Endobronchial Tuberculous--Small Airways Disease

Bronchocentric granulomatosis: Here, a small, branching airway shows destruction of wall structures and involvement of the surrounding alveoli by a necrotizing granulomatous process that also obstructs the lumens. The arteries (arrows), which show some intimal, fibrous narrowing, indicate the location of the bronchovascular bundle.

Bronchiolitis obliterans: In late stages, small airways may be completely obliterated by fibrous scar. This elastic van Gieson stain shows obliteration of the airway lumen by red-staining collagen that contains some remnants of the black-staining, elastic layers from the airway wall. The adjacent artery to the left shows the typical fibrotic, intimal thickening (endarteritis obliterans) of vessels adjacent to inflammatory scars.

After treatment, the CT may show the airway scar as a small centrilobular opacity with a surrounding alveolar mosaic hyperlucency, which indicates local air trapping and hypoperfusion.

Clinical Endobronchial Tuberculosis

Introduction: As shown above, endobronchial tuberculosis, demonstrated both histologically and by CT, regularly involves small bronchi and bronchioles in postprimary disease. In contrast, clinically, endobronchial tuberculosis is defined as tuberculosis involving the trachea, and/or main, lobar, or segmental bronchi. Before effective therapy for the disease was available, clinical endobronchial disease occurred in 10-15% of patients with active disease [1]. It is now seen mainly in countries with high rates of tuberculosis. However, in one study of HIV-infected, intravenous drug users in Spain, 6/25 (24%) had endobronchial tuberculosis. CD4 counts varied from 29-165 cells/µl [2]. In adults, endobronchial disease probably results from endobronchial spread of caseous material from active or cavitary lesions, or, less likely, from lymphatic spread from a primary parenchymal lesion or lymph nodes. In children with prominent adenopathy, a direct lymphogenous spread to the mucosa from nodes is thought to be more likely than spread from the primary focus [1].

Clinical symptoms: Symptoms, which may be present for up to a year before diagnosis, consist of dry cough, dyspnea due to lung collapse, local wheeze, hemoptysis, hoarseness (from laryngitis), anorexia, weight loss, chest pain, or fever [3]. Symptoms and signs are often mistaken for other types of bronchitis, for asthma, or for lung cancer [1].

Radiologic findings: Lung opacities are not uniformly present in these patients. In one series of 20 patients, consolidation was present in 7 (35%), collapse in 7, cavitation in 1, a miliary pattern in 1, and a clear chest in 4 (20%) [3]. In AIDS patients, mediastinal/hilar adenopathy was present in 5/6 and the lung parenchyma was often clear [2].

Diagnosis: Bronchoscopy is necessary to find the endobronchial lesions, which appear as gelatinous, granulation tissue; nodular, reddened lesions; or ulcerated mucosa. The main bronchi are involved more frequently than the trachea, and upper and lower lobe bronchi are involved roughly equally. Biopsy may show necrotizing granulomas, but culture of suspicious lesions for mycobacteria needs to be done even when the diagnosis is thought to be cancer. Sputum culture is often negative--17 of 20 in one series. Flow-volume curves are often normal [3].

Follow-up after chemotherapy: At reexamination of 12 patients after a mean of 27 months following the completion of therapy, 11 had bronchostenosis of varying severity. Non-invasive methods such as chest radiograph and flow-volume loops were insensitive for diagnosis [3]. In another study, bronchoscopic follow-up of 56 endobronchial tuberculous lesions within 3 months of completion of chemotherapy showed no change in degree of stenosis in lesions that were initially cicatricial, and a tendency to progress to stenosis of lesions that appeared to result from extrinsic compression by involved lymph nodes. Simple exudative or ulcerative lesions improved [4]. In contrast, in 6 AIDS patients, some with airway compression by lymph nodes, bronchoscopy following therapy showed no endobronchial abnormalities [2].

Short-term follow-up, however, may not be sufficient to define outcome. A case report of a 75-year-old woman who presented with a 4-year history of severe cough that did not respond to antihistamines, bronchodilators, antibiotics, or prednisone illustrates this point. She had a clear chest radiograph. Bronchoscopy showed tracheal and bronchial reddening, thickening, and whitish plaques. Cultures were positive for M. tuberculosis. Two years after effective therapy, cough and dyspnea recurred. Bronchoscopy showed marked stenosis, but there was no evidence of active tuberculosis, and cultures for organisms were negative [5,6]. Late stenosis has been reported in two other cases [7].

Late outcome: Both the bronchial and bronchiolar lesions described above are likely to contribute to the late-occurring, chronic obstructive airways disease that has been described up to 16 years following treatment of tuberculosis in 48 of 71 (68%) of subjects [8].

Treatment of late stenoses: When proximal endobronchial disease progresses to stenosis despite therapy, surgical procedures can be used to treat the lesion. In many cases, simple lobectomy or bronchoplastic procedures of main bronchi, which remove the stenotic region and lobe and reanastomose the remaining portions (sleeve lobectomy), preserve lung parenchyma [9].

Bronchocentric granulomatosis: This entity is a histologic pattern (not a disease) consisting of granulomas (necrotizing or non-necrotizing) around small bronchi and bronchioles. It has many different causes, the best known of which is allergic bronchopulmonary aspergillosis, but the pattern may also occur in other fungal diseases, as well as in rheumatoid arthritis, or mycobacterial infections. In the last, it accounts for the small branching structures seen on CT. Histologically, there is a mixture of necrosis with PMNs and granulomatous inflammation [10]. Bronchiolitis obliterans may result.

References

1. Matthews J, Matarese S, Carpenter J. Endobronchial tuberculosis simulating lung cancer. Chest 1984; 86:642-644.

2. Calpe J, Chiner E, Larramendi C. Endobronchial tuberculosis in HIV-infected patients. AIDS 1995; 9:1159-1164.

3. Ip M, So S, Lam W, Mok C. Endobronchial tuberculosis revisited. Chest 1986; 89:727-730.

4. Kim Y, Kim H, Lee K, Uh S, Cung Y, Park C. Serial fiberoptic bronchoscopic observations of endobronchial tuberculosis before and early after antituberculosis chemotherapy. Chest 1993; 103:673-677.

5. Pierson D, Lakshminarayan S, Petty T. Endobronchial tuberculosis. Chest 1973; 64:537-539.

6. Albert R, Petty T. Endobronchial tuberculosis progressing to bronchial stenosis. Fiberoptic bronchoscopic manifestations. Chest 1976; 70:537-539.

7. Mariotta S, Guidi L, Aquilini M, Tonnarini R, Bisetti A. Airway stenosis after tracheo-bronchial tuberculosis. Respir Med 1997; 91:107-110.

8. Willcox P, Ferguson A. Chronic obstructive airways disease following treated pulmonary tuberculosis. Respir Med 1989; 83:195-198.

9. Watanabe Y, Murakami S, Oda M, Hayashi Y, Ohta Y, Shimizu J, Kobayashi K, et al. Treatment of bronchial stricture due to endobronchial tuberculosis. World J Surg 1997; 21:480-487.

10. Maguire G, Lee M, Rosen Y, Lyons H. Pulmonary tuberculosis and bronchocentric granulomatosis. Chest 1986; 89:606-608.

Clinical summary Inactive TuberculosisDiscussion

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