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Asbestosis Workup

  • Author: Basil Varkey, MD, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Dec 31, 2015
 

Approach Considerations

The diagnosis of asbestosis is based on the following[20] :

  • A reliable and significant (ie, dose x time) history of asbestos exposure and an appropriate latency period between exposure and detection of disease
  • Characteristic changes of pulmonary fibrosis on imaging studies
  • Absence of other fibrotic diseases that mimic asbestosis
  • Dyspnea upon exertion
  • Bilateral basilar inspiratory crackles
  • Restrictive pattern on pulmonary function studies associated with impaired gas exchange

Blood tests for antinuclear antibodies (ANAs), rheumatoid factor, and erythrocyte sedimentation rate lack diagnostic specificity and are not useful in diagnosis or in activity assessment.

A lung scan with gallium citrate (67 Ga) is a nonspecific test that may detect areas of inflammation in the lungs. However, the results do not always correlate with other measurements of inflammation. This test is no longer recommended.

Physicians often make the diagnosis without histopathologic confirmation. Errors may occur because other, more common interstitial diseases (eg, idiopathic pulmonary fibrosis) mimic the clinical, radiologic, and pulmonary functional features of asbestosis. Bear in mind the long latency period that exists between patient exposure and the manifestation of symptoms and signs of asbestosis.

When lung tissue is available for histopathologic examination, confirmation of diagnosis requires both fibrosis and accumulation of fibers or asbestos bodies (ie, ferruginous bodies; these are asbestos fibers that develop a ferritin-protein coat and have a characteristic long-beaded appearance). Asbestos bodies alone are not diagnostic for disease, because occasionally examiners find asbestos bodies in people without known exposure.

Pleural plaques may coexist with asbestosis, but these plaques alone are usually not associated with impaired pulmonary function. Nonetheless, pleural plaques are a reliable indicator of asbestos exposure.

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Radiography

Chest radiographs (ie, posteroanterior and lateral views) are basic and required diagnostic imaging studies. However, the diagnosis of asbestosis requires multiple elements. A chest radiograph alone has only a modest positive predictive value for the condition, but when it is combined with abnormal signs (rales) and pulmonary function test results, the positive predictive value is markedly increased.[21]

Typical findings include diffuse reticulonodular infiltrates, which are observed predominantly at the lung bases. The diffuse lung infiltrates cause the appearance of shaggy heart borders.

In early disease, an increase in interstitial markings, mostly linear, is seen. Honeycombing, with cystic spaces surrounded by coarse interstitial infiltrates and small lung fields, characterizes advanced disease.

Bilateral pleural thickening may be observed. Asbestos-related pleural thickening more often involves the middle third of the pleura as opposed to the upper third, which is affected by tuberculosis, or the lower third, which can be damaged by empyema, trauma, or past pleurodesis therapy. (An oblique-view radiograph may be helpful in recognizing pleura-based abnormalities.)

A calcified pleural plaque located in the diaphragmatic pleura is a reliable indicator of asbestos exposure but is not a required element for the diagnosis of asbestosis. Besides the diaphragmatic pleura, other common sites for plaque formation in the parietal pleura are along the sixth through the ninth ribs. Noncalcified plaques may not be detected on chest radiographs. (See the image below.)

Asbestos pleural plaques. Asbestos pleural plaques.

Rarely, pleural adhesions may cause peripheral atelectasis with a rounded border (rounded atelectasis) that may simulate a lung tumor.[22]

The International Labor Office standardized classification of radiographic abnormalities is useful in grading the extent of disease in asbestosis and in other pneumoconioses.

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CT Scanning

Computed tomography (CT) scanning is useful in the delineation of pleural or pleura-based abnormalities (eg, effusion, thickening, plaque, malignant mesothelioma, rounded atelectasis) and in the delineation of a parenchymal density that is suggestive of bronchogenic carcinoma.[23]

A high-resolution CT (HRCT) scan allows better definition of interstitial infiltrates and may be helpful in diagnosing asbestosis in the early stages.

Typical HRCT findings in asbestosis include subpleural linear opacities seen parallel to the pleura; basilar lung fibrosis and peribronchiolar, intralobular, and interlobular septal fibrosis; honeycombing; and pleural plaques.

In a minority of cases, HRCT abnormalities may be seen in individuals with normal chest radiographic findings.

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Pulmonary Function Test

Diffusing capacity reduction precedes lung volume changes, but findings from a diffusing capacity measurement are not specific. Besides diffusing capacity reduction, the earliest physiologic abnormality is exertional hypoxemia. Total lung capacity is reduced in asbestosis as in other restrictive disorders.

Using spirometry, vital capacity on a pulmonary function test typically appears reduced, without a reduction in the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1 to FVC).

Small-airway flow rates (eg, midexpiratory forced expiratory flow [FEF25-75]) are reduced but are nonspecific for a diagnosis of small-airway obstructive disease.

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Oximetry

The evaluation of oxygenation is important because uncorrected hypoxemia causes pulmonary hypertension and may lead to cor pulmonale.

Physicians can use a noninvasive test of pulse oximetry as a screening test, especially if oximetry is performed during rest and during exercise (eg, 6-minute walk test).

Obtain accurate information through measurement of arterial blood gases, which requires an arterial puncture. In selected cases, an exercise study may demonstrate desaturation during exercise.

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Bronchoalveolar Lavage and Bronchoscopy

Bronchoalveolar lavage

Bronchoalveolar lavage (BAL) has only limited application in the diagnosis and management of asbestosis. BAL is helpful in diagnosing infections that may present with diffuse infiltrates and simulate asbestosis, and the procedure may aid in the diagnosis of a coexisting bronchogenic carcinoma. In workers who are exposed to asbestos, BAL can provide quantitative information through asbestos fiber counts. More than 1 asbestos body (ie, coated asbestos fiber) per milliliter of lavage effluent suggests significant exposure.[7]

Bronchoscopy

Fiberoptic bronchoscopy is performed to facilitate BAL. In addition, bronchoscopy is indicated for airway examination when radiologic studies are suggestive of bronchogenic carcinoma. Transbronchoscopic lung biopsy is not recommended for diagnosis of asbestosis. This procedure yields inadequate tissue and may cause crush alterations to the tissue.

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Histologic Findings

In most cases, physicians diagnose asbestosis without a histopathologic examination of lung tissue. A pathologic diagnosis of asbestosis requires visualization of both fibrosis and asbestos bodies through light microscopy or a significant quantity of asbestos fibers observed through electron microscopy.

The American College of Pathologists' scheme for assessing the severity of asbestosis grades fibrosis in the following 4 categories:

  • Grade 1 - Fibrosis in the wall of a respiratory bronchiole without extension to distant alveoli
  • Grades 2 and 3 - These define more extensive disease
  • Grade 4 - Alveolar and septal fibrosis with spaces larger than alveoli, ranging up to 1cm (ie, honeycombing)

Asbestos bodies (ie, ferruginous bodies) are asbestos fibers that develop a ferritin-protein coat and have a characteristic long-beaded appearance. Asbestos bodies alone are not diagnostic for disease, because occasionally examiners find asbestos bodies in people without known exposure.

Lung biopsy

Open lung biopsy is not indicated in most cases. However, this procedure provides sufficient tissue for the pathologist to make a definitive diagnosis.

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Contributor Information and Disclosures
Author

Basil Varkey, MD, FCCP Professor Emeritus, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital

Basil Varkey, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Coauthor(s)

Anita B Varkey, MD Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center

Anita B Varkey, MD is a member of the following medical societies: American College of Physicians, Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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