Undiagnosed patent foramen ovale with bi-atrial thrombus in transit: A case of pulmonary embolism and refractory hypoxia Free

Background: Pulmonary embolism (PE) is a potentially life-threatening condition that can cause hypoxia, hemodynamic instability, and, rarely, paradoxical embolism through intracardiac shunts. While a patent foramen ovale (PFO) is present in approximately 20–30% of the adult population, the presence of a bi-atrial thrombus in transit across a PFO is extremely rare. Its presence often reflects elevated pulmonary pressures due to a large or chronic thrombotic burden. If not promptly recognized and treated, this condition carries a high risk of systemic embolization and mortality.

Case Presentation: An otherwise healthy 37-year-old female was admitted to a tertiary care academic center in Canada with an acute proximal left leg deep vein thrombosis (DVT) and saddle PE. Her risk factors for venous thromboembolism (VTE) included obesity and a laparoscopic hernia repair performed two months prior to admission. She was started on weight-based low-molecular-weight heparin (dalteparin) without dose capping.

Despite therapeutic anticoagulation, the patient remained persistently hypoxic throughout her hospitalization, requiring 4 L/min of supplemental oxygen via nasal cannula to maintain oxygen saturation above 92%. A transthoracic echocardiogram on admission revealed normal LV systolic function (LVEF 56%), moderate enlargement of the RV, moderate impairment of RV systolic function, moderate pulmonary hypertension (RVSP 66 mmHg), and moderate tricuspid regurgitation. A thrombophilia screen was negative for both inherited and acquired causes of VTE.

On day seven post-admission, the patient acutely decompensated and developed rapid atrial flutter, chest pain, and hypotension. Repeat bedside echocardiography demonstrated persistent right ventricular systolic dysfunction and a large, highly mobile thrombus extending from the right to left atrium across a previously undiagnosed PFO. The patient was transferred to the Cardiovascular Surgery service, where she underwent sternotomy and cardiotomy. Intraoperatively, a thrombus measuring 11.5 cm was found lodged across the PFO. The fossa ovalis was incised, the thrombus was removed in its entirety, and the PFO was closed. The patient's postoperative course was complicated by infective endocarditis involving her pulmonic valve; however, she recovered and was transitioned to warfarin for ongoing anticoagulation. Discussion: This case illustrates the rare but life-threatening occurrence of a bi-atrial thrombus in transit through a patent foramen ovale, resulting from elevated right heart pressures that permit paradoxical right-to-left shunting. The presence of this intracardiac thrombus likely accounted for the patient's refractory hypoxia despite anticoagulation. Although echocardiography is key for diagnosis, intracardiac shunts may be undetected without early imaging, especially in patients with PE and unexplained hypoxemia. In these cases, surgical thrombectomy with PFO closure tends to lead to better outcomes compared to anticoagulation or thrombolysis alone by decreasing the risk of systemic embolization and death. In cases of PE accompanied by persistent hypoxia or clinical deterioration, a thrombus in transit should be considered early in the diagnostic process to guide timely, definitive treatment.