What should a general practitioner know about the management of patients with venous thromboembolism?

The era of the Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) virus has shown that non-core specialists can be involved in the treatment of epidemic diseases. However, the entire burden for the prevention and treatment of venous thromboembolism (VTE) falls on doctors – cardiovascular surgeons, phlebologists. It should be borne in mind that most of the thromboses – more than 2 million cases per year – are asymptomatic, and only a small part has pulmonary embolism, pulmonary hypertension, and death. The survival rate of patients with deep vein thrombosis (DVT) for 8 years is 65 %, with a combination of DVT with pulmonary embolism; the survival rate does not exceed 34 %, so a doctor of any specialty should know how to suspect VTE. The clinical picture of DVT is not always pronounced. Most often, with DVT, patients complain of swelling and pain in the affected lower limb, a decrease in the volume of active movements, and skin cyanosis. Diagnosis of DVT and thromboembolic complications at the non-specialized level should initially consist of assessing the risk of VTE using special scales, among which the Wales scale is of the greatest importance. The gold standard for diagnosing DVT is duplex ultrasound. Among the main indicators for hospitalization is not the fact of the established diagnosis of DVT, but the presence of comorbid pathology, chronic lung diseases, and old age. Additional risk factors include extended DVT, suspected pulmonary embolism, and pregnancy. The goal of anticoagulant therapy is to stop the process of pathological hypercoagulability, the progression of thrombus formation and create conditions for restoring vascular patency, while the pathological idea is that anticoagulants “dissolve the thrombus”. In this regard, anticoagulant therapy is the mainstay of treatment for DVT. To determine the duration of anticoagulant therapy, the etiology of thrombosis is of particular importance – the trigger that led to the formation of thrombotic masses.

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