Any complication of chronic bronchitis is dangerous. Bronchial asthma

Bronchitis is an inflammatory disease characterized by damage to the mucous membrane of the bronchial tree (bronchi) and manifested by cough, shortness of breath (feeling of lack of air), fever and other symptoms of inflammation. This disease is seasonal and worsens mainly in the autumn-winter period, which is due to the activation of a viral infection. Children of preschool and primary school age are especially often affected, as they are more susceptible to viral infectious diseases.

Pathogenesis (mechanism of development) of bronchitis

The human respiratory system consists of the airways and pulmonary tissue (lungs). The respiratory tract is divided into upper (which includes nasal cavity and pharynx) and lower (larynx, trachea, bronchi). The main function of the respiratory tract is to provide air to the lungs, where gas exchange occurs between the blood and air (oxygen enters the blood and carbon dioxide is removed from the blood).

The air inhaled through the nose enters the trachea - a straight tube 10 - 14 cm long, which is a continuation of the larynx. In the chest, the trachea is divided into 2 main bronchi (right and left), which go to the right and left lungs, respectively. Each main bronchus is divided into lobar bronchi (directed to the lobes of the lungs), and each of the lobar bronchi, in turn, is also divided into 2 smaller bronchi. This process is repeated more than 20 times, resulting in the formation of the thinnest airways (bronchioles), the diameter of which does not exceed 1 millimeter. As a result of the division of bronchioles, the so-called alveolar ducts are formed, into which the lumens of the alveoli open - small thin-walled vesicles in which the process of gas exchange occurs.

The bronchial wall consists of:

Mucous membrane. The mucous membrane of the respiratory tract is covered with a special respiratory (ciliated) epithelium. On its surface there are so-called cilia (or threads), the vibrations of which ensure cleansing of the bronchi (small particles of dust, bacteria and viruses that enter the respiratory tract get stuck in the mucus of the bronchi, after which, with the help of cilia, they are pushed up into the pharynx and swallowed).
Muscle layer. The muscle layer is represented by several layers of muscle fibers, the contraction of which ensures the shortening of the bronchi and a decrease in their diameter.
Cartilaginous rings. These cartilages provide a strong framework that ensures airway patency. Cartilaginous rings are most pronounced in the area of large bronchi, however, as their diameter decreases, the cartilage becomes thinner, completely disappearing in the area of bronchioles.
Connective tissue membrane. Surrounds the bronchi from the outside.

The main functions of the mucous membrane of the respiratory tract are cleansing, humidifying and warming the inhaled air. When exposed to various causative factors (infectious or non-infectious), damage to the cells of the bronchial mucosa and its inflammation can occur.

The development and progression of the inflammatory process is characterized by the migration of cells of the body's immune (protective) system (neutrophils, histiocytes, lymphocytes and others) to the site of inflammation. These cells begin to fight the cause of inflammation, as a result of which they are destroyed and release many biologically active substances (histamine, serotonin, prostaglandins and others) into the surrounding tissues. Most of these substances have a vasodilator effect, that is, they expand the lumen of the blood vessels of the inflamed mucous membrane. This leads to its swelling, resulting in a narrowing of the lumen of the bronchi.

The development of the inflammatory process in the bronchi is also characterized by increased formation of mucus (this is a protective reaction of the body that helps cleanse the airways). However, in conditions of edematous mucous membrane, mucus cannot be secreted normally, as a result of which it accumulates in the lower respiratory tract and clogs smaller bronchi, which leads to impaired ventilation of a certain area of the lung.

In an uncomplicated course of the disease, the body eliminates the cause of its occurrence within a few weeks, which leads to complete recovery. In more severe cases (when the causative factor affects the airways for a long time), the inflammatory process can extend beyond the mucous membrane and affect the deeper layers of the bronchial walls. Over time, this leads to structural changes and deformation of the bronchi, which disrupts the delivery of air to the lungs and leads to the development of respiratory failure.

Causes of bronchitis

As mentioned earlier, the cause of bronchitis is damage to the bronchial mucosa, which develops as a result of exposure to various environmental factors. Under normal conditions, various microorganisms and dust particles are constantly inhaled by humans, but they linger on the mucous membrane of the respiratory tract, are enveloped in mucus and are removed from the bronchial tree by the ciliated epithelium. If too many of these particles penetrate the respiratory tract, the protective mechanisms of the bronchi may not cope with their function, resulting in damage to the mucous membrane and the development of an inflammatory process.

It is also worth noting that the penetration of infectious and non-infectious agents into the respiratory tract can be facilitated by various factors that reduce the general and local protective properties of the body.

The development of bronchitis is promoted by:

Hypothermia. Normal blood supply to the bronchial mucosa is an important barrier to viral or bacterial infectious agents. When inhaling cold air, a reflex narrowing of the blood vessels of the upper and lower respiratory tract occurs, which significantly reduces the local protective properties of tissues and contributes to the development of infection.
Poor nutrition. Malnutrition leads to a lack of proteins, vitamins (C, D, group B and others) and microelements in the body that are necessary for normal tissue renewal and the functioning of vital systems (including the immune system). The consequence of this is a decrease in the body's resistance to various infectious agents and chemical irritants.
Chronic infectious diseases. Foci of chronic infection in the nasal or oral cavity create a constant threat of bronchitis, since the location of the source of infection near the airways ensures its easy penetration into the bronchi. Also, the presence of foreign antigens in the human body changes the activity of its immune system, which can lead to more pronounced and destructive inflammatory reactions during the development of bronchitis.

Depending on the reason, there are:

viral bronchitis;
bacterial bronchitis;
allergic (asthmatic) bronchitis;
smoker's bronchitis;
professional (dust) bronchitis.

Viral bronchitis

Viruses can cause diseases in humans such as pharyngitis (inflammation of the pharynx), rhinitis (inflammation of the nasal mucosa), sore throat (inflammation of the palatine tonsils) and so on. With a weakened immune system or with inadequate treatment of these diseases, the infectious agent (virus) travels through the respiratory tract to the trachea and bronchi, penetrating into the cells of their mucous membrane. Once in a cell, the virus integrates into its genetic apparatus and changes its function in such a way that viral copies begin to form in the cell. When a sufficient number of new viruses are formed in a cell, it is destroyed, and viral particles infect neighboring cells and the process repeats. When the affected cells are destroyed, a large amount of biologically active substances are released from them, which affect the surrounding tissues, leading to inflammation and swelling of the bronchial mucosa.

Acute viral bronchitis itself does not pose a threat to the patient’s life, however, a viral infection leads to a decrease in the protective forces of the bronchial tree, which creates favorable conditions for the addition of a bacterial infection and the development of serious complications.

Bacterial bronchitis

In case of bacterial infectious diseases of the nasopharynx (for example, with purulent sore throat), bacteria and their toxins can enter the bronchi (especially during night sleep, when the severity of the protective cough reflex decreases). Unlike viruses, bacteria do not penetrate the cells of the bronchial mucosa, but are located on its surface and begin to multiply there, which leads to damage to the respiratory tract. Also, during their life, bacteria can release various toxic substances that destroy the protective barriers of the mucous membrane and aggravate the course of the disease.

In response to the aggressive effects of bacteria and their toxins, the body's immune system is activated and a large number of neutrophils and other leukocytes migrate to the site of infection. They absorb bacterial particles and fragments of damaged mucosal cells, digest them and break down, resulting in the formation of pus.

Allergic (asthmatic) bronchitis

Allergic bronchitis is characterized by non-infectious inflammation of the bronchial mucosa. The cause of this form of the disease is the increased sensitivity of some people to certain substances (allergens) - plant pollen, fluff, animal hair, and so on. In the blood and tissues of such people there are special antibodies that can interact only with one specific allergen. When this allergen penetrates the human respiratory tract, it interacts with antibodies, which leads to the rapid activation of cells of the immune system (eosinophils, basophils) and the release of a large amount of biologically active substances into the tissue. This, in turn, leads to swelling of the mucous membrane and increased mucus production. In addition, an important component of allergic bronchitis is spasm (pronounced contraction) of the muscles of the bronchi, which also contributes to the narrowing of their lumen and disruption of ventilation of the lung tissue.

In cases where the allergen is plant pollen, bronchitis is seasonal and occurs only during the flowering period of a certain plant or a certain group of plants. If a person is allergic to other substances, the clinical manifestations of bronchitis will persist throughout the entire period of the patient’s contact with the allergen.

Smoker's bronchitis

Smoking is one of the main causes of development chronic bronchitis in the adult population. Both during active (when a person smokes a cigarette) and during passive smoking (when a person is near a smoker and inhales cigarette smoke), in addition to nicotine, more than 600 different toxic substances (tars, combustion products of tobacco and paper, and so on) enter the lungs ). Microparticles of these substances settle on the bronchial mucosa and irritate it, which leads to the development inflammatory reaction and secretion of large amounts of mucus.

In addition, the toxins contained in tobacco smoke negatively affect the activity of the respiratory epithelium, reducing the mobility of cilia and disrupting the process of removing mucus and dust particles from the respiratory tract. Also, nicotine (which is part of all tobacco products) causes a narrowing of the blood vessels of the mucous membrane, which leads to a violation of local protective properties and contributes to the addition of a viral or bacterial infection.

Over time, the inflammatory process in the bronchi progresses and can move from the mucous membrane to the deeper layers of the bronchial wall, causing irreversible narrowing of the airway lumen and impaired ventilation of the lungs.

Occupational (dust) bronchitis

Many chemical substances with which industrial workers come into contact can penetrate into the bronchi along with the inhaled air, which under certain conditions (with frequently repeated or prolonged exposure to causative factors) can lead to damage to the mucous membrane and the development of an inflammatory process. As a result of prolonged exposure to irritating particles, the ciliated epithelium of the bronchi may be replaced by flat epithelium, which is not characteristic of the respiratory tract and cannot perform protective functions. There may also be an increase in the number of glandular cells that produce mucus, which can ultimately cause blockage of the airways and impair ventilation of the lung tissue.

Occupational bronchitis is usually characterized by a long, slowly progressive, but irreversible course. That is why it is extremely important to detect the development of this disease in time and begin treatment in a timely manner.

The following are predisposed to the development of occupational bronchitis:

wipers;
miners;
metallurgists;
cement industry workers;
chemical plant workers;
workers of woodworking enterprises;
millers;
chimney sweeps;
railway workers (inhale large amounts of exhaust gases from diesel engines).

Symptoms of bronchitis

Symptoms of bronchitis are caused by swelling of the mucous membrane and increased mucus production, which leads to blockage of small and medium-sized bronchi and disruption of normal ventilation of the lungs. It is also worth noting that the clinical manifestations of the disease may depend on its type and cause. So, for example, with infectious bronchitis, signs of intoxication of the whole body (developing as a result of activation of the immune system) may be observed - general weakness, fatigue, headaches and muscle pain, increased heart rate, and so on. At the same time, with allergic or dust bronchitis, these symptoms may be absent.

Bronchitis can manifest itself:

cough;
discharge of sputum;
wheezing in the lungs;
shortness of breath (feeling of lack of air);
increased body temperature;

Cough with bronchitis

Cough is the main symptom of bronchitis, occurring from the first days of the disease and lasting longer than other symptoms. The nature of the cough depends on the period and nature of bronchitis.

A cough with bronchitis can be:

Dry (without sputum discharge). A dry cough is characteristic of the initial stage of bronchitis. Its occurrence is caused by the penetration of infectious or dust particles into the bronchi and damage to the cells of the mucous membrane. As a result, the sensitivity of cough receptors (nerve endings located in the wall of the bronchi) increases. Their irritation (by dust or infectious particles or fragments of destroyed bronchial epithelium) leads to the appearance of nerve impulses that are sent to a special part of the brain stem - the cough center, which is a collection of neurons (nerve cells). From this center, impulses travel along other nerve fibers to the respiratory muscles (diaphragm, muscles abdominal wall and intercostal muscles), causing their synchronous and sequential contraction, manifested by coughing.
Wet (accompanied by sputum production). As bronchitis progresses, mucus begins to accumulate in the lumen of the bronchi, which often sticks to the bronchial wall. During inhalation and exhalation, this mucus is displaced by the air flow, which also leads to mechanical irritation of the cough receptors. If during a cough the mucus breaks away from the bronchial wall and is removed from the bronchial tree, the person feels relief. If the mucus plug is attached tightly enough, during a cough it fluctuates intensely and irritates the cough receptors even more, but does not come off the bronchus, which often causes protracted bouts of painful coughing.

Sputum discharge during bronchitis

The cause of increased sputum production is increased activity goblet cells of the bronchial mucosa (which produce mucus), which is caused by irritation of the respiratory tract and the development of an inflammatory reaction in the tissues. In the initial stage of the disease, there is usually no sputum. As the pathological process develops, the number of goblet cells increases, as a result of which they begin to secrete a larger than normal amount of mucus. The mucus mixes with other substances in the respiratory tract, resulting in the formation of sputum, the nature and quantity of which depend on the cause of bronchitis.

With bronchitis, the following may be released:

Mucous sputum. They are colorless, transparent, odorless mucus. The presence of mucous sputum is characteristic of the initial stages of viral bronchitis and is caused only by increased secretion of mucus by goblet cells.
Mucopurulent sputum. As mentioned earlier, pus is cells of the immune system (neutrophils) that have died as a result of fighting a bacterial infection. Consequently, the release of mucopurulent sputum will indicate the development of a bacterial infection in the respiratory tract. In this case, sputum consists of lumps of mucus, inside of which there are streaks of gray or yellowish-green pus.
Purulent sputum. The release of purely purulent sputum during bronchitis is rare and indicates a pronounced progression of the purulent-inflammatory process in the bronchi. Almost always this is accompanied by the transition of a pyogenic infection to the lung tissue and the development of pneumonia (pneumonia). The sputum released is an accumulation of gray or yellow-green pus and has an unpleasant, foul odor.
Sputum with blood. Blood streaks in sputum can form as a result of damage or rupture of small blood vessels in the bronchial wall. This can be facilitated by an increase in the permeability of the vascular wall, observed during the development of the inflammatory process, as well as a prolonged dry cough.

Wheezing in the lungs due to bronchitis

Wheezing in the lungs occurs as a result of disruption of air flow through the bronchi. You can listen for wheezing in the lungs by placing your ear to the patient's chest. However, doctors use a special device for this - a phonendoscope, which allows you to pick up even minor breathing sounds.

Wheezing with bronchitis can be:

Dry whistling (high-pitched). They are formed as a result of narrowing of the lumen of the small bronchi, as a result of which a peculiar whistle is formed when an air flow passes through them.
Dry buzzing (low pitch). They are formed as a result of air turbulence in large and medium-sized bronchi, which is due to the narrowing of their lumen and the presence of mucus and sputum on the walls of the respiratory tract.
Wet. Wet wheezing occurs when there is fluid in the bronchi. During inhalation, the air flow passes through the bronchi at high speed and foams the liquid. The resulting foam bubbles burst, which is the cause of moist rales. Moist rales can be fine-bubble (heard when small bronchi are affected), medium-bubble (when medium-sized bronchi are affected) and large-bubble (when large bronchi are affected).

A characteristic feature of wheezing during bronchitis is its inconstancy. The nature and location of wheezing (especially buzzing) may change after coughing, after tapping on the chest, or even after a change in body position, due to the movement of sputum in the respiratory tract.

Shortness of breath with bronchitis

Dyspnea (feeling of lack of air) with bronchitis develops as a result of obstruction of the airways. The reason for this is swelling of the mucous membrane and the accumulation of thick, viscous mucus in the bronchi.

In the initial stages of the disease, shortness of breath is usually absent, since the patency of the airways is preserved. As the inflammatory process progresses, swelling of the mucous membrane increases, resulting in a decrease in the amount of air that can penetrate the pulmonary alveoli per unit of time. The deterioration of the patient's condition is also facilitated by the formation of mucus plugs - accumulations of mucus and (possibly) pus that get stuck in the small bronchi and completely block their lumen. Such a mucus plug cannot be removed by coughing, since during inhalation, air does not penetrate through it into the alveoli. As a result of this, the area of lung tissue ventilated by the affected bronchus is completely excluded from the gas exchange process.

