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Treatment of acute bronchitis

In acute bronchitis, it is necessary to systematically ventilate the ward or room in which the patient is located. Given that the disease can be caused by a viral bacterial or bacterial infection, antibiotics are indicated for children, especially for infants and infants (ampicillin, oxacillin, methicillin, ampiox, carbenicillin, kefzol – p. 232). With viral etiology bronchitis, the use of antibiotics is less justified, although in such cases they can be effective in order to prevent bacterial complications.

Children older than three years and with a mild course of acute bronchitis can be prescribed bactrim, erythromycin, oleandomycin phosphate, sulfonamide drugs (0.15 – 0.1 g / kg / day for 4 or 6 doses).
When applying symptomatic therapy, it is important to take into account that in patients with profuse sputum, antitussive agents can make it difficult to evacuate and worsen bronchial obstruction.
If there is a thick viscous secretion in the tracheobronchial ducts, measures are shown that contribute to its dilution and evacuation. To dilute sputum, reduce inflammatory edema of the bronchial mucosa, inhalations of 1–2% sodium bicarbonate solution are prescribed 2–3 times a day. Humidification and warming of the inhaled air is shown, best of all with the help of ultrasonic humidifiers, aeroionizers, aerosol devices. If they are absent, central heating radiators are used to humidify the air in the room where the patient is located, covering them with a wet, thick cloth.

Apply therapeutic baths for 5 to 10 minutes, daily increase the water temperature from 37 ° C to 40 ° C, warm wraps, distracting agents (mustard, jars, mustard foot baths), warm drink, expectorant medicines, etc.
With an abundance of sputum, postural drainage, contributing to the outflow of it from the affected bronchi. The patient is in Quincke position (with the head down) for 15 to 20 minutes (intermittently). In this position, coughing movements are desirable. The procedure is repeated 2 to 3 times a day. The effectiveness of the drainage increases when it is combined with a vibration massage, which in older children is performed by patting the chest over the affected area with a palm folded in a “boat”. In young children, this procedure is performed by applying rhythmic hits with the ends of the fingers of one hand on the chest or on the finger of the other hand, located along the intercostal space.

To relieve bronchospasm, aminophylline and ephedrine are used. Eufillin is administered orally in a single dose of 2–4 mg / kg 2–3 times a day, intravenously in the form of a 2.4% solution at the rate of 0.1–0.15 ml / kg, but not more than 5–7.5 ml in 150 – 200 ml of 5% glucose solution. Ephedrine is prescribed orally for children up to 1 year old – at 0.002 – 0.003 g; 2 – 5 years – 0.003 – 0.01 g; 6 – 12 years old – 0.15 – 0.02 g; older – 0.025 g 2 to 3 times a day. Prescribe combined powders of ephedrine, diphenhydramine and aminophylline in age doses.

The prognosis of acute bronchitis is favorable, but complications are possible – bronchiolitis, pneumonia. Prevention of acute bronchitis boils down to the prevention of acute respiratory viral infections and increase nonspecific resistance of the body by hardening, proper care of the child, compliance with the indoor air regime, rational nutrition, etc. 

Bronchial asthma due to physical stress

Bronchial asthma due to physical stress is a variant of bronchial asthma, characterized by the obligatory development of asthma attacks 1-10 minutes after exercise. Asthma due to physical stress is especially often observed in children.

Etiology of bronchial asthma due to physical exertion

The type of physical activity matters. Most often, asthma attacks occur when running, playing soccer, basketball, mountain climbing, less often – with intermittent loads (weight lifting); swimming is well tolerated. The formation of an attack is more affected by the duration of the load than its intensity.

Pathogenesis of bronchial asthma due to physical stress

In connection with the rapid and complete reverse development of asthma attacks due to physical stress, it is believed that bronchial obstruction is caused by bronchospasm without the presence of inflammation, swelling, and mucus secretion. Bronchospasm is not associated with immunological mechanisms. In the pathogenesis of asthma attacks due to physical stress, various regulatory disorders are expected to be involved: a relative decrease in the functions of adrenergic B receptors due to the hyperreactivity of adrenergic a receptors in combination with the peculiarities of the release of catecholamines during exercise. The participation of adrenergic mechanisms is confirmed by the effectiveness of adrenergic drugs (3-stimulating in the prevention and relief of bronchospasm induced by physical stress, as well as by provoking bronchospasm with a-adrenoreceptor stimulants and the preventive effect of a-blocking adrenergic drugs in people who are sensitive to stress; isolation of mediators of immediate allergy, which is proved by the following facts: the presence of a refractory period after an attack (depletion of copper reserves is assumed tori under load); Protective effect Intalum and calcium antagonists preventing mast cell degranulation, and antihistamines; sensitization cells of patients to degranulation and release of mediators; hyperstimulation irritant vagal receptors due to rapid cooling of the upper respiratory tract and hyperventilation during the loading process Participation. of these mechanisms is confirmed by: a pronounced correlation between the sensitivity of the bronchi to vagotonic agents and to physical. stress; the preventive effect of atropine and lidocaine (pharyngeal ring anesthesia); increased sensitivity of the bronchi to anticholinergics in some patients; heat loss during breathing. It is assumed non-immunological stimulation of the release of mediators due to mechanical irritation (body shake during exercise), direct action of physical. factors, in particular cooling, on the peripheral respiratory tract, the effect of catecholamines and acetylcholine. In the genesis of bronchospasm on physical. metabolic acidosis and impaired fatty acid utilization also matter . The central and peripheral airways are involved in the pathological reaction to the load, however, obstruction of the large bronchi most often dominates.

