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Pneumoconiosis
Last reviewed: 23.04.2024
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Pneumoconiosis (from the Greek pneumon - lung, conis - dust) is the reaction of the lung tissue to the accumulation of dust in it.
Pneumoconiosis is a pathology of the lungs of chronic course, the cause of which is the prolonged inhalation of industrial dust, which causes the development of widespread pulmonary fibrosis.
There are several types of the disease, depending on the causative factor, but still highlight the most common clinical manifestations of pneumoconiosis.
So, a person is concerned about dry cough, increasing shortness of breath, pain in the chest, which is due to the development of deforming bronchitis and severe respiratory failure.
In the process of diagnosing the disease, the professional experience and harmfulness are taken into account, which provoke damage to the lung tissue. In addition to these physical examinations, spirometry, X-ray examination, determination of the gas composition of blood and CBS are used.
The main direction in the treatment is the elimination of the harmful factor that caused the onset of pneumoconiosis. In addition, drugs are used to alleviate the patient's condition and reduce the area of lung tissue damage. They include bronchodilators, expectorants, hormones, as well as the use of physiotherapy procedures, oxygen inhalations and hyperbaric oxygenation.
Among occupational pathologies, pneumoconiosis occupies a leading position. Most often it is observed in workers in the production of glass, machinery, coal and asbestos industry, when the professional experience exceeds 5-15 years, depending on working conditions.
Aggressive dust particles can stimulate the formation of connective tissue in the pulmonary parenchyma. This leads to lung fibrosis and impairment of respiratory function. Diseases caused by exposure to dust, as a rule, are classified as occupational diseases. Their diagnosis and treatment is carried out by pathologists.
The most common cause of progression of pneumoconiosis after the termination of dust exposure is the complication of its tuberculosis. Central to pneumoconiosis in the frequency of joining a specific infection is silicosis. The emerging disease - silicotuberculosis - is a qualitatively new nosology, which has features of both silicosis and tuberculosis.
The pace of pneumoconiosis has changed significantly due to improved working conditions, so now it is very rare to diagnose progressive forms of silicosis and silicotuberculosis, which were identified in the 50's.
ICD-10 codes
Silicosis (J62)
Pneumoconiosis caused by inhalation of dust containing free silicon dioxide (SiO 2 ), in the form of a finely divided aerosol with a particle size of 0.5 to 5 microns. Silicosis is revealed in the workers of the mining and metalworking industry (slaughterers, sinkers). The likelihood of developing silicosis depends on the amount of dust deposited in the lungs, on the size, surface characteristics and crystal structure of the silicon oxide particles. As a result of the reaction of the lung tissue to the dust, interstitial fibrosis develops in the form of silicic clutches along the course of small vessels. Progression of the process leads to the formation of silicic nodules, which can increase up to 1-1.5 cm or more. When histologically examined, fibrotic and cell-fibrous nodules with a concentric arrangement of collagen and argyrophilic fibers are found, dust particles are located in the center of the nodule. The same nodules are located in the regional lymph nodes. Silicosis is characterized by a progression even after exposure to dust has ceased, as well as a frequent complication of its tuberculosis.
Separately, a group of diseases associated with accumulation in light dust containing a small amount of free silica (J.62.8): kaolinosis, cement, mica, nepheline and other pneumoconiosis.
Pneumoconiosis, caused by talc dust, is talcosis (J62.0). Morphological feature of diseases - the development of connective tissue without the formation of nodules in the parenchyma of the lungs and lymph nodes of the mediastinum. The course of diseases is favorable.
Anthracosis (J60)
Anthracosis - pneumoconiosis of the coal miner; the disease is caused by the accumulated in the coal dust. At a histological examination, accumulations of coal dust (anthracotic nodules) are found. The lung has a gray (sometimes black) color. Dust deposits are found in the lymph nodes of the mediastinum, liver, spleen.
