Abstract Introduction Tracheobronchomalacia (TBM) is a condition characterized by abnormal collapsibility of the cartilaginous airways. TBM mainly affects the central airways and may mimic common obstructive lung diseases. In this case, cardiopulmonary exercise testing (CPET) and Airway Oscillometry (AOS) were used to further characterize a patient’s complex airway dysfunction. Case description A 51-year-old female with a history of smoking and seronegative polyarthritis presented with two years of dry cough and exertional dyspnea. Initial pulmonary function testing demonstrated severe airflow obstruction without bronchodilator responsiveness (post-bronchodilator FEV1 45%, z-score -3.95). FVC and diffusing capacity were preserved. Cardiac work-up was negative and symptoms were refractory to a therapeutic trial of bronchodilator therapy. Flexible bronchoscopy revealed 50% collapse of the trachea, right mainstem, and left mainstem bronchi during exhalation. Bronchoalveolar lavage revealed normal cellular counts and microbiological data was negative. Dynamic CT chest demonstrated high-grade narrowing of the trachea and proximal bronchi on expiratory phase, thickening of cartilaginous structures of the trachea and medium sized airways, and mucus plugging in the small airways. To further characterize this patient’s dyspnea in the setting of complex airways disease, she underwent cardiopulmonary exercise testing (CPET). AOS was performed pre- and immediately post-CPET. The CPET was a submaximal test due to effort, but indicated dynamic hyperinflation and expiratory flow limitation. Pre-exercise AOS revealed abnormal resistance and reactance. Post-exercise AOS revealed decreased reactance (X5, reactance at 5 Hz; AX, area under the reactance curve), increased resonant frequency (Fres), increased low-frequency resistance (R5, resistance at 5 Hz), and increased frequency dependence of resistance (R5-R20) compared to pre-CPET AOS. Resistance at high frequency (R20, resistance at 20 Hz), which is more suggestive of large airway dysfunction, did not significantly change post-exercise (Figure 1). The AOS findings indicated that small airways dysfunction may be a more significant contributor to the patient’s exertional dyspnea than dysfunction of the larger airways. She was ultimately diagnosed with relapsing polychondritis. Dyspnea, cough, and FEV1 improved following treatment with prednisone, mycophenolate, and infliximab. Discussion Post-CPET AOS revealed significant changes to resistance and reactance associated with the small airways, but no significant change in resistance associated with the large airways. These findings may indicate that the patient’s exertional dyspnea did not primarily originate from large airway collapse but may have been predominately due to small airways dysfunction. More study is needed to determine if AOS can reliably discriminate between symptoms arising from large airway collapse and small airways dysfunction. This abstract is funded by: None.
Glozman et al. (Fri,) studied this question.