What is silicosis?

General situation of silicosis is the most serious type of pneumoconiosis, which is caused by long-term inhalation of dust containing free silica. Extensive nodular fibrosis in the lungs seriously affects lung function and loses the ability to work. Pathogenic silicon is widely distributed in nature, and about 95% of ores are pure-time (containing more than 97% free silica). Silicon is also the main component of the earth's crust. Therefore, when mining, quarrying and tunneling, workers are engaged in rock drilling and blasting. Have more opportunities to contact with dust; Stone rolling, crushing and mixing in the manufacture of glass, enamel and refractory materials, sand grinding, sand mixing, modeling, furnace building, sand blasting and sand cleaning in the foundry industry. , have access to silica dust (commonly known as silica dust). Free silica is usually represented by time. The contact time depends on many factors. In addition to its physical and chemical characteristics, the content of free silica in dust, the concentration of dust in the air, the particle size of dust, contact time and the body's defense function all affect the occurrence and severity of silicosis. Generally speaking, dust containing more than 80% free silica often causes typical diffuse collagen fiber changes in the lungs, and the disease progresses rapidly and is prone to fusion. When the free silica content is lower than 80%, the lesion is atypical and the disease progresses slowly. When it is lower than 10%, it mainly causes interstitial fiber changes and develops slowly, which is classified as other pneumoconiosis. A large amount of dust with high content of free silica is inhaled into the lungs, which often cannot be completely removed from the respiratory tract in time. Sometimes, although there are no signs of silicosis, silicosis reappears several years after leaving work. This situation is usually called "advanced silicosis"; Early silicosis patients will continue to develop even if they leave dust work. If there are no complications, patients can survive for a long time, but they often lose their ability to work. Therefore, in order to protect workers' health, China stipulates that the maximum allowable concentration of dust containing more than free silica 10% in workplace air is 2 mg/m3; When it exceeds 80%, it is 1mg/m3. If this requirement can be met, silicosis will not occur. In addition, there are chronic diseases of respiratory system, such as chronic rhinitis, chronic bronchitis, emphysema and tuberculosis. Patients have poor defense function and weak airway mucus-cilia activity, which makes them more susceptible to illness than healthy people in the same environment. Pathogenic silicon is widely distributed in nature, and about 95% of it is all kinds of pure time (containing more than 97% free silicon dioxide). Silicon is also the main component of the earth's crust. Therefore, when mining, quarrying and tunneling, workers are engaged in rock drilling and blasting. Have more opportunities to contact with dust; Stone rolling, crushing and mixing in the manufacture of glass, enamel and refractory materials, sand grinding, sand mixing, modeling, furnace building, sand blasting and sand cleaning in the foundry industry. , have access to silica dust (commonly known as silica dust). Free silica is usually represented by time. The contact time depends on many factors. In addition to its physical and chemical characteristics, the content of free silica in dust, the concentration of dust in the air, the particle size of dust, contact time and the body's defense function all affect the occurrence and severity of silicosis. Generally speaking, dust containing more than 80% free silica often causes typical diffuse collagen fiber changes in the lungs, and the disease progresses rapidly and is prone to fusion. When the free silica content is lower than 80%, the lesion is atypical and the disease progresses slowly. When it is lower than 10%, it mainly causes interstitial fiber changes and develops slowly, which is classified as other pneumoconiosis. A large amount of dust with high content of free silica is inhaled into the lungs, which often cannot be completely removed from the respiratory tract in time. Sometimes, although there are no signs of silicosis, silicosis reappears several years after leaving work. This situation is usually called "advanced silicosis"; Early silicosis patients will continue to develop even if they leave dust work. If there are no complications, patients can survive for a long time, but they often lose their ability to work. So, to protect private burdens? At night? Hey? Stop by Zhang Qi? Diarrhea? The maximum allowable concentration of free silica dust above 0% is 2 mg/m3; When it exceeds 80%, it is 1mg/m3. If this requirement can be met, silicosis will not occur. In addition, there are chronic diseases of respiratory system, such as chronic rhinitis, chronic bronchitis, emphysema and tuberculosis. Patients have poor defense function and weak airway mucus-cilia activity, which makes them more susceptible to