Macklin and Macklin qa^ 



technically as "compensatory emphysema."* In this condition the individual 

 air spaces are overdistended; and this means that the bases of alveoli lying 

 against connective tissue, particularly that of the sheaths of the blood vessels, 

 as we have seen, are strained and may become ruptured, allowing air to leak 

 into the interstitium. Factor "A," with its downgradient from alveolus to 

 vascular sheath, is then operative. 



Atelectasis— It is, then, quite possible for PIE to originate in any local, or 

 alveolar, emphysematous area; and this brings strongly to the fore the im- 

 portance of atelectasis as an initiatory cause of PIE. Atelectasis, as is well 

 known, is found under a variety of conditions, but obstruction of the bronchus 

 supplying the atelectatic region is a generally recognized immediate cause. 

 An obstruction can arise suddenly, as by impaction of a foreign body in the 

 bronchus; or gradually, in the course of disease, as in bronchopneumonia, 

 when it results from inflammatory tumefaction and exudate. The last type 

 is usually multiple in locale. Thus, atelectasis may be in one or many regions 

 of the lung: it may involve a large area of lung substance or a small one. We 

 feel that, if all human PIE cases could be searched through to their origin, it 

 would be found that atelectasis, by inducing compensatory alveolar emphy- 

 sema, is at the bottom of many, if not most, of them. 



Contrihiitory Causes— Now it is, perhaps, too much to say that all cases of 

 local overstrain of the air container are followed by PIE, even in minute 

 degree, and it would seem that something more than simple alveolar ectasia 

 is usually necessary to induce a leakage of air into the interstitium. It is prob- 

 able that the strain upon the alveolar bases is severe when the extent of the 

 stretching is great, and particularly when it is accompanied by elevation of 

 pressure, as in coughing and intense muscular effort. Where there is inflam- 

 mation the alveolar bases may be presumed to be weakened from this state, 

 and so may be more easily ruptured. In some individuals the bases are ap- 

 parently naturally weaker, and so confer a predisposition to what may be 

 termed "idiopathic" PIE. Then, too, Factor "B" must be kept in mind. It 

 operates when, for any reason, the volume of blood in the pulmonary vessels 

 is reduced, for then the internal buttress of the vascular sheath gives way, 

 creating a further downward gradient from alveolus to sheath. It seems quite 

 likely that if these vessels are overswollen the tendency to PIE resulting from 

 alveolar ectasia may be warded off. Such a protection may be operating when, 

 for instance, a lobe, or even one entire lung, is removed, for then the blood 

 vessels of the remaining parts are carrying not only their own quota of blood 

 but that from the parts which have been removed, and are thus engorged. 

 Augmented in size in this way they encroach upon the space of their surround- 

 ing sheaths and so tend to make up for the out^vard pull of the surroimding 



* It is unfortunate that pathologists and chnicians use the same term, "emphysema," for 

 two different entities: (i) alveolar ectasia and (2) interstitial emphysema. Emphysema means 

 to blow up or inflate. By using qualifying adjectives and speaking of "alveolar" emphysema 

 on the one hand and "interstitial" emphysema on the other, \\c can do nuuh to avoid 

 confusion. 