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Asbestosis (J61)
The development of asbestosis is associated with the accumulation of light asbestos fibers. Morphological manifestations are fibrosing alveolitis and interstitial fibrosis. With minor and short-term exposure to asbestos dust, individual lesions are identified, asbestos bodies are found in these zones.
In ICD-10, a large group of pneumoconiosis is caused by another (non-silicic) inorganic dust (J63): aluminosis (J63.0), berylliosis (J63.2). Sidereosis (J63.4), stannosis (J63.5), graphitic fibrosis (J63.3), etc. The histological picture and clinical manifestations depend on the effect factor.
Pathogenesis of pneumoconiosis
Due to the serious air pollution exceeding the permissible level, and the mucociliary apparatus is not functioning properly, dust particles enter the alveoli of the lungs. Later they can be absorbed by macrophages or penetrate into the interstitial tissue.
The pathogenesis of pneumoconiosis is based on the presence of the cytotoxic effect of dust particles on macrophages, as a result of which peroxide oxidation of fats develops and lysochondrial and lysosomal enzymes are secreted. Thus, the proliferation of fibroblasts and the appearance of collagen fibers in the lung tissue are activated.
In addition, the presence of immunopathological processes in the development of pneumoconiosis has been demonstrated. Fibrosis of tissues can be characterized by nodular, nodal or interstitial localization. Nodular fibrosis includes sclerotized nodules from macrophages filled with dust, and accumulations of connective tissue elements.
Interstitial type of pneumoconiosis is observed in the absence of nodules from fibrous tissue. However, there are thickened alveolar septa, perivascular and peribronchial fibrosis.
The pathogenesis of pneumoconiosis can cause the appearance of large nodes due to the fusion of smaller ones, as a result of which a significant part of the lung loses its ventilating capacity.
The companion of the fibrous process is emphysema (focal or common), which can take a bullous character. In addition to the defeat of lung tissue, pathological processes in the bronchi are observed with the development of inflammation of bronchial mucosa and bronchioles.
Pneumoconioses pass through several stages, in particular they undergo an inflammatory reaction, dystrophic and sclerotic effects.
Symptoms of pneumoconiosis
The peculiarity of silicotuberculosis is the scarcity of clinical manifestations. In the initial stages of the process, symptoms are mild and nonspecific: dyspnoea with physical exertion, dry cough, increased fatigue can be manifestations of uncomplicated silicosis and concomitant chronic nonspecific pathology.
The clinical picture of tubercular bronchoadenitis against silicosis is due to severe intoxication: fever, weakness, sweating. The formation of the lymphoblocchial fistula is accompanied by a debilitating, unproductive cough. In the absence of treatment, secondary pneumonia develops, and the course of the disease is aggravated. With the progression of massive silicotuberculosis, pulmonary-cardiac failure develops.
Tuberculous pleurisy with pneumoconiosis can be the first manifestation of a specific process, a complication of tuberculosis bronchoadenitis or pulmonary destruction with massive silicotuberculosis.
Massive silicotuberculosis, corresponding to the III stage of silicosis, is characterized by the formation in the upper lobes of light large foci of a heterogeneous structure due to calcification of individual areas and the appearance of zones of destruction. Unlike the tuberculosis of the destruction zone, they can remain stable for a long time. These pulmonary changes are formed due to the fusion of individual foci and nodal formations or with lymphoblochial complications of tuberculous lesions of the lymph nodes. When the process progresses, the zone of destruction increases, and focal seeding appears.
Pneumoconiosis in electric welders
In the process of electric welding particles of dust of iron and other metals, silicon dioxide and toxic gases are formed. When these components are exposed to the respiratory tract, their lesions are observed, including pulmonary edema.
When contact with allergens occurs bronchitis with an asthmatic component. In most cases, pneumoconiosis is characterized by a benign course. In the case of welding in a closed room, the concentration of dust is significantly increased, and the hydrogen fluoride produced by its toxic effect provokes the development of pneumonia and frequent respiratory diseases.
Pneumoconiosis in electric welders is formed more often after the expiration of 15 years. Typical forms of silicosis are noted in workers in contact with dust with silica.
