coal worker pneumoconiosis
Introduction
Introduction to coal workers' pneumoconiosis Coal miner's pneumoconiosis (coalminer's spneumoconiosis) is a general term for lung disease caused by coal mine workers' long-term inhalation of dust in the production environment, including coal and lungs caused by coal and coal-making workers inhaling pure coal dust, accounting for about 10%; The silicosis caused by the excavation of the dust by the excavator accounts for less than 10%; and the coal silt caused by the inhalation of mixed dust such as coal dust and dust, mainly occurs in the mixed work of both excavation and coal mining, accounting for about 80%. the above. Coal mines are most common in coal mines. Coal workers' pneumoconiosis mainly occurs in underground miners. The prevalence rate of open pit coal miners is very low. Coal miners can also occur in other workers who are in contact with pulverized coal in large quantities, such as dock unloading workers and briquettes. Due to the insignificant labor capacity, there is not much research. basic knowledge Probability ratio: probability of suffering from coal workers 0.0062% Susceptible people: coal mining and coal workers Mode of infection: non-infectious Complications: chronic bronchitis emphysema respiratory tract infection spontaneous pneumothorax chronic pulmonary heart disease tuberculosis
Cause
Cause of coal worker's pneumoconiosis
Cause of the disease (80%):
There have been different opinions for many years. At first, it was thought that coal dust was only in the lungs. The so-called coal-based pneumoconiosis was caused by dust in the coal dust. Later, some people were working on dockers who were simply engaged in coal unloading. In addition to coal dust deposition, there is still progressive bulk fibrosis, so it is believed that coal dust itself can cause pneumoconiosis.
Pathogenesis
According to the different time of contact with coal dust, the general anatomical appearance of simple coal worker's pneumoconiosis is also different. Usually, except for melanin on the surface of the pleura, there is no obvious abnormality in the lungs. Unless there is chronic bronchitis, there is no obvious abnormality in the trachea and bronchus. Lymph nodes tend to increase, uniform pigmentation and hard and no fibrosis. There are many pigmentation lesions adjacent to the terminal and respiratory bronchioles in the lung section. The air cavity adjacent to the dust accumulation is often slightly dilated, called the stove. Emphysema.
The basic lesions of the coal under the microscope include coal dust (or coal spots, 5 mm pigmentation), pericardial emphysema or interstitial diffuse fibrosis, coal dust and macrophage aggregation that devours coal dust. In the alveolar space, alveolar wall, bronchus and perivascular tissue, coal dust and coal dust cells are formed, mostly around the secondary respiratory bronchioles. As the lesion progresses, irregularly arranged reticular fibers appear, and later There may be a small amount of collagen fibers interwoven, which constitutes a coal dust fiber stove, and there is emphysema around the stove. It is one of the main pathological features of coal workers' pneumoconiosis, and different degrees of fibrous tissue proliferation can be seen in the pulmonary interstitial.
In addition to the basic pathological changes of coal lung and silicosis in coal sputum lungs, there are pathological changes in the presence of mixed coal dust and dust, that is, the formation of coal gangue mixed nodules, in addition to reticular fiber proliferation in the nodules, there is collagen The fibers are interwoven, but the latter are irregularly arranged. There are coal dust cells and quartz particles in the nodules. Large fibrous lesions can be seen in the late stage. Other features include subpleural coal dust deposition, hilar and mediastinal lymph nodes and their causes. A pleural-like change in the parietal wall caused by coal dust.
Prevention
Coal worker's pneumoconiosis prevention
It is necessary to emphasize the strict implementation of the national maximum dust concentration standard. The maximum allowable concentration of coal dust containing less than 10% free silica in China is 10 mg/m3. The main measures are free from the dust working environment. Do a good job of work protection, reasonable environmental protection, stay away from dusty environment, improve lung function reasonably, exercise actively, do not eat spicy food, avoid alcohol and tobacco, and ensure sleep. Improve environmental sanitation, do personal labor protection, eliminate and avoid the effects of smoke, dust and irritating gases on the respiratory tract.
