A48-07 Superior Vena Cava Compression in Thoracic Air Leak Syndrome: A Rare Cause of Preload Failure Compression

Abstract Thoracic air-leak syndrome (TALS) is a rare, noninfectious pulmonary complication after allogeneic hematopoietic cell transplantation (HCT), often arising in patients with bronchiolitis obliterans syndrome (BOS) (1, 2). While TALS typically presents with respiratory compromise due to pneumomediastinum and subcutaneous emphysema, hemodynamic effects from mediastinal air have rarely been described. We present a unique case of superior vena cava (SVC) compression secondary to TALS and demonstrated by right heart catheterization (RHC). A 19-year-old man with mixed-phenotype acute leukemia underwent three allogeneic HCTs unfortunately complicated by BOS. One year later, he developed TALS with progressive pneumomediastinum and exertional dyspnea. During admission, patient had positional tachycardia and dizziness. Computer tomography of chest revealed extensive pneumomediastinum with extrinsic compression of the bilateral internal jugular veins and lower superior vena cava, raising concern for impaired venous return. Right heart catheterization was performed and showed a baseline mean right atrial pressure (mRA) of 9 mmHg and cardiac output (CO) of 5.14 L/min (cardiac index 2.81 L/min/m²). During Valsalva maneuver, mRA increased to 28 mmHg and CO fell to 1.76 L/min (CI 0.96 L/min/m²), consistent with preload limitation from SVC compression. A mediastinal drain was placed with gradual radiographic and symptomatic improvement. The patient was ultimately discharged home on room air a couple weeks later. This case highlights a rare cardiovascular manifestation of TALS with SVC compression causing preload failure and reversible low-output physiology. Although prior literature describes TALS primarily as a respiratory process (1, 2), this case demonstrates that mediastinal air can also produce significant mechanical vascular compromise, detectable only through invasive physiologic testing. To our knowledge, this is the first report documenting RHC-proven hemodynamic instability due to TALS. Recognition of this mechanism is critical in post-HCT patients with unexplained dyspnea or hypotension, as early drainage may be lifesaving. RHC with provocative maneuvers may confirm diagnosis, guide decompression, and inform transplant timing in refractory BOS and TALS. References 1. Moon MH, et al. Thoracic air-leak syndrome after allogeneic hematopoietic stem-cell transplantation: incidence, risk factors, and clinical outcomes. Transplantation. 2010;89(10):1347-1354. PMCID: PMC28588212.Vogel M, et al. Bronchiolitis obliterans and thoracic air-leak syndromes after bone marrow transplantation. Eur Respir J. 2006;27(3):526-532. This abstract is funded by: None