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SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: The mechanisms by which the novel SARS-CoV-2 coronavirus causes coagulopathy are still being studied (1,2) Herein we present a case of a 38-year-old man admitted to the intensive care unit for severe COVID-19 infection Work-up for fever of unknown origin revealed bilateral deep venous thromboses, and a mechanism of hypercoagulability in COVID-19 infection that is not well-defined in the emerging literature CASE PRESENTATION: A 38-year-old man with a history of morbid obesity (BMI 71 5 kg/m2) presented to the emergency room with fevers, malaise and myalgias for three days He endorsed shortness of breath and cough Vitals on presentation were temperature 38 8 °C, heart rate 124 beats/min, respiratory rate 24 breaths/min, blood pressure 91/79 mmHg and SpO2 55 % On non-rebreather SpO2 was 88% with increased work of breathing and crackles on examination of the chest He was intubated and admitted to the intensive care unit Vancomycin, cefepime and azithromycin were started as empiric coverage for multifocal pneumonia He tested positive for SARS-COV-2 and parainfluenza Hydroxychloroquine was started PaO2/FiO2 ratio worsened from 99 to 73 Interleukin 2 and 6 were 2371 pg/mL and 173 pg/mL respectively Hemodynamics improved with Tocilizumab, pressor support and stress-dose steroids However he had persistent fever and tachycardia after antibiotics were broadened to vancomycin and meropenem Repeat work-up was negative for new infectious source of fever Doppler ultrasound revealed deep vein thromboses in bilateral popliteal veins CTPE was not done due to patient’s BMI of 71 5 kg/m2 High-intensity heparin drip was started Hypercoagulability work up revealed Antithrombin Activity 71 0%, Antithrombin Antigen 56% ANA screen and lupus anticoagulant were negative There was clinical improvement and he tested negative for SARS-COV-2 on day 16 of treatment He was stable for discharge by day 37 There was normalized Antithrombin Activity 93 0% and Antithrombin Antigen 85% DISCUSSION: This case provides evidence that antithrombin 3 deficiency should be included as a differential for hypercoagulability in patients with COVID-19 infection Other previously identified causes of hypercoagulability, such as lupus anticoagulant (3), were negative Though fevers may occur in COVID-19 infection, this case shows the benefit of excluding other potential sources High intensity heparin was started once deep vein thromboses were discovered However other cases of antithrombin 3 deficiency may be resistant to the heparin therapy that is being used to treat venous thromboembolism in COVID-19 CONCLUSIONS: Antithrombin 3 Deficiency is a mechanism for hypercoagulability and fever of unknown origin in patients with COVID-19 Recognition of these roles of antithrombin 3 deficiency, can better guide therapy in future cases as there may be resistance to the standard heparin therapy being adopted in COVID-19 Reference #1: Klok FA, Kruip MJHA, van der Meer NJM, et al Incidence of thrombotic complications in critically ill ICU patients with COVID-19 Thromb Res 2020 April 10 (Epub ahead of print) Reference #2: Helms J, Tacquard C, Severac F, Leonard-Lorant I, Ohana M, Delabranche X, Merdji H, Clere-Jehl R, Schenck M, Fagot Gandet F, Fafi-Kremer S High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study Intensive Care Medicine 2020 May 4:1-0 Reference #3: Bowles L, Platton S, Yartey N, Dave M, Lee K, Hart DP, MacDonald V, Green L, Sivapalaratnam S, Pasi KJ, MacCallum P Lupus Anticoagulant and Abnormal Coagulation Tests in Patients with Covid-19 New England Journal of Medicine 2020 May 5 DISCLOSURES: No relevant relationships by Eric Chang, source=Web Response no disclosure on file for Michelle Lee;No relevant relationships by Krystal Mills, source=Web Response No relevant relationships by Ifedolapo Odebunmi, source=Web esponse No relevant relationships by Timothy Sobukonla, source=Web Response
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