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* From the Department of Pulmonary and Critical Care Medicine, Thomas Jefferson University Hospital, Philadelphia, PA.
Correspondence to: Bobbak Vahid, MD, 1015 Chestnut St, Suite M-100, Philadelphia, PA 19107; e-mail: Bobbak.vahid{at}mail.tju.edu
An 18-year-old woman presented to the emergency department with chest pain, dyspnea, and dry cough for 1 day. Dry cough was the initial symptom accompanied with fever and malaise. Approximately 12 h before presentation, shortness of breath developed. Dyspnea rapidly progressed; at the time of presentation, she was in respiratory distress. The patient also complained of diffuse chest pain at presentation. Her medical history was significant for Lyme disease at age 8 years. She denied using illicit drugs. The patient also had no exposure to animals and had no risk factors for HIV infection. She reported smoking a few cigarettes a day for several weeks before presentation. She was not taking any medications. Occupational exposure and family histories were noncontributory.
Physical Examination
On presentation, the patient was alert but in moderate respiratory distress. Vital signs were remarkable for a temperature of 39°C, heart rate of 137 beats/min, respiratory rate of 30 breaths/min, and systolic/diastolic BP of 122/72 mm Hg. Oxygen saturation by digital pulse oximetry was 84% while breathing ambient air. The sclera was anicteric. No lymphadenopathy was detected. Chest auscultation revealed bilateral crackles. Cardiac, abdominal, and skin examinations were unremarkable. There was no ankle edema.
Laboratory and Radiographic Findings
WBC count was 28.4 x 103/dL with 91% neutrophils. Hemoglobin was 15.4 g/dL. Serum electrolytes and renal functions were normal. Chest radiography showed bilateral infiltrates and pleural effusions (Fig 1 ).
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Shortly after hospital admission, progressive respiratory failure developed requiring intubation and mechanical ventilation. Due to profound hypoxemia, the ventilator was set to deliver 100% inspired oxygen and positive end-expiratory pressure of 15 cm H2O. Arterial blood gas analysis on these ventilator settings showed PO2 of 50 mm Hg. The patient was placed on paralytics while on the ventilator. Differential diagnosis included severe community-acquired pneumonia, acute interstitial pneumonia, alveolar hemorrhage, acute hypersensitivity pneumonitis, and acute eosinophilic pneumonia. Cardiogenic pulmonary edema was excluded by normal B-type natreuritic peptide and normal left ventricular systolic function on echocardiography. The patient was started empirically on ceftriaxone and azithromycin IV. Further workup revealed normal antinuclear antibody, erythrocyte sedimentation rate, and anti-neutrophil cytoplasmic antibody. Findings on blood culture, tracheal aspirate culture, and serology for infection were negative. Bronchoscopy with BAL was done. BAL return was not bloody. Total cell count of BAL was 11,300/µL and differential cell count showed 72% eosinophils (Fig 2 ). BAL bacterial, viral, Legionella, Mycobacterial, and fungal culture findings were negative. Three samples of stool were negative for ova and parasites.
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What is the treatment of choice?
Answer: Idiopathic acute eosinophilic pneumonia
Answer: Systemic steroids
Discussion
Idiopathic acute eosinophilic pneumonia is a cause of acute respiratory failure characterized by the following: (1) acute onset of febrile respiratory disease (< 30 days); (2) bilateral infiltrates on chest radiography; (3) hypoxemia; (4) alveolar eosinophilia with BAL differential cell count > 25% eosinophils; and (5) no other causes of eosinophilic pneumonia.
Idiopathic acute eosinophilic pneumonia has been reported in patients from 15 to 86 years old and of either gender. Idiopathic acute eosinophilic pneumonia manifests as an acute febrile illness of 1 to 5 days in duration. Thirty-eight percent of patients may have allergic rhinitis prior to onset of disease. Prominent symptoms are cough, abdominal pain, myalgias, chest pain, and progressive hypoxemic respiratory failure requiring intubation and mechanical ventilation. Patients with acute eosinophilic pneumonia, unlike chronic eosinophilic pneumonia, have no history of atopy or asthma. Physical examination may reveal high temperatures, respiratory distress, bibasilar or diffuse crackles, or transient wheezing.
