of choice for relieving bronchospasm during exacerbation of asthma, as well as for preventing exercise-induced bronchospasm. Should be used only as needed, with the smallest possible doses and frequency of inhalations.
Increasing, especially daily, use of these drugs indicates a loss of control over asthma and the need to review therapy. If there is no rapid and stable improvement after inhalation of a β2-agonist during an exacerbation of asthma, the patient should also be monitored further and, possibly, given a short course of therapy with oral corticosteroids.
The use of oral β2-agonists in standard doses is accompanied by more pronounced undesirable systemic effects (tremor, tachycardia) than when using inhaled forms.

Oral short-acting β2-agonists(refer to emergency medicine) can be prescribed only to a few patients who are unable to take inhaled drugs. Side effects are observed more often.

Theophylline 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 daily.
Based on available data, sustained-release theophylline has little effectiveness as a first-line agent for maintenance treatment of bronchial asthma.
The addition of theophylline may improve treatment outcomes for patients in whom monotherapy with inhaled corticosteroids does not achieve asthma control.
Theophylline has been shown to be effective as monotherapy and therapy prescribed in addition to inhaled or oral corticosteroids in children over 5 years of age.
When using theophylline (especially in high doses - 10 mg/kg body weight per day or more), significant side effects are possible (usually decrease or disappear with long-term use).
Undesirable effects of theophylline:
- nausea and vomiting are the most common side effects at the beginning of use;
- disorders of the gastrointestinal tract;
- loose stools;
- heart rhythm disturbances;
- convulsions;
- death.

Sodium cromoglycate and nedocromil sodium(cromones) have limited value in long-term therapy of asthma in adults. There are known examples of the beneficial effect of these drugs in mild persistent asthma and bronchospasm caused by physical activity.
Cromones have a weak anti-inflammatory effect and are less effective compared to 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 of which is not achieved with inhaled corticosteroids.
In a small number of patients, the emergence of an underlying disease (Churg-Strauss syndrome) was observed when GCS was discontinued due to anti-IgE treatment.

System GCS for severe uncontrolled asthma, they are indicated in the form of long-term therapy with oral medications (recommended use for a longer period than with the usual two-week course of intensive therapy with systemic corticosteroids - standard 40 to 50 mg of prednisolone per day).
The duration of use of systemic corticosteroids is limited by the risk of developing serious undesirable effects (osteoporosis, arterial hypertension, suppression of the hypothalamic-pituitary-adrenal axis, obesity, diabetes mellitus, cataracts, glaucoma, muscle weakness, stretch marks and a tendency to bruise due to thinning of the skin). Patients taking any form of systemic corticosteroids for a long time require medications to prevent osteoporosis.

Oral antiallergic drugs(tranilast, repirinast, 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 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 asthma is usually lifelong. It should be borne in mind that drug therapy does not replace measures to prevent the patient’s contact with allergens and irritants. The approach to treating a patient is determined by his condition and the goal currently facing the doctor.

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

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

Basic anti-relapse therapy: 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 (SGC) and bronchodilators with the correction of acid-base metabolism and blood gas composition using medicinal and non-medicinal means.

Long-term maintenance therapy for asthma:

1. Assessment of the level of control over asthma.
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 treatment options that can serve as alternatives when choosing maintenance therapy for asthma. The effectiveness of therapy increases from step 1 to step 5.

Stage 1
Includes use of emergency medications as needed.
Intended only for patients who have not received maintenance therapy and who occasionally experience short-term (up to several hours) asthma symptoms during the day. For more frequent symptoms or episodic deterioration, patients should receive regular maintenance therapy (see step 2 or higher) in addition to rescue medications as needed.

Recommended rescue medications in step 1: rapid-acting inhaled β2-agonists.
Alternative drugs: inhaled anticholinergics, short-acting oral β2-agonists, or short-acting theophylline.

Stage 2
Emergency 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.

Stage 3

3.1. Rescue drug + one or two disease control drugs.
At stage 3, children, adolescents and adults are recommended: a combination of a low dose of inhaled corticosteroids with a long-acting inhaled β2-agonist. Administration is carried out using one inhaler with a fixed combination or using different inhalers.
If control of asthma 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 for the management of children) is to increase the doses of inhaled corticosteroids to medium doses.

3.3. Treatment option at step 3: a combination of low-dose inhaled corticosteroids with an antileukotriene drug. A low dose of sustained-release theophylline may be prescribed instead of an anti-leukotriene drug (these options have not been fully studied in children 5 years of age and younger).

Stage 4
Rescue drug + two or more disease control drugs.
The choice of drugs in step 4 depends on previous prescriptions in steps 2 and 3.
The preferred option: a 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 moderate-dose inhaled corticosteroids and a β2-agonist and/or a third maintenance drug (eg, an anti-leukotriene drug or sustained-release theophylline), the use of high-dose inhaled corticosteroids is recommended, but only as a trial therapy lasting 3-6 months.
With long-term use of high doses of inhaled corticosteroids, the risk of side effects increases.

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

The treatment effect is increased by the addition of 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 also increase the effectiveness of therapy.

Level 5
Emergency drug + additional options for using drugs to control the course of the disease.
The addition of oral corticosteroids to other maintenance therapy drugs can increase the effect of treatment, but is accompanied by severe adverse events. In this regard, this option is considered only in patients with severe uncontrolled asthma on the background of therapy corresponding to step 4, if the patient has daily symptoms that limit activity and frequent exacerbations.

Prescribing anti-IgE in addition to other maintenance therapy drugs improves control of allergic asthma if it is not achieved during treatment with combinations of other maintenance therapy drugs, which include high doses of inhaled or oral corticosteroids.

Well antibacterial therapy indicated in the presence of purulent sputum, high leukocytosis, accelerated ESR. Taking into account the antibiograms, the following is prescribed:
- spiramycin 3,000,000 units 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 intravenously.

Forecast

The prognosis is favorable with regular follow-up (at least 2 times a year) and rationally selected treatment.
Death 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 dysfunction 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 treatment, the disease can develop into a more severe form;

In severe and moderate severity of asthma, the prognosis depends on the adequacy of treatment and the presence of complications;
- concomitant pathology 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 case of asthma that began in childhood, about The long-term prognosis is favorable. As a rule, by puberty, children “outgrow” asthma, but they still have impaired pulmonary function, bronchial hyperreactivity, and abnormalities in the immune status.
With asthma that begins in adolescence, an unfavorable course of the disease is possible.
In asthma that begins in adulthood and old age, the nature of development and prognosis of the disease are more predictable.
The severity of the course depends on the form of the disease:
- allergic asthma is milder and has a more favorable prognosis;
- “pollen” asthma, as a rule, has a milder course compared to “dust” asthma;
- in elderly patients, a primarily severe course is observed, especially in patients with aspirin-induced asthma.

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

Hospitalization

Indications for hospitalization:
- severe attack of bronchial asthma;

There is no rapid response to bronchodilators and the effect lasts less than 3 hours;
- no improvement within 2-6 hours after starting oral corticosteroid therapy;
- further deterioration is observed - an increase in respiratory and pulmonary-cardiac failure, a “silent lung”.

Patients at high risk of death:
- having a history of conditions close to lethal;
- requiring intubation and artificial ventilation, which leads to an increased risk of intubation during subsequent exacerbations;
- who have already been hospitalized or sought emergency care due to bronchial asthma over the past year;
- taking or recently stopped taking oral medicationsglucocorticosteroids;
- using inhaled rapid-acting β2-agonists in excess quantities, especially more than one package of salbutamol (or equivalent) per month;
- with mental illness, a history of psychological problems, including abuse of sedatives;
- poor compliance with the treatment plan for bronchial asthma.

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 a patient from the clinical manifestations of atopic asthma by identifying the causative factor and eliminating contact with it in the future).

Patients should be taught proper administration of medications and the correct use of drug administration devices and peak flow meters to monitor peak expiratory flow (PEF).

The patient must be able to:
- control PSV;
- understand the difference between drugs of basic and symptomatic therapy;
- avoid asthma triggers;
- identify signs of worsening of the disease and independently stop attacks, as well as promptly seek medical help to stop severe attacks.
Control of asthma over a long period requires a written treatment plan (patient action algorithm).

List of preventive measures:

Stopping contact with cause-related allergens;
- termination of contact with nonspecific irritating environmental factors (tobacco smoke, exhaust gases, etc.);
- exclusion of occupational hazards;
- in the 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 medications;
- 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;
- premedication before invasive examination methods and surgical interventions - parenteral administration of drugs: corticosteroids (dexamethosone, prednisolone), methylxanthines (aminophylline) 20-30 minutes before the procedure. The dose should be determined taking into account age, body weight, severity of asthma and volume 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 (revision 2011) / ed. Belevsky A.S., M.: Russian Respiratory Society, 2012
2. Russian therapeutic reference book / edited by Academician of the Russian Academy of Medical Sciences Chuchalin A.G., 2007
   1. pp. 337-341
3. http://lekmed.ru
4. http://pulmonolog.com

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1. Exacerbation.

2. Fading exacerbation.

3. Remission.

VI. Complications

1. Pulmonary: emphysema, pulmonary failure, atelectasis, pneumothorax, etc.

2. Extrapulmonary: myocardial dystrophy, cor pulmonale, heart failure, etc.

However, at present, first of all, bronchial asthma should be classified according to severity, since this is what determines the tactics of patient management. The severity level is determined by the following indicators: 1. Number of nighttime symptoms per week. 2. Number of daytime symptoms per day and per week. 3. Frequency of use of short-acting b 2 -agonists. 4. The severity of physical activity and sleep disorders. 5. PEF values ​​and its percentage with the proper or best value. 6. Daily fluctuations of PSV. 7. Volume of therapy provided. There are 5 degrees of severity of bronchial asthma: mild intermittent, mild persistent; moderate persistent, severe persistent, severe persistent steroid dependent. (see table). Bronchial asthma of intermittent course. Asthma symptoms less than once a week; short exacerbations from several hours to several days. Night symptoms 2 times a month or less often; absence of symptoms and normal lung function between exacerbations. PEF>80% of expected and PEF fluctuations less than 20%. Bronchial asthma of mild persistent course. Symptoms once a week or more often, but less than once a day. Exacerbations of the disease can interfere with activity and sleep. Nighttime symptoms occur more often than twice a month. PEF is more than 80% of the expected value; PSV fluctuations are 20-30% of the expected value. Bronchial asthma of moderate severity. Daily symptoms. Exacerbations disrupt activity and sleep. Nighttime symptoms occur more than once a week. Daily use of short-acting b2-agonists. PSV is 60-80% of what it should be. PEF fluctuations are more than 30%. Severe bronchial asthma. Persistent symptoms, frequent exacerbations, frequent nighttime symptoms, physical activity limited by asthma symptoms; PEF is less than 60% of the expected value; fluctuations of more than 30%. It should be noted that determining the severity of asthma using these indicators is possible only before starting 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 based on the clinical picture, but at the same time he receives drug treatment corresponding to severe persistent asthma, then this patient is diagnosed with severe bronchial asthma. Severe bronchial asthma is steroid dependent. Regardless of the clinical picture, a patient receiving long-term treatment with systemic corticosteroids should be regarded as suffering from severe bronchial asthma and assigned to stage 5.

Criteria for diagnosing bronchial asthma 1. History and symptom assessment The most common symptoms of the disease are episodic attacks of suffocation, shortness of breath, wheezing, a feeling of heaviness in the chest, and cough. An important clinical marker of bronchial asthma is the disappearance of symptoms spontaneously or after the use of bronchodilators and anti-inflammatory drugs. When assessing and collecting anamnesis, factors that provoke exacerbations should be assessed, as well as seasonal variability of symptoms and the presence of atopic diseases in the patient or his relatives. 2. Clinical examination Due to the variability of obstruction, characteristic symptoms of the disease are not necessarily detected during physical examination outside of an exacerbation of bronchial asthma. During an exacerbation of the disease, the patient experiences the following symptoms: expiratory shortness of breath, swelling of the wings of the nose when inhaling, intermittent speech, agitation, activation of auxiliary respiratory muscles, orthopnea, constant or intermittent cough. During auscultation, the doctor most often listens to dry rales. It must be remembered that even during an exacerbation, wheezing may not be heard during auscultation, despite significant bronchial obstruction due to the predominant involvement of the small airways in the process. 3. Pulmonary function test Examining the function of external respiration greatly facilitates the diagnosis. Measuring respiratory function provides an objective assessment of bronchial obstruction, and measuring its fluctuations provides an indirect assessment of airway hyperresponsiveness. The most widely used measurements are the measurement of forced expiratory volume in 1 s (FEV 1) and the associated measurement of forced vital capacity (FVC), as well as the measurement of forced (peak) expiratory flow (PEF). An important diagnostic criterion is a significant increase in FEV 1 (more than 12%) and PEF (more than 15%) after inhalation of short-acting b 2 agonists. Every patient with bronchial asthma is recommended to undergo daily peak flowmetry. Monitoring asthma using a peak flow meter gives the doctor the following opportunities: determine the reversibility of bronchial obstruction; assess the severity of the disease; assess bronchial hyperreactivity; predict asthma exacerbations; identify occupational asthma, evaluate the effectiveness of treatment. 4. Assessment of allergological status The most commonly used are prick, intradermal and prick (prick) tests. However, in some cases, skin tests lead to false negative or false positive results. Therefore, specific IgE antibodies in blood serum are often tested. Eosinophilia in blood and sputum also indicates an allergic process. Thus, the diagnosis of asthma is based on an analysis of symptoms and medical history, as well as a study of external respiratory function and allergy examination data. The most important spirometric functional tests are to identify the response to inhaled b 2 -agonists, change the variability of bronchial patency by monitoring PEF, and provoke with physical activity in children. An important criterion in diagnosis is the determination of allergological status (although the absence of signs of atopy in the presence of other symptoms does not exclude the diagnosis of asthma). 5. For the purpose of differential diagnosis, the following is carried out:

X-ray of the lungs (to exclude pneumothorax, space-occupying processes in the lungs, pleural lesions, bullous changes, interstitial fibrosis, etc.);

ECG (to exclude myocardial damage);

clinical blood test (to identify undiagnosed anemia, detect gross abnormalities);

general sputum analysis (MBT, fungi, atypical cells).

Broncho-obstructive syndrome (BOS) is a symptom complex found in the clinical picture of various congenital and acquired, infectious and non-infectious, allergic and non-allergic diseases of early childhood as one of the manifestations of respiratory failure (RF), which is caused by obstruction of small bronchi and bronchioles due to hypersecretion, mucosal edema and/or bronchospasm.

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

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

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

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

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

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

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

The cause of obstruction may be tumors, foreign body, stenosis, aortic aneurysm. Greatest value in production diagnosis belongs to tomographic examination of the chest and bronchoscopy.

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

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

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

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

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

Bronchial asthma, a modern stepwise approach to therapy. Carrying out basic therapy for the disease. Treatment of exacerbations of bronchial asthma. Indications for the prescription of inhaled and systemic glucocorticosteroids. Clinical observation of patients with bronchial asthma, indications for hospitalization of patients. Definition of temporary and permanent disability. Indications for referral to MSEC.

Treatment of bronchial asthma Treatment of patients with bronchial asthma is complex, it includes drug and non-drug treatment in compliance with the antiallergic regimen. All drugs for drug treatment of the disease are divided into two types: drugs for use as needed and relief of exacerbations and drugs for basic (continuous) therapy. Currently, given the persistent nature of inflammation in bronchial asthma, the basis of treatment for this disease is the prescription of anti-inflammatory anti-asthmatic therapy. Both the level of obstruction and the degree of its reversibility make it possible to subdivide asthma according to severity into intermittent, mild persistent, moderate and severe. Currently used in the treatment of asthma "stepped" approach, in which the intensity of therapy increases as the severity of asthma increases. A stepwise approach to asthma therapy is recommended because there is wide variation in asthma severity among different individuals and within the same patient over different time periods. The goal of this approach is to achieve asthma control using the fewest drugs possible. The amount and frequency of medications taken increases ( step up), if asthma worsens, and decrease ( step down), if asthma is well controlled. The step approach also involves avoiding or controlling triggers at each step. It should be taken into account whether the patient is taking medications at the appropriate level correctly, and whether there is 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;

the need for the use of short-acting bronchodilators increases;

the spread of PEF indicators increases.

