E-CIGARETTE-ASSOCIATED LUNG INJURY IN A HEALTHY FEMALE: A CASE REPORT

Abstract

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: This is a case of a 30-year-old woman presenting with four days of dyspnea found to have E-cigarette or vaping-associated lung injury (EVALI). CASE PRESENTATION: The patient reported having 1 week dyspnea on exertion. She noted to have fevers, intermittent chills, night sweats, dry persistent cough, and diarrhea. Patient had history of asthma during childhood. She had been using electronic cigarettes with marijuana 4 days a week for at least 6 months, however due to news reports she recently stopped prior to presentation. Cartridges would last unaltered for 1 week from dispensaries. Vitals signs were notable for tachycardia and pulse oximetry of 86% on ambient air. Pulmonary exam showed scattered rales with no wheezing. Laboratory results showed a leukocytosis of 28,000 cells/mm3, procalcitonin was 0.64 ng/mL (normal < 0.08 ng/mL), and nasopharynx swab detected human rhinovirus/enterovirus on polymerase chain reaction (PCR). Due to continued oxygen desaturation on ambient air and tachycardia for two-day duration despite antibiotics and supportive care a high-resolution computed topography (HRCT) of the chest was obtained. HRCT demonstrated widespread ground glass opacities and scattered septal thickening bilaterally without lobar predominance, with diffuse subpleural sparing. There were dense consolidations seen bilaterally. Bronchoalveolar lavage (BAL) with a transbronchial biopsy were performed. Right middle and left upper lobe BAL pathology revealed oil-red O stain showing intracytoplasmic lipid droplets in alveolar macrophages consistent with lipid laden-macrophages. Transbronchial biopsy showed pneumonitis; there was interstitial edema, inflammation, mild fibrosis, hyperplasia of type II pneumocytes. Patient was treated with corticosteroids resulting in improved oxygenation. DISCUSSION: EVALI is becoming a more prevalent, being formally recognized in 2019 as non-combustible aerosol inhalation injury. Patients frequently present with hypoxia and ground glass opacities marked by subpleural sparing consistent with an inhalation injury. However bronchoscopy may be needed for diagnosis. Histopathology can vary widely; generally there is fibrinous pneumonitis and oil-red-O staining lipid-laden macrophages. Despite evidence of viral infection, the patient's clinical, radiological, and histopathological findings were consistent with EVALI. No single agent has been implicated in the pathogenesis of EVALI. However an agent of interest that has been implicated in in the pathogenesis of EVALI is vitamin E acetate which has been associated with impairment of pulmonary surfactant. The impaired surfactant and fibrinous pneumonitis frequently seen could explain the severity of this disease process. CONCLUSIONS: Further investigations are needed to determine histopathological implications, treatment options, and the use of E-cigarettes as an alternative to traditional smoking. Reference #1: Layden J, Ghinai I, Pray I, et al. Pulmonary Illness Related to E-Cigarette Use in Illinois and Wisconsin - Preliminary Report. New England Journal of Medicine. (2019) Sept 6 Reference #2: Hartmann-Boyce J, McRobbie H, Bullen C, Begh R, Stead LF, Hajek P. Electronic cigarettes for smoking cessation. Cochrane Database of Systematic Reviews (2016), Issue 9. Reference #3: Maddock SD et al. Pulmonary Lipid-Laden Macrophages and Vaping. New England Journal of Medicine. 381.15 (2019):1488. DISCLOSURES: No relevant relationships by Mario Fonseca-Paricio, source=Web Response No relevant relationships by Alan Gandler, source=Web Response No relevant relationships by Boyd Hehn, source=Web Response