Complication
Coal worker pneumoconiosis complications Complications chronic bronchitis emphysema respiratory tract infection spontaneous pneumothorax chronic pulmonary heart disease pulmonary tuberculosis
The main complications or complications of coal worker's pneumoconiosis are chronic bronchitis and emphysema, respiratory infection, spontaneous pneumothorax and chronic pulmonary heart disease are also common complications of coal workers' pneumoconiosis. Coal workers' pneumoconiosis and tuberculosis are also more common. The rate is about 22%. Combined with tuberculosis, the lesions are obviously aggravated, especially in simple coal workers' pneumoconiosis, which can rapidly progress to progressive bulk fibrosis, and the anti-tuberculosis treatment is poor. Rheumatoid pneumoconiosis (Caplan syndrome) is in coal. The incidence of pneumoconiosis is higher than that of other pneumoconiosis. The patient has rheumatoid arthritis. The chest X-ray is a circular shadow with clear lungs in both circles. The diameter is 0.5-5 cm, which occurs almost simultaneously and increases rapidly. After that, it will no longer increase, and serum rheumatoid factor can be positive, but this complication is rare in China.
Symptom
Coal worker's pneumoconiosis symptoms Common symptoms, shortness of breath, rough hemoptysis, difficulty breathing, dry cough, coal dust or cholesterol knot... Dry sputum, short hair, lung fibrosis
First of all, attention should be paid to the duration of exposure to dust and occupational history. Generally, the development time for simple coal workers' pneumoconiosis is 10 to 12 years. In this period, the lung function usually has no abnormal changes, and the clinical manifestations are non-specific. Asymptomatic, the symptoms will appear in patients with bronchitis or pulmonary infection, cough, usually a mild dry cough, but the prevalence of chronic bronchitis in coal workers is higher, the general miners also see cough, combined with lung infection When the cough is aggravated, accompanied by cough, it can cough up the sputum containing coal dust or cholesterol crystals, and there is little hemoptysis. Most of the coal workers' pneumoconiosis patients have different degrees of chest tightness or chest pain, which is characterized by intermittent pain or acupuncture pain. After the cough or cough is more obvious, sudden severe chest pain accompanied by dyspnea, should consider spontaneous pneumothorax may be, gradually progressive dyspnea, and some cases of respiratory symptoms and X-ray performance is not commensurate, X-ray film The performance is mild, but the symptoms of shortness of breath are very serious.
As the time of exposure to dust increases, shortness of breath and cough may increase, and the performance of chest radiographs will also be obvious. The increase in dyspnea is often consistent with the development of large pulmonary fibrosis. The sputum is black and the amount is large. A site of ischemic necrosis and the formation of a cavity often cough up a large number of black sputum, can also cough up a large number of purulent sputum when combined with acute infection.
Most coal workers' pneumoconiosis patients have no positive signs even in stage II and III. Occasionally, hairpins and clubbings are rare. In a few patients, the lungs can smell rough or weakened and dry vocal sounds, and there are various complications. Signs.
Examine
Coal worker's pneumoconiosis inspection
Pulmonary function test
Although early coal workers' pneumoconiosis patients had diffuse interstitial fibrotic lesions and mild emphysema, there was no significant change in lung function, only in the late stage of pneumoconiosis, or in the dynamic observation, it could be seen earlier. Trends, the type of ventilatory dysfunction of coal workers' pneumoconiosis is mainly characterized by restrictive ventilatory dysfunction in the early stage, the most common type of obstructive type in the middle and late stage, followed by mixed type. The average values of FEV1, FVC, VC and MMF are usually low in coal workers' pneumoconiosis patients. In normal people or dust-collecting workers, and basically progressive decline with the progress of the lesions, the most predictive values of FEV1, FEV1/FVC and FEV1/VC in the indicators are the most sensitive to pulmonary emphysema. The total amount, lung compliance increased, in the pure coal workers, the pneumoconiosis diffusion function can be in the normal range, the progressive bulk fibrosis patients can be reduced to the expected value of less than 50%, the diffusion function is progressively reduced, the decline may also be related to obstructive Pulmonary disease or associated with silicosis, stage III and part II stage coal workers pneumoconiosis patients at rest, arterial oxygen partial pressure and oxygen saturation decreased, arterial blood carbon dioxide partial pressure usually in the normal range or slightly lower.
2. X-ray inspection
The characteristics of coal worker's pneumoconiosis chest radiographs are: reticular changes; nodular changes; nodular fusion; block shadows and multiple villous changes.
