www.mingyihui.net Silicosis Medical Treatment Guide (Introduction)

A Guide to Medical Treatment for Silicosis (Introduction) http://www.mingyihui.net/article_433.html Silicosis (also known as silicosis disease, silicon lung, pulmonary siderosis, silicon disease, grinder's disease, or pneumoconiosis) What is silicosis? Silicosis (silicosis) is the most severe type of pneumoconiosis caused by long-term inhalation of dust containing free silica (SiO2). It leads to extensive nodular fibrosis in the lungs. In severe cases, it affects lung function and results in loss of labor capacity. What are the symptoms and signs of silicosis? What are the early symptoms of silicosis?

1. Clinical Manifestations

In the early stages, silicosis patients may have no symptoms or only mild ones. As the condition progresses, symptoms increase, mainly including the following:

Depending on the concentration of dust exposure, the content of silica dust, and the duration of exposure, silicosis can be classified into three clinical types: chronic silicosis, acute silicosis, and accelerated silicosis that lies between the two (Table 1).

In the early stages of silicosis, patients often have no symptoms or only mild ones. Even if there are already obvious signs on the X-ray chest film, they may still not show any symptoms, and are only discovered during regular health check-ups or chest X-rays taken for other reasons, showing typical silicotic nodule changes, or even reaching stage II silicosis changes. As the disease progresses or complications arise, varying degrees of symptoms may appear. The severity of the symptoms does not always correspond to the severity of the lesions in the lungs.

(1) Dyspnea: Gradually developing dyspnea with slow progression, especially after activity. Initially, the patient feels shortness of breath or chest pressure, which then occurs with slight effort. Rarely happens at rest, mostly due to lung fibrosis, especially when combined with emphysema, or caused by concurrent infections. The presence and severity of dyspnea do not necessarily correlate with the degree of pulmonary function impairment or X-ray findings. In late-stage patients, dyspnea can become extremely severe, leading to shortness of breath even with minor activities or at rest, preventing lying flat.

(2) Cough and Sputum Production: Patients with a smoking history may experience coughing and sputum production similar to bronchitis symptoms. Coughing mainly occurs in the morning, sometimes intermittently day and night. In later stages, there is often persistent paroxysmal coughing, possibly due to stimulation of the trachea and bronchi nerve receptors by silicotic nodules. There may be no sputum or only a small amount of sticky sputum. During secondary infections, purulent sputum may appear, worsening the cough. Hemoptysis is rare in simple silicosis. Wheezing is generally absent unless combined with chronic bronchitis or allergic asthma, but some patients develop wheezing due to tracheal narrowing, twisting, and fixation from fibrosis, particularly in late-stage patients or during forceful breathing.

(3) Hemoptysis: Occasionally hemoptysis occurs, usually with blood streaks in the sputum. When combined with tuberculosis or bronchiectasis, there may be repeated hemoptysis or even massive hemoptysis.

(4) Chest tightness and chest pain: Often presents as needle-like pain or continuous dull pain in the upper-middle part of the front chest. It usually appears during rainy weather or climate changes and is unrelated to respiration, movement, or body position.

(5) General Damage Condition: Not obvious unless combined with pulmonary tuberculosis or congestive heart failure. If dyspnea occurs at rest, it should raise suspicion of severe emphysema or extrapulmonary diseases. Besides respiratory symptoms, late-stage silicosis patients often experience reduced appetite, physical weakness, weight loss, and night sweats.

2. Signs

In early silicosis, there are often no signs. In late-stage patients, signs of chronic obstructive pulmonary disease may appear, such as barrel chest, hyperresonance on percussion, prolonged expiration on auscultation, weakened breath sounds, etc. Crackles and wet rales may be heard in both lungs during infection. In late-stage patients with cor pulmonale and heart failure, a series of corresponding signs may be observed.

3. Diagnosis

Diagnosis should be based on:

① Dust exposure history, including the content of free silica 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 Detailed occupational history and past health status;

③ Clinical symptoms, signs, and X-ray examination;

④ Past and current disease conditions of workers in the same occupation.

