Incidence of Deep Venous Thrombosis in Patients WithCOVID-19 and Pulmonary Embolism Compression Ultrasound COVID Study

Objectives Several reports had observed a high risk of pulmonary embolism (PE) in patients with coronavirus disease 2019 (COVID-19), most of them in the intensive care unit. Reported findings indicate that a direct viral-mediated hyperinflammatory response leads to local thromboinflammation. According to those findings, the incidence of deep venous thrombosis (DVT) in patients with COVID-19 and PE should be low. The objective of this study was to evaluate the incidence of DVT in patients with COVID-19 who developed PE. Methods In this prospective observational study, consecutive patients hospitalized in the internal medicine ward with a diagnosis of COVID-19 who developed PE were screened for DVT in the lower extremities with complete compression ultrasound. Results The study comprised 26 patients. Fifteen patients (57.7%) were male. The median age was 60 years (interquartile range, 54-73 years). Compression ultrasound findings were positive for DVT in 2 patients (7.7%; 95% confidence interval, 3.6%-11.7%). Patients with DVT had central and bilateral PE. In both, venous thromboembolism was diagnosed in the emergency department, so they did not receive previous prophylactic therapy with low-molecular-weight heparin. Patients without DVT had higher mediand-dimer levels: 25,688 mu g/dL (interquartile range, 80,000-1210 mu g/dL) versus 5310 mu g/dL (P < .05). Conclusions Our study showed a low incidence of DVT in a cohort of patients with COVID-19 and PE. This observation suggests that PE in these patients could be produced mainly by a local thromboinflammatory syndrome induced by severe acute respiratory syndrome coronavirus 2 infection and not by a thromboembolic event.

Automated summary

Several reports have noted a high risk of pulmonary embolism in COVID-19 patients, particularly in the intensive care unit. This study found a low incidence of deep venous thrombosis in COVID-19 patients with PE, suggesting that the primary cause of PE in these patients may be a local thromboinflammatory response induced by the virus.