Severe refractory arterial blood desaturation in the course of acute pulmonary embolism successfully reversed with catheter-directed therapy

Right-to-left shunting through a patent foramen ovale (PFO) caused by increased right atrial (RA) pressure in the setting of acute pulmonary embolism (PE) may, in some patients, lead to severe hypoxemic respiratory failure refractory to oxygen therapy,¹ and is associated with adverse outcomes. Prompt identification of such a PE scenario may warrant early pulmonary artery reperfusion intervention, which can help reduce the thrombus burden and right heart overload, and improve blood oxygenation.^2-4

A 38-year-old woman with a history of polycystic ovary syndrome treated with oral contraceptives was admitted to the hospital due to acute bilateral PE (Figure 1A). On admission, she had resting dyspnea with respiratory rate over 36/min, blood pressure of 140/80 mm Hg, and severely decreased arterial oxygen saturation (SaO₂) of 75%, refractory to oxygen therapy with both a reservoir mask (15 l/min) and high-flow nasal cannula (60 l/min). Partial pressure of carbon dioxide on arterial blood gas analysis was 25.8 mm Hg. The patient had tachycardia of 110 bpm, normotension, elevated cardiac troponin of 0.282 ng/ml (reference range <⁠0.014 ng/ml), and the right-to-left ventricular ratio of 1.6 on computed tomography–angiography (angioCT). In light of these findings, she was considered at intermediate-high risk of early death, and unfractionated heparin was administered. Since no improvement in SaO₂ was achieved, continuous positive airway pressure noninvasive ventilation was used, which did not prevent further deterioration of SaO₂. Due to no signs of lung disease on CT, intracardiac shunting was suspected. Transthoracic echocardiography (TTE) revealed enlargement of the right heart cavities, with interatrial septum shift toward the left atrium (LA), and a visible right-to-left shunt on color Doppler imaging (Figure 1B). Intravenous bolus of agitated saline was used to confirm migration of microbubbles from the RA to the LA through a septal defect (Figure 1C). Despite hemodynamic stability, due to severe hypoxia the Pulmonary Embolism Response Team referred the patient for urgent reperfusion with catheter-directed, low-dose local thrombolysis to reduce the right heart pressures and prevent the right-to-left shunt. The aim was to improve oxygenation and minimize the risk of paradoxical emboli (Figure 1D) due to the presence of deep vein thrombosis. The catheter-based technique was chosen to avoid possible shunting of the systematically delivered thrombolysis to the LA. The treatment resulted in gradual reduction of dyspnea and improvement of SaO₂ to 99% on the nasal cannula with 2 l/min of oxygen flow after 3 hours of recombinant tissue plasminogen activator infusion. TTE performed after 24 hours showed reversed shifting of the interatrial septum toward the RA (Figure 1E). Transesophageal echocardiography performed over the next few days showed a PFO, without right-to-left shunting at rest (Figure 1F). The patient was discharged home after 8 days with no limitation in exercise tolerance. She was prescribed extended-duration oral anticoagulation with rivaroxaban at a full dose for the first 6 months, followed by a half-dose thereafter.¹

This case shows that in the setting of acute PE, severe hypoxemia refractory to oxygen supplementation should warrant investigation for intracardiac right-to-left shunting. Early reperfusion treatment using catheter-directed therapy led to rapid reversal of the shunt and improvement of SaO₂. Our patient did not present symptoms of paradoxical embolism during the acute phase of PE or in the next few days, and the desaturation was reversible; therefore, she was not found eligible for PFO closure.⁵