A Case of Saddle Pulmonary Embolism in the Recovery Phase of COVID-19 Infection

Abstract

Introduction: COVID-19 is an infection caused by severe-acute-respiratory syndrome coronavirus-2 (SARS-CoV-2).1 Many recent reports have shown an increased risk of venous thromboembolism (VTE)4-5. Despite therapeutic anticoagulation with elevated D-dimer is widely described7, data on post-discharge prophylactic anticoagulation is limited.Case report: A 52-year-old female presented with 1-day mid-sternal chest pain and difficulty breathing. Her medical history included type-2-Diabetes Mellitus, obesity, and a hospital admission 4 weeks prior for COVID-19. She received Ceftriaxone, Azithromycin, Hydroxychloroquine, and prophylactic anticoagulation. She remained stable, with no fever or oxygen requirements and was discharged home to selfquarantine. She returned to the hospital, describing pain as sharp, constant, mild, radiating to left chest and back, aggravating on lying down and alleviating on leaning forward. Physical exam was normal, with no tachycardia, tachypnea, or hypoxemia. D-dimer was elevated (6834ng/dL), with normal troponin-T and pro Btype natriuretic peptide. In light of the findings, a contrasted Chest-CT was performed, showing a saddle pulmonary embolus (PE) in left pulmonary artery and non-obstructing thrombus in right main pulmonary artery. Electrocardiogram showed sinus rhythm and right-bundle-branch block, but no “S1Q3T3 pattern”.Patient was admitted to ICU and received enoxaparin. COVID-19 was negative. She remained hemodynamically stable. Lower extremities venous duplex scan was negative for DVT, echocardiogram reported normal ventricular function and dilation of inferior vena cava, consistent with elevated right atrial pressure. Patient was discharged on apixaban.Discussion: Several COVID-19 case-studies have highlighted the association with VTE4-5. During SARSCoV-1 epidemic the reported incidence of DVT and PE was 20% and 11% respectively10. The underlying pathophysiology is probably related to excessive inflammatory response “cytokine storm” and microvascular thrombosis. It is known that infections, either viral, bacterial or fungal can activate immune-thrombotic pathways as initial inflammatory response. However, in COVID-19, such response is disproportioned. McGonagle6 described that the tropism for angiotensin-converting enzyme 2 expressed on type-II pneumocytes and the proximity of these cells to vasculature, combined with the aforementioned inflammation may play the main role. Is COVID-19 a risk factor for PE at the recovery phase of the disease? When are the patients at the highest risk for VTE? Should COVID-19 PE be treated as provoked? Can D-dimer be relied upon as indicator for anticoagulation initiation in these settings? and if so, at what levels? Should COVID-19 patients be discharged on prophylactic anticoagulation? As more patients are being treated, COVID-19's role as risk factor for VTE in the recovery is still unclear.