C46-04 Airway Hemosiderosis in Untreated Lung Segments Following Endobronchial Valve Therapy With Surgical Fissure Completion

Introduction Endobronchial valves (EBVs) are an established therapy for patients with severe emphysema and absent collateral ventilation, offering improvements in lung function, exercise capacity, and quality of life. However, the success of bronchoscopic lung volume reduction (BLVR) depends on complete lobar isolation, which can be limited by incomplete fissures that allow interlobar collateral ventilation. To address this limitation, artificial fissure completion using surgical or energy-based techniques has emerged as a strategy to expand EBV eligibility in patients previously deemed unsuitable for valve therapy. While this approach can optimize target lobe collapse, it also introduces new anatomic and physiologic changes whose downstream effects are not yet fully characterized. We report a case of airway hemosiderosis visualized on bronchoscopy and confirmed with histopathology following artificial fissure completion and EBV therapy. Case Presentation A 76-year-old male with severe centrilobular emphysema (FEV1 29% predicted, RV 237%, DLCO 13%) underwent Video-Assisted Thoracoscopic Surgery (VATS) fissure completion followed by EBV placement in the left upper lobe as part of the COMPLETE-1 trial. Post-procedural imaging confirmed successful target lobe atelectasis without pneumothorax or valve migration. The patient demonstrated initial symptomatic improvement and stable pulmonary function on follow-up. At a routine 9-month surveillance bronchoscopy, diffuse brown mucosal discoloration with a beaded, stippled appearance was noted within the bronchus intermedius and right lower lobe bronchi, regions anatomically distant from the treated lobe (Figure 1). Endobronchial biopsies revealed hemosiderin-laden macrophages confirmed by Prussian blue staining, without evidence of granulomas, vasculitis, malignancy, or infection. Discussion Known complications of EBV therapy—such as pneumothorax, COPD exacerbation, valve migration, and granulation tissue formation—are generally confined to the treated lobe. Airway hemosiderosis affecting untreated segments has not been previously described following combined fissure completion and BLVR. Hemosiderin-laden macrophages indicate prior alveolar hemorrhage, typically arising from capillary stress, vascular congestion, or microvascular injury. In this case, their distribution in non-targeted lobes suggests a localized hemodynamic or mechanical process rather than systemic inflammation. Altered pleural pressure and ventilation-perfusion redistribution following valve-induced lobar collapse may generate shear forces or vascular engorgement in adjacent lobes. Surgical fissure completion could further amplify interlobar pressure gradients, leading to subtle microvascular disruption and mucosal hemosiderosis. Such findings underscores the need for continued endoscopic surveillance and physiologic monitoring after artificial fissure completion.