Comprehensive measures should be taken for silicosis patients, including dust removal, normal work according to work schedule, strengthening nutrition and proper rehabilitation exercise, so as to enhance their physical fitness. Prevent respiratory tract infections and complications.
With regard to the drug treatment of silicosis, a lot of research has been done in China for many years, and some drugs have been tried in clinic through animal experiments and achieved certain results.
(1) clozapine (poly (2- vinylpyridine) nitroxide, abbreviated as P204) is a macromolecular nitroxide. Experiments show that it plays a protective role in the process of silica dust destroying macrophages, and can prevent or delay the progress of silicosis. After the clinical trial of clozapine, the chest X-ray showed that the development of the disease was delayed, so it had a certain effect on stage ⅰ and ⅱ silicosis, but it had no obvious effect on stage ⅲ silicosis. The general condition and respiratory symptoms of patients were improved obviously. Usage: Take 8- 10 ml of 4% silicone aqueous solution, spray and inhale 1 time, once a day, and 3 months is 1 course of treatment. Interval 1-2 months, then retreatment for 2-4 courses, and then retreatment for 2 courses every year. The side effects of spray inhalation of this medicine are few.
(2) Other drugs include piperaquine (mainly piperaquine phosphate and piperaquine hydroxyphosphate), tetrandrine and aluminum preparations (aluminum citrate, aluminum sorbitol). After treatment, the subjective symptoms of silicosis patients have been improved to varying degrees, and some can delay the progress of the disease.
prognosis
Once diagnosed, silicosis patients should be separated from dust work and given active comprehensive treatment. Their life span can be extended to the average life span of ordinary people, but their labor force may be lost to varying degrees. The death of silicosis is often caused by severe tuberculosis, spontaneous pneumothorax and respiratory failure.
prevent
Dust prevention is the key to control or reduce the incidence of silicosis. Industrial and mining enterprises should pay attention to comprehensive dust prevention measures such as reforming production technology, wet operation, sealing dust sources, ventilation and dust removal, and equipment maintenance and repair. Strengthen personal protection and observe dust-proof operation procedures. Regularly monitor the dust concentration in the air of production environment and strengthen publicity and education. Have a physical examination before employment, including X-ray chest film. All patients with active pulmonary tuberculosis and various respiratory diseases should not take part in silica dust operations. Strengthen the regular physical examination of workers exposed to silica dust, including X-ray chest film. The interval of examination depends on the content of exposed silica dust and the concentration of air dust. It is also necessary to strengthen the prevention and treatment of tuberculosis in industrial and mining areas. Those with negative tuberculin test should be vaccinated with BCG; Preventive anti-tuberculosis chemotherapy for positive patients can reduce the incidence of silicosis complicated with pulmonary tuberculosis.
clinical picture
Generally, there are no symptoms or obvious symptoms in the early stage, and the symptoms get worse with the development of the disease. Reflex cough is caused by inhaling silica dust, but the degree and sputum volume of cough are closely related to respiratory tract infection, but not the degree of silicosis. A few patients may have phlegm and blood. If there is repeated massive hemoptysis, tuberculosis or bronchiectasis should be considered. In the early stage, I often feel acupuncture-like pain in the middle and upper chest, which has nothing to do with breathing posture and labor, and mostly occurs when the climate is changeable. The degree of chest tightness and shortness of breath is related to the scope and nature of the lesion. If the lesion is extensive and progresses rapidly, shortness of breath will be obvious and gradually aggravated. Patients can still have dizziness, fatigue, insomnia, palpitations, loss of appetite and other symptoms.
Early silicosis can have no abnormal signs. In stage III silicosis, lung tissue contracts due to a large amount of fibrosis, which leads to tracheal displacement and voiced sound. If complicated with chronic bronchitis, emphysema and pulmonary heart disease, there may be corresponding signs.
survey fee
Because of the strong compensatory ability of lung tissue, the damage of lung function in early patients is not obvious. With the aggravation of pulmonary fibrosis, lung elasticity decreases, and restrictive ventilation changes may occur, such as decreased vital capacity, total lung capacity and residual volume, while forced vital capacity and maximum ventilation volume are still normal. If accompanied by obstructive ventilation, the vital capacity, forced vital capacity and maximum ventilation capacity all decrease, while the residual capacity and its percentage in total vital capacity increase, and the diffusion function is impaired. In severe cases, hypoxemia and/or carbon dioxide retention may occur. The measurement of respiratory function is of little significance in diagnosis, and it is mainly used as the basis for labor ability appraisal.
diagnose
The patient has a close contact history with silica dust and a detailed occupational history. Combined with clinical manifestations, according to the comprehensive analysis of X-ray chest films, the diagnosis stages were made.
