Studies on COVID-19 patients have demonstrated PE in central pulmonary artery locations (main and lobar pulmonary arteries) 13, 19, 21 - 24 as well as in a peripheral distribution.9, 25 - 28 Lung autopsies of COVID-19 patients revealed microangiopathy of alveolar capillaries with 69% - 91% of thrombi in segmental and subsegmental pulmonary arteries.9, 25 - 28 Interestingly, in patients with known PE, there is a lower incidence of deep vein thrombosis (DVT) (6.9% - 13.6%) in COVID-19 patients9, 14, 17 compared to non-COVID-19 patients (45% - 70%) .9, 14, 17, 25, 26 Also, unlike non-COVID-19 patients, COVID-19 patients often lack many traditional risk factors and comorbidities for PE. 14, 17, 20 These observations have facilitated the theory that in situ microthrombi in the small peripheral pulmonary vasculature may play an important role in COVID-19 associated PE. 9, 27, 28 Thrombotic microvascular injuries have also been described in other organs (eg, kidneys and skin) despite adequate anticoagulation in COVID-19 patients.28 - 30 In addition, lower extremity DVT was found in 85.4% of COVID-19 patients admitted to the ICU (study of 48 patients) despite prophylactic anticoagulation highlighting the severity of the hypercoagulable state.31 Hence, researchers currently believe that the combination of microvascular thrombus and SARS-CoV-2 viral-induced endothelial damage leads to a systemic inflammatory reaction and progressive multisystem prothrombotic state, resulting in multiorgan failure and death.32 D-dimer considerations The root cause of increased D-dimer levels in COVID-19 illness is unclear.