Presentation
Progressive shortness of breath.
Patient Data
Dual lead pacemaker in situ. Median sternotomy wires and mediastinal clips in keeping with previous coronary artery bypass graft. Patchy infiltrates in the right mid and lower zones, as well as in the left lower zone. The heart borders are indistinct.
On the soft tissue windows, the liver and spleen are of high density on this non-contrast scan. The heart is enlarged. Basal predominance of reticular opacities, with ground glass shadowing, traction bronchiectasis and architectural distortion. Suggestion of honeycombing along the anterior subpleural surface of the left upper lobe. Large area of air trapping in the right middle lobe. There is also pneumomediastinum and small bilateral pneumothoraces.
Case Discussion
Amiodarone lung toxicity can occur at any time from the initial dose of amiodarone to more than a decade into treatment. Although not seen in this case, the presence of high density consolidation or masslike opacities are highly suggestive of this diagnosis.
The most common histologic manifestations are diffuse alveolar damage, organizing pneumonia and NSIP. Less commonly, eosinophilic pneumonia and pulmonary hemorrhage can occur. A distinctive feature of amiodarone lung is the presence of foamy histiocytes which contain intracytoplasmic osmiophilic lamellar bodies. However, this feature is also seen in patients with amiodarone exposure with no evidence of toxicity.
The presence of hepatic and splenic high density does not imply amiodarone hepatoxicity. This can be seen in the absence of toxicity.
In this case, pneumomediastinum and pneumothorax is presumably secondary to rupture of a small honeycomb or bleb. Traction bronchiectasis is indicative of established fibrotic changes. Ground glass opacification (GGO) in this context is non-specific. GGO is due to displacement of air at a resolution beyond HRCT, and may be due to reversible causes such as fluid and inflammatory cells, or irreversible causes ie fibrosis.
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