STRIDOR IN A PATIENT WITH PULMONARY TB: CHASING A TRACHEAL RODENT

Abstract

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: TB is an airborne infectious disease caused by Mycobacterium tuberculosis with the respiratory system being the most commonly involved. The involvement of airways is much less common than the lung parenchyma CASE PRESENTATION: A 38-year-old female patient with a past medical history of asthma and recently diagnosed with active pulmonary tuberculosis 6 months prior, on treatment with pyrazinamide, isoniazid, and rifampicin presented with c/o noisy breathing for 3 months. Was initially treated with bronchodilator and steroids with marginal improvement. Radiological evaluation revealed multiple cavitary lung nodules with tracheal stenosis as well right bronchus intermedius stenosis. Bronchoscopy revealed a stenotic segment measuring 2.5 cm, in the proximal trachea with residual airway which was not amenable to be passed through by bronchoscope. The stenotic lesion was biopsied and sequentially dilated to permit further advancement of the scope. There were no other stenotic segments. Several areas most notably at the distal main trachea and right main stem had what appeared to be caseating material coming through the wall of the airway with significant inflammation. Microbiological examination of bronchial washings and tissue samples did not reveal acid-fast bacilli. And this was not unexpected as the patient has already been on antituberculous treatment. Differentials of the tracheal stenosis including wegners, and other connective tissue disorders were ruled out after extensive serological testing DISCUSSION: During the pre-antibiotic era tracheobronchial tuberculosis was reported in 10-20% of all patients with pulmonary tuberculosis. The development of effective antitubercular drugs paralleled the decline in the incidence of tuberculosis in general and that of the trachea and bronchus. The pathophysiological mechanism of tracheal involvement includes implantation of organisms from infected sputum, extension to the peribronchial region by lymphatic drainage from parenchymal infection, direct extension from adjacent parenchymal infection, lymph node erosion, or hematogeneous spread. The disease progress in stages from simple erythema and edema with lymphocytic infiltration of the submucosa followed by tubercle formation. The end result is trachea bronchial narrowing secondary to fibrosis ensuing from extensive mucosal and submucosal tissue destruction. The common CT findings in the acute stage are smooth or irregular wall thickening causing. The role of steroids in the treatment is controversial with variable reports of efficacy during the early granulomatous phase. The mainstay of treatment remains to be antituberculous chemotherapy. Airway patency can be achieved by serial staged bronchoscopic-guided dilatation or stent insertion. CONCLUSIONS: A high index of suspicion will aid in early diagnosis and possible prevention of debilitating airway narrowing in tracheobronchial Tuberculosis. REFERENCE #1: Lee JH, Park SS, Lee DH, et al. EndobronchialTuberculosis: Clinical and Bronchoscopic Features in 121Cases. Chest 1992;102:990-4. REFERENCE #2: Jung SS, Park HS, Kim JO, et al. Incidence and clinicalpredictors of endobronchial tuberculosis in patients withpulmonary tuberculosis. Respirology 2015;20:488-95. REFERENCE #3: Kashyap S, Solanki A. Challenges in EndobronchialTuberculosis: From Diagnosis to Management. Pulm Med2014;2014:594806. DISCLOSURES: No relevant relationships by Muhammad Ahsan, source=Web Response No relevant relationships by Nadish Garg, source=Web Response No relevant relationships by Killol Patel, source=Web Response No relevant relationships by ARCHANA SREEKANTAN NAIR, source=Web Response