0829 Workup of Nocturnal Hypoxemia Leads to Diagnosis of Patent Foramen Ovale

Abstract

Introduction Patent foramen ovale (PFO) in adults often remains asymptomatic until clinical manifestations such as cryptogenic stroke, migraine headache, air embolism, hypoxemia, or platypnea-orthodeoxia syndrome occur. In this case, prior workup of cryptogenic stroke failed to identify a PFO that was diagnosed after further investigation of polycythemia which revealed nocturnal hypoxemia on polysomnogram. Report of Cases: A 60-year-old male with history of recurrent venous thromboembolic events (VTE), secondary polycythemia, and cryptogenic strokes was referred for a polysomnogram during the evaluation of polycythemia. Over the span of six years, he had multiple cryptogenic strokes and VTEs in the setting of polycythemia and normal hypercoagulability labs. Further evaluation suggested secondary polycythemia after serum erythropoietin and JAK2 mutation testing were negative. The patient was a never smoker without evidence of malignancy or renal disease leading to suspicion that his polycythemia was due to hypoxemia despite normal oxygen saturations during point of care evaluations. He frequently reported shortness of breath during appointments. During a polysomnogram, the patient was found to have a total apnea-hypopnea index of fewer than 5 events per hour but demonstrated hypoxemia with 49.7% of total sleep time spent below an oxygen saturation of 90%. He was referred to pulmonology for further evaluation that showed normal resting oxygen saturation, no desaturation on a six-minute walk test, mild restrictive defect on pulmonary function testing, and a normal chest computed tomography with angiography. Prior transthoracic echocardiogram had demonstrated an atrial septal aneurysm without communication between the atrial chambers. No evidence suggestive of a right-to-left shunt was found on lateral imaging of the brain during a ventilation-perfusion scan. Further evaluation of the aneurysmal atrial septum on transesophageal echocardiogram with an agitated saline bubby study demonstrated a patent foramen ovale with a right-to-left shunt. In the setting of hypoxia leading to secondary polycythemia, the patient was scheduled for PFO closure. Conclusion Hypoxemia out of proportion to sleep-disordered breathing on polysomnogram should prompt further evaluation. Despite multiple prior strokes, our patient’s PFO had gone undiagnosed until polycythemia prompted a polysomnogram that demonstrated isolated nocturnal hypoxemia and prompted a further workup. Clinically significant hypoxemia is an indication for PFO closure. Support (If Any)