Clinic of bronchial asthma due to physical stress

Attacks of suffocation induced by physical. load, mainly observed in atopic asthma and are not observed in chronic bronchitis. They occur 1-2 minutes after the load is stopped and in mild cases they stop spontaneously after
5-10 minutes (increase in individuals within 30-60 minutes), in severe cases, the attack begins during the load and lasts more than 1 hour (without treatment ); bronchospasm progresses with alternating different loads with an interval of less than 1 hour. The initial condition of the patient is not critical: in sensitive individuals, an attack may appear during complete remission, while in resistant individuals it does not develop even with initial bronchial obstruction. The initial level of obstruction affects the severity of bronchospasm, which can be short-term and asymptomatic (subclinical form of bronchial asthma due to physical stress) in 25% of cases, especially in children, moderate bronchospasm is observed in 25-30% of patients, and severe bronchospasm in 15-25%.

Diagnosis of bronchial asthma due to physical stress

Reaction to physical. the load is established using clinical observation and pulmonary function tests, studied before and after the standard load –
6-8 minutes of running on the treadmill (p-stimulating adrenergic drugs are canceled in 3-4 hours, intal is removed in 8-12). A decrease in FVC1 by more than 15% of the initial level indicates the development of bronchospasm. In the first 24 minutes, FVC increases, then decreases, reaching 40-50% of the initial value in individuals. In mild cases, two-, three-fold testing is necessary before a reaction is detected. Diagnostic value is the constant nature of the reaction – the mandatory occurrence of bronchospasm on the physical. voltage. Load tests are not performed for concomitant heart diseases.

Treatment of bronchial asthma due to physical exertion

Attacks of suffocation due to physical. loads can prevent aerosols of adrenergic drugs that stimulate p2-adrenergic receptors, intala, methylxanthines (the latter are prescribed 30 minutes before the load, intal – immediately before or at the same time as the load).
Glucocorticosteroid drugs are relatively ineffective. In certain cases, certain sports are allowed (swimming). Before sports, it is recommended
to prophylactically take theophylline and intal, the appointment of p-stimulating adrenergic drugs is prohibited. Recently, reports appeared about the effectiveness of calcium antagonists (nifedipine, 20 mg sublingually) and a-adrenergic receptors (prazosin, 2 mg, inhalation).

Bronchial asthma

Bronchial asthma is a disease characterized by the development of reversible bronchial obstruction under the influence of various stimuli and caused by hyperreactivity of the bronchi. With bronchial astmenus, a triad of clinical symptoms is observed – asphyxiation, cough and shortness of breath, in a small part of patients the only manifestation of the disease may be a paroxysmal cough. More often, young people are sick: in half of patients, asthma develops in childhood, in 1/3 – under the age of 40. There is no single classification of bronchial asthma. Two main types of bronchial asthma are distinguished – exogenous (atopic, allergic) and endogenous, which is believed to be caused by non-immune mechanisms. Endogenous bronchial asthma includes asthma of physical effort, aspirin psychogenic, infectious, hypereosinophilic asthma, asthma associated with environmental pollution, as well as many cases of occupational bronchial asthma. The main differences between the two types of bronchial asthma are given below.

Etiology and pathogenesis of bronchial asthma

To date, the most fully studied mechanisms of development of atopic bronchial asthma. An allergen (pollen, house dust, fungal spores, food, medicines), when ingested, causes the production of antibodies of the IgE class, which are fixed on the membrane of mast cells. With repeated exposure to the allergen, antibodies combine with it, causing mast cells to release a number of biologically active substances – histamine, eosinophilic anaphylaxis factor, neutrophilic chemotactic factor. Following degranulation, mast cells synthesize a slow-reacting anaphylaxis substance (which includes leukotrienes), a platelet activating factor and, possibly, prostaglandins, some mast cell mediators (histamine, most leukotrienes, prostaglandins E1 and E2, platelet activating factor) cause bronchospasm increase vascular wall permeability and mucus secretion. Others (eosinophilic, lymphocytic, neutrophilic chemotactic factors, leukotriene B4) attract neutrophils, lymphocytes, eosinophils and thrombodites.

