Panlobular Emphysema: Anatomy and Pathodynamics

Abstract

Based upon the structural concept of the secondary lobule of Miller, it is apparent that a common anatomic pattern of emphysema involving principally the terminal air ducts and sacs may be recognized on a localized or generalized basis. This form of emphysema we have labelled the panlobular type, as the entire secondary lobule of Miller shows overdistension and air sac rupture, and in advanced cases uniform bullous fields. An accompaniment of advancing degrees of emphysema is the presence of numerous alveolar fenestrations of major importance in the progression of this form of irreversible lung distension. Panlobular emphysema is a morphologic denominator common to such heterogeneous conditions as primary kyphotic chest deformities, localized hilar scleroses or neoplastic states producing laryngeal or large bronchial airway deformities and congenital lobar emphysema. Less well-defined is the airway obstruction in chronic bronchitis and bronchiectasis observed in many cases of established panlobular emphysema. An additional emphysematous group without structural bronchial deformity was also found. These were usually associated with lesser degrees of emphysema. Bronchial disturbances may produce not only an obstructive airway mechanism leading to air trapping, but indirectly influence surface tension phenomena within the lung or impair clearance of entrapped pollutants and in this way initiate erosion of the air sac membranes. Hypertrophy of the right ventricle was a frequent companion of established cases of generalized panlobular emphysema. The air-to-blood exchanging surface—the pulmonary contribution to homeostasis—is progressively destroyed through alveolar sac dissolution with the concurrent loss of the perfusing lung bed being responsible for the common clinical manifestations of cor pulmonale. Other determinants involved in the development of cor pulmonale are pathologic by-passes from artery to vein, bronchopulmonary shunting particularly in emphysema with fibrosis and a decompensating portal azygos-pulmonary vein system. These morphologic findings reflect the primary importance of the pulmonary-cardiac disease in the natural history of this form of emphysema.