Amiodarone induced lung toxicity: a radiological overview that simulating COVID19 infection disease

Abstract

Amiodarone-induced pulmonary toxicity (AIPT) is among the most serious adverse effects and is one of the leading causes of death associated with its use. It is a clinical pathology that is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. Those effects reach a plateau at a cumulative dose bigger than 150g. Patient’s comorbidities; oxygen therapy, invasive procedures or surgical interventions can trigger the pulmonary symptoms induced by amiodarone toxicity. The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Despite significant advances in the understanding of AIPT, its aetiology and pathogenesis remain incompletely understood. The role of steroids in the management of pulmonary toxicity from amiodarone is debatable, however, most reports of improvement after amiodarone withdrawal di"er little from those in which concomitant steroid therapy was employed. Therefore, the addition of therapeutic doses of corticosteroids in amiodarone induced pneumopathy may be indicated. Typically, prednisone is started in doses of 40 to 60 mg/day orally and slowly reduced. Again, the pharmacodynamics of amiodarone dictate a treatment period of four to 12 months. The case report describes a patient with AIPT who after therapy with Prednisone at a dosage of 50mg/day by gradually scaling down the doses as reported in the above clinical studies, had a clinical, functional and CT radiological picture that was markedly improved with disappearance of most of the scattered ground glass areas and the previously reported thickening with associated bi-apical fibrotic outcomes.

Keywords

• amiodarone-induced pulmonary toxicity
• amiodarone
• hyper-reactivity
• ocs
• ground glass opacity