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Epoprostenol for Worsening Hypoxemia of Hepatopulmonary Syndrome After Lung Transplantation
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A5168 - Epoprostenol for Worsening Hypoxemia of Hepatopulmonary Syndrome After Lung Transplantation
Author Block: E. Randhawa1, S. Bhandari2, N. Hinds3, D. Reich2; 1Internal Medicine Residency Program, Drexel University, Philadelphia, PA, United States, 2General Surgery, Drexel University, Philadelphia, PA, United States, 3Internal Medicine, Drexel College of Medicine, Philadelphia, PA, United States.
Introduction: Hepatopulmonary syndrome (HPS) is characterized by abnormal gas exchange caused by intrapulmonary vascular dilatation in the setting of liver disease; for which liver transplantation is the only known cure. Patients with a preoperative large alveolar-arterial oxygen gradient are at increased risk for post-operative hypoxemia. We report a case where a patient benefitted from Epoprostenol for severe hypoxemia after liver transplantation in the setting of HPS. Case Presentation: The patient is a 63 year old male with a history significant for NASH cirrhosis and HPS, on home oxygen 6L via nasal cannula, had presented for an Orthotopic Liver Transplant. Most recent pulmonary function tests showed normal spirometry with a severe diffusion abnormality and PaO2 on RA 41.6mmHg. Previous echocardiogram showed findings consistent with right to left shunting. Immediately post-operation, the patient was noted to be severely hypoxic; PaO2 60 on a PEEP of 10 and FiO2 of 100%. A CTA was done which was negative for a PE however pulmonary artery vasculature appeared dilated; Swan-Ganz Catheter located in RV showed systolic pressures of 30-35mmHg. Findings on repeat echocardiogram with bubble study were consistent with extracardiac shunting. The patient was placed in supine and started on Intravenous Epoprostenol at 0.21 mg/hr to improve V/Q matching. Post operative day 4 the patient had worsening hypoxia refractory to increases in PEEP and continued Epoprostenol. On Day 7, inhaled nitrous oxide and intravenous methylene blue were started and Epoprostenol stopped. There was an initial improvement in PaO2 followed by another worsening hypoxia. At this point the Epoprostenol was restarted. After 19 days of continued treatment, the Epoprostenol was weaned along with the ventilator settings to a PEEP of 8 and FiO2 50%. The patient eventually went for a tracheostomy and PEG tube placement and was able to be discharged to a LTAC. Conclusion: Severe hypoxia in HPS post liver transplant is a rarely documented entity. It is hypothesized that patients with severe hypoxia pre-transplant are at increased risk to be persistently hypoxic post transplant due to pulmonary vascular changes which may be more permanent. Treatment strategies should be aimed at improving V/Q matching while the pulmonary vasculature recovers.
Author Block: E. Randhawa1, S. Bhandari2, N. Hinds3, D. Reich2; 1Internal Medicine Residency Program, Drexel University, Philadelphia, PA, United States, 2General Surgery, Drexel University, Philadelphia, PA, United States, 3Internal Medicine, Drexel College of Medicine, Philadelphia, PA, United States.
Introduction: Hepatopulmonary syndrome (HPS) is characterized by abnormal gas exchange caused by intrapulmonary vascular dilatation in the setting of liver disease; for which liver transplantation is the only known cure. Patients with a preoperative large alveolar-arterial oxygen gradient are at increased risk for post-operative hypoxemia. We report a case where a patient benefitted from Epoprostenol for severe hypoxemia after liver transplantation in the setting of HPS. Case Presentation: The patient is a 63 year old male with a history significant for NASH cirrhosis and HPS, on home oxygen 6L via nasal cannula, had presented for an Orthotopic Liver Transplant. Most recent pulmonary function tests showed normal spirometry with a severe diffusion abnormality and PaO2 on RA 41.6mmHg. Previous echocardiogram showed findings consistent with right to left shunting. Immediately post-operation, the patient was noted to be severely hypoxic; PaO2 60 on a PEEP of 10 and FiO2 of 100%. A CTA was done which was negative for a PE however pulmonary artery vasculature appeared dilated; Swan-Ganz Catheter located in RV showed systolic pressures of 30-35mmHg. Findings on repeat echocardiogram with bubble study were consistent with extracardiac shunting. The patient was placed in supine and started on Intravenous Epoprostenol at 0.21 mg/hr to improve V/Q matching. Post operative day 4 the patient had worsening hypoxia refractory to increases in PEEP and continued Epoprostenol. On Day 7, inhaled nitrous oxide and intravenous methylene blue were started and Epoprostenol stopped. There was an initial improvement in PaO2 followed by another worsening hypoxia. At this point the Epoprostenol was restarted. After 19 days of continued treatment, the Epoprostenol was weaned along with the ventilator settings to a PEEP of 8 and FiO2 50%. The patient eventually went for a tracheostomy and PEG tube placement and was able to be discharged to a LTAC. Conclusion: Severe hypoxia in HPS post liver transplant is a rarely documented entity. It is hypothesized that patients with severe hypoxia pre-transplant are at increased risk to be persistently hypoxic post transplant due to pulmonary vascular changes which may be more permanent. Treatment strategies should be aimed at improving V/Q matching while the pulmonary vasculature recovers.
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