Subtle interstitial infiltrates are the common initial radiographic findings. These interstitial infiltrates usually progress to extensive alveolar and interstitial infiltrates involving all lobes within several hours. Chest CT scan shows diffuse alveolar infiltrates, pronounced septal markings, normal lymph nodes, and bilateral small pleural effusions.2 Laboratory findings of leukocytosis with neutrophil predominance and severe hypoxemia with PaO2/fraction of inspired oxygen ratio < 200 are common. Only one third of patients have an elevated peripheral eosinophils count.
The main pathologic finding is presence of acute and organizing diffuse alveolar damage with marked interstitial and to a lesser extent alveolar eosinophilic infiltrates. Fibrinous membranes are seen commonly. Granulomas are not seen in acute eosinophilic pneumonia. Airway involvement with mucous plugging with or without neutrophilic exudates has also been described. Alveolar hemorrhage is not characteristic of acute eosinophilic pneumonia. Eosinophilic pleural inflammation can be seen in approximately 10% of cases. The etiology of idiopathic acute eosinophilic pneumonia is not known. Occupational exposures (eg, indoor renovation, gasoline tank cleaning), exposure to dust and sand, and cigarette smoking may play a role in the pathogenesis.
Differential diagnoses of idiopathic acute eosinophilic pneumonia are summarized in Table 1 . Fungal infections and parasite infestations can cause pulmonary infiltrates with eosinophilia. Bronchoscopy, stool examination for ova and parasite, and serologic testing when appropriate are necessary to exclude fungal and parasitic causes. Many drugs have also been associated with eosinophilic pneumonia. The radiographic and histologic features of drug-induced eosinophilic pneumonia are indistinguishable from idiopathic eosinophilic pneumonia. Detailed history regarding use of medications is necessary to differentiate the idiopathic acute eosinophilic pneumonia from drug-induced eosinophilic pneumonia. History and physical examination also can guide the clinician to evaluate the patient for other secondary causes of pulmonary eosinophilia such as rheumatoid arthritis, AIDS, and complication of bone marrow transplantation.
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Our patient was stared on methylprednisolone, 125 mg IV q6h; within 4 days, she showed remarkable clinical improvement. Subsequently, sedation and paralytics were stopped, and she was successfully extubated after 5 days of mechanical ventilation. Steroid therapy was changed to oral prednisone, 60 mg/d. Two weeks after presentation, the chest radiograph infiltrates had resolved and the patient did not require supplemental oxygen. The prednisone dosage was reduced to 40 mg qd. Three weeks after presentation, the patient was admitted to rehabilitation center for muscle weakness secondary to steroid-induced myopathy. High-dose corticosteroids can cause significant myopathy with preferential loss of the fast twitch glycolytic-type 2B fibers. The reported incidence of steroid-induced myopathy has varied from 7 to 60% in different studies. There is no relationship between the duration or dose of corticosteroid therapy and occurrence of myopathy. Female gender, concomitant administration of IV paralytic agents, and prednisone doses 
30 mg/d (or equivalent doses of corticosteroids) are reported to be risk factors for steroid-induced myopathy. We tapered the prednisone therapy for the subsequent 3 weeks. The patient improved markedly after 2 weeks of in-house rehabilitation and was able to return to school 3 months after presentation.
Clinical Pearls
Footnotes
The authors have reported to the ACCP that no significant conflicts of interest exist with any company/organization whose products may be discussed in this article.
Received for publication February 28, 2006. Accepted for publication March 12, 2006.
Suggested Readings
ska, M, Orszulak-Michalak, D Drug-induced myopathies: an overview of the possible mechanisms. Pharmacol Rep 2005;57,23-34[ISI][Medline]
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