Abstract Introduction Negative-pressure pulmonary edema (NPPE) is a rare but potentially life-threatening form of non-cardiogenic pulmonary edema, occurring in approximately 0.05-0.1% of surgical patients. It results from forceful inspiratory efforts against a collapsed airway. Although literature primarily reports rapid resolution of NPPE with supportive care, progression to acute respiratory distress syndrome (ARDS) is exceedingly uncommon. We describe a severe case of NPPE evolving into ARDS in a high-risk patient following outpatient general anesthesia, emphasizing the importance of careful peri-extubation airway management in susceptible individuals. Case Report A 39-year-old woman with morbid obesity (BMI 48.7 kg/m²), obstructive sleep apnea (poor CPAP adherence), chronic kidney disease IV, hypertension, and diastolic dysfunction underwent an elective outpatient bilateral breast excisional biopsy under general anesthesia. The intraoperative course was uneventful. Immediately post-extubation, she developed acute dyspnea, pink frothy sputum, and severe hypoxemia. Arterial blood gas on 100% supplemental oxygen showed pH 7.20, PaCO2 65 mmHg, PaO2 140 mmHg. Imaging revealed diffuse pulmonary edema with preserved cardiac function. Despite non-invasive ventilation, respiratory failure worsened, requiring re-intubation, high positive end-expiratory pressure (PEEP 25 cm H2O), inhaled epoprostenol, and vasopressor support. Aggressive diuresis and lung-protective ventilation led to gradual improvement without extracorporeal membrane oxygenation (ECMO) or renal replacement therapy. She was extubated on day 11 and discharged on nocturnal bilevel positive airway pressure (BiPAP). Surgical pathology confirmed benign papillomas with no malignancy. Discussion Airway collapse from residual anesthetic effects and incomplete neuromuscular recovery may have led to sustained negative intrathoracic pressures, which drove hydrostatic capillary transudation and subsequent alveolar damage. Comorbidities such as morbid obesity, untreated OSA, and diastolic dysfunction may have amplified mechanical stress on alveoli, predisposing to barotrauma and secondary diffuse alveolar damage, thereby transforming a reversible NPPE episode into full-spectrum ARDS. NPPE may not follow the benign trajectory often described. Clinicians should maintain a high index of suspicion for NPPE in the peri-extubation period, especially in obese or OSA patients, and consider early airway support and monitoring. Conclusion Risk stratification and vigilant extubation practices are essential in patients with limited pulmonary reserve or OSA. Complete neuromuscular reversal, semi-upright positioning, immediate positive-pressure support, and extended post-anesthesia monitoring are critical preventive strategies. Early recognition and aggressive management are essential when negative-pressure pulmonary edema advances to secondary ARDS, as timely intervention can reduce morbidity and mortality. This abstract is funded by: None
Sorathia et al. (Fri,) studied this question.