Over a certain period of time, the insufficient supply of oxygen to the body is compensated by the unaffected areas of the lungs. However, this compensatory mechanism is very limited and when it is depleted, the body develops hypoxemia (lack of oxygen in the blood) and tissue hypoxia (lack of oxygen in the tissues). At the same time, the person begins to experience a feeling of lack of air.

To ensure normal delivery of oxygen to tissues and organs (primarily to the brain), the body launches other compensatory reactions, which consist of increasing the respiratory rate and heart rate (tachycardia). As a result of an increase in the respiratory rate, more fresh (oxygenated) air enters the pulmonary alveoli, which penetrates into the blood, and as a result of tachycardia, oxygenated blood is distributed faster throughout the body.

It is worth noting that these compensatory mechanisms also have their limits. As they become exhausted, the breathing rate will increase more and more, which without timely medical intervention can lead to the development of life-threatening complications (even death).

Shortness of breath with bronchitis can be:

Inspiratory. It is characterized by difficulty in inhaling, which may be due to blockage of the medium-sized bronchi with mucus. The inhalation is noisy and can be heard from a distance. During inhalation, patients tense the auxiliary muscles of the neck and chest.
Expiratory. This is the main type of shortness of breath in chronic bronchitis, characterized by difficulty in exhaling. As mentioned earlier, the walls of the small bronchi (bronchioles) do not contain cartilaginous rings, and in the straightened state they are maintained only due to the elastic force of the lung tissue. With bronchitis, the mucous membrane of the bronchioles swells, and their lumens can be clogged with mucus, as a result of which, in order to exhale air, a person needs to make more effort. However, pronounced contraction of the respiratory muscles during exhalation contributes to an increase in pressure in the chest and lungs, which can cause collapse of the bronchioles.
Mixed. Characterized by difficulty in inhalation and exhalation of varying degrees of severity.

Chest pain due to bronchitis

Chest pain with bronchitis occurs mainly as a result of damage and destruction of the mucous membrane of the respiratory tract. Under normal conditions, the inner surface of the bronchi is covered thin layer mucus, which protects them from the aggressive effects of air flow. Damage to this barrier results in the air flow irritating and damaging the walls of the airways during inhalation and exhalation.

Also, the progression of the inflammatory process contributes to the development of hypersensitivity of nerve endings located in the large bronchi and trachea. As a result, any increase in pressure or increase in the speed of air flow in the respiratory tract can lead to pain. This explains the fact that pain in bronchitis occurs mainly during coughing, when the speed of air passage through the trachea and large bronchi is several hundred meters per second. The pain is acute, burning or stabbing, intensifies during a coughing attack and subsides when resting the respiratory tract (that is, during quiet breathing with moistened warm air).

Temperature with bronchitis

An increase in body temperature during the clinical manifestations of bronchitis indicates the infectious (viral or bacterial) nature of the disease. The temperature reaction is a natural protective mechanism that develops in response to the introduction of foreign agents into the body tissues. Allergic or dust bronchitis usually occurs without an increase in body temperature or with a slight low-grade fever (the temperature does not rise above 37.5 degrees).

The direct increase in body temperature during viral and bacterial infections is caused by contact of infectious agents with cells of the immune system (leukocytes). As a result of this, leukocytes begin to produce certain biologically active substances called pyrogens (interleukins, interferons, tumor necrosis factor), which penetrate the central nervous system and affect the center of temperature regulation, which leads to an increase in heat generation in the body. The more infectious agents that have penetrated the tissue, the greater the number of leukocytes that are activated and the more pronounced the temperature reaction will be.

With viral bronchitis, the body temperature rises to 38 - 39 degrees from the first days of the disease, while with a bacterial infection it rises to 40 degrees or more. This is explained by the fact that many bacteria, in the course of their life activity, release large amounts of toxins into the surrounding tissues, which, along with fragments of dead bacteria and damaged cells of their own body, are also strong pyrogens.

Sweating due to bronchitis

Sweating in infectious diseases is a protective reaction of the body that occurs in response to an increase in temperature. The point is that the temperature human body above temperature environment, therefore, to maintain it at a certain level, the body needs to constantly cool down. Under normal conditions, the processes of heat generation and heat transfer are balanced, however, with the development of infectious bronchitis, body temperature can increase significantly, which without timely correction can cause dysfunction vital organs and lead to the death of a person.

To prevent the development of these complications, the body needs to increase heat transfer. This is done through the evaporation of sweat, during which the body loses heat. Under normal conditions, about 35 grams of sweat evaporates from the surface of the skin of the human body per hour. This consumes about 20 kilocalories of thermal energy, which leads to cooling skin and the whole body. With a pronounced increase in body temperature, activation occurs sweat glands, as a result of which more than 1000 ml of liquid per hour can be released through them. All of it does not have time to evaporate from the surface of the skin, as a result of which it accumulates and forms drops of sweat in the back, face, neck, and torso.

Features of the course of bronchitis in children

The main features of the child’s body (relevant for bronchitis) are increased reactivity of the immune system and weak resistance to various infectious agents. Due to the weak resistance of the child’s body, a child may often suffer from viral and bacterial infectious diseases of the nasal cavity, sinuses and nasopharynx, which significantly increases the risk of infection entering the lower respiratory tract and developing bronchitis. This also explains the fact that viral bronchitis in a child can be complicated by the addition of a bacterial infection already from 1–2 days of illness.

Infectious bronchitis in a child can cause excessively expressed immune and systemic inflammatory reactions, which is due to the underdevelopment of the regulatory mechanisms of the child's body. As a result, symptoms of the disease can be expressed from the first days of bronchitis development. The child becomes lethargic, tearful, body temperature rises to 38–40 degrees, shortness of breath progresses (up to the development of respiratory failure, manifested by pale skin, bluish skin in the area of the nasolabial triangle, impaired consciousness, and so on). It is important to note that the younger the child, the faster symptoms of respiratory failure may occur and the more severe the consequences for the baby may be.

Features of the course of bronchitis in older people

As the human body ages, the functional activity of all organs and systems decreases, which affects the general condition of the patient and the course of various diseases. A decrease in the activity of the immune system may increase the risk of developing acute bronchitis in older people, especially those who work (or have worked) in unfavorable conditions (janitors, miners, etc.). The body's resistance in such people is significantly reduced, as a result of which any viral disease of the upper respiratory tract can be complicated by the development of bronchitis.

At the same time, it is worth noting that the clinical manifestations of bronchitis in older people can be very poorly expressed (a weak dry cough, shortness of breath, and slight chest pain may be noted). Body temperature may be normal or slightly elevated, which is explained by impaired thermoregulation as a result of reduced activity of the immune and nervous systems. Danger this state is that when a bacterial infection occurs or when the infectious process moves from the bronchi to the lung tissue (that is, with the development of pneumonia), the correct diagnosis may be made too late, which will significantly complicate treatment.

Types of bronchitis

Bronchitis can vary in clinical course, as well as depending on the nature of the pathological process and changes occurring in the bronchial mucosa during the disease.

Depending on the clinical course, there are:

acute bronchitis;
Chronical bronchitis.

Depending on the nature of the pathological process, there are:

catarrhal bronchitis;
purulent bronchitis;
atrophic bronchitis.

Acute bronchitis

The cause of the development of acute bronchitis is the simultaneous impact of a causative factor (infection, dust, allergens, etc.), resulting in damage and destruction of the cells of the bronchial mucosa, the development of an inflammatory process and impaired ventilation of the lung tissue. Most often, acute bronchitis develops against the background of a cold, but it can be the first manifestation of an infectious disease.

The first symptoms of acute bronchitis may be:

general weakness;
increased fatigue;
lethargy;
soreness (irritation) of the throat mucosa;
dry cough (may occur from the first days of the disease);
chest pain;
progressive shortness of breath (especially during physical activity);
increase in body temperature.

With viral bronchitis, the clinical manifestations of the disease progress over 1 to 3 days, after which there is usually improvement general well-being. The cough becomes productive (mucous sputum may be produced for several days), body temperature decreases, and shortness of breath goes away. It is worth noting that even after the disappearance of all other symptoms of bronchitis, the patient may suffer from a dry cough for 1 to 2 weeks, which is due to residual damage to the mucous membrane of the bronchial tree.

When a bacterial infection occurs (which is usually observed 2–5 days after the onset of the disease), the patient’s condition worsens. Body temperature rises, shortness of breath progresses, and mucopurulent sputum begins to be released with coughing. Without timely treatment, pneumonia may develop, which can cause the patient's death.

Chronical bronchitis

In chronic bronchitis, irreversible or partially reversible obstruction (blocking of the lumen) of the bronchi occurs, which is manifested by attacks of shortness of breath and painful cough. The cause of the development of chronic bronchitis is frequently recurring, incompletely treated acute bronchitis. The development of the disease is also facilitated by prolonged exposure to adverse environmental factors (tobacco smoke, dust and others) on the bronchial mucosa.

As a result of the influence of causative factors, a chronic, sluggish inflammatory process develops in the mucous membrane of the bronchial tree. Its activity is not enough to cause classic symptoms acute bronchitis, and therefore at first a person rarely seeks medical help. However, prolonged exposure to inflammatory mediators, dust particles and infectious agents leads to the destruction of the respiratory epithelium and its replacement by multilayer epithelium, which is not normally found in the bronchi. Damage to the deeper layers of the bronchial wall also occurs, leading to disruption of its blood supply and innervation.

Multilayer epithelium does not contain cilia, therefore, as it grows, the excretory function of the bronchial tree is disrupted. This leads to the fact that inhaled dust particles and microorganisms, as well as mucus formed in the bronchi, are not released out, but accumulate in the lumens of the bronchi and clog them, leading to the development various complications.

In the clinical course of chronic bronchitis, there are periods of exacerbation and periods of remission. During the period of exacerbation, the symptoms correspond to those of acute bronchitis (cough with sputum production, increased body temperature, deterioration in general condition, and so on). After treatment, the clinical manifestations of the disease subside, but cough and shortness of breath usually persist.

An important diagnostic sign of chronic bronchitis is the deterioration of the patient’s general condition after each subsequent exacerbation of the disease. That is, if previously the patient experienced shortness of breath only during severe physical exertion (for example, when climbing to the 7th - 8th floor), after 2 - 3 exacerbations he may notice that shortness of breath occurs already when climbing to the 2nd - 3rd floor. This is explained by the fact that with each exacerbation of the inflammatory process, a more pronounced narrowing of the lumen of the small and medium-caliber bronchi occurs, which complicates the delivery of air to the pulmonary alveoli.

With a long course of chronic bronchitis, ventilation of the lungs can be impaired to such an extent that the body begins to lack oxygen. This can be manifested by severe shortness of breath (which persists even at rest), cyanosis of the skin (especially in the area of the fingers and toes, since the lack of oxygen primarily affects the tissues most distant from the heart and lungs), and moist rales when listening to the lungs. Without appropriate treatment, the disease progresses, which can cause various complications and death of the patient.

Catarrhal bronchitis

It is characterized by inflammation (catarrh) of the lower respiratory tract, occurring without the addition of a bacterial infection. The catarrhal form of the disease is characteristic of acute viral bronchitis. The pronounced progression of the inflammatory process leads to the activation of goblet cells of the bronchial mucosa, which is manifested by the release of large quantities (several hundred milliliters per day) of viscous mucous sputum. Symptoms of general intoxication of the body may be mild or moderate (body temperature usually does not rise above 38 - 39 degrees).

Catarrhal bronchitis is mild form disease and usually resolves within 3 to 5 days with adequate treatment. However, it is important to remember that the protective properties of the mucous membrane of the respiratory tract are significantly reduced, so it is extremely important to prevent the addition of a bacterial infection or the transition of the disease to chronic form.

Purulent bronchitis

Purulent bronchitis in most cases is a consequence of untimely or improper treatment of the catarrhal form of the disease. Bacteria can enter the respiratory tract along with inhaled air (during close contact of the patient with infected people), as well as during aspiration (sucking) of the contents of the pharynx into the respiratory tract during night sleep (under normal conditions, the human oral cavity contains several thousand bacteria).

Since the bronchial mucosa is destroyed by the inflammatory process, bacteria easily penetrate through it and infect the tissues of the bronchial wall. The development of the infectious process is also facilitated by high air humidity and temperature in the respiratory tract, which are optimal conditions for the growth and reproduction of bacteria.

IN short time bacterial infection can affect large areas of the bronchial tree. This is manifested by pronounced symptoms of general intoxication of the body (the temperature can rise to 40 degrees or more, there is lethargy, drowsiness, rapid heartbeat, and so on) and cough, accompanied by the release of a large amount of purulent sputum with a fetid odor.

If untreated, progression of the disease can lead to the spread of pyogenic infection into the pulmonary alveoli and the development of pneumonia, as well as the penetration of bacteria and their toxins into the blood. These complications are very dangerous and require urgent medical intervention, since otherwise the patient may die within a few days due to progressive respiratory failure.

Atrophic bronchitis

This is a type of chronic bronchitis in which atrophy (that is, thinning and destruction) of the mucous membrane of the bronchial tree occurs. The mechanism of development of atrophic bronchitis has not been fully established. It is believed that the onset of the disease is facilitated by prolonged exposure to unfavorable factors (toxins, dust particles, infectious agents and inflammatory mediators) on the mucous membrane, which ultimately leads to disruption of its recovery processes.

Atrophy of the mucous membrane is accompanied by a pronounced disturbance of all functions of the bronchi. During inhalation, the air passing through the affected bronchi is not moistened, not warmed, and not cleared of dust microparticles. The penetration of such air into the respiratory alveoli can lead to their damage and disruption of the process of enriching the blood with oxygen. In addition, with atrophic bronchitis, damage to the muscular layer of the bronchial wall is noted, as a result of which muscle is destroyed and replaced by fibrous (scar) tissue. This significantly limits the mobility of the bronchi, the lumen of which under normal conditions can expand or contract depending on the body’s needs for oxygen. The consequence of this is the development of shortness of breath, which first occurs during physical exertion, and then can appear at rest.

In addition to shortness of breath, atrophic bronchitis can manifest itself as a dry, painful cough, pain in the throat and chest, a disturbance in the general condition of the patient (due to insufficient oxygen supply to the body) and the development of infectious complications caused by a violation protective functions bronchi.

Diagnosis of bronchitis

In classic cases of acute bronchitis, the diagnosis is made based on the clinical manifestations of the disease. In more severe and advanced cases, as well as if chronic bronchitis is suspected, the doctor may prescribe to the patient the whole complex additional research. This will determine the severity of the disease and the severity of damage to the bronchial tree, as well as identify and prevent the development of complications.

In the diagnosis of bronchitis the following are used:

auscultation (listening) of the lungs;
general blood analysis ;
sputum analysis;
X-rays of light;
spirometry;
pulse oximetry;

Auscultation of the lungs with bronchitis

Auscultation (listening) of the lungs is carried out using a phonendoscope - a device that allows the doctor to detect even the quietest breathing sounds in the patient’s lungs. To conduct the study, the doctor asks the patient to expose the upper part of the body, after which he successively applies the phonendoscope membrane to various areas chest (to the front and side walls, to the back), listening to breathing.

When listening to the lungs of a healthy person, a soft noise of vesicular breathing is detected, resulting from stretching of the pulmonary alveoli when they are filled with air. With bronchitis (both acute and chronic), there is a narrowing of the lumen of the small bronchi, as a result of which the air flow moves through them at high speed, with turbulence, which is defined by the doctor as hard (bronchial) breathing. The doctor can also determine the presence of wheezing over various parts of the lungs or throughout the chest. Wheezing can be dry (their occurrence is caused by the passage of air flow through narrowed bronchi, the lumen of which may also contain mucus) or wet (occurring when there is fluid in the bronchi).

Blood test for bronchitis

This study allows us to identify the presence of an inflammatory process in the body and suggest its etiology (cause). For example, in acute bronchitis of viral etiology, the CBC (complete blood count) may show a decrease in the total number of leukocytes (immune system cells) of less than 4.0 x 10 9 /l. In the leukocyte formula ( percentage various cells of the immune system), there will be a decrease in the number of neutrophils and an increase in the number of lymphocytes - cells that are responsible for fighting viruses.

