Silicosis laboratory findings
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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. When chronic silicosis is suspected due to the onset of respiratory symptoms (eg, dyspnea, productive cough) or typical chest imaging findings, the evaluation is aimed at confirming the exposure history, assessing the degree of respiratory impairment, and excluding other causes. A careful occupational history is essential, as described above. (See 'Silica in the work environment' above.)
Laboratory testing — There are no laboratory tests for the diagnosis of chronic silicosis. As mycobacterial infection is often in the differential diagnosis or may develop as a complication, testing for latent tuberculosis via skin test or interferon release assay is often obtained. In addition, sputum smear and culture for mycobacteria are obtained in the presence of fever, weight loss, hemoptysis, or complicated silicosis on radiographic imaging.
●High resolution computed tomography – HRCT is usually not necessary in simple silicosis unless atypical clinical or radiographic features are noted (eg, fever, spiculated nodules, a single nodule of substantially larger size than the others). However, HRCT has been shown to improve sensitivity and significantly reduce inter-reader variability compared to conventional radiography [74,75]. The typical HRCT findings in simple silicosis are bilateral, symmetric, centrilobular, and perilymphatic nodules with sharp margination (image 5). These nodules calcify in 10 to 20 percent of patients.
HRCT is superior to conventional chest radiography for documentation of conglomerate lesions and emphysematous changes associated with complicated silicosis (image 6) [68-71,76-78]. (See "High resolution computed tomography of the lungs".)
Although pleural effusions are unusual, pleural thickening appears to be common, especially among patients with more severe disease. In a series of 110 patients with biopsy proven silicosis followed for a mean of 14 years, pleural effusions were noted in 12 patients (11 percent), but pleural thickening was present in 64 patients (58 percent) [79].
●FDG-PET scan – Fluorine-18-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) scans are often used to differentiate benign from malignant lung lesions. However, FDG-PET is often positive in PMF in the absence of malignancy or infection. The uptake of PMF lesions on FDG-PET scans was evaluated in a series of nine patients with 14 masses, ranging in size from 1.2 to 6.4 cm in maximum diameter [80]. The maximal standard uptake value (SUV) ranged from 3.1 to 14.6 and mean SUV ranged from 1.4 to 8.5. An SUV exceeding 2.5 is generally considered highly suggestive of malignancy or active inflammation. (See "Computed tomographic and positron emission tomographic scanning of pulmonary nodules", section on 'Positron emission tomography (PET)'.)
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'.)