Silicosis
Overview
Silicosis (silicosis) is the most serious type of pneumoconiosis. It is caused by long-term inhalation of chemicals containing free silica (SiO2). Caused by dust. There is extensive nodular fibrosis in the lungs, which in severe cases affects lung function and results in loss of working ability.
Cause
Silicon is widely distributed in nature. About 95% of the ores are pure quartz in various forms (containing more than 97% of free silica); silicon is also found in the earth's crust. Main ingredients. Therefore, when mining, quarrying, and tunneling, workers engaged in rock drilling, blasting, and other operations have many opportunities to be exposed to dust; stone rolling, crushing, mixing materials when making glass, enamel, and refractory materials, and sand grinding in the foundry industry , sand mixing, modeling, furnace building, sand blasting and sand cleaning and other types of work, all have the opportunity to be exposed to silica dust (commonly known as silica dust). Quartz is often used to represent free silica.
Whether the disease develops after exposure to quartz depends on many factors. In addition to its physical and chemical properties, the content of free silica in the dust, the concentration of dust in the air, the size of the dust particles, the contact time and the body's defense function all affect The occurrence and severity of silicosis. Generally speaking, dust containing more than 80% of free silica often causes typical diffuse collagen fiber changes in the lungs, mainly nodules. The disease progresses quickly and is prone to fusion. When the free silica is less than 80%, the lesions are less typical and the disease progresses more slowly. When it is less than 10%, it mainly causes interstitial fiber changes, develops more slowly, and is classified as other pneumoconiosis.
A large amount of dust containing high levels of free silica is inhaled into the lungs and often cannot be cleared promptly and completely by the respiratory tract. Sometimes, although there are no signs of silicosis, silicosis reappears several years after leaving work, which is often called "late-onset silicosis". In patients with early-stage silicosis, the disease will continue to develop even if they leave dust work. If there are no complications, the patient can They survive for a long time, but often lose the ability to work. Therefore, in order to protect the health of workers, my country has stipulated that the maximum allowable concentration of free silica dust in workshop air containing more than 10% is 2mg/m3; when it exceeds 80%, it is 1mg/m3. If this requirement is met, silicosis will not occur.
In addition, patients with chronic diseases of the respiratory system, such as chronic rhinitis, chronic bronchitis, emphysema, tuberculosis, etc., have poor defense functions and weak airway mucus-cilia activity. In the same environment, Healthy people are more susceptible to the disease.
Pathogenesis
Silicon is widely distributed in nature, and about 95% of the ores are pure quartz in various forms (containing more than 97% of free silica); silicon is also present in the earth's crust main ingredients. Therefore, when mining, quarrying, and tunneling, workers engaged in rock drilling, blasting, and other operations have many opportunities to be exposed to dust; stone rolling, crushing, mixing materials when making glass, enamel, and refractory materials, and sand grinding in the foundry industry , sand mixing, modeling, furnace building, sand blasting and sand cleaning and other types of work, all have the opportunity to be exposed to silica dust (commonly known as silica dust). Quartz is usually used to represent free silica.
Whether the disease develops after exposure to quartz depends on many factors. In addition to its physical and chemical properties, the content of free silica in the dust, the concentration of dust in the air, the size of the dust particles, the contact time and the body's defense function all affect The occurrence and severity of silicosis. Generally speaking, dust containing more than 80% of free silica often causes typical diffuse collagen fiber changes in the lungs, mainly nodules. The disease progresses quickly and is prone to fusion. When the free silica is less than 80%, the lesions are less typical and the disease progresses more slowly. When it is less than 10%, it mainly causes interstitial fiber changes, develops more slowly, and is classified as other pneumoconiosis.
A large amount of dust containing high levels of free silica is inhaled into the lungs and often cannot be cleared promptly and completely by the respiratory tract. Sometimes, although there are no signs of silicosis, silicosis reappears several years after leaving work, which is often called "late-onset silicosis". In patients with early-stage silicosis, the disease will continue to develop even if they leave dust work. If there are no complications, the patient can They survive for a long time, but often lose the ability to work. Therefore, in order to protect the private sector, the maximum allowable concentration of free silica dust exceeding 0% is 2mg/m3; when it exceeds 80%, it is 1mg/m3. If this requirement is met, silicosis will not occur.
In addition, patients with chronic diseases of the respiratory system, such as chronic rhinitis, chronic bronchitis, emphysema, tuberculosis, etc., have poor defense functions and weak airway mucus-cilia activity. In the same environment, Healthy people are more susceptible to the disease.
