JRSM >
Volume 98, Number 1 >
Pp. 26-28
Department of Thoracic Surgery, Guy's Hospital, London, UK
Correspondence to: Mr A S Coonar, Cardiothoracic Surgery, 6th Floor East Wing, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK E-mail: Aman.Coonar{at}gstt.sthames.nhs.uk
The major cause of acquired benign tracheobronchial stenosis in the UK is prolonged intubation or tracheostomy. Infective causes include tuberculosis (TB).
CASE HISTORY
A recent immigrant from China, age 36, was admitted with weight loss, dyspnoea, stridor and pyrexia. Acid-fast bacilli were identified in his sputum and he was started on antibiotics for tuberculosis (TB). CT scan showed tracheal and right-main-bronchus stenosis. Peak expiratory flow rate (PEFR) was 40 L/min. He deteriorated and rigid bronchoscopy revealed a narrow stricture 10 cm below the vocal cords (Figure 1), which was dilated. He was transferred to our centre shortly after.
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A relapsing course followed, and six dilatations were performed over the next three months. To maintain tracheobronchial patency, stenting was undertaken. Under general anaesthesia the trachea was intubated with a rigid bronchoscope. The distance between the vocal cords and the level of obstruction was noted and a silicone Y stent (Hood) was sized and prepared (Figure 1). Bougies were inserted in both main bronchi. After preoxygenation the bronchoscope was removed and the stent was slid over the bougies and its position confirmed on bronchoscopy. Postoperatively the patient did well, and with nebulisers and physiotherapy his PEFR remained above 200 L/min.
Three months later he returned with dyspnoea and stridor. Bronchoscopy revealed intra-stent granuloma and dilatation was performed. A further dilatation was needed one week later; therefore, reconstructive surgery was planned. However, the patient returned to China and we have no information on his subsequent course.
COMMENT
Tracheobronchial stenosis is not a frequent complication of pulmonary TB. It was present, for example, in only 114 (5.9%) of 1938 cases managed in a tertiary centre in Korea.1 Factors in pathogenesis include implantation of mycobacteria in the airway from a parenchymal lesion, direct infiltration from an adjacent node, and peribronchial extension through lymphatic drainage or haematogenous spread. Stenosis may arise from extrinsic compression, from a large mural lesion or from excessive inflammatory and fibrous reaction affecting the airway wall. In many cases it will respond to antituberculosis drugs together with steroids to suppress the inflammation; however, additional measures are sometimes needed. We looked at the published experience by searching PubMed and Ovid using the terms 'tracheobronchial stenosis' or 'tracheal stenosis' and 'tuberculosis'. 38 reports were identified, two-thirds of which came from East Asia. 7 were relevant (Table 1). Dilatation seems an effective and safe treatment. Of 59 patients in one series, 83% reported substantial improvement in symptoms.2 Complications were few: in a total of 101 dilatations there were two cases of deep mucosal lacerations (both of which had healed at one month), and one of bronchospasm. However recurrence was common: 80% of patients had a primary relapse of airway stenosis and 43% had a secondary relapse. Recurrence is the usual reason for stent insertion. Since retrieval of metallic stents can be difficult, non-metallic stents are preferred for the management of benign disease; they can be left in situ for long periods. Complications of stents include migration, granuloma formation and obstruction.9 In some cases surgical resection of the stenotic segment together with bronchoplastic reconstruction is a possibility.
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With the increasing incidence of TB, UK clinicians need to be sensitive to this cause of stridor, especially in groups at high risk.
Acknowledgments
Our thanks to Mr Jules Dussek FRCS, emeritus consultant thoracic surgeon.
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