Silicosis other diagnostic studies
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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. Spirometry is performed for the evaluation of possible functional lung deterioration[1][2]
- Spirometry shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio [61]
- Diffusion capacity is affected in the complicated forms of the disease and is sensitive to the presence of fibrosis.14
- Static lung volumes can demonstrate a reduction in total lung volume .
- 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 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.
- 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) [61,68]. Pulmonary function, on average, worsens in association with worsening radiographic abnormalities of chronic or accelerated silicosis; cigarette smoking is often contributory [67].In a number of studies using chest CT scan to evaluate lung parenchyma in chronic or accelerated silicosis, lung function abnormalities correlated better with the emphysematous changes of silicosis than the nodular changes of silicosis [69-71].
Bronchoscopy — Flexible bronchoscopy has a limited diagnostic role in chronic silicosis, and, for most patients, bronchoscopy to confirm the diagnosis is not indicated. However, bronchoscopic washings, brushing, or bronchoalveolar lavage may be used to obtain samples for microbiologic studies and cytology when infection and/or malignancy are in the differential diagnosis based on the imaging results. In general, transbronchial biopsy is avoided in chronic silicosis due to the presumed risk for pneumothorax and the small sample size.
Diagnosis — The diagnosis of acute silicosis is based upon the history of an acute, high dose silica exposure, imaging findings of diffuse nodular and patchy consolidative opacities, a milky, lipoproteinaceous bronchoalveolar lavage effluent, and exclusion of other potential explanations (infection, pulmonary edema, alveolar hemorrhage, eosinophilic pneumonia, primary pulmonary alveolar proteinosis). A lung biopsy is not necessary in the setting of a definite exposure history and these characteristic findings.
Once lipoproteinaceous fluid has been obtained by BAL or observed on biopsy, other causes of alveolar proteinosis or lipidosis are usually identified by history of inhalational exposure (eg, titanium, indium-tin oxide, or aluminum), testing for GM-CSF antibodies, lipid-laden macrophages in bronchoalveolar lavage fluid (suggest lipoid pneumonia), stains and/or cultures obtained from bronchoscopy (eg, Pneumocystis jirovecii or Nocardia), or presence of leukemic cells in the peripheral blood. (See "Diagnosis and treatment of pulmonary alveolar proteinosis in adults", section on 'Evaluation and diagnosis' and "Clinical presentation and diagnosis of Pneumocystis pulmonary infection in HIV-infected patients", section on 'Bronchoalveolar lavage' and "Clinical manifestations and diagnosis of nocardiosis" and "Aspiration pneumonia in adults", section on 'Lipoid pneumonia'.)
- 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 [3] In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax .
- Lung biopsy — 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 [57]. 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 (picture 1) [44]
References
- ↑ 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.
- ↑ 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.