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Asbestosis is a form of pneumoconiosis characterized by diffuse interstitial fibrosis. It can develop as long as 15 to 20 years after regular exposure to asbestos has ended. Asbestos also causes pleural plaques and mesotheliomas of pleura and the peritoneum. A potent co-carcinogen, asbestos increases the risk of lung cancer in cigarette smokers.
Causes and incidence
Asbestosis results from the inhalation of respirable asbestos fibers (50 microns or more in length and 0.5 microns or less in diameter), which assume a longitudinal orientation in the airway and move in the direction of airflow. The fibers penetrate respiratory bronchioles and alveolar walls. Sources include the mining and milling of asbestos, the construction industry, and the fireproofing and textile industries. Asbestos was also used in the production of paints, plastics, and brake and clutch linings.
Asbestos-related diseases develop in families of asbestos workers as a result of exposure to fibrous dust shaken off workers’clothing at home. Such diseases develop in the general public as a result of exposure to fibrous dust or waste piles from nearby asbestos plants, but exposures for occupants of typical buildings are quite low and not in a range associated with asbestosis.
Inhaled fibers become encased in a brown, proteinlike sheath rich in iron (ferruginous bodies or asbestos bodies), found in sputum and lung tissue. Interstitial fibrosis develops in lower lung zones, causing obliterative changes in lung parenchyma and pleurae. Raised hyaline plaques may form in parietal pleura, diaphragm, and pleura contiguous with the pericardium.
Asbestosis occurs in 4 of every 10,000 people.
Signs and symptoms
Clinical features may appear before chest X-ray changes. The first symptom is usually dyspnea on exertion, typically after 10 years’exposure. As fibrosis extends, dyspnea on exertion increases until, eventually, dyspnea occurs even at rest. Advanced disease also causes a dry cough (may be productive in smokers), chest pain (commonly pleuritic), recurrent respiratory infections, and tachypnea.
Cardiovascular complications include pulmonary hypertension, right ventricular hypertrophy, and cor pulmonale. Finger clubbing commonly occurs.
Diagnosis
The patient history reveals occupational, family, or neighborhood exposure to asbestos fibers. Physical examination reveals characteristic dry crackles at lung bases. Chest X-rays show fine, irregular, and linear diffuse infiltrates; extensive fibrosis results in a “honeycomb” or “ground-glass” appearance. X-rays may also show pleural thickening and calcification, with bilateral obliteration of costophrenic angles. In later stages, an enlarged heart with a classic “shaggy” heart border may be evident. Computed tomography scan of the lungs also aids in diagnosis.
Pulmonary function tests show:
❑ Vital capacity, forced vita capacity, and total lung capacity — decreased
❑ Forced expiratory volume in 1 second — decreased or normal
❑ Carbon monoxide diffusing capacity — reduced when fibrosis destroys alveolar walls and thickens alveolocapillary membranes.
Arterial blood gas analysis reveals:
❑ Partial pressure of arterial oxygen — decreased
❑ Partial pressure of arterial carbon dioxide — low due to hyperventilation.
Treatment
The goal of treatment is to relieve respiratory symptoms and, in advanced disease, manage hypoxemia and cor pulmonale. Respiratory symptoms may be relieved by chest physiotherapy techniques, such as controlled coughing and segmental bronchial drainage, chest percussion, and vibration. Aerosol therapy, inhaled mucolytics, and increased fluid intake (at least 3 qt [3 L] daily) may also relieve symptoms.
Diuretics, cardiac glycosides, and salt restriction may be indicated for patients with cor pulmonale. Hypoxemia requires oxygen administration by cannula or mask (1 to 2 L/minute) or by mechanical ventilation if arterial oxygen can’t be maintained above 40 mm Hg. Respiratory infections require prompt administration of antibiotics.
Special considerations
❑ Teach the patient to prevent infections by avoiding crowds and persons with infections and by receiving influenza and pneumococcal vaccines.
❑ Improve the patient’s ventilatory efficiency by encouraging physical reconditioning, energy conservation in daily activities, and relaxation techniques.
Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
