Thorax 1990;45:210-212

Unilateral post-tuberculous lung destruction: theleft bronchus syndrome

M Ashour, L Pandya, A Mezraqji, W Qutashat, M Desouki, Naser Al-Sharif,A Al-Jaboori, Ali Marie

AbstractIn a prospective study of 13 patientsrequiring pneumonectomy for unilateralpost-tuberculous lung destruction the leftside was found to be affected in 12. Reviewofa further 172 cases showed the left lungto have been destroyed in 109 (63%). It issuggested that this predominance of theleft side is due to the anatomicalcharacteristics of the left main bronchusand that disordered haemodynamics alsoappear to play a part.

Unilateral total post-tuberculous lung destruc-tion is a well recognised cause ofmorbidity andmortality.' 2 In Saudi Arabia late presentationand poor compliance with treatment fortuberculosis (as low as 30%') account for anappreciable number of patients presenting inthis way, but very few studies have dealt withthe problem in detail.4 We report the clinico-pathological and haemodynamic findings in 13patients coming to surgery at King KhalidUniversity Hospital. The left lung was affectedmore frequently than the right, and we discussthe reasons for this predilection.

Patients and methodsWe studied 13 patients with unilateral lungdestruction before elective pneumonectomy,by bronchoscopy, bronchography, pulmonaryangiography, thoracic aortography, ven-

King KhalidUniversity Hospital,RiyadhM AshourA MezraqjiM DesoukiW QutashatAl-JabooriSahary ChestHospital, Riyadh,Kingdom of SaudiArabiaN Al-SharifL PandyaA MarieAddress for reprint requests:DrM Ashour,Department of Surgery,King Khalid UniversityHospital, P Box 7805,Riyadh 11472, Kingdom ofSaudi Arabia.Accepted 21 November 1989

tilation-perfusion scanning, and computedtomography. Indications for surgery includedextensive cavitation with persistently positivesputum for six to 15 years (nine patients),repeated large haemoptyses (two patients), andgiant bullae (two patients). The resected lungswere submitted for histopathological examina-tion. To assess the prevalence of the conditionin the right and left lung, we reviewed therecords and radiographs of 1600 patients withproved pulmonary tuberculosis seen during1983-7.

ResultsThe left lung was destroyed in 12 of the 13patients who underwent surgery (fig 1). Bron-choscopic examination showed stenosis of theright bronchus intermedius in the singlepatient with destruction of the right lung.There was ulceration of the left main bronchusin two other cases and mucosal thickening andcongestion of the left bronchus in four. Pul-monary angiography showed no pulmonaryarterial flow on the affected side in any patient(fig 2); thoracic aortography showed bronchialarterial proliferation and systemic inflow to thepulmonary arterial tree from the bronchialcirculation (fig 3). Ventilation-perfusion scan-ning showed no perfusion and poor ventilation.

Total destruction of the parenchyma in eachof the resected specimens was apparent fromgross examination. The main bronchus in the12 left lungs was patent, but two had ulcerative

Figure I Chest radiograph showing left lung destruction.

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Unilateral post-tuberculous lung destruction

Figure 2 Pulmonaryangiogram showing nopulmonary flow on the sidewith lung destruction.

lesions and in one of these the ulceration wascontinuous with a parabronchial tuberculousmass. In the single right sided specimen thebronchus intermedius was stenosed. Histo-logically, there was extensive active tuber-culosis with fibrosis, widespread cavitation,and bronchiectasis. The lymph nodes fromthree specimens were examined; tuberculousgranulomas were found in one case but onlycarbon pigmentation in the other two.Obliteration of pulmonary arteries and endar-teritic changes were seen in the fibrocaseousareas. Bronchial arteries were dilated andpatent.

In the 1600 cases of pulmonary tuberculosisthat were available for review, we considered

Figure 3 Thoracicaortography showingsystemic inflow to thepulmonary arteryfrom thebronchial circulation.

post-tuberculous lung destruction to have beenpresent in 172 (llI%). The left lung wasdestroyed in 109 (63%) and the right in 63(370/0).DiscussionAlthough the apical and posterior segments ofthe upper lobes are the site of predilection withabout equal incidence on the two sides,5 totallung destruction is more frequent on the left. Acombination of anatomical factors may makethe left lung more vulnerable to this type ofdamage, and disordered haemodynamics alsoappear to play a part.The left main bronchus is considerably

longer and about 15% narrower than theright,67 and the peribronchial space is limitedby its proximity to the aorta,8 so that it is moreprone to obstruction by enlargement ofadjacent lymph nodes. Such obstruction wasnot evident in the lungs we examined, probablybecause we were seeing the end stage of thedisease process-it is likely to have beenpresent in the initial stages because mediastinaland hilar node enlargement is common inAfrican and Asian patients with post-primarytuberculosis.910 In addition, the more horizon-tal course of the left main bronchus than of theright may have an effect on drainage ofsecretions,"1 as has been shown recently bybronchoscintigraphy. 2

