Case Presentation: A 69-year-old female with a history of Takotsubo cardiomyopathy, atrial fibrillation on Amiodarone since 2 months prior, type 2 diabetes who presented to the primary care clinic due to shortness of breath. She was diagnosed with community-acquired pneumonia 3 weeks ago that was treated with Doxycycline without improvement. She continued to spike fevers to 101.4 degrees Fahrenheit, accompanied by dry cough, orthopnea, and leg edema. She was admitted to the hospital as she was found to be tachypnic and hypoxic to 78% on room air with diffuse rales, 1+ leg edema, and bilateral grand glass opacities on computed tomography of the chest. Initial laboratory tests were remarkable for white blood cell of 11.4 K/μL, N-terminal-pro BNP of 2213 pg/mL (reference 0-899), and Creatinine of 1.63 mg/dL. Since her hypoxia worsened despite broad-spectrum antibiotics for presumable multifocal pneumonia as well as diuretics for pulmonary edema, she was transferred to intensive care unit on the day 5. Bronchoalveolar lavage (BAL) showed normal cell count with 4% lymphocytes and no eosinophil. As cultures remained negative from blood, sputum, and BAL, organizing pneumonia was suspected and Prednisone 1mg/kg/day was started on the day 6. Her oxygen was weaned from high-flow nasal cannula to nasal cannula on the day 9. She was discharged home on home oxygen therapy on the day 16.

Discussion: Amiodarone is an effective antiarrhythmic drug with a variety of side effects. Pulmonary toxicity can occur in up to 15% of patients. Interstitial pneumonitis (IP) is the most common form of the pulmonary toxicity that typically occurs after 2 months of the therapy as cytotoxic active metabolites accumulate in the lungs over time. 25% of Amiodarone-induced pulmonary toxicity can present as organizing pneumonia (OP). OP often mimics infectious pneumonia because OP may present as acute onset fever, cough, and pleuritic pain, refractory to antibiotics. BAL fluid analysis of OP vary from normal cell counts to lymphocytosis, neutrophilia, or eosinophilia, thus tissue biopsy may be required when the diagnosis is unclear. Our patient presented with fevers, dry cough, and shortness of breath with bilateral opacities consistent with infectious pneumonia refractory to oral antibiotics, but the onset (3 weeks ago) and the timing of starting Amiodarone (a few months prior) raised a concern of IP/OP when she worsened on broad-spectrum antibiotics. After clinical response is confirmed, steroid can be tapered slowly over 2-6 months.

Conclusions: Amiodarone-induced organizing pneumonia can mimic acute bacterial pneumonia. As the incidence of pulmonary toxicity is high, practitioners should keep the high index of suspicion in patients who present with respiratory symptoms on Amiodarone.