A 58-year-old man who was an active smoker was admitted twice to the intensive care unit (ICU) of a tertiary referral thoracic center for severe hypercapnic acute respiratory failure and persistent bilateral chest radiograph opacities that were unchanged over the course of the two ICU admissions within a 3-month period (Fig 1). He had obesity (body mass index, 36 kg/m2), stage 3 vascular chronic renal insufficiency, and hebephrenic schizophrenia treated with haloperidol, carbamazepine, and cyamemazine. He reported chronic dyspnea on exertion, which worsened for 6 months. At the second ICU admission, he was afebrile, with a blood pressure of 160/72 mm Hg and pulse oximetry of 93% on 6 L/min oxygen therapy through a nonrebreathing mask. Physical examination showed signs of respiratory failure with wheezing and active abdominal expiration, bilateral pulmonary crackles without chest pain, hemoptysis, clubbing, or signs of cardiac failure. He had no peripheral lymphadenopathy and no enlarged spleen. Blood gases (on 6 L/min oxygen) showed respiratory acidosis (pH, 7.15 [normal range, 7.38–7.42]; Pao2 level, 67 mm Hg [normal range, 80–100 mm Hg]; Paco2 level, 102 mm Hg [normal range, 38–42 mm Hg]; Hco3 − level, 29 mmol/L [normal range, 22–27 mmol/L]). Noninvasive ventilation was initiated. Imaging performed during the second ICU hospitalization included noncontrast chest CT (Fig 2), MRI of the chest without contrast enhancement (Fig 3), and fluorine 18 fluorodeoxyglucose PET/CT (Fig 4).Chest radiographs showed ill-defined lower lung consolidations without substantial change in severity across the two ICU admissions (Fig 1). Noncontrast chest CT showed focal areas of fat attenuation within a left upper lobe masslike consolidation and mediastinal adenopathy in the right paratracheal 4R chain (measuring up to 20 mm on the short axis) with diffuse and heterogeneous multifocal punctate hypoattenuation (Fig 2). These findings were confirmed on chest MRI scans that showed T1 in-phase hyperintense signal intensity similar to subcutaneous fat in the masslike lung opacities, with focal signal drop on the out-of-phase image and complete signal drop on the water T1 image. MRI also showed similar patchy fat signal T1 in-phase hyperintense signal intensity in the 4R lymphadenopathy. Few areas of focal signal drop on the out-of-phase acquisition within the 4R lymphadenopathy was suggestive of fat signal with a punctuated distribution, termed patchy fatty nodes (Fig 3). At 18FFDG PET/CT , hypermetabolism of the left upper lobe masslike consolidation (maximum standardized uptake value [SUVmax], 6.5) and the mediastinal adenopathy (SUVmax, 3.2) was shown in the 4R lymphadenopathy (Fig 4). Endobronchial US-guided transbronchial needle aspiration (EBUS-TBNA) of the 4R station through the endotracheal tube (Fig 5A), without complications, showed a profusion of lipid-laden macrophages (Fig 5B) and extramacrophagic oil droplets (Fig 5C) without any tumoral cells, leading to the diagnosis of exogenous lipoid pneumonia. Bronchial biopsy specimens obtained during EBUS-TBNA showed vacuoles within the bronchial chorion (Fig 5D), which confirmed the diagnosis of exogenous lipoid pneumonia. Focused patient questioning revealed 15-year oral exposure to paraffin for neurolepticinduced constipation. What is your diagnosis?