illness than healthy people in the same environment. Clinical manifestations Silicosis patients generally have no symptoms or obvious symptoms in the early stage. With the development of the disease, the symptoms are aggravated, mainly manifested as: (1) cough, expectoration, cough caused by dust stimulation and respiratory inflammation, or reflex cough. Cough degree and sputum volume are closely related to bronchitis or secondary lung infection, but not to silicosis degree. A few patients may have bloody sputum. If there is repeated massive hemoptysis, tuberculosis or bronchiectasis should be considered. (2) 40% ~ 60% patients with chest pain have needle chest pain. Most of them are located on one or both sides of the middle and upper part of the chest, which has nothing to do with breathing, posture and labor, and often appears in rainy days and changeable climate. (3) The degree of chest tightness and shortness of breath is related to the scope and nature of the lesion. When the lesion is extensive and progresses rapidly, shortness of breath is obvious and gradually aggravated. This is the result of extensive fibrosis of lung tissue, massive destruction of alveoli, bronchial stenosis and thickening and adhesion of pleura, which leads to impaired ventilation and ventilation function. Patients can still have dizziness, fatigue, palpitation, loss of appetite and other symptoms. Early silicosis patients often have no abnormal findings in physical examination. Severe silicosis, due to nodule fusion, lung tissue contraction, tracheal displacement and purring. Pathology shows that the basic pathological changes of silicosis are the formation of silicon nodules and extensive fibrosis of pulmonary interstitium, and its development process is as follows: (1) The formation of silicon nodules is typical collagen fibers arranged in concentric circles, similar to the section of onion (Figure 12-2). There may be silica dust in the middle of collagen fibers, which can flow to other places with tissue fluid to form new nodules. Because of the slow action of silica dust, silicosis can continue to progress after leaving silica dust. Silicon nodules are grayish white, with a diameter of about 0.3 ~ 0.8 mm Many small nodules can fuse into large nodules or form large masses, which are more common in the upper lobes of both lungs. If the diameter exceeds 1mm, a circular or quasi-circular shadow can be displayed on the X-ray chest film. Silicon nodules are often formed around blood vessels, so the blood vessels are squeezed, the blood supply is poor, and the collagen fibers are necrotic and glassy. Necrotic tissue is discharged through the bronchus, forming a cavity. Silicosis cavities are generally small and rare. Most of them appear in the most serious part of fusion lesions. (2) Pulmonary interstitial changes alveolar septa, and a large amount of dust deposits around blood vessels and bronchi and dust cells gather, which leads to alveolar septa thickening. After that, fibrous tissue proliferated and lung elasticity decreased. The fusion of small nodules increased, resulting in alveolar collapse between nodules. Compensatory emphysema can appear around the fibrous mass, and even form pulmonary bullae. Perivascular fibrous tissue hyperplasia, perivascular silicon nodules, distortion. At the same time, due to the fibrosis of the vascular wall itself, the lumen becomes narrow and even occluded. The damage of arterioles is more obvious. The decrease of pulmonary capillary bed promotes the increase of blood flow resistance and aggravates the burden on the right heart. If lung lesions continue to develop, hypoxia and pulmonary arteriolar spasm can lead to pulmonary hypertension and even pulmonary heart disease. Because of nodular fibrosis around bronchi at all levels, or because of the contraction of plexiform fibers, bronchial compression, distortion and lumen stenosis, piston-like ventilation disorder is caused, which leads to over-inflation of alveoli, and then alveolar rupture and emphysema. A lot of fibrosis is surrounded by lobular emphysema, and respiratory bronchioles are surrounded by lobular emphysema. Emphysema is mostly distributed in the middle and lower lobes of both lungs. Sometimes the lumen is completely occluded, leading to alveolar collapse or atelectasis. The bronchioles can be dilated to varying degrees. (3) The changes of pulmonary dust cells' lymphatic system enter the lymphatic system through its amoeba-like movement, which leads to the proliferation of lymph node fibrous tissue, especially the enlargement and sclerosis of hilar lymph nodes. Followed by lymphatic countercurrent, dust cells accumulate around from hilum with lymph and reach pleura. (4) Pleura changes the stagnation of dust cells and silica dust on pleura, which can also cause fibrosis and form silica nodules; Pleural thickening and adhesion. In severe cases, spontaneous pneumothorax is often limited because of pleural adhesion when diaphragm bullae and pleura rupture. The diagnosis should be based on: ① dust exposure history, including free silica content in raw materials and finished