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{{Silicosis}} | {{Silicosis}} | ||
==Overview== | |||
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]], [[DLCO|diffusing capacity for carbon monoxide]] (DLCO), and resting [[Pulse oximetry|pulse oxygen saturation]] are obtained. | |||
===Lung Function Tests=== | ===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. | *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, [[DLCO|diffusing capacity for carbon monoxide]] (DLCO), and resting [[Pulse oximetry|pulse oxygen saturation]] are obtained. | ||
*[[PMF]] is associated with the worst pulmonary function abnormalities, including | *[[PMF]] is associated with the worst pulmonary function abnormalities, including [[compliance|decreased compliance]], [[FEV1|decreased FEV1]] and [[FEV1/FVC ratio]], and [[DLCO|decreased diffusing capacity for carbon monoxide]] (DLCO) <ref name="pmid11094786">{{cite journal| author=Wang XR, Christiani DC| title=Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts. | journal=J Occup Environ Med | year= 2000 | volume= 42 | issue= 11 | pages= 1076-84 | pmid=11094786 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11094786 }} </ref><ref name="pmid3409733">{{cite journal| author=Bégin R, Ostiguy G, Cantin A, Bergeron D| title=Lung function in silica-exposed workers. A relationship to disease severity assessed by CT scan. | journal=Chest | year= 1988 | volume= 94 | issue= 3 | pages= 539-45 | pmid=3409733 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3409733 }} </ref>. Pulmonary function, on average, worsens in association with worsening radiographic abnormalities of chronic or accelerated silicosis; [[smoking|cigarette smoking]] is often contributory<ref name="pmid21178627">{{cite journal| author=Santo Tomas LH| title=Emphysema and chronic obstructive pulmonary disease in coal miners. | journal=Curr Opin Pulm Med | year= 2011 | volume= 17 | issue= 2 | pages= 123-5 | pmid=21178627 | doi=10.1097/MCP.0b013e3283431674 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21178627 }} </ref>. | ||
====Spirometry==== | ====Spirometry==== | ||
*Spirometry is performed for the evaluation of possible functional lung deterioration<ref name="pmid22433119">{{cite journal| author=Mirabelli MC, London SJ, Charles LE, Pompeii LA, Wagenknecht LE| title=Occupation and three-year incidence of respiratory symptoms and lung function decline: the ARIC Study. | journal=Respir Res | year= 2012 | volume= 13 | issue= | pages= 24 | pmid=22433119 | doi=10.1186/1465-9921-13-24 | pmc=PMC3352304 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22433119 }} </ref><ref name="pmid23568145">{{cite journal| author=Hochgatterer K, Moshammer H, Haluza D| title=Dust is in the air: effects of occupational exposure to mineral dust on lung function in a 9-year study. | journal=Lung | year= 2013 | volume= 191 | issue= 3 | pages= 257-63 | pmid=23568145 | doi=10.1007/s00408-013-9463-7 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23568145 }} </ref> | *[[Spirometry]] is performed for the evaluation of possible functional lung deterioration<ref name="pmid22433119">{{cite journal| author=Mirabelli MC, London SJ, Charles LE, Pompeii LA, Wagenknecht LE| title=Occupation and three-year incidence of respiratory symptoms and lung function decline: the ARIC Study. | journal=Respir Res | year= 2012 | volume= 13 | issue= | pages= 24 | pmid=22433119 | doi=10.1186/1465-9921-13-24 | pmc=PMC3352304 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22433119 }} </ref><ref name="pmid23568145">{{cite journal| author=Hochgatterer K, Moshammer H, Haluza D| title=Dust is in the air: effects of occupational exposure to mineral dust on lung function in a 9-year study. | journal=Lung | year= 2013 | volume= 191 | issue= 3 | pages= 257-63 | pmid=23568145 | doi=10.1007/s00408-013-9463-7 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23568145 }} </ref> | ||
*Spirometry shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio <ref name="pmid11094786">{{cite journal| author=Wang XR, Christiani DC| title=Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts. | journal=J Occup Environ Med | year= 2000 | volume= 42 | issue= 11 | pages= 1076-84 | pmid=11094786 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11094786 }} </ref> | *[[Spirometry]] shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio <ref name="pmid11094786">{{cite journal| author=Wang XR, Christiani DC| title=Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts. | journal=J Occup Environ Med | year= 2000 | volume= 42 | issue= 11 | pages= 1076-84 | pmid=11094786 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11094786 }} </ref> | ||
*Diffusion capacity is affected in the complicated forms of the disease and is sensitive to the presence of fibrosis. | *[[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 . | *[[Static lung volumes]] can demonstrate a reduction in [[total lung volume]] . | ||