With purulent bronchitis, there will be an increase in the total number of leukocytes of more than 9.0 x 10 9 / l, and in the leukocyte formula the number of neutrophils, especially their young forms, will increase. Neutrophils are responsible for the process of phagocytosis (absorption) of bacterial cells and their digestion.

Also, a blood test can reveal an increase in ESR (the sedimentation rate of erythrocytes placed in a test tube), which indicates the presence of an inflammatory process in the body. With viral bronchitis, ESR may be slightly increased (up to 20–25 mm per hour), while the addition of a bacterial infection and intoxication of the body is characterized by a pronounced increase in this indicator (up to 40–50 mm per hour or more).

Sputum analysis for bronchitis

Sputum analysis is carried out to identify various cells and foreign substances in it, which in some cases helps to determine the cause of the disease. The sputum released when the patient coughs is collected in a sterile jar and sent for examination.

When examining sputum, the following may be found in it:

Bronchial epithelial cells (epithelial cells). They are found in large quantities in the early stages of catarrhal bronchitis, when mucous sputum begins to appear. As the disease progresses and a bacterial infection occurs, the number of epithelial cells in the sputum decreases.
Neutrophils. These cells are responsible for the destruction and digestion of pyogenic bacteria and fragments of bronchial epithelial cells destroyed by the inflammatory process. Especially many neutrophils in the sputum are found in purulent bronchitis, but a small number of them can also be observed in the catarrhal form of the disease (for example, in viral bronchitis).
Bacteria. Can be detected in sputum during purulent bronchitis. It is important to take into account the fact that bacterial cells can enter the sputum from the patient’s mouth or from the respiratory tract of medical personnel during material collection (if safety rules are not followed).
Eosinophils. Cells of the immune system responsible for the development of allergic reactions. A large number of eosinophils in the sputum indicates allergic (asthmatic) bronchitis.
Red blood cells. Red blood cells that can penetrate into sputum when small vessels of the bronchial wall are damaged (for example, during coughing attacks). A large amount of blood in the sputum requires additional research, as it may be a sign of damage to large blood vessels or the development of pulmonary tuberculosis.
Fibrin. A special protein that is formed by cells of the immune system as a result of the progression of the inflammatory process.

X-ray for bronchitis

The essence of an x-ray examination is to scan the chest with x-rays. These rays are partially blocked by various tissues that occur along their path, with the result that only a certain proportion of them passes through the chest and ends up on a special film, forming a shadow image of the lungs, heart, large blood vessels and other organs. This method allows you to assess the condition of the tissues and organs of the chest, on the basis of which conclusions can be drawn about the condition of the bronchial tree during bronchitis.

X-ray signs of bronchitis may include:

Strengthening the pulmonary pattern. Under normal conditions, bronchial tissues weakly block x-rays, so the bronchi are not visible on an x-ray. With the development of an inflammatory process in the bronchi and swelling of the mucous membrane, their radiopacity increases, as a result of which clear contours of the middle bronchi can be distinguished on the x-ray.
Enlargement of the roots of the lungs. The X-ray image of the roots of the lungs is formed by the large main bronchi and lymph nodes of this area. Expansion of the roots of the lungs can be observed as a result of migration of bacterial or viral agents into the lymph nodes, which will lead to activation immune reactions and an increase in the size of the hilar lymph nodes.
Flattening of the diaphragm dome. The diaphragm is respiratory muscle, separating the chest and abdominal cavities. Normally, it is dome-shaped and convex upward (towards the chest). In chronic bronchitis, as a result of blockage of the airways, a larger than normal amount of air may accumulate in the lungs, as a result of which they will increase in volume and push the dome of the diaphragm down.
Increased transparency of the lung fields. X-rays pass almost entirely through air. With bronchitis, as a result of blockage of the airways by mucus plugs, ventilation of certain areas of the lungs is impaired. With intense inhalation, a small amount of air can penetrate into the blocked pulmonary alveoli, but can no longer escape, which causes the expansion of the alveoli and an increase in pressure in them.
Expansion of the shadow of the heart. As a result of pathological changes in the lung tissue (in particular due to narrowing of blood vessels and increased pressure in the lungs), the flow of blood through the pulmonary vessels is disrupted (impeded), which leads to increased blood pressure in the chambers of the heart (right ventricle). An increase in the size of the heart (hypertrophy of the heart muscle) is a compensatory mechanism aimed at increasing the pumping function of the heart and maintaining blood flow in the lungs at a normal level.

CT scan for bronchitis

Computed tomography is a modern research method that combines the principle of an X-ray machine and computer technology. The essence of the method is that the X-ray emitter is not located in one place (as with a regular X-ray), but rotates around the patient in a spiral, taking many X-ray images. After computer processing of the received information, the doctor can obtain a layer-by-layer image of the scanned area, in which even small structural formations can be distinguished.

In chronic bronchitis, CT can reveal:

thickening of the walls of medium and large bronchi;
narrowing of the lumen of the bronchi;
narrowing of the lumens of the blood vessels of the lungs;
fluid in the bronchi (during an exacerbation);
compaction of lung tissue (with the development of complications).

Spirometry

This study is carried out using a special device (spirometer) and allows you to determine the volume of inhaled and exhaled air, as well as the exhalation rate. These indicators vary depending on the stage of chronic bronchitis.

Before the study, the patient is advised to refrain from smoking and heavy physical work for at least 4 – 5 hours, as this may distort the data obtained.

To conduct the study, the patient must be in an upright position. At the doctor’s command, the patient takes a deep breath, completely filling the lungs, and then exhales all the air through the mouthpiece of the spirometer, and the exhalation must be done with maximum force and speed. The counter device records both the volume of exhaled air and the speed of its passage through the respiratory tract. The procedure is repeated 2–3 times and the average result is taken into account.

During spirometry, the following is determined:

Vital capacity of the lungs (VC). It is the volume of air that is released from the patient's lungs during a maximum exhalation, preceded by a maximum inhalation. The vital capacity of a healthy adult man is on average 4 - 5 liters, and for women - 3.5 - 4 liters (these indicators may vary depending on the person’s physique). In chronic bronchitis, small and medium bronchi are blocked by mucus plugs, as a result of which part of the functional lung tissue ceases to be ventilated and vital capacity decreases. The more severe the disease and the more bronchi are blocked by mucus plugs, the less air the patient will be able to inhale (and exhale) during the study.
Forced expiratory volume in 1 second (FEV1). This indicator displays the volume of air that the patient can exhale in 1 second with forced (maximally fast) exhalation. This volume is directly dependent on the total diameter of the bronchi (the larger it is, the more air can pass through the bronchi per unit of time) and in a healthy person it is about 75% of the vital capacity of the lungs. In chronic bronchitis, as a result of the progression of the pathological process, the lumen of the small and medium bronchi narrows, as a result of which FEV1 will decrease.

Other instrumental studies

Carrying out all the above tests in most cases allows you to confirm the diagnosis of bronchitis, determine the extent of the disease and prescribe adequate treatment. However, sometimes the doctor may prescribe other tests necessary for a more accurate assessment of the condition of the respiratory, cardiovascular and other body systems.

For bronchitis, the doctor may also prescribe:

Pulse oximetry. This study allows you to assess the saturation (saturation) of hemoglobin (a pigment contained in red blood cells and responsible for transporting respiratory gases) oxygen. To conduct the study, a special sensor is put on the patient’s finger or earlobe, which collects information within a few seconds, after which the display displays data on the amount of oxygen in the patient’s blood in this moment. Under normal conditions, the blood saturation of a healthy person should be between 95 and 100% (that is, hemoglobin contains the maximum possible amount of oxygen). In chronic bronchitis, the delivery of fresh air to the lung tissue is disrupted and less oxygen enters the blood, as a result of which saturation can drop below 90%.
Bronchoscopy. The principle of the method is to insert a special flexible tube (bronchoscope) into the patient’s bronchial tree, at the end of which a camera is attached. This allows you to visually assess the condition of the large bronchi and determine the nature (catarrhal, purulent, atrophic, and so on).

Before use, you should consult a specialist.

This is their tendency to penetrate deeply and affect not only the bronchial mucosa, but also the muscle wall and peribronchial tissue (meso- and peribronchitis). It is mainly the small bronchi that undergo changes; their walls are swollen, infiltrated, the capillaries are stretched and overflowing with blood. Interstitial tissue takes a significant part in the inflammatory process, which was established by Rokitansky.

The inflammatory process in the interstitial tissue of the lungs progresses with each relapse of pneumonia in early childhood. It is of great importance to have wide lymphatic vessels. Subsequently, granulation tissue develops, followed by the formation of fibrosis and sclerosis, resulting in narrowing of the bronchi. Along with this, atelectatic foci easily develop due to blockage of the lumen of the bronchi with exudate and a decrease in their elastic properties associated with the death (complete or partial) of elastic fibers. According to M.A. Skvortsov, any prolonged catarrh of the upper respiratory tract is accompanied by the accumulation of protein fluid under the respiratory epithelium, followed by its detachment and disintegration. In the future, when repeated diseases, the inflammatory process can proceed either in a sequential way - from the mucous membrane of the bronchioles to the alveolar ducts and alveoli with the formation of foci of bronchopneumonia, or in a centrifugal way (in relation to the lumen of the bronchi) through the interstitial tissue (peribronchial pneumonia). When the muscular and elastic framework of the airways is destroyed during peribronchitis, their evacuation, i.e., self-cleaning ability, decreases. The exudate is organized and can give rise to carnification in more or less significant areas of the lungs.

Subsequently, a necrotic process often forms in the bronchi due to the loss of elasticity of their walls during increased exhalation; Diffuse bronchiectasis easily develops in connection with cough. With measles peribronchial pneumonia, such bronchiectasis sometimes develops within 1-2 days.

If necrosis of the bronchial wall occurs in the respiratory tract, which is still passable for air, then bronchiectasis develops faster. In more limited areas of pneumonia, separate bronchiectasis cavities are formed.

A. I. Abrikosov considers that chronic pneumonia is characterized by retention of exudate in the alveoli with subsequent fatty degeneration of its cells. Subsequently, the interstitial tissue grows with sclerosis of the lung tissue and obliteration of the bronchi and blood vessels.
A. N. Rubel considers diffuse or focal proliferation of connective tissue (scar, fibrous, sclerotic) to be the basis of chronic non-tuberculous processes in the lungs.

A number of authors classify bronchiectasis as only one of the phases of development of chronic pneumonia, identifying a number of concepts - chronic nonspecific pneumonia, nonspecific pulmonary consumption, pneumonitis, pulmonitis, cirrhosis of the lung, indurative pneumonia. A. Ya. Tsigelnik considers the most correct term “pneumonitis”, given the diffuse damage to the lung tissue in chronic pneumonia and the tendency of the latter to relapse.

With so-called chronic bronchitis, the bronchial mucosa is slightly changed. It is hyperemic and edematous, but in the thickness of the bronchial wall and surrounding interstitial tissue there is always a proliferation of connective tissue, its scar degeneration (fibrous peribronchitis).

These changes, according to A.N. Rubel, are secondary, since they are caused by pneumonia, prolonged influenza, measles, whooping cough, i.e. processes involving intralobular connective tissue in the form of peribronchitis. From this point of view, the origins of the chronic non-tuberculous process are quite understandable. It is in early childhood, when primary interstitial pneumonia often occurs, that during the process of tissue wrinkling, nested or continuous pneumosclerosis develops. In some cases, collapse of the alveoli, formation of atelectasis and carnification occur. It can be assumed that with each exacerbation of a chronic process in the lungs, perivasculitis develops with the formation of atrophic processes in the thickness of the bronchi (in cartilage, muscles) and with the consistent expansion of the bronchi themselves.

This condition creates favorable conditions for the proliferation of microbes. The atrophic process contributes to the formation of cylindrical or saccular expansions with the subsequent occurrence of necrosis.

Panbronchitis occurs especially easily in small children in small bronchi lacking cartilage. Such changes were described by Leschke under the name bronchiectasis of the terminal bronchial system, and even earlier by Yutinel. In the walls of the bronchi, along with the development of granulation and scar tissue, significant expansions also occur as a result of increased intrabronchial pressure. According to S.I. Volchok and A.Ya. Tsygelnik, the development of bronchiectasis is often based on atelectasis, in which deep necrotic processes develop. Behind Lately There is especially much talk about the influence of chronic sinusitis and tonsillitis on the formation of bronchiectasis. According to Yu. F. Dombrovskaya, chronic processes in the nasopharynx almost always accompany chronic pneumonia and especially bronchiectasis (sinus bronchitis, sinus pneumopathy) even in early childhood.

Ruptures of the walls of bronchioles and alveolar septa that occur during necrosis with the spread of air along the lymphatic vessels lead to interstitial emphysema. According to M.A. Skvortsov, such ruptures are most often observed near the anterior edge of the lungs, where at autopsy one can see air bubbles under the pleura - subpleural emphysema. With further spread of emphysema under the influence of incoming air along large vessels and bronchi through the root of the lung, mediastinal emphysema is formed. More rarely, subcutaneous emphysema is observed due to the release of air through the jugular fossa.

If we take into account such a variety of morphological changes, it becomes clear why in chronic pneumonia various forms of changes are found in the lung tissue: pneumonic foci, sclerosis, emphysema, atelectasis, bronchiectasis. This is explained by the simultaneous involvement of the entire lung, bronchi, interstitial tissue, alveoli, and blood vessels in the process. But the leading process in the lungs is damage to interstitial tissue with the development of granulations and foci of pneumosclerosis.

Most bronchiectasis is a consequence of chronic pneumonia. They may occur due to deformation of the bronchus located in the area of cirrhotic compaction of the lungs.

Atelectatic bronchiectasis develops most often in the lower lobes of the lungs, usually after measles, whooping cough and influenza pneumonia, as well as with severe rickets. Atelectasis is formed due to weakness of respiratory excursion, blockage of the bronchi with secretions.

The circulatory and lymphatic pathways also undergo changes - productive exo-meso-periarteritis, sclerosis and thickening of the walls develop, resulting in compression of the lymphatic vessels.

Changes in the bronchi can be both atrophic and hypertrophic in nature. In pediatric pathology, atrophic processes with thinning of the walls of the small bronchi are more common. In large bronchi, hypertrophic processes with hyperplasia of the mucous membrane and glands predominate. It is difficult to say which of the two processes - hypertrophic or atrophic - leads to the development of bronchiectasis. Most likely, both processes occur simultaneously, since during section, along with the described changes in the walls of the bronchi, atrophy of the interalveolar septa and emphysema are usually found. These changes are especially pronounced in the presence of rickets blooming form. For severe chronic interstitial pneumonia ulceration of the bronchial mucosa with metaplasia of their epithelium is observed.

We can distinguish: a) confluent, b) diffuse forms of chronic pneumonia. Both of them are accompanied by emphysema and pulmonary sclerosis.

Thus, morphological changes in chronic pneumonia in children are characterized by predominant damage to interstitial tissue, which is why they are most often called chronic interstitial pneumonia.

Changes in interstitial tissue can also explain asymptomatic microabscesses, accompanied by periodic outbreaks of temperature and increased leukocytosis without specific clinical symptoms. The development of the process in the connective tissue around the bronchi and bronchioles creates a fluoroscopy picture of the so-called cellular, or honeycomb, lung, and the predominant damage to the bronchi is characterized by a number of morphologists as panbronchitis, deforming bronchitis, etc.

There are observations by some authors about the relationship between the shape of the chest and the nature of the spread of the process. Thus, with the nested nature of the process, a barrel-shaped chest shape is more often observed, while with a continuous one, a narrowed shape is observed. The barrel-shaped shape of the chest with localized pneumosclerosis is explained by the presence of compensatory emphysema.

Mechanisms of bronchial obstruction

From a formal point of view, the lumen of the bronchus, which is a hollow tube, can change only for three reasons: 1) a decrease in diameter (spasm); 2) thickening of the wall (swelling of the mucous membrane) and 3) mechanical obstruction (blockage) of the lumen with a plug of mucus.