Step down. A reduction in maintenance therapy is possible if asthma remains under control for at least 3 months. This helps reduce the risk of side effects and increases the patient's sensitivity to the planned treatment. Therapy should be tapered “stepwise”, reducing or eliminating the last dose or additional drugs. It is necessary to monitor symptoms, clinical manifestations and indicators of respiratory function. It should be taken into account that the least severity of asthma is presented in stage 1, and the greatest - in stage 5. Stage 1. Patients with mild intermittent (episodic) asthma- these are atopics in whom asthma symptoms appear only upon contact with allergens (for example, pollen or animal hair) or are caused by physical activity, as well as children in whom wheezing occurs during a respiratory viral infection of the lower respiratory tract. The possibility of exacerbations should be taken into account. The severity of exacerbations can vary significantly between patients at different times. Sometimes exacerbations can even be life-threatening, although this is extremely rare with the intermittent course of the disease. Long-term therapy with anti-inflammatory drugs is usually not indicated for these patients. Treatment includes prophylactic medication before exercise if necessary (inhaled b2-agonists or cromogicate or nedocromil). Anticholinergics, short-acting oral beta agonists, or short-acting theophyllines may be suggested as alternatives to inhaled short-acting b 2 -agonists, although these drugs have a delayed onset of action and/or a higher risk of side effects. Stage 2. Patients with mild persistent asthma require daily long-term preventive medication. Daily:

or inhaled corticosteroids 200-500 mcg, or sodium cromoglycate, or nedocromil.

If symptoms persist despite the initial dose of inhaled corticosteroids, and the physician is confident that the patient is using the drugs correctly, the dose of inhaled drugs should be increased from 400-500 to 750-800 mcg per day of beclomethasone dipropionate or equivalent. A possible alternative to increasing the dose of inhaled hormones, especially for control of nocturnal asthma symptoms, may be the addition (to a dose of at least 500 mcg of inhaled corticosteroids) of a long-acting bronchodilator at night. If asthma control is not achieved, as evidenced by more frequent symptoms, increased need for short-acting bronchodilators, or decreased PEF levels, then step 3 treatment should be initiated. Stage 3. Patients with moderate severity of asthma require daily use of prophylactic anti-inflammatory drugs to establish and maintain asthma control. The dose of inhaled corticosteroids should be 800-2000 mcg of beclomethasone dipropionate or its equivalent. It is recommended to use an inhaler with a spacer. Long-acting bronchodilators may also be prescribed in addition to inhaled corticosteroids, especially to control nocturnal symptoms. Long-acting theophyllines and long-acting oral and inhaled b2-agonists can be used. Treat symptoms with short-acting b2-agonists or alternative drugs. For more severe exacerbations, a course of oral corticosteroids should be given. If asthma control cannot be achieved, as reflected by more frequent symptoms, increased need for bronchodilators, or a fall in PEF, then step 4 treatment should be started. Stage 4. Patients with severe bronchial asthma Asthma cannot be completely controlled. The goal of treatment is to achieve the best possible results: the minimum number of symptoms, the minimum need for short-acting β 2 -agonists, the best possible PEF values, the minimum variability in PEF, and minimal side effects from taking medications. Treatment is usually done with a large number of asthma-controlling medications. Primary treatment includes high-dose inhaled corticosteroids (800 to 2000 mcg per day of beclomethasone dipropionate or equivalent). Long-acting bronchodilators are recommended in addition to inhaled corticosteroids. You can also use short-acting b 2 -agonists once a day to achieve an effect. An anticholinergic drug (ipratropium bromide) may be tried, especially in patients who experience side effects when taking b2-agonists. Short-acting inhaled b 2 -agonists can be used as needed to relieve symptoms, but the frequency of dosing should not exceed 3-4 times per day. More severe exacerbations may require a course of oral corticosteroids. Stage 5. Patients with severe bronchial asthma receiving long-term therapy with systemic steroids, therapy with inhaled drugs should be prescribed, as in step 4. Thus, although bronchial asthma is an incurable disease, it is reasonable to expect that control of the disease can and should be achieved in most patients. It should be recalled once again that one of the central places in the treatment of asthma is currently occupied by the educational program of patients and clinical observation.

The level of asthma control is determined by the following parameters:

 minimal severity of chronic symptoms, including night ones;

 minimal (infrequent) exacerbations;

 no need for emergency care;

 minimal (ideally no) use of ß2-agonists “on demand”;

 no restrictions on activity, including physical activity;

 daily fluctuations in PEF less than 20%;

 normal or close to normal PEF indicators;

 minimal manifestations or absence of undesirable effects of drugs.

Drugs for use as needed and relief of exacerbations:1. Short-acting beta-2 agonists (salbutamol, fenoterol, terbutaline) cause relaxation of bronchial smooth muscles, increased mucociliary clearance, and decreased vascular permeability. The preferred route of administration of these drugs is inhalation. For this purpose, b 2 -agonists are available in the form of metered aerosols, dry powder and solutions. If long-term inhalation is necessary, salbutamol solutions are used through a nebulizer. 2. Anticholinergic drugs (ipratropium bromide): Less potent bronchodilators than b2-agonists and usually have a later onset of action. It should be noted that ipratropium bromide enhances the effect of b 2 -agonists when used together. Method of administration: inhalation (metered-dose aerosol, nebulizer solution). 3. Berodual - a combination drug containing a b 2 -agonist and an anticholinergic drug. Method of administration: inhalation (metered-dose aerosol, nebulizer solution). 4. Systemic glucocorticosteroids (prednisolone, methylprednisolone, triamsinalone, dexamethasone, betamethasone). Method of administration: parenteral or oral. Oral therapy is preferred. 5. Short-acting theophyllines - bronchodilators, which are generally less effective than inhaled b 2 -agonists. They have significant side effects that can be avoided with proper dosing and monitoring. It should not be used without determining the concentration of theophylline in the blood plasma if the patient is receiving drugs with slow release of theophylline.

Basic therapy drugs

Basic therapy for asthma in adults

Severity	Daily medication intake for disease control	Other Treatment Options
Stage 1: Intermittent asthma	IGKs are not always shown	Elimination activities
Stage 2: Mild persistent asthma	IGC benacort 200-400 mcg in 2 doses, constantly, oral long-acting β2-agonist (saltos) situationally during exacerbation	Elimination activities
Stage 3: Persistent asthma of moderate severity	IGC benacort 400-1000 mcg in 2-3 doses,	Elimination activities
Stage 4: Severe persistent course	IGC benacort 1000-2000 mcg in 3-4 doses, oral long-acting β2-agonist (saltos) continuously	Elimination measures

The basis of treatment for bronchial asthma are inhaled glucocorticosteroids.1. Inhaled corticosteroids (beclomethasone dipropionate; budesonide; flunisolide; fluticosone propionate) are used as anti-inflammatory drugs for a long time to control the course of bronchial asthma. Doses are determined by the severity of bronchial asthma. Treatment with high-dose aerosolized inhaled corticosteroids is given through a spacer, which improves asthma control and reduces some side effects, or by using a "breathing" inhaler. In severe cases of bronchial asthma, the use of budesonide through a nebulizer may be more effective. Inhaled corticosteroids occupy a crucial place in the treatment of asthma. They have the following advantages over systemic GCS:

 High affinity for receptors;

 Pronounced local anti-inflammatory activity;

 Lower (about 100 times) therapeutic doses;

 Low bioavailability.

Inhaled corticosteroids are the drug of choice for patients with persistent BA of any severity.

Undesirable effects of inhaled corticosteroids include: oropharyngeal mycosis, dysphonia, and sometimes cough.

The risk of uncontrolled asthma significantly exceeds the risk of adverse events from inhaled corticosteroids.

2. Systemic glucocorticosteroids (methylprednisolone, prednisolone, triamsinolone, betamethasone) for severe bronchial asthma should be prescribed in the lowest effective dose. With long-term treatment, an alternating prescription regimen and administration in the first half of the day cause the least number of side effects. It should be emphasized that in all cases of prescribing systemic steroids, the patient should be prescribed high doses of inhaled glucocorticoids. 3. Long-acting beta-2 agonists (salmeterol; formoterol; salbutamol hemisuccinate) are widely used in the treatment of severe asthma. The drugs are used both orally and inhalation, as well as parenterally. However, in pulmonological practice, the most common and effective is the inhalation route of drug delivery. The advantage of inhalation forms is due to the speed of development of the maximum effect, the local (topical) nature of the action, and the absence of a pronounced effect on internal organs when used in therapeutic doses. The drugs are also effective in preventing nighttime asthma attacks. Used in combination with anti-inflammatory anti-asthmatic drugs. Currently, there are two drugs belonging to the group of long-acting b 2 -agonists: formoterol fumarate and salmeterol xinafoate. Formoterol is the most active long-acting b 2 -agonist and is found in two dosage forms: oxis and foradil. Salmeterol is represented by such drugs as Serevent, Salmeter. The drugs improve the function of external respiration, reduce the need for short-acting b 2 -agonists, and are effective in preventing bronchospasm provoked by allergens and physical activity. Salmeterol and salbutamol hemisuccinate are used only as basic therapy.

These drugs are not used to relieve acute symptoms or exacerbations. Formoterol fumarate is a drug characterized by a unique combination of pharmacological properties:

high efficiency combined with high b 2 -selectivity, which provides a unique safety profile of the drug;

rapid onset of action (within 1-3 minutes);

duration of effect for 12 hours;

the absence of an antagonistic effect in relation to short-acting b 2 -agonists and a significant influence on their effects, which is of great clinical importance in situations involving the combined use of long-acting and short-acting adrenergic agonists;

lack of accumulation in therapeutic doses.

High safety indicators allow the use of formoterol as needed, and the rapid onset of action allows it to be used as a drug that relieves symptoms (rescue medication). Thus, formoterol may be the only bronchodilator needed by the patient in any situation. Particularly noteworthy is the potentiation of long-acting b 2 -agonists, and in particular formoterol and salmeterol, the effects of glucocorticosteroids. If the symptoms of bronchial asthma are insufficiently controlled, it is therapeutically more beneficial to prescribe a combination of low doses of inhaled glucocorticoids and long-acting b2-agonists than doubling the dose of steroids.

The presence of one of the severity indicators allows the patient to be classified into one of the categories. When determining severity, the amount of therapy needed to control asthma symptoms must be taken into account.

Clinical picture before treatment	Basic therapy
Step 5. Regular use of corticosteroid tablets
As a rule, it corresponds to stage 4, but it must be borne in mind that, regardless of the clinic, any patient receiving regular therapy with systemic steroids should be regarded as a seriously ill patient and assigned to stage 5	Basic therapy stage 4 + regular use of systemic steroids for a long time. b 2 -Short-acting agonists as needed
Stage 4. Severe course
Constant presence of symptoms. Frequent exacerbations. Frequent night symptoms. Limiting physical activity due to asthma symptoms. PEF or FEV1 less than 60% of expected	Basic therapy: high doses of inhaled glucocorticoids in combination with regular use long-acting bronchodilators High doses of inhaled glucocorticoids plus one or more of the following: inhaled long-acting b 2 -agonists oral extended-release theophylline inhaled ipratropium bromide oral long-acting b 2 -agonists b 2 -Short-acting agonists as needed
Stage 3. Moderate course
Daily symptoms. Exacerbations can lead to disruption of physical activity and sleep. Nighttime symptoms more than once a week. Daily use of short-acting b2-agonists. PEF or FEV1 60–80% of expected daily variation of indicators is more than 30%	Basic therapy: high doses of inhaled glucocorticoids (800–2000 mcg) or standard doses in combination with long-acting b2-agonists. b2-agonists, short-acting as needed
Stage 2. Mild persistent course
Symptoms range from 1 time per week to 1 time per day. Exacerbations can reduce physical activity and disrupt sleep. Night symptoms more than 2 times a month. PEF or FEV1 not less than 80% of the required the spread of indicators is 20–30%.	Basic therapy: daily intake of anti-inflammatory drugs. Cromones or standard doses of inhaled glucocorticoids (200–800 mcg), long-acting b2-agonists can be added (especially to control nighttime symptoms). b 2 -Short-acting agonists as needed.
Stage 1. Intermittent flow
Short-term symptoms less than once a week. Short exacerbations (from several hours to several days). Night symptoms less than 2 times a month. Absence of symptoms and normal respiratory function between exacerbations. Џ PEF or FEV1 not less than 80% of the required indicators, the spread of indicators is less than 20%	b 2 -Short-acting agonists as needed (no more than 1 time per week). Prophylactic use of short-acting b2-agonists or cromones before exercise or allergen exposure. The intensity of treatment depends on the severity of the exacerbation: oral steroids can be prescribed for severe exacerbation even at this stage

4. Long-acting theophyllines. Oral administration: thanks to the prolonged action, they reduce the frequency of nocturnal attacks, slow down the early and late phases of the asthmatic response to allergen exposure. The use of theophyllines can cause severe side effects: headache, tremor, nausea, vomiting, tachycardia, cardiac arrhythmias, abdominal pain, loose stools. It is necessary to monitor the content of theophyllines in plasma. 5. Leukotriene receptor antagonists (zafirlukast, montelukast) is a new group of anti-inflammatory anti-asthma drugs. Directions for use: tablets. The drugs improve the function of external respiration, reduce the need for short-acting b 2 -agonists, and are effective in preventing bronchospasm provoked by allergens and physical activity. In the treatment of severe bronchial asthma, they are especially indicated for those forms of bronchial asthma, the severity of which is associated with increased metabolism of leukotrienes (aspirin, post-exert bronchospasm syndrome, reactions to cold air and allergen exposure). 6. M-anticholinergics - anticholinergic drugs (ipratropium bromide) are not first-line drugs in the treatment of bronchial asthma, since they are inferior in effectiveness to sympathomimetics. However, in some cases, their use in combination with b 2 -agonists can be effective in patients who are refractory to b 2 -agonists. 7. Combination drugs . Currently, great importance is attached to combination drugs (combinations of long-acting b 2 -agonists and inhaled glucocorticoids). There are two dosage forms: Seretide (a combination of salmeterol and fluticasone propionate) and Symbicort (a combination of formoterol and budesonide). It should be noted that these drugs potentiate the effect of each other and together have a pronounced anti-inflammatory effect. 8. Sodium cromoglycate and nedocromil: non-steroidal anti-inflammatory drugs for long-term control of bronchial asthma. Effective in preventing bronchospasm provoked by allergens, physical activity and cold air.

Treatment of asthma exacerbations in adults

Exacerbation of asthma is an episodic condition accompanied by increased coughing, shortness of breath, the appearance of wheezing, suffocation, and a feeling of lack of air. Exacerbation of asthma is accompanied by a decrease in peak expiratory flow rate and forced expiratory volume in the first second.

There are two options for the development of severe exacerbation of asthma:

 Severe exacerbation of asthma with a slow rate of development, when an increase in respiratory syndromes is observed over several days, despite an increase in the dose of bronchodilators;

 Severe exacerbation of asthma with sudden onset is more rare, and only 1-3 hours may pass from the onset of the first symptoms to respiratory arrest and death.

Risk factors for life-threatening exacerbation of asthma

(asthmatic status):

 A history of life-threatening exacerbation of asthma.

 Exacerbation of asthma due to long-term use of systemic corticosteroids and/or their recent withdrawal.

 Hospitalization due to exacerbation of asthma during the past year in the intensive care unit.

 A history of an episode of artificial ventilation due to exacerbation of asthma.

 Mental illness or psychosocial problems.

 Failure of the patient to comply with the asthma treatment plan.

 The presence of persistent asthma symptoms for a long time (more than 3 hours) before actually seeking medical help.

