^62 Pulmonic Interstitial Emphysema 



arteries and veins. Ruptures may also occur in the paraseptal and subpleural 

 alveolar bases, but have never been found in those around the airway. Various 

 features of these ruptures have been discussed. Atelectasis, by inducing com- 

 pensatory alveolar ectasia, predisposes to air leakage. Interalveolar pores tend 

 to prevent atelectasis by allowing air to diffuse into threatened parts whose 

 bronchus is plugged, and also to minimize the degree of stretching of the af- 

 fected alveolar bases by widening the areas of periatelectatic alveolar ectasia, 

 and so appear to have some influence, though often ineffective, in warding 

 off PIE. 



Once these multiple minute rupture openings have been made, the likeli- 

 hood is that air will continue to leak into the pulmonic interstitium. The 

 bubbles become larger through coalescence, and most of them move on to the 

 mediastinum, but some remain in various parts of the connective tissue where 

 they interfere with normal lung movements. The conception of the opening 

 and closing action of the extensible pulmonary broncho-vascular "framework" 

 or "skeleton," essential to lung inflation and deflation, enables us to see how, 

 when this action is interdicted by filling of the interstitium with air bubbles, 

 the lung is splinted or locked. Until this happens, the lengthening, and espe- 

 cially the shortening, movements of the broncho-vascular rays may assist in 

 the migration of the bubbles, which are impelled by more recently invading 

 bubbles continuing to be driven through the ruptures by augmented pressure 

 heads in the affected alveoli, as in coughing. The pulmonic connective tissue 

 is seen as a funnel that gathers in air bubbles from the periphery and leads 

 them to the root, from which they debouch into the mediastinum. The his- 

 tological character of the connective tissue explains the preferred courses of 

 the air burrows. A most serious blocking of the pulmonary arteries and veins, 

 by impingement of air bubbles in their sheaths, is indicated in microscopic 

 sections made by approved methods. 



Pneumomediastinum, or mediastinal emphysema, is a direct consequence 

 of PIE. The biomechanics of pressure elevation beyond that of the atmosphere 

 are considered, and emphasis is laid on the pernicious effect of the air bubbles 

 here on the circulatory mechanism. The syndrome may simulate that of 

 angina pectorit.. The aerogenous escape channels are traced, through which 

 pneumatization of the subcutaneous tissues of the neck, head, upper extremity 

 and chest, the opposite lung, and the pleural cavity is effected. The panemphy- 

 sema field has been surveyed. It is noted that in this air canalization the 

 vascular sheaths are followed by preference not only in the lung, but also in 

 the mediastinum and adnexa, the hiatus aorticus being freely used by air in- 

 vading the abdomen. In all of this, a knowledge of the anatomy of working 

 parts is invaluable. The pool of air in the anterior mediastinum gathers from 

 increments following lines of least resistance from the posterior mediastinum. 

 The selection of these lines, traversing the loose connective tissue between the 

 parietal layers of the pleura and pericardium, is explained by the embryology 

 of the parts. This precordial pool is of particular importance clinically for 



