Abstract Introduction Re-expansion pulmonary edema (RPE) is a rare but potentially fatal complication of rapid lung re-inflation with mortality reported up to 20%. It typically develops within hours of thoracentesis or pneumothorax evacuation and involves pulmonary microvascular injury, inflammatory mediator release, and increased capillary permeability associated with mechanical stress on the re-expanding lung. While transient pulmonary pressure elevations have been described, to our knowledge, severe acute pulmonary hypertension (PH) with right ventricular (RV) failure has not previously been reported. Description of Case A 54-year-old woman with metastatic triple-negative breast cancer undergoing palliative chemoradiotherapy presented with progressive dyspnea and edema. Chest radiograph showed a large left pleural effusion with near-complete lung collapse and mediastinal shift. Two liters of pleural fluid were drained via vacuum bottles. Within one hour, she developed acute hypoxemic respiratory failure; imaging revealed new bilateral opacities consistent with RPE, prompting intubation and ICU transfer. Despite lung-protective ventilation, deep sedation, neuromuscular blockade, dexamethasone, and diuresis, she progressed to circulatory shock. Echocardiography demonstrated a dilated RV (6.0 cm) and severe PH (PASP 125 mmHg) with preserved LV function, consistent with an acute RV afterload crisis. She was treated with inhaled nitric oxide (max 45 ppm) and intravenous epoprostenol (max 2 ng/kg/min), achieving rapid improvement in oxygenation and hemodynamics. By day 3, PASP fell to 84 mmHg and RV size decreased to 4.3 cm. By day 5, epoprostenol was weaned to 1.5 ng/kg/min and sildenafil 20 mg TID was initiated as bridging therapy, and epoprostenol weaned off over 32 hours. By day 10, she was extubated to high-flow nasal cannula and off vasopressors. Repeat echocardiogram showed normal RV, LV and PASP (28 mmHg), and she was downgraded on nasal cannula to the medical wards to complete a 2-week sildenafil taper. She was subsequently discharged to skilled nursing facility. Discussion This case demonstrates RPE driving catastrophic but reversible PH with complete resolution within two weeks. Although the presentation met Berlin ARDS criteria, the primary insult was vascular rather than parenchymal—an acute, reversible RV afterload crisis. Recovery depended on early recognition and targeted pulmonary vasodilator therapy. Key lessons include: (1) RPE can mimic ARDS but represents a distinct, rapidly reversible pathophysiology; (2) echocardiography is essential to identify acute PH and guide therapy; and (3) pulmonary vasodilators such as inhaled nitric oxide, epoprostenol, and sildenafil can be lifesaving. Preventive measures include limiting pleural effusion drainage to ≤ 1.5 L and avoiding high-vacuum suction. This abstract is funded by: none
Rose et al. (Fri,) studied this question.
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