Silicosis CT

Jump to navigation Jump to search

Silicosis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Silicosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Chest X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Silicosis CT On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Silicosis CT

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Silicosis CT

CDC on Silicosis CT

Silicosis CT in the news

Blogs on Silicosis CT

Directions to Hospitals Treating Silicosis

Risk calculators and risk factors for Silicosis CT

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

CT

A CT scan can also provide a mode detailed analyses of the nodules, and can reveal cavitation due to concomitant mycobacterial infection. However, 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)[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] 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].

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].

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'.)

References

Template:WH Template:WS