Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect?

Several forms of pulmonary disease occur among patients treated with amiodarone, i.e. chronic interstitial pneumonitis, organizing pneumonia, ARDS, a solitary pulmonary mass of fibrosis. The prevalence is estimated to be about 5%. Two major hypotheses of amiodarone-induced pulmonary injury include direct cytotoxicity and a hypersensitivity reaction. Given the frequency and potential severity of amiodarone-induced pulmonary toxicity, early detection is desirable. Unfortunately, there are no adequate predictors of pulmonary toxicity due to amiodarone. Patients who should benefit from amiodarone should be carefully selected and the lowest effective dosage of amiodarone should be taken. Amiodarone-induced pulmonary toxicity is a diagnosis of exclusion. Pulmonary evaluation with chest X-ray and pulmonary function testing, including diffusion capacity for carbon monoxide is recommended when amiodarone is started. A documented decline in the diffusing capacity of greater than 20% is useful in suggesting the need for closer monitoring or for further diagnostic testing. Although the optimal frequency of follow-up has not been determined, most cases of amiodarone-induced lung injury develop during the first 2 years of treatment and disease onset usually is slow. Pulmonary function tests and imaging may be performed every 3–6 months, depending on the presumed individual risk. Treatment of amiodarone pulmonary toxicity consists primarily of stopping amiodarone. Corticosteroid therapy can be life-saving for severe cases and for patients with less severe disease in whom withdrawal of amiodarone is not desirable. Due to its accumulation in fatty tissues and long elimination half-life, pulmonary toxicity may initially progress despite drug discontinuation and may recur after steroid withdrawal. The prognosis of amiodarone lung disease is generally favourable.