Increasing Prevalence of Sars-cov2 Related Eosinophilic Pneumonia

Introduction: As the pandemic sweeps on, it is important to recognize some of the unique outcomes of the still very abstract SARS-COV2 viral pneumonia. In this case, we describe a patient that developed acute eosinophilic pneumonia secondary to COVID19 infection. Case Presentation: A 65-year-old Hispanic female with history of osteoporosis, fibromyalgia and depression presented to the ER with dyspnea and non-productive cough for two days. She was hypoxic at 91% on room air. Chest X-ray showed bilateral reticular infiltrates. COVID 19 PCR was positive. Lactate dehydrogenase, Ferritin, C-reactive protein were elevated. Initial treatment consisted of supplemental oxygen, ceftriaxone, azithromycin, hydroxychloroquine, therapeutic anticoagulation, tocilizumab and methylprednisolone, and convalescent plasma. However, she had worsening hypoxia despite maximizing noninvasive ventilation leading to Endo-Tracheal Intubation. She also developed septic shock requiring empiric coverage with meropenem, vancomycin and micafungin. Blood cultures grew MRSA. Urine culture grew E. coli. 2D Echo and Transesophageal Echo were negative for endocarditis. Gallium scan, and CT abdomen and pelvis were negative for other sources of infection. As her hypoxia worsened, CT thorax was done which revealed diffuse ground glass appearance, interstitial lung disease, fibrosis and bronchiectasis. Complete blood count with differential demonstrated new peripheral eosinophilia (2630/mm3). Serum antigens, sputum, and stool cultures for fungal agents, parasites, and Giemsa staining returned negative. Other triggers of peripheral eosinophilia such as smoking, parasitic infections, allergies, allergic interstitial nephritis, medications were ruled out. Broncho alveolar lavage, although planned, was not performed due to hemodynamic instability and severe hypoxemia. Based on acutely worsening respiratory status and significant peripheral eosinophilia, we considered the diagnosis of acute eosinophilic pneumonia and started her on high dose methylprednisolone. She had significant improvement in oxygen requirement, chest X-ray and subsequent thoracic CT scans. She then had a tracheostomy and was discharged to acute care facility. Discussion: The SARS-COV2 infection is thought to be a TH1 type response with IL-2 activation. However, in this case, TH2 mediated responses with IL-13/IL-5 activation and eosinophil release, which are the predominant mechanisms behind acute eosinophilic pneumonia, must be explored. There have been at least 2 reported cases of eosinophilic pneumonia in COVID19 infected patients. It is important to further our understanding of the pathophysiology behind SARS-COV2 related eosinophilic pneumonia to plan for efficacious treatment, and reduce excessive work up in search for other causes. It is also relevant to understand the role of high dose steroids in its treatment.