THE ENIGMATIC CASE OF RECURRENT VENTILATORY DEPENDENT RESPIRATORY FAILURE

Abstract

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Amiodarone, one of the most frequently prescribed antiarrhythmic medications in the United States, is associated with serious side effects including amiodarone-induced pulmonary toxicity (APT). One needs high suspicion to diagnose APT as the presentation can be misdiagnosed as pneumonia and heart failure. CASE PRESENTATION: A 74-year-old Caucasian female presented to the emergency department with progressively worsening shortness of breath and dry cough. She had a past medical history of left ventricular diastolic dysfunction, atrial fibrillation (on amiodarone 200mg/day), rheumatoid arthritis (RA), and 2 prior episodes of ventilatory dependent respiratory failure. On examination, the patient was hypoxemic on room air and had bibasilar lung crackles. BNP was elevated and Chest x-ray showed vascular congestion and perihilar infiltrates. The patient was placed on BiPAP for respiratory support and admitted to CCU for acute hypoxic respiratory failure secondary to CHF exacerbation. Diuretics did not improve the patient's condition and subsequent infectious workup was negative. CT chest showed patchy air-space consolidation and ground-glass opacities. Upon further interrogation, it was found that she was started on amiodarone 4 years back and multiple intubations for respiratory failure reported within the previous 2 years which responded to steroids. Amiodarone-induced pulmonary toxicity was diagnosed based on surgical lung biopsy revealing vacuolated foamy macrophages in alveolar pneumocytes, bronchial epithelial cells, and endothelial cells with diffuse interstitial pneumonitis and fibrosis. Amiodarone was discontinued and steroids were started at 1 mg/kg with a slow taper. The patient was subsequently extubated. DISCUSSION: Though APT can occur at any time after treatment is initiated, patients on a daily dose of 400 mg for >2 months or 200 mg daily for >2 years are at high risk. The reported incidence rate varies from 1.6 to 15% for daily doses of 400mg or less. The risk factors include > 60 years, high levels of des-ethyl metabolite, pre-existing lung disease, history of cardiothoracic surgery, use of iodinated contrast media, and/or use of high oxygen mixtures. Pathophysiology is direct cytotoxicity due to reactive oxygen species and the angiotensin enzyme system activation. In this patient, the diagnosis was delayed because the respiratory decompensation was attributed to heart failure. Despite adequate diuresis with central venous pressure of 6 cm H20 and negative infectious workup, her respiratory symptoms did not resolve. We were able to pinpoint the culprit behind her respiratory failure with a surgical lung biopsy and a history of amiodarone exposure. CONCLUSIONS: Strong index of suspicion for APT is necessary for prompt diagnosis in patients receiving amiodarone and presenting with respiratory symptoms. Reference #1: Schwaiblmair M, Berghaus T, Haeckel T, Wagner T, Von Scheidt W. Amiodarone-induced pulmonary toxicity: an under-recognizedand severe adverse effects?.Clin Res Cardiol 2010; 99:693–700 Reference #2: Kitaichi M. Differential diagnosis of bronchiolitis obliterans organizing pneumonia. Chest 1992; 102 (suppl.):44S-49S Reference #3: Marchlinski FE, Gansler TS, Waxman HL, Josephson ME. Amiodarone pulmonary toxicity. Ann Intern Med 1982; 97: 839-845. DISCLOSURES: No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Mashrutee Maharaul, source=Web Response No relevant relationships by SHREY SHAH, source=Web Response No relevant relationships by ARCHANA SREEKANTAN NAIR, source=Web Response