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Acutely ill medical patients are at heightened risk for venous thromboembolism, a term that combines deep vein thrombosis (DVT) and its more severe complication, pulmonary embolism.1,2 Although the incidence of venous thromboembolism inmedical patientsmight have been overestimated in some instances, according to a recent study,3 treatment by low, prophylactic doses of low molecular weight heparin (LMWH) is recommended for these patientswhen additional risk factors coexist.1,2 COVID-19 is an acute, complex disorder that is associated with SARS-CoV-2 infection, which, in its most severe presentation, is characterized by the development of interstitial pneumonia and acute respiratory distress syndrome.4 According to many reports, COVID-19 exposes patients to a particularly high risk for venous thromboembolism.5–8 Hence, hospitalized COVID-19 patients are generally treated with higher LMWH doses than recommended for thromboprophylaxis. A recent document by the Italian Drug Agency (AIFA) suggested the use of 80 to 100mg enoxaparin daily, instead of the usual 40mg, while in some hospitals, even higher, up to full anticoagulant doses of LMWH or unfractionated heparin9 are used. In our hospital we use 40mg enoxaparin daily, as recommended for high-risk, acutely ill medical patients.1,2 From the COVID-19 outbreak in Northern Italy until April 14, 388patientshavebeenadmitted toour non-intensive care unit (ICU) wards, none of whom developed symptomatic DVTduring theirhospital stay.AsDVTmaybeasymptomatic in a proportionof patients at risk,we performed leg compression ultrasonography, which failed to detect DVT in any of the 64 tested patients, independently of the severity of their condition and length of in-hospital bed rest (►Table 1). The absence of reports in the literature of DVT in COVID-19 patients under LMWH thromboprophylaxis confirms our experience. This is apparently in contrast with the relatively frequent reports of pulmonary embolism in hospitalized COVID-19 patients,5–8 which is diagnosed based on the clinical observation of rapid worsening of respiratory insufficiency and blood oxygenation that is outof proportion to theextentof pulmonary infiltration and on the evidence of pulmonary vessel occlusions, generally interpreted as caused by pulmonary emboli, when computed tomography angiography (CTA) is performed. These patients, however, usually do not have symptoms or signs of DVT. As an example, a study of 184 severe COVID-19 patients, all hospitalized in ICU and treated mostly with standard doses of LMWH for thromboprophylaxis, reported a high incidence of venous thromboembolism (n1⁄4 28).5 However, only one patient had DVT (diagnosed by compression ultrasonography), while pulmonary embolism (diagnosed by CTA)was by far the most frequent thrombotic event (n1⁄4 25) (highlighting the importanceofperformingCTA in symptomatic patientswhenever possible), followed by two cases of catheter-related upper extremity venous thrombosis.5 The discrepancy between the frequencies of pulmonary embolism and DVT is surprising, because, although pulmonary embolism may occur in the absence ofdetectableDVT, this happens in onlyapproximately 20% of studied patients.10 Therefore, we questionwhether the observed pulmonary vessels occlusions that have been described in reports onCOVID-19patients are exclusively caused by pulmonary embolism. In our experience and in some reports,11,12 filling defects of pulmonary vessels that are detectedbyCTA scans are inmany instancesmore reminiscent of pulmonary thrombi rather than emboli, because they are not fully occlusive. This observation is compatible with postmortem descriptions of “...presence of manifestations of

Pulmonary Embolism or Pulmonary Thrombosis in COVID-19? Is the Recommendation to Use High-Dose Heparin for Thromboprophylaxis Justified?