INFECTED WITH ACUTE EOSINOPHILIC PNEUMONIA

Abstract

SESSION TITLE: Chest Infections 1 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Acute eosinophilic pneumonia (AEP) is an uncommon presentation of acute respiratory illness that can be fatal and may mimic acute respiratory distress syndrome (ARDS) or community-acquired pneumonia (CAP) at onset. It remains idiopathic in most cases, however, some identifiable causes implicated are smoking or resumption of it, medicines, recreational drugs, inhalational exposures, and infections. CASE PRESENTATION: A 58-year-old female former smoker of 25 pack years who had quit 15 years ago presented to an outside hospital with shortness of breath ongoing for one day associated with chills and night sweats. Chest X-Ray showed bilateral patchy opacifications. She got intubated for hypoxic respiratory failure before transfer. On presentation, she was hypotensive requiring vasopressor support. Initial labs were significant for leukocytosis (WBC 17.1 X10E3/uL) with 88% neutrophils and mini-Bronchoalveolar lavage (BAL) showing WBC 101 cells/cmm with 44% eosinophils. The mini-BAL culture grew pan-sensitive Streptococcus pneumoniae with 2000 colony/ml colony count. She received antibiotics, and the following day, a therapeutic trial of high dose steroids was initiated as her PaO2/FiO2 ratio worsened requiring paralysis. Her oxygenation status improved in the next 3 days. She was liberated from the ventilator on day 7. Upon getting more history, it became apparent that she had restarted smoking cigarettes 2 days prior to onset. During a 4 week follow up visit, complete resolution of symptoms and peripheral eosinophilia were seen, and steroids were gradually tapered off. DISCUSSION: Since first described in 1989, AEP is believed to be a hypersensitivity reaction to an unidentified inhaled antigen leading to rapid infiltration of eosinophils into lung parenchyma causing diffuse pulmonary infiltrates and an increase in BAL eosinophils.Peripheral eosinophilia was absent at presentation in our patient but appeared later and improved with treatment which is typical of AEP. Many case reports have included smoking as a risk factor; mostly initiation of smoking, resumption or increase in the consumption of cigarettes. A few case reports have linked AEP to infectious agents especially in lung allograft recipients. To our knowledge, no prior case of Streptococcus pneumoniae associated with AEP has been documented. It would be early to suggest Streptococcus pneumoniae as a causal agent, and more research is needed in this area because if it doesn't cause AEP, it certainly makes the presentation much more complicated. CONCLUSIONS: Smoking-related AEP should be considered in a patient showing significant eosinophilia in BAL along with history suggestive of either initiation of smoking, tobacco resumption or increase in the number of cigarettes. We should look out for possible infectious agents causing or worsening presentation of AEP. Reference #1: Badesch DB, King TE, Jr., Schwarz MI. Acute eosinophilic pneumonia: a hypersensitivity phenomenon? The American review of respiratory disease. 1989;139(1):249-52. Reference #2: Jeon EJ, Kim KH, Min KH. Acute eosinophilic pneumonia associated with 2009 influenza A (H1N1). Thorax. 2010;65(3):268-70. Reference #3: De Giacomi F, Decker PA, Vassallo R, Ryu JH. Acute Eosinophilic Pneumonia: Correlation of Clinical Characteristics With Underlying Cause. Chest. 2017;152(2):379-85 DISCLOSURES: No relevant relationships by Sabin Bista, source=Web Response No relevant relationships by Muhammad Saeed, source=Web Response no disclosure on file for Svien Senne