B53-30 Liver Transplant as a Cure for Hypoxia

Abstract Introduction Hepatopulmonary syndrome (HPS) is a pulmonary complication of chronic liver disease characterized by hypoxemia secondary to dilated intrapulmonary vasculature. HPS has a progressive course and is associated with a two-fold increased risk of mortality compared to cirrhosis without HPS. The pathogenesis is multifactorial, involving impaired hepatic clearance of pulmonary vasodilators, increased production of vasoactive mediators, as well as release of vasoactive substances from translocated gut bacteria due to portal hypertension. Liver transplantation is the only definitive treatment shown to improve long-term survival in patients with severe HPS. Improvement of hypoxemia has been observed in most patients within 6 to 12 months post liver transplant. Case Report A 67-year-old female with a history of hepatitis C and alcohol-related cirrhosis presented with progressive dyspnea. Initial evaluation with stress echocardiography and CT chest were negative. She was referred to pulmonology for further workup. Pulmonary function testing (PFT) revealed reduced diffusion capacity and transthoracic echocardiogram (TTE) with bubble study revealed a patent foramen ovale (PFO). Despite PFO repair, she continued to require 6L of supplemental oxygen. Repeat TTE with agitated saline confirmed PFO closure but demonstrated late left-sided bubbles, suggesting extracardiac shunting. Arterial blood gas (ABG) analysis revealed a partial pressure of oxygen (PaO2) of 55 mmHg and an alveolar-arterial oxygen gradient (A-aO2) of 56.9 mmHg, consistent with severe hepatopulmonary syndrome (HPS). The patient was referred for and proceeded with living donor liver transplantation. At her pulmonary follow-up 4 months post-transplantation, she showed marked clinical improvement with complete resolution of hypoxemia and supplemental oxygen was discontinued. A 6-minute walk test demonstrated an oxygen saturation of 96% on room air, compared with 85% pre-transplant. Discussion HPS is characterized by the presence of underlying liver disease, intrapulmonary vascular dilatation on contrast-enhanced echocardiography, and arterial oxygenation abnormalities, defined by a PaO2 less than 80mmHg or an A-aO2 gradient greater than 15mmHg on room air (or greater than 20mmHg in patients over 64). Liver transplantation remains the only definitive treatment shown to reverse hypoxemia and improve survival in patients with HPS. Although medical therapies have been explored as bridging options, none show consistent benefit, and evidence is limited by lack of randomized controlled trials. Conclusion This case demonstrates complete resolution of severe HPS after liver transplantation, highlighting its curative potential. Clinicians should maintain a high index of suspicion for HPS in patients with hypoxemia and underlying liver disease to ensure timely diagnosis and management. This abstract is funded by: None