Bronchial asthma severe treatment. Drug prevention of bronchial asthma attacks

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

T.A. Pertseva, Corresponding Member of the Academy of Medical Sciences of Ukraine, Doctor of Medical Sciences, Professor, E.Yu. Gashinova, Candidate of Medical Sciences, Department of Faculty Therapy and Endocrinology, Dnepropetrovsk State Medical Academy

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

Epidemiology
General practitioners and pulmonologists who care for patients with asthma every day know first-hand the seriousness of the disease, its increasing prevalence and the ever-increasing economic costs associated with it.
Data on the prevalence of severe asthma are inconsistent, partly due to the lack of a universal definition of this form of the disease. However, along with the widespread increase in the total number of patients with asthma, there has been a steady trend towards an increase in the number of patients in need of assistance. emergency care, often hospitalized due to the severe course of the disease, the exacerbation of which is often life-threatening.

Definition
IN Global strategy treatment and prevention of asthma (GINA, 2005) is considered a severe disease, which is characterized by daily symptoms that limit physical activity, frequent exacerbations and nighttime manifestations, as well as a decrease in FEV1 less than 60% of the expected values and daily fluctuations in peak expiratory flow (PEF) over 30 %.
The British Thoracic Society classifies severe asthma, with adequate medical therapy, as a condition that can only be controlled with high doses of inhaled and/or systemic corticosteroids.
In 2000, the American Thoracic Society defined “refractory asthma” as a condition with the presence of one or more major and two or more minor criteria that take into account the need for medications, asthma symptoms, frequency of exacerbations, and degree of airway obstruction.
In the European Community study ENFUMOSA, patients with persistent asthma symptoms and recurrent exacerbations despite high doses of inhaled corticosteroids and long-acting bronchodilators were diagnosed with severe asthma; patients with asthma who require constant use of systemic corticosteroids to achieve disease control; patients with a history of life-threatening asthma attacks.
The most accurate definition should be considered in which severe asthma is considered as difficult to control, treatment-resistant, refractory asthma, poor control of which is confirmed by persistent symptoms, frequent exacerbations and constant variable bronchial obstruction, despite the use of high doses of corticosteroids in the form of inhalation or systemic action.

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

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

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

3. Severe asthma with steroid resistance or steroid dependence
Another form of severe asthma is “steroid-dependent” and “steroid-resistant” or “therapy-resistant” bronchial asthma. Patients with steroid dependence do not always experience frequent exacerbations or have poorly reversible severe airway obstruction. However, to maintain asthma control, they constantly require high doses of inhaled or systemic corticosteroids. Reducing the dose of basic drugs leads to a progressive deterioration in the condition of such patients, and increasing the dose can reduce the severity of symptoms and stabilize the course of the disease. It has been proven that this form of severe asthma develops more often in patients who become ill at an older age and do not have signs of atopy.
A possible mechanism for the development of steroid resistance in severe asthma may be secondary dysregulation of glucocorticosteroid receptors due to uncontrolled long-term administration of systemic hormones or a decrease in the number of steroid receptors. Reduced effectiveness of glucocorticosteroids in severe forms asthma is associated with changes in the spectrum of inflammatory cells accumulating in the mucous membrane of the respiratory tract. Eosinophilic infiltration gives way to a predominant neutrophilic infiltration, which may affect the biological effects of steroids.
Another explanation for the development of resistance may be that glucocorticosteroids not only do not affect the hypertrophy of bronchial smooth muscles, but also aggravate myopathy of the respiratory muscles (diaphragm, intercostal muscles and muscles of the upper shoulder girdle). The cause of secondary steroid resistance can also be long-term use of β 2 -agonists, viral infection and endogenous disturbances in the level of female sex hormones. Complete steroid unresponsiveness in asthma (no effect from taking 40 mg of prednisolone per day for 14 days) is rare and is most likely due to a congenital abnormality of glucocorticosteroid receptors.

Severe asthma: reasons for lack of control
Not all patients with symptoms of severe asthma actually have this form of the disease. In this section we would like to consider the main reasons why it is not possible to establish adequate control over the symptoms of the disease.

1. Incorrect diagnosis
Since the symptoms of asthma (choking attacks, shortness of breath, wheezing in the lungs) are not strictly specific, the possibility that the patient has another disease should not be denied. The list of pathological conditions that most often masquerade as difficult-to-control asthma is given in Table 1.
The large number of diseases that need to be differentially diagnosed in the presence of symptoms of severe asthma determines the thoroughness and large scope of examination of such patients (Table 2). The diagnosis of severe asthma must be confirmed by objective evidence of reversible bronchial obstruction or airway hyperresponsiveness.

