Pneumoconiosis are a number of chronic lung diseases resulting from prolonged inhalation of industrial dust and characterized by the development of diffuse fibrosis of the lung tissue. The course of pneumoconiosis is accompanied by a dry cough, progressive shortness of breath, chest pain, the development of deforming bronchitis, and an increase in respiratory failure. When diagnosing pneumoconiosis, the presence and type of occupational hazards, physical data, results of spirometry, X-ray examination, ABB and blood gas composition are taken into account. Treatment includes the exclusion of contact with harmful compounds, the use of bronchodilators and expectorants, corticosteroids, physiotherapy, oxygen inhalation, hyperbaric oxygenation.
ICD 10
J60 J61 J62 J63
Meaning
Pneumoconiosis in pulmonology include various chronic occupational lung diseases that occur due to inhalation of harmful industrial dust and lead to pronounced development of connective tissue – diffuse primary fibrosis. Pneumoconioses occupy one of the leading places in the structure of occupational diseases. Pneumoconiosis is most often found in workers of coal, asbestos, machine-building, glass and other industries exposed to harmful industrial dust for 5-15 years or more.
What causes pneumoconiosis
The factors determining the development of pneumoconiosis are the composition, prolonged exposure and high concentrations of inhaled dust of inorganic (mineral) or organic origin.
Depending on the chemical composition of the dust, the following groups of occupational lung diseases are distinguished:
- silicosis – pneumoconiosis, which develops when exposed to dust containing silicon dioxide (SiO2);
- silicatoses are a group of pneumoconioses that develop against the background of inhalation of silicates – compounds of silicic acid with metals (asbestos, kalinosis, talcosis, nephelinosis, etc.);
- metalloconiosis – pneumoconiosis caused by exposure to metal dust (aluminum – aluminosis; barium – barinosis; beryllium – berylliosis; iron – siderosis, etc.);
- carboconiosis – pneumoconiosis caused by inhalation of carbonaceous dust (anthracosis, sooty pneumoconiosis, graphitosis);
- pneumoconiosis associated with exposure to mixed dust (siderosilicosis, anthracosilicosis, pneumoconiosis of gas cutters and electric welders);
- pneumoconioses that develop with prolonged inhalation of dust of organic origin (flax, cotton, wool, sugar cane, etc.). This group of pneumoconioses more often resembles allergic alveolitis or bronchial asthma; at the same time, the development of diffuse pneumofibrosis is not noted in all cases. Therefore, diseases caused by exposure to organic dust are only conditionally attributed to the group of pneumoconioses.
The depth of dust penetration into the airways and the intensity of its elimination depend on the size (dispersion) of aerosol particles. The most active fraction is highly dispersed particles with a size of 1-2 microns. They penetrate deeply and mainly settle on the walls of terminal bronchioles, respiratory passages and alveoli. Larger particles are retained and removed by the mucociliary apparatus of the bronchi; smaller fractions are eliminated with exhaled air or through the lymphatic pathways.
Pathogenesis
The high pollution of the inhaled air combined with the insufficient efficiency of mucociliary clearance causes the penetration and settling of aerosol particles in the alveoli. From there, they can independently penetrate the interstitial lung tissue or be absorbed by alveolar macrophages. The absorbed particles often have a cytotoxic effect on macrophages, causing the process of lipid peroxidation. The lysochondrial and lysosomal enzymes released in this case stimulate the proliferation of fibroblasts and the formation of collagen in the lung tissue. Immunopathological mechanisms have been proven to be involved in the pathogenesis of pneumoconiosis.
Fibrous changes in the lung tissue in pneumoconiosis can be nodular, interstitial and nodular in nature. Nodular fibrosis is characterized by the appearance of small sclerotic nodules consisting of macrophages loaded with dust and bundles of connective tissue. In the absence of fibrous nodules or a small number of them, an interstitial form of pneumoconiosis is diagnosed, which is accompanied by thickening of the alveolar septa, perivascular and peribronchial fibrosis. The fusion of individual nodules can give rise to large nodes that occupy a significant part of the lung tissue, up to an entire lobe.
The fibrous process in the lungs is accompanied by small-focal or widespread emphysema, sometimes acquiring a bullous character. In parallel with changes in the lung tissue in pneumoconiosis, pathological processes develop in the bronchial mucosa of the type of endobronchitis and bronchiolitis.
In its development, pneumoconioses undergo a period of inflammatory-dystrophic and productive-sclerotic changes. Most pneumoconioses, as a rule, are radiologically detected only in the second period.
Symptoms of pneumoconiosis
The course of pneumoconiosis can be slowly progressing, rapidly progressing, late, regressing. A slowly progressive form of pneumoconiosis develops 10-15 years after the beginning of contact with industrial dust. Manifestations of a rapidly progressive form manifest 3-5 years after the start of contact with dust and increase over the next 2-3 years. With late pneumoconiosis, symptoms usually appear only a few years after the cessation of contact with the dust agent. A regressive form of pneumoconiosis is spoken of if dust particles are partially removed from the respiratory tract after the cessation of exposure to a harmful factor, which is accompanied by a regression of radiological changes in the lungs.
