A46-33 Resolution of Pleural Effusion After Amiodarone Withdrawal Without Diuresis - A Diagnostic Clue

Introduction Amiodarone, a class III antiarrhythmic, is well known for its pulmonary toxicity, including interstitial pneumonitis, organizing pneumonia, alveolar hemorrhage, and nodules/masses (1). Pleural involvement, however, is rare and underreported (2, 3). There is limited data on isolated fissural effusions secondary to amiodarone. Early recognition is important, as management depends on addressing the underlying cause (4, 5, 6). Case Report A 73-year-old man, lifelong non-smoker, was referred to pulmonology for abnormal imaging. His history included myocardial infarction treated with angioplasty and deceased-donor kidney transplant after latent tuberculosis treatment. In 2022, he developed atrial fibrillation and was started on amiodarone and apixaban. Prior to the pulmonary appointment, the patient was experiencing low-grade fever, mild dyspnea, and productive cough. CT chest demonstrated fluid confined to the horizontal and oblique fissures, with adjacent ground-glass opacities and tree-in-bud changes (Figure 1). He had stable weight, appetite; no peripheral edema, orthopnea, or paroxysmal nocturnal dyspnea, and reported mask use at work. Concerned about side effects, he independently discontinued amiodarone and apixaban. At the pulmonology appointment, he was stable. No antibiotics or diuretics were initiated given lack of infectious or heart failure features. The plan was to monitor the patient and repeat imaging in two months. At follow-up two months later, the patient reported complete symptom resolution. Repeat CT showed complete clearing of fissural effusion and parenchymal findings. No further interventions were required. Discussion This case is suggestive of amiodarone-induced pleural effusion isolated to the horizontal and oblique fissures, rather than heart failure. The patient’s imaging showed a loculated fissural effusion with ground-glass and tree-in-bud infiltrates (figure 1), consistent with prior reports of amiodarone-induced pleural disease without significant parenchymal involvement (2). Other alternative causes of isolated fissural effusion, including heart failure, infection, malignancy, pulmonary embolism, or other drug-induced etiologies, were considered but deemed unlikely given the absence of clinical signs, imaging features, and rapid resolution following amiodarone discontinuation (4, 5, 6).The absence of heart failure is supported by the lack of clinical signs such as volume overload, orthopnea, paroxysmal nocturnal dyspnea, or peripheral edema. Patient had stable body weight and no diuretic therapy. This case adds to the limited body of literature documenting amiodarone-associated pleural effusions and highlights the importance of considering drug-induced pleural disease in patients who develop unexplained effusions.