– A chronic obstructive pulmonary disorder characterized by permanent anatomic alteration of the airway spaces distal to the conducting airways.
Causes and Incidence
Any factor that leads to chronic alveolar inflammation can serve as a precursor for the formation of emphysematous lesions. Common precursors are tobacco smoking; air pollution, particularly in an occupational setting; underlying respiratory disease; and severe respiratory infection in early childhood. A rare congenital alpha1-antitrypsin deficiency also is a precursor. Emphysema is the leading cause of death from respiratory disease in the United States. The incidence increases with age and is highest in white, male, blue-collar workers.
Recurrent alveolar inflammation leads to degradation of the elastin in the distal airways because of an imbalance in the elastase-antielastase mechanism. As the degradation proceeds, elastic recoil is lost, the alveolar walls are destroyed, blood vessel density is reduced, the air spaces enlarge, and the peripheral bronchioles collapse; this leads to air trapping and impaired gas exchange.
Emphysema is thought to begin in early adulthood and remain asymptomatic until middle age. Gradual progressive exertional dyspnea is the most common presenting complaint. Chronic productive coughing, wheezing, recurrent respiratory infection, and fatigue may also be present. Severe dyspnea and cyanosis are late signs.
Alveolar blebs and bullae may form and rupture, leading to pneumothorax. Cor pulmonale and heart failure may also occur.
History of smoking, occupational exposure
Normal in early disease; localized radiolucency with decreased vascular markings
Total lung capacity, residual volume, functional residual capacity, increased compliance; decreased forced vital capacity and forced expiratory volume
Arterial blood gases
Decreased PaO2; normal PaCO2 until late in disease, when it increases
Bronchodilators to promote mucus clearance; antiinfective drugs to treat secondary bacterial infection; flu and pneumonia vaccines for prophylaxis; antitrypsin replacement therapy for individuals with demonstrated deficiency (experimental).
Removal of irritants; chest physiotherapy, vaporizer to loosen secretions; lowlevel oxygen to treat hypoxemia, with careful monitoring of blood gases for rise in PaO2 without rise in PaCO2; consistent exercise to improve ventilatory and cardiac function; counseling for depressive episodes.