A 70-year old man with a history of paroxysmal atrial fibrillation, diabetes mellitus, and arterial hypertension presented to the Emergency Department with the symptoms of dyspnoea, cough, and fever lasting for five days. The patient had symptomatic paroxysmal atrial fibrillation and was treated with amiodarone 200 mg daily for the previous five years. His vital signs at the arrival were as follows: blood pressure 160/110 mmHg, respiratory rate 34/min with decreased oxygen saturation (89%). Electrocardiogram (ECG) showed atrial fibrillation with a fast ventricular response rate of 110/min and no signs of ischemia. Physical examination revealed diminished pulmonary sounds with right side basal crackles. Laboratory workup revealed increased levels of white blood cell count (WBC) 13,100/ml with 83% neutrophils, creatinine (180mg/dl), C-reactive protein (CRP) 296.4 mg/dl and slite elevation of gamma-glutamyl transferase (GGT) 80 mg/dl and lactate dehydrogenase (LDH) 315 mg/dl. Chest X-ray showed diffuse bilateral perihilar nonhomogeneous infiltrates (Fig. 1). Due to the acute clinical deterioration, he was immediately admitted into the intensive care unit (ICU) and treated with high-flow oxygen. Empirical antibiotic therapy with amoxicillin-clavulanic acid and levofloxacin was started. Considering the potential toxicity, the therapy with amiodarone was discontinued. A repeated chest X-ray study one week later did not show any resolution of pulmonary infiltrates. Blood and urine cultures were taken and found to be sterile. Further investigation included a high-resolution computed tomography (HRCT) scan of the chest that showed diffuse interlobar septal thickening with the extensive ground-glass opacities in the upper lungs and consolidation in the anterior segment of the right upper lobe (Figure 2. (A and B)). The differential diagnosis considered at the time included cryptogenic organizing pneumonia (COP) but based on the imaging features, there was also a suspicion of amiodarone-induced pulmonary toxicity (AIPT). HRCT also revealed bilateral pleural effusions with paratracheal and subcarinal enlargement of lymph nodes. Transthoracic echocardiography demonstrated hypertrophic interventricular septum with normal left ventricular systolic function and no valvular abnormalities. Mitral inflow showed a pseudonormal left ventricular filling pattern consistent with elevated LV filling pressures and grade II diastolic dysfunction. Right-sided thoracocentesis was done and bacterial cultures of the pleural fluid were negative. Legionella antigen was negative. Due to the worsening of respiratory function noninvasive ventilation (NIV) was applied. After clinical stabilization, he was transferred to the Department for further investigation and treatment. After that, bronchoscopy with aspiration and transbronchial biopsy (TBB) was performed to confirm a definitive diagnosis. Bacterial cultures of the bronchial aspiration fluid were negative. Transbronchial lung tissue biopsy showed morphological findings suggestive of amiodarone exposure and indicative of its toxicity. Two small samples of lung tissue demonstrated organizing pneumonia and diffuse interstitial pneumonitis with the widening of alveolar septae infiltrated with chronic inflammatory cells and mild to moderate interstitial fibrosis. The histologic finding of hyaline membranes as seen in diffuse alveolar damage was indicative of adult respiratory distress syndrome. Reactive hyperplasia of type II pneumocytes, some of them with lipid vacuoles, were present. The intra-alveolar foamy macrophages with cytoplasmic vacuolization were characteristic of amiodarone lung toxicity (Fig. 3, Fig. 4, Fig. 5.) One week after patient's clinical condition improved and he was discharged from the hospital. A follow-up chest X-ray six weeks later showed no previously detected pulmonary infiltrates.