2. Presence of concomitant pathology
Some accompanying illnesses may cause an increase in the incidence and severity of exacerbations of bronchial asthma (Table 3). Correct diagnosis and treatment for these conditions improves control of severe asthma symptoms.

3. Constant exposure to irritating factors
Constant exposure to allergens even in low concentrations helps maintain inflammation in the airways, exacerbating the severity of asthma symptoms. Most common reasons atopies include house dust, mold, pet hair, cockroaches, pollen, and food allergens.
Inorganic irritants, such as tobacco smoke, sulfur and nitrogen dioxides, and ozone, can also cause insufficient effectiveness of inhaled corticosteroid therapy.
Taking some medicines(nonsteroidal anti-inflammatory drugs, beta-blockers) may cause severe exacerbation of bronchial asthma in some patients.
Avoiding contact with allergens, industrial and household pollutants, quitting smoking and controlled therapy significantly improve the condition of patients with bronchial asthma.

4. Don't adequate treatment
The reason for the persistence of symptoms of severe asthma may be an underestimation of the severity of the patient's condition and, as a result, an insufficient amount of anti-asthma therapy. In 15-20% of cases, the cause of severe asthma is inadequate treatment tactics. An indispensable condition proper treatment there should be a sufficient (up to high) dose of inhaled corticosteroids.
The patient's willingness and ability to cooperate plays a major role in achieving asthma control. Factors predisposing to poor adherence to treatment include: psychological problems in patients, irregularity in seeking medical help, lack of faith in traditional methods of treatment for excessive enthusiasm traditional medicine, a large number of prescribed medications, patients underestimating the severity of their condition.
Another reason for poor asthma control may be poor inhalation technique. In this regard, preference should be given to easier-to-use delivery devices with a spacer or powder inhalers.
To exclude the influence of inadequate treatment on the course and prognosis of asthma, a reasonable and clear diagnostic and treatment program should be followed.

