360 Pulmonic Interstitial Emphysema 



is concerned, are functional on only one side. It is these "one-sided," "non- 

 partitional," "sessile," or "marginal" bases that concern us, for air, in break- 

 ing through them, passes, not innocuously into neighboring alveoli, but 

 dangerously into the underlying connective tissue. 



The nature of the lining of the alveoli has long been a moot problem, and 

 it is important for us here, for it is in this lining that the rupture openings 

 occur. A basic layer of fibers and ground substance is admitted by all. One 

 modern view^ recognizes in the lining a few surviving epithelial cells or "epi- 

 cytes" in the capillary meshes, but in ordinary histological sections no epi- 

 thelium is visible on the "bare areas" which make up most of the total area 

 of the alveolar wall and which overlie the capillaries. Both epicytes and bare 

 areas have been marked out by silver lines, the former more clearly. The final 

 point at issue is the nature of the air-protoplasmic interface in these bare areas. 

 There are some who hold that it is a thin, ordinarily invisible derivative or 

 extension from epithelium; and there are others who think that it is a speciali- 

 zation of mesoderm. It is through this thin film that diffusion of oxygen and 

 carbon dioxide takes place, so that it may be regarded as a vital tissue. It seems 

 to be through this film that minute bubbles of air pass into the capillaries to 

 form emboli when the intra-alveolar pressure is too high. Ordinarily, of course, 

 no leakage of air occurs in it. More work is needed as to the exact situation, 

 in the marginal alveolar bases, of the rupture sites through which minute air 

 freshets pass to cause PIE. It is clear that, if such a base be abnormally spread 

 out, then the fibers of connective tissue in it are separated and the ground 

 substance thinned so that it will be weakened and may become air-pervious. 

 These bases are not built to stand air pressures much above that of the atmos- 

 phere. More experimental work needs to be done on pressures required to 

 rupture these bases in the different laboratory animals. The breaking strain 

 seems to be less in young children than in adult human subjects. In the experi- 

 ments the break-through made itself apparent suddenly, as though many alveo- 

 lar ruptures had occurred simultaneously; we are dealing with Factor "B" 

 here, as well as Factor "A." Once the ruptures are formed the air continues 

 to leak into the connective tissue through them and increase the PIE. When 

 the intra-alveolar pressure is high the capillaries of the base may apparently 



become torn. 



Prevention, Diagnosis, and Treatment 



At first blush it would seem futile to seek to prevent PIE, for it arises so fre- 

 quently under natural circumstances; but a survey of possibilities indicates 

 that something can be done. As with any other ailment, we should try to re- 

 move the causes. The artificially induced overstrain cases would seem pre- 

 ventible, and the avoidance of overly high intra-alveolar pressures, for instance 

 in intratracheal anesthesia and artificial respiration, will suggest itself. The 

 dangers underlying the various predisposing activities, such as heavy lifting, 

 straining at stool, and violent and continuous coughing, should be pointed out 

 to patients by clinicians wherever possible, particularly if there is a history 