====Pulse oximetry and arterial blood gases==== | ====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. | *[[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==== | ||
*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.<ref name="pmid22717312">{{cite journal| author=Lopes AJ, Costa W, Thomaz Mafort T, de Sá Ferreira A, Silveira de Menezes SL, Silva Guimarães F| title=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. | journal=Rev Port Pneumol | year= 2012 | volume= 18 | issue= 6 | pages= 260-6 | pmid=22717312 | doi=10.1016/j.rppneu.2012.04.006 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22717312 }} </ref> | *Complete cardiopulmonary exercise testing may be helpful in evaluating patients with respiratory symptoms, particularly [[dyspnea|exertional dyspnea]], who have a history of exposure to [[silica]] and whose resting lung function is normal.<ref name="pmid22717312">{{cite journal| author=Lopes AJ, Costa W, Thomaz Mafort T, de Sá Ferreira A, Silveira de Menezes SL, Silva Guimarães F| title=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. | journal=Rev Port Pneumol | year= 2012 | volume= 18 | issue= 6 | pages= 260-6 | pmid=22717312 | doi=10.1016/j.rppneu.2012.04.006 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22717312 }} </ref> | ||
===Bronchoscopy=== | ===Bronchoscopy=== | ||
*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 <ref name="pmid2817609">{{cite journal| author=Nugent KM, Dodson RF, Idell S, Devillier JR| title=The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis. | journal=Am Rev Respir Dis | year= 1989 | volume= 140 | issue= 5 | pages= 1438-41 | pmid=2817609 | doi=10.1164/ajrccm/140.5.1438 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2817609 }} </ref> In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax . | *[[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 <ref name="pmid2817609">{{cite journal| author=Nugent KM, Dodson RF, Idell S, Devillier JR| title=The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis. | journal=Am Rev Respir Dis | year= 1989 | volume= 140 | issue= 5 | pages= 1438-41 | pmid=2817609 | doi=10.1164/ajrccm/140.5.1438 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2817609 }} </ref> In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax . | ||
===Lung biopsy=== | ===Lung biopsy=== | ||
*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 <ref name="pmid4352308">{{cite journal| author=Hoffmann EO, Lamberty J, Pizzolato P, Coover J| title=The ultrastructure of acute silicosis. | journal=Arch Pathol | year= 1973 | volume= 96 | issue= 2 | pages= 104-7 | pmid=4352308 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4352308 }} </ref>. 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<ref name="pmid5775743">{{cite journal| author=Buechner HA, Ansari A| title=Acute silico-proteinosis. A new pathologic variant of acute silicosis in sandblasters, characterized by histologic features resembling alveolar proteinosis. | journal=Dis Chest | year= 1969 | volume= 55 | issue= 4 | pages= 274-8 | pmid=5775743 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5775743 | *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 [[periodic acid-Schiff|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 <ref name="pmid4352308">{{cite journal| author=Hoffmann EO, Lamberty J, Pizzolato P, Coover J| title=The ultrastructure of acute silicosis. | journal=Arch Pathol | year= 1973 | volume= 96 | issue= 2 | pages= 104-7 | pmid=4352308 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4352308 }} </ref>. 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<ref name="pmid5775743">{{cite journal| author=Buechner HA, Ansari A| title=Acute silico-proteinosis. A new pathologic variant of acute silicosis in sandblasters, characterized by histologic features resembling alveolar proteinosis. | journal=Dis Chest | year= 1969 | volume= 55 | issue= 4 | pages= 274-8 | pmid=5775743 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5775743 }} </ref> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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Overview
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.
- PMF is associated with the worst pulmonary function abnormalities, including decreased compliance, decreased FEV1 and FEV1/FVC ratio, and decreased diffusing capacity for carbon monoxide (DLCO) [1][2]. Pulmonary function, on average, worsens in association with worsening radiographic abnormalities of chronic or accelerated silicosis; cigarette smoking is often contributory[3].
Spirometry
- Spirometry is performed for the evaluation of possible functional lung deterioration[4][5]
- Spirometry shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio [1]
- 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.[6]
Bronchoscopy
- 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 [7] In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax .
Lung biopsy
- 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 [8]. 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[9]
References
- ↑ 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.