An 84‐year‐old cattle farmer presented to the emergency room with a 5‐day history of dry cough, progressive shortness of breathb and temperature to 39.4°C. Past medical history included coronary artery disease and atrial fibrillation. Amiodarone, pravastatin, warfarinb and isosorbide mononitrate were prescribed medications prior to hospital admission. His initial blood pressure was 81/49 mm Hg, pulse 76 bpm, temperature 36.4°C, oxygen saturation 88% while breathing ambient air. Serum studies showed neutrophilpredo‐minate leukocytosis, hemoglobin 10.7 (from 15 g/dL), and INR 5.9. Chest radiograph disclosed diffuse right lung infiltrates. Supplemental oxygen and antibiotics were initiated for community‐acquired pneumonia. The patient developed progressive infiltrates, dyspnea, and scant hemoptysis over the next 5 days. His antibiotic coverage was broadened and corticosteroids initiated. The patient was intubated for hypoxic respiratory failure 2 days later. Blood and sputum cultures were negative along with serologic testing for Brucella, Q fever, respiratory syncytial virus, histoplasma, and aspergillus; antinu‐clear antibody was normal. Amiodarone was discontinued, and bronchoscopy revealed blood in the small airways bilaterally. High‐resolution computed tomography scan showed bilateral alveolar consolidation most pronounced in the right upper lobe with increase attenuation in the areas of significant disease. Patient was extubated after the family requested discontinuation of care and was discharged with hospice 22 days after admission.
Amiodarone toxicity infrequently present as acute pneumonitis with fevers, pulmonary infiltrates, and leukocytosis, mimicking pneumonia. Differentiation is imperative, as the mainstay of management involves early discontinuation of amiodarone and use of corticosteroids. Despite these measures, once acute respiratory distress syndrome (ARDS) develops in this setting, mortality is as high as 50%. This is partially a result of the long half‐life of this highly lipid‐soluble drug that allows distribution in soft tissues and fat. Another important aspect of treatment is avoidance of high‐flow oxygen, as it can accelerate respiratory failure through free‐radical injury to the alveolar lining cells. This may have contributed to our patient's demise. The adverse effect of supplemental oxygen is 1 method by which amiodarone is believed to cause diffuse alveolar damage and ARDS in patients after cardiac and pulmonary surgery. Interestingly, recent publications have postulated that amiodarone may be the cause of ARDS in medical intensive care units more often than previously believed.
Rapidly progressive acute pneumonitis is a less frequent but serious manifestation of amiodarone‐induced lung disease. High‐flow oxygen should be avoided in these patients.
K. Khosa ‐ none; L. Pilar ‐ none; F. Biscardi ‐ none
To cite this abstract:Khosa K, Pilar L, Biscardi F. Another Cause of Pneumonitis and Ards. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 312. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/another-cause-of-pneumonitis-and-ards/. Accessed January 24, 2020.