Macklin and Macklin ^gg 



when, for any reason, the normal volume of blood is not received from the 

 right ventricle) without there being an equivalent narrowing of the alveolar 

 envelope. These leakage-favoring factors are spoken of, respectively, as "A" 

 and "B." When they act together there is even more tendency for air to leak 

 into the vascular sheaths than when either is actino: alone. 



Much could be said as to the efficiency of the lung as an air container, and 

 the safeguards against leakage of air into the pulmonic connective tissues 

 usually obtaining, but this is not the place to say it. The air holder is not always 

 impervious. We admit, too, that air may break out from the lung at other 

 points than the perivascular alveolar bases, under abnormal conditions, as into 

 the interlobular septa, or even through the pleura. We feel confident, how- 

 ever, that the perivascular zone is an important one from the point of view 

 of leakage of air and are convinced that a knowledge of the functional anatomy 

 of these parts has done much to explain the mode of origin of PIE. From the 

 \ascular sheaths the air can spread into the other parts of the lung connective 

 tissue. It is through pressure upon the blood vessels by air bubbles, and through 

 interference by air incarcerated in the connective tissues with the ventilational 

 action of the lungs that PIE exerts its damaging influence on the vital func- 

 tions of circtdation and respiration. 



Human Pulmonic Interstitial Emphysema, Pneumomediastinum^ Etc. 



This is just what happens in the human subject when air, in damaging quan- 

 tity, enters the interstitial tissue of the lung. It is an "accident" of surprisingly 

 frequent occurrence, and is found under a wide variety of clinical conditions. 

 The initial step, pulmonary interstitial emphysema, is seldom recognized 

 clinically, and not always at autopsy. Even emphysema of the mediastinum, 

 the next point of invasion by the air, is only now beginning to be diagnosed 

 clinically with any degree of frequency.""" The further extension of air into 

 the subcutaneous tissues of the neck, face, chest, etc., has been recognized, of 

 course, although the source of the air has not been well understood. It has 

 usually been thought to be a laceration in the mucosa of the upper airway, in 

 those cases in which intratracheal anesthesia has been used or in which some 

 instrument has been introduced into the trachea. Unexplained entry of air 

 into the pleural cavities has long been known as "spontaneous" or "idiopathic" 

 pneumothorax, although here, again, the source and rotue of the air have not 

 been correctly visualized in the majority of instances. Spontaneous pneumo- 

 thorax has often been regarded as arising through rupture of subpleural 

 blebs," the origin of which has been variously interpreted, rather than as oc- 

 curring from the rupture of an air-distended mediastinum" which has received 

 its air by extension from a PIE. Berkley and Coffen,'" however, recognized 

 that subcutaneous emphysema and pneumothorax, arising in patients •with 

 influenza, had a common source of origin, namely air in the mediastinum. 

 Pneumoretroperitoneum has been looked upon as due to the extension of air 

 from the mediastinum, although PIE as the origin of the mediastinal air has 