In recent years, new data have been obtained that better understand the role of mediators in the occurrence of bronchial asthma. The metabolism of arachidonic acid 5 and the synthesis of slow-reacting anaphylaxis substances were studied. Arachidonic acid is a product of the phospholipid membrane of a mast cell activated by a phospholipase under the influence of the antigen-antibody reaction. There are two ways of converting arachidonic acid – cyclooxygenase, which results in the formation of prostaglandins E2 and E2a and thromboxanes, and lipoxygenase, leading to the synthesis of leukotrienes, some of which form slowly reactive anaphylaxis substances. Leukotrienes and thromboxanes have a stronger effect on the smooth muscles of the bronchi than histamine and prostaglandins, while their point of application is mainly small bronchi.

It is assumed that the process of bronchial obstruction passes through two phases, the first, which occurs several minutes after inhalation of the allergen and lasts from 30 to 60 minutes, due to mediators that directly act on the vessels and bronchial wall; the second (repeated wave of bronchial obstruction several hours after the end of the first phase) is caused by the action of chemotactic factors and the effector cells attracted by them. The leading role in this period is played by eosinophils, the proteins of which damage the ciliary epithelium of the respiratory tract and increase the permeability of the mucous membrane, bronchi for allergens. At the same time, eosinophils secrete substances that inhibit histamine, platelet activating leukotrienes. Factor release of bronchospasm mediators depends on the ratio of cAMP and cGMP content in mast cells. cAMP inhibits the release of histamine, slow-reacting anaphylaxis, other mediators, while cGMP has the opposite effect. B-adrenoreceptors are known to activate adenylate cyclase, which is involved in the synthesis of cAMP. Drugs that stimulate a-adrenergic receptors increase the content of intracellular cAMP, which is destroyed by phosphodiesterase. Methylxanthines, potent phosphodiesterase inhibitors, also increase cAMP levels in cells. The synthesis of cAMP is enhanced by the excitation of H2 receptors and prostaglandin receptors, which respond to increased levels of histamine and other mediators. Cholinergic receptors are responsible for the activation of guanyl cyclase, which is involved in the synthesis of cGMP, so cholinolytic agents can also prevent the release of mediators. The role of calcium ions in the occurrence of bronchospasm is not fully understood. Moving them from the outer membrane of the cell and dealing with the cytoplasm is a sign of mast cell activation. It is also known that a decrease in the content of calcium ions in the smooth muscle cells of the bronchi contributes to the expansion of the latter.

The pathogenesis of endogenous bronchial asthma is not well understood. In development, it attaches importance to violations of the parasympathetic innervation of the bronchial tree, leading to the development of bronchospasm and a change in the secretion of bronchial glands, as well as a decrease in the threshold of sensitivity of the vagus nerve receptors to irritants. However, it is not possible to explain the development of various forms of endogenous bronchial asthma using a single hypothesis.

In the pathogenesis of asthma, physical effort suggests the importance of cooling the bronchial tree as a result of hyperventilation and inhalation of cold air. In this case, the excitation of specific temperature receptors in the airways that respond to a decrease in temperature occurs. Other mechanisms for the development of this form of asthma are discussed, in particular, IgE-independent mast cell degranulation with the release of mediators, activation of cholinergic receptors.

Exacerbation of bronchial asthma can be triggered by an infection of the upper respiratory tract, and the main role in the occurrence of bronchospasm is played not by bacteria, but by viruses (influenza, parainfluenza). Possible causes of bronchospasm are virus replication in the epithelium of the respiratory tract, causing cell damage and the release of arachidonic acid metabolites, as well as a decrease in the sensitivity threshold of bronchial tree receptors to various external stimuli under the influence of a viral infection, “Aspirin” or prostaglandin, asthma is observed in patients with polyposis nasal cavity and intolerance to acetylsalicylic acid, indomethacin, phenacetin or yellow food coloring (yellow tartrazine). Its development is associated with a violation of the synthesis of prostaglandins and an increase in the synthesis of leukotrienes due to a violation of the metabolism of arachidonic acid under the action of acetylsalicylic acid and its derivatives.

Occupational bronchial asthma occurs when in contact with various substances: 1) metal salts (chromium, nickel, manganese); 2) wood (dust of pine, oak) and vegetable (cotton, linen) dust; 3) industrial chemicals (phthalic anhydride, ethylenediamine, formaldehyde); 4) drugs (antibiotics, cimetidine, piperazine); 5) enzymes; 6) animal proteins (bird droppings, fish isolations, beekeeping products). Occupational factors can induce an immune response (metal salts, animal proteins, certain types of plant dust), act on specific cellular receptors (cotton, a substance that promotes the release of histamine, organophosphorus insecticides with anticholinesterase effects) and irritate, causing inflammation mucous membrane of the bronchi (silicon dioxide, ammonia, hydrochloric acid). Psychogenic bronchial asthma was described as early as the 17th century. In its pathogenesis, an increase in vagus nerve activity plays a role.