Uncomplicated course of pneumoconiosis is characterized by a cough with scant sputum, a pain syndrome in the chest and shortness of breath during physical activity. In addition, pharyngitis, rhinitis, dry wheezing and signs of emphysema are revealed during a more detailed examination.
Pneumoconiosis in electric welders is recorded after an X-ray study. In contrast to silicosis in the picture, radiopaque iron dust is released. At the end of contact with dust after 3-5 years, pneumoconiosis can be "cured" by cleansing of iron dust. However, these cases are possible only in the absence of complications in the form of obstructive bronchitis and tuberculosis.
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Stages of pneumoconiosis
The formation of pneumoconiosis can be characterized by a slow or rapidly progressive, late or regressive course. The slow development of pathology occurs as a result of dust exposure for 10-15 years.
The more rapidly progressive form begins to appear after a few (up to 5 years) from the onset of contact with the dust factor with an increase in symptoms within 2-3 years. The late form is characterized by the onset of manifestations only after a few years after the termination of contact with the pathological factor. Regression of pneumoconiosis is noted in the case of removing particles of dust from the respiratory system after the exposure to dust.
Despite the various causes of pneumoconiosis, the stages of development in most cases have a similar characteristic. The initial stages of pneumoconiosis are presented by shortness of breath, a cough dry or with the separation of scant sputum, pain syndrome with movements in the chest, under and between the shoulder blades.
As the process progresses, pain becomes permanent in the second stage of pneumoconiosis. In addition, the weakness grows, the temperature (from 37.0 to 37.9 degrees) appears, sweating increases, weight gradually decreases and dyspnea increases.
In the third stage of pneumoconiosis, the cough is worried constantly, sometimes paroxysmally, dyspnea is noted at rest, respiratory insufficiency is increasing, "blue" lips, changes in the shape of the fingers and nail plates are noted.
Further, the pulmonary heart develops and the pressure in the pulmonary artery increases. Of the complications, it is necessary to isolate chronic bronchitis (obstructive, with asthmatic component), tuberculosis (silicotuberculosis), damage to the walls of blood vessels with pulmonary hemorrhage, and the formation of bronchial fistulas.
In addition, in some cases, you can identify bronchiectasis, emphysema, asthmatic component, spontaneous pneumothorax and systemic diseases (rheumatoid arthritis, scleroderma). The presence of silicosis or asbestosis increases the likelihood of developing bronchial or lung cancer, as well as pleural mesothelioma.
Types of pneumoconiosis
Based on the damaging factor, it was decided to distinguish some types of pneumoconiosis, for example, silicosis, carcanconiasis, silicosis, metalloconiosis. In the case of exposure to mixed dust, anthracosilicosis, siderosilicosis, and diseases due to organic dust damage are released.
The most common and severe disease is silicosis, which occurs as a result of the action of dust with silicon dioxide. This type of pneumoconiosis is observed in workers of the foundry, mines, the manufacture of refractory materials and ceramics.
Silicosis is a chronic pathology, the severity of which is due to the duration of the impact of the aggressive factor. First, there is shortness of breath for physical activity, pain in the chest and periodic dry cough.
As the progression joins the signs of emphysema, the cough acquires a more severe shade, wheezing appears, and the pain worries even at rest. Gradually the cough becomes frequent and wet with sputum discharge.
On the basis of X-ray study, the degree and form of pathology is established. It is accepted to distinguish 3 degrees of severity, as well as nodular, nodal and interstitial form of silicosis.
In the absence of treatment and the presence of an affecting damaging factor, complications may develop. Among them, the most common are respiratory, cardiovascular, bronchial asthma, tuberculosis, obstructive bronchitis and pneumonia.
The next type of pneumoconiosis is asbestosis, the cause of which is asbestos dust. In addition to chemical exposure to dust, asbestos particles are destroyed by pulmonary tissue.
This species is found in workers involved in the production of pipes, slate, braking bands, as well as in the shipbuilding, aviation and construction industries.
