A study of the pathology and pathogenesis of bronchiectasis.

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234Middle Lobe Lower Lobe Specimens No. ofCollapse only Atelectatic bronchiectasis 2Atelectatic bronchiectasis Collapse only IAtelectatic bronchiectasis Atelectatic bronchiectasis 3Atelectatic bronchiectasis Saccular bronchiectasis ICollapse only Follicular bronchiectasis 1Atelectatic bronchiectasis Follicular bronchiectasis 1Collapse only Unclassified bronchiectasis IF. WHITWELLSEGMENTAL DISTRIBUTION.-In all segments of anaffected lobe the bronchi show similar histologicalchanges. It is very difficult to assess calibre differencesin collapsed specimens, but usually thedegree of dilatation appeared about equal in eachsegment.BRONCHIAL OBSTRUCTION.-The lobar, bronchihave been examined for stenoses and other lesionsthat might cause bronchial obstruction. None ispresent in lobes showing bronchiectasis, but inspecimens of simple collapse the bronchi are alsocollapsed and therefore obstructed.Sections have been examined microscopically forobstructing lesions of the peripheral bronchial tree.In contrast to follicular and saccular bronchiectasis,in which peripheral obstruction is invariable, thebronchioles are patent and can be followed into thepulmonary lobules, where the air cells are partlycollapsed (Fig. 34).HILAR LYMPH-GLAND CHANGES.- In many specimensthe lymph-glands around the hilar bronchiare greatly enlarged, and on section showed nonspecificchronic lymphadenitis, often with fibroticchanges. These glands are indistinguishable fromthe hilar glands in follicular bronchiectasis.In three of the middle with lower lobe specimensthere are small partly-calcified caseous foci in theperiphery of one lobe (two in middle lobes and onein a lower lobe), and a similar focus is present inthe periphery of a left lower lobe. In two ofthese specimens the hilar lymph-glands containcalcified caseous foci. Except for two specimens oftuberculous bronchiectasis and a saccular bronchiectasiswith tuberculosis in the non-bronchiectaticpart of the lobe, these are the only tuberculouslesions seen in the whole series.BRONCHIAL TREE.-The bronchi in collapsedspecimens show similar histology throughout alobe. There may be (1) moderate inflammationwithout any destruction of supporting tissues.This was also always seen in specimens of simplecollapse. (2) Slight superficial inflammation, butbronchial walls show dense fibrous thickening, andcontain no elastic tissue, muscle, or cartilage(Fig. 33). (3) Severe inflammatory changes withepithelial ulcerations and destruction of supportingtissues.The bronchioles show similar lesions, but are lessseverely affected. In some specimens inflamedbronchial walls contain numerous lymph follicles,but interstitial pneumonia is absent.The type of histological change in the bronchiappears to be unrelated to the degree of dilatation.ALVEOLI.-In spite of the gross reduction in sizeof the lobes, and the apparent total alveolar collapse,the microscopic appearances are usuallythose of incomplete absorption collapse.Many lobes seem to be infarcted; in these thereis extravasation of red cells into interstitial tissues,and the partly collapsed alveoli, and some bronchioles,are distended with blood (Fig. 34). MostFIG. 35.-Development of atelectaticbronchiectasis (a) smallfocus in periphery of middleand lower lobe; (b) enlargedhilar glands and lobar col-(t }~ 1 tlapse; (c) atelectatic bronchiectasiswith calcified foci inhilar glands.abc