Bronchial asthma resulting from environmental pollution has become widespread in recent years. In its pathogenesis, along with the effect on the bronchial mucosa of irritating substances that pollute the atmosphere (sulfur oxides, ozone, carbon oxides, nitrogen dioxide), bronchial hyperreactivity plays a role. Hypereosinophilic bronchial asthma is also distinguished, which may be one of the manifestations of periarteritis nodosa (asthmatic variant). Its peculiarity is the presence of a large number of eosinophils in the blood (40-60% or more) and sputum.

Clinic of bronchial asthma

In most patients, asthma attacks begin with an unproductive cough. Usually they occur upon contact with allergen 1} at night, after exercise, in the cold, when inhaling substances with irritating properties or a pungent odor. Attacks can last up to several hours and stop on their own or under the influence of treatment. The end of the attack is preceded by the discharge of sputum in the form of mucous plugs. During an attack of suffocation, exhalation is difficult, wheezing can be heard at a distance during both phases of the respiratory cycle; with a more severe attack, an increase in shortness of breath is sometimes accompanied by a decrease or disappearance of wheezing. The patient occupies a forced position – he usually hoarsens, resting his hands on his knees or the edge of the bed and thus fixing the shoulder girdle. The auxiliary muscles actively participate in the act of breathing; the chest is enlarged (“swollen”), its anteroposterior dimensions are enlarged, percussion sound with a box-like tint or box-like sound, the lower borders of the lungs are omitted; sharply elongated exhalation and a large number of dry rales are heard in the lungs, after the discharge of sputum, the exhalation is shortened, the number of dry snores decreases, but the last two symptoms can persist for some time after the attack of suffocation.

Frequent asthma attacks or in time an uncured, prolonged asthma attack can go into asthmatic status (status asthmaticus). In many patients, the development of it is preceded by uncontrolled (up to tens of times) use of inhalers of B-adrenergic agonists (drug blockade of B-adrenergic receptors). Asthmatic status is characterized by an increase in bronchial obstruction with tachypnea and shallow breathing and the lack of effect in the treatment of adrenomimetic drugs. As a result of the formation of mucous plugs, clogging the lumen of the boronchus and disrupting the conduct of sound to the surface of the chest, the sonority and the number of dry rales are reduced (until they disappear, the “dumb” lung). The progression of respiratory failure leads to the development of decompensated respiratory acidosis and hypercapnia. Death occurs with hypoxemic coma due to paralysis of the respiratory center. Bronchial asthma can be complicated by obstructive pulmonary emphysema, pulmonary heart, pneumothorax, pneumomediastinum.

Diagnosis and differential diagnosis of bronchial asthma

Eosinophilia is detected in the blood during attacks of suffocation or with their increased frequency. With atopic bronchial asthma, the level of IgE is increased in the blood. Kurshman spirals (elements of mucus), Charcot-Leiden crystals (decay products of eosinophils), a large number of eosinophils are found in sputum. An X-ray examination of the chest organs increased the transparency of the pulmonary fields. In severe cases, atelectasis may develop due to obstruction of the bronchi with mucous plugs.
Examination of the function of external respiration is an important method for determining the severity of an attack, as well as the effectiveness of the treatment used. In the acute period, there is a significant decrease in FEV1, other speed indicators, in addition, a decrease in VC and an increase in residual lung volume can be recorded. In the interictal period, especially at the beginning of the disease, only a decrease in FEV1 is detected . In patients with a severe or protracted attack of suffocation, hypoxemia is observed, usually accompanied by hypocapnia, and an increase in the pH of arterial blood. Hypocapnia and respiratory alkalosis are caused by hyperventilation. Normalizing or increasing PaCO2, indicating severe bronchial obstruction or progressive respiratory failure, is considered a poor prognostic symptom.

Bronchospastic syndrome also occurs in congestive heart failure (cardiac asthma), pulmonary thromboembolism, chronic bronchitis, and airway volume formations. Attacks of shortness of breath with cardiac asthma occur when lying down and can be stopped with nitroglycerin. Cough usually does not appear at the beginning, but at the end of the attack. During auscultation of the lungs, moist rales are heard, mainly in the lower sections. Distinctive features of recurrent thromboembolism of the pulmonary artery are pleural pain, signs of overload of the right heart chambers (ECG). Crucial for the diagnosis are the data of scanning and angiography of the lungs. Volumetric formations of large bronchi (tumors, polyps, foreign bodies) are detected using bronchoscopy and X-ray examination. For chronic asthmatic bronchitis, a long-term cough is characteristic. Eosinophilia is not observed; there are no elements of bronchial asthma in sputum.

Bronchiectasis in children

Bronchiectasis is an irreversible local expansion of the bronchi, accompanied by infection.