Clinical symptoms are expressed by chronic bronchitis, emphysema and pneumosclerosis. Most often, coughing with sputum, where "asbestos bodies" are found, growing dyspnoea, and asbestos warts are present on the skin.
Of the possible complications, it is necessary to isolate pneumonia, severe respiratory failure, as well as the formation of neoplasms of different locations - pleura, lungs or bronchi.
To relatively benign silicosis it is customary to include such types of pneumoconiosis, as talcosis, which develops as a result of inhalation of talc dust. This pathology is characterized by the appearance of bronchitis, the severity of which is significantly less than with asbestosis. In addition, talcosis is less prone to progression, but not in the case of inhaling cosmetic powder.
Metalloconiosis is caused by the destruction of the lung tissue by beryllium dust with the development of berylliosis, iron - siderosa, aluminum - aluminosis or barium - barite. Benign form of the flow has metalloconiosis, the cause of which has become radiopaque dust (barium, iron, tin).
In this case, there is a development of moderate fibrosis, the progression of which is not noted. In addition, when eliminating the negative effects of dust, regression of the disease is observed as a result of self-purification of the lungs.
Aluminosis is characterized by interstitial diffuse-shaped fibrosis. As for beryllium and cobalt, then due to their influence, toxic and allergic lung damage is possible.
Carboconiosis occurs due to inhalation of carbon-containing dust, for example, from soot, graphite or coal. It is characterized by a moderate fibrosis of pulmonary tissue with small-focal or instertial localization.
Separately, carbonic acid is released, caused by exposure to coal dust with the development of anthracosis. Pathology is observed in the workers of the concentrating mill or mines after 15-20 years of experience.
Fibrous process has the form of widespread sclerosis. However, with the combined damage of coal and rock dust, development of anthracosilicosis is noted, which is a more severe form with progressive fibrosis.
The defeat of pulmonary tissue as a result of exposure to organic dust only conditionally relates to pneumoconiosis, in view of the fact that in some cases there is no diffuse process with the development of pneumofibrosis. Most often there is bronchitis with an allergic component, for example, when inhaled cotton dust.
Inflammatory character with elements of an allergy can be observed at a defeat by a dust of a flour (torment), a sugar cane, plastic products, and also an agricultural dust with presence of a fungus.
Complications of pneumoconiosis
In the case of prolonged exposure to a harmful factor and the lack of proper treatment for pneumoconiosis, the risk of complications increases. They exacerbate the clinical picture of the pathological process and, as they progress, involve all new tissues in the process.
Complications of pneumoconiosis are the development of pulmonary heart, pneumonia, obtuscative form of bronchitis, bronchial asthma, the formation of bronchiectasis, the onset of cardiac and pulmonary insufficiency.
Often there is a connection of tuberculosis to the pathological process, which causes silicotuberculosis. The most important is the differential diagnosis of these diseases, which determines the tactics of patient management and treatment.
It must be remembered that tuberculosis is a contagious disease that leads to infection of surrounding people. A person with an open form of tuberculosis is subject to isolation and specific treatment.
With silicosis, there are no clinical symptoms of intoxication, manifestations of moderate activity on the part of the respiratory organs, and a typical kinetic pattern is also observed.
Complications of pneumoconiosis in rare cases can also be expressed in transformation into a malignant process. The tumor-like appearance of silicosis differs from cancer by its slow growth and the relatively satisfactory state of the patient.
Diagnosis of pneumoconiosis
Diagnosis of pneumoconiosis is established on the basis of several diagnostic criteria:
- data of a professional anamnesis:
- assessment of the dustiness of the working area:
- X-ray picture at the time of examination and in dynamics over several years,
- indicators of the function of external respiration.
Laboratory diagnostics of pneumoconiosis
With active silicotuberculosis, the leukocyte formula and biochemical blood parameters change: a moderate increase in ESR, a shift of the leukocyte formula to the left, lymphopenia, an increase in the level of γ-globulins, haptoglobin, and protein.
