Coagulopathy accompanying severe forms of coronavirus infection (COVID-19) - incidence of thrombotic complications, how to prevent and treat them
Abstract
COVID-19 coronavirus infection has a number of clinical manifestations. More serious course is accompanied by hypercoagulation status and endothelial damage, with a higher risk of venous thrombotic and thrombo- embolic complications (VTE).
These complications significantly increase the risk of death. The incidence of VTE at COVID-19 differs in subpopulations, could be present in a quarter to a third of hospi- talized patients.
Conversely, thrombotic events in the arterial bed (myocardial infarction, ischemic stroke or peripheral embolism) occur in about 5% of patients with a serious course. In the pathogenesis of thrombo- embolic disease many factors are involved - inflammation, i.e. release of a number of prothrombotic acute phase reactants (e.g.
C -reactive protein, fi brinogen) and platelet activation, as well as damage of the endo- thelial lining usual in viral infection and inserted catheters, along with slowing flow during bed rest. In the pathogenesis of myocardial infarction or ischemic strokes associated with SARS-CoV-2 infection, damage of the endothelium and the deeper layers of the artery wall is likely to be dominantly affected.
The importance of thrombotic complications on the course and prognosis of coronavirus infection is also evidenced by the large negative significance of the presence of fibrin degradation products, especially D-dimers.