Rice. Bronchus on a cross section: a - normal; b - for asthma;
1 - mucous membrane, 2 - submucosal membrane and 3 - muscular membrane, 4 - mucous plug

The figure shows that due to inflammation and edema, the mucous and submucosal layers are thickened, the bronchial muscles are spasmed, and the bronchial lumen is partially blocked by a mucus plug (4). These disorders are due to the fact that for various reasons a chronic inflammatory process develops in the bronchial tree. Special substances (in medicine they are called inflammatory mediators), released during allergic or other reactions, trigger all of the above mechanisms. At the very beginning of the disease, the obstruction of the bronchial tubes is caused mainly by their spasm, inflammation and swelling of the mucous and submucosal layers of the respiratory tract. Many people with the flu experienced difficulty in nasal breathing due to swelling of the nasal mucosa - in the same way, the bronchial mucosa swells, further narrowing their lumen. Impaired bronchial patency impedes the movement of mucus, and this is manifested by the fact that after an attack a cough occurs and sputum in the form of mucus plugs is coughed up from the bronchi.
The main substances that cause the process of chronic inflammation in the bronchial tree are: histamine; serotonin; various chemotactic factors - eosinophilic and neutrophilic (attracting various cells to the site of inflammation); bradykinin; platelet activating factor; leukotrienes; prostaglandins; polypeptides of various nature; proteases, etc. The role of many mediators is not clear in detail, but it is absolutely known that some of them, for example histamine, as well as acetylcholine, acting on the smooth muscles of the bronchi, cause their contraction and the development of bronchospasm. In addition, histamine and other mediators are able to expand the microvessels of the submucosal layer, which causes an increase in their permeability and leads to swelling and edema of the bronchial mucosa. The effect of inflammatory mediators on the mucous membrane leads to damage to the villi of the ciliated epithelium and disruption of the tight contact between cells, which further increases the swelling of the mucous membrane.

Rice. Damage to the bronchial mucosa during acute inflammation:
1 - ciliated cells; 2 - eyelashes; 3 - goblet cells;
4 - basal cells; 5 - layer of mucus

Damage to the cilia leads to disruption of the mucociliary escalator and accumulation of mucus in the lumen of the bronchi. In addition, the release of mediators and the subsequent inflammatory reaction of the mucous membrane lead to irritation of sensitive nerve endings and the development of bronchospasm through a neuro-reflex - cholinergic mechanism. This bronchospasm, on the one hand, is aggravated by the presence of primary bronchial hyperreactivity, which was mentioned above. On the other hand, the chronic inflammatory process itself is the cause of hyperreactivity, but this is secondary. Imagine that you have applied several crystals of table salt to the healthy (intact) skin of your hand. Will you feel anything? Hardly. What if you apply the same amount of salt to wounded or inflamed skin? You will feel its pathological effects: burning, pain and increased inflammation. The influence of mediators on the bronchial tree is realized in the same way: by causing an inflammatory reaction of the mucous membrane, they increase its sensitivity (reactivity) to various external influences. And this increased reactivity is called secondary hyperreactivity.
Thus, bronchospasm in asthma develops in two ways: 1) with the direct effect of inflammatory mediators on the smooth muscles of the bronchi (primary bronchospasm) and 2) with irritation of the sensitive endings vagus nerve(secondary - reflex bronchospasm). In both the first and second cases, this is the result of the release of various inflammatory mediators.
What is the reason for this? What factors provoke the release of mediators and the formation of the process of chronic inflammation? There are two main pathways: immunological, associated with allergies, and non-immunological, associated with a number of different mechanisms.

Immunological pathway for the release of inflammatory mediators

The immunological, or allergic, path of release of inflammatory mediators, as the name implies, is realized as a result of the formation of allergies (hypersensitivity) to various substances in the body. As you probably know, there is a whole spectrum of allergic substances: plant pollen (grass, flowers and trees), house dust (the main component of which is a microscopic mite that lives in a person’s home), some chemicals (which a person encounters in the process of professional activities), components of a number of food products, etc. Some of them are true allergens, that is, when they enter the body, they immediately trigger allergic reactions. Others are called haptens (conditionally they can be called pre-allergens, since when they enter the human body, they cause allergic reactions only when combined with proteins in the blood or body tissues). As a rule, allergens are substances of a protein nature, and haptens are various non-protein compounds: chemical, medicinal, and others. The most common substances that cause allergies are shown in the table.

Table. Substances that most commonly cause allergic reactions

Allergen groups	Main representatives
Household	House dust, library dust
Epidermal	Wool of domestic animals (cats, dogs, sheep, etc.), feather pillows, feathers of poultry (parrots, canaries, etc.)
Vegetable	Pollen from trees (birch, hazel, Dubai, etc.), grass pollen (timothy, hedgehog, fescue, quinoa, wormwood, etc.)
Food	Protein of milk, chicken egg, fish; citrus fruits, wheat, etc.
Fungal	Various molds, yeasts
Chemical	Isocyanates; compounds of platinum, chromium, nickel; dyes (eg Ursol, some hair dyes)
Medicinal	Penicillin preparations, sulfonamides, etc.

The allergic process develops when the allergen interacts with the body's immune system. And this process starts due to the fact that all allergic substances are foreign to the body into which they enter. Upon contact with an allergen, the body’s immune system produces special antibodies (in medicine they are called immunoglobulins). Moreover, specific antibodies are produced for each specific allergen, and the body acquires increased sensitivity to them (becomes sensitized). Repeated contact with an allergen leads to the binding of specific antibodies to their allergens. This reaction is aimed at protecting the body from the introduction of foreign proteins. But the result of this protection is often catastrophic: the complex formed by the allergen and its corresponding antibody causes a reaction of damage and destruction of special cells (they are called mast cells, or mast cells), from which various inflammatory mediators are released, triggering all the pathological mechanisms of asthma.
Thus, protective mechanisms of the immune system are involved in the development of allergic (atopic) asthma. But this immunity, in a certain sense, is vulnerable, since it ultimately leads to the formation of an allergic disease - asthma. And this happens because in the process of interaction of the allergen with the immune system, antibodies are formed that both protect the body and harm it.
During the interaction of an allergen with the immune system, antibodies (immunoglobulins) are formed with different properties or, as immunologists say, different classes. The main immunoglobulins of key importance in the pathogenesis of asthma are classes E and G (they are designated Ig E and Ig G, respectively). Class G immunoglobulins are called blocking because, by binding to allergens, they protect the body from their pathological effects. There are several varieties (subclasses) of Ig G, but the role of each of them in the pathogenesis of asthma has not been studied in detail and reliably. Class E immunoglobulins are called reagins. It is they, by binding to the corresponding allergens (antigens) and forming an antigen-antibody complex, that cause damage to mast cells and the release of mediators allergic inflammation.
The process of antibody formation is quite complex. It is determined by the coordinated interaction of a number of specialized cells: lymphocytes various types, macrophages and others, localized in various organs and tissues. I will not dwell on this issue in detail, since this could be the topic of a separate book.

Non-immunological pathway for the release of inflammatory mediators

The non-immunological pathway for the release of inflammatory mediators is determined by the fact that, due to some biochemical defects (or characteristics!), metabolism in individuals is disrupted (or, as biochemists say, metabolism) various substances. A classic example of this is the so-called aspirin, which you may have heard of. In people suffering from aspirin asthma, the metabolism of a special compound is disrupted - arachidonic acid. Due to this circumstance, taking aspirin (acetylsalicylic acid) and a number of similar drugs: analgin, indomethacin, etc., causes the release of inflammatory mediators without the participation of immunological mechanisms and the formation of antibodies.
Arachidonic acid is formed during the breakdown of phospholipids - substances from which the membranes (walls) of various cells are built. As you know, in the process of life, various cells from which tissues and organs are built are continuously replaced with new ones. Cells that have outlived their “age” are destroyed, and the substances that make them up are used to form new compounds. And one of these substances is arachidonic acid. There are two main pathways for the biochemical oxidation of arachidonic acid: cyclooxygenase and lipoxygenase. The cyclooxygenase pathway leads to the formation of a number of substances: prostaglandins, prostacyclins and others, which carry out the physiological regulation of the tone of the smooth muscles of the bronchi, blood vessels and other organs and tissues. The lipoxygenase pathway of arachidonic acid oxidation leads to the formation of other substances - leukotrienes, chemotactic mediators, the so-called slow-reacting allergy substance (MRSA) and a number of mediators of allergic inflammation that trigger asthma.
The effect of acetylsalicylic acid and other similar compounds is that they inhibit (block) the cyclooxygenase pathway of arachidonic acid oxidation, thereby activating the lipoxygenase pathway. The trouble with this pathological path is that it can also stimulate the Ig E-mediated (immunological) mechanism for the release of inflammatory mediators. That is why intolerance to aspirin and other non-steroidal anti-inflammatory drugs occurs both in non-atopic asthma (not associated with allergies) and is combined with the atopic form of the disease (caused by sensitization to various allergens).
There are other mechanisms described for the non-immunological release of inflammatory mediators, which occur after inhalation of cold air, physical activity (with the so-called exercise asthma syndrome), exposure to toxic chemicals, etc. Many of the currently studied and described mechanisms are not fully understood, often data from different authors contradict each other. Moreover, of the several dozen described mediators, many have so far been found only in animal experiments, and their role in the pathological mechanisms of asthma in humans has not been clarified. Generally speaking, to the extent that the immunological pathway for the release of inflammatory mediators in asthma has been studied in detail and systematically, non-immunological pathways are so unclear, haphazardly studied and presented. This issue is confused to such an extent that many scientists seriously believe that finally there will be that very main factor, the elimination of which with the help of some procedure or one medicine can cure asthma. Unfortunately, this is fundamentally impossible. An example proving the validity of such a statement is the discovery by the English scientist R.E.C. Altounyan of the famous drug intala. As stated earlier, asthma is triggered by damage to mast cells and other cells, followed by the release of various inflammatory mediators. Intal, “coating” the surface of cell membranes, protects them from damage and, preventing the release of mediators, blocks the further development of all pathological processes in the bronchial tree, leading to asthmatic symptoms. However, a beautiful and impeccable idea from a theoretical point of view does not always lead to the desired result in practice. And the progression of asthma, despite the ongoing inhalation of Intal and the absence of breathing difficulties and suffocation against this background, can continue unnoticed by the patient and his doctor. And sometimes this is discovered quite unexpectedly - a severe attack that cannot be relieved by any medications. Why is this happening? Yes, because it is impossible to protect millions of cells from damage. And the mediators breaking through the “intala defense”, without encountering the “second echelon of defense” on their way, contribute to the imperceptible and inevitable progression of the inflammatory process, which is the basis of the disease. In this regard, it should be noted that success in treatment cannot be achieved by any one means. But we will discuss this in the part concerning the treatment of asthma.
At the same time, all so-called inflammatory mediators are actually physiologically active substances that regulate various functions of organs and systems. Histamine, for example, is one of the regulators capillary circulation and gastric secretion. Its formation in the body occurs in a normal biochemical way - decarboxylation of histidine, an amino acid used in the synthesis of proteins. Unfortunately, the regulatory role of most mediators has been studied incompletely and unsystematically. However, some of them, such as prostaglandins, are beginning to be used in medicine in physiological quantities. And these substances have a pathological effect in cases where their quantity exceeds physiological norm(which, by the way, can fluctuate greatly).
THUS, IN THE IMPLEMENTATION OF PATHOPHYSIOLOGICAL MECHANISMS OF ASTHMA, NOT SOME FOREIGN AGENTS PARTICIPATE (SUCH AS MICROBES AND THEIR TOXINS IN INFECTIOUS DISEASES), BUT PHYSIOLOGICALLY ACTIVE REGULATORS OF OP FUNCTIONS GANISM. And bronchospasm, inflammation and swelling of the mucous membrane with all asthmatic manifestations develop only when they are excessively formed or released. I once again emphasize this fact due to the fact that in recent years in medical practice A new generation of drugs is beginning to be introduced: blockers of the so-called leukotriene receptors, as well as inhibitors of leukotriene synthesis. Leukotrienes, among many biologically active substances, play a role in the pathophysiological mechanisms of asthma. It is possible that anti-leukotriene substances (which reduce the synthesis of these compounds or competitively bind the corresponding receptors) can resist the pathological effects of leukotrienes, but those who see in them another panacea for asthma have probably “forgotten” that an excess of histamine and acetylcholine is quite enough for the appearance of all asthma symptoms - from coughing to choking. In this regard, we can confidently say that such drugs may be useful, but will not solve the problem. I will talk about specific representatives of this group of anti-asthmatic drugs further.
The above can be summarized as follows: REGARDLESS OF THE PATH OF RELEASE, MEDIATORS OF ALL TYPES, WHEN INFLUENCED ON THE BRONCHIAL TREE IN QUANTITIES EXCEEDING THE PHYSIOLOGICAL NORM, CAUSE SPASMS OF SMOOTH MUSCLE, INFLAMMATION AND SWELLING OF THE MUCOUS STIFFUS AND ALSO ACCUMULATION OF MUCUUS IN THE RESPIRATORY TRACT. AT THE SAME TIME, DEPENDING ON THE RATIO OF CERTAIN MEDIATORS, THE DEGREE OF SPASMS, INFLAMMATORY EDEMA AND OBTURATION OF THE bronchial mucus CHANGES.
Therefore, some patients cough up more sputum, while others cough up less. Bronchodilator aerosols help some, but are ineffective for others. Many patients receive anti-inflammatory (hormonal) drugs in the form of aerosols, for others they do not help, and there is a need to prescribe tablet drugs, etc. But all this is determined not only by the difference in the formation and progression of bronchial obstruction, but also by the individual characteristics of each patient’s body , his living conditions, environmental conditions and other factors.
So, due to a number of reasons - external (allergies, chemical and occupational hazards) and internal (intolerance to aspirin and its analogues, physical activity, various biochemical disorders) - a large number of inflammatory mediators are released, the damaging effect of which causes bronchospasm, swelling of the mucous membrane and accumulation of sputum. This leads to obstruction of the bronchi and causes asthma symptoms.
But perhaps not all of you know that from 20 to 35% healthy people are allergic to house dust, grass and tree pollen, and all those substances that we talked about earlier, and, nevertheless, do not suffer from asthma. To illustrate, I present data from a foreign manual on asthma for practitioners (R. Pauwels, P.D. Snashall. A practical approach to. CBA Publishing Services. Printed by Adlard & Son Ltd., Dorking, 1986).

Table. Frequency of positive skin tests for allergens in healthy subjects

According to scientific research, in 50% of healthy people, taking aspirin causes swelling and swelling of the mucous membranes of the upper respiratory tract, but they do not feel it and do not suffer from asthma. Almost the entire population inhales environmentally polluted air, filled with the “aromas” of oxides of sulfur, nitrogen, exhaust gases and other “delights” of the chemicalization of the national economy. However, only 5-10% of the population suffers from asthma! And finally, many subjects, having been in contact with occupational hazards for many years, nevertheless do not suffer from asthma.
In order for asthma to form, the targeted influence of various mechanisms is necessary - they are called trigger, that is, triggering. Trigger mechanisms can be compared to methods of starting a car engine: using a starter, a crank, or self-starting the engine when accelerating, for example, from a hill. But the result, regardless of the method, is always the same: the engine starts and the car starts moving on its own. The situation is similar when “triggering” asthma. One or another trigger mechanism triggers the disease, and it begins its life and its movement. What are the trigger mechanisms that trigger asthma? And what are the patterns that determine the progression of the disease after it has started?

Bronchiectasis in the lungs is a fairly rare phenomenon that occurs in representatives of various age groups and gender. From the experience of specialists, it follows that men suffer from the disease 2.5-3 times more often than women.

Despite the fact that the pathology is diagnosed only in 5 out of 100,000 cases, the lack of timely diagnosis and treatment can lead to the gradual destruction of all elements respiratory system with subsequent cessation of their functioning.

What is bronchiectasis

Bronchiectasis is deformed areas of the bronchi that form as a result of exposure to the inflammatory process. Such changes are irreversible and can develop either against the background of chronic diseases of the respiratory system or be independent.