Different types of pneumoconioses have similar clinical symptoms. In the initial stages, complaints of shortness of breath, cough with a meager amount of sputum, stabbing pains in the chest, scapular and interscapular areas are presented. Initially, the pain is irregular, intensifying with coughing and deep breathing; later, the pain becomes constant, oppressive.
The progression of pneumoconiosis is accompanied by an increase in weakness, subfebrility, sweating; a decrease in body weight, the appearance of shortness of breath at rest, cyanosis of the lips, deformation of the terminal phalanges of fingers and nails (“drumsticks” and “watch glasses”). With complications or a far-reaching process, signs of respiratory failure appear, pulmonary hypertension and a pulmonary heart develop.
A significant part of pneumoconioses (anthracosis, asbestos, etc.) is complicated by chronic bronchitis (non-obstructive, obstructive, asthmatic). Tuberculosis often joins the course of silicosis; it is possible to develop silicotuberculosis, which is aggravated by erosion of the pulmonary vessels, pulmonary bleeding and the formation of bronchial fistulas.
Frequent complications of pneumoconiosis are bronchiectasis, bronchial asthma, pulmonary emphysema, spontaneous pneumothorax, rheumatoid arthritis, scleroderma and other collagenoses. With silicosis and asbestos, it is possible to develop alveolar or bronchogenic lung cancer, pleural mesothelioma.
Diagnosis
When recognizing pneumoconioses, it is extremely important to take into account the patient’s professional route and the presence of contacts with industrial dust. In mass examinations of occupational risk groups, the role of primary diagnosis of pneumoconiosis is performed by large-frame fluorography. At the same time, a characteristic strengthening and deformation of the pulmonary pattern, the presence of fine-focal shadows are revealed.
In-depth examination (lung x-ray, computed tomography, MRI of the lungs) allows you to clarify the nature of pneumoconiosis (interstitial, nodular and nodular) and the stage of changes. With the progression of pneumoconiosis, the area of the lesion increases, the size and number of shadows, areas of massive fibrosis, compensatory emphysema, thickening and deformation of the pleura, etc. are revealed. Assessment of blood flow and ventilation in various areas of lung tissue is carried out using zonal rheopulmonography and lung scintigraphy.
The complex of studies of the function of external respiration (spirometry, peak flowmetry, plethysmography, pneumotachography, gas analysis) makes it possible to distinguish between restrictive and obstructive disorders. Microscopic examination of sputum in pneumoconiosis reveals its mucous or mucopurulent nature, dust impurities and macrophages loaded with dust particles. In cases difficult to diagnose, bronchoscopy with a transbronchial biopsy of lung tissue, puncture of the lymph nodes of the lung root are resorted to.
Treatment of pneumoconiosis
If any form of pneumoconiosis is detected, it is necessary to stop contact with a harmful etiological factor. The purpose of treatment of pneumoconiosis is to slow down or prevent the progression of the disease, correct symptoms and concomitant pathology, and prevent complications.
Important importance in pneumoconiosis is attached to nutrition, which should be rich in vitamins and proteins. To increase the nonspecific reactivity of the body, it is advisable to take various adaptogens (tinctures of eleutherococcus, Chinese lemongrass). Wellness and tempering procedures are widely used: physical therapy, massage, therapeutic showers (Charcot shower, circular shower). In uncomplicated forms of pneumoconiosis, ultrasound or electrophoresis with calcium and novocaine is prescribed for the chest area, inhalation of proteolytic enzymes and bronchodilators, oxygen therapy (oxygen inhalation, hyperbaric oxygenation). Miners are shown to carry out general ultraviolet irradiation, which increases the body’s resistance to bronchopulmonary diseases. Treatment and prophylactic courses for pneumoconiosis are recommended to be conducted twice a year in a hospital or sanatorium-dispensary.
Patients with a complicated course of pneumoconiosis with anti-inflammatory and antiproliferative purposes require the appointment of glucocorticoids for 1-2 months under tuberculostatic protection. With the development of cardiopulmonary insufficiency, the use of bronchodilators, cardiac glycosides, diuretics, anticoagulants is indicated.
Prognosis and prevention
The prognosis of pneumoconiosis is determined by its form, stage and complications. The most unfavorable course of silicosis, berylliosis, and asbestos, since they can progress even after cessation of contact with harmful dust.
The prevention of pneumoconiosis is based on a set of measures to improve working conditions, comply with production safety requirements, and improve technological processes. To prevent pneumoconiosis, it is necessary to use individual (anti-dust respirators, protective glasses, anti-dust clothing) and collective protective equipment (local supply and exhaust ventilation, ventilation and humidification of industrial premises).
Persons in contact with harmful production factors are subject to preliminary and periodic medical examinations in accordance with the established procedure. Employment related to contact with industrial dust is contraindicated for persons with allergic diseases, chronic diseases of the bronchopulmonary system, curvature of the nasal septum, chronic dermatoses, congenital anomalies of the heart and respiratory organs.
Literature
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