COXSACKIE B2 VIRUS: FROM A SOCCER GAME TO FULMINANT MYOCARDITIS

Abstract

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: The presentation of viral myocarditis ranges from no symptoms to devastating illness.1 This is an unfortunate case of Coxsackie B2 virus induced Fulminant Myocarditis (FM); which despite aggressive medical and mechanical circulatory support progressed to fatality. CASE PRESENTATION: A 20-year-old male patient was transferred to our hospital with respiratory failure and shock. He presented to his local hospital with dyspnea, fever, myalgias and arthralgias that started after an indoor soccer game two weeks earlier. Prior to admission he was treated with inhalers, steroids and antibiotics without improvement. The TTE showed an LVEF 30% and Chest CT Scan showed bilateral consolidations and multiple nodules surrounded by ground glass opacities. Mechanical ventilation, vasopressors and inotropes were initiated prior to transferring him to our hospital. Upon arrival he required paralysis and pronation to improve his hypoxia. He was started on broad spectrum antimicrobials. However, the initial infectious workup was negative. Further workup obtained due to persistent fever revealed portal vein thrombosis which was treated with heparin. Hypercoagulability, malignancy and rheumatology tests were unrevealing. Expanded infectious workup was most notable for positive Coxsackie B2 serology with titers that increased 4-fold during hospitalization to 1:320, consistent with viral myocarditis. TEE showed persistent LV dysfunction, global LV wall motion abnormalities, increased septal wall thickness, severe mitral regurgitation and moderate tricuspid regurgitation. After receiving diuretics, vasopressors and inotropes he improved and was extubated. He subsequently decompensated requiring reintubation and resumption of inotropes. ECMO was initiated with biventricular assist device support. Heart transplant was considered but his hospital course was complicated by severe deconditioning and went on to develop GI bleeds, acute renal failure, fungemia, pulmonary abscess status post decortication and contained pulmonary artery rupture. On ICU day #97, his illness was deemed not survivable and his family withdrew care. DISCUSSION: Coxsackie B serotypes are among the more common causes of viral myocarditis, which may evolve into FM.2 FM is defined as 2-4 weeks of acute illness, followed by cardiogenic shock, needing hemodynamic support; and myocardial inflammatory infiltrates on histology. FM has a dramatic and progressive clinical course, with a severely impaired LVEF.3 It often requires prolonged hemodynamic support and referral for heart transplant.4 In general, in-hospital outcomes are poor; with increased morbidity and up to 32% reported mortality.5 CONCLUSIONS: Coxsackie B induced Fulminant Myocarditis portends increased morbidity and mortality, even after aggressive medical and mechanical circulatory support. Reference #1: Kindermann et al. J Am Coll Cardiol. 2012;59:779–92. Reference #2: Mehta et al. Case Reports in Infectious Diseases. 2018;ID 4258296:1-4. Reference #3: Ammirati et al. Circulation. 2017;136:529-45. DISCLOSURES: No relevant relationships by Stefanie DiGiandomenico, source=Web Response No relevant relationships by Tirsa Ferrer Marrero, source=Web Response No relevant relationships by Javeria Haque, source=Web Response No relevant relationships by Christopher Roberts, source=Web Response No relevant relationships by Gabriel Ryan, source=Web Response no disclosure on file for Jonathon Truwit; No relevant relationships by Krista Tuomela, source=Web Response No relevant relationships by Jane Wainaina, source=Web Response