Amiodarone-induced pulmonary toxicity presenting as pulmonary alveolar proteinosis.
Recommended Citation
Pinto J, Stone C, Jennings J, and Thavarajah K. Amiodarone-induced pulmonary toxicity presenting as pulmonary alveolar proteinosis. Am J Respir Crit Care Med 2015; 191.
Document Type
Conference Proceeding
Publication Date
2015
Publication Title
Am J Respir Crit Care Med
Abstract
Amiodarone-induced pulmonary toxicity (APT) has been described as presenting wih organizing pneumonia, diffuse alveolar damage, nodules, usual interstitial pneumonia, desquamative interstitial pneumonia and diffuse alveolar hemorrhage. We present a case of APT presenting with secondary pulmonary alveolar proteinosis (PAP). Case: A 74-year-old female, never-smoker with past medical history significant for congestive heart failure, hypertrophic obstructive cardiomyopathy and atrial fibrillation, at which time she was treated with cardioversion and amiodarone. She was readmitted 6 weeks later with dyspnea and hypoxia despite outpatient diuresis. Rheumatologic review of systems was unremarkable. She denied culprit occupational or environmental exposures or history of recurrent infections. Physical exam showed diffuse crackles and lower extremity edema. Laboratory values were notable for white blood cel count of 11.7 K/uL (neutrophil predominant), sedimentation rate 116 mm/hr, BNP 577, negative antinuclear, cyclic-citrullinated peptide and anti-neutrophilic cytoplasmic antibodies and rheumatoid factor. Chest x-ray showed interstitial opacities mildly progressed compared to chest imaging 1 and 6 months prior. Chest Computed Tomography revealed bilateral patchy ground glass opacities and consolidation, irregular septal thickening, air bronchograms, and air-trapping. Right heart catheterization revealed pulmonary artery pressure 45/16 (mean 26) mmHg, pulmonary capillary wedge pressure14 mmHg and cardiac output of 3.08 L/min. Subsequent bronchoalveolar lavage (BAL) was turbid-appearing with 329 white blood cells cu/mm (47% neutrophils, 47% macrophages, 4% eosinophils.) BAL bacterial, fungal, mycobacterial stains and cultures, pneumocystis antigen and viral cultures were negative. Transbronchial biopsies were aborted due to significant hypoxemia and hypervascular-appearing bronchial mucosa. BAL cytology was remarkable for foamy macrophages positive for Periodic-acid Schiff (PAS) staining. Electron microscopy showed uniform-appearing lamellar bodies within the macrophages. The patient declined surgical lung biopsy. She was treated with discontinuation of amiodarone and systemic corticosteroids prior to pursuing further workup for secondary PAP or whole lung lavage. She was seen in follow up two weeks later with improving dyspnea, exercise tolerance, and oxygenation. Subsequent chest imaging revealed clearing of pulmonary infiltrates. Discussion: BAL findings of foamy macrophages and lamellar bodies on electron microscopy are used to support a diagnosis of APT. These features are also seen in secondary PAP, providing a challenge to reaching a definite diagnosis. We share a case of APT with clinical features of PAP to highlight this under-recognized manifestation of APT.
Volume
191