Bronchiectasis is accompanied by the following disturbances in the structure and functioning of the lungs:

pathological expansion of the bronchi, which do not have cartilaginous bases, due to an increase in the volume of connective tissues;
blockage of the bronchus as a result of adhesion of its walls, swelling of the pulmonary lobes;
accumulation of mucous contents in the bronchioles;
inflammation of the structures of the bronchial tree and swelling of the mucous membrane due to the development of infection, accumulation of purulent masses;
the formation of foci of pneumosclerosis - areas of the organ in which connective tissue replaces muscle tissue, which excludes the possibility of their participation in the respiratory process.

The occurrence of bronchiectasis is most often observed in areas of small and medium-sized bronchi, but in some cases the pathology may involve first-order elements. Dilatation of the bronchi is often accompanied by pathological changes in other structures of the respiratory system, leading to the development of bronchitis, pneumonia, and in severe cases, bleeding and lung abscess.

Reasons for the development of the disease

Experts distinguish two ways of occurrence of bronchiectasis - congenital or primary, and acquired (secondary). As a result of this division, two groups of causes for the development of the disease are considered.

Reasons for the formation of congenital bronchiectasis

In congenital bronchiectasis, the key factor in the occurrence of pathology is considered to be a change in the DNA molecule, entailing various defects in the formation and formation of the bronchial tree during intrauterine development child. In addition, such disorders can result from the impact on the developing fetus of such negative factors as maternal smoking, alcohol intake and narcotic drugs, the course of some chronic and infectious diseases, treatment with certain medications.

The following disorders of the structure and functioning of the organs of the respiratory system as a result of the development of a congenital disease are distinguished:

a small number or complete absence of smooth muscle cells;
increased weakness of smooth muscle tissue in the elements of the bronchial tree;
excessive elasticity of connective tissue;
reduced immune resistance of the membranes and organs of the respiratory system;
weakness of the cartilaginous bases of the bronchi.

As a result of the combination of these factors, prerequisites for the formation of bronchiectasis develop. Experts also note that in this situation, the formation of pathology in the structure of the pulmonary structures is primary, and the development of inflammatory processes can occur against the background of formed bronchial defects.

Factors causing the development of acquired bronchiectasis

Research by specialists indicates that the main cause of acquired bronchiectasis is injury to the elements of the bronchial tree as a result of infectious and inflammatory processes occurring in the lungs. The following diseases can contribute to this:

bronchitis;
tuberculosis;
measles;
whooping cough;
pneumonia;
connective tissue pathologies;
formation of oncological neoplasms in lung structures;
damage to the bronchi as a result of foreign objects entering the respiratory system.

In addition to pathologies occurring in the lungs, the formation of bronchiectasis can be caused by diseases associated with adjacent organs and systems: ulcerative colitis, staphylococcal infection, Crohn's disease, rheumatoid arthritis. Often the impetus for the development of the process is given by the abuse of smoking and drinking alcohol, taking narcotic drugs, and intoxication with toxic substances.

Types of pathology

Depending on the nature of the change in the structure of the bronchi, experts distinguish the following types of bronchiectasis:

Cylindrical. The cause of this form of the disease is sclerosis of the walls of the bronchi. The expansion of the lumen of the lungs is uniform and is present over a significant area of the lungs. Cylindrical bronchiectasis does not cause a significant accumulation of purulent masses, which has a beneficial effect on the treatment process.
Fusiform bronchiectasis is a tapering expansion that gradually turns into an unchanged area of tissue. This form of the disease is the easiest to treat, since it does not lead to the formation of pus deposits and difficulty breathing.
Bead-shaped formations. With this form of pathology, several rounded areas of deformation form on one bronchus. This entails the accumulation of a large amount of mucous or purulent contents in them.
Saccular traction bronchiectasis is one of the most severe forms of the disease. With it, large expansions of the round or oval shape which fill with pus and sputum.

In addition to the listed pronounced forms of bronchiectasis, experts identify a mixed variant of the course of the disease, which combines several types of expansion of the lung elements. Most often, this form of pathology is formed as a result of severe inflammatory processes in the respiratory system - pneumonia, tuberculosis, lung abscess. The prognosis in this case depends on the number and size of formations, as well as the timeliness of medical care.

Stages of development and symptoms of the disease

Symptoms and treatment methods for bronchiectasis depend not only on its type, but also on the phase of development of the disease. For this reason, there are two stages of bronchiectasis:

Exacerbation stage. This phase is characterized by the penetration of infection into the lung area and the development of a pronounced inflammatory process in them. At this time, the symptoms of the disease manifest themselves most clearly. A person complains of the following phenomena:

Remission stage. At this phase of the disease, signs of pathology most often disappear due to the absence of obstacles to free breathing. At the same time, multiple dilations of the bronchi can cause a dry cough and respiratory failure.

Experts insist: the prolonged presence of a cough with sputum production, the frequent occurrence of pneumonia is a reason for urgent treatment medical institution to exclude the presence of bronchiectasis in the lungs.

Treatment

The basis for effective treatment of pulmonary bronchiectasis is an integrated approach, including a variety of therapeutic techniques and a combination of medications used.

Conservative therapy

Drug treatment in the presence of bronchiectasis is the most common option to combat the pathology. It allows you to destroy pathogenic microflora, remove phlegm from the bronchi, get rid of the inflammatory process and cleanse the body of the products of microorganisms.

In the conservative treatment of bronchiectasis, the following groups of drugs are used:

anti-inflammatory – relieve inflammation, lower body temperature;
antibiotics – prevent the growth and reproduction of pathogenic microflora, contribute to its destruction;
mucolytics – thin sputum and help remove it from the lungs;
beta-adrenergic agonists - improve bronchial patency, facilitate sputum separation.

The use of cough suppressants in the treatment of bronchiectasis is strictly contraindicated, as it can lead to a worsening of the patient's condition.

Surgical intervention

Bronchiectasis is not always treated with medications - a severe form of the disease requires surgical intervention. It is justified when there is a significant dilation of one or two bronchi in one pulmonary lobe and the ineffectiveness of conservative treatment methods.

Surgical intervention involves removal of a single formation, resection of several affected areas of the bronchi, or complete removal lobes of the lung. The procedure has many contraindications, so it is not suitable for all patients.

Physiotherapy and diet

The use of physiotherapeutic procedures is indicated in the remission stage of the disease to prevent its relapse. The following methods are most effective:

electrophoresis using sodium chloride;
microwave exposure;
inductometry.

An important method of preventing periods of exacerbation of bronchiectasis is adherence to diet No. 13 according to Pevzner. It increases the body’s overall resistance to the disease and reduces the degree of intoxication.

Experts in the field of otolaryngology note that bronchiectasis in the lungs is a formation that cannot be completely eliminated. However, timely treatment in compliance with all medical recommendations allows you to prevent the progression of bronchiectasis, stop the further process of lung damage and eliminate the risk of complications.

Bronchitis is an inflammatory disease of the bronchi with a predominant lesion of their mucous membrane. The process develops as a result of a viral or bacterial infection - influenza, measles, whooping cough, etc.

In terms of frequency of occurrence, it ranks first among other respiratory diseases. Bronchitis mainly affects children and the elderly. Men get sick more often, which is due to occupational hazards and smoking. Bronchitis is more common in people living in areas and countries with cold and humid climates, in damp stone rooms or working in drafts.

Bronchitis is generally divided into primary and secondary. Primary bronchitis includes those in which the clinical picture is caused by isolated primary damage to the bronchi or combined damage to the nasopharynx, larynx and trachea. Secondary bronchitis is a complication of other diseases - influenza, whooping cough, measles, tuberculosis, chronic nonspecific diseases lungs, heart diseases and others. Inflammation can be primarily localized only in the trachea and large bronchi - tracheobronchitis, in the bronchi of medium and small caliber - bronchitis, in the bronchioles - bronchiolitis, which occurs mainly in infants and young children. However, such isolated local inflammation of the bronchi is observed only at the beginning of the development of the pathological process. Then, as a rule, the inflammatory process from one area of the bronchial tree quickly spreads to neighboring areas.

There are acute and chronic forms of bronchitis.

Acute form characterized by inflammation of the bronchial mucosa. Most often found in young children and the elderly. The disease is accompanied by a dry and sharp cough that gets worse at night. After a few days, the cough usually softens and is accompanied by sputum production.

Acute bronchitis, as a rule, occurs as a result of infection and occurs against the background of rhinitis, laryngitis, pharyngitis, tracheitis, influenza, catarrh, pneumonia and allergies. Bronchitis can be triggered by weakening of the body due to other diseases, addiction to alcohol and smoking, hypothermia, prolonged exposure to dampness, and high air humidity.

Harbingers of acute bronchitis are a runny nose, sore throat, hoarseness and sometimes temporary loss of voice, and a dry, painful cough. The temperature may rise, chills, body aches and general weakness may appear.

Acute inflammation of the bronchi can occur under the influence of many factors - infectious, chemical, physical or allergic. It occurs especially often in spring and autumn, since at this time hypothermia, colds and other diseases reduce the body's resistance.

Acute bronchitis occurs when an irritant or infection causes the tissue lining the bronchioles to become inflamed and swollen, narrowing the air passages. When the cells lining the air passages are irritated beyond a certain degree, the cilia (sensitive hairs) that normally catch and expel foreign objects stop working. Excessive mucus is then produced, which clogs the air passages and causes the characteristic bronchitis coughing. Acute bronchitis is common and symptoms usually go away within a few days.

Acute bronchitis can be either primary or secondary. It occurs mainly with catarrh of the upper respiratory tract and influenza, when the inflammatory process from the nasopharynx, larynx and trachea spreads to the bronchi. Acute bronchitis most often occurs in persons with foci of chronic inflammation in the nasopharynx - chronic tonsillitis, sinusitis, rhinitis, sinusitis, which are a source of constant sensitization of the body, changing it immunological reactions.

Most the usual reason acute bronchitis are viral infections (including the common cold and flu). Bacterial infections can also lead to the development of bronchitis.

Irritants such as chemical fumes, dust, smoke and other air pollutants can trigger an attack of bronchitis.

The risk of severe attacks of bronchitis is increased by smoking, asthma, poor nutrition, cold weather, congestive heart failure and chronic lung disease.

In general, acute bronchitis can develop:

When activating saprophytic microbes that are constantly present in the upper respiratory tract (for example, Frenkel pneumococci, Friedlander pneumobacilli, streptococci, staphylococci and others);

For acute infectious diseases - influenza, whooping cough, diphtheria and other infections;

Due to hypothermia, a sudden sharp change in body temperature, or when inhaling cold, moist air through the mouth;

When inhaling vapors of toxic chemicals - acids, formaldehyde, xylene, etc.

Most often, acute diffuse bronchitis develops under the influence of provoking factors: cooling of the body, acute infectious diseases of the upper respiratory tract, exposure to exogenous allergens (allergic bronchitis). A decrease in the body’s protective reactions also occurs with overwork and general exhaustion, especially after suffering mental trauma and against the background of serious illnesses.

At the beginning of the development of acute bronchitis, hyperemia (redness, indicating a sharply increased blood supply) and swelling of the bronchial mucosa with pronounced hypersecretion of mucus containing leukocytes and, less often, red blood cells occur. Then, in more severe cases, damage to the bronchial epithelium develops and the formation of erosions and ulcers, and in some places inflammation spreads to the submucosal and muscular layer of the bronchial wall and interstitial tissue (which surrounds the bronchi).

Those who suffer from diseases such as rhinitis, tonsillitis, sinusitis, and sinusitis are more likely to develop acute bronchitis. Bronchitis often occurs during acute infectious diseases (influenza, measles, whooping cough, typhoid fever). With increased sensitivity to the protein substance, acute bronchitis can develop when inhaling dust from animals or plants.

From the first day of the disease, antibiotics and sulfonamides are prescribed. To relieve bronchospasm, aminophylline, ephedrine, isadrine and other bronchodilators are used. Cupping, mustard plasters, and hot foot baths give a good effect, especially in the first days of the disease. Alkaline inhalations, inhaling steam, and frequent drinking of hot tea, hot milk with Borjomi or soda soften the cough.

For a dry, painful cough, stoptussin, codterpine, tusuprex, glaucine should be used (the drugs are used as prescribed by a doctor). If sputum is difficult to cough up, expectorants are given: bromhexine, potassium iodide, Doctor MOM, etc.

To treat acute bronchitis, mustard plasters, hot foot baths with mustard, drinking plenty of fluids, rubbing the chest, and inhalations are used. It is useful to drink marshmallow root syrup and licorice root infusion. Linden tea (sold in pharmacies) is effective.

For chronic bronchitis changes are observed in all structural elements of the bronchial wall, and the inflammatory process also involves lung tissue. The first symptom of chronic bronchitis is persistent cough, with which a lot of mucus is released, especially in the morning. As the disease progresses, breathing becomes increasingly difficult, especially during physical activity. Low oxygen levels in the blood cause the skin to appear bluish. If acute bronchitis lasts from several days to several weeks, then chronic bronchitis lasts for months and years. If acute bronchitis is not treated, it can lead to complications - cardiac and respiratory failure, pulmonary emphysema.

Chronic bronchitis can develop as a complication after acute or frequent repetition of acute bronchitis. In chronic bronchitis, not only the mucous membrane becomes inflamed, but also the walls of the bronchi themselves, along with the surrounding lung tissue. Therefore, chronic bronchitis is often accompanied by pneumosclerosis and emphysema. Main sign chronic bronchitis - dry paroxysmal cough, especially often appearing in the morning after a night's sleep, as well as in damp and cold weather. When coughing, purulent greenish sputum is coughed up. Over time, a patient with chronic bronchitis develops shortness of breath and pale skin. Heart failure may develop.

A common cause of chronic bronchitis is prolonged, repeated inhalation of irritating dusts and gases. The causes of chronic bronchitis can also be diseases of the nose, chronic inflammatory processes in the paranasal sinuses. The addition of this infection worsens the course of chronic bronchitis, causing the transition of the inflammatory process from the mucous membrane of the nose and sinuses to the walls of the bronchi and peribronchial tissue. Chronic bronchitis can be a consequence of acute bronchitis.

At the onset of the disease, the main symptom of chronic bronchitis is a cough, which gets worse in cold and damp weather. In most patients, cough is accompanied by sputum production. It occurs in attacks only in the morning or bothers the patient all day and even at night.

Symptoms of bronchitis also include increased fatigue, pain in the muscles of the chest and abdomen (caused by frequent coughing). Body temperature, usually normal, may rise during periods of exacerbation. Increased sensitivity to microflora and protein breakdown products in patients with chronic bronchitis can lead to bronchial asthma.

In the treatment of chronic bronchitis, especially in early period, it is important to eliminate all factors that irritate the bronchial mucosa: prohibit smoking, change professions associated with inhalation of dust, gases or vapors. The nose, paranasal sinuses, tonsils, teeth, etc., where there may be foci of infection, should be carefully examined and appropriate treatment should be carried out. It is important to ensure that the patient breathes freely through the nose.

Antibiotics are prescribed during periods of exacerbation of the disease after determining the sensitivity of microbes isolated from sputum to them. The duration of antibiotic treatment varies - from 1 to 3-4 weeks.

Sulfonamides occupy an important place in treatment, especially in cases of intolerance to antibiotics or the development of fungal diseases.

For the treatment of cough syndrome in chronic bronchitis, the following groups of drugs are used: - mucolytics (help thin the sputum) - acetylcysteine, ambroxol, bromhexine, etc.;

— mucokinetics (promote the removal of sputum) — thermopsis, potassium iodide, “Doctor MOM”;

- mucoregulators (have mucokinetic and mucolytic properties) - erispal, flui-fort;

- drugs that suppress the cough reflex. Bronchitis must be treated under the supervision of a doctor, but preparations with mustard can promote a speedy recovery.

Treatment of the disease is carried out only by a doctor. In addition to basic therapy, compresses, rubbing, teas for better mucus separation and inhalation are useful, especially those prepared on the basis of medicinal plants.

According to the severity of inflammation of the bronchi, bronchitis is distinguished as catarrhal, mucopurulent, purulent, fibrous and hemorrhagic; according to the prevalence of inflammation - focal and diffuse.

Symptoms

Deep, persistent cough producing grey, yellowish or green sputum.

Shortness of breath or difficulty breathing.

Fever.