Treatment of patients with severe asthma
Patients with symptoms of difficult-to-control asthma should be treated in specialized pulmonary centers by highly qualified specialists. Only in such medical institutions there is an opportunity for differential diagnosis using laboratory and instrumental examination methods not used in routine practice (determining the level of nitric oxide in exhaled air, studying cellular composition bronchoalveolar lavage, biopsy samples of the bronchial mucosa, computed tomography, immunological research and genetic testing). In addition, during hospitalization, you can avoid exposure to allergens and inorganic irritants that provoke exacerbation of the disease. The algorithm for managing patients with symptoms of severe asthma is presented in the figure.
It is necessary to draw up an individual treatment plan for each patient. After differential diagnosis, it is important to identify the causative factor in the development of exacerbations and, if possible, eliminate it: stop smoking, identify causally significant allergens, prevent infections, sanitize the infection in paranasal sinuses ah nose, normalize sleep, influence gastroesophageal reflux, etc.
It is imperative to evaluate and maximize the collaboration between physician and patient. Patient education is important. The patient should be trained in the elements of self-control (in particular peak flowmetry) and behavioral tactics during a developing exacerbation of the disease.
Among other measures to establish asthma control, the correct use of delivery devices and inhalation techniques should be assessed.
Patients with severe asthma should undergo rehabilitation measures. Many patients are weakened by the disease, suffer from side effects of anti-inflammatory therapy, and are forced to change their lifestyle. Prescribing a program of physical exercises and psychological correction helps improve exercise tolerance and the quality of life of patients.
In drug therapy of asthma, according to modern recommendations A stepped approach is used, in which the intensity of therapy increases as the severity of the disease increases.
For severe asthma, the mainstay of therapy is high-dose inhaled corticosteroids (for example, fluticasone, beclamethasone, mometasone). These drugs are usually taken twice a day, although there is evidence that four times a day is more effective. In some cases, administering medications in high doses via a nebulizer can significantly improve asthma control. However, it should be remembered that in severe asthma, monotherapy with inhaled corticosteroids is not sufficiently effective, and if their dose is increased to >800 mcg/day, the likelihood of systemic effects increases with a not always pronounced increase in clinical effectiveness.
Long-acting β 2 -agonists (salmeterol, formoterol) for severe asthma are necessarily prescribed in addition to inhaled corticosteroids. They help improve respiratory function, reduce the frequency of exacerbations, and reduce the use of β 2 agonists short acting and reduce the dose of inhaled corticosteroids. Considered more effective and convenient to use combination drugs containing inhaled corticosteroids and long-acting β2-agonists (for example, Seretide, Seroflo, Symbicort*).
As with any severity of asthma, in severe cases short-acting β2-agonists (salbutamol, fenoterol) are taken only “on demand”. Their frequent use leads to decreased effectiveness, which means loss of asthma control. In the second phenotype of fragile asthma, parenteral administration of adrenaline is possible in extreme situations.
Corticosteroids that have a systemic effect (prednisolone, dexamethasone, triamcinolone) are prescribed for severe persistent symptoms of severe asthma and severe exacerbation of the disease with further stepwise withdrawal. Patients who develop frequent exacerbations despite taking high-dose inhaled corticosteroids may also be advised to intermittently use high-dose systemic medications followed by maintenance at minimum doses.
If symptoms of severe asthma persist despite continued use of systemic corticosteroids, consideration should be given to increasing the daily dosage.
In patients (especially women) receiving systemic corticosteroids, correction is necessary due to severe side effects mineral metabolism and hormonal status.
Methylxanthines (theophylline) in some cases may be prescribed in addition to basic drugs. In some patients, their use can reduce the dose of inhaled and/or systemic corticosteroids. However, due to the toxicity of methylxanthines, regular monitoring of theophylline levels in blood plasma is necessary when using them.
Antileukotrienes (zafirlukast*, montelukast*) are used together with steroidal anti-inflammatory drugs. They are especially effective for aspirin-induced asthma.
The widespread use of immunosuppressants and antimetabolites for the treatment of bronchial asthma is limited by their severe toxicity. In addition, clinical trials using inhaled forms do not currently provide convincing data on their clinical effectiveness.
A promising group of drugs prescribed for severe asthma are monoclonal antibodies (omalizumab*). They have proven themselves as an effective addition to traditional basic therapy, improving respiratory function and the quality of life of patients. When using these drugs, the consumption of short-acting β 2 -agonists is also reduced. Monoclonal antibodies are included in the latest revision of recommendations for the treatment of severe bronchial asthma.
Today there is information about the pronounced anti-inflammatory effect of phosphodiesterase type 4 inhibitors (rolipram*, roflumilast*, cilomilast*) in severe asthma.

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

Bronchial asthma is classified into types, forms, phases according to several criteria (cause, degree of controllability, degree of manifestation of bronchial obstruction). But one of the most important classifications that determine the treatment of the disease is the classification according to the severity of the disease. In accordance with it, there are four forms of bronchial asthma, the most dangerous of which is severe persistent.

Classification of the disease by severity

The severity of bronchial asthma is determined by:

Number of attacks per week at night;
Number of attacks per week during the daytime;
Frequency and duration of use of short-acting beta2-agonists;
Indicators of peak expiratory flow, its daily changes;

The patient is diagnosed with:

1. Episodic bronchial asthma, or mild intermittent asthma;

This form of the disease is characterized by episodic short exacerbations (from several hours to several days). Attacks of suffocation (shortness of breath or cough) occur no more than once a week during the day, and 2 times a month at night. The peak expiratory flow rate is 80% of the expected value; during the day it fluctuates by no more than 20%.

During the period between exacerbations of bronchial asthma light form does not manifest any symptoms, the person’s lungs function normally.

Unfortunately, it is not always possible to identify the disease in this form. Firstly, its impact on a person’s life is small; he can simply ignore the symptoms and not consult a doctor. Secondly, signs of asthma episodic course similar to signs of other respiratory diseases, such as chronic bronchitis. Thirdly, most often episodic asthma is mixed, that is, allergic and infection-related factors play an equal role in its occurrence. The disease can occur in adults upon contact with allergens, in children - during infectious diseases of the lower respiratory tract.

To confirm the diagnosis, the patient is examined:

They will take general blood and urine tests;
They will do skin allergy tests;
An x-ray examination of the organs will be carried out chest;
Examine respiratory function with a beta2-agonist.

Adequate treatment, undertaken even when the disease has not gained momentum, will help to contain it and achieve stable remission. It involves taking short-acting beta2-agonists and short-acting theophyllines to stop or prevent episodic attacks (medicines are taken by inhalation or orally before physical activity, possible contact with allergens). People with mild intermittent asthma also need to adhere to the regimen established for asthmatic patients. They usually do not require treatment with anti-inflammatory drugs.