Chest X-ray manifestations of silicosis show that patients exposed to dust with high silica content and concentration often have circular or quasi-circular shadows, which appear in the middle and lower lungs of both lungs in the early stage, and then gradually expand upwards, or appear in the upper and lower lungs first. The amount of silica dust is low or mixed dust is mostly round or irregular shadow. Large shadows usually appear in the middle and outer bands of the upper fields of both lungs, often in the form of symmetrical crossed leaves, and the transparency of the surrounding lungs is high. Due to a lot of pulmonary fibrosis and contraction, the hilum moves up. The shadow density of hilum increases, and sometimes "eggshell calcification" lymph nodes can be seen. Pleura may be thickened, adhered or calcified.
In China, the diagnostic criteria and treatment principles of pneumoconiosis were published in February, 1986. At present, the X-ray diagnosis and staging standards of pneumoconiosis are as follows:
A, no pneumoconiosis (code 0)
(1) Pneumoconiosis has no X-ray manifestation.
(2) The X-ray findings are not enough to diagnose me.
Second, pneumoconiosis (code I)
(a) I have the density of class I, that is, it is certain. There are 10 small circular shadows (< 1 cm) with a diameter less than 2cm, which are distributed in at least two lung regions (one in the upper and lower * * 6 regions of the left and right lungs); Or irregular small shadows with density grade I (a group of dense shadows with different thickness, length and shape), whose distribution range is not less than two lung areas, and the lung texture is clearly visible.
(2)I+ small shadows increased obviously, but one of the density and distribution range was not enough to be classified as "II".
The third and second pneumoconiosis (code Ⅱ)
(1) Grade II density is Grade 2, that is, a large number of small round or irregular shadows are distributed in four lung areas, and the fine lung lines are still recognizable or partially disappeared; Or there is a density of 3, that is, there are many circular or irregular shadows, the distribution range reaches 4 lung areas, and the lung texture disappears partially or completely.
(2) Ⅱ+has a small shadow, the density is grade 3, and the distribution range exceeds four lung areas; Or a big shadow is not enough for ⅲ.
Fourth and third stage silicosis (code ⅲ)
(a) Ⅲ has a big shadow, the long diameter is not less than 2cm, and the wide diameter is not less than 65438±0cm.
(II)III+ single large shadow area or the sum of multiple large shadow areas exceeds the right upper lung area.
Etiology and pathology
The cause of disease
About 95% of ores contain different proportions of quartz sand, and in some industrial production, raw materials also contain different amounts of quartz sand, such as glass, refractories, enamels, ceramics and so on. It contains more than 97% free silica, so miners, workers, workers and farmers who are exposed to silica dust (dust-exposed work in railway construction and township industries) may develop silicosis.
Whether the dust will cause disease depends on many factors, such as the higher the content of free silica in the dust, the higher the concentration in the ambient air, the smaller the dust particles (0.5-2um), and the longer the contact time, the worse the respiratory defense function (chronic rhinitis, bronchitis, tuberculosis, etc.). ), the faster the occurrence and development of silicosis. It can also be caused by inhaling a large amount of free silica dust in a short time. Even if it is out of contact, delayed silicosis may occur several years later. Dust exposure time can be less than 1 year, and silicosis can occur if it is slower than1year.
pathogenesis
Silica dust particles (silica dust) are inhaled into alveoli and swallowed by pulmonary macrophages (dust cells), and the phagocytes containing silica dust fuse with lysosomes to form secondary lysosomes. Silicon dioxide has obvious toxic effect on macrophages. The hydroxyl group on the surface forms hydrogen bonds with phospholipids or protein in lysosomal membrane, which leads to the disintegration of lysosomes in phagocytes. Finally, the cell membrane itself is destroyed, releasing silica dust, which is then swallowed by other macrophages. So repeatedly. Damaged or destroyed macrophages release "fibroblasts" and activate fibroblasts, resulting in collagen fiber proliferation. When macrophages decompose, they release antigens (silica, stimulate immunocompetent cells and produce antibodies. The antigen-antibody reaction produces complex and complement, forming glassy substance deposited on collagen fibers, making the newly formed connective tissue transparent. During the development of silicon nodules, there are many plasma cells around them
pathology
Silicosis nodule is the characteristic focus of silicosis, and the accumulation of dust cells is the basis of silicosis nodule formation. When dust cell clusters are formed, fibroblasts proliferate and reticular fibers appear around them. The latter thickened and degenerated into collagen fibers, and finally formed collagen nodules with vitreous degeneration in the center. Microscopically, silicon nodules are located around bronchi and blood vessels, with a diameter of 0.3-1.5 mm. Typical silicon nodules are concentric circles of glassy collagen fibers. There may be silica dust particles between collagen fibers, and silica dust can flow with tissue fluid to other places to cause new silica nodules. So silicosis can continue to develop after dust removal. Many nodules aggregate into large nodules, and many large nodules fuse into large glassy masses.