Etiology and pathogenesis of bronchiectasis

The disease is polyetiological. The main factors contributing to the formation of bronchiectasis: congenital lung defects; recurrent non-specific inflammatory diseases of the respiratory system; childhood infectious diseases (measles, whooping cough) foreign bodies of the tracheobronchial tree, tuberculosis, some hereditary diseases and systemic lesions (cystic fibrosis, Cartagener syndrome, agammaglobulinemia); bacterial destruction of the lungs. There are various theories of the pathogenesis of bronchiectatic disease. Some authors consider the main significance of chronic bronchitis, others consider pneumosclerosis to be primary, and others – malformations and inferiority of the bronchopulmonary system. The main importance in the pathogenesis of bronchiectasis is the interaction of two factors: the inflammatory process and the violation of the drainage function of the bronchi. An important role in the occurrence of bronchiectasis is played by atelectases of various genesis (congenital, aspiration, pneumonic, with foreign bodies, bronchial tumors, with cystic fibrosis, with compression by bronchial lymph nodes). It is not excluded that nasopharyngeal diseases (rhinosinusopathies) are associated with bronchiectasis. With joint inflammation of the nasopharynx and lungs, a reactive increase in the lymph nodes of the submandibular region, neck, mediastinum, paratracheal and bronchopulmonary arises. Enlarged lymph nodes are not only a source of infection, but also a factor that disrupts pulmonary blood flow, which contributes to the development of chronic pneumonia. Thus, the pathogenesis of bronchiectasis is a chain of pathological processes that interact and affect each other.

Classification of bronchiectasis

Classification of bronchiectasis. F. Isakov, E. A. Stepanov, V. I. Geraskin (1978).
By origin:
congenital (dysontogenetic), acquired (atelectatic, emphysematous, mixed).
In shape:
cylindrical, bubble-frequent, brush-like.
For distribution:
unilateral, bilateral (large, non-distributed), – with an indication of the segment.
By the severity of bronchitis:
localized, diffuse.
With the course:
with exacerbations (frequent, rare).

Clinic of bronchiectasis

The clinical picture depends on the spread of the lesion, the severity and spread of bronchitis in the unaffected areas of the lung, on the presence of exacerbation or remission. The general condition may be slightly impaired, but with a common process, symptoms of intoxication join early. Children quickly tire, vststayuturouroz-turn. Hemoptysis is rare. With limited bronchiectasis, shortness of breath at rest is usually not observed, with bilateral damage – severe shortness of breath with little physical exertion. Some children complain of headache, bone pain. During periods of exacerbation, the amount of sputum increases, coughing throughout the day is constant, shortness of breath intensifies or appears, fever, more often to subfebrile numbers. One of the most important diagnostic signs of chronic pulmonary disease is chest deformity – chest retraction on the side of the lesion, its lag in the act respiration, a slight omission of the angle of the scapula, rapprochement of the ribs, narrowing of the intercostal spaces. Auscultatory moist rales of various sizes, decreasing after expectoration of sputum.

Diagnosis of bronchiectasis

An X-ray examination of the chest can reveal a spotted eclipse of the affected lobe of the lung, the presence of bronchiectasis is further confirmed by computed tomography. However, the main method to establish a diagnosis of bronchiectasis is bronchography – a contrast study of the bronchial tree. Evaluation of the bronchogram allows you to determine the localization of bronchiectasis, their distribution , form. Changes found during angiopulmonography of children with bronchiectasis depend on the depth and prevalence of pa process in the bronchi and lung parenchyma. The complete absence of blood flow in the affected areas of the lung indicates a functional failure and the need to remove these areas, which are only cells of purulent intoxication.

Treatment of bronchiectasis

Conservative treatment is used as a preoperative preparation in the postoperative period and is aimed at maximizing the rehabilitation of the tracheobronchial tree, as well as all associated foci of inflammation. For the rehabilitation of the trachea and bronchi, bronchoscopy is used, which is repeated 2-3 times. Inhalations, exercise therapy are prescribed. postural drainage, bronchial and mucolytics, vitamins, desensitizing agents. During surgical treatment, the volume of resection is determined according to bronchography and is specified during the operation. Resection of the lobe, several segments of two lobes of the lung is performed (with localization on the right), very rarely it is necessary to remove the entire lung – pulmonectomy. In case of bilateral localization of bronchiectasis, the operation is performed in 2 stages at intervals of 6-12 months.

Bronchogenic cysts

Pathological anatomy of bronchogenic cysts

Bronchogenic cysts are a malformation. As a rule, they are single-chamber, ovoid or rounded. The thickness of the cyst wall is not more than 5 mm, inside it is shiny, lined with a multi-row cylindrical epithelium, often ciliary. The structure of the wall repeats the structure of the normal wall of the trachea or bronchus – loose connective tissue, mucous glands, hyaline cartilage, but the wall of the cyst can be represented only by any one tissue. The average size of the cyst is 6-10 cm. Most bronchogenic cysts have a radical localization, are adjacent to one of the main or lobar bronchi. Often, cysts are located in the area of ​​Karina, often associated with the anterior wall of the esophagus, they can cause compression of the trachea and bronchi. Paratracheal cysts are attached to the tracheal wall on the right near the bifurcation. Bronchogenic cysts can be located parapericardially, paraesophageally, in the wall of the esophagus, as well as in any part of the mediastinum.

