A 56‐year‐old woman presented with 2 days of shortness of breath, cough, and fatigue. She denied sick contacts, chest pain, orthopnea, or extremity swelling. Her only change in daily routine was spending the weekend cleaning. She was febrile and breathing 32x per minute with a SaO2 of 84% on room air. She had good air movement without prolonged expiratory phase. Inspiratory crackles at the base of the right lung with increased tactile fremitus were appreciated. Initial laboratory studies were notable for a leukocytosis with a segmented neutrophilia. Chest x‐ray revealed consolidation of the right lower lobe and patchy air space disease throughout the rest of the lungs. Sputum and blood cultures were negative. She was admitted and treated empirically for community‐acquired pneumonia. After a couple of days she was still requiring 40% FiCte via ventimask. A CT of the chest revealed diffuse bilateral geographic ground glass appearance of both lungs with associated small bilateral effusions. Bronchoscopy revealed 40% eosinophils; a concomitant CBC revealed a peripheral eosinophilia not found during the original presentation. The patient was diagnosed with eosinophilic pneumonia and treated with prednisone with rapid improvement of her oxygenation status. She was ultimately discharged 2 days later and sent home with a steroid taper.
Acute eosinophilic pneumonia is a disease of unknown etiology that is thought to be linked to atopic diseases and exposures to new allergens. lt presents with an acute onset of dyspnea, cough, and fever that usually lasts 1 week. Imaging studies typically reveal diffuse interstitial infiltrates and sometimes small bilateral pleural effusions. Serum white blood cell counts tend to show a predominantly neutrophilic leukocytosis initially with eosinophilia occurring during the recovery phase. The definitive diagnosis is achieved with bronchoscopy revealing > 25% eosinophils in the bronchoalveolar lavage fluid and leukocytotic interstitial infiltrates. Treatment is prednisone with rapid recovery often in 12‐48 hours. Steroids must be tapered over 2‐4 weeks after the resolution of symptoms. There is little long‐term morbidity or mortality associated with the disease, although it may recur and require maintenance inhaled steroid treatments.
In this case, the presentation of hypoxemic respiratory failure was initially thought to be caused by a typical case of pneumonia. However, when the patient's condition failed to improve with a full course of broad‐spectrum antibiotics, an alternative explanation for the patient's persistent hypoxemia was needed. Although rare, this case of acute eosinophilic pneumonia, thought to be triggered by the exposure to cleaning supplies, suggests the need for further investigation of hypoxemic respiratory failure that doesn't improve with conventional treatment as expected and supports Ihe utility of bronchoscopy in the diagnosis of interstitial lung diseases.
L. Leung, none; H. Hefler, none.