Silicosis other diagnostic studies
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In silicosis, the pulmonary function worsens with the worsening radiology. Pulmonary function testing (PFTs) are a key component for the diagnosis and to guide the future occupational choices. Typically, spirometry before and after bronchodilator, lung volumes, diffusing capacity for carbon monoxide (DLCO), and resting pulse oxygen saturation are obtained.
Lung Function Tests
- Pulmonary function testing (PFTs) are a key component in the diagnosis and follow-up of patients to detect extent of lung involvement, severity of the disease, and guide future occupational choices. Typically, spirometry before and after bronchodilator, lung volumes, diffusing capacity for carbon monoxide (DLCO), and resting pulse oxygen saturation are obtained.
- Progressive massive fibrosis is associated with the worst pulmonary function abnormalities including
- Pulmonary function, on average, worsens in association with worsening radiographic abnormalities of chronic or accelerated silicosis; cigarette smoking is often contributory.
- Spirometry is performed for the evaluation of possible functional lung deterioration
- Spirometry shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio 
- Diffusion capacity is affected in the complicated forms of the disease and is sensitive to the presence of fibrosis.
- Static lung volumes can demonstrate a reduction in total lung volume .
Pulse oximetry and arterial blood gases
- Pulse oximetry and arterial blood gases are useful for the detection of respiratory failure (PaO2<60 mmHg with SpO2<90%) in the more advanced cases.
Complete cardiopulmonary exercise testing
- Complete cardiopulmonary exercise testing may be helpful in evaluating patients with respiratory symptoms, particularly exertional dyspnea, who have a history of exposure to silica and whose resting lung function is normal.
- Bronchoscopy to confirm the diagnosis is not indicated for most patients. However, bronchoscopic washings, brushing, or bronchoalveolar lavage (BAL) is used to exclude infection, eosinophilic pneumonia, and alveolar hemorrhage when acute silicosis is suspected. In acute silicoproteinosis, BAL yields a thick, opaque (milky) effluent similar to that seen in pulmonary alveolar proteinosis. On cytologic examination, the macrophages in the BAL are foamy and the lipoproteinaceous material stains brightly positive with periodic acid-Schiff (PAS) reagent  In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax .
- A lung biopsy is not necessary in the setting of a definite exposure history and characteristic clinical findings.The histopathology of acute silicosis is different from that of chronic or accelerated silicosis. Silicotic nodules are rarely seen, and, if present, are usually poorly developed. As described for BAL fluid, proteinaceous material fills the alveoli and consists largely of phospholipids or surfactant (or surfactant-like material) and stains with PAS reagent. The interstitium is thickened with inflammatory cells; a minimal amount of pulmonary fibrosis is typically present. Alveoli may be lined with prominent epithelial cells, the majority of which are hypertrophic type II pneumocytes . In addition, desquamated pneumocytes, macrophages, and silica particles are found in the alveolar spaces. The histologic appearance of acute silicosis resembles that of idiopathic alveolar proteinosis
- Biomarkers such as Serum NSE and CA125 concentrations would provide valuable clinical information to assess disease severity in silicosis. Research is going on the use of various other biomarkers in silicosis.
- ↑ 1.0 1.1 Wang XR, Christiani DC (2000). "Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts". J Occup Environ Med. 42 (11): 1076–84. PMID 11094786.
- ↑ Bégin R, Ostiguy G, Cantin A, Bergeron D (1988). "Lung function in silica-exposed workers. A relationship to disease severity assessed by CT scan". Chest. 94 (3): 539–45. PMID 3409733.
- ↑ Santo Tomas LH (2011). "Emphysema and chronic obstructive pulmonary disease in coal miners". Curr Opin Pulm Med. 17 (2): 123–5. doi:10.1097/MCP.0b013e3283431674. PMID 21178627.
- ↑ Mirabelli MC, London SJ, Charles LE, Pompeii LA, Wagenknecht LE (2012). "Occupation and three-year incidence of respiratory symptoms and lung function decline: the ARIC Study". Respir Res. 13: 24. doi:10.1186/1465-9921-13-24. PMC 3352304. PMID 22433119.
- ↑ Hochgatterer K, Moshammer H, Haluza D (2013). "Dust is in the air: effects of occupational exposure to mineral dust on lung function in a 9-year study". Lung. 191 (3): 257–63. doi:10.1007/s00408-013-9463-7. PMID 23568145.
- ↑ Lopes AJ, Costa W, Thomaz Mafort T, de Sá Ferreira A, Silveira de Menezes SL, Silva Guimarães F (2012). "Silicosis in sandblasters of shipyard versus silicosis in stone carvers in Brazil: a comparison of imaging findings, lung function variables and cardiopulmonary exercise testing parameters". Rev Port Pneumol. 18 (6): 260–6. doi:10.1016/j.rppneu.2012.04.006. PMID 22717312.
- ↑ Nugent KM, Dodson RF, Idell S, Devillier JR (1989). "The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis". Am Rev Respir Dis. 140 (5): 1438–41. doi:10.1164/ajrccm/140.5.1438. PMID 2817609.
- ↑ Hoffmann EO, Lamberty J, Pizzolato P, Coover J (1973). "The ultrastructure of acute silicosis". Arch Pathol. 96 (2): 104–7. PMID 4352308.
- ↑ Buechner HA, Ansari A (1969). "Acute silico-proteinosis. A new pathologic variant of acute silicosis in sandblasters, characterized by histologic features resembling alveolar proteinosis". Dis Chest. 55 (4): 274–8. PMID 5775743.
- ↑ Fang SC, Zhang HT, Wang CY, Zhang YM (2014). "Serum CA125 and NSE: biomarkers of disease severity in patients with silicosis". Clin Chim Acta. 433: 123–7. doi:10.1016/j.cca.2014.03.005. PMID 24642341.
- ↑ Pandey JK, Agarwal D (2012). "Biomarkers: A potential prognostic tool for silicosis". Indian J Occup Environ Med. 16 (3): 101–7. doi:10.4103/0019-5278.111746. PMC 3683176. PMID 23776317.