This is a 55‐year‐old woman who presented to our facility with worsening dyspnea and a productive cough. She was hospitalized more than 4 times recently for the same symptoms and was managed as a COPD exacerbation, but her symptoms were partially refractory to therapy. She had a history of hypertension on lisinopril 10 mg daily. She denied any family history of lung diseases. She was afebrile, with a pulse rate of 88, a blood pressure of 150/80, and a respiratory rate of 18. Chest auscultation revealed bilateral expiratory wheezing and rhonchi: the rest of the physical exam was unremarkable. A chest X‐ray revealed increased radiolucency of the lung, a flat diaphragm, and a long, narrow heart shadow. She was diagnosed with a COPD exacerbation and started on IV solumedrol 40 mg every 8 hours, albuterol, and iatropium every 4 hours via nebulization, and levaquin 500 mg IV daily. Pulmonary function tests (PFTs) showed a diminished expiratory flow, with notching on the flow‐volume loop. The diffusing lung capacity for carbon monoxide was normal. After 1 week of therapy, the patient did not improve, and her PFT results remained unchanged. A decision for bronchoscopy was made, and the test disclosed a more than 50% decrease in the airway cross‐sectional area during expiration because of an excessive bulging of the posterior membrane of the trachea and bronchi. She was therefore diagnosed with extensive dynamic airway collapse (EDAC) and placed on noninvasive positive pressure ventilation (NIPPV), with clinical improvement and subsequent discharge with a home CPAP machine.
EDAC is a rather frequent but underrecognized entity that can mimic COPD or asthma. Most published studies since 1960 have been case series and retrospective studies. To date, there are no classification, diagnosis, or management guidelines. It has been described as congenital or associated with chronic infections, smoking, endotracheal intubations, and long‐term ventilation. The presence of stridor or an obstructive flow‐volume curve with a notch should increase the suspicion of this pathology. The diagnosis is established during bronchoscopy, which unravels the invagination of the posterior membrane of the trachea and bronchus during expiration, leading to a reduction of the airway lumen by 50% or more (normal < 35%). Whereas steroids and bronchodilators improve COPD/asthma, they can theoretically worsen EDAC, as they decrease bronchial tone by soft‐tissue thinning and smooth muscle relaxation, respectively. In symptomatic cases, NIPPV represents the mainstay of treatment; it acts as a pneumatic stent to the collapsing airways. Smoking cessation and treatment of any underlying conditions are recommended. Support of the trachea and the main bronchi with a stent has been used in recalcitrant cases.
The purpose of reporting this case is to increase awareness of this entity as a COPD/asthma imitator while providing an up‐to‐date literature review
M. Kreidy, none; E. Kupersmith, none.
To cite this abstract:Kreidy M, Kupersmith E. Extensive Dynamic Airway Collapse: A COPD/Asthma Imitator. Abstract published at Hospital Medicine 2009, May 14-17, Chicago, Ill. Abstract 167. Journal of Hospital Medicine. 2009; 4 (suppl 1). https://www.shmabstracts.com/abstract/extensive-dynamic-airway-collapse-a-copdasthma-imitator/. Accessed November 11, 2019.