Silicosis laboratory findings: Difference between revisions
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There are no laboratory tests for the diagnosis of acute silicoproteinosis. However, a complete blood count and differential, brain natriuretic peptide, granulocyte macrophage-colony stimulating factor (GM-CSF) antibodies, and cultures of blood and sputum are helpful in excluding processes in the differential diagnosis. | |||
Assessment of oxygenation is important, either with pulse oxygen saturation or arterial blood gas, to determine the severity of respiratory impairment and whether the patient will be able to tolerate diagnostic procedures. | |||
The HRCT findings consist of numerous bilateral centrilobular nodular opacities, focal ground glass opacities, and patchy areas of consolidation [54]. In a small series that compared pulmonary alveolar proteinosis (PAP) and acute silicosis, the most common HRCT finding in PAP was “crazy paving”, while the most common finding in acute silicosis was dependent consolidation and nodular calcification [55]. (See "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults".) | |||
Hilar lymph node enlargement may be apparent on HRCT, which is a typical feature of silicosis, but not of PAP [53]. In a series of 13 patients, calcified lymph nodes were noted on HRCT in 11 (85 percent) [54]. (See "Imaging of occupational lung diseases", section on 'Silicosis'.) | |||
Bronchoalveolar lavage — When acute silicosis is suspected, bronchoalveolar lavage (BAL) is used to exclude infection, eosinophilic pneumonia, and alveolar hemorrhage. 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 [56]. (See "Basic principles and technique of bronchoalveolar lavage" and "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults", section on 'Bronchoalveolar lavage'.) | |||
Histopathology — 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]. (See "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults".) | |||
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'.) | |||
==References== | ==References== | ||
Revision as of 12:53, 19 June 2015
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There are no laboratory tests for the diagnosis of acute silicoproteinosis. However, a complete blood count and differential, brain natriuretic peptide, granulocyte macrophage-colony stimulating factor (GM-CSF) antibodies, and cultures of blood and sputum are helpful in excluding processes in the differential diagnosis.
Assessment of oxygenation is important, either with pulse oxygen saturation or arterial blood gas, to determine the severity of respiratory impairment and whether the patient will be able to tolerate diagnostic procedures.
The HRCT findings consist of numerous bilateral centrilobular nodular opacities, focal ground glass opacities, and patchy areas of consolidation [54]. In a small series that compared pulmonary alveolar proteinosis (PAP) and acute silicosis, the most common HRCT finding in PAP was “crazy paving”, while the most common finding in acute silicosis was dependent consolidation and nodular calcification [55]. (See "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults".)
Hilar lymph node enlargement may be apparent on HRCT, which is a typical feature of silicosis, but not of PAP [53]. In a series of 13 patients, calcified lymph nodes were noted on HRCT in 11 (85 percent) [54]. (See "Imaging of occupational lung diseases", section on 'Silicosis'.)
Bronchoalveolar lavage — When acute silicosis is suspected, bronchoalveolar lavage (BAL) is used to exclude infection, eosinophilic pneumonia, and alveolar hemorrhage. 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 [56]. (See "Basic principles and technique of bronchoalveolar lavage" and "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults", section on 'Bronchoalveolar lavage'.)
Histopathology — 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]. (See "Clinical manifestations and etiology of pulmonary alveolar proteinosis in adults".)
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'.)