Amiodarone toxicity mimicking metastatic lung disease and liver findings: The continuing diagnostic challenge

Learning Objectives The most serious adverse reaction of amiodarone is pulmonary toxicity which may manifest as chronic interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome, pulmonary mass or nodules. The presence of foamy macrophages on biopsy confirms exposure to amiodarone but not necessarily prove causation. Most patients with AIPT respond well to drug withdrawal. The diagnosis is of exclusion. Multiple cardiac abnormalities, liver hyper density and pattern of lung lesions on PET-CT should alert the clinician for possible diagnosis of amiodarone toxicity without clinical information.

Amiodarone induced pulmonary toxicity may typically present as nonspecific interstitial pneumonia, patchy interstitial inflammation or nodular areas of densities with differential diagnosis on CT and PET-CT including neoplasm. The diagnosis largely relies on imaging. Presentation can be variable, as high CT attenuation nodular or mass-like lung densities with increased FDG uptake because of the presence of iodine-rich amiodarone in type II pneumocytes and may mimic neoplasm. Typically biopsies show foamy histiocytes with absence of malignant cells which confirms exposure to amiodarone but not necessarily prove causation. Most patients with AIPT respond well to the withdrawal of amiodarone and addition of corticosteroids. However, symptoms and radiological abnormalities may take months (2-12 months) to resolve completely owing to the long half life of the amiodarone metabolites. High uptake of FDG is similar to false positive PET scans occasionally reported in lipoid pneumonia as well as in other inflammatory or infectious lung disorders. The mechanisms involved in AIPT are not well defined. Hypotheses include direct dose related toxic reaction, membrane disrupting toxic drug-phospholipid complex accumulation and toxic oxygen species generation by amiodarone.