1291 Persistent Obstructive Sleep Apnea After Marked Post-Bariatric Surgery Weight Loss: A Case Report from the Miami VA

Abstract Introduction Weight loss following bariatric surgery is associated with substantial improvement in obstructive sleep apnea (OSA), with prior studies demonstrating that a ≥10% reduction in body weight may decrease the apnea–hypopnea index (AHI) by up to 50%. Despite these improvements, complete resolution of OSA is uncommon, and many patients do not undergo repeat sleep evaluation after significant weight loss. This case highlights the importance of reassessing sleep-disordered breathing following major post-bariatric weight reduction, particularly when obesity hypoventilation syndrome (OHS) was previously suspected. Report of case(s) A 61-year-old veteran was diagnosed in 2015 with severe OSA on home sleep apnea testing, demonstrating a respiratory event index (REI) of 66 events/hour (supine REI 93 events/hour), oxygen saturation nadir of 48% and 78 minutes with SpO₂ < 88% at a body mass index (BMI) of 56. An in-laboratory positive airway pressure (PAP) titration revealed persistently severe residual respiratory events across all tested pressures (titration AHI 98.5 events/hour; supine AHI 121.5 events/hour), profound REM-related hypoxemia (nadir 56%), treatment-emergent central sleep apnea, and limited pressure tolerance, precluding identification of effective settings. Auto–bilevel PAP was initiated empirically. In the absence of arterial blood gas data, severe nocturnal hypoxemia and mildly elevated serum bicarbonate (26–27 mmol/L) raised concern for OHS. Following Roux-en-Y gastric bypass surgery, the patient achieved a sustained 57.3% total body weight reduction (440 lb to 188 lb; BMI 56 to 27). After a nine-year lapse in follow-up, he re-presented in 2025 with persistent hypersomnolence (Epworth Sleepiness Scale 16) and insomnia (Insomnia Severity Index 25). Serum bicarbonate was 23 mmol/L. Repeat polysomnography demonstrated residual moderate OSA (AHI 25.2 events/hour; supine AHI 41.9 events/hour; non-supine AHI 8.8 events/hour), oxygen saturation nadir 78%, and 6 minutes with SpO₂ < 90%, representing a 61.8% reduction from baseline. Conclusion Despite profound weight loss and normalization of biochemical markers previously suggestive of hypoventilation, clinically significant OSA persisted. Weight reduction alone is an unreliable marker of OSA resolution. Repeat polysomnography after weight stabilization is essential to reassess residual disease, evaluate hypoventilation risk, and optimize long term therapy. Support (if any)