asbestosis
Introduction
Introduction to asbestosis Asbestosis is a chronic, progressive, diffuse, irreversible pulmonary interstitial fibrosis, pleural plaque formation, and pleural hypertrophy caused by long-term inhalation of asbestos dust, which seriously impairs the lung function of patients and can cause lung and pleural malignancies. The incidence has increased significantly. Most of the symptoms appear in the dust for 7 to 10 years, but a few also have symptoms only 1 year after the dust. The typical symptoms of asbestosis are slow-occurring and gradually increasing dyspnea. The early stage is labor-related, and the severity is related to the time and concentration of exposure to dust. Generally, it is a dry cough. Severe smokers tend to have a heavy cough and are accompanied by mucus sputum. Chest pain is often light, often dull pain in the back or sternum, hemoptysis is less common, such as combined tumors can occur hemoptysis, combined with infection, fever, cough and phlegm. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: lung cancer, tuberculosis, laryngeal cancer, emphysema
Cause
Asbestosis
Asbestosis is caused by the deposition of asbestos fibers in the respiratory bronchioles and alveolar walls. The virulence of asbestos fibers is related to the amount of inhalation, fiber size, shape and solubility. Asbestos fibers are available in both spiral and straight shapes. Spiral fibers are often excreted by the respiratory mucosa after inhalation. Straight fibers are hard and brittle, and have strong penetrating power in the respiratory tract, so the pathogenicity is also strong.
Interstitial inflammation of the lungs (30%):
Early inhaled asbestos fibers stayed in the respiratory bronchioles, only partially reaching the alveoli, passing through the alveolar wall into the pulmonary interstitium and being phagocytosed by macrophages, releasing proinflammatory cytokines and fibrotic factors, causing interstitial inflammation and extensive fibers. Chemical.
Direct stimulation (30%):
Asbestos fibers directly stimulate the synthesis of fibroblasts and secrete collagen to form fibrosis.
Toxicity (30%):
Asbestos has toxic effects on macrophages, alveolar epithelial cells, and mesothelial cells in lung tissues, resulting in fibrosis of the lungs and pleura.
Pathogenesis
Asbestos dust particles are needle-shaped. When inhaled into the lungs, they easily enter the lower lobe along the bronchus. Asbestos fibers with a diameter of less than 3 m are deposited in the respiratory bronchioles, partially reaching the alveoli, causing bronchioloalveolitis and asbestos through mechanical stimulation and chemical action. Dust deposits in the lungs to form a dusty foci, macrophages phagocytize, followed by fibrous tissue hyperplasia, leading to alveolar septum, interlobular septal vessels, peri-bronchial and visceral pleural diffuse pulmonary fibrosis, tissue culture results show that asbestos Macrophages are less toxic than silica and less toxic to fibroblasts, indicating that pulmonary fibrosis is caused by asbestos directly stimulating fibroblasts, promoting conversion of proline to hydroxyproline, accelerating collagen synthesis, and promoting fibrosis. Formation, animal experiments show that long fibers have tumorigenic activity, and the incidence of lung and pleural malignant tumors is significantly increased.
Asbestos damage to the respiratory tract can be divided into three categories: pleural plaque or exudate; pulmonary fibrosis is involved in the pulmonary parenchyma; bronchial or pleural tumors, these lesions can occur alone or in combination, the same patient often has pleural plaque and lung Substantial lesions, pleural plaque can also be seen in patients without pulmonary parenchymal disease, lung cancer can become a complication of asbestosis, mesothelioma can occur in patients without obvious asbestosis or pleural plaque.
Early asbestosis lung mainly occurs in the middle and lower parts of both lungs, the appearance is gray, the hardness of lung tissue is increased, accompanied by pleural fibrosis adhesion and thickening. More than half of patients have localized pleural plaque in the parietal pleura, which is characterized by adhesion only to the wall layer. The pleura has no adhesion to the visceral pleura. The boundary is clear, the surface is smooth and shiny, similar to cartilage. It is symmetrically distributed on the posterolateral side of the bilateral middle and lower chest wall. The subpleural lung fibrosis thickens and the middle and late stage pulmonary fibrosis. More obvious, extensive, to the development of the two upper lung areas, the lungs become hard, pale, pleural pericardial adhesion, microscopic observation of pleural plaque is a cell-free avascular transparent collagen, occasionally fibroblasts, lung Asbestos dust dust in the tissue can cause desquamative occlusive alveolitis, dusty inflammation changes in the alveolar wall and respiratory bronchioles, macrophage accumulation, collagen fibrosis, sometimes formation of foreign body granuloma, alveolar epithelial shedding, obstruction The bronchioles block the alveolar occlusion and disappear, and the reticular fibers surround the alveolar epithelial hyperplasia, causing the alveolar wall to thicken, which in turn causes the bronchioles to Fibrosis around the tube, the lesion is usually the most severe subpleural and lung base, late extensive subpleural lung tissue damage, fibrosis and occlusion, alveolar collapse and inflammatory mechanism, so that the subpleural lung tissue is almost completely fibrous tissue Substitute, the interlobular septal fiber cord and the grid are large, and there is a large area of lung tissue damage or honeycomb changes, during which asbestos bodies are scattered, due to thickening of the vascular muscle layer and fibrosis of the intima, resulting in thickening of the pulmonary arteriole wall, thus Usually accompanied by pulmonary hypertension.
