A Case of Submassive Pulmonary Embolism in COVID-19 Patient

Abstract

Observational studies have suggested that respiratory failure in COVID-19 is not solely driven by the development of ARDS but also concomitant micro-and macrovascular thrombosis. Many patients with COVID-19 develop a hypercoagulable state that has been associated with an increased risk of death. Current treatment guidelines do not support the use for or against empiric anticoagulation. We present a case of a 57-year-old Caucasian male with COVID-19 who was started on full-dose anticoagulation empirically based on an elevated D-Dimer level and was later found to have bilateral pulmonary emboli with right heart strain and pulmonary infarction. Patient had a medical history significant for diabetes mellitus type II, hypertension, hyperlipidemia, and presented to the hospital on 4/18/20 with fever, fatigue, myalgias, weakness, productive cough, shortness of breath, non-bloody diarrhea, abdominal pain, after testing positive for COVID-19 outpatient on 4/1/20. His O2 saturation was 72% on pulse oximetry. He had no prior pulmonary history. In the ED, chest x-ray demonstrated no abnormality (image 1) and D-dimer was 5325 ng/mL. In light of significantly elevated D-dimer, the patient was started empirically on systemic anticoagulation with unfractionated heparin drip. Due to low pre-test probability and trying to limit further exposure to COVID-19, doppler ultrasound of bilateral lower extremities was chosen to rule out VTE. It was negative. Patient clinically improved over the next day and was subsequently transferred out of the ICU. Prior to discharge the patient underwent CTA to rule out PE on 4/21/20. Results demonstrated acute bilateral pulmonary emboli, including large saddle embolism left main pulmonary artery distally, with right heart strain and pulmonary infarction. Since the patient was hemodynamically stable, no systemic or catheter-based thrombolysis was indicated. Patient was started on a DOAC and discharged on 4/23/20 with oxygen only at night. Although the exact etiology of VTE associated with COVID-19 remains unclear, the available data has shown it to cause a prothrombotic state. Studies have shown the risk of VTE in COVID-19 patients admitted to the ICU to be around 2.5-5 times higher than the general ICU population. Our case serves to highlight the need for heightened vigilance for VTE as well as question the utility of common risk stratification tools such as the Well's score in COVID-19. Further studies are needed to identify when and how to anticoagulate patients with COVID-19 in addition to validating risk stratification tools that may aid clinicians in these situations.