Clinical manifestations
Patients with silicosis are generally asymptomatic or have subtle symptoms in the early stages. As the disease progresses, symptoms increase. The main manifestations are as follows:
(1) ) Coughing and expectoration Coughing due to dust irritation and respiratory inflammation, or reflex coughing. The degree of cough and the amount of sputum are closely related to bronchitis or secondary lung infection, but are not consistent with the degree of silicosis. A few patients may have bloody sputum. If there is repeated massive hemoptysis, tuberculosis or bronchiectasis should be considered.
(2) Chest pain 40% to 60% of patients have acupuncture-like chest pain. It is usually located on one or both sides of the middle and upper part of the chest, and has nothing to do with breathing, posture, or labor. It often appears on rainy days and when the climate changes.
(3) The degree of chest tightness and shortness of breath is related to the scope and nature of the disease. If the lesions are extensive and progress rapidly, the shortness of breath will be obvious and progressively worsen.
This is due to extensive fibrosis of lung tissue, massive destruction of alveoli, bronchial stenosis, and pleural thickening and adhesions, leading to damage to ventilation and ventilation functions. Patients may still have symptoms such as dizziness, fatigue, palpitations, and loss of appetite.
Physical examinations of patients with early silicosis often show no abnormal findings. In severe silicosis, due to the fusion of nodules and the contraction of lung tissue, there may be tracheal displacement and dull percussion.
Pathological description
The basic lesions of silicosis are the formation of silicium nodules and extensive fibrosis of the lung interstitium. The development process is as follows:
(1) Silicium nodules Formation of Nodules Typical silicon nodules are collagen fibers arranged in concentric circles, resembling the cross-section of an onion (Figure 12-2). There may be silica dust in the middle of the collagen fibers, and the silica dust may flow to other places with tissue fluid to form new nodules. Because silica dust acts slowly, silicosis lesions can continue to progress after working without silica dust. Silicon nodules are gray-white in color and have a diameter of approximately 0.3 to 0.8 mm. Multiple small nodules can fuse into large nodules or form large masses, which are more common in the upper lungs. Those with a diameter of more than 1 mm may show round or nearly round shadows on chest X-rays. Silicon nodules often form around blood vessels, so the blood vessels are squeezed and the blood supply is poor, causing collagen fiber necrosis and hyaline degeneration. The necrotic tissue is excreted through the bronchi, forming a cavity. Silicotic cavities are generally small and rare. It often occurs in the most severe areas of fusion disease.
(2) Lung interstitial changes: A large amount of dust deposition and accumulation of dust cells in the alveolar septa and around blood vessels and bronchi, resulting in thickening of the alveolar septa. Later, fibrous tissue proliferates and lung elasticity decreases. The small nodules fuse and enlarge, causing the alveoli between the nodules to collapse. Compensatory emphysema may occur around the fibrous mass, and bullae may even form.
Perivascular fibrous tissue hyperplasia and silica nodules surround the blood vessels, and the blood vessels are twisted and deformed. At the same time, due to the fibrosis of the blood vessel wall itself, the lumen is reduced or even occluded. Damage to small arteries is more pronounced. The pulmonary capillary bed is reduced, which increases blood flow resistance and increases the burden on the right heart. If lung lesions continue to develop, hypoxia and spasm of pulmonary arterioles can lead to pulmonary hypertension and even pulmonary heart disease.
Due to nodular fibrosis around the bronchus at all levels, or due to the contraction of mass fibers, the bronchus is compressed, twisted and deformed, and the lumen is narrowed, causing a piston-like ventilation disorder, resulting in overinflation of the associated alveoli, and then The alveoli rupture, forming emphysema. Panlobular emphysema surrounds large fibrosis, and centrilobular emphysema surrounds respiratory bronchioles. Emphysema is mostly distributed in the middle and lower lobes of both lungs. Sometimes the lumen is completely occluded, causing the alveoli to collapse or the lobules to become atelectatic. Bronchioles can dilate to varying degrees.
(3) Changes in the lymphatic system of the lungs. Dust cells enter the lymphatic system through their amoebic movement, causing lymph node fibrous tissue proliferation, especially hilar lymph node enlargement and sclerosis. Lymphatic reflux ensues, and dust cells accumulate from the hilum to the periphery with lymph fluid and reach the pleura.
(4) Pleural changes: Dust cells and silica dust stasis on the pleura can also cause fibrosis and the formation of silica nodules; pleural thickening and adhesion. In severe cases, spontaneous pneumothorax is often localized due to pleural adhesions when the bullae of the diaphragm pleura rupture.