Chest pain that gets worse with coughing.

Clinical picture. At the onset of the disease, patients note rawness in the throat and chest, hoarseness, cough, pain in the muscles of the back and limbs, weakness, and sweating. The cough at first is dry or with a scant amount of viscous, difficult to separate sputum; it can be rough, sonorous, often “barking” and appears in the form of attacks that are painful for the patient. During coughing attacks, a small amount of viscous, mucous sputum, often “vitreous,” is released with difficulty.

On the second or third day of the disease, during coughing attacks, pain is felt behind the sternum and in the places where the diaphragm is attached to the chest, sputum begins to be released more abundantly, first mucopurulent, sometimes mixed with streaks of scarlet blood, and then purely purulent. Subsequently, the cough gradually decreases and becomes softer, as a result of which the patient feels noticeable relief.

Body temperature at mild flow bronchitis can be normal or sometimes elevated for several days, but only slightly (low-grade fever). In severe cases of bronchitis, the temperature rises to 38.0-39.5 ° C and can remain this way for several days. The respiratory rate is usually not increased, but in the presence of fever it is increased slightly. Only when diffuse lesion small bronchi and bronchioles, severe shortness of breath occurs: the number of respirations can increase to 30, and sometimes up to 40 per minute, and an increase in heart rate (tachycardia) is often observed.

When percussing (tapping) the chest, the percussion sound is usually not changed, and only with diffuse inflammation of the small bronchi and bronchioles does it acquire a boxy tint. When listening, hard breathing and dry buzzing and (or) wheezing wheezing are detected, which may change (increase or decrease) after coughing.

During the period of “resolution” (subsidence) of the inflammatory process in the bronchi and liquefaction under the influence of proteolytic enzymes of viscous sputum, along with dry wheezing, moist, silent wheezing can be heard. X-ray examination does not reveal significant changes; only sometimes there is an increase in the pulmonary pattern in the hilar zone of the lungs.

Leukocytosis (up to 9000-11,000 in 1 μl) and acceleration of ESR can be detected in the blood.

In most cases, by the end of the first week, clinical signs of the disease disappear, and after two weeks, complete recovery occurs. In physically weakened individuals, the disease can last up to 3-4 weeks, and in some cases - with systematic exposure to harmful physical factors (smoking, cooling, etc.) - or the absence of timely and competent treatment - it can take a protracted, chronic course. The most unfavorable option is the development of a complication such as bronchopneumonia.

Diagnostics

A medical history and physical examination are necessary.

Chest X-rays and sputum and blood tests may be done to look for other lung diseases.

Treatment

Take aspirin or ibuprofen to reduce fever and pain.

Take a cough suppressant if you have a persistent dry cough. However, if you cough up phlegm, suppressing your cough can cause mucus to build up in your lungs and lead to severe complications.

Stay indoors in a warm area. Breathe steam, use a humidifier, take frequently hot shower to soften the mucus.

Drink at least eight glasses of water a day to help the mucus become less dense and easier to clear.

If your doctor suspects a bacterial infection, he may prescribe antibiotics.

Smokers should give up cigarettes.

Call your doctor if symptoms do not improve after 36 or 48 hours or if bouts of acute bronchitis recur.

Contact your doctor if you have a pulmonary condition or congestive heart failure and experience symptoms of acute bronchitis.

Call your doctor if you cough up blood, have shortness of breath, or have a high fever during a bout of bronchitis.

Prevention

Don't smoke and try to avoid secondhand smoke.

People with a predisposition to the disease should avoid being in areas where the air contains irritating particles such as dust, and avoid physical activity on days when the weather conditions are poor.

Acute bronchitis in children

As we already know, acute bronchitis is one of the manifestations of a viral infection with localization of the process in the bronchi. Due to the fact that acute bronchitis usually does not occur in isolation, but is combined with damage to other parts of the respiratory system, the disease essentially “dissolved” in diagnoses of acute respiratory viral infection or pneumonia. Very approximately, the share of acute bronchitis accounts for 50% of all respiratory diseases in children, especially in the first years of life.

The main pathological factor in the development of acute bronchitis can be practically equally both viral and bacterial, as well as mixed infection. However, viruses have highest value, and first of all - parainfluenza, respiratory syncytial and adenoviruses. Rhinoviruses, mycoplasmas and influenza viruses are relatively rare in this regard. It should also be noted that acute bronchitis in children is quite naturally observed with measles and whooping cough, but with rhino- or enterovirus infection- extremely rare.

Bacteria play the least role. The most common are staphylococcus, streptococcus and pneumococcus. It should be borne in mind that the bacterial flora is activated secondarily against the background of a previous viral infection. Except

In addition, bacterial bronchitis is observed when the integrity of the mucous membrane of the airways is disrupted (for example, by a foreign body). It should also be taken into account that a viral disease of the respiratory tract in the very first days takes on a viral-bacterial character.

Features of the development of the disease in childhood are, in fact, inextricably linked with the anatomical and physiological characteristics of the child’s upper respiratory tract. These, first of all, include: a significantly more abundant blood supply to the mucous membrane compared to adults, as well as age-related looseness under the mucous structures. Against the background of infection, these features ensure the rapid spread of the exudative-proliferative reaction along the continuation of the respiratory tract in depth - the nasopharynx, pharynx, larynx, trachea, bronchi.

As a result of exposure to viral toxins, the motor activity of the ciliated epithelium is suppressed. Infiltration and swelling of the mucous membrane, increased secretion of viscous mucus further slow down the “flickering” of the cilia, thereby turning off the main mechanism of cleansing the bronchi. The consequence of viral intoxication, on the one hand, and the inflammatory reaction, on the other, is a sharp decrease in the drainage function of the bronchi - difficulty in the outflow of sputum from the underlying parts of the respiratory tract. Which ultimately contributes to the further spread of infection, while simultaneously creating conditions for bacterial embolism into bronchi of a smaller diameter.

From the above, it is clear that acute bronchitis in childhood is characterized by a significant extent and depth of damage to the bronchial wall, as well as a pronounced inflammatory reaction.

It is known that the following forms of bronchitis are distinguished by extent:

Limited - the process does not extend beyond the segment or lobe of the lung;

Widespread - changes are observed in segments of two or more lobes of the lung on one or both sides;

Diffuse - bilateral damage to the airways.

Based on the nature of the inflammatory reaction, the following are distinguished:

Catarrhal;

Purulent;

Fibrinous;

Necrotic;

Ulcerative;

Hemorrhagic;

Mixed bronchitis.

In childhood, catarrhal, catarrhal-purulent and purulent forms of acute bronchitis are most common. Like any inflammatory process, it is composed of three phases: alterative, exudative and proliferative. A special place among diseases of the respiratory tract is occupied by bronchiolitis (capillary bronchitis) - a bilateral widespread inflammation of the final sections of the bronchial tree. Based on the nature of inflammation, bronchiolitis is divided in the same way as bronchitis. In the most common catarrhal bronchiolitis, swelling and inflammatory infiltration of the walls of the bronchioles are combined with complete or partial blockage of the lumen with mucous or mucopurulent discharge.

Clinical picture. For different variants of infection, the disease picture may have its own specific features. For example, parainfluenza is characterized by the formation of proliferations of the epithelium of small bronchi, and adenoviral bronchitis is characterized by an abundance of mucous deposits, loosening of the epithelium and rejection of cells into the bronchial lumen.

Here it should be emphasized once again that the decisive role in the development of narrowing of the airways in children does not belong to bronchospasm, but to increased secretion of mucus and swelling of the bronchial mucosa. And it should be noted that, despite the widespread prevalence of the disease and its well-known clinical picture, the doctor is often overcome by serious doubts when making a diagnosis due to the variety of symptoms, as well as the often present component of respiratory failure. The latter circumstance can play a decisive role in interpreting the process as pneumonia, which later turns out to be incorrect.

Acute bronchitis is a disease that manifests itself during an acute respiratory viral infection. Therefore, it is characterized by:

Connection with an infectious process;

The evolution of the general condition corresponds to the evolution of the infectious process;

Catarrhal phenomena in the nasopharynx and pharynx, preceding the onset of bronchitis.

The temperature reaction is usually due to an underlying infectious process. Its severity varies in each specific case depending on individual characteristics, and the duration ranges from one day to a week (on average 2-3 days). It should always be remembered that children lack elevated temperature does not exclude the presence of an infectious process.

Cough, dry and wet, is the main symptom of bronchitis. In the initial period it is dry and painful. Its duration varies. Usually, at the end of the first week or at the beginning of the second, the cough becomes wet, with sputum, and then gradually disappears. In young children, cough often persists for more than 14 days, although the total period rarely exceeds three weeks. A prolonged dry cough, often accompanied by a feeling of pressure or pain in the chest, indicates involvement of the trachea in the process (tracheitis, tracheobronchitis).

The “barking” tone of a cough indicates damage to the larynx (laryngitis, laryngotracheitis, laryngotracheobronchitis).

During a physical examination, either a clear pulmonary sound or a pulmonary sound with a box-like tint is determined by percussion, which is determined by the presence or absence of bronchial constriction and its degree. During auscultation, all types of wheezing, dry and wet, including fine bubbling, are heard. It should be borne in mind that fine bubbling moist rales indicate only damage to the smallest bronchi. The origin of these wheezes, as well as dry, large- and medium-bubbly wet ones, is exclusively bronchial in nature.

X-ray changes manifest themselves as an intensification of the pattern of the lungs, small shadows are visible - most often in the lower and hilar zones, symmetrically on both sides. The inflammatory process in the mucous membrane of the respiratory tract is accompanied by vascular hyperemia and increased lymph production. As a result, the pattern becomes stronger along the bronchovascular structures, which makes it more and more abundant, the shadows become wider, and the clarity of the contours deteriorates. The increased outflow of lymph, directed towards the regional lymph nodes, creates a picture of a basal strengthening of the pattern, in which blood vessels also take part. The roots of the lungs become more intense, their structure moderately deteriorates, i.e., the clarity of the elements that make up the root pattern. The smaller the bronchial branches involved in the process, the more abundant and indistinct the enhanced pattern appears.

Reactive enhancement of the lung pattern lasts longer than the clinical manifestations of bronchitis (on average 7-14 days). Infiltrative changes in the lungs that cover or blur small elements of the pulmonary pattern are absent in bronchitis.

Changes in the blood during bronchitis in a child are determined by the nature of the infection - predominantly viral or bacterial.

Acute simple bronchitis is one of the manifestations of a respiratory viral infection that occurs sequentially in a descending direction, affecting the nasopharynx, larynx, trachea and occurring in the absence of clinical signs of airway obstruction.

The main complaints are fever, runny nose, cough, and often pain in the throat when swallowing. Characteristic is the evolution of a cough, sometimes accompanied (with tracheobronchitis) by a feeling of pressure or even pain in the chest. Dry, obsessive at the beginning of the disease, this cough becomes wet in the second week and gradually disappears. Its persistence for more than two weeks is observed in young children with certain types of ARVI (acute respiratory viral infection), more often caused by adenoviruses. Longer persistence of a cough should be alarming and serve as a reason for a more in-depth examination of the patient, searching for possible aggravating factors (it should be remembered that the persistence of a cough for 4-6 weeks (without signs of bronchitis or other pathology) is observed after tracheitis.

Acute obstructive bronchitis is a disease characterized clinically pronounced signs obstruction of the respiratory tract: noisy breathing with prolonged exhalation, whistling, audible at a distance, wheezing and persistent cough (dry or wet). The terms “spastic bronchitis” or “asthmatic syndrome,” which are sometimes used to denote this form, are narrower, since they associate the development of narrowing of the bronchi only with their spasm, which is, however, not always observed.

The clinic of obstructive bronchitis occupies an intermediate position between simple and bronchiolitis. The complaints are basically the same. Objectively, during an external examination, attention is drawn to the phenomena of moderately severe respiratory failure (shortness of breath, cyanosis, participation of auxiliary muscles in the act of breathing), the degree of which is usually low. The general condition of the child, as a rule, does not suffer.

A boxy tint of the sound is noted by percussion; During auscultation, a prolonged exhalation, sounds on exhalation, dry, large- and medium-bubbly moist rales, mainly also on exhalation, are heard. All the phenomena determined by the course of a viral infection are also present.

Acute bronchiolitis is a type of disease of the terminal sections of the bronchi in young children, accompanied by clinically pronounced signs of airway obstruction.

Typically, the first symptoms of a respiratory disease appear: serous runny nose, sneezing. The deterioration of the condition may develop gradually, but in many cases it occurs suddenly. In this case, as a rule, a cough occurs, which is sometimes paroxysmal in nature. The general condition is disturbed, sleep and appetite worsen, the child becomes irritable. The picture develops more often at a slightly elevated or even normal temperature, but is accompanied by tachycardia and shortness of breath.

Upon examination, the child gives the impression of being seriously ill with clear signs of respiratory failure. The flaring of the wings of the nose during breathing is determined, the participation of auxiliary muscles in the act of breathing is manifested by retraction of the intercostal spaces of the chest. With pronounced degrees of obstruction, an increase in the anteroposterior diameter of the chest is clearly visible.

Percussion reveals a box tone over the lungs, a decrease in the zones of dullness over the liver, heart, and mediastinum. The liver and spleen are usually palpated several centimeters below the costal arch, which is a sign not so much of their enlargement as of displacement as a result of swelling of the lungs. Tachycardia is pronounced, sometimes reaching a high degree. In both lungs, multiple fine rales are heard over the entire surface, both during inhalation (at the end of it) and during exhalation (at the very beginning).

This picture of a “wet lung” can be supplemented by medium- or large-bubbly wet, as well as dry, sometimes wheezing wheezing, changing or disappearing with coughing.

Treatment of bronchitis in children

The so-called etiotropic (that is, directly affecting the pathogenic agent, for example, bacterial) for bronchitis includes the following groups of drugs:

Antibiotics;

Antiseptics (sulfonamides, nitrofurans);

Biological nonspecific protective factors (interferon).

As mentioned earlier, the advisability of using antibiotics in the treatment of bronchitis, and in particular in children, is disputed by many authors today, but we will not raise this issue here: it is quite specific, and therefore there is no point in discussing it in this book. However, there are very specific indications for prescribing the above remedies for bronchitis in children, which boil down to three main points, namely:

Possibility or direct threat of developing pneumonia;

Prolonged temperature reaction or high temperature in a child;

Development of general toxicosis,

Finally, the lack of a satisfactory effect from all types of therapy carried out previously.

Let's consider the features of antibiotic therapy in childhood, since a child's body reacts to some medications differently than a fully formed adult. Therefore, adequate (in other words, necessary and sufficient) treatment in terms of dosages is especially important, so as not to cause harm and to avoid some complications that are possible with irrational therapy with drugs from the above pharmacological groups.

Antibiotics

Penicillin group drugs

Benzylpenicillin potassium and sodium salts: children under two years old - 50,000-100,000-200,000 (maximum, according to special indications) IU/kg body weight per day; from two to five years - 500,000 units, from five to ten years - 750,000 units and, finally, from 10 to 14 years - 1000,000 units per day. The frequency of administration is at least 4 times and no more than 8, respectively, every 3-4-6 hours. It must be remembered that if there are indications for intravenous administration, then only the sodium salt of benzylpenicillin can be injected into the vein.

Methicillin sodium salt - for children up to three months - 50 mg/kg body weight per day, from three months to two years - 100 mg/kg per day, over 12 years - adult dose - (from 4 to 6 g per day). It is administered intramuscularly and intravenously. The frequency of administration is at least two and no more than four times, respectively, every 6-8-12 hours.

Oxacillin sodium salt - children up to one month - 20-40 mg/kg body weight per day, from one to three months - 60-80 mg/kg, from three months to two years - 1 g per day, from two to six years - 2 g, over six years - 3 g. Administered intramuscularly and intravenously. The frequency of administration is at least twice a day and no more than four times, respectively, every 6-8-12 hours. It is given orally 4-6 times a day 1 hour before meals or 2-3 hours after meals in the following doses: up to five years - 100 mg/kg per day, over five years - 2 g per day.