Clinic of bronchogenic cysts

Bronchogenic cysts are often asymptomatic. Clinically characterized by symptoms of compression of the trachea and large bronchi, sometimes the esophagus. Noisy breathing, wheezing, shortness of breath, cough, dysphagia, chest pain are the most common symptoms. With a complicated course – suppuration of the cyst, breakthrough of purulent contents in the bronchi, trachea – there may be a fever, purulent intoxication, hemoptysis, purulent sputum, aspiration pneumonia, chronic bronchitis. Possible malignancy. Physical data are nonspecific.

Diagnosis of bronchogenic cysts

Radiologically, the cyst is a smooth, round or oval darkening of medium intensity. The vertical dimensions prevail over the horizontal, the contours are clear. The inner surface of the dimming is intimately connected with the trachea and bronchi, rarely a leg is found that goes to the trachea or bronchus. Changing the shape of the cyst during breathing and the displacement of the cyst associated with the trachea when swallowing are functional radiological symptoms. When contrasting the esophagus, its displacement or compression can be detected. The presence of a fluid level indicates a message with the bronchus or trachea. X-ray CT expands the capabilities of the X-ray method, allows you to reliably differentiate the cyst from tumor formation, establish the relationship of the cyst with surrounding organs.
With an intimate connection with the trachea and bronchi, tracheobronchoscopy is indicated both for the purpose of differential diagnosis and for the purpose of establishing the degree of inflammatory changes in the wall of organs. Due to the possibility of infection, a transtracheal or transbronchial puncture biopsy is not indicated.
A differential diagnosis should be carried out with lung neoplasms, teratomas, neurogenic mediastinal tumors, coelomic cysts, paramediastinal pleurisy.

Treatment of bronchogenic cysts

Surgical treatment. Possible complications and malignancy determine the active tactics.

Plastic bronchitis

Plastic bronchitis (pseudomembranous bronchitis, fibrinous bronchitis, bronchial croup) is rare. Characteristic is the coughing of a sick child with fibrinous casts, reminiscent of the structure of the bronchial tree. Microscopy of casts reveals fibrin, mucus, lymphocytes, eosinophils, plasma cells and banal coccal flora. The presence of eosinophils in the casts of the bronchi, Shar-Ko-Leiden crystals, and Kurshman spirals was the basis to consider this disease as a manifestation of an allergy.

Etiology of plastic bronchitis

The etiology of the disease is not clear. They allow the possibility of developing primary chronic idiopathic plastic bronchitis and its occurrence as a secondary disease in various bronchopulmonary pathologies (tuberculosis, bronchiectasis, bronchial asthma, etc.).

Clinic of Plastic Bronchitis

In addition to coughing bronchial casts, patients have a cough, mainly paroxysmal, shortness of breath, pain and discomfort in the chest. The severity of these symptoms is determined by the extent of the lesion of the obstructed bronchial tree. This also determines the prevalence of atelectasis, which is one of the constant and characteristic symptoms of plastic bronchitis.
The course of the disease can be acute or relapsing. The intervals between relapses are different (from several days to several years). There are cases of a single manifestation of the disease, without relapse in the future.
In the acute period of the disease, dense white or gray masses are completely obstructed in their lumen in the main and lobar bronchi of the affected side. The prognosis for plastic bronchitis is mostly favorable. After isolation of the cast of bronchi, atelectasis is straightened.

Plastic bronchitis treatment

In the period of exacerbation, agents are used that help dilute the bronchial contents. The main method of treatment is bronchoscopy, which allows using bronchoscopic forceps to remove fibrinous deposits that are tightly soldered to the bronchial wall. Antibiotics are indicated.

Tuberculosis of the intrathoracic lymph nodes (Bronchoadenitis)

Tuberculous bronchoadenitis can occur as without pronounced symptoms, i hk and with obvious symptoms of tuberculous intoxication. In modern conditions, “small forms” of tuberculosis of the intrathoracic lymph nodes are increasingly observed. They are determined by the main OSROM during tomographic examination. Their clinical symptoms are scarce. Bronchoadenitis can be infiltrative and tumor-like. Infiltrative forms of bronchoadenitis usually occur with severe signs of intoxication, with a prolonged increase in temperature from 37.5 to 38 ° and higher, complaints of dry cough, which is sometimes bitonal (pertussis-like) due to compression of large bronchi. Tuberculous bronchoadenitis can be accompanied by pleurisy, often interlobar. In the presence of enlarged tumor-like lymph nodes, a violation of bronchial obstruction may occur as a result of compression of the bronchus from the outside or as a result of a breakthrough of the caseous contents of the lymph node into the lumen of the bronchus (bronchofistulosis syndrome) with the formation of atelectasis and bronchogenic seeding.