Diagnostic instructions
Diagnosis should be based on: ① Dust exposure history, including free silica content in raw materials and finished products, dust concentration in the production environment, dust particle size, production operation methods and Protective measures (including personal protection); ② the patient’s detailed occupational history and past health conditions; ③ clinical symptoms, physical signs and X-ray examination; ④ past and current illnesses of workers in the same type of work.
(1) X-ray examination At present, the diagnosis of silicosis, in addition to the above-mentioned basis, is mainly based on the X-ray chest X-ray performance. my country announced the "Diagnostic Standards and Treatment Principles of Pneumoconiosis" in December 1986, among which the X-ray diagnostic standards for pneumoconiosis are applicable to all types of pneumoconiosis legally mandated by the state. The specific standards are as follows:
1. No pneumoconiosis (code 0)
(1)0 X-ray manifestations of no pneumoconiosis.
(2) X-ray findings are not enough to diagnose as "I".
2． Stage I pneumoconiosis (code I), (see Figure 12-3).
(1) I have round-like small shadows with density level 1, distributed in at least one place in each of the two lung areas, and the diameter of each place is not less than 2cm; or there is density level 1 Irregular-shaped small shadows, whose distribution range is no less than two lung areas.
(2) The number of I+ small shadows increases significantly, but one of the density and distribution range is not enough to be classified as "II".
3. Stage II pneumoconiosis (code II), (see Figure 124)
(1) II has round or irregular small shadows with density level 2, and the distribution range exceeds four lung areas; or The small shadows with density level 3 are distributed in four lung areas.
(2) II+ has small shadows with a density of level 3, and its distribution range exceeds four lung areas; or there are large shadows that are not enough to be classified as "Ⅲ".
4. Stage III pneumoconiosis (code III), (see Figure 125)
III has a large shadow, its long diameter is not less than 2cm, and its wide diameter is not less than 1cm.
Ⅲ+ The area of ??a single large shadow or the sum of the areas of multiple large shadows exceeds the area of ??the right upper lung area.
When using the above standards, the following concepts should be used:
(1) Lung area division method: Divide the vertical distance from the lung apex to the top of the diaphragm into three equal parts, and use equal The horizontal line of dividing points divides the lung field on each side into upper, middle and lower regions.
(2) Small shadow: refers to a shadow whose diameter or width does not exceed 1cm. It can be divided into two types: ① Round (R), which is round or nearly round in shape, with neat or irregular edges; ② Irregular (IR), which refers to a group of dense shapes of different thickness, length, and shape. Shadows, they can be disconnected, or they can be haphazardly intertwined, appearing as a mesh or sometimes a honeycomb. Both types of small shadows can be called p (diameter about 1.5mm or less), q (diameter about 1.5~3mm), r (diameter 3~10mm) according to their size or thickness; irregular shapes are called s (width is about 1.5mm or less), t (width is about 1.5~3mm), u (width is about 3~10mm).
(3) Small shadow density: refers to the number of small shadows within a certain range, which can be divided into 3 levels:
Density of round-like small shadows:
Level 1 is a certain amount of small round shadows. The lung texture is clearly visible (if it is p, there are about 10 up and down within a diameter of 2cm).
Level 2: A large number of small round shadows, and the lung texture is generally identifiable.
Level 3: A large number of small round shadows, and the lung texture is partially or completely disappeared.
Intensity of small irregular shadows:
Level 1: A considerable amount of small irregular shadows, and the lung texture is generally identifiable.
Level 2: A large number of small irregular shadows. The lung markings are often partially lost.
Level 3: A large number of irregular small shadows, and the lung texture usually disappears.
The density and range determination method requires a comprehensive determination of the density of all small shadows appearing in each lung area: 1. To determine the lung area, the small shadow must account for two-thirds of the area; 2. The distribution range is the number of lung areas with small shadows; 3. The main judgment basis is based on the density in most lung areas; 4. The main basis for determination is the higher-level density with a distribution range of no less than two lung areas.
(4) Large shadow: refers to a shadow with a longest diameter of more than 1cm. Large shadows that are not enough to be classified as "Ⅲ" refer to: ① Small shadows gather and have not yet formed a uniform and dense block shadow; ② The block shadow does not reach 2cm × 1cm; ③ "Patch strips" or "white areas" appear.
(5) Pleural changes (including thickening, adhesion, calcification), pneumoconiosis complications or other diseases (such as rheumatoid pneumoconiosis) will be recorded with corresponding codes.
(6) Regarding each stage (+), in order to facilitate the dynamic observation of the disease, , Ⅰ+, Ⅱ+, Ⅲ+ are added in each stage, which is not an independent stage.