 Unfavorable home conditions.

 Socio-economic factors (low income, inaccessibility of medicines).

Treatment of exacerbation involves avoiding contact with causally significant allergens, using short-acting inhaled bronchodilators (β2-agonists or β2-agonists + m-anticholinergics) for rapid relief of bronchospasm, inhaled and systemic corticosteroids, short-acting theophyllines.

Short-acting β2-agonists are first-line drugs in the treatment of exacerbations of asthma, which is associated with the speed of their action and a relatively high safety profile.

Anticholinergic drugs are classified as second-line drugs in the treatment of exacerbations of BA, since they are inferior in effectiveness to β2-agonists, but practically do not cause complications, and in combination with β2-agonists they provide a greater bronchodilator effect compared to monotherapy.

If the patient has a burdened premorbid background in the form of coronary artery disease, cardiac arrhythmias, COPD, then the role of anticholinergic drugs in the symptomatic treatment of asthma increases significantly; they become first-line bronchodilators.

Short acting theophylline are classified as second-line drugs for the treatment of exacerbations of asthma and are recommended for use no earlier than 4 hours after the β2-agonist. Among bronchodilators, theophylline is the least effective drug , and its therapeutic dose is almost equal to the toxic one; in addition, it has the largest number of side effects (nausea, headache, insomnia, electrolyte disorders, arrhythmias, convulsions).

Glucocorticosteroid hormones As the most powerful anti-inflammatory drugs, they are mandatory for the treatment of exacerbations of asthma. It has been proven that the effectiveness of oral and parenteral forms of systemic corticosteroids in the treatment of exacerbations of asthma is almost the same. The inhalation method of administering a nebulized solution or suspension of budesonide (Benacort, Pulmicort) provides a more rapid onset of anti-inflammatory action than systemic corticosteroids, and a more pronounced improvement in clinical parameters is noted.

Currently, the inhalation route of drug administration during exacerbation of asthma is the main one at any stage of medical care (outpatient, emergency team, in hospital). The rate of development of bronchodilation is comparable to parenteral administration of the drug. The possibility of using a smaller dose of the drug and eliminating the entry of the drug into the general bloodstream with this technique reduces the risk of developing side effects of bronchodilators and corticosteroids (Table 8).

Table 8

Algorithm for the treatment of exacerbations of asthma

(Order No. 300 of the Ministry of Health of the Russian Federation dated 09.10.98)

Uncontrolled asthma	Severe exacerbation	Life-threatening exacerbation
1. Assessing the severity of an exacerbation
Speech is not impaired; NPV<25 дых/мин; PEF>50% of best; Pulse<110 уд/мин.	Shortness of breath when talking; RR>25 breaths/min; PSV<50% от лучшего; Pulse>110 beats/min.	"Mute lung"; PSV<33% от лучшего; Bradycardia, impaired consciousness
2. Further treatment tactics
Treatment at home is possible, but the answer must be received before the doctor leaves the patient	Take the issue of hospitalization seriously	Immediate hospitalization
3. Treatment
5 mg salbutamol, 10 mg Berotec via nebulizer	5 mg salbutamol, 10 mg Berotec, Benacort, Atrovent via nebulizer; prednisolone 30-60 mg per os or IV	Benacort, Atrovent, Salbutamol, Berotec via nebulizer; prednisolone 30-60 mg peros or IV, oxygen therapy, intravenous aminophylline (2.4% 20-40 ml). Stay with the patient until the SP arrives
4. Monitoring the condition 15-30 minutes after nebulizer therapy
If PEF is from 50 to 70% of the best nebulization of benacort or prednisolone 30-60 mg peros, “move up” one step according to the stepwise BA treatment regimen	If symptoms persist: hospitalization. While waiting for “SP”, repeat nebulization of β-agonists together with Atrovent 500 mcg or intravenous aminophylline 250 mg (slowly). If there is a good response after the first nebulization (symptoms have decreased, PEF>50%): move up one step according to the stepwise approach.	N.B.: If you don't have a nebulizer, take two puffs of a β-agonist, atrovent, or berodual through a small spacer
Strengthen ongoing therapy; Observation for 48 hours.	Monitor symptoms and PEF; Strengthen ongoing therapy; Create an outpatient treatment plan according to asthma treatment guidelines; Monitoring for 24 hours.

Oxygen therapy during exacerbation of asthma is vitally important, since the immediate cause of death in this case is hypoxia. Oxygen therapy is carried out in the form of inhalations, oxygen is used as a carrier gas in nebulizers. In case of life-threatening attacks, artificial ventilation of the lungs is effective. Non-invasive ventilation is recognized as optimal, but the experience of its use in severe exacerbations of asthma is still insufficient.

 Antihistamines;

 Sedatives;

 Herbal medicines;

 Mustard plasters, jars;

 Calcium preparations, magnesium sulfate;

 Mucolytics;

 Antibacterial agents (can only be indicated in the presence of pneumonia or other bacterial infection);

 Long-acting β2-agonists.

Tactics for managing patients with exacerbation of BA in a hospital setting

To provide assistance to a patient with an exacerbation of asthma, the setup of the emergency team should contain:

 Oxygen inhaler, peak flow meter;

 Nebulizer chamber complete with compressor;

 Disposable syringes;

 Set of medicines (Table 9);

 Venous tourniquet;

 Butterfly needles and/or infusion cannulas

Table 9

Mandatory and additional medicines for the treatment of exacerbations of asthma

Medicine	Severity of asthma exacerbation			Life-threatening exacerbation of asthma
Mandatory assortment	Inhaled rapid-acting β2-agonists (Salgim, Berotec)	Inhaled fast-acting β2-agonists (Salgim, Berotec)	Inhaled rapid-acting β2-agonists + ipratropium bromide (Berodual) GCS (benacort solution, prednisolone)	Oxygen Inhaled rapid-acting β2-agonists + ipratropium bromide (Berodual) GCS (benacort solution, prednisolone)
Additional assortment		Ipratropium bromide (atrovent solution) Theophylline	Theophylline	Theophylline Non-invasive ventilation

Indications for emergency hospitalization:

 Unsatisfactory response to treatment (POSvyd<50% от должного после применения бронходилятаторов);

 Symptoms of exacerbation of asthma increase or there is no clear positive dynamics of symptoms within 3 hours from the start of emergency treatment measures;

 No improvement is observed within 4-6 hours after the start of treatment with systemic corticosteroids.

After transferring a patient from the ICU to the pulmonology (therapeutic) department, it is necessary to:

 Carry out a 7-10 day course of treatment with GCS, subject to continued treatment with bronchodilators;

 Start or continue treatment with inhaled corticosteroids in a daily dose corresponding to the severity of asthma;

 It is necessary to check the skills of using an inhaler, a peak flow meter to monitor the condition.

There are no absolute criteria for discharge from hospital. Before discharge, the patient should receive medications as an outpatient treatment regimen for 12-24 hours to ensure its effectiveness.

An increase in drug consumption and the introduction of new drugs with high biological activity into medical practice lead to a significant increase in the complications of pharmacotherapy. Any drug, in addition to the direct pharmacological effect, often has negative effects on both affected and intact organs and tissues, which may cause changes in the course of the underlying disease, therefore pharmacotherapy for asthma must be balanced and justified.

Since bronchial asthma is a chronic disease with periods of exacerbation and remission, patients require constant monitoring. Drug treatment also requires constant adjustment depending on the severity of the disease. For mild and moderate cases, it is necessary to be examined by a pulmonologist or therapist 2-3 times a year, and for severe cases - once every 1-2 months. An allergic reaction to infectious and other agents plays an important role in the development of bronchial asthma, so such patients are advised to consult an allergist (once a year). With bronchial asthma, disorders of the nervous system are noted, so it is advisable to be examined by a psychotherapist once a year. To sanitize foci of chronic infection, you need to visit an otolaryngologist and dentist regularly (at least once a year). It is necessary to take a general blood and sputum test 2-3 times a year to identify the inflammatory process in the bronchopulmonary tissue. To determine the functional state of the respiratory system, spirography must be performed 2 times a year.

The need to conduct a labor examination and determine the disability group in patients with bronchial asthma arises with frequent, recurrent or prolonged attacks of asthma, clinically pronounced pulmonary or pulmonary-heart failure. And also when the course of the underlying disease is complicated by hormonal dependence, status asthmaticus, or bronchial asthma occurs against the background of a chronic recurrent inflammatory process in the lungs.

A characteristic feature of bronchial asthma is complete or partial reversibility, spontaneously or under the influence of treatment. Therefore, bronchial asthma is not initially classified as a disease that steadily leads to permanent loss of ability to work and the development of disability. The combination of modern treatment methods and measures to limit contact with provoking factors (primarily tobacco smoke and causal allergens) makes it possible to achieve control of the disease in most patients. However, referrals for medical and social examination (MSE) for asthma often occur. First of all, this is due to the need to change working conditions: in the presence of contraindications in the conditions and nature of work and the impossibility of employment in an accessible profession without reducing qualifications or a significant reduction in the volume of production activity. In the presence of long-term disability, even with a good prognosis, the patient is sent to MSEC to decide on further treatment or establishment of a disability group. The establishment of a disability group should be accompanied not only by the issuance of a certificate, but also by the preparation of an individual rehabilitation program. The question of establishing a disability group also arises in cases of severe asthma, hormone dependence (continuous use of hormones in tablets), severe concomitant diseases or complications, the formation of irreversible bronchial obstruction (developing with a combination of asthma and COPD or with a long uncontrolled course of the disease in the absence of proper treatment ). List of documents required to be submitted to MSEC to undergo examination to obtain a disability group: form No. 88; KEC certificate; outpatient card from the clinic; certificate from place of work; passport; accident report (if any); referral to % disability; military ID and military medical documents (if any); ITU certificate (during re-examination). The issue of granting a disability group is always decided individually. The mere presence of a diagnosis of bronchial asthma is not a basis for establishing a disability group.

Complications of bronchial asthma (status asthmaticus). Clinic, diagnostics. Emergency treatment of status asthmaticus.

Complications

A.Respiratory tract infections- a common complication of bronchial asthma. They can occur both during exacerbation and during remission of the disease and often provoke attacks of bronchial asthma. Dry wheezing, heard at a distance, during an acute respiratory illness may be the first manifestation of bronchial asthma in children. Bronchial asthma should be excluded in all children with frequent bronchitis and acute respiratory diseases.

1. Acute respiratory diseases most often cause attacks of bronchial asthma. The most common infections are caused by respiratory syncytial virus, parainfluenza and influenza viruses, rhinoviruses and adenoviruses. It is assumed that these viruses directly act on the bronchi, increasing their reactivity. It is possible that the occurrence of bronchial asthma attacks during acute respiratory diseases is caused by IgE specific to this virus, or by a virus-induced decrease in the sensitivity of beta-adrenergic receptors and the release of inflammatory mediators.

2. Bacterial infections rarely provoke attacks of bronchial asthma. The exceptions are chronic sinusitis and mycoplasma infection.

3. Pneumonia usually develops secondary, after prolonged or frequent attacks of bronchial asthma, when a large amount of mucus accumulates in the bronchi. At the age of up to 5 years, viral pneumonia occurs more often, at 5-30 years - mycoplasma pneumonia, after 30 years - pneumococcal and other bacterial pneumonia.

B.Atelectasis- lobar, segmental and subsegmental - can occur during both exacerbation and remission. Usually their appearance is associated with blockage of the bronchi with mucus plugs. Atelectasis is characterized by increased cough, constant wheezing, shortness of breath, fever, weakened vesicular breathing and dullness of percussion sound in the atelectasis area. Atelectasis of the middle lobe of the right lung is most often observed. Often they are not diagnosed. If atelectasis is suspected, a chest x-ray is indicated. Atelectasis is typical for young children and often recurs, usually affecting the same areas of the lung.

IN.Pneumothorax and pneumomediastinum

1. Pneumothorax- a rare complication of bronchial asthma. If pneumothorax recurs, a cyst, congenital lobar emphysema and other lung diseases are excluded. Pneumothorax can occur with severe coughing and during mechanical ventilation. This complication should be suspected when there is a sudden appearance of pain in the side, aggravated by breathing and accompanied by shortness of breath, tachypnea, and sometimes cough. The diagnosis is confirmed by chest x-ray. For small pneumothorax (less than 25% of the volume of the pleural cavity) in the absence of severe shortness of breath and pain, bed rest and observation are indicated. The air in the pleural cavity resolves on its own. In other cases, drainage of the pleural cavity is required.

2. Pneumomediastinum and subcutaneous emphysema observed more often than pneumothorax. Patients, as a rule, do not complain, so these complications are discovered by chance during chest x-ray, examination and palpation of the neck and chest. Sometimes pneumomediastinum is manifested by chest pain, less often by shortness of breath, tachypnea, tachycardia, arterial hypotension and cyanosis of the upper half of the body. A characteristic sign of pneumomediastinum is Hamman's sign (a crepitant murmur upon auscultation of the heart). Pneumomediastinum and subcutaneous emphysema usually occur during severe coughing and mechanical ventilation. Treatment in most cases is not required; in severe cases, the mediastinum is drained.

G.Bronchiectasis- a rare complication of bronchial asthma. They usually occur when bronchial asthma is combined with chronic bronchitis, prolonged atelectasis or allergic bronchopulmonary aspergillosis. With bronchiectasis, a prolonged cough, purulent sputum, hemoptysis, and a symptom of drumsticks are observed. It should be noted that with uncomplicated bronchial asthma, the last sign is absent. Sometimes the diagnosis can be made based on a chest x-ray, but in most cases an x-ray tomography or CT scan is required. In rare cases, bronchography is performed.

D.Allergic bronchopulmonary aspergillosis. The causative agent is Aspergillus fumigatus. Allergic reactions caused by the pathogen play a role in the pathogenesis of the disease. It is observed mainly in adult patients with bronchial asthma.

E.Cardiovascular complications in bronchial asthma, they most often manifest themselves as arrhythmias - from rare ventricular extrasystoles to ventricular fibrillation. Arrhythmias are more often observed in patients with cardiovascular diseases. The severity of arrhythmias increases with hypoxemia and abuse of beta-agonists. During an attack of bronchial asthma, overload of the right parts of the heart may occur. Right ventricular failure develops very rarely - only in cases of prolonged severe hypoxemia and volume overload. During an attack of bronchial asthma, pulmonary hypertension is often observed, but cor pulmonale occurs only when bronchial asthma is combined with COPD. To reduce hypoxemia, oxygen inhalations are prescribed. Limit the use of beta-agonists (both inhaled and systemic) and theophylline. For severe arrhythmias and right ventricular failure, cardiac glycosides (if the arrhythmia is not caused by these drugs) and other antiarrhythmic drugs are prescribed. In this case, be sure to take into account whether they cause bronchospasm.

AND.Status asthmaticus and respiratory failure .

Status asthmaticus (AS) is a syndrome of acute respiratory failure that develops in patients with bronchial asthma due to airway obstruction, resistant to therapy with aminophylline and sympathomimetics, including selective P2 stimulants.

Asthma is considered severe if it responds poorly to standard treatment regimens, such as inhaled corticosteroids or.

Asthma affects tens of millions of people across the planet. About 5 to 10% of them have severe asthma.

Because symptoms are usually less controllable in severe asthma, attacks with this condition pose a greater threat to health and life. In part, through close collaboration with a doctor, people with severe asthma can usually find ways to manage their symptoms.

In addition to taking specific medications, it is important for asthma patients to identify factors that contribute to flare-ups (triggers) and subsequently avoid them. In this way, the development of severe asthma attacks can be prevented.

In this current article, we will look at the causes, symptoms and treatments for severe asthma.

Severe asthma causes symptoms that are recurring and difficult to control

Doctors classify the severity of asthma based on how well the disease responds to treatment. With severe asthma, people find it difficult to control symptoms with conventional treatments.

Severe asthma involves the presence of symptoms that recur periodically throughout the day and even night. This type of asthma can interfere with daily activities and make it difficult to sleep, as symptoms often worsen at night.

