ABC | Volume 115, Nº1, July 2020

Case Report SARS-Cov-2 Infection and Pulmonary Thromboembolism – The Prothrombotic State in COVID-19 Hellen Dutra Passos, 1 Mariana Carvalho Alves, 1 Leonardo Baumworcel, 1 João Paulo Cerqueira Vieira, 1 Juliane Dantas Seabra Garcez, 1, 2 Antônio Carlos Sobral Sousa 1,2,3, 4 Clínica e Hospital São Lucas/Rede D’Or, 1 São Luiz, Aracaju, SE - Brazil Divisão de Cardiologia do Hospital Universitário da Universidade Federal de Sergipe, 2 São Cristovão, Sergipe, Brazil Departamento de Medicina da Universidade Federal de Sergipe, 3 São Cristovão, SE - Brazil Programa de Pós-Graduação em Ciências da Saúde da Universidade Federal de Sergipe, 4 São Cristovão, Sergipe, Brazil Introduction The COVID-19 caused by new coronavirus, named by the World Health Organization as Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2), has spread all over the world with astonishing speed. 1 In Brazil, the spread risk (R0) of COVID-19 has been 3.0, which explains its rapid dissemination all over the states. 2 Individuals with cardiovascular diseases, systemic arterial hypertension, diabetes mellitus, chronic obstructive pulmonary disease, and immunosuppressed patients are at higher risk for adverse outcomes. 3 A relatively high incidence of thrombotic and thromboembolic disease has been observed in COVID-19 carriers, probably due to direct effects of the SARS-CoV-2 or indirect mechanisms of the infection. Interactions between COVID-19 therapies and antiplatelet agents or anticoagulants and the inadvertent use of anticoagulants may contribute to the prothrombotic state of the disease. 4 Objectives Here we describe a patient diagnosed with SARS-CoV-2 progressing with pulmonary thromboembolism and no evidence off peripheral thrombosis. Methods The data here reported were obtained by review of electronic medical records, complementary tests, and literature review. Case Report Patient I.M.S., male, aged 66 years, self-referred to the emergency department of a general hospital in Aracaju, Brazil, onMarch 28, 2020, with nasal congestion, dry cough, asthenia, nausea and fever (40 o C) for eight days, with worsening in the last 48 hours. The patient reported having been to Rio de Janeiro for a dental implant surgery in the beginning of March and returned to Aracaju on March 18, 2020. History of osteosynthesis of the left humerus 16 years before, former smoker (quit > 10 years ago), physically active. On physical examination, the only abnormal finding was diffuse inspiratory snoring and siblings on pulmonary auscultation. The patient had normal skin color and breathing, and hemodynamically stable. The hypothesis of COVID-19 was raised and the following tests were performed: 1) laboratory routine tests, showing slightly elevated C-reactive protein levels and the other parameters within normal ranges (including myocardial injury markers); 2) RT-PCR by oropharyngeal swab; and 3) chest tomography (Figure 1) which revealed ground-glass opacities, mainly in peripheral areas and more evidently in lower segments, affecting less than 50% of the pulmonary parenchyma. Electrocardiogram (ECG) with normal sinus rhythm and heart rate of 65 bpm. Since the patient was an elderly man and had impaired pulmonary function, the patient stayed in isolation of an intensive care unit, with diagnosis of viral pneumonia, probably caused by the SARS-CoV-2 infection. A therapy with Oseltamivir (150 mg/day), Azithromycin 500 mg/day and Ceftriaxone 2g/day was initiated, combined with prophylactic enoxaparin 40mg/day for venous thrombosis. After 24 hours of hospitalization, the patient showed progressive worsening of respiratory function, culminating with acute respiratory failure, requiring orotracheal intubation on the second day of hospitalization. The patient also developed shock, and vasoactive drug was used. With worsening of hemodynamics and the negative RT- PCR for SARS-CoV-2, a transesophageal echocardiogram (TEE) was performed to rule out the possibility of infectious endocarditis. The TEE, performed on April 02, 2020, revealed: a) enlargement of the left ventricle, which showed diffuse hypokinesis predominantly of the antero-apical wall and apical septum, grade 1 diastolic function and moderated global diastolic dysfunction, with ejection fraction of 41%; b) enlargement of the right chambers, with diffuse hypokinesis of the right ventricle, and moderate global systolic dysfunction by subjective evaluation; c) mild-to-moderate pulmonary hypertension (pulmonary artery systolic pressure of Mailing Address: Antônio Carlos Sobral Sousa • Centro de Ensino e Pesquisa do Hospital São Lucas/Rede D’Or - São Luiz, Av. Gonçalo Prado Rollemberg, 211, Sala 208. Postal Code 49010-410, Aracaju, SE - Brazil E-mail: acssousa@terra.com.br Manuscript received May 04, 2020, revised manuscript May 06, 2020, accepted May 14, 2020 Keywords Coronavirus; COVID-19; Pulmonary Embolism; Severe Acute Respiratory Syndrome; Anticoagulants; Diagnostic, Imaging. DOI: https://doi.org/10.36660/abc.20200427 142