Ampicillin sodium salt - up to 1 month of life - 100 mg/kg body weight per day, up to 1 year - 75 mg/kg body weight per day, from one to four years - 50-75 mg/kg, over four years - 50 mg /kg. It is administered intramuscularly and intravenously. The frequency of administration is at least two times and no more than four times a day, respectively, every 6-8 or 12 hours.

Ampiox - up to one year - 200 mg/kg body weight per day, from one to six years - 100 mg/kg, from 7 to 14 years - 50 mg/kg. It is administered intramuscularly and intravenously. The frequency of administration is at least two and no more than four times a day, respectively, every 6-8-12 hours.

Dicloxacillin sodium salt - up to 12 years - from 12.5 to 25 mg/kg body weight per day in four doses, orally, 1 hour before meals or 1-1.5 hours after meals.

Macrolide drugs

Erythromycin (at one dose) up to two years - 0.005-0.008 g (5-8 mg) per kilogram of body weight, from three to four years - 0.125 g, from five to six years - 0.15 g, from seven to nine - 0.2 g, from ten to fourteen - 0.25 g. Used orally four times a day 1-1.5 hours before meals.

Erythromycin ascorbate and phosphate are prescribed at the rate of 20 mg/kg body weight per day. It is administered intravenously slowly after 8-12 hours, 2 or 3 times, respectively.

Oleandomycin phosphate - up to three years - 0.02 g/kg body weight per day, from three to six years - 0.25-0.5 g, from six to fourteen years - 0.5-1.0 g, over 14 years -1.0-1.5 g per day. Taken orally, 4-6 times a day. Can be administered intramuscularly and intravenously to children under three years of age - 0.03-0.05 g/kg body weight per day, from three to six years - 0.25-0.5 g, from six to ten years - 0.5- 0.75 g, from ten to fourteen years - 0.75-1.0 g per day. It is administered 3-4 times, respectively, every 6-8 hours.

Drugs of the amipoglycoside group

Gentamicin sulfate - 0.6-2.0 mg/kg body weight per day. It is administered intramuscularly and intravenously 2-3 times a day, respectively, after 8-12 hours.

Preparations of the chloramphenicol group - chloramphenicol sodium succinate - the daily dose for children under one year of age is 25-30 mg/kg of body weight, for children over one year of age - 50 mg/kg of body weight. It is administered intramuscularly and intravenously twice a day, respectively, after 12 hours. Contraindicated in children with symptoms of hematopoietic suppression and under the age of one year.

Cephalosporins

Cephaloridine (synonym - ceporin), kefzol - for newborns the dose is 30 mg/kg body weight per day, after one month of life - an average of 75 mg/kg body weight (from 50 to 100 mg/kg). It is administered intramuscularly and intravenously 2-3 times a day, respectively, after 8-12 hours.

Antibiotics of other groups

Lincomycin hydrochloride - 15-30-50 mg/kg body weight per day. It is administered intramuscularly and intravenously twice a day every 12 hours.

Fuzidin sodium: prescribed orally in doses: up to 1 year - 60-80 mg/kg body weight per day, from one to three years - 40-60 mg/kg, from four to fourteen years - 20-40 mg/kg.

On average, the course of antibiotic therapy in children with bronchitis is 5-7 days. For gentamicin, chloramphenicol - no more than 7 days, and only for special indications - up to 10-14 days.

In addition, in some cases it may be advisable to use combinations of two or three antibiotics (specially designed tables exist to determine their mutual compatibility and chemical compatibility). Such expediency is determined by the patient’s condition, often severe.

Sulfonamides

The most commonly used are: biseptol-120 (bactrim), sulfadimethoxine, sulfadimezin, norsulfazole.

Biseptol-120, containing 20 mg of trimethoprim and 100 mg of sulfamethoxazole, is prescribed to children under two years of age at the rate of 6 mg of the first and 30 mg of the second of these drugs per 1 kg of body weight per day. From two to five years - two tablets in the morning and evening, from five to twelve years - four. Bactrim, which is an analogue of Biseptol, is recalculated taking into account the fact that one teaspoon of it corresponds to two tablets of Biseptol No. 120.

Sulfadimethoxine is prescribed to children under four years of age once: on the first day - 0.025 mg/kg body weight, on subsequent days - 0.0125 g/kg. Children over four years old: on the first day - 1.0 g, on subsequent days - 0.5 g daily. Take 1 time per day.

Sulfadimezin and norsulfazole. Children under two years of age - 0.1 g/kg body weight on 1 day, then 0.025 g/kg 3-4 times every 6-8 hours. Children over two years old - 0.5 g 3-4 times a day.

Niftrofurans (furadonin, furazolidone) are used much less frequently. The daily dose of the drug is 5-8 mg/kg body weight for children under two years of age. Take 3-4 times a day.

The general course of sulfonamide or nitrofuran therapy averages 5-7 days and in rare cases can be extended to 10.

Chronic bronchitis

Chronic bronchitis is one of several lung diseases that are collectively called chronic obstructive diseases. Chronic bronchitis is defined as the presence of a cough with mucus that continues for at least three months, two years in a row. This cough occurs when the tissues lining the bronchi (the branches of the trachea through which air is inhaled and exhaled air passes) become irritated and inflamed. Although the onset of the disease is gradual, as it progresses relapses become more frequent and the cough may become persistent as a result. Long-term chronic bronchitis causes the air passages of the lungs to become irreversibly narrow, making breathing very difficult. Chronic bronchitis cannot be completely cured, but treatment nevertheless relieves symptoms and prevents complications from occurring.

Chronic bronchitis is a long-term inflammatory disease of the mucous membrane of the bronchi and bronchioles.

Infection plays an important role in the development and course of the disease. Chronic bronchitis can develop due to acute bronchitis or pneumonia. An important role in its development and maintenance is also played by long-term irritation of the bronchial mucosa by various chemicals and dust particles inhaled in the air, especially in cities with a damp climate and sudden changes in weather, in industries with significant dust or increased saturation of the air with chemical vapors. Autoimmune allergic reactions that occur due to the absorption of protein breakdown products formed in areas of inflammation also play a certain role in the maintenance of chronic bronchitis.

Smoking is no less important in the development of chronic bronchitis: the number of people suffering from bronchitis among smokers is 50-80%, and among non-smokers - only 7-19%.

Causes

Smoking is the main cause of chronic bronchitis. About 90 percent of patients smoked. Passive smoking also affects the development of chronic bronchitis.

Substances that irritate the lungs (gas emissions from industrial or chemical plants) can harm the respiratory tract. Other air pollutants also contribute to the development of the disease.

Repeated lung infections can damage the lungs and make the disease worse.

Symptoms

Constant cough with mucus, especially in the morning.

Frequent lung infections.

Clinical picture. At the very beginning of the disease, the bronchial mucosa is congested, hypertrophied in places, and the mucous glands are in a state of hyperplasia. Subsequently, inflammation spreads to the submucosal and muscular layers, in place of which scar tissue forms; the mucous and cartilaginous plates atrophy. In places where the bronchial wall is thinned, their lumen gradually expands - bronchiectasis is formed.

The process may also involve peribronchial tissue with further development interstitial pneumonia. The interalveolar septa gradually atrophy and pulmonary emphysema develops.

The clinical picture as a whole is quite characteristic and well studied, however, all manifestations of chronic bronchitis strongly depend on the extent of inflammation throughout the bronchi, as well as on the depth of damage to the bronchial wall. The main symptoms of chronic bronchitis are cough and shortness of breath.

Cough may have different character and change depending on the time of year, atmospheric pressure and weather. In summer, especially dry, the cough is insignificant or completely absent. With high air humidity and in rainy weather, the cough often intensifies, and in the autumn-winter period it becomes strong and persistent with the release of viscous mucopurulent or purulent sputum. More often, a cough occurs in the morning, when the patient begins to wash or get dressed. In some cases, the sputum is so thick that it is released in the form of fibrous strands that resemble casts of the lumen of the bronchi.

Dyspnea in chronic bronchitis is caused not only by impaired drainage function of the bronchi, but also by secondary developing pulmonary emphysema. It is often of a mixed nature. At the beginning of the disease, difficulty breathing is observed only during physical activity, climbing stairs or uphill. In the future, with the development of pulmonary emphysema and pneumosclerosis, shortness of breath becomes more pronounced. With diffuse inflammation of the small bronchi, shortness of breath takes on an expiratory nature (predominant difficulty in exhaling).

Observed and general symptoms illnesses - malaise, fatigue, sweating, body temperature rarely rises. In uncomplicated cases of the disease, palpation and percussion of the chest do not reveal any changes. Auscultation reveals vesicular or harsh breathing, against which dry buzzing and whistling sounds, as well as silent moist rales, are heard. In advanced cases, upon examination, palpation, percussion and auscultation of the chest, changes characteristic of pulmonary emphysema and pneumosclerosis are determined, and signs of respiratory failure appear.

Changes in the blood occur only during exacerbations of the disease: the number of leukocytes increases, the ESR accelerates.

X-ray examination of uncomplicated bronchitis usually does not reveal pathological changes. With the development of pneumosclerosis or emphysema, corresponding radiological signs appear. Bronchoscopy reveals a picture of atrophic or hypertrophic bronchitis (i.e., with thinning or swelling of the bronchial mucosa).

The obstructive nature of chronic bronchitis is confirmed by data from a functional study (in particular, spirography).

Improvement in pulmonary ventilation and respiratory mechanics with the use of bronchodilators indicates bronchospasm and reversibility of bronchial obstruction.

Differential diagnosis of chronic bronchitis is carried out primarily with chronic pneumonia, bronchial asthma, tuberculosis, lung cancer and pneumoconiosis.

Treatment of patients with chronic bronchitis should begin at the earliest possible stage. It is important to eliminate all factors that cause irritation of the bronchial mucosa. It is necessary to sanitize any chronic foci of infection and ensure free breathing through the nose. It is often more appropriate to treat patients with exacerbation of bronchitis in a hospital.

Further course and complications. One of the most unfavorable manifestations of chronic bronchitis, which largely determines its prognosis, is the development of obstructive disorders in the bronchial tree. The causes of this type of pathology may be changes in the mucous and submucous membranes of the bronchi, which develops due to a fairly long-term inflammatory reaction with infiltration of the walls and spasm of not only large bronchi, but also the smallest bronchi and bronchioles, narrowing of the lumen of the entire bronchial tree big amount secretions and sputum. The described disturbances in the bronchial tree lead, in turn, to disturbances in ventilation processes. With an unfavorable development of the process, arterial hypertension of the pulmonary circulation subsequently develops and a picture of the so-called “chronic pulmonary heart” is formed.

Bronchospastic syndrome can occur in any form of chronic bronchitis and is characterized by the development of expiratory shortness of breath, and if bronchospasm occupies the main place in the overall clinical picture of the disease, chronic bronchitis is defined as asthmatic.

Symptoms and clinical picture depend on the caliber of the affected bronchi. The first symptoms of chronic bronchitis: cough with or without sputum, more typical for damage to large bronchi, progressive shortness of breath, more often with damage to small bronchi. The cough may occur paroxysmally only in the morning, or it may bother the patient all day and then at night. More often, the inflammatory process first affects the large bronchi and then spreads to the small ones. Chronic bronchitis begins gradually, and for many years, except for an occasional cough, nothing bothers the patient. Over the years, the cough becomes constant, the amount of sputum produced increases, and it becomes purulent in nature. As the disease progresses, it becomes involved in pathological process increasingly smaller bronchi, which leads to pronounced disturbances in pulmonary and bronchial ventilation. During periods of exacerbation of chronic bronchitis (mainly in the cold and damp seasons), cough, shortness of breath, fatigue, weakness intensify, the amount of sputum increases, body temperature rises, often slightly, chilliness and sweating appear, especially at night, pain in various muscle groups caused by frequent cough. Exacerbation of obstructive bronchitis is manifested by an increase in shortness of breath (especially during physical exertion and the transition from heat to cold), the release of a small amount of sputum after a paroxysmal painful cough, prolongation of the exit phase and the appearance of wheezing dry rales on exhalation.

The presence of obstruction determines the prognosis of the disease, since it leads to the progression of chronic bronchitis, to emphysema, the development of cor pulmonale, the occurrence of atelectasis (areas of compaction in the lung tissue), and, as a consequence, to pneumonia. In the future, the clinical picture is determined by developing changes in the lungs and heart. Thus, when the disease is complicated by chronic pulmonary heart disease, during an exacerbation the symptoms of heart failure increase, pulmonary emphysema appears, and severe respiratory failure occurs.

At this stage, the development and progression of bronchiectasis is possible; when coughing, a large amount of purulent sputum is released, and hemoptysis is possible. Some patients with asthmatic bronchitis may develop bronchial asthma.

In the acute phase, both weakened vesicular and harsh breathing can be heard, and the number of dry whistling and moist rales over the entire surface of the lungs often increases. Outside of an exacerbation, they may not exist. There may be no changes in the blood even during an exacerbation of the disease. Sometimes moderate leukocytosis, shift leukocyte formula left, small increase in ESR. Macroscopic, cytological and biochemical examination of sputum is of great importance. With a severe exacerbation of chronic bronchitis, the sputum is purulent in nature, mostly leukocytes, DNA fibers, etc. are found in it; in case of asthmatic bronchitis, eosinophils, Kurschmann spirals, and Charcot-Leyden crystals, characteristic of bronchial asthma, may be observed in the sputum.

At the same time, radiological symptoms in most patients are not detected for a long time. In some patients, radiographs show uneven enhancement and deformation, as well as changes in the contours of the pulmonary pattern; with emphysema, an increase in the transparency of the pulmonary fields.

During the course of chronic bronchitis, significant variability is observed in different patients. Sometimes people suffer from bronchitis for many years, but functional and morphological disorders are less pronounced. In another group of patients, the disease gradually progresses. It worsens under the influence of cooling, most often in the cold season, in connection with influenza epidemics, in the presence of unfavorable professional factors etc. Repeated exacerbations of bronchitis lead to the development of bronchiectasis, emphysema, pneumosclerosis, signs of respiratory and then pulmonary heart failure appear.

Chronic bronchopulmonary respiratory failure is designated by the term “chronic pulmonary failure” and its three degrees are distinguished, depending on the severity of clinical manifestations.

Patients with severe pulmonary insufficiency are characterized by a cough with the release of a significant amount of sputum, constant shortness of breath, signs of heart failure: cyanosis, liver enlargement (on average, usually 2-3 cm), sometimes edema lower limbs. X-ray of the chest reveals significant emphysema in all patients, and the nature of ventilation disorders is of a mixed type.

Diagnostics

A medical history and physical examination help make the diagnosis of chronic bronchitis.

To confirm weakened lung function in a patient, a lung function test is performed (measurement of the volume of air held).

X-rays can detect damage to the lungs and help identify other diseases, such as lung cancer.

To determine the oxygen content and carbon dioxide An arterial blood test is performed in the blood.

General condition at simple bronchitis is caused by a reaction to infection (in the absence of toxicosis - satisfactory or moderate), and with obstructive bronchitis it is also determined by the degree of obstruction, and, consequently, the severity of respiratory failure.

The cough with simple bronchitis is usually dry; it becomes wet at the end of the first or beginning of the second week of the disease. With obstructive bronchitis, the cough is dry, persistent, painful in the first week, and deep, moist, rich in overtones in the second. Cough with bronchiolitis is frequent, painful, deep, increasing as it resolves.

Respiratory failure: absent in simple bronchitis; with obstructive respiratory failure, respiratory failure of the first, rarely second degree is possible, and with bronchiolitis it is pronounced, and is more often of the second or third degree.

Character of shortness of breath: absent in simple bronchitis, expiratory in the presence of obstruction.

Percussion: pulmonary sound in case of simple bronchitis, box tone in the presence of obstruction.

Auscultation: breathing is harsh or vesicular in simple bronchitis with the usual ratio of inhalation and exhalation phases. With obstructive bronchitis, bronchiolitis, exhalation is difficult and prolonged. Wheezing in simple bronchitis is scattered, a few dry and mostly large-bubbly - wet, disappearing almost completely after coughing. With obstructive bronchitis - a large number of dry and moist rales (both small and medium bubble), numerous, heard symmetrically throughout the entire length of the lungs. Their quantitative dynamics are almost independent of cough.