If the disease is difficult to manage, people are at increased risk of developing serious complications.

According to the US National Institutes of Health guidelines, severe asthma has the following symptoms:

• symptoms that occur throughout the day;
• waking up at night due to symptoms (often people aged 5 years and older wake up 7 nights a week, and children under age 5 wake up more than once a week);
• symptoms requiring treatment with short-acting beta-2 agonists several times a day;
• symptoms that significantly limit daily life activities;
• forced expiratory volume in the first second (FEV1) is less than 60% of normal (for people aged 5 years and older).

FEV1 is a measure of the amount of air a person can forcefully exhale in one second. By measuring FEV1, doctors get an idea of ​​the quality of lung function.

• inhaled corticosteroids and additional medications, including long-acting inhaled beta-2 agonists, theophylline and montelukast;
• oral corticosteroids taken for at least six months over a one-year period.

Symptoms

Severe asthma can cause chest tightness and pain

Every person with asthma experiences symptoms differently. For many people they can be simply unpredictable. Therefore, it is difficult to name the characteristic signs of severe asthma. However, there are medical problems that are common to this condition.

Severe asthma can make it difficult to carry out everyday life tasks. If a person is not treated effectively, the disease may ultimately limit his or her ability to work.

Asthma symptoms may occur throughout the day and even at night. In the latter case, people are forced to awaken.

Asthma symptoms can range in severity from minor inconvenience to life-threatening attacks that cause a sudden exacerbation of all symptoms at once.

Symptoms of asthma include the following:

• cough;
• feeling of tightness in the chest;
• dyspnea.

Diagnostics

Doctors diagnose severe asthma when standard asthma treatments do not control symptoms.

That is, to make such a diagnosis, some time must pass, during which doctors try to improve the patient’s condition using various therapeutic strategies.

Typically, the diagnosis of asthma consists of the following steps:

• conversation about the patient's medical history;
• performing a physical examination;
• checking respiratory function using special tests.

In addition, the doctor may check for other medical conditions that may have symptoms similar to asthma.

Causes

The medical community does not yet know the exact causes of asthma, but it is known that certain factors, such as allergies, can contribute.

In 2013, American scientists conducted a study showing that more than 75% of asthma patients aged 20 to 40 also suffer from allergies.

Another study confirmed the link between cigarette smoking and an increased risk of asthma and other respiratory problems. Children who spend time with adults who smoke also have an increased risk.

In addition, various environmental factors can contribute to asthma symptoms. In 2017, Argentine researchers showed that air pollution leads to more frequent asthma outbreaks and increases the frequency of patient visits to the hospital.

A 2014 study found a link between asthma and obesity. Based on the findings of this study, experts from the American Academy of Allergy, Asthma and Immunology stated that "in general, increasing obesity can be considered a contributing factor to the increased prevalence of asthma."

Treatment

People should see a doctor immediately if they develop severe asthma attacks

Asthma treatment includes measures to control symptoms. These measures include managing your airways, minimizing the risk of developing future asthma symptoms, and preventing lung damage.

People with severe asthma need to take medications more frequently than those with normal asthma. In addition, doctors usually prescribe higher dosages for them. How to manage specific symptoms should be discussed with your healthcare provider.

If a severe asthma attack occurs, people should go to hospital immediately as it can be life-threatening, especially if the symptoms are difficult to treat.

Asthma experts say the best way to prevent asthma attacks and uncontrolled symptoms is to avoid triggers as much as possible and take prescribed medications as directed by your doctor.

Medicines

Your doctor may suggest medications for both quick relief of symptoms and long-term treatment of asthma.

For rapid symptom relief

The main medications used to quickly relieve asthma symptoms are short-acting beta-2 agonists. These medications can be taken when symptoms begin to develop.

Examples of short-acting beta-2 agonists include the following:

• orciprenaline;
• albuterol (Ventolin, Proventil, Proair);
• levalbuterol (Xopenex).

For long-term treatment

For long-term treatment of asthma, doctors suggest taking daily medications to prevent flare-ups. Inhaled corticosteroids are considered the most effective long-acting medications used to control asthma.

Inhaled corticosteroids can cause side effects, including oral thrush, which is a yeast infection that develops in the mouth. To reduce the risk of developing this problem, you should rinse your mouth after using inhalers.

Conclusion

Asthma is a common medical condition affecting millions of people across the planet. Asthma can be mild or severe.

While most asthma responds well to treatment, the symptoms of severe asthma are not relieved by standard treatment strategies.

With severe asthma, people should make every effort to avoid triggers of attacks. You should also work closely with your doctor to find the most effective treatments.

Bronchial asthma is a chronic inflammatory disease of the airways, accompanied by their hyperresponsiveness, which is manifested by repeated episodes of shortness of breath, difficulty breathing, chest tightness and coughing, occurring mainly at night or in the early morning. These episodes are usually associated with widespread but not permanent bronchial obstruction, which is reversible either spontaneously or with treatment.

EPIDEMIOLOGY

The prevalence of bronchial asthma in the general population is 4-10%, and among children - 10-15%. Predominant gender: children under 10 years old - male, adults - female.

CLASSIFICATION

Classifications of bronchial asthma according to etiology, severity and characteristics of the manifestation of bronchial obstruction are of greatest practical importance.

The most important division of bronchial asthma into allergic (atopic) and non-allergic (endogenous) forms, since specific methods that are not used in the non-allergic form are effective in the treatment of allergic bronchial asthma.

International Classification of Diseases, Tenth Revision (ICD-10): J45 - Bronchial asthma (J45.0 - Asthma with a predominance of an allergic component; J45.1 - Non-allergic asthma; J45.8 - Mixed asthma), J46. - Asthmatic status.

Asthma severity is classified by the presence of clinical signs before treatment and/or the amount of daily therapy required for optimal symptom control.

◊ Severity criteria:

♦ clinical: number of night attacks per week and daytime attacks per day and week, severity of physical activity and sleep disorders;

♦ objective indicators of bronchial patency: forced expiratory volume in 1 s (FEV 1) or peak expiratory flow (PEF), daily fluctuations of PEF;

♦ therapy received by the patient.

◊ Depending on the severity, there are four stages of the disease (which is especially convenient for treatment).

♦ stage 1 : light intermittent (episodic) bronchial asthma. Symptoms (cough, shortness of breath, wheezing) occur less than once a week. Night attacks no more than 2 times a month. During the interictal period, there are no symptoms, lung function is normal (FEV 1 and PEF more than 80% of the expected values), daily fluctuations in PEF are less than 20%.

♦ stage 2 : light persistent bronchial asthma. Symptoms occur once a week or more often, but not daily. Night attacks more often than 2 times a month. Exacerbations can interfere with normal activity and sleep. PEF and FEV 1 outside an attack are more than 80% of the required values, daily fluctuations in PEF are 20-30%, which indicates increasing reactivity of the bronchi.

♦ stage 3 : persistent bronchial asthma average degrees gravity. Symptoms occur daily, exacerbations disrupt activity and sleep, and reduce quality of life. Night attacks occur more than once a week. Patients cannot do without daily intake of short-acting β 2 -adrenergic agonists. PEF and FEV 1 are 60-80% of the required values, fluctuations in PEF exceed 30%.

♦ stage 4 : heavy persistent bronchial asthma. Constant symptoms throughout the day. Exacerbations and sleep disturbances are frequent. Manifestations of the disease limit physical activity. PEF and FEV 1 are below 60% of the expected values ​​even outside an attack, and daily fluctuations in PEF exceed 30%.

It should be noted that the severity of bronchial asthma can be determined using these indicators only before treatment begins. If the patient is already receiving the necessary therapy, its volume should be taken into account. If a patient's clinical picture corresponds to stage 2, but he receives treatment corresponding to stage 4, he is diagnosed with severe bronchial asthma.

Phases of bronchial asthma: exacerbation, subsiding exacerbation and remission.

♦ Asthmatic status (status asthmaticus) - a serious and life-threatening condition - a prolonged attack of expiratory suffocation that is not relieved by conventional anti-asthmatic drugs within several hours. There are anaphylactic (rapid development) and metabolic (gradual development) forms of status asthmaticus. Clinically manifested by significant obstructive disorders up to the complete absence of bronchial conduction, unproductive cough, severe hypoxia, and increasing resistance to bronchodilators. In some cases, signs of overdose of β 2 -agonists and methylxanthines are possible.

Based on the mechanism of bronchial obstruction, the following forms of bronchial obstruction are distinguished.

◊ Acute bronchoconstriction due to smooth muscle spasm.

◊ Subacute bronchial obstruction due to swelling of the mucous membrane of the respiratory tract.

◊ Sclerotic bronchial obstruction due to sclerosis of the bronchial wall with a long and severe course of the disease.

◊ Obstructive bronchial obstruction, caused by impaired discharge and changes in the properties of sputum, the formation of mucus plugs.

ETIOLOGY

There are risk factors (causally significant factors) that predetermine the possibility of developing bronchial asthma, and provocateurs (triggers) that realize this predisposition.

The most significant risk factors are heredity and contact with allergens.

◊ The likelihood of developing bronchial asthma is related to a person’s genotype. Examples of hereditary diseases accompanied by manifestations of bronchial asthma are increased production of IgE, a combination of bronchial asthma, nasal polyposis and intolerance to acetylsalicylic acid (aspirin triad), hypersensitivity of the respiratory tract, hyperbradykininemia. Gene polymorphism in these conditions determines the readiness of the respiratory tract for inadequate inflammatory reactions in response to trigger factors that do not cause pathological conditions in people without a hereditary predisposition.

◊ Of the allergens, the waste products of house dust mites are the most important ( Dermatophagoides pteronyssinus And Dermatophagoides farinae), mold spores, plant pollen, dander, components of saliva and urine of some animals, bird fluff, cockroach allergens, food and drug allergens.

Provoking factors (triggers) can be respiratory tract infections (primarily acute respiratory viral infections), taking β-blockers, air pollutants (sulfur and nitrogen oxides, etc.), cold air, physical activity, acetylsalicylic acid and other NSAIDs in patients with aspirin bronchial asthma, psychological, environmental and professional factors, strong odors, smoking (active and passive), concomitant diseases (gastroesophageal reflux, sinusitis, thyrotoxicosis, etc.).

PATHOGENESIS

The pathogenesis of bronchial asthma is based on chronic inflammation.

Bronchial asthma is characterized by a special form of inflammation of the bronchi, leading to the formation of their hyperreactivity (increased sensitivity to various nonspecific irritants compared to the norm); The leading role in inflammation belongs to eosinophils, mast cells and lymphocytes.

Inflamed hyperreactive bronchi respond to triggers with spasm of airway smooth muscle, hypersecretion of mucus, edema and inflammatory cell infiltration of the mucous membrane of the airways, leading to the development of an obstructive syndrome, clinically manifested as an attack of shortness of breath or suffocation.

. ◊ The early asthmatic reaction is mediated by histamine, prostaglandins, leukotrienes and is manifested by contraction of smooth muscles of the respiratory tract, hypersecretion of mucus, and swelling of the mucous membrane.

. ◊ Late asthmatic reaction develops in every second adult patient with bronchial asthma. Lymphokines and other humoral factors cause the migration of lymphocytes, neutrophils and eosinophils and lead to the development of a late asthmatic reaction. Mediators produced by these cells can damage the epithelium of the respiratory tract, maintain or activate the process of inflammation, and stimulate afferent nerve endings. For example, eosinophils can secrete most of the major proteins, leukotriene C 4 , macrophages are sources of thromboxane B 2 , leukotriene B 4 and platelet activating factor. T lymphocytes play a central role in the regulation of local eosinophilia and the appearance of excess IgE. In the bronchial lavage fluid of patients with atopic asthma, the number of T-helper cells (CD4 + lymphocytes) is increased.

. ♦ Prophylactic administration of β 2 -adrenergic agonists blocks only the early reaction, and inhaled GC drugs only block the late one. Cromones (eg, nedocromil) act on both phases of the asthmatic response.

. ◊ The mechanism of development of atopic bronchial asthma is the interaction of antigen (Ag) with IgE, activating phospholipase A 2, under the influence of which arachidonic acid is cleaved from the phospholipids of the mast cell membrane, from which prostaglandins (E 2, D 2, F 2 α) are formed under the action of cyclooxygenase , thromboxane A 2 , prostacyclin, and under the action of lipoxygenase - leukotrienes C 4 , D 4 , E 4 , through specific receptors increasing the tone of smooth muscle cells and leading to inflammation of the airways. This fact provides justification for the use of a relatively new class of antiasthmatic drugs - leukotriene antagonists.

PATHOMORPHOLOGY

In the bronchi, inflammation, mucus plugs, swelling of the mucous membrane, smooth muscle hyperplasia, thickening of the basement membrane, and signs of its disorganization are detected. During the attack, the severity of these pathomorphological changes increases significantly. There may be signs of emphysema (see Chapter 20 “Pulmonary Emphysema”). Endobronchial biopsy of patients with stable chronic (persistent) bronchial asthma reveals desquamation of the bronchial epithelium, eosinophilic infiltration of the mucous membrane, and thickening of the basement membrane of the epithelium. Bronchoalveolar lavage reveals a large number of epithelial and mast cells in the lavage fluid. In patients with nocturnal attacks of bronchial asthma, the highest content of neutrophils, eosinophils and lymphocytes in the bronchial lavage fluid was observed in the early morning hours. Bronchial asthma, unlike other diseases of the lower respiratory tract, is characterized by the absence of bronchiolitis, fibrosis, and granulomatous reaction.

CLINICAL PICTURE AND DIAGNOSTICS

Bronchial asthma is characterized by extremely unstable clinical manifestations, so a careful history taking and examination of external respiration parameters are necessary. In 3 out of 5 patients, bronchial asthma is diagnosed only in the late stages of the disease, since during the interictal period there may be no clinical manifestations of the disease.

COMPLAINTS AND HISTORY

The most characteristic symptoms are episodic attacks of expiratory shortness of breath and/or cough, the appearance of distant wheezing, and a feeling of heaviness in the chest. An important diagnostic indicator of the disease is the relief of symptoms spontaneously or after taking drugs (bronchodilators, GCs). When collecting anamnesis, attention should be paid to the presence of repeated exacerbations, usually after exposure to triggers, as well as seasonal variability of symptoms and the presence of allergic diseases in the patient and his relatives. A thorough collection of allergy history is also necessary to establish the connection between the occurrence of difficulty breathing or coughing with potential allergens (for example, contact with animals, eating citrus fruits, fish, chicken, etc.).

PHYSICAL EXAMINATION

Due to the fact that the severity of the symptoms of the disease changes throughout the day, at the first examination of the patient, characteristic signs of the disease may be absent. An exacerbation of bronchial asthma is characterized by an attack of suffocation or expiratory shortness of breath, flaring of the wings of the nose when inhaling, intermittent speech, agitation, participation of auxiliary respiratory muscles in the act of breathing, constant or episodic cough, there may be dry whistling (buzzing) rales, intensifying on exhalation and heard at distance (distant wheezing). During a severe attack, the patient sits, bending forward, resting his hands on his knees (or the headboard, the edge of the table). With a mild course of the disease, the patient maintains normal activity and sleeps in a normal position.

With the development of pulmonary emphysema, a boxy percussion sound is noted (hyper-airiness of the lung tissue). During auscultation, dry rales are most often heard, but they may be absent even during an exacerbation and even in the presence of confirmed significant bronchial obstruction, which is presumably due to the predominant involvement of small bronchi in the process. Characterized by prolongation of the expiratory phase.

ASSESSMENT OF ALLERGOLOGICAL STATUS

During the initial examination, provocative tests with probable allergens are used, including scarification, intradermal and prick tests. Please be aware that sometimes skin tests give false negative or false positive results. Detection of specific IgE in blood serum is more reliable. Based on an assessment of the allergological status, it is highly likely that atopic and non-atopic bronchial asthma can be distinguished (Table 19-1).

