A CRAZY CAUSE OF CRAZY PAVING: AN UNUSUAL CASE OF AMIODARONE INDUCED LUNG TOXICITY

SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Amiodarone induced pulmonary toxicity is a well described entity that can present with an array of histopathologic and radiologic findings. The exact incidence of amiodarone pulmonary toxicity is estimated to between 1-10% of patients [1]. Radiologic findings vary and can include ground glass opacities, interlobular septal thickening, pulmonary nodules, reticulation, fibrosis and honeycombing [2]. Isolated unilateral findings of amiodarone pulmonary toxicity, as described in the case below, is far less common and not well described. CASE PRESENTATION: A 78 year old man with non-ischemic cardiomyopathy and atrial fibrillation on amiodarone, presented with dyspnea on exertion and a non-productive cough. He was afebrile and hemodynamically stable but was hypoxemic with an oxygen saturation of 80% on ambient air. His chest X-ray at the time showed diffuse reticular opacifications on the right side. A follow up CT of the chest showed extensive interlobular septal thickening and ground glass opacities in a “Crazy Paving” pattern on the right side only. On physical examination, the patient had bilateral lower extremity pitting edema and an elevated NT-ProBnp of 6660. Given constellation of clinical and radiologic findings, there was suspicion for cardiogenic pulmonary edema and the patient was treated with diuresis. Despite maintenance of negative fluid balance, the patient had increasing oxygen requirements and did not improve clinically. His radiologic findings had persisted as well, and a decision was made to pursue a surgical lung biopsy. Pathology of the biopsy showed acute organizing process as well as lipid laden or “foamy” macrophages. A diagnosis of unilateral amiodarone lung toxicity was made. The patient was started on glucocorticoids, amiodarone was discontinued and the patients clinical status improved. DISCUSSION: This case highlights a unique presentation of amiodarone induced pulmonary toxicity in that the findings on CT were quite significant but only found unilaterally. The pathology findings, in particular the foamy macrophages, are consistent with the diagnosis of pulmonary toxicity from amiodarone 3. This highlights the importance of recognizing amiodarone induced lung toxicity as prompt cessation of the drug and if indicated steroid therapy can result in significant clinical improvement CONCLUSIONS: Although less common, unilateral amiodarone pulmonary toxicity can occur. If the clinical timeline, symptoms, and radiologic features are otherwise consistent, consideration should be given to amiodarone induced pulmonary toxicity even with unilateral findings. Reference #1: Jackevicius CA, Tom A, Essebag V, et al. Population-level incidence and risk factors for pulmonary toxicity associated with amiodarone. Am J Cardiol. 2011;108(5):705-710. https://doi.org/10.1016/j.amjcard.2011.04.024 Reference #2: Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48. https://doi.org/10.1155/2009/282540 Reference #3: Schwaiblmair M, Berghaus T, Haeckel T, Wagner T, von Scheidt W. Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect? Clin Res Cardiol Off J Ger Card Soc. 2010;99(11):693-700. https://doi.org/10.1007/s00392-010-0181-3 DISCLOSURES: No relevant relationships by Erica Altschul, source=Web Response No relevant relationships by Nader Ishak Gabra, source=Web Response No relevant relationships by Oki Ishikawa, source=Web Response No relevant relationships by Omar Mahmoud, source=Web Response No relevant relationships by Bushra Mina, source=Web Response No relevant relationships by Maly Oron, source=Web Response No relevant relationships by Varun Shah, source=Web Response