For silicosis, when exposed to dust with high silica content and high concentration, round and quasi-round shadows often appear, which first appear in the inner and middle zones of the middle and lower fields of both lungs, and gradually Expands upward; some also appear first in the two upper lungs. When the silicon content is low or mixed dust is inhaled, round shadows are the dominant form (the so-called mesh shadows). The large shadow of silicosis is a local shadow that increases, becomes dense, and finally merges. It is common in the upper outdoor zone of both lungs. It has a clear outline and the two lungs are symmetrical and have a "wing-like" or figure-eight shape. The fusion mass shrinks inward and upward, pulling and displacing the hilum. The hilar shadows often become enlarged and dense, and sometimes "eggshell-like calcification" of lymph nodes appears, which is caused by calcium deposition under the lymph node capsule. The lung texture increases and thickens.
(2) Laboratory examination Routine examination of silicosis has no special significance. Serum protein hexoses, aminohexoses, mucins, immunoglobulins, ceruloplasmin, and urinary hydroxyproline often tend to increase, but most of them are non-specific, and the normal range fluctuates greatly, so their clinical value is not great.
(3) Pulmonary function measurement Because the lung tissue has a strong compensatory function, the damage to the lung function of patients in the early stages is not obvious. As lung fibrous tissue increases and elasticity decreases, lung capacity decreases. As the disease progresses, forced expiratory volume in one second and maximum ventilation also decrease, while residual volume and its ratio to total lung volume increase. The more severe the emphysema, the more obvious these changes are and cause diffusion dysfunction. The partial pressure of oxygen in arterial blood at rest can be reduced to varying degrees. Pulmonary function measurement is of little diagnostic significance, but it can be used as a basis for identification of the working ability of silicosis patients.
Differential diagnosis
1. The diseases that need to be distinguished from silicosis nodules include the following: acute miliary tuberculosis, pulmonary hemosiderosis, bronchioloalveolar carcinoma, sarcoidosis, alveolar microlithiasis and connective tissue diseases.
2． The massive lesions of silicosis need to be differentiated from tuberculosis balls and lung cancer masses: please refer to the relevant chapters for the above types of diseases that need to be differentiated.
Treatment Instructions
Comprehensive measures should be taken for patients diagnosed with silicosis, including moving away from silica dust operations, strengthening nutrition, insisting on medical exercise, and increasing the body's ability to resist infection. At the same time, we provide symptomatic treatment according to the patient's condition.
The four drugs used clinically are tetrandrine, piperaquine hydroxyphosphate, silicopine and aluminum citrate. They act on different aspects of the occurrence and development of silicosis, but the exact mechanism for treating silicosis is not yet complete. Clearly.
(1) Gramsilicon (poly2-vinylpyridine oxynitride) is a polymer compound with a molecular weight of about 100,000.
It has the function of protecting and phagocytosis, and can form hydrogen bonds with silica dust for adsorption, thereby reducing the fibrosis caused by silica dust. Clinical application: 8ml (320mg) of 4% aqueous solution for aerosol inhalation, 6 times a week. A course of treatment is 3 months, with an interval of 1 month between each course. It can be treated for 2 to 3 years. After treatment, respiratory symptoms can be improved, respiratory infections can be reduced, and the development of lesions can be delayed or stabilized.
(2) Aluminum citrate Aluminum citrate can tightly cover the surface of quartz dust particles, protect macrophages, and weaken the fibrosis caused by quartz. Usage: Injection 10 mg (Al) intramuscularly once a week, or aqueous solution 50 mg (Al) weekly, atomized and inhaled in divided doses, continuous treatment for 6 months, followed by 2 months off, as one course of treatment.
(3) Experiments of piperaquine hydroxyphosphate (anti-silicon No. 1) have shown that it can inhibit collagen synthesis, protect and activate macrophages, and improve the body's immune status. Tablets are taken orally, 2 times a week, 0.5g each time, double the first dose. Take it continuously for 6 months and stop for 1 to 3 months, which is a course of treatment. After application, 50% of patients' symptoms improved, most of the chest X-ray lesions were stable, and the shadows became lighter or smaller in a few cases.
(4) Tetrandrine (Tetrandrine) can bind to collagen macromolecules and break them down; improve macrophage activity; promote the degradation of collagen macromolecules and proteins The phagocytosis of polysaccharides affects the polymerization of collagen fibers; it also protects alveolar surfactants. Clinical application: Take 300 mg orally daily, 6 days a week, for 3 months, then stop for 1 month, which is a course of treatment. After 2 to 3 years of treatment, respiratory symptoms are reduced, chest X-ray lesions are stable, and a few lesions become lighter and smaller. Side effects include skin pigmentation and itching, about 1/5 patients suffer from anorexia and abdominal distension, and about 9.8% develop abnormal liver function.
