Silicosis is a occupational disease characterized by the development of severe pneumofibrosis due to prolonged inhalation of dust with a high content of free silicon dioxide. The symptoms are progressive: shortness of breath first occurs during exercise, then at rest, periodic coughing is replaced by a constant cough, chest pain increases, in the later stages, pulmonary heart failure develops. The decisive diagnostic criteria are the data of professional anamnesis in combination with typical radiological signs of silicosis. Therapeutic measures include bronchoalveolar lavage, drug therapy, oxygen therapy; in some cases, lung transplantation.
J62.8 Pneumoconiosis caused by other dust containing silicon
Silicosis is a form of pneumoconiosis that develops when inhaled and deposited in the lungs of fibrogenic dust containing crystalline silicon dioxide (silica). Silicosis became most widespread in the late XIX – first half of the XX century. in connection with the rapid development of the mining industry, machine tools and mechanical engineering, where workers were exposed to dust containing free silicon dioxide. Nowadays, the disease is a thing of the past, although employment in certain industries is still associated with an increased risk of silicosis. As a result of silicosis, massive pulmonary fibrosis develops, which can progress even after the cessation of exposure to fibrogenic dust. Pulmonology and occupational pathology are engaged in the clinical study of silicosis.
Causes of silicosis
Silicosis occurs due to the inhalation of particles of free silicon dioxide in crystalline form, mainly quartz dust, less often – cristobalite and tridymite. Silicosis can be an occupational disease for the following industries: mining (extraction of minerals from rocks containing quartz), mechanical engineering and metallurgy, manufacture of glass, ceramics, porcelain, etc. Miners, sinkers, foundry workers, sandblasters, glass blowers, stone carvers, potters are more likely to suffer from silicosis. Miners may have a mixed disease caused by exposure to quartz and coal dust – silicoanthracosis.
The rate of development of the disease, the prevalence and severity of the lesion depends on the length of service, working conditions, the intensity of dust exposure, individual properties of the body. From the beginning of work in hazardous production to the detection of silicosis, it may take from 3-5 to 15-20 years. The size of dust particles is essential – for penetration into the alveoli and the interstitial tissue, the diameter of the dust particles should be less than 5 microns. Several theories of the pathogenesis of silicosis are discussed. The earliest of them, mechanical, explains the pathological changes by mechanical damage to the lung tissue by fine dust. According to the toxico-chemical theory, quartz dust dissolves in tissues with the release of silicic acid, which has a cytotoxic effect. However, these and other theories cannot fully explain all aspects of pathogenesis.
Currently, the most popular is the immunological theory of the development of silicosis. In it, special importance is attached to the phagocytosis of quartz particles by alveolar macrophages. Absorbed silicon particles cause damage to lysosomal membranes with the release of enzymes into the cytoplasm and the death of macrophages. The silicon particles released from the dead cells are re-captured by other macrophages, again and again leading to the death of phagocytes. At the same time, when macrophages are destroyed, biologically active substances are released into the lung tissue, among which is a lipid fibrogenic factor that stimulates the formation of silicotic nodules. In addition, adsorbed on the surface of the lungs, silicon dust particles change the properties of protein particles, as a result of which the latter acquire autoantigenic properties. Dead pulmonary macrophages can also act as autoantigens. The role of the immune factor in the genesis of silicosis allows some authors to consider this disease in a number of collagenoses.
There are three main clinical and morphological forms of silicosis – nodular, diffuse-sclerotic and mixed. In the nodular form of silicosis, silicotic granulomas are formed in the lungs, represented by bundles of connective tissue. Granulomas can be arranged concentrically or vortically, sometimes merge into a large node (nodular or tumor-like form of silicosis). Nodules can undergo necrotic changes and form silicotic cavities when they break into the bronchus. The diffuse-sclerotic form proceeds with the development of interalveolar, perivascular and peribronchial fibrosis; the formation of bronchiectasis, emphysema, pleural mooring. With a mixed form of silicosis, nodular granulomas are detected against the background of widespread sclerosis.
Silicosis can occur in an acute, chronic (classical), progressive, accelerated form. Acute silicosis develops with massive exposure to silicon dust in less than 2 years. It proceeds violently with severe shortness of breath, general symptoms (weakness, weight loss). Chronic silicosis usually makes itself felt 15 or more years after contact with silica. It develops asymptomatically, gradually, and the increase in shortness of breath and cough is often attributed to other diseases or the natural aging process. It proceeds in the form of nodular fibrosis.
Progressive massive fibrosis is characterized by increased shortness of breath, cough with sputum, recurrent purulent bronchitis, pronounced pulmonary ventilation disorders. Typical complications of this form of silicosis are pneumothorax, tuberculosis, pulmonary heart disease. An accelerated version of silicosis occurs after 5-10 years of contact with quartz dust. Clinical manifestations are similar to the chronic form, but progress faster. It is often combined with mycobacterial infection, autoimmune diseases (scleroderma).
