Amiodarone-induced pulmonary toxicity (APT) is a severe side effect that can lead to lung fibrosis or fatal respiratory failure. Usually APT occurs during long term therapy after administration of prolonged loading doses or high cumulative doses. We present the case of a 58 year old woman who underwent thoracic surgery with lobe resection. She developed atrial fibrillation with hemodynamic-instability on the first post-operative day. We initiated amiodarone therapy and four days later she developed respiratory failure. The pulmonary function further deteriorated showing signs of an acute respiratory distress syndrome (ARDS). We therefore started mechanical ventilation, but still the gas exchange did not improve. A computer tomography-(CT)-scan presented bilateral interstitial and alveolar infiltrations. The patient also presented with leukocytosis, elevated C-reactive protein (CRP) levels however without elevated procalcitonin (PCT) concentrations. In the tracheal secretion we only harvested foam cells, but got no evidence for pathogens causing pneumonia. We immediately started glucocorticoid therapy with prednisolone 50 mg/d for five days. Almost instantaneously the gas exchange ameliorated. We were able to wean the patient from the respirator within five days. Pulmonary infiltrations were nearly vanished in a CT-scan few days later and completely disappeared in follow up examinations. This case demonstrates a per-acute onset of APT caused by a low loading dose in association with thoracic surgery. The initiation of glucocorticoid therapy in parallel to amiodarone withdrawal led to full recovery of the patient. One should consider APT when signs of pulmonary failure occur during brief periods of amiodarone therapy especially after thoracic surgery.