(1) X-ray Examination: Currently, silicosis diagnosis is mainly based on X-ray chest film manifestations. In December 1986, China announced the "Diagnostic Criteria and Management Principles for Pneumoconiosis," among which the X-ray diagnostic criteria for pneumoconiosis apply to various types of pneumoconiosis recognized by national law. The specific criteria are as follows:

1. No pneumoconiosis (Code 0)

(1) 0 No X-ray manifestations of pneumoconiosis.

(2) 0+ X-ray manifestations are insufficient to diagnose as "I."

2. Stage I pneumoconiosis (Code I), (see Figure 12-3).

(1) I Has grade 1 density round-shaped small shadows, distributed in at least two lung zones each with a diameter not less than 2 cm; or has grade 1 density irregular-shaped small shadows, distributed in not less than two lung zones.

(2) I+ Small shadows significantly increase, but either the density or distribution range does not meet the criteria for "II."

3. Stage II pneumoconiosis (Code II), (see Figure 124)

(1) II Has grade 2 density round-shaped or irregular-shaped small shadows, distributed in more than four lung zones; or has grade 3 density small shadows, distributed in four lung zones.

(2) II+ Has grade 3 density small shadows, distributed in more than four lung zones; or large shadows not yet meeting the criteria for "III."

4. Stage III pneumoconiosis (Code III), (see Figure 125)

III Large shadows appear, with a long diameter not less than 2 cm and a wide diameter not less than 1 cm.

III+ The area of a single large shadow or the total area of multiple large shadows exceeds the area of the right upper lung zone.

When using the above standards, the following concepts should be considered:

(1) Lung Zone Division Method: Divide the vertical distance from the lung apex to the diaphragm top equally into three parts, and use the horizontal lines through the equal division points to divide each side of the lung field into upper, middle, and lower zones.

(2) Small Shadows: Refers to shadows with a diameter or width not exceeding 1 cm. They can be divided into two types: ① Round-shaped (R), with a shape of a circle or nearly circular, with neat or uneven edges; ② Irregular-shaped (IR), referring to dense shadows of varying thicknesses, lengths, and shapes, which may be unconnected or intertwined in a disorderly manner, appearing as a network, sometimes in a honeycomb pattern. Both types of small shadows can be classified according to their size or thickness as p (diameter approximately 1.5 mm or less), q (diameter approximately 1.5~3 mm), r (diameter 3~10 mm); irregular-shaped ones are classified as s (width approximately 1.5 mm or less), t (width approximately 1.5~3 mm), u (width approximately 3~10 mm).

(3) Density of Small Shadows: Refers to the quantity of small shadows within a certain range, which can be divided into 3 levels:

Density of round-shaped small shadows:

Level 1 Definite, a certain amount of round-shaped small shadows. Lung texture is clearly visible (for example, if it is p, about 10 within a 2 cm diameter range).

Level 2 A large number of round-shaped small shadows, lung texture is generally recognizable.

Level 3 A very large number of round-shaped small shadows, lung texture partially or completely disappears.

Density of irregular-shaped small shadows:

Level 1 A considerable amount of irregular-shaped small shadows, lung texture is generally recognizable.

Level 2 A large number of irregular-shaped small shadows. Lung texture usually partially disappears.

Level 3 A very large number of irregular-shaped small shadows, lung texture usually completely disappears.

Methods for determining density and range: Comprehensive judgment should be made on the density status of all small shadows appearing in each lung zone: 1. To determine the lung zone, small shadows must occupy two-thirds of the area of that zone; 2. Distribution range refers to the number of lung zones where small shadows appear; 3. The majority of lung zones' densities serve as the main basis for judgment; 4. The higher level of density with a distribution range of not less than two lung zones serves as the main basis for judgment.

(4) Large Shadows: Refers to shadows with a longest diameter greater than 1 cm. Shadows not meeting the criteria for "III" include: ① Aggregation of small shadows, not yet forming a uniformly dense mass shadow; ② Mass shadow not reaching 2 cm x 1 cm; ③ Appearance of "patchy strips" or "whitened areas."

