*Surgical aspects

PulmonaryTuberculosis inA frican children

of

by

G. R. Crawshaw, B.Sc., M.D. (V.U.Manc.),F.R.C.S. (Eng.), Bulawayo.

The Role of Surgery in the Relief of Bronchial Obstructionand in the Prevention o`f its Effects

The main purpose of this paper is to present a pleafor a rational approach to hilar lymphadenectomy in theprevention of bronchiectasis, destroyed lung, emphysemaand a massive tally of crippling respiratory disease.Operation should be considered at an early stage if drugtherapy and physiotherapy are not clearly relievingbronchial compression or perforation by mediastinallymph glands, either where the bronchial obstructionin itself is causing symptoms or where the resultingpulmonary lesion may be regarded as still reversible.This is an infinitely more attractive proposition to me as asurgeon than to be presented with the late effects ofbronchostenosis and to be asked to salvage a respiratorycripple. I want to condemn in the strongest possibleterms the indiscriminate use of drugs and bed rest inpulmonary tuberculosis when an obvious mechanicalproblem exists.

The Prinary Complex and Bronchial Obstruction.

In the lung the glandular component of the primarytuberculous complex in young Africans is often florid in

MEDICAL JOURNAL OF ZAMBIA J¢„k¢r}J, 1969

Figure I. The florid, bilateral hilar lymphadeno-pathy often seen in African patients with primary

tuberculous infections in the lung.

the extreme. Figure I. demonstrates a not unusualradiological appearance of this florid nature and italso demonstrates the common bilateral distributionof the lymph node enlargement. These features, thefloridity and the bilateralcy of the lymph node involve-ment, in primary tuberculosis, together with thehigh incidence in African children help to explain theremarkable frequency of pathological states due tobronchial obstruction.

The Effects of Bronchial Obstruction by Enlarged LymphNodes .

Some examples of the pathological states seen inthe thoracic surgical clinic at Mpilo Central Hospitalare illustrated in Figures II-VII. The lesions represent,in the main, changes which in themselves are not tuber-culous but are the consequence of bronchial obstructionby enlarged lymph nodes.(1).

Bronchiectasis. The role of bronchial obstruction bytuberculous hilar lymph nodes has long bee+1 re3ogniscdjn the causation of bronchie3tasis. (2)(3)(4). The vulner-ability of the soft, pliable bronchial walls of childre:1 is an

*This article was prepared for, but not read at the medicalcongress in Kitwe (1968).

169

Figure IV. Bronchiectasis in the left lower lobe andlingula The hilar lymph nodes were tuberculous.

Figure VI. Stricture of the might intermediatebronchus due to compression by caseating tuberl

culous lymph nodes.

Figure V. Stricture of the left main bronchus, due to ulce-ration by infection from caseating tuberculous lymph nodes.

Figure VII. So called "destroyed lung" most often due tostenosis of the left main bronchus by dubercu]ous hilar

lymph nodes.

Figure VIH. The left main bronchus in a normal broncho-gram. It is narroVler and four times as long as the right

main bronchus.

Figure 11. Collapse of the middle lobe due to bronchialobstruction by enlarged tuberculous lymph nodes

additional factor at play. It is also well to remember thatwhat appears to be a `healed primary tuberculouscomplex' is not necessarily so for reactions around evencalcified lesions in lung parenchyma or in the lymphnodes in the hilum can occur and do so after the lesionhas been quiescent for a considerable numbers of years.(1)

The appearances in Figure Ill of "radiographic

Figure HI. "Radiographic" bronchiectasis in the middlelobe. This, as bronchiectasis elsewhere, is reversible in the

early stages -

}1EDICAL JOURNAL OF ZAMBIA J¢##¢rjJ, 1969

bronchiectasis" can be explained as due to either thedistension of the bronchi after the damming up ofmucus or a compensatory mechanism for the loss ofvolume of the collapsed lobe.(5). Whatever may be thetrue explanation, in the early stages, before infectionof retained secretion with consequent mucosal ulceration,submucosal inflammation and weakening, erosion anddistortion of the bronchial wall the changes are reversibleprovided the bronchial obstruction is relieved.

In many instances adequate drug therapy togetherwith adequate physiotherapy will achieve the re-expan-sion of the collapsed lung tissue if they are promptlyinstituted. If time is lost in starting treatment the conditionbecomes irreversible. Moreover, in not a few instances,the glandular component of the primary complex maygo on enlarging in spite of drug therapy.(6)(7)(8). I havewatched the development of bronchiectasis over aperiod of eighteen months in` such a patient underbronchographic control. She subsequently required alobectomy in addition to hilar gland resection for theprotection of the remaining lobe. Measles is a well knownfactor enhancing the risk of bronchial 'obstruction inchildren with primary tuberculous infections.(9).

