Discussion
Diagnosis With Brief Discussion
- Diagnosis
- Amiodarone-induced pulmonary toxicity
- Radiologic Findings
- Fig. 1. Chest radiograph showing diffusely increased interstitial markings and ground-glass opacities (GGOs) in the left lung and right middle lung zones.
Figs. 2
- Brief Review
- Amiodarone is an iodinated benzofuran derivative used to suppress ventricular and supraventricular tachyarrhythmias. Pulmonary toxicity is one of the most serious adverse effects of amiodarone. Several forms of pulmonary disease occur among patients treated with amiodarone, including interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome, diffuse alveolar hemorrhage, pulmonary nodules and solitary masses, and pleural effusion. Other adverse effects of amiodarone include photosensitivity, blue-gray discoloration of the skin, thyroid dysfunction, corneal deposits, liver dysfunction, and bone marrow suppression.
Interstitial pneumonitis is the most common presentation of amiodarone-induced pulmonary disease. Interstitial pneumonitis usually presents after 2 months of therapy, especially in patients whose amiodarone dose exceeds 400 mg/day.
On chest radiography, interstitial pneumonitis due to amiodarone typically shows new, diffuse or localized, reticular, ground-glass, or mixed opacities. These changes may be migratory and can occur in the absence of symptoms. Pleural effusion is rare.
The computed tomography (CT) images of patients with amiodarone-induced interstitial pneumonitis may show areas of high attenuation in the lungs, liver, and spleen owing to the accumulation of iodinated amiodarone in tissue macrophages. Although this finding is specific to amiodarone use, it is not necessary for the diagnosis of amiodarone pneumonitis and may be seen in the absence of lung toxicity. Other high-resolution CT findings related to amiodarone-induced interstitial pneumonitis include diffuse (usually bilateral) ground-glass opacities and septal thickening. Honeycombing and traction bronchiectasis can also be seen.
The treatment of amiodarone-induced interstitial pneumonitis primarily consists of stopping amiodarone and, in more symptomatic patients, initiating systemic glucocorticoids. Owing to the accumulation of amiodarone in fatty tissues and its long elimination half-life (approximately 45 days), pulmonary toxicity may initially progress despite drug discontinuation.
Amiodarone is not recommended in patients who have recovered from amiodarone-induced pulmonary toxicity because of the risk of recurrent disease and progressive pulmonary fibrosis.
- Please refer to
Case 1054, Case 704, Case 593, Case 330, Case 176, Case 114, -
- References
- N Wolkove, m Baltzan. Amiodarone pulmonary toxicity. Can respir J 2009;16(2):43
Edward D Chan, Talmadge E King Jr, Amiodaron pulmonary toxicity. https://www.uptodate.com/contents/amiodarone-pulmonary-toxicity
- Keywords
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