SESSION TITLE: Critical Care Student/Resident Case Report Posters III
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: Acute Eosinophilic Pnemonia (AEP) was first described in 1989. The underlying pathophysiology is currently unknown. It has been associated with change is smoking habit, cocaine and heroin use, and environmental factors . It usaully occurs in the age group of 20-40 years. Diagnostic criteria include an acute febrile illness, hypoxemic respiratory failure, diffuse pulmonary opacities on chest X-ray, and BAL eosinophilia >25% OR lung biopsy showing eosinophilic infiltrates. Treatment is based on early initiation of steroids, to which it often shows a rapid and dramatic response.
CASE PRESENTATION: We report a case of AEP in a 29 year old white woman with recent use of a ‘flea bomb’ (contains pyrethroids) at home while remaining indoors, about 48 hours prior to presentation. She also restarted smoking 2 weeks prior, after having quit for 10 years. She presented with 2 days of worsening fever, shortness of breath, productive cough, and developed hypoxemic respiratory failure and ARDS. She was intubated and required a PEEP of 20 and 100% FiO2 to maintain oxygenation. BAL showed 36% Eosinophils. She was started on IV steroids with dramatic clinical and radiological improvement. She was extubated on day 6 and discharged the next day.
DISCUSSION: AEP has unknown etiology and pathophysiology. Hypothesized mechanisms involve the role of GM-CSF and IL-5 (potent chemotaxin for eosinophils) produced by Th-cells . Our patient used a ‘flea bomb’ about 48 hours prior to presentation, while remaining indoors. To the best of our knowledge, there is just one case report associating eosinophilic pneumonia and pyrethrum exposure1, and ours is the first report of pyrethroid induced AEP presenting as ARDS. In addition, a study done on mice concluded that diesel and pyrethroid induced lung hyper-responsiveness was associated with increased eosinophils in blood and lung.2
CONCLUSIONS: Acute eosinophilic pneumonia has been recognized for many years, but the pathophysiology is only recently being understood. While our patient’s recent change in smoking habit may have played a role in her eosinophilic response, the temporal relationship to significant pyrethroid exposure, in light of previous cases, compels us to consider it a major contributor. Awareness of this is critical to expedite diagnostic studies that can be lifesaving. The exposure to the ‘flea bomb’ was a key historical element that proved to be vital in establishing her diagnosis, and the subsequent prompt initiation of steroid therapy. Further studies in animal models may help refine our understanding of pyrethroids and their role in AEP.
Reference #1: Carlson JE, Villaveces JW. Hypersensitivity Pneumonitis Due to Pyrethrum: Report of a Case. JAMA. 1977;237(16):1718-1719.
Reference #2: Garcia MLB, Santos UP, Perini A, Acencio MMP, Lopes FDTQS, Bueno HMS, et al. Eosinophilic pneumonitis induced by aerosol-administered diesel oil and pyrethrum to mice. Rev Panam Salud Publica. 2009;25(6):518-23.
DISCLOSURE: The following authors have nothing to disclose: Kevin Kuriakose, Jagpal Klair, Andrew Johnsrud, Mohan Rudrappa, Nikhil K. Meena
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