Diagnosis of bronchoadenitis

Recognition of bronchoadenitis requires a comprehensive clinical and radiological examination, taking into account anamnestic data, the nature of tuberculous intoxication, the presence of severe tuberculin reactions. Often, an incorrect assessment of radiological data entails overdiagnosis of these forms of tuberculosis.
The most convincing for the radiological diagnosis of bronchoadenitis are data from a tomographic study of the roots of the lungs. Changes in the roots of the lungs have to be differentiated mainly from lymphogranulomatosis, malignant neoplasms in the mediastinum, Beck sarcoidosis. In typical cases with bronchoadenitis, dullness of percussion sound in the interscapular space at the level of IV-V thoracic vertebrae (Korani symptom) and in the parasternal region can be determined.
During auscultation, altered breathing, scanty rales in the interscapular space and at the angle of the scapula are established.
Blood changes are expressed in accelerated ESR, a neutrophilic shift to the left. The white blood cell count is usually either normal or slightly increased. Accelerated ESR in combination with a pronounced tuberculin breakdown indicates the continued activity of the process. When bronchoadenitis has lost activity, changes in the blood, like tuberculin tests, are normalized. An X-ray examination in these cases reveals compaction of the lymph nodes and their petrification.
Tuberculous mycobacteria are usually detected with infiltrative bronchoadenitis, a breakthrough of the caseous lymph node in the bronchus – bronchofistulous forms (often in old age), and specific damage to the bronchial pathways. Mycobacterium tuberculosis is more often found in the study of bronchial lavage by sowing or flotation.
Patients with active tuberculosis of the intrathoracic lymph nodes need long-term treatment in a sanatorium using antibacterial drugs, and in some cases, surgical removal of caseous degenerated large lymph nodes. They need constant monitoring of the dispensary and treatment until a lasting clinical cure is established.

Complicated bronchial asthma

Complicated bronchial asthma – bronchial asthma, aggravated by the consequences of this disease or associated infectious and inflammatory process in the lungs. The most common complications are: asthmatic status, emphysema, pneumothorax, mediastinal and subcutaneous emphysema, pulmonary heart, lung atelectasis. Emphysema, observed in 2/3 of patients with bronchial asthma, has different developmental periods. It can be acute reversible (formed during an attack due to obstruction of the bronchi) and chronic irreversible (formed during repeated exacerbations of asthma). The progression of concomitant chronic bronchitis causes secondary obstructive emphysema. Due to emphysema, the value of irreversible airway obstruction increases significantly, which worsens the course and prospects of therapy for bronchial asthma. In patients, the rhythm of breathing during an attack is disturbed, the excursion of the chest decreases, its configuration changes. The main link in the formation of the pulmonary heart in bronchial asthma is a diffuse violation of bronchial obstruction leading to a series of consecutive changes: a decrease in the clearance of the pulmonary capillaries and arterioles, an increase in pressure in the pulmonary artery, uneven ventilation of the lungs, alveolar hypoventilation, a reduction in the blood vessels of the lungs, arterial hypoxemia, and an increase in work right ventricle of the heart. Immediate allergy mediators (serotonin) are involved in the pathogenesis of pulmonary hypertension, and disorders of the androgenic and glucocorticosteroid functions of the adrenal cortex are observed. The presence of severe pulmonary hypertension, overload of the right ventricle of the heart in combination with the hypokinetic type of central hemodynamics, a change in pulmonary volumes (a steady increase in OOL and its relationship to OEL) are signs of a formed pulmonary heart. Segmental atelectasis can form during an acute attack of asthmatic status or in case of bronchial obstruction with Aspergillus fumigatus plug in case of allergic bronchopulmonary aspergillosis. The signs of this complication are different depending on the cause, location and severity of pulmonary collapse. The range of symptoms ranges from a mild cough with lack of physical data to tachypnea, cyanosis, displacement of the heart and mediastinum, elevation of the diaphragm on the side involved in the process. Persistent atelectases in the right middle lobe of the lung are manifested by constant or intermittent shortness of breath (right middle lobe syndrome). The diagnosis is established by x-ray examination. In unclear cases , additional research is indicated: bronchoscopy, bronchography. Bronchial asthma is also accompanied by hemodynamic disorders. During the attack in most patients, the pressure in the pulmonary artery system is increased, and the contractility of the right ventricle of the heart is reduced; sinus tachycardia (120 strokes or more in 1 min), various ECG disturbances, paradoxical pulse are noted. These disorders correspond to the severity of bronchial obstruction. During the period of remission, the pressure in the ductal artery remains elevated and disturbances in the phase structure of the heart remain (hypodynamia of the I – II degree of the right and left ventricles) depending on the severity of the course. Pneumothorax, mediastinal and subcutaneous emphysema can occur during asthmatic status. Treatment of complications is given according to the general rules of therapy for these conditions. Particular attention should be paid to the rehabilitation of the infectious and inflammatory focus in the lungs, which is most often represented by chronic obstructive bronchitis.