2. Bronchial asthma of persistent (constant) course. In turn, persistent asthma can be mild, moderate or severe.

If the disease occurs in a mild persistent form, the patient’s peak exhalation flow is 80% of the expected rate, and can fluctuate by 20-30% during the day. He has attacks of coughing, shortness of breath, and suffocation during the day from once a day to once a week. Attacks at night recur more often than 2 times a month. Symptoms of the disease during an exacerbation affect the patient’s quality of life and may interfere with daytime activity or nighttime sleep.

A patient with mild persistent asthma requires daily treatment. To prevent attacks, he needs to use inhaled corticosteroids, sodium cromoglycate, nedocromil, and theophyllines. Initially, corticosteroids are prescribed at a dose of 200-500 mcg per day, but if bronchial asthma progresses, it is advisable to increase them to 750-800 mcg per day. Before going to bed, it is recommended to use a long-acting bronchodilator, for example, Clenbuterol, Salmeterol or Formoterol.

Moderate persistent bronchial asthma is characterized by frequent manifestations of symptoms that significantly disrupt the patient’s daytime activity and nighttime sleep. At night, attacks of coughing, choking, and shortness of breath occur once a week or more often. The peak expiratory flow rate fluctuates between 60% and 80% of predicted.

If a person is diagnosed with this form of asthma, he needs to take beta2-agonists and anti-inflammatory drugs daily to control the disease. Beclomethasone dipropionate or an analogue inhaled corticosteroid at a dose of 800-2000 mcg is recommended. In addition, it is necessary to take long-acting bronchodilators, especially if attacks often occur at night. Typically, theophyllines are used, for example, Theophilus.

How to treat severe bronchial asthma?

Severe persistent asthma is often mixed. Frequent exacerbations, repeated daily and almost nightly attacks, are provoked by asthma triggers of an allergic and infectious nature. The patient's peak expiratory flow rate is less than 60% of normal, fluctuating by 30% or more. Because of serious condition he is forced to limit his own physical activity.

Severe persistent bronchial asthma is difficult to control or not controlled at all. To assess the severity of the patient's condition, daily peak flow measurements are necessary.

Treatment of this form of the disease is carried out to minimize the manifestation of symptoms.

The patient is prescribed high doses of corticosteroids daily (which is why severe persistent asthma is sometimes called steroid-dependent). He can take them through an inhaler or spacer.

A spacer is a flask (reservoir) used in addition to an aerosol inhaler to enhance the effectiveness of its effect. Using a pocket can with a spacer, a patient even with a severe attack of suffocation will be able to help himself. He will not need to coordinate inhalation and pressing. It is better for children to use a spacer with a mask.

A person diagnosed with severe persistent bronchial asthma is recommended to:

Obviously, a patient with severe persistent asthma is forced to take a huge number of medications to control its symptoms. Unfortunately, they are not always effective, but side effects from taking them are observed quite often. Severe mixed asthma is mainly treated in a hospital, so drug therapy is selected exclusively by an experienced doctor. Any amateur activity in treatment is excluded, as it is fraught with aggravation of the condition, including death.

After treatment has begun and it gives results, the patient is diagnosed with a mixed clinical picture of the disease, since in response to therapy its symptoms are blurred. But it will be possible to change the diagnosis from severe persistent asthma to moderate asthma only when the patient begins to receive drug therapy characteristic of this degree of severity.

Video: Bronchial asthma in children and adults. Who is at risk?

Persistent asthma is a serious pathology. Symptoms can develop in a person for years, which limits his life activity. However, some patients experience periods of remission.

Persistent asthma is a chronic disease. Bronchial spasms occur systematically. This is the most common form of AD. Against the background of inflammation of the respiratory tract, exacerbations constantly occur. Mucous secretion (required to protect the body) is produced in large quantities.

In the presence of such a pathology, the patient cannot inhale air full breasts. He is also unable to exhale it completely. Some patients face problems with either inhalation or exhalation.

Classification of persistent asthma

There are four forms of this disease. The degree of severity is determined based on the symptoms and condition of the patient. The course of the pathology is determined in order to prescribe the most effective therapy. High-quality treatment helps achieve long-term results.

Here are the forms of persistent asthma.

