Discussion
Diagnosis With Brief Discussion
- Diagnosis
- Amiodarone pulmonary toxicity
- Radiologic Findings
- (Fig. 1-2) Chest computed tomography (CT) scans with lung window show interstitial thickening, subpleural ground-glass opacities and partial consolidation in both lower lobes.
(Fig. 3) Noncontrast CT scan with mediastinal window shows slightly increased attenuation of the liver relative to the spleen.
(Fig. 4-5) Follow up chest CT images show improved interstitial thickening and GGOs in both lungs.
- Brief Review
- The patient had a history of atrial fibrillation treated with amiodarone. After discontinuation of amiodarone, interstitial thickening, and GGOs improved on CT scan.
Pulmonary drug toxicity is a common and possibly underdiagnosed cause of acute and chronic lung disease. Amiodarone is an antiarrhythmic agent commonly used to treat supraventricular and ventricular arrhythmias. This drug is an iodine-containing compound that tends to accumulate in several organs, including the lungs. Amiodarone pulmonary toxicity (APT) occurs in approximately 5% - 10% of patients usually within months of starting therapy. Although there is no correlation between the development of drug toxicity and the duration of therapy or total accumulative dose, the risk is increased if the daily maintenance dose is greater than 400mg and if the patient is elderly. Although the incidence of this complication has decreased with the use of lower doses of amiodarone, it can occur with any dose.
Radiology plays a central role in diagnosis. Chest x-rays reveal patchy of diffuse infiltrates, which are commonly bilateral. Nonspecific interstitial pneumonia (NSIP) pattern is the most common manifestation of amiodarone-induced lung disease. Pleural inflammation is an accompanying feature and can manifest as pleural effusion. Organizing pneumonia (OP) pattern is less common and typically occurs in association with NSIP. Focal, homogeneous pulmonary opacities are typically peripheral in location and of high attenuation at CT due to the incorporation of amiodarone into the type II pneumocytes.
Patients usually have dyspnea, hypoxemia, exertional desaturation and sometimes weight loss. Diffuse crackles are heard on auscultation.
With early detection, the prognosis is good, with most patients improving after discontinuation of therapy and administration of corticosteroids. A minority of patients experience acute, severe lung injury resulting in death.
- References
- 1. Rossi SE, Erasmus JJ, McAdams HP, Sporn TA, Goodman PC. Pulmonary drug toxicity: radiologic and pathologic manifestations. Radiographics. 2000;20(5):1245-1259. doi:10.1148/radiographics.20.5.g00se081245
2. Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48. doi:10.1155/2009/282540
- Keywords