So-called hypertrophic emphysema.

Before discussing the pathogenesis and clinical aspects of this disease, clarification of some of the pertinent terminological definitions may be in order. Hypertrophic emphysema is the most commonly used designation of this disease. Also, it is known under the following names: genuine emphysema, idiopathic emphysema, diffuse vesicular emphysema, obstructive emphysema, dystrophlc emphysema, pulmonary hypertrophy, pulmonary dilatation, chronic large lung, and pneumonectasis. Inasmuch as loss of the elastic fibers and more or less extensive destruction of the alveoli are cardinal aspects of this disease, one may designate it as destructive emphysema. Still a more appropriate term, pseudohypertrophic emphysema, may be offered for the nomenclature of this condition. Hypertrophy of the lung in genuine emphysema is far from being similar to muscular hypertrophy of the extremities seen in men engaged in athletics or in occupations which entail heavy physical work. Although in genuine emphysema the lung is larger than normal, there is neither an increase in the number of functionally competent alveoli nor a proportionate augmentation in the number, size and functional capacity of corresponding capillary vessels. During the course of development of genuine emphysema a great many interalveolar septums are destroyed. Consequently, large, cyst-like air spaces appear in the lung. Cyst-like formations of this type are designated as blebs when they are localized subpleurally. The ones localized in other parts of the lung are conventionally referred to as bullae. Concepts vary relative to the pathogenesis of genuine emphysema. I am of the opinion that the following factors are of cardinal importance in this respect: (1) Increased intrapulmonary pressure during strenuous coughing. (2) Infections and other pathologic changes which result in extensive degenerative alterations in the elastic elements of the lung. (3) Partial bronchial occlusion of the check-valve type. Familiarity with the role of each of these items in the pathomechanics of genuine emphysema is helpful in the satisfactory management of this disease. During the compressive phase of cough which is strenuous, the intrapulmonary pressure may be as high as from 80 to 200 mm. of mercury over and above atmospheric pressure. This aerodynamic trauma, when sustained for a prolonged period of time, is likely unduly to stretch and to damage the elastic fibers of the lung. Chronic lung infections may lead to destructive changes in the elastic elements of the lung in two ways: (1) through direct toxic influences; (2) through consequent fibrosis. The latter causes constriction or complete obliteration of some of the nutritional blood vessels. The consequent diminished blood flow exerts an untoward influence upon the implicated lung