The reticular change is considered to be the earliest manifestation of coal worker's pneumoconiosis, with diffuse fine mesh shadows in the lung field. At this time, there is no clinical symptom. As the nodule expands, the lesion merges into an opaque progressive mass. Fibrosis, usually located in the upper lungs of the lungs, can also be fused to the middle and lower lung fields, sometimes only in one side of the lung field, usually in large, uniform, well-defined shadows, often in simple The coal worker's pneumoconiosis occurs on the background of the shadow of the nodules.
The coal worker's pneumoconiosis with rheumatoid arthritis, ie the chest X-ray of Caplan syndrome, tends to have multiple round, clear, well-distributed nodules, even in the lungs and even around the lung field. The diameter of the round nodule can range from 0.5 to 5 cm, but usually about 1 cm. Sometimes the lesion has no obvious correlation with arthritis, or the disease develops rapidly after the onset of arthritis. The central cavity can be calcified in the lung lesion of Caplan. And the phenomenon of lesion fusion.
In patients with progressive massive fibrosis or those with a history of severe smoking, emphysema is often combined. Severe emphysema often leads to unclear punctate and small nodules in the lungs, which may lead to clinicians' underestimation of lesions. Lymph node enlargement is less common.
Diagnosis
Diagnosis and identification of coal workers' pneumoconiosis
diagnosis
Mainly based on chest X-ray film, combined with professional history to make a corresponding diagnosis.
Differential diagnosis
Should be identified with the following diseases such as pulmonary hemosiderosis, idiopathic diffuse pulmonary interstitial fibrosis, miliary pulmonary TB, alveolar microlithiasis, alveolar cancer, foreign aid allergic alveolitis.
1. Idiopathic pulmonary hemosiderosis is a disease whose cause is still unclear. The lesion is characterized by alveolar capillary hemorrhage. The formation of hemoglobin after hemoglobin breakdown is deposited in the alveolar stroma. Eventually leads to pulmonary fibrosis. The age of onset is mainly in childhood, and the majority of the onset age is in infants and preschools. The pathogenesis may be related to autoimmunity, but the specific link is still unclear. The disease has a long course, repeated attacks, and a long-term prognosis.
2. Idiopathic pulmonary interstitial fibrosis (IPF) is a diffuse inflammatory disease of the lower respiratory tract of unknown cause. Inflammation invades the alveolar wall and adjacent alveolar spaces, causing alveolar septal thickening and pulmonary fibrosis.
3. Pulmonary miliary tuberculosis, also known as hematogenous disseminated tuberculosis. Acute miliary tuberculosis is often part of whole body miliary tuberculosis. Have low fever, fatigue, loss of appetite, cough and a small amount of hemoptysis. However, most patients have mild lesions, often no obvious symptoms, a few patients with acute onset, highly toxic symptoms and obvious respiratory symptoms, and occasionally, the lesions can be confined to both lungs.
4. Alveolar microlithiasis is a rare chronic lung disease that can occur in childhood, but clinical symptoms begin several years later. It is characterized by disseminated small stones that are widely present in the alveoli.
The lungs are hard and the cut surface has a grainy feel.
5. Alveolar cell carcinoma: originated from the bronchial mucosa epithelium, also known as bronchioloalveolar cell carcinoma or bronchioloalveolar carcinoma, or abbreviated alveolar carcinoma. The part is around the lung field. In all types of lung cancer, the incidence is low, and women are more common. Generally, the degree of differentiation is higher and the growth is slower. The cancer cells grow along the bronchioles, alveolar ducts and alveolar walls without invading the alveolar septum. Lymphatic and hematogenous metastases occur later, but can spread to other lungs or invade the pleura via the bronchus.
6. Exogenous allergic alveolitis (EAA), also known as hypersensitivity pneumonia (HP), is an immune-mediated lung caused by repeated inhalation of organic dust or chemically active substances. Disease, clinical manifestations of fever, cough, dyspnea, hypoxemia and systemic muscle and joint pain, the basic histopathological changes are early pulmonary interstitial, diffuse mononuclear cell infiltration of alveolar and terminal bronchioles , granulomas often appear later, and advanced interstitial fibrosis can develop.
