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An Unusual Case of Bilateral Pulmonary Infiltrates FREE TO VIEW

Ariella Reinherz*, MD; Tariq Cheema, MD
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Allegheny General Hospital, Pittsburgh, PA

Chest. 2012;142(4_MeetingAbstracts):960A. doi:10.1378/chest.1381407
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SESSION TYPE: Miscellaneous Cases I

PRESENTED ON: Monday, October 22, 2012 at 01:45 PM - 03:00 PM

INTRODUCTION: Common etiologies for diffuse bilateral airspace opacities include infection, acute respiratory distress syndrome, or alveolar hemorrhage. However, in a patient who recently started smoking, acute eosinophilic pneumonia (AEP) must be included in the differential diagnosis.

CASE PRESENTATION: Our patient is a 45 year old female who presented to emergency department with complaints of cough (productive with thick sputum), fever, chills, pleuritic chest pain, and shortness of breath that started two days prior to admission. She revealed that she began smoking six weeks prior to admission. She was admitted with a diagnosis of community acquired pneumonia ,however her dyspnea worsened despite coverage with appropriate antibiotics. She also had progressive hypoxia despite oxygen supplementation and eventually required intubation for mechanical ventilation.Her chest x-ray revealed bilateral pulmonary infiltrates. Rescue methods were started for refractory hypoxemia and she was placed on Pressure Control Ventilation as well as prone ventilation. Bronchoscopy with BAL was performed. This revealed a white blood cell count of 230/ mcL of which 1% were neutrophils, 19% lymphocytes, 27% macrophages, and 53% eosinophils. All culture data was negative. The patient was diagnosed with Acute Eosinophilic Pneumonia and was started on high dose intravenous steroid therapy. Her oxygenation improved dramatically.She was extubated and eventually discharged from the hospital with no restrictions.

DISCUSSION: The cause of eosinophilic pneumonia remains unknown. It is suggested that AEP is an acute hypersensitivity reaction to an inhaled antigen in an otherwise healthy patient. It is thought that the pathogenesis of AEP starts with antigenic stimulation of T-lymphocytes. High levels of macrophage-derived cytokines are also found in the bronchoalveolar lavage fluid in patients with AEP. Various drugs and inhalation exposures have been reported to be associated with AEP. These include BCG vaccination, minocycline, fludarabine, sertraline, firework smoke, World Trade Center demolition dust, tear gas, and plant repotting. Cigarette smoke has been the most frequently proposed possible trigger to AEP. A causal relationship is supported by the creation of eosinophilic lung infiltration in patients rechallanged with cigarette smoking after their initial cessation. Our case supports the suggestion that AEP is the result of a hypersensitivity reaction to an inhaled antigen. In our patient ,we feel that her recent smoking history was the trigger.

CONCLUSIONS: In patients who present with bilateral airspace disease, it is important to obtain a detailed history, especially pertaining to home medications and recent inhalation exposure.

1) Allen J. Acute Eosinophilic Pneunomia. Semin Respir Crit Care Med. 2006 Apr;27(2):142-7.

DISCLOSURE: The following authors have nothing to disclose: Ariella Reinherz, Tariq Cheema

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Allegheny General Hospital, Pittsburgh, PA




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