products, dust concentration in production environment, dust particle size, production operation methods and protective measures (including personal protection); ② The patient's detailed occupational history and past health status; ③ Clinical symptoms, signs and X-ray examination; (4) The past and present incidence of workers of the same type of work. (a) X-ray diagnosis of silicosis, in addition to the above basis, mainly based on X-ray chest film performance. In February 1986, China announced the diagnostic criteria and treatment principles of pneumoconiosis, among which the X-ray diagnostic criteria of pneumoconiosis are applicable to all kinds of pneumoconiosis stipulated by the state, and the specific criteria are as follows: 1. No pneumoconiosis (code 0) (1)0 No X-ray manifestations of pneumoconiosis. (2) The X-ray findings are not enough to diagnose me. 2. Primary pneumoconiosis (code I) (see figure 12-3). (1)I There are small circular shadows with the density of 1, which are distributed in at least one place in each lung area, and the diameter of each place is not less than 2 cm; Or there are irregular small shadows with the density of 1, and their distribution range is not less than two lung areas. (2) The number of I+small shadows has obviously increased, but the density and distribution range of one of them is not enough to be classified as "II". 3. Secondary pneumoconiosis (code Ⅱ), (see figure124) (1) Ⅱ has round or irregular small shadows, with a density of Grade 2, distributed in four lung areas; Or there are small shadows with a density of 3, and the distribution range reaches four lung areas. (2) Ⅱ+has a small shadow, the density is grade 3, and the distribution range exceeds four lung areas; Or there is a big shadow that is not enough for "ⅲ". 4. Stage III pneumoconiosis (code III), (see figure125) Stage III has a large shadow, the length and width of which are not less than 2cm and 1cm respectively. ⅲ+The sum of single large shadow area or multiple large shadow areas exceeds the right upper lung area. When using the above standards, we should follow the following concepts: (1) lung division method: divide the vertical distance from the apex of lung to the top of diaphragm into three parts, and divide each lung field into upper, middle and lower parts with the horizontal line of bisector. (2) Small shadow: refers to the shadow whose diameter or width does not exceed 1cm. It can be divided into two types: ① quasi-circular (R) with circular or nearly circular shape and regular or irregular edges; (2) Irregular shape (IR) refers to a group of dense shadows with different thickness, length and shape. They can be disconnected from each other, or they can be intertwined in disorder, in a network and sometimes in a honeycomb shape. According to the size or thickness, these two kinds of small shadows can be called P (diameter about 1.5 mm or less), Q (diameter about 1.5 ~ 3 mm) and R (diameter 3 ~ 10 mm). Irregular shapes are called S (width about 1.5 mm or less), T (width about 1.5 ~ 3 mm) and U (width about 3 ~ 10 mm) respectively. (3) Small shadow density: refers to the number of small shadows in a certain range, which can be divided into three levels: small-class circle shadow density: 1 level, and a certain amount of small-class circle shadows. The lung texture is clearly visible (if it is P, there are about 10 up and down within 2cm in diameter). Grade 2 has a large number of quasi-circular shadows, and the lung texture is generally recognizable. At grade 3, there were a lot of small round shadows, and the lung texture disappeared partially or completely. The density of irregular small shadows: 1, a considerable number of irregular small shadows, and the lung texture is generally recognizable. 2-level multi-quantity irregular small shadows. Lung markings usually partially disappear. There are a lot of irregular small shadows in the third grade, and the lung texture generally disappears completely. The density and range determination method should comprehensively determine the density of all small shadows in each lung area: 1. Determine that the small shadow in the lung area accounts for two-thirds of the area; 2. The distribution range is the number of lung areas with small shadows; 3. The density of most lung areas is the main criterion; 4. Take the higher horizontal density with the distribution range not less than two lung areas as the main standard. (4) Large shadow: refers to the shadow with the maximum diameter of 1cm. The big shadow that is not defined as "ⅲ" refers to: ① Small shadows gather and have not yet formed a uniform and dense block shadow; ② The mass shadow did not reach 2 cm×1cm; (3) There are "patches" or "whitish areas". (5) Pleural changes (including thickening, adhesion and calcification), pneumoconiosis complications or other diseases (such as rheumatoid pneumoconiosis) were recorded with corresponding codes. (6) About each period (+) In order to facilitate the dynamic observation of diseases, 0+, I+, II+ and III+ are added in each period, which is not independent staging. For silicosis, when exposed