An unconditional sign of silicotuberculosis is the presence in the sputum of a patient with mycobacterium tuberculosis, detectable by bacterioscopy or by seeding on nutrient media, but the specific gravity of bacterial liberators does not exceed 10%.
Immunological shifts: a decrease in the absolute number of T-lymphocytes due to the CD4 population, sometimes an increase in IgA and IgM.
The informative nature of provocative samples with tuberculin is not sufficient for reliable diagnosis of silicotuberculosis.
X-ray methods for pneumoconiosis
The blackouts resulting from coniotic pneumofibrosis are classified according to shape, size, location and intensity. The stage of the process is determined by comparing the obtained X-ray diffraction patterns with the standards: depending on the severity of the process, four categories (0, I, II, III) are distinguished.
For a detailed assessment of the condition of the lung parenchyma, vessels of the small circle of circulation, lymph nodes of the mediastinum, the pleura are mainly used CT of the thorax.
Limited (small) forms of silicotuberculosis: focal tuberculosis, limited disseminated tuberculosis, limited infiltration and tuberculosis. When these changes are identified, the patient with an interstitial form of silicosis does not have difficulty in establishing the diagnosis. Diffuse interstitial changes in the lung parenchyma and areas of emphysema suggest pneumoconiosis, and a limited process in the form of small and large foci or foci occurring in the intact pulmonary field is regarded as a manifestation of tuberculosis. Further clinical and radiological monitoring allows to confirm the diagnosis.
If new focal or focal changes localized in the apical-posterior segments of the lungs are found, it is necessary to clarify the background of silicosis, what caused such changes: the progression of silicosis or the complication of its tuberculosis. To establish the diagnosis, study the archival documentation and evaluate the dynamics of the process (the rate of development of new elements and growth of focal formations): the faster the changes, the higher the probability of tuberculosis etiology. Progression of the silicic process, as a rule, uniformly in all parts of the lungs. The appearance of asymmetry, the increase in the severity of changes in the posterior regions indicate the attachment of a specific process. With the help of CT, there are signs of destruction, which do not happen at small sizes of silicic nodes. Assess the dynamics of the process under the influence of a specific treatment for 3 months or more.
Silicotuberculoma on the background of nodular silicosis - a special form of lesion (does not correspond to the classification of silicosis), detected on the background of diffuse nodular pneumoconiosis in the form of rounded formations. They are formed due to the fusion of individual foci, localized more often in the cortical parts of the lungs. Distinguish tuberculoma in a stable state (its magnitude does not change, and the periphery forms a fibrous capsule). In the active phase, a depletion zone is revealed with the help of a CT closer to its lower inward pole. The progression of silicotuberculosis is accompanied by an increase in the decay zone, the appearance of focal seeding and the growth of the focus of the lesion.
Bronchological methods for pneumoconiosis
In the diagnosis of silicotuberculosis, bronchial examinations are sometimes used in combination with cytological and cytochemical studies of lavage fluid.
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Diagnosis of lymph node involvement
Tuberculosis of the intrathoracic lymph nodes is a frequent complication of silicosis, which is usually not diagnosed for a long time. Both silicosis and silicotuberculosis are characterized by the defeat of all groups of intrathoracic lymph nodes, however, the number of calcification foci and the nature of calcium deposition are different. Tuberculosis and silicic processes in the lymph nodes occur simultaneously, and a specific process quickly undergoes hyalinosis, so even by biopsy it is not always possible to confirm the diagnosis; nevertheless, a massive enlargement of the lymph nodes of one or two groups, the presence of a lymphoblocchial fistula, and the further development of inflammatory stenosis of the bronchus indicate a comprehensive lesion. To confirm the diagnosis, it is necessary to establish the fact of bacterial excretion and repeatedly (in dynamics) to study the endoscopic picture. If there is a fistula in order to prevent the development of secondary inflammation in the pulmonary parenchyma, sanation is constantly carried out. Sometimes with silicotuberculosis, multiple fistulas are identified, the healing of which occurs with the formation of characteristic pigmented, retracted scars.