In order to improve drug efficacy and reduce toxic effects, it is proposed to use drugs in combination. For example: 100 mg of Hanjia, 2 times a day, 6 days a week, plus 0.5g of Anti-Si No. 1, once a week, 3 months as one course of treatment*** 6 courses of treatment; Hanjia plus 1% grams of silicon 144ml should be instilled under the introduction of fiberoptic bronchoscope, once a year, ***2 times; Aluminum citrate should be injected intramuscularly 20mg weekly, plus 0.25g anti-silicon No. 1, taken orally twice a week, ***6 times Treatment course. Treatment results showed significant improvement in respiratory symptoms and infections. X-ray films showed that the improvement rate and condition stabilization rate were higher than those of the control group; and the effect was obvious in cases with rapid disease progression, which was also related to the nature of the work. Combination medication reduces the dosage of medication, thereby reducing side effects.
Complications
(1) Tuberculosis is a common complication of silicosis, accounting for about 20% to 50%. More were found in autopsies than in antemortem X-rays, about 36% to 75%. As silicosis worsens, the complication rate increases. Tuberculosis often leads to death in silicosis patients. According to domestic and foreign reports, 46.3% to 50.8% of silicosis patients die from tuberculosis.
The reason why silicosis patients are prone to tuberculosis may be related to the following factors: ① Silicosis patients have reduced resistance and are susceptible to tuberculosis infection; ② Extensive pulmonary interstitial fibrosis causes blood and lymph circulation disorders and reduces lung tissue Defense function against tuberculosis bacteria; ③ Silica dust has certain toxicity to macrophages, weakens the phagocytosis and sterilization capabilities of macrophages, and promotes the growth and spread of tuberculosis bacteria in tissues.
Laboratory tests show accelerated erythrocyte sedimentation rate, and Mycobacterium tuberculosis can be found in the sputum. Tuberculosis cavities are often large, irregular in shape, mostly eccentric, with papillary protrusions on the inner wall, shaped like a cave. Pleural thickening around tuberculosis lesions. Due to extensive fibrosis in both lungs, which affects blood supply, anti-tuberculosis drugs are very ineffective.
(2) Chronic obstructive pulmonary disease and pulmonary heart disease are prone to secondary bacterial and viral infections and complications due to reduced body resistance and diffuse fibrosis in both lungs, resulting in bronchial stenosis and poor drainage. Chronic bronchitis and emphysema, reduced lung function, leading to severe hypoxia and carbon dioxide retention, leading to respiratory failure. Severe silicosis can be accompanied by pulmonary hypertension, leading to pulmonary heart disease. Severe infection can cause right heart failure.
(3) Spontaneous pneumothorax: After holding your breath hard or coughing violently, the lung bullae rupture, causing tension spontaneous pneumothorax. Due to pleural adhesion, pneumothorax is mostly localized and often masked by the original symptoms of dyspnea. Sometimes it is only discovered after X-ray examination. Pneumothorax can occur repeatedly or alternately on both sides. Due to fibrosis of lung tissue and pleura, the breach is often difficult to heal and gas absorption is slow.
Prevention Instructions
To control silicosis, the key is prevention. Factories and mines across my country have adopted comprehensive dust prevention measures such as wet operations, airtight dust sources, ventilation and dust removal, equipment maintenance and overhaul, coupled with personal protection, regular monitoring of dust concentration in the air and strengthening publicity and education, which has greatly reduced the incidence of silicosis. The age at onset of disease is prolonged and the progression of lesions is delayed.
All factories and mines must conduct pre-employment physical examinations, including chest X-rays, for new workers involved in dust operations. Anyone with active internal and external pulmonary tuberculosis and various respiratory diseases (chronic rhinitis, asthma, bronchiectasis, chronic bronchitis, emphysema, etc.) should not participate in silica dust work. Workers in factories (mining) should undergo regular physical examinations, including chest X-rays. The examination interval depends on the exposure to silica content and dust concentration in the air, once every one to two or three years. If suspected silicosis is found, close observation and regular re-examination should be focused on; if silicosis is diagnosed, silicosis operations should be immediately removed, appropriate work arrangements should be made based on labor ability assessment, and comprehensive treatment should be given.
Factories and mines with silica dust should do a good job in preventing tuberculosis to reduce the incidence of silicosis combined with tuberculosis.
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