Practice

Endobronchial Tuberculosis: About Itself & Beyond

Background

Tuberculosis is one of the top infectious diseases in our country with an incidence of 322 per 100,000 population. It remains a challenge for us because of the increasing burden of drug resistant tuberculosis and HIV-associated tuberculosis, on top of the high prevalence of drug susceptible tuberculosis.1

The presentations of pulmonary tuberculosis range from the typical cough and constitutional symptoms with the CXR finding of parenchymal lesions to some specific forms of tuberculosis like endobronchial tuberculosis, intrathoracic lymphadenopathy and pleural tuberculosis where further investigations are needed to reach the microbiological and or histopathology confirmation.

On the other hand, there are many respiratory complications even after active tuberculosis infection has been successfully treated. Tracheobronchial stricture and stenosis, post tuberculous bronchiectasis, fibrosis of the pleura and lung parenchyma, recurrent hemoptysis and new development of obstructive airway disease are common post tuberculous complications encountered in respiratory medicine practice.

Case presentation

A 20-year-old woman was referred to Respiratory Medicine outpatient clinic for cough associated with tightness of chest for two months. Her cough was mostly non-productive and not much relieved by cough remedies and courses of antibiotics. She felt breathless and chest tightness for which she did not find any triggers but relieved by inhalers. She noticed weight loss but denied fever, loss of appetite and night sweats. She did not have haemoptysis or chest pain. She was previously healthy with no similar illness in the past. She did not have any comorbidities nor contact with anyone known or suspected of tuberculosis. On clinical examination she was rather thin, alert but tachypnoeic. General examination had no abnormal findings including lymphadenopathy and clubbing. Respiratory examination revealed trachea in midline, vesicular breath sounds on both lungs with increased vocal resonance with ronchi mostly in the left middle zone.

Laboratory tests showed normal total WBC with normal differential counts and platelet count. Hb was 10 g/dl and inflammatory markers were high; CRP of 35 mg/L and ESR of 56 mm/1st hr. Liver and renal function were normal. Sputum examination for acid-fast bacilli (AFB) was negative, few gram-positive cocci seen on gram stain but no growth of pathogenic organism on sputum C & S. Chest X- ray showed nodular and linear infiltrates in left middle zone with loss of lung volume of left lower lobe, obscured left heart border and medial part of left diaphragm (Figure 1a). Her spirometric values; FEV1-1.52 L (59% predicted), FVC – 1.82 L (63 % predicted), FEV1/FVC – 83.5, all of which were consistent with poor expiratory effort.

Eventually, bronchoscopy was performed to find out the exact endobronchial pathology and to obtain the microbiological and histology samples. There was no tumour growth, foreign body and active bleeding. However, left main bronchus had mucopurulent secretion, hyperemic bronchial mucosa and its distal part had whitish friable cheesy tissue (Figure 1b). Endobronchial biopsy and bronchial washing were taken from left main bronchus. Bronchial washing for cytology was negative for malignancy but was positive for acid- fast bacilli (AFB) and high load of Mycobacterium tuberculosis detected with no rifampicin resistance on Gene X-pert (X-pert MTB/RIF) test. Histopathology of bronchoscopic biopsy taken from distal left main bronchus was found to have typical features of tuberculosis: caseating granuloma with lymphocytes and Langerhans giant cells. As a result, she was confirmed to have endobronchial tuberculosis.

She was given treatment as per National Tuberculosis Program Guideline (isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months followed by isoniazid and rifampicin for subsequent 4 months). During initial two months follow ups, she was reported steady improvement in general well- being without drug side effect. However, her cough, chest tightness, breathlessness with episodes of wheezing were not much improved. Bronchial stenosis was very likely to develop as a complication, so she was advised for 2nd time bronchoscopy to proceed necessary bronchoscopic intervention.

A 3D CT-generated virtual bronchoscopy was done for intraluminal evaluation prior to actual bronchoscopic intervention (Figure 2a). Interventional bronchoscopy was performed with BF 1TH 190 Olympus broncho videoscope under local anesthesia. Left main bronchus demonstrated more than 75% concentric narrowing leaving a pin head size opening at its distal part just before bifurcation to segmental bronchi (Figure 2b, 3a). Stenotic left main bronchus was dilated with 3 ATM inflation pressure, stepped up to 5.5 ATM pressure then to 9 ATM pressure for 2 minutes cycles. Integrated inflation device (Alliance II, Boston Scientific) and CRE balloon dilatation catheter 8/9/10 mm (Boston Scientific) were used for balloon dilation procedure (Figure 3b, 3c). After a total of 4 cycles of balloon dilation, the left main bronchus stenotic area was able to accept 10 mm balloon.

On followup reviews after bronchoscopic balloon dilation procedure, her symptoms of cough, chest tightness and exercise tolerance were much improved. Sputum AFB assessment after five and six months of antiTB treatment were negative. CXR recheck was also improved without residual lobar collapse. Follow up bronchoscopy was carried out after completing 6 months of antiTB treatment. She again required second session of 3 cycles of bronchoscopic balloon dilation. At that time, broncho videoscope Olympus BF1TH 190 could pass through the stenotic left main bronchus and able to inspect lobar bronchi (Figure 3d). On 1 year follow up, she resumed premorbid exercise tolerance, well-being without needing further intervention bronchoscopy.

Discussion

Endobronchial tuberculosis (EBTB) is defined as infection of the tracheobronchial tree by Mycobacterium tuberculosis with microbial and histopathological evidence. EBTB accounts for 10- 40% of active pulmonary tuberculosis. Most of the patients are aged less than 40 years with female preponderance 2. It is classified into seven different subtypes: actively caseating, edematous hyperemic, fibro stenotic, tumorous, granular, ulcerative and nonspecific bronchitis.

