COVID-19 disease results in a wide spectrum of clinical manifestations including flu-like symptoms, difficulty in breathing, blood and circulatory complications, gastrointestinal symptoms, hepatocellular injury, hyperglycaemia and ketosis, neurological illnesses, ocular symptoms and dermatological complications. [1] These effects are thought to occur as a result of angiotensin-converting enzyme 2-mediated cellular viral entry, tissue damage, dysregulation of the renin-angiotensin-aldosterone system, systemic release of cytokines, and dysfunctions in the microcirculation. [2,3] Several reports have documented an increased incidence of venous thromboembolic events, including pulmonary embolism (PE), among critically ill patients with COVID-19 admitted to hospitals, including intensive care units (ICUs). [2,[4][5][6][7][8][9][10][11] The mechanism of thromboembolic events seems to be stimulated by excessive thrombin production, inhibition of fibrinolysis and deposition of antiphospholipids and thrombi, as well as microvascular dysfunction in multiple vascular beds including the lungs, brain, kidneys and heart. [1] COVID-19 is also known to predispose patients to systemic inflammation, which has been reported to increase the risk of deep-vein thrombosis, with PE seen in 16.7 -47% of patients admitted to ICUs. [2] Little is known about the incidence or prevalence of PE in nonhospitalised patients diagnosed with a milder form of the disease.