to dust with high silicon content and concentration, circular and quasi-circular shadows usually appear first in the middle zone of the middle and lower fields of both lungs and gradually expand upward; There are also those that first appeared in the two upper lungs. When the silicon content is low or mixed dust is inhaled, the quasi-circular shadow (so-called mesh shadow) is the main one. The big shadow of silicosis is the increase, density and final fusion of local shadows, which is common in the upper field of both lungs. The outline is clear, and the lungs are symmetrical in a "wing" shape or a figure of eight. The fusion block contracts inward and upward, causing the hilum to be pulled and displaced. The hilar shadow often increases, the density increases, and sometimes there is "eggshell calcification" of lymph nodes, which is caused by calcium deposition under the capsule of lymph nodes. Lung markings increased and thickened. (2) Laboratory examination of silicosis has no special significance. Serum proteins such as hexose, hexosamine, mucin, immunoglobulin, ceruloplasmin and urinary hydroxyproline tend to increase, but most of them are nonspecific, and their normal range fluctuates greatly, so their clinical value is not great. (3) Measurement of lung function Because the compensatory function of lung tissue is very strong, the damage of lung function in early patients is not obvious. With the increase of lung fibrous tissue and the decrease of elasticity, vital capacity decreases. With the progress of the disease, the forced expiratory volume and the maximum ventilation in one second also decreased, while the residual volume and its proportion in the total lung volume increased. The more serious emphysema is, the more obvious these changes will be, which will cause diffuse sexual dysfunction. At rest, arterial oxygen partial pressure can be reduced to varying degrees. The determination of lung function is of little significance in diagnosis, but it can be used as the basis for the identification of labor ability of silicosis patients. Differential diagnosis 1. Diseases that need to be differentiated from silicosis nodules include: acute miliary tuberculosis, pulmonary hemosiderosis, bronchioloalveolar carcinoma, sarcoidosis, alveolar microlithiasis and connective tissue disease. 2. Large lesions of silicosis should be differentiated from pulmonary tuberculoma and lung cancer lump: please refer to the relevant chapters for the above diseases that need to be differentiated. The treatment shows that comprehensive measures should be taken for the diagnosed silicosis patients, including removing silica dust, strengthening nutrition, persisting in medical exercise and improving the body's anti-infection ability. At the same time, according to the patient's condition, symptomatic treatment. Tetrandrine, praziquantel hydroxyphosphate, clozapine and aluminum citrate are four commonly used drugs in clinic, which act on different links in the occurrence and development of silicosis, but the exact mechanism of treating silicosis is not completely clear. (1) silicone (poly (2- vinylpyridine) oxynitride) is a high molecular compound with a molecular weight of about 654.38+ million. It can protect phagocytosis, form hydrogen bonds with silica dust and adsorb it, thus reducing fibrosis caused by silica dust. In clinical application, 8ml(320mg) of 4% aqueous solution was inhaled by atomization, 6 times a week. A course of treatment lasts for 3 months, and the interval of each course of treatment is 1 month. Can be treated for 2-3 years. After treatment, it can improve respiratory symptoms, reduce respiratory infection and delay or stabilize the development of the disease. (2) Aluminum Citrate Aluminum Citrate can closely cover the surface of timely dust particles, protect macrophages, and weaken timely-induced fibrosis. Usage: Injection 10mg(Al) is injected intramuscularly once a week, or aqueous solution of 50mg(Al) is atomized and inhaled in batches, with a course of treatment of 6 months and withdrawal of medication for 2 months. (3) Praziquantel Hydroxyphosphate (anti-silicon 1) has been proved to inhibit collagen synthesis, protect and activate macrophages, and improve the immune status of the body. The tablet is taken orally twice a week, 0.5g each time, and the first dose is doubled. Take it for 6 months and stop taking it 1 ~ 3 months, which is a course of treatment. After application, 50% patients' symptoms improved, most X-ray lesions were stable, and the shadows in a few cases became lighter or smaller. (4) Tetrandrine (tetrandrine) can combine with collagen macromolecules and decompose; Improve the activity of macrophages; Promote the phagocytosis of degraded collagen macromolecules and proteoglycans, and affect the polymerization of collagen fibers; It also has the function of protecting pulmonary surfactant. Clinical application: oral 300mg daily, 6 days a week, for 3 months, and drug withdrawal for 65438 0 months. As a course of treatment, after 2 ~ 3 years of treatment, respiratory symptoms were relieved, X-ray chest film lesions were