The diagnosis of EBTB is often missed or delayed because it is not always evident on initial clinical assessment, CXR and sputum microscopy for acid fast bacilli. The most common presenting symptom is prolong cough. Patients may also present with symptoms secondary to complications. In case of tracheobronchial stenosis, the presentations can be confused with other problems such as bronchial asthma or foreign body aspiration. These patients may have symptoms of chest tightness, wheezing and clinical sign of ronchi with its peculiar unilateral inspiratory nature.

In terms of radiological investigations, CXR may be normal in 10- 20% of EBTB. High resolution computed tomography (HRCT) has been found to be superior to CXR and standard CT to pick up radiological abnormalities of EBTB: parenchymal infiltrates, consolidation, segmental or lobar collapse, bronchial stenosis3. Virtual bronchoscopy is a CT based imaging technique that allows a noninvasive intraluminal evaluation of tracheobronchial tree. Bronchoscopy along with histopathological and or microbiological investigations is the most useful diagnostic tool for confirmation as well as for evaluation of complications when develop.

The treatment of EBTB is the same as pulmonary tuberculosis. Systemic corticosteroid treatment in addition to antiTB treatment has good outcome in early stages by resolution of inflammation and edema but regression of established fibrostenotic lesions is not possible. The role of corticosteroid in EBTB is therefore still controversial.

EBTB has variable clinical course, ranging from complete resolution to residual complications. The common complications are tracheobronchial stenosis, post obstructive bronchiectasis and lobar or segmental lung collapse. Tracheobronchial stenosis may develop in 60 to 95% of EBTB cases despite adequate antituberculous therapy4. Further intervention is required for those patients who develop severe tracheobronchial stenosis causing significant symptoms such as dyspnea or repeated post obstructive pneumonia. Advancement in interventional bronchoscopy has emerged with promising outcome in the management of post tuberculous tracheobronchial stenosis. There are various bronchoscopic techniques to relieve airway stenosis including laser, cryosurgery, balloon dilatation and stent insertion. Surgery is considered for refractory cases when other modalities fail.

Balloon dilatation for tracheobronchial stenosis was first described by Cohen et al 5 and was accomplished using rigid bronchoscopes or guide-wires under fluoroscopy guidance in the past. In recent years, it has been established the safety of the procedure, using flexible bronchoscope under conscious sedation or local anaesthesia6. The deflated balloon is introduced via the working channel of the flexible bronchoscope, placed across the stenosed airway segment, and is inflated to stretch and expand the stenotic bronchus radially using a pressure syringe device, thereby increasing luminal dimension of stenotic or stricture airway. This method is usually straightforward and much more cost effective compared with other interventions such as airway stenting or surgery.

Conclusion

The tricky nature of endobronchial tuberculosis, validity of investigations to reach the diagnosis and its airway compromising complications especially in the form of tracheobronchial stenosis are highlighted here to get clinicians’ awareness. Regarding the management aspect, in addition to anti-tuberculous medication, appropriate timely airway intervention therapy is often needed to overcome its troublesome complications. Among treatment options of bronchial stenosis, bronchoscopic balloon dilatation strategy is a low cost, minimally invasive interventional procedure and effective to relive symptoms of central airway obstruction and improve lung function. Such kind of therapeutic bronchoscopic procedures have been successfully carried out in upper and lower Myanmar Respiratory Medicine Bronchoscopy centers.

References

  1. World Health Organization, 2019. The sixth Joint TB Monitoring Mission report (2019) of National TB Program, Myanmar.
  2. Shahzad, T. & Irfan, M. (2016). Endobronchial tuberculosis – a review. J Thoracic Diseases: 8(12); p. 3797-3802.
  3. Kassam, N., M. et al (2000). Endobronchial Tuberculosis: A Rare Presentation. Cureus J of Med Science: 12(5); e8033. Doi: 10.7759/cureus.8033
  4. Casali, M, & Crapa, M., E. (2012). Endobronchial Tubercolosis: a peculiar feature of TB often underdiagnosed. J Multidisciplinary Respiratory Medicine: 7:35. doi:10.1186/2049-6958-7-35.
  5. Cohen, M., D. et al (1984). Balloon dilatation of tracheal and bronchial stenosis. American J Roentgenology: 142 (3); p. 477-478.
  6. Masayuki Tanahashi et al (2012). Bronchoscopic Balloon Dilation (BBD) for Benign Tracheobronchial Stenosis. In Global Perspectives on Bronchoscopy, ed. Sai P. Haranath; p. 135-148. ISBN: 978-953-51-0642-5, InTech.

Fig 1.(a) CXR of EBTB patient: nodular and linear infiltrates in left upper and middle zone with left lower lobe collapse. b) bronchoscopic finding; left main bronchus has mucopurulent secretion, hyperemic mucosa and whitish friable cheesy tissue in distal part.

Fig.(2a) CT-generated virtual bronchoscopy performed prior to bronchoscopic intervention demonstrates severe distal left main bronchus stenosis. b) bronchoscopic view from carina showing stenotic left main bronchus

Fig 3.(a) pre-balloon dilation bronchoscopic view shows severe stenosis of the left main bronchus at the distal end. b, c) during bronchoscopic balloon dilation procedure: left main bronchus was dilated with balloon dilatation catheter and inflation device. d) bronchoscopic view six months after demonstrates healing of laceration with significant regaining of luminal diameter of left main bronchus.

Author Information

Yin Mon Thant
Professor/Senior Consultant Chest Physician,
Department of Respiratory Medicine, Thingangyun General Hospital

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