A study of the pathology and pathogenesis of bronchiectasis.

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230F. WHITWELLFIG. 29.-Saccules surrounded by rims of compression collapse (CasHaematoxylin and eosin x 7.5.monary tuberculosis; Willis's statement cannottherefore be accepted.THE PRE-SACCULAR BRONCHI.-NO dilatationoccurs in the bronchi and there is little destructionof supporting tissues, despite the severe inflammatoryreaction in the bronchial walls. The mainabnormality is polyposis of the bronchial epithelium,often extensive enough to produce considerablebronchial obstruction.In the present material this change has been seenonly in saccular bronchiectasis, but similar lesionsare to be found in the bronchi draining chroniclung abscesses and secondarily infected tuberculouscavities.The bronchoscopic and histological features ofthis polypoid change have been described byJackson and Jackson (1932), who thought that itwas an inflammatory reaction produced by continualirritation from pus, an opinion supported bythe present study. Peroni (1934) considered thatthe polyps occurred first, and then producedbronchiectasis by obstruction. Samsonj (1940) described a severe case and thought2 the cause was an individual susceptibilityto mucin. Many accounts of the pathologyof bronchiectasis mention the hypertrophicbronchial epithelium, but the site andassociation with saccules have not beenstressed.COLLATERAL AIR CIRCULATION IN. DISEASED SEGMENTS.-Tfle observation thatall bronchi in the diseased segments end inblind saccules, and that these segmentsare well aerated, is considered to be ofsome importance. It provides histologicalconfirnation of the existence of a collateralair circulation in bronchiectasis, whichchallenges the validity of certain populartheories of pathogenesis.i Hf Collateral air circulation was originallya theoretical conception based upon a* belief in the existence of alveolar pores.it, Later this theory was tested and confirmedby animal experiments (Van Allen andJung, 1931), and more recently by Baarsmaand Dirken (1948) using healthy rabbits,and by Baarsma, Dirken, and Huizinga(1948) in normal human lungs. Theseworkers considered that a collateral aircirculation occurred only in the absence ofinflammatory change in the obstructedsegments.;e 451). The importance of this mechanism indiseased lungs has only recently receivedany attention. Churchill (1949), describing theradiological appearances of isolated bronchiectaticlobes in which the bronchi had been filled withlipiodol, mentioned dilated bronchi extending intoair-containing parenchyma but in no way communicatingwith it. These segments contained trappedair, as they did not deflate when the lobes wereremoved from the body and left the bronchi open.This trapped air serves the function of filling upspace but it has no oxygenating value.In the two examples of saccular bronchiectasisthe air must have reached the basal parenchymathrough the normal apical segments. This suggeststhat the intersegmental and interlobular fibroussepta are really incomplete fibrous networks whichoffer no barrier to air. Alveolar pores have beenseen in the aerated alveoli of most specimenswhenever sought in thick sections (Fig. 31).Although collateral air circulation is most easilydemonstrated in the saccular cases, it occurs inmost forms of bronchiectasis which do not involveentire lobes.
PATHOLOGY AND PATHOGENESIS OF BRONCHIECTASIS 231CLINICAL FEATURES OF SACCULAR BRONCHIECTASISThe age distribution of all these patients is shownin Fig. 4. Sixteen case-records were available for \\NORMAL APICALSE\.analysis, and the details are tabulated.XAGE AT OFERATIONUnder 5 yrs. 0 patients 'il15 0yrs. 5 ,\_26-30yrs.7., 21-25yrs.52| 1 9 $ 9 ''_31 35 Nrs.. . I36-40yrs.I patientOver 40 yrs.AGE AT ONSET OF SYMPTOMS ORMAL BASAL SEGACough " all life time "...patientsUnder 9 vrs. (except above) 09-12yrs .. .. I patient13-18 yrs. .. 6 patients19-25yrs...Over 25 yrs. ..I patientPRE-OPERATIVE DURATION OF SYMPTOMSUnder 2 yrs.3 patien is2-6yrs. 87l1O0 rs. 211-15yrs.Ipatient16 20yrs. IOver 20yrs.INATURE OF ILLNESS AT ONSET-OF SYMPTOMS )'Measles and, or whooping cough0 patientsBronchopneumonia .. 9Fairly recent insidious onset 4 -I'Cough all life but no severe childhoodillnesses.3FINGER CLtJBBINGPresent.10 patients FIG. 30.-Development of collateral air circulation in saccularDoubtful 2 ,. bronchiectasis.Absent. 2Not recorded.2 All patients had copious purulent sputum.PARANASAL SINUS INFECTIONS No correlation was found between the extent,Present*9 patients severity, and duration of the disease, and theDoubtful .. 2Absent .. 3 " presence of finger clubbing.Not recorded .. 2It is impossible to correlate theulj|jdegree A of polyposis and squamousmetaplasia to the duration of illness.PATHOGENESIS OF SACCULARBRONCHIECTASISAs the changes in pre-saccularbronchi are considered secondaryto the saccular lesions any discussionon pathogenesis amount,tothe question, "From what and howdo the saccules arise?""SrrE OF THE SACCULES. -Writershave variously suggested that theW iw dilatations ^ w of bronchiectasis originatefrom the bronchi (Robinson,1933; Ogilvie, 1941; Mallory, 1947),the bronchioles (Lander and Davidson,1938), and the parenchyma(Opie, 1928; Erb, 1933; McNeil,~ _ 4 R Macgregor, and Alexander, 1929;IFIG. 31.-Alveolar pores seen in thick sections. Elastic stain with pyronin x 600. Lisa and Rosenblatt, 1943).
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A study of the pathology and pathogenesis of bronchiectasis.

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