(5) Pleural Changes (including thickening, adhesion, calcification), complications of pneumoconiosis, or other diseases (such as rheumatoid pneumoconiosis), all have corresponding code records.

(6) Regarding each phase (+): To facilitate dynamic observation of the condition, additions of 0+, I+, II+, III+ are made within each phase, not as independent phases.

For silicosis, when exposed to high-silica and high-concentration dust, the main manifestations are round and round-shaped shadows, first appearing in the inner-middle bands of the mid-lower fields of both lungs and gradually extending upwards; they may also first appear in the upper lungs. In low-silica or mixed-dust inhalation situations, round-shaped shadows predominate (i.e., so-called reticular shadows). Large shadows in silicosis result from the aggregation, densification, and eventual fusion of local shadows, commonly seen in the outer zones of the upper lungs of both sides, with clear contours, symmetrical in both lungs presenting as "wing-like" or eight-shaped. Fusion blocks contract inward and upward, pulling the hilum out of place. Hilum shadows often enlarge and densify, sometimes showing lymph node "eggshell-like calcification" due to calcium deposition under the lymph node capsule. Lung markings increase and thicken.

(2) Laboratory Tests: Routine tests for silicosis generally have no special significance. Serum protein hexose, amino hexose, mucoprotein, immunoglobulin, ceruloplasmin, and urinary hydroxyproline often show increasing trends, but most are non-specific, with large fluctuations within normal ranges, making their clinical value limited.

(3) Pulmonary Function Testing: Due to the strong compensatory function of lung tissue, early-stage patients show no significant damage to pulmonary function. With increased fibrous tissue and reduced elasticity, vital capacity decreases. As the condition progresses, forced expiratory volume in one second and maximum ventilation volume also decrease, while residual gas volume and its percentage of total lung capacity increase. The more severe the emphysema, the more obvious these changes, leading to diffusion dysfunction. Resting arterial oxygen partial pressure may have varying degrees of reduction. Pulmonary function testing has little diagnostic significance but can serve as a basis for assessing the labor capacity of silicosis patients.

After understanding the manifestations of silicosis, what checks should we perform?

What tests should be done for silicosis? Blood and urine routine tests for silicosis patients are generally within the normal range. In late-stage silicosis, erythrocyte sedimentation rate may increase, and blood silicon and urine silicon measurements fluctuate widely. Silicosis patients often have reduced serum albumin and increased globulin, with an increase in globulin being more common.

In recent years, bronchoalveolar lavage as a diagnostic and therapeutic method for pneumoconiosis has been promoted and applied clinically. Through the detection of cellular components, biochemical immunity, and etiological characteristics of bronchoalveolar lavage fluid (BALF), it plays an important role in auxiliary diagnosis and differential diagnosis of pneumoconiosis. BALF cell count in normal non-smokers is (5~10)10^6, with alveolar macrophages (AM) accounting for about 95%, lymphocytes <5%, neutrophils, and eosinophils <1%. Lymphocyte counts in acute silicosis patients can increase to 40%~60%. PaCO2 is generally normal. However, when severe obstruction or restrictive ventilatory dysfunction occurs, PaO2 decreases, even significantly at rest, resulting in hypoxemia.

1. Pulmonary Function Test: There is no significant correlation between X-ray manifestations and pulmonary function impairment in silicosis patients. In early-stage silicosis patients without complications, pulmonary function often shows no significant change, even when severe lesions appear on X-ray chest films, the patient's pulmonary function decline may not be significant.

(1) Pulmonary function changes in silicosis patients are mainly characterized by changes in lung volume, mostly manifesting as restrictive ventilatory dysfunction, with decreased vital capacity (VC).

(2) Forced vital capacity (FVC) decreases in silicosis patients.

(3) Total lung capacity (TLC) decreases in silicosis patients.

(4) Residual volume (RV) decreases in silicosis patients.

(5) The degree of decrease in 1-second forced expiratory volume (FEV1) parallels FVC.