PATHOLOGY AND PA THOGENESIS OF BRONCHIECTASISof this haemorrhage consists of fresh red cells, but(leposits of haemosiderin in cells of the alveolarwalls and in intra-alveolar heart-failure cells showsthat some bleeding must have occurred beforeoperation. This intra-alveolar haemorrhage wasrarely seen in other forms of bronchiectasis. Theoperative technique was similar in all cases.In the lobes showing simple collapse elastictissue in alveolar walls appears to be thickened,probably because of its relaxed state. In atelectaticbronchiectasis the alveolar wall elastic tissue iseither represented by a few short thick curls, or itis completely absent. A variable amount ofinter-alveolar fibrosis is seen but there are noother signs of inflammation.CLINICAL FEATURES OF ATELECTATICBRONCHIECTASISThe age distribution of all cases is shown inFig. 4. The case-records of 15 patients wereavailable for analysis, and provided the followingdetails.AGE AT OPERATIONUnder 5 yrs.5-10 yrs.11-1 5 yrs.16-20yrs.21-25yrs.26-30yrs.Over 30 yrs.AGE AT ONSET OF SYMPTOMSUnder 3 yrs.3-6yrs.15yrs.21-23yrs.Not stated0 patients6 332 -I patient0 ,3 patients7I patientpatients2PRE-OPERATIVE DURATION OF SYMPTOMSUnder I yr. 0 patients1-3 yrs. 54-5 yrs. 36-10 yrs. 3II-I 5 yrs. 2Not stated 2NATURE OF ILLNESS AT ONSET OF SYMPTOMSMeasles and/or whooping cough7 patientsPrimary bronchopneumonia 3Insidious onset .. 2Pleurisy .. I patientNotstated.2 patientsFINGER CLUBBINGPresent (recorded as mild)Absent . .Not statedPresentDoubtfulAbsentPARANASAL SINUS INFECTIONS5 patients9 .,I patient3 patients48Three patients who had tuberculous foci in thelobes and hilar lymph-glands dated their symptomsfrom whooping-cough or measles in early childhood.There was a close correlation between the amountof inflammatory change seen in the bronchi and235the quantity and nature of the sputa; in manycases there was a complete absence of sputum.PATHOGENESIS OF ATELECTATIC BRONCHIECTASISThe following features, which are characteristic ofatelectatic bronchiectasis and not of other forms ofthe disease, suggest how atelectatic bronchiectasismay arise: (1) the generalized distribution ofcollapse and bronchiectasis in the lobes; (2) theabsence of central or peripheral bronchial obstructionin the lobes at the time of operation; (3) thepresence of tuberculous foci in some lobes andhilar lymph-glands; (4) the frequency of involvementof the right middle lobe, either alone or withthe lower lobe; (5) the variability of bronchialchanges, and the absence of inflammation in thecollapsed parenchyma; (6) the absence of fingerclubbing, sinus infections, and foul sputum inmany patients.The bronchiectasis must either be the cause, orthe result, of collapse. If collapse were secondaryto bronchiectasis one would expect the segmentaldistribution of the lesions, and their histology, tobe the same as in aerated forms of the disease.This was not so, so the collapse is probablythe primary condition. There were a few exceptionsto this generalization; they may have beensecondarily-collapsed follicular bronchiectases.If the theory that collapse is caused by peripheralbronchial obstruction is accepted, in these casesone is forced to conclude that simultaneous obstructionsoccurred in all peripheral bronchi; otherwisethe bronchiectasis could not affect all branches,and collateral air circulation would prevent alveolarcollapse. The improbability of such an occurrence,and the complete absence of peripheral obstructioni most of the specimens, suggests that there is nosound basis for this theory.There is far more evidence supporting the viewthat collapse is caused by obstruction of lobarbronchi. Although no obstructive lesions of theproximal bronchi were found in these specimens, orseen in pre-operative bronchograms, the frequentfinding of enlarged, fibrotic, or caseous hilar lymphglandssuggests that collapse arose from occlusionby these glands of the lobar bronchi. This theoryreceives further support from the high incidence ofright middle lobe specimens in atelectatic bronchiectasis,for Brock (1946) has demonstrated thepeculiar vulnerability of the middle lobe bronchusto compression from enlargement of the surroundinglymph glands.Recently Brock (1950) has described suppurativechanges, bronchiectasis, and collapse in middlelobes as a sequel to tuberculous hilar adenitis. He
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A study of the pathology and pathogenesis of bronchiectasis.

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