Several studies have shown that pulmonaryhaemodynamics play a part in the pathogenesisand spread of tuberculous infections. Thecharacteristic localisation of pulmonary tuber-culosis seems to be associated with lymph stasissecondary to reduced arterial flow at the apexand also with increased oxygen tension at thatsite.'3 Pulmonary arterial flow is reduced orabsent when there is bronchial obstruction,'4stasis of secretions,'5 or parenchymal infec-tion.'6 Ligation of the pulmonary artery ofpatients'7 and experimental animals'8 with pul-monary tuberculosis is reported to exacerbatethe disease, as does anastomosis of a majorsystemic vessel to the pulmonary artery.'9 Inour patients angiography showed pulmonaryarterial flow to be absent, bronchial arterieswere prominent, and there was radiologicalevidence of systemic flow into the pulmonaryarterial tree. It seems likely that these factorsled to lymph stasis and a raised oxygen tension,favouring progression of the disease andeventual lung destruction.

1 Cockshott P, Middlemiss H. Clinical radiology in the tropics.Edinburgh: Churchill Livingston, 1979:160-2.

2 Adebnojo SA, Adebo OA, Osinowa 0, Grillo IA. Man-agement of tuberculous destroyed lung in Nigeria. J NatlMed Assoc 1981;73:39-42.

3 Aneja KS. Assignment report of World Health Organization:tuberculosis in Saudi Arabia. Geneva: WHO, 1984.

4 Onadeko BO, Awotedu AO. Destroyed Lung Syndrome. Anend stage dilemma in patients with pulmonary tuber-culosis. A 5 year experience in a teaching hospital inNigeria [abstract]. In: XXV International Union AgainstTuberculosis World Conference on Tuberculosis and Res-piratory Disease. Singapore: 1986.

5 Kolawol TM, Onadeko BO, Sofowora EO. Radiologicpatterns of pulmonary tuberculosis in Nigeria. Tropicaland Geographical Medicine 1975;27:339-50.

6 Hollinshead WH. Anatomy for surgeons. Vol 2. New York:Harper and Row, 1979:44-51.

7 Last RJ. Anatomy, regional and applied. London: ChurchillLivingstone, 1978:226-7.

8 Williams PL, Warwich R. Gray's Anatomy. 36th ed.London: Churchill Livingstone, 1980:1241-7.

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Ashour, Mezraqji, Desouki, Al-Shanf, Pandya, Qutashat, Al-Jaboori, Marie

9 Humphries MJ, Nun AJ, Byfield SP, et al. National surveyof tuberculosis notification in England and Wales in 1983:characteristics of disease. Tubercle 1987;68:19-32.

10 Kent DC, Schwartz R. Hilar lymphadenopathy in tuber-culosis. Am Rev Respir Dis 1967;96:435-9.

11 Leigh Collis J, Clark DB, Aby Smith R. d'Abreul's Practiceof cardiothoracic surgery. London: Edward Amold,1976:107-21.

12 Groth S, Mortensen J, Lange P, et al. Imaging ofairways ofbronchoscintigraphy for the study of mucociliaryclearance. Thorax 1988;48:360-5.

13 Goodwin RA, Des Perez RM. Apical localisation ofpulmon-ary tuberculosis, chronic pulmnonary histoplasmosis andprogressive massive fibrosis of the lung. Chest 1983;83:801-5.

14 Grant JL, Naylor RW, Crandel WB. Bronchial adenomaresection with relief of hypoxis pulmonary vaso-constric-

tion. Chest 1980;77:446-9.15 Gordon I, Helms P, Fazio F. Clinical application of radio-

nuclide lung scanning in infants and children. Br J Radiol1981;54:576-85.

16 Charles BT, Rama R. Lung imaging-unilateral absence ornear absence of pulmonary perfusion on lung scanning.Semin Nucl Med 1983;13:388-90.

17 RienhoffWF Jr. A clinical analysis and follow-up study of502 cases of carcinoma of the lung. Dis Chest 1950;17:33-54.

18 Scott J, Hanlon CR, Olson BJ. Experimental tuberculosis(2). Effects of ligation ofpulmonary artery in tuberculosisin monkeys. J Thorac Surg 1950;20:761-73.

19 Rollins C, Hanlon HW, Scott Jr, Olson BJ. Experimentaltuberculosis: effects of anastomosis between systemic andpulmonary arteries on tuberculosis in monkeys. Surgery1950;28:209-24.

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the left bronchus syndrome.Unilateral post-tuberculous lung destruction:

al-Jaboori and A MarieM Ashour, L Pandya, A Mezraqji, W Qutashat, M Desouki, N al-Sharif, A

doi: 10.1136/thx.45.3.2101990 45: 210-212 Thorax

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