It is usually not difficult to distinguish severe bronchiolitis from milder obstructive bronchitis: with bronchitis there are no signs of severe respiratory failure. At the same time, there is an adjacent zone where it can be difficult to differentiate these two forms. In these cases, one should be guided by the presence of abundant fine wheezing, which is typical for bronchiolitis. This is important when differentiating from pneumonia, whereas in patients with obstructive bronchitis without moist rales, the main diagnostic problem is to exclude bronchial asthma.

Treatment

The progression of the disease may slow down as a result of smoking cessation. It is also recommended to avoid second-hand smoke and other lung irritants.

Moderate outdoor exercise can help prevent the disease from developing and will generally increase your ability to exercise.

Drinking plenty of fluids and breathing moist air (such as using a humidifier) will help make the mucus less dense. Cold, dry air should be avoided.

To make breathing easier, a bronchodilator may be prescribed, which dilates the bronchi.

If bronchodilators do not work, a steroid may be prescribed to take by mouth or as an inhaler. Patients taking steroids should be monitored by a doctor to determine whether breathing improves. If there is no response to the medication, steroid therapy may be interrupted.

Additional oxygen supply helps patients with low oxygen levels in the blood; for them it can help prolong life.

Antibiotics are prescribed to treat new infections to help prevent symptoms from getting worse. Permanent treatment antibiotics are not recommended.

Certain exercises can help clear mucus from your lungs and improve your breathing. Your doctor can give you instructions on how to do the exercises.

Call your doctor if you have a persistent cough that produces mucus and the amount of mucus increases, the color darkens, or you notice blood in the mucus.

Contact your doctor if you have a persistent cough in the morning.

Contact your doctor if you experience shortness of breath or other types of difficulty breathing.

Seek immediate medical attention if the skin on your face turns bluish or purple.

Treatment of bronchitis should be based on the etiology, pathogenesis and clinical picture of the disease. Depending on severity clinical picture Prescribe more or less strict rest, and at high temperatures, bed rest. It is necessary to strictly prohibit the patient from smoking and humidify the dry air in the room. Food should be easily digestible and rich in vitamins. At the same time, drinking plenty of fluids is recommended, and diaphoretic infusions (linden blossom, raspberries, black elderberry, and others) are advisable. Mustard plasters or jars at night are useful, especially in the initial stages of the disease.

Interferon is prescribed in the first 2 days (no later) 1-2 drops in both nostrils 4-6 times a day, up to 5 days.

If a painful cough occurs, antitussives are prescribed for 3-4 days. A good drug is glaucine hydrochloride; An infusion of ipecac root (pharmaceutical form) is also prescribed, 1 tablespoon every 3-4 hours for three days.

For bronchospasm, bronchodilators are also used: theophedrine (1/2, 1 tablet 3 times a day), aminophylline (0.15 g 3 times a day) are effective.

In general, we can say that pathogenetic therapy for bronchitis should be aimed at:

Restoring the drainage function of the bronchi,

In the presence of obstruction - to restore their patency.

Taking into account the above, drug therapy for bronchitis mainly consists of the following:

Expectorants and sputum thinners (mucolytics);

Bronchodilators;

Means of increasing oxygenation (supplying the body with oxygen).

Expectorants and sputum thinners are administered orally or by inhalation. A separate chapter is devoted to inhalation therapy for bronchitis; here we will focus only on the group of enzyme preparations.

Trypsin is a proteolytic enzyme, 2-5 mg of which is dissolved in 2-4 ml of isotonic sodium chloride solution and used as an aerosol once a day; the course lasts from 7 to 10 days. Chymotrypsin is more persistent than trypsin and inactivates more slowly. Indications for use, method, doses are the same as for crystalline trypsin. Another enzyme preparation is ribonuclease. 10-25 mg of the drug is dissolved in 3-4 mg of isotonic sodium chloride solution or 0.5% novocaine. The course is 7-8 days. Deoxyribonuclease - 2 mg per 1 ml of isotonic sodium chloride solution, 1-3 ml per inhalation for 10-15 minutes 3 times a day. Course 7-8 days.

Experimental and clinical observations have shown that enzyme preparations help reduce the viscosity of tracheobronchial secretions, cleanse the respiratory tract of purulent exudate, mucus, necrotic masses, regeneration and epithelization of the respiratory tract mucosa.

At home, steam inhalation of a 2% solution of sodium bicarbonate or essential oils is effective. In addition, anise oil is taken as an expectorant, 2-3 drops in a spoon of warm water per dose (up to six times a day).

Concerning internal funds, among mucolytics, widely known prescriptions for complex expectorant mixtures based on marshmallow root or thermopsis herb are used (respectively: 3.0 per 100.0 ml or 6.0 per 180.0 ml, 0.6 per 180.0 ml or 1.0 per 200.0 ml). To a recipe containing an infusion of marshmallow or thermopsis, add sodium bicarbonate up to 3-5 g, ammonia-anise drops and sodium benzoate 2-3 g each, syrup up to 20 g. The mixture is prescribed one teaspoon, dessert or tablespoon, depending on age .

Breast preparations No. 1 and No. 2 have proven themselves well (standard dosage forms, available in retail pharmacies). Collection No. 1 contains 4 parts of marshmallow root, 4 parts of coltsfoot leaves and 2 parts of oregano herb, and No. 2 contains 4 parts of coltsfoot leaves, 3 parts of plantain leaves, and 3 parts of licorice roots. The infusion is prepared at the rate of one tablespoon of the mixture per glass of boiling water.

In case of difficult to separate sputum (especially in the case of tracheobronchitis), expectorants are prescribed, including mucaltin - in tablets of 0.05, glaucine hydrochloride in tablets of 0.1. The dosage varies depending on the age of the patient and the degree of clinical manifestations. The mucolytic ACC (M-acetyl-1 cysteine (usually in soluble tablets or powders) is also widely used). The drug has the property of destroying the disulfide bonds of sputum mucoproteins and thus reduces their viscosity.

A number of expectorants have bronchodilator, antispastic, anti-inflammatory and sedative effects. Therapy with expectorants is assessed by the dynamics of changes in the amount of sputum per day or secreted in the first hour after waking up.

Taking into account that the inflammatory process can contribute to the development of bronchospasm (secondarily), it is necessary in some cases to use bronchodilators. Preference is given to aminophylline, mainly given its mild and multifaceted effect (improvement of pulmonary, coronary and cerebral circulation, diuretic effect). It is prescribed intravenously in a slow stream alone or in an isotonic solution of sodium chloride; 2.4% solution 10.0 ml (or 2-5 mg/kg per dose). For intramuscular administration, 12% and 24% solutions are used.

Oxygen therapy is carried out with humidified oxygen through a mask for 10-15 minutes every 2-3 hours with initial manifestations of respiratory failure, and through nasal catheters every 1-2 hours for 10-15 minutes with increasing symptoms of respiratory failure.

However, it should be remembered that oxygenation with positive pressure on exhalation (according to Martin Boyer or Gregory) for any form of obstructive bronchitis is strictly contraindicated (acute emphysema is possible).

Symptomatic treatment of acute bronchitis is determined by the clinical picture of the underlying disease - acute respiratory viral infection and includes the prescription of antipyretics and sedatives. In children with toxicosis, multidisciplinary infusion therapy is used, but this is a rather specialized issue, and we will not consider it in detail here.

The complex of therapeutic measures for chronic bronchitis is determined by its stage. General therapeutic measures for all forms of chronic bronchitis: absolute prohibition of smoking, elimination of substances that constantly irritate the mucous membrane of the respiratory tract (at home and at work), lifestyle regulation, sanitation of the upper respiratory tract, increasing the body's resistance, therapeutic physical training, physiotherapy, inhalations , expectorants.

For viscous sputum, enzyme preparations (trypsin, chymopsin) are used endobronchially, modern mucolytic agents (acetylcysteine, bromhexine) endobronchially and orally.

Well-known expectorants also contribute to the removal of sputum. plant origin with their rational selection and acceptance.

Expectorant medications make coughing easier, thin mucus, or reduce secretion. They are appointed:

When secretion is delayed or when very copious discharge secretion, threatening pulmonary edema; in this case it is necessary to induce a cough;

With a cough that greatly bothers the patient;

With a dry cough and no sputum; when sputum is produced, the cough should become soft and wet;

For foul-smelling sputum as a result of decomposition processes in the lungs and bronchi for disinfection, deodorization and reduction of secretions.

It should be borne in mind that there are certain contraindications for prescribing expectorants for chronic bronchitis:

Hemoptysis;

If the respiratory tract is dry, you should not take medications that reduce secretion;

In case of threatening pulmonary edema, medications that suppress cough or increase and dilute secretion should not be prescribed;

Caution is also necessary when prescribing expectorants to pregnant women.

Medicines of the next group tend to be secreted by the bronchi, causing dilution of bronchial secretion, increasing it and facilitating expectoration, as well as enhancing the resorption capacity of the lungs. They are often used simultaneously with emollients or mild secretomotor agents.

Ammonia and its salts. Ammonia salts taken orally are secreted by most of the bronchial mucosa in the form of carbonates, which have the property of enhancing and diluting bronchial secretion (mucin). The use of these salts is most indicated in the presence of acute and subacute inflammatory processes of the respiratory tract and bronchitis. With the existing abundant and liquid bronchial secretion (in chronic cases), taking them becomes useless. The effect of ammonia preparations is short-lived, so it is necessary to use them every 2-3 hours.

Ammonium chloride. It is secreted by part of the bronchial mucosa in the form of ammonium carbonate, which acts as a base, enhancing the secretion of mucous glands and diluting phlegm, which facilitates the movement of secretions outward. Prescribed mainly for bronchitis with scanty secretion orally - adults 0.2-0.5 g, children 0.1-0.25 g per dose every 2-3 hours (3-5 times a day) at 0.5- 2.5% solution, or in powder form in capsules. The drug should be taken after meals. In large doses, the local action may be accompanied by reflex stimulation of the vomiting center, coming from the gastric mucosa, sometimes accompanied by a feeling of nausea.

Ammonia-anise drops. Ingredients: anise oil 2.81 g, ammonia solution 15 ml, alcohol up to 100 ml. (1 g of drug = 54 drops). Transparent, colorless or slightly yellowish liquid with a strong anise or ammonia odor. 1 g of the drug with 10 ml of water forms a milky-turbid liquid of an alkaline reaction. Used as an expectorant, especially for bronchitis. Prescribe 10-15 drops every 2-3 hours 5-6 times a day on their own (diluted in water, milk, tea); often added to expectorant mixtures: ipecac, thermopsis, primrose, senega. Children: 1 drop per year of life, 4-6 times a day (every 2-3 hours). Incompatible with codeine salts and other alkaloids, with acidic fruit syrups, iodine salts.

Alkalis and sodium chloride. The main indication for the use of alkaline-salty mineral waters is catarrh of the mucous membranes of the pharynx and respiratory tract. The use of alkalis is based on their ability to dissolve mucin.

Sodium bicarbonate. Resorbing even in small quantities, sodium bicarbonate increases the alkaline reserve of the blood; the secretion of the bronchial mucosa also becomes alkaline, which leads to the dilution of sputum. Prescribed orally 0.5-2 g several times a day in powders, solution, or more often together with sodium chloride (table salt), in a ratio similar to some mineral waters. Sodium bicarbonate reduces the excitability of the respiratory center while increasing the alkaline reserve of the blood. The drug is contraindicated in case of copious liquid sputum.

Iodine salts. Iodine salts, released by the mucous membranes of the respiratory tract, cause hyperemia and increased secretion of sputum. Potassium iodide is used as an expectorant; it irritates the gastric mucosa less than other iodine preparations. The advantage of potassium iodide over other expectorants is its longer action, the disadvantage is its irritating effect on other excretory pathways (nasal mucosa, lacrimal glands). Iodine salts often have a beneficial effect on chronic bronchitis in older people. Prescribed for prolonged chronic bronchitis with viscous, difficult to expectorate sputum, in addition, for dry bronchitis, for catarrh in those suffering from emphysema, and especially for simultaneous asthmatic complaints. There are contraindications: acute inflammatory processes of the lungs and respiratory tract, early stages of pneumonia.

In many cases, emollients such as marshmallow root preparations are effective.

For bronchitis with the release of a large amount of serous sputum, terpinhydrate is used in a daily dose of up to 1.5 g. For putrefactive sputum, terpinhydrate is used in a dose of 0.2 g 3-4 times a day, often together with antibiotics.

With an increased cough reflex and bronchial obstruction, it is advisable to prescribe dosage forms from the herb thyme, which contains a mixture of essential oils, some of which have sedative properties. The combination of a central calming effect with an expectorant and some bactericidal activity makes thyme an effective drug for obstructive bronchitis.

Among the preventive measures for chronic bronchitis to increase the body's resistance, along with respiratory therapeutic exercises, hardening procedures are great importance general tonic. Pantocrine, Eleutherococcus, Schisandra, and vitamins have adaptive properties. It has a promising effect on allergic reactivity and immunobiological defense mechanisms.

Pantocrine is prescribed 30-40 drops 30 minutes before meals for 2-3 weeks. Eleutherococcus extract is recommended 20-40 drops 3 times a day 30 minutes before meals in courses of 25-30 days. Tincture Chinese lemongrass take 20-30 drops per dose 2-3 times a day on an empty stomach for 2-3 weeks. Therapy with saparal 0.05 g 2-3 times a day is also indicated for 15-25 days.

For purulent bronchitis, antibacterial therapy is additionally prescribed, and for obstructive bronchitis, antispasmodics and, in some cases, strictly according to indications, glucocorticoids.

Long-acting sulfonamide drugs are also used: sulfapyridazine 12 g/day, sulfadimethoxine 1 g/day. Bactrim is effective (2 tablets 2 times a day). Of the quinoxaline derivatives, quinoxidine is prescribed 0.15 g 3 times a day. Acetylsalicylic acid, calcium chloride and other drugs are prescribed as anti-inflammatory drugs.

In general, for the effective treatment of chronic bronchitis, the identification and treatment of rhinitis, tonsillitis, and inflammation of the paranasal cavities is essential.

It is also necessary to prescribe vitamins: ascorbic acid 300-600 mg/day, vitamin A 3 mg or 9900 IU per day, B vitamins (thiamine, riboflavin, pyridoxine) - 0.03 g per day throughout the course of treatment. Vitamin infusions are shown - from rose hips, black currants, rowan berries, etc.

The advisability of using antibiotics is disputed by many authors. However, when positively deciding the question of indications for their use in bronchitis, it is necessary to be guided by the following general rules: the possibility of pneumonia, a long-lasting increase in temperature or high temperatures, toxicosis, as well as the lack of effect from previously carried out therapy.

On average, the course of antibiotic therapy for bronchitis is 5-7 days. For gentamicin, chloramphenicol - a week, according to indications - 10 days, in severe cases up to two weeks.

In some cases, guided by the patient’s condition, it is advisable to use combinations of two or even three antibiotics, which is determined by existing compatibility tables for this group of drugs.

Sometimes, for antibacterial therapy, a choice may be made in favor of sulfonamides or drugs of the nitrofuran group. The general course of sulfonamide therapy lasts on average, as a rule, from five days to a week, less often it can be extended to ten.

Prevention

The best way to prevent chronic bronchitis is to quit or not start smoking.

Avoid contact with lung irritants and areas with polluted air.

Drink raspberry tea as a diaphoretic;

Drink an infusion of coltsfoot leaves (a tablespoon of leaves per glass of boiling water, sip throughout the day), or a mixture of coltsfoot with wild rosemary and nettle in equal parts;

Drink an infusion of pine buds (a teaspoon in a glass of water, boil for 5 minutes, leave for 1.5-2 hours and drink in 3 doses after meals);

Drink onion juice and radish juice as a strong expectorant;

For the same purpose, drink milk boiled with soda and honey.

The risk of bronchitis can be minimized by regular hardening of the body and frequent cleaning of the house to prevent the accumulation of household dust. Prolonged exposure to air in dry weather is beneficial. Treatment of chronic bronchitis is especially successful on the sea coast, as well as in dry mountainous areas (for example, in the resorts of Kislovodsk).