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Venous thromboembolism (VTE) is a well-known complication in hospitalised patients [1–5]. Risk factors include older age, obesity, immobilisation, active malignancy, systemic inflammatory response syndrome (SIRS), (major) surgery, thrombophilia, and a history of thromboembolism [2, 5]. Rudolph Virchow first described in 1884 its underlying pathophysiological mechanism and consists of endothelial cell dysfunction/inflammation, low blood flow, and blood hypercoagulability. Current guidelines recommend the use of thromboprophylaxis in acutely ill medical patients who are at high risk for VTE (Padua score≥4, IMPROVE score≥2) [6]. However, in medical practice, less than half of the patients at risk receive adequate thromboprophylaxis [4]. In light of the current worldwide SARS-CoV-2 outbreak, medical wards are confronted with increased numbers of acute severely ill patients. It is estimated that one in five SARS-CoV-2 infected patients require hospitalisation with a median stay of 11 days [7]. Together with older age (>65 years) and higher SOFA-score (>4), elevated D-dimer levels (>1 µg/mL) are associated with in-hospital death [7]. D-dimer levels are a well-known but non-specific biomarker for VTE, and they could indicate hypercoagulability. Elevated D-dimer levels also indicate inflammation. D-dimer levels are elevated in many other conditions than VTE, and its specificity for VTE diagnosis is low [7]”. Among hospitalised SARS-CoV-2 patients, 68% had D-dimer levels above the upper limit of normal, suggesting hypercoagulability in these patients [7]. Up to now, there is no clear association between SARS-CoV-2 infection and the presence of VTE besides a few case reports [9, 10]. Nevertheless, it seems that these patients are at increased risk for VTE. Firstly, elevated levels of pro-inflammatory cytokines are found in patients infected with SARS-CoV-2 leading to a highly inflammatory state in these patients [7]. Secondly, similar to the previous SARS-coronavirus epidemic, angiotensin receptor 2 has been identified as a receptor SARS-CoV-2 uses for cellular entry [11]. This receptor is highly expressed on the membrane of endothelial cells, and this could lead to endothelial cell-specific inflammation/dysfunction due to viral replication in these cells [12]., The insidious VTE seems mainly a problem in the ICU ventilated patients, while patients in the general ward, treated with thromboprophylaxis (0.5 mg/kg), had a low incidence of insidious VTE.