Heavy. Choking occurs systematically, occurring both at night and during the day. It is important to limit physical activity. Only special medications help.
Average. Attacks occur at night more often than once or twice a week. During the day they happen less often. Due to respiratory failure, a person's quality of life decreases.
Easy. Attacks occur once or twice a week, mostly during the day. Sleep may be disturbed.

Identify the provoking allergen in a timely manner and take appropriate measures.
Conduct timely vaccinations for children.
Carefully choose a profession (it is important to reduce the influence of negative external factors to zero).
Eat right.
Lead a healthy lifestyle and regularly.
Visit regularly fresh air, long walk.

Attention! Qualified treatment is of great importance. This will prevent complications.

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 analysis blood, general urine analysis, determination of general and specific IgE, chest x-ray, 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 large quantity asthma-controlling drugs.

Primary treatment includes high-dose inhaled corticosteroids (800 to 2000 mcg per day of beclomethasone dipropionate or its 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 assistance, then 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, severity 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 thought to have mild or medium degree severity that does not require emergency treatment in full. 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 side effect 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 causing an allergic reaction and acting without participation 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

Generally accepted classification bronchial asthma does not exist. 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 reasons(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 last 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 respiratory apparatus. 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; known, for example, exacerbations of the disease in menopause among women. 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. allocated to increased quantities a special substance 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 effector endings 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 neuroses that occur in patients with B. a. are often a consequence rather than a cause of the disease. Currently, there is no sufficient reason to classify psychogenic asthma as a separate form, but complex treatment 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 paroxysmal cough(dry or with the release of a small amount of mucous, viscous sputum), which is not relieved by conventional antitussives 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. When auscultating the lungs, it is sometimes determined 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. Difficulty in breathing, which the patient initially experiences only when exhaling, increases, which forces the patient to take sitting position to engage 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 may occur from respiratory arrest or acute disorders heart rate 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 - allergic rhinitis, atopic dermatitis. Attacks of suffocation in atopic B. a. often preceded by prodromal symptoms: itching in the nose and nasopharynx, nasal congestion, sometimes itching in the chin, neck, 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. relatively typical 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. observed in persons different ages, but adults get sick more often. 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 pulmonary heart, with the 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 protracted attack coughing is possible; short-term loss of consciousness ( 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 due to long-term therapy 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 in relatively short term(sometimes within 3-5 weeks) a hormone-dependent course of B. a. is formed; withdrawal of glucocorticoids can cause severe status asthmaticus, which can be fatal.

Analysis 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 ( a sharp decline) and outside of 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 FVD; 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 FVD research 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. Last method is very simple and can be used by a doctor on a regular 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 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 features clinical course, the presence of concomitant manifestations of atopy (hay fever, atopic dermatitis, food allergies etc.), family and allergy history data. The diagnosis is confirmed by identifying the patient's sensitization of the reagin type (see. Allergy ) And positive results 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 between infection-related and atopic form B. a. In favor of infection-dependent B. a. evidenced by the slow onset and long duration of attacks of suffocation, the frequent connection of their increase with 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 .

Persistent bronchial asthma is an inflammatory disease airways With chronic course, the only manifestation of which is a reversible narrowing of the lumen of the bronchi. Bronchial hyperreactivity occurs against the background of chronic inflammation of the mucous membrane and is manifested by bronchospasm and hyperproduction of thick sputum. All this leads to the appearance of characteristic symptoms.

Persistent asthma

Causes

Groups of factors causing the development of persistent asthma:

internal;
external;
triggers (provoke exacerbation of the disease).

Internal factors determine the development of the disease. These include:

Genetic predisposition

genetic predisposition (it has been proven that the risk of inheriting bronchial asthma is about 70%);
atopy (increased IgE titer in response to contact with an allergen);
high activity of the airways (strong narrowing of the lumen of the airways, in response to the action of an allergen or trigger);
obesity (affects the mechanism of respiration and promotes the development of an inflammatory response).

External factors provoke the appearance of symptoms of the disease:

Factors that provoke exacerbation of asthma:

rapid breathing;
natural factors (high or low temperature air, wind);
pharmacological drugs (NSAIDs, beta receptor antagonists);
smell of paints and varnishes;
psycho-emotional stress.

Manifestations of the disease

An exacerbation of the disease occurs after the allergen enters the body and manifests itself in the form of shortness of breath, bouts of unproductive coughing, wheezing, and chest congestion. Sometimes exacerbation can be caused by increased physical activity.

