Abstract
Coronavirus infection covid-19 has a number of clinical manifestations. The more severe course of the infection is accompanied by a hypercoagulable state, arising from a complex mechanism.
Venous thromboembolic disease (VTE) is present in about a quarter of hospitalized covid-19 patients, but it can be found in up to a half of the patients with more severe course of the infection. In contrast, arterial thrombotic events (myocardial infarction, ischemic stroke or peripheral thrombosis) are rare.
Both the virus-damaged endothelium with the activation of a number of procoagulant factors and the release of a number of cytokines, interleukins and procoagulants act in the etiopathogenesis of VTE. In addition to the activation of the coagulation cascade, platelet activation also occurs.
The importance of thrombotic complications for the course and prognosis of coronavirus infection is also evidenced by the great negative prognostic significance of high levels of D-dimers. The condition is further complicated by the immobilization of patients, the need for invasive vascular access and impaired diagnostic options for patients in severe condition in intensive care.
Adequately, it is necessary to start the administration of leastwise preventive doses of low-molecular-weight heparins in hospitalized patients, a higher dose should be individually considered in patients in more severe condition. If VTE is suspected or the diagnosis is confirmed, the full therapeutic dose is indicated according to the patient's weight, renal function and risk of bleeding.
In patients with a milder course of infection in outpatient treatment, anticoagulant prophylaxis is indicated only with a history of VTE or an overall higher risk of thrombosis.