Table 19-1. Some criteria for diagnosing atopic and non-atopic bronchial asthma

LABORATORY RESEARCH

A general blood test reveals eosinophilia. During an exacerbation, leukocytosis and an increase in ESR are detected, and the severity of the changes depends on the severity of the disease. Leukocytosis can also be a consequence of taking prednisolone. A study of the gas composition of arterial blood in the late stages of the disease reveals hypoxemia with hypocapnia, which is replaced by hypercapnia.

Microscopic analysis of sputum reveals a large number of eosinophils, epithelium, Kurschmann spirals (mucus that forms casts of small respiratory tracts), Charcot-Leyden crystals (crystallized eosinophil enzymes). During the initial examination and in case of non-allergic asthma, it is advisable to conduct a bacteriological examination of sputum for pathogenic microflora and its sensitivity to antibiotics.

INSTRUMENTAL RESEARCH

Peak flowmetry (measurement of PSV) is the most important and accessible technique in the diagnosis and control of bronchial obstruction in patients with bronchial asthma (Fig. 19-1). This study, carried out daily 2 times a day, allows you to diagnose bronchial obstruction in the early stages of the development of bronchial asthma, determine the reversibility of bronchial obstruction, assess the severity of the disease and the degree of bronchial hyperreactivity, predict exacerbations, determine occupational bronchial asthma, evaluate the effectiveness of treatment and carry out its correction . Every patient with bronchial asthma should have a peak flow meter.

Rice. 19-1. Peak flow meter. a - peak flow meter; b - rules of application.

FEV study: an important diagnostic criterion is a significant increase in FEV 1 by more than 12% and PSV by more than 15% of the proper values ​​after inhalation of short-acting β 2 -adrenergic agonists (salbutamol, fenoterol). An assessment of bronchial hyperreactivity is also recommended - provocative tests with inhalation of histamine, methacholine (for mild cases of the disease). The standard for measuring bronchial reactivity is the dose or concentration of the provoking agent causing a decrease in FEV 1 by 20%. Based on the measurement of FEV 1 and PEF, as well as daily fluctuations in PEF, the stages of bronchial asthma are determined.

A chest x-ray is performed primarily to rule out other respiratory diseases. Most often, increased airiness of the lungs is detected, sometimes quickly disappearing infiltrates.

◊ When pleuritic pain appears in a patient with an attack of bronchial asthma, radiography is necessary to exclude spontaneous pneumothorax and pneumomediastinum, especially if subcutaneous emphysema occurs.

◊ If asthma attacks are combined with elevated body temperature, an X-ray examination is performed to exclude pneumonia.

◊ In the presence of sinusitis, it is advisable to have an x-ray examination of the nasal sinuses to detect polyps.

Bronchoscopy is performed to exclude any other causes of bronchial obstruction. During the initial examination, it is advisable to assess the cellular composition of the fluid obtained from bronchoalveolar lavage. The need for therapeutic bronchoscopy and therapeutic bronchial lavage for this disease is assessed ambiguously.

An ECG is informative in severe cases of bronchial asthma and reveals overload or hypertrophy of the right heart, conduction disturbances along the right branch of the His bundle. Sinus tachycardia is also characteristic, decreasing during the interictal period. Supraventricular tachycardia may be a side effect of theophylline.

NECESSARY STUDIES AT DIFFERENT STAGES OF BRONCHIAL ASTHMA

. stage 1 . General blood test, general urinalysis, FVD study with a test with β 2 -adrenergic agonists, skin provocative tests to detect allergies, determination of general and specific IgE, chest radiography, sputum analysis. Additionally, in a specialized institution, to clarify the diagnosis, it is possible to conduct provocative tests with bronchoconstrictors, physical activity and/or allergens.

. stage 2 . General blood test, general urinalysis, respiratory function test with a test with β 2 -adrenergic agonists, skin provocative tests, determination of general and specific IgE, chest radiography, sputum analysis. Daily peak flow measurement is advisable. Additionally, in a specialized institution, to clarify the diagnosis, it is possible to conduct provocative tests with bronchoconstrictors, physical activity and/or allergens.

. steps 3 And 4 . General blood test, general urinalysis, respiratory function test with a test with β 2 -adrenergic agonists, daily peak flowmetry, skin provocative tests, if necessary, determination of general and specific IgE, chest radiography, sputum analysis; in specialized institutions - study of blood gas composition.

VARIANTS AND SPECIAL FORMS OF BRONCHIAL ASTHMA

There are several variants (infectious-dependent, dishormonal, dysovarian, vagotonic, neuropsychic, variant with pronounced adrenergic imbalance, cough variant, as well as autoimmune and aspirin-induced bronchial asthma) and special forms (occupational, seasonal, bronchial asthma in the elderly) of bronchial asthma .

INFECTION-DEPENDENT VARIANT

The infection-dependent variant of bronchial asthma is characteristic primarily of persons over 35-40 years of age. In patients with this variant of the course, the disease is more severe than in patients with atopic asthma. The cause of exacerbation of bronchial asthma in this clinical and pathogenetic variant is inflammatory diseases of the respiratory system (acute bronchitis and exacerbation of chronic bronchitis, pneumonia, tonsillitis, sinusitis, acute respiratory viral infections, etc.).

Clinical painting

Attacks of suffocation in such patients are characterized by less acute development, last longer, and are less easily controlled by β 2 -adrenergic agonists. Even after the attack has stopped, harsh breathing with prolonged exhalation and dry wheezing remain in the lungs. Often the symptoms of bronchial asthma are combined with the symptoms of chronic bronchitis. Such patients have a constant cough, sometimes with mucopurulent sputum, and body temperature rises to subfebrile levels. Often in the evening there is a chill, a feeling of chilliness between the shoulder blades, and at night - sweating, mainly in the upper back, neck and back of the head. These patients are often diagnosed with polyposis-allergic rhinosinusitis. Noteworthy is the severity and persistence of obstructive changes in ventilation, which are not completely restored after inhalation of β-adrenergic agonists and relief of an attack of suffocation. In patients with infectious-dependent bronchial asthma, emphysema and cor pulmonale with CHF develop much faster than in patients with atopic asthma.

Laboratory And instrumental research

X-rays show that, as the disease progresses, signs of increased airiness of the lungs appear and increase in patients: increased transparency of the pulmonary fields, expansion of the retrosternal and retrocardial spaces, flattening of the diaphragm, and signs of pneumonia may be detected.

In the presence of an active infectious-inflammatory process in the respiratory organs, leukocytosis against the background of pronounced blood eosinophilia, an increase in ESR, the appearance of CRP, an increase in the content of α- and γ-globulins in the blood, and an increase in acid phosphatase activity by more than 50 units/ml are possible.

Cytological examination of sputum confirms its purulent nature by the predominance of neutrophils and alveolar macrophages in the smear, although eosinophilia is also observed.

Bronchoscopy reveals signs of inflammation of the mucous membrane, hyperemia, mucopurulent nature of the secretion; in bronchial washings during cytological examination, neutrophils and alveolar macrophages predominate.

Required laboratory research

Laboratory tests are needed to establish the presence and role of infection in the pathological process.

Determination of antibodies to chlamydia, moraxella, and mycoplasma in blood serum.

Sowing of fungal microorganisms from sputum, urine and feces in diagnostic titers.

Positive skin tests with fungal allergens.

Detection of viral Ags in the epithelium of the nasal mucosa using immunofluorescence.

A fourfold increase in blood serum antibody titers to viruses, bacteria and fungi when observed over time.

DISHORMONAL (HORMONE DEPENDENT) OPTION

In this option, systemic use of GCs is mandatory for the treatment of patients, and their cancellation or dosage reduction leads to a worsening of the condition.

As a rule, patients with a hormone-dependent variant of the disease take GCs, and the formation of hormonal dependence is not significantly related to the duration of use and the dose of these drugs. In patients receiving GCs, it is necessary to check for complications of therapy (suppression of adrenal cortex function, Itsenko-Cushing syndrome, osteoporosis and bone fractures, hypertension, increased concentrations of glucose in the blood, gastric and duodenal ulcers, myopathies, mental changes).

Hormonal dependence may be a consequence of GC deficiency and/or GC resistance.

Glucocorticoid insufficiency, in turn, can be adrenal or extra-adrenal.

. ◊ Adrenal glucocorticoid insufficiency occurs with a decrease in the synthesis of cortisol by the adrenal cortex, with a predominance of synthesis by the adrenal cortex of the much less biologically active corticosterone.

. ◊ Extra-adrenal glucocorticoid insufficiency occurs with increased binding of cortisol by trascortin, albumin, disturbances in the “hypothalamus-pituitary-adrenal cortex” regulation system, with increased clearance of cortisol, etc.

GC resistance can develop in patients with the most severe course of bronchial asthma; this reduces the ability of lymphocytes to adequately respond to cortisol.

Required laboratory research

Laboratory studies are needed to identify the mechanisms that form the hormone-dependent variant of bronchial asthma.

Determination of the level of total 11-hydroxycorticosteroids and/or cortisol in blood plasma.

Determination of the concentration of 17-hydroxycorticosteroids and ketosteroids in urine.

Daily clearance of corticosteroids.

Cortisol uptake by lymphocytes and/or number of glucocorticoid receptors in lymphocytes.

Minor dexamethasone test.

DISOVARIAL OPTION

The disovarial variant of bronchial asthma, as a rule, is combined with other clinical and pathogenetic variants (most often with atopic) and is diagnosed in cases where exacerbations of bronchial asthma are associated with the phases of the menstrual cycle (usually exacerbations occur in the premenstrual period).

Clinical painting

Exacerbation of bronchial asthma (renewal or increased frequency of asthma attacks, increased shortness of breath, cough with viscous, difficult-to-discharge sputum, etc.) before menstruation in such patients is often accompanied by symptoms of premenstrual tension: migraine, mood swings, pasty face and limbs, algomenorrhea. This variant of bronchial asthma is characterized by a more severe and prognostically unfavorable course.

Required laboratory research

Laboratory tests are needed to diagnose ovarian hormonal dysfunction in women with bronchial asthma.

Basal thermometry test in combination with a cytological examination of vaginal smears (colpocytological method).

Determination of the content of estradiol and progesterone in the blood using the radioimmune method on certain days of the menstrual cycle.

SIGNIFICANT ADRENERGIC IMBALANCE

Adrenergic imbalance is a violation of the relationship between β - and α -adrenergic reactions. In addition to an overdose of β-adrenergic agonists, factors contributing to the formation of adrenergic imbalance are hypoxemia and changes in the acid-base state.

Clinical painting

Adrenergic imbalance most often occurs in patients with atopic bronchial asthma and in the presence of viral and bacterial infections in the acute period. Clinical data suggesting the presence of adrenergic imbalance or a tendency to develop it:

Worsening or development of bronchial obstruction with the administration or inhalation of a β-adrenergic agonist;

Absence or progressive decrease in effect upon administration or inhalation of a β-adrenergic agonist;

Long-term use (parenterally, orally, inhaled, intranasally) of β-adrenergic agonists.

Required laboratory research

The simplest and most accessible criteria for diagnosing adrenergic imbalance include a decrease in the bronchodilation response [according to FEV 1, instantaneous inspiratory volumetric flow rate (IVR), expiratory MVR and maximum pulmonary ventilation] in response to inhalation of β-adrenergic agonists or a paradoxical reaction (an increase in bronchial obstruction by more than by 20% after inhalation of a β-adrenergic agonist).

CHOLINERGIC (VAGOTONIC) OPTION

This variant of the course of bronchial asthma is associated with impaired acetylcholine metabolism and increased activity of the parasympathetic division of the autonomic nervous system.

Clinical painting

The cholinergic variant is characterized by the following features of the clinical picture.

Occurs mainly in older people.

Forms several years after contracting bronchial asthma.

The leading clinical symptom is shortness of breath not only during physical activity, but also at rest.

The most striking clinical manifestation of the cholinergic variant of bronchial asthma is a productive cough with the release of a large amount of mucous, foamy sputum (300-500 ml or more per day), which gave rise to calling this variant of bronchial asthma “wet asthma”.

Rapidly onset bronchospasm under the influence of physical activity, cold air, strong odors.

Impaired bronchial obstruction at the level of the medium and large bronchi, which is manifested by an abundance of dry wheezing over the entire surface of the lungs.

Manifestations of hypervagotonia are nocturnal attacks of suffocation and coughing, increased sweating, hyperhidrosis of the palms, sinus bradycardia, arrhythmias, arterial hypotension, and a frequent combination of bronchial asthma with peptic ulcer disease.

NEUROPSYCHIC OPTION

This clinical and pathogenetic variant of bronchial asthma is diagnosed in cases where neuropsychic factors contribute to the provocation and fixation of asthmatic symptoms, and changes in the functioning of the nervous system become mechanisms of the pathogenesis of bronchial asthma. In some patients, bronchial asthma is a unique form of pathological adaptation of the patient to the environment and solving social problems.

The following clinical variants of neuropsychic bronchial asthma are known.

The neurasthenia-like variant develops against the background of reduced self-esteem, inflated demands on oneself and a painful consciousness of one’s inadequacy, from which an attack of bronchial asthma “protects”.

A hysteria-like variant can develop against the background of an increased level of claims by the patient towards significant persons in the microsocial environment (family, production team, etc.). In this case, with the help of an attack of bronchial asthma, the patient tries to achieve satisfaction of his desires.

The psychasthenic variant of the course of bronchial asthma is characterized by increased anxiety, dependence on significant persons in the microsocial environment and low ability to make independent decisions. The “conditional pleasantness” of an attack lies in the fact that it “relieves” the patient of the need to make a responsible decision.

The shunt mechanism of an attack ensures the release of neurotic confrontation among family members and the receipt of attention and care during an attack from a significant environment.

Diagnosis of the neuropsychiatric variant is based on anamnestic and test data obtained by filling out special questionnaires and questionnaires.

AUTOIMMUNE ASTHMA

Autoimmune asthma occurs as a result of sensitization of patients to pulmonary tissue Ag and occurs in 0.5-1% of patients with bronchial asthma. Probably, the development of this clinical and pathogenetic variant is due to allergic reactions of types III and IV according to the classification of Coombs and Jell (1975).

Main diagnostic criteria for autoimmune asthma:

Severe, continuously relapsing course;

Formation of GC-dependence and GC-resistance in patients;

Detection of antipulmonary antibodies, increasing the concentration of CEC and the activity of acid phosphatase in the blood serum.

Autoimmune bronchial asthma is a rare, but most severe variant of bronchial asthma.

"ASPIRIN" BRONCHIAL ASTHMA

The origin of the aspirin variant of bronchial asthma is associated with a disturbance in the metabolism of arachidonic acid and an increase in the production of leukotrienes. In this case, the so-called aspirin triad is formed, including bronchial asthma, nasal polyposis (paranasal sinuses), intolerance to acetylsalicylic acid and other NSAIDs. The presence of the aspirin triad is observed in 4.2% of patients with bronchial asthma. In some cases, one of the components of the triad - nasal polyposis - is not detected. There may be sensitization to infectious or non-infectious allergens. Anamnesis data on the development of an attack of suffocation after taking acetylsalicylic acid and other NSAIDs are important. In specialized institutions, these patients undergo a test with acetylsalicylic acid to assess the dynamics of FEV 1.

SPECIAL FORMS OF BRONCHIAL ASTHMA

. Bronchial asthma at elderly. In elderly patients, both the diagnosis of bronchial asthma and the assessment of the severity of its course are difficult due to the large number of concomitant diseases, for example, chronic obstructive bronchitis, pulmonary emphysema, and coronary artery disease with signs of left ventricular failure. In addition, with age, the number of β 2 -adrenergic receptors in the bronchi decreases, so the use of β -adrenergic agonists in the elderly is less effective.