Symptoms of silicosis
In most cases, the disease develops gradually, while subjective clinical symptoms of silicosis appear later than radiological changes in the lungs. Based on clinical and radiological signs, three stages of silicosis are distinguished.
At stage I, shortness of breath is present only in conditions of physical exertion, the patient is concerned about periodic dry cough, moderate tingling pains in the chest. Radiologically, the strengthening of the pulmonary pattern, the initial signs of emphysema are determined.
Stage II of silicosis is accompanied by shortness of breath with minimal exertion, a persistent cough, constant chest pains. Dry scattered wheezing, hard breathing are heard. The images reveal nodular elements, pleural layers, bullous emphysema.
At the last, III stage of silicosis, shortness of breath becomes constant (including at rest), cough with sputum, hemoptysis, tachycardia worries; cyanosis of the face is detected. In the later stages, pulmonary hypertension and cardiopulmonary insufficiency develop. Radiological signs include massive pneumofibrosis, emphysema, atelectasis, mediastinal displacement.
The course of silicosis is often aggravated by obstructive bronchitis, bronchial asthma, bacterial pneumonia, bronchiectatic disease, spontaneous pneumothorax, lung cancer. In the case of complications of silicosis with articular syndrome, they talk about silicoarthritis. In 30-80% of cases, tuberculosis develops, which leads to a mixed form of the disease – silicotuberculosis. A simultaneous combination of silicosis, tuberculosis and rheumatoid arthritis is possible. The cause of death of patients can be both concomitant disease and decompensation of the pulmonary heart.
The reliability of the diagnosis of “silicosis” is confirmed after clarifying the professional route, conducting X-ray diagnostics, examining the FER, consulting the patient with a professional pathologist and a pulmonologist. Auscultative data are variegated: hard, weakened, bronchial breathing, dry cracking and wet wheezing, pleural friction noise can be heard over different parts of the lung.
The main radiological signs of silicosis are silicotic nodules – small–focal shadows of rounded shape ranging from 1 to 10 mm in size, located in the upper pulmonary fields; additional – emphysema, mesh or cellular structure of the pulmonary pattern, thickening of the pleura. High-resolution lung CT or MSCT have higher sensitivity. Spirography data reveal mixed violations of pulmonary ventilation. The study of blood gases, pulse oximetry allows to control the dynamics of the development of silicosis. In some patients, anti-nuclear antibodies, C-reactive protein, positive rheumatoid factor are detected.
Diagnosis of silicosis should be carried out with sarcoidosis, hemosiderosis, anthracosis, asbestos, miliary tuberculosis, metastatic lung cancer, Wegener’s granulomatosis, fungal lung lesions. An additional set of studies (sputum analysis, bronchoscopy, tuberculin test, PET and CT of the chest) helps to distinguish silicosis from these diseases.
Radical methods of treatment of silicosis have not been developed. When confirming the diagnosis, the first step should be to stop contact with quartz dust. Protein and vitamin-rich nutrition, therapeutic gymnastics, distance walking are prescribed. The main goal of therapy is to inhibit the progression of fibrous changes, prevent and eliminate complications.
In some cases, treatment begins with total bronchoalveolar lavage – this technique helps to reduce the overall dust pollution of the lungs. With the rapid progression of silicosis, corticosteroid hormones (prednisone) are used. A positive effect is noted from inhalations of proteolytic enzymes that improve bronchial patency, and hyaluronidase, which increases the permeability of tissues for the medications used.
The complex therapy of silicosis includes bronchodilators (berotec, salbutamol), expectorants, antihistamines, oxygen therapy. In case of joining the tuberculosis process, treatment with a phthisiatrician is indicated. Measures of physiotherapeutic rehabilitation include ultrasound, UFO, electrophoresis, respiratory gymnastics, spa treatment. Patients with silicosis need a categorical refusal to smoke, preventive vaccination against influenza, pneumococcus. In severe, rapidly progressing pulmonary fibrosis, lung transplantation can serve as the only salvation.
Prognosis and prevention
Timely recognized, uncomplicated silicosis may not have a significant impact on the quality and duration of life. However, in all cases, the changes in the lungs are irreversible, and the disease will progress at one rate or another. Adverse outcomes are recorded in rapidly progressive and complicated forms of pneumoconiosis.
The basis of preventive measures is the improvement of sanitary conditions (sealing of equipment, automation of production processes, exhaust ventilation, use of personal protective equipment, etc.). Preventive measures of a medical nature include periodic occupational examinations with mandatory X-ray examination of the lungs. Persons with silicosis are exempt from working in harmful industries, depending on the severity of the disorders, they are assigned a disability group.
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