A 37-year-old woman presented with progressive dyspnea of 2 weeks' duration, a low-grade fever, and night sweats. She had been a healthy marathon runner until her exercise tolerance recently declined.
The patient had no significant medical history and was not a smoker. She denied hemoptysis, weight loss, or exposure to tuberculosis and other illnesses. She reported having felt well while traveling extensively in the United States during the past 6 months.
Blood pressure was 116/69 mm Hg; pulse rate, 108 beats per minute; respiration rate, 28 breaths per minute; and temperature, 37.2°C (99°F). Oxygen saturation on room air was 98%, and 99% on 3 liters of oxygen.
Examination of head, ears, eyes, nose, and throat; abdomen; and all extremities was unremarkable. Neurologic findings were normal; review of symptoms was negative. The patient's neck was supple; there was no lymph adenopathy. Tachycardia with a regular rhythm was noted. Coarse breath sounds with expiratory wheezing was heard.
The patient was admitted to the hospital. A chemistry panel and a complete blood cell count were normal. White blood cell (WBC) count was 17,800/µL with 80% neutrophils, 13% lymphocytes, 5% monocytes, and 2% eosinophils. Erythrocyte sedimentation rate was 112 mm/h.
A chest film revealed patchy air-space disease that involved the upper lobes bilaterally with multiple, thick wall cavities with irregular walls. Small pleural effusions were seen bilaterally (Figure A).
Ceftriaxone, 2 g/d, was initiated, and the patient was placed in respiratory isolation. A computed tomography (CT) scan of the chest showed bilateral peripheral fluffy alveolar opacities primarily in the upper and middle lobes (Figure B). Blood cultures and acid-fast and Gram stains of sputum were negative.
A bronchoalveolar lavage (BAL) yielded the follow ing: slightly bloody color; red blood cell count, 7900/µL; WBC count, 13,800/µL; neutrophils, 6%; lymphocytes, 29%; histiocytes, 3%; and eosinophils, 62%. Gram, acid-fast, and viral stains were negative. Giemsa and other stains revealed a mild increase in eosinophils. Chronic idiopathic eosinophilic pneumonia was diagnosed.
Drs Deepa Vasudevan and Trevor R Allison of the University of Texas-Houston Medical School report that eosinophilic lung diseases comprise a heterogeneous group of disorders that are characterized by large numbers of eosinophils in inflammatory cellular infiltrates of the airways and/or the parenchyma of the lungs. This group includes acute eosinophilic pneumonia, drug-induced eosinophilic pneumonia, and chronic idiopathic eosinophilic pneumonia.
Acute eosinophilic pneumonia is an idiopathic acute febrile illness of less than 7 days' duration. It features hypoxemia, diffuse puhnonary infiltrates that are demonstrated on the chest film, and an increased percentage of eosinophils in BAL fluid. The disease either improves spontaneouslyor responds promptly to corticosteroids with no relapse.
Drug-induced eosinophilic pneumonia is a common acute febrile illness that has some respiratory symptoms. The chest film shows diffuse puhnonary infiltrates, and BAL fluid contains an elevated percentage of eosinophils. Cessation of the causative drug results in prompt improve ment. Symptoms recur with drug challenge.
Chronic idiopathic eosinophilic pneumonia is a rare disorder that occurs more often in women and in persons with atopy. Predominant respiratory symptoms include cough and progressive dyspnea; the most common systemic complaints are asthenia, fever, and weight loss.
The chest film shows puhnonary infiltrates that have the appearance of a photographic negative of x-ray findings in puhnonary edema. CT scanning of the lungs may reveal bilateral puhnonary opacities. The peripheral eosinophilic count may be elevated; however, it can vary throughoutthe course of the disease and may be normal. In nearly all patients, the eosinophil level in BAL fluid is strikinglyhigh. Many experts believe that evidence of pul monary eosinophilia obtained by either BAL or lung biop sy is needed to confirm the diagnosis of chronic idiopathic eosinophilic pneumonia.
The differential diagnosis includes bronchitis obliterchopuhnonary aspergillosis, which is characterized by bronchiectasis with migratory infiltrates and puhnonary eosinophilia.
Clinical and roentgenographic evidence of the disease dramatically resolves with oral corticosteroid thera py. The duration of treatment varies; however, prolonged corticosteroid therapy (about 6 months) is recommended for most patients because of the potential for relapse and the possibility of developing severe asthma. Relapses are common. Although it is difficult to recommend a particu lar regimen to treat recurrences, oral corticosteroids have been effective.
Because of the severity of her disease, this patient was given intravenous methylprednisolone sodium succi nate. Her condition improved dramatically; the symptoms nearly resolved after 3 doses of the medication. A 6-week course of high-dose oral prednisone was prescribed after discharge from the hospital.