Cough reflex

Mechanism of symptoms:

irritation of the bronchial cough receptors leads to a cough reflex;
spasm of the smooth muscles of the bronchi contributes to the formation of wheezing, due to the turbulent flow of air through the spasmodic airways;
due to increased work of the respiratory system, shortness of breath occurs.

Severity

According to severity, persistent asthma is divided into:

Mild persistent asthma. Symptoms of the disease occur two or more times a week, but not daily. The occurrence of attacks that disrupt the quality of sleep, more than 2 times a month. Exacerbations negatively affect motor activity. FEV in the first second outside of an attack is more than 80% of normal values.
Persistent asthma of moderate severity. Manifests itself as daily symptoms, nighttime manifestations occur more often than once every 7 days, exacerbations are reduced motor activity and impair sleep. Daily use of short-acting beta-2 adrenergic agonists is necessary.
Severe persistent asthma. It is characterized by regular manifestations of symptoms, more than once a day, frequent exacerbations and impaired sleep quality, and significant limitation of motor activity.

Diagnostics

Stages of diagnosing asthma:

Spirometry

Collecting patient complaints and clarifying medical history.
Functional diagnostic methods (spirometry, peak flowmetry).
Collection of allergy anamnesis.
Skin allergy tests.
Test with an allergen for the purpose of provocation.
Laboratory diagnostic methods.

When analyzing complaints, pay attention to:

shortness of breath that occurs when inhaling;
bouts of unproductive cough;
heaviness and feeling of constriction in the chest;
wheezing.

The reversibility of bronchial obstruction is assessed using spirometry. To confirm the diagnosis, the forced expiratory volume in the first second is important. First, this indicator is assessed without the use of drugs, then the patient is administered a bronchodilator drug. After 15-20 minutes, the study is repeated. An increase in FEV1 of more than 12% supports the presumptive diagnosis.

Peak flowmetry

Peak flowmetry is used to determine peak air velocity. This method used when spirometry is impossible and to monitor the dynamics of the disease. The device is small in size, so it is convenient to use to identify the influence of provoking factors at work and at home.

When collecting allergy history, it is necessary to establish the presence allergic diseases in the family, identify the connection between the occurrence of symptoms and the effect of allergens (contact with animals, cold season, symptoms after presence in certain rooms).

To identify a specific allergen, skin tests with allergens. Samples are carried out in late autumn or winter to exclude the influence of plant pollen on the test results.

Which doctor should I contact?

If symptoms of the disease appear, you should contact your local physician. After making a preliminary diagnosis, the local doctor will refer the patient to specialized specialists:

pulmonologist;
allergist;
gastroenterologist.

Necessary tests

To confirm the disease, it is necessary to donate blood to determine general and specific immunoglobulin E. You also need to donate sputum or bronchoalveolar fluid to analyze the content of eosinophils.

Sputum examination

Treatment methods

Pharmacotherapy for persistent asthma is divided into 2 types:

continuous maintenance therapy;
drugs used for exacerbation.

Maintenance (basic) therapy is aimed at reducing the frequency of attacks, up to their complete absence. For this purpose, drugs with anti-inflammatory activity (inhaled and systemic corticosteroids), long-acting beta-2 agonists are prescribed.

Salbutamol

In case of exacerbation, drugs are used with the maximum fast time development of effects: Salbutamol, Fenoterol.

Forecast

Provided a correct diagnosis is made and effective therapy is prescribed, it is possible to achieve a completely controlled course of the disease. The quality of life of such patients is almost no different from healthy people.

Preventive measures

Food allergens

To prevent exacerbation of asthma, patients are advised to exclude food products causing them to develop an allergic reaction. Obese patients need to reduce body weight, which will improve their health and reduce the risk of exacerbation. Additionally, it is necessary to eliminate active and passive smoking to minimize harmful effects to the lungs. Moderate exercise improves cardiopulmonary function. Patients are recommended to go swimming to train the muscles involved in the act of inhalation.

Possible complications

The asthmatic condition is the most severe complication of persistent bronchial asthma. It represents an acute respiratory failure and resistance to bronchodilators. Frequent exacerbations of the disease can lead to the development of emphysema due to overextension lung tissue due to the inability to exhale. It is possible to develop hypertrophy of the right ventricle of the heart due to pulmonary hypertension.

Asthma is a serious disease with the possibility of developing severe complications. But timely diagnosed disease and properly selected treatment reduce the occurrence of exacerbations to a minimum and prevent possible complications, maintaining a high quality of life for patients.