In the diagnosis of silico-tubercular bronchoadenitis, timely bronchial examination of the patient, collection of material for research (bacteriological, cytological and histological) is of great importance.
The diagnosis of pneumoconiosis
At present, there is no generally accepted classification of silicotuberculosis. Doctors use a descriptive formulation of the diagnosis, including a statement of the presence of the disease and the subsequent characterization of the silicic and tuberculosis process in accordance with the current classifications of these diseases.
The diagnosis of pneumoconiosis contains an assessment of the radiographic morphology of the lungs, the prevalence and intensity of the lesion, the stage of the process, the functional characteristics of external respiration, the course of the disease and the presence of complications, for example:
Silicotuberculosis. Silicosis of the first stage (s). Infiltrative tuberculosis of the second segment of the right lung in the phase of decay and seeding (BK +).
This approach to the formulation of the diagnosis has a number of limitations: if the X-ray picture of silicotuberculosis does not differ from its classical manifestations in the initial stages of the development of the process, it is often impossible to distinguish between the silicotic and tubercular process (disseminated and conglomerate silicotuberculosis) in stages II and III.
As a special form of the disease, acute silicosis (a rapidly progressing process, develops after the inhalation of finely dispersed silicon particles at very high concentrations) is isolated.
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Treatment of pneumoconiosis
An important aspect in the therapy of pneumoconiosis is the elimination of the harmful factor that caused the disease. Treatment of pneumoconiosis consists in slowing or completely stopping the progression of the pathological condition, reducing the activity of the process, reducing clinical symptoms and preventing the development of complications.
Important attention is paid to the nutritional regime, which must be enriched with protein products and vitamins. In order to increase the body's resistance to infection, it is necessary to increase immune defenses. For this purpose, the administration of immunomodulators of plant origin (echinacea, Chinese magnolia vine) is recommended.
Treatment of pneumoconiosis must necessarily include health and tempering procedures, for example, exercise therapy, massage, various kinds of shower - Charcot, circular.
Uncomplicated pneumoconiosis can be treated with ultrasound, electrophoresis with calcium and novocaine on the chest.
To improve the clearance of sputum, bronchodilators and expectorants are used to reduce the viscosity of the bronchial secretion and activate the mucociliary system. In addition, it is desirable to use inhalations with bronchodilators and proteolytic enzymes, as well as oxygen therapy (HBO, inhalation of oxygen).
A preventive course to prevent the progression of pneumoconiosis is carried out twice a year in a hospital or in a sanatorium. In the case of a complicated course of the disease, additional use of hormonal drugs is required to reduce the severity of the inflammatory reaction and the antiproliferative purpose.
As the increase in respiratory and heart failure, it is advisable to use diuretics, bronchodilators, cardiac glycosides and anticoagulants that affect the coagulation of blood.
Prevention of pneumoconiosis
Specific prophylaxis of pneumoconiosis consists in the modernization of equipment in the workplace to reduce the time of human stay in contact with the damaging factor. In addition, a set of measures should be developed to improve working conditions and ensure occupational safety.
Individual protection refers to the use of respirators that protect against dust, eyeglasses and special clothing. It is also necessary to take care of collective protection in the form of a supply-and-exhaust type of ventilation, ventilation and humidification of premises in production.
Prevention of pneumoconiosis requires mandatory regular preventive examination of people who are constantly in contact with a harmful factor. In addition, before the device for production, it is necessary to undergo a medical examination for contraindications.
They consist of the following diseases: allergic pathology, diseases of the bronchial system in the chronic stage, curvature of the nasal septum, chronic dermatosis, as well as congenital anomalies of the cardiac and respiratory system.
Pneumoconiosis refers to occupational pathology, the cause of which is industrial dust. Depending on working conditions and length of service, the degree of damage to lung tissue can be expressed in different degrees. Despite this, some types of pneumoconiosis can be treated well, but only if the harmful effect is removed.