Other pleural lesions caused by asbestos damage include pleural effusion, pleural adhesions and extensive pleural fibrosis. The onset of bronchial lung cancer is more concealed. It is usually found clinically after exposure to asbestos dust for 20 to 30 years. The tumor cell type is adenocarcinoma. Many, squamous cell carcinoma is not uncommon. Some patients do not show asbestosis when lung cancer occurs. The incubation period of mesothelioma is longer than that of lung cancer, which can occur from the beginning of dust collection for 30 to 40 years.
Prevention
Asbestosis prevention
The maximum allowable concentration of asbestos dust and dust containing more than 10% asbestos in China is 2mg/m3, and the highest concentration of other silicates is asbestos dust containing 10% or less is 4mg/m3. The reduction of asbestos dust concentration is to prevent workshops and The foundation of pneumoconiosis occurs on the construction site, the closed machine is equipped with aeration dust removal equipment, and attention is paid to prevent pollution of the surrounding environment due to ventilation. When mixing with other products and spinning, the fiber should be wetted beforehand to effectively reduce the generation of dust. Workers should change clothes and clean them when they go to work. It is forbidden to wear work clothes to leave the workplace and prevent pollution of the family environment. Use less toxic substances instead of asbestos.
Complication
Asbestosis pulmonary complications Complications lung cancer tuberculosis laryngeal cancer emphysema
Lung cancer
The main complication of asbestosis is lung cancer. The incidence of lung cancer in asbestosis is increased by 2 to 10 times. The smoker is even worse. About 50% of asbestosis patients die from lung cancer. It is difficult to find early lung cancer due to pulmonary fibrosis, and because of lung function. It is also difficult to withstand surgery.
2. Thoracic, peritoneal mesothelioma
The incidence rate is significantly higher than that of the general population. Mesothelioma often occurs after exposure to asbestos for many years, and multiple concealment often requires biopsy to confirm the diagnosis. Treatment is as common as lung cancer.
3. Tuberculosis
Asbestosis and pulmonary tuberculosis are not as common as silicosis, and most of the patients are milder and have better curative effect. At present, domestic asbestosis and pulmonary tuberculosis account for about 10%.
4. Bronchial, lung infections.
5. Obstructive emphysema, pulmonary heart disease and spontaneous pneumothorax.
6. Gastrointestinal tumors and laryngeal cancer.
Symptom
Asbestosis lung symptoms common symptoms gas diffusion function decline dull pain dyspnea snoring hemoptysis chest pain shortness dry cough
Asbestosis can be asymptomatic and X-ray changes in the early stage. Only after the activity, the air is short. The patients are more insidious. The symptoms appear more than 7 to 10 years, but a few of them have symptoms only 1 year after the dust. The typical symptoms of asbestosis are slowly appearing, gradually increasing the difficulty of breathing. The early stage is mainly labor. The severity is related to the time and concentration of exposure to dust. It is usually dry cough. The severe cough is often heavier and accompanied by mucus. Chest pain is often light, often dull pain in the back or sternum, hemoptysis is less common, such as combined tumors can occur hemoptysis, combined with infection, fever, cough and sputum, early physical examination often no abnormal findings, sometimes two lungs can be Hearing sputum pronunciation, or dry, wet voice, occasional pleural friction sound, late patients may have clubbing (toe), can be seen in 75% of patients, may have cyanosis, signs of cor pulmonale, asbestos fibers penetrate the skin An asbestos or corns occurs, which is seen on the sides of the fingers, the palms and the soles of the feet.