Bronchial asthma during pregnancy

Features of the course of bronchial asthma during pregnancy . Pregnancy can cause an improvement and worsening of the course of bronchial asthma. Approximately 40% of women experience remission, 35 – the course does not change, in 25% there is an exacerbation; sometimes the first attack occurs during pregnancy. A certain prognostic value is the severity of the disease before pregnancy. The course of a mild form of bronchial asthma does not change or improve; severe bronchial asthma is prone to exacerbation. Deterioration is most often observed and most pronounced in the last months of pregnancy. The effect of pregnancy on the subsequent course of the disease is variable. In 25-30% of patients, it noticeably worsens. Responsible for the immediate period after childbirth. Mothers with asthma have an increased risk of antenatal and neonatal fetal death. The mechanism of the effect of pregnancy on the course of bronchial asthma is not precisely established. Several factors are attached importance: a gradual increase in the level of plasma glucocorticosteroids by 2-2.5 times (positive factor), with which, possibly, an increase in the level of cAMP in the plasma of pregnant women, which is a good prognostic sign; increased progesterone content. having a different effect – a weak bronchodilating effect and increased shortness of breath due to excitation of the respiratory center; a decrease in the function of cellular immunity with possible consequences in the form of a change in the severity of allergies and an increase in the likelihood of an exacerbation of a bacterial infection of the respiratory tract; an increase in the size of the fetus and the associated increase in the diaphragm and a change in the respiratory volume of the lungs (the hormonal or metabolic nature of these changes is also assumed); allergic mothers with fetal antigens, which causes the development of an immunological conflict involving the lungs. The basic principles of treating bronchial asthma during pregnancy are the minimum risk for the mother and the fetus, the prevention of complications in the neonatal and perinatal periods. In the early stages of pregnancy, drugs that can stimulate uterine contractions should be avoided. Adrenergic drugs (3-stimulating drugs are well tolerated, however, since the initial clinical trials of these substances did not study their effect on pregnant women, it is not recommended to use them in the first trimester . The same applies to intal. Antibiotics of the tetracycline group for the treatment of bronchial asthma during pregnancy. contraindicated due to teratogenic effects Methylxanthines are safe and can be used, although they can increase nausea and vomiting in the first trimester of pregnancy. idnye drugs are prescribed, if necessary; the risk of complications for the mother as a result of glucocorticosteroid therapy does not increase, but may develop transient suppression of fetal adrenal glands, resulting in the glucocorticosteroid insufficiency in neonates with stress (eg, infection). In the first six weeks after birth.

Exogenous Allergic Bronchioloalveolitis

Exogenous allergic bronchioloalveolitis (synonyms of the disease: hypersensitive pneumonitis) – diseases caused by inhalation of organic dust with a particle diameter of up to 5 μm, characterized by an inflammatory process (mainly in the alveoli and bronchioles) with interstitial infiltration and the formation of granulomas, which tend to fibrosis with repeated prolonged contact antigen. For the first time, a lung disease similar to exogenous allergic bronchioalveolitis was described in 1713 by Ramazzini, in more detail in 1932, Campbell (“farmer’s lung”). The name “exogenous allergic alveolitis”, proposed by Pepis in 1967 due to the frequent involvement of bronchioles in the process, is not entirely accurate, the term “exogenous allergic bronchioloalveolitis” is considered more correct . This is a relatively rare disease, but incidence can be high in certain areas. Outbreaks of it are most often observed in years with wet summers, usually a lot of snow falls.

Etiology of exogenous allergic bronchioloalveolitis

Organic substances that cause exogenous allergic bronchioloalveolitis are very diverse. The most common cause of the disease is thermophilic actinomycetes, bacteria with a morphological characteristic of fungi that are ubiquitous and are found in earth, compost, hay, straw dust, grain, sawdust and other wet organic materials that can mold and heat up to a temperature of 40-60 ° C optimal for mushroom growth. Actinomycetes also reproduce in the heating, cooling and air conditioning systems of the recirculating type. Many microorganisms have been identified in compressors and water from vacuum pumps that can cause the disease. The most important representative of thermophilic actinomycetes is Micropolyspora faeni, whose spores with a diameter of less than 5 microns can penetrate the periphery of the lung. Actinomycetes contain three antigens: A, B, C. Antigens A and B are proteins that cross-react with antigens of fungi of other species (Aspergillus, Mucor), C is a polysaccharide that is most specific. An important group of etiological factors of the disease is whey proteins and dust from the droppings of various birds (pigeons, parrots, chickens, ducks, turkeys). Bird droppings extract (a mixture of soluble proteins, glycoproteins and polysaccharides) is a species-specific antigen – serum g-globulin. Antigens of the gastrointestinal tract of birds, cross-react with serum proteins. The frequency of exogenous allergic bronchioloalveolitis due to bird proteins is low; more often, the disease is caused by the proteins of pigeons and parrots. Exogenous allergic bronchioloalveolitis can also provoke other animal proteins, in particular, inhalation of rat serum droplets is described as the cause of the disease in laboratory workers. The disease can cause plant dust (from cotton, hemp, hemp, cork) and some medications: pituitary powder in patients with diabetes insipidus, sometimes Intal.