. Professional bronchial asthma accounts for an average of 2% of all cases of this disease. More than 200 substances used in production (from highly active low-molecular compounds, such as isocyanates, to known immunogens, such as platinum salts, plant complexes and animal products) are known to contribute to the occurrence of bronchial asthma. Occupational asthma can be either allergic or non-allergic. An important diagnostic criterion is the absence of symptoms of the disease before the start of a given professional activity, a confirmed connection between their appearance at the workplace and their disappearance after leaving it. The diagnosis is confirmed by the results of measuring PEF at work and outside the workplace, and specific provocative tests. It is necessary to diagnose occupational asthma as early as possible and stop contact with the damaging agent.

. Seasonal bronchial asthma usually combined with seasonal allergic rhinitis. During the period between seasons when exacerbation occurs, manifestations of bronchial asthma may be completely absent.

. Tussive option bronchial asthma: dry paroxysmal cough is the main, and sometimes the only symptom of the disease. It often occurs at night and is usually not accompanied by wheezing.

ASTHMATIC STATUS

Status asthmaticus (life-threatening exacerbation) is an asthmatic attack of unusual severity for a given patient, resistant to bronchodilator therapy that is usual for a given patient. Status asthmaticus also refers to severe exacerbation of bronchial asthma, requiring medical care in a hospital setting. One of the reasons for the development of status asthmaticus may be blockade of β 2 -adrenergic receptors due to an overdose of β 2 -adrenergic agonists.

The development of status asthmaticus can be facilitated by the inaccessibility of constant medical care, the lack of objective monitoring of the condition, including peak flowmetry, the patient’s inability to self-control, inadequate previous treatment (usually the absence of basic therapy), a severe attack of bronchial asthma, aggravated by concomitant diseases.

Clinically, status asthmaticus is characterized by pronounced expiratory shortness of breath, a feeling of anxiety up to the fear of death. The patient takes a forced position with the torso tilted forward and emphasis on the arms (shoulders raised). The muscles of the shoulder girdle, chest and abdominals take part in the act of breathing. The duration of exhalation is sharply prolonged, dry whistling and buzzing rales are heard, and as the patient progresses, breathing becomes weakened to the point of “silent lungs” (absence of breathing sounds on auscultation), which reflects the extreme degree of bronchial obstruction.

COMPLICATIONS

Pneumothorax, pneumomediastinum, pulmonary emphysema, respiratory failure, cor pulmonale.

DIFFERENTIAL DIAGNOSTICS

The diagnosis of bronchial asthma should be excluded if, when monitoring external respiration parameters, no disturbances in bronchial obstruction are detected, there are no diurnal fluctuations in PEF, bronchial hyperreactivity and coughing attacks.

In the presence of broncho-obstructive syndrome, differential diagnosis is carried out between the main nosological forms that are characterized by this syndrome (Table 19-2).

Table 19-2. Differential diagnostic criteria for bronchial asthma, chronic bronchitis and emphysema

. Signs	. Bronchial asthma	. COPD	. Emphysema lungs
Age at onset of disease	Often less than 40 years of age	Often over 40 years	Often over 40 years
History of smoking	Not necessary	Characteristic	Characteristic
Nature of symptoms	Episodic or constant	Episodes of exacerbations, progressive	Progressive
Sputum discharge	Little or moderate	Constant in varying quantities	Little or moderate
Presence of atopy
External triggers
FEV 1, FEV 1 /FVC (forced vital capacity of the lungs)	Normal or reduced
Hyperreactivity of the respiratory tract (tests with methacholine, histamine)			Sometimes possible
Total lung capacity	Normal or slightly increased	Normal or slightly increased	Sharply reduced
Diffusion capacity of the lungs	Normal or slightly increased	Normal or slightly increased	Sharply reduced
	Variable
Hereditary predisposition to allergic diseases		Not typical	Not typical
Combination with extrapulmonary manifestations of allergy		Not typical	Not typical
Blood eosinophilia		Not typical	Not typical
Sputum eosinophilia		Not typical	Not typical

When carrying out differential diagnosis of broncho-obstructive conditions, it is necessary to remember that bronchospasm and cough can be caused by certain chemicals, including drugs: NSAIDs (most often acetylsalicylic acid), sulfites (found, for example, in chips, shrimp, dried fruits, beer, wines, as well as in metoclopramide, injectable forms of epinephrine, lidocaine), β-blockers (including eye drops), tartrazine (yellow food coloring), ACE inhibitors. The cough caused by ACE inhibitors, usually dry, poorly controlled by antitussives, β-adrenergic agonists and inhaled glucocorticosteroids, completely disappears after discontinuation of ACE inhibitors.

Bronchospasm can also be triggered by gastroesophageal reflux. Rational treatment of the latter is accompanied by the elimination of attacks of expiratory dyspnea.

Symptoms similar to bronchial asthma occur with dysfunction of the vocal cords (“pseudoasthma”). In these cases, consultation with an otolaryngologist and phoniatrist is necessary.

If infiltrates are detected during chest radiography in patients with bronchial asthma, differential diagnosis should be made with typical and atypical infections, allergic bronchopulmonary aspergillosis, pulmonary eosinophilic infiltrates of various etiologies, allergic granulomatosis in combination with angiitis (Churg-Strauss syndrome).

TREATMENT

Bronchial asthma is an incurable disease. The main goal of therapy is to maintain a normal quality of life, including physical activity.

TREATMENT TACTICS

Treatment goals:

Achieving and maintaining control of disease symptoms;

Preventing exacerbation of the disease;

Maintaining lung function as close to normal as possible;

Maintaining a normal level of activity, including physical activity;

Elimination of side effects of anti-asthma drugs;

Prevention of the development of irreversible bronchial obstruction;

Preventing asthma-related mortality.

Asthma control can be achieved in most patients and can be defined as follows:

Minimal severity (ideally absence) of chronic symptoms, including night ones;

Minimal (infrequent) exacerbations;

No need for ambulance or emergency care;

Minimal need (ideally none) for the use of β-adrenergic agonists (as needed);

No restrictions on activity, including physical activity;

Daily fluctuations in PEF are less than 20%;

Normal (close to normal) PEF indicators;

Minimal severity (or absence) of undesirable effects of the drug.

Management of patients with bronchial asthma has six main components.

1. Education of patients to form partnerships in the process of their management.

2. Assess and monitor the severity of the disease, both by recording symptoms and, if possible, measuring lung function; For patients with moderate and severe disease, daily peak flowmetry is optimal.

3. Elimination of exposure to risk factors.

4. Development of individual drug therapy plans for long-term patient management (taking into account the severity of the disease and the availability of anti-asthmatic drugs).

5. Development of individual plans for relieving exacerbations.

6. Ensuring regular dynamic monitoring.

EDUCATIONAL PROGRAMS

The basis of the educational system for patients in pulmonology is asthma schools. According to specially developed programs, patients are explained in an accessible form the essence of the disease, methods of preventing attacks (elimination of triggers, preventive use of drugs). During the implementation of educational programs, it is considered obligatory to teach the patient to independently manage the course of bronchial asthma in various situations, to develop for him a written plan for recovering from a severe attack, to ensure access to a medical professional, to teach how to use a peak flow meter at home and to maintain a daily PEF curve, as well as correctly use metered dose inhalers. Asthma schools are most effective among women, nonsmokers, and patients with high socioeconomic status.

DRUG THERAPY

Based on the pathogenesis of bronchial asthma, bronchodilators (β 2 -adrenomimetics, m-anticholinergics, xanthines) and anti-inflammatory anti-asthmatic drugs (GCs, mast cell membrane stabilizers and leukotriene inhibitors) are used for treatment.

ANTI-INFLAMMATORY ANTI-ASTMATIC DRUGS (BASIC THERAPY)

. GK: the therapeutic effect of the drugs is associated, in particular, with their ability to increase the number of β 2 -adrenergic receptors in the bronchi, inhibit the development of an immediate allergic reaction, reduce the severity of local inflammation, swelling of the bronchial mucosa and the secretory activity of the bronchial glands, improve mucociliary transport, reduce bronchial reactivity .

. ◊ Inhalation GK * (beclomethasone, budesonide, fluticasone), unlike systemic ones, have a predominantly local anti-inflammatory effect and practically do not cause systemic side effects. The dose of the drug depends on the severity of the disease.

* When taking drugs in the form of dosing cans, it is recommended to use a spacer (especially with a valve that prevents exhalation into the spacer), which contributes to more effective control of bronchial asthma and reduces the severity of some side effects (for example, those associated with the drug settling in the oral cavity, entering the stomach) . A special form of aerosol delivery is the “light breathing” system, which does not require pressing on the can; the aerosol dose is issued in response to negative pressure on the patient’s inhalation. When using drugs in powder form with cyclohaler, turbuhaler, etc., a spacer is not used.

. ◊ System GK(prednisolone, methylprednisolone, triamcinolone, dexamethasone, betamethasone) are prescribed for severe bronchial asthma in minimal doses or, if possible, every other day (alternating regimen). They are prescribed intravenously or orally; the latter route of administration is preferable. Intravenous administration is justified if oral administration is not possible. The prescription of depot drugs is permissible only for seriously ill patients who do not follow medical recommendations, and/or when the effectiveness of other drugs has been exhausted. In all other cases, their use is recommended to be avoided.

. Stabilizers membranes mast cells (cromoglycic acid and nedocromil, as well as drugs combined with short-acting β 2 -adrenergic agonists) act locally, preventing degranulation of mast cells and the release of histamine from them; suppress both immediate and delayed bronchospastic response to inhaled Ag, prevent the development of bronchospasm when inhaling cold air or during physical activity. With long-term use, they reduce bronchial hyperreactivity, reduce the frequency and duration of bronchospasm attacks. They are more effective in children and young adults. Drugs in this group are not used to treat an attack of bronchial asthma.

. Antagonists leukotriene receptors(zafirlukast, montelukast) is a new group of anti-inflammatory anti-asthma drugs. The drugs reduce the need for short-acting β 2 -adrenergic agonists and are effective in preventing bronchospasm attacks. Use internally. Reduces the need for HA ("sparing effect").

BRONCHODILATES

It should be remembered that all bronchodilators in the treatment of bronchial asthma have a symptomatic effect; the frequency of their use serves as an indicator of the effectiveness of basic anti-inflammatory therapy.

. β 2 - Adrenergic agonists short actions(salbutamol, fenoterol) are administered by inhalation; they are considered the drug of choice for stopping attacks (more precisely, exacerbations) of bronchial asthma. When administered by inhalation, the effect usually begins within the first 4 minutes. The drugs are produced in the form of metered aerosols, dry powder and solutions for inhalers (if long-term inhalation is necessary, the solutions are inhaled through a nebulizer).

◊ To administer drugs, metered-dose inhalers, powder inhalers, and nebulization are used. To correctly use metered dose inhalers, the patient needs certain skills, since otherwise only 10-15% of the aerosol enters the bronchial tree. The correct application technique is as follows.

♦ Remove the cap from the mouthpiece and shake the can well.

♦ Exhale completely.

♦ Turn the can upside down.

♦ Place the mouthpiece in front of your mouth wide open.

♦ Start inhaling slowly, at the same time press the inhaler and continue taking a deep breath until the end (the inhalation should not be sharp!).

♦ Hold your breath for at least 10 seconds.

♦ After 1-2 minutes, inhale again (you only need to press the inhaler once for 1 breath).

◊ When using the “easy breathing” system (used in some dosage forms of salbutamol and beclomethasone), the patient must open the mouthpiece cap and take a deep breath. There is no need to press the canister or coordinate inhalation.

◊ If the patient is unable to follow the above recommendations, a spacer (a special plastic flask into which an aerosol is sprayed before inhalation) should be used or a spacer with a valve - an aerosol chamber from which the patient inhales the drug (Fig. 19-2). The correct technique for using a spacer is as follows.

♦ Remove the cap from the inhaler and shake it, then insert the inhaler into the special hole in the device.

♦ Place the mouthpiece in your mouth.

♦ Press the canister to receive a dose of the drug.

♦ Take a slow and deep breath.

♦ Hold your breath for 10 seconds and then exhale into the mouthpiece.

♦ Inhale again, but without pressing on the can.

♦ Move the device away from your mouth.

♦ Wait 30 seconds before taking the next inhalation dose.

Rice. 19-2. Spacer. 1 - mouthpiece; 2 - inhaler; 3 - hole for inhaler; 4 - spacer body.

. β 2 - Adrenergic agonists long-term actions used inhalation (salmeterol, formoterol) or orally (slow-release dosage forms of salbutamol). Their duration of action is about 12 hours. The drugs cause dilatation of the bronchi, increased mucociliary clearance, and also inhibit the release of substances that cause bronchospasm (for example, histamine). β 2 -Adrenergic agonists are effective in preventing asthma attacks, especially at night. They are often used in combination with anti-inflammatory anti-asthma drugs.

M- Anticholinergics(ipratropium bromide) after inhalation they act within 20-40 minutes. The method of administration is inhalation from a can or through a spacer. Specially produced solutions are inhaled through a nebulizer.

. Combined bronchodilators drugs, containing a β 2 -adrenomimetic and an m-anticholinergic blocker (a can and a solution for a nebulizer).

. Drugs theophyllineA short actions(theophylline, aminophylline) as bronchodilators are less effective than inhaled β 2 -adrenergic agonists. They often cause significant side effects, which can be avoided by prescribing the optimal dose and monitoring the concentration of theophylline in the blood. If the patient is already taking long-acting theophylline preparations, intravenous administration of aminophylline is possible only after determining the concentration of theophylline in the blood plasma!

. Drugs theophyllineA prolonged actions used internally. Methylxanthines cause bronchial dilation and inhibit the release of inflammatory mediators from mast cells, monocytes, eosinophils and neutrophils. Due to their long-term effect, the drugs reduce the frequency of nocturnal attacks and slow down the early and late phases of the asthmatic response to allergen exposure. Theophylline preparations can cause serious side effects, especially in older patients; Treatment is recommended to be carried out under the control of theophylline content in the blood.

OPTIMIZATION OF ANTI-ASTMATIC THERAPY

For the rational organization of anti-asthma therapy, methods for its optimization have been developed, which can be described in the form of blocks.

. Block 1 . The patient’s first visit to the doctor, assessment of the severity of bronchial asthma [although it is difficult to accurately establish it at this stage, since accurate information about fluctuations in PEF (according to home peak flow measurements during the week) and the severity of clinical symptoms is required], determination of patient management tactics. If a patient needs emergency care, it is better to hospitalize him. It is imperative to take into account the volume of previous therapy and continue it in accordance with the degree of severity. If the condition worsens during treatment or inadequate previous therapy, additional use of short-acting β 2 -adrenergic agonists can be recommended. An introductory one-week period of observation of the patient's condition is prescribed. If the patient presumably has mild or moderate bronchial asthma and there is no need to immediately prescribe treatment in full, the patient should be observed for 2 weeks. Monitoring the patient's condition involves the patient filling out a diary of clinical symptoms and recording PEF indicators in the evening and morning hours.

. Block 2 . Visit the doctor 1 week after the first visit. Determining the severity of asthma and choosing appropriate treatment.

. Block 3 . A two-week monitoring period during therapy. The patient, as well as during the introductory period, fills out a diary of clinical symptoms and records PEF indicators with a peak flow meter.

. Block 4 . Evaluation of therapy effectiveness. Visit the doctor after 2 weeks during treatment.

DRUG THERAPY ACCORDING TO THE STAGES OF BRONCHIAL ASTHMA

The principles of treatment of bronchial asthma are based on a stepwise approach, recognized in the world since 1995. The goal of this approach is to achieve the most complete control of the manifestations of bronchial asthma using the least amount of drugs. The quantity and frequency of taking drugs increases (step up) as the course of the disease worsens and decreases (step down) as therapy is effective. At the same time, it is necessary to avoid or prevent exposure to trigger factors.

. stage 1 . Treatment of intermittent bronchial asthma includes prophylactic administration (if necessary) of drugs before physical activity (inhaled short-acting β 2 -adrenergic agonists, nedocromil, their combination drugs). Instead of inhaled β 2 -adrenergic agonists, m-anticholinergic blockers or short-acting theophylline preparations can be prescribed, but their effect begins later and they are more likely to cause side effects. With an intermittent course, it is possible to carry out specific immunotherapy with allergens, but only by specialists, allergists.