Examine
Asbestosis lung examination
Asbestos bodies can be found in sputum or bronchoalveolar lavage fluid, which is evidence of exposure to asbestos, positive for serum rheumatoid factor, positive for antinuclear antibody, and pleural effusion for sterile serous or serous bloody exudate.
1. Changes in lung function
Asbestos lung and lung function changes are typical of lung volume reduction and impaired function, abnormal gas exchange, early asbestosis lung, fibrosis around the alveoli, before the X-ray changes, the amount of lung diffusion is reduced, along with interstitial fibers of the lung Development, lung contraction, lung compliance decreased, restrictive ventilation dysfunction, FVC, VC, TLC decreased, RV normal or slightly increased, lung ventilation / blood flow ratio imbalance, late mixed dysfunction, some cases Combined with obstructive emphysema, FEV1 decreased and RV/TLC increased slightly.
In patients with asbestosis, PaO2 often decreased at rest, and decreased significantly when forced, while PaCO2 rarely increased.
2. X-ray performance
The X-ray manifestations of asbestosis have two parts: pleural changes and changes in lung parenchyma. In recent years, pleural plaques have been found to appear earlier and more distinctly than lung parenchymal changes.
(1) reticular shadow: it is the main change of asbestosis lung, with medium mesh in the middle and lower lung field in the early stage. The diameter of the mesh is <3mm, and the coarse mesh is formed in the later stage. The thick and dense mesh shadow of the late whole lung is honeycomb. Shape, lung field transmittance is reduced, forming a ground glass shape, irregular small dot shadows are often seen in the lung field.
(2) fusion foci: more common in the base of the lungs, is a slab-like shadow with unclear borders and a small range.
(3) pleural changes: can appear early.
1 pleural plaque: symmetrical triangular shadows in the middle and lower parts of the chest wall, the inner edge is clear, occasionally unilateral irregularities, some pleural plaques have calcification.
2 pleural thickening, adhesion, apical pleura, lateral chest wall, pleural angle, interpleural pleural thickening, parietal pleural thickening is common in the front chest wall and the top of the iliac crest, the pericardium and parietal pleural adhesion can form a "pocket" Heart shape."
3 exudative pleural effusion: bilateral chest recurrence.
(4) The density of hilar structural disorder increased, but no lymphadenopathy.
There is still debate about the role of conventional CT scans in the diagnosis of asbestosis. Some people think that conventional CT scans have significantly higher sensitivity to pleural thickening and pulmonary parenchymal fibrosis in people exposed to asbestos than in conventional X-ray films. The diagnostic value of high-resolution CT (HRCT) may be greater. Aberle et al compared the value of HRCT with conventional CT in the diagnosis of asbestosis in 29 patients with a history of occupational asbestos exposure. These 29 patients were standard. There are mild to severe abnormalities on the chest radiograph, suggesting that the diagnosis of asbestosis lungs, they found that HRCT showed higher sensitivity than conventional CT in showing pleural plaque and pulmonary fibrosis, and some studies also showed some HRCT Patients with normal chest radiographs can find abnormalities in the pleura and in the lung parenchyma.
The characteristic manifestations of asbestosis in HRCT include:
1 line-like shadows of varying length and parallel to the pleura;
2 The lungs are lined with a line shadow of 2 to 5 cm in length and can extend to the surface of the pleura;
3 thickening of the interlobular septal line and thickening of the secondary pulmonary lobule structure;
4 Honeycomb-like lung changes.
Diagnosis
Asbestosis diagnosis
Diagnostic criteria
Mainly rely on asbestos dust contact history and chest X-ray performance.
1. History of long-term exposure to asbestos, such as miners, processing workers, people around the asbestos factory, etc.
2. Chest X-ray examination: Diagnostic criteria and staging refer to the silicosis appendix. When the lung changes to 0, if the chest wall is limited to pleural plaque on both sides, it can be set as I; if the lung lesion is I, The pleural changes involve partial palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebral palpebrae Set to "III".
Differential diagnosis
It should be differentiated from various interstitial diseases and pleural diseases.
The pleural plaque caused by asbestos is mostly bilateral, and the trauma, tuberculosis, collagen vascular disease and other causes are mostly unilateral, the lesion size is often fixed, and can be changed for several months, which is helpful for the differential diagnosis of pleural tumor.
The pleural thickening needs to be differentiated from inflammatory reactive fibrosis caused by tuberculosis, thoracic surgery, and hemorrhagic thoracic trauma. For example, combined with lower interstitial lung dysplasia, pleural plaque and pleural calcification support the diagnosis of pleural thickening caused by asbestos.
