The
clinical course of
coronavirus disease 2019 (COVID-19) is often complicated by the onset of
venous thrombosis and
thromboembolism (VTE), encompassing also pulmonary
thrombosis. Recent statistics attests that the cumulative frequency of VTE can be as high as 30% in
COVID-19 hospitalized patients, increasing to nearly 40 to 70% (depending on systematic screening) in those with severe illness,
mechanical ventilation, or intensive care unit admission. The risk of
venous thrombosis seems mostly limited to the active phase of disease, and is directly associated with some genetic (i.e., inherited prothrombotic predisposition) and demographical factors (male sex,
overweight/
obesity), disease severity (risk increasing progressively from hospitalization to development of severe illness, being the highest in patients needing
mechanical ventilation and/or
intensive care), presence and extent of
pulmonary disease, coexistence of multiple risk factors (immobilization,
mechanical ventilation, co- or
superinfections), along with increased values of inflammatory and thrombotic
biomarkers. At least three different phenotypes of pulmonary
thrombosis may develop in
COVID-19 patients, one caused by typical embolization from peripheral
venous thrombosis (e.g.,
deep vein thrombosis), a second type triggered by local
inflammation of nearby pulmonary tissue, and a third one mostly attributable to the prothrombotic state consequent to the pronounced systemic inflammatory response (i.e., the so-called
cytokine storm) that is frequently observed in
COVID-19. Although the pathogenesis of these three conditions has different features, their discrimination is essential for diagnostic and therapeutic purposes. The prognosis of
COVID-19 patients who develop pulmonary
thrombosis is also considerably worse than those who do not, thus probably needing frequent monitoring and more aggressive therapeutic management.