(6) FEV1/FVC (%) can be within the normal range, heavy smokers and those with emphysema may show obstructive ventilatory dysfunction or mixed ventilatory dysfunction.

Due to widespread fibrosis of alveoli and interstitium, capillary closure, reduced blood flow, emphysema formation, uneven gas distribution, and reduced diffusion area in silicosis, diffusion function often decreases, especially significantly in cases with mass formation. Blood pH is generally normal.

2. X-ray Manifestations: Chest X-rays are the main basis for diagnosing silicosis. Main manifestations include nodular shadows, reticular shadows, and/or large fused lesions. Secondary changes include hilar changes, lung texture changes, and pleural changes.

(1) Typical nodular shadows: The earliest manifestation of silicosis on X-ray films is the appearance of round or round-shaped shadows, often referred to as nodules. Nodules can be scattered or clustered to form overlapping shadows. They are similar in size, consistent in shape, and relatively close in density, with a diameter generally of 1~3 mm, mostly distributed in the outer zones of the middle and lower fields of both lungs, more on the right side, but can also first appear in the upper fields of both lungs.

The amount of dust exposure and the content of free silica in the dust are related to the manifestation of silicotic nodular shadows. High concentrations of dust often form high-density typical silicotic nodules, round or round-shaped shadows, progressing rapidly once they appear, manifested by an increase in the size and density of nodular shadows. Nearby nodules aggregate into clusters, come closer together, and develop into mass-like shadows. When the content of free silica in the dust is moderate, the nodular shadows are smaller and more densely packed, eventually forming large shadows, but not as quickly as the former.

(2) Late-stage silicotic nodules: Lesions fuse into mass-like large shadows, with clear edges, accompanied by linear shadows connecting to the hilum or pleura. Surrounding areas show emphysema or bullae, mainly due to the fibrous proliferation of silicotic nodules. Initially, nodules cluster locally within the lungs, gradually fusing into masses, with deeper density in the center and lighter edges. As the lesion develops, the density becomes gradually uniform, the contour clearer, and the density increases to form large mass-like shadows. Fused masses can appear singly or multiply, commonly in the outer zones of the upper lungs of both sides, often in an eight-shaped, wing-like, or sausage-like pattern. Masses can also be asymmetrical or appear in only one lobe.

(3) Contraction of masses causes tracheal mediastinal displacement, deformation, and twisting. The heart is pulled and displaced, with the hilum moving upward, causing the thickened lung texture to appear "willow leaf-like." Linear shadows connect between the mass shadows and the hilum. The pleura adheres and contracts, presenting a tent-like shadow. Large masses may form cavities due to ischemic necrosis. Cavities formed by silicotic masses are rare, often due to concurrent tuberculosis caseous necrosis.

(4) Enlarged hilar lymph nodes, manifested by enlarged hilar shadows, increased density, and unclear edges. Characteristic manifestations include lymph node calcification, forming a thin and dense "eggshell-like" ring-shaped calcification shadow on the edge of the lymph node. Some may appear in clusters. Multiple lymph nodes can fuse into "mulberry-like" patterns, characteristic images of silicosis. The degree of calcification is unrelated to the severity of silicosis or the existence of tuberculosis, and can even appear without obvious silicosis signs or without late-stage silicosis. Although not unique to silicosis, eggshell-like lymph node calcification often suggests silicosis or a history of free silica exposure.

(5) Pulmonary interstitial fibrosis type: In cases with low content of free silica in the dust, nodular shadows are sparse, presenting as irregular dense linear shadows. When these shadows increase, the lung field becomes blurred or appears "ground-glass-like."

(6) In late-stage silicosis chest films, pleural thickening and adhesions, narrowed rib spaces, disappearance of costophrenic angles, and mediastinal pericardial adhesions may also be observed.

3. Chest CT recognition of small round shadows and fused shadows exceeds ordinary chest X-rays. High-resolution CT (HRCT) can improve diagnosis by 10%.

After completing the tests and confirming the diagnosis, how should we treat it? http://www.mingyihui.net/article_433.html