The anatomical distribution of bronchiectatic lesiorisis of great interest and is further evidence for the role ofbronchial obstruction by enlarged lymph nodes in theiretiology. Brock(10) has written about the dispositionof the lymph glands around the middle lobe bron-chusrendering it liable to compression as a result of diseaseand enlargement of the sentinel gland. "As the very acuteangle formed by the origin of the middle lobe bronchusfrom the main stem begins to widen it is occupied by ;alymph gland as is usual with all such angles formed by thebranching of bronchi" (My underlining)., Herein lies anexplanation of the common distribution of bronchi-ectasis-middle lobe, left lower lobe and lingula-allfed by bronchi branching at very acute angles. This is fnmarked contrast with the distribtition of lung abscesswhich predominantly involves segments of the lungsfed by bronchi originating at 90° or `more from theparent bronchi.(11). The acute angle predisposes tocompression of the bronchi by the enlargement of thelymph node wedged in the dependent angle. .

The "destroyed lung" syndrome` inigure VII) or``chronic fibroid lung" (12) is tragically common in young

Africans and usually it is not, as it is often stated to be,the result of extensive "adult" or "fibrocaseous" pulmonarytuberculosis. There may indeed be a focus of old tuber-culosis to be found in the resected specimen but I belieiethat this is only the pulmonary component of a prima`rytuberculous complex and that the extensive bronchiectati,Clesion of the lung is due essentially to the mechanicallyobstructive effects of the accompanying lymph nodecomponent. `

Here again anatomical considerations are of\ great

::]dueitFifumr:n¥t[r[a[te£§:h:0::ian[erbarb°iTi:;0::a:o~:6::sCsT;I:of the left main bronchus by reason of its length, com-paratively small 1umen and its course between theuny_ielding _.aortic arch _on ~the one hand_ _and _.-.the_ =1Oft

171

tracheo-bronchial lymph nodes on the other. When thesenodes enlarge the left main bronchus is at risk and sureenough "destroyed lung" occurs on the left side in ninecases out of ten. It is clear that t'ie right main bronchusby contrast with the left is shorter, wider and relativelyunfixed.

i When caseating tuberculous lymph nodes become'adherent to the wall of a bronchus and the disease

process invades it ulceration and stricture formation mayoccur. This process is illustrated in Figures V and VI.Attempts at the removal of caseous material or calcificmatter through a bronchoscope are fraught with dangeruniformly unsuccessful and usua[]y make matters worse.(3)(12). Obviously when the lung beyond the stricture ispermanently damaged resection is indicated but thereis a time when the surgical removal of the diseasedlymph nodes by thoracotomy can save valuable lungtissue from destruction. (13)(14)(15).

Surgery in the Prevention of Pulmonary Tuberculosisin Children.

The final point I want to make in discussing thesurgical aspects of pulmonary tuberculosis in Africanchildren takes us back to first principles. Preventionis preferable to having to cure. It seems to me question-able that it is wise to persist with antituberculous drugtherapy alone beyond six months in the face of persistentcavities jn adult patients in developing countries. Thesepatients become the reservoir of infection in the commun-ity. I do not refer to those confined to hospital withgross bilateral disease but rather to those who become"the good chronics" and are "treated" as out patiquts.

The term "good chronic" is too often a euphemism for"fit positive tuberculotic" (16) aridhisnumbers increasewith

a rising standard of living. Surgical resection offers avaluable measure(17) of rendering such patients lessmenacing to the uninfected children of the community.(18).

REFERENCES

1. Macpherson M., (1948) Proc roy soc Med xli. 60,2. Brock R. C., Cann R. J. and Dickinson J. R,

(1937) Guy's Hospit Rep. 87. 295.3. Hutchison J. H., (1951) Tubercle (Lond.) 32. 271.

4. Valledor T. and Navarrete A., (1952) Dis. Chest.22. 46.

5. Lander F. P. Lee, (1946) Thorax 1.198.

6. Daly F. J., Brown D. S., Lincoln E. M. andWilking V. M., (1952) Dis. Chest. 22. 380.

7. Wissler H., (1953) In: `Therapie der Lungen-tuberkulose" Hans Haber, Berlin.

8. Lincoln E. M., Harris L. C., Bovornkitti S. andCarretero R. (1955) Am. Rev. Tub. Pulm. Dis.74/11. 246.

9. Dijkman J. H., (1967) Selected Papers. RoyalNetherlands Tuberculosis Association. 10. 5.

10. Brock R. C., (1947) In: `The anatomy of thebronchial tree, O.U.P. London.

MEDICAL JOURNAL OF ZAMBIA Jcz#z/ar);, 1969