After silica dust enters alveoli, it is swallowed by macrophages. Dust cells can enter the lymphatic system and reach hilar lymph nodes. Due to the continuous accumulation of dust cells, lymphatic vessels are blocked, lymphatic stagnation and reflux to subpleural lymphatic vessels. Therefore, alveolar septa and dust cells around blood vessels and bronchi gather and nodular fibrosis occurs. The extrusion or contraction of fiber blocks distorts interstitial lung, narrows bronchioles and capillaries, and affects ventilation and blood flow.
Dust cells gather in hilar lymph nodes, leading to fibrous tissue proliferation and formation of silicon nodules, hilar lymph nodes swelling and hardening, calcium deposition in or around lymph nodes, and "eggshell calcification" of hilar lymph nodes on X-ray chest film.
Silicon nodules can also be formed on the pleura, and collagen fibers proliferate and become transparent. Pleural fibrosis causes pleural thickening and adhesion. differential diagnosis
First, acute miliary tuberculosis
Stage Ⅱ silicosis should be differentiated from acute miliary tuberculosis. The latter has no history of contact with silica dust and obvious symptoms of systemic poisoning. Chest X-ray showed that the shadow of miliary lesions in both lungs was dense and the size was the same, and the upper part of lung apex was denser, without reticular and lung texture changes. Millet focus can be absorbed after anti-tuberculosis treatment.
Second, bronchioloalveolar carcinoma
Alveolar carcinoma with diffuse nodules in both lungs should be differentiated from stage ⅱ and ⅲ silicosis. The X-ray manifestations of alveolar carcinoma are nodular or invasive lesions, with uneven distribution and different sizes, no lump or large fusion, less reticular shadows and emphysema, rapid progress of the disease and lesions, and cancer cells can be seen in sputum. The patient has no history of exposure to silica dust.
Third, pulmonary hemosiderosis
This disease can be seen in bicuspid stenosis of rheumatic heart disease. Patients with recurrent heart failure have no history of exposure to silica dust. X-ray showed diffuse nodules in both lungs, similar to stage ⅱ silicosis, but the shadow near the hilum was dense, the middle and outer bands became thinner, and the left atrium in the heart shadow increased.
Fourthly, alveolar microlithiasis.
As a rare disease with unknown etiology, it often has a family history. No dust contact history. X-ray chest film shows that both lungs are covered by fine sand granular nodules with a size of about 1mm, with clear edges, especially in the inner lung, with few hilar shadows and no change in lung texture. The course of the disease progresses slowly, which can last for decades. complication
First, tuberculosis
It is a common complication of silicosis, up to 20%-50%. Autopsy found more than before, about 36%-75%. The incidence of this complication increases with the progress of silicosis staging, with 20%-40% in patients with stage I-II tuberculosis and 70%-95% in stage III. Tuberculosis accounts for 45% of the direct death cause of silicosis. When silicosis complicated with pulmonary tuberculosis, it affects each other and accelerates the deterioration. Symptoms of tuberculosis poisoning can occur, and mycobacterium tuberculosis can 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.
II. Chronic bronchitis and obstructive emphysema
Long-term inhalation of dust will damage the ciliated epithelium of bronchi. Because of diffuse nodular fibrosis of both lungs, bronchial stenosis and poor drainage, it is prone to viral and bacterial infections, complicated by chronic bronchitis and emphysema, and in severe cases, secondary pulmonary heart disease. Respiratory tract infection often induces respiratory failure and right heart failure.
Third, spontaneous pneumothorax.
Spontaneous pneumothorax is caused by the rupture of pulmonary bullae during severe cough or overwork in advanced silicosis. Because of pleural adhesion, common localized pneumothorax can often be covered up by the original symptoms of dyspnea, which was discovered only during X-ray examination. Pneumothorax can occur repeatedly or alternately on both sides. Due to the fibrosis of lung tissue and pleura, the rupture is difficult to heal and the gas absorption is slow.