. stage 2 . In case of persistent bronchial asthma, daily long-term preventive use of drugs is necessary. Inhaled GCs are prescribed at a dose of 200-500 mcg/day (based on beclomethasone), nedocromil or long-acting theophylline preparations. Inhaled short-acting β 2 -agonists continue to be used as needed (with proper basic therapy, the need should decrease until they are discontinued).

. ◊ If, during treatment with inhaled GCs (and the doctor is sure that the patient inhales correctly), the frequency of symptoms does not decrease, the dose of the drug should be increased to 750-800 mcg/day or prescribed in addition to GCs (at a dose of at least 500 μg) Long-acting bronchodilators at night (especially to prevent night attacks).

. ◊ If control of the manifestations of bronchial asthma cannot be achieved with the help of prescribed drugs (symptoms of the disease occur more often, the need for short-acting bronchodilators increases or PEF values ​​decrease), treatment should be started according to step 3.

. stage 3 . Daily use of anti-asthmatic anti-inflammatory drugs. Inhaled GCs are prescribed at 800-2000 mcg/day (based on beclomethasone); It is recommended to use an inhaler with a spacer. Long-acting bronchodilators can be additionally prescribed, especially to prevent nocturnal attacks, for example, oral and inhaled long-acting β 2 -agonists, long-acting theophylline preparations (under monitoring the concentration of theophylline in the blood; therapeutic concentration is 5-15 μg/ml). Symptoms can be relieved with short-acting β2-adrenergic agonists. For more severe exacerbations, a course of treatment with oral GCs is carried out. If control of the manifestations of bronchial asthma cannot be achieved (symptoms of the disease occur more frequently, the need for short-acting bronchodilators increases or PEF values ​​decrease), treatment should be started according to step 4.

. stage 4 . In severe cases of bronchial asthma, it is not possible to completely control it. The goal of treatment is to achieve the maximum possible results: the least number of symptoms, the minimum need for short-acting β 2 -adrenergic agonists, the best possible PEF indicators and their minimum scatter, the least number of side effects of the drugs. Typically, several drugs are used: inhaled GCs in high doses (800-2000 mcg/day in terms of beclomethasone), GCs taken orally continuously or in long courses, long-acting bronchodilators. You can prescribe m-anticholinergic drugs (ipratropium bromide) or their combination with a β 2 -adrenergic agonist. Inhaled short-acting β 2 -agonists can be used if necessary to relieve symptoms, but not more than 3-4 times a day.

. stage up(deterioration). They move to the next stage if treatment at this stage is ineffective. However, it should be taken into account whether the patient is taking the prescribed drugs correctly, and whether he has contact with allergens and other provoking factors.

. stage down(improvement). Reducing the intensity of maintenance therapy is possible if the patient's condition is stabilized for at least 3 months. The volume of therapy should be reduced gradually. The transition to a downward stage is carried out under the control of clinical manifestations and respiratory function.

The basic therapy outlined above should be accompanied by carefully performed elimination measures and supplemented with other drugs and non-drug treatment methods, taking into account the clinical and pathogenetic variant of the course of asthma.

Patients with infectious-related asthma require sanitation of foci of infection, mucolytic therapy, barotherapy, and acupuncture.

In addition to GCs, patients with autoimmune changes can be prescribed cytostatic drugs.

Patients with hormone-dependent asthma require individual regimens for the use of GCs and monitoring for the possibility of developing complications of therapy.

Patients with dysovarian changes can be prescribed (after consultation with a gynecologist) synthetic progestins.

Psychotherapeutic methods of treatment are indicated for patients with a pronounced neuropsychic variant of the course of bronchial asthma.

In the presence of adrenergic imbalance, GCs are effective.

In patients with severe cholinergic variants, the anticholinergic drug ipratropium bromide is indicated.

Patients with physical exertion bronchial asthma need exercise therapy methods and antileukotriene drugs.

All patients with bronchial asthma need various methods of psychotherapeutic treatment and psychological support. In addition, all patients (in the absence of individual intolerance) are prescribed multivitamin preparations. When the exacerbation subsides and during remission of bronchial asthma, exercise therapy and massage are recommended.

Particular attention should be paid to teaching patients the rules of elimination therapy, inhalation techniques, individual peak flowmetry and monitoring their condition.

PRINCIPLES OF TREATMENT OF EXACERBATIONS OF BRONCHIAL ASTHMA

Exacerbation of bronchial asthma - episodes of a progressive increase in the frequency of attacks of expiratory suffocation, shortness of breath, coughing, the appearance of wheezing, a feeling of lack of air and chest compression, or a combination of these symptoms, lasting from several hours to several weeks or more. Severe exacerbations, sometimes fatal, are usually associated with the doctor’s underestimation of the severity of the patient’s condition and incorrect tactics at the onset of an exacerbation. The principles of treatment of exacerbations are as follows.

A patient with bronchial asthma should know the early signs of exacerbation of the disease and begin to stop them on their own.

The optimal route of drug administration is inhalation using nebulizers.

The drugs of choice for rapid relief of bronchial obstruction are short-acting inhaled β 2 -adrenergic agonists.

If inhaled β 2 -adrenergic agonists are ineffective, as well as with severe exacerbations, systemic GCs are used orally or intravenously.

To reduce hypoxemia, oxygen therapy is performed.

The effectiveness of therapy is determined using spirometry and/or peak flowmetry by changes in FEV 1 or PEF.

TREATMENT FOR ASTHMATIC STATUS

It is necessary to examine the respiratory function every 15-30 minutes (at least), PEF and oxygen pulse. Hospitalization criteria are given in table. 19-3. Complete stabilization of the patient's condition can be achieved within 4 hours of intensive therapy in the emergency department; if it is not achieved during this period, observation is continued for 12-24 hours or hospitalized in the general ward or intensive care unit (with hypoxemia and hypercapnia, signs fatigue of the respiratory muscles).

Table 19-3. Spirometric criteria for hospitalization of a patient with bronchial asthma

State	Indications To hospitalization
Primary examination	Inability to perform spirometry FEV 1 ‹ 0.60 l
Peak flowmetry and response to treatment	No effect of bronchodilators and PSV ‹ 60 l/min Increase in PEF after treatment ‹ 16% Increase in FEV 1 ‹ 150 ml after subcutaneous administration of bronchodilators FEV 1 ‹ 30% of predicted values ​​and not > 40% of predicted values ​​after treatment lasting more than 4 hours
Peak flowmetry and response to the course of treatment	PEF ‹ 100 l/min initially and ‹ 300 l/min after treatment FEV 1 ‹ 0.61 l initially and ‹ 1.6 l after the full course of treatment Increase in FEV 1 ‹ 400 ml after using bronchodilators Decrease in PEF by 15% after an initial positive reaction to bronchodilators

In case of status asthmaticus, as a rule, inhalation of β 2 -adrenomimetics is first carried out (in the absence of a history of overdose), this can be in combination with an m-anticholinergic agent and, preferably, through a nebulizer. In most patients with a severe attack, additional GCs are indicated. Inhalation of β 2 -adrenergic agonists through nebulizers in combination with systemic GCs, as a rule, stops the attack within 1 hour. In case of a severe attack, oxygen therapy is necessary. The patient remains in the hospital until the nocturnal attacks disappear and the subjective need for short-acting bronchodilators decreases to 3-4 inhalations per day.

GCs are prescribed orally or intravenously, for example, methylprednisolone 60-125 mg intravenously every 6-8 hours or prednisolone 30-60 mg orally every 6 hours. The effect of the drugs with both methods of administration develops after 4-8 hours; The duration of treatment is determined individually.

. β 2 -Short-acting adrenergic agonists (in the absence of anamnestic data on overdose) are used in the form of repeated inhalations in severe condition of the patient in the form of dosing cans with spacers or long-term (within 72-96 hours) inhalation through a nebulizer (7 times more effective than inhalations from a can). , safe for adults and children).

You can use a combination of a β 2 -adrenergic agonist (salbutamol, fenoterol) with an m-anticholinergic blocker (ipratropium bromide).

The role of methylxanthines in emergency care is limited, since they are less effective than β 2 -agonists, are contraindicated in older patients, and, in addition, monitoring their concentration in the blood is necessary.

If the condition has not improved, but there is no need for mechanical ventilation, inhalation of an oxygen-helium mixture is indicated (causes a decrease in resistance to gas flows in the respiratory tract, turbulent flows in the small bronchi become laminar), intravenous administration of magnesium sulfate, and auxiliary non-invasive ventilation. Transfer of a patient with status asthmaticus to mechanical ventilation is carried out according to vital indications in any setting (outside a medical institution, in the emergency department, in the general ward or intensive care unit). The procedure is performed by an anesthesiologist or resuscitator. The purpose of mechanical ventilation for bronchial asthma is to support oxygenation, normalize blood pH, and prevent iatrogenic complications. In some cases, mechanical ventilation of the lungs requires intravenous infusion of sodium bicarbonate solution.

BRONCHIAL ASTHMA AND PREGNANCY

On average, 1 in 100 pregnant women suffers from bronchial asthma, and in 1 in 500 pregnant women it has a severe course that threatens the life of the woman and the fetus. The course of bronchial asthma during pregnancy is very variable. Pregnancy in patients with a mild course of the disease can improve the condition, while in severe cases it usually aggravates it. An increase in attacks is more often noted at the end of the second trimester of pregnancy; severe attacks rarely occur during childbirth. Within 3 months after birth, the course of bronchial asthma returns to the original prenatal level. Changes in the course of the disease during repeated pregnancies are the same as during the first. Previously, it was believed that bronchial asthma is twice as likely to cause pregnancy complications (preeclampsia, postpartum hemorrhage), but recently it has been proven that with adequate medical supervision, the likelihood of their development does not increase. However, these women are more likely to give birth to children with low body weight, and there is also a greater need for surgical delivery. When prescribing anti-asthmatic drugs to pregnant women, the possibility of their effect on the fetus should always be taken into account, however, most modern inhaled anti-asthmatic drugs are safe in this regard (Table 19-4). In the US FDA * developed a guide according to which all drugs are divided into 5 groups (A-D, X) according to the degree of danger of use during pregnancy * .

* According to the FDA classification (Food and Drug Administration, Committee for the Control of Drugs and Food Additives, USA), drugs according to the degree of danger (teratogenicity) for fetal development are divided into categories A, B, C, D, X. Category A (for example, potassium chloride) and B (eg, insulin): adverse effects on the fetus have not been established either in animal experiments or in clinical practice; category C (eg, isoniazid): adverse effects on the fetus have been established in animal experiments, but not from clinical practice; category D (for example, diazepam): there is a potential teratogenic risk, but the effect of the drug on a pregnant woman usually outweighs this risk; category X (for example, isotretinoin): the drug is definitely contraindicated during pregnancy and if you want to become pregnant.

Among patients undergoing operations with inhalation anesthesia, an average of 3.5% suffer from bronchial asthma. These patients are more likely to have complications during and after surgery, so assessing the severity and ability to control the course of bronchial asthma, assessing the risk of anesthesia and this type of surgery, as well as preoperative preparation are extremely important. The following factors should be considered.

Acute airway obstruction causes ventilation-perfusion disturbances, increasing hypoxemia and hypercapnia.

Endotracheal intubation can provoke bronchospasm.

Drugs used during surgery (for example, morphine, trimeperidine) can provoke bronchospasm.

Severe bronchial obstruction in combination with postoperative pain syndrome can disrupt the coughing process and lead to the development of atelectasis and nosocomial pneumonia.

To prevent exacerbation of bronchial asthma in patients with a stable condition with regular GC inhalations, it is recommended to prescribe prednisolone at a dose of 40 mg/day orally 2 days before surgery, and give this dose in the morning on the day of surgery. In severe cases of bronchial asthma, the patient should be hospitalized several days before surgery to stabilize the respiratory function (intravenous administration of glucocorticosteroids). In addition, it should be borne in mind that patients receiving systemic GCs for 6 months or more are at high risk of adrenal-pituitary insufficiency in response to surgical stress, so they are shown prophylactic administration of 100 mg hydrocortisone intravenously before, during and after surgery .

FORECAST

The prognosis of the course of bronchial asthma depends on the timeliness of its detection, the patient’s level of education and his ability to self-control. Elimination of provoking factors and timely seeking qualified medical help are of decisive importance.

DISPANSERIZATION

Patients need constant monitoring by a therapist at their place of residence (with complete control of symptoms at least once every 3 months). For frequent exacerbations, constant monitoring by a pulmonologist is indicated. According to indications, an allergological examination is carried out. The patient should know that the Russian Federation provides free (with special prescriptions) provision of anti-asthmatic drugs in accordance with lists approved at the federal and local levels.

Factors that determine the need for close and continuous monitoring, which is carried out in an inpatient or outpatient setting, depending on available facilities, include:

Insufficient or decreasing response to therapy in the first 1-2 hours of treatment;

Persistent severe bronchial obstruction (PSV less than 30% of the proper or individual best value);

Recent history of severe asthma, especially if hospitalization and intensive care unit stay were required;

Presence of high risk factors for death from bronchial asthma;

Long-term presence of symptoms before seeking emergency care;

Insufficient availability of medical care and drugs at home;

Poor living conditions;

Difficulties in obtaining transportation to the hospital in case of further deterioration.

Constant symptoms throughout the day. - Frequent exacerbations. - Frequent nighttime symptoms.

Physical activity is limited by asthma symptoms.

PEF is less than 60% of the expected value; fluctuations of more than 30%.

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

Treatment: Stage 4: Patients with severe asthma cannot fully control their asthma. The goal of treatment is to achieve the best possible results: minimal symptoms, minimal need for short-acting beta-2 agonists, best possible PEF, minimal variation in PEF, and minimal drug side effects. Treatment is usually done with a large number of asthma-controlling medications.

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

Oral corticosteroids continuously or in long courses.

Long-acting bronchodilators.

An anticholinergic drug (ipratropium bromide) may be tried, especially in patients who experience side effects with 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 to 4 times daily.

It should be noted that determining the severity of asthma using these indicators is possible only before starting treatment. If the patient is already receiving the necessary therapy, then its volume should also be taken into account. Thus, if a patient’s clinical picture is determined to have mild persistent asthma, but he receives drug treatment corresponding to severe persistent asthma, then this patient is diagnosed with severe bronchial asthma.

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

Block 1. The patient’s first visit to the doctor, assessment of severity, determination of patient management tactics. If the patient's condition requires emergency care, it is better to hospitalize him. At the first visit, it is difficult to accurately determine the degree of severity, because This requires fluctuations in PEF during the week and the severity of clinical symptoms. Be sure to consider the amount of therapy performed before your first visit to the doctor. Continue therapy during the monitoring period. If necessary, additional short-acting beta-2 agonists may be recommended.

An introductory one-week monitoring period is prescribed if the patient is suspected to have mild or moderate asthma that does not require emergency full therapy. Otherwise, it is necessary to provide adequate treatment and monitor the patient for 2 weeks. The patient fills out a diary of clinical symptoms and records PEF indicators in the evening and morning hours.

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

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

Block 4. Evaluation of therapy effectiveness. Visit after 2 weeks during therapy.

Step up: Increased therapy should be done if asthma control cannot be achieved. However, it should be taken into account whether the patient is taking medications at the appropriate level correctly and whether there is 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 bronchodilator use

short action.

The spread of PEF indicators is increasing.

Step down: A reduction in maintenance therapy is possible if asthma remains under control for at least 3 months. This helps reduce the risk of side effects and increases the patient's sensitivity to the planned treatment. Therapy should be reduced “stepwise”, lowering or eliminating the last dose, or additional drugs. It is necessary to monitor symptoms, clinical manifestations and indicators of respiratory function.

Thus, although bronchial asthma is an incurable disease, it is reasonable to expect that control of the disease can and should be achieved in most patients.

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 for the creation of flexible plans and special treatment programs depending on the availability of anti-asthmatic drugs, the regional healthcare system and the characteristics of the individual 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 clinical observation.

