NON-CARDIOGENIC PULMONARY EDEMA FOLLOWING CARDIAC ABLATION: WILL THE REAL CULPRIT PLEASE STAND UP?

Abstract

TOPIC: Diffuse Lung Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Non-cardiogenic pulmonary edema (NCPE) is an entity with a variety of etiologies and pathology that include alveolar damage due to direct toxicity or catecholamine surge. We present a case of non-cardiogenic pulmonary edema 48 hours following ablation for atrial fibrillation. CASE PRESENTATION: A 72-year-old woman with a history of atrial fibrillation, coronary artery disease with bypass grafting, and heart failure with preserved ejection fraction presented with sudden onset shortness of breath for a few hours. She had undergone cardiac ablation with pulmonary vein isolation and cavotricuspid isthmus line 2 days prior, with no periprocedural complications. She was tachypneic and hypoxic (oxygen saturation 51% on room air), with reduced breath sounds on auscultation but no peripheral edema or jugular venous distension. Laboratory workup was notable for leukocytosis, elevated N-terminal proBNP (9,853 pg/mL), elevated C-reactive protein (257 mg/L), with normal procalcitonin and negative viral panel, including SARS-CoV-2. Electrocardiography showed no acute abnormalities. Computed tomography (CT) of the chest did not show pulmonary embolism but demonstrated bilateral ground glass opacities. Oxygen was administered via high-flow nasal cannula, and diuresis was initiated in the inpatient setting. Echocardiography revealed mild left ventricular diastolic dysfunction, with left atrial enlargement and mild pulmonary hypertension (39 mm of Hg). Right heart catheterization demonstrated normal filling and pulmonary artery pressures (pulmonary capillary wedge pressure (PCWP) of 6 mm Hg and mean pulmonary artery pressure or 16 mm Hg). Systemic corticosteroids were empirically initiated for suspicion of an inflammatory etiology. The combination of steroids and diuresis produced symptomatic and radiographic improvement, and she was discharged with supplemental oxygen. Her oxygen was unable to be completely weaned off as of follow-up 6 weeks later. DISCUSSION: Catheter ablation for atrial fibrillation is a widely adopted rhythm control strategy with a favorable safety profile. NCPE appears to be an exceedingly rare complication of ablation, with only a few cases being reported in our literature review. The diagnosis of NCPE can be challenging to make, as it must be distinguished for cardiogenic edema. The lack of peripheral edema or jugular venous distension in our patient suggested the absence of cardiac etiology, but a right heart catheterization demonstrating normal PCWP definitively excluded it. Hypotheses for mechanisms for this reaction include a systemic inflammatory response syndrome, autoimmune reaction to ablation, and vagus nerve injury with consequent dysregulation of immunomodulation. Treatment is primarily supportive, including adequate ventilation, with consideration for diuresis and corticosteroids. CONCLUSIONS: NCPE is a rare adverse effect of ablation, and treatment is primarily supportive. REFERENCE #1: Weber R, Minners J, Restle C, et al. Pulmonary edema after extensive radiofrequency ablation for atrial fibrillation. J Cardiovasc Electrophysiol. 2008 Jul;19(7):748-52. DISCLOSURES: No relevant relationships by Dan Kazmierski, source=Web Response No relevant relationships by jacob miller, source=Web Response No relevant relationships by Pius Ochieng, source=Web Response No relevant relationships by NISHANT SHARMA, source=Web Response