A study of the pathology and pathogenesis of bronchiectasis.

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232F. WHlTWELLNeoprene casts, reconstruction models, anddissections of the bronchial tree show that sacculesare the bulbous terminations of the first to thirdbranchings of the segmental bronchi. As adultbronchioles arise only after about 18 branchingsfrom the segmental bronchi (Broman, 1923; Reid,1950). the saccules clearly cannot be of bronchiolarorigin.Saccules are the direct continuations of largebronchi, they are encased within extension of'theperibronchial fibrous septa, and they are placedclose to and parallel with branches of pulmonaryarteries. Their situation suggests that they wereoriginally bronch:, and not bronchopulmonaryexcavations.CAUSE OF DILATATION. First, it is possible toeliminate certain of the factors that are oftensuggested as causes of dilatation. Alveolar collapseis negligible in these specimens and cannot beconsidered as a possible cause, in spite of absoluteperipheral bronchial obstruction. Fibrous tissuefound in the saccular walls occurs only as a replacementof original bronchial structures. This fibrosisis concentric with the saccules, and not in a planewhere, by contracting, it could exert any dilatingforce on the bronchi. Most writers link togetherfibrosis and contraction, especially when discussingbronchiectasis. However, the behaviour of fibroustissue is perverse, and many examnples occur of itsproperty of ungoverned stretching, e.g., aorticaneurysms and in repaired hernias. Probably thestretching of fibrous tissue in saccular walls is afactor in the production of dilatation.The clinical findings of this group of patientsshow that while in many cases the bronchiectasisdated from an attack of bronchopneumonia, innearly half the patients the disease had an insidiousonset which escaped notice.It is considered that saccular bronchiectasisbegins as a chronic mural inflammation of themedium-sized bronchi. This condition destroysbronchial wall structures and obliterates peripheralbranches (Fig. 30), but is not sufficiently acute ordiffuse to produce parenchymal scarring or tointerfere with the establishment of a collateral air.circulation, provided all segments of a lobe arenot affected.The saccular shape of the diseased brolnchi isprobably produced after the destruction of supportingtissues and occlusion of peripheral branches,and results from distension by contained pus, thepressure of which is increased by the partial occlusionof pre-saccular bronchi (see Fig. 28). Support islent to this theory by the compression-collapseseen in several specimens in perisaccular alveoli(Fig. 29) suggesting that an expansile force iscentred within the saccules.The theory that dilatation is produced throughdistension of the bronchi by pus was originally putforward by Laennec, but only a few (Riviere, 1905)have shared his opinion. As early as 1838 Williamsdiscredited Laennec's theory by arguing that mostpatients with copious sputum do not developdilatation, and many patients with bronchiectasishave little sputum. Williams's argument was falsebecause it did not take into account the conditionof the bronchial walls. Andrus (1937) discussedthis subject and said:" As a problem in physics it is sufficient to noteat this time that in order to exert a dilating force itwould be necessary that the secretion occupy the grosssection of the lumen of the bronchus; such a conditionwould, however, necessarily result in atelectasis,and its possible effects be indistinguishable from thelatter."His theoretical aerodynamics did not allow forcollateral air circulation, and the illustrated examples.do not support his statement.ATELECTATIC BRONCHIECTASISIn recent years there have been many accountsof the association of lobar and segmental collapsewith bronchiectasis, and it has become widelyaccepted that the collapse leads to the bronchiectasis.In this condition, which has been calledatelectatic bronchiectasis (although it is recognizedto be an acquired disease), the collapse is usuallythought to be caused by peripheral bronchialobstruction. Many writers have gone even furtherand stated that all bronchiectasis, even whencongenital, is caused in this way.The specimens which have here been classifiedas follicular and saccular rarely showed collapse,even on microscopic exa-mination; where collapsewas found it appeared to be consequent to thebronchiectasis. However, some others of thespecimens did show severe alveolar collapse, sathey have been examined as a group in an attemptto find out whether the collapse or the bronchiectasiscomes first, and how this condition arises.The specimens lack homogeneity; in some thebronchi are collapsed, in others there is grossdilatation, and in most of them the bronchi arethickened but only moderately dilated (Fig. 32).However, the grouping has been of some valuebecause it has shown that " atelectatic bronchiectasis"differs from other forms of the disease inits lobar and segmental distribution, and in the
PATHOLOGY AND PATHOGENESIS OF BRONCHIECTASIS 233r-2L ~ ~~~~~ '.1 ~ ~~~~ S+. 1*2-.X~~~~~~\&"AI~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ J%--4s~'''| ~ 1.4'~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~'- '>.P'w^* wq. -1 f\0ziSl v*) FE p 1-4-0-1M#vi *ffhQ\Bs -#--pqee"4 "'" ~*specimens form only a quarter of the whole series,'they represent three-quarters of the collapsed tspecimens.*Specimens consisting of middle with lower lobes 5 .'-^ . ;>r *-3 ido not always show atelectatic bronchiectasis in FIG. 34.-Atelectatic bronchiectasis with intra-bronchiolarboth lobes. The findings are as follows. and intra-alveolar haemorrhage with patent bronchioles..... -..- I I --.
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A study of the pathology and pathogenesis of bronchiectasis.

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