Acute Interstitial Pneumonitis Secondary to Amiodarone

INTRODUCTION-Amiodarone pulmonary toxicity risk is estimated to be around 1 to 5 percent, depending on risk factors like daily dose exceeding 400mg/day, intake of drug for more than two months, age above 60 years, duration of treatment of 6 to 12 months and prior history of lung disease. CASE -A 70-year-old white male with diabetes, chronic kidney disease, hypertension and obstructive sleep apnea, presented with atrial fibrillation with rapid ventricular response and acute hypoxic respiratory failure. SARS-CoV-2 RNA test was negative and pulmonary embolism was ruled out by CT Angiogram of chest. He underwent Transesophageal Echocardiogram guided cardioversion showing low normal left ventricular function and absence of left atrial appendage or thrombus. He was discharged on a anticoagulant and a diuretic. 2 weeks later he was readmitted with recurrent atrial fibrillation with rapid ventricular response. He was loaded with amiodarone intravenously and then transitioned to oral Amiodarone 400 mg orally twice daily. After 5 days he deteriorated requiring intubation for respiratory failure. CT Chest on day 5 of amiodarone administration showed new changes in form of bilateral ground glass attenuation, septal thickening and bilateral airspace consolidation when compared to previous admission. Laboratory findings included: white blood count 14000/uL, procalcitonin 0.28ng/ml, CRP 90 mg/L, BNP and negative respiratory viral panel. Flexible Bronchoscopy was performed which showed edematous airways and thin secretions. RESULT-Bronchoscopic alveolar lavage showed normal cell count, foamy macrophages, no malignant cells, and no growth on any culture. Biopsy was held given the acuity of his condition. His blood cultures, infectious work up and autoimmune workup was negative. Amiodarone was stopped and 60 mg oral prednisone was started for possible amiodarone induced acute interstitial pneumonitis and he responded well. He was extubated by day 10 and was on tapering oral steroid schedule for 6 months. CONCLUSION-Amiodarone pulmonary toxicity is usually recognized after 2-3 months of treatment, especially in patients taking dosages higher than 400 mg/day. This case is unique given the acute onset. The major hypothesis suggested include cytotoxic injury due to drug phospholipid complexes, alteration of phospholipid bilayer and free radical induced cellular injury and indirect Immunologic reaction. Currently there are no guidelines to prevent it. Acute pneumonitis although presents rarely, needs high index of suspicion for early diagnosis and immediate treatment with high dose intravenous steroids because of increased risk of mortality.