Monthly Archive November 2019

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.

Pathogenesis of exogenous allergic bronchioalveolitis

Allergic predisposition factors in patients with exogenous allergic bronchioalveolitis have not been established, although HLA-BW40 and HLA-B8 are more common. Immunological and non-immunological mechanisms are involved in the development of the disease. Allergic reactions of various types are expected to be involved: delayed-type hypersensitivity, immune complexes, immediate-type allergic reactions caused by antibodies related to immunoglobulin E, mediated by cytotoxicity antibodies. There is currently no evidence of a predominance of a particular type of immunological reaction.
Existing ideas about exogenous allergic bronchioloalveolitis as a disease caused by the immune complex are questioned for the following reasons: there is no parallelism between the level of precipitating antibodies related to immunoglobulin G and the severity of the disease; precipitins are found in a large number of healthy individuals in contact with the antigen; in the acute period of the disease, granulomas are formed that are uncharacteristic of the Arthus phenomenon; skin reactions according to the type of Arthus phenomenon to specific antigens are not constantly detected in patients;
deposits of immune complexes in biopsies of human lungs are noted only at an early stage of the process; histological signs with exogenous allergic bronchioalveolitis are more characteristic of cellular reactions, fibrinoid necrosis of the vascular walls and perivascular infiltration by segmented cells. Many authors assign the leading role of HRT. The role of GNT due to immunoglobulin E is not clear, antibodies related to immunoglobulin E have not been identified, although certain antigens (pigeon proteins, pituitary powder) can cause GNT. It is assumed that immunoglobulin E does not participate in the development of a typical granulomatous lesion, but can mediate GNT. The question of the role of immunoglobulin E needs to be studied in connection with recent data on late-type allergic reactions caused by immunoglobulin E and characterized by mononuclear cell infiltration without the presence of vasculitis. Perhaps the participation of a secondary autoimmune cytotoxic mechanism associated with chronic inflammation and tissue destruction. Non-immunological mechanisms are associated with the characteristics of disease-causing antigens that are resistant to lysosomal enzymes, are not destroyed by alveolar macrophages, are able to activate the complement system in an alternative way and have a nonspecific adjuvant effect on the induction of cell-mediated reactions and activation of alveolar macrophages. Immuno-non-immunological mechanisms activate alveolar macrophages, which, through soluble mediators, induce inflammation and stimulate the activity of fibroblasts, which leads to fibrosis. There is an opinion that it is activated alveolar macrophages that occupy a central place in the pathogenesis of exogenous allergic bronchioloalveolitis.

Pathomorphology of exogenous allergic bronchioalveolitis

With the fulminant form of exogenous allergic bronchioalveolitis, ending with the rapid death of the patient, intense inflammatory exudate in the alveolar septa, hemorrhagic edema inside the alveoli, necrosis of the bronchioles with obliteration are detected. In the acute period, infiltration of the alveoli and bronchioles with lymphocytes, plasma cells and a large number of alveolar macrophages is detected. Noncaseating sarcoid-like granulomas, consisting of lymphocytes, activated macrophages, epithelioid and giant cells, are characteristic. In a very early period of the disease, deposits of immune complexes on the alveolar membrane and necrotizing vasculitis are found. In the chronic form, infiltration by lymphocytes and plasma cells is less pronounced, granulomas are scattered in areas of interstitial fibrosis, destruction of the bronchioles mural structure with macrophage obliteration of the lumen, hypertrophy of the cuboid epithelium of the alveoli, and sometimes of the “emphysema” zone due to uneven destruction of the alveoli are observed. At the final stage, destruction of the alveoli, fibrosis, and the picture of the “cell lung” develop.

Clinic of exogenous allergic bronchioloalveolitis

Clinical signs of the disease depend on the nature of the organic particles, the intensity and frequency of inhalation, and the characteristics of the immunological response of the patient. The allergy period is different – from several months to several years. Usually, 4-6 hours after inhalation of organic dust, a cough appears, dry or with viscous yellow sputum, which may contain blood; there is an increase in temperature to 38-40 ° C, heavy sweat, chills, myalgia, weakness, retrosternal pain. Inspiratory dyspnea progresses rapidly. Over the lungs, dullness of the sound and crepitus are determined. In the acute period, tachycardia and bronchial obstruction resistant to the action of bronchodilators may occur, which indicates the prevalence of inflammation over increased bronchial tone. Fever lasts up to 24 hours, shortness of breath and weakness sometimes lasts up to several weeks. In other cases, the symptoms spontaneously disappear within a day. Upon contact with certain antigens (pigeon proteins, pituitary powder), HNT can occur, which occurs rarely if actinomycetes are the cause of exogenous allergic bronchioloalveolitis. With repeated exposures of the antigen, shortness of breath intensifies, anorexia, weight loss are noted – the disease acquires a chronic course, which can develop without an acute attack – in cases of prolonged contact with small stumps of antigen. This form is formed by bird lovers, especially budgerigar owners, workers in contact with heating and conditioning systems, and is characterized by progressive shortness of breath, coughing, weakness, malaise, and emaciation. Wet cracking rales (“cracking cellophane”) are heard over the lungs, but this is less typical of a disease than an idiopathic fibrosing alveolitis; in 10% of patients, after a gradual onset, subsequent antigen inhalations cause acute symptoms and GNT. Rare clinical signs of exogenous allergic allergic bronchioalveolitis are also described: chest tightness, impaired consciousness, changes in sensitivity and paralysis of the facial nerve.

The course of the disease is usually acute or subacute when inhaled enough antigen; with massive inhalation, the disease can last no more than a day. In cases of prolonged exposure to small doses of antigen, the disease progresses with the development of fibrosis.

The prognosis for acute and subacute currents is favorable, elimination of antigen and glucocorticosteroid therapy lead to the reverse development of the process. The prognosis is less favorable if the disease lasts several years, especially in the elderly.