stable, and a few lesions became lighter and smaller. The side effects are skin pigmentation and itching, about 1/5 patients have anorexia and abdominal distension, and about 9.8% patients have abnormal liver function. In order to improve the curative effect and reduce the toxic effect of drugs, combined medication was proposed. For example, tetrandrine 100mg, twice a day, 6 days a week, plus anti-silicone 1 0.5g, once a week, 3 months for 1 course, a total of 6 courses; Tetrandrine plus 1% g-Si-Ping 144ml was dripped under the guidance of fiberbronchoscope, once a year, twice in total; 20mg of aluminum citrate was injected intramuscularly every week, and anti-silicon 1 0.25g was given orally twice a week, for a total of 6 courses of treatment. The treatment results showed that respiratory symptoms and infections were significantly improved. X-ray film showed that the improvement rate and stability rate of the disease were higher than those of the control group. And the effect is obvious in cases with rapid progress of lesions, which is also related to the nature of work. Combined medication reduces the dosage, thus reducing the side effects. Complications (1) Tuberculosis is a common complication of silicosis, accounting for about 20% ~ 50%. Autopsy found more x-rays than before death, about 36% ~ 75%. With the aggravation of silicosis, the combined rate increased. Tuberculosis often leads to the death of silicosis patients. According to reports at home and abroad, 46.3% ~ 50.8% of silicosis patients died of tuberculosis. Silicosis patients are prone to tuberculosis, which may be related to the following factors: ① the resistance of silicosis patients is decreased and they are prone to tuberculosis; ② Extensive fibrosis of pulmonary interstitial tissue leads to the disorder of blood and lymph circulation, which reduces the defense function of lung tissue against tuberculosis; ③ Silica dust is toxic to macrophages, which weakens the phagocytosis and sterilization ability of macrophages and promotes the growth and diffusion of tuberculosis in tissues. Laboratory examination showed that ESR was accelerated and mycobacterium tuberculosis could be found in sputum. Tuberculosis cavity is often large, irregular in shape, mostly eccentric, with papillae on the inner wall, which looks like a cave. Pleural thickening around pulmonary tuberculosis. Because of extensive fibrosis of both lungs, which affects blood supply, anti-tuberculosis drugs have poor curative effect. (2) Chronic obstructive pulmonary disease and cor pulmonale, due to decreased body resistance and diffuse fibrosis of both lungs, make bronchus narrow, poor drainage, easy to be infected by bacteria and viruses, complicated with chronic bronchitis and emphysema, decreased lung function, leading to severe hypoxia and carbon dioxide retention, and respiratory failure. Severe silicosis can be accompanied by pulmonary hypertension, leading to pulmonary heart disease. Severe infection can lead to right heart failure. (3) Spontaneous pneumothorax: After holding one's breath forcibly or coughing violently, the pulmonary bullae rupture, leading to tension spontaneous pneumothorax. Because of pleural adhesion, pneumothorax is mostly limited, which is often covered up by the original symptoms of dyspnea, and sometimes it is discovered by X-ray examination. Pneumothorax can occur repeatedly or alternately on both sides. Due to the fibrosis of lung tissue and pleura, the rupture is often difficult to heal and the gas absorption is slow. Prevention shows that prevention is the key to control silicosis. Factories and mines all over the country have adopted comprehensive dust prevention measures such as wet operation, dust source sealing, ventilation and dust removal, equipment maintenance and personal protection, regularly monitoring the dust concentration in the air, and strengthening publicity and education, which greatly reduced the incidence of silicosis, prolonged the service life of the disease and delayed the progress of the disease. All factories and mines should do a good job of pre-job physical examination for new workers engaged in dust operations, including X-ray chest films. Anyone suffering from active tuberculosis and various respiratory diseases (chronic rhinitis, asthma, bronchiectasis, chronic bronchitis, emphysema, etc.). ) should not participate in silica dust operations. Workers in factories (mines) should have regular physical examinations, including taking X-ray chest films. The inspection interval depends on the contact silica content and dust concentration in the air, once a year to once every two or three years. If suspected silicosis is found, it should be closely observed and reviewed regularly; If silicosis is diagnosed, you should leave the silica dust operation immediately, and arrange appropriate work according to the labor ability appraisal to carry out comprehensive treatment. Factories and mines with silica dust should do a good job of tuberculosis prevention to reduce the incidence of silicosis complicated with tuberculosis. /special/29/9/2004/08/252242304 1 . html