Bronchial asthma

Bronchial asthma(asthma bronchiale; Greek asthma, heavy breathing, suffocation) is a disease the main symptom of which is attacks or periodic states of expiratory suffocation caused by pathological hyperreactivity of the bronchi. This hyperreactivity manifests itself when exposed to various endo- and exogenous irritants, both those that cause an allergic reaction and those that act without the participation of allergic mechanisms. The given definition corresponds to the idea of ​​B. a. as a nonspecific syndrome and requires coordination with the tendency to preserve in diagnostic and treatment practice what developed in the USSR in the 60-70s. isolation from this syndromic concept of allergic B. a. 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 time, B. a. divided into those caused by external factors (asthma extrinsic) and those 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 system, endocrine and psychogenic factors. The so-called aspirin asthma and exercise asthma are distinguished as separate options. In the classification of A.D. Ado and P.K. Bulatov, adopted in the USSR since 1968, distinguishes two main forms of B. a.: atopic and infectious-allergic. Each of the forms is divided into stages into pre-asthma, the stage of attacks and the stage of asthmatic conditions, and the sequence of stages is not mandatory. Based on the severity of the course, they distinguish between mild, moderate and severe B. a. In recent years, in the light of the approach to B. a. As a syndrome, this classification, as well as the terminology used, raises objections. In particular, it is proposed to isolate the non-immunological form of B. a.; 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; identification of dishormonal and neuropsychic variants of B. a.

Etiology

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

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

Predisposing factors for the development of B. a., first of all, include heredity, the significance of which is more pronounced in atopic B. a., inherited in a recessive manner with 50% penetrance. It is assumed that the ability to produce allergic IgE antibodies (immunoglobulin E) in atopic asthma, as in other manifestations of atopy, is associated with a decrease in the number or decrease in the function of suppressor T lymphocytes. There is an opinion that the development of B. a. contribute to some endocrine disorders and dysfunction of the pituitary gland - adrenal cortex system; For example, exacerbations of the disease during menopause in women are known. Probably, predisposing factors include a cold, damp climate, as well as air pollution.

Pathogenesis

Pathogenesis of any form of B. a. consists in the formation of bronchial hyperreactivity, manifested by spasm of the 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 irritants - 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. The specific mechanisms of the formation of bronchial hyperreactivity have not been sufficiently studied and are probably different for different etiological variants of B. a. with a different ratio of the role of congenital and acquired disorders of regulation of bronchial tone. Great importance is attached to the defect of b-adrenergic regulation of the tone of the bronchial wall; the role of hyperreactivity of a-adrenergic receptors and cholinergic receptors of the bronchi, as well as the so-called non-adrenergic-noncholinergic system, cannot be excluded. Acute bronchial obstruction in the case of atonic B. a. develops when the bronchial walls are exposed to mediators of a type I allergic reaction (see. Allergy ). The possible pathogenetic role in the reaction of immunoglobulins G (subclass IgG 4) is discussed. Using inhalation provocation tests with atopic allergens, it has been established that they can induce a typical immediate reaction (after 15-20 min after contact with the allergen), and late, which begins after 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 attraction of neutrophils and eosinophils by chemotactic factors of a type I allergic reaction. There is reason to believe that it is the late reaction to the allergen that significantly increases the hyperreactivity of the bronchi to nonspecific stimuli. In some cases, it is the basis for the development of status asthmaticus, but the latter can also be caused by other reasons, occurring, for example, after taking non-steroidal anti-inflammatory drugs in patients with aspirin asthma, with an overdose of adrenergic agonists. after improper withdrawal of glucocorticoids, etc. In the pathogenesis of status asthmaticus, the most significant are considered to be blockade of b-adrenergic receptors and mechanical obstruction of the bronchi (viscous mucus, as well as due to edema and cellular infiltration of their walls).

Pathogenesis of aspirin B. a. not entirely clear. In most cases there is pseudoallergy To a number of non-steroidal anti-inflammatory drugs. It is believed that the disruption of arachidonic acid metabolism by these drugs is of key importance.

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

The pathogenetic mechanisms of physical exertion asthma have not been established. There is a point of view that the leading factor in pathogenesis is irritation of the effector endings of the vagus nerve. The reflex may be caused, in part, by heat loss from the lungs due to forced breathing. The influence of cooling through a mediator mechanism is more likely. It has been noted that exercise-induced asthma is more easily provoked by inhaling dry air than humidified air.

In many patients with B. a. psychogenic attacks of suffocation are noted, occurring, 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 in fact the patient inhaled saline solution), etc. Acute, severe stressful situations are more likely to cause a temporary remission of AD, while chronic psychotrauma usually worsens its course. Mechanisms of influence of psychogenic influences on the course of B. a. remain unclear. Various types of neuroses that occur in patients with B. a. are often a consequence rather than a cause of the disease. At present, there is no sufficient reason to classify psychogenic asthma as a separate form, but in the complex treatment of patients with B. a. the significance of psychogenics should be taken into account.

Clinical picture

In the pre-asthma stage, many patients develop allergic or polypous rhinosinusitis. Manifestations of preasthma proper include a paroxysmal cough (dry or with the release of a small amount of mucous, viscous sputum), which is not alleviated by conventional antitussive drugs and is eliminated by means of treating B. a. Coughing attacks usually occur at night or in the early morning hours. Most often, a cough remains after a respiratory viral infection or an exacerbation of chronic bronchitis or pneumonia. The patient does not yet experience breathing difficulties. Auscultation of the lungs sometimes reveals hard breathing, very rarely dry wheezing during forced exhalation. Eosinophilia is detected in blood and sputum. When examining external respiratory functions (ERF) before and after inhalation of a b-adrenergic agonist (izadrin, Berotek, etc.), a significant increase in expiratory power can be detected, indicating the so-called latent bronchospasm.

In subsequent stages of development of B. a. Its main manifestations are attacks of suffocation, and in severe cases also states of progressive suffocation, referred to as status asthmaticus.

Attack of bronchial asthma develops relatively suddenly, in some patients following certain individual precursors (sore throat, itchy skin, nasal congestion, rhinorrhea, etc.). There is a feeling of chest congestion, difficulty breathing, and a desire to cough, although the cough during this period is mostly dry and aggravates shortness of breath. The difficulty in breathing, which the patient initially experiences only when exhaling, increases, which forces the patient to take a sitting position to engage the auxiliary respiratory muscles ( cm. Respiratory system ). Wheezing appears 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 (distance wheezing) as a combination of different pitches of the voices of a playing accordion (musical wheezing). At the height of the attack, the patient experiences severe suffocation, difficulty not only in exhaling, but also in inhaling (due to the placement of the chest and diaphragm in the deep inhalation position during the respiratory pause).

The patient sits, resting his hands on the edge of the seat. The chest is expanded; exhalation is significantly lengthened and is achieved by visible tension in the muscles of the chest and torso (expiratory shortness of breath); the intercostal spaces retract during inspiration; The neck veins swell during exhalation and collapse during inhalation, reflecting significant changes in intrathoracic pressure in the inhalation and exhalation phases. Percussion of the chest reveals a box sound, drooping of the lower border of the lungs and limitation of the respiratory mobility of the diaphragm, which is confirmed by x-ray examination, which also reveals a significant increase in the transparency of the pulmonary fields (acute swelling of the lungs). Auscultation of the lungs reveals harsh breathing and abundant dry wheezing 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 increased. Heart sounds are often difficult to detect due to swelling of the lungs and the muffled volume of audible dry rales.

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

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

There are three possible onset of status asthmaticus: the rapid development of coma (sometimes observed in patients after discontinuation of glucocorticoids), the transition to status asthmaticus of an asthma attack (often against the background of an overdose of adrenomimetics) and the slow development of progressive suffocation, most often in patients with infectious-dependent B. a . Based on the severity of the patient’s condition and the degree of gas exchange disturbances, three stages of status asthmaticus are distinguished.

Stage I is characterized by the appearance of persistent expiratory shortness of breath, against the background of which frequent attacks of suffocation occur, forcing patients to resort to repeated inhalations of adrenergic agonists, but the latter only briefly relieve suffocation (without completely eliminating expiratory shortness of breath), and after a few hours this effect is lost. The patients are somewhat agitated. Percussion and auscultation of the lungs reveal changes similar to those during an attack of asthma, but dry wheezing is usually less abundant and high-pitched wheezing predominates. As a rule, tachycardia is detected, especially pronounced during intoxication with adrenergic agonists, when tremor of the fingers, pallor, increased systolic blood pressure, sometimes extrasystole, and dilated pupils are also detected. The tension of oxygen (pO 2) and carbon dioxide (pCO 2) in arterial blood is close to normal, there may be a tendency to hypocapnia.

Stage II of status asthmaticus is characterized by a severe degree of expiratory suffocation, fatigue of the respiratory muscles with a gradual decrease in the minute volume of breathing, and increasing hypoxemia. The patient either sits, leaning on the edge of the bed, or reclines. Excitement is replaced by increasingly lengthening periods of apathy. The tongue, skin of the face and body are cyanotic. Breathing remains rapid, but it is less deep than in stage I. Percussion reveals a picture of acute swelling of the lungs, and auscultation reveals weakened, hard breathing, which may not be audible at all over certain areas of the lungs (zones of the “silent” lung). The number of audible dry wheezing is significantly reduced (fine and quiet wheezing is detected). There is tachycardia, sometimes extrasystole; ECG shows signs of pulmonary hypertension (see. Hypertension of the pulmonary circulation ), reduction of the T wave in most leads. Arterial blood pO2 drops to 60-50 mmHg Art., moderate hypercapnia is possible.

Stage Ill of status asthmaticus 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 acidosis coma. Severe diffuse cyanosis is noted. Dry mucous membranes and decreased tissue turgor (signs of dehydration) are often detected. Breathing gradually slows down and becomes less and less deep, which during auscultation is reflected by the disappearance of wheezing and a significant weakening of respiratory sounds with the expansion of zones of the “silent” lung. Tachycardia is often combined with various cardiac arrhythmias. Death can occur from respiratory arrest or acute cardiac arrhythmias due to myocardial hypoxia.

Certain forms of brochial Asthma has characteristics of anamnesis, clinical manifestations and course.

Atopic B. a. often begins in childhood or adolescence. In more than 50% of cases, the family history reveals asthma or other atonic diseases; the patient’s history includes allergic rhinitis and 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, and interscapular area. The attack often begins with a dry cough, then quickly develops a typical picture of expiratory suffocation with distant dry rales. Usually the 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 disappear completely or remain minimal.

For atopic B. a. characterized by a relatively mild course, late development of complications. Severe course and 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 common. Complete recovery in atopic B. a. It is rare in adults.

Infection-dependent B. a. It is observed in people of different ages, but adults are more often affected. A family history of asthma is relatively common, and atopic diseases are rare. The combination of B. a is characteristic. with polypous rhinosinusitis. The onset of the disease is usually associated with acute, often viral infections or with exacerbations of chronic diseases of the respiratory system (sinusitis, bronchitis, pneumonia). Attacks of suffocation are characterized by less acute development than in atopic asthma, longer duration, less clear and rapid resolution in response to the use of adrenergic agonists. After the attack has stopped, auscultation of the lungs reveals hard breathing with prolonged exhalation, dry wheezing, and, in the presence of inflammatory exudate in the bronchi, moist rales. With this form of B. a. A severe course with repeated asthmatic statuses is more common, and complications develop faster.

Aspirin asthma in typical cases it is characterized by a combination of B. a. with recurrent polyposis of the nose and 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 are more often affected, but the disease also occurs in children. It usually begins with polypous rhinosinusitis; polyps quickly recur after their removal. At some stage of the disease, after another polypectomy or taking aspirin or analgin, B. a. is added, 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 severe status asthmaticus with a fatal outcome. Polypectomies are also often accompanied by severe exacerbations of B. a. Most clinicians believe that for aspirin B. a. characterized by a severe course. Atopy is rare among these patients.

Exercise asthma, 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 attack of suffocation after 2-10 min after the end of the load. Attacks are rarely severe and last 5-10 min, sometimes up to 1 h; pass without the use of drugs or after inhalation of a b-adrenergic agonist. Exercise asthma is more common in children than in adults. It has been noted that certain types of physical exertion (running, playing football, basketball) especially often cause post-exertional bronchospasm. Lifting weights is less dangerous; Swimming and rowing are relatively well tolerated. The duration of physical activity also matters. Under the conditions of a provocative test, loads are usually given for 6-8 min; with a longer load (12-16 min) the severity of post-load bronchospasm may be less - the patient seems to jump over bronchospasm.

Complications

Long lasting 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 arise much faster in the infection-dependent form than in the atopic form of the disease. At the height of an attack of suffocation or a prolonged coughing attack, a short-term loss of consciousness is possible ( bettolepsy ). In severe attacks, lung ruptures are sometimes observed in areas of bullous emphysema with the development pneumothorax and pneumomediastinum (see. Mediastinum ). Complications are often observed in connection with long-term therapy with B. a. glucocorticoids: obesity, arterial hypertension, severe osteoporosis, which can cause the occurrence of B. a during attacks. spontaneous rib fractures. With continuous use of glucocorticoids, a hormone-dependent course of B. a. is formed in a relatively short period of time (sometimes within 3-5 weeks); withdrawal of glucocorticoids can cause severe status asthmaticus, which can be fatal.

Analysis of the clinical picture and targeted examination of the patient make it possible to solve three main diagnostic problems: confirm (or reject) the presence of B. a., determine its form, establish the spectrum of allergens (for allergic B. a.) or pseudoallergens (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 distant wheezing; significant differences in expiratory power during an attack (sharp decrease) and outside an attack: the effectiveness of b-adrenergic agonists in relieving asthma attacks; eosinophilia of blood and especially sputum; the presence of concomitant allergic or polypous rhinosinusopathy. Confirm the presence of B. a. characteristic changes in respiratory function; X-ray data outside an asthma attack are less specific. 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 swelling of the mucous membrane, polypous, and sometimes purulent process. With atopic B. a. X-ray changes in the lungs outside of an attack of suffocation may be absent even years after the onset of the disease.

From studies of FVD, the main significance for the diagnosis of B. a. 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 a 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 during a routine outpatient appointment, incl. to identify the so-called hidden bronchospasm, often found in patients with B. a. If the expiratory power measured before and after 5, 10 and 20 min after inhalation of one dose of Alupent (or another b-adrenomimetic 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 provide 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-adrenergic blocking drugs. These studies, sometimes necessary when the diagnosis of B. a. is questionable, 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. a is provoked. A positive acetylcholine test confirms the diagnosis of B. a., a negative one allows it to be rejected with a high degree of probability.

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

Aspirin asthma is suspected with a high probability in the case of a clear connection between the attacks and the use of aspirin or other non-steroidal anti-inflammatory drugs, as well as if asthma is the first manifestation of intolerance to these drugs, especially in women over 30 years of age who do not have atopy in their personal or family history and suffer from pansinusitis or nasal polyposis, complementing the aspirin triad. The diagnosis is more reliable if during attacks of B. a. 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 widespread use of this test cannot be recommended due to the possibility of severe reactions.

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

Atopic B. a. recognized by the characteristics of the clinical course, the presence of concomitant manifestations of atopy (hay fever, atopic dermatitis, food allergies, etc.), family and allergological history. The diagnosis is confirmed by identifying the patient's sensitization of the reagin type (see. Allergy ) and positive results of elimination tests (cessation of contact with suspected allergens), as well as provocative tests with certain allergens. For atonic B. a. characterized by an increased content of total IgE in the serum, as well as the presence of allergen-specific IgE. Relatively often there is a decrease in the number of T-lymphocytes, especially suppressor T-lymphocytes.

Infection-dependent B. a. It is assumed primarily in cases 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 infection-dependent and atopic forms of B. a. In favor of infection-dependent B. a. evidenced by the slow onset and long duration of asthma attacks, the frequent connection of their frequency with a previous acute or aggravated chronic respiratory infection, a tendency to develop status asthmaticus, 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 .